PATHO - Term Test III (Respiratory System) Flashcards

Question

The shared alveolar and capillary walls makes up the \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. What occurs here and how much blood runs through the alveolar surface area?

Answer 1

**alveolocapillary membrane** gas exchange occurs across this membrame, and under normal conditions ~100mL is spread over 70-100 m² of alveolar SA

Answer 2

connection where everything goes in (blood vessels, bronchus, nerves) and pulmonary veins go out

Answer 3

* part of systemic circulation * moistens inspired air and supplies nutrients to the conducting airways, large pulmonary vessels, and pleural membranes * some of its capillaries draiwn into own venous system, some contribute to the normal venous mix of oxygenated and deoxy blood (right to left shunt) * DOES NOT participate in gas exchange

Answer 4

smooth muscle

Answer 5

**Structure:** * deep and superficial pulmonary lymphatic capillaries present * fluid and alveolar macrophages migrate from alveoli to terminal bronchioles which then enters lymphatic system * vessels leave lung at hilum through series of mediastinal lymph nodes **Function:** immune defense, keeping lung free of fluid

Answer 6

decreases; increases

Answer 7

**local humoral conditions** (even though pulmonary circulation is innervated by ANS) * relating to body fluids, especially with regard to immune responses involving antibodies in body fluids as distinct from cells * basically in response to hormones, immunity factors

Answer 8

* most important cause: **low alveolar PO₂ (P_AO₂)** * caused by pulmonary venous hypoxia aka **_hypoxic pulmonary vasoconstriction_** * results from ↑ intracellular calcium levels in vascular smooth muscle cells in response to low [O₂] and presence of oxygen radicals * can be reversible if alveolar PO₂ is corrected * Other causes: **acidemia** (also reversible) * note that an elevated PaCO2 with no drop in pH will not cause constriction * Other biochemical factors affecting vessel diameter: **histamine, prostaglandins, serotonin, NO, bradykinin**

Answer 9

* can occur in one portion or entire lung * **if one segment:** arterioles constrict locally, shunting blood to other well-ventilated areas in lung (reflexively improves efficiency by ↑ ventilation and perfusion matching) * **if all segments:** vasoconstriction throughout pulmonary vasculature, results in pulmonary hypertension * chronic alveolar hypoxia = permanent structural changes, pulmonary HTN, eventually leads to RHF (cor pulmonae)

Answer 10

**Structure:** skin, ribs, intercostal muscles **Function:** protects lungs from injury * intercostal muscles: muscular work of breathing (in conjunction with diaphragm, accessory muscles, and abdominal muscles)

Answer 11

contained by: chest wall encases: lungs

Answer 12

**Pleura:** serous membrane that adheres to the lungs (visceral pleura) and folds over itself to attach to chest wall (parietal pleura) **Parietal pleura:** lines interior surface of thoracic wall and diaphragm; has costal, diaphragmatic, and mediastinal parts **Visceral pleura:** adheres to surface of the lung **Pleural space/cavity:** the area between the two pleurae, normally filled by a thin layer of intrapleural fluid secreted by pleura to lubricate pleural surfaces (\<0.02mm thick, to allow them to slide over each other without separating); intrapleural pressure is usually -ve/subatmospheric (-4 to -10mmHg) * usually the space is a potential space rather than a real space

Answer 13

1) ventilates alveoli 2) diffuses gases into and out of blood 3) perfuses lungs so that organs and tissues of the body receive blood rich in oxygen and deficient in CO₂

Answer 14

**Ventilation:** the mechanical movement of gas or air into and out of lungs **Respiration:** the exchange of oxygen and CO₂ during cellular metabolism

Answer 15

ventilatory rate/number of times gas is inspired and expired per minute

Answer 16

ventilatory rate (breaths per min) x amount of air per breath (tidal volume) expressed as litres per minute

Answer 17

the amount of air that moves in or out of the lungs with each respiratory cycle avg: 500cc of air per breath

Answer 18

500cc (tidal volume) x 12 breaths per min = 6000 mL (or 6L)

Answer 19

10 000 mEq 200 ml/min

Answer 20

volume of air per breath that does not participate in gas exchange (i.e. ventilation without perfusion)

Answer 21

**Anatomic dead space:** volume of air in the conduct airways (~150mL) **Alveolar dead space:** volume of air in unperfused alveoli dead space is ~ equivalent to the ideal body weight in lbs

Answer 22

(ventilatory rate x tidal volume) - dead space

Answer 23

the exchange of gas between the alveoli and the external environment (O₂ in and CO₂ out)

Answer 24

talking, singing, laughing, and deliberately holding one's breath

Answer 25

**Location:** brainstem **Function:** controls respiration by transmitting impulses to respiratory muscles to cause them to relax/contract **Components:** made of several groups of neurons * dorsal respiratory group (DRG) * ventral respiratory group (VRG) * pneumotaxic center * apneustic center

Answer 26

DRG - dorsal respiratory group Receives afferent input from: * peripheral chemoreceptors (in carotid and aortic bodies) * mechanical, neural, and chemical stimuli * lung receptors

Answer 27

Nope. It's go tboth inspiratory and expiratory neurons but it usually inactive during normal breathing; becomes active with increased ventilatory effort

Answer 28

**Location:** pons **Function:** not part of generating primary rhythm; act as modifiers of the rhythm established

Answer 29

emotion, pain, disease

Answer 30

* they all send impulses from lungs to DRG **1) Irritant receptors (C fibers)** - found in epithelium of all conducting airways * sensitive to vapors, gases, and particulate matter (like inhaled dust) * causes cough reflex * also cause bronchoconstriction and increased ventilatory rate **2) Stretch receptors** - in smooth muscles of airways * sensitive to increases in size/volume of lungs * decreases ventilatory rate and volume when stimulated (aka **Hering-Breuer expiratory reflex**) **3) J-receptors** - aka juxtapulmonary capillary receptors (sensory nerve endings) found near capillaries in alveolar walls/septa * innervated by vague nerve * sensitive to increased pulmonary capillary pressure (*_reflex response:_* _apnea (? noted in carolyn's notes) followed by_ _rapid, shallow breathing, hypotension, and bradycardia_) - pulmonary chemoreflex * respond to things like ex. pulmonary edema, PE, pneumonia, CHF, barotrauma, hyperinflation of lung, IV/intracardiac administration of chemicals like capsaicin

Answer 31

a reflex triggered to prevent the over-inflation of the lung reflex is active in newborns to help with ventilations; in adults, this reflex kicks in during high tidal volumes (ex. exercise) to protect excess lung inflation

Answer 32

**1) Sympathetic division:** branches from upper thoracic and cervical ganglia of the spinal cord * contributes to smooth muscle tone, causes it to relax **2) Parasympathetic division:** nerve fibers travel in vagus nerve to the lung; main controller of airway caliber (diameter of airway lumen) under normal conditions * receptors under this division when stimulated, will cause smooth muscle contraction

Answer 33

**Structure/location:** near resp center **Function:** monitor arterial blood (indirectly) via pH changes of CSF (i.e. sensitive to very small changes in H+ concentration and pH in CSF) * CSF pH reflects arterial pH beccause CO₂ can diffuse across BBB into CSF until Pco₂ is equal on both sides * CO₂ entered into CSF combine with H₂O to make carbonic acid which gives away its H+ causing stimulation of central chemoreceptors * _increases in Paco₂ cause chemoreceptors to sense it and stimulate resp center to increase depth and rate of ventilation ⇒ Pco₂ in arterial blood 2 diffuses out of CSF ⇒ pH returns to normal_

Answer 34

* with inadequate ventilation/hypoventilation that is LONG TERM (like COPD), central chemoreceptors become insensitive to these small changes

Answer 35

**Location:** carotid bodies and aortic arch **Function:** * sensitive to Pao₂ * when Pao₂ and pH decrease, these receptors stimualte resp center to increase ventilation (but Pao₂ has to be \<60 mmHg to have influence on the ventilation changes) * become the major stimulus to ventilation when central chemoreceptors become insensitive to chronic hypoventilation

Answer 36

normal healthy: CO₂ chronic high levels of CO₂ patients: O2 (using a hypoxic drive to stimulate breathing)

Answer 37

hyperventilate because it's acidic (acetylsalicylic acid) so body tries to blow it off

Answer 38

* hypoventilate * it tells your resp center that it doesn't need to breathe anymore so you stop breathing

Answer 39

Hyperventilate - because they have too much sugar causing creation of acid (from metabolism)

Answer 40

1) major and accessory muscles of inspiration and expiration 2) elastic properties of the lungs and chest wall 3) resistance to airflow through conducting airways

Answer 41

**Major:** diaphragm, external intercostal muscles **Accessory muscles:** sternocleidomastoid, scalene muscles

Answer 42

**Structure:** dome-shaped muscle separating abdominal and thoracic cavities * motor nerves of diaphragm exit from spinal cord from C3-C5 and run downward as phrenic nerve **Function:** changes size of the chest cavitiy - increases volume when it contracts and flattens doward (creates a negative pressure that draws gas into lungs) * contraction of external intercostal muscles elevate anterior portion of ribs and increase thoracic cavity volume via front to back diameter (from anterior - posterior) * inspiration at rest USUALLY assisted by diaphragm only

Answer 43

intercostal nerves which leave the spinal cord between T1-T11, corresponding with muscle position

Answer 44

* enlarge thorax by increase A-P diameter (but not as efficiently as diaphragm) * assist inspiraiton when minute volume (volume of air inspired and expired per min) is high (exercise, disease causing increased work of breathing)

Answer 45

trick question! there are none because normal, relaxed expiration is passive and requires no muscular effort

Answer 46

abdominal and internal intercostal muscles **function:** assist expiration when minute volume is high, during coughing, or when airway obstruction is present * abdominal muscles contract to increase intra-abdominal pressure which pushes the diaphragm up and decreases the thoracic volume = expiration * internal intercostal muscles pull down the anterior ribs to decrease AP diameter

Answer 47

resp muscle paralysis: above C3 some ventilation: below C5

Answer 48

refers the the tendency for liquid molecules that are exposed to air to adhere to one another, occurs at any gas-liquid interface (think when you fill the glass with water to the top and it looks like it's going to spill over but it doesn't even if you've filled more than the glass you can hold - that's surface tension)

Answer 49

Law of Laplace: P = 2T/r Pressure (P) equals to 2 x surface tension divded by radius of sphere so the smaller the alveolar radius, the more and more pressure is requirerd to inflate it which were make taking breathes EXTREMELY dificult

Answer 50

* a lipoprotein (90% lipids, 10% protein) produced by type II alveolar cells that allow for alveolar ventilation because it lowers surface tension by coating the air-liquid interface of the alveoli * includes two groups of surfactant proteins * 1) has small hydrophobic molecules with detergent-like effect to separate liquid molecules (this decreases alveolar surface tension) * 2) **collectins** - large hydrophilic molecules capable of inhibiting foreign pathogens * allow alveoli to expand uniformly (on inspiration) and prevents it from collapsing on itself (on expiration)

Answer 51

starts ~2 weeks after they are born major complication in preemies as their bodies don't make enough surfactant so alveoli cannot open completely and trouble breathing

Answer 52

alveolar surface tension increases which causes alveolar collapse, decreased lung expansion, increased work of breathing, and severe gas-exchange abnormalities

Answer 53

1) elastin fibers in alveolar walls and surrounding the small airways and pulmonary capillaries 2) surface tension at alveolar air-liquid interface

Answer 54

its bone and musculature configuration

Answer 55

**tendency of the lungs to return to resting state after inspiration** * normal elastric recoil allows for passive expiration but may be insufficient for labored breathing (accessory muscles of expiration kick in here) * ^ muscles also kick in in diseases like emphysema when disease compromises the elastic recoil/blocks conducting airways

Answer 56

**1) tendency for chest wall to recoil by expanding outward** **2) tendency for lungs to recoil/inward collapse around the hila** these opposing forces create the small negative intrapleural pressure; happens at the end of expiration (resting level) where functional residual capacity is reached (volume remaining in lungs after normal passive expiration) * we just overcome the the tendencies when we breathe in and out (i.e. overcome lung's resistance to expand out by use of diaphragm and intercostal muscles)

Answer 57

* measure of lung and chest wall distensibility; defined as volume change per unit of pressure change (or the amount of pressure that is must be generated to expand the lungs with a given volume) * represents the relative ease of structures to be stretched (OPPOSITE of elasticity) * ex. if compliance is improving = you need to exert less pressure to move the same volume of air; if a patient has decreased compliance for whatever reason (like increasing pulmonary edema) you'll need to ventilate harder to build more pressure to move that same amount of air

Answer 58

lungs and chest wall are easier than normal to inflate and has lost some elastric recoil

Answer 59

**Compliance increases with:** normal aging, disorders like emphysema **Compliance decreases with:** those with ARDS, pneumonia, pulmonary edema, fibrosis

Answer 60

length, radius/diameter, cross-sectional area of airways density, viscosity, and velocity of gas (Poiseuille law)

Answer 61

R = P/F (aka Ohm law) Pressure (P) rate of flow (F)

Answer 62

* airway resistance normally very low * 1/2 - 2/3rd of total airway resistance occurs in the nose * next highest resistance is in oropharynx and larynx * very little resistance in conducting airways of lungs (due to large cross-sectional area)

Answer 63

**Inspiratory reserve volume (IRV):** amount of air that can be inspired forcefully after normal tidal volume inspiration, ~3300mL **Expiratory reserve volume (ERV):** amount of air that can be forcefully expired after normal tidal volume expiration, ~ 1000mL **Vital Capacity (VC):** the largest volume of air that can be moved in and out during ventilation, ~4500 - 5000mL

Answer 64

by muscular effort (therefore oxygen and energy) required for ventilation

Answer 65

* muscular effort increases * happens when lung compliance decreases in diseases like pulmonary edema * chest wall compliance decreases (in spinal deformity, obesity) * obstructed airways via bronchospasm or mucous plugging * this increase can result in marked increase in o2 consumption and inadbility to maintain adequate ventilation

Answer 66

the delivery of oxygen to the cells of the body and removal of CO₂

Answer 67

**1) ventilation of the lungs** - air in and out of lungs **2) diffusion of oxygen from alveoli into capillary blood** - high [O2] to low [O2] **3) perfusion of systemic capillaries with oxygenated blood** - no exchange happening yet! **4) diffusion of oxygen from systemic capillaries into cells** - blood to interstitial fluid and into the cells

Answer 68

1) diffusion of CO2 from cells into systemic capillaries 2) perfusion of pulmonary capillary bed by venous blood 3) diffusion of CO2 into the alveoli 4) removal of CO2 from lung by ventilation

Answer 69

**1) provides a route for water loss and heat elimination** - i.e. panting **2) enhances venous return** - pressure in lungs puts pressure on vena cava to increase venous return **3) contributes to maintaining normal acid base balance** - CO₂ and pH levels regulating RR **4) enables speech, singing, and other vocalization** **5) defends against inhaled foreign material** - thanks to long trachea and nasal passageways that gives lots of SA to stop foreign material getting into the lungs **6) removes, modifies, activates or inactives various materials passing through pulmonary circulation** - interacts with kidneys and RAAS (i.e. low oxygen may cue body to think that there is low Hb and stimulate kidney to make more erythropoietin to sitmulate bone marrow to make more RBCs)

Answer 70

aka atmospheric pressure; the pressure exerted by gas molecules in air at specific altitudes sea level: 760mmHg (the sum of pressures exerted by each gas in the air at sea level)

Answer 71

describes the portion of the total pressure exerted by an individual gas **Main gases (at sea level):** oxygen (20.9%); nitrogen (78.1%), and the few other trace gases

Answer 72

20.9% (% of oxygen in the air) x barometric pressure (P_B which is 760 mmHg) = 159mmHg **note:** you have to take into consideration water vapor as it will always exert a pressure when gas enters the lungs and becomes humidifed (so partial pressure of oxygen may be lower)

Answer 73

a) temperature of the gas

Answer 74

(760 - 47) x 0.21 = 149 mmHg water vapor has to be taken into account because when gas enters the lungs, it becomes saturated with water vapor (humidified) as it passes through the upper airways

Answer 75

% of O₂ in the inspired air (20.9%)

Answer 76

(Barometric pressure - water vapor) x FIO₂ - (PaCO₂/respiratory quotient) (760 - 40) x 0.209 - (40/0.8) = 99mHg available for diffusion into blood The adequacy of ventilation to deliver O2 to the alveoli can't be measured directly, so it's estimated by measuring the removal of CO2 from the blood (which is calculated by dividing the PaCO2 by the respiratory quotient (0.8))

