Diseased and Failing Lung Flashcards
What is bronchoconstriction mediated by?
1: PNS & immune response (IgE)
2: Mast cells
•Histamine
•Prostaglandin D2 and F2
•Leukotrienes C4, E4, and D4
•Platelet activating factor•Bradykinin
3: Non-cholinergic c-fibers
•Substance P
•Neurokinin A
•Calcitonin
What is the process of bronchoconstriction?
Vagas nerve (X) innervates smooth muscle → cholinergic nerve endings release AcH to muscarinic receptors → G protein coupling → IP3 (2nd messenger) → stimulates iCa from sarcoplasmic reticulum → increased calcium activates myosin light chain kinase
What is bronchodilation mediated by?
–Mediated by circulating catecholamines and NO
Three mechanisms of airway obstruction:
- partial occulusion
- wall thickening
- outside of airway disease
CHRONIC OBSTRUCTIVE AIRWAY DISEASE (COPD) - diseases
- Chronic bronchitis
- Emphysema
- Cystic fibrosis
- Asthma
- Bronchiectasis = Repeated infection/inflammation - - Permanent dilation of bronchi/oles destroying muscle elastin supporting tissue
Types of Chronic Obstructive Pulmonary Disease
- Centriacinar: destruction confined to the terminal and respiratory bronchioles
- Panacinar: the terminal and respiratory bronchioles & peripheral alveoli are involved
Two types of Pulmonary Emphysema
Type A and Type B
CHARACTERISTICS OF TYPE A PULMONARY EMPHYSEMA
“PINK PUFFER”
•Smoking history
•Age of onset: 40 – 50 years
•Often dramatic barrel chest
•Weight loss
•Decreased breath sounds
•Normal blood gases until late in disease process
•Cor pulmonale only in advanced cases
•Slowly debilitating disease
CHARACTERISTICS OF
TYPE B CHRONIC BRONCHITIS
“BLUE BLOATER”
•Smoking history
•Age of onset 30–40 years
•+/- Barrel chest may be p
•Shortness of breath predominant early s/s
•Sputum frequent early manifestation
•Rhonchi often present
•Often dramatic cyanosis
•Hypercapnia and hypoxemia may be present
•Frequent Cor pulmonale (RIGHT CHF) and polycythemia
•Numerous life-threatening episodes due to acute exacerbations
Changes w/ COPD
- Reductions of FEV1, FVC, and the ratio of FEV1/FVC are the hallmark of airflow limitation
- Flow-volume loops show a concave pattern in the expiratory tracing
CXR: flat diaphragm, lungs are hyperinflated d/t air trapping, heart size increased
COPD Overview
Causes: tobacco and air pollution → continual bronchial irritation and inflammation → chronic bronchitis: bronchial edema, productive cough, bronchospasm
OR → alpha-1 antitrypsin deficiency → breakdown of elastin in connective tissue of lungs → emphysema: destruction of alveolar walls, lung fibrosis, and air trapping
→ airway obstruction/air trapping, dyspnea, frequent infections → abnormal V/Q, hypoxemia and hypoventilation
Cystic Fibrosis
Mutation of CFTR gene = cystic fibrosis transmembrane conduction receptor regulator
- regulates sweat, digestive juices, and mucous → lung congestion and infection, + malabsorption of nutrients by the pancreas
Cystic Fibrosis Changes
- ABG – hypoxemia
- FVC decreased
- FEV1 decreased
- FEV1/FVC decreased
- FEF25-75 decreased
- RV - INCREASED
- RV/TLC - INCREASED
Asthma Characteristics
- Airway Hyperreactivity:
•Various noxious stimuli: cold air, allergens, chemicals, exercise, drugs (aspirin, NSAIDs, sulfites), instrumentation of the airway
•Bronchial smooth muscle constricts in response to irritants
•Asymptomatic asthmatic patients also possess airway hyperreactivity - Airway Wall Inflammation:
•Presence of mucus, edema and inflammatory cells leads to reduction of airway size or obstruction of the airway. - Reversible Expiratory Airflow:
•Bronchodilator therapy can cause a 15% or greater increase in airflow
Asthma Process diagragm
Asthma Attack w/ Spirometry
Residual volume = NORMAL
RV, ERV, IRV air trapping = ?
Asthma PFTs
–FEV1: direct reflection of the severity of expiratory airflow obstruction
•Little or no sx with FEV1 > 50%
–FEF 25-75%: also measures severity of expiratory airflow obstruction
–FRC increases by 1-2L as expiratory obstruction retains air in lungs, but overall lung capacity remains within normal limits
Asthma Flow Volume Loops
–Expiratory loop is smaller
–with a “scooped-out” appearance
Asthma: Diffusing Capacity & Blood Gases
•Diffusing Capacity–Not decreased in asthmatics
•Blood Gases
–PaO2: normal in mild to moderate asthma
•Decreases with marked asthma and severe asthma (i.e. status asthmatics)
–PaCO2: normal in mild asthma
•Increases slightly in moderate asthma and more substantially in marked and severe asthma
Interventions for intraop bronchospasm
- 100% O2
- Deepen anesthetic (volatile agent or propofol)
- Ketamine
- Lidocaine
- Short acting inhaled Beta-2 agonist (albuterol)
- Inhaled ipratropium (atrovent)
- Epinephrine 1 mcg/kg
- Hydrocortisone 2-4 mg/kg•(not acute symptoms)
- Aminophylline
- Heliox
Bronchospasm vs. Laryngospasm
If you have secured your airway, then have a sudden loss of TV, its likely bronchospasm. don’t automatically assume it is laryngospasm and do NOT remove your airway. try all other interventions before adjusting the airway
Mechanical Ventilation Targets
- Respiratory rate 7-8 breaths per minute
- Slow inspiratory flow helps gas redistribute from high compliance areas to those with longer time constants –Maximizes V/Q matching
- FiO2 adjusted to prevent hypoxemia•Smaller Vt (6 – 8 mL/kg)
- PEEP maintains patency in alveoli: 2-5 normal
- Increased expiratory times to minimize air trapping
Different Restrictive Lung Diseases
•Lung Parenchyma
–Pulmonary Fibrosis
–Sarcoidosis
–Pneumonitis
•Pleura
–Pneumothorax
–Pleural Effusion
•Chest Wall
–Scoliosis
–Ankylosing Spondylitis
- Neuromuscular Disorders
- *Obesity
Restrictive Lung Disease Characteristics
–VC = decreased
–Resting lung volume = decreased
–Normal Airway Resistance