Author:
NaomiGeorge
Robert A.Partridge
Description
- CHF, now referred to simply as “heart failure” (HF), is a heterogeneous clinical syndrome resulting from either impaired filling or ejection of blood from the ventricle
- HF often results in progressive debility, episodes of acute decompensation
- High (>50%) 5-yr mortality
- Affects ∼5.1 million Americans
- Estimated 2013 cost of CHF is >$30 billion
- Leading Medicare diagnosis for hospitalized patients ≥65 yr old
- Acute decompensated heart failure (ADHF): Acute onset of new or worsening symptoms of HF (hr-days)
- Common reason for presentation to the ED:
- 70% are recurrent exacerbations of chronic HF
- 15% are new diagnosis of HF
- 5% end-stage/terminal event
- ADHF may result from worsening cardiac pump function, or from changes in preload or afterload:
- Precipitating events include rapid increase in sympathetic tone, concomitant illness, arrhythmia, myocardial ischemia, progressive valve disease, intravascular volume increase
- 4 common phenotypical presentations based on adequacy of perfusion (warm versus cold) and presence of congestion (wet vs. dry)
- Chronic HF is a progressive failure state (mo-yr) characterized by structural and functional changes, with two main subclasses:
- Heart failure with reduced ejection fraction (HFrEF):
- Impaired contractility or pump function causing decreased ejection fraction (EF <40%)
- Estimated prevalence 50%
- Many have concomittent diastolic dysfunction
- Heart failure with preserved ejection fraction (HFpEF) EF >50%
- Impaired ventricular relaxation and compliance resulting in decreased cardiac filling
- More common in older patients, women, patients with HTN
- ACCF/AHA stages: Progressive stages denote nonreversible cardiac dysfunction. A-D, where A = risk but no disease, and D = refractory HF
- NYHA classification: Functional classes I-IV, where I has no limit on physical ability and IV has symptoms of HF at rest. Patients may improve class with therapy
Etiology
Underlying causes and acute precipitants:
- HF may result from disorders of the heart valves, endocardium, myocardium, pericardium, and metabolic derangements
- Decreased myocardial contractility:
- Ischemic cardiomyopathy
- Nonischemic cardiomyopathies:
- Familial, obesity, diabetic
- Endocrine: Hypothyroid, acromegaly,
- Pregnancy-related dilated CMP
- Toxin-related (alcohol, cocaine, chemotherapy)
- Inflammatory: Infectious and noninfectious myocarditis (viral, Chagas, SLE, HIV)
- Tachycardia-induced
- Amyloidosis
- Cardiac sarcoidosis
- Increased pressure states:
- HTN
- Valvular abnormalities
- Congenital heart disease
- RH failure due to pulmonary hypertension: Primary PAH, OSA, COPD, CTEPH, IPF, and others
- Pulmonary embolism
- Volume overload:
- Dietary indiscretion (sodium overload)
- Drugs leading to sodium retention (glucocorticoids, NSAIDs)
- Overload due to transfusion or IV fluid
- High demand states:
- Hyperthyroidism, thyrotoxicosis
- Pregnancy
- A-V fistula
- Beriberi (thiamine deficiency)
- Paget disease
- Severe anemia
- Aortic insufficiency
- Pediatric etiologies: Volume/pressure overload lesions vs. acquired HD:
- First 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
Signs and Symptoms
- Poor perfusion:
- Fatigue, somnolence, lightheadedness
- Palpitations, or irregular pulse
- Shortness of breath
- Cool extremities
- Worsening renal function
- Worsening liver function, gut ischemia (ominous)
- Congestion:
- Dyspnea
- Cough
- Orthopnea
- Paroxysmal nocturnal dyspnea
- Decreased exercise tolerance
- Elevated JVD or abdominojugular reflex
