Pulmonary Physiology Flashcards

1
Q

OSA: ____________ secondary to reduction in ___________ tone during sleep

A

mechanical obstruction, pharyngeal muscle

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2
Q

OHS: _________________ with no mechanical, neuromuscular, or metabolic etiology

A

obesity/sleep-disordered breathing/daytime hypoventilation

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3
Q

Most significant risk factor

A

Obesity

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4
Q

______ of obese patients and
_______ of patients presenting for bariatric surgery
Increasing prevalence in _________ patients

A

40%, 80%, pediatric

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5
Q

OSA is associated with increased ____________ in hospitalized patients

A

morbidity/mortality

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6
Q

OSA results in chronic _________ leading to an inflammatory state

A

hypoxemia and hypercarbia

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7
Q

OSA inflammatory state promotes the development of:

A

atherosclerosis, hypertension, stroke, insulin resistance/diabetes mellitus, dyslipidemia, etc.

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8
Q

T/F: OSA decreases FRC

A

True- decreased apneic oxygen reserve, contributes to hypoxemia and hypercarbia

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9
Q

Hallmark of OSA

A

daytime somnolence due to habitual snoring and fragmented sleep

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10
Q

_________ provides definitive objective diagnosis and gradation of severity

A

Polysomnography

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11
Q

What is the Apnea Plus Hypopnea (AHI) Index?

A

number of abnormal respiratory events per hour of sleep

READ THIS:
>5 with sleep-related symptoms or >15 without sleep-related symptoms
Moderate OSA: >15
Severe OSA: >30

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12
Q

What does STOP stand for?

A

S- Snoring
T- tiredness
O-observed apnea
P- high blood pressure

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12
Q

What does BANG stand for?

A

B- Body mass index >35 kg/m2
A- Age > 50 years
N- Neck circumference > 40 cm
G- Gender, male

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13
Q

Lifestyle treatment for OSA

A

Weight loss

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14
Q

Medical treatment for OSA

A

CPAP, airway devices, medications (modafinil, methylxanthines, tricyclic antidepressants)

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15
Q

Surgical treatment for OSA

A

adenotonsillectomy, uvulopalatopharyngoplasty, hypoglossal nerve stimulator

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16
Q

Induction considerations for OSA

A
  • Anticipate difficult mask ventilation/laryngoscopy
  • decreased FRC= decreased apneic oxygen time
  • Elevate head and shoulders (ramping)
  • Have airway adjuncts (LMA/videolaryngoscope) available
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16
Q

Preoperative considerations for OSA:

A
  • Bring CPAP on day of surgery
  • Airway examination- anticipate difficult mask ventilation/laryngoscopy
  • Mallampati and neck circumference
  • Consider regional anesthesia or multimodal analgesia (minimize need for meds that produce sedation)
  • Minimize/avoid sedatives (patient with OSA may be more sensitive to sedative effects)
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17
Q

Emergence considerations for OSA

A
  • Consider awake extubation
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18
Q

Postoperative considerations for OSA

A
  • Monitor ventilation and oxygenation
  • Consider CPAP in PACU
  • Consider prolonged monitoring (6 -24 hours)
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19
Q

What is preventable and treatable disease state characterized by airflow limitation that is not fully reversible. The airflow limitation is usually progressive and is associated with an abnormal inflammatory response of the lungs to noxious particles or gases

A

COPD

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20
Q

Chronic bronchitis: ____________ of expiratory airflow by excess ____________.

A

Obstruction, mucous secretion

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21
Q

Chronic bronchitis occurs most days for at least __________ per year for at least ______ successive years

A

3 months, 2

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22
Q

Emphysema is _________ abnormal enlargement of air spaces distal to the terminal bronchioles accompanied by irreversible destruction of _________ ________.

