Peripheral Vascular Surgery: Tutorials in Postgraduate Medicine

Canberra

Chapter One

Physiology

John Ludbrook and John A. Walsh

Publisher Summary

This chapter discusses physiology. The term biophysics includes all cardiovascular functions that are fulfilled mainly as a result of the physical properties of blood and blood vessels. The cardiovascular phenomena that attend a great many bodily activities are biophysically determined and that reflex action of the central nervous system and tissue auto regulatory mechanisms merely add sublety and precision. When considering the function of the cardiovascular system, there is merit in disregarding anatomic nomenclature in favour of a classification that is based on biophysical attributes—chiefly pressure, cross-section, wall compliance, and permeability or diffusion characteristics. The blood in systemic arteries is at high pressure, but arteries accommodate only a small proportion of the blood volume. Their chief function is as distributive conduits. The arterial blood is at high pressure is not merely because of the action of the heart, but also to peripheral resistance to outflow from the arterial tree.

It is impossible to practice peripheral vascular surgery without some knowledge of the factors that determine flow in blood vessels; of the inter-relationships between the vascular system and the volume of blood it contains; of the control systems that influence blood vessels; and of the techniques that can be used to make measurements of blood pressure, flow, and volume. The purpose of this chapter is to provide such an understanding, to suggest in what way physiologic mechanisms are relevant to disease states, and to indicate where further information can be sought. It should be pointed out that the account that follows is strictly human-oriented, and is based on data that has been gathered from study of the cardiovascular dynamics of man in health and disease, rather than that obtained from animal experiments. Because the subject of this book is peripheral vascular surgery, emphasis has been placed on the function of the peripheral vasculature. Nevertheless this chapter would be incomplete without a consideration of more general cardiovascular functions.

BIOPHYSICS OF BLOOD AND BLOOD VESSELS

In the account that follows there has been a liberal interpretation of the term biophysics, to include all cardiovascular functions that are fulfilled mainly as a result of the physical properties of blood and blood vessels. It is becoming increasingly clear that the cardiovascular phenomena that attend a great many bodily activities are biophysically determined and that reflex action of the central nervous system, and tissue autoregulatory mechanisms merely add sublety and precision.

The Determinants of Blood Flow

Certain biophysical concepts in regard to blood and blood vessels are essential to the understanding of their biological functions. The treatment of these will be at a fairly non-mathematical level: more sophisticated information can be obtained elsewhere.

) in a tube is as:

where Δρ = the pressure difference between the ends of a tube, and R = the resistance to flow between these points.

(where r = tube radius, l = tube length, and η = viscosity of the fluid). Alternatively, flow may be described as the product of perfusion pressure and conductance, the latter being the reciprocal of resistance:

Blood is no ordinary fluid, and blood vessels are not straight, rigid, nor of uniform bore. Nevertheless, the Poiseuille equation constitutes a useful starting point from which to consider the flow of blood in blood vessels.

The Poiseuille equation describes laminar flow, in which the wave front is of a constant paraboloid form (Fig. 1.1). This description fits the flow of blood fairly accurately in most circumstances. However, the particulate composition of blood results in one form of deviation from the ideal: there is a cell-free boundary layer adjacent to the vessel wall that assumes importance in small vessels (Fig. 1.6). Nor is blood flow laminar in all circumstances: in straight, uniform-bore tubes turbulent flow (Fig. 1.1) occurs when the Reynolds number (Re) exceeds a critical level, this number being a function of tube radius (r), velocity of flow (V), density of the fluid (ρ), and an inverse function of its viscosity (η). That is:

FIG. 1.1 The paraboloid wave-front that is a feature of laminar arterial blood flow, and its distortion by transient turbulence at the origin of a branch.

FIG. 1.6 Diagrammatic representation of red cell behaviour, and the changes of blood viscosity, in the microcirculation. A: 100 μ arteriole, with random orientation of red cells. B: 15 μ terminal arteriole, with more regular orientation of red cells, relatively large boundary plasma zone, and drop in apparent viscosity (Fahreus-Lindqvist effect). C: capillary, with paraboloid deformation of red cells.

