Partial Right Atrial Inflow Occlusion for Transient Systemic Hypotension During Deployment of Thoracic Stentgrafts

Purpose Temporary balloon occlusion of the inferior vena cava to lower cardiac output is a relatively infrequently used technique to induce controlled systemic hypotension. In this technical note, we describe the feasibility, reliability, and safety of partial occlusion of right atrial inflow and the effect on systemic blood pressure during the deployment of a thoracic stentgraft. Materials and Methods Twenty consecutive patients undergoing thoracic endovascular aortic repair, with proximal landing in zone 0–3 of the thoracic aorta, were prospectively included. Right atrial inflow occlusion was performed with a compliant occlusion balloon. Results Median time to reach a mean arterial pressure of 50 mmHg was 43 s. Median recovery time of blood pressure was 42 s. Conclusion Partial right atrial inflow occlusion with an occlusion balloon is feasible with reliable results and without procedure-related complications.

Ventilatory response to hypercapnia is increased after 4 h of head down bed rest

Head-down bed rest (HDBR) has previously been shown to alter cerebrovascular and autonomic control. Previous work found that sustained HDBR (≥ 20 days) attenuates the hypercapnic ventilatory response (HCVR); however, little is known about shorter-term effects of HDBR nor the influence of HDBR on the hypoxic ventilatory response (HVR). We investigated the effect of 4-h HDBR on HCVR and HVR and hypothesized attenuated ventilatory responses due to greater carotid and brain blood flow. Cardiorespiratory responses of young men (n = 11) and women (n = 3) to 5% CO2 or 10% O2 before and after 4-h HDBR were examined. HDBR resulted in lower HR, lower cardiac output index, lower common carotid artery flow, higher SpO2, and higher pulse wave velocity. After HDBR, tidal volume and ventilation responses to 5% CO2 were enhanced (all P < 0.05), yet no other changes in cardiorespiratory variables were evident. There was no influence of HDBR on the cardiorespiratory responses to hypoxia (all P > 0.05). Short-duration HDBR does not alter the HVR, yet enhances the HCVR, which we hypothesize is a consequence of cephalic CO2 accumulation from cerebral congestion.

Ectothermy and cardiac shunts profoundly slow the equilibration of inhaled anaesthetics in a multi-compartment model

The use of inhalational anaesthesia is ubiquitous in terrestrial vertebrates. Given the dependence of these agents on delivery by the cardiorespiratory system, we developed a new computational model predicting equilibration of inhaled anaesthetics in mammalian and ectotherm conditions including the ability of reptiles to maintain vascular shunts. A multi-compartment model was constructed from simultaneously-solved equations, verified by comparison to the literature for endo and ectotherm physiology. The time to 90% equilibration of anaesthetic in arterial blood (t90) is predicted and used to compare anaesthetics and physiologies. The five to tenfold lower cardiac output and minute ventilation of ectothermic vertebrates is predicted to slow equilibration times by five to ten times leading to 90% equilibration in ectotherm arterial blood of over 200 min, compounded by reduction in body temperature, and the extent of right-to-left vascular shunts. The impact of these findings is also influenced by the solubility coefficient of the anaesthetic, such that at net right-to-left shunt fractions of over 0.8, sevoflurane loses the advantage of faster equilibration, in comparison with isoflurane. We explore clinical strategies to regulate anaesthetic uptake in ectotherms by managing convectional flow especially by supportive ventilation and reduction of the right-to-left shunt.

P793 Is gender a key determinant of exercise tolerance in moderate-to-severe aortic stenosis?

