Respiratory failure Flashcards
What is acute respiratory failure and what are the conditions for mechanical ventilation?
Inadequate gas exchange leading to hypoxemia (PaO2 <60 mmHg) or hypercapnia (PaCO2 >50 mmHg), inability to protect airway, respirations > 30 RR, inability to maintain oxygen levels at 90% on 0.6 FiO2, metabolic acidosis with a pH of 7.25, or pCO2 levels greater than 50 mmHg.
What are the two main types of acute respiratory failure?
- Hypoxemic (PaO2 <60 mmHg)
- Hypercapnic (PaCO2 >50 mmHg)
What causes hypoxemic respiratory failure?
- Ventilation-perfusion (V/Q) mismatch
- Shunting
- Impaired diffusion secondary to ARDS, pneumonia, pulmonary edema, atelectasis
What causes hypercapnic respiratory failure?
- Hypoventilation due to decreased respiratory rate
- Hypoventilation due to minute ventilation,
- Increased dead space (e.g., COPD, neuromuscular disease, CNS depression).
What are the clinical signs of acute respiratory failure?
Dyspnea, tachypnea, use of accessory muscles, inability to complete sentences, and hypoxemia.
How is acute respiratory failure diagnosed?
Low oxygen saturation on pulse oximetry or arterial blood gas (ABG) showing hypoxemia or hypercapnia.
What are the oxygen delivery methods and their FiO2 ranges?
- Nasal cannula (FiO2 24-40%)
- Simple face mask (FiO2 30-50%)
- Venturi mask (FiO2 30-60%)
- Non-rebreather (FiO2 60-80%)
- High-flow nasal cannula (FiO2 up to 100%).
What is the benefit of high-flow nasal cannula (HFNC)?
Provides heated humidified oxygen at high flow rates (10-60 L/min) with up to 100% FiO2, reducing work of breathing.
When is noninvasive ventilation (NIV) indicated?
CPAP/BiPAP is used for COPD exacerbations, cardiogenic pulmonary edema, and mild ARDS before intubation.
What are the common reasons for nasotracheal intubation?
Nasotracheal intubation (NTI) is a technique in which an endotracheal tube is inserted through the nose and advanced into the trachea. It is typically used in specific clinical scenarios where oral intubation is difficult or contraindicated. Nasotracheal intubation is preferred in cases of limited mouth opening (trismus, jaw fractures) and cervical spine precautions from neck trauma, as well as respiratory distress and stridor secondary to anaphylaxis. Nasotracheal intubation is contraindicated in severe nasal trauma or basilar skull fractures (risk of intracranial tube placement).
What is a reasonable option for establishing an airway in a patient with a difficult airway?
Patients with acute onset of respiratory distress, angioedema, and shock following likely allergen exposure leading to anaphylaxis and an unstable respiratory status (eg, tachypnea, hypoxia, stridor, wheezing) that are worsening despite appropriate treatment. This situation necessitates a definitive airway. Airways can be performed with the patient still awake and in contrast to rapid sequence intubation (RSI), awake intubation (either nasotracheal or orotracheal) is the preferred method of intubation for patients with difficult airways with an upper airway obstruction (eg, swollen lips/tongue, stridor). In awake intubation, the patient independently maintains upper airway tone and spontaneous ventilation while the airway is visualized (typically using a fiberoptic endoscope) to determine whether intubation is possible. During RSI, a patient is fully anesthetized and paralyzed, causing loss of all upper airway tone, protective airway reflexes, and respiratory drive. If intubation is unsuccessful, as can occur in patients with difficult airways, the patient can rapidly become hypoxic and experience cardiac arrest.
Which agent is used for intubations with the patient still awake, when would this be appropriate?
Ketamine, a phencyclidine derivative, is the preferred agent to use for awake intubations because it provides dissociation, amnesia, and analgesia (ie, dissociative anesthesia) while maintaining upper airway tone, protective airway reflexes, and respiratory drive. It also causes a sympathetic surge (by inhibiting reuptake of catecholamines) that increases blood pressure and causes bronchial smooth muscle relaxation, which are additional benefits in patients with hypotension and bronchospasm.
What is the best way to establish an airway when attempts have failed in an awake patient?
