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neuro resp 3

Case Context and Core Pathophysiology

  • A young man in South Australia experiences a severe asthma attack with airway obstruction due to an allergic trigger triggering an immune overreaction.
  • Key triad in asthma mechanisms (as discussed):
    • Bronchospasm (constriction of bronchioles) → exhalation difficulty
    • Edema of airway walls (swelling) → narrowed airways
    • Increased mucus production → mucus plugging
  • The term “reactive airway disease” is used to describe this reactive pattern to triggers.
  • The patient reports inability to breathe and presents in a tripod/airway–protective position; without medical intervention, airway collapse and hypoxia can occur.
  • Respiratory emergency flagged as potentially fatal if not treated promptly.
  • The audience is reminded to take patient-reported distress seriously when they state they may die or cannot breathe.

Clinical Presentation and Assessment Elements

  • Signs/symptoms to look for in severe asthma: dyspnea, use of accessory muscles, wheeze, cyanosis, reduced air movement, possibly a silent chest if airways are severely blocked.
  • If a patient has a history of asthma and reports a severe attack, escalate care rapidly.
  • Assessment goals: establish airway patency, ensure adequate oxygenation, identify need for pharmacologic escalation, monitor for deterioration.
  • Objective measurements discussed include:
    • End-tidal waveform analysis (waveforms can indicate obstruction/air trapping and ventilation effectiveness)
    • Oxygen saturation (SpO2) trends
    • Respiratory rate and work of breathing
    • Ability to speak in short phrases or count numbers as a functional benchmark

Airway and Breathing: Immediate Interventions and Observations

  • When airways are severely constricted and mucus is present, inhaled bronchodilators may fail to reach the blood due to mucus acting as a barrier.
  • Observed condition in Chris: mucus blocks drug delivery and airway patency despite bronchodilators; this necessitates alternatives to ensure drug delivery.
  • If a patient cannot be ventilated effectively with inhaled therapies, escalate to systemic or alternative routes of bronchodilation.
  • Ventilation goals include improving oxygenation, reducing bronchospasm, and allowing exhalation to occur without dangerous air trapping.

Pharmacologic Treatments for Acute Severe Asthma (Thorugh the Transcript)

  • Albuterol (Ventolin) via nebulizer (inhaled beta-2 agonist)
    • Dosing guidance discussed: 5 mg per neb; nebulization typically at 8-10 L/min flow; some students suggested 8-10 L/min as a preferred setting.
    • Nebulizer therapy aims to relax airway smooth muscle around small airways to open them up.
  • Epinephrine (EPI)
    • Indications: alternative/adjunct bronchodilator when albuterol is insufficient due to mucus/edema.
    • Route and dosing discussed:
    • IM epinephrine: $0.3-0.5$ mg IM (1:1000) administered intramuscularly, typically in the thigh.
    • Nebulized epinephrine mentioned as an option in the discussion; the emphasis is on epinephrine as a potent bronchodilator with beta-2 agonist properties.
    • Pharmacologic property: epinephrine is a beta-2 agonist that dilates airways and also provides vasoconstriction to reduce mucosal edema.
  • Magnesium sulfate (MgSO4)
    • Role: a bronchodilator with smooth muscle relaxation effects; helps reduce bronchial constriction and improve airflow.
    • Administration discussed: IV infusion over approximately 10-15 ext{ minutes}; rapid onset and relatively quick effect.
  • Systemic corticosteroids
    • Methylprednisolone (Solu-Medrol): discussed dose 125 ext{ mg IV} as a standard early intervention in severe asthma.
    • Dexamethasone: dosing mentioned in pediatrics 0.5 ext{ mg/kg} (for pediatrics); adults often have a fixed dose protocol (e.g., 5–10 mg) depending on setting.
  • Anticholinergic bronchodilator
    • Ipratropium bromide (Atrovent) via nebulization: discussed as an adjunct; often given with albuterol in a combination neb.
    • Typical approach is to add ipratropium to beta-agonist therapy when response to albuterol alone is suboptimal.
  • Inhaled/Oral adjuncts and cautions
    • Consideration of ketamine in RSI scenarios for reactive airway disease when RSI is indicated; ketamine may provide bronchodilation but is not a first-line bronchodilator for asthma control.
    • The discussion notes that ketamine can be considered for RSI in refractory cases, but not as a routine asthma treatment.

