10: Pathophysiology of Heart Failure Flashcards
What is the effect of the valsalva maneuver?
- ↑intrathoracic pressure –> ↓venous return –> ↓preload
- ↓intensity of most heart murmurs
- ↑intensity of MVP, HTCM murmurs
What is capacitance?
Volume at a specified pressure; the slope at that point is stiffness = 1/compliance
What is arterial elastance?
- Ea = ESP/SV
- Ea = HR*TPR
What is the basic pathophysiology of heart failure?
- Myocardial insult/stimuli/damage causes pump dysfunction.
- Pump dysfunction activates neurohormones:
- Catecholamines
- Angiotensin II
- Cytokines
- Heart remodels by hypertrophy, fibrosis and apoptosis
- Process cycles
Describe the neurohormonal activation in heart failure.
- Initial fall in LV performance –> ↑wall stress
- Activates RAS and SNS
- Remodeling and progressive worsening of LV function leads to arrhythmias, pump failure, death
- Fibrosis, apoptosis, hypertrophy, cellular/molecular alterations, myotoxicity
- Peripheral vasoconstriction, sodium retention and hemodynamic alterations lead to heart failure Sx:
- Fatigue
- Activity altered
- Chest congestion
- Edema
- SOB
Describe the adrenergic pathway in heart failure progression.
- ↑CNS sympathetic outflow
- ↑Cardiac sympathetic activity
- Beta-1
- Beta-2
- Alpha-1
- Myocyte hypertrophy
- Myocyte injury
- ↑arrhythmias
- ↑vascular sympathetic activity
- Alpha-1
- Vasoconstriction
- Alpha-1
- ↑renal sympathetic activity
- Beta-1
- Activation of RAS
- Vasoconstriction
- Activation of RAS
- Alpha-1
- Sodium retention
- Beta-1
- ↑Cardiac sympathetic activity
Describe the neurohormonal balance in heart failure.
Vasoconstrictive hormones (endothelin, aldosterone, angiotensin II, epinephrine) outweigh naturitic peptides (ANP, BNP).
Describe the pathophysiology of myocardial remodeling.
- Insult/remodeling stimuli
- ↑wall stress, cytokines, neurohormones, oxidative stress
- Myocyte hypertrophy
- Altered interstitial matrix
- Ventricular enlargement
- Fetal gene expression
- Diastolic dysfunction
- Altered calcium handling proteins
- Myocyte death
- Systolic dysfunction
What are the four basic mechanisms of heart failure?
- ↑blood volume (XS preload)
- ↑resistance to flow (XS afterload)
- ↓contractility
- ↓filling
What are the etiologies of increased blood volume? What do they result in?
Mitral or aortic regurgitation, volume overload (IV fluid), L to R shunts, chronic kidney disease
Reduced CO to peripheries results in sodium retention, vasoconstriction –> increased preload –> ventricular remodeling (eccentric).
What are the etiologies of increased afterload? What do they result in?
Caused by aortic stenosis, aortic coarctation, HTN.
Reduced CO from diastolic dysfunction results in sodium retention, vascoconstriction and concentric remodeling.
What are the etiologies of decreased contractility? What do they result in?
Caused by ischemic cardiomyopathy (infarcion or ischemia), myocarditis, or toxins (anthracycline, alcohol, cocaine).
Reduced CO results in sodium retention and vasoconstriction, resulting in eccentric ventricular remodeling.
What are the etiologies of decreased filling? What do they result in?
Caused by mitral stenosis, constriction, restrictive cardiomyopathy, cardiac tamponade, HTCM, ICM
Concentric ventricular remodeling causes a decrease in filling pressure, reduced capacitance.
Systolic vs. diastolic heart failure
- Systolic
- Impaired contraction
- Eccentric remodeling
- All ages
- 2/2 CAD, MI
- Decreased EF
- Third heart sound
- Diastolic
- Impaired filling
- Concentric remodeling
- >60y/o, women
- 2/2 HTN
- Unchanged EF
- Fourth heart sound
What is evidence for low perfusion?
- Narrow PP
- Pulsus alterations
- Cool forearms/legs
- Sleepy/obtunded
- ACEI-related
- Symptomatic HoTN
- Declining serium sodium level
- Worsening renal function