Shock

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Shock - a global energy deficit at a cellular level

most often due to inadequate tissue perfusion

high morbidity and mortality condition

presents as the final common pathway of a large number of critical patients

cells not receiving enough energy/oxygen

Metabolic shock = tissues are unable to use energy and oxygen resulting in mitochondrial damage

Hypoxic shock:

inadequate cellular oxygen delivery due to decreased oxygen content of arterial blood

Can be due to:

- inadequate/dysfunctional haemoglobin (anaemia, carbon monoxide toxicity)

- failure of gas exchange in the lungs (resulting in hypoxaemia)

Hypovolaemic Shock:

most common type of shock

results from loss of intravascular volume (blood loss, severe dehydration)

very common in trauma patients

low preload reduces cardiac output

Cardiogenic shock:

failure of the pump to pump blood around the body caused by:

heart disease

cardiac tamponade

arrhythmias

myocardial infarction

Distributive shock:

cardiac function and blood volume not affected but there is a failure of the vascular tree to allow appropriate delivery

loss of vascular tone

sepsis/endotoxaemia

anaphylaxis

venous blockage of blood (obstructive shock)

pulmonary thromboembolism

inability of blood to perfuse and distribute

Baroreceptor mediated responses:

detects decreased blood pressure

increase in sympathetic tone (plus decrease in parasympathetic tone)

increase in heart rate

increase in SVR

sympathetic response occurs almost instantly

Humoral responses:

activation of the renin-angiotensin system

promotes vasoconstriction

sodium and water retention via aldosterone release

ADH release fro hypothalamus = vasoconstriction and renal water reabsorbtion

need to attain as much salt water as possible

Clinical signs of classic shock: reflection of animal trying to compensate

tachycardia as part of sympathetic response

poor pulse quality - vasoconstriction and lack of blood volume

decreased extremity pressure

pale mucous membranes

prolonged capillary refill time

decreased mentation - inadequate brain perfusion

Exemption from the rule:

Septic (distributive) shock

- due to vasodilation animals may have brick red mucous membranes, warm extremities and bounding pulses

- Cats may have increased heart rates in early shock but frequently present with bradycardia in more severe shock (unpredictable reaction)

Decompensation = irreversible shock

*seen in very severe hypovolaemic shock (losses greater than 35-45% blood volume)

When animal stops being able to compensate they die quickly

*blood lactate can act as prognostic investigation - useful thing to measure

lack of oxygen = lack of energy

increased calcium = apoptosis and death of cell

Gut = shock organ

Sequelae of circulatory shock:

sock can be rapidly fatal due to hypoperfusion

shock can be fatal in the minutes/hours following the insult if decompensation occurs

animals can survive the initial shock episode and develop reperfusion injury and SIRS = leading to multiple organ failure

Septic shock = characterised by systemic vasodilation and widespread endothelial activation and inflammation

Aims of circulatory shock treatment:

rapid yet judicious use of intravenous fluid therapy to restore vascular volume, normalise tissue perfusion and reduce secondary injuries

aggressive, early fluid resuscitation is associated with significantly reduced morbidity and mortality

identification and control of any haemorrhage is an important component of treatment in hypovolaemic shock

Additional shock therapies:

- Broad Spectrum bacteriocidal antibiotics

- Treat the cause

- GI protectants

- Vasopressors/Inotropes (noradrenaline)

- Bicarbonate

- Activated protein C (Septic shock)

- Glucocorticoids