Definition: A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body

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1 Definition: A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body HF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood.

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3 Heart Failure vs. Congestive Heart Failure Because not all patients have volume overload at the time of initial or subsequent evaluation, the term heart failure is preferred over the older term congestive heart failure.

4 Etiology It is a common end point for many diseases of cardiovascular system It can be caused by : -Inappropriate work load (volume or pressure -Restricted filling -Myocyte loss overload)

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6 Causes of chronic left ventricular failure Volume overload: Pressure overload: Loss of muscles: Restricted Filling: Valve regurgitation High output status Systemic hypertension Outflow obstruction Post MI, Chronic ischemia Connective tissue diseases Infection, Poisons (alcohol,cobalt,doxorubicin) Pericardial diseases, Restrictive cardiomyopathy, tachyarrhythmia

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9 Pathophysiological mechanisms

10 Pathophysiological mechanisms

11 Pathophysiology Hemodynamic changes Neurohormonal changes Cellular changes

12 Pathophysiology: The inciting event in HF is inadequate adaptation of the cardiac myocytes to increased wall stress in order to maintain adequate cardiac output following myocardial injury whether of acute onset or over several months to years whether a primary disturbance in myocardial contractility or an excessive hemodynamic burden placed on the ventricle.

13 Pathophysiology: compensatory mechanisms (1) Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance (2) myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented (3) release of norepinephrine (NE) by adrenergic cardiac nerves, which augments myocardial contractility activation (RAAS)

14 Pathophysiology: The primary myocardial response to chronic increased wall stress includes myocyte hypertrophy and remodeling, usually of the eccentric type. The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS.

15 Pathophysiology: The release of epinephrine (E) and NE, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin (V), causes vasoconstriction, which increases afterload.

16 Pathophysiology: Increase in cyclic adenosine monophosphate (camp), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy).

17 Pathophysiology: Calcium overload induce arrhythmias and lead to sudden death. Increase in afterload and myocardial contractility (known as inotropy)+ myocardial lusitropy= increase myocardial energy expenditure and decrease in cardiac output. Myocardial cell death, increased neurohumoral stimulation, adverse hemodynamic and myocardial responses.

18 Pathophysiology: RAAS activation: preload and myocardial energy expenditure. in renin= delivery of chloride to the macula densa, and beta1-adrenergic activity as a response to cardiac output, angiotensin II and aldosterone levels. Ang II, along with ET-1, is crucial in maintaining effective intravascular homeostasis mediated by vasoconstriction and aldosterone-induced salt and water retention.

19 The role of Ang II in the progression of HF Coronary artery disease Cardiomyopathy Cardiac overload Left ventricular dysfunction Peripheral organ blood flow Arterial blood pressure Renin release Angiotensin II Aldosterone release Vasoconstriction Na+ and water retention Inotropy and hypertrophy of vascular and cardiac cells Cardiac remodelling Skeletal muscle blood flow Renal blood flow Left ventricular dilation & hypertrophy Exercise intolerance Oedema Pump failure

20 Pathophysiology: Neurohumoral factors lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss.

21 Pathophysiology: Remodeling process leads to early adaptive mechanisms: Augmentation of stroke volume (Starling mechanism) Increasing venous return to the LV increases LVEDP and volume, thereby increasing ventricular preload. This results in an increase in stroke volume (SV). The normal operating point is at LVEDP of 8 mmhg, and a SV of 70 ml/beat.

22 Pathophysiology: Remodeling process leads to early adaptive mechanisms: Decreased wall stress (Laplace mechanism; P= T/R, where P= pressure, T=tension in the wall, R= radius). A dilated ventricle requires more tension in the wall to generate the same pressure. Increased myocardial oxygen demand, myocardial ischemia, Impaired contractility, and arrhythmogenesis.

23 Pathophysiology: Heart failure advances and/or becomes progressively decompensated and cause decline in the counterregulatory effects of endogenous vasodilators: NO PGs BK atrial natriuretic peptide (ANP) B-type natriuretic peptide or brain natriuretic peptide (BNP).

24 Pathophysiology: ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure expansion. ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload.

25 Pathophysiology: BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. BNP inhibits renin and aldosterone release and, possibly, adrenergic activation as well. ANP and BNP are elevated in chronic heart failure. BNP has potentially important diagnostic, therapeutic, and prognostic implications

26 Pathophysiology: The level of BNP in the blood increases when heart failure symptoms worsen, and decreases when the heart failure condition is stable. The BNP level in a person with heart failure even someone whose condition is stable is higher than in a person with normal heart function. BNP levels below 100 pg/ml indicate no heart failure BNP levels of suggest heart failure is present BNP levels above 300 pg/ml indicate mild heart failure BNP levels above 600 pg/ml indicate moderate heart failure. BNP levels above 900 pg/ml indicate severe heart failure.

27 Pathophysiology: Other vasoactive systems in CHF ET receptor system adenosine receptor system tumor necrosis factor-alpha (TNF-alpha). ET, a substance produced by the vascular endothelium, may contribute to the regulation of myocardial function, vascular tone, and peripheral resistance in CHF.

