PHYSIOLOGY A

Respiratory Physiology 3 & 4 Dr. Cruz

EXCHANGE AND TRANSPORT OF CARBON DIOXIDE AND OXYGEN

PHYSICS OF GAS DIFFUSION

Boyles law
P1V1=P2V2
K=PV

At constant temperature, increasing the pressure will decrease

the volume

Charles law
V1/V2 = T1/T2
K = V/T

ANATOMIC AND PHYSIOLOGIC CONSIDERATIONS

Capillary surface area
Large surface area
2
o Respiratory membrane-pulmonary capillary: 70 m
2
o Systemic capillary-tissue : 40 m
The transport of gases from one chamber to another follows a
partial pressure gradient
Diffusion properties of gases
Respiratory membrane
Layers of the respiratory membrane (from air to blood)
o Fluid, surfactant
o Alveolar epithelium
o Epithelial basement membrane
o Interstitial space
o Capillary basement membrane
o Capillary endothelial cell
0.2-0.6 micrometer thick
2
Surface area: 70 m
At any given point in time, from the pulmonary artery to the
pulmonary vein, the blood volume is about 500mL. Of this 500
mL, 60-140 ml blood is given to the pulmonary capillaries
o Clinical significance: the 60-140 mL of blood is evenly
2
distributed in the 70m area of the membrane. Each RBC
will now be receiving oxygen and giving of carbon dioxide
Diameter of pulmonary capillary: 5um
Average size of RBC: 7.8 um
o Since the RBC needs to pass through a small diameter
capillary, it needs to distort its shape and form a rouleaux
formation
Every single red cell should be in contact with the respiratory
membrane to ensure proper distribution of oxygen and carbon
dioxide

At constant pressure, increasing the temperature will increase the

volume

Ideal gas law

PV = nRT
P pressure, mmHg
V volume, L
n mass of gas
R constant, 62.36
T temperature, absolute degrees

Combination of Boyles and Charles law

Daltons law
PT = P1 + P2 + P3 +
The total pressure of air is equal to the summation of the
individual pressure of gases that comprises the air
Example: The total pressure of air at sea level is 760 mmHg. That
pressure is summation of the pressures of nitrogen, oxygen, and
other different gases present in the air
Henrys law
Weight of gas absorbed by liquid is directly proportional to
pressure of gas to which the liquid is exposed
Example: if you have a gas and a liquid, how much liquid will be
absorbed by the gas? It depends on the amount of pressure being
exerted by the gas on the fluid. The higher the pressure, the more
amount of gas will be dissolved in the fluid
Grahams law
Rate of diffusion is directly proportional to solubility coefficient,
and inversely proportional to the square root of molecular weight
The higher the solubility coefficient, the higher the rate of
diffusion
The greater the molecular weight, the lower the rate of diffusion
Carbon dioxide has the higher solubility coefficient, which means
that carbon dioxide will have a higher rate of diffusion
Solubility Coefficient
CO2
0.57
O2
0.024
N
0.012
He
0.008

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Combining Henrys and Grahams Law

V=PxS
V amount of gas
P pressure
S solubility coefficient

Amount of gas that will be dissolved in H2O is directly proportional

to the pressure and solubility coefficient of the gas

Ficks Law

V = [AD (P1-P2)]/T
A- area
D- diffusion constant
P1-P2- pressure gradient
o T- thickness
In pneumonia, there is inflammation of the lung thus the
respiratory membrane thickens. Rate of diffusion will decrease
In emphysema, there is destruction of the alveolar wall. Surface
area goes down, rate of diffusion decreases

Diffusing capacity
DL = V / (P1-P2)
V = [AD (P1-P2)]/T
DL = AD/T
V = DL (P1-P2)
DL = V / (P1-P2)

