The rate of global warming has accelerated over the past 50 years. Increasing surface temperature is melting glaciers and raising the sea level. More flooding, droughts, hurricanes, and heat waves are being reported. Accelerated changes in climate are already affecting human health, in part by altering the epidemiology of climate-sensitive pathogens. In particular, climate change may alter the incidence and severity of respiratory infections by affecting vectors and host immune responses. Certain respiratory infections, such as avian influenza and coccidioidomycosis, are occurring in locations previously unaffected, apparently because of global warming. Young children and older adults appear to be particularly vulnerable to rapid fluctuations in ambient temperature. For example, an increase in the incidence in childhood pneumonia in Australia has been associated with sharp temperature drops from one day to the next. Extreme weather events, such as heat waves, floods, major storms, drought, and wildfires, are also believed to change the incidence of respiratory infections. An outbreak of aspergillosis among Japanese survivors of the 2011 tsunami is one such well-documented example. Changes in temperature, precipitation, relative humidity, and air pollution influence viral activity and transmission. For example, in early 2000, an outbreak of Hantavirus respiratory disease was linked to a local increase in the rodent population, which in turn was attributed to a two- to threefold increase in rainfall before the outbreak. Climate-sensitive respiratory pathogens present challenges to respiratory health that may be far greater in the foreseeable future.

An epidemiological link between respiratory infection and acute myocardial infarction (AMI) has been suggested, and recent data indicate that there is an association between AMI and pneumococcal community-acquired pneumonia (CAP) in hospitalized patients. The objective of this study was to investigate the association of AMI with the severity of pneumonia at hospitalization and clinical failure during hospitalization among patients with CAP. An observational, retrospective study involving consecutive patients hospitalized with CAP was performed at the Veterans Hospital of Louisville, Kentucky. Patients admitted to the intensive care unit were defined as having severe CAP. Clinical failure was defined as the development of respiratory failure or shock. AMI was diagnosed on the basis of abnormal troponin levels and electrocardiogram findings. Propensity-adjusted models that controlled for clinical and nonclinical factors were used to investigate the association between AMI and pneumonia severity index and between AMI and clinical failure. Data for a total of 500 patients were studied. At hospital admission, AMI was present in 13 (15%) of 86 patients with severe CAP. During hospitalization, AMI was present in 13 (20%) of 65 patients who experienced clinical failure. Following risk adjustment, significant associations were discovered between AMI and the pneumonia severity index score (modeled with a restricted cubic spline) (P = .05) and between AMI and clinical failure (P = .04). A combined diagnosis of CAP and AMI is common among hospitalized patients with severe CAP. In cases in which the clinical course of a hospitalized patient with CAP is complicated by clinical failure, AMI should be considered as a possible etiology.

Hemolysis is common in all extracorporeal circuits as evident by the elevated plasma free hemoglobin (PFHb) level. We investigated whether increased hemolysis during extracorporeal membrane oxygenation (ECMO) is an independent mortality predictor. We performed a retrospective observational study of consecutive subjects who received ECMO at a tertiary care facility from 2007-2013 to investigate independent predictors of in-hospital mortality. We examined variables related to patient demographics, comorbidities, markers of hemolysis, ECMO characteristics, transfusion requirements, and complications. 24-hour PFHb> 50 mg/dL was used as a marker of severe hemolysis. 154 patients received ECMO for cardiac (n= 115) or pulmonary (n=39) indications. Patients’ mean age was 51 years and 75.3% were males. Compared to nonsurvivors, survivors had lower pre-ECMO lactic acid (p=0.026), lower 24-hour lactic acid (p=0.023), shorter ECMO duration (P=0.01), fewer RBC transfusions on ECMO (p=0.008) and lower level of PFHb 24-hours post ECMO implantation (p=0.029). 24-hour PFHb> 50 mg/dL occurred in 3.9 % versus 15.5% of survivors and nonsurvivors, respectively, p=0.002. A Cox proportional hazard analysis identified PFHb> 50 mg/dL 24-hours post ECMO as an independent predictor of mortality (OR= 3.4, 95% confidence interval: 1.3 – 8.8, p= 0.011). PFHb> 50 mg/dL checked 24-hour post ECMO implantation is a useful tool to predict mortality. We propose the routine checking of PFHb 24-hours after ECMO initiation for early identification and treatment of the cause of hemolysis.