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 canresult from any structural or functionalcardiac disorder that impairs the ability of

the ventricle to fill with or eject blood.

“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.”

Etiology

� It is a common end point for many diseases of cardiovascular system

� It can be caused by :

-Inappropriate work load (volume or pressure overload)

-Restricted filling

-Myocyte loss

Causes of chronic left ventricular failure

• Volume overload: Valve regurgitation

High output status

• Pressure overload: Systemic hypertension

Outflow obstruction

• Loss of muscles: Post MI, Chronic ischemia

Connective tissue diseases

Infection, Poisons (alcohol,cobalt,Doxorubicin)

• Restricted Filling: Pericardial diseases, Restrictive

cardiomyopathy, tachyarrhythmia

Pathophysiological mechanisms

Pathophysiological mechanisms

Pathophysiology

� Hemodynamic changes

� Neurohormonal changes

� Cellular changes

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.

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)

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.

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.

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).

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.

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.

The role of Ang II in the progression of HFCoronary artery disease Cardiac overloadCardiomyopathy

Left ventricular dysfunction

↓ Arterial blood pressure

↑ Angiotensin II

↓ Peripheral organ blood flow

↓ Skeletal muscleblood flow

Exercise intolerance

↓ Renalblood flow

Oedema

Cardiac remodelling

Renin release

Aldosterone release

Vasoconstriction Na+ and water retention Inotropy and hypertrophy ofvascular and cardiac cells

Left ventriculardilation & hypertrophy

Pump failure

Pathophysiology:

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

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.

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.

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).

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.

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

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 100-300 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.

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.

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.

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.

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).

Pathophysiology:

Pathophysiology:

In systolic dysfunction, left ventricular contractility is depressed, and the end-systolic 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.

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.

Neurohormonal changes

↑ After loadVasoconstriction→↑ VR↑↑↑↑Endothelin

ApoptosisMay have roles in myocyte hypertrophy

↑↑↑↑ interleukins &TNFαααα

Same effectSame effect↑↑↑↑ Vasopressin

Vasoconstriction →

↑ after load

Salt & water retention→↑ VR↑↑↑↑ Renin-Angiotensin –

Aldosterone

Arteriolar constriction →

After load →↑ workload

→↑ O2 consumption

↑ HR ,↑ contractility,

vasoconst. → ↑ V return,

↑ filling

↑↑↑↑ Sympathetic activity

Unfavor. effectFavorable effectN/H changes

Cellular changes

•••• Changes in Ca+2 handling.

•••• Changes in adrenergic receptors:

• Slight ↑ in α1 receptors

• β1 receptors desensitization → followed by down regulation

• Changes in contractile proteins

• Program cell death (Apoptosis)

•••• Increase amount of fibrous tissue

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

Stages of Heart Failure

• Designed to emphasize preventability of HF

• Designed to recognize the progressive nature of LV dysfunction

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

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

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%)

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

Framingham Criteria for Diag. of Heart Failure

� Major Criteria:

� Paroxysmal nocturnal dyspnoea

� JVD

� Rales

� Cardiomegaly

� Acute Pulmonary Edema

� S3 Gallop

� Positive hepatic Jugular reflex

� ↑ venous pressure > 16 cm H2O

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

Initial Clinical Assessment of Pts Presenting With HF

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 natriureticpeptides (BNP and NT-proBNP) can be helpful in risk stratification.

Measurement of BNP and Noninvasive Imaging

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Modified

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

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)

Differential Diagnosis

Other causes of shortness of breath on exertion

� Pulmonary disease

� Obesity

� Unfitness

� Volume overload from renal failure or nephrotic syndrome

� Angina

� Anxiety.

Differential Diagnosis

Other causes of peripheral oedema

� dependent oedema

� nephrotic syndrome

� pericardial diseases

� liver diseases

� protein losing enteropathy.

Differential Diagnosis

Non-cardiac diseases causing high-output cardiac failure

� Anaemia

� Thyrotoxicosis

� Septicaemia

� Paget's disease of bone

� Arteriovenous fistulae.

Diff.Diag.APE

Laboratory Findings

Recommendations for the Hospitalized PatientNew 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

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 co-morbidities

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.

The Hospitalized Patient

New

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Diagnosis of HF

Chest radiographs,

echocardiogram, and echocardiography are key tests in this assessment.

The Hospitalized Patient

Diagnosis of HF

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New

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.

The Hospitalized Patient

New

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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.

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New

Patients Being Evaluated for Dyspnea

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:

• acute coronary syndromes/coronary

ischemia

• severe hypertension

• atrial and ventricular arrhythmias

• infections

• pulmonary emboli

• renal failure

• medical or dietary noncompliance

The Hospitalized Patient

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Precipitating Factors for Acute HF

ECG

Types of Rhythms Associated with CHF

Chest X-ray

� Size and shape of heart

� Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema)

� Pleural effusion

Echocardiogram� Function of both ventricles

� Wall motion abnormality that may signify CAD

� Valvular abnormality

� Intra-cardiac shunts Sist.HF

Echocardiogram

Diast.HF

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

Adams KF, Lindenfeld J, et al. HFSA 2006 Comprehensive Heart Failure Guideline. J Card Fail 2006;12:e1-e122.

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.

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

Cardiac Catheterization

� When CAD or valvular is suspected

� If heart transplant is indicated

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, cardiacoutput, 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.