Extent Of Shunting Research Articles

Patent Foramen Ovale and Infarct Volume in Cryptogenic Stroke

The causal relationship between patent foramen ovale (PFO) and stroke is controversial. We hypothesized that if PFO is a pathway of embolic source, there might be a correlation between PFO characteristics (ie, size or extent of shunt) and ischemic lesion burden (ie, infarct volume and number). From ischemic stroke patients admitted to Asan Medical Center between January 2000 and October 2007, we identified those who had (1) acute ischemic lesion on diffusion-weighted imaging within 5 days of symptom onset and (2) cryptogenic stroke and only PFO detected by transesophageal echocardiography. PFO characteristics on echocardiographic studies included size, shunt grade, shunt pattern, and the presence of atrial septal aneurysm (ASA). Enrolled were 75 patients (male, 56%; mean age, 45.3±13.9 years), including 10 patients (13.3%) with ASA. In univariable analysis, PFO size was positively correlated with log-transformed infarct volume (LIV) (regression coefficient=.469, P=.009). After adjusting for hypertension, stroke history, and migraine (all P<.2), PFO size remained independently associated with LIV (regression coefficient=.481, P=.007). Lesion number was negatively correlated with PFO size (Spearman coefficient rho=-.251, P=.03). The initial National Institutes of Health Stroke Scale scores tended to be positively correlated with PFO size (Spearman coefficient rho=.223, P=.054). In cryptogenic stroke, PFO size and ischemic lesion burden were positively correlated. These results support that PFO may play a role as a pathway of embolic source in cryptogenic stroke.

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Introduction: Alveoli in the acutely injured lungs may repetitively collapse and expand at expiration having a negative impact on ventilation/perfusion match. Hypothesis: Low tidal ventilation with PEEP optimized to maintain the end-expiratory transpulmonary pressure?0 cmH2O will improve oxygenation and shunt fraction, as compared to strategies that may allow for negative expiratory transpulmonary pressures. Methods: Ten Yorkshire pigs were instrumented and mechanically ventilated using transpulmonary pressure measurements. Baseline lung mechanics were obtained for the following parameters: Vt=10mL/kg, PEEP=5cmH2O, and FiO2 = 0. 21. Lungs were injured by instilling 5% Tween-20 (3ml/kg), and ARDS was established when PF ratios fell <200. After a single recruitment maneuver (40 cmH2O x 40sec.), the animals were randomized into a PtpPEEP Group with PEEP adjusted to maintain the end-expiratory transpulmonary pressure?0 cmH2O, or the Control Group where PEEP was adjusted based on the lower PEEP scale as per ARDSNet guidelines. Cardiovascular and respiratory parameters were recorded hourly for 24hr. Results: After 12hr, the PtpPEEP Group started separating from the Control Group, maintaining, as per protocol, PtpPEEP pressures?0 cmH2O, while the Control Group showed negative values 48% of time. Overall, the PtpPEEP Group had an odds ratio of 4.3 for normal oxygenation (PF ratio>300), and intrapulmonary shunting significantly lower than the Control Group (p<0.01). Regression analysis showed that shunt fractions increased with time (p<0.01) associated with decreasing PF ratios (<0.01); however, for the same PF ratios, the PtpPEEP Group showed lower shunt fractions than the Control (p<0.01). Conclusions: In our study, the extent of shunting was a consequence of the PEEP optimization strategy. The PtpPEEP Group improved the oxygenation and shunt fractions, indicating that maintaining a PtpPEEP?0 cmH2O may have a significant impact on ventilation/perfusion matching.

Spontaneous improvement of a haemodynamically significant ventricular septal defect produced by blunt chest trauma in a child

We describe the progress of a girl aged 5 years, who suffered blunt trauma to the chest producing a ventricular septal defect of 1 centimetre in diameter. The shunt generated a mild dilation of the left-sided chambers, and exertional dyspnoea. Three months later, therapeutic catheterisation revealed important diminution in the extent of shunting. We decided, therefore, not to close the defect, and she has since remained asymptomatic.

Intrapulmonary vascular dilatation and nitric oxide in hypoxemic rats with chronic bile duct ligation

Background/Aims : Nitric oxide (NO) has been suggested as the major cause of pulmonary vascular dilatation and hypoxemia in hepatopulmonary syndrome (HPS). The aim of this study was to assess the effect of NO on arterial oxygenation in rats with common bile duct ligation (CBDL rats), a model of HPS. Methods : Arterial blood gases were measured in 44 CBDL rats and 44 Sham rats under unrestrained conditions. Intrapulmonary shunting was assessed with 141Ce-labeled microspheres (15-μm diameter) and serum nitrate/nitrite levels were measured by HPLC. The effect of NOS inhibition on A-aDO 2 was studied using L-NAME. Results : A decrease of PaO 2 below 82.7 mmHg (the mean value−2σ in Sham rats) was seen in 43% of CBDL rats. Intrapulmonary shunting was greater in CBDL rats than in Sham rats ( P<0.001). A correlation between the extent of shunting and A-aDO 2 was found in all animals studied ( r=0.89, P<0.001, n=16). Serum levels of nitrate/nitrite increased significantly across the lungs, and the increase was significantly correlated with A-aDO 2 in the total population of animals studied. Administration of L-NAME to CBDL rats achieved a significant improvement of A-aDO 2. Conclusions : These results suggest that pulmonary vascular dilatation due to NO leads to hypoxemia in CBDL rats.

Diagnosis and treatment of hepatic encephalopathy

Hepatic encephalopathy arises from the combination of hepatocellular dysfunction and portal-systemic shunting. Encephalopathy is more prominent in advanced stages of liver cirrhosis and signals the presence of fulminant hepatic failure in patients with acute liver injury. As important as the extent of shunting is the presence of large spontaneous collaterals. Ammonia continues to be a leading toxin influencing brain function. Endogenous benzodiazepines and cytokines may contribute to one of ammonia’s key effects in the brain: astrocyte swelling. The diagnosis of hepatic encephalopathy is a diagnosis of exclusion; the search for a precipitating factor should be started immediately in all cases of encephalopathy. The treatment of hepatic encephalopathy has three aims: decrease the nitrogenous load from the gut, improve the extra-intestinal elimination of ammonia and counteract central abnormalities of neurotransmission. The mainstay of treatment is directed at the colon. Newer approaches targeting the brain, such as flumazenil, have become available.