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Acute Respiratory Failure
 

Acute Respiratory Failure

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    Acute Respiratory Failure Acute Respiratory Failure Presentation Transcript

    • ACUTE RESPIRATORY FAILURE 高雄長庚醫院胸腔內科 王逸熙
    • EFFECTIVE GAS EXCHANGE
      • Sufficient surface area for gas exchange
      • Adequate airways to conduct air to and from the gas-exchange surface
      • Ability to move gas in and out of the lungs
    • WHAT IS ACUTE RESPIRATORY FAILURE ? Rapid and significant compromise in the system’s ability to adequately exchange carbon dioxide and /or oxygen
    • Definition of respiratory failure
      • Respiratory failure is a condition in which the respiratory system fails in its gas exchange function
      • Respiratory failure is a syndrome rather than a disease
      • Respiratory failure may be acute or chronic
    • Distinctions Between Acute and Chronic Respiratory failure Category Characteristic Hyercapnic Paco2 > 45 mmHG Respiratory failure Acute Develops in min to h Chronic Develops over several days or longer Hypoxemic PaO2 < 55 mmHg,when FiO2≧0.60 Respiratory Failure Acute Develops in min to h Chronic Develops over several days or longer
    • RESPIRATORY FAILURE HYPERCAPNIA HYPOXEMIA ACUTE CHRONIC ACUTE CHRONIC
    • Definition of Acute respiratory failure
      • Acute hypoxemic respiratory failure
        • PaO2 < 55 mmHg, FiO2≧ 0.60
      • Acute hypercapnic respiratory failure
        • PaCO2 > 45 mmHg, PH < 7.3
      • In many cases, hypoxemic respiratory failure and hypercapnic respiratory failure coexist
    • Two types of respiratory failure HYPERCAPNIA ( “PUMP FAILURE” ) HYPOXEMIA ( “LUNG FAILURE” ) Central Nerve System Component Peripheral Nerve System/ Chest Bellows component Airways Component Alveolar Component
    • Type 1 Acute Respiratory Failure
      • Primary problem is impaired gas exchange
      • Primary gas exchange abnormality seen in this setting is hypoxemia
    • Type 2 Acute Respiratory Failure
      • Abnormality in type 2 ARF is impaired ventilation
      • Unable to generate sufficient minute ventilation to clear CO2---hypercapnia
    • Causes of Acute Respiratory Failure Type 1 respiratory failure Type 2 respiratory failure Parenchymal process Increased load Pneumonia Upper airway obstruction Pulmonary edema Asthma cadiogenic COPD noncardiogenic Pulmonary hemorrhage Neurological etiology Progressive interstitial process Central respiratory depression Pulmonary vascular Spinal cord injury Pulmonary embolism Peripheral nerve Pulmonary hypertension Neuromuscular junction
    • Etiology of Acute Respiratory Failure
      • 1950s--- polio
      • 1960s--- COPD
      • 1970-1980--- surgery
      • 1990s--- postoperative:20-30 %
      • nonoperative:70-80 %
        • Respiratory conditions:20-25%
        • Cardiac conditions: 20 %
        • Infection or sepsis: 20%
        • Trauma and neurological disorders: 10-15%
    • Acute Respiratory Distress Syndrome
      • Acute onset
      • Bilateral pulmonary infiltrate on CxR
      • PaO2/ FiO2 <200
      • Absence of left heart failure
    • Risk Factor of ARDS Sepsis Aspiration of gastric contents Pulmonary contusion Pneumonia Near drowning Smoke inhalation/burn Trauma Pancreatitis Multiple transfusions Pulmonary embolism Disseminated intravascular coagulation
    • Clinical Disorders Associated with ARDS Direct Lung Injury Indirect Lung Injury Aspiration of gastric contents Severe sepsis Pulmonary contusion Major trauma Toxic gas (smoke) inhalation Multiple long-bone fractures Near-drowning Hypovolemic shock Diffuse pulmonary infection Hypertransfusion Acute pancreatitis Drug overdose Reperfusion injury Post-lung transplantation Post-cardiopulmonary bypass
    • Outcome of ARDS
      • Short term mortality--- 40-60%
        • No significant improvement in recent days
      • Prognosis with ARDS vary in relation to premorbid factors
        • Cirrhosis, HIV, organ transplantation, malignancy
      • Development of nonpulmonary organ dysfunction---poor prognostic sign
      • ARDS patients generally die from multiple organ dysfunction rather than progressive respiratory failure
