Respiratory Flashcards
50% decrease in airflow, >10 seconds, more than 15 seconds/hour of sleep, results in 4% decrease in O2 sats
hypopnea
Snoring, complete or partial obstruction of the airway during sleep + frequent episodes of apnea or hypopnea
Obstructive sleep apnea
Obesity, awake arterial hypercapnia, insufficient alveolar impairment indecent of any other pulmonary disease
Obesity hypoventilation syndrome
Obesity, awake arterial hypercapnia, insufficient alveolar impairment indecent of any other pulmonary disease
Obesity hypoventilation syndrome
What is hepatopulmonary syndrome?
Hypoxemia due to liver disease
What are the defining characteristics of hepatopulmonary disease?
- Presence of portal hypertension
- Increase Aa gradient
- Intrapulmonary vasodilation
Bronchoconstriction pathway
PNS- vagal stimulation
released Ach acts on M3 to stim Gq
phospholipase C is activated
converts PIP2 to IP3
IP3 stims Ca release from sarcoplasmic reticulum
bronchoconstriction results
How is bronchoconstriction from PNS stimulation turned off
IP3 phosphatase deactivates IP3 to IP2
How do mast cells promote bronchoconstriction:
Coughing, allergy, or infection activate IgE, cytokines, and complement -> amplification of allergic response
Do non-cholinergic C-fibers promote bronchodilator or bronchoconstriction?
bronchoconstriction
Identify Mast Cell mediators and their respective receptors
Histamine -> Histamine 1
Prostaglandins D2 and F2 -> Thromboxane-specific prostanoid receptor
Leukotrienes C4, D4, and E4 -> CysLT1
Platelet activating factor -> PAF
Bradykinin -> Bradykinin 2
Name C-fiber mediators and their respective receptors:
Substance P -> Neurokinin-2
Neurokinin A -> GCRP
Calcitonin gene related peptide
Bronchodilation pathway due to Circulating Catecholamines
B2 Receptors activated by circulating catecholamines
Gs protein activated
adenylate cyclase activated
cAMP activated
cAMP and protein kinase A reduce Ca release from sarcoplasmic reticulum
smooth muscle contraction decreased
bronchodilation results
How is bronchodilation from circulating catecholamines turned off
Phosphodiesterase 3 deactivates cAMP by converting it to ATP
NO and bronchodilation
potent smooth muscle relaxant
vasoactive intestinal peptide released onto airway smooth muscle by non-cholinergic PNS nerves
NO production increased
stimulates cGMP
smooth muscle relaxation and bronchodilation result
Two ways B2 Agonists cause bronchodilation:
B2 stim -> increased cAMP -> decreased iCa+2
Stabilizes mast cell membranes -> decreased mediator release
B2 agonist examples and side effects
Albuterol, salmeterol, metproteronol
tachycardia, dysrhythmias, hypoK, hyperglycemia, tremors
How do anticholinergics promote bronchodilation:
Antagonize M3R -> decrease IP3 -> decrease iCa+2
Two ways inhaled corticosteroids cause bronchodilation:
Stimulate intracellular steroid receptors
Regulate inflammatory protein synthesis (results in decreased airway inflammation and decreased airway hyperresponsiveness
Cromolyn and bronchodilation
Mast cell membrane stabilizer
(blocks cytokines, leukotrienes, histamine)?
Leukotriene modifier MOA
Inhibit 5-lipooxygenase enzyme (decreased leukotriene synthesis)
Three ways methylxanthines work and give an example
Theophylline
Inhibit PDE -> increase cAMP
Increase endogenous catecholamine release
Inhibit adenosine receptors
Define static lung volumes
How much air the lungs can hold at one time
Define Dynamic lung volumes
How quickly air can be moved in and out of the lungs over time
Normal Tidal Volumes
500 mL
Normal inspiratory reserve volume
3,000 mL
Normal end residual volume
1,100 mL
Normal residual volume
1,200 mL
Define FEV1 and the normal value
Forced Expiratory Volume in 1 second
Volume let out in 1 second after a maximum inhalation
-depends on patient effort
-declines with age
normal= >80% predicted value
Define forced vital capacity and its normal value
Volume of air exhaled after a maximum inhalation
Male = 4.8 L
Female = 3.7 L
FEV1 to FVC ratio normal value and use
75 - 80% predicted value
Used to distinguish between restrictive and obstructive
<70% = obstructive
normal with restrictive
Forced expiratory flow at 25-75% vital capacity is:
aka Mid maximal expiratory flow rate
Measure airflow in the middle of FEV
Normal: 100 +/- 25% predicted value
What is FEV25-75% used to indicate?
