32 - Bilirubin,urobilinogen, jaundice explained

KYJ32- The Yellow Family

Meet Billy and Rubin, these guys are responsible for the yellow discolouration of skin (Jaundice and bruising) the colour of urine, bile and faeces.

Of course I am talking about Bilirubin.  To understand bilirubin, we need to go back to its origins.

Your red blood cells live for about 120 days, then disintegrate. A large part of the red blood cell is haemoglobin the oxygen carrying protein in all RBCs.

Haemoglobin when broken down yields a protein (Globin) that is further recycled into it's basic amino acids.
The haeme pigment is turned in to Biliverdin by white blood cells gobbling up the fragments of red blood cell.

An enzyme in the liver, spleen and other body tissues, converts the biliverdin into Bilirubin.  About 4 mg /kg is produced daily.  It is insoluble at this point so the liver conjugates bilirubin into a soluble form and releases it to the gut via the gall bladder as Bile.  It is a strongly yellow green pigment which stains bile and subsequently faeces.

Gut bacteria break down the bilirubin as bile into a deep yellow pigment called  urobilinogen. Some of this is reabsorbed into the blood stream and excreted via kidneys giving the urine it's characteristic straw yellow colour.  Much of the urobilinogen in the gut is further broken down to stercobilin and makes poo yellowy-brown.

This is all normal physiology. But when things go wrong in the liver, the insoluble bilirubin can't be processed, and accumulates in the blood stream.  The higher the level of bilirubin, the more yellow will be the skin and eyeballs (sclera) appear.  This is called Jaundice.
It is not a disease but a symptom of hepatic dysfunction.
In new born babies, their blood brain barrier is immature and poorly formed.  Bilirubin can cross the BBB and cause lethargy, seizures and coma in the extreme.

Jaundice we have described here is an accumulation of unprocessed bilirubin.
A second type is Cholestatic Jaundice.  In this type, bilirubin is conjugated to water soluble bilirubin, released as bile, but a blockage in the biliary system (eg gall stones) causes this bile pigments to back up into
The liver and spill into systemic blood. These bile pigments stain blood yellow causing jaundice, but also irritates the skin causing itching. Incessant scratching can damage the skin in these people.  The unbearable itching is called pruritis.

There we have it more jargon:
Haemoglobin into biliverdin into unconjugated (insoluble) bilirubin.

Bilirubin into bile into urobilinogen into urine (urobilin) and faeces (stercobilin)

Accumulation of unconjugated bilirubin causing yellowing (jaundice)

Accumulation of bile in blood causing Cholestatic jaundice and itching (pruritis).

Happy new Year... Don't drink too much or it just might be ..... "All yellow"

31- Exercise induced Asthma

KYJ 31- Exercise induced Asthma.

In this series "knowing your Jargon" we explore in plain English, the meaning of some of the words we throw around as jargon.

Sitting in a high end respiratory lecture one day the speaker (who obviously new their stuff, but was hopeless at sharing the knowledge in any meaningful way), addressed the topic of asthma and the pathophysiology.

One subject that caught my interest was bronchospasm caused by exercise.  Hard physical exercise is a known trigger for asthma, it is not an allergen that sets off the broncho spasm, but breathing itself.

First let's recap Asthma
A chronic disease that is characterised by a narrowed constricted bronchioles (bronchospasm), cough with sputum, wheeze, breathlessness.
Usually triggered by known allergens, eg house dust mites, smoke, pollens, food allergens.

More rarely exercise and sudden change from humid to dry air environments.  This post will focus on the non allergenic triggers being exercise and dry air.

Physiologically we are nasal breathing beings. Our nose anatomy is physiologically crafted to clean, warm and humidify the air we breathe.
Convoluted, moist mucous covered walls of your nasal cavity are densely serviced with shallow blood vessels that, together trap dust and foreign particles (mucous-snot), humidify the air coming in (mucous-snot), and warm the ambient air to body temperature (dense network of capillaries).

At rest, you effortlessly inhale through your nose and by the time this air travels down your trachea and into the lower airways (bronchioles) it is all nice and warm and humidified.

But when you breathe hard and fast because of vigorous exercise initiating mouth breathing, or, when there is a sudden climatic change from humid to dry or air conditioned air, then this optimal warming and humidification of inhaled air is not adequate.

Dry air arrives at the bronchioles where sensors detect the temperature and humidity being too low.  As a reflex, bronchiole smooth muscles and cells lining the inside of the airways, are stimulated to increase blood flow.  This increases perfusion to goblet cells (that secrete sputum), and the overload induces an expectorating cough.
The increase in blood flow to the capillaries lining the bronchioles now results in an increase of capillary blood pressure (hydrostatic pressure), forcing plasma to leak out of capillaries into the interstitial spaces of the bronchioles.  We call this swelling and engorgement, oedema, and as it swells into the bronchiole, it constricts the passage of air causing wheeze and shortness of breath.  The engorgement stimulates the parasympathetic nervous system to activate, which gives rise to smooth muscle constriction (bronchospasm), and further goblet cell secretions.

Sound familiar??  The pathophysiology of asthma, without the trigger being an immune response (Immuniglobulin E allergic ) inflammatory trigger.

Treatment?
Rest for most.
Humidity helps, but to open the airways, and relax those spasming muscles, salbutamol.
To dry up those secretions (atrovent / ipratropium ) or atropine.

Pathophys the ECT4Health way. Hope this helped your understanding of the differences between conventional and exercise /climate induced bronchospasm/asthma.

Share this with your colleagues.

30- Heat Stroke / exhaustion

KYJ- 30- Heat Stroke v Heat Exhaustion

With Australian temps this week going crazy, it is timely that we review the real possibility that people will die from dehydration and heat stress related conditions.

Young children, pets and elderly are at increased risk as their thermoregulation is unable to
maintain adequate intrinsic cooling with air temperatures in the low to mid 40s.

The symptoms of heat stroke are rapid, and occur as the body's ability to keep cool is overloaded by high air temp, humidity and exercise. Dehydration is rapid .

Early heat exhaustion symptoms include headache, lethargy, dizziness, and  muscle weakness and cramps.
Tachycardia (>120 in kids, >140 in babies, > 110 in adults).
And rapid breathing without exertion. This is especially diagnostic in kids, and a symptom of dehydration.

Nausea with vomiting compounds dehydration by eliminating a will to drink.

Heat stroke,
This morph or deterioration of heat exhaustion can be life-threatening.

In heat stroke the body’s temperature mechanism fails.

The skin is usually hot and dry .
The person is febrile- often above 41.
Collapse and fitting may occur in small children

Pyrexia (high fever) is the diagnostic feature that separates heat exhaustion from heat stroke.

Treatment
Step 1- Cooling
Remove unnecessary clothing, shade, swimming, cool showers, shopping centres and cinema can be life saving as a prevention agent.
Limit exercise.

Step 2 -Hydrate!!!
At least
1500ml non sugary fluids PLUS 20 -30 ml / kg body weight
Avoid energy drinks, caffeinated beverage and alcohol.

If symptoms of heat stroke are apparent, IV fluids and active cooling using cool mats may be needed.

Panadol, nurofen and aspirin DO nothing for this type of fever. !!! So don't use them . The patients care centres on hydration and active cooling.

Elderly patients may suffer electrolyte shifts causing muscle twitching and cramps, and cardiac failure. Arrest.
Baseline ECG and monitor blood Biochem, urine output and specific gravity.

Stay cool.
Rob Timmings

29- Pneumonia v atelectasis v pneumonitis

KYJ29- Pneumonia
Back to basics with today's Knowing Your Jargon episode.
Many nurses have a skewed understanding of respiratory terminology and sometimes even the simplest terms can be misunderstood.

This episode looks at three common terms.
Pneumonia
Atelectasis
Consolidation

First let's review normal lungs.
Air is drawn in to our alveoli (the smallest single cell thick air sacs of our lungs).  Inside each alveolus, exists two specialised lung cells (pneumocytes), the Type 1 and type 2 pneumocytes. Type 1 is squamous epithelium and literally forms the walls of the alveolus. Type 2, the Great Alveolar Cell, has the task of producing surfactant.

Surfactant lubricates the inside  of alveoli. It is a soap like function lowers the surface tension on the wall of each alveolus, and in doing so, it allows the walls of a collapsed (empty) alveolus, to easily pop open with the next breath.  It also serves a role in promoting gas exchange across the alveolar-vascular space (the gap between lung and blood).

Surfactant is produced from approx 36 weeks gestation, making the ventilation and gas exchange in preterm babies problematic.

Pneumonia is an absence of surfactant.  And is a function of either no production or damage/disease to the Type 2 cell.

When a baby is born preterm, or a person has suffered an immersion (drowning), or, most commonly, they get a lower respiratory tract infection (chest infection), surfactant is reduced or absent.  This loss is called Pneumonia.

Pneumonia (because of a surfactant loss) then causes the alveoli to collapse and stick shut.  The term for this is atelectasis.

In multiple alveoli undergoing atelectasis, a segment of lung or a whole lobe of lung may be affected.  This is termed segmental or lobar pneumonia, and frequently called consolidation.  Eg Right lower lobe consolidation and right lower lobe pneumonia are one in the same.

In chest infections an inflammatory process causes pneumonia and the resulting bacterial or viral cell damage leads to a inflammatory mediated proliferation of white blood cells to flood the infected area to fight infection and mop up dead cells.  This engorgement of blood converging on the infected tissue  is called pneumonitis (literally inflammation of the lung).

