Shock

• Shock describes circulatory failure resulting in inadequate tissue perfusion and insufficient delivery of oxygen.
• There are many causes with different underlying pathophysiological processes, normally they are divided into four categories:

  • Hypovolaemic
  • Distributive
  • Cardiogenic
  • Obstructive
• Oxygen delivery is determined by two major factors; cardiac output and arterial oxygen content.
• Cardiac output:

  • Determined by the heart rate and stroke volume
  • Stroke volume = amount of blood pumped out of the heart from each contraction
  • Cardiac output is the amount of blood pumped out of the heart in 1 minute
  • CO = HR x SV
• Stroke volume is determined by a complex interplay of preload, myocardial contractility and afterload:

  • Preload - stretching of cardiomyocytes at the end of diastole.
  • Myocardial contractility - changes to stroke volume can be brought about through changes to contractility.
  • Afterload - pressure or load against which the ventricles must contract.
• Oxygen is carried in the blood in two ways:

  • Bound to haemoglobin
  • Dissolved in plasma (small amount)
• Clinical features of compensation:

  • Baroreceptors - found in the carotid sinus and aortic arch - respond to drop in blood pressure - increased sympathetic output = increased HR and vasoconstriction
  • RAAS - reduction in renal perfusion - release of angiotensin II causes vasoconstriction and aldosterone causes reabsorption of fluid by kidneys
  • Chemoreceptors - increased lactic acid decreased pH which activates chemoreceptors = increased respiratory rate
• Respiratory rate is a sensitive sign of systemic upset, tachypnea often occurs as a compensatory mechanism in patients with a metabolic acidosis secondary to inadequate tissue perfusion.
• Urine output is essential to monitor - oliguria is common - reduced urine output reflecting the compensatory and fluid preserving actions of aldosterone and vasopressin.
• Decompensation:

  • When normal compensatory mechanisms are overwhelmed
  • Increasing anaerobic respiration results in greater acid production but reduced renal perfusion prevents excretion of hydrogen ions
  • In severe cases a fall in BP results in vascular stasis and release of inflammatory mediators - widespread clotting leads to consumptive coagulopathy causing DIC
  • End-organs begin to fail
  • Ischaemic liver injury results in release of hepatic enzymes (very raised ALT and AST)