Presentations mixture of highlights!!!!!!!! Flashcards
I am just putting together a mixture of topics from the power points presented!!!!!!!!!!!
Asthma and bronchospasms
this is the first topic!!!!!!!!!!
what is asthma?
a chronic pulmonary disease characterized by airway inflammation, airflow obstruction, and bronchial hyper-reactivity
5 manifestations of asthma
dyspnea
wheezing
chest tightness
cough
2 types of asthma
Atopic
non-atopic
which asthma is the most common type?
atopic
Which asthma is:
type I IgE mediated hypersensitivity reaction
usually beings in childhood
triggered by environmental allergens
skin test with antigen shows wheel and flare reation
Atopic
Which type of asthma is:
viral respiratory infections are common trigger
inflammation associated hyperirritability
family hx less common
no evidence of allergen sensitization
non-atopic
Patho of atopic Asthma
big ass slide just read over be familiar with different phases and basic process!!!
-initial exposiure to the allergen stimulates the TH2 cells to:
—-secrete inflammatory cytokins
—- trigger the B cells to produce IgE
- IgE coated mast cells
-repeated exposure to allergen triggers the mast cells to release granule contents and produce cytokines and other mediators
-EARLY PHASE
-bronchoconstriction, increased mucus production, vasodilation with increased vascular pearmeability
LATE PHASE
- epithelial damage and additional inflammation and airway constriction
You can do it!!
just a word of encouragement!!!!
Bronchoactive drugs! give examples of each category B2-adrenergic agonist? Anticholinergics? MastCell stabilizers? Corticosteroids? Luekotriene receptor antagonist?
B2-adrenergic agonist? ----albuterol; terbutaline; metaproternol Anticholinergics? ---- ipratropium bromide MastCell stabilizers? ---- cromolyn, nedocromil Corticosteroids? you know them there is a million Luekotriene receptor antagonist? ----- Muontelukast, Zafirlukast, and Zileuton
Quickly how do each of the following drug categories work for asthma (should know incase our pt's get asthma attack in OR) don;t go deep (lol) please give it a try you'll surprise yourself!!!! B2-adrenergic agonist? Anticholinergics? MastCell stabilizers? Corticosteroids? Luekotriene receptor antagonist?
B2-adrenergic agonist?
–directly relax smooth muscle of airway
Anticholinergics?
—- antimuscarinic bronchodilating effects in bronchial smooth muscle and blocking constriction of vagal efferent stimulation
MastCell stabilizers?
—- prevention and reduction of inflammation
Corticosteroids?
—- anti-inflammatory
Luekotriene receptor antagonist?
—- inhibits leukotriene production (part or thr arachidonic acid pathway)
GA implications with ASTHMA::
- GA may trigger asthma exacerbation
- alteration of diaphragmatic function
- impaired ability to cough
- decreased mucociliary function
- stimulation/irritation of airway by ETT
_______ and _______ of the most recent asthma attacks are the most significant predictors of bronchospasms!
proximity and severity
Changes in lung function can also leas to ______, _____ ______, and ________ postoperatively
atelectasis
mucus plugging
wheezing
Asthma exacerbation intra-op can also lead to what?
prolonged intubation
hypoxemia
pneumonia
Recent studies have found NO links between higher risks postop complications and pts with asthma? true or false
true
from a study!!!!
pt’s with asthma who are well controlled and who have a peak flow measurement of > __% of predicted or personal best can proceed to surgery at average risk!!
