Pulm

Question 1

Conducting airway

Answer 1

Nose, pharynx, larynx (extra thoracic)
Trachea, bronchi, bronchioles (intrathoracic)

Question 2

Respiratory zone

Answer 2

Terminal bronchi, alveoli, alveolar capillaries
Oxygenation

Question 3

Factors that affect the muscles in the bronchi/bronchioles

Answer 3

-Transpulmonary pressure- keep smooth muscle areas open
-Smooth muscle- sympathetic (beta 2 receptors, relax smooth muscle and epi) and parasympathetic innerration, vagus nerve (acetylcholine causes contractions of bronchiolar smooth muscle and bronchoconstriction)
-Lung cells and endothelium=leukotrienes=constriction
-Histamine and substances from mast cells anaphylaxis and constriction
-Airway resistance-amp changes in diameters increase difficulty of breathing

Question 4

Tidal volume TV

Answer 4

Volume of inspired and expired air with each normal breathe

Question 5

Inspiratory reserve volume IRV

Answer 5

Max effort of air inspired after normal inspiration

Question 6

Expiratory reserve volume ERV

Answer 6

Max effort of air expired after normal expiration

Question 7

Residual volume

Answer 7

Air left in lungs at the end of expiratory reserve volume

Question 8

Inspiratory capacity

Answer 8

Residual volume
Tidal vine plus Inspiratory reserve volume
75-120%

Question 9

Functional residual capacity

Answer 9

Expiratory reserve volume plus residual volume
75-120%

Question 10

Vital capacity

Answer 10

Inspiratory reserve volume plus tidal volume plus expiratory residual volume
(TV plus ERV is measurement)

Question 11

Total lung capacity

Answer 11

Vital calcite plus residual volume
Max lung expansion.
80-120%

Question 12

Forced expiratory volume

Answer 12

FEV and FEV1 (expired in one second)
80-120%

Question 13

Normal PFT curve

Answer 13

Normal oval
Pressure necessary to get into lungs
Normal homeostasis

Question 14

Increase in lung compliance in PFT

Answer 14

Wide oval curve
Increase pressure necessary for exhale
Obstructive disease-destruction of airway loss of elastin
COPD emphysema asthma

Question 15

Decrease lung compliance curve in PFT

Answer 15

Compliance curve in side and narrow small curve
Increase pressure required to get air in and when air is in it’s usually less
Restrictive disease PNE, pulmonary edema, fibrosis

Question 16

Intrathroacic pressure changes that result in air movement in and out of alveoli

Answer 16

-pleural pressure (between lining of pleura) negative -5 cm H20, inspiration (expansion) -7.5 cm H20 increase suction pulling lungs with ribs
-alveolar pressure- measure of respiratory tree, when glottis is open (atmospheric pressure is at 0) with chest expansion pressure decrease to 1cm H20 and air moves out, recoil-alveolar pressure increase to 1cm and air moves out
Transpulmonary- difference between pleural and alveolar pressure, elastic forces:PEEP, surfactant, and closed epiglottis

Question 17

Pneumothorax

Answer 17

Breach of pleural spaces, atmospheric air enters and equalizes pressure to atmospheric at 0(-4 mm of Hg is lost) lungs cannot expand, air gets in but not out
S/s: SOB, tachypnea, deviated trachea, decreased breathe sounds on affected side, hyper resonance to percussion

Question 18

Brain stem and breathing

Answer 18

Brain stem
Medulla-dorsal respiratory group (or neurons) for inspiration, ventral respiratory group (or neurons) for expiration
DRN-back and gloss pharyngeal nerve transmits signs from chemo baroreceptors which signals diaphragm and intercostal muscles
VRN basic autonomic rhythm of respiration, inactive during normal breathing, medullary rhythm of inspiration and expiration, fires during hypo ventilation and signals inspiration, which stimulates and muscle contraction for expiration
Pons
Pneumotaxic center responsible for respiratory rate and pattern
Pontine group modifies rhythm set by VRG

