In evaluating patients with heart failure, the clinician should ask about the following comorbidities and/or risk factors: Show
The New York Heart Association (NYHA) classification of heart failure is widely used in practice and in clinical studies to quantify clinical assessment of heart failure (see ). Breathlessness, a cardinal symptom of left ventricular (LV) failure, may manifest with progressively increasing severity as the following:
Other cardiac symptoms of heart failure include chest pain/pressure and palpitations. Common noncardiac signs and symptoms of heart failure include anorexia, nausea, weight loss, bloating, fatigue, weakness, oliguria, nocturia, and cerebral symptoms of varying severity, ranging from anxiety to memory impairment and confusion. Findings from the Framingham Heart Study suggested that subclinical cardiac dysfunction and noncardiac comorbidities are associated with increased incidence of heart failure, supporting the idea that heart failure is a progressive syndrome and that noncardiac factors are extremely important. [31, 32, 57] Older patients with heart failure frequently have preserved ejection fraction and an atypical and/or delayed presentation. [58] Exertional dyspneaThe principal difference between exertional dyspnea in patients who are healthy and exertional dyspnea in patients with heart failure is the degree of activity necessary to induce the symptom. As heart failure first develops, exertional dyspnea may simply appear to be an aggravation of the breathlessness that occurs in healthy persons during activity, but as LV failure advances, the intensity of exercise resulting in breathlessness progressively declines; however, subjective exercise capacity and objective measures of LV performance at rest in patients with heart failure are not closely correlated. Exertional dyspnea, in fact, may be absent in sedentary patients. OrthopneaOrthopnea is an early symptom of heart failure and may be defined as dyspnea that develops in the recumbent position and is relieved with elevation of the head with pillows. As in the case of exertional dyspnea, the change in the number of pillows required is important. In the recumbent position, decreased pooling of blood in the lower extremities and abdomen occurs. Blood is displaced from the extrathoracic compartment to the thoracic compartment. The failing LV, operating on the flat portion of the Frank-Starling curve, cannot accept and pump out the extra volume of blood delivered to it without dilating. As a result, pulmonary venous and capillary pressures rise further, causing interstitial pulmonary edema, reduced pulmonary compliance, increased airway resistance, and dyspnea. Orthopnea occurs rapidly, often within a minute or two of recumbency, and develops when the patient is awake. Orthopnea may occur in any condition in which the vital capacity is low. Marked ascites, regardless of its etiology, is an important cause of orthopnea. In advanced LV failure, orthopnea may be so severe that the patient cannot lie down and must sleep sitting up in a chair or slumped over a table. Cough, particularly during recumbency, may be an "orthopnea equivalent." This nonproductive cough may be caused by pulmonary congestion and is relieved by the treatment of heart failure. Paroxysmal nocturnal dyspneaParoxysmal nocturnal dyspnea usually occurs at night and is defined as the sudden awakening of the patient, after a couple of hours of sleep, with a feeling of severe anxiety, breathlessness, and suffocation. The patient may bolt upright in bed and gasp for breath. Bronchospasm increases ventilatory difficulty and the work of breathing and is a common complicating factor of paroxysmal nocturnal dyspnea. On chest auscultation, the bronchospasm associated with a heart failure exacerbation can be difficult to distinguish from an acute asthma exacerbation, although other clues from the cardiovascular examination should lead the examiner to the correct diagnosis. Both types of bronchospasm can be present in a single individual. In contrast to orthopnea, which may be relieved by immediately sitting up in bed, paroxysmal nocturnal dyspnea may require 30 minutes or longer in this position for relief. Episodes may be so frightening that the patient may be afraid to resume sleeping, even after the symptoms have subsided. Dyspnea at restDyspnea at rest in heart failure is the result of the following mechanisms:
Pulmonary edemaAcute pulmonary edema is defined as the sudden increase in PCWP (usually >25 mm Hg) as a result of acute and fulminant LV failure. It is a medical emergency and has a very dramatic clinical presentation. The patient appears extremely ill, poorly perfused, restless, sweaty, tachypneic, tachycardic, hypoxic, and coughing, with an increased work of breathing and using respiratory accessory muscles and with frothy sputum that on occasion is blood tinged. Chest pain/pressure and palpitationsChest pain/pressure may occur as a result of either primary myocardial ischemia from coronary disease or secondary myocardial ischemia from increased filling pressure, poor cardiac output (and, therefore, poor coronary diastolic filling), or hypotension and hypoxemia. Palpitations are the sensation a patient has when the heart is racing. It can be secondary to sinus tachycardia due to decompensated heart failure, or more commonly, it is due to atrial or ventricular tachyarrhythmias. Fatigue and weaknessFatigue and weakness are often accompanied by a feeling of heaviness in the limbs and are generally related to poor perfusion of the skeletal muscles in patients with a lowered cardiac output. Although they are generally a constant feature of advanced heart failure, episodic fatigue and weakness are also common in earlier stages. Nocturia and oliguriaNocturia may occur relatively early in the course of heart failure. Recumbency reduces the deficit in cardiac output in relation to oxygen demand, renal vasoconstriction diminishes, and urine formation increases. Nocturia may be troublesome for patients with heart failure because it may prevent them from obtaining much-needed rest. Oliguria is a late finding in heart failure, and it is found in patients with markedly reduced cardiac output from severely reduced LV function. Cerebral symptomsThe following may occur in elderly patients with advanced heart failure, particularly in those with cerebrovascular atherosclerosis:
Next: Physical ExaminationPatients with mild heart failure appear to be in no distress after a few minutes of rest, but they may be obviously dyspneic during and immediately after moderate activity. Patients with left ventricular (LV) failure may be dyspneic when lying flat without elevation of the head for more than a few minutes. Those with severe heart failure appear anxious and may exhibit signs of air hunger in this position. Patients with a recent onset of heart failure are generally well nourished, but those with chronic severe heart failure are often malnourished and sometimes even cachectic. Chronic marked elevation of the systemic venous pressure may produce exophthalmos and severe tricuspid regurgitation, and it may lead to visible pulsation of the eyes and of the neck veins. Central cyanosis, icterus, and malar flush may be evident in patients with severe heart failure. In mild or moderate heart failure, stroke volume is normal at rest; in severe heart failure, it is reduced, as reflected by a diminished pulse pressure and a dusky discoloration of the skin. With very severe heart failure, particularly if cardiac output has declined acutely, systolic arterial pressure may be reduced. The pulse may be weak, rapid, and thready; the proportional pulse pressure (pulse pressure/systolic pressure) may be markedly reduced. The proportional pulse pressure correlates reasonably well with cardiac output. In one study, when pulse pressure was less than 25%, it usually reflected a cardiac index of less than 2.2 L/min/m2. [59] Ascites occurs in patients with increased pressure in the hepatic veins and in the veins draining into the peritoneum; it usually reflects long-standing systemic venous hypertension. Fever may be present in severe decompensated heart failure because of cutaneous vasoconstriction and impairment of heat loss. Increased adrenergic activity is manifested by tachycardia, diaphoresis, pallor, peripheral cyanosis with pallor and coldness of the extremities, and obvious distention of the peripheral veins secondary to venoconstriction. Diastolic arterial pressure may be slightly elevated. Rales heard over the lung bases are characteristic of heart failure that is of at least moderate severity. With acute pulmonary edema, rales are frequently accompanied by wheezing and expectoration of frothy, blood-tinged sputum. The absence of rales does not exclude elevation of pulmonary capillary pressure due to LV failure. Systemic venous hypertension is manifested by jugular venous distention. Normally, jugular venous pressure declines with respiration; however, it increases in patients with heart failure, a finding known as the Kussmaul sign (also found in constrictive pericarditis). This reflects an increase in right atrial pressure and, therefore, right-sided heart failure. In general, elevated jugular venous pressure is the most reliable indicator of fluid volume overload in older patients, and thorough evaluation is needed. [58] The hepatojugular reflux is the distention of the jugular vein induced by applying manual pressure over the liver; the patient's torso should be positioned at a 45° angle. The hepatojugular reflux occurs in patients with elevated left-sided filling pressures and reflects