Cardiac excitability and resuscitation

Cardiac Edited

Resuscitation

by PALUEL J.

New York,

FLAGG, M.D., F.A.c.c.*

New York

Cardiac

Excitability

and Resuscitation

ROBERT M. HOSLER? Cleveland,

0

NE OF SEVERAL inherent and overlapping properties of cardiac muscle is excitAnother is the all or none law. This ability. declares that the weakest effective stimulus will produce the maximum contraction. There is thus no proportionality between strength of A stimulus stimulus and force of contraction. is any environmental change that can evoke a reaction. Both of these properties as well as many additional phenomena must be considered in order to comprehend fully the restoration of the heart beat. Nevertheless, the fundamental problem in cardiac resuscitation is to keep the The resuscitation procedure is brain viable.’ thus divided into two separate and distinct chronologic steps: (1) the re-establishment of the oxygen system and (2) the restoration of the heart beat. CARDIAC

EXCITABILITY AND STIMULATION

RESPONSE

Director,

National

Resuscitation

TO

Society,

Ohio

is a breakdown of labile chemical substances Unfortunately, oxygen followed by resynthesis. as an essential component cannot be stored in the cells or tissues. With a lack of oxygen within a short lapse of time, incomplete microaerobic or anerobic metabolic reactions probably come into limited operation and these are Oxygen is one of the prinquickly exhausted. cipal agents which has a profound influence on the permeability of the cell membrane and consequently upon the excitability period. It would appear that considerable study has been carried out2 pertaining to the effects of extracellular concentrations of ions (Ca and K), pH, temperature, drugs and others, which have a direct influence on an increase or decrease It also appears that there has in excitability. been a paucity of detailed investigation of the effects of hypoxia, hypercapnia and anoxia upon this important cardiac property, particularly at the onset of cardiac arrest. Anoxia and Excitability: An arrested heart with its oxygen-depleted cardiac muscle bvill completely lose its excitability in the matter of When this a relatively short period of time. point is reached, the heart will not respond to a physical or natural stimulus and reaches absolute refractoriness although electrical activit) remains which is usually indicated on the electroRodeo and Porter3 report that cardiogram. lack of oxygen is more important than lack of substrate in producing irreversible cardiac arrest. Anoxia has more effect on disrupting the permeability of the cell membrane than various ions and agents. This condition ma!. also doubtlessly result in some intrinsic chan;e.

Descriptions and explanations of this excitatory process are given almost entirely in terms of resistance, polarization, repolarization and others, which are referred to as electrical propIt seems that present erties of the cell membrane. knowledge of the metabolic process underlying excitability and the response to stimulation is The excitability of the heart still quite limited. It changes as neural does not remain constant. and humoral influences operate upon the heart as well as modifications during the cardiac cycle and during arrest. The role of cellular metabolism markedly influences excitability. Upon contraction there * Executive

M.D.

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Cardiac

It is probable that the intrinsic excitator) process, which initiates a contraction of heart muscle, act< in the same manner as do applied stimuli. Electrical monophasic stimulation of the anterior surface of the left ventricle4 produces a reduction in threshold voltage during moderate hypoxia until severe hypoxia has its onset which is promptl). followed by a rapidly rising threshold. Significant threshold changes occur at about 15 volumes per cent of oxygen. Belo\\ 6.4 volumes per cent of oxygen the threshold rises quickly and the conduction rate rapid]) In moderate hypoxia the function;:1 increases. capacity of the heart muscle is not impaired. Following stagnant anoxia for thirty to sixt) seconds, a point can be reached where there is a I jsolute refractoriness. The previous significant facts are of singular importance in considering cardiac resuscitatioll, particularly in the restoration or initiation of tllc heart Ijcat I,)- physical stimulation, such as pounding upon the chest, the application of an csternal pacemaker stimulus or the employment of an external defibrillating shock. After cessation of the coronary circulation the nlammalian heart appears to lose the proFert)of excitability \\-ithin thirty to sixty seconds and Some rapid functional deterioration follows. means of re\.crxillx this process and restoring cellular metabolism must be provided after this Perfusion of the coronaries will time limit. adequately restore its chemical metabolic energ) sources e\~n after many minutes of arrest. At present there are two practical means for tile accomplishment of this? (1) manual cardiac massage and (3) intra-arterial transfusion under pressure. DRAWBACKS

OF

CLOSED

CHEST

905

Resuscitation

RESUSCITATION

Observation of a great many hearts in our laboratory which have been deliberately arrcstcd by weak currents and thus placed in a state of ventricular fibrillation indicates that cvanosis can be detected bv the naked eye wiithin seven seconds after ’ its onset. After the lapse of thirty seconds the heart is markedl) blue: \,et the blood trapped in the main coronar! arteries remains bright red. Extunal Defibrillation: Accomplishment of external defibrillation in animals has been successful for many years. Nevertheless, it has not proved practical in restoring circulation to an arrested fibrillating heart after forty-five to fifty-five seconds’ duration of such an ar-

