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Concealed conduction due to potassium
Concealed CHARLES
Conduction
FISCH, M.D., ~.A.c.c., HARVEY
FEIGENBAW,
Indianapolis,
T
Due to Potassium*
CONCEPT of concealed conduction dates back to 1925 when Lewis and Master’ postulated from their classic studies of .4-V conduction the existence of incomplete penetration (concealed conduction) of the A-V This conduction system by atria1 impulses. concept, although based on indirect evidence, was found extremely useful in interpretation of complex clinical arrhythmias.‘13 Hoffman and his associates” s5 using the microelectrode technic were able to provide direct evidence for the existence of concealed conduction. In the electrocardiogram, incomplete penetration of the A-V node is manifest by (I) unexpected prolongation of the P-R interval, (2) unexpected block of atria1 conduction and (3) unexpected displacement of the A-V nodal pacemaker in the presence of A-V nodal rhythm. The term unexpectedis applicable because the above phenomena cannot be explained bychanging R-P or R-R relationships. The purpose of this report is (1) to describe for the first time concealed conduction as a result of potassium-induced depression of A-V conduction and (2) to give added support to the concept of concealed conduction by producing this phenomenon experimentally.
M.D.
and JOHN A. BOWERS,
M.D.
Indiana
ment was monitored with an oscilloscope, and when advisable, permanent records were obtained by using standard lead II connections. Frequent plasma potassium determinations were made by using the Beckman flame photometer.
HE
RESULTS AND DESCRWTION OF ELECTROCARDIOGRAMS A-\’ block was produced in 76 of 78 experiments6 and concealed conduction was demonstrated in 27 instances. The average plasma potassium at the time concealed conduction became apparent was 8.29 with a range from 7.5 to 10.1 mEq./L. Figure 7 (Experiment 44-780) is an example of the simplest forms of concealed conduction, namely, sudden and unexpected prolongation of the P-R interval. Strip A is a control tracing showing slight sinus arrhythmia with a rate of about 100 beats per minute and a P-R interval of 0.10 sec. In strip B the rhythm is S-A in origin with a rate of 120 beats per minute and a 1: 1 A-V response. There are rounding and broadening of P waves; the P-R is prolonged and measures from 0.24 to 0.36 sec. Parts of this strip demonstrate A-V alternans with a paradoxic relation of P-R to R-P, the shorter R-P being followed by a shorter P-R, and the longer R-P by longer P-R (e.g., first five cycles of the strip). The diagram under .rtrip C is conventional representing, from above down, the P waves, A-V conduction and the QRS complexes. The sinus rate is now 120 beats per minute with first and second degree A-V block. P9 through PI4 with their respective QRS complexes demonstrate the classic Wenckebach structure. The P5-R, PB-R, P14-R and P18-R intervals measure 0.16 to 0.18 sec., and their respective R-P intervals are 0.62, 0.68> 0.60 and 0.60 sec. The P7-R with an R-P of 0.76 sec. is unexpectedly prolonged to 0.32 sec. One would expect that P7-R with its R-P7 longer than R-P5. R-P9, R-P14 and R-P18 should, if anything, have a P-R as short if not shorter than the P-R intervals following P5, P9, P14 and P18. The unexpected prolongation of P7-R can be explained
METHOD AND RESWTS Mongrel dogs weighing 9 to 15 kg. were used in these experiments. The animals were anesthetized with either 30 mg./kg. of sodium pentobarbital given intraperitoneally or with 2.5 mg./kg. of morphine given intramuscularly followed by 15 mg.,/kg. of sodium pentobarbital given intravenously. Potassium was administered through a femoral vein catheter in the form of isotonic solution (155 mEq./L.) of buffered potassium phosphate at a rate of 1.0 to 1.2 mEq./min. The uniform rate of infusion was assured through the use of a flowmeter. Each experi-
* From the Krannert Heart Research Institute, Marion County General Hospital, the Department of Medicine and Heart Research Center, Indiana University School of Medicine, Indianapolis, Indiana. Supported by the Herman C. Krannert Fund, the Indiana Heart Association, Indiana State Board of Health and (in part) by the U. S. Public Health Service Training Grant 5363 and (in part) with facilities provided by Cardiovascular Clinical Research Center Grant H-6308 from the National Heart Institute, National Institutes of Health, U. S. Public Health Service. 72
THE AMERICAN JOURNAL. OF
CARDIOLOGY
73
Concealed Conduction Due to Potassium
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FIG. 1 (Experiment 44-180). Str;p C demonstrates conduction of P6. For details see text.
