[Anesthetic considerations in mast-cell proliferative disease (urticaria pigmentosa and mastocytosis)].
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Biomedical subjects
Publications and source records attributed to A Perel.
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The intraoperative arousal test is used to detect potential damage to the spinal cord during spine fusion. We determined whether a continuous midazolam infusion, the effects of which are antagonized by flumazenil when the arousal test is needed, is associated with good control of the timing of arousal and with no adverse reactions. In a randomized study of 20 patients (10 in each group), we compared arousal with flumazenil during midazolam-narcotic anesthesia with an arousal test done during halothane-nitrous oxide anesthesia, both under conditions of controlled hypotension. Motor responses to verbal command were obtained 39.1 +/- 36.0 s (mean +/- SD) after the injection of flumazenil in eight patients. Two patients form this group awoke spontaneously 6 and 8 min after terminating the administration of nitrous oxide and midazolam but remained sedated up to the time of the test itself. In the halothane group, arousal occurred 26 +/- 8.3 min after halothane administration was terminated and 10.1 +/- 3.3 min after nitrous oxide was stopped. Two of the patients in this group moved, owing to early arousal 5 and 8 min before the scheduled time and needed reinstatement of anesthesia. In four patients in the halothane group, we had to wait 3-11 min after the scheduled time before satisfactory arousal was achieved. One of the patients in the halothane group showed a motor deficit of the lower limbs during the wake-up test that disappeared after decreasing the spine correction. There were no adverse reactions except for occasional shivering in the recovery period.(ABSTRACT TRUNCATED AT 250 WORDS)
Malignant hyperthermia syndrome (MHS) is rare, inherited, and triggered by volatile anesthetics and depolarizing muscle relaxants. While potentially fatal, if recognized and treated early recovery is usual. However, the condition is often not recognized until an extreme increase in temperature develops with profound circulatory depression. In this stage the syndrome is irreversible, despite specific treatment with dantrolene. At present, the only reliable diagnostic test for susceptibility to malignant hyperthermia requires sampling of viable muscle for in vitro contracture tests with caffeine and halothane. Until our malignant hyperthermia diagnostic center was opened, such tests could not be performed in Israel. Since then we encountered a 22-year-old man who developed the partial picture of malignant hyperthermia syndrome during anesthesia for inguinal herniorrhaphy. He received dantrolene and recovered. 4 months later in vitro contracture tests with caffeine and halothane performed on biopsied muscle confirmed the diagnosis.
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In paired experiments, we studied the effects of high-dose methylprednisolone on the acute pulmonary injury caused by 4 h of venous air embolization in 19 chronically instrumented, unanesthetized sheep with lung lymph fistulas. We compared the effect of methylprednisolone (30 mg/kg intravenous bolus) given before embolization, early (1 H) in the course of embolization, late (3 h) in the course of embolization, or after embolization (at the beginning of the recovery period). We measured pulmonary hemodynamics and lymph dynamics. In six sheep we also fixed lung tissue for semiquantitative histology, and in some we measured leukocyte concentrations in blood and in pulmonary lymph. Methylprednisolone did not significantly affect pulmonary hemodynamics but it largely prevented lung injury when it was given before embolization. It also lessened the degree of lung injury when it was given during embolization, although this effect became less marked as treatment was delayed. Methylprednisolone had no effect on lung injury when given after embolization was completed (4 h). We found fewer leukocytes attached to air emboli and fewer endothelial cell gaps in the lungs of sheep given methylprednisolone as prophylaxis. Leukocyte counts were lower in lung lymph and higher in the circulating blood of methylprednisolone-treated sheep. We conclude that methylprednisolone has a preventive effect on air embolism lung injury, such that its effect is greater when given earlier during the development of injury.
Both tidal volume and effective blood volume may affect the variation in the arterial pressure waveform during mechanical ventilation. The systolic pressure variation (SPV), which is the difference between the maximal and minimal systolic pressure values following one positive pressure breath was analyzed in 10 anesthetized and ventilated dogs, during ventilation with tidal volumes of 15 and 25 ml/kg. The dogs were studied during normovolemia, hypovolemia (after bleeding of 30% of estimated blood volume) and hypervolemia (after retransfusion of shed blood with additional 50 ml/kg of plasma expander). The SPV reflected hemodynamic changes and was maximal during hypovolemia and minimal during hypervolemia. Unlike all other hemodynamic parameters it was also affected by the tidal volume and significantly increased at higher tidal volumes during each volume state. We conclude that the SPV and its components are useful parameters in evaluating the intravascular volume state. They also reflect the magnitude of the tidal volume employed.
High frequency ventilation has been claimed to improve the efficiency of extracorporeal shock wave lithotripsy (ESWL) by minimizing the movement of urinary stones during the procedure. A ventilatory mode, QRS-activated ventilation, was developed in which the stones remain motionless during the delivery of shock waves. As the shock wave is triggered to occur approximately 20 milliseconds after the R wave of the QRS complex, the mechanical breath was synchronized to occur approximately 150 ms later. QRS-activated ventilation is used in 16 patients undergoing ESWL under general anesthesia. Tidal volume was set at 3 ml/kg (234 +/- 36 ml; mean +/- SD) at a rate that equaled the heart rate (71 +/- 9 beats/min). The time between the R wave and the initiation of mechanical breath (T1) was 124 +/- 25 ms, time of mechanical breath itself (T2) was 431 +/- 67 ms, and time between end of T2 and next R wave (T3) was 264 +/- 84 ms. End-tidal CO2 measured by the large breath technique was 28.1 +/- 4.8 mmHg. During the clinical use of QRS-activated ventilation and during earlier studies using an EKG simulator and a test lung, the shock wave occurred invariably at end-expiration even at high heart rates.
