Is psychiatry being harmed by involuntary hospitalization and treatment?
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Adolescent↗
Biomedical subjects
B F Hoffman
Publications and source records attributed to B F Hoffman.
Passive properties and membrane currents of canine ventricular myocytes.
The membrane potential and membrane currents of single canine ventricular myocytes were studied using either single microelectrodes or suction pipettes. The myocytes displayed passive membrane properties and an action potential configuration similar to those described for multicellular dog ventricular tissue. As for other cardiac cells, in canine ventricular myocytes: (a) an inward rectifier current plays an important role in determining the resting membrane potential and repolarization rate; (b) a tetrodotoxin-sensitive Na current helps maintain the action potential plateau; and (c) the Ca current has fast kinetics and a large amplitude. Unexpected findings were the following: (a) in approximately half of the myocytes, there is a transient outward current composed of two components, one blocked by 4-aminopyridine and the other by Mn or caffeine; (b) there is clearly a time-dependent outward current (delayed rectifier current) that contributes to repolarization; and (c) the relationship of maximum upstroke velocity of phase 0 to membrane potential is more positive and steeper than that observed in cardiac tissues from Purkinje fibers.
Animals↗
Electrical restitution process in dispersed canine cardiac Purkinje and ventricular cells.
Rate-dependent changes in cardiac action potential duration (APD) have been related to ion accumulation and depletion in restricted extracellular spaces. Isolated cardiac cells lack intercellular clefts and thus are less likely than intact tissue to experience ionic transients immediately outside the plasma membrane. Furthermore, isolated Purkinje cells lack the T tubules found in ventricular tissue and cells, which also can be a site of ion accumulation and depletion. We therefore employed single canine ventricular and Purkinje cells to investigate the contribution of restricted spaces to the electrical restitution process. In both cell types, abrupt changes in cycle length do not alter resting potential, but APD alters with a time constant of approximately 1 min. In addition, both preparations exhibit two components to the electrical restitution process of the APD. The rapid component has a time constant of 66 +/- 17 ms in the ventricle cells and 186 +/- 43 ms in the Purkinje cells. The slower component is both smaller and more variable. These values are similar to those reported in intact canine ventricular and Purkinje tissue. Thus the restitution process of APD, as measured in these isolated cardiac cells, is not markedly dependent on the presence or absence of restricted extracellular spaces.
Action Potentials↗
Circus movement in the canine atrium around the tricuspid ring during experimental atrial flutter and during reentry in vitro.
A Y-shaped lesion in the right atrium allows induction of atrial flutter in dogs. We recorded the activation sequence during this tachycardia from 96 endocardial bipolar electrodes using intracavitary electrode arrays during 12 separate episodes in three isolated perfused hearts. In each case a reentrant impulse circulated around the tricuspid valve orifice in either a clockwise or counter-clockwise direction. Cutting the pathway terminated the rhythm and prevented its reinduction. There was no discrete segment of markedly slow conduction in the reentrant circuit. The tachycardia cycle length was decreased by methacholine and increased by lidocaine. Reentry was also induced in atrial tissue around the tricuspid orifice when this structure was isolated and superfused in vitro. Tachycardia cycle lengths varied from 205 to 399 msec, depending on the circumference of the ring and temperature. Induction of tachycardia by premature stimulation depended on differences in the duration of the effective refractory period among parts of the ring. Conduction velocity was relatively uniform and was slower during tachycardias than during pacing at long cycle lengths. Analysis of the response to premature stimuli that reset the tachycardia provided evidence for incomplete recovery of excitability between depolarizations during the tachycardia. Fast-response action potentials were recorded throughout the pathway and up to six to eight cell layers deep. Histologic studies showed the supravalvular lamina, a circumferential band of fibers several cell layers below the endocardial surface, to be continuous around the tricuspid orifice. Propagation through this layer best explains the conduction velocities observed in the intact heart during flutter in this preparation.
Action Potentials↗
Effect of procainamide and N-acetylprocainamide on atrial flutter: studies in vivo and in vitro.
