Cardiovascular Research 1991; 25: 118-124
118
Reflection as a cause of mid-systolic deceleration of pulmonary flow wave in dogs with acute pulmonary hypertension: comparison of pulmonary artery constriction with pulmonary embolisation Youichiroh Furuno, Yasuo Nagamoto, Masasuke Fujita, T o h r u Kaku, Syugo Sakurai, Akio Kuroiwa early negative peak in the backward flow wave. Conclusion - Mid-systolic deceleration of pulmonary flow wave is likely to be related to reflection. Tahara et al' have shown, in dogs with acute pulmonary hypertension due to pulmonary artery constriction, that a transient decrease in pulmonary artery flow is related to a transient reversal of the pulmonary artery-right ventricular pressure gradient in mid-systole. On Doppler echocardiogram, a transient deceleration with a secondary slow rise in pulmonary flow wave has been shown to occur commonly in patients with pulmonary hyper-
It has been suggested that several mechanisms are involved in the genesis of this transient decrease or deceleration with a secondary slower rise in the pulmonary flow wave; one possibility is that these phenomena are due to a vortex: while another is that they are due to reflection.' Okamoto et a16 have shown that prominent reversal of flow in the right posterior part of the pulmonary trunk occurs during mid-systole and early diastole in pulmonary hypertension, indicating the presence of a vortex. Feigenbaum' has speculated that a vortex partially closes the valve in mid-systole. In contrast, Westerhof et a18 reported that the flow wave in the aorta was separated into forward and backward (reflected) waves. Van den Bos et al showed in dogs that aortic -~ occlusion caused larger reflected waves, that the The Second Department of Internal Medicine, University of Occupational and Environmental Health, School of measured pressure and flow waves were due to the summation of forward and backward waves, and that Medicine, Kitakyushu 807, Japan Y Furuno the backward waves contributed to the secondary Y Nagamoto pressure rise and the mid-systolic deceleration of aortic M Fujita flow wave. However, in pulmonary hypertension it has T Kaku never been shown that the mid-systolic deceleration of S Sakurai A Kuroiwa pulmonary flow wave is related to a backward flow wave (reflection). Accordingly, we examined whether Correspondence to: Dr Furuno Key words: pulmonary hypertension; mid-systolic notch; a mid-systolic deceleration of the pulmonary flow wave reflection; input impedance; pulmonary constriction; pul- occurred in acute pulmonary hypertenson resulting monary embolisation from pulmonary artery constriction or pulmonary Submitted 24 May 1990 embolisation, and if so whether it was related to Accepted 31 July 1990 backward flow wave. ~
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Abstract Study objective - The aim was to examine whether mid-systolic deceleration of the pulmonary flow wave occurred in acute pulmonary hypertension due to pulmonary artery constriction and pulmonary embolisation, and if so whether it was related to reflection. Design - Various degrees of pulmonary hypertension were induced by both pulmonary artery constriction and pulmonary embolisation in dogs. During control periods and during pulmonary artery constriction and pulmonary embolisation, pulmonary flow and pulmonary artery pressure were recorded, and the forward and backward (reflected) flow waves were separated from the measured pulmonary flow wave by the method of Westerhof et al. Materials - 20 adult mongrel dogs were used and 10 dogs qualified for analysis. The other 10 dogs, which died before both interventions were completed, were excluded. Measurements and main results - During pulmonary artery constriction, a distinct mid-systolic deceleration of the pulmonary flow wave was observed in five of the 10 dogs, while during pulmonary embolisation, no mid-systolic deceleration was found in these five dogs. The distinct deceleration of the pulmonary flow wave was related to a steep fall and
Reflection as cause of pulmonary flow deceleration in acute pulmonary hypertension
recording (control 1). We then put snares around both the right and left pulmonary arteries at the site wherc each artery gave off the fEst branch. We constricted the pulmonary arteries by tightening both the snares around them. We constricted both the snares in 5-6 steps until arrhythrmas became frequent, aortic pressure decreased to less than 70 mm Hg, or pulmonary artery pressure began to fall. Then we released the constriction to allow the pulmonary artery pressure to return to its resting level. Fifteen minutes later we made a control recording (control 2). To produce pulmonary embolisation, we injected glass beads through an injecter in the right auricle. We repeatedly injected 0.5 g doses of 150 pm diameter glass beads so that the pulmonary artery pressure could increase stepwise(5-6 steps). During control 1, during each step of pulmonary artery constriction, during control 2, and during each step of pulmonary embolisation, the ventilator was stopped at end expiration and a recording was made in a stable state. Among the 20 dogs, there were 10 in which the interventionswere not completed because of death due to poor technique and a fall in aortic or pulmonary pressure; the results in the remaining 10 dogs were d y d . CALCULATION