,...
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FIG. 2 (Experiment 50-216). In strip C the unexpected failure of P6 and P12 to conduct is the result of concealed conduction of P5 and P6. For details see text. Strip A is a control tracing. Strip B shows prolongation of P-R as the plasma potassium was rising. Strips D and E were recorded after infusion was discontinued.
by concealed conduction (incomplete penetration) of P6 producing a state of prolonged refractoriness The and causing a delay of the subsequent impulse. assumption of deep penetration into the A-V node of P6 seems valid because a number of P waves, both JANUARY
1963
preceding and following P6 and with shorter R-P intervals, conduct to the ventricles. In addition to concealed conduction, strip C demonstrates the supernormal phase of A-V conduction.? This phenomenon is manifest by conduction
Fisch, Feigenbaum
and Bowers
FIG. 3 (Experiment 48-177). Strifi A is a control tracing. &$J B shows prolonged P-R interval and A-V alternans with a paradoxic relationship of R-P to P-R (supernormal phase of A-V conduction). In strif C the unexpected prolongation of P-R after P6, P12, P14 and failure of P22 to conduct are due to concealed conduction of P5, Pll, P13 and P21, respectively. Strip D shows a 1: 1 response, first degree block and A-V alternans with an R-P and P-R relationship similar to that in strip B, but this time the plasma level of potassium was declining.
of P R-P (P4, may
waves (PI, P2, P3, Pll. P12, P16) following an that is shorter than the R-P of the blocked beats P6, P8, PI3 and P17). Dual A-V conduction also explain such a paradoxic relationship of
P-R and R-P.8
Figure 2 (Experiment 50-276) demonstrates unexpected failure of conduction of an atria1 impulse due to concealed penetration of the preceding atria1 impulse. The control tracing (A) shows a mild sinus arrhythmia and a P-R of 0.09 sec. In strip B the P waves are somewhat broader, the P-R measures from 0.16 to 0.22 sec., and A-V alternans with a paradoxical R-R and P-R relationship is clearly visible. Strip C, recorded when plasma potassium was 7.1 mEq./L., demonstrates an A-V block varying from simple prolongation of P-R interval to a 3: 1 block. The unexpected failure of P6 and PI2 to conduct, in spite of the fact that PI, 2, 3, 4, 8, 9, 10, 14, 15 and 16 conduct after a shorter R-P, can be explained by concealed conduction (incomplete penetration) of P5 and Pl 1. Both impulses? invading the A-V conduction system, produce a state of refractoriness and interfere with conduction of the succeeding P6 and P12. The R-P of impulses preceding the blocked P5 and P12 shortens gradually (P3, P4 and again P9, PlO) but the P waves conduct to the ventricle. The third P wave of each of these cycles (P5 and Pll) has a still shorter R-P and can be assumed, because the immediately preceding impulse excites the ventricle, to penetrate deeply into the A-V node. Such a penetration results in a refractory state and causes a block of conduction of P6 and P12. Strip D was recorded when the plasma potassium was 6.5 mEq./L. and shows a 1: 1 A-V response with a P-R of 0.40 sec.; it is included as supporting evidence that P3, P4, P9, PlO and Pl6 in strip C reach the ventricles in spite of the unusually long P-R. Strip E shows re-
turn to normal contour of the P wave and of the P-R intervals. Failure to recognize concealed conduction as a cause of the block of P6 and PI2 with their relatively long R-P intervals might lead to the erroneous conclusion that the P waves after a much shorter R-P (e.g., P3, P4, P9, PIO) were able to conduct because of the supernormal phase of A-V conduction. Figure 3 (Experiment 48-777). Strip A represents the control tracing. In strip B and D first degree block with A-V alternans is recorded as the plasma potassium is rising during the infusion (strip B) and declining shortly after injection was stopped (strip D). In strib C unexpected prolongation of P-R occurs after P6, PI2 and P14. Considering the fact that R-P6, R-PI2 and R-P14 are longer than, for example, R-PI, R-P2 or R-P17, one wouldexpect P6, P12, P14 to be followed by a shorter P-R than PI, P2, P17. This unexpected prolongation of P-R of P6, P12 and P14 can be easily explained by concealed conduction of P5, Pl 1 and PI 3. Such an assumption is valid because P waves with a similar relation to their immediately preceding R waves (e.g., P3, P4 or P7) are conducted. Complete block of transmission of P22 is the result of concealed conduction of P21 and represents a phenomenon identical to that described in Figure 2. Figure 3 (Experiment 45-272) demonstrates second degree A-V block with a 3: 1 atrioventricular response due to concealed conduction. The three strips were recorded at different plasma potassium levels and should be considered as separate entities. In strip A the unexpected prolongation of P20-R, after a relatively long R-P20, is due to incomplete penetration of P19, a phenomenon similar to that described in Figure 3. The failure of P19 to conduct with an R-P similar in duration to that of P3, P7, Pll, PI5 and THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Concealed Conduction Due to Potassium
FIG. 4 (Experiment
45-212).
