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213 Cards in this Set
- Front
- Back
Rate of diffusion
|
is proportional to 1/Square Root of MW
|
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What molecule diffuse faster?
Co2, Co or O2 and why? |
CO2 is a bigger molecule than O2 so CO2 diffuses slower than O2.
Net result is that O2 diffuses faster than CO2. |
|
Diffusion of a gas within a liquid, equation and which gas diffuse faster?
|
Rate of diffusion is proportional to solubility/Square Root of MW.
CO2 is 20 times more soluble in water than O2. Net result is that CO2 diffuses faster than O2 in solution. |
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Fick's Law of Diffusion equation:
|
.
V gas = (A * D * deltaP) / T Vgas = volume flow of gas or diffusion rate A = area D = Diffusion Constant = solubility /square root of MW delta P = pressure gradient T = thickness of membrane |
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diffusion limited means what? What gas?
|
Carbon Monoxide (CO) is transferred from alveoli to RBCs very
rapidly due to the great affinity between CO and hemoglobin. As a result, the partial pressure of arterial CO (PaCO) never equilibrates with the partial pressure inside the alveoli (PACO). Thus, CO is said to be diffusion limited (i.e. the transfer of CO depends mostly on its diffusion properties and not on the amount of available blood flow) |
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Perfusion-Limited Oxygen Exchange means what?
How can u improve? |
It means there are excess O2 but not enough capillaries/blood to carry the O2.
N2O is perfusion limited. O2 is also perfusion limited due to it is also equilibrates with alveolar pressure in 4 millisecond. The only way to improve oxygen transfer is by increasing the the blood flow (i.e. cardiac output). |
|
Diffusion-Limited Oxygen Exchange means what?
How can u improve it? |
Not enough O2 to fill the blood.
Co2 is diffusion limited. It does not reach alveolar P Diffusion rate must be increased. It can be increased by increasing the PAO2 (i.e. the driving force of diffusion). |
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What is the driving force in Fick's diffusion equation?
|
Is delta P which is the A-a gradient.
|
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When can be O2 diffusion limited?
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If you have a barrier like interstitial fibrosis O2 will have an increased (A-a) gradient and than you have an O2 that is for sure diffusion limited and you have a problem with gas exchange
Or In NORMAL PERSON if excercising in high altitude |
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Diffusion capacity (DL)is defined as the volume
|
the volume of gas that
diffuses across the respiratory membranes (the blood-air barrier) per min per mm Hg. . DL = Vgas / delta P Vgas= Diffusion rate of a gas P1= alveolar pressure P2= pulmonary capillary pressure (plasma not RBC) delta P= P1- P2 = pressure difference (less than 11 mm Hg for O2) |
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In a normal individual at rest, the DL Of oxygen is ____
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is about 31 ml/min/mm Hg
|
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During exercise this DL of oxygen
|
increases to
65 ml/min/mm Hg due to ..... 1)increased pulmonary blood flow (perfusion) 2)increased alveolar ventilation |
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Determination of Diffusion Capacity (DL)for Oxygen
and for Co2 |
To determine the diffusion capacity for oxygen, we must use
the carbon monoxide method for DL determination (DL for CO=V gas/ PACO-PaCO. Because carbon monoxide has such a great affinity for hemoglobin, there is no time for the PaCO to build up. If PaCO=0, then ΔP= PaCO. So, DLCO=V gas/ PACO. A known amount of carbon monoxide is inhaled over a given Once the DL for carbon monoxide has been determined (normally around 25 ml/min/mmHg) we can multiply it by 1.25 (oxygen diffuses 1.25 time faster than carbon monoxide). The DL for oxygen can also be corrected for lung volume and is expressed as DL/VA, where VA is the alveolar volume and is essentially the same as the TLC. Get CO2 diffusion constant by multiply O2 diffusion constant by 20 and you get around 620 ml/min/mmHg |
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Variables that can affect DL
Posture |
- DL is 10% to 15% higher in the recombinant
position. V/Q inbalance |
|
Variables that can affect DL
Body size |
DL increases proportionately to body size.
|
|
Variables that can affect DL
excercise |
-DL is about 25% higher during exercise. Increase of SA by recruiting more vessels
|
|
Variables that can affect DL
Pulmonary Disease - |
DL fluctuates as A and T (from
Fick's Equation) are altered. Due to decrease in SA |
|
Variables that can affect DL
Hemoglobin Concentration - |
DL increases proportionately to
the concentration of hemoglobin. |
|
Resistance to diffusion equation
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R=1/DL
|
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How do you correct for lung volume?
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To correct for lung volume divide the
diffusion capacity (DL) by the alveolar volume (VA) |
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describe the various ways oxygen is transported in
blood. |
Oxygen can be transported in blood either in chemical combination
with hemoglobin or in physical solution |
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Oxygen diffusing capacity determined by P or concentration gradient?
|
Oxygen diffuses from an area of high pressure to an area of
low pressure regardless of concentration gradient. |
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Henry's Law states what?
|
Henry's Law states that a
[gas] = kgasPgas [gas] = concentration of a particular gas in solution kgas = solubility constant for a particular gas Pgas = the partial pressure of a particular gas |
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Normal concentration of
hemoglobin in blood is_____ and each gram of hemoglobin can combine with about ______ of oxygen. |
15 g/dl
1.36 ml |
|
The relationship of oxygen chemically combined with hemoglobin is
_____. The shape of the curve is _______. |
nonlinear
sigmoidal. |
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At PaO2 of 100 mm Hg Hb saturation is________
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98%
|
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At PvO2 of 40 mm Hg Hb saturation is _____
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75 %
|
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What is the total arterial and venous [O2]?
|
Arterial:
CaO2= Hb concentration x O2 per gram Hb x .98 (O2's % saturation in Hb) Venous: CvO2= Hb concentration x O2 per gram Hb x .75 (which is % PvO2 of 40 mmHg Hb saturation) |
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What is the total DO2 to the tissues?
