Outline
Introduction and Goals of Clinical Evaluation, 403
History and Physical Examination: the Core of the Evaluation, 403
Medical History, 404
Symptoms, 404
Information About Past Medical History and Comorbidities, 405
Social and Family History, 406
Familial Cardiomyopathy and Genetic Testing, 406
Physical Examination, 406
Cardiovascular System, 406
Laboratory, 408
The Electrocardiogram, 409
Chest X-Ray, 409
Echocardiography, 409
Cardiac Structure and Systolic Function, 409
Left Ventricular Volumes and Systolic Function, 409
Right Ventricular Systolic Function, 410
Cardiac Volumes, 410
Diastolic Function and Hemodynamics, 410
Determination of Pressures, 410
Valvular Disease, 411
Structural Abnormalities, 411
Pericardial Disease, 411
Dyssynchrony Assessment, 411
Detection of Cardiac Thrombi, 411
Performing Repeat Echocardiograms, 411
Other Imaging Modalities, 411
Ischemic Evaluation: Coronary Anatomy and Myocardial Viability, 411
Morphologic and Functional Evaluation, 412
Imaging for Nonischemic Causes of Cardiac Dysfunction, 412
Imaging to Determine Prognosis, 413
Right-Heart Catheterization, 415
Endomyocardial Biopsy, 415
Assessing Exercise Capacity, 416
Introduction and Goals of Clinical Evaluation
Optimal implementation of heart failure therapy requires expeditious and accurate diagnosis as well as determination of the severity of the disease and, wherever possible, identification of its cause. The earlier in the clinical course that providers recognize the presence and stage of heart failure, the more likely that appropriate treatments will be initiated in a timely manner. In addition, since the clinical course of heart failure and the response to therapy are greatly influenced by a wide variety of risk factors and comorbid conditions, establishing a comprehensive medical, psychological, and social profile of the patient is essential for deciding on the most appropriate management strategies. As outlined in Table 31.1 , the primary goals of the clinical evaluation are to confirm that the constellation of signs and symptoms that brought the patient to medical attention are indeed due to heart failure, determine the cause and severity of cardiac dysfunction, assess functional limitations and impairment in lifestyle, define the underlying etiology of heart failure, consider the various comorbidities and psychosocial issues that could influence the natural history of the disease, and also determine the success of various therapies and assess prognosis. There is no single symptom, physical finding, or test that can achieve all these goals. Recognition and staging of heart failure is compounded by the influence of age, gender, etiology, comorbidities, the time course over which cardiac dysfunction develops, and both physiologic and psychologic adaptations to the presence of this disease. The clinical evaluation of heart failure is based on integrating information from a variety of sources, and when done effectively, it enables clinicians to initiate appropriate therapies in an expeditious and cost-effective manner. In the remainder of the chapter, we describe the modalities used for the clinical assessment of heart failure. The recommendations that are offered are based on information in the medical literature, available guidelines, and our own clinical experience in managing heart failure patients over the years.
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History and Physical Examination: the Core of the Evaluation
Performance of a thorough history and physical examination received a class I recommendation in both the American College of Cardiology/American Heart Association (ACC/AHA) and the European Society of Cardiology (ESC) heart failure guidelines based predominantly on expert opinion (Level of Evidence, C) in both documents. In fact, it is hard to imagine defining management strategies for a heart failure patient without information gleaned from the history and physical examination, and even harder to envision these strategies being successful without knowledge of who the patient is and how they live their life. In addition, the encounter between provider and patient during which the history is taken and physical examination is performed is essential for establishing a level of comfort and trust that will almost certainly be needed by both parties as decisions are made during the course of the patient’s disease.
The signs and symptoms of heart failure are typically caused by either congestion or impaired perfusion of vital organs. As abnormalities in cardiac function progress, increases in right and left ventricular filling pressures lead to the development of congestion in the pulmonary and systemic circulations, respectively. Impaired perfusion may become manifest in virtually any organ system in heart failure patients but is most often detected clinically by abnormalities in cerebral, cardiac, renal, hepatic, and skeletal muscle function. Tissue perfusion is determined by the pressure difference between the arterial and venous systems. Pressures within these vascular beds are in turn influenced by both the total intravascular volume and the ambient level of vasomotor tone.