28 Pathophysiology: Other vasoactive systems in CHF Elevated levels of ET-1 closely correlate with the severity of heart failure. ET-1 is a potent vasoconstrictor and has exaggerated vasoconstrictor effects in the renal vasculature, reducing renal plasma blood flow, glomerular filtration rate (GFR), and sodium excretion. TNF-alpha levels seem to correlate with the degree of myocardial dysfunction. Local production of TNF-alpha have toxic effects on the myocardium.

29 Pathophysiology: In systolic dysfunction, neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. Neurohormonal responses accelerate myocardial dysfunction in the long term.

30 Pathophysiology: In diastolic heart failure, altered relaxation of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occurs in response to an increase in ventricular afterload (pressure overload). The impaired relaxation of the ventricle leads to impaired diastolic filling of the left ventricle (LV).

31 Pathophysiology:

32 Pathophysiology: In systolic dysfunction, left ventricular contractility is depressed, and the endsystolic pressure volume line is displaced downward and to the right; as a result, there is a diminished capacity to eject blood into the high-pressure aorta. The ejection fraction is depressed, and the end-diastolic pressure is normal.

33 Pathophysiology: In diastolic dysfunction, the diastolic pressure volume line is displaced upward and to the left; there is diminished capacity to fill at low left-atrial pressures. The ejection fraction is normal and the end-diastolic pressure is elevated.

34 Neurohormonal changes N/H changes Favorable effect Unfavor. effect Sympathetic activity Renin-Angiotensin Aldosterone Vasopressin HR, contractility, vasoconst. V return, filling Salt & water retention VR Same effect Arteriolar constriction After load workload O 2 consumption Vasoconstriction after load Same effect interleukins &TNFα May have roles in myocyte hypertrophy Apoptosis Endothelin Vasoconstriction VR After load

35 Cellular changes Changes in Ca +2 handling. Changes in adrenergic receptors: Slight in α 1 receptors β 1 receptors desensitization followed by down regulation Changes in contractile proteins Program cell death (Apoptosis) Increase amount of fibrous tissue

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37 Factors aggravating heart failure Myocardial ischemia or infarct Dietary sodium excess Excess fluid intake Medication noncompliance Arrhythmias Intercurrent illness (eg infection) Conditions associated with increased metabolic demand (eg pregnancy, thyrotoxicosis, excessive physical activity) Administration of drug with negative inotropic properties or fluid retaining properties (e. NSAIDs, corticosteroids) Alcohol

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39 Stages of Heart Failure Designed to emphasize preventability of HF Designed to recognize the progressive nature of LV dysfunction

40 Stages of Heart Failure COMPLEMENT, DO NOT REPLACE NYHA CLASSES NYHA Classes - shift back/forth in individual patient (in response to Rx and/or progression of disease) Stages - progress in one direction due to cardiac remodeling

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46 Acute Heart Failure/Acute Pulmonary Edema) Often precipitated by a myocardial infarction. Signs include: Severe breathlessness Frothy pink sputum Cold clammy skin Tachycardia Low blood pressure Lung crepitations Raised jugular venous pressure Third heart sound Confusion

47 Chronic Heart Failure The likelihood of heart failure in the presence of suggestive symptoms and signs is increased if there is a history of myocardial infarction (MI) or angina, an abnormal ECG, or a chest X-ray showing pulmonary congestion or cardiomegaly. Symptoms include: Shortness of breath on exertion (sensitivity 66%, specificity 52%) Decreased exercise tolerance (often simply 'fatigue') Paroxysmal nocturnal dyspnoea (sensitivity 33%, specificity 76%) Orthopnoea (sensitivity 21%, specificity 81%) Ankle swelling (sensitivity 23%, specificity 80%)

48 Chronic Heart Failure The most specific signs are: Laterally displaced apex beat Elevated jugular venous pressure Third heart sound Less specific signs include: Tachycardia Lung crepitations Hepatic engorgement (tender hepatomegaly) Peripheral oedema Anorexia,nausea, abdominal fullness Rt hypochondrial pain

49 Framingham Criteria for Diag. of Heart Failure Major Criteria: Paroxysmal nocturnal dyspnoea JVD Rales Cardiomegaly Acute Pulmonary Edema S 3 Gallop Positive hepatic Jugular reflex venous pressure > 16 cm H 2 O

50 Diag. of Heart Failure (cont.) Minor Criteria LL edema, Night cough Dyspnea on exertion Hepatomegaly Pleural effusion vital capacity by 1/3 of normal Tachycardia 120 bpm Weight loss 4.5 kg over 5 days management

51 Initial Clinical Assessment of Pts Presenting With HF Measurement of BNP and Noninvasive Imaging I IIa IIb III Measurement of natriuretic peptides (B-type natriuretic peptide (BNP) or N-terminal pro- B-type natriuretic peptide (NT-proNBP) can be useful in the evaluation of patients presenting in the urgent care setting in whom the clinical diagnosis of HF is uncertain. Measurement of natriuretic peptides (BNP and NT-proBNP) can be helpful in risk stratification. Modified

