homework if you did not complete hw turn in by monday email: [email protected] read all handouts,...

Homework

• If you did not complete HW turn in by Monday EMAIL: [email protected]

• Read all handouts, pages 181-194• Write a minimum of 2 pages summarizing all

gas laws, include examples of each gas law to a real life example

• 4-18-14• Read all handouts, pages 287-302• Write a two page summary of Bernoulli’s

Principle, provide examples of its use

Gas Exchange

Gas Exchange

• Ventilation – The mechanical movement of air into and

out of the lungs• Respiration

– The interchange of gases between an organism and the medium in which it lives

– the taking in of oxygen, its use by the tissues, and the giving off of carbon dioxide

Oxygen Exchange

• FIO2 – fractional inspired oxygen concentration expressed as decimal

100% is written as 1.00

• PAO2 – partial pressure of oxygen in the alveolus expressed in mmHg

• PB – barometric pressure expressed in mmHg

Oxygen Exchange

• PaO2 – partial pressure of oxygen in the arterial blood expressed in mmHg

• SaO2 – saturation of the hemoglobin by oxygen expressed as a percentage

• Hb – hemoglobin

Oxygen Exchange

• PACO2 – partial pressure of carbon dioxide in the alveolus expressed in mmHg

• PaCO2 – partial pressure of carbon dioxide in the arterial blood expressed in mmHg

• PvO2 – partial pressure of oxygen in the venous blood expressed in mmHg

Oxygen Exchange

• PvCO2 – partial pressure of carbon dioxide in the venous blood expressed in mmHg

• R – respiratory quotient– Total exchange of oxygen for carbon

dioxide expressed as a ratio of carbon dioxide produced to the volume of oxygen consumed; normal value is 0.8

Diffusion

• Gas movement between the lungs and the tissues occurs via simple diffusion

• The partial pressure of inspired 02 (PI02) = 159mmHg, Capillary Ca02 = 40 mmHg, intracellular P02 is approx. 5 mmHg. This pressure gradient allows for the diffusion of oxygen from the lungs to the cell.

• Called the “Oxygen Cascade”

Oxygen Cascade

Oxygen Cascade

• The oxygen cascade describes the process of declining oxygen tension from atmosphere to mitochondria.

• The purpose of the cardio-respiratory system is to extract oxygen from the atmosphere and deliver it to the mitochondria of cells. Oxygen, being a gas, exerts a partial pressure, which is determined by the prevailing environmental pressure.

• At sea level, the atmospheric pressure is 760mmHg, and oxygen makes up 21% of inspired air: so oxygen exerts a partial pressure of 760 x 0.21 = 159mmHg. This is the starting point of the oxygen cascade, as one moves down through the body to the cell, oxygen is diluted down, extracted or otherwise

lost, so that at cellular level the PO2 may only 5 or so mmHg.

Oxygen Cascade

• The first obstacle that oxygen encounters is water vapor, which humidifies inspired air, and dilutes the amount of oxygen, by reducing the partial pressure by the saturated vapor pressure (47mmHg). This will, obviously, affect the PIO2 (the partial pressure of inspired oxygen), which is recalculated as: (760 - 47) x 0.2094 = 149mmHg.

• Air consists of oxygen and nitrogen, but as gas moves into the alveoli, a third gas, carbon dioxide, is present. The alveolar carbon dioxide level, the PACO2, is usually the same as the PaCO2, which can be measured by a blood gas analyzer. The alveolar partial pressure of oxygen PAO2 can be calculated from the following equation: PAO2 = PIO2 – PaCO2/R. R is the respiratory quotient, which represents the amount of carbon dioxide excreted for the amount of oxygen utilized, and this in turn depends on the carbon content of food (carbohydrates high, fat low). For now let us assume that the respiratory quotient is 0.8, the PAO2 will then be 149 – (40/0.8) = 100mmHg (approx).

