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Leading causes of death in Industrialized Societies
- 1. Cardiovascular Diseases
- 2. Cancer
- 3. Pulmonary Diseases: Asthma, cystic fibrosis, pulmonary disease
What is respiration?
transfer of oxygen and carbon dioxide between body and external enviornment
How is gas exchange achieved?
by diffusion (passive movement) of oxygen and carbon dioxide from blood to alveoli and vise versa
Where does gas exchange take place?
In terminal air sacs called alveoli
How do alveoli exchange gases?
Are air bubbles and because of increases surface area so air can diffuse into blood stream
What is importance of hemoglobin?
Ability of blood to carry oxygen and get to tissues of body
What are the important components of respiration?
Blood flow of oxygen and carbon dioxide, profuse organs by vessels, and hemoglobin carrier for oxygen
process of obtaining oxygen and releasing the cellular waste product, carbon dioxide into the environment
What are parenchyma?
alveoli, airways, and blood vessels tied together by extracellular matrix of collagen and elastin.
glue alveoli together to form organ
What is the "respiratory membrane"
alveolar cell + endothelial cell
What is the importance of the respiratory pump?
continually replenishes oxygen and discards carbon dioxide in alveoli
What is ventilation and where does it take place?
provides fresh air to respiratory membrane, which is process of inspiration, and expels air that is low in oxygen and high in carbon dioxide, the process of expiration
In respiratory pump
What are other functions of respiratory system?
acid-base balance, speech, and endocrine and metabolic functions such as conversion of angiotensin I to angiotensin II
What happens when there is increased CO2 in the blood?
Increases H+ and decreases pH levels making blood more acidic. Affects enzyme activity and metabolic problems can occur if too much or too little of CO2.
How does repiration effect speech?
forced experation across vocal cords to speak
What causes changes in values of lung volumes and capacities?
body position, age, and respiratory disease
Tidal Volume (VT)
volume of air entering or leaving nose or mouth in each breath
Expiratory Reserve Volume (ERV)
volume of gas expelled during a maximal forced expiration that starts at the end of a normal tidal expiration
Inspiratory Reserve Volume (IRV)
volume of air that is inhaled during a maximal forced inspiration starting at the end of a normal tidal inspiration
Inspiratory Capacity (IC)
volume of air that is inhaled during a maximal inspiratory effort that starts at the end of a normal tidal expiration (the FRC)
IC = VT + IRV
Vital Capacity (VC)
volume of gas expelled during a maximal forced expiration starting after a maximal forced inspiration
VC = VT + IRV + ERV
Residual Volume (RV)
volume of gas left in the lungs after a maximal forced expiration
Functional Residual Capacity (FRC)
volume of gas remaining in lungs at the end of a normal tidal expiration
FRC = ERV + RV
also called the equilibrium volume
Total Lung Capacity (TLC)
volume of gas in the lungs after a maximal inspiratory effort
TLC = VC + RV
What are some direct measurements of lung volumes?
What are some indirect measurements of lung volumes?
helium dilution technique and body plethysmography
What is spirometry?
direct measurement of volume of air exhaled into a drum
VT, IRV, ERV, VC
What measures lung volume that cannot be expired?
Helium dilution technique- for determination of residual volume
What does it mean when the airway is blocked in helium dilution technique?
problem in lungs (diease). A result in the test is a false measurement.
Why is helium used in a helium dilution technique?
insoluable in H2O so can't diffuse into blood and be carried out into pulmonary circulation
Helium dilution measures what?
volume of air in lung that can communicate with outside air at time lung airflow is opened to aparatus (residual volume)
What is body plethysmography?
more accurate measure of actual lung volume. measures total volume of air in the lung at FRC including air trapped behind obstructed airways. Applies Boyle's Law: P1V1 = P2(V1+changeV)
What is the importance of measuring lung volumes? comparing FRC measured by two techniques (Helium Dilution Technique and Body Plethysmography)
determine whether a measureable amount of air is trapped in lung due to obstructed airways
FRC (body pleth.) - FRC(helium dilution) = air trapped in lung
What is passive force acting on lung?
