Download RESPIRATION

III SEMESTER BOTANY
MODULE II
RESPIRATION
Lung Capacities and Volumes
•
Tidal volume (TV) – air that moves into and out of the lungs with each breath
(approximately 500 ml)
•
Inspiratory reserve volume (IRV) – air that can be inspired forcibly beyond the
tidal volume (2100–3200 ml)
•
Expiratory reserve volume (ERV) – air that can be evacuated from the lungs
after a tidal expiration (1000–1200 ml)
•
Residual volume (RV) – air left in the lungs after strenuous expiration (1200 ml)
•
Inspiratory capacity (IC) – total amount of air that can be inspired after a tidal
expiration (IRV + TV)
•
Functional residual capacity (FRC) – amount of air remaining in the lungs after
a tidal expiration (RV + ERV)
•
Vital capacity (VC) – the total amount of exchangeable air (TV + IRV + ERV)
•
Total lung capacity (TLC) – sum of all lung volumes (approximately 6000 ml in
males)
Dead Space
•
Anatomical dead space – volume of the conducting respiratory passages (150
ml)
•
Alveolar dead space – alveoli that cease to act in gas exchange due to collapse
or obstruction
•
Total dead space – sum of alveolar and anatomical dead spaces
Oxygen Transport
Transport of oxygen during external respiration:
With its low solubility, only approximately 1.5% of the oxygen is transported dissolved
in plasma.
The remaining 98.5% diffuses into red blood cells and chemically combines with
hemoglobin.
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Hemoglobin
Within each red blood cell, there are approximately 250 million hemoglobin molecules.
Each hemoglobin molecule consists of:
1. A globin portion composed of 4 polypeptide chains.
2. Four iron-containing pigments called heme groups.
Each hemoglobin molecule can transport up to 4 oxygen molecules because each iron
atom can bind one oxygen molecule.
When 4 oxygen molecules are bound to hemoglobin, it is 100% saturated; when there
are fewer, it is partially saturated.
Oxygen binding occurs in response to the high partial pressure of oxygen in the lungs.
When hemoglobin binds with oxygen, it is called oxyhemoglobin.
When one oxygen binds to hemoglobin, the other oxygen molecules bind more readily.
This is called cooperative binding. Hemoglobin's affinity for oxygen increases as its
saturation increases.
Oxyhemoglobin and Deoxyhemoglobin
The formation of oxyhemoglobin occurs as a reversible reaction, and is written as in
this chemical equation:
In reversible reactions, the direction depends on the quantity of products and
reactants present.
In the lungs, where the partial pressure of oxygen is high, the reaction proceeds to the
right, forming oxyhemoglobin.
In organs throughout the body where the partial pressure of oxygen is low, the
reaction reverses, proceeding to the left. Oxyhemoglobin releases oxygen, forming
deoxyhemoglobin, which is also called reduced hemoglobin.
The affinity of hemoglobin for oxygen decreases as its saturation decreases.
Oxygen-Hemoglobin Dissociation Curve
The degree of hemoglobin saturation is determined by the partial pressure of oxygen,
which varies in different organs throughout the body.
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When these values are graphed, they produce
produ
the oxygen-hemoglobin
hemoglobin dissociation
curve. The
he axes on the graph are: partial pressure of oxygen and percent saturation of
hemoglobin.
In the lungs, the partial pressure of oxygen is approximately 100 millimeters of
mercury. At this partial pressure, hemoglobin has a high affinity for oxygen, and is
98% saturated.
In the tissues of other organs, a typical partial pressure of oxygen is 40 millimeters of
mercury. Here, hemoglobin has a lower affinity for oxygen and releases some but not
all of its oxygen to the tissues. When hemoglobin leaves the tissues it is still 75%
saturated.
The oxygen-hemoglobin
hemoglobin dissociation curve is an S-shaped
S shaped curve, with a nearly flat
slope at high PO2's and a steep slope at low PO2's.
A closer look at the flat region of the oxygen-hemoglobin
oxy
hemoglobin dissociation curve between 80
and 100 millimeters of mercury:
In the lungs at sea level, a typical PO2 is 100 millimeters of mercury. At this PO2,
hemoglobin is 98% saturated.
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In the lungs of a hiker at higher elevations or a person with particular
cardiopulmonary diseases, the PO2 may be 80 millimeters of mercury. At this PO2,
hemoglobin is 95% saturated.
