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OPACCA > Resp > Flashcards

Resp Flashcards

0
Q

What is the hilum?

A

root of the lungs

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1
Q

What is the total adult lung volume?

A

3.5-8.5L

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2
Q

What is the difference between visceral pleura and parietal pleura?

A

visceral adheres to the lungs, pleural lines thoracic cavity

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3
Q

What is the main muscle of inspiration?

A

diaphragm. 80% of inspiration, controlled by the medulla via the phrenic nerve.

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4
Q

Where does the phrenic nerve exit?

A

C3, 4, 5

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5
Q

Describe the mechanical process of inspiration.

A

diaphragm contracts and flattens, pulls down the parietal pleura which decreases pressure and draws air into lungs. 80% of the work. the remaining 20% is done by accessory muscles such as external intercostals, actively moving rib cage up and out

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6
Q

Describe the process of expiration.

A

Not a passive process diaphragm relaxes, elastic recoil of the lungs, chest wall, and abdominal structures compress the lungs, exhalation longer than inspiration intercostals assist with inward movement of the ribs

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7
Q

What are the accessory muscles?

A

Scalene from neck to first two ribs, Sternoclediomastoid raises the sternum, and pectoral is major and minor

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8
Q

What are the conducting airways?

A

nasal cavity, nasopharynx, oropharynx (soft palate to hyoid), laryngopharynx

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9
Q

Characteristics of the trachea

A

smooth muscles, 11cm long, c shaped cartilagenous rings

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10
Q

Characteristics of the carina

A

Tracheal bifurcation site, right main stem bronchus, important anatomical landmark 2-3 cm above carina for ett placement

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11
Q

Characteristics of alveoli

A

primary site of gas exchange

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12
Q

Type 1 alveolar epithelial cells

A

90% functioning alveoli, gas exchange

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13
Q

type 2 alveolar epithelial cells

A

greater number vs type 1 cells, a supporting cell, produce , store and secrete surfactant

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14
Q

functions of surfactant

A

decrease surface tension, stabilizes alveoli, prevents collapse, increases lung compliance, eases WOB

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15
Q

What are the two vascular systems of the pulmonary alveoli.

A

pulmonary (pulmonary arteries, divides into right and left branches, receives venous blood from the right side of the heart) and bronchial( no gas exchange)

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16
Q

Bronchial circulation

A

functions to distribute blood to the airways, does not participate in gas exchange

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17
Q

Alveolar capillary membrane

A 
5 layers thick
no air in the blood
no blood in the alveoli
diffusion of oxygen and carbon dioxide
Co2 is 20x faster than o2
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18
Q

What is the maximum peak pressure

A

35mmHg

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19
Q

The rate of diffusion is influenced by

A

thickness of the alveolar capillary membrane
surface area of the alveolar capillary membrane
diffusion coefficient of the gas

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20
Q

Why is CO2 faster than O2 to perfuse?

A

because it is more soluble

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21
Q

What can impair diffusion through AC membrane?

A

pulmonary edema, ARDS, pulmonary fibrosis Thickens alveolar membrane

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22
Q

Function of pulmonary lymphatic circulation

A

removal of foreign matter, cell debris, remove fluid to help keep alveoli clear, produce antibody and cell mediated immune response
eventually drains into the primary lymph nodes located at the hila

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23
Q

two forms of oxygen

A

bound to hemoglobin 97% oxyhemoglobin, 4 oxygen molecules, SaO2
plasma oxygen PaO2diffuses to the cellular level, which the stimulates haemoglobin to offload its oxygen.

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24
Q

What determines o2 delivery?

A 
cardiac output 4-8l/min
hemoglobin concentration
oxygen binding capacity of the hemoglobin
am
ount of oxygen int he blood SaO2
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25
Q

how much oxygen is extracted every minute?