      • Prognosis according to disease---pneumonia, sepsis
      • Better prognosis according to disease---multiple trauma
      • Old age related to poor prognosis
    • Long-Term survival of ARDS
      • 90-day mortality: 41.2%
      • Younger patients and patient with trauma
        • Little increase in long term mortality
      • Underlying malignancy and other comorbidity
        • Significant increase long term mortality
    • Long-Term Morbidity of ARDS
      • Reduction in lung volumes
      • Reduction in diffusing capacity
      • Increase in airway resistance
      • Improvement in lung function within 1 year
      • Significant impairment of lung function in long term in 4 % of patient
      • Factors related to long term impairment
        • Prolong positive pressure ventilation
        • High FiO2
        • Increasing age
        • Severity of hypoxemia during acute illness
    • Quality of Life after ARDS
      • 43% of patients met criteria for depression
      • 43% of patient---significant functional limitations
        • Physical function
        • Respiratory symptoms
      • Significant poorer quality of life than general population
    • Short-Term mortality of COPD with Acute Respiratory Failure
      • Hospital mortality– 26 % before 1975
      • 10 % after 1975
      • Major predictor of hospital mortality
        • Prior comorbid illness & underlying nutrition
        • Baseline degree of COPD
        • Severity of acute respiratory failure upon onset
        • Etiology of acute exacerbation
        • CxR infiltration---pneumonia
        • dysrhythmia
    • Long Term survival of COPD
      • 50% of 1-year survival rate
      • 70% of long term survival with use of noninvasive ventilation
      • Poor prognostic sign
        • Persistent hypercapnia
        • Poor nutrition status
        • Increase age
    • Quality of Life after COPD Exacerbation
      • 50% of patients considered their quality of life to be good
      • 50% of patients considered their quality of life to be poor
    • ACUTE RESPIRATORY FAILURE IN THE SURGICAL PATIENT
    • Risk Factors for Postoperative Pulmonary Complication Factors related to the patient COPD Advance age Extensive (and recent) smoking history Obesity Factors related to the surgery Thoracic and upper abdominal procedures Emergency surgery Prolonged anesthesia time (>3 h) Large intraoperative blood transfusion requirements
    • Incidence of Respiratory failure Following surgery Procedure Incidence of postoperative Respiratory Failure TAAA repair 8-33 % AAA repair 5-24 % Lung resection 4-15 % CABG 5-8% All types 0.8 %
    • COPD and Postoperative Pulmonary Complication
      • 1960s, 2/3 patient with COPD had postoperative pulmonary complication, 3% of normal PFT had postoperative pulmonary complication
      • 5 % of COPD had postoperative respiratory failure
      • Preoperative FEF 25-75% < 50% and FVC <75% predicted, defined at high risk of postoperative respiratory failure – low specificity
      • Recent study with 107 consecutive operations
        • 29 % developed respiratory complication
        • 5.6 % of respiratory failure
    • COPD and Postoperative Pulmonary Complication
      • 50% of respiratory failure and death in patients with postresection FEV1< 40% of normal
      • Post- repair of thoracoabdominal aortic aneurysm
        • Respiratory failure developed in 53% of COPD
        • Respiratory failure developed in 23 % of non-COPD
      • Post- CABG
        • A significant higher percentage of Pt with COPD required mechanical ventilation in excess of 48 hours ( 18.9 vs 3.7 %) and reintubation ( 13.5 vs 3.7 %)
    • COPD and Postoperative Pulmonary Complication
      • Severe COPD affect the outcome of lung resection adversely
        • Predicted postoperative EEV1< 30-40 %--- high risk of postoperative respiratory failure
      • Undergoing cardiac procedure
        • COPD– a independent risk factor for postoperative pulmonary morbidity
      • Even severe COPD, is not a independent risk factor for postoperative respiratory failure in patients undergoing abdominal and nonresectional thoracic procedures