A

permanent, alveolar walls

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23
______lobular: predominantly affects respiratory bronchioles in upper lung lobes
Centrilobular
24
______lobular: widespread destruction of acini
Panlobular
25
What is the most significant risk factor for COPD?
Cigarette smoking (Others: Environmental pollutants, genetics)
26
COPD is ______ leading cause of death; ~___% of American adults
3rd, 5 Death may be secondary to respiratory failure or related comorbidities (e.g., heart disease, lung cancer)
27
COPD pathophysiology: * _________ in intrinsic size of bronchial lumina * _________ in collapsibility of bronchial walls * __________ in elastic recoil of the lungs
Decrease, increase, decrease
28
COPD pathophysiology:
1. Increased size of acini/alveoli causes compression of adjacent small airways, thereby increasing resistance to airflow 2. Consolidation of alveoli leads to loss of alveolar surface area and impaired gas diffusion 3. Mismatched ventilation/perfusion due to heterogeneity of the disease 4. Loss of alveolar walls decreases the number of pulmonary capillaries, which increases right ventricular workload
29
Hallmark for COPD
chronic productive cough and progressive exercise limitations
30
Clinical manifestations for COPD
dyspnea, wheezing
31
Pulmonary Function Testing (i.e., GOLD Classification) FEV1 >80%(or equal to) = ________ FEV1 50%-79% = ________ FEV1 30%-49% = ________ FEV1 <30% = ________
mild, moderate, severe, very severe
32
ABG of someone with COPD
PaO2 <60 mm Hg PaCO2 >45 mm Hg
33
Lifestyle treatment for COPD
smoking cessation, influenza vaccination
34
Medical treatment for COPD
bronchodilation: B2-agonists, anticholinergics, corticosteroids
35
Surgical treatment for COPD
bullectomy, lung volume reduction surgery (LVRS), lung transplantation
36
Preoperative considerations for COPD
* Assess symptoms, severity of airflow limitation, history of exacerbations, and comorbidities * Cough, dyspnea, chest discomfort, and fatigue are signs/symptoms of acute exacerbation * Consider regional anesthesia
36
Maintainence for COPD
* Volatile anesthetics promote bronchodilation * Consider humidification of inspired gas * Ventilation * Maintain adequate oxygenation * Eliminate CO2 * Avoid barotrauma (high PIP) * Avoid alveolar injury secondary to atelectasis * Avoid volutrauma secondary to high Vt or auto-PEEP
37
Postoperative Considerations
* Consider postoperative mechanical ventilation * Incentive spirometry
38
Chronic inflammatory disorder of the airways in which many cells and cellular elements play a role… In susceptible individuals, this inflammation causes recurrent episodes of coughing (particularly at night or in the early morning), wheezing, breathlessness, and chest tightness. These episodes are usually associated with widespread but variable airflow obstruction that is often reversible either spontaneously or with treatment.”
Asthma
39
What are the four pathophysiological alterations of asthma?
1. Bronchoconstriction – bronchial smooth muscle contraction that narrows airways in response to variety of stimuli 2. Airway hyperresponsiveness – exaggerated bronchoconstrictor response to stimuli 3. Mucous secretion – hypersecretion of mucin 4. Airway edema
40
Allergic asthma is triggered by
presentation of antigens
41
(Asthma) Antigens provoke
T-lymphocytes to generate an IgE-mediated immune response
42
(Asthma) Proinflammatory cascade results in
proliferation of eosinophils, neutrophils, mast cells, and macrophages
43
(Asthma) results in
1. increased smooth airway muscle tone (bronchoconstriction) 2. increased mucous secretion 3. submucosal edema 4. pulmonary vasoconstriction and increased vascular permeability
44
Type of asthma that may be related to high minute ventilation or low temperature/humidity of inspired gas
Exercise
45
Type of asthma that causes inhaled irritants to stimulate vagal nerve endings in the airway epithelium
Occupational
46
(Asthma) Secondary to acute inflammation due to viral/bacterial/mycoplasmal infection
Infection (I know this is redundant lol)
47
Type of asthma that results in inhibition of cyclooxygenase results in greater production of leukotrienes
