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Copyright of Canadian Journal of Anaesthesia / Journal Canadien d'Anesthésie is the property of Springer Nature and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Control of blood pressure in severe pregnancy-induced hypertension has often relied on agents with an unpredictable onset and duration of action. Because intravenous nitroglycerin is a potent, rapidly acting agent with a hemodynamic half-life measured in minutes, we evaluated its cardiovascular effects with and without volume expansion in six patients with severe pregnancy-induced hypertension. Nitroglycerin alone reduced mean arterial pressure by 27.5% without any significant changes in heart rate, central venous pressure, or stroke volume. The pulmonary capillary wedge pressure fell from 9 +/- 3 to 4 +/- 2 mm Hg (p less than 0.05) while the cardiac index decreased from 3.51 +/- 0.67 to 2.87 +/- 0.76 L/min X m2. Oxygen delivery fell significantly (p less than 0.05), from 617 +/- 78 to 491 +/- 106 ml/min X m2. While volume expansion alone had no effect on mean arterial pressure, the combination of blood volume expansion and nitroglycerin resulted in a marked resistance to the hypotensive effect of nitroglycerin. Cardiac index, pulmonary capillary wedge pressure, and oxygen utilization were not significantly different from baseline values when volume expansion preceded nitroglycerin. We conclude that the ease with which nitroglycerin reduces blood pressure is dependent on the individual patient's volume status. Although volume expansion allows one to maintain cardiac index, pulmonary capillary wedge pressure, and oxygen utilization when used in combination with nitroglycerin, this benefit may be offset by a concomitant reduction in hypotensive capability.

Fifteen primigravid patients with severe pregnancy-induced hypertension were studied by catheterization of the right side of the heart. A hemodynamic protocol was implemented that required maintaining colloid osmotic pressure above 17 millimeters of mercury, pulmonary capillary wedge pressure below 15 millimeters of mercury and the mean arterial pressure in a very narrow range throughout labor and delivery and for 48 hours postpartum. The initial colloid osmotic pressures and pulmonary capillary wedge pressures were 18.0 +/- 2.6 and 10.5 +/- 4.0 millimeters of mercury, respectively, and remained essentially unchanged throughout the post partum period. The only benefit derived from volume expansion in these patients appeared to be the absence of acute fetal distress after the initiation of antihypertensive therapy. Six of 15 patients had late fetal stress develop during labor, suggesting that aggressive volume repletion and colloid osmotic pressure correction in pregnancy-induced hypertension does not effect the over-all incidence of fetal distress. We recommend that correction of colloid osmotic pressure be restricted to instances in which extremely low values (less than 12 millimeters of mercury) or a prolonged negative colloid osmotic pressure to pulmonary capillary wedge pressure gradient are identified. Finally, the benefit of volume expansion in pregnancy-induced hypertension appears to be the prevention of sudden and profound drops in blood pressure with antihypertensive therapy--not the prevention of fetal distress during labor.

Intravenous nitroglycerin would appear to be an ideal agent for the treatment of severe pregnancy-induced hypertension complicated by cardiogenic pulmonary edema. Nitroglycerin infusion effectively reduces preload by venous dilatation and, at higher doses, results in arterial vasodilatation. Because of these pharmacologic properties, the effects of intravenous nitroglycerin were studied in three patients with severe pregnancy-induced hypertension complicated by pulmonary edema. The major cardiovascular effects of nitroglycerin were to reduce the mean pulmonary capillary wedge pressure from 27 +/- 4 to 14 +/- 6 mm Hg, which result in a change in the colloid osmotic pressure to pulmonary capillary wedge pressure gradient from -10 to 2 mm Hg. No significant changes occurred in heart rate, central venous pressure, or cardiac index. Analysis of oxygen-related parameters revealed a significant (p less than 0.05) increase in oxygen delivery and extraction accompanied by a 53% increase in oxygen consumption. The changes in oxygen-related variables appeared to be secondary to a fall in mixed venous oxygen tension from 39 +/- 4 to 33 +/- 1 torr. These changes occurred without any significant improvement in arterial oxygen tension. We conclude that while intravenous nitroglycerin expeditiously corrects the hydrostatic derangements of pulmonary edema seen in pregnancy-induced hypertension, a rapid improvement in arterial oxygenation does not occur.

Regional anaesthesia is a suitable technique for the management of the asthmatic parturient. We report the case of an asthmatic gravida in labour in whom prompt institution of bupivacaine-fentanyl epidural analgesia was associated with enhancement of the effectiveness of concurrent medical therapy for bronchospasm. Prior to the initiation of epidural blockade, inhaled atropine was employed in an effort to reduce parasympathetic tone in the bronchial smooth muscle. Sustained clinical improvement did not occur until after delivery of the fetus and placenta.