Medical History
Symptoms
Patients seek medical advice because they don’t feel well and their activities are impaired. Table 31.2 contains a list of symptoms associated with heart failure. Since heart failure can affect virtually all organs in the body, the symptoms described by patients are protean. It is important to recognize that these symptoms alone are insufficient to define the presence or severity of heart failure. A specific symptom should always be viewed in the context of other symptoms, physical signs, and the clinical setting in general. How somatic symptoms are appreciated by the patient and how they are related to the provider can vary considerably. The description of symptoms can be influenced by a variety of factors, including the patient’s threshold for detecting and relating discomfort, their age and previous level of functioning, individual performance goals, and the time course over which symptoms develop. Psychological issues, socioeconomic factors, and differences in the level of education between the patient and the examiner can also influence how a patient relates their symptoms. Needless to say, all these factors should be taken into account when evaluating an individual patient. Many patients have difficulty defining the impact of their symptoms on their activities. We find that the questions outlined in Table 31.3 are helpful in eliciting the full extent of a patient’s impairment. Another tried and true method of determining the severity of a patient’s symptoms is to seek confirmation whenever a family member or significant other accompanies the patient to the examination. The divergence in opinion of the extent of limitation described by the patient and that offered by a more objective source can be quite substantial.
| Fatigue Shortness of breath at rest or during exercise Discomfort while breathing (dyspnea) Rapid breathing (tachypnea) Difficulty in breathing while bending (bendopnea) Orthopnea Paroxysmal nocturnal dyspnea Cough Wheeze Diminished exercise capacity Nocturia Weight gain or weight loss Abdominal pain (particularly confined to the right upper quadrant) Loss of appetite or early satiety Increasing abdominal girth or bloating Edema (of the extremities, scrotum, or elsewhere) Palpitations Syncope History of Cheyne-Stokes respirations during sleep (often reported by the family rather than by the patient) Somnolence, confusion or diminished mental acuity Depression |
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Although none of the symptoms listed in Table 31.2 are sufficient by themselves for determining that heart failure is the cause of the patient’s complaints, some are more specific than others. When present, paroxysmal nocturnal dyspnea (PND) is a very strong indicator that symptoms are due to heart failure, particularly when other conditions that result in nocturnal awakening, including postnasal drip, esophageal reflux, and orthopedic issues, are excluded. PND may also be confused with shortness of breath (SOB) that occurs when patients walk to the bathroom at night after having been awakened by the need to urinate. When PND is suggested, the clinician should confirm that the episodes involve abrupt awakening due to “air hunger”—a sensation that causes the patient to move from a recumbent position to a more upright one, remaining upright for at least several minutes in order to catch their breath. Another helpful clue for defining PND is that PND tends to recur nightly at a relatively constant time after the patient lies down. Another congestive symptom that has recently attained prominence is bendopnea, which is defined as SOB when bending forward, as when a patient puts on their shoes. Bendopnea has been reported in 28% of heart failure patients. When present, it is associated with higher levels of pulmonary artery wedge (PAW) and right atrial (RA) pressures. Symptoms due to impaired cerebral perfusion, including somnolence, confusion, diminished mental acuity, or depression, though common in heart failure patients, are not often related by the patient during the interview. As with functional impairment, it is often the patient’s family member or significant other who describes the presence of these symptoms.
