Heart Failure AHMED M. ALJABRI Prof. Dr. OSAMA M. IBRAHIM Done by :

Heart Failure AHMED M. ALJABRI Prof. Dr. OSAMA M. IBRAHIM Done by :
Under supervision of : Prof. Dr. OSAMA M. IBRAHIM

Outlines Introduction & Epidemiology. Pathophysiology.
Classifications. Signs & Symptoms. Diagnosis. Treatment. Key points.

Introduction Heart Failure ( HF ) : a progressive , complex clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body. Heart failure is the final common pathway for numerous cardiac disorders including those affecting the pericardium, heart valves, and myocardium.

Introduction ( cont.) The primary manifestations of the syndrome are dyspnea, fatigue, and fluid retention. Diseases that adversely affect ventricular diastole (filling , relaxation), ventricular systole (contraction), or both can lead to heart failure. The leading causes of heart failure are coronary artery disease and hypertension.

Introduction ( cont.) For many years it was believed that reduced myocardial contractility, or systolic dysfunction (i.e., reduced left ventricular ejection fraction [LVEF]), was the sole disturbance in cardiac function responsible for heart failure.

Introduction ( cont.) However, it is now recognized that large numbers of patients with the heart failure syndrome have relatively normal systolic function (i.e., normal LVEF). This is now referred to as heart failure with preserved LVEF and is believed to be primarily caused by diastolic dysfunction of the heart. ( 20% to 60% of patients with heart failure )

Introduction ( cont.) However, regardless of the etiology of heart failure, the underlying pathophysiologic process and principal clinical manifestations (fatigue, dyspnea, and volume overload) are similar and appear to be independent of the initial cause.

Introduction ( cont.) Historically, this disorder was commonly referred to as congestive heart failure; the preferred nomenclature is now heart failure because a patient can have the clinical syndrome of heart failure without having symptoms of congestion.

Introduction ( cont.) These disorders activate a number of cardiac and peripheral neurohormonal compensatory adaptive responses which with continued stimulation become maladaptive and ultimately affect fluid retention , mortality , disease progression. However, a subgroup of patient with LV dysfunction are asymptomatic ( HF without symptoms ).

Epidemiology Approximately 5 million Americans have heart failure with an additional 550,000 cases diagnosed each year. (1) Unlike most other cardiovascular diseases, the incidence, prevalence, and hospitalization rates associated with heart failure are increasing and are expected to continue to increase over the next few decades as the population ages. 1. Gheorghiade M, Sopko G, De Luca L, et al. Navigating the crossroads of coronary artery disease and heart failure. Circulation 2006;114:1202–1213..

Epidemiology (cont.) A large majority of patients with heart failure are elderly, with multiple comorbid conditions that influence morbidity and mortality. The incidence of heart failure doubles with each decade of life and affects nearly 10% of individuals older than age 75 years.(2) 2. Rosamond W, Flegal K, Friday G, al. Heart disease and stroke statistics—2007 update: A report from thet e American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation 2007;115:e69–e171

Epidemiology (cont.) Heart failure is more common in men than in women until age 65 years. Current estimates suggest annual expenditures for heart failure of approximately $33 billion, with the majority of these costs spent on hospitalized patients. (2)

Epidemiology (cont.) Although the mortality rates have declined over the last 50 years, the overall 5-year survival remains approximately 50% for all patients with a diagnosis of heart failure, with mortality increasing with symptom severity.(2)

Excessive work demands Impaired cardiac function
Increased pressure work : Systemic hypertension Pulmonary hypertension Coarctation of the aorta Loss of myocardial tissues (Myocardial diseases) : Cardiomyopathies √ Myocarditis Coronary insufficienc √ Myocardial infarction Increased volume work : Arteriovenous shunt Excessive administration of intravenous fluids Valvular diseases : Stenotic valvular diseases Regurgitant valvular diseases Increased perfusion work : Thyrotoxicosis Anemia Congenital pericarditis : Constructive pericarditis Etiology

Pathophysiology To understand the pathophysiologic processes in heart failure, a basic understanding of normal cardiac function is necessary. The relationship between CO and mean arterial pressure (MAP) is MAP = CO × systemic vascular resistance (SVR)

Pathophysiology (cont.)
Cardiac output (CO) is defined as : the volume of blood ejected per unit time (L/min) and it is the product of heart rate (HR) and stroke volume (SV): CO = HR × SV Heart rate is controlled by the autonomic nervous system.

