Lecture 1 Flashcards
(16 cards)
Heart failure
a common, usually progressive clinical syndrome that develops when the heart is unable to pump blood at a rate sufficient to meet the metabolic demands of the tissues or can do so only at an elevated filling pressure
acute etiology
- acute hemodynamic stress
- fluid overload
- acute vascular dysfunction
- a large MI
chronic etiology
- IHD
- chronic work overload (HTN, valve diseases)
intrinsic regulation of cardiac mechanisms
- frank starling mechanisms & stretch of the right atrial wall
very specific for the heart - can increase strength of contraction due to large volume
- in response to changes in volume of blood flowing into the heart
extrinsic regulation of cardiac mechanisms
- HR & strength of contraction by the autonomic nervous system
cardiac function impairment (IHD) or an increase in workload (HTN) leads to
activation of compensatory mechanisms to maintain arterial pressure & perfusion of vital organs
compensatory mechanisms
- frank-starling mechansisms
- myocardial adaptations
- activation of neurohumoral systems
frank starling mechanism
- increased filling volumes dilate the heart and thereby increases functional cross-bridge formation within the sarcomeres, enhancing contractility
myocardial adaptations
- hypertrophy w/ or w/out cardiac chamber dilation
- ventricular remodeling- more than hypertrophy- collective molecular, cellular, & structural changes that occur as a response to injury or changes in work loading conditions
activation of neurohumoral systems
- release NE which increase HR & augments myocardial contractility & vascular resistance
- activation of RAAS
- release of atrial natriuretic peptide
pathological changes that occur as a result of adaptive changes causes functional & structural problems
- myocyte apoptosis
- cytoskeletal alterations
- fibrosis (ECM-deposition)
increased volume of blood:
- stretches the ventricular wall, causing cardiac muscle to contract more forcefully
- frank-starling
myocardial hypertorphy
- myocyte size increase (# is not changed)
- protein synthesis increase
- enlarged nuclei
- numerous mitochondria
- increase in DNA ploidy
myocardial hypertrophy
- increase in size and weight of the heart
- work (hydrostatic pressure & volume overload)
- throphic signals (activation of beta receptors)
- pressure- wall thickness
- volume- ventricular dilation
cardiac dysfunction mechanisms
- adnormal myocardial metabolism
- alteration of intracellular Ca
- apoptosis of myocytes
- reprogramming of gene expression (miRNAs)
physiologic hypertrophy
- beneficial
- aerobic exercise associated with volume-load hypertrophy & increases in capillary density & decreases HR & BP
