Heart Failure Flashcards
“definition” of heart failure
inability of the heart to meet the metabolic needs of the body
- to be distinguished from cardiac dysfunction with successful adaptation
- when adaptation fails and becomes part of the problem
- clinical diagnosis w/ no one single finding, but a complex of findings
what are 2 causes of heart failure and examples?
- decreased circulatory supply to the body
- coronary heart disease (myocardial infarction, ischemic cardiomyopathy)
- valvular heart disease (aortic stenosis, mitral regurgitation)
- cardiomyopathy - increased circulatory demand from the body
- HTN (increased resistance)
- thyrotoxicosis (overactive thyroid)
- anemia (decreased O2 carrying capacity)
- AV fistula (manmade or on dialysis)
what are 3 adaptive mechanisms for heart failure?
compensations that maintain pump function in presence of heart disease or increased demand
- Frank-Starling (short term)
- Neuro-hormonal (intermediate; renal)
- Hypertrpohy (long term)
how does Frank-Starling help heart failure?
if one exercises or increases sympathetic stimulation with heart failure, the decreased contractile state of the myocardium can increase ventricular performance, not as good as normal non-exercising, but much better than plain heart failure
what happens to B1 receptors in sympathetic stimulation in heart failure?
B1 receptors are exhausted due to chronic stimulation
-receptor synthesis decreases
plasma NE levels and heart failure survival
increasing levels of PNE are associated with decreasing length of survival in heart failure
-since PNE is a rough estimate of the sympathetic stimulation, increasing sympathetic stimulation can still be bad
how does blood flow to muscles compare in heart failure?
less CO to muscle if CHF
-less CO in general, but from what is left, maintain flow to the heart and brain at expense of skin, skeletal muscle, gut, and kidneys
what are the renal adaptations to heart failure?
stimuli: less GFR and renal blood flow, more aldosterone (there is also more AII)
response: increased Na and H2O retention, plasma volume, venous return, and venous pressure
how do beta1 and beta2 receptor density differ in heart failure?
B1 receptor density is reduced by heart failure, but not B2 receptor densities
atrial and brain natriuretic factors in heart failure
both are counter-regulatory (BNF is actually from ventricles)
-both promote vasodilation, natriuresis, and suppress RAS
what are 5 hormones that are higher in heart failure than normal?
plasma NE plasma renin-angiotensin vasopressin atrial natriuretic factor endothelin
hypertrophy and heart failure
increase in myocardial mass - remodeling
- if abnormality can be corrected, hypertrophy will regress
- if not corrected, myocardial dysfunction will worsen and become permanent
- poorer contractile function
2 causes of hypertrophy
pressure overload (stenosis w/ increased systolic wall stress) and volume overload (regurgitation with increased diastolic wall stress)
- effort to return wall stress toward normal
- though individual muscles show reduced contractility, maintained pump function (CO) by keeping wall stress near normal
types of ventricular remodeling (3 kinds and what they’re caused by)
parallel sarcomeres - concentric hypertrophy (shorter and fatter, with smaller lumen; from pressure overload) series sarcomeres - eccentric hypertrophy (longer and skinnier, with thinner walls; from volume overload) physiologic hypertrophy (longer; from volume overload) CH and EH cause increased expression of embryonic genes
what are heart failure adaptation disadvantages for:
- Frank-Starling
- Neurohumoral
- Renal
- Myocardial hypertrophy remodeling
- high left ventricle end diastolic pressure causes pulmonary edema
- increased myocardial O2 consumption, arrythmias, diminished response to sympathetic stimulation, blunted baroreceptor function, increased systemic vascular resistance
- peripheral/organ edema, decreased renal function
- decreased contractility, necrosis/apoptosis, decreased coronary reserve, changes in diastole (matrix)
right VS left ventricle heart failure diseases
RV: pulmonary embolism, cor pulmonale, mitral stenosis
LV: mitral insufficiency, aortic stenosis/insufficiency, HTN, cardiomyopathy
acute VS chronic CHF in heart failure diseases
acute: myocardial infarction, endocarditis
chronic: cardiomyopathy, HTN
low VS high cardiac output in heart failure diseases
low: cardiomyopathy, coronary heart disease
high: thyrotoxicosis, anemia, and AV fistula
forward VS backward flow in heart failure diseaes
forward: due to low CO
backward: due to high venous pressure
systolic VS diastolic in heart failure diseases
S: myocardial infarction
D: preserved EF of 40-5-% in patients
-delayed relaxxation (elterly, HTN), early ischemia
-increased stiffness (rare), infiltrative disease, amyloidosis
therapy choices for heart failure
- treat underlying cause (surgery/transplantation)
- inotropic agents
- diuretics
- venodilator (reduce pre-load)
- atrial vasodilation (reduce afterload)
- beta-blockers (blunt sympathetic stimulation)
- aldosterone antagonists
- resynchronization (bi or uni-ventricular pacing)
- internal cardiac defibrillator
- LV assist device (LVAD)
examples of inotropic agents
used to treat heart failure
-digitalis, dobutamine
examples of diuretics
used to treat heart failure
- loop
- distal tubule
- furosemide
- thiazide
examples of venodilators and arterial vasodilators
used to treat heart failure
- venodilators: nitrates, brain natrial peptide
- vasodilators: ACE inhibitors, angiotensin receptor blockers
