Efficacy of oral nifedipine in the treatment of reflex sympathetic dystrophy.
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Biomedical subjects
Publications and source records attributed to D S Prough.
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Hypertonic saline (2400 mOsm/L) has been used successfully for fluid resuscitation of dogs subjected to severe hemorrhagic shock. This study compared the effects of resuscitation with hypertonic saline vs. lactated Ringer's solution on intracranial pressure (ICP) in dogs subjected to 30 min of sustained hypovolemic shock. Hypotension was produced by rapid withdrawal of blood until mean arterial pressure was 50 mm Hg, maintained at that level by withdrawal or infusion of blood over the next 30 min as necessary. Eight animals were resuscitated with hypertonic saline solution and nine with lactated Ringer's solution. Both solutions restored systolic blood pressure and cardiac output to control values. However, diastolic blood pressure and mean arterial pressure did not return to control values. The most prominent difference between the two groups was in ICP measured after resuscitation. ICP was lower in dogs resuscitated with hypertonic saline than in dogs resuscitated with lactated Ringer's solution (p = .029). Hypertonic saline fluid resuscitation may represent a potential alternative when aggravation of intracranial hypertension during resuscitation would place a patient at greater risk.
We investigated the accuracy with which pulmonary artery wedge pressure (WP) reflected left ventricular end-diastolic pressure (LVEDP) in dogs with oleic acid-induced pulmonary edema. We compared hemodynamic variables before and during edema, as measured from a pulmonary artery catheter placed before oleic acid (PA-1) and from a second catheter (PA-2) placed 2 h after oleic acid infusion. Oleic acid decreased arterial oxygen saturation and cardiac output and increased pulmonary vascular resistance and phasic pulmonary artery pressure. LVEDP did not change after oleic acid, although WP measured by both catheters was increased. In addition, WP measured by PA-2 (7.1 +/- 0.7 mm Hg) was greater than that measured by PA-1 (5.6 +/- 0.5 mm Hg) (p less than or equal to 0.037). Using PA-1, we found that WP increased in a linear manner with LVEDP both before and after pulmonary injury (r2 = 0.91, 0.68, respectively). There was no relationship between LVEDP and WP using PA-2 (r2 = 0.07). We conclude that oleic acid-induced pulmonary edema lessens the accuracy with which WP reflects LVEDP, and that WP from a catheter placed after edema less accurately reflects LVEDP than does WP from a catheter placed before edema.
Vasoactive drugs may increase intrapulmonary shunt in patients with permeability edema. Because 7.5% hypertonic saline solution has cardiotonic properties, we studied its hemodynamic and pulmonary effects in a canine model of oleic acid-induced lung injury. Immediately after saline infusion, there were increases in cardiac output (2.0 +/- 0.1 to 3.4 +/- 0.2 L/min; p less than .001) and intrapulmonary shunt (50.3 +/- 4.4 to 57.3 +/- 3.2%; p less than .01) without alteration in arterial or mixed venous oxygen tension. Although arterial oxygen content decreased from 16.4 +/- 1.1 to 14.4 +/- 0.9 ml/dl (p less than .001), paralleling the change in hemoglobin concentration, oxygen delivery to the tissues increased from 327 +/- 23 to 486 +/- 36 ml/min (p less than .001). These effects were transient, inasmuch as all values returned to preinfusion levels within 30 min. Tissue oxygen consumption increased proportionately with cardiac output, and the directional change in arterial oxygenation was similar to the change in mixed venous oxygen tension. We conclude that tissue oxygen delivery improves after hypertonic saline infusion despite changes in intrapulmonary shunt and oxygen consumption. However, any benefit appears to be transient.
This study was carried out to determine whether 7.5% hypertonic saline (HSS) and lactated Ringer's solution restore cerebral hemodynamics comparably when used for resuscitation from endotoxic shock. Endotoxic shock was produced in 13 dogs by the iv administration of 1.5 mg/kg Escherichia coli endotoxin. After 90 min of shock, seven animals were resuscitated with lactated Ringer's solution, 60 ml/kg iv, and six with 7.5% HSS, 6 ml/kg iv. Both solutions increased cardiac output and mean arterial pressure. With HSS, intracranial pressure was lower immediately after resuscitation (p less than .001) and one hour later (p less than .01). However, cerebral blood flow was not increased by either fluid and, due to hemodilution, cerebral oxygen transport decreased during resuscitation in both groups of animals. Thus, HSS restored systemic hemodynamics and maintained a lower intracranial pressure during resuscitation from endotoxic shock, but failed, as did lactated Ringer's solution, to restore cerebral blood flow and oxygen transport.
Nimodipine, a calcium entry blocking agent similar in structure to nifedipine but with selective cerebrovascular dilating effects, has potential use in the therapy and prevention of cerebral vasospasm after intracranial hemorrhage. The authors summarize the effects of calcium entry blockers, review the pharmacology of nimodipine, and discuss both the known and possible interactions of oral nimodipine with physical and pharmacological interventions that neuroanesthesiologists employ for patients with cerebral vasospasm during craniotomy for aneurysm clipping. In a series of 26 patients undergoing aneurysm clipping, the authors found that intraoperative blood pressure tended to be reduced by nimodipine. Although the number of patients was limited by the fact that they were enrolled in a multi-center nimodipine aneurysm study and thus had to meet the criteria for that study, it is concluded that prophylaxis of cerebral vasospasm with nimodipine in patients with ruptured intracranial aneurysm results only in a favorable tendency toward lower systemic blood pressure during craniotomy.
From 1969 through 1982, 185 carotid endarterectomies were performed under regional anaesthesia on 153 patients. Of these patients, 38 (25 per cent) had suffered a previous myocardial infarction, 63 (41 per cent) had documented coronary artery disease, and 115 (75 per cent) had hypertension. Anaesthesia was provided by a superficial cervical plexus block. Monitoring consisted of measurement of direct arterial pressure and continuous display of the electrocardiogram. Oxygen was administered by nasal cannula throughout the procedure. Mean arterial pressure was elevated when necessary by infusion of phenylephrine. No patient in this study suffered an acute myocardial infarction. The only cardiac complications consisted of eight episodes of non-life-threatening dysrhythmias. We conclude that regional anaesthesia for carotid endarterectomy is associated with a low risk of perioperative myocardial infarction.
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Positive-pressure ventilation can increase dead space by trapping gas, especially at high frequencies. Under conditions of high airway resistance and high pulmonary compliance, gas trapping can increase alveolar pressure without affecting proximal airway pressure, due to impedance to expiratory gas flow. The difference between alveolar pressure and proximal airway pressure at end-expiration has been called auto-PEEP. Using a mechanical test lung, we altered compliance and resistance under a variety of high-frequency jet ventilator settings to evaluate the generation of auto-PEEP. High driving pressures and prolonged inspiratory times significantly increased gas trapping. This effect was most pronounced when both airway resistance and pulmonary compliance were elevated. These findings support the concept that high-frequency jet ventilation (HFJV) may have deleterious side-effects in patients with chronic obstructive pulmonary disease.
A case of cyanide poisoning from laetrile ingestion is presented as an illustration of the recognition and treatment of cyanide intoxication. The pharmacology of laetrile, of cyanide, and of antidotes to cyanide intoxication are discussed as they relate to the acute management and successful treatment of this patient after this highly lethal ingestion.
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