Congestive Heart Failure, Emergency Medicine

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Congestive Heart Failure, Emergency Medicine

Basics

Description

Underlying causes and acute precipitants

ACEi and ARBs are associated with multiple fetal abnormalities and should be held

Consider ICD and/or BV pacer in advanced HF

A clinical syndrome in which the heart fails to maintain adequate circulation for metabolic needs, characterized by chronic debility, acute decompensation, and high mortality.
Acute Decompensated Heart Failure (ADHF) is a rapidly progressive failure state (hr-days)Common reason for presentation to the EDUsually caused by a precipitating event in which the heart does not have the reserve to compensate for the added burden
Chronic HF is a progressive failure state (mo-yr) characterized by cardiac remodeling and neurohormonal changes, with multiple subclasses:Systolic heart failureImpaired contractile or pump function causing decreased ejection fractionDiastolic heart failureImpaired ventricular relaxation resulting in decreased cardiac fillingLow-output failureDecreased cardiac outputHigh-output failure:Normal or increased cardiac output, but insufficient to meet metabolic demandsLeft-sided failureSystolic or diastolic (or both) dysfunction of the left ventricleResultant pulmonary congestionRight-sided heart failureDue to either intrinsic dysfunction or secondary to left heart failure or pulmonary hypertension (cor pulmonale)Hepatic enlargement, JVD, and dependent edema can occur
CHF affects ~5.8 million Americans.
Estimated 2012 cost of CHF is $40 billion
ADHF is the leading Medicare diagnosis for hospitalized patients ≥65 yr old.

Common reason for presentation to the ED
Usually caused by a precipitating event in which the heart does not have the reserve to compensate for the added burden

Systolic heart failureImpaired contractile or pump function causing decreased ejection fraction
Diastolic heart failureImpaired ventricular relaxation resulting in decreased cardiac filling
Low-output failureDecreased cardiac output
High-output failure:Normal or increased cardiac output, but insufficient to meet metabolic demands
Left-sided failureSystolic or diastolic (or both) dysfunction of the left ventricleResultant pulmonary congestion
Right-sided heart failureDue to either intrinsic dysfunction or secondary to left heart failure or pulmonary hypertension (cor pulmonale)Hepatic enlargement, JVD, and dependent edema can occur

Impaired contractile or pump function causing decreased ejection fraction

Impaired ventricular relaxation resulting in decreased cardiac filling

Decreased cardiac output

Normal or increased cardiac output, but insufficient to meet metabolic demands

Systolic or diastolic (or both) dysfunction of the left ventricle
Resultant pulmonary congestion

Due to either intrinsic dysfunction or secondary to left heart failure or pulmonary hypertension (cor pulmonale)
Hepatic enlargement, JVD, and dependent edema can occur

Etiology

Decreased myocardial contractility:Myocardial ischemia/infarctionCardiomyopathy (including, alcoholic and pregnancy-related)MyocarditisDysrhythmiasDecreased contractile efficiency:Drug related (negative inotropes)Metabolic disorders
Pressure overload states:HTNValvular abnormalitiesArrhythmiaCongenital heart diseasePulmonary embolismPrimary pulmonary hypertension, sleep apnea syndromes (right heart failure)
Restricted cardiac output:Myocardial infiltrative disease
Volume overload:Dietary indiscretion (sodium overload)Drugs leading to sodium retention (glucocorticoids, NSAIDs)Overload due to transfusion or IV fluid
High demand states:Hyperthyroidism, thyrotoxicosisPregnancyA-V fistulaBeriberi (thiamine deficiency)Paget diseaseSevere anemiaAortic insufficiency
Pediatric etiologies: Volume/pressure overload lesions vs. acquired HD:1st 6 mo: VSD and PDAOlder children: Subvalvular aortic stenosis, coarctationAcquired dysfunction: Nonspecific age of onset, including myocarditis, valvular disease, and cardiomyopathies; cocaine/stimulant abuse in adolescents

Myocardial ischemia/infarction
Cardiomyopathy (including, alcoholic and pregnancy-related)
Myocarditis
Dysrhythmias
Decreased contractile efficiency:Drug related (negative inotropes)Metabolic disorders

Drug related (negative inotropes)
Metabolic disorders

HTN
Valvular abnormalities
Arrhythmia
Congenital heart disease
Pulmonary embolism
Primary pulmonary hypertension, sleep apnea syndromes (right heart failure)

