Drug interactions and creatinine levels are associated with QTc prolongation in intensive care units: a prospective, observational study.

Background Prolongation of the QTc interval may lead to life threatening arrhythmias. QTc prolongation is common in intensive care unit (ICU) patients. The objectives of this study were to identify the role of drug-drug interactions (DDIs) and other predictors (age, sex, cardiovascular diseases, and electrolyte abnormalities) in life threatening QTc prolongation in patients admitted to medical (M), surgical (S) and emergency (E) ICUs. Methods This prospective, observational study included patients above the age of 18 years who were admitted to SICU, EICU, and MICU at a tertiary respiratory referral center. Electrocardiogram (ECG) monitoring was performed during the first 5 days of ICU admission. Risk factors and DDIs which were anticipated to be associated with the prolongation of the QTc interval were assessed for all patients. Results Two hundred patients were included in the study. QTc prolongation occurred in 10.7% of patients and the majority of patients presenting with QTc prolongation had creatinine levels above 1.3 mg/dL during their 5 days of ICU admission. Incidence of pharmacodynamic (PD) DDIs was significantly higher in patients with QTc prolongation vs. other patients. Creatinine levels above 1.3 mg/dL and PD DDIs were associated with QTc prolongation during 5 days of ICU admission. Conclusions High serum creatinine and PD DDIs can increase the risk of QTc prolongation in patients admitted to the ICU. QTc interval measurements should be performed prior to initiation or after starting any drug that is associated with QT prolongation, specifically in patients with the known risk factors.

Pulmonary Hypertension in Intensive Care Units: An Updated Review.

Pulmonary hypertension (PH) is a condition associated with high morbidity and mortality. Patients with PH who require critical care usually have severe right ventricular (RV) dysfunction. Although different groups of PH have different etiologies, pulmonary vascular dysfunction is common in these groups. PH can lead to increased pulmonary artery pressure, which can ultimately cause RV failure. Clinicians should be familiar with the presentations of this disease and diagnostic tools. The contributing factors, if present (e.g., sepsis), and coexisting conditions (e.g., arrhythmias) should be identified and addressed accordingly. The preload should be optimized by fluid administration, diuretics, and dialysis, if necessary. On the other hand, the RV afterload should be reduced to improve the RV function with pulmonary vasodilators, such as prostacyclins, inhaled nitric oxide, and phosphodiesterase type 5 inhibitors, especially in group 1 PH. Inotropes are also used to improve RV contractility, and if inadequate, use of ventricular assist devices and extracorporeal life support should be considered in suitable candidates. Moreover, vasopressors should be used to maintain systemic blood pressure, albeit cautiously, as they increase the RV afterload. Measures should be also taken to ensure adequate oxygenation. However, mechanical ventilation is avoided in RV failure. In this study, we reviewed the pathophysiology, manifestations, diagnosis, monitoring, and management strategies of PH, especially in intensive care units.

Spirometry, cardiopulmonary exercise testing and the six-minute walk test results in sarcoidosis patients.

Background: The 6-minute walking test, cardiopulmonary exercise testing, and spirometry are useful tools for evaluation of respiratory impairment and functional capacity in patients with lung disease. Sarcoidosis is a multisystem granulomatous disease of unknown etiology. Objectives: Since the pulmonary involvement can affect the quality of life in sarcoidosis patients, this study is aimed to evaluate the tests mentioned above in order to examine the functional capacity of sarcoidosis patients in different stages as well as the cause of exercise intolerance. Methods: This cross-sectional study was carried out on 50 Iranian patients with sarcoidosis. Patients were classified into three groups based on the findings of the chest radiography as well as the pulmonary CT scan, reported by an expert radiologist. Pulmonary, cardiac, and activity function have been evaluated in the patients, using cardiopulmonary exercise testing, the 6-minutes walking test, and spirometry. Results: In cardiopulmonary exercise testing, percent-predicted peak VO2 (57.75±15.49, p=0.015) and percent-predicted O2 pulse (70.54±17.37, p=0.013) were significantly lower in the third group, in comparison with the others. Also, VE/CO2 (AT) (34.99±5.67, p=0.000) was significantly higher in the third group, in comparison with the other ones. Percent-predicted VO2 showed a strong positive correlation with age (r=0.377, p=0.009), TSH (r= 0.404, p=0.007), and percent-predicted FVC (r=0.443, p=0.002). In addition, O2 pulse had a positive correlation with BMI (r=0.324, p=0.026), percent-predicted FVC (r=0.557, p= 0.000), and percent-predicted FEV1 (r=0.316, p=0.032). Conclusions: According to this study, ventilatory limitation, pulmonary involvement, and deconditioning are the main causes of activity limitations in sarcoidosis patients.

