KYJ 83 - Nitrogen in lungs
I was asked .... "In air we breathe, does nitrogen have a role"?
Let's recap. Air is 21% oxygen and 78% nitrogen (the other 1% is water, argon, and traces of many gases including CO2).
When we breath in, oxygen in air diffuses into the blood across the respiratory membrane. This occurs because blood in the lung is low in oxygen, so there is a one way flow from high oxygen concentration in alveoli, to low concentration in blood.
As arterial blood rich in oxygen perfuses tissues, cells consume oxygen depleting it. Hence it needs constant replacement.
Nitrogen is not consumed by tissues so it's blood concentration is consistent. It is called an "inert gas" meaning no physiological role.
Nitrogen in the alveoli doesn't diffuse into the blood because it's concentration in blood and in alveoli is the same. It is not being used by calls nor created by cells. The only way we can really remove it from blood is to reduce the concentration of it in the air we breathe... Remember that point.
Now back to the alveoli. That air sac with nitrogen and oxygen in it. Oxygen is leaking out, nitrogen is staying in the sac.
The sac collapses slightly. No big deal. Nitrogen's role in the lung is therefore to splint the alveoli open so they can't fully collapse but they do shrink a little.
Exercise: do this!
Take the deepest breath you can and hold it for 15 sec. At the 10-15second mark, just try and breathe in some more. ....
I bet you could. By loosing oxygen into your blood, you made a bit more space inside your lungs. Cool hey!!
Now, what do you suppose happens when you breathe in less nitrogen? We do this to a patient when we put on oxygen. Someone on a face mask at 8 lpm is breathing 50% oxygen, but by pure mathematics they are also breathing about 50% nitrogen.
Oxygen diffuses into blood, and as it does less nitrogen in the alveoli causes less splinting and more alveolar collapse- this is called atelectasis. The higher the O2 a person breathes, the greater is this atelectasis, and it can be bad.
As someone breathes high oxygen therapy, their blood nitrogen (now relatively higher than lung nitrogen), starts to drop. This off gassing of nitrogen is one of the mechanisms by which hyperbaric therapy works on divers with the Bends, but in others, the longer they breathe oxygen in high concentrations, the lower their blood nitrogen becomes.
Eventually you will take them off O2. Now both blood oxygen and nitrogen levels are reduced, meaning that when a person breathes in, the diffusion of both nitrogen and oxygen occurs... Collapsing the alveoli even worse than oxygen alone.
This is one reason that weaning off O2 slowly is needed. Widespread collapse leads to pneumonia.
Summary: the more oxygen you put on your patient, the more lung collapse you cause.
Oxygen is a potentially dangerous and, at times, toxic gas, use it wisely, never routinely.
Friday, 28 March 2014
82 - Pupil Response - neuro obs
KYJ 82. What do pupils add to a neuro assessment?
Consider a neurological assessment. It includes Glascow Coma Score, vital signs, a limb power assessment and pupils.
But what does the pupil check actually achieve? Response of pupils is actually a test of the second and third cranial nerve function (Optic & Occulomotor).
In a head injured patient. Or anyone with raised intracranial pressure, brainstem compression can reduce the efficiency of this pupil response to light either because they can't sense light (CN II) or they can't constrict to the stimuli (CN III). The sensitivity of pupil response is really only of importance in an unconscious patient when determining if the cause of altered consciousness is brain related.
When assessing pupil response we are looking for
- brisk pupil constriction to bright light
- consensual response (ie both eyes constrict irrespective of which eye the light is shone into)
- rapid return to a dilated state.
Size of the pupils ranges between people and ambient light. In a dark room everyone's pupils appear large, and in bright sunlight we have narrow pupils. The assessment of size is therefore essentially meaningless as there is no "normal" size. That said 75-80% of humans have pupils which are the same size. For the rest of the 20-25% of population a size difference of up to 1mm may be a variation of normal. This is called Anisicoria.
So let's take a patient who is unconscious, you assess pupils, and his right eye is size 5 and sluggish to light, left is size 5 and brisk to light. This is a sinister and abnormal finding, and it would lead to a high index of suspicion for a cerebral event (raised ICP, bleed or swelling).
The asymmetry in this scenario was the difference between light reflex briskness. Sluggish pupils mean pressure=bad.
At its worst, fixed dilated non reacting pupils are an indicator of severe raised intracranial pressure, and imminent brain death is probable.
Final practice tip. Use a dedicated pupil torch for this. Don't use that big red dolphin torch that you illuminate the ward on night shift with.
Pupil check is also used as part of a vision and eye test, in this instance the pupil should be clearly visible through a clear cornea, and no opacity in the lens would be a normal and expected finding.
Consider a neurological assessment. It includes Glascow Coma Score, vital signs, a limb power assessment and pupils.
But what does the pupil check actually achieve? Response of pupils is actually a test of the second and third cranial nerve function (Optic & Occulomotor).
In a head injured patient. Or anyone with raised intracranial pressure, brainstem compression can reduce the efficiency of this pupil response to light either because they can't sense light (CN II) or they can't constrict to the stimuli (CN III). The sensitivity of pupil response is really only of importance in an unconscious patient when determining if the cause of altered consciousness is brain related.
When assessing pupil response we are looking for
- brisk pupil constriction to bright light
- consensual response (ie both eyes constrict irrespective of which eye the light is shone into)
- rapid return to a dilated state.
Size of the pupils ranges between people and ambient light. In a dark room everyone's pupils appear large, and in bright sunlight we have narrow pupils. The assessment of size is therefore essentially meaningless as there is no "normal" size. That said 75-80% of humans have pupils which are the same size. For the rest of the 20-25% of population a size difference of up to 1mm may be a variation of normal. This is called Anisicoria.
So let's take a patient who is unconscious, you assess pupils, and his right eye is size 5 and sluggish to light, left is size 5 and brisk to light. This is a sinister and abnormal finding, and it would lead to a high index of suspicion for a cerebral event (raised ICP, bleed or swelling).
The asymmetry in this scenario was the difference between light reflex briskness. Sluggish pupils mean pressure=bad.
At its worst, fixed dilated non reacting pupils are an indicator of severe raised intracranial pressure, and imminent brain death is probable.
Final practice tip. Use a dedicated pupil torch for this. Don't use that big red dolphin torch that you illuminate the ward on night shift with.
Pupil check is also used as part of a vision and eye test, in this instance the pupil should be clearly visible through a clear cornea, and no opacity in the lens would be a normal and expected finding.
81 - Hepatic First Pass and Enterohepatic Recirculation
KYJ 81- Hepatic First Pass
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this episode, we look at the concepts of hepatic first pass, and a related term called enterohepatic recirculation.
Now let's go on a journey. You and I are an antibiotic (say Trimethoprim). It's 10pm and Sally the patient has been diagnosed this afternoon with UTI and Dr Tinkle prescribed a three day blast of Triprim, to be commenced tonight at bedtime.
Sally switches of "Gator people" the latest in classy reality TV shows to hit the small screen, has her last whoofy stinging wee for the night. Pops the Antibiotic and goes off to sleep.
As Sally swallows you, you dissolve almost immediately. Your transit through the stomach reduces you to mere particles in a slurry as you pass into the small intestine.
Here you are absorbed through the Villi, small finger like projections that line the rugated mucosa of the bowel. Absorbed into the blood supply, your very next port of call is the Liver. There you are metabolised into other molecular compounds. This movement from gut to liver is called Hepatic First Pass. It literally means that all ingested medicines are first passed through the liver before systemic circulation.
Now some drugs or their metabolites are released into systemic blood, where they exert their action by being transported to the sites of action. Some drugs or metabolites are secreted by the liver into Bile. This is manufactured in the liver and stored and concentrated in the Gall Bladder. During Sally's next meal, fat in her food will stimulate the Gall Bladder to contract and secrete bile into the duodenum to mix with the food bolus.
Many drugs, (eg antibiotics) after hepatic metabolism are bound to bile salts, where normal bowel bacteria release them for reabsorption. They again undergo hepatic metabolism and the cycle repeats until the drug is eventually eliminated.
This process of drug going round and round between gut and liver is called Enterohepatic Recirculation.
The drugs can be eliminated by many means, but that is a post for another day.
Hope these Pharmakokinetic KYJ posts are helping you hone your pharmacology knowledge.
If you are getting anything from these, let me know and tag a bunch of your nursing crew.
Share the love.
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this episode, we look at the concepts of hepatic first pass, and a related term called enterohepatic recirculation.
Now let's go on a journey. You and I are an antibiotic (say Trimethoprim). It's 10pm and Sally the patient has been diagnosed this afternoon with UTI and Dr Tinkle prescribed a three day blast of Triprim, to be commenced tonight at bedtime.
Sally switches of "Gator people" the latest in classy reality TV shows to hit the small screen, has her last whoofy stinging wee for the night. Pops the Antibiotic and goes off to sleep.
As Sally swallows you, you dissolve almost immediately. Your transit through the stomach reduces you to mere particles in a slurry as you pass into the small intestine.
Here you are absorbed through the Villi, small finger like projections that line the rugated mucosa of the bowel. Absorbed into the blood supply, your very next port of call is the Liver. There you are metabolised into other molecular compounds. This movement from gut to liver is called Hepatic First Pass. It literally means that all ingested medicines are first passed through the liver before systemic circulation.
Now some drugs or their metabolites are released into systemic blood, where they exert their action by being transported to the sites of action. Some drugs or metabolites are secreted by the liver into Bile. This is manufactured in the liver and stored and concentrated in the Gall Bladder. During Sally's next meal, fat in her food will stimulate the Gall Bladder to contract and secrete bile into the duodenum to mix with the food bolus.
Many drugs, (eg antibiotics) after hepatic metabolism are bound to bile salts, where normal bowel bacteria release them for reabsorption. They again undergo hepatic metabolism and the cycle repeats until the drug is eventually eliminated.
This process of drug going round and round between gut and liver is called Enterohepatic Recirculation.
The drugs can be eliminated by many means, but that is a post for another day.
Hope these Pharmakokinetic KYJ posts are helping you hone your pharmacology knowledge.
If you are getting anything from these, let me know and tag a bunch of your nursing crew.
Share the love.
Monday, 10 March 2014
80 - Protein Binding (pharmacokinetics series)
KYJ 80 - Drug transport and Protein Binding
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In the last episode we looked at absorption. Once absorbed into the blood stream a drug is considered to be bioavailable.
Today we look at transport. Drugs travel in blood in 2 ways.
First of all they can be carried in their active state, or an inactive state needing to be converted in the liver to have an action.
Blood as a cocktail of cells and plasma (salts, water and protein).
Drugs are dissolved in the plasma water, or they bind to protein. While the most abundant drug carrier is Albumin, there are other proteins called globulins, glycoproteins, or lipoproteins that act as secondary transporters.
Think of a blood as being like a drug smuggler and their luggage, travelling to Bali. The dope is either bound to the boogie board (all taped up for later use) or in the smuggler's pocket, for quick access.
When bound to plasma proteins, the drug is not immediately usable, but when dissolved in the plasma water (in solution), it is available for immediate use. Given any absorbed drug, it is important to know that a drug's action is largely related to the fraction or percentage of a drug that is bound to protein vs the unbound fraction.
Some drugs have high protein binding eg Warfarin is about 98% protein bound, meaning only 2% is usable. In contrast morphine is about 25-30% protein bound, meaning that up to 75% of this drug is available to exert its effects.
If a drug is highly bound then we generally say it has a low volume of distribution and a long half life.
Suppose you gave me an antibiotic: "Robicillin" that was 60% protein bound.
You gave 1000mg
400mg is working at killing "Timmingsosis"
As the drug is used up or metabolised, it is being released from the plasma in proportion. At all times that drug is 60% protein bound and 40% is doing the work. The unbound vs bound fraction stays in balance. Thus the protein acts like a reservoir steadily releasing the drug. Eventually the concentration of unbound drug will dwindle requiring that another dose of the drug is administered to maintain effectiveness.
But if I had a medical condition where I had low albumin in my body (nephrotic syndrome, liver failure, malnutrition), then once all that albumin is saturated or bound to Robicillin, then it stays in the water of the plasma in a higher concentration. Effectively becoming toxic like being overdosed. Say I only had half my albumin. The drug normally 60% plasma protein bound (PPB) can now only bind half to protein (eg 30% PPB) meaning instead of 40% being available, now 70% or 700mg is exerting its action.
It is probable therefore that once a drug is given in a high enough dose, it has fully saturated the healthy person's plasma proteins, and is now toxic.
Toxicity can also occur when two drugs compete for plasma binding. If drug A is administered at the same time as drug B, then proteins could become saturated earlier giving rise to inadvertent potency or toxicity.
A common example is Warfarin and antibiotics (like Ciprofloxacin and clarithromycin). If these are given then the AB bind to plasma proteins reducing the PPB of Warfarin, hence more warfarin in solution increasing bleeding potential. Even Panadol, aspirin and other anti inflammatories, make this happen.
In this episode we touched on the issue of transporting drugs bound to plasma proteins. In summary the bound fraction of the drug is not used or active. Any situations that make more drug available in unbound form can potentate the drug, and some drugs will potentiate others as they compete to bind to plasma proteins.
Albumin is the principle plasma protein, and manufactured in the liver.
...
Time now to diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption - (covered KYJ79)
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In the last episode we looked at absorption. Once absorbed into the blood stream a drug is considered to be bioavailable.
Today we look at transport. Drugs travel in blood in 2 ways.
First of all they can be carried in their active state, or an inactive state needing to be converted in the liver to have an action.
Blood as a cocktail of cells and plasma (salts, water and protein).
Drugs are dissolved in the plasma water, or they bind to protein. While the most abundant drug carrier is Albumin, there are other proteins called globulins, glycoproteins, or lipoproteins that act as secondary transporters.
Think of a blood as being like a drug smuggler and their luggage, travelling to Bali. The dope is either bound to the boogie board (all taped up for later use) or in the smuggler's pocket, for quick access.
When bound to plasma proteins, the drug is not immediately usable, but when dissolved in the plasma water (in solution), it is available for immediate use. Given any absorbed drug, it is important to know that a drug's action is largely related to the fraction or percentage of a drug that is bound to protein vs the unbound fraction.
Some drugs have high protein binding eg Warfarin is about 98% protein bound, meaning only 2% is usable. In contrast morphine is about 25-30% protein bound, meaning that up to 75% of this drug is available to exert its effects.
If a drug is highly bound then we generally say it has a low volume of distribution and a long half life.
Suppose you gave me an antibiotic: "Robicillin" that was 60% protein bound.
You gave 1000mg
400mg is working at killing "Timmingsosis"
As the drug is used up or metabolised, it is being released from the plasma in proportion. At all times that drug is 60% protein bound and 40% is doing the work. The unbound vs bound fraction stays in balance. Thus the protein acts like a reservoir steadily releasing the drug. Eventually the concentration of unbound drug will dwindle requiring that another dose of the drug is administered to maintain effectiveness.
But if I had a medical condition where I had low albumin in my body (nephrotic syndrome, liver failure, malnutrition), then once all that albumin is saturated or bound to Robicillin, then it stays in the water of the plasma in a higher concentration. Effectively becoming toxic like being overdosed. Say I only had half my albumin. The drug normally 60% plasma protein bound (PPB) can now only bind half to protein (eg 30% PPB) meaning instead of 40% being available, now 70% or 700mg is exerting its action.
It is probable therefore that once a drug is given in a high enough dose, it has fully saturated the healthy person's plasma proteins, and is now toxic.
Toxicity can also occur when two drugs compete for plasma binding. If drug A is administered at the same time as drug B, then proteins could become saturated earlier giving rise to inadvertent potency or toxicity.
A common example is Warfarin and antibiotics (like Ciprofloxacin and clarithromycin). If these are given then the AB bind to plasma proteins reducing the PPB of Warfarin, hence more warfarin in solution increasing bleeding potential. Even Panadol, aspirin and other anti inflammatories, make this happen.
In this episode we touched on the issue of transporting drugs bound to plasma proteins. In summary the bound fraction of the drug is not used or active. Any situations that make more drug available in unbound form can potentate the drug, and some drugs will potentiate others as they compete to bind to plasma proteins.
Albumin is the principle plasma protein, and manufactured in the liver.
...
Time now to diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
79 - Drug Absorption (Pharmacokinetics series)
KYJ 79- Drug Absorption
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this session: Absorption and transport of a drug in our bodies.
Consider three different drugs, orally ingested Warfarin. Intravenous Morphine and a topical tinea (ringworm/athletes foot) cream like Miconizole. All different drugs yet totally different routes of administration.
Absorption refers to the way that a drug gets from where we give it, to the site in the body where the drug will exert its influence. For most drugs, the drug is carried in the blood an exception would be a topical drug delivered directly to the site of action eg the tinea cream. When a person has a fungal lesion, Miconizole cream can be applied directly to affected skin where it exerts it's action topically. It is not absorbed into the blood stream.
Other examples include ear or eye drops, even salbutamol given by nebuliser or metered aerosol, is delivered topically at the site in smooth muscular bronchiole tissue, where is causes smooth muscle relaxation.
Systemic absorption
Some topical drugs are absorbed into the skin where it diffuses into the capillaries and enters the circulating blood. Examples include GTN (Transiderm) patches, Fentanyl and nicotine patches. Steroids like oestrogen, progesterone, hydrocortisone and non-steroid anti-inflammatory rubbing gels are systemically absorbed into the blood, eg Diclofenac (Voltaren Emulgel), and Ibuprofen.
When a drug is administered directly into the blood, it doesn't need absorption. These drugs are called parenteral drugs. Any drug given intravenously, intramuscular or subcutaneously fall into this category. Once injected, intravenous morphine is immediately into the blood stream and available to be carried to the brain where it binds to Mu receptors and exerts it's action centrally to inhibit pain sensation. In recent years other drugs eg Ondanzetron and Midazolam have been administered into the mouth or nose where they are absorbed directly into systemic blood through a dense network of blood vessels.
Other drugs are slower to be absorbed. When swallowed the medication packaged usually in a pill (sugar film coated) , capsule (protein film coated), or tablet (compressed powder), is swallowed, where it is broken down and digested. The drug is absorbed from blood vessels lining the stomach or most commonly the small intestine. Once entering the gut blood, this drug is transported directly to the liver and metabolised. This is called Hepatic First Pass (HFP). More on HFP in a later session.
For many drugs this HFP destroys the drug, making some drugs less active when taken orally (Pethidine, diazepam) or completely inappropriate for oral ingestion (eg insulin, heparin, GTN), for other drugs, this hepatic metabolism is necessary to metabolise a drug into an active chemical that exerts an action.
An example is Metronidazole (Flagyl) , paracetamol (Panadol), Enalpril and even codeine all need conversion into an activated new chemical to do their job.
Absorption is how a drug enters the blood stream. In our next episode, we will look at transportation and protein binding.
Now diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
In this series of Knowing your Jargon (KYJ) we will look at Phamacokinetics (what our body does to drugs).
