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A recent 24-hour ambulatory electrocardiogram recording demonstrated multiple episodes of severe sinus bradycardia associated with pre-syncopal symptoms. Monitored anesthesia care is requested in light of the patient’s advanced age and associated medical conditions. The infiltration of local anesthesia and isolation of the cephalic vein in the left deltopectoral groove proceeds uneventfully. During placement of the ventricular pacing lead, ventricular ectopy occurs as the lead encounters the right ventricular endocardium. Subsequently, as the lead is repositioned, ventricular tachy-cardia is induced and rapidly deteriorates into ventricular fibrillation.

The initial response to a witnessed cardiac arrest is to confirm the diagnosis. Patients in arrest are unresponsive, apneic, and pulseless. Assistance should be called for immediately prior to any intervention. In the past, it was recommended to call for assistance after the initiation of cardiopulmonary resuscitation (CPR), but since 80–90% of patients with sudden cardiac arrest have ventricular fibrillation (VF), which is the most treatable dysrhythmia but which requires urgent defibrillation, the rescuer is advised to call first so that a defibrillator can be brought to the scene. The only exception is in the case of children less than 8 years of age, who usually arrest because of airway problems. In that case, an attempt at securing the airway should first be made.

It used to be assumed that chest compressions produced a cardiac output by directly compressing the ventricles against the vertebral column. This was thought to produce systole, with forward flow out of the aorta and pulmonary artery, and backward flow prevented by closure of the atrioventricular (AV) valves.

Echocardiographic images during arrest show that the AV valves are not closed during chest compressions. There are reports of patients who, during episodes of monitored VF, have developed systolic pressures capable of maintaining consciousness by coughing.

Animal models of CPR have shown that the optimal blood flows are achieved when chest compressions are performed at 80–100 times per minute and the chest is compressed 1.5 to 2 inches (3–5 cm). The new Guidelines for Cardiopulmonary Resuscitation published by the American Heart Association in 2000 recommend a chest compression rate of 100 times per minute. The proportion of time spent during the compression phase should be 50% of the relaxation phase.

Complications of CPR include skeletal injuries, espe-cially rib fractures, visceral injuries, airway injuries, and skin and integument damage (skin, teeth, lips). Less than 0.5% of the complications are considered life-threatening. These include injuries to the heart and the great vessels. However, a significant number of complications could be expected to require therapy and prolong the hospitalization. These include rib and sternal fractures, myocardial and pul-monary contusions, pneumothorax, blood in the pericar-dial sac, tracheal and laryngeal injuries, liver and spleen ruptures, and gastric perforation and dilatation.

Preoperative evaluations begin with basic information required before all anesthetics. A determination is then made as to whether the patient is in optimal condition for the planned procedure or whether further preoperative preparation is indicated. Finally, an assessment is formu-lated to predict lung function following resection. The specific pulmonary evaluation will include history of cough, sputum production, chest pain (possibly pleuritic), dyspnea, wheezing, arm pain (resulting from Pancoast tumor involving the brachial plexus), weakness (resulting from myasthenic syndrome), other endocrine syndromes (caused by tumors secreting hormones), and weight loss (hypoproteinemia).

The purpose of ventilation is to remove carbon dioxide (CO2) from the lungs. The average 70-kg man produces approximately 220 mL/min of CO2 and normally maintains an arterial CO2 (PaCO2) of 40 mmHg. If removal of CO2 is impaired, or if production increases, and ventilation does not increase, the PaCO2 rises. Arterial blood gas analysis provides the ultimate monitor of ventilation: PaCO2. In the lungs, CO2 diffuses into alveoli, and in those areas where ventilation and perfusion are well matched, alveolar CO2 (PACO2)