80
preop assessment for asthma
inspection auscultation questions -age of onset -triggering events -allergies -cough sputum characteristics Current meds (and effectiveness) smoking HX Anesthetic HX -asthma related complications Hospitalizations for asthma -freq of ER visits -Hx of intubation and mechanical ventilation
Preop management and interventions for the asthmatic
Chest PT
antibiotic therapy
Bronchodilator therapy (continue day of SX)
corticosteroids (stress dose if indicated)
—-stress dose hydrocortisone 100mg IV
Asthma classifications Intermittent asthma- Mild persistent asthma- mod persistent asthma- severe persistent asthma-
really way to much for a slide!!!! see ppt slide 23 if you want
Intraop management for asthma
- regional if not contraindicated
- Avoid non-selective BB (propranolol and Labetalol)
- Avoid NSAIDs (toradol)
- Avoid histamine releasing drugs ( morphine, atricurium, suxs, mivacurium, demerol, thiopental)
Intraop agents (tell me their effects) propofol- Ketamine- Lidocaine- VAAs-
propofol- bronchodilator
Ketamine- smooth muscle relaxant and decreased airway resistance
Lidocaine-supress airway reflexes (inhaled can assist)
VAAs- all are potent bronchodilators (sevo least irritating)
Extubation for Asthma-
deep- controversal
bronchodilator- albuterol
IV lidocaine
S/S of bronchospasm
- high inflation pressures
- expiratory upsloping on ETCO2
- prolonged expiration
- decreased O2 sat
- expiratory wheezing
- decreased breath sounds
treatment for bronchospasm
100% O2 Increase anesthestic beta agonist (terbutaline 0.25mg SQ; albuterol) anticholinergic ( ipratropium bromide) Lido IV Epi- corticosteroids
Next section is COPD!!!
Great job on the last section!!!!!!!!!
Name 5 common obstructive disorders
Emphysema Chronic bronchitis Asthma Bronchiectasis OSA
______ and ________ are often clinically grouped together and refered to as COPD
emphysema
chronic bronchitis
Emphysema and chronic bronchitits are often clinically grouped together and refered to as COPD, since many people have overlapping features of damage at both the acinar level and bronchial level, almost certainly because of the extensive trigger _______ _______ is common in both
cigarette smoking
about ___% of people with COPD are NON-smokers
10%
COPD is commonly diagnosed how
PFTs via spirometry
the PFT findings GOLD criteria for COPD is
Low FEV1/FVC= 70%
What is the severity of COPD based on the FEV1/FVC mild moderate severe very severe
mild- >80%
moderate- 50-79%
severe- 30-49%
very severe- <30%
Define emphysema
abnormal permanent enlargement of airspace distal to the terminal bronchiole,
Acinar refers to what?
emphysema
2 types of emphysema? (most prominant 95%)
centiacinar
panacinar
which type of emphysema is:
central lobes of acini are primarily affected, distal alveoli are spared, seen predominately in heavy smokers
Centiacinar
which type of emphysema is:
entire acinus is affected, associated with alpha1-antitrypsin deficiency
panacinar
s/s of emphysema
dyspnea @ rest dry cough pursed lip breathing wheezes with auscultation long expiratory pause barrel shaped chest
Define chronic bronchitis
mild chronic inflamation throughout the airways, parenchyma, and pulmonary vasculature
S/s of chronic bronchitis
Impressive cough productive sputum
wheezes or crackles
dyspnea (late)
cor pulmonale/ right sided heart failure (late)
Define brochiectasis
disease characterized by permanent dilation of bronchi and bronchioles caused by destruction of the muscle and elastoc tissue, resulting from or associated with chronic necrotizing infections
COPD pre-op eval
questions to ask
ADLs presence of infections sputum triggering agents meds and effectiveness time of symptoms (day night) previous anesthesia hx OSA
smoking is associated with __-_____ deficiency
alpha1-antitrypsin
COPD peri-op management
supress neural reflexes Inhibit increased intracellular Ca++ Control airway inflammation eliminate secretions maintain VQ
COPD anesthetics
VAAs-
IV agents-
avoid what???
VAAs- iso or sevo (greater broncho=dilators)
IV agents- propofol (direct vagal mediated relaxation of airway smooth muscle)
-Ketamine- bronchodilatory effects
avoid what- barbiturates (histamine release)
Peri-op mechanical ventilation
Increase expiratory time --- can also increase inpsiratpory time --- I:E 1:6 Auto peep- --- detection with expiratory hold .5-1 sec --- detect with auscultation Reduce MV --- decreased TV --- Decreased RR
Periop COPD with O2
maintain PaO2 at 55-75 mmHg or near the pts norm, with FiO2 less than .5
Keep PCO2 where
normal range 50-60 mmHg (pH .3-7.4)
Wonderful job.. Now of to pneumona
PNE=pneumona
Yeahhhhhhh!!!!!