Myocardial infiltrative disease

Dietary indiscretion (sodium overload)
Drugs leading to sodium retention (glucocorticoids, NSAIDs)
Overload due to transfusion or IV fluid

Hyperthyroidism, thyrotoxicosis
Pregnancy
A-V fistula
Beriberi (thiamine deficiency)
Paget disease
Severe anemia
Aortic insufficiency

1st 6 mo: VSD and PDA
Older children: Subvalvular aortic stenosis, coarctation
Acquired dysfunction: Nonspecific age of onset, including myocarditis, valvular disease, and cardiomyopathies; cocaine/stimulant abuse in adolescents

Diagnosis

Signs and Symptoms

Poor perfusion:Fatigue, somnolence, lightheadednessPalpitations, or irregular pulseShortness of breathCool extremitiesWorsening renal function
CongestionDyspnea, coughOrthopneaParoxysmal nocturnal dyspneaEvidence of sleep disordered breathingDecreased exercise toleranceElevated JVD or abdominojugular reflexDependent edema (poor sensitivity and specifity)Rales and/or wheezing, (absent in 80% with chronically elevated filling pressure due to compensatory lymphatic drainage)Pleural effusion, dullness at lung basesS3 gallop and/or S4.Laterally displaced apical impulseHepatic enlargement/tendernessNauseaAscites
ADHF with hemodynamic instability:Confusion, anxiety, syncopeTachypneaTachycardiaHypotensionCool, pale or cyanotic extremitiesNarrow pulse pressure or pulsus alternansCheyne-Stokes respirations

Fatigue, somnolence, lightheadedness
Palpitations, or irregular pulse
Shortness of breath
Cool extremities
Worsening renal function

Dyspnea, cough
Orthopnea
Paroxysmal nocturnal dyspnea
Evidence of sleep disordered breathing
Decreased exercise tolerance
Elevated JVD or abdominojugular reflex
Dependent edema (poor sensitivity and specifity)
Rales and/or wheezing, (absent in 80% with chronically elevated filling pressure due to compensatory lymphatic drainage)
Pleural effusion, dullness at lung bases
S3 gallop and/or S4.
Laterally displaced apical impulse
Hepatic enlargement/tenderness
Nausea
Ascites

Confusion, anxiety, syncope
Tachypnea
Tachycardia
Hypotension
Cool, pale or cyanotic extremities
Narrow pulse pressure or pulsus alternans
Cheyne-Stokes respirations

Essential Workup

The CXR is important in confirming the diagnosis and assessing severity.
12-hr radiographic lag from onset of symptoms may occur.
Radiographic findings may persist for several days despite clinical improvement.

Diagnosis Tests & Interpretation

Chemistry/electrolytes:Establish baseline renal function when initiating diuretics, or ACE inhibitorsHyperkalemia possible with low outputHyponatremia associated with poor prognosis
CBC:Anemia can cause or exacerbate failureInfection can cause or exacerbate failure
Liver function tests:Increase suggests hepatic congestion, or ischemia.
Thyroid function tests:Specifically in patients >65 yr old or in a-fib
Cardiac enzymes:Evaluate for ischemia or infarction
ANA and rheumatoid factor: Suspected lupus
Viral panel: Suspected myocarditis
BNP:Useful for distinguishing cardiac vs. pulmonary cause of dyspneaBNP >500 pg/mL, HF likely (ppv 90%)BNP <100 pg/mL, HF unlikely, (npv 90%)BNP 100-500 pg/mL, consider PE, cor pulmonale, renal failure, or stable underlying HF.REDHOT II Study: BNP levels are better than physicians at predicting which patients are more likely to have bad outcomesEPs were blinded to BNP values. 78% of patients discharged from ED had BNP >400.Of those discharged with a BNP >400, 90-day mortality was 9%BNP levels rise with age and are affected by gender, comorbidity, and drug therapy and should not be used in isolationBNP levels may be low in acute pulmonary edema (<1-2 hr) and obesity (BMI >30).
NT-proBNP: Cleavage product of prohormone.NT-proBNP >1,000 pg/mL predictive of HFNT-proBNP <300 pg/mL unlikely to be HF

Establish baseline renal function when initiating diuretics, or ACE inhibitors
Hyperkalemia possible with low output
Hyponatremia associated with poor prognosis

Anemia can cause or exacerbate failure
Infection can cause or exacerbate failure

Increase suggests hepatic congestion, or ischemia.