Oxygen Cascade

• The next step is the movement of oxygen from alveolus to artery, and as you would expect, there is a significant gradient, usually 5 –10 mmHg, explained by small ventilation perfusion abnormalities, the diffusion gradient and physiologic shunt (from the bronchial arteries).

• Oxygen is progressively extracted thru the capillary network, such that the partial pressure of oxygen in mixed venous blood, PVO2, is approx 46 mmHg.

• What is essential to understand about the oxygen cascade is that if there is any interference to the delivery of oxygen at any point in the cascade, significant injury can occur downstream. The most graphic example of this is ascension to altitude.

Oxygen Cascade

• At 19,000 feet (just above base camp at Mount Everest, the barometric pressure is half that at sea level, and thus, even though the FiO2 is 21%, the PIO2 is only 70mmHg, half that at sea level. Conversely, if the barometric pressure is increased, such as in hyperbaric chambers, the PIO2 will actually be higher.

• Four factors influence transmission of oxygen from the alveoli to the capillaries 1. Ventilation perfusion mismatch, 2. Right to left shunt, 3. Diffusion defects, 4. Cardiac output.

Oxygen Cascade

• The amount of oxygen in the bloodstream is determined by the oxygen carrying capacity, the serum hemoglobin level, the percentage of this hemoglobin saturated with oxygen, the cardiac output and the amount of oxygen dissolved

• The PVO2 is determined by whole body oxygen demand, and the capacity of the tissues to extract oxygen. In sepsis there appears to be a fundamental

abnormality of tissue oxygen extraction.

Alveolar Gas Tensions

The partial pressures of all gases within the normal alveoli:

PO2 = 100 mmHgPCO2 = 40 mmHgPN2 = 573 mmHgPH2O = 47 mmHg100% O2 for >12-24 hours can cause

absorption atelectasis from Nitrogen washout

Total = 760 normal barometric pressure at sea level


– CO2 gradient : from an intracellular CO2 ~60 mm Hg to the atmosphere where it is <1 mm Hg

• Determinants of alveolar CO2

– PACO2 will increase with increases in

metabolic CO2 production or decreased

alveolar ventilation

– PACO2 is equal to PaCO2

– PaCO2 equals 35-45 mmHg

– Normal CO2 production = 200 ml/min.


• Alveolar oxygen tension is affected primarily by the PO2 in the inspired gas (PIO2)

• Oxygen in the alveoli is diluted by both water vapor and CO2

• Therefore to determine the alveolar oxygen tension, we use the Alveolar Air Equation.

Calculation of Alveolar Oxygen

• Simplified Alveolar Air Equation

• PAO2 = FIO2(PB - 47) – PaCO2

(.21 x 713) - 40 = 110 mmHg

• Even in the face of hyperventilation, the PaO2 of a patient breathing room air should not exceed 120 mmHg (detects erroneous ABG results)

• A patient with normal lungs breathing 100% O2 would have a PaO2 of approx. 673 mmHg with a PB of 760

• Tachypnea = fast RATE of breathing• Hyperventilation= fast RATE and INCREASED

Volume

Diffusion of Oxygen

• Barriers to diffusion:– Alveolar epithelium– Interstitial space– Capillary endothelium– Erythrocyte membrane

Diffusion of Oxygen

• Fick’s First Law of DiffusionVgas = (A x D) (P1 – P2)

T• Vgas is the movement of a volume of gas through

a biological membrane • A is the cross-sectional area available for

diffusion• D is the diffusion coefficient • T is the thickness of the membrane• (P1 – P2) is the partial pressure gradient across

the membrane

Diffusion of Oxygen

• Fick’s First Law of Diffusion

– All this to say: The greater the surface area for diffusion, the more diffusion will occur.

– In normal healthy people, diffusion mainly depends on the gas pressure gradients.

