3. Physiology
        3.1. Acid and base
            3.1.4. From Kerry's book Respiratory alkalosis

Causes of Respiratory Alkalosis
1. Central Causes (direct action via respiratory centre)
    * Head Injury
    * Stroke
    * Anxiety-hyperventilation syndrome (psychogenic)
    * Other 'supra-tentorial' causes (pain, fear, stress, voluntary)
    * Various drugs (eg analeptics, propanidid, salicylate intoxication)
    * Various endogenous compounds (eg progesterone during pregnancy, cytokines during sepsis, toxins in patients with chronic liver disease)
2. Hypoxaemia (act via peripheral chemoreceptors)
    * Respiratory stimulation via peripheral chemoreceptors
3. Pulmonary Causes (act via intrapulmonary receptors)
    * Pulmonary Embolism
    * Pneumonia
    * Asthma
    * Pulmonary oedema (all types)
4. Iatrogenic (act directly on ventilation)
    * Excessive controlled ventilation


Hyperventilation due to respiratory centre stimulation is a feature of salicylate toxicity, especially in adults, and results in a mixed disorder (metabolic acidosis and respiratory alkalosis).


A respiratory alkalosis is the commonest acid-base disorder found in patients with chronic liver disease.


# Hyperventilation syndrome related to anxiety can cause alkalosis severe enough to cause carpopedal spasm.

# A mild fairly well compensated respiratory alkalosis is the usual finding in pregnancy.

# Any condition which decreases pulmonary compliance causes a sensation of dyspnoea. Respiratory alkalosis is commonly found in patients with asthma, pneumonia & pulmonary embolism.



Effects of Hypocapnia
1. Neurological effects
    * Increased neuromuscular irritability (eg paraesthesias such as circumoral tingling & numbness; carpopedal spasm)
    * Decreased intracranial pressure (secondary to cerebral vasoconstriction)
    * Increased cerebral excitability associated with the combination of hypocapnia & use of enflurane
    * Inhibition of respiratory drive via the central & peripheral chemoreceptors
2. Cardiovascular effects
    * Cerebral vasoconstriction (causing decreased cerebral blood flow) [short-term only as adaptation occurs within 4 to 6 hours]
    * Cardiac arrhythmias
    * Decreased myocardial contractility
3. Other effects
    * Shift of the haemoglobin oxygen dissociation curve to the left (impairing peripheral oxygen unloading)
    * Slight fall in plasma [K+]
    * Most of these effects decrease with time. A chronic hypocapnia is associated with few symptoms because of the compensation that occurs.
    * The underlying cause will also have effects other than hyperventilation & these may dominate the clinical picture - for example, the adverse effects of hypoxaemia


Particular Effects of Hypocapnia in Anaesthetised Patients
    * Decreased cerebral blood flow (CBF) [This effect may be beneficial]
    * Depression of myocardial contractility
    * Cardiac arrhythmias
    * Cerebral excitability may occur in association with high levels of enflurane
    * Shift of the oxygen dissociation curve to the left (impairing oxygen unloading peripherally)
    * Fall in plasma potassium (usually slight only)
    * Obligatory hypoventilation at end of the operation (This is exacerbated by residual drug effects as well)


One argument for routine intraoperative use of hypocapnia  is to use the induced cerebral vasoconstriction to counteract the cerebral vasodilator effects of volatile anaesthetic agents. A particular disadvantage of this is the hypoventilation at the end of the operation which delays recovery from general anaesthesia.




Compensation in an ACUTE Respiratory Alkalosis
    * Mechanism: Not really compensation but changes in the physicochemical equilibrium of the bicarbonate buffer system occur due to the lowered pCO2 and this results in a slight decrease in HCO3-. There is insufficient time for the kidneys to respond so this is the only change in an acute respiratory alkalosis.
    * Magnitude: There is a drop in HCO3- by 2 mmol/l for every 10mmHg decrease in pCO2 from the reference value of 40mmHg.
    * Limit: The lower limit of 'compensation' for this process is 18mmol/l - so bicarbonate levels below that in an acute respiratory alkalosis indicate a co-existing metabolic acidosis. (Alternatively, their may be some renal compensation if the alkalosis has been present longer than realised.)
Compensation in a CHRONIC Respiratory Alkalosis
    * Mechanism: Renal retention of acid causes a further fall in plasma bicarbonate (in addition to the acute drop due to the physicochemical effect).
    * Magnitude: Studies have shown an average 5 mmol/l decrease in [HCO3-] per 10mmHg decrease in pCO2 from the reference value of 40mmHg. This maximal response takes 2 to 3 days to reach.
    * Limit: The limit of compensation is a [HCO3-] of 12 to 15 mmol/l.



Hypoxaemia is an important cause of respiratory stimulation and consequent respiratory alkalosis.
The decrease in arterial pCO2 inhibits the rise in ventilation. The hypocapnic inhibition of ventilation (acting via the central chemoreceptors) may leave the patient with an impaired state of tissue oxygen delivery. Adaptation occurs over a few days and the central chemoreceptor inhibition is lessened and ventilation increases.

e.g. at altitude

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