Methods for mechanical cardiac support by intermittent increases in the intrathoracic pressure have recently been described. In the present study the responses of the arterial pressure waveform to mechanical ventilation with and without synchronized external chest compression (SEC) in the presence of acute ventricular failure (AVF) were evaluated by measuring the systolic pressure variation (SPV). SPV, the difference between the maximal and minimal values of systolic blood during a single positive pressure breath, consists of delta up and delta down components when systolic blood pressure during a short apnea is used as reference value. During intermittent positive pressure ventilation (IPPV) alone, AVF caused SPV to decrease significantly from 8.8 +/- 4.0 to 5.7 +/- 1.9 mm Hg, and further to 3.1 +/- 1.1 mm Hg after volume loading (P less than 0.02). The decrease in SPV was due to a significant decrease in the delta down component, whereas the delta up became the major component of the reduced SPV. The application of SEC caused significant increases in the delta down, delta up, and overall SPV during AVF without volume loading. However, during AVF with volume loading, SEC increased only the delta up component of the SPV, signifying a transient increase in the left ventricular stroke output. It is concluded that the disappearance of the delta down component of the SPV is characteristic of congestive heart failure. Analysis of the arterial waveform offers a readily available monitoring tool for the differentiation of the possible effects on increased intrathoracic pressure.(ABSTRACT TRUNCATED AT 250 WORDS)
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The systolic pressure variation (SPV), which is the difference between the maximal and minimal values of the systolic blood pressure (SBP) after one positive-pressure breath, was studied in ventilated dogs subjected to hypotension. Mean arterial pressure was decreased to 50 mm Hg for 30 minutes either by hemorrhage (HEM, n = 7) or by continuous infusion of sodium nitroprusside (SNP, n = 7). During HEM-induced hypotension the cardiac output was significantly lower and systemic vascular resistance higher compared with that in the SNP group. The systemic, central venous, pulmonary capillary wedge pressures, and heart rates, were similar in the two groups. Analysis of the respiratory changes in the arterial pressure waveform enabled differentiation between the two groups. The SPV during hypotension was 15.7 +/- 6.7 mm Hg in the HEM group, compared with 9.1 +/- 2.0 mm Hg in the SNP group (P less than 0.02). The delta down, which is the measure of decrease of SBP after a mechanical breath, was 20.3 +/- 8.4 and 10.1 +/- 3.8 mm Hg in the HEM and SNP groups, respectively, during hypotension (P less than 0.02). It is concluded that increases in the SPV and the delta down are characteristic of a hypotensive state due to a predominant decrease in preload. They are thus more important during absolute hypovolemia than during deliberate hypotension.
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Systolic pressure variation (SPV) is defined as the difference between the maximum and minimum values of systolic blood pressure following a single positive pressure breath. An increase in the SPV is known to occur clinically during hypovolemia. This study aims to quantify SPV during graded hemorrhage in ventilated dogs, and to compare its reliability relative to other hemodynamic indicators of hypovolemia. Ten anesthetized dogs were mechanically ventilated with a fixed tidal volume. A continuously inflated vest was applied around the chest to maintain the ratio of lung to chest wall compliance similar to that of humans (0.83 +/- 0.12). SPV was further divided into delta up and delta down components relative to apneic (5 s) systolic blood pressure. Dogs were bled 5, 10, 20, and 30% of their estimated blood volume. The measured parameters best correlated to the amount of bleeding were SPV (rs = 0.993), delta down (rs = 0.981), and cardiac output (rs = 0.976). The SPV and its delta down component correlated to the degree of hemorrhage as well as the CO and the pulmonary capillary wedge pressure, and significantly better than the central venous pressure and the mean systemic blood pressure. Thus, SPV and its delta down component are accurate indicators of hypovolemia in ventilated dogs subjected to hemorrhage.
We studied the relationship between oxygen consumption (Vo2) and cardiac output in 17 hemodynamically stable, septic and eight nonseptic ICU patients. Each received 300 ml of fresh-frozen plasma or 25% albumin with up to 500 ml of crystalloids, in addition to regular maintenance fluids; this treatment increased pulmonary wedge pressure (WP) by 3 to 4 mm Hg. Measurements were performed before and after approximately 5 h of volume loading. Because cardiac index (CI) decreased as WP increased in four septic and three nonseptic patients, we grouped the data according to the state of flow instead of the recording time sequence. From low to high flows, mean CI increased in septic patients and nonseptic patients. Oxygen delivery (Do2) increased in septic and nonseptic patients. Vo2 remained unchanged in nonseptic patients, while it increased in septic patients. Accordingly, arteriovenous oxygen difference narrowed in nonseptic patients from 4.46 +/- 1.62 to 3.59 +/- 1.21 ml/dl (p less than .05) but did not change in septic patients. In the septic group, the difference in CI between high and low flows was significantly (p less than .05) greater in survivors than in nonsurvivors. We conclude that the septic state is accompanied by a peripheral oxygen deficit, which can be partially reversed by maintaining an above-normal CI and Do2.
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