Brainscape's Knowledge GenomeTM

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


See full index

GI/Pulm > Pulm > Flashcards

Pulm Flashcards

1
Q

Obstructive impairment

A 
Resistive properties of respiratory system--> airway limitation: LACE
Local obstruction
Asthma
Chronic bronchitis
Emphysema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Restrictive impairment

A

Loss of volume capacity due to loss of air space/inability to expand: PAINT
Pleural disease
Alveolar filling process (CHF)
Interstitial lung disease (sarcoidosis)
Neuromuscular disease (Myasthenia gravis)
Thoracic cage abnormalities (kyphoscoliosis)

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

Volume Spirometers

A

Device to measure volume displacement by exhalation of lung contents. Older device types:
- Bellows, water seal, rolling, diaphragm

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

Flow spirometers

A 
Pneumotach systems (more commonly used now)
- Measures flow over time= volume
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Spirometry maneuver

A
  • Forced expiratory maneuver while sitting upright in a chair
  • Lips around mouthpiece
  • Maximal inspiration–> forced, rapid expiration
  • Quality: start at zero, exhale for 6 seconds, maximal effort
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Spirometry Measurements

A
  • FVC= forced vital capacity
  • FEV1= forced expiratory volume in 1st second (lower levels= obstructive disease)
  • FEV1/FVC
  • FEF-25-75 (flow rates at two intervals), TET (total expiratory time- maneuver done well)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Interpretation of spirometry

A
  • Most commmonly performed/useful screen test
    Restrictive lung:
  • FVC and FEV1 decreased
  • FEV1/FVC= normal (ratio maintained- 71)
  • FEV1= main distinguishing feature
Obstruction:
- FEV1 decreased
- FVC normal
- FEV1/FVC LOW ( 80% predicted value
Mild= 65-79%
Moderate= 50-64%
Severe= < 50%
* For obstructive lung disease- FEV1 determines severity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Flow volume loops

A

Inspiratory loops can also be obtained to evaluate for LARGE airway obstruction

  • Theory: decrease in pressure inside thoracic cage with inhalation–> but pressure outside trachea increases (trachea collapases)
  • Trachea pressure (internal) increases with exhalation–> pushes out
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Extrathoracic obstruction

A

Pressure on trachea may be visible by flow volume loops–> decreased inspiratory/expiratory loop

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

Fixed obstruction

A

Intra and extrathoracic obstruction

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

Measuring lung volumes

A

What is total lung capacity? These techniques measure functional residual capacity (FRC)
FRC= Expiratory reserve volume (ERV) + Residual volume (RV)
1 Nitrogen washout
2. Body plethysmography
3. Helium dilution technique

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

Helium dilution technique

A

Helium dilution technique= uses inert gas (won’t exchange)- allow it to come to equilibrium in closed circuit, then measure amount inhaled/inhaled
- Take deep breath in- find vital capacity, FRC (everything else calculated)

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

Body Plethsymography

A

In sealed box with fixed volume:

  • Uses Boyle’s law when patient breathes in a seled box, changes in pressure bought about by changes in volume (lung)
  • FRC directly measured, SVC measured
  • TLC and RV are assessed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Nitrogen washout

A

Determine FRC by multiple breath open circuit nitrogen washout

  • Inhale 100% O2 for several min
  • Monitor N2 concentrations until it falls below 1%
  • May underestimate bullous disease
  • High resistance airway disease= takes longer to clear nitrogen out of lungs
Concept: C1V1= C2V2
C1= nitrogen conc at start
V1= FRC volume
C2= N2 concentration in exhaled volume
V2- total exhaled volume in O2 breathing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Interpretation of Lung volume measurement

A

Restrictive lung disease:
- TLC reduced significantly (decrease in all lung volumes)

Obstructive lung disease:
- Increase in RV and TLC

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

Diffusing capacity

A

Info about transfer of gas from alveoli/capillary bed

  • ONLY non-invasive test of gas exchange
  • Perfomed by single breath technique, uses CO as freely diffusible gas (uptake only limited by interface, not pulmonary blood flow/CO conc. in blood)
  • DLCO= diffusion capacity/diffusion of lung for CO= mL CO diffuse across membrane per minute

Technique:

  • Patient exhales fully
  • Inhales air with 0.25% CO
  • Hold breath for 10 seconds
  • Exhales- measures CO exhaled

Normal result= > 80% diffusion

  • Can be reduced in interstitial disease, emphysema, pulmonary vascular disease
  • False low measurements in anemia, lung resection
  • False elevation in alveolar hemorrhage (blood in alveoli takes up CO)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Rate abnormalities in breathing

A

Normal: 20 bpm
Bradypnea: 8 bpm or less
Tachypnea: > 25 bpm

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

Tachypnea

A

Moderate to severe cardio-respiratory distress
- Absence makes pulmonary embolism less likely
- Pneumonia: both for in and out-patients
-

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

Rate and depth abnormalities

A

Cheyne-stokes respiration: Hypernea–> apnea alternations

  • periodic breathing due to sluggish breathing, or heart failure
  • Swings in cerebral flw characterized by alternating hyperpnea, hypopnea
  • May be seen in normal people as a result of aging sleep
  • Bad prognostic sign in disease
Kussmaul's respiration= rapid and deep (hypernea/hyperventilation)
- Increased respiratory rate/tidal volume due to:
MAKEUPL
- Methanol
- Aspirin
- Ketones
- Ethylene glycol
- Uremia
- Paraldehyde
- Lactic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Hypopnea

A

Shallow respirations due to:

  • Impeding respiratory failure
  • Obesity- Hypoventilation (Pickwickian syndrome)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Apnea

A

Absence of respiration (more than 10 seconds)

- Due to either central/obstructive processes

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

Pursed lips on exhalation

A

Lost elasticity in lungs (emphysema)- splint expiratory flow (resistance) to keep alveoli for squashing

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

Sighs

A

Deep breath due to “squashed alveoli” after shallow breathing

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

Orthopnea

A

Breathing “erect”

  • Pulmonary edema due to heart failure
  • Can also be due to ascites- pushes up on lungs
  • Pulmonary diseases: emphysema in apices, send blood to bases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Paroxysmal nocturnal dyspnea

A

PND - wake up due to respiratory arrest- blood in lungs while supine- becoming vertical drains blood out of lungs, improves respiration

  • due to heart failure
  • L ventricular failure
  • Pulmonary diseases (bi-apical)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Clubbing

A

Shunting of blood from finger tips

  • does NOT occur in emphysema
  • Seen in chronic bronchitis, tetralogy of Fallot, endocarditis
  • 4/5 patients with clubbing–> underlying respiratory disorder (inflammatory or neoplastic)

Signs:
Floating nails (ballottability of nail bed)
Abnormal phalangeal depth ratio
Lovibond angle disappears (at cuticle)
- Differentiate from severe nail curvature= illness
* Malignancy can increase periosteum–> tenderness in shins, clubbing (pulmonary hyperperiostrophy)

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

Hepatopulmonary syndrome

A

Cirrhosis–> AV fistulas–> standing feeds fistulas–> hypoxia

Lying down drains AV fistulas–> normoxic

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

Platypnea

A

Breathing “flat” due to orthodeoxia when upright

  • Left to Right to Left shunt (often ASD with pulmonary hypertension)
  • Cirrhotics
  • Bi-basilar processes (embolisms, pneumonia, pleural effusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Teleangiectasia-Ataxia (Osler-Weber-Rendu)

A
  • Epistaxis
  • Tongue bleeds
  • Telengectasias
  • Visceral AVMs

AV fistulas throughout body (including lung)
Arterial beds die–> release PGF–> clubbing

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

Trepopnea

A

“Twisted respiration”

  • Have to be on one side to breath better
  • Inability to lie supine or prone, preference for lateral decubitus
  • Lung is squashed by massive effusion
  • Lie down on good lung side to ensure perfusion
  • UNLESS effusion “spills”, hemoptysis, pneumonia, pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Abdominal paradox

A

Abdomen sucking in while patient inhales= sign of respiratory distress

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

Signs of respiratory distress

A

Hemodynamic instability= needs INTUBATION

  • Accessory Respiratory Muscle (ARM) use (SCM, intercostals, trapezius, scalenes)- > 90% patients hospitalized for COPD with ARM use
  • Abdominal paradox
  • Respiratory Alernans
  • Patient can’t speak completely
  • May also use ARM to exhale
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Respiratory alternans

A

Abdominal paradox alternating with diaphragm moving with chest wall (resting)

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

Tirage

A

Inspiratory retraction of suprasternal and supraclavicular fossa and intercostal spaces

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

Lung’s tripod

A

Leaning up, sitting forward on knees, pursed lips (Emphysematous breathing)
- Can see patch on thighs

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

Hoover’s sign

A

Diaphragm flattened by hyperinflated lungs–> pulls inward with inspiration
- 90% specific for COPD

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

Laryngeal height

A

Distance between adam’s apple and suprasternal notch

  • Should be > 4 cm
  • Emphysema/smoking–> decreased laryngeal height
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Predictor of COPD

A
  • Self-reported age of 45+
  • Self-reported history of COPD
  • Smoker
  • Reduced laryngeal height (< 4cm)

+ Bad outcomes after surgery

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

Presence of COPD

A

Self-reported history

- breath sounds greater than 6 seconds (should be less than 5 in nL): prolonged expiratory time (FEV1< 40)

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

Emphysema signs

A 
Slender
"puffing breathing"
long distance runner
- Must destroy lungs before getting cor pulmonale
No clubbing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

