PANCE Prep- Pulmonary Flashcards

1
Q

What does a low V:Q ratio mean?

A

low ventilation with increased or normal perfusion ==> impaired gas exchange

*there is a physiologic low V:Q ratio at the base of lungs (due to gravity, the bases receive greater perfusion and more ventilation but perfusion exceeds ventilation still)

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2
Q

What are pathologic causes of low V:Q ratio and high V:Q ratio

What do you expect to see their pO2 and CO2 level

A

Low V:Q: (low ventilation, good perfusion) asthma, chronic bronchitis, acute pulmonary edema
*High CO2, low pO2

High V:Q: (Poor perfusion, good ventilation) emphysema, PE, FB
*High pO2, low CO2

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3
Q

An area with no ventilation but perfusion is termed a ___

Areas with no perfusion and normal ventilation is termed ___

A

shunt

dead space

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4
Q

How do diseases with a low V:Q ratio lead to RHF

A

the hypoxemic response to decreased paO2 is local hypoxic vasoconstriction ==> pulmonary HTN (if persistent)

then the right ventricle has to pump against higher pressures to pump into pulm. arteries= RVH and RAE, which eventually leads to RHF (cor pulmonale)

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5
Q

What is the only medical treatment to reduce mortality in COPD

A

oxygen

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6
Q

Describe the control of respiration

A
  • Ventilation is strictly regulated primarily by changes in PaCO2
  • Ventilation is controlled by:
    1. Central chemoreceptors in medulla (increased PaCO2 in CSF ((meaning decreased pH in serum)) stimulates medulla–> + phrenic nerve–> increased rate/depth of breathing to decrease PaCO2
  1. Peripheral chemoreceptors in carotid bodies and aortic bodies in arterial blood (increased PaCO2 ((decreased pH)) + afferent neurons affecting medulla–> + increased rate/depth of breathing
    And: significant decreased PaO2 (<60mmHg) stimulates medulla as well via peripheral chemoreceptors
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7
Q

the volume in the lungs at the max inspiration

A

TLC (Vital capacity + Residual volume)

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8
Q

The volume of air remaining in the lungs after max expiration. It functions to maintain alveolar patency esp. during end expiration

A

Residual volume (RV)

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9
Q

the volume of air moved into or out of the lungs during quiet breathing

A

tidal volume (TV)

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10
Q

the volume of air that can be further exhaled at the end of normal expiration

the volume of air that can be further inhaled at the end of normal inhalation

A

Expiratory reserve volume (ERV)

inspiratory reserve volume (IRV)

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11
Q

What is FRC and when do we see it increased or decreased?

A

FRC (Functional residual capacity): voume of gas in the lungs at normal tidal volume end expiration (ERV + RV). This is the air in which gas exchange takes place

Increased: disorders w/ hyperinflation (due to loss of elastic recoil, PEEP)

Decreased: restrictive lung disease

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12
Q

What is FEV1 and FVC

A

FEV1 (forced expiratory volume in 1 sec): the volume of air that has been exhaled at the end of the first second of forced expiration

FVC (forced vital capacity): measurement of the volume of air that can be expelled from a maximally inflated lung, with the patient breathing as hard and fast as possible

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13
Q

maximum volume of air that can be exhaled following maximum inspiration

A

Vital capacity (VC) (IRV + TV + ERV)

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14
Q

Describe Wheezing and what it is commonly heard with

A
  • HIGH-PITCHED, whistling, continuous musical sound (usually louder during expiration)
  • produced by narrowed/obstructed airways

Seen w/ obstructive disease: asthma, COPD, exercise induced bronchospasm, bronchiectasis, bronchiolitis, lung CA, OSA, CHF, GERD, anaphylaxis, FB

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15
Q

Describe rhonchi and what it is commonly heard with

A

continuous, rumbling (rattling), coarse, LOW-PITCHED (sounds like snoring)

  • may be cleared w. cough or suction
  • caused by increased secretions or obstruction in the bronchial airway

Seen w/ obstructive disease: asthma, COPD, exercise induced bronchospasm, bronchiectasis, bronchiolitis, lung CA, OSA, CHF, GERD, anaphylaxis, FB

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16
Q

Describe crackles and what it is commonly heard with

A

aka rales

  • discontinuous HIGH-PITCHED sounds heard during inspiration (usually not cleared by coughing)
  • due to popping open of collapsed alveoli and small airways from fluid, exudates, or lack of aeration

-seen w/ PNA, atelectasis, bronchitis, bronchiectasis, pulmonary edema, pulmonary fibrosis

17
Q

Describe stridor and what it is commonly heard with

A
  • monophonic sound usually loudest over the anterior neck
  • due to narrowing of the larynx or anywhere over the trachea
  • can be heard in inspiration, expiration or throughout cycle

-seen w/ croup, FB, pertussis, epiglottitis

18
Q

What is asthma

A

REVERSIBLE hyperirritability of the tracheobronchial tree–> airway inflammation and bronchoconstriction

3 main components:

  1. airway hyperreactivity
  2. bronchoconstriction (decreased expiratory airflow and increased airway resistance)
  3. inflammation
19
Q

Describe HX question to ask and PE findings you’d expect with asthma

A

HX: dyspnea, wheezing, cough (esp. at night), triggers, recent steroid use/hospitalization

PE:
1. Prolonged expiration w/ wheezing or decreased breath sounds
2. hyperresonance to percussion
3. tachypnea, tachycardia, use of accessory muscles
Severe: AMS, pulsus paradoxus, silent chest

20
Q

Diagnostic studies for asthma

A
  1. PFTs (gold standard)
  2. bronchoprovacation (methacholine challenge test, bronchodilator test, exercise challenge test)
  3. Peak Expiratory Flow Rate (PEFR)- best and most objective way to assess asthma exacerbation severity and patient response in ED***
  4. Pulse Ox (O2<90% = resp. distress)
  5. ABG
  6. CXR to r/o other etiologies
21
Q

