Shock Syndromes

Question 1

Perfusion defects

Answer 1

Perfusion can be decreased globally or locally.

A local perfusion defect is due to localised vessel occlusion eg stroke or a myocardial infarction.

A global perfusion reduction is due to a reduction in the perfusion pressure (arterial BP) and effects all tissues/organs.

• Compensatory mechanisms ensure that some organs are affected before others.
• Local vessel disease may make tissues less tolerant of a drop in perfusion pressure. Eg if blood pressure falls, an individual with cronary vessel disease will experience myocardial ischaemia at a higher BP than someone with normal coronary vessels.

Question 2

What is shock?

Answer 2

Difficult to clearly define, because it is not a single disease.

Key features of the shock syndrome:

• Inadequate tissue perfusion
• Includes impaired cellular oxygenation
• Affects multiple organ systems
• If severe enough, becomes self sustaining and progressive.

Question 3

Progression of shock

Answer 3

1. Compensated shock
2. Progressive stage: reversible if treated.
3. Irreversible stage: decompensated shock where irreversible multi-organ damage occurs.

Question 4

What are the downstream complications of reduced perfusion?

Answer 4

• Anaerobic metabolism
• Inflammation
• Increased production of reactive oxygen species (free radical)
• Coagulation abnormalities.

Question 5

Types of shock

Answer 5

1. Hypovolaemic: inadequate circulating volume e.g. haemorrhage
   
   1. _​_Haemorrhagic
   2. Non-haemorrhagic
2. Cardiogenic: failure of the heart as a pump e.g. decreased myocardial contractility after MI.
3. Distributive: vasodilation with increased vascular capacity, maldistribution of blood flow and volume eg septic shock
4. Obstructive: extracardiac obstruction of blood flow eg cardiac tamponade or massive PE

Question 6

Haemorrhagic shock

Answer 6

Concealed: eg ruptured spleen; or

Revealed: eg. limb injury

Question 7

Non-haemorrhagic shock

Answer 7

Loss of total body water eg severe dehyydration from diarrhoea/vomiting; or

**Redistribution **from vascular to extravascular space (called third spacing) eg pancreatitis.

Question 8

Why does fall in BP lag behind the fall in CO?

Answer 8

If cardiac output falls, then we would expect MAP to fall. In reality we can remove 20-30% of the blood volume without a significant fall in BP.

This is because of the blood pressure control mechanisms which affect HR, SV and TPR.

Baroreceptor reflex and chemoreceptors

Increased SNS

• Tachycardia
• Increased contractility
• Increased arteriolar vasoconstriction in most of the systemic circulation increases TPR
• Venoconstriction increases venous return

​Decreased PNS

• Increased HR

​Renin angiotensin system

• Increased vasoconstriction
• Increased renal Na+ reabsorption
• Aldosterone release from adrenal cortex

Question 9

What causes the secon plateau in arterial BP?

Answer 9

The CNS ischaemic reflex.

If BP is low enough, cerebral perfusion pressure will fall and result in CNS ischaemic. Local concentration of CO2 incresaes.

High CO2 in the medulla stimulates the vasomotor centers to result in massive SNS output to the heart, vessels and adrenals.

Therefore, very low BP produces a massive SNS activation.

This is not a normal control mechanism for day to day BP control, but rather a last ditch method of salvaging some cerebral perfusion when BP is very low (<40mmHg).

Question 10

Long term compensatory mechanisms in shock.

Answer 10

Arteriolar constriction and reduced venous pressure results in reduced capillary hydrostatic pressure. Net reabsorption of fluid from interstitium to capillary occurs. Takes severeral hours for maximal effect.

Renal salt and water conservation helps to preserve blood voluem but takes hours to days. It is mediated by

• Direct effect of reduced arterial BP and renal perfusion (reverse of the renal pressure diuresis)
• Antidiuretic hormone (ADH) released form pituitary (also a vasoconstrictor)
• Angiotensin II and aldosterone

Question 11

Severity of shcok

Answer 11

Compensatory changes

• Tachycardia
• Reduced end organ perfusion (non-vital)
• Reduced renal perfusion and low urine output

Reduced BP

Reduced perfusion of the heart

Reduced perfusion of the brain

Question 12

Decompensated shock

Answer 12

In compensated shock, negative feedback mechanisms (short and long term BP control) attempt to maintain BP and perfusion of critical organs.

