Brainscape's Knowledge GenomeTM

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


See full index

NUNA 684 Advanced Pathophysiology > Pulmonary Pathophysiology > Flashcards

Pulmonary Pathophysiology Flashcards

1
Q

Primary purpose is NOT _________ but supplying necessary O2 to the tissues and excreting ____

A

arterial saturation of 100%
CO2

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

“the respiratory system delivers gas and the circulatory system delivers liquid. However, both systems deliver the same molecules, namely ____ and ____ from the body”

A

oxygen
carbon dioxide

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

Obstructive Disease Characteristics

A
  • more common than restrictive dz
  • airway resistance increased
  • air trapping & obstruction impedes airflow out - extended expiration times
  • lung volumes increase (RV and TLC)
  • turbulent airflow leads to expiratory wheezing
  • impaired gas exchange (VQ imbalance)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Restrictive disease characteristics: decreased _____ ______, reduced _____ _____, and ______ resistance is not increased

A
  • decreased lung compliance - lung expansion restricted impedes airflow in
  • lung volumes reduced
  • air resistance is not increased
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

post op morbidity/mortality is _______ with restrictive and obstructive pulm disease

A

increased

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

increased airway resistance leading to obstructed air flow is caused by 3 mechanisms:

A
  1. excessive secretions in bronchial lumen
  2. airway thickening, edema, hypertrophy of mucous glands, bronchitis, asthma
  3. destruction of lung parenchyma which leads to loss of airway radial traction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chronic airway inflammation with acute exacerbations

A

asthma

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

bronchial airways are hyper reactive to stimuli with asthma causing ____________________

A

airway narrowing at all levels and varying severity of narrowing

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

with asthma, ______ becomes obstructed therefore categorizing it as an _____________

A

expiratory airflow
obstructive disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

asthma is reversible with

A

bronchodilators

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

asthma category - extrinsic

A

allergic category
- family history of allergic/immunologic dz
- allergic related (allergen identified)
- immune system activation
- elevated IgE levels
- elevated serum eosinophils

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

asthma category - intrinsic

A

non allergic
- idiosyncratic (specific to individual)
- exacerbations with triggers
- non-immune related, no allergen identified
- normal IgE levels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Asthma periodic acute exacerbations

A
  • mild to severe attacks
  • bronchospasm
  • mucosal edema/secretions
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

asthma patients live with ______________ lasting for weeks

A

mild airway obstruction

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

with asthma, increased airway resistance to gas flow leads to a common symptom:

A

wheezing

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

asthma patients have

A

productive cough, dyspnea

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

with asthma, hypertrophied airway smooth muscle contracts during an attack causing _________

A

bronchoconstriction

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

asthma mucous gland hypertrophy leads to:

A
  • increased secretions, usually white and scant (bc of absence of infection)
  • thick, slow moving
  • mucous plugs leading to obstruction
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

asthma pathology

A
  • hypertrophied airway smooth muscles
  • mucous gland hypertrophy
  • bronchial wall edema
  • infiltration of eosinophils and lymphocytes
  • remodeling/scar tissue leading to subepithelial fibrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

etiology of asthma

A
  • allergy induced (atopy is greatest risk factor)
  • respiratory viruses
  • occupational/environmental irritants
  • drugs - aspirin, beta2 blockers, NSAIDS, and drugs that release histamine
  • exertional exercise (turbulent air causing tracheal inflammation)
  • stress: emotional and psychological
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

asthma inflammatory mediators

A
  • cytokines associated with Th-2, helper T cells, IL-4, IL-5, IL-9, IL-13
  • arachidonic acid metabolites - leukotrienes, prostaglandins
  • platelet-activating factor (PAF)
  • neuropeptides
  • reactive oxygen species
  • kinins
  • histamine
  • adenosine
  • serotonin
  • chemotactic factors
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

allergen binds to _____ on _____ causing degranulation

A

IgE
mast cell

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

following degranulation, there is a release of __________

A

inflammatory mediators

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

bronchoconstriction happens via __________ cAMP, __________ cGMP, ___________ PNS activity, and ________ cholinergic sensitivity

A

decreased cAMP
increased cGMP
increased PNS
increased cholinergic sensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

balance between _____ and ______ regulates ________ ____

A

PNS
SNS
bronchial tone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

_____ stimulation via vagal activation causes activation of the muscarinic receptors in bronchial smooth muscle

A

PNS

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

__________ receptors cause an increase in intracellular levels of cGMP

A

muscarinic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Increased intracellular _____ increases protein kinases that cause bronchoconstriction

