2 Exam- Palazzolo 3

Front 1

Rate of diffusion

Back 1

is proportional to 1/Square Root of MW

Front 2

What molecule diffuse faster?
Co2, Co or O2 and why?

Back 2

CO2 is a bigger molecule than O2 so CO2 diffuses slower than O2.
Net result is that O2 diffuses faster than CO2.

Front 3

Diffusion of a gas within a liquid, equation and which gas diffuse faster?

Back 3

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.

Front 4

Fick's Law of Diffusion equation:

Back 4

.
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

Front 5

diffusion limited means what? What gas?

Back 5

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)

Front 6

Perfusion-Limited Oxygen Exchange means what?
How can u improve?

Back 6

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).

Front 7

Diffusion-Limited Oxygen Exchange means what?
How can u improve it?

Back 7

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).

Front 8

What is the driving force in Fick's diffusion equation?

Back 8

Is delta P which is the A-a gradient.

Front 9

When can be O2 diffusion limited?

Back 9

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

Front 10

Diffusion capacity (DL)is defined as the volume

Back 10

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)

Front 11

In a normal individual at rest, the DL Of oxygen is ____

Back 11

is about 31 ml/min/mm Hg

Front 12

During exercise this DL of oxygen

Back 12

increases to
65 ml/min/mm Hg due to .....
1)increased pulmonary blood flow (perfusion)
2)increased alveolar ventilation

Front 13

Determination of Diffusion Capacity (DL)for Oxygen
and for Co2

Back 13

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

Front 14

Variables that can affect DL
Posture

Back 14

- DL is 10% to 15% higher in the recombinant
position.
V/Q inbalance

Front 15

Variables that can affect DL
Body size

Back 15

DL increases proportionately to body size.

Front 16

Variables that can affect DL
excercise

Back 16

-DL is about 25% higher during exercise. Increase of SA by recruiting more vessels

Front 17

Variables that can affect DL
Pulmonary Disease -

Back 17

DL fluctuates as A and T (from
Fick's Equation) are altered.
Due to decrease in SA

Front 18

Variables that can affect DL
Hemoglobin Concentration -

Back 18

DL increases proportionately to
the concentration of hemoglobin.

Front 19

Resistance to diffusion equation

Back 19

R=1/DL

Front 20

How do you correct for lung volume?

Back 20

To correct for lung volume divide the
diffusion capacity (DL) by the alveolar
volume (VA)

Front 21

describe the various ways oxygen is transported in
blood.

Back 21

Oxygen can be transported in blood either in chemical combination
with hemoglobin or in physical solution

Front 22

Oxygen diffusing capacity determined by P or concentration gradient?

Back 22

Oxygen diffuses from an area of high pressure to an area of
low pressure regardless of concentration gradient.

Front 23

Henry's Law states what?

Back 23

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

Front 24

Normal concentration of
hemoglobin in blood is_____
and each gram of
hemoglobin can combine
with about ______ of
oxygen.

Back 24

15 g/dl

1.36 ml

Front 25

The relationship of oxygen chemically combined with hemoglobin is
_____. The shape of the curve is _______.

Back 25

nonlinear
sigmoidal.

Front 26

At PaO2 of 100 mm Hg Hb saturation is________

Back 26

98%

Front 27

At PvO2 of 40 mm Hg Hb saturation is _____

Back 27

75 %

Front 28

What is the total arterial and venous [O2]?

Back 28

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)

Front 29

What is the total DO2 to the tissues?

Back 29

DO2 = CaO2 * Q

Front 30

What is the total [O2] returned to the lungs?

Back 30

total [O2] returned to the Lungs = CvO2 * Q

Front 31

What is the O2 uptake by the tissues? Formula

Back 31

VO2 = (CaO2 – CvO2)* Q

or

VO2 = DO2 - O2 returned to the lungs

Front 32

What is the rate of O2ER by the tissues?

Back 32

O2ER = VO2/DO2

Front 33

What is P50?

Back 33

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.

Front 34

Affect of T on P50 and curve

Back 34

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.

Front 35

Affect of Acidity on P50 and curve

Back 35

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.

