You are working as an FY1 when one of the nurses on one of the surgical wards asks you to urgently review one of the patients, who has a blood pressure of 80/40mmHg. The patient seems confused and the nurse is very worried about them.
- Understand what ‘shock’ is and why it is so important.
- Consider the physiology of shock and how this may guide our management.
- Think about the main causes of shock.
For this we are going to go back to high school and cellular biology. I know – perhaps not the most exciting thing, but like many topics in medicine the more we understand about physiology the better our patient care will be.
The textbook definition is this
Shock is a life-threatening condition of circulatory failure, causing inadequate oxygen delivery to meet cellular metabolic needs and oxygen consumption requirements, producing cellular and tissue hypoxia.https://www.uptodate.com/contents/definition-classification-etiology-and-pathophysiology-of-shock-in-adults
Why does this matter? Well, if we don’t have oxgen going to the cells, we cannot glucose into ATP. Not effectively anyway. Remember cellular respiration?….
Step 1 – Glycolysis (with or without oxygen)
All of this magic happens in our cells. The first step – glycolysis – we can do without oxygen and occurs in the cytoplasm.This is where glucose (“glyco”) is broken down (“lysed”) into two new molecules, pyruvate and lactic acid and two molecules of ATP.
Step 2 – The Citric Acid or “Krebs” Cycle
The most important parts of this ATP production take place in the mitochodria of the cell. First, the pyruvate made during glycolysis is converted into Acetyl CoA (by the removal of CO2 and the combination of that acetyl group with coenzyme A) . At the end of Step 2 we now have two more ATP and a bunch of FADH2 and NADH (which we need for the final part).
Step 3 – The Electron Transport Chain
As you’ll remember – this is the really clever bit. The main thing we have to achieve is the formation of the covalent bond between the second and third phosphate groups as this is where all the energy is stored and released.
During this step (still in the mitochodrion), electrons are passed down this chain and ADP is converted to the energy storing ATP. At the end of the chain there has to be oxygen to accept the electrons that have been passed down, or it simply cannot function and ATP will not be formed.
Throughout a lot of our discussion of resuscitation we will return to one equation.
Blood Pressure = Heart Rate x Stroke Volume x Systemic Vascular Resistance
Whenever you assess a patient with low blood pressure we need to consider each of these variables in turn. It must be due to a decrease in one (or more) of these causing the hypotension.
We can now use all of this information to consider about the causes of shock and therefore how we got about treating them.
Any loss of intravascular volume will cause a decrease in the stroke volume, and a drop in blood pressure. We know that he body does all it can to compensate for this, by an increase in adrenaline and noradrenaline and subsequent rise in both heart rate and systemic vascular resistance. THis is why patients who are hypovolaemic get grey, sweaty and clammy as blood is diverted away from the skin to vital organs.
Whilst our bodies try to fight the infection, we produce cytokines to dilate the blood vessels and increase the white cells and other mediators in the affected area. In sepsis this process has gone into overdrive and the body gets overwhelmed, with a widespread drop in systemic vascular resistance.
This is not dissimilar to sepsis, but here it is the histamine that is causing the decrease in systemic vascular resistance.
There are two mechanisms in which the heart can cause a drop in blood pressure.
- Poor myocardial contractility: the heart itself hasn’t been receiving enough oxygen and thus the cardiac muscle cells are dying. The heart is no longer able to pump effectively and so there is drop in stroke volume. It could also be to an acute rupture of one of the heart valves. Again, the body tries to compensate with an off load of adrenaline and noradrenaline, but it’s trying to force a failing pump to work. It will increase the SVR even further and drive the heart even faster. This is a downhill spiral that without prompt action will be unrecoverable.
- Tachyarrythymia: the faster the heart goes, the less the ventricles have time to fill and thus stroke volume falls.
This is due to a disruption of the normal autonomic nervous system pathways, usually as a result of spinal cord or traumatic brain injury. The loss of sympathetic tone, causes a drop in systemic vascular resistance and slowed heart rate, as there is no balance to the vagal tone. We should just note here that neurogenic shock is different to ‘spinal shock’, which is a description of the lack of nerve function and may herald as temporary or permanent paralysis. e.