elevated capillary wedge pressure and left-sided heart failure. Although edema is a cardinal manifestation of heart failure, it does not correlate well with the level of systemic venous pressure. In patients with chronic LV failure and low cardiac output, extracellular fluid volume may be sufficiently expanded to cause edema in the presence of only slight elevations in systemic venous pressure. Usually, a substantial gain of extracellular fluid volume (ie, a minimum of 5 L in adults) must occur before peripheral edema develops. Edema in the absence of dyspnea or other signs of LV or right ventricular (RV) failure is not solely indicative of heart failure and can be observed in many other conditions, including chronic venous insufficiency, nephrotic syndrome, or other syndromes of hypoproteinemia or osmotic imbalance. Hepatomegaly is prominent in patients with chronic right-sided heart failure, but it may occur rapidly in acute heart failure. When hepatomegaly occurs acutely, the liver is usually tender. In patients with considerable tricuspid regurgitation, a prominent systolic pulsation of the liver, attributable to an enlarged right atrial V wave, is often noted. A presystolic pulsation of the liver, attributable to an enlarged right atrial A wave, can occur in tricuspid stenosis, constrictive pericarditis, restrictive cardiomyopathy involving the right ventricle, and pulmonary hypertension (primary or secondary). Hydrothorax is most commonly observed in patients with hypertension involving both the systemic and pulmonary circulation. It is usually bilateral, although when unilateral, it is usually confined to the right side of the chest. When hydrothorax develops, dyspnea usually intensifies because of further reductions in vital capacity. Cardiac findingsProtodiastolic (S3) gallop is the earliest cardiac physical finding in decompensated heart failure in the absence of severe mitral or tricuspid regurgitation or left-to-right shunts. The presence of an S3 gallop in adults is important, pathologic, and often the most apparent finding on cardiac auscultation in patients with significant heart failure. Cardiomegaly is a nonspecific finding that nonetheless occurs in most patients with chronic heart failure. Notable exceptions include heart failure from acute myocardial infarction, constrictive pericarditis, restrictive cardiomyopathy, valve or chordae tendineae rupture, or heart failure due to tachyarrhythmias or bradyarrhythmias. Pulsus alternans (during pulse palpation, this is the alternation of one strong and one weak beat without a change in the cycle length) occurs most commonly in heart failure due to increased resistance to LV ejection, as occurs in hypertension, aortic stenosis, coronary atherosclerosis, and dilated cardiomyopathy. Pulsus alternans is usually associated with an S3 gallop, signifies advanced myocardial disease, and often disappears with treatment of heart failure. Accentuation of the P2 heart sound is a cardinal sign of increased pulmonary artery pressure; it disappears or improves after treatment of heart failure. Mitral and tricuspid regurgitation murmurs are often present in patients with decompensated heart failure because of ventricular dilatatation. These murmurs often disappear or diminish when compensation is restored. Note that the correlation is poor between the intensity of the murmur of mitral regurgitation and its significance in patients with heart failure. Severe mitral regurgitation may be accompanied by an unimpressively soft murmur. Cardiac cachexia is found in long-standing heart failure, particularly of the RV, because of anorexia from hepatic and intestinal congestion and sometimes because of digitalis toxicity. Occasionally, impaired intestinal absorption of fat occurs and, rarely, protein-losing enteropathy occurs. Patients with heart failure may also exhibit increased total metabolism secondary to augmentation of myocardial oxygen consumption, excessive work of breathing, low-grade fever, and elevated levels of circulating tumor necrosis factor (TNF). Previous Next: Predominant Right-Sided Heart FailureAscites, congestive hepatomegaly, and anasarca due to elevated right-sided heart pressures transmitted backward into the portal vein circulation may result in increased abdominal girth and epigastric and right upper quadrant (RUQ) abdominal pain. Other gastrointestinal symptoms, caused by congestion of the hepatic and gastrointestinal venous circulation, include anorexia, bloating, nausea, and constipation. In preterminal heart failure, inadequate bowel perfusion can cause abdominal pain, distention, and bloody stools. Distinguishing right-sided heart failure from hepatic failure is often clinically difficult. Dyspnea, prominent in left ventricular failure, becomes less prominent in isolated right-sided heart