What is the differential for weakness as it pertains to cardiac disease? The most common diseases for which dogs are presented with this complaint when the underlying cause is cardiogenic include dilated cardiomyopathy, pericardial effusion, advanced AV valve regurgitation, or cardiac arrhythmias. Other causes that are less common include congenital heart disease that affects cardiac output or oxygenation.

What are the diagnostics that are done in the evaluation of weakness and collapse? Radiography will reveal evidence of pulmonary pathology and usually give an appreciation of cardiac size. Electrocardiography will provide the evidence for the diagnosis of the rhythm disorder. Echocardiography will give the structure and functional characteristics to determine the specific disease. Finally, blood pressure and laboratory tests will clear the animal of other diseases and provide the foundation to know that drug therapy is not contraindicated if underlying organ dysfunction is severe. When these tests do not provide the answer then 24-hour ambulatory (Holter) monitoring, event recorders, or implantable recording devices can reveal the abnormal rhythm.

What are the rhythm abnormalities that can result in weakness or collapse? When the heart rate is too slow or too fast, weakness can occur. The degree of these extremes dictate the severity of the clinical signs. The parameters include both the rate and the duration of the extreme in rate. Critical to this factor is the generation of the systemic blood pressure. For example a heart rate of greater than 260 bpm is more devastating than a rate of 200 bpm, but if the faster rate persist for only a few seconds and the latter for hours the bad consequences are greater. This same thought follows through with the length and rate of bradycardias. When the extreme rates cause a loss of cerebral blood flow (inadequate pressure) for more than 8 seconds, then collapse or syncope will result. The most common tachycardias that can cause weakness include atrial fibrillation, atrial tachycardia, and ventricular tachycardia. The most common bradycardias include third degree heart block, advanced second degree heart block, and sick sinus syndrome.

Often dogs with dilated cardiomyopathy are seen with heart failure and atrial fibrillation. This combination can be a challenge to manage medically. The control of excessive heart rate in atrial fibrillation is critical.

What are the problems when striving for rate control? Remember, you can get the heart to slow down if you use enough drug. But there lies the problem. There is a 'ceiling' effect with digoxin. That is, the therapeutic/toxic dose of digoxin prevents titrating up to get the desired slowing in some dogs. The amount of digoxin required to slow the heart enough is beyond the therapeutic level. With calcium channel blockers or beta-blockers there is more room for titration; however, at the doses needed to reach the heart rate goal the negative inotropic effect or drop in systemic blood pressure can bring disappointment to reaching the target heart rate. The latter is not as much of a problem in dogs that have lone atrial fibrillation with maintained myocardial function. In these dogs the dose of either diltiazem or atenolol can be titrated to achieve the desired heart rate. We have most commonly found a good rate control with a combination of diltiazem (extended-release) and digoxin. Most dogs even with myocardial failure tolerate this drug combination. It may be that the negative inotropic effect is offset by the dramatic improvement in myocardial perfusion that occurs with adequate rate control.

In a dog with acute heart failure due to dilated cardiomyopathy and marked tachycardia due to atrial fibrillation the goals must be prioritized. Most of the time severe dyspnea is present in addition to the tachycardia of the atrial fibrillation. The dog must breath before all else. Aggressive, short term treatment with diuretics is given with acute treatment with nitroglycerin, and some may use nitroprusside in those handful of places that have continuous monitoring. The dilemma is whether to treat the dog with dobutamine or diltiazem. The dobutamine for the inotropic support or diltiazem to slow the heart rate (some of these dogs have rates greater than 240 bpm). A second dilemma concerns the route of drug administration. In the dog that is in complete distress the intravenous route is obvious, but not all dogs are in this most dire position. Some could be treated orally. Response to oral diltiazem can be rapid; however, if there is a negative response the effects can be more protracted if the long acting preparations are used such as Dilacor®. The effects of regular diltiazem do not last long in the dog and require frequent administration; however, this can be an advantage in a dog where the IV route is not selected, but the long acting medication is not desirable as yet. The unfortunate problem is that with calcium channel blockers and beta-adrenergic blockers the heart rate control comes with the price of hypotension in many dogs with myocardial failure. This is why a combination of treatment with digoxin can be advantageous, but the dog must live long enough to have all the medications achieve adequate blood levels. The role of other drugs such as pimobendan or levosimendan in these acute situations needs to be explored too. It has been our experience that if a dog is not in severe myocardial failure, the dose of diltiazem is higher than expected to achieve heart rate control. We commonly use 3 to 4 mg/kg twice daily of extended release diltiazem for long-term treatment. Some dogs may require even higher doses. We monitor patients with 24-hour electrocardiographic monitoring.