Steve Stone Cold Austin's Stone Cold Respiratory Facts Flashcards
Conducting zone
large airways consist of nose, pharynx, larynx, trachea, and bronchi;
small airways consist of bronchioles and terminal bronchioles (large numbers in parallel leading to least airway resistance);
Warms, humidifies, and filters air but does not participate in gas exchange leading to anatomic dead space;
Cartilage and goblet cells extend to end of bronchi;
pseudostratified ciliated columnar cells (beat mucus up and out of lung) extend to beginning of terminal bronchioles, then transition to cuboidal cells;
airway smooth muscles extend to end of terminal bronchioles (sparse beyond this point)
Respiratory zone
Lung parenchyma;
consists of respiratory bronchioles, alveolar ducts, and alveoli;
participates in gas exchange;
mostly cuboidal cells in respiratory bronchioles, then simple squamous cells up to alveoli;
no cilia;
alveolar macrophages clear debris and participate in immune respone
type I pneumocyte
97% of alveolar surface;
line the alveoli;
squamous;
thin for optimal gas diffusion
Type II pneumocyte
secrete pulmonary surfactant causing decreased alveolar surface tension and prevention of alveolar collapse (atelectasis);
cuboidal and clustered;
also serve as precursors to type I cells and other type II cells;
Type II cells proliferate during lung damage
Club or Clara cells
Nonciliated; low-columnar/cuboidal with secretory granules; secrete component of surfactant; degrade toxins; act as reserve cell
Collapsing pressure equation
Collapsing pressure= 2(surface tension)/radius;
alveoli have the tendency to collapse during expiration as radius decreases (law of Laplace);
Surfactant
from type II pneumocytes;
mix of lecithins, the most important one being dipalmitoylphosphatidylcholine;
surfactant synthesis begins around week 26 of gestation, but mature levels not reached until week 35;
Lecithin to sphingomyelin ratio of >2 in amniotic fluid indicates fetal lung maturity
Aspirate a peanut, where will it go when you are standing and laying down
upright- lower portion of right inferior lobe;
supine- superior portion of right inferior lobe
Structures that perforate the diaphragm that are important
at T8= IVC;
at T10= esophagus, CN X;
at T12= aorta, thoracic duct, azygos vein (12 is red, white, and blue);
innervation of diaphragm
C3, 4, 5, innervate (phrenic);
pain from diaphragm can be referred to shoulder (C5), and the trapezius ridge (C3, 4)
determination of physiologic dead space
Vd= Vt x (PaCO2-PeCO2)/PaCO2
minute ventilation (Ve)
total amount of air entering the lung in one minute;
Ve=Vt x respiratory rate
Alveolar ventilation (Va)
Volume of gas per unit time that reaches the alveoli;
Va= (Vt-Vd) x RR
hemoglobin
2 alpha, 2 beta subunits;
T (Taut) form has low O2 affinity (unloads O2);
R (Relaxed) form has high O2 affinity (loads O2);
Fetal Hb has 2 alpha, 2 gamma with lower affinity for 2,3 BPG leading to increased O2 affinity
Methemoglobin
Oxidized form of Hb (ferric, Fe3+) that does not bind O2 as readily, but has increased affinity for cyanide;
iron in hemoglobin should be ferrous, Fe2+, or reduced state;
may present with cyanosis and chocolate-colored blood;
treat this with METHylene blue
how do you treat cyanide poisoning
give nitrites to turn Fe2+ into ferric Fe3+ because methemoglobin bind cyanide more readily;
give thiosulfate to bind this new cyanide forming thiocyanate, which is renally excreted;
Carboxyhemoglobin
form of Hb bound to CO in place of O2;
causes decreased Oxygen binding capacity with a left shift in the oxygen hemoglobin dissociation curve;
decreased O2 unloading in tissue;
Oxygen hemoglobin dissociation curve: what shifts it to the right
Right shift is a decrease in Hb’s affinity for O2 so we get unloading of O2;
Right shift is BAT ACE;
2,3 BPG, Altitude increase, Temperature increase, Acidic, CO2, Exercise;
how to calculate O2 content in blood
O2 content= (O2 binding capacity x % saturation) + dissolved O2
What are profusion limited gases
O2 in a healthy person, CO2, and N2O;
gas equilibrates early along the length of the capillary;
diffusion can be increased only if blood flow increases
What are diffusion limited gases
O2 in a emphysema or fibrosis patient), CO;