Answer 77

gas and blood ventilation, perfusion (your V and Q)

Answer 78

**upper portion alveoli (in the apices) more difficult to inflate!** * when upright, gravity pulls the lungs down towards the diaphragm and compresses the bases of the lungs * the alveoli in the apices have greater residual volume of gas, are bigger and less ness numerous compared to the bases * surface tension increases as alveoli become larger, so the upper portions of the lungs are more difficult to inflate (less compliant) than the smaller alveoli in the lower portions of the lungs * so during **ventilation, most of the tidal volume is distributed to the bases of lungs where compliance is greater (ventilation is better in the basesssss)**

Answer 79

**greater perfusion in the bases of the lungs!** * in a standing position, heart has to pump against gravity to perfuse pulmonary circulation but some of that BP is dissipated when trying to go against gravity * so BP at the apices is \< at the bases and ↑ BP = ↑ perfusion so the bases would be better perfused

Answer 80

the areas that are most gravity-dependent (lower lobes that are also closer to the ground)

Answer 81

depending on the gas pressure in the alveoli and pressure in the capillary bed in the venous/arterial side. If alveolar pressure \> BP in capillary, then the capillary collapses and no blood flows through (this is most likely to happen in the areas of the lungs where BP is the lowest and gas pressure is the highest) most likely to occur in the _apices_ of the lungs

Answer 82

**Zone I:** P_A \> P_a \> P_v * alveolar pressure is the greatest so capillary bed collapses and normal blood flow ceases * usually a very small part of the lung at the apex **Zone II:** P_a \> P_A \> P_v * alveolar pressure is greater than venous pressure but not arterial pressure * blood flows through this area but somewhat impeded by alvelar pressure * normally above level of left atrium **Zone III:** P_a \> Pv \> PA * arterial and venous pressures are greater than alveolar pressure * blood flow throug here not affected * base of the lung

Answer 83

V/Q aka **respiratory quotient** - the relationship between ventilation and perfusion expressed as a ratio (explains the effectiveness of gas exchange i.e. how much oxygen and CO₂ trade places) - IDEALLY 1:1 exchange but **normal is 0.8** meaning that under normal conditions, this it the amount by which perfusion exceeds ventilation (perfusion is somewhat greater than ventilation in lung bases and some blood is normally shunted to the bronchial circulation)

Answer 84

**a) V/Q = 1** - means with every breath, you will get all the air available for perfusion (ideal world where there is not anatomical dead space) **b) V/Q \< 1** - ventilation ↓, normal perfusion (seen in those with respiratory conditions characterized by bronchospasm, ex.) OR 0.8 would be normal conditions due to anatomical dead space **c) V/Q = 0** - no ventilation, normal perfusion (occlusion happening)

Answer 85

1000 mL (1L)

Answer 86

in two forms: 1) small amount dissolved in plasma (3%) - this creates the partial pressure of oxygen 2) bound to Hb (97%)

Answer 87

1) large SA (70 to 100 m²) 2) very thin (0.5 um) 3) partial pressure of oxygen molecules in alveolar gas (P_AO₂ ~100mmHg) \>\> than that in capillary blood (Pvo₂~40mmHg) so this promotes rapid diffusion down the concentration gradient 4) Oxygen is quick quick quick to get across the alveolocapillary membrane (blood remains in pulmonary capillary for ~0.75 secs but oxygen only needs 0.25 sec for its concentration to equalize across membrane so has ample time to get into blood)

Answer 88

PaO₂ (oxygen dissolved in plasma) and P_AO₂(oxygen in alveolus) equilibrate (no more pressure gradient) note that while oxygen is diffusing through the membrame, it's also hopping onto RBCs to bind with Hb until all the binding sites are full/saturated then the O₂ starts chilling in the blood until the pressures in plasma and alveoli equalize to stop diffusion

Answer 89

% of available Hb that is bound to oxygen (measured using an oximeter)

Answer 90

when Hb molecules bind with oxygen (oxyhemoblogin association) opposite/reverse is called disassociation

Answer 91

describes the relationship between partial pressure of oxygen in the blood Hb saturation; is a distinctive S-shaped curve on a graph shows us what factors increase and decrease Hb's affinity for oxygen

Answer 92

* represents oxyhemoglobin association and occurs in the lungs * This part of the curve is flat because partial pressure changes of oxygen between 60-100 mmHg do not siginificantly alter % SaO2 (allows adequate Hb saturation at a variety of altitudes)

Answer 93

* shows inadequate saturation Hb with oxygen * happens in the systemic capillary area * it represents rapid dissociation of oxygen from Hb that occurs in the tissues (oxygen diffusion into tissue cells)

Answer 94

* The PaO₂ at which Hb is 50% saturated (normally 26.6 mmHg) * a lower than normal P₅₀ means increased affinity of Hb for O₂ * a high P₅₀ means decreased affinity of Hb for O₂ * ^ this variation is dependent on availability of O₂ to the tissues

Answer 95

**Means:** Hb has decreased affinity for oxygen, facilitates increased ease of oxygen to offload from Hb into the tissue cells **Causes:** acidosis (low pH) and hypercapnia (↑ Paco₂) * increased CO2 and H+ levels decrease the affinity of Hb for oxygen * it's done to compensate for increased CO2 (you want to pick up more CO₂ to bring back to the lungs by letting go of more O₂ * **Other causes:** hyperthermia, increased 2,3-DPG, increase in exercise level (bc increased metabolic activity) mneumonic to remember the causes: _CADET, face right_ (CO₂, acidity, DPG, exercise, tempreature)

Answer 96

**Means:** Hb has increased affinity for oxygen, promoting assocaition in the lungs and inhibiting dissociation in the tissues **Causes:** alkalosis (high pH) and hypocapnia (decreased Paco₂) * in the lungs, CO₂ diffuses from blood into alveoli so blood CO₂ level is reduced and affinity of Hb for oxygen is increased so that more O₂ can be transported from lungs into the tissues * **Other causes:** hypothermia, decreased 2,3-DPG (substance normally present in erythrocytes)

Answer 97

**the shift in oxyhemoglobin dissociation curve caused by changes in CO₂ and [H+] in the blood** * as [H+] increases, oxygen affinity decreases causing release of more oxygen to the tissue (one of the most important buffer systems in the body)

Answer 98

phenomenon describe the increasing affinity of oxygen to Hb as each subsequent oxygen molecule binds to Hb

Answer 99

1) **dissolved in plasma (Pco2)** - 10% carried this way in venous blood; 5% carried this way in arterial blood 2) **as bicarbonate (HCO3-)** - in this form: 60% of CO₂ in venous blood & 90% of CO₂ in arterial blood 3) **as carbamino compounds** 30% of CO₂ in venous blood, 5% in arterial blood

Answer 100

1) CO₂ moves into the blood (from tissues) and diffuses into RBCs 2) CO₂ + H₂O become carbonic acid (with help with enzyme carbonic anhydrase) 3) carbonic acid quickly dissociates into H+ and HCO3- 4) H+ binds to Hb where it is buffered, and HCO3- moves out of RBC into the plasma

Answer 101

~6 mmHg (venous PCO2 is 46 mmHg, alveolar PCO2 is 40 mmHg) but CO2is 20x more soluble than O2 so it can quickly diffuse into the alveoli and be removed from the lung with expiration

Answer 102

**the effect that oxygen has on CO₂ transport** * oxygen binding with Hb displaces CO₂ from the blood and into the lungs * As Hb binds with O2, the amount of CO2 carried by the blood decreases resulting int release into the alveoli IN SUMMARY: **In the tissue capillaries, O2 dissociation from Hb facilitates CO2 pickup. In lungs, O2 association with Hb faciliates release of CO2 from the blood**

Answer 103

**1) Decreased chest wall compliance** - because ribs become ossified, joints stiffen = ↑ work of breathing **2) Kyphoscoliosis** - may curve vertebral colum, decrease lung volumes **3) Intercostal muscle strength decreases** **4) Elastic recoil diminishes** - possibly from loss of elastic fibers (they are able to hold more air but not expel it as easily **RESULT:** * increased lung compliance, residual volume (RV) * decreased ventilatory capacity (VC), ventilatory reserves, V/Q * no change: total lung capacity (TLC)

Answer 104

**1) Pulmonary capillary network decreases** **2) Alveoli dilate, peripheral airways lose supporting tissues** **3) SA for gas exchange decreases** **4) pH and PCO₂ don't change, but PO₂ declines** **5) decreased sensitivity of resp centers to hypoxia and hypercapnia** **6) Decreased ability to initiate immune response against infection** Max PaO₂ at sea level can be estimated by 100- (age x 0.3)

Answer 105

Alveolar complement and surfactant are altered, as well as an increase in proinflammatory cytokines - this increases risk of pulmonary disease and infection

Answer 106

**1) Decreased exercise tolerance** - due to decreased PaO₂, diminished ventilatory reserve **2) Early airway closure inhibits expiratory flow** **3) Resp muscle strength and endurance decrease** - can be enhanced by exercise (someone who is physically fit will have fewer changes in pulmonary function than sedentary individual - considerations on activity and fitness levels earlier in life)

Answer 107

1) acute or chronic 2) obstructive or restrictive 3) infectious or non-infectious

Answer 108

**1) dyspnea** **2) cough** (^these two are the most common) 3) abnormal sputum 4) hemoptysis 5) altered breathing patterns 6) hypoventilation and hyperventilation 7) cyanosis 8) clubbing 9) chest pain

Answer 109

**subjective experience of breathing discomfort** comprised of qualitatively distinct sensations in varying intensities (individualized experiences depending on many factors) * _descriptions_: * breathlessness, air hunger, SOB, labored breathing, preoccupation with breathing * _Causes:_ can be from pulmonary disease or other things like pain, crying, heart disease, trauma, and psychogenic disorders * can be transient or chronic * severity of the experience of dyspnea **_may not directly correlate_** with severity of underlying disease * stimulation of various receptors contribute to sensation of dyspnea * afferent receptors in cortex and medulla (in the brain) * mechanoreceptors in chest wall * upper airway receptors * central and peripheral chemoreceptors

Answer 110

1) nasal flaring 2) use of accessory muscles of respiration * common in children - retraction (pulling back) of supercostal or intercostal muscles

Answer 111

dyspnea that occurs during heart failure when an individual lies flat (causes abdominal contents to exert pressure on diaphragm & decreases efficiency of resp muscles)

Answer 112

occurs when ppl with pulmonary or cardiac disease wake in the night gasping for air and have to sit/stand to relieve dyspnea

Answer 113

**What is it:** protective reflex to clear airways by an explosive expiration * initiated by inhaled particles, mucus, inflammation, foreign body via stimulation of irritant receptors * BUT there are few irritant receptors in the most distal bronchi and alveoli so it's possible to have ++amounts of shit accumulating there without initiation of cough **Consists of:** inspiration ⇒ closing of glottis and vocal cords ⇒ contraction of expiratory muscles ⇒ reopening of glottis = sudden forceful expiration to remove whatever it is * effectiveness of cough depends on depth of inspiration and how narrow the airways go (that determines velocity of expiratory gas) * those who can't cough effectively = greater risk for pneumonia

Answer 114

**Acute cough:** resolves within 2-4 weeks of onset OR resolves c/ tx of underlying condition * commonly due to URTI, allergic rhinitis (hay fever/allergies), acute bronchitis, pneumonia, CHF, PE, aspiration **Chronic cough:** cough that is persistant and in those who do not smoke * commonly due to postnasal drainage syndrome, asthma, eosinophilic bronchitis, laryngeal hypersensitivity, and GERD or unknown * in those who smoke, chronic bronchitis is the most common cause of chronic cough * also due to those taking ACE inhibitors (dry tickly cough) - resolves with stopping use of drug

Answer 115

changes in amount, colour, and consistency of sputum may indicate diseease progression and effectiveness of therapy

Answer 116

**coughing up of blood or bloody secretions** * not hematemesis - blood that is vomited is dark, has acidic pH and mixed with food particles (this is from stomach not airway) * hemoptysis - usually bright red, alkaline pH, mixed with frothy sputum **Causes:** * infection or inflammation that damages the bronchi (bronchitis, bronchiectasis) or lung parenchyma (pneumonia, TB, lung abscess) * Cancer, PE, pulmonary venous stenosis **Confirmation of site of bleeding:** via Bronchoscopy and CT

Answer 117

**1) Sigh breaths:** these are normal, you're just taking an occasionally deeper breath to maintain normal lung function; happens 10-12 every hour and is usually 1.5-2x normal tidal volume **2) Kussmaul respirations (hyperpnea):** slightly increased ventilatory rate, very large tidal volumes, and no expiratory pause * Causes: strenuous exercise, metabolic acidosis * sweet acetone breath with metabolic acidosis **3) Laboured breathing:** occurs whenever there is an increased work of breathing (especially when airways are obstructed) * in _large airway obstruction_ you will typically see: slow ventilatory rate, large tidal volume, increased effort, prolonged inspiration and expiration, stridor/audible wheezing) * in _smaller airway obstruction_ (asthma, COPD) you will typically see: rapid ventilatory rate, small tidal volume, increased effort, prolonged expiration, wheezing **4) Restricted breathing:** common caused by disorders like pulmonary fibrosis that stiffen the lungs or chest wall and decrease compliance; will see small tidal volumes and tachypnea **5) Cheyne-Stokes respirations:** alternating periods of deep and shallow breathing; apnea may last 15-60 seconds and then increase ventilation volume until a peak and then decreases again to apnea (literally looks like Torsades on a graph but for breathing) * occurs in those with brain injuries due to reduced bloow flow to brainstem which slows impulses sending info to resp centers * so instead it depends on rising and falling of CO₂ levels (increased CO₂ = hyperventilation; decreased CO₂ = hypoventilation) and then it just cycles

Answer 118

**Hypoventilation:** inadequate alveolar ventilation in relation to metabolic demands * occurs when minute volume (tidal volume x RR) is reduced * caused by alterations in pulmonary mechanics or in neurologic control of breathing * **CO₂ increases (hypercapnia - over 44mmHg**) because its removal cannot keep up with its production * results in respiratory acidosis * pronounced hypoventilation can cause secondary hypoxemia, somnolence, or disorientation **Hyperventilation:** alveolar ventilation exceeding metabolic demands * lungs are removing CO₂ faster than it's being produced by cell metabolism * leads to **hypocapnia (\< 36mmHg)** * results in respiratory alkalosis * can be with severe anxiety, acute head injury, pain, and in response to hypoxemia both can be determined by ABG analysis

Answer 119

bluish discolouration of skin and mucous membranes due to increased amounts of deoxyengated or reduced Hb in the blood generally develops when 5g of Hb is desaturated regardless of [Hb]

Answer 120

**Description:** slow blood circulation in fingers and toes (best seen in nail beds) **Causes:** most often due to poor circulation resulting from intense peripheral vasoconstriction * Raynaud disease * cold environments * severe stress

Answer 121

**Descpription:** decreased arterial oxygenation (low PaO₂) - best seen in buccal mucous membranes and lips **Causes:** pulmonary diseases or pulmonary/cardiac right to left shunts

Answer 122

Late (it's not evident until severe hypoxemia is pressent so it's a pretty insensitive indication of respiratory failure) * also note that lack of cyanosis does not necesarily mean that there is normal oxygenation (think severe anemia where there is inadequate [Hb] or CO poisoning) * at the same time, polycythemia ppl can have cyanosis even when oxygenation is adequate because they have more Hb which can easily hit the 5g of Hb desaturation to be cyanotic

Answer 123

selective bulbous enlargement of the distal segment of a digit (fingers or toes), painless * severity grading from 1-5 based on extent of nail bed hypertrophy and amount of changes in nails themselves * rarely reversible * **Causes:** common diseases that disrupt normal pulmonary circulation and cause chronic hypoxemia (bronchiectasis, CF, pulmonary fibrosis, lung abscess, congenital heart disease * potentially also lung cancer without hypoxemia due to inflammatory cytokines (hypertrophic osteoarthropathy) * **Mechanism: unknown but potentially** whole megakaryocytes enter systemic circulation and become impacted in the fingertip circulation ⇒ fragments that activated to release platelet derived growth factor (PDGF) which promotes growth, vascular permeability, and monocyte/neutrophil chemotaxis ⇒ more vascular smooth muscle cells and fibroblasts ⇒ periosteal changes near nail bed

