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Intramyocardial pressure
Intramyocardial pressure The persistence of its transmural gradient in the empty heart and its relationship to myocardial oxygen consumption Ronald J. Baird, M.D.,* Martin M. Goldbach, M.D.,** and Alberto de la Rocha, M.D.,*** Toronto, Ontario, Canada
J—/rrors inherent in described techniques of measuring systolic intramyocardial pressure have led to distrust of this measurement as an indicator of myocardial function and to inadequate evaluation of its relationship to other measureable parameters of cardiac function. Following the recent development of a simple and accurate technique of recording local peak systolic intramyocardial pressure, we have reported its relationship to systolic intraventricular pressure in normal myocardium, 1 ' 2 in myocardium from which the epicardium has been removed,3 and in ischemic myocardium.4 The purpose of this article is to report our observations on the persistence of the transmural gradient in systolic intramyocardial pressure in the empty heart and to describe the relationship From the Department of Surgery of the University of Toronto and The Toronto Western Hospital. Supported by an Ontario Heart Foundation Grant. Received for publication April 27, 1972. Address for reprints: Dr. R. J. Baird, Suite 305, Toronto Western Hospital, 399, Bathurst Street, Toronto, Ontario, Canada. •Associate Professor of Surgery, University of Toronto; Research Associate, Ontario Heart Foundation. *'Former Research Fellow of the University of Toronto and The Ontario Heart Foundation; Present Resident in Surgery, University of Toronto. **'Research Fellow of the University of Toronto and The Ontario Heart Foundation.
of changes in systolic intramyocardial pressure in this preparation to changes in myocardial oxygen consumption. In the normal heart, there is a gradient in systolic intramyocardial pressure from a low value near the epicardium to a higher value near the endocardium, where it approaches but does not exceed peak systolic intraventricular pressure.2 This definite, predictable, and consistent percentage relationship to intraventricular pressure was changed by interventions such as local epicardiectomy or local ischemia.3-4 These local manipulations produced gross local decreases in systolic intramyocardial pressure without reducing systolic intramyocardial pressure in more remote areas of the ventricle and without significantly changing "global" parameters of ventricular function such as the magnitude or rate of development of systolic intraventricular pressure. 3 - 4 Thus measurement of systolic intramyocardial pressure provided a quantitative index which could indicate local changes in myocardial contractility that were not adequately reflected by the hemodynamic measurements currently used to assess ventricular function. Peak systolic intramyocardial pressure at any point in the intact working left ventricular wall presumably is a result of the con635
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NEEDLE A 0 FLOW -
NEEDLE B 0 FLOW -
NEEDLE C PERFUSION PRESSURE
0 FLOW 200 MM
-
100
ho 0
AORTIC MM PRESSURE hq
LEFT VENTRICLE PRESSURE M M hg
CALIBRATION OF NEEDLE
Fig. 1. Three pressure sensors within the intraventricular cavity all record the same peak systolic intraventricular pressure as the direct measurement. The arrow indicates the initial point of zero flow in systole.
traction of the myocardium surrounding the pressure sensor plus the transmural transmission of the intraventricular pressure. Thus, in the intact working heart, it was impossible to study changes in peak systolic intramyocardial pressure in isolation from changes in systolic intraventricular pressure. If the influence of intraventricular pressure was eliminated by means of a preparation in which it remained zero, would the gradient in peak systolic intramyocardial pressure from epicardium to endocardium still persist? Does a change in local peak systolic intramyocardial pressure indicate a change in local contractility and myocardial oxygen
consumption? Our experiment was designed to answer these two questions. The preparation consisted of a perfused, temperature-controlled, atrium-paced, beating, innervated heart in which preload (intraventricular diastolic pressure) and afterload (intraventricular systolic pressure) were maintained at zero. Placement of pressure sensors at various depths allowed determination of regional variations in peak systolic intramyocardial pressure. Preliminary experiments indicated that the peak systolic intramyocardial pressure at any given site could be increased by increasing the coronary perfusion pressure or by giving inotropic agents such as glucagon or isoproterenol. We elected to use changes in coronary perfusion pressure to produce changes in peak systolic intramyocardial pressure and to observe if there was any correlation between the myocardial oxygen consumption and a change in systolic intramyocardial pressure. The cardiac surgeon frequently works on the empty, beating heart; with cardiopulmonary bypass he has control of the coronary perfusion pressure; postoperatively he occasionally encounters poorly understood low-output syndromes and subendocardial hemorrhagic necrosis. Thus awareness of the persistence of the gradient in systolic intramyocardial pressure in the empty heart and of the relationship between local intramyocardial pressure and oxygen consumption is of surgical importance. Method Accuracy of the pressure sensor. The pressure sensor is fashioned, as described previously, by placing a small segment of femoral vein on a No. 18 needle which has a 1 cm. gap bridged by a wire support.2"4 Positive air pressure forces saline through the sensor and then out to the atmosphere. The perfusion pressure of the sensor is monitored via a Sanborn 267 AC pressure transducer (Sanborn Co., Waltham, Mass.) and the flow via a 1.5 mm. Micron flow probe (Micron Instruments, Inc., Los Angeles, Calif.).
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Intramyocardial pressure
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CHAMBER PRESSURE Fig. 2. The chamber for testing the accuracy of the pressure sensors.
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Fig. 3. The method in which the pressure sensors are perfused.
Originally, the sensors were tested against simultaneously recorded intraventricular pressure (Fig. 1). The sensor was placed in the left ventricular cavity of a normal dog, and the peak systolic intraventricular pressure simultaneously was recorded by the sensor and by direct recording via a largebore needle and a pressure transducer. Fig. 1 shows three sensors being tested simultaneously in this manner, and each exhibits acceptable accuracy. A search for a more simple method of testing sensor accuracy led to the development of an in vitro technique that used a sensor-testing chamber. The chamber, illustrated in Fig. 2, consists of an airtight Plexiglas box, with dimensions of 12 by 8 by 7 inches. The ends contain inlet and outlet tubes for perfusion lines supplying the sensor. The top is removable so that the sensor can easily be connected and the chamber filled with saline to cover the sensor. An inlet in the top allows the application of the desired air pressure, and an inlet on the
side (at the same level as the sensor) allows direct recording of chamber fluid pressure. Chamber pressure is raised to "systolic" levels by compressed air, and a 30 to 50 mm. Hg fluctuation is produced by opening and closing a valve on the line, thus producing a pulsatile chamber pressure with a "systolic" peak and a "diastolic" trough. The pressure within the perfusion bottle is then raised above "systolic" pressure, and a slow fall of pressure is allowed while sensor flow and pressure are monitored. As the perfusion pressure falls, the initial point of zero flow is easily recorded (as shown in Fig. 4 ) , at which time sensor pressure and chamber pressure should be identical. The sensor error was usually less than 1 mm. Hg, and any sensor with an error over 3 mm. Hg was discarded. All sensors were constructed immediately before the experiment and tested in this fashion prior to their use for measurement of intramyocardial pressure. Experimental technique. Mongrel dogs weighing 20 to 30 kilograms were anesthe-
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SENSOR FLOW
PERFUSION PRESSURE mmHg
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Fig. 5. The experimental preparation.
