Unit 1 - Respiratory Pathophysiology Flashcards
3 categories of predictors for postoperative pulmonary complications for pts undergoing pulmonary surgery
- lung parenchymal function (gas exchange)
- respiratory mechanics (airflow)
- cardiopulmonary reserve
DLCO that predicts postop pulmonary complications in pts undergoing pulmonary surgery
< 40% predicted
FEV1 that predicts postop pulmonary complications in pts undergoing pulmonary surgery
< 40% predicted
normal VO2 max
normal male = ~35-40 mL/kg/min
normal female = 27-31 mL/kg/min
VO2 max that predicts postop pulmonary complications in pts undergoing pulmonary surgery
< 15 mL/kg/min
when is split lung V/Q function testing indicated
when preoperative assessment suggests an increased risk of postop pulmonary complications
(DLCO < 40% predicted, FEV1 < 40% predicted, or VO2 max < 15 mL/kg/min)
what can you ask the patient in the place of VO2 max value
ask the patient if she/he can climb 2 flights of stairs
when might a right sided DLT be used
- distorted anatomy of left main bronchus (tumor, TAA)
- left pneumonectomy
- left lung transplant
- left sleeve resection
absolute indications for OLV
- isolation of 1 lung to avoid contamination (infection, hemorrhage)
- control distribution of ventilation (bronchopleural fistula, surgical opening of major airway, large unilateral lung cyst or bulla, life threatening hypoxia d/t lung disease)
- unilateral bronchopulmonary lavage
relative indications for OLV
- surgical exposure (high priority): TAA, pneumonectomy, thoracoscopy, upper lobectomy, mediastinal exposure
- surgical exposure (low priority): middle/lower lobectomy, esophageal resection, thoracic spine surgery
- pulmonary edema s/p CABG or robotic mitral valve surgery
- severe hypoxemia r/t lung disease
DLT size for females
< 160 cm = 35 french
> 160 cm = 37 french
DLT size for males
< 170 cm = 39 french
> 170 cm = 41 french
DLT depth
female ~ 27 cm
male ~ 29 cm
pediatric DLT sizes
8-9 yrs old = 26
10+ = 28 or 32
DLT alternatives for kids under 8 yrs
- bronchial blocker
- single lumen ETT advanced into mainstem bronchus
when is DLT contraindicated
< 8 years
complication of left sided DLT placed too far on right side with clamped tracheal lumen
absent right breath sounds
complication of left sided DLT placed too far on left side with clamped tracheal lumen
left breath sounds absent
complication of left sided DLT tip in trachea with clamped tracheal lumen
left and right breath sounds heard
where on the alveolar compliance curve is alveolar ventilation best
steepest part of the curve (where alveolar compliance is best)
how does lateral positioning in awake pt affect V/Q matching
alveoli remain on the same part of the alveolar compliance curve as awake upright position
how does lateral positioning affect V/Q matching under GA
reduced lung volumes and diaphragmatic excursion is better on the dependent side
results in V/Q mismatching
how is alveolar ventilation affected in the nondependent lung of an anesthetized patient in lateral position
- alveoli move from upper, flatter region of curve to the slope
- alveolar ventilation better in non-dependent lung
how is alveolar ventilation affected in the dependent lung of an anesthetized patient in lateral position
- alveoli move to lower compliance, less ventilation (lower, flatter region of slope)
- alveolar perfusion better in dependent lung
why is there an increased risk of hypoxemia during OLV
V/Q mismatch and increased A-a gradient
how do NMBs affect V/Q
- worsen mismatch
- abdominal contents shift towards thorax
how does positive pressure ventilation affect V/Q
worsens mismatch
how does the body compensate for V/Q mismatch
HPV
what color is the bronchial cuff of a DLT
blue
where should the clamp be placed for a DLT
- to connector piece going to lumen of operative lung
- place distal to y-piece and proximal to cap
FiO2 to use for OLV
- some say 100%
- some say 80% or less to minimize absorption atelectasis
ideal RR for OLV
12-15 breaths/min to maintain PaO2 35-45 mmHg
lab that should be checked serially after OLV is started
ABGs
benefit of PEEP in OLV
- increases FRC by pushing the lung up the compliance curve
- prevents excess shearing stress of repeated alveolar opening and closing
potential downside of PEEP in OLV
may increase shunt flow to non-depdenent lung
vent settings for OLV in COPD patients
longer expiratory time (I:E 1:3) and less extrinsic PEEP will improve gas removal from lung (decreased auto-PEEP)
how do volatiles affect HPV
impaired > 1.5 MAC
why do procedures that rely on left lung for OLV have a higher incidence of hypoxemia with OLV
right lung is larger than the left
steps to take if pt becomes hypoxemic during OLV
- verify 100% FiO2
- check tube position
- r/o physiologic causes (dec. CO, bronchospasm, mucus pluc, PTX, etc)
- apply CPAP to nondependent lung starting at 2 cm H2O up to 10 cm H2O
- PEEP to dependent lung
surgical method to reduce shunt flow to non-dependent lung in pneumonectomy patients
early clamping or ligation of pulmonary artery
can the lumen of a bronchial blocker be used for suctioning?
