Can a pt hyperventilate themselves into resp failure?

tryingtohaveitall · Apr 13, 2013

He was intubated after 5 seconds of "apnea"? That's not considered apnea even in babies. Why did they intubate?

turnforthenurse, MSN, NP · Apr 13, 2013

The only thing I can think of is respiratory failure secondary to muscle fatigue due to persistent hyperventilation. That or he had some other underlying pathology, but it's strange because everything else was normal aside from being tachypneic and hypertensive.

emtb2rn, BSN, RN, EMT-B · Apr 13, 2013

White coat syndrome? Tubed after apneic x5 seconds?!?!?! Isn't that jumping the gun a bit?

hodgieRN · Apr 13, 2013

It might be possible that he was able to do that, but he wouldn't be able to do anything severe enough to be an actual emergency. Eventually, he would have to stop the act to start breathing again. It could be possible that his schizophrenia was causing him to have some break in reality, having some type of stress reaction from his anxiety, or if you really wanted to think outside the box, sometime of partial seizure activity (but I don't think this is what happened). I think what he was doing was holding is breath on purpose and then hyperventilating because he was holding his breath. If he was holding his breath long enough to start turning gray, then it makes sense that he would hyperventilate, fill back up and then purposefully hold his breath for attention. He acted out and got the attention he wanted.

It doesn't sound like there was anything wrong metabolically. If his oxygen saturation was fine, then some haldol and a psych consult would fix that right up. He probably knew that if he held his breath long enough, the monitor would start beeping. And that means attention from the medical staff. Pts get very good at faking a decrease in LOC and have learned all sorts of tricks to make the staff think something is going on. I just took care of a lady with pseudoseizures and she was very good. She knew to say "something doesn't feel right" and knew to stare off to the left and not respond when asked a question. Best one to date I've seen yet. While she was having one of her pseudoseizures, I told her that I would remove the narcotics from the MAR if she continued to act out and she immediately agreed that was fair trade. Labs and monitors don't lie. I'm sure your pt has done this before. That's my theory. Schizophrenia, anxiety, and the episodes magically stopping while he was getting some food in his stomach, I think it's obvious.

rn/writer, RN · Apr 13, 2013

Five seconds of not breathing does not constitute apnea. Think about it. A low-normal respiratory rate of 12 breaths per minute would mean five seconds between one breath and the next, and that certainly isn't apnea. If the patient had been hyperventilating, that five-second gap could have seemed quite a contrast without presenting any actual threat.

Hyperventilating can cause something called circumoral cyanosis, meaning the area around the mouth can look bluish, or in the right lighting, even gray. Taking small, shallow breaths for more than a few minutes can by physically taxing and the patient would very possible work up a sweat.

The fact that the patient could stop and start this behavior at will (when asked to, when no one else was in the room); his ability to wander the halls, eat and converse with others; and his removal of O2 suggest a problem rooted in anxiety rather than physical pathology.

I DO question why the patient was intubated if the "apnea" lasted for only five seconds. Diminished level of consciousness is not the same as loss of consciousness, and if the patient resumed breathing on his own, why would the doc perform something so invasive and unnecessary. Even if the patient passed out, I would hope the doc would wait longer than five seconds to determine the need for intubation.

Hyperventilating blows off too much CO2. This, in turn, lowers blood pressure. If the blood pressure drops too far, the person can pass out. Even though his initial blood pressure reading was elevated, it may well have dropped after his lengthy bout of hyperventilating. The ABGs bear this process out, as you said his O2 level was fine but his CO2 was low.

I'm thinking you witnessed a good old-fashioned panic attack followed by a fainting spell. It doesn't matter if the patient was or was not intentionally manipulating the situation. The result would have been the same either way.

The treatment, as you described it, seems questionable, at best. Unless there was underlying pathology--contraindicated by the labs and other diagnostic tests--normal breathing would have resumed as the CO2 level built up in the patient's blood stream.

This is the flip side of the little kid who holds his breath and turns blue when he doesn't get his way. Breathing too much or two little can cause you to faint. But then the homeostatic drive kicks in and the body works to regain its normal balance. Intubating someone who is hyperventilating makes about as much sense as it does for the stubborn child. It is simply not necessary and introduces a lot of potential for more problems.

gcupid · Apr 14, 2013

How about 2liters of Oxygen via nasal cannula, 2mg of Ativan IVP and remote tele? If the md's want to play inspector gadget, let them. As a nurse with other patients that probably all want something done from me at the same time, I have to go. Don't nobody have time for that...

LakeEmerald · Apr 14, 2013

Yeah, I did not have time for all that. :) But the weird thing was, by the time he had the 2 apneic episodes, he wasn't talking, moving, or responding to pain. We started another IV before we gave the Etomidate and Vec, and he did not flinch or groan at all. Then, after we intubated him, he did not require Versed or any sedation for the 1.5 hours I had him before I took him to ICU. If I'm able to get more info I'll update.