We studied the effects of procainamide and N-acetylprocainamide (NAPA) in a conscious dog preparation of atrial flutter resulting from circus movement around the tricuspid orifice. We also recorded transmembrane potentials of atrial tissues from the circus path in vitro. In 12 instrumented dogs, average flutter cycle length was 157 msec, the duration of the excitable gap was 73 msec, and conduction velocity was 0.75 m/sec. At 4 and 8 mg/kg, procainamide moderately prolonged cycle length, but did not terminate the flutter. At a cycle length of 300 msec procainamide increased effective refractory period (ERP) by 12% and 20% and conduction time by 8% and 19%. At 16 and 32 mg/kg procainamide prolonged cycle length, ERP, and conduction time by 60% to 80% and stopped the flutter in all trials. NAPA, at 16, 32, and 64 mg/kg, increased flutter cycle length by 16%, 16%, and 31%, ERP by 14%, 28%, and 41%, and conduction time by less than 15%. NAPA terminated the flutter in two of six dogs given 32 mg/kg, and three of five dogs given 64 mg/kg. The excitable gap was lengthened by both procainamide and NAPA. Transmembrane potentials showed that at a cycle length from 1000 to 300 msec procainamide (10 mg/liter) increased action potential duration and decreased the first time derivative of phase O of the action potential (Vmax), whereas NAPA (20 mg/liter) increased action potential duration without changing Vmax. These findings show the difficulty of relating drug effects on transmembrane potentials to efficacy in vivo since the former do not necessarily indicate which changes in cellular electrical activity are responsible for efficacy against a particular arrhythmogenic mechanism.
Acecainide↗
Clinical features and basic mechanisms of quinidine-induced arrhythmias.
Quinidine therapy is one of the most common causes of the acquired long QT syndrome and the morphologically distinctive tachyarrhythmia torsade de pointes. Clinical data from our institution and others have revealed a number of characteristic features: quinidine plasma concentrations are generally low, marked QRS prolongation is absent, hypokalemia is frequent and abrupt heart rate slowing just before the initiation of a paroxysm is almost invariable. The lack of correlation between plasma quinidine concentrations and this adverse drug effect raises the possibility either that external factors (for example, hypokalemia) modulate the response to quinidine in vivo or that one or more unmeasured active metabolites play a role. Therefore, the effect of alterations in extracellular potassium and stimulation rate on the electrophysiologic effects of quinidine were examined in canine Purkinje fibers. It was found that a form of triggered automaticity, early afterdepolarizations, is reliably produced in the presence of quinidine when extracellular potassium is lowered and the stimulation rate is slowed. More recently, the effects of a number of quinidine metabolites, as well as the commonly found impurity dihydroquinidine, were characterized in canine Purkinje fibers in a similar fashion. Although quinidine was the most potent of the substances tested, both dihydroquinidine and 3-hydroxyquinidine prolonged action potential and produced early afterdepolarizations as did quinidine at long cycle lengths. Quinidine-induced torsade de pointes is a potentially lethal adverse drug effect, occurring in 1 to 3% of patients. Hypokalemia and slow heart rates are commonly observed in a clinical setting and, in the tissue bath, quinidine and several of its metabolites induce abnormal automatic behavior when extracellular potassium is lowered and stimulation rate is slowed.(ABSTRACT TRUNCATED AT 250 WORDS)
Acecainide↗
The role of antiarrhythmic drugs in sudden cardiac death.
Antiarrhythmic drugs may either decrease or increase the likelihood of ventricular fibrillation. Although reliable data suggest reasonable mechanisms for the antiarrhythmic action of several drugs, much less information is available to indicate the mechanisms by which drugs are arrhythmogenic. Antiarrhythmic action may result from suppression of precipitating events such as inappropriately timed premature impulses or runs of excessively rapid impulses and from modification of the conditions predisposing to random reentry. Increases in the likelihood of fibrillation may result from opposite effects on precipitating events or from drug-induced increase in the likelihood of random reentry. One factor that very likely is involved in the latter is the presence of local differences in the electrical activity of myocardial cells that cause significant local differences in the tonic and use-dependent actions of antiarrhythmic drugs.
Action Potentials↗
Atrial reentry around an anatomic barrier with a partially refractory excitable gap. A canine model of atrial flutter.
We have characterized, in dogs, a model of inducible regular atrial tachycardia that resembles atrial flutter. The model involves creating a Y-shaped lesion comprised of an intercaval incision and a connected incision across the right atrium. It is suitable for serial studies of the effects of pacing or antiarrhythmic drugs in chronically instrumented animals studied in the awake state for at least several months. The postoperative cycle length of the induced tachycardia varies from 143 to 188 msec, depending on the size of the dog. The tachycardia cycle length was consistent for each dog, and the rhythm--once induced--was very stable until terminated by pacing. The mechanism of the tachycardia was reentry due to circus movement based on the ability to induce and terminate it by premature impulses or overdrive, the ability to reset the tachycardia by single premature stimuli, the pattern of entrainment during overdrive stimulation, and the ability to terminate the tachycardia by interrupting the conduction pathway. The window of reset determined by the range of coupling intervals of premature stimuli that were able to enter and reset the tachycardia ranged from 56 to 82 msec. There appears to be incomplete recovery of excitability by the end of the excitable gap as evidenced by the fact that even late premature impulses that enter the reentrant circuit conduct more slowly than the tachycardia impulse, and because stimulation of muscarinic receptors that shortens the duration of the action potential and refractoriness also reduces the cycle length of the tachycardia. Epicardial and endocardial activation mapping during tachycardia showed the reentrant pathway does not merely encircle the lesion, particularly over the left atrial epicardium near the intercaval lesion. Rather, the impulse appears to travel around the atrial tissue just above the tricuspid ring, including a portion that travels through the right side of the lower intraatrial septum. Thus, the model involves circus movement around an anatomic barrier through normal tissue that contains no depressed segments. During the circus movement, there is a relatively long excitable gap during which there is incomplete recovery of excitability. This model should be useful for studies of the mechanism of antiarrhythmic drug action and the responses to premature stimulation in this particular subclass of reentrant rhythms, and for comparison with the behavior and responses of other forms of reentry.
Animals↗
How to write a psychiatric report for litigation following a personal injury.
Psychiatrists are frequently asked to assess the psychiatric complications of personal injury cases for individuals who are seeking damages from third parties as the result of an accident. A selective review of the literature concerning the etiology and diagnoses applicable to psychiatric morbidity following personal injury is summarized. The author presents one outline of the medical-legal consultation. The reasons for inclusion of each category of information are discussed, and practical suggestions are made on how the data can be interpreted and used to educate the judicial system about the emotional consequences of accidents.
Consultants↗
The Canadian Constitution and its impact on psychiatry.
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Canada↗
Contemporary ethical issues surrounding electroconvulsive therapy.
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Coercion↗
The impact of new ethics and laws on electroconvulsive therapy.
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Electroconvulsive Therapy↗
A survey of interdisciplinary differences in attitudes and morale within a psychiatric hospital.
This survey has examined a number of job-related attitudes. Staff members in a traditional, hierarchically organized psychiatric hospital were the respondents. Differences between disciplines may be greater in this type of organization. It would be of interest to compare our sample with samples from hospitals structured along less traditional lines, such as in hospitals experimenting with program rather than discipline budgeting. These organizations, while creating unique problems of their own, might eliminate some of the differences found between disciplines in our survey.
Attitude of Health Personnel↗
Effects of verapamil and lidocaine in a canine model of sudden coronary death.
The efficacy of verapamil and lidocaine for treating ischemia-induced arrhythmias was determined in a conscious canine model with a previous myocardial infarction remote from the ischemic area. Temporary (up to 5.5 minutes) occlusion of the circumflex coronary artery was made in eight conscious dogs that had sustained an anterior myocardial infarction 13 to 35 days previously. Each dog served as its own control. Ventricular arrhythmias were observed in 100% of control experiments but in only 25% of experiments after verapamil pretreatment at 0.4 mg/kg body weight. Repetitive ventricular complexes, defined as two or more consecutive ventricular complexes terminating spontaneously in sinus rhythm, were seen in 88% of control experiments and 13% of verapamil experiments, whereas ventricular fibrillation was seen in 6% of control experiments but in no verapamil experiment. Thus, verapamil abolished arrhythmias or reduced the grade of arrhythmias in all dogs. Six of the eight dogs were also tested with lidocaine pretreatment at one or two doses resulting in mean plasma levels of 3.8 +/- 2.0 micrograms/ml. Ventricular arrhythmias were seen in 92% of control experiments and 100% of lidocaine experiments. The incidence of ventricular fibrillation increased from 8% in control to 60% in lidocaine experiments. It is concluded that verapamil may prevent severe ischemia-induced arrhythmias after a recent myocardial infarction, whereas lidocaine may in some cases aggravate arrhythmias.