Aspirin
48
Clinical manifestations of asthma
Recurrent wheezing, dyspnea, cough, tachypnea, chest tightness, fatigue
49
Asthma attacks are short-lived, lasting ______ long symptom-free periods between attacks
minutes to hours
49
Airflow obstruction that is refractory to bronchodilator therapy is known as
Status asthmaticus
50
During exacerbations, airflow obstruction is indicated by
decreased FEF25-75%
51
Asthma preoperative considerations
* Review symptom control prior to surgery (pulmonary function, medication use) * Consider canceling the procedure if optimization is necessary * Consider regional anesthesia
52
Asthma induction considerations:
* Avoid endotracheal intubation if possible; consider supraglottic airway if appropriate * Ketamine> Propofol > Etomidate/Barbiturates
53
Asthma maintenance considerations
* Consider use of sevoflurane, least irritating volatile anesthetic * Avoid atracurium, mivacurium, morphine, B-antagonists, Hemabate, NSAIDs
54
Asthma emergence considerations
* Consider deep extubation * Consider use of Sugammadex; anticholinesterase reversal agents have risk of bronchospasm * Verify adequate reversal of neuromuscular blockade
55
Intraoperative Bronchospasm: (Way to remember- a1b2eca)
1. Administer additional anesthetic agents 2. Increase FiO2 to 1.0 (100%) 3. Administer short acting B2-agonist (albuterol) 4. Consider administering epinephrine 10 mcg/kg 5. Administer a corticosteroid (hydrocortisone 2-4 mg/kg) 6. Consider administering aminophylline
56
PH is defined as:
Mean Pulmonary Artery Pressure >25 mm Hg
57
PH has Rapid disease progression; _______ mortality rate is 79%
5-year Mortality is primarily related to the integrity of the right ventricle, which is in turn related to the degree of increase in pressure in the pulmonary circulation
58
PH: Factors predictive of perioperative mortality include
major surgery, emergency surgery, long operative time, use of general anesthesia, and increased NYHA functional class (May be caused by COPD, connective tissue disorders, sarcoidosis, drug effects, and genetics/idiopathic)
59
PH Patho: * __________ vascular tone * Growth and proliferation of _________________ * Irreversible increase in PVR/PAP * Right ventricular overload culminating in cor pulmonale
Increased, pulmonary vascular smooth muscle
60
Hallmark for PH
dyspnea/ exercise intolerance
61
PH Induction considerations
* Consider ECG, echocardiogram, chest x-ray and ABG * Continue medications for PAH * Consider regional anesthesia
61
Diagnosis for PH (Studies)
* Doppler echocardiography- velocity of tricuspid regurgitation correlates with invasive PAP measurements * Cardiac catheterization- provides information about pressures in the pulmonary system and heart * Vasodilator challenge- administration of pulmonary vasodilator (nitroglycerin, isoproterenol) to assess reversibility of PAH
62
PH Maintenance considerations
* Neuraxial anesthesia may cause significant hemodynamic alterations * Etomidate or high-dose opioids may be preferable to minimize cardiac depression * Consider arterial blood pressure monitoring * Consider central venous catheter for major procedures
63
Cause of acute cor pulmonale
PE
63
What is Cor Pulmonale
Right heart failure secondary to pulmonary pathology
64
Cor pulmonale is ______ most common cardiac disorder in people greater than 50 years of age
third (Five times more prevalent in males)
65
Cause of chronic cor pulmonale
COPD
66
Clinical manifestations of cor pulmonale
Cough, dyspnea, weakness, fatigue, hemoptysis, jugular venous distension, S3 gallop, S4 heart sound, murmur, hepatomegaly, ascites, dependent edema
67
Preoperative considerations for cor pulmonale
Consider regional anesthesia
67
(PH) Doppler echocardiography and cardiac catheterization
velocity of tricuspid regurgitation correlates with invasive PAP measurements provides information about pressures in the pulmonary system and heart
68
Medical and surgical treatment for cor pulmonale
Administer O2, Medications (prostanoids, endothelin receptor antagonists, phosphodiesterase inhibitors, diuretics) heart/lung transplant
69