These are mechanical causes that are causing the heart to be unable to pump out the stroke volume effectively. There are two main causes usually seen as a consequence of trauma:
- Tension Pneumothorax: An increase in intrathoracic pressure prevents the heart from emptying fully on contraction
- Cardiac tamponade: Again the pressure around the heart stops effective emcontraction of the ventricle
Type of Shock
We can now focus on the treatments for each of these causes of shock, thinking about what it is that we need to reverse. Remember that medicine is simple…
Aim: Increase stroke volume
If we are losing the capability of getting a decent stroke volume due to a fall in the intravascular volume then we need to replace that volume. The are a couple of caveats to this:
- The fluid we give has to be able to maintain all the other functions of blood including oxygen carriage and to aid clotting
- The is ‘no point in turning on the tap, if there is no plug in the bath’
Therefore, of our patients is ion sdhock due to bleeding we need to simultaneoulsy stop that bleeding whilst giving blood back. Other intravenous solutions will work as a stop gap, but in the end the patient has to be able to carry oxygen and clot. This means giving red blood cells and plasma (and further down the line other components like cryoprecipitate and fibrinogen.
Treatment: Stop bleeding; give blood products
Aim: Increase systemic vascular resistance
The approach here aims to stop the production of the inflammatory cytokines (by giving suitable antibiotics) and to increase the SVR. We can do the latter first by giving crystalloids. Remeber in this case the body has enough oxygen carrying capaciy, but just not enough to generate a good SVR. Imagine the amount of air that comes out of a balloon when it is partially inflated vs when it is blown up completely.
Once we have tried to fill up those capacitance vessels we may need to add an extra agent to ‘squeeze’ them (like pressing on the outside of the balloon). We have a variety of options, all of which act on the adrenergic receptors and you may hear being called ‘pressors’: noradrenaline is often the agent of choice.
Treatment: antibiotics; intravenous fluid; pressors.
Aim: Increase systemic vascular resistance
Here the drop in blood pressure is only part of the equation and the widespread histamine release can also effect the lungs and other organs. We want to be able to increase the SVR, but also dilate the bronchi, which can go into spasm.
The agent of choice is adreanaline (often given intramuscularly). This will acts on all the adrenergic receptors, dilating the bronchi, whilst vasoconstricting the dilated blood vessels increasing SVR.
Treatment: Adrenaline; oxygen; intravenous fluids.
- Aim: Restore myocardial oxygenation.
- Much of what we are able to do for these patients is only temporary, and they need the urgent attention of a cardiologist or cardiothoracic surgeon. Unless blood flow is restored to the muscle it will die and the situation will be irreversible. Much of what we are able to do for these patients is only temporary, and they need the urgent attention of a cardiologist or cardiothoracic surgeon. Unless blood flow is restored to the muscle it will die and the situation will be irreversible
- Treatment: Urgent revascularisation
- Aim: Restore sinus rhythm (or at least slow the heart rate)
- If the patient has a compromised blood pressure due to a tachyarrhythmia then we follow the ALS guidelines (which we will cover in depth later in the series)Treatment: Rate control with drugs or DC cardioversion
- Treatment: Rate control with drugs or DC cardioversion
Aim: Maintain blood pressure despite the lack of sympathetic tone
Continuing our balloon analogy here the is the right about of air, but the rubber has got all saggy: we have the right amount of blood, but the vessles are dilated.
- Tension Pneumothorax:
- Aim: Relieve pressure preventing a decent stroke volume being pumped.
- Treatment: Let the air that is trapped between the pleura out: either via a needle decompression or a thorocostomy (a larger hole)
- Cardiac tamponade:
- Relieve pressure preventing a decent stroke volume being pumped.
- Treatment: Let the blood that is trapped in the pericardium out that is trapped out either via a needle (pericardiocentesis) or a thorocotomy (a much larger hole)
Type of Shock
Stop the bleeding
Cardiogenic – ischaemia
Restore myocardial perfusion
Cardiogenic – tachyarrythmia
Slow the heart rate
Release pressure around lungs or heart