S11: haemodynamic shock Flashcards

1
Q

Describe the essential characteristics of haemodynamic shock

A

Acute condition of inadequate blood flow throughout the body
Catastrophic fall in arterial BP leads to circulatory shock (mean aBP = CO x TPR)
Shock can be due to fall in CO or fall in TPR beyond capacity of the heart to cope

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2
Q

Define the three different types of shock due to fall in cardiac output

A

Cardiogenic shock = ventricle cannot empty properly
Mechanical shock = ventricle cannot fill properly
Hypovolaemic shock = reduced blood volume leads to poor venous return

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3
Q

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

A

Distributive shock: sepsis 6, adrenaline EpiPen
Mechanical shock: pericardiocentesis
Hypovolaemic shock: blood transfusion
Cardiogenic shock: vasopressors, aspirin, blood-thinning medication

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4
Q

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

A

Impairs tissue perfusion
Tissue damage due to hypoxia
Release of chemical mediators -> vasodilators
TPR falls, BP falls
Vital organs can no longer be perfused -> multi system failure

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5
Q

List the causes of cardiogenic shock

A

Acute failure of the heart to maintain cardiac output – pump failure

1) Following MI – damage to the left ventricle
2) Due to serious arrhythmias
3) Acute worsening of heart failure

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6
Q

Describe cardiogenic shock

A

Heart fills, but fails to pump effectively
CVP may be normal/raised
Dramatic drop in arterial BP
Tissues poorly perfused:
1) Coronary arteries may be poorly perfused – exacerbates problem
2) Kidneys may be poorly perfused – reduced urine production = oliguria

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7
Q

Describe the management of a cardiac arrest

A

Basic life support – chest compression & external ventilation
Advanced life support – defibrillation
Adrenaline – enhances myocardial function & increases peripheral resistance

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8
Q

Describe mechanical shock – cardiac tamponade

A

Cardiac tamponade – blood/fluid build up in pericardial space
Restricts filling of the heart – limits EDV
High CVP
Low aBP
Heart attempts to beat – continued electrical activity

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9
Q

Describe mechanical shock – pulmonary embolism

A

Embolus occludes a large pulmonary artery – increases pressure in the artery
RV can’t empty -> CVP high
Reduced return of blood to left heart -> limits filling of left heart (left atrial pressure low)
SHOCK, also chest pain & dyspnoea

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10
Q

How can an embolus reach the lungs?

A

Due to deep vein thrombosis
Portion of thrombus breaks off
Travels in venous system to right side of the heart
Pumped out via pulmonary artery to lungs

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11
Q

What is hypovolaemic shock?

A

Reduced blood volume (haemorrhage)
30-40% substantial decrease in mean aBP = serious shock response
Severity of shock related to amount and speed of blood loss
Can also result from: severe burns & severe diarrhoea/vomiting

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12
Q

Describe hypovolaemic shock – haemorrhage

A

Venous pressure falls, CO falls (Starling’s law)
Arterial pressure falls
Detected by baroreceptors

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13
Q

Describe the compensatory response in hypovolaemic shock

A
Increased sympathetic stimulation 
Tachycardia 
Increased force of contraction 
Peripheral vasoconstriction
Venoconstriction 
Increased peripheral resistance reduces the capillary hydrostatic pressure – net movement of fluid into capillaries
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14
Q

Describe the clinical presentation of hypovolaemic shock

A

Tachycardia
Weak pulse
Pale skin
Cold, clammy extremities

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15
Q

What is distributive shock?

A

Low resistance shock
Profound peripheral vasodilation – decreased total peripheral resistance
Blood volume is constant, but volume of the circulation has increased

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16
Q

Describe distributive shock – sepsis

A

Septic shock
Endotoxins are released by circulating bacteria -> profound vasodilation
Dramatic fall in TPR
Fall in arterial pressure
Impaired perfusion of vital organs
Capillaries also become leaky -> reduced blood volume

17
Q

Describe the body’s response to septic shock

A

Decreased arterial pressure is detected by baroreceptors
Increased sympathetic output
Vasoconstrictor effect overridden by mediators of vasodilation
Heart rate and stroke volume increased

18
Q

Describe the clinical presentation of septic shock

A

Tachycardia
Warm, red extremities INITIALLY
-later stages of sepsis, there is vasoconstriction causing localised hypo-perfusion

19
Q

Describe distributive shock – anaphylactic shock

A

Severe allergic reaction – release of histamine from mast cells -> powerful vasodilator effect
Dramatic drop in arterial pressure – increased sympathetic response but can’t overcome vasodilation
Impaired perfusion of vital organs
Mediators also cause bronchoconstriction & laryngeal oedema – difficulty breathing

20
Q

Describe the clinical presentation of anaphylactic shock

A

Difficulty breathing
Collapsed
Rapid heart rate
Red, warm extremities