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Heart Failure

Mohammed Khasawneh Ru2ia Group 29 / 04 / 2010


Heart failure:
Pathophysiologic state in which an abnormality in cardiac muscle which is responsible for failure of the heart to pump blood to meet the metabolic demand of the body.. so there is increase in the metabolic demand and the heart cannot pump enough blood. Chronic heart failure in another word if there is a chronic situation its actually a clinical syndrome not one disease in which the different heart diseases can produce decrement in cardiac output and this will cause increase in venous return (increase venous pressure in the systemic venous pressure and pulmonary venous pressure) and this is accompanied by some molecular abnormality and will cause progressive deterioration in the failing heart and premature death of the myocardial cells when there is chronicity we are talking about progression its not only an acute thing that the heart fail actually this failure will cause some mechanisms working so the heart get worse and there will be damage to myocardial cells and more failure.

So how can the heart fail?

1- too much preload a lot of volume to the heart and at the end this will cause heart failureby stretching to the muscles at some point the muscle will lose its contractility as obvious by frank starling law and many causes in children can cause this like: a- left to right shunt in VSD which cause too much volume and the ventricle fail b- mitral regurgitation is non shunt problem because much of the volume that is pumped by the heart is going backward to the left atrium and back to left ventricle and back and forth btw the left atrium and left ventricle so the heart dilated then failure happen . c- complete heart block which cause sever bradycardia because of increase filling time of the ventricles so they dilate to accommodate all the blood and this will cause stretching of heart muscles then failure happen. 2- Too much after load which is a lot of resistance to the heart pumping out blood so this will cause increase in work load not increase stretching of heart muscles but increase work stress. a- hypertension. b- Coarctation of the aorta c- Obstructed or stenotic aortic arch. d- aortic stenosis. 3- Impaired contractility i.e. disease in the muscle itself the heart failure developed.. a- dilated cardiomyopathy so the problem is not the preload not the after load its actually the muscle itself. b- Myocarditis in adult very frequent example is ischemic heart disease.

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4- Impaired filling of the heart so the heart cannot pump enough blood because not receiving enough blood from the atrium to the left ventricle. a- hypertrophic cardiomyopathy can produce symptoms of heart failure because hypertrophic heart cannot fill enough so very thick heart and the lumen is very small so this will produce the symptoms of heart failure (tachypnia, difficulty in breathing and pulmonary edema). b- Constrictive pericarditis: if there is something restricting the heart from filling this will produce the fail symptoms of the heart like if the heart is fibrosis and stuked. Note: In dilated cardiomyopathy the lumen is dilated but the wall is normal or thin and the systolic function is failed in hypertrophic cardiomyopathy the wall is hypertrophied and the lumen decrease also the diastolic function is failed here.. Franck starling law: The x axis for the length of the muscle or stretch of the muscle which is proportional to the end diastolic pressure so how much u put volume u end up with high pressure in the atrium and in the y axis the cardiac output or the contractility in which more volume to the heart improve contractility up to a limit then we lose it if we stretch too much.. What are the causes of heart failure? 1- Congenital heart disease : A-volume overload like VSD and large ASD. b- Pressure overload like aortic stenosis and coarctation of the aorta. c- post operative patient with residual lesions so if u have a patient who underwent VSD closure they cut in the muscle through the heart so u have a heart with sutures the muscles is weaker and u have a residual lesion so more volume overload then heart failure. D-pulmonary vascular disease like pulmonary hypertension due to congenital heart disease e-chronic hypoxia and decrease saturation in pt who have cyanotic heart disease to below 60 and this might lead to diseased muscle or ischemia to the heart itself then heart fail. 2- Coronary artery disease is not that common but we have an entity of congenital coronary artery disease where u have the coronary coming out from the pulmonary artery or coming of as acute angle so this will induce ischemic changes to the heart and then failure developed. Acquired diseases of the coronary arteries the common ex is Kawasaki disease which can cause diseases in the coronary arteries. 3- Endocarditis might produce HF in different mechanisms most common is valvar dysfunction so if there is sever mitral regurgitation 2nd to endocarditis then HF developed because of volume load. 4- Incessant arrhythmia and this mean something that is really hidden you cannot detect it easily so you have a pt with heart rate is always 120 or above when you