Front 36

Affect of CO2 on P50 and curve

Back 36

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.

Front 37

What is Bohr effect?

Back 37

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.

Front 38

Affect of 2,3-bisphosphoglycerate (BPG) on P50 and curve

Back 38

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

Front 39

Affect of Fetal Hb on P50 and curve

Back 39

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.

Front 40

list factors that affect the DL.

Back 40

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.

Front 41

How do you calculate R of diffusion?

Back 41

R = delta P/Q
DL = Q/ deltaP
therefore:
R= 1/DL

Front 42

At the tissues, the
___________ becomes the most
critical componet of
Fick’s Law.

Back 42

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

Front 43

list the compensatory mechanisms evoked by anemia**

Back 43

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).

Front 44

CO2 is produced in the body as _____

Back 44

a product of cellular metabolism.

Front 45

The partial Pressure of carbon dioxide (PCO2) is greatest?

Back 45

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.

Front 46

How is Co2 carried?

Back 46

Carbon dioxide is carried in the blood in physical solution, as
carbamino compounds, and as bicarbonate.

Front 47

The
solubility coefficient (kCO2) of Co2 is

Back 47

(kCO2) is 0.06 ml/dl *1/mm Hg.

Front 48

How do you calculate CO2 concentration in physical solution and what is it?

Back 48

[CO2] = kCO2PCO2
= (0.06 ml/dl * 1/mm Hg) * 40 mm Hg
= 2.4 ml/dl

Front 49

Why CO2 diffuses readily from the tissues, through the
capillary endothelium, and through erythrocyte cell membranes?

Back 49

Because the partial pressure of CO2 is greater in the tissue than in
capillary blood

Front 50

How can Co2 form Carbamino Compounds?

Back 50

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.

Front 51

The affinity of deoxyhemoglobin for CO2 is_________ than the affinity
of oxyhemoglobin for CO2.

Back 51

greater

Front 52

What is the principle carrier of CO2?

Back 52

bicarbonate anion

Front 53

How does the CO2-
hemoglobin dissociation curve look like?

Back 53

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.

Front 54

What is the Haldane Effect?

Back 54

the Haldane effect promotes the transport of CO2 away from
tissues and promotes elimination of CO2 through the lungs.

Front 55

What promotes the transport of CO2 away from
tissues and promotes elimination of CO2 through the lungs?

Back 55

Haldane Effect

Front 56

What is the principle form by which CO2 is transported in
blood.

Back 56

Bicarbonate

Front 57

formation
of carbonic acid takes place where?

Back 57

Carbonic anhydrase is not present in the plasma so formation
of carbonic acid takes place mainly in the RBC

Front 58

Where is more bicarbonate and why?

Back 58

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.

Front 59

What is electrical nonequilibrium?

Back 59

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.

Front 60

what is chloride shift?

Back 60

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.

Front 61

What is Hb a vasoconstrictor or dilator?

Back 61

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.

Front 62

What is necessary
for normal respiration?

Back 62

Intact innervation of the respiratory muscles is necessary
for normal respiration. Neuronal brain centers in the
brainstem ensure proper innervation of these respiratory
muscles

Front 63

The primary neurons responsible for respiration are
located in the reticular formation of__________

Back 63

medulla
oblongata.

Front 64

Medullary Centers

Back 64

The primary neurons responsible for respiration are
located in the reticular formation of the medulla
oblongata.

Front 65

There are two groups of neurons in the medulla.

Back 65

1) Dorsal respiratory group (DRG)
2) Ventral respiratory group (VRG)

Front 66

There are two groups of neurons in the medulla.
1) Dorsal respiratory group (DRG):

Back 66

These neurons fire
primarily during inspiration. The DRG is contained
with the nucleus of the tractus solitarius.

Front 67

There are two groups of neurons in the medulla.
2) Ventral respiratory group (VRG)

Back 67

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.

Front 68

The DRG is contained
with what?

Back 68

the nucleus of the tractus solitarius

Front 69

The caudal VRG is contained within

Back 69

the nucleus ambiguus and the nucleus retroambiguus.

