POS is a syndrome of hypoxia accompanied by postural changes. POS has no clear diagnostic criteria. Based on the literature review, possible criteria include :(1) decreased noninvasive oxygen saturation in the upright position and recovered in the supine position[1];(2) Arterial PO2 was significantly lower in the upright position compared to the supine position[2]
However, cases of decreased oxygen saturation in the lateral recumbent position had also been reported and very few cases of intraoperative lateral hypoxia had been reported. In the present case, there was insufficient evidence of hypoxia in the upright position, but the mechanism of lateral recumbent hypoxia was consistent with POS. We discuss the pathophysiology of this case in terms of POS pathophysiology.
The possible pathophysiological causes are intracardiac shunt (PFO, ASD, or atrial septal aneurysm(ASA) with fenestration), pulmonary diseases with ventilation/perfusion mismatch(High V/Q ratio, and low V/Q ratio[3].
Additionally, the possible pathophysiological cause is the right-to-left shunt due to PFO in the right lateral position. Due to the low diagnostic sensitivity of TTE for PFO as well as shunts, the prevalence of PFO observed by TTE contrast was reported to be lower than that observed by TEE (14.9% vs. 24.3%)[4]. This could explain the failure of preoperative TTE to detect PFO.
Factors without pulmonary hypertension that the right-to-left shunt include:(1) During positive pressure ventilation in the right lateral position, Intrathoracic positive pressure results in right heart compression, increased right atrial pressure, and appeared right-to-left shunt. Possible causes of right heart compression are short stature, diaphragm elevation, liver compression, and positive pressure ventilation. From the CT mediastinal window, we can see the smaller right atrium and the compression of the right atrium by the liver(Fig. 3). As well, the right deviation of the mediastinum was observed. (Fig. 4) (2) Dilation of the aortic root may lead to a leftward shift of the interatrial septum, which may widen the gap in the PFO as well as provide for increased right atrial pressure, thereby increasing the right-to-left shunt[5]. We can see the dilated aortic root from the intraoperative TEE examination as well as the mediastinal window of the chest CT.
In the absence of pulmonary hypertension, PFO causes a left-to-right shunt due to higher left heart pressure than the right heart. In right de-cubitus, the liver was in full contact with the right atrium resulting which increased right heart pressure. The patient had no previous history of liver disease, but on CT the liver was found to be in close apposition to the right atrium, which may be associated with the right diaphragm elevation. A few case studies reported POS with hemidiaphragmatic elevation, especially triggered by hemidiaphragmatic paralysis[6]. After the onset of muscle relaxants, the patient's diaphragm was relaxed and the postural pad elevated the relaxed diaphragm in the right lateral position. This may be the cause of diaphragm elevation in this case. Likewise, the above was aggravated by the rightward deviation of the mediastinum and aortic root dilation. In addition, smaller right atria were more likely to be compressed. These are why right heart pressure increases in the right lateral decubitus position and a right-to-left shunt occurs.
The strange phenomenon of reduced oxygen saturation but normal blood pressure occurred intraoperatively. This may be because a large amount of unoxygenated blood flow reached the left heart directly through the PFO, and the normal output of the left heart ensured normal blood pressure. After 45 minutes, prolonged hypoxia resulted in decreased cardiac pump function, decreased cardiac output, and a rapid drop in blood pressure.
During the patient's hypoxia, we tried to raise the blood pressure to a higher level using ephedrine, and oxygen saturation was briefly improved. Ephedrine has an α agonist effect, the pharmacological effect that causes pulmonary vasoconstriction and reduces intrapulmonary shunts as well as temporarily increasing left atrial pressure and reducing intracardiac right-to-left shunts. Successful reversal of right-to-left shunt to improve oxygen saturation has been reported in an elderly patient with POS using 5 µg/hr norepinephrine[7].
However, intracardiac shunts can only be resolved by PFO closure. PFO closure was rejected due to the patient's advanced age and good post-operative recovery.
In conclusion, PFO-related POS syndrome should be highly suspected in posture-related hypoxia.