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    IADVL Color Atlas of Dermatopathology - Book

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    65gken
    John Smith, a 55-year-old male with COPD, presented with worsening shortness of breath and confusion. He had a respiratory rate of 30 breaths/min, heart rate of 110 beats/min, and oxygen saturation of 88% on room air. An arterial blood gas showed a pH of 7.27, PCO2 of 60 mmHg, and HCO3 of 32 mEq/L, consistent with respiratory acidosis. The causes of respiratory acidosis include decreased ventilation due to COPD exacerbation, thoracic cage disorders, central nervous system depression, and upper airway obstruction. Initial management involves airway support, arterial blood gas analysis, treating any underlying causes, and cautious oxygen therapy to avoid

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    IADVL Color Atlas of Dermatopathology - Book

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    65gken
    75 views41 pages
    John Smith, a 55-year-old male with COPD, presented with worsening shortness of breath and confusion. He had a respiratory rate of 30 breaths/min, heart rate of 110 beats/min, and oxygen saturation of 88% on room air. An arterial blood gas showed a pH of 7.27, PCO2 of 60 mmHg, and HCO3 of 32 mEq/L, consistent with respiratory acidosis. The causes of respiratory acidosis include decreased ventilation due to COPD exacerbation, thoracic cage disorders, central nervous system depression, and upper airway obstruction. Initial management involves airway support, arterial blood gas analysis, treating any underlying causes, and cautious oxygen therapy to avoid

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    IADVL Color atlas of Dermatopathology - Book

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    John Smith, a 55-year-old male with COPD, presented with worsening shortness of breath and confusion. He had a respiratory rate of 30 breaths/min, heart rate of 110 beats/min, and oxygen saturation of 88% on room air. An arterial blood gas showed a pH of 7.27, PCO2 of 60 mmHg, and HCO3 of 32 mEq/L, consistent with respiratory acidosis. The causes of respiratory acidosis include decreased ventilation due to COPD exacerbation, thoracic cage disorders, central nervous system depression, and upper airway obstruction. Initial management involves airway support, arterial blood gas analysis, treating any underlying causes, and cautious oxygen therapy to avoid

    Copyright:

    © All Rights Reserved
    Download as PPTX, PDF, TXT or read online from Scribd
    Download as pptx, pdf, or txt
    75 views41 pages

    IADVL Color Atlas of Dermatopathology - Book

    Uploaded by

    65gken
    John Smith, a 55-year-old male with COPD, presented with worsening shortness of breath and confusion. He had a respiratory rate of 30 breaths/min, heart rate of 110 beats/min, and oxygen saturation of 88% on room air. An arterial blood gas showed a pH of 7.27, PCO2 of 60 mmHg, and HCO3 of 32 mEq/L, consistent with respiratory acidosis. The causes of respiratory acidosis include decreased ventilation due to COPD exacerbation, thoracic cage disorders, central nervous system depression, and upper airway obstruction. Initial management involves airway support, arterial blood gas analysis, treating any underlying causes, and cautious oxygen therapy to avoid

    Copyright:

    © All Rights Reserved
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    Download as pptx, pdf, or txt
    of 41

    RESPIRATORY

    ACIDOSIS
    Case scenario

    Patient Information
    Name: John Smith
    Age: 55
    Gender: Male
    Medical History: Chronic obstructive pulmonary disease (COPD)
    Current Medications: Albuterol inhaler, tiotropium inhaler
    Presenting Complaint:
    John Smith, a 55-year-old male with a history of COPD, presents to the emergency department with worsening shortness of
    breath and confusion over the past 24 hours.
    Respiratory Rate: 30 breaths per minute
    Heart Rate: 110 beats per minute
    Oxygen Saturation: 88% on room air
    Initial Laboratory Values (ABG):
    pH : 7.27 | (7.35-7.45)
    PCO2 : 60 mmHg | (35-45 mmHg)
    • HCO3 : 32 mEq/L | (22-28 mEq/L)
    Regulation of respiration

    NEURAL REGULATORY MECHANISM CHEMICAL REGULATORY MECHANISM

    AUTONOMIC VOLUNTARY PERIPHERAL CHEMORECEPTORS

    MEDULLA PONS CEREBRAL CORTEX MEDULLARY OR CENTAL


    CHEMORECEPTORS

    DORSAL RESPIRATORY NUCLEUS APNEUSTIC CENTER

    PNEUMOTAXIC CENTER
    VENTRAL RESPIATORY NUCLEUS
    AUTONOMIC NEURAL
    REGULATORY MECHANISM OF
    RESPIRATION
    PONS

    • Apneustic Center:
    The Apneustic center can stimulate the DRG in the medulla,
    primarily assisting with duration and depth of each breath. .

