RESPIRATORY PATHOPHYSIOLOGY modules 1-14 Flashcards
What mediates bronchoconstriction (2)
PNS (muscarinic-3 receptors)
immune response
What mediates bronchodilation
Catecholamines VIP receptors (NO pathway)
What is the most significant contribution to airflow resistance in the airways
Radius of airway
What physiologic systems determine airway diameter (4)
How: bronchoconstriction/dilation
PNS (Vagus) = bronchoconstriction
Mast cells and non-cholinergic PNS = bronchoconstriction
Non-cholinergic PNS (NO) = bronchodilation
SNS (catecholamines) = bronchodilation
Which nerve supplies PNS innervation to airway smooth muscles and what is the result?
Vagus n (CN 10) = M3 receptors
Result = bronchoconstriction
What effect do mast cells and non-cholinergic C-fibers produce in the airway
Bronchoconstriction
How do sympathetic nerve endings affect airway smooth muscle
They DON’T
Sympathetic nerve endings do not exist in airway smooth muscle
How does sympathetic response occur in airway smooth muscle? What is the response
B2 receptors in the airway are activated by circulating catecholamines
response = bronchoconstriction
What product does non-cholinergic PNS stimulation produce in the airway? What is the response
Nitric Oxide
Result = bronchodilation
What is the physiologic result of decreased airway radius and how
smooth muscle contraction => decreased airway diameter => increased airway resistance => reduced airflow
How = PNS vagus n., mast cells, and non-cholinergic C-fibers
What is the result of increased airway radius and how
smooth muscle relaxation => increased airway diameter => decreased airway resistance => improved airflow
how = Non-cholinergic PNS NO, SNS circulating catecholamines at B2 receptors
Which nerve provides PNS innervation to airway smooth muscles
Vagus N
How doe cholinergic nerve endings function in the airway
Release ACh on to M3 receptors
Describe the M3 receptor response to ACh
M3 is coupled to Gq protein.
M3 activation turns ON the Gq protein which activates phospholipase C (PLC)
What activates phospholipase C in the airway and what is PLC response
Activation = Gq protein is turned on by the M3 receptor activating PLC
Response = inositol triphosphate (IP3) is activated as a second messanger
What is IP3 role in the airway and what activates it?
Activation = PLC via Gq protein and M3 receptor
Role = stimulation of Ca++ release from sarcoplasmic reticulum
What is the role of Ca++ and how is it released
Release = IP3 stimulation of sarcoplasmic reticulum
Role = activates myosin light chain kinase. This enzyme enables the contractile mechanism leading to bronchoconstriction
How is the bronchoconstriction pathway deactivated?
When IP3 phosphatase deactivates IP3 to IP2
How do mast cells mediate airway radius
High concentrations of mast cells in smooth airway epithelium = Bronchoconstriction
What are the mast cell and pro-inflammatory mediators that alter airway radius and how? Result
mediators = IgE, cytokines, complement, histamine, PG, leukotrienes, bradykinin, plt activating factor
How = cough, allergy, or infection activate mediators and amplify the inflammatory process
Bronchoconstriction
How do non-cholinergic C-fibers affect airway radius?
Release chemicals that promote bronchoconstriction
What receptors respond to mast cells and other pro-inflammatory cells in the airway? result
Histamine-1 Thromboxane-specific prostanoid receptor CysLT1 PAF Bradykinin-2
Bronchoconstriction
What C-fiber mediators are released in the airway? Result
Substance P
Neurokinin A
Calcitonin gene related peptide
Bronchoconstriction
Which receptors respond to C-fiber mediator release? Result
Neurokinin-2
CGRP
Bronchoconstriction
Describe the process of how circulating catecholamines affect airway radius?
B2 receptors present in airway smooth muscle
B2 receptors activated by circulating catecholamines NOT sympathetic nerve endings
Bronchodilation is effect
What activates the B2 receptor in the airway? Function of B2 receptor?
ACtivation = circulating catecholamines
Function = B2 receptor coupled to Gq protein which is turned on thus activating adenylate cyclase.
Second messanger cAMP is activated by adenylate cyclase and, with PK, decreases Ca++ release from SR.
