Brainscape's Knowledge GenomeTM

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


See full index

Platelet and Bleeding Disorders > Week 6 > Flashcards

Week 6 Flashcards

1
Q

Pulmonary physical exam and middle lobe

A

right middle lobe can only be examined on anterior side of ches

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

Trachea deviation

A

indicates enlargement of space in left lung area pushing mediastinum to right or collapse of lobe on right (lung cancer)

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

Increased resonance

A

more hollow sounding: pneumothorax or advanced empysema

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

Dullness to percussion

A

more dense area (fluid, tissue)

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

auscultation of lungs bell or diaphragm?

A

only use diaphgragm because of high pitch sounds

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

Bronchial breath sounds

A

normal sounds over trachea

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

vesicular breath sounds

A

normal sounds over lung fields (opening and closing of alveoli)

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

crackles (rales)

A

fluid in alveoli

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

wheezing

A

narrow airways (COPD, asthma)-hhg pitched continuous sound during expiration (sometimes inspiration)

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

vocal resonance

A

increased or decreased (increased if consolidation)

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

whispered pectoriloquy

A

increased in pneumonia and consolidation

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

egophony

A

increased in pneumonia and consolidation

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

when assessing a CXR

A

ABCDE: air, bones, cardiac, diaphragm, effusion

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

Pneumothorax (air in pleural space)

A

increased volume of involved side (taking up extra space)
percussion: more air so hyper resonance (hollow)
Auscultation: decreased breath sounds, decreased vocal resonance
heart may be pushed over on CXR

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

Pleural effusion (fluid in pleural space)

A

inspection: decreased expansion
Percussion: dullness
Auscultation: absent breath sounds (fluid in way), decreased vocal resonance

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

Pneumonia

A

Inspection: splinting (not taking deep breaths due to pain)
Percussion: dullness
auscultation: crackles, bronchial breath sounds, increased vocal resonance, ego phony, whispered pectorliquy

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

Emphysema

A

loss of normal alveoli (impaired airflow), air can get in but not out of alveoli so air trap
barrel chested appearance

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

COPD

A

Inspection: AP diameter increased, accessory muscle use
Percussion: increased resonance all throughout, decreased diaphragm movement
Auscultation: decreased breath sounds and heart sounds, wheezes, prolonged expiration
CXR: flatter diaphragm and larger lungs

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

CHF

A

crackles/rales usually in dependent lung fields

wheezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Respiratory system functions

A

provide oxygen and eliminate O2
Regulates blood’s hydrogen ion concentration (pH)
form speech sounds
defend against microbes
influence arterial concentrations of chemical messengers by adding/removing
trap and dissolve blood clots arising from systemic veins (legs)

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

Produced and Added by lung cells

A

bradykinin, histamine, serotonin, heparin, prostaglandin E2, F2alpha, endoperoxidases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Metabolized, cleared by lung cells

A

prostaglandins E1, E2, F2alpha, NE

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

Conducting zone

A

trachea through terminal bronchioles

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

Respiratory zone

A

Respiratory bronchioles through alveolar sacs

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

Cartilaginous rings

A

Trachea and bronchi for maximal air flow

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

Air filtration

A

mechanical/chemical stimulation of airway receptors can cause bronchoconstriction
stimulation of nose receptors: sneeze
stimulation trachea receptors: cough
mucuciliary escalator

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

Inspiratory muscles: Diaphragm

A

Diaphragm: contraction leads to inspiration (downward movement, increasing thoracic cavity size)

relaxation leads to expiration (abdominal pressure forces muscle to resting position to decrease cavity size)

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

Inspiratory muscles: paradoxical movement

A

if hemiparalyzed, diaphragm that is paralyzed moves up with inspiration due to negative inter thoracic pressure pulling upwards

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

Inspiratory muscles: external intercostal muscles

A

connect adjacent ribs, slope down and forward

during contraction, pulled upward and forward to increase thoracic cavity

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

Inspiratory muscles: Accessory muscles

A

scalene and sternocleidomastoid which elevate first two ribs and sternum (exercise to assist inspiration)

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

Expiratory muscles: abodominal wall muscles

A

during contraction, increase intra abdominal pressure to force diaphragm upward

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

Expiratory muscles: internal intercostal muscles

A

pull ribs down and inward (decrease intrathoracic cavity size)

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

Innervation of respiration

A

C345 phrenic nerve for diaphragm

External and internal intercostal nerves

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

Pressure volume breathing

A

Muscle contraction–>intrathoracic volume increases–>intrathoracic pressure decreases–> air enters alveoli (boil’s law)

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

Factors of lung mechanics

A 
Elastic recoil
surface tension
alveolar interdepencence
intrapleural pressure
lung compliance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Elastic recoil

A

tendency of structure to return to its natural state

CW outward (increase volume)
lung: alveoli inward (decrease volume)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Pulmonary parenchyma

A

gas exchanging part of the lung-composed of elastin and collage fibers

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

Functional residual capacity

A

chest wall elastance=lung elastance and Palveolar=Patm=0

seen at end expiration

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

Surface tension

A

elastic tendency of fluid surface to acquire least SA possible (liquid cohesive forces)

