Case
A 65 year old female came to ER
with sudden onset breathlessness.
HR: 110/min
BP 180/90
RR 30/min
SpO2 90% on room air.
Examination was characterised by bilateral coarse crepitations. She was known
case of ischemic heart disease and hypertension, not compliant with her
medications.
The first differential that was unanimously thought was acute
heart failure resulting in pulmonary edema. ECG showed sinus tachycardia, Chest
X-ray confirmed diffuse pulmonary edema.
These cases form the bread and butter
of Emergency Physician. Treating them wisely and quickly with appropriate drugs
gives immediate relief. Many different drugs have been given as an early
intervention - ranging from morphine, furosemide and nitroglycerin. But what
actually works?
Imagine the lung being the bucket with
the tap as pre-load and hose (a flexible tube) as after-load. Increase in pre-load causes more
water flowing in through faucet, thus filling the bucket. Similarly, an increase in
afterload by reduced water out through the hose will lead to increased fluid in
the bucket i.e. pulmonary edema. The third possibility being left ventricular dysfunction
i.e. defects in the pump.
Causes of cardiogenic pulmonary edema
- Excessive
venous return (i.e increased preload) i.e. Tap is left open
- Excessive
systemic vascular resistance (i.e. increased afterload) i.e. Hose is narrow
- LV
dysfunction: a disorder of contractility or a disorder of rate and rhythm i.e. Pump
failure
Pathophysiology for cardiogenic pulmonary edema- a self-perpetuating cycle
GOALS OF TREATMENT
1. Turning
the faucet (tap) off: Decreasing Preload
Traditional treatment: Morphine,
Furosemide and Nitroglycerin
Morphine:
Action: Histamine release cause
decrease in preload; anxiolysis may decrease catecholamine reducing afterload
(As per studies by Vismara et al Circulation,1976)
Side-effects: Increase catecholamines:
rash/urticarial; respiratory depression in high doses; direct myocardial
depression
Mythbuster:
Timmis et al (BMJ 1980), gave 0.2mg/kg
morphine to acute myocardial infarction patients with severe left ventricular
failure found that 15min and 45 mins later, the heart rate, BP and cardiac index reduced and there was no decrease
in preload.
Hoffman et al (Chest 1987), morphine
given in prehospital pulmonary edema patients had both subjective and objective
deterioration.
From Acute decompensated heart failure
national registry (ADHERE), Peacock WF et al (Emerg Med J 2008); compared
morphine versus no morphine in acute decompensated heart failure. They observed
that morphine administration increased the need for mechanical ventilation, ICU
admission and prolonged hospital stay. Morphine was an independent predictor of
mortality (OR: 4.84)
VERDICT: Morphine has NO ROLE in modern
management of cardiogenic pulmonary edema
Furosemide
Action: Diuresis and venodilation
Increased afterload decreases renal
blood flow, hence the action of furosemide is delayed by 30-120minutes in
cardiogenic edema patients. The most common myth is doubling the dose of
furosemide if the patient does not diurese, as a result after couple of hours
the patient ends up becoming hypotensive. Diuretics work only when kidneys are
perfused by reducing afterload.
Mythbuster:
Kiely et al (Circulation 1973), 15 post
MI CHF patients, showed no drop in preload reduction due to veno-dilation, the
drop occurred post diuresis.
Ikram et al (Clin Sci, 1980) showed a
drop in cardiac output in 17% in first 90 minutes after furosemide
administration. The cardiac output returned to baseline only after diuretic
effect started.
Nelson et al (European Heart Journal 1983)
showed a similar finding. The found a drop in cardiac output and stroke volume
in first 30-60 minutes which returned to baseline after 60-90minutes.
Kraus et al Chest 1990, treated
patients with furosemide, furosemide with nitrates and nitrates plus captopril
before giving furosemide. If pre-medicated with nitrates and captopril,
furosemide had an immediate and sustained effect on pulmonary capillary wedge
pressure.
