Cardiology

Diagnosis of Heart Failure by History and Physical Examination

I. Disease Heart Failure: What every physician needs to know.

Heart failure is a clinical syndrome and is best defined as a condition in which patients have "symptoms of heart failure: typically shortness of breath at rest or during exertion, and/or fatigue; signs of fluid retention, such as pulmonary congestion or ankle swelling; and objective evidence of abnormality of the structure or function of the heart at rest."

This definition, proposed by the Task Force for the Diagnosis and Treatment of Acute and Chronic Heart Failure of the European Society of Cardiology, lays a particular emphasis on the presence of signs and symptoms that are important in making the diagnosis of heart failure at bedside. No clinical symptom or sign is specific to this syndrome, and obtaining a meticulous history and performing a thorough physical examination is therefore of paramount importance.

II. Diagnostic Confirmation: Are you sure your patient has Heart Failure?

Clinical Presentation

Patients with heart failure present with one of three common clinical profiles. The first and the most common presentation is with volume overload that manifests as pulmonary or systemic congestion. In the second group, evidence of hypotension and compromised end-organ perfusion, a consequence of low cardiac output, are the main features. The third group has features of both volume overload and systemic hypoperfusion.

A. History Part I: Pattern Recognition:

HISTORY TAKING:

A proper history taking should not only include a careful assessment of the symptoms but also attempt to identify the etiology and common precipitating factors of heart failure (Table I and Table II).

Table I.

Potential etiologic or risk factors for heart failure that can be identified by history
Coronary artery disease (CAD)HypertensionDiabetesDyslipidemiaValvular heart diseaseObesityHistory or symptoms of sleep disordered breathingExposure to cardiotoxic agents (e.g., chemotherapy, excessive alcohol use)SmokingHistory of irradiation to the chestMyopathy

Table II.

Common precipitating factors for heart failure
Acute coronary syndromeInfectionsArrhythmiaNoncompliance to medicationsDietary indiscretionsAnemiaIatrogenic (e.g., excess use of intravenous fluid)Thyroid disordersAcute valvular dysfunctionPregnancy

B. History Part 2: Prevalence:

Symptoms of Heart Failure

Dyspnea, orthopnea, and paroxysmal nocturnal dyspnea

Dyspnea is one of the common symptoms of heart failure and refers to the awareness of discomfort while breathing. It is often described as shortness of breath, breathlessness, difficulty in breathing, etc.

During the early stages of heart failure, dyspnea usually occurs only during physical activity, but later dyspnea could occur even at rest. Orthopnea (derived from the Greek word ortho meaning straight and pnoia meaning breath) is dyspnea at rest in the supine position and it is commonly attributed to pulmonary congestion that occurs during recumbency.

Paroxysmal nocturnal dyspnea (PND) refers to the sensation of shortness of breath that awakens the patient within the early hours of falling asleep and usually resolves within 15 to 30 minutes of assuming an upright posture. Because dyspnea is a common symptom in numerous conditions that affect other organ systems such as the lungs, it is not surprising that it has been found to have high sensitivity and positive predictive value but a low specificity for the diagnosis of heart failure.

In contrast, orthopnea and PND are more specific for heart failure. The absence of either of these symptoms is reported to have a high negative predictive value. The exact mechanisms for the development of dyspnea in heart failure are not known, but activation of J receptors in the pulmonary interstitial space by edema fluid could contribute to the sensation of dyspnea.

Fatigue and exercise intolerance

Fatigue and exercise intolerance are also common and nonspecific symptoms of heart failure. Patients with heart failure have reduced peak exercise capacity and increased skeletal muscle fatigability.

Reduced skeletal muscle perfusion from low cardiac output as well as intrinsic changes in the skeletal muscle, endothelial dysfunction, and altered microcirculation all play an important role in the genesis of fatigue and exercise intolerance. Patients sometimes might not be aware of their functional limitations. Making specific queries with regards to the type activities they can or cannot perform often aids in the subjective assessment of their functional capacity.