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

LaPlace’s law

A

P=2T/r T=surface tension and r= radius
so if surface extension were constant in 2 differently sized alveoli: pressure in smaller alveoli would be much greater than large and this would cause air to move to larger alveoli and promote lung collapse

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

Surfactant and surface tension

A

PL secreted by Type II alveolar epithelial cells (85% lipid and 15% protein)-detergent and reduces surface tension at air fluid interface-keeps lungs open

reduces elastic recoil of lung
reduces hydrostatic pressure in tissue outside the capillary (preventing pulmonary edema)

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

Alveolar interdependence

A

structural support of individual alveolus by surrounding alveoli via elastic tissue network

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

Intrapleural Pressure

A

pleura: normal pressure created by elastic recoil is -3-5 cmH20

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

Intrapleural and alveolar pressure during inspiration

A

intrapleural pressure -8 cmH20

alveolar pressure -1 cmH20

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

transpulmonary pressure

A

pressure difference across whole lung (keeps lung open) Ptp=Palv-Pip
it it equals 0 lungs will collapse

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

Lung compliance

A

ease with which lung is distended for a given force C=V/P

at low lung volumes, highly compliant

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

hysteresis

A

slopes of lung compliance different in expiration and inspiration. surfactant may have decreased effects of decreasing surface tension on inspiration (takes higher P to get to same TLC)

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

Total compliance

A

1/total= 1/lung compliance +1/CW compliance

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

Measurements of Oxygen

A

Hb-O2 oxyhemoglobin: % saturation
dissolved arterial oxygen: PaO2
arterial O2 saturation: SaO2 % saturation
peripheral O2 saturation (most common)

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

absorption spectra of oxygen

A

Deoxyhemoglobin: absorbs red (600-750 nm)
oxyhemoglobin: absorbs infrared (850-1000 nm)

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

Pulse ox confounding factors

A 
anemia, vasoconstriction, low bP
increased venous pulsation
external lights ources
dyes and pigments (methylene blue, nail polish)
dyshemoglobinemias (carboxyhbg, methb)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Hemoglobin spectra

A

oxyhemoglobin and carboxyhemoglobin absorbed at same spectra-gives spuriously elevated SpO2

methhb absorbs same as reduced hbg=high concentrations of meting low SpO2 but patient asymptomatic

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

Oxygen delivery

A

DO2=COxCaO2 (oxygen content) volume of oxygen delivered to systemic vascular bed permit minute
oxygen content: 1.36 x Hbg x SaO2/100 +0.003 PaO2 (dissolved O2 in plasma)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Hypoxia

A

PaO2 less than 60 mmHg (or less than 80)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Aa gradient not affected

A

alveolar hypoventilation

decreased O2 tension

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

Aa gradient affected

A

VQ mismatch
shunt
diffusion impairment

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

Aa gradient normal range

A

Age in years/4 +4

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

VQ mismatch

A

most common: mismatch between ventilation and perfusion

will partially correct with supplemental O2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Shunt

A

extreme version of VQ mismatch
adequate blood flow, poor ventilation
ex: intracardiac spatial defects VSD, ASD, PFO
ex: intrapulmonary: arteriovascular malformations ,ARDS

Does NOT correct with oxygen

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

Diffusion impairment

A

increased thickness of alveolar capillary membrane
decreased are for diffusion (less SA emphysema)
decreased blood transit time (exercise)

HYPOXIA ONLY WITH EXERTION

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

Alveolar hypoventilation

A

PAO2=PiO2 - (1.25xPaCO2) so if you retain more CO2 you will decrease oxygen. ex: advanced COPD, neuromuscular disease, drug overdose

Aa gradient normal because PAO2 decreases s the PaCO2 increases

Improves with oxygen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Decreased oxygen tension

A

altitude decreased barometric pressure

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

Acute mountain sickness (high altitude illness

A

headache, fatigue, lightheaded, anorexia, nausea
via vasogenic brain edema from disruption of blood brain barrier induced by hypoxemia at high elevation
typically above 2000m

not protected by youth/fitness but obesity and heavy exertion increase risk

Tx: supplemental oxygen, acetazolamide, descent

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

High altitude cerebral edema

A

ataxia, decline in mental function/consciousness

elevation above 3000-3500 m

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

High altitude pulmonary edema

A

occurs 2-4 days after ascent above 2500m, most common cause of death at high altitude, high risk of recurrence

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

Periodic breathing of altitude

A

mirrors Cheyne Stokes

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

Hemoglobin T state

A

open state- binds O2 with low affinity

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

Hemoglobin R state

A

closed state- binds O2 with high affinity

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

hemoglobin vs myoglobin

A

myoglobin can only bind one oxygen molecule
release O2 at very low PO2 (storage protein in muscles)

hemoglobin: sigmoidal curve: multiple oxygens can bind
Release O2 in tissues at 20-30 torr (low pressures)
binding is cooperative

