1Department of Anaesthesia and Intensive Care, 2 Department of Clinical Physiology, Sahlgrenska University Hospital, S-413 45 Göteborg, Sweden. 3Department of Cardiology, St Vincents Hospital, University of New South Wales, Darlinghurst NSW 2010, Australia*Corresponding author
Declaration of interest. Professor M. F. ORourke is a Director of PWV Medical, Sydney. PWV Medical provided funds and facilities for analysis of the data, and markets apparatus that uses the methods used in this study.
Accepted for publication: November 16, 2001
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Abstract |
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Methods. Ascending aortic pressure waves were synthesized and comparisons were made between the synthesized aortic waveforms, the measured aortic and radial arterial waveforms. Ascending aortic pressure waves (catheter-tip manometer) and radial artery pressure waves (short fluid-filled catheter) were recorded simultaneously in 12 patients with angina pectoris (age 6276 years) undergoing cardiac catheterization. Patients were studied at rest, following midazolam, sublingual nitroglycerin and during Valsalva manoeuvres.
Results. Both midazolam and nitroglycerin lowered mean arterial pressure but nitroglycerin caused a more selective decrease in the measured and synthesized aortic systolic pressures than in the radial artery pressure. The synthesized aortic systolic pressure was less, by 68 mm Hg (SD 23) and the synthesized aortic diastolic pressure greater, by 4 mm Hg (SD 2). Despite these differences in pulse pressure, the synthesized waveform tracked the measured waveform before and during interventions.
Conclusions. By deriving an aortic waveform from the radial pulse, monitoring of left ventricular afterload can improve without more invasive means.
Br J Anaesth 2002; 88: 4818
Keywords: arterial pressure; hypnotics, benzodiazepine, midazolam; anaesthetic techniques, hypotensive; pharmacology, nitroglycerin
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Introduction |
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Methods |
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Aortic recordings were obtained with an 8F Cordis catheter-tip manometer with a pressure interface (Sentron, The Netherlands).16 The catheter has a flat frequency response up to 180 Hz. Following local anaesthesia, the catheter was introduced from the femoral artery and positioned in the ascending aorta just proximal to the brachiocephalic trunk. The right radial artery was cannulated with a 45 mm Ohmeda (Swindon, UK) arterial cannula (inner diameter 1.0 mm) and connected to an external pressure transducer (Peter van Berg, Kirschseeon, Germany) by high-pressure tubing that was only 10 cm long to minimize signal distortion. When tested in our laboratory according to Gardner17 this pressure measurement system had a natural frequency of 25 Hz and a damping coefficient of 0.350.5. This implies that the signal has minimal distortion. The Siemens Sirecust 1281 cardiovascular monitoring system (Siemens Medical Electronics Inc., Danvers, MA) that we used had a high-pass filter with a cut-off at 16 Hz.
The Valsalva manoeuvre was accomplished by a prolonged forced exhalation through a facemask with an attached resistance. Airway pressure was measured at the mask and a positive airway pressure of 1070 mm Hg was generated. In relation to the Valsalva manoeuvres, measurements of systolic and diastolic pressures were made on individual pulse waves because the SphygmoCor software is based on averaging 8 s of stable pulse waves. Pressures were measured immediately before and during the peak effect of the manoeuvre, with arterial pressure at its nadir.
All signals (ECG, radial arterial, aortic and airway pressures) were digitized (MP 100, Biopac, Cal., USA) at 200 Hz and processed in the data acquisition software (Acqknowledge, Biopac, USA). Data were later processed off-line in the SphygmoCor 128 Hz. The generalized transfer function used by SphygmoCor is based on data from Karamanoglu et al.,11 who studied patients with coronary artery disease. This is virtually identical to the generalized transfer function described by Chen et al.9 During each period of measurement a recording of a stable 8 s wave train was ensemble-averaged by the SphygmoCor into a single waveform for each of MA, SA and MR, and timing and pressure data (systolic, diastolic and end systolic pressures) calculated. End systolic pressure (ESP) was determined by identification of the cardiac insicura through use of differentials. Indices were: timepressure area during systole (As) and diastole (Ad) and their ratio (Ad/As), systolic pressure augmentation index (AI), which defines the relation between the first (P1) and second (P2) systolic shoulder/peak (i.e. AI=100x(P2P1)/pulse pressure).18 19
Since the exact sagittal position of the aortic catheter in relation to the zero level of the external pressure transducer was unknown, mean values of both synthesized and measured pressures were set to be the same as in the pressure in the radial artery. All aortic pressure values were then adjusted arithmetically.
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Experimental plan |
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Statistical analysis |
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Results |
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Systolic AI in SA approximated that in MA. The magnitude of the changes in pulse wave parameters induced by midazolam and the further addition of nitroglycerin were always similar in the measured and synthesized aortic pulse waves (Table 1).
Individual values are shown as BlandAltman plots in Fig. 4AD. Figure 4A shows a consistent underestimation of the SA systolic pressure compared with MA and a large scatter in MR compared with MA systolic pressures during nitroglycerin. The resemblance between MA and SA is good with regard to ESP and AI (Fig. 4BC). SA consistently underestimated systolic and overestimated diastolic pressure areas compared with MA.
