General examination and vital signs provide insight into the presence and severity of heart failure. Patients may have evidence of respiratory distress with tachypnea, hypoxemia on pulse oximetry, inability to speak in full sentences, inability to lie flat, agitation, and use of accessory muscles of respiration. Observation of coughing or wheezing, especially with walking or while recumbent suggests the presence of pulmonary congestion. Respiratory rate is important and should be counted rather than estimated. Tachypnea may reflect severe pulmonary congestion, pulmonary edema and/or respiratory failure. The presence of Cheyne-Stokes respirations suggests that the patient has chronic severe heart failure.

Tachycardia may reflect low cardiac output, sympathetic nervous system activation, or a supraventricular arrhythmia that may be a heart failure precipitant. An irregular pulse may be due to premature ventricular beats or preexisting or new onset atrial fibrillation. An elevated temperature suggests infection as a possible contributor to heart failure decompensation. Temperature < 36 °C has been shown to be associated with a 51 % higher risk of the composite of HF rehospitalization or CV death when compared with the index group of patients with temperature >36.5 °C in the Efficacy of Vasopressin Antagonism in Heart Failure Outcome Study with Tolvaptan (EVEREST) trial [13].

In acute heart failure, systolic and mean blood pressures are important in guiding the choice of initial therapies including vasodilators, inotropic agents, vasopressors, intra-aortic balloon pump therapy or mechanical circulatory support. Low blood pressure, especially if associated with low pulse pressure, tachycardia and cool distal extremities, is a sign of low cardiac output and inadequate systemic perfusion. Low blood pressure is unusual in patients with ADHF but when present, identifies a patient at high risk of in-hospital mortality who may need more intensive care including admission to the CCU, treatment with inotropic agents (or vasopressors), and/or support with an intra-aortic balloon pump [6, 14]. As heart failure progresses, systolic blood pressure decreases, diastolic blood pressure is unchanged and pulse pressure (systolic blood pressure-diastolic blood pressure) decreases. A pulse pressure/systolic pressure ratio (referred to as the “proportional pulse pressure”) of less than 0.25 suggests that the patient has a cardiac index of less than 2.2 L/min/m² [15].

Approximately half of patients with ADHF have an initial systolic blood pressure of >140 mmHg. Patients who present with hypertension may have pulmonary congestion related to volume redistribution due to a mismatch between rapidly increasing blood pressure and impaired contractile reserve rather than total body fluid accumulation. These patients may have more severe pulmonary congestion and less volume overload than normotensive patients with ADHF. These patients generally benefit from parenteral diuretics but may also benefit from early initiation of vasodilator therapy [16–22].

Agitation or altered mental status should raise concern about brain hypoperfusion due to severely reduced cardiac output, even in the setting of normal blood pressure. Patients with low cardiac output may also have cool distal extremities, diaphoresis, pallor, tachypnea, dyspnea at rest, low systolic blood pressure, low pulse pressure, and low proportional pulse pressure. Feeling the skin of the hands and feet can give important information about systemic perfusion and the presence of systemic vasoconstriction. The temperature of the hands/feet should be compared to that of the upper arm/leg. Relative coolness of the distal extremities suggests low cardiac output [15, 23]. Some authors have suggested that feeling the temperature of the forearms and calves rather than hands and feet (which may be cool from anxiety) may be more specific for assessment of systemic perfusion [15].

An important goal of the initial physical exam is to identify and quantitate pulmonary and systemic venous congestion. Historically, four signs have been used to determine whether cardiac filling pressures are elevated including the presence of: jugular venous distention, pulmonary rales, a ventricular gallop (S3) and lower extremity edema.

Lung examination provides insight into the cause of dyspnea, volume status and the presence of pulmonary congestion. Percussion of the posterior chest may elicit dullness at one or both bases indicating the presence of a pleural effusion. Patients may also have associated decreased breath sounds. Pleural effusion is generally a manifestation of elevated right and left sided filling pressures. Bilateral pleural effusions are more common than unilateral effusions. When a unilateral effusion is present in a patient with ADHF, it is generally on the right. An isolated left pleural effusion is an unusual manifestation of decompensated heart failure.