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

O2 affects hemoglobin

A

O2 binds iron and pulls it up in the plane of the heme which tugs on the histidine-leads to alterations and local changes in structure of hemoglobin subunit the destabilize contacts formed in t state –allows hemoglobin to form R state

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

Factors affecting gas transport by hemoglobin

A

2,3 BPG, H+, CO2, CO, fetal hemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

2-3 BPG and hemoglobin

A

stabilizes the T state–highly negatively charged small molecule-binds central pocket in T state to stabilize and promote O2 release

shift saturation curve to the right–promotes O2 release so you can release O2 at higher PO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

23BPG and fetal hemoglobin

A

gamma chain in fetal hemoglobin is less positively charged than beta chain so this means HbF has lower affinity for negatively charge 23BPG. Has a higher O2 affinity (good for fetal rbc transfer)

shifts curve left compared to maternal oxyhemoglobin–lower PO2 results in higher saturation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

H+ bohr effect

A

binding of H+ favors T state- H+ protonates the histidine side chain promoting oxygen dissociation from hemoglobin

shifts curve right-able to release at higher PO2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

CO2 Haldane effect

A

favors T state

  1. preferentially binds T state-weakens oxygen binding
  2. CO2+H2O–>H2CO3–>H +HCO3- so CO2 leads to increase in H+ which decrease pH contributing to Bohr effect
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

CO effects on hemoglobin

A

binds hbg 200 times stronger than O2 and dissociates slowly–can be fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Conducting airways

A

Nasal cavity, pharynx (shared passage), larynx, and trachea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Respiratory Epithelium

A

lines most of the conducting airways
pseudostratified columnar ciliated epithelium with goblet cells
lamina propria and submucosa contain numerous seromucous glands-water mucous to cilia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Respiratory epithelium cell types

A 
Ciliated
Goblet
Granule
Brush
Basal
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Respiratory epithelium changes throughout airways

A 
From columnar to cuboidal
height of epithelium decreases
goblet/glands decrease
cartilage decrease
relative amounts of smooth muscle and elastic fibers INCREASE
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

Larynx function and landmarks

A

maintain airway (cartilage) and close off airway (muscles)

close: swallow, cough, speech (vocal folds on lateral walls)
landmarks: epiglottis and vocal folds

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Vocal folds

A

not lined by respiratory epithelium–instead stratified squamous epithelium (resist high friction)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

True and false vocal folds

A

True: stratified squamous epithelium, overlie vocal ligaments (inferior to false)

False or vestibular: respiratory epithelium, overlie vestibular ligaments, contain glands (lubricate vocal vibrations), not involved in sound production)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

Three regions of Larynx

A
  1. Vestibule: opening of larynx to vestibular folds
  2. Ventricle: between the vestibular and vocal folds
  3. infraglottic cavity: vocal folds to trachea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Laryngeal cartilages

A
  1. Epiglottis (elastic)
  2. thyroid (hyaline, shield, doesn’t cover posterior)
  3. cricoid (hyalin, only complete ring of cartilage)
  4. arytenoid (hyaline, sits on cricoid, attach vocal ligaments)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Laryngeal muscles

A

skeletal muscles (attach to arytenoids) close off airway and regulate vocal ligaments

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Larynx innervation

A

recurrent laryngeal (vagus nerve cranial nerve X)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Vocal sounds

A

Tenser/shorter vocal cord: fast vibration and high pitch

Losser/longer vocal fold: slower vibration and lower pitch

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Trachea

A

branches t4/5 for carina at sternal angle, superior to heart

forms the right and left primary main bronchi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

Histology of trachea

A

16-20 C shaped hyaline cartilages-patent airway
smooth muscle on posterior side to allow esophageal expansion
lined with respiratory epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

Histology of tracheas

A

Respiratory epithelium
seromucous glands
hyaline cartilage

same pattern through bronchi with smooth muscle around cartilage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Lingula

A

tongue shaped projection in super lobe of left lung above the oblique fissure.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Hilus of lung

A

only place where structures enter/exit

  1. bronchi
  2. blood vessels (pulmonary A/V, bronchia A/V)
  3. lymphatics
  4. nerves

RALS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

pulmonary arteries and veins

A

Arteries follow bronchia tree (segmental)

veins travel between bronchopulmonary segments (intersegmental)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Right lung superior lobe segments

A

Apical, Anterior, Posterior

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Right lung middle lobe segments

A

lateral, medial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Right lung inferior lobe segments

A

Superior, Anterior basal, medial basal, lateral basal, posterior basal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Left lung superior lobe segments

A

apicoposterior, anterior, superior lingular, inferior lingular

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

Left lung inferior lobe segments

A

superior, anterior basal, medial basal, lateral basal, posterior basal

100
Q

Bronchi vs bronchiole histology

A

Bronchi: CARTILAGE, conducting system only
Bronchiole: NO cartilage, smooth muscle more prominent, conducting and respiratory system

101
Q

Bronchioles and respiratory bronchiole histology

A

Conducting: respiratory epithelium, smooth muscle, elastic fibers, no cartilage

Respiratory: directly lead to alveoli, smooth muscle, elastic fibers, no cartilage