Over the next few days we look at :
Absorption
Transportation
Hepatic First Pass
Protein binding
Bioavailability
Half life
Distribution
Metabolism and metabolites
Excretion
In this session: Absorption and transport of a drug in our bodies.
Consider three different drugs, orally ingested Warfarin. Intravenous Morphine and a topical tinea (ringworm/athletes foot) cream like Miconizole. All different drugs yet totally different routes of administration.
Absorption refers to the way that a drug gets from where we give it, to the site in the body where the drug will exert its influence. For most drugs, the drug is carried in the blood an exception would be a topical drug delivered directly to the site of action eg the tinea cream. When a person has a fungal lesion, Miconizole cream can be applied directly to affected skin where it exerts it's action topically. It is not absorbed into the blood stream.
Other examples include ear or eye drops, even salbutamol given by nebuliser or metered aerosol, is delivered topically at the site in smooth muscular bronchiole tissue, where is causes smooth muscle relaxation.
Systemic absorption
Some topical drugs are absorbed into the skin where it diffuses into the capillaries and enters the circulating blood. Examples include GTN (Transiderm) patches, Fentanyl and nicotine patches. Steroids like oestrogen, progesterone, hydrocortisone and non-steroid anti-inflammatory rubbing gels are systemically absorbed into the blood, eg Diclofenac (Voltaren Emulgel), and Ibuprofen.
When a drug is administered directly into the blood, it doesn't need absorption. These drugs are called parenteral drugs. Any drug given intravenously, intramuscular or subcutaneously fall into this category. Once injected, intravenous morphine is immediately into the blood stream and available to be carried to the brain where it binds to Mu receptors and exerts it's action centrally to inhibit pain sensation. In recent years other drugs eg Ondanzetron and Midazolam have been administered into the mouth or nose where they are absorbed directly into systemic blood through a dense network of blood vessels.
Other drugs are slower to be absorbed. When swallowed the medication packaged usually in a pill (sugar film coated) , capsule (protein film coated), or tablet (compressed powder), is swallowed, where it is broken down and digested. The drug is absorbed from blood vessels lining the stomach or most commonly the small intestine. Once entering the gut blood, this drug is transported directly to the liver and metabolised. This is called Hepatic First Pass (HFP). More on HFP in a later session.
For many drugs this HFP destroys the drug, making some drugs less active when taken orally (Pethidine, diazepam) or completely inappropriate for oral ingestion (eg insulin, heparin, GTN), for other drugs, this hepatic metabolism is necessary to metabolise a drug into an active chemical that exerts an action.
An example is Metronidazole (Flagyl) , paracetamol (Panadol), Enalpril and even codeine all need conversion into an activated new chemical to do their job.
Absorption is how a drug enters the blood stream. In our next episode, we will look at transportation and protein binding.
Now diarise a few notes and reflect on this revision - all our KYJs are claimable for 0.25 CPD for RNs , ENs and Scheduled Medicines endorsed RNs; but you have to make reflective notes and keep as evidence.
These KYJs meet NMBA standards
3.2 Uses best available evidence, nursing expertise and respect for the values and beliefs of individuals/groups in the provision of nursing care:
• uses relevant literature and research findings to improve current practice
4.2 Participates in professional development to enhance nursing practice
...
Please Share this with your nurse networks.
Smashing that CPD, a few minutes at a time.
78 - Nitrites in urine
KYJ 78 - Nitrites on a urine test.
When we test urine using the colour coded dip stick there are many reagents that can indicate abnormality. One of the common illness to screen for is urinary tract infection (UTI). This problem is most common in women and relates to the simple fact that a female urethra is much shorter than a male's. It has been estimated that 50% of all women will experience a UTI at least once.
Bacteria and other flora can ascend the urethra and invade the bladder causing inflammation (cystitis) then, in severe cases, ascend the ureters, and infect the kidneys (pyelonephritis).
The most common organism is Escherichia coli or E.coli to his mates. This is a gram negative bacteria that normally lives in the bowel and are often referred to as "Normal Flora". They serve a good function of preventing "bad bacteria" proliferation and they manufacture Vit K.
Things turn nasty when they take leave from poo central, and migrate north to the sprinkle fields. Once invading the urethral meatus, the are usually flushed with every pee, but poor hydration, high sugar diet and other factors can provide the perfect environment to proliferate and cause inflammation.
As these bacteria multiply they attach to the bladder wall and secrete a gel that acts like a shield to hide from the immune system. Here they proliferate and overwhelm the immune defence causing symptoms of stinging, burning, frequency, urgency and offensive urine odour. Occasionally urine may be pink tinged, or cloudy in appearance. In severe pyelonephritis, it can almost look like pea-soup.
Diagnosis is usually clinically based on the history and these symptoms, but urine testing for blood, especially leukocytes (white blood cells WBC), and Nitrites is all suggestive of UTI.
As inflammation sets in, bladder capillaries engorge and become permeable to white and red blood cells leaching into the bladder. In infections this proliferation serves to cause more immune fighting neutrophils, and phagocytes to fight the bacterial invasion. This clouds the urine and pus is produced as dead WBC and bacteria accumulate.
Bacteria like E. coli secrete a chemical waste called Nitrite during their proliferative stage, and this accumulation of nitrites in urine is always a strong indicator of UTI. Long before leukocytes are seen on a dipstick test, nitrites will be present.
Occasionally the bacteria can turn the urine acidic which gives rise to the symptoms of stinging and burning during voiding. If you encourage water intake this has a soothing and acid dilution effect, as well as assisting to flush the bacteria away. Urinary alkalinisers are also effective for comfort, (Ural or Citravescent ) but don't kill the bacteria.
Treatment includes antibiotics, most commonly Trimethoprim taken once/day, at bedtime for 3 -7 days.
Trimethoprim is a bacteriostatic agent which doesn't kill E.coli, but prevents them from reproducing. They then die out or are flushed out.
Trimethoprim use is indiscriminate. It sterilises the E.coli in the UTI, but also affects all your good E.coli in the gut serving their important function. People on Trimethoprim, like other similar antibiotics should consider recolonising their gut simultaneously with a Probiotic (good bacteria) and /or a few tubs of yoghurt.
When we test urine using the colour coded dip stick there are many reagents that can indicate abnormality. One of the common illness to screen for is urinary tract infection (UTI). This problem is most common in women and relates to the simple fact that a female urethra is much shorter than a male's. It has been estimated that 50% of all women will experience a UTI at least once.
Bacteria and other flora can ascend the urethra and invade the bladder causing inflammation (cystitis) then, in severe cases, ascend the ureters, and infect the kidneys (pyelonephritis).
The most common organism is Escherichia coli or E.coli to his mates. This is a gram negative bacteria that normally lives in the bowel and are often referred to as "Normal Flora". They serve a good function of preventing "bad bacteria" proliferation and they manufacture Vit K.
Things turn nasty when they take leave from poo central, and migrate north to the sprinkle fields. Once invading the urethral meatus, the are usually flushed with every pee, but poor hydration, high sugar diet and other factors can provide the perfect environment to proliferate and cause inflammation.
As these bacteria multiply they attach to the bladder wall and secrete a gel that acts like a shield to hide from the immune system. Here they proliferate and overwhelm the immune defence causing symptoms of stinging, burning, frequency, urgency and offensive urine odour. Occasionally urine may be pink tinged, or cloudy in appearance. In severe pyelonephritis, it can almost look like pea-soup.
Diagnosis is usually clinically based on the history and these symptoms, but urine testing for blood, especially leukocytes (white blood cells WBC), and Nitrites is all suggestive of UTI.
As inflammation sets in, bladder capillaries engorge and become permeable to white and red blood cells leaching into the bladder. In infections this proliferation serves to cause more immune fighting neutrophils, and phagocytes to fight the bacterial invasion. This clouds the urine and pus is produced as dead WBC and bacteria accumulate.
Bacteria like E. coli secrete a chemical waste called Nitrite during their proliferative stage, and this accumulation of nitrites in urine is always a strong indicator of UTI. Long before leukocytes are seen on a dipstick test, nitrites will be present.
Occasionally the bacteria can turn the urine acidic which gives rise to the symptoms of stinging and burning during voiding. If you encourage water intake this has a soothing and acid dilution effect, as well as assisting to flush the bacteria away. Urinary alkalinisers are also effective for comfort, (Ural or Citravescent ) but don't kill the bacteria.
Treatment includes antibiotics, most commonly Trimethoprim taken once/day, at bedtime for 3 -7 days.
Trimethoprim is a bacteriostatic agent which doesn't kill E.coli, but prevents them from reproducing. They then die out or are flushed out.
Trimethoprim use is indiscriminate. It sterilises the E.coli in the UTI, but also affects all your good E.coli in the gut serving their important function. People on Trimethoprim, like other similar antibiotics should consider recolonising their gut simultaneously with a Probiotic (good bacteria) and /or a few tubs of yoghurt.
77- Brugada and SUDS
KYJ 77 - Brugada and SUDS
A recent image that went viral on the internet, showed an ECG that demonstrated a newish abnormality. Brugada syndrome is a genetically inherited ST elevation pattern in V1 and V2.
It was named after two brothers in the early 1990s who discovered the rhythm was associated with sudden unexplained death syndrome (SUDS).
Affecting boys and men with no other cardiac risk factors, Brugada strikes with no warning because, usually young fit men would have had no need to have an ECG previously. It is therefore diagnosed by accident or routine pre-op ECG in mining, military or other industries that require a rigid medical screening pre-employment. It is also seen post successful resuscitation of men who were "a near miss" for SUDS.
The course of illness manifests as collapse and sudden cardiac arrest (SCA) with victims found to be in ventricular fibrillation.
If detected, prophylactic use of an implantable defibrillator is often the treatment.
Brugada is perhaps the most common cardiac cause of sudden death in healthy men.
A recent image that went viral on the internet, showed an ECG that demonstrated a newish abnormality. Brugada syndrome is a genetically inherited ST elevation pattern in V1 and V2.
It was named after two brothers in the early 1990s who discovered the rhythm was associated with sudden unexplained death syndrome (SUDS).
Affecting boys and men with no other cardiac risk factors, Brugada strikes with no warning because, usually young fit men would have had no need to have an ECG previously. It is therefore diagnosed by accident or routine pre-op ECG in mining, military or other industries that require a rigid medical screening pre-employment. It is also seen post successful resuscitation of men who were "a near miss" for SUDS.
The course of illness manifests as collapse and sudden cardiac arrest (SCA) with victims found to be in ventricular fibrillation.
If detected, prophylactic use of an implantable defibrillator is often the treatment.
Brugada is perhaps the most common cardiac cause of sudden death in healthy men.
Tuesday, 25 February 2014
76 - Tension Pneumothorax.
KYJ 76 - Tension Pneumothorax
Pay attention to a tension
Off all chest injuries, Tension Pneumothorax is the most frequent killer. In this episode of trauma pearls, I'll review what differentiates a Tension pneumothorax from a pneumothorax.
First we review what s pneumothorax is. Five lobes of lung are encased in a dual layered protective membrane called Pleura. Between these two layers exists 5-15ml of lubricating fluid. During inspiration and expiration the plural layers slide across each other like two sheets of wet glass . With ease and little friction. Between the pleural layers, there is a relative vacuum ( less pressure than in the lung) and this ensures that the lungs don't fully collapse after expiration. Lung has a natural tendency to recoil to 80% of its volume if this negative pleural layer is breeched.
In a closed pneumothorax this is exactly what happens. The pleura adhered to the lung surface (visceral pleura) pops, and air from damaged alveoli moves into the relative low pressured intrapleural space. Lung recoils and function of the lung on the affected side is lost. Small pneumothorax of up to 20% result in a sharp localised pain, some shortness of breath, and a rise in respiratory rate, but are rarely life threatening, and indeed are often conservatively managed with rest. These heal ofer 48 hours and rarely need to be drained or aspirated.
Larger pneumothorax or open pneumothorax result in respiratory distress, compromise to sustainable gas exchange and potential for pneumonia. These are respiratory emergencies, and two options exist to treat. Needle aspiration can be used, but more common is the insertion of an intercostal catheter (chest drain) and attachment to an underwater seal +/- suction.
In a pneumothorax patient where every breath delivers more air into the pleural space, pressure builds. As this occurs it severely compromises the ability to ventilate the lung, ultimately collapsing it. Pleural pressure now rises, squashing the lung, and placing pressure on the opposite lung, heart and great vessels. at this point the patient has no air entry on the affected side, is severely distressed, exhibits altered consciousness, tachycardia and desaturation. As the heart is displaced it kinks off the vena cava preventing blood return to the right heart. The trachea becomes displaced (pushed) toward the unaffected side, jugular veins bulge due to blood being unable to return from the head, cyanosis and cardiac arrest ensues due to an obstructive shock- no cardiac output.
At the point of loss of cardiac output, the pneumothorax is called a Tension Pneumothorax .
PThx is an immediately life threatening cardiovascular catastrophe and must be urgently treated by releasing the pressure from the pleura.
An emergency needle decompression is utilised to achieve this. A 14g IV cannula is placed into the patient's chest at the landmark of the 2nd intercostal space, in the mid clavicular line. Pressure is immediately released allowing the heart to resume its normal position in the mediastinum, and most importantly, blood to circulate. Cardiac output is restored within seconds.
Summary:
Pneumothorax is a respiratory emergency characterised by decreased air entry and respiratory distress.
Tension pneumothorax is an extension.
It is a cardiovascular catastrophe, characterised by loss of blood pressure, cardiac output, tracheal deviation, jugular vein distension, cyanosis, and cardiac arrest in minutes, if not decompressed.
Pay attention to a tension
Off all chest injuries, Tension Pneumothorax is the most frequent killer. In this episode of trauma pearls, I'll review what differentiates a Tension pneumothorax from a pneumothorax.
First we review what s pneumothorax is. Five lobes of lung are encased in a dual layered protective membrane called Pleura. Between these two layers exists 5-15ml of lubricating fluid. During inspiration and expiration the plural layers slide across each other like two sheets of wet glass . With ease and little friction. Between the pleural layers, there is a relative vacuum ( less pressure than in the lung) and this ensures that the lungs don't fully collapse after expiration. Lung has a natural tendency to recoil to 80% of its volume if this negative pleural layer is breeched.
In a closed pneumothorax this is exactly what happens. The pleura adhered to the lung surface (visceral pleura) pops, and air from damaged alveoli moves into the relative low pressured intrapleural space. Lung recoils and function of the lung on the affected side is lost. Small pneumothorax of up to 20% result in a sharp localised pain, some shortness of breath, and a rise in respiratory rate, but are rarely life threatening, and indeed are often conservatively managed with rest. These heal ofer 48 hours and rarely need to be drained or aspirated.
Larger pneumothorax or open pneumothorax result in respiratory distress, compromise to sustainable gas exchange and potential for pneumonia. These are respiratory emergencies, and two options exist to treat. Needle aspiration can be used, but more common is the insertion of an intercostal catheter (chest drain) and attachment to an underwater seal +/- suction.
In a pneumothorax patient where every breath delivers more air into the pleural space, pressure builds. As this occurs it severely compromises the ability to ventilate the lung, ultimately collapsing it. Pleural pressure now rises, squashing the lung, and placing pressure on the opposite lung, heart and great vessels. at this point the patient has no air entry on the affected side, is severely distressed, exhibits altered consciousness, tachycardia and desaturation. As the heart is displaced it kinks off the vena cava preventing blood return to the right heart. The trachea becomes displaced (pushed) toward the unaffected side, jugular veins bulge due to blood being unable to return from the head, cyanosis and cardiac arrest ensues due to an obstructive shock- no cardiac output.
At the point of loss of cardiac output, the pneumothorax is called a Tension Pneumothorax .
PThx is an immediately life threatening cardiovascular catastrophe and must be urgently treated by releasing the pressure from the pleura.
An emergency needle decompression is utilised to achieve this. A 14g IV cannula is placed into the patient's chest at the landmark of the 2nd intercostal space, in the mid clavicular line. Pressure is immediately released allowing the heart to resume its normal position in the mediastinum, and most importantly, blood to circulate. Cardiac output is restored within seconds.
Summary:
Pneumothorax is a respiratory emergency characterised by decreased air entry and respiratory distress.
Tension pneumothorax is an extension.
It is a cardiovascular catastrophe, characterised by loss of blood pressure, cardiac output, tracheal deviation, jugular vein distension, cyanosis, and cardiac arrest in minutes, if not decompressed.
75 - Diaphragm rupture -Gastrothorax
KYJ 75 - Gastrothorax
There is a rule in the pit. "All penetrating trauma below the level of the nipple line, is abdominal trauma as well as thoracic."
This rule is based on two anatomical truisms. The first truth is that the diaphragm is the muscular boarder separating abdomen from chest cavity.
The second is that the diaphragm is located as high in the chest as the Xiphoid, at the 4th intercostal space.
A penetrating injury may cause breech or rupture to the diaphragm which is some circumstances, may allow for abdominal organs to herniate into the chest.
A characteristic finding of a loop of bowel in the chest, is bowel sounds heard in the chest during auscultation. This is referred to as Gastrothorax, and is a rare finding.
For patients with Gastrothorax, associated abdominal pain, epigastric pain, nausea and vomiting are all common symptoms. Naturally shortness of breath, tachypnoea, tachycardia and ventilation compromise are expected.
As bowel takes up space where lung needs to inflate; gas exchange is impaired.
Initial treatment is symptomatic ventilation management. A patient is usually intubated, and positive pressure ventilation recruits thoracic real-estate, and minimises herniation. It also allows greater oxygenation of lung on the affected side and prevents collapse.
Surgery is usually needed to repair the penetrating tissue injury, and diaphragmatic rupture.
Prognostically, there is a high mortality rate, as bowel ischaemia, lung parenchyma injuries, and haemorrhage all take their toll.
There is a rule in the pit. "All penetrating trauma below the level of the nipple line, is abdominal trauma as well as thoracic."
This rule is based on two anatomical truisms. The first truth is that the diaphragm is the muscular boarder separating abdomen from chest cavity.
The second is that the diaphragm is located as high in the chest as the Xiphoid, at the 4th intercostal space.
A penetrating injury may cause breech or rupture to the diaphragm which is some circumstances, may allow for abdominal organs to herniate into the chest.
A characteristic finding of a loop of bowel in the chest, is bowel sounds heard in the chest during auscultation. This is referred to as Gastrothorax, and is a rare finding.
For patients with Gastrothorax, associated abdominal pain, epigastric pain, nausea and vomiting are all common symptoms. Naturally shortness of breath, tachypnoea, tachycardia and ventilation compromise are expected.
As bowel takes up space where lung needs to inflate; gas exchange is impaired.
Initial treatment is symptomatic ventilation management. A patient is usually intubated, and positive pressure ventilation recruits thoracic real-estate, and minimises herniation. It also allows greater oxygenation of lung on the affected side and prevents collapse.
