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I completed my medical school and background EM training from India (Christian Medical College, Vellore and Apollo Hospitals, Hyderabad) where I worked for 4 years. Following this, I devoted (with all my heart) about 1.5 years to do US Medical Licensing Exams. My stint towards an EM Residency in States did not work but it took me to places and it has been quite a journey. I then relocated to London, England to work as a Registrar (Non-Trainee) in A&E. This gave me an opportunity to better understand NHS, EM training pathways and more importantly the EM Mindsets in the United Kingdom. 

Currently, I am pursuing Higher Specialist Training in Emergency Medicine at South East Scotland Deanery where I have the honour and privilege of training under some of the most innovative brains in the field of Emergency Medicine. Over the past few years, I have realised that LEARNING and UNLEARNING (which can be challenging!) is equally important to deliver cutting edge care to our patients.And through this blog, I aspire to disseminate knowledge, assist trainees with exams and stay up to date with contemporary EM literature. I have always been an avid FOAMed supporter because FOAMed has always played an indispensable role during my training. 

Lakshay Chanana
ST4 EM Trainee 
Edinburgh, Scotland

Monday, August 1, 2016

Cardiogenic Pulmonary Edema: Hold on before pushing Diuretics!!


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  
  1. Excessive venous return (i.e increased preload) i.e. Tap is left open
  2. Excessive systemic vascular resistance (i.e. increased afterload) i.e. Hose is narrow
  3. 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


     1. Turning the faucet (tap) off: Decreasing Preload

Traditional treatment: Morphine, Furosemide and Nitroglycerin

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

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


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.

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.


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!

  • 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 
  1. 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.
  2. 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.
  3. Buseman W, Schupp D. Effect of sublingual nitroglycerin in emergency treatment of severe pulmonary edema. Am J Cardiol 1978;41:931-6.
  4. 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.
  5. Figueras J, Weil MH. Blood volume prior to and following treatment of acute cardiogenic pulmonary edema. Circulation 1978;57:349-55.
  6. Gammage M. Treatment of acute pulmonary oedema: diuresis or vasodilatation? Lancet 1998;351:382-3.
  7. Kraus PA, Lipman J, Becker PJ. Acute preload effects of furosemide. Chest 1990;98:124-8.
  8. Mattu A, Sharma S, Perkins AM, Zevitz ME: Pulmonary edema, cardiogenic. eMedicine Journal 2002;3(2)
  9. Mattu A. Pulmonary edema. Emergency Physicians Monthly 2002;9(9):1,4-8,12,16,22.
  10. Tei C, Horikiri Y, Park JC, et al. Acute hemodynamic improvement by thermal vasodilation in congestive heart failure. Circulation 1995;91:2582-90. 
  11. Barnett JC, Zink KM, Touchon RC. Sublingual captopril in the treatment of acute heart failure. Curr Ther Res 1991;49:274-81.
  12. Avoiding Common Errors in the Emergency Department: Mattu, Shanmugam, Swadron, Tibbleg, Woolridge
  13. Cardiovascular Emergencies : Amal Mattu
  14. Heart Failure, Clinical Pathways in Emergency Medicine: Prof. Suresh S David 


Nikhil N. Tambe - @nikhil16mar

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.