Respiratory Acidosis Question. Help please.

Butterfly6890 · Apr 15, 2013

Tell the difference to what? Hyperventilating to hypo or just respiratory acidosis?

SCSTxRN · Apr 15, 2013

Respiratory Acidosis is a condition - it's defined by low blood pH and high CO2. CO2 buildup secondary to poor ventilation (for whatever reason) is the cause of the low blood pH.

I'm going to assume that you're a generally healthy person who's never really struggled for air. Have you ever had a hold your breath contest while swimming? Know that feeling when you come up and all you can do is suck air for a few minutes? That's your body exchanging the CO2 build up for oxygen. If something were going on in your lungs (say asthma or pneumonia) that made your mad air sucking less effective, your CO2 levels would continue to rise, your blood pH would continue to drop, and you would continue to become more desperate for air. You'd breathe harder, faster, as your body tried to restore homeostasis. If it didn't work, eventually, you'd die.

That same breath holding contest, if you try hyperventillating first, you can hold your breath longer before the CO2 buildup makes you come up for air. To a point, assuming that a patient's lungs are functioning and airways are open, increasing the O2 saturation helps the patient hold better saturation.

Excess CO2 is seen when the patient is having trouble exchanging gasses in the lungs. COPD patients typically carry higher CO2 levels with less compensatory mechanisms than the 'average' patient, because their body has gotten used to a less than ideal oxygenation level over time.

Patients with respiratory suppression secondary to drug overdose have, at least temporarily, lost some of the air sucking drive that keeps the buildup from happening - so they will go into respiratory acidosis without the accompanying tachypnea to reverse it.

Tacypnea is a rapid respiration. It can be shallow, or it can be deep. Typically, deep rapid respiration is what we call hyperventilation. Rapid, shallow respirations can be signs of asthma attack, lower lobe pneumonia, pneumothorax, and I'm sure several other things that won't come to me at 5 a.m.... but they very rarely, if ever, result in hyperventilation.

Both can be (but are not always) signs of respiratory acidosis, though. Does that make sense?

Esme12, ASN, BSN, RN · Apr 15, 2013

A few weeks before our respiratory lecture, I had a patient in the ICU who I observed was becoming very tachypnic and restless. She was an elderly woman. I told the nurse and when she noticed that the patient saturation ( I know you said those aren't the most reliable was going into the 70's and the patient was clearly distressed, she bumped the O2 from 2-10. In short, they were able to avoid intubation and keep her on a CPAP machine ( or PEEP? I know it was just positive pressure being put into her lungs, not 2 different pressures. I'm still not sure what the right term for it is. The nurse said it was to assist her with ventilation, not make her ventilate). Upon a chest xray, it was determined that she had pneumonia and I think it was causing sepsis. They also got an ABG and I believe it was respiratory acidosis ( the textbook says that pneumonia can lead to resp. acidosis). I also had a COPD patient who demonstrated the same signs of my first patient (increased RR, increased HR, very distressed)

OK.....without knowing the ABG's it is impossible to know for sure how to explain this to you but I will try. respiratory acidosis is hypoventialtion not necessarily cause by respiratory depression. http://fitsweb.uchc.edu/student/selectives/TimurGraham/Etiology_Respiratory_Acidosis.html

Causes of respiratory acidosis

A) CNS depression

1. Opioids

2. Oxygen in patient with chronic hypercapnia

3. Central sleep apnea

4. CNS lesion

5. Extreme obesity (Pickwickian syndrome)

B) Neuromuscular disorders

1. Myasthenia gravis

2. Guillain-Barre

3. ALS

4. Poliomyelitis

5. Muscular dystrophy

6. Multiple Sclerosis

C) Chest wall or Thoracic Cage Abnormality

1. Kyphoscoliosis

2. Flail Chest

3. Myxedema

4. Rib Fracture

5. Scleroderma

4) Disorders affecting gas exchange

1. COPD

2. Severe asthma or pneumonia

3. Pneumothorax or Hemothorax

4. Acute pulmonary edema

5) Airway obstruction

1. Aspiration of foreign body

2. Obstructive sleep apnea

3. Laryngospasm

You had a patient that was having trouble breathing that was having an increasingly harder time breathing. O2 sat's are a reliable (most of the time) indicator of the patients O2 saturation especially when you can document trends. This patient was decompensating and exhibiting signs of increasing distress.....restlessness and tachypnea accompanied by O2 Sats in the 70's.