Question 19

Chemoreceptors and breathing

Answer 19

-Center (near resp center)
Sense changes in pH of CSF, carbon dioxide crosses the BBB and H20, bicarbonate is formed, very sensitive to increase in CO2, and will change rate and depth of respiration, exceptions is in chronic conditions compensated acidosis by renal compensation
-Peripheral (aortic and carotid bodies)
Sense changes in O2 concentration decrease p02 and increase in RR

Question 20

Lung intervention and breathing

Answer 20

-irritarion receptors (epithelium)
When lungs are irritated by inhalation of particulate matter-cough induced causes bronchospasms and increased RR
-stretch receptors
Smooth muscles stretch in bronchi, bronchioles, king parenchyma, signals DRN to switch off inspiration (prevents over inflation)
-pulmonary C fiber receptors (J receptors)
C fibers are sensitive to increases pulmonary capillary pressures (CHF) initiate shallow rapid breathing, laryngeal vasoconstriction, mucus secretion

Question 21

Other mechanisms for breathing

Answer 21

Voluntary breathing with breathe techniques
CNS depression by brain injury or anesthesia

Question 22

Blood flow zones

Answer 22

Deoxygenated RV->PA-> capillary bed
Oxygenated PV->LA
Bronchial vessels->systemic circulation->Trach->bronchi->lungs->esophagus->visceral pleura->PA
Not involved in gas exchange but maintain cellular function

Question 23

Oxygen disassociation curve

Answer 23

Right
High pCO2, low affinity for 02, high hydrogen, low pH, high 2-3 DPG, high temp
Left
Low pCO2, low hydrogen, low 2,3 DPG, low temp

Question 24

VQ mismatching

Answer 24

Failure in alveoli oxygen concentration
Shunts blood away from alveoli by constriction to higher concentrated oxygenated alveoli occurs within 10 minutes of hypoventilation
Results in differences in alveolar 02 concentration and paCO2, CO2 in expired air (end tidal CO2) and paCO2
Hypoxia pulmonary vasoconstriction maximizes ventilation and perfusion
Due to asthma, chronic bronchitis, PNE, atelectasis, PE

Question 25

Physiological shunting

Answer 25

VQ less than normal and causes inadequate ventilation to oxygenated blood going to alveolar capillaries poor shunting

Question 26

Minute ventilation

Answer 26

Air moved in and out in one minutes TVXRR Alveolar ventilation:rate new air reaches alveoli for gas exchange

Question 27

Dead space

Answer 27

Space in respiratory system where no gas exchange occurs Conducting zone is about 30% of total lung capacity and is non wiring inherently all the time- anatomical dead space Physiological draws space- anatomical dead space plus alveoli without blood flow due to pathology On exhalation air in dead space is expired first before air from alveoli and causes CO2 harder to blow off

Question 28

Pediatric respiratory system

Answer 28

Infants have no epiglottis flap movement between breathing and eating risk for aspiration More susceptible to problems with restrictive distresses due to changes in diameter of lungs, airway Child thoracic cage less pressures needed for expansion recoils and collapses easily

Question 29

Adult respiratory system

Answer 29

Adults thoracic cage less expansion and construction restricted and limited recoil

Question 30

Measure severity of respiratory failure

Answer 30

Alveolar arterial oxygen gradient: defines oxygenation disorders PF ratio: most helpful, ratio of partial pressure of o2 in arterial blood to the fraction of Inspiratory oxygen concentration (Fi02), use this to classify ARDS

Question 31

Obstructive lung diseases

Answer 31

Increase in lung volume Croup, acute epiglottis, cystic fibrosis, chronic bronchitis (COPD), emphysema (COPD), asthma

Question 32

Croup

Answer 32

Upper airway issue due to acute viral infection Barky seal cough, strider Subglottic edema narrows airway causes respiratory distress Humidified 02 watch from away decrease stress

