CARDIOPULMONARY PHYSIOLOGY (Resp 210) class notes Edited by CK Blaine, Fall, 2000
Copyrighted by Catherine K. Blaine and Francis M. Alsis, September, 2000 All rights reserved. Duplication without permission from the authors is forbidden.
Definitions/Physiological Math
Mechanics of VentilationSummary/Review Compliance and Resistance
Tests of Small Airways Disease
Diffusion vs. Perfusion Limited Gases
Pulmonary vs. Systemic Circulation
Hypoxemic vs. Hypercapnic Failure
OxyHemoglobin Dissociation Curve
Function of the lung is to arterialize the venous blood i.e., to provide oxygenation while removing carbon dioxide.
Structure of the lung-Trachea-R and L Mainstem bronchi-Lobar Bronchi-Segmental bronchi-Sub-segmental Bronchia-Bronchioles-Terminal bronchioles-Respiratory Bronchioles-alveolar ducs-alveolar sacs-alveoli.
Terminal bronchioles -the last division (16th) of the conducting airways. Respiratory bronchiole-first division involved in gas exchange.
Conduction zone-first 16 divisions of airways from trachea to terminal bronchioles: no gas exchange-Bulk Flow.
Respiratory Zone-last six to seven divisions (17-23) -External respiration or gas exchange takes place via diffusion.
Respiration: External-Alveolar Capillary level
Internal-Tissue/Cellular level
Ventilation: mechanical movement of air into and out of the lungs in a cyclic fashion. Inspiration and Expiration are under automatic (Brainstem) and Voluntary control (cerebral input).
Diffusion: movement of gas from areas of higher partial pressure to an area of lower partial pressure.
Alveolar-Air Equation: 2 components
1. P102 = [(PB-PH20) x FI02}
[(760 nun Hg-47mm Hg) x.2 I]
P102 = 150 min Hg
2. PA02 -must is lower than P102 because of the now significant increase in PAC02 (Where does this increase come from?)
PA02 = PI02 - (PaCO2)
R = (.8)
r is the respiratory quotient amount of C02 produced by the body in one-minute amount of 02 consumed by the body in one minute
200 ml = .8 (normal protein diet only) 250 ml In the hospital as most patients are on CHO diets, r =1, thus the equation is made simpler.
Important Math Fact -Dividing by .8 is the same as multiplying by 1.25
PAC02 =n PaC02 (Why?)
Thus PAC02 =n = 40mm Hg, thus
PA02 = P102 - (PaC02)
---------------
r 150 - 40
---------
.8
=100 mm Hg
A-a gradient = Alveolar to Arterial gradient =P(A-a)02 or D(A-a)02 = PA02 - Pa02 Exon.21 (l00mmHg-90mmHg) = 10mmHg Ex. On 100% A-a 02 difference is 90 nun Hg
A Good Rule of Thumb-The (A-a) 02 difference should be 10 mm Hg less than the F102 in a normal patient.
In disease the (A-a) 02 difference increases!
You can't compare A-a 02 differences at different F102s!
At the same F102, a larger A-a difference means the patient's disease is getting worse, while a smaller A-a difference indicates that the patient is improving.
Anatomic Dead Space-(VD anat.) gas or amount of VT not involved in gas exchange. I cc/lb. up to 200 cc. If a patient weight more than 200 lbs., VD Anat. is assumed to be 200 cc's (example Morbidly Obese patients).
Physiological Dead Space (VD phis.)Volume not involved in gas exchange including anatomical dead space. In a normal person, the anatomical dead space approximately physiological dead space-Why?
What about in a hospital patient?
Mechanical Dead, Space-Volume of rebreathed gas in a patient circuit, e.g., in a ventilator circuit, mechanical dead space is the volume of the y-connector. Each six inches of flex tubing added to the circuit between the wye and the patient adds 50 cc of mechanical dead space.
Alveolar Ventilation = VT - VD anat. or phis.
Dead Space Ventilation-2 calculation methods
1. Fowler's method -anatomical dead space-Nitrogen washout (volume recorder and N2 meter)-Patient breathes 100% 02-as patient exhales. Initially N2 % is 0. It then gradually rises up to an alveolar plateau.
2. Bohr's Equation-measure physiological dead space. Measurement of anatomical dead space plus a portion of alveolar space that does not take place in gas exchange. In disease, physiological dead space increases.
VD = PAC02 - PEC02 =PaC02 - PEC02 Takes into account the ability
----------------------------------
VT PaC02 PasC02 of the lung to eliminate C02, thus
in disease, the impairment of C02 elimination will alter VD/VT
PaC02-arterial blood gas results PEC02-capnograph to measure end tidal C02 or collect gas in a Douglas bag x 3 minutes and measure sample in ABG machine.
Normal VD/VT =.33 (.25-.4). If a patient has a VDNT ratio> =.6, this indicate he/she should be on a ventilator.
Inspiration: active process requiring work of breathing, a slight increase in negative pressure to inflate the lungs.
Expiration: normally passive due to the elastic recoil of the lungs. Examples of when expiration is active-exercise, COPD.
The respiratory muscles accomplish Work of Breathing.
A. Inspiration
1. Diaphragm : 2 hemi-diaphragms. Attached to lower ribs in a circumferential manner. Contraction occurs via stimulation of the phrenic nerve-origins cervical 3,4,5. Neck injury (example-MVA or diving accident) may compromise diaphragmatic function. Contraction causes an increase in the vertical diameter of the thorax. I t also causes an increase of the transverse thorax diameter at the lower ribs. Together these increases cause an increase in intra-thoracic volume.
Movement is approximately I cm in tidal breathing but as much as 10 cm when necessary (heavy exercise, ventilatory failure).
Sniff test -is used to measure paradoxical movement of the diaphragm with paralysis.
Relaxation- dome shaped with right hemidiaphragm. higher than left due to the liver.-Clue on X-ray for Atelectasis.
1. External Intercostal Muscle attached to the lower ribs' surfaces and the upper side of the rib below. Contraction causes the rib cage to be lifted up and out creating an increase in the A-P diameter of the chest. This also increases the intra-thoracic volume.
Innervation is via the intercostal nerves, which arise from the CNS at the same level. e.g., at the 4th intercostal in the spine, an intercostal nerve arise that goes to the fourth intercostal muscle. Loss of intercostal movement does not significantly alter tidal ventilation as long as the diaphragm is working.
A. Expiration
I. Abdominal muscles-Rectus Abdominus, Internal Oblique, External Oblique, Transervus Abdominus
Contraction of abdominal muscles causes the abdominal contents to be forced up and in, causing the diaphragm to be forced up, lowering the intra-thoracic volume.
2. Internal intercostals-attachment is the same as externals, causing the ribs to be pulled down and in, reducing intra-thoracic volume.
3. Accesso1y Muscles-primarily involved in inspiration during respiratory disease.
Diffusion -Gas must cross blood-gas barrier or alveolar capillary membrane.
Fick's Law-The amount of gas that can penetrate a barrier is directly proportional to the following:
Diffusion is directly proportional to solubility but inversely proportional to the molecular weight, i.e., the more a molecule weights, the less its diffusion.
3. Pressure drop across the barrier -the driving pressure-(P I -P2). Gas moves from an area of higher pressure to one of lower partial pressure. The greater the driving pressure, the greater the diffusion.
Diffusion is inversely proportional to:
2. Molecular Weight -see above (Diffusivity constant)
Fick's Law: V gas
a ( Area x D(P1-P2)--------------------------
Thickness D= Sol.
Ö
M.W.
The lung is ideal for diffusion-alveolar capillary membrane's surface area is 50-100 meters, thickness = 1/2 g (micron).
Elastic Properties of the Lung
Lung expansion is in relation to the transpulmonary pressure. Transpulmonary pressure is the difference between the pressure within the lung and the pressure surrounding the lung
Initially, a great transpulmonary pressure is needed to increased lung volume. Volume change improves with increase in transpulmonary up to a point of full expansion. (balloon inflation).
