Gas Exchange Quiz 3

is a measure of the amount of available hemoglobin that is actually carrying oxygen.

SaO2 = [HbO2/total Hb] x 100

Changed in PO2

97%

75%

the sum of that dissolved and chemically combined with hemoglobin.

(1) PO2, (2) total hemoglobin content (g/dl), and (3) hemoglobin saturation.

CxO2 = (0.003 X PxO2) + (Hbtotal x 1.34 X SxO2)

16-20 ml/dl

[ C(a-v)O2 ]

about 5 ml/dl and is the amount of oxygen given up by every 100 mls of blood on each pass through the tissues

the amount of oxygen removed in relation to blood flow. Along with total body consumption of oxygen, you can calculate cardiac output.

Fick's equation

Qt =VO2

____________

C(a-v)O2 X 10

250 ml/min

4 to 8 L/min in adult patients

If the oxygen consumption remains constant, a decrease in cardiac output will increase the C(a-v)O2 and if the cardiac output rises, the C(a-v)O2 will fall proportionately.

 blood pH,  body temperature,  erythrocyte concentration of certain organic phosphates (2,3 DPG),  Hb structure variations  Other substances combining with Hb (ex. carboxyhemoglobin)

Right

Left

the % Hb sat for a given PO2 falls (decreased affinity for oxygen).

% Hb sat for a given PO2 rises (increased affinity of Hb for oxygen).

alters the position of the HbO2 dissociation curve due to changes in blood pH. These changes enhance oxygen loading in the lungs and oxygen unloading in the tissues.

As blood in the tissues picks up CO2, pH falls, the curve shifts to the right. With lower affinity for oxygen, Hb more readily gives up its oxygen to the tissues.

Venous blood returning to the lungs, pH goes up to 7.40 and shifts the HbO2 curve back to the left to aid loading at the lungs.

hifts the curve to the left, increasing Hb affinity for oxygen.

the curve shifts to the right, and the affinity of Hb for oxygen decreases.

Areas of increased temperature in the body will have increased temperature, hence increased unloading (Hb decreased affinity).

A decreased temperature decreases the need for O2, decreased unloading (Hb increased affinity)

In the red blood cells.

It stabilizes the deoxygenated Hb molecule, reducing its affinity for oxygen. Without 2,3-DPG normal oxygen unloading would be impossible.

right, increased oxygen unloading or decreased affinity of Hb for oxygen.

left, increased loading or affinity of Hb for oxygen.

alkalosis

chronic hypoxemia

Anemia

This increase promotes O2 unloading and decreases the affinity of Hb for oxygen

acidosis results in a lower intracellular 2,3-DPG and a greater affinity for oxygen banked blood (stored blood)-

In banked blood the concentrations of 2,3-DPG decreased by a third of the normal value in a weeks time. Large transfusions of blood more than a few days old can severely impair oxygen delivery to the tissue, even with normal PO2.

the shape, of the molecule, and therefore alter its affinity for oxygen (loading and unloading of oxygen).

Problems occur when the amino acid sequence in the polypeptide chains vary from normal.

There are more than 120 abnormal hemoglobins.

15% to 40% abnormal Hb.

HbS has less affinity for oxygen.

Deoxygenated HbS is less soluble than oxygenated and normal Hemoglobin.

it can crystallize inside the erythrocyte, causing the characteristic deformation in the cell shape.

The crystalline form is more fragile, leading to hemolysis and increased risk of thrombosis.

The heme complex normal ferrous iron ion (Fe2+) loses an electron and is oxidized to its ferric state (FE3+).

In the ferric state the iron ion cannot combine with oxygen and this type of anemia is called: methemoglobinemia

nitrite poisoning (meds: nitric oxide, nitroglycerine, lidocaine)

Blood looks brownish in color.

Skin color: grayish.

Treated with reducing agents like methylene blue or ascorbic acid

Identify with spectrophotometry

It is the chemical combination of hemoglobin with carbon monoxide.

Affinity of Hb for carbon monoxide (CO) is 200 times greater than oxygen

HbCO cannot carry oxygen, creates loss of oxygen carrying capacity.

the left, creating more problems with unloading of oxygen

increasing oxygen concentration to decrease the half life of CO and to supersaturate the plasma to keep oxygen going to the tissues.

Hyperbaric oxygen (HBO) is recommended for use, usually with patients of 25% or greater HbCO. (Room air, 1 atm., it takes more than 5 hours to remove half of HbCO, 100% O2, 1 atm., it takes 80 min, and HBO at 3 atm., 100%, is only 20 to 30 min)

It has a greater affinity for oxygen than normal adult Hb

Curve is shifted to the left.

This affinity is needed in fetal life

Replaced usually during the first year of life with normal adult hemoglobin

is the partial pressure of oxygen at which the Hb is 50% saturated, at 7.40 pH.

about 27 (26.6) mm Hg.

right, increased unloading, decreased affinity of Hb for O2.

increased affinity of Hb for O2 and decreased unloading.