Answer 124

* pain originates in pleurae, airways, or chest wall * _Infection and inflammation of parietal pleura_: **sharp, stabbing pain (pleurodynia)** on inspiration when the pleura stretches * localized to a portion of the chest wall, creating **pleural friction rub** over the painful area * laughing, coughing makes pain worse * common with pulmonary infarction (like PE) * _Infection and inflammation of trachea/bronchi:_ **central chest pain, pronounced after coughing** (hard to differentiate from cardiac pain * _pulmonary HTN:_ **pain during exercise** (mistaken for angina) * _Excessive coughing, rib fractures, thoracic surgery:_ **chest wall/muscle pain, rib pain** * _Inflammation of costochondral junction (costochondritis)_: **chest wall pain, reproducing with pressing on sternum or ribs**

Answer 125

**Description:** Increased [CO₂] in arterial blood (Paco₂) caused by hypoventilation of alveoli **Causes:** most common due to decreased drive to breathe or inadequate ability to respond to ventilatory stimulation (most people are driven to breathe by high CO₂ levels, not low O₂ levels except in chronic lung disease patients) * 1) depression of resp center by drugs * 2) disease of medulla including infections of CNS or trauma * 3) abnormalities of spinal conducting pathways (spinal cord disruption/poliomyelitis) * 4) diseases of NMJ or of resp muscles themselves (muscular dystrophy, myasthenia gravis) * 5) thoracic cage abnormalities (chest injury, congenital deformity) * 6) large airway obstruction (tumors, sleep apnea) * 7) increased work of breathing or physiologic dead space (emphysema) **Symptoms:** dysrhythmias (electrolyte imbalances from resp acidosis); somnolence/coma due to ICP changes from high levels of arterial CO2 causing cerebral vasodilation

Answer 126

**Hypoxemia:** reduced oxygenation of arterial blood (reduce PaO₂) - caused by respiratory alterations (changes in breathing) * hypoxemia can lead to hypoxia * can occur with blood flow bypassing the lungs (due to intracardiac defects causing right-to-legt shunting or because of intrapulmonary arteriovenous malformations) * often associated with compensatory hyperventilation resultant respiratory alkalosis (decreased Paco₂ and increased pH) * S/S: cyanosis, confusion, tachycardia, edema, and decreased renal output **Hypoxia (ischemia):** reduced oxygenation of cells in tissues * tissue hypoxia can result from other abnormalities unrelated to alterations of pulm. function (like low cardiac output or cyanide poisoning)

Answer 127

V - amount of air that enters the alveoli Q - amount of blood perfusing the capillaries around the alveoli

Answer 128

**1) oxygen delivery to the alveoli** * minute ventilation (RR x tidal volume) *- is the minute ventilation adequate??* * oxygen content of inspired air (Fio₂) - *is there enough oxygen in the inspired air??* **2) Diffusion of oxygen from the alveoli into the blood** * balance between alveolar ventilation and perfusion (V/Q match) * Diffusion of oxygen across the alveolar capillary barrier *-* *is the membrane thickened or decreased SA* **3) Perfusion of pulmonary capillaries** * *is the blood flow bypassing the lungs?*

Answer 129

P_AO₂ Two factors: a) presence of adequate oxygen content of the inspired air (FiO₂ which is 21%) b) amount of alveolar minute volume (tidal volume x RR)

Answer 130

**1) Normal V/Q** * abnormal V/Q is the most common cause of hypoxemia **2) alveolocapillary membrane** * thickened membrane or decreased SA impairs diffusion of oxygen * **thickened membrane** from edema (tissue swelling), fibrosis (formation of fibrous lesion) increase the time it takes for oxygen to diffuse into the capillaries ⇒ if too slow, then blood doesn't stay there long enough for O₂ to diffuse and levels of alveolar gas and capillary blood do not have time to equilibrate * **Decreased SA:** emphysema leading to destruction of alveoli

Answer 131

abnormal distribution of ventilation and perfusion

Answer 132

* low V/Q (inadequate ventilation of well-perfused areas of the lungs) * occurs in atelectasis, asthma due to bronchoconstriction, pulmonary edema & pneumonia when alveoli are filled with fluid * when blood passes through portions of the pulmonary capillary bed that receive no ventilation, pulmonary capillaries in that area constrict causing a **right to left shunt** (no oxygen picked up and it just continues on to back to the LA) resulting in decreased systemic PaO₂ and hypoxemia

Answer 133

* poor perfusion of well-ventilated portions of the lung resulting in wasted ventilation * most commonly cause is PE that impairs blood flow to a segment of the lung

Answer 134

an area where alveoli are ventilated but not perfused

Answer 135

**Description:** defined as inadequate gas exchange such as PaO₂ ≤ 60mmHg (hypoxemic resp failure) and/or Paco₂ ≥ 50mmHg with pH ≤ 7.25 (acidotic; hypercapnic resp failure) **Causes:** direct injury to the lungs, airways, or chest wall * indirectly due to disease/injury involving another body system (brain, spinal cord, heart) * others can be in those with normal resp system OR chronic pulmonary disease * major surgeries - most common problems (atelectasis, pneumonia, PE, pulmonary edema) * risks: smokers, infection, limited cardiac reserve, neruollogical disease, chronic renal failure, chronic hepatic disease **Treatment:** * if resp failure is primarily hypercapnic, it's due to inadequate alveolar ventilation (treatment: BVM, noninvasive +ve pressure ventilation, intubation and placement on mechanical ventilation) * if resp failure is primarily hypoxemic, it's due to inadequate exchange of oxygen between alveoli and capillaries (treatment: supp oxygen) * prevention: deep breathing exercises and early ambulation to prevent atelectasis and secretion accumulation

Answer 136

* frequent turning, position changes * deep breathing exercises * early ambulantion to prevent atelectasis and accumulation of secretions * humidified oxygen * antibiotics for infection

Answer 137

* deformity, trauma, immboilization, heavy accumulation of fat * grossly obese ppl are often dyspneic on exertion or when recumbent (lots of fat around chest wall) * kyphoscoliosis distorts thoracic cage - presents with dyspnea on exertion that can progress to resp failure * MSK abnormalities (ankylosing spondylitis, pectus excavatum- depressed sternum) * Resp muscles can be impaired in neuro muscular diseases (polio, muscular dystrophy, myasthenia gravis, Guillain-Barré syndrome)

Answer 138

1. Airway Obstruction 2. Flail Chest 3. Open pneumothorax 4. Massive hemothorax 5. Tension pneumothorax 6. Cardiac tamponade 7. Myocardial contusion 8. Traumatic aortic rupture 9. Tracheal or bronchial tree injury 10. Diaphragmatic tears 11. Pulmonary contusion 12. Blast injuries

Answer 139

**Description:** fracture of several consecutive (two or more adjacent) ribs in two or more places OR fracture of the sternum and several consecutive ribs causing instbaility of the chest wall and paradoxical movement of the flail segment **S/S:** on inspiration, unstable portion moves inward while chest expands; on expiration it moves outward while chest wall falls (**paradoxical movement**) * you will also see movement of mediastinum towards opposite lung during inspiration * decreased tidal volume so increased RR to compensate (TEMPORARILY) but many progress to hypercapnic respiratory failure **Treatment:** hand on injury * SPLINT x VENTILATION * possible intubation * stabilize flail segment * load and go * Monitor for: * pulmonary contusion/cardiac contusion (which can contribute to hypoxia) * hemothorax * pneumothorax

Answer 140

**Dx:** pulmonary function testing (reduction in forced vital capacity FVC will be seen), ABG measurement (hypercapnia), radiographs **Treatment:** reversing underlying cause if possible, otherwise supportive; mechanical ventilation for severe cases

Answer 141

**Description:** presence of air or gas in pleural space due to rupture in visceral pleura (the one that surrounds the lungs) or parietal pleura and chest wall **Physiology:** air separates the visceral and parietal pleurae which destroys the negative pressure in the pleural space and disrupts eqm b/w elastic recoil forces between lung and chest wall * lung tends to recoil by collapsing toward hilum

Answer 142

**Description:** occurs unexpectedly in healthy individuals (usually men in their 20s-40s) and caused by spontaneous rupture of blebs (blister-like formations) on the visceral pleura **Physiology:** bleb rupture can occur during sleep, rest, or exercise; usually in the apices of the lungs * cause of the bleb formation is unknown but many have been found to have emphysema-like changes in their lungs even without history of smoking and no known genetic disorder * approx 10% of those ppl have family hx of pneumothorax linked to mutations in follivulin gene * can present as either open or tension pneumo **S/S:** pleural pain, tachypnea, dyspnea, potential absent/decreased breath sounds, hyperresonance to percussion on affected side Dx and Treatment same as all the other pneumos **Dx:** chest radiographs, ultrasound, CT **Treatment:** aspiration (inserting chest tube attached to a water-seal drainage system) with suction/catheter and one-way valve * those with persistent air leaks may need thoracoscope surgery, pleurdesis (substance placed into pleural space to obliterate it)

Answer 143

**Description:** pneumo that can caused by chest trauma (fractured ribs, stabbing, GSW) that tear the pleura; bleb or bulla (large vesicle) rupture like in emphysema; mechanical ventilation (overventilation, especially if it includes positive end-expiratory pressure PEEP or in pediatrics) * can present as open or tension pneumo **S/S:** pleural pain, tachypnea, dyspnea, potential absent/decreased breath sounds, hyperresonance to percussion on affected side Dx and Treatment same as all the other pneumos **Dx:** chest radiographs, ultrasound, CT **Treatment:** aspiration (inserting chest tube attached to a water-seal drainage system) with suction/catheter and one-way valve * those with persistent air leaks may need thoracoscope surgery, pleurdesis (substance placed into pleural space to obliterate it)

Answer 144

a traumatic pneumothorax that results from injury to the pleura, with air introduced into the pleural space secondary to diagnostic or therapeutic medical intervention ## Footnote **most commonly caused by transthoracic needle aspiration**

Answer 145

**Description:** aka sucking chest wound * air pressure in the pleural space = barometric pressure because air drawn into the pleural space during inspiration is forced back out during expiration * ventilation impaired and hypoxia results * if the pneumo is \>3cm in diameter it will remain open to the atmosphere equalizing intrathoracic pressure and atm pressure leading to lung collapse * if the opening is greater than diameter of trachea, air will follow path of least resistance **S/S:** proportional to size of defect; diminished breath sounds on affected side, tachypnea, tachycardic, pain, hyperresonant sound with percussion **Treatment:** * ****ensure open airway * manually splint injury until treated * asherman or 3-sided occlusive dressing * load and go * oxygen

Answer 146

**Description:** condition where air continuously leaks out of lung and into pleural space; continues to accumulate but cannot exit (like a one-way valve) resulting in increaseding intrathoracic pressure on the affected side and eventual collapse lung (+ SVC and IVC) **Pathophysiology:** air accumulates in pleural space so much to the point where it's pushing against the already recoiled lung, causing compression atelectasis * also pressing against mediastinum, compressing and displacing heart, great vessels, and trachea (**mediastinal shift**) * pressure on heart = decreased contraction and hypotension **S/S:** resp distress and cyanosis, loss of radial pulse, decreased LOC, tracheal deviation away from affected side (rare, late finding) * dyspnea, anxiety, tachypnea (small short breaths to try and inflate lungs) * JVD - due to pressure on SVC and IVC * hyperresonance if percussed (more echo-y because no lung tissue absorbing the sound) * shock with hypotension **Dx:** chest radiographs, ultrasound, CT **Treatment:** * high flow oxygen * decompress affected side or correct the cause * watch for compliance * re-ax treatment!!! covering an open pneumo and not following up on treatment can lead to a tension pneumo * LOAD AND GO * ACP skill: needle decompression

Answer 147

**Closed:** spontaneous or secondary pneumothorax **Open:** trauma

Answer 148

**Description:** the pressence of at least 1500mL of blood loss into the pleural space of the thoracic cavity **S/S:** * ventilatory insufficiency (hypoxia, agitation, anxiety, tachypnea, dyspnea) * confusion * flat neck veins - hypovolemia; rarely distended due to mediastrinal compression * breath sounds decreased and dull to percussion (blood absorbs the sound) * hypovolemic shock (from blood loss or compression of heart/great vessel) **Treatment:** * high flow oxygen * treat for shock * fluid administration - titrate to preserve a peripheral pulse by maintaining their BP around 80-90 systolic * you want to give fluids so that it's just enough to perfuse tissues but not too much tot he point where more fluid is being pushed into the same place where the blood is pooling in to make the problem worse) * monitor for tension hemopneumothorax

Answer 149

**Description:** condition where there is fluid/blood that fills up in the pericardial sac **Signs/Symptoms:** Beck's triad * _JVD:_ backed up blood due to heart not pumping blood out * _Hypotension:_ can't build up pressure because heart cannot stretch out so cannot pump out (Frank Starling's Law) * _Muffled Heart Sounds:_ sounds like "underwater", sound has to travel through fluid * **Paradoxical pulse** - an exaggeration of the normal variation of pulse strength on inhalation, where BP decreases (on inhale) and increases (on exhale) * in cardiac tamponade, there is decreased CO and the drop is so exaggerated that the radial pulse disappears on inspiration * Equal breath sounds (no fluid in lungs, this is a problem with fluid in the heart) **Treatment:** * high flow oxygen * load and go * treat for shock * fluid administration * titrate to peripheral pulse (80-90mmHg) * monitor and treat dysrhythmias - V-tach, V-fib, asystole * minitor for: hemothorax, pneumothorax

Answer 150

**Description:** bruise to the heart muscle; the most common cardiac injury and typically due to blunt anterior chest injury * includes a number of dx including MI, dysrhythmias, acute heart failure, valvular injury or cardiac rupture * usually injury tot he RA and RV * can be acute or develop over time **S/S:** same as MI (may mimic cardiac ischemia) * chest pain (usually sharp, retrosternal chest pain) * dysrhythmias - PVCs, maybe STEMIs, elevation in II, III, aVF, V1 and aVR * cardiogenic shock (rare) **Dx:** perform 12-lead ECG **Treatment:** treat as cardiac tamponade (high flow O2, treat for shock, fluid titration to 80-90 mmHg, monitor for dysrhythmias and hemothorax, pneumothorax, LOAD AND GO)

Answer 151

**Description:** tear in the aorta wall; most common cause of IMMEDIATE deaath **Cause:** MVCs, fall from heights (80% die immediately, most die on scene) - MOI with rapid deceleration * situations where they have stopped but the heart and internal structures kept going, and got ruptured/ripped out of their attachment points) **Pathophysiology:** 85% occur at the ligamentum arteriosum or the branch off point of left subclavian artery **S/S:** Asymmetric BP (HTN in UE, hypotension in LE but this is rare), widened pulse pressure, pain in chest or scapula, no obvious signs of chest trauma **Dx:** SCENE OBSERVATIONS and history

Answer 152

**Description:** result in a partial/complete disruption of the airway, usually localized within 2cm of the carina in up to 80% of cases **S/Sx:** subQ emphysema (chest, face neck), dyspnea, deformed chest **Dx:** usually cannot be dx in the field **Treatment:** ensure adequate airway (Cuffed ET tube past site of injury) * Monitor for: pneumothorax, hemothorax

Answer 153

**Description:** tears in the diaphragm; may allow herniation of abdo organs and structures into thoracic cavity * more common on the left because liver protects the right hemidiaphragm **Causes:** severe blow to the abdomen, sudden increase in intraabdominal pressure (like seat belt or kick to abdomen); cause also be from penetrating trauma these tend to be small (and usually it's blunt force trauma) **S/S:** diminished breath sounds, bowel sounds ausculated in chest (rare); abdomen appears scaphoid (sunken); respiratory distress **Tx:** ensure adequate airway, ventilation, high flow oxygen, treat for shock, transport!

