Hospital Medicine

Congestive heart failure

Congestive heart failure

I. Problem/Condition

Heart failure (HF) is a major public health problem in the United States and one of the most common diagnoses that hospitalists encounter. According to the National Health and Nutrition Examination Survey (NHANES) 2009-2012, an estimated 5.7 million adult Americans had HF. Projections show that by the year 2030, this number will increase by about 46% resulting in more than 8 million adult Americans with heart failure. About 917,000 new cases of heart failure are diagnosed annually. It is the number 1 discharge diagnosis in elderly patients. It has a 50% readmission rate in 6 months and an absolute mortality rate of 50% in 5 years. Management of HF is expensive with costs in US exceeding $40 billion per year and mean cost being about $23,000 per hospitalization per patient.

HF is a complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or eject blood. Patients with heart failure may present with dyspnea on exertion, exercise limitations, signs of left- or right-sided congestive symptoms (pulmonary edema or peripheral edema), palpitations (secondary to extrasystolic beats or supraventricular or ventricular tachycardia) or syncope. In this section, we will mainly discuss the general diagnostic and management approach to heart failure.

A. What is the differential diagnosis for this problem?

Heart failure has been classified according to various different criteria: etiology, mechanism, stages, function and degree of compensation.

Etiologically, the most common predisposing conditions of Heart failure in the descending order of the population attributable risk are coronary artery disease, cigarette smoking, hypertension, obesity, diabetes and valvular heart disease. The less common ones include myocarditis, infiltrative disease, postpartum cardiomyopathy, HIV infection, substance abuse, drug-induced and others.

Patients with left ventricular dysfunction are often classified into two groups depending on their left ventricular ejection fraction (LVEF): heart failure with reduced ejection fraction HFrEF (EF < 40%)or heart failure with preserved ejection fraction (HFpEF) (EF>40%). Why is it important to categorise a patient with heart failure in this way? Most of the medications like B-blockers, ACE-inhibitors that have shown to improve survival in HF were studied in patients with reduced ejection fraction, whereas for patients with preserved ejection fraction, the management is mostly directed towards the underlying cause, for example, controlling hypertension in HFpEF from hypertensive heart disease.

HFpEF comprises about one third of all cases of HF and is due to impaired left ventricular relaxation or impaired ventricular compliance. Although the ejection fraction is preserved in HFpEF, patients may still have depressed stroke volume as their end-diastolic volume is lower than normal. HFpEF is more commonly associated with aging, LV hypertrophy, hypertension, diabetes mellitus, infiltrative cardiomyopathy, sleep apnea and coronary artery disease.

Patients may also present with predominant right heart failure syndrome. This may be seen in patients with pulmonary arterial hypertension and congenital heart disease affecting the right ventricle such as tetralogy of Fallot. Patients with HF and left ventricular function may also present clinically with signs of right-sided heart failure. High output states may also lead to heart failure. Causes of high output state include thyrotoxicosis, sepsis (especially from gram negative bacteremia), arteriovenous (AV) fistula, beriberi, anemia, carcinoid (rarely), Paget’s disease, and hepatic hemangiomas.

The progressive nature of the HF has been classified into 4 stages by the American College of Cardiology Foundation/ American Heart Association:

Stage A: High risk for HF but without structural heart disease or HF symptoms (e.g., DM, metabolic syndrome, CAD, obesity, hypertension, history of familial CM, or use of cardiotoxin)

Stage B: Structural heart disease but without history of HF signs or symptoms (e.g., asymptomatic valve disease, LVH, reduced LVEF, MI)

Stage C: Structural heart disease + prior / current HF symptoms or signs

Stage D: Advanced HF: HF refractory to maximal medical therapy, often requiring specialized interventions

Functionally, New York Heart Association puts patients with HF into 4 classes:

NYHA I: no symptoms currently with ordinary activity

NYHA II: symptoms of HF with ordinary activity

NYHA III: symptoms of HF with less than ordinary activity

NYHA IV: symptoms of HF with any activity or at rest

Furthermore, heart failure may also be classified according to the level of compensation into stable or acutely decompensated heart failure syndrome. Hospitalists most often encounter acute heart failure syndromes (AHFS) or newly diagnosed heart failure. Each time a patient is admitted for heart failure, a clinician must investigate causes that can lead to decompensation. These include anemia, infection, tachycardia, pulmonary embolism, and noncompliance to medication(s) that interfere with the cardiorenal balance such as non-steroidal anti-inflammatory agents.

