Type II Respiratory Failure

1. Type II Respiratory Failure COPD and Status Asthmaticus

2. Outline • COPD • Pathophysiology • Dynamic Hyperinflation • Approach to the Patient • Status Asthmaticus • Pathophysiology • Presentation • Therapy

3. Chronic Obstructive Pulmonary Disease Acute on Chronic Respiratory Failure

4. Pathophysiology • Alveolar ventilation is maintained by the CNS, which acts through nerves and the respiratory muscles. • The three subsets of ventilatory failure are loss of drive, impaired neuromuscular competence, and excessive load. • Few patients have a loss of drive and usually occurs in the setting of drug/alcohol overdose or physician-directed sedation.

5. Pathophysiology • Inspiratory muscle fatigue is the primary mechanism. • A muscle fatigues when its energy consumption exceeds that supplied by blood flow. • In an acute exacerbation, respiratory muscle oxygen consumption can rise to 17-46% of total body consumption. • The most significant contributor to elastic load is dynamic hyperinflation.

6. Dynamic Hyperinflation • Airflow obstruction prolongs expiration. • When the rate of alveolar emptying is slowed, expiration cannot be completed before the next inspiration. • Therefore, the lung fails to reach FRC at the end of each breath and there remains a positive elastic recoil pressure which is called intrinsic PEEP (PEEPi). • Greater effort must be generated to initiate a breath due to the PEEPi.

8. Dynamic Hyperinflation • At the same time that the load is increased, the respiratory muscles are forced to operate in a disadvantageous position of the force-length relationship. • Diaphragm strength is only 2/3 normal in stable COPD patients which is due diaphragm position and not inherent muscle weakness.

9. Dynamic Hyperinflation • Patients with dynamic hyperinflation also frequently have other conditions such as malnutrition and steroid induced myopathy that causes intrinsic muscle weakness. • Patients with severe COPD live a balanced life between increased load and diminished neuromuscular competence. • Any minor decrement in strength or increase in load are enough to precipitate muscle fatigue and respiratory failure.

10. Other Causes of Increased Load • Resistive load • Airway resistance is increased by bronchospasm, airway inflammation, and mucous plugging. • Superimposed heart failure may also increase airway resistance. • Tracheal stenosis should be considered in patients with previous intubations. • Sleep-disordered breathing commonly coexists with COPD also needs to be excluded.

11. Other Causes of Increased Load • Increased lung elastic load • Pulmonary edema, pneumonia, interstitial fibrosis, tumor, and atelectasis all contribute to increased lung stiffness. • Minute ventilation load • An increase in CO2 production from caloric intake, fever, agitation, muscular exertion, and hypermetabolism from injury or inflammation imposes a higher excreation load. • Worsened dead space may be caused by pulmonary embolism, hypovolemia, PEEP, or shallower breathing (raises the dead space fraction, Vd/Vt)

12. Approach to the Patient: Early Acute on Chronic Failure • The goal in the patient not yet intubated is to avoid mechanical ventilation when possible and to recognize progressive respiratory failure when it is not. • NIPPV is a proven therapy that can avert intubation in up to 75% of patients with ACRF. • It is not a cure but buys the physician time to treat the precipitants of ACRF and for the patient to improve. • Current guidelines recommend NIPPV as first-line therapy for COPD-related acute on chronic respiratory failure (ACRF).

13. Approach to the Patient: Early Acute on Chronic Failure • NIPPV has been shown to relieve symptoms, reduce respiratory rate, increase tidal volume, improve gas exchange and reduce diaphragmatic work. • Complications are few and minor; local skin breakdown from the mask is simple to treat. • Careful patient selection is essential for successful NIPPV.

14. Selection Criteria for NIPPV • Establish need for assistance • Moderate/severe respiratory distress • Tachypnea • Use of accessory muscles • pH<7.35, PaCO2>45, or P/F ratio<200 • Exclusions • Respiratory arrest • Medically unstable • Unable to protect airway • Excessive secretions • Severe agitation • Unable to fit mask • Recent upper airway or GI surgery

15. NIPPV • A risk of NIPPV is its potential to lull the team into a sense of comfort while the patient continues to worsen. • Time spent trying NIPPV may potentially lead to a later, more urgent intubation in an exhausted patient with greater tissue hypoxia. • Avoiding intubation is always dependant on discerning the cause of ACRF and reversing it.

16. Oxygen • One of the greatest myth of mankind is that patients rely on hypoxic drive to breathe. • As a result, oxygen is withheld and the underlying hypoxia is left untreated. • This leads to worsening acidemia, fatiguing respiratory muscles, failing right ventricle, arrhythmias, myocardial ischemia, cerebral injury, and respiratory arrest.

