Ventricular fibrillation pacemaker

Myocardial infarction (MI) is caused by the acute thrombotic occlusion of a coronary artery. The myocardial region that has been cut off from its blood supply dies within a short time owing to the lack of 02 and glucose. The loss in functional muscle tissue results in reduced cardiac performance. In the infarct border zone, spontaneous pacemaker potentials may develop, leading to fatal ventricular fibrillation. The patient experiences severe pain, a feeling of annihilation, and fear of dying. 

Four prisoners drank a decoction of yew needles (T. baccata) (12). Two died in prison with cardiac arrest. One went into deep coma, and had several episodes of ventricular fibrillation, controlled by defibrillation after return of consciousness his general condition deteriorated suddenly, he lost consciousness again, his circulation stopped, and he died on the fourth day. The other patient drank a much smaller amount of the decoction he was conscious, had bradycardia requiring transient pacemaking, and had a mild ventricular dysrhythmia he recovered after 10 days. In both cases there was excessive diuresis and severe hypokalemia and atropine was effective for a short time in the control of bradycardia. 

Cardiovascular System Following systemic absorption, local anesthetics decrease electrical excitabdity, conduction rate, and force of contraction. Most local anesthetics also cause arteriolar dilation. Untoward cardiovascular effects usually are seen only after high systemic concentrations are attained and effects on the CNS are produced. However, on rare occasions, lower doses of some local anesthetics wUl cause cardiovascular collapse and death, probably due to either an action on the pacemaker or the sudden onset of ventricular fibrillation. Ventricular tachycardia and fibrillation are relatively uncommon consequences of local anesthetics other than bupivacaine. The use of local anesthetics as antiarrhythmic drugs is discussed in Chapter 34. Untoward cardiovascular effects of local anesthetic agents may result from their inadvertent intravascular administration, especially if epinephrine also is present. 

Pacemakers are used for cKents in symptomatic sinus bradycardia or asystole. This client is in ventricular fibrillation therefore, the nnrse wonld qnestion this order. 

The implantable cardioverter defibrillator (ICD) is a cardiac pacemaker. It can be used to pace one or both chambers on the right side of the heart It has an additional feature, though. ICDs can also impart powerful shocks to the heart if it is beating too fast (tachycardia) or goes into ventricular fibrillation. Either condition means that blood cannot be pumped very efficiently, if at all. A number of major clinical studies were done that identified various categories of heart patients who could benefit from the therapies delivered by devices like the ICD. 

Vulnerability to ventricular arrhythmias. There is the theoretical risk of ventricular fibrillation whenever a pacemaker stimulus is delivered into the vulnerable period of the ventricle. Experimentally, the ventricular fibrillation threshold is lower with bipolar stimulation than with conventional unipolar cathodal stimulation. Despite these laboratory observations, no clinical differences between permanent unipolar and bipolar systems have been reported with respect to the risk of inducing ventricular arrhythmias. 

Fig. 20.8 Top Noise detected on the ventricular channel leads to false detection of ventricular fibrillation. Bottom Daily monitoring of lead impedance in the same patient shows a sudden increase in resistance. In this case the patient was notified remotely via a home monitoring system and came to the pacemaker clinic before an inappropriate shock was delivered.

Defibrillation serves to counteract ventricular fibrillation, i.e. to re establish the correct heartbeat. Pacemaker batteries, e.g., are checked 100% during several weeks at 37 °C (body temperature) for their function and are only then released for service. 

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 ]. 

Contraindications Atrial fibrillation or flutter, second-or third-degree AVblock or sick sinus syndrome (with functioning pacemaker), ventricular tachycardia... 

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. 

Sweeney MO, Hellkamp AS, Ellenbogen KA, et al. Adverse effect of ventricular pacing on heart failure and atrial fibrillation among patients with normal baseline QRSd in a clinical trial of pacemaker therapy for sinus node dysfunction. Circulation 2003 23 2932-7. 