COPD/chronic bronchitits

A

Bigger
Sprinter- can deal with hypoxia better
Cor pulmonale
Clubbing fingers

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

Toe clubbing

A

Pulmonary hypertension

  • Fingers normal, pink
  • Toes bluer, clubbed
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Vesicular breath sounds

A 
Lower pitched/soft breath sounds
FETo maneuver (obstruction)

Breath sounds in chronic bronchitis- increased intensity of breath sounds in mouth, decreased in chest

Pleural effusion:

Pneumothorax: everything is SILENT

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

Asthma

A

Longer wheezes, the worse
Length of wheexing/total length of breath= severity correlation
- Not a good predictor of asthma

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

Crackles

A

Timing is crucial:

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

Findings of pneumonia

A

Posturally-induced crackles

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

Bradypnea

A

Slow breathing (< 8 bpm) due to:

  • hypothyroidism
  • CNS depression
  • Narcotics/sedatives
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Kussmaul’s respiration

A 
Rapid and deep (hypernea/ hyperventilation- increased rate and tidal volume)
- Differs from hyperventilation of cardiac/respiratory disorders= shallow (less effective)
MAKEAL
- Methanol
- Aspirin
- Ketones
- Ethylene glycol
- Uremia
- Paraldehyde
- Lactic acidosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Accessory Respiratory Muscles (ARM)

A

Normal= only diaphragm contracts on inspiration, exhalation is passive

  • Recruit scalenes, trapezius, SCM
  • Seen in > 90% patients hospitalized for COPD
  • SCM may lift clavicles, first ribs
  • Upper lift > 5mm–> Forced expiratory volume in 1st second of 0.6L
  • Chronic use–> hypertrophy
  • See inspiratory retraction of suprasternal/supraclavicular fossa, intercostal spaces (tirage)
  • May use abdominal muscles to aid with exhalation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Causes of clubbing

A 
Intrathoracic:
- AV malformations
- Lung cancers
- Mesothelioma
- Bronchial problems
- Cystic fibrosis
Cardiovascular
- Congenital cyanotic heart disease
- Subacute bacterial endocarditis
- Infected aortic bypass graft
Hepatic/GI: 
- Cirrhosis
- IBD
- GI cancer
*10% benign (AAs, idiopathic, pregnancy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Hypertrophic Osteoarthropathy

A

Systemic disorder of bones, joints, soft tissue; associated with intrathoracic neoplasm (bronchogenic)
- Also called Hypertrophic pulmonary osteoarthropathy
- Painful, tender periosteal bone proliferation usually associated with clubbing
- Seen in long bones of extremities: pre-tibial aches (shining, thickened warm skin)
Diagnosis: imaging
Treatment: resection

*Can also occur in non-neoplastic pulmonary disorders (CF, bronchiectasia, empyema, lung abscesses)

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

Breath Sounds in methacholine challenge (asthma)

A
  • Decreased intensity (reduced airflow)
  • Increased pitch with airway narrowing (precedes full-on wheezing)
  • Wheezing on maximal forced exhalation is NOT predictive of asthma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Breath sounds in pneumothorax

A

reduced or silent

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

Breath sounds in pleural effusion

A
  • Vesicular on top
  • Bronchial in middle
  • Absent on bottom
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

Breath sounds in chronic bronchitis

A

increased intensity of breath sounds in mouth, decreased in chest

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

Reduced Breath Sound Intensity (BSI)

A

Airflow obstruction

  • COPD: reduced transmission of sound (not production)
    • fever and localized sound= pneumonia with effusion
  • Confirm obstruction with FETo maneuver
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

Wheezes

A

Length of wheezing correlates with severity of airflow obstruction (Time of wheeze/T of total expiration)

  • Intensity + polyphonic components does not correlate with obstruction
  • Pitch is not related to site of production–> more severe asthmatics have higher pitched wheezes

Cardiac asthma= asthma in L ventricle failure

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

Crackles

A

Early= large central airways (low pitched, coarse)–> bronchitis

Mid-inspiratory= medium-sized airways (pathognomonic of bronchiectasis)

Late crackles= peripheral airways snapping open, predominates at bases, fine, high-pitched–> fluid or scarring in interstitium

  • Crackles of heart failure valuable if posturally-induced (PICS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Obstructive Atelectasis

A 
Excessive secretion due to: 
- asthma
- chronic bronchitis
Foreign body aspiration
Blood
Bronchial neoplasms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Compressive atelectasis

A

Expansion of the pleural space

  • By fluid: effusion (CHF, neoplasms), blood (rupture of aneurysm)
  • By air: pneumothorax
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Patchy atelectasis

A

Loss of surfactant due to:

  • neonatal RDS
  • adult respiratory distress syndrome (ARDS)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Contraction atelectasis

A

Irreversible fibrosis of lung tissue: parenchymal or pleural fibrosis

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

Broncial arteries

A
  • Secondary circulatory supply to pulmonary system (from systemic circulation)
  • Comes from internal thoracic arteries
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Bronchial veins

A

drain to azygous/hemiazygous vains

- Abundant anastomoses with pulmonary veins

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

Pulmonary artery

A

Emanates from R ventricle–> venous blood to arteries, arterioles, capillaries–> gas exchange ONLY (no blood supply to lung tissue)–> drain oxygenated blood into pulmonary veins–> L atrium

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

Pulmonary arterial pressure

A

Systolic/Diastolic/Mean
ex: 25/10/15

Precapillary pressure: before blood enters alveoli
Post-capillary pressure: measures L heart pressure (backs up into pulmonary vein

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

Mean pulmonary arterial pressure

A

(PA systolic pressure + 2(PA diastolic pressure))/3

Mean PAP > 25 mmHg–> pulmonary HTN

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

Pulmonary vascular resistance

A 
PVR= (Pulmonary arterial pressure- pulmonary venous pressure)/ pulmonary blood flow
-PVR= (Pa-Pla)/Qt

Pla= pulmonary venous pressure= Left atrial pressure

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

Effects of vascular pressure increases on lung

A

Lung circulation:

  • Recruitment of closed vessels
  • Distension= increase in caliber of vessels

Lung volume:

  • low lung volumes–> high resistance (extra-alveolar vessels narrow)
  • High lung volumes–> low resistance (extra-alveolar vessels stretched out)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

Measurement of pulmonary blood flow

A
  • Oxygen consumption (VO2)= measured in L/min
  • O2 concentration in blood entering lungs= CvO2
  • O2 concentration in blood leaving lungs (CaO2)

Fick equation:
V02= Q (CaO2- CvO2)
* Oxygen consumed related to flow across capillary bed multiplied by O2 difference

*Pulmonary blood flow is dependent on position

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

Hypoxic pulmonary vasoconstriction

A

Systemic arteriole: dilates in response to hypoxia (try to get as much oxygenated blood to tissue as possible)

Pulmonary arteriole: constricts due to hypoxia
- Adaptive mechanism: shunting–> avoid wasting flow through “Dead space”

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

Pulmonary hypertension

A

Normal mean PAP= 15 mm Hg
Pathologically increased PA pressure–> pulmonary hypertension

Three mechanisms for development of PH:

  1. Increase in L atrial pressure (post-capillary)
  2. Increase in pulmonary blood flow
  3. Increase in pulmonary vascular resistance (PVR)

Over time, high pressure distends arterioles, increases inflammation, causes architectural remodeling

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

Pulmonary HTN: increase in L atrial pressure

A

Post-capillary pulmonary HTN
- Passive pulmonary HTN

  • Aortic stenosis
  • L-sided Heart failure
  • Mitral valve stenosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Pulmonary HTN: pulmonary edema

A

Stages:
0= normal alveolar walls, no excess fluid in perivascular connective tissue spaces
1= Initial fluid leak; bronchovascular space around conducting vessels and airways
2= interstitial edema; spaces between alveoli and capillaries fill with fluid
3= alveolar edema: fluid extravasates from interstital spaces into alveoli

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

Pulmonary HTN: increase in pulmonary blood flow

A
  • Initially: rise in PA pressure small (pulmonary capillaries accomodate high flows via recruitment and distension)
  • Sustained high flows–> histologic changes in walls of small arteries, arterioles
  • Eventually, PA pressures may reach systemic levels–> R to L shunting (Patent foramen ovale, anastomoses of bronchial vein to pulmonary vein), Systemic shunting

Can initially start out as L to R shunt (arterio-venous)–> increased flow through pulm circulation:

  1. Intra-cardiac
    - Congenital heart disease: VSD, ASD, Patent ductus arteriosus (aorta to pulmonary artery)
    - Anomalous pulmonary venous return: pulmonary vein return to R atrium instead of L atrium
  2. Extra-cardiac shunts (L to R)
    - AV malformations (advanced liver disease, telangiectasia)
    - Dialysis fistulas (man-made)
    - Paget’s disease

Non-shunt examples:
- Anemia (chronic, severe), thryotoxicosis, sepsis (acute), thiamine deficiency

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

Pulmonary HTN: increase in pulmonary vascular resistance

A
  1. Vasoconstrictive
    - Alveolar hypoxia (altitude, emphysema, bronchitis)
    - Chemical mediators
    - Vasoconstrictors: serotonin, endothelin-1
    - Vasodilator deficiency: nitric oxide (NO), prostacyclin
  2. Obstructive:
    - Embolism in pulmonary arterial system (thrombo, fat, air, amniotic fluid, lymph spread of tumor)
    - Thrombosis in situ (sickle cell anemia, antiphospholipid syndrome)
    - Foreign bodies (talc powder, schistosomiasis)
  3. Obliterative:
    - Destruction of capillary bed (emphysema)
    - Diseases of pulmonary arterioles (connective tissue diseases: scleroderma, SLE)
    - Disease of pulmonary venules (connective tissue diseases, pulmonary veno-occlusive disease (PVOD))
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Pulmonary arterial hypertension (PAH)