At any given pressure, there is always a greater volume on expiration than at the same point and pressure during inspiration. This phenomenon is called hysteresis of the pressure/volume curve.
Transpulmonary Pressure change will cause volume change regardless of the cause of the pressure change, if it changes from 0 to+10 or from -10 to 0, it doesn't matter, its still an absolute change of 10.
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Work of Breathing
: Related to lung compliance and airway resistance.
-------
Pressure
Normal Compliance of the lung is 200 n-A/cwp or .2 L/cwp However Normal Compliance of the Lung and Chest Wall (what we must measure clinically) is 100 ml/cwp or .1 L/cwp. Most ventilator patients have a compliance of between 30-50 ml/cwp. Decreased compliance indicates that the lungs are stiff or difficult to inflate, (ex., pulmonary edema, and scar tissue), while increased compliance means the lungs are easy to inflate(ex., emphysema).
Factors influencing compliance of the Lungs
A. Lung tissue
1. Elasten fibers of the lung. Fibers that stretch quite easily.
2. Collagen -does not stretch easily. The more collagen in the lung, the more difficult it is to stretch.
A. Surface tension Forces
The cohesive (attractive) forces between adjacent water molecules will be stronger than cohesive forces between adjacent water and air molecules. In the lungs the surface is liquid lined, and the air within the alveoli causes a pressure difference that would cause the alveoli to collapse. During ventilation, these surface tension forces must be overcome in order to inflate the alveoli.
Because the lungs are a series of alveoli, the surface tension forces in each alveoli effects the others. La Place's law explains this.
La Place's Law-If surface tension forces (T) remain constant in adjacent, the pressures within the alveolus is dependent on the radius of the alveolus.
P=4T r = 2 (large alveolus) P = 4T =2T
-- ----
r 2
P=4T r = 1 (small alveolus) P 4T =4T
--- ----
r 1
Therefore, the small alveolus (r = 1) has a greater pressure than the larger one, and the smaller alveolus would collapse and fill the larger alveoli. If this were to occur, this would create Atelectasis. In normal lungs, however this is not permitted to occur because of the presence of SURFACTANT, a product of the Type II alveoli pneumocytes, which reduces alveolar surface tension caused by the air-liquid interface, thereby stabilizing the alveoli. Surfactant is dipalmitoyl phospholipid.
Advantages of Surfactant
1. Surface tensions are lowered increasing the compliance of the lung. This results in decreased expanding pressures which means less Work of Breathing (wob). 2. Adds to the stability of the alveoli preventing the emptying of smaller alveoli into larger ones, thus prevents Atelectasis. 3. Helps to keep the alveoli dry, i.e., prevents transudation of fluid into the alveoli.
Artificial Surfactants on Market
1. Exosurf- Burroughs Welcome
2. Survanta-Ross
3. Infasurf-Forrest Medical
The newer surfactants are more chemically like the original as they contain many of the proteins attached to natural surfactant.
Another factor, which contributes to the stability of the lungs, is the geometric arrangement of the Alveoli. Adjacent alveoli tend to keep each other open due to their shared interstitial tissue and the Pores of Kohn. This mutual support is called INTERDEPENDANCE.
D. Compliance of the Thorax (Chest Wall)
The elastic nature of the chest wall has a tendency to spring out. This, in conjunction with the elastic recoil of the lungs, whose tendency would be to collapse, creates a normally negative intrapleural pressure. If this negative pressure is abolished, e.g. in pneumothorax, the lungs will collapse upon a drop in intrapulmonary pressure (Inhalation). Refer to West's Respiratory Physiology. (page 102 Figure 7.11) -for explanation of resting levels of chest wall, lungs and chest wall and lungs.
-resting level of lungs, alone- minimum volume (less than residual volume)
-resting level of the chest wall- normal 80% of TLC -resting level of lungs/chest wall is FRC' therefore the FRC is the equilibrium volume when the elastic recoil of the lung (inward) is balanced by the normal tendency of chest wall to spring out.
In diseases contributing to stiffness of the lungs, the following occurs to offset decreasing compliance:
This allows the patient to maintain an adequate minute ventilation with a checked increase in the patient's work of breathing. This check is not an indefinite one, however, and most likely will lead to ventilatory failure.
II. Resistance to airflow within the lungs, also contributes to the amount of work necessary to ventilate the lungs.
In order for the flow to occur, a pressure drop must occur within the tube,
therefore, R=
D P-----
D
V (flow)
Types of Flow
1.) Laminar flow: molecules move linearly, parallel to one another. Less pressure to move air = less W of B.
2.) Turbulent flow: non-linear, swirling flow. More pressure to move air = greater W of B.
3.) Transitional: a combination of 1 & 2, due generally to numerous bifurcation's of the airways. Most flow in the lungs is of this type.
Poiseuille's Law : flow is related to the pressure times a constant (
P ) times the 4th power of the radius of a tube, divided by 8 times the viscosity and length of the tube.
V= P
P r4-----
8nl Rearranged to show Resistance (R) relationship:
R = 8nl
--------
P
r 4V = flow
P= pressure difference
R = radius
N = Viscosity
1= length of tube
P
= the constant
Most flow factors in this law are constant with the exception of the radius. If radius decreases, resistance increases, e.g., if radius is 1/2, R increases 16 fold ( =2x2x2x2=16) Pressure is greater when resistance increases.
Therefore W of B increases with turbulent flow and increased Resistance (increased P). W of B decreases with laminar flow and decreased Resistance (decreased P.).
Characteristics of flow depends on Reynold's number:
Re= 2rvd
--------- r= radius d= density
n n= viscosity v= velocity
When Resistance is high -flow is more likely turbulent. e.g. Trachea- Re-- >2000 due to the velocity of flow and airway is large. Average diameter of trachea- 18 mm.
When Resistance is low -flow tends to be laminar, e.g., Small Airways- Re = <1 due to low velocity of flow and airway is small. Average diameter of terminal bronchiole = 0.7 nun.
Because most airways are transitional, most airways have a Resistance between 1 and 2000.
Resistance
Factors Controlling Resistance - by influence on the diameter of the airway.
A. Volume - as lung volume increase, the diameters of the airways increase or dilate therefore increasing radius causing decreasing Resistance. Resistance therefore decreases initially during inspiration. Conversely, Resistance increases during exhalation and may lead to an obstructive process, e.g., in COPD.
B. Tone of Bronchial Smooth Muscle- Tone is under autonomic control. Drugs, e.g., alter tone. Reflex changes also cause changes in tone. An increase in tone causes bronchoconstriction or narrowing of the bronchi, thus increasing airway resistance resulting in increased W of B. Bronchodilators cause a decrease in tone, allowing relaxation of smooth muscle and increase in airway diameter.
C. Density and Viscosity of Gas-less dense or viscous gases cause a decrease in resistance.
D. Diseases causing an increase in secretion production of increased edema decreased airway diameter. *Note CPT to remove secretions.
E. Dynamic Compression
1.) Flow- Volume Relationships
A-Normal
B-Bad Effort
C-Restrictive
D- Moderate Obstructive
Regardless of curve, the terminal portion of curve is effort independent. Why?
This phenomenon is a result of dynamic compression of the airways causing a limitation of flow. At some point during forced exhalation, pressure surrounding the airways becomes greater than pressure within the airway causing airway collapse- limiting expiratory flow. This dynamic compression causes an increase in R during exhalation.
2. Tissue Resistance- tissue viscous Resistance. Small amount of resistance met by virtue of tissue mass and structure.
Muscles of Ventilation cause a greater negative drop in intrapleural pressure with a subsequent drop in intrapulmonary pressure causing lungs to inflate. Pressure change needed to cause volumes to increase is related to Compliance and Resistance. Therefore, any decreased C or increased R, due to disease, will cause an increased W of B.
Review of Compliance normal .2 I/cmH20
P= 30cmH20 V= 500n-A
500/30 .017 l/cwp) = decreased compliance
e.g. Pulmonary Fibrosis. ARDS. Due to decreased compliance, W of B increases in these conditions.
Review of Resistance: Airway resistance (primary)and tissue resistance (small) must be overcome for ventilation to occur.
