Patent Foramen Ovale (PFO)

Debubble every line - A PFO is a one-in-four finding in adults, so treat every venous line as a possible route to the brain. Clear air from tubing, stopcocks, syringes, and injectate before anything goes in. A bubble the lung would normally filter can cross the septum and embolize systemically instead.

What opens the shunt - The flap only leaks when right atrial pressure beats left. Valsalva, coughing and straining on emergence, high airway pressures and PEEP, and anything that raises PVR — hypoxia, hypoventilation and hypercarbia, acidosis, airway obstruction, pulmonary hypertension — all push it that way. Keep the patient full, keep gas exchange clean, and use the least PEEP that does the job.

Confirming it - Bubble-contrast echocardiography is the test. TEE with agitated saline injected during a cough or Valsalva is the most sensitive. TTE with bubble contrast is sensitive enough to pick up a clinically significant PFO and avoids the sedation TEE requires. Transcranial Doppler tells you a right-to-left shunt exists but not where it sits.

Watching for venous air - Precordial Doppler is the most sensitive noninvasive monitor in routine use, and gives the textbook mill-wheel murmur. End-tidal nitrogen is very sensitive. A sudden fall in ETCO2 is real but nonspecific — it also drops with pulmonary embolism, major blood loss, hypotension, and arrest. A PA catheter shows a rise in PA pressure. With a PFO in the picture, venous air is not only a pulmonary problem.

If air gets in - Tell the surgeon, flood the field with saline and wax the bone edges, stop nitrous oxide, go to 100% oxygen, aspirate air back through the central line, and support the pressure with volume, vasopressors, and ACLS as needed. Jugular compression or a Valsalva raises venous pressure at the field, and repositioning to left lateral decubitus is part of the standard response.

Nitrous oxide - Leave it out of cases where venous air is plausible, and turn it off the moment air is suspected. It also markedly raises pulmonary vascular resistance, which is the wrong direction for a septum you want to stay shut.

Hypoxemia that does not fit - Unexplained desaturation that does not correct with FiO2 should raise a right-to-left atrial shunt, including platypnea-orthodeoxia syndrome. Chasing it with oxygen alone will not work; the fix is lowering right atrial pressure and PVR.

After device closure - Percutaneous closure is now the usual route, and these patients arrive on aspirin or clopidogrel, or on an anticoagulant. Atrial arrhythmias follow closure in roughly 3% to 5% and are usually transient; atrial fibrillation has run 5% to 6% with some devices. Get the closure date and the current antithrombotic from the cardiology note rather than from the patient. Endocarditis prophylaxis applies for six months after repair of a cardiac defect.

The foramen ovale is a flap-like tunnel between the septum primum and septum secundum at the fossa ovalis. In utero it carries oxygenated placental blood from the right atrium to the left, bypassing collapsed, non-functioning lungs. At birth the lungs expand, left atrial pressure rises above right, and the flap is pressed shut, fusing in about 75% of infants. In roughly 25% of adults it stays probe-patent.

Usually that costs nothing — left atrial pressure exceeds right, so the flap stays closed. But it is a valve, not a seal. Anything that pushes right atrial pressure above left — Valsalva, coughing, straining, positive-pressure ventilation, a rise in pulmonary vascular resistance — opens a right-to-left conduit, and venous thrombus or air crosses into the systemic circulation without ever passing the pulmonary filter. That is paradoxical embolism, and it is the mechanism behind the association of PFO with cryptogenic stroke and with decompression sickness in divers.