physiological consequences of respiratory centre
TRANSCRIPT
Causes and Consequences of Respiratory Centre Depression and
Hypoventilation
Lou Irving Director Respiratory and Sleep Medicine, RMH
Capacity of the Respiratory System
At rest During exercise supplies 250 ml / min O2 supplies > 4000 ml / min O2 removes 200 ml / min CO2 removes > 4000 ml / min CO2
Inadequate function causes 1. Hypoxaemia 2. Hypercapnoea and respiratory acidosis
Can sustain about 0.1 horse power
Glucose + O2 ® energy + H2O + CO2
Aerobic metabolism RQ = 0.8
Aerobic & anaerobic metabolism
Pyruvate ® Lactate + Energy RQ 1.2 -1.5
Functional Organization of the Respiratory System
Respiratory centre &
peripheral chemoreceptors Maintain blood
PaO2 » 100mHg
PaCO2 = 40mmHg
pH = 7.40
CONTROLLER
PUMP GAS EXCHANGER
Alveolar – capillary membrane Capacity VO2 & VCO2 > 4 L/min
Respiratory muscles, chest wall and airways Capacity VE > 100 L/min
Respiratory Control System
Central controller
Sensors Effectors
1. Chemoreceptors 2. Lung receptors 3. Other receptors
Respiratory muscles
1. Brain stem (pons and medulla) 2. Cortex
Central Controller
• Brainstem – neurones in medulla and pons – automatic rhythmic inspiratory stimuli, and sometimes expiratory stimuli – in-put from peripheral sensors – can be over-ridden by cortex – major output is to the phrenic nerves
• Cortex
– voluntary hyperventilation ® hypocapnoea – to a lesser extent, hypoventilation ® hypercapnoea
Sensors • Central chemoreceptors
– situated on ventral surface of medulla, surrounded by CSF – respond to CSF [H+] – CSF [H+] is a reflection of CO2 in cerebral capillaries – PaCO2 ® CSF [H+] ® ventilation – do not respond to PaO2
• Peripheral chemoreceptors
– situated in carotid bodies at bifurcation of common carotid arteries in neck, and aortic bodies around arch of aorta
– rapid responses – respond to ¯ PaO2, ¯ pH, PaCO2 ® ventilation
• Lung and other receptors
– pulmonary stretch, irritant and J receptors – upper airway receptors, joint and muscle receptors, painful stimuli
Carbon dioxide tension
Ventilation
1.5l/min/mmHg
40 60 80
10
20
30
L/min
mmHg
Ventilatory Response to Carbon Dioxide
Small in CO2 ® rapid in ventilation
Significant individual variability
Large fall in PaO2 before any significant in ventilation
Significant individual variability
Stimuli for Ventilation
• Increased metabolic activity
• VE matched to O2 consumption and CO2 production
VE
Metabolic activity Work
PaO2
PaCO2
pH
40 mmHg
7.40
> 80 mmHg
Other Stimuli for Ventilation
• Metabolic acidosis
• VE excessive for O2 consumption and CO2 production, and is aimed at correcting the acidosis
VE
Metabolic acidosis Acidosis
PaO2
PaCO2 < 40 mmHg
> 100 mmHg
pH returns to just below normal
Ventilatory Response to Exercise
• Ventilation increases with work to maintain PaO2 and PaCO2 at baseline. Beyond the anaerobic threshold, relative increase in VE because of extra H+ production from lactic acid
• VE matched to O2 consumption and CO2 and H+ production
VE
Work Work
PaO2
PaCO2
pH
33 mmHg
7.32
> 80 mmHg
Other Stimuli for Ventilation
• Anxiety
• VE excessive for O2 consumption and CO2 production. • Results in a respiratory alkalosis
VE
Anxiety Anxiety
PaO2
PaCO2 < 40 mmHg
> 100 mmHg
pH > 7.45
Hypoventilation
• Situation where rate of alveolar ventilation is not meeting metabolic requirements for oxygen consumption and carbon dioxide production
® ¯ PaO2 and PaCO2
• If acute causes a respiratory acidosis
• If chronic, there is a compensatory metabolic alkalosis
Causes of Hypoventilation
• Reduced respiratory centre activity – Reduced drive (eg low CO2 or high pH) – Suppression of activity by drugs, trauma, vascular accidents etc
• Neuromuscular disease – nerve paralysis (drugs, polio, Guillian- Barre, trauma etc) – muscle weakness (drugs, motor neurone disease, muscular dystrophy)
• Chest wall deformity (gross) • Obesity (gross)
• Sleep disordered breathing
Sleep Disordered Breathing
1. Obstructive sleep apnoea
2. Central sleep apnoea 3. Obesity hypoventilation syndrome
Obstructive Sleep Apnoea (OSA)
• Transient obstruction of the throat during sleep preventing breathing, and disturbing sleep
• Occurs in people who snore (but not all snorers have OSA)
• Obstruction occurs during sleep because of : – Airway muscles relax (floppy throat - esp REM) – Throat already narrowed (obesity, tonsils etc) – Tongue falls backwards ( esp if supine)
OSA - Cycle of Events
1. Snoring in light sleep 2. Complete obstruction (apnoea) in deep sleep 3. Reduced blood O2, increased CO2, other stimuli 4. Brain “wakes” to lighter sleep (arousal) 5. Muscles contract, airways opens, breathing
recommences 6. Back into deep sleep, obstructs again……. Often more than 60 events every hour throughout sleep Very fragmented sleep ® sleep deprivation Bed partner often makes diagnosis
OSA – When to Suspect
1. Snoring 2. Witnessed apnoeas 3. Arousals 4. Choking 5. Symptoms of disturbed sleep
EDS, mood change, poor memory, ¯ libido 6. Difficult to treat hypertension, unexplained respiratory failure etc
OSA - Respiratory Signals from Polysomnogram
Apnoeas
Desaturation during apnoeas
Chest and abdominal wall movement showing paradoxical movement when upper airway obstruction
Arousals
EEG, EMG, ECG snoring and body position not shown
Management
• Nasal CPAP
• Others - mandibular advancement splint surgery lie on side
4-20 cm H2O pressure
85% compliance
for moderate + OSA
Other Forms of Sleep Disordered Breathing
• Less common than OSA
• Central sleep apnoea – several forms, eg Cheyne Stokes breathing – manage underlying heart failure etc +/- CPAP or BiPAP
• Obesity hypoventilation
– usually presents as ventilatory failure +/- right heart failure – “sensitive” to supplemental oxygen – manage with BiPAP and weight reduction (gastric banding)
• Hypoventilation associated with neuromuscular diseases
– Prolonged and improved life with non-invasive ventilatory support in selected cases
Consequences of Chronic Severe Sleep Apnoea
• “Sleep or die” • Hypoventilation during sleep with consequent re-setting of
the respiratory centre ® day-time hypoventilation
• This can also occur with other conditions, such as severe COPD, severe pulmonary fibrosis and neuromuscular disease in which there is less ventilation during sleep than when awake
• These patients develop chronic hypoxia, chronic hypercapnoea, and a compensated respiratory acidosis
Patients with Chronic Hypercapnoea
Are dependent on hypoxic drive (ie not stimulated by chronic hypercapnoea) What happens if give large amount of supplemental oxygen?
PaO2 = 56 mmHg, PaCO2 = 52 mmHg, pH = 7.36