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BACKGROUND The pressure rate quotient (PRQ; mean arterial pressure/heart rate [MAP/HR]) less than one (PRQ or = 1 mm) lasting for > 1 min. Transesophageal echocardiography determination of ischemia was worsening of wall motion > or = 1 grade and lasting > 1 min. PRQ < 1 was compared to ECG and/or TEE as a predictor or indicator of myocardial ischemia. RESULTS Electrocardiography ischemia occurred during 230 intervals in 10 patients, and in only 41 of 230 (18%) was PRQ < 1. Transesophageal echocardiography-defined ischemia occurred during 592 intervals in 9 patients, and in 119 of 592 (20%) PRQ < 1. Compared to ECG and TEE, PRQ < 1 had a low sensitivity (21%) and poor positive predictive value (25%). CONCLUSIONS Pressure rate quotient < 1 is an unreliable indicator and predictor of myocardial ischemia when evaluated by ECG, TEE, and the combination of these modalities in patients undergoing coronary artery bypass graft surgery.

A 42-YR-OLD man with marfanoid syndrome was scheduled for repair of thoracoabdominal aneurysm. Sevoflurane/oxygen was used as the primary anesthetic. At the completion of the operation (9 h and 42 min), the temperature had decreased to 33.9°C (blood), and sinus bradycardia (heart rate 56 beats/min) was noted (Lead II) and seemed to periodically decrease to 42 beats/min. (The preoperative electrocardiogram demonstrated normal sinus rhythm, heart rate of 84 beats/min, and left ventricular hypertrophy.) During this episode of bradycardia, blood pressure and cardiac output remained unchanged from previously recorded measurements. Arterial blood gas analysis did not reveal any acid–base or electrolyte abnormality that might explain the presence of bradycardia. After intravenous administration of 0.4 mg atropine, there was only a minimal increase in heart rate (60 beats/min). On admission to the cardiothoracic intensive care unit (33.0°C blood temperature), bradycardia was still present; Osborn waves (J-waves) and a prolonged QT interval were noted on the electrocardiogram (fig. 1A). The Osborn waves disappeared 8 h postoperatively (36.8°C blood temperature; fig. 1B). The electrocardiographic abnormalities associated with hypothermia are Osborn waves, prolonged PR and QT interval, sinus bradycardia, atrial and ventricular dysrhythmias, and shivering artifacts (muscular tremor). Hypothermia induces a difference between epicardial and endocardial potassium channel currents. The Osborn waves represent the electrocardiographic reflection of this transmural voltage gradient. The amplitude and the duration of the Osborn waves are inversely related to body temperature. The Osborn waves can persist 12–24 h after resumption of normothermia. The differential diagnosis of Osborn waves includes hypercalcemia, central nervous system lesions, coronary vasospasm, left ventricular hypertrophy, Brugada syndrome, and drug abuse, and it can appear as a normal variant (early repolarization). As shown in this case, the electrocardiogram provides early and important end-point core organ information regarding the electrophysiologic effect of a potentially lifethreatening degree of hypothermia.

Perioperative myocardial ischemia is associated with an increased risk of perioperative myocardial infarction (PMI). Several attempts have been made to define intraoperative hemodynamic predictors of myocardial ischemia. In a canine preparation with coronary stenosis, a pressure rate quotient (PRQ = mean arterial pressure/heart rate) less than one (PRQ less than 1) indicated subendocardial myocardial ischemia. The authors tested this hypothesis in patients undergoing elective coronary artery bypass graft operation (CABG), using electrocardiogram (ECG) ST-segment changes (leads II/V5) to diagnose myocardial ischemia. Sixty (n = 60) patients having CABG surgery were prospectively studied before initiation of cardiopulmonary bypass. Calibrated ECG leads II and V5 (diagnostic mode) were monitored continuously and recorded with the use of a Hewlett-Packard computer ST-segment analyzer. In addition, arterial and pulmonary artery pressures were monitored. Ischemia was defined as new-onset ST deviation (greater than or equal to 1 mm from the baseline ECG). ECG and hemodynamic data were stored at 2-min intervals for subsequent computer analysis. Serial creatinine phosphokinase (CPK) X MB (%) determinations and 12-lead ECGs were collected for the initial 3 postoperative days. Of the 3,463 intervals (2 min) available for study, 3,322 (96%) were satisfactorily recorded for 60 patients. Ischemia occurred during 65 intervals in 9 patients (9 of 60), of which only 34% (22 of 65) were associated with a PRQ less than 1 (P less than 0.01). In contrast, there were 466 intervals during which PRQ was less than 1, but without ECG evidence of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

