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PCIV > Vol.3-Ch.1 "Pulmonology" > Flashcards

Vol.3-Ch.1 "Pulmonology" Flashcards

1
Q

What are Intrinsic risk factors VS Extrinsic risk factors and what is the major example of each for pulmonary diseases?

A

Intrinsic Risk Factors are those that are influenced by or from within the patient. The most important one is Genetic Predisposition

Extrinsic Risk Factors are those that are external to the patient. The most important on is cigarette smoking (another big one is environmental pollution)

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2
Q

What are the 3 parts of the upper airway?

What is the major function of the upper airways?

A
  • Nasal Cavity
  • Pharynx
  • Larynx

The are mostly in charge of humidifying, warming, and purifying the air we breath.

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3
Q

How is air filtered and warmed in the nose?

A

It is filtered by a combo of the nose hairs in the anterior portion of the nose and by mucus on the walls of the posterior, the mucus is constantly made by the goblet cells in the mucous membrane and moved toward the posterior portion of the nose via Cilia (thin fingerlike projections that contract one way) until it reaches the back and is swallowed.

Air is warmed because the air flows over the Kiesselbach’s Plexus in the lower nasal septum (a rich supply of blood vessels, also the most common cause of nose bleeds)

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4
Q

What are the 4 sinuses of the upper airway?

A
  • Frontal
  • Ethmoid
  • Sphenoidal
  • Maxillary
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5
Q

What are the 3 divisions of the Pharynx?

A
  • Nasopharynx
  • Oropharynx
  • Laryngopharynx
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6
Q

What are the 3 pairs of cartilage that form the larynx?

How are the vocal cords formed?

A
  • Thyroid Cartilage
  • Cricoid Cartilage
  • Epiglottis

The vocal cords (there are two pairs) are formed by folds in the internal lining of the larynx. The upper ones (Vestibule) form the false vocal chords and the lower pair form the True Vocal Chords.

During inspiration both cartilage pairs are wide open and separated and the epiglottis sits upright allowing air in, but when swallowing the epiglottis tips backwards and the cartilage pairs close, opening the esophagus.

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7
Q

How can smoking negatively affect the trachea?

A

It destroys the Cilia that help to move the mucus that trap foreign particles moving it towards the pharynx (backwards in this case, and makes it to where coughing is the only safety mechanism to remove foreign particles

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8
Q

What is the Carina?

A

It is where the trachea deviates into the left and right mainstem Bronchi.

It has a lot of nerve endings and stimulation of these will produce a violent cough

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9
Q

Starting from the Trachea, what is the flow of tissues/organs that air flows down to for gas exhange?

A
  • Trachea
  • Carina
  • Right and Left Mainstem Bronchi
  • Secondary (Lobar) Bronchi
  • Tertiary (Segmental) Bronchi
  • Bronchioles
  • Terminal Bronchioles (approx. 22 divisions of
    bronchioles)
  • Respiratory Bronchioles (at this level, gas exchange
    can occur)
  • Alveolar Ducts
  • Alveoli or Alveoli Sacs
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10
Q

After how much damage to surface area in the alveoli is there no longer enough area for gas exchange for a resting patient?

A

2/3

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11
Q

What is the difference between the right and left mainstem bronchi?

A

The right bronchi essentially is just a continuation of the trachea (does angle off much) whereas the left mainstem bronchi angles more acutely.

This is why most food or liquids aspirated go into right lung as well as an ET tube pushed too far may pass the carina and will often go into right mainstem bronchi

**So if you don’t hear left side air flow on auscultation, it may be because you are too far

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12
Q

Approximately how many alveoli are there in the lungs?

What 3 things make up the Respiratory Membrane?

A

300 million

The alveolar lining, supportive tissue (elastin fibers), and capillaries

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13
Q

What is surfactant in the lungs and what does it do?

A

It is a chemical secreted by type II cells on the alveolar surface that keeps the alveoli moist and open

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14
Q

What is a physiologic shunt?

A

It is when blood passes through alveoli without gas exchange and is normal in small amounts, (approximately 2% of blood flow to the lungs)

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15
Q

How many lobes are in the right and left lungs?

A

The right lung has 3 divisions

The left lung has 2 divisions

(b/c it has the heart it leans against)

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16
Q

Visceral Pleura VS Parietal Pleura?

A

Visceral Pleura is the pleura that lines the lung tissues and contains no nerves.

Parietal Pleura is the pleura that lines the thoracic cavity and contains nerves

A small amount of fluid separates the two to reduce friction by lubrication

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17
Q

Where does the lungs pleural lining actually connect to the lungs?

A

At the Hilum, where the bronchi and blood vessels enter the lungs

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18
Q

Pulmonary Vessels vs Bronchial Vessels?

A

The pulmonary vessels are the pulmonary veins and arteries that transport blood from the heart for gas exchange and then back to the heart (left atrium).

The Bronchial vessels are the bronchial arteries and veins that supply blood to the muscles of the lungs themselves via an extension off the aorta, and the veins drain back into the superior vena cava

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19
Q

What are the 3 major processes that allow for gas exchange to occur?

