Terry W. Latson

Autonomic Reflex Dysfunction in Patients Presenting for Elective Surgery Is Associated with Hypotension after Anesthesia Induction

BackgroundAutonomic reflex dysfunction in patients with diabetes is associated with an increased incidence of hypotension after induction of anesthesia. Whether this finding can be extrapolated to patients with autonomic dysfunction from other causes (e.g., advanced age, hypertension, altered ventricular function) has not been established. MethodsThe authors investigated whether autonomic reflex dysfunction in a more generalized patient group (26 consecutively consenting day-surgery patients older than 39 yr) was similarly associated with the occurrence of hypotension after induction. Preoperatlve tests of autonomic function included: Valsalva maneuver, change in heart rate with forced breathing, change in heart rate and blood pressure with standing, and spectral analysis of heart rate variability. Anesthesia was induced with 3–5 mg/kg thiopental, 2 μg/kg fentanyl, and 60% N2O; 0.1 mg/kg vecuronium was used for paralysis; 0–1.5% isoflurane was added for maintenance of anesthesia after intubation. Noninvasive measurements of mean blood pressure were obtained every minute for 10 min after induction and then every 3 min until skin incision. ResultsTwelve patients developed hypotension (mean blood pressure < 70 mmHg), and 14 patients did not. Measurements of autonomic reflex function were significantly more abnormal in the patients who developed hypotension (P < 0.006 for Valsalva measurements, heart rate variability parameters, and change in heart rate with forced breathing). Using critical test values for autonomic tests, the incidence of hypotension was 67–83% in patients with autonomic nervous system dysfunction versus 9–17% in other patients. ConclusionsThe results document that: (1) some degree of autonomic reflex dysfunction is not uncommon in patients older than 39 yr presenting for elective surgery, and (2) such dysfunction is associated with an increased incidence of hypotension when using the described induction technique.

Effects of three anesthetic induction techniques on heart rate variability

STUDY OBJECTIVE To investigate the effects of different clinical induction techniques on heart rate variability (HRV). DESIGN Two studies are reported. Study 1 prospectively compared the effects of two induction techniques (etomidate vs. thiopental sodium) known to have widely disparate effects on cardiovascular reflexes. Study 2 specifically investigated whether the vagotonic effects of sufentanil cause an increase in vagally mediated HRV. SETTING Elective surgery in a university-affiliated hospital. PATIENTS Study 1: 18 ASA physical status I patients having minor surgery; Study 2: 10 ASA physical status III and IV patients having cardiac surgery. INTERVENTIONS In Study 1, anesthesia was induced with either etomidate 0.3 mg/kg or thiopental sodium 4 mg/kg with 60% nitrous oxide in oxygen. In Study 2, anesthesia was induced with a sufentanil infusion (total dose 2.9 +/- 0.2 micrograms/kg). MEASUREMENTS AND MAIN RESULTS The electrocardiogram-derived heart rate signal was subjected to power spectral analysis (similar to electroencephalographic analysis) to obtain measurements of (1) absolute HRV power [units of (beats per minute)2] within defined frequency ranges (HRVLO = power between 0 and 0.125 Hz; HRVHI = power between 0.126 and 0.5 Hz; HRVTOT = HRVLO + HRVHI) and (2) normalized HRV power (the percentage of total power) within these same frequency ranges [e.g., %HRVHI = (HRVHI/HRVTOT) x 100%]. In Study 1, both techniques caused large reductions in HRVTOT. The reduction caused by the thiopental sodium technique (-89% +/- 2%) significantly exceeded that caused by the etomidate technique (-58% +/- 13%, p less than 0.02). In Study 2, sufentanil decreased absolute power measurements of vagally mediated HRV (-69 +/- 12 change in HRVHI) but increased corresponding normalized measurements of vagally mediated HRV (90% +/- 30% increase in %HRVHI). CONCLUSIONS In Study 1, the greater reduction in HRV with the thiopental sodium technique provides evidence that the depressant effects of anesthetics on HRV are related in part to their effects on cardiovascular reflexes. However, the significant depression in HRV caused by the etomidate technique suggests that mechanisms other than baroreflex depression (e.g., impaired consciousness) also are important in these depressant effects. In Study 2, the decrease in HRVHI caused by sufentanil documents that absolute power measurements of vagally mediated HRV are not correlated with changes in parasympathetic tone during a potent opioid induction. This lack of a correlation may result from the decrease in total HRV observed with loss of consciousness. The increase in %HRVHI suggests that normalized measurements of HRV may still provide an index of changes in sympathetic-parasympathetic balance, even when total HRV is decreased following anesthetic administration.