The three strips were recorded
at somewhat different levels of plasma potassium.
In
strip A the unexpected prolongation of P20-R and block of P17 are due to concealed conduction of P19 and Pl6, respectively. Similarly, in strip B, concealed conduction of P7 and P20 explains the unexpected block of P8 and prolongation of P21-R. In sn$~ C concealed conduction of PlO and P12 causes prolongation of Pll-R and block of P13, respectively.
P21 is the result of prolongation of the preceding R-R interval; consequently the subsequent refractory period is longer.Q Concealed conduction of Pi6 accounts for failure of P17 to conduct, and 3:l A-V block results. The assumption of deep penetration of A-\’ node by P16 and P19 is valid because atria1 waves in comparable positions in respect to their preceding R waves (e.g., P3, Pll and P21) conduct to the ventricles. In strip B the unexpected prolongation of P6-R, P21-R and block of P8 are the results of concealed conduction of P5, P20 and P7, respectively. In strip C the prolongation of Pl 1-R and block of P13-R arc again the results of concealed conduction of PlO and P12. Figure 5 (Experiment 48-227) is an example of A-V nodal tachycardia with displacement of the A-V nodal pacemaker by incomplete penetration of an JANUARY
1963
atria1
impulse.
Strip A is a control
tracing
while
strip B shows first and second degree A-V block. Strip C demonstrates an A-V nodal tachycardia with an R-R interval of 0.58 sec. Pl: P6, P9, P21, P26 and P29 are conducted to the ventricles after an R-P of 0.08 to 0.12 sec. and a P-R varying from 0.28 to 0.36 sec. In view of the fact that the A-V node discharges regularly with an R-R interval of 0.58 sec., the sudden prolongation of distance between the eighth and ninth QRS to 0.80 sec. is unexpected and Concealed penetration of P12 has to be explained. with premature discharge of the ectopic A-V nodal pacemaker makes it possible for P13 to arrive at a time when the A-V conduction system is excitable and penetrates the ventricles with a P-R of 0.36 sec. Assumption of incomplete but deep penetration of P12 is valid because P waves with identical or
Fisch, Feigenbaum
76
and Bowers
FIG. 5 (Experiment 48-221). strip rl is a control tracing. In strip B second degree A-V block was produced by potassium. .%ip C demonstrates a nodal tachycardia with an R-R of 0.58 sec. Pl, Pb, P9. P21, P26 and P29 are conducted after an R-P varying from 0.08 to 0.12 sec. Concealed conduction of P12 “dislocates” the nodal pacemaker and allows for P13 to conduct. This explains the unexpected prolongation of the distance between the eighth and ninth QRS from the nodal interval of 0.58 to 0.80 sec. Strip D shows 1 : 1 conduction with a P-R of 0.26 sec.
shorter R-P intervals conduct to the ventricles (Pl. P6, P21, P29). A’trip D demonstrates 1: 1 conduction with an R-P of 0.08 and P-R of 0.28 sec., respectively. COMMENTS
The frequent demonstration of concealed conduction during infusion of potassium is not The same mechanisms that produce surprising. ordinary A-V block are also responsible for deep but incomplete penetration of the A-V conducting system with unexpected changes of the refractory period following nonconducted atria1 impulses. Despite the fact that as early as 1911 Mathison’O described A-V block due to potassium, the subsequent literature bearing on this subject is confusing.“-” Under the conditions of our experiments, with the exception of peaking of T wave, varying A-V block with clearly defined P waves is the most consistent abnormality produced.‘xa1g The mean plasma potassium level at which the block was observed in 76 experiments6 was 8.33 mEq. with a standard deviation of 0.76. Hoffman and his associates4 have shown that concealed conduction with failure of A-V transmission can take place anywhere along the A-V conduction system between the atria and the ventricles. The failure of propagation may result from either decremental conduction or from difference in the duration of the action potential of the different components of the A-V transmission system. Reduction of resting membrane potential with decrease in velocity of the rise of action potential lowers the ampli-
tude of action potential and may result in decremental conduction. Potassium is known to produce all of these described changes in the resting and action potential. In the surface electrocardiogram these alterations may result in A-V block with or without the phenomenon of concealed conduction. SUWIARY 1. Concealed conduction (incomplete penetration of the atrioventricular node) was observed in 27 of 79 instances of potassium-induced atrioventricular block in dogs. 2. This phenomenon can be explained b) the known effects of potassium on the resting membrane potential and on the speed of the rise and the amplitude of action potential. REFERENCES
1. LEWIS, T. and malian
2.