Answer 154

**Description:** hemorrhaging into the lung tissue from blunt force trauma or penetrating trauma; very common chest injury (especially with flail or multiple rib fractures in elderly) * may cause marked hypoxemia seoncdary to bleeding into alveoli and interstitium of th lung * kids have more flexible bones so even with the same MOIs, they have pulmonary contusions without rib fractures **S/S:** hours to develop (delayed finding, or during secondary transport); frequently with fractures ribs **Treatment:** assisted ventilation (if indicated), oxygen, transport, IV insertion

Answer 155

**Description:** those that result from explosion injuries and can have a myriad of effects on the body systems; can also present with penetrating trauma as a result of the blast * difficult to assess in the field and may be lethal if not recognized **Stages of the blast: note that not every blast has all stages** **1) Primary** - initial air blast, caused solely by the direct effect of blast overpressure on tissue * almost always affects air-filled structures (lungs, ears, GI tract) because air is easily compressible * may also have pulmonary contusions, pneumos, tension pneumo, arterial gas embolus **2) Secondary:** when patient is struck by material that's propelled by the blast through the air (shrapnel) **3) Tertiary:** body is thrown by the pressure of the blast/wave; pt makes impacts with the ground or other object (getting thrown) **4) Quaternary:** burns from exploration, radiation from radiological, or respiratory injuries from smoke inhalation **5) Quinary:** hyperinflammatory state caused by chemicals used in bombs (or any reaction that the body has as a result of the trauma itself)

Answer 156

* DO NOT REMOVE * stabilize object * monitor for: * tension pneumothorax * hemothorax * cardiac tamponade

Answer 157

**Description:** severe compression injury to the chest (i.e. steering wheel, conveyer belt, heavy object); not actually asphyxia * sudden compression of the heart and mediastinum transmits force to the capillaries of the neck and head * ruptures capillaries **S/S:** looks strangulated, cyanosis (above crush) and swelling of head and neck, lips/tongue swollen and eyes (conjunctival) hemorrhage * skin below the level of the crush injury will remain pink and notmal in appearance unless there are other associated injuries **Tx:** ensuring an airway, treat for shock

Answer 158

* fractures to sternum * caused by significant blunt trauma to the anterior chest (can also be caused by CPR in the elderly) * S/S: signs of fracture on palpation * you can presume that myocardial contusion is present

Answer 159

* most frequent injury to the chest (most commonly seen in lateral aspect of rib 3-8) * S/S: pain, dyspnea, fracture evident on palpation * monitor for pneumothorax and hemothorax

Answer 160

**Causes:** fracture ribs; others: blunt/penetrating trauma **Symptoms:** pleuritic chest pain (some air may leak out but not lifet hreatening unless progresses to tension pneumo) * dyspnea (does not acutely compromise breathing though) * decreased breath sounds on affected side * tympany if percussed (sounds like a drum, more hollow sound but there is still some lung tissue to absorb some of the sounds) **Treatment:** monitor for tension pneumo; self-heals

Answer 161

less 1) alveolar pressure can be lowered below atmospheric pressure (by increasing chest cavity size, mechanics of breathing) 2) Atmospheric pressure can be increased above normal resting alveolar pressure (BVM, CPAP, any ventilation that we do as paramedics)

Answer 162

Not sginificantly, its purpose is more to raise PaO₂

Answer 163

rapid recognition and intervention (with possible surgical intervention)

Answer 164

**Blunt:** rapid deceleration, shearing forces, crush injuries * **1) Direct compression:** direct impact to the area ⇒ fracture of solid organs, blow out of hollow organs * **2) Deceleration forces:** quick speed changes ⇒ shearing of organs and blood vessels

Answer 165

* direct trauma to organ and vasculature * energy becomes trnasmitted from mass and velocity

Answer 166

* inadequate oxygen delivery **Causes:** * hypovolemia - no blood to circulate around * **ventilation/perfusion (V/Q) mismatch** - if you don't have blood, you can ventilate as much as you want but there will be no perfusion to the tissue * **pleural pressure changes** - ex. pneumothorax; individual will not be able to create same negative pressure as a healthy individual * **pump failure** - heart failure (heart not pumping = no blood circulation)

Answer 167

smooth muscle (no skeletal muscle)

Answer 168

**Description:** presence of fluid in the pleural space **Causes:** source of fluid usually from blood vessels/lymphatic vessels beneath pleural space; also abscess or other lesion that may drain into pleural space **Types:** from intact blood vessels: * _transudative_ (watery fluid → due to CV disease like heart failure causing increased pulmonary capillary pressure; liver or kidney disease or low protein count like lack of albumin so no pressure to keep fluid in vasculature) * _exudative_ (high [WBC] and plasma proteins → due to infection, inflammation, malignancy) * presence of pus (_empyema_) - due to pulmonary infections (pneumonia); lung abscesses; infected wounds; (covered in another flashcard) * blood (_hemothorax_) - due to traumatic injury, surgery, rupture, malignancy damaging blood vessels * chyle (_chylothorax_) - milky fluid containing lymph and fat droplets moving from lymphatic vessels into pleural space, typically should drain from lacteals of small intestine into lymphatic system during digestion → due to traumatic injury, infection, or disorder that dsirupts lymphatic transport **Pathophysiology:** small collections of fluid is fine, no dysfunction (most will be removed by lymphatic system once underlying condition resolved) **S/S:** larger effusions cause dyspnea, compression atelectasis with impaired ventilation, and pleural pain are common; mediastinal shift and CV manifestations * decreased breath sounds and dull percussion on affected side; pleural friction rub heard over areas of inflamed pleura **Diagnosis:** chest X-ray **Treatment:** thoracocentesis (needle aspiration) for Sx relief * if large, drainage done with placing a chest tube and surgery to prevent recurrence of the effusion

Answer 169

**Description:** infected pleural effusion characterized by the presence of pus in pleural space, develops when pulmonary lymphatics become blocked leading to an outpout of contaminated lymphatci fluid into the pleural space **Prevalence:** most common in older adults and children **Causes:** usually complication of pneumonia, surgery, trauma, or bronchial obstruction from a tumor * *S. aureus, E. coli,* anaerobic bacteria, and *Klebsiella pneumoniae* **S/S:** cyanosis, fever, tachycardia, cough, and pleural pain * decreased breath sounds directly over empyema **Diagnosis:** chest radiographs, thoracentesis, sputum culture **Treatment:** antimicrobials; draining pleural space with chest tube; ultrasound-guided pleural drainage, instillation of fibrinolytic agents, DNase into pleural space, surgical debridement (if severe)

Answer 170

* characterized by **decreased compliance (stiffness) of lung tissue** (meaning more effort to expand lungs during inspiration, increased work of breathing) * **decrease in total volume of air that the lungs are able to hold,** often due to decreased elastricity of lungs themselves or caused by a problem related to expansion of chest wall during inspiration * these people have dyspnea, ↑ RR, ↓ tidal volume, ↓ FVC * can cause V/Q mismatch, affect alveolocapillary membrane = ↓ oxygen diffusion resulting in hypoxemia * Common conditions: * aspiration * atelectasis * bronchiectasis * bronchiolitis * pulmonary fibrosis * inhalation disorders * pneumoconiosis * allergic alveoliis * pulmonary edema * acute respiratory distress syndrome (ARDS)

Answer 171

**Description:** the passage of fluid and solid particles in to the lung **Risk/Predisposing factors:** tends to occur in those with impaired normal swallowing mechanism and cough reflex * predisposing factors: alterd LOC (from substance use, sedation, anesthesia) * seizure disorders * stroke, neuromuscular disorders causing dysphagia * feeding through NG tube **Pathophysiology:** * R lung (particulary R lower lobe) is more susceptible to apiration than L length because R bronchus is anatomically straighter * serious consequences with aspirting on _large food particles or gastric fluid pH \<2.5_ (can obstruct bronchus leading to bronchial inflammation and airway collapse distal to obstruction) * may also lead to recurrent infection and bronchiectasis (permanent dilation of the bronchus) * _gastric fluid_ may cause severe pneumonitis * acidic fluid can damage alveolocapillary membrane (which allows plasma and blood cells to move into alveoli = hemorrhagic pneumonitis) * _aspiration of oral or pharyngeal secretions:_ can lead to aspiration pneumonia * _tracheal intubation:_ can lead to aspiration and bacterial pneumonia * Bronchial damage includes inflammation, loss of ciliary function, and bronchospasm * lung becomes stiff and noncompliant due to disrupted surfactant production = edema and lung collapse → leads to hypoventilation due to less SA for gas exchange, and maybe hypotension **Signs/Symptoms:** sudden onset of choking, uncontrolled cough with/without vomiting, fever, dyspnea, and wheezing * some may have no acute symptoms but recurrent lung infections, chronic cough, persistent wheezing over months/years **Treatment:** preventative measures (using semirecumbent position - sitting half upright; surveillance of enteral feeding, use of promotility agents to stimulate smooth muscle contractions, avoid excessive sedation) * NG tubes may prevent aspiration but may also cause regurgitation as tube is being placed (so beware) * for _aspiration pneumonitis_: oxygen and ventilation with PEEP + corticosteroids * fluid restriction to decreased blood volume and minimize pulmonary edema * antimicrobials if bacterial pneumonia develops as a complication

Answer 172

**Description:** collapse of lung tissue; 3 types * **1) Compression atelectasis:** caused by external pressure exerted by tumor, fluid, air in pleural space or by abdominal distention pressing on a portion of lung, causing alveoli to collapse * **2) Absorption atelectasis:** results from removal of air from obstructed or hypoventilated alveoli (gradually absorbed out and into the blood, and then the lungs collapse) or from inhalation of concentrated oxygen (replacing nitrogen) or anesthetic agents * **3) Surfactant impairment (adhesive) atelectasis:** results from decreased production or inactivation of surfactant (can't reduce surface tension can't prevent lung collapse after expiration) → can occur due to premature birth, aspiration, ARDS, anesthesia induction, or mechanical ventilation **Pathophsyiology:** tends to occur after surgery especially in those who have been given general anesthesia (post-op ppl often in pain, breathe shallowly, don't wanna move and thus producing viscous secretions that tend to pool in dependent portions of the lungs i.e. thoracic and upper abdominal surgery * atelectasis causes ↑ shunt, ↓ compliance, V/Q mismatch may lead to perioperative hypoxemia **S/S:** dyspnea, cough, fever, leukocytosis (Easily mistaken with infection) **Treatment:** prevention of post-op atelectasis * deep breathing exercises - promotes ciliary clearance of secretions; stabilizes alveoli by redistributing surfactant, promotes collateral ventilation through pores of Kohn (promotes expansion of collapse alveoli) * frequent position changes * early ambulation * Post-op noninvasive positive pressure ventilation (NIPPV) in high risk individuals

Answer 173

**Description:** persistent abnormal dilation of the bronchi **Causes:** potentially genetic predisposition or defect in host defense; usually occurs with other resp conditions associated with chronic bronchial inflammation (airway obstruction with mucous plugs, atelectasis, foreign body aspiration, infection, CF, TB, congenital weakness of bronchial walls, immunocompromised) * can be idiopathic (no known cause) * could be associated with rheumatologica disease, inflammatory bowel disease, immunodeficiency syndromes (AIDS) **Pathophysiology:** chronic inflammation of bronchi leads to destruction of elastic and muscular components of their walls, obstruction of bronchial lumen, traction from adjacent fibrosis, and permanent dilation **S/S:** _chronic productive cough_ that may stem from childhood illness/infection * often with recurrent lower resp tract infections * expectoration of big amounts of purulent (pus) sputum that's super smelly * hemoptysis * clubbing of fingers (due to chronic hypoxemia) * decreased FVC and expiratory flow rates * hypoxemia eventually leads to cor pulmonae **Dx:** CT **Treatment:** sputum culture, antibiotics anti-inflammatory drugs, bronchodilators, chest physio, oxygen

Answer 174

**Description:** diffuse, inflammatory obstruction of small airways or bronchioles occurring most commonly in children (in adults, usually happens with chronic bronchitis or health ppl with upper/lower _viral_ RTI or inhalation of toxic gases), or unknown cause * serious complication of stemi cell and lung transplantation - can progress to _bronchiolitis obliterans_ (fibrotic process that occludes airways and cause permanent scarring of the lungs) **S/S:** * ****rapid ventilatory rate * marked use of accessory muscles * low grade fever * dry, nonproductive cough * hyperinflated chest * can cause decreased V/Q lead to hypoxemia **Diagnosis:** spirometry and bronchoscopy with biopsy **Treatment:** appropriate antibiotics, corticosteroids, immunosuppressive agents, chest physical therapy (humidified air, coughing and deep breahing exercises, postural draining)

Answer 175

complication of bronchiolities obliterans in which alveoli and bronchioles become filled with plugs of connective tissue

Answer 176

**Description:** excessive amount of fibrous or connective tissue in the lung **Causes:** * by formation of scar tissue after active pulmonary disease (ARDS, TB, etc.) * autoimmune disorders (RA, progressive systemic sclerosis, sarcoidosis) * inhalation of harmful substances (eg coal dust, asbestos) * if unknown - **idiopathic pulmonary fibrosis (IPF)** **Pathophysiology:** chronic inflammation leads to fibrosis and causes a marked loss of lung compliance * lungs become stiff, difficult to ventilate, and diffusing capacity of alveolocapillary membrane may decrease causing hypoxemia * poor prognosis for diffuse pulmonary fibrosis **S/S:** _increasing dyspnea on exertion_ (primary sx); diffuse inspiratory crackles **Dx:** pulmonary function testing (decreased FVC), X-rats, CT, biopsy **Treatment:** oxygen, corticosteroids, antifibrotic and cytotoxic drugs, lung transplantation

Answer 177

**Description:** PF with no known cause; the most common idiopathic interstitial lung disorder and characterized by chronic inflammation **Prevalence:** M \> W, most after 60 y.o. **Pathophysiology:** results from multiple injuries at different lung sites with aberrant healing responses to alveolar epithelial cell injury (probably happens in response to environment x genetic factors) ⇒ leads to fibroproliferation of interstitial lung tissue around alveoli, causing decreased oxygen diffusion across membrane and hypoxemia * disease progression goes from decreased lung compliance to increased WOB, decreased tidal volume, resultant hypoventilation with hypercapnia **S/S:** similar sx and tx as normal PF

Answer 178

* Exposure to toxic gases * pneumoconiosis * allergic alveolitis

Answer 179

**Common toxic gases:** smoke, ammonia, hydrogen chloride, sulfur dioxide, chlorine, phosgene, and nitrogen dioxide * inhalation injuries can result from any of these as well as household/industrial combustants, heat, and smoke particles **Effects:** * damage to airway epithelium * promote mucus secretion, inflammation, mucosal edema, ciliary damage, pulmonary edema, and surfactant inactivation * acute toxic inhalation frequently complicated by ARDS and pneumonia **Signs/Symptoms:** burning of eyes, nose, throat; coughing; chest tightness; dyspnea * hypoxemia **Treatment:** oxygen, mechanical ventilation with PEEP, supporting CV system; sometimes corticosteroids

Answer 180

* Prolonged exposure to high concentrations of supplemental oxygen * **Mechanism/Effects:** * due to severe inflammatory response mediated by oxygen free radicals * damage to alveolocapillary membrane ⇒ disruption in surfactant production, produces interstitial and alveolar edema, and reduction in lung compliance * in infants, can lead to _bronchopulmonary dysplasia_ (severe scarring of lung) * **Treatment:** ventilatory support, reduction of inspired [O₂] \<60% as soon as tolerated

Answer 181

**Description:** any change in the lung caused by inhalation of inorganic dust particles, usually from workplace **Common causes:** silica, asbestos, coal (Others: talc, fiberglass, clays, mica, slate, cement, metals (cadmium, beryllium, tungsten, cobalt, aluminum, iron) **Patho:** often occurs after years of exposure to offending dust with progressive fibrosis of lung tissue * particles depositing in the lugns causes release of proinflammatory cytokines ⇒ leads to chronic inflammation with scarring of alveolocapillary membrane ⇒ pulmonary fibrosis and progressive pulmonary deterioration **S/S:** cough, chronic sputum production, dyspnea, decreased lung volmes, and hypoxemia **Dx:** requires hx of exposure to particles (occupational history); X-ray or CT **Treatment:** usually palliative; prevent further exposure and improve working conditions; pulmonary rehab; management of hypoxemia and bronchospasm

