L45 Pathophysiology of Heart Failure

Question 1

What is forward failure CHF?

Answer 1

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

Question 2

What is backward failure CHF?

Answer 2

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.

Question 3

CO = ?

Answer 3

SV * HR

Question 4

What are the components of SV?

Answer 4

Contractility, preload, and afterload

Question 5

What is preload?

Answer 5

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

Question 6

What is afterload?

Answer 6

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

Question 7

What is contractility?

Answer 7

The innate ability of the heart to contract

Question 8

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

Answer 8

Frank-Starling contractility curve

Question 9

SV = ?

Answer 9

EDV - ESV

Question 10

EF = ?

Answer 10

[(EDV-ESF)/EDV] * 100

Question 11

What are the effects of increasing preload on SV?

Answer 11

Increasing preload increases SV

Question 12

What are the effects of decreasing afterload on SV?

Answer 12

Decreasing afterload increases SV

Question 13

What are the effects of increasing contractility on SV?

Answer 13

Increasing contractility increases SV

Question 14

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

Answer 14

Move along the curve (increase)

Question 15

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

Answer 15

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

Question 16

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

Answer 16

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

Question 17

What are some disorders of impaired contractility?

Answer 17

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

Question 18

What are some disorders of markedly increased afterload?

Answer 18

1. Severe aortic stenosis

2. Uncontrolled hypertension

Question 19

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

Answer 19

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

Question 20

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

Answer 20

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

Question 21

Describe the neurohormonal model beginning with reduced CO.

Answer 21

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

Question 22

Describe the sympathetic nervous system response to decreased CO.

Answer 22

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

Question 23

What are the negative effects of chronic NE stimulation?

Answer 23

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

Question 24

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

Answer 24

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

Question 25

Describe the RAAS.

Answer 25

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.

Question 26

Chronic sympathetic/RAAS activation leads to what effects?

Answer 26

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

Question 27

What happens in pressure-overload LVH?

Answer 27

Concentric LVH

Question 28

What causes pressure-overload LVH?

Answer 28

Aortic stenosis and systemic hypertension

Question 29

What happens in volume-overload LVH?

Answer 29

Eccentric LVH with progressive dilation

Question 30

What causes volume-overload LVH?

Answer 30

Mitral regurgitation, AV fistula, and hyperthyroidism

Question 31

What are three ways to classify heart failure?

Answer 31

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

Question 32

What is the most accurate way to classify heart failure?

Answer 32

HF with reduced ejection fraction (traditionally systolic) HF with preserved ejection fraction (traditionally diastolic)

Question 33

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

Answer 33

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

Question 34

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

Answer 34

SV decreases, EDV increases, EF decreases

Question 35

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

Answer 35

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

Question 36

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

Answer 36

SV decreases, EDV decreases, EF stays the same Contractility does not change

Question 37

How is the RV different from the LV?

Answer 37

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

Question 38

What are the cardiac causes of right-sided HF?

Answer 38

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

Question 39

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

Answer 39

1. COPD 2. Interstitial lung diseases 3. ARDs

Question 40

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

Answer 40

1. Pulmonary embolism | 2. Primary pulmonary hypertension

Question 41

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

Answer 41

L: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue R: peripheral edema, RUQ discomfort

Question 42

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

Answer 42

L: diaphoresis, tachycadia, tachypnea, pulmonary rales, loud P2, S3 gallop (systolic dysfunction), S4 gallop (diastolic dysfunction) R: jugular venous distension, peripheral edema, hepatomegaly

Question 43

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

Answer 43

Precedes

Question 44

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

Answer 44

Growth

Question 45

What will prevent/delay the development of CHF?

Answer 45

Efforts directed at preventing or slowing the progression of ventricular remodeling

Question 46

What are some drugs that prevent ventricular remodeling?

Answer 46

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

Question 47

What are some drugs that prolong survival in CHF?

Answer 47

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