Even though the PO2 differs by 20 millimeters of mercury there is almost no difference
in hemoglobin saturation. This means that although
althou
the PO2 in the lungs may decline
below typical sea level values, hemoglobin still has a high affinity for oxygen and
remains almost fully saturated.
Factors that affect the affinity of hemoglobin for oxygen include:
Temperature: A higher temperature cause
c
a decrease in affinity. In more active tissue
with a higher temperature O2 unloads more easily.
pH: Hydrogen ion increases (pH decreases) in more active tissue. This decreases the
affinity of hemoglobin by the Bohr effect which can be expressed in this
is equation
Hb
+
O2
-->
Hb-O2
+ H+
In more active tissue pH decreases and O2 is more easily unloaded
PCO2 : CO2 binds reversibly with Hb to form carbaminohemoglobin a molecule which
has a lesser affinity for O2 . This decrease in the affinity of Hb for oxygen in the
presence of CO2 is called the carbamino effect
These first three factors work together to promote O2 unloading in respiring tissues
and O2 loading in the lungs.
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The hemoglobin oxygen disassociation curve can shift
shift either to the left or to the
right.. When the curve shifts to the right, the affinity of oxygen for hemoglobin
decreases and oxygen can be more easily unloaded. When the curve shifts to the left,
the affinity of oxygen for hemoglobin increases and oxygen can be more easily loaded.
CO2 Transport
1. Carbon dioxide is produced by cells throughout the body.
2. It diffuses out of the cells and into the systemic capillaries, where
approximately 7% is transported dissolved in plasma.
3. The remaining carbon dioxide diffuses into the red blood cells. Within the red
blood cells, approximately 23% chemically combines with hemoglobin, and 70%
is converted to bicarbonate ions, which are then transported in the plasma.
CO2Transport: Carbaminohemoglobin (Tissues)
Of the total carbon dioxide in the blood, 23% binds to the globin portion of the
hemoglobin molecule to form carbaminohemoglobin, as written in this equation:
Carbaminohemoglobin forms in regions of high PCO2, as blood flows through the
systemic capillaries in the tissues.
CO2Transport: Carbaminohemoglobin (Lungs)
The formation of carbaminohemoglobin is reversible.
In
the
lungs,
which
have
a
lower
PCO2,
carbon
dioxide
carbaminohemoglobin, diffuses into the alveoli, and is exhaled.
exhaled
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dissociates
from
CO2 Transport: Bicarbonate Ions (Tissues)
1. Of the total carbon dioxide in the blood, 70% is converted into bicarbonate ions
within the red blood cells, in a sequence of reversible reactions. The bicarbonate
ions then enter the plasma.
2. In regions with high PCO2, carbon dioxide enters the red blood cell and
combines with water to form carbonic acid. This reaction is catalyzed by the
enzyme carbonic anhydrase. The same reaction occurs in the plasma, but
without the enzyme it is very slow.
3. Carbonic acid dissociates into hydrogen ions and bicarbonate ions. The
hydrogen ions produced in this reaction are buffered by binding to hemoglobin.
This is written as HHb.
4. In order to maintain electrical neutrality, bicarbonate ions diffuse out of the red
blood cell and chloride ions diffuse in. This is called the chloride shift.
5. Within the plasma, bicarbonate ions act as a buffer and play an important role
in blood pH control.
CO2 Transport: Bicarbonate Ions (Lungs)
1. In the lungs, carbon dioxide diffuses out of the plasma and into the alveoli. This
lowers the PCO2in the blood, causing the chemical reactions to reverse and
proceed to the left.
2. In the lungs, the bicarbonate ions diffuse back into the red blood cell, and the
chloride ions diffuse out of the red blood cell. Recall that this is called the
chloride shift.
3. The hydrogen ions are released from hemoglobin, and combine with the
bicarbonate ion to form carbonic acid.
4. Carbonic acid breaks down into carbon dioxide and water. This reverse reaction
is also catalyzed by the enzyme carbonic anhydrase.
Tobacco Smoking
Considering the globe, the adverse effects of tobacco smoking out number all
the effects of other pollutants. It is considered as one of the most important
preventable causes of death. Tobacco smoking affects not only those who are actively
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smoking but it also has an adverse consequence on the health of those who are by the
vicinity of the smoker. These individuals are termed as passive Smokers.
