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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

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2
Q

Key mediators of CO

A

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

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3
Q

Preload, two ways

A

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

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4
Q

Afterload, two ways

A

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

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5
Q

Contractility

A

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

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6
Q

Frank-Starling Curve axes

A

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

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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

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8
Q

Between D and A? Between B and C?

A

Isovolumetric relaxation; isovolumetric contraction

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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
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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
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11
Q

Increased afterload could be caused by… (2)

A
  1. Advanced aortic stenosis; 2. Uncontrolled severe hypertension
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12
Q

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

A

Impaired contractility and increased afterload; systolic dysfunction

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13
Q

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

A

Impaired diastolic filing; diastolic dysfunction

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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)

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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

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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%)

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17
Q

Three compensatory mechanisms of failing heart

A

Frank-Starling mechanism, ventricular hypertrophy, neurohormonal activation

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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

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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

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20
Q

Concentric hypertrophy is what? What could cause this?

A

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

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21
Q

Eccentric hypertrophy is what? What could cause this?

A

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

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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

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23
Q

Neurohormal activation (3)

A
  1. Increased sympathetic nervous system; 2. Increased Renin-Angiotensin system; 3. Increased ADH
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24
Q

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

A

TPR; CO

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25
On a very basic level, heart failure is what?
A CLINICAL syndrome
26
HFrEF
Heart failure with reduced ejection fraction
27
HFprEF
Heart failure with preserved ejection fraction
28
What triggers the adrenergic nervous system during HF?
Fall in CO sensed by baroreceptors in carotid sinus/aortic arch
29
What is the result of the adrenergic nervous system during HF?
Increased HR and ventricular contractility (directly increase CO) and arteriol vasoconstriction (increases MAP) and venous vasoconstriction (increases preload --> increased stroke volume)
30
Alpha receptor distribution allows for what phenomenon during HF?
During sympathetic stimulation, blood flow is redistributed to vital organs at the expense of the skin, splanchnics and kidneys
31
What stimulates renin release? (3)
1. Decreased renal artery perfusion; 2. Decreased salt delivery to macula densa; 3. Direct stimulation of juxtaglomerular beta-receptors via sympathetics
32
What does renin do? Then what?
Cleaves angiotensinogen --> angiotensin I which is cleaved to form angiotensin II by ACE
33
What is the main effect of angiotensin II?
It is a potent vasoconstrictor, raises TPR to maintain BP
34
What else does angiotensin II do? What happens then?
Increase thirst (hypothalamus) and aldosterone release (adrenals); increase in intravascular volume --> increase preload --> increased CO
35
At what point does increasing preload stop working?
At the flat portion of the ventricular performance curve
36
What pituitary hormone is released during HF? What does it do?
ADH --> increases water reabsorption from the kidneys--> increased intravascular volume --> increase preload --> increased CO
37
Two ways in which compensatory mechanisms are not beneficial in the long run
1. Increased intravascular volume can worsen pulmonary congestion; 2. Increased arteriolar resistance increases afterload against failing ventricle
38
