Ventilation-Perfusion Matching and Mismatching

distribution of blood flow is uneven due to

gravity

ratio of ventilation to blood flow for single alveolus

Va/capillary blood flow

ratio of ventilation to blood flow for entire lung

total Va/cardiac output

if ventilation > perfusion,

V/Q > 1

if perfusion > ventilation,

V/Q < 1

where is V/Q highest?

zone 1, at 3.0

where is V/Q lowest?

zone 3, at 0.6

V/Q mismatching is the most frequent cause of

arterial hypoxemia (reduced blood PO2) in cardiopulmonary disease

ventilation increases more slowly than blood flow from apex to base, so

V/Q ratio at apex > 1 and decreases as move down lung

regional differences in VQ produce

regional differences in PaO2 and PaCO2, with regional differences in PaO2 being much greater than those of PaCO2

normal flow (without shunt)

2 normal, parallel lung units, both receiving equal quantities of fresh air and blood flow

blood and alveolar gas partial pressures are typical for a resting individual

right-to-left shunt flow

mixed venous blood bypasses the gas exchange unit and goes directly into arterial blood

thebesian vessels

tiny veins in the wall of the heart chambers

of left ventricular myocardium, coronary venous blood drains directly into left ventricle rather than right atrium via these vessels

this is an example of how normally some blood always bypasses gas exchange units

arterial hypoxemia

result from additional defects that can occur

deoxygenated blood from right atrium or ventricle crosses septum and mixes with blood from left atrium or ventricle

cannot necessarily be corrected by administering 100% O2—shunted blood never exposed to enriched O2

final PaO2 will depend on size of shunt

a PaO2 less than 80mmHg in an adult breathing room air at sea level

bronchial circulation

1-2% total cardiac output, contains oxygenated blood, arises from aorta

supplies support tissue of lungs, including connective tissue, lower trachea, and bronchi

empties into pulmonary veins e.g. pleurohilar bronchial veins into the axygous vein which passes into vena cava

shunt

blood that enters the arterial system without going through ventilated areas of the lung

example of anatomic shunt

some of the bronchial circulation also passes directly (via deep bronchial veins) to the pulmonary veins

other abnormalities related to bronchial circulation

connection between pulmonary artery and vein (pulmonary arteriovenous fistula)

congenital defects can lead to right-to-left shunting after birth e.g. teratology of fallot (hole between ventricles)

result is to slightly depress arterial PO2 (since no gas exchange)

atelectasis

obstruction to ventilation of a gas exchanging unit with subsequent collapse- an example where the V/Q ratio = 0

causes include mucous plugs, foreign bodies, tumours

physiological shunt

ventilation to lung units is impaired in the presence of normal perfusion

lung unit with no ventilation has a V/Q ratio of 0

blood perfusing this unit is mixed venous blood and in the absence of gas exchange, the blood leaving is still mixed venous blood

deoxygenated blood bypasses the opportunity to exchange gas via contact with a gas exchange unit

dead space

V/Q = infinity

ventilation without perfusion (e.g. pulmonary embolism)

no gas exchange because there is no blood flow to receive O2 from alveolar gas

alveolar gas will have same composition as humidified, inspired air (PAO2= 150 mmHg; PACO2= 0 mmHg)

what happens to alveolar-arterial gradient during ventilation-perfusion mismatch on gas exchange?

will increase because relative over-ventilation of one area will not compensate for under-ventilation of another area

pulmonary embolism

blood clots that lodge in pulmonary arteries, often arise from detached portions of venous thrombi formed in lower extremities

thrombi cause shortness of breath, cough, hemoptysis (coughing up blood), tachycardia (increased heart rate), fall in blood oxygenation

example of V/P mismatching

restrict blood supply to alveoli being ventilated

high V/P and hypoxemia (low PAO2)

factors leading to venous thrombi

stasis of blood (e.g. immobilization after surgery)

alterations on the blood coagulation system (e.g. increased coagulability seen in sickle cell disease)

abnormalities in the vessel wall (e.g. due to local trauma or inflammation)

very large thrombi impact in

large arteries, but more common to break up and block several smaller vessels

pulmonary hypertension

mean pulmonary arterial pressure is approx 15 mmHg, increases are this

pulmonary hypertension causes

increase in left atrial pressure

increase in pulmonary blood flow

increase in pulmonary vascular resistance (most common)

pulmonary hypertension causes- increase in left atrial pressure

e.g. mitral stenosis (narrowing of the mitral valve opening that slows blood flow from left atrium to left ventricle) or left ventricular failure

sustained increases in left atrial pressure lead to structural changes in the walls of small pulmonary arteries (thickening)

result: dyspnea, hemoptysis, pulmonary edema

pulmonary hypertension causes- increase in pulmonary blood flow

e.g. congenital heart disease, patent ductus arteriosis- DA shunts most of blood from pulmonary artery to descending aorta in fetus. failure of the DA to close following birth results in left-to-right shunt

sustained high flow through pulmonary circulation results in recruitment/distention mechanisms being overwhelmed and structural changes in wall occur

pulmonary hypertension causes- increase in pulmonary vascular resistance

e.g. vasoconstrictive, like high altitude

obstructive, like thromboembolism

obliterative, like emphysema in which capillary bed is partly destroyed

effectiveness of gas exchange determined by

alveolar-arterial PO2 difference; A-a gradient

usually between 5-10mmHg in healthy person

value rises approx 3mmHg per decade of life

very upper limit of normal is 25mmHg

abnormalities in PaO2 may or may not

be associated with VQ inequality

hypercapnia

defined as an increase in arterial PCO2 above the normal range (40 ± 2mmHg)

hypocapnia

defined as an abnormally low arterial PCO2 (less than 35mmHg)

A-a gradient or alveolar-arterial PO2 difference (AaDO2)

subtract arterial PO2 (easily measured from blood gas analysis) from the ideal alveolar PO2, in absence of any inequality (derived from alveolar gas equation)

PAO2= PIO2 - (PACO2/R) + F (can ignore F)

mechanisms of hypoxemia

1. ventilation perfusion mismatch (most common)

2. shunt

3. diffusion abnormalities

4. alveolar hypoventilation (seen in overdoses of sedative/narcotic drugs, neuromuscular disease, etc)

5. low atmospheric oxygen (seen at high altitude)

VQ and hypercapnia

mismatching should cause both hypoxemia and this (CO2 retention)

but pts with mismatching often show normal arterial PCO2 since there is a reflex increase in ventilation rate triggered by chemoreceptors

increased dead space can also increase PaCO2 in absence of compensation, but local bronchoconstriction usually occurs immediately to redistribute perfusion

occurs in cases of hypoventilation

what kind of relationship between alveolar ventilation and alveolar CO2?

inverse, hypoventilation always causes decreased PaO2 and increased PaCO2