Radius- r4- resistance increases on exhalation because elastic recoil causes a decrease in radius of airway.
R = D P (P1-P2)
---- -------
D
V or (flow)
Increased resistance also increases W of B because additional pressure work is needed to move adequate volume.
Therefore, W of B increases due to increased resistance and/or decreased compliance. In addition, conditions such as emphysema, characterized by an increased compliance, also cause problems in that increased dynamic compression occurs because of active exhalation. Active exhalation is necessary because of the decreased elastic recoil of the lungs. This premature collapse of the airways results in air trapping. Increased W of B in this case due to increased airway resistance caused by dynamic compression. N.B. - aging process also causes increased compression of airways due to decreased elastic recoil.
Examples of conditions contributing to increased airway resistance
e.g. Asthma- increased resistance of both inspiration and expiration
Emphysema- due to dynamic compression
Cystic Fibrosis- due to increased secretions
Chronic bronchitis- increased secretions, inflammation
Bronchogenic Tumors- most common cause-smoking
Bronchospasm-allergens, chemicals
Work = Force x Distance (physics)
W of B = Pressure x Volume (respiratory application) (Curve page 115, West)
OAECDO -area indicating W of B to overcome lung compliance
AECBA -additional work necessary to overcome Resistance
OABCDO -total of W of B
AECFA - work to cause exhalation. Does not normally require added W of B
Decreased compliance would require more pressure to achieve same volume therefore indicating increased W of B.
Increased inspiratory resistance requires even more work (hatched area) Area to left of graph indicates increased work due to expiratory resistance (Xed area.)
Compliance problems primarily indicative of a restrictive disease in the lung parenchyma
Airway Resistance problems primarily indicative of an obstructive process in the airways
Oxygen Consumption
Lung Ventilation (muscular work) responsible for approximately 5% of 02 consumption. Increased W of B creates an increased 02 demand to ventilate, as much as 40% or more of Total 02 consumption therefore W of B can also be measured in terms of oxygen consumption.
Not normally even, in upright position. Ventilation preferentially distributes to the bases Zone 3- West) Why?
1. Intrapleural P is not uniform throughout pleural space.
e.g. at apex of lung Intrapleural P= - l0cmH20 at bases is approximately - 2.5 cmH20 (this -2.5 due to greater P below lung base)
At apex, at FRC, the transpulmonary P is the difference between 0 & -10 therefore 10 cml-120, At base, at FRC, the transpulmonary P is the difference between 0 & 2.5 therefore equals 2.5cmH.20,therefore at rest, the basal alveoli are less expended than the apical alveoli (10). The basal alveoli have a greater capacity to expand, resulting in increased distribution of ventilation during inspiration from resting level (FRC.)
If patient were to inhale from RV, Ventilation would be preferential to the apices, because bases would have a + intrapleural P due to airway closure with exhalation to RV. This preference would continue until volumes reach FRC level, then preference would become normal, that is, first to the bases, then up to the apex.
Summary
From RV, ventilation, initially is greater to the apex of the lung.
From FRC (normal), ventilation is initially greater to the bases.
Significance is seen with discussion of V/Q ratios. Alteration of V/Q in disease, equates to alteration of the arterial blood gases.
e.g. Restrictive disease causes decreased volumes on inspiration, therefore decreased volume, creating an abnormal V/Q ratio and altered ABG's.
Obstructive disorders also lead to reduced volumes, again altering V/Q and ABG's.
Volume alteration with obstruction depends on severity of disorder creating uneven distribution of ventilation. Obstructive diseases, because of the associated uneven distribution of ventilation, more often lead to V/Q abnormalities than restrictive disorders.
-Reasons for use: 5 major categories
A. Medical Diagnostics
1. Diagnostic-determine disease-restrictive vs. obstructive
2. Determine extent or severity of the disease
3. Follow course of a disease. Serial PFT's. Is therapy helping?
4. Evaluation of Pulmonary Symptoms
5. Evidence of abnormal CXR, but patient is asymptomatic
B. Surgical Diagnostics
C. Disability Evaluation
1 . Evaluation by e.g. Medicare to determine disability by virtue of pulmonary disease.
2. Evaluations also are done to determine possibility of rehabilitation.
D. Public Health- Epidemiology
Survey of large populations for statistical data.
E. Research - other than Epidemiology
Essentially, PFTs are performed to determine whether the patient's disorder is obstructive, restrictive, or a combination.
Obstructive -airway resistance disorder is determined by a decrease in flow rates.
Restrictive - compliance disorder is determined by a decrease in all volumes
Obstructive Restrictive O&R
FVC ¯ or N (mild) ¯ ¯
FEVI ¯ or N (mild) ¯ ¯
FEV 1%/ FVC ¯ N ¯
FRC or N ¯ ¯ N (low)
Depends on severity
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Normal FRC=40% of TLC
FRC & RV not determined by normal spirometry. Three techniques generally employed.
1. Nitrogen Washout - Open Circuit - Uses normal existence of N2 in lung. Patient breathes 100% 02, over a period of time (up to 7 minutes), at tidal volume. Exhaled air is analyzed during collection. Initially, N2 levels are high, but with washout, N2 levels are zero on exhalation. Measures gas communicating with airways.(page 6 West)
2. Helium Dilution - Closed Circuit - Helium used because it is inert and not absorbed into the pulmonary capillary system. (page 9 West)
% Helium is introduced into the closed circuit. Patient breathes into this closed system At test's end, helium is in lung and spirometer and a final helium % is read.
The initial and final helium readings, in conjunction with volume in the spirometer at the beginning of test will allow FRC to be calculated.
3. Plethysmography - 2 types of plethysmographs(body boxes)( page 12 West)
1. Pressure Boxes D P
2. Volume boxes D V
Here, FRC is actually the Thoracic Gas Volume and the body box measures true thoracic gas volume in that it measures the gas that communicates with the airways plus that gas which does not ( e.g. gas trapped in bullous area.) In normal, healthy lungs, the FRC
measured by the pletysmograph will be equal to that measured by He or N2. In disease, e.g. COPD, cystic or bullous disorders, the FRC measured higher (more accurate) than FRC measured by He or N2. Therefore, plethysmograph is more accurate in presence of disease in that it measures thoracic gas volumes.
Patient placed in box, and breathes through a mouthpiece, for a few minutes until pressures stabilize in box. A shutter, within mouthpiece, is the closed so that patient must exhale (pant) against this closed shutter. At this point, i.e. at period of no flow, pressures are measured at the mouth and within box. Employing Boyle's Law, (T constant) allows FRC to then be calculated.
1.Maximal Mid-Expiratory Flow Rate- Flow rate during the mid-portion of the expiratory curve. Calculation done one time-volume curve.( page 47-52-Ruppel)
2.FEF 25-75- flow rate, again, during mid-portion of expiratory phase. Done on flow volume loop or time-volume curve.
FEF 75-85-very small airways
3. Closing Volume- used for determination of early, small airway disease in light of normal spirometry and flow volume loops (MWFR &FEF 25-75). Single-breath nitrogen washout, started from Residual Volume. Beginning at RV, patient inhales 100% 02 up to TLC. During exhalation, initially N2 is 0, then gradually increases. (Ruppel, pp. 83-87)
Phase I: Pure dead space
Phase II: Dead space and alveolar gas
Phase III: Alveolar gas
Phase IV. Apical alveolar gas, because basal airways have closed, Apical alveoli have greater % of N2 than bases, because during inhalation of 100% 02, most 02 goes to bases, less to apex, because of distribution pattern.
In disease, CV is greater, i.e., occurs sooner than normal. Normal is 10% of volume i.e., 10% of VC. If greater, indicates premature small airway collapse.
Increases with age, obstructive disease and even with restrictive disorders, e.g., in fibrosis/obesity.
Closing Capacity - closing volume plus the residual volume. Usually expressed as a % of the TLC. Normal- 30%.
