Hellenic J Cardiol 2015; 56: 285-301 Review Article Clinical Assessment in Acute Heart Failure 1 2 NIKOLAOS S. KAKOUROS , STAVROS N. KAKOUROS 1University of Massachusetts, MA, USA; 2Cardiac Department, “Amalia Fleming” General Hospital, Athens, Greece Key words: eart failure (HF) is defined as “a clear precipitant or trigger. It is very im­ Heart failure, complex clinical syn drome that portant to establish the precipitating diagnosis, physical examination, H can result from any structural or causes, which may have therapeutic and congestion. functional cardiac disorder that impairs the prognostic implications. Approximate­ ability of the ventricle to fill with, or eject ly 60% of patients with AHF have doc­ blood.” HF has an estimated overall prev­ umented CAD. Myocardial ischemia in alence of 2.6%. It is becoming more com­ the setting of acute coronary syndromes mon in adults older than 65 years, because is a precipitant or cause, particularly in of increased survival after acute myocar­ patients presenting with de novo AHF.4 dial infarction (AMI) and improved treat­ AHF is also often precipitated by medica­ ment of coronary artery disease (CAD), tion and dietary non­compliance, as well val vular heart disease and hypertension.1 as by many other conditions, which are Acute HF (AHF) is an increasingly com­ summarized in Table 1. Once the diagno­ mon cause of hospitalizations and mortality sis of AHF is confirmed, initial therapy in­ worldwide. In the majority of patients, AHF cludes removal of precipitants; if this can Manuscript received: can be attributed to worsening chronic HF, be carried out successfully, the patient’s August 25, 2014; and approximately 40­50% of this group have subsequent course may be stable. Accepted: a preserved ejection fraction. The remaining Approximately 80% of AHF admis­ November 13, 2014. cases present with de novo AHF, often sec­ sions initially present to the emergency ondary to acute coronary syndromes.2 department. Patients usually arrive with Address: Symptoms are predominantly the result the classic symptoms (e.g. dyspnea, fa­ Stavros N. Kakouros of systemic and pulmonary congestion due tigue) or signs (e.g. peripheral edema) of to elevated left ventricular (LV) filling pres­ HF. It is critical to establish the diagnosis 26, Paritsi St. sures. Signs and symptoms usually improve of AHF early, as delays in diagnosis and 15451 Athens, Greece 5 [email protected] markedly during hospitalization; however, treatment may lead to worse outcomes. mortality during that period remains high, The immediate assessment of patients ranging from 5­15%. Of those patients who presenting with AHF should include a survive to discharge, a further 10­15% will thorough history and physical examination die within 3 months. Most patients have that should be complemented by ECG, one or more serious comorbid conditions chest X­ray and the necessary initial labo­ that contribute to a poor outcome.3 ratory investigations (Table 2). Echocar­ diography is most useful in patients with 6 Initial assessment and phenotype suspected HF, when it is available. Es­ classification tablishing the HF diagnosis, according to ESC guidelines, requires the conditions In patients with AHF, there is often a shown in Table 3.2 (Hellenic Journal of Cardiology) HJC • 285 N.S. Kakouros, S.N. Kakouros Table 1. Common precipitants of hospitalization for acute heart failure. Acute coronary syndrome Cardiac tamponade Uncontrolled hypertension Acute pulmonary embolism Tachyarrhythmia / bradyarrhythmia Aortic dissection Concurrent infections Anemia Exacerbation of COPD or asthma Alcohol abuse Renal dysfunction Peripartum Thyroid dysfunction Perioperative problems Dietary and medication non­compliance Drugs (NSAID, corticosteroid, negative inotropic agents, illicit drugs) COPD – chronic obstructive pulmonary disease; NSAID – nonsteroidal anti­inflammatory drugs. Table 2. Immediate Emergency Department assessment of heart Table 3. Diagnostic requisites for heart failure (ESC HF Guide­ failure. lines 2012). History HF with reduced EF Symptoms typical of HF Clinical examination Signs typical of HF ECG Reduced EF HF with preserved EF Symptoms typical of HF Chest X­ray Signs typical of HF Initial laboratory studies: Normal or only mildly reduced Blood biochemistry LVEF and LV not dilated Cardiac biomarkers Relevant structural heart disease Natriuretic peptides (LV hypertrophy, LA enlargement) Markers of renal impairment and/or diastolic dysfunction Oxygen saturation EF – ejection fraction; HF – heart failure; LA – left atrium; LV – left Echocardiogram (portable echo) ventricle. Once the diagnosis of AHF has been made, pa­ are predominantly the result of systemic and pulmo­ tients may be broadly categorized into phenotypes of nary congestion