Rob on Haemostasis Part 2 Clotting

Rob on Haemostasis Part 3 Coagulation

#Snakebite

Originally published in social media in Nov 2018...

That bite of summer has well and truly come early this year and with that heat, comes snakes.
Our neighbors (Toowoomba region) have reported many sightings.

3000 bites are reported annually.
300-500 hospitalisations
2-3 deaths annually.

Average time to death is 10-14 hours  (many references cite between 4 - 24 hours). The point is that the urban myth that you are bitten in the yard and die before you can walk from your chook pen back to the house is a load of rubbish.  It can happen but it is an epic case of rare!!

While not new, the management of snake bite (like a flood/fire evacuation plan or CPR) should be refreshed each season.

Let’s start with a
Basic overview.

There are five genus of snakes that will harm us (seriously)  (Disclaimer:  these are the ones for which there is antivenin.  Other snakes eg copperheads and whips , small eyed etc still make us sick)
Browns, Blacks, Adders, Tigers and Taipans.

All snake venom is made up of huge proteins (like egg white). When bitten, a snake injects some venom into the meat of your limb  (NOT into your blood).

This venom can not be absorbed into the blood stream from the bite site directly.  

It travels in a fluid transport system in your body called the lymphatic system (not the blood stream).

Now this fluid (lymph) is moved differently to blood.
Your heart pumps blood around, so even when you are lying dead still, your blood still circulates around the body. Lymph fluid is different. It moves around with physical muscle movement like bending your arm, bending knees, wriggling fingers and toes, walking/exercise etc.

Now here is the thing. Lymph fluid becomes blood after these lymph vessels converge to form one of two large vessels (lymphatic trunks)which are connected to veins at the base of the neck.

Back to the snake bite site.
When bitten, the venom has been injected into this lymph fluid (which makes up the bulk of the water in your tissues).

The only way that the venom can get into your blood stream is to be moved from the bite site in the lymphatic vessels. The only way to do this is to physically move the limbs that were bitten.

Stay still!!! Venom can’t move if the victim doesn’t move.  (disclaimer - gravity plays a role, and some lymph can very slowly move...but super slow)
Stay still!!

Remember people are not bitten into their blood stream.

In the 1980s a technique called Pressure immobilisation bandaging was developed to further retard venom movement. It completely stops venom /lymph transport toward the blood stream.

A firm roll bandage is applied directly over the bite site (don’t wash the area).

Technique:
Three steps: keep them still
Step 1
Apply a bandage over the bite site, to an area about 10cm above and below the bite.
Step 2:
Then using another elastic roller bandage, apply a firm wrap from Fingers/toes all the way to the armpit/groin.

The bandage needs to be firm, but not so tight that it causes fingers or toes to turn purple or white. About the tension of a sprain bandage.

Step 3:
Splint the limb so the patient can’t walk or bend the limb.

Do nots:
Do not cut, incise or suck the venom.
Do not EVER use a tourniquet
Don’t remove the shirt or pants - just bandage over the top of clothing.
Remember movement (like wriggling out of a shirt or pants) causes venom movement.

DO NOT try to catch, kill or identify the snake!!! This is important.

In hospital we NO LONGER NEED to know the type of snake; it doesn’t change treatment.

5 years ago we would routinely do a test on the bite, blood or urine to identify the snake so the correct anti venom can be used.
BUT NOW...
we don’t do this as often. Our newer Antivenom neutralises the venoms of all the 5 listed snake genus, so it doesn’t matter what snake bit the patient.

Read that again- one injection for all snakes!
Polyvalent is our one shot wonder, stocked in almost all hospitals, so many hospitals no longer stock specific Antivenins. Regional differences (Tassie, Victoria, south of Perth, outer islands)use region specific antivenins.

Australian snakes tend to have 3 main effects in differing degrees.

Bleeding - internally and bruising.
Muscles paralysed causing difficulty talking, moving & breathing.
Pain
In some snakes severe muscle pain in the limb, and days later the bite site can break down forming a nasty wound.