- Dependent edema (poor sensitivity and specificity)
- 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
- Ascites
- ADHF with hemodynamic instability:
- Confusion, anxiety, syncope
- Tachypnea
- Tachycardia
- Hypotension
- Cool, pale, or cyanotic extremities
- Narrow pulse pressure or pulsus alternans
- Cheyne-Stokes respirations
Essential Workup
Diagnosis is often challenging and dependent on test findings as well as clinical gestalt
Diagnostic Tests & Interpretation
There is no single diagnostic test. HF is a clinical diagnosis
Lab
- Electrolytes:
- Establish baseline renal function when initiating diuretics, or ACE inhibitors
- Hyperkalemia possible with low output
- Hyponatremia associated with poor prognosis
- CBC:
- Anemia can cause or exacerbate failure
- Infection can cause or exacerbate failure
- Liver function tests:
- Thyroid function tests:
- Specifically in patients >65 or in new a-fib
- Cardiac enzymes:
- Evaluate for ischemia or infarction
- Mild elevation of troponin common
- Viral panel: Suspected myocarditis
- BNP:
- Useful to support clinical judgement to diagnose HF, particularly if cause of dyspnea is unknown:
- BNP >500 pg/mL, HF likely (ppv 90%)
- BNP <100 pg/mL, HF unlikely, (npv 90%)
- BNP 100-500 pg/mL, indeterminate
- BNP is elevated with age, afib, cardioversion, anemia, renal failure, sleep apnea, sepsis, severe burns, drug therapy, and others and should not be used in isolation
- BNP 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 HF
- NT-proBNP <300 pg/mL unlikely to be HF
- Must use NT-proBNP if patient is on an ARNI
Imaging
- CXR:
- Poor accuracy for ADHF
- Cardiomegaly cannot be assessed on supine film
- Specific signs of CHF:
- Cephalization (vascular prominence in the upper lungs due to fluid overload)
- Interstitial edema/Kerley B lines
- Alveolar edema
- Effusions
- 12-hr lag from onset of symptoms may occur
- Radiographic findings may persist for several days despite clinical improvement
- Bilateral confluent perihilar infiltrates leading to classic butterfly pattern:
- ECG:
- Normal ECG has high negative predictive value
- Underlying cardiac ischemia
- Presence of dysrhythmias
- Left-ventricular hypertrophy
- Heart block
- Bedside US: Cardiac, pulmonary, and IVC:
- Cardiac basic:
- Visual estimates of EF
- RV strain
- Pericardial tamponade
- Cardiac advanced:
- Measurement of EF
- Diastology
- Acute valvular pathology
- Ventricle dilation or hypertrophy
- Regional wall motion abnormalities
- IVC:
- >2 cm with minimal respirophasic changes
- Pulmonary:
- B lines in >2 rib spaces bilaterally
- Identify large effusions
Differential Diagnosis
- HFpEF, HFrEF, mixed HF
- Arrhythmia
- Acute coronary syndrome
- Anemia
- Malnutrition
- Pericardial tamponade
- Pneumothorax
- Thoracic aortic dissection
- Constrictive pericarditis
- Congenital heart disease (pediatric)
- Septic cardiomyopathy
- Mitochondrial:
- BB and CCB overdose
- Cyanide, CO poisoning
- Right-sided HF:
- Renal failure
- Cirrhosis
- Left-sided HF
- Venous stasis
- Primary pulmonary disease:
- Pulmonary embolism
- COPD exacerbation
- Asthma exacerbation
- IPF exacerbation
- Acute respiratory distress syndrome
- Pneumonia
Prehospital
- IV access
- Supplemental oxygen
- Cardiac monitor and pulse oximetry
- ECG
- Sublingual nitrates if no hypotension
- Noninvasive ventilation (NIV)
- Endotracheal intubation may be required
Initial Stabilization/Therapy
- IV access
- Supplemental oxygen
- Cardiac monitor and pulse oximetry
- ECG: Assess for acute MI, arrhythmia:
- Initiate cardiac cath lab for possible reperfusion