This patient was suffering from hypoxia...not getting enough oxygen. So the nurse increased this patient oxygen by increasing her supplemental O2 to 10Lmp. This patient had an order for CPAP, or continuous positive airway pressure. This uses mild air pressure to keep the airways open....The mild pressure from CPAP can prevent the airway(aveolar beds) from collapsing or becoming blocked. This makes it easier to get a deep breath all the way in and get the oxygen into the lungs.

Example.....have you ever tried blowing up a brand new balloon and it just won't inflate? Then you try to blow up a balloon that someone has inflated partially already a little and it's easy to get more air in? CPAP

So your CXR shows pneumonia. Your saturation is indicating hypoxia so your patient is hyperventilating to get more oxygen (a hypoxic/hypo-ventilated state) therefore your body is in a state of acidosis. It then attempts to compensate and get more oxygen in by breathing faster.http://georgiahealth.edu/itss/edtoolbox/GeorgiaLabs/AcidBase/hyper_hypoventilate/HyperHypoventilation.html

Respiratory acidosis is an acid-base balance disturbance due to alveolar hypoventilation (using CPAP to get more O2 deeper in to the lungs). Production of carbon dioxide occurs rapidly and failure of ventilation promptly increases the arterial carbon dioxide. Acute respiratory acidosis is present when an abrupt failure of ventilation occurs

Respiratory Acidosis: Acid Base Tutorial, University of Connecticut Health Center

Your COPD patient was in the same stae for a different reason.

nurseprnRN, BSN, RN · Apr 15, 2013

I understand that respiratory acidosis is clinically manifested as respiratory depression ( this is what they say happens with drug overdose). But is it that sometimes, the first signs might be a hyperventilating patient ( like mine who RR was going up, HR was going up) and if we did not quickly intervened, they would have eventually hypoventilated?

I am just thinking of the compensatory mechanisms that pt's demonstrate when they have resp. acidosis. I might be confusing hyperventilating with tachypnea. But to me they look the same! How can you tell the difference especially since you have to treat the underlying cause?

You're on the right track and I think that clearing up one or two misconceptions will get you going.

Ventilation refers to the amount of air being moved in and out-- think of a musty room that needs a lot of air exchange to ventilate it. Little bits of air won't do the job well.

Tachypnea means "fast breath(ing)" (remember the tachometer in your car? Engine speed and pnea/pneu, lungs/breath.

Respiratory depression isn't a symptom of respiratory acidosis. (That's what "manifested as" means, being evidence-- you would say, "Too much sun exposure as manifested by a burn," not "A burn as manifested by too much sun exposure.")

So let's put this all together.

Respiratory depression causes respiratory acidosis. Respiratory acidosis is the result of a higher-than-normal arterial CO2 level (PaCO2), and this happens because respiratory efforts are not enough to move CO2 (which functions as an acid) out of the lungs. The body senses this decreased pH and tries, sometimes ineffectively, to increase ventilation to move more CO2 out, but increased respiratory rate in a crummy chest does not translate into better ventilation if alveoli are full of gunk or inflammation. Therefore you see tachypnea but not hyperventilation.

Here's a bit of a tutorial on ABGs (and why hyperventilating does not increase your blood oxygen levels) that may help you. Remember: The lungs' first job is to excrete CO2, not to pul in oxygen. That's because regulating CO2 happens rapidly and is the prime way your body regulates its pH.

