L45 Pathophysiology of Heart Failure Flashcards
What is forward failure CHF?
The inability of the heart to pump blood forward at a sufficient rate to meet the metabolic demands of the body?
What is backward failure CHF?
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.
CO = ?
SV * HR
What are the components of SV?
Contractility, preload, and afterload
What is preload?
The tension/wall stress in the ventricle at the end of diastole (related to venous return and intrinsic compliance)
What is afterload?
The tension/wall stress in the ventricle during contraction (the pressure against which the ventricle contracts
What is contractility?
The innate ability of the heart to contract
What describes the relationship of myocyte/ventricular stretch to the pressure generated during systole?
Frank-Starling contractility curve
SV = ?
EDV - ESV
EF = ?
[(EDV-ESF)/EDV] * 100
What are the effects of increasing preload on SV?
Increasing preload increases SV
What are the effects of decreasing afterload on SV?
Decreasing afterload increases SV
What are the effects of increasing contractility on SV?
Increasing contractility increases SV
What happens on the Frank-Starling curve with increased preload?
Move along the curve (increase)
What happens on the Frank-Starling curve with increased contractility?
Move up to a new curve (increased CO) at the same pressure
What are the three types of disorders that incite heart failure?
- Disorders of impaired contractility
- Disorders of markedly increased afterload
- Disorders with impaired ventricular relaxation/decreased filling
What are some disorders of impaired contractility?
- MI/ischemic cardiomyopathy
- Chronic mitral regurgitation
- Dilated cardiomyopathy
What are some disorders of markedly increased afterload?
- Severe aortic stenosis
2. Uncontrolled hypertension
What are some disorders with impaired ventricular relaxation/decreased filling?
- Restrictive cardiomyopathy
- Acquired or familial hypertrophic cardiomyopathy
- Infiltrative diseases
- Constrictive pericarditis
What are the compensatory mechanisms employed to maintain CO in HF?
- Length-dependent activation (Frank-Starling mechanism) - seconds
- Baroreceptor response of ANS - seconds
- Renal compensation via RAA system - seconds to hours
- Ventricular remodeling via myocardial hypertrophy and/or dilation - weeks to years
Describe the neurohormonal model beginning with reduced CO.
- Compensatory responses
- Increased systemic vascular resistance
- Increased afterload
- Depressed ventricular performance
- Reduced CO (repeat)
Describe the sympathetic nervous system response to decreased CO.
- Increased sympathetic/decreased parasympathetic tone
- Increased NE (increased secretion, decreased reabsorption)
- Increased beta 1 receptor activation
- Increased contractility and HR
What are the negative effects of chronic NE stimulation?
Increased ischemia and arrhythmia (heart) and increased renin, sodium/water reabsorption, and vascular resistance (afterload - kidneys)
Renin is released in response to a decrease in cardiac output. What happens next?
Decreased stretch of the glomerular afferent arteriole, reduced delivery of chloride to the macula densa, and increased beta 1 adrenergic activity
Describe the RAAS.
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.
Chronic sympathetic/RAAS activation leads to what effects?
- Myocyte hypertrophy
- Re-expression of fetal isoforms
- Myocyte apoptosis
- Changes in interstitial matrix
This all leads to worsening cardiac performance due to progressive hypertrophy and/or dilation
What happens in pressure-overload LVH?
Concentric LVH
What causes pressure-overload LVH?
Aortic stenosis and systemic hypertension
What happens in volume-overload LVH?
Eccentric LVH with progressive dilation
What causes volume-overload LVH?
Mitral regurgitation, AV fistula, and hyperthyroidism
What are three ways to classify heart failure?
- Forward vs. backward
- LV. vs. RV vs. biventricular
- Systolic vs. diastolic
What is the most accurate way to classify heart failure?
HF with reduced ejection fraction (traditionally systolic)
HF with preserved ejection fraction (traditionally diastolic)
Describe the Frank Starling curve in heart failure with reduced ejection fraction.
Curve drops down and to the right; for a given preload, there is less CO
Describe the pressure-volume loop in heart failure with reduced ejection fraction.
SV decreases, EDV increases, EF decreases
Describe the Frank Starling curve in heart failure with preserved ejection fraction.
Curve drops down and to the right; for a given preload, there is less CO (same as reduced ejection fraction)
Describe the pressure-volume loop in heart failure with preserved ejection fraction.
SV decreases, EDV decreases, EF stays the same
Contractility does not change
How is the RV different from the LV?
- RV is more compliant than LV
- RV can tolerate much larger changes in filling without major change in pressure
- RV is susceptible to acute changes in pulmonary vascular resistance
What are the cardiac causes of right-sided HF?
- LV failure
- Mitral stenosis/regurgitation
- Acute MI with RV infarction
- Pulmonic stenosis
What are the pulmonary parenchymal causes of right-sided HF?
- COPD
- Interstitial lung diseases
- ARDs
What are the pulmonary vascular causes of right-sided HF?
- Pulmonary embolism
2. Primary pulmonary hypertension
Compare the symptoms of left-sided heart failure and right-sided heart failure.
L: dyspnea, orthopnea, paroxysmal nocturnal dyspnea, cough, fatigue
R: peripheral edema, RUQ discomfort
Compare the physical findings of left-sided heart failure and right-sided heart failure.
L: diaphoresis, tachycadia, tachypnea, pulmonary rales, loud P2, S3 gallop (systolic dysfunction), S4 gallop (diastolic dysfunction)
R: jugular venous distension, peripheral edema, hepatomegaly
Remodeling often ___ the development of symptoms of CHF by months to years.
Precedes
Remodeling is predominantly a ___-mediated response and results from an interplay between mechanical, systemic, and locally derived neurohormonal factors.
Growth
What will prevent/delay the development of CHF?
Efforts directed at preventing or slowing the progression of ventricular remodeling
What are some drugs that prevent ventricular remodeling?
- ACEI/ARB/ARNI
- Beta blockers
- Aldosterone antagonists
What are some drugs that prolong survival in CHF?
- ACEI/ARB/ARNI
- Beta blockers
- Aldosterone antagonists
- Hydralazine + nitrates
