Barbara W. Palmisano

Transcutaneous PCO2 and PO2: a multicenter study of accuracy.

A multicentcr study used 756 samples from 251 patients in 12 institutions to compare arterial (PaO2, PaCO2) with transcutaneous (PsO2, PsCO2) oxygen and carbon dioxide tensions, measured usually at 44°C. Of these samples, 336 were obtained from 116 neonates, 27 from 25 children with cystic fibrosis, and 140 from 40 patients under general anesthesia. Ninety-one patients were between 4 weeks and 18 years of age, 32 were between 18 and 60 years, and 12 were over 60. The ratio of transcutaneous to arterial P(s/a)CO2 was 1.01 ±0.11 with PaCO2 less than 30 mm Hg, increasing to 1.04 ±0.08 at PaCO2 greater than 40 mm Hg. Mean bias and its standard deviation (PsCO2 — PaCO2) were + 1.3 ± 3.9 mm Hg in the entire group, + 1.8 ± 4.2 mm Hg in neonates (NS). Bias was +0.2 ± 2.7 mm Hg when PaCO2 was less than 30 mm Hg (N = 175, NS), 1.0 ± 3.4 with 30 < PaCO2 < 40 (n = 329,p < 0.001), and +2.04 ± 4.00 mm Hg with 40 < PaCO2 < 70 (n = 229,p < 0.001). These data suggest that, using transcutaneous PCO2 monitors with inbuilt temperature correction of 4.5%/‡C, the skin metabolic offset should be set to 6 mm Hg. The linear regression was PsCO2 =1.052(PaCO2)-0.56, Sy·x = 3.92, R = 0.929 (n = 756); and PsCO2 = 1.09(PaCO2)-1.57, Sy·x = 4.17, R = 0.928 in neonates (n = 336). The use of vasopressors and vasodilators had no significant effect on bias or its standard deviation or on regression slope and intercept (n = 78). In cystic fibrosis patients, bias and standard deviation were 0.0 ± 1.7 mm Hg (n = 27). Under anesthesia, PsCO2 = 1.07PaCO2-1.58, with bias and standard deviation = 0.6 ± 3.5 (n = 140). For oxygen, at PaO2 ≤ 80 the ratio P(s/a)O2 = 1.05 ± 0.16 in nconates and 0.93 ± 0.21 in older patients, but when PaO2 > 80, P(s/a)O2 fell to 0.88 ± 0.18 in neonates and 0.74 ± 0.21 in older patients. The errors were significantly greater (p < 0.001) in older patients than in neonates above but not below 80 mm Hg, and within both groups errors were significantly greater above than below 80 mm Hg.

Direct Myocardial Effects of Halothane and Isoflurane: Comparison between Adult and Infant Rabbits

Background:Infants may be more sensitive than adults to myocardial depression by potent inhalation anesthetics. Most studies of cardiovascular effects of inhalation agents in infants are performed in vivo with multiple factors producing the observed effects. The purpose of this study was to determine if newborns are more sensitive than adults to the direct actions of halothane and isoflurane on global electrophysiologic, contractile and metabolic functions of the heart. Methods:Direct myocardial effects of the agents were determined using isolated rabbit hearts perfused at constant pressure. Three doses of halothane and isoflurane were administered to 37 Infant (3-8 days old) and 36 adult rabbit hearts. Heart rate and rhythm, atrioventricular conduction time, left ventricular function (systolic, diastolic, and developed pressures; maximum and minimum values of the differential wave (dP/dt); and time constant of isovolumic LV relaxation), coronary flow and O2 consumption, and fractional O2 extraction were measured and compared between age and anesthetic groups. Results:Halothane was a more potent depressant of cardiac function than isoflurane and developmental differences were more evident with this agent. The most striking developmental differences in anesthetic effects were the significantly greater prolongation of atrioventricular conduction time and the time constant of isovolumic LV relaxation by halothane in infant compared with adult hearts. Infant hearts were also more sensitive to depression of left ventricular developed pressure and maximum value of the differential wave and to elevation of diastolic pressure by halothane. For both agents heart rate was less depressed in infants than in adults. There were no developmental differences in anesthetic effects on coronary flow and O2 metabolism. Conclusions:Developmental changes in myocardial physiology make the newborn less sensitive to direct depression of heart rate by halothane and isoflurane, but more sensitive to depression of contraction-relaxation and atrioventricular conduction by halothane.