B. Describe a diagnostic approach/method to the patient with this problem

A thorough history and physical examination followed by laboratory and imaging studies including echocardiography usually lead to the diagnosis of the underlying etiology of congestive heart failure (CHF). The diagnostic approach is discussed in detail below.

1. Historical information important in the diagnosis of this problem.

Common presenting symptoms include fatigue and weakness (due to decreased cardiac output) and weight gain, swelling of legs, shortness of breath (due to fluid overload) exacerbated by exertion. Also common are nocturia, paroxysmal nocturnal dyspnea, orthopnea, anorexia, right upper quadrant abdominal discomfort due to hepatic congestion. At times, patients can present with altered mental status due to cerebral hypoperfusion.

Important history questions include acuity of onset (acute pulmonary embolism), presence of chest pain (due to cardiac ischemia, acute pulmonary embolism), recent blood loss (anemia-induced CHF), presence of risk factors of coronary arterial disease, exposure to toxins and infectious agents, past medical history (thyrotoxicosis, human immunodeficiency virus (HIV), liver or kidney dysfunction), previous surgery (congenital cardiac disease), recent use of medicines (cardiotoxic drugs), use of tobacco (increase likelihood of CAD), drugs (cocaine and methamphetamine can cause DCM and worsen underlying compensated HF), excessive alcohol (can lead to DCM), family history of cardiac disease (congenital heart disease, sudden death, or history of cardiomyopathy) and recent travel (Chagas disease is a well-known cause of HF).

Patients who present with acute HF exacerbation should be asked about factors that can lead to acute decompensation. These include any recent infection, dietary non compliance (excess use of fluids, alcohol, or salt), medication noncompliance (especially diuretics), presence of chest pain (CAD is well known to exacerbate acute cardiac decompensation).

2. Physical Examination and manoeuvres that are likely to be useful in diagnosing the cause of this problem.

Most CHF patients who present to the emergency department (with CHF exacerbation) usually have low oxygen saturation and rapid respiratory rate, which may or may not be associated with altered mental status, excessive sweating, use of accessory muscles of respiration, and cyanosis based on severity of dyspnea. It is important to know that these patients usually remain normotensive (mainly congestive heart failure decompensation or “wet” decompensation). Approximately 5-10% of acute heart failure hospitalization may be hypotensive and have signs of low cardiac output (“cold” decompensation).

Findings of fluid overload such as lower extremity pitting edema, bilateral pulmonary crackles or rales with hepatomegaly, jaundice, ascites, jugular venous distension (JVD) (high specificity but low sensitivity finding), displaced point of maximum impulse (representing increased cardiac size), and S3 on cardiac examination are common in patients with congestive heart failure.

Characteristic physical examination maneuvers that can guide towards the underlying etiology of dyspnea include pulsating liver (usually associated with tricuspid regurgitation), S4 in patients with diastolic heart failure, thyrotoxicosis (goiter, exophthalmos, excessive sweating, cachectic appearance, and a pulsatile thyroid mass) and presence of murmurs (of valvular dysfunction). Hepatojugular reflux cannot diagnose cause of dyspnea but can help establish diagnosis of fluid overload.

It is important to know that pulmonary rales may be absent in patients with chronic CHF and lower extremity swelling may not be apparent in chronically bedridden patients (who should be evaluated for sacral edema).

In patients with well-compensated CHF all the above mentioned signs and symptoms may be absent and the patient may appear totally asymptomatic.

Cardiac cachexia, confusion and altered mental status may be present in severe cases.

3. Laboratory, radiographic and other tests that are likely to be useful in diagnosing the cause of this problem.

A series of laboratory and radiographic tests may be needed to evaluate dyspnea. These include complete blood count (CBC), comprehensive metabolic panel (CMP), brain natriuretic peptide (BNP) also known as B-type NP and brain NP, D-dimer, serial cardiac markers and 12-lead electrocardiogram (ECG), chest X-ray (CXR), lower extremity ultrasound (to rule out deep vein thrombosis), and transthoracic echocardiography.