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examine him he is 120 and he is 3 years old which is normal so you did not detect him until the heart fail because the heart does not restthere is tachycardia but its close to normal range so nobody detect it until HF happen. 5- Cardiomyopathy: a- Dilated. b- Hypertrophic. c- Constrictive where u have abnormality in the filling of the heart. d- Noncompaction which is common in neonate with metabolic disorders the myocardium here like a sponge full of holes and defects its a very primitive form of cardiomyopathy. e- Chronic anemia can cause HF because with chronic anemia the heart have to compensate by dilation and hypertrophy and tachycardia so HF happen bcoz the heart did not rest f- Eissenmengaer syndrome where you have a shunt that got through there all the time bcoz of pulmonary vascular disease those pt can have HF and primary pulmonary hypertension which might lead to HF in right and left ventricles. g- Corpulmonal which is HF 2nd to chronic lung disease. h- Rheumatic heart disease. i- Acquired dilated cardiomyopathy in pt who taking chemotherapy. What are the compensatory mechanisms in HF? 1- increase in the sympathetic tone cause increase in heart rate , vasoconstriction and increase in contractility so all of those are cause the heart to compensate for defect in cardiac muscle but with time this will induce problem increase heart rate obviously will increase cardiac output , vasoconstriction will maintain normal blood pressure so that is good initially and increase contractility those 3 things actually will increase cardiac work so the heart will need more o2 to himself with time ca+2 depletion happen in the myocyte because the sympathetic NS work by increase the availability of ca+2 so this will deplete it in cardiac muscles and decrease in contractility happenmore failure 2- rennin-angiotensin aldosteron system : salt and water retention with improvement of contractility through frank starling law angiotensin is also a potent vasoconstrictor so increase after load to maintain pressure and this will cause the renal system to be hyper responsive to natrioritic peptide that work to dauresis but the rennin a a system actually suppress this response of dauresis so this will cause increase in myocardial work again increase o2 needs with time this will cause pulmonary and venous congestion because of more fluid and over load so decrease contractility.. 3- Inflammatory response due to increase work stress but those mechanisms will cause the production of cytokines and free radicals so cause apoptosis or programmed cell death then fibrosis and decrease contractility. Why does dilation help?

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If u imagine the outer circle is the left ventricle in diastoly but the inner is systoly so when the heart contract there will be shortening in the diameter let us say about 50% the diameter was 1 then become 0.5 and let us say this shortening instead of being 50% become 25% so if the heart dilate then its actually maintain a normal cardiac output hear you have to think of volume if u have ejection fraction of 30% compared to ejection fraction of 70% one will say ohhh this is really bad but because the heart is dilated this will actually increase volume so the strok volume become normal or close so dilation helps but with time become a problemi.e. normal heart volume is let us say 100cc ejection fraction is 70%*100cc=70cc each beat the heart is pumbing..if ejection fraction now become 35%so the heart function is really bad so it will dilate and more volume in the heart lets say 200cc instead so 200cc*35%=70cc so its the same strok volume but with time those 200cc will actually fail.. Clinical features: 1- Tachycardia, cardiomegaly and gallop rhythm some of this is 2nd to sympathetic ns. 2- Cold extremities due to decrease perfusion. 3- Hypertension and skin mottling.. 4- Metabolic acidosis, decrease perfusion. Dyspnea, retraction and grunting because of hypertension in pulmonary vascular bed this is due to fluid overload. 5- Poor feeding and poor growth 2nd to difficulty in breathing. 6- Central cyanosis if there is pulmonary edema in the non compensated phase. 7- Peripheral cyanosis if you have only decrease perfusion but no pulmonary edema. 8- Hepatomegaly and peripheral edema because of increase venous pressure in systemic veins. 9- Exercise intolerance in older children. X ray in HF: 1-cardiomegaly. 2- Pulmonary edema (infiltrate the lung). Investigations: 1- ECG: cannot diagnose the cause of HF except you can detect if there is arrhythmia, ischemia and heart block. 2- BNP; brain natriuritic peptide in the diagnose. Follow up and management of HF it have a very good predictive value 90%+ for HF. 3- Exercise testing might help in some pt if u want to know there tolerance, peak o2 consumption, progression and improvement in HF . 4- Echocardiography can give u radio information in HF u see dilation in most pt so this picture is actually an m mode btw diastolic diameter and systolic one so this dimension is v big and the difference btw this dimension and the systolic one is v small that mean the contractility is v small this is the ventricular septum with time so here is diastoly systoly diastoly .and there is a posterior wall measure the diameter of the ventricle so u measure the diastolic dimension and the systolic one the difference btw the 2 is the shortening or the diameter shortening (contraction)

