acute respiratory failure
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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 mmHGRespiratory 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” )
CentralNerve SystemComponent
PeripheralNerveSystem/Chest Bellowscomponent
AirwaysComponent
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--- polio1960s--- COPD1970-1980--- surgery1990s--- 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
SepsisAspiration of gastric contents Pulmonary contusionPneumoniaNear drowningSmoke inhalation/burnTrauma PancreatitisMultiple transfusionsPulmonary embolismDisseminated intravascular coagulation
Clinical Disorders Associated with ARDS
Direct Lung Injury Indirect Lung InjuryAspiration of gastric contents Severe sepsisPulmonary contusion Major traumaToxic gas (smoke) inhalation Multiple long-bone fracturesNear-drowning Hypovolemic shockDiffuse 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 ObesityFactors 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
ProcedureIncidence 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 apneaFactors 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
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