Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BioScience I-Josh > Presentations mixture of highlights!!!!!!!! > Flashcards

Presentations mixture of highlights!!!!!!!! Flashcards

I am just putting together a mixture of topics from the power points presented!!!!!!!!!!!

1
Q

Asthma and bronchospasms

A

this is the first topic!!!!!!!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is asthma?

A

a chronic pulmonary disease characterized by airway inflammation, airflow obstruction, and bronchial hyper-reactivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

5 manifestations of asthma

A

dyspnea
wheezing
chest tightness
cough

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

2 types of asthma

A

Atopic

non-atopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

which asthma is the most common type?

A

atopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A

Atopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Which type of asthma is:
viral respiratory infections are common trigger
inflammation associated hyperirritability
family hx less common
no evidence of allergen sensitization

A

non-atopic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Patho of atopic Asthma

big ass slide just read over be familiar with different phases and basic process!!!

A

-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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

You can do it!!

A

just a word of encouragement!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q 
Bronchoactive drugs! 
give examples of each category
B2-adrenergic agonist?
Anticholinergics?
MastCell stabilizers?
Corticosteroids?
Luekotriene receptor antagonist?
A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q 
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?
A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

GA implications with ASTHMA::

A
  • GA may trigger asthma exacerbation
  • alteration of diaphragmatic function
  • impaired ability to cough
  • decreased mucociliary function
  • stimulation/irritation of airway by ETT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

_______ and _______ of the most recent asthma attacks are the most significant predictors of bronchospasms!

A

proximity and severity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Changes in lung function can also leas to ______, _____ ______, and ________ postoperatively

A

atelectasis
mucus plugging
wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Asthma exacerbation intra-op can also lead to what?

A

prolonged intubation
hypoxemia
pneumonia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Recent studies have found NO links between higher risks postop complications and pts with asthma? true or false

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

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!!

A

80

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

preop assessment for asthma

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Preop management and interventions for the asthmatic

A

Chest PT
antibiotic therapy
Bronchodilator therapy (continue day of SX)
corticosteroids (stress dose if indicated)
—-stress dose hydrocortisone 100mg IV

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q 
Asthma classifications 
Intermittent asthma-
Mild persistent asthma-
mod persistent asthma-
severe persistent asthma-
A

really way to much for a slide!!!! see ppt slide 23 if you want

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Intraop management for asthma

A
  • regional if not contraindicated
  • Avoid non-selective BB (propranolol and Labetalol)
  • Avoid NSAIDs (toradol)
  • Avoid histamine releasing drugs ( morphine, atricurium, suxs, mivacurium, demerol, thiopental)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q 
Intraop agents (tell me their effects)
propofol-
Ketamine-
Lidocaine-
VAAs-
A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Extubation for Asthma-

A

deep- controversal
bronchodilator- albuterol
IV lidocaine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

S/S of bronchospasm

A
  • high inflation pressures
  • expiratory upsloping on ETCO2
  • prolonged expiration
  • decreased O2 sat
  • expiratory wheezing
  • decreased breath sounds
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

treatment for bronchospasm

A 
100% O2
Increase anesthestic
beta agonist (terbutaline 0.25mg SQ; albuterol)
anticholinergic ( ipratropium bromide)
Lido IV
Epi- 
corticosteroids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Next section is COPD!!!

A

Great job on the last section!!!!!!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name 5 common obstructive disorders

A 
Emphysema
Chronic bronchitis
Asthma
Bronchiectasis
OSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

______ and ________ are often clinically grouped together and refered to as COPD

A

emphysema

chronic bronchitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

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

A

cigarette smoking

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

about ___% of people with COPD are NON-smokers

A

10%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

COPD is commonly diagnosed how

A

PFTs via spirometry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

the PFT findings GOLD criteria for COPD is

A

Low FEV1/FVC= 70%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q 
What is the severity of COPD based on the FEV1/FVC 
mild
moderate
severe
very severe
A

mild- >80%
moderate- 50-79%
severe- 30-49%
very severe- <30%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Define emphysema

A

abnormal permanent enlargement of airspace distal to the terminal bronchiole,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Acinar refers to what?

