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 HYPOXEMIA
( “PUMP FAILURE” ) ( “LUNG FAILURE” )

Central Peripheral
Airways Alveolar
Nerve Nerve
Component Component
System System/
Component Chest Bellows
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
Aspiration of gastric contents
Pulmonary contusion
Toxic gas (smoke) inhalation
fractures
Near-drowning
Diffuse pulmonary infection
Indirect Lung Injury
Severe sepsis
Major trauma
Multiple long-bone
Hypovolemic shock
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
Incidence of postoperative
Procedure 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