The amount of oxygen in the atmosphere is 20.8%, we get the

20.8% of 760mmHg in order to get the amount of oxygen in the
atmosphere
When we inhale air in the atmosphere, the pressure of oxygen
partially drops (humidified air)
o Why humidified? Because when we inhale water vapor is
added to the mixture
In the alveoli, the pressure becomes much lower which will
facilitate the diffusion of oxygen from the atmosphere to the
alveoli
The pressure gradient between alveoli and venous blood
facilitates the diffusion of oxygen towards the venous blood,
giving now your arterial blood
Since the tissues have a high consumption for oxygen, it has a low
pressure creating now a pressure gradient between the tissue and
arterial blood driving the oxygen towards the cell
In carbon dioxide, the pressure gradient between arterial blood
and the cell will facilitate transport of carbon dioxide towards the
blood, giving rise to your venous blood. The carbon dioxide from
the venous blood will be transported in your alveoli and then back
into the atmosphere

The transport of oxygen and carbon dioxide is passive and based on

simple diffusion
O2 diffusion

Unit for diffusing capacity: ml/min/mmHg

Diffusing capacity is the amount of gas that diffuses thru the
respiratory membrane per minute, per mmHg of pressure
gradient
DLCO: 20-30
DLO2: 21
DLCO2: 20x > O2

O2 diffusing capacity
Diffusing capacity for oxygen: 21ml/min/mmHg
Average pressure gradient between the alveoli and pulmonary
capillary: 11 mmHg
Rate of diffusion: 230ml/min
CO2 diffusing capacity
Not measured accurately because carbon dioxide easily
equilibrates (zero net flux)
Diffusing capacity: 400-500ml/min/mmHg
o There is a high diffusing capacity because carbon dioxide has
a high solubility coefficient so it easily pass thru the
respiratory membrane
o Diffusing capacity is 20x more than O2
Partial pressure of gases at different compartments:
The values obtained is based on Daltons law

ABG: PaO2: 80-100 mmHg

The numbers in green is your arterial blood
When the PaO2 of the patient is 80-100mmHg, it is presumed that
the oxygen saturation is 100%
At the level of pulmonary capillaries, partial pressure of oxygen is
100mmHg. When it reaches the left side of the heart, it drops to
95mmHg
o What happens to the 5mmHg?

Arterial blood coming from the lungs goes to the left

ventricle, this blood will be ejected to the aorta.

In the aorta, you have a bronchial artery that will go to

the conducting zone of the lungs.

The conducting zone needs supply of oxygen and

nutrients because no gas exchange occurs there. From
there, blood will drain to the bronchial vein

Bronchial vein contains unoxygenated blood and will

drain into your pulmonary vein

Pulmonary vein contains oxygenated blood

There will be mixing of blood in the pulmonary vein

This mixing of blood is the cause for the 5mmHg drop

in the partial pressure of oxygen

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CO2 diffusion

GAS DIFFUSION
Equilibration
Occurs in < 0.75 sec
o In that span of time, there is zero net flow of gases
Two types of equilibration
o Perfusion limited

Dependent in blood flow

Observed in insoluble gas, oxygen and carbon dioxide

Respiratory membrane can easily allow the oxygen

and carbon dioxide to pass through such that the
factor that will determine the equilibration is the
blood flow

O2, CO2: 0.25 sec equilibration

o Diffusion limited

Dependent on the ability of a respiratory membrane

to allow a particular gas to pass through

Diffusion of highly soluble gas and carbon monoxide

Carbon monoxide do not diffuse through the

membrane easily

When gases has a high affinity to Hgb, it is said to be

diffusion limited

Prevents equilibration
Oxygen and carbon dioxide is perfusion limited under normal
circumstances. However, during exercise, there is increased blood
flow to the lungs. Oxygen and carbon dioxide slowly shifts to
perfusion limited to diffusion limited

HgbA
Adult hemoglobin
22
HgbF
Fetal hemoglobin
22
o 2,3 DPG (diphosphoglycerate which is a byproduct of
glycolysis)
o O2 affinity
o Clinical significance: in a pregnant mother, when she
inhales, oxygen from the alveoli goes to the adult
hemoglobin. When the red cell passes thru the placental
circulation, since HgbF has higher affinity to oxygen, there
will be transfer of oxygen from HgbA to HgbF
O2 affinity
Hgb abnormalities
o Sickle cell disease
Carbon monoxide, nitric oxide and cyanide poisoning
o Converts iron from ferrous to ferric
o The affinity to oxygen decreases
Hemoglobin
14-15g/100ml blood
NV in females: 12-14 g/dL
NV in males: 14-16 g/dL
1g : 1.34ml O2
Oxyhemoglobin Hgb combined with oxygen
O2 in blood
19.4ml O2/100ml arterial blood
14.4ml O2/100ml venous blood
5ml O2 is given off to the tissues each cycle
o Utilization coefficient
O2 dissociation curve

