Differentiating AV Blocks

Tropes and Pressors - Part 2 of a 3 part series.

Tropes and Pressors  -A 3 part series.

Part 2 of 3  # KYJ (Knowing your jargon)

This episode – The Pressors

Recap from yesterday …

Vasopressors are drugs we give to squeeze arteries (and veins) to increase SVR (Afterload and Blood pressure, and subsequently MAP.

Inoptopes :more correctly – positive inotropes, are drugs we give to increase the force of the cardiac contraction. This increases SV, and CO which of course increases MAP.  Its all about that MAP!!.

So when are each indicated?

God I wish it was that simple, but it comes down to etiology (cause) and type of shock occurring in the patient.

If you didn’t already view the post on shock, or watch my Video on shock;  then perhaps that might be a good place to refresh.

Remembering there are 4 main types of shock: hypovolemic, distributive, cardiogenic, and obstructive. Vasopressors and inotropes may be indicated for all types, and though most of the medications can be used in each type, we do need to tackle the specifics of each one.

So….here goes.

The major vasopressors include phenylephrine, norepinephrine, vasopressin and Metaraminol.

Drugs like Adrenaline and Dopamine are vasopressors, but they also exert inotrope properties.

Then  out on a limb (good choice of words really) Dobutamine and Milrinone are obligate inotropes.

So Last bit of FIZZ (physiology before we dive into the drugs)

Receptors to consider for this post :

Adrenergic - Alpha 1 – Cause Vasoconstriction

Adrenergic - Beta 1  - Causes increase Chronotropy and Inotropy

Vasopressin Receptors – V1 = vasoconstriction, V2= reduced urine output.

The Vasopressors

By redistributing blood back to the heart, vasopressors help increase CO directly with an increase in blood return to the heart (Preload), and  and increase in SVR. through arterial vasoconstriction peripherally. There are  main groups are catecholamines, Smooth Muscle and dopaminergic receptors

The Vasopressors are ‘Boss of the Pit’ when distributive shock (Sepsis, Neurogenic disruption or anaphylaxis) is the dominant cause of drop in Cardiac output.  The goal of vasopressors is to increase the SVR by direct constriction of the vessels.

Two distinct physiologies are happening in distributive shock.  

First a loss of nerve messages to blood vessel walls  causes them to relax – dilate, and blood pools in the peripheries.  With the maldistribution of volume between central and peripheral circulation, (blood stuck out in the veins of Arms and legs), there is little perfusing the core vital organs.  Remember at any given moment in time your 5.5 litres of blood is parked 30% in your arteries, and 70% in your veins.  Increases in that venous pooling causes a dramatic drop in arterial flow/volume and of course, pressure (SVR and MAP).

Secondly, as blood in peripheral areas pools, and causes congestion, this vasodilation extends to the capillaries, and these little guys are super leaky.   As they congest, and spill their plasma into the peripheral tissues, you see oedema forming and drop in blood volume, which is now becoming thick and viscous as plasma leaves, the haemoconcentrated blood now has a tenacious sticky vibe going on.  Bad bad bad.   You can see why we fluid resuscitate these people.  In fact, a fluid load, is frequently the First line treatment; and only after some sauce is given to we then squeeze the pie – ok bad visual.

Note to Americans – in Australia we eat real pies with meat inside – sauce “dead horse”  or what you mob call “ketchup” is a must have.

Right Back to it…

Remembering that that Magic MAP of 60 to 65 mm Hg is required to perfuse organs (American College of Critical Care Medicine (ACCM) guidelines). If fluid resuscitation doesn’t get that MAP up to 60 mm Hg, it is recommended that vasopressors be next in line.

So what do we select? 

Norad (Noradrenaline) / Norepinephrine

The first of our Catecholamines, and a favourite in the Sepsis world (Surviving Sepsis Campaign recommendation).

We follow this with Adrenaline (epinephrine) or Vasopressin  as a back up plan

Norepinephrine is recommended as the initial pressor for  because it lights up those Alpha  receptors.  In blood vessels, these receptors act like switches that open Calcium gateways into the smooth muscle cells lining the vessel walls.   As they get turned on, Calcium rushes in, causing the muscles to contract (constrict) pushing up the pressure, and squeezing the blood out of those naughty veins, back to the heart and central core circulation.   By increasing the venous return, then you increase the Preload, and the heart now has volume it can use to pump with.  They also act on the arteries (remember that constriction here increases SVR and MAP)  … And that is the game changer.

