HCP 7: Bob Coffman Chronic Bronchitis + Pneumonia Flashcards
Mechanism of Cough Reflex
Innate mechanism that helps remove mucus, noxious substances, & bacteria from larynx, trachea & large bronchi
Stimulation of Rapidly Acting Receptors (RARs)
Afferent signal thru vagal fibers
Nucleus tractus solitarius “Cough center”
Motor output to respiratory muscles (diaphragm, intercostals, abs, laryngeal muscles)
Inspiratory phase: deep inspiration
Compressive: expiratory muscles contract; strong expiration against closed glottis
Expulsive: open glottis & expulsive flow of air
Recovery: restorative inspiration
DDX of Cough
- COPD (Smoking, productive cough, barrel chest, wheeze, cyanosis)
- Pneumonia (COPD, alcoholism, crackles, consolidation on CXR)
- Influenza (Fever, myalgia, winter, elderly, close quarters)
- TB (Contact, immunosuppression, fatigue, weight loss, +PPD)
- Asthma (Atopy, chest tightness)
- Cystic Fibrosis (Ashkenazi Jew, salty sweat, pancreatic insufficiency)
- Pulmonary Embolism (immobilization, pleuritic chest pain, hemoptysis)
- CHF (MI, CAD, valve disease, S3/S4)
Explain why someone who has chronic bronchitis would also have heart problems
Smoking -> ROS -> Inflammation.
Triggers bronchiole SMC hypertrophy (causing hyperresponsiveness), fibroblast migration, & goblet cell hyperplasia (increase mucus production). The smoke itself destroys cilia so that it is unable to clear the mucus. All these factors cause airway occlusion, increasing the blood/air barrier-according to Fick’s law of diffusion, increased thickness inversely related to rate of diffusion. Hypercapnia & HYPOXEMIA. 1. Erythropoiesis->polycythemia->viscosity.
2. Hypoxic vasoconstriction.
3. Destruction of pulmonary vasculature.
All cause pulmonary HTN -> Loud P2, RVH, RAA, sternal lift, JVD.
Explain how someone with chronic bronchitis might faint if you give them 100% O2
Chronic bronchitis patients are used to hypercapnia due to thickened blood/air barrier, causing blunted response of central (& peripheral to lesser extent) over time. O2 becomes main driving force for breathing. O2 mainly detected by peripheral chemoreceptors (only when below 60), and he’s chronically hypoxic.
Giving him O2 would cause his PO2 to be >60, taking away his drive to breathe. He would stop breathing, CO2 would accumulate. There’s also the Haldane effect (Increased oxyHb, decrease affinity for CO2, increase dissolved CO2) & loss of hypoxic vasoconstriction (increase perfusion to less-ventilated areas & vice versa) that also cause CO2 to accumulate.
What is chronic bronchitis?
COPD characterized by airflow limitation & NOT fully reversible
“Presence of productive cough for >3mo. during at least 2 consecutive years”
What are some risk factors for chronic bronchitis?
Smoking, male, alpha-1 anti-trypsin deficiency, history of chronic pulmonary infections
How would you diagnose chronic bronchitis?
Spirometry (Decreased FEV1 <0.70)
CXR: Flattened diaphragm, hyperinflation, air trapping, rapid tapering of pulmonary vasculature
ABG: V/Q mismatch (hypoxia, hypercapnia)
How do you treat chronic bronchitis?
Lifestyles changes (smoking cessation) Bronchodilators (Ipratropium, albuterol, salmeterol) Corticosteroids Pulmonary rehab O2 therapy Lung transplant
Why shouldn’t we give barbiturates, opioids, benzodiazepines, or general anesthetics to patients with chronic bronchitis?
The main MOA is to make medullary respiratory center less responsive to increases in PaCO2 and suppress respiration. This would allow even more CO2 build up, causing CO2 narcosis.
What is the MOA for erythromycin?
When would you use it?
How do bacteria become resistant?
Macrolide, allergy to penicillin, CAP
Irreversibly binds to 50S subunit of ribosomal DNA
Inhibit translocation of tRNA
Inhibit protein synthesis
Bacteriostatic effects (bacteriocidal if higher dose)
Resistance if methylate 50S (drug not able to bind)
What is the effect of alcohol on pulmonary disease?
Clearly linked to prevalence & mortality due to pneumonia
Increased risk for ARDS
Increases inflammation & impairs immune response
-alter oropharyngeal flora & esophageal motility
-Blunted cough/gag reflex
-Decrease mucociliary clearance
-Impaired innate immunity in alveolar space (macrophage, chemokines, chemotaxis)
-Dehydrates epithelial lining fluid
Describe Physiology of gas exchange & O2 delivery
Fick’s law of diffusion: Volume of gas =Area x Diffusivity x Pressure difference / thickness
O2 carried by Hb (positive cooperativity)
Release of O2 if increased CO2, decrease pH, increase temp, or increase 2, 3 BPG
What is the purpose of O2 therapy and what are the delivery methods?
Relive hypoxemia & work of breathing
Increases O2 diffusion gradient across alveolar-capillary membrane
Low flow systems (nasal cannula) - FiO2 max 20-40%
High flow (Venturi mask) - FiO2 max 50%
What would you expect to see in the LFTs of an alcoholic?
AST:ALT is 2:1 or greater, esp. elevated GGT
AST not specific, ALT more specific
GGT elevated in patients with chronic viral hepatitis or alcoholic liver disease
Describe what the A-a gradient is and its clinical significance.
Measure of difference in partial pressure between alveoli (A) and arterial (a) blood. Normally 0-10 (highly efficient) & increases after 30. BUT >25mmHg implies pulmonary disease that causes impaired diffusion of alveolar across pulmonary membrane