Answer 182

**Description:** aka extrinsic allergic alveolitis; it's an allergic inflammatory disease of the lungs caused by inhalation of organic particles of fumes * can be acute, subacute, or chronic (see symptoms below) **Causes:** many allergins (grains, silage, bird poop, wood dust, cork dust, animal pelts, coffee beans, fish meal, mushroom compose, and molds on sugarcane/barley/straw **Pathophysiology:** lung inflammation is a hypersensitivity response that occurs after repeated, prolonged exposure to allergen causing pneumonitis * lymphocytes and inflammatory cells infiltrate interstitial lung tissue which cause release of automimmune and inflammatory cytokines **S/S:** Acute causes fever, cough, chills a few hours after exposure; tachypnea and inspiratory cracks on lower lung lobes * Continued exposure = chronic, pulmonary fibrosis develops (also dyspnea, fatigue, weight loss) **Diagnosis:** hx taking of allergen exposure; serum antibody test; chest x-ray; bronchoalveolar lavage; CT; lung biopsy **Treatment:** remove allergen; corticosteroids

Answer 183

via lymphatic draining and balancing between capillary hydrostatic pressure, capillary oncotic pressure, and capillary permeability surfactant lining the alveoli also repels water, keeping fluid from entering the alveoli

Answer 184

**Description:** excess water in the lung **Predisposing factors:** heart disease, ARDS, inhalation of toxic gases **Pathophysiology:** * 1) most common cause: _L sided heart disease_ → when LV fails, filling pressures on this side of the heart increase causing an increase in pulmonary capillary hydrostatic pressure → when hydrostatic pressure \> oncotic pressure in capillaries, fluid moves from capillay into interstitial space (between alveoli and capillary) * when lymphatic system cannot keep up with removing fluid, pulmonary edema occurs * 2) second cause: _capillary injury that increases capillary permeability_ (ARDS, inhalation of toxic gases) → capillary injury and inflammation causes water and plasma proteins to leak out of capillary and move into interstitial space (↑ interstitial oncotic pressure) → water moves out of capillary and into lung * 3) another cause: _obstruction of lymphatic system by tumors/fibrotic tissue; by increased systemic venous pressure_ **S/s:** dyspnea, hypoxemia, increased WOB; inspiratory crackles (rales), dullness to percussion over lung bases * if severe edema: pink frothy sputum, hypoxemia worsens, hypoventilation with hypercapnia may develop **Treatment:** depends on cause * if due to ↑ hydrostatic pressure due to HF: improving cardiac output (diuretics, vasodilators, improving cardac muscle contraction) & oxygen * If due to ↑ capillary permeability resulting from injury: removing offending agent, support and maintain adequate ventilation and circulation & oxygen * potentiall mechanical ventilation is

Answer 185

**Description:** represent a spectrum of acute lung inflammation and diffuse alveolocapillary injury * Defined as: * 1) acute onset of bilateral infiltrates on chest radiograph * 2) low raito of PaO₂ to FIO₂ under positive airway pressure * 3) not derived from hydrostatic pulmonary edema **Predisposing factors/causes:** genetic factors, sepsis, multiple trauma * other causes: pneumonia, burns, aspiration, cardiopulmonary bypass surgery, pancreatitis, blood transfusions, drug OD, inhalation of smoke/noxious gases, fat emobli, high supplemental [O₂}, radiation therapy, DIC * high mortality rate * \>30% of ICU cases are complicated by ARDS **Pathophysiology:** causes acute injury to alveolocapillary membrane ⇒ massive pulmonary infection, increased capillary permeability, severe pulmonary edema, shunting, V/Q mismatch, and hypoxemia * ARDS can occur directly (gastric acids, toxic gases) or indirectly (sepsis, trauma, etc.); progresses through 3 overlapping phases: * **1) Exudative phase (within 72 hours):** neutrophils and other cells release inflammatory cytokines which damage alveolocapillary membrane + ↑ capillary permeability ⇒ fluid and shit leaks out from capillary to pulmonary interstitium and flood alveoli (hemorrhagic exudate) * surfactant inactivated * causes pulmonary edema and hemorrhage ⇒ decreased lung compliance and imapred alveolar ventilation * inflammatory cytokines also cause pulmonary vasoconstriction = V/Q mismatch * **2) Proliferative phase (within 4-21 days):** pulmonary edema resolves; type II pneumocytes, fibroblasts, and myofibroblats proliferate * exudate becomes a cellular granulation and looks like hyaline membranes * progressive hypoxemia * **3) Fibrotic phase (within 14-21 days):** remodeling and fibrosis of lung tissue * fibrosis progressively obliterates alveoli, resp bronchioles, and interstitium leading to ↓ in FRC and continuing V/Q mismatch with severe RL shunt * acute respiratory failure **Clinical Manifestations:** progressive from 1-6 1. dyspnea and hypoxemia c/ poor response to supplemental oxygen 2. hyperventilation and resp alkalosis 3. ↓ tissue perfusion, metabolic acidosis, and organ dysfunction 4. ↑ WOB, ↓ tidal volume, hypoventilation 5. hypercapnia, resp acidosis, worsening hypoxemia 6. resp failure, ↓CO, hypotension, 💀 **Diagnosis:** hx of lung injury, physical exam, blood gas analysis, radiologic exam, measurement of serum biomarkers **Treatment:** EARLY DETECTION, supportive therapy, preventing complications * supportive therapy * maintaining adequate oxygenation and ventilation while preventing infection

Answer 186

* characterized by airway obstruction that is worse with expiration * more force (use of accessory muscles of expiration) needed to expire a given volume of air and empyting lungs is slowed * unifying symptom: **dyspnea** * unifying sign: **wheezing** * ppl have increased WOB, V/Q mismatch, decreased forced expiratory volume in 1 sec (FEV₁) * most common diseases: * asthma * chronic bronchitis * emphysema * last two^ often called together as COPD

Answer 187

**Description:** chronic inflammatory disorder of the bronchial mucosa causing bronchial hyperresponsiveness, airway constriciton, REVERSIBLE variations in airflow obstruction **Prevalence:** all ages **Prediposing factors/causes:** familial disorder (genetic component) * other risk factors: age of onset of disease, levels of allergen exposure, urban residence, exposure to indoor and outdoor air pollution, tobacco smoke, recurrent respiratory tract viral infections, GERD, obesity * high level of exposure to allergens during childhood increases risk for asthma but also decreased exposure to certain infectious organisms creates an immunological imbalance favouring development of allergies and asthma (**hygiene hypothesis**) **Pathophysiology: *i****t's all really about air going in but cannot be pushed out due to swelling so we really need to use accessory muscles to push out leading to wheezes* * airway exposure to antigen intiates innate and adaptive immune response in sensitized ppl * bronchial mucosa gets inflamed, airways are hyperresponsive (thanks to our lymphocyte and leukocyte friends) * there is an immediate (early) and late (delayed) response * **early asthmatic response:** APCs present antigen to T-helper cells → differerentiate into Th2 cells releasing inflammatory cytokines and ILs that activate B lymphocytes and eosinophils →IgE made! & bind to mast cells → more stuff released from mast cell (inflammatory mediators like histamine, bradykinin, PAF, prostglandins) → vasodilation, increased capillary permeability, mucosal edema, bronchospasm, mucus secretion → airways narrowed and airflow obstructed * **late response:** 4-8 hours after early response; eosinophils, neutrophils and lymphocytes cause a latent release of inflammatory mediators again causing bronchospasm, edema, and mucus secretion * leukotrienes cause prolonged smooth muscle contraction * eosinophils cause direct tissue injury with fibroblast proliferation and airway scarring * impaired mucociliary function + mucus accumulation and cell debris forming plugs in the airway * untreated inflammation can lead to LT damage (irreverisble) - i.e. airway remodeling * airway obstruction increases resistance to airflow, decreases flow rates (esp expiratory flow) → leads to air trapping, hyperinflation distal to obstructions and increased WOB * airflow isn't distributed evenly in the lungs due to varying resistance and continued air trapping increases intrapleural and alveolar gas pressures, causes decreased perfusion of alveoli (so your V/Q is shit and all over the place in different parts of the lung) * lung receptors notice increased lung volume and obstruction, so it triggers hyperventilation (this results in early hypoxemia without CO2 retention) → hypoxemia further increases hyperventilation through stimulation of resp center (PacO2 decreases, H increases = resp alkalosis) * too much **air trapping** eventually leads to lungs/thorax being hyperexpanded, resp muscles are now also very stretched (so decreased tidal volume with increasing CO2 retension and resp acidosis) = resp failure **Clinical Manifestations:** asymptomatic between attacks w/ normal pulmonary function tests * During an attack: starts with chest constriction, expiratory wheezing, dyspnea, nonproductive coughing, prolonged expiration, tachycardia, and tachypnea * severe attacks: accessory muscle use, wheezing hear on inspiration and expiration * pulsus paradoxus (decrease in SBP during inspiration of more than 10mmHg) * hypoxemia with associated resp alkalosis * status asthmaticus (if bronchospasm not reversed and becomes severe) - hypoxemia worsens, expiratory flows and volumes decrease further and ventilation decreases (acidosis develops) - life threatening * silent chest (no audible air mvoement ) and PaCO2 \>70mmHg = you're fucking dead soon so you better get epi because ventolin isn't going anywhere **Dx:** peak flor measurements, ABG, history of allergies and recurrent episodes of wheezing, dyspnea, cough or exercise intolerance; spirometry * during acute attacks: assess for triggers, hypoxemia and resp alkalosis that may turn into hypercapnia with resp acidosis = ventilate **Treatment:** oxygen, inhaled beta-agonist bronchodilators; oral corticosteroids (epi) * Management of asthma: avoid triggers, use of peak flow meter, short-acting beta-agonist inhalers, anti-inflammatory meds and inhaled corticosteroids * if corticosteroids don't work, luekotriene antagonists * if more severe, long acting beta agonists to control persistent bronchospasm * be mindful when bagging these patients, you might push a lot of air in that won't come out leading to potential damage and pneumos

Answer 188

The hygiene hypothesis proposes that childhood exposure to germs and certain infections helps the immune system develop. This teaches the body to differentiate harmless substances from the harmful substances that trigger asthma. In theory, exposure to certain germs teaches the immune system not to overreact. When children are exposed to highly hygienic environment and receive vaccinations to prevent certain infections, this may increase their chances of developing infections/diseases

Answer 189

respiratory distress AND suspected bronchoconstriction

Answer 190

Bronchodilator - opens up airways

Answer 191

Epinephrine is a chemical that narrows blood vessels and opens airways in the lungs. These effects can reverse severe low BP wheezing, severe skin itching, hives, and other symptoms of an allergic reaction

Answer 192

**Description:** common preventable and treatable disease characterized by persistent airflow limitation that is usually progressive and associated with enhanced chronic inflammatory response in airways and lung to noxious particles/gases **Prevalence:** the most common chronic lung disease in he world, 4th leading cause of death in US and globally * higher in women throughout lifespan **Risk factors:** tobacco smoke (cig, pipe, cigar, environmental tobacco smoke), occupational dusts and chemicals (vapors, irritants, fumes), indoor air pollution from biomass fuel (in cooking and hearing), outdoor air pollution, and anything really that affects growth during gestation and childhood (low birth weight, resp tract infections) * inherited mutation of a₁-antitrypsin gene results in development of COPD at early age even without smoking **Conditions under COPD:** chronic bronchitis and emphysema

Answer 193

**Description:** hypersecretion of mucus and chronic productive cough for at least 3 months of the year (usually winter) for at least 2 consecutive years **Pathophysiology:** * inspired irritants result in airway inflammation with neutrophils, macrophages, and lymphocytes into the bronchial wall * inflammation leads to bronchial edema, more and bigger mucous glands and goblet cells in airway epithelium, smooth muscle hypertrophy with fibrosis, and airway narrowing * thick and strong ass mucus produced and can't be cleared due to impaired ciliary function * lung defences become less effective = high risk of pulm infection and injury (bacteria collecting here) * leads to airway osbtruction (hypertrophied smooth muscle constricts especially on expiration), air trapping (airways collapse early in expiration; expands thorax and resp muscles stretched so mechanical disadvantage), loss of SA for gas exchange, frequent exacerbations (infections, bronchospasms) → leads to cough, dyspnea, decreased tidal volume, hypoxemia, hypercapnia, cor pulmonale * obstruction causes V/Q mismatch with hypoxemia * process starts with affecting larger bronchi and then eventually all airways **S/S:** productive cough, dyspnea (late), intermittent wheezing, occasional barrel chest, always prolonged expiration, cyanosis, chronic hypoventilation, polycythemia, cor pulmonale (RHF); history of smoking * also note these people don't use their PaCO₂ to stimulate breathing changes cause it's chronically elevated * note that chronic bronchitis and emphysema are collectively called COPD so some of the stuff here may also overlap with emphysema **Diagnosis:** history of symptoms, physical exam, chest imaging, pulmonary function tests (FEV₁ /FVC ratio \<0.7), blood gas analysis **Treatment:** stop smoking to prevent further disease progression * bronchodilators, mucolytics (expectorants), antioxidants, anti-inflammatory drugs ⇒ controls cough and reduces dyspnea * chest physicala therapy (deep breathing, postural draining) * during acute exacerbations (infection and bronchospasm): antibiotics, steroids, potentially mech. ventilation * last resort: chronic use of oral steroids * home oxygen therapy (those with severe hypoxemia)

Answer 194

**Description:** abonrmal permanent enlarge of gas exchange airways (acini) accompanied by destruction of alveolar walls without obvious fibrosis * Obstruction results in changes in lung tissues * major mechanism of airflow limitation: **loss of elastic recoil** **Causes:** * _primary emphysema_ (1-3% cases of emphysema) commonly linked to an inherited deficiency of the enzyme, α₁- antitrypsin which typically inhibits action of many proteolytic enzymes so a deficiency increases likelihood of developing emphysema due to proteolysis in lung tissues not inhibited * _secondary emphysema_ major cause is inhalation of **cigarette smoke** (contributing factors: air pollution, occupational exposures, and childhood respiratory tract infections) **Pathophysiology:** characterized by destruction of alveoli through breakdown of elastin within septa by an imbalance btween proteases and antiproteases, oxidative stress, and apoptosis of lung structural cells * leads to creation of large air spaces within the lung parenchyma (called bullae) and air spaces adjacent to pleurae (blebs) → these are not effective in gas exchange leading to ++ V/Q mismatch and hypoxemia * expiration becomes difficult due to loss of elastic recoil reducing the volume of air that can be expired passively & air trapped in lungs * Air trapping - causes hyperexpansion of the chest, muscle of respiration now at a mechanical disadvantage (↑ WOB and eventually develop hypoventilatio and hypercapnia) * persistent inflammation in airways can result in hyperreactvitiy of bronchi with bronconstriction * destruction of alveolar walls and pulmonary capillary cause pulmonary artery hypertension and cor pulmonale **Clinical Manifestations:** productive cough (with infection); dyspnea, wheezing, history of smoking * classic sign: barrel chested * prolonged expiration * chronic hypoventilation, polycythemia, cor pulmonale (all these late in course) **Diagnosis:** based on pulmonary function measures * pulmonary function tests indicate obstruction to gas flow during expiration with marked decreased in FEV₁ **Treatment:** stop smoking; pharmacologic tx depends on clinical severity (mild, mod, severe, or very severe) * Bronchodilators (inhaled anticholinergic agents and beta agonists) * inhaled corticosteroids for severe COPD (but try to avoid this for LT use) * pulmonary rehab, improved nutrition, breathing techniques * home oxygen - for progressive pulmonary dysfunction with hypoxemia and hypercapnia * phosphodiesterase E4 (PDE4) inhibitor and mucolytics

Answer 195

False. They are the MOST common cause

Answer 196

very young, very old, impaired immunity ppl

Answer 197

**Description:** acute infection or inflammation of the airways or bronchi; usually self-limiting **Causes:** virus (most common) **Clinical Manifestations:** similar to pneumonia (fever, cough, chills, malaise) * viral bronchitis: nonproductive cough often occurs in paroxysms (acute spasms), aggracated by cold, dry or dusty air; sometimes purulent sputum; chest pain - from coughing effort **Dx:** physical exam will not show signs of pulmonary consolidation (lung full of mucus), chest radiographs no infiltrates (so you know it's not pneumonia) **Treatment:** Viral ⇒ rest, aspirin, humidity, cough suppressant (codeine) * Bacterial ⇒ rest, antipyretics, humidity, antibiotics

