Cardiac emergencies (Proceedings)

Emergencies related to cardiac disease are common, and can be difficult to differentiate from non cardiac diseases with similar clinical signs. The emergency clinician must be able to differentiate between cardiac and non-cardiac diseases using subtle clues obtained from a brief physical examination, and an understanding of common cardiac conditions.

Congestive heart failure

Congestive heart failure (CHF) is the most common heart-related emergency in both dogs and cats. Congestive heart failure implies impaired cardiac function leading to increased venous pressures, with resulting congestion and edema. In response to a diseased heart (most commonly chronic valvular disease leading to mitral regurgitation), a fall in cardiac output is sensed by baroreceptors in the aorta and carotid sinus. The baroreceptors then signal the brain to increase heart rate and to constrict arterioles and veins. Reduced renal perfusion also stimulates the release of renin from the kidney, ultimately causing the following major changes:

     1. Vascular smooth muscle constriction

     2. Vasopressin release (water retention and vasoconstriction)

     3. Increased thirst

     4. Production of aldosterone (salt retention, water retention)

Thus, congestive heart failure is a state of volume overload resulting from neuroendocrine responses to reductions in cardiac output. The most common cause of congestive heart failure in dogs is chronic valvular disease (mitral regurgitation), with other causes including dilated cardiomyopathy, severe arrhythmias, and congenital heart diseases such as patent ductus arteriosus (PDA).

Dogs and cats with CHF commonly have a history of acute onset of shortness of breath. Dogs sometimes have a history of a dry cough especially at night, due to compression of the trachea by the enlarged left atrium. Coughing in cats is generally associated with asthma. Exercise intolerance and polyuria/polydipsia can also be reported in dogs with CHF. Physical examination findings consist mostly of shortness of breath. The presence of a cardiac murmur (or gallop in cats) certainly supports a diagnosis of CHF. Pulmonary crackles on auscultation suggest the presence of pulmonary edema, though causes of non-cardiogenic pulmonary edema including seizures, strangulation, contusion, and electrocution must be considered. In dogs, breed (i.e. Doberman) and auscultation (cardiac murmur) are often sufficient to create an index of suspicion for CHF. Cats with CHF are much less tolerant of handling, and the stress of the physical examination may be life-threatening. In our experience, the physical examination in cats that present with dyspnea consists of brief auscultation (i.e. murmur/gallop Yes or No) and rectal temperature. Cats with CHF are typically hypothermic from reduced perfusion, which other diseases such as asthma and chronic lung disease are more commonly associated with normothermia or even hyperthermia.

Diagnostic imaging consisting of thoracic radiography is commonly used to identify dogs and cats with congestive heart failure. Cardiomegaly, pulmonary vessel distension, and an alveolar infiltrate are commonly observed in dogs with underlying cardiac failure. In dogs, perihilar edema along with pronounced left atrial enlargement are commonly observed. In cats, distribution of pulmonary infiltrates are more variable. While radiography is used to identify whether congestive heart failure is likely, echocardiography is used to determine the nature of the underlying cardiac disease.

Treatment of dogs and cats with CHF consists first and foremost of an oxygen rich environment such as an oxygen cage (which produces up to 40-50% FIO2). There should be minimal handling, as these animals have a reduced tolerance of stress. Diuretics (Furosemide 2mg/kg) are the mainstay of therapy and can be administered intravenously or intramuscularly to reduce blood volume. Subcutaneous administration will not be effective due to reduced perfusion. As multiple injections are often necessary, a bowl of water should always be available, to prevent the development of pre-renal azotemia. Doses of furosemide can be administered every 1-2 hours until signs of dyspnea less, after which it can be administered at 2-4mg/kg q8-12hours in dogs, 1-2mg/kg q 8-12hrs in cats. Excessive dosing can lead to dehydration, electrolyte changes, and renal failure. Vasodilators can also be useful to reduce congestion. Nitroglycerine paste is a venodilator that is sometime applied to the inner ear or the groin area. Since perfusion to those areas is questionable in CHF, the efficacy of this therapy is questionable. In cases of severe CHF that does not respond to furosemide, sodium nitroprusside (0.5-1ug/kg/min to start) can be administered as a continuous infusion and titrated to effect. Sodium nitroprusside causes vascular smooth dilation of veins and arteries, thus reducing venous return to the heart as well as afterload (promoting forward flow of blood). The use of nitroprusside requires close monitoring, and should be used cautiously. In cases of DCM, dobutamine may be used to increase cardiac contractility (5-15ug./kg.min), and to control signs of CHF. Once signs of CHF are controlled, maintenance therapy is selected based on the underlying disease detected by echocardiogram. Some advocate the use of analgesics to reduce the anxiety associated with dyspnea. In general the use of any medication that cause hypotension and reduced cardiac output should be avoided. While I do not do this in practice, if you choose to do so, it is important to select drugs that are reversible (opioids), or that have minimal cardiovascular effects (diazepam). The use of Pimobendan is rapidly gaining popularity in the United States. Pimobendan increases myocardial contractility, and causes both peripheral and coronary vasodilation. As it increases cardiac output without increased energy demand, Pimobendan is thought to have beneficial effects on the treatment of heart failure and has potential to prolong the life span in animals with cardiac disease.

