. Clinical and pharmacological approaches in the treatment of chronic heart failure Flashcards
chronic heart failure defiinition
syndrome, due to systolic and/or diastolic dysfunction of the cardiac muscle, leading to dyspnea and fatigue as a result of reduced CO
types of
According to the output:
-low output/ high output
According to the affected side
-LHF/RHF
According to the clinical course
- acute/ chronic
which type of output is most common
Low-output heart failure - 95%
can be systolic or diastolic
describe systolic low output HF
heart muscle loses its ability to contract (systolic dysfunction).
Characterised by;
-decreased cardiac output
-decreased left ventricular ejection fraction (LVEF)
describe diastolic low output HF
heart muscle becomes stiff and doesn’t fill with blood easily (diastolic dysfunction)
characterised by:
- elevated left and right ventricular end-diastolic pressures (heart muscle wont relax)
- normal LVEF
conditions causing High-Output Heart Failure
peripheral shunting (A-V fistula), - heart pumps more but blood is still lost
low-systemic vascular resistance,
hyperthyroidism,
anemia,
pregnancy, etc
what is Left-sided heart failure
inefficient contraction of the left ventricle to supply oxygenated blood to body
- chronic hypertension
- valve defects
what is Right-sided heart failure
failure of the right ventricle:
2nd to LHF / pulm diseases
Acute HF
Dramatic drop in cardiac output
short course of hours to days
causes
- sepsis
- acute mi
Chronic HF
long term processes assoc w/ comp changes of the heart that no longer produce sufficient EF
new york heart assoc of heart failure
Class 0- no complaints
Class 1- without symptoms in heavy exercise
Class 2- decreased physical capacity and complaints of fatigue with usual physical exercises
Class 3- significantly decreased physical capacity and complaints of fatigue and dyspnea with low intensity physical efforts
Class 4- complaints at rest
CHF Stages-according to the structural changes of the heart
Stage A- no structural or functional changes in the heart, no symptoms, but the patient is at high risk of developing HF
Stage B- minimal structural or functional changes in the heart, but no symptoms
Stage C
C1- changes in the heart, plus present symptoms of CCF
C2- advanced changes in the heart, plus present symptoms of CCF
Stage D- patient with advanced cardiac disease and marked symptoms of CCF at rest, who’s given the maximal therapy needed, but remains uncompensated.
Pathophysiological mechanisms of compensation in HF
4
Neurohormonal activation
RAAS activation
Frank-Starling mechanism
Ventricular remodeling-
Neurohormonal activation in CHF (sympathetic)
Increases ventricular contractility and heart rate
Systemic and pulmonary vasoconstriction
Stimulates secretion of renin from juxtaglomerular apparatus of the kidney
effect of angiotensin in CHF
- V.C
norepinephrine (symp activity)
-synthesis and secretion of aldosterone which leads to: sodium and water retention