Maintenance for cor pulmonale
* Maintain adequate oxygenation * Avoid acidosis * Avoid stimuli that increase sympathetic tone * Avoid hypothermia
70
Pulmonary Embolism (PE)
Occlusion of pulmonary blood flow by embolic material, resulting in obstruction of pulmonary blood flow and resultant mismatch of ventilation and perfusion
71
PE Occurs in ____% of surgical patients
1%
72
PE occurs in ___% of orthopedic surgical patients
30%
73
PE is usually caused by a DVT from the __________ vessels
PE is usually caused by a DVT from the **ileofemoral vessels**
74
Causes of PE
1. DVT 2. Air 3. CO2 4. Tumor 5. Bone 6. Fat 7. Amniotic fluid 8. catheter fragments
75
Virchow's Triad
1. Venous stasis 2. Venous Injury 3. Hypercoaguable state
76
List the stepwise pathophysiology of PE:
1. thrombus formation 2. release of thrombus into circulation 3. Occlusion of pulmonary circulation 4. Increased PVR proximal to occlusion, decreased perfusion distal to occlusion 5. V/Q mismatch 6. Alveolar Damage
77
Hallmark signs of PE:
1. sudden onset of dyspnea 2. sudden decrease in EtCO2
78
Clinical manifestations of PE
1. hypotension 2. tachycardia 3. hypoxemia 4. wheezing 5. tachypnea
79
PE clinical presentation is primarily determined by [...]
PE clinical presentation is primarily determined by the **size of the embolus**
80
Treatment of PE:
1. Medical: thrombolytic agents; anticoagulation 2. embolectomy; IVC filter insertion
81
Anesthetic Management of PE: Induction: _______ (cardiac stable) Avoid _____ & _____ (increase PVR) Maintenance: high _____ monitor ____ & ____
Anesthetic Management of PE: Induction: Etomidate (cardiac stable) Avoid Ketamine & N2O (increase PVR) Maintenance: high Fio2; monitor CVP/PAP
82
Treatment for Intraoperative PE: 1. Increase _____ 2. Discontinue _____ 3. Administer ___ & ___ as needed 4. Administer ___ & ____ for ventricular dysrhythmias 5. Prepare for ____ or _____ 6. Consider ____ as a temporizing measure
Treatment for Intraoperative PE: 1. Increase Fio2 2. Discontinue anesthetic agents 3. Administer sympathomimetics & IVF/blood as needed 4. Administer lidocaine & amiodarone for ventricular dysrhythmias 5. Prepare for thrombolysis or pulmonary embolectomy 6. Consider CPB as a temporizing measure
83
Restrictive Pulmonary Disease (Pulmonary Edema):
Conditions that interfere with normal lung expansion during inspiration
84
Acute intrinsic causes of restrictive pulmonary disease
1. pulmonary edema 2. aspiration pneumonitis 3. ARDS
85
Chronic intrinsic causes of restrictive pulmonary disease
1. idiopathic pulmonary 2. fibrosis 3. sarcoidosis 4. radiation injury
86
Chronic extrinsic causes of restrictive pulmonary disease
1. flail chest 2. pneumothorax 3. pleural effusion
87
Pulmonary edema refers to [...]
Pulmonary edema refers to **accumulation of excess fluid in interstitium and alveoli**
88
in pulmonary edema, Accumulation of excess fluid is usually caused by
1. increased pulmonary capillary hydrostatic pressure 2. decreased intravascular colloid oncotic pressure
89
Negative-pressure pulmonary edema may result from
acute airway obstruction
90
Risk Factors for negative pressure pulmonary edema:
1. young patients 2. male gender 3. delayed recognition/prolonged treatment of airway obstruction 4. excessive administration of intravenous fluids
91
Pathophysiology of pulmonary edema:
1. Imbalance of Starling’s forces leads to pulmonary edema
92
Cardiogenic pulmonary edema pathophysiology
Cardiogenic - high pulmonary capillary pressure (i.e. CAD, HTN, cardiomyopathy, mitral valvular disease)
93
Non-cardiogenic pulmonary edema pathophysiology
Non-cardiogenic - increased permeability of the alveolar-capillary membrane (i.e. Sepsis, ARDS)
94
hallmark sign of pulmonary edema:
pink frothy sputum
95
Clinical Manifestations of Pulmonary Edema
1. tachypnea 2. accessory muscle use' 3. tachycardia 4. hypertension 5. diaphoresis 6. basilar crackles on auscultation
96
Pulmonary edema CXR:
* Enlargement of cardiac silhouette * ‘White-out’ appearance
97
Treatment for pulmonary edema:
Medical: administer O2, consider CPAP or mechanical ventilation, restrict fluid administration, medications (morphine, nitroprusside, inotropes)