OK, as to why the lungs do CO2 first, a little background. Your CO2 levels vary considerably over the course of a day, whether you are sitting quietly (not generating a lot of CO2 in muscle work) or running up the stairs with a big bag of heavy laundry (lots of CO2 manufacture going on). Why do you breathe heavily when exercising? To blow off that new CO2 load, that's why. Yes, you use the oxygen, too. However, there are two sensors in your respiratory controls that tell your body when to breathe. One, the primary one, is an acid/base sensor. When it sees increasing acid levels of whatever origin, it makes you breathe faster and more deeply to engage that compensatory mechanism for acidosis: Blow off CO2. It's fast, it's effective, and it's a great bit of engineering. This is why you breathe fast and deep with exercise OR, if, for example, you have diabetic ketoACIDosis or eat a bottle of aspirin (acetylsalicylic ACID). The respiratory drive is primarily CO2-driven.

If your CO2 level is chronically elevated, as in, oh, lung disease, that sensor kinda feeps out. Fortunately, you have a back-up. It's an oxygen sensor, and in chronic lungers, low oxygen levels are what drives their respiration. Increased CO2 doesn't do it anymore.

This all makes for some interesting clinical things. But first, a brief chemistry review. Remember semipermeable membranes? A substance diffuses from the area of higher concentration to an area of lower concentration? Diffusion pressure, that's called.

Think about your alveolus-- blood on one side of the membrane, air on the other. The air you have in your alveolus has an oxygen pressure (at sea level) of about 80-100 torr (mmHg). So if the blood on the other side of it has less oxygen than that, which of course venous blood does, oxygen will slide over there to be picked up by red cells. Good so far? What that means is that you can NEVER have a higher blood oxygen than what's being inhaled, else how would it get there? You can breathe as fast and as deep as you want but the PaO2 (pressure of arterial oxygen) will never exceed that of the air you breathe. (As a quick-and-dirty estimate, PaO2 should be roughly 4-5x inspired oxygen concentration in a healthy lung-- at 21% O2 for room air, that's...80-100. Neat. If you breathe 50% oxygen, your arterial oxygen should be 200-250; you never see it that high in hospitals because people in hospitals getting oxygen DON'T HAVE NORMAL LUNGS. The difference between what it ought to be and what it is is called the "arterial-alveolar gradient," A-a gradient. That's mostly it for oxygen.

OK, now the CO2 part. Remember the diffusion gradient, the difference between one side of the membrane and the other. Well, for practical intent and purpose, there's not much CO2 in your alveolus if you are breathing, so ANY CO2 on the other side will leap at the chance to leave the RBCs and fly out there. This is why you can hyperventilate yourself into dizziness (respiratory alkalosis)...and why we give people who are hyperventilating a paper bag to rebreathe their exhaled air; its higher CO2 level makes it harder for them to keep blowing off more and more, and eventually it all equilibrates.

The architecture of your lungs makes it easier to lose CO2 than to take in O2, because it's more important in the greater scheme of things to regulate your body pH rapidly. So... you can have crappy lungs, giving you a very low PaO2 even on supplementation, and still have the CO2-excreting thing working relatively well. This is why you see people with pneumocystis pneumonia (blessedly not as prevalent as it was in past years) with ABGs showing PaO2 of 50 and CO2 of 30. They're breathing hard, not because their CO2 drive demands it, but because their hypoxic drive demands it. The CO2 loss is the result.

Last: This whole thing is why kids drown in pools all the time having thought they'd play a joke on their buddies and go hide in the deep end. They intentionally hyperventilate, thus driving down their CO2 levels but not, as we saw above, loading themselves with extra oxygen. Then they go down to the deep end and sit. Alas, they pass out from lack of oxygen before their CO2 elevates enough to alert them to being literally short of breath, so by the time their CO2 drive kicks in they're already asleep, and they take a big breath of water. Finis.

I LOOOOVE physiology.

sunnybabe · Apr 15, 2013

Thanks so much. I am so much happier! :geek: