Causes and Consequences of Respiratory Centre Depression and Hypoventilation Lou Irving Director Respiratory and Sleep Medicine, RMH louis.irving@mh.org.au
Capacity of the Respiratory System At rest During exercise supplies 250 ml / min O 2 supplies > 4000 ml / min O 2 removes 200 ml / min CO 2 removes > 4000 ml / min CO 2 Glucose + O 2 fi energy + H 2 O + CO 2 Aerobic metabolism RQ = 0.8 Aerobic & anaerobic metabolism Pyruvate fi Lactate + Energy RQ 1.2-1.5 Can sustain about 0.1 horse power Inadequate function causes 1. Hypoxaemia 2. Hypercapnoea and respiratory acidosis
Functional Organization of the Respiratory System Respiratory centre & CONTROLLER peripheral chemoreceptors Maintain blood PaO 2» 100mHg PaCO 2 = 40mmHg ph = 7.40 PUMP Respiratory muscles, chest wall and airways Capacity VE > 100 L/min GAS EXCHANGER Alveolar capillary membrane Capacity VO 2 & VCO 2 > 4 L/min
Respiratory Control System Central controller 1. Brain stem (pons and medulla) 2. Cortex Sensors Effectors 1. Chemoreceptors 2. Lung receptors 3. Other receptors Respiratory muscles
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 fi hypocapnoea to a lesser extent, hypoventilation fi hypercapnoea
Sensors Central chemoreceptors situated on ventral surface of medulla, surrounded by CSF respond to CSF [H + ] CSF [H + ] is a reflection of CO 2 in cerebral capillaries PaCO 2 fi CSF [H + ] fi ventilation do not respond to PaO 2 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 fl PaO 2, fl ph, PaCO 2 fi ventilation Lung and other receptors pulmonary stretch, irritant and J receptors upper airway receptors, joint and muscle receptors, painful stimuli
Ventilatory Response to Carbon Dioxide 30 1.5l/min/mmHg Ventilation L/min 20 10 40 60 80 Carbon dioxide tension mmhg Small in CO 2 fi rapid in ventilation Significant individual variability
Large fall in PaO 2 before any significant in ventilation Significant individual variability
Stimuli for Ventilation Increased metabolic activity PaO 2 > 80 mmhg V E PaCO 2 ph 40 mmhg 7.40 Metabolic activity Work V E matched to O 2 consumption and CO 2 production
Other Stimuli for Ventilation Metabolic acidosis PaO 2 > 100 mmhg V E PaCO 2 ph < 40 mmhg returns to just below normal Metabolic acidosis Acidosis V E excessive for O 2 consumption and CO 2 production, and is aimed at correcting the acidosis
Ventilatory Response to Exercise Ventilation increases with work to maintain PaO 2 and PaCO 2 at baseline. Beyond the anaerobic threshold, relative increase in V E because of extra H + production from lactic acid PaO 2 > 80 mmhg V E PaCO 2 ph 33 mmhg 7.32 Work Work V E matched to O 2 consumption and CO 2 and H + production
Other Stimuli for Ventilation Anxiety PaO 2 > 100 mmhg V E PaCO 2 ph < 40 mmhg > 7.45 Anxiety Anxiety V E excessive for O 2 consumption and CO 2 production. Results in a respiratory alkalosis
Hypoventilation Situation where rate of alveolar ventilation is not meeting metabolic requirements for oxygen consumption and carbon dioxide production fi fl PaO 2 and PaCO 2 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 CO 2 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 O 2, increased CO 2, 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 fi 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, fl libido 6. Difficult to treat hypertension, unexplained respiratory failure etc
OSA - Respiratory Signals from Polysomnogram Apnoeas Arousals Desaturation during apnoeas Chest and abdominal wall movement showing paradoxical movement when upper airway obstruction EEG, EMG, ECG snoring and body position not shown
Management Nasal CPAP 4-20 cm H2O pressure 85% compliance for moderate + OSA Others - mandibular advancement splint surgery lie on side
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 fi 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? PaO 2 = 56 mmhg, PaCO 2 = 52 mmhg, ph = 7.36