KIN 3515- FINAL

ventilation

mechanical drawing in and expelling of air via breathing

external respiration

sequence of events in exchange of O2 and CO2 between the external environment and cells

cellular respiration

the intracellular metabolic processes carried out within the mitochondria with uses O2 and produces CO2 to generate energy from nutrients

TV

tidal volume, volume of inspired or expired air per breath; volume 0.4-1 L

IRV

inspiratory reserve volume; maximum volume can inspire over and above resting tidal volume; volume 2.5-3 L

ERV

expiratory reserve volume; maximum volume can expire over and above resting tidal volume; volume 1-1.5 L

RLV

residual lung volume; volume remaining in lungs after maximum expiration; volume 0.8-1.2 L

IC

inspiratory capacity; maximum volume of air that can be inspired; volume 3-4 L

FRC

functional residual capacity; volume remaining in lungs after resting tidal expiration; volume 2-2.2 Lq

respiration

sum of all physiologic processes that accomplish ongoing passive movement of O2 from the atmosphere to the tissue in support of cell metabolism and continual passive movement of CO2 from the tissues to the atmosphere

FVC

forced vital capacity; maximum volume fo air that can be expired after maximum inspiration; volume 4-5 L

TLC

total lung capacity; maximum volume of air lungs can hold; volume 4-7 L
minute ventilation (Ve)- volume of air moving past the mouth and nose per minute; Ve=TVbreathing rate=mL/breathbreath/min

alveolar ventilation (Va)

volume of air reaching the alveoli each minute; Va=breathing rate*(TV-anatomic dead space)=breaths/min(mL/breath-mL/breath)

anatomic dead space

the volume of air remaining in the conduction zone of the pulmonary system, a fairy set volume of are (30% of the tidal volume); increasing the rate of depth of breathing increases Ve; increasing depth of the breathing increases Va; tidal volume (depth of breathing) rarely exceeds 60% of FVC (comes from reducing IRV or ERV)

physiological dead space

portion of alveolar volume with a V:P ration of near 0; no gas exchange can occur in these spaces; due to under perfusion of blood inadequate ventilation relative to alveolar surface, can change in volume

hyperventilation

increase in pulmonary ventilation that exceeds O needs of metabolism, causes hypocapnia (low blood CO2) and acidosis

hypocapnia

low blood CO2

hypoventilation

reduced pulmonary ventilation, causes hypercapnia

hypercapnia

high blood CO2

apnea

transient cessation of breathing

hyperpnea

increased pulmonary ventilation due to exercise-rate matches need

dyspnea

shortness of breath, often associated with hypercapnia and acidosis

hypoxia

insufficient O2 at cellular level

-O2 deliver
-CO2 removal
-acid-base balance-blood pH
-facilitates speech and sound
-defends against microbes
-particle filtration
-traps and dissolves blood clots
-adds or removes chemicals

what are the functions of the pulmonary system?

-Ventilation: the mechanical drawing in and expelling of air via breathing
-respiration: the sum of all physiological processes that accomplish ongoing passive movement of O2 from the atmosphere to the tissue in support of cell metabolism and continual passive movement of CO2 from the tissues to the atmosphere
-So in other words.. ventilation is a very active process of drawing in and expelling O2 and CO2 whereas respiration is a passive process of moving O2 from the atmosphere to the tissues to support cell metabolism and passively moving CO2 from the tissues back to the atmosphere.

what is the difference between ventilation and respiration?

-External respiration: the sequence of events in exchange of O2 and CO2 between the external environment and cells
-cellular respiration: the intracellular metabolic processes carried out within the mitochondria which uses O2 and produces CO2 to generate energy from nutrients
-So external respiration is a sequential exchange of O2 and CO2 between the external environment and the cells and cellular respiration is respiration within the cells to the cell's metabolic processes within the mitochondria which uses O2 to produce CO2 to generate energy from nutrients.

what is the difference between external and cellular respiration?

conductive zone --> transitional zone --> respiratory zone

what is the importance of the functional organization of the pulmonary system?

