An unusual cause of carbon dioxide rebreathing in a circle absorber system.
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Adolescent↗
Biomedical subjects
M R Salem
Publications and source records attributed to M R Salem.
Effect of intracoronary infusions of amrinone and dobutamine on segment shortening, blood flow, and oxygen consumption in in situ canine hearts.
Previous in vivo studies assessing the effects of amrinone on myocardial contractility used intravenous infusions, and thus were complicated by varying cardiac loading conditions. Accordingly, the present study was performed in 15 open-chest, anesthetized (fentanyl and midazolam) dogs using infusions of amrinone and dobutamine directly into the left anterior descending artery (LAD). In the LAD bed, percentage of segment shortening (%SS), an index of local myocardial contractility, was assessed with ultrasonic crystals. Coronary blood flow was measured electromagnetically and used to calculate myocardial oxygen consumption and infused drug concentrations. Amrinone and dobutamine were infused separately into the LAD at rates yielding calculated arterial blood concentrations in the clinical range (100, 150, and 200 micrograms/min, and 2.5, 5.0, and 7.5 micrograms/min, respectively). A mixture of amrinone and dobutamine was also infused into LAD and changes in %SS compared with the sum of the their individual effects. In six of the dogs, an extracorporeal system was used to maintain constant coronary blood flow during amrinone infusions. Amrinone and dobutamine caused individually increases in %SS that were comparable (range, 20%-45%). Myocardial oxygen consumption increased in parallel with %SS for both amrinone and dobutamine. For amrinone, coronary blood flow increased more than myocardial oxygen consumption, resulting in a modest (at highest dose approximately 10%) decrease in oxygen extraction; whereas for dobutamine, coronary blood flow increased in proportion to myocardial oxygen consumption, resulting in no change in oxygen extraction.(ABSTRACT TRUNCATED AT 250 WORDS)
Amrinone↗
Effects of hypertonic saline solutions in the coronary circulation.
UNLABELLED: The use of small-volume injections of hypertonic saline solutions (HSS) in resuscitation from hemorrhagic shock is accompanied by well-maintained and pronounced increases in coronary blood flow (CBF) and by increases in myocardial contractility. The present study was performed in open-chest, anesthetized dogs to evaluate the contribution of direct coronary vasodilator and positive inotropic effects of HSS to these therapeutic responses. The left anterior descending coronary artery (LAD) was cannulated and perfused at constant pressure (100 mm Hg) with normal arterial blood. CBF in LAD was measured electromagnetically, and used to calculate myocardial oxygen consumption (MVO2) and coronary arterial plasma osmolality. Percent segmental shortening in LAD bed (% SS) was evaluated with ultrasonic crystals. Measurements were obtained during infusion into LAD of 2.5, 5.0, and 7.5% HSS at 2 ml/min. These HSS solutions yielded calculated plasma osmolalities of 329 +/- 3, 361 +/- 8, and 378 +/- 10 mOsm/kg, respectively. The increases in plasma osmolality by 2.5% HSS were in the therapeutic range, whereas those by 5.0 and 7.5% HSS were supertherapeutic. HSS caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve modest steady-state increases within 2-3 min. The magnitude of the peak and steady-state increases in CBF by HSS correlated to osmolality. The 2.5% HSS had no effect on MVO2 and % SS, whereas the 5.0% and 7.5% HSS increased these variables in an osmolality-dependent manner. CONCLUSIONS: (1) intracoronary infusions of HSS caused modest steady-state coronary vasodilation, (2) Supertherapeutic elevations of plasma osmolality by HSS were required for direct positive inotropic effects, and (3) the present findings suggest that the direct cardiac actions of HSS contribute minimally to the increases in coronary blood flow and myocardial contractility that follow the use of these solutions for resuscitation from hemorrhagic shock.
Animals↗
Right and left ventricular O2 uptake during hemodilution and beta-adrenergic stimulation.