Also, the 5 seconds felt like 5 minutes. There was a clicking in his throat that seemed to indicate trouble. He deserves an award if still acting then! Thanks for all the great responses!

nrsang97, BSN, RN · Apr 14, 2013

A few months ago I was doing my rapid response rounds. I was leaving the rehab building, and this man was walking in. He appeared to be looking for something/ was lost. I approached and asked him if there was anything I could do to help. He told me he wanted to see someone and had been tired for the last few weeks. I asked him if he wanted me to walk him to the ER. He at first declined, but when I told him that was the only way he could be seen by a doctor he went with me. He was at first walking with me and talking fine. As time went on he started getting weak and diaphoretic on me. I got him to a place where I cold sit him down and some house keepers came by and got me a wheel chair, and some transporters helped me get him into the wheel chair. We took him to the ER. By that time he could not even tell me his name. He handed me his wallet and I looked at his driver's license, and started calling his name and he quit talking to me. We ran him to triage, and then to the trauma room.

ER did a workup and absolutely nothing was wrong with him at least physically that they could find. CXR negative, CT negative for PE or brain bleed, tumor, etc.

I was sure there was something wrong with him, but in fact there was not. So strange. He even tried claiming he didn't speak English. His family said he had done this before and nothing was wrong with him. He did have a history of a mental disorder, but they didn't keep him in they psych unit, just sent him back to outpatient therapy.

Sounds like the OP's patient had a huge panic attack. I don't understand intubating him.

Esme12, ASN, BSN, RN · Apr 14, 2013

Yeah, I did not have time for all that. :) But the weird thing was, by the time he had the 2 apneic episodes, he wasn't talking, moving, or responding to pain. We started another IV before we gave the Etomidate and Vec, and he did not flinch or groan at all. Then, after we intubated him, he did not require Versed or any sedation for the 1.5 hours I had him before I took him to ICU. If I'm able to get more info I'll update.
Also, the 5 seconds felt like 5 minutes. There was a clicking in his throat that seemed to indicate trouble. He deserves an award if still acting then! Thanks for all the great responses!

There are 2 theories.....maybe he wasn't hyperventilating and there was something neurological going on...maybe a head CT would have been helpful.

While 5 seconds of apnea seem like a long time it isn't and the patient could have passed out or was siezing as you mentioned a "clicking sound".......but hyperventilation can cause seizures and cardiovascular collapse when extreme as in neurological situation like with tumors of the brain stem, medulla and pons. Or lesion in the brain cause by conditions like MS. It's called crental neurogenic hyperventilation.....CNH

Symptoms of CNH have been observed to vary according to the progression of CNH. The initial symptoms of CNH include a low arterial partial pressure of carbon dioxide, a high or normal arterial partial pressure of oxygen, high arterial pH, and tachypnea. The partial pressure of carbon dioxide has been noted by Yushi et al. to drop as low as 6.7 mmHg, while oxygen saturation remains at 99-100%. Respiratory alkalosis is induced in people affected with CNH, which stimulates the hyperpnea to attempt to compensate the rise of the blood’s pH. Some of the reported cases of CNH claim alkaline cerebral spinal fluid (CSF). However, not all of the cases experience this effect and other cases of CNH have a local increase in the pH surrounding the tumor that causes the condition. The hyperventilation of CNH patients persists during sleep.Those affected have been observed to not be able to voluntarily control their breathing in order to slow it down and the hyperventilation is predominantly controlled by the diaphragm.
CNH has been found to affect people of all ages, ranging from children at the age of seven to adults at the age of eighty-seven. It has affected people while they have been both conscious and unconscious. After Plum and Swanson's initial discovery of CNH it was thought that CNH was rare in conscious patients. More cases of CNH have been observed in conscious patients since then. Additional symptoms of conscious CNH include loss of appetite, difficulty concentrating, poor memory, difficulties in eating or talking, cachexia, vomiting, disorientation, and a generalized confused state that varies from patient to patient. It is generally seen, however, that the mood changes, anxiety, and difficulty concentrating progress as the tumor increases in severity and, in effect, CNH persists. All of these symptoms are not present in each reported case of CNH, and symptoms seem to vary on a case to case basis. Other symptoms that have been associated with CNH are transient epileptic episodes with a temporary loss of consciousness. This condition is thought to result from severe hypocapnia that induces blood vessels in the brain to constrict, leading to brain ischemia. Other symptoms caused by CNH are electrolyte dysequilibrium and mood changes that primarily include anxiety due to the hyperventilation.
Once CNH is diagnosed, the condition generally progresses until the patient becomes unconscious or lapses into a coma. Most patients are seen to enter this state two to three months after the onset of CNH. Lange et al. cited a patient that experienced pulmonary edema, bronchitis, and pneumonia prior to death, though all reported cases of CNH describe various progressions of the condition until it worsens to the point of death.