A

mPAP> 25 mmHg at rest

  • Pulmonary vascular resistance > 3 wood units
  • Pulmonary arterial wedge pressure (Left Atrial Pressure) < 15 mm Hg (need to rule-out L-sided causes of increased pressure)
  • Right heart failure (advanced cases)- may need new valve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Epidemiology of idiopathic PAH

A

Female
Young to middle age
Now may be more common in middle age to older men

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

Genetics: heritable PAH

A
  • 6-10% of cases of PAH: see bone morphogenic receptor protein 2 (BMRP2)
  • Need yearly echocardiogram
  • Genetic anticipation
  • Incomplete penetrance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Pathogenesis of PAH

A

Arteriolar vascular remodeling: excessive cell proliferation, reduced rates of apoptosis
- Excessive rates of vasoconstriction

Histology: 1 + of the following:

  • Intimal hyperplasia
  • Medial hypertrophy
  • Adventitial hypertrophy
  • Plexiform arteriopathy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

PAH effects on R ventricle

A

Hypertrophy: pushing against resistance

  • In advanced cases–> dilation of decreased stroke volume
  • Myocardial ischemia due to: thinning of RV wall causing stretch/narrowing of coronary arteries, reduced cardiac output

Symptoms:
- Dyspnea, fatigue, syncope, dizziness, chest pain

Physical exam in RV dysfunction:

  • JVD, RV heave (PA pulsation), Tricuspid regurgitation murmur, Loud pulmonic valve closure (P2)
  • Liver findings: Hepatosplenomegaly, Hepatojugular reflux, Hepatic pulsation, ascites, peripheral edema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Cor pulmonale

A

Altered structure of R ventricle (hypertrophied or dilated)
- Impaired function of RV

Diseases associated with cor pulmonale:

  • Lung (COPD, fibrosis)
  • Pulmonary vasculature (IPAH)
  • respiratory pump (obesity hypovent, sleep apnea)
  • Thoracic cage (kyphoscoliosis)

*NOT cor pulmonale: R-sided heart disease due to L-sided heart disease (mitral stenosis)

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

Mechanisms of excessive pleural fluid formation

A

Transudative (not inflammatory)

  • increased hydrostatic pressure
  • decreased oncotic pressure
  • decreased lymphatic drainage

Exudative (inflammatory)
- increased endothelial permeability due to cancer, infections

Decreased pleural pressure: vacuum
- Endobronchial obstruction–> lung collapses–> pleural space pulls thins in

Movement from peritoneal space: pressure in abdomen higher than in chest–> small discontinuities in diaphragm–> ascites moves

Thoracic duct rupture

Iatrogenic (catheter in pleural cavity instead of vein)

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

Symptoms of pleural effusion

A
  • Chest Pain (Pleuritic)
  • Dyspnea
  • Cough and Sputum production
  • Symptoms related to the underlying disease (e.g. fever, weight loss…)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

Physical findings of pleural effusion

A
  • Tracheal shift
  • Decreased thoracic excursion
  • Decreased to absent tactile fremitus
  • Flat percussion note
  • Decreased-to-absent vesicular breath sounds overlying bronchial breath sounds (a three-layered gradient)- massive effusion–> no sound throughout (vs smaller effusion, sounds at apex)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Limitations of chest x-ray in identifying pleural effusion (compensations)

A
  • Large amount may accumulate in the diaphragmatic ‘gutter’ before becoming visible on PA view
  • Need to resort to decubitus films to see if fluid is present and tappable
  • 1 cm of fluid (1 fingerbreadth) enough for tap
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Causes of pleural effusion

A 
CHF
Pneumonia
Malignancy
Pulmonary embolism
Viral
Cirrhosis with ascites
GI diseases
Asbestos/mesothioloma
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Differential diagnosis of hemothorax (bloody)

A 
4 Ts:
Trauma (25%)
Tumor (50%)
Thromboembolism (15%)
Tuberculosis (5%)
  • Post-cardiotomy syndrome (ex: after bypass surgery)
  • Benign asbestos effusion (asymptomatic)- 5%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Differential diagnosis of white exudate in pleural space

A

Pus: centrifuge–> pellet
Lipids: TGs (chylothorax), Cholesterol (pseduochylothorax)

Cause of chylothorax: Thoracic duct has been damaged:

  • 55% tumor= lymphoma
  • 25% trauma= surgical, other
  • 15% idiopathic (congenital, other)

Diagnosis of chylothorax: Pleural fluid TGs: > 110, not < 50
- Values in between–> electrophoresis to look for chylomicrons

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

Yellow-green pleural fluid

A

Rheumatoid

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

Brown pleural fluid

A

Amebic

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

Black pleural fluid

A

Aspergillus

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

Light’s criteria

A

3 consistant predictors of whether effusion was exudate (bad) or transudate (benign):

Exudative:

  1. Pleural fluid protein/serum protein > 0.5
  2. Pleural fluid LD > 0.67 of upper limits of normal serum serum LDH
  3. Pleural fluid LDH divided by serum LDH > 0.6
  • Pleural fluid LDH divided by serum LDH > 0.6
  • Pleural fluid LDH greater than two-thirds the upper limit of normal for the serum LDH.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

Laboratory studies of pleural effusion

A

Chemistry:

  • Protein, LDH, Glucose
  • Amylase (perforated esophagus or pancreatic process spilling through diaphragm)
  • Lipids
  • pH

Cell count and differential

  • Acute: PMNs
  • Chronic: lymphocytes

Cytology: rule out cancer

Microbiology: look for organisms

Biopsy (closed needle via video-assisted thoracoscopy)

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

Low glucose/low pH effusions

A

Lots of metabolically active cells in effusion:

  • Glucose converted to lactate and CO2
  • Acidifies cavity

Therefore, they must both go in same direction (increased glucose, increased pH, decreased glucose, more acidic)

Normal pH of pleural space= 7.6
- Acidic < 7.2

States of low glucose/low pH:

  • Empyema: PMNs
  • Esophageal rupture: PMNs
  • Hemothorax: PMNs
  • Rheumatoid effusion: Lymphocytes
  • Lupus effusion: Lymphocytes
  • Malignancy–> bad prognostic sign: Lymphocytes
  • Tuberculosis: Lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Diagnostic thoracentesis indications in suspect CHF

A

Conduct thoracocentesis b/c suspicion that it’s not cancer:

  • Fever
  • Pain
  • Unilateral effusion
  • Left effusion > right (supposed to be R > L)
  • Effusions of disparate size
  • PaO2 inconsistent with clinical presentation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Hepatic hydrothorax

A
  • Occurs in 5% of patients with clinical ascites (ascites all in chest)
  • Can occur in absence of clinical ascites
  • Definitive diagnosis by radionuclide study
  • 70% of effusions are right-sided; can also be unilateral on the left
  • Chest tube drainage contraindicated: reaccumulate
  • Refractory effusion: TIPS (transjugular intrahepatic portosystemic shunt) or VATS (video-assisted thoroscopy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Anasarca

Causes of pleural transudates

A

Transudates seen in:

Heart failure, cirrhosis, nephrosis, protein-losing enteropathy

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

Parapneumonic effusion

A

Common complication of pneumonia
Proper managment necessary

  • Uncomplicated: free-flowing effusion that resolves with antibiotics= exudative
  • Complicated: loculated (not free-flowing) effusion that requires pleural space drainage–> resolve pleural sepsis= fibrinopurulent
  • Empyema: end-stage complication (drain!)= organizational

Ominous symptoms:

  • Prolonged symptoms
  • Anaerobic infection, virulent pathogen
  • Not getting better with antibiotics

Ominous radiologic findings:

  • Large effusion
  • Air-fluid level
  • Loculation
  • Multiple loculations
  • Size of loculations
  • Pleural enhancement/thickening on CT

Ominous fluid findings:

  • Gross pus (empyema)
  • Positive stain or culture
  • Low pH
  • Low Glucose
  • High LDH
  • (Cell count not as much of an issue)
100
Q

Empyema thoracis

A
  1. Pus in the pleural space (thick, yellow-white, opaque coagulum, containing fibro-collagen deposits, but above all cells and bugs)
  2. No pus, but organisms on gram stain
  3. No organisms on gram stain, but + cultures
  4. None of the above, but concerning chemistries: glucose, pH low

Causes:

  • Pulmonary infection
  • Surgical procedure
  • Trauma
101
Q

Treatment of empyema

A

Therapeutic thoracentesis
Chest tube + fibrinolysis (break up goop)
Image-guided catheter + fibrinolysis (break up pus)–> surgery earlier vs later

Surgery:

  • Video-thoracoscopy with decortication
  • Thoracotomy with decortication
  • Open drainage
102
Q

Malignant pleural effusion

A

4 most common causes:

  • Lung
  • Metastatic: breast, lymphoma, ovary
  • Symptoms of cancer

Radiographic findings:

  • Massive effusion with contralateral shift
  • Large homogeneous density without contralateral shift (lung cancer)
  • Bilateral effusion with normal heart size (non-lung primary)
103
Q

Causes of massive effusion

A 
Tumor
Trauma 
Empyema
Hepatic hydrothorax
CHF (if bilateral)
104
Q

Biochemistry of malignant effusion

A
  • Exudative
  • High proteins
  • Consider Cancer when exudative by LDH only
  • Glucose < 60 mg/dl (30-50) in 30% of cases (bad omen)
  • pH < 7.30 (7.05-7.29) in 30% of cases (bad omen)
  • Amylase-rich (salivary) in 10-14% of cases PF/S = 5:1
  • Cytology diagnostic only in 40-60% of cases
  • Closed pleural biopsy adds only another 10-20%
105
Q

Asbestos

A

Ferruginous bodies:
- Fibers coated with hemosiderin and glycoproteins. The hallmark of asbestos exposure. More abundant in patients with pleural plaques.