elastic recoil- potential energy within the walls of expandable chamber that opposes distension or stretch
What are 2 major recoil forces act to pull lungs inward? (elastic recoil of lung)
- 1. interstitial elastin and collagen
- 2. surface tension of H2O lining alveolar wall exposed to air
What 2 major recoil forces act to pull lungs outward? (elastic recoil of thoracic cage)
- 1. attachment of rib cape to spine due to ligaments and cartilage at joints
- 2. Elasticity (elastin and collagen) in relaxed diaphragm muscle
Balance b/t recoil forces of lung and thoracic cage is the measurement of what lung volume?
functional residual capacity (FRC) or equilibrium volume
when integrity of thoracic cage is breached (stab or bullet wound to chest), pressure in pleural space equilibrates with atmosphere and lungs collapse and stops ventilation and gas exchange
What are the active forces (respiratory muscles) in inspiration?
contraction of diaphragm and external intercostal muscles that opposes elastic recoil of lungs
when muscle force exceeds lung recoil force, lungs expand
What is inspiratory work?
contracting inspiratory muscles consume energy, expressed as work (W = change in P * change in V)
What happens during expiration?
normal quiet breathing (expiring back to FRC). No force opposing elastic recoil of lung, so lung tissue pulls the lung back toward equilibrium volume. No expiratory work
What happens during strenuous exercise or disease states (expiring below FRC)?
Necessary to increase tidal volume more than inspiratory capacity allows (due to heavy exercise). Begin to exhale below FRC, so expiratory mucles (abdominal and internal intercostal muscles) must contract pulling the chest wall inward below FRC. Expiratory muscles oppose passive chest wall recoil forces.
What does surfactant do?
counteracts surface tension of water, reducing elastance and increasing compliance of the lung to usable 'physiological' level.
What is surfactant?
mixture of substances composed mostly of dipalmitoyl phosphatidylcholine, a phospholipid produced by alveolar type II cells and secreted on alveolar surface where it floats to air/water interface. Polar molecule with hydrophilic and hydrophobic ends. Hydrophilic end (+ charge) is submerged in water at air interface. Hydrophobic tails float above water (like oil on water), producing a monolayer of surfactant molecules. ***charged ends of surfactant molecules tend to repel one another when they are squeezed together in the monolayer. THus repelling force of surfactant molecules balances the tendency of water molecles to reduce surface area and contract the alveolus***
True or False: Normally, we use inspiratory muscles to inspire and expiratory muscles to expire when breathing at rest
False: in normal healthy lung, we expire passively at rest, using elastic recoil of the lung to deflate the lung and expire
What is active recoil?
Inspiratory muscles increase thoracic cage recoil and expiratory muscles decrease thoracic cage recoil
What are the 3 functional advantages of surfactant?
- 1. It substantially reduces tremendous surface tension in alveoli, thus increasing lung compliance to an optimal level. Without surfactant, tremedous energy would be requried to expand the lung. Surfactant minimizes the inspiratory work of breathing.
- 2. It helps to keep alveoli from filling with fluid (retards alveolar edema)
- 3. It stabilizes alveoli and prevents alveolar collapse (atelectasis) due to Lapalce's Law
Why do alveoli tend to collapse?
tendency of small alveoli to collapse is much greater than larger alveoli due to Laplace's law (P = 2T/r). Surfactant lowers tension of alveolar walls at low lung volumes, but transpulmonary pressure of large and small communicating airspaces is the same. Without surfactant the surface tension remains constant as lung volumes change, and recoil pressure of small airspaces exceeds that of larger onces. Result is that small alveoli tend to empty into larger ones. Without opposing mechanisms, pressure in small alveoli would be greater than the pressure in large alveoli b/c of smaller r. Greater pressure in small alveoli would cause air to move out of them into the larger units, thus resulting in alveolar collapse.
What 2 factors counteract alveolar collapse?
