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Narcosis, other pharmacologic influences,
hypoxia, and pathologic processes ->
reduce excitability of respiratory neurons
-> respiratory failure

  • Narcotic drugs & respiratory depression:
Leads to reduced PaO2 & increased PaCO2.
Carries best prognosis & amenable to Rx.
Narcotic drugs also diminish metabolism.
Complications of narcotic poisoning-

2.Microbial infections
3.Circulatory depression
4.Renal functional derangements
5.Hypo or hyperthermia
6.Consequences of therapeutic measures

  • Asphyxia- depression of PaO2 and elevation of PaCO2; assisted ventilation.
  • Circulatory depression- due to central vasomotor depression, hypoxemia, and direct narcotic effects on blood vessels; blood supply of brain is maintained due to hypercapnia induced cerebral vasodilatation; support of circulation.
  • Hypothermia- due to reduced metabolism & deranged heat regulating mechanisms; hyperthermia in case of infections
  • Renal impairment- due to hypotension
  • Respiratory insufficiency due to pulmonary pathologies:
(i) Pulmonary Emphysema
(ii) Pneumonia
(iii) Atelectasis
(iv) Asthma
(v) Tuberculosis

Pulmonary Emphysema

  • Excessive air in lungs
  • Causes- chronic infections, chronic smoking.
  • Physiologic abnormalities-

1.Increased airway resistance
2.Destruction of alveolar walls - reduced diffusing capacity - increased PaCO2 & reduced PaO2
3.Reduced alveolar capillaries - pulmonary hypertension - right heart failure


  • Inflammatory condition of respiratory membrane
  • Alveoli are filled with fluid and blood cells
  • Most common- bacterial- pnemococcal
  • Reduction in total available area for gas exchange
  • Decreased VA/Q
  • Hypoxemia and hypercapnia


  • Collapse of alveoli / lobe / lung
  • Causes- (i) Airway obstruction and (ii) lack of surfactant
  • Hyaline Membrane Disease is fatal


  • Airway hyper-responsiveness
  • Allergic hypersensitivity- pollen
  • Older people- pollution
  • Histamine, SRS-A, ecf, bradykinin are released from mast cells
  • Localized edema in walls of airways and spasm of bronchiolar smooth muscles
  • Reduced PEFR and FEV1
  • Increase in FRC and RV


  • Mycobacterium tuberculosis
  • Tubercle- due to walling off of infection
  • Cavitation- in untreated cases
  • Fibrosis- in late stages

1.Reduced VC
2.Reduced surface area and increased thickness of respiratory membrane
3.Abnormal VA/Q


  • Cessation of breathing (generally temporary)

1.Reduction in stimulus to respiratory centre
2.Active inhibition of respiratory neurons- prolongation of Hering-Breuer reflex
3.Decreased ability of respiratory neurons to react to stimuli- narcotics


  • Labored, distressful breathing with conscious effort
  • Factors leading to dyspnea -

1.Abnormality of respiratory gases in body fluids
2.Amount work to be performed by respiratory muscles
3.State of mind

Disorders of rhythm

  • Cheyne-Stokes respiration:
  • Periodic breathing
  • Seen in congestive heart failure, uremia, brain disease and sleep.
  • Prolongation of circulation time
  • Increased sensitivity to CO2

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