Con: continuous blood gas monitoring should not be a standard during cardiopulmonary bypass.
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Blood Gas Analysis↗
Biomedical subjects
R G Merin
Publications and source records attributed to R G Merin.
Comparative effects of halothane, enflurane, and isoflurane at equihypotensive doses on cardiac performance and coronary and renal blood flows in chronically instrumented dogs.
In order to compare equihypotensive effects of the three available volatile anesthetics, halothane, enflurane, and isoflurane, dogs were chronically instrumented for measurement of: arterial, left ventricular, and left atrial blood pressures; rate of rise of left ventricular blood pressure; myocardial wall thickening (pulsed Doppler); cardiac output (pulmonary artery electromagnetic flow meter); and coronary and renal blood flows (pulsed Doppler flow meters). All three anesthetics were administered on different days in random order to each dog (n = 10) at doses necessary to decrease mean arterial pressure to 70 and 45 mmHg and two intermediate arterial blood pressures. Changes in cardiac function and regional blood flows were compared to the awake resting state and between anesthetics using analysis of variance and paired t tests. All three anesthetics produced increases in heart rate and decreases in left ventricular dP/dt, myocardial thickening fraction, and stroke volume with the hypotension. The decreases in cardiac performance were similar among the anesthetics except at the high dose (mean arterial pressure = 45 mmHg). During this profound hypotension, cardiac performance was better maintained during isoflurane anesthesia and most depressed by enflurane anesthesia. Coronary and renal blood flows were well preserved with all three anesthetics even at mean arterial pressures of 45 mmHg. Our results suggest that isoflurane may be more beneficial than halothane or enflurane for producing profound intentional hypotension (less than 50 mmHg mean arterial pressure), although extrapolation from animal experiments to the clinical situation should be used with caution.
Animals↗
Effects of sevoflurane and isoflurane on hepatic circulation in the chronically instrumented dog.
To compare the effects of sevoflurane and isoflurane on hepatic circulation, eighteen dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic and portal blood flows. Each animal was studied while awake and during 1.2 and 2 MAC of either isoflurane or sevoflurane. Both anesthetics induced tachycardia and a dose-dependent decrease in mean aortic blood pressure (isoflurane -27% and -39%; sevoflurane -22% and -37%). Cardiac output decreased only at the highest concentration (isoflurane -10%; sevoflurane -21%). During sevoflurane, portal blood flow decreased at both 1.2 and 2 MAC (-14 and -33%, respectively), whereas an increase in hepatic arterial blood flow was recorded at 2 MAC (+33%). During isoflurane, the only significant change was a decrease in portal blood flow (-16%) at 1.2 MAC. Neither anesthetic significantly changed renal blood flow. Therefore, both anesthetics led to similar systemic and hepatic vasodilation.
Anesthetics↗
Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in conscious, chronically instrumented dogs and their interactions with ganglionic blockade.
To assess the hemodynamic effects of acute changes in extracellular ionized calcium concentration, [Ca2+], seven dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) pressures, cardiac output, and coronary and renal blood flows. [Ca2+] was lowered 0.35 mmol.l-1 by citrate infusion and then increased 0.35 mmol.l-1 above control level by CaCl2 infusions. This protocol was performed in the conscious dogs with and without ganglionic blockade (chlorisondamine 2 mg.kg-1). LV dP/dtmax decreased at low [Ca2+] and increased at high [Ca2+] during all conditions. The other hemodynamic variables measured were only slightly changed by changing [Ca2+] without ganglionic blockade and surprisingly even less with ganglionic blockade. Therefore, the lesser hemodynamic effects induced by acute changes in [Ca2+] in the conscious compared with anesthetized dogs cannot be explained by the depressant effects of the anesthetics upon the autonomic nervous system. We have suggested that the binding of Mg2+ to citrate may be of importance for the minor hemodynamic effects in the conscious dogs.
Animals↗
Hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration and enflurane, halothane or isoflurane in chronically instrumented dogs.
