Rolf M. Gunnar

Cardiac Conduction in Patients with Symptomatic Sinus Node Disease

Cardiac conduction was investigated at the time of pacemaker insertion in 15 patients with symptomatic sinus node disease. Techniques included recording of His bundle potentials, atrial pacing at various heart rates, and atropine administration. Atrioventricular (AV) conduction was impaired in eight patients who manifested one or more of the following: P-R prolongation, P-H prolongation, and development of second degree AV block with atrial pacing at heart rates below 130 beats/min. Five patients had intraventricular conduction defects diagnosed electrocardiographically; none of these had H-Q prolongation. One of these five, with left bundle-branch block, subsequently developed complete heart block and had a calcific lesion involving the His bundle. Depression of cardiac automaticity was noted in four patients, with asystolic periods greater than 2 sec after sudden cessation of atrial pacing at rates of 100-160 beats/min. Responses to 1 mg of intravenous atropine were varied, but no patient developed sinus rates greater than 90 beats/min, suggesting the presence of primary sinus node dysfunction.In conclusion, abnormalities of conduction and automaticity in specialized tissue in addition to the sinus node are common in patients with symptomatic sinus node disease. These abnormalities should be recognized when present, so that the ideal site for permanent pacing may be chosen.

Paroxysmal Ventricular Fibrillation in Two Patients with Hypomagnesemia Treatment by Transvenous Pacing

Paroxysmal ventricular fibrillation unassociated with heart block occurred in two patients with hypomagnesemia. In neither patient were other causes of the arrhythmia apparent. Temporary transvenous pacing successfully suppressed the episodes after drug therapy failed. Prolongation of the Q-T interval was a prominent electrocardiographic feature in both patients and is postulated to have resulted from a loss of intracellular potassium secondary to hypomagnesemia.

Acute Hemodynamic Effects of Dopamine in Patients with Shock

The hemodynamic effects of dopamine were studied in 62 patients with clinical shock. In 36 patients with infection dopamine increased mean arterial pressure (MAP) 30%, and cardiac output (CO) 37%. Urine flow (UF) increased from 0.5 ml/min to 1.6 ml/min. Norepinephrine (NE) in 26 patients resulted in a higher MAP, lower CO, and similar UF. Isoproterenol (Isp) in 19 patients resulted in a lower MAP, higher CO, and a significantly lower UF. In 13 patients with cardiogenic shock dopamine increased MAP 6%, and CO 40%. UF increased from 0.6 ml/min to 1.1 ml/min. NE in eight patients resulted in a lower CO than during dopamine infusion, and Isp in five patients resulted in a higher CO. Dopamine improves MAP pressure, CO, and UF when shock is due to infection and is superior to Isp which does not increase perfusion pressure to adequate levels and does not improve UF. In patients with cardiogenic shock who have reduced CO and increased systemic vascular resistance, perfusion pressure tended to be adequate, and improved CO occurred with dopamine and Isp but not with NE. Although Isp increased CO more than dopamine, differences in regional perfusion are important in selection of the best inotropic agent and in most patients make dopamine the preferred agent.

Pseudo A-V Block Secondary to Premature Nonpropagated His Bundle Depolarizations Documentation by His Bundle Electrocardiography

His and right bundle electrograms were recorded in a patient with unexplained P-R prolongations and periods suggestive of both type I and II second degree A-V block. The mechanism of these conduction disturbances was shown to be due to multiple nonpropagated premature His bundle depolarizations (H′) which produced their effects on the subsequent cycle by virtue of concealed conduction into the A-V junction. The effects on A-V conduction were related to the time of occurrence of H′ in relation to the subsequent P wave: If H′-P was short, a more profound conduction defect occurred. H′ was generally undetectable on the ECG because of both antegrade and retrograde block, but a few propagated H′ produced typical junctional premature contractions. Propagation of H′ depended on a short preceding cycle length and a late occurrence of H′. The site of origin of H′ appeared to be in the bundle of His. The mechanism of production of H′ did not appear to be either reentry or parasystole.The term pseudo A-V block is used to describe the arrhythmia because there was no evidence of an intrinsic abnormality of A-V conduction. It is expected that other unusual electrocardiographic phenomena may be explainable with intracardiac recordings of specialized conduction tissue potentials.