Surgery is usually needed to repair the penetrating tissue injury, and diaphragmatic rupture.
Prognostically, there is a high mortality rate, as bowel ischaemia, lung parenchyma injuries, and haemorrhage all take their toll.
74 - Quinsy -peritonsilar abscess
KYJ 74 - Quinsy (peritonsilar abscess).
Looking in throats is an in exact science, but with some understanding of some basic terms, it can be a simple part of an ENT assessment.
In the walls of the back of the mouth, beneath the uvula and adjacent to the tongue, lay the tonsils. These structures are lymphatic tissue with a unique capacity to filter lymph fluid. The tonsils harbour mature and immature lymphocytes and neutrophils. When deep caverns in their surface called "crypts" fill with pus, the patient is diagnosed with follicular tonsillitis. Usually bacterial, follicular tonsillitis differs from inflammation alone seen in URTI.
While tonsils frequently become inflamed (tonsillitis), it is only when pus forms (follicular tonsillitis) that it is usually considered bacterial. It is only then, that antibiotics are considered as an adjunct to management.
Inflamed tonsils swell and as they do, they occasionally meet in the oropharynx, threatening airway obstruction.
Occasionally an abscess forms in behind one of the tonsils, this is called a peritonsilar abscess (PTA) or Qunisy . It is considered a surgical emergency.
Recognising this potentially life threatening condition and being able to differentiate it from tonsillitis is important. The fundamental difference is speed of presentation. Quincy develops fast; in hours.
In Quinsy, the throat pain is usually unilateral, and much worse if the patient tries to open their mouth. Sometimes they have earache on the affected side.
The breath is foetid, and other lymph nodes in the neck are often tender (lymphadenopathy). The patient's voice is often muffled and has been described as "hot potato voice", or "mouth full of marbles"
They often can't swallow (even saliva), and will often drool.
They will be febrile above 39.5C.
The management, like any abscess is Cut n drain.
Incision and drainage followed up with antibiotics. As many PTAs are resistant to penicillins, a macrolide like Clindamycin are used post op.
Rarely is tonsillectomy used these days. This goes for tonsillitis also.
Quinsy is an emergency, and airway patency is the top priority.
Remember : FLU SHAVE
Febrile
Lymphadenopathy
Unilateral pain
Swallowing difficulty
Halitosis
Acute onset
Voice change
Energy depleted (lethargic)
Looking in throats is an in exact science, but with some understanding of some basic terms, it can be a simple part of an ENT assessment.
In the walls of the back of the mouth, beneath the uvula and adjacent to the tongue, lay the tonsils. These structures are lymphatic tissue with a unique capacity to filter lymph fluid. The tonsils harbour mature and immature lymphocytes and neutrophils. When deep caverns in their surface called "crypts" fill with pus, the patient is diagnosed with follicular tonsillitis. Usually bacterial, follicular tonsillitis differs from inflammation alone seen in URTI.
While tonsils frequently become inflamed (tonsillitis), it is only when pus forms (follicular tonsillitis) that it is usually considered bacterial. It is only then, that antibiotics are considered as an adjunct to management.
Inflamed tonsils swell and as they do, they occasionally meet in the oropharynx, threatening airway obstruction.
Occasionally an abscess forms in behind one of the tonsils, this is called a peritonsilar abscess (PTA) or Qunisy . It is considered a surgical emergency.
Recognising this potentially life threatening condition and being able to differentiate it from tonsillitis is important. The fundamental difference is speed of presentation. Quincy develops fast; in hours.
In Quinsy, the throat pain is usually unilateral, and much worse if the patient tries to open their mouth. Sometimes they have earache on the affected side.
The breath is foetid, and other lymph nodes in the neck are often tender (lymphadenopathy). The patient's voice is often muffled and has been described as "hot potato voice", or "mouth full of marbles"
They often can't swallow (even saliva), and will often drool.
They will be febrile above 39.5C.
The management, like any abscess is Cut n drain.
Incision and drainage followed up with antibiotics. As many PTAs are resistant to penicillins, a macrolide like Clindamycin are used post op.
Rarely is tonsillectomy used these days. This goes for tonsillitis also.
Quinsy is an emergency, and airway patency is the top priority.
Remember : FLU SHAVE
Febrile
Lymphadenopathy
Unilateral pain
Swallowing difficulty
Halitosis
Acute onset
Voice change
Energy depleted (lethargic)
73 - Virus- the great undead.
KYJ 73 - Virus the great undead.
Of recent years there has been a Hollywood buzz topic explored in a few films. The Zombie apocalypse. You know the plot. A creature or creatures that were neither dead nor alive sought human hosts with which to inhabit, biologically enslave and ultimately conquer.
Sound familiar? We already have a zombie apocalypse on our hands. It is called the Flu. It is called Herpes. It is called HIV, or Hepatitis, or croup or the common cold.
All these diseases are caused by a non living yet not dead particle called a Virus.
Viruses are protein shells with a single strand (usually) of genetic matter. Typically, they are very very small when compared with human cells. Eg If a white blood cell was a 50m Olympic swimming pool, a virus by comparison would be a 2 year old child swimming in that pool.
We're talking small.
A virus is incapable of reproducing itself (the definition of a living organism is that it can reproduce), so it is not considered alive or living. It is either active or inactive.
To replicate a virus attaches to a host cell. It bonds with the membrane of the cell and expels its genetic (RNA) material inside the cell. The genetic code penetrates the host cells own DNA, joins to it and reprograms the cell to cease being what it was before infection, and become a factory to manufacture more viral particles.
It's a zombie.
Let's look at a Flu virus- Influenza A. "Flu" has many surface proteins that are categorised as Hs and Ns. You've heard of H5N1, or H1N1 flu, bird flu, swine flu?
The H is a protein called hemagglutinin and it is responsible for letting a virus stick onto and penetrate a cell.
The N is a protein enzyme called Neurominidase which is responsible for the release of a new viral particle from a host cell.
When you have the vaccination for flu, you are getting the Antigen (signature of a weakened virus). Your immune system then makes antibodies to "attack" the real infection flu virus when it invades you in the flu season. The Antibody actually attaches to the H disabling the virus and stopping it from endearing and infecting the cell.
Anti viral drugs (Relenza, Tamiflu) in converse attack the virus's N protein, stopping the newly created viruses from being released by the slave cell.
Signalling invasion by a virus the cell releases a chemical scent (cytokines) called interferon, that calls macrophages (white blood cells) to destroy the infected cell.
...
These viruses are tricky wee things. Small, un-dead, efficient killers that inhabit the bodies of cells and convert them into slaves.
Zombies to the max!!
Of recent years there has been a Hollywood buzz topic explored in a few films. The Zombie apocalypse. You know the plot. A creature or creatures that were neither dead nor alive sought human hosts with which to inhabit, biologically enslave and ultimately conquer.
Sound familiar? We already have a zombie apocalypse on our hands. It is called the Flu. It is called Herpes. It is called HIV, or Hepatitis, or croup or the common cold.
All these diseases are caused by a non living yet not dead particle called a Virus.
Viruses are protein shells with a single strand (usually) of genetic matter. Typically, they are very very small when compared with human cells. Eg If a white blood cell was a 50m Olympic swimming pool, a virus by comparison would be a 2 year old child swimming in that pool.
We're talking small.
A virus is incapable of reproducing itself (the definition of a living organism is that it can reproduce), so it is not considered alive or living. It is either active or inactive.
To replicate a virus attaches to a host cell. It bonds with the membrane of the cell and expels its genetic (RNA) material inside the cell. The genetic code penetrates the host cells own DNA, joins to it and reprograms the cell to cease being what it was before infection, and become a factory to manufacture more viral particles.
It's a zombie.
Let's look at a Flu virus- Influenza A. "Flu" has many surface proteins that are categorised as Hs and Ns. You've heard of H5N1, or H1N1 flu, bird flu, swine flu?
The H is a protein called hemagglutinin and it is responsible for letting a virus stick onto and penetrate a cell.
The N is a protein enzyme called Neurominidase which is responsible for the release of a new viral particle from a host cell.
When you have the vaccination for flu, you are getting the Antigen (signature of a weakened virus). Your immune system then makes antibodies to "attack" the real infection flu virus when it invades you in the flu season. The Antibody actually attaches to the H disabling the virus and stopping it from endearing and infecting the cell.
Anti viral drugs (Relenza, Tamiflu) in converse attack the virus's N protein, stopping the newly created viruses from being released by the slave cell.
Signalling invasion by a virus the cell releases a chemical scent (cytokines) called interferon, that calls macrophages (white blood cells) to destroy the infected cell.
...
These viruses are tricky wee things. Small, un-dead, efficient killers that inhabit the bodies of cells and convert them into slaves.
Zombies to the max!!
Sunday, 16 February 2014
72 Hyperbaric Oxygen Therapy (HBOT)
KYJ 72 - Hyperbaric Oxygen
ALERT!!! Nerdy sciency post.
Imagine giving 240%-280% oxygen. Possible? Yes of course, but only in a hyperbaric chamber. Lets review what you understand of 100% oxygen.
Right now, if you are sitting at sea level in and you place a tight fitting bag-valve-mask on your face and run it at 15lpm; you will be giving yourself 100% oxygen.
That means- 100% oxygen at 760mmHg. (Seal level or atmospheric pressure).
Atmospheric pressure =1 Atm = 760mmHg.
Our atmosphere is made up of gases. Mostly nitrogen 78% and oxygen 21% and a 1% mix of other gases.
Breathing air we are breathing is therefore 21% of 760mmHg
Meaning O2 pressure on room air is 159mmHg (0.21x760=159)
When you're breathing 50% O2 then this is the same as saying you are breathing 50% of 760mmHg = 380mmHg Oxygen pressure.
100% of 1 atmosphere (760) is the same as PO2 = 760mmHg.
....
Now... The highest concentration of a gas is 100%, but what if you could breath that same gas at higher atmospheric pressure? Well this is the principle of Hyperbaric Oxygen Therapy (HBOT).
Typically in a HBOT chamber a patient breathes 100% at higher than 760mmHg (1atm).
Common examples are diabetic and other chronic would patients, or those with radio necrosis, who are treated at 14 metres of seawater (msw).
And... Divers with bends, or carbon monoxide poisoning, and gangrene infections who are treated at 18msw.
No!!! They don't wear togs, and they don't get wet. The term msw means that they are subjected to the equivalent pressure in a chamber, as a person diving at a depth of 14 or 18 msw.
The deeper you dive under water, the greater the pressure.
For every 10 msw the atmospheric pressure doubles our atmosphere.
Sea level = 760mmHg (1 atm)
10msw = 1520mmHg (2 atm)
14msw = 1824mmHg*
18msw = 2128mmHg*
20msw = 2280mmHg (3 atm).
In rare cases of cerebral arterial gas embolism (CAGE) or severest cases of the "Bends" , a patient might be treated at 30msw which is 4 times the pressure on land (3040mmHg).
So, now we do some very simple maths. If 100% O2 at sea level is 760, then the pO2 at 14msw (2.4 atm) would be 1824mmHg or the equivalent of 240% oxygen.
At this pressure (concentration) oxygen changes in its physiological effects. It now dissolves into blood plasma exerting paO2 of 1700-1800mmHg (normal = 80-100)!!
When this high, oxygen is a remarkable antibiotic. It destroys anaerobic bacteria. It also initiates a wound healing process called angioneogenesis.
Angio= blood vessels,
Neo = new
Genesis = creation of
Angioneogenesis is the process of budding new blood vessels into previously avascular tissue, stimulating new cell growth and subsequently, switches on wound healing in previously indolent wounds like venous ulcers, diabetic foot wounds and arterial ulcers.
In divers affected with the bends (nitrogen bubbles in the blood and joints), the effect of pressure literally squeezes these bubbles (shrinking their size), and the high concentration of oxygen helps them off gas their bubbles.
In Carbon monoxide (CO) poisoning, HBOT forces CO off haemoglobin and reduces the half life of CO from 4-6 hours in air, to 23 mins in a HBO chamber.
Does it treat sports injuries... No!
Does it treat MS, CP or Autism? No?
It has been used by quacks and crack pots over 50 years for everything from fertility to longjevity. But reputable HBO treatment facilities are governed by a code of conduct to treat only those conditions for which their is robust RCT research data to support its use.
Fancy a high pressure job? Hyperbaric nursing was a fun departure from any other role, I'd done. And I recommend it for nurses looking for something different, and don't suffer with asthma, or claustrophobia.
With 11 or so reputable chambers in Australia alone, it is worth looking into.
ALERT!!! Nerdy sciency post.
Imagine giving 240%-280% oxygen. Possible? Yes of course, but only in a hyperbaric chamber. Lets review what you understand of 100% oxygen.
Right now, if you are sitting at sea level in and you place a tight fitting bag-valve-mask on your face and run it at 15lpm; you will be giving yourself 100% oxygen.
That means- 100% oxygen at 760mmHg. (Seal level or atmospheric pressure).
Atmospheric pressure =1 Atm = 760mmHg.
Our atmosphere is made up of gases. Mostly nitrogen 78% and oxygen 21% and a 1% mix of other gases.
Breathing air we are breathing is therefore 21% of 760mmHg
Meaning O2 pressure on room air is 159mmHg (0.21x760=159)
When you're breathing 50% O2 then this is the same as saying you are breathing 50% of 760mmHg = 380mmHg Oxygen pressure.
100% of 1 atmosphere (760) is the same as PO2 = 760mmHg.
....
Now... The highest concentration of a gas is 100%, but what if you could breath that same gas at higher atmospheric pressure? Well this is the principle of Hyperbaric Oxygen Therapy (HBOT).
Typically in a HBOT chamber a patient breathes 100% at higher than 760mmHg (1atm).
Common examples are diabetic and other chronic would patients, or those with radio necrosis, who are treated at 14 metres of seawater (msw).
And... Divers with bends, or carbon monoxide poisoning, and gangrene infections who are treated at 18msw.
No!!! They don't wear togs, and they don't get wet. The term msw means that they are subjected to the equivalent pressure in a chamber, as a person diving at a depth of 14 or 18 msw.
The deeper you dive under water, the greater the pressure.
For every 10 msw the atmospheric pressure doubles our atmosphere.
Sea level = 760mmHg (1 atm)
10msw = 1520mmHg (2 atm)
14msw = 1824mmHg*
18msw = 2128mmHg*
20msw = 2280mmHg (3 atm).
In rare cases of cerebral arterial gas embolism (CAGE) or severest cases of the "Bends" , a patient might be treated at 30msw which is 4 times the pressure on land (3040mmHg).
So, now we do some very simple maths. If 100% O2 at sea level is 760, then the pO2 at 14msw (2.4 atm) would be 1824mmHg or the equivalent of 240% oxygen.
At this pressure (concentration) oxygen changes in its physiological effects. It now dissolves into blood plasma exerting paO2 of 1700-1800mmHg (normal = 80-100)!!
When this high, oxygen is a remarkable antibiotic. It destroys anaerobic bacteria. It also initiates a wound healing process called angioneogenesis.
Angio= blood vessels,
Neo = new
Genesis = creation of
Angioneogenesis is the process of budding new blood vessels into previously avascular tissue, stimulating new cell growth and subsequently, switches on wound healing in previously indolent wounds like venous ulcers, diabetic foot wounds and arterial ulcers.
In divers affected with the bends (nitrogen bubbles in the blood and joints), the effect of pressure literally squeezes these bubbles (shrinking their size), and the high concentration of oxygen helps them off gas their bubbles.
In Carbon monoxide (CO) poisoning, HBOT forces CO off haemoglobin and reduces the half life of CO from 4-6 hours in air, to 23 mins in a HBO chamber.
Does it treat sports injuries... No!
Does it treat MS, CP or Autism? No?
It has been used by quacks and crack pots over 50 years for everything from fertility to longjevity. But reputable HBO treatment facilities are governed by a code of conduct to treat only those conditions for which their is robust RCT research data to support its use.
Fancy a high pressure job? Hyperbaric nursing was a fun departure from any other role, I'd done. And I recommend it for nurses looking for something different, and don't suffer with asthma, or claustrophobia.
With 11 or so reputable chambers in Australia alone, it is worth looking into.
71 Carbon Monoxide poisoning
KYJ 71 - Carbon Monoxide (CO)
In knowing your jargon (KYJ) blogs we explore commonly heard terms in the clinical environment. It is ECT4Health's little way of contributing to #FOAMed.
Today, the noxious gas Carbon Monoxide (CO) is our topic.
First a story. As a kid I was into motocross. I loved bikes and motors and would spend hours tinkering in the shed tuning and playing with my bike. One afternoon in the closed up shed with the bike idling away, I started developing a thumping headache and a sudden burst of dizziness. Not making the connection between a closed up shed and an engine spewing out fumes, I learned the hard way about carbon monoxide and some of the early adverse effects.
CO is a colourless odourless tasteless gas produced when organic matter (carbon fuel) is burned. It is present in all hydrocarbon combustion (diesel, petrol, kerosine,oils), and when natural fibers like wood, paper and cotton burn.
The colour of smoke is deceptive, as smoke contains many gases and particulate matter that gives off colour and odour. CO is invisible.
CO has a remarkable ability to bind to haemoglobin at the same receptor site as oxygen. The sinister thing is, CO's affinity to bind to Hb is 240-320 times greater than oxygen. So if there is even the slightest hint of CO in the air you breathe, it will kick off any oxygen from your red blood cells.
Now CO is able to be measured in blood using a venous or arterial blood gas. Carboxyhaemoglobin (HbCO) levels are considered abnormal when elevated above 3%.
The average smoker may have a HbCO of 5-10%, and values over 25% are pathological.
At the cellular level CO shuts down a cells energy (ATP) production causing hypoxia, and lactic acidosis.
Headaches, shortened clotting times (note that DVT risk is high in smokers), sleepiness, and alteration in consciousness leading to coma and death by asphyxia.
Being so good at sticking to Hb, CO has a slow half life of about 5 hours, but if the patient is administered 100% oxygen, it can be reduced to under an hour. It is no surprise then that the treatment for CO poisoning is oxygen therapy .
Initially 100% should be applied on suspicion, and an ABG taken to determine levels.
Always take a Neuro obs baseline, and 12 lead ECG.
If severe, treatment may consider Hyperbaric oxygen therapy. The standard is 18 meters of pressure for 90 minutes.
Every year many people die from deliberate or accidental exposure to Carbon monoxide. Suicide intent, building fires, car fires, bush fires and blocked flues in caravans/campers are all common.
Less common causes are the use of paint strippers in poorly ventilated areas (methylene chloride) as the liver metabolises these stripper fumes into CO.
Another cause is poorly maintained air compressors being used to fill SCUBA tanks on dive charter boats. If the exhaust pipe is downwind of the air intakes on a compressor, then CO is sucked into the intake and compresses CO gas into the Scuba tank.
