HEART FAILUREBY

DR.ARSHAD FUAD ) الباطني ) الطب في دكتور�اه عراقي بورد ) الباطني ) الطب في دكتوراه عربي بورد

) أمراض ) في دقيق تخصص دكتوراه عراقي بوردوالشرايين القلب وقسطرة

MBCHB, FIBMS (MEDICINE), CABM (MEDICINE),

FIBMS(CARDIOLOGY)

DEFINITION Heart failure (HF) is a clinical syndrome

that occurs in patients who, because of an inherited or acquired abnormality of cardiac structure and/or function, develop a constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales) that lead to frequent hospitalizations, a poor quality of life, and a shortened life expectancy.

EPIDEMIOLOGY The overall prevalence of HF in the adult population in developed

countries is 2%. rising with age, and affects 6–10% of people over age 65.

Although the relative incidence of HF is lower in women than in men, women constitute at least one-half the cases of HF because of their longer life expectancy.

The overall prevalence of HF is thought to be increasing, in part because current therapies for cardiac disorders, such as myocardial infarction (MI), valvular heart disease, and arrhythmias, are allowing patients to survive longer.

Although HF once was thought to arise primarily in the setting of a depressed left ventricular (LV) ejection fraction (EF), epidemiologic studies have shown that approximately one-half of patients who develop HF have a normal or preserved EF (EF >50%).

Accordingly, HF patients are now broadly categorized into one of two groups: (1) HF with a depressed EF (commonly referred to as systolic failure) or (2) HF with a preserved EF (commonly referred to as diastolic failure).

ETIOLOGYDepressed Ejection Fraction (<40%)

Preserved Ejection Fraction (>50%)

Coronary artery disease• Myocardial infarction• Myocardial ischemia

Pathologic hypertrophy• Primary (hypertrophic

cardiomyopathies)• Secondary (hypertension)

Chronic pressure overload• Hypertension• Obstructive valvular disease

Aging

Chronic volume overload• Regurgitant valvular disease• Intracardiac shunting (L to R)• Extrracardiac shunting

Restrictive cardiomyopathy• Infiltrative disorders (amyloidosis,

sarcoidosis)• Storage diseases

(hemochromatosis)• Fibrosis• Endomyocardial disorders

Nonischemic dilated cardiomyopathy• Familial or genetic disorders• Toxic or drug-induced damage• Metabolic disorder• Viral or other infectious agents

Disorders of rate and rhythm• Chronic bradyarrhythmias• Chronic tachyarrhythmias

Pulmonary Heart Disease High-Output States Cor pulmonale Metabolic disorders

• Thyrotoxicosis• Nutritional disorders

(beriberi)Pulmonary vascular disorders Excessive blood-flow requirements

• Systemic arteriovenous shunting

• Chronic anemia• In 20–30% of the cases of HF with a depressed EF, the exact etiologic basis is not known. These patients are referred to as having nonischemic, dilated, or idiopathic cardiomyopathy if the cause is unknown

PROGNOSIS Despite many recent advances in the evaluation

and management of HF, the development of symptomatic HF still carries a poor prognosis.

Although it is difficult to predict prognosis in an individual, patients with symptoms at rest [New York Heart Association (NYHA) class IV] have a 30–70% annual mortality rate, whereas patients with symptoms with moderate activity (NYHA class II) have an annual mortality rate of 5–10%.

Thus, functional status is an important predictor of patient outcome

NEW YORK HEART ASSOCIATION CLASSIFICATION

PATHOGENESIS HF may be viewed as a progressive disorder that is

initiated after an index event either damages the heart muscle, with a resultant loss of functioning cardiac myocytes, or, alternatively, disrupts the ability of the myocardium to generate force, thereby preventing the heart from contracting normally.

This index event may have an abrupt onset, as in the case of a myocardial infarction (MI); it may have a gradual or insidious onset, as in the case of hemodynamic pressure or volume overloading; or it may be hereditary, as in the case of many of the genetic cardiomyopathies.

