Hemodynamic Depression Research Articles

Improved Hemodynamic Outcomes With Glycopyrrolate Over Atropine in Carotid Angioplasty and Stenting

Prophylactic atropine traditionally has been used to prevent CAS-associated hemodynamic depression. Glycopyrrolate may serve as an alternative with decreased cardiac effects. This study aims to compare the efficacy of prophylactic glycopyrrolate to atropine in preventing CAS-induced hemodynamic instability and cardiac complications. 115 consecutive CAS patients from 2004-2010 were evaluated. Primary endpoints were stroke, MI, bradycardia (HR<60 beats/min), and hypotension (systolic BP <90 mm Hg). Additional outcomes included tachycardia (HR >100 beats/min), hypertension (systolic BP >160 mm Hg), pre- and postoperative systolic BP difference, vasopressor use, arrhythmias, cardiac enzyme elevations, and access site complications. Of 115 patients, 65 (56.5%) patients who received atropine or glycopyrrolate prior to CAS were analyzed [40 (61.5%) patients received glycopyrrolate, 25 (38.5%) received atropine]. Mean age was 70.0 ± 8.5 years (range, 48-86 years). Mean stenosis was 86.2 ± 7.4% (range, 70-99%). No MI, major stroke, or death was observed in the 30-day postoperative period. Baseline systolic BP and HR were equivalent between groups. Postoperative bradycardia and hypotension were significantly lower in glycopyrrolate patients compared with atropine patients (30% vs 72%, P = .002; 2.5% vs 36%, P < .001, respectively). Postoperative hypertension was also significantly lower in the glycopyrrolate cohort (2.5% vs 16%, P = .047), whereas tachycardia, pressure changes, vasopressor use, and cardiac complications did not differ significantly. No significant differences in neurologic and access site complications were observed. Prophylactic glycopyrrolate, compared with atropine, reduces hemodynamic instability during CAS. The authors recommend glycopyrrolate use to prevent CAS-induced bradycardia and hypotension.

The hemodynamic effects of medetomidine continuous rate infusions in the dog

ObjectiveTo characterize the hemodynamic effects of continuous rate infusions (CRI) of medetomidine administered at doses ranging from 0 to 3 μg kg−1 hour−1. Study designProspective, blinded, randomized experimental trial. AnimalsSix adult purpose-bred mongrel dogs. MethodsAnesthesia was induced with sevoflurane for placement of arterial and venous catheters. Dogs recovered from anesthesia after which baseline hemodynamic measurements were obtained via lithium dilution cardiac output (CO) determination, with subsequent measurements via pulse power analysis to provide continuous CO determinations. Medetomidine, 1, 2, or 3 μg kg−1 hour−1 or a volume equivalent placebo, was administered via CRI for 60 minutes. Systolic, mean, and diastolic arterial pressure, heart rate (HR), CO and stroke volume were measured and stroke index (SI), cardiac index (CI), total peripheral resistance (TPR), and total peripheral resistance index (TPRI) were calculated at 3, 7, 10, 20, 30, 45, 60, 90, and 120 minutes from the start of the infusion. ResultsIncrease in dose decreased SI by 25%, 19%, and 30%, HR by 33%, 57%, and 60%, CI by 50%, 65%, 70% and increased TPRI by 109%, 235%, and 222% from baseline to the 60-minute measurement for the 1, 2, and 3 μg kg−1 hour−1 doses, respectively. HR, TPRI, and CI all showed significant differences over the duration of the study from the placebo treatment. ConclusionsMedetomidine CRI produces clinically relevant changes in CO, TPR, and HR. The demonstrated decrease in CO is largely because of bradycardia and the degree of cardiovascular depression appears to be dose-dependent. These findings are consistent with previously described hemodynamic changes with single bolus administration of medetomidine. Clinical relevanceLow-dose medetomidine CRIs produce clinically relevant hemodynamic depression at doses as low as 1 μg kg−1 hour−1 and should be used cautiously in dogs.