A

emphysema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

2 types of emphysema? (most prominant 95%)

A

centiacinar

panacinar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

which type of emphysema is:

central lobes of acini are primarily affected, distal alveoli are spared, seen predominately in heavy smokers

A

Centiacinar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

which type of emphysema is:

entire acinus is affected, associated with alpha1-antitrypsin deficiency

A

panacinar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

s/s of emphysema

A 
dyspnea @ rest
dry cough
pursed lip breathing
wheezes with auscultation
long expiratory pause
barrel shaped chest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Define chronic bronchitis

A

mild chronic inflamation throughout the airways, parenchyma, and pulmonary vasculature

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

S/s of chronic bronchitis

A

Impressive cough productive sputum
wheezes or crackles
dyspnea (late)
cor pulmonale/ right sided heart failure (late)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Define brochiectasis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

COPD pre-op eval

questions to ask

A 
ADLs
presence of infections
sputum
triggering agents
meds and effectiveness
time of symptoms (day night)
previous anesthesia hx
OSA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

smoking is associated with __-_____ deficiency

A

alpha1-antitrypsin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

COPD peri-op management

A 
supress neural reflexes
Inhibit increased intracellular Ca++ 
Control airway inflammation
eliminate secretions
maintain VQ
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

COPD anesthetics
VAAs-
IV agents-
avoid what???

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Peri-op mechanical ventilation

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Periop COPD with O2

A

maintain PaO2 at 55-75 mmHg or near the pts norm, with FiO2 less than .5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Keep PCO2 where

A

normal range 50-60 mmHg (pH .3-7.4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Wonderful job.. Now of to pneumona

PNE=pneumona

A

Yeahhhhhhh!!!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Define pneumonia

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Pro-op assesment for PNE

s/s of PNE

A 
fever/chills
N/V
Cough
Chest pain
diaphoresis
cyanosis in nailbeds/lips
AMS
headache
muscle pain
weakness
crackles
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Etiology of PNE

A 
advanced age
immunocompromised
underlying lung disease
alcoholism
impaired swallowing
AMS
immobilization
ETT
malnutrition
CV or liver disease
Chronic exposure to irritants
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

immunocompromised pt’s at risk for PNE

A 
HIV
Cystic fibrosis
Meds from transplants
autoimmune diseases
Asplenia
pregnancy
DM
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

4 main causitive agents for PNE

A

bacterial
viral
Fungal
Parasitic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Most common type of bacterial PNE

A

streptococcus pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Bacterial PNE s/s: the pt may present with a cough and what color sputum???

A

green, yellow, rust colored

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

common types of viral PNE

A 
rhinovirus
coronavirus
INFLUENZA VIRUS
RSV
CMV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Fungal PNE is seen in pts with what

A

AIDS (PCP)

chemotherapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Parasitic PNE is most common in what patients

A

Immigrants
immune deficient
people after traveling

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

PNE can be classified as what 5 categories?

A 
atypical
community acquired
nosocomial
aspiration
ventilator associated
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

PNE is also classified by the area of lung affected and divided into what 2 classes

A

Lobar

bronchial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

What is atypical PNE

A

aka walking PNE
sicker than they appear
caused by atypical organisms
atypical symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

CAP

A

Pt has not been in hospital

most common pathogen is streptococcus pneumoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Nosocomial PNE occurs when

A

> 48 hrs after admission

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Anesthetic considerations for PNE

A 
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

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!!

A

I meant smart ass!!! but none-the-less you still got this shit!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

define PE

A

impaction of foreign material into the pulmonary circulation, specifically the pulmonary arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

Etiology of PE

A

90% DVT
Less common
– air, bone, tumor, amniotic fluid, fat, CO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Etiology of PE r/t hereditary conditions

A

factor V leidan
protein C deficiency
Protein S deficiency
Antithrombin Deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

Other less popular PE etiology

A

Contraceptives
HRT
Air travel
Cancer

72
Q

What is the process that leads to DVT/ PE

A

venous stasis
hypercoagulbility
Vessel wall injury
====virchow’s triad

73
Q

Patho of PE

A 
virchow's triad
thrombus
dislofgement
occlusion of pulmonary circulation
vascular changes
symptoms
74
Q

S/S of PE

A 
dyspnea
tachypnea
tachycardia
hypotension
cyanosis
hemoptysis
chest pain
syncope
JVD
75
Q

Anesthesia implications:

for pts at risk for PE

A 
minimize myocardial depression
high fiO2
Monitor PAP
intotropes/vasopressors
etomidate or ketamine induction
76
Q

Anesthesia implications:

how to detect PE during anesthesia??

A 
Decreased ETCO2
Tachycardia
Decreased SaO2
Increase in PAP or CVP
decreased B/P
bronchospasm
EKG
77
Q

Anesthesia implications:

treatment intraop

A 
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
78
Q

Anesthesia implications:

PE postop concerns

A

persistant hypoxia

reperfusion edema

79
Q

Anesthesia implications:

PE prevention

A

LMWH 12 hours before sx
SCDs
Warfarin (INR 3)
inferior vena cava filter

80
Q

A good drug for PE treatment ( to better ventilate)

A

Inhaled Nitric oxide

81
Q

Inhaled nitric oxide (facts)

A

specific to lungs
effective dose 10-20ppm
pulmonary vasodilation
decreases RV afterload

82
Q

Ok chicken fuckers 4 presentations down!!!! not bad, only 24 to go haha!!