The New York Heart Association (NYHA) functional classification ( Table 31.4 ) is used to quantify symptomatic limitation in heart failure patients and has proved useful for assessing the adequacy of therapy and determining prognosis. It offers a simple and rapid means of detecting changes in the patient’s symptomatic status over time or in response to treatment. As such, it has become the “lingua franca” for communication between providers about the patient’s clinical status. Evaluation of the NYHA functional class also provides important prognostic information, as there is a stepwise increase in morbidity and mortality risk with increasing functional class. While other means of assessing symptoms such as cardiopulmonary exercise testing more accurately determine whether the patient’s subjective complaints are caused by heart failure and can provide a more precise indication of the patient’s limitation, NYHA functional class determination is a standard for assessing and communicating symptomatic status because of its ease and economy.
| Class | Symptoms |
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| Class I (mild) | No limitation of physical activity Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath) |
| Class II (mild) | Slight limitation of physical activity Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea |
| Class III (moderate) | Marked limitation of physical activity Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea |
| Class IV (severe) | Unable to carry out any physical activity without discomfort Symptoms of cardiac insufficiency at rest If any physical activity is undertaken, discomfort is increased |
Patients are also classified according to the stage of heart failure, as depicted in Fig. 31.1 . In contrast to NYHA functional classification, which is based on symptoms alone, the ACC/AHA Heart Failure Staging system incorporates risk factors and changes in the heart’s structure and function into the equation. Whereas patients frequently move to higher or lower NYHA classes as their disease waxes and wanes, a patient’s stage of heart failure can only advance. Also, within stages C and D heart failure, symptoms can vary considerably over time. For instance, a stage C patient hospitalized for an episode of decompensation may have symptoms that improve from NYHA class IV on admission to class I or II at the time of discharge. The use of this staging system has helped alert providers to the substantial numbers of patients who are at risk for developing heart failure. In a community-based survey carried out in the United States, 56% of adults ≥45 years of age were found to have stage A or B heart failure. Striking differences in mortality as the stage advances were also noted in this population, emphasizing the need for risk factor modification and early intervention in order to prevent progression of disease and improve outcomes.
Information About Past Medical History and Comorbidities
Heart failure patients tend to be older and often have comorbidities that influence the presentation, clinical course, prognosis, and response to therapy. Comorbid conditions may also interfere with the diagnostic process, aggravate symptoms, and contribute to a reduction in quality of life. Comorbidities of particular importance in the management of heart failure patients are listed in Table 31.5 . As part of the diagnostic evaluation and, in particular, for designing appropriate management strategies, it is essential for the clinician to have full knowledge of the patient’s comorbidities and how they are being treated.
| Angina Coronary artery disease Frailty Cachexia Malignancies Stroke Peripheral vascular disease Depression Diabetes Gout Arthritis Hyperlipidemia Hypertension Iron deficiency Anemia Chronic kidney disease Chronic obstructive pulmonary disease Asthma Sleep disordered breathing Obesity Thyroid disorders (both hypo- and hyperthyroidism) |
Social and Family History
Understanding the social fabric of the patient’s life, including their cultural background, education, work history, current living situation, and social support, will allow the clinician to gain a more thorough assessment of why they may have developed heart failure (e.g., work exposure, travel experience), and how they perceive their current limitations. It will also provide a context for various therapeutic strategies, particularly those that can be offered to patients with advanced heart failure (i.e., mechanical circulatory support and heart transplantation).
Information from family history can provide clues about etiology of heart failure. A history of cardiovascular risk factors or the presence of heart failure in other family members can influence the direction of the diagnostic evaluation. For instance, knowledge that multiple family members have had myocardial infarctions would direct the clinician toward determining whether coronary artery disease is the cause of the patient’s heart failure.
Familial Cardiomyopathy and Genetic Testing (see also Chapter 24 )
Dilated cardiomyopathy (DCM) is considered to be idiopathic in around half of the cases and approximately a third of these are hereditary. Overall, more than 50 genes have been identified as causes of DCM, with the most common ones being genes related to the cytoskeleton (e.g., titin, lamin, and desmin). For patients with DCM, the ACC/AHA Heart Failure Guideline gives a class I recommendation for obtaining a three-generational family history. A history of early onset heart failure or sudden cardiac death in first-degree family members should trigger genetic testing to determine if a familial cardiomyopathy (defined as the presence of DCM in ≥2 relatives) is present.
