Clinical Nugget: Acute (on Chronic) Heart Failure in the Emergency Department.
Harry Elizaga, EDSS
A 65 y/o man presents with shortness of breath. He has bilateral lung wheezes and bibasal crackles. He is known to have COPD and has been using his puffers more often for the past few days. He denies having fever or increased sputum production. He has PND and orthopnea with no peripheral oedema.
His medical history revealed admissions in hospital with both COPD exacerbations and Congestive heart failure.
Both respiratory and cardiology teams are refusing to take the patient. Does this sound familiar?
Shortness of breath diagnosis in ED can be complex and the primary diagnosis can co-exist with another illness. Acute heart failure may be the cause of the ED presentation or just the tip of the iceberg for an underlying issue waiting to be addressed or missed!
We need to think of the causes to address the problem appropriately. Here is a simple visual which runs through the causes in broad terms: 1. Preload(salt intake, missed diuretics, unrestricted intake) 2. After load (hypertension) 3. Arrhythmia (AF) 4. Muscle (AMI, myocarditis) and 5. Valvular (AS, Valve rupture)
Traditionally, heart failure has been dichotomised
into systolic vs diastolic, low output vs high output, right vs left etc.
A pragmatic way of viewing this is related to the patient’s haemodynamic state: A normotensive patient, A hypertensive or A hypotensive patient with heart failure. This classification along with identifiable causes is what we care for in the emergency department as it allows us to tailor initial treatment accordingly.
No single historical, examination or laboratory parameter can suggest the diagnosis. It is best interpreted as a whole. However, there are some features that are more predictive than others. I’ve included only the ones that are pertinent in terms of likelihood ratios as follows:
**(LR > 10 great predictor! LR> 5 good) _____________________+ve likelihood ratio_______________
Heart failure 5.8
Myocardial infarction 3.1
Examination s3 gallop 11 !
Hepato-Jugular Reflux 6.4
Elevated JVP 5.1
Pulmonary Venous congestion 12 !
Interstitial oedema 12 !
Alveolar oedema 6
Pleural effusion 3.2
Atrial Fibrillation 3.8
New T wave changes 3.0
“Fortunately, our medical student was able to elicit a previous background of heart failure and AMI. On examination, he heard an S3 Gallop! JVP was < 3 cm so, he pressed on the patient’s RUQ which showed +ve hepato-jugular reflux. CXR showed signs consistent with heart failure and ECG showed atrial fibrillation with T wave changes.”
The cardiology registrar reviewed the patient and discovered the patient is being worked up for pulmonary fibrosis. Now what?
Luckily, the ED registrar thought of doing a lung ultrasound.”
Bedside thoracic US for B-lines can be a useful test for diagnosing CHF. Predictive accuracy is greatly improved when studies are totally positive or totally negative. A two-zone protocol performs similarly to an eight-zone protocol
When you see > 3 B-lines (like rays of the sun in a dark field) using the curvilinear probe. You’re golden! It’s worthwhile looking at the heart while you’re there.
“The cardiology registrar read about B lines in heart failure and accepted the patient’s care. But, then he also read that BNP can exclude a heart failure diagnosis and advised not to transfer the patient unless a BNP has been done.”
B-Type Natriuretic Peptide (BNP)
BNP is released when myocardial cells are stretched. This is true for heart failure. A BNP value <100 pg/mL essentially rules out heart failure as the cause of dyspnea, whereas values >400 pg/mL indicate a 95% likelihood of heart failure.
However, values between 100 and 400 pg/mL warrant further investigation. Unfortunately, the patients in the middle are the exact patients we want answers for. Before getting a result of >400 pg/mL, our patients are more likely already on NIV.
specialist knew that BNP wasn’t available in our local hospital and made the cardiology registrar aware of this fact. Besides, the constellation of symptoms suggests the diagnosis, why bother with a test that won’t change your impression or immediate management?”
Management questions (as Per ACEP policy 2007 for adult CCF patients -acep.org)
1. Is there a role for noninvasive positive-pressure ventilatory support in the ED management of patients with acute heart failure syndromes and respiratory distress?
Patients with acute heart failure syndrome who are dyspneic, but not necessarily in need of emergent intubation, may be candidates for noninvasive ventilatory assistance with either CPAP or BiPAP. CPAP provides a constant end-expiratory pressure, and BiPAP provides the same constant end-expiratory pressure, as well as added positive pressure at the onset of inspiration to assist ventilation.