CO is a dangerous poison, and one that is insideous. The sad reality is that it is impossible for the victim to know they are dangerously affected, because they just drift off to sleep (or never wake up).
In knowing your jargon (KYJ) blogs we explore commonly heard terms in the clinical environment. It is ECT4Health's little way of contributing to #FOAMed.
Today, the noxious gas Carbon Monoxide (CO) is our topic.
First a story. As a kid I was into motocross. I loved bikes and motors and would spend hours tinkering in the shed tuning and playing with my bike. One afternoon in the closed up shed with the bike idling away, I started developing a thumping headache and a sudden burst of dizziness. Not making the connection between a closed up shed and an engine spewing out fumes, I learned the hard way about carbon monoxide and some of the early adverse effects.
CO is a colourless odourless tasteless gas produced when organic matter (carbon fuel) is burned. It is present in all hydrocarbon combustion (diesel, petrol, kerosine,oils), and when natural fibers like wood, paper and cotton burn.
The colour of smoke is deceptive, as smoke contains many gases and particulate matter that gives off colour and odour. CO is invisible.
CO has a remarkable ability to bind to haemoglobin at the same receptor site as oxygen. The sinister thing is, CO's affinity to bind to Hb is 240-320 times greater than oxygen. So if there is even the slightest hint of CO in the air you breathe, it will kick off any oxygen from your red blood cells.
Now CO is able to be measured in blood using a venous or arterial blood gas. Carboxyhaemoglobin (HbCO) levels are considered abnormal when elevated above 3%.
The average smoker may have a HbCO of 5-10%, and values over 25% are pathological.
At the cellular level CO shuts down a cells energy (ATP) production causing hypoxia, and lactic acidosis.
Headaches, shortened clotting times (note that DVT risk is high in smokers), sleepiness, and alteration in consciousness leading to coma and death by asphyxia.
Being so good at sticking to Hb, CO has a slow half life of about 5 hours, but if the patient is administered 100% oxygen, it can be reduced to under an hour. It is no surprise then that the treatment for CO poisoning is oxygen therapy .
Initially 100% should be applied on suspicion, and an ABG taken to determine levels.
Always take a Neuro obs baseline, and 12 lead ECG.
If severe, treatment may consider Hyperbaric oxygen therapy. The standard is 18 meters of pressure for 90 minutes.
Every year many people die from deliberate or accidental exposure to Carbon monoxide. Suicide intent, building fires, car fires, bush fires and blocked flues in caravans/campers are all common.
Less common causes are the use of paint strippers in poorly ventilated areas (methylene chloride) as the liver metabolises these stripper fumes into CO.
Another cause is poorly maintained air compressors being used to fill SCUBA tanks on dive charter boats. If the exhaust pipe is downwind of the air intakes on a compressor, then CO is sucked into the intake and compresses CO gas into the Scuba tank.
CO is a dangerous poison, and one that is insideous. The sad reality is that it is impossible for the victim to know they are dangerously affected, because they just drift off to sleep (or never wake up).
Friday, 14 February 2014
70 Rhabdomyolysis & myoglobin
KYJ 70 Rhabdomyolysis
Was asked in class what Rhabdomyolysis was today. So I thought that would be a good KYJ topic.
Rhabdo = stripy
Myo = muscle
Lysis = destroy
Rhabdomyolysis is skeletal muscle damage.
In cases of crush injury, hyperthermia, over extreme muscle exercise, and electrocution, it is probable that muscle tissue can be injured.
Muscle yields a high concentration of proteins and electrolytes that are released when Muscle cells are damaged.
Myoglobin
Myoglobin is the large red protein in muscle, which transports oxygen. It is essentially the same as haemoglobin in the red blood cell, in that it carries oxygen.
When injured (rhabdomyolysis), muscle cells spill or leak this from their cytoplasm. It is picked up in lymphatic fluid and extruded into blood. As it is filtered out in urine, it shows up by making the urine appear blood stained. Urine will test positive for blood and is called myoglobinuria. The sad consequence is renal failure as myoglobin clogs up the renal tubules.
Potassium
Potassium (K+) is the principle intra cellular cation (positive charged electrolyte). It exists in low quantities in blood, but high concentration inside cells.
As muscle cells are damaged, it leaches out into the blood causing a dangerous elevation in serum potassium (hyperkalaemia). If too high, it becomes cardiotoxic. Spiking potassium after crush injuries is the likely cause of sudden cardiac arrest in the minutes following rescue.
Creatine Kinase
CK is an enzyme that is used in the process of converting glucose to energy in muscle cells. When muscles are subject to rhabdomyolysis, they release this enzyme which may be detected in blood and used as a gauge as to how severe the tissue damage is.
Rhabdomyolysis alone is a deadly killer. It's cardiac effects and kidney damage are sinister sequelae of a large injury to muscles.
Was asked in class what Rhabdomyolysis was today. So I thought that would be a good KYJ topic.
Rhabdo = stripy
Myo = muscle
Lysis = destroy
Rhabdomyolysis is skeletal muscle damage.
In cases of crush injury, hyperthermia, over extreme muscle exercise, and electrocution, it is probable that muscle tissue can be injured.
Muscle yields a high concentration of proteins and electrolytes that are released when Muscle cells are damaged.
Myoglobin
Myoglobin is the large red protein in muscle, which transports oxygen. It is essentially the same as haemoglobin in the red blood cell, in that it carries oxygen.
When injured (rhabdomyolysis), muscle cells spill or leak this from their cytoplasm. It is picked up in lymphatic fluid and extruded into blood. As it is filtered out in urine, it shows up by making the urine appear blood stained. Urine will test positive for blood and is called myoglobinuria. The sad consequence is renal failure as myoglobin clogs up the renal tubules.
Potassium
Potassium (K+) is the principle intra cellular cation (positive charged electrolyte). It exists in low quantities in blood, but high concentration inside cells.
As muscle cells are damaged, it leaches out into the blood causing a dangerous elevation in serum potassium (hyperkalaemia). If too high, it becomes cardiotoxic. Spiking potassium after crush injuries is the likely cause of sudden cardiac arrest in the minutes following rescue.
Creatine Kinase
CK is an enzyme that is used in the process of converting glucose to energy in muscle cells. When muscles are subject to rhabdomyolysis, they release this enzyme which may be detected in blood and used as a gauge as to how severe the tissue damage is.
Rhabdomyolysis alone is a deadly killer. It's cardiac effects and kidney damage are sinister sequelae of a large injury to muscles.
69 Interferon
KYJ 69 - Interferon & cytokines
To communicate with each other, many cells in your body release chemical signals called cytokines. There are many cytokines, and their function differs greatly. An example of cytokines include interleukins, lymphokines, and interferons.
Often clinicians hear these jargon words, but few know what they are. This post will explore interferon.
Interferons are cytokines that are released by cells infected by virus, bacteria, parasites or tumour. And they have a few jobs. They are called interferon because they interfere with the virus proliferation.
1
Suppose a cell lining the throat should be invaded by a virus. It becomes the Host for the virus.
Ordinarily a virus would alter the throat cell's DNA and force the cell to replicate the virus genetic matter. Hence, the cell is converted into a virus factory.
It is not recognised by the immune system as foreign, because it is one of the body's own cells. So how does this virus get destroyed???
Signalling its distress, the host cell releases a chemical signal called interferon. This alerts the immune system that it has been taken hostage by the virus, and in the ultimate act of sacrifice, instructs the immune system to destroy the cell. Macrophages are activated to move in and eat the host cell. Now that's taking one for the team!!
2
A second task of the interferon is that the healthy cells around the diseased Host cell are "warned" that it's neighbour has been infiltrated by the baddies and to resist getting invaded.
3
In response to interferon the healthy cells around the infection can produce an enzyme that destroys the protein shell that the virus comes packaged in.
Whilst not an Antibiotic, interferon sure behaves like one in viral infections. You'll know about them early because when they are released they often cause muscle aches and pains (myalgia) and lethargy in the prodrome to a full infection.
Have you ever felt a bit Fluy? Well that yuk feeling is (in part), interferon.
There are 10 or so different interferons, and some are specific to viral invasion and some prevent tumour proliferation. In a nutshell, they are cytokines that act on enhancing our immune fight against invasion.
Are you liking these KYJ posts. Click on share . It's like releasing interferon to share the love.
To communicate with each other, many cells in your body release chemical signals called cytokines. There are many cytokines, and their function differs greatly. An example of cytokines include interleukins, lymphokines, and interferons.
Often clinicians hear these jargon words, but few know what they are. This post will explore interferon.
Interferons are cytokines that are released by cells infected by virus, bacteria, parasites or tumour. And they have a few jobs. They are called interferon because they interfere with the virus proliferation.
1
Suppose a cell lining the throat should be invaded by a virus. It becomes the Host for the virus.
Ordinarily a virus would alter the throat cell's DNA and force the cell to replicate the virus genetic matter. Hence, the cell is converted into a virus factory.
It is not recognised by the immune system as foreign, because it is one of the body's own cells. So how does this virus get destroyed???
Signalling its distress, the host cell releases a chemical signal called interferon. This alerts the immune system that it has been taken hostage by the virus, and in the ultimate act of sacrifice, instructs the immune system to destroy the cell. Macrophages are activated to move in and eat the host cell. Now that's taking one for the team!!
2
A second task of the interferon is that the healthy cells around the diseased Host cell are "warned" that it's neighbour has been infiltrated by the baddies and to resist getting invaded.
3
In response to interferon the healthy cells around the infection can produce an enzyme that destroys the protein shell that the virus comes packaged in.
Whilst not an Antibiotic, interferon sure behaves like one in viral infections. You'll know about them early because when they are released they often cause muscle aches and pains (myalgia) and lethargy in the prodrome to a full infection.
Have you ever felt a bit Fluy? Well that yuk feeling is (in part), interferon.
There are 10 or so different interferons, and some are specific to viral invasion and some prevent tumour proliferation. In a nutshell, they are cytokines that act on enhancing our immune fight against invasion.
Are you liking these KYJ posts. Click on share . It's like releasing interferon to share the love.
68 Alcohol and the myth of IV Rehydration
KYJ 68 Alcohol overdose
Whilst alcohol is diuretic, and causes dehydration most noticeably cerebral (hence hangover), the patient's diuresis is osmotic, so doesn't reduce blood volume.
Alcohol filtered into renal tubules causes the increase in urine output, by osmosis. It prevents reabsorption in the ascending loop and distal tubes.
The patient may be dehydrated, but they are not volume depleted.
Giving IV Normal saline in these patients who are hung over or still intoxicated, compounds their hypervolaemia, but because their blood is still full of ethanol, they continue to suck water from their interstitial space and cells.
IV fluids in the acute alcohol ingestion just worsens the need to use the bottle or pan more frequently.
Normally in sober blood, 65% of a litre of NS is shifted into the ISS within 15 mins, but in drunk folk, (because of the osmotic pull of alcohol in blood), this ISS replenishment doesn't happen and all we do is overload them.
Fine if you are 22 and full of Yagerbombs, but potentially dangerous if you have an older type with the beginnings of heart failure. That hypervolaemia can induce a hypertensive crisis, and systolic failure, not to mention a heap of unwanted preload.
Whilst alcohol is diuretic, and causes dehydration most noticeably cerebral (hence hangover), the patient's diuresis is osmotic, so doesn't reduce blood volume.
Alcohol filtered into renal tubules causes the increase in urine output, by osmosis. It prevents reabsorption in the ascending loop and distal tubes.
The patient may be dehydrated, but they are not volume depleted.
Giving IV Normal saline in these patients who are hung over or still intoxicated, compounds their hypervolaemia, but because their blood is still full of ethanol, they continue to suck water from their interstitial space and cells.
IV fluids in the acute alcohol ingestion just worsens the need to use the bottle or pan more frequently.
Normally in sober blood, 65% of a litre of NS is shifted into the ISS within 15 mins, but in drunk folk, (because of the osmotic pull of alcohol in blood), this ISS replenishment doesn't happen and all we do is overload them.
Fine if you are 22 and full of Yagerbombs, but potentially dangerous if you have an older type with the beginnings of heart failure. That hypervolaemia can induce a hypertensive crisis, and systolic failure, not to mention a heap of unwanted preload.
67 Adrenaline / Epinephrine
KYJ 67 - Adrenaline /Epinephrine
In Knowing Your Jargon (KYJ) posts, you never know where the next topic will come from. I was teaching a trauma course today and the topic of adrenaline (the hormone) came up, which generated questions about what is does. So here we go.
Adrenaline or epinephrine as it is also known, is a hormone. It is made in the Adrenal gland and is one of a number of chemicals that are collectively called catecholamines.
Catecholamines are hormones that excite certain biological processes in the body.
Epinephrine is a neuromodulator which means it modulates a nerve response, specifically the sympathetic nervous system.
So to fully grasp what epinephrine does, we must understand what the sympathetic nervous system does, because epinephrine is an SNS stimulator.
You've heard of "flight or fight"? That primitive response that if attacked or threatened, a person will respond with a neurohormonal surge of chemicals from many glands to prepare to stand and fight or flee the threat. Either way there is a phenomenon of superhuman strength, speed and endurance.
The sympathetic nervous system effects do the following:
Increase mental alertness.
Increase heart rate (chronotropy).
Increase strength of contraction (inotropy).
Increase electrical nerve transmission speed (dromotropy).
Relax bronchiole smooth muscles- opening the lungs for greater gas exchange.
Open iris to let in more light.
Constricts veins to push more blood into arterial circulation (perfuses tissues/muscles, and increases BP).
Stimulates the breakdown of glycogen in the muscles and the liver, into glucose (we increase our blood sugar).
So, given these effects are all typical of the SNS; and, given that epinephrine modulates this response, it is also correct to say that epinephrine (adrenaline) causes these symptoms. It is therefore called an Adrenergic response.
...
Now consider these effects. And think of why or when we'd desire stimulating these effects...
... Can u see that we would want to give epinephrine to patients at a time that we wanted to :
manage slow heart beats,
Or raise low BPs
Or cause vasoconstriction in tissues that are swollen.
Or open up constricted airways or lungs.
In cardiac arrest, adrenaline is used for three reasons:
First: peripheral vaso constriction. Pushing volume into the central vessels making CPR more effective
Second: to cause a fine undetectable cardiac electrical rhythm to become faster and coarser, so it may respond to defibrillation.
Third: to attempt to stimulate some cardiac activity. A slim hope that the SNS might miraculously initiate an electrical stimulus.
In croup or upper airway oedema, the administration of adrenaline constricts blood vessels thereby reducing plasma leakage into tissues (oedema). And dries up salivary secretions.
As an additive in local anaesthetic (Lignocaine with Adrenaline), the profound vasoconstriction aids in bloodless incisions or suture lines.
As a soak on nose packing gauze, the vasoconstrictive effect assists with severe epistaxis (nose bleeding).
As an IV infusion, adrenaline is used to increase heart rate and force of contraction of the heart (inotropy). This therefor maintains cardiac output and subsequently, increases BP in patients in shock.
As an IM or SC injection, (EpiPen) is used to reverse the life threatening cascade in anaphylactic shock (allergic reaction). It reduces airway oedema, and assists to redistribute venous blood to improve arterial perfusion.
In nurses and paramedics it is a hormone surge that many of is crave. That buzz you get is the best rush on Mother Earth. You get that call - the Red phone goes off. Your breathing rate increases, your pupils dilate, your heart races, and you feel it pounding in your chest. Your mouth goes dry. You feel super alert, clear of thought, senses are hyperalert, and you are super strong physically.
All hunger you had disappears, and those sore feet you've been on for hours, or that nursing back pain that seems persistent seems to have disappeared.
You are on the high of your life time... Whoa what a ride. Then someone yells ..."MVA rollover...ETA 3 mins!!"
And you are high as a kite thinking ....."yeah..... Bring it on"
...
That is flight or fight!!!
That my friends is the nectar of the Gods.
That is Adrenaline!!!
In Knowing Your Jargon (KYJ) posts, you never know where the next topic will come from. I was teaching a trauma course today and the topic of adrenaline (the hormone) came up, which generated questions about what is does. So here we go.
Adrenaline or epinephrine as it is also known, is a hormone. It is made in the Adrenal gland and is one of a number of chemicals that are collectively called catecholamines.
Catecholamines are hormones that excite certain biological processes in the body.
Epinephrine is a neuromodulator which means it modulates a nerve response, specifically the sympathetic nervous system.
So to fully grasp what epinephrine does, we must understand what the sympathetic nervous system does, because epinephrine is an SNS stimulator.
You've heard of "flight or fight"? That primitive response that if attacked or threatened, a person will respond with a neurohormonal surge of chemicals from many glands to prepare to stand and fight or flee the threat. Either way there is a phenomenon of superhuman strength, speed and endurance.
The sympathetic nervous system effects do the following:
Increase mental alertness.
Increase heart rate (chronotropy).
Increase strength of contraction (inotropy).
Increase electrical nerve transmission speed (dromotropy).
Relax bronchiole smooth muscles- opening the lungs for greater gas exchange.
Open iris to let in more light.
Constricts veins to push more blood into arterial circulation (perfuses tissues/muscles, and increases BP).
Stimulates the breakdown of glycogen in the muscles and the liver, into glucose (we increase our blood sugar).
So, given these effects are all typical of the SNS; and, given that epinephrine modulates this response, it is also correct to say that epinephrine (adrenaline) causes these symptoms. It is therefore called an Adrenergic response.
...
Now consider these effects. And think of why or when we'd desire stimulating these effects...
... Can u see that we would want to give epinephrine to patients at a time that we wanted to :
manage slow heart beats,
Or raise low BPs
Or cause vasoconstriction in tissues that are swollen.
Or open up constricted airways or lungs.
In cardiac arrest, adrenaline is used for three reasons:
First: peripheral vaso constriction. Pushing volume into the central vessels making CPR more effective
Second: to cause a fine undetectable cardiac electrical rhythm to become faster and coarser, so it may respond to defibrillation.
Third: to attempt to stimulate some cardiac activity. A slim hope that the SNS might miraculously initiate an electrical stimulus.
In croup or upper airway oedema, the administration of adrenaline constricts blood vessels thereby reducing plasma leakage into tissues (oedema). And dries up salivary secretions.
As an additive in local anaesthetic (Lignocaine with Adrenaline), the profound vasoconstriction aids in bloodless incisions or suture lines.
As a soak on nose packing gauze, the vasoconstrictive effect assists with severe epistaxis (nose bleeding).
As an IV infusion, adrenaline is used to increase heart rate and force of contraction of the heart (inotropy). This therefor maintains cardiac output and subsequently, increases BP in patients in shock.
As an IM or SC injection, (EpiPen) is used to reverse the life threatening cascade in anaphylactic shock (allergic reaction). It reduces airway oedema, and assists to redistribute venous blood to improve arterial perfusion.