102
Q

Alveolar cell types

A

Type I pneumocytes; flat make diffusion barrier with capillary endothelial cells
Type II pneumocystis (5%) surfactant
Macropage dust cells

103
Q

Gas exchange membrane

A

surfactant layer–>Type I pneumocyte epithelium–>shared basement membrane–>endothelial cell of capillary

104
Q

Parts of the parietal pleura

A
  1. costal pleura : adjacent to ribs
  2. diaphragmatic pleura: adjacent to diaphragm
  3. mediastinal pleura: adjacent to pericardial sac
105
Q

Pleural recesses

A
  1. Costomediastinal recess: between heart percardium and ribs
  2. costodiaphragmatic recess: between ribs and diaphragm

become larger during expiration–can get fluid for infection/bleeding

106
Q

Diaphragm

A 
dome shaped central tendon (pulls down during contraction)
moves 4-6 cm with each breath
vena cava (T8), esophageal hiatus T10, aortic hiatus T12, are the three foramen
107
Q

Vagus nerve Cranial nerve X

A

originates in brainstem
superior laryngeal and recurrent laryngeal nerves innervate larynx. (right loops around subclavian and left loops around aortic arch)

108
Q

Intrapleural and alveolar pressure

A

Intrapleural: during inspiration, decrease from -5 to -8 creates gradient for breathing

Alveolar: at mid inspiration -1, end of inspiration/expiratoin 0, and mid expiration +1

109
Q

Situations where Intrapleural pressure is increased

A

Forced exhalation (dynamic compression)
stiff chest wall (decreased CW compliance, lose outward elastic recoil)
fluid or air in pleural space (pleural effusion or pneumothorax)

110
Q

Pneumothorax symptoms and exam

A

chest pain, dyspnea, asymptomatic

decreased breath sounds, decreased chest excursion, hyperresonnant to percussion, decreased/absent tactile fremitus

111
Q

Pneumothorax causes:

A

Primary: no known lung disease (rupture of apical sub pleural blebs shear force, tall young smokers)
Secondary: underlying lung disease
Iatrogenic
traumatic: GSW, broken rib

112
Q

penetrative pneumothraox

A

puncture chest wall, air into intrapleural space which increases the intrapleural pressure (Alveolar pressure still 0. Tp is O or negative.

don’t die right away

113
Q

Non penetrative pneumothorax (tension)

A

trapped air in pleural space that can’t get out

hemodynamic instability-elevated intrapleural pressure impairs venous return to heart-die

114
Q

Pneumothorax management

A

small and asymptomatic: observe (maybe oxygen)
symptomatic moderate to large: chest tube
tension: needle decompression 2nd intercostal space in mid clavicular line

115
Q

Vital capacity

A

Inspiratory reserve volume, tidal volume and expiratory reserve volume

116
Q

alveolar gas equation

A

PAO2= [(Pb-PH2O)xFiO2] -(PaCO2/RQ)

no CO2 in inspired air
inert uses in equilibrium(nitrogen)
alveolar and arterial CO2 are in equilibrium
ignore change in volume between inspired and expired air

117
Q

Simplified alveolar gas equation

A

PAO2=(760-47)x.21 - (40/.8) =99

118
Q

PACO2

A

PACO2= CO2 production/alveolar ventilation

119
Q

minute ventilation effects on PACO2 and PAO2

A

hyperventilation: decrease PACO2 and increase PAO2 (indirectly via PCO2)
hypoventilation: increase PACO2 (direct) and decrease PAO2 (indirect)

120
Q

diffusion factors

A

area of membrane, difference in partial pressure of gases, diffusion constant (membrane properties and gas properties ie. MW, solubility)

inversely proportional to membrane thickness

121
Q

Blood-gas (capillary/alveolar) interface

A

oxygen in alveoli–>epithelium–>interstitial space and basement membrane–>endothelium–>plasma (PaO2)–>erythrocyte membrane–>RBC cytoplasm–>Hemoglobin (SO2)

122
Q

limitations of oxygen diffusion

A

transit time of blood in pulmonary capillary

  1. disease states thickening membrane
  2. low inspired PO2 (decrease pressure gradient takes longer for equilibrium to occur)
  3. exercise (decreased time)
123
Q

CO2 diffusion across alveolar membrane

A

CO2 diffuses 20x more rapidly (higher solubility), small difference in partial pressure

124
Q

CO2 transport in blood

A
  1. dissolved (5-10%)
  2. bicarbonate (in RBC via carbonic anhydrase) 60-90%
  3. carbaminohemoglobin (HHb-CO2) Haldane 5-30%
125
Q

Conditions affecting gas diffusion due to less surface area

A

ventilation perfusion matching

decrease in lung parenchyma

126
Q

conditions affecting gas diffusion due to alveolar interstitum wall thickening

A

edema, inflammation, fibrosis, sarcoidosis, hypersensitivity pneumonitis, radiation, busulfan, collage disorders

127
Q

conditions affecting gas diffusion due to smaller differences in partial pressure