Small airway disease - most sensitive indicator
Usually reduced with obstructive
Usually normal with restrictive
Maximum voluntary ventilation is:
Endurance test
Max volume of air inhaled and exhaled over 1 minute
Normal Male= 140-180L
Normal Female = 80-120L
Another name for FEV 25-75%
Mid maximal expiratory flow rate (MMEF)
Another name for FEV 25-75%
Mid maximal expiratory flow rate (MMEF)
Postop pulmonary comp risk factors: patient
age > 60
ASA > 2
CHF
COPD
Cigarette smoking (>40 pack years
Postop pulmonary comp risk factors: procedure
aortic > thoracic > upper abdominal ~ neuro ~ peripheral vascular > emergency
general anesthesia
duration of surgery > 2 hours
Postop pulmonary comp risk factors: diagnostic testing
albumin < 3.5 g/dL
-indicates poor nutritional status
Factors NOT shown to increase postop pulmonary comps
mild/moderate asthma
arterial blood gas analysis
pulmonary function testing
Smoking: respiratory effects
increase risk for pulmonary disease
decreased mucociliary clearance
airway hyperactivity
reduced pulmonary immune function
Smoking: CV effects
leads to CV disease
carbon monoxide -> decreased DO2
catecholamine release
coronary vasoconstriction
decreased exercise healing
Smoking: effects
impaired wound healing
Smoking: short term effects of stopping
carbon monoxide t1/2 = 4-6 hours
P50 returns to near normal in 12 hours
short term cessation not effective in reducing pulmonary complications
Smoking: intermediate term effects of stopping
Pulmonary function return takes at least 6 weeks. Includes:
airway function
mucociliary clearance
sputum production
pulmonary immune function
hepatic enzyme induction subsides after 6 weeks
What is the best way to reverse anesthesia-induced atelectasis?
Alveolar recruitment methods
How do you perform an effective alveolar recruitment method?
Peak airway pressure 30 cm H2O required to initially reopen atelectatic region
Then increase PIP to 40 cm H2O for 8 seconds
Apply method to open alveoli, then apply PEEP to keep open
Most common ABG finding in asthma
respiratory alkalosis with hypocarbia
What does an elevated PaCO2 in an asthmatic suggest?
Air trapping -> respiratory muscle fatigue -> impending respiratory failure
What EKG changes may occur in a patient with asthma?
Right axis deviation due to RV strain and increased workload from increased PVR
Is tracheal intubation the first choice in a patient with asthma?
No! Use regional, mask, or LMA if appropriate.
If tube, consider deep extubation.
What drugs can be given to decrease airway reactivity on extubation?
Opioids
Lidocaine 1-1.5 mg/kg 1-3 mins prior to extubation
Ventilator settings in asthmatic
Limit inspiratory time
Prolong expiratory time
Tolerate moderate permissive hypercapnia
What drugs do you avoid in an asthmatic?
Histamine releasing drugs:
Sux, atracurium, morphine, meperidine, etc.
What is the role of H1 and H2 antagonists in the patient with asthma?
An H2 antagonist (ranitidine and famotidine) allows for unopposed H1 stimulation which can lead to bronchospasm.
However, an H2 antagonist may be used in GERD-induced asthma.
List differential diagnoses concerning intraop bronchospasm and wheezing.
Mechanical obstruction of ETT (biting, kinked, secretions, cuff overinflation)
Light anesthesia (coughing + straining -> decreased FRC)
Bronchospasm
Acute asthmatic attack
Pulmonary embolism
Pulmonary edema
Pulmonary aspiration
Endobronchial intubation
Pneumothorax
How does bronchospasm present?