Background Gender-related differences are known about pathophysiology and clinical outcome of aortic stenosis (AS). Nevertheless, the impact due to gender on effort intolerance as well as its mechanisms has not been defined. We sought to assess functional capacity in AS labelling gender differences. Methods Sixty patients [age 69(63-76)years; female 24(40%)] with at least moderate AS (rest Vmax &gt;3 m/s) underwent to rest and exercise echocardiography with simultaneous cardiopulmonary exercise test (CPET) during maximal symptom-limited exercise. Differences on echocardiographic and CPET variables were assessed according to gender. Results Women showed lower effort tolerance [female vs male: workload 51(46.5-72.5) vs 92.5(74-118.5)watts, p&lt;.0001; peakVO2 13.2(12-15.2) vs 17.7(14.2-22-7)mL/kg/min, p=.002; Predicted peakVO2 63.5(53.5-74) vs 76(61.5-101)%, p=.006; anaerobic threshold 11.4(9.8-13.2) vs 12.8(11.4-15-7)mL/kg/min, p=.01; VE/VCO2 29.5(26.1-30.2) vs 26.2(24.3-28.5), p=.008] characterized by lower chronotropic reserve [age-predicted heart rate (HR) reserve 69.5(58.6-78.9) vs 82.8(74.6-89.7)%, p=.003; HR reserve 40.5(33.6-51) vs 47.5(39-67.5), p=.02; HR recovery at 1 min 9(4-12) vs 14(8.5-20), p=.002)], lower cardiac output (CO) response [exercise CO 7.9(6.4-8.8) vs 8.6(7.9-9.9) L/min, p=.01; CO reserve 2.9(2.1-3.6) vs 4.3(3.2-5.4)L, p=.0008] and lower peripheral extraction [C(A-V)VO2 12(9.7-14.2) vs 15.4(13.8-16.6)mL/100mL, p=.0007]. At 12 months follow up, the incidence for AVR was 0.55(0.31-0.73) in women and 0.29(0.15-0.45) in men, while at 60 months it was respectively 0.69(0.44-0.85) and 0.59(0.11-0.35). Conclusions in women, moderate-to-severe AS generates a higher degree of functional limitation compared to men. A lower CO reserve, mainly determined by an impaired chronotropic response and lower C(A-V)O2, plays a central role. This unfavourable phenotype is associated with a less advanced LV remodelling pattern and an earlier incidence of AVR.

Impaired central hemodynamics in chronic obstructive pulmonary disease during submaximal exercise

It is unknown whether central hemodynamics are impaired during exercise in chronic obstructive pulmonary disease (COPD) patients. We hypothesized that, at a similar absolute V̇o2 during exercise, COPD patients would have a lower stroke volume and cardiac output compared with healthy controls. Furthermore, we hypothesized that greater static hyperinflation [ratio of inspiratory capacity to total lung capacity (IC/TLC)] and expiratory intrathoracic pressure would be significantly related to the lower cardiac output and stroke volume responses in COPD patients. Clinically stable COPD ( n = 13; FEV1/FVC: 52 ± 13%) and controls ( n = 10) performed constant workload submaximal exercise at an absolute V̇o2 of ~1.3 L/min. During exercise, inspiratory capacity maneuvers were performed to determine operating lung volumes and cardiac output (via open-circuit acetylene rebreathe technique) and esophageal pressure were measured. At similar absolute V̇o2 during exercise ( P = 0.81), COPD had lower cardiac output than controls (COPD: 11.0 ± 1.6 vs. control: 12.2 ± 1.2 L/min, P = 0.03) due to a lower stroke volume (COPD: 107 ± 13 vs. control: 119 ± 19 mL, P = 0.04). The heart rate response during exercise was not different between groups ( P = 0.66). FEV1 (%predicted) and IC/TLC were positively related to stroke volume ( r = 0.68, P = 0.01 and r = 0.77, P < 0.01). Last, esophageal pressure-time integral during inspiration was positively related to cardiac output ( r = 0.56, P = 0.047). These data demonstrate that COPD patients have attenuated cardiac output and stroke volume responses during exercise compared with control. Furthermore, these data suggest that the COPD patients with the most severe hyperinflation and more negative inspiratory intrathoracic pressures have the most impaired central hemodynamic responses. NEW & NOTEWORTHY Chronic obstructive pulmonary disease leads to cardiac structural changes and pulmonary derangements that impact the integrative response to exercise. However, it is unknown whether these pathophysiological alterations influence the cardiac response during exercise. Herein, we demonstrate that COPD patients exhibit impaired central hemodynamics during exercise that are worsened with greater hyperinflation.