    • COPD and Postoperative Pulmonary Complication
      • COPD should undergo a preparatory pulmonary regimen– optimize lung function and minimize airway secretions
        • Smoking cessation
        • Institution of inhaled bronchodilator
        • Oral antibiotics in the presence of purulent secretion
        • Use of incentive spirometry
    • Smoking and postoperative pulmonary complication
      • Smoking—a risk factor for postoperative pulmonary complication, prolonged mechanical ventilatory support
      • Detrimental effects of smoking
        • Bronchial irritation with resultant excessive airway secretions
        • Impairment in mucociliary clearance, elevation of carboxyhemoglobin level
          • Impaired oxygen uptake and tissue oxygen utilization
      • Preoperative smoking cessation—reduced postoperative pulmonary complication
        • At least 8 weeks abstinence is required
    • Impact of anesthesia on pulmonary function
      • Administration of general anesthesia---either inhaled or intravenous route
        • Immediate loss of diaphragmatic and intercostal muscle tone
        • 20 % reduction of FRC
        • Development of compressive atelectasis
          • Atelectasis area make up 2-10 % of total lung volume, disappear with application of PEEP
          • Increase in shunt fraction up to 15 %
    • Impact of anesthesia on pulmonary function
      • Inhaled anesthetic agents ---respiratory depressants
        • Blunt the response to both hypoxemia and hypercapnia
        • Deposition of these agents in muscle and fat may depress hypoxic drive persist for several hours after termination of anesthesia
    • Impact of surgery on postoperative pulmonary function
      • Upper abdominal surgery
      • Cardiac surgery
      • Lung resection
    • Upper abdominal surgery
      • Within 24 h of surgery, vital capacity declines by 50 %-- persist as long as 7 days
        • Development of diaphragmatic dysfunction
          • Local irritation, inflammation, surgical trauma and pain
          • Diminished phrenic nerve output
      • Vital capacity falls only 25 % after lower abdominal surgery
    • Cardiac surgery
      • Lung volumes decreases about 30 % after CABG – return to preoperative value may take several months
      • Lung function decline to a greater degree when internal mammary harvesting and grafting
      • Shunt fraction increase from 3 % to 19 %
        • Atelectasis
        • Alteration in chest wall compliance and motion
          • Division of the sternum, harvest of internal mammary artery,
        • Injure LLL due to intraoperative lung retraction
          • Atelectasis, lung contusion
    • Cardiac surgery
      • Injury to left phrenic nerve
        • Diaphragmatic paralysis
        • About 10 % of patient
      • Cardiopulmonary bypass
        • Duration of bypass linked to the severity of postoperative atelectasis
    • Lung resection
      • Loss of lung function due to removal of lung parenchyma
      • Chest wall trauma due to thoracotomy, transection of muscle, rib retraction
      • Atelectasis
    • Causes of Postoperative Respiratory Failure Factors extrinsic to the lung Depression of central respiratory drive(anesthetics, opioids, sedatives) Phrenic nerve injury/ diaphragmatic paralysis Obstructive sleep apnea Factors intrinsic to the lung Atelectasis Pneumonia Aspiration Acute lung injury (ARDS) Volume overload/ congestive heart failure Pulmonary embolism Bronchospasm/ COPD
    • Management of Acute Respiratory failure
      • Airway Management
      • Correction of Hypoxemia and Hypercapnia
      • Search for an Underlying Cause
    • Airway Management
      • Assurance of an adequate airway
        • Whether emergent intubation or not?
    • Correction of Hypoxemia and Hypercapnia
      • Assure adequate oxygen delivery to tissue
        • achieved with a PaO2 of about 60 mmHg
        • Slight higher PaO2 in patient with CVA or CAD
      • Correct of hypercapnia
        • Less urgent in COPD with partly compensated respiratory acidosis
        • More urgent in profound respiratory acidosis in patient with drug overdose