Investigations into the mechanisms of coronary vasodilation by contrast media in dogs.

RATIONALE AND OBJECTIVES: The study was performed to clarify the mechanisms underlying contrast-induced coronary vasodilation. METHODS: The left anterior descending coronary artery of 14 open-chest dogs was perfused at constant pressure. Coronary blood flow (CBF) was measured electromagnetically and used to calculate myocardial oxygen consumption (MVO2). Responses were evaluated during intracoronary infusions (2 mL/ minute) of the ionic contrast medium, Hypaque-76, and the nonionic contrast medium, Isovue-370, and compared with those caused by hypertonic saline solutions with comparable osmolarities. Studies also were conducted using Isovist-300, which is a new nonionic and iso-osmolar contrast medium. RESULTS: Hypaque-76 and Isovue-370 caused initial peak increases in CBF (reflecting decreases in coronary vascular resistance), which waned rapidly to achieve more modest steady-state increases within 2 to 3 minutes. Both the peak and steady-state increases in CBF were greater during Hypaque-76 than during Isovue-370. The increases in CBF caused by the contrast medium were greater than those caused by the corresponding saline solution. Neither Hypaque-76 nor Isovue-370 changed MVO2-Isovist-300 had no effect on CBF or MVO2. CONCLUSIONS: The coronary vasodilation by contrast media is the result of a direct vasorelaxing effect rather than secondary to a metabolic mechanism. Hyperosmolarity can account only in part for contrast-induced coronary vasodilation.

Nitric oxide does not modulate whole body oxygen consumption in anesthetized dogs.

The effects of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) and the NO donor sodium nitroprusside (SNP) on whole body O2 consumption (VO2) were assessed in 16 dogs anesthetized with fentanyl or isoflurane. Cardiac output (CO) and mean arterial pressure (MAP) were measured with standard methods and were used to calculate VO2 and systemic vascular resistance (SVR). Data were obtained in each dog under the following conditions: 1) Control 1, 2) SNP (30 microg. kg-1. min-1 iv) 3) Control 2, 4) L-NAME (10 mg/kg iv), and 5) SNP and adenosine (30 and 600 microg. kg-1. min-1 iv, respectively) after L-NAME. SNP reduced MAP by 29 +/- 3% and SVR by 47 +/- 3%, while it increased CO by 39 +/- 9%. L-NAME had opposite effects; it increased MAP and SVR by 24 +/- 4% and 103 +/- 11%, respectively, and it decreased CO by 37 +/- 3%. Neither agent changed VO2 from the baseline value of 4.3 +/- 0.2 ml. min-1. kg-1, since the changes in CO were offset by changes in the arteriovenous O2 difference. Both SNP and adenosine returned CO to pre-L-NAME values, but VO2 was unaffected. We conclude that 1) basally released endogenous NO had a tonic systemic vasodilator effect, but it had no influence on VO2; 2) SNP did not alter VO2 before or after inhibition of endogenous NO production; 3) the inability of L-NAME to increase VO2 was not because CO, i.e., O2 supply, was reduced below the critical level.

Controlled hypotensive anesthesia in scoliosis surgery.

In a retrospective study comparing normotensive (twenty-two patients) and controlled hypotensive (forty-four patients) anesthesia for spine fusion and Harrington instrumentation, the use of hypotensive anethesia was found to decrease the need for blood replacement and total blood loss by an average of 40 per cent and to reduce the average operating time by more than thirty minutes. No complications attributable to the anesthetic technique occured.

The influence of halothane and nitroprusside on canine spinal cord hemodynamics.

Regional spinal cord blood flow was measured in 12 halothane-anesthetized mongrel dogs by means of 15 +/- 3 u radiolabeled microspheres under (1) control conditions, (2) 60-torr mean arterial blood pressure (MAP) using sodium nitroprusside (NPS), (3) 50-torr MAP using NPS, and (4) after reestablishment of normotension. With the onset of either level of hypotension, there were nonsignificant decreases from control conditions in cardiac output and pulmonary capillary wedge pressure (PCWP). A rise in heart rate was seen at 50 torr MAP. There were no significant changes in spinal cord blood flow (SCBF) under either hypotensive condition in any region of the cord, indicating an intact autoregulatory response. Sensitivity of SCBF to changes in the PaCO2 was shown to be 1.02 ml/min/100 g tissue per torr PaCO2. These data showed that (1) deliberate hypotension with NPS did not change SCBF in the dog; (2) sensitivity to PaCO2 was high under halothane anesthesia; and (3) SCBF was relatively homogeneous throughout the length of the cord.