Front 70

The rostral VRG is also known as

Back 70

the Botzinger
Complex (BOT)and are contained within the retrofacial
nucleus.

Front 71

What is Botzinger
Complex (BOT)?

Back 71

The rostral VRG is also known as the Botzinger
Complex (BOT)and are contained within the retrofacial
nucleus.

Front 72

What is located in the the retrofacial
nucleus?

Back 72

The rostral VRG is also known as the Botzinger
Complex (BOT)and are contained within the retrofacial
nucleus.

Front 73

The cells of the pre-Botzinger complex do what?

Back 73

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.

Front 74

appear to act as pacemakers that can generate the
spontaneous respiratory rhythm much like the SA node
generates the spontaneous cardiac rhythm.

Back 74

The cells of the pre-Botzinger complex
in VRG

Front 75

What is in the nucleus ambiguus and the nucleus retroambiguus?

Back 75

VRG

Front 76

Pontine Centers, do what?

Back 76

Centers in the pons modulate the activity of medullary
centers.

Front 77

There are two groups of neurons in the pons.

Back 77

1) Pontine respiratory group (PRG)
2) Apneustic Center

Front 78

Pontine respiratory group (PRG) in pons

Back 78

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.

Front 79

Apneustic Center in pons

Back 79

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.

Front 80

What contained
within the nucleus parabrachialis medialis and the
Kolliker-Fuse nucleus?

Back 80

Pontine respiratory group (PRG) in pons

Front 81

Higher Brain Centers do what?

Back 81

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.

Front 82

Higher brain centers
voluntarily control activity of respiratory muscles
through the what?

Back 82

corticospinal pathway.

Front 83

If the vagi are transected below the medullary centers?

Back 83

level 4
all spontaneous breathing will cease (apnea).
Thus, vagal afferents to the medullary centers are required for
spontaneous breathing to occur.

Front 84

If the vagi are transected above the medullary and below the
apneustic center?

Back 84

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.

Front 85

If the vagi are transected above the apneustic center and below the
pneumotaxic center?

Back 85

(level 2 in the diagram above) apneusis will
occur. Thus vagal afferents to the apneustic center appear to
prevent apneusis.

Front 86

If the vagi are transected above the pneumotaxic center

Back 86

(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.

Front 87

Inspiratory neurons from the
DRG receive

Back 87

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.

Front 88

Inspiratory and Expiratory
neurons from the VRG

Back 88

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.

Front 89

Inspiratory and Expiratory
neurons from, but primarily
serve as efferents innervating
muscles of inspiration.

Back 89

the VRG

Front 90

Inspiratory neurons from

Back 90

DRG

Front 91

innervate
the internal intercostals
and abdominal muscles

Back 91

The
expiratory efferents innervate
the internal intercostals
and abdominal muscles by way
of vagus nerve during active
expiration. VRG

Front 92

innervate the
external intercostals and
the accessory muscles of
inspiration

Back 92

The inspiratory
efferents innervate the
external intercostals and
the accessory muscles of
inspiration by way of the
vagus nerve.VRG

Front 93

send collaterals
to the DRG and are known to
inhibit

Back 93

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.

Front 94

These neurons also serve as
the primary innervators
of the diaphragm by way of

Back 94

the phrenic nerve. DRG

Front 95

relaying
information about stretch
and other lung receptors.

Back 95

In
addition the DRG also receives
vagal afferents

Front 96

In addition to normal control of breathing, Pulmonary reflexes
serve two additional functions.

Back 96

1) influence the normal pattern of breathing
2) protect the respiratory system from harmful stimuli

Front 97

The pulmonary Reflex Arc

Back 97

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)

Front 98

Pulmonary Stretch Receptors

Back 98

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.

Front 99

Muscle Proprioceptors

Back 99

(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.

Front 100

Irritant and Juxtacapillary Receptors

Back 100

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.

Front 101

Irritant receptors are distributed in

Back 101

the epithelial lining
of the large and small airways and the juxtacapillary receptors are
located in the lung parenchyma close to alveolar capillaries.

Front 102

Irritant receptors respond to

Back 102

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.