• Any disease process that decreases the surface area available for diffusion decreases the V/Q ratio and decreases PaO2 and increases PaCO2

Diffusion of Oxygen

• Time Limits to Diffusion– Red blood cells (RBC’s) are normally in

contact with the alveolus in the pulmonary capillary for 0.75 seconds. During heavy exercise, a 0.25 sec. transit time is still sufficient for full equilibration of gas diffusion.

– Saturation of the RBC is normally accomplished in < 0.5 seconds

– The time available for diffusion in the lung is mainly a function of the rate of pulmonary blood flow

Diffusion of Oxygen

• Time Limits to Diffusion– Diffusion time decreases in conditions of

increased cardiac output e.g.: • heavy exercise, high fever and septic

shock• CO2 diffuses 20x faster across the A/C

membrane than O2 because of its increased solubility in plasma

Gas Exchange

Diffusion of Oxygen

• A-a Gradient– Difference in partial pressure between the

alveolar gas and the arterial value– Expressed as P(A-a)O2

• P(A-a)O2 = PAO2-PaO2– Normal = (on 21%) less than 4mmhg for

every 10 years in age– Normal value: 5-10mmHg on R/A and

< 65mmHg on 100% – On 100% 02 every 50mmhg difference in

P(A-a)02 = 2% shunt

Diffusion of Oxygen

• A-a Gradient– Two factors account for the normal PAO2 –

PaO2 gradient:• Right to left shunts in the pulmonary and cardiac

circulation: bronchial venous drainage and the thebesian venous drainage

• Regional differences between pulmonary ventilation and blood flow

Hypoxic Pulmonary Vasoconstriction

• A 17 year old male presents to the emergency room after being stabbed in the chest, on chest x-ray his right lung was fully collapsed, and yet his SpO2 was 94% on room air - why?

• hypoxic pulmonary vasoconstriction• Hypoxic Pulmonary Vasoconstriction is a physiologic

protective mechanism which prevents right to left shunting of blood.

• Right to left shunt causes hypoxemia unresponsive to oxygen therapy

Hypoxic Pulmonary Vasoconstriction

• One would expect that this patient would have a 50% shunt due to perfusion but no ventilation of the right lung; this does not happen. Hypoxic pulmonary vasoconstriction takes place. Many of the tissues in the body are capable of regulating their own blood flow – the heart, the kidney, the brain and the gut all autoregulate blood flow. It appears that HVP is a similar mechanism within the lung, to prevent right to left intrapulmonary shunting, and thus the presence of deoxygenated blood in the peripheral circulation. This process is most florid in utero, when blood is diverted away from the lungs through the ductus arteriosis, due to high pulmonary arterial pressures. We know that pulmonary smooth muscle cells are extremely sensitive to alveolar oxygen tensions, but the mechanism of vasoconstriction is unknown. HPV is probably multifactorial in origin and modulated by a variety of endothelium dependent factors (nitric oxide, endothelin, prostacyclin etc).

What are the effects of diffusion defects

• What are the effects of diffusion defects and ventilation-perfusion mismatches on arterial oxygenation?

• Diffusion defects and ventilation perfusion mismatches cause hypoxemia, responsive to exogenous oxygen and positive pressure ventilation.

• Oxygen diffuses from the alveoli to the pulmonary capillaries along a partial pressure gradient – there is less oxygen in the blood, the higher the inspired concentration of oxygen, the more rapidly the gases diffuse. For most individuals, an equilibrium position occurs early in inspiration, when the arterial blood becomes fully saturated with oxygen, and the rate of uptake of oxygen depends on capillary blood flow.

