the ICU, he receives large doses of furosemide(80 mg every six hours), IV nitroglycerin and IVVasotec (for afterload reduction). He eventuallystabilizes, is extubated and later discharged.

Case reviewPulmonary edema is an accumulation of fluidwithin the pulmonary tissues. Although mostcommonly caused by CHF, it can also resultfrom narcotic overdose, renal disease, severe liverdisease, exposure to high altitudes and toxic gasinhalation.

Pulmonary edema most frequently occurswhen the left ventricle begins to fail as an effec-tive forward pump. Causes of left ventricular fail-ure include acute myocardial ischemia orinfarction, dysrhythmias and exacerbation ofchronic CHF. Vascular pressures in the pul-monary tissues begin to increase as blood to theleft side of the heart is supplied from the pul-monary circulation. This results in an increase inpulmonary hydrostatic pressure.

When the hydrostatic pressure exceeds thepressure that normally holds fluid within the vas-cular system (oncotic pressure), fluid moves intothe spaces between the cells of the pulmonarysystem (interstitial space).

Initially, the lymphatic system removes thefluid between the cells. But the capacity of thelymphatic system is limited and, eventually, thefluid is forced into the alveoli, where gas exchangetakes place. The presence of fluid in the interstitialspace and alveoli significantly affects respiratorygas exchange, leading to hypoxia and dyspnea.

The term flash pulmonary edema describespulmonary edema that develops rapidly—oftenover a few minutes. Flash pulmonary edemaalmost always occurs in patients with a history ofCHF and pulmonary edema.

These patients normally remain stable on suchmedications as diuretics, digitalis, nitrates andantihypertensives. However, on occasion, theycan rapidly decompensate and develop acute pul-monary edema in a matter of minutes. Causes ofthis decompensation can include myocardialischemia, cardiac dysrhythmias, a change in med-ications or diet (e.g., eating foods high in sodi-um) or worsening renal insufficiency. Often, theexact cause remains unknown.

Most patients with flash pulmonary edemarespond to aggressive diuresis and vasodilatortherapy. Emergency treatment of pulmonaryedema is directed at correcting the underlyingcause, removing excess fluid and providing sup-plemental oxygenation. However, the first thera-py should always be administration of 100%

oxygen via the appropriate device. Facial continuous positive air-

way pressure (CPAP) devices canhelp increase oxygen tension andairway pressures, which candecrease the amount of fluid thatenters the alveoli. If this fails,emergent intubation and mechan-ical ventilation are indicated.

If the cause is myocardialischemia or infarction, therapy,such as thrombolytics, should beprovided. If the patient is sufferingan exacerbation of chronic CHF,efforts should be made to elimi-nate excess fluid through the useof potent diuretics, such asfurosemide (Lasix).

If the patient’s blood pressure is normal or ele-vated, vasodilators, such as nitroglycerin, can beused. They decrease cardiac preload and, thus,cardiac work. In severe cases, nitroglycerinshould be administered intravenously, if allowedby local protocols. Alternatively, and in patientswho are in less severe distress, nitroglycerin pastecan be applied to the patient’s chest.

Morphine can also be used in the treatment ofacute pulmonary edema. Morphine sulfate acts asa venous vasodilator and can decrease theamount of blood being delivered to the heart(preload), which can decrease pulmonary pres-sures. In addition, some patients may benefitfrom the use of agents that increase the force ofthe cardiac contraction, thus increasing theheart’s cardiac output. Such agents includedobutamine (Dobutrex), dopamine (Intropin)and amrinone (Inocor).

ConclusionPatients with advanced heart disease and CHFoften develop flash pulmonary edema. EMS per-sonnel must always keep this in mind and be alertfor early indicators of respiratory distress, such asincreased respiratory rate, heart rate, cyanosis anda fall in oxygen saturation. Often, intubation andmechanical ventilation can be avoided by earlyrecognition and prompt prehospital therapy. JEMS

Bryan Bledsoe, DO, FACEP, EMT-P, is an emergencyphysician, paramedic and EMS author fromMidlothian, Texas. He is the author of numerousEMS textbooks, including Paramedic Care: Principlesand Practices and Essentials of Paramedic Care.Contact him via e-mail at bbledsoe@earthlink.net.

Paul Bojan, EMT-P, is a firefighter/paramedicwith the Summit (Ill.) Fire Department.

WWW.JEMS.COM | JANUARY 2004 | JEMS 5554 JEMS | JANUARY 2004

Early recognition & prompt prehospital therapy improve patient outcomes

By Bryan E. Bledsoe, DO, FACEP, & Paul Bojan, EMT-P

Hear Dr. Bledsoe discuss the treat-ment of pain and the management ofeye injuries at EMS Today in Salt LakeCity, March 2–6, 2004.

PHO

TOS

CO

URT

NEY

McC

AIN

The term flash pulmonary edemadescribes pulmonaryedema that developsrapidly—often over a few minutes. Italmost always occursin patients with ahistory of congestiveheart failure & pulmonary edema.

Evaluation & treatmentThe patient, a 52-year-old, obese (weight 325lbs./148 kg.) male in no acute distress, had abrief syncopal episode while standing.Bystanders report he was unconscious for about10 seconds. He’s alert, and his skin is dry withnormal color. Initial vital signs reveal a regularpulse of 100; blood pressure of 200/130 torr;normal, non-labored respirations of 18; and aSpO2 of 98% on room air. The ECG reveals apaced rhythm.

The patient has a history of congestive heart

failure (CHF), hypertension, cardiac dysrhyth-mias, elevated cholesterol, renal insufficiencyand a below-knee amputation (BKA) of his leftleg due to vascular insufficiency. He has animplanted pacemaker and an automated internalcardiac defibrillator (AICD). Current medica-tions include Lasix, Coumadin, Pravachol,Coreg, Cordarone, Vasotec, Viagra andLanoxin. When questioned, the patient statesthat he hasn’t taken the Viagra “in several days.”

You provide supportive care, including sup-plemental oxygen, IV access and cardiac moni-toring. The patient initially does well duringtransport to the hospital of his choice. Suddenly,he develops difficulty breathing, cyanosis andaltered mental status. His SpO2 drops into the50s. You immediately detect the patient’s dete-rioration, divert to a closer hospital and haveyour communications center alert that hospital.

Hospital evaluationOn arrival at the hospital, you move the patientto the emergency department (ED), where thestaff is assembled and awaiting his arrival. Thepatient is deteriorating by the minute. Rales areheard in all lung fields, and he begins coughingup pink, frothy sputum.

Because of the patient’s rapid respiratoryfailure, the ED physician elects to performemergent rapid sequence intubation (RSI).He’s given 6 mg midazolam (Versed) and 150mg succinylcholine (Anectine). Following ade-quate relaxation, he’s intubated and placed ona mechanical ventilator. Paralysis is maintainedwith vecuronium (Norcuron), and sedation ismaintained with additional doses of midazo-lam. The ED physician also puts him on IVnitroglycerin and starts diuresis with IVfurosemide (Lasix).

The patient is moved to the ICU, where heremains on a ventilator for 48 hours. Lab andother diagnostic tests exclude recent cardiacischemia. He’s diagnosed with acute respiratoryfailure secondary to flash pulmonary edema. In

Medic 1534 and ALS Quint 1542 are dispatched to a“man down” at a local car dealership. The responsetime is short. On arrival, EMS personnel are shown to

an office where they find a man in his mid-50s, conscious, alertand without complaint. The patient reports that he was leaningagainst a car when he felt dizzy and passed out.