Question 33

Acute epiglottis

Answer 33

Associated with H influenza Inspiratory strider, drooling, tripod Rapid edema of epiglottis and it is severe and life threatening Protect airway

Question 34

Cystic fibrosis

Answer 34

Autosomal recessive genetic disease that affects chloride ion transport in respiratory and GI tract Cough, wheezing, expiratory sputum, PNE, clubbing, barrel chest, rales, recurrence infection like pseudomonas Mucus plugs with submucosal glands and goblet cells Chronic inflammation with excessive cytokines and neutrophil activation

Question 35

Chronic bronchitis

Answer 35

Hyper secretion of mucus and chronic persistent cough (3 mths for 2 years) Usually acquired, generic alpha 1 anti tripsin deficiency Looks worse when exhaling, decreased FEV, wheezing in low airway strider in high airway, SOB, hypoxia, mild cyanosis, blue bloater, poor exercise tolerance, May cause polycythemia Large airway but can affect all smooth muscles, bronchial inflammation causes edema causes increase number and size of mucosal glands, goblet cells, air trapping, VQ mismatch, chronic hyper capnia

Question 36

Emphysema

Answer 36

Enlargement of respiratory zone and destruction of alveolar walls SOB, barrel chest, tripod, purses lip breathing, wheezing, pink puffer, hyper resonance Breakdown of elastin causes loss of recoil causes air trapping causes SOB causes decreased RR causes retention of CO2 and structural changes and loss of alveolar cells decreased area for gas exchange and bulbs and blend, VQ mismatch, hypoxia, inflammation and risk for infection

Question 37

Asthma

Answer 37

Chronic inflammation bronchial mucosa, hyperresponse, constriction, and obstruction Same ss as chronic bronchitis Early in due to antigen response, cytokines reinsert; increase capillary permeability, mucosal edema, mucus production, bronchospasm Late constriction VQ mismatch hypoxemia, CO2 retention, acidosis, resp failure

Question 38

Pulmonary edema

Answer 38

In the lungs and alveoli Differences in pressure gradient, excess fluid in alveoli including heart, pulmonary circulation, including pulmonary capillary permeability can’t drain to lymphatics HF, ARDS, toxic gases SOB, increased RR, crackles, pink frothy sputum, CP, orthopnea, PND Gas exchange impaired due to decreased lung compliance fluid in pulmonary alveolar sacs

Question 39

Pleural effusion

Answer 39

Excess fluid in pleural space, blocked by lymph node, heart failure, decreased oncotic pressure, increased vascular permeability of pleural membrane Fatigue, SOB, high RR Impaired gas exchange

Question 40

Hypoxemia respiratory failure

Answer 40

Decreased pa02 with or without hypoxia Resp failure less than or equal to 50 mm Hg Tachycardia, cyanosis, confusion Hypoventilation, VQ mismatch, increased alveolar capillary membrane thickness like in CHF, PE, pulm edema, PNE

Question 41

Hypercarbic respiratory failure

Answer 41

Increases CO2 paCO2 over 50 mm Hg and decreased pH less than or equal to 7.25 Confusion, lethargy Hypoventilation, decreased respiratory drive,, neuromuscular dz, airway obstruction, dead space, chest wall deformity

Question 42

Restrictive disease

Answer 42

Decreased compliance and lung volume Structural, aspiration, atelectasis, bronchiolitis, pulmonary fibrosis

Question 43

Structural restrictive disease

Answer 43

Kyphosis, scoliosis, muscular, dystrophy, obesity, increased shortness of breath, increase respirations, difficulty with secretion clearance, increased effort to expand lungs

Question 44

Aspiration

Answer 44

Fluid or solid and lung, dysphasia Bronchial inflammation causes decreased Cilia function, and bronchospasm, alveolar capillary membrane damage causes hemorrhagic, pneumonitis, and a stiff noncompliant lung