can’t suction blood, pus, or mucus from non-ventilated lung
can suction air from non-ventilated lung
can O2 insufflation be used with a bronchial blocker
yes
youngest age a DLT can be used
8 years old (size 26 Fr)
how can OLV be accomplished in a pt requiring nasal intubation
single lumen tube with bronchial blocker
how can OLV be accomplished in a pt with a trach
bronchial blocker
best choice for OLV when lung must be isolated for contamination concerns
DLT - not bronchial blocker
which lung is ventilated when using a bronchial blocker
the lung on the opposite side of the blocker
2 most common serious complications of mediastinoscopy
- hemorrhage
- pneumothorax (usually R side)
most common approach for mediastinoscopy
- small incision at midline of lower neck at suprasternal notch
- scope placed anterior to trachea and posterior to innominate artery and thoracic aorta
risk of mediastinoscopy r/t thoracic aorta
- hemorrhage
- reflex bradycardia
7 vital structures at risk for injury during mediastinoscopy
- thoracic aorta
- innominate artery
- vena cava
- trachea
- thoracic duct
- phrenic nerve
- RLN
consequence of innominate artery injury during mediastinoscopy
decreased carotid blood flow and cerebral blood flow
consequence of thoracic duct injury during mediastinoscopy
chylothorax
consequence of phrenic or right laryngeal nerve injury during mediastinoscopy
paresis
only absolute contraindication to mediastinoscopy
previous mediastinoscopy d/t scarring
relative contraindications of mediastinoscopy
- tracheal deviation
- thoracic aortic aneurysm
- SVC obstruction
what should you consider in regards to NMBs in pts having a mediastinoscopy
- procedure used to diagnose & stage lung cancer
- assoc. between oat cell carcinoma and eaton-lambert syndrome
- ELS pts sensitive to all NMBs
vascular anatomy from heart to brain
innominate (brachiocephalic) artery → R common carotid → R internal carotid → R cerebral circulation at circle of willis
consequence of innominate artery compression
- compromises circulation to right side of circle of Willis
- detrimental to pts with cerebrovascular disease
where should pulse ox be placed for mediastinoscopy
right upper extremity - of scope compresses innominate artery, waveform will dampen
where should NIBP placed in mediastinoscopy
LUE - if scope compresses innominate a., BP reading on L arm wont be affected
why might it be helpful to have a lower extremity IV in a mediastinoscopy in the event of bleeding
fluids and blood given in an upper extrmity will pass through vascular injury and enter mediastinum
indications for tracheal resection
- tracheal stenosis
- tracheomalacia
- tumor
- vascular lesions
- congenital malformations
sequence of ETT management in a patient undergoing lower tracheal resection
- place ETT in trachea above lesion
- after surgeon opens trachea, 2nd ETT place in L mainstem bronchus (used to ventilate L lung)
- surgeon sutures posterior tracheal anastomosis
- endobronchial ETT removed and tracheal ETT is advanced past anastomosis and positioned in L bronchus
what artery is at risk for compression during tracheal resection
brachiocephalic - follow same rules as mediastinoscopy for NIBP and pulse ox measurement
complication of neck positioning after tracheal resection surgery
tetraplegia - pt must maintain flexed position for several days after surgery to reduce tension on tracheal anastomosis
best choice for reintubation post tracheal resection
flexible fiberoptic bronch
2 core lung protective ventilation strategies
- low Vt
- PEEP
Berlin definition: onset of ARDS
within 1 week of initial insult or new/worsening respiratory symptoms
Berlin imaging criteria for ARDS
CXT or CT - bilateral opacities not fully explained by effusions, lonar/lung collapse, or nodules
Berlin definition of ARDS: edema origin
resp failure NOT fully explained by cardiac failure or fluid overload
Berlin criteria for mild ARDS
PaO2/FiO2 ratio 201-300 mmHg with PEEP or CPAP ≥ 5 cm H2O
Berlin criteria for moderate ARDS
PaO2/FiO2 ratio < 101-200 mmHg with PEEP ≥ 5
Berlin criteria for severe ARDS
PaO2/FiO2 ratio < 100 mmHg with PEEP ≥ 5
pulmonary causes of ARDS
which is the most common?
