Michels Phys Flashcards
Tidal volume
(VT): amount of air that enter or leaves the lung in a single cycle ~500 ml (normal breath)
Functional residual capacity
(FRC): volume of gas that remains in the lung at then end of a passive expiration (equilibrium point for lung)
Inspiratory capacity
(IC): maximal volume of air that can be inhaled from FRC
Inspiratory reserve volume
(IRV): volume of air that can be inhaled after a normal inspiration
Expiratory reserve volume
(ERV): volume that can be exhaled after a normal expiration
Residual volume
(RV): volume of air that remains in the lungs after maximal expiration (cannot be measured by spirometry)
Vital capacity
(VC): maximal volume that can be expired after maximal inspiration
Total lung capacity
(TLC): amount of air in the lung after maximal inspiration
PIgas
Fgas(Patm-Ph20)
For PIO2=150mmHg
Method to determine FRC
Helium Dilution
- helium allowed to diffuse into lungs once valve is open
Body Plethysmography
- airtight box, subject inside,close mouthpiece valve at FRC
- subject tries to inhale against closed valve, changing lung by changing volume and box by - changing volume and lowering/raising pressure in lung box
Anatomical dead space
volume of conducting airways (about 150ml)
- define conducting airways
Alveolar dead space
alveoli containing air but not participating in gas exchange
Physiologic dead space
total dead space for the system (1/3 total)
alveolar ventilation
room air delivered to the respiratory zone per minute
VA = (VT – VD)f
VT = tidal volume VD = dead space f = respiratory rate
total ventilation is
tidal volume x respiratory frequency
How can alveolar ventilation be increased
by increasing tidal volume or respiratory volume
Where is expired CO2 derived from
all expired CO2 derives from the alveolar space and none from the dead space.
What is the relationship between CO2 concentration and alveolar ventilation
CO2 concentration is inversely related to alveolar ventilation
Where is ventilation highest
Ventilation is highest at the base of the lung due to gravitational effects.
What factors influence diffusion rate
Pressure gradient
Thickness or diffusion distance
Area of barrier
Diffusion constant
Perfusion limited
: amount of gas transported is limited by blood flow (partial pressure gradient is not maintained)
O2 is perfusion limited
Diffusion limited
: amount of gas that is transported depends on the diffusion process (diffusion will continue as long as the partial pressure gradient is maintained
CO is diffusion limited
Normal uptake of O2 in the Pulmonary Capillary
PVO2 = 40 mm Hg
Under normal conditions, the PaO2 nearly equals the PAO2 by the time the RBC is 1/3 through the capillary bed
Abnormal uptake of O2 in Pulmonary Capillary
Decreasing the PIO2 will result in increased time to equilibrate PAO2 and PaO2 (diffusion equilibrium)
CO2 Transfer
The diffusion for CO2 is approximately 20X higher than O2.
However, the concentration gradient for CO2 is lower than O2 and the reaction of CO2 with blood is complex.
Generally, hypercapnia is rare but there is a potential for elevated levels of CO2 due to thickening of the blood-gas barrier.
Diffusion Capacity
Diffusing capacity of the lung includes the distance that a gas travels across membranes into the blood and the time it takes to react with hemoglobin
Diffusing capacity is measured by the uptake of CO in the lung measured in mL•min-1•mm Hg-1 (assays lung structural features)
Normal diffusing capacity for CO is 25 mL•min-1•mm Hg-1
Pathological Changes that Reduce DL
Diffuse interstitial pulmonary fibrosis - Thickening of the interstitium, alveolar wall and destruction of capillaries Chronic obstructive pulmonary disease - Loss of lung elastic tissue and pulmonary capillaries (decreases surface area and total Hb content) Loss of functional lung tissue - Decreases surface area and Hb content Anemia - Fall in Hb content
Diffusion of gas across a barrier
is proportional to the area of the barrier and the partial pressure difference, and inversely proportional to the thickness
Muscles of Inspiration
Diaphragm
External intercostals
Accessory muscles of inspiration include the scalenus and sternomastoids and the pectoralis
Muscles of Expiration
Passive during rest
Forced expiration can involve the internal intercostals and abdominal muscles
Transmural pressure
Transmural pressure is the pressure measured from inside to out.