Pneumonitis, like all inflammation, gives rise to capillary leakage.  This exudate, and the dead bodies of bacteria or cellular debris is what we cough out as sputum.

Wow... We covered some jargon this episode. Don't forget to share the post and check all the posts out on the blog www.knowingyourjargon.blogspot.com

Like and share our page.
KYJ not to be confused with KYJelly, but still lubricating the minds of the multitudes.

Shock Series - part 6 of 6 Cardiogenic

Part 6 of 6 -Cardiogenic Shock

Recapping: Shock is a syndrome characterised by poor cellular perfusion. It can be preceded by

1. blood volume loss (Hypovolaemia),
2. obstruction of blood flow into the heart (obstructive),
3. failure to pump (cardiogenic), or
4. available blood being maldistributed (distributive).

In this final instalment we review Cardiogenic shock. As the name implies, cardio (heart)- genic (originates) is a form of shock that results in poor perfusion of cells secondary to the dysfunction of the heart.
Causes of mechanical pump failure are many and varied, but in the context of the trauma patient, a blunt or penetrating injury to the myocardium (heart muscle), or a traumatic myocardial infarction are all examples of a traumatic induced cardiogenic shock.
At the core of this type of shock is a patient with normal vascular tone and normal circulating volume, but with failure to effectively pump blood, cardiac output, blood pressure and tissue perfusion suffers.
Penetrating trauma is a surgical emergency. Ventricular lacerations require repair, and prognosis is poor. With normal healing process post trauma, inflammation causes altered cardiac compliance and force of contraction (inotropy), so outcomes are not good for traumatic cardiogenic shock patients.
Treatment for cardiogenic shock focuses on enhancing contractility, to improve cardiac output.
Positive inotropic infusions such as adrenaline and dopamine are used to increase cardiac contractility.
Anti arrhythmia medication is used to prevent arrhythmias, and nitrates to promote coronary perfusion.
Judicious IV fluids are used, as haemodilution and vascular overload are an unwanted complication.
In Summary:
Cardiogenic shock is a mechanical pump failure resulting in poor cardiac output.
Irrespective of the type of shock, all shock is life threatening. Be it a pump fail, loss of volume, obstruction or one of three types of maldistribution, cellular perfusion suffers, which is fundamentally, and quintessentially; shock.

Shock series part 5 of 6- Obstructive Shock

Part 5 of 6 - Obstructive Shock

Recapping: Shock is a syndrome characterised by poor cellular perfusion. It can be preceded by

1. blood volume loss (Hypovolaemia),
2. obstruction of blood flow into the heart (obstructive),
3. failure to pump (cardiogenic), or
4. available blood being maldistributed (distributive).

Over the last week we have covered Distributive shock and hypovolaemia.
Today we will review obstructive shock.
As the name implies, obstructive shock is a poor tissue perfusion because of a blockage (obstruction) to blood returning to the heart. Unlike maldistribution related distributive shock, where poor venous return is caused by vasodilation; the size of the venous space plays no role in obstructive shock.
A physical blockage to blood entering the right heart can manifest in chest trauma patients due to two primary conditions.
Tension pneumothorax and Pericardial Tamponade

In both conditions the heart is compressed or shifted by pressure that inhibits blood return. The mechanical pumping of the heart continues in vane , but with no blood coming into the heart, then cardiac output is all but impossible.
Treatment of obstructive shock is to remove the obstruction. In tension pneumothorax a needle is placed into the chest to release trapped pleural pressure (thoracentesis). In pericardial tamponade, blood collects in the space between the fibrous pericardial membranes, and compresses the Vena Cava and myocardium.

 Doctors trained in the technique can perform pericardiocentesis, which involves the insertion of a needle below the ribs, and into the engorged pericardial sac.  Alternatively, an open thoracotomy is performed to open the pericardial sac .
There, blood (or serous fluid) is aspirated to release pressure.

Obstructive shock occurs quickly, but with rapid assessment, it's cause can be quickly identified and managed. Restoration of cardiac output, and blood pressure is the aim of treatment. Secondary management may include surgery to repair bleeding pericardium, or a formal chest drain to aid in the recovery of pneumothorax.

Shock Series- part 4 of 6 hypovolaemia

Part 4 of 6 - Hypovolaemic Shock

Hypovolaemic Shock part 4 of a 6 part shock series

Recapping: Shock is a syndrome characterised by poor cellular perfusion. It can be preceded by

• blood volume loss (Hypovolaemia),
• obstruction of blood flow into the heart (obstructive),
• failure to pump (cardiogenic), or
• available blood being maldistributed (distributive).

This trauma pearl edition looks at blood loss as a cause of shock.
Haemorrhagic or Hypovolaemic shock is poor tissue perfusion due to a decrease in circulating blood volume. It is the most common type of shock in trauma patients.
Recapping our physiology, blood is s suspension of particles, cells, electrolytes, proteins and water. An average adult has about 60-65 ml/kg... Approximately 5.5 litres.
Hypovolaemia literally means low volume of blood and is classified into four stages according to the percentage of blood loss. A nice easy way to remember the stages is by recalling the game of tennis.
Stage 1 = 0-15% volume loss Stage 2 = 15-30% (750-1500ml) Stage 3 = 30-40% Stage 4 = more than 40% ( >2L)
With out stopping bleeding I guess it's "game, set, match!!"
Most hypovolaemia is caused through bleeding, but other causes can be dehydration, diarrhoea and severe burns where plasma leakage can be acutely life threatening.
Treatment for this shock focuses mostly on stopping bleeding. Door to theatre times in major trauma centres have improved, as have our accessory treatments. The old surgical adage that the only effective way to stop bleeding was "bright lights and sharp steel" still rings true, however a lot can be said for direct pressure, and elevation. Judicial use of tourniquet devices remain a valid option if there is delay to life saving surgery.
Therapy with clot activating mesh has proved successful, with products like Quickclot, Oxicel etc.
Drug therapy with Tranexamic Acid, and VitK, fresh frozen plasma (FFP) infusions, and platelet infusions has improved outcomes.
Fluid resuscitation IV or IOss has featured as a primary survey intervention for decades, however this is being challenged by the newest school of thought; is that of permissible hypotension. We have dedicated a trauma pearl to this topic; see below.
The gold standard management is to insert 2 x large bore IV cannulas, and attach the patient to a crystalloid (normal saline or Hartmann's (lactated Ringers).
Where 5-10 years ago it was commonplace to rapidly infuse 1-2litres; today the standard fluid bolus is 100-200 aliquots of saline to titrate systolic BP of 80-90 mmHg.
Fear of haemodilution, acidosis, coagulopathy, inadvertent cooling of the patient, and disruption of a haemostatic clot is rationale enough to be judicious with fluid resuscitation. In head trauma patients with potentially raised ICP, maintaining a SBP up to 100 mmHg is standard management.
Maintaining a balance of colloids, crystalloids and Blood products is an ongoing area of research, and whilst experts can't agree on any one protocol, a ratio of 3:1 crystalloid to colloid, appears to be most common. A blood product replacement regime using a ratio of 1:1:1 or for every bag of packed RBC, give a bag of FFP, and a bag of Platelets, yields favourable outcomes, but nigh impossible in remote and some rural areas.
Burns patients loose massive volumes of plasma. Special fluid resuscitation regimes include large volume replacment.
The Parkland formula is the most commonly used regimen.
Parkland is:

• 3-4ml X. Kg X. % of burn.
• Half of the volume given in the first 8 hours post burn ( back dated to the time of the injury)
• Remainder of volume over the following 16 hours.
• Eg: a 75kg man is 50% burnt at 10am.
• 4ml x 75= 300ml
• 300ml x 50 = 15000ml
• So by 6pm tonight he will require 7500ml.

Summary: Hypovolaemic shock is the most common of the shock syndromes in trauma, the principles of treatment are simple: stop bleeding, replace loss. However there is no one protocol to achieve this goal, and treatment is tailored to the individual on a case by case basis.

Shock Series 3 of 6 Anaphylaxis

Part 3 of 6 - Anaphylaxis a Distributive Shock 

Anaphylactic Shock part 3 of a 6 part shock series

Recapping: Shock is a syndrome characterised by poor cellular perfusion. It can be preceded by

• blood volume loss (Hypovolaemia),
• obstruction of blood flow into the heart (obstructive),
• failure to pump (cardiogenic), or
• available blood being maldistributed (distributive).

This trauma pearl edition continues to explore distributive shock; specifically anaphylactic shock.
Anaphylactic shock, is the severest manifestation of an allergic reaction. As a shock, it characteristically results in life threatening cellular hypoxia. It is classified as a type of distributive shock because it causes a wide spread vasodilation resulting in severe hypotension.
Similar to sepsis discussed in part 2, anaphylactic shock vasodilates because of immune system activation the difference I'd that in sepsis the endotoxins released from bacteria are the stimulus, but in anaphylactic reactions, it is the activation of immunoglobulin E.
When the body is exposed to an allergen (antigen), the plasma protein Immunoglobulin E, binds to it.
This activates white blood cells in the blood stream (basophils) and in tissue (Mast cells) to degranulate or burst open. These cells are full of Histamine and Heparin. Once released, heparin slows down coagulation (promoting blood glow locally), and histamine is a potent vasodilator. Blood vessels dilate and become engorged, causing plasma water to leak into the interstitial spaces between cells.
Oedema is experienced as hives and angioedema as seen in the image.
In severe swelling, airway obstruction is the rapid killer. A wide spread vasodilation doesn't just result in maldistribution of blood volume, but capillary leakage can result in Hypovolaemia, giving a dual shock syndrome resulting in catastrophic loss of blood pressure.
Anaphylaxis is life threatening and treated using :

• Antihistamine medication counters the vasodilation effect of histamine released by basophils and mast cells.
• IV or IO Fluid resuscitation may be required to restore volume.