- pneumonia (most common)
- COVID 19
- aspiration
- smoke inhalation
- near-drowning
extrapulmonary causes of ARDS
which is the most common
- sepsis (most common)
- hematologic (TRALI, TACO, massive transfusion)
- trauma/shock
- burns
- CPB
what causes ARDS
neutrophil and platelet mediated inflammation injury that leads to diffuse alveolar destruction
4 key pathophysiologic features of ARDS
- protein-rich pulmonary edema
- loss of surfactant
- hyaline membrane formation
- possible long-term lung injury
stage 1 of ARDS
- onset
- duration
exudative
- onset ~6-72 hours after initial insult
- duration ~7 days
which phase of ARDS triggers inflammatory cascade and causes diffuse alveolar destruction
phase 1
what happens to type 1 pneumocytes in stage 1 of ARDS
injury disrupts integrity of tight junctions
- leads to capillary leak and protein-rich fluid traverses the alveolar capillary membrane
consequences of capillary leak in stage 1 of ARDS
- protein-rich fluids traverse alveolar capillary membrane
- surfactant damage increases alveolar surface tension
- alveolar collapse leads to dec. gas exchange
- inc. WOB d/t decreased alveolar compliance
role of hyaline membranes in stage 1 of ARDS
- alveoli collapse when there’s not enough surfactant
- damaged cells accumulate in airways and form hyaline membranes
common diagnostic findings in stage 1 of ARDS
- bilateral alveolar infilitrates on CXR
- hypoxemia despite increased supplemental O2
- increased A-aDO2 gradient
- spontaneously breathing pt may have respiratory alkalosis (tachypnea)
- pHTN in setting of low/normal LV filling pressure
hallmark of ARDS
hypoxemia despite increased supplemental O2
phase 2 of ARDS
duration?
proliferative phase
duration 7-21 days
how does the body attempt to repair itself in phase 2 of ARDS
- new pulmonary surfactant
- new type 1 pneumocytes
- tight junctions restored
- alveolar fluid drained by lymphatics
lasting damage from phase 2 of ARDS
fibrotic scarring
phase 3 of ARDS
extensive fibrotic changes causes irreversible changes to lung archtitecture
fibrosis of pulmonary vasculature leads to irreversible pHTN
typical cause of death in ARDS
not from respiratory failure but from underlying complications like sepsis or multiorgan failure
how does ARDS affect alveoli
some become very stiff, some maintain normal compliance
why is low Vt important in ARDS
Vt follows the path of least resistance - the stiff alveoli have poor compliance and fill minimally, normal compliance alveoli fill too much
alveolar overdistention causes volutrauma and barotrauma
what is biotrauma
excessive stretch stimulus in alveoli stimulates release of inflammatory mediators and exacerbates existing ARDS inflammation
superior ventilator mode in ARDS
pressure control - may offer superior pattern of flow distribution vs. volume control
ideal Vt for ARDS
4-6 mL/kg IBW
target plateau pressure for mechanically ventilating ARDS pts
< 30
reduce Vt to as low as 4 mL/kg IBW to achieve
RR for ARDS ventilation
6-35 breaths/min to target pH 7.3-7.45
risk of high RR in ventilating ARDS pts
dynamic hyperinflation
how to evaluate RV function in setting of PEEP adjustments
point of care echocardiography
PaCO2 goal for ventilating ARDS pts
permissive hypercapnia may be required
(the body will retain bicarb to compensate for respiratory acidosis)
how does prone positioning improve severe ARDS
- may improve V/Q matching and allow higher PaO2 for given FiO2
- greater number of functional lung units
max FiO2 for a regular nasal cannula
40%
how does conservative fluid management help in ARDS pts
supports oxygenation by reducing hydrostatic pressure in pulmonary capillaries
