Clinical Evaluation of Heart Failure

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.

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.

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.

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.

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.