Congestive Heart Failure

Congestive heart failure (CHF) is one of the most commonly encountered entities in the Emergency Department. Because the prevalence of CHF increases with age, the enormous burden of this disease is also on the increase. Currently, CHF costs the health care system about $20 billion per year in the U.S. and it accounts for more hospitalizations than any other disease in patients older than 65.

Definitions

• Congestive heart failure (CHF) exists when the heart is unable to pump sufficient blood to meet the metabolic requirements of the body’s tissues. Because of natural compensatory mechanisms in response to heart failure, it most commonly is associated with abnormal retention of fluid.
• CHF is classified in many ways. Although in some respects, these classifications are artificial because they do not exist as independent entities, they are nonetheless very helpful distinctions to make in the evaluation and treatment of Congestive heart failure (CHF)patients:
• High output failure versus low output failure: In low output failure there is an inherent problem with the contractility of the heart. In high output failure, an intact myocardium is unable to keep up with excess functional demands secondary to hypermetabolic states such as thyrotoxicosis, anemia or AV shunts. Low output failure is much more common.
• Left-sided versus right-sided failure: Left-sided failure is usually due to mechanical overload or ischemia. The most common cause of right-sided failure is pulmonary hypertension secondary to left-sided failure.
• Systolic versus diastolic failure: Systolic failure is more common and is due to impaired contractility during systole. Diastolic failure occurs when impaired relaxation prevents adequate filling of the ventricles during diastole. Diastolic failure is less well understood and appears to be due to hypertension, as well as other less common causes such as restrictive cardiomyopathy or aortic stenosis.
• Backward versus forward failure: Backward failure refers to the accumulation of fluid behind the ventricles (e.g., edema and hepatic congestion in right-sided failure, pulmonary edema in left-sided failure). Forward failure refers to the failure of the heart to provide adequate perfusion of the tissues, which is usually manifested by some degree of hypotension, whether relative or absolute.
• Acute and chronic heart failure essentially involve the same process, although when heart failure develops over a short period of time, it tends to involve more forward failure and hypotension and less accumulation of fluid. In chronic failure, there is more time for the evolution of compensatory processes.
• Cardiogenic pulmonary edema refers to the accumulation of fluid in the interstitial and alveolar spaces as a result of CHF. It is a severe form of left-sided CHF.

Epidemiology

At the present time, nearly 5 million patients are diagnosed with CHF in the U.S. with 500,000 new cases identified each year. Almost 300,000 patients die from CHF or its complications every year.

Pathophysiology

• The most common underlying pathology in CHF is ischemic heart disease. Other causes of low output failure include valvular disease, myocarditis, chronic hypertension and cardiomyopathies (such as those caused by ethanol and cocaine abuse). Anemia and thyrotoxicosis are causes of high output failure. Table 2C.1 lists common processes that
  

  Common precipitants of congestive heart failure

  Myocardial infarction/ischemia	Dietary and fluid excesses
  Dysrhythmia	Valvular heart disease
  Infection	Non-compliance with medications
  Thyrotoxicosis	Uncontrolled hypertension
  Pulmonary embolism

  can precipitate CHF. The causes in the first column are especially important to identify because they have specific therapy that can be initiated in the ED.

• In CHF, elevated left ventricular filling volumes exceeds the threshold over which increased preload increases efficiency and instead, the heart begins to pump more inefficiently, with decreasing stroke volume. This relationship is described by the Frank-Starling curve. Decreasing stroke volume leads to the clinical effects of both backward and forward failure.
• Neurohormonal compensatory responses play an important role in the pathophysiology of CHF. Alterations in adrenergic tone redistribute blood flow to the brain and heart and reduce flow to other organs. The reduction in flow to the kidneys increases stimulation of renin-angiotensin-aldosterone axis which leads to an increased secretion of ADH, renin and angiotensin II. This leads to increased sodium and water retention and a rise in both preload and afterload. Increased adrenergic tone leads to arteriolar vasoconstriction, which also contributes to increased afterload.