TABLE I Closrd Chest Defibrillation

rhvthmia. Failure occurs not from the inability to accomplish defibrillation of the heart. but from the inability to restore a blood pressure compatible with life. Electrocardiographic evidence is readily obtained which indicates that the heart has been defitjrillated (Table I). However, after one minute a pulse or a systemic blood pressure is seldom recordable; and upon promptly opening the thorax, one will find the heart in a state of standstill or asystole. In the meantime the heart is dying although scceptable complexes are recorded upon the electronic It is clear that electrical activity as monitor. recorded by the electrocardiograph is not necessarily related to the effecti\reness of thr However, most of US are reluctant circulation.6 to accept the fact that electrical activity can persist long after mechanical activit), has ceased. Experimental Closed Chest Resurcitation: \Yc have carried out many animal experiments based upon restarting arrested hearts which are intimately associated with the practical time limit of the excitability of cardiac muscle. These experiments are summarized in Tables I to IV. As indicated in Table I! somewhere around fifty seconds is the dividing line Ijetween 3atisfactor)- and unsatisfactory defibrillation by the external application of countershock in these experiments. This is in general agreement with Dow and Wiggers’ report’ in 1940. Beyond this point it was found that the heart could always be defibrillated as indicated by the electrocardiogram (Tables I and III), but there was seldom return of a satisfactory blood

Cardiac

996

Resuscitation mended for successful defibrillation that the myocardium be pink and \vell ox!-genated before applying a shock with internal electrodes (compare Tables II and III). Another problem in closed chest defibrillation is that of obtaining a current flow of sufficient density in all parts of the cardiac musculature. The anatomy of the organs of the thorax and mcdiastinum does not lend itself to constant dee;rres of tissue conduction and resistance.

TABLE 11 Electrodes

Applied

Electrodes

Applied

Directly

to Myocardium

TABLE m Directly

to Myocardium

1_..__.:__ D:i%‘iit”, _r

1 n_o_ 1Return

Return

/

xrdiogram

Circula-

before Masag?

tion

1p-l

I-70

t<>

120

70

I

0

)

70

70

TABLE IV External

Defibrillation

Dog

Arterial Perfusion after (sec.)

Duration of Fibrillation (sec.)

Experiments (no.)

and Supplemental

Methodq

-

-

0

Total Arrest 8fCirculation (sec.)

Return of Circulation

45 55 120 125

:

_ 45 55 65 65 75 85 90 105 120

-

-/

0 0 120 125 150 150 150 180 180

150 150

I

: +

1x0

i

f

In this situation it was pressure or pulse. found that rapid surgical exposure of the heart, followed by a short manual pumping of that readily and successfully restored the organ, heart beat, blood pressure and the circulation to a normal level. In other experiment9 (Table IV), after electrical defibrillation had been recorded and no return of systemic circulation occurred within 120 to 150 seconds, the administration of an intra-arterial infusion of saline and 1 :lO,OOO dilution of adrenalin under pressure of 300 mm. Hg resulted in a satisfactory return of systemic circulation without opening the chest. Mammalian hearts arrested for sixty to 120 seconds lose their excitability and ability to respond to a stimulus (Tables I and III). Supplemental methods for restoring the cellular metabolism must be employed. During the past twenty years we have empirically recom-

There is a complex relationship bettveen the cellular metabolic processes and the recovery of excitability which is initiated as soon as an adequate coronary circulation or perfusion is resumed or instituted. The heart as a muscular organ bvill remain viable as long as sixty to but in order for it one hundred minutes: to function as an hydrodynamic pump, it must have oxygenated blood circulated in its coronary system under an adequate pressure.* To prevent death before it occurs and to reverse clinical death after it occurs is perhaps the most important problem at this time in the twentieth century. As of today, resuscitation is still in its infancy. The unpleasant and forbidding task of opening the chest remains the surest means of reversing clinical death. Other reliable and acceptable methods are universally To initiate successfully a heart being sought. beat by a physical stimulus alone, this stimulus must be apphed or delivered before the period of excitation of the anoxic cardiac muscle cells has been terminated. This vital period is less than one minute.

1. HOSLER, R. hf. A Manual of Cardiac Resuscitation, 2nd ed. Springfield, 1958. Charles C Thomas. 2. CRANEFIELD, P. F. and HOFFMAN, B. F. Electrophysiology of cardiac cells. Physiol. Rrrm., 38: 41, 1958. 3. RODEO, S. F. and PORTER, B. V. The role of lack of su r,c. oxygen in irreversible cardiac arrest. Gynec. & Obsf., 109: 431, 1959. Effects of 4. HARRIS, A. S. and MATLOCK, W. P. An!. .J. Physiol., anoxemic anoxia on excitability.

150: 493, 1947. R. M. and WOLFE, K. Open chest versus closed chest cardiac resuscitation. Am. J. Surg., 97: 739,1959. 6. FOGELSON, I,. The electrocardiogram of the dying heart. J. Med. - biol., Moscow, 6: 3, 1928. 7. Dow, P. and WIGGERS, C. J. Limitations of myocardial rrcovery from fibrillation through countershock. Proc. Sac. Exper. Biol. G? Med., 45 : 355, 1940. 8. HOSLER, R. M. and WOLFE, K. Closed chest resuscitation. .4rch. SUY~., 79: 31, 1959.

5.

HOSLER,

* This is presurnrd THE

to be 40 mm. Hg as a minimum. AMERICAN

JOURNAL

OF

CARDIOLOGY