Clinical, electrophysiologic and hemodynamic profile of patients resuscitated from prehospital cardiac arrest.
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Biomedical subjects
Publications and source records attributed to S M Mallon.
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The various patterns resulting from stimulation through the catheter electrodes recording His bundle activity were evaluated in 30 patients using intracardiac electrograms from the right ventricular apex (RVA), posterosuperior wall of the left ventricle (LV), high right atrium (HRA) and left atrium (LA) in the vicinity of the coronary sinus. His bundle pacing was characterized by a QRS complex and stimulus (St)-V, St-RVA and St-LV intervals that equated the QRS configuration, H-V, H-RVA and H-LV intervals of sinus beats. Right septal pacing produced pattern of "complete" left bundle branch block (with normal electrical axis) associated with St-V intervals of 0 msec, and St-RVA and St-LV intervals of different duration from that of the H-RVA and H-LV intervals recorded during sinus rhythm. Fusion beats resulting from simultaneous activation of His bundle and right septal muscle were characterized by St-V intervals of 0 msec and St-RVA or St-LV intervals of similar duration to that of the H-RVA or H-LV intervals of sinus beats. Fusion QRS configuration depended on the type of ventricular complex present during sinus rhythm. Analysis of the retrograde atrial activation intervals permitted differentiation among impulse initiation at the low right atrium, His bundle or right septal muscle. Simultaneous recording of multiple atrial and ventricular electrograms has enhanced understanding of the complex patterns observed during attempted His bundle pacing in man.
Intra-atrial Wenckebach patterns of stimulus-to-response intervals coexisting with distal, A-V nodal, and His-Purkinje, blocks occurred in eight patients during high right atrial stimulation at rapid rates. In two patients with 2:1 St-H block and in two patients with 4:1 St-V block, an increase in the degree of block occurred when the proximal intra-atrial Wenckebach cycle was completed with the stimulus which otherwise would have been propagated to the distal levels. However, the degree of block did not increase when the intra-atrial Wenckebach terminated in distally blocked stimuli. In one patient progression of 4:1 into 5:1 St-V block was due to the association of intra-atrial Wenckebach with alternating 2:1 block at the A-V nodal, and His-Purkinje, levels. Contrasting with most reports dealing with the mechanisms of alternating Wenckebach in a single structure, this study permitted the determination of the boundaries between proximal and more distal levels. It also showed that alternating Wenckebach cycles (of St-H intervals) ending with two consecutively blocked stimuli could result from the association of proximal intra-atrial Wenckebach with distal, A-V nodal Wenckebach, or abortive AW, cycles. The electrophysiology of documented two, or three, level block in different structures has validated previously made assumptions regarding multilevel block in a single structure.
Ambulatory rhythm monitoring and chronic arrhythmia management were studied in 16 patients resuscitated from prehospital cardiac arrest. Asymptomatic complex ventricular arrhythmias (ACVA) occurred in 12 patients (75%) entering long-term follow-up during the first 12 months (average follow-up, 13.25 months). The patients' therapy consisted of a dose-adjusted, membrane-active antiarrhythmic drug regimen monitored by blood levels. While there has been little change in the frequency of ACVAs despite carefully controlled antiarrhythmic management, only one death has occurred during 212 patient-months of postarrest follow-up, a 6% one-year mortality. This compares favorably to our previous experience in survivors of prehospital cardiac arrest not receiving a controlled antiarrhythmic program. Despite the failure to suppress ACVAs, the drug-monitored population is showing a trend toward a decreased frequency of recurrent cardiac arrest.
Pseudo bundle branch block, a previously unreported arrhythmia produced by concealed premature impulses arising in the bundle branches, was seen in two patients with sick sinus node syndrome. Although concealed conduction was not apparent in either the surface or intracardiac leads, the latter were essential in localizing the site of manifest impulse formation. Patient 1, with left bundle branch extrasystoles, had pseudo bundle branch block and pseudo atrioventricular block that depended on the timing and extent of concealment of premature depolarization. Because of the coexisting sinus bradycardia in this patient, electrical stimulation and the recording of the right ventricular apical electrograms gave additional information that helped corroborate the postulated mechanisms. Patient 2 had right bundle branch extrasystoles with sinus beats that showed a right bundle branch block pattern possibly caused by pseudo bundle branch block. In this case the possibility that both the automaticity and the conduction disturbance had a mechanical origin could not be excluded.
