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Biomedical subjects

J A Shaver

Publications and source records attributed to J A Shaver.

At least 55 records · Page 3Linked to original sources
PubMed1976

Undesirable cardiac arrhythmias associated with rate hysteresis pacemakers.

The introduction of the ventricular inhibited pulse generator with the feature of rate hysteresis has been associated with a variety of rhythm disturbances, some causing serious concern. This pulse generator has two different pacing rates: (1) the automatic rate, which is the interval between two successive paced beats (usually 860 msec or 70/min), and (2) the hysteresis interval, which results in a 1,000 msec delay between a sensed cardiac contraction and the next pacemaker discharge. The hysteresis interval after a sensed signal may result in long pauses that may predispose to the development of serious cardiac arrhythmias. Two examples of this type of complication were recently observed. One patient had bigeminal rhythm with mechanically ineffective cardiac contractions and an effective cardiac rate of 35/min; he experienced dyspnea and weakness during these prolonged episodes. Another patient had repeated episodes of ventricular fibrillation. The cardiac arrhythmias were not controlled by antiarrhythmic agents, and both patients required replacement of the pulse generator. The proposed advantages of pulse generator hysteresis are (1) prolongation of battery life, and (2) maintenance of effective atrial transport; these advantages may be outweighed by undesirable cardiac arrhythmias that may be associated with this mode of pacemaker function. Rate hysteresis cardiac pacemakers should be reserved for patients having predominantly sinus rhythm without ventricular irritability. In patients with frequent ectopic ventricular activity, atrial fibrillation or high degree atrioventricular block, the rate hysteresis pacemaker offers no advantage over the conventional demand pacemaker. For patients with frequent ectopic ventricular activity not easily controlled by antiarrhythmic agents, consideration should be given to the use of a permanent demand pacemaker with external rate control, which may provide greater flexibility in arrhythmia management.

Aged↗
PubMed1976

Surgical treatment of acute aortic regurgitation in infective endocarditis.

During a six-year period 15 consecutive patients with isolated aortic regurgitation due to infective endocarditis were encountered. None had prior significant aortic valve disease. Elective valve replacement was performed in 13 patients; emergency operation was needed in only 1 patient because of intractable pulmonary edema. One patient died suddenly from acute heart block while undergoing medical treatment. Preoperative cardiac catheterization studies in 10 of the 14 patients revealed gross elevations of left ventricular end-diastolic pressure, pulmonary hypertension, depressed cardiac output, and 3 to 4+ aortic regurgitation. There was 1 early and 1 late postoperative death, both due to systemic embolism, yielding an overall surgical mortality of 14%. After a mean follow-up of 18 months, 10 of the 11 patients are in New York Heart Association Functional Class I. Most patients with acute aortic regurgitation secondary to infective endocarditis have clinically observable congestive heart failure and will eventually require valve replacement. If congestive heart failure can be stabilized by a medical regimen, a course of antibiotic therapy can be administered and elective valve replacement can be performed. The time taken for preoperative antibiotic treatment is not associated with irreversible myocardial damage sufficient to influence the results of operation.

Adolescent↗
PubMed1976

Mobitz II atrioventricular block due to infra-Hisian block and bundle branch extrasystoles.

An asymptomatic elderly male presented with complete right bundle branch block, left anterior fascicular block and Mobitz Type II second degree atrioventricular block. In addition, he was noted to have ventricular premature systoles. Electrophysiologic studies demonstrated two apparently different mechanisms for the second degree A-V block--infra-Hisian block and A-V block due to bundle branch extrasystoles arising in the affected right bundle branch. Concealed conduction of the bundle branch extrasystoles as the proximate cause of infra-Hisian block could not be excluded. However, both forms of A-V block were evidently dependent upon significant distal conduction system disease; this consideration was felt to warrant permanent pacemaker implantation.

Aged↗
PubMed1976

Sound pressure correlates of the Austin Flint murmur. An intracardiac sound study.