Pulmonary crackles (or rales) are caused by transudation of fluid from the pulmonary capillaries into the alveolar space. Crackles due to heart failure generally are audible from the base upward and do not clear with cough or deep inspiration. Patients with chronic heart failure may not have rales despite significantly elevated pulmonary capillary wedge pressure and clinical decompensation [8]. The absence of rales in patients with chronic heart failure does not exclude decompensated heart failure as a cause of worsening dyspnea. Rales may be due to other pulmonary pathology. Rales associated with atelectasis are generally coarse and clear with cough or deep inspiration. Rales associated with pneumonia may be heard at locations other than the bases, are frequently unilateral and commonly associated with fever, leukocytosis, and other findings of pulmonary consolidation such as bronchial breath sounds and egophony. Patients with ADHF may present with “cardiac asthma” with wheezing and decreased airflow. Cardiac asthma is probably caused by a combination of reflex bronchoconstriction in response to elevated pulmonary and bronchial vascular pressure, obstruction from intraluminal edema fluid, and bronchial mucosal swelling [24].

Lower extremity edema is a common finding in patients with ADHF. In patients with chronic heart failure, edema may be absent despite symptoms of dyspnea and elevated pulmonary capillary wedge pressure [8]. Edema is not a specific finding for heart failure as patients may have edema from other causes including venous insufficiency, cirrhosis, hypoalbuminemia, kidney disease including nephrotic syndrome, pregnancy, and treatment with a number of medications including calcium channel blockers (particularly dihydropyridines, e.g. amlodipine, nifedipine), thiazolidinediones, docetaxel, gabapentin, pregabalin, nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, fludrocortisone, and vasodilators (hydralazine, minoxidil, diazoxide; less frequent – alpha1 blockers, and methyldopa). However, edema is a specific finding of heart failure when associated with elevated jugular venous pressure [10, 11].

The jugular venous pressure (JVP) is the single most important finding in the assessment of intravascular volume status. JVP provides a direct measurement of right atrial (RA) pressure, an estimate of right ventricular filling pressure and some insight into pulmonary capillary wedge and left atrial pressures. JVP is measured as the vertical distance from the mid right atrium to the top of the observable column of blood (or meniscus) in the internal jugular vein and is expressed in centimeters of water.

A number of methods have been suggested to estimate JVP. Assessment of JVP may be made with the upper torso of the patient elevated at 30–45°. When assessing JVP, it is important that the height of the meniscus of the internal jugular vein be clearly identified. In patients with ADHF, a meniscus may not be seen at 30–45° because of high JVP. It is recommended that JVP be assessed at both 30–45° and 90° (sitting upright) to avoid underestimating filling pressures [15, 25]. The position of the right atrium can be estimated to be at the intersection of the fourth or fifth intercostal space and the mid-axillary line. The JVP can be estimated by measuring the vertical distance from the position of the right atrium to the top of the meniscus. Alternatively, the position of the right atrium can be estimated to be 5 cm below the angle of Louis. Using this method, JVP can be estimated to be the vertical distance from the angle of Louis to the meniscus plus 5 cm of water.

Another alternative is to measure JVP in the upright sitting position. In most patients, the distance from the right atrium to the clavicle is 10 cm in the upright position. If a meniscus is seen above the clavicle, the patient has an elevated JVP. The JVP is 10 cm plus the measured distance from the clavicle to the observed meniscus. This method gives JVP <10 cm of water, 10–12 cm, 12–14 cm, etc. This method is less cumbersome, is more accurate, and has less intra- and inter-observer variability and avoids underestimating JVP. If a meniscus is not observed in the upright position, assessment of JVP should then be made at progressively decreasing elevations of the torso above supine. If a meniscus is not seen while lying flat, the patient may be volume depleted [15, 25].

Some studies have found poor inter-observer reliability in the assessment of JVP by ED physicians [26]. A study of patients with heart failure that compared estimates of JVP by exam, estimates of RA pressure by echo and RA pressure measured by a pulmonary artery catheter in patients with heart failure found that clinical assessment of JVP accurately estimated normal RA pressure but tended to underestimate RA pressure in patients with elevated RA pressure [27]. Others have suggested that physical examination is helpful in determining whether central venous pressure is high or low but not in assessing a specific pressure [28, 29].

