on more than one occasion i’ve been called to a patients room for hypoxia. The patient is sleeping and the waveform is terrible. I find where the patients probe is and ensure there is no pressure on that point (i.e, reposition their hand) and boom, hypoxia cured. Thank you for the video!
id like to add shunts are not exclusively intracardiac. patients with small airway pathologies like pulmonary edema and ARDS have pulmonary shunts where blood flow to diseased portions of the lungs that are not ventilating are preserved, leading to admixing of non-oxygenated ang oxygenated blood.
What’s the mechanism for hypoxia in PE? V/Q mismatch doesn’t quite make sense to me that even a large infarct could cause enough hypoxia to cause a measurable change in the O2sats
sometimes the PE causes a degree of reactive pulmonary hypertension that is enough to back up into the RA and open a PFO, causing shunting and mixing of deoxygenated blood into the left heart.
When a large pulmonary vessel is occluded, two things happen: - The portion of the lung that is downstream from the occlusion continues to be ventilated, but now has zero perfusion - The blood that normally would have gone to that portion of the lung is redirected elsewhere. Some of it gets redirected to portions of the lung which do not receive good ventilation. While the lung has a natural mechanism to vasoconstrict vessels going to areas with poor ventilation, it does not have an adaptation to deal with the opposite problem (i.e. bronchioles going to areas with poor perfusion). Your instinct is correct though that it would need to be a relatively large PE to cause hypoxemia via this mechanism in the sense that many relatively small PEs do not cause low O2 sats. There are a number of studies showing that the presence or absence of hypoxemia has minimal to no impact on the probability a patient with suspected PE or presenting with dyspnea actually has a PE. Here's just one that isn't non-paywalled: www.atsjournals.org/doi/10.1164/ajrccm.162.6.2004204
Unless mild, hypoxemia otherwise always leads to hypoxia. However, a number of situations exist in which hypoxia occurs without hypoxemia. Oxygen delivery to peripheral tissues is approximately equal to the product of cardiac output, O2 sat, and hemoglobin concentration. So for example, in cardiogenic shock where the cardiac output is markedly reduced, or in profound anemia resulting in very low hemoglobin concentration, patients can experience hypoxia despite no hypoxemia. Cyanide poisoning can have the same end result by interfering with cells' ability to utilize oxygen. And hypoxia can occur more locally due to a focal obstruction of blood flow from an embolus or from compartment syndrome.
I know, I'm sorry. The CV exam videos are taking a while to edit. I've got a one-off, general interest video coming in 2 days, hopefully followed by weekly CV exam videos for the next 4 weeks after that.
Sorry, it's a scheduled release for Sunday morning. I do this so I don't need to worry about uploading it and entering in all of the information (including references) Saturday night. This also allows colleagues to vet them ahead of time if it's something that I'd like more feedback on.
on more than one occasion i’ve been called to a patients room for hypoxia. The patient is sleeping and the waveform is terrible. I find where the patients probe is and ensure there is no pressure on that point (i.e, reposition their hand) and boom, hypoxia cured. Thank you for the video!
Essential information for any medical professional brilliantly explained. Thank you.
From an RT"s point of view, always look at the patient clinical presentation when in doubt of the pulse oximetry value.
Thank you so much for mentioning pulse oximetry and black skin. I feel like this isn't talked about enough.
I absolutely love this video. Beautifully and simply explained. This one goes into my must watch playlist :)
Absolutely awesome Doctor Strong, awesome!!
A great lecture, it would be helpful if there's a lecture about supplemental O2 therapy
Here's an old one about the impact of supplemental O2 on the ABG: ua-cam.com/video/9klrDCall9M/v-deo.html
Excellent information and insights! Much appreciated.
this underscores the need for nurse rounding to observe the patient and not rely on the monitor for any patient who has a condition WORTH monitoring.
Wonderful videos.please make videos on General Practioner's Daily OPD patients.dealing with common problems.
I wish you can upload more 🙏
Thank You So Much.... Circulating Haemoglobin .... have much better understanding now...
id like to add shunts are not exclusively intracardiac. patients with small airway pathologies like pulmonary edema and ARDS have pulmonary shunts where blood flow to diseased portions of the lungs that are not ventilating are preserved, leading to admixing of non-oxygenated ang oxygenated blood.
What’s the mechanism for hypoxia in PE? V/Q mismatch doesn’t quite make sense to me that even a large infarct could cause enough hypoxia to cause a measurable change in the O2sats
sometimes the PE causes a degree of reactive pulmonary hypertension that is enough to back up into the RA and open a PFO, causing shunting and mixing of deoxygenated blood into the left heart.
When a large pulmonary vessel is occluded, two things happen:
- The portion of the lung that is downstream from the occlusion continues to be ventilated, but now has zero perfusion
- The blood that normally would have gone to that portion of the lung is redirected elsewhere. Some of it gets redirected to portions of the lung which do not receive good ventilation. While the lung has a natural mechanism to vasoconstrict vessels going to areas with poor ventilation, it does not have an adaptation to deal with the opposite problem (i.e. bronchioles going to areas with poor perfusion).
Your instinct is correct though that it would need to be a relatively large PE to cause hypoxemia via this mechanism in the sense that many relatively small PEs do not cause low O2 sats. There are a number of studies showing that the presence or absence of hypoxemia has minimal to no impact on the probability a patient with suspected PE or presenting with dyspnea actually has a PE. Here's just one that isn't non-paywalled: www.atsjournals.org/doi/10.1164/ajrccm.162.6.2004204
Doc, as far as hypoxia and hypoxemia, can you have one without the other?
Unless mild, hypoxemia otherwise always leads to hypoxia. However, a number of situations exist in which hypoxia occurs without hypoxemia. Oxygen delivery to peripheral tissues is approximately equal to the product of cardiac output, O2 sat, and hemoglobin concentration. So for example, in cardiogenic shock where the cardiac output is markedly reduced, or in profound anemia resulting in very low hemoglobin concentration, patients can experience hypoxia despite no hypoxemia. Cyanide poisoning can have the same end result by interfering with cells' ability to utilize oxygen. And hypoxia can occur more locally due to a focal obstruction of blood flow from an embolus or from compartment syndrome.
Waiting for new videos😫
I know, I'm sorry. The CV exam videos are taking a while to edit. I've got a one-off, general interest video coming in 2 days, hopefully followed by weekly CV exam videos for the next 4 weeks after that.
Your last video isn't accessible...it is somehow private
Sorry, it's a scheduled release for Sunday morning. I do this so I don't need to worry about uploading it and entering in all of the information (including references) Saturday night. This also allows colleagues to vet them ahead of time if it's something that I'd like more feedback on.