23 June 2012

ELECTROCONVULSIVE THERAPY =ECT

E.C.T .


SINUSOIDAL WAVE ECT
An understanding of the electrical aspects of ECT is necessary for any psychiatrist who advises this treatment to his patients. A short series of articles will therefore examine important aspects of the role of electricity in ECT. A more detailed discussion is available elsewhere (Sackeim et al, 1994; Andrade, 2009).

Electrical currents differ in their fundamental waveform, and are prototypically sinusoidal wave or brief-pulse in nature. Each waveform may be monophasic (unidirectional) or biphasic (bidirectional) . Further modifications have also been described (Gordon, 1982). Sinusoidal wave stimuli are generally administered using constant voltage ECT devices, and brief-pulse stimuli using constant current devices.

Sinusoidal (sine) wave stimuli are similar to the electricity in the domestic mains, which is supplied at the constant voltage of 110 or 220 volts, depending on the country. The sinusoidal wave stimulus waxes and wanes in amplitude, and the distance between two adjacent points in the same phase comprises one cycle. Descriptors of a sinusoidal wave stimulus include the following:
1. Amplitude (measured in volts [v])
2. Frequency (measured in Hertz [Hz]; that is, cycles per second) 3. Duration (measured in seconds [s])
Sinusoidal wave stimuli administered during ECT are typically set at 110-160v in amplitude and 0.5-0.8s in duration. The frequency is 50-60 Hz, depending on the electrical mains frequency in the country.

Disadvantages of sinusoidal wave stimuli
Sinusoidal wave stimuli carry three important disadvantages. The first disadvantage is that, because the voltage remains constant, the quantity of current delivered to the brain (by Ohm's law) varies as an inverse function of the resistance in the circuit. Since this resistance (impedance) varies widely across patients, and also in the same patient across time (Sackeim et al, 1991), it follows that the same electrical stimulus may be associated with widely differing electrical currents, and therefore with widely different potential for efficacy and adverse effects.

From the preceding paragraph, it is obvious that, with sinusoidal wave ECT devices, the clinician cannot set and administer a planned electrical dose quantified in units of charge. Therefore, a second disadvantage with sinusoidal wave stimuli is that ECT stimulus dosimetry is not feasible.



The third disadvantage is that, with sinusoidal wave stimuli, current is constantly flowing (except momentarily, when the wave is at isoelectrical points); the brain therefore continues to receive electrical stimulation even after the stimulated neurons have fired and are in a refractory state. Unnecessary charge is thus delivered, and this may be the reason why sinusoidal wave ECT has been associated with an increased prevalence and magnitude of cognitive deficits.

ECT was originally administered using constant voltage, sinusoidal wave stimuli. In recent years, however, the use of the more efficient constant current, brief-pulse stimulus has become almost universal.



BRIEF-PULSE ECT
Brief-pulse stimuli comprise trains of rectangular- shaped pulses of electricity; descriptors include the following:
1. Pulse height (measured in milliamperes [mA])
2. Pulse width (measured in milliseconds [ms])
3. Pulse frequency (measured in pulses per second [pps])
4. Stimulus duration (measured in seconds)


Common values for these descriptors are 500-800 mA for pulse height, 0.75-1.5 ms for pulse width, 80-150 pps for pulse frequency and 0.4-4 s for stimulus duration.

Stimulus dose calculations
As already mentioned, the administration of a preset stimulus dose is feasible only with constant current, brief-pulse ECT devices. To calculate the ECT dose, the clinician must first summate the time for which current is flowing. Thus, when the stimulus settings are 1.5 ms pulse width, 125 pps frequency, and 0.4 s stimulus duration, it is apparent that 125*0.4 (that is, 50) pulses will be delivered, and that current will flow for 1.5*125*0.4 (that is, 75) ms.

Multiplying duration of current flow by the strength of the current gives the delivered charge in units of millicoulombs (mC). Thus, if the pulse amplitude setting was 800 mA (that is, 0.8 amperes [A]) in the preceding example, the delivered charge would be 1.5*125*0.4* 0.8 (that is, 60) mC.