tized with 28 mg. per kilogram of sodium pentobarbital, intubated, and ventilated with air under intermittent pressure. The chest was opened via a transstemal thoracotomy through the fifth intercostal space. Heparin, 2 mg. per kilogram, was given, and total cardiopulmonary bypass was instituted via cannulas in the superior vena cava, inferior vena cava, and femoral artery. The Bentley Temptrol bubble oxygenator (Bentley Laboratories, Inc., Santa Ana, Calif.) was primed with 500 ml. of Normosol (Abbot Laboratories, Montreal), 30 mEq. of sodium bicarbonate, 500 ml. of 1-day-old acid-
citrate-dextrose blood, and 50 mg. of heparin. The heat exchanger was set at 37.5° C. Blood was pumped to the femoral artery by a Sarns standard pump and to the coronary perfusion bottle by a Sarns coronary perfusion pump (Sarns Inc., Ann Arbor, Mich.). In order to decompress the right side of the heart completely, a separate catheter drained the right ventricle. The pulmonary artery was ligated, and the ventilator was turned off. Pressure in the aortic arch was monitored via a catheter inserted through the left femoral artery (Fig. 5). Two purse-string sutures were inserted on the ascending aorta, and the aorta was clamped just cephalad to them. During a 5 minute period of anoxic arrest, the left atrium was opened widely and the mitral valve was completely excised. This maneuver ensured that the left ventricle remained empty and its systolic and diastolic pressure stayed at zero. A catheter was then placed in the coronary sinus with its tip placed so as to sample from the left of the entrance of the posterior interventricular vein. Two cannulas, one for perfusing and the other for recording pressure in the aortic root, were then inserted through the purse-string sutures, and the aortic root was perfused with nonpulsatile flow at a mean pressure of 50 mm. Hg. The aortic root pressure was monitored via a Sanborn 267 AC transducer,
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and the aortic root flow was monitored by a Statham 5 mm. extracorporeal flow probe on the perfusion line (Statham Instruments, Inc., Oxford, Calif.). The heart usually began to beat spontaneously as soon as coronary flow was established; if not, electrical defibrillation was employed. The temperature of the right ventricular myocardium was monitored via a tissue probe and thermometer (Model 2505, Yellow Springs Instrument Co., Yellow Springs, Ohio). A pacemaker electrode was sewn to the right atrial appendage, and the atrium was paced at a rate sufficient to "capture" the atria and ventricles (Model 5800, Medtronic, Inc., Minneapolis, Minn.). Thus the experimental preparation was an innervated and metabolically supported heart in which coronary perfusion pressure, heart rate, and temperature could be controlled and coronary flow rate and coronary arterial and venous oxygen content could be observed. The absence of left atrial inflow and the removal of the mitral valve allowed zero preload and zero afterload in the left ventricle. The left ventricular lumen always remained empty except for a slight ooze from the myocardium. The body of the animal, apart from the heart, was perfused by means of the usual cardiopulmonary bypass. Pressure sensors, previously tested as above, were then inserted at desired depths in the anterolateral wall of the left ventricle. An attempt was made to place one sensor in the inner and one in the outer half of the myocardium. Simultaneous measurement of peak systolic intramyocardial pressure at the site of the sensor was then obtained by perfusing each sensor with saline at a slowly falling pressure and then observing the flow pattern at each sensor by means of separate flow probes, as shown in Fig. 3. The perfusion pressure at which flow through a sensor first becomes zero during systole is the peak systolic intramyocardial pressure at that area of the myocardium.2-4 All pressure systems had uniform frequency responses up to 30 cycles per second, and all pressure transducers (for aortic root pressure, aortic arch pressure, and sen-
Intramyocardial pressure
639
sor perfusion pressure) were calibrated and flushed from the same bottle.5 The coronary artery flow and the flow through each myocardial pressure sensor were recorded via a 4-channel sine-wave electromagnetic flowmeter (Statham M-4000). Mechanical zero flow calibration was performed before and after each experimental run. The three pressures, three flows, and the electrocardiogram were all recorded on an 8-channel directwriting Sanborn recorder at a paper speed of 10 mm. per second. The experiment consisted of measuring peak systolic intramyocardial pressure and myocardial oxygen consumption at three separate levels of coronary perfusion pressure: 50, 100, and 150 mm. Hg. Measurements were not begun until perfusion pressure had stabilized for 5 minutes at the desired level, and once they had begun the perfusion pressure was not adjusted regardless of any slight variation. Blood was taken simultaneously from the coronary perfusion catheter and coronary sinus catheter, drawn into heparinized syringes, capped, placed in ice, and analyzed immediately after the experiment for oxygen content, pH, Pco 2 , and base deficit. Oxygen content and capacity were determined on the first arterial and venous samples by the classical manometric technique. All further samples were analyzed for oxygen saturation by precision spectrophotometry, and the oxygen content was determined graphically. Hematocrit values were determined on the first and last samples. If the hematocrit had changed from its initial value, the experiment was eliminated from the series. All arterial oxygen samples exhibited oxygen saturations of 100 per cent. The pH of arterial blood did not vary beyond 7.31 to 7.45. Myocardial temperature remained at 37.5 ± 1° C. Myocardial oxygen consumption was calculated from the known coronary artery flow, arterial oxygen content, and venous oxygen content. At the end of the experiment, the left ventricle was dissected from other parts of the heart and weighed. Myo-
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Table I. The gradient in intramyocardial pressure at a coronary perjusion pressure of lOOmg.Hg PSIMP ( mm. Hg) Depth of
sensors
Sensor I Sensor 2
Mean difference (per cent)
Standard deviation
Significance
Sensor 1 in outer and sensor 2 in middle third
4 34 29 28
23 131 64 65
+353
166
p <
0.05
Sensor 1 in middle and sensor 2 in inner third
60 63 66 70 22 30 59 55 83
170 202 142 103 38 105 139 87 125
+225
77
p <
0.001
Sensor 1 in outer and sensor 2 in inner third
16 20
116 121
+665
85
-
Legend: Data are from fifteen separate experiments with thirty observations. Standard deviation is the standard deviation of mean percentage increase. PSIMP, Peak systolic intramyocardial pressure.
cardial oxygen consumption was then expressed as milliliters per minute per 100 grams of left ventricular muscle. The exact depth of each pressure sensor and the total thickness of the myocardium at that point were determined at postmortem examination, thus allowing the depth of the sensor to be expressed as a percentage of wall thickness. Values for peak systolic intramyocardial pressure from the inner, middle, and outer thirds of the myocardial wall were grouped separately for analysis. The experiment was technically satisfactory in 20 dogs. Results In Table I, thirty observations of the peak systolic intramyocardial pressure at two separate depths in the ventricular wall during coronary perfusion at 100 ± 5 mm. Hg in 15 dogs are displayed. It is obvious that there was a gradient in peak systolic intramyocardial pressure from a lower value in the outer third to a higher value in the inner third despite the fact that intraventricular pressure was always zero. A similar gradient was also present at coronary perfusion pressures of 50 and 150 mm. Hg. (At 50 mm.