gas does not equilibrate by the time blood reaches the end of the capillary;
Equation for pulmonary vascular resistance
PVR= (Ppulm artery- Pleft atrium)/ cardiac output;
Pleft atrium= pulmonary wedge pressure
Alveolar gas equation
PAo2= PIo2 - (Paco2)/R; usually that means PAo2= 150- Paco2/0.8; PAo2= alveolar Po2; PIo2= Po2 in inspired air; Paco2= arterial Pco2; R= respiratory quotient= CO2 produced/O2 consumed; normal A-a gradient= 10-15; increased A-a gradient could mean hypoxia, causes include shunting, V/Q mismatch, fibrosis
hypoxemia
decreased Pao2;
With a normal A-a gradient look for high altitude or hypoventilation;
with an increased A-a gradient look for V/Q mismatch, diffusion limitation, R to L shunt
Hypoxia
decreased O2 delivery to tissue;
causes can be decreased cardiac output, hypoxemia, anemia, CO poisoning
Ischemia
loss of blood flow;
impeded arterial flow or decreased venous drainage
V/Q mismatch
V= ventilation (how much gas getting there);
Q= perfusion (how much blood is getting there);
base of lung= 0.6 (wasting perfusion);
apex of lung= 3 (wasting ventilation);
V/Q= 0 means airway obstruction;
V/Q= infinity means blood flow obstruction
Remember that V and Q are both highest at the base, but Q is just much higher at the base;
CO2 transport
3 forms: 1) HCO3- (90%), 2) carbaminohemoglobin or HbCO2 (5%) CO2 is bound to N-terminus of globin not the heme and favors taut Hb form, 3) Dissolved CO2 (5%)
When CO2 in a RBC is turned into HCO3- and is transported out of the RBC, what comes into the cell
HCO3- is pumped out while Cl- is pumped in
Bodies response to high altitude
decrease in atmospheric oxygen leads to decreased Pao2 causing increased ventilation and decreased Paco2;
get a chronic increase in ventilation;
increased EPO causing increased hematocrit and Hb;
increased 2,3BPG (increasing release of O2 from Hb);
increased mitochondria in cells;
Increased renal bicarb excretion to compensate for respiratory alkalosis (give acetazolamide if you need to stop this);
Chronic hypoxic pulmonary vasoconstriction can cause RVH;
Response to exercise
Increased CO2 production;
increased O2 consumption;
increased ventilation rate to meet O2 demand;
V/Q ratio from apex to base becomes more uniform;
increased pulmonary blood flow due to increased cardiac output;
decreased pH during strenuous exercise (secondary to lactic acidosis);
no change in Pao2 and Paco2, but increase in venous CO2 content and decrease in venous O2 content
Rhinosinusitis
obstruction of the sinus drainage into nasal cavity leading to inflammation and pain over affected area;
typically maxillary sinus in adults;
most common acute cause is viral URI;
may cause superimposed bacterial infection, most commonly S. pneumoniae, H. influenzae, and M. catarrhalis
Deep venous thrombosis
predisposed by Virchow triad (1. stasis 2. hyper-coagulability (e.g. factor V leiden) 3. endothelial damage (exposed collagen activates clotting cascade);
About 95% of PEs come from deep leg veins;
Homan sign- dorsiflexion of foot leading to calf pain;
Use heparin for prevention and acute management;
use warfarin for long-term prevention of DVT recurrence
Pulmonary emboli
V/Q mismatch leading to hypoxemia causing respiratory alkalosis;
sudden onset dyspnea, chest pain, tachypnea;
Types are: Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor (FAT BAT);
If Fat you see long bone fractures or liposuction (also get triad of hypoxemia, neuro abnormalities, and petechial rash);
Amniotic fluid emboli can lead to DIC especially postpartum;
Gas emboli- nitrogen bubbles precipitate in ascending divers, treat with hyperbaric oxygen
Obstructive lung diseases
obstruction of air flow resulting in trapping air in the lungs;
airways close prematurely at high lung volumes;
increased RV and decreased FVC;
PFTs- greatly decreased FEV1, and decreased FVC causing a decreased FEV1/FVC ratio (hallmark), V/Q mismatch;
chronic, hypoxic pulmonary vasoconstriction can lead to cor pulmonale;
Chronic Bronchitis, Emphysema, Asthma, Bronchiectasis
Chronic bronchitis
blue bloaters;
a form of COPD along with emphysema;
hyperplasia of mucus secreting glands in the bronchi (Reid index > 50%;
productive cough > 3 months per year for >2 years;
