Allowing the novice to succeed: transitional support in critical care.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J J Kane.
Explore the source record for details and available documents.
Three groups of 10 extracted endodontically treated mandibular molars were mounted in acrylic resin. The occlusal surface was reduced until a 4 mm pulp chamber height remained. A peripheral shelf 2 mm deep and 1.4 mm wide was placed on one group, while four TMS Minim pins were placed 45 degrees to the long axis of the tooth into the facial and lingual walls of the second group. The final group served as the control and had no further treatment. All teeth were then restored with amalgam. An Instron testing machine was used to apply a controlled force to the beveled amalgam at a crosshead speed of 2 mm/min until fracture occurred. A peripheral shelf did not improve the fracture resistance of the coronal-radicular restorations tested. The specimens with semihorizontal pins were significantly stronger than specimens from the other groups. Placement of pins into the pulp chamber is recommended when adequate dentin remains.
The effect of pulp chamber depth and extension into the root canal space on fracture resistance was examined on endodontically treated teeth with coronal-radicular amalgam restorations. Six groups of 10 mandibular molars were mounted in acrylic resin, and crowns were ground apically until the wall height of the pulp chamber was 2, 4, or 6 mm. Three millimeters of gutta-percha was removed from the three canals of one-half the teeth and amalgam was condensed into the canal space to a height 7.5 mm above the cementoenamel junction (CEJ). The remaining teeth had amalgam condensed from the floor of the chamber to 7.5 mm above the CEJ. The amalgam restorations were loaded with an Instron instrument (Instron Corp., Canton, Mass.) until failure. Amalgam extension into the root canal space contributed minimally to the fracture resistance of the amalgam coronal-radicular restoration with four or more millimeters of chamber wall. If less than 4 mm of chamber wall height remained, however, the fracture load was substantially increased. Amalgam extension into the root canal space should be confined to teeth with limited remaining pulp chambers.
Explore the source record for details and available documents.
In order to determine the relationship of paroxysmal ventricular tachycardia (PVT) to any antecedent (premonitory) ventricular arrhythmias during the early phases of acute myocardial infarctions, 24-hour Holter monitoring was begun on 52 male patients an average of 12.6 hours after the onset of prolonged chest pain that was documented as acute infraction. Twenty-four patients had PVT and 28 did not. We analyzed in detail the incidence of frequency of premature ventricular complexes (PVCs), prematurity and pairing during the 10 minutes immediately preceding PVT from a continuous 10-minute rhythm strip. There was no positive correlation between PVT and the number or complexity of PVCs in the 10 minutes immediately before ventricular tachycardia. These findings suggest that there is no consistent pattern or frequency of ventricular arrhythmia that could be identified as premonitory for PVT during the immediate pre-PVT period, even during the acute phase of myocardial infarction in man.
The long-term prognosis of paroxysmal ventricular tachycardia (PVT) complicating acute myocardial infarction remains unevaluated. Significant ventricular arrhythmia in the patient after infarction is said to carry a poor prognosis with regard to survival. To evaluate these two important aspects of myocardial infarction in man, 56 patients with documented myocardial infarction had Holter monitoring performed during the initial 24 hours and prior to hospital discharge. In 38 of the 45 survivors, Holter monitoring was repeated an average of 19 months after infarction. There were eight cardiac deaths during follow-up. Data analysis revealed that of 18 patients with PVT during the acute phase, one died during follow-up and 17 survived long-term. Even though the incidence of complex PVCs prior to hospital discharge and at long-term follow-up was higher in patients with PVT during the acute phase than in those without PVT, survival appeared unaffected. Thus, PVT during the acute phase of myocardial infarction and complex PVCs at the time of hospital discharge are not incompatible with long-term survival.
In order to evaluate the effect of digitalis on the effective refractory period of the human ventricle, 14 patients were studied with atrial or ventricular pacing and with the introduction of ventricular extra-stimuli. The ventricular effective refractory period (VERP) was recorded before and after 1.0 to 1.25 mg ouabain given intravenously and the results compared with similar changes in the Q-T interval. During atrial pacing (eight patients) at rates of 70 to 110 beats per minute, ouabain reduced the mean ventricular effective refractory period from 290 +/- 13 ms to 260 +/- 16 ms (P less than 0.01) and the mean Q-T interval was reduced from 372 +/- 18 ms to 359 +/- 19 ms (P less than 0.01); the mean VERP/Q-T ratio was 0.79 +/- 0.04 before ouabain and 0.73 +/- 0.04 after ouabain (P less than 0.01). Utilising ventricular drive pacing (six patients) the mean ventricular effective refractory period was reduced from 245 +/- 16 ms to 226 +/- 13 ms (P less than 0.01) and the mean Q-T interval reduced from 382 +/- 18 ms to 360 +/- 29 ms (P less than 0.01). There was no significant change in the mean VERP/Q-T ratio (0.63 +/- 0.04 before vs 0.63 +/- 0.04 after ouabain). The results demonstrate that clinically effective doses of ouabain produce a significant reduction of the effective refractory period of the human ventricle. This change is accompanied by a reduction in the VERP/Q-T ratio during atrial pacing.
Since both propranolol therapy and saphenous-vein bypass surgery have become accepted treatments for patients with symptomatic coronary-artery disease, it is important to determine if either influences the prevalence of ventricular arrhythmias in these patients. Six-hour dynamic electrocardiography was done on 130 patients with chronic stable angina pectoris at least 1 year after being randomized to surgical or medical therapy. All surgical patients had saphenous-vein grafting; 90% of the medical patients received propranolol. Data analysis showed that even though the overall prevalence of premature ventricular contractions was no different in medical and surgical patients, the prevalence of complex premature ventricular contractions was significantly higher in surgically treated patients not receiving propranolol than in propranolol-treated medical patients (p less than 0.05). However, the survival rate was no different in either group, and the quality of life in the surgical patients remained superior.
Bongkrekic acid and atractyloside, inhibitors of adenine nucleotide translocase, do not inhibit Ca2+ uptake and H+ production by pig heart mitochondria. However, bongkrekic acid, but not atractyloside, inhibits dinitrophenol-induced Ca2+ efflux and H+ uptake. Conversely, ruthenium red blocks Ca2+ uptake and H+ production but does not prevent dinitrophenol-induced Ca2+ efflux and H+ uptake by mitochondria. These results suggest that mitochondrial Ca2+ uptake and release exist as two independent pathways. The efflux of Ca2+ from mitochondria is mediated by a bongkrekic acid sensitive component which is apparently not identical to the ruthenium red sensitive Ca2+ uptake carrier.
An interpolated premature ventricular contraction (PVC) may produce either complete block of the next sinus impulse or depression of A-V nodal conduction with a prolonged A-H interval. When a PVC results in partial depression of a A-V nodal conduction, the effect on subsequent premature atrial stimuli is unknown. The authors have recently observed three patients in which the effect of a premature ventricular stimulus with interpolation on the functional refractory period of the A-V node could be measured. In case one an interpolated PVC sufficient to prolong the A-H interval from 80 to 120 msec was followed by programmed premature atrial stimuli which resulted in no additional A-V nodal delay, and the apparent functional refractory period of the A-V node was reduced from 420 to 330 msec when compared with the atrial extrastimulus technique. In case two a programmed ventricular extrastimulus prolonged the A-H interval in the following sinus beat from 120 to 240 msec; atrial extrastimuli then resulted in only minimal increments in A-V nodal delay and the apparent functional refractory period of the A-V node was reduced from 590 msec. A ventricular extrastimulus in case three increased the resting A-H interval from 60 to 115 msec; conduction of atrial extrastimuli then resulted in a reduction in the functional refractory period of the A-V node from 465 to 400 msec. In each case an interpolated premature ventricular stimulus produced (1) depression of A-V nodal conduction in the ensuing sinus beat A1 and (2) relative facilitation of A-V nodal conduction of a subsequent premature atrial stimulus (A2). The functional refractory period of the A-V node was reduced when compared with the atrial extrastimulus technique alone.
Analysis of clinical ventricular ectopy has provided deductive evidence for the existence of concealed ventricular rhythms. Studies in the experimental animal have demonstrated that when ventricular extrastimuli are applied near the ventricular effective refractory period of consecutive sinus beats, extrastimuli may not be conducted after sinus beats immediately following the post-estrasystolic pause. This sequence may be due to a prolongation of the effective refractory period of ventricular muscle produced by the increased cycle length resulting from the post-extrasystolic pause. The purpose of this study was to extend these observations to the human ventricle in an attempt to produce concealed ventricular rhythms by programmed ventricular extrastimuli. Twelve patients with normal PR intervals and QRS complexes with a mean age of 49 years were studied with ventricular extra-stimuli at programmed intervals following normally conducted sinus impulses. Premature ventricular impulses were introduced after every sinus beat at intervals 10 to 120 msec outside the effective refractory period. In eleven patients without ventricular interpolation, stimuli applied within 40 msec of the effective refractory period produced from one to three concealed (non-conducted) ventricular stimuli following the post-extrasystolic pause; stimuli applied greater than 40 msec outside the effective refractory period at identical current levels produced manifested bigeminy in all cases. In one patient with interpolated premature ventricular beats without a compensatory pause, programmed ventricular extrastimuli produced manifest bigeminy at all coupling intervals. This study demonstrates the experimental production of concealed and manifest ventricular rhythms in man and confirms the importance of the relationship between the ventricular effective refractory period, the timing of the premature ventricular impulse, and the occurence of a compensatory pause.
Explore the source record for details and available documents.
The effectiveness of Holter monitoring is compared to modified treadmill exercise for detecting ventricular arrhythmia in 54 patients during the third week after a documented myocardial infarction. Treatment with digoxin and antiarrhythmic agents had been discontinued for 48 hours. Whereas 76% of the patients had no PVCs during treadmill exercise, only 7% were free of PVCs during Holter monitoring. Complex PVCs occurred in 37% of the subjects during Holter monitoring and in 4% of the subjects during treadmill stress. Although Holter monitoring was significantly more reliable in detecting ventricular arrhythmia, assessment of exercise tolerance and angina status during modified treadmill stress makes both technics desirable in carefully selected patients awaiting discharge from the hospital after myocardial infarction.
Explore the source record for details and available documents.
The use of digitalis in pulmonary heart disease has been a topic of great interest for a number of years. The physician's decision to use or not to use digitalis in pulmonary disease has often been an emotional rather than a reasoned one. The diagnostic difficulties from a clinical point of view in separation of pulmonary from cardiac symptoms and findings have also been confusing. The fact that small doses of digitalis may have an inotropic effect on the cardiac muscle has been a difficult concept for many physicians to adopt. On the other hand, the larger doses of digitalis that are often necessary to control the ventricular response in supraventricular arrhythmias sometimes gives rise to confusion. We shall attempt to review the subject in detail and examine indications, contraindications, toxicity, dosage, assessment of benefit, and role of digitalis serum levels in patient management.
The pharmacokinetics of digoxin, the most frequently used digitalis preparation, are reviewed. The dominate serum turnover time is about 34 hours, and is not affected by the route of administration. Excretion is largely as unchanged digoxin in the urine and this excretion is compromised in renal failure. Serum levels of digoxin (determined by radioimmunoassay) are generally available and are useful clinically in assessment of both toxicity and the state of underdigitalization, even though significant overlap exists. Special problems are presented in patients with myocardial infarction, pulmonary heart disease, and thyroid disease.
Continuous tape recordings of cardiac rhythm were made in 51 male patients with acute myocardial infarction within 24 hours of their infarction. These tracings were analyzed for the incidence of paroxysmal ventricular tachycardia (PVT) and the sinus rate immediately preceding each episode of PVT. In 26 patients, 112 episodes of PVT at a rate greater than 100 beats/min were documented. Although 67 per cent of the episodes of PVT were preceded by sinus rates between 60 and 100 beats/min, 15 per cent occurred at sinus rates below 60 beats/min and 18 per cent occurred at sinus rates above 100 beats/min. The data remained essentially unchanged regardless of whether ventricular tachycardia was defined at rates in excess of 100, 120 or 140 beats/min. The results of this study show that during the early phases of acute myocardial infarction in man, PVT was most common during sinus rates generally thought to be within the normal range (60 to 100 beats/min). A lower, but close to equal incidence of PVT was observed during sinus bradycardia and sinus tachycardia.
Although sinus node function has been evaluated during premature atrial stimulation, no study of retrograde ventriculoatrial sinus node activation following premature ventricular stimuli has been reported. The purpose of this study was to investigate the production of compensatory and noncompensatory pauses by premature ventricular contractions through a comparison of the effects of atrial and ventricular stimulation on sinus node function. Eleven patients in sinus rhythm were studied with programmed introduction of premature atrial and ventricular stimuli outside the ventricular vulnerable period. The onset of sinus node reset, duration of return sinus cycle (A2-A3) during reset, and estimated sinoatrial conduction times were recorded. Sinus node function during premature ventricular stimulation was approximated by utilizing the interval between the last sinus beat and onset of retrograde atrial depolarization (A1-A2 interval). The return cycle length (A2-A3) during sinus reset compared at equal A1-A2 intervals was significantly less with ventriculoatrial conduction (1,145 +/- 52 msec. atrial vs. 1,076 +/- 52 msec ventriculoatrial; P less than 0.01 by paired t test) and the estimated sinoatrial conduction time was significantly less with ventriculoatrial conduction (71 +/- 7 msec. atrial vs. 25 +/- 7 msec. ventriculoatrial; P less than 0.01 by paired t test). Ventriculoatrial sinus reset occurred later in the sinus cycle than atrial reset in three of seven patients with sinus reset produced by both atrial and ventricular prematures. This study shows that the effects of ventriculoatrial conduction on sinus node function are significantly different from those of atrial stimulation alone. The return sinus cycle length during reset and estimated sinoatrial conduction time are significantly reduced with ventriculoatrial conduction. Although the zones of sinus reset with atrial and ventricular stimulation are approximately equal, ventriculoatrial depolarization may produce sinus reset later in the sinus cycle in some cases.