Time Course Of Hemodynamic Changes Research Articles

Ascertaining the Value of Noninvasive Measures Obtained Using Color Duplex Ultrasound and Central Aortic Pressure Monitoring During the Management of Cerebral Arteriovenous Malformation Resection: Protocol for a Prospective, Case Control Pilot Study.

BackgroundDramatic hemodynamic changes occur upon removal of an arteriovenous malformation of the brain (bAVM) with a number of potentially serious perioperative complications, such as intracranial hemorrhage and venous occlusive hypertensive syndrome. As these complications largely occur in the postoperative inpatient period, a rapid, repeatable noninvasive investigation to serially monitor relevant intracranial hemodynamics may be of benefit. Though, transcranial Doppler (TCD) and transcranial color duplex (TCCD) are techniques used and available to provide hemodynamic measurements postoperatively, the time course of hemodynamic sequences following bAVM resection remains uncertain.ObjectiveThis is a prospective, case control pilot study conducted in participants having elective bAVM resection surgery.MethodsEach participant will undergo a preoperative color duplex ultrasound (CDU) of the bilateral extracranial carotid arteries, a CDU of the circle of Willis including the bAVM vessels, and a central aortic pressure measurement, repeated daily, postoperatively, for a 2-week period.ResultsPatient accrual has commenced with anticipation of first results in 2018.ConclusionsThis protocol aims to strengthen the work of previous authors by providing documentation of the time course of hemodynamic changes following bAVM resection. The protocol is designed to determine whether noninvasive technology, including CDU imaging of the extracranial carotid and intracranial arteries in the form of TCCD along with central aortic pressure measurements, can determine whether there are any hemodynamically significant prognostic markers that may provide insight into the process of vessel remodeling, including insight into venous changes following bAVM resection.

Glossopharyngeal Insufflation and Breath-Hold Diving: The More, the Worse?

The glossopharyngeal insufflation maneuver (lung packing) is largely performed by competitive breath-hold divers to improve their performance, despite observational evidence of fainting and loss of consciousness in the first seconds of apnea. We describe here the time course of hemodynamic changes, induced by breath-holding with and without lung packing, in 2 world-class apnea competitors. When compared with apnea performed after a deep breath (100% vital capacity), lung packing leads to a decrease in cardiac output, blood pressure, and cerebral blood flow during the first seconds after the beginning of apnea. The major hemodynamic disorders were observed in diver 1, who exhibited the greater increase in pulmonary volume after lung packing (+22% for diver 1 vs +10% for diver 2). After the initial drop in both cardiac output and blood pressure, the time course of hemodynamic alterations became quite similar between the two apneas. Some recommendations, such as limiting the number of maneuvers and performing lung packing in the supine position, should be expressed to avoid injuries secondary to the use of glossopharyngeal insufflation.

The importance of blood pressure variability in rat aortic and left ventricular hypertrophy produced by sinoaortic denervation.

The main objective was to examine the role of hemodynamics in rat aortic and left ventricular hypertrophy produced by sinoaortic denervation (SAD). Rats were examined at different times after SAD or sham operation (Sham). Hemodynamics were recorded continuously in conscious unrestrained rats. The time course of hemodynamic changes and cardiovascular hypertrophy was observed and linear regression analysis was performed to study the role of hemodynamics in SAD-induced aortic and left ventricular hypertrophy. Long-term mortality, water and food intake, and body weight were also determined after operation. High mortality (40%), dramatic reduction of water and food intake, and weight loss occurred within 1 week after SAD. Chronic SAD rats exhibited a marked increase in blood pressure variability (BPV), with no change in the average level of blood pressure (BP), as compared with the Sham control rats. Increased BPV was higher at 2 weeks (about threefold) than 16 weeks (about twofold) after SAD. Aortic hypertrophy existed in all three kinds of examined rats: 2-, 10- and 16-week SAD rats. Left ventricular hypertrophy was found only in 10- and 16-week SAD rats. Both aortic hypertrophy and left ventricular hypertrophy were significantly and positively correlated with BPV, but not with BP level. Persistent high BPV following SAD can lead to aortic and left ventricular hypertrophy. The aorta is more sensitive to increased BPV than the heart.

Time course of hemodynamic changes and improvement of exercise tolerance after cardioversion of chronic atrial fibrillation unassociated with cardiac valve disease

This study prospectively assessed the time course, magnitude and mechanism of the hemodynamic changes after restoration of sinus rhythm in patients with chronic atrial fibrillation (AF) unassociated with valvular disease. Severe cardiac dysfunction may occur after chronic supraventricular tachycardia in patients with and without underlying cardiac disease. Improvement may follow abolishment of the arrhythmia or adequate slowing of the ventricular rate. Eight patients were studied with a mean previous duration of AF of 10 ± 9 months. Ejection fraction, exercise capacity and the atrial contribution to the left ventricular filling (only during sinus rhythm) were studied before cardioversion, after cardioversion and 1 week, 1 month and 6 months thereafter. A significant improvement in ejection fraction from 36 ± 13 to 53 ± 8% (p < 0.05) occurred at 1 month after cardioversion. Concomitantly, peak oxygen consumption had increased at 1 month, from 20.1 ± 7 to 25.2 ± 6 ml/min/kg (p < 0.05). Thereafter, no further improvement in hemodynamic parameters occurred. The atrial systole improved already at 1 week (from 3 ± 5 to 16 ± 11%, p < 0.05) and remained unchanged thereafter. Thus, restoration of sinus rhythm was associated with a delayed improvement in ejection fraction and maximal exercise capacity, preceded by an early restoration of atrial contractility and an acute slowing of the heart rate. The discrepancy in time course of restoration of atrial and ventricular function parameters suggests that an intrinsic left ventricular cardiomyopathy is present in patients with AF.

Time course of hemodynamic changes in rats with healed severe myocardial infarction

Male rats were monitored for 8 mo after severe myocardial infarction (MI) to chronicle hemodynamic and left ventricular (LV) functional changes. Blood pressure (BP), heart rate (HR), cardiac output index (CO), regional blood flow, and systemic vascular resistance (SVR) were measured with catheters and radiolabeled microspheres at 4, 7, 10, 20, and 35 wk after coronary artery ligation (n = 10-16/group) or sham operation (control; n = 9-14/group). At 4 wk, 43 +/- 1% of the LV circumference was scarred, peak LV BP, LV dP/dtmax, mean BP, SVR, and HR were 11-38% less than control (P less than 0.05), and LV end-diastolic pressure (LVEDP) was increased by 313% (P less than 0.05). Mean BP, LVEDP, LVBP, and LV dP/dtmax did not further deviate after 4 wk. However, CO and SVR changed progressively and were 67 and 33%, respectively, of control by 35 wk (P less than 0.05) when blood flow to stomach, small intestine, and kidney was 55, 38, and 27% of control. Lung and heart weights were significantly increased by 148 and 22% at 4 wk, and remained elevated, and lung dry weight-to-wet weight ratio was reduced at 7 and 10 wk. Thus the trajectory of rats with healed severe MI reflects progressive cardiac decompensation, cardiac output redistribution, and terminal heart failure.