Dr. Mazzaferro is a staff critical care specialist who manages all patients in the critical care unit, including those who present on emergency with congestive heart failure.
Congestive heart failure (CHF) is unfortunately a common problem that presents to the veterinary small animal practitioner. Clinical signs may include weakness and exercise intolerance, cough, lethargy, inappetance, vomiting, diarrhea, and syncope or collapse. A presumptive diagnosis often is made on the patient's primary presenting complaints, signalment, a thorough history, and physical examination findings. One of the most important concepts to remember in the diagnosis and management of any patient with CHF is to minimize patient stress and do no harm.
A careful physical examination is essential in the diagnosis and management of the patient in CHF. In some cases, the patient should be placed in an oxygen cage or receive flow-by oxygen supplementation, and observed carefully from a distance. Observe the patient's respiratory rate and effort, and posture from afar. Next, approach the patient, and perform a systematic examination, and evaluate the mucous membrane color and capillary refill time? Look carefully at the thoracic inlet and jugular groove for jugular venous distension or a jugular pulse? Auscult the heart for murmurs or dysrhythmias. Simultaneously palpate the inguinal region for a femoral pulse, checking for synchrony and pulse quality. Auscult all lung fields for pulmonary crackles or wheezes. Palpate the abdomen for hepatomegaly and a ballotable fluid wave. Does compression of the cranial abdomen and liver result in jugular venous distension? Palpate the distal extremities. Are they warm to the touch, or do they feel cold due to poor peripheral circulation?
Patients with fulminant pulmonary edema from left-sided CHF may have blood-tinged fluid coming from the nares and mouth and have concomitant pulmonary crackles and a rapid restrictive respiratory pattern. A cardiac murmur or dysrhythmia is often present in cases of severe mitral insufficiency, but in some cases, the heart may be difficult to hear beyond harsh pulmonary crackles. Pulse quality may be supportive of low output cardiac failure. Pulses may be absent in cases of severe low output failure, or in cases of arterial embolism. Jugular venous distension and jugular pulses may be visible in cases of right-sided heart failure. Heart sounds may be muffled to absent in cases of pleural or pericardial effusion. Hepatomegaly and a fluid wave may be present on abdominal palpation in cases of right-sided heart failure. Distal extremity coolness and hematochezia on rectal examination may be present due to low cardiac output.
Emergency management of the patient in CHF consists improving systemic oxygen delivery and minimizing patient stress. Oxygen delivery is a function of both oxygen uptake by the respiratory system, cardiac output, and hemoglobin concentration. The mainstay of therapy for treatment of congestive heart failure is to provide supplemental oxygen and decrease fluid buildup within the lungs.
Flow-by oxygen should be administered to patients with congestive heart failure as a physical examination is taking place. Flow-by oxygen is well-tolerated, and requires minimal physical restraint. Because flow-by is a relatively inefficient method of providing an increase in the fraction of inspired oxygen, other methods including oxygen hoods, oxygen cages, nasal, nasopharyngeal and tracheal oxygen insufflation should be considered for long-term therapy. Humidified oxygen flow rates can be administered at 50–100 ml/kg/minute.
Aside from supplemental oxygen, furosemide is one of the most important therapies for management of the patient with congestive heart failure and pulmonary edema. Furosemide can be administered as a bolus (4–8 mg/kg IV or IM), or as a constant rate infusion (0.66–1 mg/kg/hour IV) to promote diuresis and decrease pulmonary vascular overload and pulmonary edema. The goal of diuretic treatment is to repeat the therapy every 30–60 minutes until the patient's body weight has decreased by 5–7%. Once the patient's respiratory rate and effort has normalized, oral furosemide can be started.
Nitric Oxide Donors
Nitric oxide donors should be initiated as a primary initial therapy in any patient with fulminant congestive heart failure. Nitric oxide donors cause dilation of the pulmonary vasculature and a relative decrease in pulmonary vascular pressures. Nitroglycerine paste is not absorbed as readily across the skin as was once previously thought, and has largely fallen out of favor for use in veterinary patients with CHF. In patients with refractory pulmonary edema that is not responding to traditional diuretic therapy, sodium nitroprusside should be considered, as long as the patient is not hypotensive. Sodium nitroprusside is a balanced arteriolar and venous dilator that decreases both pulmonary and systemic vascular resistance. The drug is administered as a constant rate infusion (2–10 mcg/kg/minute IV, titrated to effect). Because of its potent hypotensive effects, arterial blood pressure must be monitored closely throughout the infusion.
Morphine is an opioid agonist that is useful in patients with congestive heart failure. In dogs, low dose (0.025–0.05 mg/kg IV) morphine dilates the splanchnic vasculature and increases venous capacitance, allowing drainage of fluid from the pulmonary parenchyma. Morphine provides the additional benefits of allowing slower, deeper respirations, and decreasing anxiety in patients with congestive heart failure.
Dobutamine is a synthetic beta-adrenergic agonist that is used as a positive inotrope, specifically in patients with DCM. At lower doses, dobutamine improves cardiac contractility with minimal effects on chronotropy or heart rate. At higher doses, however, dobutamine can be pro-arrhythmogenic. Dobutamine can be administered at a dose of 2–20 mcg/kg/minute. Potential side effects include tachyarrhythmias (at higher doses), facial twitching, and seizures.
Pimobendan (0.25 mg/kg PO BID) has been used with success in dogs with CHF secondary to DCM and mitral valve insufficiency. Pimobendan is a phosphodiesterase-III inhibitor that sensitizes the myocardium to calcium, and improves inotropic activity in addition to causing arteriolar and venous dilation. In addition to its use as a long-term inodilator in the treatment of dogs with CHF, Pimobendan is also recommended for use in emergency therapy of CHF, as it can have an onset of effects within one hour.
Irrespective of the underlying cause, patients with CHF must be managed carefully and aggressively following initial diagnosis. Supplemental oxygen, potent diuretics, and nitric oxide donors continue to be the mainstay of therapy in both cats and dogs during the initial management of CHF. Patients that do not respond to standard therapies may require additional drug protocols, including positive inotropic and intravenous vasodilatory drugs. Careful monitoring of the patient's heart rate and rhythm, arterial blood pressure, respiratory rate and effort, and pulse oximetry or arterial oxygen saturation should be performed to evaluate the patient's response to therapy.
References are available upon request.