A

altitude, gases added to inspired air (helium, nitrogen, anesthetics)

128
Q

conditions affecting gas diffusion due to changes in perfusion

A

fast pulmonary capillary transit times (exercise)

129
Q

conditions in oxygen reaction with Hbg

A

altered by other gases binding with Hb (CO)
abnormal hemoglobin structure (methHbg)
oxygen reaction with hemoglobin is not linear
changes in the oxygen dissociation curve

130
Q

normal PaO2

A

at sea level: PaO2=104-(.27xage)

131
Q

in healthy person, small Aa gradient is normal

A

50% due to VQ mismatch

50% due to true shunt (thebesian and bronchial circulations)

132
Q

hypoxemia and Aa gradient

A

Normal aA gradient-you would have to start with low alveolar PO2

increased Aa gradient-alveolar PO2 is normal but arterial Po2 is low

133
Q

Aa gradient alternatives

A

P:F ration: PaO2/FIO2

oxygenation index: mean airway pressure x FIO2 x 100/PaO2

134
Q

minute ventilation

A

volume of air leaving lung each minute
Ve=fB x VT (RR x tidal volume)

Ve=Vd+VA (dead space ventilation + alveolar ventilation)
alveolar ventilation is volume of air leaving alveoli each minute that has participated in gas exchange

135
Q

Tidal volume has 2 components

A

Vt=Vd+VA

136
Q

measuring alveolar ventilation

A

VA=VCO2/FACO2

carbon dioxide production/exhaled alveolar CO2

137
Q

Measuring anatomic dead space (Fowler’s method)

A

inhale 100% oxygen, start at expiration there is no nitrogen because you just inhaled oxygen. point where nitrogen and oxygen are mixed (area under curve) is the anatomic dead space.

138
Q

Physiologic dead space

A

anatomic dead space+alveolar dead space (air going in and out but no blood going by it)-no CO2 excretion.

139
Q

Bohr Equation for estimating physiologic dead space using dead space fraction Vd/Vt

A

Vd/Vt=PaCO2-PECO2/PaCO2
PECO2-mixed expiration CO2 (use end tidal CO2)
normal 0.2-0.3

140
Q

Alveolar PCO2 determined by

A

VCO2=CO2 production=O2 consumption x RQ
CO2 eliminated through ventilation of alveoli
VA=VE (1-Vd/Vt)
assume no CO2 inspired, inert gases equilibrium

141
Q

Calculating Alveolar PACO2

A

PACO2= VCO2/VE(1-Vd/Vt)

increased PACO2: increased Co2 production, decreased minute ventilation, increased dead space fraction

142
Q

How to increase alveolar ventilation

A

increasing total minute ventilation (increasing tidal volume, increasing respiratory rate), decreasing dead space ventilation

143
Q

alveolar dead space

A

where alveoli is normal and ventilated, but not perfused (not participating in gas exchange)

144
Q

lower lung

A

ventilates and perfuses better

145
Q

diffusion limited CO2

A

very soluble gas, moves from alveoli to RBC with no increase in partial pressure so it is only limited by diffusion properites

146
Q

perfusion limited NO

A

not soluble, as it moves into RBC, partial pressure quickly equals the alveolar pressure and there is no additional movement, depends on blood flow

147
Q

Both diffusion and perfusion limited O2

A

oxygen is soluble, but not fully, still a rise in partial pressure in rBC. Resting conditions: perfusion dependent, abnormal: diffusion depednet

148
Q

what happens when alveolar pressure>capillary pressure

A

capillary collapse (transmural pressure is difference between inside and outside of capillaries)

149
Q

Uneven distribution of blood flow (lower more) due to pressures (IN abnormal circumstances)

A

Zone 1: PA>Pa>Pv (collapse capillaries)
Zone 2: Pa>PA>Pv (blood flow determine by arterial/alveolar pressure differences)
Zone 3: Pa>Pv>PA (blood flow determined by arterial-venous differences)

150
Q

Concentration of gas in lung/cap

A

depends on both ventilation and perfusion

151
Q

Normal V/Q ratio

A

1

152
Q

dead space

A

area ventilated but not perfused

153
Q

VQ ratios and alveolar gas

A

Shunt: VQ=0
Normal: 1
Dead space infinity

154
Q

VQ ratios at different lung levels

A

VQ ratio HIGHEST at top of lung. Both ventilation and perfusion increase toward bottom, perfusion at a faster rate so it make the VQ ratio smaller at lower lung levels

155
Q

high VQ can not compensate for low VQ units

A

high VQ means not perfusion so you have a low contribution to oxygen content

156
Q

Causes of uneven ventilation

A

regional changes in elasticity, regional obstruction, regional check valves, regional disturbances in expansion

157
Q

Causes of uneven perfusion

A

embolization, occlusion, compression, fibrosis, loss of capillary surface area

158
Q

VQ mismatch and CO2/O2

A

as you increase PaCO2, the concentration of CO2 increases in linear fashion.
as you increase PaO2, relationship of concentration is less linear.

