Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Cardiology > Lectures 3-4: Heart Failure > Flashcards

Lectures 3-4: Heart Failure Flashcards

1
Q

Heart failure (definition)

A

Structural or functional cardiac disorder that impairs the ability of ventricles to eject blood (forward failure) or fill with blood (backward failure) or both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Key mediators of CO

A

CO = HR x SV (preload, afterload, contractility)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Preload, two ways

A

Ventricle wall tension at end of diastole. End-diastolic volume/pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Afterload, two ways

A

Ventricular wall tension during contraction. Systolic ventricular (or arterial) pressure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Contractility

A

Property of heart muscle that accounts for changes in the strength of contraction. Independent of preload and afterload.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Frank-Starling Curve axes

A

X-axis = preload; Y-axis = stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Pressure-Volume Loop points

A

A: MV opens, LV filling begins; B: LV contraction, MV closes; C: AV opens, ejection beings: D: AV closes, ejection ends

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Between D and A? Between B and C?

A

Isovolumetric relaxation; isovolumetric contraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Impaired contractility could be caused by… (3)

A
  1. Coronary artery disease (MI or ischemia); 2. Chronic volume overload (mitral/aortic regurgitation); 3. Dilated cardiomyopathies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Impaired diastolic filing could be caused by… (5)

A
  1. Left ventricular hypertrophy; 2. Restrictive cardiomyopathy; 3. Myocardial fibrosis; 4. Transient myocardial ischemia; 5. Pericardial constriction or tamponade
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Increased afterload could be caused by… (2)

A
  1. Advanced aortic stenosis; 2. Uncontrolled severe hypertension
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What two impairments lead to reduced ejection fraction? What else is this called?

A

Impaired contractility and increased afterload; systolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What impairment leads to preserved ejection fraction? What else is this called?

A

Impaired diastolic filing; diastolic dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What does systolic dysfunction look like on the PV loop?

A

Shifts ESVPR line down –> down and left shift of the loop (increased EDP and EDV AND end systolic volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe diastolic dysfunction. What does it look like on a PV loop?

A

HF with preserved ejection fraction, ventricle is stiff, which impairs ejection; upward shift of EDVPR line –> at any volume, ventricular pressure is higher and there is decreased stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Define ejection fraction (and %s)

A

Fraction of end-diastolic volume ejected from the ventricle during each systolic contraction (normal range=55%-75%)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Three compensatory mechanisms of failing heart

A

Frank-Starling mechanism, ventricular hypertrophy, neurohormonal activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Frank-Starling Mechanism

A

Reduced stroke volume at given preload causes increase in EDV due to normal venous return –> slight increase in stroke volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ventricular hypertrophy and what happens in the short-term and eventually

A

Thicker ventricle, decreased wall stress to maintain contractile force via decreased workload; eventually could lead to functional decline

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Concentric hypertrophy is what? What could cause this?

A

Pressure overlaod –> narrowing of lumen; new sarcomeres in parallel; hypertension or aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Eccentric hypertrophy is what? What could cause this?

A

Volume overload –> widening of lumen; new sarcomeres in series (elongation); regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Pathophysiologic consequences of compensation

A

Both increased ventricular end-diastolic volume and myocardial hypertrophy can lead to increased atrial pressure which causes symptoms of HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Neurohormal activation (3)

A
  1. Increased sympathetic nervous system; 2. Increased Renin-Angiotensin system; 3. Increased ADH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Rise in ____ enduced by compensatory mechaisms can balance fall in ____ in early stages of HF

A

TPR; CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

On a very basic level, heart failure is what?

A

A CLINICAL syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

HFrEF

A

Heart failure with reduced ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

HFprEF

A

Heart failure with preserved ejection fraction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What triggers the adrenergic nervous system during HF?

A

Fall in CO sensed by baroreceptors in carotid sinus/aortic arch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What is the result of the adrenergic nervous system during HF?

A

Increased HR and ventricular contractility (directly increase CO) and arteriol vasoconstriction (increases MAP) and venous vasoconstriction (increases preload –> increased stroke volume)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Alpha receptor distribution allows for what phenomenon during HF?

A

During sympathetic stimulation, blood flow is redistributed to vital organs at the expense of the skin, splanchnics and kidneys

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What stimulates renin release? (3)

A
  1. Decreased renal artery perfusion; 2. Decreased salt delivery to macula densa; 3. Direct stimulation of juxtaglomerular beta-receptors via sympathetics
32
Q

What does renin do? Then what?

A

Cleaves angiotensinogen –> angiotensin I which is cleaved to form angiotensin II by ACE

33
Q

What is the main effect of angiotensin II?

A

It is a potent vasoconstrictor, raises TPR to maintain BP

34
Q

What else does angiotensin II do? What happens then?

A

Increase thirst (hypothalamus) and aldosterone release (adrenals); increase in intravascular volume –> increase preload –> increased CO

35
Q

At what point does increasing preload stop working?

A

At the flat portion of the ventricular performance curve

36
Q

What pituitary hormone is released during HF? What does it do?

A

ADH –> increases water reabsorption from the kidneys–> increased intravascular volume –> increase preload –> increased CO

37
Q

Two ways in which compensatory mechanisms are not beneficial in the long run

A
  1. Increased intravascular volume can worsen pulmonary congestion; 2. Increased arteriolar resistance increases afterload against failing ventricle
38
Q

How could natriuretic peptides be beneficial?

A

Opposite of other hormone systems: excretion of sodium and water, vasodilation, inhibition of renin, and antagonism of angiotensinogen II on aldosterone and vasopressin levels

39
Q

Ventricular ESV depends on what and what, but not on what?