Physical Examination
Cardiovascular System
Despite the plethora of blood chemistries, biomarker analyses, imaging studies, and other diagnostic tests that all heart failure patients are subjected to in today’s medical environment, a carefully performed physical examination provides unique information to the clinician. Oversights in the physical examination are a major contributor to missed or delayed diagnosis, and they lead to exposure to unnecessary tests, initiation of incorrect treatments, and other adverse consequences. In a review of 208 case vignettes, Verghese et al. concluded that physical examination inadequacies are a preventable source of medical error and that adverse events are caused mostly by failure to perform the relevant examination. Clinical signs of congestion have also been shown to be independent predictors of prognosis in heart patients. In a post-hoc analysis of 1376 patients with symptomatic left ventricular systolic dysfunction and a documented recent episode of atrial fibrillation, congestive signs on the physical examination (i.e., peripheral edema, jugular venous distension, a third heart sound, and pulmonary rales) were associated with worse prognosis. Physical findings in heart failure patients have been extensively described by a group of expert clinicians, and Table 31.6 lists the ones that have been found to be most helpful by the authors. A discussion of these signs follows.
- 1.
General. The exam begins when the clinician enters the room, and it uses multiple senses. Visual examination of the patient’s body habitus, noting the presence of obesity, cachexia, a neurologic deficit, or orthopedic problem, provides valuable diagnostic information. Vertical head bobbing due to a forceful pulse is seen in patients with chronic aortic insufficiency, while lateral movement from side to side may indicate the presence of severe tricuspid insufficiency. Shortness of breath during normal conversation or when the patient moves to the examining table suggests the presence of pulmonary congestion or underlying lung disease. The clinician should note whether the patient is pale, flushed, perspiring, or in pain, and be alerted to the presence of unusual odors indicating poor personal hygiene, tobacco, or alcohol use. The astute examiner can detect ketoacidosis by its characteristic fruity odor or advanced liver disease by the “mousy” smell of fetor hepaticus.
- 2.
Vital signs provide extensive information about the patient’s current level of well-being, and they may provide clues into the etiology of heart failure. Normal heart rate, blood pressure, respiratory rate, and oxygen saturation are associated with clinical stability, whereas rapid heart rate, low blood pressure (usually below 90 mm Hg), and rapid shallow breathing with reduced oxygen saturation are indicators of decompensation. The patient’s pulse rate and characteristics may provide clues regarding etiology of heart failure (e.g., tachycardia induced cardiomyopathy) or the presence of cardiac arrhythmias (e.g., atrial fibrillation). A narrow pulse pressure (less than 25% of systolic blood pressure) is a sign of reduced left ventricular stroke volume, while a wide arterial pulse suggests the presence of a high output state, chronic aortic insufficiency or a stiff, noncompliant vascular bed (as in heart failure with preserved ejection fraction [HFpEF] patients). Peripheral findings indicating a wide pulse pressure (e.g., Quincke or water hammer pulse) are often found in patients with chronic aortic insufficiency, while evidence of poor capillary refill suggests low cardiac output/and or severe vasoconstriction.
- 3.
A low volume carotid pulse is consistent with reduced cardiac output or (when there is delayed rise) aortic stenosis, while a bounding pulse indicates a large stroke volume, stiff noncompliant vascular bed, or (particularly when there is rapid falloff) chronic aortic insufficiency. The contour of the carotid pulse may also contain clues about etiology. A notch or shudder during the upstroke (anacrotic shoulder of aortic stenosis), a double bump in its midportion (bisferiens pulse of chronic aortic insufficiency), or an initially normal carotid upstroke that slows midway through (spike and dome pulse of hypertrophic obstructive cardiomyopathy) are pathognomonic physical findings.
- 4.