Front 103

Juxtacapillary receptors respond to

Back 103

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.

Front 104

is the most important constituent in blood regulating
respiration.

Back 104

CO2

Front 105

Any increase in the partial pressure of CO2 will
_____ ventilation, where as a decrease in the partial
pressure of CO2 will ________ventilation.

Back 105

increase
decrease

Front 106

Any increase in the partial pressure of CO2 will lead to a
__________ in pH which is sensed by chemoreceptors.

Back 106

decrease

Front 107

80% of the
chemoreceptors are located

Back 107

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).

Front 108

Plasma levels of H+ and HCO3
- cannot influence chemoreceptors in
the brain because

Back 108

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.

Front 109

Peripheral Chemoreceptors represent____ % of the total
chemoreceptors,

Back 109

Peripheral Chemoreceptors represent only 20 % of the total
chemoreceptors, but are more rapidly activated than the central
chemoreceptors.

Front 110

Peripheral chemoreceptors are located in the

Back 110

carotid and aortic bodies

Front 111

Carotid and Aortic body chemoreceptors

Back 111

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.

Front 112

Peripheral chemoreceptors are sensitive to

Back 112

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.

Front 113

What happens to repiratory drive during end-stage emphysema?

Back 113

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.)

Front 114

Why does ventilation rate is altered
very little under normal circumstances?

Back 114

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.

Front 115

if the PACO2 is increased ventilatory rate _______

Back 115

increases

Front 116

If the PAO2 increases the ventilatory rate ________

Back 116

decreases

Increasing the PAO2 lowers the ventilatory rate and the slope of
the ventilation/PACO2 curve.

Front 117

How is ventilatory response to CO2 influenced by sleep, and increasing age?

Back 117

decreased

Front 118

Ventilatory Response to Oxygen

Back 118

(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.

Front 119

Ventilatory Response to pH

Back 119

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.

Front 120

Ventilatory Response to Exercise

Back 120

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.

Front 121

Although exercise increases the rate of ventilation 3 things remain stable

Back 121

1) PCO2 remains stable
2) PO2 remains stable
3) plasma pH remains stable

Front 122

Two possible types of mechanisms for hyperpnea

Back 122

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.

Front 123

Abnormal Breathing Patterns

Back 123

Obstructive vs Central Sleep Apnea

Front 124

In obstructive apnea

Back 124

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.

Front 125

In central apnea

Back 125

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.

Front 126

Cheyne-Stokes Respiration

Back 126

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.

Front 127

Biot’s Breathing

Back 127

Type of central apnea
Periods of normal breathing are interupted by periods of apnea.
CNS problems can precipitate this type of breathing.

Front 128

Eupnea

Back 128

Normal quite breathing

Front 129

Normal quite breathing

Back 129

Eupnea

Front 130

Dyspnea

Back 130

Literally means "air-hunger". Difficulty in breathing
usually accompanies strenuous exercise or certain disease
states.

Front 131

Literally means "air-hunger". Difficulty in breathing
usually accompanies strenuous exercise or certain disease
states.

Back 131

Dyspnea

Front 132

Hyperpnea

Back 132

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.

Front 133

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.

Back 133

Hyperpnea

Front 134

Hypocapnia

Back 134

decreased CO2 in blood. Opposite of Hypercapnia

Front 135

decreased CO2 in blood.

Back 135

Hypocapnia
Opposite of Hypercapnia

Front 136

Cyanosis

Back 136

Means blueness of the skin due to excessive amounts of
deoxygenated hemoglobin.

Front 137

Means blueness of the skin due to excessive amounts of
deoxygenated hemoglobin.

Back 137

Cyanosis

Front 138

Tachypnea

Back 138

rapid shallow breathing

Front 139

rapid shallow breathing

Back 139

Tachypnea

Front 140

Kussmaul Breathing

Back 140

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.

Front 141

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.

Back 141

Kussmaul Breathing

Front 142

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

Back 142

Ataxic Respirations

Front 143

Ataxic Respirations

Back 143

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

Front 144

Agonal Respiration

Back 144

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.

