Test 3: Pulmonary Flashcards

Question

What is functional residual capacity (FRC)?

Answer 1

expiratory reserve volume + residual volume the volume of air remaining in the lungs after a normal exhalation INCREASED OBSTRUCTIVE LUNG DISEASE DECREASED RESTRICTIVE LUNG DISEASE 1149

Answer 2

inspiratory reserve volume + tidal volume + expiratory reserve volume the maximum volume that can be exhaled after a maximum inhale. the maximum amount of air that can enter and leave the lungs during respiration DECREASE RESTRICTIVE LUNG NORMAL OR INCREASED OBSTRUCTIVE ~2400mL 1148

Answer 3

Inspiratory reserve+ tidal volume+ expiratory reserve+ residual volume maximum volume the lungs can be expanded. INCREASED OBSTRUCTIVE DECREASED RESTRICTIVE ~6L 1149

Answer 4

Forced vital capacity (FVC) Forced expiratory volume in 1 second (FEV1) ------------FEV1/FVC Ratio Early detection of of restrictive or obstructive deficits, severity classification, monitoring progression Restrictive lung diseases restrict volume; the lungs are unable to expand normally diminishing the amount of gas that can be inspired therefore reducing the FVC. Obstructive disease affects gas flow; airflow into and out of the lungs is obstructed reducing the FEV1 Ratio: Diagnostic tool RESTRICTIVE DISEASE: FVC DECREASED OBSTRUCTIVE DISEASE: FEV1 DECREASED 1148

Answer 5

maximum amount of air that can be displaced from the lung during a forced expiration. 1149

Answer 6

Rate of ventilations/min x the volume or amount of air per breath in L= _____L/min OR Tidal volume x ventilation rate the total amount of air moved into the lungs each minute Clinical significance: -Key indicator how well lungs are functioning -Hypoxia/hypercapnia monitoring: can indicate gas exchange issue (hypoventilation leading to hypoxia or hypercapnia) 1137

Answer 7

rate new air reaches the gas exchange areas of the lungs the rate can not be accurately determined by observation of rate, pattern, or effort. If adequacy of ventilation needs to be determined ABG or capnography must be used to determine if there is CO2 retention. 1138

Answer 8

-The volume of air per breath that does not participate in gas exchange. It is ventilation without perfusion. -on exhalation the air in the dead spaces is expired first before air from the alveoli which decreases CO2 removal. Diseases causing dead space make CO2 harder to blow off (COPD/asthma) Anatomic dead space= volume of air in the conducting airways (no gas exchange) about 30% of tidal volume Alveolar dead space= volume of air in unperfused alveoli 1138

Answer 9

Physiologic dead space = anatomic dead space + alveolar dead space PNA, PE lecture and organizer

Answer 10

a wedge-shaped depression in the center of each lung where the bronchi, arteries, veins, and nerves enter and exit the lungs. The hilum is located in the mediastinal surface of the lung, in front of the 5th through 7th thoracic vertebrae. 1133*

Answer 11

provide oxygenated blood from the systemic circulation to: moisten inspired air and supply nutrients to the conducting airways, large pulmonary vessels, lymph nodes, and membranes (pleura), that surround the lungs. 1136

Answer 12

very thin membrane made up of the alveolar epithelium, the alveolar basement membrane, an interstitial space, the capillary basement membrane and the capillary endothelium. Gas exchange occurs across this membrane. The extremely thin alveolar walls are easily damaged and can leak plasma and blood into the alveolar space. Any disorder that thickens the membrane impairs gas exchange. 1136 Not in lecture but super important

Answer 13

A reaction to a low alveolar partial pressure of O2 (PaO2) causing increased pulmonary vascular resistance in the lung area (can be unit, lobe etc.) that is not well ventilated, causing a shunting of pulmonary blood flow to areas of the lung that are adequately ventilated therefore have a normal PaO2. Attempt to maximize ventilation/Perfusion and avoid mismatch. 1137

Answer 14

Alteration of ventilation(V)/perfusion(Q) ratio An imbalance in the alveolar ventilation and the alveolar blood flow. Normal: 0.8-1 Most common cause of hypoxemia Asthma, chronic bronchitis, PNA, atelectasis, pulmonary embolism 1145-1146

Answer 15

Ventilation/perfusion= V/Q= 0.8 normal represents the amount by which perfusion exceeds ventilation under normal conditions 1146