Pleural plaques:

  • Absent at 10 years from initial exposure
  • Present in 10% after 20 years
  • Half cases have them at 40 years
  • Calcifying within years of radiologic appearance
106
Q

Mesothelioma

A
  • Typically presenting with chest pain and a pleural mass
  • Often locally destructive and locally metastatic
  • Exudative and hemorrhagic effusion
  • Diagnosis usually requires open biopsy via thoracoscopy
  • Prognosis is typically poor
  • Benign mesotheliomas are associated with Hypertrophic Pulmonary Osteoarthropathy in 20% of cases and symptomatic hypoglycemia in 5%
107
Q

Pulmonary embolism- Pleural effusions

A

Pleural effusion common in PE- “the big masquerader”

  • Bloody or straw-colored
  • Exudate and transudative
  • Lymphocytic or neutrophilic
  • Small, can be medium
  • Associated with fever, rapidly abating
  • Resolves quickly*
  • Unilateral effusion
  • Pleural effusions can increase after 72 hours in PE due to:
  • Recurrent embolization
  • Infected pulmonary infarction
  • Hemothorax on heparin
108
Q

Radiologic features of pleural effusion that are NOT due to pulmonary embolism

A
  • Massive effusion
  • Bilateral effusion
  • Delayed in onset
  • Increases after 72 hours
  • Unaccompanied by chest pain
109
Q

Tuberculosis pleurisy

A
  • Acute illness to indolent disease
  • Cough (80%); Chest pain (76%);
  • Temperature 100-104o
  • Unilateral small-to-moderate effusion
  • Parenchymal infiltrate in a third of cases on CXR
  • PPD negative in up to 30% of cases
  • Self-remitting initially, but eventually resulting in pulmonary tuberculosis
110
Q

Pleural fluid analysis in TB pleurisy

A
  • Heavy exudate (protein > 4 g/dl) – occasionally bloody
  • pH < 7.40 (< 7.30 in 20% of cases)
  • PF glucose = serum (< 60 mg/dl in 20% of cases)
  • Nucleated cells < 5,000/ul
  • 90-95% lymphocytes in tipical cases
  • Acute TB pleurisy and TB empyema have PMN’s
  • > 10% mesothelial cells make TB unlikely
  • PF/blood esosinophils > 10% make TB unlikely
    ADA can be diagnostic (if available)
111
Q

Pleuropulmonary manifestations of rheumatoid arthritis

A
  • Infections of lung and pleura
  • Pleurisy
  • Interstitial disease
  • Pulmonary nodules
  • Pulmonary vasculitis
  • Combination of pleural/parenchymal disease
  • Rare complications
112
Q

Rheumtoid pleurisy diagnostic criteria

A 
Appearance: turbid, yellow green, debris
100-15,000 nucleated cells
Usually lymphocytes
Total protein > 0.5, up to 7.3 g/dL
LDH < 1000 IU/L
Glucose low
pH 7.0
Complement: low
RF (rheumatoid factor) present
113
Q

FEV1 in Asthma

A

FEV1/FVC= 50% (should be 80% in normal)

  • Sign of airflow obstruction
  • Absolute ratio, not compared to normal*
114
Q

Diagnosing asthma when spirogram is normal

A

Spirogram can be normal (asthma comes and goes)

Challenge testing= methacholine; negative predictive value

  • Normal patients react at about 16 mg/mL
  • Reaction defined as 20% fall in FEV1 (asthma when dose is low)
  • Absence rules out asthma, but presence could be due to another airway issue (specific, not sensitive)
  • Contraindications=
  • Advanced age
  • FEV1 < 50% normal
  • Recent MI, suspected cardiac disease
  • Inability to coordinate/cooperate with testing
115
Q

Medical managment of asthma

A
  • Diagnosis
  • Monitor course
  • Control factors that worsen asthma
  • Pharmacotherapy: symptom therapy, controller therapy (day to day treatment to keep symptoms under control)
  • 10-15% improvement after bronchodilator administration
116
Q

Drug therapy in asthma: Symptomatic drugs

A 
Beta-adrenergic agents (short acting)
Anticholinergic agents (short acting)
Oral prednisone (burst for flares)
- Can have bad long-term effects--> ONLY for short term flares
117
Q

Inhaled medication delivery devices

A
  • Metered-dose inhaler (MDI)
  • Dry powder inhaler (DPI)
  • Spacer/holding chamber
  • Nebulizer
118
Q

Drug therapy in asthma- controller therapy

A

Principle:

  • Inhaled glucocorticoids: kills eosinophils
  • Oral glucocorticoids for severe exacerbations (long term use–> osteoporosis, muscle catabolism)
  • Reduce risk of adverse events by rinsing mouth, lowest possible dose, monitor growth in children
  • Benefits: long term control of symptoms, reduced mortality from asthma symptoms

Alternatives:

  • Anti-leukotriene drugs (oral)
  • Theophylline (oral and IV)
  • Cromolyn sodium (inhaled)
  • Allergen immunotherapy: antigen extracts to desensitize allergic patients
119
Q

Managing chronic asthma

A

Rule of 2s:
If short-acting dilator needed more than 2 times per week, more than 2 night-time awakenings per month= poorly controlled (need inhaled corticosteroid)
- Can add anti-leukotrienes, theophylline as symptoms get worse

Symptoms infrequent, lung function normal–> just use short-acting inhaler as needed

120
Q

Long-acting bronchodilator as monotherapy

A

Study examined if patients could be placed on long-acting bronchodilators only
- Rate of treatment failure (hospitalization rates) much higher than those on inhaled steroids

121
Q

Compliance with asthma medications

A
  • For controller therapy to work, patient must take it!
  • Compliance is 54% for inhaled steroids
  • Takes 1+ week for effectiveness to begin
  • Use of short-acting inhalers markedly declines with compliance
122
Q

Exercise-induced asthma

A

Inflammatory cells activated while NE and epi pumping through body during exercise

  • As soon as exercise stops for a minute, NE and epi decline–> overwhelm lungs with inflammatory response (no longer dilated by epi/NE)
  • Asthma symptoms kick in
123
Q

Nocturnal asthma attacks

A

NE and epi at lowest level during sleep–> symptoms can kick in due to lack of dilation
- Nocturnal attacks more common in uncontrolled patients

124
Q

Moderate asthma poorly controlled with inhaled steroid

A

Control GERD
Control Rhinitis
Eliminate mycoplasma, chlamydia infections

125
Q

COPD

A

Group of chronic lung diseases characterized by chronic airflow limitation:

  • Chronic bronchitits
  • Emphysema
  • fist appeared in Europe in industrial revolution
126
Q

Chronic bronchitis

A

Definition:

  • Daily productive cough
  • 3 mos/yr for 2 years
  • Airway disease

Histo:

  • Edema, inflammation
  • Goblet cell hyperplasia
  • Mucous, pus in airway
  • Smooth muscle hypertrophy
  • No obstruction= simple bronchitis
127
Q

COPD- Asthmatic bronchitits

A

Overlap of bronchitis (COPD- smoking induced) and asthma

  1. Exposure to tobacco+ features of asthma
  2. Begin with asthma–> chronic irreversible airflow obstruction (no smoking history)
128
Q

COPD emphysema

A 
Path: 
- distal airspace destruction
- more prominent in apices
Physio: 
- loss of surface area (less O2 transfer)
- decreased elastic recoil
- Airway collapse
129
Q

Obstructive lung diseases

A

MOST patients have concomittant emphysema and bronchitis

  • Solely emphysema= shortness of breath
  • Solely bronchitis= productive mucous cough
130
Q

Epidemiology of COPD

A
  • 10 million adults diagnosed
  • 24 million Americans have impaired lung function

Risk factors:

  • Cigarette smoking
  • Age
  • Childhood respiratory infections
  • Family history
  • Exposure to air pollution
  • Smoking rates have declined from 40-50%, still 22-25% (1/5 will get COPD)
  • Women have surpassed men with lung cancer and COPD death rates
131
Q

Clinical presentation of COPD

A

Chronic bronchitis: wheezing rhonchi, edema, cyanosis

  • Cough apparent after URI
  • Cough worsens and progresses

Emphysema: breathlessness, thin, barrel chest

  • Insiduous onset
  • Cor pulmonale (R ventricular heave, increased P2, dependent edema)
  • Cyanotic digits
  • NO clubbing
132
Q

Differential diagnosis of COPD

A

Asthma
CHF
Bronchiectasis
Tuberculosis

133
Q

Pathogenesis of COPD

A

Anti-proteases (A-1 anti-trypsin)- 1/6000 caucasians
Genetic factors
Smoking- no matter how much decline in function has occurred, quitting can dramatically slow decline in FEV1 (decline is normal in all people- aging, loss of elastase)
Pollution

134
Q

Chest radiographs in COPD

A 
Barreling of chest
Diaphragm flattens
Diminished lung markings
Bullae formation
Chronic bronchitis--> "dirty lung" appearance (bronchovascular markings)
135
Q

Physiology of COPD

A 
Absolute FEV1/FVC ratio declines
- Obstruction (FEV1 declines)
Loss of elastic recoil/ airway collapsibility
- elevated TLC, RV/TLC ratio (hyperinflation, air trapping)
Airway inflammation and bronchospasm
- Increased resistance
Reduced DLCO
Loss of surface area
Hyperinflation
136
Q