159
Q

examples of shunt

A

lobar pneumonia and ARDS

160
Q

examples of VQ mismatch with high VQ ratio

A

COPD: increased VQ ratio, increased physiologic dead space, wasted ventilation, high frequency low tidal volume breathing.
Pulmonary embolism
Compression of pulmonary capillaries due to high alveolar pressure
shock (pulmonary vascular hypotension)

161
Q

examples of VQ mismatch with low VQ ratio

A 
asthma
chronic bronchitis
acute pulmonary edema
airway obstruction (aspiration)
cystic fibrosis
162
Q

airway resistance in small vs large airways

A

in smaller airways, flow is more laminate, larger-more turbulent

163
Q

resistance is inversely proportional to

A

the radius of a tube (smaller radius=larger resistance)

164
Q

airway resistance is inversely proportional to

A

lung volume (higher lung volume, lower resistance)

165
Q

How does lung volume affect airway resistance

A

as inspiring, create large negative intrapleural pressure which increase transpulmonary pressure-airway distension, dilating the airways drops the resistance

dynamic compression-forced expiration makes the intrapleural pressure positive, decreasing transpulmonary pressure (can overcome the alveolar elastic recoil and traction on bronchiolar wall-collapse airway)

166
Q

alveolar dead space due to poor blood flow

A

decreased cardiac output due to CHF and obstruction to blood flow due to PE

167
Q

Measure anatomic dead space

A

Fowler’s method or 1 mL/lb of ideal body weight

168
Q

Measure physiologic deadspace via estimation through

A

Bohr equation

169
Q

dead space fraction

A

Vd/Vt normal 1:3 or .30

170
Q

dead space fraction during exercise

A

anatomic dead space increases during inspiration due to distending airways
however, Vd/Vt decreases during inspiration due to increase in Vt (during exercise)
alveolar dead space decreases (Due to increased CO)

physiologic dead space decreases

171
Q

dead space fraction in exercise with cardiopulmonary disease states

A

elevated Vd/Vt ratio
CHF: lower CO (inadequate blood flow ares increase Vd)
COPD, ILD, PH: already have issues with ventilation and can’t increase Vt enough

172
Q

cardiopulmonary exercise test

A

use to evaluate unexplained dyspnea, exercise intolerance, pt with cardio or pulmonary disease, disability, pre op

173
Q

what are PFTs

A

spirometry, lung volumes, and diffusion capacity

174
Q

FEV1, FVC, FEV1/FVC ratio

A

FVC: forced vital capacity
FEV1: forced expiratory volume at 1 second
ratio of the two normal above 70%

175
Q

spirometry in obstructive

A

reduced FEV1 and FEV1/FVC ratio

176
Q

spirometry in restrictive

A

FVC is surrogate for TLC. TLC is reduced in restrictive lung disease. the ratio is relatively normal

177
Q

peak expiratory flow loops effort

A

effort dependent at high lung volumes
effort independent at low lung volumes due to dynamic compression from increase Pip and less alveolar elastic recoil leading to less traction on airways

178
Q

Flow volume curve obstructive

A

FEV1 reduced relative to FVC due to increased airway resistance

reduced peak flow, curvilinear effort independent phase (scoop), vital capacity possibly reduced from hyperinflation

179
Q

Flow volume curve restrictive

A

steep descent in effort independent phase, vital capacity reduced (due to disease specific factor limiting TLC)

180
Q

Variable extrathoracic obstruction

A

during inspiration, airway pressure is less than atmospheric pressure (creating obstruction by collapsing airway?) giving truncation of inspiratory limb

expiration is normal: airway pressure exceeds atm pressure

ex: paradoxical movement of vocal cords

181
Q

Variable intrathoracic obstruction

A

inspiration is normal: airway pressure is larger than pleural pressure

expiration: pleural pressure exceeds airway pressure decreasing airflow and flattening of the expiratory loop,
ex: tumor in trachea

182
Q

fixed airway obstruction

A

truncation of both limbs (exp and insp)

ex: tracheal stenosis

183
Q

Inspiratory reserve volume vs inspiratory capacity

A

IRV: amount of air breathed in on top of TV
IC: IRV and TV

184
Q

Expiratory reserve volume and FRC

A

ERV: amount that can be breathed out on top of tidal volume
FRC: ERV and RV

185
Q

Measuring lung volumes: body plethysmography

A

breathing in increase the pressure in the chamber and they can calculate the volume

186
Q

Measuring lung volumes: helium dilution or nitrogen washout

A 
measures FRC (breathing in helium) 
Nitrogen washout-fowler's method
187
Q

Measure diffusion capacity

A

CO (b/c purely diffusion limited) DLCO

188
Q

Determinants of DLCO

A

alveolar cap SA and pulmonary cap volume (reduced in emphysema)
alveolar cap thickness (increased in Pulm fibrosis)
lung volume/SA (reduced in obesity)
Hbg concentration ( reduced in anemia)
carboxyhemoglobin concentration (elevated in smokers)
distribution of VQ in lung

189
Q

Bronchial smooth muscle innervation in airways

A

smooth muscle from trachea to alveoli, controlled by cholinergic parasympathetic and adrenergic sympathetic