A

25% arterial oxygen every minute

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26
Q

what changes hemoglobin binding capacity

A

hypoxemia, altered rbc morphology

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27
Q

describe the relationship between extraction an consumption

A

once maximum extraction is reached, further increase in demand or decrease in supply leads to hypoxia
then anerobic metabolism and lactic acidosis

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28
Q

what are the three forms of CO2 in the blood

A

plasma 10%
hemoglobin 30%
bicarbonate 60% can accept or reject components to maintain acid base balance

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29
Q

What is the v in the vq balance

A

ventilation
movement of air into and out of alveolus
normal alveolar ventilation 4L/min

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30
Q

what is the q in the vq balance

A

perfusion
flow of blood thru a pulmonary capillary bed
normal alveolar perfusion 5L/minute

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31
Q

what is a normal vq

A

4:5 or 0.8

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32
Q

what problems can cause vq mismatch

A

ventilation, perfusion, or a combo

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33
Q

shunt

A

normal blood flow with decreased ventilation
anything that Impedes or blocks airflow
less than 0.8

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34
Q

dead space

A

ventilation without perfusion greater that 0.8

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35
Q

what are the normal and pathological percentages of wob

A

normal 3%

critical illness, 30% or more

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36
Q

how does the body compensate for vq mismatch?

A

hypoxic vasoconstriction around the alveoli with decreased oxygenation or bronchoconstriction in the presence of alveolar deadspace

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37
Q

Which two factors must be overcome for lung expansion?

A

elastic recoil, compliance, and resistance (impedance to airflow by conducting airways)

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38
Q

what causes increased wob

A

change in compliance
decreased chest wall compliance
increased airway resistance
decreased lung recoil

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39
Q

what are the key factors in lung compliance

A

lung volume- greatest at moderate volumes
tissue elastic recoil - aging decreases elastic tissue, increased compliance
pulmonary surfactant- decrease surface tension of alveoli, increased copmliance

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40
Q

elastic recoil

A

expiration

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41
Q

resistance key factors

A

under normal conditions, frictional interference to flow of air thru airways
adult icu increased resistance- leads to increased wob to move air in and out of the lungs

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42
Q

what might increase resistance

A

increased airway secretions
bronchospams
the smaller diameter, the increased resistance to airflow

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43
Q

changes in compliance

A

lungs are stiffer, difficult to inflate, increased effort or vent pressure to achieve volume
emphysema lungs are floppy, easy compliance

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44
Q

changes in resistance

A

increased effort to get air into lungs

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45
Q

What are the triad controllers of ventilation

A

controller - cns autonomic control
effector - muscles of ventilation
sensors - chemoreceptors( central and peripheral)
mechanoreceptor (chest and wall of lung)

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46
Q

components of the control of ventilation controllers

A

brainstem-medulla and pons, apneustic length of resp, pneumotaxic rate and depth
cerebral
cortex - voluntary ventilation to override autonomic control

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47
Q

the central and peripheral chemoreceptor control of ventilation

A

sensitive to changes in paCO2 and hydrogen ions
medulla and pons
not affected by paO2
CO2 is your drive to breathe

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48
Q

peripheral chemoreceptors respond to

A

paO2 primarily, but does respond to paCO2 and hydrogen.
any paO2 less than 60 increases ventilation
found in the bifurcation of common carotid, and above and below aortic arch

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49
Q

Dissociation curve

A

a relationship between paO2 and SaO2
dissolved oxygen and hemoglobin-bound oxygen
hemoglobin has a steady and predictable affinity for oxygen, occasionally events occur that change the affinity relationship
the curve shifts

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50
Q

what does a shift in the curve mean and what influences it?

A 
how O2 is taken up by Hgb alveolar level
how o2 is delivered tissue level
four major factors
-pH
-paCO2
-Temperature
-2,3 Diphosphoglycerate (unable to measure, increase response to  tissue hypoxia
51
Q

what does a shift to the left mean?

A

left hemoglobin “latches on”
higher arterial saturation for any given paO2
oxygen delivery to the tissue is impaired
hemoglobin: increased affinity for oxygen
hypothermia
alkalosis
decreased paO2
increase in pH
decrease in DPG
decrease temp

52
Q

what does a shift to the right mean?

A 
right "releases"
for any given pao2 we have a lower sa02
delivery of oxygen to the tissue level is enhanced
hemoglobin has less affinity for oxygen
fever
acidosis
increased paCO2
increased DPG
53
Q

alveolar hypoventilation

A

reflected by a decrease in paO2 and an increase in PaCO2

example:respiratory depression

54
Q

diffusion impairment

A

related to thickness of the alveolar wall, area available for gas exchange, and partial pressure difference between sides ie pulmonary edema

55
Q

what can cause respiratory impairment to a critical level

A

alveolar hypoventilation, diffusion impairement, VQ mismatch

56
Q

You are admitting a COPD exacerbation to icu. Where would observe for accessory muscle use?