  Diagnosis and Evaluation

  Clinical Features
  

• Left-sided failure symptoms include dyspnea (particularly with exertion), orthopnea, paroxysmal nocturnal dyspnea, fatigue and nocturia.
• Physical examination features in left-sided failure include tachypnea, tachycardia, pulmonary rales and/or wheezing ("cardiac asthma"), dullness to percussion, diaphoresis, poor peripheral perfusion causing pale and cool extremities, S3 and S4 gallop rhythms and in severe pulmonary edema secondary to CHF, abnormal breathing patterns, such as Cheyne-Stokes.
• Right-sided failure symptoms include lower extremity edema and right upper quadrant pain and anorexia due to liver congestion.
• Examination features in right-sided failure include jugular venous distention, hepatojugular reflux, hepatomegaly, RUQ abdominal tenderness, and peripheral edema.

  Diagnostic Studies

• In addition to establishing the diagnosis of CHF, the EP must focus on the identifying and correction of its underlying causes. Important precipitating causes are listed in Table 2C.1.
• Chest X-ray (CXR) findings are mostly a function of left-sided failure, which results in increased pulmonary venous pressures.
• Because of the higher resistance to flow in the lower regions, blood flow is initially shunted to the upper pulmonary vasculature. This appearance of engorged vessels in the upper lung fields is known as "cephalization" and is the earliest finding of CHF on the chest X-ray.
• As the vascular pressure increases, fluid starts to move to the gravity-dependent lower zones of the lungs, which is known as "caudalization".
• Interlobular edema creates short horizontal linear markings in the lung periphery at the bases which are known as Kerley B lines.
• With increasing severity, a bat-wing pattern may be seen, representing interstitial edema in both upper and lower regions of the lungs
• In its most severe form, edema fluid spills from the interstitial spaces into the airspaces, causing opacification of the lung fields on CXR
• Cardiomegaly is usually evident on the CXR, especially in patients with chronic CHF.
  In those cases where CHF occurs acutely in a previously healthy individuals, the EP must distinguish cardiogenic from noncardiogenic causes of pulmonary edema, such as the adult respiratory distress syndrome (ARDS) Pleural effusion may also be seen in CHF. It is often bilateral.
• A 12-lead EKG should be obtained immediately in patients presenting with signs and symptoms suggestive of CHF because an important precipitant of CHF is ischemia and infarction.
• In chronic CHF, changes such as ventricular hypertrophy and conduction abnormalities can be seen. These changes invariably make the identification of acute coronary syndromes more difficult, underscoring the importance of performing serial EKGs in the ED and obtaining previous EKGs for comparison. The presence of dynamic or new changes in the 12-lead EKG should raise the suspicion for ACS.
• Bedside echocardiography performed by EPs may be very valuable in ruling out the presence of a pericardial diseases effusion in the setting of a patient with signs of failure and an enlarged heart on CXR. Formal echocardiography yields a great deal of valuable information to help guide the management of patients with CHF but is not necessarily required during the course of ED management.
• Basic laboratory investigations such as CBC, electrolytes, urea and creatinine are indicated in CHF. Anemia is an important contributing factor in CHF. Electrolyte disturbances are common and potentially life-threatening. These are often the result of chronic diuretic therapy and renal insufficiency associated with CHF.
• In most cases, serum troponin or other cardiac markers should be measured during the ED evaluation because of the strong association between CHF and ischemic heart disease.
• A digitalis level should be obtained in those patients receiving digoxin therapy.
• B-type natriuretic peptide (BNP) is an endogenous cardiac peptide produced in the ventricles that is released from the heart in response to fluid overload. Recently, an assay of BNP has been introduced to assist in the diagnosis of CHF. It is both sensitive and specific for the presence of CHF; however, its clinical role has yet to be determined. At present, it appears that this test may have a role in a limited subset of patients in whom the diagnosis of CHF may be clouded by coexisting pulmonary disease such as chronic obstructive pulmonary disease (COPD) or sleep apnea.