Relationship between Serum Uric Acid Levels and the Severity of Pulmonary Hypertension.

BACKGROUND: Right heart catheterization is the gold standard test for diagnosis and clinical assessment of the patients with pulmonary hypertension (PH). In recent years, the usefulness of cheaper and non-invasive tests in the follow-up of PH patients is being studied. The aim of the present study was to evaluate the relationship between serum uric acid level and severity of pulmonary hypertension in PH patients. MATERIALS AND METHODS: In a cross-sectional study, serum uric acid was measured in 110 patients with PH (63 women; mean age [±SD] was 52.83±17.88 years). Pulmonary arterial pressure and severity of right ventricular dysfunction were assessed using RHC and echocardiography, respectively. RESULTS: Serum uric acid was higher in PH patients with severe RV dysfunction, compared to mild and moderate dysfunction (7.8mg/dl [IQR: 5.8-9.2] in severe dysfunction, versus 4.7 mg/dl [3.87-5.82] in mild dysfunction and 5 mg/dl [3.5-6.95] in moderate dysfunction. Serum uric acid was significantly correlated with pulmonary artery systolic pressure (r=0.51, P<0.001). Serum uric acid level also had a significant positive correlation with the World Health Organization functional class of the patients (r=0.49, P<0.001). Serum uric acid level greater than 5.7 mg/dl was found to be the most sensitive and specific points for predicting severe RV dysfunction in PH patients (sensitivity 76.6%, specificity 71.4%; AUC=0.79, P<0.001) . CONCLUSION: Serum uric acid is correlated with the severity of symptoms and RV dysfunction in patients with pulmonary hypertension. Further studies are recommended with larger sample size in this regard.

Syncope paradox in the outcome of patients with pulmonary thromboembolism: short-term and midterm outcome.

BACKGROUND AND AIM: We compare the early and midterm outcomes of pulmonary thromboembolism (PTE) in patients with and without syncope in our single-center registry. METHOD: Between December 2006 and May 2013, 351 consecutive patients (mean age = 60.21 ± 16.91 years, 55.3% male) with confirmed acute symptomatic PTE were divided in with and without syncope groups. Groups were compared in terms of the effect of syncope on 30-day mortality and adverse events, and mortality in a median follow-up time of 16.9 months. RESULTS: From 351 patients, 39 (11.1%) had syncope and 312 (88.9%) did not. Syncope group had less frequently chest pain (30.8% vs 51.4%; P value = 0.015). Also, the rates of 30-day adverse events and mortality were 12.8% and 5.1% for the group with syncope, and 14.4% and 10.3% for the group without syncope, respectively, with no significant difference. At follow up, 65 patients died and mortality was 18.5% for 351 patients (5.1% in the group with syncope and 20.2% for the other group). After adjustment for confounding factors, the effect of syncope on 30-day adverse events and mortality remained non-significant and on the midterm mortality was significant, showing that the presence of syncope was associated with lower midterm mortality (P value = 0.038). CONCLUSION: Among PTE patients in our registry, 11.1% presented with syncope. Relationship between syncope and 30-day adverse events and mortality remained non-significant after adjustments for other factors. However, in midterm follow up, patients with syncope were significantly at decreased risk of mortality compared to those without syncope.

Correlates of syncope in patients with acute pulmonary thromboembolism.

Identification of pulmonary thromboembolism (PTE), as a cause of syncope, is important and may be life saving. We prospectively analyzed data on 335 patients with acute PTE. Relationships between syncope secondary to acute PTE and clinical findings, risk factors, and imaging modalities were analyzed. Of the 335 patients, 36 (10.7%) had syncope at presentation. Compared to patients without syncope, those with syncope had a higher frequency of right ventricular (RV) dysfunction (94.3% vs 72.1%, respectively; P value = .004) and saddle embolism (24.2% vs 10.9%, respectively; P value = .044). Frequency of RV dysfunction was similar between patients with and without saddle embolism. Although not significant, more patients with syncope had a history of previous PTE (P value = .086). By multivariable analysis, RV dysfunction and saddle embolism were independent correlates of syncope in patients with PTE. In-hospital mortality was not significantly different between the groups. In conclusion, among patients with PTE, RV dysfunction and saddle embolism were the independent correlates of syncope.