Change in HW• DUE MAY 9th (GROUP PROJECT) WORTH 10 POINTS• Read all handouts• Write a 5 page summary on 1 of the following:• Gas Laws: provide real life applications• Gas Exchange and the Oxygen cascade• Bernoullis Principle/application to medical devices• Laminar vs turbulent flow in relation to the airway• Posieuille’s Law and it’s application in the airway• Osmosis/osmotic pressure, using blood as an example• Intro to electricity/voltage, amperage, resistance• Reference sources and use APA format. Include a power point

presentation (minimum 10 slides demonstrating content of paper). Print a copy of your power point (6 slides per page) include with your paper ; email me a copy, present in class, 20 min per group

• WATCH Fluid Mechanics in Medicine videos on website for review

• EXAM 2 in two weeks• Review: • (we will be covering this next week)• Fluid Dynamics pg 287-294• Bernoulli/Venturi Principle pg 294-302• Reynolds Number pg 332-333• Laminar &Turbulent flow pg 306-309• Viscosity pg 327• Poiseuilles Law pg 328-332

Exam 2 also includes:

• Def: Ventilation, respiration

• Shunting/deadspace• Normal values for:

PaO2, PAO2, PvO2, PaCO2, PACO2, SaO2, Respiratory quotient

• Oxygen Cascade• 4 influences of oxygen

from alveoli to capillaries

• DO2 formula• O2 consumption

• Absorption ATX• Normal CO2 production• Barriers to diffusion• Ficks Law• Time limits to diffusion• Natural Shunts• HPV• A-a ratio• V/Q mismatch• How is O2 carried in

the blood• Hyperbaric chamber

indications

What are the effects of diffusion defects

• The diffusion capacity depends on the thickness of the alveolar wall, the area available for gas exchange and the partial pressure difference between the two sides. If the thickness of the wall increases – such as in pulmonary fibrosis, chronically, or pulmonary edema, acutely, the diffusion capacity is lower.

• Moreover, with increasing heart rate, the time for equilibration may be shorted, and the patient may become hypoxemic. The treatment is to increase the partial pressure gradient for oxygen by administering exogenous oxygen to the patient. If the patient has pulmonary edema, the surface area may be increased by increasing the transalveolar pressure (and marginalizing fluid), through administration of continuous positive airway pressure (CPAP).

Diffusion of Oxygen

• a/A Ratio– Ratio between the partial pressure of the

alveolar gas and the partial pressure of the arterial gas or how much oxygen is getting from the alveoli to the blood

– Expressed as: PaO2/PAO2

– Normal value: > 75%– Low value = V/Q mismatch

V/Q mismatch vs. Shunt

• V/Q mismatch: Ambiguous term, simply means there is a problem with either ventilation or perfusion or both resulting in hypoxemia. Initial treatment it to give Supplemental O2; assess via pulse-ox

• If the V/Q mismatch does not improve with Oxygen, it is deemed a “shunt” and will require positive pressure.

• Refractory hypoxemia (V/Q that doesn’t respond to O2 alone, = shunt = positive pressure)

Diffusion of Oxygen

Remember: If blood flow to an area of the lung increases, CO2

coming from the tissues will be delivered faster, causing a rise in alveolar CO2. Also, alveolar O2 will decrease because of the faster uptake at the pulmonary capillary. The opposite occurs if blood flow decreases.

If blood flow to an area of the lung remains constant, but alveolar ventilation decreases then: PAO2 should decrease and CO2 should increase.

Diffusion of Oxygen

Remember: If an area of the lung is ventilated but has no

blood flow then: the area represents alveolar dead space, has alveolar gas similar to atmospheric and V/Q is elevated.

If an area of the lung has no ventilation but is normally perfused by the pulmonary circulation then: The area represents an alveolar shunt, alveolar gas will have a PO2 and PCO2 like that of mixed venous blood and V/Q is lower

R in the alveolar gas equation is equal to the ideal V/Q ratio of 0.8 with an ideal alveolar pO2 of 100mmHg and CO2 of 40mmHg

SHUNT

• Perfusion without effective ventilation• Treatment: Positive pressure• Example of Shunt: Scar tissue/ATX, PN,

Pneumo, Pulm. Edema

DEAD SPACE• Ventilation without perfusion• Treatment depends on cause• Heart not pumping effectively• Pulmonary emboli (blood clot preventing

blood flow, vasoconstriction)

Diffusion of Oxygen

Remember: At the apex of the lung, the blood flow is less than

ventilation resulting in a high V/Q At the base of the lung the blood flow is greater

than ventilation resulting in a low V/Q

Transport of Oxygen

• Blood carries oxygen in two forms:– Plasma

• Oxygen first dissolves in plasma• Relates to Henry’s Law which states that there is

a direct relationship between the partial pressure of the gas over the liquid

• Amount of oxygen carriage = 0.03 x PaO2

• At 3 atmospheres breathing 100% O2, the amount of oxygen dissolved in the plasma would meet the resting tissue demands of the body!

