Respiratory Failure

    .

    Post-ICU neuropsychiatric impairment

    • Common (75%)
    • Studies shown at 1 and 5 years post-intubation for ARDs or severe sepsis.
    • High risk of depression, anxiety, loss of executive function.
    • Depends on:
      • Age
      • Length of ventilator
      • Poor glucose control
      • hypoxemia

     

    Respiratory Failure

    • 3 types
      • Hypoxic - decline in oxyhemoglobin
      • Hypercapnic
      • Upper Airway

     

    Hypoxemic

    • Acute decline in oxyhemoglobin level that does not readily correct with supplemental O2.
    • Ambient air arterial pO2 <60
    • Arterial pO2 to FiO2 ratio is 200 or less.
    • Arterial pCO2 can be either normal, or reduced (compensatory hyperventilation).
    • Caused by ongoing perfusion of lung units that no longer receive ventilation due to alveolar collapse or flooding from:
      • Edema, puss, blood.
      • Creates Intra-pulmonary shunt that does not correct with increased alveolar ventilation or supplemental O2.
    • Reversed by application of PEEP --> opens up (recruits) flood or collapsed alveoli. 


    Heart Failure

    • Manifests as acute cardiogenic pulmonary edema.
      • 50% have normal ejection fraction.
      • Look for diastolic dysfunction, infarction, valve lesions, etc...
    • Radiographically indistinguishable from ARDS.
    • Cardiogenic edema can improve rapidly with diuretics. 
    • Investigations:
      • Echocardiography is #1.
      • Tropinin, ECG, BNP can be useful.  
      • (BNP: Helps distinguish cardiogenic from non-cardiogenic, but do not diagnose or exclude heart failure)

     

    Atelectasis

    • Important cause of hypoxemic respiratory failure.
    • More common post-anesthesia, and invasive mechanical vents.
    • Encompasses ~50% of acute post-op hypoxemia, can last days.
      • Important cause of peri-operative death, esp in obese patients undergoing bariatic surgery.
    • Risk Factors:
      • Morbidly obese patients
      • Ventilated patients:
        • Supine, absence of larger side-breathes, low tidal volumes predispose to bibasillar atelectasis.
      • Mucous plugging and R-mainstem intubation --> can cause lobar collapse
    • Management:
      • Chest physiotherapy
      • Incentive spirometry
      • Early mobilization
      • Continuous positive pressure (CPAP)

     

    Pneumonia

    • Consolidation creates a physiologic shunt (simlar to cardiogenic/ ARDS).
      • Pneumonia is the most common trigger for ARDS for non-hospitalized patients.
    • Unilateral pneumonia can cause hypoxemia, focal areas of atelectatic lung are harder to recruit with PEEP.
      • PEEP can worsen hypoxemia by overdistending normal lung.
    • Positioning patient in lateral-decubitous position with "good lung" at the deep end, helps reduce intrapulmonary shunt.

     

     

     

    Hypercapnic (Ventilatory) Failure

    • Ventilatory respiratory failure --> hypoventilation and hypercapnia.
    • Elevation of pCO2 due to increased production or alveolar ventilation.
    • Increased CO2 production
      • Metabolic demands, fever, muscle activity, agitation.
    • Decreased alveolar ventilation
      • 1. Increased mechanical load
      • 2. Decreased respiratory drive (sedating drugs)
      • 3. Respiratory muscle weakness (increase work of breathing, neuromuscular disease, kyphoscoliosis).
      • 4. Increase Dead-Space Ventilation
        • (i.e. COPD or ARDS have increased deadspace, ongoing ventilation of lung units with injured vascular beds).
      • 5. Neuromuscular Weakness. 
    • Ventilation without perfusion is happening.
    • Hypoxemia often concominant, but (unlike physiologic shunt) corrects with supplemental O2.
      • However, hypoxemic and ventilatory failures often occur together.

     

    Sedating Drugs

    • Opioids are potent respiratory depressors, but any sedating medication can do it.
      • Opioid intoxication: miosis, encephalopathy, hypotension, hypothermia, hyporeflexia
      • Think alternative diagnosis if do not respond to total of 10mg naloxone (mean half-life 1 hour), continuous infusion may be needed.
      • All respiratory depressant drugs with worsening respiratory depression require intubation except opioids, which respond well to naloxone.
      • Chronic opioid users receiving naloxone should be watched for withdrawal:
        • Delirium, agitation, diaphoresis, tremulousness, hypertension, fever, seizures
    • Benzodiazepines
      • Flumazenil can reverse resp depression in benzo overdose, but rarely given due to risk of seizures in chronic benzo users.
      • Benzo overdose usually does not cause life-threatening respiratory depression without co-ingestion of other drugs (i.e. narcotics).
    • Stroke can cause respiratory depression.
    • Hypothyroidism (rare)

     

    ​Muscle Weakness

    • Normal lungs, but respiratory failure = "bellows failure"

    • Often neuromuscular weakness

    • Findings:

      • Weak cough, excessive respiratory muscle use, orthopnea, rapid/shallow breathing.