A
  • Ventilation: the mechanical process of moving air in
    and out of the lungs
  • Diffusion: Process by which gases move between the
    alveoli and the pulmonary capillaries
  • Perfusion: the circulation of blood through the lungs
    or more specifically the pulmonary capillaries
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20
Q

Why is oxygen so important to our bodies?

A

It allows for aerobic respiration required for healthy cellular metabolism

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21
Q

What body structures must be intact for ventilation to occur? (5x)

A
  • chest wall
  • nerve pathways
  • diaphragm
  • pleural cavity
  • brainstem
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22
Q

What part of the brain controls ventilation and what nerve sends that signal to the diaphragm?

A

The Medulla; since expiration is mostly passive the inspiration center of the medulla is much more active.
(the hypothalamus, pons and other voluntary portions of the brain can effect this, the medulla is just responsible for at rest, involuntary breathing)

The Phrenic Nerve sends the impulse to the diaphragm

**the Intercostal Nerves also receive the impulse

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23
Q

On what side of the rib do the associated artery, vein, and nerve lay?

A

The inferior side

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24
Q

Inspiration VS Expiration

The two divisions of ventilation

A

INSPIRATION:
- Diaphragm contracts (flattens)
- Intercostal muscles contract, expanding the chest
cavity both laterally and anteroposteriorly
- Decreases chest cavity pressure by 1-2mmHg below
ATM
- It is always an ACTIVE process, requiring energy

EXPIRATION:
- Chest wall and diaphragm relax
- Increases chest cavity pressure by 1-2 mmHg above
ATM
- It is a passive process requiring no energy (unless
patient has emphysema or is exercising)

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25
Q

What is the pressure of the pleural space and why is it necessary?

A

The pleural space has a negative pressure of 4-8 mmHg in order to ensure that the chest wall and lungs move in concert

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26
Q

Airway Resistance VS Lung Compliance

Another two factors to ventilation

A
  • Airway Resistance: is the drag to the flow of air coming into or out of the lungs. The greatest factor here are the medium sized bronchi which are made of smooth muscle and can constrict when irritated as will asthma or anaphylaxis
  • Lung Compliance: is the ease with which the chest expands aka the change in volume of the chest cavity that results from a specific change in pressure within the chest cavity.
    The two major factors here are Age, as you get older you loose elasticity in the muscles, ribs, and cartilage of the chest wall which result in a shrunken chest wall. And Emphysema patients who have damage to the elastic tissue holding alveoli together and small so they have very high compliance which means little pressure change occurs even with large lung volume expansion
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27
Q

What are the different lung volumes? (x7)

What factors effect lung volumes?

A
  • Total Lung Capacity: 6,000ml
  • Vital Capacity: 4,800mL
    a) Inspiratory Reserve: 3,000mL
    b) Tidal Volume: 500mL
    c) Expiratory Reserve: 1,200mL
  • Residual Volume: 1,200mL
  • Dead space: 150mL

Inspiratory Capacity = insp. res. + tidal
Functional Residual Capacity = exp. res. + residual vol.
Vital Capacity = insp. res. + tidal + exp. res.
(the total air inhaled and exhaled in one breath)

Volume of air entering is dependent on metabolic needs of pt.
Age, sex, physical conditioning, medical illness can alter lung volumes

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28
Q

How do you calculate the Minute Respiratory Volume of a patient?

Minute Alveolar Volume?

A

Min. Resp. Vol. = Tidal Volume X Respiratory Rate

Min. Alveolar Vol. = (tidal - dead space) X Resp Rate

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29
Q

Alveolar Dead Space VS Anatomical Dead Space

A

Alveolar Dead Space is air that is in alveoli that are damaged or dead and cannot be used for gas exchange

Anatomical Dead Space is air that is in the trachea, mainstem bronchi, and bronchioles during inspiration or expiration that cannot be used for gas Exchange (approx. 150mL)

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30
Q

What is the Hering-Breuer Reflex?

A

It is the mechanism the prevents over inflation of the lungs; this is achieved by the Stretch Receptors in the visceral pleura and on the walls of the bronchi/bronchioles that are directly responsible for shutting off the Medulla’s impulses for inflation when the lungs are adequately inflated.

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31
Q

In a healthy Pt what is the most important determinant of the ventilatory rate?

What senses this?

A

Arterial PCO2 is the most important factor for ventilatory rate

As arterial PCO2 levels increase (more CO2) the pH of blood drops or becomes more acidic. As blood pH decreases this is also reflected in the pH of the cerebrospinal fluid (which bathes the brain and spinal cord) which is sensed by the MEDULLA that initiates increased vent rate.

There are also specific sensors in the aorta and carotid artery that are sensitive to PCO2 and will send a chemical messenger to the medulla.

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32
Q

What Pt is not as sensitive to PCO2 changes and therefore relies more on PO2 to get feedback for vent changes?