  ED Management

  Emergency Resuscitation
  

• In severe cases, emergent management may involve aggressive intervention to maintain airway, breathing and circulation.
• All patients require vascular access, cardiac monitoring and pulse oximetry.
• All patients should be placed on oxygen therapy. The specific technique of delivery (nasal cannula, face mask, non-rebreather mask) should be guided by the severity of presentation and pulse oximetry values.
• Aggressive airway management should be initiated in the setting of severe respiratory distress, with or without hypoxia. Endotracheal intubation will be necessary in patients who become so somnolent that they are unable to protect their airway or in those who have tired of breathing and may have begun to have periods of apnea.
• Noninvasive ventilation techniques such as continuous positive airway pressure (CPAP) or biphasic positive airway pressure (BiPAP) have been used in many instances where intubation and mechanical ventilation were once considered inevitable. They are used as a bridging therapy in the patient with severe cardiogenic pulmonary edema until pharmacologic therapy takes effect. These devices provide continuous or biphasic positive airway pressure through a tight-fitting face mask. This positive pressure improves cardiac output by decreasing venous return and excessive preload. It also improves oxygenation by increasing alveolar recruitment and decreases the work and metabolic requirement of breathing.
• Heart rate is extremely important in CHF and both inappropriately slow and fast rates will decrease the ability of the heart to work efficiency. Brady- and tachydysrhythmias should be treated according to ACLS guidelines in the setting of CHF.
• When frank shock is present, vasopressor therapy may need to begin immediately. An inotropic agent such as dopamine is preferred. These agents all increase myocardial oxygen consumption and ischemia, creating an additional risk for dysrhythmias.
• Although pressors may raise arterial blood pressure, this alone does not guarantee sufficient perfusion, if cardiac output is too low. Adequate perfusion must always be assessed by using clinical indicators such as urine output, skin appearance and mental status.
• Interventional therapies may be possible in the event that acute exacerbation is due to ACS (e.g., percutaneous coronary intervention) or a related structural problem (e.g., valvular or myocardial rupture repair).
• Intra-aortic balloon counterpulsation (IABP) can be used as a bridge to other interventional therapies such as cardiac transplantation.

