Temporary pacemaker

Platiaum and its alloys are also used as biomedical electrodes, eg, platiaum—indium wires for permanent and temporary pacemaker leads and defibrillator leads. Electrophysiology catheters, which contain platinum electrodes and marker bands, have been used to map the electrical pathways of the heart so that appropriate treatment, such as a pacemaker, can be prescribed. 

Alternatively, a continuous magnesium infusion may be initiated after the first bolus, at a rate of 0.5 to 1 g/hour. Alternative treatments include transvenous insertion of a temporary pacemaker for overdrive pacing, which shortens the QT interval and may terminate torsades de pointes intravenous isoproterenol 2 to 10 mcg/minute, to increase the heart rate and shorten the QT interval intravenous lidocaine, which may shorten the duration of ventricular repolarization or intravenous phenytoin, which may also shorten the duration of ventricular repolarization, administered at a dose of 10 to 15 mg/kg infused at a rate of 25 to 50 mg/minute. 

Class 111, for example, prosthetic heart valves, rechargeable non-active drug delivery systems, absorbable sutures, spinal stents, neurological catheters, temporary pacemaker leads. 

Antiarrhythmic treatment with intravenously administered phenytoin as well as correction of the electrolyte balance (K+, Ca " ", Na+) should be performed. AV block may require a temporary pacemaker. Digitalis antibodies may be used as a specific antidote. 

Temporary pacemaker 4 Staphylococcus epidermidis Staphylococcus aureus... 

A 32-year-old woman took 800 mg of citalopram, 20 times her usual daily dose, in a suicide attempt. On admission to hospital she had a sinus bradycardia (41/ minute) but the electrocardiogram was otherwise normal, with a QT interval of 430 ms. Treatment with atropine failed to increase her heart rate and she had hypotension and syncope. A temporary pacemaker was inserted and was required for the next 6 days before it could be safely removed. 

Rothenhausler HB, Hoberl C, Ehrentrout S, Kapfhammer HP, Weber MM. Suicide attempt by pure citalopram overdose causing long-lasting severe sinus bradycardia, hypotension and syncopes successful therapy with a temporary pacemaker. Pharmacopsychiatry 2000 33(4) 150-2. 

During an episode of lithium toxicity (serum concentration 3.86 mmol/1), a 42-year-old woman developed sinus bradycardia that required a temporary pacemaker (124). There was marked prolongation of sinus node recovery time. Lithium was withdrawn and the patient underwent hemodialysis once daily for 3 days sinus node recovery time normalized. The presence of nontoxic concentrations of carbamazepine may have contributed to the condition. 

Heart block is the most serious consequence of digitalis poisoning and should be anticipated by the insertion of a temporary pacemaker. If this is postponed until heart block or dysrhythmias occur, there may be difficulty in inserting the pacemaker (because of ventricular excitability), and delay in treatment can be deleterious. 

Timolol was withheld and a temporary pacemaker was inserted. Rechallenge with timolol was associated with recnrrence of third-degree AV block. She subseqnently had a permanent dnal chamber pacemaker implanted. 

Devices that contact circulating blood (intravascular catheters, temporary pacemaker electrodes, oxygenators, dialyzers,... 

Repeated doses of activated charcoal may enhance elimination. Serum electrolytes should be monitored in all serious exposures. Intravenous administration of sodium bicarbonate may decrease toxicity. Hypotension can be treated with fluids and vasopressors if needed. Ventricular dysrhythmias can be treated with class IB antiarrhythmics such as phenytoin or lido-caine. Persistent bradycardia and third-degree heart block are indications for insertion of a temporary pacemaker. Seizures can be treated with diazepam. If seizures are uncontrolled, phenobarbital or phenytoin can be administered. 

Serious ingestions require cardiac monitoring in an intensive-care setting. Hypotension may be resistant to dopamine and dobutamine. Norepinephrine can also be used. Bradycardia can be treated with atropine and a temporary pacemaker as needed. Digoxin-specific FAB antibody fragments have been used with some success for cardiac conduction abnormalities after a yew exposure. If no contraindication, lido-caine, amiodarone, or procainamide may be used for ventricular dysrhythmias. 

Patients may present with a slow ventricular response (in the absence of AV nodal-blocking drugs) and thus do not require therapy with digoxin, verapamil, or esmolol. This type of presentation should alert the clinician to the possibility of preexisting SA or AV nodal conduction disease such as sick sinus syndrome. DCC should not be attempted in these patients without a temporary pacemaker in place (see below). 

Treat bradycardia or heart block with atropine, 0.5-2 mg IV (see p 412) a temporary pacemaker may be needed for persistent symptomatic bradycardia. 

Two patients with supraventricular tachycardia (180 bpm) were treated, firstly with intravenous practolol (20 and 10 mg respectively) and shortly afterwards with disopyramide (150 and 80 mg respectively). The first patient rapidly developed sinus bradycardia of 25 bpm, lost consciousness and became profoundly hypotensive. He did not respond to 600 micrograms of atropine, but later his heart rate increased to 60 bpm while a temporary pacemaker was being inserted. He was successfully treated with disopyramide 150 mg alone for a later episode of tachycardia. The second patient also developed severe bradycardia and asystole, despite the use of atropine. He was resuscitated with adrenaline (epinephrine) but later died. ... 

