pulmonary: restrictive, obstructive diseases and PE Flashcards
(71 cards)
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
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
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
4
Q
describe restrictive disease
A
- decreased lung compliance
- lung expansion restricted, impeding air flow in
- lung volumes reduced
- air resistance NOT increased
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)
6
Q
what are pulmonary function tests?
A
spirometry and flow volume loops to distinguish between obstructive and restrictive conditions
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
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%
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%
10
Q
describe normal PFT results
A
- FEV: 4.0
- FVC: 5.0
- ratio: 80%
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
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
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
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
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
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
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
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
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
20
Q
what are the goals of asthma treatment?
A
- prevent bronchial inflammation
- maintain patent airways
21
Q
what type of therapy is used for asthma treatment?
A
- long term control of airway narrowing
- rescue for acute bronchospasm attacks
22
Q
what anti inflammatory drugs are used for asthma?
A
- glucocorticoids
- leukotriene blockers
- mast cell-stabilizing agents
23
Q
what bronchodilator drugs are used for asthma?
A
- beta2 agonists (rescue)
- methylxanthines
- anticholinergics (antimuscarinics)
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
25
what are common glucocorticoids used in asthma treatment?
- IV hydrocortisone, methylprednisolone
- fluticasone (Flovent)
- salmeterol (Advair)
- budesonide (Pulmicort)
- triamicinolone (Azmacort)
- beclomethasone (Beclovent)
26
describe leukotriene blockers for asthma treatment
- 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
27
what are common leukotriene blockers used in asthma treatment?
- monotelukast (Singulair)
- zafirlukast (Accolate)
- pranlukast (Zyflo)
- zileuton (Ultair)
28
describe mast cell stabilizers for asthma treatment
* effective only with extrinisic (allergic) asthma
- block airway inflammation
- inhibits mediator release from mast cells
- stabilizes membranes inhibiting mast cell degranulation
29
what is a common mast cell stabilizer used in asthma treatment?
cromolyn
30
describe beta adrenergic agonists for asthma treatment
- 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
what are common beta 2 agonists used in asthma treatment?
- albuterol (Ventolin)
- metaproterenol (Alupent)
- terbutaline (Brethaire)
32
what are side effects of beta 2 agonists?
- hypokalemia (ATP K+ pumps drives it into cell)
- tachycardia
- vasodilation
33
describe methylxanthines for asthma treatment
- 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
what are common methyxanthines for asthma treatment?
- ipratropium (Atrovent)
- atropine (anticholinergic)
- glycopyrolate (anticholinergic)
35
describe status asthmaticus
- life threatening
- may last for hours or days
- attack unresponsive to bronchodilator treatment
* *exhaustion, dehydration, tachycardia
36
what is treatment for status asthmaticus?
- repeated high doses of glucocorticoids
| - beta 2 agonists
37
describe recommended management for mild intermittent asthma
Step 1
- anti-inflammatory: no daily medication needed
- short-acting bronchodilator: inhaled beta2 agonist as needed for symptoms
38
describe recommended management for mild, persistent asthma
Step 2
- anti-inflammatory: inhaled steroid (low dose) or cromolyn or nedrocromil
- short-acting bronchodilator: inhaled beta2agonist as needed for symptoms
39
describe recommended management for moderate, persistent asthma
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
describe recommended management for severe, persistent asthma
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
describe bronchospasm and reactive airway disease (RAD)
- 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
what are common triggers of bronchospasms and RAD?
- 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
what are common causes of acute bronchospasm in anesthetized patients?
- 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
describe management of bronchospasm and RAD
- 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
describe management of COPD
- 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
describe chronic bronchitis
- 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
describe emphysema
- 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
describe pathogenesis of emphysema
- 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
compare and contrast characteristics of chronic bronchitis and pulmonary emphysema
```
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
describe restrictive lung disease
- 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
what are causes of acute intrinsic restrictive lung disease (pulmonary edema)?
- 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
what are causes of chronic intrinsic restrictive lung disease?
- fibrosis (radiation, occupational toxin)
- O2 toxicity
- sarcoidosis
- scleroderma
53
what are causes of extrinsic restrictive lung disease?
- 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
describe acute intrinsic restrictive disease (pulmonary edema)
- primarily b/c of an increase in intravascular lung water: increased pulmonary capillary pressure, increased pulmonary capillary permeability
- results in reduced lung compliance
55
what are causes of pulmonary edema?
- cardiogenic pulmonary edema: increased hydrostatic pressure
- pulmonary aspiration
- infection
56
describe management of pulmonary edema
- 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
describe chronic intrinsic lung disease or interstitial lung disease
- 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
what are common causes of chronic intrinsic lung disease?
- chronic inflammation of alveolar walls and perialveolar tissue
- most commonly d/t pulmonary fibrosis (fibrotic elastic tissue)
59
describe sarcoidosis
- 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
describe diffuse interstitial pulmonary fibrosis
- 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
describe management of chronic intrinsic disease
- 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
describe chronic extrinsic restrictive disease
- 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
describe management of chronic extrinsic disease
- 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
describe intraop pulmonary embolism
- 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
what are predisposing factors to thromboembolism?
- 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
what are the three primary factors causing venous thrombi?
* Virchow triad
- venous stasis
- hypercoagulability
- vascular (venous) injury
67
what are causes of venous stasis?
- CHF
- cor pulmonale
- general anesthesia
- immobility
- obesity
- varicose veins
- prior venous thrombi
- long surgery
68
what are causes of hypercoagulability?
- DIC
- infection
- malignancy
- pregnancy
- oral contraceptions
- thrombophilias
69
what are causes of venous injury?
- trauma
- surgery
- lower extremity fracture
70
what are clinical signs of PE?
- reduced ETCO2 and capnograph wave
- unexplained hypoxemia
- sudden CV collapse with hypotension
- tachycardia, right bundle branch block
- bronchospasm
71
describe management of intraop PE
- 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
