Steps for eval:
1. To test or not to test? Use PERC criteria (only low risk pts). If score zero, don’t test.
2. If testing: is pt is low-risk or not? Use Wells criteria. If low-risk, send D dimer. If not, CTA.
3. If by clinical gestalt determine high suspicion, forget criteria and CTA.

-a-massive PE (large central clot burden causing RV failure) is equivalent to submassive PE (RV dysfunction) in pt with poor cardiopulmonary reserve

-primary indication for surgical/catheter embolectomy is failure of hemodynamic improvement after fibrinolysis, however can consider it early in pts for whom you are considering giving fibrinolytic

-Geneva criteria for PE risk assessment – does not have vague criteria of “PE most likely diagnosis”

-Note: TWI in inferior and anteroseptal leads are highly suspect for PE

-MOPPET trial: low dose tPA reduces pulmonary HTN in pts with moderate PE (in terms of size and location) immediately after and the effect is present months afterwards but does not affect mortality or recurrent PE as
early heparin in PE pts reduces in-hospital and 30 day mortality (2010 Chest)

-a normal A-a gradient does NOT rule out PE
-hypoxemic has NPV of 70% (30% of pts with PE will NOT be hypoxemic)
-chart in the ICU book for PPV and NPVs of findings
-ICU book: p130 chart central line insertion depth
-new pleural effusion after central line placement – suspect SVC perforation! Must tap and sent analysis
-the MAP is more accurate estimate of aortic pressure (SBP increases closer to periphery)
-septic shock = defect in mitochondrial use of O2 -> elevated lactate (>2 is abnl). Also the respiratory burst adds to O2 demand.
-P/F ratio (PaO2:FiO2) = estimate of shunting. <200 = >20% shunting of deoxygenated blood through lungs
-PaO2 measures gas exchange in the lungs (NOT arterial O2 content bc doesn’t account for Hb). Pulse ox measures arterial O2 content.
-pulse ox not as accurate for black or brown nail polish – put oximeter on sides of finger
-*supplemental O2 can be safely withheld if SpO2 92% or greater on room air**
—which kind of pts are exceptions??? (given O2 dissociation curve)
-clinical studies: SpO2 accurately shows hypoventilation (low PaO2) if pt is on room air, but NOT if on supplemental O2
-pulse ox and ETCO2 can replace ABGs
-in cardiac arrest, the lack of color change from purple to yellow on a capnometer can occur even if ETT is in the trachea – representing low CO
-continuous ETCO2 almost identical to PaCO2 unless in cases of impaired gas exchange such as increased dead space (hypoventilation, obstructive lung disease) or low CO (PE, lung overinflation)
–changing the vent settings will change how well ETCO2 and PaCO2 correlate, so should repeat ABG to determine the difference each time the vent settings are changed
–can also use continuous ETCO2 to determine change in CO as a result of giving a fluid challenge or aggressively diuresing
-low flow O2 systems provide a variable FiO2 (depends on multiple factors, incl pt’s inspiratory flow rate), whereas high flow provide constant

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