Granted these patients have some organic issue but I can see schizophrenia as an organic issue to cause a patient to compulsively hyperventilate. Not always a wiki fan but this is a great explanation.....http://en.wikipedia.org/wiki/Central_neurogenic_hyperventilation

This is similar to "The choking game" (also known as the fainting game and a wide variety of local slang names), refers to intentionally cutting off oxygen to the brain with the goal of inducing temporary syncope and euphoria. There are two distinct methods used to achieve oxygen deprivation: strangulation (stroke and choke/auto-eroticism) and self-induced hypocapnia (plain ole hyperventilation)

Self-induced hypocapnia
The second mechanism requires hyperventilation (forced overbreathing) until symptoms of hypocapnia such as tingling, light-headedness or dizziness are felt, followed by a breath-hold. This alone is enough to cause a blackout, but it is widely believed that the effect is enhanced if lung air pressure is increased by holding the breath "hard" or "bearing down" (tightening the diaphragm as in a forced exhalation while allowing no air to escape or having an assistant apply a bear-hug). These latter actions may augment the effects of hypoxia by approximating the Valsalva maneuver, causing vagal stimulation.
The hyperventilation leads to an excessive elimination of carbon dioxide (CO₂) whereas no significant additional amounts of oxygen can be stocked in the body. As only carbon dioxide is responsible for the breathing stimulus, after hyperventilation, breath can be held longer until cerebral hypoxia occurs. The blood also becomes abnormally alkaline as a result of the excessive elimination of carbon dioxide; this subsequent rise in blood pH is termed alkalosis. Alkalosis interferes with normal oxygen utilization by the brain. The symptoms of alkalosis are: neuromuscular irritability, muscular spasms, tingling and numbness of the extremities and around the mouth, and a dizziness, or giddiness, often interpreted as a sense of euphoria.
In the body alkalosis generally induces vasodilatation (widening of the blood vessels) but in the brain alone it causes vasoconstriction (narrowing of the blood vessels). This vasoconstriction appears to be made even worse by a sudden increase in blood pressure caused by squeezing or holding the breath ‘hard’. The alkalosis induced euphoria can be followed rapidly by hypoxia-induced unconsciousness. The sequence of events leading to unconsciousness from hyperventilation is as follows:
Decrease in partial pressure of alveolar CO₂.
Decrease in partial pressure of arterial CO₂.
Increase in blood pH, (respiratory alkalosis).
Vasoconstriction of blood vessels supplying brain.
Pooling of the blood present in the brain at the time.
Brain rapidly uses up oxygen (O₂) available in the pooled blood.
O₂ concentration in the brain drops.
Unconsciousness from hypoxia of cerebral tissue.
Because the brain cannot store reserves of oxygen and, unlike other organs, has an exceedingly low tolerance of oxygen deprivation, it is highly vulnerable if vasoconstriction is not reversed. Normally, if the brain is hypoxic, autonomous systems in the body divert blood to the brain at the expense of other organs; because the brain is vasoconstricted this mechanism is not available. Vasoconstriction is only reversed by the build-up of carbon dioxide in the blood through suspension of breathing.
In some versions the bear-hug is replaced by pressure on the neck in which case blackout is a hybrid of strangulation and self-induced hypocapnia.

Wiki is batting a thousand today......http://en.wikipedia.org/wiki/Choking_game

Hyperventilation/hypocapnia can cause numbness and tingling, muscle spasms of the face, hands and legs and can progress to the chest causing a paralysis/stunning of the chest wall muscles. It can progress to cause "hypoxia" due to the body to unload O2 at the tissue level causing circumoral pallor and seizures from hypoxia in the brain.

This patient didn't need O2 for their O2 is usually fine but the needed a simple mask to allow them to re-breathe their own CO2...or a paper bag. However usually patient won't breathe into a paper bag....I have used a Non-rebreather and sealed one of the flutter vents.....not inflated with O2 and under close observation allowed the patient to rebreathe their own CO2.

So this is a long winded answer to your question ......yes I have seen this phenomenon

OP I'll be curious to see any updates!

http://www.instructorscorner.org/media/resources/SAC/Vol%20Hyper%20Preceding%20Unde%20Swim.pdf

Altra, BSN, RN · Apr 14, 2013

Great information provided above. To me this sounds like an MD who thought "ain't nobody got time for that" when faced with a probable psych issue and took the "safest" (though most aggressive/invasive) approach in making sure the patient wouldn't circle the respiratory drain.

imintrouble, BSN, RN · Apr 14, 2013

I have absolutely no scientific evidence to back up my opinion. I DO have almost 20 yrs of nursing experience. COPDers can "anxiety" themselves right into the ICU if you don't get a handle on their breathing.

They're absolutely my worst patients. They expect/demand every single spare second I have after taking care of everybody else. They know, and I know, what will happen if I don't give extensive 1-1. I almost feel like I'm held hostage by these patients.