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His bundle electrocardiography was helpful in the diagnosis of impulse formation in the right bundle branch. Ten patients with narrow QRS complexes had ectopic beats with an "incomplete" left bundle branch pattern and almost simultaneous activation of His bundle and ventricles. Both QRS morphology and H- - V intervals depended on the more proximal or distal location of the ectopic focus. In four patients with "complete" right bundle branch block the morphology of ectopic ventricular complexes and H- - V intervals also depeneded on the presence or absence of retrograde block and differential degrees of forward and/or retrograde conduction delays. Nine patients with "complete" right bundle branch block and four with "complete" left bundle branch block had premature beats which could have originated in the proximal right bundle branch, proximal left bundle branch, or distal His bundle. In one patient with "complete" left bundle branch block, "concealed" His bundle depolarizations (probably originating in an ectopic focus located in the right bundle branch) produced pseudo Type II (Mobitz) A-V block. Although lidocaine appeared to have been more effective in patients with bundle branch block than in those with narrow QRS complexes, further studies are necessary to corroborate this impression.
His bundle recordings were performed in 2 patients in whom AV nodal bypass tracts coexisted with intermittent AV conduction disturbances occurring below the site from which the His bundle deflection was recorded. Case 1 had: (a) tachycardia dependent right bundle-branch block, (b) persistent HV prolongation, and (c) bradycardia dependent AV block. Case 2 showed: (a) intra-atrial conduction delay, (b) tachcardia dependent left bundle-branch block with HV prolongation, (c) bradycardia dependent HV conduction disturbance, (d) tachycardia-bradycardia syndrome of an unusual type; the latter presumably resulted, during atrial flutter, from the alternation of rapid AH conduction through the bypass tract with intermittent (complete) distal His bundle block or bilateral bundle-branch block.
Ventricular ectopic activity occurred only after premature atrial beats in a patient with an acute inferior wall myocardial infarction. The ventricular ectopic activity occurred only when the coupling interval between the premature atrial beats and preceding sinus beat was less than or equal to 0-44 s. The sinus cycle length, however, appeared to influence the form of expression of ventricular ectopic activity independent of coupling intervals, with single premature ventricular contractions occurring at cycle lengths greater than or equal to 0-72 s, couplets at cycle lengths of 0-68 to 0-71 s, and ventricular tachycardia at cycle lengths less than or equal to 0-67 s.
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A 47-year-old man experienced ventricular fibrillation three times during a 3 1/2-year period. Each episode was preceded by an auditory aura, and no ventricular irritability was identified between episodes. The results of coronary arteriographic, hemodynamic, and intracardiac electrophysiologic studies were all normal. Hypokalemia and abnormal oxyhemoglobin dissociation were present. The possible relationships of these unusual features to the patient's disturbances in rhythm are discussed.
His bundle recordings and premature atrial stimulation from coronary sinus, mid-right atrium and high-right atrium were performed in a patient with repetitive supraventricular tachycardias. Regardless of the paced site, there was a range of coupling intervals during which testing stimuli elicited short runs of premature beats. The corresponding P waves were positive in leads I, II and III and had a high-to-low right atrial activation sequence. Their morphology was similar to that of sinus beats. However, sustained tachycardia occurred only when pacing was performed from the coronary sinus. Therefore, it is postulated that the site of stimulation might be important in the genesis and (perhaps) perpetuation of this arrhythmia by changing the site and (or) mode of entry into the area where this type of tachycardia occurs. Though sinus node reentry was the most likely mechanism, it could not be determined whether the circuit involved the sinus node per se or the so called perinodal fibers.
In a patient with idiopathic hypertrophic subaortic stenosis, propagated responses followed testing stimuli (St2) delivered within the wide QRS complexes elicited by driving stimuli (St1). This phenomenon was not seen at all St1-St2 which produced the minimal V1-V2 interval. It appeared at St1-St2 intervals which resulted in the largest difference between St1-St2 intervals, probably because of the marked asymmetry of propagation occurring very early in the cycle. More studies are required to determine whether this was due to a shift of the vulnerable period toward early systole (suigenesis to idiopathic hypertrophic subaortic stenosis) or to more complex types of intraventricular reentry. In other clinical conditions a similar mechanism could explain the multiple responses produced by pacemaker stimuli falling at the end of ventricular depolarization and also by "properly synchronized' low intensity transthoracic electrical discharges.