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DO2 = CaO2 * Q
|
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What is the total [O2] returned to the lungs?
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total [O2] returned to the Lungs = CvO2 * Q
|
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What is the O2 uptake by the tissues? Formula
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VO2 = (CaO2 – CvO2)* Q
or VO2 = DO2 - O2 returned to the lungs |
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What is the rate of O2ER by the tissues?
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O2ER = VO2/DO2
|
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What is P50?
|
partial
pressure of oxygen in which Hb is 50 % saturated. The magnitude of a shift to the right or a shift to the left of an O2-Hb dissociation curve can be expressed in terms of P50. An increase in P50 denotes a decrease in the Hb affinity for oxygen and a decrease in the P50 denotes an increase in the Hb affinity for oxygen. |
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Affect of T on P50 and curve
|
As temperature increases, there is an increased probability that
the shape of the Hb structure will be altered due to an increase in kinetic energy. This will have the effect of lowering the affinity of Hb for oxygen. Consequently, increased temperature at the tissue level of exercising muscle contributes significantly to the release of oxygen from Hb. This is indicated by a shift to the right of the O2-Hb dissociation curve. |
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Affect of Acidity on P50 and curve
|
The lower the pH (increased acidity) the more oxygen will be driven
off the Hb. This is referred to as the Bohr Effect. The more H+ (increased acidity) the more these ions will interact with the Hb molecule altering its structure. If the structure of hemoglobin is altered then it cannot bind oxygen as effectively. The lower pH at the tissue level (compared to the lungs) contributes to the releasing of oxygen from Hb and the O2-Hb dissociation curve shifts to the right. |
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Affect of CO2 on P50 and curve
|
Increases in the partial pressure of CO2 (PCO2) leads to an increase
in acidity As carbon dioxide produced by tissues is taken up by the blood it is converted to carbonic acid (with the aid of carbonic anhydrase) which then dissociates to bicarbonate and hydrogen ions. This isthe most common reason for the O2-Hb dissociation curve to shift to the right. |
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What is Bohr effect?
|
The lower the pH (increased acidity) the more oxygen will be driven
off the Hb. This is referred to as the Bohr Effect. The more H+ (increased acidity) the more these ions will interact with the Hb molecule altering its structure. If the structure of hemoglobin is altered then it cannot bind oxygen as effectively. The lower pH at the tissue level (compared to the lungs) contributes to the releasing of oxygen from Hb and the O2-Hb dissociation curve shifts to the right. |
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Affect of 2,3-bisphosphoglycerate (BPG) on P50 and curve
|
This compound (found in RBCs) decreases the affinity of Hb for
oxygen. BPG is a by-product of glycolysis (glucose breakdown). As BPG binds deoxyhemoglobin, it stabilizes the Taut form of Hb so that its affinity for oxygen is decreased. Increased blood levels of BPG will result in a shift to the right of the O2-Hb dissociation curve |
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Affect of Fetal Hb on P50 and curve
|
Fetal Hb has a higher affinity for oxygen than does maternal Hb.
The reason for this is that the fetal Hb does not bind BPG as effectively as the maternal Hb. Oxygen saturation in the placenta is quite low. The higher affinity of the fetal (compared to maternal) Hb for oxygen helps insure that the fetus does not suffer undue hypoxia. |
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list factors that affect the DL.
|
Posture - DL is 10% to 15% higher in the recombinant
position. Body Size - DL increases proportionately to body size. Exercise -DL is about 25% higher during exercise. Pulmonary Disease - DL fluctuates as A and T (from Fick's Equation) are altered. Hemoglobin Concentration - DL increases proportionately to the concentration of hemoglobin. |
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How do you calculate R of diffusion?
|
R = delta P/Q
DL = Q/ deltaP therefore: R= 1/DL |
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At the tissues, the
___________ becomes the most critical componet of Fick’s Law. |
distance of diffusion
(L) Time of diffusion increases as a function of the square of the distance of diffusion. The result is that diffusion over a short distance is fast, but diffusion over a long distance is slow |
|
list the compensatory mechanisms evoked by anemia**
|
1) increase the amount of oxygen extracted from the blood by
the tissue since tissue oxygen concentration is lower in anemic patients. 2) increase cardiac output (more blood flows through tissues per unit time). |
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CO2 is produced in the body as _____
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a product of cellular metabolism.
|
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The partial Pressure of carbon dioxide (PCO2) is greatest?
|
PP of Co2 is greater in the
tissue than in capillary blood, therefore, carbon dioxide will tend to diffuse from the tissue to the blood. |
|
How is Co2 carried?
|
Carbon dioxide is carried in the blood in physical solution, as
carbamino compounds, and as bicarbonate. |
|
The
solubility coefficient (kCO2) of Co2 is |
(kCO2) is 0.06 ml/dl *1/mm Hg.
|
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How do you calculate CO2 concentration in physical solution and what is it?
|
[CO2] = kCO2PCO2
= (0.06 ml/dl * 1/mm Hg) * 40 mm Hg = 2.4 ml/dl |
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Why CO2 diffuses readily from the tissues, through the
capillary endothelium, and through erythrocyte cell membranes? |
Because the partial pressure of CO2 is greater in the tissue than in
capillary blood |
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How can Co2 form Carbamino Compounds?