Transport of Oxygen

HBO

• Hyperbaric oxygen therapy is used to increase the amount of oxygen dissolved in the plasma, by increasing the ambient pressure.

• At normal atmospheric pressure, the amount of oxygen dissolved in the blood is so low, that we don’t even bother to quantify it. However, increasing the environmental pressure, using a hyperbaric chamber, increases the solubility of oxygen in the blood. If 100% oxygen is inspired at 3 atmospheres, the inspired PO2 is over 2000mmHg, and this should increase the volume of oxygen in solution in the blood to approximately 6ml/100ml of blood.

HBO

• Diseases for which hyperbaric oxygen therapy is indicated:

• Arterial gas embolism• Decompression sickness (the bends)• Severe carbon monoxide poisoning• Osteoradionecrosis• Clostridial myonecrosis• Wound healing

Transport of Oxygen

• Blood carries oxygen in two forms– Red Blood Cell

• The major source of oxygen carriage• Each red blood cell consists of 4 Heme

complex’s, each with its own iron ion. • Oxygen molecules bind to these Heme

complexes via the iron ion.• When all the Heme complex’s are bound with O2,

the Hb is converted to its oxygenated state and referred to as: Oxyhemoglobin (HbO2)

• Each gram of normal Hb can carry approx. 1.34 ml of oxygen.

http://www.youtube.com/watch?v=TKKW9VIrgtU

Transport of Oxygen

• Amount of oxygen carriage = 1.34 x Hb x SaO2

• Hemoglobin saturation: Saturation is a measure of the proportion of available Hb that is actually carrying oxygen.

• Calculated: SaO2 = (HbO2 ÷ Total Hb) x 100• Expressed as SaO2

• Clinically, HbO2 and SaO2 are measured directly

• Hb affinity refers to how well Hb carries and releases oxygen

• http://www.youtube.com/watch?v=V1FAnE31AYs

http://www.youtube.com/watch?v=V1FAnE31AYs

CaO2

• Oxygen is carried in the blood in two forms: dissolved and bound to hemoglobin. Dissolved oxygen obeys Henry’s law – the amount of oxygen dissolved is proportional to the partial pressure. For each mmHg of PO2 there is 0.003 ml O2/dl (100ml of blood). If this was the only source of oxygen, then with a normal cardiac output of 5L/min, oxygen delivery would only be 15 ml/min. Tissue O2 requirements at rest are somewhere in the region of 250ml/min, so this source, at normal atmospheric

pressure, is inadequate.

CaO2

• Hemoglobin is the main carrier of oxygen. Each gram of hemoglobin can carry 1.34ml of oxygen. This means that with a hemoglobin concentration of 15g/dl, the O2 content is approximately 20ml/100ml. With a normal cardiac output of 5l/min, the delivery of oxygen to the tissues at rest is approximately 1000 ml/min: a huge physiologic reserve.

CaO2

• Hemoglobin has 4 binding sites for oxygen, and if all of these in each hemoglobin molecule were to be occupied, then the oxygen capacity would be filled or saturated. This is rarely the case: under normal conditions, the hemoglobin is 97% to 98% saturated. The amount of oxygen in the blood is thus related to the oxygen saturation of hemoglobin.