- 1. Surfactant: reduce water surface tension
- 2. Interdependence: alveoli are tethered to one another b/c adjacent alveoli share common spetal walls and the alveolar walls are supported by an interstitial fibrous network. This alveolar 'framework' helps to prevent collapse.
What is elastance?
one measure of the ability of a substance to maintain its original shape (stiffness)
What is compliance?
Is a measure of the ease with which an object is distended (distensibility). Used to measure the elastance of pulmonary and cardiovascular vessels. It is the inverse of elastance.
What is lung compliance and how is it measured?
it is measured as the slope of the pressure-volume curve of the lung. Compliance of the lungs is least at high lung volumes and greatest at low lung volumes
What is dynamic lung compliance (Cdyn)?
compliance measured over the course of a normal tidal volume
What factors decrease lung compliance below normal?
- 1. Deposition of scar tissue (pulmonary fibrosis): scar tissue is composed mostly of collagen which has very high elastance (stiff). Lung becomes stiffer and compliance decreases
- 2. Insufficient secretion of surfactant from type II cells in infants (infant respiratory distress syndrome, IRDS, or hyaline membrane disease). Type II cells are too immature to produce surfactant in premature birth
- 3. Destruction of type II cells due to prolonged hypoxemia or to inhalation of toxins (adult respiratory distress syndrome, ARDS). Results in atelectasis (massive collapse of alveoli) and then death
- 4. Excessive accumulation of water in alveolar space (alveolar edema)
- 5. Prolonged quiet breathing: surfactant secretion is stimulated by inflation of lung, but during quiet breathing the lung does not expand sufficiently to stimulate secretion at a rate to keep up with normal metabolic removal of surfactant from alveolar surface and complience decreases. Pulomnary sensory nerves cause sigh or yawn to restore normal surfactant concentrations on alveolar surface
What are factors that increase lung compliance above normal?
- 1. Destruction of lung tissue by protease and collagenase enzymes formed during chronic inflammation (emphysema)
- 2. Excessive secretion of surfactant (rare)
- 3. Chronic Obstructive Pulmonary Disease (COPD)
What are consequences to lungs with decreased compliance?
- 1. TLC and VC are reduced becasue a stiff lung cannot be expanded as readily
- 2. B/c more force must be generated by inspiratory muscles to expand a stiff lung, work of breathing increases
What are some consequences to lungs with increased compliance?
- 1. TLC is increased but due to dynamic compression of airways during expiration the VC of lung actually decreases
- 2. A highly compliant lung has little recoil force for deflation during expiration. Thus expriatory muscles must be used to help delfate the lung. Increases the work of breathing
True of False: Sighing and yawning play an important role in maintaining normal lung compliance?
True: hyperinflation (stretching) of the lungs stimulates type II cells in alveoli to secrete surfactant to maintain normal compliance of lung
What are some determinants of laminar flow?
- occurs during quiet breathing (low air velocities), obeys derivative of Ohms law: V = PA - Pao / RaoAlso occus at small airways
What are determinants of airway resistance?
- 1. resistance to laminar airflow obeys Poiseuille's law: Raw = (8*n*l) / (pi *r4)
- 2. Turbulence adds to resistance to airflow as air velocity increases in upper airways. Reynold's number: Re = 2rvd / n
Where is the major site of resistance to airflow?
Major site is in larger airways, upper airways (nose, mouth, larynx, and trachea) and in medium sized lobar, segmental, and subsegmental bronchi. Due to Reynolds factor b/c air velocity is much greater in larger airways vs. bronchioles b/c their total cross sectional area is much smaller than accumulative area of millions of tiny bronchioles, and resistance to laminar flow in the distal airways is greatly diminished by resistances being in parallel
An increase in resistance does what to work of breathing?
Increases work of breathing b/c inspiratory muscles must develop additional force to overcome the resistance to airflow
What are factors that determine airway resistance?
