Factors Affecting Ventilation

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Changes in Posture[edit]

  • Change from an erect to a supine position cause blood flow changes:
  • Posterior areas of the lung to receive increased perfusion, as well as becoming more compressed
  • V/Q ratios are similar as in healthy lungs both ventilation and perfusion undergo similar changes
  • Being supine also increases pulmonary blood volume by almost a third due to return of blood from the periphery
  • When supine, the abdominal contents push the diaphragm superiorly, causing a reduction in FRC
  • As closing capacity increases with age, closing capacity will exceed FRC at age 44 in an average person
  • This is partially counteracted by increased diaphragm stretch capacity
  • Change in posture reduces anatomical deadspace by one third
  • This reduces VD/VT ratio when supine from 34% to 30%
  • Diffusing capacity is improved in the supine position due to increased pulmonary blood volume


  • Ventilation can reach 15x resting level - ~120 L/min in young fit healthy people during strenuous exercise
  • PCO2 stays constant during exercise, but may fall at very high work levels
  • PO2 may increase slightly, but can fall at high work levels
  • Arterial pH remains nearly constant, but can fall during heavy exercise due to lactic acid liberation in anaerobic glycolysis
  • Passive movement of limbs stimulates ventilation at initiation of exercise
  • Exact mechanism of increased ventilatory response to exercise not exactly known - ?if due to oscillations in PCO2 and PO2
  • May also be due to changes in CO2 load
  • Increase in body temperature and impulses from motor cortex may play a role


  • Barometric pressure decreases at altitude (760 -> 380 at 5500m), while partial pressure of O2 remains at 21% and saturated vapour pressure remains 47mmHg at body temperature. therefore alveolar PO2 tends towards zero
  • Response to hypoxia occurs in 3 phases:
  • Acute response - increasing ventilation rapidly due to carotid body chemoreceptor feedback to hypoxia - increases for 5-10 minutes
  • Hypoxic ventilatory decline - lasts 10-20 minutes. Minute ventilation reaches a peak and then begins to decline due to pCO2 falling causing respiratory alkalosis, then an unknown mechanism called HVD causes a further significant fall in ventilation and arterial PO2. This is responsible for many of the symptoms seen in the first few hours at altitude
  • The third phase is a gradual increase in ventilation to a new increased minute ventilation baseline over eight hours. PCO2 decrease blunts the hypoxic response, however a reset in central chemoceptors leads to a lower baseline PCO2. DPG driven right shift of the Hb-O2 curve occurs to improve O2 offloading in the tissues.
  • Ongoing ascent leads to central hypoxic depression of respiratory centres and ultimately apnoea and death
  • Long term adaptation to increased altitude is polycythaemia, left shift in Hb-O2 curve to encourage O2 uptake and increased vascularity in heart/muscles
  • Hypoxic pulmonary vasoconstriction causing pulmonary hypertension can occur, which cause right heart strain and hypertrophy (along with increased viscosity from polycythemia)
  • Acute Altitude sickness occurs due to hypoxia and alkalosis
  • Initially: headache, nausea, insomnia, fatigue, dyspnoea
  • Severe AAS: Pulmonary oedema → secondary HPV → HTN and Cerebral oedema → ADH secretion


  • Anaesthesia diminishes pulmonary ventilation causing hypercapnia if spontaneous breathing is preserved
  • This is due mainly to reduced CO2 sensitivity, which moves the ventilation/PCO2 curve progressively down and to the right as MAC is increased


  • Low concentrations of inhaled anaesthetics result in smaller tidal volumes at higher frequencies resulting in reduced ventilation and mildly increased CO2
  • Higher concentrations of inhaled anaesthetics result in very slow breathing and large decreases in minute volume and large increases in CO2
  • Apnoeic threshold PCO2 - the threshold at which a patient becomes apnoeic
  • The acute hypoxic ventilatory response is reduced in volatile and propofol anaesthesia, even at 0.1 MAC, although this decrease only occurs in hypercapnic conditions
  • Patients therefore cannot respond to hypoxia with hyperventilation
  • Patients who have lost their sensitivity to PCO2 may stop breathing altogether after induction due to loss of hypoxic drive
  • Post-op patients have obtunded hypoxic drives even at very low MACs
  • Anaesthesia has a specific pattern of alteration of respiratory muscle activity:
  • The pharynx shape is changed by the soft palate falling against the posterior pharyngeal wall
  • The inspiratory muscles in the chest are depressed at low MACs, while diaphragmatic activity is preserved up until higher MACs
  • Expiratory muscles have increased activity
  • FRC is reduced with all anaesthetic drugs by ~20%
  • Chest shape changes due to changes in muscle activity
  • Diaphragm relaxation causes cephalad movement which decreases FRC
  • Decreased FRC causes increased airway resistance, however this is largely offset by the bronchodilator effect of the GA's
  • Closing capacity approaches FRC as FRC is reduced during anaesthesia causing collapse and atelectasis
  • Compliance is decreased because of:
  • Decreased lung volume
  • Decreased FRC
  • Pulmonary collapse in dependent regions
  • Minute volume is reduced due to depression of central control centres and reduced metabolic rate MRO2
  • Physiological dead space is roughly the same fraction during anaesthesia as it is during normal conditions


  • Compliance has no measurable difference as patients age.
  • As patients age they have more variable patterns when sleeping with more apnoeic periods, variations in upper airways resistance and episodes of transient hypoxaemia down as low as 75%.
  • Anatomical dead space is increased in infants due to their large head and neck, with on average of 3.3ml/kg. This reduces down to 2 ml/kg as a young adult and then gradually increases by roughly a ml per year.
  • The diffusing capacity of the lung gradual worsens throughout life in a linear fashion. Functional residual capacity gradual increases throughout life, and may increase markedly in disease states such as COPD.
  • The closing capacity increases more rapidly then FRC and as a result will equal FRC in a supine patient (gravity decreases FRC) at the age of 44 and an erect patient in their seventies. This leads to a worsening of V/Q ratios with age as gas trapped by a CC>FRC constitutes a shunt. The end result is that arterial PO2 values gradually decline with age.

Morbid Obesity[edit]

  • Decreased FRC & ERV, especially when supine
  • Elevated work of breathing, respiratory muscle inefficiency and diminished respiratory compliance.
  • The decreased FRC and ERV, with a high closing volume to FRC ratio of obesity, are associated with the closure of peripheral lung units, ventilation to perfusion ratio abnormalities and hypoxemia, especially in the supine position
  • Commonly develop sleep apneoa and hypoventilation syndromes, which in turn lead to chronic hypoxia and pulmonary hypertension