OXYGEN TRANSPORT
Oxygen is transported in two ways, either dissolved in plasma or
with hemoglobin
Dissolved O2
PaO2: 80-100 mmHg
If the PaO2 is between 80-100mmHg, it is presumed that the Hgb
is 100% saturated
Determined by ABG
Oxy-Hgb
Have a high affinity for oxygen
Hgb is able to carry 4 O2 molecules
1RBC carries 280 million Hgb
1 g Hgb is able to transport 1.34 ml O2
Measured by O2 saturation
Myoglobin
Another form by which Hgb is stored in the body
Not a transported oxygen but merely a stored oxygen that is
present in muscle tissue

Partial pressure of oxygen is plotted against %Hgb saturation

The graph will tell you how many Hgb will be saturated in a given
pressure
Example: the pressure of oxygen is 27mmHg, 50% Hgb is
saturated. This means that 1 Hgb molecule carries 2 oxygen
molecules. Why? Because 1 Hgb molecule can carry 4 oxygen
molecules and 50% of that 2
If the partial pressure of oxygen is 100mmHg, the %saturation is
almost 100%. If the partial pressure of oxygen is 80mmHg, the
%saturation is around 95%

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This proves that if the partial pressure of oxygen in around

80-100mmHg, the Hgb is 100% saturation
If the partial pressure of oxygen is 60mmHg, the %Hgb saturation
is still around 90%. But below that, the %saturation drastically
drops

Oxy-Hgb
When one oxygen binds to hemoglobin it will exhibit cooperativity
effect
o When one oxygen molecule binds to hemoglobin, it will
facilitate further binding of other oxygen molecules to
hemoglobin
More sensitive to ventilation compared to PaCO2
PAO2: 100-104 mmHg (pressure of oxygen in the alveoli)
1 g Hgb: 1.34 ml O2
Bohr effect
O2 affinity
Shift to the right in the curve
o There is a decrease in %saturation, which means there is a
decrease in oxygen affinity
o Oxygen is given off
o Observed in increase temp, carbon dioxide, 2,3 DPG and
decreased pH
Occurs in the tissues
Haldane effect
O2 affinity
Shift to the left in the curve
o There is an increase in %saturation
o Hgb will take in oxygen
o Observed in decreased temp, carbon dioxide, 2,3-DPG and
increase in pH
Occurs in the lungs

2,3 DPG
By product of glycolysis
Allosteric binding
When it binds to Hgb, it prevents oxygen binding
Observed at the tissue level
o When the tissue continuously use glycolysis to produce
energy, more 2,3 DPG is produced and will bind to
hemoglobin
CO (carbon monoxide)
Competitive binding
At lower concentration, Hgb has a higher affinity to oxygen
o When oxygen binds to Hgb in low carbon monoxide
concentrations, since the affinity of oxygen to Hgb is so high

Hgb will not give the oxygen it contains when it passes

through the systemic circulation
o Prevents O2 release
At higher concentrations, prevents further O2 binding
Normally, Hgb-CO (carboxyhemoglobin) is <2%
Hazard levels are around Hgb-CO 5-7%
Hgb-CO 10% is exhibited in chronic smokers

Dyspnea
Difficulty of breathing
Anoxemia
O2 in body fluids
Measured in PaO2
Hypoxia
O2 supply to tissues
Cyanosis
Bluish discoloration of skin due to deoxyhemoglobin
In the clinics, it is observed in the oral cavity and the tongue
Hypoxia
Hypoxic
o PaO2: <60 mmHg
Circulatory
o blood flow
Anemic
o O2 binding to Hgb
Histotoxic
o O2 utilization
o Cyanide poisoning
EPO
Production is induced by hypoxia
Renal cortical interstitial cells

EXCHANGE OF GASES
Utilization coefficient
% of blood that gives off O2 to the tissues
5ml given off from 19.4 ml O2
o 25% of blood
Increase utilization coefficient
o Strenuous exercises
Decrease utilization coefficient
o Cryogenics (tissue transplant)