In the ESCAPE trial, estimates of JVP by physical exam recorded on initial history and physical exam were compared with RA pressure on invasive hemodynamic monitoring in 194 patients with chronic severe symptomatic heart failure randomized to the PA catheter group [9]. Estimated JVP (in cm of water) was converted to RA pressure (in mmHg) by multiplying JVP (in cm of water) by 0.736, the ratio of the density of water relative to the density of mercury. (1 cm of water equals 0.736 mmHg.) Measured right atrial pressure was less than 8 mmHg in 82 % of patients (9/11) who had an estimated JVP of less than 8 mmHg. Measured RA pressure was ≥8 mmHg in 82 % (149/181) of patients who had an estimated JVP ≥8 mmHg. Measured right atrial pressure was >12 mmHg in 70 % (80 of 114) of patients who had an estimated JVP of >12 mmHg.

Elevated JVP is helpful in predicting elevated pulmonary capillary wedge pressure. In the ESCAPE trial, estimated RA pressure ≥12 mmHg was strongly associated with PCWP ≥30 mmHg with an odds ratio of 4.6 [9]. In a study of 1000 patients with advanced heart failure undergoing transplant evaluation, 79 % of patients had concordance of right atrial and pulmonary capillary wedge pressures defined as an RAP ≥10 mmHg with a PCWP ≥22 mmHg [30]. An RA pressure of ≥10 mmHg had a positive predictive value of 88 % to identify a PCWP ≥22 mmHg. In another study of 4079 potential transplant candidates, elevated pressures were defined as RAP ≥10 mmHg and PCWP ≥22 mmHg. Pressures were described as “concordant” if the RA and PCWP were both either high or low. The frequency of concordant pressures over three sequential 4 year periods was 74 %, 72 %, and 73 % [31]. In another study of 537 patients hospitalized for ADHF who underwent right heart catheterization, 36 % of patients had concordant low filling pressures (RA <10 mmHg; PCWP <22 mmHg) and 36 % of patients had concordant high filling pressures (RA ≥10 mmHg; PCWP ≥22 mmHg [32]. Fifteen percent of patients had RA <10 with PCWP ≥22 mmHg (“High-Left Mismatch”) and 13 % of patients had RA ≥10 mmHg and PCWP <22 mmHg (“High-Right Mismatch”).

On multivariate analysis, patients with a history of symptomatic heart failure who were enrolled in the Studies of Left Ventricular Function (SOLVD) treatment trial and who had elevated JVP had an increased risk of hospitalization for heart failure, death or hospitalization for heart failure, and death from pump failure [33].

In patients with chronic severe heart failure, findings of volume overload (rales, elevated JVP and lower extremity edema) identify patients with an elevated PCWP. However, rales, elevated JVP and rales may be absent despite an elevated PCWP. In a study of 50 patients with chronic heart failure, physical findings of heart failure were compared with hemodynamic measurements. All 10 patients with lower extremity edema had an RA pressure ≥10 mmHg. All patients with an RA pressure ≥10 mmHg had an elevated PCWP ≥22 mmHg. JVP was the most sensitive finding on exam for elevated PCWP. No patient with edema, rales or elevated JVP had a wedge pressure <22 mmHg. However, 18/43 patients (42 %) with PCWP ≥22 mmHg and 8/18 (44 %) of patients with PCWP ≥35 mmHg had no findings of volume overload on physical exam [8].

In ADHF, the apical impulse may be displaced leftward indicating cardiac enlargement. A late diastolic gallop (S4) may be heard, especially in patients with heart failure with preserved systolic function in sinus rhythm. An early diastolic gallop (S3) may be heard in patients with heart failure and systolic dysfunction. There is conflicting evidence whether an S3 is specific for elevated LVEDP [8, 34] but its presence reliably predicts the presence of left ventricular dysfunction [8, 34]. A holosystolic murmur of functional mitral regurgitation is common in patients with ADHF and systolic dysfunction. Patients with biventricular dysfunction, pulmonary hypertension or isolated right heart failure may have a murmur of tricuspid regurgitation. This can be distinguished from a murmur of mitral regurgitation by the location of the murmur at the left sternal border and an increase in the intensity of the murmur with inspiration.