A

cGMP

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

someone with significant wheezing pre-op will get an inhaler with _________ agonist which increases ______ causing _______

A

beta2
cAMP
bronchodilation

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

Mast cell degranulation releases mediators: ________, __________, ___________, and __________, which cause increased capillary permeability and other inflammatory changes

A

histamine
leukotrienes
chemotactic factors
bradykinin

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

bronchodilation is promoted by ___________

A

cAMP

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

intracellular levels of cAMP can be increased by beta adrenoceptor agonists which increase the rate of its synthesis by _____ or by _________ which slow the rate of its degredation

A

adenylyl cyclase
phosphodiesterase inhibitors (such as theophylline)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

bronchoconstriction can be inhibited by ___________ antagonists and possibly by ___________ antagonists

A

muscarinic
adenosine

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

goal of asthma treatment is to prevent ________ ________ and maintain patent airways

A

bronchial inflammation

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

2 types of drugs for asthma treatment

A

long term control of airway narrowing
rescue acute bronchospasm attacks

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

anti-inflammation drugs for asthma (3)

A

glucocorticoids
leukotriene blockers
mast cell-stabilizing agents

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

bronchodilation drugs for asthma (3)

A

beta 2 agonists
methylxanthines
anticholinergics (antimuscarinics)

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

Glucocorticoids are administered _____, decrease bronchial hypersensitivity and inflammatory response, ________- stabilizing, most effective ___________ drugs, and are effective as __________ _______ drugs

A

IV/inhaler
membrane-stabilizing
anti-inflammatory
prophylactic pre-op

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

glucocorticoid drugs:

A

IV hydrocortisone, methylprednisone
fluticasone (flovent), salmeterol (advair)
budesonide (pulmicort)
triamicinolone (azmacort)
beclomethasone (beclovent)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

leukotriene blockers
leukotrienes mediate __________ in asthma. These drugs inhibit the __________ _________ pathway, and reduce the synthesis of ____________. Only 50% of patients have beneficial response and these ARE effective for ________ induced asthma

A

inflammation
5-lypoxygenase enzymatic pathway (5-LO inhibitors)
leukotrienes
aspirin induced asthma

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

leukotriene blocker drugs:

A

monotelukast (singulair)
zafirlukast (accolate)
pranlukast (zyflo)
zileuton (ultair)

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

Mast cell stabilizer drug

A

cromolyn

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

cromolyn - effective only with _________ asthma, blocks airway ___________, inhibits mediator release from ______ ______, and stabilizes ___________.

A

extrinsic (allergic)
inflammation
mast cells
membranes (inhibits mast cell degranulation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

beta adrenergic agonists are the most ______ __________

A

potent bronchodilators

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

stimulation of beta2 receptors in the lungs cause increased _____ _______, which causes increased intracellular _______, leading to decreased ________

A

adenylyl cyclase
cAMP
Ca++

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

beta adrenergic agonist drugs: (3) and side effects: (3)

A

Drugs: albuterol (ventolin), metaproterenol (alupent), terbutaline (brethaire)
Side effects: hypokalemia, tachycardia, vasodilation

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

beta2 agonist activates _________ which activates __________ which activates _________ and __________

A

adenylate cyclase
cAMP (by ATP)
phosphodiesterase and bronchodilation

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

methylxanthines moa:
inhibits __________________ which
inhibits __________________
catecholamine ____________
__________ blocking actions

A

phosphodiesterase enzyme (which degrades cAMP) resulting in increased cAMP
inhibits prostaglandins
catecholamine release
histamine blocking actions

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

methylxanthines are for ______ _______ and __________, NOT for _________ bronchospasm attacks

A

chronic control and management
acute bronchospasm attacks

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

methylxanthine drugs and side effects

A

theophylline (elixophyllin, theo-24, uniphyl)
seizures, v-ectopy, agitation, N/V

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

anticholinergics/antimuscarinics decrease ______ ______, inhibit production of _______, results in _____________, and inhibits ______________ ____________

A

vagal tone
cGMP
bronchodilation
tracheobronchial secretions

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

anticholinergic/antimuscarinic drugs: (3)

A

ipratropium (atrovent)
atropine
glyco (robinul)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

status asthmaticus is considered ______-_________, can last for _________, attacks are unresponsive to _________

A

life-threatening
hours to days
bronchodilator Rx

54
Q

status asthmaticus results in ____________, _____________, and _____________. treatment regimen is repeated __________, ___________.