Hg, the values were somewhat lower and at 150 mm. Hg somewhat higher than at 100 mm. Hg.) This gradient in peak systolic intramyocardial pressure is similar to that described in the intact working ventricleand must, therefore, result from the inherent structure and function of the myocardium and not from the transmission of intraventricular pressure. In this situation, it is also obvious that the systolic intramyocardial pressure in the inner third of the ventricle often is greater than the coronary perfusion pressure. At a perfusion pressure of 100 mm. Hg, the mean values for intramyocardial pressure were as follows: inner third, 123 ±43 mm. Hg; middle third 61 ± 28 mm. Hg; and outer third 22 + 11 mm. Hg. The data from five separate experiments, in which changes in coronary flow, peak systolic intramyocardial pressure and myocardial oxygen consumption were all satisfactorily observed following a change in coronary perfusion pressure from 50 to 100 to 150 mm. Hg, are displayed in Table II. An increase in coronary perfusion pressure was invariably accompanied by an increase in coronary flow, peak systolic intramyo-
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Table II. Intramyocardial pressure and myocardial oxygen consumption Experiment No.
Heart rate (beats/ min.)
Range
Mean
Range
MVO, (ml./lOO Gm.)
1
150
48 105 150
40- 52 100-116 148-150
24.2 53.5 102.0
Steady 48.5-63.5 Steady
2.74 4.57 5.41
65 86 122
63 82 125
162
32 107 144
24- 40 106-108 142-147
26.6 240.0 434.0
20.0-30.0 Steady Steady
2.72 7.44 8.23
56 87 135
27 55 83
132
48 117 157
46- 52 112-120 145-158
55.0 126.0 168.0
Steady 124-128 166-172
2.57 3.65 3.03
88 142 137
44 66 85
138
47 90 144
42- 50 84- 94 138-150
39.3 63.0 117.5
Steady Steady Steady
3.73 4.77 6.02
72 85 113
144
54 104 154
52- 56 100-104 Steady
35.9 78.7 148.0
33.0-38.6 76.0-84.0 Steady
1.38 2.08 2.33
12 22 38
Coronary perfusion pressure (mm. Hg) Mean
Coronary flow (ml. /min.)
PSIMP PSIMP at site 1 at site 2 (mm. Hg) (mm. Hg)
Legend: PSIMP, Peak systolic intramyocardial pressure. MVO:, Myocardial oxygen consumption per 100 grams of left ventricular myocardium.
cardial pressure, and myocardial oxygen consumption. (The values observed when coronary perfusion pressure was decreased from 150 to 100 to 50 mm. Hg were essentially similar to those observed during the increase and are not displayed.) A record from a typical experiment is shown in Fig. 6. As the coronary perfusion pressure is raised, the peak systolic intramyocardial pressure at both the outer and the inner measuring sites also rises. In Fig. 7, the relationship of coronary pressure to coronary flow in two experiments is displayed graphically to illustrate the typical linear increase in coronary flow which accompanies an increase in nonpulsatile coronary pressure in this preparation. Fig. 8, A illustrates the typical linear increase in systolic intramyocardial pressure which accompanies the increase in coronary pressure in three separate experiments. In Fig. 8, B the change in myocardial pressure at two separate sites in the wall of the left ventricle is displayed. Fig. 9 illustrates the relationship between the change in systolic intramyocardial pressure and myocardial oxygen consumption in the experiments detailed in Table II. It can
be seen that myocardial oxygen consumption has a positive relationship to systolic intramyocardial pressure: It tends to increase with increasing systolic intramyocardial pressure in all cases. In Fig. 9, the rate of increase is given for each experiment (on the supposition that there is a linear relationship). The average rate of increase over the five experiments is 0.045 MV0 2 unit per unit of peak systolic intramyocardial pressure. The standard error of this average slope is 0.011. This indicates that there is a definite tendency for the one variable to increase with the other (p < 0.05). In general terms, this means that every 10 mm. Hg rise in systolic intramyocardial pressure is accompanied by a rise in myocardial oxygen consumption of 0.45 ml. of oxygen per 100 grams of left ventricular myocardium. The observations may be summarized as follows: 1. In this preparation, in instances in which intraventricular pressure remains zero, there is still a gradient in systolic intramyocardial pressure from a low value near the epicardium to a higher value near the endocardium.
Baird, Goldbach,
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The Journal of Thoracic and Cardiovascular Surgery
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Intramyocardial pressure
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2. In the empty beating heart, the systolic intramyocardial pressure in the inner third of the left ventricle frequently exceeds the coronary perfusion pressure. 3. In this preparation, in which temperature, heart rate, preload, and afterload remain constant, the level of coronary artery pressure and flow is an important determinant of myocardial contractility. 4. A change in systolic intramyocardial pressure in this preparation is accompanied
by a similar change in myocardial oxygen consumption. Discussion The demonstration of an increasing level of systolic intramyocardial pressure from the epicardium to the endocardium despite the presence of zero intraventricular pressure is of great interest. The presence of this gradient in the normal working heart has been frequently demonstrated.2"4- c>7 Its
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Baird, Goldbach, de la Rocha
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Fig. 9. The positive relationship between myocardial oxygen consumption (MVO;) and peak systolic intramyocardial pressure (PSIMP) as peak systolic intramyocardial pressure is increased by increasing coronary perfusion pressure and flow. Average slope 0.045. S.E., ± 0.011. p < 0.05.
presence in the empty heart must indicate that it is not caused by the mural transmission of the resultant intraventricular pressure. We are unable to say whether it is caused by the complicated interrelationship of the myocardial fibers (i.e., anatomy) or reflects an inherent difference in the inner as compared to the outer layers of the myocardium (i.e., contractility). The report of Sponitz and colleagues,8 which indicates that the sarcomeres in the inner layers are longer than those in the outer layers, provides some support for the latter hypothesis. The presence of a large gradient in systolic pressure across the myocardium suggests that discussions of over-all myocardial "tension" or "stress" based on modifications of the law of Laplace or on isolated measurements with strain gauges attached to the outer layers are open to criticism.
