- Author: Amy Pound, MD, University Hospitals Case Medical Center, Case Western Reserve University, School of Medicine
- Editor: Rahul Patwari, MD, Rush University, Chicago Illinois
- Last Update: 2017
Upon finishing this module, the student will be able to:
- Discuss the classifications of heart failure
- Identify the signs of symptoms for acute exacerbation of congestive heart failure
- Identify key findings of congestive heart failure on chest xray
- Compare various ED treatment options for acute exacerbations of congestive heart failure
Congestive Heart Failure (CHF) is one of the most common illnesses treated in the Emergency Department. It affects about 2% of the US population or roughly 4.8 million Americans. For patients over the age of 65, it remains the most common inpatient diagnosis, comprising 20% of hospital admissions.
CHF arises when the ventricles fail to maintain blood circulation, often when the cardiac demand increases. Such precipitating events include cardiac ischemia or dysrhythmias, infection, PE, physical or emotional stress, noncompliance in medication or diet, volume overload. The heart has no reserve to compensate for the increased burden and blood circulation becomes congested. Typical chief complaints include shortness of breath and peripheral edema.
Classification & Terminology
NYHA CHF Classification
- Class I – Ordinary activity not limited by symptoms
- Class II – Ordinary activity leads to dyspnea, fatigue, etc
- Class III – Marked limitation of ordinary activity
- Class IV – Symptoms at rest or with any physical activity
Systolic vs Diastolic Dysfunction
Systolic dysfunction includes a dilated left ventricle with impaired contractility, typically caused by ischemia, infarction cardiomyopathy, myocarditis, or dysrhythmias. Contrasted with diastolic dysfunction in which the left ventricle remains intact and normal in size, but has an impaired ability to relax, such as with infiltrative cardiomyopathy. Diastolic dysfunction has a better prognosis that systolic dysfunction.
High vs Low Output
In low output failure, there is decreased cardiac output secondary to myocardial damage, such as with ischemia, dilated cardiomyopathy, valvular disease or chronic hypertension. In high output failure, the cardiac output is high or normal, but remains insufficient to supply oxygen demands. This can be found in hyperthyroidism, pregnancy, anemia, AV fistulas, beriberi or paget’s disease.
Right vs Left Failure
Right sided failure can lead to congestion of pressure and fluid into the right ventricle, resulting in hepatic enlargement, increased JVD and dependent edema. Left sided heart failure will cause congestion of pressure and fluid into the left ventricle, resulting in pulmonary congestion.
Potentially life-threatening illnesses included in the differential diagnosis are: COPD, PE, pneumothorax, anaphylaxis, asthma, pneumonia, foreign body obstruction, acute coronary syndrome.
Initial Actions and Primary Survey
- Cardiac monitor, pulse oximetry, IV access with 2 large bore IVs
- If the patient is hypoxic, give oxygen via 100% NRB facemask and consider more invasive methods of oxygenation including CPAP, BiPAP or intubation if needed.
- Elevate the head of the bed. You may need to have the patient dangle their legs over the side of the stretcher to reduce venous return and decrease preload.
- If patient is having chest pain, obtain an EKG and consider medicating with nitroglycerin.
- Order a portable CXR.
- Draw labs for CBC with differential, CMP, Troponin, PT/PTT, BNP. May want to include lactate and blood cultures x2 if patient is febrile.
The most classic presentation for CHF includes dyspnea, especially with exertion. Dyspnea on exertion has a sensitivity of 100% and specificity 17%. And the absence of exertional dyspnea decreases the likelihood of CHF. In addition, the patient may complain of orthopnea (sensitivity 88%, specificity 50%) or paroxysmal nocturnal dyspnea (sensitivity 39%, specific 80%). The presence of paroxysmal nocturnal dyspnea increases the likihood of CHF.
If the patient does have a cough productive of sputum, the sputum is most often described as pink and frothy.
Most patients presenting with CHF will also complain about swelling, often in their lower extremities.
In general, the patient may have hypertensive and diaphoretic upon initial presentation.
Increased JVD, greater than 4 cm, is highly specific for CHF (98%, with 17% sensitivity).
Auscultation of the lungs will most likely reveal rales secondary to alveolar edema (sensitivity 29%, specificity 77%). The absence of rales decreases the likelihood of CHF. Wheezing may also be present, caused by peribronchial edema.
The patient may be tachycardic, and may have an S3 gallop (sensitivity 24%, specificity 99%). Presence of an S3 increases the likelihood of CHF.
Finally, edema may be present, most often in the lower extremities (sensitivity 20%, specificity 86%) Edema is often characterized as pitting, and may extend through the legs and include the abdomen.
Most common findings are cardiomegaly and effusions. CXR findings may lag by 12 hours from onset of symptoms, and subsequently CXR findings may persist for several days despite clinical improvement. 1 out of 5 patients admitted for CHF showed lack of any pulmonary congestion on CXR.
Cardiomegaly – cardiothoracic ration greater than 50% diameter. Patients with diastolic failure may have normal heart size.
Peribronchial Cuffing – thickened bronchial walls secondary to edema. Indicated by arrow in above image.
Perihilar congestion – large hila with indistinct margins suggest pulmonary vasculature edema.
Cephalization – redistribution of blood flow to upper lobes. Only seen on upright films. Circled area in following image.
Pleural effusion – meniscus at the angle of the diaphragm. Arrow in above image.