Answer 16

V/Q below normal --> inadequate ventilation to oxygenate blood flowing through alveolar capillaries V/Q < NORMAL organizer/lecture From Google: a type of blood recirculation that occurs when blood bypasses the pulmonary circulation and mixes with deoxygenated blood in the systemic circulation A small amount of physiologic shunting is normal and is caused by vessels that supply the bronchi. However, shunting can also be caused by disease in the heart, pulmonary vasculature, or alveolar air space. A key characteristic of shunting is that it doesn't respond to supplemental oxygen. This is because the supplemental oxygen can't reach the blood that has already bypassed the alveoli

Answer 17

dependent regions of the lung get more blood flow due to compression of capillaries in the low pressure areas. Changing positions changes flow distribution. example: a person standing has less blood flow to the apices than the lower lobes. 1146

Answer 18

Works in all areas of the lung, depending on positioning. zone 3 (best) blood flow in all or most of lungs during exercise due to increased cardiac output. doesn't work: zone 1 blood flow (worst) occurs when PA pressures are too high (pulmonary HTN), or alveolar pressures are too high (hyperinflation-> asthma/COPD), or in the least dependent area of the lung at any given time. Seriously a picture is much easier to understand! 1146 Fig 34.05 Mostly slide

Answer 19

shift in the oxyhemoglobin dissociation curve cased by changes in the CO2 and hydrogen ion concentrations in the blood. 1147

Answer 20

the property of hemoglobin that allows it to carry more carbon dioxide (CO2) when it's deoxygenated than when it's oxygenated 1148

Answer 21

net fluid movement from alveoli to interstitial space that drains into the lymphatic system. Helps prevent pulmonary edema. Book?? According to Google: Pulmonary capillary pressure (Pcap) is the average hydrostatic pressure in the small pulmonary vessels where filtration occurs. It's the filtration point in the capillary bed and determines how much interstitial fluid builds up in the lung

Answer 22

excessive fluid in alveoli due to a failure of one of the clearing mechanisms: -lymphatic drainage, capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability. impedes gas exchange 1165

Answer 23

MOST: Left sided heart disease pulmonary over-circulation Increased pulmonary capillary permeability (inflammation, ARDS, or inhalation of toxic gases) Obstruction of the lymphatic system 1165

Answer 24

Dyspnea tissue hypoxia increased WOB Crackles, pink frothy sputum 1166

Answer 25

Excess fluid in the pleural space 1. Transudative 2. Exudative 3. Empyema 4. Hemothorax 5. Chylothorax: tear in the thoracic duct leading to the leakage of chyle (lymph formed in the GI system) into the pleural space. (rare complication of surgery and some malignancies)

Answer 26

Transudative: clear or slightly discolored, contain few cells and little protein. 1160

Answer 27

Exudative: response to inflammation, infection or malignancy. Leukocytes and plasma proteins migrate out into affected tissue. Parapneumonic effusions (PNA) 1160

Answer 28

Empyema: contains infectious microorganisms 1160

Answer 29

Hemothorax: blood (trauma, surgery, cancer, PE or TB) 1160

Answer 30

Chylothorax: tear in the thoracic duct leading to the leakage of chyle (lymph formed in the GI system) into the pleural space (rare complication of surgery and some malignancies) 1160

Answer 31

Percent of Hgb saturated with O2 in arterial blood Normal 97-100 1145 34.2

Answer 32

Percent Hbg saturated with O2 in mixed venous blood Normal 75 1145 34.2

Answer 33

Acidosis, increased CO2, Increased Temp, Increased DPG decreased affinity of Hbg for O2, O2 readily released in tissue More common for a right shift

Answer 34

Alkalosis, decreased CO2, decreased temp, decreased DPG increased affinity of Hgb for O2, Less O2 to tissues Less common

Answer 35

Medulla oblongata and pons Medulla: --Dorsal - inspiration --Ventral- expiration Pons: pneumotaxic center- controls rate and pattern 1138

Answer 36

Rate and inspiration time Vagal and glossopharyngeal nerves Chemoreceptors and baroreceptors Diaphragm and intercostal muscles 1138