VERDICT: Diuretic effect is delayed if
administered alone and can be detrimental in first 30-60 minutes. Furosemide
activates the renin angiotensin aldosterone system and increases the afterload,
causing more harm than good in pulmonary edema patients. So, when the patients
undergo preload and afterload reduction, furosemide works immediately as the
kidneys are perfused.
Nitroglycerin
Action: Immediate drop in preload and
afterload
Advantages: Moderate to high doses
bring significant reduction in systemic vascular resistance. It has a short
half-life, can be titrated easily. Multiple modes of administration-
sublingual, oral, intravenous and topical.
Side-effect: Head ache
Take caution if the patient is
hypotensive, acute mitral regurgitation, aortic stenosis, pulmonary
hypertension and patients on sildenafil
Being Aggressive! Starting at
50-60 microgram/min (NOT at 2.5-5mcg/min) and escalating 10-20mcg/min (upto 400mcg/min). Another way of optimising hemodynamics is thru a NTG bolus of 0.5 - 2mg. Multiple studies like Cotter et al 1998, Beltrame et al
1998, Kruas et al 1990, Hoffman et al 1987, Nelson et al 1983 have proved the
importance of high dose nitroglycerin over smaller dosages.
The oral dose of NTG is 0.4mg or 400mcg is approximately equal to 80mcg/min infusion. Therefore, starting an infusion at 5mcg/min after administering 0.4mg sublingual dose leads to a dramatic dose reduction.
VERDICT: Nitroglycerin should be the
FIRST line drug for treatment of moderate CHF and pulmonary edema.
2. Using
a bigger/ wider hose: Decreasing afterload
Nitroglycerin, nitroprusside,
hydralazine and ACE-I
Nitroprusside can be used in acute
mitral regurgitation and severe hypertension. But it has shown to have high
fluctuations in BP and is not easily titrable. Similarly hydralazine is
difficult to titrate.
ACE-I like captopril 25mg dipped in
water placed sublingually for BP>110, has shown to be an excellent pre-load
reducer in 10 minutes (Barnett et al, Curr Ther Research 1991), without any
effect on heart rate and mean arterial pressure.
Langes et al (Current Ther Research
1993), showed that giving captopril infusion in moderate CHF with pulmonary
edema decreases preload and afterload in 6 minutes, improves cardiac output
without any adverse effects.
Varriale et al (Clin Cardiology 1993),
showed that intra venous enalaprilat in severe CHF and mitral regurgitation,
increased cardiac output and stroke volume, decreased preload and afterload,
also decreased the magnitude of mitral regurgitation.
Saccheti et al (Am J Em Med 1999),
showed that sublingual captopril significantly dropped the need for intubation
or ICU admission in severe CHF patients (0.28:1).
Non-compliant dialysis patients who
developed pulmonary edema showed improved outcome with sublingual captopril. (Saccheti
et al Am J Em Med 1993).
VERDICT: Sublingual or intravenous
ACE-I showed hemodynamic and subjective improvement in 6-12 minutes.
Combination with IV nitroglycerin exceeds benefit with either drug alone. It
can be used as an acceptable alternative to IV nitroglycerin.
Non Invasive Ventilation
Action: decreases preload and
afterload, maintains positive airway pressure during respiration by keeping the
stiff alveoli open and promoting gas exchange.
VERDICT: NIV decreases work of
breathing, improves O2/ CO2 exchange, reduces length of stay, reduces hospital
costs, reduces need for intubation, and may decrease mortality. Early NIV usage
is a must!
3. Improving
pump function: using ionotropic support
Patients with STEMI, where pump
function is affected, there arises a need for ionotropic support.
Catecholamines: dobutamine, dopamine,
phosphodiesterase inhibitors : milrinone, IABP (bridging device before
PTCA/CABG)
No good literature to establish
superiority of one over another.
VERDICT: Use what you are comfortable
with. Use milrinone in cardiogenic pulmonary edema patients unresponsive to
dobutamine/ dopamine.