CBC can help establish underlying cause of HF (such as leukocytosis in pulmonary infection or low hematocrit in anemic patients). CMP can help evaluate underlying renal and hepatic status. Elevated liver function tests (LFTs) can be due to vascular congestion. High blood urea nitrogen (BUN) and creatinine and low sodium reveal inadequate perfusion to peripheral organs.

Brain natriuretic peptide (BNP) is usually elevated in hypervolemic patients, such as in CHF or renal failure. BNP levels correlate with ventricular stress. N-terminal pro-brain natriuretic peptide (NT-BNP) levels are more susceptible to renal function. Both BNP and NT-BNP may be lower in obese patients.

ECG and cardiac biomarkers (troponin, CK-MB enzymes) are the first-line test to evaluate cardiac ischemia. It is important to know that a normal ECG does not rule out non-ST elevation myocardial infarction (NSTEMI) or unstable angina, which can be a cause of precipitating heart failure. Also, the first set of cardiac biomarkers are neither sensitive nor specific in cases of acute myocardial infarction (MI). An ECG can also give clues regarding other conditions such as pericardial tamponade (electrical alternans), pulmonary embolism (right-sided strain pattern), and heart blocks. It is important to know that patients with muscular dystrophy and sinus rhythm can have atrial electromechanical dissociation and mechanical electrical activity should be observed on echocardiography as they can be at high risk of thromboembolic complications.

Chest x-ray is essential to evaluate dyspnea. Findings such as Kerley B lines, interstitial edema, pleural effusion and dilated cardiac shadow (in cases of fluid overload), consolidation (such as in pneumonia and aspiration), pleural effusion (in CHF or pneumonia), discrete loss of vascular markings (in pneumothorax), water-bottle heart (in pericardial effusion), and hyperinflation (in chronic obstructive pulmonary disease (COPD) and asthma) can all give clues to diagnosis.

Echocardiography remains the cornerstone of diagnosis and it can also help determine the cause and mechanism of heart failure, type (systolic versus diastolic) and etiology of CHF. Echocardiography can also comment on chamber size, ejection fraction, stroke volume, abnormalities in myocardium (dilated CMP, hypertrophic obstructive cardiomyopathy [HOCM]) and pericardium (constrictive pericarditis, tamponade, pericardial effusion), and valvular abnormalities.

Cardiac endomyocardial biopsy may only be needed in some patients with rapidly progressive heart failure (for example, in suspected cases of giant cell myocarditis, as therapy can significantly modify outcome in this case). In other cases, the role of myocardial biopsy is still unclear and mainly reserved for research protocols.

Cases where HF etiology cannot be established should be screened for hemachromatosis, sleep-related disturbed breathing and HIV. Noninvasive imaging may be considered to define CAD. Holter monitoring might be considered with suspicion of arrhythmia.

C. Diagnostic criteria

Framingham criteria are well known for the diagnosis of congestive heart failure. Diagnosis of CHF needs at least two major criteria or one major criterion in conjunction with two minor criteria. The major criteria include paroxysmal nocturnal dyspnea, neck venous distention, acute pulmonary edema, increased central venous pressure, positive hepatojugular reflux on clinical exam, rales and S3 gallop on auscultation, cardiomegaly on imaging, and weight loss of greater than 4.5kg in 5 days during treatment. Minor criteria include extremity edema, night cough, dyspnea on exertion, hepatomegaly, pleural effusion, decrease in vital capacity by one third from normal, and tachycardia. The sensitivity of Framingham’s score for diagnosis of congestive heart failure is almost 100%.

It is important to know that at times initial diagnosis of heart failure can be difficult as patients can present with minimal symptoms.

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

Common over-utilized tests used by hospitalists include multiple thyroid stimulating hormone (TSH), serial BNP levels and frequent CXR. Repeat cardiac echocardiography is also not needed unless a patient’s clinical condition changes.

Although CXR and BNP can be useful initial tests, repetition of these tests during hospitalization may not always be necessary. It is important to understand that CXR may take several weeks to show improvement. BNP may be useful on admission or discharge.