- Elevate head of bed to reduce venous return
- Control airway:
- NIV: CPAP vs. BiPAP
- Reduce work of breathing, improve oxygenation, decrease need for intubation, mortality benefit
- Intubation for impending respiratory failure
- Treat underlying illness(es)
ED Treatment/Procedures
- Congestion with adequate perfusion: Reduce preload, control afterload, consider fluid restriction and diuresis:
- Reduce preload in acute pulmonary edema:
- Sublingual or IV nitroglycerin
- Nitro paste (less reliable, IV preferred)
- Sodium nitroprusside: Powerful veno and arterial dilator, requires arterial line
- IV diuretics (less rapid/effective in patients with poor renal perfusion):
- Consider starting at 2x home dose
- Avoid aggressive preload reduction in ADHF when suspected etiology is aortic stenosis, HOCM, or pulmonary hypertension
- HOCM: Consider BB use to lower HR
- Poor perfusion with hypotension:
- No first-line pressor for cardiogenic shock
- Norepinephrine:
- Dopamine often recommended, however SOAP II investigators found trend toward increased adverse events with dopamine
- Dopamine
- Dobutamine:
- Inotropic agent, may cause vasodilation
- Milrinone:
- Inotropic agent, may cause vasodilation
- Associated with arrhythmia
- Avoid vasodilators (nitrates, morphine)
- Cautious initiation of diuretics after inotropes in select cases
- Mechanical cardiac support (MCS) devices are indicated in select cases; obtain early involvement/transfer to cardiac intensivist or HF specialist
- Nondurable MCS devices (ECMO, LVAD, impella, balloon pump) may offer a bridge in certain cases and when recovery or transplant is likely
- Caution:
- ACEi, ARBs, ARNIs, BB, and aldosterone antagonists may be indicated once stabilized; however often safest to avoid in the ED given risk of hypotension, acute renal failure, and hyperkalemia
- Calcium channel blockers suppress contractility and have no role in HF management
Pediatric Considerations |
- Neonates (first weeks of life):
- Suspect ductal-dependent cardiac lesions if clinical CHF and no improvement with O2:
- PGE1 to maintain patent ductus
- Children:
- IV furosemide, dopamine, or milrinone
- IV nitroglycerin for pulmonary edema
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Medication
- Aspirin: 325 mg PO/PR if AMI is suspected
- Bumetanide (Bumex): 1-3 mg IV, max 10 mg/d
- Dobutamine: 2-10 mcg/kg/min IV, max of 40 mcg/kg/min
- Dopamine: 2-20 mcg/kg/min IV, max of 50 mcg/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 mcg/kg IV load; 0.375-0.75 mcg/kg/min IV
- Nesiritide: 2 mcg/kg bolus, then infusion of 0.01 mcg/kg/min
- Nitroglycerin: 0.4 mg sublingual; 1-2 in of nitro paste; 5-20 mcg/min IV, max of 100-200 mcg/min IV. USE NON-PVC tubing
- Nitroprusside: 0.3-10 mcg/kg/min IV (starting dose), max of 10 mcg/kg/min
Pregnancy Prophylaxis |
ACEi and ARBs are associated with multiple fetal abnormalities and should be held:- Oxygen
- Nitroglycerin
- Furosemide
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Disposition
Admission Criteria
- ICU:
- Pulmonary edema requiring NIV or ETT
- Cardiogenic shock
- Concomitant MI or ischemia
- Medical wards:
- New-onset CHF
- Symptoms not relieved by ED therapy
Discharge Criteria
- Mild exacerbation of chronic CHF:
- Responds to ED treatment
- No other cardiac and pulmonary findings
- Close follow-up should be arranged with continuation of diuretic, vasodilator, or ACE inhibitor therapy and patient lifestyle education
Issues for Referral
Consider ICD and /or BV pacer in advanced HF:
- 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