Allergy to snakes is rarer than winning lotto twice.

Final tips: not all bitten people are envenomated and only those starting to show symptoms above are given antivenom.

Did I mention to stay still.
Call help (000 or 112)
You need hospital!!!

Rob Is a writer and teacher for ECT4Health. This snake /spider envenomation material is included in our Emergency courses called #whatMergency and found here...www.ect4health.com.au/whats

GTN In Inferior MI

#KYJ- #Dogmalysis

Myth or fact??

GTN and inferior MI

In a post on another forum I was asked why GTN shouldn’t be used in Inferior MI patients.

In this post I want to explore why you may have learned this relative truism.

To unpack this blanket dogma I’ll say at the outset that there are circumstances where using nitrates in patients is discouraged, but realistically, many of us do and will.

First in our quest is to understand, that more than 70% of blood in your body is currently sitting inside your veins.   Like arteries, veins are muscular, and subject to dilation (relaxation), when influenced by drugs like nitrates (Anginine, nitrates, nitro lingual etc).

When taking a nitrate, all blood vessels simultaneously relax, reducing the pressure (blood pressure) inside the vessel.   So after a nitrate, blood pressure inside arteries drops, as does venous pressure, resulting in poor venous flow (venous pooling).  This results in a reduction of blood returning to the heart (venous return), and subsequent cardiac filling (preload) before the next contraction.

Now heart attacks (Myocardial Infarctions)  are, far more often, a left heart injury.  Much less frequently, is the Right Ventricle is injured. 

A right heart MI, is seen concomitantly in about a third of the Inferior MIs.  These are injuries to the apex of the left ventricle (the pointy bit at the bottom of a heart), often caused from a blocked artery called the Left Anterior Descending (LAD) artery; that has some distal branches that perfuse portions of the Right ventricle. 

Ok... if you are still with me.

Glyceryl Trinitrate (GTN) (eg Anginine, nitrolingual etc) are often given first line in patients with chest pain.  Frequently, in acute presentations, this is prior to an ECG having been performed yet.  In these chest pain patients, the premise is to restore cardiac muscle perfusion by vasodilating the coronary arteries- letting more oxygen in.

GTN is therefore first line and precedes Diagnosis of the cause of the chest pain, rendering its use as pre-emptive, or diagnostic rather than curative.

That first GTN dose must be evaluated carefully.  If it doesn’t have immediate effect (1-5 mins of dramatic improvement) then no more should be used until you can exclude an Inferior ECG change, or Right heart MI.

Why?

Remember that GTN vasodilator effect reduces blood flow in veins.  So if their Right Heart (which is responsible for oxygenation of blood) should fail, then the GTN actually worsens the whole heart muscle perfusion by dramatically dropping preload.

Now this occurs in about 35% of Inferior MI patients and you’d never see it on an ECG unless you did a Right Sided ECG, or moved the V4 electrode to the Right chest and ran the trace again.  This is called a V4R trace.

V4R lead looks at the Right Ventricle.  So should always be performed in Inferior MI (ST elevation in leads II, III, and or AVF).

To suspect a Right Heart MI the V4R lead needs to show  1mm or more elevation.

So knowing NitroG is more venous dilatory than coronary, this Vasodilation drops preload, in a struggling R)heart which further drops pulmonary blood oxygenation and preload into the left.

Worsens cardiac hypoxia .   Rule is - dont use GTN in known Right MIs and extreme caution in those with inferior Type 1 MIs (STEMI).

But if you didn’t have an ECG yet, and that is usually the case; then you couldn’t have known.

Worsening pain and hypotension after GTN is the Red Flag.

Cardiac Seminars are filling fast.

Book one at your hospital by talking to your DON/NUM or Educator.

#ECT4Health. 

Www.Ect4Health.Com.Au/whats 

Proton Pump Inhibitors not good long term.

