Respiratory P2 Flashcards

1
Q

O2 content in the blood depends on 3 things

A

PO2
RBC #
Hemoglobin

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2
Q

Normal Hb ranges

A

Males: 13-18 g/dl
Female: 12-16 g/dl

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3
Q

Each Hb carries

A

1.34 ml O2 if fully saturated
4 binding sites for O2

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4
Q

A normal person will carry…

A

20 ml O2

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5
Q

a person with anemia

A

has a decrease in RBC mass or amount of Hb
will only have 13.4 ml O2
O2 dissolved in plasma .2 ml/dl

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6
Q

S/S of Anemia

A

decreased endurance
tachycardia
pallor
shortness of breath
dizziness
cold hands/feet

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7
Q

At rest, what can we expect the SPO2 of a pt who has anemia to be?

A

likely normal
not measuring absolute hemoglobin, but a ratio

remember that SPO2 is not a complete measure of circulatory sufficiency or O2 content in blood

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8
Q

Why is less than 90% PO2 a critical clinical point with regards to SaO2?

A
  1. it is when the slope begins to drastically change
  2. clinical signs of hypoxemia
  3. cut-off point for safe mobility or exercise
  4. supplemental O2
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9
Q

RV/LV output in an adult

A

5.5L
rate of blood flow through the pulmonary circulation is equal to the rate of blood flow through systemic circulation

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10
Q

Driving pressure in pulmonary circulation

A

-10 mmHG
-it HAS to be low for pulmonary circulation to equal systemic circulation. lungs would fill with fluid if it was higher
-low pressure and low resistance produces less filtration then systemic capillaries

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11
Q

V/Q

A

ratio of the amount of air getting to the alveoli (alveolar ventilation) and the amount of blood being sent to the lungs (cardiac output)

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12
Q

Why is VQ ratio is important ?

A

it is one of the major factors affecting alveolar (arterial) levels of O2 and CO2

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13
Q

upright lung V/Q

A

Physiological dead space: V>Q
Mid: V/Q = 1
shunt: V<Q

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14
Q

What is the average V/Q ratio across the lungs?

A

.8
this means that there is more perfusion vs ventilation
autoregulation causes the lungs to try to match V & Q by altering the size of pulmonary arterioles

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15
Q

V/Q mismatch

A

contributes to the 5 mmHg difference between PO2 in alveolar air and PO2 in arterial blood

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16
Q

Which lung are you more likely to aspirate?

A

right

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17
Q

High V/Q ratio

A

pulmonary embolism
Q is the pathology

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18
Q

Low V/Q ratio

A

pneumonia
ventilation is the pathology

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19
Q

Goal of turning schedule

A

allow for drainage of different areas of the lungs via gravity to ensure better ventilation/perfusion ratio

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20
Q

CO2 Transport

A

CO2 must be removed from living tissues via diffusion out of cells, movement into blood, excretion by lungs

Transported in blood via
1. dissolved CO2
2. carbamino compounds
3. HCO3

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21
Q

What happens to CO2 within RBCs in systemic capillaries?

A
  1. reaction is catalzyed by carbonic anhydrase in RBCs
  2. CO2 combines with water to make carbonic acid
  3. build up of carbonic acid dissociates and becomes bicarbonate
  4. release of bicarbonate is buffered by Hb
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22
Q

What happens to CO2 in lung capillaries?

A
  1. Deoxy-Hb is converted into oxy-Hb
  2. oxy-Hb has weak affinity for H+, H+ is released within the RBCs
  3. Eventually forms carbonic acid, which becomes O2 and CO2
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23
Q

Blood pH norm

A

7.35 to 7.45

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24
Q

Blood pH is maintenance

A

Lungs, maintains PaCO2
Kidneys, maintains bicarbonate (base) and hydrogen (acid) levels

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25
Q

Types of acids in body

A

Volatile acids
Nonvolatile acids

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26
Q

Volatile acids

A

can leave solution and enter atmosphere as a gas
carbonic acid
carbonic acid is controlled by lungs

