Cardiovascular Research, 1976, 10, 474-481,
Alterations of the Frank orthogonal scalar leads induced by anaphylactic shock in the rabbit and J . P . B L E U S From the Institut L. Frerlericq 17, Place Delcour, 4000 Ligge, Belgium J . B O L A N D , J . TROQUET,
A U T H O R S ' S Y N O P S I S The anaphylactic shock of the rabbit is characterized by an acute right ventricular overload, accompanied by severe alterations of cardiac electrogenesis. During shock, the mean QRS vector, as measured from the algebraic sum of the Q, R, and S deflections an the three leads, shifts to the right, inferiorly and anteriorly. An injury current quickly appears. The TQ vector points away from the right ventricle. A progressive depolarization on the right ventricular wall is displayed by suction electrodes and the suppression of right ventricular hypertension by a cross circulation produces an almost immediate disappearance of the injury current. The geneses of these electrical alterations are briefly discussed. The possibility of an anaphylactic reaction at the level of the coronary arterial wall, previously mentioned in the literature, seems unlikely. The role of the haemodynamic changes and of the increased right ventricular blood pool is thought to be predominant.
Anaphylactic shock in the rabbit is characterized by severe cardiocirculatory effects which have been widely investigated. The main contributions to this subject were summarized by Halpern (1962) in a symposium on shock. An intense vasoconstriction of pulmonary arterioles, taking place in less than 1 min, results in a sudden increase of pulmonary artery and right ventricular pressures: the right ventricle becomes dilated and quickly decompensates. A very significant drop of cardiac output follows together with a severe although sometimes reversible decrease of aortic pressure. The lowering of systemic arterial pressure is partially prevented by a peripheral vasoconstriction which was demonstrated as early as 1935 by Vallery-Radot et a1 by angiographic data and confirmed more recently by means of a radiocardiographic method (Merchie et al, 1965). Electrocardiographic changes and rhythm disturbances appear very early during this sensitization shock (Mikulicich, 1951 ; Halpern et a/, 1958) which, in the rabbit, may actually
be considered as an experimental model of acdte 'cor pulmonale'. The purpose of the present investigation was to analyse the electrical modifications associated with this form of acute right ventricular strain and to try and determine the factors accounting for the evolution of the Frank scalar leads in those experimental conditions. The electrical and haemodynamic parameters of the animal in shock were first analysed. In another group of experiments, it was then attempted to repeat the measurements after having suppressed the right ventricular hypertension during the shock by a cross circulation. Finally, recordings of surface action potentials by means of suction electrodes were used with a view to determine the actual part taken by each ventricle in the overall electrical alterations.
Material and methods Group 1 A first group of 1 1 rabbits, with an average weight of 2200 g, were sensitized by three consecutive
415 Orthogonal ECG and anaphylactic shock 1 Cross circulation between the cardiovascular system of the animal in shock (sensitized) and the healthy one (not sensitized). The arrows show the direction of the circulation. RA=right atrium; LA= IeJi atrium; RV=right ventricle; L V= IeJi ventricle; CE=a carotis externa; Ao= aorta; J=jugular vein; VCI= veiia cava inferior; r=adjustable resistance; cl=arterial clamp; PVD and PAo=right ventricular and aortic pressure transducers.
FIG.
Non-sensitized rabbit
daily subcutaneous injections of 5 ml of hen albumin. The anaphylactic shock was induced 3 weeks later. The animals were anaesthetized by intravenous administration of pentobarbital (30 mg/kg). A tracheotomy was performed. Through the femoral vein, a radio-opaque catheter was inserted under fluoroscopy into the right ventricular cavity. The femoral artery was used to measure the aortic pressure, both pressures being recorded by means of Elema strain gauge pressure transducers. The three orthogonal scalar leads were recorded using the Frank network (1956) and seven hyperdermic needle electrodes of 1 cm length. The shock was induced by the intravenous injection of 0.5 ml of a solution (20%) of ovalbumin in isotonic sodium chloride (9%,). The five parameters mentioned were continuously monitored on a Mingograph 42B at a speed of 10 mm/s. Every minute, a sample was taken at 100mm/s. Group 2 A second group of five rabbits were sensitized and anaesthetized in the same way. Artificial respiration was secured by a Palmer pump after intravenous injection of 4-5 mg/kg of gallamine. Through a median thoracotomy, the pericardium was exposed and opened; the edges were sutured to the chest wall in such a way that the heart laid on a cradle made of the posterior part of the pericardium. A water suction pump was used to attach a suction electrode to the epicardium of each ventricle (Hoffman et al, 1959). The anaphylactic shock was induced in the same way as in the first part of the experiment and five parameters were continuously recorded, ie, two pressure curves, two suction potentials, and a standard bipolar lead.
