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 For this reason, a blood test called CK-MB was once used to diagnose MI, but due to insensitivity, it has been replaced by Troponin testing.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.
Friday 24 January 2014
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.
Saturday 18 January 2014
49 - Understanding Blood gases part 6 of 6
KYJ 49 - Blood Gas series -part 6
Base Excess.
The Base excess is a measure of how radically deviated the metabolic system is. The base excess (BE) normal value is between -2 to +2 ( some texts site -3 - +3).
It is loosely influenced by bicarbonate (base or alkali). Many authors suggest that BE is the better value used to determine metabolic acidosis or alkalosis. One colleague of mine in the #FOAMed world (Chris Nickson who writes for "Life in the Fast Lane") states that
"Bicarbonate levels are not an ideal indicator of either metabolic or respiratory components of acid-base disturbance because it is affected by both.
Furthermore the relationship between metabolic acidosis and bicarbonate is neither consistent nor linear."
This essentially means that the more acidotic a person is, the bicarb does not necessarily change in a predictable way. And I agree. But it is nonetheless an indicator as to whether the acidosis is respiratory or metabolic.
Unlike pH or CO2, the concentration of the bicarbonate ion (HCO3-) (in mEq/L) is not measured, it is calculated from the PCO2 and pH.
As more less bicarb is excreted, the BE swings further into negative ( less than -3. Eg -5 or -7). The opposite occurs with accumulation of bicarb (base). The more there is, the more positive will be the BE. (>+3)
There it is BE or HCO3- for me Bicarb is quick and easy and does the job. But BE could be used as a well accepted alternative.
And that is Blood gases in 6 easy posts. I do teach these in a face to face workshop, and if you are interested in a respiratory seminar including ABGs in your town, let me know. I travel anywhere for 10 or more.
What's our next topic?
Base Excess.
The Base excess is a measure of how radically deviated the metabolic system is. The base excess (BE) normal value is between -2 to +2 ( some texts site -3 - +3).
It is loosely influenced by bicarbonate (base or alkali). Many authors suggest that BE is the better value used to determine metabolic acidosis or alkalosis. One colleague of mine in the #FOAMed world (Chris Nickson who writes for "Life in the Fast Lane") states that
"Bicarbonate levels are not an ideal indicator of either metabolic or respiratory components of acid-base disturbance because it is affected by both.
Furthermore the relationship between metabolic acidosis and bicarbonate is neither consistent nor linear."
This essentially means that the more acidotic a person is, the bicarb does not necessarily change in a predictable way. And I agree. But it is nonetheless an indicator as to whether the acidosis is respiratory or metabolic.
Unlike pH or CO2, the concentration of the bicarbonate ion (HCO3-) (in mEq/L) is not measured, it is calculated from the PCO2 and pH.
As more less bicarb is excreted, the BE swings further into negative ( less than -3. Eg -5 or -7). The opposite occurs with accumulation of bicarb (base). The more there is, the more positive will be the BE. (>+3)
There it is BE or HCO3- for me Bicarb is quick and easy and does the job. But BE could be used as a well accepted alternative.
And that is Blood gases in 6 easy posts. I do teach these in a face to face workshop, and if you are interested in a respiratory seminar including ABGs in your town, let me know. I travel anywhere for 10 or more.
What's our next topic?
48 - understanding ABGs part 5. Compensation.
KYJ 48 - Blood Gases series. Part 5.
In the last episode we looked at basic analysis of ABGs, normal values and some ABG examples. Two sets of homework ABGs were offered : did you have a go??
A).
pH 7.54
paCO2 =24
HCO3 = 24
This is Respiratory Alkalosis (The Justin Beiber effect)
And
B).
pH 7.61
PaCO2 = 42
HCO3 = 28
This is Metabolic Alkalosis commonly caused by Hyperemesis in morning sickness.
Plug: in all my two day Respiratory nursing seminars, I do a two hour face to face session in ABGs with 20 examples.
Today we start to tackle the term "compensation".
Compensation is the process of bringing an abnormal pH back into the normal range. Now we talked about the range being 7.35-7.45, but if you had to pin one number to absolute normal, then 7.4 is absolute. So less than 7.4 (7.35-7.4) would be the acidic side of normal, and higher than 7.4 (7.4-7.45) is the alkaline side of normal.
In the last episode we mentioned that abnormal pH (acidosis and alkalosis) is either caused by an abnormal CO2 or an abnormal HCO3.
Remember if the problem is abnormal CO2 then it is called "respiratory". If the HCO3 is abnormal it is called "metabolic".
Compensation is where the respiratory system fails to excrete CO2, the kidneys (metabolic) adjust the amount of HCO3 to balance pH. And visa versa,
If the HCO3 is the cause of abnormality, the lungs will adjust CO2 levels to balance pH close to 7.4.
So let's start with a simple set of Respiratory Acidosis values.
The patient has had a heavy dose of morphine post op, and not breathing up well. He is not blowing off adequate CO2 which accumulates and drops his pH.
pH 7.31
paCO2 50
HCO3 25
Now over time (60-90 mins) his kidneys will start retaining alkali (HCO3) to buffer his acidic pH. This early compensation is seen in the next set of gases.
pH 7.34
PaCO2 50
HCO3 29. **
Note the increase of bicarb which has dragged his pH up close to normal. At this stage, because pH is still technically acidotic, the diagnosis of the gases is called:
Respiratory Acidosis with partial compensation.
10 mins later the gases are :
pH 7.36
PACO2 50
HCO3 31**
Note HCO3 has risen further bringing pH into normal range.
- this is called
Fully Compensated Respiratory Acidosis.
...
Let's look
At another example:
pH 7.22
PaCO2 36
HCO3 18 very low
Metabolic Acidosis ( this girl is a diabetic with DKA. Note how fast and deep she is breathing (Kussmaul respirations) (video)
5 minutes lapse
pH 7.34
PaCO2 28* (blowing off her CO2)
HCO3 18
You can see her lungs are compensating - but this is still a Metabolic Acidosis with partial compensation.
5 more mins
pH 7.36
paCO2 24 (blown more off)
HCO3 18
Fully compensated metabolic acidosis. The pH has corrected by excreting all the acidic CO2 by rapid deep breathing.
Remember the difference between partially compensated and fully compensated is directly related to the pH value.
If it's a HCO3 problem the lungs try to compensate
If it's a CO2 problem the Kidneys try to rescue.
In the final episode, we will look at the often unused value called Base Excess (BE). What we have covered to date has served me well for my whole career, and every exam, and I have never needed to look at BE for ABG analysis, however many of you would have covered it at some point in your education or practice, so I will address this forgotten ABG value. Then I think we are done.
In the last episode we looked at basic analysis of ABGs, normal values and some ABG examples. Two sets of homework ABGs were offered : did you have a go??
A).
pH 7.54
paCO2 =24
HCO3 = 24
This is Respiratory Alkalosis (The Justin Beiber effect)
And
B).
pH 7.61
PaCO2 = 42
HCO3 = 28
This is Metabolic Alkalosis commonly caused by Hyperemesis in morning sickness.
Plug: in all my two day Respiratory nursing seminars, I do a two hour face to face session in ABGs with 20 examples.
Today we start to tackle the term "compensation".
Compensation is the process of bringing an abnormal pH back into the normal range. Now we talked about the range being 7.35-7.45, but if you had to pin one number to absolute normal, then 7.4 is absolute. So less than 7.4 (7.35-7.4) would be the acidic side of normal, and higher than 7.4 (7.4-7.45) is the alkaline side of normal.
In the last episode we mentioned that abnormal pH (acidosis and alkalosis) is either caused by an abnormal CO2 or an abnormal HCO3.
Remember if the problem is abnormal CO2 then it is called "respiratory". If the HCO3 is abnormal it is called "metabolic".
Compensation is where the respiratory system fails to excrete CO2, the kidneys (metabolic) adjust the amount of HCO3 to balance pH. And visa versa,
If the HCO3 is the cause of abnormality, the lungs will adjust CO2 levels to balance pH close to 7.4.
So let's start with a simple set of Respiratory Acidosis values.
The patient has had a heavy dose of morphine post op, and not breathing up well. He is not blowing off adequate CO2 which accumulates and drops his pH.
pH 7.31
paCO2 50
HCO3 25
Now over time (60-90 mins) his kidneys will start retaining alkali (HCO3) to buffer his acidic pH. This early compensation is seen in the next set of gases.
pH 7.34
PaCO2 50
HCO3 29. **
Note the increase of bicarb which has dragged his pH up close to normal. At this stage, because pH is still technically acidotic, the diagnosis of the gases is called:
Respiratory Acidosis with partial compensation.
10 mins later the gases are :
pH 7.36
PACO2 50
HCO3 31**
Note HCO3 has risen further bringing pH into normal range.
- this is called
Fully Compensated Respiratory Acidosis.
...
Let's look
At another example:
pH 7.22
PaCO2 36
HCO3 18 very low
Metabolic Acidosis ( this girl is a diabetic with DKA. Note how fast and deep she is breathing (Kussmaul respirations) (video)
5 minutes lapse
pH 7.34
PaCO2 28* (blowing off her CO2)
HCO3 18
You can see her lungs are compensating - but this is still a Metabolic Acidosis with partial compensation.
5 more mins
pH 7.36
paCO2 24 (blown more off)
HCO3 18
Fully compensated metabolic acidosis. The pH has corrected by excreting all the acidic CO2 by rapid deep breathing.
Remember the difference between partially compensated and fully compensated is directly related to the pH value.
If it's a HCO3 problem the lungs try to compensate
If it's a CO2 problem the Kidneys try to rescue.
In the final episode, we will look at the often unused value called Base Excess (BE). What we have covered to date has served me well for my whole career, and every exam, and I have never needed to look at BE for ABG analysis, however many of you would have covered it at some point in your education or practice, so I will address this forgotten ABG value. Then I think we are done.
47 - understanding ABGs part 4
KYJ 47 - blood gas series part 4.
We measure blood gases for two reasons. First to determine pH of blood and secondly to look at gas exchange of oxygen. Low oxygen values are called Hypoxaemia.
Normal values are
pH = 7.35 - 7.45
PaO2 = 80-100mmHg
PaCO2 = 35-45mmHg
HCO3 = 22-26 mEq
If pH drops below normal (acidosis) the cause is too much acidic CO2, or not enough HCO3.
High pH (alkalosis) is caused by too much HCO3 or not enough CO2.
