pulmonary: restrictive, obstructive diseases and PE Flashcards
what is the primary purpose of the pulmonary system?
supplying necessary O2 to the tissues and excreting CO2
*don’t need 100% O2 to fulfill purpose
what is the difference in how the respiratory system delivers O2 and CO2 molecules opposed to the circulatory system?
respiratory system delivers gas and the circulatory system delivers liquid
describe obstructive disease
- 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
describe restrictive disease
- decreased lung compliance
- lung expansion restricted, impeding air flow in
- lung volumes reduced
- air resistance NOT increased
with obstructive disease, what 3 mechanisms cause an increase in airway resistance that leads to obstructed air flow?
- 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)
what are pulmonary function tests?
spirometry and flow volume loops to distinguish between obstructive and restrictive conditions
describe pulmonary function tests
- FEV1: volume forcefully exhaled in one second
- FVC: total volume that can be forcefully exhaled
- FEV1/FVC: ratio used to distinguish obstructive vs. restrictive
describe pulmonary function test results with obstructive diseases
-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%
describe PFT results with restrictive diseases
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%
describe normal PFT results
- FEV: 4.0
- FVC: 5.0
- ratio: 80%
describe characteristics of asthma
- 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
describe extrinsic asthma
- allergic asthma
- family hx of allergic/immunologic disease
- allergic related (allergen identified)
- immune system activation
- elevation of IgE levels and serum eosinophils
describe intrinsic asthma
- non-allergic asthma
- idiosyncratic (specific to the individual)
- exacerbations with triggers
- non-immune related (no allergen identified)
- normal IgE levels
what are signs and symptoms of asthma?
- 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
describe pathology of asthma
- 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
what are common etiologies of asthma attacks?
- 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
what are inflammatory mediators associated with asthma?
- 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
describe the immune mediated process of asthma
- 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
describe PNS role in bronchoconstriction
- 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
what are the goals of asthma treatment?
- prevent bronchial inflammation
- maintain patent airways
what type of therapy is used for asthma treatment?
- long term control of airway narrowing
- rescue for acute bronchospasm attacks
what anti inflammatory drugs are used for asthma?
- glucocorticoids
- leukotriene blockers
- mast cell-stabilizing agents
what bronchodilator drugs are used for asthma?
- beta2 agonists (rescue)
- methylxanthines
- anticholinergics (antimuscarinics)
describe glucocorticoids for asthma treatment
- 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
what are common glucocorticoids used in asthma treatment?
- IV hydrocortisone, methylprednisolone
- fluticasone (Flovent)
- salmeterol (Advair)
- budesonide (Pulmicort)
- triamicinolone (Azmacort)
- beclomethasone (Beclovent)
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
what are common leukotriene blockers used in asthma treatment?
- monotelukast (Singulair)
- zafirlukast (Accolate)
- pranlukast (Zyflo)
- zileuton (Ultair)
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
what is a common mast cell stabilizer used in asthma treatment?
cromolyn
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
what are common beta 2 agonists used in asthma treatment?
- albuterol (Ventolin)
- metaproterenol (Alupent)
- terbutaline (Brethaire)
what are side effects of beta 2 agonists?
- hypokalemia (ATP K+ pumps drives it into cell)
- tachycardia
- vasodilation
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
what are common methyxanthines for asthma treatment?
- ipratropium (Atrovent)
- atropine (anticholinergic)
- glycopyrolate (anticholinergic)
describe status asthmaticus
- life threatening
- may last for hours or days
- attack unresponsive to bronchodilator treatment
- *exhaustion, dehydration, tachycardia
what is treatment for status asthmaticus?
- repeated high doses of glucocorticoids
- beta 2 agonists
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
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
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
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
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
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
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
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)
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
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)
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
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
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
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
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
what are causes of chronic intrinsic restrictive lung disease?
- fibrosis (radiation, occupational toxin)
- O2 toxicity
- sarcoidosis
- scleroderma
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
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
what are causes of pulmonary edema?
- cardiogenic pulmonary edema: increased hydrostatic pressure
- pulmonary aspiration
- infection
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)
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
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)
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)
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
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
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
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
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
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
what are the three primary factors causing venous thrombi?
- Virchow triad
- venous stasis
- hypercoagulability
- vascular (venous) injury
what are causes of venous stasis?
- CHF
- cor pulmonale
- general anesthesia
- immobility
- obesity
- varicose veins
- prior venous thrombi
- long surgery
what are causes of hypercoagulability?
- DIC
- infection
- malignancy
- pregnancy
- oral contraceptions
- thrombophilias
what are causes of venous injury?
- trauma
- surgery
- lower extremity fracture
what are clinical signs of PE?
- reduced ETCO2 and capnograph wave
- unexplained hypoxemia
- sudden CV collapse with hypotension
- tachycardia, right bundle branch block
- bronchospasm
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