Specifically in patients >65 yr old or in a-fib

Evaluate for ischemia or infarction

Useful for distinguishing cardiac vs. pulmonary cause of dyspneaBNP >500 pg/mL, HF likely (ppv 90%)BNP <100 pg/mL, HF unlikely, (npv 90%)BNP 100-500 pg/mL, consider PE, cor pulmonale, renal failure, or stable underlying HF.
REDHOT II Study: BNP levels are better than physicians at predicting which patients are more likely to have bad outcomesEPs were blinded to BNP values. 78% of patients discharged from ED had BNP >400.Of those discharged with a BNP >400, 90-day mortality was 9%
BNP levels rise with age and are affected by gender, comorbidity, and drug therapy and should not be used in isolation
BNP levels may be low in acute pulmonary edema (<1-2 hr) and obesity (BMI >30).

BNP >500 pg/mL, HF likely (ppv 90%)
BNP <100 pg/mL, HF unlikely, (npv 90%)
BNP 100-500 pg/mL, consider PE, cor pulmonale, renal failure, or stable underlying HF.

EPs were blinded to BNP values. 78% of patients discharged from ED had BNP >400.
Of those discharged with a BNP >400, 90-day mortality was 9%

NT-proBNP >1,000 pg/mL predictive of HF
NT-proBNP <300 pg/mL unlikely to be HF

CXR:Cardiomegaly (sensitive)Specific signs of CHF:Cephalization (vascular prominence in the upper lungs due to fluid overload)Interstitial edema/Kerley B linesAlveolar edemaEffusions (usually right sided)Bilateral confluent perihilar infiltrates leading to classic butterfly pattern:May be asymmetric and mistaken for pneumonia
EKG:Underlying cardiac ischemiaPresence of dysrhythmiasLeft-ventricular hypertrophyHeart blockNormal EKG has high negative predictive value for systolic dysfunction.
2-D Cardiac Echo:Ejection fractionAcute valvular pathologyPericardial tamponadePericardial thickening in constrictive pericarditisVentricle dilation, or hypertrophyRegional wall motion abnormalities

Cardiomegaly (sensitive)
Specific signs of CHF:Cephalization (vascular prominence in the upper lungs due to fluid overload)Interstitial edema/Kerley B linesAlveolar edema
Effusions (usually right sided)
Bilateral confluent perihilar infiltrates leading to classic butterfly pattern:May be asymmetric and mistaken for pneumonia

Cephalization (vascular prominence in the upper lungs due to fluid overload)
Interstitial edema/Kerley B lines
Alveolar edema

May be asymmetric and mistaken for pneumonia

Underlying cardiac ischemia
Presence of dysrhythmias
Left-ventricular hypertrophy
Heart block
Normal EKG has high negative predictive value for systolic dysfunction.

Ejection fraction
Acute valvular pathology
Pericardial tamponade
Pericardial thickening in constrictive pericarditis
Ventricle dilation, or hypertrophy
Regional wall motion abnormalities

Differential Diagnosis

Left-sided CHF:Acute exacerbation of COPDAsthma exacerbationAcute respiratory distress syndromePneumonia, bronchitisConstrictive pericarditisAnemia, malnutritionPericardial tamponadeCoarctation of aorta
Right-sided HF:Nephrotic syndrome, chronic renal failureCirrhosisLeft-side heart failurePulmonary embolismSleep disordered breathingVenous stasis

Acute exacerbation of COPD
Asthma exacerbation
Acute respiratory distress syndrome
Pneumonia, bronchitis
Constrictive pericarditis
Anemia, malnutrition
Pericardial tamponade
Coarctation of aorta

Nephrotic syndrome, chronic renal failure
Cirrhosis
Left-side heart failure
Pulmonary embolism
Sleep disordered breathing
Venous stasis

Treatment

Pre-Hospital

IV access
Supplemental oxygen
Cardiac monitor and pulse oximetry
EKG
Sublingual nitrates for active chest pain without hypotension
Furosemide
Endotracheal intubation may be required.