Define pneumonia
an infection of the lower respiratory tract caused by bacteria, viruses, fingi, protazoa, or parasites; results in an inflammatory response and fluid accumulation in the alveoli
Pro-op assesment for PNE
s/s of PNE
fever/chills N/V Cough Chest pain diaphoresis cyanosis in nailbeds/lips AMS headache muscle pain weakness crackles
Etiology of PNE
advanced age immunocompromised underlying lung disease alcoholism impaired swallowing AMS immobilization ETT malnutrition CV or liver disease Chronic exposure to irritants
immunocompromised pt’s at risk for PNE
HIV Cystic fibrosis Meds from transplants autoimmune diseases Asplenia pregnancy DM
4 main causitive agents for PNE
bacterial
viral
Fungal
Parasitic
Most common type of bacterial PNE
streptococcus pneumoniae
Bacterial PNE s/s: the pt may present with a cough and what color sputum???
green, yellow, rust colored
common types of viral PNE
rhinovirus coronavirus INFLUENZA VIRUS RSV CMV
Fungal PNE is seen in pts with what
AIDS (PCP)
chemotherapy
Parasitic PNE is most common in what patients
Immigrants
immune deficient
people after traveling
PNE can be classified as what 5 categories?
atypical community acquired nosocomial aspiration ventilator associated
PNE is also classified by the area of lung affected and divided into what 2 classes
Lobar
bronchial
What is atypical PNE
aka walking PNE
sicker than they appear
caused by atypical organisms
atypical symptoms
CAP
Pt has not been in hospital
most common pathogen is streptococcus pneumoniae
Nosocomial PNE occurs when
> 48 hrs after admission
Anesthetic considerations for PNE
Semi-recumbent position (when able) NGT-OGT secretion management NPO status ensure proper cuff pressure (20-30 cm H20 TCDB H2 blockers Antiemetics higher FiO2 may be needed (if active) watch for airway irritation
ok next is PE you are on a good tract, just keep reading and flipping it will all come to you!!! you are smart you can do this this!!
I meant smart ass!!! but none-the-less you still got this shit!!!
define PE
impaction of foreign material into the pulmonary circulation, specifically the pulmonary arteries
Etiology of PE
90% DVT
Less common
– air, bone, tumor, amniotic fluid, fat, CO2
Etiology of PE r/t hereditary conditions
factor V leidan
protein C deficiency
Protein S deficiency
Antithrombin Deficiency
Other less popular PE etiology
Contraceptives
HRT
Air travel
Cancer
What is the process that leads to DVT/ PE
venous stasis
hypercoagulbility
Vessel wall injury
====virchow’s triad
Patho of PE
virchow's triad thrombus dislofgement occlusion of pulmonary circulation vascular changes symptoms
S/S of PE
dyspnea tachypnea tachycardia hypotension cyanosis hemoptysis chest pain syncope JVD
Anesthesia implications:
for pts at risk for PE
minimize myocardial depression high fiO2 Monitor PAP intotropes/vasopressors etomidate or ketamine induction
Anesthesia implications:
how to detect PE during anesthesia??
Decreased ETCO2 Tachycardia Decreased SaO2 Increase in PAP or CVP decreased B/P bronchospasm EKG
Anesthesia implications:
treatment intraop
airway established (if not already) D/c anesthetic 100% fiO2 PEEP Circulatory support Sympathominetics/Inotropes Anticoagulation -----heparin 5000-1000 units bolus gtt 1000-1500 units an hour
Anesthesia implications:
PE postop concerns
persistant hypoxia
reperfusion edema
Anesthesia implications:
PE prevention
LMWH 12 hours before sx
SCDs
Warfarin (INR 3)
inferior vena cava filter
A good drug for PE treatment ( to better ventilate)
Inhaled Nitric oxide
Inhaled nitric oxide (facts)
specific to lungs
effective dose 10-20ppm
pulmonary vasodilation
decreases RV afterload
Ok chicken fuckers 4 presentations down!!!! not bad, only 24 to go haha!!
keep it up Lets go onto pulm HTN ps this is the 2 person one may be long but I am going to keep it condensed!!!!!!!
