respiratory insufficiency & other clinical conditions

8/14/2019 Respiratory Insufficiency & Other Clinical Conditions

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Dr. Niranjan Murthy H LAsst Professor of Physiology

SSMC, Tumkur


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RESPIRATORY INSUFFICIENCY

Narcosis, other pharmacologic influences,

hypoxia, andpathologic processes

reduce excitability of respiratory neurons respiratory failure


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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


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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 tohypercapnia induced cerebral

vasodilatation; support of circulation.

Hypothermia- due to reduced metabolism& deranged heat regulating mechanisms;

hyperthermia in case of infections


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Renal impairment- due to hypotension

Respiratory insufficiency due to

pulmonary pathologies:

(i) Pulmonary Emphysema

(ii) Pneumonia(iii) Atelectasis

(iv) Asthma

(v) Tuberculosis


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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


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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


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Tuberculosis

Mycobacterium tuberculosis

Tubercle- due to walling off of infection

Cavitation- in untreated cases

Fibrosis- in late stages

Reduced VC

Reduced surface area and increasedthickness of respiratory membrane

Abnormal VA/Q


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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


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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 byrespiratory muscles

(v) State of mind


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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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respiratory insufficiency & other clinical conditions

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