respiratory pathophysiology Flashcards
chemicals that contribute to increased airway resistance include (3)
inositol triphosphate (CN10–>Ach–>M3–>Gq–>PLC–>IP3–>Ca2+–>MLCK–>bronchoconstriction)
phospholipase C
leukotrienes
which nerve supplies parasympathetic innervation to airway smooth muscle
vagus nerve
how M3 receptor in airway smooth muscle creates bronchoconstriction (PSNS)
- cholinergic nerve endings release Ach to M3 receptors (a Gq protein)
- Gq protein activated, which activates phospholipase C (PLC)
- PLC activates ionsitol triphosphate (IP3), which is the second messenger
- IP3 stimulates calcium release from SR
- myosin light chain kinase activates and bronchoconstriction occurs
how M3 receptor in airway smooth muscle is inactivated
when IP3 phosphatase deactivates IP3 to IP2
are there sympathetic nerve endings in airway smooth muscle?
no, so B2 receptors are activated via catecholamines circulating systemically
how B2 receptors in airway smooth muscle creates bronchodilation (SNS)
- B2 receptor activation is via circulating catecholamine
- B2 (Gs receptor) activates adenylate cyclase
- adenylate cyclase activates cAMP
- along with protein kinase A, cAMP reduces Ca2+ release from SR
- this reduces smooth muscle contraction and produces bronchodilation
how B2 receptor in airway smooth muscle is inactivated
PDE3 turns off cAMP by converting it to AMP
pathway that NO follows to create bronchodilation
- non cholinergic PNS nerves release vasoactive intestinal peptide into airway smooth muscle
- this increases NO production
- NO stimulates cGMP, which fosters smooth muscle relaxation and bronchodilation
beta 2 agonists (3)
albuterol
metaproterenol
salmeterol
MOA of beta 2 agonists
stimulate B2, increase cAMP, decrease iCa2+
-stabilizes mast cell membranes and decreases mediator rerlease
SE of B2 agonists (5)
increased HR
dysrhythmias
hypokalemia (stimulates Na/K pump)
hyperglycemia
tremors
anticholinergics
atropine, glycol, iatropium*
MOA of anticholinergics
M3 antagonism, decreased IP3, decreased iCa2+
SE of anticholinergics (5)
inhibits secretions (dry mouth)
urinary retention
blurred vision
cough
increased IOP with narrow angle glaucoma
corticosteroid examples (5)
beclomethasone
budesonide
flunisolide
fluticasone
triamcinolone
MOA of corticosteroids (4)
stimulates intracellular steroid receptors
regulates inflammatory protein synthesis
decreases aw inflammation
decreases aw hyperresponsiveness
SE of corticosteroids (4)
dysphonia
myopathy of laryngeal muscles
oropharyngeal candidiasis
possible adrenal suppression
cromolyn MOA
stabilizes mast cell membranes (negligible SE’s)
leukotriene modifiers (4)
zileuton
monteuklast
pranlukast
zafirlukast
MOA of leukotriene modifiers
inhibits lipoxygenase enzyme, decreases leukotriene synthesis (negligible SE’s)
theophylline (methylxanthine) MOA
inhibits PDE, increases cAMP available
increases endogenous catecholamine release, inhibits adenosine receptors
SE’s of theophyllin (depending on plasma concentration)
-at a plasma concentration of 20mcg/mL: n/v/d, HA, disrupted sleep
-at a plasma concentration of 30mcg/mL: sz, tachydysrhythmias, CHF
most sensitive PFT for small airway disease (obstruction)
FEV 25-75%
FEV1 measurement and normal value
volume of air that can be exhaled after maximum inhalation in 1 second (declines with age)
>80% predicted value
FVC measurement and normal value
volume of air that can be exhaled after max inhalation
male: 4.8L
female: 3.7L
FEV1/FVC measurement and normal value
compares volume of air expiration in 1 second and total volume expiration
-useful in obstructive versus restrictive disease
-<70% = obstructive
- normal = maybe restrictive
75-80% predicted value is normal
MMEF (mid maximal expiratory flow rate) OR FEV 25-75% measurement and normal value
normal with restrictive disease and reduced with obstructive disease
100 +/- 25% predicted value
MMV (maximum voluntary ventilation) measurement and normal value
max volume of air that can be inhaled and exhaled over the course of 1 minute. best test of endurance
male: 140-180L
female: 80-120L
DLCO measurement and normal value
(based on which law?)