98
Aspiration Pneumonitis
Movement of gastric contents from the stomach to the lungs that results in chemical injury to the lung tissue
99
Overall incidence of aspiration pneumonitits
~1/3000 anesthetics ~1/1500 emergency anesthetics or cesarean deliveries
100
Aspiration pneumonitis Occurs when protective _____ _______ are inhibited; usually occurs after ______ or gastroesophageal reflux
Occurs when **protective airway reflexes** are inhibited; usually occurs after **vomiting** or gastroesophageal reflux
101
Risk factors for aspiration pneumonitis:
1. emergency surgery with a full stomach 2. bowel obstruction 3. pregnancy 4. acute trauma
102
List the stepwise pathophysiology of aspiration pneumonitis:
1. Immediate damage to lung parenchyma by caustic aspirate 2. Atelectasis develops within minutes, leading to airway closure and decreased compliance 3. Alveolar macrophages release inflammatory cytokines (IL-8, TNF-alpha), which attract neutrophils that in turn release oxygen radicals and proteases 4. Secondary injury results from fibrin deposition and alveolar necrosis
103
Aspiration Pneumonitis causes:
Damage to alveolar-capillary membrane * Impaired gas exchange * Hypoxemia * Initial hypocarbia due to hyperventilation * Subsequent hypercarbia * Capillary leak * Flooding of interstitium and alveoli with protein rich fluid * Protein-rich fluid may inactivate surfactant, further contributing to decreased compliance
104
Aspiration Pneumonitis hemodynamic changes
* Myocardial ischemia and acidosis secondary to hypoxemia * Reduced CO and hypotension
105
Hallmark of aspiration pneumonitis:
arterial hypoxemia
106
Clinical Manifestations of aspiration pneumonitis:
1. tachypnea 2. dyspnea 3. cyanosis 4. tachycardia 5. hypertension
107
Diagnosis of aspiration pneumonitis is made by ____ and ______
Diagnosis is made by **ABG and chest radiography** * Chest radiography demonstrates aspirate in perihilar and dependent lung regions
108
Differential Diagnosis for aspiration pneumonitis:
have high concern in an otherwise healthy patient who develops unexplained/sudden hypoxemia intra- or postoperatively
109
Treatment for aspiration pneumonitis:
Medical- ventilation (consider low FiO2, consider PEEP), consider steroids, consider lidocaine 1.5 mg/kg, avoid routine administration of antibiotics, avoid routine use of deep tracheal suctioning/bronchoscopy
110
Preoperative considerations for aspiration pneumonitis:
* NPO * Recognize risk factors * Pharmacologic prophylaxis * Nonparticulate antacid (sodium citrate with citric acid) * H2 receptor antagonist (famotidine) * PPI (pantoprazole) * antiemetics (ondansetron)
111
Induction for aspiration pneumonitis:
Induction * Consider RSI with cricoid pressure * Consider videolaryngoscopy * If vomiting, reflux, or aspiration occur during induction * Tilt the patient’s head downward or turn the patient to the left side * Suction the oropharynx/ETT * Consider applying PEEP * Consider postponing surgery
112
Maintenance for aspiration pneumonitis:
Maintenance * Avoid excessive administration of sedating medication * Evacuate the stomach
113
Emergence for aspiration pneumonitis:
* Awake extubation * Verify adequate reversal of neuromuscular blockade
114
Acute Respiratory Distress Syndrome (ARDS)
Condition occurring in critically ill patients in which fluid accumulates in the alveoli, resulting in a mismatch of ventilation and perfusion
115
* Risk for developing ARDS is additive 1 risk factor- __% 2 risk factors- __% 3 risk factors- ___%
* Risk for developing ARDS is additive 1 risk factor- 25% 2 risk factors- 42% 3 risk factors- 85%
116
Major Risk Factors for ARDs
1. sepsis 2. bacterial pneumonia 3. trauma 4. aspiration pneumonitis
117
Other risk factors for ARDs:
Miscellaneous- disease of the central nervous system, pancreatitis, uremia, DIC, anaphylaxis, coronary artery bypass grafting, transfusion reactions
118
ARDS has a mortality rate of ___ %
ARDS has a mortality rate of ~50%
119
List the stepwise pathophysiology of ARDs:
1. Damage to the alveolar-capillary membrane leads to diffuse inflammatory response 2. Capillary endothelium- releases cytokines and membrane-bound phospholipids, complement system- activates leukocytes and macrophages, produces microemboli 3. Pulmonary vasoconstriction, bronchoconstriction, altered vascular reactivity/permeability 4. Increased PVR with possible development of cor pulmonale
120
Hallmark feature of ARDs:
noncardiogenic pulmonary edema
121
Clinical Manifestations of ARDs:
1. dyspnea, hypoxemia 2. diffuse bilateral pulmonary infiltrates 3. decreased pulmonary compliance
122
ARDS is precipitated by [...]
ARDS is precipitated **by a noxious event (e.g., trauma, bacterial pneumonia)**
123
Treatment for ARDs:
Medical- 1. Lung protective ventilation (supplemental O2) 2. afterload reduction/inotropic support, 3. prone positioning 4. iNO
124
Anesthetic Management for ARDs:
Maintenance * Ventilation * Consider Vt 6-8 mL/kg IBW * Consider PEEP * Avoid PIPs >30 cm H2O * Avoid excessive administration of IV fluids * Consider monitoring arterial blood pressure, central venous pressure, cardiac output, urinary output
125
Simple Pneumothorax- define
accumulation of air in pleural space; no communication between plural space and atmosphere | treatment: catheter aspiration & tube thoracostomy
126
Tension Pneumothorax- define
progressive accumulation of air in pleural space that results in mediastinal shift | Tx: * needle thoracostomy * tube thoracostomy
126
Communicating Pneumothorax- define
accumulation of air in pleural space due to communication between pleural space and atmosphere | tx: * semi-occlusive dressing * supplemental O2 * tube thoracostomy
127
Hemothorax- define
accumulation of blood in pleural space | Tx: * tube thoracostomy * consider blood transfusion
128
Hallmark signs of Tension Pneumothorax:
1. decreased SpO2 2. increased peak inspiratory pressures 3. tachypnea 4. hypotension 5. tachycardia
129
Clinical Manifestions of Tension Pneumothorax:
1. asymmetric chest wall movement 2. tracheal shift 3. hyperresonance
130
Differential diagnosis for tension pneumothorax:
have high concern in patient with history of chest trauma who develops acute decrease in pulmonary compliance
131
Atelectasis:
Pathologic condition characterized by abnormal alveolar gas exchange due to airway collapse
132
Atelectasis occurs in ~___% of patients who receive general anesthesia
Atelectasis occurs in **90% of patients who receive general anesthesia** ## Footnote Develops within minutes; may persist for hours or days * Usually subclinical and resolves within 24-48 hours
133
Ateletasis is most common after _____/______ surgery Most common cause of postoperative ______ ________
Most common after **thoracic/upper abdominal surgery** Most common cause of **postoperative respiratory dysfunction**
134
List the stepwise pathophysiology of atelectasis:
1. Blockage or obstruction of airways results in: 2. closure of small airways, 3. with absorption of alveolar oxygen, 4. eading to alveolar collapse 5. which prevents alveolar gas exchange V/Q mismatch
135
In atelectasis, blockage or obstruction of airways may result from:
1. compression of lung tissue 2. impaired surfactant, 3. absorption of oxygen from nitrogen-free alveoli
136
Anesthetic Management of atelectasis:
Ventilation * Conside Vt 6-8 mL/kg IBW * Consider PEEP * Consider low FiO2 * Consider vital capacity maneuver * Consider open-lung ventilation
137
Postoperative Considerations for atlectasis:
* Incentive spirometry * Consider CPAP in PACU
137
Pleural Effusion
Accumulation of excess pleural fluid within the pleural space, secondary to disease or pathology of adjacent structures
138
List the stepwise pathophysiology of pleural effusion:
1. Blockage of lymphatic drainage from the pleural cavity 2. Increased pulmonary capillary pressure (secondary to cardiac failure) with eventful transudation of fluid into pleural cavity 3. Decreased plasma colloid osmotic pressure 4. Infection/inflammation of pleura resulting in altered capillary membrane permeability
139
Treatment of pleural effusion:
Surgical- tube thoracostomy, thoracentesis, pleurodesis
140
NPO guidelines: 1. Clear liquids 2. Breast milk 3. Nonhuman Milk/ infant formula 4. Light meal 5. Fried food/Fatty meal or meat