Non-protected carotid artery stent without angioplasty in high-risk patients with carotid and coronary artery disease undergoing cardiac surgery

Hemodynamic depression (HD) is a frequent complication related to carotid endartherectomy or carotid artery stenting (CAS), often not well tolerated in patients with coronary artery disease. The purpose of this study is to assess whether CAS without angioplasty is beneficial in patients with severe carotid artery disease before coronary revascularization surgery (CABG) regarding the occurrence of HD. Between October 2002 and August 2006, 39 CAS were performed in 35 patients before cardiac surgery. Outcome measures, including periprocedural and 30-day post stenting and cardiac surgery complications, were assessed. Twenty-seven patients underwent CABG and eight combined CABG and valve replacement. During or immediately after CAS there was no episode of bradycardia or hypotension necessitating medical treatment. In the period between CAS-CABG, there was no case of HD. We also found no myocardial infarction. There were five neurological complications, two of them in the period between CAS-CABG (one transitory ischemic attack (TIA) and one minor stroke) and three after CABG (one TIA and two strokes). Three of them were discharged symptom-free. CAS without angioplasty can be a safe alternative to treat patients with coexistence of carotid and cardiac disease, since does not produce hemodynamic depression, therefore diminishing the cardiac complications.

Simultaneous Bilateral Carotid Stenting in High-Risk Patients

The safety and efficacy of SBCAS have not been evaluated in detail. The purpose of our study was to evaluate the outcome after SBCAS in high-risk patients compared with unilateral stent placement. Between March 2002 and October 2008, a total of 205 consecutive high-risk patients underwent CAS at our institution. Of these patients, 30 (14.6%) underwent SBCAS (n = 24) and staged SBCAS (n = 6). Patients who underwent unilateral CAS (n = 175) during the same period served as controls. The stroke risk factors, procedural results, and outcome at 30 days and 6 months, as well as the restenosis rate at 6 months, were compared by using either the chi(2) test or the Kruskal-Wallis equality-of-populations rank test. Our data revealed no significant differences in the stroke risk factors between the SBCAS and the control group. HPS occurred more commonly in SBCAS (ie, 16.7%, 4/24) compared with 2.9% (5/175) in the control group (P = .014). However, there was no statistical significance between 2 groups in the event rate of stroke (minor and/or major stroke), death, or restenosis at 6 months. There was no significant difference in outcome at 6 months following stent placement between SBCAS and unilateral CAS in the high-risk patient group, even though HPS occurred more commonly after SBCAS.

Stent-based off-pump creation of an apico-aortic conduit

An apico-aortic conduit (AAC) is an alternative therapy in patients with aortic valve stenosis and severe concomitant disease. We investigated whether it is feasible to create an apico-aortic conduit off-pump with a newly developed, stent-based coring- and cannulation-device in the animal model. A new self-expandable, stent equipped and hooked prosthesis and a sheath enabling both airtight removal of tissue and introduction of the prosthesis were designed and experimentally investigated in six pigs. Hemodynamic- and echocardiographic investigations were performed without and with aortic stenosis. In three animals MRI was performed. There was no significant blood loss, no relevant contamination with air and no hemodynamic depression during the whole procedure. It was possible to yield the entire cardiac output through the conduit after creating a high grade aortic stenosis. Autopsy revealed an excellent anchorage of the prosthesis. Neither relevant intracavitary injury nor thrombotic formation was seen. This study proves the feasibility of a stent-based, off-pump creation of an AAC. The principle of this approach might be used for other purposes.