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Respiratory quotient
Ratio between the amount of CO2 being given off to the amount
of O2 taken in
o CO2:O2
80 CO2 molecules expired:100 O2 molecules into the pulmonary
capillaries
0.8 respiratory exchange ratio
Changes in respiratory quotient
o Interstitial pulmonary fibrosis

There is scarring of respiratory membrane

Which one will be deranged first? The diffusion of

oxygen. Because carbon dioxide has a higher solubility
coefficient so it can easily pass through the membrane

Respiratory coefficient goes up

CO2 TRANSPORT
Transported in five forms
Dissolved CO2
Dissolved in plasma
PaCO2: 35-45 mmHg
0.2ml/100ml

Explaining the picture

Carbon dioxide being produced by the cell can easily diffuse
through the membrane (dissolved in plasma form)
When it diffuses into the plasma it combines with water forming
your carbonic acid
Carbon dioxide goes into the plasma and combines with the
plasma proteins
Carbon dioxide goes in to the red cell, combines with water and
forms carbonic acid. The hydrogen atoms dissociate forming
bicarbonate which goes out into the plasma
o Bicarbonate is negatively charge, when it goes out it will
render the cell positive. To counteract this, chloride goes in
(chloride shift)
Carbon dioxide goes into the red blood cell and combines with
hemoglobin that will force oxygen to be released into the tissue
When blood goes into the pulmonary capillaries, all reactions go
reverse.
CO2 dissociation curve

H2CO3 (carbonic acid)

Most volatile acid
The only acid being handled by the lungs
0.1-0.3ml/100ml
HCO3 (bicarbonate)
Most important
Majority of carbon dioxide is transported through this
3ml/100ml
22-26 mmol/L (amount of bicarbonate in ABG)
Carbamino-Hgb
CO2 bound in hemoglobin (CO- carboxy-Hgb)
1.5ml/100ml
CHON-bound
Carried by plasma proteins

As you increase the pressure of CO2 , the content also increases

(directly related)
If O2 is absent, the content of CO2 is higher compared to when
oxygen is present

Deoxy-Hgb
Has a higher affinity to CO2 and H ions
Blood pH and CO2 Transport

CO2 transport will alter the blood pH such that at the tissue level,
CO2 is transported from the cells to the blood
CO2 is transported in the blood reduces pH, primarily due to
H2CO3
pH increases as CO2 is released to the lungs, (H2CO3 decreases)
ABG pH: 7.35-7.45

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CONTROL OF RESPIRATION
VENTILATORY CONTROL
Respiratory rate
12-18 cpm 12yrs adult
14-22 cpm 6-12yrs
20-25 cpm 3-6yrs
20-30 cpm 1-3yrs
Lower rates during sleep

25-40 cpm 6-12mos

30-45 cpm 3-6 mos
35-55 cpm 0-3 mos
40-70 cpm premature

pH
7.4 97.35-7.45
A decrease in pH will increase ventilation up to 4x
: 400% ventilation
PaO2
Should be maintained around 80-100 mmHg
a decrease in oxygen : 75% ventilation
Ventilatory response to CO2

Goal of breathing
Minimize work
Maintain blood gases
Maintain acid-base balance
Automatic respiration begins at birth. In utero, the placenta, not the
lung, is the organ of gas exchange in the fetus. Its microvilli
interdigitate with the maternal uterine circulation, and O2 transport
and CO2 removal from the fetus occur by passive diffusion across the
maternal circulation
There are four major sites of ventilation control:
Respiratory center
o Located in the medulla oblongata
o Ventilatory pattern generator
o Integrator receive all other impulses coming from the
different parts of the body, interpret it and make
appropriate adjustments for the respirator center for the
ventilator pattern
Central chemoreceptors
o Located at the ventrolateral surface of the medulla
oblongata
o Detects the pH of the cerebrospinal fluid
o Indirectly detect the PCO2 content of the CSF
Peripheral chemoreceptors
o Aortic and carotid bodies