The jugular venous pulse is the most useful physical finding for determining a patient’s volume status. It has been shown to have better sensitivity and specificity than other signs, such as pulmonary rales or the presence of an S 3 . Not only does an elevated JVP detect systemic congestion, but there is good sensitivity (70%) and specificity (79%) between high JVP and elevated left-sided filling pressure. Changes in JVP with therapy usually parallel changes in left-sided filling pressure. Significant interobserver variability regarding the extent of JVP elevation, however, has been noted. Both sensitivity and specificity of the JVP in detecting congestion can be improved by exerting pressure on the right upper quadrant of the abdomen while assessing venous pulsations in the neck (i.e., hepatojugular or abdominojugular reflux). The jugular pulse is best assessed in a warm, well-lighted room with the patient comfortably seated on the exam table with the head elevated at 45 degrees. The venous pulse can be identified by its predominant inward movement that distinguishes it from the sharply outward bounding carotid pulse. When the meniscus of the pulse is identified, the vertical distance to the angle of Louis is measured and 5 cm added to account for the distance to the midpoint of the right atrium. A normal venous pressure is less than 8 cm H 2 O. While the position of the meniscus of the venous pulse in the neck will vary according to the patient’s degree of elevation, the actual vertical height remains relatively constant so that determination of pulse is theoretically independent of the patient’s position. However, at lesser degrees of elevation, the meniscus of the venous pulse may rise to the angle of the jaw, thereby obscuring the true extent of elevated venous pressure. Increasing the elevation of the head of the bed will overcome this limitation. Also, observation for venous pulsation along the side of the ear above the angle of the jaw can help detect very high levels of venous pressure.
- 5.
Lung examination is used to assess for presence of pulmonary congestion that can be manifest as dullness and diminished breath sounds due to a pleural effusion, fine crackles (rales) due to fluid in the intra-alveolar space, or wheezes due to bronchospasm. When present, rales are specific in confirming that heart failure is present. However, in patients with chronic disease, lymphatic hypertrophy serves to remove fluid buildup in the lungs so that rales are often absent, even when filling pressures are elevated. Rubs indicative of inflammation of the pleural surface can also often be detected by auscultation or even palpation during a deep inspiration.
- 6.
Cardiac examination starts with observation, palpation, and percussion of the chest, which is then followed by auscultation. Chest wall deformities, particularly bowing of the left chest, may occur in patients with congenital abnormalities. The presence of cardiomegaly can often be detected by observing an apical impulse that is displaced laterally in the left precordium. Pulsations in the apical impulse during early and late diastole are the visual analogues of the S 3 and S 4 heart sounds. A visible sternal lift can be appreciated in many patients with pulmonary hypertension, but can also be caused by anterior displacement of the heart by the posteriorly situated left atrium as it fills rapidly during systole, as occurs in patients with severe mitral regurgitation. Percussion of the left cardiac border >8 cm to the left of the midsternal line indicates that the heart is enlarged. Palpation of the precordium builds on the visual evaluation of pulsations at the cardiac apex and over the sternum. It is also used to detect an accentuated second heart sound (as occurs in pulmonary hypertension) and the presence of thrills associated with turbulent flow across a heart valve or due to a structural abnormality such as a ventricular septal defect (VSD). Auscultation for murmurs, gallops, and rubs completes the cardiac examination. While a complete overview of cardiac auscultation is beyond the scope of the chapter, the general focus is to detect the presence of valve abnormalities that could be the cause (e.g., aortic stenosis) or consequence (e.g., mitral or tricuspid insufficiency) of heart failure, get an insight into ventricular filling patterns by listening for the presence of an S 3 and S 4 , and determine if other abnormalities (e.g., VSD) or pericardial disease are present. The intensity of heart sounds may also help indicate the presence of cardiac abnormalities. The intensity of S 1 can be diminished by a long PR interval or other conditions (e.g., aortic insufficiency) that lead to left ventricular volume overload while P 2 intensity is increased in patients with pulmonary hypertension.
- 7.
Abnormal physical findings on the abdominal examination due to heart failure are mostly consequences of congestion and include hepatomegaly, splenomegaly, and ascites. The latter is best assessed by testing for shifting dullness, particularly in patients where detection of a fluid wave may be obscured by obesity.
- 8.
