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Heart Failure

Heart Failure. Done by : AHMED M. ALJABRI Under supervision of : Prof. Dr. OSAMA M. IBRAHIM. Outlines. Introduction & Epidemiology. Pathophysiology . Classifications. Signs & Symptoms. Diagnosis. Treatment. Key points. Introduction.

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Heart Failure

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

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

  3. 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.

  4. 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.

  5. 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.

  6. 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 )

  7. 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.

  8. 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.

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

  10. 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..

  11. 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

  12. 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)

  13. 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)

  14. Etiology

  15. 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)

  16. 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.

  17. Pathophysiology(cont.) • 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 

  18. Pathophysiology(cont.) • 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.

  19. Pathophysiology(cont.) • 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.

  20. Pathophysiology(cont.) • 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.

  21. Pathophysiology(cont.) • 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 )

  22. Pathophysiology(cont.) • 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

  23. Pathophysiology(cont.) • 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 :

  24. Pathophysiology(cont.) (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.

  25. Pathophysiology(cont.) (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).

  26. Pathophysiology(cont.) (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.

  27. Key elemnts involved in ventricular remodeling

  28. Pathophysiology(cont.) • 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.

  29. Pathophysiology(cont.) • 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.

  30. 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

  31. 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.

  32. Classifications (cont.) • 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.

  33. Classifications (cont.) • In term of function : • 1)- Systolic dysfunction : There is impaired ejection of blood from the heart during systole & cardiac contractility

  34. Classifications (cont.) • 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 , Valvularstenosis.

  35. Classifications (cont.) • 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.

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

  37. Classifications (cont.) • 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.

  38. Classifications (cont.) • 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.

  39. Classifications (cont.) • 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.

  40. Classifications (cont.) • 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.

  41. Classifications (cont.) • 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.

  42. 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 IAsymptomatic CStructural heart disease with prior or current HF symptoms IISymptoms with minimal exercise IIISymptoms with moderate exercise. DRefractory HF requiring specialized interventions IVSymptomatic at rest

  43. 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.

  44. SIGNS & Symptoms 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

  45. 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.

  46. 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.

  47. 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).

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

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