A

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!!!!!!!

83
Q

Management strategies for PULM HTN

A 
TREAT THE CAUSE
O2
diuretics in RV failure
vasodilators
CCB
ACEi
Epoprostenol, trespitinil
Sildenafil
prostacyvlin
Nitric oxide
atrial septostomy
transplant
anticoagulation
84
Q

Phosphodiesterase inhibitors MOA

A

inhibit nitric oxide degradation

85
Q

Phosphodiesterase examples and effects (2)

A 
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
86
Q

Endothelien receptor antagonist:

drug and MOA?

A

Endothelin-1

  • neurohormone that casuses pulm vasoconstriction, smooth muscle proliferation, and fibrosis
  • stimulates endothelin receptors A and B
  • -A- vasoconstriction
  • -B- vasodilation
87
Q

anesthetic considerations:

recommended test pre-op

A 
CBC, Coags, LFTs
EKG
CXR
ABG
Echo
Cardiac Cath
88
Q

anesthetic considerations:

assessment

A 
type of sx
METS
Severty of Pulm HTN
RV function
Comorbidities
89
Q

anesthetic considerations: Pulm HTN

you want to optimize what?

A 
O2
Brinchodilation
antibiotics
steroids
vasodilators
inotropes
90
Q

anesthetic considerations: Pulm HTN

Goals to maintain:

A 
preload
SVR
Contractility
CO
NSR
91
Q

anesthetic considerations: Pulm HTN

Goals to prevent

A

MI
hypotension
Increased PVR

92
Q

anesthetic considerations: Pulm HTN

Monitoring

A

ASA standards
A-line
CVP
TEE

93
Q

anesthetic considerations: Pulm HTN

regional benefits and precautions

A 
Maintain spont breathing
postop analgesia
continuous vs bolus
plexus/nerve catheters
anti-coagulation???
Reduce LA dose
94
Q

anesthetic considerations: Pulm HTN

GA benefits

A 
Method of choice for major sx
Airway management
systemic vasodilation
mechanical ventilation
reduced coronary perfusion
95
Q

anesthetic considerations: Pulm HTN

pre-medication

A

Small doses of midazolam (avoid hypoventilation)

96
Q

anesthetic considerations: Pulm HTN

induction

A

opiods (blunt DL)
Lido (blunt DL)
prop, etomidate (either)
muscle relaxants (avoid histamine releasing)

97
Q 
anesthetic considerations: Pulm HTN
meds:
propofol
etomidate
ketamine
A 
PROPOFOL
decrease SVR
Decrease Venouse return
Decrease contractility
ETOMIDATE
maintain hemodynamics
no PVR effect
KETAMINE (CONTROVERSIAL)
INCREASES PVR???
98
Q 
anesthetic considerations: Pulm HTN
Isoflurane-
Des-
Sevo-
Nitrous Oxide
A 
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
99
Q

anesthetic considerations: Pulm HTN

maintenance

A

maintain opioids
maintain muscle relaxation
Avoid histamine releasing drugs

100
Q

anesthetic considerations: Pulm HTN

Ventilatory management!

A

high O2
Moderate TV
HYPOcarbia (increase rate)
low PEEP (5-10)

101
Q

anesthetic considerations: Pulm HTN

HTN crisis treatment

A 
inhaled NO (20-40 ppm)
Milirone (50 mcg/kg bolus)
102
Q

ok another one down!!!! stay with me!!! lets do TB

A

Here is goes

103
Q

Define TB

A

an infection caused by mycobacterium tuberculosis (an acid fast bacillus) that infects pulmonary tissues and other organs

104
Q

What is a definitive test for TB

A

acid-fast sputum test

105
Q

What are the stages of TB

A 
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
106
Q

how does TB spread

A

airborne droplets 1-5 mcg

107
Q

Anesthetic implications for TB:

infection control

A

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

108
Q

pretty short and sweet!!!!! kinda shitty presentation but well take it!!!

A

oh well!!!

109
Q

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

A

ok one more big breath!!!!

110
Q

lung transplant today is a standard alternative to manage what?

A

end stage lung disease, refractory to standard medical or sugical therapy, to pts with NO other significant functional impairment

111
Q

current life expectancy post lung transplant?>

A

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!!