Smooth muscle contraction is reduced = bronchodilation
How is adenylate cyclase activated and what is the subsequent role in airway?
Activation = B2 receptor turning on Gq protein
Role second messenger cAMP is activated
How is cAMP activated and what is the subsequent role in airway?
Activation = adenylate cyclase, PK
Role = reduces Ca++ release from SR, reducing smooth muscle contraction and promotes bronchodilation
How is the B2 receptor pathway deactivated?
Phosphodiesterase 3 deactivates cAMP by converting to AMP
What is the role of NO is the airway and how?
Role = bronchodilation
How = non-cholinergic PNS nerves release vasoactive intestinal peptide onto airway smooth muscles
This increases NO production
NO stimulates cGMP which leads to smooth muscle relaxation
Examples of leukotriene modifier drugs
usually end in KAST
Montelukast
Zafirlukast
Zileuton
Example of methylxanthine
Theophylline
Example of mast cell stabilizer drugs
Cromolyn
Examples of corticosteroids for respiratory diseases
Fluticasone
Budesonide
Beclomethasone
Triamcinolone
What are the classes for each drug Theophylline Zafirlukast Budesonide Cromolyn Triamcinolone Montelukast
Theophylline = methylxanthine Budesonide/Triamcinolone = corticosteroids Cromolyn = mast cell stabilizer Zafirlukast/Montelukast = leukotriene modifier
3 classes of pulmonary medications
direct acting bronchodilators
anti-inflammatories
methylxanthines
2 categories of direct acting bronchodilators
Beta 2 agonists
Anticholinergics
What are examples of Beta 2 agonists for respiratory diseases. Effect?
albuterol, metaproterenol, salmeterol
Bronchodilation
Examples of anticholinergics for respiratory disease. Effect?
atropine, glycopyrrolate, ipatropium, tiotropium
Bronchodilation
3 categories of anti-inflammatory drugs used for bronchodilation
Inhaled corticosteroids
Cromolyn
Leukotriene modifiers
Which 2 anesthetic agents have bronchodilating effects?
Volatile anesthetics
Ketamine
2 MOA of bronchodilating beta-2 agonists
B2 stimulation => increased cAMP => decreased Ca++
Stabilizes mast cell membranes => decreases mediator release
Side effects of beta-2 agonists for bronchodilation
tachycardia dysrhythmias HYPOkalemia HYPERglycemia Tremors
MOA of anticholinergic bronchodilators
M3 antagonism => decreased IP3 => decreased Ca++
Side effects of anticholinergic bronchodilators
Dry mouth from decreased secretions Urinary retention Blurred vision Cough Increased IOP
MOA of corticosteroids for bronchodilation
Stimulates intracellular steroid receptors
Regulates inflammatory protein synthesis
-decreasing airway inflammation
-decreasing airway hyperresponsiveness
Side effects of corticosteroids for bronchodilation
Dysphonia
Myopathy or laryngeal muscles
Oropharyngeal candidiasis
Adrenal suppression
MOA of cromolyn for bronchodilation
stabilizes mast cells
MOA of leukotriene modifiers for bronchodilation
Inhibition of 5-lipoxygenase enzymes which decreases leukotriene synthesis
MOA of methylxanthines for bronchodilation
Inhibition of phosphodiesterase => increased cAMP
Increased endogenous catecholamine release
Inhibition of adenosine receptors
Side effects of methylxanthines
Low plasma concentrations:
- N/V/D
- HA
- disrupted sleep
High plasma concentrations >30 mcg/mL:
- Seizures
- Tachydysrhythmias
- CHF
Which PFT is the most sensitive indicator of small airway disease
Forced expiratory flow 25 - 75%
What does forced expiratory flow measure
The average forced expiratory flow during the middle half of the FEV measurement
What do static lung volumes measure and examples
Measures how much air the lungs can hold at a single point in time
Examples = RV, ERV, Vt, IRV, FRV, IC, VC, TLC
What does dynamic lung volume measure and examples
Measures how quickly air can be moved in and out of the lungs over time
Examples: FEV1, FVC, FEV1/FVC ratio, MMEF
Measure of how much air the lungs can hold
Static lung volume
Measure of how quickly air can be moved in an out of the lungs over time
Dynamic lung volume
Measure of how well the lungs transfer gas across the alveolar-capillary membrane
Diffusion capacity
What is the normal FEV1 value
> 80% of predicted value
What is the normal FEV1/FVC ratio
> 75-80% of predicted value
How are lung volumes and capacities measured
Spirometry
What does spirometry measure
Lung volumes and capacities
Can reserve volume and FRC be measured by spirometry
no
What does dynamic lung volume assess?
