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122 Cards in this Set
- Front
- Back
Saturation |
is a measure of the amount of available hemoglobin that is actually carrying oxygen. |
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Hemoglobin saturation eq |
SaO2 = [HbO2/total Hb] x 100 |
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Hb saturation with oxygen varies with |
Changed in PO2 |
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Normal arterial SaO2 |
97% |
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Normal venous SvO2 |
75% |
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Total oxygen content equals |
the sum of that dissolved and chemically combined with hemoglobin. |
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Total oxygen content must have 3 variables: |
(1) PO2, (2) total hemoglobin content (g/dl), and (3) hemoglobin saturation. |
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Total oxygen content equation |
CxO2 = (0.003 X PxO2) + (Hbtotal x 1.34 X SxO2) |
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Normal CaO2 |
16-20 ml/dl |
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arteriovenous oxygen content difference equation |
[ C(a-v)O2 ] |
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The normal arteriovenous oxygen content difference [ C(a-v)O2 ] is normally how much? |
about 5 ml/dl and is the amount of oxygen given up by every 100 mls of blood on each pass through the tissues |
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The C(a-v)O2 indicates |
the amount of oxygen removed in relation to blood flow. Along with total body consumption of oxygen, you can calculate cardiac output. Fick's equation |
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Cardiac output equation |
Qt =VO2 ____________ C(a-v)O2 X 10
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Normal VO2 |
250 ml/min |
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Nirmal cardiac output |
4 to 8 L/min in adult patients |
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Significance of the C(a-v)O2 |
If the oxygen consumption remains constant, a decrease in cardiac output will increase the C(a-v)O2 and if the cardiac output rises, the C(a-v)O2 will fall proportionately. |
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Factors Affecting Oxygen Loading and Unloading |
blood pH, body temperature, erythrocyte concentration of certain organic phosphates (2,3 DPG), Hb structure variations Other substances combining with Hb (ex. carboxyhemoglobin) |
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A low pH (acidity) shifts the curve to the |
Right |
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a high pH (alkalinity) shifts the curve to the |
Left |
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When the pH of blood curve shifts to the right what happens? |
the % Hb sat for a given PO2 falls (decreased affinity for oxygen). |
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When the pH of blood curve shifts to the left, what happens? |
% Hb sat for a given PO2 rises (increased affinity of Hb for oxygen). |
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What does the pH Bohr effect do |
alters the position of the HbO2 dissociation curve due to changes in blood pH. These changes enhance oxygen loading in the lungs and oxygen unloading in the tissues. As blood in the tissues picks up CO2, pH falls, the curve shifts to the right. With lower affinity for oxygen, Hb more readily gives up its oxygen to the tissues. Venous blood returning to the lungs, pH goes up to 7.40 and shifts the HbO2 curve back to the left to aid loading at the lungs. |
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How does a drop of body temp affect the HbO2 curve? |
hifts the curve to the left, increasing Hb affinity for oxygen. |
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How does an increase in body temp affect the HbO2 curve? |
the curve shifts to the right, and the affinity of Hb for oxygen decreases. |
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How does increased body temp affect unloading? |
Areas of increased temperature in the body will have increased temperature, hence increased unloading (Hb decreased affinity). |
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How does decreased body temp affect unloading? |
A decreased temperature decreases the need for O2, decreased unloading (Hb increased affinity) |
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Organic Phosphates (2,3-DPG)2,3-diphosphoglycerate (2,3-DPG) Is found where? |
In the red blood cells. |
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What does Organic Phosphates (2,3-DPG)do? |
It stabilizes the deoxygenated Hb molecule, reducing its affinity for oxygen. Without 2,3-DPG normal oxygen unloading would be impossible. |
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Increased 2,3-DPG shifts the HbO2 curve to the... |
right, increased oxygen unloading or decreased affinity of Hb for oxygen. |
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Decreased 2,3 DPG shift the curve to the |
left, increased loading or affinity of Hb for oxygen. |
