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MHD 1 > L45 Pathophysiology of Heart Failure > Flashcards

L45 Pathophysiology of Heart Failure Flashcards

1
Q

What is forward failure CHF?

A

The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body?

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2
Q

What is backward failure CHF?

A

The ability to pump blood forward at a sufficient rate to meet the metabolic needs of the body ONLY if the cardiac filling pressures are abnormally high.

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3
Q

CO = ?

A

SV * HR

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4
Q

What are the components of SV?

A

Contractility, preload, and afterload

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5
Q

What is preload?

A

The tension/wall stress in the ventricle at the end of diastole (related to venous return and intrinsic compliance)

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6
Q

What is afterload?

A

The tension/wall stress in the ventricle during contraction (the pressure against which the ventricle contracts

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7
Q

What is contractility?

A

The innate ability of the heart to contract

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8
Q

What describes the relationship of myocyte/ventricular stretch to the pressure generated during systole?

A

Frank-Starling contractility curve

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9
Q

SV = ?

A

EDV - ESV

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10
Q

EF = ?

A

[(EDV-ESF)/EDV] * 100

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11
Q

What are the effects of increasing preload on SV?

A

Increasing preload increases SV

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12
Q

What are the effects of decreasing afterload on SV?

A

Decreasing afterload increases SV

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13
Q

What are the effects of increasing contractility on SV?

A

Increasing contractility increases SV

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14
Q

What happens on the Frank-Starling curve with increased preload?

A

Move along the curve (increase)

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15
Q

What happens on the Frank-Starling curve with increased contractility?

A

Move up to a new curve (increased CO) at the same pressure

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16
Q

What are the three types of disorders that incite heart failure?

A
  1. Disorders of impaired contractility
  2. Disorders of markedly increased afterload
  3. Disorders with impaired ventricular relaxation/decreased filling
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17
Q

What are some disorders of impaired contractility?

A
  1. MI/ischemic cardiomyopathy
  2. Chronic mitral regurgitation
  3. Dilated cardiomyopathy
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18
Q

What are some disorders of markedly increased afterload?

A
  1. Severe aortic stenosis

2. Uncontrolled hypertension

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19
Q

What are some disorders with impaired ventricular relaxation/decreased filling?

A
  1. Restrictive cardiomyopathy
  2. Acquired or familial hypertrophic cardiomyopathy
  3. Infiltrative diseases
  4. Constrictive pericarditis
20
Q

What are the compensatory mechanisms employed to maintain CO in HF?

A
  1. Length-dependent activation (Frank-Starling mechanism) - seconds
  2. Baroreceptor response of ANS - seconds
  3. Renal compensation via RAA system - seconds to hours
  4. Ventricular remodeling via myocardial hypertrophy and/or dilation - weeks to years
21
Q

Describe the neurohormonal model beginning with reduced CO.

A
  1. Compensatory responses
  2. Increased systemic vascular resistance
  3. Increased afterload
  4. Depressed ventricular performance
  5. Reduced CO (repeat)
22
Q

Describe the sympathetic nervous system response to decreased CO.

A
  1. Increased sympathetic/decreased parasympathetic tone
  2. Increased NE (increased secretion, decreased reabsorption)
  3. Increased beta 1 receptor activation
  4. Increased contractility and HR
23
Q

What are the negative effects of chronic NE stimulation?

A

Increased ischemia and arrhythmia (heart) and increased renin, sodium/water reabsorption, and vascular resistance (afterload - kidneys)

24
Q

Renin is released in response to a decrease in cardiac output. What happens next?

A

Decreased stretch of the glomerular afferent arteriole, reduced delivery of chloride to the macula densa, and increased beta 1 adrenergic activity

25
Q

Describe the RAAS.

A

Renin converts angiotensinogen to angiotensin I. ACE converts I to II.

II is a vasoconsrictor, which increases afterload.

II activates aldosterone, which increases sodium and water retention, thus increasing preload.

II also activates ADH, which vasoconstricts and retains water. This increases afterload and preload.

26
Q

Chronic sympathetic/RAAS activation leads to what effects?

A
  1. Myocyte hypertrophy
  2. Re-expression of fetal isoforms
  3. Myocyte apoptosis
  4. Changes in interstitial matrix

This all leads to worsening cardiac performance due to progressive hypertrophy and/or dilation

27
Q

What happens in pressure-overload LVH?

A

Concentric LVH

28
Q

What causes pressure-overload LVH?

A

Aortic stenosis and systemic hypertension

29
Q

What happens in volume-overload LVH?

A

Eccentric LVH with progressive dilation

30
Q

What causes volume-overload LVH?

A

Mitral regurgitation, AV fistula, and hyperthyroidism

31
Q

What are three ways to classify heart failure?

A
  1. Forward vs. backward
  2. LV. vs. RV vs. biventricular
  3. Systolic vs. diastolic
32
Q

What is the most accurate way to classify heart failure?

A

HF with reduced ejection fraction (traditionally systolic)

HF with preserved ejection fraction (traditionally diastolic)

33
Q

Describe the Frank Starling curve in heart failure with reduced ejection fraction.

A

Curve drops down and to the right; for a given preload, there is less CO

34
Q

Describe the pressure-volume loop in heart failure with reduced ejection fraction.

A

SV decreases, EDV increases, EF decreases

35
Q

Describe the Frank Starling curve in heart failure with preserved ejection fraction.

A

Curve drops down and to the right; for a given preload, there is less CO (same as reduced ejection fraction)

36
Q

Describe the pressure-volume loop in heart failure with preserved ejection fraction.

A

SV decreases, EDV decreases, EF stays the same

Contractility does not change

37
Q

How is the RV different from the LV?

A
  1. RV is more compliant than LV
  2. RV can tolerate much larger changes in filling without major change in pressure
  3. RV is susceptible to acute changes in pulmonary vascular resistance
38
Q

What are the cardiac causes of right-sided HF?

A
  1. LV failure
  2. Mitral stenosis/regurgitation
  3. Acute MI with RV infarction
  4. Pulmonic stenosis
39
Q

What are the pulmonary parenchymal causes of right-sided HF?

A
  1. COPD
  2. Interstitial lung diseases
  3. ARDs
40
Q

What are the pulmonary vascular causes of right-sided HF?

A
  1. Pulmonary embolism

2. Primary pulmonary hypertension

41
Q

Compare the symptoms of left-sided heart failure and right-sided heart failure.

A

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

R: peripheral edema, RUQ discomfort

42
Q

Compare the physical findings of left-sided heart failure and right-sided heart failure.

A

L: diaphoresis, tachycadia, tachypnea, pulmonary rales, loud P2, S3 gallop (systolic dysfunction), S4 gallop (diastolic dysfunction)

R: jugular venous distension, peripheral edema, hepatomegaly

43
Q

Remodeling often ___ the development of symptoms of CHF by months to years.

A

Precedes

44
Q

Remodeling is predominantly a ___-mediated response and results from an interplay between mechanical, systemic, and locally derived neurohormonal factors.

A

Growth

45
Q

What will prevent/delay the development of CHF?

A

Efforts directed at preventing or slowing the progression of ventricular remodeling

46
Q

What are some drugs that prevent ventricular remodeling?

A
  1. ACEI/ARB/ARNI
  2. Beta blockers
  3. Aldosterone antagonists
47
Q

What are some drugs that prolong survival in CHF?

A
  1. ACEI/ARB/ARNI
  2. Beta blockers
  3. Aldosterone antagonists
  4. Hydralazine + nitrates

MHD 1 (58 decks)

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