Answer 37

Basic rhythm Diaphragm & intercostals 1138

Answer 38

Medulla Sense change in pH or CSF as CO2 crosses the BBB. As pH decreases they stimulate the respiratory center to increase the depth and rate of ventilation. Become insensitive to small changes in CO2 with CO2 retaining pathology like COPD. 1139

Answer 39

Carotid and aortic bodies senses changes in O2 concentration. lower PO2 increases respiratory rate. Accompanied by dyspnea 1138

Answer 40

aka the Hering-Breuer EXPIRATORY reflex stretch receptors in the smooth muscle are sensitive to the increases in size or volume of the lungs. When stimulated they decrease the ventilitory rate and volume NOTE: this reflex is active in newborns and assists with ventilation. In adults it's only active at high tidal volumes such as exercise and mechanical ventilation, may protect against excess lung inflation 1140

Answer 41

receptors sensitive to increased pulmonary capillary pressure, which stimulates them to initiate rapid, shallow breathing; laryngeal constriction on expiration; mucus secretion; hypotension; and bradycardia. Associated with dyspnea Located: near the capillaries in the alveolar septa and other airway locations as nociceptors. 1140

Answer 42

Full or partial occlusion of the pulmonary artery. -Clot/DVT (venous thromboembolism) -Fat -Amniotic fluid -Air NOTE: 25% of people with PE will have the first symptom as sudden death Symptoms: Tachypnea Dyspnea Chest pain Low Sat 1179

Answer 43

Diagnosis: -CTA/MRA (GOLD STANDARD HAHA!) -D-dimer -ABG (evaluate for hypoxemia) -BNP & Troponin (markers for R ventricular dysfunction) -EKG (look for R heart strain) Treatment: -Anticoagulation therapy if stable --Xa inhibitors or lovenox If unstable: -IV fibrinolytic -Catheter directed therapy (EKOS??) -Thrombectomy 1180

Answer 44

Occlusion causes --> -Hypoxic vasoconstriction -Decreased surfactant -Release of neurohumoral and inflammatory substances -Pulmonary edema -Atelectasis 1180

Answer 45

Pressures in the PA > 25 at rest Causes: 5 main categories with many subcategories 1. idiopathic, heritable, drug and toxin, connective tissue disease 2. Left sided heart disease 3. lung diseases and/or hypoxia 4. chronic thromboembolic 5. unclear multifactorial mechanism (tumors, metabolic disorder, renal failure etc.) --Not sure what category to put these but slides say chronic hypoxia, and valve disease MOST common: Left sided heart failure 1181

Answer 46

Symptoms: -May be asymptomatic until late in the disease process -Fatigue -Chest pain -tachypnea -dyspnea (especially with exertion) -cyanosis -syncopy Assessment findings: -peripheral edema -JVD -precordial heave -accentuation of the pulmonary component of the second heart sound (???) -Kidney problems -Liver congestion Diagnosis: -CXR (usually first indication) showing enlarged R heart -EKG with right ventricular hypertrophy -CT

Answer 47

Patho: endothelial disfunction with overproduction of vasoconstrictors (thromboxane & endothelin) and decrease in production of vasodilators (prostacyclin & nitric oxide) --> resistance to flow increases R heart strain causing hypertrophy --> cor pulmonale (right ventricular hypertrophy, dilation or both) Treatment: - O2 (treat underlying disease process) - Diuretics - Anticoagulants - Avoid contributing factors (air travel, decongestants, NSAIDS, pregnancy, tobacco etc) -Vasodilators (calcium channel blockers, inhaled nitric oxide) -Refractory to treatment may need lung transplant 1181

Answer 48

- Dyspnea - Wheezing (lower airway) - Stridor (upper airway) - Prolonged expiration (long FEV1) 1167

Answer 49

Early: -Exposure to an antigen causes a major immune response with HISTAMINE, LEUKOTRINES, CYTOKINE, CHEMOKINE, PROSTAGLANDIN, IgE, PLATELET ACTIVATING FACTOR, TRYPTASE AND CHYMASE -Mucosal edema and mucus production increases -Bronchospasm, THROMBOXANES increased contractile response of bronchial smooth muscle. Late: -4-8 hours after exposure -Chemotactic recruitment of eosinophils (and friends) release more inflammatory mediators restarting the inflammatory response ----causing mucosal edema, mucus production, bronchospasm, contractility of smooth muscle If untreated long term inflammation causes airway damage and airway remodeling that becomes permanent INCREASED RV, FRC AND TLC NORMAL OR DECREASED VC AND IRV 1170