what are the 3 stages of ARDS
- exudative
- proliferative
- fibrotic
2nd messenger in pathway of bronchodilation induced by catecholamines
cAMP
2nd messenger in pathway of bronchoconstriction induced by PNS
IP3
what factor has the most significant contribution to airflow resistance
radius
how does smooth muscle contraction affect airflow
decreased airway diameter = increased airway resistance = decreased airflow
how does smooth muscle relaxation affect airflow
increased airway diameter = decreased airway resistance = improved airflow
nerve that supplies parasympathatic innervation to airway smooth muscle
vagus
releases ACh to M3 receptors in airway smooth muscle
cholinergic nerve endings
effects of M3 receptor activation in airway smooth muscle
= Gq activation = phospholipase C activation = IP3 activation = Ca2+ release from SR = MLK activation = contraction = bronchoconstriction
when does the PNS mediated bronchoconstriction pathway turn off
when IP3 phosphatase deactivates IP3 to IP2
in what part of airway are mast cells highly concentrated
smooth airway epithelium
proinflammatory mediators involved in bronchoconstriction
- prostaglandins (D2 & F2)
- leukotrienes (C4, E4, D4)
- platelet activating factor
- bradykinin
chemicals released by non-cholinergic C fibers that promote bronchoconstriction
- substance P
- neurokinin A
- calcitonin gene related protein
how are beta 2 receptors in airway smooth muscle activated
catecholamines in systemic circulation
how does beta 2 activation lead to bronchodilation
activation = Gs protein activation = adenylate cyclase activation = cAMP activation = decreased Ca2+ from SR = decreased smooth muscle contraction = bronchodilation
how is the pathway of bronchodilation from beta 2 receptor agonism turned off
PDE3 deactivates cAMP by converting it to AMP
how does vasoactive intestinal peptide affect airway smooth muscle
release by noncholinergic PNS nerves = increased NO production = cGMP stimulated = smooth muscle relaxation and bronchodilation
MOA of beta-2 agonists
beta 2 stim = increased cAMP = decreased Ca2+ = bronchodilation
SEs of beta 2 agonists
- tachycardia
- dysrhythmias
- hypokalemia
- hyperglycemia
- tremors
MOA of anticholinergics for bronchodilation
M3 antagonism = increased cAMP = decreased Ca2+ = bronchodilation
SEs of anticholinergics
- dry mouth
- urinary retention
- blurred vision
- cough
- increased IOP with narrow angle glaucoma
SEs of cortocosteroids
- dysphonia
- laryngeal muscle myopathy
- oropharyngeal candidiasis
- possible adrenal suppression
SEs of methylxanthines if plasma conc. > 20 mcg/mL
- N/V/D
- headache
- disrupted sleep
SEs of methylxanthines if plasma conc. > 30 mcg/mL
- seizures
- tachydysrhythmias
- CHF
what is FEV1
volume of air that can be exhaled in 1 second after maximal inhalation
normal FEV1
> 80% of predicted value
what is FVC?
what’s normal?
volume that can be exhaled after maximal inhalation
o Normal male = 4.8 L
o Normal female = 3.7 L
what is the FEV1:FVC ratio
when does it suggest obstructive vs. restrictive disease
compares volume of air expired in 1 second and total volume of air expired
- < 70% suggests obstructive disease
- Usually normal in restrictive disease
normal FEV1:FVC
75-80% predicted value
what is FEF 25-75%
measures airflow in the middle of FEV
most sensitive indicator of small airway disease
FEF 25-75%
FEF 25-75% in obstructive vs. restrictive disease
what is considered normal
o Usually ↓ with obstructive disease
o Usually normal with restrictive disease
o Normal: 100 +/- 25% predicted value
what is MMV
normal values?