Management strategies for PULM HTN
TREAT THE CAUSE O2 diuretics in RV failure vasodilators CCB ACEi Epoprostenol, trespitinil Sildenafil prostacyvlin Nitric oxide atrial septostomy transplant anticoagulation
Phosphodiesterase inhibitors MOA
inhibit nitric oxide degradation
Phosphodiesterase examples and effects (2)
sildenafil (PDE-5 inhibitor) --- decreases PAP/PVR --- min effects on systemic vasculature --- synergistic with NO --- Reduction in RV mass-prevention or reversal of RVH Milrinone (PDE-3 inhibitor) --- decreases PVR/PAP/SVR --- nebulized form minimizes systemic vasodilation
Endothelien receptor antagonist:
drug and MOA?
Endothelin-1
- neurohormone that casuses pulm vasoconstriction, smooth muscle proliferation, and fibrosis
- stimulates endothelin receptors A and B
- -A- vasoconstriction
- -B- vasodilation
anesthetic considerations:
recommended test pre-op
CBC, Coags, LFTs EKG CXR ABG Echo Cardiac Cath
anesthetic considerations:
assessment
type of sx METS Severty of Pulm HTN RV function Comorbidities
anesthetic considerations: Pulm HTN
you want to optimize what?
O2 Brinchodilation antibiotics steroids vasodilators inotropes
anesthetic considerations: Pulm HTN
Goals to maintain:
preload SVR Contractility CO NSR
anesthetic considerations: Pulm HTN
Goals to prevent
MI
hypotension
Increased PVR
anesthetic considerations: Pulm HTN
Monitoring
ASA standards
A-line
CVP
TEE
anesthetic considerations: Pulm HTN
regional benefits and precautions
Maintain spont breathing postop analgesia continuous vs bolus plexus/nerve catheters anti-coagulation??? Reduce LA dose
anesthetic considerations: Pulm HTN
GA benefits
Method of choice for major sx Airway management systemic vasodilation mechanical ventilation reduced coronary perfusion
anesthetic considerations: Pulm HTN
pre-medication
Small doses of midazolam (avoid hypoventilation)
anesthetic considerations: Pulm HTN
induction
opiods (blunt DL)
Lido (blunt DL)
prop, etomidate (either)
muscle relaxants (avoid histamine releasing)
anesthetic considerations: Pulm HTN meds: propofol etomidate ketamine
PROPOFOL decrease SVR Decrease Venouse return Decrease contractility ETOMIDATE maintain hemodynamics no PVR effect KETAMINE (CONTROVERSIAL) INCREASES PVR???
anesthetic considerations: Pulm HTN Isoflurane- Des- Sevo- Nitrous Oxide
ISOFLURANE - attenuate magnitude of HPV -potentiates vasodilator response to B1 -No effect on Alpha 1 DESFLURANE - potentiates pulm vasoconstriction SEVO- -can be used safely NITROUS OXIDE- -depresses myocardial contractility -increased PVR and RAP -Caution
anesthetic considerations: Pulm HTN
maintenance
maintain opioids
maintain muscle relaxation
Avoid histamine releasing drugs
anesthetic considerations: Pulm HTN
Ventilatory management!
