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Sudden Death > Physiology of Shock > Flashcards

Physiology of Shock Flashcards

1
Q

What is shock?

A

Condition of inadequate perfusion to sustain normal organ function

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2
Q

What are the five classes of shock?

A

Hypovolaemic, cardiogenic, obstructive, distributive, cytotoxic

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3
Q

What is cytotoxic shock?

A

Uncoupling of tissue oxygen delivery and mitochondrial oxygen uptake = CO poisoning, CN- poisoning

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4
Q

What is hypovolaemic shock?

A

Insufficient circulating volume = loss of circulating volume causes reduced preload and CO

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5
Q

What are some causes of hypovolaemic shock?

A

Bleeding, third space losses, severe dehydration (rare) = clinical features depend on degree of hypovolaemia

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6
Q

What are some compensatory mechanisms for hypovolaemia?

A

Baroreceptor reflexes
Sympathetic mediated neurohormonal response Capillary absorption of interstitial fluid
HPA axis response

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7
Q

Where are stretch sensitive receptors located?

A

Carotid sinus (CN IX) and aortic arch (CN X)

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8
Q

How does the baroreceptor reflex respond to decreased stretch?

A

Decreased afferent input to medullary CV centres = inhibition of parasympathetic (CN X) and enhanced sympathetic output

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9
Q

In what ways can the sympathetic nervous system increase cardiac output?

A

Via chronotropy and inotropy

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10
Q

How does the sympathetic neurohormonal response correct hypovolaemia?

A

Release of circulating vasoconstrictors to redirect fluid from peripheral and secondary organs

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11
Q

What effect does the redirection of fluids from peripheral organs have?

A

Causes lactic acidosis which drives chemoreceptors to enhance response
Circulating vasodilators also increased

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12
Q

What are some features of the capillary absorption of interstitial fluid to correct hypovolaemia?

A

Reduced capillary hydrostatic pressure

Inward net filtration

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13
Q

What occurs in the HPA axis response to hypovolaemia?

A

Intra-renal baroreceptors mediate renin release from JGA = resulting ang II enhances vasoconstriction and ADH secretion to enhance renal reabsorption of water and Na

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14
Q

What are the three ways the heart can increase cardiac output?

A

Increase heart rate
Increase stroke volume
Both of the above

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15
Q

What is the Frank Starling relationship?

A

Greater volume loading of ventricle during diastole results in greater ventricular ejection in systole

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16
Q

What effect does inotropy have on the Frank Starling curve?

A

Shifts curve up

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17
Q

What effect does a failing heart have on the Frank Starling curve?

A

Shifts curve down = has less contractility so EDV increases to maintain SV resulting in pulmonary congestion

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18
Q

What are some ways to ensure good fluid practice?

A

Treat them as a drug
Consider individual patient
Consider both fluid and electrolyte requirements
Consider difference between resuscitation and maintenance

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19
Q

What is cardiogenic shock?

A

Inability of the heart as a pump to meet circulatory demands = causes reduction in systolic function and cardiac output

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20
Q

What does cardiogenic shock commonly occur as a complication of?

A

Acute MI

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21
Q

What are some other causes of cardiogenic shock?

A

Acute valve dysfunction, myocarditis, cardiomyopathy, myocardial contusion

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22
Q

What are the clinical signs of cardiogenic shock?

A

Poor forward flow = hypotension, shock, fatigue, syncope

Backpressure = pulmonary oedema, elevated JVP, hepatic congestion

23
Q

What is positive inotropy?

A

Increase in force of cardiac contraction for any given preload

24
Q

How can positive inotropy be achieved?

A

Physiologically by sympathetic nervous system

Using beta and dopaminergic stimulation = dobutamine, adrenaline, dopamine, dopexamine

25
Q

What is the purpose of the intra-aortic balloon pump?

A

Provides counterpulsation

26
Q

What does an intra-aortic balloon pump do?

A

Inflates during ventricular diastole (augmented diastole)

Deflates during ventricular systole (reduced afterload)

27
Q

What is obstructive shock?

A

Physical obstruction to filling of heart reducing preload and cardiac output = may be obstruction to heart or great vessels

28
Q

What part of the cardiac cycle does obstructive shock affect?

A

Mainly affects cardiac filling (rather than cardiac ejection)

29
Q

What are some causes of obstructive shock?

A

Pulmonary embolism, tamponade, tension pneumothorax

30
Q

How is obstructive shock treated?

A

By treating the underlying cause:
PE = anticoagulation +/- thrombolysis
Tamponade = pericardial drainage
Tension pneumothorax = decompression + drainage

31
Q

What are some x-ray signs of a massive PE?

A

Dilated hypokinetic right ventricle
Bowing of interventricular septum
Hyperkinetic right ventricular apex (McConnell’s sign)

32
Q

What are some features of tamponade?

A

Fluid accumulation in the pericardial sac

Each chamber is compressed so impaired cardiac filling and contraction

33
Q

What are some features of a tension pneumothorax?

A

Air trapped in pleural cavity under positive pressure to create one way valve
Lung collapses due to increased pressure

34
Q

Why does a tension pneumothorax impair cardiac filling and function?

A

Due to the displacement of mediastinal structures

35
Q

What are the other names for distributive shock?

A

Vasodilatory or warm shock

36
Q

What occurs in distributive shock?

A

Significant reduction in SVR beyond the compensatory limits of increased cardiac output

37
Q

What is the cardiac output like in distributive shock?

A

Initially high but insufficient to maintain forward perfusion

38
Q

What are the three types of distributive shock?

A

Septic, anaphylactic and neurogenic

39
Q

What is septic shock?

A

Bacterial endotoxin mediated capillary dysfunction

40
Q

What indicates hypoperfusion in septic shock?

A

Rising lactate levels = usually before hypotension occurs

41
Q

Why is quick administration of antibiotics important in septic shock?

A

Every hour delay of appropriate antibiotics increases mortality by 75%

42
Q

Why are vasopressors used in septic shock?

A

Early use of vasopressors improves perfusion and minimises excessive fluid volumes

43
Q

What causes anaphylactic shock?

A

Uncontrolled activation and degranulation of mast cells = release of histamine causes uncontrolled vasodilation

44
Q

How does adrenaline act in anaphylactic shock?

A

As both a vasoconstrictor and mast cell stabiliser

45
Q

How is anaphylactic shock diagnosed?

A

By measuring serum mast cell tryptase levels

46
Q

What does neurogenic shock usually follow?

A

Spinal cord or central trauma

47
Q

What are some features of neurogenic shock?

A

Hypotension follows loss of descending sympathetic tone

Inappropriate bradycardia generally occurs due to unopposed vagal tone

48
Q

How is neurogenic shock treated?

A

Dopamine and vasopressors

49
Q

What is the traditional view of how CPR works?

A

Physically pushes blood out of the heart to maintain vital organ perfusion

50
Q

What is the more modern view of how CPR works?

A

Cyclical changes in intrathoracic pressure alternately push blood out of and suck blood into chest

51
Q

What are the shockable rhythms?

A

Ventricular fibrillation and pulseless ventricular tachycardia

52
Q

What are the non-shockable rhythms?

A

Asystole and pulseless electrical activity

53
Q

How long does it take for significant cerebral damage to occur after cardiac arrest?

A

4-5 minutes

54
Q

What are the reversible causes of cardiac arrest?

A

Hypovolaemia, hypoxia, hyperkalaemia (metabolic), hypothermia, tamponade, thrombosis, tension pneumothorax, toxins

Sudden Death (10 decks)

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