Development of Baroreflex Control of Heart Rate in Swine

ABSTRACT: The purpose of this study is to describe the developmental course of arterial baroreflex control of heart rate in swine. Tests of baroreflex function were performed with eight conscious piglets serially over their first 2 mo of life. Systemic blood pressure was raised with phenylephrine (pressor test) and lowered with nitroprusside (depressor test), and stimulus-response curves relating heart rate to mean blood pressure were constructed. Baroreflex sensitivity was determined as the slope of the linear portion of the curve. Baroreflex sensitivity decreased with increasing age. Baroreflex sensitivity was not different between pressor and depressor tests except when the piglets were >52 d old and sensitivity was greater with the depressor test. The heart rates at threshold and saturation, and therefore the heart rate response range, shifted to lower heart rates with increasing age. This shift was more than can be accounted for by the simultaneously decreasing resting heart rate.

Dose-response for Atropine and Heart Rate in Infants and Children Anesthetized with Halothane and Nitrous Oxide

The dose recommendations for atropine in anesthetized children vary, and the dose-response for heart rate has not been defined. We determined the dose-response for atropine and heart rate in 181 healthy children anesthetized with halothane and nitrous oxide. After induction of anesthesia, atropine in a dose of 5, 10, 20, 30, or 40 micrograms.kg-1 was administered by rapid intravenous infusion of each subject. The effects of atropine on heart rate, heart rhythm, and systolic blood pressure were compared among dosage groups, and a dose-response curve for peak heart rate was constructed. The effects of atropine were compared also between younger and older subjects. For the group of all 181 subjects, atropine increased heart rate in a dose-related manner up to 30 micrograms.kg-1. Fifty percent maximal response corresponded to 9 micrograms.kg-1, and 90% maximal response corresponded to 26 micrograms.kg-1. Some subjects had nonsinus supraventricular rhythms before atropine, but none had nonsinus rhythm after atropine except after the smallest dose, 5 micrograms.kg-1. Systolic blood pressure increased significantly after all doses of atropine except 5 mu.kg-1. Subjects less than 6 months old had higher control and peak heart rates than did subjects greater than or equal to 2 yr old, but the older subjects had greater change in heart rate after atropine. For subjects greater than or equal to 2 yr old, all doses of atropine produced a significant increase in heart rate. The same was true for younger subjects, less than 6 months old, except that 5 micrograms.kg-1 did not increase heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

The Effect of Paralysis on Oxygen Consumption in Normoxic Children after Cardiac Surgery

To determine whether paralysis reduces oxygen consumption (VO2) after cardiac surgery in infants, the authors measured VO2 before and after paralysis in 17 sedated infants who were ventilated mechanically after cardiac surgery. Oxygen consumption was determined as being the difference between oxygen content of inspired and expired gases. The absence or presence of “movement” (breathing or repeated movement of the extremities) before paralysis was noted. For eight infants who did not “move” before paralysis, VO2 was similar before (9.1 ± 1.2 ml · kg-1 · min-1, mean ± SD) and after (9.0 ± 1.5 ml · kg-1 · min-1) paralysis (P = 0.81). However, for nine infants who did “move” before paralysis, VO2 decreased from 9.2 ± 1.4 ml · kg-1 · min-1 before paralysis to 8.0 ± 1.4 ml · kg-1 · min-1 after paralysis (P < 0.05). One infant in each group had an increase in VO2 greater than 10% of the baseline value (i.e., 12% and 14%). In conclusion, if breathing or repeated movement is present before paralysis, paralysis decreases VO2 by 13% in sedated infants after cardiac surgery. If repeated or regular movement is not present before paralysis, paralysis does not decrease VO2. These data suggest that in normoxic patients, muscle paralysis does not significantly alter VO2 and therefore should not be used for this purpose.

Depression of baroreflex control of heart rate by halothane in growing piglets

The purpose this study was to examine the effects of halothane on baroreflex control of heart rate in developing swine. Serial tests of baroreflex function were performed over the first 2 months of life in eight piglets in the conscious state and during anesthesia with 0.45, 0.9, and 1.35% halothane. Systemic blood pressure was increased with phenylephrine (pressor test) and decreased with nitroprusside (depressor test), and stimulus-response curves relating mean blood pressure to heart rate were constructed. Baroreflex sensitivity was determined as the slope of the linear portion of the curve. Halothane markedly depressed baroreflex sensitivity at all ages in a dose-dependent manner (conscious greater than 0.45% greater than 0.9%, 1.35%). Increasing age was accompanied by decreasing baroreflex sensitivity in both the conscious and the anesthetized states. The difference in baroreflex sensitivity between conscious and anesthetized states did not change with age for the depressor test (tachycardia response), but it did change with age for the pressor test (bradycardia response). For this test, conscious values converged toward anesthetized values at higher ages; therefore, there was relatively less depression by halothane at older ages. Halothane also decreased resting heart rate and decreased the limits and narrowed the range of the baroreflex heart rate response. Increasing age was accompanied by a decreasing resting heart rate and by decreasing limits and a narrowing range of the baroreflex response. The effect of halothane on heart rate variables was similar at all ages. Halothane decreased resting blood pressure and decreased the lower limit and widened the span of the baroreflex blood pressure range.(ABSTRACT TRUNCATED AT 250 WORDS)