Drug of choice (first line)

• Adrenaline IM or SC as a chemical vasoconstrictor, thus restoring vascular tone and BP, and reducing capillary leakage, plasma loss.
• Adrenaline dose: over 13yrs
• 0.5ml of 1:1000 =500mcg

Dose is age dependant and doses recommended by the NH&MRC, and the Australian Resuscitation council, can be found here for children.
The patients vital signs should be closely monitored, and repeat adrenaline doses can be given every 5 minutes.

Shock series 2 of 6 Neurogenic

In part Two we look at Neurogenic Shock
One of the three in the distributive shock family.

Recapping: Shock is a syndrome characterised by poor cellular perfusion. It can be preceded by

• blood volume loss (Hypovolaemia)
• obstruction of blood flow into the heart (obstructive)
• failure to pump (cardiogenic), or
• available blood being maldistributed (distributive)

This trauma pearl edition continues to explore distributive shock; specifically neurogenic shock.
Neurogenic means : originated in the nerves. It is a form of volume maldistribution caused through loss of venous return , where the sympathetic nervous controller of vessel diameter has been injured.
Lets go back a bit. The autonomic nervous system regulates many functions including heart rate, blood pressure, blood vessel and bronchial diameter.
Two branches: sympathetic = vasoconstriction, increase heart, increase BP.
Parasympathetic does the opposite! It slows the heart, drops BP, and dilates blood vessels.
I spinal injured patients, an injury to the spinal cord at or above the T6 vertebrae, can disrupt or sever the sympathetic influence on the heart.
Loss of sympathetic control, means the the parasympathetic influence over whelms.
Like a red army fighting a blue army on a battlefield: remove one side, and the other charges forward. This is seen in the neurogenic shock patient as bradycardia (slow heart rate) a widespread vasodilation, causing a maldistribution of volume, and results in ineffective circulation (loss of Blood pressure). Another feature of neurogenic shock is poikilothermia - which is an inability to sweat, shiver or regulate temperature. Poikilothermia patients get cold fast as the start to assume the temperature of the room. In neurogenic shock patients, hypothermia is a silent killer and one of the deadly triad. The clinician needs to aggressively keep these patients warm.
So neurogenic shock is not caused by the parasympathetic nervous system misbehaving, it is just that there is limited sympathetic tone to offer resistance. Loss of sympathetic tone therefore is the route cause of neurogenic shock. Venous pooling is treated using positioning, judicious fluid resuscitation (remember they have all their blood just maldistributed), and vasopressor drugs. Pharmacological agents like norepinephrine (noradrenaline), Aramine, and Epinephrine can offer assistance in countering vasodilation.
Neurogenic shock is not the same as spinal shock. Whilst the cause of both is a spinal cord injury, spinal shock is a symptom set that includes flaccidity of muscle tone below the level of injury, loss of reflexes, sensation and movement.
Spinal shock is not really a form of shock at all. Yet it can coexist with neurogenic shock in the same patient.
In Summary: neurogenic shock is a life threatening loss of sympathetic nerve tone caused through a spinal injury above the level of T6. It is a true shock in that it causes poor cellular perfusion secondary to maldistribution of circulating blood.
Keep the patient warm, flat and well oxygenated.

Shock part 1 of 6

Part 1 of 6 - Septic Shock (Distributive Shock 1 of 3)

SHOCK – classifications ( 1 of 6)

Put in the simplest way, Shock is the poor oxygenation of tissue, and cellular compromise that results.
Classified into four types:
SHOCK VIDEO

• Distributive – Sepsis, Neurogenic, anaphylactic
• Hypovolaemic
• Obstructive
• Cardiogenic

Today’s part 1 session will focus on the first of these and specifically Sepsis.
A photo is circulating the net at present. it depicts a man with severe gas gangrene to his right thigh. The story is a sad one, in that it resulted in the man’s death a short time after the image was taken, and emergency surgery had been performed.
Gas Gangrene is a fulminate anaerobic bacterial invasion of Muscle and skin tissue, resulting in characteristic discolouration and the formation of gas. The organism most responsible is Clostridia Perfringens a soil inhabiting cousin of Tetanus, and Botox.
When opportunistically invading tissue through a laceration, abrasion or the like, this anerobe produces an alphatoxin or endotoxin that vasoconstricts locally, causing tissue deoxygenation to support it’s multiplication. This results in necrosis of tissue and gas formation characteristic of the presentation.
Locallised sepsis such as gangrene causes catastrophic tissue loss, but perhaps more worrisome is the potential of septicaemia, or blood stream invasion of microbes.
This leads to Septic shock, and the topic that the rest of this Trauma Pearl will focus.
In septic shock, bacterial invasion leads to an enormous immune response to fight infection. Release of immunoglobulins other vasoactive cellular chemicals results in a global wide spread vasodilation of the venous network in the patient.
If veins dilate, the balance of blood volume left in arterial and capillary beds (where tissue oxygenation takes place) is reduced leading to hypotension (arterial) and hypoxaemia (capilliary) – Shock.
In addition, certain bacteria release endotoxins which bind to white blood cells and endothelium stimulating the release of cytokines that alter coagulation and initiate relaxation of vascular smooth muscle – Vasodilation.
The result of septic shock is that there is a wide spread maldistribution of the blood volume. This in the true sense is a distributive shock. Antibiotics do little to manage the shock once it has commenced. Judicial fluid replacement, positioning, Heparinisation, oxygen supplementation and redistribution using vasopressors continues to be the side game while assisting the patient to fight infection.
Sadly, septic shock has a poor prognosis, and nurses, paramedics and doctors should understand that all trauma patients are somewhat immunicompromised and at risk of developing septic shock, if not from their injuries, then from the myriad of invasive procedures we perform in haste to support A, B , Cs.

Check out the video summary
or read through the other 5 parts to the 6 episode series.
2 - Neurogenic Shock
3 - Anaphylaxis
4 - Hypovolaemic Shock
5 - Obstructive Shock
6 - Cardiogenic shock


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Kids tubes and numbers

Trauma Pearl #6
Kids, tubes and numbers.
Today's trauma pearl is more of a tip than an article. In the heat of a trauma resuscitation, many clinicians struggle to remember sizes of tubes (ETT, gastric, urinary catheter etc.) this quick pearl is a simple and easy formula to remember.

Start with ETT (endotracheal tube)
Using the child's age
(Age/4)+4= ETT
Eg
A 6 year old boy will require a size 5.5 tube.

Once we have a tracheal time size, other sized tubes can be calculated using a simple 2x3x4x rule. Lets use the example of an 8 year old child, who is hit by a car crossing the street.  She needs a size 6 ETT.

Now apply the 2x3x4x rule.
2x
Y-suction Catheter=2 x 6 =12
IDC (urine catheter)=2x6=12
Gastric (NG) tube = 2x 6 = 12
3x
How far to insert the ETT measured at the teeth is 3x ETT size
3x 6= 18. The tube should measure 18cm at the teeth.
4x
If the child needs a chest drain the standard size is 4x ETT
8 year old needs size 6 ETT
4x6 = 24g Intercostal catheter.

This simple tool is effective for adults too. When seconds count, and the team needs to function like a well oiled machine, tips and tricks like this are gold. Can you think of any? Why not contribute them here for us all to benefit from.

Cardiac Drugs 5 of 5 - calcium channel blocker

Cardiac Drugs Series- #5

In this series we briefly overview those drugs that our cardiac patients take for blood pressure control.
Check out our first four episodes on
ACE inhibitors (prils)
Ang2Receptor blockers (Sartans)
Beta blockers (lols)
Loop diuretics

Continuing in the same Antihypertensive (blood pressure lowering) theme, this episode looks at Calcium Channel Blockers. (Ca2+ blockers)

Before we start, we should review the normal role of calcium in our heart and blood vessels.   Muscle in the heart and smooth muscle in the walls of arteries (where blood pressure is regulated), requires calcium to flush into muscle cells to contract.

 Reflecting on basic electrolyte and cell physiology, you may recall that calcium ion concentrations outside cells is about 10 thousand times higher than Ca2+ levels inside cells.
At a microscopic level, the membrane of muscle cells (all cells) have tiny gates that open and close to allow specific substances into (influx) and out of (efflux) the cell.  As expected, cells have calcium specific gates (channels), which open when electrically stimulated (action potential).

Once these channels (gates) open, calcium influxes into the muscle cell and is used by the muscle cell to initiate a conformational change (muscle cell contraction).

Recognising that a contracted muscular wall of an artery results in an increase of pressure (blood is squeezed), it stands to reason that if I can give you a drug that blocks or prevents these calcium gates (channels) opening.

The result is impaired ability for the artery to contract or constrict .
The resulting relaxation of the artery causes there to be more space for blood= less arterial pressure. For all the same physiological reasons, calcium channel blocker act on cardiac muscle to reduce the force of the heart contraction.

A secondary effect that causes the reduction of heart rate is that calcium blockade reduces the speed of electrical impulses through the heart.

Examples of these drugs include verapamil and nifedipine.

Some (nifedipine) are fast acting, and effective in inhibiting smooth muscle contraction in hypertensive crisis, or premature labour.

Others are longer acting and used as another weapon against hypertension, and tachyarrythmias like SVT.

If you are enjoying these #FOAMed #ECT4Health medutorials, please share this post on your page or with your networks.

