I'm a med-surg nurse that floated to my hospital's CCU the other night. Another nurse's pt was in respiratory acidosis and had to be intubated. It was caught when the pt's morning ABGs were drawn. I've been doing some reading on clinical signs, most of which are difficult to assess in a sleeping pt. I did see that tachycardia and hypotension are signs, which is something that they were treating, but this had apparently been an ongoing problem for the pt, not new onset.
Are there other outward, physical signs that I as a nurse could assess that would lead me to start thinking about respiratory failure, especially when the pt was sleeping on night shift?
Since it's so hard to read tone online, I feel compelled to add, I'm asking this just for my own education, since this is an area where I'm not strong, not to blame the other nurse for missing something. From what I've been reading, it would have been hard for her to catch this without the lab draw.
Your body wants to blow off the excess carbon dioxide so tachypnea is an early sign. Along with tachycardia as the heart tries to increase it's output to meet an inadequately supplied metabolic demand.
You're mixing a couple different things here. Respiratory acidosis tends to result from hypoventilation, and often respiration will be decreased (hard to assess in a sleeping patient). If there is a diffusion impairment the patient may be tachypneic. The acidemia causes vasodilation, to which the heart responds by increasing CO (HR and SV).
Remember one of the important things about blood pH is that it affects the oxyhemoglobin dissociation. when the blood becomes acidic, the RBC has an increased affinity for oxygen and won't exchange gas at the cellular level as effectively. So if you have a patient that is ventilating well and complaining of "smothering", one of the first things to consider is an ABG. these problems are often vicious circles and the patient will continue to decompensate until we intervene. Because of this, the O2 saturation is often of little use because the hemoglobin is well-saturated with oxygen but it doesn't release it to the cells in exchange for CO2. Hence the build up in the blood reflected in the ABG.
Actually during acidemia the oxyhemoglobin dissocation curve shifts to the right and hemoglobin has a DECREASED affinity for oxygen (higher PO2 required for normal SaO2-hemoglobin gives O2 away). Alkalemia causes an INCREASED affinity (lower PaO2 required for normal SaO2-hemoglobin likes to keep O2), which causes a decrease in DO2 to the tissues (high ScvO2).
In acidemia, the body tries to maintain by attempting to increase DO2 and decrease H+ ion concentration: vasodilation, increased CO, decreased hemoglobin affinity (RBCs release O2 more readily to tissues), increase RR (if possible), decrease buffer (bicarb) excretion, increase fixed acid excretion.
Classic signs of mild acidemia are flushing of skin, tachycardia, feeling lightheaded, bounding pulses, sweating, etc. As the acidemia worses, you will have a decrease in CO due to negative inotropism (decrease SV), reflex vasoconstriction, cold clammy skin, tachycardia or bradycardia, and thready/weak pulses.
Last edit by PetERNurse on Dec 9, '11
: Reason: Typo