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What Things tend to increase 2,3-DPG concentration? |
alkalosis chronic hypoxemia Anemia This increase promotes O2 unloading and decreases the affinity of Hb for oxygen |
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What are Things that decrease 2,3-DPG? |
acidosis results in a lower intracellular 2,3-DPG and a greater affinity for oxygen banked blood (stored blood)- In banked blood the concentrations of 2,3-DPG decreased by a third of the normal value in a weeks time. Large transfusions of blood more than a few days old can severely impair oxygen delivery to the tissue, even with normal PO2. |
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Structural abnormalities in the hemoglobin molecule alters what? |
the shape, of the molecule, and therefore alter its affinity for oxygen (loading and unloading of oxygen). |
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When do problems occur with hemoglobin? How many abnormal hemoglobins are there? |
Problems occur when the amino acid sequence in the polypeptide chains vary from normal. There are more than 120 abnormal hemoglobins. |
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Healthy individuals have what percent of abnormal Hb? |
15% to 40% abnormal Hb. |
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Abnormal Hemoglobin Sickle cell hemoglobin (HbS) |
HbS has less affinity for oxygen. Deoxygenated HbS is less soluble than oxygenated and normal Hemoglobin. |
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Because HbS is less soluble, what can it do? What does this lead to? |
it can crystallize inside the erythrocyte, causing the characteristic deformation in the cell shape. The crystalline form is more fragile, leading to hemolysis and increased risk of thrombosis. |
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Methemoglobin (metHb) |
The heme complex normal ferrous iron ion (Fe2+) loses an electron and is oxidized to its ferric state (FE3+). In the ferric state the iron ion cannot combine with oxygen and this type of anemia is called: methemoglobinemia |
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Most common cause of methemoglobinemia are? |
nitrite poisoning (meds: nitric oxide, nitroglycerine, lidocaine) |
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Physical presentation of metHb are? How do you identify it? Treat it? |
Blood looks brownish in color. Skin color: grayish. Treated with reducing agents like methylene blue or ascorbic acid Identify with spectrophotometry |
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Carboxyhemoglobin (HbCO) |
It is the chemical combination of hemoglobin with carbon monoxide.
Affinity of Hb for carbon monoxide (CO) is 200 times greater than oxygen HbCO cannot carry oxygen, creates loss of oxygen carrying capacity. |
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HbCo shifts the curve |
the left, creating more problems with unloading of oxygen |
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Treatment for HbCo |
increasing oxygen concentration to decrease the half life of CO and to supersaturate the plasma to keep oxygen going to the tissues. Hyperbaric oxygen (HBO) is recommended for use, usually with patients of 25% or greater HbCO. (Room air, 1 atm., it takes more than 5 hours to remove half of HbCO, 100% O2, 1 atm., it takes 80 min, and HBO at 3 atm., 100%, is only 20 to 30 min) |
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Fetal Hemoglobin (HbF) During fetal life and for up to 1 year after birth. |
It has a greater affinity for oxygen than normal adult Hb Curve is shifted to the left. This affinity is needed in fetal life
Replaced usually during the first year of life with normal adult hemoglobin |
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What is P50? |
is the partial pressure of oxygen at which the Hb is 50% saturated, at 7.40 pH. |
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What is normal P50? |
about 27 (26.6) mm Hg. |
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Increased P50 means that the curve is shifted to the |
right, increased unloading, decreased affinity of Hb for O2. |
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Decreased P50 hemoglobin affinity curve.. |
increased affinity of Hb for O2 and decreased unloading. |
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How much carbon dioxide is normally carried in the blood? |
45 to 55 ml/dl |
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carbon dioxide is normally carried in the blood in the following three forms: |
1.dissolved in physical solution 2.chemically combined with protein 3.ionized as bicarbonate |
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Carbon Dioxide Dissociation Curve |
the loading and unloading of CO2 in the blood can be illustrated in graphic form. Unlike the S-shaped O2 dissociation curve, the carbon dioxide curve is almost linear. This means that there is more direct relationship between partial pressure of CO2 and the amount of CO2 content in the blood. |
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In the Carbon Dioxide Dissociation Curve, high SaO2... |