Regardless of the nature of the inciting event, the feature that is common to each of these index events is that they all in some manner produce a decline in the pumping capacity of the heart.

Although the precise reasons why patients with LV dysfunction may remain asymptomatic is not certain, one potential explanation is that a number of compensatory mechanisms become activated in the presence of cardiac injury and/or LV dysfunction allowing patients to sustain and modulate LV function for a period of months to years.

The list of compensatory mechanisms that have been described thus far include:

(1) activation of the renin-angiotensin-aldosterone (RAA) and adrenergic nervous systems, which are responsible for maintaining cardiac output through increased retention of salt and water

and (2) increased myocardial contractility. In addition, there is activation of a family of countervailing vasodilatory

molecules, including the atrial and brain natriuretic peptides (ANP and BNP), prostaglandins (PGE2 and PGI2), and nitric oxide (NO), that offsets the excessive peripheral vascular vasoconstriction.

Thus, patients may remain asymptomatic or minimally symptomatic for a period of years; however, at some point patients become overtly symptomatic, with a resultant striking increase in morbidity and mortality rates.

the transition to symptomatic HF is accompanied by increasing activation of neurohormonal, adrenergic, and cytokine systems that lead to a series of adaptive changes within the myocardium collectively referred to as LV remodeling.

PATHOPHYSIOLOGICAL CHANGES INHEART FAILURE

Ventricular dilatation Myocyte hypertrophy Increased collagen synthesis Altered myosin gene expression Altered sarcoplasmic Ca2+-ATPase density Increased ANP secretion Salt and water retention Sympathetic stimulation Peripheral vasoconstriction

TYPES OF HEART FAILURE

Left-sided heart failure. There is a reduction in the left ventricular output and an increase in the left atrial or pulmonary venous pressure.

Right-sided heart failure. There is a reduction in right ventricular output for any given right atrial pressure. Causes of isolated right heart failure include chronic

lung disease (cor pulmonale), multiple pulmonary emboli and pulmonary valvular stenosis.

Left, right and biventricular heart failure

Biventricular heart failure. Failure of the left and right heart may develop because the disease process, such as dilated

cardiomyopathy or ischaemic heart disease, affects both ventricles

or because disease of the left heart leads to chronic elevation of the left atrial pressure, pulmonary hypertension and right heart failure.

Diastolic and systolic dysfunctionHeart failure may develop as a result of impaired myocardial contraction (systolic

dysfunction) but can also be due to poor ventricular filling and

high filling pressures caused by abnormal ventricular relaxation (diastolic dysfunction). The latter is caused by a stiff non-compliant ventricle

and is commonly found in patients with left ventricular hypertrophy.

NB: Systolic and diastolic dysfunction often coexist, particularly in patients with coronary artery disease.

Acute and chronic heart failure Heart failure may develop suddenly, as

in MI, or gradually, as in progressive valvular heart disease.

When there is gradual impairment of cardiac function, a variety of compensatory changes may take place.

High-output failure Conditions such as large arteriovenous

shunt, beri-beri , severe anaemia or thyrotoxicosis can occasionally cause heart failure due to an excessively high cardiac output.

Stages of HF Stage A: patients at high risk for developing heart

failure but without structural disorders of the heart Stage B: patients with a structural disorder of the

heart but no symptoms of heart failure Stage C: patients with past or current symptoms of

heart failure associated with underlying structural heart disease

Stage D: patients with end-stage disease who require specialized treatment strategies such as mechanical circulatory support, continuous inotropic infusions, cardiac transplantation, or hospice care

Heart Failure Clinical Stages

Symptoms not controlled with treatment

NORMAL

Asymptomatic LV Dysfunction

Compensated

Decompensated

No symptomsNormal exerciseNormal LV fxn

No symptomsNormal exerciseAbnormal LV fxn

No symptoms ExerciseAbnormal LV fxn

Symptoms ExerciseAbnormal LV fxn

Refractory

ATA-01-SK-0416-0418-NE

Clinical ManifestationsSymptoms

The cardinal symptoms of HF are fatigue and shortness of breath. Although fatigue traditionally has been ascribed to the

low cardiac output in HF, it is likely that skeletal-muscle abnormalities and other noncardiac comorbidities (e.g., anemia) also contribute to this symptom.