A

Nasal flaring, gasping, tracheal tug, suprasternal indrawing, intercostal, scalene retractions, sternocliedomastoid tug, paradoxical breathing/ flail chest, abdominal breathing, pectorals, serratus anterior (to help rib expansion 1-8 ribs to the back)

57
Q

Neck and chest inspection

A 
palpate trachea to see if it is midline or deviated (will deviate towards collapse or atelectatsis)
chest wall configuration
respiratory effort
respiratory rate
additional inspections
58
Q

in a pneumo thorax where would you expect the trachea to deviate?

A

away from the injury

59
Q

what will be detected when you palpate the chest wall?

A

tenderness, abnormailities, symmetrical chest excursion, subcutaneous emphysema

60
Q

describe bronchovesicualar breath sounds

A

at airway bifurcations
softer
hollow, tubular

61
Q

describe vesicular breath sounds

A

peripheral lung fields

low pitched, rustling

62
Q

describe crackles as they relate to pathology, sound, and classifications

A

pathology- small amount of fluid in the airways
sound-popping or crackling, heard on both inspiration and expiration
classifications-fine(soft, high pitched), coarse(louder, slightly longer, lower pitched

63
Q

where can you listen for the various lobes of the lungs?

A

1&2 intercostal space for anterior upper lobes
3-5 anterior intercostal space right mid lobe
6-7 anterior intercostal space lower lobes

T1-3 posterior upper lobes
T4-8 RLL LLL

64
Q

describe the pathology, and sound characteristics of wheezes

A

pathology- air moving through narrowed airways, constriction, swelling, or partial obstruction
sound - high or low pitched, a musical quality, heard mainly on expiration, can be heard through the entire respiratory cycle

65
Q

describe the pathophysiology and sound of stridor

A

pathology - turbulent airflow through a partially obstructed upper airways
sound - high pitched, harsh, primarily on inspiration

66
Q

what do you have if the crackles clear with a cough?

A

atelectasis

67
Q

describe the pathophysiology and sound of a plural friction rub

A

pathology- inflamed pleural surfaces rub together, inflamation, trauma, neoplasms
sound - low pitched, grating or creaking sound
heard more often inspiratory, not affected by coughing
sharp pain, patient will splint chest

68
Q

Describe techniques available to critical care to assist with evaluation of an adult ICU patient’s oxygenation and ventilation?

A

Assessing WOB, auscultation, ABG, SpO2, FiO2 requirements, CXR, end tidal monitoring,

69
Q

How does pulse oximetry work?

A

sensor absorbs different wavelengths of light
unit calculates a percentage of hemoglobin that is saturated with oxygen
SpO2 less 70% is inaccurate

70
Q

What are the phases of end-tidal carbon dioxide monitoring capnogram?

A

phase 1- beginning of expiration
phase 2- exhalation of CO2 rise of the wave
phase 3- CO2 elimination plateau of the wave
phase 0- beginning of inspiration down wave

must be greater than 17mmHg

71
Q

How can you determine if it is a pleural or pericardial rub?

A

Have the patient hold their breath. If it goes away, then it’s pericardial

72
Q

index of arterial oxygen efficiency

A

PaO2/FiO2
Interpretation <200= ARDS
indicates hypoxemia

73
Q

Describe a thoracentesis

A

needle inserted into the pleural space
-diagnostic- obtain sample
-therapeutic- remove fluid - effusion
requires cooperation of patient
complications- pain, pneumothorax, hypotension
post-test care- send labelled specimens to lab
post-test

74
Q

Your patient is to have a bronchoscopy in the next hour. Describe preparation for this procedure.

A 
explain the procedure and make sure consent is obtained
preoxygenate
patent IV
oral chlorhexidine wash
vital signs
assess tolerance
analgesia
sedation
75
Q

Is it normal to see the diaphragm uneven in adults?

