Transesophageal atrial pacing for intraoperative sinus bradycardia or AV junctional rhythm: feasibility as prophylaxis in 200 anesthetized adults and hemodynamic effects of treatment.

Sinus bradycardia (SB) or atrioventricular junctional rhythm (AVJR) may produce circulatory insufficiency in anesthetized surgical patients, especially those with cardiovascular disease. Chronotropic drugs have been the preferred initial treatment, except when epicardial pacing is available. Alternative methods include transvenous or transcutaneous pacing. Drugs may be ineffective or have undesirable effects. Transvenous pacing is time consuming and risky, and transcutaneous pacing is not universally applicable or effective. Transesophageal atrial pacing (TAP) lacks these disadvantages, but unavailability of equipment and unfamiliarity with the method has discouraged widespread use. Feasibility of TAP as prophylaxis for intraoperative SB or AVJR was tested with approved or investigational devices in 200 anesthetized surgical patients, not necessarily with cardiovascular disease or having cardiac surgery. Of these, 84 later had incidental SB < or = 60 beats/min, and 23 of these 84 had SB < or = 50 beats/min. Thirteen patients had AVJR (72 +/- 4 beats/min; mean +/- SEM). TAP at 80 beats/min for SB, or at a rate sufficient to overdrive AVJR, was effective initial treatment in all patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Evaluation of transesophageal atrial pacing stethoscope in adult surgical patients under general anesthesia.

Sinus bradycardia (SB) and atrioventricular junctional rhythm (AVJR) commonly cause circulatory insufficiency in anesthetized surgical patients. Treatment is usually with drugs, which can be ineffective or have adverse effects. Cardiac pacing might be preferred, but the transvenous or epicardial routes are too invasive for routine use, and transcutaneous pacing fails to preserve atrial transport function. Transesophageal atrial pacing (TAP) lacks these disadvantages, yet unavailability of inexpensive products has prevented more widespread use. Therefore, a pacing esophageal stethoscope (PES) fabricated by addition of bipolar electrodes to disposable esophageal stethoscopes routinely used for intraoperative monitoring, was evaluated in 100 anesthetized adults. TAP thresholds (10-msec pulses) and hemodynamic effects of TAP as treatment for incidental SB (< or = 60 beats/min) or AVJR were determined. Minimum TAP thresholds (mean +/- standard error) in 48 males were 7.3 +/- 0.3 mA and in 51 females were 8.5 +/- 0.4 mA. Corresponding inferior alveolar ridge-to-electrode distances were 32.5 +/- 0.2 and 30.4 +/- 0.2 cm. For 48 patients with SB < or = 60 beats/min (54 +/- 1 beats/min), TAP (81 +/- 1 ppm) produced average 15, 11, and 14 mmHg increases in systolic, diastolic, and mean arterial pressure, respectively (P < 0.001). For 11 patients with AVJR (71 +/- 5 beats/min), TAP (92 +/- 3 ppm) produced average 23 and 15 mmHg increases in systolic and mean arterial pressure, respectively (P < 0.05). There were no apparent complications of TAP. TAP with a PES appears practical, safe, and effective for prophylaxis and treatment of SB or AVJR in anesthetized surgical patients.

Atrial pacing thresholds measured in anesthetized patients with the use of an esophageal stethoscope modified for pacing.