Other findings associated with congestion include scrotal edema (grossly underreported, particularly by trainees), presacral edema, and edema of the lower extremities. For the latter, both the depth of indentation caused by pressure of the examiners thumb and how long the pit remains are used determine the grade, which ranges from 1 to 4.
- 9.
While low cardiac output (which may be further accentuated by peripheral arterial constriction) can lead to an abnormally low body temperature, it is more commonly associated with localized reduction in temperature in peripheral tissues. The examiner may detect cool hands, feet, or nose in patients with low cardiac output. Marked reductions in tissue perfusion are characterized by a dusky mottled appearance of the extremities. Milder degrees of hypoperfusion, however, may be manifest by reduced temperature only in watershed areas such as the knee caps.
- 10.
Low cardiac output and decreased cerebral hypoperfusion can lead to drowsiness, forgetfulness, and other signs of reduced mental acuity. In extreme cases, patients may be judged as having dementia, but the real cause of altered mentation becomes apparent as the patient recovers with treatments that raise cerebral perfusion.
| Tachycardia Extra beats or irregular rhythm Narrow pulse pressure or thready pulse a Pulsus alternans a Tachypnea Elevated jugular venous pressure Positive hepatojugular reflux Dullness and diminished breath sounds at one or both lung bases Rales, rhonchi, or wheezes Cardiac apex displaced leftward or inferiorly Sustained apical impulse Parasternal lift S 3 or S 4 (either palpable or audible) Tricuspid or mitral regurgitant murmur Hepatomegaly (often accompanied by right upper quadrant discomfort) Ascites Presacral edema Anasarca a Cool or mottled extremities a Pedal edema Chronic venous stasis changes |
Laboratory
Essential
A list of routine diagnostic tests used for the evaluation of patients with heart failure is provided in Table 31.7 . The goal of this testing is to detect reversible or treatable causes of heart failure, determine the patient’s suitability for particular therapies, and reveal the presence of comorbidities that might affect treatment strategies. Repeated determination of electrolyte values, renal function, and other variables is also required as the clinical course evolves over time.
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Selective
There are a variety of uncommon causes of heart failure, including exposure to toxic substances (e.g., recreational substance abuse, heavy metals), infections (e.g., HIV/AIDS, Chagas disease), infiltrative diseases (e.g., amyloidosis, glycogen storage diseases, lysosomal storage diseases), hormonal abnormalities (e.g., growth hormone, pheochromocytoma), and nutritional deficiencies (e.g., thiamine, L-carnitine, selenium). Testing for these causes for heart failure should be considered when one of them is suspected. The ACC/AHA Guidelines give class IIa recommendations for screening for hemochromatosis or HIV in selected patients who present with heart failure and for obtaining diagnostic tests for rheumatologic diseases, amyloidosis, or pheochromocytoma when there is clinical suspicion of these diseases.
Biomarkers (see also Chapter 33 )
Natriuretic peptides, troponins, and numerous additional biomarkers related to inflammation, oxidative stress, vascular dysfunction, and myocardial matrix remodeling have been implicated in heart failure. Natriuretic peptides in particular have assumed an important role in the clinical evaluation of patients. Their measurement in ambulatory patients with dyspnea are given a class I recommendation to support clinical decision making regarding the diagnosis of heart failure. They are most helpful in making the diagnosis in cases where information obtained from the history and physical examination leaves the examiner uncertain about whether or not heart failure is present. As patients with levels below the diagnostic cut-point are highly unlikely to experience heart failure, natriuretic peptide levels are useful in excluding heart failure. In the nonacute setting, values of 35 pg/mL for B-type natriuretic peptide (BNP) and 125 pg/mL for NT-proBNP are considered the upper limit of normal, while in the acute setting these values are increased to 100 pg/mL and 300 pg/mL, respectively. While discordance between natriuretic peptide levels and the rest of the clinical assessment should alert the clinician to the possibility that they may have erred in diagnosing heart failure, it is important to recognize that a number of factors can alter natriuretic peptide levels. These are summarized in Table 31.8 . Thus natriuretic peptide levels should always be interpreted in the context of the clinical setting. Measurement of natriuretic peptides are also given a class 1 recommendation for use in patients presenting with dyspnea to help support the diagnosis of heart failure and establish disease prognosis or severity in both ambulatory and acutely ill heart failure patients. Measurement of biomarkers of myocardial injury or fibrosis may be considered (class IIb recommendation) for added risk stratification.
