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pulmonary: restrictive, obstructive diseases and PE Flashcards

1
Q

what is the primary purpose of the pulmonary system?

A

supplying necessary O2 to the tissues and excreting CO2

*don’t need 100% O2 to fulfill purpose

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2
Q

what is the difference in how the respiratory system delivers O2 and CO2 molecules opposed to the circulatory system?

A

respiratory system delivers gas and the circulatory system delivers liquid

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3
Q

describe obstructive disease

A
  • more common than restrictive
  • airway resistance increased
  • air trapping and obstruction impedes air flow out (extended expiration times)
  • lung volumes increase (RV and TLC)
  • turbulent air flow leading to wheezing
  • impaired gas exchange leading to VQ mismatch
  • more amendable to treatment than restrictive
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4
Q

describe restrictive disease

A
  • decreased lung compliance
  • lung expansion restricted, impeding air flow in
  • lung volumes reduced
  • air resistance NOT increased
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5
Q

with obstructive disease, what 3 mechanisms cause an increase in airway resistance that leads to obstructed air flow?

A
  • excessive secretions partly blocking bronchial lumen
  • airway thickening by edema, hypertrophy of mucous glands, bronchitis, or asthma
  • destruction of lung parenchyma (loss of airway radial traction narrows airway)
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6
Q

what are pulmonary function tests?

A

spirometry and flow volume loops to distinguish between obstructive and restrictive conditions

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7
Q

describe pulmonary function tests

A
  • FEV1: volume forcefully exhaled in one second
  • FVC: total volume that can be forcefully exhaled
  • FEV1/FVC: ratio used to distinguish obstructive vs. restrictive
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8
Q

describe pulmonary function test results with obstructive diseases

A

-both FEV1 and FVC are low and ratio is less than 0.7
0.6-0.7: mild
0.4-0.6: moderate
less than 0.4: severe
ex: FEV: 1.3, FVC: 3.1, ratio 42%

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9
Q

describe PFT results with restrictive diseases

A

both FEV1 and FVC are low and ratio is greater than or equal to 0.7
ex: FEV: 2.8, FVC: 3.1, ratio 90%

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10
Q

describe normal PFT results

A
  • FEV: 4.0
  • FVC: 5.0
  • ratio: 80%
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11
Q

describe characteristics of asthma

A
  • chronic airway inflammation with periodic acute severe exacerbations
  • bronchial airways are hyper-reactive to stimuli
  • airway narrowing at all levels with varying severity
  • expiratory airflow becomes obstructed (obstructive disease)
  • reversible with bronchodilators
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12
Q

describe extrinsic asthma

A
  • allergic asthma
  • family hx of allergic/immunologic disease
  • allergic related (allergen identified)
  • immune system activation
  • elevation of IgE levels and serum eosinophils
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13
Q

describe intrinsic asthma

A
  • non-allergic asthma
  • idiosyncratic (specific to the individual)
  • exacerbations with triggers
  • non-immune related (no allergen identified)
  • normal IgE levels
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14
Q

what are signs and symptoms of asthma?

A
  • periodic acute exacerbations: mild to severe attacks; bronchospasm; mucosal edema/secretions
  • mild airway obstruction lasting for weeks
  • increased airway resistance to gas flow: wheezing
  • productive cough, dyspnea
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15
Q

describe pathology of asthma

A
  • hypertrophied airway smooth muscle contracts during an attack causing bronchoconstriction
  • mucous gland hypertrophy causes increased secretions, usu. white and scant (thick, slow moving; mucous plugs leads to obstruction)
  • bronchial wall edema
  • infiltration of eosinophils and lymphocytes
  • remodeling leads to subepithelial fibrosis
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16
Q

what are common etiologies of asthma attacks?

A
  • allergy induced
  • respiratory viruses (children)
  • occupational and environmental irritants (adults): airborne pollens, animal danders, dust, pollutants, chemicals
  • drugs: aspirin, beta2blockers, NSAIDS, drugs causing histamine release
  • exertional exercise
  • stress, emotional, psychological
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17
Q

what are inflammatory mediators associated with asthma?