|
Dissolved CO2 can react with free amino groups of plasma proteins to
form carbamino compounds. Inside the RBC CO2 can combine with Hemoglobin to form a carbamino compound. |
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The affinity of deoxyhemoglobin for CO2 is_________ than the affinity
of oxyhemoglobin for CO2. |
greater
|
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What is the principle carrier of CO2?
|
bicarbonate anion
|
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How does the CO2-
hemoglobin dissociation curve look like? |
has no plateau (remember a plateau
would indicate hemoglobin saturation with CO2). The CO2 - hemoglobin dissociation curve is affected by the partial pressure of O2 just as the O2 – hemoglobin dissociation curve is affected by the partial pressure of CO2. |
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What is the Haldane Effect?
|
the Haldane effect promotes the transport of CO2 away from
tissues and promotes elimination of CO2 through the lungs. |
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What promotes the transport of CO2 away from
tissues and promotes elimination of CO2 through the lungs? |
Haldane Effect
|
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What is the principle form by which CO2 is transported in
blood. |
Bicarbonate
|
|
formation
of carbonic acid takes place where? |
Carbonic anhydrase is not present in the plasma so formation
of carbonic acid takes place mainly in the RBC |
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Where is more bicarbonate and why?
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Since the concentration of bicarbonate is great inside the cell,
bicarbonate is able to diffuse across the RBC cell membrane, which is very permeable to anions (negatively charged ions). Once the plasma and RBC concentrations of bicarbonate anions equilibrate (chemical equilibrium) there is more bicarbonate in the plasma compared to the RBC since the ratio of plasma to RBC is 55 : 45. This represents an electrical nonequilibrium. |
|
What is electrical nonequilibrium?
|
Since the concentration of bicarbonate is great inside the cell,
bicarbonate is able to diffuse across the RBC cell membrane, which is very permeable to anions (negatively charged ions). Once the plasma and RBC concentrations of bicarbonate anions equilibrate (chemical equilibrium) there is more bicarbonate in the plasma compared to the RBC since the ratio of plasma to RBC is 55 : 45. |
|
what is chloride shift?
|
Although the RBC is
permeable to anions, it is impermeable to cations (K+, Na+, H+, etc.). To balance the loss of bicarbonate ions and correct for the electrical nonequilibrium, chloride anions rush into the RBC. This is known as the chloride shift. |
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What is Hb a vasoconstrictor or dilator?
|
Hb by itself is a vasoconstrictor.
Hb is carrying its own vasodilator to the tissues in a form of SNO. The SNO is converted to NO which serves as a vasodilator and facilitates O2 diffusion into the tissues. |
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What is necessary
for normal respiration? |
Intact innervation of the respiratory muscles is necessary
for normal respiration. Neuronal brain centers in the brainstem ensure proper innervation of these respiratory muscles |
|
The primary neurons responsible for respiration are
located in the reticular formation of__________ |
medulla
oblongata. |
|
Medullary Centers
|
The primary neurons responsible for respiration are
located in the reticular formation of the medulla oblongata. |
|
There are two groups of neurons in the medulla.
|
1) Dorsal respiratory group (DRG)
2) Ventral respiratory group (VRG) |
|
There are two groups of neurons in the medulla.
1) Dorsal respiratory group (DRG): |
These neurons fire
primarily during inspiration. The DRG is contained with the nucleus of the tractus solitarius. |
|
There are two groups of neurons in the medulla.
2) Ventral respiratory group (VRG) |
Some neurons of this
group fire during inspiration and others fire during active expiration. The caudal VRG is contained within the nucleus ambiguus and the nucleus retroambiguus. The rostral VRG is also known as the Botzinger Complex (BOT)and are contained within the retrofacial nucleus. These neurons fire primarily during expiration. The cells of the pre-Botzinger complex now appear to act as pacemakers that can generate the spontaneous respiratory rhythm much like the SA node generates the spontaneous cardiac rhythm. |
|
The DRG is contained
with what? |
the nucleus of the tractus solitarius
|
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The caudal VRG is contained within
|
the nucleus ambiguus and the nucleus retroambiguus.
|
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The rostral VRG is also known as
|
the Botzinger
Complex (BOT)and are contained within the retrofacial nucleus. |
|
What is Botzinger
Complex (BOT)? |
The rostral VRG is also known as the Botzinger
Complex (BOT)and are contained within the retrofacial nucleus. |
|
What is located in the the retrofacial
nucleus? |
The rostral VRG is also known as the Botzinger
Complex (BOT)and are contained within the retrofacial nucleus. |
|
The cells of the pre-Botzinger complex do what?
|
Part of VRG and The cells of the pre-Botzinger complex
now appear to act as pacemakers that can generate the spontaneous respiratory rhythm much like the SA node generates the spontaneous cardiac rhythm. |
|
appear to act as pacemakers that can generate the
spontaneous respiratory rhythm much like the SA node generates the spontaneous cardiac rhythm. |
The cells of the pre-Botzinger complex
in VRG |
|
What is in the nucleus ambiguus and the nucleus retroambiguus?
|
VRG
|
|
Pontine Centers, do what?
|
Centers in the pons modulate the activity of medullary
centers. |
|
There are two groups of neurons in the pons.
