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"