Answer 198

**Description:** infection of the lower resp tract caused by bacteria, viruses, fungi, protozoa, or parasites * the 6th leading cause of death in US * categorized as: **community-acquired (CAP), health care-associated (HCAP), hospital-acquired (HAP), or ventilator-associated VAP** **Types:** 1. **HCAP:** occuring in those with recent hospitalizations, living in nursing home or extended care facility, home infusion therapy, chronic dialysis, or home wound care 2. **HAP:** 2nd most common nosocomial infection (hospital acquired) but has GREATEST mortality 3. **VAP:** nosocominal infection occurring in 9-27% of individuals who require intubation and mechanical ventilation - most common is influenza and resp syncytial virus (RSV) 1. bacterial colonization of oropharynx occurs after ET tube palaced with subsequent aspiration and pooling of bacteria near ET tube cuff (and then create a biofilm) - this can be reduced with raising head of bed, improval oral hygiene, suctioning 4. **CAP:** one of the most common reasons for hospitalizations - most common microorganism (*Streptococcus pnumoniae*) The causative microorganism influences the clinical presentation of the individual, the treatment plan and the prognosis. **Incidence/Prevalence:** highest in elderly **Risk Factors:** advanved age, compromised immunity, underlying lung disease, alcoholism, altered consciousness, impaired swallowing, smoking, endotracheal intubation, malnutrition, immobilization, underlying cardiac or liver disease, and living at nursing home **Modes of infection:** aspiration of oropharyngeal secretions - the most common route of lower RTI * inhalation of microorganisms that have been released into the air when an infected individual coughs, sneezes, talks; or from aerosolized water * ET tubes become colonized with bacteria that form biofilms (protected colonies of bacteria that are are resistant to host defences and antibiotics) * infection anywhere in the body or from IV drug use (can lead to bacteremia that causes bacteria from the blood to spread to the lung) **Pathophysiology:** in healthy lungs, pathogens that get to the lung normally just get expelled/controlled * ptahogens recognized by alveolar macrophages stimulate T & B cells causing widspread inflammation in the lung and recruitment of typical immunity cells * resulting inflammatory mediators and immune complexes can damaged bronchial mucous membranes and alveolocapillary membrane, resulting in acini and terminal bronchials to fill with infectious debris and excudate * some pathogens cause release toxins that further damage lungs and consolidation of lung tissue (mucus filled) * the accumulation of exudate in the acinus leads to dyspnea and to V/Q mismatch and hypoxemia * _Most common and lethal cause_ of outpatient and inpatient pneumonias: **pneumococcus** ⇒ can infect the lungs through inhalation of aerosolized bacteria or more commonly by aspiration or colonized oropharyngeal secretions (these bacteria have capsules that makes phagocytosis hard and release toxins) * Viral pneumonia: seasonal, usually self limiting CAP ⇒ destroys ciliated epithelial cells (which usually expel pathogens) and invade goblet cells and bronchial mucous glands; bronchial walls become edematous and infiltrated with leukocytes **Clinical Manifestations:** most cases preceded by viral UTRI * fever, chills, productive or dry cough, malaise, pleural pain, dyspnea and hemoptysis * pulmonary consolidation (on physical exam) demonstrated by dull percussion, inspiratory crackles, increased tactile fremitus (palpable chest vibrations when someone speaks), egophony (prolonged "a" heard on auscultation over consolidated lung tissue when person says "e"), whispered pectoriloquy (also on auscultation) * potential S/S of underlying systemic disease or sepsis **Diagnosis:** hx taking and physical exam (tachypnea, tachycardia, cracks, bronchial breath sounds, pleural effusion findings); WBC count (elevated); oxygenation and pH, chest X-rays (show infiltrates in the lungs), stains and cultures of resp tract secretions, and blood cultures **Treatment:** _prevention_ - avoidance of aspiration, resp isolation of immunocompromised people, vaccination * _management:_ establishing adequate ventilaion and oxygenation * adequate hydration and good pulmonary hygiene (e.g. deep breathing, coughing, chest physical therapy) * antibiotics given within 4 h to treat bacterial pneumonia * viral pneumonia: treated with supportive therapy alone (potentially antivirals if severe)

Answer 199

**Description:** infection caused by *Mycobacterium tuberculosis* (acid-fast bacillus) that usually affects the lungs but may invade other body systems * leading cause of death from a curable infectious disease in the world **Risk factors:** emigration of infected individuals from high prevalence countries, transmission in crowded institutional settings, homeslessness, substance use, lack of access to screening and medical care **Pathophysiology:** high contagious, transmitted from person to person in airborne droplets * in immunocompetent individuals, microorganism usually contained by inflammatory and immune response systems (results in **latent B infection [LTBI]** and has no clinical evidence of disease) * once bacilli is inspired, it lodges in the lung periphery (usually upper lobe) and causes localized nonspecific pneumonitis (lung inflammation); som emay migrate through lymphatics and initiate immune response * inflammation in lungs = activation of alveolar macrophages and neutrophils ⇒ phagocytosis BUT they can resist lysosomal killing and form **tubercles** (granulomatous lesions) * infected tissues within tubercle die forming cheeselike material (caseation necrosis) * collagenous scar tissue then grows around tubercle which completely isolates bacilli * immune reponse is complete ~10 days after (preventing further multiplication of bacteria) * once bacilli are isolated in tubercles and immunity develops, TB may stay dormant for life ⇒ reactivated if immune system sucks and may spread through blood and lmyphatics to other organs * _infection with HIV is the single greatest risk factor for reactivation of TB infection_ * other causes that amy reactivate TB: cancer, immunosuppressive meds (i.e. corticosteroids), poor nutritional status, renal failure **Clinical Manifestations:** LTBI is asymptomatic * Sx of active disease often develop so gradually that they are not noticed until disease is advanced * fatigue, weight loss, lethargy, anorexia (loss of appetite), low grade fever that usually occurs in the afternoon * cough with purulent sputum develops slowly and becomes more frequnt over several weeks/months * night sweat and general anxiety * dyspnea, chest pain, and hemoptysis (later in course) * extrapulmonary TB is common in HIV ppl and may cause neuro deficits, meningitis symptoms, bone pain, and urinary symptoms **Dx:** +ve tuberculin skin test (TST; purified protein derivative [PPD]), sputum culture, immunoassays, chest radiographs * +ve test = yearly chest radiographs to detect active disease * those who have received TB vaccine with bacille Calmette-Guérin (BCG) will have + TST even if they have never had TB * when active disease, the culture you take will show bacillus in acid-fast stain **Treatment:** combination antibiotic therapy to control active disease or prevent reaction of LTBI * some TB categories are now arising to be resistant to tx ("multidrug-resistant TB" and "extensively resistant TB"

Answer 200

**Description:** circumscribed area os suppuration (pus) and destruction of lung parenchyma; follows consolidation of lung tissue leading to inflammation that causes alveoli to fill with fluid, pus, and microorganisms * _Aspiriation abscess_: can occur from aspiration of anaerobes; usually associated with alcohol abuse, seizure disorders, general anesthesia, and swallowing disorders * Necrosis of consolidated tissue may progress proximally until it communicates with a bronchus

Answer 201

* process of abscess emptying into a bronchus and cavity formation * Abscess communication with bronchus causes production of copious amounts of foul-smelling sputum and occasionally hemoptysis * **S/S**: fever, cough, chills, pleural pain * **Dx:** made with chest radiography * **Treatment:** appropriate antibiotics and chest physical therapy (chest percussion and postural drainage); bronchoscopy to drain abscess

Answer 202

* Blood flow disruption through the lungs can occlude the vessels, increase pulmonary vascular resistance and destroy the vascular beds * Effects of altered pulmonary flow may range from insignificant to life threatening changes in V/Q * Major disorders: * pulmonary embolism * pulmonary HTN * cor pulmonale

Answer 203

**Description:** occlusion of a portion of pulmonary vascular bed by an embolus **Causes:** most commonly results from a DVT involving their lower leg; less common: tissue fragments, lipids (fats), foregin body, air bubble, or amniotic fluid **Risk factors: VIRCHOW TRIAD** * conditions/disorders that promote blood clotting as a result of _venous stasis_ (immobolization, heart failure); * _hypercoagulability_ (inherited coagulation disorders, malignancy, hormone replacement therapy, oral contraceptives) * _injuries to endothelial cells that line the vessels_ (trauma, infection, caustic IV infusions) * genetics (factor V Leiden, antithrombin II, protein S, protein C, prothrombin gene mutations) **Pathophysiology:** pulmonary emboli can result in: * 1) _embolus with infarction:_ embolus that causes infarction (death) of a portion of lung tissue ⇒ leads to shrinking and scarring in the affected area of the lung * _2) embolus without infarction:_ an embolus that does not cause permanent lung injury (perfusion of the affected lung segment is maintained by bronchial circulation) ⇒ clot is dissolved by fibrinolytic system and pulmonary function returns to normal * _3) massive occlusion:_ an embolus that occlusdes a major portion of the pulmonary circulation (i.e. main pulmonary artery embolus) * _4) multiple pulmonary emboli:_ multiple embolic may be chronic or recurrent * ++obstruction to pulmonary vasculature will ↑ pulm artery vasoconstriction, pulm HTN, and RV dilation and afterload **Clinical Manifestations:** nonspecific (so you gotta look at risk factors and predisposing factors) & also DVT is often asymptomatic and hard to detect with clinical exam * sudden onset of pleuritic chest pain, dyspnea, taachypnea, tachycardia, unexplained anxiety * occasionally syncope or hemoptysis * _large emboli:_ pleural friction rub, pleural effusion, fever, leukocytosis * _recurrent small emboli:_ may not be detected until progressive incapacitation, precordial pain, anxiety, dyspnea, RV enlargement * _Massive occlusions:_ severe pulmonary HTN and shock **Diagnosis:** chest radiographs, pulmonar function tests, d-dimer levels (elevated; a product of thrombus degradation) + CT or MRI * level of brain natriuretic peptide and troponin useful when PE is associated with RV dysfunction **Treatment:** prevention - elimination of predisposing factors for those at risk * venous stasis people: leg elevation, bed exercises, position changes, early post op ambulation, pneumatic calf compression * prophylactic low dose anticoagulant therapy to prevent clot formation * **Primary tx:** anticoagulant therapy (low molecular weight heparin) and factor Xa inhibitors * if life-threatening PE: use fibrinolytic agent (streptokinase) * filter in IVC to prevent emboli from reaching the lungs

Answer 204

**Description:** as defined as a mean pulmonary artery pressure (MPAP) \>25mmHg at rest (normal is 15-18mmHg) **Classifications:** * 1) No known cause OR associated with inheritance, drugs or toxin, connective tissue disease or infection * 2) PAH attributable to left heart disease * 3) PAH caused by chronic lung disease or hypoxia, or both * 4) Chronic thromboembolic PAH * 5) PAH caused by other multifactorial mechanisms including blood, metabolic, and systemic factors **Causes:** COPD (most common lung disease associated with PAH); interstitial fibrosis; but any condition causing chronic hypoxemia can lead to PAH **Pathophysiology:** * ***Idiopathic pulmonary arterial hypertension (IPAH)*** aka the 5th category (above) is characterized by endothelial dysfunction with overproduction of vasoconstrictors (eg. thromboxane, endothelin) and decreased production of vasodilators (NO, prostacyclin) * vascular growth factors released ⇒ fibrosis and thickening of vessel walls (**remodeling**) with luminal narrowing and abnormal vasoconstriction * leads to resistant to pulmonary artery blood flow = pressure increases here + in RV * Gas exchange reduced with restriction in lung volumes * As resistance and pressure ↑, RV has to work harder = RV hypertrophy (cor pulmonale) followed by right HF * Category 3: PAH associated with lung resp disease or hypoxia is serious complication of conditions like COPD, hypoventilation with obesity (these also have hypoxic pulmonary vasoconstriction that further increase pulm artery pressure) **Clinical Manifestations:** may not be detected until quite severe * Sx masked by other forms of pulm or CV disease * first indication: abnormality seen in chest radiography (enlarged R heart border) or ECG showing RVH * Fatigue, chest discomfort, tachypnea, dyspnea (particularly with exercise) * peripheral edema, JVD, precordial heave, accentuation of pulmonary component of the 2nd heart sound **Diagnosis:** Right heart catheterization * to determine cause: chest x-ray, ECHO, CT * IPAH dx made when all other causes ruled out **Treatment:** oxygen, diuretics, anticoagulants, avoiding contributing factors (air travel, decongestant meds, NSAIDs, pregnancy, tobacco use) * Meds (not curative): prostacyclin, endothelin antagonists, PDE-5 inhibitors, guanylate cyclas activator * lung transplant (if no remission) * most effective tx for PAH associated with lung resp disease/hypoxia or both: _treatment of primary disorder_ (and supp oxygen to reverse hypoxic vasoconstriction)

Answer 205

* condition where severely overweight people fail to breathe rapidly enough or deeply enough which results in low blood oxygen levels and high CO₂ levels * many also frequently stop breathing altogether for short periods of time during sleep, resulting in partial awakenings during the night followed by continual sleepiness during the day * puts strain on heart which eventually may lead to symptoms of HF, leg edema, and others * Most effective tx: weight loss * Others: noctural ventilation with postive airway pressure (CPAP)

Answer 206

**Description:** defined as right ventricular enlargement (hypertrophy, dilation or both) caused by PAH **Pathophysiology:** develops as PAH exerts chronic pressure overload in RV * pressure overload increases work of RV and causes hypertrophy of normally thin-walled heart muscle * eventuall progresses to dilation and failure of the ventricle **Clinical Manifestations:** may be obscured by underlying respiratory or cardiac disease and appear only during exercise testing * heart may appear normal at rest but CO falls with exercise * ECG may show RVH * pulmonary component of second heart sound (represents closure of pulmonic valve) may be accentuate; pulmonic valve murmur may be present * Tricuspid valve murmur may also occur * JVD, hepatosplenomegaly, peripheral edema - due to increased pressures in systemic venous circulation **Diagnosis:** physical exam, imagine, ECG or ECHO **Treatment:** goal: to decrease workload of RV by lowering pulmonary artery pressure * same tx as for pulmonary hypertension (reverse underlying lung disease if possible)

Answer 207

**Description:** cancer of the larynx **Prevalence/Risk Factors:** \<1% cancers in US; primary risk factor is _tobacco_ _smoking_ which is further heightened with smoking x alcohol consumption combo * HPV (6 and 11) also linked to both benign and malignant laryngeal disease * highest incidence: men 50-75 y.o. **Pathophysiology:** * carcinoma of true vocal cords (glottis) more common than of supraglottic structures (epiglottis, aryepiglottic folds, arytenoids, false cords) * tumors of subglottic area rare * squamous cell carcinoa the most common cell type * metastasis develops by spreading to draining lymph nodes; distant metastasis is rare **Clinical Manifestations:** * hoarseness (that can lead to voice loss if progress), dyspnea (rare with supraglottic tumors but can be severe in subglottic), cough (may following swallowing) * laryngeal pain with supraglottic lesions **Diagnosis:** external inspection and palpation of larynx and lymph nodes of neck; indirect laryngoscopy (imaging procedures) & biopsy; **Treatment:** combined chemo and radiation or surgical resection * swallowing and speech difficulties may occur aftter tx (sequelae) - swallowing and speech therapy * extensive lesions need total laryngectomy

Answer 208

**Description:** refers to tumors arising from epithelium of respiratory tract (i.e. cells that line the bronchi; bronchogenic carcinomas aka primary lung cancers) * second most common cancer is the US, low survival (17%) **Causes/risk factors:** most common - tobacco smoking (and those who smoke and have obstructive lung disease are at much greater risk) * heacy smokers have 20x greater chance of developing lung cancer than nonsmokers * smoking related to cancers of larynx, oral cavity, esophagus, and urinary bladder * other risk factors: radon gas exposure, secondhand (environmental) smoke, occupational exposures to certain workplace toxins, radiation, and air pollution * genetic risks: polymorphism of genes responsible for growth factor receptors, angiogenesis, apoptosis, DNA repair, and detox of inhaled smoke **Classifications:** based on cell type and molecular profiling _(see other flashcard)_ **Pathophysiology:** tobacco smoke contains \>30 carcinogens, responsible for causing 80-90% of lung cancers ⇒ lead to tumor development (and growth factors and inflammatory mediators continue to promote tumor development) * changes go from metaplasis to carcinoma in situ to invasive carcinoma * tumor further progresses by invading surrounding tissues and metastasize to distant sites (brain, bone marrow, liver) **Clinical manifestations:** covered in other flashcards; sx often attributed to side effects of smoking; usually advanced when the sx are bad enough for someone to go to the doc **Diagnosis:** sputum cytologic studies, chest imaging, viral bronchoscopy, endobronchial ultrasound, biopsy, electromagnetic navigational broncoscopy * non-small cell cancer staging via TNM classification (T- denotes extent of primary tumors; N - nodal involvement, M - extent of metastasis) * small cell lung cancer staging - limited (confined to area of origin in lung) or extensive **Treatment:** stop smoking, avoid environmental toxins * early stage lung carcinoma - surgical resection (more difficult to do once metastasis has occurred) * for non-small cell carcinoma with metastasis: add on radiation and chemo