Max. Voluntary Ventilation - max volume of air that can be inhaled & exhaled over 1 minute
o Normal male = 140-180 L
o Normal female = 80-120 L
PFT that is the best test of endurance
MMV
PFTs that measure dynamic lung volumes
- FEV1
- FVC
- FEV1:FVC
- FEF 25-75%
- MMV
what is DLCO?
normal values?
diffusing capacity: measures alveolocapillary membrane’s ability to exchange gas
• Volume of CO that can transverse alveolocapillary membrane per a given alveolar partial pressure of CO
Normal: 17-25 mL/min/mmHg
how can airway resistance be measured
dynamic pulmonary function testing
which lung volume is represented by the width of the flow volume loop
Vital capacity
patient related risk factors for postop pulmonary complications
- age > 60
- ASA > 2
- CHF
- COPD
- smoking
procedures at highest risk for postop pulmonary complications
- aortic
- thoracic
- upper abd ~ neuro ~ peripheral vascular
anesthesia time assoc. with increased postop pulmonary complications
2+ hours
lab test indicative of risk for postop pulmonary complications
albumin < 3.5 g/dL
respiratory risks of smoking
- risk for pulm disease
- decreasd mucociliary clearance
- airway hyperreactivity
- decreased pulmonary immune function
CV risks of smoking
- CV disease
- decreased DO2
- catecholamine release
- coronary vasoconstriction
- exercise intolerance
short term effects of smoking cessation
- CO t1/2 = 4-6 hours
- P50 to near normal in 12 hours
- decreased carboxyhemoglobin within 24 H
- does not reduce pulmonary complications
intermediate-term effects of smoking cessation
return of pulmonary function takes at least 6 weeks
- airway function
- mucociliary clearance
- sputum production
- pulmonary immune function
hepatic enzyme induction subsides (6 wks)
Best way to reverse anesthesia-induced atelectasis
ARM
how to perform ARM
hold PIP of 40 cm H2O for 8 seconds (best to apply PEEP to keep re-recruited alveoli open)
values in obstructive disease:
- FEV1
- FVC
- FEV1:FVC
- FEF 25-75%
- RV
- FRC
- TLC
- FEV1 = decreased
- FVC = increased to decreased
- FEV1:FVC= decreased
- FEF 25-75% = decreased
- RV = normal (inc if gas trapping)
- FRC = normal (inc if gas trapping)
- TLC = normal ( inc if gas trapping)
values in restrictive disease:
- FEV1
- FVC
- FEV1:FVC
- FEF 25-75%
- RV
- FRC
- TLC
- FEV1 = decreased
- FVC = decreased
- FEV1:FVC = normal
- FEF 25-75% = normal
- RV = decreased
- FRC = decreased
- TLC = decreased
when does airway collapse occur with extrathoracic obstruction
inhalation
when does airway collapse occur with intrathoracic obstruction
exhalation
PFTs have not been shown to be predictive of pulmonary postop complications except:
lung reduction surgery
greatest risk factor for developing asthma
atopy
most common ABG finding in asthma
respiratory alkalosis
what does increased PaCo2 indicate in asthmatic pts
- air trapping
- resp muscle fatigue
- impending respiratory failure
EKG during severe asthma attack
may show RV strain with RAD r/t increased PVR/increased R heart workload
what causes tachypnea and hyperventilation in asthmatics
neural reflexes (not hypoxemia)
what does a flow volume loop with a flat inspiratory or expiratory portion suggest in a wheezing patient
upper airway obstruction (not asthma)
CXR of asthmatics
- hyperinflated lungs
- diaphragmatic flattening
vent settings for asthma
- limit inspiratory time
- prolong expiratory time
- tolerate permissve hypercarbia
how can hemabate cause adverse effects in asthmatic