A mobile dual-probe system has been developed for the rapid bedside measurement of left ventricular ejection fraction (LVEF) from the beat-to-beat count rate variations that occur during the transit of a single radionuclide bolus through the left ventricle (LV). Cardiac output, pulmonary blood volume, and left ventricular end-diastolic volume can also be calculated. The dual-probe system incorporates a central collimated probe for monitoring activity in the LV surrounded by an annular detector collimated in such a manner as to provide simultaneous real-time monitoring of the LV background activity. The LVEFs obtained from this system correlated well with LVEFs derived from conventional single-plane contrast angiography (r=0.90) in a series of 33 patients with coronary artery disease. Positioning the dual probe over the midpoint of the LV is accomplished with standard M-mode ultrasound. Since the method is noninvasive and sensitive to volume changes in the LV, the dual probe is particularly useful for monitoring seriously ill patients as well as those with segmental wall-motion abnormalities.
In the course of the evaluation of five patients with left atrial myxoma, it was noted that the movement of the myxoma was related to specific changes in left atrial hemodynamics. Prolapsing tumors, Type I, move from the left ventricle to the left atrium in early systole and from the left atrium to the left ventricle in early diastole, thereby causing prominent c and v waves accompanied by a rapid y descent. Nonprolapsing tumors, Type II, remain in the left atrium during the entire cardiac cycle, impeding flow across the mitral valve. In these latter cases, the y descent is slow and indistinguishable from that caused by mitral valvular stenosis. The cineangiocardiograms and echocardiograms corroborate these two types of hemodynamic observations. The particular value of direct echocardiographic examination of the left atrium prior to cardiac catheterization was evident in two of the three patients with nonprolapsing tumors. Since the hemodynamic pattern of nonprolapsing left atrial myxoma resembles that of mitral valvular stenosis, it is stressed that echocardiography should have an important place in precatheterization assessment of patients with mitral valve disease. If left atrial myxoma is suspected clinically or on the basis of echocardiographic findings, regardless of the pressure curve contours, transseptal cardiac catheterization should be avoided and the left atrium visualized by pulmonary angiography levophase.
Thirty patients, 20 males and 10 females, having a 50% or greater obstruction of the left main coronary artery, were evaluated. Their ages ranged from 40 to 71 years (mean 53.8 years). All patients had angina pectoris, the duration of which varied from 2 months to 20 years (mean 5.4 years). Twenty-four patients (80%) had accelerated angina pectoris; 17 (56.7%) had prior myocardial infarction, and 27 (90%) were found to have coexisting three-vessel disease and abnormal left ventricular contraction. There were no deaths or serious arrhythmias related to cardiac catheterization procedures. In the 11 unoperated patients 5 (45%) died within the first year of follow-up; however, all except one death occurred in patients with diffuse distal coronary artery disease technically unsuitable for surgery. Among the six survivors four were considered surgical candidates. These four patients have continued to have symptoms of angina pectoris with a mean follow-up period of 17.5 months (16 to 20 months). In the 19 patients who underwent aortocoronary saphenous vein bypass grafting, there was one immediate postoperative death (surgical mortality 5.3%) and one late death. The 17 survivors in the surgical group have a mean follow-up period of 17.3 months (8 to 31 months); 13 of them have clinically improved with 6 being totally free of angina pectoris. Thus, mortality is extremely high in those with poor distal vasculature technically unsuitable for surgery, but mortality is relatively low in patients who have technically bypassable lesions whether treated surgically or medically. Although saphenous vein bypass grafting appears to be more effective in providing clinical improvement, asymptomatic left main coronary obstruction may not justify surgical therapy.
Coronary angiography and hemodynamic studies were performed in a group of 13 patients who had been successfully resuscitated from unexpected ventricular fibrillation, had had angina pectoris prior to the cardiac arrest, and who had not had an acute myocardial infarction in the periarrest period. Eleven of the 13 had one or more coronary artery lesions which were amenable to surgical intervention, and eight of the 11 accepted surgery. Left ventricular end-diastolic pressure was elevated in most patients, while cardiac index and ejection fraction were depressed. Bypassable lesions were found in the main left coronary artery in one patient, and the proximal left anterior descending artery in two. Both of these patients had disease elsewhere. The remaining five patients had diffuse three-vessel disease. The eight patients have survived for periods ranging from 8 to 32 months (average = 24 months). This contrasts to an overall 1-year mortality of approximately 30% in survivors of hospitalization after unexpected ventricular fibrillation.