Jugular Vein Pressure Research Articles

Continuous retrograde hypothermic low flow cerebral perfusion during aortic arch surgery

Continuous retrograde hypothermic low flow cerebral perfusion (CRCP) with deep hypothermic systemic circulatory arrest (DHSCA) during aortic arch surgery was employed in six patients, aged 21-79 years. From August 1991 to November 1992, five of these patients were operated for ascending and arch aortic dissection type I, and one patient was operated for an aneurysm extending from the ascending aorta into the arch. Cardiopulmonary bypass (CPB) technology included a centrifugal pump and low-dose aprotinin. Venous drainage was established via the superior and inferior caval veins and arterial return via the femoral artery. Prior to CPB, a bypass line connecting the arterial line with the superior vena cava cannula was implemented. Prior to DHSCA, the patients were systemically cooled to a mean nasopharyngeal temperature of 15.2 degrees C. After induction of systemic circulatory arrest, the femoral artery cannula was clamped. Thereafter, the implemented bypass line was opened to achieve reverse flow into the superior vena cava to allow venoarterial perfusion. The perfusate was returned to the CPB circuit through drainage from the inferior caval vein and by aspiration of blood from the opened aortic arch. CRCP flow rate ranged from 250 to 450 ml/min (mean 375 ml/min) maintaining an internal jugular vein pressure between 18 and 25 mmHg. The duration of CRCP ranged from 24 to 55 minutes (mean 39 minutes). Postoperatively, one patient died of cardiac failure. The other five patients regained full consciousness without neurological deficits, as defined by the Glasgow coma score, within 48 hours after the operation. Neither did we see other major organ complications.(ABSTRACT TRUNCATED AT 250 WORDS)

Deep hypothermic systemic circulatory arrest and continuous retrograde cerebral perfusion for surgery of aortic arch aneurysm

From 1987 to February 1991, we have repaired or replaced the aortic arch in ten patients using deep hypothermic systemic circulatory arrest with continuous retrograde cerebral perfusion (CRCP). CRCP can be implemented using the bypass connecting the arterial and venous lines of the extracorporeal circuit to reverse the flow into the superior vena cava cannula after induction of circulatory arrest. CRCP flow required to maintain an internal jugular vein pressure of 20 mmHg ranged from 100 to 500 ml/min. After completion of suturing of the aortic arch graft, air is evacuated retrogradely from the open arch vessels prior to reestablishing the usual arterial return. Two patients died, one from sepsis and the other from liver cirrhosis 1 month postoperatively. CRCP times ranged from 11 to 56 min, and minimal nasopharyngeal temperatures ranged from 16 degrees to 18 degrees C. The difference in oxygen content between the perfused blood and the blood draining from the arch vessels during CRCP most likely reflected the steady-state metabolism of the brain during the deep hypothermic state. This technique offers advantages including the need for dissecting and clamping the arch branches, providing sufficient metabolic support to the brain during deep hypothermia, and eliminating embolism of particulate debris from the aortic arch.

Technique and clinical results of carotid stump back-pressure to determine selective shunting during carotid endarterectomy

A method of confirming carotid back pressure accuracy, variability during carotid clamping, and the clinical results with a modified back pressure shunt criterion were evaluated in 665 carotid endarterectomies. Mean arterial pressure, back pressure, and internal jugular vein pressure were measured. Cerebral perfusion pressure (back pressure — jugular vein pressure) and the collateral to hemisphere vascular resistance ratio, (ratio = [arterial pressure — back pressure]/[back pressure — jugular vein pressure]) were calculated. A shunt was used when cerebral perfusion pressure < 18 mm Hg. Back pressure accuracy was confirmed by test occlusion of the internal carotid artery distal to the plaque. Initial back pressure values were falsely high in 83 (12.5%) carotid endarterectomies. The mean SD (n = 665, mm Hg) were arterial pressure = 84.0 ± 9.06, back pressure = 41.0 ± 15.9, jugular vein pressure = 6.2 ± 3.9, cerebral perfusion pressure = 35.1 ± 5.7, and resistance ratio = 1.85 ± 1.44. Perfusion pressure was < 18 mm Hg in 82 (12.3%), of which 74 (11.1%) were shunted, and 8 (1.2%) had perfusion pressure increased ≥ 18 mm Hg during carotid endarterectomy with phenylephrine. Back pressure was <25 mm Hg in 107 (16.1%), ≤25 in 114 (17.1%), and <50 mm Hg in 481 (72.3%). Pressures were continuously monitored during 28 carotid endarterectomies, and all had a positive linear relationship between arterial pressure and back pressure, and minimal variability in the back pressure/arterial pressure and resistance ratios. Only two patients (0.3%) had a new neurologic deficit in the first 12 hours after carotid endarterectomy. Unless confirmation techniques are used, erroneously high carotid stump back pressure measurements may occur in 10% to 15% of carotid endarterectomies, resulting in failure to use a shunt in some depending on the pressure criterion used. Patients with cerebral perfusion pressure ≥18 mm Hg and back pressure ≥25 mm Hg can safely undergo carotid endarterectomy without a shunt.