Group 3 A third group of five pairs of rabbits of similar weight were used to establish a cross circulation between one animal in shock and one which was not sensitized (Fig. 1). The absence of blood incompatibility between both animals was first checked. The sensitized rabbit was prepared as previously described. A jugular vein and a carotid artery were exposed. The vein was used to introduce into the right atrium a big catheter which was connected to a Sigmamotor pump with a maximal output of 150 ml/min. A second strong catheter was then placed into the artery where it was tied and clamped. The non-sensitized rabbit was similarly prepared. The jugular vein was kept opened by a catheter fitted with an adjustable resistance and connected to a funnel collecting the blood coming out of the pump. An intercarotid anastomosis was established between the t w o animals. At the beginning of the experiment, the venous and arterial anastomoses were kept closed. During shock, the opening of the cross circulation allowed the correction of the right ventricular hypertension and of the systemic hypotension developing during the investigation. The usual parameters were recorded for the sensitized rabbit and the effects of correcting the arterial pressure and the right ventricular hypertension by this cross circulation were analysed. In the three groups, all the animals were heparinized (100 units USP/kg) to avoid thrombosis on or in the catheters. The magnitude and direction of the mean vectors representative of the ventricular depolarization and repolarization were determined as follows: the baseline was taken at the level of points J; the mean values of each projection on the X, Y,and Z leads
476 Boland. Troquet, and Bleus
- +
Z+
10" x+
X-
Z-
-
1
amplitudes correlate satisfactorily with the mean surfaces even when the heart rate is widely varying (Simonson et al, 1954; Boland et al, 1972). Applying Pythagoras' theorem, spatial magnitudes were considered equal to the square root of the sum of the squares of the simultaneous QRS voltages in the three orthogonal leads. The angular directions of QRS and QT vectors are characterized by three angles a, p, and y. They represent for each spatial vector the angular distance from X for u, from Y for p, and from Z for y. The angles are computed from their cosine, the latter being the ratio between the scalar lead and the spatial vector. The positivity and negativity of these three angles have been arbitrarily chosen: is positive (from 0 to 180") when located below the level of the X axis; /3 and y are positive when they are to the left of the Y and Z axes, respectively. Fig. 2 shows graphically the positivities and negativities of voltages and angles for a spatial vector M. The statistical significance of the differences between arithmetical means of magnitude, orientation, duration and pressure were checked by Student's t test. Each group of measurements, from 30s to 6 min, were compared with the values at time zero, preceeding the initiation of the sensitization shock. (I
t
OO Yt
FtG . 2
Graphic representation of a spatial vector M located in the left antero-inferior octant. It is built f r o m the simultaneous QRS voltages in the three orthogonal leads. The positivity of the leads is arbitrarily chosen to the leji for X , down f o r Y, and to the back for Z. The spatial orientation is given by the three angles u, @, and y which are the angular distances between the spatial vector M and the three orthogonal axes X , Y , and Z ; a i s positive when located below the X axis; and y are positive when orientated to the lefr of Y and Z, respectively.
were measured as in standard electrocardiography, by the algebraic sum of Q, R, and S heights. It has previously been demonstrated that these mean
Results
Group 1 One out of the I I rabbits had to be excluded because of the early appearance of an incomplete AV dissociation caused by a junctional tachycardia with aberrant conduction. The
260 Heart rate
220
. z.
2oo'80
I"100 Arterial pressure
2 0
. . . . . . r
1% ' 50
- 4 - A - L
. gT.:-18 40
Riqht pressure ventricula;
I
I
I
0 1 2 3 4 5 6 Time after triqqerinq ( m i d
a
I2
I
I
I
I
I
I
18
10
F t G . 3 Evolirtioti of the haemodynamic parameters driring t/ir anuphylactic shock. The resitlts are graphically presented with their dispersion ( i I S D ) . Conversion : traditional to S I w i t s : I mmHg= 0.133 kPa.
411
Orthogonal
ECG and anapiiylactic
shock
. . .
0.8003. -
. . r
l
l
,
,
,
,
,
0
1
2
3
4
5
6
I
i
I2
18
1
a
Time (rninl
haemodynamic results of the 10 others are presented in Fig. 3. After a mild tachycardia of short duration, a significant (P
Alterations of the Frank orthogonal scalar leads induced by anaphylactic shock in the rabbit and J . P . B L E U S From the Institut L. Frerlericq 17, Place Delcour, 4000 Ligge, Belgium J . B O L A N D , J . TROQUET,
A U T H O R S ' S Y N O P S I S The anaphylactic shock of the rabbit is characterized by an acute right ventricular overload, accompanied by severe alterations of cardiac electrogenesis. During shock, the mean QRS vector, as measured from the algebraic sum of the Q, R, and S deflections an the three leads, shifts to the right, inferiorly and anteriorly. An injury current quickly appears. The TQ vector points away from the right ventricle. A progressive depolarization on the right ventricular wall is displayed by suction electrodes and the suppression of right ventricular hypertension by a cross circulation produces an almost immediate disappearance of the injury current. The geneses of these electrical alterations are briefly discussed. The possibility of an anaphylactic reaction at the level of the coronary arterial wall, previously mentioned in the literature, seems unlikely. The role of the haemodynamic changes and of the increased right ventricular blood pool is thought to be predominant.
Anaphylactic shock in the rabbit is characterized by severe cardiocirculatory effects which have been widely investigated. The main contributions to this subject were summarized by Halpern (1962) in a symposium on shock. An intense vasoconstriction of pulmonary arterioles, taking place in less than 1 min, results in a sudden increase of pulmonary artery and right ventricular pressures: the right ventricle becomes dilated and quickly decompensates. A very significant drop of cardiac output follows together with a severe although sometimes reversible decrease of aortic pressure. The lowering of systemic arterial pressure is partially prevented by a peripheral vasoconstriction which was demonstrated as early as 1935 by Vallery-Radot et a1 by angiographic data and confirmed more recently by means of a radiocardiographic method (Merchie et al, 1965). Electrocardiographic changes and rhythm disturbances appear very early during this sensitization shock (Mikulicich, 1951 ; Halpern et a/, 1958) which, in the rabbit, may actually
be considered as an experimental model of acdte 'cor pulmonale'. The purpose of the present investigation was to analyse the electrical modifications associated with this form of acute right ventricular strain and to try and determine the factors accounting for the evolution of the Frank scalar leads in those experimental conditions. The electrical and haemodynamic parameters of the animal in shock were first analysed. In another group of experiments, it was then attempted to repeat the measurements after having suppressed the right ventricular hypertension during the shock by a cross circulation. Finally, recordings of surface action potentials by means of suction electrodes were used with a view to determine the actual part taken by each ventricle in the overall electrical alterations.
Material and methods Group 1 A first group of 1 1 rabbits, with an average weight of 2200 g, were sensitized by three consecutive
415 Orthogonal ECG and anaphylactic shock 1 Cross circulation between the cardiovascular system of the animal in shock (sensitized) and the healthy one (not sensitized). The arrows show the direction of the circulation. RA=right atrium; LA= IeJi atrium; RV=right ventricle; L V= IeJi ventricle; CE=a carotis externa; Ao= aorta; J=jugular vein; VCI= veiia cava inferior; r=adjustable resistance; cl=arterial clamp; PVD and PAo=right ventricular and aortic pressure transducers.
FIG.
Non-sensitized rabbit
daily subcutaneous injections of 5 ml of hen albumin. The anaphylactic shock was induced 3 weeks later. The animals were anaesthetized by intravenous administration of pentobarbital (30 mg/kg). A tracheotomy was performed. Through the femoral vein, a radio-opaque catheter was inserted under fluoroscopy into the right ventricular cavity. The femoral artery was used to measure the aortic pressure, both pressures being recorded by means of Elema strain gauge pressure transducers. The three orthogonal scalar leads were recorded using the Frank network (1956) and seven hyperdermic needle electrodes of 1 cm length. The shock was induced by the intravenous injection of 0.5 ml of a solution (20%) of ovalbumin in isotonic sodium chloride (9%,). The five parameters mentioned were continuously monitored on a Mingograph 42B at a speed of 10 mm/s. Every minute, a sample was taken at 100mm/s. Group 2 A second group of five rabbits were sensitized and anaesthetized in the same way. Artificial respiration was secured by a Palmer pump after intravenous injection of 4-5 mg/kg of gallamine. Through a median thoracotomy, the pericardium was exposed and opened; the edges were sutured to the chest wall in such a way that the heart laid on a cradle made of the posterior part of the pericardium. A water suction pump was used to attach a suction electrode to the epicardium of each ventricle (Hoffman et al, 1959). The anaphylactic shock was induced in the same way as in the first part of the experiment and five parameters were continuously recorded, ie, two pressure curves, two suction potentials, and a standard bipolar lead.
Group 3 A third group of five pairs of rabbits of similar weight were used to establish a cross circulation between one animal in shock and one which was not sensitized (Fig. 1). The absence of blood incompatibility between both animals was first checked. The sensitized rabbit was prepared as previously described. A jugular vein and a carotid artery were exposed. The vein was used to introduce into the right atrium a big catheter which was connected to a Sigmamotor pump with a maximal output of 150 ml/min. A second strong catheter was then placed into the artery where it was tied and clamped. The non-sensitized rabbit was similarly prepared. The jugular vein was kept opened by a catheter fitted with an adjustable resistance and connected to a funnel collecting the blood coming out of the pump. An intercarotid anastomosis was established between the t w o animals. At the beginning of the experiment, the venous and arterial anastomoses were kept closed. During shock, the opening of the cross circulation allowed the correction of the right ventricular hypertension and of the systemic hypotension developing during the investigation. The usual parameters were recorded for the sensitized rabbit and the effects of correcting the arterial pressure and the right ventricular hypertension by this cross circulation were analysed. In the three groups, all the animals were heparinized (100 units USP/kg) to avoid thrombosis on or in the catheters. The magnitude and direction of the mean vectors representative of the ventricular depolarization and repolarization were determined as follows: the baseline was taken at the level of points J; the mean values of each projection on the X, Y,and Z leads
476 Boland. Troquet, and Bleus
- +
Z+
10" x+
X-
Z-
-
1
amplitudes correlate satisfactorily with the mean surfaces even when the heart rate is widely varying (Simonson et al, 1954; Boland et al, 1972). Applying Pythagoras' theorem, spatial magnitudes were considered equal to the square root of the sum of the squares of the simultaneous QRS voltages in the three orthogonal leads. The angular directions of QRS and QT vectors are characterized by three angles a, p, and y. They represent for each spatial vector the angular distance from X for u, from Y for p, and from Z for y. The angles are computed from their cosine, the latter being the ratio between the scalar lead and the spatial vector. The positivity and negativity of these three angles have been arbitrarily chosen: is positive (from 0 to 180") when located below the level of the X axis; /3 and y are positive when they are to the left of the Y and Z axes, respectively. Fig. 2 shows graphically the positivities and negativities of voltages and angles for a spatial vector M. The statistical significance of the differences between arithmetical means of magnitude, orientation, duration and pressure were checked by Student's t test. Each group of measurements, from 30s to 6 min, were compared with the values at time zero, preceeding the initiation of the sensitization shock. (I
t
OO Yt
FtG . 2
Graphic representation of a spatial vector M located in the left antero-inferior octant. It is built f r o m the simultaneous QRS voltages in the three orthogonal leads. The positivity of the leads is arbitrarily chosen to the leji for X , down f o r Y, and to the back for Z. The spatial orientation is given by the three angles u, @, and y which are the angular distances between the spatial vector M and the three orthogonal axes X , Y , and Z ; a i s positive when located below the X axis; and y are positive when orientated to the lefr of Y and Z, respectively.
were measured as in standard electrocardiography, by the algebraic sum of Q, R, and S heights. It has previously been demonstrated that these mean
Results
Group 1 One out of the I I rabbits had to be excluded because of the early appearance of an incomplete AV dissociation caused by a junctional tachycardia with aberrant conduction. The
260 Heart rate
220
. z.
2oo'80
I"100 Arterial pressure
2 0
. . . . . . r
1% ' 50
- 4 - A - L
. gT.:-18 40
Riqht pressure ventricula;
I
I
I
0 1 2 3 4 5 6 Time after triqqerinq ( m i d
a
I2
I
I
I
I
I
I
18
10
F t G . 3 Evolirtioti of the haemodynamic parameters driring t/ir anuphylactic shock. The resitlts are graphically presented with their dispersion ( i I S D ) . Conversion : traditional to S I w i t s : I mmHg= 0.133 kPa.
411
Orthogonal
ECG and anapiiylactic
shock
. . .
0.8003. -
. . r
l
l
,
,
,
,
,
0
1
2
3
4
5
6
I
i
I2
18
1
a
Time (rninl
haemodynamic results of the 10 others are presented in Fig. 3. After a mild tachycardia of short duration, a significant (P
