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PathoPhys Exam 2 > PULMONARY > Flashcards

PULMONARY Flashcards

1
Q

Which side of the lungs is a more common site for pneumonia, and why?

A

Right side - because right bronchus is a more “straight shot” to lungs than left.
Particularly for aspiration pneumonia

*Right Lower Lobe - most common site for pneumonia**

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2
Q

Describe the anatomical differences between the right and left side of respiratory system

A

Right bronchial main stem branches 3 times for each of the 3 right lobes of the lung

Left bronchial main stem branches 2 times for each of the 2 left lobes of the lung

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3
Q

When does the conducting zone end and the respiratory zone begin?

A

As the terminal bronchioles become respiratory bronchioles

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4
Q

Describe the movement of gas at the alveolar / capillary junction

A

PASSIVE DIFFUSION
net movement occurs until gas pressures are equal across the surface

  • O2 will move from high to low pressure (bronchioles to capillary)
  • CO2 will move from high to low pressure (capillary to bronchioles)
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5
Q

Is it possible to stockpile O2?

A

Yes - but only if the O2 concentration is higher than normal

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6
Q

Typical PO2 in tissue capillaries during strenuous exercise

A

PO2 = 20mmHg
with
O2Sat = 35%

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7
Q

Typical PO2 in tissue capillaries at rest

A

PO2 = 45mmHg
with
O2Sat = 75%

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8
Q

Usual PO2 in lung capillaries

partial pressure of inspired O2 in the lungs

A

PO2 = 100mmHg
with
O2Sat = 98-100%

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9
Q

At what PO2 are 2 of every 4 Fe ions bound by O2?

A

PO2 of 25mmHg
with
O2Sat = 50%

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10
Q

At what PO2 are all 4 Fe ions bound by O2?

A

PO2 = 100mmHg
with
O2 Sat = 98-100%

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11
Q

How does hyperventilation effect diffusion of O2 and CO2?

A

Hyperventilation reduces the partial pressure of CO2 in the lungs from the normal 40mmHg, thereby allowing the partial pressure of O2 to rise

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12
Q

How would these conditions affect the O2-Hg curve?

Low pH
High CO2
Higher temperature

A

Shift to the RIGHT

These conditions make Hg more apt to release O2
(Less affinity)

Tissues are in greater need of O2

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13
Q

Where in the body does the O2-Hg curve tend to shift right?

A

Skeletal muscles in use
(lactic acid, CO2 acidity - high temp - high CO2%)

Placenta

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14
Q

How would these conditions affect the O2-Hg curve?

High pH
Low CO2
Lower temperature

A

Shift to the LEFT

These conditions make Hg more apt to BIND and HOLD O2

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15
Q

Where int he body does the O2-Hg curve tend to shift left?

A

LUNGS
(dumping CO2 = low acidity/higher pH and low CO2%)
+ outside air is cooler than body temp

Fetal Hemoglobin
extremely high affinity for O2

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16
Q

4 structural abnormalities than can affect gas exchange

A
  1. Confluence of alveoli, from destroyed septae. Less surface area. (Emphysema)
  2. Thickening of septae, making gas exchange more difficult. (Pulmonary Fibrosis, Pulm Edema)
  3. Arterioles leading to septae blocked, no blood arriving for exchange (PE, fat embolus, Amniotic Fluid Embolism)
  4. Alveolis filled with fluid (asthma, pneumonia)
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17
Q

Condition associated with increased lung compliance

A

Emphysema (easy to expand the lung)

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18
Q

Condition associated with decreased lung compliance

A

Pulmonary fibrosis (hard to expand the lung)

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19
Q

Two major determinants of lung compliance

A
  1. Stretchability of lung tissues
  2. Surface tensions at air-water interfaces within alveoli
    * *surfactant increases compliance! by decreasing surface tension caused by water at alveolar surfaces**
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20
Q

Where is surfactant secreted and what does it to

A

Secreted by Type II 2 !! Alveolar Cells

“reduces surface tension” - reduces cohesive forces between molecules of water on alveolar surface&raquo_space; increases lung compliance!

Type II pneumocytes start making surfactant around 28 weeks gestation - fully functioning by 36-37 weeks

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21
Q

Group of disorders characterized by progressive scarring of the lung tissue between the alveolar sacs and surrounding capillaries.

Characterized by alveolar septal thickening, fibroblast proliferation, collagen deposition, and, if the process remains unchecked, pulmonary fibrosis

A

Interstitial Lung Diseases
aka Intrinsic Restrictive Lung Diseases

Idiopathic Interstitial Pneumonia
Eosinophilic pulmonary disease
Sarcoidosis
Pulmonary alveolar proteinosis

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22
Q

Group of disorders characterized by a narrowing of pulmonary airways. This hinders a person’s ability to completely expel air from the lungs.