Pacing in the right ventricle can have deleterious effects in terms of the development of heart failure and atrial fibrillation. This has led to the development of algorithms that minimize ventricular pacing in patients whose bradycardia is because of the dysfunction of their sinus node (which functions as the heart s natural pacemaker), rather than the dysfunction of their heart s intrinsic conduction system. Excellent discussions of this issue and other sophisticated pacemaker algorithms can be found in Al-Ahmad et al. (2010). 

Another use for defibrillators is to shock either atrial flutter or fibrillation, which are abnormally rapid atrial rhythms. These atrial rhythms are much less likely to spontaneously proceed rapidly to death than ventricular arrhythmias. Using electrical shock to treat rapid heart arrhythmias other than VF is usually referred to as cardioversion and hence some users refer to the tachycardia treatment devices as cardioverter—defibrillators. Cardiovertor and defibrillator treatment is different from pacemaker treatment (discussed elsewhere in this book) because a pacemaker stimulates a slowly beating heart and uses much weaker shocks. Pacemaking increases the rate of the relatively healthy heart, which increases blood flow. 

An implanted medical device that functions as a pacemaker and is also capable of delivering high energy shocks to the heart to treat ventricular tachycardia (abnormally fast heart rate) and fibrillation. 

If the procedure is to proceed in a smooth and expeditious fashion, careful preoperative planning is essential. The first such decision is whether the patient requires a single-chamber or dual-chamber pacemaker. As a rule, if the patient has intact atrial function, every effort is made to preserve atrial and ventricular relationships. Single-chamber ventricular pacing is usually reserved for the patient with chronic atrial fibrillation or atrial paralysis. A device is selected with acceptable size, longevity, and progranunability. If the heart is chronotropically incompetent, a device that offers some form of rate adaptation... 

Stambler BS, Ellenbogen KA, Zhang X, et al. Right ventricular outflow versus apical pacing in pacemaker patients with congestive heart failure and atrial fibrillation. J Cardiovas Electrophysiol 2003 14 1180. 

The only effective treatment for symptomatic sinus node dysfunction is cardiac pacing. Despite two decades of clinical investigation, the optimal pacing mode, pacing system and site of ventricular stimulation for bradycardia support for sinus node dysfunction remain uncertain. Selection of pacing mode may be important for the clinical outcomes of quality of life, pacemaker syndrome, atrial fibrillation, heart failure, thromboembolism, and mortality in patients with sinus node dysfunction. 

Stambler BS, Ellenbogen KA, Orav EJ, Sgarbossa EB, Estes NA, Rizo-Patron C, Kirchhoffer JB, Hadjis TA, Goldman L, Lamas GA. Predictors and clinical impact of atrial fibrillation after pacemaker implantation in elderly patients treated with dual chamber versus ventricular pacing. Pacing Clin Electmphysiol. 

Fig. 12.1 The cumulative risk of developing atrial fibrillation according to the mode of cardiac pacing. Patients with an atrial or dual chamber pacemaker were significantly less likely to develop AF compared to patients receiving a ventricular pacemaker. Reprinted with permission from Kerr CR, Connolly SJ, Abdollah MB et al. Circulation 2004 109 357-62.

Fig. 12.2 An example of atrial fibrillation (AF) organizing into atrial flutter. A. The upper strip in the top panel demonstrates the atrial electrogram (EGM) and the lower strip demonstrates the annotated markers indicating how the pacemaker classifies each atrial and ventricular event as well as the cycle length (in ms) between each interval. The atrial electrogram shows the rapid irregular atrial rhythm which subsequently transitions into an organized atrial tachycardia. B. Atrial antitachycardia pacing (ATP) therapy - a burst train followed by two premature extrastimuli is delivered restoring atrial paced rhythm. The marker channel notations indicate how the device classifies each beat. Inter-beat intervals are also shown (in ms). AP - atrial paced event VP - ventricular paced event AR - atrial event sensed in atrial refractory period FS - AF sensed event TD - tachycardia detected TS - tachycardia sensed event. Courtesy AM Gillis.

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