Now that we have established the diagnosis of acidosis or alkalosis being purely a numbers game. Let's look
At qualifying types of each extreme
Acidosis can be called Respiratory acidosis or Metabolic Acidosis.
Respiratory acidosis means the cause is high CO2 (>45). Remember CO2 makes blood acidic. You excrete CO2 by breathing. So if CO2 is too high, it is a problem with ventilating it off, hence it's called a Respiratory Acidosis.
Metabolic Acidosis is caused by an underproduction of bicarb (HCO3) or an accumulation of acids in the blood eg Lactic acid, ketones, and chloride. In these patients the pH is always low. But instead of seeing a high respiratory acid value (CO2) there is an abnormally low HCO3 value.
.....
Alkalosis
Alkalosis is the same as Acidosis but a mirror image.
Respiratory Alkalosis is a high pH with an abnormally low CO2. The patient has blown off (hyperventilated) all their CO2 (acid) leaving them alkalotic. I like to call this the "Justin Beiber Effect". Tweenies seeing a live Justin Beiber concert get hysterical and hyperventilate - and pass out wasting a $150 concert ticket!!
Metabolic Alkalosis is a high pH with abnormally high HCO3. In this alkalosis the patient has retained HCO3 ( an alkali) or excreted too many metabolic acids. A classic example is hyperemesis (vomiting) seen in early pregnancy with morning sickness. Middle ear vertigo, sea sickness, diarrhoeal illness and diuretic use, all cause the retention of bicarb, and loss of acids (eg stomach acid).
...
So let's look at some values.(normal in brackets)
pH 7.02. (7.35-7.45)
PaCO2 55. (35-45)
HCO3 24. (22-26)
Note that pH is too low (Acidosis), and the CO2 is high (Respiratory)
This is Respiratory Acidosis- this bloke needs to breathe more to vent off his CO2. Suspect this in sleepy shallow breathers waking up from anaesthetic.
Another:
pH 7.22 (7.35-7.45)
PaCO2 36 (35-45)
HCO3. 18 (22-26)
pH is too low ( acidotic again) but CO2 is normal. Bicarb is too low. There is not enough metabolic alkali (bicarb) in the blood so it becomes acidic. This is a case of metabolic acidosis, and frequently caused by diabetics with extremely high BGLs. They start melting fat, which produces large amounts of ketones. These ketone by products of fat catabolism cause the diabetic to develop this lethal diabetic ketoacidosis a type of metabolic acidosis .
What you may have noticed in these examples, is that I have not mentioned Oxygen values. The reason is, that oxygen levels are are not used in the analysis of acid/base balance when interpreting ABGs. In fact PaO2 is the last value that we are interested in. It is merely an indicator of blood oxygenation and never pH.
Look at these two next examples and have a crack at telling me what they are.
A).
pH 7.54
paCO2 =24
HCO3 = 24
And
B).
pH 7.61
PaCO2 = 42
HCO3 = 28
I'll answer these in the next post, and we will start our exploration of what Compensation means.
We measure blood gases for two reasons. First to determine pH of blood and secondly to look at gas exchange of oxygen. Low oxygen values are called Hypoxaemia.
Normal values are
pH = 7.35 - 7.45
PaO2 = 80-100mmHg
PaCO2 = 35-45mmHg
HCO3 = 22-26 mEq
If pH drops below normal (acidosis) the cause is too much acidic CO2, or not enough HCO3.
High pH (alkalosis) is caused by too much HCO3 or not enough CO2.
Now that we have established the diagnosis of acidosis or alkalosis being purely a numbers game. Let's look
At qualifying types of each extreme
Acidosis can be called Respiratory acidosis or Metabolic Acidosis.
Respiratory acidosis means the cause is high CO2 (>45). Remember CO2 makes blood acidic. You excrete CO2 by breathing. So if CO2 is too high, it is a problem with ventilating it off, hence it's called a Respiratory Acidosis.
Metabolic Acidosis is caused by an underproduction of bicarb (HCO3) or an accumulation of acids in the blood eg Lactic acid, ketones, and chloride. In these patients the pH is always low. But instead of seeing a high respiratory acid value (CO2) there is an abnormally low HCO3 value.
.....
Alkalosis
Alkalosis is the same as Acidosis but a mirror image.
Respiratory Alkalosis is a high pH with an abnormally low CO2. The patient has blown off (hyperventilated) all their CO2 (acid) leaving them alkalotic. I like to call this the "Justin Beiber Effect". Tweenies seeing a live Justin Beiber concert get hysterical and hyperventilate - and pass out wasting a $150 concert ticket!!
Metabolic Alkalosis is a high pH with abnormally high HCO3. In this alkalosis the patient has retained HCO3 ( an alkali) or excreted too many metabolic acids. A classic example is hyperemesis (vomiting) seen in early pregnancy with morning sickness. Middle ear vertigo, sea sickness, diarrhoeal illness and diuretic use, all cause the retention of bicarb, and loss of acids (eg stomach acid).
...
So let's look at some values.(normal in brackets)
pH 7.02. (7.35-7.45)
PaCO2 55. (35-45)
HCO3 24. (22-26)
Note that pH is too low (Acidosis), and the CO2 is high (Respiratory)
This is Respiratory Acidosis- this bloke needs to breathe more to vent off his CO2. Suspect this in sleepy shallow breathers waking up from anaesthetic.
Another:
pH 7.22 (7.35-7.45)
PaCO2 36 (35-45)
HCO3. 18 (22-26)
pH is too low ( acidotic again) but CO2 is normal. Bicarb is too low. There is not enough metabolic alkali (bicarb) in the blood so it becomes acidic. This is a case of metabolic acidosis, and frequently caused by diabetics with extremely high BGLs. They start melting fat, which produces large amounts of ketones. These ketone by products of fat catabolism cause the diabetic to develop this lethal diabetic ketoacidosis a type of metabolic acidosis .
What you may have noticed in these examples, is that I have not mentioned Oxygen values. The reason is, that oxygen levels are are not used in the analysis of acid/base balance when interpreting ABGs. In fact PaO2 is the last value that we are interested in. It is merely an indicator of blood oxygenation and never pH.
Look at these two next examples and have a crack at telling me what they are.
A).
pH 7.54
paCO2 =24
HCO3 = 24
And
B).
pH 7.61
PaCO2 = 42
HCO3 = 28
I'll answer these in the next post, and we will start our exploration of what Compensation means.
46 - Understanding ABGs part 3
KYJ 46 - Acidosis. ABG series part 3.
In this series I walk you through the fundamentals of analysing arterial blood gases.
Part 1 looked at partial pressure
Part 2 looks at oxygen and CO2 values.
In today's episode we look at pH of blood, and discuss acid vs alkali.
Potenz Hydrogen or pH is a measure of acidity or alkalinity.
Fun Science fact: all liquids can be measured for pH on a scale between 1 - 14. Pure sterile distilled water is neutral at 7.0
If a liquid is less than 7.0 it is called an acid, and the closer to 1 it is, the stronger acid it is. Examples include sulphuric acid in your car battery, hydrochloric acid in your stomach, vinegar and lemon juice. Some of you will remember an advert for skin cream or shampoo claiming it is pH balanced at 5.5, the same pH of your skin.
Conversely, a liquid with a pH higher than 7.0 is called a base or alkali. Bile, caustic soda, soap, and Sodium Bicarbonate that we have in our pantries for cooking. Infarct anything that is called an Antacid eg Mylanta or Gaviscon.
Arterial Blood has a pH of 7.35-7.45 but under certain circumstances may fluctuate either side of this normal range. Notice that blood is actually slightly alkaline. Despite this, it is called neutral or normal in this range (that must really irritate the nerdy Sheldon types).
If the pH of blood should drop below 7.35 it is called acidosis. If it swings above 7.45 it is called alkalosis.
Now there are a few principles to understand before we discuss how acidosis or alkalosis occurs. The first is the effect of CO2 being produced.
All cells produce two waste products at part of their normal metabolism. Carbon Dioxide and water.
These waste products must be removed from the body and we do that two ways. We urinate and we breathe.
CO2 and water form a weak acid in blood. It is called carbonic acid (CO2+H2O =H2CO3).
So blood is constantly becoming acidotic, and without being able to breathe off CO2 it would accumulate in minutes to cause dangerous levels of acid in your blood.
CO2 is also converted inside red blood cells to an alkali called bicarbonate (HCO3). This acts in blood to buffer or counteract the effect of acidic CO2 rise.
As HCO3 levels rise driving blood into the alkalosis end of normal pH, your kidneys work harder to pee off the bicarb. Normal HCO3 levels are 22-26mEq
Remember
HCO3 is alkali
CO2 is acid
We breathe off CO2 to prevent acidosis, and pee off bicarb to prevent alkalosis.
Our lungs and kidneys are therefore organs that help to keep our pH between 7.35 -7.45
In the next session we will pull these all together and look at where CO2, pH and bicarb fit into the basics of ABG analysis.
In this series I walk you through the fundamentals of analysing arterial blood gases.
Part 1 looked at partial pressure
Part 2 looks at oxygen and CO2 values.
In today's episode we look at pH of blood, and discuss acid vs alkali.
Potenz Hydrogen or pH is a measure of acidity or alkalinity.
Fun Science fact: all liquids can be measured for pH on a scale between 1 - 14. Pure sterile distilled water is neutral at 7.0
If a liquid is less than 7.0 it is called an acid, and the closer to 1 it is, the stronger acid it is. Examples include sulphuric acid in your car battery, hydrochloric acid in your stomach, vinegar and lemon juice. Some of you will remember an advert for skin cream or shampoo claiming it is pH balanced at 5.5, the same pH of your skin.
Conversely, a liquid with a pH higher than 7.0 is called a base or alkali. Bile, caustic soda, soap, and Sodium Bicarbonate that we have in our pantries for cooking. Infarct anything that is called an Antacid eg Mylanta or Gaviscon.
Arterial Blood has a pH of 7.35-7.45 but under certain circumstances may fluctuate either side of this normal range. Notice that blood is actually slightly alkaline. Despite this, it is called neutral or normal in this range (that must really irritate the nerdy Sheldon types).
If the pH of blood should drop below 7.35 it is called acidosis. If it swings above 7.45 it is called alkalosis.
Now there are a few principles to understand before we discuss how acidosis or alkalosis occurs. The first is the effect of CO2 being produced.