52 Forms of Heart Failure Systolic & Diastolic High Output Failure Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, Paget s disease Low Output Failure Acute large MI, aortic valve dysfunction--- Chronic

53 Forms of heart failure ( cont.) Right vs Left sided heart failure: Right sided heart failure : Most common cause is left sided failure Other causes included :Pulmonary embolisms Other causes of pulmonary htn. RV infarction Mitral Stenosis Usually presents with: LL edema, ascites hepatic congestion cardiac cirrhosis (on the long run)

54 Differential Diagnosis Other causes of shortness of breath on exertion Pulmonary disease Obesity Unfitness Volume overload from renal failure or nephrotic syndrome Angina Anxiety.

55 Differential Diagnosis Other causes of peripheral oedema dependent oedema nephrotic syndrome pericardial diseases liver diseases protein losing enteropathy.

56 Differential Diagnosis Non-cardiac diseases causing high-output cardiac failure Anaemia Thyrotoxicosis Septicaemia Paget's disease of bone Arteriovenous fistulae.

57 Diff.Diag.APE

58 Laboratory Findings

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62 Recommendations for the Hospitalized Patient New Recommendations Based on the 2009 Focused Update Incorporated Into the ACCF/AHA 2005 guidelines for the Diagnosis and Management of Heart Failure in Adults: A Report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines

63 The Hospitalized Patient Diagnosis of HF New I IIa IIb III The diagnosis of heart failure is primarily based on signs and symptoms derived from a thorough history and physical exam. Clinicians should determine the following: a. adequacy of systemic perfusion; b. volume status; c. the contribution of precipitating factors and/or comorbidities d. if the heart failure is new onset or an exacerbation of chronic disease; and e. whether it is associated with preserved normal or reduced ejection fraction.

64 The Hospitalized Patient Diagnosis of HF I IIa IIb III Chest radiographs, echocardiogram, and echocardiography are key tests in this assessment. New

65 The Hospitalized Patient I IIa IIb III Patients Being Evaluated for Dyspnea Concentrations of BNP or NT-proBNP should be measured in patients being evaluated for dyspnea in which the contribution of HF is not known. Final diagnosis requires interpreting these results in the context of all available clinical data and ought not to be considered a stand-alone test. New I IIa IIb III Acute coronary syndrome precipitating HF hospitalization should be promptly identified by electrocardiogram and cardiac troponin testing, and treated, as appropriate to the overall condition and prognosis of the patient. New

66 The Hospitalized Patient I IIa IIb III Precipitating Factors for Acute HF It is recommended that the following common potential precipitating factors for acute HF be identified as recognition of these comorbidities, is critical to guide therapy: New acute coronary syndromes/coronary ischemia severe hypertension atrial and ventricular arrhythmias infections pulmonary emboli renal failure medical or dietary noncompliance

67 ECG

68 Types of Rhythms Associated with CHF

69 Chest X-ray Size and shape of heart Evidence of pulmonary venous congestion (dilated or upper lobe veins perivascular edema) Pleural effusion

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71 Echocardiogram Function of both ventricles Wall motion abnormality that may signify CAD Valvular abnormality Intra-cardiac shunts Sist.HF

72 Echocardiogram Diast.HF

73 Patterns of LV Diastolic Filling as shown by standard Doppler echo.

74 Evaluation Exercise Testing Exercise testing is not recommended as part of routine evaluation in patients with HF. Exercise testing with physiologic testing for inducible abnormality in myocardial perfusion or wall motion abnormality should be considered to screen for the presence of coronary artery disease with inducible ischemia. Strength of Evidence = C Adams KF, Lindenfeld J, et al. HFSA 2006 Comprehensive Heart Failure Guideline. J Card Fail 2006;12:e1-e122.

75 Evaluation Endomyocardial Biopsy Endomyocardial biopsy should be considered in patients: With rapidly progressive clinical HF or ventricular dysfunction, despite appropriate medical therapy Suspected of having myocardial infiltrative processes, such as sarcoidosis or amyloidosis With malignant arrhythmias out of proportion to LV dysfunction, where sarcoidosis and giant cell myocarditis are considerations Strength of Evidence = C Adams KF, Lindenfeld J, et al. HFSA 2006 Comprehensive Heart Failure Guideline. J Card Fail 2006;12:e1-e122.

76 Cardiac Catheterization When CAD or valvular is suspected If heart transplant is indicated

77 Pulmonary-Artery Catheterization - used to assess the pulmonary-artery occlusion pressure, is considered the gold standard for determining the cause of acute pulmonary edema. - permits monitoring of cardiac filling pressures, cardiac output, and systemic vascular resistance during treatment. -a pulmonary-artery occlusion pressure above 18 mm Hg indicates cardiogenic pulmonary edema or pulmonary edema due to volume overload. - common complications include: hematoma at the insertion site, arterial puncture, bleeding, arrhythmias, and bloodstream infection.

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