In nurses and paramedics it is a hormone surge that many of is crave. That buzz you get is the best rush on Mother Earth. You get that call - the Red phone goes off. Your breathing rate increases, your pupils dilate, your heart races, and you feel it pounding in your chest. Your mouth goes dry. You feel super alert, clear of thought, senses are hyperalert, and you are super strong physically.
All hunger you had disappears, and those sore feet you've been on for hours, or that nursing back pain that seems persistent seems to have disappeared.
You are on the high of your life time... Whoa what a ride. Then someone yells ..."MVA rollover...ETA 3 mins!!"
And you are high as a kite thinking ....."yeah..... Bring it on"
...
That is flight or fight!!!
That my friends is the nectar of the Gods.
That is Adrenaline!!!
Tuesday, 11 February 2014
66 - Lactate and lactic acidosis
KYJ 66 - Lactic Acid
Lactic acid or lactate is an acidic byproduct of glucose which has been incompletely metabolised.
Let's review the Cell
At its simplest, cells need glucose to make energy.
The energy is a chemical called adenosine triphosphate (ATP).
Now without boring you to death... Just know that a chemical chain reaction involving oxygen is needed inside the cell to convert that glucose to energy.
Glycolysis is the first step which is where Glucose is split into two molecules of pyruvate. Next, pyruvate and oxygen combine to enter a reaction called the Krebs cycle.
But... If no oxygen is available, pyruvate is expelled from the cell, and it is converted into
Lactate.
Being acid, lactate build up causes lactic acidosis. Haemoglobin that is a acidotic is reluctant to carry oxygen to cells.
The irony is the less oxygen available to the cells, the more lactic acidosis.
I viscous cycle.
Lactate can be converted back to Glucose in the liver, but again, it is an oxygen dependant process.
Lactic acid or lactate is an acidic byproduct of glucose which has been incompletely metabolised.
Let's review the Cell
At its simplest, cells need glucose to make energy.
The energy is a chemical called adenosine triphosphate (ATP).
Now without boring you to death... Just know that a chemical chain reaction involving oxygen is needed inside the cell to convert that glucose to energy.
Glycolysis is the first step which is where Glucose is split into two molecules of pyruvate. Next, pyruvate and oxygen combine to enter a reaction called the Krebs cycle.
But... If no oxygen is available, pyruvate is expelled from the cell, and it is converted into
Lactate.
Being acid, lactate build up causes lactic acidosis. Haemoglobin that is a acidotic is reluctant to carry oxygen to cells.
The irony is the less oxygen available to the cells, the more lactic acidosis.
I viscous cycle.
Lactate can be converted back to Glucose in the liver, but again, it is an oxygen dependant process.
67 - Adrenaline - The buzz
KYJ 67 - Adrenaline / Epinephrine the hormone and the drug
In Knowing Your Jargon (KYJ) posts, you never know where the next topic will come from. I was teaching a trauma course today and the topic of adrenaline (the hormone) came up, which generated questions about what is does. So here we go.
Adrenaline or epinephrine as it is also known, is a hormone. It is made in the Adrenal gland and is one of a number of chemicals that are collectively called catecholamines.
Catecholamines are hormones that excite certain biological processes in the body.
Epinephrine is a neuromodulator which means it modulates a nerve response, specifically the sympathetic nervous system.
So to fully grasp what epinephrine does, we must understand what the sympathetic nervous system does, because epinephrine is an SNS stimulator.
You've heard of "flight or fight"? That primitive response that if attacked or threatened, a person will respond with a neurohormonal surge of chemicals from many glands to prepare to stand and fight or flee the threat. Either way there is a phenomenon of superhuman strength, speed and endurance.
The sympathetic nervous system effects do the following:
Increase mental alertness.
Increase heart rate (chronotropy).
Increase strength of contraction (inotropy).
Increase electrical nerve transmission speed (dromotropy).
Relax bronchiole smooth muscles- opening the lungs for greater gas exchange.
Open iris to let in more light.
Constricts veins to push more blood into arterial circulation (perfuses tissues/muscles, and increases BP).
Stimulates the breakdown of glycogen in the muscles and the liver, into glucose (we increase our blood sugar).
So, given these effects are all typical of the SNS; and, given that epinephrine modulates this response, it is also correct to say that epinephrine (adrenaline) causes these symptoms. It is therefore called an Adrenergic response.
...
Now consider these effects. And think of why or when we'd desire stimulating these effects...
... Can u see that we would want to give epinephrine to patients at a time that we wanted to :
manage slow heart beats,
Or raise low BPs
Or cause vasoconstriction in tissues that are swollen.
Or open up constricted airways or lungs.
In cardiac arrest, adrenaline is used for three reasons:
First: peripheral vaso constriction. Pushing volume into the central vessels making CPR more effective
Second: to cause a fine undetectable cardiac electrical rhythm to become faster and coarser, so it may respond to defibrillation.
Third: to attempt to stimulate some cardiac activity. A slim hope that the SNS might miraculously initiate an electrical stimulus.
In croup or upper airway oedema, the administration of adrenaline constricts blood vessels thereby reducing plasma leakage into tissues (oedema). And dries up salivary secretions.
As an additive in local anaesthetic (Lignocaine with Adrenaline), the profound vasoconstriction aids in bloodless incisions or suture lines.
As a soak on nose packing gauze, the vasoconstrictive effect assists with severe epistaxis (nose bleeding).
As an IV infusion, adrenaline is used to increase heart rate and force of contraction of the heart (inotropy). This therefor maintains cardiac output and subsequently, increases BP in patients in shock.
As an IM or SC injection, (EpiPen) is used to reverse the life threatening cascade in anaphylactic shock (allergic reaction). It reduces airway oedema, and assists to redistribute venous blood to improve arterial perfusion.
In nurses and paramedics it is a hormone surge that many of is crave. That buzz you get is the best rush on Mother Earth. You get that call - the Red phone goes off. Your breathing rate increases, your pupils dilate, your heart races, and you feel it pounding in your chest. Your mouth goes dry. You feel super alert, clear of thought, senses are hyperalert, and you are super strong physically.
All hunger you had disappears, and those sore feet you've been on for hours, or that nursing back pain that seems persistent seems to have disappeared.
You are on the high of your life time... Whoa what a ride. Then someone yells ..."MVA rollover...ETA 3 mins!!"
And you are high as a kite thinking ....."yeah..... Bring it on"
...
That is flight or fight!!!
That my friends is the nectar of the Gods.
That is Adrenaline!!!
In Knowing Your Jargon (KYJ) posts, you never know where the next topic will come from. I was teaching a trauma course today and the topic of adrenaline (the hormone) came up, which generated questions about what is does. So here we go.
Adrenaline or epinephrine as it is also known, is a hormone. It is made in the Adrenal gland and is one of a number of chemicals that are collectively called catecholamines.
Catecholamines are hormones that excite certain biological processes in the body.
Epinephrine is a neuromodulator which means it modulates a nerve response, specifically the sympathetic nervous system.
So to fully grasp what epinephrine does, we must understand what the sympathetic nervous system does, because epinephrine is an SNS stimulator.
You've heard of "flight or fight"? That primitive response that if attacked or threatened, a person will respond with a neurohormonal surge of chemicals from many glands to prepare to stand and fight or flee the threat. Either way there is a phenomenon of superhuman strength, speed and endurance.
The sympathetic nervous system effects do the following:
Increase mental alertness.
Increase heart rate (chronotropy).
Increase strength of contraction (inotropy).
Increase electrical nerve transmission speed (dromotropy).
Relax bronchiole smooth muscles- opening the lungs for greater gas exchange.
Open iris to let in more light.
Constricts veins to push more blood into arterial circulation (perfuses tissues/muscles, and increases BP).
Stimulates the breakdown of glycogen in the muscles and the liver, into glucose (we increase our blood sugar).
So, given these effects are all typical of the SNS; and, given that epinephrine modulates this response, it is also correct to say that epinephrine (adrenaline) causes these symptoms. It is therefore called an Adrenergic response.
...
Now consider these effects. And think of why or when we'd desire stimulating these effects...
... Can u see that we would want to give epinephrine to patients at a time that we wanted to :
manage slow heart beats,
Or raise low BPs
Or cause vasoconstriction in tissues that are swollen.
Or open up constricted airways or lungs.
In cardiac arrest, adrenaline is used for three reasons:
First: peripheral vaso constriction. Pushing volume into the central vessels making CPR more effective
Second: to cause a fine undetectable cardiac electrical rhythm to become faster and coarser, so it may respond to defibrillation.
Third: to attempt to stimulate some cardiac activity. A slim hope that the SNS might miraculously initiate an electrical stimulus.
In croup or upper airway oedema, the administration of adrenaline constricts blood vessels thereby reducing plasma leakage into tissues (oedema). And dries up salivary secretions.
As an additive in local anaesthetic (Lignocaine with Adrenaline), the profound vasoconstriction aids in bloodless incisions or suture lines.
As a soak on nose packing gauze, the vasoconstrictive effect assists with severe epistaxis (nose bleeding).
As an IV infusion, adrenaline is used to increase heart rate and force of contraction of the heart (inotropy). This therefor maintains cardiac output and subsequently, increases BP in patients in shock.
As an IM or SC injection, (EpiPen) is used to reverse the life threatening cascade in anaphylactic shock (allergic reaction). It reduces airway oedema, and assists to redistribute venous blood to improve arterial perfusion.
In nurses and paramedics it is a hormone surge that many of is crave. That buzz you get is the best rush on Mother Earth. You get that call - the Red phone goes off. Your breathing rate increases, your pupils dilate, your heart races, and you feel it pounding in your chest. Your mouth goes dry. You feel super alert, clear of thought, senses are hyperalert, and you are super strong physically.
All hunger you had disappears, and those sore feet you've been on for hours, or that nursing back pain that seems persistent seems to have disappeared.
You are on the high of your life time... Whoa what a ride. Then someone yells ..."MVA rollover...ETA 3 mins!!"
And you are high as a kite thinking ....."yeah..... Bring it on"
...
That is flight or fight!!!
That my friends is the nectar of the Gods.
That is Adrenaline!!!
65 - Reperfusion Injury
KYJ 65 - Reperfusion Injury.
The hottest of topics over recent years has included this paradox that ischaemic tissue is actually damaged as much by the restoration of oxygen than the deprivation of oxygen.
Reperfusion injury as the name implies is cellular damage that occurs to tissue when it's oxygen supply has been replenished. We see it in cardiac tissue, brain tissue, In fact, all tissue.
Recently the world has seen a reversal of the routine administration of oxygen to stroke patients , and those with cardiac chest pain and MI. Many nurses and doctors have struggled with this. At the outset, it seems counterintuitive to withhold oxygen to tissue that starves for it; but read on.
Review that all cells have a membrane made from a dual layer of fat (lipid). Technically this lipid bilayer is a water repelling wall that has tiny holes (pores or channels) that allows gases and chemicals to enter and exit cells.
The damage of those membranes makes cells lose control of these pores, allowing water to enter the cell and burst it. The death of the cell is called necrosis, and if it is water that killed it, it's called hydrolysis.
Now the damage to these cell membranes can be caused by many things. Toxins, mechanical damage or chemicals that dissolve the lipid bilayer are all examples.
Now let's look at oxygen . O2 is two atoms of oxygen. When oxygen enters cells, some of it splits into two singlet oxygen atoms that are negatively charged. These are called highly reactive oxygen species or most commonly "Oxygen free radicals".
It can form damaged O2- which is called Superoxide.
It can bond to hydrogen to form OH- (hydroxyl)
If O joins H2O is becomes hydrogen Peroxide (H2O2).
If it joins a nitrogen atom it becomes Nitric Oxide (NO).
It can even bind to another O2 causing the molecule called Ozone (O3).
All of these are oxygen free radicals and they react chemically with lipid cell membranes (lipid peroxidation) and this punches holes in the membrane of recently ischaemic cells.
The more oxygen available to tissue, the more free radicals (oxidants) are produced, which means the more cells get damaged.
In a nut shell this is called Reperfusion injury.
So you can see why oxygen delivery is now considered a double inch sword. While cells that had been starved of it, needed it; when it is restored, it actually causes further necrosis.
We can minimise this reperfusion by restoring blood flow, but not giving too much oxygen.
How much is too much?? We just don't know. But we do know that the oxygen we had been using is damaging.
Share the post on your page, and tag other nurses.
The hottest of topics over recent years has included this paradox that ischaemic tissue is actually damaged as much by the restoration of oxygen than the deprivation of oxygen.
Reperfusion injury as the name implies is cellular damage that occurs to tissue when it's oxygen supply has been replenished. We see it in cardiac tissue, brain tissue, In fact, all tissue.
Recently the world has seen a reversal of the routine administration of oxygen to stroke patients , and those with cardiac chest pain and MI. Many nurses and doctors have struggled with this. At the outset, it seems counterintuitive to withhold oxygen to tissue that starves for it; but read on.
Review that all cells have a membrane made from a dual layer of fat (lipid). Technically this lipid bilayer is a water repelling wall that has tiny holes (pores or channels) that allows gases and chemicals to enter and exit cells.
The damage of those membranes makes cells lose control of these pores, allowing water to enter the cell and burst it. The death of the cell is called necrosis, and if it is water that killed it, it's called hydrolysis.
Now the damage to these cell membranes can be caused by many things. Toxins, mechanical damage or chemicals that dissolve the lipid bilayer are all examples.
Now let's look at oxygen . O2 is two atoms of oxygen. When oxygen enters cells, some of it splits into two singlet oxygen atoms that are negatively charged. These are called highly reactive oxygen species or most commonly "Oxygen free radicals".
It can form damaged O2- which is called Superoxide.
It can bond to hydrogen to form OH- (hydroxyl)
If O joins H2O is becomes hydrogen Peroxide (H2O2).
If it joins a nitrogen atom it becomes Nitric Oxide (NO).
It can even bind to another O2 causing the molecule called Ozone (O3).
All of these are oxygen free radicals and they react chemically with lipid cell membranes (lipid peroxidation) and this punches holes in the membrane of recently ischaemic cells.
The more oxygen available to tissue, the more free radicals (oxidants) are produced, which means the more cells get damaged.
In a nut shell this is called Reperfusion injury.
So you can see why oxygen delivery is now considered a double inch sword. While cells that had been starved of it, needed it; when it is restored, it actually causes further necrosis.
We can minimise this reperfusion by restoring blood flow, but not giving too much oxygen.
How much is too much?? We just don't know. But we do know that the oxygen we had been using is damaging.
Share the post on your page, and tag other nurses.
Saturday, 8 February 2014
64 - Hypoxic drive Myth and the Haldane effect
KYJ 64 - Hypoxic drive.
Can I use oxygen on my COPD patient?
Yes. Judiciously, and under close observation, but Yes.
Hypoxic drive is a normal part of our primitive mechanism to breath. Literally hypoxic means "low oxygen". So hypoxic drive means, when oxygen levels drop off in blood, chemical receptors in your carotid arteries and Aorta, detects low oxygen, and informs the respiratory centre in the brain. This stimulates you to take another breath.
All humans have a hypoxic drive. But in the first few years of life a more powerful drive takes over.
Hypercapnic drive. If you are older than 3, and don't have severe gas trapping COPD, then you are breathing primarily because of this drive. Hypercapnic drive means high Carbon Dioxide (CO2) drive.
As CO2 rises in your blood it lowers blood pH and causes blood to become acidic. This acidic blood traveling through brain results in subtle lowering of CSF pH which, when detected in the Respiratory centre, is a powerful stimulant to initiate a breath.
In some CO2 retaining COPD patients (not many), their Hypercapnic drive ceases to function effectively, causing them to rely on their hypoxic drive . Traditionally we have been taught to avoid oxygenating these patients for fear of eliminating their will to breathe. But this is an erroneous myth. We will never completely destroy will to breathe.
So can I use oxygen on a person with hypoxic drive??? Yes. But we still want to minimise its use. Not because of respiratory suppression, but for a whole other reason. The Haldane effect.
The Haldane effect is a physics principle that states that the more oxygen that haemoglobin can carry in blood, the less it can transport CO2.
So... Now stay with me!!
So... If I push your oxygen sats up, you can't carry CO2 and excrete it. CO2 rises (is retained), exerting more and more acidosis.
Now at a point, acidic blood becomes so acidic that it then will not allow haemoglobin to bind with oxygen,
So how much is enough.
23-28 % (nasal prongs) or Venturi mask.
What indications...
In severe COPD patients who are known CO2 retainers, administer oxygen when their baseline sats drop below 88%.
All other patients - oxygenate to maintain sats over 93%
Summary
1. Hypoxic drive is normal
2. Oxygen to a patient with hypoxic drive causing respiratory rate depression is a MYTH.
3. The Haldane effect inhibits CO2 transportation for excretion in over oxygenated COPD patients.
Give Oxygen Judiciously, and have a sound reason to use this poisonous gas.
Share this with your paramedic/EMT, nurse friends and pages.
Like and share our page.
Can I use oxygen on my COPD patient?
Yes. Judiciously, and under close observation, but Yes.
Hypoxic drive is a normal part of our primitive mechanism to breath. Literally hypoxic means "low oxygen". So hypoxic drive means, when oxygen levels drop off in blood, chemical receptors in your carotid arteries and Aorta, detects low oxygen, and informs the respiratory centre in the brain. This stimulates you to take another breath.
All humans have a hypoxic drive. But in the first few years of life a more powerful drive takes over.
Hypercapnic drive. If you are older than 3, and don't have severe gas trapping COPD, then you are breathing primarily because of this drive. Hypercapnic drive means high Carbon Dioxide (CO2) drive.
As CO2 rises in your blood it lowers blood pH and causes blood to become acidic. This acidic blood traveling through brain results in subtle lowering of CSF pH which, when detected in the Respiratory centre, is a powerful stimulant to initiate a breath.
In some CO2 retaining COPD patients (not many), their Hypercapnic drive ceases to function effectively, causing them to rely on their hypoxic drive . Traditionally we have been taught to avoid oxygenating these patients for fear of eliminating their will to breathe. But this is an erroneous myth. We will never completely destroy will to breathe.
So can I use oxygen on a person with hypoxic drive??? Yes. But we still want to minimise its use. Not because of respiratory suppression, but for a whole other reason. The Haldane effect.
The Haldane effect is a physics principle that states that the more oxygen that haemoglobin can carry in blood, the less it can transport CO2.
So... Now stay with me!!
So... If I push your oxygen sats up, you can't carry CO2 and excrete it. CO2 rises (is retained), exerting more and more acidosis.
Now at a point, acidic blood becomes so acidic that it then will not allow haemoglobin to bind with oxygen,
So how much is enough.
23-28 % (nasal prongs) or Venturi mask.
What indications...
In severe COPD patients who are known CO2 retainers, administer oxygen when their baseline sats drop below 88%.
All other patients - oxygenate to maintain sats over 93%
Summary
1. Hypoxic drive is normal
2. Oxygen to a patient with hypoxic drive causing respiratory rate depression is a MYTH.
3. The Haldane effect inhibits CO2 transportation for excretion in over oxygenated COPD patients.
Give Oxygen Judiciously, and have a sound reason to use this poisonous gas.
