Feedback:Respiratory Distress Patient

[VentMedic]

If you understand the oxygen-hemoglobin dissociation curve, V/Q mismatching, shunting and deadspace you will understand "hypoxic drive" better.

If the person has significant V/Q mismatching or acute lung disease going on, they may still require large amounts of oxygen to maintain a decent PaO2. We look at A-a gradients and not "SpO2" in the acutely ill. In other words, for someone with normal lungs, the PaO2 might be 400+ mmHg on 100% O2. The pt who is distressed might still have an SpO2 above 90% on 100% O2 but have a PaO2 barely above 60 mmHg. If the person has low Hb and diminished O2 carrying capacity, you have a very ill and compromised patient that needs oxygen.

Also, 2 L by NC is not the same FiO2 for everyone. Neither is a NRBM if the pt's minute volume exceeds 15 L/Min. If a person has a rapid RR, they are entraining mostly room air diluting the O2.

I rarely worry about hypoxic drive in acute processes unless they are a chronic hypoventilator. If a person still can tell me they are short of breath, then O2 is still appropriate. If they have some neural muscular disease such as ALS or MD where they chronically retain CO2 due to muscular weakness and not lung pathology, I will be prepared to support respirations with the O2. Some people with severe obstructive sleep apnea are also prone to this. And then you have the central apneas which just require ventilation if they fall asleep such as Odine's curse or Central Hypoventilation Syndrome.

[Just Plain Ruff]

just a question here for all the providers out there, When was the last time any of us had a patient who was a copd'r and we knocked out their respiratory drive.

I'd be interested to hear the stats on this.

[JakeEMTP]

I was discussing this very topic with one of the RT's last night. I was informed that due to our minimal transport times, 1/2 hr at the most, the risk of knocking out the hypoxic drive was minimal. They also stated that if I felt that the pt. would benefit from some O2 administration, go ahead and give it.

This is where a thorough assessment of your/my patient is paramount. Some folks do not require their face blown off with 15 lpm because that is what's in the protocol. If my patient has improvement with 8, 10, 12 than that's what they will receive.

Treat the patient, not the monitor or the little finger sticky thingy. :wink:

[Just Plain Ruff]

I agree, the standard transport times I've been used to in the past have been of the 1 hour or so variety and I've never had a patient get their resp drive knocked out.

What I'm curious about is how many on this site have seen this "Phenomena"

[VentMedic]

Often, fatique is mistaken for "knocking out the hypoxic drive".

Out of all the COPD pts, which that are many different classifications and levels within each, only a small percentage can actually be classified as CO2 retainers.

http://home.pacbell.net/whitnack/The_Death...rive_Theory.htm

The Death of the Hypoxic Drive Theory

On March 15th I gave a talk at the 22nd Annual Tahoe “Odyssey” Conference, a conference for Respiratory Care Practitioners, Nurses, and Physicians. The topic was “The Death of the Hypoxic Drive Theory.

By “Hypoxic Drive Theory” I am referring to either the default assumption that any chronically compensated respiratory acidosis implies reliance on the hypoxic drive to maintain adequate gas exchange….or

…..that chronically compensated respiratory acidosis means the central chemoreceptors are defunct or deficient.

This is more than just a theory, it’s become a clinical mindset, almost a medical urban legend. “He’s a retainer”, “that’s where he lives”, “he’s in the 50/50 club”, etc., all are like so many clinical buzzwords.

There is the existence of a hypoxic drive. It normally accounts for about 10-15% of the total drive to breathe. We all have it, unless perhaps we’ve had bilateral carotid surgery. It becomes obliterated at a PaO2 above about 170, and becomes a greater stimulus as the PaO2 drops below 70, and especially below 50.

There is a hyperoxia associated hypercarbia, which can develop in certain patients while they are in crisis. But it has little, if anything, to do with respiratory drive.