CPAP and BiPAP have both been shown to improve differing respiratory, cardiac, and hemodynamic indices as well as specific outcomes among patients presenting with acute heart failure syndromes
Level B recommendation: Use 5-10 mm Hg CPAP by nasal or face mask as therapy for dyspneic patients with acute heart failure syndrome without hypotension or the need for emergent intubation to improve heart rate, respiratory rate, blood pressure, and reduce the need for intubation, and possibly reduce in-hospital mortality.
Level C recommendation: Consider using BiPAP as an alternative to CPAP for dyspneic patients with acute heart failure syndrome; however, data about the possible association between BiPAP and myocardial infarction remain unclear.
Should vasodilator therapy (e.g., nitrates, nesiritide
, and ACE inhibitors) be prescribed in the ED management of patients with acute heart failure syndromes? Multiple studies suggest that nitroglycerin is effective in treating acute heart failure by its effective venodilation
and preload reduction at low doses, and additional arteriodilation
and afterload reduction at higher doses.
Nesiritide is a recombinant form of B-type (brain) natriuretic peptide that dilates veins, peripheral arteries, and coronary arteries with resulting reductions in preload and afterload similar to nitrates. However, nesiritide
has failed to show superiority to nitrates in several studies of patients with acute heart failure syndromes. In addition, multiple meta-analyses have raised uncertainty regarding the safety of nesiritide
and its possible association with worsening renal function and higher mortality.
Angiotensin-converting enzyme (ACE) inhibitors reduce both preload and afterload, improve renal hemodynamics, impair sodium retention, maintain or enhance left ventricular function, and attenuate sympathetic stimulation. However, no adequately powered, controlled, randomized clinical trials exist that evaluate the efficacy of ACE inhibitors in acute heart failure syndromes. In addition, several studies have reported first-dose hypotension in acute heart failure syndrome patients receiving oral ACE inhibitors.
Level B recommendation: Administer intravenous nitrate therapy to patients with acute heart failure syndromes and associated dyspnea.
Level C: Angiotensin-converting enzyme (ACE) inhibitors may be used in the initial management of acute heart failure syndromes, although patients must be monitored for first-dose hypotension.
Should diuretic therapy be prescribed in the ED management of patients with acute heart failure syndromes? Although physicians have been reassured over the years by their bedside observations that loop diuretics (e.g., furosemide, bumetanide, and torsemide) appear to be effective in the treatment of patients with heart failure by increasing urine output and decreasing edema
, currently there are no randomized clinical trials evaluating the clinical benefit of furosemide alone in patients with acute heart failure syndromes.
Studies have shown that aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation, as compared with aggressive nitrate monotherapy, and may also lead to worsening renal function. However, studies have shown there may be a role for diuretics in conjunction with nitrates, with a regimen of high-dose nitrates and low-dose diuretics providing more consistent clinical improvement than a regimen of high-dose diuretic and low-dose nitrates
Level B recommendation: Treat patients with moderate-to-severe pulmonary edema
resulting from acute heart failure with furosemide in combination with nitrate therapy.
Level C recommendations: 1) Aggressive diuretic monotherapy is unlikely to prevent the need for endotracheal intubation, compared with aggressive nitrate monotherapy. 2) Diuretics should be administered judiciously, given the potential association between diuretics, worsening renal function, and the known association between worsening renal function at index hospitalization and long-term mortality.
– Before commencing nitrates and overly diuresing the patient, ensure that they do not have severe aortic stenosis or a right ventricular MI as they are preload dependent.
Recommendation for high dose nitrates (>500mcg/min) as first line is prevalent. If the patient is critically ill and severely hypertensive, its a good thought. Remember, GTN 300-600 mcg SL is equivalent to a drip rate of 40-80mcg/min (Usual chest pain drip is at 10-20 mcg/min initially). Its a good marker that the patient will tolerate the same equivalent IV dose and titrate upwards 10-20 mcg every 10 minutes. There are other reasons why the patient is hypertensive during the initial few minutes in the resuscitation room. Apply NIV, give SL GTN, alleviate pain and determine appropriate initial dose once a blood pressure trend is established. – A patient with SOB with clear lungs- think of PE, high output states (thyrotoxicosis, anaemia), metabolic(acidosis/sepsis) and toxicologic causes
– Patients with End-stage renal disease- think of dialysis. If they are not anuric, they may respond to diuretic therapy in large doses >/=160mg IV
-Wang CS et al., JAMA, 2005
-Liteplo AS et al. Acad Emerg Med. 2009 Mar;16(3):201-10. doi: 10.1111/j.1553-2712.2008.00347.x. Epub 2009 Jan 29. ETUDES,
-Maisel A. B-type natriuretic peptide measurements in diagnosing congestive heart failure in the dyspneic emergency department patient. Rev Cardiovasc Med. 2002;3(suppl 4):S10-S17.