Stroke volume, or the volume of blood ejected during systole, is equal to : the difference between the ventricular end-diastolic volume (EDV) and the end- systolic volume (ESV). SV = EDV – ESV

The EDV is : the filled volume of the ventricle prior to contraction. The ESV is : the residual volume of blood remaining in the ventricle after ejection. In a typical heart, the EDV is about 120 ml of blood and the ESV about 50 ml of blood.

The difference in these two volumes, 70 ml, represents the SV. Therefore, any factor that alters either the EDV or the ESV will change SV. SV depends on : Afterload, preload, and contractility.

Afterload : Pressure that the chamber or ventricle has to generate to eject the blood out. It is affected by : arterial blood pressure. Systemic vascular resistance is the primary determinant of Afterload load.

Preload : Pressure on ventricle after contraction during filling It is affected by : 1) venous blood pressure ( volume of blood ) 2) Rate of venous return ( vein tone )

Left ventricular end-diastolic pressure (LVEDP) is the primary determinant of preload (used in the clinical setting to estimate preload ), estimated clinically by measuring the pulmonary capillary wedge pressure ( PCWP ) with a Swan-Ganz catheter, normal level : 5-15 mmHG

The decrease in the heart’s pumping capacity results in the heart having to rely on compensatory responses ( hemodynamic and neurohormonal changes ) to maintain an adequate cardiac output. These compensatory responses include :

(1) Preload through the Frank-Starling mechanism, whereby an increase in venous return to the heart will increase the EDV of the ventricle, which stretches the muscle fibers thereby increasing their preload, This leads to an increase in the force of ventricular contraction and CO.

(2) Tachycardia and increased contractility through sympathetic nervous system (SNS) activation, primarily due to release of norepinephrine (NE) (3) Vasoconstriction: A number of neurohormones likely contribute to the vasoconstriction, including NE, angiotensin II, endothelin-1, and arginine vasopressin (AVP).

(4) Venricular hypertrophy & remodeling : Ventricular hypertrophy is a term used to describe an increase in ventricular muscle mass. Cardiac or ventricular remodeling is a broader term describing changes in both myocardial cells and extracellular matrix that result in changes in the size, shape, structure, and function of the heart.

Key elemnts involved in ventricular remodeling

These compensatory responses are intended to be short-term responses to maintain circulatory homeostasis after acute reductions in blood pressure or renal perfusion. However, the persistent decline results in long- term activation of these compensatory responses, resulting in initiation and progression o fHF.

In addition to neurohormones, several proinflammatory cytokines such as TNF-α have a role in heart failure pathophysiology. TNF-α produces multiple deleterious actions, including negative inotropic effects, increasing myocardial cell apoptosis, and stimulating remodeling via several mechanisms.

HF may be classified based on
Classifications HF may be classified based on CO Cardiac Function Side of The Heart Onset of Symptom NYHA & ACC/AHA Low output HIGH OUTPUT Rt. Sided HF Lt. sided HF Acute HF Diastolic HF Systolic HF Chronic HF

Classifications (cont.)
According to Cardiac output : 1)- High output HF : It is uncommon type of HF , The function of the heart may be supranormal but inadequate owing to excessive metabolic need for cardiac output. Causes : 1) Severe anemia. 2) Thyrotoxicosis.

2)-Low output HF : The function of the heart is inadequate to meet tissues needs of blood. caused by : disorder that impair the pumping ability of the heart such as : IHD , Cardiomyopathy.

In term of function : 1)- Systolic dysfunction : There is impaired ejection of blood from the heart during systole & cardiac contractility

ejection fraction : It's the Percent of the total amount of LV volume expelled during systole , normal EF ≥ 50 % EF misleading may occurred with mitral stenosis , aortic regurgitation. Causes : Conditions that impairs the contractile performance of the heart ex. IHD, Cardiomyopathy. Increase pressure work on the heart ex. HTN , Valvular stenosis.

2)- Diastolic dysfunction : it account for 40% of all cases of HF. There is impaired filling of the ventricles during diastole, characterized by decreased the ability to stretch during filling, so the congestive symptoms are predominate in diastolic dysfunction.

