- Email: [email protected]
Successful defibrillation with the use of left ventricular drainage after prolonged refractory ventricular fibrillation in experimental acute myocardial infarction
Successful Defibrillation with the Use of Left Ventricular Drainage after Prolonged Refractory Ventricular Fibrillation in Experimental Acute Myocardial Infarction
LESLIE A. KUHN, MD, FACC” FRED LAJAM, MDT HIDEKI SAKURAI,? MD JAIME CASTRO-BLANCO, MDT ALLEN UNGER, MD* STEPHEN NOVICK, MD* ANTHONY J. MARANO, MD* ROBERT S. LITWAK, MD, FACCt New York, New York
From the Division of Cardiology, Department of Medicine,* and the Division of Cardiothoracic Surgery, Department of Surgery,? Mount Sinai School of Medicine, New York, N.Y. This study was supported by U. S. Public Health Service Grant HE 04132, National Heart and Lung Institute. Manuscript received November 29, 1971, accepted January 21, 1972. Address for reprints: Leslie A. Kuhn, MD, Ames Coronary Care Unit, Mount Sinai School of Medicine, 5th Ave. and 100th St., New York, N.Y. 10029.
248
August 1972
To determine the efficacy of left ventricular drainage in permitting defibrillation after prolonged, refractory ventricular fibrillation, 12 dogs (7 normal, 5 with major coronary arterial ligation) with 21 episodes of either spontaneous or electrically induced ventricular fibrillation were studied before and during left ventricular drainage by means of transaortic or transatrial cannulation. After prolonged ventricular fibrillation without circulatory support (average 28, range 17 to 48 minutes), electrical defibrillation was unsuccessful despite increasing amounts of direct current. Defibrillation was then attempted during graded amounts of left ventricular drainage (200 to 1,800 ml/min; 8.7 to 57.8 ml/kg per min). Defibrillation was successful in each instance (10 watt-set), at an average left ventricular drainage flow rate of 19.7 ml/kg per min (range, 12.1 to 30.4). Successful defibrillation was obtained with either low or normal arterial pH values. Left ventricular drainage with concomitant successful defibrillation was associated with significant increments of arterial PO2. Submaximal volumes of left ventricular drainage may permit defibrillation after prolonged refractory ventricular fibrillation, both in normal animals and in those with acute myocardial infarction. Acute reduction of left ventricular volume with alteration of the form of the left ventricle, reduction of myocardial oxygen requirement and increments of coronary flow attributable to left ventricular drainage are postulated as mechanisms facilitating defibrillation. It is suggested that application of left ventricular drainage through a closed chest may be helpful in certain clinical instances of refractory ventricular fibrillation.
Some experimental studies have demonstrated that after very short periods of ventricular fibrillation, defibrillation is more often successful when the animal is receiving one of a variety of modalities of circulatory support.1*2 Delay in onset of ventricular fibrillation after coronary arterial occlusion has been obtained with left heart bypass.3v4 It has been observed that ventricular fibrillation may be prevented by counterpulsation after coronary arterial ligation2 and that the infarcted fibrillating ventricle may be defibrillated more easily during left heart bypass435 or after prefibrillatory counterpulsations than if no circulatory support is utilized. The object of our studies was to determine whether use of a technique of extracorporeal circulatory support, by producing decompression of the distended, fibrillating left ventricle, would permit de-
The American Journal of CARDIOLOGY
Volume 30
LEFT VENTRICULAR
DRAINAGE
FOR DEFIBRILLATION-KUHN
ET AL.
fibrillation when initiated after prolonged refractory ventricular fibrillation. We selected for this purpose a relatively simple method of applying left ventricular “decompression” in which a drainage catheter could be introduced by way o:f a peripheral artery.
Methods
Figure 1 demonstrates the experimental arrangement. Left ventricular “drainage” or “bypass” was employed because it provides an effective and rapid means of decompressing the distended left ventricle. In addition, newer methods of cannulation enable such a technique to be used in a clinical setting with relative ease and promptness without need to open the chest. We studied 21 episodes of ventricular fibrillation in 12 dogs. Seven were normal and 5 had ligation of a major branch of the left anterior descending coronary artery. After induction of light anesthesia with intravenously injected sodium pentobarbital (average dose 30 mg/kg), a left thoracotomy was performed in the fifth interspace. The animal breathed room air by means of an endotracheal tube and a volume respirator. The left femoral artery was catheterized and the catheter was connected to a Statham strain gauge and a multichannel recorder for pressure measurement. The right femoral artery was cannulated with a large-bore Bardic catheter to receive blood from the left ventricle by way of the extracorporeal circulatory system. A straight stainless steel cannula with a wall thickness of 0.2 mm and an outer diameter of 4.5 mm, as described by Zwart et a1.,7 was inserted by way of a carotid artery into the left ventricle. This method of extracorporeal circulation has also been described by Geddes et al.8 In a few animal,s the left ventricle could not be cannulated in this manner; instead it was cannulated through the left atrium with a large-bore flexible plastic catheter. (Since results were similar in the 2 groups of animals, they will be discussed subsequently as 1 group.) The bypass system included a reservoir into which left ventricular blood drained by gravity drainage and a Sarns roller pump. Tygon tubing connected the pump and reservoir to the femoral arterial perfusion cannula. The system was primed with about 500 ml of normal saline solution. Left ventricular pressure was measured and its blood sampled periodically ‘for pH and POs (Astrup method) by means of a stopcock connected to the drainage line. A flowmeter attached to the pump indicated the minute volume pumped. The animal was given 3 mg/kg of heparin by intravenous administration. The electrocardiogram was obtained by needle electrodes. Ventricular fibrillation usually occurred spontaneously in animals with coronary arterial ligation. In the others, it was induced by electric shocks applied directly to the exposed heart. After 15 minutes of ventricular fibrillation, during which there was no assisted circulation but lung ventilation was maintained, an attempt was made to defibrillate the ventricles with successive direct-current shocks of 10, 20, 30 and 40 watt-seconds applied to the exposed heart. If any of these was successful, ventricular fibrillation was produced again and defibrillation was attempted at the end of an additional 20 minutes of ventricular fibrillation. When it was determined that graded DC shocks could not produce defibrillation, left ventricular drainage was instituted, starting with a flow rate of 200 ml/min for 10 minutes, during which the ventricles continued to fibrillate. Mean arterial pressure ranged from 30 to 50 mm Hg during ventricular drainage. Attempts at defibrillation with DC shocks of 10 to 40 watt-seconds were
August
Figure 1. Schematic Description in text.
diagram
of experimental
arrangement.
then made and, if unsuccessful, successive 10 minute periods of left ventricular drainage with flows increasing by 200 ml/min during each period were carried out and DC defibrillation attempted again. In several animals the experiments were repeated after successful defibrillation.
Results Table I summarizes the results obtained. The duration of refractory ventricular fibrillation before institution of left ventricular drainage was 17 to 46 minutes (mean 28) for the 12 dogs. In each of the 21 instances of ventricular fibrillation, after the institution of left ventricular drainage, successful defibrillation was accomplished with current levels that were previously unsuccessful. Ranges of extracorporeal flow rate studied were 8.7 to 57.6 ml/kg per min. The average minimal flow rate permitting defibrillation was 19.7 ml/kg per min (range 12.1 to 30.4). Thus, defibrillation could be accomplished during submaximal flow rates, which were well within the capability of the system utilized. Illustrative experiments (Fig. 2): The time from coronary arterial ligation is listed in relation to each of the events portrayed with the duration of uninterrupted venTABLE
i
Results Dogs (no.) Average yeight (kg) Episodes of ventricular fibrillation (no.) Average time of ventricular fibrillation before defibrillation (min) Range of flow studied (ml/kg per min) Minimal flow permitting defibrillation (ml/kg per min)
1972
The American Journal of CARDIOLOGY
12 29.3 (z!=l.4) 21 28 (17-48) 8.7-57.6 19.7 (12.1-30.4)
Volume 30
249
LEFT
VENTRICULAR
DRAINAGE
4
DEFIBRILLATION-KUHN
v.E
ZOWW.
IOWW.
IMINUTESOFVFI
3OUKC.
~l5l_.___~161_
TIME (min.)
0
IO
4
4
CONTROL CE6;;;bRY (MINUTES OF WI
ET
4
4
COR ARTERY LIGATED
FOR
0 --
li7l_
23
VF
IO wsec
0
(131-
4
iI81 _I191
_1201_(291
24
20 wsec.
25
(14) _1151_.___
II PO2 and pH Values During Ventricular Fibrillation
Arterial
PO8
(mm Arterial
&I pH
7.38 (7.6-7.57)
Defibrillation Successful
7.17 (6.80-7.49)
During Bypass Unsuccessful
7.34 (7.0-7.8)
* P X0.01. 250
August 1972
The American Journal of CARDIOLOGY
27
42
4
4
LV BY-PPJS LV BY-PASS 200ml/mm 400mllmm (20rsec.) ~171_____ (32)--
30 wsec
Left ventricular PO2 and pH: Values obtained during the course of the experiments are listed in Table II. The low POs level noted during ventricular
Left Ventricular
4
40wsec. LVEWWSS LV BY-PASSLV BY-PASS 200mllmm 4OOmllmm BOOmllmm l3Cwsecl lM.recl
tricular fibrillation in parentheses. In Figure 2A, at the time of coronary arterial ligation, the electrocardiographic pattern of acute injury is noted. Ventricular fibrillation occurred spontaneously 10 minutes later. The animal was allowed to fibrillate for 15 minutes, after which there were attempts at defibrillation with increasing amounts of current applied directly to the heart. These were unsuccessful. After 19 minutes of ventricular fibrillation with no assisted circulation, left ventricular drainage was begun in the manner previously indicated at an initial rate of 200 ml/min. Attempts at ventricular defibrillation were unsuccessful. Increasing the flow rate to 400 ml/min also did not permit electrical defibrillation, but when the flow rate was increased to 800 ml/min, defibrillation was successful after 29 minutes of previously irreversible ventricular fibrillation. This experiment was then repeated in the same animal with the same result, ventricular fibrillation restarting spontaneously when the extracorporeal circulation was discontinued. Figure 2B illustrates a similar experiment. The first 2 panels show the electrocardiogram before and after coronary arterial ligation. Ventricular fibrillation occurred spontaneously after 10 minutes. After 15 minutes of ventricular fibrillation, attempts at defibrtllation with increasing currents were unsuccessful. Left ventricular drainage with a flow rate of 200 ml/min was initiated after 17 minutes of ventricular fibrillation. Attempts at defibrillation were unsuccessful until the flow rate was increased to 400 ml/min. At this flow rate, defibrillation was successful after 32 minutes of ventricular fibrillation. Ventricular fibrillation recurred when left ventricular drainage was discontinued.
TABLE
AL.
Figure 2. Electrocardiographic tracings in 2 typical experiments. A, dog weighing 33 kg. The time from coronary arterial ligation is listed in relation to each of the events with the duration of uninterrupted ventricular fibrillation in parentheses. Note that attempts at ventricular defibrillation were unsuccessful until extracorporeal flow rate was increased to 800 ml/min. Defibrillation was then successful after 29 minutes of previously irreversible ventricular fibrillation. B, in this experiment (with an animal weighing only 26 kg) attempts at defibrillation were unsuccessful until the flow rate was increased to 400 ml/min. At this flow rate, defibrillation was successful after 32 minutes of ventricular fibrillation. Ventricular fibrillation recurred
when left ventricular drainage was discontinued. fibrillation was raised considerably during left ventricular drainage, and there was a pronounced difference in arterial POs obtained during extracorporeal flow rates that led to successful defibrillation as compared to values obtained during flow rates that did not lead to successful defibrillation. Of course, the flow rate was higher in the group that underwent successful defibrillation. A variety of arterial pH values was obtained, usually related to a combination of metabolic acidosis and respiratory alkalosis. There was typically a base deficit and a low level of PCOz. Successful defibrillation was accomplished despite a wide range of pH values. A relatively normal value for arterial pH was not essential for successful defibrillation.
Discussion Our results indicate that left ventricular drainage permits a successful defibrillation even after prolonged, apparently refractory ventricular fibrillation. These findings are consistent with the conclusions of other investigators who have demonstrated that, in an animal with ventricular fibrillation of very short duration without circulatory support, defibrillation is more easily accomplished when a variety of methods of circulatory support are utilized.1,2 It has been well demonstrated that such techniques are considerably more efficacious in this regard than direct, manually controlled cardiac contractions.9 Our findings extend these observations to prolonged ventricular fibrillation without circulatory support, which is refractory to electrical defibrillation and which, in a clinical setting, presents a hopeless resuscitative problem. Mechanisms facilitating defibrillation after left ventricular drainage: The consistent success of left ventricular drainage in permitting defibrillation may well be related to acute reduction of the volume of the distended, fibrillating left ventricle. There is ample experimental evidence that left ventricular size is of key importance in permitting the maintenance and development of ventricular defibrillation.l”J1 This suggests that large hearts provide more reentrant pathways for perpetuation of fibrillatory “circus” rhythms than do smaller hearts in which refractory tissue may be present, thus allow-
Volume 30
LEFT VENTRICULAR
ing the rhythm to terminate. Other modes of circulatory support, previously cited, which permit defibrillation after shorter periods of ventricular fibrillation than noted in our study, also result in acute reduction of left ventricular volume, In addition to ventricular size, the form of the cardiac tissue may be important in facilitating defibrillation. GarreylO has demonstrated that long thin pieces of cardiac tissue recover promptly from ,ventricular fibrillation and, if strips of cardiac tissue are quite narrow, ventricular fibrillation may be impossible. The form of the distended fibrillating ventricle is visibly altered during left ventricular drainage. Alterations of myocardial oxygen requirement and blood flow produced by left ventricular drainage may also be of importance in permitting defibrillation after prolonged refractory ventricular fibrillation, although we could not measure these satisfactorily in our experiments. It is logical to assume that there was some reduction of myocardial oxygen requirement coincident with acute reduction of ventricular volume during left ventricular drainage. Measurement of intercoronary flow (backflow) has indicated that substantial increments are obtained during ventricular fibrillation witlh initiation of left heart bypass.12 Such increase in coronary flow may be responsible for the ease of defibrillation of the ventricles during left ventricular drainage. Experiments in the dog and pig indicate that ventricular fibrillation occurs only when a critical mass of myocardium becomes totally avascular. Therefore, measures that decrease the size of the avascular myocardium (by increasing coronary flow) can be expected to enhance the possibility of defibrillating the ischemic ventricle. Alterations of blood and myocardial electrolytes, which must also be considered factors in permitting defibrillation, were not measured in this study, but it is of interest that pH1 variation over a wide range did not influence ability to defibrillate the ventricles
DRAINAGE
FOR DEFIBRILLATION-KUHN
ET AL.
during left ventricular drainage. Although some investigators have cited potassium shifts from the intracellular compartment to the serum as a causative factor in the production of ventricular fibrillation after acute myocardial infarction, more recent investigations have indicated that such electrolyte shifts are probably not responsible for ventricular fibrillation in this experimental setting.14 Clinical implications: The clinical connotations of our results are not clear at this time. We do not know whether continued maintenance of circulatory adequacy or adequate cerebral function will be possible after defibrillation following such prolonged ventricular fibrillation. However, this modality requiring only a peripheral arterial cutdown procedure may be instituted relatively rapidly through a closed chest and may permit defibrillation even after prolonged ventricular fibrillation in clinical situations when the ventricles cannot be defibrillated by existing methods. Maintenance of circulatory support by external cardiac compression during initiation of the left ventricular catheter would, of course, enhance the possibility of restoration of circulatory adequacy after defibrillation. There are clinical settings in which left ventricular drainage may be used for relatively prolonged periods in patients with surgically remediable cardiac disease to prevent recurrent ventricular fibrillation during preparation for definitive cardiac surgery; coronary revascularization in acute myocardial infarction is one such instance. Transarterial left ventricular drainage through a closed chest has been applied clinically by Zwart et al.15 for other purposes. It is reasonable to expect advances in the future which will permit long-term application of a variety of techniques of closed chest circulatory support, particularly in regard to development of nonthrombogenic surfaces. ls This should permit extension of the indications for circulatory support to include recurrent or refractory ventricular fibrillation.
References pulsatile 1. Rosselot E, Gold H, Vyden JK, et al: Venoarterial circulatory assist in the treatment of resistant ventricular fibrillation. Amer J Cardiol 27:48-50, 1971 counter2. Fleming WH, Schultz J, Malm JR: Synchronized pulsation in the management of ventricular fibrillation following coronary artery ligation. J Thorac Cardiovasc Surg 58:253-257,1986 3. Dennis C, Carlens E, Senning A, et al: Clinical use Of a cannula for left heart bypass without thoracotomy. Ann Surg 158:823-837,1982 4. Leighninger DS, Davidson AIG, Beck CS: Left heart bypass in cardiac resuscitation. I\mer J Cardiol 15:33-37, 1985 5. Crawford FA, Willwerth IlM, Cline RE, et al: Left heart bypass following left coronary artery occlusion. Circulation 37: suppl2:12-17,1988 8. Roaensweia J. Chatterjee S, Merino F: Treatment of acute myocardial-infarction by counterpulsation. J Thorac Cardiovast Surg 59:243-250, 1970 7. Ewart HHJ, Kralios A, Collan R; et al: Transarterial closed chest left ventricular (Ta CLV) bypass. Trans Amer Sot Artif Intern Organs 15:386-390, 1989 8. Geddes LA, Schuhmann RE, Hoff HE, et al: Total maintenance of circulation in the closed chest animal with ventricular fibrillation. Baylor Cardiovasc Res Center Bull 8:33-44, 1987
9. Nachlas MM, Siedband MP, Bernstein P: Experimental technics for improving the effectiveness of cardiac resuscitation. Ann Surg 181:331-343, 1985 10. Garrey WE: The nature of fibrillary contraction of the heart. Its relation to tissue mass and form. Amer J Physiol 33:397-414, 1914 11. Szabuniewicz M, Hoff HE, McCrady JD: Spontaneous ventricular fibrillation in the armadillo. Baylor Cardiovasc Res Center Bull 8:135-147, 1970 12. Davidson AIG, Leighninger DS: Collateral flow in the heart at different aortic perfusion pressures using left heart bypass. Ann Surg 182:46-52, 1985 13. Myers MB, Cherry G: Ventricular fibrillation area thresholds in the dog and pig. J Thorac Cardiovasc Burg 59: 401412, 1970 14. Cherry G, Myers MB: The relationship to ventricular fibrillation of early tissue sodium and potassium shifts and coronary vein potassium levels in experimental myocardial infarction. J Thorac Cardiovasc Surg 81:587-598, 1971 15. Zwart HHJ, Kwan-Gett CS, Backman DK, et al: Transar-terial left ventricular bypass (abstr). Amer J Cardiol 28:687, 1970 18. Wakabayashf A, Dietrick W, Connolly JE; Closed chest left heart bypass without anticoagulation. J Thorac Cardiovasc Surg 58:81 l-820, 1989
August 1972
The American Journal of CARDIOLOGY
Volume 30
251
LESLIE A. KUHN, MD, FACC” FRED LAJAM, MDT HIDEKI SAKURAI,? MD JAIME CASTRO-BLANCO, MDT ALLEN UNGER, MD* STEPHEN NOVICK, MD* ANTHONY J. MARANO, MD* ROBERT S. LITWAK, MD, FACCt New York, New York
From the Division of Cardiology, Department of Medicine,* and the Division of Cardiothoracic Surgery, Department of Surgery,? Mount Sinai School of Medicine, New York, N.Y. This study was supported by U. S. Public Health Service Grant HE 04132, National Heart and Lung Institute. Manuscript received November 29, 1971, accepted January 21, 1972. Address for reprints: Leslie A. Kuhn, MD, Ames Coronary Care Unit, Mount Sinai School of Medicine, 5th Ave. and 100th St., New York, N.Y. 10029.
248
August 1972
To determine the efficacy of left ventricular drainage in permitting defibrillation after prolonged, refractory ventricular fibrillation, 12 dogs (7 normal, 5 with major coronary arterial ligation) with 21 episodes of either spontaneous or electrically induced ventricular fibrillation were studied before and during left ventricular drainage by means of transaortic or transatrial cannulation. After prolonged ventricular fibrillation without circulatory support (average 28, range 17 to 48 minutes), electrical defibrillation was unsuccessful despite increasing amounts of direct current. Defibrillation was then attempted during graded amounts of left ventricular drainage (200 to 1,800 ml/min; 8.7 to 57.8 ml/kg per min). Defibrillation was successful in each instance (10 watt-set), at an average left ventricular drainage flow rate of 19.7 ml/kg per min (range, 12.1 to 30.4). Successful defibrillation was obtained with either low or normal arterial pH values. Left ventricular drainage with concomitant successful defibrillation was associated with significant increments of arterial PO2. Submaximal volumes of left ventricular drainage may permit defibrillation after prolonged refractory ventricular fibrillation, both in normal animals and in those with acute myocardial infarction. Acute reduction of left ventricular volume with alteration of the form of the left ventricle, reduction of myocardial oxygen requirement and increments of coronary flow attributable to left ventricular drainage are postulated as mechanisms facilitating defibrillation. It is suggested that application of left ventricular drainage through a closed chest may be helpful in certain clinical instances of refractory ventricular fibrillation.
Some experimental studies have demonstrated that after very short periods of ventricular fibrillation, defibrillation is more often successful when the animal is receiving one of a variety of modalities of circulatory support.1*2 Delay in onset of ventricular fibrillation after coronary arterial occlusion has been obtained with left heart bypass.3v4 It has been observed that ventricular fibrillation may be prevented by counterpulsation after coronary arterial ligation2 and that the infarcted fibrillating ventricle may be defibrillated more easily during left heart bypass435 or after prefibrillatory counterpulsations than if no circulatory support is utilized. The object of our studies was to determine whether use of a technique of extracorporeal circulatory support, by producing decompression of the distended, fibrillating left ventricle, would permit de-
The American Journal of CARDIOLOGY
Volume 30
LEFT VENTRICULAR
DRAINAGE
FOR DEFIBRILLATION-KUHN
ET AL.
fibrillation when initiated after prolonged refractory ventricular fibrillation. We selected for this purpose a relatively simple method of applying left ventricular “decompression” in which a drainage catheter could be introduced by way o:f a peripheral artery.
Methods
Figure 1 demonstrates the experimental arrangement. Left ventricular “drainage” or “bypass” was employed because it provides an effective and rapid means of decompressing the distended left ventricle. In addition, newer methods of cannulation enable such a technique to be used in a clinical setting with relative ease and promptness without need to open the chest. We studied 21 episodes of ventricular fibrillation in 12 dogs. Seven were normal and 5 had ligation of a major branch of the left anterior descending coronary artery. After induction of light anesthesia with intravenously injected sodium pentobarbital (average dose 30 mg/kg), a left thoracotomy was performed in the fifth interspace. The animal breathed room air by means of an endotracheal tube and a volume respirator. The left femoral artery was catheterized and the catheter was connected to a Statham strain gauge and a multichannel recorder for pressure measurement. The right femoral artery was cannulated with a large-bore Bardic catheter to receive blood from the left ventricle by way of the extracorporeal circulatory system. A straight stainless steel cannula with a wall thickness of 0.2 mm and an outer diameter of 4.5 mm, as described by Zwart et a1.,7 was inserted by way of a carotid artery into the left ventricle. This method of extracorporeal circulation has also been described by Geddes et al.8 In a few animal,s the left ventricle could not be cannulated in this manner; instead it was cannulated through the left atrium with a large-bore flexible plastic catheter. (Since results were similar in the 2 groups of animals, they will be discussed subsequently as 1 group.) The bypass system included a reservoir into which left ventricular blood drained by gravity drainage and a Sarns roller pump. Tygon tubing connected the pump and reservoir to the femoral arterial perfusion cannula. The system was primed with about 500 ml of normal saline solution. Left ventricular pressure was measured and its blood sampled periodically ‘for pH and POs (Astrup method) by means of a stopcock connected to the drainage line. A flowmeter attached to the pump indicated the minute volume pumped. The animal was given 3 mg/kg of heparin by intravenous administration. The electrocardiogram was obtained by needle electrodes. Ventricular fibrillation usually occurred spontaneously in animals with coronary arterial ligation. In the others, it was induced by electric shocks applied directly to the exposed heart. After 15 minutes of ventricular fibrillation, during which there was no assisted circulation but lung ventilation was maintained, an attempt was made to defibrillate the ventricles with successive direct-current shocks of 10, 20, 30 and 40 watt-seconds applied to the exposed heart. If any of these was successful, ventricular fibrillation was produced again and defibrillation was attempted at the end of an additional 20 minutes of ventricular fibrillation. When it was determined that graded DC shocks could not produce defibrillation, left ventricular drainage was instituted, starting with a flow rate of 200 ml/min for 10 minutes, during which the ventricles continued to fibrillate. Mean arterial pressure ranged from 30 to 50 mm Hg during ventricular drainage. Attempts at defibrillation with DC shocks of 10 to 40 watt-seconds were
August
Figure 1. Schematic Description in text.
diagram
of experimental
arrangement.
then made and, if unsuccessful, successive 10 minute periods of left ventricular drainage with flows increasing by 200 ml/min during each period were carried out and DC defibrillation attempted again. In several animals the experiments were repeated after successful defibrillation.
Results Table I summarizes the results obtained. The duration of refractory ventricular fibrillation before institution of left ventricular drainage was 17 to 46 minutes (mean 28) for the 12 dogs. In each of the 21 instances of ventricular fibrillation, after the institution of left ventricular drainage, successful defibrillation was accomplished with current levels that were previously unsuccessful. Ranges of extracorporeal flow rate studied were 8.7 to 57.6 ml/kg per min. The average minimal flow rate permitting defibrillation was 19.7 ml/kg per min (range 12.1 to 30.4). Thus, defibrillation could be accomplished during submaximal flow rates, which were well within the capability of the system utilized. Illustrative experiments (Fig. 2): The time from coronary arterial ligation is listed in relation to each of the events portrayed with the duration of uninterrupted venTABLE
i
Results Dogs (no.) Average yeight (kg) Episodes of ventricular fibrillation (no.) Average time of ventricular fibrillation before defibrillation (min) Range of flow studied (ml/kg per min) Minimal flow permitting defibrillation (ml/kg per min)
1972
The American Journal of CARDIOLOGY
12 29.3 (z!=l.4) 21 28 (17-48) 8.7-57.6 19.7 (12.1-30.4)
Volume 30
249
LEFT
VENTRICULAR
DRAINAGE
4
DEFIBRILLATION-KUHN
v.E
ZOWW.
IOWW.
IMINUTESOFVFI
3OUKC.
~l5l_.___~161_
TIME (min.)
0
IO
4
4
CONTROL CE6;;;bRY (MINUTES OF WI
ET
4
4
COR ARTERY LIGATED
FOR
0 --
li7l_
23
VF
IO wsec
0
(131-
4
iI81 _I191
_1201_(291
24
20 wsec.
25
(14) _1151_.___
II PO2 and pH Values During Ventricular Fibrillation
Arterial
PO8
(mm Arterial
&I pH
7.38 (7.6-7.57)
Defibrillation Successful
7.17 (6.80-7.49)
During Bypass Unsuccessful
7.34 (7.0-7.8)
* P X0.01. 250
August 1972
The American Journal of CARDIOLOGY
27
42
4
4
LV BY-PPJS LV BY-PASS 200ml/mm 400mllmm (20rsec.) ~171_____ (32)--
30 wsec
Left ventricular PO2 and pH: Values obtained during the course of the experiments are listed in Table II. The low POs level noted during ventricular
Left Ventricular
4
40wsec. LVEWWSS LV BY-PASSLV BY-PASS 200mllmm 4OOmllmm BOOmllmm l3Cwsecl lM.recl
tricular fibrillation in parentheses. In Figure 2A, at the time of coronary arterial ligation, the electrocardiographic pattern of acute injury is noted. Ventricular fibrillation occurred spontaneously 10 minutes later. The animal was allowed to fibrillate for 15 minutes, after which there were attempts at defibrillation with increasing amounts of current applied directly to the heart. These were unsuccessful. After 19 minutes of ventricular fibrillation with no assisted circulation, left ventricular drainage was begun in the manner previously indicated at an initial rate of 200 ml/min. Attempts at ventricular defibrillation were unsuccessful. Increasing the flow rate to 400 ml/min also did not permit electrical defibrillation, but when the flow rate was increased to 800 ml/min, defibrillation was successful after 29 minutes of previously irreversible ventricular fibrillation. This experiment was then repeated in the same animal with the same result, ventricular fibrillation restarting spontaneously when the extracorporeal circulation was discontinued. Figure 2B illustrates a similar experiment. The first 2 panels show the electrocardiogram before and after coronary arterial ligation. Ventricular fibrillation occurred spontaneously after 10 minutes. After 15 minutes of ventricular fibrillation, attempts at defibrtllation with increasing currents were unsuccessful. Left ventricular drainage with a flow rate of 200 ml/min was initiated after 17 minutes of ventricular fibrillation. Attempts at defibrillation were unsuccessful until the flow rate was increased to 400 ml/min. At this flow rate, defibrillation was successful after 32 minutes of ventricular fibrillation. Ventricular fibrillation recurred when left ventricular drainage was discontinued.
TABLE
AL.
Figure 2. Electrocardiographic tracings in 2 typical experiments. A, dog weighing 33 kg. The time from coronary arterial ligation is listed in relation to each of the events with the duration of uninterrupted ventricular fibrillation in parentheses. Note that attempts at ventricular defibrillation were unsuccessful until extracorporeal flow rate was increased to 800 ml/min. Defibrillation was then successful after 29 minutes of previously irreversible ventricular fibrillation. B, in this experiment (with an animal weighing only 26 kg) attempts at defibrillation were unsuccessful until the flow rate was increased to 400 ml/min. At this flow rate, defibrillation was successful after 32 minutes of ventricular fibrillation. Ventricular fibrillation recurred
when left ventricular drainage was discontinued. fibrillation was raised considerably during left ventricular drainage, and there was a pronounced difference in arterial POs obtained during extracorporeal flow rates that led to successful defibrillation as compared to values obtained during flow rates that did not lead to successful defibrillation. Of course, the flow rate was higher in the group that underwent successful defibrillation. A variety of arterial pH values was obtained, usually related to a combination of metabolic acidosis and respiratory alkalosis. There was typically a base deficit and a low level of PCOz. Successful defibrillation was accomplished despite a wide range of pH values. A relatively normal value for arterial pH was not essential for successful defibrillation.
Discussion Our results indicate that left ventricular drainage permits a successful defibrillation even after prolonged, apparently refractory ventricular fibrillation. These findings are consistent with the conclusions of other investigators who have demonstrated that, in an animal with ventricular fibrillation of very short duration without circulatory support, defibrillation is more easily accomplished when a variety of methods of circulatory support are utilized.1,2 It has been well demonstrated that such techniques are considerably more efficacious in this regard than direct, manually controlled cardiac contractions.9 Our findings extend these observations to prolonged ventricular fibrillation without circulatory support, which is refractory to electrical defibrillation and which, in a clinical setting, presents a hopeless resuscitative problem. Mechanisms facilitating defibrillation after left ventricular drainage: The consistent success of left ventricular drainage in permitting defibrillation may well be related to acute reduction of the volume of the distended, fibrillating left ventricle. There is ample experimental evidence that left ventricular size is of key importance in permitting the maintenance and development of ventricular defibrillation.l”J1 This suggests that large hearts provide more reentrant pathways for perpetuation of fibrillatory “circus” rhythms than do smaller hearts in which refractory tissue may be present, thus allow-
Volume 30
LEFT VENTRICULAR
ing the rhythm to terminate. Other modes of circulatory support, previously cited, which permit defibrillation after shorter periods of ventricular fibrillation than noted in our study, also result in acute reduction of left ventricular volume, In addition to ventricular size, the form of the cardiac tissue may be important in facilitating defibrillation. GarreylO has demonstrated that long thin pieces of cardiac tissue recover promptly from ,ventricular fibrillation and, if strips of cardiac tissue are quite narrow, ventricular fibrillation may be impossible. The form of the distended fibrillating ventricle is visibly altered during left ventricular drainage. Alterations of myocardial oxygen requirement and blood flow produced by left ventricular drainage may also be of importance in permitting defibrillation after prolonged refractory ventricular fibrillation, although we could not measure these satisfactorily in our experiments. It is logical to assume that there was some reduction of myocardial oxygen requirement coincident with acute reduction of ventricular volume during left ventricular drainage. Measurement of intercoronary flow (backflow) has indicated that substantial increments are obtained during ventricular fibrillation witlh initiation of left heart bypass.12 Such increase in coronary flow may be responsible for the ease of defibrillation of the ventricles during left ventricular drainage. Experiments in the dog and pig indicate that ventricular fibrillation occurs only when a critical mass of myocardium becomes totally avascular. Therefore, measures that decrease the size of the avascular myocardium (by increasing coronary flow) can be expected to enhance the possibility of defibrillating the ischemic ventricle. Alterations of blood and myocardial electrolytes, which must also be considered factors in permitting defibrillation, were not measured in this study, but it is of interest that pH1 variation over a wide range did not influence ability to defibrillate the ventricles
DRAINAGE
FOR DEFIBRILLATION-KUHN
ET AL.
