Influence of oxygen tension on myocardial performance. Evaluation by tissue Doppler imaging

BACKGROUND: Low O(2 )tension dilates coronary arteries and high O(2 )tension is a coronary vasoconstrictor but reports on O(2)-dependent effects on ventricular performance diverge. Yet oxygen supplementation remains first line treatment in cardiovascular disease. We hypothesized that hypoxia improves and hyperoxia worsens myocardial performance. METHODS: Seven male volunteers (mean age 38 ± 3 years) were examined with echocardiography at respiratory equilibrium during: 1) normoxia (≈21% O(2), 79% N(2)), 2) while inhaling a hypoxic gas mixture (≈11% O(2), 89% N(2)), and 3) while inhaling 100% O(2). Tissue Doppler recordings were acquired in the apical 4-chamber, 2-chamber, and long-axis views. Strain rate and tissue tracking displacement analyses were carried out in each segment of the 16-segment left ventricular model and in the basal, middle and apical portions of the right ventricle. RESULTS: Heart rate increased with hypoxia (68 ± 4 bpm at normoxia vs. 79 ± 5 bpm, P < 0.001) and decreased with hyperoxia (59 ± 5 bpm, P < 0.001 vs. normoxia). Hypoxia increased strain rate in four left ventricular segments and global systolic contraction amplitude was increased (normoxia: 9.76 ± 0.41 vs hypoxia: 10.87 ± 0.42, P < 0.001). Tissue tracking displacement was reduced in the right ventricular segments and tricuspid regurgitation increased with hypoxia (7.5 ± 1.9 mmHg vs. 33.5 ± 1.8 mmHg, P < 0.001). The TEI index and E/E' did not change with hypoxia. Hyperoxia reduced strain rate in 10 left ventricular segments, global systolic contraction amplitude was decreased (8.83 ± 0.38, P < 0.001 vs. normoxia) while right ventricular function was unchanged. The spectral and tissue Doppler TEI indexes were significantly increased but E/E' did not change with hyperoxia. CONCLUSION: Hypoxia improves and hyperoxia worsens systolic myocardial performance in healthy male volunteers. Tissue Doppler measures of diastolic function are unaffected by hypoxia/hyperoxia which support that the changes in myocardial performance are secondary to changes in vascular tone. It remains to be settled whether oxygen therapy to patients with heart disease is a consistent rational treatment

Relation of tricuspid annular displacement and tissue Doppler imaging velocities with duration of weaning in mechanically ventilated patients with acute pulmonary edema

<p>Abstract</p> <p>Background</p> <p>Liberation from the ventilator is a difficult task, whereas early echocardiographic indices of weaning readiness are still lacking. The aim of this study was to test whether tricuspid annular plane systolic excursion (TAPSE) and right ventricular (RV) systolic (Sm) and diastolic (Em & Am) tissue Doppler imaging (TDI) velocities are related with duration of weaning in mechanically ventilated patients with acute respiratory failure due to acute pulmonary edema (APE).</p> <p>Methods</p> <p>Detailed quantification of left and right ventricular systolic and diastolic function was performed at admission to the Intensive Care Unit by Doppler echocardiography, in a cohort of 32 mechanically ventilated patients with APE. TAPSE and RV TDI velocities were compared between patients with and without prolonged weaning (≥ or < 7 days from the first weaning trial respectively), whereas their association with duration of ventilation and left ventricular (LV) echo-derived indices was tested with multivariate linear and logistic regression analysis.</p> <p>Results</p> <p>Patients with prolonged weaning (n = 12) had decreased TAPSE (14.59 ± 1.56 vs 19.13 ± 2.59 mm), Sm (8.68 ± 0.94 vs 11.62 ± 1.77 cm/sec) and Em/Am ratio (0.98 ± 0.80 vs 2.62 ± 0.67, p <0.001 for all comparisons) and increased Ε/e' (11.31 ± 1.02 vs 8.98 ± 1.70, p <0.001) compared with subjects without prolonged weaning (n = 20). Logistic regression analysis revealed that TAPSE (R²= 0.53, beta slope = 0.76, p < 0.001), Sm (R²= 0.52, beta = 0.75, p < 0.001) and Em/Am (R²= 0.57, beta = 0.32, p < 0.001) can predict length of weaning ≥ 7 days. The above measures were also proven to correlate significantly with Ε/e' (r = -0.83 for TAPSE, r = -0.87 for Sm and r = -0.79 for Em/Am, p < 0.001 for all comparisons).</p> <p>Conclusions</p> <p>We suggest that in mechanically ventilated patients with APE, low TAPSE and RV TDI velocities upon admission are associated with delayed liberation from mechanical ventilation, probably due to more severe LV heart failure.</p

Venous gas embolism as a predictive tool for improving CNS decompression safety

A key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. In the present review, we highlight the findings from our laboratory related to the hypothesis that VGE formation is the main mechanism behind serious decompression injuries. In recent studies, we have determined the impact of VGE on endothelial function in both laboratory animals and in humans. We observed that the damage to the endothelium due to VGE was dose dependent, and that the amount of VGE can be affected both by aerobic exercise and exogenous nitric oxide (NO) intervention prior to a dive. We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached

Occurrence, Risk Factors, Prognosis and Prevention of Swimming-Induced Pulmonary Oedema: a Systematic Review

Background: Swimming-induced pulmonary oedema (SIPE) can affect people with no underlying health problems,but may be life threatening and is poorly understood. The aim of this systematic review was to synthesise the evidence on SIPE incidence, prevalence, risk factors, short- and long-term outcomes, recurrence and effectiveness of interventions to prevent recurrences. Methods: We carried out a literature search using bibliographic databases and reference lists. Risk of bias was assessed by adapting existing quality assessment tools including those developed by the National Heart Lung and Blood Institute. Results: Nine studies met the inclusion criteria. Quantitative synthesis was not possible because of study heterogeneity. Five studies, which differed from each other in case definition, swimming environment, population characteristics and denominators, reported an incidence of 0.01% of UK triathlons raced over 5 years in unspecified swimming environments(one study, not fully reported, of men and women of unspecified age); 0.5% of river races swum over 3 days in Sweden(one study,of men and women up to the age of 70);and 1.8–26.7% of time trials in the sea around Israel (three studies of male teenage military trainees). One study reported that 1.4% of triathletes in the USA had experienced SIPE. One study found that hypertension, female sex, fish oil use, long course distance and another lower initial lung volumes and flows were risk factors for SIPE. A third study reported that higher mean pulmonary artery pressures and pulmonary artery wedge pressures, and lower tidal volumes were associated with SIPE. Three studies suggested that SIPE symptoms usually resolve within 24 h, although a restrictive deficit in lung function persisted for a week in one small study. We found no studies that reported deaths from SIPE. The single small study of longer-term outcomes reported no difference between affected and unaffected swimmers. Two studies suggested that around 30% of people report recurrences of SIPE. Two very small uncontrolled studies of the effect of sildenafil for recurrence prevention were inconclusive. Conclusions: SIPE may be an important public health problem affecting the growing number of recreational open water swimmers. Further research should clarify the frequency of SIPE among recreational open water swimmers, confirm reported risk factors and explore others, explore long-term consequences and test interventions to prevent recurrence