Airway resistance
Lung recoil
What does FVC measure and normal values
Volume of air exhaled after a maximal inhalation
Male = 4.8 L Female = 3.7 L
What does FEV1/FVC ratio measure
Normal values
Compares volume of air expired in 1 second and total volume of air expired
Normal = 75-80% predicted value
What does an abnormal FEV1/FVC indicate
<70% suggests obstructive disease
Normal in restrictive disease
Helps differentiate between obstructive vs restrictive disease
Measure of volume of air exhaled after a maximal inhalation in 1 second
FEV1
Measure of volume of air that can be exhaled after a maximal inhalation
FVC
What does FEV1 measure and normal value
Volume of air exhaled after a maximal inhalation in 1 second
> 80% predicted value
What does abnormal FEV1 indicate
Poor pt effort
Declines with age
Measures volume of air exhaled after maximal inhalation in 1 second
FEV1
What does forced expiratory flow at 45-75% VC measure and normal values
Measures airflow in the middle of FEV (@25-75%)
Normal = 100 +/-25% predicted value
Measures airflow in the middle of FEV and is most sensitive indicator of small airway disease
Forced expiratory flow at 25-75% VC
What does an abnormal forced expiratory flow at 25-75% of VC indicate
REDUCED = obstructive disease
NORMAL = restrictive or no disease
Most sensitive indicator of small airway disease
What does maximum voluntary ventilation measure and normal values
Maximum volumes of air that can be inhaled and exhaled over 1 minute
male = 140-180 mL female = 80-120 mL
Measures maximum volume of air that can be inhaled and exhaled over 1 minute
Maximum voluntary ventilation
How is diffusion capacity measured and normal value
Measured by volume of carbon monoxide that can traverse the aveolocapillary membrane per a given alveolar partial pressure of carbon monoxide
normal = 17-25 mL/min/mmHg
Measure of volume of carbon monoxide that passes thru the alveolocapillary membrane per a given alveolar partial pressure of carbon monoxide
Diffusion capacity
What law is diffusion capacity based on
Fick’s Law of diffusion
What is the importance of lung flow-volume loops
differentiation between obstructive and restrictive disease
What patient population is at risk for postop pulmonary complications
age>60 yo CHF COPD Cigarette smoker ASA >2
What procedure variables increase postop pulmonary complications
Surgical site (Aortic>thoracic>upper abd/neuro/peripheral vascular>emergency)
Procedures lasting >2.5 hrs
General anesthesia
Which diagnostic test can indicate and increased risk for postop pulmonary complications
serum albumin<3.5 g/dl
Does a history of asthma increase postop pulmonary complications?
NO
What are short-term benefits of smoking cessation
Decreased carboxyhgb, which improves P50 (affinity for O2)
From greatest impact to least, list the surgical procedures that can increase postop pulmonary complications
Aortic
Thoracic
Upper abd, neuro, peripheral vascular
emergency
6 risk reduction strategies for postop pulmonary complications
- Smoking cessation (at least 6 weeks)
- Alveolar recruitment + PEEP
- Bronchodilators and corticosteroids for expiratory airflow obstruction
- Treat active infections
- Consider options other than GA
- Teach patient pulmonary recruitment maneuvers
What is the half-life of carbon monoxide?
4-6 hours
Intermediate-term effects of stopping smoking?
Return of pulmonary function at least 6 weeks Airway function Mucociliary clearance Sputum production Pulmonary immune function Reduce hepatic enzyme induction
What peak airway pressure is required for initial reopening of atelectatic regions?