BIS monitored day‐case cardioversion: a comparison of sevoflurane with propofol

This study compared haemodynamic parameters and Bispectral Index System (BIS) values during day-case DC cardioversion of atrial fibrillation with either propofol or sevoflurane anaesthesia. After Research Ethics Committee approval and written informed consent, 60 patients scheduled for elective day-case cardioversion were randomly assigned to two groups. Both groups had a BIS electrode applied before induction of anaesthesia. Patients in one group were given intravenous propofol 2% at 67 mg.min−1 via infusion pump and the other inhaled sevoflurane 8% in 10 l.min−1 oxygen. The patients were asked to tap continuously with their index finger on their chest during induction. The induction-time endpoint was taken when the patient stopped tapping and then either the infusion of propofol was stopped or the inspired sevoflurane was reduced to 6%. One minute later, a DC shock was delivered. Eye opening to verbal command was then taken as the point of awakening. Before hospital discharge, patients completed a questionnaire that included scoring of pain on induction, postoperative nausea and vomiting and overall satisfaction. There was no difference between the mean (SD) age and weight of the propofol and sevoflurane group (respectively 70.0 (9.1) vs 70.1 (10.1) years and 80.4 (16.8) vs 86.4 (14.6) kg). The mean (SD) time taken for induction was significantly lower in the sevoflurane group (93.1 (45.0) vs 124.0 (29.6) s; p < 0.05). Mean arterial pressure was significantly lower in the propofol group after cardioversion (86.7 (15.5) vs 106.3 (21.1) mmHg; p < 0.01) and at eye opening to verbal command (83.1 (13.3) vs 104.2 (15.9) mmHg; p < 0.01). The propofol group also had correspondingly lower median (IQR) BIS values (47 (40–57) vs 65 (47–73) and 73 (69–82) vs 83 (79–87); p < 0.05). None of the patients reported awareness and satisfaction scores were similar in both groups. A previous study suggested that sevoflurane induction provided better cardiovascular stability than a target-controlled infusion of propofol for anaesthesia for cardioversions [1]. In our study, despite using less propofol (1.7 mg.kg−1 vs 2.9 mg.kg−1), patients also had significantly lower blood pressure and BIS values compared with sevoflurane. The time taken for induction in elderly patients may be longer with propofol infusion [2]. In our study, induction with propofol also appeared to take longer patients with atrial fibrillation compared with sevoflurane. A slow circulation time should speed induction with inhaled sevoflurane due to the more rapid rise in alveolar concentration compared with a normal circulation. Sevoflurane-induction anaesthesia for patients with atrial fibrillation undergoing DC cardioversion offers appropriate anaesthetic depth with less haemodynamic depression and more rapid recovery when compared with propofol. Future studies using BIS monitoring may help to refine anaesthetic administration to these patients.

Cardiopulmonary effects of diazepam-ketamine-isoflurane or xylazine-ketamine-isoflurane during abdominal surgery in foals

To evaluate cardiopulmonary effects of anesthetic induction with diazepam and ketamine or xylazine and ketamine, with subsequent maintenance of anesthesia with isoflurane, in foals undergoing abdominal surgery. 17 pony foals. Foals underwent laparotomy at 7 to 15 days of age and laparoscopy 7 to 10 days later. Foals were randomly assigned to receive diazepam, ketamine, and isoflurane (D/K/Iso; n = 8) or xylazine, ketamine, and isoflurane (X/K/Iso; 9) for both procedures. During anesthesia for laparotomy, cardiac index, and mean arterial blood pressure ranged from 110 to 180 mL/kg/min and 57 to 81 mm Hg, respectively, in the D/K/Iso group and 98 to 171 mL/kg/min and 50 to 66 mm Hg, respectively, in the X/K/Iso group. Cardiac index, heart rate, and arterial blood pressures were significantly higher in the D/K/Iso group, compared with the X/K/Iso group. During anesthesia for laparoscopy, cardiac index and mean arterial blood pressure ranged from 85 to 165 mL/kg/min and 67 to 83 mm Hg, respectively, in the D/K/Iso group, and 98 to 171 mL/kg/min and 48 to 67 mm Hg, respectively, in the X/K/Iso group. Heart rates and arterial blood pressures were significantly higher in the D/K/Iso group, compared with the X/K/Iso group. There were no significant differences between groups during either experimental period for percentage end-tidal isoflurane, arterial blood gas partial pressures, or pH values. Anesthesia of foals for abdominal surgery with D/K/Iso was associated with less hemodynamic depression than with X/K/Iso.