To assess the hemodynamic interactions when combining verapamil, acute changes in extracellular ionized calcium concentration [Ca2+] and enflurane (2.5%), halothane (1.2%) or isoflurane (1.6%), seven dogs were chronically instrumented to measure heart rate (HR), aortic, left atrial and left ventricular (LV) pressures, and cardiac output (CO). [Ca2+] was lowered 0.35 mmol.l-1 by citrate infusion and then increased 0.35 mmol.l-1 above control level by CaCl2 infusions. Verapamil was infused at 3 micrograms.kg-1 x min-1 (loading dose 200 (awake), 150 (isoflurane) or 100 (enflurane and halothane) micrograms.kg-1), giving mean verapamil concentrations around 75 (range of means: 66-84 ng.ml-1). Verapamil produced mostly minor changes in the cardiovascular effects of changing [Ca2+] in both awake and anesthetized dogs, indicating mostly additive effects. Verapamil induced a decrease in HR at high [Ca2+] and abolished an increase in mean aortic pressure at both low and high [Ca2+] awake. Verapamil exaggerated the decrease in CO and stroke volume (SV) induced by low [Ca2+] during enflurane anesthesia and abolished the increase in CO induced by low [Ca2+] and exaggerated the increase in SV and LV dP/dtmax induced by high [Ca2+] during halothane anesthesia.
Anesthesia, Inhalation↗
Physiology, pathophysiology and pharmacology of the coronary circulation with particular emphasis on anesthetics.
The normal control of coronary blood flow is through alterations in the resistance of the intramyocardial arterioles (R2). Myocardial cellular hypoxia causes increased breakdown of ATP (or decreases synthesis) resulting in increased concentrations of the purine metabolite, adenosine. This potent endogenous, vascular smooth muscle relaxant vasodilates the R2 arterioles increasing coronary blood flow and myocardial O2 delivery. This mechanism autoregulates coronary blood flow according to myocardial O2 needs. Myocardial hypertrophy (from chronic hypertension) or coronary atherosclerosis interfere with this process and result in myocardial ischemia which may cause symptoms (angina), signs (ECG changes, regional muscle dysfunction) or tissue death (myocardial infarction). In addition, coronary atheroma disrupt endothelial function in the large R1 coronary arteries predisposing to vasoconstriction, platelet aggregation and thrombosis. Therapeutic measures for controlling ischemia may include decreasing oxygen demand (especially heart rate) and maintaining supply (R1 vasodilators and anti-thrombotic drugs such as non-steroidal anti-inflammatories). Intravenous, most inhalational and regional anesthesia appear to interfere minimally in the control of both the normal and ischemic coronary circulation. Thus optimizing myocardial oxygen balance (maintaining supply and decreasing demand) during anesthesia protects the ischemic myocardium. High doses of isoflurane, sevoflurane or desflurane are potent R2 coronary vasodilators which may cause redistribution of collateral blood flow away from ischemic regions (coronary steal). However, if tachycardia and hypotension are avoided, such an effect has not been shown experimentally or clinically. Preliminary evidence suggests that halothane may preferentially dilate R1 arteries and/or interfere with platelet aggregation. If these effects are confirmed, then halothane may prove to be the anesthetic of choice in the non-failing ischemic heart.
Anesthetics↗
Effects of volatile anesthetics on the coronary circulation in chronically instrumented dogs.
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Anesthetics↗
Effects of enflurane and isoflurane on hepatic and renal circulations in chronically instrumented dogs.
