New MI classifications -MINOCA

#KYJ - knowing your jargon.

Cardiac terminology.

For some time the terms NSTEACS and STEMI have been used to describe acute cardiac conditions that frequently manifest as chest pain.

In fact the term myocardial infarction (MI) is without doubt, the alpha predator in the mortality stakes.  Our synonymous use of the term MI with the more colloquial “heart attack” has permeated medical drama and pop culture for many years.   There is sound reason too; MI and it’s gang head quarters(cardiovascular disease), have risen to be the #1 killer of adults in all 1st world countries.   

But what if our understanding of heart attack was changed, and as clinicians, we had to review not just the condition “MI“, but it’s diagnostic criteria?

Well this occurred in August 2018.  The premise that MI was caused from an ischaemic blockage in a coronary artery has been scrutinised and left falling short of the whole truth.

Myocardial infarctions have long been divided into two categories:  STEMI and Non STEMI with the focus on the ECG as the Rex of diagnosis.

Now,there is a lot to support that when the ECG shows ischaemic changes, a diagnosis of MI can be made.  Especially in the context of ST elevation ,new Q waves or a new left bundle branch block; but now, it seems that the Troponin Blood test it the king of the diagnostic castle.

MI has been recategorised into 5 different categories or three main types. 

So what is the common feature???

Troponin .   That cardiac Troponin (cTn) is inside cardiac cells, locked up like a prisoner inside a ...um Cell. 

If there was cell damage (injury) or death (infarction), that cTn leaks out and is detected as it is picked up by lymphatic vessels, and distributed into the blood stream.

So cTn rise on the background of a cardiac event is always sensitive for MI... but what type? 

Type 1 MI 

These are the traditional STEMIs.  A brittle atheroma inside a coronary vessel ruptures, and in attempt to stop bleeding from an arterial rupture, vasoconstriction, a clot and fibrin reinforcing mesh forms a solid thrombus that occludes the  blood flow.  No flow, no O- oh no!! Ischaemic heart cells soon die (necrosis) - infarction.

These blockages are often extensive, and the scar that results from a large area of muscle death, slows and alters the electrical pathway- thus, ST segment elevation and the development of a big Q wave.

Type 2 MI

These infarcts are cardiac cell death from ischaemia, but instead of a blockage in a specific vessel, there exists a vessel network spasm- construction and shutting down of a section of myocardial perfusion.

No flow- oh No, no O.!!!

Infarction!

We previously called these NSTEMI.  The damage area is not full thickness of the muscle wall, so no Q wave, and rarely an ST segment elevation.  Little cell death but extensive ischaemia in the penumbra around the dead stuff.

Types 3-5

These MIs are complex and caused from things like toxins, drugs, and physical injury like surgery, or trauma.  The injury to the heart muscle causes it to inflame (like all injuries) and some injured tissue will die (infarct).  The difference here is that they are not directly ischaemic.

So these groups of MI are called #MINOCAs - MIs with non obstructed Coronary Arteries.

The heart may be directly injured, or indirectly die off.  Think of extreme shock, or hypovolaemia/sepsis/anaemia; in these cases there is greater cardiac demand for Oxygen than the shocked or anaemic patient’s ability to supply.  Too little too late-  muscle dies but not from coronary blockage... MINOCA 

Big topic-  best addressed in our #ARRR , #Acute Deterioration and #Cardiac seminars.

All our seminars in one place here . Www.Ect4Health.Com.Au/whats 

~Rob Timmings

Bluebottle stings - Queensland 2019

#KYJ - Bluebottle stings
It’s been a summer of bites and stings, and this week droves of bluebottles have hit the southern coast of Queensland and NSW causing countless stings to waders and swimmers.

The Bluebottle (Indo-Pacific) is a smaller colony of a larger group of marine stingers that are collectively called Portuguese Man-o-war.

Unlike the Box Jellyfish and the collective cuboid jellyfishes (yes ‘jellyfishes’) I wrote about last week - the Irukandji (16 diff species), the Bluebottle is not a jellyfish at all.

All that stings is not a jellyfish, corals, fish and even some molluscs have a sting.

Bluebottles are related to coral, and interestingly, they are not even one animal, but three different animals living together.

Look carefully, there is three individual polyps living together as one .