Emphysema

A

Tethering structures around airway collapse–> airway collapse

137
Q

Bronchitis

A

Mucous and inflammation of airways (vs just inflammation in asthma)

138
Q

Prognosis of COPD

A

Predictors: age and post-bronchodilator FEV1
- FEV1 reduced to 1 L or 30% predicted, 5-year survival 50%

Poor prognostic factors

  • Resting tachycardia
  • Hypercapnea (increased PaCO2)
  • Cor pulmonale (R ventricular heave, loud P2, dependent edema)
  • Weight loss
139
Q

Treatment of COPD

A

Smoking cessation
Influenza, pneuomococcal vaccine
Control environment (avoid irritants)

Minimize airflow obstruction: smooth muscle spasm, inflammation, luminal secretions

  • Reduce exacerbations
  • Supplement oxygen
140
Q

Drug therapy in COPD

A
  1. Sympathomimetic bronchodilators: short and long-acting
  2. Anticholingergic: short and long acting
    - Reduce smooth muscle tone, mucous secretion
  3. Theophylline: no longer used
    - May reduce overnight fall in FEV1, enhance respiratory muscle function/ central drive
  4. Corticosteroids (systemic, inhaled)
    - Systemic= acute exacerbations
    - Inhaled= decrease exacerbation frequency (does not improve FEV1, but indicated when FEV1 < 50-65%)
  5. Mucolytics (thin mucous, easier to cough out)= guiafenesin
  6. Antibiotics (increased dyspnea, change in sputum color, volume)
  7. Oxygen therapy
141
Q

Oxygen therapy for COPD

A

Proven to prolong life in hypoxemic patients
Survival best for 22-24 hour use (vs 12)
Neuropsycholocial improvements
INDICATIONS:
- PO2 < 55 mmHg (2 measurements) at rest
- PO2 55-59 mm HG with evidence of cor pulmonale (ECG, polycythemia, CHF)
- Normal resting PaO2 but desaturation during sleep, exercise

142
Q

Cystic fibrosis

A

Most common lethal genetic disease in whites
Autosomal recessive, affects 70,000 ppl
- Dysfunction of cystic fibrosis transmembrane protein (CFTR)
- Mutation–> altered chloride ion channels
- Thick mucous forms that can’t be cleared–> substrate for infection (pseudomonas, burkholderia, s. aureus, haemophilus)
- Seen in lung, sweat glands, pancreas, GI tract

Histo: impaired extrusion of mucus secretion onto epithelial surface of airways in cystic fibrosis–> ciliary disfunction–> opportunistic infections

Imaging: Finger-in-glove mucous dilatation of airways

Clinical:

  • Rhonchi
  • Consolidation during pneumonia
  • Cyanotic digits, clubbing
143
Q

Bronchiectasis

A

Dilatation and damage to bronchi seen in disorders (including CF):
- Foreign body aspiration
- Chronic aspiration
- Defective host defense (hypo IgG, AIDS)
- CF (upper lobe- pseudomonas)
- Young’s syndrome (like CF but normal sweat Cl)
etcS&ER*EW&&RY

144
Q

CF therapy

A

Measures to enhance mucociliary clearance
- Bronchodilators
- Physcial measures: chest percussion
- Hydration (oral, hydrating medications)
- Osmotic measures= surfing (use inhaled salene solution to thin mucous)
Intermittent/regular antibiotics
Lung transplantation
Emerging gene therapy, molecular therapy strategies

145
Q

Hypercarbia

A

High CO2
Not moving enough air
* vs hypoxia= dysfunction of air/blood interface

146
Q

Acute respiratory failure

A

Hours to days

  • Hypoxemic respiratory failure= paO2 < 60 mmHg when breathing room air at sea level
  • Hypercapnic respiratory failure: PaCO2> 50 mm Hg (normal > 40)
147
Q

A-a gradient

A

Palveolar O2- Parterial O2 (PAO2- PaO2)

A-a gradient= FIO2 * 713- (PaCO2/R)- PaO2

PAO2= FiO2*713- (PaCO2/R)

FIO2 percent inspired oxygen (room air is 0.21)
PaCO2= arterial CO2 concentration
PaO2= arterial O2 concentration
R= respiratory quotient (0.8)

Normal= age/4 + 4 (about 12)

148
Q

Hypoxia with normal A-a gradient

A

Due to:

  1. Low O2 level
  2. Hypoventilation (opiate-induced)
149
Q

Hypoxia with increased A-a gradient

A

Increased A-a gradient:

  1. V/Q mismatch: clogged vessel or blocked airway (improves with O2 supplementation)
  2. Diffusion: disease process–> scarring/inflammation–> hard for O2 to cross alveoli (improves with O2 supplementation)
  3. Shunt: intra or extra-pulmonary (does NOT improved with O2 supplementation)
150
Q

Hypoxia resistant to O2 administration

A

Shunt: blood moving through capillary doesn’t pass alveoli (shunted past)
- Can be intra- or extra-pulmonary

151
Q

Conditions causing acute hypoxic failure

A
  • Pneumonia
  • Altitude elevation
  • Drug overdose
  • Scarring of interstitium (usually not acute)
  • Shunt (VSD= ventricular-septal defect)
  • May not be due to lung issues:
  • Heart Failure
  • Abnormal hemoglobin
  • Toxins
  • Met-hemaglobinemia
  • Cyanide
152
Q

Hypercapnia: causes

A
  • Not moving air (no drive)
  • Muscles unable to move abnormal lung: restrictive (normal FEV1 to FVC ratio) or obstructive lung disease (lowered FEV1, FE/FVC)
  • Muscles too weak to move normal lung: diaphragm injury, wasting, obesity, Guillain-Barre
  • Air interfacing with non-perfused lung (usually presents as hypoxemia)
153
Q

Definition of Systemic inflammatory response syndrome (SIRS)

A

Body temp > 38 (sepsis) or < 36 (septic shock)

  • HR > 90 bpm
  • Tachypnea, RR > 20 bpm, PaCO2 < 32 mm Hg
  • WBC > 12,000 cells/mm3, < 4000 cells/mm3 or > 10% bands

Severe sepsis= sepsis + organ dysfunction + hypoperfusion/hypotension

Septic shock= severe sepsis induced hypotension, persists despite fluid resuscitation, hypoperfusion abnormalities/organ dysfunction

154
Q

Pathogenesis of Sepsis

A
  1. Coagulation system activation: imbalance of hemostasis + activation of procoagulation pathways, down-regulation of anti-coagulant mechanisms
  2. Microcirculation and flow redistribution in sepsis: CV collapse- tachycardia, hypotension
    - Recruitment of neutrophils–> host inflammatory response (uncontrolled)–> injury, clots–> decreased glucose, oxygen delivery
  3. Down-regulation: counter-balance SIRS response with compensatory anti-inflammatory response (CARS)
    - Steroids don’t improve survival
155
Q

System involvement in sepsis

A
  1. Cardiovascular: Intravascular colume reduced (circulatory instability/collapse)
    - cytokines can cause myocardial depression–> reduced cardiac contractility, reduced cardiac output–> can mimic cardiogenic shock (suspect sepsis if no evidence of MI)
  2. Pulmonary/ARDS:
    Lungs take double hit–> pulmonary cause of sepsis (pneumonia) + SIRS effects/acidosis–> respiratory failure
  3. Renal: serious complication: mortality > 50%
    - Inflammatory-mediator induced cytotoxicity, alterations in renal perfusion, hypoxemia, apoptosis
  4. Multisystem organ dysfunction (MODS): multifactorial causes
156
Q

ARDS

A

Adult respiratory distress syndrome
Most common cause= sepsis
- Acute onset bilateral pulmonary infiltrates without heart failure (pulm capillary wedge pressure < 18 mm Hg) with poor oxygenation
- Non-compliant inflamed lungs (more work to breath)
- Profound hypoxia (PaO2/FIO2 < 200) (FIO2= fraction inspired O2)

Pathophysiology: See exudative, proliferative, fibrotic changes

  • Alveolar cells damaged–> less surfactant, capillary leakage–> inflammatory exudate-> increased inflammation
  • Dysfunctional alveoli–> shunting, V/Q mismatch
  • Hypoxemia refractive to O2
  • Decreased lung compliance
  • Mortality > 50%
157
Q

Treatment of ARDS

A

“Do no harm”

  • Minimize ventilator, allow high CO2, O2 sat 80-90% (minimize lung stretch)
  • Low tidal volume (6cc/kg body weight), minimize fluid overload (diuresis, nutrition)
  • Sepsis complicated by ARDS= 60%
158
Q

Management of Sepsis

A
  1. Source control: remove cause (antibiotics won’t work if source remains)
  2. Antibiotics
  3. Fluids to overcome:
    - distributive shock= third spacing
    - cardiogenic shock= poor cardiac function
    - Hypovolemic shock= sick patients often have decreased fluid intake or increased fluid losses (diarrhea)
  4. Hemodynamic support: catecholamine infusions (increase BP), vasoactive agents (DA< NE, neosynephrine)
159
Q

Pulmonary congestion and edema

A 
Edema in lungs due to microvascular injury:
Causes:
- infections (viruses, mycoplasma, etc.)
- inhaled gases (oxygen, cyanides, smoke, etc)
- liquid aspiration
- drugs and chemicals 
- shock, trauma, sepsis, radiation
- pancreatitis, uremia, TTP, DIC, etc.

