PACEMAKER, AICDs AND THE ANESTHESIOLOGIST

• The need for cardiac pacing results from conduction disorders of the heart, which may or may not be associated with IHD.
• Permanent Pacemakers (PPM) are classified using a five letter code( See below)
• For example DDDR means atrial and ventricular sensing (I), atrial and ventricular pacing(II) with adaptive(III) rate(IV) response
• Most modern units work in DDD mode, and provide atrial pacing in the presence of atrial bradycardia and ventricular pacing after an endogenous/paced atrial depolarization, if a spontaneous ventricular beat is absent
• KEY PERIOPERATIVE QUESTIONS: 1. Indication for pacemaker and associated cardiac comorbidities 2. Type of pacemaker; also how does the rate modulation work in that pacemaker? Chest x-ray will help to find the pulse generator siting and lead placement (atrium/ventricle/both) and number 3. When it was last checked 4. Requirement of diathermy for the procedure 5.Whether anticipating any other factor/s interfering with pacemaker function? 6. Surgical site proximity to the pacemaker 7. What is your plan to avoid inappropriate pacemaker function (e.g. change from demand to fixed rate mode) in case of interference? Cardiology/ Pacemaker programmer support may be needed for the same
• WHAT ECG CAN TELL: 1. If native rhythm predominates--> patient not PPM dependent 2. If all beats preceeded by a pacemaker spike--> pacemaker dependent 3. No evidence of pacemaker activity--> magnet might be applied over the pulse generator to switch to fixed rate pacing. If pacemaker is activated by a magnet to pace at a fixed rate, spike may fall in the refractory period and fail to stimulate the ventricle 4. If pacemaker spike is not followed by p or QRS waves --> PPM malfunction
• The characteristics of a PPM can be changed externally by application of a magnet or using radiofrequency generators, usually for a change of demand to fixed rate. Application of a magnet over a non-programmable VVI pacemaker will convert it to VVO asynchronous mode. The modern reprogrammable units need a cautious approach to the use of magnets. In this case, there is a risk of reprogramming ( with inappropriate settings), but it will remain in the asynchronous fixed rate mode, until the magnet is removed, after which the 'inappropriate' reprogrammed mode may take over
• ABOUT THE RATE RESPONSE FUNCTION: Such PPMs may sense electrical activity or vibration (e.g. shivering) and cause a tachycardia in response. Some measure respiratory rate by sensing thoracic impedence and adjust HR accordingly. Some sense blood temperature and so may cause a tachycardia when warming a hypothermic patient. With hypokalemia, there is a risk of loss of pacing capture and with hyperkalemia, there is risk of VT or VF.
• INTRAOPERATIVE STEPS: 1. If possible, avoid surgical diathermy; but if unavoidable, bipolar is safer than unipolar diathermy. 2. Monopolar where necessary, should be used in short bursts with at as low energy levels as possible 3. Diathermy plate should be kept on the same side, as far away from the PPM as possible 4. Cables from diathermy equipment also should be kept away from the PPM 5. Confirm device functionality on completion of the surgery
• Surgical diathermy can cause 1. Ventricular fibrillation 2. 'Reprogramming' of programmable PPMs 3. Inhibition of demand function 4. Unit failure 5. Asystole
• AUTOMATIC IMPLANTABLE CARDIOVERTER DEFIBRILLATORS (AICDs) and THE ANESTHESIOLOGIST: They consist of a set of lead electrode systems for sensing-pacing-delivery of shocks for cardioversion/ defibrillation; modern units can also function as DDD pacemakers. All AICDs should be deactivated with a programming device before surgery to avoid inappropriate shock delivery during electrical interference; in modern AICDs, the anti-bradycardia function can be left activated (Consult the manufacturer for this). The effect of magnets are inconsistent across devices; but modern units are inhibited by magnets. If required, external pads can be placed over the patient with external defibrillators ready to attach, for use in case any tachyarrhythmias occur during this period. Take all precautions as in the case of PPM. Postoperatively, the ICD should be checked and reactivated.

DIATHERMY AND THE ANESTHESIOLOGIST

• WHY WE SHOULD KNOW? 1.Anesthesiologist may be blamed if burns occurs due to malposition of the plate 2. It can interfere with monitors e.g. ECG and pulseoximeters 3. It can disrupt pacemaker function in a patient, having it.
• Diathermy depends on the heat generated when a current pass through a tissue and is used to coagulate blood vessels and cut through tissues
• A high frequency current is necessary for this, as myocardium is sensitive to DC and low frequency AC [the usual Mains frequency of 50 Hz will precipitate VF]. Very high frequencies have minimal tissue penetration and pass without harming the myocardium
• A 0.5 MHz alternating sinewave is used for cutting and a 1.0-1.5 MHz pulsed sinewave pattern is used for coagulation
• UNIPOLAR DIATHERMY & PROBLEMS: Here the forceps represent one electrode (small area, high current density and significant heat generation) and the diathermy plate ( indifferent electrode) over the patient represent the other electrode (large area, less heat). If the the plate is malpositioned, the current may pass through any point of metal contact* like ECG electrodes, metal poles of lithotomy, operation table etc, and may result in passage of high current density as the area of contact is small, resulting in a burn. So we should ensure that the plate is in close and proper contact with a large, highly perfused (will dissipate heat) area of skin (adhesive gels are useful). If we place it near to metal prosthesis (e.g. Hip), which has a low resistance than tissue, it will generate a high current density, resulting in burns. A unipolar diathermy can generate 150-400 Watts of energy.
• BIPOLAR DIATHERMY: Current passes between the two blades of the forceps; so requires no plate; safer in patients with pacemaker. But can generate only 40 Watts of energy. So efficacy is less and may be used for coagulation of small blood vessels
• OTHER PROBLEMS: Sometimes diathermies may cause ignition of skin preparation spirit. Newer diathermies dont have earthing; but if your machine is having earthing, an inappropriate earthing will result in current passing through other routes mentioned above*, resulting in burns.
• Cautious use of diathermy is required in patients with pacemakers:

VOCAL CORD PALSIES; a complete description

Under normal circumstances, the vocal cords meet in the midline during phonation. On inspiration, they move away from each other. They return toward the midline on expiration, leaving a small opening between them. When laryngeal spasm occurs, both true and false vocal cords lie tightly in the midline opposite each other.