More than 50% of patients in
cardiogenic pulmonary edema are euvolemic. Fluid is excess in the wrong bucket.
Hence treatment should be focussed towards ‘fluid redistribution’ and not
‘fluid removal’.
Suggested algorithm for managing heart failure based on BP on ED arrival as
normotensive failure, hypotensive failure and hypertensive failure.
Sauna for CHF patients!
Tie et al (Circulation, 1995) studied
thermal vasodilation using sauna in 34 CHF patients and found that 15 minutes
of sauna reduced preload, afterload, mitral regurgitation and significant
improvement in cardiac index, stroke volume and ejection fraction!
SUMMARY
- Treatment of pulmonary edema should be focused on ‘fluid redistribution’ and not ‘fluid removal’.
- First line: Nitroglycerin and NIV (start ASAP)
- Second line: ACE-I (in addition or
instead of NTG)
- Third line: Diuretic like furosemide
- Morphine has NO ROLE in modern management of cardiogenic pulmonary edema
Listen to Dr. Mattu's talk on Pulmonary Edema
Further Reading
- Beltrame JF, Zeitz CJ, Unger SA, et al. Nitrate therapy is an alternative to furosemide/morphine
therapy in the management of acute cardiogenic pulmonary edema. J Card Fail (1998) 4:271-9.
- Biddle TL, Yu PN. Effect of furosemide on haemodynamic and lung water in acute pulmonary
edema secondary to myocardial infarction. Am J Cardiol 1979;43:86-90.
- Buseman W, Schupp D. Effect of sublingual nitroglycerin in emergency treatment of severe
pulmonary edema. Am J Cardiol 1978;41:931-6.
- Cotter G, Metzkor E, Kaluski E, et al. Randomized trial of high-dose isosorbide dinitrate plus
low-dose furosemide versus high-dose furosemide plus low-dose isosorbide dinitrate in severe
pulmonary oedema. Lancet 1998;351:389-93.
- Figueras J, Weil MH. Blood volume prior to and following treatment of acute cardiogenic
pulmonary edema. Circulation 1978;57:349-55.
- Gammage M. Treatment of acute pulmonary oedema: diuresis or vasodilatation? Lancet
1998;351:382-3.
- Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990;98:124-8.
- Mattu A, Sharma S, Perkins AM, Zevitz ME: Pulmonary edema, cardiogenic. eMedicine Journal
2002;3(2)
- Mattu A. Pulmonary edema. Emergency Physicians Monthly 2002;9(9):1,4-8,12,16,22.
- Tei C, Horikiri Y, Park JC, et al. Acute hemodynamic improvement by thermal vasodilation in
congestive heart failure. Circulation 1995;91:2582-90.
- Barnett JC, Zink KM, Touchon RC. Sublingual captopril in the treatment of acute heart failure. Curr Ther Res 1991;49:274-81.
- Avoiding Common Errors in the Emergency Department: Mattu, Shanmugam, Swadron, Tibbleg, Woolridge
- Cardiovascular Emergencies : Amal Mattu
- Heart Failure, Clinical Pathways in Emergency Medicine: Prof. Suresh S David
Author:
Nikhil N. Tambe - @nikhil16mar
M.B.B.S., ECFMG (USA)
Emergency Medicine Resident (PGY-2)
Masters in Emergency Medicine (GWU)
Kokilaben Dhirubhai Ambani Hospital, Mumbai
Instructor (American Heart Association)
Lifesupporters Institute of Health Sciences, Mumbai
I am an Emergency Medicine enthusiast, a lifelong learner, a proponent of Evidence Based Medicine, love ECGs, resuscitation and emergency cardiology. After my graduation I worked as a Research Assistant in the USA. I have always been actively involved in teaching basic and advanced lifesaving skills to medics, paramedics and lay public since 2012. Currently I am pursuing EM Residency at Kokilaben Dhirubhai Ambani Hospital under George Washington University - Masters in Emergency Medicine Program. My vision is to create awareness about EBM and develop EM as a stand alone speciality in India.
