Pacemaker failure

In one patient carbamazepine caused pacemaker failure until the pacemaker was adjusted, no doubt because of its effects on cardiac conduction (SEDA-18, 62). 

Life-threatening hazard If a client was at risk of death due to the adverse reaction or if it is suspected that continued use of a product could cause death (e.g., pacemaker failure of an intravenous pump that could cause excessive drug dosing)... 

Gould L, Patel S, Gomes GI, Chokshi AB. Pacemaker failure following external defibrillation. Pacing Clin Electrophysiol 1981 4 575-577. 

Souliman SK, Christie J. Pacemaker failure induced by radiotherapy. Pacing Clin Electrophysiol 1994 17 270-273. 

Quertermous T, Megahy MS, Das Gupta DS, Griem ML. Pacemaker failure resulting from radiation damage. Radiology 1983 148 257-258. 

These three cases illustrate the importance of sleep studies in respiratory failure patients receiving EPR. Such studies are able to deteet pacemaker failure as well as upper airway obstruction. Patients with idiopathic primaiy hypoventilation may still maintain adequate gas exchange during wakefulness, even with dysfunctional pacers, but at night in the absence of cues to breathing, a sleep study will show a very different picture. 

Cardiac pacemaker failures within five feet (some instances of failures out to 100 feet)... 

Ivabradine is used in the treatment of angina in patients in normal sinus rhythm. It acts on the sinus node resulting in a reduction of the heart rate. It is contraindicated in severe bradycardia (heart rate lower than 60 beats/ minute), cardiogenic shock, acute myocardial infarction, moderate-to-severe heart failure, immediately after a cerebrovascular accident, second and third-degree heart block and patients with unstable angina or a pacemaker. Side-effects include bradycardia, first-degree heart block, ventricular extrasystoles, headache, dizziness and visual disturbances, including blurred vision. 

Cardiostimulation. By stimulating Pi-receptors, hence activation of ade-nylatcyclase (Ad-cyclase) and cAMP production, catecholamines augment all heart functions, including systolic force (positive inotropism), velocity of shortening (p. clinotropism), sinoatrial rate (p. chronotropism), conduction velocity (p. dromotropism), and excitability (p. bathmotropism). In pacemaker fibers, diastolic depolarization is hastened, so that the firing threshold for the action potential is reached sooner (positive chronotropic effect, B). The cardiostim-ulant effect of p-sympathomimetics such as epinephrine is exploited in the treatment of cardiac arrest Use of p-sympathomimetics in heart failure carries the risk of cardiac arrhythmias. 

Secondary hypotension is a sign of an underlying disease that should be treated first. If stroke volume is too low, as in heart failure, a cardiac glycoside can be given to increase myocardial contractility and stroke volume. When stroke volume is decreased due to insufficient blood volume, plasma substitutes will be helpful in treating blood loss, whereas aldosterone deficiency requires administration of a mineralocor-ticoid (e.g., fludrocortisone). The latter is the drug of choice for orthostatic hypotension due to autonomic failure. A parasympatholytic (or electrical pacemaker) can restore cardiac rate in bradycardia. 

Patients with decompensated cardiac failure requiring the use of IV inotropic therapy (such patients should first be weaned from IV therapy before initiating carvedilol) bronchial asthma (see Warninas) or related bronchospastic conditions second- or third-degree AV block sick sinus syndrome or severe bradycardia (unless a permanent pacemaker is in place) cardiogenic shock clinically manifest hepatic impairment hypersensitivity to the drug. 

Ideally, if symptomatic sinus node dysfunction occurs in the presence of drugs known to impair sinus node function, the first treatment is to discontinue the offending drug [29]. However, this is typically not feasible in patients with heart failure who are dependent on several medications to improve long-term outcomes, or may need antiarrhythmic drug therapy for symptomatic arrhythmias. Accordingly, the treatment usually becomes a question of whether to apply pacing to increase heart rate. This is further complicated by the appropriate pacemaker prescription once the decision to pace has been made. 

CRT is now recommended for patients with LVEF less than or equal to 35%, sinus rhythm, and NYHA functional class III or ambulatory class IV symptoms despite recommended, optimal medical therapy and who have cardiac dyssynchrony, which is currently defined as a QRS duration greater than 0.12 ms, unless contraindicated. To date, over 4,000 patients have been studied in randomized clinical trials of CRT. A recent evaluation of complications from those studies suggest a risk of implant mortality of 0.4%, failure to implant a functioning LV lead in 10%, lead malfunction or dislodgement in 8.5%, and pacemaker infection in 1.4% [123]. 

Saxon LA, Stevenson WG, Middlekauff HR, Stevenson LW. Increased risk of progressive hemodynamic deterioration in advanced heart failure patients requiring permanent pacemakers. Am. Heart J. 1993 125 1306-10. 

Oguz E, Dagdeviren B, Bilsel T, et al. Echocardio-graphic prediction of long-term response to biventricular pacemaker in severe heart failure. Eur. J. Heart Fail. 2002 4 83-90. 

Contraindications Bronchial asfhma, cardiogenic shock, prolonged QT syndrome (unless funcfioning pacemaker is presenf), second- and fhird-degree hear block, sinus bradycardia, unconfrolled cardiac failure... 