Improvement in functional recovery of the isolated guinea pig heart after hyperkalemic reperfusion with adenosine

The aim of this study was to examine the effect of initial hyperkalemic reperfusion (HKR), with and without added adenosine, on coronary flow, myocardial function, and endothelium-dependent and endothelium-independent coronary vascular function. Cardioplegic arrest was induced in 40 isolated guinea pig hearts by infusing oxygenated cardioplegic (high in potassium ion) Krebs solution for 5 minutes. Hearts were then stored at room temperature for 3.5 hours. On reperfusion, hearts were divided into four groups of 10 hearts each: control, reperfusion with regular Krebs solution (4.6 mmol/L potassium chloride); base hyperkalemic reperfusion, initial reperfusion with 37 degrees C oxygenated, cardioplegic Krebs solution for 5 minutes; hyperkalemic reperfusion with addition of 1 mmol/L adenosine during HKR; and hyperkalemic reperfusion with addition of 5 mmol/L adenosine. Coronary reserve (adenosine bolus 2 mmol/L) and responses to acetylcholine (1 mumol/L) and nitroprusside (100 mumol/L) were examined before and after ischemia and reperfusion. Flow did not return to preischemic values in any group after reperfusion. Adenosine treatment during initial reperfusion increased coronary flow (percentage of baseline +/- standard error of the mean) from 57% +/- 4% in control and 45% +/- 3% in hearts with hyperkalemic reperfusion to 79% +/- 3% and 83% +/- 5% in hearts with hyperkalemic reperfusion also treated with, respectively, 1 mmol/L adenosine and 5 mmol/L adenosine (p < 0.05). At 30 and 60 minutes of reperfusion, however, flow remained elevated only in the group treated with 5 mmol/L adenosine. Coronary reserve and responses to acetylcholine and nitroprusside were equivalently depressed in all groups after reperfusion. Recovery of left ventricular systolic and diastolic function was improved in all groups after hyperkalemic reperfusion (54% +/- 4% of preischemic value) compared with control (39% +/- 3%), and recovery was further enhanced in the group treated with 5 mmol/L adenosine (60% +/- 4%). In this ex vivo model, hyperkalemic reperfusion improved myocardial function after cardioplegic arrest and the addition of 5 mmol/L adenosine improved coronary flow. Adenosine may counteract the potassium chloride-induced vasoconstriction that occurs during hyperkalemic reperfusion and may thus improve coronary flow and myocardial function. Postischemic depression of endothelium-dependent or endothelium-independent vascular functions, however, was not alleviated by hyperkalemic reperfusion with or without adenosine.

Effects of l-Arginine and Nω-Nitro-l-Arginine Methyl Ester on Cardiac Perfusion and Function After 1-Day Cold Preservation of Isolated Hearts