Movement of Lung and Chest wall as result of pneumothrax
When intrapleural pressure is equal to atmospheric:
lung wants to recoil and chest wall wants to expand
Lung compliance
Relates to transmural pressure change required to achieve a given change in volume.
How is compliance determined
Compliance is determined by elastic recoil and surface tension.
- elastic recoil of the lung is determined by elastic tissue (elastin and collagen - geometry of meshwork conveys elasticity)
- surface tension is reduced by surfactants
What changes compliance
Obstructive (problems with exhalation) increases compliance.
Restrictive (problems with inhalation, ie fibrosis) reduces compliance.
What are the functions of surfactants
- Lowers surface tension
- Increases alveolar stability
- Keeps alveoli dry
What happens in a diseased state where surfactant is absent
- Compliance is reduced
- Collapsed region of lungs
- Wet regions
Characteristic of lung apex during ventilation
Intrapleural pressure more negative
Greater transmural pressure gradient
Alveoli larger, less compliant
Less ventilation
Characteristics of lung base during ventilation
Intrapleural pressure less negative
Smaller transmural pressure gradient
Alveoli smaller, more compliant
More ventilation
Driving pressure
Is the pressure change from one end of the tube to the other: P = flow x resistance
For the same flow, pressure of laminar flow > turbulent
Laminar flow
resistance is constant irrespective of flow
Turbulent flow
resistance increases w/flow rate
Velocity of gas in the lung
Increase airway in parallel with increase cross sectional area as move down tree
- resistance drops
Increasing velocity as move up tree to maintain flow
- turbulent pattern
Types of resistance in lung
Airway and Tissue
Tissue resistance must be overcome for lung to inflate
Over 85% of total resistance is airway
Factors that determine cross-sectional area of airways
- Lung volume - holds airways open
- Lung elasticity - contributes to tethering effect
- Bronchial smooth muscle tone
Airway resistance and lung volume
As lung volume increases, resistance decreases.
Patients with obstructive disease breathe at higher lung volumes to decrease airway resistance
Chemical factors that Affect Airway Resistance
All act by affecting smooth muscle tone of bronchioles (medium sized airways). Smooth muscle tone is the greatest determinant of resistance of the medium-sized airways.
Bronchoconstrictors
Cause constriction of SM.
Parasymp nervous system (acetylcholine and methacholine).
histamine
irritants (i.e. cigarette smoke)
Bronchodilators
Cause relaxation of SM.
Symp nervous system (NE via B2 receptors).
Agonsists for B2 receptors (i.e. isoproteronol, albuterol).
Increases PCO2 in bronchioles
Transmural pressure during quiet respiration
transmural pressure remains positive during exhalation
Transmural pressure during forced expiration
Engagement of expiratory respiratory muscles raises intrapleural pressure which is often positive
- If intrapleural pressure exceeds airway pressure the transmural pressure becomes negative and the airway will collapse unless supported by SM or cart
- Where ad if airway collapse during a forced expiration depends on the loss of pressure along the airway.
- Pressure lost as resistance is overcome
- Pressure is lost as velocity increases and flow becomes turbulent
Dynamic Airway Compression Upon Forced Expiration
Loss of pressure occurs as gas moves from the alveolus to the mouth
- Increase resistance
- Increase velocity
- Transition from laminar to turbulent flow
Elastic Forces and Airway Compression
Quiet resp: driving force is diff btwn alveolar and mouth pressure.
Airway compression: driving force is diff btwn alveolar pressure and pleural pressure.
Elastic recoil pressure is the diff btwn alveolar and pleural pressure.