|
1) Pontine respiratory group (PRG)
2) Apneustic Center |
|
Pontine respiratory group (PRG) in pons
|
Located in the upper
pons, this group of neurons was previously known as the pneumotaxic center. The PRG acts as an “offswitch” to inhibit inspiration and is contained within the nucleus parabrachialis medialis and the 104 Kolliker-Fuse nucleus. The PRG modulates or “fine tunes” the breathing pattern generated in the medullary centers. |
|
Apneustic Center in pons
|
The apneustic center is a vague area
located in the lower pons, and is named for its ability to prevent apneusis (i.e. prolonged inspiratory gasps with only minimal time for expiratory efforts). Experimental animals or humans who have had spinal cord transections in this area of the pons display apneusis. Vagus nerve transections can also induce apneusis. Neurons of the apneustic center are believed to even out respiration by acting as a “cutoff switch” to inspiratory efforts. In other words, the apneustic center projects and integrates a variety of afferent information that ultimately ends inspiration. |
|
What contained
within the nucleus parabrachialis medialis and the Kolliker-Fuse nucleus? |
Pontine respiratory group (PRG) in pons
|
|
Higher Brain Centers do what?
|
Higher brain centers modulate the medullary and pontine
respiratory centers (i.e. modulation of respiration during laughing, crying, talking, eating, adaptations to environmental temperatures, etc.) Higher brain centers voluntarily control activity of respiratory muscles through the corticospinal pathway. |
|
Higher brain centers
voluntarily control activity of respiratory muscles through the what? |
corticospinal pathway.
|
|
If the vagi are transected below the medullary centers?
|
level 4
all spontaneous breathing will cease (apnea). Thus, vagal afferents to the medullary centers are required for spontaneous breathing to occur. |
|
If the vagi are transected above the medullary and below the
apneustic center? |
level 3 in the diagram above) a spontaneous,
although uneven, breathing pattern will be generated. Thus, the vagal afferents to the medullary centers stimulate a spontaneous breathing pattern and prevents apnea. |
|
If the vagi are transected above the apneustic center and below the
pneumotaxic center? |
(level 2 in the diagram above) apneusis will
occur. Thus vagal afferents to the apneustic center appear to prevent apneusis. |
|
If the vagi are transected above the pneumotaxic center
|
(level 1 in
the diagram above) a breathing pattern with deep inspiratory efforts will be established. Thus vagal afferents to the pneumotaxic center (i.e. PRG) appear to inhibit inspiratory efforts. |
|
Inspiratory neurons from the
DRG receive |
vagal and
glosopharyngeal afferents relaying chemoreceptor information PNC APC about PaO2, PaCO2, and pH. also receives vagal afferents relaying information about stretch and other lung receptors. These neurons also serve as the primary innervators of the diaphragm by way of the phrenic nerve. Neurons of the DRG send many collateral fibers to the VRG. |
|
Inspiratory and Expiratory
neurons from the VRG |
primarily
serve as efferents innervating muscles of inspiration. The expiratory efferents innervate the internal intercostals and abdominal muscles by way of vagus nerve during active expiration. The inspiratory efferents innervate the external intercostals and the accessory muscles of inspiration by way of the vagus nerve. Expiratory neurons from the Botzinger complex are the only neurons of the VRG to send collaterals to the DRG and are known to inhibit inspiratory neurons of the DRG. |
|
Inspiratory and Expiratory
neurons from, but primarily serve as efferents innervating muscles of inspiration. |
the VRG
|
|
Inspiratory neurons from
|
DRG
|
|
innervate
the internal intercostals and abdominal muscles |
The
expiratory efferents innervate the internal intercostals and abdominal muscles by way of vagus nerve during active expiration. VRG |
|
innervate the
external intercostals and the accessory muscles of inspiration |
The inspiratory
efferents innervate the external intercostals and the accessory muscles of inspiration by way of the vagus nerve.VRG |
|
send collaterals
to the DRG and are known to inhibit |
Expiratory
neurons from the Botzinger complex are the only neurons of the VRG to send collaterals to the DRG and are known to inhibit inspiratory neurons of the DRG. |
|
These neurons also serve as
the primary innervators of the diaphragm by way of |
the phrenic nerve. DRG
|
|
relaying
information about stretch and other lung receptors. |
In
addition the DRG also receives vagal afferents |
|
In addition to normal control of breathing, Pulmonary reflexes
serve two additional functions. |
1) influence the normal pattern of breathing
2) protect the respiratory system from harmful stimuli |
|
The pulmonary Reflex Arc
|
1) Receptors (sensors)
2) Afferent Limb (Vagus nerve carries most of the afferent fibers in the pulmonary reflexes) 3) CNS Integration (central controller, see previous pages) 4) Efferent Limb (Phrenic nerve, intercostal nerves) 5) Effector (respiratory muscles) |
|
Pulmonary Stretch Receptors
|
Located throughout the smooth muscle
layers of the pulmonary airways. They provide information about lung volumes to the brain. These receptors adapt very slowly. Pulmonary reflexes utilizing these stretch receptors are called Hering-Breuer inflation reflexes. |
|
Muscle Proprioceptors
|
(i.e. muscle spindles and golgi tendon organs)
and Joint Receptors in the diaphragm and in the intercostal muscles sense the degree of stretch and the amount of movement from the limb muscles and reflexly regulate the degree of their contraction. |
|
Irritant and Juxtacapillary Receptors
|
rapidly adapt to sustained
stimuli. Irritant receptors are distributed in the epithelial lining of the large and small airways and the juxtacapillary receptors are located in the lung parenchyma close to alveolar capillaries. Irritant receptors respond to hot or cold air, and noxious chemicals. Stimulation of these receptors induces sneezing, coughing, and laryngeal spasms, constricts airways, induces shallow rapid respiratory pattern. Juxtacapillary receptors respond to anesthetic gases, mediators (such as histamine released during allergic reactions), engorgement of pulmonary capillaries and interstitial edema. Stimulation of these receptors induces shallow rapid respiratory pattern. |
|
Irritant receptors are distributed in
|
the epithelial lining
of the large and small airways and the juxtacapillary receptors are located in the lung parenchyma close to alveolar capillaries. |
|
