Background
Basic human
needs are elements that are needed by humans in defense of the balance of
physiology and psychology. One is the need for oxygen. Oxygen is one component
of gases and vital elements in the metabolism process to maintain the viability
of all body cells. Normally this element is obtained by inhaling the room O2
whenever breathing.
Oxygen is
the most vital basic need in human life, in the body, oxygen plays an important
role in the process of cell metabolism. Oxigan deficiency can cause significant
things to the body, one of which is death. Therefore, various efforts need to
be done to ensure the fulfillment of oxygen needs, to be met properly. In the
implementation of oxygen demand fulfillment is a separate nurse's duties,
therefore every nurse must be familiar with the manifestation of oxygen
fulfillment level on the client and able to overcome various problems related
to the fulfillment of the needs tesebut. Therefore, the need for oxygen is the
most important and very vital for the body.
Every human
body cell needs oxygen to perform metabolic functions, so oxygen is the most
important substance in human life. Maintaining oxygenation is an attempt to
ensure adequate supply of oxygen to tissues or cells. This of course depends
not only on adequate respiratory function, but also to be supported by adequate
circulatory function. To assess the balance of supply and oxygen demand, more
specific parameter checks are needed, and not sufficient based on clinical
examination alone. Often patients who initially improve with oxygen therapy,
acute respiratory failure can result in cardiac arrest and ending with death,
due to inadequate management of respiratory and circulatory functions.
Oxygen
enters the body through the lungs, transported to the tissue through the blood,
and is consumed at the intracellular level (mitochondria) to provide energy for
cell metabolism. The presence of interference with the respiratory system, the
cardiovascular system, or tissue can interfere with oxygenation and cause
tissue damage or death of the organism.
SUPPLY OXYGEN
Oxygen is
transported from the inspiratory air to every cell in the body. According to
the laws of physics, the gas moves from the region of high pressure
concentration to low pressure concentration.
Thus, the
movement and taking of oxygen from the lungs to the tissue can actually be
determined by four main variables:
1. Arterial
oxygen content (arterial O2 content / CaO2)
- Ventilation
- Taking oxygen
2. Oxygen
delivery (DO2)
3. Oxygen
consumption (VO2)
4. Oxygen extraction
ratio (O2 ER)
Assessment
of the adequacy of oxygen supply to the tissues, depending on three factors:
1.
Hemoglobin levels
2. Cardiac
output
3.
Oxygenation.
The amount
of oxygen available to the body in a minute is known as the oxygen supply (DO2).
The amount of oxygen is closely related to the cardiovascular system, not just
the respiratory system.
If the
supply given to our body is sufficient, then the metabolism process in the body
will run properly and normally, but if the supply is not sufficient, then the
metabolic process will go badly.
OXYGEN CONSUMPTION (VO2)
About 250 ml
of oxygen is used every minute by healthy people (oxygen consumption at rest),
thus only about 25% of the oxygen content in arteries is used every minute.
Hemoglobin in mixed venous blood (SvO) was about 73% saturated (98% minus 25%).
At rest, the supply of oxygen to the body cells exceeds the consumption of
oxygen. Preferably during exercise, oxygen consumption increases. Low cardiac
output, low hemoglobin (anemia) or low oxygen saturation will result in reduced
tissue oxygen supply, unless compensated for any of the above factors occurs.
Figure 1.
Balance between oxygen supply and oxygen
consumption. The horizontal line represents the amount of oxygen supply that
can be lowered and compensated by increased oxygen extraction (normally between
20-30%, between A-B). The point (illustrates) the point of compensation is not
enough and oxygen consumption is limited by supply (depending on supply), and
anaerobic metabolism produces lactic acid.
Hb ROLE ON O2
TRANSPORT IN BLOOD
O2 can be
transported from the lung to the tissues via two paths: physically soluble in
plasma or chemically binding to Hb as oxyhemoglobin (HbO2). The chemical bond
of O2 with Hb is reversible, and the actual amount transported in this form has
a nonlinear relationship with the partial pressure of O2 in arterial blood
(PaO2), determined by the amount of O2 that is physically soluble in the blood
plasma. Furthermore, the amount of O2 that is physically soluble in the plasma
has a direct relationship with the partial pressure of O2 in the alveolus
(PAO2). The amount of O2 also depends on the solubility of O2 in plasma. Only
about 1% of total O2 is transported in this way. This way of transport is not
sufficient to sustain life even in a resting state. Most of the O2 is
transported by Hb present in red blood cells. In certain circumstances (eg
carbon monoxide poisoning or massive haemolysis with Hb insufficiency),
sufficient O2 to survive may be transported in the form of physical solution by
giving the patient O2 a higher pressure than atmospheric pressure (hyperbaric
O2 space).
One gram of
Hb can bind 1.34 ml of O2. The mean Hb concentration in the adult male blood is
about 15 g per 100 ml so that 100 ml of blood can carry 20.1 ml of O2 (15 x
1,34) when the saturated O2 (SaO 2) is 100%. But a little mixed venous blood
from the bronchial circulation is added to the blood leaving the pulmonary
capillaries and already oxygenated. This dilution process explains why only
about 97 percent of the blood leaving the lungs becomes saturated.
At the
tissue level, O2 dissociates from Hb into the plasma and diffuses from the
plasma to the tissue cells of the body to meet the tissue requirements.
Although the need for such tissue varies, but about 75% of Hb still binds to O2
at the time Hb returns to the lung in the form of mixed venous blood. So only
about 25% O2 in arterial blood is used for tissue purposes. Hb that releases O2
at the tissue level is called reduced Hb. Hb is reduced to purple and causes a
bluish color in the venous blood, whereas HbO2 is bright red and causes a
reddish color in arterial blood.
OKSIHEMOGLOBIN
DISCIENT DISTRIBUTION
To be able
to understand O2's transport capacity it is clear that Hb to O2 must be known
as O2 supply for tissue and O2 retrieval by the lung depends on the
relationship. If full blood is exposed to various partial pressures of O2 and
the percentage of saturation of Hb is measured, then a curve of the letter S is
obtained when the two measurements are combined. This curve is known as the
oxyhemoglobin dissociation curve and states the affinity of Hb to O2 at various
partial pressures.
A very
important physiological fact about this curve is the presence of a flat top. At
the top of the flat curve, large changes in O2 pressure due to slight changes
in saturation of HbO2. This means that a relatively constant amount of O2 can
be supplied to the network even at high altitudes when PO2 can be as high as 60
mmHg or less. This also means that the administration of O2 in high
concentrations (normal air 21%) in patients with mild hypoxemia (PaO2 = 60-75
mmHg) is useless, since HbO2 can only be increased very little. The release of
O2 to the tissue can be increased by the PO2 relationship to SaO2 on the steep
curve of the venous region. In this section major changes in HbO2 are the
result of slight changes to PO2.
The affinity
of Hb to O2 is influenced by many other factors that accompany the tissue and
may be altered by the disease. A list of some of these factors and their
effects on affinity for O2 can be seen in the table below.
Table
1. Factors affecting oxyhemoglobin affinity (HbO2)
HbO2 Dissociation Curve
|
|
Shift Left
(P50 decrease)
|
Shift Right
(P50
increase)
|
pH ↑
|
pH ↓
|
PCO2 ↓
|
PCO2 ↑
|
Temperature ↓
|
Temperature ↑
|
2,3 DPG ↓
|
2,3 DPG ↑
|
P50
= oxygen voltage required to produce 50% saturation
The
curve shifts to the right when the blood pH decreases or PCO2 increases. Under
these circumstances, at a certain PO2 the affinity of Hb to O2 is reduced, so
that O2 that can be transported by blood is reduced. Pathological conditions
that cause metabolic acidosis, such as shock (excessive lactic acid formation
due to anaerobic metabolism) or CO2 retention (as found in many lung diseases)
will cause right-shift curves. The shift of the curve slightly to the right as
in the vein section of the normal curve (pH 7.38) will help the release of O2
into the tissue. This shift is known as the Bohr effect. Another factor that
causes a right curve shift is an increase in temperature and 2,3
diphosphoglycerate (2,3-DPG) is the organic phosphate in red blood cells that
binds Hb and reduces the affinity of Hb to O2. In chronic anemia and hypoxemia,
2,3-DPG red blood cells increase. Although the ability of O2 transport by Hb
decreases when the curve shifts to the right, but the ability of Hb to release
O2 to the network is made easier. Therefore, in chronic anemia and hypoxemia
the shift of the curve to the right is a process of compensation. Right-shift
curves with temperature rise, in addition to describing an increase in cell
metabolism and increased O2 demand, are also a process of adaptation and cause
more O2 to be released into the tissue from the bloodstream.
Conversely,
an increase in blood pH (alkalosis) or decreased PCO2, temperature, and 2,3-DPG
will cause a left-sided oxyhemoglobin dissociation curve. The shift to the left
causes an increase in the affinity of Hb to O2. As a result O2 pulmonary uptake
increases in a shift to the left, but discharge to the tissue is disrupted.
Hence theoretically hypoxia (tissue O2 insufficiency to meet metabolic
requirements) in severe alkalosis, especially when accompanied by hypoxemia.
This occurs during the process of overventilation mechanism with respirator or
at high site due to hyperventilation. Because hyperventilation is also known to
decrease cerebral blood flow due to a decrease in PaCO2, cerebral ischemia is
also responsible for the symptoms of dizzy that often occur in such conditions.
The stored blood will lose the activity of 2,3-DPG, so the affinity of Hb to O2
will increase. Therefore, patients receiving blood transfusions stored in large
quantities are likely to experience O2 discharge to the tissues due to a shift
in the HbO2 dissociation curve to the left.
Hb
affinity is constrained via PO2 required to produce 50% saturation (P50). Under
normal circumstances, P50 is about 27 mmHg. P50 will increase, if the
dissociation curve shifts to the right (decrease the affinity of Hb to O2)
whereas in the left curve shift, (increase of Hb affinity to O2), P50 will
decrease.
CO
2 homeostasis is also an important aspect in the adequacy of respiration.
Transport of CO2 from tissue to lung for disposal is done in three ways. About
10% of CO2 is physically soluble in plasma, because unlike O2, CO2 is easily
soluble in plasma. About 20% of CO2 binds to the amino group in Hb (carbaminohemoglobin)
in red blood cells, and about 70% is transported in the form of plasma
bicarbonate (HCO3-). CO2 binds to water in the following reaction:
This
reaction is reversible and is called the buffer equation of bicarbonate-carbonic
acid. The body's acid-base balance is strongly influenced by lung function and
CO2 homeostasis. In general, hyperventilation (alveolar ventilation in the
state of excessive metabolic needs) causes alkalosis (increased blood pH
exceeds the normal pH of 7.4) due to excessive CO2 excretion of the lung;
Hypoventilation (alveolar ventilation that can not meet metabolic requirements)
causes acidosis due to CO2 retention by the lungs. A decrease in PCO2 as occurs
in hyperventilation will cause the reaction to shift to the left causing the
concentration of H + (increase in pH), and the increase in PCO2 leads to a
right-sided reaction, resulting in an increase in H + (decrease in pH).
Just
like O2, the amount of CO2 in the blood is related to PCO2. The dissociation
curve of CO2 is almost linear on the physiological boundaries of PCO2. This
means that the CO2 content in the blood is directly related to PCO2. In
addition, there is no meaningful barrier to CO2 diffusion. Therefore PaCO2 is a
good clue to the adequacy of ventilation.
GAS BLOOD ANALYSIS
To
adequately assess respiratory function, it is also necessary to study things
outside the lung such as volume and distribution of gas transported by the
circulatory system.
PaCO2
is the best VA instruction. When PaCO2 increases, the immediate cause is always
alveolar hypoventilsai. Hypoventilation causes respiratory acidosis and a
decrease in blood pH. The direct cause of the decrease in PaCO2 is always
alveolar hyperventilation. Hyperventilation causes resiratory alkalosis and an
increase in blood pH.
When
PaO2 falls below normal values, hypoxemia occurs. In severe respiratory
failure, PaO2 decreases to 30-40 mmHg. Hypoxemia due to lung disease is caused
by one or more of the following mechanisms:
1.
an imbalance between the
ventilation-perfusion process (the most common cause),
2.
alveolar hypoventilation,
3.
diffusion gangguang,
4.
intrapulmonary anatomic shunts.
Hypoxemia
due to the first three disorders can be corrected by administering O2. But the
intrapulmonary anatomic shunt (arteriovenous shunt) can not be treated with O2
therapy.
Arterial
blood gas changes are critical in the diagnosis of respiratory failure or
ventilation that may arise slowly. If the levels of PaO2tutun below normal,
respiratory insufficiency occurs, and respiratory failure occurs when PaO2
drops to 50 mmHg. PaCO2 may increase or fall below the normal value of
insufficiency or respiratory failure.
Table
2. Normal Value of Arterial Blood Gas
Cardiac output
Cardiac
output is the amount of blood pumped from the left ventricle / right ventricle
to the aorta / kepulmonal every minute. Cardiac output is equal to stroke
volume multiplied by heart rate.
CO = SV X HR
Description: SV = The amount of blood pumped by the ventricles per contractionHR
= Number of heartbeats per minute. In normal resting men, stroke volume
averaged 70 ml / beat and HR was about 75 x pulse / min. So the average cardiac
out put CO = 70 ml / pulse x 75 x / mnt = 5250 ml / mnt = 5.25 L / mnt. This
volume is close to the total blood volume, in an adult male of about 5 L which
will flow through the pulmonary circulation and systemic circulation every
minute. When the body tissue deficiency or oxygen excess cardiac out put turns
to meet its needs. This factor can increase stroke volume and HR causing
increased cardiac out put.
STROKE VOLUME
Three
factors that affect stroke volume:
1. Preload
(stretching)
The more
hearts are filled when the diastole, the greater the power of contraction
during systolic, in this connection is known as Frank-Starling's law. In
Preload's body is the volume of blood that fills the ventricle at the end of
diastolic End Diastolic Volume (EDV). Normally the greater the EDV (preload)
the stronger the contraction. The duration of ventricular diastole and venous
pressure are two key factors that determine EDV when the heart rate increases,
the duration of diastole shortens. Shortening filling time means that EDV is
reduced and the ventricles can contract before the ventricle is adequately
filled. When venous pressure increases the greater amount of blood is pushed
into the ventricles and EDV increases.
2. Contractility
The second
factor that affects stroke volume is contractility ie contraction force. Things
that increase contractility are called positive inotropic agents. Positive
inotropicagent encourages the inclusion of calcium in the potential action of
the heart, which strengthens muscle fibers contract. The sympathetic symmetes
of ANS (Automatic Nervous System) include epinephrine and nepepinephrine,
increasing the level of calcium in extra cellular fluids, and all digitalism
drugs have a positive effect. Conversely, sympathetic inhibition of ANS,
anoxia, acidosis, some anesthetic agents (eg Halothane) and increased
extra-cellular potassium have negative inotropic effects. Calcium channel
blockers have a negative inotropic effect by reducing the inclusion of calcium,
reducing heart rate.
3. Afterload
Ejection of
blood from the heart begins when the right diventricular pressure exceeds the
pressure in the pulmonal trunk and when the pressure in the left ventricle
exceeds the pressure in the aorta (about 80 mmHg). Higher pressure in the
ventricles causes blood to drive the opening of the semilunar valve. The
pressure to be overcome before the opening of the semilunar valve is named
afterload. Increased afterload causes a decreased volume stroke and more blood
is left in the ventricle at the end of systolic. Conditions that can increase
afterload include hypertension and atherosclerosis.
This is
related with the process of tissue oxygenation can be concluded that all the
processes that resulted in cardiac output will result in a decrease in the
supply of oxygen in the body which ultimately will interfere with the process
of oxygenation. Both the structure of the heart muscle, the electrical
disturbance of the heart and the amount of cardiac output itself.
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