When COPD patients are in acute respiratory failure they are usually breathing somewhere near their maximum limit. When 100% O2 is applied the CO2 can be driven up by 3 factors…

The Haldane Effect. Unsaturated hemoglobin carries CO2. A patient in crisis may arrive in the ER with an SpO2 on room air of 75%, the unmeasured mixed venous saturation may then in turn also be much lower than the 75% norm. All this unsaturated hemoglobin is then carrying an extra CO2 load. This is in the setting whereby the patient has an already elevated PaCO2, perhaps has an elevated Hgb after years of hypoxemia, and is “topped off” on their ability to ventilate. So for every rise in their SpO2 we are driving more CO2 into the plasma. If this were you or I, we would simply then ventilate this extra CO2 out via the lungs. But their lungs can’t and don’t, therefore the CO2 shows up in the “downstream” ABG.

The release of hypoxic pulmonary vasoconstriction. Imagine the worst ventilated alveoli. The local CO2 pressure there may be 100 or more. On room air the local O2 pressure will surely be less than 60 torr. At this level of local hypoxemia, the adjacent pulmonary vasculature will constrict. Blood will then be sent to the alveoli which is ventilating more effectively. Ventilation/perfusion matching is enhanced. But if 100% O2 is given the O2 pressure will not drop below 60, the pulmonary vasculature will not constrict, and V/Q matching will not be optimized. Just as giving Nipride may drop the PaO2 as hypoxic pulmonary vasoconstriction is released, so giving 100% O2 may also raise the PaCO2. This also can happen to patients in an asthmatic crisis given 100% O2. It’s not that we knock out a hypoxic drive, so much as we drive in a hypercarbic potential. Then further compromise ventilation through increased V/Q mismatching.

A small amount of the CO2 retainers whom are in acute failure, and whom have their PaCO2 increased further from the two mechanisms listed above, will then reduce their minute ventilation further by about 15-20%. Usually the PaO2 will have been about 40 on room air, the PaCO2 70. Given 100% O2 the PaO2 rises well above the 170 range whereby all hypoxic drive is obliterated, and the PaCO2 rises to 90 or more. But is this a result of a central drive deficiency? Or of central wisdom? When the PaO2 is 40 the patient can’t let their PaCO2 go up to 90. If they did the PaO2 would plummet to about 20 and rapid death would ensue (per the alveolar air equation). But when the hypoxic drive “gun to the head” is removed, the patient then titrates their respiratory effort such that the ventilatory effort and work is proportioned out for the long haul. It is not a drive deficiency. We may view this as patient permissive hypercapnea, may apply non-invasive ventilation, may simply realize that hypoxemia kills and hypercapnea does not, or may intubate them. Or hypoxemia may be used as a respiratory stimulant. But if this is the tactic chosen, it should be viewed as akin to giving epinephrine to an already compromised myocardium in order to maintain adequate perfusion pressure. Just as if we were to see this same patient arrive in stable condition for a clinic condition later we wouldn’t insist they needed an epi drip to maintain a sufficient cardiac output, so too should we not insist that a CO2 retainer not in crisis needs hypoxemia in order to stimulate adequate respiratory drive.

In the May 98 issue of Clinical Pulmonary Medicine is an article titled Acute Respiratory Failure in Chronic Obstructive Pulmonary

Disease” by Schiavi. In it the author concludes that…… “....The traditional idea that oxygen

induces hypoventilation by suppressing hypoxic ventilatory drive at the

level of peripheral chemoreceptors is no longer tenable.”

MUCH MORE INCLUDING REFERENCES:

http://home.pacbell.net/whitnack/The_Death...rive_Theory.htm

[Just Plain Ruff]

exceptional paper vent excellent post. thanks that taught me a lot.

[a918emt]

just a question here for all the providers out there, When was the last time any of us had a patient who was a copd'r and we knocked out their respiratory drive.

I'd be interested to hear the stats on this.

personally just 1 in 3 years as an E, working with a medic and fire based ems (6 people on every ems scene).

