Dr.

Niranjan Murthy H L
Asst Professor of Physiology
SSMC, Tumkur
 RESPIRATORY INSUFFICIENCY
• 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-
(vi) Asphyxia
(vii)Microbial infections
(viii)Circulatory depression
(ix) Renal functional derangements
(x) Hypo or hyperthermia
(xi) 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-
(i) Increased airway resistance
(ii) Destruction of alveolar walls  reduced
diffusing capacity  increased PaCO2 &
reduced PaO2
(iii) Reduced alveolar capillaries  pulmonary
hypertension  right heart failure
 Pneumonia
• 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
 Atelectasis
• Collapse of alveoli / lobe / lung
• Causes- (i) Airway obstruction and (ii) lack
of surfactant
• Hyaline Membrane Disease is fatal
 Asthma
• 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
 Tuberculosis
• Mycobacterium tuberculosis
• Tubercle- due to walling off of infection
• Cavitation- in untreated cases
• Fibrosis- in late stages
• Reduced VC
• Reduced surface area and increased
thickness of respiratory membrane
• Abnormal VA/Q
 Apnea
• Cessation of breathing (generally
temporary)
(ii) Reduction in stimulus to respiratory
centre
(iii) Active inhibition of respiratory neurons-
prolongation of Hering-Breuer reflex
(iv) Decreased ability of respiratory neurons
to react to stimuli- narcotics
 Dyspnea
• Labored, distressful breathing with
conscious effort
• Factors leading to dyspnea -
(iii) Abnormality of respiratory gases in body
fluids
(iv) Amount work to be performed by
respiratory muscles
(v) 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