Ventilation, Thermal Noise, and Errors in Cardiac Output Measurements after Cardiopulmonary Bypass

BackgroundThe authors observed transient increases in the amplitude of respiratory variations in pulmonary artery blood temperature in many patients after cardiopulmonary bypass (CPB). This increased “thermal noise” may significantly influence measurements of thermodilution cardiac outputs (TDCO) performed during this time. MethodsThe authors recorded the peak-to-peak amplitude of respiratory variations in pulmonary artery blood temperature in 15 patients during the first 35 min after CPB. Possible relationships between the amplitude of these variations and the magnitude of temperature differences between commonly monitored body temperature sites (nasopharyngeal, rectal, bladder, and pulmonary artery) were also examined. In ten additional patients, the authors investigated the influence of these increased respiratory variations on TDCO measurements by correlating the maximum variation in three successive TDCO measurements with the peak-to-peak amplitude of the respiratory variations in pulmonary artery blood temperature. Potential error in TDCO measurements caused by these increased respiratory variations in pulmonary artery blood temperature were also examined using model calculations of the effects of respiratory variations in pulmonary artery blood temperature on measured TDCO thermal areas. ResultsIn the first 15 patients, the mean amplitude of respiratory variations in pulmonary artery blood temperature after CPB (mean ± SEM) were: (1) within 5 min after CPB, 0.037 ± 0.004°C; (2) 10 min after #1, 0.025 ± 0.003°C; (3) 20 min after #1, 0.019 ± 0.003°C; and (4) 30 min after #1, 0.012 ± 0.002°C. There were no significant correlations between the magnitude of the respiratory variation in pulmonary artery blood temperature and the observed temperature differences between body sites. Four patients had pulmonary artery blood temperature variations in excess of the maximum amplitude previously reported in man (0.05°C). In the next ten patients, the maximum variation between three successive TDCO measurements taken at specified times in the respiratory cycle (end Inspiration, end exhalation, and 3 s after end exhalation) was significantly correlated with the amplitude of respiratory variations in pulmonary artery blood temperature (r = 0.83, P < 0.001). Four patients with increased respiratory variations in pulmonary artery blood temperature had variations in TDCO measurements exceeding 21/min. Subsequent model calculations demonstrated that the magnitude of potential error in TDCO measurements is dependent on both the amplitude of the respiratory variations in pulmonary artery blood temperature and the baseline cardiac output. On the basis of these thermal area calculations, potential errors of 15–50% could be caused by respiratory variations in pulmonary artery blood temperature > 0.05°C. ConclusionsThe authors concluded that respiratory variations in pulmonary artery blood temperature are transiently increased in many patients after CPB, and that this increased “thermal noise” may cause significant errors in TDCO measurements.

Influence of ketorolac tromethamine on clot elastic strength in humans as assessed by thromboelastography