A. Management of HFrEF

See Figure 1.

Figure 1.

Management of HFrEF

Stage A

This include patients who are at risk of heart failure but without structural heart disease and it involves patients with risk factors such as hypertension, diabetes, metabolic syndrome, history of use of cardiotoxins, and family history of cardiomyopathy.

At this stage, the goal is to reduce risk factorsvia life style modifications including achieving normal body weight, regular exercise, healthy diet, giving up smoking, controlling blood pressure, glucose and cholesterol. This applies to patients with both HFrEF and HFpEF. Controlling hypertension alone in the elderly has been shown to decrease the HF incidence by about 40%.

Stage B

This includes patients with structural heart disease but without any sign or symptoms of heart failure. This can be due to previous myocardial infarction, left ventricular hypertrophy and/or asymptomatic reduced LVEF.

-Given coronary artery disease is the most common cause of heart failure, all patients without an obvious cause should be evaluated for coronary artery disease.

-All patients with HFrEF should be started on an evidence-based b-blocker (carvedilol or bisoprolol or sustained release metoprolol only) and ACE-I or ARB as tolerated. ARB is best used in ACE-I intolerant patients. Only 3 ARBs have been studied on HF patients – valsartan, losartan and candesartan.

-If a patient cannot tolerate ACE-I and ARB or are contraindicated, then hydralazine-nitrate combination can be used instead.

-Early diagnosis and intervention here can delay the onset of symptomatic heart failure and improve survival. For example, the use of ACE-I in asymptomatic HFrEF patients has been shown to reduce the incidence of death or symptomatic heart failure from 39 to 30%.

Stage C

Patients with prior or current symptomatic heart failure are included in Stage C.

-B blocker and ACE-I or ARB are continued as above.

-Diuretics are used in all cases of fluid retention as tolerated.

-NYHA class II-IV patients should also be started on a low dose aldosterone antagonist (spironolactone 12.5-25 mg or eplerenone 25-50 mg).

-Hydralazine and nitrate combination should be considered in African-American patients with NYHA class III-IV HFrEF.

-Combination of ACE-I and ARB may be considered in persistently symptomatic patients with HFrEF who are already being treated with an ACE-I and a beta blocker in whom an aldosterone antagonist is not indicated or tolerated (combination of all 3 potassium elevating medications – ACE-I, ARB and aldosterone antagonist is best avoided).

-Digoxin can be used in HFrEF patients with persistent NYHA II-IV symptoms despite medical management as above to reduce rehospitalization. Maintain digoxin level between 0.5-0.9.

-Patients with chronic HF with permanent/ persistent/ paroxysmal AF and an additional risk factor for cardioembolic stroke (history of hypertension, DM, previous stroke or TIA, or > 75 years of age) should receive chronic anticoagulant therapy. Omega-3 polyunsaturated fatty acid (PUFA) supplementation is reasonable to use as adjunctive therapy in patients with NYHA class II-IV symptoms and HFrEF or HFpEF, unless contraindicated to reduce mortality and cardiovascular hospitalizations.

-ICD therapy is recommended for primary prevention of sudden cardiac death to reduce total mortality in selected patients optimized on guideline directed medical management with persistent LVEF< 35% and NYHA II or III symptoms (extended to NYHA I only for patients with CAD and LVEF<30%, also post-MI patients need to wait for at least 40 days before being considered for ICD).

-Cardiac resynchronisation therapy with a BiVICD is indicated for patients who have LVEF< 35%, with a QRS duration of > 120 msec, and NYHA class III-IV on guideline directed medical management (extended for NYHA II only with LBBB and QRS > 150 msec, never indicated for NYHA I).

Stage D

When patients have symptoms of heart failure despite maximal medical therapy they are included in this stage. It calls in for specialised interventions such as ultrafiltration, intravenous inotropic support, mechanical circulatory support like left ventricular assist device (LVAD), or cardiac transplantation. Transplantation remains the most definitive treatment. Those who are waiting for transplant could use bridge LVAD. Those who not candidates for transplant can be considered for destination LVAD. The rest should be counselled for palliative measures.