conductive zone

air enters via the nose and mouth when it enters the ____ zone of the system. the air is adjusted to body temp., filtered by mucus, and humidifies; trachea-bronchi-bronchioles-smaller terminal bronchioles

transitional zone

as the branching of the bronchioles gets smaller and smaller the air moves from the conduction zone through the _____ zone. a very small amount of gas exchange can occur. respiratory bronchioles-alveolar ducts

respiratory zone

as branching increases in the transitional zone; we end up at the ____ zone where most the gas exchange is occurring and alveolar sacs are located

alveoli/alveolar sacs

elastic, thin walled (1 cell layer), membranous sacs, lined by surfactant; vital surface for gas exchange between lung tissue and blood; LARGEST blood supply of any organ

-diaphragm contracts, flattens, and moves downward into the abdominal space
-contraction of the scalene and external intercostal muscles rotates and lift that ribs up and away from the body
-elongation and enlargement of chest cavity expands the volume in the lungs causing the intra-alveolar pressure to decrease below atmospheric
-air is sucked in through nose and mouth filling and inflating the lungs
-ends with thoracic cavity expansion ceases causing intra-alveolar pressure to equal atmospheric

explain the mechanical and muscular aspects of INSPIRATION

-Results from the natural recoil of the stretched lung tissue and relaxation of the inspiratory muscles
-Chest cavity volume is decreased, and alveolar gas is compressed causing air to move out of the respiratory zone and into the atmosphere
-During strenuous exercise utilizing internal intercostals and abdominal muscles
-Ends when the compressive force of the expiratory musculature ends, and intro-alveolar pressure decreases to back atmospheric

explain the mechanical and muscular aspects of EXPIRATION

-As volume decreases pressure increases AND the inverse as volume increases pressure decreases
-Changes in the volume of the chest during ventilation creates pressure gradients that drive air flow (atmosphere 760 mmHg)
-Chest volume increase, alveolar pressure falls (759 mmHg), air flows into the lungs
-Chest volume decreases, alveolar pressure increases (761 mmHg), air flows out of the lungs

how does Boyle's Law relate to pulmonary function?

Alveolar ventilation and pulmonary blood flow are highly regulated and well matched at rest and light exercise; at rest Va = 4.2L/min and 5L of blood flows through pulmonary capillaries = 0.84

How do the mechanical and muscular aspects of inspiration and expiration differ from rest to high intensity exercise?

surfactant

lipoprotein mixture produces by alveolar epithelial cells
-reduces the alveolar membrane's surface tension which reduces the energy requirement for alveolar inflation
-makes breathing easier

-Increasing the rate or depth of breathing increases Ve
-Increasing depth of breathing increases Va.
-Ve is the volume of air moving past the mouth and nose per min
-Va is the volume of air reaching the alveoli each min.

How do VE, VA, ventilation-perfusion ratio, anatomic and physiologic dead space interact to impact pulmonary function at rest and during exercise. Why is it important for the ventilation-perfusion ratio to be balanced?

physiologic dead space is the sum of anatomic and alveolar dead space. alveolar dead space is the conducting airways not lined with respiratory epithelium. dead space is the portion of the lung where no gas exchange is occurring.

What is the difference between anatomic and physiologic dead space?

they work together since at rest and light exercise alveolar ventilation and pulmonary blood flow are well matched and regulated

How is each of the earlier factors impacted by changes in the rate or depth of breathing?

PAO2

partial pressure of O2 in alveolar chambers

PaO2

partial pressure of O2 in arterial blood

SaO2%

percent saturation of Hb in arterial blood with O2

PvO2

partial pressure of O2 in venous blood

PACO2

partial pressure of CO2 in alveolar chambers

PaCO2

partial pressure of CO2 in arterial blood

PvCO2

partial pressure of Co2 in venous blood

SvCO%

percentage saturation of Hb in venous blood with O2

a-vO2 diff

arterial-venous oxygen difference

oxyhemoglobin

normal Hb with iron in reduced for (Fe++); Fe++ shares electrons and bonds with O2. in blood vessels leaving the lungs and going to the body

deoxyhemoglobin

when oxyhemoglobin dissociated and releases O2. irons is still in the Fe++ state. in blood vessels in the periphery and returning to the lungs

carbaminohemoglobin

normal Hb combined with Co2. in blood vessels in the periphery and returning to the lungs

carboxyhemoglobin

normal Hb combined with carbon monoxide. the carbon monoxide bond with Hb is 210x stronger than the bond with O2. transport of O2 to tissue is impaired

methemoglobin

iron is oxidized (Fe+++) and cannot find O2 in this state

anemia

reduced Hb due to low iron stores

polycythemia

over production of Hb

Bohr effect

any change in plasma acidity; PCO2 or temperature shifts the oxyhemoglobin dissociation curve. more acidic and higher temp shift down and right and less acidic and low temp shift up and left