minimcs action of F2 alpha prostaglandin
s/s bronchospasm
- wheezing
- ↓ breath sounds
- ↑ airway resistance
- ↑ PIP with normal plateau pressure
- ↓ dynamic pulmonary compliance
- ↑ alpha angle on capnograph (expiratory upsloping)
treatment of bronchospasm
- 100% FiO2
- deepen anesthetic
- albuterol
- inhaled ipratropium
- epi 1 mcg/kg IV
- hydrocortisone 2-4 mg/kg IV (doesn’t help acutely)
- aminophylline
- Heliox
factors that contribute to air trapping in COPD
- decreased elastic recoil
- decreased airway rigidity & collapse during exhalatoin
- decreased airway pressures & airway collapse
common COPD findings
- flattened diaphragm
- increased AP diameter
- pulmonary bullae
- increased WOB
why are COPD patients at risk for severe alkalosis if PaCO2 normalized via ventilator settings
- chronically elevated PaCO2 = respiratory acidosis
- kidneys reabsorb bicarb and cause compensatory metabolic alkalosis
- changing vent settings doesn’t get rid of excess bicarb
most efficacious treatment for improving pHTN and preventing erythrocytosis in chronic bronchitis
o2 therapy
why do chronic bronchitis patients have erythrocytosis
RBCs overproduced to compensate for V/Q mismatch
why do chronic bronchitis patients have cor pulmonale
chronic hypoxemia & hypercarbia increase PVR and cause right heart strain/RAD
why do chronic bronchitis patients have ascites
weak right heart creates back pressure on liver/liver congestion
assoc. with enlargement and destruction of airways distal to terminal bronchioles
emphysema
assoc. with hypertrophied bronchial mucus glands & inflammation limited airflow during exhalation
chronic bronchitis
what contributes to pHTN in emphysema patients
• Destruction of pulmonary capillary bed
• same amount of blood must travel to a smaller network of blood vessels)
how do emphysema patients develop right heart failure
Late in disease, hypoxemia & hypercarbia further increase PVR
PaO2 & PaCO2 in emphysema
• Generally normal or slightly reduced PaO2
• Generally normal or decreased PaCO2 (r/t hyperventilation)
what causes cirrhosis in alpha 1 antitrypsin deficiency
abnormal enzymes can’t be secreted from hepatocyte - accumulation causes cell death and cirrhosis
how does alpha 1 antitrypsin deficiency cause emphysema
alpha-1 antitrypsin deficiency allows overactivity of alveolar elastase, which breaks down pulmonary connective tissue
causes destruction of pulmonary connective tissue
lab values in COPD:
- RV
- FRC
- TLC
- FEV1
- FEV/FVC
- FEF 25-75%
• Increased: RV, FRC, TLC
• Decreased: FEV1, FEV/FVC, FEF 25-75%
PFTs diagnostic of COPD
FEV1/FVC ratio of < 70% after bronchodilator therapy
best practice for supplemental O2 in COPD pt
Titrate supplemental O2 to maintain arterial O2 sat of 88-92%
when should neuraxial anesthesia be avoided in pts with COPD
when pt requires sensory blockade > T6
why is an interscale block not the best choice for a pt with COPD
causes paralysis of ipsilateral hemidiaphragm
ideal b:g solubility in a COPD pt
low - to minimize postop ventilatory depression
how does slower inspiratory time help COPD pts
helps gas redistribute from high compliance area to those with longer time constants (matches V/Q throughout lung)
expiratory time for COPD pts
Increase to minimize air trapping and auto-PEEP
how can N2O contribute to PTX in COPD pt
can cause rupture of pulmonary blebs
flow volume loop that suggests air trapping
Flow volume loop that doesn’t return to 0 at end expiration
what is auto-PEEP?
