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 neuronsprolongation 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