112
Q

% most common diseases treated with lung transplantation

A 
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
113
Q

Anesthetic implications for lung transplant:

donor pro-op

A

PaO2/FiO2 >300
clear Chest X-ray
Negative bronchoscopy (minimal to no secretions)
age < 20 years

114
Q

Anesthetic implications for lung transplant:

recipient pre-op

A 
H&P
EKG
CxR
labs-ABG, Coags, lytes, CBC
Type and Cross -PRBCs, PLTs, FFP
IV
Review- ECHO, Cath, VQ
immunosupression
115
Q

Anesthetic implications for lung transplant:

donor intra-op

A

Lungs must be visualized and deemed acceptable.

CROSS CLAMPING TIME DECLEARED–starts ischemia time

116
Q

Anesthetic implications for lung transplant:

recipient intra-op

A 
Induction
intubation
ventilate 
ASA monitoring
A-line
CVL
PA line
warming blankets
TEE???
117
Q

Anesthetic implications for lung transplant:

Obstructive lung disease

A 
I:E ration 1:4 or 1:5
check for auto peep
avoid hyperinflation (Pnemo)
permissive hypercarbia
bronchodilators (if indicated)
118
Q

Anesthetic implications for lung transplant:

restrictive lung disease

A 
NO inhaled
Low volume ventilation 
high RR
Minimal PEEP
AUTO PEEP= NOT A CONCERN
119
Q

Anesthetic implications for lung transplant:

suppurative lung disease

A

agressive pulmonary toilet
avoid hyperinflation
NO inhaled

120
Q

Anesthetic implications for lung transplant:

intra-op recipient once lung implanted

A 
end ischemia time
record ischemia time
ventilate
intra-op bronch for anastomosis check
avoid reprofusion injury (NO)
protective ventilation(PCV < 25 mmHg)
121
Q

Anesthetic implications for lung transplant:

post lung transplant in OR

A 
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
122
Q

Not too bad!!!! alot of info!!

A

ok her we go!!

123
Q

ok next is bronchoscopy and Chest xray

A

this should be interesting get ready set and go!!!!!!!!!!!

124
Q

Indications for a bronchoscopy

A 
cough 
wheeze
hemoptysis
diaphragmatic paralysis
unexplained hoarsness
vocal cord paralysis'
suspected TEF
airway obstruction
chest trauma
intubation
abnormal cXr
125
Q

Anesthetic implications for Bronchoscopy:

preop-assessment

A

airway assessment
respiratory CV focus
dental
premedication - antisialogogue, sedative

126
Q

rigid bronchoscope highlights (scaled way down from ppt to hit highlights)

A

trachea and proximal/central airways
GA needed
analyzes expired gases

127
Q

rigid bronch indications

A 
tumor
foreign body removal
stent placement
dilation
viscous secretions
128
Q

rigid bronch side note (just look and read)

A

in a picture in the ppt it shows a side port where the anesthesia circuit can connect!! ( no need for ETT (?????)

129
Q

Flexible bronchoscopy

A 
most common
visualizes to segmental bronchi (3rd generation)
LA
conciuos sedation
GA
suction, bx, and irrigation channels
need large diameter ETT
130
Q

flexible bronchoscopy indications

A 
clearing secretions
hemoptysis control
tumor staging
stent placement
topical placement (meds)
131
Q

Anesthetic implications for Bronchoscopy:

contraindications to bronch

A 
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
132
Q

Anesthetic implications for Bronchoscopy:

complications

A 
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
133
Q

Anatomy!!!!!!!
larynx location?
composed of

A
  • epiglottis to cricoid cartilage

- 3 single cartilages, 3 paired cartilages

134
Q

Anatomy!!!!!!!
trachea
length?
RMB and LMB angles

A

-10-15 cm long
- RMB 25-30 degrees
LMB 45 degrees

135
Q

Anatomy!!!!!!!

right bronchial anatomy and left bronchial anatomy

A

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!!!

136
Q

CxR how to interperate?

A

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!!!

137
Q

ok that is done!!! are you still with me

A

you bet your ass you are!!!!!

138
Q

rudy and jake please upload any information you think WE should KNOW for your lung presentations!!!!!!! I won’t be adding those here!!!