Wang et al. reviewed 22 studies of patients who presented to the emergency department with dyspnea to assess the usefulness of history, symptoms, physical findings, and routine diagnostic studies (chest radiograph, electrocardiogram and serum B-type natriuretic peptide) to differentiate heart failure from other causes of dyspnea. Many clinical characteristics increased the probability that dyspnea was caused by heart failure. The finding in each category that best predicted that dyspnea was due to heart failure was the presence of: a past history of heart failure; the symptom of paroxysmal nocturnal dyspnea; sign of a third heart sound; chest radiograph showing pulmonary venous congestion; and electrocardiogram showing atrial fibrillation. The finding in each category that best predicted that dyspnea was not due to heart failure was the absence of: a past history of heart failure; the symptom of dyspnea on exertion; rales on physical exam; chest radiograph showing cardiomegaly; and any abnormality on electrocardiogram [35].

Many heart failure practitioners have found a 2 × 2 dichotomous matrix based on a clinical assessment of volume status (congestion/no congestion) (“wet” or “dry”) and systemic perfusion (adequate perfusion/clinically important hypoperfusion) (“warm” or “cold”) to be useful in characterizing the clinical status of patients with ADHF and in developing a therapeutic plan [36]. See Fig. 2.1 in Chap. 2 [37]. Signs, symptoms and laboratory data that suggest a patient is congested or “wet” include: orthopnea, jugular venous distention, rales, ascites, peripheral edema, dyspnea at rest or with exertion, orthopnea, PND, peripheral edema, abdominal distention, unexplained weight gain, rales, jugular venous distention, hepatojugular reflux, hepatomegaly, and elevated B-type natriuretic peptide (BNP) or n-terminal pro-BNP. Signs and symptoms that suggest a patient has compromised perfusion or is “cold” include: a narrow pulse pressure, a proportional pulse pressure of <0.25, pulsus alternans, symptomatic hypotension (without orthostasis), cool distal extremities, anxiety and impaired mentation.

A prospective analysis of 452 patients admitted to an academic heart failure service found that clinical assessment of a patient’s hemodynamic profile could be used to predict outcomes. Patients with initial “warm-wet” and “cold-wet” profiles had an increased risk of death or urgent transplant on multivariate analysis (HR 2.48; P = 0.003). These profiles were also associated with an increased risk of death or urgent transplant when patients with NHYA FC III (HR 2.23, p = 0.026) and NYHA FC IV (HR 2.73, p = 0.009) symptoms were analyzed separately [23]. In the ESCAPE trial, clinician determined “cold” vs. “warm” profile was associated with a lower median measured cardiac index in the “cold” patients (1.75 vs. 2.0 L/min/m²; p = 0.004). On Cox regression analysis, “cold” or “wet” profiles at the time of discharge conveyed a 50 % increased risk of death or rehospitalization [9].

Patients with right heart failure may have a right-sided S3, increased intensity of the pulmonic component of the second heart sound (in patients with pulmonary hypertension), a murmur of tricuspid regurgitation, hepatomegaly and ascites. A pulsatile liver may be palpable in patients with severe tricuspid regurgitation.

Minor abnormalities of serum electrolytes are common in patients with ADHF and may be due to neurohormonal activation, low cardiac output, or heart failure medications. The reported incidence of hyponatremia defined as a serum sodium ≤ 135 mEq/L varies widely between 7.7 and 45 % [38, 39]. In EHFS I, 20 % of patients were hyponatremic [37]. Hypokalemia is common in patients treated with loop diuretics. Hyperkalemia occurs in approximately 8 % of patients with ADHF in the setting of chronic heart failure and is associated with treatment with angiotensin converting enzyme inhibitors (ACEIs), angiotensin receptor blockers (ARBs), mineralocorticoid antagonists (MRAs), potassium supplementation, potassium sparing diuretics, and chronic or acute renal insufficiency [39, 40]. Diabetes is common in patients with ADHF (44 % in ADHERE; 41.5 % in OPTIMIZE) and poor glycemic control may accompany or contribute to ADHF [41].