Initial Stabilization/Therapy

IV access
Supplemental oxygen
Cardiac monitor and pulse oximetry
EKG
Elevate head of bed to reduce venous return.
Control airway as needed:Noninvasive positive pressure ventilationCPAP vs. BiPAPReduce work of breathing, improve oxygenation, decrease need for intubation, possible mortality benefitSome studies report higher incidence of MI with BiPAP over CPAP in acute CHF; studies not conclusiveIntubation for impending respiratory failure

Noninvasive positive pressure ventilationCPAP vs. BiPAPReduce work of breathing, improve oxygenation, decrease need for intubation, possible mortality benefitSome studies report higher incidence of MI with BiPAP over CPAP in acute CHF; studies not conclusive
Intubation for impending respiratory failure

CPAP vs. BiPAP
Reduce work of breathing, improve oxygenation, decrease need for intubation, possible mortality benefit
Some studies report higher incidence of MI with BiPAP over CPAP in acute CHF; studies not conclusive

Ed Treatment/Procedures

General: Oxygenate, ventilate, treat underlying condition when possible
Congestion with adequate perfusion: Reduce preload, consider fluid restrictionRapidly reduce preload in acute pulmonary edema:Sublingual or IV nitroglycerinNitro pasteIV diuretics (less rapid/effective in patients with poor renal perfusion)Avoid preload reduction in ADHF when suspected etiology is aortic stenosis, HOCM, or pulmonary hypertension.Cautious afterload reduction in ADHF: Avoid ACEi and ARBs in cases of hypotension, acute renal failure, and hyperkalemia.NesiritideLimited benefit, may cause hypotension
Poor perfusion with hypotension:Agents that increase contractility:DobutamineDopamineMilrinoneAvoid vasodilators (nitrates, morphine)Initiate diuretics after inotropes.
Initiate venous thromboembolism prophylaxis in those with ADHF without contraindications

Rapidly reduce preload in acute pulmonary edema:Sublingual or IV nitroglycerinNitro pasteIV diuretics (less rapid/effective in patients with poor renal perfusion)
Avoid preload reduction in ADHF when suspected etiology is aortic stenosis, HOCM, or pulmonary hypertension.
Cautious afterload reduction in ADHF: Avoid ACEi and ARBs in cases of hypotension, acute renal failure, and hyperkalemia.Nesiritide
Limited benefit, may cause hypotension

Sublingual or IV nitroglycerin
Nitro paste
IV diuretics (less rapid/effective in patients with poor renal perfusion)

Nesiritide

Agents that increase contractility:DobutamineDopamineMilrinone
Avoid vasodilators (nitrates, morphine)
Initiate diuretics after inotropes.

Dobutamine
Dopamine
Milrinone

Neonates (1st weeks of life):Suspect ductal-dependent cardiac lesions if clinical CHF and no improvement with O2:PGE1 to maintain patent ductus
Children:IV furosemide, and dopamine or milrinoneIV nitroglycerin for pulmonary edema

Suspect ductal-dependent cardiac lesions if clinical CHF and no improvement with O2:PGE1 to maintain patent ductus

PGE1 to maintain patent ductus

IV furosemide, and dopamine or milrinone
IV nitroglycerin for pulmonary edema

Medication

Aspirin: 325 mg PO/PR if AMI is suspected
Bumetanide (Bumex): 1-3 mg IV, max. 10 mg/day
Dobutamine: 2-10 Î¼g/kg/min IV, max. of 40 Î¼g/kg/min
Dopamine: 2-20 Î¼g/kg/min IV, max. of 50 Î¼g/kg/min
Enalapril: 0.625-1.25 mg IV; 2.5-20 mg/d PO
Furosemide (Lasix): No prior use: 40 mg IVP; prior use: Double 24-hr dose (80-180 mg IV); no effect in 30 min: Redouble dose
Milrinone: 50 Î¼g/kg IV load; 0.375-0.75 Î¼g/kg/min IV
Nesiritide: 2 Î¼g/kg bolus, then infusion of 0.01 Î¼g/kg/min
Nitroglycerin: 0.4 mg sublingual; 1-2 in of nitro paste; 5-20 Î¼g/min IV, max. of 100-200 Î¼g/min IV. USE NON-PVC tubing.
Nitroprusside: 0.3-10 Î¼g/kg/min IV (starting dose), max. of 10 Î¼g/kg/min

