Changes In Blood Flow Patterns Research Articles

The role of intracranial pressure in the arrest of hemorrhage in patients with ruptured intracranial aneurysm.

✓ Intracranial epidural pressure (EDP) was recorded in 29 patients admitted with ruptured saccular aneurysms, but unfit for immediate surgery. In 10 patients a total of 13 recurrent hemorrhages were recorded; the average time before rerupture was 7.7 days after the last hemorrhage. Ten of the rebleedings started from intracranial pressure levels at or below 400 mm H2O whereas three started from higher prerupture levels. The observations indicate an increasing risk of rebleeding as the epidural pressure decreases toward normal pressure. Most repeat hemorrhages are arrested at EDP levels about that of the diastolic blood pressure. The resulting reduced pressure gradient across the aneurysm wall is important in the arrest of hemorrhage and the maintenance of hemostasis. Measurement of internal carotid artery blood flow during the acute stage of recurrent hemorrhage shows marked changes in blood flow pattern. Arrest of blood flow occurred only at the end of diastole; forward flow occurred only during systole. The effect of intracranial-pressure-buffering mechanisms on the increased EDP after rupture is discussed. Activation of these mechanisms may reduce the EDP to acceptable pressure levels within minutes and should be awaited before decompressive management is considered. Continuous recording of the EDP in patients unfit for immediate aneurysm surgery is important in the selection of the optimal time for operation.

COARCTATION OF THE AORTA AND PREGNANCY. OBSTETRIC AND CARDIOVASCULAR COMPLICATIONS BEFORE AND AFTER SURGICAL CORRECTION.

THE ALTERED cardiovascular hemodynamics associated with coarctation of the aorta are well understood. The changes in blood-flow pattern in the abdominal aorta and its pelvic branches produced by coarctation have considerable significance to the obstetrician who cares for the woman with coarctation who becomes pregnant. The essential physiologic alterations produced by coarctation (Figure) are as follows: (1) decreased pulse pressure (or damping) of the pulse contour in the aorta and all arterial branches originating below the coarcted segment in the descending thoracic aorta; (2) increased arterial blood pressure in the aortic arch proximal to the coarctation and in the branches of the aortic arch; (3) increased left ventricular work because of hypertension in the proximal aorta; (4) extensive collateral arterial circulation, carrying blood from the hypertensive branches proximal to the coarctation to the abdominal aorta distally. Usually, these collaterals provide a fairly normal mean arterial pressure and a near normal