Causes : Conditions that increase ventricular wall thickness ( ex. Myocardial hypertrophy ), conditions that delay diastolic relaxation ex. IHD , aging ( ventricular stiffness )

According to the side of the heart : 1)- Right sided HF : Impairs the ability to move deoxygenated blood from the systemic circulation into pulmonary circulation, consequently, a dam back of blood occurs, leading to its accumulation in the systemic venous system.

A major effect of Rt.sided HF is peripheral edema. Causes : Persistence left sided heart HF. Acute or chronic pulmonary diseases ex. pulmonary HTN. Conditions that weaken the heart muscle or restrict blood flow into lung ex. tricuspid or pulmonary valve regurgitation.

2)- Left sided HF : Impairs the pumping of blood from pulmonary circulation into arterial side of the systematic circulation, as a results : There is a decrease in CO, Increase in LVEDP, Congestion in the pulmonary circulation.

Pulmonary edema symptoms often occur at night after the person has been reclining & gravitational force has been removed from the circulatory system, the edema fluid that had been sequestered in lower extremities is redistributed into the pulmonary circulation.

Based on onset of symptoms : Acute HF : sudden onset of signs and symptoms of HF. Chronic HF : secondary to slow structural changes occurring in the stressed myocardium. Acute decompensation : sudden exacerbation or worsening of symptoms in chronic HF.

II Symptoms with minimal exercise
ACC/AHA HF stage NYHA functional class A At high risk for HF but without structural heart disease or symptoms None B Structural disease but without HF I Asymptomatic C Structural heart disease with prior or current HF symptoms II Symptoms with minimal exercise III Symptoms with moderate exercise. D Refractory HF requiring specialized interventions IV Symptomatic at rest

SIGNS & Symptoms Although most patients initially have LVF, and because LVF increases the workload of the right ventricle, both ventricles eventually fail and contribute to the heart failure syndrome. Because of the complex nature of this syndrome, it has become exceedingly more difficult to attribute a specific sign or symptom as caused by either RVF or LVF.

SIGNS & Symptoms Systemic or peripheral tissues congestion
Rt. Sided HF Lt. Sided HF Systemic or peripheral tissues congestion Pulmonary congestion & CO Impaired gas exchange Pulmonary edema Jugular venous distension Ascites Hepatomegaly Splenomegaly Lower limb edema Cyanosis Activity intolerance Signs of hypoxia Orthpnea Paroxismal nocturnal dyspnea Bibasilar rales

Diagnosis (cont.) No single test is available to confirm the diagnosis of heart failure. Heart failure often is suspected initially in a patient based on the symptoms & history. Measurement of B-type natriuretic peptide (BNP) may assist in differentiating dyspnea caused by heart failure from other causes.

Diagnosis (cont.) BNP is elevated in patients with heart failure and thought to balance the effects of the RAA system by causing natriuresis, diuresis, vasodilation, decreased aldosterone release, decreased hypertrophy.

Diagnosis (cont.) There are no specific ECG findings associated with heart failure. The echocardiogram can determine the presence of systolic and/or diastolic dysfunction and the left ventricular ejection fraction (LVEF).

Goals of treatment Improve the patient’s quality of life.
Reduce symptoms & hospitalizations. Slow progression of the disease process.

Goals of treatment (cont.)
Prolong survival. Identification of risk factors for heart failure and preventing the development of this disorder.

Treatment ( non pharmacological )
The first step in the management of chronic heart failure is to determine the etiology and/or any precipitating factors. Treatment of underlying disorders such as anemia or hyperthyroidism may avoid the need for treatment of heart failure.

Restriction of fluid intake and dietary sodium is an important intervention. Restriction of physical activity reduces cardiac workload and it is recommended for virtually all patients with acute congestive symptoms.

However, once the patient’s symptoms have stabilized and excess fluid is removed, restrictions on physical activity are discouraged.

Treatment ( pharmacological )
Although dietary sodium and water restriction should be instituted in all heart failure patients, pharmacologic therapy is required for slowing disease progression and prolonging survival and usually is necessary for control of symptoms.