Answer 50

Familial or environmental. More commonly familial Can also be indoor or outdoor pollution, tobacco, obesity, GERD etc. Occurs at all ages, more common in women and those below the poverty level 1167

Answer 51

Symptoms: -asymptomatic between attacks, pulm function tests are normal. -chest constriction -expiratory wheezing -dyspnea -nonproductive cough -prolonged expiration -use of accessory muscles -Tachycardia -tachypnea Treatment: -Avoid allergens and irritants -inhaled low dose corticosteroids (pulmicort) -Beta 2 agonists (albuterol) - should only be used when necessary is associated with increased risk for severe exacerbations -Anticholinergic stimulators (Ellipta or atrovent) -Antihistamine (zyrtec etc.) -Antileukotrienes (singulair) -Steroids 1171-1172

Answer 52

Typically acquired Genetic: alpha1-antitrypsin deficiency, more common in those with European descent and results in early age COPD without smoking. Most common lung disease in the world INCREASED RV, FRC AND TLC NORMAL OR DECREASED VC AND IRV 1173

Answer 53

Hypersecretion of mucus and chronic productive cough that continues at least 3 months of the year, and for at least 2 consecutive years. 1173

Answer 54

-Bronchial inflammation caused by inspired irritants causing edema---> -Increased size and number or mucous glands and goblet cells --> -smooth muscle hypertrophy with fibrosis and narrowing of airways--> -Thick tenacious mucus is produced and cannot be cleared because of impaired ciliary function compromising defense mechanisms, and air trapping 1173

Answer 55

Symptoms: -Dyspnea on exertion (eventually as it gets worse marked dyspnea even at rest) -persistent productive cough -Wheezing -Barrel chest -cyanosis -hypoxemia -polycythemia -cor pulmonale -CO2 -V/Q mismatch -Chronic hypercarbia (blue bloaters- obese, cough, cyanosis) 1173

Answer 56

Destruction of alveolar walls results in permanent enlargement of gas exchange airways. (large alveoli instead of smaller ones with more surface area for gas exchange) -Obstruction results from inflammatory changes -inflammation and imbalance in proteases and antiproteases, oxidative stress and apoptosis of lung structural cells -destruction of alveoli produces large air spaces within the lung (BULLAE) and air spaces adjacent to pleurae (BLEBS) ------V/Q mismatch and hypoxia --Malnutrition -no mucous like chronic bronchitis (pink puffers- pink skinny) 1173

Answer 57

Abnormal, permanent enlargement of gas exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis. Associated with enhanced chronic inflammatory response in airway to noxious particles or gases. 1173

Answer 58

obstruction of the upper airway in children, subglottic edema causing narrowing of airway and respiratory distress 6mo- 3yrs Symptoms: -barky cough -inspiratory stridor Treatment: -oral or inhaled glucocorticoids -nebulized epi -rarely intubation -supportive care Not common thanks to vaccination (diphtheria, RSV, rhinovirus, adenovirus, rubella) USUALLY RESOLVES IN 3-7 DAYS 1191

Answer 59

Usually affects children 2-6 caused by H. influenzae type B (HiB). -life threatening edema of the epiglottis possibly causing obstruction of the upper airway Symptoms: -inspiratory stridor -sudden development of high fever -severe respiratory distress -drooling -tripod Treatment: -Keep them calm -Intubation -broad spectrum abx & corticosteroids Not common thanks to vaccination, increasingly an issue for adults now. :( 1193-1194

Answer 60

-autosomal recessive genetic disorder, defective epithelial chloride ion transport (CFTR gene) -Multiorgan (lungs, GI & reproductive) disease -chloride and water are not transported appropriately across epithelial membranes. Chronic inflammation with excessive cytokines and neutrophils Symptoms: -thick dehydrated mucus secretions (mucus plugging) -persistent cough or wheeze -excessive sputum production -recurrent or severe PNA -chronic sinusitis -malnutrition -intestinal obstruction -eventually barrel chest and digital clubbing Recurrent Infections: -Pseudomonas most common -PNA bacterial, fungal and viral Treatment: -Chest cpt -pancreatic enzymes -bronchodilators -hypertonic saline inhalation (break up secretions) -High dose NSAID > 6 yrs old. (emerging) 1205-1206