In the normal vascular tree the Reynolds number rarely exceeds the critical level for turbulence except for brief periods of time and where the vascular geometry is complex (as at the aortic valve, or at the take-off of arterial branches). Only when there is pathologic irregularity, stenosis or dilation of an arterial lumen does prolonged turbulence occur. Among the consequences of turbulence is a sharp rise in energy-loss (and thus resistance to flow), and the production of audible murmurs that may be of diagnostic value. Finally, blood flow is pulsatile (rather than steady) in many blood vessels. This introduces a further complexity into the relation of pressure and flow, especially because of dynamic interaction with the visco-elastic arterial wall, and in regard to the production of turbulence. One effect of the elasticity of the central arteries is that at some points in the distal arterial tree flow may not be undirectional but is transiently reversed during cardiac diastole. This phenomenon is most apparent when peripheral resistance is high.

Pressure

The actual, or measured, pressure at any point in the vasculature is made up of hydraulic and hydrostatic components.

Hydraulic Pressure is the force that drives blood through the vasculature (Fig. 1.2). This force is normally generated by cardiac action (although subsidiary musculovenous pumps contribute to hydraulic pressures in the venous system of the lower limb). In the arterial tree the hydraulic pressure is pulsatile, though for simplicity of analysis this driving force is often approximated to the mathematically-derived mean hydraulic pressure. The timing and shape of the hydraulic pressure waves that originate from the heart are considerably modified by the visco-elastic properties and geometric shape of the arterial tree (Fig. 1.3). The proximal aorta constitutes an elastic reservoir into which the left ventricular contents are discharged, and which dampens the central pressure pulse. Proceeding distally in the arterial tree the increasing rigidity of the vessel walls causes an exaggeration of the systolic peak and diastolic trough, of pressure. Arterial branching and the high resistance offered by the peripheral microvasculature cause reflection of pressure waves, so that at some points there is superposition of direct and reflected pressure peaks and troughs (standing waves). For the above reasons, at some points in the arterial tree distal-proximal pressure gradients may be transient (Fig. 1.3), and these account for the transient reversal of flow mentioned earlier. Nevertheless, there is a consistent downward gradient of mean pressure (hydraulic pressure gradient or ΔP) in the direction of mean blood-flow.

FIG. 1.2 Definitions of pressure. Hydraulic pressure gradients generated by the interaction of the cardiac pump with the resistance offered by arterial, microvascular, and venous elements of the vascular tree. Hydrostatic pressure in the venous system in the upright posture, resulting from the weight of a column of blood in a system that is rendered open-ended by collapse of the veins above heart level. Transmural (distending) pressure: the difference between intravascular and tissue pressure.

FIG. 1.3 Intravascular pressure pulses in the human aortic arch, femoral artery, and dorsalis pedis artery. The stippled area is the time-period during which back-flow can occur in the dorsalis pedis artery. (After Remington, J. W. and Wood, E. H., J. Appl. Physiol. 9: 433, 1956).

The hydrostatic component of intravascular pressure is analogous to that derived from the height of a column of blood (Fig. 1.2). The vasculature is of course a closed system of tubes (rather an open-ended system) and it is only the pliability of its walls that allows hydrostatic pressures to be generated. For instance, the collapsibility of the walls of veins creates an effective water-level (zero-pressure reference point) in the venous system, that is located in the thorax (Figs. 1.11, 1.12). The consequence is that the actual pressure at any point in the venous system is a sum of the hydraulic pressure (driving force) and of an hydrostatic pressure that is approximately equal to the vertical distance of the point below the heart. In the case of arteries, elasticity allows the creation of hydrostatic pressures. In fact, hydrostatic pressures are approximately equal in arteries and veins at the same horizontal level, and therefore do not contribute to the determination of blood flow.

FIG. 1.11 Venous pressure gradients through abdominal inferior vena cava, right atrium, superior vena cava, brachiocephalic and internal jugular veins. HIP = hydrostatic indifferent points, at which no pressure change occurs during the appropriate postural manoeuvres. (From Ludbrook, J. (Ed.) The venous system in Cardioangiological flow methods. Ed. Korner, P. I., International Society of Cardiology, 1972.)

FIG. 1.12 Normal range of central venous pressures in the supine posture in relation to the sternomanubrial junction (SMJ). (After Debrunner, F. and Bhüler, F., Brit. med. J. 3. 148, 1969.)

A third way of describing pressure should be mentioned in passing. It is the pressure-difference between the inside and outside of a blood vessel—the transmural or distending pressure (Fig. 1.2). The cross-sectional area of the lumen of a blood vessel is determined by the interaction of transmural pressure with the physical properties of its wall.