Cardiac Drugs 4 of 5 Loop Diuretics

Cardiac Drugs 4- loop diuretics

This is the 4th drug in my popular cardiac drug series.

Not strictly cardiac drugs, classes of diuretics have been used first and second line in cardiac patients since before the 80s.   This edition looks at the loop diuretics and specifically the drug Frusemide (Furosemide) marketed as Lasix for decades. Quite simply tradenamed because it lasts six hours.

This drug causes a reduction of sodium reabsorption in the ascending limb of the loop of Henle in the nephrons of the kidney.
If sodium is reabsorbed from the nephron, so to is water as it is osmotically attracted to salt.  Lasix inhibits this process causing the patients kidneys to lose or excrete sodium and consequently, water as urine. The process is called a diuresis.

Now let's explore why you would want to remove water from someone...

1.  Too much pressure in the veins causing overfilling and inefficiency in the patients heart. By removing water, we remove blood pressure making the heart work using less energy and oxygen. Doing this can improve the efficiency of a heart in a patient with congestive heart failure.

2.  After administering a unit of packed cells (RBCs) the osmotic pressure in the vascular space increases.  This drags water via osmosis into the blood stream.  Fluid overload here can make hard work for the heart, so Lasix pulls off this excess vascular water, and promotes its excretion via the kidneys.

3. Acute blood pressure control.
Less circulating blood volume means less pressure in the closed vascular system.    In patients with high blood pressure, the removal of a modest volume of water can reduce blood pressure.  Blood pressure that the heart has to pump against... For this reason is assists to
Reduce afterload, an inhibitor of the cardiac output.

4.  Pulmonary oedema and ankle swelling. As vascular volume is depleted, the interstitial fluid shifts into the vascular space to balance it.  So in a patient with oedema, Lasix can help strip the swelling excess fluid making breathing more comfortable, improving gas exchange, and survivability from an oedematous event often caused by heart failure.

Adverse effects:
Ototocicity or deafness caused by neural damage in the ears has been linked to high rapid doses of Lasix.

Hypotension.  It's effects can be dramatic on blood pressure.  Especially when first started on this drug, and when standing up, they can get a case of the dizzies.

Potassium depletion. In allowing excretion of sodium, occasionally potassium can be depleted too. For this reason, often they need a supplement of potassium.

Frequency.  Naturally these class of drugs makes someone want to pee more often. The patient needs to be told to expect this.

There you have it, a short yadda yadda on the loop diuretic Frusemide.

#FOAMed. #ECT4Health
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Cardiac Drugs 3 of 5 beta-blockers

Beta Blockers (Lols)
Cardiac Drugs Series #3 of 5

In this third edition on getting to know your cardiac drugs, we cover the B-blockers, or more correctly the
Beta- Adrenoreceptor antagonists.

Examples of these drugs include :
Propranolol
Metoprolol
Atenolol

To grasp these antiarrythmic and anti hypertensive drugs, you first need to review the relationship between stress, or shock and BP.

In shock when tissue is poorly perfused, or stress (fight or flight) the Adrenal Medulla releases a cocktail of hormones that aim to elevate BP.
Two such hormones are Adrenaline (or Epinephrine by another name), and Norepinephrine.

Their effects are many and varied, but happen because they bind to specialised receptors called alpha 1 & 2, beta1 and beta2 and Beta 3 adrenergic receptors.

As the name (beta blocker) implies, this class of drugs inhibits the beta 1,2and 3 effects, but newer more beta2 selective blockers have a dramatic effect.

Beta 2 receptors increase the force of cardiac contraction and blood flow to muscle, liver and brain.  But in doing so, this places a lot of demand on the heart.  In a patient with heart failure the use of a drug to inhibit this taxing effect of adrenaline and norepinephrine can assist the heart to reduce its workload, and pump more efficiently.

Beta blockers work on vascular smooth muscle, cardiac muscle and smooth muscle in the lungs.

Where lungs bronchiole smooth muscle is normally opened by adrenaline, beta blockers can actually cause bronchoconstriction , which is a serious side effect worsening ventilation and gas exchange.  In patients with severe restrictive lung diseases (COPD or asthma), this class of drug is best avoided.

Another effect is slowing down of the heart, so in patients who are Beta blocked, they have a reduced capacity to compensate in states of shock.

When expecting tachycardia in a stressed, anxious or shocked patient, the pulse rate barely elevates in those on these medications.  It is for this effect that this class of drugs is used to
inhibit tachyarrythmias.

Other strange effects of these drugs include insomnia, vivid nightmares and dreams, and blood sugar/lipid disturbances.

Cardiac Drugs 2 of 5 ARBs Sartans

Cardiac Drugs 2
In this 5 part series on cardiac drugs, we look at the "Sartans".

Sartans are anti hypertensives in a class of drugs known as Angiotensin2 receptor blockers or ARBs for short.

Recapping our physiology, low blood flow through the kidneys initiate a humoral cascade where ACE in lungs converts inactive Angiotensin into Angiotensin 2.
This potent substance increases blood pressure by stimulation arterial vasoconstriction, and stimulation of the Aldosterone secretion.

Receptors in vessels called AT-1 receptors are activated by Angiotensin 2 causing constriction, and hence , hypertension.

Sartan drugs are a family of drugs which compete at the AT1 receptor and effectively block the action of Angiotensin 2 from working.

Their direct effects are vasodilation, which reduces pressure inside the blood vessel. Used therefore as an anti hypertensive, Sartan drugs are a powerful weapon in the management of chronic heart failure.

Indirectly Sartans also inhibit Vasopressin (ADH) and promote sodium excretion by inhibiting aldosterone.  Where sodium is excreted via the kidneys, water (urine) follows.  This effect prevents venous overload (preload) which makes the hearts job to pump more efficient.

Examples of these drugs include Irbesartan, Telmisartan, and Losartan.

They are usually second line after ACE inhibitors. Side effects include headache and dizziness especially when standing up quickly. They don't tend to have the irritating cough that ACE inhibitors have, but a potentially worrying issue is the unconfirmed reports that ARBs increase risk of MI.
To date, there is no consensus and further investigations are underway.

If you are getting anything from these little snippets, please feel free to share our post and tag your nursing, medical and paramedic friends.

Our next edition will be beta blockers.

Cardiac Drugs 1 of 5 ACE inhibitors

Cardiac Drugs.
Part 1 of 5

Starting a new series on some of those cardiac drugs that we all give and probably take for granted.

Let's start with some physiology of hypertension.   We all know that blood vessels stiffen and become hardened (sclerosis) with age. With a reduction in flow, arteries in kidneys detect low flow, and stimulate the release of a protein called Renin from the juxtoglomerular cells.

Renin converts a protein in plasma to Angotensin.

Angiotensin in plasma is converted to an active state by Angiotensin Converting Enzyme (ACE) secreted in the lungs.

This conversion by ACE to angiotensin 2 causes potent chemical constriction of blood vessels , and elevates BP.

...
In patients with Heart Failure , high blood pressure makes the heart have to work so much harder to pump blood, that it actually fails, and heart failure worsens.

Less blood being pumped = Lower output = Lower kidney flow =  More Renin!!!   It is a viscous cycle.

So a class of drug that impairs this situation is an ACE inhibitor.

***pril
These drugs all have the suffix 'pril in their generic name.
Lisinopril
Perindopril
Ramipril
Captopril
Enalpril

All examples of these ACE inhibitor drugs.   By stoping ACE , these drugs inhibit the conversion of Angiotensin 1 into the active Angiotensin 2 which causes high blood pressure.

These drugs are not without their side effects. In fact, the side effects like annoying dry cough are often the reason for non compliance with this therapy.
An Increase of inflammatory pain caused by the release of Bradykinin when ACE is inhibited can make these drugs literally a Pain to take.  This problem usually results in a need to  switch therapy to the Sartan drugs.
And that is our next article.

26 - MAHA

KYJ26 - MAHA Microangiopathic Haemolytic Anaemia.

I love big medical words or long Latin terms that sound cool but are really very simple.  I'm such a geek that way.

A recent post on the snakebite condition VICC (KYJ25), prompted today's post.

Microangiopathic haemolytic anaemia is a condition seen in snakebites where coagulation is disrupted. In Australia this is almost exclusively Brown snakes.

It is literally the cutting up of red blood cells in the smallest peripheral blood vessels.
Microangiopathic (very small blood vessel disease) haemolytic (blood cutting or splitting) anaemia (literally without blood).

MAHA is caused during a disease that causes clotting and coagulation in the capillary beds in tissues and organs.  When fibrin clots form these fine stringy strands of mesh "dam" up the small blood vessels and as blood tries to squeeze past these fibrin strands they get shredded into fragments. It doesn't just happen to RBCs , but platelets and white blood cells causing "thrombocytopenia" and "leukopenia" respectively.

With wide spread RBC destruction, there exists, an anaemia and subsequent reduction in oxygen transport.

MAHA is most common in Aortic Stenosis where the stiff aortic valve fractures and breaks blood cells being ejected with force from the heart's left ventricle.

It is always present in a Disseminated Intravascular Coagulation (DIC), and as such the cellular debris that is left in the blood vessels as a result of MAHA, may lead to death by multiple organ dysfunction syndromes (previously called "multi-organ failure").

Summary:
MAHA is a haemolytic anaemia seen in the context of Brown snake bites, where fibrin destroys blood cells squeezing past clots.

25 - VICC

KYJ25 - VICC Venom induced Consumptive Coagulopathy

Snake bites have always interested me. Perhaps it was my teen experiences with having a pet snake, or the fascination with them being so lethal, but I've always been interested.

