Are orthostatics useful?

Yes. But only in certain situations. Read on.

Typical case: 80-year old woman with severe ILD and pulmonary hypertension on 6 L nasal cannula coming in with dizziness and presyncope. “I feel fine now,” she says after one day of being in the hospital (her son warns you she is eager to get home to see a new grandchild). She has been on Lasix for several months for leg edema (which on exam is 3+), and despite saying she’s not dizzy anymore, her orthostatic vital signs (VS) are positive by SBP and DBP. Should you stop Lasix? Can you send her home?

Orthostatic symptoms include lightheadedness, dizziness, confusion, weakness, blurry vision, etc. Orthostatic VS are positive if after 1-3 minutes, the heart rate increases >30, systolic BP decreases >20, diastolic BP decreases >10 (the 30-20-10 rule). For patients who have hypertension, using a cutoff of systolic BP decreases >30 is more specific. This paper provides a great physiologic review of orthostatic hypotension (OH). In up to 1/3 of cases, the cause of orthostasis will not be identified.

Studies such as this meta-analysis and this prospective population study have linked OH to increased all-cause mortality as well as stroke, CHF, and MI. Positive orthostatic VS can be linked to serious chronic illnesses, but these studies showed patients with OH had worse outcomes independently of other conditions.

Just some of the diseases associated with OH:

  • Neurodegenerative disease: primary autonomic failure, MSA, Parkinson’s, MS
  • Neuropathies: diabetes, amyloidosis, renal failure, stroke
  • Cardiovascular disease: heart block, pulmonary HTN, heart failure
  • Endocrinopathies: adrenal insufficiency, hypothyroidism
  • Cancer: paraneoplastic syndromes, multiple myeloma

Known factors that can make OH worse:

  • Fever
  • Dehydration, excessive urination
  • Increased venous pooling
  • Immobilization and deconditioning
  • Post-prandial state
  • Certain medications (diuretics, some antipsychotics, etc…)

The above information shows that not all orthostasis will be fixed by fluids. Don’t overload patients if they’re not responding.

More recently, orthostatic VS have been critiqued. Anand Swaminathan’s presentation on the “urban legend” of orthostatics in the ED is very informative. He cites a study showing that in a population of 900 nursing home residents, 50% had orthostatic VS changes. The numbers are similar for young, healthy adults. Positive orthostatics could indicate a new problem…or not. See this: a letter to the editor on the lack of evidence showing positive orthostatic VS in syncope require additional diagnostic testing/admission. For triaging purposes, orthostatic VS are not as useful as orthostatic symptoms (getting so lightheaded they might fall or injure themselves at home).

Orthostatic VS should only be obtained if they will change decision-making or result in new treatment. I propose that orthostatic VS are useful for:

  • in certain presenting complaints, like pre-syncope or syncope, which based on a patient’s background, may lead to cardiac testing (I say this as an internal medicine doctor dealing with patients already admitted to the hospital)
  • determining how aggressively someone’s supine hypertension should be treated
  • determining if someone’s lightheadedness, dizziness, or hypotension should be treated with compression stockings or meds like droxidopa or midodrine
  • evaluating functional status or quality of life in patients with above-mentioned chronic illnesses (very specific situations)

Returning to the case: the patient’s positive orthostatic VS were thought to be due to underlying pulmonary HTN and deconditioning. Lasix was thought to be necessary for pulmonary and peripheral edema. She was sent home. She was re-admitted <48 hrs later with syncope and found to be normotensive lying on her back, but profoundly hypotensive (SBP 50s) with just turning in bed; this failed to improve with IV fluids. TTE showed new RV dilation and a thrombus vs. vegetation on a pacemaker lead. In retrospect, this TTE should have been performed during her first hospitalization. This case is a good example that the significance of positive orthostatics depends on the clinical context, and while you may not need to treat the orthostatics per se, they can be a warning sign of a high-risk patient or a brewing problem.

Interpreting hypoxia on an ABG: PaO2 and SaO2

Let’s say you have a 57 year old patient breathing comfortably on room air, and when you walk in the next morning, he’s suddenly on 6 L O2 by nasal cannula. He doesn’t look like he’s in respiratory distress, but you decide to investigate by getting an ABG.

Result: 7.27/47/68

He is satting 93% on 6 L NC. Is that good? Is that bad? How does his O2 sat compare to the PaO2 on his ABG?

Normal PaO2=80-100 mm Hg. PaO2 is affected by age (tends to be lower) and altitude (tends to be lower).

PaO2 and O2 sat can be related through the oxygen-hemoglobin dissocation curve! See this table for PaO2 to O2 sat conversion. Remember that from first year of med school?

Straight from Wikipedia

As you can see, under normal conditions, an O2 sat of 90% correlates with a PaO2 of 60 mm Hg  (bonus points if this makes you realize an O2 sat  of 90% is not totally normal, although for sick, hospitalized patients,  it is acceptable). This curve is useful because it shows that giving supplemental O2 is most useful when someone has an O2 sat <90%. The curve also shows that O2 sat falls slower than the PaO2–a change in PaO2 from 96 to 70 may only show up as a change in O2 sat from 97% to 92%.

FiO2 can also affect an ABG reading. The PaO2 on your ABG should equal FiO2 x 500. If it doesn’t, there’s probably an A-a gradient. The PaO2/FiO2 ratio (or P/F ratio) is useful for categorizing hypoxia as potentially severe (when applied to ARDS).

So what about the patient above? His PaO2 of 68 mm Hg correlated perfectly with an O2 sat of 93%. However, he was also on 6 L NC, and the FiO2 was 40%. This implied that there was a significant A-a gradient

Random notes below:

Why are air bubbles bad? The PO2 of room air is 150 mm Hg, which means any air bubbles trapped in the ABG sample will shift the oxygen value towards 150 mm Hg.

When does the ABG have to be put on ice? If it can’t be processed in 15 minutes. (Residual blood cells will continue to use oxygen and make the PaO2 seem lower than it really is.) An ABG on ice can still be analyzed for up to an hour after collection.

If I get a value like PaO2=213, what does that mean?! At least you know the patient’s not hypoxic? PO2 is measured directly via electrode. The electrode is calibrated for values between 0-140. Therefore values >150 are of unclear accuracy. Remember that FiO2 affects the value as well.


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