during left ventricular drainage. Although some investigators have cited potassium shifts from the intracellular compartment to the serum as a causative factor in the production of ventricular fibrillation after acute myocardial infarction, more recent investigations have indicated that such electrolyte shifts are probably not responsible for ventricular fibrillation in this experimental setting.14 Clinical implications: The clinical connotations of our results are not clear at this time. We do not know whether continued maintenance of circulatory adequacy or adequate cerebral function will be possible after defibrillation following such prolonged ventricular fibrillation. However, this modality requiring only a peripheral arterial cutdown procedure may be instituted relatively rapidly through a closed chest and may permit defibrillation even after prolonged ventricular fibrillation in clinical situations when the ventricles cannot be defibrillated by existing methods. Maintenance of circulatory support by external cardiac compression during initiation of the left ventricular catheter would, of course, enhance the possibility of restoration of circulatory adequacy after defibrillation. There are clinical settings in which left ventricular drainage may be used for relatively prolonged periods in patients with surgically remediable cardiac disease to prevent recurrent ventricular fibrillation during preparation for definitive cardiac surgery; coronary revascularization in acute myocardial infarction is one such instance. Transarterial left ventricular drainage through a closed chest has been applied clinically by Zwart et al.15 for other purposes. It is reasonable to expect advances in the future which will permit long-term application of a variety of techniques of closed chest circulatory support, particularly in regard to development of nonthrombogenic surfaces. ls This should permit extension of the indications for circulatory support to include recurrent or refractory ventricular fibrillation.
References pulsatile 1. Rosselot E, Gold H, Vyden JK, et al: Venoarterial circulatory assist in the treatment of resistant ventricular fibrillation. Amer J Cardiol 27:48-50, 1971 counter2. Fleming WH, Schultz J, Malm JR: Synchronized pulsation in the management of ventricular fibrillation following coronary artery ligation. J Thorac Cardiovasc Surg 58:253-257,1986 3. Dennis C, Carlens E, Senning A, et al: Clinical use Of a cannula for left heart bypass without thoracotomy. Ann Surg 158:823-837,1982 4. Leighninger DS, Davidson AIG, Beck CS: Left heart bypass in cardiac resuscitation. I\mer J Cardiol 15:33-37, 1985 5. Crawford FA, Willwerth IlM, Cline RE, et al: Left heart bypass following left coronary artery occlusion. Circulation 37: suppl2:12-17,1988 8. Roaensweia J. Chatterjee S, Merino F: Treatment of acute myocardial-infarction by counterpulsation. J Thorac Cardiovast Surg 59:243-250, 1970 7. Ewart HHJ, Kralios A, Collan R; et al: Transarterial closed chest left ventricular (Ta CLV) bypass. Trans Amer Sot Artif Intern Organs 15:386-390, 1989 8. Geddes LA, Schuhmann RE, Hoff HE, et al: Total maintenance of circulation in the closed chest animal with ventricular fibrillation. Baylor Cardiovasc Res Center Bull 8:33-44, 1987
9. Nachlas MM, Siedband MP, Bernstein P: Experimental technics for improving the effectiveness of cardiac resuscitation. Ann Surg 181:331-343, 1985 10. Garrey WE: The nature of fibrillary contraction of the heart. Its relation to tissue mass and form. Amer J Physiol 33:397-414, 1914 11. Szabuniewicz M, Hoff HE, McCrady JD: Spontaneous ventricular fibrillation in the armadillo. Baylor Cardiovasc Res Center Bull 8:135-147, 1970 12. Davidson AIG, Leighninger DS: Collateral flow in the heart at different aortic perfusion pressures using left heart bypass. Ann Surg 182:46-52, 1985 13. Myers MB, Cherry G: Ventricular fibrillation area thresholds in the dog and pig. J Thorac Cardiovasc Burg 59: 401412, 1970 14. Cherry G, Myers MB: The relationship to ventricular fibrillation of early tissue sodium and potassium shifts and coronary vein potassium levels in experimental myocardial infarction. J Thorac Cardiovasc Surg 81:587-598, 1971 15. Zwart HHJ, Kwan-Gett CS, Backman DK, et al: Transar-terial left ventricular bypass (abstr). Amer J Cardiol 28:687, 1970 18. Wakabayashf A, Dietrick W, Connolly JE; Closed chest left heart bypass without anticoagulation. J Thorac Cardiovasc Surg 58:81 l-820, 1989
August 1972
The American Journal of CARDIOLOGY
Volume 30
251