The physiology of their venom effects is something that we have come to understand over the last 30 years, and it is surprising that it is just on 30
years since pressure immobisation was introduced.

So let's spend a few episodes of KYJ to grasp the major venom effects of our Australian snakes.

Most common, is the widely known effect of bleeding.

More correctly coagulopathies are classified into consumptive (pro coagulant) coagulopathy and anticoagulant effects.

Classically, species of Taipan, Brown snake and Tiger snakes, cause early wide spread clotting which ironically then leaves the victim unable to coagulate .

This is called venom induced consumptive coagulopathy (VICC).

Snake venom causing VICC has a protein that activates prothrombin to convert to thrombin. Which then causes fibrinogen to be consumed by conversion into fibrin.
Widespread microscopic disseminated micro vascular coagulation takes place and claggs up brain, heart,lung , renal ,hepatic and other organs, leading to organ failure.
 Once all the fibrinogen had been used up, the patient (often still living) now had nil capacity to coagulate, and starts to bleed as though they have had an overdose of Warfarin.

While antivenin halts this process, the danger period is in the hours and days to follow as they are left coagulopathic.

The other form of bleeding effects (seen in Black snakes), is an anticoagulant effect preventing thrombin formation, but other venom effects of these black snakes like myotoxicity and renal impairment (addressed next episode) bear more clinical concerns.

In summary : VICC is early wide spread coagulation, followed by rapid inability to coagulate because of fibrinogen consumption,
Taipans (particularly the Inland Taipans) are the most potent venoms of any snake,

24 - tPA

KYJ24- tPA. Tissue plasminogen Activator.
One of our social media mates impactednurse.com (Ian Miller) crafted a fantastic step by step guide to the use of tenectoplase, a common tPA.

I thought I'd dedicate this post to helping you develop a greater understanding of this family of drugs.

First some normal physiology.
For years Japanese car manufacturers dreamed of producing a car tyre that when punctured, would automatically detect air leak and seal the hole.

Our blood vessels have done this for thousands of years. Constantly, your vessels endothelial cell linings become damaged and expose the underlying collagen layer to the blood circulating within. When this occurs, platelets stick to the exposed puncture site and activate a clotting cascade that attracts other platelets, and initiate fibrinogen (a plasma protein ) to convert to Fibrin strands. This latter chemical reaction exists to repair vessel damage but is initiated to stop bleeding. The process is simply the symphony of clotting and coagulation.

This process happens hundreds or thousands of times/day in your body.  You are making clots, and probably did it while you read this sentence.

So there are substances that these endothelial cells (lining your blood vessels) make. One such chemical is called tissue plasminogen activator (tPA).

TPA is released when a clot is detected. It's job is to convert a plasma protein called Plasminogen into an enzyme that gobbles up clots, and particularly Fibrin.  The enzyme is called Plasmin.

Summary: tPA released from Vessel wall cells, converts plasminogen into the active enzyme Plasmin, which dissolves fibrin clots.

Now... Let's look at Tenectoplase.  This is a tPA. Genetically manufactured from Chinese Hamster Ovarian cells.

When injected into the blood stream of patients suffering Myocardial infarction, Stroke, or Pulmonary Embolism, the tPA goes to work converting the patient's plasminogen into the enzymatic Plasmin.  This intern indiscriminately seeks and destroys all clots in the patient's body.

Can you imagine the patient who has had a recent wound, surgery or injury?  They could start bleeding from these areas, as the Plasmin is not fussy which clots it dissolves.  Catastrophic haemorrhage, wound dehiscence and strokes are potential complications from treatment with tPA. Look for ALOC, signs of shock and frank bleeding in the urine/faeces.

Minor side effects are things like microscopic haematuria, bleeding gums, and ready bruising.  If the patient had had venepunctures, they may ooze blood from these sites.

This tPA is a genetically modified version of your own natural ability to dissolve your own clots, but in appropriate conditions, is a life saver.

23 - Peritonism

KYJ23- Peritonism

Peritonism- and assessing the Abdomen

During a secondary assessment of a drowsy  patient post road traffic crash, a colleague reports that the abdomen is distended, rigid, and has rebound tenderness. There is no obvious bruising, but bowel sounds are absent.  How would you interpret this information?

Assessing an abdomen uses the three techniques of Inspection, Auscultation and Palpation in that order - think -  "look, listen , feel"

Look- Inspection
First observe the skin surface of the abdomen. Look for scars, bruises, lacerations and abrasions. Inspect contour of the abdomen and determine if it is symmetrical. Is there distension?
Presence of abdominal distension is seen in drowning victims, intraabdominal bleeding (organ rupture), or very distressed young children after crying.
Upper abdomen distension is usually less significant than lower abdo distension, which is sinister. In these circumstances you should maintain a high index of suspicion for a large intra peritoneal haemorrhage . Finally make an educated guess if the abdominal enlargement is trauma related, pregnancy or simply lifestyle girth enlargement ( beer gut ).

Listen - auscultation
Using the umbilicus as a land mark, mentally divide the abdomen left to right, and upper to lower quadrants .
Place the diaphragm on each quadrant to determine if bowel sounds are present. Normal finding is that within 60 seconds in each quadrant, bowel sounds should be heard. In stress and shock, the trauma patient's cardiovascular system will reduce blood flow to the gut. Peristalsis will reduce or stop, giving rise to a silent abdomen.
Bowel sounds also switch off if there is abdominal organ injury, so a silent abdomen is an unreliable piece of data to confirm intraabdominal pathology.  Still, it is valuable in the context of a thorough assessment.

Feel - Palpation
During trauma palpation, you are assessing for the following 3 things:
Pain- :
pain on pressing into each quadrant or on rebound ( ie when pressure  is released) the sensation of pain or tenderness is restricted to a patient who is conscious enough to feel it. Both pain on palpation and rebound tenderness is an ominous symptom of intraperitoneal bleeding , or organ damage, leakage of bowel contents.
Guarding:
Is the tensing up of a muscle group when a painful stimulus is expected. If you were to threaten to tickle a toddlers tummy, they would tense up their abdominal muscles.  This voluntary guarding is a normal finding. It is however abnormal for a patient to exhibit involuntary guarding. This finding is referred to as Rigidity. And is an ominous sign, especially if the patient is unconscious and technically can't perceive pain.
Organ Symmetry:
When systematically palpating each quadrant, feeling the size and contour of large organs is a skill best practiced. An enlarged liver or spleen can indicate a sub capsular haemorrhage, but is subtle and difficult to assess on palpation alone.

Peritonism refers to the rigid, tender to palpate, or rebound tenderness, and involuntary guarding. It is an important finding in the trauma patient and is highly suggestive of abdominal bleeding. Coupled with absent bowel sounds +\- distension, and this is a patient going for a Laparotomy or CT scan at the very least.

The normal abdomen is soft, non tender to palpate, has bowel sounds in 3 of 4 quadrants and no new distension.
Know normal so you can recognise abnormal. Practice on your kids, your partner or even healthy patients during a routine assessment, and hone your skills in Abdominal Assessment.

22 - Hypoxia Series 4 of 4

KYJ22- Ischaemic Hypoxia
Part 4 of our 4 part miniseries on poor cellular oxygenation (Hypoxia).

This final episode looks at hypoxia as a result of Ischaemia.

Ischaemia is a multifaceted term. It refers to a lack of blood flow to tissues whose cells subsequently become hypoxic.
In Ischaemia, the blood has enough oxygen in it, but for one or more reasons, the blood flow is reduced or obstructed, and can't reach distal cells/organs.

Excellent examples of Ischaemia include coronary arterial blockage that we know of as Myocardial Infarction (MI). Classically in  MI, the patients blood is well oxygenated, but a fibrin clot has blocked blood flow , so down stream cardiac tissue becomes hypoxic or ischaemic.

Another example might be a CVA where a clot occluded a cerebral vessel effectively cutting off oxygen delivery to a section of brain.  A third example is a DVT.  Finally a crush injury or compressive force applied to a body part, restricts blood flow and therefore oxygenation of tissues.  Such is the mechanism that underpins decubitus ulcers or pressure sores.

All these hypoxic tissues are concomitantly referred to a ischaemic.  Most correctly, ischaemic hypoxia.

Treatment is to identify the cause of reduced blood flow, and alleviate the blockage or compression.

Remember Hypoxia is lack of cellular oxygen:
It could be :
Cellular toxicity - Histotoxic
Low blood oxygen- Hypoxaemic
Low RBC or Hb count- Anaemic
A low blood flow- Ischaemic

But all result in dysfunction in cells.

21- hypoxia series- 3 of 4

KYJ21- Anaemic Hypoxia
In this 4 part miniseries on hypoxia, session 3 talks about Anaemic Hypoxia.

Recapping, hypoxia is the term used to describe poorly oxygenated cells.  This can occur through many mechanisms.  One such mechanism is loosely called anaemia. Literally anaemia means "without blood".  Anaemic hypoxia is similar but refers to two states of the blood's capacity to transport oxygen to cells.  In our last post we spoke of the reduced oxygen level in the blood (hypoxaemia), meaning that a percentage of the haemoglobin was unsaturated with oxygen.

Well what if you were fully saturated (100%) yet still didn't deliver adequate oxygen to tissues? One such situation occurs when there is :
1- less red blood cells
Or
2- less Haemoglobin in each Red blood cell.

1-  less red blood cells
This form of anaemia is seen in blood loss, or blood district ice diseases.  Given you have some 75 trillion RBC delivering your oxygen, it is reasonable to assume that if you had a massive trauma/surgery and lost a lot of blood, you would have less capacity to transport oxygen.  Haemorrhage or haemolytic anaemia is therefore a cause.