B. Management of HFpEF

Management of HFpEF differs from that of HFrEF in that it is limited to managing the underlying cause or associated conditions, apart of symptomatic management. B-blockers, ACE-I/ ARB or cardiac resynchronisation have not shown any definitive improvement in survival in HFpEF patients.

-Systolic and diastolic blood pressure should be tightly controlled.

-Diuretics should be used for relief of symptoms due to volume overload in patients with HFpEF.

-Any underlying ischemic heart disease should be evaluated and managed.

-Management of AF according to published clinical practice guidelines in patients with HFpEF is reasonable to improve symptomatic HF.

C. Management of acutely decompensated heart failure

The priority in patients with congestive heart failure in the emergency department is to rule out severe decompensation, i.e. in acute respiratory failure or in cardiogenic shock. In acute respiratory failure, stabilization of airway should be considered a priority with oxygen support, bilevel positive airway pressure (BPAP), or intubation. In the case of cardiogenic shock and low cardiac output, inotropic support should be initiated rapidly. In some cases of low cardiac output, immediate transfer to the cardiac catheterization laboratory is needed to revascularize and initiate percutaneous mechanical support, such as intra-aortic balloon pump, percutaneous assist devices, or, more rarely, extracorporeal membrane oxygenator (ECMO). In both cases, transfer to the appropriate level of care should be initiated.

Second, congestive symptoms are acutely managed with intravenous diuresis as oral absorption of diuretics is decreased due to bowel wall edema from congestion. Use of morphine is indicated, not only to improve pain but also as it decreases afterload and improves dyspnea. Oxygen is known to improve mortality in cases of acute HF. Other measures such as use nitrates (venodilators) and changing position of the patient (sitting up) can decrease the preload and can improve symptoms of dyspnea in acute cases. Dose of the diuretics is based on multiple factors including vital signs, chronic outpatient dose, renal functions, and electrolytes status.

Third, diagnostic work-up is often initiated simultaneously with the goal of excluding decompensating factors and determining the etiology of heart failure. In cases, when the underlying cause of CHF is known, treatment should be directed towards the cause. These include revascularization of viable myocardium if the etiology is ischemia and stabilization of blood pressure in hypertensive cardiomyopathy.

Conditions that can precipitate acute CHF and should be considered include myocardial ischemia, dietary indiscretion or medical noncompliance, systemic infection (including endocarditis), atrial fibrillation, volume overload (such as in renal failure), toxins (such as alcohol and cocaine), medications (high dose beta-blockers, calcium channel blockers), acute pulmonary embolism (PE), pregnancy, severe anemia (high cardiac output failure), uncontrolled hypertension, surgical stress, and uncontrolled thyroid dysfunction. If CAD is the cause of CHF, aspirin and sublingual nitroglycerin should be added to the regimen. Beta-blockers are recommended to be started once the acute phase of CHF exacerbation is resolved. If a patient was already on beta-blockers as an outpatient, it is recommended to decrease the dose rather than, as previous recommendations advised, discontinue the medicine.

Once a patient is admitted to the hospital, predischarge planning should be initiated right away. This includes addressing exacerbating factors, obtaining optimal fluid status, managing transition from intravenous to oral diuretics and HF education. An oral medication regimen should be stable for 24 hours before discharging the patient from hospital. Once stabilized and discharged from hospital, treatment of chronic heart failure includes diet and exercise with recommendation for less than 2g per day of sodium intake and decreasing daily fluid intake. Patients who are ambulatory should also go through exercise training.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

In order not to miss the key management points, we have divided them into three areas, covering diagnostic approach, treatment management, and discharge.

With regards to diagnostic approach

The cause and mechanism of heart failure should always be determined.

Amyloidosis or infiltrative causes should be considered in patients with low voltage on ECG and heart failure.

Decompensating factors should be evaluated for and treated.

Atrial electromechanical dissociation should be considered in patients with muscular dystrophy. Patients in sinus rhythm and muscular dystrophy can still have strokes if in atrial electromechanical dissociation.

In cases of rapidly progressive heart failure and when giant cell myocarditis or cardiac amyloidosis is suspected, cardiac biopsy should be considered.