4. D V max 50- (Ruppel, page 55 and 61)maximum flow at 50%of the vital capacity. In disease or disorders affecting small airways, the AV max 50 is decreased as compared to predicted normals. Patient is allowed to breathe a 20% 02- 801/o helium mixture, decreasing the resistance met in medium and larger airways. In normal individuals, you would expect a 40-50% change in the AV max 50 when breathing this mixture. In small airways disease, the AV max 50 would be less than 40-50% change. This test could also be applied to disorders of large or medium airway involvement, e.g. Asthma. In this instance, the AV max 50 would be normal or greater because resistance in large airways is overcome by 02-He mixture.
5.Visoflo -(page 111, figure 7.17) point on two curves when flow volume loops come together. In small airway's disease, the volume of isoflow occurs sooner.
6.Frequency Dependence Compliance
Compliance = D Volume
D Pressure
How can compliance be measured in the laboratory setting? ( If plethysmograph unavailable)
1. Volume- patient -spirometer system
2. Pressure - measure esophageal pressure with esophageal balloon intrapleural pressure. Catheter, with balloon, introduced via nose into esophagus. Catheter attached to pressure manometer. Patient instructed to inhale from FRC at 300ce intervals (approximately) hold breath, with glottis open, taking pressure readings at each volume change. Compliance is then calculated for each interval.
In Frequency Dependence Compliance, compliance is measured in much the same way as just described, but the patient is asked to breathe rapidly. In normal lungs, compliance's at slow and fast rates should be close, but in small airway disease, this test, (which is actually a dynamic test.) the measured compliance would be decreased. This test actually measures resistance in the small airways. Therefore, compliance measured dynamically, in small airway's disease, will be considerably less than compliance measured statistically. (Normally C dynamic is approximately 80% of C static.). When breathing at 60 breaths/min, if C is less than 75% of value at 20 breaths/in, small airway's disease is present.
7. Resistance
In laboratory, esophageal balloon can also be used to measure resistance. R is more easily measured by body plethysmograph. ( R page 71)
Normal R = .6 to 2.4 cmH20/ I /see
Flow, in testing, is measured by pneumotachograph -2 types.
A. Pressure Transducer- element in device to creates a fixed resistance. P. measured before resistance and after resistance, and change of P is used to calculate flow.
B. Temperature Pneumotach- heated wire, which will cool with flow. Device will attempt to keep wire at constant temperature. The energy necessary to maintain temperature is directly related to the flow rate.
Tests of Pulmonary Mechanics
1. FVC 6. F-V loops
1. FEV timed 7. V of Isoflow
3. FEF 200-1200 8. V max 50
4. FEF 25-75 9. MVV-page 64
5. PEFR 10. Compliance
11. R & GAW (conductance)-Conductance is the reciprocal of R
- comparison of flow to volume change, requiring an X-Y recorder to give flow in 2 directions (expiration, inspiration). Test begun at RV to TLC to RV.
Refer to Handout, for F-V loop patterns
1. Single Breath N2 Washout - To determine gas distribution, Phase III of the curve is examined. 500cc are studied, after the first 700 cc have been exhaled. If gas is evenly distributed, the normal N2 is 1.5-3%. ( Ruppel, page 84 and 750-1250)
If N2 is increased 3% indicates maldistribution of gas. In COPD, e.g., N2 is greater than 10%.
2. Seven minute N2 Washout- Patient breathes 100% 02 for 7 minutes. At the end of 7 minutes, patient performs a forced exhalation and N2% in end sample is analyzed. Normal is less than 2% in end sample. In maldistribution , N2% is greater than 2%. (19889 IDI-Index of Distribution of Ideal Gas) ( Ruppel, page 88)
Distribution index (slope line): Ideal - 1
Normal - 1.8
Abnormal- 3.4
3. Inhalation of radioactive Xenon, with lung scan (Ruppel, page 90-94) (V/Q scans--99MTEC)
Diffusion- REVIEW
Fick's Law - Amount of gas that can penetrate a barrier is proportional to several factors:
1. Area of barrier - if area increases, the amount of gas that diffuse is increased. (A-C membrane destruction in emphysema = decreased area therefore decreased diffusion)
2. Diffusivity constant- related to the solubility of and the square root of the molecular weight of a gas. D = Sol
þ
M.W.
Diffusion is proportional to solubility. Diffusion is inversely proportional to M.W., i.e. the larger the molecule, the less is its Diffusivity.
1.Pressure drop across barrier (P I -P2)- driving pressure. Gas moves from an area of high to lower partial pressure. The greater the driving P, the greater the diffusion
2. Thickness of barrier- inversely proportional. The thicker the barrier, the less the diffusion. The thinner the barrier, the more the diffusion.
Fick's Law - Vgas = A.D.(P1-P2) D=Sol
T þ M-W.
The lung is the ideal for diffusion - alveolar-capillary membrane, e.g., area 50-100 meters
Thickness = 1/2 m
Diffusion Limited vs. Perfusion limited - gases act somewhat differently in their ability to enter blood, e.g.:
N20- diffuses readily into blood because there is no partial pressure in venous; blood but on inhalation of N20, there is a partial pressure in alveolus. There is a driving pressure PAN20--+-+PaN20, and diffusion occurs until the gas reaches equilibrium This occurs quite rapidly as N20 does not bind with Hb but rather dissolves in plasma causing a rapid rise in PaN20. The only way, therefore, to increase N20 levels in blood is that perfusion would have to increase. Therefore, N20 is perfusion limited.
C0- very little in blood (negligible). If CO is inhaled, it will readily diffuse because if driving pressure (0 in blood, increased in alveolus). PaCO will not rise rapidly, however, because CO attaches immediately to Hb with very little dissolving in plasma. Equilibrium is never reached, driving pressure remains significant and diffusion is continuous. If one wanted to increase the amount of CO diffusing across A/C membrane, the A/C membrane would need to be altered to increase diffusion. Therefore CO is diffusion limited.
02 - does have an affinity for Hb, but some does dissolve in plasma, Blood entering lung has Pa02 if 40, alveolar 02, e.g., =100. Therefore driving pressure exists and diffusion will occur with equilibrium occurring in .25 sec. Therefore, in healthy lungs, 02 is perfusion limited, because the only way to increase 02 diffusion would be to increase blood flow or perfusion. In disease, equilibrium takes a much longer time because of an abnormal A/C membrane and therefore in disease 02 is perfusion and diffusion limited.
This helps to explain dyspnea on exercise, in mild disease, in that, with exercise, blood velocity increases not allowing ample time for equilibrium to occur, with a subsequent drop in Pa02, even in light of a normal Pa02 at rest.
Fick's law can further be applied to a test for measuring the diffusing capacity of the lung.
1. Single breath method . Initially patient with a known amount of Helium breathes in CO% of .3% (for FRQ. Patient holds breath for 10 seconds, then patient exhales and CO% is again measured. The difference between what was inhaled and then exhaled is the amount that diffused. ( Ruppel, page 98-99)
Normal = 25 ml/min/-mmHg (STPD) - less that 25 indicates that inability of gas to diffuse across the alveolar/capillary membrane.
2. Steady state method- several, as many as 12 breaths taken to create an equilibrium if Cardiac output is normal. (CO%=O.1-0.2%) Filey method for steady state.
Problems other than an altered A/C membrane- can cause an abnormal DLC
1. Anemia- causes a decreased DLCO therefore know patient's Hb count so that correction factors can be used in calculation.
2. Pneumonectomy- decrease in area for diffusion
3. COPD- small airway disease which alters distribution of gas. Hampering CO from reaching alveolar level. Causes a decreased DLCO.
4. Large tumors
5. Hypoventilation- PaC02, ¯ Pa02
6. Altered Hb or Hct levels
7. Body Position-Standing/Sitting vs. Supine
8. Altitude
Diffusion defects will ultimately cause hypoxemia. But because of its solubility (C02 diffused approximately 20X faster than 02), C02 will diffuses even with diffusion defects. Therefore, C02 retention is not generally a result of a diffusion problem. Diffusion will result in decreased Pa02 however. If diffusion is severely impaired and does lead to a rise in PaC02, the peripheral chemoreceptors will be stimulated to increased ventilation. A chronic adjustment to gradual increases in C02 leads to blunting of this response.