Front 145

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

Back 145

Agonal Respiration

Front 146

Apnea

Back 146

Absence of breathing

Front 147

Absence of breathing

Back 147

Apnea

Front 148

Draw the Feedback loop for Decreased ventilation

Back 148

Palazzolo lecture 12 slide 16

Front 149

Compare Hyperventilation and Hyperpnea during excercise

Back 149

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)

Front 150

Normal excercise vs Severe excercise

Back 150

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

Front 151

mechanism of action for hypernea is unclear but appears to involve both....

Back 151

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.

Front 152

What situations you see Cheyene Stokes apnea?

Back 152

- heart disease
-CNS disease
- high altitude

Front 153

What situations you see Biot;s breathing?

Back 153

- CNS damage

Front 154

What is the principle carrier of CO2?

Back 154

bicarbonate anion

Front 155

What is the plateau indicate in the HB O2 curve

Back 155

Hb saturation with O2

Front 156

What Co2-Hb dissociation curve has no plateau?

Back 156

plateau
would indicate hemoglobin saturation with CO2).

Front 157

The maternal
blood supply arrives via the _______to the ______

Back 157

uterine arteries
intervillous sinusoids.

Front 158

Oxygen is picked up by the ______ arteries and
returned to the fetus via the ____ vein.

Back 158

umbilical and umbilical

Front 159

Blood-Blood Barrier
between the mother and the fetus is about ___thick.

Back 159

3.5 microns

Front 160

Partial pressure of O2 of blood in the umbilical vein is about ___ mmHg.

Back 160

30

Front 161

Fetus lives in a very ____ environment.

Back 161

hypoxic

Front 162

At birth, the fetus is cut off from the placental gas exchange
resulting in _____ and ____

Back 162

hypoxemia
hypercapnia.

Front 163

At birth ________increases (not clear why) and this leads to the first
gasps of air.

Back 163

chemoreceptor
sensitivity

Front 164

Since the alveoli are
not totally collapsed (pre-inflated with fluid), _____pressure is
needed for inflation.

Back 164

less

Front 165

Intrapleural pressure _______at birth

Back 165

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.

Front 166

The remaining
fluid in the lungs at birth is taken up by ________

Back 166

the lymphatic system and
production of surfactants help to reduce the surface tension.

Front 167

When is Respiratory Distress syndrome occur in newborns?

Back 167

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.

Front 168

Pulmonary vascular resistance ____at birth

Back 168

Pulmonary vascular resistance decreases at birth, as the airways
open up and fluid is emptied out of the lungs.

Front 169

The partial pressure
of O2 in the lungs is ____ at birth.

Back 169

increased.

Front 170

What leads to the closure of the foramen ovale?

Back 170

There is an increase in the left
atrial pressure which leads to the closure of the foramen ovale.

Front 171

The ductus arteriosus is closed primarily due to

Back 171

increase in
partial pressure of O2, an increase in circulating levels of
bradykinin, and a decrease in circulating levels of prostaglandins

Front 172

What is hypoxia?

Back 172

Hypoxia is a decrease in oxygen tension, whereby cells do not get
the amount of oxygen that is required.

Front 173

decrease in oxygen tension, whereby cells do not get
the amount of oxygen that is required.

Back 173

hypoxia

Front 174

Symptoms include impaired judgement, disorientation, headache,
anorexia, nausea, vomiting, and tachycardia.

Back 174

hypoxia

Front 175

Causes of Hypoxia

Back 175

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.

Front 176

Hypoxic Hypoxia

Back 176

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)

Front 177

Inadequate ventilation of the lungs lead to hypoxia, due to what?

Back 177

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)

Front 178

Pulmonary disease resulting in hypoxemia due to uneven
V/Q ratio or diffusion barrier lead to hypoxia, due to what?

Back 178

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.

Front 179

Inadequate transport of Oxygen lead to hypoxia due to what?

Back 179

Anemia or abnormal Hb (Also Known As Anemic Hypoxia),
general or localized circulatory deficiencies (Also
Known As Circulatory Hypoxia), tissue edema.

