Heart failure Flashcards
describe Ejection fraction and how it represents HF
- EJECTION FRACTION = (STROKE VOLUME / END DIASTOLIC VOLUME) * 100%
- HF with a preserved EF suggests the compensatory mech are able to sustain circulatory demands
- Conversely a low EF denotes cardiac congestion (more volume is staying in the ventricular chamber with each heart beat)
Describe the role of calcium cycling in HF
- calcium cycling impairs the contraction and relaxation of the myocytes and can contribute to the EXERCISE INTOLERANCE SUFFERED by patients with HF
–> upon exertion, the heart is functionally UNABLE to match the increased demand
describe RAAS
- becomes activated to mitigate the reduction in cardiac output by increasing sodium and water retention, vasoconstriction, and thirst
–> Long term, the RAAS also initiates remodeling processes within the heart and vasculature, promotes CNS dysfunction (sustained SNA) and can lead to electrolyte disturbances)
Role of angiotension II
- AngII activates ATI receptors and ATII receptors
- AT1 recetpors: –> vasoconstriction, hypertrophy, proliferation, increase thirst and sodium retention
- AT2 receptors: –> activate the adrenal gland to produce aldosterone
–> Heart –> fribrosis –> HF
–> kidney –> salt and fluid retention –> increase in blood pressure
Describe the activation of sympathetic nervous system in response to Cardiac failure
- Cardiac failure the metabolic demand is not met, the sympathetic nervous system is activated
- Sympathetic nervous system releases Epinephrine leading to INCREASE IN PERIPHERAL VASCULAR RESISTANCE which results in a reduction of perfusion (blood is centralized to body), increase in HR and contractility
Describe humoral changes in response to cardiac failure
- humoral changes include activation of vasoconstrictors, vasodilators, anti-natriuretic and anti-diuretic substances
- Contribute to the fluid retention, sustained sympathetic hyperactivitya nd futher cellular remodeling processes characteristic of decompensated HF
Systolic Dysfunction
- IMPAIRED CONTRACTILITY which causes REDUCTION IN CARDIAC OUTPUT
- Compensatory Mechanisms:
–> Increase preload (gets back to a better SV
–> increase contractility (Sympathetic;)
–> ventricular hypertrophy, elasticity (remodelling)
- patient with systolic dysfunction and low stroke volume can be given VASODILATOR to REDUCE AFTERLOAD allowing heart to eject a larger SV
Describe diastolic dysfunction
- DIASTOLIC DYSFUNCTION does NOT REDUCE stroke volume, but GENERATES HIGHER DIASTOLIC PRESSURES within ventricles leading to IMPAIRED FILLING (heart has to work harder to pump
- Occurs over time as hypertrophy and remodeling (fibrosis) compromises ventricular relaxation
- DIASTOLIC FUNCTION is IMPAIRED as a result of calcium cycling, decreased tissue compliance, increase ventricular stiffness and depressed ATP levels
- Initial reduction in Cardiac output reduces venous return and increases venous pressure (A–> B)
- Sympathetic nervous system is activated acutely to increase venous tone and increase cardiac output through increased fluid returning to heart (B–>C)
- Further neurohumoral activation, more fluid is retained and venous pressure increases (C–>D)
- As more and more fluid is retained, the failing heart cannot match the volume demand, causing greater increases in venous pressure (D–>E)
- This causes a downward spiral of fluid retention and cardiac congestion
HF symptoms
- Pulmonary and peripheral edema –> fluid accumulation in body (RAAS)
- Fatigue/exercise intolerance –> reduction in ejection fraction (Cardiac output)
- Confusion –> inadequate perfusion of the brain
- SHortness of breath –> pulmonary edema resulting in excessive ventilation
- Cachexia –> reduction of anabolism/increase in catabolism throughout the body
Describe treatment for HF
- Diruet = reduce volume
- ACEi, ARB = reduce remodeling, afterload, myocardial metabolic demand
- B-blocker = counter sympathetic effects
- statins = dyslipidemia + pleiotropic effects