Transesophageal atrial pacing (TAP) with the use of standard, thermistor-equipped, esophageal stethoscopes, modified for pacing by incorporation of a 4-French, bipolar TAP probe (pacing esophageal stethoscope [PES]), was evaluated in 100 adult patients under general anesthesia. A commercially available TAP pulse generator supplied 10-ms pulses with current variable between 0 and 40 mA. Pacing distances (in centimeters) were measured from the infraalveolar ridge to midway between PES electrodes (1.5-cm interelectrode distance). Pacing thresholds (milliamperes) were measured at the point of a maximum-amplitude P-wave (PMAX) in the bipolar esophageal electrogram and points 1 cm proximal or 1, 2, or 3 cm distal to PMAX. TAP (70-100 beats per min) was used for sinus bradycardia less than or equal to 60 beats per min (36 patients) or atrioventricular (AV) junctional rhythm (2 patients) and blood pressure changes with TAP documented. In male patients (n = 49), PMAX was 32.7 +/- 0.3 cm (mean +/- SE) and minimum pacing threshold 5.1 +/- 0.4 mA (range, 1-13 mA) at 33.6 +/- 0.3 cm (range, 30-37 cm). In female patients (n = 51), PMAX was 30.4 +/- 0.4 cm and minimum pacing threshold 4.4 +/- 0.4 mA (range, 2-14 mA) at 31.1 +/- 0.4 cm (range, 26-40 cm). TAP produced an average 13-16 mmHg increase in systolic, diastolic, or mean arterial pressure in patients with sinus bradycardia or AV junctional rhythm. There were no subjective patient complaints (epigastric discomfort, dysphagia) that could be attributed to TAP; objective evaluation (esophagoscopy) was not performed.(ABSTRACT TRUNCATED AT 250 WORDS)

Increased intraoperative cardiovascular morbidity in diabetics with autonomic neuropathy.

Thirty-eight consenting subjects scheduled for elective ophthalmologic surgery were classified as nondiabetics (n = 21) or diabetics (n = 17) and were tested preoperatively for autonomic dysfunction. The autonomic tests consisted of respiratory sinus arrhythmia and heart rate responses to the Valsalva maneuver to test cardiac vagal function and diastolic blood pressure responses to head-up tilt and cold pressor test to assess sympathetic efferent integrity. At a separate time, anesthesia was established with fentanyl (2 micrograms/kg), sodium thiopental (3-5 mg/kg), and vecuronium (0.1 mg/kg), and maintained with isoflurane, oxygen, and nitrous oxide. An anesthesiologist, blinded to the autonomic test results, recorded perioperative blood pressure and heart rate. The autonomic test results revealed significant autonomic dysfunction among the diabetics. Heart rate and blood pressure declined to a greater degree (P less than 0.05) during induction of anesthesia in diabetics compared with controls and there was less of an increase in these same parameters following tracheal intubation in diabetic patients. Thirty-five percent of diabetics required intraoperative vasopressors compared with only 5% of control patients (P less than 0.05). A major finding was that the diabetics who required intraoperative blood pressure support had significantly greater impairment of autonomic test results compared with those diabetics who did not need vasopressors. Diabetics are at increased risk for cardiovascular lability during anesthesia and preoperative screening of diabetics with simple noninvasive autonomic tests may be useful in identifying those at high risk for perioperative cardiovascular instability.

Halothane anesthesia attenuates cardiopulmonary baroreflex control of peripheral resistance in humans.

The effects of halothane anesthesia on cardiopulmonary (low pressure) baroreflex control of peripheral resistance were studied in 10 ASA class I young men. Graded (-5, -7.5, -10, -12.5 mmHg) lower body negative pressure (LBNP) was used to produce progressive decreases in thoracic blood volume and central venous pressure. These stimuli activate reflexes from cardiopulmonary baroreceptors. Volunteers were studied while awake and during 1 MAC (0.75%) and 1.25 MAC (0.93%) halothane anesthesia. Hetastarch (6%) in 0.9% normal saline was infused into patients before baseline recordings were initiated. Blood pressure, stroke volume, cardiac output, and systemic and forearm vascular resistance decreased and forearm blood flow increased during halothane anesthesia. In awake subjects, LBNP did not alter heart rate or blood pressure, but stroke volume and cardiac output decreased. Blood pressure was maintained by cardiopulmonary baroreflex-mediated increases in peripheral resistance. In anesthetized subjects, decreases in stroke volume and cardiac output during LBNP were similar to awake responses, however, hypotension occurred because reflex resistance increases were markedly attenuated. The authors conclude that halothane anesthesia blunts cardiopulmonary baroreflex resistance responses provoked by mild decreases in thoracic blood volume in humans.