Seven dogs were chronically instrumented for measurements of mean aortic blood pressure and cardiac output and for simultaneous measurements of hepatic, portal, and renal blood flows. Each animal was studied on two separate occasions, awake and during 1.2, 1.4, 1.75, and 2.0 MAC isoflurane and enflurane. Both anesthetics induced tachycardia; to a greater degree than isoflurane, enflurane lowered mean aortic blood pressure in a dose-dependent manner (-37, -45, -48, and -62% vs. -19, -25, -41, and -44%, respectively) and cardiac output (-20, -26, -41, and -48% vs. -3, -5, -11, and -15%, respectively). With isoflurane, cardiac output decreased only at 1.75 and 2.0 MAC, and portal blood flow did not change significantly, whereas hepatic arterial blood flow increased at 1.75 and 2 MAC (by 28 and 33%, respectively). With enflurane, no significant changes were recorded in hepatic arterial blood flow, whereas portal blood flow decreased in a dose-dependent manner. Except at 2 MAC, hepatic circulation did not differ between anesthetics. Likewise, neither anesthetic significantly changed renal blood flow, except for enflurane at 2.0 MAC, which was associated with a 35% reduction. Both anesthetics led to similar systemic, hepatic, and renal vasodilations. Our data suggest that high concentrations of enflurane are associated with decreases in portal, total hepatic, and renal blood flows, most likely as a result of an anesthetic-induced cardiac depression.
Animals↗
Comparison of the effects of isoflurane and desflurane on cardiovascular dynamics and regional blood flow in the chronically instrumented dog.
Seven mongrel dogs were chronically instrumented for the measurement of aortic and left ventricular blood pressures, cardiac output, left ventricular wall thickening, left ventricular dP/dt, and circumflex coronary, renal, hepatic and portal blood flows under the influence of desflurane (D) and isoflurane (I). Administration of the two anesthetics, was randomized, as was the order of the concentrations administered. Each dog was studied awake and at 1.2, 1.4, 1.75, and 2.0 MAC of each anesthetic on different days. Both anesthetics decreased mean arterial pressure, stroke volume, systemic vascular resistance, left ventricular dP/dt, and wall thickness. The decreases were dose-dependent for mean arterial pressure (percent of awake values: D 78, I 85 at 1.2 MAC, and D 67, I 69 at 2.0 MAC); stroke volume (D 66, I 72 at 1.2 MAC, and D 52, I 57 at 2.0 MAC); dP/dt (D 61, I 64 at 1.2 MAC, and D 46, I 49 at 2.0 MAC); and WT (D 68, I 70 at 1.2 MAC, and D 47, I 60 at 2.0 MAC). Systemic vascular resistance decreased approximately the same at 1.2 MAC (D 71, I 87%) as at 2.0 MAC (D 71, I 79%). Heart rate increased but also not in a dose-dependent fashion (percent of awake values: D 177, I 145 at 1.2 MAC, and D 176, I 155 at 2.0 MAC). Coronary blood flow was increased by both anesthetics at all concentrations (percent of awake values: I 136 at 1.2 MAC and 161 at 2.0 MAC of awake, and D 131 at 1.2 MAC and 138 at 2.0 MAC.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Cardiovascular effects of acute changes in extracellular ionized calcium concentration induced by citrate and CaCl2 infusions in chronically instrumented dogs, conscious and during enflurane, halothane, and isoflurane anesthesia.
To study the cardiovascular effects of low blood ionized calcium ion concentrations [Ca2+] induced by citrate infusion followed by high [Ca2+], induced by CaCl2 infusion awake and during enflurane (2.5% ET), halothane (1.2% ET), and isoflurane (1.6% ET) anesthesia, dogs were chronically instrumented to measure heart rate, aortic, left atrial, and left ventricular (LV) blood pressures, and cardiac output. In conscious dogs low [Ca2+] (decreased 0.35 mM); increased heart rate (HR) and mean aortic pressure (MAP) and decreased stroke volume (SV) and LV dP/dtmax. Low [Ca2+] increased HR during all three anesthetics and decreased LV dP/dtmax except during isoflurane anesthesia. Low [Ca2+] produced more hemodynamic depression during enflurane anesthesia than during anesthesia with halothane or isoflurane increasing left atrial pressure and decreasing MAP and SV. The differences seen were partially related to decreased systemic vascular resistance during halothane and isoflurane anesthesia. In conscious dogs following high [Ca2+] (increased 0.37 mM); only MAP and LV dP/dtmax increased. LVdP/dtmax was also increased by high [Ca2+] during all three anesthetics without a change in MAP. Cardiac output increased during halothane and isoflurane anesthesia but was unchanged during enflurane. It would appear that the hemodynamic sensitivity for the effects of changing [Ca2+] was enflurane greater than halothane greater than isoflurane greater than awake. The results suggest that the effects of changes in [Ca2+] induced by citrate and CaCl2 infusion are modified by the three volatile anesthetics.