Edema

Edema is the quintessential symptom and sign of heart failure. Swelling of the feet and ankles, abdominal fullness due to swelling and distention of the liver, abdominal distention from ascites, scrotal swelling, and anasarca are different manifestations of fluid retention. Although not specific, edema is an integral sign to make the diagnosis of decompensated heart failure.

Wheezing and cardiac asthma

Heart failure patients can present with wheezing, which is often referred to as cardiac asthma. Although the exact mechanisms are unclear, congestion and edema of the bronchial wall and increased bronchial hyperresponsiveness can lead to airflow obstruction, which could explain the presence of wheezing.

It is not uncommon for heart failure patients to present with cardiac asthma, which can potentially lead to misdiagnosis. In addition patients with heart failure often complain of a cough, particularly in the recumbent position.

Cheyne-Stokes respiration

Cheyne-Stokes breathing refers to a waxing and waning pattern of breathing where periods of central apnea or hypopnea alternate with periods of hyperventilation. This symptom is more often reported by a family member rather than by the patient and is prevalent in advanced stage of heart failure.

Weight loss/cardiac cachexia

Nonedematous weight loss is a well-known feature of end-stage heart failure. Unintentional weight loss of more than 6% in heart failure has been used to define cardiac cachexia. Multiple factors including neurohumoral and immune abnormalities, anorexia, malabsorption, and depression contribute to the development of cachexia of heart failure. Cardiac cachexia is an independent predictor of increased mortality.

Declining cognitive function

A significant portion of patients with heart failure exhibit some degree of cognitive impairment, including memory and attention deficits. The mechanism is not clear but reduced cardiac output, coexistent cerebrovascular disease, and depression are thought to play a role. Patients with low output heart failure could present with altered sensorium and this might be one of the foremost complaints offered by the patient or the family.

C. History Part 3: Competing diagnoses that can mimic Heart Failure.

Assessment of severity of symptoms of heart failure

History taking is also important in determining the functional limitations in patients with heart failure. The New York Heart Association classification is widely used to classify patients into four groups (Class I-IV).

Class I refers to patients with structural heart disease who do not have any functional limitation; class II patients develop symptoms during ordinary activity to which they are previously accustomed; class III patients develop symptoms on less-than-ordinary exertion, and class IV patients have symptoms at rest. The NYHA functional class can fluctuate during the course of heart failure and sustained improvement in functional class can be seen with treatment.

D. Physical Examination Findings.

Physical examination in Heart Failure

Vital Signs

Pulse: A careful assessment of the arterial pulse rate, rhythm, volume, or character can provide information about the underlying LV pump function, valvular abnormalities, and hemodynamics.

Pulse Rate: Sinus tachycardia (pulse rate >100 beats/min) is a common feature in patients with acute heart failure and reflects activation of the sympathetic nervous system in response to reduced cardiac output. However, tachycardia may not be prominent in patients who have been adequately beta-blocked.

Chronic tachyarrhythmia in patients with left ventricular dysfunction should raise the suspicion of tachycardia-mediated cardiomyopathy. Bradycardia (pulse rate <60 beats/min) can result from the use of beta-blockers or may be related to heart block that can occasionally be a precipitating factor for heart failure.

Pulse Rhythm: Sinus arrhythmia is a variation of the pulse rate with breathing (an increase in pulse rate on inspiration and a decrease on expiration) and is common in children and adolescents, as well as the physically fit. An irregularly irregular rhythm, often occurring with changing pulse volume, could indicate atrial fibrillation, which is common in patients with heart failure.

Frequent ventricular ectopies are another source of irregular pulse. If they occur frequently as in bigeminy or trigeminy, the pulse can be regularly irregular and the pulse deficit in this setting can be appreciated by simultaneous precordial auscultation and palpation of a peripheral pulse. Rhythm abnormalities, if suspected, need to be confirmed by an electrocardiogram.

Pulse Character and Volume: The pulse character refers to an impression of the pulse waveform and volume derived during palpation of the arterial pulse. The character and volume of the pulse are best assessed by palpating one of the larger arteries (e.g., carotid, brachial, or femoral) and may provide useful information regarding the presence of several underlying conditions.