After several attempts to secure a definitive airway via awake intubation have failed, and the patient has severe hypoxia and signs concerning for impending cardiac arrest (eg, severe hypotension, falling heart rate), cricothyrotomy should be performed immediately to bypass the upper airway obstruction and restore ventilation and oxygenation. Especially given cases of rapidly progressive airway edema (which further airway instrumentation will only increase), additional intubation attempts are unlikely to succeed and will only increase the risk of deterioration. The procedure involves incising the cricothyroid membrane and inserting an endotracheal or tracheostomy tube, which can be used for mechanical ventilation. Management of the failed airway (ie, airway that cannot be intubated on initial attempts) is determined by the ability to oxygenate the patient using mask ventilation. In patients who cannot be adequately oxygenated (“can’t intubate, can’t oxygenate”) due to upper airway obstruction, a surgical airway (ie, cricothyrotomy) should be performed. In contrast, patients who can be oxygenated via bag valve mask ventilation (“can’t intubate, can oxygenate”) may tolerate further intubation attempts. Adjunctive airway techniques (eg, video laryngoscopy) may increase the chance of success.
What are the indications for mechanical ventilation?
Apnea, acute respiratory failure, impending respiratory failure, or need for airway protection.
What initial ventilator settings are used in volume control?
Tidal volume (6-8 mL/kg), respiratory rate (12-16), FiO2 (100%), PEEP (5 cm H2O).
What are the different ventilator modes?
- Volume control (set tidal volume, variable pressure)
- Pressure control (set pressure, variable volume)
- Pressure support (patient-triggered breaths)
What sedative agents are used during mechanical ventilation?
Opioids (fentanyl, hydromorphone), sedatives (propofol, midazolam, dexmedetomidine).
How do you correct respiratory acidosis (high CO2)?
Increase respiratory rate or tidal volume to enhance ventilation.
How do you correct respiratory alkalosis (low CO2)?
Decrease respiratory rate or tidal volume to reduce ventilation.
How do you correct hypoxemia (low O2)?
Increase FiO2 or PEEP in increments to achieve PaO2 >60 mmHg.
Why is PEEP avoided with patients with intracardiac shunts?
PEEP raises intrathoracic pressure, which compresses pulmonary capillaries and raises pulmonary vascular resistance. This increases pressure within the right heart chambers and can increase right-to-left shunting through an existing intracardiac shunt (eg, atrial or ventricular septal defect), worsening hypoxemia.
How do you wean a patient off mechanical ventilation?
FiO2 <50%, PEEP <5 cm H2O, spontaneous breathing trial (the rapid shallow breathing index RSBI [RR/Vt] <105).
What is ARDS?
Severe hypoxemic respiratory failure due to alveolar injury and proteinaceous fluid accumulation in alveoli. When patients have diffuse pulmonary edema (inspiratory wet crackles, bilateral patchy infiltrates), the sources can be either cardiogenic or noncardiogenic ARDS occurs due to noncardiogenic causes. With either, the ensuing pulmonary edema cause the alveoli become flooded and unable to fill with gas (ventilation: V = 0). However, they are still being perfused (Q), resulting in many alveoli with ventilation-perfusion (V/Q) ratios approaching zero. Because blood passing through the lungs returns to the left atrium without being oxygenated, this situation is analogous to a **true right-to-left anatomic shunt similar to an atrial septal defect with flow from the right to the left atrium. In ARDS, this is an intrapulmonary shunt effect. Increasing the fraction of inspired oxygen (FiOz) to 100% does not improve oxygenation because the shunted blood never “sees” the alveolar gas. Because pure oxygen alone cannot improve hypoxemia, treatment depends on reducing the shunt effect. This can be done by pressurizing the inspired gas in a closed circuit (eg, mechanical ventilator). Positive end-expiratory pressure (PEEP) reduces the shunt by propping the collapsed alveoli open, displacing extracellular lung fluid and exposing more alveolar surface area for gas exchange/oxygen uptake.
What are common causes of ARDS?
Sepsis, aspiration, pneumonia, trauma, transfusion-related acute lung injury (TRALI), and pancreatitis.
What is the Berlin definition for diagnosing ARDS?
- Acute onset (<1 week)
- Bilateral infiltrates
- Pulmonary edema not due to heart failure (PCWP <18 mmHg)
- PaO2/FiO2 ratio <300
What is the classification of ARDS based on PaO2/FiO2 ratio?