Anesthesia, Inhalation↗
Effects of sevoflurane and isoflurane on cardiac and coronary dynamics in chronically instrumented dogs.
To assess the hemodynamic properties of the new inhalational anesthetic sevoflurane, 22 dogs were chronically instrumented for measurement of heart rate, aortic, left ventricular and left atrial pressures, cardiac output, and coronary blood flow. Dogs were randomly assigned to two groups, receiving either 1.2 and 2 MAC of sevoflurane (n = 11) or isoflurane (n = 11). At 1.2 and 2 MAC, sevoflurane produced an increase in heart rate (+60 +/- 12% and +54 +/- 9%, respectively), dose-dependent aortic hypotension (-22 +/- 4% and -38 +/- 4%, respectively), systemic vasodilation (-22 +/- 5% and -19 +/- 5%, respectively), dose-dependent decrease in stroke volume (-31 +/- 6% and -48 +/- 4%, respectively), and left ventricular dP/dt (-40 +/- 4% and -61 +/- 10%, respectively). Cardiac output decreased only at 2 MAC (-17 +/- 6%). Finally, coronary blood flow increased at 1.2 MAC of sevoflurane (+29 +/- 8%). Except for heart rate, sevoflurane and isoflurane produced similar effects. At 1.2 MAC, sevoflurane produced a greater increase in heart rate than isoflurane (+60 +/- 12% vs. +33 +/- 9%). The authors conclude that, except for heart rate, the effects of sevoflurane on cardiac function and coronary blood flow are almost identical to those induced by isoflurane in the chronically instrumented dog.
Anesthetics↗
Influence of hypertension on MAC of halothane in rats.
This study was designed to assess the relationship between MAC and hypertension. To this purpose, MAC of halothane was determined in fully inbred spontaneously hypertensive rats (SHR) and Wistar Kyoto rats (WKY). Because MAC determination was performed in animals whose lungs were mechanically ventilated, the adequacy of the ventilation was initially established in 20 rats equally divided into SHR and WKY, and instrumented with catheters in the abdominal aorta. Subsequently, MAC of halothane was determined in 40 rats equally divided into SHR and WKY, including those instrumented. There were no differences in MAC of halothane between SHR (n = 20) and WKY (n = 20) (1.08 +/- 0.02% vs. 1.11 +/- 0.02%). Subgroup analysis indicated that MAC of halothane was not affected by the presence of an arterial catheter in the abdominal aorta (SHR 1.09 +/- 0.06% vs. 1.08 +/- 0.02%; WKY 1.15 +/- 0.04% vs. 1.08 +/- 0.02%). The authors' data provide experimental evidence that MAC is not affected by either chronic hypertension or limited instrumentation.
Anesthesia, Inhalation↗
Myocardial protection: what the anesthesiologist does.