DOSE CALCULATIONS

Consider the following facts:
1. Brief-pulse ECT delivers a train of identical pulses of electricity.
2. Each pulse has a certain amplitude (pulse height). This is measured in units of current; that is, amperes (A) or milliamperes (mA).
3. Each pulse has a certain duration (pulse width). This is measured in milliseconds (ms).
4. There is a specific number of pulses delivered each second. This is computed from the stimulus frequency, which is measured in Hertz (Hz) or cycles per second (cps). If the stimulus is unidirectional, the number of pulses per second is the same as the stimulus frequency. If the stimulus is bidirectional, the number of pulses per second is double the stimulus frequency (this is because each cycle is made up of one positive and one negative pulse). Most constant current, brief-pulse ECT devices deliver bidirectional pulses.
5. The ECT stimulus is passed for a specific duration. This is known as the stimulus duration, or the duration of the stimulus train, and is measured in seconds (s).

Step 1:
To calculate the ECT dose, the first step is to determine the following:
1. Current, or pulse amplitude (A or mA)
2. Pulse width (ms)
3. Number of pulses per second (obtained from the stimulus frequency)
4. Stimulus duration (s).

Some ECT devices allow the clinician to choose all these settings. Some devices have certain of these settings fixed, and certain of these settings under the clinician's control. The manual of the device and its control panel usually provide the necessary information about the values of the settings that are fixed and the values of the settings that the clinician can manipulate.

In the event that the clinician is unable to determine any of the above values from the manual, the control panel, and the manufacturer, a visit to any electronics establishment which owns an oscilloscope can quickly and accurately determine not only the values of the fixed and variable parameters but also the nature of the stimulus delivered by the instrument, and the fidelity of the settings. Clinicians would be wise to check the fidelity of their instruments periodically, such as every 6-12 months, even if they know all the values.

Step 2
The second step is to calculate the number of pulses delivered. This is done as follows:
Number of pulses delivered = (number of pulses per second) x (stimulus duration in s).


Step 3
The third step is to calculate the total time for which current is flowing. This is done as follows:
Total time in ms = (Pulse width in ms) x (number of pulses delivered)

Step 4
The fourth and final step is to calculate the ECT dose that is set, measured in units of electrical charge; that is, millicoulombs (mC). The dose is calculated using the formula:
Charge = current x time.
Thus,
Dose in mC = (current in A) x (total time in ms).

Worked example
Calculating the ECT dose is actually far easier than it may appear from the preceding instructions. Here is a sample calculation for an ECT device which delivers bidirectional pulses with the following settings:
Pulse amplitude (current) = 800 mA (that is, 0.8 A)
Pulse width = 1.2 ms
Stimulus frequency = 60 Hz
Stimulus duration = 2 s

Since the apparatus delivers 60 bidirectional pulses a second, the total number of pulses per second is 60 x 2 = 120.

The number of pulses delivered during the 2 second stimulus is 120 x 2 = 240.

The total time for which current flowed is 240 x 1.2 = 288 ms.

The charge delivered is 0.8 x 288 = 230.4 mC.

Some practical recommendations for brief-pulse ECT are:
1. Set pulse width at 0.5-1.0 ms
2. Set pulse frequency at 100-200 pulses per second
3. Set pulse amplitude at 0.5-1.0 A
4. Set stimulus duration at whatever length is necessary to create the charge that is desired. The stimulus duration can be as long as even 4-6 seconds.

What dose should a clinician choose?
Most patients have an initial seizure threshold of about 50-100 mC. Clinicians should choose stimulus settings in this range for the initial stimulus if they wish to administer threshold ECT, and stimulus settings at higher values if they wish to administer suprathreshold ECT. When increasing the ECT dose, an increase in stimulus duration is usually the best way to increase the charge of the stimulus.

Here are two exercises for practice.
1. An instrument delivers bidirectional pulses. Current is set at 800 mA. Pulse width is set at 0.75 ms. Stimulus frequency is set at 70 Hz. Stimulus duration is set at 0.75 s. What is the electrical charge delivered?
(Answer, 63 mC).

2. An instrument delivers unidirectional pulses. Current is set at 500 mA. Pulse width is set at 1 ms. Stimulus frequency is set at 80 Hz. Stimulus duration is set at 4 s. What is the electrical dose delivered?
(Answer, 160 mC).