Answer 61

decreased compliance (stiffness) of lung tissue, resulting in increased WOB to expand lungs during inspiration Examples: -Scoliosis -muscular dystrophy -morbid obesity -aspiration -atelectasis -bronchiectasis -pulmonary fibrosis -pulmonary edema -ARDS -bronchiolitis TYPICALLY DECREASED VC, IC, FRC, AND TLC NORMAL OR DECREASED RV NORMAL FEV1/FVC 1161

Answer 62

diffuse injury of the bronchioles resulting in inflammation and fibrosis. Primary usually in children due to viral infection. Adults smoking (asbestos/coal) and chronic bronchitis, pulmonary fibrosis but can be in healthy people. Symptoms: -hypoxemia -decreased minute ventilation (increased accessory muscle use) -hypercarbia -tachypnea -nonproductive cough 1163

Answer 63

excessive amount of fibrosis or connective tissue in the lung. -chronic inflammation -fibrosis around the alveoli (stiffness), myofibroblast proliferation, causes decreased oxygen diffusion and hypoxemia. -progressive increase in WOB as compliance decreases -hypoventilation and hypercapnia -idiopathic, ARDS/TB, RA/sarcoidosis, coal/asbestos 1163

Answer 64

inadequate gas exchange. Generally a result of direct injury to lungs, airways or chest wall; or indirectly because of disease or injury involving another body system (brain/spine/heart). Hypoxemic PaO2 <60 (<50 on the slides) Hypercapnic/Hypercarbia PaCO2> 50 AND pH < 7.25 1158

Answer 65

Hypoxemic: -low PaO2 (slides with or without hypoxia?) -inadequate O2 exchange between alveoli and capillaries -tachycardia, cyanosis, confusion --Give O2! ----------(slides: heart failure, increased alveolar membrane thickness, hypoventilation) Hypercapnic -high CO2 -inadequate alveolar minute ventilation (hypoventilation) -confusion & lethargy --Ventilatory support! Bipap, bag mask, vent/intubation ---------(slides: neuromuscular disease, airway obstruction, physiologic dead space, chest wall deformity) 1158

Answer 66

PaO2/FiO2 Assesses for the severity of hypoxemic respiratory failure. MUST be only part of the evaluation -active inflammatory process -acute (<7 days) -resp failure not from cardiac cause or overload Acute Lung Injury

Answer 67

Exudative Phase- inflammatory stage where fluid/edema builds up in alveoli preventing gas exchange Proliferative Phase- early signs of healing. edema beings to drain (lymphatic) may have increased pleural effusions, pulm edema improves. Capillary alveolar barrier begins to restore. Fibrotic Phase- Does NOT always occur, but very likely with ARDS at least in some part. Can have interstitial or capillary fibrosis as well. Risk for pulm HTN. Lecture

Answer 68

External: lungs and environment Internal: blood and cells Organizer

Answer 69

The rate of diffusion is influence by surface area, thickness or alveolar membrane and the partial pressure gradients of gasses. Organizer

Answer 70

Nose Pharynx Larynx Trachea Bronchi Bronchioles 1131-1132

Answer 71

Terminal bronchioles Alveoli Alveolar capillaries 1133-1134

Answer 72

resistance is directly related to tube length and blood viscosity, and inversely related to the radius of the tube to the 4th power. 1043 Works for airways too. The smaller the tube the higher to the 4th power the resistance. lecture and organizer

Answer 73

Starts at 0 drops below atmospheric pressure during inspiration rises above atmospheric pressure during exhalation lecture & organizer

Answer 74

A cluster or respiratory bronchioles, alveolar ducts and alveoli, DISTAL to a single terminal bronchiole 1133

Answer 75

-Alveoli- loss of wall tissue & enlargement decreasing the surface area for diffusion, increased stiffness Pulmonary capillaries- decrease in number and complexity of alveolar capillaries. -Chest wall- decreased compliance and elastic recoil, reducing respiratory reserve, decreased strength, postural changes -Vital capacity decreases and residual volume increases without a change in total lung volume -Aging can cause the PaO2 to decrease but does not affect CO2 ----Results in increased risk for PNA, COPD & other resp infections 1151 & organizer

Answer 76

Alveolar- arterial gradient lecture & organizer Google: a measurement of the difference in oxygen concentration between the alveoli and the arterial system. It's a useful tool for diagnosing hypoxemia and determining its severity

