acute respiratory failure

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


• 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 %)


• 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 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

acute respiratory failure

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