Serial BNP should be avoided during hospital stay although it may be useful to order this test on admission and on discharge to monitor baseline level of patients.

CHF exacerbation can be due to a combination of etiologies and concentrating on one may lead to missing other underlying etiologies. Always consider multiple causes that can lead to decompensation of heart failure.

With regards to management

Patients may decompensate quickly. Pitfalls include failure to identify signs of respiratory failure and inability to take appropriate immediate action such as securing airway and transfer to cardiac care unit (CCU). Some of the alarming signs include hypotension, respiratory distress, and diaphoresis.

Inotropic support should be considered in certain cases of low cardiac output and systemic organ hypoperfusion.

The use of calcium channel blockers, beta-blockers, and digoxin are contraindicated in cardiac amyloidosis.

During the hospital stay, diuretic naïve patients can become dehydrated easily, leading to acute renal failure. In these patients the dose of diuretics should be monitored closely.

Unmonitored anticoagulation can at times lead to life-threatening bleeding.

Common side effects of medicines used for the treatment of CHF exacerbation include hypotension, hyponatremia, hypokalemia, and hypomagnesemia.

Cough and angioedema are well-known side effects of ARBs and ACEIs and should be monitored.

Medication with drug-drug interactions should be avoided, patients should be advised on medication interactions.

Placement of implantable cardioverter defibrillator (ICD) and biventricular (BV) pacing is known to improve mortality but can be easily forgotten. BV pacemaker is considered in patients with refractory HF, ejection faction (EF) less than 35% and QRS greater than 120 msec. ICD is used in cases of decreased EF as secondary prophylaxis.

It is important to differentiate patients who present with congestive symptoms of HF (majority of the cases) from patients with hypotensive shock and low cardiac output needing ionotropic support.

Always rule out digoxin toxicity in patients with HF presenting with tachyarrhythmia or gastrointestinal symptoms.

For discharge

Patients with acute decompensation should be closely followed up after hospital discharge to minimize rehospitalization.

Referral for heart transplantation or destination mechanical support should be considered in selected patients with advanced heart failure.

Management of heart failure involves change in diet (low sodium diet), close monitoring to detect early signs of volume overload, avoidance of any factors that can lead to decompensation, and use of medication known to improve survival or symptoms.

Medications for CHF are divided into two groups: medications that are known to prolong survival and others that are beneficial for symptomatic relief. Medications that have been shown to improve survival include ACEIs, ARBs, hydralazine and nitrates, beta-blockers, and spironolactone. Medications that are used for symptomatic treatment include digoxin and diuretics.

ACEIs are known to improve mortality and decrease hospital admission rates. However, it is necessary to monitor for side effects such as hyperkalemia or allergic reactions such as angioedema. Not only are ACEIs known to improve outcomes in symptomatic patients, they also improve mortality in asymptomatic patients with HF (stage B).

Hydralazine and nitrates are mostly used in African American patients with class 3 or class 4 CHF on the New York Heart Association’s classification or in patients who cannot tolerate ACEIs or ARBs. In patients of African American race, they have been shown to improve survival.

Beta-blockers also improve mortality and lower hospital admissions rate. They should be stopped or administered at lower doses in patients admitted with acutely decompensated heart failure. Beta-blockers reduce oxygen demand of the myocardium by decreasing heart rate, increase diastolic blood supply, act as antiarrhythmic agent and decrease the rate of sudden cardiac death. In patients with HF, beta-blocker therapy should be started at a low dose and titrated up slowly.

Aldosterone antagonists are used in cases of symptomatic heart failure. In patients with symptomatic CHF, these medications are known to have significant morbidity and mortality benefits. Close monitoring of potassium levels are warranted if used in combination with ACEI.

Digoxin is known to decrease hospital admissions rates but it does not have any mortality benefits. Digoxin has a narrow therapeutic window and clinicians should keep a high index of suspicion for toxicity. Monitoring of digoxin level once a patient has reached a steady statemay be useful to avoid toxicity, especially in the elderly population.

Biventricular pacing and defibrillator therapy have both been shown to improve survival of patients with symptomatic heart failure (stage C).

Selected patients with refractory heart failure should be referred for consideration for heart transplantation or destination ventricular assist device therapy.

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