30 cmH2O
What benefits could PIP of 40 cm H2O for 8 seconds provide
Reverse anesthesia-induced atelectasis
How can anesthesia-induced atelectasis be reversed almost completely?
PIP of 40 mmH2O for 8 seconds
What is the relationship between FiO2 and atelectasis
FiO2 significantly contributes to absorption atelectasis
Use lowest FiO2 the patient can tolerate
Preoperative risk reduction strategies to decrease postop pulmonary complications
Treat expiratory airflow obstruction with bronchodilators and corticosteroids
Treat active infxn with antibiotics
Educate on pulmonary recruitment maneuvers
Treat RV failure
Intraoperative risk reduction strategies to decrease postop pulmonary complications
Consider RA vs GA
Minimally invasive surgical procedures over open procedures
Avoid procedures >3 hours
Postoperative risk reduction strategies to decrease postop pulmonary complications
Utilize effective analgesia (NB, Neuraxial opioids, PCA)
Pulmonary recruitment measures (IS, deep breathing, pulm toilet, CPAP)
What characteristics (2) define obstructive lung disease
Small airway obstruction
Increased expiratory flow
Getting air out is the problem
What characteristics (2) define restrictive disease
Proportionate reduction in all lung volumes
Poor compliance
Problem is small lung volumes
What lung measures are decreased in restrictive disease
FEV1 and FVC
RV, FRC, TLC
Which lung measure is normal in restrictive disease
FEV1/FVC
FEF 25-75%
Which lung measures are decreased in COPD with gas trapping
FEV1, FVC, FEV1/FVC, FEF 25-75%
Which lung measures are increased in COPD with gas trapping
RV, FRC, TLC
What is an example of a fixed respiratory lesion. How does the flow-volume loop appear
Ex: tracheal stenosis
Inspiratory and expiratory limbs are flat
Describe the effect of an extrathoracic obstruction on inhalation and expiration
Inhalation = airway collapse, decreased flow
Expiration = pushes obstruction open. Normal flow
Describe the effect of an intrathoracic obstruction on inhalation and expiration
Inhalation = obstruction is pulled open, normal flow
Expiration = airway collapse, reduced flow
Describe the effect of extrathoracic vs intrathoracic obstruction on the flow-volume loop
Extrathoracic = inspiratory limb is flat
Intrathoracic = expiratory limb is flat
Definition of asthma
Acute, reversible airway obstruction accompanied by airway inflammation and bronchial hyperreactivity
Which obstructive lung disease is reversible
Asthma
What airway measures are improved in asthma after bronchodilators
FEV1, FEV1/FVC, FEF25-75%
What ABG findings may be found in the asthmatic patient
respiratory alkalosis
Hypocarbia
What does hypercarbia indicate in the asthmatic patient
Air trapping, respiratory muscle fatigue and impending respiratory failure
What anesthetic measures can be taken with the asthmatic patient (6)
- Suppress airway reflexes during instrumentation
- Limit inspiratory time, prolong expiratory time, permissive hypercapnia
- Avoid non-selective beta-blockers (beta-1 are best)
- Deep extubate if possible
- Chose anesthetics that promote bronchodilation
- Avoid histamine releasing drugs
Which histamine releasing drugs should be avoided in the asthmatic patient
Succinylcholin
Atracurium
Morphine
Meperidine
Which anesthetic agents promote bronchodilation in the asthmatic patient
Volatiles (sevo, iso)
Ketamine
Propofol
Lidocaine
Which beta blockers should be avoided and which ones used if needed in the asthmatic patient
Avoid = non-selective beta-blockers, beta-2
Ok to use = beta-1 selective
Ventilator settings that should be used in the asthmatic patient
Limit inspiratory time
Prolong expiratory time
Permissive hypercapnia
What alternatives should be considered in lieu of airway instrumentation in the asthmatic patient
LMA
Regional techniques
Which spirometry measures are altered in the asthmatic patient and how
FEV1, FEV!/FVC, FEF 25-75%
All decreased but reversible
Why might there be EKG changes during an severe asthmatic attack? What are the changes?