      • Diaphragmatic weakness = paradoxical inward motion of abdomen during inspiration

    • Usually involves acute trigger of decompensation (fever, focal atelectasis, small PE).

      • Find the trigger.

    • Weakness causes other complications: i.e. atelectasis, aspiration, pneumonia.

    • Respiratory Complications of Neuromuscular Weakness

      Complication

      Risk Factors

      Treatment

      Chronic ventilatory failure

       

       

      Pulmonary hypertension

      Chronic ↓ arterial PO2, ↑ arterial PCO2

      Ventilatory support

      Sleep-disordered breathing

      ↓↓ Arterial PO2, ↑↑ arterial PCO2 with sleep

      Ventilatory support

       

      Upper airway obstruction due to bulbar dysfunction

      Ventilatory support

      Atelectasis

      Reduced lung volumes

      Ventilatory support

       

      Mucus plugging

      Chest physiotherapy

      Pneumonia

      Dysphagia with aspiration

      Dietary modification

       

      Impaired cough, atelectasis

      Chest physiotherapy

    • Can measure bedside:

      • lung volumes

      • Maximum inspiratory pressure (more negative = more diaphragm strength) -30cmH2O = normal.

      • Maximum expiratory pressure (more positive = more abdo/intercostal strength) <40 = impaired cough and secretion retention.

      • Poor predictive values, use of serial values to compare is best.

    • Causes:

      • see below

    • Management:

      • (See above table)

      • Chest physiotherapy (incl. incentive spirometry, postural drainage, manual/mechanical assisted cough)

      • Ambulation

     

    Neuromuscular Disease

    • Spinal cord injury (phrenic nerve, C3,4,5).

      • If above C3 injury = complete ventilatory loss, require life long ventilation or diaphgragmatic pacing, high risk of atelectasis + pneumonia.

      • Incomplete injury above C3 or C3/4/5 injury = initially require support, but often recover (acc. muscles, improvement in strength, oncent of rigidity all help).  Most recover independent ventilation.

    • Generalized Neuromuscular Weakness

      • Guillain-Barré Syndrome (GBS) - acute immune mediated polyneuropathies cause ventilatory failure and bulbar dysfunction.

        • Acute Demyelinating Inflammatory Polyneuropathy - 90% of GBS cases - progressive symmetric weakness + hyporeflexia (lower ext. first).  1/4 requires mechanical ventilation.

        • Plasmapheresis or IVIG (no role for steroids). 

      • Myesthenia Gravis (Myesthenic Crisis)

        • Oropharyngeal weakness often accompanies (may need intubation).  Triggered by infection, medications, surgery, pregnancy or natural hx.

        • Plasmapheresis or IVIG, steroids for sustained control.

      • ALS

        • Motor neuron disease, can present with acute vent failure.

        • Usually in context of well established disease.

    • Management:

      • Early identification --> respiratory support, minimize aspiration risk.

     

    Restrictive Lung Disease

    • Extra-pulmonary
      • Kyphoscoliosis (can develop hypercapnea with pulmonary HTN)
        • Decompensation usually precipitated by infection, PE, volume overload.
        • NIPPV often has a role to improve entilation (esp during sleep).
      • Increased intra-abdominal pressure
        • Ascites, bowel edema, gas insufflation.
    • Pulmonary
      •  (i.e. fibrotic lung disease).
      • Usually causes hypoxemia
      • Immunesuppression is generally not effective, evaluate for reversible causes. (infection, VTE, HF)
      • Acute Exacerbation: diffuse alveolar damage superimposed on baseline fibrosis. --> causes death.

     

    Obstructive Lung Disease

    • Lower Airway
      • Decompensation in Asthma/COPD caused by increased work of breathing (not much hypoxemia).
      • Worsening obstruction, increased minute ventilation --> air trapping --> dynamic hyperinflation.
        • Increases lung volumes --> higher positive PEEP (auto-PEEP aka Intrinsic PEEP).
        • Elevated intrathoracic pressures --> risk of pneumothorax, hypotension (reduced venous return to R-heart).
        • Chronic --> Elevated dead space ventilation.
      • Management: (COPD, Asthma)
        • Hypoxia usually easily correctible with O2. 
        • If no response to O2, consider other dx: HF, PE, pnomothorax, pneumonia.
        • Bronchodilators, steroids etc.. (See COPD/Asthma sections).
    • Upper Airway
      • Less common.
      • Epiglottitis and deep neck infection (Ludwig's angina), retropharyngeal abscess, peritonsillar abscess.
      • Overt signs: Inspiratory stridor, retraction, cyanosis --> Intubation!
      • Less severe: Drooling, dysphagia, hoarseness  -->
        • close monitoring (Low threshold for intubation --> hard to place tube in obstructed airway).
      • Paradoxical vocal cord motion is upper airway obstruction mimicing asthma exacerbation.