    • Pneumotaxic Center:
    It inhibits the apneustic center, helping to control the duration and
    depth of each breath.

    The antagonistic interaction between the apneustic and pneumotaxic centers helps fine-tune breathing patterns .
    Medulla Oblongata
    • Pre- Botzinger complex (PACEMAKER NEURONS)
    Initiate the respiration

    • Dorsal Respiratory Group (DRG):


    It generates the rhythmic contractions of the diaphragm and
    intercostal muscles responsible for inspiration.

    • Ventral Respiratory Group (VRG):


    It becomes active during forced Expiration (as expiration is a
    passive process)
    INSPIRATION MAINTAINANCE EXPIRATION
    _
    Initiation by Pre- Apneustic center Pneumotaxic center
    _
    Botzinger complex Activation of
    (medulla) (DRG) in medulla . Vagal
    afferents
    Spinal cord
    Inspiration
    Stretch receptors
    (Phrenic nerve)
    Phrenic nerve(c3, c4, c5)

    Diaphragm contracts Tidal volume (>500ml)

    Inspiration initiates

    MEDULLA : Initiates respiration


    PONS : Reguates Respiration
    CHEMICAL REGULTORY
    MECHANISM OF RESPIRATION
    • CENTRAL CHEMORECEPTORS (medulla) – ventral surface of the 4th ventricle

    Sensitive to co2 levels in blood and increase in H+ ions in CSF


    [ hypercapnia ] & [acidosis]
    i.e.,

    Chemo reflex

    Stimulate DRN

    Hyperventilation
    • Peripheral chemoreceptors (carotid and aortic bodies)

    Sensitive to o2 levels in the blood and increase in H+ ions


    [ hypoxia ] & [acidosis]
    i.e.,

    Stimulate VAGUS and GLOSSOPHARYNGEAL nerve

    DRN

    Hyperventilation
    RESPIRATORY ACIDOSIS

    •Respiratory acidosis is a acid base disorder characterized by an increase in the


    levels of carbon dioxide (CO2) in the bloodstream, leading to a decrease in
    blood pH.(acidic)

    •Due to res. Acidosis there is renal retention of bicarbonate partially


    compensates for acidosis, therefore there is increase in plasma bicarbonate
    concentration is also seen.
    • This condition primarily occurs due to

    Impaired ventilation

    Resulting in the retention of CO2

    Acidosis
    RESPIRATORY ACIDOSIS
    (HYPERCAPNIA)

    Increased carbon
    Increased dead space Decreased dioxide production
    ventilation &Abnormal
    transport of carbon
    dioxide
    Decreased central
    Anatomic respiratory drive

    Primary spinal
    Alveolar cord/lower motor
    neuron/muscle
    disorders
    Thoracic cage &
    lung disorders
    Metabolic
    disorders
    Toxins,
    poisoning, drugs
    Increased dead space (gas exchange abnormalities;
    pulmonary parenchymal causes or airway disorders)
    • ANATOMIC - Short shallow breathing

    • ALVEOLAR - Pulmonary embolism (usually severe)


    Pulmonary vascular disease LIKE PULMONARTY HYPERTENSION (usually severe)
    Dynamic hyperinflation ( EXPIRATION TIME) (COPD (chronic) , severe asthma (acute) ).
    End stage interstitial lung disease (SARCODOSIS, IPF)
    REDUCED PERFUSION TO ALVEOLI THAT ARE
    VENTILATED
    DECREASED VENTILATION
    • CNS
    • THORACIC CAGE DISORDERS
    • METABOLIC
    • TOXINS
    • DRUGS
    Decreased central respiratory
    drive

    • Sedative overdose (opioids, benzodiazepines , Anesthetics , Barbiturates,


    tricyclic antidepressants)
    (acute)

    • Encephalitis
    • Stroke
    • Tumours
    • Central and obstructive sleep apnoea
    • Obesity hypoventilation syndrome
    • Brainstem disease
    Primary spinal cord/lower motor neuron/muscle disorders

    • Cervical spine injury


    • Guillain-Barre syndrome
    • Myasthenia gravis
    • Muscular dystrophy
    • Tetanus
    • Multiple sclerosis
    • Acute intermittent porphyria
    • Eaton Lambert syndrome
    • Glycogen storage and mitochondrial diseases
    Thoracic cage disorders
    • Kyphoscoliosis
    • Thoracoplasty
    • Flail Chest
    • Ankylosing spondylitis
    • Pectus excavatum
    • Fibrothorax
    Metabolic disorders
    • Hypermagnesaemia
    • Hypokalemia
    • Hypercalcemia
    • Hypothyroidism
    Toxins, poisoning, drugs