The Rees system in infants: fresh gas flow and PaCO2.

Fresh gas flow from the anaesthetic machine can be set to determine the low level of PaCO2 that is achieved during anaesthesia using Rees variation of the T-piece. It does not however set the upper limits for PaCO2 which is more reliant upon the minute ventilation. For a PaCO2 of 40 mm Hg, it is suggested that the fresh gas flow from the machine be 220 cc/kg. For small infants, a higher flow rate is necessary.

Tracheal intubating conditions and apnoea time after small-dose succinylcholine are not modified by the choice of induction agent.

BACKGROUND: In a randomized, double-blind clinical trial, we studied the effect of different i.v. induction drugs on tracheal intubation conditions and apnoea time after small-dose (0.6 mg kg(-1)) succinylcholine used to facilitate orotracheal intubation at an urban, university-affiliated community medical centre. METHODS: One hundred and seventy-five ASA I and II adult patients scheduled to undergo surgical procedures requiring general anaesthesia and tracheal intubation were allocated to one of five groups according to i.v. anaesthetic induction drug used. General anaesthesia was induced by i.v. administration of lidocaine 30 mg and propofol 2.5 mg kg(-1) (Group 1), thiopental 5 mg kg(-1) (Group 2), lidocaine 30 mg and thiopental 5 mg kg(-1) (Group 3), etomidate 0.3 mg kg(-1) (Group 4), or lidocaine 30 mg and etomidate 0.3 mg kg(-1) (Group 5). After loss of consciousness, succinylcholine 0.6 mg kg(-1) was given i.v. followed by direct laryngoscopy and tracheal intubation after 60 s. Measurements included intubation conditions recorded during laryngoscopy 60 s after succinylcholine administration, and apnoea time. RESULTS: Overall, clinically acceptable intubation conditions were met in 168 out of the 175 patients studied (96%). They were met in 35/35 patients in Group 1, 33/35 patients in Group 2, 34/35 patients in Group 3, 33/35 patients in Group 4, and 33/35 patients in Group 5. Mean (SD) apnoea time was 4.0 (0.4), 4.2 (0.3), 4.2 (0.6), 4.1 (0.2) and 4.1 (0.2) min respectively in Groups 1-5. There were no differences in the intubation conditions or apnoea times between the groups. CONCLUSIONS: The use of succinylcholine 0.6 mg kg(-1) produced the same favourable intubation conditions and a short apnoea time regardless of the induction drug used.

Verification of endotracheal tube position.

The goals of tracheal intubation are to place the tube in the trachea and to position the tube at an appropriate depth inside the trachea. Various clinical signs and technical aids are described to verify tracheal intubation and to diagnose esophageal intubation. Many of these methods fail under certain circumstances. Not all these methods can be applied in every intubation, but it is essential that the clinician involved in tracheal intubation have the necessary airway management skills, perform these tests accurately, and interpret the results correctly. Prioritization of these tests depends on many factors, including familiarity, availability of monitors, and the location of intubation. Viewing the tube passing between the cords during direct laryngoscopy and visualization of the tracheal rings and carinae with a fiberoptic scope after intubation are the only fullproof methods of confirming tracheal intubation. In the nonarrested patient, carbon dioxide monitoring quickly can differentiate tracheal from esophageal intubation. In the arrested patient, however, carbon dioxide monitoring can be unreliable, although it can be useful as a prognostic indicator of the efficacy of resuscitation. Devices such as [figure: see text] the self-inflating bulb and esophageal detector device may be more useful in patients with cardiac arrest, but they also can yield false results. Placing the distal tip of the tube in the middle of the trachea can be accomplished by positioning the upper end of the cuff 2 cm below the cords during direct laryngoscopy or by placing the distal tip of the tube 4 cm above the carinae with the aid of a fiberoptic scope. The position of the tube always should be verified by clinical assessment (e.g., auscultation). If direct visualization cannot be done, referencing the marks on the tube, transillumination techniques, or cuff maneuvers can be helpful. In the emergency and critical care settings, a chest radiograph easily can detect malpositioned tracheal tubes that may not be detected by routine clinical assessment. Other techniques (e.g., use of fiberoptic scopes, cuff maneuvers, transillumination) can decrease the need for frequent chest radiographs. Based on available information, two algorithms are proposed: one for emergency intubation (Fig. 9) and the other for verification of tracheal tube position in elective intubation (Fig. 10). These algorithms are designed [figure: see text] to assist the clinician and should not be substituted for clinical judgment. Under no circumstances should clinical signs be ignored in the presence of conflicting information from monitors and technical aids.

