Objective Evaluate the association between carbon dioxide (pCO 2), cerebral blood flow (CBF), and cerebral autoregulation (CA) in preterm infants. Study design Cerebral saturations (rScO 2, surrogate for CBF using NIRS) and mean arterial blood pressure (MAP) monitored for 96 h in infants <29 weeks gestation. Relationship between rScO 2 , the rScO 2-MAP correlation (CA analysis) and pCO 2 category assessed by mixed effects modeling. Results Median pCO 2 differed by postnatal day (p < 0.0001)-pCO 2 increased between day 1 and 2, and low variability seen on day 4. A 5% increase in rScO 2 was noted when pCO 2 was >55 mmHg on each postnatal day (p < 0.001). No association observed between the overall rScO 2-MAP correlation and pCO 2. On day 1 only, the correlation coefficient decreased from 0.26 to −0.09 as pCO 2 category increased (p = 0.02). Conclusions CBF increased above a pCO 2 threshold of 55 mmHg, but overall, no association between pCO 2 and CA was noted.

Barosinusitis, or sinus barotrauma, is a well-described condition associated with changes in barometric pressure during flight and diving that can result in sinonasal mucosal injury. In this case report, we present an adolescent who experienced barosinusitis during scuba diving and subsequently developed Pott's puffy tumor (PPT), characterized by frontal sinusitis, frontal bone osteomyelitis, and overlying subperiosteal abscess. This unique case of PPT following scuba diving provides the opportunity to review the pathophysiology of both barotrauma-induced sinus disease and PPT, a rare and unreported serious complication of barosinusitis. Furthermore, we discuss how scuba diving and associated barosinusitis can be considered a risk factor in the development of PPT.

Electrocardiograph-gated blood pool scans (anteroposterior and left anterior oblique projections) were recorded in 30 patients seven to 10 days after myocardial infarction. Left ventricular ejection fractions (mean 0.26 +/- 0.10) were lower on average than values previously obtained in 11 normal subjects (mean 0.52 +/- 0.06) and correlated broadly with the clinical assessment of left ventricular performance. Ejection fractions were lower in anterior (mean 0.21 +/- 0.09) than inferior (mean 0.32 +/- 0.08) infarcts. Abnormal wall motion was detected in 11 of 15 anterior infarcts and in six of 13 inferior infarcts: mean ejection fractions associated with global asynergy, segmental asynergy, and normal wall motion were 0.15, 0.26, and 0.36, respectively. Twenty-four patients were reinvestigated two months later. Though there was some change in the clinical status of eight patients, wall motion and ejection fraction were unchanged (mean difference -0.005 +/- 0.036). Twelve patients were reinvestigated six months after infarction. The ejection fraction for the group was significantly lower than the values obtained at 10 days and two months, and four individual changes were significant when compared with the first study. Changes in wall motion were observed in one patient. From this radionuclide study, we conclude that ejection fraction and wall motion do not improve after the early convalescent phase of myocardial infarction.

An elevated cardiac troponin is a negative prognostic indicator in acutely decompensated heart failure (ADHF). In addition, sleep disordered breathing (SDB) is common in this patient population, and benefits to early diagnosis and treatment are increasingly being recognized. Multiple pathophysiologic mechanisms (recurrent arousals with sympathetic surges, intrathoracic pressure changes that increase wall stress, repetitive hypoxemia) exist by which sleep apnea may cause myocardial injury. Although this does not occur in patients with compensated heart failure (or those without cardiovascular disease), added stressors such as increased left ventricular filling pressures and hypoxemia may create at-risk myocardium that is sensitive to these perturbations. We report preliminary results of an observational study to determine the association between sleep apnea and overnight, changes in high-sensitivity troponin in patients with ADHF. Methods: Adult patients admitted to the cardiology service of a large academic medical center with a primary diagnosis of ADHF were included. Subject demographics, medical history, heart failure characteristics, and sleep questionnaires, were collected at the time of enrollment. Portable sleep apnea testing (Apnea Link, ResMED) was then performed on all subjects within 48 hours of admission to determine presence, type and severity of SDB as determined by 4% desaturation criteria. Pre and post-sleep serum samples were analyzed for high-sensitivity cardiac troponin (hs-cTn) T and I levels by immunoassay. This procedure was performed twice for each subject, once at the time of enrollment and again before hospital discharge. The primary outcome was overnight percentage change in high-sensitivity cardiac troponin T and I. Results: 13 subjects have been studied to date (planned N=40). On average subjects were 66 years of age (range 49-78), 30% of subjects were female, and the average BMI was 31 kg/m 2. 85% of subjects met criteria for sleep apnea, and of those patients OSA was more common (predominantly OSA 73% vs. predominantly CSA 27%). Overnight percentage change in hs-cTnT by subject is shown in figure 1 with subjects divided into cohorts no-mild sleep apnea (AHI <15 events/hr) and moderate-severe sleep apnea (AHI ≥ 15 events/hr). Conclusions: Home sleep apnea testing is feasible and well-tolerated in patients with ADHF. Consistent with previous studies both obstructive and central sleep apnea are highly prevalent in this patient population. We hypothesize that sleep apnea may cause subclinical myocardial damage as demonstrated by overnight high-sensitivity troponin release, and this may be one mechanism linking early intervention for SDB with favorable heart failure outcomes.