1925.
MASTER, A. M.
heart;
Conduction in mamHeart, 12: 209,
A-V conduction.
D. and SHOOKHOFF, gcn in Bundel. I. W&z.
SCHERF,
C.
Reitzleitungstovun10: 97,
Arch. Inn. Med.,
1925. 3. LANGENDORF, R. and PICK, A.
Concealed conduction. Further evaluation of a fundamental aspect of propagation of cardiac impulse. Circulation,
13: 381, 1956. 4. HOFFMAN, B. F. and CRANEFIELD, P. F.
physiology of the Heart, p. 219. McGraw Hill Book Company.
ElectroNew York, 1960.
5. HOFFMAN, B. F., CRANEFIELD, P. F. and STUCKEY, Circulation
Res.,
6. FISCH, C., FEIGENBAUM,H. and BOWERS, J. A.
The
J. H.
Concealed
conduction.
9: 194, 1961.
THE AMERICAN JOURNAL OF CARDIOLOGY
Concealed Conduction Due to Potassium
7.
8.
9.
10.
11.
12.
13.
effect of potassium on atrioventricular conduction of normal dogs. Am. J. Cardiol., in press. FISCH, C. and STEINMETZ,E. F. Supernormal phase of atrioventricular (A-V) conduction due to potassium. A-V alternans with first degree A-V block. Am. Heart J., 62: 211, 1961. MOE, G. M., PRESTON, J. B. and BURLINGTON,H. Physiologic evidence for a dual A-V transmission system. Circulation Res., 4: 357, 1956. GOUAUX,J. L. and ASHMAN,R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am. Heart J., 34: 366, 1947. MATHISON,G. C. The effect of potassium salts upon the circulation and their action on plain muscle. J. Physiol., 42: 471, 1911. WIGGERS, C. J. Studies on ventricular fibrillation produced by electric shock. Am. J. Physiol., 93: 197, 1930. WINKLER, A. W., HOFF, H. E. and SMITH, P. K. Electrocardiographic changes and concentration of potassium in serum following intravenous injection of potassium chloride. Am. J. Physiol., 124: 478,1938. CHAMBERLAIN,F. L., SCUDDER, J. and ZWEIMER, R. L. Electrocardiographic changes associated with experimental alterations in blood potassium in cats. Am. Heart J., 18: 458, 1939.
JANUARY 1963
77
14. CRISMON,J. M., CRISMON,C. S., CALABRESI, M. and DARROW, D. C. Electrolyte redistribution in cat heart muscle and skeletal muscle in potassium poisoning. Am. J. Physiol., 139: 667, 1943. 15. BELLET, S., GAZES, P. C. and STEIGER, W. A. The effect of potassium on the electrocardiogram in normal dogs and in dogs with myocardial infarction. Am. J. M. SC., 220: 237, 1950. 16. BUTCHER, W. A., WAKIM, K. G., ESSEX, H. E., PRUITT, R. D. and BURCHELL,H. B. The effect of changes in concentration of cations on the electrocardiograms of the isolated perfused heart. Am. Heart J., 41: 801, 1952. 17. MULLER, 0. F., DELEON, A. C. and BELLET,S. The effect of hyperpotassemia on the idioventricular pacemaker in complete A-V heart block and comparison with its effect on the heart rate in normal sinus rhythm. Am. J. Cardiol., 7: 817, 1961. 18. FISCH, C., MARTZ, B. L. and PRIEBE, F. H. Transient effect of potassium on A-V conduction and ventricular tachycardia produced by acetyl strophanthidin: demonstration of supernormal conduction. Am. Heart J., 60: 212, 1960. 19. FISCH, C., MARTZ, B. L. and PRIEBE, F. H. Enhancement of potassium-induced atrioventricular block by toxic doses of digitalis drugs. J. Clin. Invest., 39: 1885, 1960.