Pericardial effusion

Pericardial effusion, or fluid accumulation within the pericardial space, is also common. Though not truly a type of cardiac disease, consequences of fluid accumulation in the pericardial space are signs of right sided heart failure. Pericardial effusion is common in large breed dogs, though it can occur in any size dog of any breed. The most common cause of pericardial effusion is neoplasia, followed by idiopathic pericardial effusion. Other non-neoplastic causes include anticoagulant rodenticide toxicity and left atrial tear secondary to severe chronic valvular disease). Right atrial hemangiosarcoma (commonly found in large breed dogs) is the most common type of neoplasia followed by chemodectoma and mesothelioma. Less common types of neoplasia reported as causes of pericardial effusion include lymphoma and osteosarcoma. Pericardial effusion occurs less commonly in cats, and can be caused by feline infectious peritionitis, lymphoma, or a volume overloaded state such as congestive heart failure (though this rarely causes tamponade).

Clinical signs of pericardial effusion occur when the intrapericardial pressure, which is normally very low, rises above the right ventricular filling pressure, causing a reduction in cardiac output, a rise in systemic venous pressure, and signs of congestion. Clinical signs associated with this state occur most commonly when intrapericardial pressure rises slowly, and include pleural effusion, jugular venous distension, and ascites. Signs of left sided failure are not apparent, because the left side of the heart is a higher pressure system than the right side. On the other hand, small volume effusions that accumulate suddenly cause profound circulatory compromise before signs of congestion become apparent.

Dogs presenting with pericardial effusion can have vague signs of lethargy, or may present with signs of cardiovascular collapse. Pericardial effusion should be ruled out in any large breed dog presenting with signs of weakness. Physical examination findings consistent with pericardial effusion include jugular venous distension, tachypnea (due to pleural effusion), abdominal effusion, and tachycardia with muffled heart sounds. Palpation of femoral pulses may reveal pulsus paradoxus, which is essentially an exaggeration of a normal phenomenon. Under normal conditions, the surge of venous return to the heart during inspiration causes the right side of the heart to fill at the expense of the left side of the heart, so that left ventricular stroke volume falls slightly and the femoral pulse feels weaker than during expiration. This becomes exaggerated when right ventricular pressure rises, and is often easily discerned during palpation of the femoral pulse. Electrocardiography may also be useful in raising the index of suspicion for pericardial effusion. In addition to sinus tachycardia, ECG findings consistent with pericardial effusion include small amplitude QRS complexes and electrical alternans, which is a beat to beat variation in the size of the QRS complex that occurs as the heart swings within the fluid filled pericardial sac. Radiographs often show a large, globoid heart, pleural effusion, and an enlarged caudal vena cava due to venous congestion.

Pericardial effusion can be confirmed using echocardiography, where an anechoic space (fluid) is seen between the heart and the pericardium. Documentation of a right atrial mass is often easier when the pericardial fluid is present. Pericardiocentesis is the treatment of choice for cardiovascular stabilization. Under light sedation, the animal can be positioned in left lateral recumbency or in sternal recumbency. Ultrasound can be used to determine the best location to perform pericardiocentesis, the best site typically being the right 5th intercostal space at the level of the costochondral junction. The site is clipped and aseptically prepared. While monitoring the ECG, a large over the needle catheter (4-5 inches long) is inserted toward the heart. When fluid is obtained, the stylette is removed and fluid is drained. Most effusions are bloody or blood tinged, and a small amount should be placed in a red top tube to assess for clotting before large volumes of pericardial effusion are drained. If arrhythmias are detected, the catheter may be withdrawn slightly and if severe ventricular arrhythmias develop, lidocaine may need to be administered (2 mg/kg IV). In cases of severe ventricular arrhythmias, the procedure may need to be aborted. Typically there is noticeable improvement in femoral pulse quality and normalization of heart rate within a few minutes of successful pericardiocentesis. Pericardial fluid should be submitted for cytologic evaluation, though negative cytologic findings should be interpreted cautiously as many tumors do not readily exfoliate.