Heart pacing, temporary

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. 

Following septal ablation, patients should be monitored in a coronary care unit for 24 to 48 hours and the temporary pacing wire should be removed at the end of this period in the absence of atrioventricular block. Patients may then be transferred to a telemetry unit for monitoring of arrhythmias. Total hospitalization is usually for three to five days to monitor for occurrence of complete heart block that would require a permanent pacemaker. A sizeable infarction is induced with alcohol ablation and causes creatinine phosphokinase to peak at 1000 to 1500 one day after the ablation. Patients should be maintained on aspirin indefinitely. 

After venous access, some consideration should be given to the sequence of lead placement. Some operators prefer to place the RV electrode first for emergency RV pacing, should heart block ensue because the heart failure patients commonly have a left bundle branch block and any trauma to the conduction system or right bundle may result in complete heart block. Other operators choose to place the coronary sinus lead first and, if necessary, depend on heart rate support via a temporary transvenous pacemaker placed via the femoral vein. The issue of failure speaks for placing the coronary sinus lead first. Should the procedure fail with unsuccessful left-sided left ventricular lead placement and the patient has already received right-sided electrodes, a pacing system may be left without an indication unless a future second attempt is considered. As more and more systems are placed for a primary prevention indication like MADIT II, this has become less problematic (153). 

Pandian NG, et al. Transfemoral temporary pacing and deep venous thrombosis. Am Heart J 1980 100 847. 

Lever N, Ferguson JD, Bashir Y, Channon KM. Prolonged temporary pacing using subcutaneous tunneled axtive-fixation permanent pacing leads. Heart 2003 89 209-210. 

Del Nido P, et al. Temporary epicardial pacing after open heart surgery complications and prevention. J Cardiac Surg 1989 4 99. 

Isoproterenol increases heart rate due to nonselective pi/p2-a0renoceptor agonist actions, thereby shortening the QT interval and the effective refractory period. While there are no randomized controlled trials of isoproterenol use for torsades in humans (it has prevented quinine-induced torsades in a dog model), occasional case reports suggest benefit (Omar et al. 2014). It is probably particularly useful as a bridge to temporary pacing in patients unresponsive to magnesium sulfate. 

In a prospective study of 42 patients (33 men median age 49 years) who had been hospitalized with mad honey intoxication, all had nausea, vomiting, dizziness, fainting, and sweating five had syncope [106"]. The mean blood pressure was 73/52 mmHg and the mean heart rate 38/minute 18 had sinus bradycardia, 15 had complete atrioventricular block, and nine had nodal rhythm. None needed temporary pacing and all were discharged without complications. 

Management Muscarinic M2 receptors in the vagus are involved in the cardiotoxicity of grayanotoxin [112", 113" ], and bradycardia and heart block in these cases respond to atropine, as in toxicity with vera-trum alkaloids. However, temporary pacing may sometimes be required [114 ]. 

Management Solution (i) Advanced cardiac life support (ACLS) protocol for complete heart block (CHB) and (ii) turn off tachycardia therapies (iii) turn on temporary pacing in a VOO mode if available (iv) if temporary VOO pacing not available or ineffective, then continue ACLS protocol for CHB as a bridge to emergent reoperation to tighten set screw. 

In extreme cases, if all other therapies fail, temporary pacing should be considered as a viable option [28]. In the case of irreversible third-degree heart block the placement of a pacemaker may be needed. 

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 ]. 

RED FLAG All invasive temporary pacing has the potential to deliver a shock directly to the heart along the pacing wire, resulting in ventricular tachycardia or fibrillation. 

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