Answer 77

PSP -No apparent cause or lung disease (usually young males 20-40) caused by spontaneous rupture of blebs on the visceral pleura, possible genetic component SSP -Pre-existing lung disease which integrity of the visceral pleura is compromised. Traumatic -punctures by fractured rib or knife/bullet wounds, or iatrogenic (caused by medical procedure) such as needle aspiration, mechanical ventilation (barotrauma). Frequently involves BOTH visceral and parietal pleura Tension -site of pleural rupture acts as a one way valve, permitting air to enter the pleural space on inspiration but preventing escape during expiration. More air enters pleural space the pushes against the lung, causing compression atelectasis, mediastinal shift, severe respiratory distress, hypotension, and eventually death. 1159

Answer 78

-Young adult (15-34) -Lung disease -Tall/Thin (esp males and esp PSP) -Hx of PTX -Smokers -Having invasive medical procedures (central line/thora/biopsy etc) -Trauma Organizer

Answer 79

-Sudden pleural pain -Tachypnea -Dyspnea -decreased breath sounds -hyperresonance -severe hypoxemia (tension) -tracheal deviation away from affected lung (tension) -hypotension (tension) Treatment: -One way chest valve (PSP) -Aspiration/chest tube with water seal and suction -Surgery 1159

Answer 80

volume of air inhaled or exhaled with each normal breath RESTRICTIVE LUNG DISEASE ISSUE ~500 mL

Answer 81

Ratio often seen as percent Normal 70-80% (0.7-0.8) varies based on age, size etc. Obstructive: <70% (COPD/Asthma) Restrictive: >75% (Pulm fibrosis, Pna) Notes: Obstructive Severity Scoring ------Mild FEV1>80% ------Moderate FEV1 50-79% ------Severe FEV1 <50% Organizer

Answer 82

Adult: -Normal Epiglottal movement -More rigid/less space for expansion, other contributing factors such as obesity Child/Infant: -Hypoactive epiglottal movement (risk for aspiration) -More compliant airways/smaller airways can collapse due to easy recoil -Particularly vulnerable to airway obstruction organizer

Answer 83

Zone 1: Dead Space ---alveolar pressure exceeds arterial pressure causing little to no blood flow in pulm capillaries. Normal, worse with things like hypotension. Zone 2: Fluid Exchange ---arterial pressure exceeds alveolar pressure allowing pulsatile flow. Favorable for gas exchange. Zone 3: Optimal Gas Exchange ---both arterial and venous pressures exceed alveolar pressure leading to continuous flow. Ideal for gas exchange as blood flow is constant allowing for continuous exchange. 1146

Answer 84

occurs when the lungs are suddenly damaged, leading to inflammation, fluid accumulation in alveoli, and impaired oxygen exchange. Alveolar capillary membrane injury, inflammation and endothelial dysfunction (considered a less severe version of ARDS) Cause: -Pna -Aspiration -toxic inhalation -pulmonary edema -sepsis -trauma -pancreatitis Diagnosis: P:F ratio- PaO2/FiO2 ratio of 200-300mmHg Features: -lung injury -pulmonary edema -inflammation -compensatory mechanisms may function for a period -cyanosis PEEP: Moderate PEEP, should improve oxygenation without hemodynamic compromise organizer

Answer 85

the more advanced, critical stage of lung injury Causes: -PNA -Aspiration -Toxic inhalation -Sepsis -TRALI -Severe pancreatitis Diagnosis: P:F ratio- PaO2/FiO2 ratio < 200mmHg Features: -Severe pulmonary edema -widespread atelectasis -decreased lung compliance -severe hypoxemia -diffuse alveolar damage PEEP: HIGH PEEP, watch for decreased cardiac output from decrease in venous return.... also PTX but they don't seem to care about that one HAHAHAHA!

Answer 86

Rare disorder in which the automatic control of breathing is impaired, particularly during sleep. People with this condition fail to breathe normally because the brain's autonomic centers do not properly respond to hypoxemia or hypercapnia levels in the blood, especially during sleep when breathing is largely under involuntary control Can be congenital (genetic mutation) see in infants or in early childhood Can be acquired due to brainstem injury, trauma, stroke, tumors, MS or post infection autoimmune response

Test 3: Pulmonary Flashcards

(110 cards)