decreases the blood’s capacity to hold CO2, helping it unload at the lungs |
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In the Carbon Dioxide Dissociation Curve, lower SvO2.. |
increases the bloods capacity for CO2 aiding uptake at the tissues |
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Hypoxemia |
is a condition in which there is an inadequate amount of oxygen in arterial blood (decreased PaO2, SaO2, or hemoglobin content) |
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Hypoxia |
(low O2 content, low cardiac output or low oxygen uptake at the tissue level) occurs whether hypoxemia is present or not. a condition which signifies low oxygen tissue content or cells resulting from inadequate oxygen delivery to meet their oxidative requirements. Therefore, the end result of ineffective gas exchange is hypoxia, which is manifested by hypoxemia. |
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MAIN CAUSES OF HYPOXIA |
Hypoxic (anoxic) Anemic Stagnant Histotoxic
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ABNORMALITIES OF GAS EXCHANGE AND TRASPORT |
Gas exchange is abnormal when either tissue oxygen delivery or carbon dioxide removal is impaired |
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Impaired oxygen delivery equation |
DO2 = CaO2 x Qt O2 Delivery to tissue = Arterial O2 content x Cardiac output |
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Hypoxia occurs when DO2 falls short of cellular needs. This is due to: |
(1) decreased of arterial blood content (hypoxemia), (2) decreased cardiac output or perfusion (shock or ischemia), (3) Abnormal cellular function prevents proper uptake of O2 (dysoxia)
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Causes of Hypoxemia - indicated by low PaO2 |
Low PIO2 Hypoventilation V/Q imbalance (Low V/Q) Anatomic shunt Physiologic shunt Diffusion defect Normal aging |
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Low PIO2 Low PAO2 |
Low PAO2 Caused by: (From alveolar air equation [PB-PH2O] FIO2 ) Low PB Low FIO2 |
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Low PIO2 primary indicators |
Low PAO2Low PaO2 |
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Low PIO2 primary indicators |
Low PAO2 Low PaO2 |
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Low PiO2 Assessment of Hypoxia |
PaO2 is low
P(A-a)O2 gradient on room air and supplemental O2 are normal
CaO2 is low
CvO2 is normal (if cardiac output increases to compensate)
Example: travel to high altitudes; low barometric pressure, creating mountain sickness. |
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Hypoventilation |
-As alveolar PCO2 rises the alveolar PO2 will fall. (FIO2 constant)- more noticeable at room air. Caused by: hypoventilation |
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Primary indicators of hypoventilation |
Low PaO2 High PaCo2 (Ventilation is the problem.. not oxygenation.) |
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Hypoventilation: assessment of hypoxia |
PaO2 decreased Normal P(A-a)O2 on room air and supplemental O2 CaO2 decreased CvO2 normal (if cardiac output increases to compensate) |
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Diffusion defect |
Due to thickening of the alveolar-capillary membrane, gas exchange is impeded; as seen by Fick’s first law of diffusion. |
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Diffusion defect caused by |
Disorders of the alveolar-capillary membrane such as; pulmonary fibrosis, interstitial edema, and interstitial lung disease |
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Primary indicators of diffusion defect |
Low PaO2 High P(A-a)O2 on air; resolves with O2 |
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Diffusion defect: hypoxia |
PaO2 low P(A-a)O2 gradient increased on room air, resolving when placed on supplemental oxygen CaO2 decreased CvO2 normal (if cardiac output increases to compensate) |
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VENTILATION/PERFUSION IMBALANCES (Low V/Q) |
Low V/Q’s are the most common cause of hypoxemia in patients with lung disease |
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Low V/Q caused by |
Perfusion in excess of ventilation; such as with bronchospasm, secretions in airway, and low volumes. |
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Low V/Q indicators |
Low PaO2 High P(A-a)O2 on air; decreases with O2 |
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Low V/Q assessment of hypoxia |
PaO2 decreased P(A-a)O2 widened on room air but decreased widening with supplemental oxygen CaO2 is decreased CvO2 is normal (if cardiac output increases to compensate) |
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Anatomical shunt is what kind of shunt? What is it caused by? |
*a true shunt Caused by: Blood flow between right and left sides of circulation; congenital heart disease. |
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Indications for an anatomical shunt |
Low PaO2 High P(A-a)O2 on room air; does not resolve with O2 |
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Anatomical shunt: Assessment of Hypoxia |