All cells produce two waste products at part of their normal metabolism. Carbon Dioxide and water.
These waste products must be removed from the body and we do that two ways. We urinate and we breathe.
CO2 and water form a weak acid in blood. It is called carbonic acid (CO2+H2O =H2CO3).
So blood is constantly becoming acidotic, and without being able to breathe off CO2 it would accumulate in minutes to cause dangerous levels of acid in your blood.
CO2 is also converted inside red blood cells to an alkali called bicarbonate (HCO3). This acts in blood to buffer or counteract the effect of acidic CO2 rise.
As HCO3 levels rise driving blood into the alkalosis end of normal pH, your kidneys work harder to pee off the bicarb. Normal HCO3 levels are 22-26mEq
Remember
HCO3 is alkali
CO2 is acid
We breathe off CO2 to prevent acidosis, and pee off bicarb to prevent alkalosis.
Our lungs and kidneys are therefore organs that help to keep our pH between 7.35 -7.45
In the next session we will pull these all together and look at where CO2, pH and bicarb fit into the basics of ABG analysis.
Thursday 16 January 2014
45 - Understanding ABGs part 2
KYJ 45 - Blood Gas series -part 2.
In part one of this series on understanding Blood gases, we reviewed the principle of partial pressure (Dalton's Law).
We also touched on Henry's law that (in part) helps us understand gas dissolving into plasma.
This episode we look at oxygen and CO2 in blood.
Abbreviations
pp= partial pressure
A = Alveoli
a = Arterial
v = Venous (upper case V= ventilation)
p = pressure
O2 = oxygen
CO2 = carbon dioxide
mmHg = millimeters of Mercury
Diffusion = gas particles moving from one area to another eg lungs to blood or blood to cells.
Normal values
The partial pressure (pp) of oxygen in blood varies between arterial and venous blood. When freshly oxygenated in the lungs, arterial blood has a normal value of 80-100 mmHg. In depleted venous blood, the oxygen pressure (tension) is approximately 35-45 mmHg.
Clearly you see that the arterial oxygen tension is more than twice that of venous blood.
The opposite effect happens with Carbon dioxide. Normal tension in arterial blood is 35-45 mmHg, but in venous blood rises to 42-52mmHg. Slightly higher but not as dramatic as the difference in venous vs arterial Oxygen.
For the purpose of this series we will focus on Arterial blood as measured during Arterial Blood Gases.
First Oxygen:
When oxygen is inhaled, it is drawn in with a partial pressure of 159 mmHg (room air 21% of 760 mmHg)
After humidification and mixing with gases inside the lung's alveoli, the partial pressure (pp) has reduced to about 105-110 mmHg. This pressure is abbreviated as pAO2 (uppercase "A" = Alveolar) .
Oxygen diffuses into the blood stream where it dissolves first into plasma exerting pressure in the blood. Any given volume of blood only comes into close contact with alveoli for 0.7 of a second, so time to fully equilibrate gas pressure in both blood and lung is not possible.
Given that blood entering the lung capillaries has a pp oxygen in venous blood of ~40mmHg, the difference in pressure between blood and lung is steep (40 in venous blood vs 105 in alveoli).
Gas diffuses from high pressure to low pressure, so oxygen will migrate from lungs to blood in attempt to balance the pressure.
After a split second, the oxygen pressure in blood has risen from 40 ish to 90 ish, and makes its way back to the left heart to be pumped out to all those starving cells in the body.
At the exodus from the lungs arterial blood has a predictable oxygen tension (paO2) of 80-100mmHg.
Less than 80 is deemed Hypoxaemia. Less than 60 is called Respiratory Failure.
The difference between oxygen pp in alveoli and arterial blood is called the Aa Gradient, and it should be about 7-12 mmHg difference. It slightly increases with age, but a high Aa gradient is an indicator of lung deterioration.
CO2.
CO2 is the waste gas produced by cell metabolism and must be excreted. Most efficiently, carbon dioxide is exhaled. Transported by venous blood, to the lungs, and blown off by breathing. Some is also excreted by kidneys converted into bicarbonate, but let's not get ahead of ourselves.
Diffusion of CO2 from blood into alveoli happens simultaneously with oxygen diffusion.
With almost no measurable CO2 in the air you breathe (shhh don't tell the Greenies) and high CO2 pressure in blood returning to the lungs (42-52), it isn't any surprise that CO2 will diffuse out of the blood and into the lungs to be breathed off. Arterial blood therefore has slightly less CO2 at 35-45mmHg. If CO2 accumulates in our blood, it causes the blood to become acidic (Acidosis). Breathing therefore allows us to maintain a beautiful balance.
We will leave this session here, and tomorrow look at acidosis in greater detail.
Memorise your paO2 80-100
And paCO2 35-45 normal values.
In part one of this series on understanding Blood gases, we reviewed the principle of partial pressure (Dalton's Law).
We also touched on Henry's law that (in part) helps us understand gas dissolving into plasma.
This episode we look at oxygen and CO2 in blood.
Abbreviations
pp= partial pressure
A = Alveoli
a = Arterial
v = Venous (upper case V= ventilation)
p = pressure
O2 = oxygen
CO2 = carbon dioxide
mmHg = millimeters of Mercury
Diffusion = gas particles moving from one area to another eg lungs to blood or blood to cells.
Normal values
The partial pressure (pp) of oxygen in blood varies between arterial and venous blood. When freshly oxygenated in the lungs, arterial blood has a normal value of 80-100 mmHg. In depleted venous blood, the oxygen pressure (tension) is approximately 35-45 mmHg.
Clearly you see that the arterial oxygen tension is more than twice that of venous blood.
The opposite effect happens with Carbon dioxide. Normal tension in arterial blood is 35-45 mmHg, but in venous blood rises to 42-52mmHg. Slightly higher but not as dramatic as the difference in venous vs arterial Oxygen.
For the purpose of this series we will focus on Arterial blood as measured during Arterial Blood Gases.
First Oxygen:
When oxygen is inhaled, it is drawn in with a partial pressure of 159 mmHg (room air 21% of 760 mmHg)
After humidification and mixing with gases inside the lung's alveoli, the partial pressure (pp) has reduced to about 105-110 mmHg. This pressure is abbreviated as pAO2 (uppercase "A" = Alveolar) .
Oxygen diffuses into the blood stream where it dissolves first into plasma exerting pressure in the blood. Any given volume of blood only comes into close contact with alveoli for 0.7 of a second, so time to fully equilibrate gas pressure in both blood and lung is not possible.
Given that blood entering the lung capillaries has a pp oxygen in venous blood of ~40mmHg, the difference in pressure between blood and lung is steep (40 in venous blood vs 105 in alveoli).
Gas diffuses from high pressure to low pressure, so oxygen will migrate from lungs to blood in attempt to balance the pressure.
After a split second, the oxygen pressure in blood has risen from 40 ish to 90 ish, and makes its way back to the left heart to be pumped out to all those starving cells in the body.
At the exodus from the lungs arterial blood has a predictable oxygen tension (paO2) of 80-100mmHg.
Less than 80 is deemed Hypoxaemia. Less than 60 is called Respiratory Failure.
The difference between oxygen pp in alveoli and arterial blood is called the Aa Gradient, and it should be about 7-12 mmHg difference. It slightly increases with age, but a high Aa gradient is an indicator of lung deterioration.
CO2.
CO2 is the waste gas produced by cell metabolism and must be excreted. Most efficiently, carbon dioxide is exhaled. Transported by venous blood, to the lungs, and blown off by breathing. Some is also excreted by kidneys converted into bicarbonate, but let's not get ahead of ourselves.
Diffusion of CO2 from blood into alveoli happens simultaneously with oxygen diffusion.
With almost no measurable CO2 in the air you breathe (shhh don't tell the Greenies) and high CO2 pressure in blood returning to the lungs (42-52), it isn't any surprise that CO2 will diffuse out of the blood and into the lungs to be breathed off. Arterial blood therefore has slightly less CO2 at 35-45mmHg. If CO2 accumulates in our blood, it causes the blood to become acidic (Acidosis). Breathing therefore allows us to maintain a beautiful balance.
We will leave this session here, and tomorrow look at acidosis in greater detail.
Memorise your paO2 80-100
And paCO2 35-45 normal values.
44 - Understanding Arterial Blood Gases part 1
KYJ 44 understanding Blood gases. Part 1.
In this series of "knowing your jargon (KYJ)", we explore the blood gases, and explain some of the terminology used in interpretation.
We start with some fundamental science and a physics principle called Dalton's Law.
Dalton said that the pressure exerted by a mixture of gases is equal to the sum of all gases in the mix. Air exerts pressure (air pressure).
Air is a mixture of gases, mostly nitrogen (78%) oxygen (21%), and a minute quantity of CO2, argon, xenon, water vapour, and traces of other environmental contaminants make up the last 1%.
All these gases exert their cumulative pressure in the mix that we call Air, but individually these gases all exert their own pressure. This is called Partial Pressure, abbreviated to "pp".
Now air pressure as a whole, or atmospheric pressure is relatively constant at sea level but reduces with altitude. At sea level our atmospheric pressure is 760 mmHg (101.3 KPa).
But if you were at Everest base camp at 5000metres, the air is so thin that atmospheric pressure is about half that at sea level (380 mmHg), and only a third at the summit some 8.3km high.
Now back to Dalton's law. The pressure of a mixed gas is the sum of its parts.
So air pressure (760), is the sum of the pressure of nitrogen, oxygen, argon , CO2 etc.
When we know the percentage of a gas in air, we can calculate its partial pressure. Oxygen makes up 21% ( actually 20.9% but let's not split hairs), of air
If Air is 760mmHg and Oxygen is 21% (or 0.21 of air), then
760 x 0.21 = 159.6
Oxygen at sea level then has a partial pressure of 159.6mmHg.
Expressed as ppO2 = 159.6.
...
Take a sip of your coffee/wine
And do these quick calculations.
...
1. What would the partial pressure of nitrogen (78% of air) be at sea level?
2. What would the partial pressure of Oxygen be at Everest Base Camp?
...
Ok. Answers at the end of this blog session.
Read on:
Now another physics principle is that many gases are soluble in liquids. An excellent example is oxygen and carbon dioxide(CO2).