How could natriuretic peptides be beneficial?
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
Ventricular ESV depends on what and what, but not on what?
Afterload and contractility but NOT on preload
40
If you hold afterload and contractility constant, but increase preload, what happens in the PV loop?
Increased stroke volume but constant ESV
41
If you old preload and contractility constant, but increase afterload, what happens in the PV loop?
Increased ESPVR along line (higher ESV), decreased stroke volume
42
If there is a positive inotropic intervention, what happens in the PV loop?
Shifts ESPVR line upward and leftward resulting in larger stroke volume and smaller ESV
43
The most common manifestation of L ventricular failure is
Dyspnea on exertion (can manifest at rest if HF worsens)
44
What are some other symptoms f L ventricular failure? (4)
Orthopnea, cough, PND, fatigue
45
What are some symptoms of R ventricular failure? (3)
Edema (peripheral, ascites), R upper quadrant pain (engorged liver), anorexia (edema in GI tract)
46
The NYHA chronic HF classification has how many levels? What is it based on?
4 (I - IV); dyspnea and level of physical activity impairment (none, mild, moderate, and severe [symptoms present at rest])
47
Stages of chronic HF classification has how many levels? Describe each.
A: at risk, no symptoms; B: heart disease, no symptoms of HF; C: disease + symptoms; D: symptoms despite interventions
48
LV failure is associated with what signs (7, 4 are heart sounds)
Tachycardia, tachypnea, rales; loud P2, S3, S4, mitral regurgitation murmur
49
Describe what S3 and S4 are related to
S3: systolic dysfunction, abnormal filling of dilated chamber; S4: dystolic dysfunction, forceful atrial contraction into stiffened ventricle
50
RV failure is associated with what signs (6, 3 are heart sounds)
JVD, hepatomegaly, peripheral edmea; S2, S3, tricuspid regurgitation murmur
51
T/F: Pleural effusion can be see in R or L heart failure
True! Pleural veins drain into systemic and pulmonary beds
52
In HR, chest x-ray may reveal (4)
Cardiomegaly, vascular redistribution/interstitial edema (Kerley B lines), alveolar edema (opacification), bilateral pleural effusion
53
What does coronary ateriography measure?
CO, degree of LV dysfunction, and LV end-diastolic pressure
54
Five goals of HF treatment w/ reduced EF
1. Identify underlying cause; 2. Eliminate precipitating cause; 3. Manage symptoms (decrease congestion, increase CO); 4. Modulate neurohormonal response; 5. Prolongation of survival
55
What systemic factors could contribute to HF? (4)
Thyroid dysfunction, infections, uncontrolled diabetes, HTN
56
What lifestyle modifications could improve HF?
Lower salt intake, alcohol cessation, medication compliance
57
What does maximizing medications mean?
Discontinuing drugs that contribute to HF (NSAIDs, antiarrhythmias, etc)
58
What do diurectics do in regards to the heart? When should they be used? Do they confer a mortality benefit?
Reduce venous return; in patients w/ congestion/edema; no, only symptomatic
59
What do venous vasodilators do?
Increase venous compliance, decrease venous return to the heart + preload, taking someone off the flat, pulmonary congestion part of the F-S curve
60
What do arterial vasodilators do?
Decrease SVR, afterload, and increase SV
61
What are two examples of arteriolar + venous dilators?
ACE inhibitors and angiotensin II receptor blockers (ARBs)
62
What are the effects of ACEIs?
Decreases vasoconstriction, aldosterone (improves Na+ elimination) --> reduced intravascular volume --> reduced congestion
63
What do ACEIs prevent?
Maladaptive ventricular remodeling
64
Beta blockers can be used in patients who are...
Stable (w/out recent deterioration or volume overlaod)
65
Beta blockers should be avoided in patients...
Who are bradycardic, hypoperfused, with chronic long disease, or AV block
66
What is the thought behind positive inotropic treatment? Works for systolic or dystolic dysfunction?
Increases contractility --> increase SV and CO at any given EDV; systolic
67
Chronic aldosterone in HF can contribute to...Describe effectiveness of rx
Ventricular remodeling; aldosterone antagonists have been shown to improve mortality
68
What is a treatment of arrhythmias that can cause sudden death?
Implantable cardiac defibrillator
69
Who might get a biventricular pacemaker? What does this intervention do?
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
Two goals of HF treatment w/ preserved EF
1. Reduce congestion/edema; 2. Treat underlying cause (hypertension, etc)
71
Describe the use of diruetics for volume overload in these patients
With caution: the stiff ventricle requires high filling pressure to maintain CO
72
Are the other drugs discussed for HFrEF useful for HFprEF?
No
73
What does "wet" vs "dry" mean? What does "warm" vs "cold" mean?
Wet = volume overload; cold = reduced CO and vasoconstriction
74
What is a frightening presentation of acute decompensated HF?
Cardiogenic pulmonary edema
75
Treatment for decompensated HF? (pneumonic)
L (loop diuretics), M (morphine --> anxiety and venous dilation), N (nitrates --> venous vasodilators), O (O2), P (position)

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