High volume pulse is a feature of a large stroke volume and is classically seen in patients with severe aortic regurgitation (AI). Several fanciful names, such as collapsing pulse, water hammer pulse, or Corrigan's pulse, have been given to the high volume pulse of aortic regurgitation.

In severe aortic regurgitation, the collapsing pulse may be associated with other features, such as de Musset's sign (nodding of the head with each pulse) and Quincke's sign (pulsation of the nail bed capillaries). The severity of AI correlates well with the ratio of pulse pressure to systolic pressure: a ratio less than 50% indicating mild AI; ratio between 50% and 75% suggests moderate AI; and ratios above 75% are indicative of severe AI.

High volume pulse is also be seen in high cardiac output states, such as arteriovenous fistulae, chronic severe anemia, thyrotoxicosis, and other hyperdynamic circulatory states. Pulsus bisferiensis a difficult pulse to recognize and is characterized by two systolic peaks. It is seen in aortic regurgitation with or without aortic stenosis, and in some patients with hypertrophic cardiomyopathy (HCM). In HCM with obstruction, there is "spike and dome" pulse with a rapid early wave followed by a more slowly rising second component of the pulse.

Dicrotic pulse also has two peaks, one in systole and the other reflected wave from the periphery in early diastole. It may be seen after the administration of nitrates in otherwise normal subjects, in febrile patients, or in cardiac tamponade, congestive cardiac failure, or shock.

The exact mechanism of the dicrotic pulse is unclear. It is often difficult to differentiate between pulsus bisferiens and dicrotic pulse without invasive or noninvasive pulse recording.

Low volume pulse (pulsus parvus) is seen in low output cardiac states, such as shock and hypovolemia, as well as in aortic stenosis. The low volume pulse in severe aortic stenosis, also called anacrotic pulse,refers to a slow rising and generally flat volume pulse wave associated with a low cardiac output and prolonged left ventricular ejection time.

Pulsus alternans is a regular pulse that alternates between a larger and smaller volume on a beat-to-beat basis and is seen in severe cardiac failure. In pulsus paradoxus there is an abnormally large decrease in pulse volume during inspiration.

Its presence suggests either a restricted left ventricular filling during inspiration (associated with increase in pericardial pressure and increased right heart filling that shifts the interventricular septum towards the left ventricle impairing left-sided filling), such as pericardial tamponade, or exaggerated changes in intrathoracic pressure as in severe asthma. Other causes of pulsus paradoxus include right ventricular infarction, large pulmonary embolus, and tense ascites or obesity.

Pulsus paradoxus can be confirmed by a change in systolic blood pressure from inspiration to expiration of greater than 10 mm Hg or 10% of systolic pressure.

Blood Pressure: A range of blood pressure values may be seen in patients presenting with acute heart failure. A "crush and burn" presentation with cardio genic shock and hypotension requiring prompt treatment with inotrope, vasopressors, or mechanical assist devices is a rare presentation of heart failure.

In the majority of patients with acute decompensated heart failure, the systolic blood pressure is normal or elevated (>140 mm Hg). Patients with low systolic blood pressure (<120 mm Hg) at admission are at increased risk of a higher in-hospital mortality. In most patients with well-compensated chronic heart failure, the blood pressure is in the low normal range.

Pulse pressure: The difference between the systolic and diastolic blood pressure, the pulse pressure, is indicative of stroke volume and vascular compliance or stiffness. The normal pulse pressure is around 40 mm Hg.

Low pulse pressure suggests reduced stroke volume in heart failure. Both low and elevated pulse pressures are associated with adverse cardiovascular outcomes. In patients with chronic systolic heart failure, proportional pulse pressure (defined as pulse pressure divided by the systolic pressure) of less than or equal to 25% correlates well with a cardiac index of less than 2.2 L/min/m2.

Respiration

Tachypnea or an increase in respiratory rate above 18 per minute indicates respiratory distress in heart failure and suggests pulmonary congestion. Cheyne-Stokes breathing (discussed above) is an ominous sign and is associated with poor outcomes in heart failure.