Five consecutive beats from a record of about 10 beats are shown in fig 1. The recordings of pulmonary flow wave and pulmonary pressure in the five consecutive beats were stable, and the beat with the least noise was used for the calculation of the pulmonary flow and pressure waves. The pulmonary flow wave and pressure wave in one of several beats which were stored in the magnetic tape recorder were sampled every 10 ms, and converted to digital data with an A-D converter to be analysed with a microcomputer (NEC PC-9801). Artifacts on the flow wave resulting from the P and QRS waves of the ECG and the pacing stimulation were eliminated by assuming that pulmonary flow was o litres*min-’after the pulmonary flow wave had crossed the zero level three times in early diastole. The methods for calculatinginput impedance using Fourier analysis have been reported previously.‘&I3 The characteristic impedance was estimated by averaging the impedance moduli of 8 Hz or more, with the noise level of the moduli of harmonics being set at 40 ml-min-’ for pulmonary artery flow and at 0.1 mm Hg for pulmonary artery pressure, and the moduli which were less than these levels being discarded. Thus the characteristic impedance was calculated between 8 and 24 Hz. Forward and backward (= reflected) waves in the pulmonary artery were calculated from measured flow and pressure waves using the characteristic impedance by the method of Westerhof et and the calculated waves were PROTOCOL After a steady state had been reached, we had a control depicted using the NEC-9801 computer system.
Downloaded from by guest on April 10, 2016
Methods This study was performed in accordance with the standards laid down for the care and use of laboratory animals in the Japanese “Guidelines for Animal Experimentation”. Twenty mongrel dogs weighing 12-19 kg were anaesthetised with intravenous pentobarbitone (30 mg-kg-’). The dogs were intubated and ventilated with a Harvard pump. The heart was exposed through a mid-sternal thoracotomy, and the pericardium was partially incised across the origin of great vessels. The pulmonary artery was then carefully isolated by blunt dissection. A cuff type electromagnetic flow probe (Nihon Kohden) driven by an electromagnetic flow meter (Nihon Kohden) was placed around the proximal pulmonary artery about 3 cm above the valve. A 7F microtip pressure transducer (Millar Micro-Tip) was advanced into the pulmonary artery through a stab wound in the right ventricular outflow tract. The pressure sensor of the microtip transducer was positioned 5 mm distal to the distal rim of the flow probe. The microtip transducer was attached to a control unit amplifier (Millar). A lumen catheter attached to a pressure transducer (Gould) was then advanced into the left atrium through a stab wound in the left ventricular apex, and another was positioned in the ascending aorta from the femoral artery. The flow and pressure signals were amplified by DC amplifiers (Nihon Kohden). ECG electrodes were attached to the pericardium of the left ventricular lateral wall and to the limbs. The leads were then connected to an electrocardiograph(Nihon Kohden). Recordingswere stored in a seven channel magnetic tape recorder (Sony) and replayed so that selected sections could be rerecorded at a paper speed of 100 mm-s-’. ECG, pulmonary artery flow and pressure, ascending aorta pressure, and left atrial pressure were recorded. The system used for measurement of pulmonary artery flow and pressure had adequate frequency response: DC amplifiers 100 &-3dB, electromagnetic flow meter 100 Hz-3dB (at high response mode); the frequency response of the recording systemwas satisfactoryin the range of 0-30 Hz. The sinus node was destroyed by an injection of 30% formalin and electrodes were attached to the right auricle. To keep the heart rate constant, pacing was performed at 120 beatsemin-’ using a cardiac stimulator (San-ei). When the heart rate did not decrease below 120 beats*&-’, pacing was performed at 150 beats-mid. To put snares around both the right and left pulmonary arteries, we dissected them bluntly. We instrumented the right auricle with an injector to inject glassbeads through a stab wound. After completing the instrumentation, we waited 20 min for the dogs to stabilise.
119
Youichiroh Furuno, Yasuo Nagamoto, Masasuke Fujita, Tohru Kaku, Syugo Sakurai, Akio Kuroiwa
I- igure 1 Actual recordings of ECG pulmonaty ariety flow wave, andpulmona y artety pressure dunng control. Atnal pacing was performed at a rate of 120 beats m i n d Artifacts on the flow wave resultfrom P and QRS waves ofECG and from pacingstimuh. PA =pulmonary a r m y
deceleration was observed during pulmonary artery constriction, the degree of which was not increased even at a maximum step of pulmonary artery constriction (data not shown), while during pulmonary embolisation no mid-systolic deceleration was observed. There were similar findings in all of these five dogs. In fig 4, the phase (upper part of each panel) and the impedance modulus (lower part of each panel) of the input impedance are indicated (left panel: the dog in fig 2; right panel: the dog in fig 3). Pulmonary artery constriction increased both the input resistance (impedance modulus at 0 Hz) and the characteristic impedance, while pulmonary embolisation increased only the input resistance. During control periods, and during pulmonary artery constriction and pulmonary embolisation, the input was initially negative and then became positive. As shown in the table, input resistance significantly increased at the maximum step during both pulmonary artery constriction and pulmonary embolisation in comparison with control periods 1 and 2. Characteristic impedance significantly increased during pulmonary artery constriction in
Haemodynamic and impedance data in 10 dogs. Data are means ( S D ) ___
Control I
Svstolic PAP (mm Hg) 24.4fS.O) Dias:olic PAP (mm Hg) 10.2(3.4) Mean PAP (mm Hg] 16.q3.7) PA flow (litresmin- ) 1.32(0.47) Input resistance (dyn.sxm-') 753(258) Characteristic impedance (dyn.s,cm-') 118(42)
Maximum step of PAC
Control 2
Maximum step of P E
48 X 7 . 9 ) 14.X5.7) ZS.Z(S.4) 1.04(0.41) 1856(645)t 235(87)t
22.7(5.O) 9.5(2.6) 15.2(3.0) 1.21(0.46) 759(217) 129(41)
43.0(10.1)* 26.1(8.2)*' 33.0(8.7)* 1.02(0.34) 2012(628)§ 151(40)
PAP=pulrnonary artery pressure; PA=pulmonary artery; PAC=pulmonary artery constriction; PE=pulmonary embolisation. *p'0.05; **p
118
Reflection as a cause of mid-systolic deceleration of pulmonary flow wave in dogs with acute pulmonary hypertension: comparison of pulmonary artery constriction with pulmonary embolisation Youichiroh Furuno, Yasuo Nagamoto, Masasuke Fujita, T o h r u Kaku, Syugo Sakurai, Akio Kuroiwa early negative peak in the backward flow wave. Conclusion - Mid-systolic deceleration of pulmonary flow wave is likely to be related to reflection. Tahara et al' have shown, in dogs with acute pulmonary hypertension due to pulmonary artery constriction, that a transient decrease in pulmonary artery flow is related to a transient reversal of the pulmonary artery-right ventricular pressure gradient in mid-systole. On Doppler echocardiogram, a transient deceleration with a secondary slow rise in pulmonary flow wave has been shown to occur commonly in patients with pulmonary hyper-
It has been suggested that several mechanisms are involved in the genesis of this transient decrease or deceleration with a secondary slower rise in the pulmonary flow wave; one possibility is that these phenomena are due to a vortex: while another is that they are due to reflection.' Okamoto et a16 have shown that prominent reversal of flow in the right posterior part of the pulmonary trunk occurs during mid-systole and early diastole in pulmonary hypertension, indicating the presence of a vortex. Feigenbaum' has speculated that a vortex partially closes the valve in mid-systole. In contrast, Westerhof et a18 reported that the flow wave in the aorta was separated into forward and backward (reflected) waves. Van den Bos et al showed in dogs that aortic -~ occlusion caused larger reflected waves, that the The Second Department of Internal Medicine, University of Occupational and Environmental Health, School of measured pressure and flow waves were due to the summation of forward and backward waves, and that Medicine, Kitakyushu 807, Japan Y Furuno the backward waves contributed to the secondary Y Nagamoto pressure rise and the mid-systolic deceleration of aortic M Fujita flow wave. However, in pulmonary hypertension it has T Kaku never been shown that the mid-systolic deceleration of S Sakurai A Kuroiwa pulmonary flow wave is related to a backward flow wave (reflection). Accordingly, we examined whether Correspondence to: Dr Furuno Key words: pulmonary hypertension; mid-systolic notch; a mid-systolic deceleration of the pulmonary flow wave reflection; input impedance; pulmonary constriction; pul- occurred in acute pulmonary hypertenson resulting monary embolisation from pulmonary artery constriction or pulmonary Submitted 24 May 1990 embolisation, and if so whether it was related to Accepted 31 July 1990 backward flow wave. ~
~~
~~~
Downloaded from by guest on April 10, 2016
Abstract Study objective - The aim was to examine whether mid-systolic deceleration of the pulmonary flow wave occurred in acute pulmonary hypertension due to pulmonary artery constriction and pulmonary embolisation, and if so whether it was related to reflection. Design - Various degrees of pulmonary hypertension were induced by both pulmonary artery constriction and pulmonary embolisation in dogs. During control periods and during pulmonary artery constriction and pulmonary embolisation, pulmonary flow and pulmonary artery pressure were recorded, and the forward and backward (reflected) flow waves were separated from the measured pulmonary flow wave by the method of Westerhof et al. Materials - 20 adult mongrel dogs were used and 10 dogs qualified for analysis. The other 10 dogs, which died before both interventions were completed, were excluded. Measurements and main results - During pulmonary artery constriction, a distinct mid-systolic deceleration of the pulmonary flow wave was observed in five of the 10 dogs, while during pulmonary embolisation, no mid-systolic deceleration was found in these five dogs. The distinct deceleration of the pulmonary flow wave was related to a steep fall and
Reflection as cause of pulmonary flow deceleration in acute pulmonary hypertension
recording (control 1). We then put snares around both the right and left pulmonary arteries at the site wherc each artery gave off the fEst branch. We constricted the pulmonary arteries by tightening both the snares around them. We constricted both the snares in 5-6 steps until arrhythrmas became frequent, aortic pressure decreased to less than 70 mm Hg, or pulmonary artery pressure began to fall. Then we released the constriction to allow the pulmonary artery pressure to return to its resting level. Fifteen minutes later we made a control recording (control 2). To produce pulmonary embolisation, we injected glass beads through an injecter in the right auricle. We repeatedly injected 0.5 g doses of 150 pm diameter glass beads so that the pulmonary artery pressure could increase stepwise(5-6 steps). During control 1, during each step of pulmonary artery constriction, during control 2, and during each step of pulmonary embolisation, the ventilator was stopped at end expiration and a recording was made in a stable state. Among the 20 dogs, there were 10 in which the interventionswere not completed because of death due to poor technique and a fall in aortic or pulmonary pressure; the results in the remaining 10 dogs were d y d . CALCULATION
Five consecutive beats from a record of about 10 beats are shown in fig 1. The recordings of pulmonary flow wave and pulmonary pressure in the five consecutive beats were stable, and the beat with the least noise was used for the calculation of the pulmonary flow and pressure waves. The pulmonary flow wave and pressure wave in one of several beats which were stored in the magnetic tape recorder were sampled every 10 ms, and converted to digital data with an A-D converter to be analysed with a microcomputer (NEC PC-9801). Artifacts on the flow wave resulting from the P and QRS waves of the ECG and the pacing stimulation were eliminated by assuming that pulmonary flow was o litres*min-’after the pulmonary flow wave had crossed the zero level three times in early diastole. The methods for calculatinginput impedance using Fourier analysis have been reported previously.‘&I3 The characteristic impedance was estimated by averaging the impedance moduli of 8 Hz or more, with the noise level of the moduli of harmonics being set at 40 ml-min-’ for pulmonary artery flow and at 0.1 mm Hg for pulmonary artery pressure, and the moduli which were less than these levels being discarded. Thus the characteristic impedance was calculated between 8 and 24 Hz. Forward and backward (= reflected) waves in the pulmonary artery were calculated from measured flow and pressure waves using the characteristic impedance by the method of Westerhof et and the calculated waves were PROTOCOL After a steady state had been reached, we had a control depicted using the NEC-9801 computer system.
