Last edited: 9/1/2021

3. RESPIRATORY ALKALOSIS
Respiratory Alkalosis Medical Editor: Jan Camille Santico

OUTLINE III) PATHOPHYSIOLOGY OF RESPIRATORY

ALKALOSIS
I) INTERPRETING THE ABG
II) PHYSIOLOGY OF RESPIRATORY ALKALOSIS Respiratory alkalosis is caused by either:
III) PATHOPHYSIOLOGY OF RESPIRATORY o Increased removal of CO2 / Low CO2 levels in the
ALKALOSIS blood
IV) DIFFERENTIALS o Low oxygen levels in the blood
V) TREATMENT
Recall: CO2 + H2O ↔ H2CO3 ↔ H+ + HCO2
VI) REVIEW QUESTIONS
VII) REFRENCES o According to Le Chatelier’s principle, when a
reactant/substrate is in excess, the reaction will shift
to the opposite side to maintain equilibrium. Likewise,
I) INTERPRETING THE ABG
when a reactant/substrate is deficient, the reaction
Table 1. Sample ABG Case will shift to maintain equilibrium.
ABG Result Normal Values o When there is deficient CO2, the reaction will shift to
pH 7.48 7.35 – 7.45 the left, decreasing the protons in the blood and
pCO2 28 mmHg 35 – 45 increasing the pH

HCO3 18 mEq/L 22 – 26 IV) DIFFERENTIALS

pO2 45 mmHg >90
Note: Please refer to the lecture video on “Acid Base Disorders and ABG
Interpretation” to understand this section better.
The pH is high; there is alkalemia
The CO2 is low; there is hypocarbia
The HCO3 is low
The pO2 is low; there is moderate hypoxia
To determine the primary cause of the alkalemia, check
the bicarbonate and carbon dioxide levels
o If the HCO3 is going in the same direction as the pH=
Metabolic
o If the pCO2 is going in the opposite direction as the
pH= Respiratory
Since the carbon dioxide is going in the opposite
direction, it is respiratory alkalosis
To compensate for the alkalemia, the body employs
mechanisms to reduce bicarbonate and increase the
protons (H+)
o Since the bicarbonate level is lower than normal, we
can say that there is partial metabolic compensation
 Full compensation – bicarbonate falls within the
normal range
 Partial compensation – bicarbonate does not fall
within the normal range
Table 2. Oxygen Saturation Values
Oxygen Saturation Interpretation
80 - 100 Normal
60 - 80 Mild Hypoxia
40 - 60 Moderate Hypoxia
<40 Severe Hypoxia
II) PHYSIOLOGY OF RESPIRATORY ALKALOSIS
In the medulla, there is a ventral and dorsal respiratory
group, which function as respiratory centers that
regulate our rate and depth of breathing.
When the neurons of these respiratory centers fire, they
send signals to the lower motor neurons in the spinal
cord
The action potentials then travel through the peripheral
nerves that innervate the muscles for breathing
o Diaphragm
o External intercostals
When these muscles contract, they increase the
space/volume of the thoracic cavity, helping pull oxygen
in the lungs and blow carbon dioxide out
This section gives an overview of the possible
causes/differentials of respiratory alkalosis, arranged
anatomically.
(A) RESPIRATORY CENTERS
When there is increased activity of the respiratory
centers, they increase the respiratory rate, which
increases the clearance of CO2
(1) Drugs
Some drugs/medications stimulate the respiratory centers
Examples: salicylates (e.g. aspirin), methylxanthine,
nicotine
(2) Infections
Sepsis secondary to Gram negative bacteria can lead to
respiratory alkalosis
o The lipopolysaccharides and toxins of Gram negative
bacteria can stimulate the respiratory centers
(3) Liver Failure
Recall: Liver breaks down ammonia to urea
Liver failure results in a buildup of ammonia
o Can lead to hepatic encephalopathy
o Ammonia is also a strong stimulant
(4) Hyperthyroidism
Elevated thyroid hormone levels  increased basal
metabolic rate  increased activity of respiratory centers
Thyrotoxicosis – severe form of hyperthyroidism
(5) Pregnancy
The hormone progesterone, which is typically elevated
during pregnancy, can stimulate respiratory centers
This is a physiologic change in pregnancy, so it is not
alarming
(6) Hypothalamus
The hypothalamus is part of the limbic system
Pain, anxiety, and fear can stimulate the hypothalamus 
activate the respiratory centers
o Oxygen intake is increased in response to
pain/fear/anxiety
o However, increased removal of CO2