It’s a Trinity!  These polyps are attached to one another and are not able to survive independently.
This is called obligate symbiosis.   It’s like nurses and coffee, or accountants and calculators, or Trump and his Wall.
Each polyp works together to function like an individual animal.  The sail or float, the Gauci and the Tenticles. Each start live as a separate animal, then “find” each other in a moment of serendipity or is that SEArendipity- sea what I did there!!

Anyhoo-  the Bluebottle recently hit the news as weather patterns in East Coast of Australia caused armadas of thousands of these stingers into coastline locations.  Thousands of reported and unreported stings have compounded a 10 year spike in suspected Irukandji stings.

What is important to note is that the venoms of these animals is very different.   For our #Irukandji article scroll back to last week .

Bluebottle stings are intensely and immediately painful.   The pain is described a whip like, and burning, unlike the Irukandji sting that is a deep muscular ache and delayed for 5-30 mins after sting.

Bluebottles have very few recorded deaths, but of those, it is thought to be anaphylactic airway swelling in people stung on their throat or neck.

Bluebottles stinging tentacles can survive days after they have been chopped up by passing boat propellers. This means that fragments of tentacle floating in water with swimmers congregate can still provide stings despite no intact bluebottles being seen washed up on the beach. Bluebottles either have a left or a right sided sail. This insures that irrespective of which way the wind blows half of the armada will be blown in that direction, insuring survival and distribution of the species .

Treatment:
We really don’t know what is the best treatment for bluebottles -many different reports and studies will have differing ideas. The standard first aid management is to first pick off or wash off the remaining tentacles with seawater. Must be seawater!!!

It is not recommended to use vinegar on bluebottle stings and  is not recommended to use fresh water to wash off the sting, both of these have been demonstrated to increase the firing of undischarged stinging cells.

Hot water  Vs  Ice packs
The recommended first aid after decontamination is to immerse the stunning area in hot water. The water should be as hot as the person can stand without causing burning. For most people this means expediting them to a nice hot shower. Because the sting is immediately intense, and sensation in the stung limb is altered, it is reasonable to assist the stung victim by testing water temperature to avoid scalding- especially in children.

And alternate approach to the application of hot water, is the application of ice. If ice is to be used it must be covered with a wet cloth and applied for no more than 20 minutes at a time inspecting the skin regularly for the potential of ice burns.
Now the astute reader is going to be looking at the use of either hot water or ice as being almost completely opposite each other, the point of these treatments however, is to denature the venom which is a delicate heat sensitive protein.
My personal experience with bluebottles has revealed that the hot water option is fast and superior to using ice packs. It is also convenient to use hot water as all other fish stings require a hot water immersion as a first aid treatment.

In most first aid courses when the bites and stings session comes up, a first aid instructor will teach a simplified first aid management.  My preference is to teach “if you were bitten on land or stung on the land use ice, if you were stung or bitten in the water use hot water as your first aid treatment, now this is just a rule of thumb, and of course doesn’t apply to deadly snakes spiders or box jellyfish. But as a general rule , Fish stings, fish bites,stingray barbs coral stings, anemone &  ascidians stings and all jellyfish with the exception of box jellyfish, it is easy to simply remember one first aid strategy-hot water.

Exceptions.
Box Jelly fish /Irukandji- vinegar & hospital.
Sharks -  well they are not venomous and so haemorrhage control is the focus.
Octopus/molluscs eg cone shell-  treat as a snake bite with pressure immobilisation bandaging.

Clinical management:
There is evidence supporting ongoing ice application, and dermatitis topical treatments like hydrocortisone cream.
Analgesia should be liberal, and antihistamine use is very common and well supported.
Treat any anaphylactoid reactions with usual airway management and adrenaline protocols.

Blue bottles and their stings are a part of life in many coastal areas.  Listed to and heed local weather forecasts and lifeguard warnings.
Have a first aid plan and obviously, if there are bluebottles washed up on the beach, don’t go swimming that day.

Be safe in the sun.
#RobTimmings
#Bluebottle
#ECT4Health
Our emergency management seminar “Whatmergency” covers common stings and bites :-  more www.ect4health.com.au/whats

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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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 

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Spider bites and other creepy crawlers

#KYJ-  Spider bite.

In the last great act of defiance look at where this spider decided to sit.  We hear a lot about creepy crawleys in our area. Spiders, scorpions, ants, wasps and centipedes (and that is just my yard).