A

A COPD patient will have decreased responsiveness to changes in arterial PCO2, and will therefore lean on a delicate balance between PO2 levels being low enough to stimulate the medulla and high enough for maintenance of body function. This can be seen as low as 50-60mmHg in COPD patients

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33
Q

What is the concentration of O2 and CO2 in:

  • Alveoli
  • Arterial Blood (going to lungs)
  • Venous Blood (going to heart from lungs)
A

Alveoli:
104mmHg O2
40mmHg CO2

Arterial Blood/Capillaries:
40mmHg O2
45mmHg CO2

(Remember gases will diffuse from high to low concentration)

Venous Blood Returning to the heart from the lungs post gas exchange will have:
104mmHg O2
40mmHg CO2

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34
Q

Lung Perfusion is dependent on what 3 things?

A
  • Adequate Blood Volume (& hemoglobin
    concentration)
  • Intact Pulmonary Capillaries
  • Efficient pumping of blood via heart
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35
Q

What is Hemoglobin?

A

It is a protein transport unit which has 4 Iron containing Heme molecules and a protein containing globin portion. The O2 binds to the heme, and once one O2 binds to it, the hemoglobin changes so that it can more readily take up other O2 molecules and vice versa when releasing. This is seen by the Oxygen Dissociation Curve

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36
Q

What % of O2 is transported via hemoglobin?

A

98% is transported via hemoglobin

2% is transported by O2 diffusion into plasma

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37
Q

What can change the O2 dissociation curve? (4x)

A

Right Shift occurs in: (decreased O2 affinity)

  • Decrease pH
  • increase CO2
  • increase Temp
  • increase 2,3-BPG

Left Shift occurs in: (increase O2 affinity)

  • Increase pH
  • Decrease CO2
  • Decrease pH
  • Decrease 2,3-BPG
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38
Q

Bohr Effect VS Haldane Effect?

A

Bohr Effect:
When hemoglobin are at a tissue site and saturated with oxygen, a CO2 molecule will bind to the hemoglobin, which makes the hemoglobin have a higher affinity for CO2 and will thus release it’s O2 for more CO2

The Haldane Effect:
When the CO2 rich hemoglobin get to the lungs, it is released into the alveoli b/c of the lower concentration there. As O2 then take the place of the CO2, the hemoglobin becomes more acidic which causes the release of more of the CO2.

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39
Q

At what mmHg is O2 more readily binding to the hemoglobin?

At what mmHg is O2 is there not much change in saturation of hemoglobin b/c it is already near 100% sat

A

10-50mmHg

70mmHg

40
Q

What are the 3 ways that CO2 is transported from the cells to the lungs?

A
  • As a Bicarbonate Ion: (70%)
    As CO2 is released into the capillaries, it enters the red blood cell where an enzyme Carbonic Anhydrase combines CO2 with water to form two ions, H+ and HCO3- (bicarbonate). Bicarbonate is then released from the RBCs and transported in plasma. In the lungs the reverse process takes place which produces water and CO2 to be diffused into the alveoli. Basically the CO2 must be converted into bicarbonate in order to transport safely (less acidic) where it is then reversed back into CO2 to be exhaled.
  • Bound to the globin portion of the hemoglobin (23%)
    CO2 can bind to the amino acid protein chain that makes up the hemoglobin (Not on the Heme). This turns hemoglobin into Carbaminohemoglobin which then travels to the lungs to be diffused into the lower CO2 concentrated alveoli to be exhaled.
  • As a CO2 gas itself which is very acidic (7%)
41
Q

Perfusion is the system used for _____?

A

Respiration- the exchange of gases between a living organism and its environment

42
Q

Breathing Patterns:

  • Cheyne-Stokes
  • Kussmaul’s Resp
  • Central Neurogenic Hyperventilation
  • Ataxic (Biot’s) Resp
  • Apneustic Resp
A
  • Cheyne-Stokes:
    Progressively increasing tidal flow, followed by a
    declining volume and separated by period of apnea.
    Typically seen in older pts with terminal illness or
    brain injury
  • Kussmaul’s Resp:
    Deep, rapid breaths that result as a corrective
    measure against conditions such as diabetic
    ketoacidosis that produce metabolic acidosis
  • Central Neurogenic Hyperventilation:
    Deep, rapid respirations that are caused by strokes or
    injury to the brain stem. Stemmed from a loss of
    normal ventilatory regulation and respiratory alkalosis
    is often seen
  • Ataxic (Biot’s) Resp:
    Repeated episodes of gasping separated by periods
    of apnea. Seen in pts with ICP
  • Apneustic Resp:
    Long, deep breaths that are stopped during the
    inspiratory phase and separated by periods of apnea.
    Seen in pts with a stroke or severe central nervous
    system disease
43
Q

What types of things will disrupt diffusion?

A
  • Anything that changes a concentration of oxygen in
    the alveoli such as high altitude
  • Destruction of the alveoli
  • Alteration of thickness of the respiratory membrane.
    This is most often caused by accumulation of fluid
    and inflammatory cells in the interstitial space:
    a) a Cardiogenic cause of this is Left sided heart
    failure
    b) a Non-Cardiogenic cause of this is a change in
    pulmonary capillary permeability such as in
    respiratory distress syndrome
44
Q

What are 5 things to assess in the primary general assessment of a possible respiratory patient?