Ponder the bubbles in your bottle of champagne / soft drink or beer. These are CO2 bubbles coming out of solution and returning to gas. Under pressure the CO2 formed during fermentation (grog) or manufacture (soft drink), dissolves into the liquid. When you pop the top off these beverages, pressure is released and the dissolved gas reforms into bubbles and fizzes or "off gases".
Blood or more correctly, plasma is the same. It dissolves oxygen and CO2 into solution. Of course these gases don't travel in the blood in bubbles do they- they'd get stuck. That is what happens to divers with the bends. But that is another post.
In our next edition we will explore more about oxygen and CO2 gas dissolved in blood.
Answer 1= ppN2 is 600.4 mmHg
Answer 2= ppO2 base camp is only about 80mmHg
In this series of "knowing your jargon (KYJ)", we explore the blood gases, and explain some of the terminology used in interpretation.
We start with some fundamental science and a physics principle called Dalton's Law.
Dalton said that the pressure exerted by a mixture of gases is equal to the sum of all gases in the mix. Air exerts pressure (air pressure).
Air is a mixture of gases, mostly nitrogen (78%) oxygen (21%), and a minute quantity of CO2, argon, xenon, water vapour, and traces of other environmental contaminants make up the last 1%.
All these gases exert their cumulative pressure in the mix that we call Air, but individually these gases all exert their own pressure. This is called Partial Pressure, abbreviated to "pp".
Now air pressure as a whole, or atmospheric pressure is relatively constant at sea level but reduces with altitude. At sea level our atmospheric pressure is 760 mmHg (101.3 KPa).
But if you were at Everest base camp at 5000metres, the air is so thin that atmospheric pressure is about half that at sea level (380 mmHg), and only a third at the summit some 8.3km high.
Now back to Dalton's law. The pressure of a mixed gas is the sum of its parts.
So air pressure (760), is the sum of the pressure of nitrogen, oxygen, argon , CO2 etc.
When we know the percentage of a gas in air, we can calculate its partial pressure. Oxygen makes up 21% ( actually 20.9% but let's not split hairs), of air
If Air is 760mmHg and Oxygen is 21% (or 0.21 of air), then
760 x 0.21 = 159.6
Oxygen at sea level then has a partial pressure of 159.6mmHg.
Expressed as ppO2 = 159.6.
...
Take a sip of your coffee/wine
And do these quick calculations.
...
1. What would the partial pressure of nitrogen (78% of air) be at sea level?
2. What would the partial pressure of Oxygen be at Everest Base Camp?
...
Ok. Answers at the end of this blog session.
Read on:
Now another physics principle is that many gases are soluble in liquids. An excellent example is oxygen and carbon dioxide(CO2).
Ponder the bubbles in your bottle of champagne / soft drink or beer. These are CO2 bubbles coming out of solution and returning to gas. Under pressure the CO2 formed during fermentation (grog) or manufacture (soft drink), dissolves into the liquid. When you pop the top off these beverages, pressure is released and the dissolved gas reforms into bubbles and fizzes or "off gases".
Blood or more correctly, plasma is the same. It dissolves oxygen and CO2 into solution. Of course these gases don't travel in the blood in bubbles do they- they'd get stuck. That is what happens to divers with the bends. But that is another post.
In our next edition we will explore more about oxygen and CO2 gas dissolved in blood.
Answer 1= ppN2 is 600.4 mmHg
Answer 2= ppO2 base camp is only about 80mmHg
Tuesday 14 January 2014
43- Troponin and the Sarcomeres
KYJ-43 Troponin.
Let's zoom down deep
Into a muscle cell.
The muscle cell of Striated muscle (striped muscle) has molecular structures called Sarcomeres.
These are strands of proteins wrapped around each other that physically shorten in length when electrically stimulated. The two primary filaments are called Actin (thin filaments) and Myocin (thick filaments).
These Sarcomeres may number in the thousands inside each muscle cell.
Binding these Sarcomeres together is a protein glue called Troponin. Think of it as cheese melted on a pizza gooing all the other stuff together.
There are three types of troponin. They are called T, C and I. All striped muscle including cardiac muscle and skeletal muscle has Troponin C. But types of Troponin I and T are specific to cardiac muscle cells.
If a heart muscle cell is injured or damaged, this troponin leaks out of the damaged cell, and stains the interstitial fluid surrounding the cell. It leaches into the lymphatic system which drains eventually into the blood stream.
If detected in the blood (on blood tests) it is a direct indicator that cardiac muscle injury/ damage has occurred.
Normal blood troponin is functionally zero- ie, troponin is an intramuscular substance, not an intravascular substance. That said, a tolerance of less than 0.04 mcg/L is considered ok.
If Troponin I&T are elevated >0.04 then this is highly suggestive of cardiac damage, and one of three diagnostic criteria for myocardial infarction. The other two criteria being ST elevation on ECG, and or a pain history that sounds cardiac typical.
Troponin can take 4-6 hours to reach the blood, and up to 12 hours to peak during a cardiac episode. Once elevated, can be present in blood for 5-14 days.
The I-Stat point of care blood test is a common method to test for troponin at the bedside, and in around 10 mins can support a diagnosis of MI.
For those with an unclear ECG based diagnosis, the patient can be admitted onto a ward for serial enzymes at 6 and 12 hours or 4 and 9 hours post onset of pain.
Because of troponin's ability to linger in the blood, it is a handy test for those patients that state they had chest pain yesterday or last week.
It is, to date, our most sensitive blood test for MI diagnosis.
Let's zoom down deep
Into a muscle cell.
The muscle cell of Striated muscle (striped muscle) has molecular structures called Sarcomeres.
These are strands of proteins wrapped around each other that physically shorten in length when electrically stimulated. The two primary filaments are called Actin (thin filaments) and Myocin (thick filaments).
These Sarcomeres may number in the thousands inside each muscle cell.
Binding these Sarcomeres together is a protein glue called Troponin. Think of it as cheese melted on a pizza gooing all the other stuff together.
There are three types of troponin. They are called T, C and I. All striped muscle including cardiac muscle and skeletal muscle has Troponin C. But types of Troponin I and T are specific to cardiac muscle cells.
If a heart muscle cell is injured or damaged, this troponin leaks out of the damaged cell, and stains the interstitial fluid surrounding the cell. It leaches into the lymphatic system which drains eventually into the blood stream.
If detected in the blood (on blood tests) it is a direct indicator that cardiac muscle injury/ damage has occurred.
Normal blood troponin is functionally zero- ie, troponin is an intramuscular substance, not an intravascular substance. That said, a tolerance of less than 0.04 mcg/L is considered ok.
If Troponin I&T are elevated >0.04 then this is highly suggestive of cardiac damage, and one of three diagnostic criteria for myocardial infarction. The other two criteria being ST elevation on ECG, and or a pain history that sounds cardiac typical.
Troponin can take 4-6 hours to reach the blood, and up to 12 hours to peak during a cardiac episode. Once elevated, can be present in blood for 5-14 days.
The I-Stat point of care blood test is a common method to test for troponin at the bedside, and in around 10 mins can support a diagnosis of MI.
For those with an unclear ECG based diagnosis, the patient can be admitted onto a ward for serial enzymes at 6 and 12 hours or 4 and 9 hours post onset of pain.
Because of troponin's ability to linger in the blood, it is a handy test for those patients that state they had chest pain yesterday or last week.
It is, to date, our most sensitive blood test for MI diagnosis.
42- the Reticuloendothelial System
KYJ42- Reticuloendothelial system.
If you are one of those nurses who learned stuff once upon a time for exams, then forgot most of it, then we are probably kindred spirits.
The numbers of times I have learned, forgotten and relearned stuff is astounding, so you are not alone.
I once learned, forgot and relearned about the Reticuloendothelial System (RES) and thought I would do a simple KYJ on it.
Let's start by saying it is no longer called the Reticuloendothelial system any more. The new name is the Mononuclear Phagocyte System (MPS).
The new name is helpful, because it offers an inkling into its function.
The MPS is part of our greater immune system. It is responsible for removing dead and dying cells and debris resulting from an immune response and programmed cell deaths (apoptosis). For an example. A few posts ago we spoke about bilirubin and it's precursor being the natural death of Red Blood Cells. The MPS has s role in the mopping up of this cell debris.
Reflecting on our greater immune system we can use the analogy of a cake.
The cake is made up of many ingredients. So too is our immune system.
Consisting of proteins in plasma (antibodies and complement proteins), and white blood cells (macrophages, monocytes, basophils, mast cells, lymphocytes, eosinophils, phagocytes, neutrophils)
These ingredients all bring a different function to the fight against disease, cell death, pathogens, and allergens.
That part of our immune system that physically digests the foreign and dead cells. Is what we formerly called the Reticuloendothelial system.
Specifically monocytes.
These cells are types of white blood cell (leukocyte). Their role is uniquely different to lymphocytes and granulocytes. Where lymphocytes manufacture chemicals to kill nasties, but monocytes actually engulf and digest particles like "The Pacman". Monocytes, are the largest of all the white blood cells and it is perhaps surprising to note that more than half of all the monocytes live in the spleen. Monocytes have an innate ability to migrate out of the blood stream and into tissues. They do this in response to chemical signals released by damaged or infected tissues. When they migrate to the site of infection they change form and become macrophages- a type of phagocyte (phago= to eat, cyte=cell).
Macrophages are the largest of the phagocytes, and are thus named- macro=big, phage=eater.
If you are one of those nurses who learned stuff once upon a time for exams, then forgot most of it, then we are probably kindred spirits.
The numbers of times I have learned, forgotten and relearned stuff is astounding, so you are not alone.
I once learned, forgot and relearned about the Reticuloendothelial System (RES) and thought I would do a simple KYJ on it.
Let's start by saying it is no longer called the Reticuloendothelial system any more. The new name is the Mononuclear Phagocyte System (MPS).
The new name is helpful, because it offers an inkling into its function.
The MPS is part of our greater immune system. It is responsible for removing dead and dying cells and debris resulting from an immune response and programmed cell deaths (apoptosis). For an example. A few posts ago we spoke about bilirubin and it's precursor being the natural death of Red Blood Cells. The MPS has s role in the mopping up of this cell debris.
Reflecting on our greater immune system we can use the analogy of a cake.
The cake is made up of many ingredients. So too is our immune system.
Consisting of proteins in plasma (antibodies and complement proteins), and white blood cells (macrophages, monocytes, basophils, mast cells, lymphocytes, eosinophils, phagocytes, neutrophils)
These ingredients all bring a different function to the fight against disease, cell death, pathogens, and allergens.