Myocardial O2 uptake (MVO2) and related variables were compared in right and left ventricles (RV and LV, respectively) during isovolemic hemodilution (HD) alone and combined with isoproterenol (Iso) infusion in 13 isoflurane-anesthetized open-chest dogs. Measurements of myocardial blood flow (MBF) obtained with radioactive microspheres were used to calculate MVO2. Lactate extraction (Lacext) was determined. The study consisted of two experimental series: 1) graded HD (dextran) to hematocrit (Hct) of 10% and 2) Iso (0.1 microgram.kg-1.min-1 iv) during moderate HD (Hct = 18 +/- 1%). In series 1, arteriovenous O2 content difference in both ventricles decreased in parallel with reduced arterial O2 content caused by HD, i.e., percent O2 extraction was constant; MVO2 was maintained by proportional increases in MBF. In series 2, Iso during moderate HD raised MVO2 (RV, +156%; LV, +80%). Higher MVO2 was satisfied by combination of increased MBF and O2 extraction in RV and by increased MBF alone in LV. Lacext remained consistent with adequate myocardial O2 delivery throughout study. Conclusions were that 1) both RV and LV tolerated extreme HD (Hct = 10%) because blood flow reserves were sufficient to fully compensate for reduced arterial O2 content; 2) significant cardiac reserve was evident during HD, which could be recruited Iso; and 3) because increase in MVO2 in RV caused by Iso in presence of HD was partially satisfied by increased O2 extraction, the absence of augmented O2 extraction during HD alone was not due to impaired release of O2 from diluted red blood cells.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Use of the self-inflating bulb for detecting esophageal intubation after "esophageal ventilation".
This present investigation tests the efficacy of the self-inflating bulb for detecting esophageal intubation after intentional "esophageal ventilation" to mimic gastric insufflation after bag-and-mask ventilation. In 72 anesthetized patients, the trachea and esophagus were intubated with identical tubes. The efficacy of the bulb was tested by a second anesthesiologist before and after the delivery of three breaths at a tidal volume of 300-350 mL each. The pressures generated by the bulb connected to esophageally placed tubes were measured in 10 patients. In all patients, the second anesthesiologist reported no reinflation of the bulbs when connected to esophageally placed tubes and instantaneous reinflation when connected to tracheally placed tubes, thus correctly identifying the location of each tube. The mean negative pressure generated when compressed bulbs were connected to esophageally placed tubes was 55.4 +/- 1.2 mm Hg before esophageal ventilation and 59.0 +/- 0.68 mm Hg after esophageal ventilation. We conclude that insufflation of the stomach as a result of esophageal ventilation, to the extent demonstrated in this study, does not interfere with the effectiveness of the bulb in differentiating esophageal from tracheal intubation.
Adult↗
Direct effects of propofol on myocardial contractility in in situ canine hearts.
The pronounced decrease in arterial blood pressure evident during anesthetic induction with propofol has raised the possibility that propofol has a direct negative inotropic effect. Previous attempts to evaluate this mechanism in vivo have been inconclusive because of confounding variables associated with intravenous administration of propofol. Accordingly, in the current study, steady-state changes in myocardial contractility and related hemodynamic parameters were assessed during intracoronary infusions of propofol in seven open-chest dogs anesthetized with fentanyl and midazolam. The left anterior descending coronary artery (LAD) was cannulated and perfused at controlled pressure (100 mmHg) with normal arterial blood. In LAD-perfused myocardium, contractility was evaluated from measurements of percent segmental shortening (%SS) obtained with ultrasonic crystals. Coronary blood flow in LAD was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2; Fick principle) and coronary propofol concentration. Propofol was infused into the LAD at 150, 300, 600, and 1,200 micrograms/min (P-150, P-300, P-600, P-1,200). These infusion rates yielded calculated blood concentrations of 7 +/- 1, 15 +/- 1, 26 +/- 2, and 50 +/- 5 micrograms.ml-1, respectively. The calculated blood concentrations at P-150 were in the clinical range, whereas those at P-300, P-600, and P-1,200 were supratherapeutic. P-150 had no effect on %SS, whereas higher infusion rates caused decreases in %SS. Changes in MVO2 by propofol generally paralleled changes in %SS. At P-150 and P-300, coronary blood flow was proportional to MVO2, whereas at P-600 and P-1,200, coronary blood flow was in excess of the prevailing MVO2, resulting in increased coronary venous oxygen tension.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Oxygen extraction ratio: a valid indicator of transfusion need in limited coronary vascular reserve?