Haldane effect

increased capacity of hemoglobin the carry CO2 under conditions of decreased O2 saturation of hemoglobin

Dalton's law

mixture's total pressure is the sum of all partial pressures of the individual gases in the mixture

Henry's law

oxygen and other gases will diffuse from an area of high pressure to an area of low pressure

Fick's Law

diffusion rate across a membrane is:
-direction proportional to tissue area, diffusion constant and the pressure differential of the gas on each side of the membrane
-inversely proportional to the thickness fo the tissue

solubility

dissolving power of a gas determines the number of molecules moving into or out of a fluid
-expressed as mL of gas/100mL of fluid
-coefficients for blood CO2>>O2-(57.03mL>>2.26mL>1.30mL)
-quantify dissolved (mL has/100mL fluid)=solubility coefficient*(partial pressure/total barometric pressure)

oxyhemoglobin, carboaminohemoglobin, an carboxyhemoglobin

what hemoglobins are a part of normal gas exchange process?

deoxyhemoglobin and methemoglobin

what hemoglobins forms hamper the normal gas exchange process?

-dissolved in the fluid portion of blood -1.5%
-in combination with hemoglobin in RBC-98.5% making this form the most predominant

what the ways oxygen is transported in blood? which is more predominant?

blood does not loose all O2 or CO2 as a minimum level is needed to drive ventilation and acid base balance

What chemical and protein interactions and partial pressures/pressure gradients are involved that enable oxygen to be transported?

-tense state: subunits of hemoglobin are held together by electrostatic forces when deoxygenated
-loading of 1 O2 molecule to 1 hemoglobin binding site causes the iron molecule and peptide attached to move slightly and interrupt the electrostatic forces
-relaxed state: hemoglobin becomes looser and more readily binds O2 into the 3 remaining sites. when O2 is bound we have oxyhemoglobin

how does cooperative binding impact the ability of hemoglobin to carry oxygen?

PO2 determines the amount of O2 carried by either mechanism in the blood.
-dissolved O2: linear relationship between PO2 and O2 content in blood
-HbO2: sigmoidal relationship between PO2 and O2 content in blood based on cooperative binding

How does the s-shape of the oxyhemoglobin dissociation curve indicate how oxygen is loaded at lungs and unloaded at the muscles?

-Bohr Effect maximizes O2 transport
-any change in plasma acidity, PCO2 or temperature shifts the oxyhemoglobin dissociation curve
-more acidic and higher temp shift down and right. less acidic and lower temp shift up and left.
-downward right shift indicated an altered Hb molecular structure which reduces the ability to hold O2 particularly within the 20-50 mmHg PO2 range

What is the Bohr effect, what factors are involved, how does the oxyhemoglobin dissociation curve change, and how does it facilitate oxygen loading or unloading?

1. pH is increased H+ ions (7.4-7.35 ions shift)
2. PCO2 (40mmHg to 43 mmHg)
3. temperature (lungs-37 C, muscles 38 C)
4. 2,3 diphoshoglycerate (DPG)

-increases in PCO2, pH, temp, and DPG decreases the affinity of Hb for O2 (causes Hb to assume a tense confirmation and the O2 dissociation curve shifts down and right)
-increases in PCO2, pH, temp, and DPG are found in the areas of tissues (muscles) and facilitates unloading of O2

How do 4 factors near the muscles change the oxyhemoglobin dissociation curve to benefit oxygen release to muscles during physical activity?

-iron containing globular protein in skeletal and cardiac muscle providing intramuscular O2 storage (can on store 1 molecule of O2)
-facilitates delivery of O2 to mitochondria
-has higher affinity for O2 than Hb
-loads and retains O2 at much lower PO2
-unloads O2 at super low PO2 found at the areas of mitochondria
-affinity for O2 not influenced by pH, CO2, or temperature

what is the role of myoglobin in oxygen transport in the tissue?

myoglobin has higher affinity for O2 than Hb. Loads and retains O2 at much lower partial pressure of O. unloads O2 at super low PO2 found at the areas of the mitochondria. Affinity for O2 not influenced by pH, CO2, or temperaure

How is myoglobin different from hemoglobin and how does it facilitate increased intensity of physical activity?