Vessel Radius

The Poiseuille thesis that volume-flow is a function of the fourth power of tube-radius is a concept that is central to the understanding of peripheral resistance, and of the effects of stenotic lesions on blood flow.

The element of the vasculature that is the major determinant of peripheral resistance to blood flow is the terminal arteriole. This is partly due to its size. Thus the relative resistances to flow offered by the diameters of the thoracic aorta, brachial artery, and a terminal arteriole are approximately as 1:10,000:15,000,000,000,000. Size is not the only determinant, for capillaries are a good deal smaller (6–7μ) than terminal arterioles (15–50μ), and are shorter by a factor of one half to one quarter; however each terminal arteriole gives off up to 30 capillaries. It is the integrated effect of the radii, lengths, and series-parallel arrangements of the different sections of the vascular tree that are responsible for the actual, measured, hydraulic pressure gradient (Fig. 1.4).

FIG. 1.4 Schematic drawing of hydraulic pressure gradients in the vascular tree of the lower limb, derived from published data.

A = artery; AC = arterial capillary;

VC = venous capillary; FoV = small foot vein;

GSV–A, –K: great saphenous vein at ankle, knee;

FeV = femoral vein at groin; RA = right atrium.

Closed circles, continuous line: neutral resting conditions.

Open circles, interrupted line: with maximal arteriolar dilatation. (After Ludbrook, J. Aspects of venous function in the lower limbs, Thomas, Springfield, 1966.)

A major difference between the resistance vessels in man and the rigid tubes of Poiseuille, is that the radii of the resistance vessels are not fixed. Their elastic walls cause radius to be dependent on the distending (transmural) pressure. Moreover the action of the innervated smooth muscle of their walls can cause profound changes in radius, providing a mechanism for the active regulation of both the magnitude and anatomic location of regional peripheral resistance (see p. 11).

Blood Viscosity

The coefficient of viscosity (η) is defined as the ratio of shear stress to shear rate. A paraphrase of this definition, applicable to tubes of fixed geometry, is the ratio of hydraulic pressure to the flow rate. The Poiseuille equation holds true only for fluids that are Newtonian in behaviour (constant viscosity at all rates of flow). Water and electrolyte solutions are Newtonian, plasma nearly so, but blood is distinctly non-Newtonian. At high rates of shear (rapid flow), the viscosity of normal blood is near-constant and approximately five times that of water, but at low rates of shear (slow flow) its viscosity progressively increases towards infinity (Fig. 1.5). The main determinants of this anomalous behaviour of blood are the concentration of red cells in the plasma and the interaction of red cells with certain plasma proteins (particularly fibrinogen, but also normal and abnormal globulins). Blood viscosity is also an inverse function of temperature, though this effect is small in the physiologic range.

FIG. 1.5 The non-Newtonian behaviour of whole blood at different levels of haematocrit (Ht), compared with the near-Newtonian behaviour of blood plasma. Data from in vitro measurements with a cone-in-cone viscometer. (After Cairncross, D. et al., Med. J. Austr. 1: 1348, 1969.)

In an altogether different sense, blood is non-Newtonian. When blood flows in vitro through fine (< 100μ) tubes its apparent viscosity diminishes (Fahreus-Lindqvist effect). This may be because of single-file red cell progression, and also because the cell-free, low-viscosity, plasma layer adjacent to the wall assumes greater importance (Fig. 1.6). However, in life, red cells squeeze through capillaries by assuming a jellyfish-like paraboloid form: it has been suggested that the internal viscosity of the red cell itself may be of paramount importance in this circumstance. No meaningful equation of in vitro measurements of blood viscosity with the in vivo situation has yet been accomplished. In general, only gross changes in red cell concentration, or gross alterations in plasma constituents (macroglobulins, cryoglobulins, higher molecular weight dextrans), can and do affect blood flow in small vessels.

The Properties of Blood Vessel Walls

Some of the ways in which these may affect blood flow have been already considered. Two other properties of the vessel wall are important: compliance and tension.

Compliance

This may be loosely defined as the visco-elastic property of a vessel wall. It can be examined by determining the relationship of change in cross-sectional area (or volume) to change in transmural pressure: i.e. Δ volume/Δ pressure.

An isolated artery retains its circular cross-section when the transmural pressure is zero, and as the pressure across its elastic wall is increased there is a corresponding and nearly linear increase in luminar cross-sectional area (Fig. 1.7). It appears stiffer when the pressure changes are pulsatile rather than static. Isolated veins behave very differently. When the transmural pressure is zero they collapse (Fig. 1.7). As it is increased, there are at first large increments of volume for small increments of pressure, until a circular cross-section is attained. Then further volume increments are small, as the largely-collagenous wall becomes taut. These simple, in vitro, pressure-volume relationships are more complex in life for both anatomic and physiologic reasons. For instance, the wall of a vein may be rendered rigid by the surrounding tissue (e.g. bone). A hydrostatic rise in intravenous pressure may be paralleled by a rise in extravenous pressure, whether hydrostatic (cerebrospinal fluid, abdominal contents) or dynamic (skeletal muscle contraction). Active change in wall compliance can be effected in many vessels by change in smooth muscle tone. In the case of arterioles, this effect is much greater than any passive changes in cross-section that can be produced by changes in transmural pressure. In the walls of central arteries elastic elements predominate, but substantial active changes in calibre can occur in muscular peripheral arteries. Venules greater than 50 μ in diameter and subcutaneous veins have muscular walls and can undergo active changes in compliance (venous tone). However, most deeply-placed veins contain little or no smooth muscle and their compliance is determined only by the transmural pressure and by the physical properties of their walls.

FIG. 1.7 Diagrammatic representation of the relation of transmural pressure and luminal cross-sectional area for the abdominal aorta (continuous line) and common iliac vein (interrupted line). Cross-sectional areas are assumed to be identical at 10 mm Hg transmural pressure.

Stippled band: normal working pressure-range for iliac vein.

Matched band: normal working pressure-range for abdominal aorta.

Tension

The tension (T) in the wall of a blood vessel (i.e. the tangential stretching force) is described by Laplace’s law:

T = Pr

That is, the force tending to stretch the wall is not merely a function of the pressure (P) across the wall of a vessel, but also of its radius (r). Several deductions can be made from this. Laplace’s law provides an explanation of how the 05μ thick wall of a capillary can withstand the hydrostatic pressure of 90 mm Hg to which it may be exposed (for instance in the foot, in the standing posture). At an identical pressure, the wall tension of a capillary is only about 1/10,000 of that in the ascending aorta. Laplace’s law is also relevant to the tendency of the wall of an arterial aneurysm to disrupt (see Fig. 1.23).

FIG. 1.23 The application of Laplace’s law to the tendency for an arterial aneurysm to rupture (i.e. wall tension/wall thickness).

Functional Classifications of Blood Vessels

When considering the function of the cardiovascular system there is merit in disregarding anatomic nomenclature in favour of a classification that is based on biophysical attributes: chiefly pressure, cross-section, wall compliance, and permeability or diffusion characteristics.

The blood in systemic arteries is at high pressure, but arteries accommodate only a small proportion (15%) of the blood volume. Their chief function is as distributive conduits.

That arterial blood is at high pressure is not merely due to the action of the heart, but also to peripheral resistance to outflow from the arterial tree. Resistance vessels are those along which there is a steep hydraulic gradient: they are of small cross-section and have walls of low (but variable) compliance. These characteristics are possessed by arterioles and terminal arterioles, though when there is full arteriolar dilatation, capillaries and even collecting venules may act as resistance vessels (see Fig. 1.4).

The greater part of the blood volume is accommodated at low hydraulic pressure, in vessels that have extremely pliable walls and are of large cross-section. These capacity vessels are, collectively, venules, systemic veins, right atrium, right ventricle, pulmonary vasculature, and left atrium.

There remain the vessels concerned with exchange of water and solutes between blood and tissues, or between blood and the external environment. These are the capillaries. The control of this exchange function is complex. It is in part invested in precapillary sphincters that determine flow versus no-flow in individual capillaries (and thus exchange or no-exchange). In some vascular beds such as the skin there are specialized shunt vessels; blood flowing through these by-passes capillaries, and is not available for tissue-exchange. The tissue lymphatics also participate in exchange with the tissues, though in a more restricted fashion.

Blood Volume and Vascular Capacity

There are no hard facts about the distribution of blood volume among the various elements of the vasculature, but there are certain well-agreed presumptions. Only about 15% of the blood volume is contained by systemic arteries, while 65% lies in systemic veins. Eighty per cent lies within the capacity vessels of high compliance that collectively make up the low-pressure compartment. There is less agreement as to the distribution of blood volume between the macroscopic components of this compartment and its microscopic elements (venules). All parts of the low pressure compartment are in free intercommunication (at least in steady-state situations), and offer a low resistance to blood flow. An implication of this is that in all parts of the compartment at the same horizontal level, the blood pressures are identical, and principally of hydrostatic origin: this is approximately true.

A related concept is that the region of the heart is a circulatory null-point, in that right atrial (central venous) pressure is near-constant regardless of body posture or activity. This is closely true for man. Only very small changes in central venous pressure result from postural change within the range 10° head-down to 60° foot-down, or are caused by the extremes of cardiac output from sudden cardiac arrest to that which obtains during exercise.

The introduction of the cardiac pump into the low pressure compartment has remarkably little effect on the freedom of intercommunication, or on the pressures, within it. Following sudden pump failure (cardiac arrest) in animals and in man there is almost no change in central venous pressure: while there is a profound pressure-drop in the left ventricle and arterial tree, the shift of blood volume into the highly compliant low-pressure compartment is trivial. Conversely, when cardiac arrest occurs in a patient with congestive (biventricular) heart failure, central venous pressure remains at a higher than normal level: the antemortem venous congestion is due to an increase in blood volume, and not directly to cardiac pump failure. Grossly abnormal differentials in mean pressure between elements of the low-pressure compartment arise only when there is severe obstruction to flow between them (massive pulmonary embolism, severely stenotic cardiac valve disease), and usually a compensatory hypervolaemia is necessary before these pressures can be generated.

It is implicit that the one means of producing a change in central venous pressure is by altering blood volume. When this has been done in normal humans the change in central venous pressure with acute changes in blood volume of ± 750 ml are quite regularly predictable (Fig. 1.8). The vasculature behaves like an inert plastic bag of constant and high compliance. Whether the compliance of the low pressure compartment can be altered by the activity of the smooth muscle that is present in the walls of some of its elements (i.e. by changes in venous tone) will be discussed later (p. 30).

FIG. 1.8 Effect of alteration in blood volume (produced by bleeding or auto-transfusion) on central venous pressure in normal, recumbent, human subjects. (After Gauer, O. H. et al., Circulat. Res. 4: 79, 1956.)

Musculovenous Pumps

These are highly developed in man, presumably as an adaptation to his upright posture. In the lower limbs the valved deep veins, enclosed within the deep fascia of the enveloping muscles, constitute a parallel-series arrangement of reciprocating pumps (Fig. 1.9). The deep veins constitute the pump chambers, especially the large, specialized, venous sinuses in the soleus muscle. Blood is driven in a proximal direction by the contraction of the surrounding muscles, within which pressures of up to 250 mm Hg can be generated in the lower leg. When phlebography is performed during muscle contraction the intramuscular veins can be shown to be obliterated, while the intermuscular veins are merely narrowed. During the phase of muscle relaxation the deep veins are refilled by muscle throughflow, by upflow from distal deep veins, and by inflow from subcutaneous veins via the one-way-valved perforating veins.

FIG. 1.9 Musculo-venous pumps of the lower limb, during reciprocal thigh-calf contraction-relaxation as in walking. Note effects of muscle contraction on venous volume, valve position, and flow through superficial communicating, and deep veins.

Three identificable effects result from the action of the lower limb musculovenous pumps. During ambulatory activity the venous blood volume of each lower limb is reduced by 100–150 ml, because the compliance of this portion of the low pressure compartment is reduced, as is also the mean hydrostatic venous pressure. This blood is redistributed within the low-pressure compartment (especially to the pulmonary vasculature). Second, the reduction in mean deep venous pressure (Fig. 1.10) causes a corresponding increase in perfusion pressure in the exercising muscles In this sense the musculovenous pumps act as cardiac boosters or superchargers, for by a trivial diversion of the energy-output of the leg muscles, the maximum rate of blood flow through them can be boosted by up to 50%. Third, the increase in lower limb venous hydrostatic pressure that results from assuming the upright posture causes a marked increase in the rate of production of tissue-fluid; the venous pressure-lowering action of the musculovenous pumps reverses this tendency.

FIG. 1.10 Schematic representation of the behaviour of superficial (great saphenous) and deep (posterior tibial) venous pressure at the ankle before, during, and after ambulatory exercise. Note the deep-superficial venous pressure gradient during muscle relaxation. (From Ludbrook, J. (Ed.) The venous system in Cardioangiological flow methods. Ed. Korner, P. I., International Society of Cardiology, 1972.)

Lymphatics

Of all the components of the vascular system, the lymphatics have been most difficult to investigate. This is chiefly because of their small size and their transparency.

Four anatomic elements of the lymphatic system are worthy of note. Lymphatics begin as blind, 5–10 μ diameter terminal capillaries in the tissue spaces. The endothelial cells that comprise the walls of these terminals have intercellular gaps that are notably greater than those between the endothelial cells of venous capillaries. These gaps may be several micra wide and allow the passage of macromolecules up to a molecular weight of 6000. The intercellular gaps (or open junctions) also act as inlet valves, permitting protein or other macromolecules to pass into the lymphatics but not to escape. In tissue oedema these intercellular gaps are held open by fine fibrils that pull on the endothelial cells, thus facilitating the entry of excess tissue fluid. The second element comprises the 05–1 mm diameter, valved, lymphatic trunks of the limbs or mesentery that carry lymph to regional lymph nodes. Then come the lymph nodes themselves, through the sinuses of which lymph flows, and by means of which the contents of lymph come into immediate contact with the reticuloendothelial system. Finally, lymph is gathered into larger, valved, trunks (thoracic duct, right lymphatic duct) of up to 5 mm in diameter, the walls of which contain a small amount of smooth muscle.

The flow of lymph is engendered by a number of factors. The first is the rate of production and amount of tissue fluid. The rate of accumulation of tissue fluid is governed principally by the interaction of intravascular pressure, tissue pressure, permeability of the blood capillaries, and the osmotic gradient across their walls. Entry of substances into lymphatics is by two main methods: firstly, through the intercellular gaps described above; and secondly by pinocytosis (the transcellular route). Because of the large gaps between the endothelial cells in the blind lymphatic endings, and the free exchange of crystalloids through the cells, osmotic pressure gradients between tissue spaces and lymphatics are insignificant. Thus the rate of entry into the lymphatic terminals is largely governed by the magnitude of tissue pressure, and by the rate at which lymph is propelled proximally. While there is under resting conditions a modest distal-proximal hydraulic gradient in the lymphatic system, the chief mechanism for onward propulsion of lymph is by extrinsic pumps. Muscular activity is the main pumping mechanism, creating hydraulic forces not only within the muscles but also in subcutaneous tissues and the body cavities. The pulsation of adjacent arteries and arterioles aids lymph flow. Flow in splanchnic lymphatics is boosted by visceral smooth muscle activity, including that in the small intestinal villi. The effectiveness of these pumps is greatly increased by the lymphatic valves. Finally, the smooth muscle of the major lymphatic ducts has been observed to undertake spontaneous, rhythmic, propulsive activity. This peristalsis is enhanced by stimulation of the sympathetic nervous system and by catecholamines, and inhibited by barbiturates.

Several major functions of lymphatics have been identified. They act as a device for removing excess tissue fluid. In the small bowel, they participate in the absorptive process by acting as a transport pathway for lipids (in the form of chylomicrons). However, these two functions may in a sense be accidental, for the most important activity of lymphatics is as afferents to, and efferents from, lymph nodes. By means of the afferent lymphatics large, foreign, antigenic, protein molecules and microorganisms are first brought into contact with the reticuloendothelial system.

Methods of measuring flow-rate in lymphatics are of relevance to the study of lymphatic obstruction. They are relatively crude. Thoracic duct outflow has been measured in man by cannulation. The total flow in 24 hours is approximately equal to plasma volume. At the other end of the scale, tissue clearance by lymphatics has been measured by the disappearance-rate of ¹³¹I-labelled albumin from an injected depot. Crude qualitative estimates of lymphatic flow can be made by the rate of travel of intra-dermally injected dyes and by the rate of clearance of radiocontrast medium from lymphatic trunks.

METHODS OF MEASURING CARDIOVASCULAR FUNCTIONS

Intravascular Pressure Measurement

There are three aspects to this topic: the measuring devices, the means of access to the interior of blood vessels, and the clinical applications.

MEASURING DEVICES

Indirect methods of measurement are largely of historic interest, except for the brachial sphygmomanometer. That this is still in use is a tribute to its simplicity and to certain accidents of anatomy (the shape of the arm, the superficial location of the brachial artery) and of haemodynamics (the Korotkow sounds). Its limitations are that it is only accurate in the upper arm, gives an unreliable indication of diastolic pressure, and inter- and intra-observer errors are inherent in the method.

The simplest device for direct pressure measurement is the saline manometer. It is practical only to the measurement of venous (i.e. low) pressure. The other inherent limitations of the saline manometer are that it has a poor frequency-response and that the pressure cannot easily be directly recorded. Nevertheless it is widely used in clinical practice for central venous pressure measurement.

Direct methods of measurement that permit the accurate reproduction of intravascular pressure and its changes depend on devices that transduce pressure into an electrical signal. The transducers in common use are the strain gauge, the semi-conductor transducer, and inductance and capacitance manometers. There are some variations among these in physical robustness, frequency-response and stability, but the differences are rarely critical in clinical practice. They may be used with a variety of amplifier and display systems (pen-writer, ultraviolet recorder, oscilloscope). Most reputable commercially available instrument systems have a sufficiently high frequency-response, sufficient baseline stability, and sufficiently linear input-output characteristics, for clinical purposes. The sources of error mostly relate to the method of cannulating the vessel, the choice of zero-pressure reference-point, differences between end- and lateral-pressure, and in the selection of tubing (length, diameter and consistency) to produce critical-damping. Many of these sources of error can be minimized by the use of a catheter-tip mounted electromanometer, though a major present limitation of this device is its size (2–3 mm in diameter).

ACCESS TO THE VASCULATURE, REFERENCE POINTS AND CLINICAL APPLICATIONS

Peripheral venous pressure is most often measured in the lower limbs, and in the portal system. Lower limb venous pressure measurements may be used to study the musculovenous pumps, to detect venous obstruction and to detect or locate arteriovenous fistulae. A catheter can be readily introduced transcutaneously into the great and small saphenous veins, the femoral vein, or the popliteal vein (by way of the small saphenous). The posterior tibial vein can be cannulated only by surgical exposure (though the intracalcanean pressure is close to the mean pressure in the posterior tibial vein).

Portal vein pressure is measured to test for portal vein obstruction. Direct measurement can be made by operative cannulation of a small bowel mesenteric tributary and in exceptional circumstance by reopening the obliterated umbilical vein, or by transcutaneous transhepatic puncture. However, certain indirect methods of measurement are possible and correlate closely with direct: transcutaneous puncture of the spleen and catheterization of the splenic pulp, or the wedging of a catheter into an hepatic vein tributary. In practice, the most commonly used methods are splenic puncture, and per-operative mesenteric venous cannulation.

Central venous pressure monitoring is used with increasing frequency during surgery and intensive care. The term is usually used as a synonym for right atrial pressure or a close approximation to it. A catheter is introduced into the venous system transcutaneously, through or over a needle, and advanced into a brachiocephalic vein, the superior vena cava or the right atrium. The site of venipuncture may be an antecubital vein, the external jugular vein, or (less often) the cephalic, internal jugular or subclavian veins. By whatever route the catheter is introduced, it is critically important that its tip lies in one of the intrathoracic veins. This should be checked by chest radiography, or by using the catheter as an electrocardiographic lead.

Reference points are particularly important in venous pressure measurement, because pressure changes of a few centimetres of water from normal may reflect dramatic changes in circulatory homeostasis. Only when the pressure transducer is mounted in the catheter tip and when the anatomic location of the tip is accurately known, is a truly direct measurement of intravascular pressure obtained. The more usual circumstance is that the pressure transducer is connected to the external end of an intravascular catheter, so that only when the transducer is placed on exactly the same horizontal level as the catheter-tip is pressure meaningfully measured. There is little difficulty in accomplishing this in the case of peripheral limb veins, but rather more of a problem in the case of intrathoracic and intra-abdominal veins.