A
  • position
  • color
  • mental status
  • ability to speak
  • respiratory effort
45
Q

What are a few important questions to ask about a respiratory patient?

A
  • has this happened before? if so what care was given?
  • have you been intubated before?
  • do you have a preexisting respiratory problem? if so
    what medications do you take?
  • do you have any cardiac problems? if so what
    medications do you take?
46
Q

Sputum and what different colors can mean?

A
  • Thick green and brown sputum can mean there is an
    infection in the lungs or bronchial passages
  • Yellow or Pale sputum can mean inflammation or
    allergies
  • Pink, frothy sputum is a sign of severe pulmonary
    edema
  • Bloody sputum (hemoptysis) may be seen with
    cancer, tuberculosis, and bronchial infection
47
Q

What is tactile fremitus?

A

It is the vibration made when speaking and can be used to compare each side of the chest

48
Q

What might it mean if you hear a hollow sounds vs a dull sound upon percussion of the chest?

A

A hollow sound may mean a pneumothorax or emphysema. A dull sound is indicative of pulmonary edema, hemothorax, or pneumonia

49
Q

What are normal breath sounds for bronchi?

Bronchovesicular? Vesicular?

A

Bronchial (or tubular):

  • Loud, high pitched breath sounds heard over trachea
  • expiratory phase last longer

Bronchovesicular:

  • Softer, medium pitch heard over the mainstem bronchi
  • expiratory and inspiratory phases are equal length

Vesicular:
- soft, low pitched breath sounds hear in the lung periphery

50
Q

Abnormal Breath sounds?

  • Snoring
  • Stridor
  • Wheezing
  • Rhonchi
  • Crackles
  • Pleural Friction Rub
A
  • Snoring: Upper airway is partially obstructed, often by
    tongue
  • Stridor: Harsh, high pitched sound heard on
    inspiration and can mean upper airway
    obstruction such as croup
  • Wheezing: Whistling sound due to narrowing of
    airways by edema, bronchoconstriction, or
    foreign materials
  • Rhonchi: Rattling sounds in the larger airways
    associated with excessive mucus or other
    material
  • Crackles: (aka Rales) Fine, moist crackling sound
    associated with fluid in the smaller airways
  • Pleural Friction Rub: Sounds like dried pieces of
    leather rubbing together, occurs when the
    pleura become inflamed, as in pleurisy
51
Q

What signs and symptoms might be indicative of a venous clot like a deep vein thrombosis?

A

Extremity swelling, redness, hard/firm

52
Q

What is Pulsus Paradoxis?

A

It is a drop in blood pressure 10mmHg during each inspiration and is indicative of COPD or cardiac tamponade. However as a rule you should never take the time to check for it during prehospital care.

53
Q

What does pulse oximetry measure? How does it measure it?

A

It measures the amount of oxygen saturation on hemoglobin (does not reflect the amount of hemoglobin) and it does so by sending two wave lengths of light, red light and infrared light.

Deoxyhemoglobin absorb more red light and Oxyhemoglobin absorb more infrared light. The ratio of the two lights is calculated and gives you a Hemoglobin Oxygen Saturation or SpO2

54
Q

SpO2 VS SaO2

A

SpO2 is oxygen saturation % given by a pulse oximeter but SaO2 is oxygen saturation % attained by blood gas analysis

55
Q

What is a Wright Spirometer?

A

It is a hand held device that a pt can blow into as hard as they can that will give a patient’s “Peak Expiratory Flow Rate” or PEFR. The test should be done twice and take the higher number which is in mL/min.

It is dependent upon patients sex, age, and height and requires a cooperative patient who understands how to use it

56
Q

Hyper/Hypocarbia?

A

high or low levels of CO2

57
Q

What is a colorimetric device?

A

It is a type of CO2 measuring device in which a chemical coated piece of paper sits in a plastic device that when breathed upon with H+ ions it change the paper’s color

58
Q

PG 22 HAS CAPNO VERBAGE TO LOOK OVER!

A

PG 22 HAS CAPNO VERBAGE TO LOOK OVER!

59
Q

Are most CO2 measuring electronic devices qualitative or quantitative?

A

Most are quantitative b/c they can measure exactly how much CO2 is present

(Qualitative devices only detect the presence)

60
Q

Describe the 4 phases of a wave on a capnography machine pleth

A

+ A-B = Phase I:
Respiratory baseline, it is flat b/c there is no CO2 present and corresponds to the late phase of inspiration and early part of expiration when there is dead space gases without CO2 released.

+ B-C = Phase II:
The respiratory upstroke. Reflects the appearance of CO2 in the alveoli.

+ C-D = Phase III:
The respiratory plateau. This is the max amount of CO2 exhaled and is where the ETCO2 measurement is taken.