     

     

     

    ARDS

    • Acute Respiratory Distress Syndrome
    • Non-Cardiogenic form of pulmonary edema.
    • Acute persistent diffuse lung inflammation that injures the alveolar epithelial cells and pulmonary capillary endothelial cells.
      • --> increased vascular permeability and cytokine release --> leakage of protein, fluid, neutrophils into the interstitium and alveoli --> creates oncotic gradient to move further fluid into the lung airspace. 
      • Decreased surfactant function causes atelectasis --> further impairs gas exchange. 
      • Alveolar flodding reduces lung compliance and therefore increase work of breathing.
    • This creates hypoxemic respiratory failure from shunt, but eventually can cause hypercapnic failure (work of breathing).
    • Pathology:
      • Diffuse alveolar damage. (diagnosis is clinical!)
    • Diagnose:
      • Historically: classified by arterial pO2:FiO2 ratio
        • P:F ratio < 300 = Acute Lung Injury.
        • P:F ratio < 200 = ARDS
        • Also involved PA catheters for wedge pressure
      • NEWER: 2012 Berlin Definition of ARDS
        (consensus statement by European Society of Intensive Care Medicine, American Thoracic Society, Society of Critical Care Medicine).
        • Changes:
          • Removed PA catherers from criteria (studies show their use does not improve outcomes in lung injury, so they are removed from new guidelines).
          • Heart failure and volume overload can coexist in ARDS (exclusion of cardiogenic edema does not require objective assessment with echo or PCWP) unless no risk factors for ARDS.
          • Can now use CT or CXR for bilateral opacity criteria.
             
        • Classify ARDS into mild/mod/severe by level of oxygenation, eliminating "Acute Lung Injury".
        • 2012 Berlin Definition of ARDS 

              1. Acute onset within 1 week of an apparent clinical insult or development and

                  progression of respiratory symptoms

           

              2. Bilateral opacities on chest imaging not explained by other pulmonary pathology

                  (such as pleural effusions, lung collapse, nodules, etc..)

           

              3. Respiratory failure not explained by heart failure or volume overload 

           

          • Severity Arterial pO2 / FiO2 Ratio (P:F Ratio)
            MILD 201 to 300 mmHg (26.7-39.9 kPa)
            MODERATE 101 - 200 mmHg (13.4-26.6 kPa)
            SEVERE < 100 mmHg (<13.3 kPa)

             
          • NOTE: All 3 categories require P:F ratio measured with a PEEP of at least 5cm
            of H2O (Can be non-invasively w/ CPAP in mild ARDS).

     

    Causes

    • More than 60 disorders can precipitate ARDS (direct or indirect lung injury).
      • Severe sepsis from pneumonia or non-pulmonary lung sources are majority of cases.
    • Common Causes of Acute Respiratory Distress Syndrome

      Direct Pulmonary Injury

      Pneumonia

      Aspiration

      Near drowning

      Inhalational injury

      Trauma or lung contusion

      Indirect Pulmonary Injury

      Sepsis

      Severe trauma

      Multiple blood transfusions

      Pancreatitis

    • (See R-side)

     

    Prognosis

    • Mortality rate is 40%, varies by cause:
      • Best prognosis: trauma.
      • Worst prognosis: Severe sepsis from pulmonary source.
    • Deaths are caused by underlying precipitant of lung injury or subsequent nosocomial infections
      • Not by direct lung injury.

     

    Management

    • Mechanical ventilation / POSITIVE PRESSURE is primary supportive treatment. (less applicable in focal disease.
      • NOTE: key pathologic change: flooding of alveoli by membrane disruption.
      • NOTE: Latest trial: NIPPV did not improve survival or need for intubation in ARDS pts.
        (May be beneficial in select pts with pneumonia).
    • Limit intravascular volume to level enough to maintain perfusion.
      • Additional volume will cause leaky capillaries to be more leaky.
      • Multi-Center Study: relatively complex fluid strategy improved lung function, shortened duration of mechanical ventilation and ICU stay, but did not change mortality.
        • Conservative strategy: lower CVP pressures. (less boluses, more furosemide)
        • vs. Liberal strategy.
    • Many therapies trialed:
      • Most shown to improve oxygenation, but not survival.
         
    • Nonventilator Management of Acute Respiratory Distress Syndrome (Source:MKSAP16)

      Intervention

      Comments

      Inhaled vasodilators

      ↑ O2 saturation; no proven survival benefit

      Systemic corticosteroids

      ↑ O2 saturation; may reduce duration of invasive ventilation; no survival benefit; optimal patient selection, timing, dose, and duration uncertain

      Neuromuscular blockade

      Used in early severe ARDS; may improve mortality but limited published experience and not widely used in North America

      Conservative fluid strategy

      ↑ O2 saturation and reduced duration of invasive mechanical ventilation in single large National Institutes of Health study

      Prone positioning

      ↑ O2 saturation; no survival benefit in individual trials (signal towards mortality improvement)

      Extracorporeal membrane oxygenation

      (After H1N1, limited expr)

      May improve mortality in severe ARDS but limited published experience, limited availability

      ARDS = acute respiratory distress syndrome.

    Tag page (Edit tags)
    • No tags
    Page statistics
    15735 view(s), 10 edit(s) and 24347 character(s)

    Comments

    You must login to post a comment.

    Attach file

    Attachments