[MedicEllis]

A small amount of the CO2 retainers whom are in acute failure, and whom have their PaCO2 increased further from the two mechanisms listed above, will then reduce their minute ventilation further by about 15-20%. Usually the PaO2 will have been about 40 on room air, the PaCO2 70. Given 100% O2 the PaO2 rises well above the 170 range whereby all hypoxic drive is obliterated, and the PaCO2 rises to 90 or more. But is this a result of a central drive deficiency? Or of central wisdom? When the PaO2 is 40 the patient can’t let their PaCO2 go up to 90. If they did the PaO2 would plummet to about 20 and rapid death would ensue (per the alveolar air equation). But when the hypoxic drive “gun to the head” is removed, the patient then titrates their respiratory effort such that the ventilatory effort and work is proportioned out for the long haul. It is not a drive deficiency. We may view this as patient permissive hypercapnea, may apply non-invasive ventilation, may simply realize that hypoxemia kills and hypercapnea does not, or may intubate them. Or hypoxemia may be used as a respiratory stimulant. But if this is the tactic chosen, it should be viewed as akin to giving epinephrine to an already compromised myocardium in order to maintain adequate perfusion pressure. Just as if we were to see this same patient arrive in stable condition for a clinic condition later we wouldn’t insist they needed an epi drip to maintain a sufficient cardiac output, so too should we not insist that a CO2 retainer not in crisis needs hypoxemia in order to stimulate adequate respiratory drive.

In the May 98 issue of Clinical Pulmonary Medicine is an article titled Acute Respiratory Failure in Chronic Obstructive Pulmonary

Disease” by Schiavi. In it the author concludes that…… “....The traditional idea that oxygen

induces hypoventilation by suppressing hypoxic ventilatory drive at the

level of peripheral chemoreceptors is no longer tenable.”

MUCH MORE INCLUDING REFERENCES:

http://home.pacbell.net/whitnack/The_Death...rive_Theory.htm

can I say AMEN!!!!!

hypoxemia kills and hypercapnea does not

I have always lived by this and always will.

As for the call, from all the information you have given (and mind you I didn't assess the pt) you did fine and CPAP was not needed. With diff. breathers if you are having a hard Tx choice between CHF/Rales and COPD/Wheezing, pt Spo2/EtCo2 is fine and not showing respiratory failure, let the ER do there job with a chest x-ray and Tx decision based on that. If pt is stable and not decompensating CPAP would not be my 1st choice on this call. I may have choose to give the pt a neb Tx or two based on physcial exam, PMHx and Hx of current illness (ie, not sudden onset, fever/chills, sputum production, Hx of pneumonia in the past).

[DirtJerZ]

Well, was the patient febrile? was he in acute distress, what was he doing when it started, how was his bloodpressure? Was there any jvd, peripheral edema, was he diaphoretic, mild, moderate, severe distress. It sounds like pneumonia too me, from what little info you did give, if it was pneumonia in my state he would be going bls to the hospital, 99% spo2 is better than mine. And too many questions about what his actuall level of distress was? are you a paramedic?

[VentMedic]

It sounds like pneumonia too me, from what little info you did give, if it was pneumonia in my state he would be going bls to the hospital, 99% spo2 is better than mine.

That would depend on the overall medical conditions and assessment of the patient before assuming PNA is "BLS". In the ED, if a patient has bilateral PNA, which is generally determined by CXR and other differential tests, they are placed on a sepsis protocol which gets them a higher level of care bed. Crackles in only one area does rule out PNA in other lobes.

99% on a NRBM tells very little if the A-a gradient is significant. I hope you understand the difference in PAO2 (partial pressure of oxygen in the alveolar gas) for a person on O2 as opposed to room air and what V/Q mismatching is. PaO2 is oxygen pressure in the arterial blood. Of course, even that does not tell us much about the content of oxygen in the blood until SaO2 and Hb are known.

The Alveolar-Arterial gradient (PAO2-PaO2 gradient) for the average young healthy adult at sea level, will be 5 - 10 mm Hg. If they are on a nonrebreather it should be over 400 mmHg.

Since you don't always have access to an ABG machine in the field, you have to rely on other signs to assess the respiratory status. A pulse oximeter number should not be used to determine the severity of distress since a good number can be misinterpreted to being "all is well" or mislead the rest of your assessment.