- 1. Density of the gas (not usually major factor unless deep sea diving). However, reducing air density reduces turbulent flow and decreases airway resistance to some degree
- 2. Radius of airways (most important) and influenced by: airway smooth muscle contrication, secretion of mucus onto airway surface can reduce airway caliber and increase airway resistance, swelling of airway mucosa caused by inflammation (bronchiolitis), and lung volume- airway resistance is less at high lung volumes
Where is turbulent airflow most common?
in large airways and branch points (high air velocity)
Airway resistance is lower where?
in distal airways due to large cross sectional area (effective radius is large)
Airway resistance is high where?
In upper airways due to high airflow velocity and development of turbulent airflow
True or False: Less work is requried to breath at the top of a mountain than at sea level?
True: at high altitude, air is less dense than at sea level which reduces turbulent airflow when we breath. Thus total resistance to airflow is reduced making it easier to breath air in and out of the lungs
When is there dynamic compression of airways?
- 1. During forced expiration, small bronchioles collapse due to elevation of pleural pressure necessary to deflate the lung rapidly
- 2. dynamic compression increases the resistance to airflow during expiration, adding to expiratory work of breathing
- 3. rarely occurs during normal quiet breathing in healthy subjects and can exhibited only by a large forced expiration. It is quite common in emphysema
What diseases contribute to airway obstruction and affect airway radius?
Chronic bronchitis (mucus, inflammation), asthma (smooth muscle spasm), and COPD which is a combination of emphysema and chronic bronchitis
What prevents dynamic compression?
tethering of thoracic airways to lung parenchyma
True or False: A person with significant emphysema will have no difficulty blowing out birthday candles?
False: Loss of lung tissue will make thoracic airways susceptible to collapse with a forced expiration and thus reduce airflow needed to blow out candles
What is restrictive lung disease?
all conditions that decrease lung compliance and increase elastance or recoil force of the lung
What are causes of restrictive lung disease?
- 1. scar tissue deopsition
- 2. lack of surfactant
- 3. flooding of alveoli with water
What are the names of problems that cause restrictive lung disease?
- 1. Pulmonary fibrosis
- 2. Respiratory distress syndrome
- 3. Pulmonary edema
What are some consequences of restrictive lung disease?
- 1. decrease in FRC, TLC, VC, IC
- 2. Anything making lung stiff
- 3. Respiratory fatigue- more inspiratory work needs to be done to inflate the lung then leads to failure of inspiratory muscles
- 4. Atelectasis
What is obstructive lung disease (emphysema type)?
conditions that increase lung compliance and decrease elastance or recoil force of lung
What are causes of obstructive lung disease (emphysema type)?
- 1. loss of lung tissue
- 2. old age (gradual loss of elastin and collagen in lung)
- 3. loss of supportive lung tissue and mesenchymal cells due to disease
- 4. decrease in elastic recoil of lung
What are the names of problems that cause obstructive lung disease (emphysema type)?
- 1. enphysema
- 2. antitrypsin deficiency (enzyme destroys protease enzymes that degrade elastin and collagen)
- 3. Smoking is #1 cause
What are some consequences of obstructive lung disease (emphysema type)?
- 1. active expiration needed to deflate the lung (abdominal breathing)- less IC for inspiration
- 2. Work of expiration excessive (leading to failure of expiratory muscles)
- 3. Air trapped in lung due to dynamic compression (RV markedly increased, VC impiared)
- 4. Expired air impaired
- 5. decrease in elastic recoil of lung allow chest wall to pull lung outward at rest results in increased FRC and TLC
What are some causes (and name disease) of obstructive lung disease (airway disease type)?
- 1. mucus hypersecretion or immoble (cystic fibrosis)
- 2. Inflammation of airway (bronchitis)
- 3. airway smooth muscle spasm (asthma)
What are some consequences of obstructive lung disease (airway disease type)?
- 1. marked increase in airway resistance
- 2. inspiraed and expired airflow impaired
- 3. Work of inspiration and expiration elevated
- 4. RV elevated due to trapped air in lung so VC compromised
Why are there pulmonary function test of lung volumes?
lung volumes are altered in restrictive and obstructive lung diseases
What are pulmonary function tests for forced expiration?