The ability of changes in coronary pressure and flow to change myocardial contractile force and oxygen consumption has been demonstrated frequently.11'13 Preliminary experiments had shown that an increase in peak systolic intramyocardial pressure and myocardial oxygen consumption in this preparation could be produced by isoproterenol or glucagon. The use of a simple change in coronary perfusion pressure seemed to be a more controllable and less complex means of observing any correlation between peak systolic intramyocardial pressure and myocardial oxygen consumption and was the method chosen. The techniques described in this report do not allow us to distinguish between the separate effects of increased pressure or increased flow. The illustrated relationship between the changes in peak systolic intramyocardial
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Intramyocardial pressure
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pressure and myocardial oxygen consumption indicate that a recorded change in local intramyocardial pressure indicates a similar change in energy utilization by the myocardium. Measuremement of intramyocardial pressure thus assumes the status of a technique capable of assessing one aspect of myocardial contractility. The main advantages of using a measurement of systolic intramyocardial pressure as an index of contractility are that it is quantitative and can be used to assess the function of individual regions of the myocardium. The current parameters of contractility, which are based on the rate of change and magnitude of intraventricular pressure, can only assess the total function of the ventricle. Several diseases (in particular coronary artery occlusive disease) have regional rather than global effects on the myocardium. This form of assessment of contractility should be particularly applicable to studies of their effects. In the experimental preparation, a change in systolic intramyocardial pressure was always accompanied by a similar change in myocardial oxygen consumption. Thus it is possible to suggest that regions of the myocardium having a high systolic intramyocardial pressure have higher energy requirements than regions with lower systolic intramyocardial pressures. This hypothesis would then suggest that the inner layers of the heart have a higher energy utilization than the outer layers and thus provides another reason for the subendocardial preponderance of ischemic damage. It would also suggest that events such as the procedure of epicardiectomy or the occurrence of coronary occlusion and reduced local coronary perfusion pressures, by reducing the local systolic intramyocardial pressure, also reduce the local energy requirements.'• * Awareness of the gradient in systolic intramyocardial pressure in the beating but empty heart is of importance to surgeons. It is routine in many open-heart operations to vent the left ventricle, which may be beating or fibrillating. (We elected not to use a standard vent in this experiment because
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we wondered whether the presence of a rigid structure fixing the apex of the left ventricle might create artifacts in the intramyocardial pressure of the surrounding regions and also because it was necessary to be certain that the left ventricular lumen was empty.) The higher intramyocardial pressure in the inner layers of the heart, frequently exceeding the coronary perfusion pressure, must lead to less perfusion of these areas. The response of systolic intramyocardial pressure to inotropic agents (sympathetic nervous stimulation, catecholamines,10 and coronary pressure and flow changes) adds to the complexity. The higher oxygen consumption of the deeper layers must mean a higher demand for perfusion. Thus these observations provide further insights into the possible cause of low-output syndromes and subendocardial necrosis which are occasionally encountered after open-heart surgery.1" The equipment that we have used to measure intramyocardial pressure in the canine heart is too cumbersome for clinical use. However, with suitable modification or miniaturization, such as recently described by Armour and Randall,10 measurement of myocardial pressure could become available to the surgeon. It would provide knowledge of local myocardial function which would be useful in the surgery of coronary artery disease and myocardial dyskinesia. The availability of an accurate technique of measuring local systolic intramyocardial pressure and knowledge of its direct relationship to the myocardial oxygen consumption should encourage further studies of its value as an index of myocardial function. Summary Peak systolic intramyocardial pressure was observed in the beating heart with zero preload and afterload. A gradient in systolic intramyocardial pressure from a low value in the outer third to a high value in the inner third, which has already been described in the working heart, was also found in the empty heart. Thus this gradient cannot result from the mural transmission of systolic intraventricular pressure but must result
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from the inherent structure and function of the left ventricular myocardium. Systolic intramyocardial pressure was increased by increasing coronary perfusion pressure, and the change in intramyocardial pressure was correlated with the change in myocardial oxygen consumption. There was a close positive correlation between a change in myocardial systolic pressure and myocardial oxygen consumption. Awareness of the presence of a high systolic intramyocardial pressure in the inner third of the beating but empty heart is important for the surgeon. The systolic intramyocardial pressure in the inner layers of the left ventricle in this situation frequently exceeds the coronary perfusion pressure. The subsequent high oxygen requirement and difficulty of local perfusion may be a factor in postoperative subendocardial hemorrhagic necrosis or low-output syndromes. Measurement of systolic intramyocardial pressure allows a quantitative assessment of myocardial function in specific regions of the left ventricle. In the surgery of coronary artery disease and myocardial dyskinesia, it should have advantages over current techniques of assessing myocardial function. REFERENCES 1 Baird, R. J., Manktelow, R. T., Cohoon, W. J., Williams, W. G., and Spratt, E. H.: Improved Pressure Gradients and Flow Rates in Myocardial Vascular Implants, Ann. Surg. 168: 730, 1968. 2 Baird, R. J., Manktelow, R. T., Shah, P. A., and Ameli, F . M.: Intramyocardial Pressure: A Study of its Regional Variations and its Relationship to Intraventricular Pressure, J. THORAC.
CARDIOVASC. SURG. 59:
810,
1970.
3 Baird, R. J., and Ameli, F . M.: The Decrease in Intramyocardial Pressure Following Epicardiectomy, Ann. Surg. 174: 950, 1971.
Thoracic and Cardiovascular Surgery
4 Baird, R. J., and Ameli, F. M.: The Changes in Intramyocardial Pressure Produced by Acute Ischemia,
I.
THORAC.
CARDIOVASC. SURG.
62:
87, 1971. 5 Manktelow, R. T., Baird, R. I.: A Practical Approach to Accurate Pressure Measurements, J.
THORC.
CARDIOVASC. SURG. 58:
122,
1969.
6 Kirk, E. S., and Honig, C R.: An Experimental and Theoretical Analysis of Myocardial Tissue Pressure, Am. J. Physiol. 207: 361, 1963. 7 Kreutzer, H., and Shoeppe, H.: The Behaviour of Pressure in the Myocardial Wall, Pfluegers Arch. 278: 181, 1963. 8 Sponitz, H. M., Sonnenblick, E. H., and Spiro, D.: Relation of Ultrastructure to Function in the Intact Heart, Circ. Res. 28: 49, 1966. 9 Mirsky, I.: Left Ventricular Stresses in the Intact Human Heart, Biophys. J. 9:189, 1969. 10 Streeter, D . D., Vaishnau, R. N., Patel, D. J., Sponitz, H. M., Ross, I., and Sonnenblick, E. H.: Stress Distribution in the Canine Left Ventricle During Diastole and Systole, Biophys. J. 10: 345, 1970. 11 Salisbury, P. F., Cross, C. E., and Rieben, P. A.: Intramyocardial Pressure and Strength of Left Ventricular Contraction, Circ. Res. 10: 608, 1961. 12 Opie, L. H.: Coronary Flow Rate and Perfusion Pressure as Determinants of Mechanical Function and Oxidative Metabolism of Isolated Perfused Rat Heart, I . Physiol. 180: 529, 1965. 13 Abel, R. M., and Reis, R. L.: Effects of Coronary Blood Flow and Perfusion Pressure on Left Ventricular Contractility in Dogs, Circ. Res. 27: 961, 1970. 14 Kaye, M. P., and Randall, W. C : Mechanism of Decreased Myocardial Contractile Force After Epicardiectomy, Cardiovasc. Res. 5: 154, 1970. 15 Najafi, H., Lai, R., Khalil, M., Serry, C , Rogers, A., and Haklin, M.: Left Ventricular Hemorrhagic Necrosis, Ann. Thorac. Surg. 12: 400, 1971. 16 Armour, J. A., and Randall, W. C : Canine Left Ventricular Intramyocardial Pressures, Am. I. Physiol. 22: 1833, 1971.
J—/rrors inherent in described techniques of measuring systolic intramyocardial pressure have led to distrust of this measurement as an indicator of myocardial function and to inadequate evaluation of its relationship to other measureable parameters of cardiac function. Following the recent development of a simple and accurate technique of recording local peak systolic intramyocardial pressure, we have reported its relationship to systolic intraventricular pressure in normal myocardium, 1 ' 2 in myocardium from which the epicardium has been removed,3 and in ischemic myocardium.4 The purpose of this article is to report our observations on the persistence of the transmural gradient in systolic intramyocardial pressure in the empty heart and to describe the relationship From the Department of Surgery of the University of Toronto and The Toronto Western Hospital. Supported by an Ontario Heart Foundation Grant. Received for publication April 27, 1972. Address for reprints: Dr. R. J. Baird, Suite 305, Toronto Western Hospital, 399, Bathurst Street, Toronto, Ontario, Canada. •Associate Professor of Surgery, University of Toronto; Research Associate, Ontario Heart Foundation. *'Former Research Fellow of the University of Toronto and The Ontario Heart Foundation; Present Resident in Surgery, University of Toronto. **'Research Fellow of the University of Toronto and The Ontario Heart Foundation.
of changes in systolic intramyocardial pressure in this preparation to changes in myocardial oxygen consumption. In the normal heart, there is a gradient in systolic intramyocardial pressure from a low value near the epicardium to a higher value near the endocardium, where it approaches but does not exceed peak systolic intraventricular pressure.2 This definite, predictable, and consistent percentage relationship to intraventricular pressure was changed by interventions such as local epicardiectomy or local ischemia.3-4 These local manipulations produced gross local decreases in systolic intramyocardial pressure without reducing systolic intramyocardial pressure in more remote areas of the ventricle and without significantly changing "global" parameters of ventricular function such as the magnitude or rate of development of systolic intraventricular pressure. 3 - 4 Thus measurement of systolic intramyocardial pressure provided a quantitative index which could indicate local changes in myocardial contractility that were not adequately reflected by the hemodynamic measurements currently used to assess ventricular function. Peak systolic intramyocardial pressure at any point in the intact working left ventricular wall presumably is a result of the con635
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NEEDLE A 0 FLOW -
NEEDLE B 0 FLOW -
NEEDLE C PERFUSION PRESSURE
0 FLOW 200 MM
-
100
ho 0
AORTIC MM PRESSURE hq
LEFT VENTRICLE PRESSURE M M hg
CALIBRATION OF NEEDLE
Fig. 1. Three pressure sensors within the intraventricular cavity all record the same peak systolic intraventricular pressure as the direct measurement. The arrow indicates the initial point of zero flow in systole.
traction of the myocardium surrounding the pressure sensor plus the transmural transmission of the intraventricular pressure. Thus, in the intact working heart, it was impossible to study changes in peak systolic intramyocardial pressure in isolation from changes in systolic intraventricular pressure. If the influence of intraventricular pressure was eliminated by means of a preparation in which it remained zero, would the gradient in peak systolic intramyocardial pressure from epicardium to endocardium still persist? Does a change in local peak systolic intramyocardial pressure indicate a change in local contractility and myocardial oxygen
consumption? Our experiment was designed to answer these two questions. The preparation consisted of a perfused, temperature-controlled, atrium-paced, beating, innervated heart in which preload (intraventricular diastolic pressure) and afterload (intraventricular systolic pressure) were maintained at zero. Placement of pressure sensors at various depths allowed determination of regional variations in peak systolic intramyocardial pressure. Preliminary experiments indicated that the peak systolic intramyocardial pressure at any given site could be increased by increasing the coronary perfusion pressure or by giving inotropic agents such as glucagon or isoproterenol. We elected to use changes in coronary perfusion pressure to produce changes in peak systolic intramyocardial pressure and to observe if there was any correlation between the myocardial oxygen consumption and a change in systolic intramyocardial pressure. The cardiac surgeon frequently works on the empty, beating heart; with cardiopulmonary bypass he has control of the coronary perfusion pressure; postoperatively he occasionally encounters poorly understood low-output syndromes and subendocardial hemorrhagic necrosis. Thus awareness of the persistence of the gradient in systolic intramyocardial pressure in the empty heart and of the relationship between local intramyocardial pressure and oxygen consumption is of surgical importance. Method Accuracy of the pressure sensor. The pressure sensor is fashioned, as described previously, by placing a small segment of femoral vein on a No. 18 needle which has a 1 cm. gap bridged by a wire support.2"4 Positive air pressure forces saline through the sensor and then out to the atmosphere. The perfusion pressure of the sensor is monitored via a Sanborn 267 AC pressure transducer (Sanborn Co., Waltham, Mass.) and the flow via a 1.5 mm. Micron flow probe (Micron Instruments, Inc., Los Angeles, Calif.).
Volume 64 Number 4 October, 1972
Intramyocardial pressure
CONTROLLABLE n ff= AIR PRESSURE —HJ_li_
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CHAMBER PRESSURE Fig. 2. The chamber for testing the accuracy of the pressure sensors.
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Fig. 3. The method in which the pressure sensors are perfused.
Originally, the sensors were tested against simultaneously recorded intraventricular pressure (Fig. 1). The sensor was placed in the left ventricular cavity of a normal dog, and the peak systolic intraventricular pressure simultaneously was recorded by the sensor and by direct recording via a largebore needle and a pressure transducer. Fig. 1 shows three sensors being tested simultaneously in this manner, and each exhibits acceptable accuracy. A search for a more simple method of testing sensor accuracy led to the development of an in vitro technique that used a sensor-testing chamber. The chamber, illustrated in Fig. 2, consists of an airtight Plexiglas box, with dimensions of 12 by 8 by 7 inches. The ends contain inlet and outlet tubes for perfusion lines supplying the sensor. The top is removable so that the sensor can easily be connected and the chamber filled with saline to cover the sensor. An inlet in the top allows the application of the desired air pressure, and an inlet on the
side (at the same level as the sensor) allows direct recording of chamber fluid pressure. Chamber pressure is raised to "systolic" levels by compressed air, and a 30 to 50 mm. Hg fluctuation is produced by opening and closing a valve on the line, thus producing a pulsatile chamber pressure with a "systolic" peak and a "diastolic" trough. The pressure within the perfusion bottle is then raised above "systolic" pressure, and a slow fall of pressure is allowed while sensor flow and pressure are monitored. As the perfusion pressure falls, the initial point of zero flow is easily recorded (as shown in Fig. 4 ) , at which time sensor pressure and chamber pressure should be identical. The sensor error was usually less than 1 mm. Hg, and any sensor with an error over 3 mm. Hg was discarded. All sensors were constructed immediately before the experiment and tested in this fashion prior to their use for measurement of intramyocardial pressure. Experimental technique. Mongrel dogs weighing 20 to 30 kilograms were anesthe-
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SENSOR FLOW
PERFUSION PRESSURE mmHg
CHAMBER PRESSURE mmHg
200
|_
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SENSORS
Fig. 5. The experimental preparation.
tized with 28 mg. per kilogram of sodium pentobarbital, intubated, and ventilated with air under intermittent pressure. The chest was opened via a transstemal thoracotomy through the fifth intercostal space. Heparin, 2 mg. per kilogram, was given, and total cardiopulmonary bypass was instituted via cannulas in the superior vena cava, inferior vena cava, and femoral artery. The Bentley Temptrol bubble oxygenator (Bentley Laboratories, Inc., Santa Ana, Calif.) was primed with 500 ml. of Normosol (Abbot Laboratories, Montreal), 30 mEq. of sodium bicarbonate, 500 ml. of 1-day-old acid-
citrate-dextrose blood, and 50 mg. of heparin. The heat exchanger was set at 37.5° C. Blood was pumped to the femoral artery by a Sarns standard pump and to the coronary perfusion bottle by a Sarns coronary perfusion pump (Sarns Inc., Ann Arbor, Mich.). In order to decompress the right side of the heart completely, a separate catheter drained the right ventricle. The pulmonary artery was ligated, and the ventilator was turned off. Pressure in the aortic arch was monitored via a catheter inserted through the left femoral artery (Fig. 5). Two purse-string sutures were inserted on the ascending aorta, and the aorta was clamped just cephalad to them. During a 5 minute period of anoxic arrest, the left atrium was opened widely and the mitral valve was completely excised. This maneuver ensured that the left ventricle remained empty and its systolic and diastolic pressure stayed at zero. A catheter was then placed in the coronary sinus with its tip placed so as to sample from the left of the entrance of the posterior interventricular vein. Two cannulas, one for perfusing and the other for recording pressure in the aortic root, were then inserted through the purse-string sutures, and the aortic root was perfused with nonpulsatile flow at a mean pressure of 50 mm. Hg. The aortic root pressure was monitored via a Sanborn 267 AC transducer,
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and the aortic root flow was monitored by a Statham 5 mm. extracorporeal flow probe on the perfusion line (Statham Instruments, Inc., Oxford, Calif.). The heart usually began to beat spontaneously as soon as coronary flow was established; if not, electrical defibrillation was employed. The temperature of the right ventricular myocardium was monitored via a tissue probe and thermometer (Model 2505, Yellow Springs Instrument Co., Yellow Springs, Ohio). A pacemaker electrode was sewn to the right atrial appendage, and the atrium was paced at a rate sufficient to "capture" the atria and ventricles (Model 5800, Medtronic, Inc., Minneapolis, Minn.). Thus the experimental preparation was an innervated and metabolically supported heart in which coronary perfusion pressure, heart rate, and temperature could be controlled and coronary flow rate and coronary arterial and venous oxygen content could be observed. The absence of left atrial inflow and the removal of the mitral valve allowed zero preload and zero afterload in the left ventricle. The left ventricular lumen always remained empty except for a slight ooze from the myocardium. The body of the animal, apart from the heart, was perfused by means of the usual cardiopulmonary bypass. Pressure sensors, previously tested as above, were then inserted at desired depths in the anterolateral wall of the left ventricle. An attempt was made to place one sensor in the inner and one in the outer half of the myocardium. Simultaneous measurement of peak systolic intramyocardial pressure at the site of the sensor was then obtained by perfusing each sensor with saline at a slowly falling pressure and then observing the flow pattern at each sensor by means of separate flow probes, as shown in Fig. 3. The perfusion pressure at which flow through a sensor first becomes zero during systole is the peak systolic intramyocardial pressure at that area of the myocardium.2-4 All pressure systems had uniform frequency responses up to 30 cycles per second, and all pressure transducers (for aortic root pressure, aortic arch pressure, and sen-
Intramyocardial pressure
639
sor perfusion pressure) were calibrated and flushed from the same bottle.5 The coronary artery flow and the flow through each myocardial pressure sensor were recorded via a 4-channel sine-wave electromagnetic flowmeter (Statham M-4000). Mechanical zero flow calibration was performed before and after each experimental run. The three pressures, three flows, and the electrocardiogram were all recorded on an 8-channel directwriting Sanborn recorder at a paper speed of 10 mm. per second. The experiment consisted of measuring peak systolic intramyocardial pressure and myocardial oxygen consumption at three separate levels of coronary perfusion pressure: 50, 100, and 150 mm. Hg. Measurements were not begun until perfusion pressure had stabilized for 5 minutes at the desired level, and once they had begun the perfusion pressure was not adjusted regardless of any slight variation. Blood was taken simultaneously from the coronary perfusion catheter and coronary sinus catheter, drawn into heparinized syringes, capped, placed in ice, and analyzed immediately after the experiment for oxygen content, pH, Pco 2 , and base deficit. Oxygen content and capacity were determined on the first arterial and venous samples by the classical manometric technique. All further samples were analyzed for oxygen saturation by precision spectrophotometry, and the oxygen content was determined graphically. Hematocrit values were determined on the first and last samples. If the hematocrit had changed from its initial value, the experiment was eliminated from the series. All arterial oxygen samples exhibited oxygen saturations of 100 per cent. The pH of arterial blood did not vary beyond 7.31 to 7.45. Myocardial temperature remained at 37.5 ± 1° C. Myocardial oxygen consumption was calculated from the known coronary artery flow, arterial oxygen content, and venous oxygen content. At the end of the experiment, the left ventricle was dissected from other parts of the heart and weighed. Myo-
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Table I. The gradient in intramyocardial pressure at a coronary perjusion pressure of lOOmg.Hg PSIMP ( mm. Hg) Depth of
sensors
Sensor I Sensor 2
Mean difference (per cent)
Standard deviation
Significance
Sensor 1 in outer and sensor 2 in middle third
4 34 29 28
23 131 64 65
+353
166
p <
0.05
Sensor 1 in middle and sensor 2 in inner third
60 63 66 70 22 30 59 55 83
170 202 142 103 38 105 139 87 125
+225
77
p <
0.001
Sensor 1 in outer and sensor 2 in inner third
16 20
116 121
+665
85
-
Legend: Data are from fifteen separate experiments with thirty observations. Standard deviation is the standard deviation of mean percentage increase. PSIMP, Peak systolic intramyocardial pressure.
