Sunday 30 December 2018

Cardiogenic shock and Frank Starling

#KYJ - Cardiogenic Shock

Let’s unpack this common type of shock we see in our clinical deteriorating patient’s.

I edit, proof and English polish nursing and paramedic assignments as a side service to my seminar and cruise boat education sessions.
In many recent case studies, pathophysiology is a common theme that needs a bit of work to schmooze the passing paper in to an A Grade masterpiece.   The last 3 months was full of shock, and especially cardiogenic, so I thought I’d dedicate this episode of #KnowingYourJargon (KYJ) to this topic.

Let’s commence with nomenclature.  Cardio = heart.  Genic = to originate/create (think Genesis as the book of creation from Old Testament Judeo/Christian and Islam mythology) .

Shock- is fundamentally a state of imbalance between cellular oxygen demand vs delivery of oxygen to cells .   In a nutshell, shock is “relative global cellular hypoxia” (Timmings 2004) 
Then cardiogenic shock therefore means :
Global cellular hypoxia that originated from heart failure.

To unpack this further we need to understand heart pumping function, and it’s discourse- heart failure.

Given the adult heart pumps blood; the volume it pumps measured over a minute is termed Cardiac output.  Normally this equates to 4.2-7 litres/min which is pretty awesome given its size.

Now when there is injury, or death of heart muscle, or  degenerative changes occur with lifestyle challenges and the encroachment of the autumn years; the efficiency of the heart as a pump wanes.

This is called heart failure and can occur in with left or right heart or both, termed congestive heart failure (CHF)
These slow changes over years are called “chronic” , but after a cardiac event such as a myocardial infarction (commonly termed heart attack), or a traumatic injury to the heart eg stabbing, or blunt crushing trauma, then the cardiac failure is called Acute.  Irrespective of aetiology, a heart in failure wont pump adequate oxygenated blood around the body to meet the demand of cells-  this is shock. Cardiogenic shock.

Now read on if you are interested in diving deeper.
This is where you and I get our geeky on!!

Frank -Starling Mechanism(Law)

Otto Frank and Ernest Starling were a couple of turn of the century early 1900s geekoids that had a hankering for the dynamics of the heart pumping function- Otto loved playing with frogs, and Ernest was a Dog man, so armed with their work on Frogs n Dogs, they went and got a whole mechanism named after themselves.

Essentially what they asserted was two monumental principles.

First that a heart needs to fill up with blood before it can pump out any blood . . .

Yep, I know- crickets...

Their second assertion is that not only does the heart need to fill up with blood, but it’s chambers must actually be stretched a little to get a good strong elastic contraction.
I know these seem obvious, but in the world of medicine and cardiology especially, that fill up the heart till it’s a bit stretched like a balloon part is called “Preload”. You have to have preload the ventricles before an output from the pump will be efficient.

Think of a rubber band .
It’s elastic potential is only realised when you stretch it, and heart muscle is the same.  If you don’t pull back on a rubber band you can’t ‘feeyonnnng’ (real word*) it across the room at your loved one.
*ok that was t a real word- but you get it hey?   Stretch The rubber and whoosh there is a release of tension.
In cardiac ventricles this preload works like a partially inflated balloon.   Let it go and the elasticity causes the air you blew into the balloon to propel it across the room.

Hearts need to fill with blood and preload.

Now Frank and Starling also said that too much stretch (preload) is going to work against the pump.  Preload is a good thing but overload causes failure .

Like Tim Tams- some = good , but the whole packet = bad.

In heart failure the pump has lost its inotropy (force of contraction) so if the weak muscle can’t pump the reservoir of blood out efficiently= cardiogenic shock happens.
Likewise in MIs, or acute muscle injury.
A secondary mechanism is the hypoxia of heart muscles itself.  Muscle needs oxygen to pump (contract) but also to relax and fill.   So ischaemic (hypoxic) hearts are stiff and non compliant-  remember Starlings first principle ?   Heart has to fill up with blood first.