A

Afterload and contractility but NOT on preload

40
Q

If you hold afterload and contractility constant, but increase preload, what happens in the PV loop?

A

Increased stroke volume but constant ESV

41
Q

If you old preload and contractility constant, but increase afterload, what happens in the PV loop?

A

Increased ESPVR along line (higher ESV), decreased stroke volume

42
Q

If there is a positive inotropic intervention, what happens in the PV loop?

A

Shifts ESPVR line upward and leftward resulting in larger stroke volume and smaller ESV

43
Q

The most common manifestation of L ventricular failure is

A

Dyspnea on exertion (can manifest at rest if HF worsens)

44
Q

What are some other symptoms f L ventricular failure? (4)

A

Orthopnea, cough, PND, fatigue

45
Q

What are some symptoms of R ventricular failure? (3)

A

Edema (peripheral, ascites), R upper quadrant pain (engorged liver), anorexia (edema in GI tract)

46
Q

The NYHA chronic HF classification has how many levels? What is it based on?

A

4 (I - IV); dyspnea and level of physical activity impairment (none, mild, moderate, and severe [symptoms present at rest])

47
Q

Stages of chronic HF classification has how many levels? Describe each.

A

A: at risk, no symptoms; B: heart disease, no symptoms of HF; C: disease + symptoms; D: symptoms despite interventions

48
Q

LV failure is associated with what signs (7, 4 are heart sounds)

A

Tachycardia, tachypnea, rales; loud P2, S3, S4, mitral regurgitation murmur

49
Q

Describe what S3 and S4 are related to

A

S3: systolic dysfunction, abnormal filling of dilated chamber; S4: dystolic dysfunction, forceful atrial contraction into stiffened ventricle

50
Q

RV failure is associated with what signs (6, 3 are heart sounds)

A

JVD, hepatomegaly, peripheral edmea; S2, S3, tricuspid regurgitation murmur

51
Q

T/F: Pleural effusion can be see in R or L heart failure

A

True! Pleural veins drain into systemic and pulmonary beds

52
Q

In HR, chest x-ray may reveal (4)

A

Cardiomegaly, vascular redistribution/interstitial edema (Kerley B lines), alveolar edema (opacification), bilateral pleural effusion

53
Q

What does coronary ateriography measure?

A

CO, degree of LV dysfunction, and LV end-diastolic pressure

54
Q

Five goals of HF treatment w/ reduced EF

A
  1. Identify underlying cause; 2. Eliminate precipitating cause; 3. Manage symptoms (decrease congestion, increase CO); 4. Modulate neurohormonal response; 5. Prolongation of survival
55
Q

What systemic factors could contribute to HF? (4)

A

Thyroid dysfunction, infections, uncontrolled diabetes, HTN

56
Q

What lifestyle modifications could improve HF?

A

Lower salt intake, alcohol cessation, medication compliance

57
Q

What does maximizing medications mean?

A

Discontinuing drugs that contribute to HF (NSAIDs, antiarrhythmias, etc)

58
Q

What do diurectics do in regards to the heart? When should they be used? Do they confer a mortality benefit?

A

Reduce venous return; in patients w/ congestion/edema; no, only symptomatic

59
Q

What do venous vasodilators do?

A

Increase venous compliance, decrease venous return to the heart + preload, taking someone off the flat, pulmonary congestion part of the F-S curve

60
Q

What do arterial vasodilators do?

A

Decrease SVR, afterload, and increase SV

61
Q

What are two examples of arteriolar + venous dilators?

A

ACE inhibitors and angiotensin II receptor blockers (ARBs)

62
Q

What are the effects of ACEIs?

A

Decreases vasoconstriction, aldosterone (improves Na+ elimination) –> reduced intravascular volume –> reduced congestion

63
Q

What do ACEIs prevent?

A

Maladaptive ventricular remodeling

64
Q

Beta blockers can be used in patients who are…

A

Stable (w/out recent deterioration or volume overlaod)

65
Q

Beta blockers should be avoided in patients…

A

Who are bradycardic, hypoperfused, with chronic long disease, or AV block

66
Q

What is the thought behind positive inotropic treatment? Works for systolic or dystolic dysfunction?

A

Increases contractility –> increase SV and CO at any given EDV; systolic

67
Q

Chronic aldosterone in HF can contribute to…Describe effectiveness of rx

A

Ventricular remodeling; aldosterone antagonists have been shown to improve mortality

68
Q

What is a treatment of arrhythmias that can cause sudden death?

A

Implantable cardiac defibrillator

69
Q

Who might get a biventricular pacemaker? What does this intervention do?

A

Continued symptoms of HF on maximum medical therapy, LVEF 120msec); been shown to augment left ventricular systolic function, improve exercise capacity, and reduce the frequency of heart failure exacerbations and mortality

70
Q

Two goals of HF treatment w/ preserved EF

A
  1. Reduce congestion/edema; 2. Treat underlying cause (hypertension, etc)
71
Q

Describe the use of diruetics for volume overload in these patients

A

With caution: the stiff ventricle requires high filling pressure to maintain CO

72
Q

Are the other drugs discussed for HFrEF useful for HFprEF?

A

No

73
Q

What does “wet” vs “dry” mean? What does “warm” vs “cold” mean?

A

Wet = volume overload; cold = reduced CO and vasoconstriction

74
Q

What is a frightening presentation of acute decompensated HF?

A

Cardiogenic pulmonary edema

75
Q

Treatment for decompensated HF? (pneumonic)

A

L (loop diuretics), M (morphine –> anxiety and venous dilation), N (nitrates –> venous vasodilators), O (O2), P (position)

Cardiology (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions