Ventricular tachycardia with pulse

Arterial pulses are an accurate measure of the ventricular rate in healthy persons with good ventricular function. In patients with a rapid ventricular rate—because of supraventricular tachyarrhythmias such as atrial flutter or fibrillation or rapid ventricular rates (e.g., ventricular tachycardia or premature ventricular beats)—extremity pulses (e.g., radial pulse) may be considerably slower than the true ventricular rate. A more accurate ventricular rate is determined by listening to the ventricles with the stethoscope (usually at the apex) or counting from an ECG. In patients with atrial fibrillation and a fast ventricular rate, a pulse deficit (measure of the difference in true ventricular rate and peripheral pulse rate) may exist. This may be as much as 10 to 20 beats per minute. Thus the location of the pulse (radial or apical) should be recorded. The pulse deficit will be reduced as the ventricular rate is controlled with drug therapy or normal sinus rhythm is restored. 

B. Complications. Ventricular tachycardia in patients with a pulse may be associated with hypotension or may deteriorate into pulseless ventricular tachycardia or ventricular fibrillation. 

A 63-year-old man with paralysis below C4 developed chest pain but had no positive evidence of myocardial infarction. His pulse rate suddenly fell to 24/minute and he collapsed. He was given intravenous adrenaline 1 mg and atropine 0.4 mg, after which he developed a supraventricular tachycardia at 156/minute followed very soon after by ventricular tachycardia and then fibrillation. Resuscitation was unsuccessful. 

A. The earliest symptoms of acute caffeine poisoning are usually anorexia, tremor, and restlessness. These are followed by nausea, vomiting, tachycardia, and confusion. With serious intoxication, delirium, seizures, supraventricular and ventricular tachyarrhythmias, hypokalemia, and hyperglycemia may occur. Hypotension is caused by excessive beta-2-mediated vasodilation and is characterized by a low diastolic pressure and a wide pulse pressure. 

A 21-year-old woman, who used cocaine regularly and occasionally other drugs of abuse, took moclobemide 1800 mg at 15.00 h and venlafaxine 1800 mg at 18.00 h. At 20.14 h she was conscious but restless and agitated. She had excessively clammy skin with a normal body temperature, increased symmetrical reflexes, ataxia, increased muscle tone, and dilated pupils her blood pressure was 180/120 mmHg, pulse rate 105/minute, and respiratory rate 16/minute. She deteriorated at around 23.30 h, with loss of verbal contact, severe agitation, hallucinations, periodic coma, continuously dilated pupils, a tachycardia of 124/minute and a blood pressure of 105/90 mmHg. Two hours later, her respiratory rate was 34/minute, and her temperature 41-42 °C. She had bloody respiratory secretions and loose bloody stools. Her heart rate increased to 170/minute and she developed ventricular fibrillation. Deflbrillation was unsuccessful and she died. 

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