FEV/FVC
Normally around 80%
Obstructive (increased airflow resistance): drops as FEV decreases
Restrictive (increase elastic resistance): increases as both FEV and FVC decrease disproportionately
Pulmonary pressure
Can be altered by
1. Recruitment
2. Distension
Recall pulmonary arteries contain relatively little smooth muscle- ensures arteries are highly compliant
Behavior of Alveolar and Extra-alveolar Vessels
Pulmonary capillaries- exposed to alveolar pressures and have the propensity to collapse when alveolar pressure exceeds capillary pressure
Extra-alveolar vessels- Include pulmonary arteries and veins; diameter increases when lung tissue expands
Do contain some smooth muscle- tone can be effected by pharmacologic agents
Vasodilation of pulmonary capillaries- acetylcholine, isoproterenol, NO, prostacyclins
Vasoconstriction of pulmonary capillaires- serotonin, histamine, norepinephrine
Pulmonary Vascular Resistance (PRV)
Pulmonary Vascular Resistance- normally very low
- Recruitment and distension of pulmonary capillaries can lower the pulmonary vascular resistance
- Exercise
- Increased pressure
- gravity
- PVR Increases at high and low lung volumes
- Increases with alveolar hypoxia due to hypoxic pulmonary vasoconstriction
Chemicals and PRV
nitric oxide (NO) and prostacyclins cause vasodilation
Viagra: a selective inhibitor of cGMP-specific phosphodiesterase type 5 (PDE5)
Capillary recruitment and distension
Recruit in parallel
Distension increases capillary diameter
Both recruitment and distension usually occur at the same time
Changes in pulmonary resistance with changes in lung volume
Resistance increases at high lung volumes due to increased alveolar pressure, and stretching of the capillary wall.
Diameter increases with expanding lung tissue and decreases at low lung volume.
Hypoxic Vasoconstriction
Note it is alveolar PO2 that controls hypoxic vasoconstriction.
An example of hypoxic vasoconstriction is travel to high altitude where the PIO2 is less.
Mechanical influences that increase PVR
Increased lung volume (above FRC) - lengthening and compression of pulmonary caps Decreasing lung volume - compression and loss of traction of extra-alveolar vessels Increased interstitial pressure - compression of vessels Increased blood viscosity - increased resistance
Mechanical influences that decrease PVR
Increased pulmonary artery pressure, left atrial pressure, pulmonary blood volume, cardiac output
- recruitment and distension
Gravity
- recruitment and distension due to hydrostatic effects
Positive-Pressure Ventilation
Impact on PVR: Increases PVR Increased alveolar pressure - compression of alveolar vessels Positive intrapleural pressure - compression of extra-alveolar vessels; decreased in pulmonary blood flow
Endogenous Chemicals and Effects on Vascular SM (Extra-alveolar vessels)
Vasoconstrictors→ serotonin, histamine, norepinephrine
- Increases vascular resistance
Vasodilators→ acetylcholine
- Decreases vascular resistance
Causes of pulmonary edema
Increased cap hydrostatic pressure
- MI, mitral stenosis, fluid overload, pulmonary veno-
occlusive disease
Increased cap permeability
- Inhaled or circulating toxins,sepsis, radiation, O2
toxicity; ARDS
Reduced lymph drainage
- Increased central venous pressure, lymphangitis
carcinoma
Decreased interstitial pressure
- Rapid removal of pleural effusion or pneumothorax,
hyperinflation
Decreased colloid osmotic pressure
- Overtransfusion, hypoalbuminemia, renal disease
Uncertain etiology
- high altitude, neurogenic, overinflation, heroin
Control of circulation
- Hypoxic vasoconstriction limits pulmonary blood flow with PIO2 is reduced (hypoxic vasoconstriction limits pulmonary blood flow in fetuses which is quickly reversed upon delivery)
- Nitric oxide (NO) is an endothelium-derived factor that relaxes pulmonary vessels and capillaries
Endothelins are endothelium-derived factors that constrict pulmonary vessels and capillaries. - Sympathetic stimulation (ex. Norepinephrine) acts as a vasoconstrictor.
Metabolic functions of Pulmonary Circulation
- Angiotensin I is converted to angiotensin II by angiotensin-converting enzyme (ACE) found on the surface of capillary endothelial cells
- Bradykinin is inactivated by ACE in the lung
Serotonin is inactivated by uptake and storage in the lung - Prostaglandins E1, E2, and F2α are inactivated in the lung
- Norepinephrine is partly taken up by the lung
- Other substances such as epinephrine, prostaglandins A1 and A2, angiotensin II, and vasopressin are not metabolized by the lung