Renal dysfunction is common in patients with ADHF. In the ADHERE Registry, chronic renal insufficiency was reported in 30 % of patients. 9 % of patients had a creatinine on admission of >3.0 mg/dL and 21 % had a creatinine >2.0 mg/dL. Five percent were on chronic dialysis [1]. In OPTIMIZE-HF, the mean creatinine was 1.8 mg/dL [6]. In EHFS I, renal dysfunction was reported to have complicated management in 18 % of patients. Serum creatinine was ≥150 μmol/l (1.7 mg/dL) in 16 % of patients and ≥200 μmol/l (2.3 mg/dL) in 7 % [2]. In a nationwide, prospective, observational study of 206 cardiology centers with intensive cardiac care units in Italy, 47 % of patients admitted with acute heart failure had renal dysfunction defined as creatinine ≥1.5 mg % (mg/dL) [39].

Patients with HF commonly have risk factors associated with both heart and kidney disease including diabetes mellitus, hypertension and vascular disease. Elevated BUN and creatinine may be manifestations of renal hypoperfusion in the setting of low cardiac output or in the setting of marked neurohormonal activation even in the face of normal cardiac output and normal or elevated filling pressures. Elevated BUN and creatinine may also be a manifestation of hypovolemia with low filling pressures in the setting of diuretic therapy. The BUN/creatinine ratio may be elevated in the setting of low cardiac output, neurohormonal activation or volume depletion. In each of these conditions, the proximal tubular absorption of sodium is increased. This is accompanied by reabsorption of BUN but not creatinine. Treatment with ACEIs or ARBs may also contribute to renal dysfunction particularly in the setting of renal artery stenosis, severe chronic heart failure or volume depletion [42, 43]. It has been our observation that lower urinary tract obstruction is a common reversible cause of abnormal renal function in older men with ADHF.

Anemia is common in patients with ADHF. The World Health Organization defines anemia as hemoglobin (Hgb) <13.0 g/dL in men and <12.0 g/dL in women. In clinical trials and large HF registries, the prevalence of anemia has ranged from 15 to 61 % overall and from 14 to 70 % among hospitalized patients [44]. In a meta-analysis of 34 cohort studies or retrospective analyses of randomized controlled trials in HF which included 153,180 patients, 37.2 % of patients were anemic. Anemia was associated with an increased risk of mortality in patients with HFrEF and HFpEF with an adjusted hazard ratio of 1.46 [45].

In the OPTIMIZE – HF registry, half of the patients had a hemoglobin <12.1 g/dL and 25 % had a hemoglobin of 5–10.7 g/dL. Patients with low hemoglobin tended to be older, female, and Caucasian and more commonly had preserved systolic function and elevated creatinine. Low hemoglobin was associated with higher in-hospital mortality, longer hospital length of stay and more readmissions at 90 days [46]. In EHFS I, a hemoglobin <11 g/dL was reported in 18 % of men and 23 % of women [2]. In patients with ADHF in Italy, a hemoglobin <12 g/dL was present in 46 % of patients [39]. In a large population-based cohort of Canadian patients discharged after hospitalization for new onset HF, 17 % had anemia, 58 % of whom had anemia of chronic disease. Anemic patients were more likely to be older, female, and have a history of chronic renal insufficiency or hypertension. Anemic patients had a significantly greater risk-adjusted mortality (HR = 1.34) compared with non-anemic patients [47]. In the EVEREST Trial, 34 % of patients with systolic dysfunction hospitalized for ADHF were anemic at baseline. 73 % of patients who were anemic at baseline were anemic at discharge or day 7 and 6 % of patients without anemia developed anemia by discharge or day7. Anemia at discharge but not on admission was associated with an increased risk of long-term all-cause mortality and short-term (≤100 days post-discharge) cardiovascular mortality or CHF hospitalization [48].