Temperature

Cold peripheries and peripheral cyanosis may suggest low cardiac output, whereas cold and clammy skin is a feature of cardiogenic shock and reflects intense vasoconstriction associated with acute decompensated heart failure. Low core temperature correlates with low cardiac output and is an independent predictor of poor outcomes.

E. What diagnostic tests should be performed?

Physical examination in Heart Failure

Assessment of congestion in Heart Failure

Jugular venous distention and abdominojugular or hepatojugular reflux

Examination of the neck veins is perhaps the most important physical skill that has to be learned to help assess the volume status of a patient with heart failure. The internal rather than the external jugular vein should be examined to assess jugular venous distention (JVD) because the latter has valves and is not directly aligned with the superior vena cava and right atrium.

Jugular venous pulsation (JVP) has two upward deflection waves (a and v waves) and two downward deflections or descents (x and y descents). The JVP can be obliterated with gentle pressure applied at the base of the neck and is not generally palpable.

The 'a' wave (atrial contraction) occurs just before the first heart sound (S1) and is associated with the fourth heart sound (S4) when present. The 'v' or atrial venous filling wave occurs at the end of ventricular systole and just after the second heart sound (S2). The 'x' descent occurs as the right atrium relaxes and the tricuspid valve moves downward.

The 'y' descent follows the peak of the 'v' wave as the tricuspid valve opens and the right atrium empties. Prominent 'a' wave is seen when the right ventricular end-diastolic pressure is increased or the right ventricular compliance is reduced.

A large or 'cannon a' wave is seen during atrial-ventricular dissociation when the right atrium contracts against a closed tricuspid valve. A prominent 'v' wave is seen in tricuspid regurgitation. A steep 'y' descent is seen when the ventricle fills early and rapidly during diastole (e.g., constrictive pericarditis), whereas a blunted 'y' descent is noted if diastolic ventricular filling is impaired (e.g., tamponade).

A paradoxical increase in the JVP with inspiration (instead of the expected decrease) is referred to as Kussmaul's sign and indicates impaired filling of the right ventricle as seen in constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, and severe right-sided heart failure. The central venous pressure is considered to be elevated when JVP is greater than 3 cm vertical height above the sternal angle (angle of Louis) while the patient is positioned at an angle of 45 degrees.

Adding 5 cm to the height of the JVP above the sternal angle with the patient at 45 degrees can assess the actual right atrial pressure. A sustained increase in jugular venous pulsation (>3 cm) on applying steady abdominal pressure constitutes a positive abdominojugular reflux or hepatojugular reflux (AJR).

A positive AJR is the most effective test for fluid overload in heart failure and suggests a pulmonary wedge pressure of 15 mm Hg or higher in the absence of isolated right ventricular failure. Presence of JVD with or without presence of the third heart sound (S3) is associated with adverse outcomes in patients with heart failure.

Systolic blood pressure response to Valsalva maneuver

The normal systolic blood pressure (SBP) response during the Valsalva maneuver consists of four phases (sinusoidal response). Phase 1 is the initial transient increase in SBP above baseline at the beginning of strain resulting from transmission of elevated intrathoracic pressure to the vasculature.

During phase 2, there is reduction in SBP from baseline that is largely due to decreased venous return with continued strain. During phase 3 there is a sudden decline of SBP when strain is released and intrathoracic pressure falls. The last phase, phase 4, is characterized by an overshoot of SBP above baseline together with reflex bradycardia.

In patients with heart failure, SBP remains elevated throughout phase 2 because the elevated filling pressure enables the heart to fill despite decreased venous return from increased intrathoracic pressure (square wave response). In addition, overshoot of blood pressure is not seen during phase 4 when strain is released (absent overshoot).

Phases 2 and 4 of the SBP response to the Valsalva maneuver can usually be assessed at the bedside using a sphygmomanometer and by carefully listening to the presence and absence of Korotkoff sounds while cuff pressure is held and maintained 15 mm Hg above the normal SBP. Korotkoff sounds are only heard during release of straining (phase 4) in healthy subjects, whereas absence of Korotkoff sounds in both phases 2 and 4 (absent overshoot) can be appreciated in patients with mild heart failure.