A
  • cytokines associated with Th-2 and helper T cells: IL 4, 5, 9, 13
  • arachidonic acid metabolites: leukotrienes, prostaglandins
  • platelet-activating factor (PAF)
  • neuropeptides
  • reactive oxygen species (ROS)
  • kinins (bradykinin)
  • histamine
  • adenosine
  • serotonin
  • chemotactic factors
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18
Q

describe the immune mediated process of asthma

A
  • allergen binds to IgE on mast cell causing degranulation
  • release of inflammatory mediators from mast cell
  • bronchoconstriction via multiple mechanisms: decreased cAMP, increased cGMP increases PNS activity increasing cholinergic sensitivity causing vagal afferents sensitivity to histamine, noxious stimuli, cold air, irritants, and ET intubation
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19
Q

describe PNS role in bronchoconstriction

A
  • balance between PNS and SNS regulates bronchial tone
  • PNS stimulation via vagal activation causes activation of muscarinic receptors in bronchial smooth muscle
  • muscarinic receptors cause increase in intracellular levels of cyclic guanosine monophosphate (cGMP)
  • increased intracellular cGMP increases protein kinases that cause bronchoconstriction
  • antimuscarinics promote dilation
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20
Q

what are the goals of asthma treatment?

A
  • prevent bronchial inflammation

- maintain patent airways

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21
Q

what type of therapy is used for asthma treatment?

A
  • long term control of airway narrowing

- rescue for acute bronchospasm attacks

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22
Q

what anti inflammatory drugs are used for asthma?

A
  • glucocorticoids
  • leukotriene blockers
  • mast cell-stabilizing agents
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23
Q

what bronchodilator drugs are used for asthma?

A
  • beta2 agonists (rescue)
  • methylxanthines
  • anticholinergics (antimuscarinics)
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24
Q

describe glucocorticoids for asthma treatment

A
  • not rapid acting, usu. 1-3 hours onset
  • admin. IV or inhaler
  • decreased bronchial hypersensitivity, inflammatory response
  • membrane-stabilizing
  • most effective anti-inflammatory drugs
  • effective as prophylactic pre-op drugs
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25
Q

what are common glucocorticoids used in asthma treatment?

A
  • IV hydrocortisone, methylprednisolone
  • fluticasone (Flovent)
  • salmeterol (Advair)
  • budesonide (Pulmicort)
  • triamicinolone (Azmacort)
  • beclomethasone (Beclovent)
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26
Q

describe leukotriene blockers for asthma treatment

A
  • leukotrienes mediate inflammation in asthma
  • blocker inhibit the 5-lipoxygenase enzymatic pathway (5-LO inhibitors)
  • reduce the synthesis of leukotrienes
  • only 50% of patients with beneficial response
  • effective for aspirin-induced asthma
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27
Q

what are common leukotriene blockers used in asthma treatment?

A
  • monotelukast (Singulair)
  • zafirlukast (Accolate)
  • pranlukast (Zyflo)
  • zileuton (Ultair)
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28
Q

describe mast cell stabilizers for asthma treatment

A
  • effective only with extrinisic (allergic) asthma
  • block airway inflammation
  • inhibits mediator release from mast cells
  • stabilizes membranes inhibiting mast cell degranulation
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29
Q

what is a common mast cell stabilizer used in asthma treatment?

A

cromolyn

30
Q

describe beta adrenergic agonists for asthma treatment

A
  • most potent bronchodilators
  • stimulation of beta 2 receptors in the lungs cause increased cyclase leading to increased cAMP which increases Ca++ promoting tracheobronchial smooth muscle relaxation
  • inhibits inflammatory cell function
31
Q

what are common beta 2 agonists used in asthma treatment?

A
  • albuterol (Ventolin)
  • metaproterenol (Alupent)
  • terbutaline (Brethaire)
32
Q

what are side effects of beta 2 agonists?

A
  • hypokalemia (ATP K+ pumps drives it into cell)
  • tachycardia
  • vasodilation
33
Q

describe methylxanthines for asthma treatment

A
  • MOA poorly understood
  • inhibits phosphodiesterase enzyme which degrades cAMP, resulting in increased cAMP
  • inhibits prostaglandins
  • catecholamine release (epi is a beta2 agonist)
  • histamine blocking actions
  • chronic control and management
  • not for acute bronchospasm attack
34
Q

what are common methyxanthines for asthma treatment?