That part of our immune system that physically digests the foreign and dead cells. Is what we formerly called the Reticuloendothelial system.
Specifically monocytes.
These cells are types of white blood cell (leukocyte). Their role is uniquely different to lymphocytes and granulocytes. Where lymphocytes manufacture chemicals to kill nasties, but monocytes actually engulf and digest particles like "The Pacman". Monocytes, are the largest of all the white blood cells and it is perhaps surprising to note that more than half of all the monocytes live in the spleen. Monocytes have an innate ability to migrate out of the blood stream and into tissues. They do this in response to chemical signals released by damaged or infected tissues. When they migrate to the site of infection they change form and become macrophages- a type of phagocyte (phago= to eat, cyte=cell).
Macrophages are the largest of the phagocytes, and are thus named- macro=big, phage=eater.
41- Coagulation part 7 of 7
KYJ 41- Coagulation series part 7.
Rob's Pizza analogy
Factors 8, 5 and 13.
As we draw to the end of our marathon series on coagulation, we must address the coagulation factors that have been missing from previous discussion.
In earlier sessions we discussed that:
9 activates to 9a under the influence of 11a.
9a then binds with 10 using calcium. Where calcium is the glue, Factor 8 is the protein that allows 10 to activate.
The same relationship occurs between factor 10a and 2. Using calcium, prothrombin (F2) is activated to become Thrombin, but there must be Factor 5 present for this reaction to occur.
Thrombin (2a) is like a Food processor . It chops fibrinogen in the plasma (factor 1) in to tiny strands called Fibrin. These fibrin strands use Factor 13 to weave and inter tangle with the platelet plug, and stabilise the thrombus.
Think of a block of cheese (fibrinogen) being placed into a food processor (Thrombin), turned on (Calcium and Factor 5) and it comes out grated (Fibrin).
Now, sprinkled on the pizza (platelets plug) the cheese is all loose.
It is grilled in the pizza oven (Factor 13). And the cheese melts into and forms a topping on the pizza (Stabilised Thrombus).
So where did the Cheese come from?? Well it was once Milk (factor 9a) using rennet (factor 8) separated in to curds (10) and with calcium gummed together to set into cheese (10a).
Without milk or rennet you can't have cheese. Without cheese you can't make pizza.
Rob's Pizza analogy
Factors 8, 5 and 13.
As we draw to the end of our marathon series on coagulation, we must address the coagulation factors that have been missing from previous discussion.
In earlier sessions we discussed that:
9 activates to 9a under the influence of 11a.
9a then binds with 10 using calcium. Where calcium is the glue, Factor 8 is the protein that allows 10 to activate.
The same relationship occurs between factor 10a and 2. Using calcium, prothrombin (F2) is activated to become Thrombin, but there must be Factor 5 present for this reaction to occur.
Thrombin (2a) is like a Food processor . It chops fibrinogen in the plasma (factor 1) in to tiny strands called Fibrin. These fibrin strands use Factor 13 to weave and inter tangle with the platelet plug, and stabilise the thrombus.
Think of a block of cheese (fibrinogen) being placed into a food processor (Thrombin), turned on (Calcium and Factor 5) and it comes out grated (Fibrin).
Now, sprinkled on the pizza (platelets plug) the cheese is all loose.
It is grilled in the pizza oven (Factor 13). And the cheese melts into and forms a topping on the pizza (Stabilised Thrombus).
So where did the Cheese come from?? Well it was once Milk (factor 9a) using rennet (factor 8) separated in to curds (10) and with calcium gummed together to set into cheese (10a).
Without milk or rennet you can't have cheese. Without cheese you can't make pizza.
40 - Coagulation part 6 of 7
KYJ40-Series on Coagulation part 6- the role of calcium.
As a young ICU nurse in a big tertiary hospital more than 20 years ago, we had these blokes (4) who were burned in a caravan fire, all came into our unit. It was one of the most interesting (physiology) experiences of my life. The daily grind of bathing these guys, drug paralysed, sedated and fully ventilated became monotonous and the relentless surgeries, skin harvests and grafts made one wing of our ICU look nothing short of a macabre scene from some horror movie.
Daily these blokes seemed to return from theatre, and the dressing of choice was a product called Kaltostat. A calcium rich mesh that filled with blood oozing from graft sites, and became a clot.
Two points will be addressed in today's post. The first is the difference between a clot and a thrombus, the second is the role of calcium in this dressing and in the coagulation system in general.
First the Jargon. Clot vs Thrombus.
When platelets stick to the damaged inside wall of a vessel. This is called Platelet Adhesion.
When platelets stick to each other like a snow flakes in a snow ball, this is called Platelet Aggregation.
When platelets release substances to signal new tissue to grow eg- (Platelet Derived Growth Factor (PDGF)), or to signal other platelets to come (Thromboxane A2, ADP), or to initiate the coagulation cascade (PGI and calcium, factor V and VIII). This is all collectively called Platelet activation.
All these processes (adhesion, aggregation and activation) occur in the intravascular space. Ultimately this leads to a plug of solid matter at the site of vessel injury. This is called a thrombus.
When a thrombus breaks away from its attachment on a vessel wall and travels in the blood stream, it is called an embolus or embolism.
A clot is a thrombus, but outside the blood vessel.
A scab is a dehydrated or dried clot- usually over an external wound. The active mushy slough at the base of the scab and the wound bed is often active platelets, releasing PDGF stimulating the growth of new granulation tissue .
Now let's focus on Calcium.
Fundamentally a positively charged ion (cation) abbreviated to Ca++ .
Calcium is present in plasma, and interstitial fluid, but also specialised granules inside platelets called Delta granules. When a platelet is activated it releases the contents of its Delta granules which among other chemicals, includes Calcium onto its surface and into the surrounding plasma.
Factoid: sleeping (dormant) plasma coagulation factors like 7,9,10 and prothrombin(F2), are all negatively charged proteins. They therefore readily accept a positive charged particle to bind with. Calcium does this.
It is like the glue that makes factor 7 activate Factor 10.
It is the glue that activates 9 to 9a, and the glue that activates 10 to 10a, and the glue which converts (2) prothrombin into (2a) thrombin.
In a simplified way, think of calcium a positively electrically charged particle that "electrically" flicks a switch to start these protein chemical reactions.
Now back to my burns patient covered in calcium rich impregnated gauze mesh; do you appreciate Kaltostat and products like it a little more?
As a young ICU nurse in a big tertiary hospital more than 20 years ago, we had these blokes (4) who were burned in a caravan fire, all came into our unit. It was one of the most interesting (physiology) experiences of my life. The daily grind of bathing these guys, drug paralysed, sedated and fully ventilated became monotonous and the relentless surgeries, skin harvests and grafts made one wing of our ICU look nothing short of a macabre scene from some horror movie.
Daily these blokes seemed to return from theatre, and the dressing of choice was a product called Kaltostat. A calcium rich mesh that filled with blood oozing from graft sites, and became a clot.
Two points will be addressed in today's post. The first is the difference between a clot and a thrombus, the second is the role of calcium in this dressing and in the coagulation system in general.
First the Jargon. Clot vs Thrombus.
When platelets stick to the damaged inside wall of a vessel. This is called Platelet Adhesion.
When platelets stick to each other like a snow flakes in a snow ball, this is called Platelet Aggregation.
When platelets release substances to signal new tissue to grow eg- (Platelet Derived Growth Factor (PDGF)), or to signal other platelets to come (Thromboxane A2, ADP), or to initiate the coagulation cascade (PGI and calcium, factor V and VIII). This is all collectively called Platelet activation.
All these processes (adhesion, aggregation and activation) occur in the intravascular space. Ultimately this leads to a plug of solid matter at the site of vessel injury. This is called a thrombus.
When a thrombus breaks away from its attachment on a vessel wall and travels in the blood stream, it is called an embolus or embolism.
A clot is a thrombus, but outside the blood vessel.
A scab is a dehydrated or dried clot- usually over an external wound. The active mushy slough at the base of the scab and the wound bed is often active platelets, releasing PDGF stimulating the growth of new granulation tissue .
Now let's focus on Calcium.
Fundamentally a positively charged ion (cation) abbreviated to Ca++ .
Calcium is present in plasma, and interstitial fluid, but also specialised granules inside platelets called Delta granules. When a platelet is activated it releases the contents of its Delta granules which among other chemicals, includes Calcium onto its surface and into the surrounding plasma.
Factoid: sleeping (dormant) plasma coagulation factors like 7,9,10 and prothrombin(F2), are all negatively charged proteins. They therefore readily accept a positive charged particle to bind with. Calcium does this.
It is like the glue that makes factor 7 activate Factor 10.
It is the glue that activates 9 to 9a, and the glue that activates 10 to 10a, and the glue which converts (2) prothrombin into (2a) thrombin.
In a simplified way, think of calcium a positively electrically charged particle that "electrically" flicks a switch to start these protein chemical reactions.
Now back to my burns patient covered in calcium rich impregnated gauze mesh; do you appreciate Kaltostat and products like it a little more?
39 - coagulation series 5 of 7
KYJ39- Intrinsic Coagulation part 5.
I was over viewing the coagulation cascade that we have covered in our first 4 episodes, and also the process yet to cover, when it dawned on me that coagulation is much like the startup sequence of an aircraft. Flick that switch, twist that knob, push this button, then shift that lever. It happens with all the precision of a skilled pilot.
The intrinsic (contact activation) pathway started with Factor 12 (FXII or Hageman Factor) becoming activated by a blood contaminant, bacteria or tissue injury.
The process in now underway. Activated Hageman factor (FXIIa) catalyses the activation of factor XI (Plasma Thromboplastin). There is not much to
Be said for FXI, except that it is another liver produced protein which circulates in plasma as a dormant sleeper, and woken up by activation of Hageman Factor.
Once activated Thromboplastin, switches on factor 9 (Factor IX) also called Christmas Factor. We discussed this briefly in an earlier post (KYJ 28) if you missed it click to http://KnowingYourJargon.blogspot.com
Now Factor 9 is activated which activates Factor 10.
12 - 12a - 11 - 11a - 9 - 9a - 10 - 10a.
Do you get a sense that one inactive protein is activated, which switches on or activates the next in a "dominoes" effect like cascade. It is literally a chain reaction.
Now we have covered all the coagulation factors that are called Serine proteases. This means that they act as enzymes (*ases) that activate other chemical reactions.