Wheezing
Decreased breath sounds
Increased peak inspiratory pressure with normal plateau pressures (decreased dynamic pulmonary compliance)
Increased alpha angle on capnograph (expiratory upslope)
How do you treat bronchospasm?
100% FiO2
Deepen anesthetic (volatile agent, propofol, lidocaine, ketamine)
Short acting inhaled B2 agonist (albuterol)
Inhaled ipratroprium
Epinephrine 1 mcg/kg IV
Hydrocortisone 2-4 mg/kg IV (doesn’t treat acute, prevents problems later)
Aminophylline (theophylline not great for acute)
Heliox to reduce airway resistance
Describe the pathophysiology of COPD.
Loss of lung elasticity = decreased recoil -> air trapping -> increased residual volume
Reduced airway rigidity -> airway collapse during exhalation -> air trapping
Increase gas velocity through narrow airways -> decreased pressure in airways -> airway collapse -> air trapping
Secretions -> airflow obstruction and bronchospasm
Describe the acid base changes with COPD
Respiratory acidosis due to chronic elevation of PaCO2
Metabolic alkalosis (compensatory) due to reabsorption of bicarbonate
What results if you restore PaCO2 to normal using mechanical ventilation in a patient with COPD?
Risk of severe alkalosis due to amount of bicarb in blood not changing
Reduced O2 unloading and apnea result
How is chronic bronchitis diagnosed?
Presence of cough and sputum for more than 3 months in a span of 2 years
What lung changes occur with chronic bronchitis?
hypertrophied bronchial mucus glands
chronic inflammation
air flow is limited during exhalation
Why does erythrocytosis result from chronic bronchitis?
RBCs are overproduced in compensation of V/Q mismatch and hypoxia. Increased blood viscosity and myocardial work result.
How does chronic bronchitis lead to cor pulmonale?
Chronic hypoxemia and hypercarbia -> pulmonary HTN -> RV strain and right axis deviation -> cor pulmonale
What happens to left heart function as a result of chronic bronchitis?
It is normal (normal PAOP)
What is the most efficient drug to improve pulmonary hypertension and erythrocytosis in chronic bronchitis?
Oxygen
How does chronic bronchitis affect the liver?
A weakened right heart causes back pressure on the liver that leads to congestion and ascites
What lung changes occur with emphysema?
Enlargement and destruction of airways distal to the terminal bronchioles
Decreased surface area for gas exchange results -> dead space increases
Pulmonary capillary beds are destroyed -> contribute to pulmonary htn due to same amount of blooding traveling to smaller amount of vessels
What O2 and CO2 changes occur in emphysema?
Normal or slightly reduced PaO2
Normal or decreased PaCO2 (hyperventilation)
Late disease -> increased PVR due to hypoxemia and hypercarbia -> right heart failure
What protein deficiency can cause emphysema?
Alpha-1 antitrypsin deficiency
How does Alpha-1 antitrypsin deficiency cause emphysema?
Alpha-1 antitrypsin deficiency is an enzyme made in the liver. Alpha-1 antitrypsin usually blocks alveolar elastase breakdown in pulmonary connective tissue. Deficiency allows overactivity of breakdown and results in destruction of pulmonary connective tissue -> pan lobular emphysema
What lung spirometry changes occur in COPD?
Increased: RV, FRC, TLC
Decreased: FEV1, FEV1/FVC ratio, FEF 25-75%
What FEV1/FVC ratio after bronchodilator therapy is diagnostic of COPD?
<70%
What are the recommended ventilator settings in COPD?
Vt 6-8 mL/kg IBW
Slow inspiratory flow
PEEP to maintain airway patency in alveoli (prevent atelectasis)
Increase expiratory time -> minimize air trapping and auto-PEEP
Caution volume cycled ventilation -> higher PIP from less time to get same volume of gas in)
What can happen if using N2O in a patient with COPD?