Share this with your paramedic/EMT, nurse friends and pages.
Like and share our page.
Friday, 7 February 2014
63 - Albumin - what is it ?
KYJ 63- Albumin
Not to be confused with albumen which is egg white, albumin is the principle protein in plasma.
It is made in the liver, and is a large protein molecule in your blood that has many important functions. It carries hormones, and blood fats, and even binds to many drugs for transport around the body.
Arguably the most important task for albumin is that it acts like a water magnet assisting to maintain blood volume.
Your capillaries have tiny pores in them that leak water from plasma into the interstitial spaces between the blood vessels and cells. As blood pressure increases, this pushes more water out, just like turning up the tap on a lawn soaker hose. Albumin in your vessels exerts a counter pressure called "colloid oncotic pressure" reducing uncontrollable loss.
Being a large protein molecule, and positively charged, albumin is not excreted by the kidneys , but in kidney diseases or inflammation , albumen is excreted and may become depleted in plasma.
Another mechanism of low albumen (hypoalbuminaemia) levels is liver failure where this essential protein is not manufactured.
Irrespective of route cause of hypoalbuminaemia, less albumin equates to less oncotic pressure holding water in the blood. This allows for excessive leakage into the interstitial spaces. Resulting in swelling of ankles (with pitting), gross water weight gain, reduced urine output, and general bloating around the abdomen.
Video of Oedema
The other down side to low albumin is the inability to carry some hormones, fats and drugs that need to plasma protein bound.
Albumin (plasma protein) should not be confused with the closely named albumen, which is Egg white protein. The similarities are very obvious, both words mean "white protein". But our albumin is made in the liver, and albumen comes out of the bum of a chook. Incidentally, it tastes great as a pavlova. Albumen that is.
Knowing your Jargon (KYJ)... Lubricating the minds of the multitudes. Check our youTube channel ( ect4health ) http://youtu.be/sdWhUmUuWqc
and our blogs.
Www.knowingyourjargon.blogspot.com
My little contribution to #FOAMed
Not to be confused with albumen which is egg white, albumin is the principle protein in plasma.
It is made in the liver, and is a large protein molecule in your blood that has many important functions. It carries hormones, and blood fats, and even binds to many drugs for transport around the body.
Arguably the most important task for albumin is that it acts like a water magnet assisting to maintain blood volume.
Your capillaries have tiny pores in them that leak water from plasma into the interstitial spaces between the blood vessels and cells. As blood pressure increases, this pushes more water out, just like turning up the tap on a lawn soaker hose. Albumin in your vessels exerts a counter pressure called "colloid oncotic pressure" reducing uncontrollable loss.
Being a large protein molecule, and positively charged, albumin is not excreted by the kidneys , but in kidney diseases or inflammation , albumen is excreted and may become depleted in plasma.
Another mechanism of low albumen (hypoalbuminaemia) levels is liver failure where this essential protein is not manufactured.
Irrespective of route cause of hypoalbuminaemia, less albumin equates to less oncotic pressure holding water in the blood. This allows for excessive leakage into the interstitial spaces. Resulting in swelling of ankles (with pitting), gross water weight gain, reduced urine output, and general bloating around the abdomen.
Video of Oedema
The other down side to low albumin is the inability to carry some hormones, fats and drugs that need to plasma protein bound.
Albumin (plasma protein) should not be confused with the closely named albumen, which is Egg white protein. The similarities are very obvious, both words mean "white protein". But our albumin is made in the liver, and albumen comes out of the bum of a chook. Incidentally, it tastes great as a pavlova. Albumen that is.
Knowing your Jargon (KYJ)... Lubricating the minds of the multitudes. Check our youTube channel ( ect4health ) http://youtu.be/sdWhUmUuWqc
and our blogs.
Www.knowingyourjargon.blogspot.com
My little contribution to #FOAMed
62 _ Nephrotic Syndrome
KYJ 62 - Nephrotic Syndrome
So a middle aged fit healthy man arrived with bilateral pitting oedema to the knees. He has noted the progressing swelling from ankle oedema a week ago to this today, and mentions that he was short of breath just getting dressed.
No medical history. Fit as an ox, hard working farming labourer.
Ankle oedema is a really common symptom with lots of causes, but these can be condensed into two principles.
To understand both it is important to recap how capillaries leak. Capillaries are pipes full of microscopic pin holes. The holes are big enough to allow water and salts and other small molecules to leak from the blood stream but large molecules like protein (eg Albumen) stay inside. Albumen is like a water magnet. It attracts water, holding on to blood volume and preventing excessive volume loss (hypovolaemia).
If the blood pressure is too high (hydrostatic pressure) then plasma is pushed out of capillaries causing oedema.
Likewise if there is not enough albumen in the blood stream (oncotic pressure), then there are not enough water magnets in the capillary to hold in plasma. Water then leaks out, causing oedema.
So, low albumen levels in blood could be :
1: loss of albumen or
2: reduced production of Albumen
In Nephrotic syndrome, inflammation of the glomerular apparatus (all 1.2 million of them in your kidneys), causes these sieve like filters to allow big albumen and other proteins to slip through the kidneys and be lost into urine.
Over time albumen levels in blood drop to a critical level, allowing capillaries in the legs, abdomen and lungs to leak plasma. This causes oedema.
On pathology the Biochem shows elevated Urea and creatinine. And s markedly reduced Glomerular filtration rate (GFR).
LFTs results typically show normal LFTs but markedly reduced serum Albumen.
Urine will predictably show large protein, and, depending on inflammation, occasionally blood.
The clincher is often hypertension. As kidneys fail, they leak protein, but overall filtration of blood is reduced leaving the patient hypervolaemic. This excess vascular fluid increases blood pressure, which causes even more oedema.
Viscous cycle.
Treatment is to reduce BP, administer anti inflammatories, and if needed, give Albumen.
Interesting case. With some cool pathophysiology.
Have seen an interesting case of something recently?
So a middle aged fit healthy man arrived with bilateral pitting oedema to the knees. He has noted the progressing swelling from ankle oedema a week ago to this today, and mentions that he was short of breath just getting dressed.
No medical history. Fit as an ox, hard working farming labourer.
Ankle oedema is a really common symptom with lots of causes, but these can be condensed into two principles.
To understand both it is important to recap how capillaries leak. Capillaries are pipes full of microscopic pin holes. The holes are big enough to allow water and salts and other small molecules to leak from the blood stream but large molecules like protein (eg Albumen) stay inside. Albumen is like a water magnet. It attracts water, holding on to blood volume and preventing excessive volume loss (hypovolaemia).
If the blood pressure is too high (hydrostatic pressure) then plasma is pushed out of capillaries causing oedema.
Likewise if there is not enough albumen in the blood stream (oncotic pressure), then there are not enough water magnets in the capillary to hold in plasma. Water then leaks out, causing oedema.
So, low albumen levels in blood could be :
1: loss of albumen or
2: reduced production of Albumen
In Nephrotic syndrome, inflammation of the glomerular apparatus (all 1.2 million of them in your kidneys), causes these sieve like filters to allow big albumen and other proteins to slip through the kidneys and be lost into urine.
Over time albumen levels in blood drop to a critical level, allowing capillaries in the legs, abdomen and lungs to leak plasma. This causes oedema.
On pathology the Biochem shows elevated Urea and creatinine. And s markedly reduced Glomerular filtration rate (GFR).
LFTs results typically show normal LFTs but markedly reduced serum Albumen.
Urine will predictably show large protein, and, depending on inflammation, occasionally blood.
The clincher is often hypertension. As kidneys fail, they leak protein, but overall filtration of blood is reduced leaving the patient hypervolaemic. This excess vascular fluid increases blood pressure, which causes even more oedema.
Viscous cycle.
Treatment is to reduce BP, administer anti inflammatories, and if needed, give Albumen.
Interesting case. With some cool pathophysiology.
Have seen an interesting case of something recently?
Saturday, 1 February 2014
61 - ABO blood types and Rhesus D
KYJ 61 - Understanding Blood Groups.
Last month I got a request from a nurse working in an oncology unit with patients needing frequent transfusions. The request was "can you explain some immunology terms and the concept of blood types?"
Bang!! Let's do it.
There are 4 main blood blood groups, and each group has a positive (+) or a negative (-) attached to their group.
The blood group refers to their Red Blood Cells.
In the surface of an RBC there are many chemicals called Antigens. These antigens are like ID badges that allows the body to recognise the RBC as one of its own.
RBCs are like nurses.
Some have ID badges that say "A", some have "B" badges, and some wear both "A" & "B" badges, then there are nurses who never got a badge.
Nurses wearing type A badges are called Type A nurses (type A blood).
Nurses with a type B badge are called Type B nurses (B blood), and nurses with both are called type AB.
Those with no ID badge are called Type O, which means zero. They are not wearing any ID label.
There we have A, B , AB, and O blood groups.
Now here is where it gets tricky.
In people with type A blood, they have an immune fighting chemical in plasma called anti-B antibodies. In People with type B blood, they have anti-A antibodies.
People with type O blood have both antibodies. And AB people have none.
So if I gave you a blood transfusion with an incompatible blood type, then your immune system will attack the "foreign" blood cell's antigen with these antibodies.
B people (because they attack A blood) can't have A blood, or AB blood .
"A" people cant be given B or AB blood,
"O" people fight all other groups so can't have A , B , or AB transfusions.
But AB people can have anybody's blood, because they don't have the AntiA or antiB antibodies. AB people are the easiest to transfuse, and as such, are called the "universal recipient".
In a similar fashion, type O blood people are the "universal donor" because their blood can be given to any one. Often in trauma, when minutes count, a person is given type O blood while the crossmatch blood test is being performed.
Now another antigen on the red blood cell is called a Rhesus factor D. Abbreviated to RhD.
All RBCs may this antigen; in which case they are called RhD(+) or just "positive". If there is no RhD antigen, they are RhD(-) or just "negative".
So we have ABO blood groups and each of these can be RhD positive or negative.
When cross matching blood for transfusions, they match not only the ABO group, but the RhD antigen too.
Any RhD positive blood that is given to RhD negative people can spark a transfusion reaction called a haemolytic reaction, where blood cells explode.
RhD(-) people have an antibody to detect the D antigen and attack it. To suppress this reaction, a negative person can be given an injection of AntiD which inhibits the RhD(-) persons body from making antibodies to fight (+) blood. This really only becomes an issue in negative women giving birth to an RhD(+) baby, where there is a chance during labour that their blood should mix.
So in summary:
B+ blood means that the red blood cell has a B antigen and an RhD antigen on its surface
AB+ blood has all three A, B and RhD.
O- blood in contrast has no antigens. And so if it was given to any one there is no cause to expect a transfusion reaction.
Come and check out our Facebook group: www.facebook.com/ect4health
Last month I got a request from a nurse working in an oncology unit with patients needing frequent transfusions. The request was "can you explain some immunology terms and the concept of blood types?"
Bang!! Let's do it.
There are 4 main blood blood groups, and each group has a positive (+) or a negative (-) attached to their group.
The blood group refers to their Red Blood Cells.
In the surface of an RBC there are many chemicals called Antigens. These antigens are like ID badges that allows the body to recognise the RBC as one of its own.
RBCs are like nurses.
Some have ID badges that say "A", some have "B" badges, and some wear both "A" & "B" badges, then there are nurses who never got a badge.
Nurses wearing type A badges are called Type A nurses (type A blood).
Nurses with a type B badge are called Type B nurses (B blood), and nurses with both are called type AB.
Those with no ID badge are called Type O, which means zero. They are not wearing any ID label.
There we have A, B , AB, and O blood groups.
Now here is where it gets tricky.
In people with type A blood, they have an immune fighting chemical in plasma called anti-B antibodies. In People with type B blood, they have anti-A antibodies.
People with type O blood have both antibodies. And AB people have none.
So if I gave you a blood transfusion with an incompatible blood type, then your immune system will attack the "foreign" blood cell's antigen with these antibodies.
B people (because they attack A blood) can't have A blood, or AB blood .
"A" people cant be given B or AB blood,
"O" people fight all other groups so can't have A , B , or AB transfusions.
But AB people can have anybody's blood, because they don't have the AntiA or antiB antibodies. AB people are the easiest to transfuse, and as such, are called the "universal recipient".
In a similar fashion, type O blood people are the "universal donor" because their blood can be given to any one. Often in trauma, when minutes count, a person is given type O blood while the crossmatch blood test is being performed.
Now another antigen on the red blood cell is called a Rhesus factor D. Abbreviated to RhD.
All RBCs may this antigen; in which case they are called RhD(+) or just "positive". If there is no RhD antigen, they are RhD(-) or just "negative".
So we have ABO blood groups and each of these can be RhD positive or negative.
When cross matching blood for transfusions, they match not only the ABO group, but the RhD antigen too.
Any RhD positive blood that is given to RhD negative people can spark a transfusion reaction called a haemolytic reaction, where blood cells explode.
RhD(-) people have an antibody to detect the D antigen and attack it. To suppress this reaction, a negative person can be given an injection of AntiD which inhibits the RhD(-) persons body from making antibodies to fight (+) blood. This really only becomes an issue in negative women giving birth to an RhD(+) baby, where there is a chance during labour that their blood should mix.
So in summary:
B+ blood means that the red blood cell has a B antigen and an RhD antigen on its surface
AB+ blood has all three A, B and RhD.
O- blood in contrast has no antigens. And so if it was given to any one there is no cause to expect a transfusion reaction.
Come and check out our Facebook group: www.facebook.com/ect4health
60- Bohr Effect
KYJ 60 - Bohr Effect.
So I've been preparing for some new videos which I'll film in the next few weeks. One is going to be on CO2, and how it is transported in blood. Full of jargon.
One such term is the Bohr effect.
First know that 90% of CO2 is transported in plasma as bicarb (HCO3-), 5% is dissolved in plasma like bubbles in fizz drink.
In capillaries at the tissue end, blood is giving up
Oxygen and absorbing CO2. It is transported to the lungs and CO2 is diffused off the blood and breathed out, and oxygen is diffused into blood, and transported back to tissues where the process repeats itself.
At that tissue end of respiration, As co2 rises, blood pH and oxygen carriage falls. This is called the Bohr Effect.
The Bohr effect then shifts the oxyhaemoglobin curve to the right.
So I've been preparing for some new videos which I'll film in the next few weeks. One is going to be on CO2, and how it is transported in blood. Full of jargon.
One such term is the Bohr effect.
First know that 90% of CO2 is transported in plasma as bicarb (HCO3-), 5% is dissolved in plasma like bubbles in fizz drink.
In capillaries at the tissue end, blood is giving up
Oxygen and absorbing CO2. It is transported to the lungs and CO2 is diffused off the blood and breathed out, and oxygen is diffused into blood, and transported back to tissues where the process repeats itself.
At that tissue end of respiration, As co2 rises, blood pH and oxygen carriage falls. This is called the Bohr Effect.
The Bohr effect then shifts the oxyhaemoglobin curve to the right.
59- Antibodies and Antigens - inflammation part 4 of 4
KYJ 59 - Antigens, antibodies and basic immune function.
Getting your head around the basic immunology stuff can be daunting.
In this quick post I will explore the above terms.
.
Suppose a bacteria enters your body. On its surface are chemicals. in the same way that every human you have met has a particular scent, so to do bacteria. Strep have their own strep "taste", and E-Coli have their own E-Coli "taste", and so for all microbes (bacteria, virus, paracites); there is this unique chemical on their "skin".
That Chemical scent is called an ANTIGEN.
Microbes that cause diseases are called Pathogens. You have heard of good bacteria, and bad bacteria?? Well bad ones are pathogens, and therefore pathogenic, meaning they cause illness, infection , and some cancers - eg HPV and Cervical Cancer.
...
White blood cells called B-Lymphocytes are genetically programed to recognise these pathogens because they "smell" their Antigen (scent). When they recognise a pathogen, they secrete a substance that sticks to the Antigen on the pathogen's surface.
This chemical secreted by the B-Lymphocyte is called an ANTIBODY.
Antibodies, are also referred to by their technical name - immunoglobulin abbreviated to Ig.
Now an antibody sticks to or binds to an antigen (all on the surface of the Bacteria). This antibody/antigen then is able to be recognised by killing cells called Killer T Lymphocytes, or Cytotoxic Ts.
Think of B cells as a Forrester who chooses which trees to cut down. He doesn't cut them down, he just marks the tree for distruction.
So B Cell the Forrester (Barry) ties a pink ribbon around the trunks . The pink Ribbon is an Antibody (Ig).
Now Tom the Lumberjack (Killer T Lymphocyte) sees the trees that need destroying, and attacks them with his toxic poison (chainsaw).
Now we have dead bit of tree (bacteria) lying on the forest floor. so Phil the Phagocyte cleans up the mess.
Now lets look at vaccination.
with vaccination a person is given some antigens from weakened or dead pathogens. the B Cells recognise these antigens, and start making antibodies which stay in the body for months to years. But most importantly, some T Cells are reminded of who the bad guys are, so should they be exposed to the live pathogen, they mount a rapid all out attack quickly and effectively before the disease takes hold.
Getting your head around the basic immunology stuff can be daunting.
In this quick post I will explore the above terms.
.
Suppose a bacteria enters your body. On its surface are chemicals. in the same way that every human you have met has a particular scent, so to do bacteria. Strep have their own strep "taste", and E-Coli have their own E-Coli "taste", and so for all microbes (bacteria, virus, paracites); there is this unique chemical on their "skin".
That Chemical scent is called an ANTIGEN.
Microbes that cause diseases are called Pathogens. You have heard of good bacteria, and bad bacteria?? Well bad ones are pathogens, and therefore pathogenic, meaning they cause illness, infection , and some cancers - eg HPV and Cervical Cancer.
...
White blood cells called B-Lymphocytes are genetically programed to recognise these pathogens because they "smell" their Antigen (scent). When they recognise a pathogen, they secrete a substance that sticks to the Antigen on the pathogen's surface.
This chemical secreted by the B-Lymphocyte is called an ANTIBODY.
Antibodies, are also referred to by their technical name - immunoglobulin abbreviated to Ig.
Now an antibody sticks to or binds to an antigen (all on the surface of the Bacteria). This antibody/antigen then is able to be recognised by killing cells called Killer T Lymphocytes, or Cytotoxic Ts.
Think of B cells as a Forrester who chooses which trees to cut down. He doesn't cut them down, he just marks the tree for distruction.
So B Cell the Forrester (Barry) ties a pink ribbon around the trunks . The pink Ribbon is an Antibody (Ig).
Now Tom the Lumberjack (Killer T Lymphocyte) sees the trees that need destroying, and attacks them with his toxic poison (chainsaw).
Now we have dead bit of tree (bacteria) lying on the forest floor. so Phil the Phagocyte cleans up the mess.