Anemia in heart failure is multifactorial [44]. In patients with acute decompensation, plasma expansion due to salt and water overload may cause dilutional anemia [49, 50]. Anemia may also be caused by renal dysfunction with inappropriate erythropoietin production, pro-inflammatory cytokine activation with anemia of chronic disease, iron deficiency and defective iron utilization [44, 51]. In a community based study of patients with HF due to systolic dysfunction, the relationship between anemia and renal insufficiency was explored. Anemia was present in 32 % of patients. Low serum iron or low ferritin was found in 43 % of patients with anemia. Renal dysfunction (defined as a glomerular filtration rate <60 ml/min by the Modification of Diet in Renal Disease (MDRD) equation) was present in 54 % of patients. 41 % of patients with renal dysfunction and 22 % of patients without renal dysfunction were anemic. Anemia and renal dysfunction independently predicted mortality and the effects were additive [52]. In patients hospitalized for ADHF who had a thorough evaluation for underlying causes of anemia (defined as hemoglobin <12 g/dL in men and <11.5 g/dL in women), iron deficiency was the most common cause of anemia with depleted iron stores found in 73 % of anemic patients on bone marrow aspiration. Serum ferritin was not a reliable marker of iron deficiency in this study [53].

Low “relative lymphocyte count” or “lymphocyte ratio” (total number of lymphocytes/total number of leukocytes × 100) is an independent predictor of mortality in outpatients with heart failure [54]. In the EVEREST trial, patients with low relative lymphocyte count tended to be older, more likely to be male, had higher rates of comorbid disease and were more likely to have a history of prior myocardial infarction and coronary revascularization. Patients with low relative lymphocyte ratio had significantly lower presenting systolic and diastolic blood pressure, higher mean heart rates, lower serum sodium levels, higher blood urea nitrogen, and higher natriuretic peptide levels. These patients were less likely to receive evidence-based HF medications. After adjusting for multiple risk factors, relative lymphocyte count <15.4 % was an independent predictor of all-cause mortality and cardiovascular mortality or HF hospitalization in the first 100 days following discharge [55].

In the Preliminary study of RELAXin in Acute Heart Failure (Pre-RELAX-AHF), patients admitted with acute heart failure, SBP ≥125 mmHg, and BNP ≥350 pg/ml were randomized to the vasodilator relaxin or placebo. Patients with a lymphocyte ratio <13 % had similar baseline characteristics as patients with a lymphocyte ratio >13 % but had less improvement in dyspnea, greater worsening of HF, longer initial length of stay, fewer days alive and out of the hospital and greater risk for all-cause mortality at 60 and 180 days [56].

Up to 60 % of patients hospitalized with ADHF have mild liver function test abnormalities. Elevation of all liver function tests, and especially γ-glutamyl transferase (GGT) and total bilirubin (Tbili), are associated with high central venous pressure (CVP). Only elevated transaminases and Tbili are associated with both high CVP and low cardiac output [57].

In the EVEREST trial, the most common LFT abnormality was an elevation in GGT which occurred in 60 % of patients. Other LFT abnormalities were common and included elevation of alanine aminotransferase (ALT) in 21 % of patients, aspartate aminotransferase (AST) in 21 %, alkaline phosphatase in 23 %, and total bilirubin (Tbili) in 26 % and decreased albumin in 17 %. LFT abnormalities were minor in most patients. Tbili was the only LFT abnormality to decrease from admission to discharge. All LFTs except albumin improved following discharge. Lower baseline ALB and elevated Tbili were both associated with an increased risk for all-cause mortality. In-hospital decreases in albumin or increases in Tbili were associated with higher rates of both all-cause mortality and HF rehospitalization [58].

Two specific conditions affecting the liver, congestive hepatopathy and ischemic hepatitis (or “shock liver”) have been described in patients with heart failure. Congestive hepatopathy refers to a spectrum of chronic liver injury that is caused by chronic passive hepatic congestion in the setting of elevated right atrial pressure. Congestive hepatopathy occurs most commonly in conditions associated with chronically elevated right atrial pressure including: severe right-sided or biventricular heart failure, severe tricuspid regurgitation, cor pulmonale, severe pulmonary hypertension, restrictive cardiomyopathy, pericardial constriction, and congenital heart disease with Fontan reconstruction. Untreated congestion can result in hepatic fibrosis and, eventually cardiac cirrhosis. Laboratory testing generally shows mild non-specific increases in transaminases generally not more than 2–3 times the upper limit of normal, mildly increased Tbili generally <3 mg/dL (predominantly unconjugated), and normal or slightly elevated alkaline phosphatase (which helps differentiate congestion from biliary obstruction). Hepatic synthetic function is usually normal or only slightly impaired. Serum albumin is usually normal or slightly reduced. The international normalized ratio (INR) is rarely increased above 1.5 [59, 60].