Can rupture pulmonary bleb -> pneumothorax
Three characteristics of restrictive lung disease:
Decreased lung volumes and capacities
Decreased compliance
Intact pulmonary flow rates
Two spirometry tests diagnostic of restrictive lung disease:
FEV1 and FVC <70%
Ventilator settings for restrictive lung disease:
Minimize barotrauma
-smaller Vt (6 mL/kg IBW)
-faster RR (14-18 breaths/min)
-PIP < 30 cm H2O
-prolonged inspiratory time (I:E ratio 1:1)
Three potential problems of aspiration:
Airway obstruction due to gastric contents entering airway
Bronchospasm/impaired gas exchange due to chemical burn of airway and lung parenchyma from gastric contents
Bacterial infection due to entry of infectious material (infection does not always occur)
What is Mendelson’s syndrome?
Chemical aspiration pneumonitis first described in OB patients.
Characterized by gastric pH <2.5 and gastric volume > 25 mL
Pharmacologic prophylaxis of aspiration:
Antacids: sodium bicarb, sodium citrate, magnesium trisilicate
H2 antagonists: ranitidine, cimetidine, famotidine
GI stimulants: metoclopramide
PPIs: omeprazole, pantoprazole, lansoprazole
Antiemetics: ondansetron, droperidol
Is routine use of prophylaxis against aspiration recommended?
No
Diagnosis of aspiration:
Hallmark = hypoxemia
dyspnea, tachypnea, cyanosis, tachycardia, htn
Aspiration treatment includes:
First action - tilt head down or to side
Upper airway suction to remove debris
Lower airway suction only to remove debris; not useful for chemical burn due to gastric acid
Secure the airway, support oxygenation
PEEP to reduce shunt
Bronchodilators to decrease wheezing
IV Lidocaine to reduce the neutrophil response
When are antibiotics indicated for aspiration?
Only if WBCs are increased or if the patient develops a fever >48H after the incident
Hallmark characteristics of a pneumothorax include:
Hypoxemia
Increased airway pressures
Tachycardia
Hotn
Increased CVP
POC Ultrasound = absence of lung sliding
How does a tension pneumothorax affect hemodynamics?
Increased intrathoracic pressure compresses mediastinal structures and decreases venous return, cardiac output, and BP
What is the emergency treatment for a tension pneumothorax?
14g angiocath insertion at
-2nd intercostal space at mid-clavicular line
-4th or 5th intercostal space at anterior axillary line
What drugs can be given via ETT?
NAVEL - narcan, atropine, vasopressin, epinephrine, lidocaine
Normal vital capacity:
65-75 mL/kg
Normal inspiratory force:
75-100 cm/H2O
Normal PaO2:
> 72 mmHg
Normal A-a gradient:
<10-15
Normal PaO2 at 100% O2:
> 400 mmHg
Normal A-a gradient at 100% FiO2:
<100 mmHg
What EKG characteristics are present in Wolf-Parkinson-White?
Delta wave caused by ventricular preexcitation
Short PRI <0.12s
Wide QRS
Possible T wave inversion
Why does a delta wave appear on the EKG in Wolf-Parkinson-White syndrome?
WPW bypasses the AV node and forfeits the slowing of conduction at the node. Therefore, the impulse travels through the AV node and accessory pathway at the same time, leading to early arrival at the ventricle characterized by the upsloping delta wave.
Describe the MOA of adenosine:
Adenosine is an endogenous nucleoside that slows AV node conduction. Stimulation of the cardiac adenosine-1 receptor causes K efflux -> hyper polarizes the cell membrane -> slow AV node conduction
Discuss the concentration effect:
higher concentration of inhalation anesthetic delivered to the alveolus (FA), the faster the onset of action, aka over pressuring. (only relevant for nitrous oxide)
What two components make up the concentration effect?
- Concentrat”ing” effect
- Augmented gas inflow effect
Discuss the concentratING effect:
nitrogen is primary gas in lungs when breathing room air
nitrous oxide is ~34 times more soluble in blood than nitrogen
when N2O is introduced in lungs, the volume of N2O going from the alveolus to the pulmonary blood is much higher than the nitrogen moving in the opposite direction
this leads to alveolus shrinkage and relative increase in FA due to reduced alveolar volume
Discuss tidal breathing pressure changes:
Transpulmonary pressure = always positive (keeps airway open)
Intrapleural pressure = always negative (keeps lungs inflated)
Alveolar pressure = slightly negative during inspiration and slightly positive during expiration