45 to 55 ml/dl

1.dissolved in physical solution

2.chemically combined with protein

3.ionized as bicarbonate

the loading and unloading of CO2 in the blood can be illustrated in graphic form.

Unlike the S-shaped O2 dissociation curve, the carbon dioxide curve is almost linear.

This means that there is more direct relationship between partial pressure of CO2 and the amount of CO2 content in the blood.

decreases the blood’s capacity to hold CO2, helping it unload at the lungs

increases the bloods capacity for CO2 aiding uptake at the tissues

is a condition in which there is an inadequate amount of oxygen in arterial blood (decreased PaO2, SaO2, or hemoglobin content)

(low O2 content, low cardiac output or low oxygen uptake at the tissue level) occurs whether hypoxemia is present or not.

a condition which signifies low oxygen tissue content or cells resulting from inadequate oxygen delivery to meet their oxidative requirements. Therefore, the end result of ineffective gas exchange is hypoxia, which is manifested by hypoxemia.

Hypoxic (anoxic)

Anemic

Stagnant

Histotoxic

Gas exchange is abnormal when either tissue oxygen delivery or carbon dioxide removal is impaired

DO2 = CaO2 x Qt

O2 Delivery to tissue = Arterial O2 content x Cardiac output

(1) decreased of arterial blood content (hypoxemia),

(2) decreased cardiac output or perfusion (shock or ischemia),

(3) Abnormal cellular function prevents proper uptake of O2 (dysoxia)

Low PIO2

Hypoventilation

V/Q imbalance (Low V/Q)

Anatomic shunt

Physiologic shunt

Diffusion defect

Normal aging

Low PAO2

Caused by: (From alveolar air equation [PB-PH2O] FIO2 )

Low PB

Low FIO2

Low PAO2Low PaO2

Low PAO2

Low PaO2

PaO2 is low

P(A-a)O2 gradient on room air and supplemental O2 are normal

CaO2 is low

CvO2 is normal (if cardiac output increases to compensate)

Example: travel to high altitudes; low barometric pressure, creating mountain sickness.

-As alveolar PCO2 rises the alveolar PO2 will fall.

(FIO2 constant)- more noticeable at room air.

Caused by: hypoventilation

Low PaO2

High PaCo2

(Ventilation is the problem.. not oxygenation.)

PaO2 decreased

Normal P(A-a)O2 on room air and supplemental O2

CaO2 decreased

CvO2 normal (if cardiac output increases to compensate)

Due to thickening of the alveolar-capillary membrane, gas exchange is impeded; as seen by Fick’s first law of diffusion.

Disorders of the alveolar-capillary membrane such as; pulmonary fibrosis, interstitial edema, and interstitial lung disease

Low PaO2

High P(A-a)O2 on air; resolves with O2

PaO2 low P(A-a)O2 gradient increased on room air, resolving when placed on supplemental oxygen CaO2 decreased CvO2 normal (if cardiac output increases to compensate)

Low V/Q’s are the most common cause of hypoxemia in patients with lung disease

Perfusion in excess of ventilation; such as with bronchospasm, secretions in airway, and low volumes.

Low PaO2

High P(A-a)O2 on air; decreases with O2

PaO2 decreased

P(A-a)O2 widened on room air but decreased widening with supplemental oxygen

CaO2 is decreased

CvO2 is normal (if cardiac output increases to compensate)

*a true shunt

Caused by:

Blood flow between right and left sides of circulation; congenital heart disease.

Low PaO2

High P(A-a)O2 on room air; does not resolve with O2

PaO2 will be very low (if over 25-30% shunt)

P(A-a)O2 is very wide and widens even further with supplemental oxygen (if over 25-30% shunt)

CaO2 is decreased

CvO2 is normal (if cardiac output increases to compensate)

As the shunted blood increases to 30%; it becomes impossible to make up the oxygen of blood going by totally unventilated alveoli or moving from the right side of the heart to the left without going through the lungs.

Ex: ARDS

Caused by:Perfusion without ventilation; atelectasis, pneumonia, and pulmonary edema

Low PaO2

High P(A-a)O2 on air; does not resolve with O2

Extremely low PaO2 (as % shunt increases)

P(A-a)O2 widened with increased widening with supplemental O2 (as % shunt increases)

CaO2 is low

CvO2 is normal (if cardiac output increases to compensate)

apply the following 50/50 rule:

If the oxygen concentration is more than 50% and the PaO2 is less than 50 mmHg, significant shunting is present; otherwise the hypoxemia is mainly due to a simple V/Q imbalance

an abnormal deficiency of oxygen in the arterial blood that is resistant to treatment; usually indicates the presence of right-to-left shunting

The patient is on an FIO2 of 50% and the PaO2 is less than 50 mmHg.