Front 180

Anemic Hypoxia

Back 180

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.

Front 181

Circulatory Hypoxia

Back 181

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.

Front 182

Inadequate ability of the tissue to use oxygen lead to hypoxia due to what?

Back 182

Poisoning of cellular enzymes or diminished cellular
metabolic capacity due to a lack of vitamin, enzyme,
cofactor etc. (Also Known As Histotoxic Hypoxia)

Front 183

Histotoxic Hypoxia)

Back 183

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.

Front 184

Barometric pressure is low so the partial pressure of inspired O2 is
low. Compensate by ......

Back 184

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.

Front 185

Symptoms include headaches, fatigue, dizziness,
nausea, loss of appetite, hypoxemia and alkalosis. In severe cases,
pulmonary edema can also result.

Back 185

Mountain sickness

Front 186

Mountain sickness

Back 186

Symptoms include headaches, fatigue, dizziness,
nausea, loss of appetite, hypoxemia and alkalosis. In severe cases,
pulmonary edema can also result.

Front 187

Oxygen Toxicity

Back 187

Partial pressure of inspired O2 is extremely high

Front 188

Oxygen toxicity is directly related to the ___ and ____

Back 188

length of time and
the amount of pressure

Front 189

100% O2 at 760mmHg for 24 hrs results in

Back 189

substernal pain due to PE

Front 190

100% O2 at 760mmHg for 30 hrs results in

Back 190

permanent lung damage
absorbable atelectasis

Front 191

100% O2 at 2280 mmHg for 1 hr results in

Back 191

coma and death

Front 192

One effect of O2 toxicity is

Back 192

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.

Front 193

In high
barometric pressures are also known to inactivate _____

Back 193

high
barometric pressures are also known to inactivate supraoxide
dismutases, catalases, peroxidases, sulfhydryl dehydrogenases
and other enzymes, which normally would eliminate free
radicals.

Front 194

O2 toxicity increases the tendency towards ____

Back 194

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.

Front 195

Absorption atelectasis

Back 195

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.

Front 196

In deep sea diving Pressure increases ___mmHg for ___ft under water

Back 196

760 mm Hg (or 1 atm) for each 33 ft
under water.

Front 197

What happens with N in diving as the pressure increases the further you go under?
water,

Back 197

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.

Front 198

nitrogen narcosis

Back 198

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.

Front 199

euphoria, loss of coordination, and will lead
to coma and finally death.

Back 199

nitrogen narcosis

Front 200

What happens when u come up from diving too fast?

Back 200

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.

Front 201

decompression sickness

Back 201

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.

Front 202

joint pain, deafness, impaired
vision, and even paralysis.

Back 202

decompression sickness

Front 203

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.

Back 203

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.

Front 204

Where is higher P in the fatal lung?

Back 204

RA>LA

IVC 30 highest, lowest from tissues

Front 205

Causes of Hypoxemia

Back 205

high altitude
hypoventilation
diffusion defect
V/Q defect
R to L shunt

Front 206

Common Causes of Respiratory Acidosis

Back 206

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

Front 207

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?

Back 207

Common Causes of Respiratory Acidosis

Front 208

Common Causes of Respiratory Alkalosis

Back 208

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

Front 209

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?

Back 209

Common Causes of Respiratory Alkalosis

Front 210

Common Causes of Metabolic Acidosis

Back 210

1. Ingested drugs or toxic substances
2. Loss of bicarbonate anions
3. Lactic acidosis
4. Ketoacidosis - Diabetes
5. Inability to excrete protons (H+)

Front 211

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?

Back 211

Common Causes of Metabolic Acidosis

Front 212

Common Causes of Metabolic Alkalosis

Back 212

1. Loss of H+ (vomiting, excess aldosterone, diuretics)
2. Ingestion of bicarbonate anion (or antacids)
3. Excess administration of Bicarbonate anion

Front 213

1. Loss of H+ (vomiting, excess aldosterone, diuretics)
2. Ingestion of bicarbonate anion (or antacids)
3. Excess administration of Bicarbonate anion
Cause what?

Back 213

Common Causes of Metabolic Alkalosis