Mitral valve motion and pressure correlates of the Austin Flint murmur (AFM) were investigated in nine patients with aortic regurgitation using high fidelity catheter tip micromanometers and the mitral valve echocardiogram (MVE). External phonocardiography demonstrated a mid-diastolic murmur (MDM) in eight subjects and a presystolic murmur (PSM) in five. Maximum intensity of both AFM components was found in the left ventricular (LV) inflow tract; the murmur was not recordable in the left atrium (LA). In two patients, an apparent AFM was recorded in the intracardiac phonocardiogram when absent externally. Only one subject had a significant late diastolic "reversed" or LV to LA gradient; in this patient, presystolic mitral regurgitation was shown angiographically but no PSM was present and MVE revealed absence of atriogenic mitral valve re-opening. In two subjects, a PSM disappeared from the external phono when a "reversed" gradient occurred during the diastolic pause following a ventricular premature systole; this LV to LA gradient was associated with diastolic mitral regurgitation recordable in the left atrial phono. In two patients, LV inflow phono showed the MDM to begin 80-120 msec after the aortic second sound and during the D to E phase of the MVE. The rate of early diastolic mitral valve closure in patients (152 +/- 24 mm/sec) was not significantly different from 13 normals (232 +/- 10 mm/sec). With regard to the genesis of the AFM, the present study concludes: 1) diastolic mitral regurgitation plays no role, and 2) antegrade mitral valve flow is required but simultaneous retrograde aortic flow may also be necessary.

Aortic Valve Insufficiency↗
PubMed1976

The contribution of tricuspid valve closure to the first heart sound. An intracardiac micromanometer study.

The sound-pressure correlates of the second high frequency component of a split first heart sound (S1) were investigated in 27 patients. An external phonocardiogram was recorded with high fidelity sound and pressure from the left and right atria in 21 patients, from the pulmonary artery in 14 of these, and from the central aorta in 11. In the remaining six patients, high fidelity recordings from the central aorta and right-sided chambers were obtained with an external phonocardiogram. The external component of S1 that coincided with a left atrial C wave and "internal sound" was defined as M1. In those cases where the left atrial pressure was not recorded, this component could be identified by a low frequency transient in the central aortic pressure trace. The other external high frequency component of S1 that was synchronous with a separate right atrial C wave and "internal sound" was defined as T1; with two exceptions, M1 preceded T1. The two exceptions which caused reversal of this order, so that T1 preceded M1, were due to chronic left bundle branch block and mitral stenosis. In both cases, T1 was shown to be distinctly separated from the upstroke of pressure rise in the central aorta. This finding was also demonstrated in three cases of right bundle branch block and one case with aortic valvular disease. The usual asynchrony of ventricular contraction was altered by induction of ventricular premature systoles; the separation of externally identifiable M1 and T1 components and their internal markers was predictably altered by this maneuver. The occurrence of T1 was variable in relation to the upstroke of the pulmonary artery pressure, which suggests that it is not related to pulmonic ejection. It is concluded that micromanometrically recorded right and left atrial C waves can serve as markers for externally recordable M1 and T1 components of the first heart sound. In addition, T1 is frequently an externally recordable and audible event.

Adolescent↗
PubMed1976

Alterations of right ventricular systolic time intervals by chronic pressure and volume overloading.

Right ventricular (RV) systolic time intervals and hemodynamic parameters were determined by micromanometric techniques in 13 subjects with normal right ventricles (NRV). These data were compared to those of 16 patients with pulmonary hypertension (PH) or predominant pressure overloading and 13 individuals with uncomplicated secundum atrial septal defects (ASD) or predominant volume overloading. In PH, the QP2 interval tends to remain within the normal range due to reciprocal changes in isovolumic contraction (ICT) and ejection (RVET) times. Elevations of pulmonary artery diastolic pressure are associated with increases in the mean rate of isovolumic pressure rise (MRIPR) (r = 0.84), but the latter change does not fully compensate for the widened ventriculoarterial diastolic pressure difference and ICT becomes prolonged (P less than 0.001). Factors other than stroke index depression which may contribute to the decreased duration of RVET (P less than 0.001) include tricuspid regurgitation and elevation of pulmonary vascular impedance. In ASD, QP2 is significantly prolonged (P less than 0.025) due to a significant increase in RVET (P less than 0.005). In contrast to NRV, a linear correlation of RVET and stroke index was not present, which suggested an alteration of ejection dynamics in this group. Despite a high incidence of complete or incomplete right bundle branch block the interval from QRS onset to rapid RV pressure upstroke was not prolonged. This is most probably the result of peripheral bundle branch block of genesis of the QRS pattern by right ventricular hypertrophy.

Adolescent↗
PubMed1976

Coronary arteritis in systemic lupus erythematosus.

Acute myocardial infarction in systemic lupus erythematosus may be due to an atheromatous or arteritic process. Confirmation of the latter etiology has previously been made only at postmortem examination. A 45-year-old white woman with known systemic lupus erythematosus developed anginal pain and multiple episodes of acute myocardial infarction. During this period, there was serologic but no other clinical evidence of active systemic lupus erythematosus. Serial coronary angiographic studies were strongly suggestive of an arteritic process based upon (1) a saccular aneurysm with no obstructive lesions in a coronary artery supplying an area of recent transmural myocardial infarction and (2) the development of significant obstructive lesions in a previously normal coronary artery over a period of 18 days. This case illustrates the difficulties in distinguishing between atherosclerosis and arteritis using a single coronary angiographic study. The distinction is significant because of the different therapeutic interventions required.

Acute Disease↗
PubMed1976

Determinants of variation between Fick and indicator dilution estimates of cardiac output during diagnostic catheterization. Fick vs. dye cardiac outputs.

Simultaneous Fick and duplicate dye cardiac outputs were done in 105 patients with various cardiovascular diseases during routine cardiac catheterization. Dye was injected into the pulmonary artery and sampled from the brachial artery. Nineteen patients had mitral and/or aortic valvular regurgitation. Eighty-four per cent of the duplicate dye cardiac outputs agreed within 10 per cent variation from the line of identity, and 98 per cent were within 25 per cent. There was no systematic difference between the Fick and dye methods. Seventy-five per cent agree within 20 per cent variation from the line of identity. However, individual variation ranged from -27 to +58 per cent. There was, also, no systematic difference between Fick and dye methods either with low cardiac index or valvular regurgitation. Variation between the two methods was less with low cardiac index and greater with higher cardiac index. The variation was not increased in the presence of valvular regurgitation. The variation in the two methods could partly be explained by errors in the measurement of arteriovenous oxygen difference and oxygen consumption. When the injection is made into the pulmonary artery and sampled from the brachial artery, dye outputs are valid irrespective of the level of resting cardiac index and valvular regurgitation as long as there are enough points to draw a straight line from semilogarithmic trace of the descending limb.

Cardiac Catheterization↗
PubMed1975

Reversibility of left ventricular asynergy by nitroglycerin in coronary artery disease.

To evaluate the potential reversibility of left ventricular asynergy in patients with coronary artery disease, pre- and postnitroglycerin left ventriculography was performed in 32 subjects. In four other subjects left ventriculography was repeated without intervention of nitroglycerin. Changes in ejection fraction and percentage of systolic shortening of three minor axes from the first to the second angiogram were then calculated. Changes were not significant for the myocardial infarction group or for the control group without the intervention of nitroglycerin. Normal left ventricles showed small but significant changes (p less than 0.05). Patients with coronary artery disease but without previous myocardial infarction who demonstrated asynergy in their first angiogram showed three types of response: (1) no significant change (p less than 0.05)-irreversible asynergy; (2) significant change (p less than 0.025) with residual dysfunction-partially reversible asynergy; (3) significant change (p less than 0.001) without residual dysfunction-completely reversible asynergy. It is concluded that postnitroglycerin ventriculography is useful in assessing the reversibility of left ventricular asynergy in patients with coronary artery disease.

Adult↗
PubMed1975

Mobitz type I atrioventricular block in the ventricular specialized conduction system.

A patient with a history of multiple syncopal episodes had electrocardiographic findings of Wenckebach type of second degree atrioventricular block and left bundle branch block. He was thought to have intermittent complete heart block. His bundle recordings demonstrated the unusual occurrence of Mobitz type I block localized to the ventricular specialized conduction system. Based on the findings of this case and those of previous case reports, it is recommended that electrophysiologic studies should be performed on all patients with Mobitz type I atrioventricular block who also have bundle branch block.

Aged↗
PubMed1975

Mechanism of normal splitting of the second heart sound.

The mode of inspiratory augmentation (1A) of the A2-P2 interval was investigated in seven normal volunteers (group 1) and six patients with pulmonary hypertension of diverse etiology (group 2) using catheter-tip micromanometers. In group 1 subjects, inspiratory widening of this interval was found to average 27.2 msec, of which 7.6 plus or minus 2.7 msec (1 sd) or 27 plus or minus 7% was due to a decrease in the Q-A2 interval. The major contribution of Q-P2 interval prolongation was divided into two components: a) Q-O was measured from the onset of the QRS to the onset of the rapid descent of the right ventricular (RV) negative dp/dt, which was felt to reflect the duration of RV electromechanical systole, b) O-P2 or Q-P2 - Q-O. Increase in the Q-O interval accounted for only 7.7 plus or minus 5.0 msec or 28 plus or minus 12% of the total IA. The major single component of IA was the increase in O-P2 which averaged 11.9 plus or minus 3.0 msec. Five of six group 2 patients demonstrated significant respiratory change in Q-P2 intervals. In contrast to group 1 subjects, however, this was accomplished primarily via increases in the duration of RV electromechanical systole. The O-P2 interval is felt to primarily reflect the impedance characteristics of the pulmonary vascular bed. It is concluded that physiologic splitting of the second heart sound in normal subjects is most probably due to an inspiratory decrease in impedance of the pulmonary bed rather than the traditional explanation of prolongation of RV systole secondary to an increase in venous return. When the normal impedance characteristics of this bed are lost, as in pulmonary hypertension, IA must occur primarily via increases in the duration of RV systole. The inspiratory delay from the conclusion of RV systole to the occurrence of P2 is attributed to the inertiance of the RV stroke mass.

Adolescent↗
PubMed1975

Determination of site of infection in endocarditis.

Medical-surgical treatment of antibiotic refractory endocarditis requires determination of the site of infection, which is not always possible with conventional cardiac catheterization. The cases of two patients with right-sided endocarditis who survived after combined medical-surgical therapy are presented. One had persistent Pseudomonas aeruginosa bacteremia and three possible sites of infection. Multiple quantitative blood cultures proximal and distal to each suspected site indicated the pulmonary valve alone was infected. The second had sustained bacteremia with three enteric organisms and no apparent valvular abnormality. Quantitative cultures excluded the abdomen as the continuing source of bacteremia and suggested the tricuspid valve was infected. This was confirmed by a second catheterization using multiple cultures in conjuction with dye dilution studies, intracardiac phonocardiography, and angiography. These bacteriologic and cardiologic techniques may be especially useful in detecting right-sided endocarditis and may also be helpful in detecting concomitant infection of both sides of the heart.

Adult↗
PubMed1974

Autonomic mechanisms in hemodynamic responses to isometric exercise.

Selective autonomic blockade with intravenous propranolol, practolol, atropine, and combined atropine-propranolol was utilized to elucidate the role of the autonomic nervous system in the hemodynamic responses in young adult male volunteers to handgrip sustained at 30% of maximal voluntary contraction for 3 min. The initial 30 s of the tachycardia response was found to be mediated by withdrawal of vagal dominance, as evidenced by blockade of this response by prior atropinization. The mid and late portion of the heart rate response curve was demonstrated to be sympathetic in origin, since it was unaffected by atropine, but was suppressed by combined atropine-propranolol blockade. Sympathetic stimulation appears to be a secondary mechanism for increasing the heart rate, however, as it becomes operative only after the first mechanism of vagal withdrawal has been utilized. This was confirmed by the finding that beta adrenergic receptor blockade alone had little effect on the heart rate response curve. The pressor response to handgrip was accompanied by increased cardiac output and no change in calculated systemic vascular resistance. After propranolol, handgrip resulted in increased peripheral resistance and an equivalent rise in arterial pressure, but no increase in cardiac output. It was concluded that the increase in resistance was the result of sympathetically induced vasoconstriction. This response was shown to be independent of peripheral beta adrenergic receptor blockade by the use of practolol, a cardio-selective beta adrenergic receptor-blocking drug which caused identical hemodynamic responses to those observed after propranolol. Left ventricular ejection time (corrected for heart rate) was prolonged by handgrip. The increased afterload imposed on the left ventricle by sustained handgrip may explain the prolongation of ejection time index. Preejection period was prolonged by SHG after propranolol and shortened after atropine. In addition to confirming the previously defined role of the parasympathetic nervous system, this study delineates the role of the sympathetic nervous system in the heart rate and pressor responses to sustained handgrip.

Adult↗