Mild (200-300), moderate (100-200), severe (<100).
How is ARDS managed?
- Low tidal volume ventilation (6 mL/kg)
- High PEEP
- Prone positioning
- Neuromuscular blockade
- Conservative fluid management
Are steroids used in ARDS?
Systemic corticosteroids for the treatment of ARDS remain controversial.
When is prone positioning beneficial in the setting of ARDS?
Mechanical ventilation with patients in prone position may have mortality benefits in severe ARDS, likely due to enhanced gas exchange (through improvements in lung perfusion and transpulmonary pressure differences). However, it is generally reserved for those in whom ventilator settings have been maximized (eg, fraction of inspired oxygen of 100%) and is associated with complications (eg, nerve compression, tube dislodgment).
What are the complications of mechanical ventilation?
Barotrauma (pneumothorax), oxygen toxicity, ventilator-associated pneumonia (VAP), and auto-PEEP.
How do you recognize impending respiratory failure in ventilated patients?
- Elevated plateau pressure (>30 cm H2O) indicates poor lung compliance
- Normalizing or rising PaCO2 suggests muscle fatigue
What is the best method for ensuring proper endotracheal placement?
Capnography (measurement of COz concentration over time) is the most reliable method for verification of endotracheal tube (ETT) placement in the trachea rather than the esophagus. Clinical findings, including auscultation of breath sounds over both lung fields, chest wall rise with assisted ventilation, visualization of the ETT passing through the vocal cords, and fogging of the ETT on exhalation, are not reliable indicators of correct placement in the trachea. A normal capnogram has a characteristic rectangular waveform with 4 phases. Any variation in waveform morphology and/or end-tidal COz (EtCO2) can provide diagnostic information about ventilation/perfusion or metabolic status. A normal waveform with all 4 phases after intubation indicates proper ETT placement, whereas a flat-line waveform typically indicates improper esophageal placement. A colorimetric EtCO, detector consists of litmus paper that changes color when exposed to CO2. CO2 exhalation from an ETT properly placed in the trachea will lead to a color change (purple to yellow), whereas an ETT improperly placed in the esophagus will not deliver COz to the detector, resulting in no color change.
Why should drowning victims be monitored even if they feel well initially?
They are at risk of delayed ARDS due to aspiration of fluid into the lungs. When fluid enters the alveolar airspace (ie, pulmonary edema), the surface tension increases (due to dilution of surfactant) causing the alveolar walls to cling together and collapse (ie, atelectasis), which decreases lung compliance. PEEP props open (“recruits”) the partially flooded alveoli, improving lung compliance.
What is the role of extracorporeal membrane oxygenation (ECMO) in respiratory failure?
ECMO provides oxygenation for refractory hypoxemia when mechanical ventilation fails.
What is post-intensive care syndrome (PICS)?
Chronic physical, psychiatric, and cognitive impairments following an ICU stay, with an increase risk of occurrence in conditions that involve ARDS or prolonged mechanical ventilation. It is thought to be secondary to CNS hypoxia, neuroinflammation & metabolic disruption.
How does sepsis-related immune suppression affect ICU patients?
Leads to prolonged immunoparalysis, increasing susceptibility to nosocomial infections like VRE and hospital-acquired pneumonia. Over time, this will improve.
What psychiatric conditions accompany post-intensive care syndrome (PICS)?
Major depression, PTSD, anxiety, and sleep disturbances. These can develop within 5 years of ICU event.
What are the neurocognitive symptoms of post-intensive care syndrome (PICS)?
Impaired memory, executive function, attention, and processing speed.
What are the physical symptoms of post-intensive care syndrome (PICS)?
Decreased mobility, muscle weakness, and reduced independence, requiring early PT/OT to mitigate conditions. Most ICU survivors are impaired in ≥1 domains for several years, usually with major negative impacts on quality of life. PICS is a significant health concern: Many patients require chronic health services and are unable to return to work. These medical and financial burdens frequently extend to patients’ families and caregivers.
What are the risk factors for post-intensive care syndrome (PICS)?
ICU delirium, prolonged mechanical ventilation, ARDS, sepsis, and CNS hypoxia.
How is post-intensive care syndrome (PICS) managed?
Early physical therapy, occupational therapy, post-ICU clinic follow-up, home care, and psychiatric support.