Current American College of Cardiology/ American Heart Association(ACC/AHA) treatment guidelines are organized around the four identified stages of heart failure. This staging system emphasizes the progressive nature of the disorder and targets treatment to prevent or slow the progression of heart failure.

B C D A Treatment Description Stage
Lifestyle modification, smoking cessation; treat hyperlipidemia and use ACEI for HTN No structural heart disease and no symptoms but risk factors: CAD, HTN, DM, cardiotoxins, familial cardiomyopathy A β- blockers Lifestyle modifications, adrenergic blockers, ACEI. Abnormal LV systolic function, MI, valvular heart disease but no HF symptoms B Lifestyle modifications, ACEI, β-blockers, diuretics, digoxin Structural heart disease and HF symptoms C Therapy listed under A, B, C and mechanical assist device, heart transplantation, continuous IV inotropic infusion, hospice care in selected patients Refractory HF symptoms to maximal medical management D

STANDARD FIRST-LINE THERAPIES : Angiotensin Converting Enzyme Inhibitors ( ACEI ) β- blockers Diuretic Digoxin Alternative or for selected patients : Angiotensin II- Receptor Blockers ( ARB ) Vasodilators: (Hydralazine/Nitrate)

ACE Inhibitors ACE inhibitors are the cornerstone of pharmacotherapy of patients with heart failure. MOA : By blocking the production of angiotensin II and, in turn, aldosterone is decreased.

ACE Inhibitors This attenuates many of the deleterious effects including reducing ventricular remodeling myocardial fibrosis, cardiac hypertrophy, and Na & H2O retention.

ACE Inhibitors Vasodilatation ( arterio dilatation & venodilatation) : The endogenous vasodilator bradykinin, which is inactivated by ACE, is also increased by ACE inhibitors,along with the release of vasodilatory PG & histamine.

ACE Inhibitors The beneficial effect of ACE inhibitors on mortality has been documented conclusively, with numerous trials showing a 20% to 30% relative reduction in mortality with ACE inhibitor therapy compared with placebo.

ACE Inhibitors In addition to improving survival, ACE inhibitors also reduce the combined risk of death or hospitalization, slow the progression of heart failure, and reduce the rates of reinfarction. The benefit occurs within the first few days of therapy and persists during long-term treatment.

ACE Inhibitors The benefits are independent of the etiology of heart failure and are observed in patients with mild, moderate, or severe symptoms. ACE inhibitors clearly are superior to vasodilator therapy with hydralazine-isosorbide dinitrate.

ACE Inhibitors ACE inhibitors also are effective for prevention of heart failure. No dose-dependent differences in mortality have been reported for ACEinhibitors.

ACE Inhibitors Side effects : Dry cough. First dose hypotension. Hyperkalemia. Acute renal failure. Angioedema. Contraindications : Pregnancy. Bilateral renal artery stenosis. Hypotension.

Initial dose Target dose

ARB The current ACC/AHA guidelines recommend the use of ARBs in patients who are unable to tolerate ACE inhibitors. The primary clinical trials supporting the use of these agents in heart failure used either valsartan or candesartan.

ARB ARBs are not an alternative in patients with hypotension, hyperkalemia, or renal insufficiency secondary to ACE inhibitors because they are as likely to cause these adverse effects. For patients who are unable to tolerate an ACE inhibitor because of cough or angioedema, an ARB is recommended as the first-line alternative.

β-blockers β-blockers have been shown to prolong survival, decrease hospitalizations reduce morbidity and mortality , and cause “reverse remodeling”. Many studies show improvements in NYHA functional class, β-blockers should be used in all stable patients with heart failure and a reduced left ventricular ejection fraction in the absence of contraindication.

β-blockers MOA : It seems likely that the mechanisms of benefit include antiarrhythmic effects, slowing or reversing the detrimental ventricular remodeling caused by sympathetic stimulation, Up-regulation of β 1 receptors , decreased myocyte death from catecholamine-induced necrosis or apoptosis.

β-blockers In addition, there is evidence that response to β-blockers is dose dependent. Therapy must be instituted at low doses, with slow upward titration to the target dose.

β-blockers 1/10 the final dose is typically starting dose, with doses doubling no more frequently than every 2 weeks until the target dose is reached. Therapy is generally limited to either carvedilol or metoprolol and there is no compelling evidence that one drug is superior to the other.