failure because of the absence of pulmonary congestion. However, when cardiac output becomes markedly reduced in patients with terminal right-sided heart failure (as may occur in isolated right ventricular infarction and in the late stages of primary pulmonary hypertension and pulmonary thromboembolic disease), severe dyspnea may occur as a consequence of the reduced cardiac output, poor perfusion of respiratory muscles, hypoxemia, and metabolic acidosis. Previous Next: Heart Failure in ChildrenIn children, manifestations of heart failure vary with age. [60] Signs of pulmonary venous congestion in an infant generally include tachypnea, respiratory distress (retractions), grunting, and difficulty with feeding. Often, children with heart failure have diaphoresis during feedings, which is possibly related to a catecholamine surge that occurs when they are challenged with eating while in respiratory distress. Right-sided venous congestion is characterized by hepatosplenomegaly and, less frequently, with edema or ascites. Jugular venous distention is not a reliable indicator of systemic venous congestion in infants, because the jugular veins are difficult to observe. Also, the distance from the right atrium to the angle of the jaw may be no more than 8-10 cm, even when the infant is sitting upright. Uncompensated heart failure in an infant primarily manifests as a failure to thrive. In severe cases, failure to thrive may be followed by signs of renal and hepatic failure. In older children, left-sided venous congestion causes tachypnea, respiratory distress, and wheezing (cardiac asthma). Right-sided congestion may result in hepatosplenomegaly, jugular venous distention, edema, ascites, and/or pleural effusions. Uncompensated heart failure in older children may cause fatigue or lower-than-usual energy levels. Patients may complain of cool extremities, exercise intolerance, dizziness, or syncope. For more information, see the Medscape Drugs & Diseases article Pediatric Congestive Heart Failure. Previous Next: Heart Failure Criteria, Classification, and StagingFramingham system for diagnosis of heart failureIn the Framingham system, the diagnosis of heart failure requires that either two major criteria or one major and two minor criteria be present concurrently, as shown in Table 1 below. [1] Minor criteria are accepted only if they cannot be attributed to another medical condition. Table 1. Framingham Diagnostic Criteria for Heart Failure (Open Table in a new window) Major Criteria Minor Criteria Paroxysmal nocturnal dyspnea Nocturnal cough Weight loss of 4.5 kg in 5 days in response to treatment Dyspnea on ordinary exertion Neck vein distention A decrease in vital capacity by one third the maximal value recorded Rales Pleural effusion Acute pulmonary edema Tachycardia (rate of 120 bpm) Hepatojugular reflux Hepatomegaly S3 gallop Bilateral ankle edema Central venous pressure >16 cm water
Circulation time of ≥25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
Source: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. Previous Next: ACC/AHA StagingStage AAmerican College of Cardiology/American Heart Association (ACC/AHA) stage A patients are at high risk for heart failure; thus, this stage is now also known as "at risk for heart failure." [4, 5, 6, 7] Patients in this stage do not have structural heart disease or symptoms of heart failure. Thus, management in these cases focuses on prevention, through reduction of risk factors. Measures include the following [3] :
Patients who have a family history of dilated cardiomyopathy should be screened with a comprehensive history and physical examination together with echocardiography and transthoracic echocardiography every 2-5 years. [8] Stage BACC/AHA stage B patients are now also designated as "pre-heart failure.. [4, 5, 6, 7] These individuals are asymptomatic, with left ventricular (LV) dysfunction from previous myocardial infarction (MI), LV remodeling from LV hypertrophy (LVH), and asymptomatic valvular dysfunction, which includes patients with New York Heart Association (NYHA) class I heart failure (see for a description of NYHA classes). [3] In addition to the heart failure education and aggressive risk factor modification used for stage A, treatment with an angiotensin-converting enzyme inhibitor/angiotensin-receptor blocker (ACEI/ARB) and/or beta-blockade is indicated. Evaluation for coronary revascularization either percutaneously or surgically, as well as correction of valvular abnormalities, may be indicated. [3] Treatment with an implantable cardioverter-defibrillator (ICD) for primary prevention of sudden death in patients with an LV ejection fraction (LVEF) below 30% that is more than 40 days post-MI is reasonable if the expected survival is more than 1 year. There is less evidence for implantation of an