-difference between the amount of O2 carried in the arterial blood and carried in the venous blood
-O2 released from Hb is independent of the rate of blood flow at tissue
-at rest a-vO2 difference is 4-5mL/dL
-during aerobic exercise a-vO2 difference is 15-18 mL/dL
-release during vigorous exercise increases due to Bohr effect
-active muscle's capacity to extract O2 from blood indicated that O2 supply not O2 utilization is the limiting factor for exercise capacity

what does the a-vO2 difference tell us about oxygen transport?

1. dissolved in plasma or in RBC fluid -5%
2. combined with Hb in RBC -5-40%
3. bicarbonate (HCO3) -60-90% so it is most predominant

What are the 3 ways carbon dioxide can be transported in blood? Which transport form is most predominant?

-Transport of CO2 from blood to lungs
-Dissolved CO2 diffuses from the plasma into alveoli
-PCO2 in plasma drops
-carbaminohemoglobin dissociates and CO2 diffused into alveoli
-Bicarbonate (HCO3-) diffuses into the RBC, H+ released from Hb, carbonic acid is reformed
-Cl- moves from RBC to plasma to balance charge
-H+ binding to bicarbonate increases Hb affinity for O2
-Carbonic acid (H2CO3) in the RBC dissociates into CO2 and H2O
-CO2 diffuses into alveoli

What chemical and protein interactions and partial pressures/pressure gradients are involved that enable carbon dioxide to be transported?

increases capacity of hemoglobin to carry CO2 under conditions of decreases O2 saturation of hemoglobin

Diffusion of CO2 from the skeletal muscle into the blood is the only means for escape through the lungs.

what is the Haldane effect? what role does it have in the gas exchange process?

oxygen consumption

VO2=(volume inspired% oxygen in inspired air)-(volume air expired%oxygen in expired air) = (VI %O2I) -(VE %O2E)

maximal oxygen consumption

maximal amount of oxygen used by the body during maximal effort exercise

ventilatory threshold (Vt)

point at which pulmonary ventilation increases disproportionately with O2 consumption during graded exercise

lactate threshold

highest VO2 or exercise intensity before there is a 1mM increases in blood lactate concentration above pre-exercise level; before OBLA

onset of blood lactate accumulation (OBLA)

signifies when blood lactate concentration sysyematically increases to 4 mM

1. factors that generate the alternating inspiration-expiration rhythm
2. factors that regulate the rate and depth of breathing to match body needs
3. factors that modify respiratory activity to serve other purposes

what are the 3 distinct components regulating respiration?

1. neural circuits
2. humoral circuitd

what 2 categories of factors enable regualation of respiration?

phase 1: when exercise stops there is an abrupt decline in Ve, reflects removal fo the central command drive
phase 2: gradual diminution of the short-term increase in nerve impulse strength at the respiratory center, and removal of input from the peripheral sensors at reestablishment of the body's normal metabolic, thermal, and chemical homeostasis occurs
-a fall in blood pH signal acidosis and reflects hypercapnia, lactate accumulation, or ketone accumulation

what are the basis processes of ventilatory stimulation that return the system to normal when homeostasis is perturbed by hypercapnia or hypocapnia?

-PaO2 does not decrease to an extent to stimulate chemoreceptors
-P_AO2 rises above average resting value with increases Ve which hastens oxygenation of blood
-CO2 production thus H+ increases to stimulate chemoreceptors
-Hyperventilation reduces PaCO2 below resting concentrations which would decrease ventilatory drive from CO2

Explain the humoral control of ventilation at rest

-Cortical influence: signals from motor complex, cortical activation in anticipation of exercise - Central Command
-Peripheral influence: sensory input from joints/tendons/muscles

explain the neural control of ventilation at rest

-in medulla
-PaCO2 is the most important respiratory stimulus at rest
-The action of CO2 is not the mediatory
-H+ content which changes with CO2 content exerts a significant command over Ve
-A fall in blood pH signals acidosis and reflects hypercapnia, lactate accumulation, or ketone accumulation
-Reduced arterial pH increases inspiratory activity to eliminate CO2 to reduce arterial levels of H2CO3
-Mainly signal through minorly central chemoreceptors, minorly signal through peripheral chemoreceptors

