cardiac 3 Flashcards

1
Q

EDPVR is determined by:

A

1) ECM composition – produced by fibroblasts which produce heart size
2) myofilament relaxation (ATP availability)

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2
Q

change in compliance graph

A

pr-vol graph: increase pressure and volume therefore decreased compliance
decrease pressure volume therefore increase compliance

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3
Q

diastolic dysfunction:

A

2 reasons for not filling properly:
1) properties of ECM that make stiffer heart (decrease compliance) – impairs ability to fill therefore no CO but has force

2) relaxation is energy dependent
after myosin produces power stroke it will dissociate from actin the ATP therefore decrease oxygen to heart slows rate of producing ATP therefore slow relaxation to fill heart

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4
Q

factors that regulate inotropy

A

after load, HR, sympathetic activation all increase contractility
systolic failure and parasympathetic activation inhibit and decrease inotropic state

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5
Q

systolic dysfunction pressure-volume relationship

A

decrease ESPVR therefore thinner and larger and more compliant

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6
Q

diastolic dysfunction pr volume relationship

A

decrease compliance with increased EDPVR therefore can’t fill properly but can contract

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7
Q

histology

A

1) myocyte size –> wider and increase CSA therefore hypertrophy
2)capillary density –> density is affected by cell size therefore do ratio to tell around each cardiomyocyte the number of capillaries
3) pervascualr fibrosis: pikers series red
reactive interstitial fibrosis : masons trichrome
- specifically around vasculature so with more fibrosis around arterioles therefore can’t vasodialte and impairs blood supply to heart therefore ATP produced decreases

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8
Q

LV remodelling

A

1) concentric hypertrophy: thicker cell walls, cells added in parallel. due to pressure stress: increase BP, resistance training, RV COPD, calcified valve
2) eccentric hypertrophy: thinner cell walls, cells added in series. due to volume stress (increased CO overtime): endurance training, prego, mitral regurgitation, myocardial infarction

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9
Q

Afterload=

A

LVP therefore it is peak wall stress

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10
Q

wall stress =

A

LV pr x radius/ wall thickness

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11
Q

LV remodelling to normalize T

A

with pressure overload– concentric hypertrophy and increase thickness and reduce radius to reduce stress

with volume overload– eccentric hypertrophy and increase radius and reduce thickness to reduce stress

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