Intoxicated
MIA Man
- Nov 16, 2023
- 1,043
People who consider gas asphyxiation with simple asphyxiants (particularly, inert gases) or shallow-water blackout can sometimes overlook the essential detail that respiration can be stimulated not only by increased CO₂ levels but also hypoxemia.
Designations:
VT - tidal volume (higher tidal volumes mean deeper breaths);
fR - respiratory frequency.
The acute response to hypoxia is an immediate augmentation of ventilatory activity following the onset of a hypoxic stimulus, and typically includes increases in both fR and VT relative to baseline (321). To date, almost all animals studied exhibit such a hyperbolic increase in ventilation as a function of decreasing arterial oxygen saturation (PaO₂) (30, but see also 300); however, the underlying changes in fR versus VT are highly variable between species (36, 256). The acute HVR persists throughout any given hypoxic stimulation and terminates immediately following the removal of hypoxia, that is, it begins and ends within one breath of the detection of a change in PaO₂ at the carotid body (321).
The acute HVR is a classic reflex response to sensory input from peripheral arterial chemoreceptors. The carotid bodies are the most important arterial chemoreceptor for the acute HVR in humans and most animals (95), and their adequate and physiological stimulus is PaO₂ (198).
Source:
pmc.ncbi.nlm.nih.gov
As mentioned previously, the respiratory control center responds to altered levels of CO2 and O2 by changing the respiratory rate and pattern. Interestingly, the response to hypoxia differs from the response to hypercapnia. Hypoxia induces a breathing pattern of rapid and shallow breaths with a relatively higher increase in respiratory rate than tidal volume. The aim is to decrease the cost of breathing by avoiding the need to overcome the lungs' higher elastance at high volumes.
In simple terms, breathing with high tidal volumes requires more negative pressure generation in the intra-pleural space and, thus, more oxygen utilization by respiratory muscles, especially in an already hypoxic patient. In contrast, hypercapnia triggers a breathing pattern of deep and slow breaths with a relatively more significant increase in tidal volume than respiratory rate. This pattern aims to limit dead space ventilation and optimize carbon dioxide elimination.
Source:
Acid-base changes associated with hypoxaemia
This was the topic of Question 11 from the second paper of 2007, which was passed by 14% of the candidates (i.e. by one person). Fortunately, the college examiners left us with a small window into their thinking. In short, there are two main effects:
The effects produced by inhalation of pure N₂O:
Nitrous oxide has a peculiar sweetish taste which is by no means unpleasant. Great variation will be found to occur in the sensations which patients experience during the inhalation of this agent. When administered in the proper manner, and with due attention to details, these sensations will be more likely to be of an agreeable than of a disagreeable character. Should the apparatus possess valves which do not work easily, or should the channels through which the gas is made to pass be too small, or should the patient from want of confidence or knowledge breathe in a shallow and restricted manner, or through the nose, an unpleasant experience may result. A feeling of warmth in the lips and an indescribable though pleasant numbness over most of the body are amongst the first sensations noticed. The patient has an irresistible desire to breathe more deeply and quickly. These sensations are rapidly followed by a peculiar and pleasurable "thrilling" which hardly admits of description. Some tinnitus may be present, and curious sensations, such as fulness and expansion of the head, are occasionally experienced. As a general rule, however, loss of consciousness comes on before the patient has time, so to speak, to define his feelings. The respiration will be observed to be deepened and quickened in response to the desire of the patient just alluded to. The pulse grows fuller under the finger, probably due to constriction of the systemic arterioles. The time which elapses between the commencement of the inhalation and loss of full consciousness is extremely short, about twenty to thirty seconds on the average.
Source:
https://i.sanctioned-suicide.net/im...t_-_Anaesthetics_and_their_administration.pdf (pp. 243, 244)
Designations:
VT - tidal volume (higher tidal volumes mean deeper breaths);
fR - respiratory frequency.
The acute response to hypoxia is an immediate augmentation of ventilatory activity following the onset of a hypoxic stimulus, and typically includes increases in both fR and VT relative to baseline (321). To date, almost all animals studied exhibit such a hyperbolic increase in ventilation as a function of decreasing arterial oxygen saturation (PaO₂) (30, but see also 300); however, the underlying changes in fR versus VT are highly variable between species (36, 256). The acute HVR persists throughout any given hypoxic stimulation and terminates immediately following the removal of hypoxia, that is, it begins and ends within one breath of the detection of a change in PaO₂ at the carotid body (321).
The acute HVR is a classic reflex response to sensory input from peripheral arterial chemoreceptors. The carotid bodies are the most important arterial chemoreceptor for the acute HVR in humans and most animals (95), and their adequate and physiological stimulus is PaO₂ (198).