This post brings the Intrinsic and extrinsic pathway to a common point- Factor X.
The X Factor is therefore the start of what is called the Common Pathway.
Let's summarise:
Injured vessel releases tissue factor (F3)
F3 converts F7 to activate F10.
Or
Tissue injury allows F12 to activate, converting F11, converting F9 activating F10.
Now the pathway to clotting is the same.
Factor 10 activates F2 (prothrombin to Thrombin),
which activates Factor 1 (fibrinogen into Fibrin clots)
...
The coagulation factors that have not been covered yet include Factors 5, 8, 13, and the proteins S, C, Z and of course Calcium (Factor 4).
Stay tuned and we will fill in the gaps in the next episode.
I was over viewing the coagulation cascade that we have covered in our first 4 episodes, and also the process yet to cover, when it dawned on me that coagulation is much like the startup sequence of an aircraft. Flick that switch, twist that knob, push this button, then shift that lever. It happens with all the precision of a skilled pilot.
The intrinsic (contact activation) pathway started with Factor 12 (FXII or Hageman Factor) becoming activated by a blood contaminant, bacteria or tissue injury.
The process in now underway. Activated Hageman factor (FXIIa) catalyses the activation of factor XI (Plasma Thromboplastin). There is not much to
Be said for FXI, except that it is another liver produced protein which circulates in plasma as a dormant sleeper, and woken up by activation of Hageman Factor.
Once activated Thromboplastin, switches on factor 9 (Factor IX) also called Christmas Factor. We discussed this briefly in an earlier post (KYJ 28) if you missed it click to http://KnowingYourJargon.blogspot.com
Now Factor 9 is activated which activates Factor 10.
12 - 12a - 11 - 11a - 9 - 9a - 10 - 10a.
Do you get a sense that one inactive protein is activated, which switches on or activates the next in a "dominoes" effect like cascade. It is literally a chain reaction.
Now we have covered all the coagulation factors that are called Serine proteases. This means that they act as enzymes (*ases) that activate other chemical reactions.
This post brings the Intrinsic and extrinsic pathway to a common point- Factor X.
The X Factor is therefore the start of what is called the Common Pathway.
Let's summarise:
Injured vessel releases tissue factor (F3)
F3 converts F7 to activate F10.
Or
Tissue injury allows F12 to activate, converting F11, converting F9 activating F10.
Now the pathway to clotting is the same.
Factor 10 activates F2 (prothrombin to Thrombin),
which activates Factor 1 (fibrinogen into Fibrin clots)
...
The coagulation factors that have not been covered yet include Factors 5, 8, 13, and the proteins S, C, Z and of course Calcium (Factor 4).
Stay tuned and we will fill in the gaps in the next episode.
38 - Coagulation Series part 4 of 8
KYJ38 - Intrinsic Coagulation System. 4 of 7.
This is the 4th post in a series on Coagulation factors.
In the first three episodes we looked at the Tissue Factor Activation pathway- otherwise known as the Extrinsic pathway.
This edition of a KYJ looks at the initiation of the Intrinsic pathway, or more recently known as the Contact Activation.
Let's start with blood or more specifically Plasma.
Plasma is a cocktail of salts, glucose and proteins. Many of the proteins in plasma serve a role in coagulation, and to date, we have discussed Tissue factor 3, VonWillebrand Factor and the plasma Factors 7, 10, 2, and 1.
Well as you guessed, the numbers in between are all involved in the intrinsic pathway. Let's start with the contact (intrinsic) activation of the coagulation cascade.
If blood comes into contact with a negatively charged surface such as glass, foreign objects, bacteria, or Tissue factors released by damaged cells, it initiates the contact activation pathway.
It starts when a protein called "High-molecular-weight kininogen" (HMWK), (also known as the Williams-Fitzgerald-Flaujeac Factor ) that shares a role in both the coagulation system as well as the kinin-kallikrein system, is activated by a negatively charged contact.
Additionally, a factor called Hageman Factor (Factor XII) And another protein called Prekellikrein (PK) also activates , and together the three proteins activate Factor 12 into Factor XIIa.
Hageman Factor was named in 1955 after a Railway worker was found to be deficient in Factor XII. His blood simply wouldn't coagulate in a glass test tube. Deficiency of factor XII is a rare genetic disease and can be considered a form of a Haemophilia. The genetic link was discovered when some family members also were found to be deficient in this liver manufactured protein.
Are you developing an understanding as to why chronic liver failure patients develop clotting and coagulation disorders??
More on this system in our next edition.
This is the 4th post in a series on Coagulation factors.
In the first three episodes we looked at the Tissue Factor Activation pathway- otherwise known as the Extrinsic pathway.
This edition of a KYJ looks at the initiation of the Intrinsic pathway, or more recently known as the Contact Activation.
Let's start with blood or more specifically Plasma.
Plasma is a cocktail of salts, glucose and proteins. Many of the proteins in plasma serve a role in coagulation, and to date, we have discussed Tissue factor 3, VonWillebrand Factor and the plasma Factors 7, 10, 2, and 1.
Well as you guessed, the numbers in between are all involved in the intrinsic pathway. Let's start with the contact (intrinsic) activation of the coagulation cascade.
If blood comes into contact with a negatively charged surface such as glass, foreign objects, bacteria, or Tissue factors released by damaged cells, it initiates the contact activation pathway.
It starts when a protein called "High-molecular-weight kininogen" (HMWK), (also known as the Williams-Fitzgerald-Flaujeac Factor ) that shares a role in both the coagulation system as well as the kinin-kallikrein system, is activated by a negatively charged contact.
Additionally, a factor called Hageman Factor (Factor XII) And another protein called Prekellikrein (PK) also activates , and together the three proteins activate Factor 12 into Factor XIIa.
Hageman Factor was named in 1955 after a Railway worker was found to be deficient in Factor XII. His blood simply wouldn't coagulate in a glass test tube. Deficiency of factor XII is a rare genetic disease and can be considered a form of a Haemophilia. The genetic link was discovered when some family members also were found to be deficient in this liver manufactured protein.
Are you developing an understanding as to why chronic liver failure patients develop clotting and coagulation disorders??
More on this system in our next edition.
37 - Coagulation Factors part 3 of 7
KYJ37- Series part 3- Coagulation.
Summarising Coagulation : the solidification of liquid blood into
A solid gel is called Coagulation. It starts with either an injury to a vessel wall , or blood coming into contact with a negatively charged surface eg Bacteria, tissue injuries.
In the first two episodes we looked at the extrinsic pathway (vessel wall injury) and simplified the steps and coagulation factors (F):
F3 activates F7
F7 activates F10
F10 activates F2 (prothrombin into Thrombin)
Easy to remember if we say this simple math equation.
3+7=10 (2 Easy). A euphemism for the steps.
The activation of F10 was described as the beginning of the what is called the "Common Pathway", so named because both the extrinsic and intrinsic coagulation paths lead to the activation of F10 (Factor X).
So let's kick of from the Thrombin (factor IIa) the activated form of a Factor II.
Thrombin is a protein enzyme which is pivotal in the clotting cascade. Thrombin (FIIa) converts a plasma protein called Fibrinogen (Factor I) into the end product of coagulation, Fibrin (Factor Ia).
Fibrin are fine strands of fibres or strands which bond together in plasma to form a mesh like net.
This mesh wraps itself around and through platelets that aggregate at the site of the injured blood vessel. They sort of weave the platelet clot into a tight stable clump called a Fibrin Clot. The net like mesh further traps blood cells and more platelets together causing solidification of the blood.
Ultimately, all coagulation pathways lead to this final process of a Fibrinogen being converted (activated) into Fibrin.
Look at any scab or clot and what you are looking at is blood cells, platelets, and solidified plasma (Fibrin).
The whole process started with the exposure of blood to Tissue a Factor (FIII) and it finished with Factor I activated.
In our next edition, we will look at Factor 12 and the initiation of the Contact Pathway (Intrinsic) ,
Summarising Coagulation : the solidification of liquid blood into
A solid gel is called Coagulation. It starts with either an injury to a vessel wall , or blood coming into contact with a negatively charged surface eg Bacteria, tissue injuries.
In the first two episodes we looked at the extrinsic pathway (vessel wall injury) and simplified the steps and coagulation factors (F):
F3 activates F7
F7 activates F10
F10 activates F2 (prothrombin into Thrombin)
Easy to remember if we say this simple math equation.
3+7=10 (2 Easy). A euphemism for the steps.
The activation of F10 was described as the beginning of the what is called the "Common Pathway", so named because both the extrinsic and intrinsic coagulation paths lead to the activation of F10 (Factor X).
So let's kick of from the Thrombin (factor IIa) the activated form of a Factor II.
Thrombin is a protein enzyme which is pivotal in the clotting cascade. Thrombin (FIIa) converts a plasma protein called Fibrinogen (Factor I) into the end product of coagulation, Fibrin (Factor Ia).
Fibrin are fine strands of fibres or strands which bond together in plasma to form a mesh like net.
This mesh wraps itself around and through platelets that aggregate at the site of the injured blood vessel. They sort of weave the platelet clot into a tight stable clump called a Fibrin Clot. The net like mesh further traps blood cells and more platelets together causing solidification of the blood.
Ultimately, all coagulation pathways lead to this final process of a Fibrinogen being converted (activated) into Fibrin.
Look at any scab or clot and what you are looking at is blood cells, platelets, and solidified plasma (Fibrin).
The whole process started with the exposure of blood to Tissue a Factor (FIII) and it finished with Factor I activated.
In our next edition, we will look at Factor 12 and the initiation of the Contact Pathway (Intrinsic) ,
36- Coagulation series part 2 of 7
KYJ Series part 2 on Coagulation Factors.
In series 1, we reviewed the initiation of the Tissue Factor (extrinsic) pathway of coagulation. It used to be called extrinsic meaning external stimuli, because the cascade is initiated when Tissue Factor (Factor III) is exposed through vessel wall injury.
This session carries on with where we left off. Factor VII .
Factor VII circulates in the blood in an inactive form. It is manufactured by the liver using Vitamin K, a fat soluble nutrient found in leafy Green vegetables.
FVII is activated by tissue factor and vonWillebrand factor released by the endothelium and damaged vessel walls. Here it becomes factor VIIa.
Now this activated FVIIa causes a conversion of the first factor of the Common Pathway. So called because this is where the Tissue factor (extrinsic) initiation of coagulation converges with the contact activation (intrinsic pathway (another post)).