β-blockers Side effects : Bronchspasm. Bradycardia. Impaired glycemic control. Contraindications : Bradycardia. AV Block . Hypotension. Acute exacerbation of HF.

Initial dose Target dose

Diuretics Diuretic therapy is recommended in all patients with clinical evidence of fluid retention. Among the drugs used to manage heart failure, diuretics are the most rapid in producing symptomatic benefits.

Diuretics Because diuretics do not alter disease progression or prolong survival, they are not considered mandatory therapy. Thus patients who do not have fluid retention would not require diuretic therapy.

Diuretics The primary goal of diuretic therapy is to reduce symptoms associated with fluid retention, improve exercise tolerance and quality of life, and reduce hospitalizations from heart failure. They accomplish this by decreasing pulmonary and peripheral edema through reduction of preload.

Diuretics Diuretic therapy is usually initiated in low doses with dosage adjustments based on symptom assessment and daily body weight. Change in body weight is a sensitive marker of fluid retention or loss.

Diuretics Thiazide Diuretics: MOA : Thiazide diuretics such as hydrochlorothiazide block sodium and chloride reabsorption in the distal convoluted tubule . Consequently, the thiazides are relatively weak diuretics and infrequently are used alone in heart failure.

Diuretics Thiazide diuretics may be preferred in patients with only mild fluid retention and elevated blood pressure because of their more persistent antihypertensive effects compared to loop diuretics.

Diuretics Loop Diuretics: MOA : They act by inhibiting a Na-K-2Cl transporter in the loop of Henle, where 20% to 25% of filtered sodium normally is reabsorbed. Loop diuretics also induce a prostaglandin-mediated increase in renal blood flow, which contributes to their natriuretic effect.

Diuretics Unlike thiazides, loop diuretics maintain their effectiveness in the presence of impaired renal function. doses above the recommended ceiling doses produce no additional diuresis & thus, once the ceiling dose is reached, it is recommended to give the diuretic more frequently for additional effect rather than to give progressively higher doses.

Diuretics Side effects : Hypokalemia Hypomagnesamia. Hyperlipidemia Hyperglycemia Contraindications : Pregnancy Renal failure (only thiazide)

Diuretics Aldosterone antagonist : Spironolactone and eplerenone are aldosterone antagonists that work by blocking the mineralocorticoid receptor, the target site for aldosterone. Although the diuretic effects are minimal, the potassium-sparing effects can have significant consequences.

Diuretics Recent evidence suggests that it may improve survival in CHF patients because aldosterone antagonists inhibit cardiac extracellular matrix and collagen deposition, thereby attenuating cardiac fibrosis and ventricular remodeling.

Diuretics Side effects : Hyperkalemia. Gynecomastia. Metabolic acidosis. Contraindications : Hyperkalaemia Concurrent use of other potassium-sparing products. Renal failure

Digoxin A number of clinical trials have shown that digoxin improves LVEF, quality of life, exercise tolerance, and HF symptoms. MOA : +Ve inotropic effect by ↑ intracellular Ca. Vagotonic effect. Antrrhythmogenic effect.

Digoxin Most of the benefits from digoxin is achieved at low plasma concentrations and little additional effect is achieved with higher doses. Thus, for most patients, the target digoxin plasma concentration should be 0.5 to 1.0 ng/mL.

Digoxin This plasma concentration range can be achieved with a daily dose of mg. This target would also be expected to decrease the risk of adverse effects from digoxin toxicity.

Digoxin digoxin should not be used in patients with a normal LVEF, sinus rhythm, and no history of heart failure symptoms, because the risk is not balanced by any known benefit.

Digoxin Side effects & toxicity: Vomiting. Bradycardia. Heart block. Visual disturbance. Contraindications : Renal disease. Ventricular arrythmia. Heart block.

Vsodilators Preload : By Venodilators , ex: Nitrate “ Isosorbide dinitrate, ISDN” ( GMP ) Afterload : By arteriodilators, ex: Hydralazin (direct arteriodilator)

Vsodilators ISDN and hydralazine were combined originally in the treatment of heart failure because of their complementary hemodynamic actions. It is suggested that African Americans have less nitric oxide than do non- African Americans, and thus, may derive particular benefit from therapy that enhances nitric oxide bioavailability.