Abstract WP350: Pumping Against Gravity - Cardiac Function Affects Fluctuations in Cerebral Blood Flow Caused by Head Position Change in Acute Ischemic Stroke

Introduction: Acute ischemic stroke (AIS) patients often have the head-of-bed (HOB) elevated to 30 0 while in the Emergency Department (ED). Flat HOB positioning has been shown to impact cerebral flow. Whether this holds true in undifferentiated, ED stroke patients is unknown. Hypothesis: We tested the hypothesis that 0 0 HOB positioning improves middle cerebral artery (MCA) mean flow velocity (MFV) in AIS compared to 30 0 . We secondarily tested the hypothesis that lower cardiac output (CO) is associated with greater fluctuation of MFV. Methods: This was a quasi-experimental study with repeat measurements of MCA MFV at 30 0 and 0 0 HOB position. Patients > 18 years presenting to the ED within 12 hours of symptom onset and a NIHSS ≥ 4 were eligible. After applying non-invasive monitoring of mean arterial pressure (MAP) and CO, an investigator used transcranial Doppler to obtain bilateral MCA MFV at 30 0 and 0 0 HOB position. If a signal was unobtainable on the ischemic side, the contralateral MFV was used for analysis. The primary analysis comprised all subjects with confirmed stroke on subsequent imaging and included student t-test for continuous measures. Secondary analysis used multiple linear regression to test if baseline NIHSS, age, MAP and CO were associated with changes in MFV. Results: There were 38 subjects enrolled, of whom 32 had confirmed AIS and were included in analysis. The mean age was 66 (±15) years and NIHSS 7 (±6). Stroke location was mixed (50% lacunar, 25% posterior and 25% anterior circulation). Averaged across all subjects, the MFV did not significantly increase when changing the HOB position from a 30 0 to 0 0 (+0.7 cm/s, 95% CI -1.6 to 3.1). Nevertheless, 16% (95% CI 5-33%) of subjects had a ≥ 20% increase and 47% (95% CI 29-65%) had any increase in MFV at 0 0 compared to 30 0 HOB. Adjusting for age, NIHSS and MAP, lower CO was associated with greater change in MFV (+2 cm/s [95% CI 0.2-3.7 cm/s] for every 1 L/min lower cardiac output, p=0.03). Conclusions: In conclusion, in a mixed sample of ED AIS patients, lower HOB position does not significantly impact cerebral flow on average, yet a considerable proportion of individuals may benefit from lower HOB position. Low cardiac output may identify those that benefit most.

Sympathetic nerve activity and peripheral vasodilator capacity in young and older men

Interindividual variability in sympathetic nerve activity (SNA) has provided insight into integrative mechanisms contributing to blood pressure (BP) regulation in humans. In young people, the influence of high SNA on BP is balanced by lower cardiac output and less adrenergic vasoconstrictor responsiveness. Older people have higher SNA and higher BP. We hypothesized that SNA has a restraining effect on peripheral vasodilator responsiveness in young and older men, such that individuals with higher tonic SNA would show less forearm vasodilatation to exogenous vasodilators. We measured muscle SNA (MSNA; microneurography) and forearm vasodilator responses to intra-arterial infusions of acetylcholine (ACh; endothelium dependent) and sodium nitroprusside (SNP; endothelium independent) in 13 young (age; 27 ± 1 yr) and 16 older (61 ± 2 yr) men. Forearm vascular conductance (FVC) responses to ACh were lower in the older men at the two highest doses (2 and 4 μg·100 ml−1·min−1; Δ395 ± 81 vs. 592 ± 87% and 412 ± 87 vs. 616 ± 132%, P < 0.05), and MSNA was higher (64 ± 4 vs. 41 ± 2 bursts/100 hb; P < 0.05). There was no difference in the FVC response to SNP between young and older men ( P > 0.05). In young men, there was an inverse relationship between resting MSNA and FVC responses (%change) to both ACh and SNP ( r = −0.83 and r = −0.83, respectively; P < 0.05). In older men, however, this relationship was not observed. Tonic SNA may act to restrain vasodilator responses in young men, whereas in older men a lack of such restraint may be protective against the pressor effects of higher SNA.