high O2
Moderate TV
HYPOcarbia (increase rate)
low PEEP (5-10)
anesthetic considerations: Pulm HTN
HTN crisis treatment
inhaled NO (20-40 ppm) Milirone (50 mcg/kg bolus)
ok another one down!!!! stay with me!!! lets do TB
Here is goes
Define TB
an infection caused by mycobacterium tuberculosis (an acid fast bacillus) that infects pulmonary tissues and other organs
What is a definitive test for TB
acid-fast sputum test
What are the stages of TB
EARLY INFECTION -immune fight infection -no s/s EARLY PRIMARY PROGRESSION (ACTIVE) - immune system loses fight - inflammation ensues - NON-productive cough -fatigue weight loss fever -diagnosis difficult LATE (ACTIVE) - cough is PRODUCTIVE - more s/s -progressive weight loss anemia, rales - present on X-ray - diagnosis via sputum LATENT - Myobacteria persist on body - no s/s occuring -pt's DO NOT feel sick - infection can reappear
how does TB spread
airborne droplets 1-5 mcg
Anesthetic implications for TB:
infection control
N95 mask (except for rudy’s bad ass beard)
neg pressure air system
surgical mask for pt
all equip sterilized after use
air filter in Y peice
CHANGE OUT SODA LIME after pt
elective procedures postponed till post infection
pretty short and sweet!!!!! kinda shitty presentation but well take it!!!
oh well!!!
ok here is long winded Lo’s Lung transplant!!!! it could be scary she likes alot of info well see what happens. buckle up boys
ok one more big breath!!!!
lung transplant today is a standard alternative to manage what?
end stage lung disease, refractory to standard medical or sugical therapy, to pts with NO other significant functional impairment
current life expectancy post lung transplant?>
single 5.5 years
double 6.5 years
(i only added this b/c I thought It was odd that you have a better expectancy with 2 lungs vs one) seems tricky!!
% most common diseases treated with lung transplantation
RESTRICTIVE LUNG DISEASE - idiopathic pulmonary fibrosis, ILD OBSTRUCTIVE LUNG DISEASE -COPD, bronchitis SUPPORATIVE LUNG DISEASES - cystic fibrosis, bronchiectasis PULMONARY VASCULAR DISEASE - pulm artery HTN OTHER - sarcoidosis
Anesthetic implications for lung transplant:
donor pro-op
PaO2/FiO2 >300
clear Chest X-ray
Negative bronchoscopy (minimal to no secretions)
age < 20 years
Anesthetic implications for lung transplant:
recipient pre-op
H&P EKG CxR labs-ABG, Coags, lytes, CBC Type and Cross -PRBCs, PLTs, FFP IV Review- ECHO, Cath, VQ immunosupression
Anesthetic implications for lung transplant:
donor intra-op
Lungs must be visualized and deemed acceptable.
CROSS CLAMPING TIME DECLEARED–starts ischemia time
Anesthetic implications for lung transplant:
recipient intra-op
Induction intubation ventilate ASA monitoring A-line CVL PA line warming blankets TEE???
Anesthetic implications for lung transplant:
Obstructive lung disease
I:E ration 1:4 or 1:5 check for auto peep avoid hyperinflation (Pnemo) permissive hypercarbia bronchodilators (if indicated)
Anesthetic implications for lung transplant:
restrictive lung disease
NO inhaled Low volume ventilation high RR Minimal PEEP AUTO PEEP= NOT A CONCERN
Anesthetic implications for lung transplant:
suppurative lung disease
agressive pulmonary toilet
avoid hyperinflation
NO inhaled
Anesthetic implications for lung transplant:
intra-op recipient once lung implanted
end ischemia time record ischemia time ventilate intra-op bronch for anastomosis check avoid reprofusion injury (NO) protective ventilation(PCV < 25 mmHg)
Anesthetic implications for lung transplant:
post lung transplant in OR
If single lung - remove DL tube- place SL tube - assess chest tube -transport to ICU If double lung - turn pt to opposite lateral decubitis -switch ventilation to transplanted lung - remove next lung
Not too bad!!!! alot of info!!
ok her we go!!
ok next is bronchoscopy and Chest xray
this should be interesting get ready set and go!!!!!!!!!!!
