How does Patent Foramen Ovale cause paradoxical emboli

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GonefromTX

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Maybe I'm overthinking it, how could an embolus possibly travel from right atrium to left atrium when the LA has a higher pressure than RA after birth? The PFO is also pushed close at all times by the left atrial pressure.

Same thing for Atrial Septal Defect. Doesn't Eisenmenger syndrome need to happen (reversal to right to left shunt) for a clot to travel from right to left heart?

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I asked a neurologist about this and he basically said that a paradoxical emboli really only in situations where numerous small clots are thrown. The initial emboli would cause PEs, therefore increasing the pulmonary arterial pressure. This would eventually increase the RA pressure such that RA>LA, potentially leading to a paradoxical emboli in the presence of a PFO. Also, I would suspect it could happen in any situation where you have RA hypertrophy (Tricuspid stenosis, congenital malformations, pulmonary HTN, etc) with a PFO.
 
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I asked a neurologist about this and he basically said that a paradoxical emboli really only in situations where numerous small clots are thrown. The initial emboli would cause PEs, therefore increasing the pulmonary arterial pressure. This would eventually increase the RA pressure such that RA>LA, potentially leading to a paradoxical emboli in the presence of a PFO. Also, I would suspect it could happen in any situation where you have RA hypertrophy (Tricuspid stenosis, congenital malformations, pulmonary HTN, etc) with a PFO.
That makes perfect sense. So strange that questions in step 1 frequently ask of isolated paradoxical emboli in PFOs without any other factors. Thanks!
 
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I think the paradoxical emboli comes from the fact that emboli typically occur on right sided circulation, i.e. you can find the embolism in the pulmonary arteries from a DVT in the right leg venous circulation for example. The paradoxical part is since you have a patent foraman ovale, you get clotting in the LEFT side of the body because the emboli can cross over to the left side via the foramen.

I think that's what is paradoxical about it; the fact that it's on the left sided circulation. It need not be complicated.
 
That makes perfect sense. So strange that questions in step 1 frequently ask of isolated paradoxical emboli in PFOs without any other factors. Thanks!

It happens in isolation. I have seen it several times, including last week. Ended up having to do a BKA after two attempts at limb salvage. Otherwise healthy individual with PFO and lower extremity DVT that ended up with clot in her leg. Also, keep in mind that RA and LA pressures are dynamic. The range between the two in normal function is overlapping (commonly quoted 2-6mmHg for RA and 4-12mmHg for LA). I've heard people say that PE is a prerequisite for paradoxical embolism, but at least anecdotally, I have seen otherwise.
 
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That makes perfect sense. So strange that questions in step 1 frequently ask of isolated paradoxical emboli in PFOs without any other factors. Thanks!
If memory serves, UW says it can can happen in times of straining that increase right sided pressure (coughing, bowel movements, valsalva). My UW is expired but what I got out of it is that if something were to increase RA pressure enough it is possible. I agree that along with other PE makes it more possible than a coincidental increase in RA pressure.
 
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If memory serves, UW says it can can happen in times of straining that increase right sided pressure (coughing, bowel movements, valsalva). My UW is expired but what I got out of it is that if something were to increase RA pressure enough it is possible. I agree that along with other PE makes it more possible than a coincidental increase in RA pressure.

This.
 
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I've heard the same re: dynamic pressures in RA vs. LA and also the idea that blood entering the RA from the IVC flows preferentially toward the septum, perhaps transiently sweeping a clot through a PFO in the "current," as it were.
 
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All good answers. Medscape says that right-to-left shunting must be present in order for PFO to be of potential significance in the presence of paradoxical embolus. This makes sense given the special anatomy of the PFO valve tract. They then provide the following situations as potential causes of RLS in the setting of PFO:
  • Right atrial hypertension
  • Right ventricular hypertension
  • Right ventricular failure with increased end-diastolic pressure; positive-pressure ventilation
  • Positive end-expiratory pressure
  • Pulmonary hypertension from hypoxemia
  • Myocardial infarction (MI) of the right side of the heart
  • Valsalva-type maneuvers (forced expiration against a closed glottis), including urination, defecation, and sneezing
So I think it is safe to assume that all patients with PFO will, at least transiently, have some flow from right atrium to left atrium and that this flow is necessary for movement of an intracardiac embolus from right to left circulation because of the anatomy of the defect. The probability of such an embolus moving from right to left circulation should be proportional to the frequency and duration of the right-to-left shunting through the PFO.

EDIT: Just for additional helpful info, valsalva maneuver decrease venous return and increases right atrial pressure via direct compression of the vena cavae and cardiac chambers. Left-sided heart dimension also changes.
 
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