Well in stiff poorly filled hearts, output will drop.
Again - cardiogenic shock.

Are we done?
Credit: Robert Timmings 
#ECT4Health 
@ECT4Health 
#RobTimmings

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Saturday 29 December 2018

Irukandji syndrome

#KYJ - Irukandji Syndrome

They only live for about 6 months, they have 24 eyes, 4 stomachs, each with their own anus, and are no bigger than your thumb nail; but , they punch way above their weight by packing a sting that places them into the top 10 deadly venomous animals in the world.

Only a handful of deaths have been attributed to a collection of jellyfish stings known collectively as Irukandji, but the syndrome that their stings invoke always require hospital admission for analgesia, and cardiac monitoring. 

The most common offender Carukia barnesi, (identified in 1964 and named after its discoverer, Jack Barnes, is one of up to 16 species all thought to inflict the sting with venom causing what is now called Irukandji Syndrome.   There isn’t one “Irukandji jellyfish”, so with similar biology but different genetic features, it is tangible to see their venom effects can be difficult to pin down.

What is known is that these jellyfish uniquely have stinging cells (nematocysts) on not only their tentacles (of which there are four), but also in their Bell.  There is no safe place to handle them.

Their venom is thought to contain a nerve agent that acts to modulate sodium channels.  The effects cause rapid nerve firing .

Symptoms
5-30 minutes after a sting, the victim will experience severe generalised pain or cramps, 
GI symptoms of Diarrhoea, nausea and vomiting, 
Sympathetic symptoms localised or general sweating, restlessness, anxiety, headache,large muscle cramps and painful back spasms, and a classic sense of doom.
Pain from Irukandji can last weeks, and has been reported as the proverbial “10 out of 10”

Irukandji Syndrome can cause pulmonary oedema (likely cardiogenic) as acute hypertensive crisis is a frequent symptom, that has lead to stroke.

These stings hospitalise dozens of people world wide, and in Australia.  

The flourish in warm waters where hard coral is abundant (reefs). They are a family of jelly fish that actively hunt fish in the reef ecosystem, and are attracted to light.   What is sinister is that their annual blooms are being recorded as far south in the Australian east coast as Hervey Bay, and the southern migration each year correlated with warmer ocean currents.   The estimate from researcher is that their impact on the massive Gold and Sunshine Coast tourist industry will be inevitable as they march down our coast line.

Treatment.
Phase 1 - First aid
The first aid for suspected Irukandji stings is DRSABCD, and liberal dousing with vinegar.
While the vinegar does nothing for the pain or symptoms from stinging cells that have shot their load, the acid is thought to disable the unfired cells from further envenomation.
A few years ago Associate Professor Jamie Seymour from the Australian Institute of Tropical Health and Medicine (JCU in Cairns) reported that vinegar can actually cause discharge of stinging cells worsening the envenomation buy up to 50%, he stated "That's a big amount, and that's enough to make the difference, we think, between someone surviving and somebody dying."

That said, the Australian Resuscitation Council continues to recommend using vinegar.  So what to do?  More research is needed on the vinegar thing.

Phase 2- hospital management.

Pain and cardiovascular management is the priority.   Massive IV narcotic use and even sedation with ventilator support may be necessary.
There is no Antivenom or reversal agent.

Supportive use of Antihypertensives, and antihistamines are indicated.   Magnesium Sulphate is thought to be cardio protective and aids in the extreme haemorrhagic stroke risking hypertension.

These people go on to experience excruciating pain for days to weeks, so analgesia will be their friend.   Of the doom and dread and pain, one of my patients stated:
“For the first hour I was worried I would die, then for the next few hours, I was worried I wouldn’t!”

The jellies are coming more prevalent, and as more people are being stung in further southern parts of the coast, clinicians in places like south east Queensland will soon notch up their first Irukandji Syndrome patient in the annals of the reflective journals.

Written by Rob Timmings
@ECT4Health 
#Irukandji #ECT4Health