disease of small airways;
findings: wheezing, crackles, cyanosis (early-onset hypoxemia due to shunting), late-onset dyspnea, CO2 retention
Emphysema
pink puffer w/ barrel chest;
enlargement of airway spaces, decreased recoil, increased compliance, decreased DLCO resulting from destruction of alveolar walls;
two types- centriacinar (associated with smoking), Panacinar (associated with alpha 1 antitrypsin deficiency);
increased elastase activity leads to loss of elastic fibers and increased lung compliance;
exhalation through pursed lips to increase airway pressure and prevent airway collapse during respiration
Asthma
Bronchial hyperresponsiveness causes reversible bronchoconstriction smooth muscle hypertrophy, Curschmann spirals (shed epithelium form mucus plugs), and Charcot-Leyden crystals (formed from breakdwon of eosinophils in sputum);
Can be triggered by URIs, allergens, and stress;
test with methacholine challange;
find- wheezing, cough, tachypnea, dyspnea, hypoxemia, decreased I/E ratio, pulsus paradoxus, mucus plugging
Bronchiectasis
Chronic necrotizing infection of bronchi leading to permanently dilated airways, purulent sputum, recurrent infections, hemoptysis;
associated with bronchial obstruction, poor ciliary motility (smoking), Kartagener syndrome, cystic fibrosis, allergic bronchopulmonary aspergillosis
Finds in restrictive lung disease
Causes decreased lung volumes (decreased FVC and TLC);
PFTs show FEV1/FVC ration > 80%
Types of restrictive lung disease caused by poor breathing mechanics
see normal A-a gradient;
Poor muscular effort (polio, myasthenia gravis);
Poor structural apparatus (scoliosis, morbid obesity)
Types of restrictive lung disease caused by interstitial lung diseases
Pulmonary decrease diffusing capacity, increased A-a gradient;
ARDS, neonatal respiratory distress syndrome (hyaline membrane disease), pneumoconioses (anthrax, silicosis, asbestosis), sarcoidosis (increased ACE and Ca), idiopathic pulmonary fibrosis (repeated cycles of lung injury and healing leading to increased collagen deposition), Goodpasture, Granulomatosis with polyangitiis, Langerhans cell histiocytosis, hypersensitivity pneumonitis, drug toxicity (bleomycin, busulfan, amiodarone, methotrexate)
Hypersensitivity pneumonitis
Mixed type III/IV hypersensitivity reaction to environmental antigen leading to dyspnea, cough, chest tightness, headache;
often seen in farmers and those exposed to birds
Asbestosis
Associated with shipbuilding, roofing, and plumbing;
ivory white, calcified pleural plaques are pathognomonic of asbestos exposure, but are not precancerous;
associated with an increase incidence of bronchogenic carcinoma and mesothelioma;
affects lower lobes, asbestos (ferruginous) bodies are golden-brown fusiform rods resembling dumbbells;
Coal workers’ pneumoconiosis
Prolonged coal dust exposure leads to macrophages laden with carbon causing inflammation and fibrosis;
also known as black lung disease;
affects upper lobes;
anthracosis- asymptomatic condition found in many urban dwellers exposed to sooty air
Silicosis
associated with foundries, sandblasting, and mines;
macrophages respond to silica and release fibrogenic factors, leading to fibrosis;
it is thought that silica may disrupt phagolysosomes and impair macrophages, increasing susceptibility to TB;
also increases risk of bronchogenic carcinoma;
affects upper lobes;
eggshell calcification of hilar lymph nodes
Neonatal respiratory distress syndrome
surfactant causes increased surface tension leading to alveolar collapse;
A lecithin:sphingomyelin ratio
Acute respiratory distress syndrome
Neutrophil mediated;
May be caused by trauma, sepsis, shock, gastric aspiration, uremia, acute pancreatitis, or amniotic fluid embolism;
diffuse alveolar damage causes increased alveolar capillary permeability leading to protein-rich leakage into alveoli and noncardiogenic pulmonary edema (normal PCWP);
results in formation of intra-alveolar hyaline membrane;
initial damage due to release of neutrophilic substances toxic to alveolar wall, activation of coagulation cascade, and oxygen-derived free radicals
Pulmonary HTN
Normal pulmonary artery pressure= 10-14 mmHg;
pulmonary HTN >25 mmHg at rest;
results in arteriosclerosis, medial hypertrophy, and intimal fibrosis of pulmonary arteries;
Couse: severe respiratory distress causes cyanosis and RVH leading to death from decompensated cor pulmonale
primary pulmonary HTN
due to an inactivating mutation in the BMPR2 gene (normally functions to inhibit vascular smooth muscle proliferation);
poor prognosis
secondary pulmonary HTN
due to COPD (destruction of lung parenchyma); mitral stenosis (increased resistance causing increased pressure); recurrent thromboemboli (decreased cross-sectional area of pulmonary vascular bed); autoimmune disease (e.g. systemic sclerosis, inflammation leading to intimal fibrosis causing medial hypertrophy); left-to-right (increased shear stress causing endothelial injury); sleep apnea or living at high altitude (hypoxic vasoconstriction)
sleep apnea
repeated cessation of breathing > 10 seconds during sleep causing disrupted sleep leading to daytime somnolence;
normal PaO2 during the day;
nocturnal hypoxia leading to systemic/pulmonary HTN, arrhythmias (atrial fibrillation/flutter), and sudden death;
Central sleep apnea-no respiratory effort;
Obstructive sleep apnea- respiratory effort against airway obstruction, associated with obesity, loud snoring;
Treat: weight loss, CPAP, surgery;
hypoxia leads to increased EPO causing increased erythropoiesis
Obesity hypoventilation syndrome
obesity (BMI >30) causing hypoventilation leading to decreased PaO2 and increased PaCO2 during waking hours
Lung findings on physical exam: pleural effusion
breath sounds- decreased
Percussion- dull
Fremitus- decreased
Tracheal Deviation- none
Lung findings on physical exam: atelectasis
(bronchial obstruction) breath sounds- decreased Percussion- dull Fremitus- decreased Tracheal Deviation- toward side of lesion
Lung findings on physical exam: Spontaneous pneumothorax
breath sounds- decreased
Percussion- Hyperresonant
Fremitus- decreased
Tracheal Deviation- none
Lung findings on physical exam: Tension pneumothorax
breath sounds- decreased
Percussion- Hyperresonat
Fremitus- decreased
Tracheal Deviation- away from lesion
Lung findings on physical exam: Consolidation (lobar pneumonia, pulmonary edema)
breath sounds- bronchial breath sounds, late inspiratory crackles
Percussion- dull
Fremitus- increased
Tracheal Deviation- none
Common sites for lung cancer to metastasize to
adrenals, brain, bone (pathologic fracture), liver (jaundice, hepatomegaly)
Complications of Lung Cancer
SPHERE;
Superior vena cava syndrome, Pancoast tumor, Horner syndrome, Endocrine (paraneoplastic), Recurrent laryngeal symptoms (hoarseness), Effusions (pleural or pericardial)
Adneocarcinoma
Peripheral;
most common lung cancer in nonsmokers and overal;
activating mutations include k-ras, EGFR, and ALK;
associated with hypertrophic osteoarthropathy (clubbing);
bronchioloalveolar subtype (adenocarcinoma in situ), grows along alveolar septa leading to apparent thickening of alveolar walls;
Squamous cell carcinoma
Central;
Hilar mass arising from bronchus;
Cavitation, Cigarettes, hyperCalcemia (produces PTHrP);
Keratin pearls and intercellular bridges;
Large cell carcinoma
Peripheral; highly anaplastic undifferentiated tumor; poor prognosis; less responsive to chemo; removed surgically; Pleomorphic giant cells
Bronchial carcinoid tumor
Excellent prognosis; metastasis rare; symptoms usually due to mass effect; occasionally carcinoid syndrome (5-HT secretion causing diarrhea, flushing, wheezing); nests of neuroendocrine cells; Chromogranin A +
Mesothelioma
Malignancy of the pleura associated with asbestosis;
results in hemorrhagic pleural effusions and pleural thickening;
Psammoma bodies seen on histology
Pancoast tumor
Carcinoma that occurs in apex of lung may affect cervical sympathetic plexus, causing Horner syndrome, SVC syndrome, Sensorimotor deficits and hoarseness
Superior vena cava syndrome
An obstruction of the SVC that impairs blood drainage from head, neck, and upper extremities;
commonly caused by malignancy and thrombosis from indwelling catheters;
medical emergency;
can raise intracranial pressure (if obstruction is severe) causing headaches, dizziness, and increased risk of aneurysm/rupture of intracranial arteries
Lobar Pneumonia