+ D-E = Phase IV:
Inspiratory phase, the sudden downstroke that returns to baseline to restart the cycle

**Pg.24 Has the graphing example!!

61
Q

Normoxia VS Hyperoxia VS Hypoxia

A

Normoxia = normal, adequate O2 at 96-99% (maybe
100%)
Hyperoxia = too much oxygen

Hypoxia = not enough oxygen (less that 96%)

62
Q

Can you give too much oxygen?

A

Yes, too much oxygen (hyperoxia) can cause the formation of toxic chemicals called Free Radicals or Reactive Oxygen Species (ROS) that can damage body cells and tissues through a process called Oxidative Stress

63
Q

What is the most common cause of upper airway obstruction?

What is “Café Coronary”?

How can you tell when someone has a total upper airway obstruction?

A

The relaxed tongue is the most common upper airway obstructer.

Café Coronary is in reference to a common case of airway obstruction in which an elderly patient with dentures cant tell how well they have chewed their food so they accidentally inhale a large unchewed piece (this is made worse when alcohol is involved)

Most airway obstruction only need intervention when it is absolutely obstructed, sign of this are a silent cough, cyanosis, and the inability to speak or breath. Often you can ask “are you choking” and if they respond with hand movements instead of words then it is severe

64
Q

6 common causes of airway obstruction?

A
  • Tongue (most common)
  • Foreign matter (food, dentures, etc)
  • Trauma
  • Burns (laryngeal edema)
  • Allergic reaction (often reports itching in palate
    followed by a “lump” in the throat”, often a rash
    (urticaria) is seen
  • Infection (croup, epiglottitis, strep throat, etc)
65
Q

How to handle an airway obstruction in a conscious or unconscious patient. Laryngeal edema treatment?

A

Conscious:
- if partial block ask them to forcefully cough
- if complete block, perform abdominal thrusts first
then chest thrusts if needed. If pregnant pt go
straight to abdominal thrusts

Unconscious:
- Head tilt chin lift
- begin cpr
- each time you open airway for cpr, check for visible
foreign material
- if obstruction persists, use a laryngoscope and Magill
forceps to try to remove the block. Once removed,
begin ventilation and admin supp O2

Laryngeal Edema:
- head tilt chin lift, admin supp O2
- attempt bag valve ventilation if needed (sometimes
you can force air past)
- start IV with a crystalloid solution and IV or IM
epinephrine. Next admin diphenhydramine. ET tube
or sub tracheal air way may be needed

66
Q

What are the two main ways that you can get pulmonary edema?

A
  • Cardiogenic Pulmonary Edema which is caused by left sided heart failure in which the left ventricle is not pumping adequately so there is back pressure that goes back into the lungs and essentially pushes fluids out of the capillaries and into the interstitial spaces in the lungs
  • OR from ARDS aka Acute Respiratory Distress Syndrome in which fluid accumulates in the lungs because of increased vascular permeability and decreased fluid removal from the lung tissue. This can be caused by a very large array of things

**Basically there is Cardiogenic or Non-Cardiogenic Pulmonary Edema

67
Q

What is ARDS aka Acute Respiratory Distress Syndrome?

A

Is a form of pulmonary edema that results from fluid accumulation in the lungs because of increased vascular permeability and decreased fluid removal from the lung tissue. This can be caused by a very large array of things.

The byproduct of the different causes though ultimately result increased capillary permeability, destruction of the capillary membrane, and increase in osmotic forces that act to draw fluid into the interstitial space; combining to form a thickening of the respiratory membrane and limits oxygen diffusion. Ultimately it is a Diffusion disorder.

In severe cases enough fluid can accumulate to form in the alveoli causing a loss of surfactant, collapse of alveolar sacs, and further impaired gas exchange.

Mortality for ARDS is approx. 70%

68
Q

Signs/Symptoms and treatment for an ARDS patient?

A

Most signs and symptoms will be related to the underlying cause of ARDS, but usually there will be Crackles (Rales) or wheezing (if bronchospasm occurs), tachypnea, and tachycardia.

For treatment, unless there is hypoventilation do not give more fluids. Suction may be needed for secretions. Diuretics and Nitrates used in cardiogenic pulmonary edema are NOT helpful here.
The BEST thing you can do is give them supp O2 with CPAP and PEEP (Continuous Positive Atmo Pressure ; Positive End-Expiratory Pressure).

69
Q

What are the 3 most common Obstructive Lung Diseases? (the COPD umbrella)

A
  • Emphysema
  • Chronic Bronchitis
  • Asthma
70
Q

What three underlying diseases make up COPD?

What is directly linked as the cause for COPD?

A

Emphysema, Chronis Bronchitis, and Asthma

Smoking and Environmental toxins

71
Q

In obstructive lung disease, what are 3 major things happening in the bronchioles that make it hard to ventilate?

What is the “Hallmark” of Obstructive Lung Disease?

A
  • Bronchospasms
  • Increased Production of mucus (and damaged Cilia that are suppose to help move the excess mucus)
  • Inflammation of airway

During inspiration the bronchioles naturally dilate and when exhaling they constrict. But when you have the previously listed mechanisms in play severally reducing lumen size, air gets trapped. This is the “Hallmark” of obstructive lung disease is.

