The Mechanical Effects of the Gravid Uterus in Late Pregnancy*

Kerr, M. G.

doi:10.1111/j.1471-0528.1965.tb00061.x

Cited by 158 publications

(63 citation statements)

References 30 publications

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“…11 This is analogous to the responses of some subjects treated with nitroprusside ( Figure 2). In both instances, the initial rise in HR probably reflects activation of the sinoaortic baroreceptor reflex before the latter is overpowered by an increasingly severe hypovolemic and hypotensive stimulus.…”

Section: Supine Hypotensionsupporting

confidence: 73%

“…These include the supine hypotension syndrome of pregnancy, 11 the Bezold-Jarisch reflex, 12 and reflexive cardiac and vasomotor depression elicited by severe hemorrhage and other forms of acute/ severe hypovolemic hypotension. 2) Although hydralazine and diazoxide relax only arterial resistance vessels, nitroprusside also relaxes venous capacitance vessels.…”

Section: Mechanismmentioning

confidence: 99%

“…The supine hypotensive syndrome is defined by marked reductions in MAP and HR 11 that occur in a small percentage of late gestation gravida when they adopt the supine position. The position produces caval compression and a reduction in venous return, thereby leading to a fall in MAP.…”

Section: Supine Hypotensionmentioning

confidence: 99%

“…Shortly after MAP starts to fall, reflex reduction in HR begins. 11 Depending on baseline hemodynamic status, nitroprusside may increase or decrease cardiac output. 20 ' 21 In the context of the abnormally reduced blood volume characteristic of untreated severe preeclampsia, 22 nitroprusside-induced venodilation decreases venous return and cardiac output.…”

Section: Supine Hypotensionmentioning

confidence: 99%

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Nitroprusside in preeclampsia. Circulatory distress and paradoxical bradycardia.

Wasserstrum

1991

Hypertension

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In severe preeclampsia, short-term peripartum management of hypertension with hydralazine is complicated by relatively prolonged hypotensive episodes, resulting in fetal distress. We hypothesized that nitroprusside's rapid onset and brief antihypertensive action would permit more controlled blood pressure reduction. Nitroprusside was infused into 10 invasively monitored subjects until mean arterial pressure either 1) was gradually reduced 10-20% or 2) fell abruptly. Subjects fell into two groups, defined by whether the hypotensive effect of nitroprusside was accompanied by a fall in heart rate (group A, n=$) or a rise (group B, n=2). Group B showed the expected sinoaortic baroreceptor reflex elevations in heart rate (+17 ±6 beats/min) in response to moderate falls in mean arterial pressure (-32±9 mm Hg) elicited by moderate doses (1.03±0.23 /tg/kg/min). However in group A, steep reductions in mean arterial pressure (-75±22 mm Hg, p<0.0001), significantly greater than in group B (p<0.05), occurred at much lower doses (0.35±0.23 /ig/kg/min;/?<0.05) and were accompanied by falls in heart rate (-21±7 beats/min). The apparently paradoxical falls in heart rate and extreme hypotensive responses in group A indicate severe circulatory compromise, corresponding to the cardiac and vasomotor depression that characterizes severe hemorrhage and other forms of acute/severe hypovolemic hypotension. This hemodynamic pattern represents a cardiopulmonary baroreceptor reflex presumably related to the Bezold-Jarisch reflex. The appearance of this pattern in the present study probably reflects the imposition of nitroprusside's prominent venous dilator action on the relatively reduced blood volume that generally characterizes severe preeclampsia. (Hypertension 1991;18:79-84) P reeclampsia, a hypertensive disorder unique to pregnancy, occurs in about 7% of pregnancies that continue beyond the first trimester. 1Severe preeclampsia is distinguished from the mild form of the disease by the magnitude of hypertension (severe, systolic pressure greater than 160 mm Hg or diastolic pressure greater than 110 mm Hg) and the existence or severity of proteinuria, visual symptoms, pulmonary edema, epigastric pain, or other accompanying disturbances.1 -2 Severe preeclampsia is a major cause of maternal and fetal morbidity and mortality. Its etiology has not been established.The reduced sinoaortic baroreceptor reflex sensitivity that characterizes severe preeclampsia results in hemodynamic instability.3 This instability, manifested as markedly enhanced responses to antihypertensive drugs, is of concern with hydralazine because of the relatively long and variable intervals to its maximum effect and its relatively long durations of action. When cumulative doses of the drug exert their full effects without baroreceptor reflex buffering, severe hypotension and fetal distress frequently results. -5Intravenous nitroprusside has become the drug of choice for parenteral treatment of most hypertensive crises in nonpregnant adults and has largely supplanted di...

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Section: Supine Hypotensionsupporting

confidence: 73%

Section: Mechanismmentioning

confidence: 99%

Section: Supine Hypotensionmentioning

confidence: 99%

Section: Supine Hypotensionmentioning

confidence: 99%

See 2 more Smart Citations

Nitroprusside in preeclampsia. Circulatory distress and paradoxical bradycardia.

Wasserstrum

1991

Hypertension

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“…At term gestation, there is nearly complete obstruction of the inferior vena cava in the supine position and venous return occurs incompletely via collateral veins. 1 Because venous return is impaired, stroke volume decreases, and heart rate increases to maintain cardiac output (box 1). In a laboring patient, ϳ400 ml of blood is displaced into the central circulation with each contraction.…”

mentioning

confidence: 99%

Hemodynamic Effects of Aortocaval Compression and Uterine Contractions in a Parturient with Left Ventricular Outflow Tract Obstruction

Baird

Arkoosh²

2012

Anesthesiology

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A 21-YR-OLD parturient underwent induction of labor at 37 weeks gestation for cardiac decompensation in the setting of a bicuspid aortic valve and subaortic membrane. Cardiac evaluation revealed a left ventricular outflow tract gradient of 80 mmHg. Epidural analgesia was initiated with ropivacaine (0.1%) and fentanyl (0.0002%) (8 ml/h). As labor progressed, a phenylephrine infusion was required to maintain systolic systemic blood pressure more than 100 mmHg. Cyclic variations of maternal heart rate (red arrow) correlating with uterine contractions (blue arrow) subsequently developed. Fetal heart rate (black arrow) was unaffected. Evaluation of the parturient revealed she was normotensive with the phenylephrine infusion and resting comfortably in the supine position.The sinusoidal maternal heart rate pattern suggests the tachycardia was secondary to intermittent hemodynamic changes. Given the patient's position, aortocaval compression undoubtedly was a contributing factor. At term gestation, there is nearly complete obstruction of the inferior vena cava in the supine position and venous return occurs incompletely via collateral veins.1 Because venous return is impaired, stroke volume decreases, and heart rate increases to maintain cardiac output (box 1). In a laboring patient, ϳ400 ml of blood is displaced into the central circulation with each contraction.2 This transient fluid influx leads to an increase in preload, with a concomitant increase in stroke volume and a reflexive decrease in heart rate (box 2).Parturients with stenotic aortic lesions are extremely sensitive to changes in intravascular volume. Whereas hypovolemia leads to decreases in cardiac output, increases in preload are associated with pulmonary edema and atrial arrhythmias. Management requires meticulous attention to positioning, intravascular volume, and perfusion pressure. The cyclic heart rate pattern resolved after a 400-ml crystalloid bolus and repositioning into left uterine displacement. The remainder of labor progressed uneventfully with the vaginal delivery of a healthy fetus via a planned vacuum-assisted delivery in second stage.

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