Question 45

Atelectasis

Answer 45

Blockage of airway, pressure outside lungs, can’t expand, not enough, surfactant, common and bedbound patients, increase in pulmonary shunt increase in VQ mismatch, causing hypoxia and decrease compliance

Question 46

Bronchiolitis

Answer 46

Inflammation of bronchioles, chronic bronchitis, viral, respiratory, illness, toxic gas Atelectasis or emphysematous destruction of alveoli beyond area of inflammation, decrease VQ matching, decreased minute, ventilation, increase in carbon dioxide and tachypnea

Question 47

Pulmonary fibrosis

Answer 47

Excess fibrosis and connective tissue in lungs Scar tissue after pulmonary disease, such as ARDS or TB, autoimmune like RA or sarcoidosis, inhalation of toxins, or idiopathic Chronic inflammation causes fibrosis of alveolar epithelium causes proliferation of myofibroblast, causes stiff alveoli, causes decrease compliance, VQ, mismatch and hypoxemia

Question 48

Acute lung injury

Answer 48

Inflammatory process and lungs that leads to alveolar, epithelial and vascular endothelial injury in the lungs can be due to infection or non-infection Onset oacute less than seven days Bilateral infiltrates, respiratory distress that is not related to fluid overload Acute lung injury, PF ratio less than or equal to 300

Question 49

ARDS

Answer 49

PF ratio less than or equal to 200 When acute lung injury progresses Causes can be direct, like pneumonia, aspiration, pulmonary contusion, fat, emboli, re-perfusion, near, drowning, inhalation injury, pulmonary edema post transplant, indirect, includes sepsis, trauma, cardiopulmonary, bypass, drug overdose, pancreatitis, blood transfusion Symptoms include shortness of breath, decreased oxygen, poor response, to oxygen, hyperventilation, respiratory alkalosis, organ, dysfunction, metabolic, acidosis, decreased tidal, volume, increase, carbon dioxide, decreased, cardiac output, decreased blood pressure Three phases exudative, proliferative, fibrotic

Question 50

Exudative stage of ARDS

Answer 50

Inflammatory, first 72 hours, PF ratio 201 to 300, mild Inflammatory and exudate, increase, capillary, permeability, surfactant, and inactivated or production impaired, compliance lost

Question 51

Proliferative stage of ARDS

Answer 51

1 to 3 weeks after injury PF ratio 101 to 200, moderate Early healing, pulmonary Edema drain, increase, lymphatic drainage, increase, pleural effusion, exudates granulate and recovery of capillary, alveolar barrier, surfactant production restarts

Question 52

Fibrotic stage of ARDS

Answer 52

14 to 21 days after injury overlaps with proliferative stage PF ratio less than 100 and is severe Does not occur in everyone fibroblast proliferate in alveoli, increased risk for pulmonary hypertension

Question 53

Pulmonary embolism

Answer 53

Thrombus, fat, air, amniotic fluid postpartum Increased respiratory rate, shortness of breath, chest pain, increase in dead space, VQ, mismatch, decreased and oxygen, pulmonary infection, pulmonary, hypertension, decreased cardiac output, hypertension, shock Causes hypoxic vasoconstriction, which then causes decreased surfactant, which then causes release of neurohormones and inflammatory substances which causes pulmonary edema and atelectasis to the affected area Diagnostics include D dimer CTA, MRA, EKG changes elevated troponins

Question 54

Pulmonary artery hypertension

Answer 54

Increase in pulmonary artery pressure at greater than 25 mmHg normal is 15 to 18 Can be idiopathic, genetic, connective, tissue disease, chronic hypoxia, left, ventricular failure, valve disease, long-standing, hypertension Shortness of breath, chest pain, increase respiratory rate, cough, JVD, fatigue, palpitations, right sided heart failure Vasoconstrictors overwhelm vasodilators, causing resistance of blood flow to lungs, causing remodeling of right ventricle cor pulmonale Pulmonary artery hypertension, and pulmonary artery hypertension crisis diagnostics include an echo and a right heart Cath