CLARA AND SARAH Shock

Learning Outcomes  Define shock  List the categories of shock  Explain the physiological consequences of shock  Compare physiological short-term and long-term control of blood pressure  Explain the de-compensation of physiological consequences of shock  Correlate the physiological and pathophysiological consequences of shock with the clinical manifestations.  Outline pharmacological targets and mechanisms of actions of drugs used to treat shock. 1st December

First things first … Starling’s Law: The heart pumps out the blood that is returned to it I.e.: the force of contraction of the heart depends on how much the cardiac myocytes are initially stretched by the returning blood The more returning blood = the bigger the volume of blood in the heart (EDV) = the more the muscles are stretched = the stronger the heart will pump (SV)

Define shock 1st December “Acute circulatory failure with inadequate or inappropriately distributed perfusion, resulting in generalized cellular hypoxia and/or an inability of the cells to utilize oxygen”  Inadequate tissue perfusion (not enough blood/oxygen to the tissue) leading to organ dysfunction

What are the main types of shock? Explain each briefly Hypovolaemic : loss of circulatory volume Cardiogenic : failure of the heart to act as an effective pump Vasodilatation (Distributive): abnormalities of the peripheral circulation  Septic  Anaphylactic  Neurogenic (Obstructive : mechanical impediments to forward flow)

Hypovolaemic shock Why ?  Inadequate volume  haemorrhage, oliguria, decreased fluid intake  Fall in cardiac output : the heart cannot pump as much blood around (Starling’s Law)   Preload problem Now what?  Vasoconstriction : try to get as much blood to the target site  Tachycardia : increase heart rate to get blood there quickly, HOWEVER, decrease in CO : not enough time for the heart to fill up (so stroke volume remains low)! And finally?  Hypotension, inadequate perfusion, organ dysfunction

Cardiogenic shock = pump failure Why ?  Fall in cardiac output : something has happened to the heart which means that it cannot pump out enough blood  MI, Valve dysfunction, electrolyte disturbances   Pump failure, reduce contractility And now?  The heart cannot seem to pump out as much blood in one go like it should do. Vasoconstriction will kick in, as the heart “thinks” that by doing so (and therefore increasing blood flow), it will have a bigger blood volume coming back to the heart (increased EDV), and therefore it will be able to pump our more blood (increase in SV to compensate for shock  Starling’s Law!).  HOWEVER: the heart will quickly realise that it cannot pump out as much blood as it just cannot function well (we therefore have a failure of Starling’s Law : even though there is a lot of blood in the heart, this doesn’t matter : the heart cannot increase its CO). Rather than try and pump out as much blood in one go, it will increase its rate (tachycardia) as a means to get as much blood out that way  Increased capacitance : too much blood in the blood vessels : heart is already failing, cannot pump as hard against the resistance in the vessels, therefore there is a backlog of blood in the body, which will lead to increased JVP and oedema

Vasodilatation = Anaphylaxis, Sepsis (+Neurogenic) Why ?  Vasodilation : decrease in resistance of the blood vessels  Allergic reaction  Infection  Spinal injury   Afterload problem What now ?  The heart rate will rise to try and keep the blood flowing (tachycardia)  The heart’s force of contraction will increase (cardiac output rises) : this is not cardiogenic shock : there is nothing wrong with the heart! And finally?  Hypotension, inadequate perfusion, organ dysfunction

Clinical Signs Heart ratePerfusionExtremitiesPulseVeins C - Hypovolaemic P – Cardiogenic R - Vasodilatory

Clinical signs Heart ratePerfusionExtremitiesPulseVeins C - Hypovolaemic TachycardicIncreased cap. refill (>2 secs) Pale, cool and clammy Weak, threadyEmpty P – Cardiogenic R - Vasodilatory

Clinical signs Heart ratePerfusionExtremitiesPulseVeins C - Hypovolaemic TachycardicIncreased cap. refill (>2 secs) Pale, cool and clammy Weak, threadyEmpty P – CardiogenicPossibly Tachycardic Increased cap. refill (>2 secs) Pale, cool and clammy Weak, threadyFull (and high JVP) R - Vasodilatory

Clinical signs Heart ratePerfusionExtremitiesPulseVeins C - Hypovolaemic TachycardicIncreased cap. refill (>2 secs) Pale, cool and clammy Not enough blood getting to the extremities, as well as blood being directed to central organs Weak, threadyEmpty P – CardiogenicPossibly Tachycardic Increased cap. refill (>2 secs) Pale, cool and clammy Major vasoconstriction directing the blood to central organs Weak, threadyFull (and high JVP) R - Vasodilatory TachycardicDecreased cap. refill (<2 secs) Flushed, hot and sweaty BoundingFull

And how do we (try) and fix it? Hypovolaemic: Lack of blood!  IV Fluids (replete volume)  Vasopressors – adrenaline, noradrenaline (further vasoconstriction) Cardiogenic: The heart is not beating well!  Inotropes – e.g. isopenaline, dobutamine (increase contractility by stimulating B1-adrenoreceptors. Vasodilatory: The blood vessels are too dilated!  Vasopressors – adrenaline, noradrenaline  IV Fluids