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so if this dimension is 7cm the normal is 5 to 5.5 so this is dilated and if the shortening fraction is 10% then this is abnormal and the normal btw 25%-45%. Echo can give u an idea about valve regurgitation cases like mitral regurgitation. Treatment: 1- Improve symptoms. 2- Slow the progression of ventricular remodeling because HF bring about more HF. 3- Improve survival In children we do not have any evidence based medicine regarding HF every thing come from adult literature about tx of HF. Acute management: 1-inotrops to support the heart. 2-diuresis due to volume overload. 3-vasodilator to decrease after load so you give some rest to the heart and improve the perfusion to tissue. In chronic tx of HF: 1-diuresis : it helps because it decrease volume overload but on the other hand it stimulate the sympathetic nervous system because of less volume this will also stimulate the aldosteron system the only diuretic that is showed to improve survival in adults is aldosteron which is actually weak diuretic but decrease mortality. 2- digoxin is very old medication was used for HF by inhibition of na+ _k+ ATPase and this will increase the intracellular back k+ ..This will inhibit the na+ _ca2+ exchange so this will increase the intracellular ca2+ increase the bioavailability in the myocytes and increase the contractility.. It also decrease the sympathetic tone so improve the symptoms and decrease the hospital stay.. 4- ACE-inhibitors : Angiotensen converting enzymes inhibitors it causes vasodilatation because angiotensen 2 is vasoconstrictor it causes favorable ventricular remodeling its slows down bad remodeling so it helps in the long term causes improvement in renal function and block the hypertrophic event of angiotensen 2 so improve cardiac output improve filling pressure and improve symptoms.. 5- angiotensen receptor antagonists have the same effect of ACE inhibitor.. 6- B-blockers : decrease work stress , decrease HR , decrease myocardial demand so decrease sympathetic activity cause improvement in cardiac function but this improvement happen delayed 2-3 months after the initial therapy so if u start with b-blocker u actually make the pt worse so u give them after u stabilize the patientcarpetalol?? which is vasodilator , antioxidant and antiprolferative.. 7- BNP analogue : manufactured by recombinant DNA very helpful cause dauresis ,vasodilatation , decrease sympathetic and renien angiotensen aldosteron so protect the heart.

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8- Resynchronization therapy : If u have a pt with conduction delay and wide QRS in ECG that means the Ventricle is not contract all at the time so part of the wall contract later on the Other wall contract and this is not effective synchronization mean all the Ventricles s should contract at the same time homogenous contraction. 9- Heart transplantation for end stage HF. 10- Ventricular assessment devices. 11- Using multipotential stem cells inject them within the myocardium to produce new myocardial cells. Notes from here and there in the lecture: #dilated cardiomyopathy have nothing to do with the atrium because the atrium myocytes thin so the atrium is not really contribute to cardiac output about 20% so the myopathy happen in the ventricles and when we talk about HF its really ventricular failure not atrial failure BUT??.....its a chain primarily the ventricles fail then the atrium will dilate because of increase pressure when ventricles dilate the end systolic volume increase so the atrium will empty in an already filled ventricles so the atrial pressure increase and venous pressure increase so venous congestion happen in the lungs and body..obs! # Heart block rule in HF: Due to decrease heart rate the diastolic phase is longer so more filling of the heart so basically the heart try to pump same amount put in less heart beat and instead of pumping 5 liters in 100 beats it pump 5L in 50 beats so it has to double the volume then dilation of the heart happen then FAILUREnice!

The end! Done by: Mais jzzazi

www.SAWA2006.com

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