Direct effects on the heart are determined largely by Bi receptors, although B2 and to a lesser extent a receptors are also involved, especially in heart failure. Beta-receptor activation results in increased calcium influx in cardiac cells. This has both electrical and mechanical consequences. Pacemaker activity—both normal (sinoatrial node) and abnormal (eg, Purkinje fibers)—is increased (positive chronotropic effect). Conduction velocity in the atrioventricular node is increased (positive dromotropic effect), and the refractory period is decreased. Intrinsic contractility is increased (positive inotropic effect), and relaxation is accelerated. As a result, the twitch response of isolated cardiac muscle is increased in tension but abbreviated in duration. In the intact heart, intraventricular pressure rises and falls more rapidly, and ejection time is decreased. These direct effects are easily demonstrated in the absence of reflexes evoked by changes in blood pressure, eg, in isolated myocardial preparations and in patients with ganglionic blockade. In the presence of normal reflex activity, the direct effects on heart rate may be dominated by a reflex response to blood pressure changes. Physiologic stimulation of the heart by catecholamines tends to increase coronary blood flow. 

Procainamide INa (primary) and IKr (secondary) blockade Slows conduction velocity and pacemaker rate prolongs action potential duration and dissociates from INa channel with intermediate kinetics direct depressant effects on sinoatrial (SA) and atrioventricular (AV) nodes Most atrial and ventricular arrhythmias drug of second choice for most sustained ventricular arrhythmias associated with acute myocardial infarction Oral, IV, IM eliminated by hepatic metabolism to /V-acetylprocainamide (NAPA see text) and renal elimination NAPA implicated in torsade de pointes in patients with renal failure Toxicity Hypotension long-term therapy produces reversible lupus-related symptoms... 

Medications such as P-blockers, calcium channel blockers, digoxin, and amiodarone can be used to control cardiac conduction abnormalities (arrhythmias), and a pacemaker may be inserted to combat heart failure. The general supportive care measures used in acute stroke syndromes also should be followed. Death in patients with MELAS is usually the result of cardiac failure, pulmonary embolus, or renal failure. 

The advantages of this type of battery are its very low rate of self-discharge and its extremely high reliability. Although it has been used in tens of thousands of cardiac patients over more than a decade, there has not been a single case of failure causing internal injury of any kind. For the very special requirement of heart pacemakers the... 

Amiodarone and carvedilol have been used in combination in 109 patients with severe heart failure and left ventricular ejection fractions of 0.25 (16). They were given amiodarone 1000 mg/week plus carvedilol titrated to a target dose of 50 mg/day. A dual-chamber pacemaker was inserted and programmed in back-up mode at a basal rate of 40. Significantly more patients were in sinus rhythm after 1 year, and in 47 patients who were studied for at least 1 year the resting heart rate fell from 90 to 59. Ventricular extra beats were suppressed from 1 to 0.1/day and the number of bouts of tachycardia over 167 per minute was reduced from 1.2 to 0.3 episodes per patient per 3 months. The left ventricular ejection fraction increased from 0.26 to 0.39 and New York Heart Association Classification improved from 3.2 to 1.8. The probability of sudden death was significantly reduced by amiodarone plus carvedilol compared with 154 patients treated with amiodarone alone and even more so compared with 283 patients who received no treatment at all. However, the study was not randomized, and this vitiates the results. The main adverse effect was s)mptomatic bradycardia, which occurred in seven patients two of those developed atrioventricular block and four had sinoatrial block and/or sinus bradycardia one patient developed slow atrial fibrillation. 

A 64-year-old woman with systemic lupus erythematosus took chloroquine for 7 years (cumulative dose 1000 g). She developed sjmcope, and the electrocardiogram showed complete heart block a permanent pacemaker was inserted. The next year she presented with biventricular cardiac failure, skin hyperpigmentation, proximal muscle weakness, and chloroquine retinopathy. Coronary angiography was normal. An echocardiogram showed a restrictive cardiomyopathy. A skeletal muscle biopsy was characteristic of chloroquine myopathy. Chloroquine was withdrawn and she improved rapidly with diuretic therapy. 

Encainide has been reported to cause sinus node arrest in association with prolonged sinus node recovery time (19). It also raises the pacing threshold in patients with chronic implanted pacemakers (20), although this has not been reported to increase the failure rate of pacemakers. 

A 64-year-old man without heart failure was found dead 18 hours after a single infusion of infliximab for rheumatoid arthritis (62). No obvious cause was found at autopsy, except that the patient was known to have had frequent intervention by a pacemaker that had been implanted for several years. 

Recent studies demonstrate that cardiac resynchronization therapy (CRT) offers a promising approach to selected patients with chronic heart failure. Delayed electrical activation of the left ventricle, characterized on the ECG by a QRS duration that exceeds 120 ms, occurs in approximately one-third of patients with moderate to severe systolic heart failure. Since the left and right ventricles normally activate simultaneously, this delay results in asynchronous contraction of the left and right ventricles, which contributes to the hemodynamic abnormalities of this disorder. Implantation of a speciahzed biventricular pacemaker to restore synchronous activation of the ventricles can improve ventricular contraction and hemodynamics. Recent trials show improvements in exercise capacity, NYHA classification, quality of life, hemodynamic function, and hospitalizations. A device that combined CRT with an implantable cardioverter-defibrillator (ICD) improved survival in addition to functional status. CRT is currently indicated only in NYHA class ni-IV patients receiving optimal medical therapy (ACE inhibitors, diuretics, -blockers, and digoxin) and... 

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