Shock and critical illness Flashcards
(44 cards)
Signs of shock
Rapid and weak pulse (tachycardia with reduced stroke volume)
Mean arterial pressure may be reduced or normal, but pulse pressure reduced
Breathing is rapid and shallow
Urine output is reduced
There may be reduced mental awareness or confusion
Hypovolemic shock
Inadequate filling
Hypovolemic shock causes?
Haemorrhage, diarrhoea, vomiting, third space losses (burns)
Cardiogenic shock
Inadequate cardiac output
Cardiogenic shock causes
Stroke volume: MI, myocarditis, Takotsubo (stress induced cardiomyopathy)
Bradycardia
Tachyarrhythmias
Acute valve rupture
Distributive shock
Excessive vasodilatation
Distributive shock causes
Septic
Anaphylactic
Neurogenic
Obstructive shock causes
Cardiac tamponade
PE
IVC obstruction
Changes to Guyton graph in hypovolemic shock
CVP volume line lower on the graph, therefore intersects the starling curve at a lower CO (reduced blood supply)
How does hypovolemic shock affect CO?
Reduced preload therefore reduced contractility via the Frank-Starling mechanism
Fall in pressure leads to what immediate response
Reduction in baroreceptor and cardiopulmonary receptor activity - removes inhibitory impulses to the NTS - increase in sympathetic outflow
Increase in circulating vasoactive hormones (adrenaline, noradrenaline).
Effect of increasing the sympathetic outflow in hypovolemic shock
Myocardial contractility permits greater SV at lower filling pressure and increased HR - CO raised.
Higher starling curve means intersects with hypovolemic line at same CO as non hypovolemic (with normal starling)
Kidney response to falling blood pressure
Kidneys act like a high pressure baroreceptor: fall in pressure -pressure natriuresis, release of renin for raised levels of angiotensin II.
What happens to ADH in shock
Increased release of ADH (if >10-15% fall in ECV)
Effect of RAAS
Vasoconstriction - increased tone to capacitance vessels and retention of salt and water.
If blood loss is less than 15%..
Compensated haemorrhage
As perfusion falls what happens to chemoreceptors?
Hypoperfusion and hypoxia - carotid bodies ‘stagnant hypoxia’ - activates the chemoreceptors.
What as well as ‘stagnant hypoxia’ activates the chemoreceptors?
Anaerobic conditions -pyruvate generated from glycolysis channels into lactic acid cycle (pyruvate is converted to lactate) - type-A lactic metabolic acidosis (pH <7.35)
What is the response to the fall in pH and chemoreceptor activation?
Chemoreceptor activation contributes to the sympathetic activation (above) also targets the NTS - increase phrenic nerve firing and increase ventilation rate
How does hyperventilation compensate for metabolic acidosis?
Through loss of volatile acid CO2 (respiratory loss)
Vasculature in shock
Vasoconstricted (to raise afterload)
What happens to body fluid after hours in hypovolemic shock?
Absorption of interstitial fluid into depleted circulation
What allows fluid to move from the interstitium to the circulation?
Fall in venous pressure and sympathetic mediated rise in postcapillary resistance ratio lowers the capillary BP - (lower than interstitium) net absorption across the capillary wall
How is the patient stabilised with hypovolemic shock?
Fluid resuscitation: Isotonic glucose, isotonic saline, blood
