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Respiratory alkalosis and respiratory acidosis in mechanically ventilated patients: when to treat them and when to accept them.

July 31, 2021

Original post published on 31st July 2021 by Giuseppe Natalini


Should mechanical ventilation avoid respiratory acidosis or respiratory alkalosis

As is often true in medicine (and in life…) the answer to this question cannot be a simple “yes” or “no”, but requires a more articulate approach. The answer is in fact different in case of acidosis or alkalosis and if the mode of mechanical ventilation is controlled or assisted. 

I am going to anticipate the conclusions in Figure 1, which I will then try to justify. 



Figure 1

In this post, when we say acidosis and alkalosis we mean uncompensated disorders of acid base equilibrium, i.e. conditions with pH < 7.35 (acidemia) or pH > 7.45 (alkalemia).

Let’s be reminded that mechanical ventilation is called controlled when the patient does not contribute in any way to ventilation: the detected respiratory rate is the same as the set respiratory rate, there are no signs of inspiratory trigger nor of inspiratory activity during inspiration. Ventilation is called assisted when the respiratory rate, at least, depends on the patient: in this instance, inspiratory trigger activation can be seen and the detected respiratory rate is higher than one set on the ventilator.

Let's start to examine the four cases summarized in the table in Figure 1. 


RESPIRATORY ALKALOSIS DURING CONTROLLED VENTILATION 

This case is the simplest to understand and solve. Hypocapnia, which is at the basis of respiratory alkalosis, is a consequence of mechanical ventilation only, and the patient suffers passively its deleterious effects, which are vasoconstriction in the systemic circulation and a reduction of oxygen release to tissues due to the leftward shift in the haemoglobin dissociation curve (Figure 2).

Figure 2

The consequences can be tissue ischemia and hypoxia, which are especially fearsome for the brain and myocardium

This respiratory alkalosis must be avoided, and this is easy to do: it is sufficient to limit tidal volume to 6-8 ml/kg of ideal body weight and, in case of persisting hypocapnia, to reduce respiratory rate as much as is needed to reach and acceptable range of pH and PaCO2  (for example PaCO2 > 30 mmHg and pH < 7.5).


RESPIRATORY ALKALOSIS DURING ASSISTED VENTILATION 

In this condition, hypocapnia is a consequence of an increased activity of the respiratory centers (Figure 3).

 

 

 


Figure 3


Any modification in mechanical ventilation settings cannot solve the problem: a reduction of inspiratory support (or, even worse, a reduction of the inspiratory trigger sensitivity) will only cause an increase in the inspiratory effort that the patient has to generate in order to maintain the level of ventilation that the respiratory centers command. If a reduction of inspiratory assistance were to decrease ventilation and to increase PaCO2, it would be a sign that respiratory muscles are fatigued and have surrendered, since they are not adequately assisted anymore. In other words, PaCO2 is going to increase only when the patient is exhausted from the effort to breathe.

The only reasonable weapon we have to increase PaCO2 in a patient with respiratory alkalosis during assited ventilation is the pharmacological reduction of the activity of the respiratory centers, using sedation. 

Is it worth it? Often it is not, and we’ll try to understand the reasons.

One of the most fearsome effects of hypocapnia is cerebral vasoconstriction, which should not be a problem during assisted ventilation.

The acidity of cerebrospinal fluid (CSF) pH is the main stimulus for breathing centers, therefore it is the main cause of hyperventilation and hypocapnia.

There are also other breathing centers stimulants (cortical and peripheral), but usually their importance is secondary compared to the importance of H+ concentration in CSF.  

We can reasonably think that a hypocapnic subject in assisted ventilation has CSF acidosis (a high concentration of H+) which stimulates breathing centers, and that arterial blood hypocapnia is a consequence of hyperventilation. The presence of CSF acidosis is an excellent antidote against cerebral vasoconstriction which is induced by the opposite condition, CSF alkalosis (a low concentration of H+ in the CSF).

CSF acidosis is frequent in inflammatory, hemorrhagic and ischemic brain conditions, which are the conditions in which, during assisted ventilation, respiratory alkalosis is usually observed.

The absence of cerebral vasoconstriction can be confirmed by a neurological examination: presence of good vigilance or of unimpaired mental status  should exclude a significant brain hypoperfusion. 

We have to be aware of the fact that respiratory alkalosis in the arterial blood, even if it is without deleterious effects on the brain, maintains its systemic extracerebral side effects, independently from CSF pH. It could be an unfavourable condition in patients at risk of coronary hypoperfusion or in presence of signs of tissue hypoxia. We can therefore tolerate hypocapnia and respiratory alkalosis in patients undergoing assisted ventilation if the risk of myocardial (or other organs or tissues) hypoperfusion is absent.


RESPIRATORY ALKALOSIS DURING CONTROLLED VENTILATION

In case of respiratory acidosis during controlled ventilation, we can increase minute ventilation if it does not expose the patient to the risk of ventilator induced lung injury, for example by keeping driving pressure below 15 cmH2O and stress index around 1 (see 28/02/2015 post).

If this is not possible, we can tolerate hypercapnia, which has many favourable physiological effects, such as the increase in cardiac output, in oxygen delivery and in the transfer of oxygen to tissues (shifting to the right the haemoglobin dissociation curve).

Due to these effects, respiratory acidosis is generally well tolerated from the physiopathological point of view (surely much more than hypocapnia).


RESPIRATORY ACIDOSIS DURING ASSISTED VENTILATION

Respiratory acidosis during assisted ventilation should always be avoided, because it is a sign of insufficient inspiratory support for weak or fatigued respiratory muscles.

This is true even if there is a physiological PaCO2 (around 40 mmHg) in presence of acidosis: it's not normal to have a normal PaCO2 when there is acidosis, therefore this condition should also be seen as a sign of fatigue or weakness of the respiratory muscles.

In these cases the solution is simple: increasing inspiratory support and, if this does not resolve respiratory acidosis, starting controlled ventilation to let respiratory muscles rest temporarily.

Conclusion.

Respiratory acidosis and respiratory alkalosis can be tolerable or not, depending on the fact that they manifest during assisted or controlled ventilation. 

During controlled ventilation, respiratory alkalosis is not acceptable, while during assisted ventilation respiratory acidosis is not acceptable. 

On the contrary, hypocapnia during assisted ventilation and hypercapnia during controlled ventilation can be acceptable after evaluating their impact on other organs and parenchymas.

A smile for all of ventilab’s friends, and happy holidays!



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