• Taking all of these factors into account, we can calculate the oxygen content of blood where the PO2 is 100mmHg, and the hemoglobin concentration is 15g/L:

• [1.34 x Hb x (saturation/100)] + 0.003 x PO2 = 20.8ml

CaO2

• As one would expect, this figure changes mostly with the hemoglobin concentration: when the patient is anemic the oxygen content falls, when polycytemic, it rises. In either case the O2 saturation of hemoglobin may be 97 – 100%, but there may be a large discrepancy in content.

DO2- Delivery of O2 to Tissues

• DO2 = [1.34 x Hb x SaO2 + (0.003 x PaO2)] x Q

• The Delivery of oxygen (DO2) to the tissues is determined by:

• The amount of oxygen in the blood: the oxygen binding capacity of haemoglobin x the concentration of haemoglobin x the saturation of haemoglobin + the amount of dissolved oxygen all Multiplied by the Cardiac Output (Q).

• The cardiac output is determined by preload, afterload and contractility.

• The hemoglobin concentration is determined by production, destruction and loss.

• The SaO2 (the saturation of haemoglobin at arterial level with oxygen - as opposed to the SpO2 which is measured by pulse oximetery)

Oxygen Consumption

• Approximately 250 ml of oxygen are used every minute by a conscious resting person (oxygen consumption) and therefore about 25% of the arterial oxygen is used every minute. The hemoglobin in mixed venous blood is about 70-75% saturated

• In general there is more oxygen delivered to the cells of the body than they actually use. When oxygen consumption is high (eg. during exercise) the increased oxygen requirement is usually provided by an increased cardiac output

VO2- Oxygen Consumption

• Tissue oxygen extraction is calculated by subtracting mixed venous oxygen content from arterial oxygen content.

• This is computed by figuring out how much oxygen has been lost between the arterial side and the venous side of the circulation and multiplying the result by the cardiac output. In the following equation, VO2 is the oxygen consumption per minute, CaO2 is the content of oxygen in arterial blood, and CvO2 is the content of oxygen in venous blood:

• VO2 = Q x (CaO2-CvO2) mlO2/min

VO2

• The major difference between the two is obviously the hemoglobin saturation, which is roughly 100% on the arterial side and 75% on the venous side.

• Substituting inwards, where hemoglobin is 15g/dl: CaO2 is approx 20ml/100ml, CvO2 is 15ml/100ml: the difference is 5ml/100ml = 50 ml/l multiplied by a cardiac output of 5L = O2 consumption per minute is 250ml.

• So the mixed venous O2 saturation can be used to calculate the oxygen consumption: if SvO2 is decreasing, the O2 consumption is increasing.

Oxygen Exchange

• Oxyhemoglobin Dissociation Curve (OHDC)– Graph representing the relationship

between PaO2 and SaO2

– Position of the curve determined by P50

• Definition – The point at which the Hb is 50% saturated with oxygen

– Normal value – 26.6 mmHg

Oxyhemoglobin Disassociation Curve

90


• The steep aspect of the curve is the portion where minimal changes in PO2 normally result in large increases in O2 Saturation.

PaO2 60 equals = 90%, this is the slippery slope range. A PaO2 below 60 equals a dramatic decrease in SaO2.


• With a PO2 lower than 60mmHg, the curve steepens dramatically. Even a small drop in PO2 causes a large drop in SaO2 indicating a decreased affinity for O2. This normal decrease in affinity of Hb for O2 helps release large amounts of O2 to the tissue where the PO2 is low. This also explains why it is necessary to keep the PaO2 higher than 60mmHg in clinical practice


Shift to the Left

Shift to the Right

Shifts of the Curve

• Left Shift of the Curve– Hemoglobin has greater affinity for oxygen– Larger uptake of oxygen in the lung– Smaller amounts of oxygen released at

tissue level– P50 < 26.6

Shifts of the Curve

• Causes of Left Shift– in body temperature (decreased metabolism)– in pH– in carbon dioxide– in 2,3-diphosphoglycerate (2,3 DPG: a

stabilizing organophosphate found in RBC’S) – Abnormal hemoglobin (methemoglobin: Iron

molecule loses an electron and is unable to bind with O2(metHb), fetal hemoglobin (HbF), carboxyhemoglobin (HbCO)