72
Q

Look at ARDS Pictures on PG 28-29!

A

Look at ARDS Pictures on PG 28-29!

73
Q

What pharmacological intervention options do you have with an Obstructive Lung Disease Pt? (asthma or copd)

A

Beta-Adrenergic Receptor (B2) stimulation will help fight bronchospasms by relaxing the smooth muscles. This is done by Albuterol, Levalbuterol, and epinephrine.

Ipratropium Bromide (Atrovent) is a parasympathetic blocker and will aid in drying the bronchial secretions when there is excess mucus production.

74
Q

What is Emphysema?

A

Emphysema results from the destruction of alveolar walls distal to the terminal bronchioles. More common in men, major factor is smoking. It ultimately affects the diffusion process.

Continued exposure to toxin substances such as cigarette smoke results in damage to alveolar membrane and walls leading to decreased surface area for gas exchange. It also weakens the walls of the small bronchioles which in combo with the alveoli damage it leads to a lessened recoil of the lungs which increases the amount of air trapped in the lungs. Additionally the amount of pulmonary capillaries decrease which increase resistance to pulmonary blood flow, this puts and causes hypertension on the right side of the heart and can lead to right heart failure, cor pulmonale, and death.

As the disease progresses PaO2 decreases which leads to the overproduction of RBCs (Polycythemia) to try to make more spots for O2 to ride on (which is not the problem, its wrongly compensating). PaCO2 also chronically increases, forcing the body to depend on hypoxic drive to control respirations.

75
Q

How might you identify an Emphysema Pt?

What common symptoms might you find? (besides the obvious)

A

Emphysema Pts = Pink Puffers

  • they are barrel chested
  • skinny b/c of energy used to breath
  • pink b/c of polycythemia
  • pursed lips
  • clubbed fingers are common
  • exhibits signs of Right Sided Heart Failure (JVD,
    Peripheral edema, hepatic congestion)
  • RARELY associated with a cough, except in the
    morning
76
Q

How do you calculate how much a pt smokes when calculating for a medical purpose?

A

of packs per day X # of years

Medical problems like emphysema, chronic bronchitis, and lung cancer usually arise after a pt surpasses a 20-pack/year history

77
Q

What is Chronic Bronchitis?

A

Occurs often after prolonged smoking, and results from an increase in the number of goblet (mucus-secreting) cells in the respiratory tree. It is characterized by the large amount of sputum produced. Unlike emphysema it affects ventilation and not diffusion itself.

The hypoxia and hypercarbia associated with chronic bronchitis are caused by a decrease in ventilation or vital capacity. This can also lead to polycythemia like emphysema. It is much more likely to caused an increase in PaCO2 which causes pulmonary vasoconstriction resulting in pulmonary hypertension and, eventually, Cor Pulmonale.

78
Q

How do you assess a patient has chronic bronchitis?

A

They will produce a large amount of sputum and a productive cough. Generally they must have a productive cough for at least three months per year for two or more consecutive years.
Patients are usually overweight and can be cyanotic giving them the Blue Bloater nick name.
They may also have signs of right sided heart failure and an ECG reading will often show increased right ventricular signs

79
Q

How to treat a pt with COPD (emphysema and/or chronic bronchitis) and why might O2 be dangerous even though it is obviously needed?

A

Treatment includes O2 and reverse of bronchoconstriction if present.
However, O2 may cause a dip in the pts respiratory drive b/c the disease has caused them to become dependent on a hypoxic respiratory drive. So their respiratory drive is dependent upon the need for O2 to make them want to breath as opposed to it normally being driven by the need to breath off CO2.

After O2 is given you should be ready to take over ventilations with a bag valve mask or with a CPAP machine with PEEP set to 10cm/H2O pressure.

(If the CPAP fails, intubation may be necessary. You have to have an AIRWAY)

Often Corticosteroids (Solu Medrol) are used for longer term management

80
Q

Asthma stats

A

Only respiratory problem that is on the rise not declining

death for blacks is twice as high for whites

50% of cases end in death on route to hospital

occurs in 45yo or more

intrinsic factors tend to affect adults whereas extrinsic factors tend to affect children

81
Q

What is asthma?

A

It is a chronic inflammatory disorder of the airways. Each pt has their own set of “triggers” but typically there will be two phases:

  • Phase I: after exposure to offending agent, release of chemical mediators such as histamine occurs to which contraction of smooth muscle and leakage of fluid from peribronchial capillaries is caused (bronchoconstriction and bronchial edema) which decreases expiratory airflow. (the typical “asthma attack”) This can last 1-2 hours before naturally dissolving or can be cut short with bronchodilator meds.
  • Phase II: Occurs 6-8 hours after exposure to the trigger and happens when cells of the immune system invade the mucosa of the respiratory tract (eosinophils, leukocytes, neutrophils). Which causes another round of swelling and edema of the bronchioles. Here beta-agonist drugs don’t work well and longer lasting Corticosteroids are required.