If hypovolaemia is severe enough, decompensatory mechanisms (positive feedback) overwhelm the compensatory mechanisms and result in progressive hypotension and death.

Question 13

Decompansatory mechanisms

Answer 13

• Myocardial depression
• Acidosis
• CNS depression
• Tissue ischaemia
• Abnormal coagulation
• Vasomotor failure

Question 14

Myocardial depression

Answer 14

• Loss of contractility as coronary perfusion falls
• Results in lower BP, which lowers coronary perfusion further…

A classic positive feedback loop

Question 15

Acidosis

Answer 15

Inadequate blood flow during haemorrhage affects the metabolism of all cells in the body.

• It accelerates the production of H+.
• Impaired kidney function prevents excretion of the excess H+, and generalised metabolic acidosis results.

Acidosis

• Caused myocardial depression
• Decrease the responsiveness of the heart and vessels to SNS.

Question 16

Tissue ischaemia

Answer 16

Prolonged ischaemia eventually results in irreversible organ damage

• Gut
• Kidney
• Liver

Prolonged ischaemia also causes microvascular dysfunction

• precapillary sphincter smooth muscle relaxes
• Capillary damage and increased capillary permeability
• Results in leaking of proteins and water into interstitium.

Question 17

Abnormal clotting

Answer 17

Haemostasis is initially confined appropriately to the damaged vessel

Severe shock results in widespread inappropriate activation of platelets and coagulation cascade and causes blockage of small vessels.

Consumption and dilution (from fluid shifts, IV fluids) of clotting factors, fibrinogen and platelets can result in bleeding at the same time.

Disseminated intravascular coagulation (DIC)

Question 18

Vasomotor failure

Answer 18

• Ischaemia of the brainstem eventually depresses the vasomotor centre.
• Results in loss of SNS tone and fall in TPR and cardiac output.
• End-stage positive feedback loop

Question 19

Cardiogenic shock

Answer 19

Pump failure. Can think of it as insufficient CO despite adequate filling pressure (preload)

Can be

• Intrinsic loss of contractility
• Valve disease
• Electrical disturbance (arrhythmia)

Falls in stroke volume and cardiac output in this case are compensated for by fluid retention (higher filling pressure) and SNS effect on inotropy and HR.

How effective this is depends on how great the original impairment of contractility is and how responsive the heart is to the SNS.

Question 20

Distributive shock

Answer 20

Profound vasodilation resulting in

• Decreased TPR
• Increased vascular capacitance (causes low filling pressure and therefore low preload)

Together, these cause hypotension.

Examples are:

• Septic shock
• Anaphylactic shock
• Neurogenic shock (such as with spinal anaesthesis)

Question 21

Septic shock

Answer 21

• Involves a complex interaction between infection and and host immune response
  
  • Mediators include endotoxin (a lipopolysaccharide cell wall constituent of gram-negative bacteria)
  • TNF and IL-1 released in repsonse to endotoxin, stimulating release of other pro-inflammatory cytokines
  • Combined effects of organism and host response result in clinical pattern of septic shock.
• Early in its course, septic shock shows decreased systemic vascular resistance, normal to low cardiac filling pessures, and increased cardiac output.
• Periphery may feel warm rather than cold and shut down at this time.
• Cardiac output deteriorates further in later stages of septic shock, and mimics cardiogenic shock.
• Increased capillary permeability can also contribute to hypovolaemia

Question 22

Obstructive shock

Answer 22

Underlying pathology is a mechanical obstruction to normal cardiac output which results in reduced systemic perfusion.

Examples

• Massive pulmonary embolus (increases RV afterload)
• Tension pneumothorax (compresses large veins in chest and decreases preload)
• Pericardial tamponade (compresses heart, but particular R atrium and ventricles and therefore decreases RV preload)