CLINICAL ISSUES
It was believed for long that the electrical dose administered during ECT was immaterial to therapeusis as long as a seizure developed; this was because the seizure was erroneously considered to be an all or none phenomenon. Therefore, attempts were made to administer ECT with the smallest possible electrical doses in order to contain dose-related cognitive impairment.

Today, it is recognized that ECT seizure characteristics vary as a function of the electrical dose, and that the clinical and biological effects of ECT are likewise dose-dependent. Stimulus dosimetry with ECT has therefore assumed importance much as it has in psychopharmacology. Research during recent decades has established the following (Andrade, 2009):

1. Quantification of the ECT stimulus is biologically most appropriate with units of electrical charge (mC) as opposed to units of energy (joules) or power (watts). One reason is that energy and power computations are both confounded by the electrical impedance in the circuit during ECT; this impedance varies widely across subjects and, in the same subject, across time. Another reason is that the electrical charge delivered describes a greater variance in the seizure threshold across subjects and across time than the energy or power during ECT.

2. Brief-pulse stimuli are as effective as but cognitively less toxic than sinusoidal wave stimuli. A likely explanation is that the electrical charge in brief-pulse ECT is delivered in packets called pulses; there is therefore an economy of stimulation. In contrast, current is always flowing during sinusoidal wave ECT, even during the refractory period of the stimulated neurons; there is therefore an excessive stimulation of brain structures.

3. The lowest electrical dose for seizure induction (seizure threshold) varies several fold across subjects and, in the same subject, across time; while the threshold commonly lies within the 60-300 mC band, it may be as low as 30 mC in some patients, and as high as over 1000 mC in very rare cases. Several factors which influence the seizure threshold have been identified; these will be discussed in the next article.

4. The seizure threshold is the biological baseline with reference to which stimulus dosing is based (see below). This is best established with unilateral ECT, but may be true for bilateral treatments as well.

5. The likelihood of response to ECT (efficacy) is proportionate to the degree to which the ECT stimulus dose exceeds the seizure threshold; this is however true only with unilateral ECT.

6. The speed of response to ECT (efficiency) is proportionate to the degree to which the ECT stimulus dose exceeds the seizure threshold; this is true with both unilateral and bilateral ECT.

7. Cognitive adverse effects with ECT are proportionate to the degree to which the ECT stimulus dose exceeds the seizure threshold; this is true with both unilateral and bilateral ECT.

8. The ECT seizure is not an all or none phenomenon; several dose-dependent seizure characteristics have been described, most importantly in the EEG.


FACTORS INFLUENCING THE SEIZURE THRESHOLD
The seizure threshold is defined as the lowest electrical dose which elicits an adequate seizure. In this context, an adequate seizure is defined as one which is associated with a motor seizure duration of at least 15 s, or an EEG seizure duration of at least 20-25 s.

Factors which influence the seizure threshold are (Andrade, 2009):
Age:
Seizure threshold increases with increasing age because of the increasing resistance offered by a thickened bony cranium.

Gender:
Seizure threshold is greater in males than females because the bony cranium is thicker.

Head size:
Seizure threshold increases with increasing head size because of the greater interelectrode distance.



Diagnosis:
Seizure threshold may be lower in manic patients.

Electrode placement:
Seizure threshold is greater with bilateral relative to unilateral electrode placement because of the greater interelectrode distance.

Anesthesia:
Seizure threshold increases with higher doses of barbiturate or propofol anesthesia in the ECT premedication. However, agents such as ketamine or etomidate do not affect the threshold.

Stimulus variables:
For a set charge, the seizure threshold is lower when the stimulus duration is longer.

Concurrent medication:
Seizure threshold can be lowered by certain antidepressants (e.g. clomipramine) , neuroleptics (e.g. chlorpromazine) , xanthine alkaloids (e.g. aminophylline and caffeine), and other drugs. Seizure threshold is elevated by benzodiazepines and anticonvulsant drugs.

Previous ECT:
ECT has an anticonvulsant effect, and the seizure threshold therefore commonly rises across the ECT course, particularly in those who respond to the treatment.