Recent east coast wet weather has produced a minefield of critters that can cause harm.

This KYJ is dedicated to terrestrial arthropod bites. 

These fall into two categories.  Insects (6 legged bugs) and arachnids like Scorpians, centipede and spiders.

With the exception of the infamous Funnel web spider, all critters listed above are treated the same. 

Wash the bite with soap and water, apply an ice pack for 10-20 minutes.

Rest the patient.

Paracetamol or ibuprofen for pain.

Funnel web spiders are potentially lethal. They can cause respiratory failure and are managed as snake bites using pressure immobilisation bandaging and antivenin.

Only male Sydney Funnel Web Spiders and Redback Spiders have caused human deaths, but none have occurred since antivenoms

were made available in 1981.

The Australian funnel-web spiders are among the deadliest spiders in the world, but while they can kill us, their venom has little effect on cats n dogs.  There are many species of funnel-web spiders in Australia but only males of the species is deadly. Despite an average of 40 bites per year from funnel webs, only 13 deaths have been recorded, and none for over 35 years.

Other large hairy spiders like Mouse spiders may have venom that is as toxic as that of some funnel-webs, and while people are bitten from time to time, no-one has been recorded as having died from the effects of a mouse spider bite. Antivenoms are available for both funnel-web and Redback Spider bites.

Red Back bites occasionally get antivenin, but this is a controversy.  In 2012 an Australian study concluded that there was little point, other than a mild, hit n miss analgesic effect.  Considering the fact that no one has died from Red Back spider bites for well over 60 years, many clinicians consider a wait n watch. That said, there is fierce debate among toxicologists (http://mobile.abc.net.au/news/2013-11-22/doctors-warned-to-keep-using-redback-anti-venom/5109838)

Typically spider bites cause an neurotoxic and cytotoxic responses.  

Neurotoxic symptoms include muscle rigidity, stiffness, myalgia and at its worst, weakness and paralysis (eg funnel web).

Cytotoxic effects cause local skin irritation and blistering.  A white hypo perfused area directly onthe bite, with a wide area of redness (inflammation) around the pale bite centre is common. Sweating around the bite site is a function of the neurotoxic effects. 

Some international spider bites (brown recluse) have been associated with necrosis and muscle breakdown but we don't see this in Australian spiders despite the mythical notion of the white tail spider.  It's now widely accepted that any infection post spider bite was not due to venom it was due to soil bacteria introduced at the time of the puncture.

First aid for spider bites remains rest, ice packs, analgesia and give it a good clean.  If the patient has not had a recent tetanus shot then this should be attended to.

Scorpions and centipede in Australia are not deadly. That said and anaphylactic reaction to any bite or sting is a life-threatening emergency.  Like spider bites scorpions and centipede bites I treated using basic first aid.

Whilst this post is focused on spider bites, is important to recognise that wasps and ants stings are also treated with ice packs although much success has been gained from rubbing the freshly cut surface of an onion straight onto a wasp or ant sting.

Personally I have had tremendous success with an onion. Instant pain relief. 

DOAC reversal

Reversing the new oral anticoagulants.

Till recently reversing the “Xabans” and the Direct Factor II inhibitor medications has been a challenge.   Unlike Warfarin which is reversed using Vitamin K, and Heparins which are reversed using Protamine Sulphate; the new direct oral anticoagulants (DOACs) don’t have a magic antidote.

In this post, I’ll unpack the way these new drugs work, and then discuss how they will be reversed if your patient is bleeding from trauma, or requires surgery.

If you’ve seen my YouTube then you will have a good understanding on the differences between blood clotting and blood coagulating (you should start there if you thought they were the same thing).

Fast forward to the #DOAGs section if you’re all over this coag cascade stuff.

Ok

Ultimately the solidification of blood to form a thrombus requires these two separate processes- clotting and coagulation which is the conversion of a cocktail of proteins (coag factors) in blood, from liquid state to a solid stringy strandy dental floss like product that, like string on a birthday parcel holds a parcel of clotted cells (RBC & Platelets) together.

That string is called FIBRIN

Here is where we start. 

If you can’t make fibrin, you can’t coagulate.   The complex cascade of chemical reactions in your blood which forms fibrin, is called coagulation.  Any drug that stops that chain reaction is called an Anti-coagulant.

Simple steps in the common coagulation pathway involve 4 players.

