SAN PEDRO COLLEGE
Respiratory Therapy Department
Charisa Antonette S. Huelva – 2B
EFFECTS OF EXERCISE
VENTILATION: ALVEOLAR VENTILATION
• During strenuous exercise, this can increase to 120 l/min, a 20-
fold increase.
• Depending on the intensity and duration of the exercise, alveolar
ventilation must increase to
(1) Supply sufficient oxygen to the blood and
(2) Eliminate the excess carbon dioxide produced by the
skeletal muscles.
• The increased alveolar ventilation is produced mainly by an
increased depth of ventilation (increased tidal volume), rather
than by an increased rate of ventilation.
• During very heavy exercise, however, both an increased depth
and frequency of ventilation are seen.
• The tidal volume is usually about 60 percent of the vital capacity,
and the respiratory rate may be as high as 30 breaths/min.
• Three distinct consecutive breathing patterns are seen during
mild and moderate exercise.
(1) Increase in alveolar ventilation, within seconds after the
onset of exercise.
(2) A slow, gradual further increase in alveolar ventilation
developing during approximately the first 3 minutes of
exercise. Alveolar ventilation during this period increases
almost linearly with the amount of work performed.
(3) Alveolar ventilation stabilizes. When an individual stops
exercising, alveolar ventilation decreases abruptly
OXYGEN CONSUMPTION
• At rest, normal oxygen consumption (VO2) is about 250 mL/min.
The skeletal muscles account for approximately 35 to 40 percent
of the total VO2
• During exercise, the skeletal muscles may account for more than
95 percent of the VO2.
• During heavy exercise, the VO2 of an untrained person may be
more than 3500 ml of o2/min.
ARTERIAL BLOOG GAS LEVELS
• No significant PaO2, PaCO2, or pH changes are seen between
rest and approximately 60 to 70 percent of maximal VO2.
• During very heavy exercise, however, when lactic acidosis is
present, both the pH and PaCO2 decline.
• It is believed that arterial acidosis stimulates the carotid
chemoreceptors, causing increased alveolar ventilation and
promoting respiratory acid-base compensation.
OXYGEN DIFFUSION CAPACITY
• The oxygen diffusion capacity increases linearly in response to
the increased oxygen consumption (VO2), during exercise.
• The oxygen diffusion capacity may increase as much as
threefold during maximum exercise. It has been shown that the
increased oxygen diffusion capacity results from the increased
cardiac output during exercise.
ALVEOLAR-ARTERIAL PO2 DIFFERENCE
• Normally, there is a mean alveolar-arterial oxygen tension
difference of about 10 mm hg because of:
(1) Mismatching of ventilation and perfusion; and
(2) Right-to-left pulmonary shunting of blood.
• Despite increases in oxygen consumption (VO2), alveolar
ventilation, and cardiac output, the P(A-a) O2 remains
essentially constant until 40 percent of the maximal VO2 is
reached, beyond this point, the P(A-a) O2 begins to increase.
CIRCULATION
• Heavy exercise is one of the most stressful conditions the
circulatory system encounters.
• Blood flow to the working muscles may increase as much as 25-
fold and the total cardiac output may increase as much as 8-fold
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CARDIORESPIRATORY
CIRCULATION: SYMPATHETIC DISCHARGE
• At the onset of exercise, the brain transmits signals to the
vasomotor center in the medulla oblongata to trigger a
sympathetic discharge. This sympathetic discharge has two
circulatory effects:
(1) The heart is stimulated to increase its rate and strength of
contraction
(2) The blood vessels of the peripheral vascular system
constrict, except for the blood vessels of the working
muscles, which strongly dilate in response to local
vasodilators in the muscles themselves.
• The net result is an increased blood supply to the working
muscles while the blood flow to nonworking muscles is reduced.
• Vasoconstriction in the heart and brain does not occur during
exercise, because both the heart and the brain are as important
to exercise as the working muscles themselves
CARDIAC OUTPUT
• The increased oxygen demands during exercise are met almost
entirely by an increased cardiac output. The increased cardiac
output during exercise results from:
Increased Stroke Volume
• Due to vasodilation in the working muscles; that is, the
vasodilation in the working muscles increases the venous return
to the heart.
• The heart, in turn, pumps more oxygenated blood back to the
working muscles. Thus, the degree of vasodilation in the working
muscles directly influences the stroke volume,
• The greater the vasodilation in the working muscles, the greater
the stroke volume and cardiac output
Increased Heart Rate
• The heart rate increases linearly with oxygen consumption, the
magnitude of the change is influenced by the size of the stroke
volume; that is, when the stroke volume decreases, the heart
rate increases, and when the stroke volume increases, the heart
rate decreases.
• The stroke volume, in turn, is influenced by:
(1) The individual’s physical condition,
(2) The specific muscles that are working, and
(3) The distribution of blood flow.
• The body’s ability to increase the heart rate and stroke volume
during exercise progressively declines with age.
• An individual’s maximum heart rate is estimated by the following
formula:
Maximum heart rate = 220 – age (years)
ARTERIAL BLOOD PRESSURE
• There is an increase in arterial blood pressure during exercise
because of the:
(1) Sympathetic discharge,
(2) Increased cardiac output, and
(3) Vasoconstriction of the blood vessels in the nonworking
muscle areas.
• Depending on the physical condition of the individual, as well as
the intensity and duration of the exercise, the systolic arterial
blood pressure may increase as little as 20 mm Hg or as much
as 80 mm Hg
PULMONART VASCULAR PRESSURES
• As oxygen consumption and cardiac output increase during
exercise, the systolic, diastolic, and mean pulmonary arterial and
wedge pressures also increase linearly
MUSCLE CAPILLARIES
• At rest, approximately only 20 to 25 percent of the muscle
capillaries are dilated.