Aortic will send impulses via the vagus nerve

Carotid will send impulses via the glossopharyngeal

nerve
o Detect levels of PaCO2, PaO2 and pH in arterial blood
Pulmonary mechanoreceptors, sensory neurons
o Lungs, airways
Motor output
Efferent pathway
Common pathway will be branching out from C3-5 which will give
rise to the phrenic nerve and will innervate the diaphragm
T1-12 which will give rise to intercostal nerves: intercostal
muscles, accessory muscles for respiration
Ventrolateral tract: involuntary
Corticospinal tract: voluntary
MAIN STIMULANTS OF BREATHING
PaCO2
Most potent regulator
Most important stimulus
The purpose of ventilation is to maintain a PaCO2 of 40 mmHg
Increase in carbon dioxide content will increase ventilation up to
9x (900x)

Metabolic acidosis will increase ventilation

Sleep and certain drugs will depress the respiratory center which
will decrease ventilation thrive
o Patients with COPD have a lesser respiratory thrive which
acts as a protective mechanism to prevent premature
closure of the airways

Plots carbon dioxide content against ventilation

o An increase in carbon dioxide content will have a
corresponding increase in alveolar ventilation
o As ventilation decreases, carbon dioxide increases
Plots oxygen content
o The lower oxygen levels you have at a particular pressure
for carbon dioxide, the greater the ventilation
o Lower carbon dioxide content together will low oxygen
levels will further increase your ventilation

Respiratory Control Center

Maintains periodic breathing/ventilation
The respiratory center is not a single center but rather a collection
of different centers
Dorsal respiratory group
o Nucleus tractus solitaries dictates inspiration
Ventral respiratory group
o Rostral nucleus retrofacialis
o Caudal nucleus retroambiguus
o Nucleus paraambiguus

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Inspiratory ramp (group A in the diagram)

Functions like the SA node in which it can fire its own action
potential
Gradually increases its frequency and then stops
Sends the excitatory stimuli to the respiratory muscles, the
diaphragm contracts then you will inhale
Always active unless inhibited by something else
Accomplished by:
o Nucleus tractus solitaries
o Rostral nucleus retroambiguus
o Nucleus paraambiguus
Exhalation (group B&C)
Group B is activated by group A
Group B sends impulses to activate group C
Once group C is activated, it will send impulses to inhibit group A
o This is the reason why the inspiratory ramp stops
o When this occurs, we exhale
Accomplished by:
o Nucleus retrofacialis
o Caudal nucleus retroambiguus
o Nucleus paraambiguus both inspiratory and expiratory
roles
Hering-Breuer reflex

Pneumotaxic center
Not normally active
Upper pons
Inhibits respiration
Directly activates group C thus inhibiting group A
Best observed when there is double vagotomy
When no impulses reaches group B, the pneumotaxic center is
activated there is a longer inspiratory and expiratory phase
Regulates inspiratory volume and rate
Fine tuning of the respiratory rhythm

Apneustic center
Lower pons
Controls intensity of the respiration
Prevents the switch off of the inspiratory signals to the DRG
Deep inspiration, short (sudden and abrupt) expiratory phase
Prolonged inspiratory gasps interrupted by transient expiratory
efforts if transected
CENTRAL CHEMORECEPTORS
Ventrolateral surface of medulla
Detect CSF pH

Tells us how rhythmicity of breathing works

More evident among neonates
Group A sends stimulus, so the muscles contract and once they
expand the pulmonary stretch receptors are stimulated and will
send excitatory stimuli to group B
When group B is on, then C is on. If C is on then group A is turned
off or inhibited

Since A is off, no impulses will go to the respiratory muscles

muscles relax
Present also are your deflation receptors, this will be sending
inhibitory stimuli back to group B
Group B switched off group C is off group A is on

BBB (blood brain barrier)

o Inhibit a lot of transport of substances
o Permeable to CO2
o It will not permit diffusion of carbonic acid or any other acid,
and bicarbonate
o Carbon dioxide can easily cross the BBB
o The brain tissue metabolism also produces carbon dioxide

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CO2 in the CNS will combine with water and with the action
of carbonic anhydrase carbonic acid
o Carbonic acid is the acid that the chemoreceptors will detect
The reason why we said earlier that it can also indirectly detect
carbon dioxide is because when there is a high amount of carbon
dioxide more carbonic acid will be produced