dynamic hyperinflation or breath stacking
if the patient can’t fully exhale each breath, a portion of that previous breath remains in the lungs
flow volume loop that suggest air trapping
doesn’t return to 0 at end expiration
3 causes of auto PEEP
- increased minute ventilation
- decreased expiratory flow
- increased airway resistance
methods to treat auto PEEP
- increased expiratory time (inc. I:E - 1:2 to 1:3)
- decreased RR
- larger ETT
- suction secretions
- d/c from circuit
vent settings for pt with restrictive lung disease
- Vt 6-8 mL/kg
- RR 14-18
- prolong inspiratory time (I:E 1:1)
PFTs in restrictive lung disease
decreased FVC and FEV1 (<70%)
ratio unchanged
3 characteristics of restrictive lung disease
- decreased lung volumes and capacities
- decreased compliance
- intact pulmonary flow rates
acute intrinsic causes of restrictive lung disease
- upper airway obstruction
- aspiration
- narcan
- cocaine OD
- re-expansion of collapsed lung
- neurogenic
chronic intrinsic causes of restrictive lung disease
(interstitial lung disease)
- sarcoidosis
- amiodarone-induced pulmonary fibrosis
structural causes of restrictive lung disease
- kyphoscoliosis
- ankylosing spondylitis
- flail chest
- PTX
- pleural effusion
- pneumomediastinum
- mediastinal mass
- neuromuscular disorders
FRC in restrictive disease
decreased
3 potential problems with aspiration
1) gastric contents in airway = risk obstruction
2) gastric contents cause chemical burn to airway/lung parenchyma = risk bronchospasm
3) infectious material enters airway = bacterial infection
when is aspiration most likely to occur
most common during induction or within 5 min of extubation
what is mendelson’s syndrome & what are the risk factors
chemical aspiration pneumonitis
- gastric pH < 2.5
- gastric volume > 25 mL (0.4 mL/kg)
hallmark symptom of aspiration
hypoxemia
Most common CXR finding in aspiration pneumonitis
pulmonary edema & infiltrates in perihilar and dependent lung regions
what should you do first if you suspect your patient has aspirated
head down/to the side
when should abx be given for aspiration pneumonitis
only if pt develops fever or ↑ WBC after 48 hours
best method to prevent VAP
avoid intubation altogether
what should raise suspicion of VAP in intubated pt
↑ WBC and/or fever
what med should be used for intubated/vented pt with high risk for GI bleed prophylaxis and why
sucralfate
PPIs increase bacterial overgrowth
drug class not recommended for aspiration pneumonitis prophylaxis
anticholinergics
treatment of closed PTX
obs, catheter aspiration, chest tube
treatment of open PTX
occlusive dressing (allows air to escape but doesn’t allow air in), supplemental O2, chest tube, +/- intubation
closed PTX
Defect in pulmonary tree or lung tissue - air enters and exits pleural space through defect
open PTX
Defect in chest wall - air passes between pleural space and atmosphere
which type of PTX is described?
Lung collapses on inspiration & partially re-expands on expiration
open
what type of PTX is described?
↑ intrathoracic pressure when air enters pleural space through a ball-valve defect in chest wall (air can enter but not exit the pleural space)
tension
how does mediastinum shift in tension PTX
towards contralateral side
hallmark characteristics of tension PTX
hypoxemia, ↑ airway pressures, ↑ HR, ↓ BP, ↑ CVP
POC tension PTX US
lack of lung sliding and absence of comet tails (reverberation artifact)
emergency tension PTX treatment
insertion of 14g angiocath in a) 2nd intercostal space at MCL or b) 4th or 5th intercostal space at AAL
definitive treatment of tension PTX
chest tube
most common cause of hemothorax
bleeding intercostal vessel
indications for thoracotomy with hemothorax
o Initial drainage > 1 L
o Continued bleeding > 200 mL/hr
o White lung on CXR
o Large air leak
hemothorax patients who are candidates for VATS management
- bleeding < 150 mL/hr
- HD stable
cause of chylothorax
damage to thoracic duct, which empties lymph into L subclavian
key characteristics of flail chest
paradoxical movement of chest wall at site of rib fractures
what happens during inspiration with flail chest