#kYJ Proton pump inhibitors (PPIs)

One of the commonest drug classes we see patients taking for reflux or Gastroesophageal Reflux Disease (GORD) is the proton pump inhibitor.
You know of these drugs as Esomeprazole and Pantoprazole, Omeprazole.  In fact, so common are these drugs, that these listed are in the list of the top 10 most prescribed PBS medications in Australia.

Are they safe for long term use?  No.

Remember all drugs have costs and benefits; so if costs outweigh benefits, perhaps it’s time to wean.

One would think that being so popular and readily available, that they are safe, but this is sadly not the case for many Australians on this class of drug.  The adverse effects of these drugs (like many), are linked to a perfect storm I call the 4Ds.
Dose, duration, and drug/drug interaction (DDI) and Diet.

First let’s look at the options for managing Heart Burn/Reflux by understanding some very basic stomach physiology.

There’s three main players.
Pepsinogen
Gastrin
Hydrochloric acid.

Pepsinogen
This is a substance classified as a Zymogen or pro-enzyme (note the “ogen” suffix).  All “ogens” are enzymes that are dormant until they are activated by something. You’ve heard of Fibrinogen, and Plasminogen in the blood? Well this is an ogen in the stomach.  More in a minute on Pepsinogen.

Gastrin
Secreted directly into your blood by G-Cells in your Stomach and Duodenum when gut receptors detect protein, calcium or stretch of your stomach. Yeah!! I know, who would have thought your stomach was an endocrine gland??!!

Gastrin acts systemically to stimulate your stomach’s Parietal cells to make Hydrochloric acid.

Hydrochloric Acid (HCl)
Also called Gastric acid, this is a strong acid with a low pH of 1.5-2 that inhibits ingested fungus/bacteria— yep, remember that mouldy Cheese and craft beer you had for s’mores last week!!

As acidity in your stomach rises (pH falls) this acts as a powerful stimulus to tighten the lower oesophageal sphincter (LOS), preventing any regurgitation/refluxing of gastric acid which, when entering up into your oesophagus, irritates the mucosa- inflames it and can ulcer it.  This causes the classic heart burn or reflux symptoms.  Burn baby burn!!
Yay for stomach acid.

Other than antimicrobial, LOS tightening functions, the other vital role of Hydrochloric acid is to convert that Pepsinogen (pro-enzyme) in to the active protein digesting enzyme called Pepsin.

Now Pepsin is the darling of protein digestion.  That steak, eggs, fish, Tofu or beans you ate is getting broken down mechanically and chemically into tiny particles called Amino acids.  This symphony of chemicals listed above is like an epic startup sequence for protein digestion and absorption.

So... where does that leave PPIs (those *prazole drugs)?

Ok... if you’re still with me, PPIs are prescribed for short term (3-6weeks) inhibition if gastric acid production in the background of GORD or peptic ulcers. They are safe short term, to inhibit acid production while the inflamed oesophagus or stomach lining is healing.

They do not fix the ulcer, and actually worsen GORD over time- read back to the bit about gastric acid being a trigger to tighten the LOS sphincter.   Inhibit acid production, and you don’t close that sphincter as well, allowing acid to reflux into the same oesophagus that is irritated and inflamed!!

Short term use.   These PPIs are for short term use while your gut is healing.  But what do we see as nurses? We see people prescribed these drugs forever.  They fly under the radar and are rarely flagged for pharmacy review.

Imagine I gave you a drug that essentially stopped you digesting protein, calcium, vitamin B12 and magnesium; caused you more reflux and indirectly allows potentially harmful pathogens access to your lower GI to play gene splicing monopoly with your healthy gut flora?

You’d probably not be surprised that there would be some discourse hey?  Well you’d be right.  These drugs are not without the costs to health.  Perhaps the most sinister issue with them is the potential for Drug-Drug interactions (DDIs).

DDIs from PPIs (see what I did there?) are common.
Many drugs your patient takes rely on passage through the stomach with a predictable pH.  When altering gastric pH with PPIs, then the chemical dynamics change and alter absorption of all drugs the patient takes orally.  The effects are varied but generally fall into two categories.  Their drug may not be absorbed effectively, or conversely, it may be more absorbed than anticipated leading to toxicity.  Gastric motility can also be altered which further renders bioavailability of every oral drug as unpredictable.
Constipation or diarrhoea, malabsorption, dehydration, and altered gut flora balance opens a whole can of worms (well not actually-but eeeuuu!).