ICD in patients with nonischemic cardiomyopathy, an LVEF less than 30%, and no heart failure symptoms. There is no evidence for use of digoxin in these populations. [62] Aldosterone receptor blockade with eplerenone is indicated for post-MI LV dysfunction. Stage CACC/AHA stage C patients have structural heart disease and current or previous symptoms of heart failure; they are therefore designated as having "symptomatic heart failure." [4, 5, 6, 7] ACC/AHA stage C corresponds with NYHA class I-IV heart failure. The preventive measures used for stage A disease are indicated, as is dietary sodium restriction. Drugs routinely used in these patients include ACEI/ARBs, beta-blockers, or angiotensin receptor–neprilysin inhibitors (ARNIs), in conjunction with evidence-based beta-blockers, and loop diuretics for fluid retention. [3, 61, 63] For selected patients, therapeutic measures include aldosterone receptor blockers, hydralazine and nitrates in combination, and cardiac resynchronization with or without an ICD (see ). [3, 61, 63] A meta-analysis performed by Badve et al suggested that the survival benefit of treatment with beta-blockers extends to patients with chronic kidney disease and systolic heart failure (risk ratio 0.72). [64] The 2016 and 2017 ACC/AHA focused updates to the 2013 guidelines added a class IIa recommendation for ivabradine, a sinoatrial node modulator, in patients with stage C heart failure. [61, 63] They indicate that ivabradine may reduce hospitalization for patients with symptomatic (NYHA class II-III) stable chronic heart failure with reduced ejection fraction (LVEF ≤35%) who are receiving recommended therapy, including a beta blocker at the maximum tolerated dose, and who are in sinus rhythm with a heart rate of 70 bpm or greater at rest. [61, 63] Stage DACC/AHA stage D patients have refractory heart failure (NYHA class IV) that requires specialized interventions; they are in "advanced heart failure." [4, 5, 6, 7] Therapy includes all the measures used in stages A, B, and C. Treatment considerations include heart transplantation or placement of an LV assist device in eligible patients; pulmonary catheterization; and options for end-of-life care. [3] For palliation of symptoms, continuous intravenous infusion of a positive inotrope may be considered. Previous Differential Diagnoses
References
Media Gallery
of 29 Tables
Table 1. Framingham Diagnostic Criteria for Heart Failure Major Criteria Minor Criteria Paroxysmal nocturnal dyspnea Nocturnal cough Weight loss of 4.5 kg in 5 days in response to treatment Dyspnea on ordinary exertion Neck vein distention A decrease in vital capacity by one third the maximal value recorded Rales Pleural effusion Acute pulmonary edema Tachycardia (rate of 120 bpm) Hepatojugular reflux Hepatomegaly S3 gallop Bilateral ankle edema Central venous pressure >16 cm water
Circulation time of ≥25 seconds
Radiographic cardiomegaly
Pulmonary edema, visceral congestion, or cardiomegaly at autopsy
Source: Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. Table 2. Evidence-Based BNP and NT-proBNP Cutoff Values for Diagnosing HF Criterion BNP, pg/mL NT-proBNP, pg/mL HF Unlikely (LR-Negative) HF Likely (LR-Positive) HF Unlikely (LR-Negative) HF Likely (LR-Positive) Age, y >17 < 100 (0.13)* >500 (8.1)* - - >21 - - < 300 (0.02)† - 21-50 - - - >450 (14)† 50-75 - - - >900 (5.0)† >75 - - - >1800 (3.1)† Estimated GFR, < 60 mL/min < 200 (0.13)‡ >500 (9.3)‡ - - BNP = B-type natriuretic peptide; GRF = glomerular filtration rate; HF = heart failure; LR = likelihood ratio; NPV = negative predictive value; NT-pro-BNP = N-terminal proBNP; PPV = positive predictive value; – = not specifically defined. * Derived from Breathing Not Properly data (1586 emergency department [ED] patients, prevalence of HF = 47%). [65] † Derived from PRIDE data (1256 ED patients, prevalence of HF = 57%). [66, 75] ‡ Derived from subset of Breathing Not Properly data (452 ED patients, prevalence of HF = 49%). [74] Table 3. 2013 American College of Cardiology Foundation/American Heart Association (ACCF/AHA) Heart Failure Staging System Stage Description Examples Notes A At high risk for heart failure but without structural heart disease or symptoms of heart failure Patients with coronary artery disease, hypertension, or diabetes mellitus without impaired left ventricular (LV) function, LV hypertrophy (LVH), or geometric chamber distortion Patients with predisposing risk factors for developing heart failure No corresponding New York Heart Association (NYHA) functional classification B Structural heart disease but without signs/symptoms of heart failure Patients who are asymptomatic but who have LVH and/or impaired LV function Corresponds with patients with NYHA class I C Structural heart disease with current or past symptoms of heart failure Patients with known structural heart disease and shortness of breath and fatigue, as well as reduced exercise tolerance The majority of patients with heart failure are in this stage Corresponds with NYHA classes I, II, III and IV D Refractory heart failure requiring specialized interventions Patients who have marked symptoms at rest despite maximal medical therapy Patients in this stage may be eligible to receive mechanical circulatory support, receive continuous inotropic infusions, undergo procedures to facilitate fluid removal, or undergo heart transplantation or other procedures Corresponds with patients with NYHA class IV Table 4. 