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Cardiovascular II > Heart failure > Flashcards

Heart failure Flashcards

1
Q

Lambl excrescences

A

Fibrous thickening of valves in the aging heart

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2
Q

Brown atrophy

A

Lipofuscin deposits in aging heart

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3
Q

Causes of high output heart failure

A

Thyrotoxicosis induced
Anemia induced
tachycardia induced

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4
Q

Causes of increased afterload contributing to HF

A

Severe HTN
Severe aortic stenosis

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5
Q

Pathologic causes of increased preload contributing to HF

A

Aortic regurgitation
Mitral regurgitation
MI
Dilated cardiomyopathy

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6
Q

Physiologic cause of increased preload

A

Exercise

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7
Q

Effect of increased contractility on isovolumic P/V curve

A

Shifts left

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8
Q

Six principal mechanisms of CVS dysfunction

A

Pump failure
Flow obstruction
Regurgitant flow
Shunted flow
Disorders of cardiac conduction
Rupture of the heart or major vessel

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9
Q

Causes of systolic dysfunction causing reduced ejection fraction

A

Impaired ventricular contractility
Increased afterload

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10
Q

Change in PV loop in systolic dysfunction

A

Shifts right and SV decreases

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11
Q

PV loop in compensation by Frank Starling mechanism

A

Increased preload, SV, and contraction
Extends to the right

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12
Q

PV loop compensation by catecholamine release

A

Increased HR, contractility, SV, and filling
PV loop shifts left

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13
Q

PV loop compensation by increasing ventricular volume or elasticity

A

Increased EDV and SV, slightly right

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14
Q

Causes of diastolic relaxation or ventricular filling leading to diastolic dysfunction with preserved EF

A

LV hypertrophy
Restrictive cardiomyopathy
Myocardial fibrosis
Transient MI
Pericardial constriction or tamponade
Amyloid deposition

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15
Q

PV loop changes in heart failure with preserved ejection fraction

A

EDV decreased and increased LVEDP
Shifts up and left

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16
Q

Most common cause of RHF

A

LHF

17
Q

Compensatory response of the myocardium to increased mechanical work

A

Cardiac hypertrophy

18
Q

Collective molecular, cellular, and structural changes that occur as a response to injury or changes in loading conditions in the heart

A

Ventricular remodeling

19
Q

Arrangement of new sarcomeres in pressure overload of the heart

A

In parallel –> thicken

20
Q

Arrangement of new sarcomeres in volume overload of the heart

A

In series –> elongate

21
Q

Changes that regulate excitation-contraction that occur in the failing cardiac myocyte that contribute to depressed LV systolic function in HF

A

Decreased function of SR Ca adenosine triphosphates (SERCA2A)

Decreased Ca uptake into the SR and hyperphosphorylation of the ryanodine receptor
Ca leakage from the SR

22
Q

Changes that occur in the cross-bridges that occur in the failing cardiac myocyte that contribute to depressed LV systolic function in HF

A

Decreased expression of alpha-myosin heavy chain

Increased expression of beta-myosin heavy chain

Myocytolysis

Disruption of the cytoskeletal links between the sarcomeres and the ECM

23
Q

Activation of neurohumoral systems that occur in the failing cardiac myocyte that contribute to depressed LV systolic function in HF

A

Adrenergic nervous system
Renin-angiotensin-aldosterone system
Increased production of ADH

24
Q

Produced when ventricular myocardium is subjected to hemodynamic stress and able to be detected in the blood

A

BNP

25
Q

Effect of the release of natriuretic peptides

A

Excretion of Na and water
Vasodilation
Inhibition of renin secretion
Antagonism of the effects of ATII on aldosterone and vasopressin levels

26
Q

Function of enothelin-1, released in HF

A

Potent vasoconstrictor

27
Q

Regions of liver affected by cell death in RHF

A

Centrilobular regions

28
Q

Possible causes of high output HF

A

Hyperthyroidism
Severe anemia
Thiamine deficiency
Septic shock
Trauma
Surgical shunt - AV fistula
Paget disease

29
Q

Type of hypertrophy seen in endurance athletes

A

Eccentric

30
Q

Type of hypertrophy seen in strength athletes

A

Concentric

Cardiovascular II (29 decks)

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