Irritant receptors respond to
|
hot or cold air, and noxious
chemicals. Stimulation of these receptors induces sneezing, coughing, and laryngeal spasms, constricts airways, induces shallow rapid respiratory pattern. Stimulation of these receptors induces sneezing, coughing, and laryngeal spasms, constricts airways, induces shallow rapid respiratory pattern. |
|
Juxtacapillary receptors respond to
|
anesthetic gases, mediators (such as histamine released during
allergic reactions), engorgement of pulmonary capillaries and interstitial edema. Stimulation of these receptors induces shallow rapid respiratory pattern. |
|
is the most important constituent in blood regulating
respiration. |
CO2
|
|
Any increase in the partial pressure of CO2 will
_____ ventilation, where as a decrease in the partial pressure of CO2 will ________ventilation. |
increase
decrease |
|
Any increase in the partial pressure of CO2 will lead to a
__________ in pH which is sensed by chemoreceptors. |
decrease
|
|
80% of the
chemoreceptors are located |
centrally (ventral surface of the
medulla, location not precisely defined). These chemoreceptors do communicate with the respiratory neuronal groups in the medulla (especially the dorsal respiratory group). |
|
Plasma levels of H+ and HCO3
- cannot influence chemoreceptors in the brain because |
these ions do not cross the blood-brain
barrier. CO2 freely diffuses through capillaries and into the extracellular fluid and hence make contact with the central chemoreceptors. Alternatively, CO2 which has diffused into the CSF can also stimulate chemoreceptors since the CSF lies so close to the medullary surface. |
|
Peripheral Chemoreceptors represent____ % of the total
chemoreceptors, |
Peripheral Chemoreceptors represent only 20 % of the total
chemoreceptors, but are more rapidly activated than the central chemoreceptors. |
|
Peripheral chemoreceptors are located in the
|
carotid and aortic bodies
|
|
Carotid and Aortic body chemoreceptors
|
Carotid body chemoreceptor afferent fibers accompany carotid
baroreceptor afferent fibers centrally via the carotid sinus nerve. Aortic body chemoreceptor afferent fibers accompany aortic baroreceptor afferent fibers centrally via the vagus nerve. |
|
Peripheral chemoreceptors are sensitive to
|
partial pressures of
CO2, O2, and pH of arterial blood. The carotid body chemoreceptors are more sensitive to blood gas composition than are the aortic body chemoreceptors. |
|
What happens to repiratory drive during end-stage emphysema?
|
chemoreceptors can adapt to constant high levels of CO2
and thereby decrease hypercapnic ventilatory drive. Such is the case in end-stage emphysema. Respiratory muscle tire and ventilate less, resulting in higher levels of CO2. It is at this point that hypoxic ventilitory drive kicks in. Hypoxic ventilatory drive is not as sensitive as hypercapnic drive.) |
|
Why does ventilation rate is altered
very little under normal circumstances? |
Furthermore, under normal conditions, arterial PCO2 only varies
by as little as 3 mm Hg. Therefore ventilation rate is altered very little under normal circumstances. |
|
if the PACO2 is increased ventilatory rate _______
|
increases
|
|
If the PAO2 increases the ventilatory rate ________
|
decreases
Increasing the PAO2 lowers the ventilatory rate and the slope of the ventilation/PACO2 curve. |
|
How is ventilatory response to CO2 influenced by sleep, and increasing age?
|
decreased
|
|
Ventilatory Response to Oxygen
|
(for any given PACO2), the arterial PO2 has
very little effect on ventilatory rate until the arterial PO2 decreases to about 50 mm Hg, upon which the ventilatory rate will increase. Increasing the PACO2 has the effect of increasing the ventilatory rate and slope of ventilation/PO2 curve. |
|
Ventilatory Response to pH
|
A fall in the arterial pH will typically cause an increase in
the rate of ventilation, but it is often difficult to determine if this increase in ventilation is due to a drop in pH per se, or if it is due to an increase in PCO2. To answer this question one should observe situations in which pH is partially compensated (e.g. uncontrolled diabetes mellitus). In this type of situation there is an obvious increase in ventilatory rate and both PCO2 and pH are decreased. |
|
Ventilatory Response to Exercise
|
Exercise increases the rate and depth of ventilation while the
amount of O2 uptake and CO2 output remains closely matched. During sever exercise ventilation can increase by as much as 15 times the normal ventilatory rate. What mystifies pulmonologists is that the stimulus for exercise-induced increase in ventilation (hyperpnea) is virtually unknown. |
|
Although exercise increases the rate of ventilation 3 things remain stable
|
1) PCO2 remains stable
2) PO2 remains stable 3) plasma pH remains stable |
|
Two possible types of mechanisms for hyperpnea
|
1) neurogenic
a. sensory input from the exercising limbs stimulates the respiratory muscles either by spinal reflexes or through brain stem respiratory centers. b. input from the cerebral cortex 2) humoral continued rapid and deep ventilation after exercise suggests that some chemical or humoral factor is involved. |
|
Abnormal Breathing Patterns
|
Obstructive vs Central Sleep Apnea
|
|
In obstructive apnea
|
there is a least a partial obstruction of
the oropharynx due to decreases in skeletal muscle tone during sleep (i.e the tongue). Despite a decrease in airflow, respiratory drive is still present as seen by cycling pleural pressure. |
|
In central apnea
|
all breathing efforts cease for a
period of time. Central apnea is often referred to as periodic breathing. Examples of periodic breathing include Cheyne-Stokes and Biot’s Breathing patterns. |
|
Cheyne-Stokes Respiration
|
Type of central apnea
Severe hypoxemia can induce this type of breathing pattern which is characterized by periods of apnea (10 to 20 seconds) followed by periods of hyperventilation (10 to 20 seconds). It is often seen at high altitudes and in patients with heart disease and brain damage. |
|
Biot’s Breathing
|
Type of central apnea
Periods of normal breathing are interupted by periods of apnea. CNS problems can precipitate this type of breathing. |
|
Eupnea
|
Normal quite breathing
|
|
Normal quite breathing
|
Eupnea
|
|
Dyspnea
|
Literally means "air-hunger". Difficulty in breathing
usually accompanies strenuous exercise or certain disease states. |
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Literally means "air-hunger". Difficulty in breathing
usually accompanies strenuous exercise or certain disease states. |
Dyspnea
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Hyperpnea