Source:
Time Domains of the Hypoxic Ventilatory Response and Their Molecular Basis - PMC
Ventilatory responses to hypoxia vary widely depending on the pattern and length of hypoxic exposure. Acute, prolonged, or intermittent hypoxic episodes can increase or decrease breathing for seconds to years, both during the hypoxic stimulus, and ...
pmc.ncbi.nlm.nih.gov
As mentioned previously, the respiratory control center responds to altered levels of CO2 and O2 by changing the respiratory rate and pattern. Interestingly, the response to hypoxia differs from the response to hypercapnia. Hypoxia induces a breathing pattern of rapid and shallow breaths with a relatively higher increase in respiratory rate than tidal volume. The aim is to decrease the cost of breathing by avoiding the need to overcome the lungs' higher elastance at high volumes.
In simple terms, breathing with high tidal volumes requires more negative pressure generation in the intra-pleural space and, thus, more oxygen utilization by respiratory muscles, especially in an already hypoxic patient. In contrast, hypercapnia triggers a breathing pattern of deep and slow breaths with a relatively more significant increase in tidal volume than respiratory rate. This pattern aims to limit dead space ventilation and optimize carbon dioxide elimination.
Source:
Acid-base changes associated with hypoxaemia
This was the topic of Question 11 from the second paper of 2007, which was passed by 14% of the candidates (i.e. by one person). Fortunately, the college examiners left us with a small window into their thinking. In short, there are two main effects:
- Respiratory alkalosis, at mild hypoxaemia
- Metabolic acidosis, with severe hypoxaemia
- Acute hypoxaemia (low partial pressure of oxygen at the carotid chemoreceptors) is a potent respiratory stimulant
- At a PaO₂ around 60 mmHg, "hypoxic drive" becomes an important influence on the respiratory control centre, producing an increase in the respiratory rate and tidal volume
- This increase in minute volume produces an increase in the clearance of PaCO₂
- The decrease in PaCO₂ changes the chemical equilibrium of bicarbonate and carbonic acid, decreasing the concentration of carbonic acid and increasing the pH
- Alkalosis ensues.
- The oxygen concentration the blood is insufficient to support aerobic metabolism
- Cellular metabolism switches to anaerobic metabolism and generates lactate
- Lactate dissociates fully at physiological pH, widening the anion gap and generating hydrogen ions
- The presence of excess hydrogen ions decreases the pH
- This decreased pH serves to further stimulate the respiratory centre
The effects produced by inhalation of pure N₂O:
Nitrous oxide has a peculiar sweetish taste which is by no means unpleasant. Great variation will be found to occur in the sensations which patients experience during the inhalation of this agent. When administered in the proper manner, and with due attention to details, these sensations will be more likely to be of an agreeable than of a disagreeable character. Should the apparatus possess valves which do not work easily, or should the channels through which the gas is made to pass be too small, or should the patient from want of confidence or knowledge breathe in a shallow and restricted manner, or through the nose, an unpleasant experience may result. A feeling of warmth in the lips and an indescribable though pleasant numbness over most of the body are amongst the first sensations noticed. The patient has an irresistible desire to breathe more deeply and quickly. These sensations are rapidly followed by a peculiar and pleasurable "thrilling" which hardly admits of description. Some tinnitus may be present, and curious sensations, such as fulness and expansion of the head, are occasionally experienced. As a general rule, however, loss of consciousness comes on before the patient has time, so to speak, to define his feelings. The respiration will be observed to be deepened and quickened in response to the desire of the patient just alluded to. The pulse grows fuller under the finger, probably due to constriction of the systemic arterioles. The time which elapses between the commencement of the inhalation and loss of full consciousness is extremely short, about twenty to thirty seconds on the average.
Source:
https://i.sanctioned-suicide.net/im...t_-_Anaesthetics_and_their_administration.pdf (pp. 243, 244)
Noteworthy implications:
- Breathing inert gases like nitrogen (or non-inert gases with similar effects) may be not as easy as breathing plain air, it's very possible that you will want to breathe more frequently and more deeply as the hypoxemia develops. It seems, this urge to breathe more intensively becomes a big surprise for some people, so they're inclined to think that there's something wrong with their setup or the method.
- If something restricts respiration during the period of inducing loss of consciousness via gas asphyxiation (f.e., insufficient gas flow rate to a face mask), this may cause noticeable discomfort in presence of AHVR.
- The chances of achieving unconsciousness via the plain shallow-water blackout method (where only hyperventilation with air is used before submerging) without experiencing the urge to breathe seem very low, because even if you manage to avoid hypercapnia, the urge to breathe (possibly of a smaller intensity than that from hypercapnia) may be provoked by the lack of oxygen nevertheless.
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