Orthopnea, which is defined as dyspnea occurring in the recumbent position, is usually a later manifestation of HF than is exertional dyspnea. It results from redistribution of fluid from the splanchnic

circulation and lower extremities into the central circulation during recumbency, with a resultant increase in pulmonary capillary pressure.

Paroxysmal Nocturnal Dyspnea (PND): This term refers to acute episodes of severe shortness of breath and coughing that generally occur at night and awaken the patient from sleep, usually 1–3 hours after the patient retires. PND may be manifest by coughing or wheezing, possibly because of increased pressure in the bronchial arteries leading to airway compression, along with interstitial pulmonary edema that leads to increased airway resistance

Cheyne-Stokes Respiration( 40%) Acute Pulmonary Edema

OTHER SYMPTOMS Gastrointestinal symptoms. Anorexia, nausea, and

early satiety associated with abdominal pain and fullness are common complaints and may be related to edema of the bowel wall and/or a congested liver.

Cerebral symptoms such as confusion, disorientation, and sleep and mood disturbances may be observed in patients with severe HF, particularly elderly patients with cerebral arteriosclerosis and reduced cerebral perfusion.

Nocturia is common in HF and may contribute to insomnia.

Physical Examination

In mild or moderately severe HF, the patient appears to be in no distress at rest except for feeling uncomfortable when lying flat for more than a few minutes.

In more severe HF, the patient must sit upright, may have labored breathing, and may not be able to finish a sentence because of shortness of breath.

Systolic blood pressure may be normal or high in early HF, but generally is reduced in advanced HF because of severe LV dysfunction.

The pulse pressure may be diminished, reflecting a reduction in stroke volume.

Sinus tachycardia is a nonspecific sign caused by increased adrenergic activity.

Peripheral vasoconstriction leading to cool peripheral extremities and cyanosis of the lips and nail beds is also caused by excessive adrenergic activity.

General Appearance and Vital Signs

JUGULAR VEINS Elevated

PULMONARY EXAMINATION Pulmonary crackles (rales or crepitations)

result from the transudation of fluid from the intravascular space into the alveoli. In patients with pulmonary edema, rales may

be heard widely over both lung fields and may be accompanied by expiratory wheezing (cardiac asthma).

Pleural effusions(unilateral on the right or bilateral)

CARDIAC EXAMINATION Cardiomegaly , the point of maximal impulse (PMI) usually

is displaced below the fifth intercostal space and/or lateral to the midclavicular line, and the impulse is palpable over two interspaces.

In some patients, a third heart sound (S3) is audible and palpable at the apex.

Patients with enlarged or hypertrophied right ventricles may have a sustained and prolonged left parasternal impulse extending throughout systole.

A fourth heart sound (S4) is not a specific indicator of HF but is usually present in patients with diastolic dysfunction.

The murmurs of mitral and tricuspid regurgitation are frequently present in patients with advanced HF.

ABDOMEN AND EXTREMITIES Hepatomegaly is an important sign in patients

with HF. When it is present, the enlarged liver is frequently tender and may pulsate during systole if tricuspid regurgitation is present.

Ascites, a late sign, occurs as a consequence of increased pressure in the hepatic veins and the veins draining the peritoneum.

Jaundice, also a late finding in HF, results from impairment of hepatic function secondary to hepatic congestion and hepatocellular hypoxemia and is associated with elevations of both direct and indirect bilirubin.

Peripheral edema is a cardinal manifestation of HF, but it is nonspecific and usually is absent in patients who have been treated adequately with diuretics. Long-standing edema may be associated

with indurated and pigmented skin. Cardiac Cachexia

Diagnosis The diagnosis of heart failure should

not be based on history and clinical findings; it requires evidence of cardiac dysfunction with appropriate investigation using objective measures of left ventricular structure and function (usually echocardiography).