- 1. b/c both narrowing of airways and dynamic compression limit or suppress rate at which air can flow in and out of lungs, during forced expiration which accelerate dynamic compression, this test provides a reasonably effective means in which to distinguish obstructive vs. restricitve diseases
- 2. FEV1.03. FVC
- 4. FEV/FVC %
What is metabolic cost of breathing?
amount of respired O2 required to produce the energy for work of breathing
What happens to work of breathing in restrictive lung disease?
increased due to decreased lung compliance
What happens to work of breathing in obstructive lung disease?
increased due to increase resistance to airflow
What happens to work of breathing in emphysema?
further increased due to increased airflow resistance b/c expiratory muscles are requred to deflate the lung
What are the effects on pulmonary pressures when using mechanical ventilation?
most mondern ventilators use positive thoracic pressure to inflate the lungs. The body normally creates negative throacic pressures to dirve inspiration
What are physiology consequences of positive pressure ventilation (mechanical ventilation)?
- 1. Impedes venous return into thorax and reduces CO2
- 2. Aggravates V/Q mismatching. Postive pressure in alveoli tends to impede capillary blood flow, more in upper regions of lung. If alveolar pressure prevents alveolar capillary flow, it will increase zone 1and alveolar dead space
- 3. Increased risk of overinflating the lungs or hypo- or hyperventilating the patient (monitor premies and ARDS)
True or False: Asthma is characterized as an obstructive lung disease, but is difficult to classify using PFTs
True: Asthma is the only major pulmonary disease that is episodic: patients are usually unsymptomatic. PFT would not reveal airway obstruction unless patient is having an asthma attack at the time of testing.
Lung volumes, airflow, and work of breathing are dependent on what?
elastic and resistive properties of the lungs and airways
What determines resistance of airway?
airway caliber (radius), turbulent flow, and dynamic compression of thoracic airways during expiration are major factors impairing airflow
Mechanical ventilation of lungs impedes what?
CO2 and proper blood flow/ gas exchange through lungs
What is total minute ventilation?
- Minute ventilation VE = VT (f)
- f = breaths per min
- VT = tidal volume
- Minute respiratory volume (VT in a minute)
What is alveolar ventilation?
volume of fresh air that enters the functioning gas exchange regions of the lung per minute
- VA = (VT - VD) f
- VD = vol of dead space
What must be proportional in alveolar ventilation?
O2 consumption and CO2 production
What happens to alveolar ventilation during exercise?
alveolar ventilation must increase in proportion to the increased metabolic demands in order to insure adequate delivery of O2 and removal of CO2 from tissue
What is alveolar ventilation regulated by?
respiratory centers in brain stem that control respiratory muscles. These centers alter depth of inspiration (VT) and frequency of breathing (f) so that VA remains proportional to VO2 and VCO2
What is anatomical dead space?
is the volume occupied by the conducting zone. Conducting zone is respiratory passages down to the level of and including the terminal bronchioles. Is equivalent to a person's weight in pounds.
How is anatomical dead space determined?
Determined using Fowler's method (nitrogen washout)
What is physiological dead space?
is the total dead space of respiratory tract that includes anatomical dead space + any alveolar space in which gas exchange is not occurring (usually due either to diffusion impiarment or to absence of pulmonary capillary flow at the alveolar unit)
Physiological dead space = anatomical dead space + alveolar dead space
How is physiological dead space determined?
Bohr equation = expiration in which CO2 is diluted from dead space air
VD = [(PACO2 - PECO2) / PACO2] VT
When is physiological dead space > anatomical dead space?
when a significant # of alveoli are being ventilated but not perfused (alveolar dead space)
How can the amount of alveolar dead space in an individual be estimated?
By determination of nitrogen washout and Bohr equation
Physiological dead space = anatomical dead space when
in healthy lung
How can one calculate alveolar dead space?
can't be measured directly. One must determine anatomical and physiological dead spaces and subtract
Alveolar dead space = physiological dead space - anatomical dead space
What does the presence of alveolar dead space mean?
