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
Types of acids in body
Volatile acids Nonvolatile acids
26
Volatile acids
can leave solution and enter atmosphere as a gas carbonic acid carbonic acid is controlled by lungs
27
Nonvolatile
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
28
Buffer systems
provide or remove hydrogen to stabilize pH bicarbonate is the most important extracellular fluid buffer kidneys excrete excessive H and produce bicarbonate
29
PO2 ranges of arterial blood gases
80 mmHg to 100 mmHg
30
PCO2 range of arterial blood gases
35-45 mmHg
31
Bicarbonate range of arterial blood gases
22-26 mEq/L
32
Acceptable ranges of ABGs are generally reported in following format
PO2 PCO2 pH HCO3
33
Why and when would ABGs be performed?
lung disease with poor gas exchange, kidney disease, electrolyte problems
34
Acute disorders of acid-base
Respiratory Acidosis Respiratory alkalosis Metabolic Acidosis Metabolic Alkalosis
35
Respiratory Acidosis
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
Hypoventilation
can be caused by oversedation (opioids), chest wall deformities
37
Respiratory alkalosis
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
Hyperventilation
caused by anxiety, pain, shock, manual ventilation
39
Left shift of oxy-Hb curve
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
Pulmonary Embolism
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
Metabolic Acidosis
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
Ketoacidosis
caused by starvation
43
Prolonged diarrhea...
is losing base
44
Metabolic Alkalosis
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
Prolonged vomiting
losing acid
46
Diuretic therapy
loss of H+, causes increase pH
47
Severe potassium depletion
leads to loss or excessive excretion of H+
48
Excessive ingestion of black licorice
loss of hydrogen and potassium in urine is increased
49
What does PCO2 tell us?
alveolar ventilation
50
What does PO2 tell us?
oxygenation status, can also estimate with pulse oximetry
51
What does HCO3 tell us?
buffering capacity base excess/base deficit
52
Your patient in the hospital has had ABGs drawn. The chart is as follows = 92/49/7.31/25
1. Pt is slightly acidic 2. PCO2 is high, HCO3 is normal. Primary respiratory problem. 3. Condition is described as respiratory acidosis
53
Your patient in the hospital has had ABGs drawn. The chart is as follows: 92/40/7.32/20
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
Your patient in hospital has had ABGs drawn. They are listed in the chart 92/47/7.35/28
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
Your patient in the hospital has had ABGs drawn. They are in the chart as 92/33/7.35/21
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
Kussmaul Respirations
hyperventilation associated with diabetic ketoacidosis
57
Roles of dissolved O2 in plasma
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
Regulation of breathing occurs via
Medulla Oblongata Pons
59
Medulla Oblongata
loose collection of neurons in the reticular formation called rhythmicity center. Control autonomic breathing. has both ventral and dorsal respiratory group
60
Pons
controls rhythmicity center in medulla apneustic center (excitatory) and pneumotaxic center (inhibitory)
61
3 ways to stop breathing
stroke spinal cord injury paralyze diaphragm
62
Dorsal respiratory group
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
Ventral respiratory group
contains both expiratory and inspiratory neurons controls motor neurons to internal intercostal muscles part of medulla
64
Apneustic center
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
Pneumotaxic center
1. may inhibit apneustic center, inhibiting inspiration 2. modulates output of medullary centers 3. function still incompletely understood, likely maintains normal respiration
66
Rhythmicity Center
from the medulla made up of dorsal respiratory and ventral respiratory groups controls autonomic breathing
67
What regulates breathing?
voluntary control automatic control--> chemoreceptors that monitor changes in blood PCO2, PO2, pH
68
Peripheral chemoreceptors
carotid and aortic bodies control breathing indirectly via sensory nerve fibers to medulla
69
Chemoreceptor control
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
Chemoreceptors are more sensitive to changes in
PCO2
71
Peripheral chemoreceptors
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
Firing rate of carotid bodies increases when
arterial PCO2 increases pH decreases PO2 decreases below 60 mmHg (or lower than 89% in pulsoximeter)
73
Chemoreceptors and pH
cerebral cortex has a slower reaction to pH brainstem has the 1st response to pH
74
Central Chemoreceptors
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
Acclimatization to high altitude
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
Altitude Training
increases RBC number increases Hb concentration angiogenesis altered glucose transport, glycolysis, pH regulation