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    CLEMENT
    Thank you for the presentation on respiratory insufficiency and failure. I learned a lot about the different types, causes, clinical presentations, diagnosis and management.

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    Resp Insuff

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    105 views30 pages
    Thank you for the presentation on respiratory insufficiency and failure. I learned a lot about the different types, causes, clinical presentations, diagnosis and management.

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    Thank you for the presentation on respiratory insufficiency and failure. I learned a lot about the different types, causes, clinical presentations, diagnosis and management.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    105 views30 pages

    Resp Insuff

    Uploaded by

    CLEMENT
    Thank you for the presentation on respiratory insufficiency and failure. I learned a lot about the different types, causes, clinical presentations, diagnosis and management.

    Copyright:

    © All Rights Reserved
    Download as PPT, PDF, TXT or read online from Scribd
    Download as ppt, pdf, or txt
    of 30

    Respiratory Insufficiency

    and Failure

    Presenter: Dr Frank John

    Facilitator: Dr B. L. Mtinangi

    Physiology Group 1
    Layout
    Introduction
    Classification/types of respiratory
    insufficiency and failure
    Pathophysiology
    Some lung diseases which lead to resp.
    failure
    Clinical presentation
    Diagnosis & management
    References
    Introduction
    The aim of breathing is to supply the blood
    with adequate amount of oxygen needed for
    tissue metabolism and clear the blood
    carbondioxide from tissues.
    Therefore the level of O2 and CO2 in the
    blood must be maintained within normal
    ranges.
    Failure of the respiratory system to maintain
    those gases within normal range leads to
    respiratory insufficiency/failure.
    Types/classification of RF
    RF can be classified in various ways:
    According to duration; acute/chronic.
    According to blood gas analysis;
    Hypoxemia- O2 level below 60 mmHg
    Hypercapnea- CO2 level above 45 mmHg
    According to functional classification
    Controller RF Resp centres in brain and
    medulla.
    System RF lungs, spinal cord
    According to ventilatory pump
    partial or global
    According to origin obstructive or restrictive
    Transfer of oxygen of inhaled air into
    the blood and
    of waste carbon dioxide of blood into
    the lungs
    Ventilation

    Gas Exchange Hypercapnic respiratory failu

    Hypoxemic respiratory failure


    Respiratory Failure
    inadequate blood oxygenation or CO2 removal
    A syndrome rather than a disease
    PaO2 < 60 mmHg or PaCO2 > 50 mmHg

    Hypoxemic Hypercapnic
    PaO2 < 55~60 mmHg or SaO2 < 90%
    PaCO2 > 45~50 mmHg
    with FiO2 >= 60%

    This two types of respiratory failure always coexist

    Acute: develops in minutes to hours, pH < 7.30


    Chronic: develops over several days or longer
    Ventilation
    CNS PNS Respiratory Muscles Airways
    Efferents Chest Wall

    Dysfunction of any component


    CNS
    Afferents/
    of the ventilation system may Alveoli
    Intergration result in ventilatory failure

    Chemoreceptors PaO2 Alveolar Minute


    PaCO2 Ventilation Ventilation
    Respiratory drive
    O2 demand Motor neuron/nerve function
    CO2 production Muscle strength
    Dead space Respiratory mechanics

    VE MSV
    Minute Ventilation Maximal Sustainable Ventilation

    MSV = MVV/2
    PaCO2 = K VCO2 / VA
    VA= VE (1- VD/VT) MVV = 40 FEV1
    MVV: Maximal voluntary ventilation

    Ventilatory Demand Ventilatory Suppl

    Ventilaroty Demand > Ventilatory Supply Ventilator


    Respiratory Failure
    in a patient with Asthma

    Ventilatory Demand Ventilatory Supp


    Dead Space Ratio

    CO2 Production
    VA= VE (1-
    VD/VT)

    PaCO2 = K VCO2 /Minute


    VA Ventilation

    CO2 Hypercapnic
    Production
    Dead Space Respiratory Failu
    Ratio
    Minute
    Ventilation
    Hypercapnic Respiratory Failure

    Increase carbon dioxide production


    Fever, sepsis, seizure, obesity, anxiety
    Increase work of breath (Asthma, COPD)
    high carbohydrate diet with underlying lung
    disease
    Hypercapnic Respiratory Failure

    Decrease minute ventilation (hypovent.)


    CNS disorders
    stroke, brain tumor, spinal cord lesions, drug overdose
    Peripheral nerve disease
    Guillain-Barre syndrome, botulism, myasthenia gravis
    Muscle disorders
    muscular dystrophy, respiratory muscles fatigue
    Chest wall abnormalities
    scoliosis, kyphosis, obesity
    Metabolic abnormalities
    myxedema, hypokalemia
    Airway obstruction
    Upper airway obstruction, Asthma, COPD
    Hypercapnic Respiratory Failure

    Increase dead space


    Airway obstruction
    Upper airway obstruction
    Asthma, COPD
    Foreign body aspiration

    ARDS, Pulmonary embolism


    Chest wall disorder
    Response well to oxygen therap
    PAO2 = PiO2 PACO2/R
    A-a gradient = PAO2 PaO2