Relationship of Pulmonary Artery to Left Ventricular Diastolic Pressures in Acute Myocardial Infarction

We have measured pulmonary artery (PA) and left ventricular diastolic pressures (LVDP) in patients with acute myocardial infarction to establish the relationships of PA pressure to LVDP. Paired determinations for the various parameters showed (mean difference in mm Hg): left ventricular end-diastolic pressure (LVEDP)-LVDP pre-a + 7.9, P < 0.001; LVEDP-mean PA wedge + 6.0, P < 0.001; mean PA wedge-LVDP pre-a, + 0.8, P > 0.2; PA end-diastolic pressure (PAEDP)-mean PA wedge (in all patients) +3.3, P < 0.001; PAEDP-mean PA wedge (patients with pulmonary vascular resistance ≦2 units) +1.3, P < 0.1; LVEDP-PAEDP +4.7, P < 0.001; and LVEDP-mean PA −2.0, P < 0.02. The relationship of LVEDP to mean PA wedge was: LVEDP (y) = 1.12 mean PA wedge (x) +4.69; Sy.x = 3.42; r = 0.92.After acute myocardial infarction, PA pressures did not accurately reflect LVEDP because atrial contraction made a large contribution to ventricular filling pressure. In addition, PAEDPs were not the same as mean PA wedge pressures because of some increase of pulmonary vascular resistance in many patients. Thus, PA pressures only provided reliable information about the level of pulmonary venous pressure. LVDP pre-a correlated well with mean PA wedge pressure, and therefore measurement of LVDP (pre-a and EDP) yielded information not only about pulmonary edema, but also about LV performance.

Site of Heart Block in Acute Myocardial Infarction

Bundle of His electrograms were recorded in eight patients with acute myocardial infarction and heart block. Three patients with diaphragmatic myocardial infarction (DMI) and one with subendocardial infarction were characterized by slowing or block above the bundle of His and A-V junctional escape rhythms during periods of advanced or complete block. An additional patient with DMI had block in the His bundle itself. Intraventricular conduction in the above patients was characterized by normal H-Q intervals (35 to 60 msec) and absence of widened QRS. In contrast, three patients with anterior infarction (AMI) manifested complete block below the bundle of His and idioventricular escape. P-H intervals were normal (80 to 140 msec) and A-V conduction was considered unaffected. Our electrophysiologic observations coupled with previous clinical, anatomic, and pathologic findings suggest that the heart block in DMI is usually due to an ischemic lesion of the A-V node, while heart block in AMI is due to necrosis involving both bundle branches.

Transient and Persistent Atrial Standstill with His Bundle Lesions Electrophysiologic and Pathologic Correlations

Electrophysiologic studies, including His bundle recording and atrial pacing (AP), were performed in one patient with transient (TAS) and another with persistent atrial standstill (PAS). Both subsequently expired, and postmortem examinations with serial sections of the conduction system were obtained. The patient with TAS had left bundle-branch (LBB) block, a P-H interval of 140 msec (normal, 80-140 msec), an H-Q of 40 msec (normal, 35-55 msec), and an AP threshold of 1.2 ma. Postmortem examination revealed total left circumflex occlusion proximal to the sinoatrial (SA) nodal artery takeoff, SA nodal arteriolosclerosis without infarction, and left-sided cardiac skeletal sclerosis (LSCSS) disrupting the penetrating portion of the His bundle and the LBB. Intracardiac recordings in the patient with PAS showed absent atrial activity and an H-Q of 60 msec. The atria were inexcitable with AP up to 15 ma at multiple sites. Postmortem examination revealed a previously undescribed atrial disease characterized by arteriolosclerosis, fibroelastosis, fatty infiltration, and vacuolar degeneration of muscle cells, with only moderate SA and A-V nodal involvement. LSCSS was present, disrupting the branching portion of the His bundle. Thus, TAS reflected SA nodal ischemia without infarction; PAS reflected a new atrial degenerative disease; H-Q was normal with a lesion in the penetrating portion of the His bundle and was prolonged with a similar lesion in the branching portion.

Electrophysiological Significance of First Degree Atrioventricular Block with Intraventricular Conduction Disturbance

His bundle electrograms (H) were recorded in 27 patients with PR prolongation and intraventricular conduction disturbances. The PR interval was subdivided into P-H (normal 80-140 msec), a measure of atrioventricular (A-V) conduction, and H-Q (normal 35-55 msec), a measure of intraventricular conduction. In 12 patients with left bundle-branch block (LBBB), P-H varied from 115-410 msec (mean 173 msec), and was prolonged in eight patients. H-Q varied from 39-125 msec (mean 80 msec), and was prolonged in 10 patients. In eight patients with right bundle-branch block (RBBB), P-H varied from 146-450 msec (mean 206 msec), and was prolonged in all patients. H-Q ranged from 41-65 msec (mean 51 msec), and was slightly prolonged in three patients, all of whom had, in addition, evidence of left anterior or posterior hemiblock. Seven patients with lesser intraventricular conduction defects all had prolonged P-H intervals, with normal H-Q intervals. With atrial pacing at increased heart rates, block proximal to H occurred in all groups. Three patients with LBBB developed block distal to H with atrial pacing, and one additional patient with LBBB and one patient with RBBB and left posterior hemiblock developed block distal to H following atropine administration.In conclusion, most patients with PR prolongation and intraventricular conduction defects had prolongation of P-H, suggesting A-V nodal disease. In addition, the patients with LBBB usually had significant H-Q prolongation, suggesting bilateral bundle-branch disease. In the group with RBBB, H-Q prolongation was less common and less marked, and, when present, occurred in patients with evidence of left anterior or posterior hemiblock.

Correlation of Vectorcardiographic Criteria for Myocardial Infarction with Autopsy Findings

One hundred eight patients who had had vectorcardiograms and electrocardiograms recorded were followed to autopsy, and their hearts were carefully studied postmortem. Vectorcardiographic criteria previously proposed using the Frank corrected lead system were tested against the anatomic findings. These criteria correctly predicted the presence of infarction in 49 (92%) of 53 hearts and correctly localized the infarct in 39 (74%). In four hearts (8%) infarction could not be identified. In 18 (32%) of 55 hearts in which infarcts were not present, these criteria falsely indicated infarction. The reasons for the false positive predictions are discussed. The criteria tested will prove useful in the diagnoses and localizations of myocardial infarcts when the pitfalls of deformities of the vectorcardiogram produced by ventricular hypertrophy and bundle-branch block are avoided.

Bundle Branch and Ventricular Activation in Man A Study Using Catheter Recordings of Left and Right Bundle Branch Potentials

His (H), right bundle branch (RB), and left bundle branch (LB) potentials were recorded by electrode catheters passed into the left and right ventricles in seven patients without conduction defects. In another three patients, H and LB were recorded. Initial ventricular activation was considered to coincide with the onset of the QRS (Q). The following intervals were measured in milliseconds: H-Q, LB-Q, RB-Q, H-LB, H-RB, and LB-RB. The average and range of these was as follows: H-Q 46 (39-54), LB-Q 27 (24-30), RB-Q 25 (20-27), H-LB 20 (14-28), H-RB 21 (15-29), and LB-RB 2 (1-10). LB-RB was 3 msec or less in six of seven patients. Coupled atrial pacing produced delays in H-RB without effect on H-LB and LB-Q. The production of incomplete and complete right bundle branch block was related to increase in the LB-RB interval. One patient developed left bundle branch block (LBBB) during coupled pacing with delay of LB while RB-Q remained unchanged. H-Q intervals were measured in three additional patients with rate related LBBB during both control and block. Prolongation of H-Q was less than 3 msec during LBBB. It is concluded that the proximal left and right bundle branches are usually activated simultaneously in man, and that block of either bundle without contralateral bundle delay does not significantly delay the onset of ventricular activation.