Conduction
FISCH, M.D., ~.A.c.c., HARVEY
FEIGENBAW,
Indianapolis,
T
Due to Potassium*
CONCEPT of concealed conduction dates back to 1925 when Lewis and Master’ postulated from their classic studies of .4-V conduction the existence of incomplete penetration (concealed conduction) of the A-V This conduction system by atria1 impulses. concept, although based on indirect evidence, was found extremely useful in interpretation of complex clinical arrhythmias.‘13 Hoffman and his associates” s5 using the microelectrode technic were able to provide direct evidence for the existence of concealed conduction. In the electrocardiogram, incomplete penetration of the A-V node is manifest by (I) unexpected prolongation of the P-R interval, (2) unexpected block of atria1 conduction and (3) unexpected displacement of the A-V nodal pacemaker in the presence of A-V nodal rhythm. The term unexpectedis applicable because the above phenomena cannot be explained bychanging R-P or R-R relationships. The purpose of this report is (1) to describe for the first time concealed conduction as a result of potassium-induced depression of A-V conduction and (2) to give added support to the concept of concealed conduction by producing this phenomenon experimentally.
M.D.
and JOHN A. BOWERS,
M.D.
Indiana
ment was monitored with an oscilloscope, and when advisable, permanent records were obtained by using standard lead II connections. Frequent plasma potassium determinations were made by using the Beckman flame photometer.
HE
RESULTS AND DESCRWTION OF ELECTROCARDIOGRAMS A-\’ block was produced in 76 of 78 experiments6 and concealed conduction was demonstrated in 27 instances. The average plasma potassium at the time concealed conduction became apparent was 8.29 with a range from 7.5 to 10.1 mEq./L. Figure 7 (Experiment 44-780) is an example of the simplest forms of concealed conduction, namely, sudden and unexpected prolongation of the P-R interval. Strip A is a control tracing showing slight sinus arrhythmia with a rate of about 100 beats per minute and a P-R interval of 0.10 sec. In strip B the rhythm is S-A in origin with a rate of 120 beats per minute and a 1: 1 A-V response. There are rounding and broadening of P waves; the P-R is prolonged and measures from 0.24 to 0.36 sec. Parts of this strip demonstrate A-V alternans with a paradoxic relation of P-R to R-P, the shorter R-P being followed by a shorter P-R, and the longer R-P by longer P-R (e.g., first five cycles of the strip). The diagram under .rtrip C is conventional representing, from above down, the P waves, A-V conduction and the QRS complexes. The sinus rate is now 120 beats per minute with first and second degree A-V block. P9 through PI4 with their respective QRS complexes demonstrate the classic Wenckebach structure. The P5-R, PB-R, P14-R and P18-R intervals measure 0.16 to 0.18 sec., and their respective R-P intervals are 0.62, 0.68> 0.60 and 0.60 sec. The P7-R with an R-P of 0.76 sec. is unexpectedly prolonged to 0.32 sec. One would expect that P7-R with its R-P7 longer than R-P5. R-P9, R-P14 and R-P18 should, if anything, have a P-R as short if not shorter than the P-R intervals following P5, P9, P14 and P18. The unexpected prolongation of P7-R can be explained
METHOD AND RESWTS Mongrel dogs weighing 9 to 15 kg. were used in these experiments. The animals were anesthetized with either 30 mg./kg. of sodium pentobarbital given intraperitoneally or with 2.5 mg./kg. of morphine given intramuscularly followed by 15 mg.,/kg. of sodium pentobarbital given intravenously. Potassium was administered through a femoral vein catheter in the form of isotonic solution (155 mEq./L.) of buffered potassium phosphate at a rate of 1.0 to 1.2 mEq./min. The uniform rate of infusion was assured through the use of a flowmeter. Each experi-
* From the Krannert Heart Research Institute, Marion County General Hospital, the Department of Medicine and Heart Research Center, Indiana University School of Medicine, Indianapolis, Indiana. Supported by the Herman C. Krannert Fund, the Indiana Heart Association, Indiana State Board of Health and (in part) by the U. S. Public Health Service Training Grant 5363 and (in part) with facilities provided by Cardiovascular Clinical Research Center Grant H-6308 from the National Heart Institute, National Institutes of Health, U. S. Public Health Service. 72
THE AMERICAN JOURNAL. OF
CARDIOLOGY
73
Concealed Conduction Due to Potassium
_. C.1I..:I I I I 1 I I I I~+bl ::
:
:: :,:::...
::
::
::.
::_
:...
.:.
:::,::
:
1. I I I I I I I i i 7 k 1 i I .::
.:jj
;;j
.I
,,^
FIG. 1 (Experiment 44-180). Str;p C demonstrates conduction of P6. For details see text.
,...