PaO2 will be very low (if over 25-30% shunt) P(A-a)O2 is very wide and widens even further with supplemental oxygen (if over 25-30% shunt) CaO2 is decreased CvO2 is normal (if cardiac output increases to compensate) |
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True shunts |
As the shunted blood increases to 30%; it becomes impossible to make up the oxygen of blood going by totally unventilated alveoli or moving from the right side of the heart to the left without going through the lungs. Ex: ARDS |
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Physiologic shunt is caused by what? |
Caused by:Perfusion without ventilation; atelectasis, pneumonia, and pulmonary edema |
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Primary indicators of physiological shunt are? |
Low PaO2 High P(A-a)O2 on air; does not resolve with O2 |
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Physiologic shunt: assessment of hypoxia |
Extremely low PaO2 (as % shunt increases) P(A-a)O2 widened with increased widening with supplemental O2 (as % shunt increases) CaO2 is low CvO2 is normal (if cardiac output increases to compensate) |
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Rule of thumb To differentiate between hypoxemia caused by a V/Q imbalance and that caused by shunting |
apply the following 50/50 rule: If the oxygen concentration is more than 50% and the PaO2 is less than 50 mmHg, significant shunting is present; otherwise the hypoxemia is mainly due to a simple V/Q imbalance |
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Refractory hypoxemia |
an abnormal deficiency of oxygen in the arterial blood that is resistant to treatment; usually indicates the presence of right-to-left shunting |
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To determine refractory hypoxemia: |
The patient is on an FIO2 of 50% and the PaO2 is less than 50 mmHg. If the FIO2 is increased by 20% and the PaO2 increases less than 10 mmHg |
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As we age, the normal P(A-a)O2 gradient increases (widens) about 3 mm Hg every 10 years, from age 20 years. This is due to |
a gradual decrease in PaO2 caused by a progressive loss of elastic recoil pressure in the lung. This changes the V/Q distribution and results in mildly progressive hypoxemia. |
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HEMOGLOBIN DEFICIENCIES ABSOLUTE: caused by |
Loss of hemoglobin (Hb) anemia; due to hemorrhage or inadequate erythropoiesis |
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HEMOGLOBIN DEFICIENCIES ABSOLUTE: primary indicators |
Low Hb content Reduced CaO2 |
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HEMOGLOBIN DEFICIENCIES ABSOLUTE: assessment of hypoxia |
PaO2 may be normal or low P(A-a)O2 is normal both on and off oxygen CaO2 is low CvO2 is low |
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Progressive decreases in Hb causes? |
large drops in CaO2. The patient will be hypoxic even when the PaO2 is normal. A drop in hemoglobin of 5 g/dl would be like dropping arterial blood to venous (PaO2 of 100 mmHg to 40 mmHg). |
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Hemoglobin deficiency Relative is caused by? |
Abnormal hemoglobin; carboxyhemoglobin, methemoglobin, and abnormal hemoglobin (those causing left shift of oxyhemoglobin dissociation curve) |
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Hemoglobin deficiency Relative: primary indicator |
Abnormal SaO2 (done by co-oximeter) Reduced CaO2 |
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Hemoglobin deficiency Relative: assessment of hypoxia |
PaO2 may be normal or decreased
P(A-a)O2 gradient is normal on room air and oxygen
CaO2 is reduced (co-oximeter)
CvO2 is reduced (co-oximeter) |
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Reduced blood flow caused by? |
Decreased perfusion; (1) circulatory failure (shock) and (2) local reduction in perfusion such as MI, CVA (ischemia) |
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Reduced blood flow indicators: |
Increased (widened) C(a-v)O2 Decreased CvO2 |
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Reduced blood flow: assessment of hypoxia |
PaO2 is normal P(A-a)O2 is normal on room air and on oxygen CaO2 is normal CvO2 is decreased C(a-v)O2 is widened (increased) |
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DYSOXIA: caused by? |
Dysoxia is a form of hypoxia in which the cellular uptake of oxygen is abnormally decreased. The best example is cyanide poisoning (disruption of cellular enzymes). It can also occur when tissue oxygen consumption becomes dependent on oxygen delivery. |
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Dysoxia primary indicators |
Normal CaO2 Increased CvO2 |
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Dysoxia: assessment of hypoxia |
PaO2 is normal P(A-a)O2 on room air and supplemental oxygen is normal CaO2 is normal CvO2 is increased |
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Dysoxia may occur when..? Usually oxygen consumption equals what? What does an oxygen debt lead to? |
tissue oxygen consumption becomes dependent on oxygen delivery. Usually oxygen consumption equals oxygen demand (the flat portion of the solid line) . If delivery falls, solid line, tissue extraction reaches a maximum, the point of critical delivery. Further decreases create an oxygen debt (oxygen demand exceeds delivery (sloped line). This leads to anaerobic metabolism and lactic acid build up. Dotted line, pathological (ARDS, septic shock), the debt can occur at normal oxygen levels. Slope of dotted line indicates decreased extraction ratio (VO2/DO2). |
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Impaired Carbon Dioxide Removal |
Caused by decreased alveolar ventilation (VA) relative to metabolic need which causes: PaCO2 = VCO2 /VA hypercapnia and respiratory acidosis |
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A decrease in alveolar ventilation occurs when: |
(1) The minute ventilation is inadequate (2) The dead space ventilation per minute is increased (3) A V/Q imbalance exists |
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Inadequate Minute Ventilation Minute ventilation equation |
Vt x f = VE |
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Decreased VE is usually caused by what? |
decreased tidal volumes but could be due to decreased respiratory rates (drug overdose). Usually caused by restrictive conditions: -- Atelectasis Respiratory center depression Neuromuscular disorders Impeded thoracic expansion kyphoscoliosis |
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Decreased VE is usually caused by what? |
decreased tidal volumes but could be due to decreased respiratory rates (drug overdose). Usually caused by restrictive conditions: -- Atelectasis Respiratory center depression Neuromuscular disorders Impeded thoracic expansion kyphoscoliosis |
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How is Increased Dead Space Ventilation caused? |
ventilation without perfusion or ventilation in excess of perfusion (high V/Q) |
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Alveolar ventilation equation |
(Vt – VDS) X f = VA |
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Dead space ventilation increases due to: |
1. Rapid, shallow breathing (an increase in anatomical dead space per minute)Using the above formula: Normal:(500 ml – 150 ml) X 12=4200 ml Shallow:(250 ml – 150 ml) X 24=2400 ml2. Increased physiological dead space (V/Q = 0) Using the above formula: Normal:(500 ml – 150 ml) X 12=4200 ml DS (500 ml – 300 ml) X 12 =2400 ml |
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Clinical assessment of dead space |
1. Minute ventilation to arterial PCO2 disparity. 2. The arterial to alveolar CO2 tension gradient P(a-A)CO2) 3. Dead space to tidal volume ratio VD/Vt |
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If the patients minute ventilation doubles, the PaCO2 should |
decrease by 10 mmHg |
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If there is a disparity between the minute ventilation and the expected PaCO2, dead space is _____ |
Increased |
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if the patient has a minute ventilation of 20 L/min and the PaCO2 is 40 mmHg, the patient has |
Dead space |
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End tidal CO2 (PETCO2) is usually ______ mm Hg less than PaCO2. |
1 to 5 |
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What does it mean when the distance between the PaCO2 and PETCO2 increases? |
it means there is more dead space. The gas from ventilated but not perfused areas will be closer to atmospheric gas. It mixes with other gases from perfused areas, however the PETCO2 will be lowered. |
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Normal VDS/Vt is about how much? |
.2 to .4 (20% to 40%) |
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A patient on a ventilator can have a VDS/Vt of how much? |
up to .5 (50%) |
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What is a normal up VDS/Vt for a COPD patient? |
0.6 (60%) |
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A VDS/Vt of 0.6 to 0.8 (60 to 80%) represents what? |
is significant disease and the patient is unable to maintain spontaneous ventilation. |
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VDS/Vt calculated using Modified Bohr equation: |
VDS/Vt = (PaCO2 – PECO2 ) /PaCO2 |
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Which has a greater effect on oxygenation? V/Q imbalances or carbon dioxide? |
V/Q imbalances So, any increase in PCO2 from low V/Q units can be corrected by a reduction in PCO2 from high V/Q units. But, O2 cannot do the same because the oxygen curve is nearly flat when the PO2 is above normal. |
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To get rid of high CO2 patients must |
must increase their alveolar ventilation. Those that can increase ventilation have a normal to decreased CO2. |
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What happens if a patient cannot increase alveolar ventilation to get rid of high CO2? |
If minute ventilation cannot be increased they will become hypercapnic. Here the energy cost is prohibitive to maintain an increased minute ventilation, so the patient will opt for less work and therefore the CO2 levels will rise. |