volume of carbon monoxide that can traverse the alveocapillary membrane per a given alveolar partial pressure of CO
-based on ficks law of diffusion
-normal: 17-25mL/min/mmHg
independent risk factors for PPC’s (patient related, procedure related, diagnostic testing related)
patient: >60y, CHF*, COPD, cigarettes
procedure: surgical site (aortic >thoracic>upper abdominal> neuro/peripheral vascular), procedure >2h, GA
diagnostic: albumin <3.5g/dL
factors that have NOT been correlated with PPC’s (3)
asthma
ABG’s
PFT’s
short term effects of stopping smoking (3)
carbon monoxide t1/2 4-6h
P50 returns to normal in 12h
short term cessation does not reduce PPC’s
intermediate term effects of stopping smoking (and how long intermediate is)
(5)
return of pulmonary function takes at least 6 weeks. this includes
aw function, mucociliary clearance, sputum production, pulmonary immune function, hepatic enzyme induction also subsides after 6w
obstructive disease PFT
FEV1
FVC
FEV1/FVC
FEF 25-75%
RV
FRC
TLC
FEV1 decreased
FVC increased or decreased
FEV1/FVC decreased
FEF 25-75% decreased
RV increased or normal
FRC increased or normal
TLC increased or normal
restrictive disease PFT
FEV1
FVC
FEV1/FVC
FEF 25-75%
RV
FRC
TLC
FEV1 decrease
FVC decrease
FEV1/FVC normal
FEF 25-75% normal
RV decreased
FRC decreased
TLC decreased
label this image
label this image
label this image
for an extrathoracic obstruction, which limb of the flow volume loop is flat?
the inspiratory limb
for an intrathoracic obstruction, which limb of the flow volume loop is flat?
the expiratory limb
most common ABG finding for asthma
respiratory alkalosis with hypocarbia
treatment of bronchospasm (in order)
- 100% FiO2
- deepen anesthetic
- short acting beta 2 agonist
- inhaled iatropium
- epinephrine 1mcg/kg IV
- hydrocortisone 2-4mg/kg IV
- aminophylline
- helium oxygen
regarding emphysema, explain the pathophysiology of pHTN
(what happens to PaO2 and PaCO2)
enlargement and destruction of airways distal to terminal bronchioles
-increase in dead space
-destruction of pulmonary capillary bed
-PaO2 and PaCO2 normal to slightly decreased
alpha 1 antitrypsin deficiency
abnormal variant of A1 antitrypsin enzyme is produced. hepatocyte cannot secrete this enzyme into the blood so it builds up and causes cirrhosis. alveolar elastase breakdown is regulated by this enzyme so when the enzyme dysfunctions it allows for overactivity of alveolar elastase.
the net result is destruction of pulmonary connective tissue and pan lobular emphysema
COPD dx during PFT
FEV1/FVC < 70% after bronchodilator therapy
ways to reduce risk of breath stacking or hyperinflation (3)
increase expiratory time (I:E 1:2 or 1:3)
decrease RR
larger ETT diameter (reduces flow resistance)
diagnostic for restrictive flow disease
FEV1 and FVC <70%
best way to mechanically ventilate a patient with restrictive lung disease (3)
minimize barotrauma with smaller Vt and higher RR
PIP <30cmH2O
prolong inspiratory time (IE 1:1)
methods to reduce the incidence of ventilator associated pneumonia include (3)
minimize duration of mechanical ventilation
limit sedation
oropharyngeal decontamination
mendelsons syndrome risk factors include gastric pH and volume of
pH <2.5
volume >25mL (.4mL/kg)
treatment of aspiration pneumonitis (in order)
- tilt the head down or to the side
- upper airway suction to remove particulate matter
- lower airway suction if necessary
- secure the airway to support oxygenation
- PEEP to reduce shunt
- bronchodilators to reduce wheezing
- IV lidocaine to reduce neutrophil response
- steroids probably won’t help and abx aren’t indicated unless patient has increased WBC count after >48h
emergency tx of a tension pneumothorax is a 14g catheter inserted in one of these places
2nd intercostal space mid clavicular line
4th or 5th intercostal space at anterior axillary line
nitrous is how many times more soluble in the blood than nitrogen?