Active Smoking and disease
The cigarette smoke that is taken through the mouth into the lung has several
types of chemicals that have diverse & serious effects on our health. The composition
depends on the type of tobacco, length of the cigarette, and presence and effectiveness
of filter tips. Usually present are (1) Carcinogens whose effects have been verified in
lower animals (e.g.polycyclic hydrocarbons, betanaphthylamine, nitrosamines). (2) Cell
irritants and toxins (e.g. Ammonia, formaldehyde, and oxides of nitrogen). (3) Carbon
monoxide, and (4) nicotine, which has various effects on the sympathetic nervous
system, blood pressure, heart rate etc.
The more common adverse health effects of tobacco are lung cancer, coronary
heart disease, COPD (Chronic bronchitis, emphysema), and systemic atherosclerosis.
And the less common effects are peptic ulcer, Cancer that can originate from larynx,
esophagus, pancreas, bladder & kidneys.
Fetuses are also adversely affected by maternal smoking. Several studies have
shown that maternal smoking could cause low birth weight, prematurity, still birth
and infant mortality. Moreover other complications of pregnancy like abruptio
placentae, placenta previa, and premature rupture of membranes have been found to
be caused by maternal smoking.
The risk of mortality is dose dependent. The number of pack years i.e. number
of packs per day times number of years is directly related to mortality rate. The more
pack years of smoking the higher the risk of mortality. Coronary heart disease causes
most of the deaths when it comes to effects of cigarette smoking. Lung cancer closely
follows causing a huge number of deaths.
Involuntary smoke exposure (Passive Smoking)
The effect of passive smoking has been identified during the last few decades.
Its effect comes when non-smoking people inspire the ambient air, which is polluted
by cigarette smoke. The health impact depends on the volume of the air in the room,
number of active smokers, rate of air exchange and duration of exposure. Data from
different countries show that the risks of lung cancer increase by 1.5 due to passive
smoking. There is also increased risk of cardiovascular diseases specially MI, and high
incidence of lower respiratory tract diseases in infants & children of smoking parents.
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Children & infants of smoking mothers will have an obvious intense exposure and
hence retardation of physical and intellectual growth is likely to occur.
Benefits of cessation or reducing exposure to cigarette smoke
When a person stops smoking the risks of diseases and subsequent death start
to decline.
The risk to reach to that of non-smoking people may take 20 years of
smoke-free period. The amount of cigarettes smoked daily, and duration of smoking
determines the rate of decrease of risks. The relative risk of lung cancer and laryngeal
cancer start to decline after 1 to 2 smoke free years. However considering lung cancer
former smokers will have slightly higher risk than non-smokers even after 30 years of
smoke-free years. When it comes to coronary diseases the decline of risk is rapid and
it can level with those of non-smokers after 5 to 20 years. Once COPD has been
developed quitting does not have any significant effect in reversing the situation.
Hypercapnia and hypocapnia
An increase in partial pressure of CO2 (pCO 2) above 43 mm Hg is called hypercapnia.
Hypercapnia produces acidosis. This stimulates the chemosensitive area in the
medulla and chemoreceptors in the carotid and aortic sinuses. This activates the
inspiratory area and thereby causes hyperventilation (increase in the rate of
respiration). Hyperventilation removes more CO2 until pCO
2
is lowered to normal.
When the pCO2 is less than 37 mm Hg the condition is called hypocapnia. It is the
common cause of alkalosis. Alkalosis inhibits respiration (hyperventilation), therby
allows metabolic C 2 to accumulate in blood.
Emphysema
This disease is characterized by the irreversible distension of respiratory bronchioles,
alveolar ducts and alveoli. Distension of these structures reduces the surface area
available for exchange of gases. Hypoxia, pulmonary hypertension, heart failure etc.
are the consequences of the disease. Persistent coughing, cigarette smoking and
infections are the predisposing factors.
Apnoea
It refers to the temporary cessation of breathing. A sudden severe pain or cold can
bring about apnoea.
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Asphyxia
Asphyxia refers to oxygen starvation as result of low-atmospheric oxygen or other such
situations as drawning. Acute asphyxia involves a combination of respiratory,
circulatory and nervous system failure.
Hypoxia
Hypoxia is a condition in which the body or a region of the body is deprived of
adequate oxygen supply. Hypoxia may be classified as either generalized, affecting the
whole body, or local, affecting a region of the body. Generalized hypoxia occurs in
healthy people when they ascend to high altitude. Hypoxia also occurs in healthy
individuals when breathing mixtures of gasses with low oxygen content.
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