We have described whole body oxygen (O2) extraction ratio (ER) as a reliable indicator of transfusion need in acute normovolemic anemia. In normal hearts, myocardial lactate production (-LACT), indicating anaerobic metabolism, does not occur until the ER greater than 50% and Hct less than 10%. It is not known if the ER is valid in the setting of limited coronary vascular reserve. This study assesses the effect of a critical left anterior descending (LAD) coronary stenosis on the compensation to acute blood loss anemia. Adult dogs were anesthetized, paralyzed, and mechanically ventilated. A critical LAD stenosis was created in seven animals (STEN). There were seven controls (CON). Animals underwent isovolemic exchange transfusion with 6% HES until cardiac failure (CF). Catheters were placed in the aorta, pulmonary artery, and anterior interventricular coronary vein. Cardiac failure occurred at Hct = 8.6% +/- 0.4% in the CON and 17.0% +/- 0.5% in the STEN animals. Cardiac output increased in the CON, but not in the STEN animals. Blood flow in the LAD increased in the CON but not the STEN animals. -LACT began in the CON and STEN animals at Hct less than 20% and coincided with an ER greater than 50% in both groups. We conclude that CF occurs at a higher hematocrit with a critical LAD stenosis. The whole body ER greater than 50% remains a valid indicator of myocardial metabolism in anemia in the presence of limited coronary vascular reserve. The ER may be a useful guide to transfusion therapy.
Anemia↗
Phenylephrine does not limit myocardial blood flow or oxygen delivery during isoflurane-induced hypotension in dogs.
Experiments were performed on seven fentanyl-pentobarbital-anesthetized, open-chest dogs to determine whether stimulation of coronary alpha 1-adrenergic receptors by phenylephrine causes coronary vasoconstriction and impaired myocardial oxygen delivery when phenylephrine is infused to correct isoflurane-induced hypotension. Myocardial blood flow was measured with radioactive microspheres, and myocardial oxygen and lactate extraction were determined. The Fick equation was used to calculate myocardial oxygen consumption. Measurements were obtained (a) under control conditions, (b) after a 30-min inhalation of isoflurane sufficient to decrease mean aortic pressure by 30%, and (c) while maintaining administration of isoflurane, 5-10 min after restoration of mean aortic pressure by intravenous infusion of phenylephrine. Isoflurane-induced hypotension was accompanied by a baroreceptor-mediated increase in heart rate and by a decrease in myocardial oxygen consumption; however, myocardial blood flow was maintained, resulting in decreased oxygen extraction and increased coronary sinus PO2, thus implying a direct coronary vasodilating effect for isoflurane. Lactate extraction was unaffected. Phenylephrine infusion during inhalation of isoflurane returned mean aortic pressure and heart rate to their respective control values, and it did not change myocardial oxygen consumption, myocardial blood flow, myocardial oxygen extraction, coronary sinus PO2, or lactate extraction from values obtained during isoflurane alone. These latter findings are consistent with undiminished coronary vasodilation by isoflurane in the presence of phenylephrine. In conclusion, infused phenylephrine to restore aortic pressure during isoflurane administration had no vasoconstrictor effect in the coronary circulation and did not impair myocardial oxygen delivery. Apparently, the direct coronary vasodilating action of isoflurane completely nullified phenylephrine-induced vasoconstriction via local alpha 1-adrenergic receptors.
Animals↗
Hemodynamic responses to pancuronium and vecuronium during high-dose fentanyl anesthesia for coronary artery bypass grafting.