What PFT findings would you expect in asthma

A

Decreased FEV1 and decreased FEV1/FVC (reversible obstruction)

Intermittent: nl FEV1, FEV1 >80% predicted, FEV1/FVC nl

Mild persistent: FEV1>/= 80% predicted, FEV1/FVC nl

Mod. persistent: FEV1 60-80% predicted**, FEV1/FVC reduced by 5%

Severe persistent: FEV1<60%, FEV1/FVC reduced >5%

22
Q

Tx for acute asthma exacerbation

A
  1. Short acting B2 agonist (SABA)**: Albuterol (Proventil), Levalbuterol, Terbutaline (Brethine), Epinephrine
    - Give MDI or neb q20min x 3 doses or continuous
  2. Anticholinergics/ Antimuscarinics: Ipratroprium (Atrovent)
    - Central bronchodilators
  3. Corticosteroids (Prednisone, Methylprednisolone (Solumerdrol), Prednisolone (Prelone)
    - anti-inflammatory-onset of action 4-8hrs
    - DC w/ 3-5 day course
23
Q

SE of SABAs

A

B1 cross reactivity:

  1. tachycardia/arrhythmias
  2. muscle tremors,
  3. CNS stimulation
  4. HYPOKalemia
24
Q

SE of steroids

A
  1. immunosuppression
  2. catabolic
  3. hyperglycemia
  4. fluid retention
  5. osteoporosis
  6. growth delays
25
Q

Give examples of:

  1. Inhaled corticosteroids
  2. Long acting B2 agonists
  3. Short acting B2 agonists
  4. Mast cell modifiers
  5. Leukotriene modifiers/receptor antagonists
  6. ICS/LABA combo
A
  1. ICS: Beclomethasone (Beclovent), Flunisolide (Aerobid), Triamcinolone (Azmacort)
  2. LABA: Salmeterol (Serevent), Formoterol
  3. Albuterol (Proventil), Levalbuterol (Xopenex), Terbutaline (Brethine), Epinephrine
  4. Cromolyn (Intal), Nedocromil (Tilade)
  5. Montelukast (Singulair), Zafirlukast (Accolate), Zileuton (Zyflo)
  6. Symbicort (Budenoside/Formoterol), Advair diskus (Fluticasone/Salmeterol)
26
Q

Asthma drug of choice for long term, persistent (chronic maintenance)

A

inhaled corticosteroids

27
Q

What are the indications for LABAs (long acting B2 agonists)

A
  1. if persistent asthma is not controlled with ICS alone
  2. Once asthma control maintained (>3months), step down off LABA

CI: not a rescue drug and should not be used alone

28
Q

What medication is useful in asthmatics with allergic rhinitis/aspirin induced asthma?

A

Leukotriene modifiers/receptor antagonists (LTRA)

29
Q

How does smoking affect Theophylline levels

A

smoking decreases Theophylline levels so a HIGHER dose is needed in smokers

30
Q

Describe the classification of asthma severity

A

Intermittent: Sx and SABA use: 2x or less a week and PM sx 2 or less a month, no interference w/ normal activity

Mild persistent: Sx +2/week, SABA 2+d/week, PM 3-4 month, minor limitation

Mod. persistent: daily sx and SABA use, PM >1+/week but not nightly, some limitation

Severe persistent: Sx and SABA throughout day, PM nightly, extreme limitation

31
Q

Describe the management of intermittent, mild, mod, and severe asthma

A

Intermittent: SABA PRN

Mild persistent: SABA PRN + LD ICS

Mod persistent: SABA PRN + LD ICS + LABA or SABA + MD ICS

Severe persistent: SABA PRN + HD ICS + LABA +/- Omalizumab (anti-IgE drug)

*Step down if sx controlled >3months

32
Q

What is COPD

A

progressive, largely IRREVERSIBLE airway obstruction

2 components:

  1. loss of elastic recoil
  2. increased airway resistance
33
Q

Compare the clinical manifestations and PE findings of emphysema vs chronic bronchitis

A

Emphysema: dyspnea MC sx**, prolonged expiration, accessory muscle use
PE: HYPERinflation, HYPERresonance to percussion, decreased freitus, decreased/absent breath sounds, barrel chest, pursed lips
“cacectic, pursed lips- pink puffers”

Chronic bronchitis: productive cough** 3+ months for 2 consecutive years, prolonged expiration
PE: rales/crackles, rhonchi, wheezing, signs of cor pulmonale (peripheral edema, cyanosis)
“obese and cyanotic- blue bloaters”

34
Q

Compare the ABS/Labs and V/Q mismatch of emphysema vs chronic bronchitis

A

Emphysema: resp. alkalosis (can develop resp. acidosis in acute exacerbations),
-matched VQ defects, mild hypoxemia, often CO2 is normal

Chronic bronchitis: resp. acidosis**, increased Hct/RBC (chronic hypoxia stimulates erythropoiesis)
-severe VQ mismatch*, severe hypoxemia, hypercapnia

35
Q

Diagnostic studies for COPD

A
  1. PFTs- gold standard**
  2. CXR/CT: hyperinflated, flat diagphragm decreased vascular markings in emphysema
    - increased AP diameter, and vascular markings in chronic bronchitis
  3. EKG: cor pulmonale= longstanding PHTN esp. w// chronic bronchitis, MAT, and afib
36
Q

Describe PFT findings for COPD

A

Obstruction: decreased FEV1 and FVC, Decreased FEV1/FVC <70%

Hyperinflation: increased lung volumes, incresaed RV, TLC, RV/TLC, increase FRC