Metaraminol

Metaraminol is trade named Aramine, and Metaramin.  It is a potent alpha 1 stimulant, with weak Beta effects.  It tends to be used in spinal cord injuries that result in distributive neurogenic shock, and to bring up BP in a perianaesthetic scenario.  RFDS in Australia use it as a first line "rescue drug" for increasing BP that can occasionally plummet when performing rapid sequence induction (emergency intubation).   Dose is usually up to 10mg diluted to 20 ml and given in a good secure IV line as a slow push over 1-2 mins

Vasopressin

Vasopressin is a natural hormone also known as ADH (Antidiuretic Hormone) normally secreted from the Pituitary gland.

It fires up specific Vasopressin 1 and 2 receptors.  Remember V-1 receptors to stimulate smooth muscle contraction of the vessels , and the V-2 receptors in the kidneys stop urine production hence increased blood volume, and increased CO and MAP.

It wont cause the patient to increase heart rate, or increase force of contraction.

Phenylephrine

This is another pressor that occasionally gets bandied around, but caution in use is advised because it tends to cause a reflex bradycardia.

Ironically, as much as it fires off those alpha receptors to cause vasoconstriction, The sudden increase in BP can trigger off the vagus nerve (Parasympathetic) which is actually the nerve that tells the heart to “Go Slow – this is a school zone”.  So BP goed up, parasympathetic response kicks in and a reflex bradycardia loses the ground you gain.  Some docs love it- Im not convinced.  Many of you will know of Phenylephrine as the why bother replacement for pseudoephedrine in the old cold and flu tablets.

Phenylephrine is a pure alpha-1 agonist, inducing peripheral arterial vasoconstriction. Reflex bradycardia may occur due to selective vasoconstriction and elevation of blood pressure.

Adrenaline

Also known as Epinephrine, this hormone has essentially equivocal activity on alpha-1 and beta -1 receptors. So Epinephrine increases SVR through the Alpha 1, and the Beta effects on increasing Inotropy and  HR, boost cardiac output on both sides of the equation (CO=SVxHR).

Dopamine is a precursor of norepinephrine and epinephrine (catecholamines).  So it essentially does the same thing.  All good pies need a reliable base, so as a precursor to the catecholamines, the effects are both vasopressor and inotropic.

Controversy exists around whether differing doses of Dopamine affect different tissues. Many readers will recall that low doses increase renal perfusion(5 to 15 micrograms/kg/min), and higher doses (>15 micrograms/kg per minute), are more peripherally vasopressor.

Giving Pressors

IV.   Say it out loud.  IV.   These drugs are for intravenous (IV) use only.   They are fast acting, short duration, and epically destructive if an IV cannula through which these drugs are given, should extravasate (tissue).

It’s a brave clinician that will settle for a peripheral IV line, so as soon as possible these patients should have a central access (either CVL or PICC).  Doses are dependent on presentation but always via a pump, and the patient should be very closely monitored – especially heart rate and BP, but also Sats, JVP and breath sounds.  As BP can rise dramatically with pressors, complications like heart failure can declare itself with a surprise ankle swelling, pulmonary oedema, and breathlessness.

Next part of our series will tackle the other class of drugs, looking deeper at the Beta 1 receptor meds  - the inotropes.

Now the physiology and Jargon is out the way, stay tuned for Part 2 as we dive into the deep dark world of the "Tropes and Pressors"

 Who is Rob Timmings and ECT4Health?   Follow on Facebook

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Tropes and Pressors - Part 1 of a 3 part series

Tropes and Pressors 

Part 1 of 3  # KYJ (Knowing your jargon)

To kick off this KYJ  we first need to unpack a bit of terminology.  So this is Part 1 of 3

Shock  is a state of  oxygen deficit (hypoxia) to tissues; all tissues – and of particular concern, vital organs (heart , brain, lungs, kidneys). Shock is global cellular hypoxia.  Whilst shock can be caused by a lack of oxygen in the blood itself, most shock is actually a drop in perfusing pressure of what blood is available.  SHOCK VIDEO

MAP is Mean arterial pressure.  It is, in its most basic of descriptors the average blood pressure (mean) that perfuses vital organs.  A low MAP will therefore be consistent with shock, irrespective of how oxygenated the blood is.  Magic MAP number to aim for is 60 mmHg.  Below 60, and we struggle to perfuse our Kidneys.