S. pneumoniae, Legionella, Klebsiella;
intra-alveolar exudate leading to consolidation;
may involve entire lung
Bronchopneumonia
S. pneumoniae, S. aureus, H, influenzae, Klebsiella;
acute inflammatory infiltrates from bronchioles into adjacent alveoli;
patchy distribution involving 1 or more lobes
Interstitial pneumonia
atypical;
Viruses (RSV, influenza, adenovirus), mycoplasma, legionella, chlamydia;
diffuse patchy inflammation localized to interstitial areas to alveolar walls;
distribution involving 1 or more lobes;
generally follows a more indolent course
Lung abcess
Localized collection of pus within parenchyma;
caused by bronchial obstruction (e.g. cancer) or aspiration of oropharyngeal contents (look for LOC (drunks, epileptics));
air fluid levels often seen on CXR;
often due to S. aureus, or anaerobes (bacteroides, fusobacterium, peptostreptococcus (GI bugs))
Transudate
Decreased protein content;
due to CHF, nephrotic syndrome, hepatic cirrhosis;
watery (translucent)
Exudate
High protein content, cloudy;
due to malignancy, pneumonia, collagen vascular disease, trauma (occurs in states of increased vascular permeability);
must be drained in light of risk of infection;
protein/serum > .5;
LDH/serum > .6;
LDH > 2/3 upper limit
Spontaneous pneumothorax
Accumulation of air in the pleural space;
occurs most frequently in tall, thin, young males because of rupture of apical blebs;
Tension pneymothorax
Usually occurs in setting of trauma or lung infection;
air is capable of entering pleural space but not exiting;
trachea deviates away from affected lung
1st generation H1 blockers
Diphenhydramine, dimenhydrinate, chlorpheniramine (en/ine or en/ate);
Used for allergy, motion sickness, sleep aid;
Toxicity is sedation, antimuscarinic, anti-alpha-adrenergic
2nd generation H1 blockers
Loaradine, fexofenadine, desloratadine, cetrizine (usually end in -adine);
used for allergies;
far less sedating than 1st gens due to less CNS entry
Guaifenesin
Expectorant- thins respiratory secretions;
does not suppress cough reflex
N-acetlycystein
mucolytic can loosen plugs in CF patients;
also used as an antidote for acetaminophen overdoes
Dextromethorphan
antitussive (antagonizes NMDA glutamate receptors);
synthetic codeine analog;
has mild opioid effect when used in excess;
naloxone can be given in overdose;
mild abuse potential
Pseudoephedrine, Phenylephrine
Sympathomimetic alpha agonstic, nonprescription nasal decongestants;
Uses: reduce hyperemia, edema, and nasal congestion;
open obstructed eustachian tubes, pseudoephedrine also illicitly used to make methamphetamine;
Toxicity is HTN, can also cause CNS stimulation/anxiety (pseudoephedrine)
Albuterol, metaproterenol, pirbuterol;
SABA;
relaxes bronchial smooth muscle (beta2);
use during acute exacerbation;
Salmeterol, formoterol
LABA;
long acting agents for prophylaxis;
adverse effects are tremor and arrhythmia
Methylxanthines: Theophylline
Likely causes bronchodilation by inhibiting phosphodiesterase leading to increased cAMP levels due to decreased cAMP hydrolysis;
usage is limited by narrow therapeutic index (cardio and neuro toxicity);
metabolized by cytochrome P-450;
blocks actions of adenosine
Ipratropium
Competitive block of muscarinic receptors, preventing bronchoconstriction;
also used for COPD, as is tiotroprium (longer lasting)
Corticosteroids for asthma
Beclomethasone, fluticasone;
inhibit the synthesis of virtually all cytokines;
inactivate NF-kB, the transcription factor that induces the production of TNF-alpha and other inflammatory agents;
1st line therapy for chronic asthma
Antileukotrienes for asthma
Montelukast, zafirlukast- block leukotriene receptors, especially good for aspirin induced asthma;
Zileuton- a 5-lipoxygenase pathway inhibitor, blocks conversion of arachidonic acid to leukotrienes
Omalizumab
monoclonal anti-IgE antibody;
binds mostly unbound IgE and blocks binding to FceRI;
used in allergic asthma resistant to inhaled steroids and long-acting beta2 agonists
Methacholine
muscarinic receptor agonist;
used in bronchial provocation challenge to help diagnose asthma
Bosentan
Used to treat pulmonary arterial HTN;
competitively antagonizes endothelin-1 receptors, decreasing pulmonary vascular resistance