Answer 209

* two major categories: * **non-small cell lung carcinoma (NSCLC)** - 75-75% of all lung cancers * *squamous cell carcinoma* * *adenocarcinoma* * *large cell undifferentiated carcinoma* * **neuroendocrine tumors of the lung** - arise from bronchial mucosa * *small cell carcinoma* - most common of this category * *large cell neuroendocrine carcinoma* * *typical/atypical carcinoid tumors* * other pulmonary tumors: mesothelioma (associaed with asbestos exposure) - less common

Answer 210

* accounts for ~30% of bronchogenic carcinomas * associated with smoking and COPD * tumors typically located near hila and project into bronchi * pneumonia and atelectasis often associated with SCC * **Growth:** slow * **Metastasis:** tumors tend to stay localized and not metastasize until late in course (mostly to hilar lymph nodes) * **Diagnosis:** biopsy, sputum analysis, bronchoscopy, electron microscopy, immunohistochemistry * **S/S:** central location leads to sx of **nonproductive cough, hemoptysis,** sputum production, airway obstruction, hypercalcemia * ****chest pain is late sx (large tumors) * **Treatment:** surgery, chemo and radiation

Answer 211

* tumor arising from glands of the lung - constitutes 35-40% of all bronchogenic carcinomas * develops in a stepwise fashion through atypical adenomatous hyperplasia, adenocarcinoma in situ, and minimally invasive adenocarcinoma to invasic carcinoma * also includes bronchioalveolar cell carcinoma (rumor arises from terminal bronchioles and alveoli) - slow growing with unpredictable pattern of metastasis * **Growth rate:** Moderate * tumors usually \<4cm and more commonly arise in peripheral regions of pulmonary parenchyma * **Metastasis:** Early - to lymph nodes, pleural, bone, adrenal glands, brain * **Symptoms:** may be asymptomatic or with pleuritic chest pain and SOB from pleural involvement by tumor; pleural effusion * **Diagnosis:** radiography, fiberoptic bronchoscopy, electron microscopy * **Treatment:** surgery + chemo as adjunctive therapy

Answer 212

* consitutes ~10% of bronchogenic carcinomas * epithelial cells have transformed so much that all evidence of differentiation has been lost so considered undifferentiated non-small cell carcinoma * these tumors arise from squamous, glandular, or neuroendocrine precursor cells; arise centrally and can grow to distort trachea and cause widening of carina * **Growth rate:** rapid * **Metastasis:** early and widespread * **Means of Diagnosis:** sputum analysis, bronchoscopy, electron microscopy (by exclusion of other types) * **Clinical Manifestations:** chest wall pain, pleural effusion, cough, sputum production, hemoptysis, airway obstruction from pneumonia * **Treatment:** surgery

Answer 213

* arise from mesothelial cells that line pleura * ~80% linked to asbestos exposure but can take up to 40 years after exposure for dx of tumor * **Growth rate:** rapid * **Metastasis:** early; to lymph nodes, lungs, heart, bone * **Clinical Manifestations:** dyspnea and chest pain; chronic cough, signs of pleural effusion * **Dx:** chest wall imaging (shows pleural effusion): CT, thoracocentesis, thoracscopy, cytology * **Treatment:** surgery, chemo, radiation, immunotherapy

Answer 214

**Description:** most common type of neuroendocrine lung tumors; highest correlation with tobacco smoking * arise from neuroendocrine cells that contain neurosecretory granules * most tumors central in organ (hilar and mediastinal) * cell sizes range 6-8 um * often associated with ectopic hormone production (paraneoplastic syndromes) - hyponatremia, Cushing syndrome, hypocalcemia, gynecomastia (gonadotropins), carcinoid syncrome (serotonin), and Lambert-Eaton myasthenic syndrome (paneoplastic cerebellar degeneration) **Growth rate:** very rapid **Metastasis:** very early and widespread; to mediastinum, lymph nodes, brain, bone marrow **Clinical Manifestations:** tend to present Stage IV, worst prognosis * chest pain, cough, dyspnea, hemoptysis, localized wheezing, airway obstruction, S/S of excessive hormone secretion **Dx:** Radiogarphy, sputum analysis, bronchoscopy, electron microscopy, immunohistochemistry **Treatment:** treated by chemotherapy and ionizing radiation to thorax and CNS

Answer 215

* ~1% of all lung tumors * unusual in that they are not related to smoking, may begin in childhohod, and grow very slowly * usually discovered by chest imaging for something else * cured by local surgical or bronchoscopic resection

Answer 216

infections foreign body aspiration obstructive sleep apnea trauma

Answer 217

Croup illnesses are characterized by infection and obstruction of the upper airways: 1) acute laryngotracheobronchitis (croup) 2) spasmodic croup \*note that Diptheria can also be considered a croup illness but is now rare due to vaxx

Answer 218

**Description:** an acute laryngotracheitis, almost always occurs in children between 6 months and 5 years (peak incidence at 2 y.o.) **Causes/Incidence:** 85% cases (virus - most common parainfluenza; others: RSV, rhinvirus, adenovirus, rubella virus, or atypical bacteria) * higher in males, most common in winter months * ~15% of cases have strong family hx of croup * _spasmodic croup_ - usually in older children (unknown etiology but can be triggered by cold, allergy, or viral infection) * develops acutely usually without fever and tends to recur **Pathophysiology:** caused primarily by subglottic inflammation and edema from infection * the subglottic space is loos so allows for accumulation of mucosal and submucosal edema (vs in larynx, the mucous membranes are tightly adhered to cartilage so not as much space to swell) * cricoid cartilage also the structurally narrowest point of the airway which makes edema in this area critical * spasmodic croup also causes bronchoconstriction but with less inflammation and edema * **summary:** inflammation and edema ⇒ upper airway obstruction ⇒ increased airflow resistance ⇒ increased WOB ⇒ generates more negative intrathoracic pressure that may exacerbate collapse of upper airway ⇒ resp failure **Clinical Manifestations:** rhinorrhea, sore throat, low grade fever for a few days, then develops harsh (seal-like) barking cough, inspiratory stridor, hoarse voice * quality of voice, cough, and stridor may tell you the location of the obstruction: * **snoring:** enlarged tonsils or adenoids * **inspiratory stridor:** airway compromised at level of supraglottic larynx, vocal cords, subglottic region, upper trachea * **Expiratory stridor:** narrowing or collapse in trachea or bronchi * **noise during both inspiration and expiration:** fixed obstruction of vocal cords or subglottic space * **Hoarseness/weak cry:** obstruction at vocal crods * **croupy cough:** constriction below vocal cords * most resolve spontaneously in 24-48 hours, do not want hospital admission * severe croup may show deep retractions, stridor, agitation, tachycardia, maybe pallor/cyanosis * spasmodic croup: hoarseness, barking cough, stridor; sudden onset, usually at night and without prodromal symptoms; resolves quickly **Diagnosis:** Westley croup score (for severity) **Treatment:** Degree of symptoms determines level of treatment * most do not need tx (mild stridor cases may need outpatient tx) * glucocorticoids (injection, oral dexamethasone, or nebulized budesonide) * for acute resp distress: nebulized epinephrine which stimulates α-and β-adrenergic receptors and decreases mucosal edema and airway secretions (opens up the airway, reduces inflammation) * oxygen (or heliox- helium/oxygen mix for severe cases)

Answer 219

1) Severe resp distress AND 2) Stridor at rest AND 3) current history of URTI AND 4) Barking cough or recent history of a barking cough

Answer 220

**Description:** aka pseudomembranous croup; the most common potentially life threatening upper airway infection in children **Cause:** most often by *Staphylococcus aureus (S.aureus)* (including MRSA), *Haemophilus influenzae (H. influenzae*), or group A beta-hemolytic *Streptococcus* (GABHS) * treatment of viral croup with corticosteroids has increased risk for bacterial tracheitis **Clinical Presentation:** tachypnea, stridor, hoarse voice, fever, cough, and/or increased secrestions from nose or mouth * presence of airway edema and ++purulent secretions leads to airway obstruction that can be worsened by formation of a tracheal pseudomembrane and mucosal sloughing **Treatment:** immediate antibiotics, endotracheal intubation to prevent total upper airway obstruction

Answer 221

**Description:** severe, raipdly progressive, life threatening infection of the epiglottis and surrounding area **Causes:** historically caused by *Haemophilus influenzae* type B (HiB) - this has been reduced due to vaxx (but up to 25% of cases still caused by HiB which is now more common in adults) * current cases in children - usually due to vaxx dailure or caused by other pathogens **Pathophysiology:** epiglottis arises from the posterior tongue base and covers laryngeal inlet during swallowing * bacterial invasion of the mucosa with associated inflammation leads to rapid development of edema =\> leads to severe, life threatening obstruction of the upper airway **Clinical Manifestations:** child between 2-7 y.o. suddenly develops fever, irritability, sore throat, inspiratory stridor, and severe resp distress * child appears anxious and has muffled voice ("hot potato" voice) * drooling, absence of cough, preference to sit, dysphagia * be in tripod position to improve breathing * death can occur in a few hours * bacteria invasion can cause other things: pneumonia, cervical lymph node inflammation, otitis, meningitis (rare) or septic arhtritis (rare) **Diagnosis:** do not attempt throat exam as it may trigger laryngospasm and cause respiratory collapse **Treatment:** LIFE THREATENING * intubation to secure airway * antibiotics * racemic epinephrine and corticosteroids (temp fix) * postexposure prophylaxis with rifampin for household unvaccinated contacts after a child is dx

Answer 222

* **Description:** aka tonsillitis - can be severe enough to cause upper airway obstruction * **Causes:** group A beta-hemolytic Streptococcus (GABHS) and MRSA which have risen in past 15 years; complication of mono * can be complicated by formation of **tonsillar abscess** (further contributes to airway obstruction * **Peritonsillar abscesses:** usually unilateral and most often a complication of acute tonsillitis * abscesses need to be drained * antibiotics given * may need corticosteroids if significant obstruction in tonsillar infections * adenotonsillectomy if recurrent tonsillitis

Answer 223

* usually occurs in 1-4 y.o. * most objects expelled by cough reflex but some may lodge in the larynx, trachea, or bronchi * large objects may occlude the airway and become life threatening (particular concern with batteries and magnets) * aspiration event is commonly not witnessed or is not recognized when it happens because the coughing, choking, gagging can resolve really quicky * **Symptoms:** * Foreign bodies lodged in larynx or upper trachea cause cough, stridor, hoarseness or inability to speak, resp distress, agitation/panic * if object is small, it can get lodged in a bronchus instead - causes local irritation, granulation, obstruction and infection (coughing, wheezing, atelectasis, pneumonia, lung abscess, blood streaked sputum) * **Treatment:** Heimlich or sweep oral airway; bronchoscopic removal, antibiotics as necessary

Answer 224

**Description:** partial or intermittent complete upper airway obstruction (UAO) during sleep with disruption of normal ventilation and sleep patterns **Prevalence:** childhood OSAS is common (2-3% prevalence in 12-14 y.o., up to 13% of children between 3-6 y.o.) and 2-4x higher in vulnerable populations (blacks, Hispanics, preterm infants) * children: equal prevalence among girls and boys * obese children higher incidence * possible influences early in life: passive smoke inhalation, SES, snoring * infants at risk beween they have anatomic and physiologic predispositions towards airway obstruction and gas exchange abnormalities **Pathophysiology:** reduced airway diameter, increased upper airway collapsibility, and airway inflammation are common causes of OSAS * UAO during sleep results in cyclic episodes of increasing respiratory effort and changes in intrathoracic pressures with oxygen desaturation, hypercapnia, and arousal → child goes back to sleep and cycle repeats * **adenotonsillar hypertrophy** (one of the most common causes of OSAS in children), gastroesophagela reflux, obesity, and craniofacial anomalies associated with decreased airway diameter * reduced motor tone of upper airways (like CP, Down's, neuro disorders) can reduce airway diameter * allergy, asthma may contribute to inflammation * children with history of RSV bronchiolitis in infancy may show tendency towards upper airway inflammation **Clinical Manifestations:** * snoring and laboured breathing, sweating, restlessness during sleep (can be continuous or intermittent) * potential episodes of increased respiratory effort but no audible airflow, often terminated by snorting, gasping, respositioning, or arousal * daytime sleepiness/napping * chronic mouth breathing (terrible breath) * enuresis (bed wetting) * obese children may adopt prone position to attempt improved ventilation * _consequences:_ can lead to cog and neurobehavioural impairment, excessive daytime sleepiness, impaired school performance and poor QoL **Dx:** hx taking from parents (does their kid snore?); physical exam; imaging of upper airway to help rule out some underlying causes * polysomnographic sleep study to look at obstructed breathing and physiologic impairment **Treatment:** tonsillectomy and adenoidectomy, CPAP, anti-inflammatories, dental tx, high flow NC, weight loss

Answer 225

* surfactant deficiency disorder * bronchopulmonary dysplasia * infections * aspiration pneumonitis * asthma * acute respiratory distress syndrome (ARDS) * cystic fibrosis (CF)

Answer 226

**Description:** previously known as hyaline membrane disorder (HMD); aka surfactant deficiency disorder (SDD) - a significant cause of neonatal morbidity and mortality characterized by poor lung structure and lack of adequate surfactant * Vermont Oxford Neonatal Network definition: PaO₂ \<50mmHg on room air, central cyanosis in room air, need for supplemental oxygen to maintain PaO₂ \>50mmHg, and classic chest film appearance **Prevalence:** almost exclusively in premature infants, and incidence has increased in US over the past 2 decades; occurs in 50-60% of infants born at 29 weeks gestation and decreases significantly by 36 weeks * death rates have declined since intro of atenatal steroid therapy and postnatal surfactant therapy **Risk factors:** premature birth/low birth weight; male gender; c-section without labour; diabetic mother; perinatal asphyxia **Pathophysiology:** caused by surfactant deficiency which decreases alveolar SA available for gas exchange (without surfactant, the alveoli collapse at the end of each exhalation) * surfactant is normally not secreted by alveolar cells until ~30 weeks gestation (newer textbook says 20-24) * preemies are also born with underdeveloped and small alveoli that are difficult to inflate and have thick walls and inadequate capillary blood supply = gas exchange ++impaired * their chest walls are also weak and highly compliance so the rib cage tends to collapse inward with respiratory effort * net effect: _atelectasis_ resulting in significant hypoxemia = metabolic acidosis * atelectasis requires ++ negative inspiratory pressure to open alveoli with each breath ⇒ increased WOB ⇒ hypercapnia ⇒ hypoxemia + hypercapnia cause pulmonary vasoconstriction ⇒ increased intrapulmonary resistance and shunting ⇒ hypoperfusion of the lung & decrease in effective pulmonary blood flow * increased pulm vascular resistance may even cause partial return to fetal circulation with right to left shunting through ductus arteriosus and foramen ovale * increased pulmonary capillary permeability + need for mechanical ventilation (which damages alveolar epithelium) both result in leakage of plasma proteins into alveoli air spaces (creating appearance of hyaline membranes which looks glassy/transparent) and this causes further inactivation of surfactant **Signs and Symptoms:** appears within minutes of birth → tachypnea (RR \>60 /min), expiratory grunting, intercostal and subcostal retractions, nasal flaring, cyanosis * severity increases over first 2 days of life (newer textbook says first hours of life) * apnea, irregular respirations when baby tires * chest radiograph shows diffuse granular densities within first 6 hours of life ("ground glass" appearance associated with alveolar flooding) * clinical manifestations reach a peak within 3 days after which there is gradual improvement **Diagnosis:** basis of premature birth or other risk factors, chest radiographs, pulse ox readings, analysis of amniotic fluid or tracheal aspirates to measure lung maturity **Treatment:** prevention of premature birth (_the ultimate treatment for RDS_) * for those at risk for preterm birth: antenatal tx with glucocorticoids to induce significant and rapid acceleration of lung maturation and stimulation of surfactant production in fetus * For babies \<1000g: administration of synthetic or natural surfactant through nebulizer or nasal CPAP ventilation (start 15-30min after birth) * Supportive care: oxygen, mechanical ventilation (but before of harm this could cause) * most infants survive RDS and most recovery within 10-14 days (however may have subsequent bronchopulmonary dysplasia)

