Respiratory acidosis/failure s/s

  1. 1
    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.
    fiveofpeep likes this.
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  5. 1
    You're right, it isn't easy to pick up on subtle hints at times.

    Respiratory acidosis is a pCO2>45, regardless of the pH. If the pH is normal, then the acidosis is being compensated. 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.

    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.

    Hope this helps somewhat, I'm sure someone else can come along and give a more complete answer.
    fiveofpeep likes this.
  6. 0
    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
  7. 1
    Respiratory acidosis means they're retaining CO2, so it climbs. The higher it gets the more acidotic they get. Chronic COPDers will have higher CO2 levels with a increase in HCo3 to compensate. This is normal for them. In a patient who is uncompensated, with high c02, a big big red flag will be somnolence, very drowsy, confusion ect. If its not caught too soon, your going to run into an emergent situation where they need to be tubed now because they stop breathing, are hypo ventilating or can't protect their airway at all. If it was caught sooner and they noticed they were more somnolent but awake enough to try bipap to get them over the hump that may have helped and prevented it from getting to full on respiratory failure. It can be tough at night when were trying to promote sleep, when the patient is actually starting to get into trouble and were not realizing it immediately. Just keeping a close eye on them. Unfortunately we don't let our patients sleep long stretches in ICU, for this reason, we need to watch em close.
    fiveofpeep likes this.
  8. 0
    Respiratory acidosis is defined as a pH less than 7.35 with a PaCO2 greater than 45 mm Hg. Acidosis is caused by an accumulation of CO2 which combines with water in the body to produce carbonic acid, thus, lowering the pH of the blood. Any condition that results in hypoventilation can cause respiratory acidosis. These conditions include:
    • Central nervous system depression related to head injury
    • Central nervous system depression related to medications such as narcotics, sedatives, or anesthesia.
    • Impaired respiratory muscle function related to spinal cord injury, neuromuscular diseases, or neuromuscular blocking drugs
    • Pulmonary disorders such as atelectasis, pneumonia, pneumothorax, pulmonary edema, or bronchial obstruction
    • Massive pulmonary embolus
    • Hypoventilation due to pain, chest wall injury/deformity, or abdominal distention
    The signs and symptoms of respiratory acidosis are centered within the pulmonary, nervous, and cardiovascular systems. Pulmonary symptoms include dyspnea, respiratory distress, and/or shallow respirations. Nervous system manifestations include headache, restlessness, and confusion. If CO2 levels become extremely high, drowsiness and unresponsiveness may be noted. Cardiovascular symptoms include tachycardia and dysrhythmias.
    Increasing ventilation will correct respiratory acidosis. The method for achieving this will vary with the cause of hypoventilation. If the patient is unstable, manual ventilation with a bag- valve-mask (BVM) is indicated until the underlying problem can be addressed. After stabilization, rapidly resolvable causes are addressed immediately. Causes that can be treated rapidly include pneumothorax, pain, and CNS depression related to medications. If the cause cannot be readily resolved, the patient may require mechanical ventilation while treatment is rendered. Although patients with hypoventilation often require supplemental oxygen, it is important to remember that oxygen alone will not correct the problem.

    Taken from Interpretation of ABGs by Orlando Regional Medical Center.


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