The hemodynamic and electrocardiographic (ECG) effects of pancuronium and vecuronium were compared during high-dose fentanyl anesthesia for coronary artery bypass grafting (CABG) surgery. Forty-eight morphine-scopolamine premedicated patients scheduled for elective CABG were anesthetized with fentanyl (100 micrograms/kg) in divided doses, and either of two muscle relaxants, pancuronium (n = 26; 0.10 mg/kg) or vecuronium (n = 22; 0.09 mg/kg). Hemodynamic data, blood gas samples, and ECG tracings were obtained at the following intervals: (1) control; (2) prior to intubation; (3) 1 minute after intubation; (4) prior to sternotomy; and (5) 1 minute after sternotomy. In the pancuronium group, heart rate (HR), cardiac index (CI), and rate-pressure product (RPP) were increased after induction of anesthesia and following intubation. Eleven patients (42.3%) displayed ischemic ST segment changes. Four patients in this group developed tachycardia and hypertension to an extent requiring pharmacological intervention. Vecuronium-treated patients displayed no increases in HR, MAP, and RPP, and a decrease in CI. Only one patient (5.6%) developed evidence of ischemic ECG changes. Four patients in the vecuronium group, all receiving preoperative beta-blocker therapy, became hypotensive and bradycardic after the induction of anesthesia. The present investigation confirms the increased incidence of myocardial ischemia during high-dose fentanyl-pancuronium anesthesia. Although vecuronium was associated with fewer myocardial ischemic changes, the occurrence of bradycardia and hypotension in some patients receiving preoperative beta-adrenergic blocking drugs remains a concern.
Anesthesia, Intravenous↗
Intracoronary isoflurane causes marked vasodilation in canine hearts.
Previous studies of coronary vasomotor effects of isoflurane were complicated by changes in systemic hemodynamic conditions and in global cardiac work demands. Accordingly, in the current study, the left anterior descending coronary artery (LAD) of 11 open-chest dogs anesthetized with fentanyl and pentobarbital was cannulated and perfused with isoflurane-free arterial blood or with arterial blood equilibrated in an extracorporeal oxygenator with isoflurane (0.5, 1.0, 2.0% in 95.5% oxygen-4.5% carbon dioxide). Steady-state changes in coronary blood flow (CBF) in LAD were measured electromagnetically, and their transmural distribution (endocardium: epicardium ratio) was evaluated with 15-microns radioactive microspheres. Venous blood was obtained from the anterior interventricular vein and analyzed for oxygen tension (PO2) and oxygen content. Myocardial oxygen consumption (MVO2) was calculated using the Fick equation. Cardiac responses during isoflurane were compared to those during maximal vasodilation with intracoronary adenosine. Perfusion pressure was maintained at 100 mmHg. CBF increased 271, 279, and 503% with 0.5, 1.0, and 2.0% isoflurane, respectively, with no change in the endocardium:epicardium ratio. With 2.0% isoflurane, the increase in CBF was 80% of the maximal, adenosine-induced response. The increases in CBF caused by isoflurane were accompanied by greater than proportional increases in venous PO2 and decreases in the arteriovenous oxygen difference, reflecting the reduction (approximately 40% in MVO2. In conclusion, isoflurane has a direct, concentration-dependent relaxing effect on coronary vascular smooth muscle in the canine heart in situ. The ability of isoflurane to increase CBF nearly maximally while also significantly reducing local myocardial oxygen requirements attests to the potency of isoflurane's direct vasodilator action.
Adenosine↗
Positive end-expiratory pressure increases intraocular pressure in cats.
