As a primary care veterinarian, you may encounter patients with acute cardiogenic pulmonary edema (ACPE) on a fairly regular basis. These patients' PE is caused by elevated hydrostatic pressure in the pulmonary capillaries due to left-sided congestive heart failure, as opposed to the non-cardiogenic form of PE, which is caused by decreased colloid osmotic pressure or altered vascular permeability in the pulmonary capillaries. While some ACPE patients may benefit from transfer to a specialty clinic for evaluation or consultation, often transferring your patient suffering from ACPE is not in their best interest. This article provides some tips on stabilizing them within your own hospital, with the goal of helping you with the in-house management of ACPE patients.

The general approach to treatment usually includes a combination of a diuretic and a vasodilator. In an ACPE patient dying of heart failure, the kidney function is secondary, so I do not use IV fluids unless they are being used to deliver a continuous rate infusion (CRI).

Patient pre-treatment

Patient post-treatment

The first priority in an ACPE patient is to reduce the edema with a diuretic. I usually recommend giving furosemide at an initial dose of 3-5mg/kg IV. After the initial dose, you have a choice between an intermittent bolus method and furosemide CRI. Intermittent bolus is usually administered at 1mg/kg IV every hour, or 2mg/kg IV every two hours. The CRI is run at a rate of 0.5-1.0mg/kg/hr. Whichever method is chosen, it should be continued until the respiratory rate is < 40/min on oxygen for 2-3 hours, or until the total daily dose of furosemide exceeds 15mg/kg/day. Then switch to 2mg/kg IV every 6-8 hours for the next 12-18 hours.          

I also check on systolic blood pressure. If the pressure is >120mmHg, then I would start a nitroprusside CRI at 2mcg/kg/min. Take another blood pressure reading in 45 minutes, and increase the nitroprusside by 1mcg/kg/min increments until the systolic blood pressure is between 85 and 90mmHg, with a maximum of 5mcg/kg/min. If nitroprusside is successful, several hours are required to wean the patient off the CRI; sometimes hydralazine oral is also required to continue the afterload reduction while transitioning the patient to oral medication. I will often use a high concentration infusion so that I don't have to administer large fluid volumes intravenously. A syringe pump can be used. Note that nitroprusside is inactivated by exposure to light, so it comes with a light-protective bag.          

If the blood pressure is less than 120mmHg, then the patient would likely benefit from a dobutamine CRI starting at 5mcg/kg/min and increasing to as high as 15mcg/kg/min. The cardiac rhythm should be monitored, because dobutamine can cause ventricular arrhythmias at higher doses and is usually the limiting factor in how high you can increase the dose. Dobutamine CRI can help with the low output heart failure more common in dilated cardiomyopathy patients, and can reduce the effective regurgitant orifice area of the mitral valve for purely valve patients with congestive heart failure.

Pimobendan can be used orally to function as a combination of inotropy and vasodilator. Pimobendan is absorbed rapidly (within an hour in most patients). Excessive pimobendan can cause hypotension that could be excessive, so measuring blood pressure is still warranted. Pimobendan could potentially be used along with dobutamine, but the potential for arrhythmia would be expected to increase.

Follow-up: If the patient responds, I prescribe TID oral furosemide to go home for 2-5 days, along with an ACE inhibitor +/- pimobendan or rate control drugs for atrial fibrillation. A radiograph and renal panel should be repeated in 4-5 days after discharge.