. 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
Frank-Starling mechanism
he strength of the heart’s systolic contraction is directly proportional to its diastolic expansion
effect of Ventricular remodeling in CHF
change of heart shape structure and function to increase CO
Classification of drugs for the treatment of CCF-
drugs alleiviating symptoms
drugs reducing morbidity
Drugs affecting the mortality/morbidity ratio
ACE inhibitors
Angiotensin receptor blockers
β- blockers
Aldosterone antagonists
drugs alleiviating symptoms
diuretic - odema is major symp
Cardiac glycosides
dobutamine
drugs prescribied in NYHA Class 1
mortality drugs
ACEI
ARB- if ace is CI
Beta blockers after MI
symp
NONE
drugs prescribied in NYHA Class 2
mortality drugs
ACEI
ARB- if ace is CI
Beta blockers after MI
symp
diuretic according oedema presence
drugs prescribied in NYHA Class 3
mortality mod
ACEi/ ARB combined w.
beta blocker / aldosterone antag
symp
-cardiac glycoside or diuretic
drugs prescribied in NYHA Class 4
mortality mod
ACEi/ ARB combined w.
beta blocker / aldosterone antag
symp
- CG
- Diuretic
- inotropic drugs
- dobutamine