Now lets look at vaccination.
with vaccination a person is given some antigens from weakened or dead pathogens. the B Cells recognise these antigens, and start making antibodies which stay in the body for months to years. But most importantly, some T Cells are reminded of who the bad guys are, so should they be exposed to the live pathogen, they mount a rapid all out attack quickly and effectively before the disease takes hold.
58 - Inflammation part 3 of 4
KYJ -58 - Inflammation 3
Part 3 in our understanding of inflammation.
Today we pick up where we left off. Lymphocytes.
Lymphocytes are specialised white cells that kill microbes in a few ways. They are categorised into Natural Killers (NK cells), B-cells (made in bones) and T Cells (made in the Thymus gland).
B cells make large quantities of proteins called Immunoglobulins (antibodies) which attach to bacteria and neutralise them. A bit like fly spray killing cockroaches.
T cells are classified as Cytotoxic T cells, or Helper T cells.
CytotoxicTs produce enzymes, that kill body cells that have become infected by bacteria and viruses.
HelperTs produce chemical attractants called cytokines (think "Impulse body spray") that attracts killer cells and phagocytes to attack pathogens.
Both B and T cells are capable of remembering the antigens (nasties) that they come into contact with. The next time the same germ invades, they mount an all out attack by releasing antibodies and cytokines.
If tissues become infected by viruses or tumor cells, they release chemical signals called Interferons that attract NK Cells. These NKcells then attack and destroy cancer cells and infected tissue cells before they get out of control.
Lymphocytes are responsible for life long immunity, and are the rock stars of the vaccination world.
You may have heard of Cell-mediated immunity. This means the blood cells do the killing. Neutrophils, B-Cells, Macrophages all contribute to cell-mediated immunity. Batman, Spider-Man and the foot soldiers.
Humoral immunity is all about the chemicals- immunoglobulins (antibodies), interferons and other cytokines being released by tissue cells, and lymphocytes.
Next episode well look at the other phils. White blood cells called Eosinophils and Basophils.
Part 3 in our understanding of inflammation.
Today we pick up where we left off. Lymphocytes.
Lymphocytes are specialised white cells that kill microbes in a few ways. They are categorised into Natural Killers (NK cells), B-cells (made in bones) and T Cells (made in the Thymus gland).
B cells make large quantities of proteins called Immunoglobulins (antibodies) which attach to bacteria and neutralise them. A bit like fly spray killing cockroaches.
T cells are classified as Cytotoxic T cells, or Helper T cells.
CytotoxicTs produce enzymes, that kill body cells that have become infected by bacteria and viruses.
HelperTs produce chemical attractants called cytokines (think "Impulse body spray") that attracts killer cells and phagocytes to attack pathogens.
Both B and T cells are capable of remembering the antigens (nasties) that they come into contact with. The next time the same germ invades, they mount an all out attack by releasing antibodies and cytokines.
If tissues become infected by viruses or tumor cells, they release chemical signals called Interferons that attract NK Cells. These NKcells then attack and destroy cancer cells and infected tissue cells before they get out of control.
Lymphocytes are responsible for life long immunity, and are the rock stars of the vaccination world.
You may have heard of Cell-mediated immunity. This means the blood cells do the killing. Neutrophils, B-Cells, Macrophages all contribute to cell-mediated immunity. Batman, Spider-Man and the foot soldiers.
Humoral immunity is all about the chemicals- immunoglobulins (antibodies), interferons and other cytokines being released by tissue cells, and lymphocytes.
Next episode well look at the other phils. White blood cells called Eosinophils and Basophils.
57 - Inflammation part 2 of 4
KYJ -57 Inflammation 2
Part 2 in our understanding inflammation.
In episode 1, I briefly over viewed the typical acute inflammation symptoms. Any body part that becomes inflamed is usually given the suffix "itis". Tonsillitis is inflammation of the tonsils. Urethritis is inflammation of the urethra, cystitis is inflammation of the bladder (cyst=bladder), and Arthritis is inflammation of a joint (arthro= joint).
Spiderman to the rescue!!
So let's suppose an organism infects a site. Make it a tissue infection like a bacterial skin infection. A splinter while gardening, removed with tweezers and washed at the time of injury.
Yet bacteria got into the wound. Injured tissue releases chemicals from damaged epithelial cells inside tiny blood vessels. This chemical release of signalling chemicals is called chemotaxis. These chemicals are multiple types of proteins, and peptides that are collectively called cytokines (meaning cell attractors).
Cytokines like histamine and interleukin are secreted which causes the first in a cascade of white blood cells called Neutrophils to mobilise to the area of injury. Histamine causes vasodilation which increases blood flow to bring more neutrophils, and it forces capillaries to open their pores, allowing Neutrophils to migrate out of the blood vessel and into the site of tissue damage and bacteria.
Once at the scene of the "crime", neutrophils ingest bacteria, and dead cells. They are types of phagocytes meaning eating cells, but they also attack bacteria with chemicals that dissolve and digest their cell walls.
Finally, and most impressively, Neutrophils have the unique ability to weave spider web like nets that trap bacteria and kill them. Literally NETs , these Neutrophil Extracellular Traps (NETs) are fibrous strands of protein that is literally like a toxic spiderweb that serves as a physical barrier to wall off areas of infection. Very typical in skin infections like pimples, boils and abscesses. Neutrophils are just like SpiderMan spinning a web.
Superman follows
Clark Kent (AKA Superman) was a reporter. He could fight evil, but also report on it. And that is exactly what happens next.
Macrophages are another type of phagocyte that migrates to the area to assist neutrophils. They digest and mop up cellular debris, but in addition to the killing, they record information about the bacteria and having a taste of the bacteria (antigen), the the Macrophage reports a description to the Lymphocyte who then produces toxic killing and signalling chemicals called Antibodies (or Immunoglobulins).
And that is our next episode in the series on inflammation in "Knowing your Jargon".
Summary:
Spider-Man (neutrophils) first at the crime site. Kills bad guys, and sets NETs (traps).
Superman (Macrophage) is close second, kills more bad guys and tips off the media (Lymphocyte).
Part 2 in our understanding inflammation.
In episode 1, I briefly over viewed the typical acute inflammation symptoms. Any body part that becomes inflamed is usually given the suffix "itis". Tonsillitis is inflammation of the tonsils. Urethritis is inflammation of the urethra, cystitis is inflammation of the bladder (cyst=bladder), and Arthritis is inflammation of a joint (arthro= joint).
Spiderman to the rescue!!
So let's suppose an organism infects a site. Make it a tissue infection like a bacterial skin infection. A splinter while gardening, removed with tweezers and washed at the time of injury.
Yet bacteria got into the wound. Injured tissue releases chemicals from damaged epithelial cells inside tiny blood vessels. This chemical release of signalling chemicals is called chemotaxis. These chemicals are multiple types of proteins, and peptides that are collectively called cytokines (meaning cell attractors).
Cytokines like histamine and interleukin are secreted which causes the first in a cascade of white blood cells called Neutrophils to mobilise to the area of injury. Histamine causes vasodilation which increases blood flow to bring more neutrophils, and it forces capillaries to open their pores, allowing Neutrophils to migrate out of the blood vessel and into the site of tissue damage and bacteria.
Once at the scene of the "crime", neutrophils ingest bacteria, and dead cells. They are types of phagocytes meaning eating cells, but they also attack bacteria with chemicals that dissolve and digest their cell walls.
Finally, and most impressively, Neutrophils have the unique ability to weave spider web like nets that trap bacteria and kill them. Literally NETs , these Neutrophil Extracellular Traps (NETs) are fibrous strands of protein that is literally like a toxic spiderweb that serves as a physical barrier to wall off areas of infection. Very typical in skin infections like pimples, boils and abscesses. Neutrophils are just like SpiderMan spinning a web.
Superman follows
Clark Kent (AKA Superman) was a reporter. He could fight evil, but also report on it. And that is exactly what happens next.
Macrophages are another type of phagocyte that migrates to the area to assist neutrophils. They digest and mop up cellular debris, but in addition to the killing, they record information about the bacteria and having a taste of the bacteria (antigen), the the Macrophage reports a description to the Lymphocyte who then produces toxic killing and signalling chemicals called Antibodies (or Immunoglobulins).
And that is our next episode in the series on inflammation in "Knowing your Jargon".
Summary:
Spider-Man (neutrophils) first at the crime site. Kills bad guys, and sets NETs (traps).
Superman (Macrophage) is close second, kills more bad guys and tips off the media (Lymphocyte).
56 - Inflammation part 1 of 4
KYJ 56- Inflammation (Series)
Part 1.
One of the common pathophysiological processes central to many acute and chronic diseases is Inflammation.
Being a process, like coagulation which we covered in a previous series, the inflammatory process has many steps, and complicated cocktails of chemicals are released from many tissues to activate, sustain or inhibit the process.
Inflammation (literally to catch fire) is a process mounted by the immune system to respond to fight pathogens, clean up cellular debris after injury or infection, and repair damaged tissue.
The classic symptoms of inflammation include:
Rubor = Redness (Erythaema)
Calor = Heat
Tumor = Swelling (Oedema)
Dolor = Pain.
Typically an inflamed body part is painful, red, hot and swollen. The redness and heat is why the Latin term inflammation (to catch fire) was used to describe the syndrome.
In this first of a few parts series, we will look at the end result and pathophysiology of these four symptoms, then in subsequent episodes of KYJ, I will take you through the cellular steps.
But first: the symptoms.
Red, hot, swollen.
Erythaema or redness off tissue is seen as a direct result of an increase of blood flow. During an inflammatory response, blood vessels are stimulated by chemicals released by damaged cells, which widen the local blood vessels (vasodilation). The result is higher blood flow which blushes the local tissues giving rise to the characteristic redness and increase of temperature in inflamed tissue (red and hot)
Oedema - swollen
If you missed our video on oedema, here is the link. ( http://youtu.be/sdWhUmUuWqc ). Oedema is swelling of tissue. As a consequence of the dilation of blood vessels I just discussed, it is reasonable to assume that an increase in blood flow would result in an increase in blood pressure in the local area.
Now the smallest blood vessels in tissues are capillaries; and these blood vessels are tiny- just a single cell thick and full of little holes that allow substances (nourishment and wastes) to leak from inside the capillary. Water in the plasma of the blood leaks out of these holes (fenestrations), and this leakage is in part due to how high the pressure in the blood vessel is. This pressure is called hydrostatic pressure. The higher the blood flow through capillaries (hydrostatic pressure) the more they leak. It is just like those green soaker garden hoses you probably once played under on a hot summer day. If you turn up the tap (hydrostatic pressure) then it leaks more water, and capillaries are no different. In locally inflamed tissue however, damaged capillaries have larger holes in them, so not only do they leak more plasma, but now they also leak a blood protein called Albumen. Albumen is that plasma protein which acts like a water magnet holding volume inside the vast network of capillaries. With out albumen you would leak uncontrollably. As damaged capillaries lose albumen into the tissue spaces surrounding the blood vessel. The albumen, now in the interstitial space, attracts more plasma to leak from capillaries and surrounding cells. The accumulation of fluid in the tissues is called oedema.
Next episode we look at the cellular chemicals and funky stuff like cytokines, and chemotaxis.
Check out my other vids on the YouTube channel called, funnily enough - ECT4Health.
Part 1.
One of the common pathophysiological processes central to many acute and chronic diseases is Inflammation.
Being a process, like coagulation which we covered in a previous series, the inflammatory process has many steps, and complicated cocktails of chemicals are released from many tissues to activate, sustain or inhibit the process.
Inflammation (literally to catch fire) is a process mounted by the immune system to respond to fight pathogens, clean up cellular debris after injury or infection, and repair damaged tissue.
The classic symptoms of inflammation include:
Rubor = Redness (Erythaema)
Calor = Heat
Tumor = Swelling (Oedema)
Dolor = Pain.
Typically an inflamed body part is painful, red, hot and swollen. The redness and heat is why the Latin term inflammation (to catch fire) was used to describe the syndrome.
In this first of a few parts series, we will look at the end result and pathophysiology of these four symptoms, then in subsequent episodes of KYJ, I will take you through the cellular steps.
But first: the symptoms.
Red, hot, swollen.
Erythaema or redness off tissue is seen as a direct result of an increase of blood flow. During an inflammatory response, blood vessels are stimulated by chemicals released by damaged cells, which widen the local blood vessels (vasodilation). The result is higher blood flow which blushes the local tissues giving rise to the characteristic redness and increase of temperature in inflamed tissue (red and hot)
Oedema - swollen
If you missed our video on oedema, here is the link. ( http://youtu.be/sdWhUmUuWqc ). Oedema is swelling of tissue. As a consequence of the dilation of blood vessels I just discussed, it is reasonable to assume that an increase in blood flow would result in an increase in blood pressure in the local area.
Now the smallest blood vessels in tissues are capillaries; and these blood vessels are tiny- just a single cell thick and full of little holes that allow substances (nourishment and wastes) to leak from inside the capillary. Water in the plasma of the blood leaks out of these holes (fenestrations), and this leakage is in part due to how high the pressure in the blood vessel is. This pressure is called hydrostatic pressure. The higher the blood flow through capillaries (hydrostatic pressure) the more they leak. It is just like those green soaker garden hoses you probably once played under on a hot summer day. If you turn up the tap (hydrostatic pressure) then it leaks more water, and capillaries are no different. In locally inflamed tissue however, damaged capillaries have larger holes in them, so not only do they leak more plasma, but now they also leak a blood protein called Albumen. Albumen is that plasma protein which acts like a water magnet holding volume inside the vast network of capillaries. With out albumen you would leak uncontrollably. As damaged capillaries lose albumen into the tissue spaces surrounding the blood vessel. The albumen, now in the interstitial space, attracts more plasma to leak from capillaries and surrounding cells. The accumulation of fluid in the tissues is called oedema.
Next episode we look at the cellular chemicals and funky stuff like cytokines, and chemotaxis.
Check out my other vids on the YouTube channel called, funnily enough - ECT4Health.
Friday, 24 January 2014
55 - Creatine Kinase (CK)
KYJ 55 - CK creatine kinase.
In our KYJs (knowing your jargon), we explore terms you hear at work, but don't always understand.
Today is a blood test value called CK or creatine kinase.
First let's look at the word. 'Creatine' , it looks like 'create' and that is what it does. Creatine is an organic acid made from nitrogen. Muscles, being protein, are highly nitrogenous, and as muscle cells need a very high production of energy, creatine is needed in a reaction with the chemical that functions as cellular energy. We covered in out cell biology video.
Do you remember the name of the energy? Adenosine triphosphate (ATP).
So creatine is abundant in muscle cells.
Creatine is enzymatically broken down by an enzyme called a kinase. After being acted on by CK, it binds with a phosphate molecule. It is then referred to as phosphocreatine
Our subject today is that enzyme. Creatine Kinase = CK.
CK or more correctly CPK, is creatine phosphokinase, an enzyme that is secreted by cells to create a chemical reaction between Creatine and ATPinto its waste byproduct called creatinine...this is excreted via the kidneys. Note how similar these two words are.
In different tissues there are different types of creatine kinase Cardiac tissue has a CK with two sub categories. CK-M, and CK-B. Together these CKs are released when heart muscle tissue is injured. For this reason, a blood test called CK-MB was once used to diagnose MI, but due to insensitivity, it has been replaced by Troponin testing.
So normally CK is found in blood between 60 - 175 units/L.
It is elevated in any injury to muscle (MI, Rhabdomyolysis) where it is most abundant.
There is also elevated CK in patients with Thyroid dysfunction (low Thyroxine) . It therefore has value in monitoring patients with Hypothyroidism. One study talked about Anticholesterol drugs like Lipitor (Statins) having links to raised CK.
In patients with alcoholic liver disease /failure, the CK can be low.
So there you have it. CK is an enzyme that catalyses a reaction between ATP and Creatine, to form creatinine that gets excreted in urine.
In our KYJs (knowing your jargon), we explore terms you hear at work, but don't always understand.
Today is a blood test value called CK or creatine kinase.
First let's look at the word. 'Creatine' , it looks like 'create' and that is what it does. Creatine is an organic acid made from nitrogen. Muscles, being protein, are highly nitrogenous, and as muscle cells need a very high production of energy, creatine is needed in a reaction with the chemical that functions as cellular energy. We covered in out cell biology video.
Do you remember the name of the energy? Adenosine triphosphate (ATP).
So creatine is abundant in muscle cells.
Creatine is enzymatically broken down by an enzyme called a kinase. After being acted on by CK, it binds with a phosphate molecule. It is then referred to as phosphocreatine
Our subject today is that enzyme. Creatine Kinase = CK.
CK or more correctly CPK, is creatine phosphokinase, an enzyme that is secreted by cells to create a chemical reaction between Creatine and ATPinto its waste byproduct called creatinine...this is excreted via the kidneys. Note how similar these two words are.
In different tissues there are different types of creatine kinase Cardiac tissue has a CK with two sub categories. CK-M, and CK-B. Together these CKs are released when heart muscle tissue is injured. For this reason, a blood test called CK-MB was once used to diagnose MI, but due to insensitivity, it has been replaced by Troponin testing.
So normally CK is found in blood between 60 - 175 units/L.
It is elevated in any injury to muscle (MI, Rhabdomyolysis) where it is most abundant.
There is also elevated CK in patients with Thyroid dysfunction (low Thyroxine) . It therefore has value in monitoring patients with Hypothyroidism. One study talked about Anticholesterol drugs like Lipitor (Statins) having links to raised CK.
In patients with alcoholic liver disease /failure, the CK can be low.
So there you have it. CK is an enzyme that catalyses a reaction between ATP and Creatine, to form creatinine that gets excreted in urine.
54 - Primary Assessment- Exposure
KYJ 54. E = Expose
Part 5 of 5 part series on Primary Survey.
Expose & Environment
While some texts choose to cap primary survey at ABCD. Many trauma authors include E for exposure and environmental considerations, as part of the primary survey procedure. Irrespective of opinion it's inclusion in the end of Primary or beginning of Secondary assessment, is a foolish and meaningless semantic debate. The fact remains that if a patient is not fully exposed, visual assessment can not be accurate or complete.
This two tiered approach includes physical removal of the patients clothing. If appropriate, safe and not contraindicated (burnt to the skin), attempts should be made to remove clothing in damaged. Many patients however, require their clothing to be cut off with shears, or scissors.
Clothing removed from a patient post alleged criminal activity should be stored in a paper or breathable bag, to preserve potential forensic evidence. Label all items removed from a patient, and preferably have an itemised documentation witnessed by another colleague.
Once naked (or near naked) the patient must be covered with warm blankets. One of the three lethal silent killers in a trauma room is hypothermia.
It is Hypothermia prevention that is most detrimental, and so referred to as Environmental considerations.
Ensure that susceptible patients are kept warm, and dry.