2022 ACC/AHA/Heart Failure Society of America (HFSA) Heart Failure Staging System Proposed Terminology Stage Definition and Criteria At risk for HF A At risk of HF; asymptomatic, no structural heart disease nor cardiac biomarkers of stretch injury (eg, patients with hypertension, atherosclerotic cardiovascular disease, diabetes, metabolic syndrome and obesity, exposure to cardiotoxic agents, genetic variant for cardiomyopathy, or positive family history of cardiomyopathy) Pre-HF B No signs/symptoms of HF and evidence of one of the following: Structural heart disease
Evidence for raised filling pressures by invasive hemodynamic measurements or by noninvasive imaging that suggests elevated filling pressures (eg, Doppler echocardiography) Patients with risk factors and raised levels of B-type natriuretic peptides or persistently elevated cardiac troponin in the absence of competing diagnoses that result in such biomarker elevations (eg, acute coronary syndrome, chronic kidney disease, pulmonary embolus, or myopericarditis) Symptomatic HF C Structural heart disease with current or previous symptoms of HF Advanced HF D Marked HF symptoms that interfere with daily life and with repeated hospitalizations despite attempts to optimize guideline-directed medical therapy HF = heart failure Table 5. 2022 ACC/AHA/HFSA Classification of Heart Failure (HF) by Left Ventricular Ejection Fraction (LVEF) HF Type by LVEF Criteria HF with reduced EF (HFrEF) LVEF ≤40% HF with improved EF (HFimpEF) Previous LVEF ≤40% and a followup LVEF >40% HF with mildly reduced EF (HFmrEF) LVEF of 41%-49% Evidence of spontaneous/provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement) HF with preserved EF (HFpEF) LVEF ≥50% Evidence of spontaneous/provokable increased LV filling pressures (eg, elevated natriuretic peptide, noninvasive and invasive hemodynamic measurement)  Back to List Contributor Information and Disclosures Author Ioana Dumitru, MD Associate Professor of Medicine, Division of Cardiology, Founder and Medical Director, Heart Failure and Cardiac Transplant Program, University of Nebraska Medical Center; Associate Professor of Medicine, Division of Cardiology, Veterans Affairs Medical Center Specialty Editor Board Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Yasmine S Ali, MD, MSCI, FACC, FACP Assistant Clinical Professor of Medicine, Vanderbilt University School of Medicine; President, LastSky Writing, LLC Chief Editor Gyanendra K Sharma, MD, FACC, FASE Professor of Medicine and Radiology, Director, Adult Echocardiography Laboratory, Section of Cardiology, Medical College of Georgia at Augusta University Additional Contributors Mathue M Baker, MD Cardiologist, BryanLGH Heart Institute and Saint Elizabeth Regional Medical Center Henry H Ooi, MD, MRCPI Director, Advanced Heart Failure and Cardiac Transplant Program, Nashville Veterans Affairs Medical Center; Assistant Professor of Medicine, Vanderbilt University School of Medicine Mariclaire Cloutier Freelance editor, Medscape Drugs & Diseases Acknowledgements Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York AcademyofSciences,and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. David FM Brown, MD Associate Professor, Division of Emergency Medicine, Harvard Medical School; Vice Chair, Department of Emergency Medicine, Massachusetts General Hospital David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. William K Chiang, MD Associate Professor, Department of Emergency Medicine, New York University School of Medicine; Chief of Service, Department of Emergency Medicine, Bellevue Hospital Center William K Chiang, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Medical Toxicology, and Society for Academic Emergency Medicine Disclosure: Nothing to disclose. Joseph Cornelius Cleveland Jr, MD Associate Professor, Division of Cardiothoracic Surgery, University of Colorado Health Sciences Center Joseph Cornelius Cleveland Jr, MD is a member of the following medical societies: Alpha Omega Alpha, American Association for the Advancement of Science, American College of Cardiology, American College of Chest Physicians, American College of Surgeons, American Geriatrics Society, American Physiological