Blood Flow (Q) - significant differences exist between the pulmonary and systemic circulatory systems.
Pulmonary Circulation
Low resistance- due to pressures within pulmonary system and also because of the elastic properties of the pulmonary vasculature.
Systemic Circulation -High resistance- due primarily to the distance required to pump blood and the more rigid structures of the arterial systemic vasculature.
Illustration of the pressures found within the pulmonary and systemic circulatory systems.
Vascular Resistance = Input pressure - Output pressure
Flow (cardiac output)
Pulmonary Vascular R = 15 (mean PA pressure) - 5 (LA pressure)
6 liters
PVR= 10/6 = 1.7 mmHg/l/m (may also be expressed as dynes/second)
- measured by Swan-Ganz catheter advanced into the pulmonary artery, wedged and balloon deflated.
PAWP or PCWP or PAOP - wedge pressure - indirectly measures LA pressure. When catheter is wedged, measures back pressure in pulmonary circulation (under static conditions) caused by pressures down line. Therefore, if LA pressure increases, back pressure will increase and will be measured as an increase in the wedge pressure reading.
Swan-Ganz- inserted into the sub-clavian or internal jugular vein (any vein). Catheter is open at the tip for pressure monitoring, with balloon attached. With balloon inflated, it floats through PA into RV into PA and wedges. Wedge pressure is an indirect measurement of left atrial pressure.
Using the thermo-dilution method, the Swan-Ganz can determine CO.
Pulmonary Hypertension - characterized by an increased PAP. Chronically, this will lead to Cor Pulmonale because of the failure of RV due to increased PAP, resulting, clinically in distension of neck veins, pedal edema, etc
Systemic Vascular R = 100 (Mean aortic P) - 2 (RA pressure)
6 liters
SVR=98/6=17mmHg/l/m
Therefore SVR is approximately 10 times greater than PVR
Increased SVR leads to increased work of LV. Which, with failure = CHF
Poiseuille's Law also has a direct relationship to blood flow (radius) and resistance. If diameter decreases, resistance will increase.
Difference between pressure within vessel and outside vessel = TRANSMURAL PRESSURE
Vasculature
To understand PVR and Q. one needs to understand the 2 types of vessels within the Pulmonary Circulation
Smaller vessels-less than 50m in size. Called Alveolar Vessel known as alveolar capillaries. Factors influencing the caliber of alveolar vessels is alveolar pressure. The higher the alveolar pressure, the small the caliber if the capillaries, e.g. at Apex of lung, alveolar pressures are greater than at base. Therefore, the caliber of the capillaries is less resulting in a decrease in blood flow to lung apices.
Larger vessels- greater than 50m in size. Called Extra-alveolar vessels. Not influenced by alveolar pressure. Extra alveolar vessels are influenced, however, by lung volume. As volume increases, alveoli expand, stretching capillaries causing them to expand. During inspiration, as volume increases, vessels are opened with a drop in vascular resistance, increasing blood flow. As volume continues to increase, alveolar pressures begin to increase, causing decreasing blood flow through alveolar vessels. Therefore, PVR decreases m low lung volumes, but increases as lung volume increases.
Recruitment & Distention- come into play essentially with exercise.
Recruitment - during rest, normally, some blood vessels are closed. In exercise they will open to carry blood to increase Q. The opening of vessels normally closed to Q is called recruitment. This protects right ventricle from doing too much work.
Distention- refers to the increased Q causing an increase in the diameter of a blood vessel to further increase Q during exercise. Distension usually leads to recruitment. When open vessels can no longer distend, closed vessels will open.
PVR influenced by:
Hypoexmia & Acidosis = Pulmonary Vasoconstriction
Fick's Principle of Measuring Q or Cardiac Output
(CO) QT= V02 per min
Ca02-CvO2 (10)
(exit) (enter)
3 Methods: Utilizing the Fick Principle
1. 0xygen Consumption- as above. 02 consumption calculated and 02 content of both arterial and venous 02 measured. Values then plugged into Fick equation.
2.Dye Dilution- utilizes the change in the concentration of dye. Injected into antecubital vein. A densitometer measures concentration of dye as it goes through heart. The greater the CO, the faster dye will be pumped through heart.
3. Thermodilution- utilizes the Swan-Ganz catheter with thermistor channel at tip of catheter, Catheter sitting in PA, sensing a given temperature. Cold saline injected through catheter. Thermistor senses changes in temperature. The greater the CO, the lower the temperature change. The lower the CO, the greater the temperature change.
Perfusion
-like ventilation, blood flow through the pulmonary circulation is non-uniform. Perfusion to the bases is greater than to the apices (like ventilation) Why?
Gravity the effects of gravity on transpulmonary pressures and arterial blood pressure. In upright man, blood pressure at the apex of the lung is low, alveolar pressure is high. Therefore, Alveolar P exceeds P within capillaries or arterioles, causing a narrowing of blood vessels, causing a decreased blood flow. Apex is Zone 1. (PA> Pa >PV)
In Zone 2, mid lung, Pa > PA >Pv, level with the Heart
In Zone 3, the 1ung bases, arterial and venous P now exceeds alveolar P, increasing the size of the blood vessels, creating a greater perfusion to the bases. (Pa > Pv > PA)
Water Balance in Lung
Hydrostatic Pressure (both capillaries & interstitial)-definition Oncotic Pressure-definition Why are the lungs normally dry? Pulmonary Edema 1st Interstitial,
Peribronchial & perivascular
2nd Alveolar
Metabolic Functions of Lung
a) conversion of Angiotensin 1--> 2
potent vasoconstrictor Angiotension Converting Enzyme (ACE)
b) Bradykinen inactivated by (ACE)
c) PGE 1 E2 bronchodilator, vasoconstrictor of PDA
PGF2 bronchoconstriction
d) Serotonin
e) NE (30%)
f)Arachidonic Acid - breaks into luekotriemes
ex SRS-A
1. QS = CC02-CaO2 CC02 = CA02
QT CC02-CvO2 used with a Swan-Ganz catheter in place
3. Estimated Shunt Eq. = Ca02
CC02 - Ca02
2. Increased V/Q by virtue of decreased perfusion with normal ventilation e.g. pulmonary embolus, shock.
PA02 =150
PAC02= 0 no perfusion therefore ABGs
Approach atmospheric values
V/Q =5.1 = oo
0
As perfusion decreases with normal ventilation, V/Q increases (infinity)
Therefore as V/Q increases:
Pa02 increases approaching atmospheric values
PaC02 decreases approaching atmospheric values
= Increased V/Q
V, although less to apex than to base, exceeds Q, which is decreased in relationship to the base. Therefore V exceeds Q, therefore higher V/Q ratio.
Base = Decreased V/Q
V, although greater to the base, does not exceed Q because Q increases in a greater proportion, therefore Q exceeds V. Therefore, lower V/Q ratio -
Because of the variation of V/Q throughout the lung fields. ABG results from different lung fields will also vary. The predominant effect on the ABGs, however, will come from the bases because a greater volume of blood comes from the bases. Normally, the high P02 values at the apex balance with the low P02 form the bases. But in abnormal situations, ABGs may have low P02 even with high P02 at apex because a greater volume of blood from base, with decreasing P02, will have an overall decreasing effect on P02 (CO2 is opposite.)
Therefore, V/Q mismatch, specifically a decreasing V/Q ratio, will result in a decreased P02 and an increased PC02. The increased PaC02 of low V/Q may not be seen because with increased PaC02, central and peripheral chemoreceptors kick in and blow off C02.
Effects of V/Q on content of oxygen ( not only P02) i.e., amount dissolved in plasma plus amount bound to hemoglobin, e.g. Normal content = 20 vol. /O/o
Total 02 content = OxyHemoglobin content + Dissolved Content
OxyHemoglobin Content =Hb x 02 Capacity x Saturation
(1.34 ml/gm Hb)
Dissolved Content = P02 x.003 ml/02/mmHg
Increased V/Q may increase content
Decreased V/Q will decrease content
Because low V/Q units (bases) have a greater contribution than high V/Q units, the overall result of varying V/Q units is a decreased oxygen content.