Pathology:

  • Capillary hydrostatic pressure NOT elevated
  • primary injury to vascular endothelium or alveolar epithelium
  • leakage of fluids into interstitial space and then alveolar space
  • Can lead to ARDS= adult respiratory distress syndrome
160
Q

DAD= diffuse alveolar damage

A

Clinical ARDS

  • Pattern of acute lung injury and repair
  • Usually bilateral interstitial involvement

Causes:

  • Infections
  • Toxins
  • Drugs
  • Shock
  • Radiation
  • Misc

Early stage:

  • edema, +/- hemorrhage
  • fibrinous exudate
  • HYALINE MEMBRANES
  • mild interstitial inflammation
  • fibrin microthrombi
161
Q

Extrinsic asthma: types and causes

A
  • Atopic (allergic)= Type 1 (IgE) immune reaction
  • Occupational: type 1 immune reaction
  • Allergic bronchopulmonary aspergillosis: Type 1 and 3 immunological reactions
162
Q

Intrinsic asthma: types and causes

A
  • Non-atopic (nonreaginic): unknown etiology (infections?)

- Pharmacologic (aspirin): decreased prostaglandins, increased leukotrienes

163
Q

Atopic asthma (extrinsic)

A

Acute phase reaction: mast cells primary (histamine, chemotactic factors) and secondary mediators (leukotrienes, prostaglandin D2 cytokines, neuropeptides) induce bronchospasm, edema, mucous secretions

Late phase reaction: recruit neutrophils, basophils, eosinophils, monocytes–> persistant bronchospasm, edema and epithelial cell necrosis

164
Q

Non-atopic asthma (intrinsic)

A

Triggered by respiratory tract infections, chemicals, drugs

  • No family history
  • NO IgE mediated hypersensitivity reaction
  • Primary etiology unknown
165
Q

Kartagener syndrome

A

Inherited (autosomal recessive) defect with immotile cilia (absence of dynein arms)

  • Dextocardia (heart angled to right), sinusitis (no cilia to clear substances), bronchiectasis (inability to clear lungs–> chronic infections)
  • Recurrent respiratory tract infections
  • Sterility (abnormal cilia in vas deferens and fallopian tube)
166
Q

Definition of asthma

A

Reversible airflow obstruction: defined by FEV1 changing by > 15% of Peak expiratory flow rate
- Can resolve spontaneously or to treatment
Pathogenesis: hyperresponsiveness to stimuli–> exaggerated response
- Airway inflammation

167
Q

IL-4

A

Cytokine released by TH2 lymphocytes

  • produces IgE antibody, upregulates allergic response
  • Stimulates vascular cell adhesion molecule (VCAM)–> eosinophil migration
168
Q

IL-3

A

Cytokine released by TH2 lymphocytes

- growth factor for mast cell maturation

169
Q

IL-5

A

Cytokine released by TH2 lymphocytes

- Eosinophil maturation

170
Q

Mast cells in asthma

A

Antibodies on surface interact with allergens–> release of granules of:

  • Histamie
  • Tryptase
  • De Novo synthesis of prostaglandins, leukotrienes
171
Q

Eosinophils in asthma

A

Seen in respiratory secretions (sputum) during asthma attacks, release:

  • cysteinyl leukotrienes
  • major basic protein–> damages respiratory epithelium
172
Q

Histamine

A

released from Mast cells–> constriction, mucous secretion, vascular leak

173
Q

Tryptase

A

released from Mast cells–> Mucous secretion

174
Q

LTC4, LTD4

A

Released from mast cells–> constriction, mucous secretion, vascular leak

175
Q

Physiologic changes in acute asthma

A
  • Hypoxemia
  • Air trapping
  • Increased residual volume, fall in vital capactiy (VC)
  • Possible rise in total lung capacity (TLC)
  • Hyperinflation–> causes greater work to breathe
  • Rise in PaCO2 (BAD sign)–> increased work of breathing–> muscle fatique
176
Q

Managing severe acute asthma

A

Additional inhaled beta-2 agonists in high dose with high flow nebulizer (q 20 min- 1.5 hr)
- High dose corticosteroids to break episode

177
Q

Screening for Alpha-1 antitrypsin deficiency in COPD

A
  • COPD in non-smoker
  • Bronchiectasis without risk factors
  • Premature onset COPD, unremitting asthma as adult
  • Basilar predominence of emphysema (more common in apices)
  • Family history
  • Cirrhosis without apparent risk factors
178
Q

Histoplasma capsulatum

A
  • Small yeast- Narrow-based bud
  • Multiply within macrophages
  • Dx: direct visualization & capsular Ag in body fluids and urine
  • Endemic in Ohio and Mississippi river valleys and Caribbean (bird/bat droppings)
179
Q

Coccidioides immitis

A
  • Thick-walled nonbudding large spherule with endospores
  • Like Histoplasmosis and TB may present as asymptomatic pulmonary disease (60%), progressive pulmonary disease, or miliary disease
  • Endemic in SW US
180
Q

Blastomyces

A
  • Round to oval thick-wall yeast
  • Broad-based bud
  • Similar pathology with histoplasmosis and coccidiomycosis
  • Endemic in central and SE US
181
Q

Neural control of bronchial tone

A

5 Receptor subtypes in lung:

  • 3 Muscarininc receptors: M1+M3= bronchoconstriction; M2= inhibiti M1, M3
  • 2 Beta-adrenergic receptors: Beta-2 more common–> bronchodilation; beta-1–> bronchoconstriction
182
Q

Asthma vs COPD obstructive lung disease

A

Asthma:

  • Reversible*
  • No parenchymal destruction
  • Eosinophils, T-cells
  • Responds well to steroids

COPD:

  • Irreversible*
  • Tissue destruction
  • Smoking
  • Neutrophils
  • Less responsive to steroids
183
Q

Interstitial lung disease: Clinical presentation

A

Epidemiology:

  • Fibrosis= more common in older males
  • Sarcoidosis= younger patients
  • History of occupational/environmental exposure
  • History of a connective tissue disorder

Symptoms:

  • Dyspnea and or chronic non-productive cough
  • An abnormal chest x-ray
  • Uncommon: wheezing, chest pain, hemoptysis

Exam:

  • Clubbing= RARE (advanced disease)
  • Bilateral inspiratory crackles, basilar
  • Signs of R heart dysfunction
184
Q

Interstitial lung disease: Upper lobe disease

A 
ASSET:
Ankylosing spondylitis
Sarcoidosis
Silicosis, pneumoconiosis
Esoinophilic granuloma
Tuberculosis, fungi
185
Q

Interstitial lung disease: mid-field disease

A

Vascular disease
CHF
Lymphangitic tumor spread
Pneumocystis

186
Q

Interstitial lung disease: basilar disease

A 
Bloodborne/gravity-dependent injury
Drugs
Immune complexes (collagen vascular disease)
Idiopathic pulmonary fibrosis
Aspiration
Asbestos
187
Q

Interstitial lung disease: Pulmonary function testing

A

Typically restrictive, but non-specific

  • Decreased Lung Volumes (TLC, FVC)
  • Normal expiratory Flow Rates (FEV1)
  • High FEV1/FVC Ratio
  • Reduced DLCO
  • Widened P(A-a) O2
  • May have hypoxemia (especially with exercise)
  • Can see obstruction in LAM (lymphangioleiomyomatosis), Sarcoidosis, concomittant asthma/emphysema
188
Q

Exposure related interstitial lung disease

A 
Pneumoconiosis:
- Silicosis
- Asbestos
- Coal workers pneumoconiosis
- Berylliosis
Others: Drugs, radiation, hypersensitivity
189
Q

Silicosis

A

Caused by inhalation of crystalline silica (usually quartz)

  • Occupational hazards: mining, quarrying, stonework foundries, abrasive, ceramic, lens polishing
  • Characterized by progressive pulmonary nodules and fibrosis

Clincal presentation:
- Acute: a few weeks to a few years after the initial exposure
- Chronic: 10 to 30 years after first exposure
- Accelerated: within 10 years of initial exposure
Dose and duration of exposure important
Symptoms variable (PFT)

Associations/complications:

  • Progressive massive fibrosis (PMF)= nodules coalesce into large masses (poor prognosis)
  • Tuberculosis (2-30 fold increased incidence)
  • Lung cancer (esp. in smokers)

Diagnosis:

  • CXR: eggshell calcification
  • Histo: nodular fibrosis, collagen whorls, birefringent silica particles
190
Q

Asbestos-related pulmonary disease

A 
"unquenchable disease"
Spectrum:
- Asbestos--> fibrosis
- Pleural disease--> plaques and effusion
- Rounded atelectasis
- Malignancy: lung cancer, mesothelioma

Clinical presentation:
- 30-40 years post-exposure (pleural effusions 15 years post): dyspnea on exertion

Causes:
- Mining and milling of fibers, textiles, cement, insulation, shipbuilding; spouses clothes

Benign asbestos pleural effusion (BAPE)

  • Esosinophilic, bloody, exudative
  • Asymptomatic/dyspnea, chest pain, fever
  • Spontaneous resolution

Complications of asbestos:

  • Respiratory failure
  • Malignancy: bronchogenic carcinoma (synergistic with tobacco), mesothelioma
  • No medical therapy for asbestos-related pulmonary disease
191
Q

Coal workers pneumoconiosis (CWP)

A

Chronic inhalation of coal dust–> anthracosis

  1. Simple CWP= small nodular opacities on chest imaging (asymptomatic)
    - Coal macules (coal-dust laden macrophages, peribroncial)
    - Cough
    - Black sputum
    - no dysfunction
  2. Complicatied CWP= progressive massive fibrosis (PMF) similar to silicosis (dyspnea, cough)
    - Progressive severe fibrosis
    - Nodules > 1 cm (dense collagen/black pigment)
    - Respiratory insufficiency)