PRACTICAL ISSUES
The seizure threshold varies widely, and so different patients require different electrical doses at different times. It is common for most patients to convulse with a dose that is around 50-100 mC at the first ECT; towards the end of the course, however, a dose of 180-300 mC may be required to elicit a seizure. This is because ECT has an anticonvulsant effect, and the seizure threshold rises as the ECT course progresses.

In view of the research demonstrating greater efficacy and efficiency of ECT associated with higher electrical doses, many clinicians identify the ECT threshold by trial and error at the first treatment, starting at very low doses which prove subconvulsive and increasing until a convulsion is at last elicited; this is known as stimulus dose titration. At subsequent treatments, suprathreshold electrical doses are administered. Up to six times suprathreshold ECT may be desirable when unilateral electrode positioning is employed; at these doses, unilateral ECT may be as effective as bilateral ECT while yet retaining its cognitive advantage. With bilateral ECT, a 1.5 times suprathreshold dose is probably sufficient.

A particular electrical dose can be composed from different combinations of pulse height, pulse width, pulse frequency, and stimulus train duration. Research suggests that increasing stimulus dose delivery through an increase in the stimulus train duration identifies the lowest seizure threshold; the latter indicates that even if the seizure threshold is an important biological marker, it is not a fixed value (Andrade et al, 2002). Research also suggests that pulses wider than 1.0 to 1.5 mC are probably inefficient (Sudha et al, 2003). Currently, studies are examining the utility of ultra-brief pulse ECT where the pulse width is set at below 0.5 ms.

Resistance at the electrode-skin interface should be minimized during the ECT procedure. If the resistance is high, too low a dose is delivered with constant voltage ECT devices, and too high a voltage is developed with constant current ECT devices. In the former instance, the ECT may be subtherapeutic, and in the latter instance, skin burns may result.



ECT AND SUCCINYLCHOLINE- RELATED ASYSTOLE
The ECT stimulus results in an initial parasympathetic activation followed quickly by a more dominant and sustained sympathetic activation; changes in cardiovascular parameters (such as heart rate and blood pressure) during ECT correspond to these autonomic effects. The parasympathetic activation may dominate in certain circumstances:
1. Idiosyncratically.

2. When the patient is receiving sympatholytic medication (e.g. drugs which block alpha or beta adrenergic receptors).

3. When subconvulsive stimuli are administered (e.g. when titrating the stimulus dose to identify the seizure threshold; or when the seizure threshold is high and the administered stimulus fails to elicit a seizure).

When the parasympathetic activation dominates, the patient may experience hypotension, bradycardia, and even asystole.

Asystole during an ECT session may rarely occur even before the ECT stimulus is administered. In such instances, succinylcholine, the muscle relaxant used during the ECT procedure, is usually responsible through one or both of two possible mechanisms:

1. Hyperkalemia (this is more likely in patients with burns, paralysis, prolonged bed rest, etc.).

2. Direct cholinergic effect (because succinylcholine is essentially made up of two acetylcholine molecules).



Succinylcholine- related asystole before ECT was first reported by McCall (1996).



Recently, Arias et al (2009) described the occurrence of succinylcholine- related asystole in a 62-year-old woman who was receiving her 13th ECT for a major depressive episode. The asystole developed despite the administration of glycopyrrolate 0.1 mg i.v. 30 min prior to ECT. The asystole lasted 3-4 s and was immediately recognized and treated with i.v. atropine (0.4 mg). ECT was afterwards administered uneventfully.

Hyperkalemia as the cause of the asystole was ruled out by the presence of a normal serum potassium level. The subsequent course of ECT in this patient was also uneventful; the later treatments were administered under parenteral atropine cover.

Conclusions
Asystole in connection with ECT may rarely occur, as a consequence of succinylcholine administration, even before the ECT stimulus is administered.

Comments
1. Nondepolarizing muscle relaxants can be administered in lieu of succinylcholine, but these are far longer-acting and therefore require more intensive anesthesiological management.
2. Asystole due to hyperkalemia will not respond to parenteral atropine. Measures to treat the hyperkalemia need to be instituted.





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