MAP is determined by two things.

Cardiac output, and Systemic vascular resistance.

Cardiac output is the volume of blood you pump out in any given minute (normally 4200-7000ml).  It is made up of how much you heart pumps in one beat (Stroke volume (SV)) x the number of times/in that you beat (Heart Rate (HR)).  

The maths looks like this:  CO = SV x HR.

MAP VIDEO

Stroke Volume

Your ventricles are a muscular bag of blood.  When they contract (systole), blood is ejected in a volume called a stroke volume (SV).  We don’t eject all of our blood with every contraction, infact your heart fills with about 100ml, and pumps out 70ml. 

This stroke volume represents 70% of the ventricle’s filling volume.  That percentage (70%) is called an ejection fraction (EF). 

Stroke volume (SV) is determined by a few factors. 

·         Strength of your heart beat,  (Inotropy)

·         how much blood was in your heart, (Preload)

·         the pressure inside the artery that your heart is pumping into (Systemic Vascular Resistance – also called Afterload) and,

·         the stiffness of the ventricle. (Compliance)

CARDIAC OUTPUT & STROKE VOLUME VIDEO

Inotropy

This is a concept that refers to the strength of a heart’s contraction. 

So what if I could give you a drug that increased the force of your contraction?   Then you’d fill with 100ml, but pump out a greater SV by increasing your EF.  That drug is therefore referred to as a positive Inotrope.

Positive Inotropes are hormones or drugs that increase the strength (force) of the heart contraction (Inotropy).   Typical Inotropes include Dopamine, digoxin, adrenaline, dobutamine and others; we will discuss in detail in Part 2.

Loss of inotropy occurs after infaction, ischaemia, or with an aging stiff heart.   Collectively this is called Heart Failure.

Preload

Fundamentally, preload is about the filling and the stretching of your ventricles.  Passively the Left ventricle fills up to about 70 ml, then the atria contracts squeezing (pushing ) in another 25-30 ml.  Like, you’re your suit case is full, but some muppet says, “hey Dad, can you fit my jacket in”?   so you are there squeezing a jacket into an already full case.     The case isn’t full its now Preloaded.   It is stretched and bulging.   Preload in the heart is determined by a couple of factors.  The force of an atrial contraction (lost in AF or flutter), and the volume of blood returning to the left heart from the lungs.  So, atrial arrythmias, and hypovolaemia can dramatically lead to a reduced SV, CO, MAP and subsequently shock.

Systemic Vascular Resistance (Afterload)

As a pipe carrying fluid is compressed (narrowed), the pressure inside the pipe increases. Thus, squeezing blood through a narrower artery leads to increased in pressure.  This is called systemic vascular resistance (SVR). Increasing the SVR leads to increased blood pressure, mean arterial pressure (MAP) and increased perfusion to organs.  

Vasopressors are natural hormones, or drugs that cause an increase vasoconstriction.  Commonly these are just referred to as “pressors”.  Common drugs that fall into these categories include Noradrenaline(norepinephrine), Metaraminol, phenylephrine, vasopressin, and good old adrenaline

Now the physiology and Jargon is out the way, stay tuned for Part 2 as we dive into the deep dark world of the "Tropes and Pressors"

 Who is Rob Timmings and ECT4Health?   Follow on Facebook

Robs     Courses  -  Cruises  -   Videos   and Seminar Dates

RespPhys6 Respiratory Failure part 6 of 8

Smoke inhalation

Smoke inhalation

#KYJ #KnowingYourJargon

With so many fires in the last few days (weeks) and forecast over this coming month, I though it might be time to review smoke inhalation injury as a presentation.

The reality is that inhalation of smoke causes more deaths in fires than the burns.

It has been estimated that  greater than half, and up to 80% of fire related deaths are due to toxic exposure to products of combustion and or asphyxia .

When stuff burns it releases gases and particulate matter (smoke).   The gases are toxic, colourless and often odourless.  When you smell or see smoke, this is aerosolised ash, and incomplete or unburned product.