A

exhaustion (need to intubate), dehydration, tachycardia.
glucocorticoids, beta2 agonist

55
Q

Step 1 asthma and medications

A

mild, intermittent
- anti-inflammatory: no daily meds needed
- short acting bronchodilator: inhaled B2-agonist as needed for symptoms

56
Q

Step 2 asthma and meds

A

mild, persistent asthma
- anti-inflammatory: inhaled steroid (low dose) or cromolyn or nedrocromil
- short-acting bronchodilator: inhaled B2-agonist as needed for symptoms

57
Q

Step 3 asthma and meds

A

moderate, persistent asthma
- anti-inflammatory: inhaled steroid (medium dose) or inhaled steroid (low to medium dose) and inhaled long acting B2-agonist
- short-acting bronchodilator: inhaled B2 agonist as needed for symptoms

58
Q

Step 4 asthma and meds

A

severe, persistent asthma
- anti-inflammatory: inhaled steroid (high dose) and long-acting inhaled B2-agonist, possibly systemic steroids
- short-acting bronchodilator: inhaled B2-agonist as needed for symptoms

59
Q

Categorizing obstructive disease

A

(ABCCE)
asthma
bronchospasm
chronic bronchitis
COPD/emphysema

(all obstructive disease has trouble getting air OUT)

60
Q

bronchospasms are more common in chronic bronchitis and asthmatics with _______ __________ and patients with __________ ________

A

reactive airways
smoking histories

61
Q

adult bronchospasm triggers

A

mechanical or noxious chemical irritants

62
Q

pediatric bronchospasm triggers

A

environmental allergens
recent viral illness
URI

63
Q

bronchospasms can be caused by histamine releasing drugs such as _______ and _______

A

MSO4
atricurium

64
Q

_________ and ___________ reactions can trigger bronchospasms

A

anaphylactoid
transfusion

65
Q

bronchospasms are mediated by the _________

A

PNS

66
Q

causes of acute bronchospasms in anesthetized patients:

A
  • nonspecific bronchial hyperresponsiveness
  • allergic or anaphylactic reaction to drugs or blood transfusion
  • allergic or anaphylactic reaction to other allergens (latex)
  • exacerbation of asthma
  • pharm factors: b-blockers, prostaglandin inhibitors (remember AA pathway), anticholinersterases
  • stimulation of parasympathetic fibers and M2 and M3 muscarinic receptors
  • tracheal irritation from intubation
67
Q

with bronchospasms, avoid ______ ___________, use ______ or _________

A

airway instrumentation (ETT)
LMA
regional

tracheal intubation is the most common cause of bronchospasm

68
Q

with bronchspasms, avoid __________-__________ drugs, ________, and _____ _________.

A

histamine releasing
NSAIDs
beta2 blockers

(would still give vanco but would pre-treat)

69
Q

Bronchospasm treatment - most important to _____ _______

A

deepen anesthetic

70
Q

_______ is better than ___________ for bronchospasms and __________ has bronchodilator effects and increases catecholamines

A

propofol
thiopental/etomidate
ketamine

71
Q

IV ______ and ______ blunt airway reflexes

A

opioids and lidocaine

72
Q

increase _______ concentration

A

FiO2 (inspired oxygen)

73
Q

use periop bronchodilators such as __________

A

albuterol

74
Q

use antimuscarinics such as ______ or _______

A

robinul or atropine

75
Q

(for bronchospasms) use corticosteroids such as

A

solumedrol 125 mg IV

76
Q

(for bronchospasms) use epi dose

A

0.1-1 mg IV

77
Q

COPD management - remove ________, give __________, __________, supplemental _________, and possible diuretics if ___ _________ has developed

A

remove cause (smoking, polllutants - may be reversible with this)
bronchodilators
steroids
supplemental oxygen
cor pulmonale

78
Q

COPD management - Trelegoy Ellipta 3 different drugs:

A

inhaled long acting beta2 agonists (LABA)
inhaled long acting muscarinic antagonist (LAMA)
inhaled long acting corticosteroids

79
Q

chronic bronchitis is characterized by excessive mucous production in bronchial tree, _________ of mucous glands in large bronchi, increase in bronchial ______ _______, ___________ and environmental pollutants

A

hypertrophy
smooth muscle
smoking

80
Q

with chronic bronchitis, outward airflow ___________ results

A

obstruction

81
Q

chronic bronchitis: chronic hypoxemia leads to erythocytosis and _________ _________, which leads to ____ _____ _______, giving the appearance of a “_____ __________”

A

chronic
pulmonary HTN
right heart failure
blue bloater

82
Q

emphysema is characterized by enlarged ____ _____ distal to the terminal bronchiole caused by destruction of the _________ ________, which causes destruction and subsequent loss of _________ walls, and destruction of surrounding ________ _______.