This first factor of the Common pathway is :
Factor X (Stuart-Prower factor), named after two people who suffered a form of factor X deficiency in the 20s and 30s.
Like FVII, Factor X is a liver synthesised protein enzyme also manufactured from Vit K. It circulates in blood doing nothing until it comes into contact with activated FVII (FVIIa) , then it activates to form Factor Xa.
This activation now stimulates the conversion of prothrombin (Factor II) into Thrombin, it's activated form (FIIa).
Let's summarise :
Injury to vessel
FIII exposed to plasma
FVII activates
FVIIa converts FX to FXa
FXa activates FII (prothrombin)
Into Factor IIa (Thrombin).
Perhaps you wondered how Warfarin (Coumadin) works to
Inhibit coagulation.
Well this drug and others like it inhibit the Vit K initiated synthesis of factors VII, X and Prothrombin (FII).
We are almost there with this arm of the coagulation cascade and the Extrinsic pathway factors.
Stay tuned for our next edition of KnowingYourJargon .
In series 1, we reviewed the initiation of the Tissue Factor (extrinsic) pathway of coagulation. It used to be called extrinsic meaning external stimuli, because the cascade is initiated when Tissue Factor (Factor III) is exposed through vessel wall injury.
This session carries on with where we left off. Factor VII .
Factor VII circulates in the blood in an inactive form. It is manufactured by the liver using Vitamin K, a fat soluble nutrient found in leafy Green vegetables.
FVII is activated by tissue factor and vonWillebrand factor released by the endothelium and damaged vessel walls. Here it becomes factor VIIa.
Now this activated FVIIa causes a conversion of the first factor of the Common Pathway. So called because this is where the Tissue factor (extrinsic) initiation of coagulation converges with the contact activation (intrinsic pathway (another post)).
This first factor of the Common pathway is :
Factor X (Stuart-Prower factor), named after two people who suffered a form of factor X deficiency in the 20s and 30s.
Like FVII, Factor X is a liver synthesised protein enzyme also manufactured from Vit K. It circulates in blood doing nothing until it comes into contact with activated FVII (FVIIa) , then it activates to form Factor Xa.
This activation now stimulates the conversion of prothrombin (Factor II) into Thrombin, it's activated form (FIIa).
Let's summarise :
Injury to vessel
FIII exposed to plasma
FVII activates
FVIIa converts FX to FXa
FXa activates FII (prothrombin)
Into Factor IIa (Thrombin).
Perhaps you wondered how Warfarin (Coumadin) works to
Inhibit coagulation.
Well this drug and others like it inhibit the Vit K initiated synthesis of factors VII, X and Prothrombin (FII).
We are almost there with this arm of the coagulation cascade and the Extrinsic pathway factors.
Stay tuned for our next edition of KnowingYourJargon .
35- Coagulation series 1 of 7
KYJ Series Part1-Coagulation factors.
I've posted before about the differences between clotting and coagulation. In summary, clotting is the clumping of platelets and coagulation is the solidification of fluid blood into a solid jelly.
The subject of this mini- series of posts is Coagulation, and specifically the different proteins that cause it to happen.
There are 14 factors involved in the complex cascade that we know of as coagulation. Most of them have funky names that honour people in history who had a deficiency or a discovery of one or more factors, or some complicated chemical name. But all coag factors have a Roman numeral name , and it is these that I will refer to most.
Most nurses will remember the old intrinsic and extrinsic coagulation pathways, from 1st or 2nd year of their studies. This old theory has since been replaced by a similar "contact activation vs common coagulation pathways"
This series will tackle this as simply as possible.
Start off with the following basics:
A blood vessel is lined by dynamic cells (endothelium) that produce many substances that repel platelets, constrict vessels, and inhibit solidification of blood.
If damaged, the underlying collagen surface of the vessel is exposed, and attracts platelets to stick to the injured vessel wall. This exposed collagen also initiates the first steps of the coagulation cascade.
Here we start.
Damaged endothelium, allows platelets to stick because a substance in the collagen called Tissue factor (factor III) attracts platelets and his starts the cascade.
Enter another substance secreted by endothelium. Endothelium makes and stores von Willebrand factor (vWF). Von Willebrand factor is secreted from the endothelial cell both into the plasma and also under the endothelial layer into the subendothelial matrix. It is a large protein that acts like glue sticking platelets to one another and to the subendothelial matrix at an injury site.
The other major function of vWF is to act as a carrier protein for factor VIII (antihaemophilic factor). More on this factor in another post.
So vonWillebrand Factor (vWF) allows platelets to stick to their mates- this is called platelet aggregation and when this happens, the platelet undergoes activation and the result is a fragile and unstable clot.
The unstable clot is called a Primary platelet plug, because it aims to plug the hole in the vessel wall at the site of endothelial injury.
To stabilise and strengthen the clot, plasma is activated to form strands of insoluble fibrin, which wraps around the clot like a mesh, and traps more platelets, and blood cells floating past.
The activation of plasma takes place by the release of the tissue factor (factor III) and vWF now joining with a plasma protein called proconvertin (factor VII).
This chemical cocktail activates Factor VII into VIIa . The little "a" means activated.
This is the contact activation or (extrinsic) pathway under way.
In our next part we will
Look at the role of activated factor VII (FVIIa), and the solidification of plasma.
Summary:
Vessel injury exposes FIII to platelets and plasma.
Platelets respond by using vWF to stick together.
Plasma responds by activating FVII.
It does get exciting from here on in.
I've posted before about the differences between clotting and coagulation. In summary, clotting is the clumping of platelets and coagulation is the solidification of fluid blood into a solid jelly.
The subject of this mini- series of posts is Coagulation, and specifically the different proteins that cause it to happen.
There are 14 factors involved in the complex cascade that we know of as coagulation. Most of them have funky names that honour people in history who had a deficiency or a discovery of one or more factors, or some complicated chemical name. But all coag factors have a Roman numeral name , and it is these that I will refer to most.
Most nurses will remember the old intrinsic and extrinsic coagulation pathways, from 1st or 2nd year of their studies. This old theory has since been replaced by a similar "contact activation vs common coagulation pathways"
This series will tackle this as simply as possible.
Start off with the following basics:
A blood vessel is lined by dynamic cells (endothelium) that produce many substances that repel platelets, constrict vessels, and inhibit solidification of blood.
If damaged, the underlying collagen surface of the vessel is exposed, and attracts platelets to stick to the injured vessel wall. This exposed collagen also initiates the first steps of the coagulation cascade.
Here we start.
Damaged endothelium, allows platelets to stick because a substance in the collagen called Tissue factor (factor III) attracts platelets and his starts the cascade.
Enter another substance secreted by endothelium. Endothelium makes and stores von Willebrand factor (vWF). Von Willebrand factor is secreted from the endothelial cell both into the plasma and also under the endothelial layer into the subendothelial matrix. It is a large protein that acts like glue sticking platelets to one another and to the subendothelial matrix at an injury site.
The other major function of vWF is to act as a carrier protein for factor VIII (antihaemophilic factor). More on this factor in another post.
So vonWillebrand Factor (vWF) allows platelets to stick to their mates- this is called platelet aggregation and when this happens, the platelet undergoes activation and the result is a fragile and unstable clot.
The unstable clot is called a Primary platelet plug, because it aims to plug the hole in the vessel wall at the site of endothelial injury.
To stabilise and strengthen the clot, plasma is activated to form strands of insoluble fibrin, which wraps around the clot like a mesh, and traps more platelets, and blood cells floating past.
The activation of plasma takes place by the release of the tissue factor (factor III) and vWF now joining with a plasma protein called proconvertin (factor VII).
This chemical cocktail activates Factor VII into VIIa . The little "a" means activated.
This is the contact activation or (extrinsic) pathway under way.
In our next part we will
Look at the role of activated factor VII (FVIIa), and the solidification of plasma.
Summary:
Vessel injury exposes FIII to platelets and plasma.
Platelets respond by using vWF to stick together.
Plasma responds by activating FVII.
It does get exciting from here on in.
Saturday 4 January 2014
Why shouldn't we put Oxygen on chest pain patients
WHY NO OXYGEN ON MY CHEST PAIN PATIENT???
I've received an email from a follower to cover the oxygen on a chest pain issue from a Why we don't use oxygen any more on AMI patients.
I'll start by saying... Do what your policies /protocols say, and if they are wrong, lobby to have them changed.
Second what I'm summarising here is a distillation of literature that spans papers back to 1964.
Cabello, J. et.al. (2010). Oxygen therapy for acute myocardial infarction (Review). The Cochrane Library
http://www.thecochranelibrary.com/details/file/742697/CD007160.html
Burls et al 2011
Emergency med Journal did a meta analysis.
http://www.medscape.com/viewarticle/752314
Beazley et al 2007 who looked at
Historical perspectives
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809170/
And the article that probably started the debate early in 1900, yes 113 years ago...
Steele's article in the BMJ claiming oxygen relieved Angina.
And it does. No one is disputing this. It is like saying Crack makes you High, but does it mean that it is the right thing to use??
Oxygen in the blood of a MI / chest pain patient is (more often than not) in sufficient saturations (94-99%).
Pain is caused by a narrowing, vasospasm or clot blockage to a coronary vessel feeding oxygenated blood to a chunk of heart muscle.
When cardiac blood flow reduces, the cells suffer Ischaemia (hypoxia) not due to lack of oxygen in the blood, but lack of flow to tissue (perfusion).
The thought originally was improve O2 in blood, and we prove O2 cell delivery in what little perfusion we have. But it doesn't work.
It doesn't work.!!
When you increase O2 concentration in blood it dissolves more oxygen in plasma (Pa02). It doesn't carry more on haemoglobin. And high plasma concentrations (pressures) of oxygen exert a vasoconstrictor effect on coronary arteries.
Doesn't that seem dumb to you? In Angina, or AMI, aren't we trying to improve blood flow?!!
Effect 2
Oxygen molecules when released to previously ischaemic cardiac tissue cause physical damage to the cardiac cell membranes. This Oxidative burst results in the overproduction of oxygen free radicals. Hydrogen Peroxide, superoxide dismutase, singlet oxygen, to name a few. These substances are the route cause of the cell damage that occurs when we dissolve the clot or give GTN restoring blood flow. This lipid peroxidation of the cell membranes is called Reperfusion Injury. It destabilises action potentials in the cardiac mass , which leads to reperfusion arrhythmias.