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.

Anesthetic care of pediatric surgical patients.

Some technical aspects of intraoperative anesthetic care of pediatric surgical patients are discussed. Recent concepts of premedicant, anesthetic and muscle relaxant drugs as related to the pediatric patient are presented. Endotracheal intubation is an integral part of the pediatric anesthetic management. Adequacy of fluid and blood replacement is emphasized. Most current pediatric anesthetic systems incorporate the "T piece" principle. Maintenance of a near normal PaCO2 could be accomplished by allowing partial rebreathing during controlled ventilation. Current status of three useful techniques is presented: deliberate hypotension, hemodilution, and the rapid induction-intubation technique for children with a full stomach. Anesthetic considerations of special problems, such as neurosurgery or cardiac surgery and monitoring, are not discussed.

Myocardial oxygen consumption and segmental shortening during selective coronary hemodilution in dogs.

Experiments were conducted in 33 open chest, anesthetized dogs to evaluate direct effects of hemodilution on myocardial oxygenation and contractile function. The left anterior descending coronary artery (LAD) was perfused selectively from a controlled pressure reservoir with either normal arterial blood or arterial blood diluted with lactated Ringer's solution. Systemic hemodynamic parameters were held stable. In the LAD bed, values were obtained for coronary blood flow (CBF) with an electromagnetic flowmeter, myocardial oxygen consumption (MVO2) using the Fick principle, and percentage segmental shortening (%SS), an index of local myocardial contractility, by sonomicrometry. Studies were conducted with LAD perfusion pressure (PP) set at control (100 mm Hg) and at 50% of that level to simulate coronary insufficiency (CI). CI abolished coronary reactive hyperemia after release of a 90-second occlusion, indicating exhausted vasodilator reserve capacity. With PP at control, reductions in LAD hematocrit to as low as 10% had no effect on MVO2 or %SS, because increases in blood flow were sufficient to offset induced falls in arteriovenous oxygen content difference. However, during CI, a more modest reduction in hematocrit to 17% caused reductions in both MVO2 and %SS, because of inadequate flow responses during hemodilution. The following conclusions can be made: 1) Extreme hemodilution is well tolerated by the normal heart with a stable work requirement and; 2) Relatively modest hemodilution may compromise myocardial oxygenation and contractile function when in the presence of exhausted or severely depleted vasodilator reserve capacity.

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.

Hemodilution impairs hypocapnia-induced vasoconstrictor responses in the brain and spinal cord in dogs.

Despite the increasing use of plasma expanders in the perioperative period, there have been few studies of cerebrovascular responsiveness during hemodilution. The present study was performed to evaluate the influence of isovolemic hemodilution on vasoconstrictor responses in the brain and spinal cord during hypocapnia. Sixteen mechanically ventilated, halothane-anesthetized dogs were randomly divided into two equal groups: Group 1, control group (hematocrit [Hct], 42% +/- 2%); Group 2, isovolemic hemodilution with 5% dextran 40 (Hct, 19% +/- 2%). Hypocapnia (22 +/- 1 mm Hg) was induced in both groups by removal of dead space tubing without altering mechanical ventilation. Regional blood flow in the brain and spinal cord was measured with 15-microns radioactive microspheres and used to calculate regional vascular resistance (RVR). In Group 1, hypocapnia caused increases in RVR (ranging from 44% +/- 10% in the cerebral cortex to 93% +/- 17% in the thoracic spinal cord). In Group 2, hemodilution itself decreased RVR relatively uniformly throughout the brain and spinal cord. After hemodilution, hypocapnia had no significant effect on RVR in the cerebral cortex, cerebellum, pons, and medulla, and caused less pronounced increases in RVR within the spinal cord. We conclude that hemodilution either attenuated or completely abolished vasoconstrictor responses within the brain and spinal cord during hypocapnia. Furthermore, the present findings suggest that induced hypocapnia may be less effective as a clinical maneuver to reduce increased intracranial pressure during hemodilution.

