Pathophysiology of Congestive Heart Failure Flashcards

1
Q

Braunwald’s Definition of Congestive Heart Failure

A

The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body (forward failure)
or
The ability to do so only if the cardiac filling pressures are abnormally high (backward failure)

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2
Q

Major Determinants of Cardiac Performance

A

Heart Rate
Preload
Afterload
Contractility

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3
Q

Disorders of Impaired Contractility

A

Myocardial infarction
Ischemic cardiomyopathy
Dilated cardiomyopathy

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4
Q

Disorders of Markedly Increased Afterload

A

Severe aortic stenosis

Uncontrolled hypertension

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5
Q

Disorders with Impaired Ventricular Relaxation/Decreased Filling

A

Restrictive cardiomyopathy
Acquired or familial hypertrophic cardiomyopathy
Constrictive pericarditis

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6
Q

Heart Failure with Preserved Ejection Fraction (Diastolic Heart Failure)

A

Due to decreased diastolic compliance
Stroke volume is reduce and filling pressures are higher
EF is still normal though, makes it difficult to diagnose clinically

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7
Q

Pathophysiology of Right Sided Heart Failure

A

RV is more compliant than LV (thinner walls, pulmonary vascular resistance is less than systemic)
RV can tolerate larger changes in filling w/o change in pressure
BUT
RV is susceptible to acute changes in Pulmonary Vascular Resistance
Pulmonary disease can cause isolated RV failure

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8
Q

Causes of Right Sided Heart Failure

A

Cardiac: LV failure, mitral stenosis/regurg, acute MI wtih RV infarction, pulmonic stenosis
Pulmonary parenchymal diseases: COPD, interstitial lung diseases (silicosis, pulmonary fibrosis), ARDS (acute respiratory distress syndrome)
Pulmonary Vascular Diseases: pulmonary embolism, primary pulmonary hypertension

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9
Q

Compensatory Mechanisms to Maintain Cardiac Output in CHF

A
Frank-starling mechanism (increase in residual volume aka preload which contributes to greater output on next contraction)
Autonomic nervous system (baroreceptor response)
Renal Compensation (renin-angiotensin-aldosterone system)
Ventricular Remodeling
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10
Q

Post-MI Ventricular Remodeling

A

Any architectural or structural change that occurs after myocardial infarction in either the infarcted or non-infarcted regions of the heart

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11
Q

Alterations in Ventricular Shape and Size Following Acute MI

A

Acute alterations in ventricular dimensions (seconds)
Infarct expansion (hours-weeks)
**Hypertrophy/dilation of noninfarcted segments (weeks-years)

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12
Q

Eccentric Hypertrophy

A

Due to volume overload
Ventricular dilation and overall heart enlargement
Sarcomeres added in series

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13
Q

Concentric Hypertrophy

A

Due to pressure overload
Ventricular wall thickening
Sarcomeres added in parallel

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14
Q

Mechanisms of Post-MI Ventricular Remodeling

A
Cardiac myocyte hypertrophy
Cardiac fibroblast hyperplasia
Perivascular and interstital fibrosis
Vascular remodeling and angiogenesis
Cardiac myocyte apoptosis
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15
Q

Rx of Ventricular Dysfunction

A

Early recognition of remodeling, because months/years of remodeling will eventually lead to CHF
Remodeling is growth-mediated response and derived from mechanical and local neurohormonal factors
PREVENTING or SLOWING the progression of ventricular remodeling will prevent/delay development of CHF

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16
Q

Drugs that Prevent Ventricular Remodeling

A

ACE Inhibitors/ARBs/LCZ696
Beta Blockers
Aldosterone Antagonists

17
Q

Drugs the Prolong Survival with Ventricular Remodeling

A

ACE Inhibitors/ ARBs/LCZ696
Hydralazine and nitrates
Beta blockers (carvedilol, metoprolol, bucindolol)
Aldosterone antagonists (spironolactone, eplerenone)

18
Q

Clinical Manifestations of Left Sided Heart Failure

A

Symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue

Physical findings: diaphoresis, tachycardia, tachypnea, pulmonary rales, loud P2, S3 gallop (systolic dysfunction), S4 gallop (diastolic dysfunction)

19
Q

Clinical Manifestations of Right Sided Heart Failure

A

Symptoms: peripheral edema, RUQ discomfort

Physical findings: jugular venous distension, peripheral edema, hepatomegaly