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