The pressure rate quotient (PRQ; mean arterial pressure/heart rate [MAP/HR]) less than one (PRQ1) has been proposed as a simple, clinically available hemodynamic index of myocardial ischemia. Recent investigations using electrocardiography (ECG) detection of myocardial ischemia have not found this index reliable. We prospectively compared PRQ1 to detection of myocardial ischemia via transesophageal echocardiography (TEE) and ECG in patients undergoing elective coronary artery bypass graft.Forty-six of 50 patients admitted into the study had acceptable data acquisition. Calibrated ECG leads II and V5 were recorded with a computerized ST-segment analyzer. Hemodynamic data were stored at 2-min intervals. After tracheal intubation, a 5.0-MHz TEE probe was inserted. Electrocardiography-detected ischemia was defined as new onset ST-segment deviation (or = 1 mm) lasting for1 min. Transesophageal echocardiography determination of ischemia was worsening of wall motionor = 1 grade and lasting1 min. PRQ1 was compared to ECG and/or TEE as a predictor or indicator of myocardial ischemia.Electrocardiography ischemia occurred during 230 intervals in 10 patients, and in only 41 of 230 (18%) was PRQ1. Transesophageal echocardiography-defined ischemia occurred during 592 intervals in 9 patients, and in 119 of 592 (20%) PRQ1. Compared to ECG and TEE, PRQ1 had a low sensitivity (21%) and poor positive predictive value (25%).Pressure rate quotient1 is an unreliable indicator and predictor of myocardial ischemia when evaluated by ECG, TEE, and the combination of these modalities in patients undergoing coronary artery bypass graft surgery.

The effect of halothane on ventricular function in normal children was studied with the aid of echocardiography, which offers a noninvasive method to obtain these measurements safely. Thirteen healthy children ranging in age from 19 months to 12 years (mean=6 years), undergoing elective non-cardiac surgical procedures, were studied. Secobarbital, 4 mg/kg, and morphine, 0.1 mg/ kg, were administered intramuscularly an hour prior to induction of general anesthesia. Echocardiographic measurements were obtained while the patients breathed room air (control) and following nitrous oxide, 60 per cent, and concentrations of halothane ranging from 0.5 to 2 per cent. Increasing inspired concentrations of halothane significantly altered ventricular function in a dosedependent fashion. At halothane, 2 per cent, systolic blood pressure, pulse rate, and cardiac output decreased to 82, 94, and 72 per cent of control values, respectively. Measurements of ventricular performance, ejection fraction (EF), left ventricular enddiaslolic volume (LVEDV), and mean normalized rate of circumferential fiber shortening (Vuf) showed parallel decreases. Following atropine, 0.02 mg/kg, intravenously, improvement in cardiac output and all rate-dependent variables was observed. Although V,.r improved by 18 per cent, other indices of myocardial performance (EF, LVEDV, PEP/LVET) still showed depression. It is concluded that halothane can significantly decrease ventricular function in children undergoing surgical procedures. The accompanying decrease in cardiac output was completely offset by the administration of atropine.

The effect of sodium nitroprusside (SNP) infusion on platelet function was prospectively evaluated in 29 patients undergoing cardiac surgical procedures requiring cardiopulmonary bypass. Any patient receiving preoperative medication known to interfere with platelet function was excluded from this study. Platelet function was evaluated by measurement of platelet aggregation with both adenosine diphosphate (ADP) and epinephrine-induced aggregation tests. Ten patients served as a control population receiving fentanyl anesthesia and no SNP. Nineteen patients received SNP, as clinically indicated, following the induction of anesthesia (and prior to cardiopulmonary bypass) to maintain a mean blood pressure of 80 mmHg. The infusion rate and total dose of SNP delivered was recorded for each patient. Infusion rates of SNP greater than or equal to 3 micrograms.kg.-1 min-1 resulted in a dose-related decrease in platelet aggregation (P less than 0.05). This reduction in platelet function was accompanied by a concomitant increase in bleeding time from 5.8 +/- 0.6 to 9.3 +/- 0.4 min in the patients receiving SNP (P less than 0.05). In addition, with the administration of a total dose of SNP greater than or equal to 16 mg, a significant reduction in platelet aggregation (P less than 0.05) was observed. Platelet aggregation studies and bleeding time performed in the control group (following the administration of fentanyl (30 micrograms/kg) did not reveal any deviation from baseline values. The results from this in vivo study support previous in vitro data demonstrating a detrimental effect upon platelet function following SNP infusion.