Increased PVR increases the workload of the right heart
Changes = RV strain w/ right axis deviation
How does bronchospasm cause hypoxemia
due to V/Q mismatch
What changes occur with FRC and TLC in the asthmatic patient
FRC may increase d/t air trapping
TLC remains normal
What are chest xray changes in the asthmatic patient
Hyperinflated lungs
Diaphragm flattening
What is the dose of lidocaine for airway reflex suppression in the asthmatic patient
Lidocaine 1-1.5 mg/kg 1-3 minutes p/t extubation
How doe NMBD affect bronchospasm
They don’t
Consideration for toradol in the asthmatic patient
Avoid if the patient has aspirin-intolerant asthma
In an OB patient with asthma and poor uterine tone after delivery, which drug is most appropriate and why
Methergine
Carboprost can elicit bronchoconstriction in asthmatic patients because of the F2 alpha PG action.
How can IV hydration benefit the asthmatic patient
IVF can decrease viscosity of airway secretions
What are some anesthetic causes of wheezing
Kinked ETT end-bronchial intubation Aspiration Light anesthesia Cuff overinflation Pt biting ETT
How does intraoperative bronchospasm present (5)
Wheezing Decreased breath sounds Increased peak inspiratory pressure Decreased dynamic compliance Increased alpha angle on EtCO2 waveform (expiratory upsloping)
Treatment for bronchospasm (8)
- 100% FiO2
- Deepen anesthetic
- Short-acting inhaled beta-2 agonist
- Inhaled ipratropium
- Epi 1 mcg/kg IV
- Hydrocortisone 2-4 mg/kg IV
- Aminophylline
- Helium-O2 mixture
What does a deficiency in alpha-1 antitrypsin lead to?
Increase in alveolar protease activity
That enzyme degrades pulmonary connective tissue
Leads to development of panlobular emphysema
Cigarette smoking doubles rate of destruction
What is the treatment for alpha-1 antitrypsin deficiency
Liver transplant
Describe expiratory flow in the COPD patient
Reduction in maximal expiratory flow
Slower forced emptying of lungs
Definition of chronic bronchitis
Hypertrophied bronchial mucus glands and chronic inflammation
Definition of emphysema
Enlargement and destruction of airway distal to terminal bronchioles
What volumes and capacities are increased in COPD
RV, FRC
Metabolic changes in COPD patient and how does the body compensate
Elevated PaCO2 causing respiratory acidosis
Compensation = Kidneys reabsorb HCO3- which provides compensatory metabolic alkalosis
How does O2 administration affect CO2 in the COPD patient
Inhibition of hypoxic pulmonary vasoconstriction
Haldane effect
SaO2 goal for the COPD patient at risk for O2-induced hypercapnia
88-92%
What are components of COPD pathophysiology (4)
- Progressive deterioration of elastic components in lungs
- Reduced airway rigidity causing exhalation collapse
- Increased gas velocity decreasing airway pressures
- Secretions obstructing airflow
Why is O2 unloading affected in the COPD patient
If CO2 is returned to normal, the compensatory increase in HCO3- from kidney reabsorption remains. This reduces O2 unloading
What is a hematologic compensation for COPD and why
RBC overproduction
Compensates for V/Q mismatch (increased dead space)
Increases blood viscosity and myocardial work
How can supplemental O2 affect patients with severe COPD
It can cause O2-induced hypercapnia
How does supplemental O2 lead to O2-induced hypercapnia in the COPD patient (2)
- Inhibition of HPV increases shunt and dead space. Increased DS decreases CO2 excretion
- Haldane effect describes how O2 in the blood determines the blood’s ability to buffer O2. Well oxygenated blood has lower capacity to buffer CO2 which causes hypercapnia
When should regional anesthesia be considered in the COPD patient
For procedures involving the extremities and lower abdomen
When should neuraxial anesthesia be avoided? Why
When the patient requires sensory blockade >T6
Why = impairment of expiratory muscle function and reduced ERV, hindering cough and clearance of secretions
Effects of an interscalene block on COPD patient
IS block causes paralysis of ipsilateral hemidiaphragm d/t phrenic nerve blockade
What type of volatile agent is best for COPD patient
An agent with a low blood:gas solubility
An anesthetic that bronchodilates i.e. sev/iso>des
Considerations for the use of N2O on the COPD patient
N2O is associated with rupture of pulmonary blebs and can lead to PTX
Vt, I:E considerations, and PEEP considerations for the COPD patient
Vt = 6 - 8 mL/kg IBW I:E = longer expiratory time PEEP = use but be alert for hyperinflation
Considerations for sedation when using regional anesthesia in the COPD patient
Avoid over-sedation, which depressive ventilation
Which volatile anesthetic is least irritating to the airway?