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27
Q

Nonvolatile

A

do not leave solution, we can’t breathe these off

  1. sulfuric and phosphoric acids
  2. by products of aerobic and anaerobic metabolism during starvation

must be buffered in body fluids before excretion by kidneys

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28
Q

Buffer systems

A

provide or remove hydrogen to stabilize pH

bicarbonate is the most important extracellular fluid buffer

kidneys excrete excessive H and produce bicarbonate

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29
Q

PO2 ranges of arterial blood gases

A

80 mmHg to 100 mmHg

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30
Q

PCO2 range of arterial blood gases

A

35-45 mmHg

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31
Q

Bicarbonate range of arterial blood gases

A

22-26 mEq/L

32
Q

Acceptable ranges of ABGs are generally reported in following format

A

PO2
PCO2
pH
HCO3

33
Q

Why and when would ABGs be performed?

A

lung disease with poor gas exchange, kidney disease, electrolyte problems

34
Q

Acute disorders of acid-base

A

Respiratory Acidosis
Respiratory alkalosis
Metabolic Acidosis
Metabolic Alkalosis

35
Q

Respiratory Acidosis

A

1.reduction in pH due to primary increase in PCO2 (hypercapnia)
2. features include low pH, high PCO2, normal HCO3
3. Causes include hypoventilation, obstructive lung disorders, CNS depression

36
Q

Hypoventilation

A

can be caused by oversedation (opioids), chest wall deformities

37
Q

Respiratory alkalosis

A
  1. increase in pH due to primary decrease in PCO2 (hypocapnia)
  2. features include high pH, low PCO2, normal bicarbonate
  3. causes include hyperventilation, hypoxemia, pulmonary embolus
38
Q

Hyperventilation

A

caused by anxiety, pain, shock, manual ventilation

39
Q

Left shift of oxy-Hb curve

A

Hb has increased affinity for O2, making unloading of O2 into tissues harder

alkalosis (increased pH) can be caused by hyperventilation, vomiting, pancreatic diseases

40
Q

Pulmonary Embolism

A
  1. Blood flow to lung tissue is blocked by embolus
  2. decreased perfusion, increased V/Q ratio
  3. hypoxemia triggers increased RR, leads to alkalosis
41
Q

Metabolic Acidosis

A
  1. decrease in pH due to primary decrease in bicarbonate
  2. features include low pH, normal PCO2, low HCO3
  3. Causes include ketoacidosis, posisonings, renal failure, prolonged diarrhea
42
Q

Ketoacidosis

A

caused by starvation

43
Q

Prolonged diarrhea…

A

is losing base

44
Q

Metabolic Alkalosis

A
  1. increase in pH due to primary increase in bicarbonate
  2. features include high pH, normal PCO2, high bicarbonate
    Causes include vomiting, diuretic therapy, severe potassium depletion, excessive ingestion of black licorice
45
Q

Prolonged vomiting

A

losing acid

46
Q

Diuretic therapy

A

loss of H+, causes increase pH

47
Q

Severe potassium depletion

A

leads to loss or excessive excretion of H+

48
Q

Excessive ingestion of black licorice

A

loss of hydrogen and potassium in urine is increased

49
Q

What does PCO2 tell us?

A

alveolar ventilation

50
Q

What does PO2 tell us?

A

oxygenation status, can also estimate with pulse oximetry

51
Q

What does HCO3 tell us?

A

buffering capacity
base excess/base deficit

52
Q

Your patient in the hospital has had ABGs drawn. The chart is as follows = 92/49/7.31/25

A
  1. Pt is slightly acidic
  2. PCO2 is high, HCO3 is normal. Primary respiratory problem.
  3. Condition is described as respiratory acidosis
53
Q

Your patient in the hospital has had ABGs drawn. The chart is as follows: 92/40/7.32/20

A
  1. pt is acidic
  2. PCO2 is normal, HCO3 is low. Metabolic problem.
  3. Condition is described as acute metabolic acidosis, can be caused by type 1 diabetes
54
Q

Your patient in hospital has had ABGs drawn. They are listed in the chart 92/47/7.35/28

A
  1. pt is in acid/base balance
  2. PCO2 and HCO3 are both high, respiratory acidosis and metabolic alkalosis
  3. Can be either respiratory acidosis w/compensation of metabolic alkalosis (COPD) or metabolic alkalosis w/compensation of respiratory acidosis (vomiting w/hypoventilation)
55
Q

