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
What is the purpose of the intra-aortic balloon pump?
Provides counterpulsation
26
What does an intra-aortic balloon pump do?
Inflates during ventricular diastole (augmented diastole) | Deflates during ventricular systole (reduced afterload)
27
What is obstructive shock?
Physical obstruction to filling of heart reducing preload and cardiac output = may be obstruction to heart or great vessels
28
What part of the cardiac cycle does obstructive shock affect?
Mainly affects cardiac filling (rather than cardiac ejection)
29
What are some causes of obstructive shock?
Pulmonary embolism, tamponade, tension pneumothorax
30
How is obstructive shock treated?
By treating the underlying cause: PE = anticoagulation +/- thrombolysis Tamponade = pericardial drainage Tension pneumothorax = decompression + drainage
31
What are some x-ray signs of a massive PE?
Dilated hypokinetic right ventricle Bowing of interventricular septum Hyperkinetic right ventricular apex (McConnell's sign)
32
What are some features of tamponade?
Fluid accumulation in the pericardial sac | Each chamber is compressed so impaired cardiac filling and contraction
33
What are some features of a tension pneumothorax?
Air trapped in pleural cavity under positive pressure to create one way valve Lung collapses due to increased pressure
34
Why does a tension pneumothorax impair cardiac filling and function?
Due to the displacement of mediastinal structures
35
What are the other names for distributive shock?
Vasodilatory or warm shock
36
What occurs in distributive shock?
Significant reduction in SVR beyond the compensatory limits of increased cardiac output
37
What is the cardiac output like in distributive shock?
Initially high but insufficient to maintain forward perfusion
38
What are the three types of distributive shock?
Septic, anaphylactic and neurogenic
39
What is septic shock?
Bacterial endotoxin mediated capillary dysfunction
40
What indicates hypoperfusion in septic shock?
Rising lactate levels = usually before hypotension occurs
41
Why is quick administration of antibiotics important in septic shock?
Every hour delay of appropriate antibiotics increases mortality by 75%
42
Why are vasopressors used in septic shock?
Early use of vasopressors improves perfusion and minimises excessive fluid volumes
43
What causes anaphylactic shock?
Uncontrolled activation and degranulation of mast cells = release of histamine causes uncontrolled vasodilation
44
How does adrenaline act in anaphylactic shock?
As both a vasoconstrictor and mast cell stabiliser
45
How is anaphylactic shock diagnosed?
By measuring serum mast cell tryptase levels
46
What does neurogenic shock usually follow?
Spinal cord or central trauma
47
What are some features of neurogenic shock?
Hypotension follows loss of descending sympathetic tone | Inappropriate bradycardia generally occurs due to unopposed vagal tone
48
How is neurogenic shock treated?
Dopamine and vasopressors
49
What is the traditional view of how CPR works?
Physically pushes blood out of the heart to maintain vital organ perfusion
50
What is the more modern view of how CPR works?
Cyclical changes in intrathoracic pressure alternately push blood out of and suck blood into chest
51
What are the shockable rhythms?
Ventricular fibrillation and pulseless ventricular tachycardia
52
What are the non-shockable rhythms?
Asystole and pulseless electrical activity
53
How long does it take for significant cerebral damage to occur after cardiac arrest?
4-5 minutes
54
What are the reversible causes of cardiac arrest?
Hypovolaemia, hypoxia, hyperkalaemia (metabolic), hypothermia, tamponade, thrombosis, tension pneumothorax, toxins