Potential mechanisms of stroke by PICC Arterial PICC placement with the catheter tip central to the carotid or vertebral arteries Venous PICC placement with an existing right-to-left shunt Intrapulmonary shunt
--Pulmonary arteriovenous malformation (AVM) Intracardiac shunt --Atrial or ventricular septal defect (ASD, VSD) --Patent foramen ovale (PFO) Shunt between aorta and pulmonary artery --Patent ductus arteriosus (PDA) Thoracic venous anomalies --Persistent left SVC draining directly into the left atrium (this drainage pattern is present in < 10% of patients with a persistent left SVC)
Changes in cardiac output have been reported to positively correlate with the intrapulmonary shunt
Lung perfusion scintigraphy revealed findings suggesting intrapulmonary shunt
with a rate of 23% and lung tomography with contrast material was taken.
If and when the intrapulmonary shunt
is severe, as was seen in our cases, optimisation of factors that could affect the mixed venous saturation becomes of prime importance.
In conclusion, the origin of the hypoxaemia in consolidative forms of bronchoalveolar carcinoma is possibly secondary to intrapulmonary shunt
through dilated vessels with massive plasma leakage.
The intrapulmonary shunt
((Qs/Qt: (Cc02-CaO2)/(CcO2-CvO2)) was calculated 3 times; at the beginning of the operation and 1 and 24 hours after the operation.
It is a very useful formula in evaluating the degree of intrapulmonary shunt
and subsequent compromise of cardiopulmonary function.
2] only reflect blood flow that participates in gas exchange, and this will lead to an underestimate of cardiac output if a significant intrapulmonary shunt
The underlying mechanism mostly involves a right-to-left intracardiac or intrapulmonary shunt
2]) significantly decreased during the infusion of AVE If at a given intrapulmonary shunt
Inhaled nitric oxide therapy has been shown to improve the oxygenation in acute hypoxaemic respiratory failure by increasing the blood flow to better aerated regions of the lungs, thereby reducing intrapulmonary shunt
and improving ventilation-perfusion matching.
Siobal's excellent review of pulmonary vasodilators found that long-term use of calcium channel blockers (diltiazem and nifedipine) reduced pulmonary arterial pressure and improved survival over a 5-year period, but cautioned that oral calcium channel blockers use was limited by their dose-related systemic vasodilator effects, a potential for hypotension, worsening right-ventricular function, increased intrapulmonary shunt
, and hypoxemia.