Central chemoreceptors is said to exert a greater influence in

controlling ventilatory pattern. It has a direct connection in going
towards the respiratory center

PERIPHERAL CHEMORECEPTORS
Influences only 40% of the ventilator thrive
Carotid and aortic bodies
PaCO2, PaO2 and pH of arterial blood
40% of the ventilatory response to CO2
The peripheral chemoreceptors are the only chemoreceptors that
respond to changes in PO2
They consist of type I (glomus) cells that are rich in mitochondria
and endoplasmic reticulum.
Asphyxia
o PaCO2, PaO2
PULMONARY MECHANORECEPTORS

Receptors
Rapidly adapting pulmonary stretch receptors
o Irritant receptors
o Detects foreign material
o Can sometimes decrease ventilation and increase heart rate
o Located in the pulmonary parenchyma
Slowly adapting pulmonary stretch receptors
o Lung inflation in COPD
o The onset of the inspiratory ramp is delayed
o The expiratory phase becomes slower and prolonged
o Protective mechanism in order to prevent premature close
of the airways
o How do they work?

When we exhale the intrathoracic pressure increases

it will compress the airways

In patients with OPD, the airways are narrower than

usual. The problem occurs when they exhale. Since
the intrathoracic pressure increases during exhalation
it will further narrow the airways

What is the effect of prolonging the expiratory phase?

The increase in intrathoracic pressure becomes
gradual. The pressure that will compress the airways
will be less keeping the airway patent
o Located in the pulmonary parenchyma
Juxtaalveolar receptors (J receptor)
o Present in the respiratory membrane and pulmonary
capillaries
o Detect engorgement of blood vessels
o Located in the pulmonary parenchyma
o In pulmonary congestion

The J receptors are activated

There is a sensation of dyspnea

Ventilation increases with a concomitant increase in

heart rate
Somatic receptors
o Detect lung inflation
o Control or upraise the respiratory center lung expansion
which will initiate expiration
o Located in the thoracic wall

SPECIAL SITUATIONS

Reflexes
Hering-Breuer reflex
Diving reflex
o Protective mechanism for the airways
o Stimulated when cold water touches the face and nasal
passages
o Airways will close and stops ventilation
Aspiration reflex
o Occurs when a foreign material is found in the
nasopharyngeal wall
o There is a transient inspiration and a sudden closure of the
airways
o Purpose is to dislodge the foreign object in order for us to
expectorate or swallow it

Exercise and Respiration

During exercise, the most important stimulus for breathing would
be neural impulses from the motor cortex and impulses from the
muscles and joints
minute ventilation is achieved by the neural impulses going to
the respiratory center
Increase in minute ventilation
o Cortical radiation
o Joint, muscle proprioceptors
Exercise is remarkable because of the lack of significant changes
in blood gases.

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Treatment: hyperbaric therapy

o Gradual increase oxygen pressure forcing nitrogen back
into the solution
o Gradual decrease give time for all the nitrogen and other
gases to come out via the lungs

Abnormal Control of Breathing

Commonly exhibited in individuals with CNS lesions and metabolic
disorders

diffusing capacity of gases

o Particularly the diffusing capacity for oxygen

ventilation, perfusion, O2 utilization

o There is increased ventilation type II pneumocytes will
start producing more surfactants further dilating the alveoli
thus increasing the surface tension
o There is increased perfusion, more blood enters the wide
surface area more oxygen can transfer from the alveoli to
the blood
o At the tissue level, oxygen utilization is high because the
actively contracting muscle continuously consumes oxygen
oxygen tension drops pressure gradient between
arterial blood and tissue increases increased rate of
diffusion more oxygen can go to the tissues from the
blood
Anaerobic threshold
o Level of exercise at which sustained metabolic acidosis
begins
o When crossed, anaerobic metabolism is increased
o Flow of carbon dioxide goes up, lactate increases, pH
decreases triggers ventilation to go up
o Increase in ventilation arterial CO2 drops arterial O2
increase s