Your patient in the hospital has had ABGs drawn. They are in the chart as 92/33/7.35/21

A
  1. pt is in acid-base balance
  2. Low PCO2 and low HCO3, have both respiratory alkalosis and metabolic acidosis
  3. respiratory alkalosis comp for metabolic acidosis (hyperventilation w/diabetes ketoacidosis) OR metabolic acidosis comp w/respiratory alkalosis (hyperventilation, kidneys produce less bicarbonate)
56
Q

Kussmaul Respirations

A

hyperventilation associated with diabetic ketoacidosis

57
Q

Roles of dissolved O2 in plasma

A
  1. Establishes PO2 of blood and tissue fluids
  2. only dissolved O2 in plasma can be utilized by cells
  3. partial pressure of O2 plays role in determining loading of O2 onto Hb in lungs and unloading of O2 into cells
  4. plays role in regulation of breathing by stimulating chemoreceptors
58
Q

Regulation of breathing occurs via

A

Medulla Oblongata
Pons

59
Q

Medulla Oblongata

A

loose collection of neurons in the reticular formation called rhythmicity center. Control autonomic breathing.

has both ventral and dorsal respiratory group

60
Q

Pons

A

controls rhythmicity center in medulla
apneustic center (excitatory) and pneumotaxic center (inhibitory)

61
Q

3 ways to stop breathing

A

stroke
spinal cord injury
paralyze diaphragm

62
Q

Dorsal respiratory group

A
  1. contains inspiratory neurons that innervate both diaphragm and ventral respiratory group
  2. receives input from CN IX, X, VRG
  3. most likely integrate regulation of respiration rate and depth

a part of medulla

63
Q

Ventral respiratory group

A

contains both expiratory and inspiratory neurons
controls motor neurons to internal intercostal muscles

part of medulla

64
Q

Apneustic center

A
  1. promotes inspiration by stimulating inspiratory neurons in medulla
  2. provides constant stimulus for inspiration
  3. if no input received from the pneumotaxic center, prolonged inspiratory gasps occur
65
Q

Pneumotaxic center

A
  1. may inhibit apneustic center, inhibiting inspiration
  2. modulates output of medullary centers
  3. function still incompletely understood, likely maintains normal respiration
66
Q

Rhythmicity Center

A

from the medulla
made up of dorsal respiratory and ventral respiratory groups
controls autonomic breathing

67
Q

What regulates breathing?

A

voluntary control
automatic control–> chemoreceptors that monitor changes in blood PCO2, PO2, pH

68
Q

Peripheral chemoreceptors

A

carotid and aortic bodies
control breathing indirectly via sensory nerve fibers to medulla

69
Q

Chemoreceptor control

A

input for chemoreceptors modify rate and depth of breathing
-O2 content of blood decreases slowly because we have a reservoir
-PCO2 is more immediately affected by changes in ventilation, rate and depth is adjusted to maintain

70
Q

Chemoreceptors are more sensitive to changes in

A

PCO2

71
Q

Peripheral chemoreceptors

A

cartoid bodies are more important than aortic bodies in meditating respiratory changes in response to chemical changes in plasma

only chemoreceptors that increase ventilation in response to hypoxemia

72
Q

Firing rate of carotid bodies increases when

A

arterial PCO2 increases
pH decreases
PO2 decreases below 60 mmHg (or lower than 89% in pulsoximeter)

73
Q

Chemoreceptors and pH

A

cerebral cortex has a slower reaction to pH
brainstem has the 1st response to pH

74
Q

Central Chemoreceptors

A

within the medulla
fall in CSF pH stimulates these

responsible for 70-80% of increased ventilation that occurs in response to sustained rise in arterial PCO2

takes several minutes to respond after peripheral

75
Q

Acclimatization to high altitude

A

high altitude = cause of hypoxemia
-PaO2 decreases, carotid bodies increase RR/TV
-hypoxic ventilatory produces hyperventilation, produces initial respiratory alkalosis
-kidneys excrete bicarbonate to alter pH
-kidneys secrete EPO to trigger more RBC and increase Hb

76
Q

Altitude Training

A

increases RBC number
increases Hb concentration
angiogenesis
altered glucose transport, glycolysis, pH regulation