2- less haemoglobin
Given each RBC is stuffed with 200-300 million molecules of haemoglobin (made from iron), some people with misshaped RBC or iron deficiency, don't have as much Haemoglobin in each RBC.  Less Hb = less oxygen being transported per red blood cell.
Examples are Sickle Cell anaemia, or iron deficiency anaemia.

Summary:  in anaemic hypoxia, cells suffer because blood can't carry the quantity of oxygen to meet demand. Either too few RBC, or too little Hb in each RBC.

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20- hypoxia series 2 of 4

KYJ20- Hypoxaemic Hypoxia
This post is part 2 of a 4 part miniseries on the concept of Hypoxia.  Recapping- hypoxia is the term used to describe a cell or group of cells that do not gave adequate oxygen; literally hypoxia means low oxygen.

If you missed it our first post looked at Histotoxic hypoxia, this post looks at Hypoxaemic hypoxia.

Let's start with the concept that the cells of the body get oxygen delivered directly through diffusion from the blood stream.

This would imply that oxygen is carried in the blood, and it is. 97% of all oxygen carried in blood is bound to a red blood cell protein called haemoglobin, and is normally measured as a saturation percentage between 94-99%. The other three percent is dissolved in plasma and measured as a partial pressure between 80-100mmHg in arterial blood (40mmHg in veins).

When blood oxygen levels drop below normal, this is called Hypoxaemia.  Hypo =low, ox= oxygen, and aemia=blood.

Hypoxaemia = low blood oxygen.

Now, to ensure adequate cellular oxygen delivery, we need to ensure adequate blood oxygen concentration. Hypoxaemia will cause hypoxia.

So there you have it Hypoxaemic hypoxia is hypoxia caused because blood oxygen levels were too low.

The common cause is respiratory failure, due to lung infections, oedema or bronchial exudate, constriction and alveoli collapse (pneumonia).

Often the patient experiencing Hypoxaemic hypoxia, will have breathlessness as a central focus, but will always be poorly saturated.

Treatment... Oxygen. And manage the cause of hypoxaemia.

Go ahead... Fix dem lungs!

19 - Hypoxia 1 of 4

KYJ19- Hypoxia Types- Histotoxic

There are four types of Hypoxia.
Histotoxic
Hypoxaemic
Ischaemic
Anaemic

Today we look at Histotoxic.
But first we define hypoxia. Hypoxia is a common term yet often misunderstood in a nurses vocabulary.  It is Latin. It literally means low (hypo) oxygen (oxia)
Hypoxia -low oxygen.

As a term, it is used in medicine to refer specifically to cells.  Recapping that all cells need oxygen to be delivered constantly to drive the manufacture of energy (ATP), a cell or group of cells that is low in oxygen is said to be hypoxic.

Many reasons exist as to why a cell is how in oxygen. One such reason is that the cell is poisoned by a toxin.  Such hypoxia is called Histotoxic Hypoxia.  Literally, histo means cell, and toxic means poisoned.

In Histotoxic hypoxia a cell's ability to use oxygen has been damaged by substances that shut down the ability to manufacture energy.

Examples exist in smoke inhalation injuries, where two toxins, Carbon Monoxide, and Cyanide poison the cell.  Once affected by these toxins, the cell is disabled and unable to use oxygen.

Additionally, carbon monoxide gas displaces oxygen from the haemoglobin, rendering the red blood cells hypoxic. But that is tonight's  discussion.

Know your jargon (KYJ) .
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18 - SABA metered inhalers

KYJ18- SABA Metered Inhalers.
My princess started to develop a nocturnal cough in the last few days. Not a "little 11 year old girl" cough, but a deep "chesty old man with bronchitis" cough.

The change of the season tends to bring on a bit of bronchial hypersesponsiveness, that is characteristic of, and has essentially the same pathophysiology of, Asthma.

She (we) have always responded to SABAs and so I thought I would look at the common metered inhaler SABA.

SABAs are short acting beta-agonists. The most common in use (and over the counter in Australia) is Salbutamol marketed under the trade names of Asmol, or Ventolin. Many paramedics and nurses are familiar with the dosage forms of metered Aerosol (MA), nebulised and IV.   This post looks at the MA variety that any "Joe Lunchbox " can buy from their chemist (drug store), with no prescription.

First let's look at the action. In bronchial - hypersesponsiveness and asthma, one principle pathophysiological principle is that of bronchospasm.
Smooth muscles that surround the bronchioles constrict like snakes squeezing their prey. This restricts the air flow and stimulates over secretion of the mucous secreting cells that line the respiratory tract.  The symptoms are cough (cream sputum), and shortness of breath often with an audible wheeze as air squeezing through wet narrow tubes becomes turbulent.

Specialised adrenaline sensitive receptors in these smooth muscles, called Beta-receptors are stimulated by adrenaline (epinephrine) and instruct the muscles to relax. Thereby preventing the bronchial spasm of the muscle.  Other chemicals and drugs work on these same Beta receptors, and have this same effect. Salbutamol is one such drug.

The beta receptor or more correctly "beta Adrenergic receptors" because of their stimulation by adrenaline, are activated as part of the Sympathetic nervous system (SNS) response to stress and shock or threat (fight or flight response). If you were being chased by a deadly drop bear, your SNS would release Adrenaline to increase heart rate, contractility, stimulate glucose release into blood, open your pupils to
Let more light in, constricts blood vessels in your skin and gut to allow more blood to flow to muscles and vital organs, AND... Relaxes smooth muscle in your lungs to allow you to ventilate easier.

Parts of this sympathetic response can be mimicked by drugs that are called Sympathomimetics.  One such family of Sympsthomimetic is the Short (and long) Acting Beta Agonists (SABAs and LABAs).

Salbutamol -aka Albuterol in the USA (Ventolin) is a SABA that allows for constricted smooth bronchial muscle to relax, improving flow of air.

When buying Amy's Ventolin metered inhaler (puffer) yesterday I was very very surprised and disappointed to see the "how to use" leaflet showed images of the puffer being placed into the mouth of the model. No mention of a spacer device.

When these MA medications are used, the atomised gas is propelled at hundreds of MPH to the back of the throat or roof of the mouth where the drug is swallowed. It is not absorbed and as little as 0.2% of the dose gets to the lungs where they exert their effects topically.

It is functionally useless to use a MA puffer in your mouth. So I was astounded that the product insert showed this technique.

Used with a volume spacer device, either commercial, or makeshift with a water bottle, soda can or even an empty coffee cup, these puffers are more effective as nebulisers, and safer from an infection control point of view.

One other point. These sprays hold only two hundred (200) doses, yet contain enough compressed gas to continue making the characteristic spray sound for up to 350 squirts. The dangers inherent in this, is that a user could be using their MA with faith that they are getting medication delivered, but only getting the propellant gas.

Never use the patients own MA, always a fresh one when dosing.

In acute asthma attacks, the recommended first aid is a 4.4.4 procedure.

Sit the person up. Administer a dose via a spacer device and ask them to take 4 deep breaths. And repeat for 4 doses.
...
Wait 4 minutes and Repeat.
If no improvement in 10 minutes, or rapid deterioration occurs, they need hospital.
...
Steroids (IV Hydrocortisone, or Prednisone, betamethisone) does nothing for 4-6 hours.

Recap - 4 doses each with 4 breaths. Wait 4 minutes and repeat.

And ALWAYS use a volume spacer to allow the drug to atomise into a gas, before it is inhaled.

17- pulmonary Embolism

KYJ17- Pulmonary Embolism

Of all the causes of chest pain that are non cardiac, a pulmonary embolism (PE) has to be high on the hit list of acute killers.

A common cause is a clot in a peripheral vein breaking of and becoming liberated in blood returning to the heart.   With the venous returning blood merging into larger and larger veins enroute, the clot (now called an embolism) is free to journey all the way into the right heart, and through to the lungs.  Once in lungs, the pulmonary blood vessels become narrower and narrower, to the point where the traveling embolism gets lodged inside a lung vessel. This is a pulmonary embolism.

A person experiencing a pulmonary embolism most often experiences a classic triad of symptoms.
Shortness of breath
Tachycardia
Low oxygen saturations (Hypoxaemia)

There are other symptoms that relate to right heart failure (ankle swelling, ECG changes) in large PEs.

 The classic ECG change is a right Bundle branch block, and S1Q3T3 pattern seen in 10-50% of large PEs

S1Q3T3 is literally :
-a large S wave in lead I,
-a large Q wave in lead III and
-an inverted T wave in lead III

While it is commonly seen in those diagnosed with big PEs, it is one of those supporting signs of an already confirmed diagnosis, and is present in up to 20% of other right lung failure inducing conditions. It's value in diagnosis is negligible.

Diagnosis of PE is based on a criteria called the Wells Score.
It uses history, evaluation of risk factors, blood tests and with radiology.
The gold standard is pulmonary angiogram (CTPA) though VQ Scans are also used.

Risk factors include
Immobilisation post operatively
Long haul travel
Dehydration
Smoking
Pregnancy and hormone replacement
History of Deep Vein Thrombosis

Thus a patient who presents with these risk factors, and demonstrates the classic presentation of chest pain, shortness of breath and desaturation <94%, is a likely candidate for a CTPA.

In weak or low probability patients, a blood test called D-Dimer can be used to rule out PE. D-Dimer looks for breakdown products of a clot in the blood.  It would be present anytime someone is post op, or post injury of any kind, so s positive D-Dimer is not diagnostic.  A negative D-Dimer however, means there is no PE, do its negative predictive value is very good to rule out PE. It saves the patient from needing a risky CT scan.