Shifts of the Curve

• Right Shift of the Curve– Hemoglobin has less affinity for oxygen– Smaller uptake of oxygen in the lung– Larger amounts of oxygen available at

tissue level– P50 > 26.6

Shifts of the Curve

• Causes of Right Shift– in body temperature– in pH– in carbon dioxide– in 2,3 DPG

–http://www.youtube.com/watch?v=VIQC_tCHBBI

http://www.youtube.com/watch?v=VIQC_tCHBBI

http://www.youtube.com/watch?v=VIQC_tCHBBI

Remember!

• An increase in P50 indicates a shift of the OHDC to the right causing decreased affinity for O2 on the Hb which causes greater unloading of O2 at the tissue and decreased loading at the alveoli

• A decrease in P50 indicates a shift to the left causing increased affinity, decreased unloading of O2 at the tissue and increased loading at the alveoli

Oxygen Content

• Total Oxygen Content (CaO2) equals the sum of the dissolved O2 and the O2 chemically combined with Hb.– CaO2 = (0.003 x PaO2) + (1.34 x Hb x SaO2)

Represents dissolved O2 Represents chemically combined O2

.O3 = dissolved O2 1.34 = Carrying capacity of Hb

Normal value = 16 – 20 ml/dl

Oxygen Loading and Unloading

• If oxygen consumption remains constant, a decreased cardiac output increases the difference between arterial and venous oxygen content expressed as: C(a-v)O2.

• If oxygen consumption remains constant with an increase in cardiac output the C(a-v)O2 will decrease proportionately.


• Bohr Effect– Describes the effect of carbon dioxide

and hydrogen ions (H+) on uptake and release of oxygen

– Blood entering the pulmonary capillary bed is high in carbon dioxide with a decreased pH

– As CO2 is released at the alveolus, pH increases


– This results in a shift of the OHDC to the left, increasing the affinity of hemoglobin for oxygen, resulting in greater uptake of oxygen

– At the tissue level, CO2 excreted by the cells diffuses into the blood, lowering the ph and increasing the carbon dioxide level

– This results in a shift of the OHDC to the right, decreasing the affinity of hemoglobin for oxygen, resulting in greater release of oxygen to the tissue


• Haldane Effect– Describes the influence of hemoglobin saturation

on uptake and release of carbon dioxide

– Increase in levels of PaO2 in the pulmonary capillary bed decreases the ability of the hemoglobin to carry CO2, resulting in larger amounts of CO2 being released into the alveolus

– Decreases in levels of PaO2 at the tissue level increases the ability of the hemoglobin to carry CO2, resulting in larger amounts of CO2 being picked up by the RBC in the systemic capillary bed


In a nutshell:

The Bohr Effect affects oxygen transport by enhancing oxygen loading in the lungs and unloading in the tissues

The Haldane Effect affects CO2 transport by enhancing CO2 loading at the tissues and unloading in the lungs

Phew!

Effects of Carbon Monoxide (CO) on Oxygen Transport

• Hemoglobin has an 200x increased affinity for CO as to O2

• Presence of CO does not affect the oxygen saturation or PaO2

• CO is analyzed clinically

using CO-Oximetry

Effects of Carbon Monoxide (CO) on Oxygen Transport

• Presence of CO is not detectable by a pulse oximeter, only through analysis by a CO-Oximeter

• Treated by high concentrations of oxygen and/or hyperbaric oxygen

Carbon Dioxide Transport

• CO2 is normally carried in the blood in three different forms:

– Dissolved in a physical solution

– Chemically combined with protein

– Ionized as bicarbonate


• Dissolved in the Plasma and Intracellular Fluid– Plays a much more important role in

transport than dissolved O2 because of it’s higher solubility in plasma

– Approximately 8% of the total CO2 released in the lungs is transported in solution