Oxygen
Nitroglycerin
Furosemide

Follow-Up

Disposition

ICU:Pulmonary edemaCardiogenic shockConcomitant MI or ischemia
Medical wards:New-onset CHFSymptoms not relieved by ED therapy

Pulmonary edema
Cardiogenic shock
Concomitant MI or ischemia

New-onset CHF
Symptoms not relieved by ED therapy

Mild exacerbation of chronic CHF:Responds to ED treatmentNo other cardiac and pulmonary findings
Close follow-up should be arranged with continuation of diuretic, vasodilator, or ACE inhibitor therapy and patient lifestyle education.

Responds to ED treatment
No other cardiac and pulmonary findings

Shown to decrease mortality and hospitalization rates in select patient groups

Follow-Up Recommendations

Close follow-up within 1 wk of discharge
Medication and dietary compliance
Frequent home monitoring of body weight
Monitor electrolytes and renal function during chronic diuretic therapy

Pearls and Pitfalls

BNP may be useful if CHF diagnosis uncertain.
In severe CHF, NIPPV can improve impending respiratory compromise.
Be vigilant in searching for and treating the underlying cause of the heart failure exacerbation (e.g., MI, PE, valvular pathology).

Additional Reading

Heart Failure Society of America. Executive summary: HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010;16(6):475-535.
Singer AJ, Birkhahn RH, Guss D, et al. Rapid Emergency Department Heart Failure Outpatients Trial (REDHOTII): A randomized controlled trial of the effect of serial B-type natriuretic peptide testing on patient management. Circ Heart Failure. 2009;2:287-293.
Silvers SM, Howell JM, Kosowsky JM, et al. ACEP Clinical policy: Critical issues in the evaluation and management of adult patients presenting to the emergency department with acute heart failure syndromes. Ann Emerg Med. 2007;49(5):627-669.

Codes

ICD9

428.0 Congestive heart failure, unspecified
428.20 Systolic heart failure, unspecified
428.30 Diastolic heart failure, unspecified
428.40 Combined systolic and diastolic heart failure, unspecified
428.1 Left heart failure
428.21 Acute systolic heart failure
428.22 Chronic systolic heart failure
428.23 Acute on chronic systolic heart failure
428.2 Systolic heart failure
428.31 Acute diastolic heart failure
428.32 Chronic diastolic heart failure
428.33 Acute on chronic diastolic heart failure
428.3 Diastolic heart failure
428.41 Acute combined systolic and diastolic heart failure
428.42 Chronic combined systolic and diastolic heart failure
428.43 Acute on chronic combined systolic and diastolic heart failure
428.4 Combined systolic and diastolic heart failure
428 Heart failure

ICD10

I50.9 Heart failure, unspecified
I50.20 Unspecified systolic (congestive) heart failure
I50.30 Unspecified diastolic (congestive) heart failure
I50.40 Unsp combined systolic and diastolic (congestive) hrt fail
I50.1 Left ventricular failure
I50.21 Acute systolic (congestive) heart failure
I50.22 Chronic systolic (congestive) heart failure
I50.23 Acute on chronic systolic (congestive) heart failure
I50.2 Systolic (congestive) heart failure
I50.31 Acute diastolic (congestive) heart failure
I50.32 Chronic diastolic (congestive) heart failure
I50.33 Acute on chronic diastolic (congestive) heart failure
I50.3 Diastolic (congestive) heart failure
I50.41 Acute combined systolic and diastolic (congestive) hrt fail
I50.42 Chronic combined systolic and diastolic hrt fail
I50.43 Acute on chronic combined systolic and diastolic hrt fail
I50.4 Combined systolic and diastolic (congestive) hrt fail
I50 Heart failure

SNOMED

42343007 congestive heart failure (disorder)
10633002 acute congestive heart failure (disorder)
74960003 Acute left-sided congestive heart failure (disorder)
80479009 Acute right-sided congestive heart failure (disorder)
426263006 Congestive heart failure due to left ventricular systolic dysfunction
5375005 Chronic left-sided congestive heart failure (disorder)
66989003 Chronic right-sided congestive heart failure (disorder)
88805009 Chronic congestive heart failure
92506005 Biventricular congestive heart failure (disorder)