7. Haemodynamic Shock

Question 1

What is haemodynamic shock?

Answer 1

Acute condition of inadequate blood flow throughout the body

Question 2

What leads to circulatory shock?

Answer 2

Catastrophic fall in BP

Question 3

What can shock be due to?

Answer 3

Fall in cardiac output or total peripheral resistance beyond the capacity of the heart to cope

Question 4

What is cardiogenic shock?

Answer 4

Pump failure - heart fills but fails to pump effectively

Question 5

Give 3 causes of cardiogenic shock

Answer 5

Following an MI where there is damage to the LV
Serious arrhythmias
Acute worsening of heart failure

Question 6

What would you see clinically with cardiogenic shock?

Answer 6

Central venous pressure normal or raised.
Dramatic drop in arterial BP.
Tissues poorly perfused - eg coronary arteries, making problem worse, and kidneys, leading to oliguria

Question 7

What is a cardiac arrest?

Answer 7

Unresponsiveness associated with lack of pulse - heart has stopped

Question 8

What 3 things can cause a cardiac arrest?

Answer 8

Asystole (loss of electrical and mechanical activity).
Pulseless electrical activity (PEA).
Ventricular fibrillation (uncoordinated electrical activity) - most common, often following MI, electrolyte imbalance or some arrhythmias.

Question 9

What should be done in a cardiac arrest?

Answer 9

Basic life support - chest compressions and external ventilation.
Advanced life support - defibrillation depolarises all cells putting them into the refractory period.
Adrenaline - enhances myocardial function and increases peripheral resistance.

Question 10

What type of haemodynamic shock do cardiac tamponade and pulmonary embolisms cause?

Answer 10

Mechanical shock

Question 11

What is cardiac tamponade?

Answer 11

Blood or fluid build up in pericardial space, restricts filling of heart

Question 12

What would you see clinically in mechanical shock caused by cardiac tamponade?

Answer 12

High central venous pressure
Low arterial blood pressure
Continued electrical activity

Question 13

What is a pulmonary embolism?

Answer 13

Embolus concluding a large pulmonary artery

Question 14

How does a pulmonary embolism lead to mechanical shock?

Answer 14

Pulmonary artery pressure high, reduced return of blood to left heart, left atrial pressure low, arterial blood pressure low

Question 15

What other symptoms are present in a pulmonary embolism?

Answer 15

Chest pain and dyspnoea

Question 16

How does an embolus normall reach the lungs?.

Answer 16

DVT, some of thrombus breaks off, travels in venous system to right side of heart, pumped out via pulmonary artery to lungs

Question 17

What is hypovolaemic shock?

Answer 17

Reduced blood volume leading to inadequate venous return

Question 18

What is mechanical shock?

Answer 18

Ventricle cannot fill properly

Question 19

What is hypovolaemic shock most commonly due to?

Answer 19

Haemorrhage

Question 20

What is the severity of hypovolaemic shock related to?

Answer 20

Amount and speed of blood loss

Question 21

What would you see clinically in a patient with hypovolaemic shock?

Answer 21

Tachycardia (increased sympathetic stimulation due to decreased BP being detected by baroreceptors), increased force of contraction, peripheral vasoconstriction and venoconstriction
Weak pulse
Pale skin
Cold, clammy extremities

Question 22

What is internal transfusion?

Answer 22

Increased peripheral resistance reduces capillary hydrostatic pressure in hypovolaemic shock, and so there is net movement of fluid into capillaries

Question 23

What can hypovolaemic shock result from other than haemorrhage?

Answer 23

Severe burns

Severe diarrhoea or visiting and therefore loss of Na+

Question 24

What is it called in hypovolaemia where BP can maintain high despite blood loss?

Answer 24

Decompensation

Question 25

How does hypovolaemia lead to multi system failure?

Answer 25

Peripheral vasoconstriction, impaired tissue perfusion, tissue damage due to hypoxia, release of vasodilators, TPR falls, BP falls, vital organs no longer perfused, multi system failure

Question 26

Up to what percentage blood loss can body fluid volumes be restored within 3 days? Via what systems?

Answer 26

20%

RAAS and anti-diuretic hormone

Question 27

What is distributive shock? Give two types

Answer 27

Low resistance shock caused by profound peripheral vasodilation, so decreased TPR.
Toxic (septic) shock
Anaphylactic shock

Question 28

What is sepsis?

Answer 28

Serious life-threatening response to infection

Question 29

What causes toxic/septic shock?

Answer 29

Endotoxins released by circulating bacteria, leading to excessive inflammatory response, vasodilation, fall in TPR and arterial pressure, impaired perfusion of vital organs. Leaky capillaries of reduced blood volume. Increased coagulation and localised hypo-perfusion.

Question 30

Why is there decreased BP in septic shock, despite decreased arterial pressure being detected by baroreceptors and therefore increased sympathetic output?

Answer 30

Vasoconstriction overridden by mediators of vasodilation released in the inflammatory response, but HR and stroke volume is still increased

Question 31

What do you see clinically in a patient with septic shock?

Answer 31

Tachycardia

Warm red extremities initially, but then vasoconstriction (pale and cold) and localised hypo-perfusion

Question 32

What is anaphylactic shock?

Answer 32

Severe allergic reaction

Question 33

What causes anaphylactic shock?

Answer 33

Release of histamine from mast cells and other mediators, vasodilation, fall in TPR and arterial pressure, increased sympathetic output and cardiac output, but cant overcome vasodilation to impaired perfusion of vital organs.
Also bronchoconstriction and laryngeal oedema occur

Question 34

What would you see clinically in a patient with anaphylactic shock?

Answer 34

Difficulty breathing, collapsed, rapid HR, red and warm extremities

Question 35

What would you administer to a patient with anaphylactic shock? What does this cause?

Answer 35

Adrenaline - cause vasoconstriction via action at alpha1-adrenoceptors