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1.
Crit Care ; 13 Suppl 5: S8, 2009.
Article in English | MEDLINE | ID: mdl-19951392

ABSTRACT

INTRODUCTION: Cardiac troponin has been shown to be elevated in one-half of the parturients admitted for post-partum haemorrhage. The purpose of the study was to assess whether increased cardiac troponin was associated with a simultaneous alteration in haemoglobin tissue oxygen saturation in peripheral muscles in post-partum haemorrhage. METHODS: Tissue haemoglobin oxygen saturation of thenar eminence muscle (StO2) was measured via near-infrared spectroscopy technology. Two sets of StO2 parameters (both isolated baseline and during forearm ischaemia-reperfusion tests) were collected at two time points: upon intensive care unit admission and prior to intensive care unit discharge. Comparisons were performed using Wilcoxon paired tests, and univariate associations were assessed using logistic regression model and Wald tests. RESULTS: The 42 studied parturients, admitted for post-partum haemorrhage, had clinical and biological signs of severe blood loss. Initial cardiac troponin I was increased in 24/42 parturients (0.43 +/- 0.60 microrg/l). All measured parameters of muscular haemoglobin oxygen saturation, including Srecovery, were also altered at admission and improved together with improved haemodynamics, when bleeding was controlled. Multivariate analysis showed that muscular Srecovery <3%/second at admission was strongly associated with increased cardiac troponin. CONCLUSIONS: Our study confirmed the high incidence of increased cardiac troponin, and demonstrated the simultaneous impairment in the reserve of oxygen delivery to peripheral muscles in parturients admitted for severe post-partum haemorrhage.


Subject(s)
Muscle, Skeletal/blood supply , Muscle, Skeletal/metabolism , Oxygen Consumption/physiology , Postpartum Hemorrhage/blood , Troponin I/blood , Adult , Female , Humans , Postpartum Hemorrhage/physiopathology , Postpartum Hemorrhage/therapy , Pregnancy , Spectroscopy, Near-Infrared/methods
2.
Eur J Heart Fail ; 10(3): 291-7, 2008 Mar.
Article in English | MEDLINE | ID: mdl-18313982

ABSTRACT

BACKGROUND: Cardiac resynchronisation therapy (CRT) is a validated treatment for heart failure (HF) patients in NYHA class III-IV despite optimal medical therapy. We aimed to assess the beneficial effects of CRT in patients with catecholamine-dependent overt HF (CDOHF). METHODS: We studied 20 CDOHF patients who had undergone CRT implantation. Patients had a mean baseline QRS duration of 174+/-25 ms and/or echocardiographic asynchrony, and LVEF of 18+/-3%. Mean follow-up was 18+/-12 months. Dependence on catecholamine agents was defined as the inability to stop or reduce drug infusion without re-occurrence of hypotension, low urine output and hypoxaemia. RESULTS: After CRT implantation, catecholamine agents were mostly withdrawn within 2 days and blood pressure, urine output and BNP rapidly improved within 24 h. During follow-up, survival rates were 85% at 3 months, 80% at 6 months and 55% at 18 months. Among the 9 deaths, 5 were related to overt HF, 3 to sudden cardiac death and 1 to non-cardiac death. LVEF improved from 18+/-3% to 21+/-4% three months after CRT implantation. CONCLUSION: "Rescue" CRT implantation in CDOHF patients allowed a rapid and successful catecholamine weaning in all studied patients. Furthermore, this immediate beneficial effect is sustained for more than one year in surviving patients.


Subject(s)
Cardiac Pacing, Artificial , Heart Failure/therapy , Aged , Cardiac Output, Low/physiopathology , Cardiac Output, Low/therapy , Catecholamines/physiology , Female , Heart Conduction System/physiopathology , Heart Failure/physiopathology , Humans , Male , Middle Aged , Pacemaker, Artificial , Retrospective Studies , Stroke Volume , Treatment Outcome , Ventricular Dysfunction, Left/physiopathology
4.
Anesthesiology ; 100(1): 30-6; discussion 5A, 2004 Jan.
Article in English | MEDLINE | ID: mdl-14695721

ABSTRACT

BACKGROUND: Postpartum hemorrhage remains a major cause of global maternal morbidity and mortality, even in developed countries, despite the use of intensive care units. This study sought to (1) assess whether myocardial ischemia could be associated with and even aggravate hemorrhagic shock in young parturients admitted for postpartum hemorrhage, and (2) identify the independent risk factors for myocardial ischemia. METHODS: On their referral to the intensive care unit, a multidisciplinary team managed parturients with severe postpartum hemorrhage. Ventilation, transfusion, catecholamines, surgery, or angiography with uterine embolization were provided as clinically indicated. Plasma cardiac troponin I levels were used as a surrogate marker of acute myocardial injury and electrocardiograms of myocardial ischemia. RESULTS: A total of 55 parturients were referred with severe postpartum hemorrhage, all in hemorrhagic shock. Twenty-eight parturients (51%) had elevated serum levels of cardiac troponin I (9.4 microg/l [3.7-26.6 microg/l]), which were associated with electrocardiographic signs of ischemia and deteriorated myocardial contractility and correlated with the severity of hemorrhagic shock. Indeed, multivariate analysis identified low systolic and diastolic arterial blood pressure (< 88 and < 50 mmHg, respectively) and increased heart rate (> 115 beats/min) as independent predictors of myocardial injury. In addition, all patients who were given catecholamines also had elevated cardiac troponin I levels. CONCLUSIONS: These results suggest that treatment of postpartum hemorrhage-induced hemorrhagic shock should be coupled with concomitant prevention of myocardial ischemia, even in young parturients.


Subject(s)
Myocardial Ischemia/complications , Myocardial Ischemia/epidemiology , Postpartum Hemorrhage/complications , Postpartum Hemorrhage/epidemiology , Adult , Cohort Studies , Electrocardiography , Female , Hemodynamics/physiology , Humans , Myocardial Contraction/physiology , Myocardial Ischemia/physiopathology , Postpartum Hemorrhage/physiopathology , Pregnancy , Risk Factors , Shock, Hemorrhagic/physiopathology , Troponin I/blood
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