Hypoxia - Causes and Symptoms

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HYPOXIA: CAUSES AND SYMPTOMS
by
Kevin T. Martin
BVE, RRT, RCP
RC Educational Consulting Services, Inc.
16781 Van Buren Blvd, Suite B, Riverside, CA 92504-5798
(800) 441-LUNG / (877) 367-NURS
www.RCECS.com
HYPOXIA: CAUSES AND SYMPTOMS
BEHAVIORAL OBJECTIVES
UPON COMPLETION OF THE READING MATERIAL, THE PRACTITIONER WILL BE
ABLE TO:
1. Describe the criteria for documented hypoxemia
2. Describe the main causes of hypoxia.
3. Explain the effect of cardiac output on PaO 2
4. List a minimum of five symptoms of hypoxia.
5. Discuss oxygenation assessment
6. Evaluate hypoxia
7. Know the normal values for PaO 2 and % saturation.
8. Classify the severity of hypoxemia
COPYRIGHT © OCTOBER, 1985 By RC Educational Consulting Services, Inc.
COPYRIGHT © April, 2000 By RC Educational Consulting Services, Inc.
(# TX 1 762 726)
AUTHORED BY KEVIN T. MARTIN, BVE, RRT, RCP
REVISED 1988, 1990, 1994, 1996, BY KEVIN T. MARTIN, BVE, RRT, RCP
REVISED 1999, 2002, 2005 BY MICHAEL R. CARR, BA, RRT, RCP
ALL RIGHTS RESERVED
This course is for reference and education only. Every effort is made to ensure that the clinical
principles, procedures and practices are based on current knowledge and state of the art
information from acknowledged authorities, texts and journals. This information is not intended
as a substitution for a diagnosis or treatment given in consultation with a qualified health care
professional.
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HYPOXIA: CAUSES AND SYMPTOMS
TABLE OF CONTENTS
INTRODUCTION ...........................................................................................................................5
DOCUMENTED HYPOXEMIA.....................................................................................................5
MAIN CAUS ES OF HYPOXIA .....................................................................................................5
HYPOXIC (ANOXIC) HYPOXIA.............................................................................................5
SHUNT - DEAD SPACE COMPARISON ................................................................................7
CLINICAL IMPACT OF SHUNT .............................................................................................8
STAGNANT HYPOXIA (SHOCK, ISCHEMIA) ...................................................................10
HISTOTOXIC HYPOXIA........................................................................................................10
ANEMIC HYPOXIA ................................................................................................................10
DOES CARDIAC OUTPUT EFFECT PaO 2 ?...............................................................................12
SYMPTOMS OF HYPOXIA ........................................................................................................12
EARLY .....................................................................................................................................14
LATE ........................................................................................................................................15
ACUTE .....................................................................................................................................15
CHRONIC.................................................................................................................................16
OXYGENATION ASSESSMENT................................................................................................16
EVALUATION OF HYPOXIA ....................................................................................................18
% SATURATION.....................................................................................................................18
HEMOGLOBIN ........................................................................................................................18
CLASSIFYING THE SEVERITY OF HYPOXEMIA .................................................................18
OXYGEN CONTENT ...................................................................................................................20
OXYGEN DELIVERY TO TISSUES ......................................................................................20
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HYPOXIA: CAUSES AND SYMPTOMS
OXYGEN EXTRACTION RATIO ..........................................................................................21
REFRACTORY HYPOXEMIA ....................................................................................................21
HAZARDS OF HIGH FIO 2 IN THE TREATMEANT OF HYPOXEMIA..................................21
COMPENSATION FOR HYPOXEMIA ......................................................................................22
RESPIRATORY DISEASED PATIENTS: CAN THEY TRAVEL BY AIR? ............................22
CONDITIONS ADVERSELY AFFECTED BY HYPOXIA...................................................23
CONDITIONS ADVERSELY AFFECTED BY PRESSURE CHANGES .............................23
OTHER CONTRAINDICATIONS ..........................................................................................24
INTERACTION WITH THE PHYSICIAN .............................................................................24
INTERACTION WITH THE AIRLINE/TRAVEL AGENT ...................................................24
PERSONAL PLANNING ........................................................................................................25
INTERACTION WITH OXYGEN VENDOR.........................................................................25
CLINICAL PRACTICE EXERCISE ............................................................................................25
SUMMARY...................................................................................................................................26
PRACTICE EXERCISE DISCUSSION........................................................................................26
SUGGESTED READINGS AND REFERENCES .......................................................................27
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HYPOXIA: CAUSES AND SYMPTOMS
INTRODUCTION
T
wo terms frequently used in discussing decreased oxygen levels are hypoxia; anoxia has
become a synonymous term, and hypoxemia. The term “hypoxia” is used throughout this
course to describe 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.
Hypoxemia is a condition in which there is an inadequate amount of oxygen in arterial blood
(decreased PaO 2, SaO 2 , or hemoglobin content). Hypoxia (low O2 content, low cardia output, or
low oxygen uptake at the tissue level) occurs whether hypoxemia is present or not. However,
there are instances where there is a normal amount of oxygen in arterial blood (PaO2 )
hypoxemia, but the patient is hypoxic (low O2 content). These patients have hypoxia without
hypoxemia. This means that the total carrying capacity of the blood is reduced, while the
dissolved oxygen (PaO 2 ) continues to be at normal or above normal levels. A few examples of
this condition are patients with sickle cell anemia, carbon monoxide poisoning, severe blood loss
and Thyrotoxicosis (Grave’s Disease).
In the final analysis, it doesn’t really matter how the terms are used as long as you understand the
differences between oxygen pressure, saturation, and content. Understanding these concepts,
and you can define hypoxemia and hypoxia any way you wish.
DOCUMENTED HYPOXEMIA
In adults, children, and infants older than 28 days, hypoxemia exists when the PaO2 is less than
60 mmHg or the arterial oxygen saturation (SaO 2 ) is less than 90% when breathing room air. In
infants 28 days or younger, hypoxemia is present when the PaO 2 is less than 50 mmHg, the SaO2
is less than 88%, or the capillary oxygen tension (PCO2 ) is less than 40 mmHg.6
MAIN CAUSES OF HYPOXIA
C
auses of hypoxia can be divided into four main categories: (1) hypoxic (anoxic), (2)
stagnant, (3) histotoxic and (4) anemic. (Some textbooks place “anemic” hypoxia in the
“hypoxic” hypoxia category and refer to “histotoxic” hypoxia as “dysoxia”).
In humans, tissue hypoxia is estimated to occur when mitochondrial PO2 is less than 7 mmHg.3
Oxygen delivery (DO 2 ) to the tissues is a function of arterial oxygen content (CaO2 ) times
cardiac output (Q t ).2
DO2 = CaO 2 x Qt
Hypoxic (Anoxic) Hypoxia
Hypoxic hypoxia refers to mechanisms that decrease the average alveolar PO2 . Impaired
oxygenation in such cases as pulmonary fibrosis, or venous to arterial shunts in ARDS
characterize hypoxic hypoxia. These pulmonary conditions result in inadequate alveolar PO2 ,
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5
HYPOXIA: CAUSES AND SYMPTOMS
which causes a drop in arterial oxygen tensions and contributes to low tissue oxygenation.