Anthracosis= accumulation of coal dust in lungs, pleura, lymph nodes

  • No significant reaction
  • Smokers/urban dwellers
192
Q

Caplan’s syndrome

A

Rheumatoid arthritis & CWP

  • Faster progression/more severe
  • Nodular lesions with central necrosis, peripheral fibrohistiocytic inflammation
  • Also Seen in silicosis, asbestosis
193
Q

Berylliosis

A

Exposure to beryllium (used in industrial ceramics) causing:

  • Acute chemical pneuomonitis (DAD)
  • Chronic berylliosis (noncaseating granulomatous inflammation on pleura, septa, bronchovascular bundles)–> progresses to end stage fibrosis

Symptoms: 15+ years after exposure
* Increased risk for lung cancer

194
Q

Talcosis

A

Exposure to talc (Mg silicates: seen in mining, leather, rubber, paper)

  • Diffuse foreign body granulomas with polarizable talc particles, fibrotic nodules, interstitial fibrosis
  • Seen with IV drug abusers (cut heroin with talc)
195
Q

Drug-induced lung diseases

A

Bronchospasm
Pulmonary edema
Chronic pneumonitis / fibrosis
Hypersensitivity pneumonitis

196
Q

Radiation-induced lung diseases

A

Acute radiation pneumonitis (1-6 months post radiation)

  • Fever, dyspnea, radiologic infiltrates
  • DAD
  • Responds to steroids

Chronic radiation pneuonitis
- Progresses to interstitial fibrosis

197
Q

Post-lung transplant complications

A

Infections

Acute rejection:

  • Early weeks-months post-transplant
  • Symptoms: fever, dyspnea, cough, CXR infiltrates
  • Histo: perivascular, peribronchiolar mononuclear cell infiltrates
  • Treatment: increase immunosuppression

Chronic rejection:

  • 6-12 months post-transplant
  • Symptoms; dyspnea, cough
  • Histo: bronchiolitis obliterans (destroyed bronchioles
  • Treatment: none
  • Accelerated pulmonary atherosclerosis
  • Lymphoproliferative diseases
198
Q

Hypersensitivity pneumonitis

A

Extrinsic allergic alveolitis= cell-mediated reaction to inhaled antigens

Organic antigens:

  • Bacteria, fungi (Farmer’s lung- Actinomyces)
  • Humidifiers- thermophilic bacteria
  • Indoor hot tubs
  • Animal proteins (bird fancier’s lung)

Acute disease: dyspnea, chest pain, fevers, chills, productive cough

Chronic disease: insiduous, dyspnea, cough, fibrosis

Diagnosis: serm precipitins, pathology, history of exposure (presents like ILD)

Histo:

  • Interstitial pneumonitis (non-specific interstitial pneumonia pattern)
  • Non-caseating, poorly formed granulomas
  • BOOP reaction (bronchiolitis obliterans organizing pneumonia)
  • May progress to severe interstitial fibrosis

Treatment: steroids (symptomatic), antigen avoidance

199
Q

Sarcoidosis

A

Systemic disease of unknown etiology, affects lungs 90% of cases

  • Prevalence 10-20/100,000 (AAs, N. Europeans)
  • Most common ILD in USA

Presentation:

  • Young adults (women)
  • Asymptomatic, incidental chest x-ray finding
  • Pulmonary symptoms
  • Skin lesions
  • LOFGREN’S syndrome= Fever, arthralgia, skin (erythema nodosum), uveitis and mediastinal (hilar) adenopathy
  • Can involve multiple organs

Diagnosis:

  • Diagnosis of EXCLUSION (unknown etiology)
  • PFT: Restrictive and/or obstructive disease
  • Pathognomonic pathology (obtain tissue biopsy)
  • Hypercalcemia/hypercalciuria

Prognosis: 70% of stage 1 improve–> declines with staging
- 85% remission by 2 years

Treatment: Corticosteroid immune suppression with symptomatic/organ-involvement (cardiac, neurological, ocular)

200
Q

Erythema nodosum

A

Feature of Sarcoidosis=

  • Acute, nodular and erythematous hypersensitivity reaction that involves the subcutaneous tissue of the shins (panniculitis)
  • Often self-limited, resolving with mild residual hyperpigmentation.
  • Typically in young women (18-34)
  • May occur as drug reaction, manifestation of systemic disease, or idiopathic entity
  • Biopsy non-diagnostic
201
Q

Histopathology of sarcoidosis

A
  • Non-caseating granulomas
  • epithelioid histiocytes
  • multinucleated giant cells
  • rim of lymphocytes / collagen fibrosis
  • schaumann bodies (laminated calcified concretions)
  • asteroid bodies (stellate inclusions within giant cells)
202
Q

ILD and connective tissue diseases

A
  • Scleroderma (skin changes, fine crackles in lung bases, spirometry restriction, ground glass, reticulonodular changes)
  • Rheumatoid arthritis
  • Sjogren’s syndrome
  • Polymyositis
  • SLE
203
Q

Idiopathic interstitial pneumonias (IIP)

A

Smoking-related:

  • Idiopathic pulmonary fibrosis (IPF)
  • Desquamative interstitial pneumonia (DIP)
  • Respiratory bronchiolitis-associated ILD (RBILD)

Completely idiopathic:

  • Nonspecific interstitial pneumonia (NSIP)
  • Cryptogenic organizing pneumonia (COP)
  • Lymphocytic interstitial pneumonia (LIP)
  • Acute interstitial pneumonia (AIP)
204
Q

Idiopathic pulmonary fibrosis

A
  • Chronic progressive fibrotic disease affecting older adults > 55 years, predominantly males
  • Usually in ex-tobacco smokers
  • Relentless course and high mortality
  • Pathology is “usual interstitial pneumonia” or UIP.
  • Abnormal wound healing

Clinical presentation:

  • Dyspnea (>90%)
  • Non-productive cough (>70%)
  • Bibasilar crackles (>85%)
  • Clubbing (>25%)
  • Progressive disease: pulmonary insufficiency/cor-pulmonale, cardiac failure (poor prognosis)

PFTs consistent with restriction
Diagnosis made by clinical picture, radiology and PFTs and confirmed by open lung biopsy

Prognosis: 50-70% mortality in 5 years
Treatment: lung transplant
- Limited response to glucocorticoids
- Cyclophosphamide, azathioprine
- Interferon gamma 1B (Interferons regulate collagen production by fibroblasts)
205
Q

Desquamative interstitial pneumonia

A

Idiopathic interstitial pneumonitis

  • Chronic lung inflammation characterized by interstitial inflammation and fibrosis and accumulation of macrophages in alveolar spaces
  • Occurs almost exclusively in current or former cigarette smokers
  • Ground glass opacities on CT scans
  • 5% mortality in 5 years

Treatment: smoking cessation

206
Q

Respiratory bronchiolitis-associated interstitial lung disease (RBILD)

A

Idiopathic interstitial pneumonitis

  • Syndrome of small airway inflammation and interstitial lung disease occurring in smokers
  • Ground glass opacities on CT scans
  • Rare mortality

Treatment: smoking cessation

207
Q

Nonspecific interstitial pneumonia (NSIP)

A

Idiopathic interstitial pneumonitis

  • Diffuse inflammation of the interstitium
  • Younger patients
  • May progress to fibrosis
  • Ground glass opacities on CT scans
  • Associated with many diseases- connective tissue diseases, hypersensitivity

Prognosis: 10% mortality over 5 years
Treatment: corticosteroids

208
Q

Cryptogenic organizing pneumonia

A

Idiopathic interstitial pneumonitis
- If etiology known called BOOP- bronchiolitis obliterans and organizing pneumonia
- Young patients
- Antecedant viral illness in 1/3
Prognosis: Rare mortality- 65% make complete recovery

Treatment: corticosteroids

209
Q

Lymphocytic interstitial pneumonia

A

Idiopathic interstitial pneumonitis

  • Lymphocytes in interstitium
  • Associated with HIV, Sjogren’s syndrome

Treatment: corticosteroids

210
Q

Acute interstitial pneumonia (AIP)

A

Idiopathic interstitial pneumonitis

  • Idiopathic ARDS
  • Fevers, cough, dyspnea of sudden onset
  • Bilateral alveolar infiltrates on imaging
  • Diffuse alveolar damage on pathology
  • 60% mortality in 6 months
211
Q

Lymphangioleiomyomatosis (LAM)

A

Abnormal smooth muscle proliferation in lungs, lymph nodes, lymphatic ducts

  • Seen in Reproductive age women with tuberous sclerosis
  • Cystic spaces in the lung lined by abnormal smooth muscle (HMB-45 + , ER/PR +)
  • Leads to Progressive respiratory failure
212
Q

Eosinophilic pneumonia

A

Eosinophilic infiltration in interstitial/ alveolar spaces

  • Idiopathic: Chronic/Acute/Simple (Loeffler syndrome)
  • Secondary: Infections (parasites/fungal)
  • Drug-induced
  • Immunological or Systemic: ABA/Churg-Strauss syndrome
213
Q

Diffuse pulmonary hemorrhage

A
  • Goodpasture’s syndrome (anti-basement membrane antibodies)
  • Idiopathic pulmonary hemosiderosis
  • Vasculitis-associated hemorrhage: Wegener granulomatosis, Churg-Strauss syndrome, Lupus vasculitis
214
Q