BACKGROUND AND METHODS: The purpose of the present study was to examine the effect of various levels of positive end-expiratory pressure on intraocular pressure in cats. Fourteen healthy adult cats (2.6 to 3.7 kg) without evidence of ocular disease were anesthetized with pentobarbital, paralyzed, and placed on mechanical ventilation. Direct continuous measurements of heart rate (HR), mean arterial pressure (MAP), CVP, CSF pressure, and intraocular pressure were recorded at zero end-expiratory pressure, and at 5, 10, and 15 cm H2O positive end-expiratory pressure, applied in random order. MAIN RESULTS: There were no significant changes in pHa, Paco2, HR, MAP, hematocrit, and temperature. Intraocular pressure increased significantly from 17 (during zero end-expiratory pressure) to 20 mm Hg at 10 cm H2O positive end-expiratory pressure; at 15 cm H2O positive end-expiratory pressure, intraocular pressure increased significantly to 21 mm Hg. CVP and CSF pressure increased significantly in parallel with intraocular pressure at 5, 10, and 15 cm H2O positive end-expiratory pressure. CONCLUSIONS: We speculate that similar responses occur in man, and may be undesirable in patients with already increased intraocular pressure, when higher levels of positive end-expiratory pressure are used.
Animals↗
Myocardial and systemic hemodynamics during isovolemic hemodilution alone and combined with nitroprusside-induced controlled hypotension.
Myocardial and systemic effects of isovolemic hemodilution alone and combined with controlled hypotension induced with sodium nitroprusside (SNP) were studied in halothane-anesthetized, open-chest dogs. Regional blood flow was measured with radioactive microspheres and used to compute regional oxygen (O2) supply. Values for regional blood flow in myocardium were used to compute myocardial O2 (MVO2) and lactate uptake (MVLAC) using the Fick equation. Hemodilution to hematocrit 50% of baseline increased aortic blood flow and decreased systemic vascular resistance, although other systemic hemodynamic values were not changed. Twofold increases in myocardial blood flow were accompanied by no change in MVO2, MVLAC, or coronary sinus PO2. Hemodilution increased regional blood flow sufficiently in the pancreas, liver, duodenum, skeletal muscle, skin, and brain to preserve O2 supply whereas unchanged blood flow in the spleen and kidney reduced O2 supply. Under hemodilution, 15 min of intravenous SNP sufficient to reduce mean arterial pressure by 50% caused parallel reductions in aortic blood flow, dP/dt max, and left ventricular end-diastolic pressure; systemic vascular resistance was unaffected. Myocardial blood flow and MVO2 decreased proportionally, whereas MVLAC and coronary sinus PO2 did not change. Regional blood flow and O2 supply decreased in the kidney, spleen, liver, and skin. Extending SNP infusion to 60 min increased myocardial blood flow and MVO2, but other hemodynamic values were unchanged. Comparing previous results with adenosine-induced hypotension inferred that coronary vasodilator reserve was greatly reduced at this time. In conclusion, although myocardial O2 supply versus demand balance was well maintained during SNP-induced hypotension under hemodiluted conditions, diminished coronary vasodilator reserve suggests increased vulnerability to ischemia if stresses of augmented cardiac work demand or impaired arterial oxygenation were superimposed. The decrease in O2 supply in the kidney during combined hemodilution and SNP-induced hypotension also warrants concern. These latter findings suggest the need for extensive clinical monitoring when SNP is used for controlled hypotension under hemodiluted conditions.
Analysis of Variance↗
Hemodynamic responses to endotracheal extubation after coronary artery bypass grafting.
After coronary artery bypass grafting (CABG) surgery, patients may remain at risk for myocardial ischemia and infarction and ventricular dysrhythmias. The hemodynamic responses to endotracheal extubation and the efficacy of intravenous lidocaine pretreatment were studied after CABG surgery and overnight mechanical ventilation. Twenty-five patients were divided into two groups: group 1 (n = 13) patients who had tracheal extubation after pretreatment with a placebo; group 2 patients who received lidocaine (1 mg/kg IV) before tracheal extubation. Hemodynamic data, electrocardiographic tracings, and arterial blood gases were obtained before tracheal extubation, during suctioning, and 1, 5, and 20 min after tracheal extubation. Group 1 patients displayed significant increases in heart rate, arterial blood pressure, rate-pressure product, right atrial pressure, and cardiac index during suctioning and within 1 min of tracheal extubation, returning to preextubation level by 5 min. There were no significant changes in pulmonary and systemic resistance indices. Hemodynamic changes in group 2 patients were similar to those in group 1. Both in the absence and presence of lidocaine, tracheal extubation caused hemodynamic responses that were small in magnitude and brief in duration. These responses were not associated with electrocardiographic or enzymatic evidence of myocardial ischemia or infarction, or with ventricular dysrhythmias. Compared with the well-documented hemodynamic responses to tracheal intubation, we found that extubation of the trachea after CABG surgery was associated with less pronounced responses. This may be related to avoidance of laryngoscopy and possibly accommodation to the endo-tracheal tube. These modest hemodynamic responses of extubation of the trachea after CABG surgery were not modified by intravenous lidocaine.