- non-injured ribs move outward
- injured ribs move inward
- underlying tissue compressed
- mediastinum shifts contralateral side
what happens during expiration with flail chest
- non-injured ribs move inward
- injured ribs move outward
- underlying lung tissue doesn’t empty
- mediastinum shifts to ipsilateral side
consequences of flail chest
alveolar collapse, hypoventilation, hypercarbia, hypoxia
what causes airlock
Gas embolism of significant size can travel to R heart and lodge in pulmonary outflow tract or PA
consequences of airlock
converts distal alveoli to dead space
s/s VAE
- air on TEE
- “mill wheel” murmur with precordial
- ↓ ETCO2
- ↑ EtN2
- ↑ PAP
- ↓ BP
- pulmonary edema
- hypoxia
- cyanosis
methods to detect VAE from most to least sensitive
TEE > doppler > PAP/EtCO2 > CO, CVP > BP, EKG, stethoscope
what is durant position
L lateral decubitus position (
VAE treatment
- 100% O2
- flood field with NS
- d/c insufflation
- L lateral decubitus position (Durant maneuver)
- aspirate air from CVL
- HD support (floods, vasopressors, inotropes)
how does air trapped in the pulmonary circulation affect the left side of the heart
- decreased LV preload
- decreased CO
- asystole/CV collapse
diagnosis of pHTN
mean PAP > 25 mmHg
causes increased PVR
increased vascular smooth muscle tone, vascular cell proliferation, and/or pulmonary thrombi
consequences of increased RV afterload in pHTN
RV dilation, RVH, ultimately systolic impairment
CO in pHTN pt
relatively fixed & preload dependent
what leads to tricuspid regurg in pHTN pt
↓ RV stroke volume = ↑ RV volume at the end of diastole - stretches tricuspid
causes of pHTN
COPD, hypoxemia, hypercarbia, L heart dysfunction, mitral valve disease. CHD, connective tissue disorders, chronic thromboembolism, portal HTN
drugs that increase PVR
- n2o
- ketamine
- desflurane
causes of increased PVR
hypoxemia
hypercarbia
acidosis
SNS stim
pain
hypothermia
↑ intrathoracic pressure
mechanical ventilation
PEEP
atelectasis
drugs that decrease PVR
iNO, nitro, PDE inhibitors, PGE1, PGE2, CCBs, ACE inhibitors
how can increased RA pressure cause a shunt
how is this treated
open foramen ovale and lead to R L intracardiac shunt
Treat: reverse causes of increased pulmonary resistance
preferred neuraxial method in pHTN pts
epidural - slower sympathectomy vs. spinal
drug of choice for increased PVR r/t uterine contractions
nitroglycerin
Carbon monoxide deprives the tissues of o2 what 2 primary ways
1) CO binds to O2 binding site on hgb with affinity 200x that of O2 - displaces O2 from hgb & ↓ CaO2
2) CO causes L shift in carboxyhgb dissociation curve (less O2 at tissue level)
how does CO poisoning lead to metabolic acidosis
Impairs oxidative phosphorylation - decreased ATP - metabolic acidosis
t1/2 of carboxyhemoglobin
4-6 hours breathing room air
CO poisoning treatment
100% supplemental O2 reduces t1/2 to 60-90 min
O2 therapy continued until CoHgb < 5% for 6 hours
when is hyperbaric o2 indicated for CO poisoning
if CoHgb > 25% or pt symptomatic
risk of using dessicated soda lime with des
CO formation
VC that is a strong indicator for mechanical ventilation
what’s normal?
< 15 mL/kg
normal 65-75 mL/kg
inspiratory force that is a strong indicator for mechanical ventilation
what’s normal?
< 25 cm/H2O
normal 75-100 cm/H2O
PaO2 and A-a gradients that are strong indicators for mechanical ventilation
@ 21% FiO2:
- PaO2 < 55 mmHg
- A-a gradient > 55 mmHg
@100% FiO2:
- PaO2 < 200 mmHg
- A-a gradient > 450 mmHg
single best predictor of postop pulm complications (after pulm surgery)
VO2 max
how does the PNS affect airway diameter
causes bronchoconstriction
physiologic systems that contribute to bronchoconstriction
mast cells & noncholinergic c fibers
PNS (vagus nerve)
physiologic systems that contribute to bronchodilation
non-cholinergic PNS (NO)
SNS (circulating catecholamines)
A = expiration
B = inspiration
C = TLC
D = Residual volume
inhalation vs exhalation on flow volume loop
inhalation: waveform moves R-L with negative deflection
exhalation: waveform moves L-R with positive deflection
PaCO2 that is a strong indicator for mechanical ventilation
> 60