Look these drugs have their place for short term use.  To get a job done, but unlike antihypertensives, or chronic disease preventatives like COPD or HF meds, these drugs are not for the long term use.

Weaning is hard but well supported, and any GP that is up to date will embrace the discontinuation regimens.
If taking these drugs twice daily, a week to two weeks of step down protocols should be introduced.

BD meds down to daily for a week.
Then daily down to every second day.
Then half the dose second daily.

Using H2 blockers like Ranitadine for break through dyspepsia, and anti acids like Gaviscon or Mylanta for break through rebound pain is also toggled with a month of bland, non spicy, acid reduced food.

The stomach needs 3weeks to 6 weeks to reset its Gastrin signalling mechanism that the patient knocked off with long term PPIs.

The whole process is a painful one but long term gains like reduced risk of MI and Stroke, and electrolyte/protein absorption are undeniably important for longer term healthy gut.

GP or Gastro specialist needs to be on board, and like the Statin debates of the early 20teens, finding a doctor that is progressive and evidence based in their approach can sometimes be a challenge. So remember to tread lightly.

But really- PPIs have a role as a short term drug, not long term.

Into your Pharmy??  Check out our #RustyPills seminar
Www.Ect4Health.Com.Au/whats

Cor Pulmonale S1Q3T3

#KYJ the S1Q3T3

Cardiac Refresher on Cor Pulmonale, or Right heart strain. 

Imagine the patient presents with chest pain. 

Our go to assessment tool for any chest pain presentation is the good old ECG.  You perform the ecg and on assessment your patient shows no ST elevation or depression, no obvious widespread T wave abnormalities, and no LBBB.

Naturally the clinical assessment of their pain and any shortness of breath will be contiguous with your initial ECG.  

Your patient seems to be breathless, and holding their Sats >90%, and there is limited (if any) ankle swelling.

Pain onset was described as sudden, and SOB is a feature.

You’ve ruled out T1MI (previously called a STEMI); and have a low suspicion of a Type 2 or 3 MI (NSTEMI) 

But the patient is in pain and it seems to be eased by GTN.

Bloods for Troponin are collected among others, and sent for processing (or you ran them through the ISTAT).

Troponin - normal.

Let’s look closer at that seemingly normal ECG.

Tachy at 104

Lead I shows a larger S wave than R 

Lead III shows a Q wave and it’s T wave is flattened or inverted.

It is a classic (frequently missed pattern called #S1Q3T3 - hashtag (#) added by me.

This pattern on the ecg is indicative of an increase of Right heart distress.

Now think this through.  The Right Heart pumps into the lungs.  In situations that the lung vessels are diseased, inelastic, engorged, blocked ; the pulmonarywatson vessels become hypertensive . 

Right heart trying to pump into a high pressure area (lungs) causes strain and localised lactic acid (overwork) pain, in the Right ventricle.  As oxygen demand exceeds delivery, the Right heart becomes ischaemic (hypoxic) compounding the anginal pain.

Right gear strain/failure is called Cor Pulmonale .

It is a secondary cardiac (COR onary) issue to a primary lung (PULMONary) problem.

Really common sudden onset S1Q3T3 patterns are often seen in pulmonary embolism , pneumothorax or acute Asthma presentations.

Two of these obviously present as an initial respiratory issue (Pneumothorax and asthma), but PE usually manifests with pain as the focal complaint.

Acute cor pulmonale is summarised as an increased volume and pressure within the right ventricle due to pulmonary hypertension.  

The pain is often both localised lung pain and ischaemic aching heart pain.

It is important to keep these differentials in mind when a patient presents in chest pain, with respiratory distress and the S1Q3T3 pattern.

More?  Check out our cardiac KYJs and courses on the website www.ect4health.com.au/whats 

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