One of the complications of respiratory fatigue is the development of hypercapnia. How does the
body compensate for an increase in CO2? What are the effects of hypercapnia on the central
nervous system?
Hypercapnia is excessive carbon dioxide in the bloodstream, and it is typically caused by
inadequate respiration. As levels of CO2 in the blood begin to rise, the body can respond through
hyperventilation or hypoventilation. The blood brain barrier is permeable to CO2 and when there
is elevated amounts of CO2 this causes the pH of the cerebral spinal fluid to decrease, therefore
causing an increase in intracranial pressure. Symptoms associated with hypercapnia are
tachycardia, dyspnea, flushed skin, confusion, headaches, dizziness, seizures, depression, and
muscle twitches (Patel et al., 2022).
Patel S, Miao JH, Yetiskul E, et al. Physiology, Carbon Dioxide Retention. [Updated 2022 Jan
4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan. Available from: https://www.ncbi.nlm.nih.gov/books/NBK482456/
Identify the pharmacotherapy for management of Emmanuels asthma if he failed corticosteroid
monotherapy and explain their mechanism of action.
Emmanuels next step after his corticosteroids have failed would be to use a short acting beta2
agonist, also known as SABA. This medication can be used in an inhaler or a nebulizer. The
pathway of B2 receptor action begins when an agonist activates the receptor, causing the alpha
subunit of the Gs protein to detach and reattach to adenylate cyclase, stimulating it to catalyze
the conversion of adenosine triphosphate (ATP) into cyclic adenosine monophosphate (cAMP),
which acts as a second messenger within the cell. In turn, cAMP initiates two routes leading to
smooth muscle relaxation, the first is through freeing the catalytic subunit of protein kinase A
enzyme, whose function is to phosphorylate various enzymes contributing to the relaxation of
airway smooth muscles, and the second is by reducing calcium concentration inside the cell by
preventing its extracellular influx, inhibiting its outflow from intracellular storage, and initiating
sequestration of calcium ions in the cytoplasm, thus preventing muscle contraction (Abosamak et
al., 2022).
Abosamak NER, Shahin MH. Beta 2 Receptor Agonists/Antagonists. [Updated 2022 Jul 4]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available
from: https://www.ncbi.nlm.nih.gov/books/NBK559069/