STUDY OBJECTIVE To evaluate the effect of ketorolac tromethamine on coagulation using thromboelastography (TEG). DESIGN TEGs were performed in each patient before and after ketorolac administration. Each patients predrug results were used as control measurements for comparison with the postdrug results. SETTING Medical center surgical unit. PATIENTS Twenty ASA physical status I and II patients undergoing minor elective surgery; 12 healthy volunteers. INTERVENTIONS TEGs were performed in all subjects before and 60 minutes after the intramuscular (IM) administration of ketorolac tromethamine 60 mg. Ten surgical patients were studied in the intraoperative period, and 10 surgical patients were studied in the postoperative period. The 12 healthy volunteers did not undergo a surgical procedure. MEASUREMENTS AND MAIN RESULTS Specific parameters assessed from the TEGs were reaction time (R time), coagulation time (RK time), clot formation rate (angle of deflection), and maximum clot strength (maximum amplitude of deflection). Ketorolac administration did not cause statistically significant changes in these parameters in any of the three groups studied. CONCLUSIONS IM administration of ketorolac tromethamine 60 mg did not significantly alter the speed of formation or viscoelastic strength of clots as measured by TEG. These results provide additional support for prior clinical studies confirming the safety of ketorolac administration in the perioperative period.

Perioperative measurements of interleukin-6 and α-melanocyte-stimulating hormone in cardiac transplant patients

Interleukin-6 (IL-6) and alpha-melanocyte-stimulating hormone (alpha MSH) are important modulators of the immunologic response to tissue injury and antigenic challenge. Serial changes in the plasma concentrations of these two peptides were measured in 12 patients undergoing heart transplantation. Tissue concentrations of IL-6 in atrial samples from both donor and recipient hearts were also compared. Plasma IL-6 concentration remained stable prior to cardiopulmonary bypass (CPB), initially decreased with the onset of CPB, and then increased significantly over control values at the end of CPB (180 +/- 40 v 53 +/- 60 pg/mL). Plasma IL-6 remained elevated for at least 60 minutes after CPB, and then it returned to control values by 24 hours postoperatively (67 +/- 9 pg/mL). Examination of IL-6 changes after CPB in 10 additional patients undergoing nontransplant cardiac surgery with CPB revealed a similar elevation in IL-6 at 60 minutes after CPB (290 +/- 76 pg/mL). However, IL-6 in the nontransplant group remained significantly elevated at 24 hours (138 +/- 42 pg/mL). These combined results suggest that CPB causes a marked increase in IL-6, and that implantation of a new heart in transplant patients does not augment this increase. The return of IL-6 to control values by 24 hours in the patients who have had transplants suggests that immunosuppression has an appreciable effect on IL-6 at this time. In contrast to IL-6, plasma alpha MSH never increased above control values.(ABSTRACT TRUNCATED AT 250 WORDS)

Changes in plasma atrial natriuretic peptide concentration during heart transplantation

Examination of changes in plasma atrial natriuretic peptide (ANP) concentrations during heart transplantation may provide important information about factors influencing plasma ANP in patients with severe heart failure. Serial changes in plasma ANP during heart transplantation, and atrial content of ANP in native and donor atria, were measured in 12 patients. Preoperative plasma ANP was elevated in all patients (387 +/- 77 pg/mL), whereas atrial content of ANP in native atria was reduced (0.36 +/- 0.082 micrograms/mg protein). Preoperative plasma ANP did not correlate with hemodynamics, but was negatively correlated with creatinine clearance (r = -0.76, P < .01). Intraoperative plasma ANP prior to transplantation was strongly correlated with intraoperative plasma ANP after transplantation (r = 0.84, P < .001). Although postoperative plasma ANP was reduced from preoperative plasma ANP by 75%, these two measurements were also significantly correlated (r = 0.70, P < .02). Postoperative plasma ANP was not correlated with hemodynamics, but was negatively correlated with both creatinine clearance (r = -0.65, P < .05) and content of ANP in the native atria (r = -0.75, P < .01). Multiple linear regression analysis suggested that up to 85% of the variability of early postoperative plasma ANP could be accounted for by the variability in these latter two parameters. The decrease in native atrial ANP content, in the context of elevated plasma ANP concentration, is consistent with prior animal studies suggesting that severe heart failure induces cellular adaptations favoring accelerated ANP synthesis and secretion (with resultant reduction in tissue content).(ABSTRACT TRUNCATED AT 250 WORDS)

Management of the thrombocytopenic cardiac surgical patient - A role for aprotinin?

rophylactic aprotinin therapy reduces blood loss and transfusion requirements in patients with P intact hemostasis undergoing cardiac surgery (1). The mechanism by which aprotinin is able to limit bleeding in this particular clinical setting remains unclear; however, aprotinin appears to retain its beneficial effect in the presence of impaired primary hemostasis (i.e., the platelet defect which occurs after aspirin ingestion) (2). Therefore, the influence of aprotinin on postbypass bleeding may be partially platelet independent. We report the use of aprotinin for coagulopathy prophylaxis in a patient with persistent and refractory thrombocytopenia requiring a complex repeat cardiac surgical procedure. The unique preoperative hematologic management of the patient is reviewed.