190
Q

Bronchial smooth muscle and cholinergics

A

stimulation leads to contraction and increased glandular mucus secretion (AcH stimulates muscarinics)

191
Q

Bronchial smooth muscle and adrenergics

A

stimulation leads to relaxation and inhibition of glandular secretion (beta 2 receptors)

192
Q

Bronchodilators

A

B2 agonists: albuterol, anti cholinergic: ipratropium, NO, increased PCO2 and increased O2 in small airways

193
Q

Bronchoconstrictors

A

Ach, alpha agonists, inhaled irritants, histamine, leukotrienes, serotonin, endothelia, decreased PCO2 in small airways

194
Q

Obstructive lung disease

A

asthma, COPD, CF

195
Q

Wheezing

A

continuous adventitial lung sounds, high pitched whistling

due to fluttering of airway walls/fluid

196
Q

stridor

A

high pitched monophonic sound over anterior neck from oscillation of narrowed airway
inspiratory stridor: occurs in extrathoracic region (supraglottic and glottic/subglottic)
expiratory stridor: occurs in intrathoracic region

197
Q

Cough

A

duration (acute, subacute, chronic >8wk) chronic most likely inflammation.

198
Q

Resistance in lung airways

A

higher resistance in larger airways (even though large radius) because surface area is low. Higher surface area in small airways-less resistance because flow is dissipated.

199
Q

Mechanisms of lower airway obstruction

A 
mucous (asthma)
airway wall thickening/bronchoconstriction (asthma)
decreased tethering (emphysema)
200
Q

Where is the obstruction

A

trachea/bronchomalacia: degradation of cartilage-floppy airways
chronic bronchitis or bronchiectasis-irreversible mucus hypersecretin
asthma: smooth muscle hypertrophy/bronchoconstriction, mucus hypersecrtion, REVERSIBLE
emphysema: destruction of elastin fibers, decreased tethering, floppy airways IRREVERSIBLE

201
Q

Asthma summary

A

episodic triad: wheeze, cough, dyspnea
reversible airway obstruction, hyperactivity mucus (more goblet)
cellular inflammation eosinophilic
repetitive airway injury–>basement membrane thickening
multiple phenotypes (gene by environment)

202
Q

Hygiene hypothesis

A

Type I: exposed to infections, microbes, animals-develop tolerance-healthy
Type II: few infections, sterile environment–have an allergic reaction to same allergen

203
Q

Asthma potential protective factors

A

Contact with animals
high exposure to endotoxin (activates innate immune response)
early exposure to bacterial products

204
Q

Respiratory infections in asthma

A

healthy infant exposed to respiratory infections that cause wheezing may resolve or develop asthma (if proper genetic background)

can exacerbate symptoms, lung function

can make asthma more severe if its persistant

205
Q

Asthma is characterized by

A

airway obstruction (reversible)
hyper responsiveness (twitchiness)
inflammation
mucuous production

206
Q

Asthma and PFTs

A

low FEV1/FVC, typically corrected by bronchodilator

207
Q

Asthma and lung volumes

A

Mild: no changes
Acute or severe: increased RV (hard to exhale)
most severe: FRC and TLC usually normal, but may lose elasticity in sever (increased TLC)

208
Q

airway hyperresponsiveness in asthma

A

increased bronchoconstriction (most severe in asthma) from methacholine, cold air, exercise

209
Q

methacholine challenge

A

normal person nothing happens

asthma-casdues smooth muscle constriction and loss of FEV1

210
Q

airway inflammation in asthma

A

leukocyte infiltration–>cell activation–>damages airway epithelium–>exposes the basement membrane–>leads to increased mucus–>this happens repetitively it will cause airway remodeling

211
Q

`mast cells in asthma

A

have IgE which bind specific allegergen to activate mast cell–>produce mediators like histamin/leukotriene, cytokines (recruit eosinophils), growth factors, for angiogenesis or scarring, metalloproteinases-balance profibrotic/antifibrotics

212
Q

Eosinophils in asthma

A

cause airway hyper responsiveness, inflammation via cytokines, airway remodeling via growth factors, bronchial obstruction via leukotrienes, epithelial injury

213
Q

Histamine in asthma

A

made by mast cells and basophils, leads to bronchoconstriciton, vasodilation, edema, itching

214
Q

Eicosanoids in asthma

A

derived from phospholipase A2 activity (prostaglandins, thromboxanes, leukotrienes,) contribute to bronchoconstriction

215
Q

asthma inflammatory cascade

A

stimulus
cell activation/mediator release (recruit T cells which produce cytokines which recruit eosinophils, mast cels)
inflammation
smooth muscle hypertrophy, bronchial hyperresponsiveness

216
Q

Airway remodeling in asthma

A

more inflammation = subepithelial fibrosis, increased smooth muscle mass, new vessel formation and mucus gland hyperplasia

217
Q

Causes of airway narrowing

A

contraction of smooth muscle, cellular debris/mucus, edema of airway wall, airway remodeling (hypertrophy of smooth muscle, subepithelia fibrosis)