Square wave response is noted when Korotkoff sounds are present during phase 2 (strain phase) but not phase 4, and it is seen in severe heart failure. The cardiovascular response to the Valsalva maneuver can be quantified by using the pulse amplitude ratio, the ratio of the minimum and maximum pulse pressure at the end and beginning of the strain phase, respectively, and analysis of pressure wave forms on peripheral arteries.

Pulse amplitude ratio has been shown to have a high correlation with pulmonary capillary wedge pressure (PCWP) and left ventricular end diastolic pressure (LVEDP). Portable devices have been developed for noninvasive assessment of PAWP and LVEDP at the bedside using this principle.

Rales/crackles, wheezing

Rales/crackles and wheezing on auscultation of the lungs are signs of pulmonary edema secondary to elevated left-sided filling pressure. In longstanding chronic heart failure, rales could be absent because development of increased lymphatic drainage prevents accumulation of edema fluid. The presence of rales is not a sensitive marker of heart failure, as they may be heard in several pulmonary pathologies including pneumonia and interstitial fibrosis.

Pleural and pericardial effusions

Accumulation of fluid in body cavities often occurs in patients with heart failure due to elevated hydrostatic pressure, and the fluid is generally transudate in character. In acute decompensated heart failure, moderate to large effusions are common.

Pericardial effusions are more common in patients with a chronic increase in right-sided rather than left-sided filling pressure. In contrast, pleural effusions are equally common in patients with elevated right- or left-sided cardiac pressure.

Although in heart failure pleural effusions are usually bilateral, isolated right-sided pleural effusions are not uncommon. The mechanism of isolated right-sided pleural effusions is not well understood. Presence of isolated left-sided pleural effusion in heart failure warrants further investigation.

Edema, ascites, and other signs of congestion

Edema of the feet, ankles, or sacrum; hepatomegaly; and ascites; reflect fluid retention that is characteristic of chronic heart failure and is usually associated with elevated right atrial pressure. Edema can also occur as a result of low plasma oncotic pressure due to low serum albumin that is not infrequently seen in patients with chronic end-stage heart failure.

Distention of the abdomen due to heart failure could contribute to respiratory distress. Tense ascites and elevated venous pressure have been shown to cause diuretic resistance and development of cardiorenal syndrome. Chronic hepatic congestion from heart failure can lead to cardiac cirrhosis.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Physical examination in Heart Failure

C. Examination of the precordium in Heart Failure

Palpation of the precordium

Displacement of Apical Impulse: The normal apical impulse, also known as point of maximal impulse (PMI), lies just medial to the mid clavicular line. It is the size of a penny and does not extend beyond the first half of systole.

In the absence of mediastinal shift from any source including collection of intrathoracic air or fluid, displacement of the apical impulse to the left indicates cardiomegaly, albeit with low sensitivity. PMI is frequently difficult to palpate because of obesity and obstructive lung disease. In left ventricular hypertrophy, a wide (>3 cm diameter) sustained (more than half of systole) PMI can be palpated.

Other findings during palpation of the precordium: Right ventricular parasternal heave is seen in patients with right ventricular enlargement or hypertrophy and is best felt by placing the heal of the hand on the left sternal border. The pulmonic component of the second heart sound can be palpated in severe pulmonary hypertension.

Auscultation

Third Heart Sound: The third heart sound (S3) is a low-pitched sound, which occurs 120 to 160 msec after the second heart sound. The timing corresponds to early rapid filling phase of the ventricle.

Left-sided S3 is best heard at the apex using the bell of the stethoscope. S3 is considered to be generated by low frequency vibrations of the ventricular wall during rapid deceleration of blood in diastole. In addition to heart failure, S3 can be heard in health young adults, pregnancy, valvular heart disease, as well as high output states.

