Pathophys of Heart Failure - HF 1 Flashcards
heart failure most commonly characterized by
- fluid retention
- elevations in ventricular filling pressures
some causes of heart failure
- hypertension
- MI
- cardiomyopathy
- arrhythmia
- congenital heart disease
- valvular disease
the true problem from heart failure results from
- maladaptive neurohormonal responses to decreased cardiac performance
pathophys causes of heart failure
- impaired contractility
- increased afterload
- increased volume
- impaired ventricular filling
impaired contractility caused by
- ischemic and dilated cardiomyopathy
increased afterload caused by
- longstanding hypertension
- aortic stenosis
increased volume caused by
- aortic/mitral insufficiency
impaired ventricular filling caused by
- hypertrophy
what is the most common cause of heart failure
- MI
ischemic cardiomyopathy - the primary/secondary disease process
- primary - coronary arteries
- secondary - heart muscle
dilated cardiomyopathy - the primary disease process
- primary - heart muscle
decreasing contractility has what effect on stroke volume
effect on cardiac output
- decreasing contractility decreases stroke volume
- decreased cardiac output
physiological adaptations to decreased stroke volume
- increased preload (frank starling)
- increased wall thickness
what happens if we increase preload beyond that of the adaptive response
- we get pulmonary edema
most common symptoms of heart failure
- dyspnea
how is preload regulated
- venous tone
- blood volume
- body position
venous tone is regulated by
- sympathetic activity increasing tension in walls of veins and venules
blood volume increased by
- RAS
- Sympathetic nervous system
- ADH
- fluid intake
result of increased sympathetic tone
- beta 1 stimulation increases HR and contractility
- alpha 1 stimulation increases venous return and decreases venous compliance
- increased renin release, salt and fluid retention and vasoconstriction
cardio response to chronic beta-AR stimulation
- down regulation of beta AR
- energy starvation
- cardiomyocyte death
- ventricular arrhythmias
- fibrosis
RAAS response to decreased stroke volume
- kidneys sense decreased EABV
- increase renin from JGA
- increase angiotensin II and aldosterone levels
- increases blood volume and vasoconstriction
heart failure result on RAAS
- disrupts negative feedback loop
- excessive fluid retention
role of ANP and BNP
- counteract maladaptive hormones
how chronic hypertension leads to heart failure
- chronically elevated BP increases LV pressure
- leads to hypertrophy of ventricle
- remodeling and dilation