A

air space
alveoli septa
alveolar
capillary bed

83
Q

centriacinar emphysema - destruction of _________ ________ __ _________

A

central part of lobule

84
Q

panacinar emphysema - destruction of _________ ________

A

entire lobule

85
Q

bullous emphysema - _______ areas or bullae form

A

cystic

86
Q

with emphysema, breathing through _______ _____ delays the closure of small airways

A

pursed lips

87
Q

emphysema - _______ ________ is primary pathologic factor

A

cigarette smoking

88
Q

emphysema - ___ ___________ deficiency (inhibits elastase) leads to increased elastase, smoking causes a decrease in elastase inhibitors leading to ______ _________.

A

a1 antitrypsin
increased elastase

both a1 antitrypsin deficiency and smoking cause increased elastase

89
Q

elastase destroys _________ inside the lung

A

elastin

90
Q

elastin is essential as it supports what?

A

elastic structure of the lungs responsible for elastic recoil

91
Q

elastic recoil supports smaller airways by providing _____ _______

A

radial traction (this leads to weak, floppy walls)

92
Q

Note that in centriacinar emphysema, the destruction is confined to the ________ and ___________ bronchioles. In panacinar emphysema, the ___________ alveoli are also involved

A

terminal
respiratory
peripheral

93
Q

___________ pts will have a harder time uptaking our anesthetic/volatile gases bc they have decreased diffusion capacities

A

pulmonary emphysema

94
Q

restrictive lung disease characteristics - reduced lung ___________ and ___________

A

reduced lung compliance and volumes result

95
Q

restrictive lung disease - airway resistance is _________________

A

not increased

  • exp flow rates are normal
  • reduced FEV1 (bc low lung volumes)
  • reduced FVC
  • normal FEV1/FVC ratio
96
Q

restrictive lung disease. usually has __________ gas exchange, but breathing is ______ and ________.

A

normal
rapid and shallow (but it gets it done!)

97
Q

acute intrinsic lung disease

A

(pulm edema)
- drug/chemical pneumonitis
- aspiration pneumonitis
- pneumonia
- ARDS
- neurogenic pulm edema
- NPPE
- CHF

98
Q

chronic intrinsic disease

A
  • fibrosis (radiation, occupational toxin)
  • oxygen toxicity
  • sarcoidosis
  • scleroderma
99
Q

extrinsic lung disease

A
  • neuromuscular dz
  • muscular dystrophy
  • spinal cord transection
  • Guillain-Barre syndrome
  • Eaton-lambert syndrome
  • Myasthenia gravis
  • morbid obesity, ascites, pregnancy
  • pleural effusion
  • pleural thickening
  • mediastinal mass
  • pneumothorax
  • neuroskeletal diseases
  • scoliosis, kyphosis
100
Q

acute intrinsic restrictive dz is primarily bc of an increase in _________ _______ ________ r/t increased pulm capillary ______ and _______ which results in reduced lung compliance.

A

intravascular lung water
pressure and permeability

101
Q

acute intrinsic restrictive dz multiple causes: (3 listed)

A
  • cardiogenic pulm edema (increased hydrostatic pressure)
  • pulmonary aspiration
  • infection
102
Q

In managing edema, delay ______ _______, reduce ________ _______ _______, use ________ _________ ventilation with _________, and adjust __________ to maintain adequate oxygenation

A

elective surgery
interstitial lung water
positive pressure ventilation with PEEP
FiO2

103
Q

Reduce interstitial lung water with:

A
  • diuretic treatments, limit fluids
  • inotropes and vasodilators
104
Q

Use positive pressure ventilation with PEEP and:
lower Vt to ______ with higher _________
reduce ___________ and _____________
keep PiPs less than __________________

A
  • lower Vt (4-6ml/kg) and higher RR (>14)
  • reduce volutrauma, barotrauma
  • keep PiPs less than 30 cm H2O
105
Q

chronic intrinsic lung dz is also referred to as:

A

interstitial lung dz

106
Q

changes in intrinsic lung properties (parenchyma) include reduced _______ and _________

A

compliance and FRC

107
Q

Multiple cause contributing to formation of interstitial lung dz: Chronic inflammation of ________ _______ and _________ ________, most commonly due to pulmonary __________, which all ultimately results in gas exchange abnormalities = altered ______.