Kussmauls breathing
Evident for metabolic acidosis (ex. Diabetic ketoacidosis)
Fast and deep breathing
The drop in pH will stimulate the chemoreceptors (peripheral)
that will stimulate the inspiratory center to increase ventilation
More carbon dioxide goes out, more carbonic acid goes out thus
increasing the pH back to normal
Apnea
Cessation of breathing for about <10 sec
Sleep apnea
o OSA (obstructive sleep apnea)

The problem is anatomic

Prominent among obese patients

Occurs when the tongue falls back into the pharyngeal

wall thus obstructs the airways

Snoring

Prevented by sleeping on the side

o Central sleep apnea

More serious disorder

Central alveolar hypoventilation

The respiratory center is damaged

The breathing becomes voluntary, so when the

patient is sleeping, breathing stops

Management: sleeping with ventilator or using a

diaphragmatic pacemaker

SIDS (sudden infant death syndrome)

Neonates are abdominal breathers

When neonates sleep on their tummy, the

abdomen cannot expand therefore there is
decreased ventilation

Decompression Sickness
Happens when we rapidly ascend in the water
Rapid in total pressure of ambient gases
This force the dissolved gases in the plasma to go out of the
solution air bubbles
Formation of gas bubbles in tissues and blood
o N2 bubbles air embolus impede blood flow tissue
damage

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Apneustic breathing
Increased depth and rate of breathing
Stimulation of chemoreceptors
Prolonged inspiratory and sudden expiratory

Cheyne-Stokes ventilation
Gradual increase in ventilation and gradual decrease in ventilation
Blood gases fluctuate in this breathing pattern

Control of H concentration
Chemical buffer systems
o Most immediate to react
o Least potent
Respiratory system
o Next to react after buffers
nd
o 2 most potent
o Regulate only carbonic acid
Renal system
o Most important and most potent because it can handle a
wide variety of acid and bases
o Slowest to react (3-5 days for complete correction to occur)
Lungs
Regulates volatile acids
o H2CO3: volatile acid
Controls extracellular CO2
o Alveolar ventilation modulates PCO2
50-75% effectiveness in correcting in acid base disorders
1-2x buffering power than the chemical buffer systems
FOUR BASIC DISORDERS

ACID BASE BALANCE

Acid-Base Balance
Control of H concentration
o Extracellular concentration: 0.00004 mEq/L
o pH = -log [H]
o pH = - log [0.00000004 Eq/L]
o pH = 7.4 (7.35-7.45)
Acid: releases H ions
Base: accepts H ions
o H2CO3 H + HCO3

Henderson Hasselbach Equation

o pH = 6.1 +log [HCO3]/(0.03 x PCO2)

Respiratory acidosis
Evident in ventilation
CO2, H2CO3
pH
ABG profile for acute: pH, PaCO2
ABG profile for chronic: N pH, PaCO2
o Normal pH is due to the correction of the kidneys
Examples for acute
o Depression of the respiratory center
o Neuromuscular disease
o Airway obstruction
Examples for chronic
o COPD
o Pickwickian syndrome
o Restrictive ventilatory defects
Respiratory alkalosis
ventilation
Loss of CO2, H2CO3
pH
Examples
o Excessive mechanical ventilation
o Anxiety, hysteria, excitation
o Stroke, CVA, meningitis
o Drugs amphetamines
o High altitudes

Oxygen tension decreases less oxygen in the blood

PaO2 drops detected by the chemoreceptors
stimulates the center ventilation increases
o Fever

Ventilation increase because of the mechanism the

body has in order to dissipate heat
o Pregnancy

In a pregnant mother, when she inhales, oxygen from

the alveoli goes to the adult hemoglobin. When the
red cell passes thru the placental circulation, since Hgb
F has higher affinity to oxygen, there will be transfer
of oxygen from HgbA to HgbF

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Adult Hgb will have lower O2 tension stimulate

respiratory center increased ventilation

Metabolic acidosis
pH, HCO3
Stimulation of chemoreceptors, ventilation
Removal of CO2, H2CO3
lactic acid production
Examples:
o Ketoacidosis
o Renal pathology
o Chronic diarrhea

Bicarbonate is excreted acid is retained in the body

Metabolic alkalosis
pH, HCO3
ventilation
Retention of CO2, H2CO3
Example
o Vomiting HCl goes out
o Renal pathology
INTERPRETING ABG

Normal Values:

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