Sevoflurane
How does air trapping affect emergence from volatile anesthetic?
Theoretically prolongs emergence d/t agent trapping in alveoli
How does slow inspiratory flow improve V/Q matching in COPD patients?
It helps gas redistribute from high compliance areas to areas with longer time constants
This maximizes V/Q matching through entire lung
How does an increased expiratory time affect COPD ventilation
It minimizes air trapping and auto-PEEP
Suggested mechanical ventilation settings for patients with COPD
Vt 6-8 ml/kg IBQ
Slow inspiratory flow
PEEP
Increased expiratory time
You should select a volatile agent with a high blood:gas solubility. T/F
FALSE
All halogenated anesthetics dilate the lower airways. T/F
TRUE
Sevo is more likely than des to irritate the airway. T/F
FALSE
Turning on N2O can produce PTX. T/F
TRUE
Inhibition of HPV caused by volatile agents can be overcome by increasing FiO2. T/F
TRUE
Define dynamic hyperinflation
When a new breath is given before the patient was able to fully exhale the previous breath
AKA breath stacking
When a new breath begins before complete exhalation is…
dynamic hyperinflation aka auto-PEEP aka breath stacking
What are risk factors for dynamic hyperinflation
High minute ventilation
Increased airway resistance
reduced expiratory flow
What are consequences of dynamic hyperinflation (auto-PEEP)
Barotrauma
PTX
HoTN
Interventions for dynamic hyperinflation (auto-PEEP)
Disconnecting patient from circuit to allow for full exhalation to atmospheric pressure
Increase I:E ratio
How does high minute ventilation contribute to auto-PEEP
Large tidal volumes or fast respiratory rate don’t allow enough time for full expiration
Factors that contribute to reduced expiratory flow in the COPD patient (3)
Anything that decreases airway diameter:
- bronchoconstriction
- Airway collapse
- Inflammation
Factors that contribute to increased airway resistance in the COPD patient
Secretions
Obstructed ETT
Fighting ventilator
What pulmonary consequences may arise d/t auto-PEEP
Alveolar overdistension Barotrauma PTX INC PIP INC PP INC work of breathing
What cardiac consequences may arise d/t auto-PEEP
Impaired venous return
HoTN
Overestimation of CVP/PAOP
List 3 causes of auto-PEEP
High minute ventilation
Reduced expiratory flow
Increased airway resistance
Examples of restrictive lung disease
Sarcoidosis
Negative pressure pulmonary edema
Flail chest
Define restrictive lung disease and what structures may be restricted
Define = collection of disorders that impair normal lung expansion during inspiration
Structures = pulmonary interstitium, pleura, rib cage, abdomen
Acute causes of restrictive ventilatory deffects
aspiration
upper airway obstruction (flat inspiratory limb on flow-volume loop)
Chronic pulmonary causes of restrictive lung disease
Sarcoidosis
Pulmonary fibrosis d/t amiodarone
What defects of the chest wall, mediastinum or pleura can contribute to restrictive lung disease
Flail chest Pleural effusion Ankylosing spondylitis PTX Mediastinal mass Pneumomediastinum Neuromuscular disorders i.e. MDs, GBS SC injury
Other anatomical contributors to restrictive lung deffects
Pregnancy
Obesity
Ascites
Which lung measures are changed and how with restrictive lung disease
FEV1 and FVC are decreased
Mechanical ventilator management for patients with restrictive lung disease
Vt 6 mL/kg IBW
RR = 14 - 18 bpm
PIP < 30 cm H2O
I:E = 1:1
All increase inspiration time/volume
3 characteristics of restrictive lung disease
- Decreased lung volumes and capacities
- Decreased compliance
- Intact pulmonary flow rates
Which lung volumes are affected by restrictive lung disease
All volumes are decreased (VC, TLC, Vt…)
Remember FRC is decreased
What is the goal for mechanical ventilation in patients with restrictive lung disease and how is this accomplished