Summary
Ventilation and Perfusion both are greater at the base of the lung.
V/Q ratio greater at apex and V/Q less at base, therefore, overall effects of varying V/Q units throughout lung field is a normalization of the arterial P02 and content. Any situation that would cause V/q mismatch, specifically low V/q, would lead to arterial hypoxemia. (Theoretically PC02 would increase, but with a rise in PCO2, body will compensate by increasing ventilation).
Most pulmonary diseases precipitate a decreased V/Q ratio leading to arterial hypoxemia.
Acute Respiratory Failure PaO2 less than 50 and/or
PaC02 is greater than 50
HYPOXEMIC vs. HYPERCAPNIC FAILURE
Ventilatory Failure -Increased PCO2 and/or Decreased P02
Hypoxemia = Decreased Pa02
Hypoxia = Decreased 02 to tissue- result of hypoxemia
Degrees of Hypoxemia
Normal = 90mmHg Will alter with age. Less than normal is some degree of hypoxemia (mild, moderate, severe.)
Hypercapnia Increased PC02- Normal Range 38-42 mmHg (35-45 other refs.)
Pathophysiologic Cause of Hypercapnia is HYPOVENTILATION
Diseases Affecting:
1. Respiratory Center (Brain)
2. N-M transmission
3. Thoracic Cage
4. Lung Movement
5. Lungs
Hypoventilation related to causative disease, e.g.
1.COPD- but not all COPD patients hypoventilate
2.Disease affecting mechanics of chest wall excursion -Neuromuscular disorders: Gillian Barre Syndrome, Polio, Amylotrophic lateral sclerosis, myasthenia, gravis, and muscular dystrophy
3. Post-op - due to pain
4, Anesthesia- depression of the respiratory center
5. Head trauma, OD's - again, depression of the respiratory centers
6. Idiopathic diseases- Pickwickian Syndrome and Sleep Apnea
7., flail chest and pneumothorax
What must be appreciated is that Hypoventilation may result from any number of disorders but is always hallmarked by an increased PaC02.
Pathophysiologic Cause of HYPOXEMIA
1. V/Q mismatch
2. Decreased F102, e.g. altitude
3. Diffusion defects
4. Hypoventilation
e.g., if PaCo2= 60 mmHg ( due to Hypoventilation)
Calculate PA02 = 150 - 60/.8 150-75= 74 mmHg Therefore, because of the alveolar air equation, PaO2, at givenF102, must be reduced in the presence of the increased PaCO2.
5. Shunt- blood from right side of heart returns to the left side without becoming arterilalized. Blood shunted will have a decreased P02 which will decrease overall PaO2.
Differential Diagnosis
-Decreased F102- rarely cause of decreased P02at normal altitude
-Hypoventilation- can be determined by measuring PaCO2/FI02/ALVEOLAR AIR EQUATION
-Diffusion- most common problem associated with decreased PaO2 in interstitial diseases
-Shunt- tends to occur in congenital diseases (physiological shunt) vs. anatomic shunt
-V/Q most common problem
All, with exception of shunt, will improve with 100% 02 administration.
Signs of Hypoxemia,
Ethanol -like symptoms, confusion, loss of judgement, paranoia, restlessness, dizziness, Sympathetic response: increased heart rate, increased blood pressure, diaphoresis, pale.
Signs of C02 Narcosis
Headache, mild sedation, drowsiness, coma, vasodilatation, sweating, increased heart rate, increased blood pressure (systolic and diastolic)
Shunt - 2 types
1. Anatomic normal 3-5% of CO via thespian vessels
2. Physiologic e.g. congenital defect or occurs in severe pulmonary disorders, e.g., ARDS- causing an actual collapse of pulmonary tissue causing a shunt effect. Actually, a result of V/Q mismatch-separated because of differing mechanisms, i.e., a physiologic shunt appears as a V/Q unit with low ventilation with V/Q approaching 0.
Shunt Chart/ Shunt Equation
Gas Transport
02 consumption = 250 ml/m normally, i.e. Tissue requires 250ml/m. How is this transported? Dissolved in plasma and as OxyHemoglobin.
Oxygen transported 2 Ways to oxygenate tissue
1.Dissolved in plasma- .003ml/mmHg P02/1 00ml
2.Oxyhemoglobin-1.34 ml/gmHb
Hemoglobin in RBC
Heme: iron porphyrin complex
Globin : protein complex- made up of polypeptide chains (amino acids) made up of 2a and 2B chains (difference related to sequence of amino acids)
Types of Hemoglobin
- Hemoglobin H- normal sequences of amino acids
- Hemoglobin F- fetal hemoglobin
- Hemoglobin S-sickle cell anemia-sequence altered causing easy
breakdown of RBC-crystallization of Heme complex
-Hemoglobin G thallasemia (Mediterranean descent)
-Carboxyhemoglobin- Hb & CO
-OxyHemoglobin- Hb & 02
Oxvhemoglobin Dissociation Curve.
Expresses the relationship of all possible P02's to saturation and 02 content. The shape if the curve expresses this relationship (the curve is not linear, i.e., 02 does not combine with Hb proportionally)
Association: flat proportion
Dissociation: steep proportion
P50--PO2 at 50% Sa02
Normal = 26-27 on adult curve, 18= 19 on Fetal Hb curve
Association - 02 loading onto Hb- at lung level
Dissociation 02 unloading- at tissue level
Association Curve- a drop on P02 on this portion of the curve cause a little drop in both saturation and content, i.e., 02& Hb continue to combine effectively.
Dissociation Curve- a drop in P02 will cause a significant drop in both saturation and content. Normally, this occurs at a P02 less than 50 mm Hg. A small drop in P02 below 50 causes a great decrease in saturation and content. P02 less than 50 is, therefore, a part of acute respiratory failure.
Shifts of the, HbO2 Curve
Factors that cause of RIGHT Shift:
1. Hyperthermia. (increased temperature)
2. Hypercapnia (increased PC02)
3. Acidosis (decreased pH)
4. Normal to increased 2-3 DPG(diphosphoglycerate) levels
A right shift causes a small decrease in the ability to load 02 at the lung level. In addition, a right shift will result in a decreased saturation and content which indicates that more 02 has been unloaded at the tissue level.
Therefore, a right shift hampers loading of 02 at the lung level but favors unloading of 02 at the tissue level. This is desirable in that, in exercise, e.g., temperature in muscles increases, C02 production increases, etc., causing a right shift, unloading more 02.
Factors that cause a LEFT shift:
1. Hypothermia (decreased temperature)
2. Hypocapnia (decreased PC02)
3. Alkalosis (increased pH)
4. Decreased 2-3 DPG
A left shift causes an increase in the ability to load 02 at lung level (minor) and reduces the unloading of 02 at the tissue level.
Therefore, a left shift favors loading of 02 at lung level and hampers unloading 02 at tissue level. Desirable at lung level because C02 is reduced(blown off) etc,
2-3 DPG substance normally manufactured by the RBC. Its presence favors 02 release. Therefore, its presence tends to shift the curve to the right.
Increased 2-3 DPG - protective mechanism
-chronic hypoxemia -COPD
-altitude
-sickle cell anemia
-cyanotic congenital heart disease
-chronic cardiac insufficiency (decreased CO) CBF
Decreased 2-3 DPG
-septic shock ( even with normal or sufficient P02,tissue oxygenation is poor)
-bank blood- depletes 203 DPG levels
-CO poisoning(therefore, compound problem :
1. Hb bound with CO
2. CO poisoning decreased 2-3 DPG
Application to Clinical Situations:
Altitude Anemia COHb
P02: Decreased N N
Sa02: Decreased N Decreased
Carboxyhemoglobin
Content: Decreased(acute) Decreased Decreased
N to increase (chronic with increased Hb)
Carbon Dioxide Transport
1. As HC03 -majority
C02 + H20 ->--> H2C03**à à H+ + HC03
CA*
*Carbonic Anhydrase **Carbonic Acid
C02 produced during internal respiration combines with H20, in presence of enzyme CARBONIC ANHYDRASE, to form H+ & HC03 (Reverses at lung level)
2.Carbamino Compound -CO2 combines with terminal amine groups of protein -including hemoglobin
3.Dissolved, in Plasma
The % of C02 carried varies from arterial to mixed venous blood.