218
Q

Asthma Dx

A

episodic cough, wheezing, dyspnea with triggers
FH
during severe attacks: wheezing, tachypnea, accessory muscle use

219
Q

asthma triggers

A 
allergen exposure
viral infections
exercise
occupational exposure
medications 
circadian variation
220
Q

Confirming asthma Dx

A

low FEV1/FVC, increased airway resistance, reversible with beta agonists, hyper responsive with methacholine

increased eosinohils, IgE sensitivity (not necessary diagnostic)

221
Q

Tx asthma

A

controll inflammatory stimuli by environment control
control inflammation and hyper responsiveness with anti-inflammatory (corticosteroids and leukotriene modifiers)
control symptoms with bronchodilators (beta 2 agonists, muscarinic antagonists

222
Q

COPD characterized by

A

respiratory symptoms (cough, exertion dyspnea), airflow obstruction (reduced FEV1/FVC) and is IRREVERSIBLE

223
Q

COPD chronic bronchitis

A

smoker’s cough (cough/sputum for 3 mo)
disease of airways (bronchi/bronchioles)
srutctureal changes in airways (neutrophilic inflammation, metaplasia of epithelium, expanded mucus glands)
mucus hypersecretion

224
Q

COPD chronic bronchitis histology

A

dramatic expansion of submucosal glands

225
Q

COPD chronic bronchitis mechanisms

A

intralumenal blockage (secretions) or edema/inflammation/hypertrophy

226
Q

COPD emphysema

A 
destructive process of elastic fibers in lung parenchyma 
destroy alveolar walls and associated capillaries
enlarged airspaces (losing surface area and diffusion capacity)
227
Q

Collapsible bronchioles in emphysema

A

Losing elastic fibers that tether airway open-can collapse if put force on. reduced radial traction (airways aren’t staying open on exhalation)

228
Q

COPD pathogenesis

A

SMOKING

229
Q

Respiratory Bronchiolitis

A

earlier abnormality of COPD in smokers

inflammation, goblet cell metaplasia, smooth muscle hypertrophy, fibrosis/narrowing in bronchioles

230
Q

Emphysema pathogenesis

A

smoke induced inflammation drives alveolar destruction, respiratory infections aid this process, neutrophilic inflammation, chemokine trigger imbalance of proteases (steroid resistant)

231
Q

Emphysema: protease/antiprotease imablance

A

antiprotenase deficiency or protease excess–> leads to free protease (found in neutrophils) which destroy connective tissues (elastin)

232
Q

COPD and PFTs

A 
invariable low FEV1/FVC and low FEV1 (FVC may be normal or reduced in advanced)
normal or elevated TLC hyperinflation
normal or elevated FRC
normal or elevated RV
reduced DLCO
233
Q

emphysema and lung compliance

A

increased

234
Q

diaphragm in COPD

A

flattened and shortened muscle fiber length (less stretch-generate less tension so it’s harder to breathe when hyper inflated) leads to weakness

235
Q

COPD exacerbations

A

increased symptoms, 50% due to bacterial/viral infection, Tx: antibiotics and systemic steroids

236
Q

COPD and PA hypertension

A

result of alveolar hypoxia and resultant vasoconstriction, compensatory RV hypertrophy and RV failure (cor pulmonate) Tx: O2 supplementation

peripheral edema

237
Q

Diagnosing COPD

A

chronic symptoms, exclude asthma (see if reversible), spirometry FEV1/FVC

238
Q

COPD symptoms

A

persistent/progressive dyspnea, chronic productive cough (sputum discoloration), wheezing, lower extremity edema (cor) orthopnea, hemoptysis

239
Q

COPD physical exam

A

may be normal
barrel chest
hyper resonant percussion and low diaphragm
diminished breath sounds
prolonged expiratory phase
rhonchi (rattling), wheeze
lower extremity edema, cyanosis, cachexia

240
Q

COPD radiograph

A

hyper lucency-decreased peripheral vascular lung markings
hyperinflation (low, flat diaphragm, increase in retrosternal air space, narrow cardiac silhouette)
enlarged pulmonary arteries

241
Q

Pink puffer type a

A 
emphysematous phenotype
extertional dyspnea
little sputum
infrequent exacerbations
hyper inflated, use of accessory muscles
pursed lip breathing
normal oxygenation
thin
242
Q

Blue bloater type b

A 
bronchitic phenotype
cough and sputum
frequent exacerbations
less dyspnea
chronic hypoxemia
pulmonary HTN
corpulmonale right sided heart failure
normal habits or obese
243
Q

Tx:

A

SMOKING CESSATION
immunizations
bronchodilator with anticholinergics and beta agonists
suppress inflammation with corticosteroids (not effective)
treat hypoxia
manage exacerbations
pulmonary rehab

244
Q

COPD measures for oxygen therapy

A

PaO2<55 mmHg, sat <88%

or <60 mmHg end organ dysfunction

245
Q

Long term oxygen therapy in COPD

A

survival benefit

Platelet and Bleeding Disorders (4 decks)

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