Is calcium a coronary vasoconstrictor in vivo?

BACKGROUND: Calcium produces constriction in isolated coronary vessels and in the coronary circulation of isolated hearts, but the importance of this mechanism in vivo remains controversial. METHODS: The left anterior descending coronary arteries of 20 anesthetized dogs whose chests had been opened were perfused at 80 mmHg. Myocardial segmental shortening was measured with ultrasonic crystals and coronary blood flow with a Doppler flow transducer. The coronary arteriovenous oxygen difference was determined and used to calculate myocardial oxygen consumption and the myocardial oxygen extraction ratio. The myocardial oxygen extraction ratio served as an index of effectiveness of metabolic vasodilation. Data were obtained during intracoronary infusions of CaCl2 (5, 10, and 15 mg/min) and compared with those during intracoronary infusions of dobutamine (2.5, 5.0, and 10.0 microg/min). RESULTS: CaCl2 caused dose-dependent increases in segmental shortening, accompanied by proportional increases in myocardial oxygen consumption. Although CaCl2 also increased coronary blood flow, these increases were less than proportional to those in myocardial oxygen consumption, and therefore the myocardial oxygen extraction ratio increased. Dobutamine caused dose-dependent increases in segmental shortening and myocardial oxygen consumption that were similar in magnitude to those caused by CaCl2. In contrast to CaCl2, however, the accompanying increases in coronary blood flow were proportional to the increases in myocardial oxygen consumption, with the result that the myocardial oxygen extraction ratio remained constant. CONCLUSIONS: Calcium has a coronary vasoconstricting effect and a positive inotropic effect in vivo. This vasoconstricting effect impairs coupling of coronary blood flow to the augmented myocardial oxygen demand by metabolic vascular control mechanisms. Dobutamine is an inotropic agent with no apparent direct action on coronary resistance vessels in vivo.

Isoflurane-induced coronary vasodilation is preserved in reperfused myocardium.

Isoflurane causes vasodilation in the coronary circulation. The present study evaluated whether this action is preserved after a brief coronary occlusion followed by reperfusion. Fourteen open-chest dogs anesthetized with fentanyl and midazolam were studied. The left anterior descending coronary artery was perfused via an extracorporeal system with normal arterial blood or with arterial blood equilibrated with 1.4% (1 minimum alveolar anesthetic concentration [MAC]) isoflurane. Coronary perfusion pressure was maintained at 90 mm Hg. Coronary blood flow (CBF) was measured with a Doppler flow transducer. Steady-state changes in CBF during isoflurane, and during intracoronary infusions of acetylcholine (Ach; 20 micrograms/min), an endothelium-dependent vasodilator, and sodium nitroprusside (SNP; 80 micrograms/min), an endothelium-independent vasodilator, were compared in normal myocardium and in myocardium subjected to 15 min of ischemia (due to cessation of perfusion) followed by 30 min of reperfusion. Ischemia-reperfusion had no significant effect on the increases in CBF by isoflurane (421% +/- 88% vs 388% +/- 84%) or SNP (115% +/- 18% vs 135% +/- 19%), whereas it attenuated these increases in CBF by Ach (232% +/- 38% vs 143% +/- 21%). In conclusion, a brief period of myocardial ischemia followed by reperfusion did not affect the coronary vasodilating effects of isoflurane and SNP, although it blunted these effects of Ach. The present findings provide further evidence suggesting that the ability of isoflurane to relax coronary vascular smooth muscle is independent of the nitric oxide-cyclic guanosine monophosphate pathway.