Anesthetic Management of a Hypothyroid Cardiac Surgical Patient

lik ANY IMPORTANT anesthetic considerations exist . L ..__ rL.._.,.:rl:,.1 ‘PI____ -L. in a pZtieiii Wiih ~‘ypuulylululsul. :__1..2_. I IlCbC mcl”“~; (1) increased sensitivity to depressant drugs (which may be marked in some patients); (2) a hypodynamic cardiovascular system characterized by decreased heart rate, stroke volume, and cardiac output; (3) decreased oxygen demand; (4) slowed metabolism of drugs, particularly opioids; (5) decreased intravascular fluid volume; (6) impaired ventilatory response to arterial hypoxemia and/or elevation in partial pressure of carbon dioxide; (7) delayed gastric emptying time; (Sj impaired ciearance of free water with resultant hyponatremia; (9) hypothermia; (10) anemia; (11) hypoglycemia; (12) altered neuromuscular excitability, which may interfere with estimation of neuromuscular blockade’; and (13) multiple alterations in the adrenergic nervous system.‘.’ Adrenergic alterations include (1) unresponsive baroreceptor reflexes; (2) primary adrenal insufficiency; (3) decreased sensitivity of p-adrenergic receptors; and (4) decreased number of P-adrenergic receptors. These potential physiological alterations have significant implications regarding patient assessment, use of appropriate invasive monitors in the perioperative period, and selection of both anesthetic and cardioactive drugs. Responses to inotropic drugs may bc influcnced by the accompanying alterations in the adrenergic nervous system. In theory, an inotropic drug that does not denend on --r ---B-receptor interactions for its effects, would be particularly advantageous in these patients. Amrinone, which exerts its inotropic action via phosphodiesterase (PDE) inhibition, may warrant special consideration in these patients. A case is reported of a patient with coronaq artery disease, aortic stenosis, and concomitant hypothyroidism, who was scheduled to undergo coronary artery bypass grafting (CABG) and aortic valve replacement (AVR). The management of a cardiac surgical patient presenting with hypothyroidism is reviewed.

Perioperative measurements of IL-6 and α-melanocyte stimulating hormone in a cardiac transplant patient after ventricular assist device support.

The ventricular assist device (VAD) has been used to support circulation in patients prior to cardiac transplantation. Although the hemodynamic characteristics of VAD have been studied thoroughly, their impact on the patients immune system has not been well documented. VAD require two large-diameter tubes passing transcutaneously through the abdominal wall. Despite vigorous efforts to :maintain sterility at the cannula sites and the use of velour sleeves to allow tissue ingrowth, the risk of infection persists throughout the time an assist pump is used. McBride et al. [1] reported a significant infection rate in patient supported with an external pulsatile VAD. Interleukin-6 (IL-6) is one of the key mediators of the host response to tissue injury and invasion [2]. Induction of IL-6 synthesis is believed to be an early marker of activation of the acute phase response [3]. The a-Melanocyte-stimulating hormone (MSH), a peptide that occurs within the brain, the circulation, and other body sites, is a potent antipyretic agent when given centrally or peripherally [4]. The peptide likewise inhibits inflammation and aspects of the acute phase response [5]. Catania and Lipton [6] suggest that MSH may antagonize the effect of cytokines either directly or indirectly and play an important role in modulation of the acute phase response. Plasma concentrations of IL-6 (pIL-6) and MSH (pMSH) in patients with VAD have not been studied