Animals↗
Modification of the electrophysiologic matrix by antiarrhythmic drugs.
Evidence from many experiments and observations suggests that the likelihood of ventricular fibrillation is increased in some proportion to the magnitude of local differences in the electrophysiologic state of the ventricular myocardium. Many local anesthetic antiarrhythmic drugs have differing affinities for resting, open and inactivated fast channels. In ischemic or otherwise damaged hearts, local differences in resting potential, action potential upstroke and action potential duration will result in differing degrees of block of fast channels by local anesthetic antiarrhythmic drugs. Such drugs can be expected to add to the preexisting local inhomogeneities of electrophysiologic state and thereby increase the likelihood of fibrillation.
Action Potentials↗
The effects of single premature stimuli on automatic and triggered rhythms in isolated canine Purkinje fibers.
We studied the effects of single premature stimuli on automatic and triggered rhythms occurring in preparations of isolated canine Purkinje fibers. Preparations were made from false tendons, the subendocardial right bundle branch, and infarct zone Purkinje fibers 24 hr after occlusion of the left anterior descending coronary artery, and were studied by standard microelectrode techniques. Single premature impulses almost always produced reset of automatic rhythms, whether the pacemaker had a low (less than -60 mV), intermediate (-61 to -70 mV), or high (greater than -70 mV) maximum diastolic potential. In contrast, single premature impulses imposed on triggered rhythms sometimes were found to alter these rhythms; often, early premature impulses (i.e., during phase 3) resulted in either a shortened first return cycle or a short period of arrest of the rhythm. The results of this study indicate that it may be possible to design simple electrophysiologic tests using single premature stimuli to determine whether an arrhythmia is being caused by an automatic focus or by triggered activity.
Animals↗
Action potential prolongation and induction of abnormal automaticity by low quinidine concentrations in canine Purkinje fibers. Relationship to potassium and cycle length.
Marked QT prolongation with induction of polymorphous ventricular tachycardia ("Torsades de Pointes") is a well-described phenomenon during quinidine therapy, frequently occurring at low plasma quinidine concentrations, low serum potassium, and slow heart rates. We have therefore assessed the dose-electrophysiological effects of quinidine as a function of extracellular potassium and cycle length in canine Purkinje fibers, using standard microelectrode techniques. Quinidine (1 microM) prolonged action potential at 90% repolarization, while leaving phase zero upstroke slope (Vmax) unchanged at a cycle length 300-8000 msec; at 10 microM, Vmax depression became evident. Increases in the action potential at 90% repolarization were most marked at long cycle lengths and low extracellular potassium (in contrast to Vmax depression) and were partially reversed by tetrodotoxin (1 microM). The relationship between log of cycle length and action potential at 90% repolarization was linear (for cycle length 300-8000 msec) in the absence of quinidine. Quinidine increased the slope of this relationship in a concentration-related fashion, whereas increasing extracellular potassium shifted the curve rightward (without changing slope), regardless of the presence or absence of quinidine. Action potentials were also measured following pauses of 5-60 seconds. In the absence of quinidine, the action potential depolarization returned to its baseline value in a monoexponential fashion (time constant 36.0 +/- 4.9 sec, mean +/- SE, n = 10). In the presence of 1 microM quinidine, this return was better fit as a biexponential process (time constants 4.2 +/- 1.2 and 40.7 +/- 6.2 seconds, n = 14). At slow stimulation rates (cycle length greater than 4000 msec) in low extracellular potassium (2.7 mM), quinidine produced early afterdepolarizations in 7/14 (50%) of fibers at 1 microM and 14/18 (78%) at 10 microM. Early afterdepolarizations were eliminated by increasing stimulation rates, raising the extracellular the extracellular potassium concentration to 5 mM, or adding tetrodotoxin. These data suggest that prolongation by quinidine of action potentials at 90% repolarization is multifactorial, with both a "tonic" prolonging effect and a prominent frequency-dependent action potential shortening effect. At long cycle lengths and low extracellular potassium, low quinidine concentrations consistently produced early after-depolarizations. The parallels between this form of triggered activity and clinical arrhythmias induced by quinidine suggest that early afterdepolarizations may play a role in quinidine-induced Torsades de Pointes.
Action Potentials↗