cardial oxygen consumption was then expressed as milliliters per minute per 100 grams of left ventricular muscle. The exact depth of each pressure sensor and the total thickness of the myocardium at that point were determined at postmortem examination, thus allowing the depth of the sensor to be expressed as a percentage of wall thickness. Values for peak systolic intramyocardial pressure from the inner, middle, and outer thirds of the myocardial wall were grouped separately for analysis. The experiment was technically satisfactory in 20 dogs. Results In Table I, thirty observations of the peak systolic intramyocardial pressure at two separate depths in the ventricular wall during coronary perfusion at 100 ± 5 mm. Hg in 15 dogs are displayed. It is obvious that there was a gradient in peak systolic intramyocardial pressure from a lower value in the outer third to a higher value in the inner third despite the fact that intraventricular pressure was always zero. A similar gradient was also present at coronary perfusion pressures of 50 and 150 mm. Hg. (At 50 mm.
Hg, the values were somewhat lower and at 150 mm. Hg somewhat higher than at 100 mm. Hg.) This gradient in peak systolic intramyocardial pressure is similar to that described in the intact working ventricleand must, therefore, result from the inherent structure and function of the myocardium and not from the transmission of intraventricular pressure. In this situation, it is also obvious that the systolic intramyocardial pressure in the inner third of the ventricle often is greater than the coronary perfusion pressure. At a perfusion pressure of 100 mm. Hg, the mean values for intramyocardial pressure were as follows: inner third, 123 ±43 mm. Hg; middle third 61 ± 28 mm. Hg; and outer third 22 + 11 mm. Hg. The data from five separate experiments, in which changes in coronary flow, peak systolic intramyocardial pressure and myocardial oxygen consumption were all satisfactorily observed following a change in coronary perfusion pressure from 50 to 100 to 150 mm. Hg, are displayed in Table II. An increase in coronary perfusion pressure was invariably accompanied by an increase in coronary flow, peak systolic intramyo-
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Intramyocardial pressure
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October, 1972
Table II. Intramyocardial pressure and myocardial oxygen consumption Experiment No.
Heart rate (beats/ min.)
Range
Mean
Range
MVO, (ml./lOO Gm.)
1
150
48 105 150
40- 52 100-116 148-150
24.2 53.5 102.0
Steady 48.5-63.5 Steady
2.74 4.57 5.41
65 86 122
63 82 125
162
32 107 144
24- 40 106-108 142-147
26.6 240.0 434.0
20.0-30.0 Steady Steady
2.72 7.44 8.23
56 87 135
27 55 83
132
48 117 157
46- 52 112-120 145-158
55.0 126.0 168.0
Steady 124-128 166-172
2.57 3.65 3.03
88 142 137
44 66 85
138
47 90 144
42- 50 84- 94 138-150
39.3 63.0 117.5
Steady Steady Steady
3.73 4.77 6.02
72 85 113
144
54 104 154
52- 56 100-104 Steady
35.9 78.7 148.0
33.0-38.6 76.0-84.0 Steady
1.38 2.08 2.33
12 22 38
Coronary perfusion pressure (mm. Hg) Mean
Coronary flow (ml. /min.)
PSIMP PSIMP at site 1 at site 2 (mm. Hg) (mm. Hg)
Legend: PSIMP, Peak systolic intramyocardial pressure. MVO:, Myocardial oxygen consumption per 100 grams of left ventricular myocardium.
cardial pressure, and myocardial oxygen consumption. (The values observed when coronary perfusion pressure was decreased from 150 to 100 to 50 mm. Hg were essentially similar to those observed during the increase and are not displayed.) A record from a typical experiment is shown in Fig. 6. As the coronary perfusion pressure is raised, the peak systolic intramyocardial pressure at both the outer and the inner measuring sites also rises. In Fig. 7, the relationship of coronary pressure to coronary flow in two experiments is displayed graphically to illustrate the typical linear increase in coronary flow which accompanies an increase in nonpulsatile coronary pressure in this preparation. Fig. 8, A illustrates the typical linear increase in systolic intramyocardial pressure which accompanies the increase in coronary pressure in three separate experiments. In Fig. 8, B the change in myocardial pressure at two separate sites in the wall of the left ventricle is displayed. Fig. 9 illustrates the relationship between the change in systolic intramyocardial pressure and myocardial oxygen consumption in the experiments detailed in Table II. It can
be seen that myocardial oxygen consumption has a positive relationship to systolic intramyocardial pressure: It tends to increase with increasing systolic intramyocardial pressure in all cases. In Fig. 9, the rate of increase is given for each experiment (on the supposition that there is a linear relationship). The average rate of increase over the five experiments is 0.045 MV0 2 unit per unit of peak systolic intramyocardial pressure. The standard error of this average slope is 0.011. This indicates that there is a definite tendency for the one variable to increase with the other (p < 0.05). In general terms, this means that every 10 mm. Hg rise in systolic intramyocardial pressure is accompanied by a rise in myocardial oxygen consumption of 0.45 ml. of oxygen per 100 grams of left ventricular myocardium. The observations may be summarized as follows: 1. In this preparation, in instances in which intraventricular pressure remains zero, there is still a gradient in systolic intramyocardial pressure from a low value near the epicardium to a higher value near the endocardium.