RR5. Carotid Higlhly-calcified “De Novo” Stenosis and Cutting-balloon Angioplasty: A Tool to Prevent Haemodynamic Depression?

RR5. Carotid Higlhly-calcified “De Novo” Stenosis and Cutting-balloon Angioplasty: A Tool to Prevent Haemodynamic Depression?

Hemodynamic instability during carotid artery stenting: the relative contribution of stent deployment versus balloon dilation

Hemodynamic instability may complicate carotid angioplasty and stenting in up to 40% of patients. The authors have previously demonstrated that primary self-expanding stent placement alone can gradually dilate severely stenosed carotid arteries without the use of balloons. The authors hypothesized that eliminating the balloon would reduce carotid baroreceptor stimulation, thereby decreasing the incidence of hemodynamic instability. Ninety-seven high surgical risk patients with symptomatic, severely stenosed carotid arteries were treated with the intention of using a self-expanding stent alone. Seventy-seven arteries (79%) were treated with stenting alone, and 20 required angioplasty (21%). Intraprocedural bradycardia (heart rate < 60 bpm) developed in 29 patients (38%) and hypotension (systolic blood pressure < 90 mm Hg) occurred in 1 patient (1%) treated with stenting alone. Fourteen patients (70%) who underwent angioplasty and stenting had bradycardia, and hypotension developed in 4 (20%). Atropine, glycopyrrolate, or vasopressors were required in 8% of patients who received stenting alone, compared to 30% of patients who underwent angioplasty. In the first 24 hours after treatment, hypotension or bradycardia developed in 25 patients (32%) who had undergone stent placement alone, and in 15 patients (75%) after stent placement and balloon angioplasty. There was no difference in the occurrence of intra- or postprocedural hypertension (systolic blood pressure > 160 mm Hg) between patients treated with stenting alone or stenting and balloons. Factors independently associated with hemodynamic depression included baseline heart rate and balloon use. Hemodynamic instability during and after carotid artery stenting was observed more frequently when balloon angioplasty was required than when stent placement was performed without concurrent balloon angioplasty.

The cardiopulmonary effects of anesthetic induction with isoflurane, ketamine–diazepam or propofol–diazepam in the hypovolemic dog

ObjectiveTo evaluate and compare the cardiopulmonary effects of induction of anesthesia with isoflurane (Iso), ketamine–diazepam (KD), or propofol–diazepam (PD) in hypovolemic dogs. Study designProspective randomized cross–over trial. AnimalsSix healthy intact, mixed breed, female dogs weighing 20.7 ± 4.2 kg and aged 22 ± 2 months. MethodsDogs had 30 mL kg−1 of blood removed at a rate of 1.5 mL kg−1 minute−1 under isoflurane anesthesia. Following a 30–minute recovery period, anesthesia was reinduced. Dogs were assigned to one of three treatments: isoflurane via facemask using 0.5% incremental increases in the delivered concentration every 30 seconds, 1.25 mg kg−1 ketamine and 0.0625 mg kg−1 diazepam intravenously (IV) with doses repeated every 30 seconds as required, and 2 mg kg−1 propofol and 0.2 mg kg−1 diazepam IV followed by 1 mg kg−1 propofol increments IV every 30 seconds as required. Following endotracheal intubation all dogs received 1.7% end–tidal isoflurane in oxygen. Cardiopulmonary variables were recorded at baseline (before induction) and at 5 or 10 minute intervals following endotracheal intubation. ResultsInduction time was longer in Iso (4.98 ± 0.47 minutes) compared to KD (3.10 ± 0.47 minutes) or PD (3.22 ± 0.45 minutes). To produce anesthesia, KD received 4.9 ± 2.3 mg kg−1 ketamine and 0.24 ± 0.1 mg kg−1 diazepam, while PD received 2.2 ± 0.4 mg kg−1 propofol and 0.2 mg kg−1 diazepam. End–tidal isoflurane concentration immediately following intubation was 1.7 ± 0.4% in Iso. Arterial blood pressure and heart rate were significantly higher in KD and PD compared to Iso and in KD compared to PD. Arterial carbon dioxide partial pressure was significantly higher in PD compared to KD and Iso immediately after induction. Conclusions and clinical relevanceIn hypovolemic dogs, KD or PD, as used in this study to induce anesthesia, resulted in less hemodynamic depression compared to isoflurane.

