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Tissue Perfusion II Respiratory Pathophysiology

Tissue Perfusion II Respiratory Pathophysiology. Paul Marshall. Pathophysiology: common mechanisms Inability to maintain normal blood gases Hypoxaemia Hypercapnia Possible mechanisms:  IMPAIRED VENTILATION (hypoventilation)  neuromuscular Motor neurone disease

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Tissue Perfusion II Respiratory Pathophysiology

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  1. Tissue Perfusion II Respiratory Pathophysiology Paul Marshall

  2. Pathophysiology: common mechanisms • Inability to maintain normal blood gases Hypoxaemia Hypercapnia • Possible mechanisms:  IMPAIRED VENTILATION (hypoventilation)  neuromuscular Motor neurone disease Brain stem damage (e.g CVA)  obstruction COPD asthma bronchial tumour bronchiectasis

  3. Possible mechanisms continued:  IMPAIRED VENTILATION (cont:)  alveolar damage emphysema fibrotic lung disease  pleural damage pneumothorax  IMPAIRED GASEOUS EXCHANGE pneumonia COPD pulmonary oedema ARDS  IMPAIRED PERFUSION right to left shunts PE

  4. Asthma: • acute reversible airway disease • due to increased reactivity of smooth muscle of bronchioles (inflammatory response) • may be episodic, chronic or severe acute • result:  airway obstruction (bronchospasm and • oedema, excess sputum) - worse on • expiration •  hypoventilation • hypoxaemia • retention of CO2

  5. Asthma continued: clinical features • dyspnoea • expiratory wheeze and cough • anxiety/fear/restlessness • central cyanosis • low O2 sats < 90% • tachycardia • alteration in consciousness

  6. Chronic Obstructive Pulmonary Disease (COPD)  umbrella term which encompasses: emphysema chronic bronchitis chronic obstructive airways disease (COAD) characterised by:  airways obstruction (variable reversibility)  inflammatory/bronchitis component  emphysema  UK: 600,000 have COPD 26,000 die /year in England and Wales set to be fifth largest cause of death by 2020

  7. Pathophysiology: • bronchitis/ inflammatory component: •  major contributory factor is smoking •  bronchial inflammation & oedema •  mucous gland hypertrophy: • excess mucus production • impaired muco-ciliary clearance •  increased bacterial growth in static • mucus •  alveolar macrophages activated – • destroy alveolar wall •  result: • decrease in FEV1 (CO2 retention) • hypoventilation (V/Q mismatch)

  8. Emphysema component: • pathologically an increase in the size of air • spaces distal to terminal bronchioles with • destruction of alveolar walls •  loss of lung elastic recoil •  alveolar distension and rupture •  compliance reduced •  total lung capacity increases •  residual volume increases •  physiologic dead space increased •  reduced diffusing capacity •  Result: • hypoventilation(V/Q mismatch)

  9. Emphysema – genetic factor:  deficiency of 1-Antitrypsin (protein) 1-Antitrypsin protects against alevolar wall destruction by elastase  deficiency allows unchecked destruction of alveolar wall

  10. Overall pathophysiological effect: •  airflow obstruction ( peak flow/FEV1) • hypoventilation •  ventilation/perfusion (V/Q) mismatch •  reduced diffusing capacity •  CO2 retention (hypercapnia) • Hypoxaemia Reference: (Weinberger 1992, West 1992)

  11. BTS guidelines (1997): FEV1 Drug choice (of predicted) MILD  80% short acting 2-agonist or inhaled anticholinergic MODERATE  60% short acting 2-agonist or inhaled anticholinergic or both (COMBIVENT) consider steroid trial SEVERE  40% consider combination therapy ? home nebuliser steroid trial ? other agents

  12. Hypercapnia in COPD: additional mechanisms • fatigue of inspiratory muscles • alteration in breathing pattern ( Vt,  Vf,  dead space) • abnormalities of ventilatory drive: major stimulus is hypoxaemia complex mechanism may be reduced chemoreceptor responsiveness (Weinberger 1989, Lourenco & Miranda 1968)

  13. Respiratory failure: • inability to maintain normal arterial PaO2 and • PaCO2 • two types: • Type I: PaO2 low (< 8.0 kPa) (hypoxaemia) • PaCO2 normal or low • (normal < 6.5 kPa) • Asthma • PE • Pulmonary oedema

  14. Respiratory failure: continued Type II: PaO2 low (< 8.0 kPa) (hypoxaemia) PaCO2 raised (> 6.5 kPa) (hypercapnia) chronic bronchitis chest deformities respiratory centre depression e.g. opiates brain stem CVA

  15. References: BTS (1997) British Thoracic Society guidelines: diagnosis & Management of COPD Thorax 52(suppl 5):S1-S32 Lourenco RV & Miranda JM (1968) Drive and performance of the Ventilatory apparatus in chronic obstructive lung disease NEJM 279:53-59 Weinberger SE et al (1989) Hypercapnia NEJM 321:1223-1231 Weinberger SE (1992) Principles of pulmonary medicine 2nd ed. WB Saunders Philadelphia West JB (1992) Pulmonary physiology- the essentials 4th ed. Williams & Wilkins Baltimore

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