Treatment.
Like a clot blocking a coronary blood vessel, a PE can be dissolved directly using a lysis agent, but contraindications (eg recent surgery) exist. For large life threatening PEs, thrombolysis or surgical (Thrombectomy) treatment is available.

The most common management is supportive reoxygenation therapy, and anticoagulant medication to prevent thrombus growth (snowballing).  The aim is to inhibit fibrin formation, to allow the patient to slowly dissolve the clot over time.

There you have it. PE. A deadly killer with 25% mortality. Don't forget to walk around that plane when you are next flying home from Europe!! And if you are on the Pill, for goodness sake stay active and quit the fags!!! (Disclaimer :  in Australia Fags are cigarettes)

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16-Oxyhaemoglobin dissociation curve

KYJ16- Oxyhemoglobin Dissociation curve.

It doesn't seem to matter how many courses on respiratory or ventilation I attend, there is always a teacher who makes a hash job of explaining the difficult concept of the oxyhaemoglobin dissociation curve.  After one of you requested this poison chalice, thought I'd have a go of explaining it my way.

First, know that haemoglobin binds to oxygen and we record this as saturation percentage (normal now believed to be SaO2 = 90-98%).

The plasma also dissolves oxygen into solution, and this exerts a pressure in plasma. In arteries we measure this in the normal range of 80-100mmHg.

The OHD curve achieves three things
First
The curve predicts that if Sats are normal, then pressures are normal. There is a direct relationship between the present age of Hb that is saturated, and the amount of plasma dissolved O2.  As one goes up, so does the other and if one goes down, the other follows.

Second
Being a sigmoid shape, the curve is flat at the top, and steep in the middle. For a drop in oxygen in the top 20mmhg of PaO2, there is little effect on saturation, but once a PaO2 drops below 80, the patients saturations drop below 95% and rapidly fall.

It works backwards too. If I look at your sats and they are in the high 90% (normal) I should be able to predict that your plasma O2 is also normal.  And nurses do that every shift.  We grab a sat probe, and use this as a guide to the patients oxygenation.

What we need to understand is that a 10% drop in sats from 99-89% is no where near as dramatic as a 10% drop between 89-79%!!
In fact sats below 88% is very dangerous, because blood is not carting enough oxygen to perfuse cells. With sats lower than 88% we predict a PaO2 at below 60mmHg.  This is technically the diagnostic criteria for Respiratory Failure.

Third
The last concept of the curve is called shift.
The graph curve can be skewed to the left or right of normal prediction, by things like pH, blood temperature, CO2, and a chemical on red blood cells called 2,3 DPG which allows red blood cells to release oxygen to cells.

When the curve is shifted to the left, then haemoglobin binds tightly to oxygen and is reluctant to give it up to the cell. It means sats will be high, but cells may be hypoxic, as oxygenated blood won't give up the goods.  I like to remember that a Left Shift means that oxygen is "left hanging on" to haemoglobin.

Left shift is caused when blood is
cold (<36C),
alkaline (pH >7.45),
And when a chemical called 2,3 DPG is lacking (banked blood products).

The opposite to these
High DPG
Acidosis (pH<7.35)
Hyperthermia
Causes a shift of the curve to the right. That means that for a given PaO2 the Hb saturation is less than predicted.
We may see low saturations in these patients meaning less oxygen is being carried in the blood. Cells naturally become hypoxic if blood is reluctant to carry oxygen.

15- Traumas Lethal Triad

KYJ15- the Lethal Triad.

The Lethal Triad is what I call the dark horses of the trauma room. The silent killers that creep out from nowhere and cause catastrophic deterioration.  The Lethal triad is:
• Hypothermia
• Coagulopathy
• Acidosis

Hypothermia is a common feature of the trauma patient who is a young child, elderly, burns or spinal. Whilst many mechanisms exist to cause hypothermia in trauma patients, the most common issue is hypovolaemia, and conduction as the patient lays on a cold bed, in an often 25 degrees (air conditioned) room.
 Loss of further heat must be avoided in the trauma room.
Hypothermia affects coagulation. In a bleeding patient where there is some reliance on the patients ability to stem haemorrhage, a cold patient has impaired haemostatic ability.
Hypothermia also causes alteration in oxygen transport. When cold, haemoglobin binds tightly to oxygen (left shift) and becomes reluctant to release oxygen at the cellular end . They appear well saturated (because they are) but hypoxic at cellular level (shock). The old adage of " keep them warm with a blanket so they don't go into shock", Is as true today as it ever was.

Coagulopathy as spoken about in a previous blog.  Is an altered ability to coagulate.  Coagulation is not the same as clotting

Blood is a suspension of water, proteins and cells. Traveling through pipes that are dynamic.
Your blood vessel walls actually secrete substances that keep your blood liquid.

Plasma will coagulate unless it is told not to by blood vessels. So what is coagulation?

Coagulation is a property whereby a liquid becomes a solid. In blood, it is a series of chemical reactions that convert a protein called prothrombin into thrombin, then fibrinogen into fibrin.
the plasma turns to jelly
Fibrin forms strands that mesh together clotting platelets in a spiderweb like net.  This forms a stable or Fibrin clot

Clotting is not the coagulation. It  is a process whereby platelets are stimulated (by vessel walls) to become activated and clump together.  Clotting works in synergy with coagulation to effect haemostasis (stop bleeding).
 But
In trauma patients who have bled, haemodilution (automatic shock response), the release of a protein called Thrombomodulin , cold, and over use of fluid resuscitation agents, contribute to poor coagulation.
Don't over hydrate your trauma patient ( see our shock series ).

Finally Acidosis.
Lowering of the pH occurs in shocked patients through three primary mechanisms
• Under ventilation leads to CO2 rise, which causes more CO2 to drag pH down.
• fluid overloading with Saline can lead to hyper chloraemic  acidosis
• hypo oxygenation of cells (Ischaemia) forces the cell to use anaerobic metabolism which (recalling 1st year cellular physiology) prevents pyruvate from entering the Kreb's cycle and instead, converts to lactic acid. - metabolic acidodis.

Ventilate the trauma patient with O2, keep them warm to promote cellular oxygenation and much of the problems with acidosis can be averted.

Lethal triad had been implicated in not only killing our trauma and shock patients early, but contributes to the third peak or delayed deaths by sepsis, multiple organ dysfunction, DIC, and ARDS.

14- oxygen saturations

KYJ14- Sats
Now before you just scroll past thinking you know oximetry and that random number generator we call a Sats probe, just consider that there might be a little something in today's episode of "Knowing your Jargon".

Oxygen is carried primarily in your red blood cell. Inside your RBCs (all 75 trillion) you have millions of iron rich molecules of protein called haemoglobin.

Form a picture of delivery van. Got that image?

This van is the red blood cell.
Now imagine opening the double doors of the van- and in the back of the van are millions of small lunch boxes. Each of these is haemoglobin.

93% of all our Oxygen is carried inside the haemoglobin. Some is dissolved into the plasma (water) of our blood and exerts a pressure (partial pressure).

If I measure that little bit of plasma dissolved oxygen, it is recorded as a partial pressure of oxygen. In arteries this is expressed as paO2 and normally 80-100 mmHg. In room air at sea level in a patient with a normal temperature (36-38 deg).

Back to the Haemoglobin (Hb).
Hb bound oxygen is responsible for 93% of the oxygen carried on blood. Understanding how these boxes of Hb helps us to grasp the jargon of measuring it,

Each Hb is only capable of holding 4 oxygen molecules.  When each of the 4 receptor binding sites is attached to an oxygen then we say that this Hb is 100% "saturated", meaning it can't hold any more oxygen.

If 3 sites are attached =75% saturated.
2=50% and 1=25%.

In arterial blood, or blood fresh from the lungs- Hb is usually 100% saturated. In Venous (deoxygenated) blood, the saturations are 75% saturated.  So we really only use a quarter of the oxygen we carry.

Now when we measure our saturations "sats" we can look at blood pulsing through our finger/toes/earlobes, non-invasively using a sats probe or we can take a sample of arterial blood, and measure saturation directly on a blood gas machine or portable iStat device.

Normal sats are 95-99% and reflect an average of millions of molecules of haemoglobin, not just one (which mathematically can only be either 75% or 100%).

If measuring sats using a probe on a finger, then the value is recorded as s saturation of pulsatile oxygen (SpO2).

If measuring sats of arterial blood you are recording it as a saturation of arterial oxygen, and the lowercase "a" denotes this, or SaO2.

Summary.
Saturations (SaO2 and SpO2) measure haemoglobin (RBC) bound oxygen.

Plasma bound oxygen is measured as a pressure not percentage. The abbreviation is PaO2 and normal is 80-100mmHg.

13- FEV1- FVC

KYJ13- FEV1/FVC Ratio

In "knowing your jargon" we look at the common jargon terms that our colleagues throw around. Today it is the respiratory diagnostic term FEV1:FVC.  These diagnostics are performed as a respiratory function study using a technique called Spirometry.  Nurses often have to record Spirometry, but don't always feel confident with the result interpretation, so let's have a crack at explaining some.

Take a breath in.  Breathe in.   Now take in a big breath and exhale as fast as you can and as much as you can through open mouth.

If you played along, what you just did was blow your FVC.
Forced Vital Capacity (FVC) is the total volume of air that you can exhale after taking in a big breath, then forcibly empty your lungs.  Your normal FVC varies with Age, height and sex.  Everyone's chest is different in dimension.
Example: a 45 year old woman 170cm has a FVC of 4 litres.