    • Tetanus
    • Botulism
    • Organophosphates
    • Succinylcholine and neuromuscular blockade
    • Procainamide
    Increased carbon dioxide production
    • Fever
    • Thyrotoxicosis
    • Increased catabolism (sepsis, steroids)
    • Overfeeding
    • Metabolic acidosis
    • Exercise
    Abnormal transport of carbon dioxide
    • Decreased perfusion ( heart failure, cardiac arrest, pulmonary
    embolism)
    • Severe anemia
    • Acetazolamide (carbonic anhydrase inhibitor)
    Upper airway disorder (RARE)
    • Severe laryngeal or tracheal disorders
    (stenosis/tumors/angioedema/tracheomalacia)
    • Vocal cord paralysis
    • Epiglottitis
    • Foreign body aspiration
    • Retropharyngeal disorders
    • Obstructive goiter
    Clinical features
    ● Features of underlying disease

    ● Respiratory system

    - Stimulation of ventilation (tachypnea)


    - Dyspnea

    ● CVS
    -Tachycardia
    -Bounding pulse
    -Hypotension
    ● CNS

    - ↑ cerebral blood flow.


    - ↑ ICT
    - Papilledema
    - CO₂ Narcosis (disorientation, confusion, headache, lethargy)
    - Coma (arterial hypoxemia, ↑ ICT, anaesthetic effect of
    ↑ PCO₂ >100 mm Hg)

    ● Peripheral vasodilatation (Bounding pulse, warm, flushed, sweaty)


    Approach:

    1. Assess and stabilize the airway, breathing, and circulation


    2. Perform a brief clinical bedside assessment with vitals and oxygen
    monitoring
    3. Draw an arterial blood gas (ABG)
    4. Administer initial bedside therapies
    1. Consider ventilator support (SPO2 <90) & IV access:

    2. ABG Analysis
    Distinguishing acute and chronic RS Acidosis

    3.History ,examination & investigation


    Prescribed medications
    Drug history
    Past history of
    Chronic lung disease
    Sleep apnea
    Neuromuscular disorder
    Lab investigations

    • Serum Bicarbonate and electrolytes


    • CBC(ANEMIA,POLYCYTHEMIA)

    • Toxicology screening (OPIATES, BENZODIAZEPINES, TRICYCLIC ANTIDEPRESSANTS, BARBITURATES)

    • TFT
    Chest Imaging:

    • CXR (lung parenchymal pathology)


    • CT Chest (COPD, interstitial lung disease, thoracic cage abnormalities)

    Brain and spinal cord imaging :


    • CT (stroke ,tumour, traumatic transection)
    • MRI
    4.Initial management
    • Reversal and avoidance of sedatives
    • Naloxone for opiate overdoses
    • Flumazenil for benzodiazepine (BDZ) Overdose

    • Bag-valve mask or noninvasive ventilation -Non-invasive positive


    pressure ventilation
    [nasal mask, face mask, or nasal plugs]
    • Endotracheal Intubation and mechanical ventilation
    [Acute respiratory failure, inadequate oxygenation or ventilation even after NPPV, and airway
    protection in a patient with depressed mental status]

    • Administration of oxygen

    The target pulse oxygen saturation (SpO2) should be 90 to 93 percent /


    PaO2 of 60 to 70 mmHg.
    • Oxygen administration should be titrated carefully in patients with severe
    obstructive pulmonary disease and chronic CO2 retention who are breathing
    spontaneously . When oxygen is used injudiciously, these patients may
    experience progression of the respiratory acidosis causing severe acidemia.
    • Aggressive and rapid correction of hypercapnia should be avoided, because
    the falling Paco2, may provoke the same complications noted with acute
    respiratory alkalosis (i.e., cardiac arrhythmias, reduced cerebral perfusion,
    and seizures).
    • The Paco2, should be lowered gradually in chronic respiratory acidosis, aiming
    to restore the Paco2, to baseline levels and to provide sufficient Cl- and K+ to
    enhance the renal excretion of HCO3-.
    -Rapid infusion of alkali [NaHCO3 ] is justified only in prolonged
    cardiopulmonary arrest ,severe symptomatic metabolic acidosis,
    tricyclic antidepressant overdose. (otherwise contraindicated)
    - Sodium lactate and Sodium gluconate can be given.

    -Avoid overfeeding as changes in metabolism may worsen


    acidosis by increasing the rate of elimination of carbon dioxide
    Definitive Management:

    •Reverse the cause / Treat the etiology

    • Reverse hypercapnia
    SUMMARY
    • Primarily due to drugs, asthma, brain stem pathology, spinal cord
    disorders, Lung pathology
    • C/F : headache, confusion, disorientation ,lethargy
    • RX : O2 Administration
    THANK YOU…

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