So in a nut shell organisations are scrambling to change policies to ensure clinicians only use oxygen on patients in shock or those with desaturation. If sats are <94% Use oxygen, but if not, they don't need it, and it is probably doing damage.
ILCOR and our own Australian Resuscitation Council are on it with guideline changes in 2010 as a result of Cabello's work.
The giants of the cardiac world Am Heart Assn , Australian Heart Foundation has given it the tick!
Queensland Health is on it with policy written categorically stating to only oxygenate to maintain O2 above 93%. (PCCM 2011 page 80)
For more than 45 years we have known that oxygen delivery on chest pain patients is potentially damaging. Use it judiciously.
I've received an email from a follower to cover the oxygen on a chest pain issue from a Why we don't use oxygen any more on AMI patients.
I'll start by saying... Do what your policies /protocols say, and if they are wrong, lobby to have them changed.
Second what I'm summarising here is a distillation of literature that spans papers back to 1964.
Cabello, J. et.al. (2010). Oxygen therapy for acute myocardial infarction (Review). The Cochrane Library
http://www.thecochranelibrary.com/details/file/742697/CD007160.html
Burls et al 2011
Emergency med Journal did a meta analysis.
http://www.medscape.com/viewarticle/752314
Beazley et al 2007 who looked at
Historical perspectives
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809170/
And the article that probably started the debate early in 1900, yes 113 years ago...
Steele's article in the BMJ claiming oxygen relieved Angina.
And it does. No one is disputing this. It is like saying Crack makes you High, but does it mean that it is the right thing to use??
Oxygen in the blood of a MI / chest pain patient is (more often than not) in sufficient saturations (94-99%).
Pain is caused by a narrowing, vasospasm or clot blockage to a coronary vessel feeding oxygenated blood to a chunk of heart muscle.
When cardiac blood flow reduces, the cells suffer Ischaemia (hypoxia) not due to lack of oxygen in the blood, but lack of flow to tissue (perfusion).
The thought originally was improve O2 in blood, and we prove O2 cell delivery in what little perfusion we have. But it doesn't work.
It doesn't work.!!
When you increase O2 concentration in blood it dissolves more oxygen in plasma (Pa02). It doesn't carry more on haemoglobin. And high plasma concentrations (pressures) of oxygen exert a vasoconstrictor effect on coronary arteries.
Doesn't that seem dumb to you? In Angina, or AMI, aren't we trying to improve blood flow?!!
Effect 2
Oxygen molecules when released to previously ischaemic cardiac tissue cause physical damage to the cardiac cell membranes. This Oxidative burst results in the overproduction of oxygen free radicals. Hydrogen Peroxide, superoxide dismutase, singlet oxygen, to name a few. These substances are the route cause of the cell damage that occurs when we dissolve the clot or give GTN restoring blood flow. This lipid peroxidation of the cell membranes is called Reperfusion Injury. It destabilises action potentials in the cardiac mass , which leads to reperfusion arrhythmias.
So in a nut shell organisations are scrambling to change policies to ensure clinicians only use oxygen on patients in shock or those with desaturation. If sats are <94% Use oxygen, but if not, they don't need it, and it is probably doing damage.
ILCOR and our own Australian Resuscitation Council are on it with guideline changes in 2010 as a result of Cabello's work.
The giants of the cardiac world Am Heart Assn , Australian Heart Foundation has given it the tick!
Queensland Health is on it with policy written categorically stating to only oxygenate to maintain O2 above 93%. (PCCM 2011 page 80)
For more than 45 years we have known that oxygen delivery on chest pain patients is potentially damaging. Use it judiciously.
Friday 3 January 2014
34- Respiratory Failure 1 and 2
KYJ34 - Resp Failure 1 & 2.
Today's post is really very simple, yet complicated by jargon by the medical world.
What is your concept of Respiratory Failure?
For many nurses, the notion of RF is a simple one defined by its title. Remember "respiration" is all about the exchange of gases.
So respiratory failure is a failure to maintain normal blood gas- ultimately, normal oxygen levels.
Hence, the definition of Respiratory Failure is a patient with PaO2 < 60mmHg (normal is 80-100)
Now once RF is determined, type 2 respiratory failure includes an altered Carbon Dioxide (PaCO2) level in and a reduced pH of arterial blood.
Specifically PaCO2 > 50mmHg ( normal is 35-45)
and
Lower pH than 7.35 (acidosis).
Functionally, a type 1 RF is a fairly acute condition like pneumonia, Pulmonary Oedema, PE, asthma, or low oxygen environments like high altitude climbers.
Type 2 RF, is seen in patients with chronic lung diseases like Mesothelioma, emphysema, COPD, and lung cancers. These patients invariably started with Hypoxaemia, (the diagnostic criteria for RF) but their pathology, affects the excretion of CO2, and drop in pH in addition to the Hypoxaemia (PaO2 <60).
Recap-
RF1= low oxygen in blood
RF2= low oxygen in blood
and high CO2 (hypercapnoea)
and Low pH (acidosis)
What to do-- oxygenate.
Remember hypoxia kills, hypercapnoea happens!
Today's post is really very simple, yet complicated by jargon by the medical world.
What is your concept of Respiratory Failure?
For many nurses, the notion of RF is a simple one defined by its title. Remember "respiration" is all about the exchange of gases.
So respiratory failure is a failure to maintain normal blood gas- ultimately, normal oxygen levels.
Hence, the definition of Respiratory Failure is a patient with PaO2 < 60mmHg (normal is 80-100)
Now once RF is determined, type 2 respiratory failure includes an altered Carbon Dioxide (PaCO2) level in and a reduced pH of arterial blood.
Specifically PaCO2 > 50mmHg ( normal is 35-45)
and
Lower pH than 7.35 (acidosis).
Functionally, a type 1 RF is a fairly acute condition like pneumonia, Pulmonary Oedema, PE, asthma, or low oxygen environments like high altitude climbers.
Type 2 RF, is seen in patients with chronic lung diseases like Mesothelioma, emphysema, COPD, and lung cancers. These patients invariably started with Hypoxaemia, (the diagnostic criteria for RF) but their pathology, affects the excretion of CO2, and drop in pH in addition to the Hypoxaemia (PaO2 <60).
Recap-
RF1= low oxygen in blood
RF2= low oxygen in blood
and high CO2 (hypercapnoea)
and Low pH (acidosis)
What to do-- oxygenate.
Remember hypoxia kills, hypercapnoea happens!
Thursday 2 January 2014
33- Blood and it's products
KYJ 33- Blood products
When they bleed, why not just give them blood?
Blood is a cocktail of substances. Water, cells, salts and proteins.
Cells carry oxygen (red cells) , fight infection (white cells) and stop bleeding by forming clots (platelets).
Because capillaries are prone to leaking certain salts and proteins hold water inside the blood vessel (albumen). These large molecules of albumen can't fit through the small holes in the capillary walls, and attract water, so by staying in the vessel this holds volume.
Another role of albumen is as a carrier of chemicals bound to the protein. Many drugs, bilirubin and hormones are transported on blood bound or plasma proteins.
Other proteins help fight infection. These are called antibodies or Immunoglobulins, and they are created by white blood cells after an exposure to a wild pathogen or vaccine .
Finally a class of proteins called coagulation factors aid in the clotting process ( collectively these proteins are called factors. There are 13 of them). Ultimately these factors are activated by damage to a vessel wall, and result in the formation of insoluble strands of solid matter called fibrin, or a fibrin clot.
Once blood is donated at a blood bank (volume 500 ml) it is spun into it's separate parts.
The factors ( factor 1, 8 and 13) can be are separated off and frozen , this is called cryoprecipitate (Cryo for short), or Anti-haemophilic factor (AHF). Additionally factor 8 (VIII) can be further isolated.
The rest of the plasma is fresh frozen and hence called FFP.
Usually the FFP is thawed and given neat, but some people have allergic reactions to some of the Coagulation Factors , especially 1, 8 and 13, (cryo) so they cleave this off and deplete the FFP to make it safer for people likely to have a transfusion reaction. Some proteins are more allergenic.
This type of FFP is called cryodepleated FFP.
They harvest the red cells for people needing a haemoglobin transfusions, eg bleeding post op, or trauma, anaemic people. This blood product is called "packed cells".
White cells are binned (they would attack the person getting a transfusion) .
Platelets are kept in a separate bag alive (they die in 8 days).
Quick overview video I posted on the Subject.
When they bleed, why not just give them blood?
Blood is a cocktail of substances. Water, cells, salts and proteins.
Cells carry oxygen (red cells) , fight infection (white cells) and stop bleeding by forming clots (platelets).
Because capillaries are prone to leaking certain salts and proteins hold water inside the blood vessel (albumen). These large molecules of albumen can't fit through the small holes in the capillary walls, and attract water, so by staying in the vessel this holds volume.
Another role of albumen is as a carrier of chemicals bound to the protein. Many drugs, bilirubin and hormones are transported on blood bound or plasma proteins.
Other proteins help fight infection. These are called antibodies or Immunoglobulins, and they are created by white blood cells after an exposure to a wild pathogen or vaccine .
Finally a class of proteins called coagulation factors aid in the clotting process ( collectively these proteins are called factors. There are 13 of them). Ultimately these factors are activated by damage to a vessel wall, and result in the formation of insoluble strands of solid matter called fibrin, or a fibrin clot.
Once blood is donated at a blood bank (volume 500 ml) it is spun into it's separate parts.
The factors ( factor 1, 8 and 13) can be are separated off and frozen , this is called cryoprecipitate (Cryo for short), or Anti-haemophilic factor (AHF). Additionally factor 8 (VIII) can be further isolated.
The rest of the plasma is fresh frozen and hence called FFP.
Usually the FFP is thawed and given neat, but some people have allergic reactions to some of the Coagulation Factors , especially 1, 8 and 13, (cryo) so they cleave this off and deplete the FFP to make it safer for people likely to have a transfusion reaction. Some proteins are more allergenic.
This type of FFP is called cryodepleated FFP.
They harvest the red cells for people needing a haemoglobin transfusions, eg bleeding post op, or trauma, anaemic people. This blood product is called "packed cells".
White cells are binned (they would attack the person getting a transfusion) .
Platelets are kept in a separate bag alive (they die in 8 days).
Subscribe to:
Posts (Atom)