Right atrial-jugular venous pressure gradients during CPR in children

This study measured the internal jugular vein and right atrium pressures during pediatric CPR to detect and quantify venous pressure gradients across the thoracic inlet. Ten children from 2 months to 15 years old who underwent CPR had simultaneous pressure measurements recorded from the right atrium and jugular vein. The right atrium-jugular vein peak compression-phase gradient was 18.3 +/- 4.7 mm Hg (mean +/- SD), and the end-relaxation gradient was 0.7 +/- 0.6. Jugular vein pressure exceeded the right atrium only in the early-relaxation phase (right atrium-jugular vein = -2.1 +/- 1.2). Thoracic inlet venous valving persisted throughout the duration of CPR. There is a large venous gradient across the thoracic inlet during chest compressions in children, facilitating cerebral blood flow. This gradient reversed only in the early-relaxation phase. The data suggest that jugular venous return occurs only in the early-relaxation phase, whereas cerebral venous drainage persists throughout the CPR cycle.

Vascular responses to acute intracranial hypertension.

In 27 rhesus monkeys the cerebrospinal fluid pressure (CSFP) was raised by injections into the cisterna magna to about 40 to 50 mm Hg in steps of 5 mm Hg every five minutes. During the initial phase of the rise of the CSFP to about 15 mm Hg normal animals showed a significant fall in the systolic arterial blood pressure. With a further elevation of the CSFP the BP rose till the CSFP reached 30 to 40 mm Hg. If the CSFP were raised higher than that, a large number of the animals showed a significant fall in the BP. In animals which were shocked before the CSFP was raised there was no drop in the systolic BP during the initial phase. This study indicates that vascular decompensation occurs in the majority of animals when the CSFP goes higher than 30 to 40 mm Hg; there is a significant rise in the pulse rate, superior sagittal sinus pressure (SSP), and internal jugular vein pressure (JVP). The JVP was related to the SSP, indicating that the JVP most probably reflected the pressure changes in the intracranial venous sinuses. Four animals suddenly collapsed at the highest CSFP. In the remaining 23 animals, on a sudden lowering of the CSFP to zero from the highest level, 13 monkeys died in less than half an hour and four in about an hour, while six animals stood this elevation of the CSFP well, with a good recovery. This indicates that, once the vascular decompensation has set in, the prognosis is generally poor even after lowering the CSFP to normal. The drop of the CSFP to zero produced no significant change in the pulse rate but a significant fall in the BP. The SSP rose when its pre-lowering level was less than 7·5 mm Hg and fell when the level was at or above 7·5 mm Hg level. The JVP showed a significant correlation with the variations in the SSP. The fundus examination at the end of the experiment revealed no abnormality.

Compression of cerebral vessels by intracranial hypertension. I. Dural sinus pressures.

In the monkey, sagittal sinus pressure is a complex function of cerebral blood flow and intracranial pressure; jugular vein pressure is a qualitative measure of cerebral blood flow. In the presence of intracranial hypertension, the response of anterior sagittal sinus pressure to blood flow changes is greatly exaggerated, but there is minimal communication of these large fluctuations in pressure to the transverse sinus and jugular vein. On the basis of these observations, we postulated compression of the sagittal sinus in response to increased intracranial pressure, and evidence is presented to localize maximum compression to the region of the interaural line. Reduction in diameter of cerebral vessels proximal to the sinus also appears to occur with intracranial hypertension, and ultimately, the dynamic interaction of these two factors is responsible for sagittal sinus pressure. In the end stage of cerebral decompensation, when intracranial and arterial tensions are equal, anterior sagittal sinus pressure also approaches the diastolic pressure, indicating nearly total collapse of the sinus.

The relation between internal jugular vein pressure and cerebrospinal fluid pressure in the operation of radical neck dissection.

The relation between internal jugular vein pressure and cerebrospinal fluid pressure in the operation of radical neck dissection.