Indications for a bronchoscopy
cough wheeze hemoptysis diaphragmatic paralysis unexplained hoarsness vocal cord paralysis' suspected TEF airway obstruction chest trauma intubation abnormal cXr
Anesthetic implications for Bronchoscopy:
preop-assessment
airway assessment
respiratory CV focus
dental
premedication - antisialogogue, sedative
rigid bronchoscope highlights (scaled way down from ppt to hit highlights)
trachea and proximal/central airways
GA needed
analyzes expired gases
rigid bronch indications
tumor foreign body removal stent placement dilation viscous secretions
rigid bronch side note (just look and read)
in a picture in the ppt it shows a side port where the anesthesia circuit can connect!! ( no need for ETT (?????)
Flexible bronchoscopy
most common visualizes to segmental bronchi (3rd generation) LA conciuos sedation GA suction, bx, and irrigation channels need large diameter ETT
flexible bronchoscopy indications
clearing secretions hemoptysis control tumor staging stent placement topical placement (meds)
Anesthetic implications for Bronchoscopy:
contraindications to bronch
arrhythmia (their dead) refractory hypoxemia inability to tolerate recent MI Creatinine > 3.0 platelets < 50,000 uncorrected coagulopathy SVC obstruction Pulm HTN Unstable neck or c-spine immobility Limited ROM of TMJ
Anesthetic implications for Bronchoscopy:
complications
Bronchospasm hypoxemia hemoptysis pneumothorax hemorrhage infection edema Ok this list goes on for about another 20 answers. just know it it is bad it could happen
Anatomy!!!!!!!
larynx location?
composed of
- epiglottis to cricoid cartilage
- 3 single cartilages, 3 paired cartilages
Anatomy!!!!!!!
trachea
length?
RMB and LMB angles
-10-15 cm long
- RMB 25-30 degrees
LMB 45 degrees
Anatomy!!!!!!!
right bronchial anatomy and left bronchial anatomy
too much to make card on many different anatomical locations I feel this is more important to a pulmonoligist not anesthesia as we wont be going that deep into the lungs but if you have alot of free time and want to learn go look!!!
CxR how to interperate?
not a radiologist not going into detail.. look for big signs like why your pt is breathing maybe its a pneumothorax you know what to look for. and pulm htn or pulm edema and ARDS white out!! if you crave the need for more see ppt i don;t think it is important!!!
ok that is done!!! are you still with me
you bet your ass you are!!!!!
rudy and jake please upload any information you think WE should KNOW for your lung presentations!!!!!!! I won’t be adding those here!!!
Thanks for your cooperation
ok last pulmonary one I think!!! it is sam I am
on atelectasis and hypoxemia!! drop your socks grab your cocks!!! this will be an adventure
anesthesia induced lung collapse occurs in approximately ___% of all GA surgeries
90%
2 types of alveolar cells
type I- squamous alveolar- cells that form the structure of an alveoli
type II-(greater alveolar)- cells that secrete pulmonary surfactant
3 mechanisms of lung dysfunction
loss of lung “units”
impaired gas exchange
V/Q mismatch
the key factor involved in the origin of lung collapse is the _______ dysfunction observed in anesthesia
diaphragmatic
how does compressive atelectasis occur
abdominal pressure id transmitted into thoracic cage and compresses pulmonar parachyma in dependent areas
how does denitrogenating a pt cause atelectacis
high fiO2 induces atelectasis by absorption of )2 in oulmonary areas with low V/Q
Why don’t we leave pt’s on an fiO2 of 1.0
reabsorption atelectasis
who is at higher risk for reabsorption atelectasis?
smoker
elderly
(b/c they have pre-existing low V/Q areas)
do you give more O2 for treatment of atelectasis
not really! remember reabsorption atelectasis. increasing fiO2 is effective for treating the symptom but not the cause
so what is treatment for atelectasis and how is it done
Alveolar recruitment strategy (ARS)
controlled and step wise increment and decrement of airway pressures using fixed settings in PCV.