    PaO2 = [ FiO2(PATM-PH2O) PaCO2/R ]


    [ A-a gradient]

    Low Inspired Oxygen


    Alveolar Hypoventilation
    Shunt
    V-Q mismatch
    Diffusion impairmen

    Hypoxemic Respiratory Fail


    Hypoxic Respiratory Failure

    1. Low inspired oxygen


    High altitudes

    2. Hypoventilation
    Conditions described in hypercapnic
    respiratory failure
    Oxygen therapy improve hypoxemia but may
    worsen the hypoventilation
    Hypoxic Respiratory Failure

    3. Shunt (blood flow dont exposed to


    alveolar)
    Can be anatomical or physiological
    Anatomical eg rt to lt shunts-ASD, pulmonary arterial-
    venous shunts, blood flow through collapsed lung.
    Physiological shunts-reduced ventilation to a well perfused
    lung.
    In both PaO2 is reduced and PaCO2 may be normal or
    reduced.
    O2 therapy may or may not improve the condition in phys
    shunt.
    Hypoxic Respiratory Failure

    4. Ventilation-Perfusion Imbalance
    Pulmonary emboli- produce alveolar dead
    space
    Pulmonary edema, pneumonia, abscess-
    impair regional ventilation produce reduced
    PaO2 and Hb saturation
    COPD-increase resistive work of breathing
    affecting both V & P
    Hypoxic Respiratory Failure

    5. Diffusion Impairment
    Interstitial lung disease
    Pulmonary fibrosis, Connective tissue
    disease, Interstitial pneumonia, interstitial
    pulmonary TB
    Atelectasis due obstruction or lack of
    surfactant -RDS
    Obstructive lung disease
    Emphysema, Asthma
    Some dses which lead to
    resp. failure
    Chronic Pulmonary Emphysema:
    Excess air in the lung due to complex
    obstructive and destructive process of the
    lungs from long term smoking.
    Bronchial obstruction cause increase in
    airway resistance, work of breathing and
    difficult in expiration
    Loss of alveolar walls decrease diffusing
    capacity of the lung
    Loss of alveolar capillaries lead to increase
    vasc. resistance then pulm HT then rt heart
    failure
    Abnormal V/Q ratio with either:
    Low V/Q physiological shunt (poor aeration)
    High V/Q physiological dead space (wasted
    ventilation)
    Progress over years and lead to hypoxia and
    hypercapnea then death
    Pneumonia:
    Is any inflammatory condition of the lung, commonest
    being bacterial pneumonia
    Infection begins in the alveoli and progress in the
    membrane where it bcom inflammed and porous. This
    cause fluids and blood cells to leak out
    The alveoli become filled with blood cells and fluid

    .
    mm
    Pneumonia ct..
    The major pulmonary abnormalities are:
    Reduction in the total surface area of the
    respiratory membrane
    Decrease V/Q ratio
    Both these effects cause hypoxemia and
    hypercapnea
    Atelectasis
    Means collapse of the alveoli
    It can occur in a localized areas or in the
    entire lung
    Can be caused by total obstruction of the
    airway or due to surfactant deficiency
    Both expiratory volume and rate are reduced
    leading to severe dyspnoea
    History & Physical Examination

    Acute or Chronic
    Underlying ( heart / lung ) diseases
    Drugs history

    Wheezing? Rhonchi? Crackes?


    Diminish breath sound?
    Air-space consolidation?
    S/S of heart failure
    Clubbing finger
    Clinical Presentations of
    Acute Respiratory Failure
    Breath pattern:
    rapid-deep rapid-shallow slow-shallow
    Accessory respiratory muscles used:

    Paradoxical respiration:

    Hypoxemia
    dizziness, irritable, conscious change, tachycardia,
    cyanosis, peripheral vasodilatation, pulmonary
    vasoconstrition.
    Hypercapnia
    Headache, somnolence, conscious change
    Workup
    LAB:
    Arterial blood gas; Pulse oxymeter
    CBC,
    Cardiac enzyme
    Electrolytes: K, Pi, Mg Ca, Na.
    Biochemistry data,

    ECG (cardiac echo)


    Chest X-ray (chest CT, lung scan)
    Lung function test
    PA catherter
    Neurological exam (Brain CT, EEG)
    Management
    Establish Airway
    Establish Ventilation
    Oxygen Therapy
    Treat the circulatory failure
    NOTE: Oxygen therapy is beneficial in hypoxia
    due to: hypoventilation, high altitude, impaired
    alveolar membrane diffusion.
    The other forms of hypoxia are resistant bcoz
    the problem might be in the transport mech.
    and O2 is already available
    Airway Management

    Head tilt-chin lift / Jaw-thrust maneuver


    Artificial airway (Oral or Nasal airway)
    Laryngeal Mask Airway
    Endo-Tracheal intubation
    Tracheostomy
    Artificial respiration:
    Resuscitator
    Tank Respirator:+/- pressure
    References
    Guyton and Hall Physiology textbook
    Ganong Medical Physiology
    Essentials of respiration
    Postgraduate lecture notes 2008 by Dr B. L.
    Mtinangi
    Internet

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