Transcript Type II Respiratory Failure
Type II Respiratory Failure
COPD and Status Asthmaticus
Outline
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COPD Pathophysiology Dynamic Hyperinflation Approach to the Patient Status Asthmaticus Pathophysiology Presentation Therapy
Chronic Obstructive Pulmonary Disease
Acute on Chronic Respiratory Failure
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.
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.
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.
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.
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.
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.
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 CO load.
2 production from caloric and hypermetabolism from injury or inflammation imposes a higher excreation Worsened dead space may be caused by pulmonary embolism, hypovolemia, PEEP, or shallower breathing (raises the dead space fraction, Vd/Vt)
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).
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.
Selection Criteria for NIPPV
Establish need for assistance Moderate/severe respiratory distress Tachypnea Use of accessory muscles pH<7.35, PaCO 2 >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
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.
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.
Oxygen
When oxygen is given, the PCO 2 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.
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 B 2-selective agents should be given by MDI with spacer unless patient distress makes that impractical in which case a nebulizer may be used.
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.
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
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.
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 PaCO 2 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 VCO respiratory muscles.
2 from resting This combination can easily produce a pH >7.7 which is life threatening.
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 CO 2 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.
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.
Status Asthmaticus
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.
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
Imminent respiratory failure is marked by: Altered mental status Paradoxical respirations Bradycardia Quiet chest Absence of pulsus paradoxus
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.
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.
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 PaCO 2 rises due to inadequate alveolar production from the respiratory muscles.
2 The absence of hypercapnia does not preclude a severe attack nor the potential for respiratory arrest.
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.
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.
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
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.
Front Line Therapy
Inhaled B -agonists should be started immediately and aggressively.
Frequently, higher doses are needed.
Long acting treatment.
B -agonists are not indicated in initial 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.
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.
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.
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.
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).
Summary
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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.