Arterial: 5% Dissolved
90% HC03
5% Carbamino Compounds
Venous: 10 %Dissolved
60% HC03
30% Carbamino Compounds
Acid Base Balance
-Cellular metabolism results in the production of byproducts, composed of acids and bases. Elimination & Retention of acids and bases results in acid-base balance.
Acids - H+ ion donor
e.g. H2C03 -> -> H+ + HC03
acid base
Base - H+ ion acceptors
e.g. HC03- + H+ ->-> H2C03
base acid
pH - used to express the overall relationship of acid and bases to maintain acid/base balance
Haldane Effect - unloading of 02 causes loading of C02 (tissue)
Bohr Effect - loading of C02 causes unloading of 02 (tissue)
Henderson-Hasselbach Equation
pH = pK + log HC03 (base)/ PC02 (acid) 20/1 ratio
Illustrates that if either base or acid changes, pH will change unless balanced is maintained at a 20 to I ratio (base to acid).
Balance maintained by 2 mechanisms:
1. Chemical Buffers - 4 Groups
A. HC03- H2C03- Bicarbonate-Carbonic Acid System
Accounts for 53% of buffering
B. Hemoglobin accounts for 35%
C. Protein -other than Hb 7% (Albumin)
D. Phosphate - Buffer System 5%
HC03-H2CO3 and Hb systems account for a total of 88% of the body's buffering capabilities and is expressed as Base Excess or Base Deficit.
2. Elimination - 2 systems responsible for C02 elimination.
A.Lungs- PC02-Volatile Acid
(Respiratory Component) Lungs will eliminate up to 12,000- 18,000 mEq/day
B.Kidneys- Fixed Acid, Lactic, acetic acids, (metabolic or non-respiratory component) Kidneys will eliminate up to 40-80 mEq/day
Therefore, for immediate C02 elimination, the lungs are most important for eliminating acids rapidly. Therefore, lungs are more important than kidneys in the acute situation. In addition, death will occur more rapidly with lung dysfunction than with kidney dysfunction.
Measurement of Acid-Base Balance
pH = Base/ Acid = HC03/PCO2
Because this balance is to be maintained at a 20 to I ratio. pH and PCO2 measurements are taken directly. From these two parameters. HC03 can be calculated.
Refer to Siggaard-Anderson Nomogram
Base: Expressed in one of three ways LHC03 2.Base Excess 3.Total C02-rarely reported
Base Excess is calculated by using the Siggaard-Anderson Nomogram illustrates PC02 and pH, with calculations of Total C02, Base Excess and HC03 possible. In addition, Nomogram takes hemoglobin into consideration to calculate Base Excess. Base Excess is a little more accurate, therefore, in that it takes into consideration the buffering capabilities of both the HC03 and Hb buffering systems. As a result, both the HC03 and Base Excess calculations may differ with Base Excess more accurate, (Nomogram also incorporated in slide rule and computer application for calculation)
For Example: Use S-A Nomogram
1.Given pH=7.4 Find HC03=24Meg/l
PC02=40 BE=O
2.Given pH-7.5 Emid HC03=
PC02=50 BE=
Normals
pH = 7.38-7.42 (7.35-7.45) Narrow range makes acid-base determination easier
PC02= 38-42 mm Hg (35-45)
HC03=22-26 meg/l
B.E. = -2 to +2 (a negative BE is really a base deficit, expressed as a negative excess)
2 Major Acid-Base Disorders
Acidosis: pH less than 7.38
Alkalosis: pH greater than 7.42
Acidosis -occurs as a result of either too much acid (volatile and/or fixed) or too little base Anion Group calculation will further differentiate a metabolic acidosis that is to an accumulation of fixed acids as opposed to once due to a loss of HC03.
Alkalosis- opposite- too much base or too little acid
Acidosis
Metabolic- increase in fixed acid or increased elimination of Base (increased HC03)
Respiratory- too much volatile acid seem as increased PCO2
Alkalosis
Metabolic- too little acid leading to increased retention or decreased elimination of Base (increased HC03)
Respiratory - too little volatile acid see, as decreased PC02
pH PCO2 BE/HC03 Example
Acidosis
Metabolic ↓↓ N(acute) ↓↓↓ pH=7.2
PC02= 40mmHg
BE= -13
HC03=15Me/l
e.g. Ketoacidosis- (diabetics)
Lactic acidosis (due to anaerobic glycolysis due to hypoxemia)
Shock decreased oxygenation = hypoxemia - lactic acid
Renal Failure
Diarrhea HC03 loss
Diamox - carbonic anhydrase inhibitor (H+ retained)
Methanol - anti-freeze
Ethylene Glycol- anti-freeze
Aspirin overdose
Respiratory
pH PC02 BE/HC03 Example
↓↓ ↑↑ N(acute) pH=7.2
PC02=75mmHg
BE= -1
HC03= 26MeqlL
e.g. COPD- C02 retainers
Drug overdose, Trauma, N-M disorders, etc. anything leading to
HYPOVENTILATION)-respiratory center depression for any number of
reasons.
pH PC02 BE/HC03 Example
Metabolic ↑↑ N(acute) ↑ pH=7.55
PC02=40mmHg
BE= +11
HC03= 35MEQ/L
e.g. Vomit(loss of H+ & CL- by loss of HCL acid-bulimia)
NG tube(ditto)
Hypokalemia (causes HC03 retention)
Hypochloremia (causes HC03 retention)
Often seen in conjunction with chronic lung disease (COPD,
asthma)
Drugs e.g., Diuretics (decreased K & decreased Cl): Steroids(decreased K)
HC03 administration: Iatrogenic
pH PCO2 BE/HC03 Example
Respiratory ↑↑ ↓↓ N pH=7.6
PC02=25mmHg
BE= O mEq/L
HC03=25mEqIL
e.g. Anemia (=decreased 02 content, Hyperventilation occurs to increase 02)
Pulmonary Disease (an effect to improve V/Q= hyperventilation) pneumonia, COPD, pulmonary embolism
Fever (increased 02 demand-hyperventilation)
Drugs (alcohol, etc.- initially)
CNS disorders- stimulation =hyperventilation
Bactermia-Sepsis- respiratory alkalosis may be first sign of this disorder
Iatrogenic- ventilator patients-may be desirable, e.g., patients with increased intracranial pressure. Respiratory Alkalosis may reduce this pressure.
CHF-decreased CO
Compensation
The body's attempt to restore the pH to normal, so that enzyme systems can function effectively. Death (tissue, organ) will occur at extreme pH variations (less than 7/1 or greater than 7.6)
pH will rarely be restored to normal by body mechanisms and will never
overcompensate. Therefore, pH reading will give first indication of overall condition (acidosis or alkalosis). Review of PC02 and BE or HC03 will confirm type of condition and if acute (non-compensated) or chronic (compensated or partially compensated)
Compensatory Mechanisms
A. Metabolic problems: compensated by the lungs. Reduce volatile acid or retain volatile acid
1. Metabolic Acidosis pH=7.22
PC02=40-normal volatile acid
BE= -11- too much fixed acid
Compensating mechanism therefore, will be to blow off volatile acid ( decreasing PC02). This will begin within two hours and will compensate within six hours after start. Excellent mechanism.
Compensated Metabolic Acidosis
pH: decreased (near norm) pH =7.34
PC02: decreased PC02=25
HC03: decreased BE= -11
Although hyperventilation is an excellent mechanism, PC02 may only be reduced to no less than 8-12 mm Hg.