A

Thanks for your cooperation

139
Q

ok last pulmonary one I think!!! it is sam I am

A

on atelectasis and hypoxemia!! drop your socks grab your cocks!!! this will be an adventure

140
Q

anesthesia induced lung collapse occurs in approximately ___% of all GA surgeries

A

90%

141
Q

2 types of alveolar cells

A

type I- squamous alveolar- cells that form the structure of an alveoli
type II-(greater alveolar)- cells that secrete pulmonary surfactant

142
Q

3 mechanisms of lung dysfunction

A

loss of lung “units”
impaired gas exchange
V/Q mismatch

143
Q

the key factor involved in the origin of lung collapse is the _______ dysfunction observed in anesthesia

A

diaphragmatic

144
Q

how does compressive atelectasis occur

A

abdominal pressure id transmitted into thoracic cage and compresses pulmonar parachyma in dependent areas

145
Q

how does denitrogenating a pt cause atelectacis

A

high fiO2 induces atelectasis by absorption of )2 in oulmonary areas with low V/Q

146
Q

Why don’t we leave pt’s on an fiO2 of 1.0

A

reabsorption atelectasis

147
Q

who is at higher risk for reabsorption atelectasis?

A

smoker
elderly
(b/c they have pre-existing low V/Q areas)

148
Q

do you give more O2 for treatment of atelectasis

A

not really! remember reabsorption atelectasis. increasing fiO2 is effective for treating the symptom but not the cause

149
Q

so what is treatment for atelectasis and how is it done

A

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

150
Q

3 phases of ARS

A

hemodynamic preconditioning phase
recruitment phase
decremental phase peep titration phase

151
Q

hemodynamic preconditioning phase

A

-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

152
Q

recruitment phase

A
  • opening pressures of lung is 40cnH2O
  • once hemodynamics have been tested and stabilized
  • increase both driving pressures and PEEP to 20cmH20
153
Q

decremental phase peep titration phase

A
  • progressive decrease in PEEP of 2 cmH2O every few minutes

- identify lung closing pressures in dependent zones

154
Q

When to recruit

A

once after induction

whenever the airway is open to atm

155
Q

when not to recruit

A

LMA or facemask
hemodynamically unstable
-broonchospams, TEF, high ICP , pneumothorax

156
Q

Anatomy!!!!!!!

right bronchial anatomy and left bronchial anatomy

A

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!!!

157
Q

CxR how to interperate?

A

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!!!

158
Q

ok that is done!!! are you still with me

A

you bet your ass you are!!!!!

159
Q

rudy and jake please upload any information you think WE should KNOW for your lung presentations!!!!!!! I won’t be adding those here!!!

A

Thanks for your cooperation

160
Q

ok last pulmonary one I think!!! it is sam I am

A

on atelectasis and hypoxemia!! drop your socks grab your cocks!!! this will be an adventure

161
Q

anesthesia induced lung collapse occurs in approximately ___% of all GA surgeries

A

90%

162
Q

2 types of alveolar cells

A

type I- squamous alveolar- cells that form the structure of an alveoli
type II-(greater alveolar)- cells that secrete pulmonary surfactant

163
Q

3 mechanisms of lung dysfunction

A

loss of lung “units”
impaired gas exchange
V/Q mismatch

164
Q

the key factor involved in the origin of lung collapse is the _______ dysfunction observed in anesthesia

A

diaphragmatic

165
Q

how does compressive atelectasis occur

A

abdominal pressure id transmitted into thoracic cage and compresses pulmonar parachyma in dependent areas

166
Q

how does denitrogenating a pt cause atelectacis

A

high fiO2 induces atelectasis by absorption of )2 in oulmonary areas with low V/Q

167
Q

Why don’t we leave pt’s on an fiO2 of 1.0

A

reabsorption atelectasis

168
Q

who is at higher risk for reabsorption atelectasis?

A

smoker
elderly
(b/c they have pre-existing low V/Q areas)

169
Q

do you give more O2 for treatment of atelectasis

A

not really! remember reabsorption atelectasis. increasing fiO2 is effective for treating the symptom but not the cause

170
Q

so what is treatment for atelectasis and how is it done

A

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

171
Q

3 phases of ARS

A

hemodynamic preconditioning phase
recruitment phase
decremental phase peep titration phase

172
Q

hemodynamic preconditioning phase

A

-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

173
Q

recruitment phase

A
  • opening pressures of lung is 40cnH2O
  • once hemodynamics have been tested and stabilized
  • increase both driving pressures and PEEP to 20cmH20
174
Q

decremental phase peep titration phase

A
  • progressive decrease in PEEP of 2 cmH2O every few minutes

- identify lung closing pressures in dependent zones

175
Q

When to recruit

A

once after induction

whenever the airway is open to atm

176
Q

when not to recruit

A

LMA or facemask
hemodynamically unstable
-broonchospams, TEF, high ICP , pneumothorax

BioScience I-Josh (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions