Micro Flows in the Cardiopulmonary System: A Surgical Perspective - Bioanalysis Advanced Materials Methods and Devices - page 72

aiming at a better understanding of the pathogenesis of CMD and the development of
therapeutic principles is necessarily based on the knowledge of the physiological
principles governing microvascular control of myocardial perfusion in healthy
subjects.
A condition which is related to CMD is the observation of angina symptoms in
patients with normal results in a coronary angiogram, often called coronary syn-
drome X [ 4 , 12 ]. Recent analyses have shown that this condition may have a
significant negative influence on prognosis for cardiac events. This condition is
specifically prevalent in women [ 21 ].
CMD is also linked to non cardiac diseases with well known microvascular
implications. For example, diabetes mellitus (DM) strongly affects the microvascu-
lar system (arterioles, capillaries, venules). Also, the viscosity of the blood is
increased in hyperglycemia, with concomitant increase in resistance of the micro-
vasculature, leading to stasis and thrombosis of capillaries. Coronary heart disease
events and mortality are greater in patients with DM.

5.2 The Lung

Airflow is delivered to the lungs through bronchi, into bronchioles and then into
alveoli where the oxygen and carbon dioxide exchange takes place with the pulmo-
nary capillaries. A mean number of 480 million alveoli with a mean diameter of
200

m are found in human lungs [ 16 ]. The adequacy of gas exchange in the lungs is
determined by the balance between pulmonary ventilation and capillary blood flow
[ 3 , 7 , 11 ]. This balance is commonly expressed as the ventilation-perfusion ( V / Q )
ratio. A perfect match between ventilation and perfusion ( V / Q

m

1), which
corresponds to normal arterial oxygenation, is the reference point for defining the
abnormal patterns of gas exchange [ 1 ].
A V / Q ratio above 1.0 describes the condition where ventilation is excessive
relative to capillary blood flow, with resultant hypoxemia and hypercapnia.
The excess ventilation, known as dead space ventilation , does not participate in
gas exchange with the blood [ 2 ]. Dead space ventilation increases when the
alveolar-capillary interface architectureisdestroyedsuchasinemphysema
(Figs. 5.4 and 5.5 )
A V / Q ratio below 1.0 describes the condition where capillary blood flow is
excessive relative to ventilation. The excess blood flow, known as intrapulmonary
shunt, does not participate in pulmonary gas exchange, with resultant also hypox-
emia and hypercapnia [ 1 ]. The fraction of the cardiac output that represents
intrapulmonary shunt is known as the shunt fraction [ 7 , 11 , 2 ]. Intrapulmonary
shunt fraction increases when small airways are occluded, such as in asthma,
when alveoli are filled with fluid, such as in acute respiratory distress syndrome
(ARDS) (Figs. 5.6 and 5.7 ). The main functional mechanism to combat perfusion
ventilation mismatch is the so-called hypoxic pulmonary vasoconstriction (HPV)
[ 19 ], which leads vasoconstriction of arteriolar vessels supplying regions with low

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