BACKGROUND Coronary flow responses to endothelium-dependent (acetylcholine [ACh] or 5-hydroxytryptamine [5-HT]) and endothelium-independent (adenosine [ADE] or nitroprusside [NP]) vasodilators may be altered before and after 1-day hypothermia during the perfusion of arginine vasopressin (AVP), D-arginine (D-ARG), L-arginine (L-ARG), or nitro-L-arginine methyl ester (L-NAME). METHODS AND RESULTS Four groups of guinea pig hearts (37.5 degrees C [warm]) were perfused for 6 hours with AVP, L-ARG, L-NAME, or nothing (control). Five heart groups (cold) were perfused with AVP, D-ARG, L-ARG, L-NAME, or nothing (control), but after 2 hours they were perfused at low flow for 22 hours at 3.7 degrees C and again for 3 hours at 37.5 degrees C. ADE, butanedione monoxime, and NP were given for cardioprotection before, during, and after hypothermia. In warm groups, L-ARG did not alter basal flow or ADE, ACh, 5-HT, or NP responses, whereas L-NAME and AVP reduced basal flow and the ADE response, abolished ACh and 5-HT responses, and increased the NP response. In cold groups after hypothermia. L-ARG did not alter basal flow, but L-NAME, AVP, D-ARG, and control reduced flow. In the postcold L-ARG group, ACh increased peak flow, but NP did not increase flow in other cold groups. Effluent L-ARG and L-CIT in the cold control group fell from 64 +/- 9 and 9 +/- 1 micrograms/L at 1 hour to 36 +/- 5 and 5 +/- 1 micrograms/L at 25 hours, respectively. Left ventricular pressure and cardiac efficiency improved more in the postcold L-ARG group than in the postcold D-ARG, AVP, and L-NAME groups. CONCLUSIONS Endogenous effluent levels of L-ARG and L-CIT decrease after 24 hours in isolated hearts, whereas perfusion of L-ARG improves cardiac performance, basal coronary flow, and vasodilator responses. In contrast, L-NAME, L-ARG, and AVP limit flow and performance but maintain a partial vasodilatory response to NP. Sustained release of NO may account for improved performance after L-ARG after hypothermia.

Direct effects of halothane and isoflurane in infant rabbit hearts with right ventricular hypertrophy secondary to chronic hypoxemia

In this study we compared the direct myocardial effects of halothane and isoflurane between chronically hypoxemic and normoxemic infant hearts with an isolated, perfused, nonworking rabbit heart model.Anesthetic effects were measured on heart rate, atrioventricular time, coronary flow, O2 consumption and extraction, and left and right ventricular peak systolic and end-diastolic pressures, + and -dP/dtmax; and tau, the time constant of isovolumic relaxation. Control values were similar between chronically hypoxemic and normoxemic groups except for variables affected by right ventricular (RV) hypertrophy in chronically hypoxemic hearts. For these variables values were significantly larger in the chronically hypoxemic group (P <or=to 0.05): coronary flow (12.3 +/- 0.4 vs 10.3 +/- 0.3 mL centered dot min-1 centered dot g-1), RV peak systolic pressure (68 +/- 3 vs 53 +/- 4 mm Hg), RV + dP/dtmax (1.42 +/- 0.07 vs 1.03 +/- 0.08 mm Hg/ms), and RV - dP/dtmax (-0.99 +/- 0.04 vs -0.78 +/- 0.08 mm Hg/ms). (Values are mean +/- SEM.) With anesthesia, values were similar between chronically hypoxemic and normoxemic groups except for coronary flow, which was significantly greater in chronically hypoxemic hearts for both anesthetics (14.1 +/- 0.9 vs 11.3 +/- 0.7 mL centered dot min-1 centered dot g-1 for halothane and 15.4 +/- 1.1 vs 12.2 +/- 0.6 mL centered dot min-1 centered dot g-1 for isoflurane). The degree of depression of RV peak systolic pressure and RV + dP/dt (max) by both anesthetics, and of RV -dP/dtmax by isoflurane, was significantly larger in chronically hypoxemic hearts because these hearts had greater control values but similar anesthetic values to normoxemic hearts. In this model, indices of myocardial function when the hearts were exposed to halothane and isoflurane were similar between chronically hypoxemic and normoxemic hearts except for coronary flow, which was greater in the chronically hypoxemic hearts. (Anesth Analg 1995;80:1122-8)

Coronary Flow Response to Vasodilators in Isolated Hearts Cold Perfused for One Day with Butanedione Monoxime

Objectives Impaired tissue reperfusion may be an important limiting factor for long-term hypothermic cardiac preservation. Cardiac function and recovery of coronary responses to endothelium independent and dependent vasodilators were tested before and after one day of preservation by cold perfusion with a normal extracellular solution containing the contraction uncoupler 2,3, butanedione monoxime (BDM) with or without reperfusion with nitroprusside (NP) plus adenosine (Ade) or plus the nucleoside transport inhibitor, nitrobenzylthioinosine (NBTI).Methods Guinea pig hearts (n = 70) were isolated and perfused at constant pressure during normothermic conditions (37°C). Groups 1 and 2 were perfused for 8 hrs without cold perfusion (time control); group 2 was also infused with arginine vasopressin (AVP) for 6 hrs; groups 3–5 were infused with BDM before, during, and initially after 22 hrs of constant, low flow hypothermic (3.8°C) perfusion; group 3 was also infused with NP and Ade, and group 4 with NP and NBTI...