Postoperative Hemodynamics After Cardiopulmonary Bypass in Survived Newborn Piglets

Cardiac function and hemodynamics are frequently decreased during the first hours after heart surgery, resulting in inotropic support for treatment and prevention of further hemodynamic deterioration. The aim of this study was analysis of hemodynamics of neonatal piglets who survived early postoperative course after cardiopulmonary bypass (CPB) and cardioplegic arrest without the use of inotropic drugs. Newborn piglets (younger than 7 days) were placed on mild hypothermic CPB (32 degrees C) for 180 minutes, including 90 minutes of cardioplegic arrest. Hemodynamics were examined after termination of CPB and none of the animals received any inotropic support. After 6 hours, survived animals were euthanized (CPB group, n=4). For control, neonatal piglets were examined for the same time interval after surgery without CPB (control group, n=3). Systolic left-ventricular pressure increased after CPB, mean arterial blood pressure and amplitude of left ventricular wall thickness decreased. Compared with control group, systolic left-ventricular pressure in CPB group was higher (p<0.05). Present data demonstrated hemodynamic depression after cardiac procedures in survived neonatal animals. Although the effects may not be solely attributed to CPB and myocardial ischemia effects may be potentiate by CPB.

Is Haemodynamic Depression during Carotid Stenting a Predictor of Peri-procedural Complications?

Is Haemodynamic Depression during Carotid Stenting a Predictor of Peri-procedural Complications?

Is Haemodynamic Depression during Carotid Stenting a Predictor of Peri-procedural Complications?

The clinical significance of Haemodynamic Depression (HD) during carotid stenting (CAS) remains unclear. The aim of this study was to analyze the frequency and predictors of HD during CAS in a single centre experience. A prospective protocol for CAS was applied in a 15-month interval. Patients with restenosis, on betablockers, or with arrhythmias were excluded. A standardized dose of atropine (0.4mg) was given prior to stent deployment. Changes in heart rate, blood pressure, and neurological status were monitored and recorded. HD was defined as systolic pressure <90mmHg and/or heart rate <50 beats/min. Fifteen potential predictors of HD (age, gender, hypertension, smoking, diabetes, coronary artery disease, previous myocardial infarction, symptoms, degree of carotid stenosis contralateral CEA or CAS, calcified/hyperechoic plaque, plaque length, stent oversizing and type of stent) were tested in multivariate analysis. Two hundred and twenty three consecutive patients were enrolled. HD occurred in 98 cases (44%): in 68 cases HD required additional pharmacological support. At 30 days, any stroke rate was 3.1% (3 major and 4 minor), TIA rate 1.8%, myocardial infarction rate 0.4%. No deaths were recorded. No difference in complication rates were found in patients with or without HD. From regression analysis only the presence of calcified plaque (HR 9.5; 95% CI 5.0 to 18.2; p<0.0001) and the plaque length (HR 1.77; 95% CI 1.03 to 3.06; p=0.038) were associated significantly with HD. HD during CAS is a common, relatively benign event, without increased risk of peri-operative complications. Careful pharmacological treatment is necessary to decrease HD and the potential complications, especially in patients with more severe calcified lesions. These results require confirmation in a separate, larger cohort.