That non-functioning alveoli are present and are being ventilated but are not undergoing gas exchange with pulmonary capillary blood
What is wasted ventilation (VW)?
volume of air per minute used to ventilate the physiological dead space
VW = VD (f)
Explain VD / VT
wasted fraction of each breath. Increasing VT decreases; ventilation becomes more effecient. With pulmonary disease, an increase in alveolar dead space will significantly increase wasted fraction, making ventilation less efficient
What does increasing wasted ventilation mean?
that the body must consume more energy to ventilate the lungs for air that will not undergo gas exchange with blood. It decreases the efficiency of gas exchange.
What are some factors that promote alveolar dead space and wasted ventilation?
- 1. suppressed pulmonary blood flow: heart failure, hemorrhage, positive pressure ventilation, pulmonary emboli (blood clot (thrombus)), hypoxic pulmonary vasoconstriction (ARDS)
- 2. Imparied diffusion across respiratory membrane: pulmonary interstitial edema and pulmonary fibrosis
- 3. Gravity and posture: not major contributors but can aggravate the problem
What does gravity do with regional distribution of ventilation?
pulls the lung mass downward, causing the upper alveoli to be stretched outward to a greater extent than alveoli at the bottom of the lung (upper alveoli are stretched to a higher resting volume than lower alveoli, or closer to their maximal alveolar volume).
What happens to alveoli compliance due to gravity?
compliance is less b/c upper alveoli are stretched more than lower alveoli
When the lungs are inflated during inspiration what happens to upper and lower alveoli?
- lower- are distended with greater ease and accept more of the inspired air than upper alveoli b/c thier resting compliance is greater that upper. (> ventilation @ bottom of lung)
- upper- less accepting of inspired air
Under normal resting condition alveolar ventilation is greater where in the lungs?
at the bottom of the lungs
What happens when VT increases due to increased metabolic demand (exercise)?
alveoli at upper portion of lung are recruited to ventilation
During a hemorrhage or shock what do you do to the person?
lay them down to put lung in flat position to increase profusion and decrease alveolar dead space b/c profusion is lower. Increasing zone III and decreasing zone I
What pathological factors can influnce regional distribution of ventilation?
- 1. Regional airway obstruction (asthma) or bronchoconstriction
- 2. Regional differences in compliance (fibrosis)
- 3. Regional differences in dynamic compression (emphysema)
When do alveolar dead space and wasted ventilation increase?
- 1. conditions that impair pulmonary capillary blood flow (hemorrhage, heart failure, pulmonary embolism, and high altitude)
- 2. Conditions that impiar diffusion of O2/CO2 b/t air and blood: pulmonary fibrosis, pulmonary edema, and emphysema
How do you maintain a normal VA when alveolar dead space and wasted ventilation are increased?
VE must increase to compensate for the increase in VA
True or False: considering the optimal design of a snorkel tube, dead space is the major limiting physiological factor to consider.
True and False: dead space of snorkel is important limiting factor, but minimizing dead space by decreasing diameter of tube will increase resistence of airflow, which @ a point becomes the major limiting factor. *Also below about 1m, the pressure of water on chest makes it impossible to inhale, regardless of the snorkel dead space.
True or False: When we exercise and need to increase alveolar ventilation, is it more efficient to increase breathing frequency or tidal volume?
False: Increasing tidal volume increases alveolar ventilation w/o affecting ventilation of dead space (wasted ventilation). Increasing frequency will also increase alveolar ventilation but less efficiently b/c also increase wasted ventilation.
True or False: A person with significant emphysema often finds comfort by expiring slowly through pused lips?
True: expiring more slowly reduces force needed to deflate the lung and lessens dynamic compression. Pursing lips moves region of highest airway resistance out of the throax to the mouth and thus establishes higher pressures in throacic airways, preventing them from collapse with forced expiration