A

normal to see diaphragm, higher on the left due to the liver

76
Q

What are some diagnostic tests for respiratory?

A

bronchoscopy - direct visualization of respiratory structures
Pulmonary angiography - assess/ determine blood flow through lungs, radiopaque substance injected, observe impaired/cessation of blood flow
VQ scan - diagnose alteration in normal VQ relationship - ventilation inhaled radioactive gas, perfusion injected

77
Q

what is indicated by a dip in the end tidal waveform at the beginning of inspiration?

A

If the patient is NMB then the end of the plateau will be curved and pull down, meaning that some oxygen is pulling pass the analyzer, but doesn’t have the strength to complete the breath

78
Q

What are the important buffers?

A

bicarb, hemoglobin, proteins

79
Q

hypoxia

A

decreased amount of oxygen at the cellular level

80
Q

hypoxemia

A

insufficient amount of oxygen in the blood

81
Q

hypercapnea

A

increased concentration of carbon dioxide in arterial blood

82
Q

pH normal values

A

7.35-7.45

83
Q

PaO2 normal value

A

80-100
measure of the partial pressure of oxygen dissolved in arterial blood
pao2 less than 40 life threatening

84
Q

PaCO2 normal values

A

partial pressure of carbon dioxide
35-45
respiratory component

85
Q

Describe the effect on PaCO2 you would observe with the adult critical care patient who is hyperventilation?

A

low PaCO2 because they Re blowing off more co2 because it diffuses easier than oxygen

86
Q

normal bicarb values

A

22-26

a calculated value, the acid-base component that is regulated by kidneys

87
Q

Normal base excess values

A

identifies a metabolic disturbance
positive is alkalosis
negative is acidosis
normal -2 to +2

88
Q

SaO2 normal values

A

95-100%

Hemoglobins maximum capacity to bind to oxygen

89
Q

which acid base imbalance is the most difficult to treat?

A

correct fluid and electrolyte imbalances
sodium bicarbonate in severe acidosis only
difficult to treat because of numerous causes

90
Q

What are the symptoms of oxygen toxicity?

A

chest pain, blurry vision, hyperoxia induced seizure

91
Q

What is absorption atelectasis?

A

breathing high concentrations of O2 washes nitrogen out of alveoli, which collapses alveoli

92
Q

Describe the flow rates, FiO2 and issues associated with nasal prongs

A

1-6L/min, 24-44%, well tolerated, but can have sore ears or skin breakdown, epistaxis (nose bleed)

93
Q

Describe the flow rates, FiO2 and issues associated with a simple face mask

A

5-8L/in, 40-50%, ensure flow rates 5L/min minimum to flush out CO2 from the mask

94
Q

Describe the flow rates, FiO2 and issues associated with a non-rebreather mask

A

10-15L/min, 60-90%FiO2, need to get a tight seal to achieve maximum FiO2, flow rates must be sufficient enough to keep reservoir bag from deflating.

95
Q

What is the main difference between low and high flow systems?

A

high flow systems do not entrain air.

96
Q

Describe the flow rates, FiO2 and benefits associated with high flow nasal prongs

A

up to 15L/min, eliminate need for facemask to achieve desired FiO2, pt can eat, drink, take meds,

97
Q

What are the criteria for intubation?

A

acute respiratory failure, PaO2 >50 with pH 50

98
Q

Describe assist control?

A

AKA volume control
full support mode
pre-set resp rate, inspiratory time, and Vt
Set breaths and patient triggered breaths are at same Vt

99
Q

Describe pressure control

A

full suppot
pre-set resp rate, inspiratory pressure, inspiratory time
no set tidal volumes
trend patient volumes to ensure receiving adequate amounts

100
Q

Describe SIMV

A

synchronous Intermittent Mandatory Ventilation
partial support
pre-set resp rate, inspiratory time, tidal volume
ventilator delivers set breaths that are synchronized with pt’s own breaths, and tidal volumes.
No PS to overcome ETT resistance

101
Q

Describe Pressure Support

A

spontaneous mode
Pre-set FiO2, PEEP, Pressure support level,
no set resp rate
Pt determines RR and Vt

102
Q

Describe CPAP

A

spontaneous mode
Pre-set FiO2 and PEEP
pt does all WOB
Continuous pressure levels

103
Q

Describe the basic pathophysiology of atelectasis

A

incomplete expansion of a lung/portion of

collapse of alveolar lung tissue

104
Q

What are some causes for atelectasis?