A
  • ipratropium (Atrovent)
  • atropine (anticholinergic)
  • glycopyrolate (anticholinergic)
35
Q

describe status asthmaticus

A
  • life threatening
  • may last for hours or days
  • attack unresponsive to bronchodilator treatment
  • *exhaustion, dehydration, tachycardia
36
Q

what is treatment for status asthmaticus?

A
  • repeated high doses of glucocorticoids

- beta 2 agonists

37
Q

describe recommended management for mild intermittent asthma

A

Step 1

  • anti-inflammatory: no daily medication needed
  • short-acting bronchodilator: inhaled beta2 agonist as needed for symptoms
38
Q

describe recommended management for mild, persistent asthma

A

Step 2

  • anti-inflammatory: inhaled steroid (low dose) or cromolyn or nedrocromil
  • short-acting bronchodilator: inhaled beta2agonist as needed for symptoms
39
Q

describe recommended management for moderate, persistent asthma

A

Step 3

  • anti-inflammatory: inhaled steroids (med. dose) or inhaled steroid (low to med. dose) and inhaled long acting beta2 agonist
  • short-acting bronchodilator: inhaled beta2agonist as needed for symptoms
40
Q

describe recommended management for severe, persistent asthma

A

Step 4

  • anti-inflammatory: inhaled steroids (high dose) and long acting inhaled beta2agonist; possibly systemic steroids
  • short-acting bronchodilator: inhaled beta2agonist as needed for symptoms
41
Q

describe bronchospasm and reactive airway disease (RAD)

A
  • bronchospasm rare (2%)
  • wheezing common
  • more common in chronic bronchitis and asthmatics with reactive airways and pts. with smoking hx.
  • mediated by parasympathetic nervous system
42
Q

what are common triggers of bronchospasms and RAD?

A
  • adults: mechanical or noxious chemical irritants
  • pediatric: environmental allergens and recent viral respiratory illnesses or URI
  • histamine-releasing drugs: morphine, atricurium
  • anaphylactoid and transfusion reactions
43
Q

what are common causes of acute bronchospasm in anesthetized patients?

A
  • nonspecific bronchial hyperresponsiveness
  • allergic or anaphylactic reaction to drugs or blood transfusion
  • exacerbation of asthma
  • pharmacologic: beta blockers, prostaglandin inhibition (NSAIDS), anticholinesterases
  • stimulation of parasympathetic fibers and M2 and M3 muscarinic receptors
  • tracheal irritation from intubation
44
Q

describe management of bronchospasm and RAD

A
  • avoid airway instrumentation (ETT), use LMA or regional
  • avoid histamine-releasing drugs, NSAIDs, beta2blockers
  • deepen anesthetic level (propofol better than pentothal and etomidate; ketamine has bronchodilator effects by increasing catecholamines)
  • IV opioids and lidocaine blunt airway reflexes
  • increase FiO2
  • perioperative bronchodilators (albuterol)
  • antimuscarinics (robinul, atropine)
  • corticosteroids (solumedrol 125 mg IV)
  • epinephrine (0.1-1 mg IV) (last resort, esp. with underlying cardiac disease; increases demand and decreases supply)
45
Q

describe management of COPD

A
  • remove cause: smoking, pollutants (may have mild, reversible symptoms)
  • bronchodilators
  • steroids
  • supplemental oxygen
  • possibly diuretic therapy if cor pulmonale (right sided congestion) has developed
46
Q

describe chronic bronchitis

A
  • excessive mucous production in bronchial tree
  • hypertrophy of mucous glands in large bronchi
  • bronchial smooth muscle increases
  • caused by smoking and environmental pollutants
  • outward airflow obstruction results
  • chronic hypoxemia leads to erythrocytosis (body increases O2 carriers- hgb) and pulmonary HTN causing right heart failure (blue bloater)
47
Q

describe emphysema

A
  • enlarged air space distal to the terminal bronchiole caused by destruction of alveoli septa
  • destruction and subsequent loss of alveolar walls (destroys dividers b/w air sacs, reducing surface area for gas exchange)
  • destruction of surrounding capillary bed
  • centriacinar: destruction of central part of lobule (terminal and respiratory bronchioles only)
  • panacinar: destruction of entire lobule (peripheral alveoli also involved)
  • bullous: cystic areas or bullae form
  • breathing through pursed lips delays closure of small airways (pink puffers)
  • able to maintain O2 concentration better than chronic bronchitis pts.
  • air trappings: new air cant get in b/c old air cant get out
48
Q

describe pathogenesis of emphysema

A
  • cigarette smoking is primary pathologic factor
  • alpha1 antitrypsin deficiency (inhibits elastase): increased elastase
  • smoking decreases elastase inhibitors: increased elastase
  • elastase destroys elastin inside the lung
  • elastin essential as it supports elastic structure of the lungs responsible for elastic recoil
  • elastic recoil supports smaller airways by providing radial traction
49
Q

compare and contrast characteristics of chronic bronchitis and pulmonary emphysema