The practical result is that by the end of every breath, quite a bit of air remains in the lungs.

Exhalations take longer with obstructive lung disease, so that as the rate of breathing increases and the lungs work harder, the amount of fresh air circulated into the lungs, and spent air circulated out, decreases.

A

Obstructive Lung Disease

COPD (Emphysema, chronic bronchitis)
Asthma
Bronchiectasis
Cystic Fibrosis

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23
Q

Diseases characterized by a decrease in the total volume of air that the lungs are able to hold, is often due to a decrease in the elasticity of the lungs themselves or caused by a problem related to the expansion of the chest wall during inhalation i.e. weakened muscles or damaged nerves

Decreased lung volumes&raquo_space; decreased oxygenation

A

Restrictive Lung Diseases

Sarcoidosis
Pulmonary fibrosis
Scoliosis
Marked obesity

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24
Q

Gas diffusion in the lung depends on what three things?

A
  1. Availability / Ventilation
    (how much O2 available / able to get into alveoli)
  2. Diffusability
    (how easy it is for that O2 to cross the alveolus into the pulmonary capillaries)
  3. Perfusion
    (how well those capillaries are picking up the O2 in the alveoli)
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25
Q

Describe FIO2 - room air and 6 liters/min mask

A

Fraction of Inspired Air that is Oxygen

Room air: 0.21 (with PIO2 at 140mmHg sea level)
6 L / min mask: 100%

26
Q

What can decrease Availability / Ventilation?

A
  1. Respiratory rate - shallow, infrequent breathing brings in less O2
  2. PIO2: At higher altitudes, PIO2 drops from 140mmHg to 70mmHg, so even though FIO2 is still 21%, the low PIO2 = lowers pressure gradient, and less oxygen diffuses across alveoli to capillaries
27
Q

What can decrease diffusability?

A

Thickening of interstitium

** notably doesn’t affect diffusability of CO2 as much as O2 **

28
Q

What can decrease perfusion?

A
  1. V/Q Mismatch - COPD, some areas of the lungs have great circulation but poor oxygenation
  2. V/Q Shunting - some areas of the lung have enough oxygen but little blood flow to pick it up >
    > will carry low O2, high CO2 blood to systemic circulation
  3. Right-to-left Shunting - if low O2, high CO2 blood skips the lungs completely, via
    - hole in the heart
    - perfusing areas that have no ventilation
29
Q

Decreased PaO2 levels in bloodstream

A

Hypoxemia

30
Q

Decreased O2 delivery in tissues

A

Hypoxia

31
Q

If the A-a gradient is normal, the cause of hypoxemia must be:

A
  1. Hypoventilation ( increased PaCO2)
    * * COPD, neuromuscular, poor ventilator settings **
  2. Low Pi (extreme elevation)

normal A-a gradient is good for ruling out pneumonia, and ruling in COPD exacerbation

32
Q

If the A-a gradient is elevated, the cause of hypoxemia must be:

A
  1. V/Q Mismatch (Ventilation/Perfusion Mismatch) - corrected w FIO2 100%
  2. Shunting
  3. Impaired Diffusion (corrected w FIO2 100%)
33
Q

What would the A-a gradient in a patient w both low PaCO2 and low PaO2 be like?

A

A-a gradient must be elevated in a patient with both low PaCO2 and low PaO2

both of these numbers are shown on ABG results

34
Q

A-a gradient formula

A

A-a gradient = PA O2 - Pa O2

PA O2 (Alveolar O2 at room air) = 
[150mmHg] - [ (Pa CO2) / 0.8 ]
35
Q

What is indicated for a patient with an elevated A-a gradient that is not corrected with 100% FIO2?

A

Shunt (R>L)
V/Q ratio of 0 “absolute V/Q shunt”
Complete obstruction of alveoli, complete atelectasis, so any blood passing by that area is not oxygenated at all (blue blood sent to systemic circulation)

36
Q

Causes of Hypoxia

A

ANY HYPOXEMIA

but also:

  1. Heart failure / decreased cardiac output
    * O2 getting to blood, but bloodstream isn’t moving*
  2. Anemias of Carbon Monoxide poisoning
    * O2 arrives at bloodstream, but no taxis to carry it*
  3. Cyanide poisoning of the mitochondria
    * O2 arrives to the bloodstream and the tissues, but tissues can’t do anything with it *
37
Q

Why do COPD patients have high CO2 values?

A

Confluence / Collapse of Alveoli (atelectasis)&raquo_space; “dead space” in lungs that’s still being perfused&raquo_space; “absolute V/Q shunting”&raquo_space; CO2 rich, blue blood carried into systemic circulation

38
Q

What is “Self-PEEP” ?