17. Oxygen • When oxygen is given, the PCO2 may rise but this is due to worsened V/Q matching and the Haldane effect, not to hypoventilation. • The goal of oxygen therapy is to maintain 90% saturations which can usually be attained with 3-5 L/min. • Patients may still progress to respiratory failure despite oxygen therapy, but not because of it.

18. Pharmacotherapy • Bronchodilators are an essential part of the management even though most of the airflow obstruction is irreversible as most patients have some reversible component. • Inhaled B2-selective agents should be given by MDI with spacer unless patient distress makes that impractical in which case a nebulizer may be used.

19. Pharmacotherapy • The addition of ipratropium yields increment benefit in patients with stable COPD but does not result in improved bronchodilation in acute exacerbation. • Patients given steroids demonstrate improvement within 12 hours. • Current guidelines recommend methylprednisolone 0.5-1 mg/kg every 6 hours during the acute exacerbation with a transition to oral therapy when tolerated. • Bacterial bronchitis is a common precipitant of ACRF and appropriate coverage for CAP should be started empirically.

20. Recognizing Impending Respiratory Failure • Some patients will progress to frank respiratory failure despite aggressive attempts to find and reverse the causes. • The decision to intubate requires clinical judgment and is best assessed by the physician present AT THE BEDSIDE. • Assessment of respiratory failure based solely on results of ABGs is fraught with errors. • Useful bedside parameters include increasing respiratory rate (despite NIPPV), decreasing mentation, pattern of breathing (abdominal paradox and respiratory alternans), and the patient’s own assessment

21. Peri-intubation Risks • There are two pitfalls in the postintubation period: hypotension and alkalosis. • Hypotension is a consequence of increasing PEEPi following intubation resulting from manual hyperinflation. • PEEPi reduces venous return which is aggravated by reduced preload and right heart dysfunction. • In addition, the medications used during intubation have vasodilatory and sympatholytic properties. • The circulation can be restored by holding ventilation for 30 seconds (to reduce PEEPi) in addition to volume and bolus vasopressors as needed.

22. Peri-intubation Risks • Most patients have a minute ventilation of 10 L/min and tidal volume of 300 mL. • Higher minute ventilation can occur during bagging and inappropriate ventilator settings. • This cause the PaCO2 to be driven down in combination with a pre-existing compensatory metabolic alkalosis that produces a sever metabolic alkalosis. • This is further aggravated by a fall in VCO2 from resting respiratory muscles. • This combination can easily produce a pH >7.7 which is life threatening.

23. Improving Neuromuscular Competence • Malnutrition is a common comorbidity of advanced COPD and may contribute to respiratory muscle dysfunction. • However, excessive refeeding can cause high levels of CO2 production and should be avoided. • Once the muscles are rested, a program of exercise should be initiated in conjunction with daily readiness for liberation from mechanical ventilation screens. • The goal is to encourage muscle power, tone and co-ordination by allowing the patient to assume nonfatigueing respirations. • After a period of work, the patient is returned to full rest on the ventilator to facilitate sleep. • As strength improves, the amount of exercise is increased until the patient is liberated from the ventilator.

24. Decreasing Load • It is important to continue treatment with bronchodilators either with nebulizers or MDI. • Other contributors to increased load such as CHF, PE, and pneumonia should be sought and treated.

25. Status Asthmaticus

26. Characteristics • Asthma is characterized by wheezing, dyspnea, cough, hyper-reactive airways, and reversible airflow obstruction. • Usually, an exacerbation is managed uneventfully in an ambulatory setting. • However, severe attacks and death can occur regardless of disease classification and sometimes with little warning.

27. Severe asthma is defined as: • Dyspnea at rest • Upright positioning • Inability to speak in phrases or sentences • Respiratory rate > 30 • Use of accessory muscles • Pulse > 120 • Pulsus paradoux > 25 mmHg • Peak expiratory flow rate < 50% predicted • Hypoxemia • Eucapnia or hypercapnia

28. Imminent respiratory failure is marked by: • Altered mental status • Paradoxical respirations • Bradycardia • Quiet chest • Absence of pulsus paradoxus

29. Pathophysiology • Exacerbations often evolve over hours to days before patients seek medical care. • Airway inflammation leads to plugging of large and small airways with tenacious mucus. • Mucus plugs consists of sloughed epithelial cells, eosinophils, and fibrin that leak through the denuded epithelium.