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Increased rate and depth of breathing due to increased
metabolic needs. It is distinguished from hyperventilation in that hyperventilation leads to a decrease in PCO2 as a result of an increase in the rate of breathing. |
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Increased rate and depth of breathing due to increased
metabolic needs. It is distinguished from hyperventilation in that hyperventilation leads to a decrease in PCO2 as a result of an increase in the rate of breathing. |
Hyperpnea
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Hypocapnia
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decreased CO2 in blood. Opposite of Hypercapnia
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decreased CO2 in blood.
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Hypocapnia
Opposite of Hypercapnia |
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Cyanosis
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Means blueness of the skin due to excessive amounts of
deoxygenated hemoglobin. |
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Means blueness of the skin due to excessive amounts of
deoxygenated hemoglobin. |
Cyanosis
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Tachypnea
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rapid shallow breathing
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rapid shallow breathing
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Tachypnea
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Kussmaul Breathing
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is a form of hyperventilation described as
deep and labored breathing. Kussmaul breathing is often seen as a result of severe metabolic acidosis (such as diabetic ketoacidosis)or renal failure. |
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is a form of hyperventilation described as
deep and labored breathing. It is often seen as a result of severe metabolic acidosis (such as diabetic ketoacidosis)or renal failure. |
Kussmaul Breathing
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abnormal breathing pattern characterized by
a complete lack of respiratory rhythm (i.e. irregular pauses with increased episodes of apnea). Ataxic respiration eventually progresses to agonal respirations |
Ataxic Respirations
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Ataxic Respirations
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abnormal breathing pattern characterized by
a complete lack of respiratory rhythm (i.e. irregular pauses with increased episodes of apnea). Ataxic respiration eventually progresses to agonal respirations |
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Agonal Respiration
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abnormal breathing pattern characterized by
shallow, slow, irregular inspirations flowed by irregular pauses. It may also be characterized as gasping or labored breathing. Sometimes it is accompanied by vocalization Agonal respirations eventually progress to complete apnea. |
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abnormal breathing pattern characterized by
shallow, slow, irregular inspirations flowed by irregular pauses. It may also be characterized as gasping or labored breathing. Sometimes it is accompanied by vocalization |
Agonal Respiration
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Apnea
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Absence of breathing
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Absence of breathing
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Apnea
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Draw the Feedback loop for Decreased ventilation
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Palazzolo lecture 12 slide 16
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Compare Hyperventilation and Hyperpnea during excercise
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During excercise: In BOTH:
Rate and depth of breathing, minute ventilation, O2 consumption, Co2 production INCREASES. In Hyperventilation alkalosis (low CO2), but in Hyperpnea the acid/base status will be normal (during normal excercise) |
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Normal excercise vs Severe excercise
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During normal excercise ventilation increases, but arteial PO2, pH, lactic acid levels are constant.
During extreme excercise plasma lactic acid increases, and Ph decreases, PP of O2 will increase |
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mechanism of action for hypernea is unclear but appears to involve both....
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1. neurogenic mechanism:
excerxixing muscle →afferent fibers→CNS→efferent fibers→respiratory muscle 2. and humoral mechanisms: after excercising, it takes several minutes for the deep, rapid breathing pattern of hyperpnea to cease. |
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What situations you see Cheyene Stokes apnea?
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- heart disease
-CNS disease - high altitude |
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What situations you see Biot;s breathing?
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- CNS damage
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What is the principle carrier of CO2?
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bicarbonate anion
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What is the plateau indicate in the HB O2 curve
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Hb saturation with O2
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What Co2-Hb dissociation curve has no plateau?
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plateau
would indicate hemoglobin saturation with CO2). |
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The maternal
blood supply arrives via the _______to the ______ |
uterine arteries
intervillous sinusoids. |
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Oxygen is picked up by the ______ arteries and
returned to the fetus via the ____ vein. |
umbilical and umbilical
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Blood-Blood Barrier
between the mother and the fetus is about ___thick. |
3.5 microns
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Partial pressure of O2 of blood in the umbilical vein is about ___ mmHg.
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30
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Fetus lives in a very ____ environment.