  Specific Pharmacotherapy

• The use of pharmacotherapeutic agents is aimed at improving the unfavorable hemodynamics of acute CHF. In general, these agents share the ability to precipitate or worsen hypotension. As each successive agent is introduced (at a pace commensurate with the severity of symptoms), close attention must be paid to vital signs, fluid balance and symptomatic response to therapy.
• Nitrates cause both arterial and venous vasodilatation, reducing both preload and afterload. Nitroglycerin (NTG) is the initial agent of choice in acute CHF.
• Nitrates can be administered through many routes including sublingual, transdermal, and intravenous.
• Caution should be exercised with sublingual NTG because of its ability to cause precipitous drops in blood pressure.
• Transdermal paste (1/2-2 inches applied to chest wall) gives a slower, lower dose release of NTG but may not be effective in severe CHF when cutaneous perfusion is compromised.
• IV dosing is required in severe CHF, and IV infusions may be started at 10-20 mcg/ min and titrated to relief of symptoms while maintaining systolic BP less than 90 mm.
• Nitrates predictably cause headache, which will often require treatment with anal-gesics.
• Diuretics reduce volume overload. Loop diuretics are the preferred class, and initial treatment should begin with furosemide (Lasix) 20-80 mg IVP, depending on the patient’s previous exposure and severity of symptoms. Even with IV administration, full effect may take up to 30 min, underscoring the importance of using diuretics together with nitrates. Adverse effects of diuretics include electrolyte imbalances, prerenal azotemia, contraction alkalosis and hypotension.
• ACE inhibitors decrease afterload. Because of several trials that demonstrate reduction in morbidity and mortality in CHF, ACE inhibitors should be used in the treatment of chronic CHF unless a contraindication exists. Several agents can be given in the ED, however, captopril (Capoten) 6.25-12.5 mg PO q8h is preferred because it is the fastest acting of the various agents available. Angiotensin II receptor blockers (ARBs) inhibit the effects of angiotensin II. They decrease afterload and improve diuresis.
  Currently, they should only be used in place of ACE inhibitors in patients who are intolerant or allergic to ACE inhibitors.
• Morphine decreases catecholamine levels by decreasing anxiety, theoretically causing a decrease in preload and afterload. However, little evidence for the effectiveness of morphine exists and its use is controversial. Respiratory depression with morphine may result in unnecessary intubation—a small dose (e.g., 2 mg IV) may be beneficial without impairing respiratory effort.
• Beta-blockers have been shown in multiple well-designed, randomized studies to improve the symptoms and altered hemodynamics in chronic CHF. They inhibit the neurohormonal cascade and improve symptoms, especially in the setting of cardiac ischemia.
  They have also been shown to decrease mortality. However, they are not generally indicated in the treatment of acute heart failure and may result in acute decompensation.
  When CHF occurs within the setting of AMI, the decision to add ß-blockers to therapy should be made with the guidance of a cardiologist.
• Digoxin enhances contractility and reduces afterload by blunting the cardiac sympathetic response. It also causes AV nodal blockade which may be beneficial in patients with atrial dysrhythmias. Currently, there are no conclusive data to show that digoxin reduces mortality in CHF although it may reduce hospitalizations and improve quality of life. Because it is slow to act, its use in the ED for CHF is on the decline. IV loading may be initiated in the ED with 0.25 mg followed by further IV or PO doses over the next several hours.
• Calcium channel blockers are not currently recommended in the ED treatments for congestive heart failure, unless they are required for rate control in accordance with ACLS guidelines.
• Dobutamine is a synthetic catecholamine that unlike other pressor agents causes vasodilatation in addition to inotropy. For this reason, it is the one vasoactive catecholamine sometimes used in treatment of CHF in the absence of cardiogenic shock.
  Dobutamine must be given with close hemodynamic monitoring and may initially result in hypotension.
• Nesiritide (Beta natriuretic peptide) is an endogenous substance that acts both a vasodilator and a diuretic. It has recently been demonstrated to be effective in the treatment of acute CHF. However, its effects are more prolonged and it is less titratable than NTG. Its role as a first-line agent in the treatment of CHF and superiority over NTG has yet to be demonstrated.

Prognosis

Prognosis in CHF decreases proportionately with severity. Two commonly used classification systems for severity of heart failure are given in (Table 2C.2). Both classifications demonstrate the typical progression of chronic CHF from backward to forward failure.

Disposition

Patients diagnosed with acute heart failure or acute exacerbation of chronic heart failure most commonly require admission to hospital. Moderate or severe presentations require admission to the cardiac care unit (CCU) or monitored unit.
Mild exacerbations may be admitted to unmonitored settings in the absence of suspected ACS. It may also be appropriate to admit patients with mild exacerbations to short-stay or observational units or even to discharge them home with close follow-up when no acute serious underlying pathology is suspected and symptoms have resolved.

Table Classification of heart failure severity and prognosis

Killip Classification			1 yr
(Clinical)	Definition	Incidence (%)	Mortality (%)
Class I	No signs of pulmonary edema	30	5
Class II	Mild failure (rales, S3)	40	15-20
Class III	Frank pulmonary edema	10	40
Class IV	Cardiogenic shock	20	80
Diamond-Forrester
Classification (Based on invasive monitoring)	Cardiac Index (L/min/m2)	Pulm. Artery Wedge Pressure (mm Hg)	1 yr Mortality (%)
Class I	>2	<18	3
Class II	>2	>18	9
Class III	<2	<18	23
Class IV	<2	>18	51