Effects of Posture and Prolonged Pneumoperitoneum on Hemodynamic Parameters during Laparoscopy

The present prospective study was designed to evaluate hemodynamic changes associated with head-down positioning and prolonged pneumoperitoneum during totally endoscopic robot-assisted radical prostatectomy. Ten American Society of Anesthesiologists (ASA) physical status I-III patients undergoing totally endoscopic robot-assisted radical prostatectomy were enrolled in the study. Invasive hemodynamic parameters were measured by transpulmonary arterial thermodilution using the PiCCO system with a femoral artery catheter. Cardiac index (CI), heart rate (HR), mean arterial pressure (MAP), systemic vascular resistance index (SVRI), intrathoracic blood volume (ITBV), and central venous pressure (CVP) were recorded with the patient in the supine position, after head-down tilt, intraoperatively after 30 min, 1 h, 2 h, 3 h, and 4 h of pneumoperitoneum at an insufflation pressure of 12 mmHg, after deflation still with head-down positioning, and finally, with the patient in the supine position. Placing the patient in the Trendelenburg (head-down) position caused a significant increase in CVP (from 9.9 +/- 3.4 to 15.1 +/- 2.3 mmHg), whereas all other hemodynamic parameters remained nearly unaffected. The induction of pneumoperitoneum resulted in a significant increase in MAP (from 74.9 +/- 12.9 to 95.4 +/- 11.9 mmHg). No other parameter was affected. Even at 4 h of pneumoperitoneum only mild hemodynamic changes were observed. After release of the pneumoperitoneum with the patient still in the head-down position, HR (49.0 +/- 4 versus 63.9 +/- 12.4 min(-1)) and after placing the patient in the supine position, CI (2.4 +/- 0.2 versus 3.3 +/- 0.7 l min(-1 )m(-2)) increased significantly, whereas CVP returned to baseline values. Patients undergoing totally endoscopic radical prostatectomy with 4 h of pneumoperitoneum in the Trendelenburg position experienced no significant hemodynamic depression during posture and pneumoperitoneum.

Hemodynamic Depression During Carotid Angioplasty With Stenting

To investigate potential risk factors for hemodynamic depression (HD) in elective carotid angioplasty with stenting (CAS) by using multidetector computed tomography (MDCT) angiographic findings and clinical data. A retrospective study was conducted for 32 patients that underwent MDCT angiography before CAS in our hospital. We reviewed the MDCT angiographic findings to evaluate parameters including total plaque volume, composition and the composition ratio of plaque, degree of stenosis, and distance of the most stenotic portion from carotid bifurcation. Clinical data such as patient age, presence of neurological symptoms, underlying medical disease, smoking history, and previous stroke history were noted. The MDCT angiographic parameters and clinical data were then analyzed to determine a prediction for periprocedural HD (systolic blood pressure, <90 mm Hg; or heart rate, <40 beats/min). Periprocedural HD was observed in 9 patients (28.1%). Among the MDCT angiographic parameters, the hemodynamic unstable group of patients had a smaller total plaque volume than that of stable group of patients (P = 0.04). The other MDCT parameters and clinical data did not show statistically significant difference between 2 groups. In this study, only the total volume of plaque was a positive factor for predicting HD during CAS. Multidetector computed tomography angiography can be helpful for predicting HD during CAS.

Influence of Stent Type on Hemodynamic Depression after Carotid Artery Stent Placement