The 3 big symptoms of asthma are: dyspnea, wheezing, and coughing

82
Q

What are some good tools to use when dealing with an asthma pt?

What is the best method for manually attaining a breathing rate?

A

Peak Expiratory Flow Rate (PEFR)

Capno - they typically have a “shark fin” wave form b/c it is harder for them to empty air from the alveoli. And the ETCO2 levels will probably drop b/c they are hyperventilating but after they tire it should go back to normal.

Place fingers on radial artery, pretending to take pulse and place hand on pts chest, this will make them not alter breathing b/c they don’t think your taking that. Count for 30 seconds and then multiply by 2

83
Q

How to care for an asthma pt?

What is Status Asthmaticus?

A

The goals are to correct hypoxia, reverse bronchospasms, and reduce inflammation.

Give O2, get IV, Get ECG, Give Albuterol (or levalbuterol) and Atrovent in nebulizer; for prolonged asthma attacks give corticosteroids to help reduce inflammation.

After all this be ready for possible intubation b/c these patients can get very tired and quit breathing for themselves suddenly.

Status Asthmaticus is asthma that is a severe persistent attack even after repeated doses of bronchodilators. These pts will be exhausted, severely acidotic, and dehydrated. BE READY TO INTUBATE

84
Q

What is an Upper Airway Infection (URI)?
What is the best defense?
How do you treat it?

A

It as an infection involving the upper airway (the larynx and above). They are typically self limiting and only require treatments as needed for symptoms. The best defense is just proper hand washing and covering mouth during coughing or sneezing.

Most are caused by viruses though a few can be bacterial. The most significant is group A Streptococcus aka “strep throat”

This is not often life threatening except for cases where the infection causes pus bad enough to occlude an airway, especially in children.

85
Q

What is Pneumonia?

A

Pneumonia is an infection of the lungs. It is very common in the old and HIV pts and is a leading cause of death for immunosuppressed pts (HIV & Cancer). The unifying concept for those at an increased risk are those who have a defect in mucus production, ciliary action, or both.

It is a collection of related respiratory diseases caused when a variety of infectious agents invade the lungs, mostly viruses and bacteria. It is primarily a ventilation disorder, as fluid and inflammation cells collect in the alveoli, and may collapse. It is possible for the infection to spread beyond the lungs and get into the blood stream, causing septic shock.

The patient usually presents with:
- Ill appearance
- fever
- chills
- pleuritic chest pain
- productive cough with yellow/brown sputum with 
  possible bloody streaks
- Crackles (rales) over infected area of lung

**Any pt with chest pain, productive cough, fever, and chills should be assumed to have pneumonia

Official diagnosis requires x-ray, blood labs, ect. and will usually require antibiotics. So in the prehospital setting, just treat symptoms.

86
Q

What is Severe Acute Respiratory Syndrome (SARS)?

A

It is a viral respiratory illness aka SARS-CoV (coronavirus). It is spread by close person contact via water droplets that enter through a mucus membrane. It incubates for about 2-7 days and people are only contagious for as long as they have symptoms. Pts should quarantine for at least 10 days.

Signs and symptoms include:
- sore throat
- Rhinorrhea (runny nose)
- chills/rigors
- myalgias (muscle aches)
- headache
- diarrheic
It can progress into cough w/ sputum, respiratory distress and end in respiratory failure

Treatment is similar to pneumonia; extra protective wear should be donned and receiving facility should be notified

87
Q

What is Middle East Respiratory Syndrome (MERS)?

A

It is a viral respiratory illness and a new version of a coronavirus; MERS-CoV. It is spread through close person contact and kills 3-4 of every 10 pts infected. There is no vaccine or specific treatment. Incubation is for 5-6 days. Pts with preexisting conditions are likely to have a more severe infection.

Primary Signs and symptoms include:

  • Fever
  • Cough
  • Shortness of breath

Possible S&S’s include:

  • nausea
  • vomiting
  • diarrhea
88
Q

What are the 4 major types of lung cancer and from where do they arise?

A

Lung Cancer is the leading cause of cancer related death.
It is primarily a problem of diffusion but can also become ventilatory.
Most lung cancers are caused by carcinogens (cancer-producing substances) from cigarette smoking.

  • Most common is ADENOCARCINOMA which arises
    from glandular-type cells in the lungs and bronchioles
  • SMALL CELL CARCINOMA (“oat cell” carcinoma)
  • EPIDERMOID CARCINOMA
  • LARGE CELL CARCINOMA all the previous three arise
    from bronchiole tissues
89
Q

What are 5 common toxic inhaled substances and what can inhalation cause? How do you treat it and what are some important questions to ask x3?

A

Inhalation of the following can case pain, inflammation, or destruction of pulmonary tissue leading to edema and/or bronchospasms:

  • Ammonia (ammonium hydroxide)
  • Nitrous Oxide (nitric acid)
  • Sulfur Dioxide (sulfurous acid)
  • Sulfur Trioxide (sulfuric acid)
  • Chlorine (hydrochloric acid)

It is important to determine the duration of exposure, if it was in an enclosed space, and if consciousness was lost

Remove pt from environment and give them humidified O2, intubation may cause laryngospasm completely blocking airway. Attain IV access in preparation for drug usage b/c airway may be lost very quickly

90
Q

What is Carbon monoxide poisoning?