• Chemically Combined with Protein– Combined with plasma proteins (< 1% of CO2

transported)– Combined with Hb to form carbaminohemoglobin

• H+ ions are produced by the bonding of erythrocyte Hb to CO2 reducing gaseous CO2 and increasing H+

• This stabilizes the pH because when it is reduced by hemoglobin it becomes a weaker acid – CO2 in its gaseous state is a volatile acid

• Makes up approximately 12% of CO2 transported


• Ionized as Bicarbonate (HCO3)– Makes up approximately 80% of the CO2

transported– Undergoes hydrolysis in plasma and in the

fluid of the RBC

CO2 + H2O ↔ H2CO3 ↔ HCO3 + H+

Most hydrolysis occurs within the Hb and plasma of the RBC

Hydrolysis reverses in the lung

Hydrolysis

Carbonic Acid


• Ionized as Bicarbonate (HCO3)– Reaction is enhanced by the enzyme

catalyst - carbonic anhydrase– As HCO3 builds within the cell, it moves out

of cell to maintain the concentration equilibrium

– The HCO3 splits into Na and Cl– Chloride (Cl-) moves into the cell to

maintain the electrolyte equilibrium– The process is called the “chloride shift”

+


The Chloride Shift

RBC

Erythrocyte

Plasma

• http://www.youtube.com/watch?v=VINQnL_oVFY

http://www.youtube.com/watch?v=VINQnL_oVFY

http://www.youtube.com/watch?v=VINQnL_oVFY

Abnormalities of Gas Transport

• Gas exchange is abnormal when oxygen delivery or carbon dioxide removal is impaired.

• Oxygen delivery to the tissues is a function of arterial oxygen content and cardiac output expressed as:

DO2 = CaO2 x Q

. .

DO2 = Oxygen transport to the tissuesCaO2 = Arterial oxygen contentQ = Cardiac Output

Abnormalities of Gas Transport O2

Arterial Oxygen Content• Hypoxemia:

– Exists when PaO2 is below the predicted normal based on the age of the patient. Can be due to lung disease – Most common cause of hypoxemia is V/Q mismatch

• Expected PaO2 = 100.1 – (0.323 x age in years)


Arterial Oxygen Content• Hypoxemia:

– Also occurs with abnormalities that impair oxygen delivery e.g., anemia, carboxyhemoglobin, methemoglobin

– Can occur when ambient PO2 is low such as at high altitudes

– The most important component in the oxygen transport system is Hb.


Reduction in Blood Flow• Shock or Circulatory Failure

– Tissue oxygen deprivation throughout the body

– Can be caused by low cardiac output as in an MI or overwhelming bacteremia

– Ischemia – Localized loss of blood flow to an area of the body or organ

– Dysoxia – Form of hypoxia caused by cellular O2 uptake disruption – Cyanide poisoning, septic shock, ARDS


During conditions of reduced arterial oxygen content (hypoxemia), normal oxygen delivery to the tissues can be maintained by the body increasing cardiac output.

Abnormalities of Gas Transport CO2

• Any disorder that lowers alveolar ventilation relative to metabolic production of CO2

– Inadequate minute ventilation• Restrictive/Obstructive lung disease, Drug

induced, improper ventilator settings : These are also V/Q mismatches.

− Increased dead space ventilation• Rapid/shallow breathing or increased physiologic dead

space V/Q = 0

Abnormalities of Gas Transport CO2

– V/Q Imbalances:• V/Q relationships must be in balance for

pulmonary gas exchange to be effective

• V/Q imbalances have a greater effect on oxygenation than on CO2 removal

Formulas to Remember

• PAO2• A-a gradient• A-a ratio• CaO2• DO2• VO2• Temperature

conversions• CO• SVR

• Gas Laws• CI• SV• EF

Adios, Au revoir , Bis später

homework if you did not complete hw turn in by monday email: [email protected] read all handouts,...

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