| Cardiac |
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| Heart failure Acute coronary syndromes Pulmonary embolism Myocarditis Left ventricular hypertrophy Hypertrophic or restrictive cardiomyopathy Valvular heart disease Congenital heart disease Atrial and ventricular tachyarrhythmias Heart contusion Cardioversion, ICD shock Surgical procedures involving the heart Pulmonary hypertension Noncardiac Advanced age Ischemic stroke Subarachnoid hemorrhage Renal dysfunction Liver dysfunction (mainly liver cirrhosis with ascites) Paraneoplastic syndrome Chronic obstructive pulmonary disease Severe infections (including pneumonia and sepsis) Severe burns Anemia Severe metabolic and hormone abnormalities (e.g., thyrotoxicosis, diabetic ketosis) |
The use of natriuretic peptides to screen ACC/AHA stage A patients with risk factors for developing heart failure is given a class IIa recommendation based on the expectation that the presence of elevated levels will be followed by aggressive initiation of guideline directed medical therapy and other life-style strategies designed to prevent further progression of disease. Whether this approach will prove cost-effective and have an impact on quality of life and outcomes, however, requires further study.
The Electrocardiogram
The electrocardiogram (ECG) is an essential part of the initial evaluation of a patient with new onset or suspected heart failure. In the ACC/AHA guidelines, obtaining an ECG is given a class I recommendation, while the ESC guidelines stress the negative predictive value of a normal ECG in helping exclude the presence of heart failure. An ECG should also be obtained whenever there is an episode of acute heart failure or a heart failure patient’s condition deteriorates over time. Sinus tachycardia due to sympathetic nervous system activation is seen with advanced heart failure or during episodes of decompensation. The presence of atrial arrhythmias on the ECG may explain why heart failure has worsened, as well as provide a target for therapeutic interventions. Ventricular arrhythmias ranging from isolated PVCs to more complex arrhythmias, including runs of nonsustained ventricular tachycardia, are common in heart failure patients. The presence of ventricular arrhythmias raises concerns about electrolyte abnormalities and also the potential risk of life-threatening rhythm disturbances. A widened QRS complex exceeding 120 milliseconds (msec) in a patient with systolic dysfunction is a useful indicator of ventricular dyssynchrony. The QRS duration is essential in determining whether or not cardiac resynchronization therapy (CRT) should be recommended, with both the QRS pattern and duration used to define the strength of the recommendation for CRT, with the highest level of enthusiasm for patients who have a left bundle branch block (LBBB) pattern with QRS duration ≥150 msec. The P wave morphology helps detect left atrial enlargement (LAE). A biphasic P wave in lead V 1 is a sensitive indicator of LAE, while increased P wave duration in lead II is more specific. An increase in P wave amplitude in lead II suggests that right atrial enlargement may be present. An unusual P wave axis (particularly when coupled with a short PR interval in the setting of atrial arrhythmias) suggests that an ectopic atrial focus or accessory pathway may be present. Increased voltage in lead AVL or in the limb leads should lead to consideration of left ventricular hypertrophy and a search for its causes. A large R wave, prolonged QRS, and ST-T wave changes in the right precordial leads can be a clue that right ventricular hypertrophy is present and should trigger a search for conditions that cause primary or secondary pulmonary hypertension. The presence of Q waves suggests that heart failure may have been caused by a myocardial infarction (or possibly amyloidosis); new or reversible repolarization changes raise concerns that clinical deterioration may be due to worsening myocardial ischemia, even when chest pain is absent. Low QRS voltage suggests the presence of an infiltrative disease, particularly amyloidosis, or pericardial effusion.
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