To assess the effect of stent type on hypotension and bradycardia after carotid artery stent placement. A retrospective analysis on a prospectively maintained database was conducted in 256 patients (126 men; mean age, 71.8 years +/- 8.6; 194 de novo lesions) undergoing carotid artery stent placement between January 1996 and January 2007 by using self-expanding stents. Braided Elgiloy stents (Wallstents) were used in 44 of the 256 patients (17.2%) and slotted-tube nitinol stents were deployed in 212 (82.8%). Bivariate and multivariable logistic regression models were used to determine the influence of stent design on procedural and 24-hour hypotension and bradycardia. Procedural hemodynamic depression (HD) was encountered in 73 of the 256 patients (28.5%) due to hypotension in 24 (9.4%), bradycardia in 12 (4.7%), or both in 37 (14.5%) patients. Rates of procedural hypotension were 11.3% with nitinol stents and 0% with braided Elgiloy stents (P = .0188). Persistent postprocedural HD occurred in 91 of the 256 patients (35.5%) due to hypotension in 40 patients (15.6%), bradycardia in 23 (9.0%), or both in 28 (10.9%). Within a multivariable analysis adjusted for clinically relevant factors affecting rates of HD, the use of braided Elgiloy stents was associated with a decreased rate of procedural hypotension (odds ratio: 0.165; 95% confidence interval: 0.038, 0.721; P = .017). Procedural hypotension and bradycardia were not correlated to incidence of major adverse events but were associated with an increased duration of hospital stay (P = .0059 and P = .0335, respectively). Nitinol stents are associated with a higher risk of hypotension as compared to braided Elgiloy stents during carotid artery stent placement.

Factors associated with hypotension and bradycardia after carotid angioplasty and stenting

Acute procedurally induced hemodynamic depression can occur after carotid angioplasty and stenting (CAS). This study was performed to determine the frequency and risk factors for hypotension and bradycardia after the CAS procedure. The study reviewed clinical variables and angiographic data of all patients undergoing elective CAS with neuroprotection during a recent 5-year period. Intravenous atropine was given selectively in cases of bradycardia (heart rate <60 beats/min or a decrease of >20 beats/min). We further defined hemodynamic depression as bradycardia or severe hypotension (systolic blood pressure fall >30 mm Hg). Frequency and potential risk factors for hemodynamic depression were analyzed by logistic regression. During the study period, 416 patients (99% male; mean age, 74 +/- 11 years) underwent the CAS procedure. The median degree of stenosis was 93% (range, 60% to 99%). The frequencies of post-CAS hemodynamic depression include hypotension in 58 (14%), bradycardia in 112 (27%), or both in 21 (5%). All patients with bradycardia received intraprocedural atropine, and all heart rates returned to the baseline level. Persistent hypotension occurred in 45 patients (11%). Increased age was associated with CAS-induced bradycardia or hypotension. Adjusted risk factors associated with hemodynamic depression include age >78 years (odds ratio [OR], 5.25; 95% confidence interval [CI], 2.32 to 15.25; P = .01) and ejection fraction of <25% (OR, 3.25; 95% CI, 0.58 to 6.58; P = .02). CEA-related restenosis was associated with a reduced risk of hemodynamic depression (OR, 0.21; 95% CI, 0.12 to 0.69, P = .001). Persistent hypotension after CAS was associated with an increased risk of an adverse clinical event (44%, P = .001). Hemodynamic depression, including hypotension and bradycardia, is frequent after CAS. However, CAS-induced hemodynamic depression is rare in patients with postendarterectomy stenosis. Patients with compromised ejection fraction and increased age are at a higher risk of presenting with CAS-induced hemodynamic instability, and persistent hypotension after CAS is associated with an increased postprocedural complication rate.

Increased Cortical Cell Loss and Prolonged Hemodynamic Depression after Traumatic Brain Injury in Mice Lacking the IP Receptor for Prostacyclin

