Acute Cardiogenic Pulmonary Edema

sudden↑in pulmonary venous pressure

➡️ Acute left sided heart failure e.g. myocardial infarction. ➡️On top of chronic LSHF : MS with aggravating factor as AF. 

Clinical S/S : 

Severe dyspnea at rest & orthopnea.

Sense of impending death.

Sweating & irritability.

Cyanosis.

Crepitation . 

Cough with frothy pink sputum.

Diagnostic Testing

• Radiographic abnormalities include cardiomegaly, interstitial and perihilar vascular engorgement,

Kerley B lines, and pleural effusions.

• The radiographic abnormalities may follow the development of symptoms by several hours, and their resolution may be out of phase with clinical improvement.

Treatment 

Supplemental oxygen should be administered initially to raise the arterial oxygen tension to >60 mm Hg.

Mechanical ventilation is indicated if oxygenation is inadequate by noninvasive means or if hypercapnia coexists.

◦ Placing the patient in a sitting position improves pulmonary function.

◦ Bed rest, pain control, and relief of anxiety can decrease cardiac workload.

• Precipitating factors should be identified and corrected, as resolution of pulmonary edema can often be accomplished with correction of the underlying process. The most common precipitants are as follows:

◦ Severe HTN

◦ MI or myocardial ischemia (particularly if associated with MR)

◦ Acute valvular regurgitation

◦ New-onset tachyarrhythmias or bradyarrhythmias

◦ Volume overload in the setting of severe LV dysfunction

Medications

Morphine sulfate reduces anxiety and dilates pulmonary and systemic veins. 

Furosemide (IV) Decreases pulmonary congestion (venodilator) 

Vasodilators (IV):

Na nitroprusside IV infusion (0.5 – 5 mg / kg/ min).

Nitroglycerin is a venodilator that can potentiate the effect of furosemide. 

IV administration is preferable to oral and transdermal forms as it can be rapidly titrated.

Inotropic agents, such as dobutamine or milrinone, may be helpful after initial treatment of CPE in patients with concomitant hypotension or shock.