A

It is a tasteless, odorless, colorless gas that is emitted by incomplete burning of fossil fuels. It is the number ONE cause of poisoning and mostly occurs from automobile transmissions and home heating devices.

Hemoglobin has 200-250x higher affinity; it blocks them from transporting O2; when bound it is called Carboxyhemoglobin; it ultimately results in hypoxia and metabolic acidosis which is worsened by its ability to bind to myoglobin which stores O2 in muscles.

91
Q

How is a CO-oximeter similar and different from a pulse oximeter. What all can a CO-oximeter detect/measure?

A

It functions similarly but it uses 8 wavelengths of light instead of two. It can measure CO levels but it can also detect:

  • carboxyhemoglobin (CO)
  • methemoglobin
  • oxyhemoglobin
  • deoxyhemoglobin
92
Q

What signs and symptoms are felt at what levels of severity of CO poisoning and what is the related % of poisoning?

  • mild
  • moderate
  • severe
  • fatal
A

Mild:

  • 15-20%
  • headache, nausea, vomiting, dizziness, blurred vision

Moderate:

  • 21-40%
  • confusion, syncope, chest pain, dyspnea, tachycardia, tachypnea, weakness

Severe:

  • 41-60%
  • arrhythmias, hypotension, cardiac ischemia, palpitations, respiratory arrest, pulmonary edema, seizures, coma, cardiac arrest

Fatal:
- 60%+

93
Q

What is a pulmonary embolism?

A

It is a blood clot (thrombus) or some other particle that lodges in a pulmonary artery and blocks the flow. 1 in 5 cases of sudden death are a PE, 50K deaths annually.

Risk factors include: immobility, venous pooling during pregnancy, cancer, infections, A-Fib, sickle cell, birth control (hormone therapy)

Specific types of emboli include: air, fat, amniotic, but mostly blood clots that develop in deep veins of lower legs

Once clot has lodged the resulting effect on the lungs is they are no longer able to perform gas exchange which leads to Ventilation-Perfusion Mismatch

Signs and symptoms may include:

  • sudden onset of dyspnea
  • unproductive cough with hemoptysis
  • labored breathing
  • tachypnea & tachycardia
  • In large severe emboli you may get right side heart failure, JVD, extreme confusion, extreme hypotension, or cardiac arrest.

Up to 50% of cases a deep vein thrombosis will be evident showing a warm, swollen extremity with thick cord palpated along medial thigh and pain on palp or extension of calf

94
Q

What is a spontaneous pneumothorax?

A

It is a pneumothorax in the absence of blunt or penetrating trauma.
Typical pt is: male (5-1 male to female ratio), 20-40yo, tall, thin, smoker/COPD; most pts will have a recurrent episode within 2 years of first one.

S&S:

  • sudden sharp, pleuritic chest pain or shoulder pain
  • decreased breath sounds best noted at apex
  • hyper resonance to percussion
  • subcutaneous emphysema on palp
  • tachypnea, diaphoresis, and pallor
  • Cyanosis is RARE

all you can really do is give O2

Be wary of CPAP or intubation b/c it risks a Tension Pneumothorax; signs that this has occurred are:

  • the pt became hard to ventilate
  • hypoxic
  • cyanosis
  • hypotension
  • late signs are JVD & tracheal deviation
95
Q

What is Hyperventilation Syndrome?

A

It primarily is caused by anxiety but always assume something deeper; it is rapid breathing that is getting rid of too much CO2. Another side effect of this now respiratory alkalotic state is that it increases the amount of bound Calcium causing Hypocalcemia (less free C b/c it is being taken up by cells) causing cramping in the hands and feet aka Carpopedal Spasm.

Other signs and symptoms may include:

  • fatigue
  • dizziness
  • nervousness
  • dyspnea
  • chest pain
  • numbness of mouth, hands, & feet

Be wary of pts with a history of seizures as a hyperventilator episode can precipitate a seizure

Primary treatment is just reassuring the nervous pt and instructing for them to slow breathing on their own.
DO NOT use paper back rebreathing or breath holding techniques

96
Q

What are some causes of CNS dysfunction that affect breathing?

A
  • head trauma
  • stroke
  • brain tumors
  • certain drugs such as narcotics and barbiturates that
    lower the responsive to PaCO2 levels in the brain
97
Q

What are some causes of Spinal Cord, Nerves, or Respiratory Muscle dysfunction?

A
  • spinal cord trauma
  • polio
  • amyotrophic lateral sclerosis (ALS or Lou Gehrig’s)
  • myasthenia gravis
  • tumors
  • Guillain-Barre Syndrome (GBS) in which the myelin
    covering of the nerve is damaged, resulting in relative
    loss of nerve impulse conduction

PCIV (5 decks)

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