Inadequate amounts of O2 in the alveoli, or inadequate transfer across the alveolar-capillary
(A-C) membrane are probably the most common cause of hypoxia. A more descriptive term
might be alveolar hypoxia because there is a reduction in alveolar PO2 . Examples include:
alveolar hypoventilation, low barometric pressure (high altitude), large airway obstruction,
pneumonia, disorders of the respiratory muscles and neuromuscular junction, diseases of the
pleura and chest wall. Hypoxic hypoxia responds well to O2 therapy (with the exception of
shunts). In most cases, hypoxic hypoxia is easily remedied by providing the patient with
additional O2 to breathe.
Low alveolar oxygen (PAO2 ) is a very common cause of hypoxic hypoxia and usually
the result of simple hypoventilation. Airway obstruction also decreases the PAO 2 . Airway
obstruction is evidenced by an increased use of accessory muscles, intercostal and sternal
retractions, or abnormal breath sounds, such as, wheezing and stridor. Total airway obstruction
is associated with absent breath sounds. Hypoventilation and airway obstruction not only
decrease the PAO 2 and PaO 2 , they also increase the PaCO2 , which makes this diagnosis fairly
simple.
At high elevations, low barometric pressure is the cause of a low PAO 2 and PaO 2 . The
concentration of oxygen remains the same at high altitudes (21%), but due to a decrease in the
number of O2 molecules, there is less actual O2 available. Those who live in higher elevations
adapt to a lower number of molecules by increasing their amount of hemoglobin. Their PaO2
and PAO 2 are lower, but their O2 content is normal. This is the hypoxia that is a hazard to
aviators.
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HYPOXIA: CAUSES AND SYMPTOMS
The Shunt - Dead Space Comparison Chart
Poor or, noVentilation
Pneumonia
Atelectasis
V/Q = 0
Good Ventilation
V/Q = ∞
Poor, or no Perfusion
Good Perfusion
Decreasing Ventilation
SHUNT
Shock
Pulmonary Emboli
Normal
V/Q mismatch
Decreasing Blood Flow
V/Q = 1
V/Q mismatch
Deadspace
Ventilation
Decreased V/Q
Increased V/Q
V/Q mismatch is another common cause of hypoxic hypoxia (See Shunt – Dead Space
Comparison Chart). Lung disease, being rarely uniform, results in localized areas of pathology.
The matching of ventilation to perfusion is disrupted in these areas, resulting in a lower PaO2 .
When V/Q mismatching is chronic, the body tries to compensate for the defect. For example, if
there is poor ventilation to an area, blood flow is restricted. Blood flow is shifted to other areas
where there is better gas exchange. This improves the V/Q matching in normal areas. There is a
limit to this compensation so there usually is a certain amount of hypoxia for significant defects.
A shunt is a condition, in which, there is a direct mixing of venous and arterial blood. It is the
ultimate decreased V/Q mismatch (See Shunt – Dead Space Comparison Chart). Since blood
does not come in contact with nonventilated alveoli, there is no gas exchange. A major shunt is
quickly diagnosed at the bedside by simply placing the patient on 100% O2 for 30 to 40 minutes
and looking for a substantial rise in the oxygen saturation and PaO2 . If blood is perfusing
nonventilated alveoli, there is no appreciable rise in PaO 2 since there is no oxygen for gas
exchange. Virtually all conditions except shunt (and apnea) result in the PaO2 rising by varying
degrees. The PaO 2 cannot rise in a shunt because there is no diffusion of fresh oxygen from
alveolar air to the blood.
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HYPOXIA: CAUSES AND SYMPTOMS
CLINICAL IMPACT OF SHUNT
Shunt fraction percentage
< 10
10 – 19
20 – 29
> 30
Clinical significance
Compatible with normal lungs
Intrapulmonary abnormality; compatible with spontaneous
breathing
Significant intrapulmonary diseases: probably requires CPAP or
PEEP
Severe intrapulmonary disease; aggressive mechanical ventilatory
support with PEEP required; life threatening
100
75
PaO2
50
25
Exercise
0.25
0.50
0.75
1.0
RBC Transit Time
(Seconds)
Normal diffusion is complete within 0.3 seconds.
Impaired diffusion may be complete during RBC
transit time except during exercise.
Grossly impaired diffusion will not be completed.
These patients suffer dyspnea at rest.
Figure 1
Conditions causing a decrease in diffusion also fall in the hypoxic hypoxia category (see Figure
2). Pulmonary edema, alveolar fibrosis or thickening, and loss of alveoli are examples of
conditions that interfere with diffusion. All of these slow the passage of O2 through the A-C
membrane.
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HYPOXIA: CAUSES AND SYMPTOMS
A red blood cell (RBC) is in contact with the alveoli for 3/4 of a second (see Figure 1).
Normally, the diffusion of O2 is rapid, being completed within about 1/3 of a second. This gives
a considerable margin of safety. RBC transit time can be decreased significantly by an increase
in cardiac output. Yet diffusion will still be complete. Hypoxia in the normal patient is not
produced until contact time is decreased to 1/4 of a second. This occurs during heavy exercise
when cardiac output is increased 3-4 times normal.
If diffusion is impaired, it may not be detected because of this margin of safety. A patient may
not experience any dyspnea or hypoxia if they are at rest because diffusion is still complete.
However, should this patient exercise and increase cardiac output, there may not be enough time
for gas exchange.
HYPOXIC HYPOXIA
Airway Obstruction
Hypoventilation or
low barometric pressure
PAO 2
Alveolar fibrosis
Interstitial edema or thickening
Figure 2
This results in the “dyspnea on exertion” (DOE) so common in patients with lung disease.
Dyspnea on exertion is one of the first indicators of chronic lung disease. It is a result of
inadequate time for diffusion. As activity increases, RBC transit time decreases and hypoxia
ensues in these patients. The patient’s exercise tolerance becomes less and less as the disease
progresses. When diffusion is seriously impaired, the patient even becomes dyspneic at rest.
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HYPOXIA: CAUSES AND SYMPTOMS
Dyspnea at rest indicates severe disease.
Stagnant Hypoxia (Shock, Ischemia)
Non-transportation of O2 via the circulatory system results in stagnant hypoxia. Low cardiac
output or perfusion (shock or ischemia), severe hypotension, or low pulmonary venous outflow
(gross pulmonary embolism) are examples of conditions that reduce circulation, seriously
decreasing oxygen transport to the tissues. Simply increasing the patient’s FIO 2 has very little
benefit because the arterial oxygen content (CaO 2 ) is almost at a maximum level while the
patient is breathing room air.
Circulatory failure is the most common cause of this type of hypoxia. There may be a
generalized failure of transportation, such as, cardiac arrest, cardiogenic shock, myocardial
infarction (MI), or congestive heart failure (CHF). There may be a localized failure of
transportation, such as, an embolus. An embolus decreases or occludes blood flow to a specific
organ, or area making that organ/area hypoxic.
In circulatory failure, tissue oxygen deprivation is widespread. Although the body tries to
compensate for the lack of oxygen by directing blood flow to vital organs, this response is
limited. Thus prolonged shock ultimately causes irreversible damage to central nervous system
and eventual cardiovascular collapse.2
Even when whole-body perfusion is adequate, local reductions in blood flow can cause localized
hypoxia. Ischemia can result in anaerobic metabolism, metabolic acidosis, and eventual death of
the affected tissue. Myocardial infarction and stroke (cerebrovascular accident) are good
examples of ischemic conditions that can cause hypoxia and tissue death. 2 Other examples of
this condition are high “G” forces, prolonged sitting in one position or hanging in a harness, cold
temperatures, and positive pressure breathing. This hypoxia is usually experienced when sitting
for hours in a boring class.
Histotoxic Hypoxia
Conditions that interfere with oxygen uptake or utilization by tissue cells result in histotoxic
hypoxia. Cyanide poisoning is the most common example of histotoxic hypoxia. Cyanide
disrupts cellular enzymes (cytochrome oxidase system) responsible for O2 usage at the tissue
level. This disrupts cellular metabolism and causes death. (It is important to note that many
nitrate medications used for cardiac conditions metabolize to cyanide in the body). Histotoxic
hypoxia is an example of hypoxia without hypoxemia. There may be adequate amounts of O2 in
the blood but the tissues can’t use the O2 . Certain narcotics, chewing tobacco, and alcohol will
prevent oxygen use by the tissues. This hypoxia is usually experienced after drinking too much.
Anemic Hypoxia
The last major cause of hypoxia to be discussed is anemic hypoxia. Anemic hypoxia is a result
of reduced oxyhemoglobin content. It can be a result of an “actual” or a “relative” anemia.
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HYPOXIA: CAUSES AND SYMPTOMS
“Actual” anemia is a decrease in the amount of hemoglobin present. “Relative” anemia is a
decrease in the amount of hemoglobin available for O2 transport. The importance of hemoglobin
cannot be overemphasized in relationship to hypoxia. Of the normal 20 ml/dl of O2 carried by
the blood, 19.7 ml is bound to the hemoglobin molecule. Obviously, a decrease in hemoglobin
from the normal 15 gm leads to hypoxia. A decrease in the oxygen content level to <16 ml/dl is
generally considered hypoxia.
Numerous conditions alter the hemoglobin molecule and change its O2 carrying capacity.
Abnormal hemoglobin, such as, methemoglobin, carboxyhemoglobin, and sulfhemoglobin are
unavailable for O2 transport. The patient may have a normal overall hemoglobin amount, but it’s
the wrong kind of hemoglobin. This is described as a “relative” anemia. This hypoxia is usually
experienced by smokers.
Carboxyhemoglobin is a result of carbon monoxide (CO) combining with hemoglobin. CO
attaches to the same receptor site on hemoglobin as O2 , but with an affinity 210 times greater. In
fact, the mere pressure of 0.16 mm Hg of CO binds up to 75% of the receptor sites on
hemoglobin! CO makes hemoglobin virtually incapable of transporting O2 . It also shifts the O2 Hb curve to the left. This impedes release of any O2 actually bound to the hemoglobin
compounding the hypoxia. (One has better oxygenation with 50% less hemoglobin than one has
with 50% carboxyhemoglobin). Heavy cigarette smokers and smoke inhalation victims have
significant amounts of carboxyhemoglobin. Normal carboxyhemoglobin levels are less than 3%.
Heavy smokers may have levels of 5-10%.
Methemoglobin (HbMet) is a change in the Hb molecule from a ferrous ion to a ferric ion. This
decreases binding sites and increases the affinity of the remaining sites like carboxyhemoglobin.
Normal HbMet levels are less than 3%. Primaquine, dapsone, nitrates, local anesthetics, and
aniline can increase HbMet levels. Hereditary RBC enzyme deficiencies and Hb-M disease also
increase levels. The most common cause of acquired methemoglobinemia is toxic exposure to
drugs or chemicals (e.g., nitrites, some sulfonamides), but it is also associated with infections
such as clostridial infection and malaria. HbMet shifts the O2 -Hb curve to the left like
carboxyhemoglobin compounding the hypoxia. Infants less than 6 months old are especially
susceptible to nitrate poisoning and methemoglobinemia if they drink well water containing
nitrates.
Sulfhemoglobin also decreases O2 binding sites but decreases, rather than increases, the affinity
of the remaining sites. Sulfhemoglobin shifts the O2 -Hb curve to the right. This partially cancels
the loss of binding sites. There are less symptoms of hypoxia with sulfhemoglobin than the other
abnormal hemoglobins. Causes of sulfhemoglobin are: phenacetin, acetanilid, dapsone, sulfur
dioxide, hydrogen sulfide, and severe smog.
Fetal Hemoglobin (Hemogobin F) is the normal hemoglobin of the fetus. Most HbF is replaced
by Hemoglobin A in the first days after birth. HBF has an increased capacity to carry oxygen and
is present in increased amounts in some pathologic conditions, including sickle cell anemia,
aplastic anemia, and leukemia. Small amounts are produced throughout life.
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HYPOXIA: CAUSES AND SYMPTOMS
The lack of 2,3 DPG in HbF increases the affinity of oxygen for hemoglobin. This enables the
fetus to survive at PO2 ’s less than 40 mm Hg. The increased affinity for oxygen allows HbF to
vigorously take up oxygen from the plasma at the placenta by maintaining oxygen diffusion
gradient. By 6 months after birth, most HbF has been replaced with HbA.
Sickle Cell Hemoglobin (HbS) is much less soluble than HbA in the deoxygenated state. Thus
HbS tends to crystallize in the red blood cell to a curved, sickle-shape. The sickle-shaped cell is
fragile and subject to rupture. As the abnormal molecules become deoxygenated, because of
decreased oxygen tension in the peripheral circulation, they become sickle-shaped, move slowly,
clump together and hemolyze. If the proportion of HbS to HbA is large, as in sickle cell anemia,
local thrombosis and infarction may occur.
It is important to note that pulse oximeters and ABG machines do not differentiate between
normal and abnormal hemoglobin. They perceive abnormal hemoglobin as oxyhemoglobin.
This means a patient can be very hypoxic in the presence of excellent oximetry or ABG
measurements. The % saturation must be measured via co-oximetry for accurate readings. If
there is suspicion of abnormal hemoglobin, co-oximetry is a necessity. (Even without suspicion
of abnormal hemoglobin co-oximetry is the standard on all ABG’s).
DOES CARDIAC OUTPUT EFFECT PaO2 ?
A
decrease in cardiac output can significantly lower CaO2 and PaO 2 in people with
increased shunt fractions because it lowers CvO 2 and PvO 2 .
Arterial blood is a mixture of blood draining normally oxygenated alveoli and airless alveoli.
Shunted blood is venous unoxygenated blood. This blood mixes directly with oxygenated blood
leaving aerated alveoli. Low cardiac output lowers the mixed venous oxygen content and
therefore shunted blood oxygen content. In this way, CaO 2 and PaO 2 are decreased as the more
profoundly hypoxemic mixed venous blood mixes with arterial blood.
SYMPTOMS OF HYPOXIA
H
ypoxia is a common clinical disorder and is the result of a variety of conditions.
Detection of hypoxia is sometimes extremely difficult. In its severe form (the classical
picture of cyanotic nail beds and mucus membranes) the diagnosis is straightforward, in
less severe forms, hypoxia manifests in less obvious ways. The symptoms of hypoxia can vary
among individuals. This often makes its clinical detection difficult.
The symptoms of hypoxia vary, depending upon the severity and duration of the problem and the
individual patient response. Hypoxia impairs cellular mitochondrial function. This alters normal
oxidative metabolism and allows toxic metabolites to accumulate. This leads to tissue necrosis
and cellular death, if not reversed. The symptoms of hypoxia are due to malfunctioning hypoxic
cells.
In its most severe form, the patient has a bluish tint (cyanosis) to their skin, nail beds and mucus
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HYPOXIA: CAUSES AND SYMPTOMS
membranes. The subjective observer, lighting available, and the patient’s skin color hamper
detection of cyanosis. If cyanosis is detected, one can readily assume the patient is hypoxic.
However, one should not wait until cyanosis appears before making the diagnosis. Cyanosis is
not apparent until there is a significant amount of reduced hemoglobin, approximately 5 grams.
This is 1/3 of their total hemoglobin. The patient is severely hypoxic long before cyanosis
appears.
Smoke inhalation produces significant hypoxia with no detectable cyanosis. The patient may, in
fact, appear “pinker” than normal. The reaction of CO with hemoglobin causes the retention of
its bright red color, so there is no cyanosis. These patients do not appear blue, despite being
severely hypoxic. Likewise, cyanosis may not appear in the anemic patient if there isn’t enough
hemoglobin to produce this symptom.
Arterial blood gases may be equally deceptive. A normal PaO2 range is 80-100 mm Hg. This
varies with age and altitude, decreasing with increased age or high altitude. A useful rule of
thumb for a patient breathing room air at sea level is to subtract ½ the patient’s age from the
number 105 to predict their normal PaO 2 . For example, an 80-year-old patient has a normal
PaO 2 of 65 mm Hg (105 - 80/2 = 65). Another predictive formula is to subtract 1 mm Hg from
80 for every year over 60 years old. Another formula used for older individuals is: Predicted
PaO 2 = 100.1 - (0.323 X patient age). These predictive formulas cannot be used with chronic
lung disease patients. A “normal” PaO2 range for patients with chronic lung disease is around
60-80 mm Hg.
Using these formulas give a normal PaO2 considerably lower than the “normal” range of 80-100
mm Hg for older persons. However, this may be entirely normal for an older patient.
Conversely, an anemic patient can have a very high PaO2 and still be hypoxic. One should not
treat a patient for hypoxia based solely on the PaO 2 . One must consider the PaO 2 in conjunction
with the patients’ age, hemoglobin, and the presence of other symptoms of hypoxia. A low PaO 2
and the presence of other symptoms of hypoxia require treatment rather than just a low PaO 2
alone. (American Association of Respiratory Care clinical practice guidelines recommend
oxygen therapy for patients > 28 days old when PaO 2 is < 60 mm Hg or % saturation is < 90%.
For neonates, oxygen is recommended when PaO 2 is < 55 mm Hg or % saturation is < 88%).
A low PaO 2 and no symptoms of hypoxia may indicate a chronic condition for the patient. The
patient may be entirely compensated for the low PaO 2 and should not be considered hypoxic.
Older patients, those at high elevations, and those with chronic lung disease all have a low
“normal” PaO2 . They may exhibit no symptoms of hypoxia with this low PaO2 . By textbook
definition they are hypoxemic. However these patients require no clinical treatment for their
hypoxemia. Conversely, patients exhibiting the following symptoms of hypoxia require
treatment even if PaO2 is adequate.
The remaining symptoms of hypoxia involve many organ systems. Hypoxia is often confused
with other problems. Dyspnea, is the complaint of “shortness of breath”. Obviously, the patient
must be aware of the hypoxia to be dyspneic. This limits its validity. A patient may or may not
be hypoxic when dyspneic. Tachypnea is probably the most common symptom of hypoxia.
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HYPOXIA: CAUSES AND SYMPTOMS
Both dyspnea and tachypnea are often perceived as signs of acute anxiety instead of hypoxia.
This is compounded by the fact that hypoxia produces anxiety in the alert, conscious patient.
However, as the hypoxia increases, anxiety changes to irritability, mental confusion, lethargy,
and in extreme cases, coma.
Brain function is significantly affected by hypoxia and this provides several symptoms. A PaO2
of 50-55 mm Hg impairs judgement, alters short-term memory, and may cause euphoria.
Cognitive and motor functions deteriorate at PaO 2 ’s between 30-55 mm Hg. Loss of
consciousness occurs when PaO 2 is less than 30 mm Hg.
Initially, the body tries to compensate for hypoxia. Tachycardia, tachypnea, hyperpnea,
hypertension and increased use of the accessory muscles of breathing (neck and upper chest) are
implemented to reverse the hypoxia. As the hypoxia continues to worsen, these compensatory
mechanisms begin to fail. The body starts to “shut down”. Late stages of hypoxia cause the
opposite of the above symptoms: bradycardia, bradypnea, hypopnea, hypotension and little to no
respiratory movement. Numerous premature ventricular contractions (PVC’s) also are common.
With the advance of hypoxia, the body begins additional compensation measures. The bowels
and bladder are evacuated in severe hypoxia. Nausea is quickly followed by emesis to evacuate
the stomach. The body wants to waste no energy when hypoxic. Nonessential systems are shut
down immediately in life threatening hypoxic episodes. Blood flow is shifted to the central
nervous system (CNS) by cerebral vasodilation and peripheral vasoconstriction.
Many arrhythmias develop in addition to the PVC’s, bradycardia, and tachycardia already
mentioned. Ventricular tachycardia, ventricular fibrillation, or asystole occur in severe hypoxia.
Circulatory failure and shock occur when PaO 2 is less than 30 mm Hg or % saturation is less
than 50%. If pulmonary artery (PA) pressures are being monitored, they increase.
Chronic hypoxia causes chronic pulmonary hypertension and cor pulmonale. In the patient with
chronic hypoxia, one also finds “clubbing” of the digits and a loss of the cuticular angle. The
hematopoietic response to chronic hypoxia is to increase the number of RBC’s so these patients
are polycythemic.
COMMON SYMPTOMS OF HYPOXIA
Early:
•
Dyspnea
•
Tachypnea
•
Anxiety
•
Tachycardia
•
Hypertension
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HYPOXIA: CAUSES AND SYMPTOMS
•
Increased use of accessory muscles
•
Nausea
Late:
•
Cyanosis
•
Bradycardia
•
Little to no respiratory movement
•
Emesis
•
Ventricular arrhythmias
•
Hypotension
•
Lethargy
•
Coma
Acute:
•
Tachycardia
•
Arrhythmias
•
Increased respiratory rate
•
Dyspnea
•
Anxiety
•
Blurred vision
•
Impaired judgment
•
Euphoria
•
Lethargy/weakness
•
Tremors/hyperactive reflexes
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HYPOXIA: CAUSES AND SYMPTOMS
•
Stupor
•
Coma
•
Death
Chronic:
•
Clubbing of the digits
•
Polycythemia
•
Right ventricular hypertrophy
•
Chronic pulmonary hypertension
•
Dyspnea
•
Decreased cardiac output
•
Arrhythmias
•
Impaired judgment
•
Irritability
•
Tiredness
•
Papilledema
•
Myoclonic jerking
OXYGENATION ASSESSMENT
Step 1
Identify the PaO2 and determine whether it is below or within normal range. The normal
predicted PaO 2 is dependent on the patient’s age, FI02 , and barometric pressure. Generally, a
PaO 2 , below 80 mm Hg in a patient less than 60 years of age is abnormal, and hypoxemia is
occurring. A PaO 2 of 60 to 79 mm Hg is considered mild hypoxemia, 40 to 59 mm Hg is
considered moderate hypoxemia, and less than 40 mm Hg is considered severe hypoxemia. A
significant difference between PAO 2 , and PaO 2 , [P (A - a) O2] indicates shunt, V/Q
mismatching, or diffusion defect. Hypoxemia with a normal P (A - a) O2, may occur with an
elevated PaCO2 , and when breathing at high altitude.
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HYPOXIA: CAUSES AND SYMPTOMS
Step 2
Identify the degree of SaO 2 on the hemoglobin. SaO 2 should be maintained above 90% in the
upper flat portion of the oxyhemoglobin dissociation curve in most cases. In the upper portion of
the curve, moderate decreases in the PaO 2 do not cause significant reductions in SaO2 , and
oxygen content of the hemoglobin. If the SaO2 , is 70% in the steep part of the oxyhemoglobin
dissociation curve, small changes in PaO2 , will produce significant changes in SaO2 . SaO 2 may
be abnormally decreased with hypoxemia and carbon monoxide poisoning. Actual measurement
of SaO 2 with a co-oximeter is crucial when carbon monoxide poisoning is suspected.
SO2 %
95.80
50.0
0
PO2
26.83
80.0
180
Step 3
Identify the hemoglobin concentration and CaO2 , if available. Hemoglobin and CaO2
measurements from co-oximeters are reliable. CaO 2 measurements from laboratories without
co-oximeters are calculated and may not be accurate. A recent hemoglobin measurement from
the CBC can provide an estimation of the oxygen-carrying capacity of the blood. A normal PaO 2
and SaO 2 are of little value without an adequate hemoglobin concentration.
Step 4
Assess the adequacy of tissue oxygenation using available data. Tissue oxygenation depends on
adequate oxygenation and circulation of the arterial blood. Evaluation of circulation and tissue
oxygenation can be achieved by assessment of the sensorium, blood pressure, extremity
temperature and pulses, and mixed venous oxygen (PvO 2 )
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17
HYPOXIA: CAUSES AND SYMPTOMS
EVALUATION OF HYPOXIA
T
he process of tissue oxygenation is complex and cannot be evaluated appropriately by
examining only the PaO2 and SaO 2 . The focus in evaluating hypoxia must always be on
oxygen delivery to the tissues. This process involves inspiring an adequate concentration
of oxygen (FIO2 ), transferring oxygen across the lung efficiently (PAO2 -PaO 2 relationship),
maintaining an adequate oxygen-carrying capacity (hemoglobin [Hb] concentration), and
sustaining adequate oxygen transport to all body tissue (blood flow, or cardiac output). All these
factors must be considered during an assessment of a person’s oxygenation status. Focusing on
the ultimate goal of adequate oxygen delivery to the tissues is essential.
Arterial blood gas analysis involves objective evaluation of hypoxia. PaO2 has previously been
discussed. For most individuals, a PaO 2 less than 80 mm Hg is considered hypoxemic.
However, one should note whether there are additional symptoms of hypoxia before aggressive
treatment is implemented. As mentioned earlier, many patients have a normal PaO2 less than 80
mm Hg. Patients with chronic lung disease may be considered hypoxic when PaO 2 is less than
60 mm Hg. However many of these patients are comfortable with a PaO 2 of 50-60 mm Hg.
Treatment decisions must be based upon the PaO 2 in conjunction with clinical symptoms.
The importance of hemoglobin and its % saturation with O2 cannot be overemphasized in the
evaluation of hypoxia. Normally, hemoglobin is 95-97% saturated with O2 . Most institutions
and textbooks consider % saturation less than 90% to be hypoxemic for adults. For neonates, a
minimum of 88% is recommended instead. Many recommend 92% as the minimum %
saturation. Pulse oximetry % saturation should be correlated with an actual % saturation
measurement for monitoring purposes.
CLASSIFYING THE SEVERITY OF HYPOXEMIA
Classification
PaO2 (mmhg)
SaO2 (%)
Normal
Mild Hypoxemia
Moderate Hypoxemia
Severe
80 –100
60 – 79
40 – 59
< 40
> 95
90 – 94
75 – 89
< 75
There are 4 factors that affect the saturation (affinity) of hemoglobin with O2 : pH, PaCO2 ,
temperature, and 2,3 diphosphoglycerate (DPG). If any of these factors change from normal, the
% saturation will change for any given PaO2 . Changes that cause an increase in saturation for a
given PaO2 are: increased pH, decreased PaCO2 , decreased temperature and decreased 2,3 DPG.
The opposite conditions of decreased pH, increased PaCO2 , increased temperature and increased
2,3 DPG cause a decrease in saturation for a given PaO 2 . The former are conducive to easy
loading but difficult release of O2 from hemoglobin. The latter are conducive to difficult loading
but easy release of O2 . These should be considered when evaluating the % saturation.
NOTE: 2,3 DPG is an enzyme produced in RBC’s in response to hypoxia. Anemia and hypoxia
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18
HYPOXIA: CAUSES AND SYMPTOMS
increase DPG levels to release O2 from hemoglobin. DPG also varies directly with pH. This
partially compensates for changes in saturation caused by changes in pH. For example, a
decrease in pH that lowers % saturation is partially offset by an increase in 2, 3 DPG which
increases % saturation. It is important to note that banked blood stored in acid citrate dextrose is
deficient in DPG. Should the patient receive a transfusion of this blood it may take 18-24 hours
before DPG levels return to normal. This interferes with the normal binding and release of O2
from hemoglobin during this time.
If the PaO 2 , % saturation, and hemoglobin level are known, oxygen content can be calculated.
This calculation determines the volume of O2 present in a 100 ml sample of blood. The result is
expressed in “volumes %.” Every one mm Hg of the PaO2 measured is the result of 0.003 ml of
dissolved molecular O2 . To determine the amount of molecular O2 dissolved in plasma, multiply
0.003 times the PaO 2 . For example, if the PaO 2 is 100, 0.003 X 100 mm Hg = 0.3 ml of
dissolved O2 .
One gram of hemoglobin can bind with 1.34 ml of molecular O2 if all of its receptor sites are
bound. This is equivalent to a % saturation of 100%. (Technically, 1.39 ml of O2 can combine
with 1 gm of hemoglobin. The presence of abnormal hemoglobins makes 1.34 ml more
clinically applicable).
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HYPOXIA: CAUSES AND SYMPTOMS
OXYGEN CONTENT
O2 CONTENT = Dissolved In Plasma + Bound O2 To Hb
O2
Dissolved O2 = 0.003 x PaO2
O2
O2 -Hb
Bound O2 = 1.34 x Hb x % O2 saturation
Normally, 95-97% of the receptor sites are bound with O2 . To calculate the amount of O2 bound
to hemoglobin, multiply the factor 1.34 times the amount of hemoglobin present, times the %
saturation. For example, 1.34 X 15 gm X 97% = 19.5 ml of O2 .
The amount of bound O2 is added to the amount of O2 dissolved in the plasma for the O2 content.
In the examples used, 0.3 ml of dissolved O2 plus 19.5 ml of bound O2 is equal to 19.8 ml.
Normal arterial O2 Content is therefore around 20 ml. Normal venous O2 content is around 15
ml. One can assume hypoxemia if arterial O2 content approaches 15 ml.
Oxygen Delivery to Tissues
Oxygen delivery is expressed as cardiac output multiplied by the content of oxygen in arterial
blood:
DO2 = CaO 2 x QT x 10
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HYPOXIA: CAUSES AND SYMPTOMS
The Oxygen content is determined by PaO 2 , SaO 2 , and hemoglobin concentration:
CaO 2 = Hb x SaO 2 x 1.39 + PaO 2 x 0.003
In hypoxemic patients, the dissolved oxygen content, represented by PaO 2 x 0.003 is negligible.
Tissues are limited to varying degrees in how much of the delivered oxygen they can extract
from arterial blood. Disease states such as sepsis may limit extraction capabilities.
Oxygen extraction ratio can be calculated:
O2 Extraction Ratio = VO2 / DO 2
O2 Extraction Ratio can be estimated:
O2 Extraction Ratio = (SaO 2 - SvO 2 ) / SaO 2
Some organs with low oxygen requirements (i.e. kidneys) may only extract 5% of the available
oxygen while other organs with high oxygen requirements (heart) may extract 50% or more of
delivered oxygen. The normal global (i.e. mixed) situation is that we deliver about 1,000 ml’s of
oxygen per minute to the tissues and they extract about 250 ml’s leaving 750 ml’s of oxygen
returning to the lungs in the venous blood. In times of duress, most people can increase their
extraction ratio from the normal 25% to at least 50%.
REFRACTORY HYPOXEMIA
Refractory hypoxemia is hypoxemia that is resistant to oxygen therapy, or requires FIO2 ’s
greater than 60% to achieve a PaO 2 of at least 60 mm Hg and oxygen saturation >90%. An
example of this might be a patient that continues to have their FIO2 increased to correct their low
PaO 2 only to have the PaO 2 return to a low value in a few days. Usually this indicates the
presence of right-to-left shunting.
HAZARDS OF HIGH FIO2 IN THE TREATMEANT OF HYPOXEMIA
Unfortunately the use of high concentrations of oxygen (>60%) in the treatment of hypoxemia
can be identified as a contributing factor in the death of some patients. The delivery of high
concentrations of oxygen, while waiting for conditions, such as influenza pneumonia to resolve,
leads to an irreversible condition known as oxygen toxicity. Oxygen toxicity consequences are
from exposure of the lung tissues to free radicals that react with and damage the cell
mitochondria of lung tissue. At ambient levels of oxygen, the body has enzyme systems to
protect the tissues from this sort of damage but these systems are overwhelmed by high
therapeutic oxygen concentrations when they are delivered for long time periods. In a patient
breathing 100% oxygen, pathological changes can be demonstrated within 8 hours of exposure.
Exposure to this level of oxygen frequently becomes clinically significant within about 24 hours
of exposure. Hyperthermia, acidosis, and hypoglycemia all potentiate oxygen toxicity.
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HYPOXIA: CAUSES AND SYMPTOMS
COMPENSATION FOR HYPOXEMIA
The body has several ways of dealing with hypoxemic challenges. The first changes are
tachycardia, to increase the cardiac output, and hyperventilation. Hyperventilation increases the
PaO 2 as the PaCO2 falls. Both of these maneuvers can increase oxygen delivery greatly. A
healthy person can typically at least triple cardiac output and typically lower their PaCO2 to 20
mm Hg or lower for at least short time periods. This combination can allow the tissues to
maintain adequate oxygenation at very low PaO 2 levels without even having to increase the
extraction ratio. When combined with the above, the ability to increase the extraction ratio
greatly enhances the body’s ability to tolerate hypoxemia without tissue hypoxia.
An example of these compensatory mechanisms at work would be a patient with chronic blood
loss anemia. If we assume that this patient has normal cardiac and lung function to start with,
doubling the cardiac output would allow such a patient to maintain normal oxygen extraction at a
hemoglobin of 7 gm%. If we then double extraction ratio to 50%, this person could maintain
adequate tissue oxygenation at a hemoglobin of 3.5 gm%. Body tissues don’t care that much
whether they’re hypoxic due to a low PaO 2 or hypoxic from anemia. The patient described has a
hypoxia situation analogous to someone with a normal hemoglobin with an oxygen saturation of
15% if not for his ability to increase his PaO2 , cardiac output, and oxygen extraction ratio.
Unfortunately, most of the hypoxic patients we deal with in the intensive care unit do not have
athletic cardiac and pulmonary performance figures. Once the oxygen extraction ratio hits the
stops (usually around 50% or so), there will be at least some tissues where oxygen consumption
will become supply limited and tissue hypoxia will ensue. This will result in decreased function
of the organ in question (angina in the case of the heart, mental confusion in the case of the brain
etc.) and will result in some anaerobic metabolism and the development of lactic acidosis. Lactic
acid levels can be measured to monitor for this turn of events but if the tissue hypoxia is
localized to only a few organs (normally the ones with the highest demands) and the body’s
ability to metabolize lactate is intact, this can easily be a late and insensitive measure of tissue
hypoxia. Acidosis is a better indicator but it too only shows up when you already have
significant tissue hypoxia. Function based evaluation is better where it is available (i.e. angina or
EKG changes, mental status, etc.).
RESPIRATORY DISEASED PATIENTS: CAN THEY TRAVEL BY AIR?
There are increased opportunities for patients with COPD and other respiratory diseases that
require continuous oxygen to travel. Ongoing advances in technology are the corner stone in
allowing this growing trend. Airline personnel are adjusting to the special needs of patients with
lung disease.
In general, modern day jetliners maintain cabin pressures slightly above outside barometric
pressure. Regulations by the US Federal Aviation Administration govern cabin environment.
There is flexibility however in the desired cabin pressure which are allowed to change during
turbulence or adverse weather. Each type of aircraft is designed to fly at a different maximum
altitude and has a different cabin-pressurization capability. Healthy passengers usually have
little difficulty in tolerating moderate changes in altitude.
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HYPOXIA: CAUSES AND SYMPTOMS
Two major factors have a great influence on how well a COPD patient tolerates air travel. The
first one is the final altitude reached, which determines the maximum available oxygen pressure.
Ascent rate and the flight duration at that final altitude are important elements that may
exacerbate any preexisting clinical problems. A preflight assessment should be preformed on a
COPD to eliminate the problems that may be manifested because of atmospheric changes.
Secondly, the prolonged air travel is immobilizing, which increases the risk of developing
pulmonary thromboembolic disease.
Relative contraindications to air travel include a vital capacity or diffusing capacity of less than
50% of the predicted value, a maximum voluntary ventilation of less than 40 L/min, respiratory
acidosis, and a PaO 2 of less than 50 mm Hg.13 These values, however, may be misleading, since
they relate to the patient’s ground environment and do not take into account the use of
supplemental oxygen aloft. Measuring the PaO2 as close to the time of flight as possible is an
excellent way to predict what the PaO 2 will be at altitudes of up to 8,000 feet in normocapnic
COPD patients.12
Any destination is possible with careful preparation, sufficient oxygen supply and a medical
escort. The most important thing, when contemplating air travel, is to discuss with his or her
physician the travel plans before the flight.
Relative contraindications to air travel. (Adapted from J Respir Dis.12 )
Conditions adversely affected by hypoxia
•
Acute bronchospasm
•
Cyanosis
•
Dyspnea at rest or during exercise
•
Pneumonia or acute upper respiratory tract infection
•
Pulmonary hypertension, with or without cor pulmonale
•
Severe anemia (hemoglobin <7.5 g/dl)
•
Unstable, coexisting cardiac disorders such as arrythmias, angina pectoris, and myocardial
infarction within the previous 3 to 4 weeks
Conditions adversely affected by pressure changes
•
Thoracic surgery in the preceding 3 weeks
•
Noncommunicating lung cysts
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HYPOXIA: CAUSES AND SYMPTOMS
•
Otitis media, sinusitis, or recent middle-ear surgery
•
Pneumothorax or pneumomediastinum
•
Inadequate pulmonary function (as evidenced by one or more of the following)
Diffusing capacity <50% of predicted
Hypercapnia (PaCO2 >50 mm Hg)
Hypoxemia while breathing room air (PaO2 <50 mm Hg)
Maximum voluntary ventilation <40 L/min
Vital capacity <50% of predicted
Other contraindications
•
Contagious diseases, including active tuberculosis
Tips for patients with chronic obstructive pulmonary disease who plan to travel by air. (Adapted
from Respir Care.14 )
Interaction with the physician
•
Determine whether a need for in-flight oxygen exists.
•
Get multiple copies of a letter describing the respiratory condition, the liter flow and duration
of in-flight oxygen needed, and medication prescriptions.
•
Consider an emergency supply of antibiotics and corticosteroids.
•
Ascertain the names of physicians en route and at the destination.
Interaction with the airline/travel agent
•
Notify the airline of the need for oxygen at least 48 hours before the flight.
•
Fly nonstop, if possible.
•
Travel during business hours so vendor personnel will be available.
•
Prearrange a motorized cart or wheelchair if a stopover is scheduled.
•
Try to be seated near a restroom during the flight.
•
Call the airline at least 48 hours before the flight to confirm details.
•
Consider using a travel agent specializing in travel for patients with medical needs.
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24
HYPOXIA: CAUSES AND SYMPTOMS
Personal planning
•
Arrive at least 2 hours early for the flight.
•
Bring a nasal cannula and extra length of tubing.
•
Pack medications in carry-on luggage.
•
Have multiple copies of prescriptions.
•
Have cash to pay for oxygen at a first-aid station, if needed.
Interaction with oxygen vendor
•
Favor a company that has, or can arrange, nationwide coverage.
•
Arrange for oxygen during stopovers (if needed).
•
Try to learn what type of system will be supplied (to check adapters).
CLINICAL PRACTICE EXERCISE
The following practice exercise is discussed at the end of the course. Answers are based upon
the text material.
1. You are asked to evaluate a 68-year-old male complaining of dyspnea. He is 10 hours postop for exploratory laparotomy. He is not a smoker and has no history of pulmonary disease.
What clinical information is needed to evaluate this patient for hypoxia? Why?
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
2. Vital signs are: HR 130, BP 150/120, RR 35, and temperature 98.9. Breath sounds are equal
bilaterally but decreased. Pulse oximetry is 88%. Chest X-ray shows interstitial bilateral
infiltrates. Hemoglobin level is 10 gm. Evaluate this information.
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
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HYPOXIA: CAUSES AND SYMPTOMS
3. ABG’s on 3 lpm nasal cannula are pH 7.33, PaCO2 55, PaO 2 75, BE O, % saturation 85%.
Calculate the O2 content and list possible causes of the patient’s hypoxia.
______________________________________________________________________________
______________________________________________________________________________
______________________________________________________________________________
SUMMARY
H
ypoxia is the result of inadequate gas exchange at the A-C membrane (hypoxic),
inadequate transport or use of O2 by the tissues (stagnant, histotoxic), or inadequate
amounts/binding of hemoglobin with O2 (anemic). Initial symptoms of hypoxia include,
but are not limited to, tachycardia, tachypnea, anxiety, dyspnea, nausea, PVC’s, hypertension
and increased PA pressures. Later symptoms of hypoxia include: bradycardia, bradypnea,
hypotension, ventricular tachycardia, ventricular fibrillation, asystole, cyanosis, lethargy and
coma. Chronic symptoms include clubbing of the digits, polycythemia, pulmonary hypertension,
and cor pulmonale.
Age and chronic lung disease must be taken into account when evaluating the PaO2 . PaO 2 values
less than 80 mm Hg on room air in the normal young adult at sea level indicate hypoxia. Normal
% saturation is 95-97%. Levels below 90% with hemoglobin values of at least 15 gms% are
considered hypoxic. Both PaO 2 and % saturation should be viewed in terms of the total O2
content in arterial blood. Normal O2 content is approximately 20 ml.
Perhaps the most important thing that the patient with respiratory disease who is contemplating
air travel can do is discuss travel plans with his or her physician before the flight.
PRACTICE EXERCISE DISCUSSION
1. Vital signs are needed to determine tachycardia or tachypnea. Pulse oximetry and/or ABG’s
are needed for blood gas data and % saturation. Breath sounds are necessary to evaluate level of
ventilation and presence of obstructions. Since patient is post-op, low hemoglobin is a
possibility so hemoglobin levels need to be determined. CXR is necessary to rule out fibrosis
and edema as causes of dyspnea.
2. Tachycardia, tachypnea, hypertension, and oximetry indicate hypoxia. Low hemoglobin
indicates low O2 content further reinforcing hypoxia. Bilateral infiltrates are decreasing
diffusion and are responsible for decreased breath sounds and pulse oximetry.
3. O2 content is (.003 x 75) + (1.34 x 10 x .85) = 11.62 ml. Patient has both hypoxic hypoxia
and anemic hypoxic. Hypoxic hypoxia is from hypoventilation and decreased diffusion.
Anemic hypoxia is probably from surgical blood loss.
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26
HYPOXIA: CAUSES AND SYMPTOMS
SUGGESTED READINGS AND REFERENCES
1. Shapiro B, Kacmarek R, Cane R, Peruzzi W, Hauptman D. CLINICAL APPLICATION
OF RESPIRATORY CARE, 4th ed., 1991, Mosby Year Book Inc, pp 111-122
2. Scanlan C, Spearman C, Sheldon L. EGAN’S FUNDAMENTALS OF RESPIRATORY
CARE, 7th ed., 1999, Mosby Year-Book Inc., pp 232-239, 738-742
3. Burton G, Hodgkin J. RESPIRATORY CARE: A GUIDE TO CLINICAL PRACTICE, 4th
ed., 1997 J. B. Lippincott Co, pp 371-375
4. Barnes T. RESPIRATORY CARE PRACTICE, 1988, Yearbook Medical Publishers, Inc., pp
137-139
5. Shapiro B, Peruzzi W, Templin R. CLINICAL APPLICATION OF BLOOD GASES, 5th
ed., 1994, Mosby Year Book, Inc, pp 33-42, 63-64, 197-202, 263-273
6. AARC Clinical Practice Guideline, OXYGEN THERAPY IN THE ACUTE CARE
HOSPITAL, Dec 1991, Vol. 36, #12, pp 1410-1413
7. Wilkins R., CLINICAL ASSESSMENT in RESPIRATORY CARE, 4th ed., 2000, Mosby
Year Book, Inc, PP. 126-127, PP. 134-135
8. Fink J., CLINICAL PRACTICE IN RESPIRATORY CARE, 1999, Lippincott Williams
&Wilkins, PP. 250-255
9. Beachey W., RESPIRATORY CARE ANATOMY AND PHYSIOLOGY: FOUNDATION
FOR CLINICAL PRACTICE, 1998 Mosby Year Book inc., PP 150 – 151, PP 208-212, PP 228234
10. Sattar F., Farzan D., A CONCISE HANDBOOK OF RESPIRATORY DISEASES, 4th ed.,
1997, Appleton and Lange pp 19 - 20, 373
11. Dantzker D., MacTntyre N., Bakow E., COMPREHENSIVE RESPIRATORY CARE, 1995
Saunders Company, pp 98- 118, 337 – 338
12. Gong H Jr. Should your patient be allowed to fly? Advising COPD patients about
commercial air travel. J RespirDis. 1984; 5:28-39
13. Mortazavi A, Eisenberg MJ, Langleben D, Ernst P, Schiff RL. Altitude-related hypoxia:
risk assessment and management for passengers on commercial aircraft. Aviat Space Environ
Med. 2003; 74:922-927
14. Stoller JK, Travel for the technology-dependent individual. Respir Care. 1994;39:347-362.
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HYPOXIA: CAUSES AND SYMPTOMS
15. American Airlines. Planing ahead. Available at:
http://aa.com/content/travelinformation/travelHelp/planningAhead.jhtml.
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HYPOXIA: CAUSES AND SYMPTOMS
POST TEST
DIRECTIONS: IF COURSE WAS MAILED TO YOU, CIRCLE THE MOST
CORRECT ANSWERS ON THE ANSWER SHEET PROVIDED AND RETURN TO:
RCECS, 16781 VAN BUREN BLVD, SUITE B, RIVERSIDE, CA 92504-5798 OR
FAX TO: (951) 789-8861. IF YOU ELECTED ONLINE DELIVERY, COMPLETE
THE TEST ONLINE – PLEASE DO NOT MAIL OR FAX BACK.
1. Which of the following listed data does not meet the criteria for documented
hypoxemia?
a. PaO 2 of < 60 mmHg in adults, children, and infants older than 28 days
b. SaO 2 of < 90% on 40% oxygen, in adults, children, and infants younger than
28 days
c. PaO 2 of < 50 mmHg in infants younger than 28 days
d. Capillary oxygen tension (PcO2 ) < 40 mmHg infants younger than 28 days
2. Histotoxic hypoxia is a result of:
a.
b.
c.
d.
e.
low barometric pressure.
interference with O2 uptake or utilization.
lack of hemoglobin.
impaired diffusion.
none of the above.
3. Early symptoms of hypoxia consist of:
1.
2.
3.
4.
a.
b.
c.
d.
e.
anxiety.
lethargy.
tachycardia.
polycythemia.
1, 2, 3
3, 4
1, 2, 4
1, 3
2, 3, 4
4. CaO 2 and PaO 2 are not affected when severely shunted blood mixes with arterial
blood because of cardiac output compensation.
a. True
b. False
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29
HYPOXIA: CAUSES AND SYMPTOMS
5. Which of the following is an example of hypoxic hypoxia?
a.
b.
c.
d.
e.
hypoventilation.
low barometric pressure.
cyanide poisoning.
all the above.
a & b only.
6. What is the clinical significance of a shunt fraction that is 22%?
a.
b.
c.
d.
Compatible with normal lungs
Intrapulmonary abnormality; compatible with spontaneous breathing
Significant intrapulmonary diseases: probably requires CPAP or PEEP
Severe intrapulmonary disease; aggressive mechanical ventilatory support with
PEEP required; life threatening
7. What effect will high altitude have on the PaO2 ?
a. decreases PaO 2 .
b. increases PaO 2 .
c. altitude has no effect on PaO 2 .
8. For patients with chronic lung disease, a “normal” PaO2 is more likely to be:
a.
b.
c.
d.
e.
94-97%.
80-100 mm Hg.
60-80 mm Hg.
20 ml/dl.
none of the above.
9. The most common cause of Acquired Methemoglobinemia is toxic exposure to
drugs or chemicals:
a. True
b. False
10. For most patients (under 60 years old), a normal PaO 2 is considered to be:
a.
b.
c.
d.
e.
94-97%.
80-100 mm Hg.
60-80 mm Hg.
20 ml/dl.
none of the above.
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HYPOXIA: CAUSES AND SYMPTOMS
11. Which of the following diseases or condition will least likely cause Hypoxic
Hypoxia?
a. Pneumonia.
b. Airway obstruction.
c. Severe hypotension.
12. Chronic symptoms of hypoxia include:
1.
2.
3.
4.
a.
b.
c.
d.
e.
barrel chest.
clubbing of digits.
polycythemia.
right ventricular hypertrophy.
1, 3, 4
1, 2, 3, 4
1, 4
2, 3, 4
none of the above.
13. Normal arterial O2 content is:
a.
b.
c.
d.
e.
20 ml (volumes %).
15 ml (volumes %).
10-20 ml (volumes %).
80-100 mm Hg.
60-80 mm Hg.
14. Normal hemoglobin % saturation is:
a.
b.
c.
d.
e.
88-92%.
95-97%.
70%.
90%.
less than 90%.
15. What happens to O2 content when carboxyhemoglobin levels increase?
a. O2 content increases.
b. O2 content decreases.
c. O2 content remains the same.
KM: Test Version G
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HYPOXIA: CAUSES AND SYMPTOMS
ANSWER SHEET
NAME____________________________________ STATE LIC #_________________
ADDRESS_________________________________ AARC# (if applic.)_____________
DIRECTIONS: (REFER TO THE TEXT IF NECESSARY – PASSING SCORE FOR
CE CREDIT IS 70%). IF COURSE WAS MAILED TO YOU, CIRCLE THE MOST
CORRECT ANSWERS AND RETURN TO: RCECS, 16781 VAN BUREN BLVD,
SUITE B, RIVERSIDE, CA 92504-5798 OR FAX TO: (951) 789-8861. IF YOU
ELECTED ONLINE DELIVERY, COMPLETE THE TEST ONLINE – PLEASE DO
NOT MAIL OR FAX BACK.
1. a b c d
2. a b c d e
3. a b c d e
4. a b
5. a b c d e
6. a b c d
7. a b c
8. a b c d e
9. a b
10. a b c d e
11. a b c
12. a b c d e
13. a b c d e
14. a b c d e
15. a b c
KM: Test Version G
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HYPOXIA: CAUSES AND SYMPTOMS
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