Ect4health-KYJ-series

Friday, 15 November 2019

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

Saturday, 9 November 2019

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