Patients most at risk from hypothermia are :
• shock
• children (especially babies)
• elderly
• burns >10% BSA
• high spinal patients (above T6)
• wet (urine/water)
Hypothermia causes haemoglobin to bind tight to oxygen. Cold patients carry oxygen well, but won't pass it to the cells that need it. Their sats are good, but they are hypoxic at a cellular level, giving rise to the development of acidosis which renders haemoglobin unable to transport oxygen, worsening hypoxia.
Keep them warm or they will die!!
Part 5 of 5 part series on Primary Survey.
Expose & Environment
While some texts choose to cap primary survey at ABCD. Many trauma authors include E for exposure and environmental considerations, as part of the primary survey procedure. Irrespective of opinion it's inclusion in the end of Primary or beginning of Secondary assessment, is a foolish and meaningless semantic debate. The fact remains that if a patient is not fully exposed, visual assessment can not be accurate or complete.
This two tiered approach includes physical removal of the patients clothing. If appropriate, safe and not contraindicated (burnt to the skin), attempts should be made to remove clothing in damaged. Many patients however, require their clothing to be cut off with shears, or scissors.
Clothing removed from a patient post alleged criminal activity should be stored in a paper or breathable bag, to preserve potential forensic evidence. Label all items removed from a patient, and preferably have an itemised documentation witnessed by another colleague.
Once naked (or near naked) the patient must be covered with warm blankets. One of the three lethal silent killers in a trauma room is hypothermia.
It is Hypothermia prevention that is most detrimental, and so referred to as Environmental considerations.
Ensure that susceptible patients are kept warm, and dry.
Patients most at risk from hypothermia are :
• shock
• children (especially babies)
• elderly
• burns >10% BSA
• high spinal patients (above T6)
• wet (urine/water)
Hypothermia causes haemoglobin to bind tight to oxygen. Cold patients carry oxygen well, but won't pass it to the cells that need it. Their sats are good, but they are hypoxic at a cellular level, giving rise to the development of acidosis which renders haemoglobin unable to transport oxygen, worsening hypoxia.
Keep them warm or they will die!!
53 - Primary Assessment - Disability
KYJ 53- D= Disability
Part 4 of 5 part series on Primary Survey.
Disability- neuro assessment
Fourth step in the process of primary assessment is to determine if the patient is rousable.
The assessment is divided into two parts.
Alertness and pupils
Alertness is an assessment of the level of consciousness. Altered consciousness exists on a spectrum of wide awake/alert/orientated through to Unresponsive/comatose.
Scored on the first part of a Glascow coma scale, the assessment of LOC uses the familiar mnemonic
A.V.P.U
Alert- spontaneous awake patient
Verbal- the patient needs your voice to rouse/stir. Speak the patients name. If he responds in any way, he scores a "V" for verbal
Pain- if he won't respond to your verbal stimuli, inflict a painful gesture. There are only two acceptable stimuli.
Supra orbital pressure (if no obvious eye/face trauma)
Trapezeus pinch/twist.
Do NOT use Sternal rubs, nipple cripples, chest hair pulls, fingernail bed pressure, pinched earlobes, or any peripheral stimuli as it will not be effective if the patient had a high spinal injury. All the Sternal rubbing in the world won't wake me up if I had a severed C7. So do I not respond due to head related reasons, or because my spinal injury renders me anaesthetised from the neck down??!!
If your patient responds in any way to a painful stimulus, then they score a "P" for pain.
Finally is a patient who neither responds to voice or pain. These patients are unresponsive and score a "U".
If they are a P or a U they are in the PU ( poo ) !! This refers to the fact that patients scoring A or V can maintain their own airway, and tongue obstruction is no risk. Patients in the PU can't protect their airway, and an adjunct needs to be inserted. Hence, AVPU assessment is a life saving assessment.
The final part of this assessment is pupil response. Using a dedicated penlight, assess both eyes pupils for size , shape, and consensual reaction to light. Both pupils should constrict briskly to light irrespective of which eye you shine the torch into.
A sluggish or poorly reacting pupil is an indicator that the cause of the patients altered conscious state is cerebral and not shock, or chemical related. Despite narcotic induced constriction, pupils will still demonstrate reaction.
Note 20-25% of the population have one pupil at a different size to the other. Size is not diagnostic, reaction to light is.
Remember : AVPU- if they are a P or a U they're in the PU !
PEARL= pupils equal and reacting to light.
Remember to Share with your colleagues.
Part 4 of 5 part series on Primary Survey.
Disability- neuro assessment
Fourth step in the process of primary assessment is to determine if the patient is rousable.
The assessment is divided into two parts.
Alertness and pupils
Alertness is an assessment of the level of consciousness. Altered consciousness exists on a spectrum of wide awake/alert/orientated through to Unresponsive/comatose.
Scored on the first part of a Glascow coma scale, the assessment of LOC uses the familiar mnemonic
A.V.P.U
Alert- spontaneous awake patient
Verbal- the patient needs your voice to rouse/stir. Speak the patients name. If he responds in any way, he scores a "V" for verbal
Pain- if he won't respond to your verbal stimuli, inflict a painful gesture. There are only two acceptable stimuli.
Supra orbital pressure (if no obvious eye/face trauma)
Trapezeus pinch/twist.
Do NOT use Sternal rubs, nipple cripples, chest hair pulls, fingernail bed pressure, pinched earlobes, or any peripheral stimuli as it will not be effective if the patient had a high spinal injury. All the Sternal rubbing in the world won't wake me up if I had a severed C7. So do I not respond due to head related reasons, or because my spinal injury renders me anaesthetised from the neck down??!!
If your patient responds in any way to a painful stimulus, then they score a "P" for pain.
Finally is a patient who neither responds to voice or pain. These patients are unresponsive and score a "U".
If they are a P or a U they are in the PU ( poo ) !! This refers to the fact that patients scoring A or V can maintain their own airway, and tongue obstruction is no risk. Patients in the PU can't protect their airway, and an adjunct needs to be inserted. Hence, AVPU assessment is a life saving assessment.
The final part of this assessment is pupil response. Using a dedicated penlight, assess both eyes pupils for size , shape, and consensual reaction to light. Both pupils should constrict briskly to light irrespective of which eye you shine the torch into.
A sluggish or poorly reacting pupil is an indicator that the cause of the patients altered conscious state is cerebral and not shock, or chemical related. Despite narcotic induced constriction, pupils will still demonstrate reaction.
Note 20-25% of the population have one pupil at a different size to the other. Size is not diagnostic, reaction to light is.
Remember : AVPU- if they are a P or a U they're in the PU !
PEARL= pupils equal and reacting to light.
Remember to Share with your colleagues.
52 - Primary Assessment Circulation
KYJ 52 C = Circulation
Part 3 of 5 part series on Primary Survey.
Circulation
Third step in the Primary survey is assessing circulation.
Being the third letter of the alphabet, think of three parts to this assessment.
1. Output - pulse
2. Skin indicators - colour/warmth
3. Bleeding
First is output. You want to know if the patient has a heart beat. Check carotid and radial pulse simultaneously. The carotid pulse confirms that the patient has a cardiac output with enough pressure to perfuse brain. The radial pulse confirms that you have enough output to perfuse kidneys.
Given a normal BP of 120/80 , a patient with a Systolic pressure (SBP) of above 80mmHg is able to perfuse their kidneys. They will still have s palpable radial pulse. But should their state of shock be so advanced that SBP is less than 80, then their radial pulse can't be palpated.- severe shock.
If their SBP drops below 70 the femoral and brachial pulses can't be felt.
Carotid pulse is impalpable with an SBP below 60mmHg. At this pressure, cerebral perfusion is feeble, and the patient is technically dead. BLS, and ALS and correcting the causes (Hs &Ts) is required if the patient has any chance of surviving.
Palpate the carotid and radial together. Feel tone, and gauge the rate. Fast and strong indicates early shock, whilst a rapid weak and thready pulse is late shock.
Next is skin indicators. Is the patient demonstrating pink mucous membranes, or are they showing pallor, ashen grey, of cyanosis? Remember pink is good and blue is bad!
Feel the skin- is it cool or warm? Is it dry or clammy/moist?
The classic moderate to severe shock patient demonstrates skin which is typically, pale, cold and clammy as a result to vascular perfusion being redistributed from skin to the core or central vital organs. No blood flow = pale cold and clammy!
Finally, blood loss. Is the patient bleeding? If there is uncontrolled external bleeding, then this needs immediate direct pressure and elevation.
After assessing the state of the patient's circulation, the international standard is to establish vascular access.
Formerly this required 2 large bore IV cannulas (catheters) either 24 or 16 gauge. However recently there has been a greater focus on establishment of an intraosseous catheter for severe shock and trauma, where there has been three attempts at intravenous access or a time lapse greater than 90seconds.
Many IO devices are on the market, all with limitations. A devise that is quick, reliable and secure should be favoured.
A tibial devise is of limited use with abdominal or lower limb trauma.
A humerus device is limited with upper limb or shoulder injuries,
A manubrial (sternum) device can not be used on children under 12. Despite limitations, they are easier, and quicker than traditional IV establishment, especially in shocked patients.
What IV fluid should be hung. Well that is up to your protocol, and is the proverbial "holy grail" of answers, but most trauma research is suggesting 0.9% normal saline (NaCl).
Caution with large fluid loads should be exercised, as hyperchloraemic acidosis can occur, as can fluid overload, hypothermia, and dilutional coagulopathy.
Remember most patients are already coagulopathic and have dilutional anaemia on arrival; don't make it worse.
Part 3 of 5 part series on Primary Survey.
Circulation
Third step in the Primary survey is assessing circulation.
Being the third letter of the alphabet, think of three parts to this assessment.
1. Output - pulse
2. Skin indicators - colour/warmth
3. Bleeding
First is output. You want to know if the patient has a heart beat. Check carotid and radial pulse simultaneously. The carotid pulse confirms that the patient has a cardiac output with enough pressure to perfuse brain. The radial pulse confirms that you have enough output to perfuse kidneys.
Given a normal BP of 120/80 , a patient with a Systolic pressure (SBP) of above 80mmHg is able to perfuse their kidneys. They will still have s palpable radial pulse. But should their state of shock be so advanced that SBP is less than 80, then their radial pulse can't be palpated.- severe shock.
If their SBP drops below 70 the femoral and brachial pulses can't be felt.
Carotid pulse is impalpable with an SBP below 60mmHg. At this pressure, cerebral perfusion is feeble, and the patient is technically dead. BLS, and ALS and correcting the causes (Hs &Ts) is required if the patient has any chance of surviving.
Palpate the carotid and radial together. Feel tone, and gauge the rate. Fast and strong indicates early shock, whilst a rapid weak and thready pulse is late shock.
Next is skin indicators. Is the patient demonstrating pink mucous membranes, or are they showing pallor, ashen grey, of cyanosis? Remember pink is good and blue is bad!
Feel the skin- is it cool or warm? Is it dry or clammy/moist?
The classic moderate to severe shock patient demonstrates skin which is typically, pale, cold and clammy as a result to vascular perfusion being redistributed from skin to the core or central vital organs. No blood flow = pale cold and clammy!
Finally, blood loss. Is the patient bleeding? If there is uncontrolled external bleeding, then this needs immediate direct pressure and elevation.
After assessing the state of the patient's circulation, the international standard is to establish vascular access.
Formerly this required 2 large bore IV cannulas (catheters) either 24 or 16 gauge. However recently there has been a greater focus on establishment of an intraosseous catheter for severe shock and trauma, where there has been three attempts at intravenous access or a time lapse greater than 90seconds.
Many IO devices are on the market, all with limitations. A devise that is quick, reliable and secure should be favoured.
A tibial devise is of limited use with abdominal or lower limb trauma.
A humerus device is limited with upper limb or shoulder injuries,
A manubrial (sternum) device can not be used on children under 12. Despite limitations, they are easier, and quicker than traditional IV establishment, especially in shocked patients.
What IV fluid should be hung. Well that is up to your protocol, and is the proverbial "holy grail" of answers, but most trauma research is suggesting 0.9% normal saline (NaCl).
Caution with large fluid loads should be exercised, as hyperchloraemic acidosis can occur, as can fluid overload, hypothermia, and dilutional coagulopathy.
Remember most patients are already coagulopathic and have dilutional anaemia on arrival; don't make it worse.
51 - primary Assessment Breathing
KYJ 51 - B = Breathing
Part 2 of 5 part series on Primary Survey.
Breathing
After clearing and securing airway patency, the next step in trauma patient assessment and management, is to assess for spontaneous breathing effort and effectiveness. 10 pieces of assessment criteria can be used to assess breathing.
•Rate - should be 12-20/min
•Depth - shallow or deep breathing?
•Symmetry- is the left and right chest rising equally?
•Air entry- left =right?
•Skin colour - pink is good, blue is bad!
•Jugular veins- flat, or bulging?
•Tracheal position- midline alignment?
•Chest wall integrity- foreign bodies, wounds, bruising, redness or swelling?
•Palpate-bony crepitus? Instability?
•Laboured breathing- is there accessory muscle use?
With a selection of these assessments, the clinician is able to determine how oxygen will be administered. The international gold standard for ALL breathing TRAUMA patients , is non-rebreather bag mask (NRBM) at 12-15lpm, which delivers between 75-90% Oxygen.
All trauma patients should get this regimen, unless they have ineffective breathing and require oxygenation invasively- ETT or Surgical airway
When oxygenating COPD patients who retain CO2, recognise that few patients in this population experience Hypoxic drive, which can affect their stimulus to breathe. Hyperoxygenation in this patient can lead to respiratory depression and respiratory acidosis. Watch them carefully and monitor ABGs.
Part 2 of 5 part series on Primary Survey.
Breathing
After clearing and securing airway patency, the next step in trauma patient assessment and management, is to assess for spontaneous breathing effort and effectiveness. 10 pieces of assessment criteria can be used to assess breathing.
•Rate - should be 12-20/min
•Depth - shallow or deep breathing?
•Symmetry- is the left and right chest rising equally?
•Air entry- left =right?
•Skin colour - pink is good, blue is bad!
•Jugular veins- flat, or bulging?
•Tracheal position- midline alignment?
•Chest wall integrity- foreign bodies, wounds, bruising, redness or swelling?
•Palpate-bony crepitus? Instability?
•Laboured breathing- is there accessory muscle use?
With a selection of these assessments, the clinician is able to determine how oxygen will be administered. The international gold standard for ALL breathing TRAUMA patients , is non-rebreather bag mask (NRBM) at 12-15lpm, which delivers between 75-90% Oxygen.
All trauma patients should get this regimen, unless they have ineffective breathing and require oxygenation invasively- ETT or Surgical airway
When oxygenating COPD patients who retain CO2, recognise that few patients in this population experience Hypoxic drive, which can affect their stimulus to breathe. Hyperoxygenation in this patient can lead to respiratory depression and respiratory acidosis. Watch them carefully and monitor ABGs.
50- primary assessment Airway
KYJ 50 - Airway.
Part 1 of 5 part series on Primary Survey.
Airway and simultaneous C-Spine precautions.
Few clinical staff will refute that priority of patient assessment starts with assessing Airway.
As the first step in a primary and secondary survey, airway assessment is the Alpha priority.
Today's trauma pearl is the first instalment in a five part series that looks at this step in detail.
The arrival of a trauma patient presents many challenges to EMS and nursing staff. Exposure to fuel, chemicals, blood and other body fluids, anxious and aggressive patients or relatives, well meaning yet obstructive first responders; all these things are safely risks that need to be managed before prioritising patient assessment.
Getting down to airway assessment the emergency responder first needs to recognise that opening a patients mouth to inspect the airway requires a technique that avoids head tilt. In trauma (especially when the patient was knocked out), protecting the cervical spine integrity is vital, so opening an airway using a full head tilt (as you were taught in first aid or basic life support courses) is s No No.
Chin lift or Jaw thrust are both techniques that can be used to open the mouth, and lift the tongue away from the pharynx. With a patient lying supine, these techniques will open the airway temporarily allowing you to assess for foreign obstruction.
What are you looking for?
Anything you see in the airway will fall into one of three categories.
Wet n sloppy -(blood, secretions, vomit)
Hard n Chunky- (broken off teeth, windshield glass, food, gum, vomit)
Soft n fleshy- ( tongue, oedema, vomit)
Once an obstruction has been found, remove it.
Wet n sloppy - Yankeur or rigid sucker to gently suction the oropharynx
Hard n chunky - Magills forceps or, if safe, your gloved fingers (caution against this if broken teeth or glass is likely)
Soft n fleshy - insert an airway adjunct such as a nasopharyngeal , guedels airway(OPA), LMA, or oesophageal airway, if the patient is unable to control their own tongue.
Definitive airway security is the insertion of an Endotracheal Tube (ETT).
Failure to establish an effective patent airway, may require an emergency surgical airway (tracheostomy).
Not until the patient's airway is secure, should assessment of the patient continue.
Summary: remember, wet n sloppy, hard n chunky, & soft n fleshy.
The Airway is your top priority.
Part 1 of 5 part series on Primary Survey.
Airway and simultaneous C-Spine precautions.
Few clinical staff will refute that priority of patient assessment starts with assessing Airway.
As the first step in a primary and secondary survey, airway assessment is the Alpha priority.
Today's trauma pearl is the first instalment in a five part series that looks at this step in detail.
The arrival of a trauma patient presents many challenges to EMS and nursing staff. Exposure to fuel, chemicals, blood and other body fluids, anxious and aggressive patients or relatives, well meaning yet obstructive first responders; all these things are safely risks that need to be managed before prioritising patient assessment.
Getting down to airway assessment the emergency responder first needs to recognise that opening a patients mouth to inspect the airway requires a technique that avoids head tilt. In trauma (especially when the patient was knocked out), protecting the cervical spine integrity is vital, so opening an airway using a full head tilt (as you were taught in first aid or basic life support courses) is s No No.
Chin lift or Jaw thrust are both techniques that can be used to open the mouth, and lift the tongue away from the pharynx. With a patient lying supine, these techniques will open the airway temporarily allowing you to assess for foreign obstruction.
What are you looking for?
Anything you see in the airway will fall into one of three categories.
Wet n sloppy -(blood, secretions, vomit)
Hard n Chunky- (broken off teeth, windshield glass, food, gum, vomit)
Soft n fleshy- ( tongue, oedema, vomit)
Once an obstruction has been found, remove it.
Wet n sloppy - Yankeur or rigid sucker to gently suction the oropharynx
Hard n chunky - Magills forceps or, if safe, your gloved fingers (caution against this if broken teeth or glass is likely)
Soft n fleshy - insert an airway adjunct such as a nasopharyngeal , guedels airway(OPA), LMA, or oesophageal airway, if the patient is unable to control their own tongue.
Definitive airway security is the insertion of an Endotracheal Tube (ETT).
Failure to establish an effective patent airway, may require an emergency surgical airway (tracheostomy).
Not until the patient's airway is secure, should assessment of the patient continue.
Summary: remember, wet n sloppy, hard n chunky, & soft n fleshy.
The Airway is your top priority.
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