08 Breathlessness and Control of Breathing Flashcards
What is the effect of COPD on breathing compared to healthy individuals
Breathing is shallower and faster
- Minute ventilation is unchanged
- Although COPD patients have expiratory airway obstruction, the time taken for expiration is unchanged
- There is increased neural drive to breathing (despite VT/Ti is the same)
- During exercise, there is a slight decrease in Ti/Ttot to help COPD patient expire whereas healthy individuals have increased Ti/Ttot to give time to inspire
Describe the central coordination of breathing
- Early inspiratory initiates inspiratory flow via respiratory muscles
- Inspiratory augmenting may also dilate pharynx, larynx and airways.
- Late inspiratory may signal the end of inspiration, and “brake” the start of expiration.
- Expiratory decrementing may “brake” passive expiration by adducting larynx and pharynx.
- Expiratory augmenting may activate expiratory muscles when ventilation increases on exercise.
- Late expiratory may signal the end of expiration and onset of inspiration, and may dilate the pharynx in preparation for inspiration
State the nervous innervations that control respiratory reflex
Nose and face: CN V (irritant)
Pharynx and larynx: CN IX (irritant)
Bronchi and bronchioles: CN V (irritant and stretch)
What happens when both PaO2 and PaCO2 fall together
This happens when a fall in inspired PO2 rather than minute ventilation is the primary event.
Describe how PCO2 responses are potentiated by alkalosis and acidosis
Chemosensitivity to PCO2 is augmented by low PO2 (meaning when there is low O2, at the same level of PCO2, there is higher minute ventilation)
Acidosis causes higher sensitivity and alkalosis blunts the chemosensitivity
Describe how ventilatory responses to hypoxia is augmented by CO2
At the same level of PAO2 or Hb saturation, the higher the PCO2, the higher the minute ventilation
However, PAO2 to minute ventilation is not a linear relationship, but Hb saturation is
What causes metabolic acidosis and what are the compensatory effects
Causes: diabetic ketoacidosis, salicylate overdose and renal tubular defect
Compensation:
- Increase minute ventilation
- Increase renal excretion of weak acids (lactate and ketoacid)
- Increase renal retention of chloride to balance ion difference
What causes metabolic alkalosis and what are the compensatory effects
Causes: vomiting, diuretics and dehydrations
Compensation:
- Decrease minute ventilation
- Increase retention of weak acids (lactate and ketoacid)
- Increase excretion of chloride
What are the causes of respiratory acidosis/hypoventilation conditions
Central: Acute: metabolic centre poisoning (drugs/anaesthetics) Chronic: - Congenital hypoventilation syndrome - Obesity hypoventilation syndrome - Vascular disease of metabolic centre - Chronic mountain sickness
Peripheral:
Acute: muscle relaxant drugs, myasthenia gravis
Chronic: neuromuscular with respiratory muscle weakness
What are the causes of respiratory alkalosis
- Chronic hypoxaemia
- Excess H+ (metabolic causes)
- Pulmonary vascular disease
- Chronic anxiety (psychogenic)
What are the 3 types of breathlessness and define each of them
- Dyspnoea: difficulty breathing
- Tightness: difficulty in inspiring due to airway narrowing; a feeling that the chest is not expanding normally
- Increased work and effort: breathing at a high minute ventilation, or at a normal minute ventilation but at a high lung volume, or against an inspiratory or expiratory resistance
Define air hunger
Sensation of a powerful urge to breath
Mismatch between minute ventilation demanded / minute ventilation achieved
- Demand: central metabolic centre
- Achieved: afferents from lungs, chest wall and peripheral chemoreceptors
Is our physiological system more sensitive to oxygen or CO2
CO2 because:
For a change in minute ventilation of 30 L/min is elicited by 1kPa of PCO2 rise and 7kPa drop of PO2