Oxygenation and Delivery Devices: Practical Details

  • Oxygen delivery devices and approximate FiO2 ranges discussed:
    • Nasal cannula: 2-6 ext{ L/min}; FiO2 up to approximately 0.40
    • Simple mask: 6-10 ext{ L/min}; FiO2 0.35-0.60
    • Non-rebreather mask (NRB): 10-15 ext{ L/min}; FiO2 up to about 0.70-0.95 (practical target often ~0.60-0.90 depending on fit and inspiratory effort)
    • High-flow devices and pressure support: capable of approaching 100% FiO2 when a good seal is achieved (especially with CPAP/BiPAP or high-flow systems)
    • Venturi masks: color-coded with fixed FiO2 values for precise titration
  • CPAP/BiPAP: Continuous or biphasic positive airway pressure can provide PEEP to help keep airways open and assist with exhalation, potentially reaching near 100% FiO2 with proper seal and device settings.
  • The concept of FiO2 and device selection is tied to the patient’s tolerance, secretions, sedation status, and ability to maintain a seal with the device.

Ventilation Considerations in Severe Asthma (Status Asthmaticus)

  • When airways are severely inflamed and mucus obstructs flow, patients may develop auto-PEEP (air trapping) if exhalation is incomplete.
  • BVM use can risk barotrauma if delivered too aggressively in an auto-PEEP state; use controlled, slower ventilation to give time for exhalation.
  • End-tidal CO2 and waveform monitoring help guide ventilation strategy, but a lack of air movement can make ETCO2 less reliable; clinicians should integrate clinical signs with waveforms and SpO2.
  • Tidal volume and peak inspiratory pressures should be managed to avoid gastric distension and aspiration; use appropriate bag-valve-mask technique and consider advanced airway if ventilation is not adequate.

Advanced Airway and Equipment Considerations

  • BVM (Bag-Valve-Mask) specifics:
    • BVM sizes: adult, pediatric, and infant; ensure proper sizing for an adequate seal and ventilation.
    • EZ Flow devices and inline adapters can limit delivered pressure to protect the lungs and prevent over-ventilation.
    • Pop-off valve: prevents excessive pressure; on some BVMs, the pop-off can be disabled, increasing risk of barotrauma; EZ Flow and pop-off interactions discussed.
    • Pop-off valve engagement protects against over-pressurization, especially important in infants.
  • Critical concepts for effective bagging in asthma/COPD contexts:
    • S-E-X-D-E mnemonic for bagging logistics discussed by instructors (S = Sex? unclear in transcript; E = Elevation; X = Extra Equipment; D = Younger; E = Decanto). The gist: ensure help is available, elevation of head, have extra equipment ready, and involve a second person.
    • Use CPAP/BiPAP when indicated to aid exhalation (helps reduce air trapping and improve oxygenation).
  • Anatomic considerations for acute airway management:
    • Needle cricothyrotomy location: identify cricothyroid membrane between cricoid and thyroid cartilages for emergency airway access.
    • Laryngeal pressure (BERT maneuver) vs cricothyroid puncture: appropriate terminology when discussing airway devices.
    • Aspiration risk with poor airway management; consider advanced airway if indicated.
  • Complications to monitor for during airway management:
    • Gastric distension, aspiration, barotrauma, and tension pneumothorax risk with aggressive ventilation.
    • Ensure monitoring for signs of tension pneumothorax after chest compressions or aggressive ventilation in a severely obstructed airway.

Differential Diagnoses and Related Conditions Discussed

  • Anaphylaxis vs asthma: two-body-system involvement (e.g., skin, GI, circulatory) can help differentiate.
  • CHF with wheeze vs true bronchospasm: end-tidal waveform patterns and clinical history help differentiate; treat underlying cause accordingly.
  • Infections and asthma interplay:
    • RSV bronchiolitis and bronchiolitis in young children (under 2 years) vs bronchitis in older patients.
    • Common respiratory infections (e.g., flu, COVID-19) can trigger wheeze but are not always primarily bronchospastic.
  • COPD and its components:
    • Emphysema vs chronic bronchitis; clinical signs like barrel chest and pink puffer vs blue bloater.
    • Air trapping and auto-PEEP common in COPD; risk of right-sided heart failure (cor pulmonale).
    • Treatments often include oxygen, bronchodilators, corticosteroids, and sometimes CPAP; caution with epinephrine in CAD patients due to potential tachyarrhythmia.

COPD-Specific Notes (Overlap with Asthma Emergencies)

  • Emphysema: alveolar destruction, loss of surface area, air trapping; pink puffer phenotype with pursed-lip breathing and cachexia.
  • Chronic bronchitis: productive cough for at least 3 months in 2 consecutive years; “blue bloater” phenotype with hypoxia and cyanosis.
  • Auto-PEEP and risk of barotrauma discussed in the context of aggressive ventilation in COPD.
  • Oxygen and ventilation strategies emphasize balancing oxygenation with the risk of hyperinflation; CPAP/PEEP can help with exhalation and gas exchange.
  • Dosing considerations for COPD exacerbations often prioritize albuterol and non-invasive ventilation prior to resorting to epinephrine due to potential cardiac strain in elderly patients with CAD.