30. Pathophysiology • Smooth muscle bronchospasm occurs in all patients but a small subset have a sudden onset with intense spasm and little inflammation. • This is can be lethal but also can also improve rapidly with bronchodilators. • Triggers include NSAIDS, B-blockers, allergens, exercise, stress, sulfites, and cocaine. • Respiratory tract infections are not a usual trigger.

31. Gas Exchange Abnormalities • Airway obstruction causes V/Q mismatch. • Shunting is trivial so small amounts of oxygen corrects hypoxemia. • Refractory hypoxia is rare and suggests additional pathology. • As the severity of obstruction increases, the PaCO2 rises due to inadequate alveolar ventilation and increased CO2 production from the respiratory muscles. • The absence of hypercapnia does not preclude a severe attack nor the potential for respiratory arrest.

32. Circulatory Effects of Severe Airway Obstruction • High intrathoracic pressures during expiration: • Decrease right-sided preload • Vigorous inspiration: • Augments RV filling • Shifts the septum into the left ventricle • Diastolic dysfunction • Incomplete LV filling • Impaired LV emptying • Lung hyperinflation: • Increases RV afterload • Transient pulmonary hypertension • This is the basis for pulsus paradoxus.

33. Clinical Presentation: Medical History • Characteristics of prior exacerbations that can predict fatal or near fatal episodes include: • Intubation • Hypercapnia • Barotrauma • Hospitalization despite steroids • Psychiatric illness • Medical noncompliance • Intubation is the greatest single predictor of death.

34. Other concerning features are long symptom duration, late arrival to care, fatigue, altered mental status, sleep deprivation. • The absence of a history of asthma should prompt a search for other diagnoses: • COPD • CHF • Foreign body aspiration • Upper airway obstruction • Pneumonia • PE

35. Clinical Presentation: Physical Exam • The posture, pattern of speech, positioning, and level of alertness is the best marker of patient condition and response to therapy. • Airflow obstruction is determined by PEFR and is a good way to assess and follow patients. • < 50% predicted or personal best indicates a severe exacerbation • Hypercapnia on ABG indicates impending respiratory failure. • Anion gap acidosis is usually due to excess lactate from increased work of breathing and tissue hypoxia.

36. Front Line Therapy • Inhaled B-agonists should be started immediately and aggressively. • Frequently, higher doses are needed. • Long acting B-agonists are not indicated in initial treatment. • Subcutaneous administration is not indicated unless the patient is unable to carry out inhaled therapy but is associated with greater toxicity. • SC epinephrine may be beneficial in non-responders. • MDI with spacer and nebulizer are equally effective in delivering treatment. • Combination therapy with ipratropium and albuterol results in greater bronchodilation compared to either alone.

37. Front Line Therapy • Systemic steroids should given quickly on initial presentation. • Oral (prednisone 80 mg) or IV (methylprednisolone 125 mg) routes are equally effective, but oral should be avoided if intubation is an issue. • There is no added benefit of inhaled steroids during the acute phase.

38. Other Therapies • Magnesium: May be beneficial in severe attacks but the jury is still out. • Leukotriene modifiers: Preliminary data suggests benefit in acute attacks. • Heliox: Less dense so reduces turbulent flow to improve gas delivery. May mask worsening obstruction so there is less time and margin for error when intubation required. • Antibiotics: Infectious triggers are rare so antibiotics likely have no role. • NIPPV: Decreases work of breathing and may prevent some intubations.

39. Intubation • The goals of intubation are to maintain oxygenation and prevent respiratory arrest. • 40% of deaths in ventilated asthmatics are due to cerebral anoxia from respiratory arrest prior to intubation. • Changes in posture, mental status, speech, accessory muscle use, and respiratory rate indicate failure better than an ABG or PEFR. • The decision to intubate is best made by a clinician at the bedside based on their estimation of the patient’s ability to maintain spontaneous respiration.

40. Postintubation Hypotension • Hypotension occurs in 30% of patients and has several causes: • Loss of sympathetic tone from sedation • Prehospitalization hypovolemia • Dynamic hyperinflation (DHI) from overzealous bagging • DHI can be confirmed by a trial of hypopnea. • Improvement after this trial does not exclude tension pneumothorax (responsible for 6% of ventilated asthmatic deaths).

41. Summary • COPD exacerbations are often multi-factorial in origin. • NIPPV is proven to reduce risk of intubation and mortality. • Asthma attacks can be sudden and lethal even in patients with no past history of severe attacks. • 40% of deaths in asthma are due to anoxia in the peri-intubation phase. Do not delay intubation if it appears inevitable. • Consider dynamic hyperinflation as a cause for post-intubation hypotension.