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hypoxic
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At birth, the fetus is cut off from the placental gas exchange
resulting in _____ and ____ |
hypoxemia
hypercapnia. |
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At birth ________increases (not clear why) and this leads to the first
gasps of air. |
chemoreceptor
sensitivity |
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Since the alveoli are
not totally collapsed (pre-inflated with fluid), _____pressure is needed for inflation. |
less
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Intrapleural pressure _______at birth
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Intrapleural pressure decreases at birth (due
to the outward pull of the baby's chest wall once the newborn is out), thus aiding in the inflation of the lungs. |
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The remaining
fluid in the lungs at birth is taken up by ________ |
the lymphatic system and
production of surfactants help to reduce the surface tension. |
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When is Respiratory Distress syndrome occur in newborns?
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Respiratory Distress syndrome does not occur at the newborns first
breath, rather at the successive breaths. The first breath for all newborns is equally as hard, regardless of if respiratory distress will occur or not. |
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Pulmonary vascular resistance ____at birth
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Pulmonary vascular resistance decreases at birth, as the airways
open up and fluid is emptied out of the lungs. |
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The partial pressure
of O2 in the lungs is ____ at birth. |
increased.
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What leads to the closure of the foramen ovale?
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There is an increase in the left
atrial pressure which leads to the closure of the foramen ovale. |
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The ductus arteriosus is closed primarily due to
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increase in
partial pressure of O2, an increase in circulating levels of bradykinin, and a decrease in circulating levels of prostaglandins |
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What is hypoxia?
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Hypoxia is a decrease in oxygen tension, whereby cells do not get
the amount of oxygen that is required. |
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decrease in oxygen tension, whereby cells do not get
the amount of oxygen that is required. |
hypoxia
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Symptoms include impaired judgement, disorientation, headache,
anorexia, nausea, vomiting, and tachycardia. |
hypoxia
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Causes of Hypoxia
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1) Inadequate ventilation of the lungs.
2) Pulmonary disease resulting in hypoxemia due to uneven V/Q ratio or diffusion barrier. 3) Venous-to-arterial shunts (right to left cardiac shunts). 4) Inadequate transport of Oxygen. 5) Inadequate ability of the tissue to use oxygen. |
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Hypoxic Hypoxia
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Inadequate ventilation of the lungs.
Due to deficiency of oxygen in the atmosphere such as at high altitudes or due to some neuromuscular disorder causing hypoventilation. (Also Known As Hypoxic Hypoxia) |
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Inadequate ventilation of the lungs lead to hypoxia, due to what?
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Due to deficiency of oxygen in the atmosphere such as at
high altitudes or due to some neuromuscular disorder causing hypoventilation. (Also Known As Hypoxic Hypoxia) |
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Pulmonary disease resulting in hypoxemia due to uneven
V/Q ratio or diffusion barrier lead to hypoxia, due to what? |
Hypoventilation due to increased airway resistance (i.e.
emphysema), or decreased compliance (i.e. fibrosis) or impairments in the gas diffusion processes or physiological shunts. |
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Inadequate transport of Oxygen lead to hypoxia due to what?
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Anemia or abnormal Hb (Also Known As Anemic Hypoxia),
general or localized circulatory deficiencies (Also Known As Circulatory Hypoxia), tissue edema. |
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Anemic Hypoxia
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Inadequate transport of Oxygen lead to hypoxia
Anemia or abnormal Hb (Also Known As Anemic Hypoxia), general or localized circulatory deficiencies (Also Known As Circulatory Hypoxia), tissue edema. |
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Circulatory Hypoxia
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Inadequate transport of Oxygen lead to hypoxia
Anemia or abnormal Hb (Also Known As Anemic Hypoxia), general or localized circulatory deficiencies (Also Known As Circulatory Hypoxia), tissue edema. |
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Inadequate ability of the tissue to use oxygen lead to hypoxia due to what?
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Poisoning of cellular enzymes or diminished cellular
metabolic capacity due to a lack of vitamin, enzyme, cofactor etc. (Also Known As Histotoxic Hypoxia) |
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Histotoxic Hypoxia)
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Inadequate ability of the tissue to use oxygen lead to hypoxia
Poisoning of cellular enzymes or diminished cellular metabolic capacity due to a lack of vitamin, enzyme, cofactor etc. |
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Barometric pressure is low so the partial pressure of inspired O2 is
low. Compensate by ...... |
1) hyperventilating (increases the PO2 and decreases the PCO2)
2) increase production of RBC (more hemoglobin to carry more O2) Hypoxemia stimulates production of erythropoietin(or hemopoietin) from kidney which stimulates the bone marrow to produce more RBCs (hematopoiesis). 3) increase production of BPG, and/or increase body temperature, will cause a right shift in the oxygenhemoglobin dissociation curve. 4) Increase capillary density, improve oxidative capacity by increasing the effectiveness of the enzymes. 5) Increase maximum breathing capacity (due to a decrease in the density of air) 6) Increase pulmonary vasoconstriction (increase in pulmonary arteriole pressure, improve uniformity of lung perfusion. |
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Symptoms include headaches, fatigue, dizziness,
nausea, loss of appetite, hypoxemia and alkalosis. In severe cases, pulmonary edema can also result. |
Mountain sickness
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Mountain sickness
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Symptoms include headaches, fatigue, dizziness,
nausea, loss of appetite, hypoxemia and alkalosis. In severe cases, pulmonary edema can also result. |
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Oxygen Toxicity
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Partial pressure of inspired O2 is extremely high
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Oxygen toxicity is directly related to the ___ and ____
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length of time and
the amount of pressure |
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100% O2 at 760mmHg for 24 hrs results in
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substernal pain due to PE
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100% O2 at 760mmHg for 30 hrs results in
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permanent lung damage
absorbable atelectasis |
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100% O2 at 2280 mmHg for 1 hr results in
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coma and death
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One effect of O2 toxicity is
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make the body less able to
remove oxygen derived free radicals. Oxygen is known to form dangerous free radicals such as O2 - and H2O2. An increase in barometric pressure will result in an increased production of these free radicals. |
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In high
barometric pressures are also known to inactivate _____ |
high
barometric pressures are also known to inactivate supraoxide dismutases, catalases, peroxidases, sulfhydryl dehydrogenases and other enzymes, which normally would eliminate free radicals. |
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O2 toxicity increases the tendency towards ____
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absorption
atelectasis. Absorption atelectasis occurs due to the diffusion of oxygen into plasma down an increased pressure gradient. If the airways become obstructed by mucous, for example, the chance of atelectasis is increased. |
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Absorption atelectasis
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occurs due to the
diffusion of oxygen into plasma down an increased pressure gradient. If the airways become obstructed by mucous, for example, the chance of atelectasis is increased. |
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In deep sea diving Pressure increases ___mmHg for ___ft under water
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760 mm Hg (or 1 atm) for each 33 ft
under water. |
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What happens with N in diving as the pressure increases the further you go under?
