Howard C. Cohen

Diagnosis of cardiac tamponade by echocardiography: changes in mitral valve motion and ventricular dimensions, with special reference to paradoxical pulse.

The echocardiographic findings in three patients who presented with pericardial effusion and cardiac tamponade are described. Cyclic respiratory changes affected the diastolic movement of the anterior mitral leaflet, viz., during inspiration its anterior excursion decreased in amplitude and the E-F slope diminished. This inspiratory alteration in mitral valve motion was accompanied by an increase in right ventricular dimensions and a reciprocal decrease in left ventricular dimensions. Pericardial paracentesis confirmed the presence of effusion and relieved cardiac tamponade in all the patients. Repeat echocardiography, performed in two of the patients immediately after the pericardial tap, showed that the E-F slope had become steeper and that phasic respiratory variations in the diastolic motion of the anterior mitral leaflet were no longer present. The compatibility of our observations with the theories which endeavor to explain the mechanism of the paradoxical pulse in pericardial effusion with cardiac tamponade is discussed. We suggest that the abnormalities in anterior mitral leaflet motion defined by echocardiography constitute a useful addition to the study of patients with suspected cardiac tamponade resulting from pericardial effusion.

Intermittent Parasystole—Mechanism of Protection

Analysis of ten cases of intermittent ventricular parasystole suggested temporary loss of protection of the parasystolic focus resulting in discharge and “resetting” of the parasystole by sinus or other supraventricular beats. Parasystolic centers appear to be protected from supraventricular and other ventricular ectopic impulses early in their cycle by their refractory periods, and late in the cycle by diastolic depolarization. Between these two areas of protection is a period of “susceptibility” during which supraventricular beats can discharge the parasystolic focus. This phenomenon accounted for fixed coupling of the first parasystolic beat of a series to a preceding sinus beat. Under certain conditions all parasystolic beats may have such fixed coupling, a new and previously unconsidered mechanism for parasystole with fixed coupling.In one case of intermittent ventricular parasystole, the parasystole was shown to originate in the posterior fascicle of the left bundle branch on the basis of the shape of the standard electrocardiogram and by His bundle recordings. These parasystolic impulses produced a compensatory pause regardless of whether their discharge was manifest or concealed, and thus imitated a second degree (Type II) atrioventricular (A-V) block. This represents the first description of completely blocked atrial impulses resulting from concealed parasystolic beats arising within the ventricular conduction system.

Ventricular Tachycardia with Narrow QRS Complexes (Left Posterior Fascicular Tachycardia)

Ectopic atrial, A-V junctional, and ventricular tachycardias in man have been associated with digitalis medication. Recently it has become possible to distinguish various locations of pacemakers within the specialized conduction system of the ventricles on the basis of the form of the QRS complexes in the standard electrocardiogram. Tachycardias originating in the left bundle branch and documented by right, left, and His bundle recordings have been produced in animals given excessive digitalis. We have noted a similar tachycardia in a patient with ischemic heart disease receiving digitalis during hypokalemia. The QRS complexes were 0.10 sec in duration and by contour suggested an ectopic focus located in the posterior fascicle of the left bundle; His bundle recordings were consistent with this diagnosis. As the ectopic rhythm became synchronized with a slightly irregular sinus rhythm, bidirectional depolarization of the His bundle with fusion His potentials could be demonstrated.

Observations on second degree atrioventricular block, including new criteria for the differential diagnosis between type I and type II block☆

Abstract Since type I atrioventricular (A-V) block tends to be temporary and does not give rise to prolonged asystole, and type II A-V block tends to be progressive, ultimately leading to complete block and Adams-Stokes attacks, it is important to identify the type in each patient with acute or chronic second degree A-V block. The usual definition of these 2 types needs expansion. This new definition is given and new criteria are presented to permit differentiation of the 2 types of A-V block even in the presence of (1) incomplete A-V dissociation with single ventricular captures and (2) persistent 2:1 A-V block. The different roles and sites of concealed conduction in the 2 types of A-V block are defined. In type I, concealed conduction occurs within the region of block and depresses subsequent conduction, occasionally leading to blockage of consecutive atrial impulses. In type II, concealed conduction occurs down to the region of block, discharging subsidiary junctional pacemakers and thus preventing their escape. The frequent association of type II A-V block with bundle branch block and ventricular escapes with normal retrograde conduction (unidirectional block) is emphasized. Concealed retrograde conduction across the region of unidirectional block facilitates antegrade A-V transmission (early ventricular captures, supernormal phase of A-V conduction). The evidence is reviewed for placing the lesion causing type II A-V block below the A-V node; this is based on correlation of electrocardiographic findings, including His bundle recordings and anatomic data. Exceptions to the rule occur occasionally but should not lead to abandonment of the electrocardiographic classification of second degree A-V block into type I and type II because the distinction has proved of great value for clinical orientation.

The nature and type of arrhythmias in acute experimental hyperkalemia in the intact dog

Abstract Progressive A-V block was produced in the intact dog by rapid intravenous infusion of isotonic potassium chloride (KCl) solution. The site of the conduction disturbance was determined with electrode catheter recordings from the atria and region of the His bundle, and a simultaneous conventional ECG. First-degree and seconddegree A-V block and then complete A-V dissociation were produced, with the block above the bundle of His, the ventricles following a pacemaker originating in the bundle of His. During A-V dissociation, atrial potentials maintained their control rate. “Sinoventricular” conduction could not be produced under the conditions of the experiments. Further infusion of KCl produced conduction defects below the bundle of His with an irregular ventricular action. Unexpectedly, with the most rapid infusions of KCl, the experimental animals developed complete block below the site of the His bundle recording at a time when conduction above the junctional pacemaker was only partially blocked. Ventricular arrhythmias, including terminal tachycardias, are probably the consequence of depressed or failing propagation of the cardiac impulse.

Response of Resistant Ventricular Tachycardia to Bretylium: Relation to Site of Ectopic Focus and Location of Myocardial Disease

Ventricular tachycardias were determined to be of either right-or left-sided origin in 25 patients whose arrhythmias were life-threatening and resistant to lidocaine and other antiarrhythmic drugs. All five patients with right ventricular tachycardia responded well to bretylium and survived. Eleven of 20 patients with left ventricular tachycardia did not do well. Four did not respond to bretylium but survived, five had no response and died, and two responded but died when hypotension prevented continued treatment. Eight of these 11 had acute anterior myocardial infarction or ischemia. Of nine patients with left ventricular tachycardia who responded well to bretylium and survived, only two had anterior infarction, and none had anterior ischemia. Because bretylium was efficacious in all patients with right ventricular tachycardia or inferior myocardial infarction in this study, it seems warranted to investigate further the relationship between drug responsiveness and the site of ectopic impulse formation and the location of myocardial disease.

Echocardiography in mechanical alternans. With a note on the findings in discordant alternans within the left ventricle.

We describe the echocardiographic manifestations of mechanical alternation of left ventricular (LV) contraction during regular sinus rhythm. Chronic LV dilatation and failure existed in all our four cases. Alternation was observed with respect to the following echocardiographic variables: amplitude and rate of increase of amplitude of systolic excursions of the LV posterior wall and ventricular septum (VS); reciprocal changes in the duration of LV ejection and pre-ejection periods (on the aortic valve echo) such that the total duration of LV electromechanical systole remained constant; reciprocal changes in the duration of RV ejection and pre-ejection periods (on the pulmonic valve echo) such that the total duration of RV electromechanical systole remained constant; systolic anterior excursion of the aortic root as a whole; steepness of the mitral EF slope; septal and LV posterior wall diastolic position; and end-systolic LV diameter. In two patients, discordant alternans of the motion of the LV posterior wall and the VS was observed.

Tachycardia and bradycardia-dependent bundle branch block alternans: clinical observations.

Eleven patients with tachycardia-dependent, bradycardia dependent, or “pseudobradyeardia-dependent” bundle branch block (BBB) alternans were studied. This classification is based on the following criteria: 1) When alternans is initiated by a sudden acceleration in ventricular rate, or it appears with aberration of the second beat after a pause, the alternans is tachycardia-dependent and results from a 2: 1 bidirectional block in the affected bundle branch. 2) When alternans begins with the aberrant complex terminating a pause it is bradycardia-dependent; such an alternans results from alternating bundle branch cycle lengths and refractoriness, possibly produced by alternating transseptal retrograde penetration of the affected bundle branch. 3) In cases referred to as “pseudobradycardia dependent BBB” alternans, a change from alternans to persistent BBB occurs as the cycle lengthens; however, the disappearance of BBB with further increase of the cycle length proves the tachycardia-dependence of the conduction defect.

Flutter of left ventricular structures in patients with aortic regurgitation, with special reference to patients with associated mitral stenosis

Echocardiography was performed in 45 patients with aortic regurgitation. Forty showed a high frequency diastolic flutter of the mitral valve, which was holodiastolic in all but the patients with associated mitral stenosis. Of four patients with coexisting mitral stenosis, mitral flutter was absent in two; in the other two, in atrial fibrillation, mitral flutter occurred, but only during a fixed interval after mitral valve opening, irrespective of cycle length. A fine flutter of similar frequency was observed on the left ventricular aspect of the ventricular septum in 12 patients. In six of these it was of slight degree and restricted to early diastole and the high septum; in four others (three of whom had associated mitral stenosis), the septal flutter was more marked, holodiastolic, and present over all parts of the septum scanned; in two, it was holodiastolic over the high septum but early diastolic at lower septal levels. Aortography performed in 19 patients showed that septal flutter was present in seven of 12 patients in whom the regurgitant aortic jet was directed forward to the ventricular septum, whereas in the other seven patients with no septal flutter, the jet was directed away from the septum. Septal flutter is useful as an echocardiographic sign of aortic regurgitation, especially in the presence of mitral stenosis when mitral flutter may be absent or exceeded by septal flutter in both amplitude and duration, and when the mitral valve has been replaced by a prosthetic valve. Vibration of the septum appears to be attributable to the regurgitant aortic jet impinging on it and may contribute to the production and radiation of the characteristic diastolic murmur of aortic regurgitation.

Concealed intraventricular conduction in the His bundle electrogram.

Multiple areas of concealed intraventricular conduction are deduced on the basis of aftereffects observed in His bundle recordings. Electrocardiograms and His bundle recordings are presented from two patients with unstable bilateral bundle branch block, the instability of which depended on the interval at which ventricular depolarization was initiated by sinus or paced impulses. This circumstance allows postulation of 1) concealed transseptal retrograde penetration of the left bundle branch system; 2) concealed transseptal retrograde penetration of the right bundle branch system; 3) alternate beat Wenckebach phenomenon with two areas of block in the bundle branch system with concealed penetration of the proximal area; 4) concealed re-entry in the right bundle branch system during an H-V Wenckebach cycle with resetting of the sequence of 2:1 H-V block and return of the re-entry wave to the A-V node causing subsequent A-H block; 5) proximal 2:1 block and distal Wenckebach block producing only two consecutively blocked beats;and 6) infrahisian Wenckebach block with changes both in A-V conduction andQRS contour.