A

When COPD patients inhale through nose and exhale slowly through pursed lips, can help privet collapse of small airways

39
Q

Globulin that prevents lung damage from lysosomal enzymes

A

Alpha-1 Antitrypsin

Deficiency results in emphysema

40
Q

Does asthma have a greater impact on inspiration or expiration?

A

Expiration

“Wheezing on expiration”

41
Q

FEV 1 Predicted Value for Severe Asthma

A

35-49%

42
Q

Physiological consequences of the positive pressure into chest cavity with a PTX

A
  1. Compresses heart and blood vessels
  2. Decreases cardiac output
  3. Decreases venous return (usually dependent on negative pressure in chest cavity)
43
Q

Physiological consequences of loss of negative pressure in pleural space with a PTX

A
  1. Lung volume air escapes into pleural space (moves from high to low pressure)
  2. V/Q shunt - blood traveling from that region to the heart doesn’t get oxygenated
  3. Decreased vital capacity
  4. Decreased PaO2
44
Q

When to suspect Tension Pneumothorax:

A
  1. Distress, with rapid labored respirations
  2. Cyanosis
  3. Tachycardia
  4. Diaphoresis
    * *receiving CPR or on ventilation **
45
Q

Cranial Nerves involved in gag reflex

A

Afferent: (touching pharyngeal mucosa ) > CN IX
Efferent: CN X > (gag reflex)

46
Q

Cough reflex

A

CN X

Triggers: Chemoreceptors and Mechanoreceptors, multiple sites within reparatory tract

Lowest trigger site: @ bifurcation / trifurcations of each main stem bronchus

47
Q

Mechanoreceptors which protect against excessive lung inflation by decreasing reparatory rate and volume

A

Stretch receptors

48
Q

Baroreceptors in the capillaries of alveoli which are sensitive to increased pulmonary capillary pressure - and respond by triggering slow shallow breathing, laryngeal constriction, decreased BP and bradycardia

A

Juxtapulmonary (J) capillary receptors

49
Q

Immune cells in upper respiratory tract - down only to terminal bronchioles, none in gas exchange areas

A

IgA secreting

Dendritic cells

Cilia (to move mucus upwards)

50
Q

Infection or inflammation of the pleura, which often results from pneumonia. Result is a roughening of the pleura which creates friction and stabbing pain with each breath

A

Pleurisy

51
Q

Muscles of inspiration

SSED

A

Sternocleidomastoid
Scalenes
External intercostals
Diaphragm

52
Q

Muscles of expiration

IIRT

A

Internal Intercostals
Internale / External Obliques
Rectus Abdominis
Transverse Abdominis

53
Q

2 Nerves controlling respiratory muscles

A

Phrenic Nerve

Intercostal (Thoracic Spinal) Nerves

54
Q

Area of brain that controls timing of inspiration - rate and rhythm

A

Medulla

  • Sends inspiratory and expiratory motor signals down spinal cord to chest wall muscles and diaphragm
  • Sensitive to pH, CO2, O2 from chemoreceptors
55
Q

Area of brain that controls smoothness and coordination efforts of breathing - depth and length of each respiration

A

Pons

*Quantity of air inhaled,

56
Q

Increased depth of respiration with a decreased respiratory rate seen when this area is damaged

A

Lateral Pons, respiratory region

57
Q

Alternating periods of deep and shallow breathing; apnea lasting 15-60 seconds; occurs when bloodflow to brainstem is limited

A

Cheyne - Stokes Breathing

58
Q

Where are the central chemoreceptors and what do they detect?

A

Near pons and medulla (brainstem)

Detect concentration of H+ in CSF - which is directly proportional to PaCO2

DOMINANT CONTROL OF RESPIRATION

59
Q

Where are the peripheral chemoreceptors and what do they detect?

A

Carotid bulb and aortic arch

Detect pCO2 ** most sensitive

pO2 ** NOT TRIGGERED UNTIL pO2 IS 70-60mmHg
pH

60
Q

What two things stimulate respiration?

A

Drop in O2 (peripheral chemoreceptors - pO2 70-60mmHg)

Drop in pH (central chemoreceptors - indicative of increase in CO2)

61
Q

Normal ABG

A

pH / pCO2 / pO2 / HCO3 / SaO2

7.34-7.45 40mmHg 90mmHg 24mEql 95%

62
Q

High Anion Gap

A

> 11 ** means additional positive ions, like H+ or other acids, are present **

total cation - total anion
(Na + K+) - (CL + HCO3)

PathoPhys Exam 2 (2 decks)

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