Answer 227

**Description:** aka Chronic lung disease (CLD) of prematuriy; the major cause of pulmonary disease in infants * associated with premature birth (usually \<28 weeks' gestation), prolonged (at least 28 days) perinatal supp oxygen, and positive pressure ventilation * Bronchopulmonary dysplasia is not as common because of the availability of exogenous surfactant and antenatal glucocorticoids **Risk factors:** premature birth (especially ≤28 weeks); positive pressure ventilation; supplemental oxygen administration; antenatal chorioamniotis; postnatal sepsis or pneumonia; patent ductus arteriosus; nutritional deficiencies; early adrenal insufficiency; genetic susceptibility **Pathophysiology:** form of arrested lung development * poor formatino of alveolar structure with fewer and large alveoli and decreased SA for gas exchange * persistent inflammation contributes to pulmonary capillary fibrosis, perfusion mismatch, pulmonary HTN, and decreased exercise capacity **Clinical Manifestations:** clinical defintion of BPD: need for supplemental oxygen at 36 weeks' postmenstrual age or gestation age (time elapsed b/w first day of last normal menstrual period and day of birth); and for at least 28 days after birth * hypoxemia and hypercapnia caused by V/Q mismatch and diffusion defects * increased WOB * impaired ability to feed * intermittent bronchospasm, mucus plugging, and pulmonary hypertension * mild BPD infants: mild tachypnea, difficulty handling RTIs * most severe infants: have dusky spells (apnea) that may occur with agitation, feeding, or gastroesophageal reflux **Treatment:** need prolonged assisted ventilation; diuretics for pulmonary edema; bronchodilators to reduce airway resistance; inhaled corticosteroids

Answer 228

age of child clinical presentation season of the year

Answer 229

**Description:** common, viral RTI of the small airways occurring almost exclusively in infants and young toddlers; major reason for hospitalization * has a seasonal, yearly incidence (Nov- April) * leading cause of hospitalization fo rinfants during winter season **Cause:** RSV (most common associated pathogen); others: human metapneumovirus and human bocavirus * preemies and those who have underlying BPD or heart disease have higher risk for severe prognosis * linked with increased risk for asthma later in childhood **Pathophysiology:** viral infection causes necrosis of bronchial epithelium and destruction of ciliated epithelial cells * lymphocytes infiltrate around bronchioles and a cell-mediated hypersensitivity to the viral antigens occurs causing inflammation * submucosa becomes edematous and cellular debris and fibrin form plugs within bronchioles * edema of bronchial wall, mucus and debris accumulation, and bronchospasm narrow peripheral airways * atelectasis can occur in someareas of the lung and hyperinflation in others * mechanics of breathing disrupted - obstruction of airflow worse on expiration ⇒ leads to air trapping, hyperinflation, and increased functional residual capacity ⇒ increased WOB ⇒ hypercapnia **Signs/Symptoms:** starts with ++rhinorrhea, then tight cough over few days + decreased appetite, lethargy, fever * infants: tachypnea, respiratory distress, abnormal auscultatory findings of chest * wheezing (most common), rales, rhonchi * chest radiographs show hyperexpeanded lungs, patchy or peribronchial infiltrates, potentially atelectasis of right upper lobe * apnea * conjunctivitis, otitis media **Diagnosis:** history, S/S (rhinitis, cough, wheezing, chest retractions, taypnea) **Treatment:** depends on severity and age * _Mild:_ no specific treatment (outpatient monitoring) * Prevention: RSV-specific antibody (monthly) injection for 5 months throughout RSV season) for high-risk infants * handwashing and alcohol-based decontamination * prevention of exposure to tobacco smoke * promotion of infant breast feeding

Answer 230

**Description:** infection and inflammation in terminal airways and alveoli **Cause:** CAP major cause of morbidity and mortality in children particularly in developing countries * most common agents: viruses (2-3x more in children) than bacteria (most common post natal period) and atypical microorganisms (but clinical symptoms often do not differentiate between viral from bacterial or atypical); coinfections are common * risk factors: age \<2 y.o., overcrowded living conditions, winter season, recent antibiotic treatment, daycare attendance, passive smoke exposure * nutritional status, age and underlying disease process influence morbidity/mortality rates to CAP **Pathophysiology:** see individual flashcards for the three types (viral, bacterial, atypical pneumonia) **Diagnosis:** based on clincal and lab findings * chest x-ray in bacterial pneumonia: patchy infiltration and segmental/lobar disease * viral infection: insterstitial pattern * use of biomarkers **Treatment:** some can be outpatient; most children need oxygen supplementation (and some assisted ventilation) * adequate hydration, nutrition, and supportive pulmonary therapy * some may been enteral feeding * monitoring for aspiration * bacterial pneumonias: antibiotics

Answer 231

* 2-3x more likely to occur in children than in adults, incidence generally follows a seasonal pattern * bacterial coinfections common * most common viral pneumonia: **Respiratory syncytial virus (RSV)** * ****others: parainfluenza, influenza, human rhinovirus, human metapneumovirus, adenoviruses, and *Mycoplasma pneumoniae* * acquired by direct contact, droplet transmission, aerosol exposure * **Pathophysiology:** initial destruction of ciliated epithelium of distal airway with sloughing of cellular material → leads to inflammatory response * **S/S:** often cough with no fever

Answer 232

* most commonly result of infection with streptococci and staphylocci microorganism * pneumococcal pneumonia most common cause of community-acquired bacterial pneumonia, presents acutely with varying severity * Staph and group A streptococcal can be fulminant (sudden, severe) and necrotizing with high incident of empyema, pneumatocele (lung lesion filled with air) and sepsis * **Patho:** usually begins with aspiration of nasopharyngeal bacteria * may be preceded by viral infection somtimes which can cause epithelial damage, reduced mucocillary clearance in trachea and major bronchi and a reduced immune response (setting everything up for bacterial pneumonia) * once in alveoli, bacteria can phagocytosed by host defences and alveolar macrophages but if these fail, then the macrophages release numerous inflammatory cytokines and neutrophils will be recruited to lung = inflammation (exudate, edema, vascular engorgement) * leads to alveoli filling up and gas exchange can't occur (if severe, resp failure) * shock may occur at the same time which causes metabolic acidosis * **Signs/Symptoms:** preceding viral illness followed by chills and trigors, SOB, increasingly productive cough (potential blood streaking of sputum) * malaise, emesis, abdominal pain, chest pain * **Diagnosis:** auscultation shows crackles and decreased breath sounds; lobar pattern or patchy in chest films

Answer 233

* aka ***Mycoplasma* pneumoniae*, Chlamydophila* pneumoniae)** * the most common cause of community-acquired pneumonia for school-aged children and YA * transmission is from person to person with a 2-3 week incubation period * Mycoplasmic organisms attach to ciliated respiratory epithelial cells causing local sloughing of cells to occur * then lymphocytes infiltrate and neutrophils come along * gradual onset, resembles a URTI but with low-grade fever, cough, chest pain * usually not severe and self-limiting

Answer 234

* caused by foreign substance (food, meconium i.e. from amniotic fluid, saliva or gastric secretions, environmental compounds, entering the lung and resulting in inflammation of the lung tissue * leading cause of death in children who are neurologically compromised due to failure of protective reflexes and difficulty swallowing * children undergoing sedation/anesthesia also may aspirate oral secretions contaminated with anaerobic bacteria or acidic stomach contents * severity of lung injury after aspiration depends on volume and pH of material aspirated, and the presence of pathogenic bacteria * ++low or ++high pH will cause significant inflammatory response * ingestion of hydrocarbons: depends on volatility and viscosiry of aspirated substance (low viscosity substance would be gasoline or lighter fluid [most toxic]; high viscosity would be petroleum jelly or mineral oil [less likely to cause pneumonitis]) * **t****reatment:** * depends on material aspirated but generally broad-spectrum antibiotics with failure to improve after 48 hours * botox into salivary gland to suppress secretion (for those with lots of secretions)

Answer 235

**Description:** fibrotic obstruction of respiratory bronchioles and alveolar ducts secondary to intense inflammation * relatively rare in children * two types: * proliferative * constrictive (obstructive) - more common **Causes:** often occurs as sequela (i.e. consequence of a previous disease/injury) of a severe viral pulmonary infection (influenza, adenovirus, pertussis [whooping cough], measles) * may be secondary to parainfluenza, RSV, HIV, or *M. pneumoniae* infection or lung transplant * may occur after lung, heart-lung, or bone marrow transplantation * may be associated with collagen vascular disease, toxic fume inhalation, chronic hypersensitivity, pneumonitis, Crohn disease, and SJS **S/S:** child may appear like they are improving after acute insult, but the disease progresses and they deteriorate with symptoms of increasing tachypnea, dyspnea, cough, sputum production, crackles, wheezing, increased chest wall size (increased APD), hypoxemia **Treatment:** no specific treatment, too rare for trials; inhaled corticosteroids, bronchodilators, antibiotics, oxygen; some may need mechanical ventilation but overall no cure

Answer 236

**Description:** chronic inflammatory disease characterized by bronchial hyperreactivity and reversible airflow obstruction, usually in response to an allergen (Type I hypersensitivity reaction) **Prevalence:** most prevalent chronic disease in childhood (affects ~10% of US children between birth and 17 yo; most affected include black, American Indian (bro this book is racist af), Alaska Native, Hispanic children * those living in an urban setting * those with low SES **Causes:** genetic susceptibility x environmental factors * risk factor includes: early exposure to allergens (air pollution, dust mites, cockroach antigen, cat exposure, tobacco smoke); RTIs, preterm children; child obesity * ~70-80% of acute wheezing episodes in children with asthma are associated with viral RTI (RSV, human rhinovirus, parainfluenza) * in those \<2 y.o., most common is RSV * Older children and adults: major viral trigger is rhinovirus (the "common cold" virus) * bacterial RTIs can also trigger asthma * vitamin D insufficiency (may cause airway inflammation and wheezing because vit D suppresses Th-2 mediated allergic disease) **Pathophysiology:** similar to adults; initiated by type I hypersensitivity reaction mediated by Th2 lymphocytes whose cytokines activate mast cells, eosinophils, leukocytes, and Ig# production * mucus production in the airways lead to V/Q mismatch with hypoxemia, expiratory airway obstruction and air trapping, and increased WOB * in young children, airway obstruction can be more severe due to small diameter of airways **Clinical Manifestations:** acute attack: coughin, expiratory wheezing, SOB, faint breath sounds due to poor air movement; clipped sentences or can't speak at all due to dyspnea * hyperinflation (barrel chest) * elevated RR and HR * nasal flaring, use of accessory muscles with retractions (may look like they are "head bobbing" from sternocleidomastoid use) * pulsus paradoxus may be present * anxious, diaphoretic, exercise intolerance **Diagnosis:** often under diagnosed and undertreated becaus elooks like other resp illness in kids * dx based on wheezing as well as variety of risk factors (parental history of asthma, atopic dermatitis, sensitization to aeroallergens or foods, blood eosinophilia, wheezing not associated with upper resp tract illnesses * pulmonary function testing (spirometry) **Treatmet:** goal is LT control by reducing impairment and risk * education, avoiding allergies * caregivers should assess for nighttime awakenings, interference with functional activities, use of short-acting beta2 agonists, pulmonary function tesitng, and exacerbations requiring steroids * same tx as adults: stepwise sequence based on severity and response to tx

Answer 237

**Description:** condition where there is pulmonary edema not a result of cardiac disease (noncardiogenic pulmonary edema) * ARDS occurs in all children and is a life-threatening condition resulting from direct ALI (penumonia, aspiration, near drowning, smok inhalation) OR from systemic insult (sepsis, multi trauma) * characterized by an inflammatory response that causes alveolocapillary injury **Prevalence:** ~10% of total admissions to PICU; mortality is high (~40%) **Patho:** same as adults **Clinical Manifestations:** develops acutely after ALI (usually within 24 hours but can be delayed up to a few days) * characterized by progressive resp distress, severe hypoxemia, decreased pulmonary compliance, and diffuse densities on chest radiograph * initially: hyperventilation but CO₂ retention may happen due to inadequate functional air space and resp muscle fatigue **Treatment:** supportive; goals are to maintain adequate tissue oxygenation, minimize lung injury, avoid iatrogenic (from tx) pulmonary complications * mechanical ventilation, high levels of PEEP to promote alveolar ventilation and stabilization, and redistribution of alveolar edema fluid into interstitium

Answer 238

**Description:** autosomal recessive inherited disease that results from defective epithelial chloride ion transport * CF gene located on chromosome 7 and mutations divided into 6 classes with varying severity * Classes 1-3: more severe disease * Classes 4-6: milder pulmonary disease and pancreatic insufficiency **Prevalence:** primarily whites; median age of dx is 6 y.o.; mean age of survival ~40s; high carrier frequency **Pathophysiology:** multiorgan disease affecting the lungs, GI tract, and reproductive organs * abnnormal expression of the **cystic fibrosis transmembrane conductance regulator (CFTCR) protein** which is an activated chloride channel present on surface of many types of epithelial cells * most important effects are on the lungs and likely cause of death would be from resp failure * mucus plugging, chronic inflammation, chronic infection of the small airways * mucus plugging - due to increased production (more goblet cells and glands and bigger) and altered properties of mucus (dehydrated and viscous due to defective chloride secretion and excess sodium absoprtion) * periciliary fluid also deplete causing cilia to not be able to move = mucus adheres to the epithelium and bacteria and other WBC byproducts accumulate * lots of neutrophils in the airways releasing oxidants and proteases that damage lung structural proteins = all causing inflammation * CF airway microenvironment favours bacterial colonization (*Staphylococcus aureus, Haemophilus influenzae* common in younger children; *Pseudomonas aeruginosa* in at least 75% of children with CF) ⇒ their biofilm allows for rapid mutation and antibiotic resistant * chronic inflammation leads to microabscess formation, bronchiectasis, patch consolidation, pneumonia, peribronchial fibrosis, cyst formation; may also have pneumothorax and hemoptysis * vasculature gets remodelled due to localized chronic hypoxia and arteriolar vasoconstriction * pulmonary HTN and cor pulmonale may develop in late stages of disease **Clinical Manifestations:** respiratory or GI symptoms * Resp: persistent cough or wheeze, excessive sputum production, recurrent or severe pneumonia * over time: barrel chest and digital clubbing * chronic sinusitis, nasal polyps **Diagnosis:** immunoreactive trypsinogen (IRT) blood screening, sweat test (reveals [Cl-] \> 60 mEq/L), genotyping for mutations; sibling with CF taken into account **Treatment:** primarily focused on pulmonary health and nutrition * promoting mucus clearance (via chest physical therapy, bronchodilators, aerosolized dornase alfa enzyme and hypertonic saline to liquefy mucus) * oral, inhaled, or IV antibiotics - treat exacerbations of pulmonary infection and with antibiotic resistance * recombinant human growth hormone - improves lung function, height, and weight * lung transplantation (if end stage)

Answer 239

**Description:** aka sudden unexpected infant death (under \<1 year of age) that remains unexplained after thorough case investigation, including performance of a complete autopsy, examination of the death scene, and review of clinical history * always occurs during nighttime sleep, when infants are least likely to be observed **Cause:** unknown (probably a combination of predisposing factors that are vulnerable infant x environmental stressors); most common cause of unexplained infant death in Western countries * seasonal variation noted (higher frequencies during winter months) - related to higher rates of RTIs which have been reported to precede the death * sleeping room may also be overheated and infant overwrapped **Incidence/Prevalence:** low during first month of life with peak incidence 2-4 months; unusual after 6 months; **Risk factors:** prone and side-lying sleeping positions; sleeping on soft bedding; overheated sleeping environment; lower SES, mothers \<20 yo, Blacks/Native Americans/Alaska Natives; low birth weight or growth restricted infants; male infants; pre-term delivery; multiple gestations; siblings who died of SIDS; smoking while preggo; exposure to tobacco smoke; lack of prenatal care; illicit drug use of binge-drinking; larger family size **Treatment:** prevention by avoidance SIDS risk factors