Pathology and physiology Flashcards

1
Q

Name the reversible causes of cardiac arrest

A

4 H’s, 4 T’s

  • hypoxia
  • hypovolaemia
  • hypo / hyperkalaemia / metabolic
  • hypothermia
  • thrombosis; coronary or pulmonary
  • tamponade
  • toxins
  • tension pneumothorax
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2
Q

Wischnewski ulcers can be associated with what mode of death?

A

Hypothermia

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3
Q

Corneal arcus are associated with what?

A

Coronary artery atherosclerosis

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4
Q

Define shock

A

A condition of inadequate perfusion to sustain normal organ function - i.e. oxygen concentration cannot meet the metabolic demands of the major organs systems

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5
Q

Name the 5 classes of shock

A
  • hypovolaemic shock
  • cardiogenic shock
  • obstructive shock
  • distributive shock
  • cytotoxic shock
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6
Q

Describe cytotoxic shock

A
  • blood flow to tissues is maintained but cellular hypoxia occurs either due to a failure of oxygen delivery via haemoglobin or failure of mitochondrial respiration and use of oxygen
  • examples include CO poisoning, CN poisoning
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7
Q

Describe the physiology of hypovolaemic shock

A
  • failure of forward cardiac output due to insufficient circulating volume to fill the circuit
  • this leads to reduced preload and cardiac output
  • end organ hypoperfusion
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8
Q

Hypovolaemic shock can occur when?

A

Can be from;

  • blood loss
  • interstitial fluid loss
  • or pure water (rare) deficit
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9
Q

Describe the clinical features of hypovolaemic shock

A
  • young fit people tend to compensate well until they dont
  • dependent on the degree of hypovolaemia
  • early; modest tachycardia, pulse pressure may widen, sweaty
  • as it continues; tachycardia increases, pule pressure narrows, tachypnoeic, urine output maintained initially
  • hypotension is a late sign of haemorrhage
  • increasingly end organ hypoperfusion becomes apparent e.g. confusion, falling urine output is also a later sign
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10
Q

Name the compensatory mechanisms for hypovolaemic shock

A
  • baroreceptor reflexes
  • sympathetic mediated neurohormonal response
  • capillary absorption of interstitial fluid
  • hypothalamo-pituitary-adrenal response
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11
Q

Describe the baroreceptor reflex in hypovolaemic shock

A
  • stretch sensitive receptors in carotid sinus (CNIX) and aortic arch (CNX)
  • shock causes decrease arterial stretch which leads to decreased stimulation of baroreceptors which leads to reduction of affterent input to medullary CV centres
  • inhibition of parasympathetic and enhanced sympathetic output
  • results in the increase in CO, increase inotropic and chronotropic effect
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12
Q

Describe the sympathetic mediated neurohormonal response in hypovolaemic shock

A
  • sympathetic chronotropy and inotropy
  • release of circulating vasoconstrictors e.g. adrenaline, noradrenaline, angiotensin, norad, vasopressin
  • this raises vasomotor tone and redirects fluid from peripheral and secondary organs
  • the resulting lactic acidosis chemoreceptors to enhance response
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13
Q

Describe the capillary absorption of interstitial fluid in hypovolaemic shock

A
  • reduced capillary hydrostatic pressure, inward net filtration
  • starlings forces favour net inward filtration
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14
Q

Describe the hypothalamo-pituitary-adrenal response in hypovolaemic shock

A
  • the combined effects of hypotension and sympathetic activation results in increased secretion of renin from JGA
  • this increases conc. of angiotensin 2 which acts as a stimulus to release aldosterone and vasopressin
  • this enhances vasoconstriction, thirst and the renal reabsorption of sodium and water
  • this all aims to restore blood volume
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15
Q

What are the 3 options the heart has to increase its cardiac output?

A
  • increase HR (tachycardia)
  • increase stroke volume (inotropy)
  • increase both
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16
Q

Greater volume loading of the ventricle during diastole results in what?

A

Greater ventricular ejection in systole

17
Q

How does inotropy and heart failure affect the Frank-Starling curve?

A
  • inotropy results in an upward shift of the curve due to increased contractility
  • HF results in a downward shift of the curve due to decreased contractility
18
Q

Describe the physiology of cardiogenic shock

A
  • inability of the heart as a pump to meet circulatory demands
  • most commonly a complication of acute MI but may also follow acute valve dysfunction
  • other causes include myocarditis, cardiomyopathy, myocardial contusion
19
Q

Name clinical signs of cardiogenic shock

A
  • poor forward flow; hypotension / shock, fatigue, syncope

- backpressure; pulmonary oedema, elevated JVP, hepatic congestion

20
Q

Positive inotropic effects are achieved through what?

A

Adrenergic stimulation

21
Q

Positive inotropic effects can be replication pharmacologically using what?

A
  • beta and dopaminergic stimulation
  • dobutamine, adrenaline
  • dopamine, dopexamine
  • others e.g. milrinone, levosimendan
22
Q

What is the aim of an intra-aortic balloon pump and how does it do this?

A

Aim; provides counterpulsation to provide mechanical support of CV system

  • inflation during ventricular diastole (augmented diastole)
  • deflation during ventricular systole (reduced afterload)
23
Q

Describe obstructive shock and its treatment

A
  • involves a physical obstruction to either the heart or great vessels
  • mainly affects cardiac filling rather than cardiac ejection
  • treatment involves removing the underlying cause; pulmonary embolism, cardiac tamponade, tension pneumothorax
24
Q

Describe the physiology of distributive shock

A
  • aka vasodilatory / warm shock
  • generally initial high cardiac output but insufficient to maintain forward perfusion
  • inadequate oxygen delivery and organ perfusion due to failure of endothelial cells in the micro-circulation to vasoconstrict and direct blood flow correctly resulting in pooling in the larger vessels
25
Q

Name the 3 subtypes of distributive shock

A
  • septic; bacterial endotoxin mediated capillary dysfunction
  • anaphylactic; mast cell release of histaminergic vasodilators
  • neurogenic; loss of thoracic sympathetic outflow following spinal injury
26
Q

Describe septic shock

A
  • rising lactate levels detect hypoperfusion before hypotension occurs
  • early use of vasopressors improves perfusion and minimises excessive fluid volumes
27
Q

Describe anaphylactic shock

A
  • uncontrolled activation and degranulation of mast cells
  • release of histamine with resulting uncontrolled vasodilation
  • adrenaline acts both as a vasoconstrictor and a mast cell stabiliser
  • serum mast cell tryptase levels confirms the diagnosis
28
Q

Describe neurogenic shock

A
  • most commonly follows traumatic transection of spinal cord or central trauma
  • hypotension follows loss of descending sympathetic tone
  • inappropriate bradycardia generally occurs due to unopposed vagal tone
  • dopamine alongside vasopressors are the mainstays of treatment

Note; not the same as spinal shock