:ii
ii.1
‘.;i
:i;
ii-j
the unexpected
y::
jj:
ii_:
.I_,
I i i i i i i i i i i .i i i i I :
.:
prolongation
,j::.
:
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of P7-R
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resulting
:
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FIG. 2 (Experiment 50-216). In strip C the unexpected failure of P6 and P12 to conduct is the result of concealed conduction of P5 and P6. For details see text. Strip A is a control tracing. Strip B shows prolongation of P-R as the plasma potassium was rising. Strips D and E were recorded after infusion was discontinued.
by concealed conduction (incomplete penetration) of P6 producing a state of prolonged refractoriness The and causing a delay of the subsequent impulse. assumption of deep penetration into the A-V node of P6 seems valid because a number of P waves, both JANUARY
1963
preceding and following P6 and with shorter R-P intervals, conduct to the ventricles. In addition to concealed conduction, strip C demonstrates the supernormal phase of A-V conduction.? This phenomenon is manifest by conduction
Fisch, Feigenbaum
and Bowers
FIG. 3 (Experiment 48-177). Strifi A is a control tracing. &$J B shows prolonged P-R interval and A-V alternans with a paradoxic relationship of R-P to P-R (supernormal phase of A-V conduction). In strif C the unexpected prolongation of P-R after P6, P12, P14 and failure of P22 to conduct are due to concealed conduction of P5, Pll, P13 and P21, respectively. Strip D shows a 1: 1 response, first degree block and A-V alternans with an R-P and P-R relationship similar to that in strip B, but this time the plasma level of potassium was declining.
of P R-P (P4, may
waves (PI, P2, P3, Pll. P12, P16) following an that is shorter than the R-P of the blocked beats P6, P8, PI3 and P17). Dual A-V conduction also explain such a paradoxic relationship of
P-R and R-P.8
Figure 2 (Experiment 50-276) demonstrates unexpected failure of conduction of an atria1 impulse due to concealed penetration of the preceding atria1 impulse. The control tracing (A) shows a mild sinus arrhythmia and a P-R of 0.09 sec. In strip B the P waves are somewhat broader, the P-R measures from 0.16 to 0.22 sec., and A-V alternans with a paradoxical R-R and P-R relationship is clearly visible. Strip C, recorded when plasma potassium was 7.1 mEq./L., demonstrates an A-V block varying from simple prolongation of P-R interval to a 3: 1 block. The unexpected failure of P6 and PI2 to conduct, in spite of the fact that PI, 2, 3, 4, 8, 9, 10, 14, 15 and 16 conduct after a shorter R-P, can be explained by concealed conduction (incomplete penetration) of P5 and Pl 1. Both impulses? invading the A-V conduction system, produce a state of refractoriness and interfere with conduction of the succeeding P6 and P12. The R-P of impulses preceding the blocked P5 and P12 shortens gradually (P3, P4 and again P9, PlO) but the P waves conduct to the ventricle. The third P wave of each of these cycles (P5 and Pll) has a still shorter R-P and can be assumed, because the immediately preceding impulse excites the ventricle, to penetrate deeply into the A-V node. Such a penetration results in a refractory state and causes a block of conduction of P6 and P12. Strip D was recorded when the plasma potassium was 6.5 mEq./L. and shows a 1: 1 A-V response with a P-R of 0.40 sec.; it is included as supporting evidence that P3, P4, P9, PlO and Pl6 in strip C reach the ventricles in spite of the unusually long P-R. Strip E shows re-
turn to normal contour of the P wave and of the P-R intervals. Failure to recognize concealed conduction as a cause of the block of P6 and PI2 with their relatively long R-P intervals might lead to the erroneous conclusion that the P waves after a much shorter R-P (e.g., P3, P4, P9, PIO) were able to conduct because of the supernormal phase of A-V conduction. Figure 3 (Experiment 48-777). Strip A represents the control tracing. In strip B and D first degree block with A-V alternans is recorded as the plasma potassium is rising during the infusion (strip B) and declining shortly after injection was stopped (strip D). In strib C unexpected prolongation of P-R occurs after P6, PI2 and P14. Considering the fact that R-P6, R-PI2 and R-P14 are longer than, for example, R-PI, R-P2 or R-P17, one wouldexpect P6, P12, P14 to be followed by a shorter P-R than PI, P2, P17. This unexpected prolongation of P-R of P6, P12 and P14 can be easily explained by concealed conduction of P5, Pl 1 and PI 3. Such an assumption is valid because P waves with a similar relation to their immediately preceding R waves (e.g., P3, P4 or P7) are conducted. Complete block of transmission of P22 is the result of concealed conduction of P21 and represents a phenomenon identical to that described in Figure 2. Figure 3 (Experiment 45-272) demonstrates second degree A-V block with a 3: 1 atrioventricular response due to concealed conduction. The three strips were recorded at different plasma potassium levels and should be considered as separate entities. In strip A the unexpected prolongation of P20-R, after a relatively long R-P20, is due to incomplete penetration of P19, a phenomenon similar to that described in Figure 3. The failure of P19 to conduct with an R-P similar in duration to that of P3, P7, Pll, PI5 and THE
AMERICAN
JOURNAL
OF
CARDIOLOGY
Concealed Conduction Due to Potassium
FIG. 4 (Experiment
45-212).
The three strips were recorded
at somewhat different levels of plasma potassium.
In
strip A the unexpected prolongation of P20-R and block of P17 are due to concealed conduction of P19 and Pl6, respectively. Similarly, in strip B, concealed conduction of P7 and P20 explains the unexpected block of P8 and prolongation of P21-R. In sn$~ C concealed conduction of PlO and P12 causes prolongation of Pll-R and block of P13, respectively.
P21 is the result of prolongation of the preceding R-R interval; consequently the subsequent refractory period is longer.Q Concealed conduction of Pi6 accounts for failure of P17 to conduct, and 3:l A-V block results. The assumption of deep penetration of A-\’ node by P16 and P19 is valid because atria1 waves in comparable positions in respect to their preceding R waves (e.g., P3, Pll and P21) conduct to the ventricles. In strip B the unexpected prolongation of P6-R, P21-R and block of P8 are the results of concealed conduction of P5, P20 and P7, respectively. In strip C the prolongation of Pl 1-R and block of P13-R arc again the results of concealed conduction of PlO and P12. Figure 5 (Experiment 48-227) is an example of A-V nodal tachycardia with displacement of the A-V nodal pacemaker by incomplete penetration of an JANUARY
1963
atria1
impulse.
Strip A is a control
tracing
while
strip B shows first and second degree A-V block. Strip C demonstrates an A-V nodal tachycardia with an R-R interval of 0.58 sec. Pl: P6, P9, P21, P26 and P29 are conducted to the ventricles after an R-P of 0.08 to 0.12 sec. and a P-R varying from 0.28 to 0.36 sec. In view of the fact that the A-V node discharges regularly with an R-R interval of 0.58 sec., the sudden prolongation of distance between the eighth and ninth QRS to 0.80 sec. is unexpected and Concealed penetration of P12 has to be explained. with premature discharge of the ectopic A-V nodal pacemaker makes it possible for P13 to arrive at a time when the A-V conduction system is excitable and penetrates the ventricles with a P-R of 0.36 sec. Assumption of incomplete but deep penetration of P12 is valid because P waves with identical or
Fisch, Feigenbaum
76
and Bowers
FIG. 5 (Experiment 48-221). strip rl is a control tracing. In strip B second degree A-V block was produced by potassium. .%ip C demonstrates a nodal tachycardia with an R-R of 0.58 sec. Pl, Pb, P9. P21, P26 and P29 are conducted after an R-P varying from 0.08 to 0.12 sec. Concealed conduction of P12 “dislocates” the nodal pacemaker and allows for P13 to conduct. This explains the unexpected prolongation of the distance between the eighth and ninth QRS from the nodal interval of 0.58 to 0.80 sec. Strip D shows 1 : 1 conduction with a P-R of 0.26 sec.
shorter R-P intervals conduct to the ventricles (Pl. P6, P21, P29). A’trip D demonstrates 1: 1 conduction with an R-P of 0.08 and P-R of 0.28 sec., respectively. COMMENTS
The frequent demonstration of concealed conduction during infusion of potassium is not The same mechanisms that produce surprising. ordinary A-V block are also responsible for deep but incomplete penetration of the A-V conducting system with unexpected changes of the refractory period following nonconducted atria1 impulses. Despite the fact that as early as 1911 Mathison’O described A-V block due to potassium, the subsequent literature bearing on this subject is confusing.“-” Under the conditions of our experiments, with the exception of peaking of T wave, varying A-V block with clearly defined P waves is the most consistent abnormality produced.‘xa1g The mean plasma potassium level at which the block was observed in 76 experiments6 was 8.33 mEq. with a standard deviation of 0.76. Hoffman and his associates4 have shown that concealed conduction with failure of A-V transmission can take place anywhere along the A-V conduction system between the atria and the ventricles. The failure of propagation may result from either decremental conduction or from difference in the duration of the action potential of the different components of the A-V transmission system. Reduction of resting membrane potential with decrease in velocity of the rise of action potential lowers the ampli-
tude of action potential and may result in decremental conduction. Potassium is known to produce all of these described changes in the resting and action potential. In the surface electrocardiogram these alterations may result in A-V block with or without the phenomenon of concealed conduction. SUWIARY 1. Concealed conduction (incomplete penetration of the atrioventricular node) was observed in 27 of 79 instances of potassium-induced atrioventricular block in dogs. 2. This phenomenon can be explained b) the known effects of potassium on the resting membrane potential and on the speed of the rise and the amplitude of action potential. REFERENCES
1. LEWIS, T. and malian
2.
1925.
MASTER, A. M.
heart;
Conduction in mamHeart, 12: 209,
A-V conduction.
D. and SHOOKHOFF, gcn in Bundel. I. W&z.
SCHERF,
C.
Reitzleitungstovun10: 97,
Arch. Inn. Med.,
1925. 3. LANGENDORF, R. and PICK, A.
Concealed conduction. Further evaluation of a fundamental aspect of propagation of cardiac impulse. Circulation,
13: 381, 1956. 4. HOFFMAN, B. F. and CRANEFIELD, P. F.
physiology of the Heart, p. 219. McGraw Hill Book Company.
ElectroNew York, 1960.
5. HOFFMAN, B. F., CRANEFIELD, P. F. and STUCKEY, Circulation
Res.,
6. FISCH, C., FEIGENBAUM,H. and BOWERS, J. A.
The
J. H.
Concealed
conduction.
9: 194, 1961.
THE AMERICAN JOURNAL OF CARDIOLOGY
Concealed Conduction Due to Potassium
7.
8.
9.
10.
11.
12.
13.
effect of potassium on atrioventricular conduction of normal dogs. Am. J. Cardiol., in press. FISCH, C. and STEINMETZ,E. F. Supernormal phase of atrioventricular (A-V) conduction due to potassium. A-V alternans with first degree A-V block. Am. Heart J., 62: 211, 1961. MOE, G. M., PRESTON, J. B. and BURLINGTON,H. Physiologic evidence for a dual A-V transmission system. Circulation Res., 4: 357, 1956. GOUAUX,J. L. and ASHMAN,R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am. Heart J., 34: 366, 1947. MATHISON,G. C. The effect of potassium salts upon the circulation and their action on plain muscle. J. Physiol., 42: 471, 1911. WIGGERS, C. J. Studies on ventricular fibrillation produced by electric shock. Am. J. Physiol., 93: 197, 1930. WINKLER, A. W., HOFF, H. E. and SMITH, P. K. Electrocardiographic changes and concentration of potassium in serum following intravenous injection of potassium chloride. Am. J. Physiol., 124: 478,1938. CHAMBERLAIN,F. L., SCUDDER, J. and ZWEIMER, R. L. Electrocardiographic changes associated with experimental alterations in blood potassium in cats. Am. Heart J., 18: 458, 1939.
JANUARY 1963
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14. CRISMON,J. M., CRISMON,C. S., CALABRESI, M. and DARROW, D. C. Electrolyte redistribution in cat heart muscle and skeletal muscle in potassium poisoning. Am. J. Physiol., 139: 667, 1943. 15. BELLET, S., GAZES, P. C. and STEIGER, W. A. The effect of potassium on the electrocardiogram in normal dogs and in dogs with myocardial infarction. Am. J. M. SC., 220: 237, 1950. 16. BUTCHER, W. A., WAKIM, K. G., ESSEX, H. E., PRUITT, R. D. and BURCHELL,H. B. The effect of changes in concentration of cations on the electrocardiograms of the isolated perfused heart. Am. Heart J., 41: 801, 1952. 17. MULLER, 0. F., DELEON, A. C. and BELLET,S. The effect of hyperpotassemia on the idioventricular pacemaker in complete A-V heart block and comparison with its effect on the heart rate in normal sinus rhythm. Am. J. Cardiol., 7: 817, 1961. 18. FISCH, C., MARTZ, B. L. and PRIEBE, F. H. Transient effect of potassium on A-V conduction and ventricular tachycardia produced by acetyl strophanthidin: demonstration of supernormal conduction. Am. Heart J., 60: 212, 1960. 19. FISCH, C., MARTZ, B. L. and PRIEBE, F. H. Enhancement of potassium-induced atrioventricular block by toxic doses of digitalis drugs. J. Clin. Invest., 39: 1885, 1960.