2. Metabolic Alkalosis pH=7.55
PC02=40mmHg
BE= -11
Compensatory mechanism is respiratory. In the event of too little acid the body will attempt to add volatile acid (increased PaCO2) This mechanism is the least efficient.*
Partially Compensated Metabolic Alkalosis
PH= increased (near normal) pH=7.48
PC02= increased PCO2=50
HC03= increased BE= +11
*With increased PC02. Pa02 will decrease and when hypoxemia occurs,
mechanism halted (no more than PC02= 50 to 55)
B. Respiratory Problems: compensated by the kidneys
I. Respiratory Acidosis
pH = 7.25
PC02= 65 mm Hg
HC03= 24 mEq/L
BE= 0
Compensation will be for the kidneys to eliminate H+ or retain HCO3. Slower mechanism-L Onset within six hours, complete compensation within 72 hours.
Compensated Respiratory Acidosis
pH : Decreased (near) 7.3 6
PC02: Increased 65
BE: Increased +10
2.Respiratory Alkalosis
pH = 7.60
PC02 = 25
BE= 0
Compensation would be to retain fixed acid by reducing HC03-excretion retaining H+.
pH - increased 7.45
PC02 - decreased 25
HC03-decreased -9
BE -4
Treatment of Acidosis & Alkalosis (Metabolic/ Respiratory)
A. Acidosis
1. Metabolic Acidosis
Patient weight x .2 x ΔB.E.
(kg) (constant)
Using B.E. indicates treatment to take into account all buffering systems HC03-, H2C03, plus others)
B.E. Actual (decreased pH) to Normal (7.4)
e.g. 70 kg. Patient
B.E. of pH of 7.4= 0
B.E. of pH of 7.22 = -11
PC02 of 40
70 x.2 x 11 = 154 mEq of HCO3
e.g. pH 7.10
PC02 30
Correct to 7.40
Δ B.E. Of 11 (use Siggaard-Anderson Nomogram)
B.E = -5 TO -20
(pH is 7.4) (pH = 7. 1)
(PC02=30) (PCO2= 30)
Therefore, ΔBE = 15
One amp of HC03 equals approximately 44mEq of HC03
-Not all amps are the same.
2.Respiratory Acidosis
Improve ventilation - TX underlying cause with respiratory intervention (PD & CPT, CMV. Incentive Spirometry). In severe, chronic disorders with acute exacerbation, administration of HC03 may be helpful to increase pH for administration of drugs whose effects may be diminished in presence of low pH. Rarely done. Actually, higher doses of these drugs would work.
B. Alkalosis
1. -Metabolic Alkalosis (Cl- Na+ HC03-)
1.Administration of additional chloride salt
e.g. KCL- if caused by hypokalemia
NaCL- another chloride salt- given when K is normal or increased (renal failure). For N -G suctioning, NaCL is administered.
NH4Cl (ammonium chloride) in CHF. E.g., sodium cannot be given, so N4HCl may be given. Cannot be given in liver failure.
Argenine Hydrochloride- Hydrochloric acid
Calculation of amount of Cl. Salt to be administered utilizes the same formula as used to treat Metabolic acidosis.
e.g. pH 7.55 correct to 7.40
PC02 = 40 PC02 still at 40
B.E. = +11 corrected to 0
AB.E. = 11
70 kg. X .2 x 11= 154mEq Cl One liter of N.S.S. (.09% NaCl) contains approximately 150 mEq Cl if patient can tolerate Na
2.Respiratory Alkalosis
e.g. Sedation - e.g. Pavulon
Ventilator patients: reduce alveolar ventilation
-Decreased tidal volume
-Decreased frequency -A/C to IMV mode
-Add Mechanical Dead Space- each 6" flex tube equals 50cc dead space
Refer to Acid-Base Handout 10mmHg PC02 causes Δ pH of .07-.08
e.g. pH7.55 PCO2 from 40 to 30 =Increased pH of.07 to.08 therefore pH =7.63 This is a dangerous pH: Alkalosis may lead to seizure and sudden death due to arrhythmia. Life -threatening pH less than 7.2 or greater than 7.55 (e.g. arrhythmia's)
Control of Ventilation - 3 components
I.Respiratory Centers- brain stem: medulla & pons
2.Chemorecotor reflexes
PCO2 (primarily) P02 & pH (latent)
3. Neural reflexes
- higher centers in the brain
- peripheral centers- e.g. in lungs
I. Respiratory Centers- three centers
A.The Medullary Center
-Reticular Activating System (RAS)
-Contain cells active in both inspiration and expiration, therefore, responsible for the rhythm of ventilation.
-Activity is one of oscillation. Inspiratory neuron fires to produce inspiration, and, at the same time, fires to inhibit expiration and visa versa. These cells also receive input from other areas above and below the Medullary center to
modulate rate and depth of ventilation.
B.Apneustic Center
-located in Pons
-stimulates the inspiratory component of the Medullary center. Sends impulse to inspiratory cells in the RAS to stimulate inspiration.
C.Pneumotaxic Center
-located in upper pons-above Apneustic center -Inhibits inspiratory activity. Message to expiratory cells in RAS to inhibit inspiration
The interaction of these three centers are responsible for the regulation of ventilation. The level of ventilation is influenced by many factors.
Factors influencing the level of ventilation
1. Impulses from the pulmonary stretch receptors in the lung affect the level of ventilation
2.Input from the carotid & aortic chemoreceptors
3.Stimulation to baroreceptors (pressure)
4.Cerebral cortex input- voluntary hyperventilation & hypoventilation
5.PaC02- most important
B. Drugs e.g., Mepiridine (Demerol-narcotic) have the ability to blunt the response to increased PaCo2. Therefore, drug therapy such as this must be handled carefully in the non-ventilated patient with preexisting blunting of the PaC02 drive, e.g. COPD.
How does response to PaC02 occur?
Response is on two levels, involving the 2 types of chemoreceptor reflexes.
II. Chemoreceoptor Reflexes
A. Central Chemoreceptors
-found in the medulla of the brain stem
-bathed in CSF (cerebro-spinal fluid) and separated from the blood by the blood -brain barrier. This barrier is impermeable to H- & HC03, but is quite permeable to C02, therefore, as C02 increases n the blood, it readily diffuses in to the CSF.
In CSF, C02, under the influence of carbonic anhydrase, combines with H20 to form H2C03, which dissociates into H+ and HC03.
The H+ concentration therefore stimulates the central chemoreceptors to alter level of ventilation therefore responds to pH of CSF. This mechanism is slow, that is, does not occur for several hours. This is the reason for the 2-3 hour response time for respiratory compensation. In chronic C02 retainers, this mechanism is even slower because of chronically increased C02 levels which has already blunted C02 response.
Summary: Central chemorecptors respond to changes of pH of CSF, due
to changes of C02 of arterial blood.
3.Peripheral Chemoreceptors - located in two areas
1.Carotid bodies- (bifurcation of carotid arteries). 9th cranial
nerve/glossopharyngeal
2.Aortic bodies - (arch of aorta). 10 th cranial nerve/vagus
Stimulation of these receptors causes abrupt alteration of ventilation in acute situations. Stimulation is via changes in PCO2 primarily, and ventilation will change quite rapidly. Peripheral chemoreceptors will also respond to decrease P02, but this decrease must be significant. Increased PC02 will potentiate response when in conjunction with decreased P02 in carotid bodies only. Peripheral chemoreceptors will respond to decreases in pH. Very weak response.
III. Neural reflexes - refer to West
-Herring-Bruer Reflex
-Paradoxical Reflex
-Deflation Reflex- e.g. in pnemothorax, lung collapse sends impulse to medulla to initiate inspiration
-Gamma system- information sent from muscle spindles to spinal column, when muscles are stretched. Believed to be mechanism involved in dyspnea.
1.Cheyne-Stokes - Gradual increasing in the rate and depth of ventilation followed by a gradual decreased in both, followed by increasing periods of apnea.
Overall Ventilation and ABG's Indicates a disorder above the pons, e.g. in stroke.
2.Biots
-Due to vascular damage to brain stem
-Irregular, chaotic pattern usually with decreased VT.
-Will affect overall ventilation & ABG's
-Requires intubation & ventilatory support