A 
chronic bronchitis 
-obstruction d/t decreased airway lumen d/t mucus and inflammation
-moderate dyspnea
-decreased FEV1
-marked decrease in PaO2 (blue bloater: airway plugged by mucus)
-increased PaCO2
-normal diffusing capacity
-increased HCT
-marked cor pulmonale
-poor prognosis
pulmonary emphysema
-obstruction d/t loss of elastic recoil
-severe dyspnea
-decreased FEV1
-modest decrease in PaO2 (pink puffer)
-normal to decreased PaCO2
-decreased diffusing capacity
-normal HCT
-mild cor pulmonale
-good prognosis
50
Q

describe restrictive lung disease

A
  • reduced lung compliance
  • reduced lung volumes result
  • airway resistance is NOT increased
  • expiratory flow rates are normal
  • reduced FEV1 d/t low lung volumes
  • reduced FVC
  • normal FEV1/FVC ratio
  • usually normal gas exchange
  • breathing is rapid and shallow
51
Q

what are causes of acute intrinsic restrictive lung disease (pulmonary edema)?

A
  • drug/chemical pneumonitits (opioid OD)
  • aspiration pneumonitis
  • pneumonia
  • ARDS
  • neurogenic pulmonary edema
  • negative pressure pulmonary edema (NPPE): upper airway obstruction
  • CHF
  • high altitude
  • re-expansion of collapsed lung
52
Q

what are causes of chronic intrinsic restrictive lung disease?

A
  • fibrosis (radiation, occupational toxin)
  • O2 toxicity
  • sarcoidosis
  • scleroderma
53
Q

what are causes of extrinsic restrictive lung disease?

A
  • neuromuscular diseases
  • muscular dystrophy
  • spinal cord transection
  • Guillain-Barre syndrome
  • eaton-lambert syndrome
  • myasthenia gravis
  • morbid obesity, ascites, pregnancy
  • pleural effusion
  • pleural thickening
  • mediastinal mass
  • pneumothorax
  • neuroskeletal diseases
  • scoliosis, kyphosis
  • external pressure on respiratory pleural cavity, restricting cavity expansion, decreasing lung expansion and compliance
54
Q

describe acute intrinsic restrictive disease (pulmonary edema)

A
  • primarily b/c of an increase in intravascular lung water: increased pulmonary capillary pressure, increased pulmonary capillary permeability
  • results in reduced lung compliance
55
Q

what are causes of pulmonary edema?

A
  • cardiogenic pulmonary edema: increased hydrostatic pressure
  • pulmonary aspiration
  • infection
56
Q

describe management of pulmonary edema

A
  • delay elective surgery until cardiopulmonary function optimized
  • reduce interstitial lung water: diuretics, fluid limitation, inotropes, vasodilators
  • PPV with PEEP to drive out fluid
  • lower Vt (4-6 ml/kg) and higher RR (greater than 14): reduce volutrauma, barotrauma
  • keep PiPs less than 30 cmH2O
  • adjust FiO2 to maintain adequate oxygenation (try to keep Sat above 95% w/o 100% FiO2)
57
Q

describe chronic intrinsic lung disease or interstitial lung disease

A
  • changes in intrinsic lung properties (parenchyma): scar tissue, sarcoidosis, fibrosis, inflammation
  • reduced compliance, reduced FRC
  • ultimately results in gas exchange abnormalities: altered V/Q d/t altered ventilation in regions
58
Q

what are common causes of chronic intrinsic lung disease?