Vitamin K

Factor X (remember that ‘X’) though it’s pronounced “factor 10.”

Factors 2(Factor II) also called Prothrombin

Factor 1 (Factor I) also called Fibrinogen.

Now tissue injury and chemicals released from the platelets and vessel wall cells stimulate the coagulation chain reaction- think of a finger on dominoes.  This activates Factor X.  But this go button needs calcium and vitamin K to allow the cascade to start.

So Factor X activates now called Xa.

Xa activates Factor II Prothrombin 

Which is now called IIa (or Thrombin).

IIa activates factor I

which is technically Factor Ia (aka Fibrin).

Anticoagulants.

Warfarin deactivates vitamin K so the prices can’t start

Heparins/enoxaparin directly prevents the activation of FX into Xa and also stops Prothrombin (Factor II) activating into thrombin Factor IIa.

Now #DOACs 

Direct Oral AntiCoagulants inhibit one of two pathways.

The Xabans- (apixaban, rivaroxaban, edoxaban)

Their name with an “Xa” in indicates that they Ban the Xa-   They actually deactivate factor Xa.   

Remember once activated FX turns to FXa which converts Prothrombin FII.

The Xabans stop (ban) coagulation at that Xa step. 

Dabagatran (Pradaxa) is different.  It waits till Thrombin (IIa) forms then deactivates it so it can’t convert fibrinogen into strings of fibrin.

Now stopping these drugs is not possible, so to help the patient coagulate, we need to stimulate the Fibrinogen directly, or, in the case of Pradaxa, stimulates Prothrombin earlier in the chain reaction.

Now bleeding patients:

On warfarin we can reverse it giving a large bolts of Vitamin K.

Heparin is reversed using protamine.

DOACs are short acting (5-17 hour half lives) , so unless someone just took their dose today, reversal and severe bleeding is rare, making these anticoagulants quite safe.   But what if we don’t have that 5 hours?? 

If available, idarucizumab is recommended for reversal of anticoagulant effects for patients taking Dabigatran.

It is an antibody that binds to the drug blocking its effects on Thrombin.

For the Xabans, the reversal is harder, 

Many have tried and failed, and perhaps the fact that these drug are so short acting that motivating some research and development isn’t seen as worthwhile or profitable.  So we are left with few options; none of which are great.

Charcoal:

If taken inside 4-6 hours of last Xaban dose, activated charcoal orally can bind with Rivaroxaban and Apixaban.

Andexanet alfa, the first agent shown to reverse the anticoagulant effects of rivaroxaban and apixaban, has been approved by the FDA, according to statement from Portola Pharmaceuticals in early May 2018.  It is a factor Xa “decoy” molecule that acts by attracting and sticking to Xabans, thereby preventing them from interacting with actual factor Xa, but andexanet also has a short half life and hence the effect quickly reduces once treatment stops, so needs a complex infusion.

Factor VII - 4factor PCC

FEIBA 50 IU/kg (contains factors 2,7,9 an 10 in predominatly inactivated form as wellas activated factor 7 and 1-6 units of Factor VIII coagulant antigen (FVIII C:Ag) per mL)

Prothrombin-X

Current guidelines do not recommend use of prothrombin complex (Prothrombinex-VF in Australia) but it has been shown to normalise prothrombin time in a trial of 12 healthy male subjects at a dose of 50 IU/kg iv infusion (Eerenberg et al., 2011).

Tranexamic acid (TXA)

Not new, and scraping the bottom of the barrel, but TXA has been used in severe bleeding since Moses hunted Brontosaurus.   It is only used in bleeding patients with Xabans or Dabigatran, if bleeding is severe- ie trauma. Classified as a Plasminogen inhibitor, it really only helps you to maintain any coagulation you’ve been able to make already. So given that DOACs inhibit/slow down coagulation and don’t stop it completely, preserving any thrombus you’ve formed is what you want when you’re bleeding.  TXA does this by preventing body enzymes (plasminogen) dissolving the clots you already made.

Platelets , FFP and RBC 

Again, only if bleeding.   It stands to reason that as you bleed you also loose the DOAC drugs . So transfusions of unadulterated blood products acts to correct not only losses, but dilute the plasma bound DOACs.

Well that’s about it, so Q&A is open.

#RobTimmings #ECT4Health

This content is available in our #RustyPills pharmacology course, and #CardiacSeminars.
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