Vsodilators Hydralazine and ISDN is appropriate as first-line therapy in patients unable to tolerate either an ACE inhibitor or ARB because of renal insufficiency, hyperkalemia, or possibly hypotension.

Vasodilators Side effects : headache, dizziness, and gastrointestinal distress

Anticoagulant : ( Warfarin ) It is used in case of : Biventricular dysfunction ( Systole & Diastol ). Sever LV dilatation. Atrial fibrillation. History of embolic episodes.

Antiarrythmics : Calcium channel blockers with negative inotropic effects, such as verapamil or diltiazem, should be avoided. Amiodarone is a reasonable alternative for rate control in those patients who are not responding to digoxin and/or β-blockers or who have contraindications to these agents.

Treatment of acute decompansated HF : IV Positive inotropic agents: the drugs that improve myocardial contractility . (β adrenergic agonists, dopaminergic agents, phosphodiesterase inhibitors), dopamine, dobutamine, milrinone, amrinone, nitroglycerin. IV fuerosemide Goals of tratment : relieve congestion well as treat symptoms of low cardiac output

Nesiritide : Nesiritide is the first new drug approved for the treatment of decompensated heart failure since milrinone. Manufactured by recombinant techniques, it is identical to the endogenous human BNP.

MOA : Mimics the vasodilatory and natriuretic actions of the endogenous peptideby stimulating the natriuretic peptide receptor A which leads to increased levels of cyclic guanosine monophosphate in target tissues.

Nesiritide produces dose-dependent venous and arterial vasodilation, increases in cardiac output, natriuresis, and diuresis, and decreases cardiac filling pressures, SNS and RAAS activity.

Key Points Heart failure is a clinical syndrome caused by the inability of the heart to pump sufficient blood to meet the metabolic needs of the body. Heart failure can result from any disorder that reduces ventricular filling (diastolic dysfunction) and/or myocardial contractility (systolic dysfunction).

Key Points (cont.) There are many classifications for HF.
The primary manifestations of the syndrome are dyspnea, fatigue, and fluid retention. The leading causes of heart failure are coronary artery disease and hypertension.

Key Points (cont.) Heart failure is a progressive disorder that begins with myocardial injury. In response to the injury, a number of compensatory responses are activated which are responsible for the symptoms of heart failure and contribute to disease progression.

Key Points (cont.) Most patients with symptomatic heart failure should be routinely treated with ACE inhibitor, β-blocker, and diuretic. The benefits of these medications on slowing heart failure progression, reducing morbidity and mortality, and improving symptoms are clearly established.

Key Points (cont.) Patients should be treated with a diuretic if there is evidence of fluid retention. Treatment with digoxin may also be considered to improve symptoms and reduce hospitalizations.

Key Points (cont.) The combination of hydralazine and nitrates improves the composite end point of mortality, hospitalizations for heart failure, and quality of life in African Americans who receive standard therapy. Treatment goals for acute decompensated heart failure are directed toward restoration of systemic oxygen transport and tissue perfusion.

References Joseph T. DiPiro, et al. Pharmacotherapy :
A Pathophysiologic Approach . The McGraw-Hill Companies. Seventh Edition , 2008, Chapter 16, page : Frederic S. Bongard, Darryl Y. Sue, Janine R. E. Vintch, Current Critical Care Diagnosis and Treatment, McGraw-Hill Professional,Third edition , 2008, page: Mary Anne Koda-Kimble, Lloyd Yee Young , et al .Hand Book Of Applied Therapeutics.Lippincott Williams & Wilkins. Eighth edition, 2007, Chapter 18 , page : Daniel H. Cooper, et al. Washington Manual of Medical Therapeutics. Therapeutics. Lippincott Williams & Wilkins. 32ed Edition, 2007, Chapter 6, page:

Parameter Value end-diastolic volume (EDV) 120 ml end-systolic volume (ESV) 50 ml stroke volume (SV) 70 ml ejection fraction (Ef) 58% heart rate (HR) 70 bpm cardiac output (CO) 4.9 L/m

For example: EDV= , ESV= 50 EF = / 120 = 0.58 = 58 %

Heart Failure AHMED M. ALJABRI Prof. Dr. OSAMA M. IBRAHIM Done by :

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