A
  • chronic inflammation of alveolar walls and perialveolar tissue
  • most commonly d/t pulmonary fibrosis (fibrotic elastic tissue)
59
Q

describe sarcoidosis

A
  • systemic granulomatous disorder: granulomatous tissue is present in several other organ systems (skin, eyes, liver, spleen)
  • granulomatous tissue is prone to develop in intrathoracic lymph nodes and the lungs
  • fibrotic changes in lungs occur in alveolar walls (decreased gas exchange)
  • endobronchial sarcoid is common (decreased airflow)
60
Q

describe diffuse interstitial pulmonary fibrosis

A
  • primary feature is thickening of interstium of alveolar wall
  • infiltration of lymphocytes, plasma cells
  • followed by fibroblast which cause formation of thick collagen bundles
  • ultimately destroys the structure of the alveoli
  • final scarring occurs and air-filled cystic spaces form (referred to as “honeycomb lung”)
  • reduced compliance and impaired gas exchange
61
Q

describe management of chronic intrinsic disease

A
  • optimize cardiopulmonary status
  • unable to tolerate long periods of apnea d/t decreased FRC
  • uptake of inhaled anesthetics is faster d/t reduced FRC
  • pneumothorax risks are increased (decreased wall integrity): use lower Vt and higher RR; keep PiPs less than 30 cmH2O
  • more prone to oxygen toxicity: oxygenate with lower FiO2 if possible
  • consider regional anesthetic if not contraindicated
  • no N2O
62
Q

describe chronic extrinsic restrictive disease

A
  • disorders of thoracic cage or chest wall (may be mechanical in nature or tumor obstructing flow)
  • lung expansion is restricted
  • lungs are compressed, volumes reduced
  • increased inspiratory airway resistance from decreased lung volumes (near end expiration)
  • recurrent pulmonary infections result from ineffective cough dynamics
  • V/Q mismatches d/t low ventilated regions
63
Q

describe management of chronic extrinsic disease

A
  • avoid drugs with prolonged respiratory depressant effects
  • be cautious of N2O
  • consider regional anesthesia if not contraindicated
  • reduced lung compliance may prompt the need to deliver higher airway pressures (PiPs) in order to deliver adequate Vt to maintain oxygenation/ventilation
  • higher RR may need to be considered in order to adequately oxygenate/ventilate
64
Q

describe intraop pulmonary embolism

A
  • very rare
  • embolic material from the venous circulation occludes the pulmonary vascular bed
  • primarily originates from blood clots in the lower extremities and pelvic veins
  • 90% are DVTs from iliofemoral vessels
  • embolisms are also possible from fat, amniotic fluid, tumor cells, air, foreign material
65
Q

what are predisposing factors to thromboembolism?

A
  • venous stasis: trauma, surgery (esp. LE, pelvis, major abd), immobility, pregnancy, low CO (CHF, MI), morbid obesity, hypovolemia
  • abnormality or injury of the vessel wall: varicose veins, drug induced irritation
  • hypercoagulable state: estrogen therapy (OC), cancer, deficiencies of endogenous anticoagulants (antithrombin III, protein C, protein S), burns, surgery
  • hx of previous thromboembolism
66
Q

what are the three primary factors causing venous thrombi?

A
  • Virchow triad
  • venous stasis
  • hypercoagulability
  • vascular (venous) injury
67
Q

what are causes of venous stasis?

A
  • CHF
  • cor pulmonale
  • general anesthesia
  • immobility
  • obesity
  • varicose veins
  • prior venous thrombi
  • long surgery
68
Q

what are causes of hypercoagulability?

A
  • DIC
  • infection
  • malignancy
  • pregnancy
  • oral contraceptions
  • thrombophilias
69
Q

what are causes of venous injury?

A
  • trauma
  • surgery
  • lower extremity fracture
70
Q

what are clinical signs of PE?

A
  • reduced ETCO2 and capnograph wave
  • unexplained hypoxemia
  • sudden CV collapse with hypotension
  • tachycardia, right bundle branch block
  • bronchospasm
71
Q

describe management of intraop PE

A
  • goal: optimize cardiac output and O2 delivery
  • increase FiO2 to 100%
  • may use PEEP to help with hypoxemia
  • support circulatory system: sympathomimetics and inotropes, IV fluid boluses, treat ventricular dysrhythmias
  • phosphodiesterase inhibitors increase contractility and are pulmonary artery dilators
  • ultimately remove or dissolve embolic fragments

advanced pathophysiology (3 decks)

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