A

obstruction (most common), pleural effusion, pneumothorax

105
Q

What are the two classifications of pneumonia?

A

typical (infection from bacteria)

atypical (viral and mycoplasma infections)

106
Q

Describe the critical care management of bacterial pneumonia

A 
intubation and ventilation
antibiotics
hydration
chest physio
bronchodilators
analgesia
antipyretics (if permitted)
107
Q

What is the pathophysiology of pleural effusion?

A

abnormal collection of fluid in pleural space.

most common cause CHF

108
Q

What are the two types of pleural effusions?

A

transudative - factors affecting formation/absorption of fluid (CHF)
exudative - fluid leakage - injured capillary bed (pneumonia, metastatic disease, empyema)

109
Q

Describe decortication

A

removal of fibrous/scarred areas of the pleural membrane to facilitate lung expansion

110
Q

Describe the pathophysiology of pulmonary edema

A

fluid accumulates within the capillaries, interstitial tissues and eventually the alveoli by destroying surfactant
decreased compliance, impairs gas exchange

111
Q

What are the two classifications of pulmonary edema?

A

cardiogenic - CHF

non-cardiogenic - smoke inhalation, DIC, septic shock

112
Q

Describe the critical care management of pulmonary edema

A

reduce preload, increase contractility, and decrease afterload

113
Q

What’s the difference between primary and secondary tuberculosis?

A

primary - previous unexposed

secondary - reinfection or reactivation

114
Q

Describe the pathophysiology of COPD

A

peripheral airways are major site of obstruction of normal alveolar ventilation
inflammation: edema, mucous secretion
impaired mucocilliary clearance
as disease progresses, air “trapped” in lungs during forced expiration

115
Q

Describe the characteristics of “pink puffers”

A

emyphsema
lack cyanosis
use accessory muslces
pursed lip breathing

116
Q

Describe the characteristics of “blue bloaters”

A 
Chronic bronchitis
cyanosis
fluid retention
edema
right heart failure
diaphragm flattens
117
Q

Describe the difference in VQ mismatch between emphysema and COPD

A

emphysema - destroyed alveoli and capillary beds, where as COPD - air trapped in alveoli, low gas exchange, but okay perfusion/wasted perfusion

118
Q

What are the three classifications of Acute Respiratory Failure?

A

hypoxemic - oxygenation defect, PaO250, drug OD, stroke, spinal injury
mixed - both, pulmonary edema

119
Q

What is the difference between direct and indirect ards?

A

direct - lung epithelium incurs direct injury such as aspiration, or pulmonary infection
indirect - insult occurs elsewhere in the body, mediators transmitted via bloodstream to the lungs, pancreatitis, sepsis, trauma

120
Q

Describe the pathophysiology of ARDS

A
  • damage to the alveolar-capillary membrane, increased capillary permeability
  • fluid, plasma proteins and blood in alveoli
  • inactivation of surfactant
  • alveolar atelectasis
  • hypoventilation
  • thickening of the hyaline membrane
  • massive atelectasis
121
Q

What clinical finding separates ARDS from ARF?

A

worsening hypoxia despite increasing levels of CO2 in ARDS

122
Q

What is the critical care management of ARDS?

A
  • treat underlying cause
  • promote gas exchange
  • prevent further lung injury
  • low tidal volumes 5-6mL/kg
  • PaO2 55-80
  • SpO2 88-95%
  • plateau mean airway pressures of <30
  • pH goal 7.3-7.45
123
Q

Describe the benefits of Nitric Oxide

A

selective pulmonary vasodilator - no effect of systemic vasculature because it is neutralized by hemoglobin

124
Q

Describe the rationale behind prone positioning

A

improve oxygenation and ventilation
improves perfusion to less damaged parts
improves VQ mismatch
decreases intrapulmonary shunting

125
Q

What is the PaO2/FiO2 ratio

A

PaO2/FiO2

<100 severe ARDS

OPACCA (8 decks)

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