Session 11 ILOs - Haemodynamic shock Flashcards

1
Q

Describe the essential characteristics of haemodynamic shock

A

Haemodynamic shock is an acute condition of inadequate blood flow throughout the body, due to a catastrophic fall in arterial blood pressure, which leads to circulatory shock

Can be due to either:

  • Fall in CO
  • Fall in TPR (beyond heart’s ability to compensate)
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2
Q

Describe the characteristics of hypovolaemic, cardiogenic, mechanical and distributive shock such as anaphylactic shock

A

Haemodynamic shock due to 2 causes:

a) Fall in cardiac output:

  1. Cardiogenic shock (pump failure - ventricle can’t empty properly)
    - Defining factor is drop in arterial BP
    - Causes include myocardial infarction, serious arrhythmias or acute worsening of heart failure
    - Tissues become poorly perfused
  2. Mechanical shock (cannot fill - ventricle cannot fill properly)
    - Caused by cardiac tamponade(build up of fluid in pericardial space which restricts heart from filling properly) or massive pulmonary embolism (a embolus occludes a large pulmonary artery)
    - Cardiac tamponade = high central venous pressure and low arterial BP
    - Pulmonary embolism = high pulmonary artery pressure causing reduced emptying of right ventricle. Leads to low left atrial pressure and low arterial blood pressure
  3. Hypovolaemic shock (loss of blood or fluid volume)
    - Patients present with compensatory sympathetic stimulation e.g. tachycardia
    - Caused most commonly by a haemorrhage or pure blood loss, diarrhoea , vomitting but severity is related to amount and speed of blood loss
    - Danger of decompensation

b) Fall in TPR:

  1. Distributive shock
    - There is an excessive vasodilation, which causes fall in TPR
    - Caused by either toxic shock (i.e. sepsis) or anaphylactic shock
    - Decreased arterial BP, tachycardia and warm extremities initially but then later in sepsis you get vasoconstriction
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3
Q

Describe the general features of management of the various types of shock

A
  1. Cardiogenic
    - Help to treat the cause i.e. remove blockage if MI
  2. Mechanical
    - Cardiac tamponade = insert needle to relieve the fluid from pericardial sac (pericardiocentesis)
    - Pulmonary embolism = anticoagulants to remove the clot
  3. Hypovolaemic
    - Saline solution to increase the blood volume
  4. Excessive vasodilation
    - Toxic shock = treat underlying cause e.g. sepsis - give antimicrobial drugs to treat causative infection
    - Anaphylaxis = give adrenaline via epipen to activate vasoconstriction (alpha 1 Adrenergic Receptor activation)
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4
Q

Describe the body’s compensatory responses to hypovolaemia to maintain arterial blood pressure

A
  • Venous pressure falls due to fluid loss which causes CO to fall and consequently arterial BP falls
  • Detected by baroreceptors

Compensatory response:

  • Increased sympathetic stimulation
  • Tachycardia, increased force of contraction and increased vasoconstriction and VENOconstriction
  • Also normally at the capillaries, fluid moves out into tissue due to balance of starling’s forces however if the blood volume drops then the hydrostatic force drops and fluid moves into the capillaries

Longer term compensation = RAAS system Renin-Angiotensin-Aldosterone System

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5
Q

Explain how prolonged peripheral vasoconstriction in response to hypovolaemia can lead to decompensation

A
  • If you don’t quickly replace fluids, there is a danger of decompensation:
  • In response to hypovolaemic shock –> peripheral vasoconstriction
  • This leads to tissue damage by hypoxia, as there’s insufficient oxygen to tissues
  • Hypoxic tissue released chemical mediators - vasodilators in order to increase tissue perfusion and cause vasodilation
  • Over a prolonged period of peripheral vasoconstriction, concentration of vasodilators builds up and undos and overcomes the actions of the sympathetic nervous system
  • This causes widespread vasodilation
  • TPR falls
  • This causes BP to fall dramatically
  • Vital organs can no longer be perfused, so you get multi-organ failure and death
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