Ventricular Tachycardia

Definition and Etiology

Ventricular tachycardia (VT) is a cardiac arrhythmia characterized by a rapid rhythm originating in the ventricle. This rhythm originates below the bundle of His in the specialized conduction system, surrounding ventricular myocardium, or both.³²³ VT may be caused by disorders in impulse formation, impulse conduction, or a combination of the two.³²³ Ventricular reentry is an important mechanism in the genesis of sustained VT, whereas abnormal automaticity is probably responsible for idioventricular rhythms and parasystole.

Clinical Signs and Differential Diagnosis

The clinical signs detected depend on the ventricular rate, type of VT (uniform or multiform), duration of VT, and severity of the underlying cardiac disease.³²⁵ Large animals with VT may be asymptomatic at rest if the rhythm is relatively slow and uniform, or they may have severe CHF with rapid uniform or multiform VT.³²⁵ Exercise intolerance is common and may be so severe that the animal has frequent syncope.

Animals with sustained VT have a rapid heart rate with a regular (uniform) or irregular (multiform) rhythm.^328-331 Heart rates as high as 300 bpm have been detected in horses with VT. Heart sounds vary in intensity, with some loud booming sounds (“bruit de cannon”). Arterial pulse may be variable or uniform, with normal (slower rate) or weak (rapid rate) intensity pulses. Pulse deficits frequently occur, particularly with rapid or multiform VT.Jugular pulses are commonly detected in large animals with VT. The large pulse waves seen in the jugular vein are cannon “a” waves that occur when the right atrium and ventricle contract simultaneously. Cardiac murmurs are not commonly detected. Signs of CHF are usually present when VT is rapid and sustained but are uncommon in animals with slower or paroxysmal VT.^328-330 Signs of right-sided CHF (ventral edema, venous distention) usually predominate with sustained uniform VT and increase in severity the longer the duration and more rapid the rate of the arrhythmia. Signs of left-sided CHF (coughing, expectoration of foamy fluid, respiratory distress) usually predominate with multiform VT.

The presence of jugular pulses and bruit de cannon in an animal with a rapid regular rhythm helps distinguish VT from sinus or supraventricular tachycardia. Multiform VT can be difficult to distinguish from AF, because both arrhythmias have an irregular rhythm with heart sounds that vary in intensity.

Clinical Pathology

Electrolyte, metabolic, or toxic causes of VT may be present in large animals with primary GI disease. Hypomagnesemia and hypokalemia have also been associated with development of VT.³³¹ Serum creatinine and BUN may be elevated in horses and cattle in CHF associated with prerenal azotemia. Serum osmolality, BUN, and creatinine increase and urine osmolality decreases acutely in horses with experimental monensin toxi-

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cosis. Initial decreases in serum potassium and serum calcium have also been reported in these animals. Marked elevations of cTnI have been seen in horses with VT.^195,196,326 cTnI is a more sensitive indicator of myocardial injury; therefore cTnI is currently preferred for detection of myocardial injury in horses, cattle, South American camelids, and small ruminants. Cardiac isoenzymes of CK and LDH are often elevated if there is recent myocardial injury associated with VT. Elevation of the myocardial fraction of CK (CK-MB) in excess of 5% of the total CK is compatible with myocardial injury in horses.¹⁷⁷ A neutrophilic leukocytosis, elevated SAA, and hyperfibrino­genemia may be detected in animals with infectious myocarditis or bacterial endocarditis or may be elevated owing to the primary underlying disease. In most large animals with VT, however, hematologic findings are normal.

The diagnosis of VT is made from the ECG. A series of four or more ventricular premature complexes (VPCs) is diagnostic of VT.^324,332 The electrocardiographic appearance of the VPC may be widened and bizarre, or the QRS duration and appearance of the QRS and T may be near normal, especially in horses (Fig. 30.32).^324,325 Although the duration of QRS complexes that are ventricular in origin is usually within the normal range reported for horses, it is usually longer than the QRS duration of the horse's normal sinus beats.³²⁴ The major direction of the QRS complex is usually oriented opposite to that of the T wave.

The echocardiogram is used to determine whether cardiac disease is present. The echocardiogram is usually abnormal in large animals with primary myocardial disease and normal in large animals with secondary VT, except for the changes associated with the VT itself (see Fig. 30.15). Abnormal echocardiographic findings that may be detected in large animals with primary myocardial disease include myocardial dyskinesis, hypokinesis, and akinesis; abnormal myocardial echogenicity; decreased FS, ET, and EF; loss of the normal systolic and diastolic undulations of the aortic root; and detection of spontaneous contrast, small aortic root, and large pulmonary artery. Occasionally the echocardiographic abnormalities created by VT may be difficult to distinguish from those of primary myocardial disease. Rupture of the aortic root at the right sinus of Valsalva should be considered in horses with acute onset of uniform VT and colic.

FIG. 30.32 Lead II electrocardiogram obtained from a horse with sustained uniform venticular tachycardia (VT) and congestive heart failure before (A) and after (B) conversion to sinus rhythm. Note the abnormal QRS and T configuration and slower atrial rate during the sustained VT.

FIG. 30.33 Lead II electrocardiogram obtained from a horse with multiform ventricular tachycardia and acute onset of pulmonary edema. Note the multiple different QRS and T configurations and the elevated ventricular rate.

Cardiac catheterization may reveal severe hypotension and low cardiac output.

Pathophysiology

VT is probably initiated spontaneously by late coupled ven­tricular complexes, whereas one very early ventricular premature depolarization can often initiate VT electrically.³²³ Sympathetic stimulation may also provoke VT by increasing the amplitude of the early afterdepolarizations, culminating in a run of VT.³²³ This may be the mechanism of some of the exercise-induced VT in horses. Reentry in the ventricle is an important cause of sustained VT, particularly in human patients with dilated cardiomyopathy and ischemic heart disease. The area of reentry is reportedly small (drug for most large animal practitioners—is rapidly acting, administered IV, and has a short duration of action and minimal hemodynamic effects. However, this drug has central nervous system side effects in horses (hyperexcitability and seizures) and must be used at a lower dosage than in cattle. Quinidine gluconate (or quinidine sulfate in cattle) is effective in large animals but is less rapidly acting, has negative inotropic effects at large doses or if primary myocardial disease is present, causes hypotension, and can produce undesirable adverse or toxic reactions. Magnesium sulfate can cause hypotension but has no other recognized adverse cardiovascular effects. It is less rapidly acting than lidocaine, but in both normomagnesemic and hypomagnesemic patients it may be effective when other antiarrhythmics fail. IV procainamide, IV and oral propafenone, and IV flecainide have also been used successfully in horses with VT. IV propafenone is indicated for refractory VT and has been used successfully in several horses that did not respond to lidocaine, quinidine, procainamide, or magnesium sulfate. However, it is currently unavailable in the United States. Sotalol has been successful in several horses with VT and is available in an intravenous formulation.³³⁹ Other antiarrhythmics such as propranolol have been used with less success but have converted large animals with sustained VT.