Coronary Artery Bypass↗
Contrast media adversely affect oxyhemoglobin dissociation.
Effects of ionic (Hypaque-76) and nonionic (Isovue-370 and Omnipaque-350) contrast media on oxyhemoglobin dissociation of normal human red blood cells were evaluated. In series 1, 4-mL venous blood samples were obtained from 15 normal human volunteers. One blood sample served as control, and 1 mL of either of the three contrast media was added in vitro to the other 4-mL blood samples. P50 values were estimated from the linear portion of the oxyhemoglobin dissociation curve obtained by tonometry. Determinations of P50 were performed at either pH 7.4 or 7.2. At pH 7.4, P50 in the absence of contrast media was 26.3 +/- 0.4 mm Hg (mean +/- SEM). The contrast media caused comparable decreases in P50 from this value (Hypaque-76, 20.0 +/- 0.5 mm Hg; Omnipaque-350, 21.6 +/- 0.4 mm Hg; Isovue-370, 20.7 +/- 0.4 mm Hg). Reducing pH to 7.2 in the absence of contrast media increased P50 to 33.3 +/- 1.0 mm Hg, evidence of the Bohr effect. The presence of contrast media either completely abolished (Hypaque-76 and Omnipaque-350) or markedly attenuated (Isovue-370) this effect. In series 2 (five patients), blood samples were withdrawn from the external iliac artery during injection of Isovue-370 (60-78 mL) into the proximal abdominal aorta to evaluate peripheral vascular disease. Measurement of P50 of these samples yielded findings consistent with those of series 1. The present findings demonstrate that both ionic and nonionic contrast media increase the affinity of hemoglobin for oxygen and, therefore, that they may inhibit oxygen delivery to body tissues.
Angiography↗
Blood volume and hematocrit in regional circulations during isovolemic hemodilution in dogs.
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Animals↗
Myocardial and systemic responses to arterial hypoxemia during cardiac tamponade.
Experiments were performed on 14 anesthetized, open-chest dogs to assess myocardial and systemic responses to cardiac tamponade alone (TAMP) and combined with arterial hypoxemia (HYP). Regional blood flow (RBF) was measured with radioactive microspheres and used to compute regional O2 supply. Myocardial oxygen and lactate extraction were determined. Myocardial oxygen consumption (MVO2) was calculated with Fick equation. An increase in pericardial pressure, sufficient to reduce mean aortic pressure (MAP) by 20%, caused proportional decreases in myocardial RBF and MVO2 but had no effect on endo-to-epi flow ratio or on myocardial lactate extraction. TAMP alone decreased RBF and O2 supply in kidney, splanchnic organs, skeletal muscle, and skin, but it had no effect in brain. HYP (arterial PO2, 35 +/- 2 mmHg) during TAMP restored MAP and caused transmurally uniform increases in myocardial RBF that were adequate to maintain MVO2 and lactate extraction. RBF increased sufficiently in brain to maintain regional O2 supply, whereas unchanged or inadequate increases in RBF in other tissues accentuated reductions in O2 supply. During combined TAMP and HYP, local vasodilator mechanisms were capable of maintaining adequate oxygen supply in myocardium and brain but not apparently in the nonvital tissues where these mechanisms were antagonized by reflex vasoconstriction.
Animals↗
Hypercapnia, hypocapnia and hypoxemia.
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Anesthesia↗
An unusual foreign body in the left main bronchus after open heart surgery.
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Adult↗