In one breath
Asphyxia is hypoxia and hypercapnia together, nearly always from a mechanically blocked airway, and it kills through three stages: exaggerated breathing, convulsions, then exhaustion and collapse. Hypercapnia is retention of CO₂, almost always from hypoventilation; it first drives breathing and then depresses it, ending in respiratory acidosis. Hypocapnia is the mirror image, a CO₂ washout by hyperventilation, and its damage is mostly cerebral vasoconstriction plus respiratory alkalosis. Drowning, respiratory acidosis and respiratory alkalosis are the applied end of the same two gases.
Builds on: Carbon dioxide transport · Chemical control of breathing · Hypoxia · Leads to: Abnormal breathing patterns · Artificial respiration
Asphyxia
Definition: hypoxia combined with hypercapnia.
It usually develops from mechanical obstruction of the airway:
- suffocation
- strangulation
- drowning
- a foreign body impacted in the trachea or larynx
- traumatic compression of the chest
Asphyxia is not just hypoxia
Hypoxia on its own (high altitude, anemia, cyanide) need not raise PCO₂ at all. Asphyxia needs both — PO₂ down and PCO₂ up — which is why its features are a mixture of the two, and why the respiratory drive is enormous early on.
Stages of asphyxia
| Stage | Lasts |
|---|---|
| 1. Exaggerated breathing | 1–2 minutes |
| 2. Convulsion | about 1 minute |
| 3. Exhaustion and collapse | about 5 minutes |
Stage 1: exaggerated breathing
- Hypercapnia and hypoxia together stimulate the respiratory centers strongly.
- Breathing becomes deep and rapid, and the accessory muscles come into prominent use.
- The patient is severely dyspneic and looks intensely anxious.
- Cyanosis appears and the eyes become prominent.
Stage 2: convulsion
- Respiratory efforts turn violent.
- Generalized muscular convulsions occur.
- Increased sympathetic discharge and catecholamine release give tachycardia and a rise in blood pressure.
- Consciousness may be lost.
Stage 3: exhaustion and collapse
- Hypoxia has now reached the vital centers of the brain, and suppresses cardiorespiratory activity.
- Convulsions stop abruptly; respiration becomes gasping.
- Respiratory effort fails and blood pressure falls.
- Pupils widely dilated, pulse feeble, reflexes abolished.
- The pause between gasps grows longer until the last breath is taken.
Draw it: the three stages of asphyxia
Draw a time line of about 8 minutes along the bottom and breathing depth up the side. For 0–2 min draw tall, closely packed breaths labelled “deep + rapid, accessory muscles, cyanosis”. For 2–3 min draw very tall irregular spikes labelled “convulsions, tachycardia, BP ↑”. From 3 min on draw a few shallow gasps that get smaller and further apart, ending in a flat line labelled “BP ↓, pupils dilated, reflexes lost”. Write “PO₂ ↓ and PCO₂ ↑ throughout” above the trace, and mark where stimulation of the centers turns into depression.
Hypercapnia
Definition and causes
Definition: retention of CO₂ in the body. CO₂ is a major product of metabolism, so hypermetabolic states such as fever and a high carbohydrate intake tend to push it up.
- Hypoventilation — by far the commonest setting. Ventilation may be depressed, as in respiratory failure, brain injury or narcotic poisoning; or it may simply be inadequate — chest wall disease, myocardial failure, polyneuropathies.
- Diffusion defects. Because CO₂ is far more soluble than O₂, pulmonary fibrosis usually does not cause hypercapnia. But severe destruction or thickening of the alveolar–capillary membrane, as in emphysema or advanced fibrosis, impairs gas exchange enough to produce both hypercapnia and hypoxia. See Obstructive vs restrictive disease.
- Fever. A rise in body temperature of 1°C raises CO₂ production by 13%. Fever also stimulates breathing, so the extra CO₂ is normally blown off; hypercapnia appears only if ventilation is compromised as well.
- High carbohydrate intake. The respiratory quotient rises, so more CO₂ is produced.
Type I versus type II respiratory failure
Hypoxia with a normal PCO₂ is type I. Hypoxia with hypercapnia is type II. Only type II carries the CO₂ narcosis problem, and only type II patients are at risk from uncontrolled O₂ (see Oxygen therapy).
Effects of hypercapnia
- The first effect is stimulation of respiration.
- If severe and prolonged, it turns into respiratory depression: sensory perception is blunted and the patient becomes confused.
- This progresses to coma with further respiratory depression, which raises PCO₂ still higher — a vicious cycle.
- Deep, sustained hypercapnia ends in respiratory acidosis, with plasma bicarbonate able to climb past 40 mEq/L.