The other half of the ratio is the FEV1.  This stands for "Forced Expiratory Volume in 1second".  FEV1 is a function of how fast you can exhale all your air .  In a normally healthy lung, more than 80% of your breath should be able to be expelled in the first 1 second.

In restrictive lung diseases (asthma, bronchitis, emphysema, Ca) the ability to vent off breath fast is limited.
A diagnosis of COPD is made based on a FEV1 that is less than 70% of predicted FVC.

In these gas trapping disease states, alveolar destruction, narrowed bronchioles, and mucous production cause the passage of air to be restricted, thus slower in its ability to vent off.

An FEV1 measures the actual volume of gas inside that first 1 second, and for the exams of the 45 yo woman of 170cm that should have a FVC of 4 litres, her FEV1 should be at least 3.2 litres

FEV1/FVC ratio
Mathematically , 3.2/4 is 0.8 or 80%.

A similar quick test is the PEFR (Peak Expiratory Flow Rate) or simply, "peak flow".

Similar to FEV1 where a forceful exhalation volume is measured over one second. The peak flow looks at speed of your breath as litres per minute (L/min).

When you forcibly exhale the fastest flow of air is recorded judged on a set of predicted norms.  In the example we've used, you would predict a 45 yo 170cm woman could blow around 430-450 L/min.

Now that's a lot of wind!!

Like FEV1 a lower than predicted PEFR suggests acute worsening of exhalation ability.  It is useful to monitor asthma, especially in children who may use a peak flow meter daily as part of their written asthma plans.

Like??  Don't forget to share our page with your colleagues.

And... Breathe easy!!

12- Orthopnea

KYJ12- Orthopnea
In "knowing your Jargon", we tackle those funky terms, abbreviations and conditions that we use, but don't always understand.

Today's pearl is Orthopnea.
This is a symptom of heart failure, and other respiratory distress causing diseases. Literally, Orthopnea is Latin for "position breath", and it refers to someone who gets breathless when lying flat.

Functionally, it is a good piece of respiratory assessment.  A skilled clinician will ask the patient, "how many pillows do you sleep on at night?"
For those who experience Orthopnea, the answer will be more than two.  Some patients will claim they sleep in an arm chair or recliner. This is severe orthopnea.

Physiologically, the majority of alveoli that contribute to gas exchange are in the large bases of the lungs. These are located in the back, not on top of the diaphragms like your intuition suggests. As a consequence, lying flat allows more blood to gravitationally occupy the vascular beds of the bases, and air to occupy the apex and middle/upper lobes. With less air contacting the majority of the basal avleoli, less gas exchange occurs, giving rise to dyspnoea when lying flat.

Sitting someone up allows those big bases to fill with air and thus improve oxygenation and CO2 excretion.

Next time your breathless patient is struggling, try sitting them up... Then you can high five yourself all the way down the hallway!!

Know your jargon and share this post!!  Because that is what cool nurses do!

11- Cor Pulmonale

KYJ11- Cor Pulmonale
In this "knowing your jargon" series, we have looked at heart failure that affects the Left heart (LVF) and it's subcategories of systolic and Diastolic failure.

This episode of KYJ we look at Right heart failure also known by its Latin name Cor Pulmonale (pulmonary cardiac (failure)).

In Right heart failure, the right ventricle fails to pump volume into the pulmonary vascular network.  The most common cause is high blood pressure inside lungs (pulmonary hypertension), secondary to lung diseases both acute (pulmonary embolism) and chronic lung diseases eg COPD.

In these restrictive lung diseases, there exists a reduction in lung vessels, meaning the right heart must push harder against the resistance of fewer blood vessels.  This causes the right heart to fail.
Another common contributing factor is obstructive sleep apnoea (OSA).

With inability to clear blood returning to the right heart, venous congestion builds up giving rise to a characteristic set of symptoms.
Jugular venous distension
Ankle oedema ( sometimes pitting)
Ascites .
Breathlessness on exertion and lethargy.

As the cause of Cor Pulmonale is always respiratory, treatment focuses on managing the underlying pathology. Eg sleep
Apnoea is managed with CPAP.
PE managed with thrombolysis or heparin/warfarin.

Right heart failure often leads to
Left failure and together these conditions are called Congestive Heart Failure (CHF or CCF).

Knowing your jargon (KYJ) lubricating the minds for ... Oh.... At least 3 weeks...!!!
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10- Kussmaul breathing

KYJ10- Kussmaul Breathing.

Knowing your Jargon episode 10 looks at the characteristic breathing pattern called Kussmaul's.

Before we define it, let us review the primary stimulus to breathe.
Whilst at a superficial level breathing would appear to be about oxygen and CO2 levels, it's primary stimulus is CSF pH (potenz Hydrogen) or acidity of the cerebral spinal fluid. Blood pH influences CSF pH and the respiratory centre stimulates breathing rate and depth on this continual CSF sampling.

As waste CO2 increases, pH of blood drops (becomes acidic), this in turn drops CSF pH which stimulates the brain to drive your next breath.

...
Now let's look at severe metabolic Acidosis (blood with low pH, low HCO3, & normal CO2) .
In this situation, the cause of acidosis could be many things, but commonly diabetic ketoacidosis, aspirin poisoning, cyanide exposure, alcoholic coma, inhalant abuse, lactic acidosis and acute renal failure.

In each of these examples, the pH is low, and the CO2 is usually normal .

So what does our brain do to respond to this dropping pH?  It stimulates the lungs to breathe deeper and faster... This characteristic rapid deep breathing (hyperventillation) is called Kussmaul breathing, is involuntary, and serves to "blow" or vent off as much CO2 as possible, in attempt to raise and correct pH.

Typically the patient takes deep and rapid breaths, and appears to be doing this with no effort.  It is completely autonomic/ involuntary.

Look for Kussmaul breathing in the next diabetic ketoacidosis patient you care for.

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9- PF Ratio

KYJ9- PF Ratio

In this episode of Knowing Your Jargon we take a look at one of those funky respiratory terms called the PF ratio.

Correctly referred to as PaO2/fiO2 ratio, this calculation is a number derived from dividing the pressure of oxygen in arterial blood (in mmHg) with the concentration of oxygen that the patient is breathing.

PaO2 is normally 80-100 on room air. The fiO2 (fraction of inspired oxygen) of room air is 0.21 which is just another way of saying 21%.

To calculate the PF ratio you just divide paO2 by fiO2.

80/0.21 = 380
100/0.21= 475

Normal PF ratio is therefore 380-475.

As the number drops= badness
Infact the PF ratio is used to diagnose acute lung injury
(ALI= PF < 300 ) and the dreaded
Acute Respiratory Distress Syndrome (ARDS = PF <200)

So let's look at some predictions.  Assuming normal is 400.

1.  Assuming you have your patient on a Hudson simple face mask at 6 lpm.  It assumes oxygen delivery of 50% which is an fiO2 of 0.5.

If a blood gas was taken you would expect a paO2 of at least 200 (200/0.5=PF ratio of 400)

Predict a paO2 for any given patient by starting with a PF of 400 and multiplying it by their oxygen concentration.

Eg 400 x 0.5 predicts that s patient on 50% oxygen should have a PaO2 of about 200.

Eg - on an oxylog (air mix) at 60.5% oxygen, you'd expect that your patient should have a paO2 of at least 242 mmHg.

400 x 0.605 = 242

So next time you look at a set of ABG results, and think your patient is well oxygenated because their paO2 is between 80-100 mmHg,  consider the oxygen that they are breathing, calculate that little PF Ratio and just be sure. Remember 380-475 is normal.

Breathtaking hey?

8- systolic and diastolic failure

KYJ8 - Systolic failure vs Diastolic failure
Knowing your Jargon episode 8

In this episode of KYJ we take a look at the two categories of Left Heart Failure.  First recap blood flow-

Venous blood returns to the right heart from the body.
Right heart pumps blood to lungs
Diffusion of oxygen and CO2 takes place.
Oxygenated blood returns to left heart.
Lefty pumps blood out around the body.

Now "systolic" means the pumping stroke of the heart. It refers to the ejection or squirting of blood out of the ventricle during contraction.

"Diastolic" is an adverb that describes the relaxation phase after contraction. After systole (contraction) the squished heart now relaxes back to its resting state, and as it does it fills partially with blood.  This relaxation is what is called "diastole".

Both systole and diastole require energy.

In left heart failure, the forward momentum of blood is impaired for a variety of reasons.

Systolic failure is when the heart muscle can not contract with the "oomph" that it needs. We see systolic failure in people after cardiac injuries or heart attacks (myocardial infractions). These muscles demonstrate poor contraction (systole) and as a result the force of ejection of blood into arterial circulation is limited. Normally your heart pumps out 60-70% of it's filled volume (ie ejection fraction= 60-70%) but in a systolic failure, the volume ejected is alot lower than normal. Over the course of a minute, the cardiac output is diminished.
Systolic failure is a failure to pump.

Diastolic failure
In diastolic failure, we see a reduced cardiac output for other reasons. To first pump blood, the heart has to fill with blood. Stiff old hearts with loss of stretch don't fill well. Given that a healthy heart might fill with 100-120 ml of blood, a stiff heart might only fill with 60-80 ml or worse. If this happens then the ejection of blood over a given minute is much less than normal.

These patients are exhibiting diastolic failure. Rather than failure to contract, diastolic failure is failure to fill.

There it is.  A sentence with the word "failure" in it three times.

I hope you are enjoying these "KYJ" snippets.