Case-Specific Transcripts and Practical Pointers

  • Brittany’s scenario progresses to bradycardia and then ventricular fibrillation; management discussed includes defibrillation and vasopressor use (epinephrine) with attention to not worsening potential tension pneumothorax.
  • If a patient deteriorates into cardiac arrest from respiratory failure, standard ACLS protocols apply with consideration of reversible triggers (e.g., bronchospasm, pneumothorax).
  • In transport and field settings, the emphasis is on rapid escalation of therapy, ensuring proper device setup, and not delaying treatment while awaiting perfect imaging or tests.

Quick Reference: Key Doses, Devices, and Concepts (まとめ)

  • Albuterol (nebulized): 5 ext{ mg} per neb; flow 8-10 ext{ L/min}
  • Epinephrine (IM): 0.3-0.5 ext{ mg} (1:1000) IM; thigh injection
  • Epinephrine (nebulized) discussed as alternative; not standardized in this note
  • Magnesium sulfate (MgSO4): 1-2 ext{ g} IV over 10-15 ext{ minutes}
  • Methylprednisolone (Solu-Medrol): 125 ext{ mg IV}
  • Dexamethasone: 0.5 ext{ mg/kg} (peds) for steroids; adult dosing varies by protocol
  • Ipratropium bromide: 0.5 ext{ mg} via neb; often combined with albuterol
  • Oxygen devices and FiO2 targets:
    • Nasal cannula: 2-6 ext{ L/min}; FiO2 up to 0.40
    • Simple mask: 6-10 ext{ L/min}; FiO2 0.35-0.60
    • NRB mask: 10-15 ext{ L/min}; FiO2 up to 0.70-0.95
    • High-flow / CPAP: potential for near 100% FiO2 with good seal
  • Ventilation and monitoring concepts:
    • End-tidal waveform analysis; watch for variables indicating poor air movement or air trapping
    • Auto-PEEP and risk of barotrauma with aggressive ventilation
    • BVM management cadence: typical target around 10 ext{ breaths/min}, with slower delivery in status asthmaticus (e.g., one breath every 8-10 ext{ seconds}) to allow exhalation
    • Consider PEEP in severe obstruction to assist with exhalation during ventilation
  • COPD-focused notes:
    • Emphysema, chronic bronchitis, COPD overlap; pink puffer vs blue bloater phenotypes
    • Common treatments: oxygen, bronchodilators, corticosteroids, CPAP; careful consideration of epinephrine in CAD patients
    • Auto-PEEP risk and need for careful ventilation strategy
  • RSI and sedation considerations in asthma:
    • Ketamine considered for its bronchodilatory properties in RSI context; not a primary treatment for asthma control

Exam Preparation Connections and Practical Implications

  • Recognize that asthma is a reactive airway disease with a triad of bronchospasm, edema, and mucus; triggers can provoke life-threatening episodes.
  • In severe asthma, lack of response to inhaled bronchodilators necessitates systemic agents and supportive ventilation strategies.
  • Differentiating asthma from anaphylaxis or CHF is essential for appropriate pharmacologic approach; look for multi-system involvement and history.
  • For prehospital care, be prepared to escalate quickly: nebulized bronchodilators, systemic steroids, magnesium, epinephrine (IM), and non-invasive ventilation as appropriate.
  • In COPD, manage with bronchodilators and oxygen, and consider CPAP for air trapping; avoid unneeded epinephrine unless indicated by a concurrent anaphylactic process or severe bronchospasm with CAD risk.

Final Thoughts for the Upcoming Respiratory Exam

  • Be comfortable with the pharmacology of acute asthma management and the typical dosing ranges discussed (albuterol, ipratropium, magnesium, steroids, epinephrine).
  • Understand the rationale for each therapy and how mucus, edema, and bronchospasm interact to create different physiologic states (silent chest vs noisy chest).
  • Be able to describe oxygen delivery options and rationale for device choice based on FiO2 needs and patient ability to tolerate devices.
  • Know the signs of deterioration and when to escalate to advanced airway interventions, including the relevant airway anatomy landmarks for invasive access.
  • Review COPD pathophysiology differences and how management differs from classic asthma cases, including considerations about auto-PEEP and the use of CPAP.

If you want, I can restructure these notes into a more condensed per-topic cheat sheet or expand any section with additional clarifications or simplified mnemonics.