INVESTIGATIONS IN HEART FAILURE Blood tests: complete blood count, a

panel of electrolytes, blood urea nitrogen, serum creatinine, hepatic enzymes, and a urinalysis. Selected patients should have assessment

for diabetes mellitus (fasting serum glucose or oral glucose tolerance test), dyslipidemia (fasting lipid panel), and thyroid abnormalities (thyroid-stimulating hormone level).

BIOMARKERS Circulating levels of natriuretic peptides are useful

adjunctive tools in the diagnosis of patients with HF. Both B-type natriuretic peptide (BNP) and N-terminal

pro-BNP, which are released from the failing heart, are relatively sensitive markers for the presence of HF with depressed EF; they also are elevated in HF patients with a preserved EF,

albeit to a lesser degree. However, it is important to recognize that natriuretic

peptide levels increase with age and renal impairment, are more elevated in women, and can be elevated in right HF from any cause.

Levels can be falsely low in obese patients and may normalize in some patients after appropriate treatment.

Chest X-ray. Look for cardiomegaly, pulmonary congestion with upper lobe diversion, fluid in fissures, Kerley B lines, and pulmonary oedema.

Electrocardiogram for ischaemia, chamber enlargement or arrhythmia.

Echocardiography. Cardiac chamber dimension, systolic and diastolic function, regional wall motion abnormalities, valvular heart disease, cardiomyopathies.

Stress echocardiography. Assessment of viability in dysfunctional myocardium

Nuclear cardiology. Radionucleotide angiography (RNA) can quantify ventricular ejection fraction, single photon-emission computed tomography (SPECT)

or positron emission tomography (PET) can demonstrate myocardial ischaemia and viability in dysfunctional myocardium.

CMR (cardiac MRI). Assessment of viability in dysfunctional myocardium with the use of dobutamine for contractile reserve or with gadolinium for delayed enhancement (‘infarct imaging’).

Cardiac catheterization. Diagnosis of ischaemic heart failure (and suitability for revascularization),

Cardiac biopsy. Diagnosis of cardiomyopathies, e.g. amyloid, follow-up of transplanted patients to assess

rejection. Cardiopulmonary exercise testing. Peak

oxygen consumption (VO2) is predictive of hospital admission and death in heart failure. A 6-minute exercise walk is an alternative.

Ambulatory ECG monitoring (Holter). In patients with suspected arrhythmia.

Complications

In advanced heart failure, the following may occur: Renal failure is caused by poor renal perfusion

due to a low cardiac output and may be exacerbated by diuretic therapy, angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers.

Hypokalaemia may be the result of treatment with potassium-losing diuretics or hyperaldosteronism caused by activation of the renin–angiotensin system and impaired aldosterone metabolism due to hepatic congestion.

Hyperkalaemia may be due to the effects of drug treatment, particularly the combination of ACE inhibitors and spironolactone (which both promote potassium retention), and renal dysfunction.

Hyponatraemia is a feature of severe heart failure and is a poor prognostic sign.

Impaired liver function is caused by hepatic venous congestion and poor arterial perfusion, which frequently cause mild jaundice and abnormal liver function tests; reduced synthesis of clotting factors can make anticoagulant control difficult.

Thromboembolism. Deep vein thrombosis and pulmonary embolism

may occur due to the effects of a low cardiac output and enforced immobility,

whereas systemic emboli may be related to arrhythmias, atrial flutter or fibrillation, or intracardiac thrombus complicating conditions such as mitral stenosis, MI or left ventricular aneurysm.

Atrial and ventricular arrhythmias are very common and may be related to electrolyte changes (e.g. hypokalaemia,

hypomagnesaemia), the underlying structural heart disease, and the pro-arrhythmic effects of increased

circulating catecholamines or drugs.