Downloaded from by guest on April 10, 2016
Methods This study was performed in accordance with the standards laid down for the care and use of laboratory animals in the Japanese “Guidelines for Animal Experimentation”. Twenty mongrel dogs weighing 12-19 kg were anaesthetised with intravenous pentobarbitone (30 mg-kg-’). The dogs were intubated and ventilated with a Harvard pump. The heart was exposed through a mid-sternal thoracotomy, and the pericardium was partially incised across the origin of great vessels. The pulmonary artery was then carefully isolated by blunt dissection. A cuff type electromagnetic flow probe (Nihon Kohden) driven by an electromagnetic flow meter (Nihon Kohden) was placed around the proximal pulmonary artery about 3 cm above the valve. A 7F microtip pressure transducer (Millar Micro-Tip) was advanced into the pulmonary artery through a stab wound in the right ventricular outflow tract. The pressure sensor of the microtip transducer was positioned 5 mm distal to the distal rim of the flow probe. The microtip transducer was attached to a control unit amplifier (Millar). A lumen catheter attached to a pressure transducer (Gould) was then advanced into the left atrium through a stab wound in the left ventricular apex, and another was positioned in the ascending aorta from the femoral artery. The flow and pressure signals were amplified by DC amplifiers (Nihon Kohden). ECG electrodes were attached to the pericardium of the left ventricular lateral wall and to the limbs. The leads were then connected to an electrocardiograph(Nihon Kohden). Recordingswere stored in a seven channel magnetic tape recorder (Sony) and replayed so that selected sections could be rerecorded at a paper speed of 100 mm-s-’. ECG, pulmonary artery flow and pressure, ascending aorta pressure, and left atrial pressure were recorded. The system used for measurement of pulmonary artery flow and pressure had adequate frequency response: DC amplifiers 100 &-3dB, electromagnetic flow meter 100 Hz-3dB (at high response mode); the frequency response of the recording systemwas satisfactoryin the range of 0-30 Hz. The sinus node was destroyed by an injection of 30% formalin and electrodes were attached to the right auricle. To keep the heart rate constant, pacing was performed at 120 beatsemin-’ using a cardiac stimulator (San-ei). When the heart rate did not decrease below 120 beats*&-’, pacing was performed at 150 beats-mid. To put snares around both the right and left pulmonary arteries, we dissected them bluntly. We instrumented the right auricle with an injector to inject glassbeads through a stab wound. After completing the instrumentation, we waited 20 min for the dogs to stabilise.
119
Youichiroh Furuno, Yasuo Nagamoto, Masasuke Fujita, Tohru Kaku, Syugo Sakurai, Akio Kuroiwa
I- igure 1 Actual recordings of ECG pulmonaty ariety flow wave, andpulmona y artety pressure dunng control. Atnal pacing was performed at a rate of 120 beats m i n d Artifacts on the flow wave resultfrom P and QRS waves ofECG and from pacingstimuh. PA =pulmonary a r m y
deceleration was observed during pulmonary artery constriction, the degree of which was not increased even at a maximum step of pulmonary artery constriction (data not shown), while during pulmonary embolisation no mid-systolic deceleration was observed. There were similar findings in all of these five dogs. In fig 4, the phase (upper part of each panel) and the impedance modulus (lower part of each panel) of the input impedance are indicated (left panel: the dog in fig 2; right panel: the dog in fig 3). Pulmonary artery constriction increased both the input resistance (impedance modulus at 0 Hz) and the characteristic impedance, while pulmonary embolisation increased only the input resistance. During control periods, and during pulmonary artery constriction and pulmonary embolisation, the input was initially negative and then became positive. As shown in the table, input resistance significantly increased at the maximum step during both pulmonary artery constriction and pulmonary embolisation in comparison with control periods 1 and 2. Characteristic impedance significantly increased during pulmonary artery constriction in
Haemodynamic and impedance data in 10 dogs. Data are means ( S D ) ___
Control I
Svstolic PAP (mm Hg) 24.4fS.O) Dias:olic PAP (mm Hg) 10.2(3.4) Mean PAP (mm Hg] 16.q3.7) PA flow (litresmin- ) 1.32(0.47) Input resistance (dyn.sxm-') 753(258) Characteristic impedance (dyn.s,cm-') 118(42)
Maximum step of PAC
Control 2
Maximum step of P E
48 X 7 . 9 ) 14.X5.7) ZS.Z(S.4) 1.04(0.41) 1856(645)t 235(87)t
22.7(5.O) 9.5(2.6) 15.2(3.0) 1.21(0.46) 759(217) 129(41)
43.0(10.1)* 26.1(8.2)*' 33.0(8.7)* 1.02(0.34) 2012(628)§ 151(40)
PAP=pulrnonary artery pressure; PA=pulmonary artery; PAC=pulmonary artery constriction; PE=pulmonary embolisation. *p'0.05; **p