Society, American Society of Transplant Surgeons, Association for Academic Surgery, Heart Failure Society of America, International Society for Heart and Lung Transplantation, Phi Beta Kappa, Society of Critical Care Medicine, Society of Thoracic Surgeons, and Western Thoracic Surgical Association Disclosure: Thoratec Heartmate II Pivotal Tria; Grant/research funds Principal Investigator - Colorado; Abbott Vascular E-Valve E-clip Honoraria Consulting; Baxter Healthcare Corp Consulting fee Board membership; Heartware Advance BTT Trial Grant/research funds Principal Investigator- Colorado; Heartware Endurance DT trial Grant/research funds Principal Investigator-Colorado Shamai Grossman, MD, MS Assistant Professor, Department of Emergency Medicine, Harvard Medical School; Director, The Clinical Decision Unit and Cardiac Emergency Center, Beth Israel Deaconess Medical Center Shamai Grossman, MD, MS is a member of the following medical societies: American College of Emergency Physicians Disclosure: Nothing to disclose. John D Newell Jr, MD Professor of Radiology, Head, Division of Radiology, National Jewish Health; Professor, Department of Radiology, University of Colorado School of Medicine John D Newell Jr, MD is a member of the following medical societies: American College of Chest Physicians, American College of Radiology, American Roentgen Ray Society, American Thoracic Society, Association of University Radiologists, Radiological Society of North America, and Society of Thoracic Radiology Disclosure: Siemens Medical Grant/research funds Consulting; Vida Corporation Ownership interest Board membership; TeraRecon Grant/research funds Consulting; Medscape Reference Honoraria Consulting; Humana Press Honoraria Other Craig H Selzman, MD, FACS Associate Professor of Surgery, Surgical Director, Cardiac Mechanical Support and Heart Transplant, Division of Cardiothoracic Surgery, University of Utah School of Medicine Craig H Selzman, MD, FACS is a member of the following medical societies: Alpha Omega Alpha, American Association for Thoracic Surgery, American College of Surgeons, American Physiological Society, Association for Academic Surgery, International Society for Heart and Lung Transplantation, Society of Thoracic Surgeons, Southern Thoracic Surgical Association, and Western Thoracic Surgical Association Disclosure: Nothing to disclose. Gary Setnik, MD Chair, Department of Emergency Medicine, Mount Auburn Hospital; Assistant Professor, Division of Emergency Medicine, Harvard Medical School Gary Setnik, MD is a member of the following medical societies: American College of Emergency Physicians, National Association of EMS Physicians, and Society for Academic Emergency Medicine Disclosure: SironaHealth Salary Management position; South Middlesex EMS Consortium Salary Management position; ProceduresConsult.com Royalty Other Brett C Sheridan, MD, FACS Associate Professor of Surgery, University of North Carolina at Chapel Hill School of Medicine Disclosure: Nothing to disclose. George A Stouffer III, MD Henry A Foscue Distinguished Professor of Medicine and Cardiology, Director of Interventional Cardiology, Cardiac Catheterization Laboratory, Chief of Clinical Cardiology, Division of Cardiology, University of North Carolina Medical Center George A Stouffer III, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Heart Association, Phi Beta Kappa, and Society for Cardiac Angiography and Interventions Disclosure: Nothing to disclose. Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference Which patient assessment finding would indicate heart failure?Abnormal findings that suggest heart failure
High blood pressure (130/80 mm Hg or above) or low blood pressure is present. Low blood pressure could be a sign of late-stage heart failure. A third heart sound (indicating abnormal movement of blood through the heart) is heard. Heart murmurs may or may not be present.
What are expected findings of heart failure?Swelling in the legs, ankles and feet. Rapid or irregular heartbeat. Reduced ability to exercise. Persistent cough or wheezing with white or pink blood-tinged mucus.
Which findings will the nurse likely observe when a patient has a rightShortness of breath (dyspnea), even after only a small amount of exertion. Weakness and lethargy. Fatigue. Swelling (edema), that often involves not only the ankles and lower extremities but also the thighs, abdomen, and chest.
What assessment findings would you expect to see with leftSigns and Symptoms
Left-sided heart failure symptoms include: Awakening at night with shortness of breath. Shortness of breath during exercise or when lying flat. Chronic coughing or wheezing.
|
When the nurse is assessing a patient, which findings would be an indicator of heart failure
zusammenhängende Posts
Urheberrechte © © 2024 de.apacode Inc.