The role of the anesthesiologist in myocardial protection is to optimize myocardial oxygen balance during the perioperative period. Nonpharmacological steps that can be taken to achieve this revolve around maintaining a satisfactory hemoglobin concentration and oxyhemoglobin saturation through maximizing ventilation. In addition, alkalosis and hypothermia should be prevented since they cause a left shift of the oxyhemoglobin dissociation curve, thus interfering with tissue oxygen delivery. Hypocarbia increases coronary vascular resistance. Blood volume must be adequate with an optimal hemoglobin concentration. Pharmacological measures should also be used, and it is important to continue through the perioperative period any previously administered cardioactive drugs. Furthermore, in the prebypass period, tachycardia may not be controlled by anesthetics; unless the tachycardia is paroxysmal, beta blockers are the drugs of choice. Depending on the cause, diastolic hypotension also needs to be treated either with volume, vasoconstrictors, or inotropes. Likewise, major hypertension can produce increased demand and, again depending on the cause, either anesthetics, vasodilators, beta blockers, or calcium blockers may be useful. Finally, myocardial ischemia without obvious cause probably should be treated with nitroglycerin or calcium blockers. During surgery, the effect of the anesthetic drugs on myocardial oxygen balance is important.
Anesthesia↗
Basic physiology and pharmacology of cardiovascular function.
Cardiac function is based on the complex biochemistry of cardiac muscle contraction. Contributing factors are action potential, membrane receptors, ion channels and G proteins, the important effectors in the sarcoplasm, particularly calcium ion and protein kinase, and the interaction of the contractile proteins. These are various pharmacological approaches to cardiovascular function by modulating the myocardial biochemistry. These include beta agonists, beta antagonists, mixed adrenergic agonists, nonadrenergic inotropes (including PDE III inhibitors), and nonadrenergic vasodilators.
Cardiac Surgical Procedures↗
Cardiovascular effects of and interaction between calcium blocking drugs and anesthetics in chronically instrumented dogs: VII. Verapamil and thiopental.
To assess the role of basal anesthesia in the negative inotropic properties of verapamil, the effect of thiopental (30 mg/kg followed by 3.5 mg.kg-1.min-1) on verapamil pharmacokinetics (200 micrograms/kg iv; n = 6) and its pharmacodynamics (3 and 6 micrograms.kg-1.min-1; n = 11) in chronically instrumented dogs was studied. In the presence of thiopental, verapamil pharmacokinetics remained essentially unchanged. In contrast, anesthesia altered verapamil hemodynamic properties. In the conscious animal verapamil infusions increased heart rate (14 +/- 3 and 27 +/- 4 beats/min, respectively), cardiac output (0.22 +/- 0.07 and 0.24 +/- 0.08, l/min, respectively) and PR interval (14 +/- 2 and 25 +/- 6 ms, respectively) and slightly decreased dP/dt (-315 +/- 114 and -419 +/- 106 mmHg/s, respectively). Systemic vascular resistance (SVR) decreased at the low dose (-2.7 +/- 0.7 mmHg.1.min-1), and stroke volume decreased at the high dose (-4.4 +/- 0.6 ml). Yet the presence of thiopental resulted in an accentuation of verapamil-induced tachycardia (27 +/- 7 and 31 +/- 6 beats/min, respectively), and a decrease in stroke volume (-5.3 +/- 2.0 and -6.3 +/- 2.1 ml, respectively). At 3 micrograms.kg-1.min-1 verapamil did not increase PR interval, cardiac output, or vasodilation. Finally, at 6 micrograms.kg-1.min-1 verapamil did not decrease dP/dt and increased renal blood flow (21.8 +/- 6.4 ml/min). These data provide evidence that the negative inotropic properties of verapamil are more pronounced in the presence of thiopental. However, the role of basal anesthesia appears to be limited.
Animals↗
Etomidate myoclonus and the open globe.
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Adult↗
The isolated heart preparation.
The major advantage of the isolated heart over isolated cardiac muscle for studying the effect of anaesthetics relates to the maintenance of the anatomy and function of the heart as a pump and the use of the native coronary circulation for cardiac nutrition and oxygenation. For the latter function, perhaps the blood perfused heart-lung preparation is more physiological but less controllable, particularly for metabolic studies. However, both preparations are predominantly useful for evaluating mechanisms and comparative biochemical pharmacology, rather than being relevant for clinical management.
Anesthetics↗
Cardiac arrest following i.v. verapamil may be related to concomitant digoxin therapy as well as halothane.
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Digoxin↗