34 times
(because B:G partition coefficient of nitrous is .47 and B:G of nitrogen is 0.014)
indications for thoracotomy related to hemothorax include
blood loss >1000mL or >200 mL/h, white lung on CXR, large air leak
(<150mL/h can be managed with VATS)
treatment of flail chest
reducing pain with epidural catheter or intercostal nerve block
order of monitors for VAE according to relative sensitivities (4)
- TEE
- precordial doppler
- EtCO2
- CVP
in neurosurgical patients, list the risk of VAE according to position from highest to lowest
sitting > supine > prone > lateral
s/sx VAE
air observed on TEE
mill wheel murmur
decreased EtCO2
decreased EtN2
increased PAP’s
HoTN
dysrhythmias
p.edema
hypoxia
cyanosis
tx of VAE in order
- 100% FiO2
- flood surgical field with NS
- if surgical insufflation is used, d/c it
- place patient in left lateral decubitus (durant maneuver)
- aspirate air from CVC
- hemodynamic support with inotropes, pressors, and fluid until air is reabsorbed
PVR can be reduced by (3)
hyperventilation
nitric oxide
nitroglycerine
PVR can be increased by (5)
hypoxia
hypercarbia
nitrous oxide
Hothermia
PEEP
pHTN is define as a PAP >
25mmHg
PVR equation and normal
PVR= (mean PAP - PAOP) / CO x 80
normal: 150-250dynes/sec/cm^5
drugs that decrease PVR include (6)
inhaled nitric oxide
NTG
PDE inhibitors (sildenafil)
PGE1 and PGI2
CCB’s
ACEI’s
with PVR in the setting of decreased SVR, treat via
vasopressors
with PVR in the setting of increased SVR or RV failure
give inhaled nitric oxide or iloprost
tx of carboxyHGB
treating the patient with 100% FiO2 takes the t1/2 of carboxyHGB from 4-6h to 60-90m. do this until CoHGB is less than 5%
hyperbaric O2 is indicated if CoHGB exceeds 25% or if patient is asymptomatic
hyperbaric O2 may prevent delayed neurcognitive syndrome
what can increase the production of CoHGB (think about the gas machine)
soda lime (des is biggest offender). this happens as soda lime becomes dehydrated
which drugs can you give down ETT? pneumonic
NAVEL
Narcan
Atropine
Vasopressin
Epinephrine
Lidocaine
normal VC and indication for mechanical ventilation
65-75mL/kg
indication <15mL/kg
normal inspiratory force and indication for mechanical ventilation
75-100cmH2O
<25cmH2O
normal PaO2 (at .21 FiO2) and indication for mechanical ventilation
> 72
<55 indication
normal A-a gradient (at .21 FiO2) and indication for mechanical ventilation
<10-15mmHg
>55
normal PaO2 (at 100% FiO2) and indication for mechanical ventilation
> 400mmHg
<200mmHg
normal ? (at 100% FiO2) and indication for mechanical ventilation
<100mmHg
>450mmHg
PaCO2 that indicates mechanical ventilation
> 60
RR that indicates mechanical ventilation (adults)
> 40 or <6
3 best predictors of PPC’s for patients undergoing pulmonary surgery
- DLCO <40% of predicted
- FEV1 <40% of predicted
- VO2 max <15mL/kg/min
DLT size and insertion depth for a female
<160cm
>160cm
<160cm 35fr
>160cm 37fr
~27cm
DLT size for male and insertion depth
<170cm 39fr
>170cm 41fr
~29cm
DLT for children 8-9y
26fr (smallest i believe)
DLT size for children 10+
28 or 32fr
how to ventilate during OLV (FiO2, Vt, RR, ARM’s, PEEP, COPD consideration)
80-100% FiO2
Vt 6mL/kg
RR 12-15BPM to maintain EtCO2
perform ARM before OLV initiation
PEEP 5-10cmH2O
if COPD with auto PEEP, give longer expiratory time and maybe decrease PEEP
management of hypoxemia during OLV
- verify 100% FiO2
- check position of tube via FOB
- rule out physiologic causes
- apply CPAP 2-10cm to non dependent lung
- apply PEEP 5-10cmH2O to dependent lung
- can also reinflate surgical lung intermittently, ask to clamp p.artery, and limit any drugs that decrease HPV
what can the lumen of the bronchial blocker be used for
insufflate O2 to non ventilated lung
suction air from non ventilated lung
relative contraindications to mediastinoscopy (3)
tracheal deviation
thoracic aortic aneurysm
SVC obstruction
(the only absolute contraindication is previous mediastinoscopy)
ARDS:
Mild
Moderate
Severe
Mild: PaO2 201-300mmHg
Moderate: PaO2 101-200mmHg
Severe: PaO2 <100mmHg
key pathophysiologic features of ARDS includes (4)
- protein rich p.edema
- loss of surfactant
- hyaline membrane formation
- possible long term injury
target PaO2/SaO2 during MV for ARDS
PaO2 55-80
SaO2 88-95% (just like COPD)
HFNC can deliver flow rates up to
60L/min
NC can only deliver up to _____% O2
21-40%
compared to a normal healthy lung, which lung volume undergoes the greatest increase in a patient with emphysema?
residual volume r/t premature aw closure (also why FRC is increased in this population)
what is the dx of a patient with elevated PIP’s but normal plateau pressures
bronchospasm/something that increases airway resistance
what is the likely dx of a patient with elevated PIP and plateau pressures
decreased p.compliance
atelectasis, p.edema, endobronchial intubation
B:G of nitrous oxide versus nitrogen and comparable solubility
B:G nitrous oxide 0.34
nitrogen 0.014
nitrous oxide 34x more soluble
youngest age that can get a DLT and size
8 years old
26fr
3 stages of ARDS
- exudative: hyaline membrane formation, bilateral alveolar infiltrates on CXR,
- proliferative: 7-21d. new pulmonary surfactant and type 1 cells, tight junctions restored and alveoli drained via lymphatics
- fibrotic: if you dont recover from proliferative you progress to this. can lead to pHTN