An elderly man with long standing brady-tachycardia was successfully treated for atrial flutter firstly with a temporary pacemaker (later withdrawn) and 600 mg amiodarone daily. Ten days later, and 25 minutes after a permanent pacemaker was inserted under local anaesthesia with 15 mL of 2% lidocaine, severe sinus bradycardia and long sinoatrial arrest developed. He was effectively treated with atropine plus isoprenaline, and cardiac massage. ... 

A 63-year old woman developed torsade de pointes arrhythmia and was found to have a prolonged QT interval after taking astemizole and ketoconazole. These two drugs were withdrawn and she was successfully treated with a temporary pacemaker, magnesium sulphate and lidocaine. She was later discharged with a normal ECG. ... 

Erythromycin. An 87-year-old woman collapsed suddenly in her kitchen 4 days after starting to take astemizole 10 mg daily and erythromycin twice daily [dose unknown]. An ECG showed her to be having multiple episodes of torsade de pointes arrhythmias, the longest of which lasted 17 seconds. Her QTc was 720 milliseconds and she was mildly hypoka-laemic. She was given a temporary pacemaker and when she was eventually discharged with a normal sinus rhythm, her QTc had fallen to 475 milliseconds. ... 

In all patients, we prefer positioning a temporary pacemaker through the left femoral vein, leaving the right one available for ICE or transfemoral workstation, if required. The temporary PM should be placed far from the permanent lead tip, reducing the risk of displacement during dilatation. 

At the end of the procedure, we prefer to position a temporary PM from the ipsilateral subclavian vein before removing the femoral one, because this permits leg motion and reduces the profound venous thrombosis risk. This is particularly important in patients who need to wait some days before attending a new reimplantation procedure. We usually maintain the temporary pacemaker for at least 24 h, even if the patient s spontaneous rhythm is adequate. We prefer its removal at the end of the procedure only in case of single-day extraction/reimplantation procedures. 

Fig. 7.6 Sensitivity testing. The pacing rate is set to a rate less than the intrinsic ventricular rate and the sensitivity dial is slowly adjusted. With the sensitivity set to 7mV, the first QRS complex is sensed by the temporary pacemaker and causes inhibition of the pacing output. With the sensitivity set to 8 mV (which reduces sensitivity) the second QRS complex (arrow) is not sensed and the pacemaker delivers a pacing output at the programmed rate. The pacemaker then begins to output asynchronously the second pacing stimulus does not result in ventricular capture because it is delivered during the ventiicular refractory period. In this case the intrinsic ventricular electrogram has an amplitude between 7 and 8 mV. If no intrinsic ventricular rhjrthm is present, sensitivity testing cannot be performed.

Fig. 7.8 Chest radiograph of a patient requiring long-term temporary pacing using an active fixation permanent pacing lead with the lead tip (black arrow) in the right ventricular apex and the proximal lS-1 lead connector (white arrow) seen outside the body attached to a temporary pacemaker.

Hynes JK, et al. Eive-year experience with temporary pacemaker therapy in the coronary care unit. Mayo Clin Proc 1983 58 122. 

Prophylactic Temporary Pacemaker Insertion. Approximately 1% of patients with acute myocardial infarction develop a Type n second-degree AV block. Although this rhythm is often tolerated hemodynamically, because there can be sudden progression to complete AV block, temporary pacing should be considered. New bundle-branch block (BBB) has been associated with an 18% risk of transient complete AV block (9-11). The development of BBB usually signifies an extensive infarction, typically involving the anterior wall. Death in these patients usually results from left ventricular pump failure, although 9% of deaths have been attributable to complete AV block (9). 

Teach patient about temporary pacemaker, if indicated. 

A potential case of an interaction between quinidine and flucloxacillin was demonstrated in a 63-year-old patient with recently diagnosed dilated cardiomyopathy who was admitted to the hospital with polymorphic ventricular tachycardia and ventricular fibrillation episodes induced by bradycardia. The patient was on a heart failure regimen of furosemide, spironolactone and perindopril, and was initiated on oral quinidine in the hospital for the prevention of ventricular arrhythmias. The patient s temporary pacemaker lead was removed and an implantable cardioverter-defibrillator was placed due to continued ventricular fibrillation. The next day, the patient became febrile. Culture of pacemaker lead tip and blood cultures were positive for S. aureus. Flucloxacillin and rifampin were initiated, but rifampin was discontinued due to the development of renal insufficiency and liver test abnormalities. These were normalised after rifampin was discontinued. The patient required continuous pacing to prevent ventricular tachycardia episodes, and quinidine was increased to 2800 mg per day (maximum daily dose). Quinidine plasma levels were subtherapeutic at 1.1 mg/L. The authors speculate that this interaction was due to quinidine being a substrate of Pgp and CYP3A4, and flucloxacillin s ability to induce these enzymes. While this may be a potential mechanism, the authors do not comment on how long the patient received rifampin. Rifampin is also a CYP3A4 inducer and could have been parf of fhe reason for fhe decrease in quinidine level [46 ]. 

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