The recurrent laryngeal nerve (RLN) carries both abductor and adductor fibers to the vocal cords.

Selmon’s law: The abductor fibers are more vulnerable, and moderate trauma causes a pure abductor paralysis. Severe trauma causes both abductor and adductor fibers to be affected. N.B.:- Pure adductor paralysis does not occur as a clinical entity.

Scenario 1- PURE UNILATERAL ABDUCTOR PALSY: As adduction is still possible on the affected side, the opposite cord come and meet in the midline on phonation. However, only the normal cord abducts during inspiration.

Scenario 2- COMPLETE UNILATERAL PALSY OF THE RLN: Both abductors and adductors are affected. On phonation, the unaffected cord crosses the midline to meet its paralyzed counterpart, appearing to lie in front of the affected cord. On inspiration, the unaffected cord moves to full abduction.

Scenario 3- BILATERAL INCOMPLETE ABDUCTOR PALSY: When there is incomplete bilateral damage to the recurrent laryngeal nerve, the adductor fibers draw the cords toward each other, and the glottic opening is reduced to a slit, resulting in severe respiratory distress.

Scenario 4- COMPLETE BILATERAL PALSY OF THE RLN: With a complete palsy, each vocal cord lies midway between abduction and adduction, and a reasonable glottic opening exists.

Thus, bilateral incomplete palsy is more dangerous than the complete variety.

Scenario 5- DAMAGE TO SUPERIOR LARYNGEAL NERVE/S: Damage to the external branch of the superior laryngeal nerve or to the superior laryngeal nerve trunk causes paralysis of the cricothyroid muscle (the tuning fork of the larynx), resulting in hoarseness that improves with time because of increased compensatory action of the opposite muscle. The glottic chink appears oblique during phonation. The aryepiglottic fold on the affected side appears shortened, and the one on the normal side is lengthened. The cords may appear wavy. The symptoms include frequent throat clearing and difficulty in raising the vocal pitch.

Scenario 6- TOTAL BILATERAL PARALYSIS OF VAGUS NERVES: This affects the recurrent laryngeal nerves and the superior laryngeal nerves. In this condition, the cords assume the abducted, cadaveric position. The vocal cords are relaxed and appear wavy. A similar picture may be seen after the use of muscle relaxants.

N.B:- Topical anesthesia of the larynx may affect the fibers of the external branch of the superior laryngeal nerve and paralyze the cricothyroid muscle, signified by a “gruff” voice. Similarly, a superior laryngeal nerve block may affect the cricothyroid muscle in the same manner as surgical trauma does.

Reference: Benumof and Hagberg’s Airway Management, Third edition

NITROUS OXIDE ISOTHERM

An isotherm is a line of constant temperature

Compressed gases in a cylinder can either stay as a gas, or change state to form a liquid due to the higher pressure (both carbon dioxide and nitrous oxide do this).

A graph of pressure against time for nitrous oxide is shown below. The isothermal lines are shown for 40°C, 36.6°C and 20°C.

At 40°C, nitrous oxide is above its critical temperature and so it is a gas no matter whatever pressure is being applied.

When it is compressed (moving from right to left along the isotherm) the pressure increases smoothly. At 36.6°C (the critical temperature), as soon as the pressure reaches the critical pressure (72 bar), the gas becomes a liquid.

 At 20°C, once the pressure reaches 52 bar (the saturated vapour pressure of nitrous oxide at 20°C), some of the gas condenses so that liquid and vapour are both present. Further decreases in volume cause more vapour to condense, with no associated rise in pressure. When all the vapour has condensed to a liquid, any further reduction in volume causes a rapid rise in pressure.

In most circumstances, nitrous oxide is stored below its critical temperature of 36.4 C. It therefore exists in the cylinder as a vapour in equilibrium with the liquid below it.

To determine how much nitrous oxide remains in a given cylinder, it must be weighed, and the weight of the empty cylinder, known as the tare weight, subtracted. Using Avogadro’ s law, the number of moles of nitrous oxide may now be calculated. V/n= K, where V = volume of gas, n = amount of substance of the gas, K = a proportionality constant

Using the universal gas equation, the remaining volume can be calculated. PV = nRT, where P = pressure, V = volume, n = the number of moles of the gas, R = the universal gas constant (8.31 J/K/mol), T = temperature

CRITICAL TEMPERATURE AND PRESSURE

Critical temperature: The temperature above which a gas cannot be liquefied regardless of the amount of pressure applied. (K/°C).

At this point the specific latent heat is zero, as no further energy is required to complete the change in state of the substance.

Critical pressure: The minimum pressure required to cause liquefaction of a gas at its critical temperature. (kPa/Bar)

The latent heat of vaporisation is the heat energy required to change the state of a substance from liquid to vapour.