driving pressure of 15 cm H2O, RR 10-15 I:E 1:1 fiO2 1.0
3 phases of ARS
hemodynamic preconditioning phase
recruitment phase
decremental phase peep titration phase
hemodynamic preconditioning phase
-test hemodynamic response to high PEEP
-Change of 15-20% from base line of VS halts test
-3-5 ml/kg of crystalloid to correct hypovolemia
actual test
1) 5 cm increments of PEEP from 0-20
2) each PEEP step maintained for 5 breaths
-spend a few minutes at PEEPS 10-15 to test hemodynamic stability
recruitment phase
- opening pressures of lung is 40cnH2O
- once hemodynamics have been tested and stabilized
- increase both driving pressures and PEEP to 20cmH20
decremental phase peep titration phase
- progressive decrease in PEEP of 2 cmH2O every few minutes
- identify lung closing pressures in dependent zones
When to recruit
once after induction
whenever the airway is open to atm
when not to recruit
LMA or facemask
hemodynamically unstable
-broonchospams, TEF, high ICP , pneumothorax
Anatomy!!!!!!!
right bronchial anatomy and left bronchial anatomy
too much to make card on many different anatomical locations I feel this is more important to a pulmonoligist not anesthesia as we wont be going that deep into the lungs but if you have alot of free time and want to learn go look!!!
CxR how to interperate?
not a radiologist not going into detail.. look for big signs like why your pt is breathing maybe its a pneumothorax you know what to look for. and pulm htn or pulm edema and ARDS white out!! if you crave the need for more see ppt i don;t think it is important!!!
ok that is done!!! are you still with me
you bet your ass you are!!!!!
rudy and jake please upload any information you think WE should KNOW for your lung presentations!!!!!!! I won’t be adding those here!!!
Thanks for your cooperation
ok last pulmonary one I think!!! it is sam I am
on atelectasis and hypoxemia!! drop your socks grab your cocks!!! this will be an adventure
anesthesia induced lung collapse occurs in approximately ___% of all GA surgeries
90%
2 types of alveolar cells
type I- squamous alveolar- cells that form the structure of an alveoli
type II-(greater alveolar)- cells that secrete pulmonary surfactant
3 mechanisms of lung dysfunction
loss of lung “units”
impaired gas exchange
V/Q mismatch
the key factor involved in the origin of lung collapse is the _______ dysfunction observed in anesthesia
diaphragmatic
how does compressive atelectasis occur
abdominal pressure id transmitted into thoracic cage and compresses pulmonar parachyma in dependent areas
how does denitrogenating a pt cause atelectacis
high fiO2 induces atelectasis by absorption of )2 in oulmonary areas with low V/Q
Why don’t we leave pt’s on an fiO2 of 1.0
reabsorption atelectasis
who is at higher risk for reabsorption atelectasis?
smoker
elderly
(b/c they have pre-existing low V/Q areas)
do you give more O2 for treatment of atelectasis
not really! remember reabsorption atelectasis. increasing fiO2 is effective for treating the symptom but not the cause
so what is treatment for atelectasis and how is it done
Alveolar recruitment strategy (ARS)
controlled and step wise increment and decrement of airway pressures using fixed settings in PCV.
driving pressure of 15 cm H2O, RR 10-15 I:E 1:1 fiO2 1.0
3 phases of ARS
hemodynamic preconditioning phase
recruitment phase
decremental phase peep titration phase
hemodynamic preconditioning phase
-test hemodynamic response to high PEEP
-Change of 15-20% from base line of VS halts test
-3-5 ml/kg of crystalloid to correct hypovolemia
actual test
1) 5 cm increments of PEEP from 0-20
2) each PEEP step maintained for 5 breaths
-spend a few minutes at PEEPS 10-15 to test hemodynamic stability
recruitment phase
- opening pressures of lung is 40cnH2O
- once hemodynamics have been tested and stabilized
- increase both driving pressures and PEEP to 20cmH20
decremental phase peep titration phase
- progressive decrease in PEEP of 2 cmH2O every few minutes
- identify lung closing pressures in dependent zones
When to recruit
once after induction
whenever the airway is open to atm
when not to recruit
LMA or facemask
hemodynamically unstable
-broonchospams, TEF, high ICP , pneumothorax