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Discussion |
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Pressure
The aortic pulse pressure was underestimated using the SphygmoCor software. This was largely the result of a discrepancy in systolic pressure. The underestimation may be explained in several ways. A small but systematic bias was introduced in the study by setting measured and SA mean pressures identical to radial mean pressure. Normally the aortic mean pressure should be 13 mm Hg higher than the radial mean pressure.4 More importantly, the generalized transfer function used by the SphygmoCor is based on data from a younger population (mean age 54 years)11 than investigated in the present study (mean age 67 years). In younger individuals, pulse pressure amplification along the arterial tree results in a higher peripheral systolic pressure. The less compliant arterial system of an elderly individual will equalize peripheral and central systolic pressure. Indeed, similar resting aortic and radial systolic pressures were observed in the present study. Furthermore, the generalized transfer function is based on pooled data including pressure waveforms at rest, as well as during infusion of nitroglycerin.11 Individualized transfer functions have been evaluated previously9 and were found to be only marginally superior to the generalized transfer function in reconstructing central pressures. Further validation studies should involve young individuals with normal and compliant arterial vasculature. It can be argued that the fluid-filled radial catheter system could introduce damping and thus lower the pulse pressure in the SA wave. This seems unlikely, however, since the extremely short fluid-filled radial system had a natural frequency and damping coefficient well above monitoring standards.17 Longer extensions have so far not been validated. About 90% of the power in the aortic pressure is within the first three harmonics10 and these are unlikely to be affected by the length of the tubing. Longer extensions, however, will decrease the natural frequency of a fluid-filled external system, making it susceptible to false amplification during tachycardia. In such a system a high heart rate may introduce errors which were not encountered in the present study.
Waveform
A monophasic systolic peak was observed in the aortic pressure waveform. This pattern differs from the original work by Murgo et al.,18 who describe a late systolic peak as a result of the reflected pressure wave (type A waveform), considered typical in elderly or hypertensive individuals. Again, differences in the composition of study populations may explain the different waveforms observed. The study by Murgo et al. was of a population with a mean age of 34 years, compared with 67 years in this investigation. The pressure wave reflection in an elderly group of individuals with a less compliant arterial vascular tree is probably so fast that the incident wave meets and blends with the reflected wave very early in systole.
The waveform can be described as a supply/demand relationship. The area under the diastolic part of the pulse wave, Ad, is hence divided by the systolic area, As (i.e. Ad/As), where Ad represents the potential for coronary perfusion enabling the cardiac workload, As.22 Interestingly, in our study, this relationship was altered only by nitroglycerin, despite a more pronounced decrease in systolic pressure during midazolam. This shows that nitroglycerin can decrease not only stroke volume but also pulse wave reflection.
The AI indicates vascular stiffness, reflecting both structural vascular changes as in hypertension or diabetes23 and pharmacologically induced dynamic changes in pulse wave reflection where the second systolic peak represents the reflected pressure wave.7 Perhaps in patients with intact endothelial function24 changes in AI could indicate depth of anaesthesia and sympathetic tone.
Clinical implications
We found that systolic pressure and AI from a radial cannula should be used with caution even as a rough estimate of aortic data (Fig. 4, left-hand panels). Whereas midazolam did not affect the gradient between radial and aortic pressures, the addition of nitroglycerin did (Fig. 3). With midazolam the radial and aortic pulse wave changes suggested that midazolam elicits an arteriolar vasodilatation without major changes in stroke volume. Midazolam and nitroglycerin in combination affected the pulse waves in the same way as when nitroglycerin was given alone, which suggests dilatation of small arteries and reduced stroke volume.7 The Valsalva manoeuvre decreased transmural aortic pressure and pulse wave velocity and reduced stroke volume, with increased heart rate and vasoconstriction. The net effect of these changes on pulse wave reflection was a delay of the reflected wave into diastole.5 In the present study the agreement between measured and synthesized aortic pressure improved during the Valsalva manoeuvre. Speculatively, both reduced stroke volume and increased heart rate during the Valsalva manoeuvre could lower central systolic pressure more than radial pressure, similar to the effects of nitroglycerin.7 If this difference in pressure reduction equals the underestimation of aortic systolic pressure by the SphygmoCor, measured and SA aortic pressures would coincide. These observations are similar to those made by Chen et al.9
The information contained in arterial pressure waveforms is probably underused in anaesthesia and intensive care. The present study shows that if the radial pulse wave is continuously translated into an aortic pulse wave, the level of monitoring can improve without more invasive means. Continuous monitoring of aortic pressure and waveform gives a better estimate of left ventricular afterload than does radial monitoring and is of importance in volume and drug therapy. There is no reason why the detailed information contained in the arterial pressure waveform should be overlooked by the anaesthetists and intensivists who are regularly confronted with arterial pressure waveforms. Further studies should assess pulse wave reflection and late systolic augmentation. The present study illustrates the benefits and possible pitfalls of using a generalized transfer function in elderly patients. The SA pulse wave will be damped, causing a moderate but consistent underestimation of pulse pressure and systolic timepressure area. The underestimation of systolic pressure is not seen with an increased intrathoracic pressure.
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Acknowledgements |
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References |
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