Kerley B lines – Dilated lymphatic channels. Typically 2 cm in length and horizontal, peripherally located perpendicular to pleura. Black arrowheads in following image are kerley b lines, white arrows are septal lines
Reference: Chapman S, Nakielny R. Aids to Radiological Differential Diagnosis 4th edition. Saunders 2003
Credit: Dr Laughlin Dawes
Alveolar edema – batwing appearance
The Breathing Not Properly study found BNP to be 90% sensitive and 76% specific for the diagnosis of CHF. Release stimulated by high ventricular filling pressures. Has a diuretic effect and antihypertensive effect, by increasing the amount of sodium in the urine.
- <100 Unlikely CHF
- 100-500 Potentially CHF, although could also be PE,
- Pulmonary HTN, ESRD, cirrhosis, or hormone replacement therapy
- >500 Most likely CHF
May show underlying cardiac ischemia, dysrhythmias, LVH or heart block. A normal EKG has a high negative predictive value for systolic dysfunction.
Echocardiogram with Ejection Fraction
Normal ejection fraction is 55-75%. Patients with severe CHF may have EF less than 20%. Echocardiogram can also be used to visualize ventricular size and any wall abnormalities or valvular pathology, pericardial thickening, tamponade or constrictive pericarditis as additional contributors to CHF.
After initial actions (IV, O2, monitor, etc) have been completed, medication needs can be addressed:
- Normotensive patients: Give rapid acting nitrates to vasodilate, may be given sublingual, IV, or transdermal with nitropaste. IV Morphine can be given for chest pain and to increase vasodilation. IV diuretics, such as Lasix, can increase urine output.
- Hypertensive patients: Add Nitroprusside IV drip for severe, persistent hypertension.
- Hypotensive patients: Avoid nitrates and morphine, as they will drop the blood pressure even loser. Instead, increase myocardial contractility with dopamine, dobutamine, norepinephrine, amrinone or milrinone.
- Severe or Chronic low output CHF: Use ACE inhibitors to increase hemodynamic stability and exercise capability.
- Diastolic CHF: Calcium channel blockers may help, but do not use in patients with concurrent, depressed left ventricular function, as this may increase mortality and recurrence of CHF.
As patient’s CHF becomes more advanced, the patient may need an Automatic Internal Cardiac Defibrillator (AICD), Left Ventricular Assistance Device (LVAD) or heart transplant.
MADIT trial showed that in patients with previous MI, EF < 35%, non-sustained ventricular tachycardia, and inducible ventricular tachycardia unresponsive to procainamide, AICD placement reduced sudden death by 54% at 2 yrs.
MADIT II trial showed that patients with history of MI and EF <30% had a 29% reduction in mortality after AICD placement.
Patients may receive an LVAD as a temporizing measure until a heart transplant can be performed, or as a definitive treatment alone, if not a transplant candidate. The REMATCH study showed that patients had increased quality of life and had a 52% rate of survival at one year, compared to 25% for medical management only.
Heart transplant is the only long-term definitive treatment for congestive heart failure. Patients who receive a heart transplant have a 10-year survival rate of 50%.
Pearls and Pitfalls
- Acute CHF can rapidly progress over hours to days, commonly due to a precipitating event, leaving the patient with no reserve to compensate for increased burden on heart
- Precipitating event may be an MI! Check EKG and troponins
- CXR findings may lag by 12 hrs, treat clinical symptoms.
- Most common CXR findings are cardiomegaly and effusions
- Start with 100% O2 on NRB mask, but use noninvasive CPAP or BiPAP, or intubate when necessary
- Elevating the head of bed with patients legs dangling over side of stretcher will reduce venous return and decrease preload and improve patient symptoms
- AVOID nitrates, morphine diuretics in hypotensive patients!
A short list of important articles with the PubMed links / ID.
- PMID: 16234501, Wang CS, FitzGerald JM, Schulzer M, et al: Does this dyspneic patient in the emergency department have congestive heart failure?. JAMA 2005; 294:1944.
- PMID: 11794191, Rose EA, Gelijns AC, Moskowitz AJ, et al: Long-Term Use of a Left Ventricular Assist Device for End-Stage Heart Failure. N Engl J Med 2001; 345:1435-1443
- PMID: 12135939, McCullough PA, Nowak RM, McCord J, et al: B-type natriuretic peptide and clinical judgment in emergency diagnosis of heart failure: analysis from Breathing Not Properly (BNP) Multinational Study. Circulation. Jul 23 2002;106(4):416-22
- PMID: 16387212, Collins SP, Lindsell CJ, Storrow AB et al: Prevalence of negative chest radiography results in the emergency department patient with decompensated heart failure. Ann Emerg Med. Jan 2006;47(1):13-8
- PMID: 8960472, Moss AJ, Hall WJ, Cannom DS, et: Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators. N Engl J Med 1996; 335:1933.
- PMID: 11911755, Publication Committee for the VMAC Investigators : Intravenous nesiritide vs nitroglycerin for treatment of decompensated congestive heart failure: A randomized controlled trial. JAMA 2002; 287:1531
- PMID: 8376698, Ho KK, Pinsky JL, Kannel WB, Levy D. The epidemiology of heart failure: the Framingham Study. J Am Coll Cardiol. 1993 Oct. 22(4 Suppl A):6A-13A.
- American Heart Association. Classes of heart failure. Available at: http://www.heart.org/HEARTORG/Conditions/HeartFailure/AboutHeartFailure/Classes-of-Heart-Failure_UCM_306328_Article.jsp. Accessed: Mar 16, 2016.
- Tinley, Peter. CDEM Curriculum CHF Module (2008). https://cdemcurriculum.com/cardiovascular/congestive-heart-failure/. Accessed: May 30, 2017.