- That high bicarbonate is renal compensation: tubular reabsorption of HCO₃⁻ comes to exceed its excretion, so plasma HCO₃⁻ rises and the acidosis is partly offset.
Hypocapnia
Causes
Definition: washout of CO₂ from the body, the result of hyperventilation. Because hyperventilation also increases O₂ intake, PO₂ rises at the same time.
- Brief hyperventilation when someone is suddenly moved into the heat.
- Habitual over-breathing in the neurotic patient.
- Voluntary hyperventilation, performed as an experiment: PCO₂ may fall as low as 15 mmHg, while arterial PO₂ rises to about 140 mmHg.
Applied: the voluntary hyperventilation experiment
Over-breathe hard for two or three minutes and you reproduce the whole syndrome in yourself: PCO₂ down towards 15 mmHg, PO₂ up towards 140 mmHg, then dizziness and tingling of the lips and fingers from cerebral vasoconstriction. Stop, and breathing does not simply return to normal — it swings through cycles of apnea and over-breathing, which is periodic breathing.
Effects
- Vasoconstriction, with cerebral blood flow falling by more than 30%.
- That cerebral ischemia causes dizziness, light-headedness and sensory abnormalities, mainly paresthesia.
- Depression of the vasomotor and respiratory centers.
- Cardiac output falls, because coronary blood flow falls.
- Features of the accompanying respiratory alkalosis; plasma bicarbonate is decreased.
- Acid secretion in the renal tubule is inhibited, so HCO₃⁻ reabsorption is reduced. Ionized calcium falls, and features of hypocalcemic tetany may appear — Chvostek sign and carpopedal spasm.
Worth knowing, though not in your pages: the reason ionized calcium falls is that alkalosis makes Ca²⁺ bind more tightly to plasma albumin. Total plasma calcium is unchanged; only the free, active fraction drops. That is why the tetany is relieved as soon as PCO₂ is allowed back up.
Drowning
Definition: suffocation caused by immersion in water.
| Water | What the water does | Result in blood |
|---|---|---|
| Fresh water | Enters lungs, passes rapidly into blood | Hemodilution and hemolysis |
| Sea water | Hypertonic, draws fluid from vessels into lung | Hemoconcentration |
- In some victims the first gasp of water triggers immediate reflex laryngospasm, so water never reaches the lungs at all. These patients die of asphyxia with dry lungs.
- Seawater drowning floods the alveoli from the vascular side; see Pulmonary edema and drowning. Rescue is a matter of clearing the airway and starting Artificial respiration or Cardiopulmonary resuscitation (CPR).
Respiratory acidosis
Any condition that reduces removal of CO₂ by the lungs raises PCO₂ and so produces respiratory acidosis.
- Depression of the respiratory centers — narcotics, barbiturates.
- Diseases of the respiratory apparatus — chronic obstructive lung disease, pneumothorax, pleural effusion, chest wall deformity.
- Diseases impairing diffusion across the alveolar–capillary membrane — pulmonary fibrosis, pulmonary edema.
- Compensation: the high PCO₂ drives the respiratory centers harder, so rate and depth both rise, and blowing off the CO₂ brings pH back — provided the fault does not lie in the center itself. Where it does, this correction is simply unavailable. See Respiratory centers (neural control).
Respiratory alkalosis
- Cause: excess elimination of acid through the respiratory tract. Hyperventilation lowers PCO₂, and so lowers H⁺ concentration.
- The physiological cause is ascent to high altitude, where the hypoxic drive makes a healthy person over-breathe. See Acclimatization to high altitude.
Exam-answer skeleton: "Define asphyxia, give its causes and describe its stages" (short note)
- Definition in one line: hypoxia combined with hypercapnia.
- Causes: mechanical airway obstruction — suffocation, strangulation, drowning, foreign body, chest compression.
- Name the three stages before describing any of them.
- Stage of exaggerated breathing (1–2 min): strong stimulation of the centers, deep rapid breathing, accessory muscles, dyspnea, anxiety, cyanosis.
- Stage of convulsion (about 1 min): violent efforts, generalized convulsions, sympathetic overactivity with tachycardia and a rise in blood pressure, loss of consciousness.
- Stage of exhaustion and collapse (about 5 min): hypoxic suppression of the vital centers, convulsions stop, gasping respiration, blood pressure falls, dilated pupils, feeble pulse, reflexes abolished.
- Close with the single mechanism sentence: hypoxia and hypercapnia first stimulate and then depress the respiratory centers — that one shift explains the whole sequence.
Asked in exams
- Asphyxia: Jan 2011, 4 marks · Jan 2021, 2 marks · Jan 2023, MCQ
- Hypercapnia: Aug 2024, essay
- Hypocapnia and voluntary hyperventilation: Nov 2013, 2 marks · Sep/Oct 2019, 4 marks