S3 is more common in children and young adults and becomes less common during old age. The presence of S3 in heart failure is considered to indicate a stiff left ventricle and is associated with reduced cardiac output, elevated end-end diastolic pressure, decreased ejection fraction, and adverse outcomes. Right-sided S3 becomes louder during inspiration and is a feature of right ventricular dysfunction in patients with cor pulmonale and those with tricuspid regurgitation.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Clinical criteria used for the diagnosis of Heart Failure

Clinicians have diagnosed heart failure for decades based on carefully taken history, bedside physical examination, and chest radiograph. However, classic symptoms of heart failure, such as dyspnea at rest or during exertion, and fatigue, lack specificity and may be seen in patients with many other conditions.

Physical signs, such as S3, pulmonary rales, peripheral edema, jugular venous distention, and hepatojugular reflux, while reasonably specific in certain clinical settings are unacceptably insensitive, making their absence in an individual patient of little value in excluding heart failure. And since there is no 'gold standard' for the clinical diagnosis of heart failure, several criteria have been developed to help clinicians make a correct diagnosis in a patient with suspected heart failure.

The two most commonly used are the Framingham and Boston criteria. In the Framingham criteria (Table III), the diagnosis of heart failure is considered definite if two major or one major and two minor criteria are present.

Table III.

The Framingham criteria for the diagnosis of congestive heart failure
Major Criteria Minor Criteria Major or Minor Criteria
PND or orthopneaJVDRalesCardiomegalyAcute pulmonary edemaS3 GallopIncreased venous pressure >16 cm H2OCirculation time > or equal to 25 secHepatojugular reflux Ankle edemaNight coughDyspnea on exertionHepatomegalyPleural effusionVital capacity decreased by one third from maximumTachycardia (rate > or equal to 120) Weight loss > or equal to 4.5 kg in 5 days in response to treatment

The Boston criteria (Table IV) uses the information from history, physical examination, and chest radiography to categorize the diagnosis of heart failure into definite, possible, or unlikely depending on scores >7, 5-7, and <5, respectively. Both criteria have good diagnostic concordance but have a wide range of sensitivity and specificity depending on the population studied. The Boston criteria have been shown to have better ability in predicting clinically relevant outcomes, such as heart failure associated hospitalizations and adverse cardiovascular outcomes in the elderly.

Table IV.

Boston criteria for the diagnosis of heart failure
History Physical Examination Chest X-Ray
Criterion Score Criterion Score Criterion Score
Dyspnea at rest 4 Tachycardia (91-110 bpm: 1, >110 bpm: 2) 1-2 Pulmonary edema 4
Orthopnea 4 JVP (>6 cm H2O: 2; <6 cm H2O plus hepatomegaly or edema: 3) 2-3 Interstitial pulmonary edema 3
PND 3 Lung crackles (If basilar:1; if more than basilar: 2) 1-2 Bilateral pleural effusions 3
Dyspnea on walking level 2 Wheezing 3 Cardiothoracic ratio > or equal to 0.5 3
Dyspnea on climbing 1 S3 3 Upper zone flow distribution 2

What's the Evidence for specific management and treatment recommendations?

Dickstein, K, Cohen-Solal, Filippatos, G. "ESC guidelines for the diagnosis and treatment of acute and chronic heart failure 2008: The Task Force for the diagnosis and treatment of acute and chronic heart failure 2008 of the European Society of Cardiology. Developed in collaboration with the Heart Failure Association of the ESC (HFA) and endorsed by the European Society of Intensive Care Medicine (ESICM)". Eur J Heart Fail. vol. 10. 2008. pp. 933-989.

"2009 Focused Update: ACCF/AHA 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". J Am Coll Cardiol. vol. 53. 2009. pp. 1342-1382.

Greenberg, B, Kahn, AM, Bonow, RO, Mann, DL, Zipes, DP, Libby, P. "Clinical Assessment of Heart Failure". Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine. Elsevier Saunders. 2012. pp. 505.

Leier, C, Chatterjee, K. "The physical examination in heart failure-Part I". Congest Heart Fail. vol. 13. 2007. pp. 41-47.

Leier, C, Chatterjee, K. "The physical examination in heart failure-Part II". Congest Heart Fail. vol. 13. 2007. pp. 99-104.

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