Fortunately, in clinical situations in which central venous pressure is sought the patient is usually supine. In this circumstance, the pressures in the intrathoracic great veins (brachiocephalic, superior vena cava, inferior vena cava) and in the right atrium are closely similar (Fig. 1.11). The normal mean value is about 5 cm H2O (3·5 mm Hg). It has recently been established that a reliable external zero-pressure reference point is 1 cm behind the manubriosternal junction (range ± 4 cm) (Fig. 1.12). So that provided the catheter-tip is identified as lying in one of these central locations and the zero of the manometer scale is in a horizontal plane 1 cm behind the manubriosternal junction, a normal central venous pressure range is 1–9 cm H2O.

In the upright posture, true right atrial pressure is a little lower than when a person is supine (though the transmural pressure remains near-constant, because intrathoracic pressure also falls). Thus in this posture the zero-pressure reference point lies at the junction of a frontal plane through the mid-axillary line and a horizontal plane through the 4th chondrosternal junction (the phlebostatic axis).

It is less easy to decide on a truly appropriate zero-pressure reference point for portal venous pressure. The traditional one is the anterior surface of the lumbar vertebral column, which gives a mean normal portal pressure of 22 cm H2O (with 95% confidence limits of 12 to 32 cm H2O). However, it is more meaningful physiologically to compare portal venous pressure with central venous pressure: that is, to measure the pressure gradient across the liver.

Direct arterial pressure measurements are being used increasingly often in everyday clinical practice, not only in the course of cardiac surgery, but as part of intensive-care monitoring. The common routes of access to the arterial tree are by transcutaneous femoral artery catheterization, or by surgical cannulation of the radial artery. Brachial artery puncture may be used in the short-term. The pressure transducer must again be placed horizontal with the catheter-tip, but there is a greater margin for error.

BLOOD FLOW MEASUREMENT

A great variety of techniques are in use. They may be grouped as follows:

Detection of Marker-dilution

Until recently the marker has usually been a dye (indocyanine green), the concentration changes of which are measured by withdrawal of blood through a cuvette-densitometer and displayed by means of a chart-recorder. However, thermal dilution, using room-temperature saline as the marker and an intravascular catheter-mounted thermistor to detect temperature-change, is gaining in popularity: it has advantages of economy, and withdrawal of blood is unnecessary. Gamma-detection of radionuclide dilution comes a poor third. With any of these markers, instant bolus-injection is the most useful technique: mean volume-flow past the point of injection is calculated from the mean concentration of the marker during the time it takes to pass the sampling point (Fig. 1.13). By using suitable injection and sampling points, cardiac output and regional arterial or venous flow (limb or splanchnic) can be measured. The advantages of marker-dilution techniques are that they measure volume-flow, they are applicable to any vessel that can be catheterized, and their inherent accuracy for long-term measurements is good. Their deficiencies are that they measure mean, rather than instantaneous, flow; complete mixing of the marker in the blood stream must be assured; and it must be certain that a variable distribution of blood flow between injection and sampling points does not occur.

FIG. 1.13 Methods for measuring blood flow in clinical practice.

Injected marker dilution, using cold saline, indocyanine green, or a radionuclide. The dose of the marker is indicated as D. The actual, recorded, concentration-time curve at the sampling point (continuous line) is corrected for recirculation (broken line), allowing the calculation of mean concentration (C) during the time duration (T) of passage of the marker.

Local marker clearance, using ¹³³Xe. The rate of change of concentration of the gamma-emitting radionuclide with time is exponential, and the slope of this line when replotted semi-logarithmically is a function of tissue blood flow.

Electromagnetic flowmeter. M, electromagnet; E, electrodes across which the potential difference is a function of flow.

Doppler-effect flowmeter. G, the generator of ultrasound; R, the receiver of reflected ultrasound. The frequency-shift is a function of flow.

Venous occlusion plethysmography. P, volume-sensing forearm Plethysmograph; V, intermittent venous occlusion cuff; A, arterial occlusion cuff. An intermittent measure of mean blood flow in the limb segment is derived from the rate of change of volume with time during venous occlusion.

Directly-applied Flow Detectors

These are applied to the outside of specific vessels. The principle of the electromagnetic flowmeter is that a moving conductor in a magnetic field sets up a potential difference that is a function of flow-rate (Fig. 1.13). In practice, an alternating magnetic field is used (square-wave, chopped sine-wave) in order to minimize error from polarization at the electrodes. In the Doppler-effect flowmeter, ultrasound is beamed at a narrow angle to the vessel. When it is reflected from the moving wave-front of blood the ultrasound waves undergo a frequency-shift that is a function of the rate of blood flow (Fig.