where are the central chemoreceptors located? PaCO2 and H+

-Carotid bodies: Lie at the fork of both common carotid arteries that supply the brain
-Aortic bodies: Lie in the arch of the aorta
-PaO2 must fall below 60 mmHg before afferent impulses begin to change in increase ventilation
-The safety margin of Hb saturation enables the large reduction
-Remember PaO2 is based on dissolved O2 and not O2-Hb

where are the peripheral chemoreceptors located? PaO2

phase 1: neurogenic stimuli from motor cortex and feedback from active limbs stimulate the respiratory center to abruptly increase ventilation
phase 2: after brief plateau, ventilation increases to achieve a steady rate related to the metabolic gas exchange demands
phases 3: fine tuning of the steady rate ventilation through peripheral chemoreceptors and mechanoreceptor sensory feedback

explain the 3 phases of ventilatory phases during exercise

phase 1: when exercise stops there is an abrupt decline in Ve; reflects removal of the central command drive
phase 2: gradual diminution of the short term increase in nerve impulse strength at the respiratory center; and removal of input from the peripheral sensors as reestablishment of the body's normal metabolic, thermal, and chemical homeostasis occurs

explain the 2 phases of ventilatory changes during recovery

-cold ambient air normally does not pose a danger to respiratory passages
-significant loss of water and heat notably during strenuous exercise with large Ve
-fluid loss contribute to dehydration, dry mouth, burning in throat, irritation of respiratory passes, and triggers coughing during recovery phase
-covering nose and mouth: traps water from the exhaled air and warms the next incoming breath of aire

what are the effects of cold weather exercise and voluntary hyperventilation on pulmonary ventilation?

the progressive increase in pulmonary volume that occur under constant pressure
-in hot weather, the creep is higher

what is ventilatory creep? how is it different between cool and hot weather exercise?

VE increases linearly with O2 consumption and CO2 production during light to moderate exercise

what are the acute effects of steady rate vs graded/non-steady rate exercise on ventilation, including VO2 and VCO2?

Ventilatory equivalent - (VE/VO2)

VO2 = (volume air inspired %oxygen in inspired air) minus (volume air expired %oxygen in expired air) • = (VI %O2I ) - (VE %O2E)

Equations & Calculations: ventilatory equivalent and VO2.

VO2: the oxygen demand is equal to that consumed during steady rate; sufficient oxygen to provide the necessary ATP for the given exercise intensity
-VO2 max: the plateau in VO2 with increasing exercise intensity (graded exercise); increasing exercise intensity does not increases amounts of O2 available, represents the greats amount of ATP production by aerobic metabolism
-RER > 1.0 there is excess CO2 exhaled bc acid buffering

What are VO2 and VO2max? What does it mean when an RER is greater than 1.0?

-Lactate threshold: the highest Vos or exercise intensity before there is a 1mM increase in blood lactate concentration above pre-exercise level, reached BEFORE OBLA
-OBLA signifies when blood lactate concentration systematically increased to 4mM
Lactate threshold.. better endurance indicator than VO2max because endurance training increases the VO2 at which the lactate threshold is observed

What are the differences between lactate threshold and OBLA?

endurance training increases the VO2 at which the lactate threshold is observed

Why might lactate threshold be a better predictor of endurance performance than VO2max?

-3-5% during moderate exercise
-8-11% during maximal exercise
-15% or greater for elite-training endurance athletes

What is the energy cost (% of VO2) of breathing at rest and during different levels of exercise?

-VEmax is maximal minute ventilation and during exercise it is less than MVV
-VE at VO2max = 60-85% MVV
-ventilation does not limit performance or VO2max in normal healthy people

What is VEmax? Why does VEmax not normally limit VO2max? Why is pulmonary ventilation not the weak link in oxygen supply during maximal exercise? What is the limiting factor in oxygen supply during maximal exercise?

-Exercise induced arterial hypoxia is impaired ventilation-perfusion ration during intense exercise that compromises SaO2 and O2 transport capacity
-Possible functional causes:
-inequality in ventilation perfusion ration within the lungs
-Shunting of blood between venous and arterial circulations
-failure to achieve end capillary equilibrium and alveolar-blood gases

What is exercise induced arterial hypoxia? What are the possible functional causes?

buffer

chemical or physiologic mechanisms that prevent changes in H+