Respiratory Alkalosis RENAL PATHOLOGY: NOTE #3. 1 of 3

(7) Fever
Increased core temperature  increased basal metabolic
rate  stimulates the hypothalamus and respiratory
centers
(8) Midbrain Tumors
Lesions might stimulate the respiratory centers
(9) Induced hyperventilation to reduce intracranial
pressure (ICP)
Intracranial pressure can increase due to a tumor,
hemorrhage, or infarction
Elevated ICP  brain herniation  compressed
brainstem  disrupted function of respiratory centers
We can reduce ICP by reducing either:
o Cerebrospinal fluid (CSF)
o Edema
o Blood flow to the brain
Intervention: Temporary hyperventilation to reduce CO2
o Decreased CO2  vasoconstriction of cerebral
vessels  decreased blood flow  decreased ICP
Respiratory alkalosis may also result from iatrogenic
hyperventilation
o In patients being supported by mechanical ventilation,
the induced respiratory rate may be mistakenly set
too high
Figure 1.Differentials of Respiratory Alkalosis
2 of 3 RENAL PATHOLOGY: NOTE #3.
(B) LUNGS
Any disease disrupting the proper intake or exchange of
oxygen within the lungs can cause respiratory alkalosis
Diseases which can cause hypoxia (low oxygen levels)
include:
o Pulmonary edema
 Fluid accumulation in the interstitial spaces
(between alveoli and capillaries
 Due to the resulting poor gas exchange, oxygen
levels drop
 Causes: heart failure, liver failure
o Acute Respiratory Distress Syndrome (ARDS)
 Fluid in the lungs and in the spaces
o Pneumonia
 Pus in the interstitial spaces
o Pulmonary Embolism
 a clot obstructs blood flow through the pulmonary
vessels
Hypoxia is a strong stimulant for the respiratory centers
When peripheral chemoreceptors (carotid and aortic
bodies) detect low oxygen concentration, they send
signals to the respiratory centers via the
glossopharyngeal and vagus nerves.
Respiratory centers are stimulated  increased
respiratory rate and depth  reduced CO2 levels 
respiratory alkalosis
Respiratory Alkalosis
 V) TREATMENT
Table 3. Treatments for Respiratory Alkalosis
Differential
Salicylate overdose
Sepsis due to Gram
negative Bacteria
Hepatic Encephalopathy
Hyperthyroidism
Fever
Pain, anxiety, fear
Iatrogenic
hyperventilation
Elevated ICP
Pulmonary Embolism
ARDS
Pulmonary Edema
Pneumonia
Increased respiratory rate
while ventilated /
“breathing over the
ventilator”
Respiratory Alkalosis
VI) REVIEW QUESTIONS
Given the following ABG results, determine if the
Treatment alkalosis is respiratory or metabolic.
Sodium bicarbonate ABG Result
pH 7.48
Antibiotics
pCO2 32 mmHg
Lactulose, Rifaximin HCO3 21 mEq/L
Anti-thyroid medications pO2 91 mmHg
(methimazole,
propylthiouracil) a. Respiratory
b. Metabolic
Tylenol (anti-pyretic)
Calm down the patient Given the following ABG results, determine if the
Breathe into paper bag alkalosis is respiratory or metabolic.
Anti-anxiety medications
ABG Result
Decrease respiratory rate
pH 7.51
in ventilator settings
pCO2 46 mmHg
Reduce ICP
HCO3 32 mEq/L
Prevent herniation
pO2 72 mmHg
Heparin
Tissue plasminogen
activator a. Respiratory
Embolectomy b. Metabolic
Proper ventilation
Which of the following substances will NOT
Diuretics stimulate the respiratory center?
Antibiotics a. Salicylates
b. Ammonia
Medications for depressing
c. Opioid
the respiratory center
d. Levothyroxine
(opioids, sedatives)
Respiratory alkalosis may be a normal finding in
which demographic?
a. Teenagers
b. Pregnant women
c. Smokers
d. Elderly
Which of the following will not likely cause
respiratory alkalosis?
a. Vomiting
b. Aspirin overdose
c. Heart failure
d. Anxiety
CHECK YOUR ANSWERS
VII) REFRENCES
RENAL PATHOLOGY: NOTE #3. 3 of 3