If the FIO2 is increased by 20% and the PaO2 increases less than 10 mmHg

a gradual decrease in PaO2 caused by a progressive loss of elastic recoil pressure in the lung.

This changes the V/Q distribution and results in mildly progressive hypoxemia.

Loss of hemoglobin (Hb) anemia; due to hemorrhage or inadequate erythropoiesis

Low Hb content

Reduced CaO2

PaO2 may be normal or low

P(A-a)O2 is normal both on and off oxygen

CaO2 is low

CvO2 is low

large drops in CaO2.

The patient will be hypoxic even when the PaO2 is normal.

A drop in hemoglobin of 5 g/dl would be like dropping arterial blood to venous (PaO2 of 100 mmHg to 40 mmHg).

Abnormal hemoglobin; carboxyhemoglobin, methemoglobin, and abnormal hemoglobin (those causing left shift of oxyhemoglobin dissociation curve)

Abnormal SaO2 (done by co-oximeter)

Reduced CaO2

PaO2 may be normal or decreased

P(A-a)O2 gradient is normal on room air and oxygen

CaO2 is reduced (co-oximeter)

CvO2 is reduced (co-oximeter)

Decreased perfusion;

(1) circulatory failure (shock) and

(2) local reduction in perfusion such as MI, CVA (ischemia)

Increased (widened) C(a-v)O2

Decreased CvO2

PaO2 is normal

P(A-a)O2 is normal on room air and on oxygen

CaO2 is normal

CvO2 is decreased

C(a-v)O2 is widened (increased)

Dysoxia is a form of hypoxia in which the cellular uptake of oxygen is abnormally decreased.

The best example is cyanide poisoning (disruption of cellular enzymes).

It can also occur when tissue oxygen consumption becomes dependent on oxygen delivery.

Normal CaO2

Increased CvO2

PaO2 is normal

P(A-a)O2 on room air and supplemental oxygen is normal

CaO2 is normal

CvO2 is increased

tissue oxygen consumption becomes dependent on oxygen delivery.

Usually oxygen consumption equals oxygen demand (the flat portion of the solid line) .

If delivery falls, solid line, tissue extraction reaches a maximum, the point of critical delivery.

Further decreases create an oxygen debt (oxygen demand exceeds delivery (sloped line).

This leads to anaerobic metabolism and lactic acid build up.

Dotted line, pathological (ARDS, septic shock), the debt can occur at normal oxygen levels. Slope of dotted line indicates decreased extraction ratio (VO2/DO2).

Caused by decreased alveolar ventilation (VA) relative to metabolic need which causes: PaCO2 = VCO2 /VA hypercapnia and respiratory acidosis

(1) The minute ventilation is inadequate

(2) The dead space ventilation per minute is increased

(3) A V/Q imbalance exists

Vt x f = VE

decreased tidal volumes but could be due to decreased respiratory rates (drug overdose).

Usually caused by restrictive conditions: -- Atelectasis

Respiratory center depression

Neuromuscular disorders

Impeded thoracic expansion

kyphoscoliosis

decreased tidal volumes but could be due to decreased respiratory rates (drug overdose).

Usually caused by restrictive conditions: -- Atelectasis

Respiratory center depression

Neuromuscular disorders

Impeded thoracic expansion

kyphoscoliosis

ventilation without perfusion or ventilation in excess of perfusion (high V/Q)

(Vt – VDS) X f = VA

1. Rapid, shallow breathing (an increase in anatomical dead space per minute)Using the above formula:

Normal:(500 ml – 150 ml) X 12=4200 ml

Shallow:(250 ml – 150 ml) X 24=2400 ml2. Increased physiological dead space (V/Q = 0)

Using the above formula:

Normal:(500 ml – 150 ml) X 12=4200 ml DS (500 ml – 300 ml) X 12 =2400 ml

1. Minute ventilation to arterial PCO2 disparity.

2. The arterial to alveolar CO2 tension gradient P(a-A)CO2)

3. Dead space to tidal volume ratio VD/Vt

decrease by 10 mmHg

Increased

Dead space

1 to 5

it means there is more dead space. The gas from ventilated but not perfused areas will be closer to atmospheric gas.

It mixes with other gases from perfused areas, however the PETCO2 will be lowered.

.2 to .4 (20% to 40%)

up to .5 (50%)

0.6 (60%)

is significant disease and the patient is unable to maintain spontaneous ventilation.

VDS/Vt = (PaCO2 – PECO2 ) /PaCO2

V/Q imbalances

So, any increase in PCO2 from low V/Q units can be corrected by a reduction in PCO2 from high V/Q units.

But, O2 cannot do the same because the oxygen curve is nearly flat when the PO2 is above normal.

must increase their alveolar ventilation.

Those that can increase ventilation have a normal to decreased CO2.

If minute ventilation cannot be increased they will become hypercapnic.

Here the energy cost is prohibitive to maintain an increased minute ventilation, so the patient will opt for less work and therefore the CO2 levels will rise.