PANCE Prep- Pulmonary Flashcards
What does a low V:Q ratio mean?
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)
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
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
An area with no ventilation but perfusion is termed a ___
Areas with no perfusion and normal ventilation is termed ___
shunt
dead space
How do diseases with a low V:Q ratio lead to RHF
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)
What is the only medical treatment to reduce mortality in COPD
oxygen
Describe the control of respiration
- 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
- 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
the volume in the lungs at the max inspiration
TLC (Vital capacity + Residual volume)
The volume of air remaining in the lungs after max expiration. It functions to maintain alveolar patency esp. during end expiration
Residual volume (RV)
the volume of air moved into or out of the lungs during quiet breathing
tidal volume (TV)
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
Expiratory reserve volume (ERV)
inspiratory reserve volume (IRV)
What is FRC and when do we see it increased or decreased?
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
What is FEV1 and FVC
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
maximum volume of air that can be exhaled following maximum inspiration
Vital capacity (VC) (IRV + TV + ERV)
Describe Wheezing and what it is commonly heard with
- 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
Describe rhonchi and what it is commonly heard with
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
Describe crackles and what it is commonly heard with
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
Describe stridor and what it is commonly heard with
- 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
What is asthma
REVERSIBLE hyperirritability of the tracheobronchial tree–> airway inflammation and bronchoconstriction
3 main components:
- airway hyperreactivity
- bronchoconstriction (decreased expiratory airflow and increased airway resistance)
- inflammation
Describe HX question to ask and PE findings you’d expect with asthma
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
Diagnostic studies for asthma
- PFTs (gold standard)
- bronchoprovacation (methacholine challenge test, bronchodilator test, exercise challenge test)
- Peak Expiratory Flow Rate (PEFR)- best and most objective way to assess asthma exacerbation severity and patient response in ED***
- Pulse Ox (O2<90% = resp. distress)
- ABG
- CXR to r/o other etiologies
What PFT findings would you expect in asthma
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%
Tx for acute asthma exacerbation
- Short acting B2 agonist (SABA)**: Albuterol (Proventil), Levalbuterol, Terbutaline (Brethine), Epinephrine
- Give MDI or neb q20min x 3 doses or continuous - Anticholinergics/ Antimuscarinics: Ipratroprium (Atrovent)
- Central bronchodilators - Corticosteroids (Prednisone, Methylprednisolone (Solumerdrol), Prednisolone (Prelone)
- anti-inflammatory-onset of action 4-8hrs
- DC w/ 3-5 day course
SE of SABAs
B1 cross reactivity:
- tachycardia/arrhythmias
- muscle tremors,
- CNS stimulation
- HYPOKalemia
SE of steroids
- immunosuppression
- catabolic
- hyperglycemia
- fluid retention
- osteoporosis
- growth delays
Give examples of:
- Inhaled corticosteroids
- Long acting B2 agonists
- Short acting B2 agonists
- Mast cell modifiers
- Leukotriene modifiers/receptor antagonists
- ICS/LABA combo
- ICS: Beclomethasone (Beclovent), Flunisolide (Aerobid), Triamcinolone (Azmacort)
- LABA: Salmeterol (Serevent), Formoterol
- Albuterol (Proventil), Levalbuterol (Xopenex), Terbutaline (Brethine), Epinephrine
- Cromolyn (Intal), Nedocromil (Tilade)
- Montelukast (Singulair), Zafirlukast (Accolate), Zileuton (Zyflo)
- Symbicort (Budenoside/Formoterol), Advair diskus (Fluticasone/Salmeterol)
Asthma drug of choice for long term, persistent (chronic maintenance)
inhaled corticosteroids
What are the indications for LABAs (long acting B2 agonists)
- if persistent asthma is not controlled with ICS alone
- Once asthma control maintained (>3months), step down off LABA
CI: not a rescue drug and should not be used alone
What medication is useful in asthmatics with allergic rhinitis/aspirin induced asthma?
Leukotriene modifiers/receptor antagonists (LTRA)
How does smoking affect Theophylline levels
smoking decreases Theophylline levels so a HIGHER dose is needed in smokers
Describe the classification of asthma severity
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
Describe the management of intermittent, mild, mod, and severe asthma
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
What is COPD
progressive, largely IRREVERSIBLE airway obstruction
2 components:
- loss of elastic recoil
- increased airway resistance
Compare the clinical manifestations and PE findings of emphysema vs chronic bronchitis
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”
Compare the ABS/Labs and V/Q mismatch of emphysema vs chronic bronchitis
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
Diagnostic studies for COPD
- PFTs- gold standard**
- CXR/CT: hyperinflated, flat diagphragm decreased vascular markings in emphysema
- increased AP diameter, and vascular markings in chronic bronchitis - EKG: cor pulmonale= longstanding PHTN esp. w// chronic bronchitis, MAT, and afib
Describe PFT findings for COPD
Obstruction: decreased FEV1 and FVC, Decreased FEV1/FVC <70%
Hyperinflation: increased lung volumes, incresaed RV, TLC, RV/TLC, increase FRC