• During heavy exercise, all these capillaries dilate to facilitate the
distribution of blood.
• This reduces the distance that oxygen and other nutrients must
travel from the capillaries to the muscle fiber. At the same time,
the blood vessels of the viscera and nonworking muscles
constrict.
 SAN PEDRO COLLEGE
Respiratory Therapy Department
Charisa Antonette S. Huelva – 2B
EFFECTS OF HIGH ALTITUDE
VENTILATION
• One of the most prominent features of acclimatization is
increased alveolar ventilation, when an individual ascends
above the earth’s surface, the barometric pressure progressively
decreases and the atmospheric PO2 declines. As the
atmospheric PO2 decreases, the individual’s arterial oxygen
pressure (PaO2) also decreases.
• Eventually, the PAO2 will fall low enough (to about 60 mm Hg)
to stimulate the carotid and aortic bodies, known collectively as
the peripheral chemoreceptors. When the peripheral
chemoreceptors are stimulated, they transmit signals to the
medulla to increase ventilation.
• Because the peripheral chemoreceptors do not acclimate to a
decreased oxygen concentration, increased alveolar ventilation
will continue for the entire time the individual remains at the high
altitude.
POLYCYTHEMIA
• When an individual is subjected to a low concentration of oxygen
for a prolonged period of time, the hormone erythropoietin from
the kidneys stimulates the bone marrow to increase red blood
cell (RBC) production.
• The increased hemoglobin available in polycythemia is an
adaptive mechanism that increases the oxygen-carrying
capacity of the blood.
ACID-BASE STATUS
• Because of the increased ventilation generated by the peripheral
chemoreceptors at high altitudes, causing a secondary
Respiratory Alkalosis.
• Over a 24-to 48-hour period, the renal system tries to offset the
respiratory alkalosis by eliminating some of the excess
bicarbonate.
ALVEOLAR-ARTERIAL DIFFERENCE
• At high altitude, oxygen diffusion across the alveolar-capillary
membrane is limited and this results in an increased alveolar-
arterial oxygen tension difference (P(A-a)O2).
VENTILATION-PERFUSION RELATIONSHIPS
• At high altitude, the overall ventilation-perfusion ratio improves
as a result of the more uniform distribution of blood flow that
develops in response to the increased pulmonary arterial blood
pressure
CARDIAC OUTPUT
• During acute exposure to a hypoxic environment, the cardiac
output during both rest and exercise increases, which, in turn,
increases the oxygen delivery to the peripheral cells.
• In individuals who have acclimatized to high altitude, however,
and in high-altitude natives, increased cardiac output is not seen
PULMONARY VASCULAR SYSTEM
• As an individual ascends from the earth’s surface, pulmonary
hypertension progressively increases as a result of hypoxic
pulmonary vasoconstriction
EFFECTS OF HIGH PRESSURE
DIVING
• Because water is incompressible, the pressure increases
linearly with depth. For every 33 feet (10 m) below the surface,
the pressure increases 1.0 atmosphere (760 mm Hg).
• Thus, the total pressure at a depth of 33 feet is 2 atmospheres
(1520 mm Hg)—1.0 atmosphere (1 atm) owing to the water
column and 1.0 atmosphere pressure owing to the gaseous
atmosphere above the water
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CARDIORESPIRATORY
Breath-Hold Diving
• The simplest and most popular form of diving. The maximum
duration of a breath-hold dive is a function of:
(1) The diver’s metabolic rate, and
(2) The diver’s ability to store and transport O2 and CO2.
• A delicate balance exists between the diver’s O2 and CO2 levels
during a breath-hold dive.
The CO2-O2 Paradox
• Is caused by the pressure changes that develop around the
diver’s body during the dive.
• The CO2 paradox occurs as the diver descends, and the O2
paradox occurs as the diver ascends.
The Mammalian Diving Reflex
• It also known as diving reflex or diving response, consists of
bradycardia, decreased cardiac output, lactate accumulation in
under perfused muscles, and peripheral vasoconstriction elicited
during a breath-hold deep dive.
• The mammalian diving reflex is a set of physiologic reflexes that
acts as the first line of defense against hypoxia
Decompression Sickness
• A during a deep dive, the dissolved nitrogen in the diver’s blood
will move into body tissues. The amount of dissolved gas that
enters the tissues is a function of:
(1) The solubility of the gas in the tissues,
(2) The partial pressure of the gas, and
(3) The hydrostatic pressure in the tissue.
• When the decompression is performed at an appropriately slow
rate, the gases leaving the tissues will be transported (in their
dissolved state) by the venous blood to the lungs and exhaled.
• When the decompression is conducted too rapidly, the gases will
be released from the tissue as bubbles
HYPERBARIC MEDICINE
• The administration of oxygen at increased ambient pressures is
now being used routinely to treat a variety of pathologic
conditions and is accomplished by means of a compression
chamber (also called a hyperbaric chamber).
• Most of the therapeutic benefits of hyperbaric oxygenation are
associated with the increased oxygen delivery to the tissues.
INDICATION FOR HYPERBARIC OXYGENATION
THERAPY
Gas Diseases
• Decompression sickness
• Gas embolism
Vascular
• Radiation necrosis of bone or soft tissue
• Diabetic microangiography
• Compromised skin grafts
• Crush wounds
• Acute traumatic ischemias
• Thermal burns
Infections
• Clostridial myonecrosis
• Necrotizing soft-tissue infections
• Chronic refractory osteomyelitis
Defects in Oxygen Transport
•