due to elevated LV filling pressures. hypertensive AHF, acute coronary syndrome (ACS), Patients with AHF may present insidiously or acutely, right HF, high­output HF, pulmonary edema, and with a spectrum of clinical severity ranging from in­ cardiogenic shock (Figure 1).7 The Killip classifica­ creasing dyspnea to acute pulmonary edema or car­ tion is valid in acute de novo HF after AMI, and is diogenic shock.2 Severity at presentation does not al­ used in coronary care and intensive care units. It is ways correlate well with long­term prognosis. Patients designed to provide a clinical estimate of the severity presenting with pulmonary edema due to severe hy­ of myocardial derangement in the treatment of AMI pertension and normal LV systolic function may have (Table 4).8 an excellent prognosis. In contrast, patients present­ ing with only moderate dyspnea and severe LV dys­ Clinical evaluation of severity and congestion function, may have high mortality. Overall, however, patients demonstrating clinical or hemodynamic con­ HF is characterized by dyspnea, fatigue and signs of gestion have been shown to have significantly worse volume overload, which may include peripheral ede­ rates of mortality and HF rehospitalization.9 Clinical ma and pulmonary rales. These symptoms and signs congestion in HF is defined as a high left ventricular Table 4. Killip classification. Stage I No heart failure. No clinical signs of cardiac decompensation Stage II Heart failure. Diagnostic criteria include rales, S3 gallop and pulmonary venous hypertension. Pulmonary congestion with wet rales in the lower half of the lung fields Stage III Severe heart failure. Frank pulmonary edema with rales throughout the lung fields. Stage IV Cardiogenic shock. Signs include hypotension (systolic blood pressure ≤90 mmHg) and evidence of peripheral vasoconstriction, such as oliguria, cyanosis and diaphoresis. 286 • HJC (Hellenic Journal of Cardiology) Clinical Assessment in Acute Heart Failure Pulmonary edema (chest X-ray, dyspnea and typically O2sat<90%) Cardiogenic shock Tissue hypoperfusion Hypertensive AHF 180/100 mmHg Hypotension Pulmonary congestion Tachycardia and HFPEF Reduced urine output Acute HF De Novo HF or Decompensated Chronic HF ACS High output HF Myocardial ischemia Adequate perfusion Angina Tachycardia Cardiac enzymes, MR Pulm. congestion ± reduced EF Right HF JVD, Edema, ± Signs of LHF Figure 1. Clinical phenotypes at presentation of acute heart failure (AHF). JVD – jugular vein distension; MR – mitral regurgitation; LHF – left heart failure. diastolic pressure (LVDP) associated with signs and tion, body weight, serum sodium, natriuretic peptides, symptoms of HF, such as rales, dyspnea, orthopnea, chest X­ray and others. paroxysmal nocturnal dyspnea and edema. Eleva­ Relying on a limited set of physical examination tion of LVDP in HF patients, without overt clinical findings alone is associated with low sensitivity and congestion, has been termed “hemodynamic conges­ poor predictive value in identifying hemodynamic tion”. Often, hemodynamic congestion precedes clini­ congestion. In a study of patients with chronic HF, cal congestion by days or even weeks. In chronic HF, physical signs of congestion (rales, edema, and jugu­ even severe hemodynamic congestion rarely causes lar venous distension [JVD]), were absent in 42% of rales and/or radiographic pulmonary edema.10 This patients with a measured pulmonary capillary wedge may be related to several adaptive pathophysiologi­ pressure (PCWP) ≥22 mmHg, and the combination cal changes, such as an increase in alveolar capillary of these signs showed only a 58% sensitivity in detect­ membrane thickness, increased lymphatic drainage, ing elevated PCWP.9 In another study of chronic HF and/or pulmonary hypertension. patients, the presence of JVD, when measured care­ The gold standard for evaluating hemodynamic fully, had the best combination of sensitivity (81%), congestion in HF patients is cardiac catheterization; specificity (80%), and predictive accuracy (81%) for however, its invasive nature limits its routine use in detection of an elevation in PCWP (≥18 mmHg).11 clinical practice. Numerous tools are available for the Ultrasonography of the lungs using an echocardio­ assessment of congestion, including physical examina­ graphic probe is another potentially useful way to as­ (Hellenic Journal of Cardiology) HJC • 287 N.S. Kakouros, S.N. Kakouros sess pulmonary congestion. Thoracic impedance mea­ medical history (e.g. a potential cause of cardiac dam­ surement, using external or implanted devices, has age), whereas, conversely, certain features, particu­ been investigated in recent years in assessing conges­ larly previous AMI, greatly increase the likelihood of tion.12 Measuring the lead