Wegener Granulomatosis

A

Granulomatous vasculitis involving upper and lower respiratory tract and kidney

  • Anti-neutrophilic cytoplasmic antibodies
  • Vasculitis (hemoptysis), necrotic lung nodules, destructive lesions of nose and sinuses, glomerulonephritis

Treatment: Steroids, immunosuppresive drugs

215
Q

Churg-strauss syndrome

A

Systemic vasculitis, often associated with Asthma

  • Anti-neutrophilic cytoplasmic antibodies
  • Eosinophilic pneumonia, eosinophilic vasculitis

Treatment: Steroids

216
Q

Pulmonary alveolar proteinosis

A

Pathology:

  • Impaired activity of alveolar macrophages with overproduction of surfactant (decreased GM-CSF)
  • Association with exposure to irritants and recurrent RTI (fungi/Nocardia)
  • Progressive respiratory insufficiency or resolution

Treatment: Repeated BALs (chelation)

Clinical presentation:

  • Cough
  • Sputum (chunks of gelatinous material)
  • Progressive respiratory difficulty
  • Diffuse pulmonary opacification on chest x-ray

Histopath:

  • Alveolar spaces filled with dense, amorphous, PAS-positive, lipid containing, surfactant-like material
  • Hyperplastic pneumocytes
  • Focal necrosis
  • No inflammation
217
Q

Virchow’s triad

A
  1. Hypercoagulability
  2. Venous stasis
  3. Endothelial injury
218
Q

Large emboli

A

Lodge proximally at bifurcation of pulmonary artery (saddle embolism) or lobar branches
Cause hemodynamic compromise:
- Sudden death
- Hypotension: vascular obstruction, hypoxic vasoconstriction, inflammatory vasoconstriction
- Pulmonary hypertension
- R ventricular failure: increased pulmonary vascular resistance–> R heart gets larger–> ventricular dependence (impinges on L ventricle)–> decreased cardiac output

219
Q

Swan-Ganz catheter in normal heart vs PE

A 
Catheter= Records pressures throughout heart, pulmonary artery
Normal RA: 0-6 mmm Hg- Elevated in PE
RV: 25/6 - Elevated in PE
PA: 25/12- Elevated in PE
PCWP: 5-12 Normal in PE
220
Q

Mechanisms of hypoxemia in PE

A 
Ventilation/Perfusion mismatch
- Intrapulmonary shunting V/Q=0
- Dead space ventilation V/Q= infinity
Inflammatory mediators
Surfactant dysfunction
Atelectasis
Pulmonary edema
Pulmonary hemorrhage
221
Q

Symptoms of PE

A 
Dyspnea (most common)- sudden onset
Pleurisy
Cough 
Orthopnea
Hemoptysis
Calf pain
Calf swelling
Wheeze
* 1/3 patients have NO SYMPTOMS
222
Q

Signs of PE

A

Tachypnea, tachycardia
Rales
Accentuated S2 (pulmonary valve)

223
Q

Differential diagnosis of PE

A 
Acute coronary
Aspiration pneumonia
Valvular heart disease
Pulmonary edema
Aortic dissection
224
Q

Lab studies in PE

A

ABG: Hypoxemia

  • Elevated A-a gradient
  • Respiratory alkalosis

D-dimers: degradation products of cross-linked fibrin (high sensitivity, low specificity)

  • Also seen in infection, malignancy, pregnancy, trauma
  • Used to rule out PE in low risk groups (in ER)

Adjunctive labs:

  • Brain natriuretic peptide (BNP)
  • Troponin T and I
  • Correlates with RV dysfunction
  • Elevated in extensive PE (BAD sign)

EKG:

  • Sinus tachycardia
  • RV strain (right axis deviation, RBBB, S1Q3T3 pattern)
225
Q

Chest x-ray findings in PE

A
  • Atelectasis (subtle)
  • Pleural effusion (subtle)
  • Infiltrate (subtle)
  • May be normal
  • Hampton’s hump: peripheral, wedge shaped- implies infarction
  • Westermark’s sign: focal oligemia
  • Palla’s sign (knuckle sign): enlarged pulmonary artery with cutoff
  • Fleischner’s lines: linear discoid atelectasis (MORE COMMON SIGN)
226
Q

Doppler ultrasound of DVT

A 
TEST OF CHOICE
- Leg swelling, pain not always present
- 50-70% patients with PE have no DVT
- 1/3 patients with DVT have asymptomatic PE
Treatment: anticoagulation, IVC filter
227
Q

Echocardiography of PE

A

May diagnose central PE, intracardiac clot (PE in transit- moving through heart, not yet at lungs)

  • McConnell’s sign= RV motion abnormality sparing apex
  • RV abnormalities (hypokinesis, dilation)= worse prognosis
228
Q

Pulmonary angiography in PE

A 
GOLD STANDARD (almost completely replaced by CT angiography)
- Dye induced allergic reactions, contrast reactions (arrhythmia/renal failure)
229
Q

V/Q Scan in PE

A

Ventilation: radiolabeled xenon or Tcn
Perfusion scan: IV radiolabeled albumin

Most useful with normal chest x-ray

  • atelectasis/effusion makes interprestation difficult
  • Best used with high suspicion (pre-test probability)
230
Q

Well’s Criteria

A

Calculate clinical probability of DVT

  • Clinical symptoms of DVT
  • Other diagnosis less likely than PE
  • Heart rate > 100
  • Immobilization/surgery in previous 4 weeks
  • Previous DVT/PE
  • Hemoptysis
  • Malignancy
231
Q

CT angiography

A

TEST OF CHOICE FOR PE (replaced pulmonary angiography)

Advantages:

  • Readily available 24/7
  • High sensitivity for larger, central clots
  • May give alternate diagnosis
  • Venography can diagnose DVT

Disadvantages:

  • Can’t see small clots
  • Dye reactions (like pulmonary angiography)
232
Q

Treatment of PEs

A 
ABCs (airway, breathing, circulation)
Prevent recurrence of PEs:
- anticoagulation
- IVC filter
Rapidly remove clot:
- Thrombolysis
- Surgical embolectomy
233
Q

Anticoagulation therapy

A

unfractionated heparin: indirect thrombin inhibitor (accelerates activity of antithrombin III)
- Complications= osteoporosis, heparin induced thrombocytopenia

low molecular weight heparin: subQ injection, no lab monitoring needed,
- lower risk of heparin-induced thrombocytopenia

warfarin: oral drug for long-term therapy
- Vit K antagonist, binds and inhibitis II, VII, IX, X
- Contraindicated in pregnancy

Absolute contraindications to anticoagulation

  • Active bleeding
  • neoplasm
  • Uncontrolled bleeding
  • head trauma
  • CNS surgery within 2 months
  • Internal bleeding within 6 months

Relative contraindications:

  • Bleeding diathesis
  • Uncontrolled HTN
  • CPR
  • Non-hemorrhagic stroke within 2 months
  • Surgery within 10 days
  • Platelets < 100k

Duration:

  • First VTE with temp/reversible cause: 3-6 month
  • First VTE with no cause IDed: 6 months- indefinite
  • Irreversible cause or recurrent VTE: indefinite
234
Q

IVC filter

A

Placed via femoral/jugular approach
Indications:
- Contraindication to anti-coagulation
- Recurrent VTE despite adequate AC

Complication:

  • IVC laceration
  • Migration
  • Thrombosis

Many retrievable (after starting AC therapy)

235
Q

Thrombolytics

A

Tissue plasminogen activator (t-PA)
Rapid clot lysis
Indications:
- Refractory hypotension, hypoxemia (hemodynamic instability)
Risks: 2-3% risk of intraventricular hemorhage

236
Q

Surgical embolectomy

A

Rarely used
High mortality
Indications:
- Severe hypoxemia, hypotension with contraindication to thrombolytics

237
Q

Risk factors for increased morbidity/mortality in PE

A 
Hypotension/shock
Severe hypoxemia
RV dysfunction on echo
Elevated troponin
Elevated BNP
238
Q

Long-term complications of pulmonary embolism

A

Post-thrombotic syndrome:
- chronic leg swelling, pain
Chronic thromboembolic pulmonary HTN (CTEPH)
- 4% chronic PE
- Dyspnea, chest pain, fatique, syncope long after PE
- Echo evidence of pulmonary HTN
- Diagnosis: V/Q scan with multiple defects, angiography
- Treatment: surgical endarterectomy

239
Q

Prophylaxis for VTE (in-hospital

A
  • Mechanical: compression stockings, intermittent pneumatic compression boots, IVC filter
  • Pharmacologic: Sub-Q heparin, LMW heparin, Warfarin
  • Early ambulation
  • Limit use of femoral lines
240
Q

Asthma and pregnancy

A

Rule of 1/3:
1/3 gets better
1/3 gets worse
1/3 stays the same

  • remember: healthy mom, healthy child
241
Q

Scleroderma and PFTs

A

Dyspnea due to interstitial lung disease
See low FVC and FEV1= restrictive lung disease
Ratio normal

242
Q

Transudates

A
  • CHF
  • Cirrhosis (hepatic hydrothorax)
  • Nephrotic syndrome (low albumen–> proteinuria)
  • Atelctasis
  • Pulmonary embolism= Exudate/transudate
243
Q

Exudate

A 
Empyema
Malignancy
TB
Collagen vascular disease
Pancreatitis
Esophageal perforation
Chylothorax
Hemothorax
BAPE
244
Q

Anion gap

A

Normal= 12

Na- (Cl-+HCO3)

245
Q

Respiratory compensation

A

PaCO2 changes 10 mmHg for every 0.08 change in pH

GI/Pulm (7 decks)

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