Respiratory Function lessons 1-4

• 1. Cardiovascular Diseases
• 2. Cancer
• 3. Pulmonary Diseases: Asthma, cystic fibrosis, pulmonary disease

transfer of oxygen and carbon dioxide between body and external enviornment

by diffusion (passive movement) of oxygen and carbon dioxide from blood to alveoli and vise versa

In terminal air sacs called alveoli

Are air bubbles and because of increases surface area so air can diffuse into blood stream

Ability of blood to carry oxygen and get to tissues of body

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

alveoli, airways, and blood vessels tied together by extracellular matrix of collagen and elastin.

glue alveoli together to form organ

alveolar cell + endothelial cell

continually replenishes oxygen and discards carbon dioxide in alveoli

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

acid-base balance, speech, and endocrine and metabolic functions such as conversion of angiotensin I to angiotensin II

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.

forced experation across vocal cords to speak

body position, age, and respiratory disease

volume of air entering or leaving nose or mouth in each breath

volume of gas expelled during a maximal forced expiration that starts at the end of a normal tidal expiration

volume of air that is inhaled during a maximal forced inspiration starting at the end of a normal tidal inspiration

volume of air that is inhaled during a maximal inspiratory effort that starts at the end of a normal tidal expiration (the FRC)

IC = V_T + IRV

volume of gas expelled during a maximal forced expiration starting after a maximal forced inspiration

VC = VT + IRV + ERV

volume of gas left in the lungs after a maximal forced expiration

volume of gas remaining in lungs at the end of a normal tidal expiration

FRC = ERV + RV

also called the equilibrium volume

volume of gas in the lungs after a maximal inspiratory effort

TLC = VC + RV

spirometry

helium dilution technique and body plethysmography

direct measurement of volume of air exhaled into a drum

V_T, IRV, ERV, VC

Helium dilution technique- for determination of residual volume

problem in lungs (diease). A result in the test is a false measurement.

insoluable in H2O so can't diffuse into blood and be carried out into pulmonary circulation

volume of air in lung that can communicate with outside air at time lung airflow is opened to aparatus (residual volume)

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)

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

elastic recoil- potential energy within the walls of expandable chamber that opposes distension or stretch

• 1. interstitial elastin and collagen
• 2. surface tension of H2O lining alveolar wall exposed to air

• 1. attachment of rib cape to spine due to ligaments and cartilage at joints
• 2. Elasticity (elastin and collagen) in relaxed diaphragm muscle

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

contraction of diaphragm and external intercostal muscles that opposes elastic recoil of lungs

when muscle force exceeds lung recoil force, lungs expand

contracting inspiratory muscles consume energy, expressed as work (W = change in P * change in V)

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

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.

counteracts surface tension of water, reducing elastance and increasing compliance of the lung to usable 'physiological' level.

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***

False: in normal healthy lung, we expire passively at rest, using elastic recoil of the lung to deflate the lung and expire

Inspiratory muscles increase thoracic cage recoil and expiratory muscles decrease thoracic cage recoil

• 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

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.

• 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.

one measure of the ability of a substance to maintain its original shape (stiffness)

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.

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

compliance measured over the course of a normal tidal volume

• 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

• 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)

• 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

• 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: hyperinflation (stretching) of the lungs stimulates type II cells in alveoli to secrete surfactant to maintain normal compliance of lung

• occurs during quiet breathing (low air velocities), obeys derivative of Ohms law: V = P_A - P_ao / R_ao
• Also occus at small airways

• 1. resistance to laminar airflow obeys Poiseuille's law: R_aw = (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

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

Increases work of breathing b/c inspiratory muscles must develop additional force to overcome the resistance to airflow

• 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

in large airways and branch points (high air velocity)

in distal airways due to large cross sectional area (effective radius is large)

In upper airways due to high airflow velocity and development of turbulent airflow

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

• 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

Chronic bronchitis (mucus, inflammation), asthma (smooth muscle spasm), and COPD which is a combination of emphysema and chronic bronchitis

tethering of thoracic airways to lung parenchyma

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

all conditions that decrease lung compliance and increase elastance or recoil force of the lung

• 1. scar tissue deopsition
• 2. lack of surfactant
• 3. flooding of alveoli with water

• 1. Pulmonary fibrosis
• 2. Respiratory distress syndrome
• 3. Pulmonary edema

• 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

conditions that increase lung compliance and decrease elastance or recoil force of lung

• 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

• 1. enphysema
• 2. antitrypsin deficiency (enzyme destroys protease enzymes that degrade elastin and collagen)
• 3. Smoking is #1 cause

• 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

• 1. mucus hypersecretion or immoble (cystic fibrosis)
• 2. Inflammation of airway (bronchitis)
• 3. airway smooth muscle spasm (asthma)

• 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

lung volumes are altered in restrictive and obstructive lung diseases

• 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. FEV_1.0
• 3. FVC
• 4. FEV/FVC %

amount of respired O₂ required to produce the energy for work of breathing

increased due to decreased lung compliance

increased due to increase resistance to airflow

further increased due to increased airflow resistance b/c expiratory muscles are requred to deflate the lung

most mondern ventilators use positive thoracic pressure to inflate the lungs. The body normally creates negative throacic pressures to dirve inspiration

• 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: 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.

elastic and resistive properties of the lungs and airways

airway caliber (radius), turbulent flow, and dynamic compression of thoracic airways during expiration are major factors impairing airflow

CO2 and proper blood flow/ gas exchange through lungs

• Minute ventilation V_E = V_T (f)
• f = breaths per min
• VT = tidal volume
• Minute respiratory volume (VT in a minute)

volume of fresh air that enters the functioning gas exchange regions of the lung per minute

• V_A = (V_T - V_D) f
• VD = vol of dead space

O2 consumption and CO2 production

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

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

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.

Determined using Fowler's method (nitrogen washout)

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

Bohr equation = expiration in which CO2 is diluted from dead space air

V_D = [(P_ACO2 - P_ECO2) / P_ACO2] V_T

when a significant # of alveoli are being ventilated but not perfused (alveolar dead space)

By determination of nitrogen washout and Bohr equation

in healthy lung

can't be measured directly. One must determine anatomical and physiological dead spaces and subtract

Alveolar dead space = physiological dead space - anatomical dead space

That non-functioning alveoli are present and are being ventilated but are not undergoing gas exchange with pulmonary capillary blood

volume of air per minute used to ventilate the physiological dead space

V_W = V_D (f)

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

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.

• 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

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).

compliance is less b/c upper alveoli are stretched more than 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

at the bottom of the lungs

alveoli at upper portion of lung are recruited to ventilation

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

• 1. Regional airway obstruction (asthma) or bronchoconstriction
• 2. Regional differences in compliance (fibrosis)
• 3. Regional differences in dynamic compression (emphysema)

• 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

V_E must increase to compensate for the increase in V_A

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.

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: 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