Prostacyclin is the major arachidonic acid metabolite of the vascular endothelium and is produced mainly via the cyclooxygenase-2 pathway. By acting on the prostacyclin (IP) receptor on platelets and vascular smooth muscle cells, prostacyclin exerts vasodilatory and antiaggregative/antiadhesive effects. Previous studies have shown that prostacyclin production increases after brain trauma, but the importance of prostacyclin for posttraumatic hemodynamic alterations and neuron survival has not been investigated. This study evaluated if endogenous prostacyclin plays a role in the pathophysiologic process in the brain after brain trauma. This was performed by comparing prostacyclin (IP) receptor-deficient (IP(-/-)) mice and mice with functional IP receptor (IP(+/+)) after a controlled cortical injury regarding contusion volume, cerebral blood flow ([(14)C]iodoantipyrine autoradiography), number of perfused capillaries (fluorescein isothiocyanate-dextran fluorescence technique), the transfer constant (K(i)) for [(51)Cr]EDTA, and brain water content (wet vs dry weight) in the injured and contralateral cortex. Contusion volume was increased in IP(-/-) mice compared with IP(+/+) mice. Three hours after trauma, cortical blood flow was decreased in the injured cortex of both groups and the reduction in blood flow in the cortex of the IP(-/-) mice persisted from 3 to 24 h, whereas blood flow approached normal values in the IP(+/+) mice after 24 h. No differences could be detected between the two genotypes regarding other hemodynamic parameters. We conclude that the prostacyclin IP receptor is beneficial for neuron survival after brain trauma in mice, an effect that may be mediated by improved cortical perfusion.

Suction Due to Left Ventricular Assist: Implications for Device Control and Management

Left ventricular assist device (LVAD) overpumping is associated with hemolysis, thrombus release, and tissue damage at the pump inlet. However, the impact of LVAD suction on pulmonary circulatory function remains unknown. We investigated LVAD suction as induced by pulmonary artery banding and overpumping in experimental animals and in a computer model. In six sheep, a rotary LVAD was implanted. Before inducing suction, partial support (40-60% of cardiac output) was established and characterized by measuring pressures and flows. In the animals, pulmonary artery occlusion (PAOC) elicited LVAD suction (left ventricular pressure was from -10 to -20 mm Hg) within 5-10 heartbeats. During suction, aortic pressure dropped to 50% and LVAD flow decreased significantly. After releasing the occlusion (20 s), the collapsed state persisted for another 20 s. A similar trend was obtained by simulating PAOC in the computer model. Additional simulations showed that pulmonary vascular resistance (PVR), volume status, and right ventricular (RV) contractility are exponentially related to the persistence of collapse after a suction event. Even modest increases in predisposing factors (elevated PVR, RV dysfunction, hypovolemia) caused sustained hemodynamic collapse lasting in excess of 15 min. Both in selected animals and the computer model, comparable suction-induced collapse was obtained by increasing LVAD speed by about 33%. Attempted compensation by simply decreasing speed was not effective, but temporarily shutting down the LVAD caused rapid reversal of collapse. In conclusion, rotary LVAD suction causes unfavorable conditions for effective unloading. The use of pump interventions appears a promising tool to detect suction and to avoid the associated hemodynamic depression.

Brain Injury Secondary to Carotid Intervention

Causes of brain injury during endovascular carotid intervention are protean. Mechanisms of injury include embolic and hemodynamic events, acute carotid occlusions occurring through a variety of means, and the relatively rare contrast-induced encephalopathy. Embolic injury may result from micro- and macroembolization and most commonly causes ischemic stroke when sufficiently severe. Hemodynamic injury may proceed from hemodynamic depression and hypoperfusion (which may result in watershed infarction) or the hyperperfusion syndrome, which may, if severe, result in hemorrhagic stroke. Embolic and dynamic causes of stroke may either occur intraprocedurally or at a variable time after stent placement and may be co-related. Impaired clearance of emboli due to relative hypoperfusion may exacerbate their clinical relevance. Other causes of stroke include acute carotid occlusions, which most commonly occur procedurally due to flow-limiting spasm, acute dissection, and, if a filter-type cerebral protection device has been used, filter occlusion due to a large trapped embolic load. These scenarios may result in stroke if not recognized and dealt with appropriately. Acute stent thrombosis may occur within 24 hours of the procedure as a result of adverse hemodynamic factors or suboptimal patient response to procedural heparin and antiplatelet agents, or it may occur after the procedure, again perhaps as a result of suboptimal response to antiaggregate drugs.