GOAL = minimize risk of barotrauma
Accomplished = Small Vt (6 mL/kg) and faster RR (14-18 bpm). Keep PIP <30 cmH2O by prolonging inspiratory time
When does aspiration most commonly occur
During induction and intubation or within 5 minutes of extubation
What are the possible consequences of aspiration (4)
Airway obstruction
Bronchospasm
Impaired gas exchange
Bacterial respiratory infection
Risk factors for aspiration
Pregnancy
Trauma
Emergency surgery
GI obstruction
What is Mendelson’s syndrome
A chemical aspiration pneumonitis d/t gastric pH <2.5 and gastric volume >25 mL
List some pharmacologic prophylaxis classes for aspiration
Antacids H2 antagonists GI stimulants PPI Antiemetics
Typical signs and symptoms of aspiration
Hypoxemia Dyspnea Tachypnea Cyanosis Tachycardia HTN
Initial treatment of aspiration includes 4 interventions
head downward or to side
Suction upper airway
Secure airway if indicated
PEEP
Criteria for a patient to be discharged home from PACU after aspiration
- No new cough or wheeze
- No CXR evidence of pulmonary injury
- No decrease in SpO2 >10% of preop value on RA
- A-a gradient <300 mmHg
What CXR findings may be present on images s/p aspiration
Pulmonary edema
Infiltrates in perihilar and dependent lung regions
How do ETT contribute to VAP
ETT bypass a patients defense mechanisms including cough and mucociliary clearance
Micro-aspiration possible between ETT cuff and trachea
How does GI prophylaxis affect VAP
PPIs suppress gastric acid leading to bacterial overgrowth in the stomach
Any aspirations increase the risk of infection
Aspiration pneumonitis causes what 3 potential problems?
- Airway obstruction
- Chemical burn to airway and lung parenchyma
- Bacterial infxn
What drug class is not recommended as a prophylaxis for aspiration pneumonitis by decreasing secretions
Anticholinergics
What are 3 types of PTX
Closed
Communicating
Tension
What are hallmark characteristics of tension PTX
Hypoxemia Increased airway pressures Tachycardia HoTN Increased CVP Absent BS on affected side Tracheal shift to unaffected side
Which gas should be discontinued immediately if a PTX is suspected
N2O
What is emergency treatment of a tension PTX
14 g angiocath to 2nd IC space at mid-clavicular line or at 4-5th IC space at anterior axillary line
4 consequences of flail chest
Alveolar collapse
Hypoventilation
Hypercarbia
Hypoxia
In a closed PTX, where is the defect located?
Pulmonary tree or lung tissue
Air enters and exits the pleural space through defect
Treatment for closed PTX
Observation
Cath aspiration
CT insertion
In an open PTX, where is the defect located?
Defect in the chest wall
Air passes between pleural space and atmosphere
What happens to the lung during an open PTX
Inspiration = lung collapse Expiration = partial re-expansion
Treatment for open PTX
Occlusive, unidirectional dressing allowing air out but not in
Supplemental O2
CT insertion
Possible tracheal intubation
Where is the defect when a tension PTX occurs
It can be an open or closed defect
Consequence of tension PTX
Increased intrathoracic pressure causes mediastinal shift on contralateral side
Compression of heart and vasculature reduces VR and CO
Indications for surgical treatment of hemothorax
Initial output >1000 mL
Bleeding > 200 mL/hr
White lung on CXR
Large air leak
What can increase the risk of chylothorax
CVC insertion on left side disrupting the thoracic ducts
Describe the movement of the flail segment during respiration
Inspiration = the injured ribs move inward and collapse affected region
Expiration = Injured ribs move outward and affected region doesn’t empty
What are the pulmonary consequences of flail chest
Alveolar collapse
Hypoventilation
Hypercarbia
Hypoxia