A

alveolar walls
perialveolar tissue
pulmonary fibrosis (fibrotic elastic tissue)
altered VQ

108
Q

Sarcoidosis is a systematic _____________ disorder

A

granulomatous
granulomatous tissue is present in several other organ systems - skin, eyes, liver, spleen and is prone to develop in intrathoracic lymph nodes and the lungs

109
Q

with sarcoidosis, fibrotic changes in the lungs occur in _______ ______

A

alveolar walls

110
Q

____________ sarcoid is common

A

endobronchial

111
Q

Primary feature of diffuse interstitial pulm fibrosis is:

A

thickening of interstitum of alveolar wall

112
Q

in diffuse interstitial pulm fibrosis, thickening of the interstitium of alveolar wall is followed by infiltration of _________ and _____ ______, followed by __________ which form thick ________ _________ which ultimately destroys the structure of the alveoli.

A

lymphocytes and plasma cells
fibroblasts
collagen bundles

113
Q

final scarring occurs and air-filled cystic spaces form referred to as:

A

honeycomb lung

114
Q

diffuse interstitial pulm fibrosis results in reduced _________ and impaired ____________

A

compliance
gas exchange

115
Q

management of chronic intrinsic dz:
- decreased _______ causing inability tolerate long periods of apnea
- inhaled anesthetic uptake is ___________
- pneumothorax risks are ____________ (PiPs should be ______)
- more prone to _______ _________

A
  • decreased FRC causing inability tolerate long periods of apnea
  • inhaled anesthetic uptake is faster
  • pneumothorax risks are increased (PiPs should be <30 cm H2O)
  • more prone to oxygen toxicity (oxygenate with lower FiO2 if possible, and consider regional anesthetic if not contraindicated)
116
Q

chronic extrinsic restrictive dz is a disorder of ____________ or _____________

A

thoracic cage or chest wall (may be mechanical or tumor)

117
Q

chronic extrinsic restrictive dz: lung expansion is ____________, lungs are __________, and volume is _________.

A

restricted
compressed
reduced

118
Q

increased __________ airway resistance from decrease lung volumes

A

inspiratory airway resistance
(near end expiration)

119
Q

recurrent __________ ____________ result from ineffective cough dynamics

A

pulmonary infections

120
Q

_______ _____________ due to low ventilated regions

A

V/Q mismatches

121
Q

chronic extrinsic dz management:
- avoid drugs with ______ ________ _______ effects
- be cautious with _______
- consider _______ __________
- reduced lung compliance may prompt:
- higher _________ _________ may need to be considered

A

chronic extrinsic dz management:
- avoid drugs with prolonged respiratory depressant effects
- be cautious with N2O
- consider regional anesthesia
- reduced lung compliance may prompt: need for higher PiPs to maintain oxygenation/ventilation
- higher respiratory rates may need to be considered to maintain oxygenation/ventilation

122
Q

intra-op PE is ______. Embolic material occludes ________ _________ _________.

A

rare
pulmonary vascular bed

123
Q

Peri-op PE mortality

A

10%

PEs happen in 1% of surgical patients and 30% of ortho pts (long bones)

124
Q

PEs primarily originate from blood clots in the ______________ and _______________

A

lower extremities and pelvic veins

> 90% of DVTs are from iliofemoral vessels

125
Q

Three primary factors known as Virchow’s Triad are:

A

Virchow’s Triad

  1. venous stasis
  2. hypercoagulability
  3. vascular (venous) injury
126
Q

PE clinical signs (5)

A
  • reduced ETCO2 and capnograph wave
  • unexplained hypoxemia
  • sudden CV collapse
  • tachycardia, RBBB
  • bronchospams (lots of wheezing)
127
Q

PE intaop goal:

A

optimize cardiac output and O2 delivery

  • increase FiO2 to 100%
  • PEEP
  • support circulatory system
  • Phosphodiesterase inhibitors
  • ultimate removal or dissolution of embolic fragments
128
Q

PE - support circ system by (3 things)

A
  • sympathomimetics and inotropes
  • IV fluid boluses
  • treat ventricular dysrhythmias
129
Q

PE - phosphodiesterase inhibitors increase:

A

increase contractility and are pulmonary artery dilators

130
Q

shunt

A

perfusion without ventilation

  • atelectasis - collapsed alveoli where gas exchange ventilation is no longer occurring
131
Q

dead space

A

ventilation without perfusion

  • alveoli are adequately ventilated but perfusion is less than adequate

NUNA 684 Advanced Pathophysiology (16 decks)

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