ุนุฌุฒ ุงูููุจ ุจูู ู
ุญุงูุฑู ุูุจุดูู ู
ุจุณุท ุฌุฏุง
Heart Failure
Definition: is a condition in which the heart is unable to pump sufficient amount of blood to maintain blood flow to meet the body's demand.
-Mild to moderate degree be symptomatic during exercise.
-Sever degree symptomatic even during test.
Some classifications of heart failure:
1-according to pathophysiology :High ,low (COP) heart failure.
2-according to clinical presentation (signs,symptoms):left,right,biventricular heart failure.
3-according to management or onset :acute ,chronic heart failure.
[According to pathophysiological classification:]
Notes:
COP=Stroke volumeรHeart rate
SV=End diastolic volume -End systolic volume
EDV:called preload,the volume and pressure of blood in ventricles at the end of diastole (dilation),so is the capacity of stretching.
ESV:called afterload,the volume and pressure of blood in ventricles during systole.
So is the force of contraction .
According to starling law: Force of contraction related directly to Capacity of stretching,
So when there is increase in preload ,there is related increasing in afterload .
Contractility:is intrinsic ability of myocardium for forceful contraction at given fiber length.
SV depends on:
1-preload,
2-afterload, >>any defect in these mechanisms lead to heart failure.
3-contractility,
A-Low COP heart failure:causes,
1-increase of preload,chronic volume overload:
-aortic ,mitral valves regurgitation (Lt HF).
-VSD,ASD (Right HF).
2-decrease of preload(inflow obstruction) :mitral,tricuspid valves stenosis.
3-increase of afterload (outflow obstruction):
-hypertension, aortic valve stenosis (Lt HF).
-Pulmonary hypertension ,pulmonary valve stenosis (Rt HF).
-diastolic dysfunction:constrictive pericarditis,restrictive cardiomyopathy,cardiac lemonade.
4-decrease contractility :
-MI.
-Myocarditis.
-Cardiomyopathies
5-arrythmias:[Atrial fibrillation,CHB,tachycardia]
Mechanisms:
1-hypertrophy of smooth muscle lead to obstruct the flow of coronary arteries lead to ischemia and necrosis and increase of demand.
2-decrease the preload lead to decrease the afterload.
3-decrease the contractility .
4-tachycardia leads to fatigue of myocardium and decrease filling time,
bradycardia ,decrease the contractility leads to heart failure even SV is normal.
B-High COP heart failure:
In condition that the body gets a hyper dynamic circulation:
1-Thyrotoxicosis.
2-Chronic sever anemia.
3-Beri-beri syndrom.
4-Pagetโs disease of bone.
5-AV fistula.
In high COP Hf the pulse rate may be wide >60mmgh.
Note:Compensatory mechanism of body to activate RAAS,SNS in low COP lead to increase load on myocardium end by hypertrophy and ischemia.
[According to clinical presentation:]
1-left side HF:
Causes:[systemic HTN, valvular heart diseases,MI,CAD,AF,drugs or alcohol,myocarditis,cardiomyopathy,immune disorder]
Presentation:
-pulmonary oedem(crackles).
-hypoxia(SaPo2<90%).
-tachypnea.
-SOB.
-displaced Apex beat.
*cardiac asthma may occurs.
2-Right side HF:
Causes:[chronic lung disease^corpulmonale^,pulmonary hypertension,pulmonary valve stenosis,ASD,VSD,myocarditis,cardiomyopathy].
Pesentation:
-peripheral odema.
-ascites.
-elevated JVP.
-hepatospleenomegaly.
-ventricular heaven.
Management :
1-Investigation.
2Treatment.
Investigation:
1-X-ray: features of HF in x-ray are,
-enlargement of cardiac silhouette.
-septal or kerly B line .
-reticular shadow of alveolar odema.
-prominent of blood vessels of upper lobe of lung.
-enlargement of hilar vessels.
-cardiac-thoracislc ratio>0.5
-absence of costophrenic angle.
-splaying of carina>90degree
-convex LA appendage
-double density sign with distant from carina >7cm
2-Echo,
For assessment of severity ,determines if there is valvular heart disease,and in follow up.
3-Blood test:
-CBC.
-serum urea,creatinine.
-Hemoglobin,to exclude anemia.
-Thyroid fuction test,to exclude thyrotoxicosis,
-LFT,RFT.
-c-reactive protein.
-cardia
c markers of MI is suspected .