It’s what you can’t see or smell that is actually the killer.

Let’s look at these

Carbon dioxide (CO2) is produced in all carbon fuelled fires (wood, paper, oils, petrochemicals and any products manufactured from these).

When inhaled, CO2 displaces oxygen in the lungs, reducing gas exchange (less oxygen into blood, and dramatically less CO2 out) = profound hypoxaemia and hypercapnic acidosis (Respiratory acidosis).

Carbon monoxide (CO) is present in any incomplete carbon fuel combustion. Like CO2 it’s odourless, colourless and deadly poisonous.  When inhaled, it binds to haemoglobin in red blood cells with such high bonding affinity, that it displaces oxygen.  This means that red blood cells can’t carry oxygen, so the patient is not just hypoxaemic, but globally hypoxic.  Headaches, confusion, chest pain and altered consciousness.

When measuring Sats on these patients, the sats probe can’t differentiate between oxygen rich blood and carbon monoxide poisoned blood.   They often look pink, perfused and in severe poisoning, their sats are 100%. The probe is just looking at blood colour, and CO causes blood to turn bright red just like oxygen. Think exposure to car fumes, bush fires.

Cyanide gas

Cyanide is a cellular toxin.  It is released from burning synthetics and wool. Once breathed in, it diffuses into plasma where it off gases into cells.  It is a deadly cytotoxic that shuts down cellular metabolism and energy production.

Death is quick when cyanide (the blue death) is involved.   Think of caravan, tent, building and car fires, where synthetic textiles are abundant.

Inhalation of other pneumotoxic particles / ash that can be super heated, causes burns and inflammation in the delicate lung tissues. This rapidly leads to acute lung injury (ALI) and surfactant decrease (pneumonia) resulting in two presentations-  atelectasis (lung collapse and consolidation) and pulmonary oedema, as damaged lung swells and leaks fluid into the spaces between the alveoli and the capillaries.  In technical terms, this leads to a VQ (ventilation / Perfusion (Q)) mismatch which reduces oxygen gas exchange.

Finally asphyxia.

Asphyxia is caused when there is a lack of oxygen in the air you breathe.  In a poorly ventilated area, Fire is consuming oxygen, reducing that which is available.  As you breathe poorly oxygenated air, you asphyxiate.  Fresh Air has 21% oxygen , and as the fire burns, it consumes this  oxygen just like you and I.   As oxygen levels In the Air drops to around 15%, The concentration of oxygen still supports burning, but is too low to maintain consciousness. So when these situations occur, like in a building fire, or in a bush when you are surrounded by dense smoke and smouldering trees, you’d collapse and go unconscious before you got burned.   In a home fire, the reality is, they never wake up to smell the smoke or fire or even to respond to the smoke alarm (as controversial as that last bit may sound).

They were unconsciousness, and never felt a thing. 

So.... the patients you see with smoke inhalation are actually the lucky ones.

Any way you look at smoke inhalation, asphyxia, cyanide or CO poisoning; these conditions all represent an injury due to poor oxygenation.... this is quite simply, shock.

Management 

Oxygen is the first line treatment.  In smoke inhalation we can not rely on pulse oximetry to assess oxygen status because the probes can’t differentiate between carbon monoxide and oxygen. Formal arterial blood gases must be used. The benefit of arterial blood gas analysis, is that a carbon monoxide reading called a carboxyhaemoglobin can also measure the CO in the red blood cells.

Normal is less than 3% for non smokers.  Anything over COHb 15% is cause for concern and high flow O2 (aiming for 100% oxygen via a tight fitting mask), is recommended until COHb drops below 4-5%.

Secondary management of smoke inhalation is symptomatic.  If pulmonary oedema is manifest, then non-invasive positive pressure ventilation (Ni-PPV), Lasith and or nitrates (GTN infusion or patches) might be useful.

Acute lung injuries have high mortality and poor prognosis, so management often requires ICU admission and steroids to stem inflammation.

Like the post? Let me know, share and check out our webpage or follow the YouTube page 

and Facebook group.

#ECT4Health 

#SmokeInhalation

www.ect4health.com.au

DKA vs HHS - Why no Ketones - ECT4Health Rob Timmings

Rob on Haemostasis Part 1 Vasoconstriction

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
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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