water, |
Because of the higher pressures the further you go under
water, nitrogen which is poorly soluble in water under normal conditions is now forced into solution, and finally into the tissue. If enough nitrogen gets into the blood, a nitrogen narcosis (also known as "raptures of the deep") will develop. |
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nitrogen narcosis
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If enough nitrogen gets into the blood during diving, a nitrogen narcosis
(also known as "raptures of the deep") will develop. This is characterized by euphoria, loss of coordination, and will lead to coma and finally death. |
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euphoria, loss of coordination, and will lead
to coma and finally death. |
nitrogen narcosis
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What happens when u come up from diving too fast?
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If nitrogen is removed from the tissues slowly, no problems
will result. However, if nitrogen is removed from the tissue to fast, nitrogen bubbles will form in the body fluids causing extreme pain, causing anywhere from minor to serious damage, depending on where the bubbles form in the body. This is referred to as decompression sickness or more commonly referred to by divers as "The Bends". Symptoms of decompression sickness are joint pain, deafness, impaired vision, and even paralysis. |
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decompression sickness
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If nitrogen is removed from the tissues slowly, no problems
will result. However, if nitrogen is removed from the tissue to fast, nitrogen bubbles will form in the body fluids causing extreme pain, causing anywhere from minor to serious damage, depending on where the bubbles form in the body. This is referred to as decompression sickness or more commonly referred to by divers as "The Bends". Symptoms of decompression sickness are joint pain, deafness, impaired vision, and even paralysis. |
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joint pain, deafness, impaired
vision, and even paralysis. |
decompression sickness
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If Carbon dioxide pressure is allowed to build up beyond 80 mm
Hg, as in the case with divers that wear helmets____will start to occur, ______ will develop, respiratory centers in the CNS will begin to shut down, rather than be excited. |
If Carbon dioxide pressure is allowed to build up beyond 80 mm
Hg, as in the case with divers that wear helmets, lethargy will start to occur, respiratory acidosis will develop, respiratory centers in the CNS will begin to shut down, rather than be excited. |
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Where is higher P in the fatal lung?
|
RA>LA
IVC 30 highest, lowest from tissues |
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Causes of Hypoxemia
|
high altitude
hypoventilation diffusion defect V/Q defect R to L shunt |
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Common Causes of Respiratory Acidosis
|
1. Depression of the respiratory centers
2. Neuromuscular disorders which also affect respiratory muscles 3. Chest wall restriction 4. Lung restriction 5. Pulmonary parenchymal diseases 6. Airway obstruction |
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1. Depression of the respiratory centers
2. Neuromuscular disorders which also affect respiratory muscles 3. Chest wall restriction 4. Lung restriction 5. Pulmonary parenchymal diseases 6. Airway obstruction Cause what? |
Common Causes of Respiratory Acidosis
|
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Common Causes of Respiratory Alkalosis
|
1. Excitement
2. Anxiety 3. Drugs which stimulate respiratory centers 4. Pathologies which stimulate respiratory centers 5. Hypoxia induced by high altitude 6. Hyperventilation syndrome 7. Overventilation with a mechanical ventilator |
|
1. Excitement
2. Anxiety 3. Drugs which stimulate respiratory centers 4. Pathologies which stimulate respiratory centers 5. Hypoxia induced by high altitude 6. Hyperventilation syndrome 7. Overventilation with a mechanical ventilator Cause what? |
Common Causes of Respiratory Alkalosis
|
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Common Causes of Metabolic Acidosis
|
1. Ingested drugs or toxic substances
2. Loss of bicarbonate anions 3. Lactic acidosis 4. Ketoacidosis - Diabetes 5. Inability to excrete protons (H+) |
|
1. Ingested drugs or toxic substances
2. Loss of bicarbonate anions 3. Lactic acidosis 4. Ketoacidosis - Diabetes 5. Inability to excrete protons (H+) Cause what? |
Common Causes of Metabolic Acidosis
|
|
Common Causes of Metabolic Alkalosis
|
1. Loss of H+ (vomiting, excess aldosterone, diuretics)
2. Ingestion of bicarbonate anion (or antacids) 3. Excess administration of Bicarbonate anion |
|
1. Loss of H+ (vomiting, excess aldosterone, diuretics)
2. Ingestion of bicarbonate anion (or antacids) 3. Excess administration of Bicarbonate anion Cause what? |
Common Causes of Metabolic Alkalosis
|