Baird, Goldbach,
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The Journal of Thoracic and Cardiovascular Surgery
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Intramyocardial pressure
643
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2. In the empty beating heart, the systolic intramyocardial pressure in the inner third of the left ventricle frequently exceeds the coronary perfusion pressure. 3. In this preparation, in which temperature, heart rate, preload, and afterload remain constant, the level of coronary artery pressure and flow is an important determinant of myocardial contractility. 4. A change in systolic intramyocardial pressure in this preparation is accompanied
by a similar change in myocardial oxygen consumption. Discussion The demonstration of an increasing level of systolic intramyocardial pressure from the epicardium to the endocardium despite the presence of zero intraventricular pressure is of great interest. The presence of this gradient in the normal working heart has been frequently demonstrated.2"4- c>7 Its
644
The Journal of Thoracic and Cardiovascular Surgery
Baird, Goldbach, de la Rocha
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presence in the empty heart must indicate that it is not caused by the mural transmission of the resultant intraventricular pressure. We are unable to say whether it is caused by the complicated interrelationship of the myocardial fibers (i.e., anatomy) or reflects an inherent difference in the inner as compared to the outer layers of the myocardium (i.e., contractility). The report of Sponitz and colleagues,8 which indicates that the sarcomeres in the inner layers are longer than those in the outer layers, provides some support for the latter hypothesis. The presence of a large gradient in systolic pressure across the myocardium suggests that discussions of over-all myocardial "tension" or "stress" based on modifications of the law of Laplace or on isolated measurements with strain gauges attached to the outer layers are open to criticism.
The ability of changes in coronary pressure and flow to change myocardial contractile force and oxygen consumption has been demonstrated frequently.11'13 Preliminary experiments had shown that an increase in peak systolic intramyocardial pressure and myocardial oxygen consumption in this preparation could be produced by isoproterenol or glucagon. The use of a simple change in coronary perfusion pressure seemed to be a more controllable and less complex means of observing any correlation between peak systolic intramyocardial pressure and myocardial oxygen consumption and was the method chosen. The techniques described in this report do not allow us to distinguish between the separate effects of increased pressure or increased flow. The illustrated relationship between the changes in peak systolic intramyocardial
Volume 64
Intramyocardial pressure
Number 4 October, 1972
pressure and myocardial oxygen consumption indicate that a recorded change in local intramyocardial pressure indicates a similar change in energy utilization by the myocardium. Measuremement of intramyocardial pressure thus assumes the status of a technique capable of assessing one aspect of myocardial contractility. The main advantages of using a measurement of systolic intramyocardial pressure as an index of contractility are that it is quantitative and can be used to assess the function of individual regions of the myocardium. The current parameters of contractility, which are based on the rate of change and magnitude of intraventricular pressure, can only assess the total function of the ventricle. Several diseases (in particular coronary artery occlusive disease) have regional rather than global effects on the myocardium. This form of assessment of contractility should be particularly applicable to studies of their effects. In the experimental preparation, a change in systolic intramyocardial pressure was always accompanied by a similar change in myocardial oxygen consumption. Thus it is possible to suggest that regions of the myocardium having a high systolic intramyocardial pressure have higher energy requirements than regions with lower systolic intramyocardial pressures. This hypothesis would then suggest that the inner layers of the heart have a higher energy utilization than the outer layers and thus provides another reason for the subendocardial preponderance of ischemic damage. It would also suggest that events such as the procedure of epicardiectomy or the occurrence of coronary occlusion and reduced local coronary perfusion pressures, by reducing the local systolic intramyocardial pressure, also reduce the local energy requirements.'• * Awareness of the gradient in systolic intramyocardial pressure in the beating but empty heart is of importance to surgeons. It is routine in many open-heart operations to vent the left ventricle, which may be beating or fibrillating. (We elected not to use a standard vent in this experiment because
645
we wondered whether the presence of a rigid structure fixing the apex of the left ventricle might create artifacts in the intramyocardial pressure of the surrounding regions and also because it was necessary to be certain that the left ventricular lumen was empty.) The higher intramyocardial pressure in the inner layers of the heart, frequently exceeding the coronary perfusion pressure, must lead to less perfusion of these areas. The response of systolic intramyocardial pressure to inotropic agents (sympathetic nervous stimulation, catecholamines,10 and coronary pressure and flow changes) adds to the complexity. The higher oxygen consumption of the deeper layers must mean a higher demand for perfusion. Thus these observations provide further insights into the possible cause of low-output syndromes and subendocardial necrosis which are occasionally encountered after open-heart surgery.1" The equipment that we have used to measure intramyocardial pressure in the canine heart is too cumbersome for clinical use. However, with suitable modification or miniaturization, such as recently described by Armour and Randall,10 measurement of myocardial pressure could become available to the surgeon. It would provide knowledge of local myocardial function which would be useful in the surgery of coronary artery disease and myocardial dyskinesia. The availability of an accurate technique of measuring local systolic intramyocardial pressure and knowledge of its direct relationship to the myocardial oxygen consumption should encourage further studies of its value as an index of myocardial function. Summary Peak systolic intramyocardial pressure was observed in the beating heart with zero preload and afterload. A gradient in systolic intramyocardial pressure from a low value in the outer third to a high value in the inner third, which has already been described in the working heart, was also found in the empty heart. Thus this gradient cannot result from the mural transmission of systolic intraventricular pressure but must result
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Baird, Goldbach, de la Rocha
from the inherent structure and function of the left ventricular myocardium. Systolic intramyocardial pressure was increased by increasing coronary perfusion pressure, and the change in intramyocardial pressure was correlated with the change in myocardial oxygen consumption. There was a close positive correlation between a change in myocardial systolic pressure and myocardial oxygen consumption. Awareness of the presence of a high systolic intramyocardial pressure in the inner third of the beating but empty heart is important for the surgeon. The systolic intramyocardial pressure in the inner layers of the left ventricle in this situation frequently exceeds the coronary perfusion pressure. The subsequent high oxygen requirement and difficulty of local perfusion may be a factor in postoperative subendocardial hemorrhagic necrosis or low-output syndromes. Measurement of systolic intramyocardial pressure allows a quantitative assessment of myocardial function in specific regions of the left ventricle. In the surgery of coronary artery disease and myocardial dyskinesia, it should have advantages over current techniques of assessing myocardial function. REFERENCES 1 Baird, R. J., Manktelow, R. T., Cohoon, W. J., Williams, W. G., and Spratt, E. H.: Improved Pressure Gradients and Flow Rates in Myocardial Vascular Implants, Ann. Surg. 168: 730, 1968. 2 Baird, R. J., Manktelow, R. T., Shah, P. A., and Ameli, F . M.: Intramyocardial Pressure: A Study of its Regional Variations and its Relationship to Intraventricular Pressure, J. THORAC.
CARDIOVASC. SURG. 59:
810,
1970.
3 Baird, R. J., and Ameli, F . M.: The Decrease in Intramyocardial Pressure Following Epicardiectomy, Ann. Surg. 174: 950, 1971.
Thoracic and Cardiovascular Surgery
4 Baird, R. J., and Ameli, F. M.: The Changes in Intramyocardial Pressure Produced by Acute Ischemia,
I.
THORAC.
CARDIOVASC. SURG.
62:
87, 1971. 5 Manktelow, R. T., Baird, R. I.: A Practical Approach to Accurate Pressure Measurements, J.
THORC.
CARDIOVASC. SURG. 58:
122,
1969.
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