Chapter 3: Shock Flashcards

1
Q

Cardiac output definition

A

Stroke volume ( volume of blood ejected by the L ventricle) x HR ( ejection cycles /minute)

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2
Q

What dictates stroke volume

A

Filling volume of the ventricle( preload)
Myocardial contractility (Starling’s curve)
Systemic vascular resistance ( afterload)

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3
Q

What controls the HR

A

Vagus nerve and endogenous catecholamine release

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4
Q

In times of stress what happens with an infant’s Cv system

A

Infants have relatively less myocardial contractility - increased cardiac output depends on increasing the HR rather than stroke volume - bradycardia is not that well tolerated in infants

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5
Q

What is microcirculatory dysfunction

A

maldistribution of capillary blood flow

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6
Q

By how much does hydrostatic pressure fall by in shock states

A

30-40 %

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7
Q

What does endotoxin do to capillary beds during septic shock

A

Damages vascular endothelium
Damaged cells can then generate procoagulant activity - which may explain why fibrin is deposited into the microcirculation

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8
Q

Norepinephrine -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - hypovolemia and head trauma
Release by sympathetic NS
Effects - vascocontriction - B1 and B2 stimulation

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9
Q

Epinephrine -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - hypovolemia and hypercapnea
Release by adrenal medullae
Effects - vascocontriction - a1 and B2 stimulation

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10
Q

Angiotensin II -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - hypovolemia
Release by kidneys and brain
Effects - vascocontriction

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11
Q

Leukotrienes-stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - tumor necrosis factor
Release by macrophages
Effects - capillary permeability

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12
Q

Thromboxane A2 -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - Hypoxia
Release by Platelets
Effects - Vasoconstriction and platelet aggregation

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13
Q

Prostaglandins F2 -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - Hypoxia
Release by Platelets and vascular smooth muscle
Effects -Vasoconstriction

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14
Q

Prostaglandins I2 -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - Hypoxia
Release by Healthy vascular endothelium
Effects -Vasodilator counterbalances thromboxane A2

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15
Q

Mycocardial depressant factor -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - Ischemia/tissue damage
Release by Pancreas
Effects -Direct negative ionotropic effects

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16
Q

Opiates -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - Hypoxia
Release by Pituitary
Effects -Decreased myocardial contractility, decreased sympathetic tone
Hypotension

17
Q

Inducible Nitrous Oxide -stimulus, sources and effects as an endogenous vasoactive mediator

A

Stimulus - Inflammatory cytokines
Release by Leucocytes
Effects -Vasodilation of vascular smooth muscle

18
Q

How much ATP is produced by aerobic and anerobic respiration per mole of glucose

A

2 moles compared to 38

19
Q

What are deleterious effects of anerobic metabolism

A

Depletion of glycogen stores and accumulation of lactic and associated acidosis -
Decresed ATP lead to K efflux, Na and Ca influx with water causing cells to swell