Monday, 2 December 2019
Friday, 15 November 2019
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.
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"
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.
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)
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"
Robs Courses - Cruises - Videos and Seminar Dates
Sunday, 10 November 2019
Saturday, 9 November 2019
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.
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#ECT4Health
#SmokeInhalation
Thursday, 31 October 2019
Monday, 28 October 2019
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