Normal Cardiac Rhythm

Action potentials recorded from various cardiac cells may vary somewhat from the action potential described previously. Some cells, for instance, totally lack phase 1 and have a slower phase 0. Such cells are said to have a slow response as opposed to the fast response just described. Also, action potentials from the nodal cells (see the next section, Normal Cardiac Rhythm ) differ somewhat from the fast response cells. Nonetheless, the fundamental ionic fluxes occurring during cardiac action potentials are similar in all cardiac cells. This ionic activity is pharmacologically significant because various antiarrhythmic drugs will affect the movement of sodium and other ions in an attempt to establish and maintain normal cardiac rhythm. 

Certain cardiac cells are able to initiate and maintain a spontaneous automatic rhythm. Even in the absence of any neural or hormonal input, these cells will automatically generate an action potential. They are usually referred to as pacemaker cells in the myocardium. Pacemaker cells have the ability to depolarize spontaneously because of a rising phase 4 in the cardiac action potential (see Fig. 23-1). As described previously, the resting cell automatically begins to depolarize during phase 4 until the cell reaches threshold and an action potential is initiated. 

Pacemaker cells are found primarily in the sinoatrial (SA) node and the atrioventricular (AV) node (Fig. 23-2). Although many other cardiac cells also have the ability to generate an automatic rhythm, the pacemaker cells in the SA node usually dominate and control cardiac rhythm in the normal heart. 

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An arrhythmia can be broadly defined as any significant deviation from normal cardiac rhythm.6 Various problems in the origination and conduction of electrical activity in the heart can lead to distinct types of arrhythmias. If untreated, disturbances in normal cardiac rhythm result in impaired cardiac pumping ability, and certain arrhythmias are associated with cerebrovascular accidents, cardiac failure, and other sequelae that can be fatal.1,2 16 Fortunately, a variety of drugs are available to help establish and maintain normal cardiac rhythm. 

In a retrospective review of all dysrhythmias in children with prenatal cocaine exposure, 18 cases were detected in 554 infants who had positive urine screens for cocaine (318). In 13 neonates the dysrhythmia occurred beyond the period of direct cocaine exposure and six of the children had dysrhythmias after the neonatal period. Most of the dysrhythmias were supraventricular extra beats. Overall, the rate of consultations for dysrhythmias was higher among cocaine-exposed neonates than expected. Some cocaine-exposed children had symptomatic dysrhythmias that were persistent or recurrent and required treatment to maintain cardiac output and restore normal cardiac rhythm. Children who were exposed prenatally to cocaine appeared to be at increased risk of abnormal responses to stress, manifested by symptomatic dysrhythmias beyond the period of cocaine exposure. 

The cardiac conduction system of the horse shares many features with other species but also has some important differences. The function of the heart relies upon the presence of cells capable of spontaneous activity these form the pacemaker areas of the heart. These nodal areas generate the normal cardiac rhythm. The electrical activity of the... 

Antidysrhythmics restore normal cardiac rhythm in cardiac dysrhythmias. Cardiac dysrhythmia (arrhythmia) is deviation from the cardiac rate. These deviations are ... 

Antidysrhythmics are drugs that restore normal cardiac rhythm and are used to treat cardiac dysrhythmias. A cardiac dysrh5dhmia is a disturbed heart ihythm. It is also known as arrhythmia—absence of heart ihythm. A disturbed heart rhythm is any deviation from the normal heart rate or heart pattern including slow rates (bradycardia) and fast rates (tachycardia). The electrocardiogram (ECG) is used to identify the type of dysrhythmia. 

Here s an outline of many common cardiac arrhythmias and their features, causes, and treatments. Use a normal electrocardiogram strip, if available, to compare normal cardiac rhythm configurations with the rhythm strips shown here. Characteristics of normal sinus rhythm include the following ... 

Cardiac arrhythmias or dysrhythmias are disturbances of the normal regular rhythm which may be caused by an abnormality in the site of impulse generation, its rate or regularity, or its propagation or conduction (1,2). The more commonly encountered cardiac arrhythmias are... 

Mechanism of Action A cardiac agent that slows impulse formation in the SA node and conduction time through the AV node. Adenosine also acts as a diagnostic aid in myocardial perfusion imaging or stress echocardiography. Therapeutic Effect Depresses left ventricular function and restores normal sinus rhythm. 

Unlabeled Uses Control of hemodynamicallystableventriculartachycardia, control of rapid ventricular rate due to accessory pathway conduction in preexcited atrial arrhythmias, conversion of atrial fibrillation to normal sinus rhythm, in cardiac arrest with persistent ventricular tachycardia or ventricular fibrillation, paroxysmal supraventricular tachycardia, polymorphic ventricular tachycardia or wide complex tachycardia of uncertain origin, prevention of postoperative atrial fibrillation... 

D 10 Cardiac resynchronization if wide QRS interval is present in normal sinus rhythm... 

Digoxin is indicated in patients with heart failure and atrial fibrillation. It is also most helpful in patients with a dilated heart and third heart sound. It is usually given only when diuretics and ACE inhibitors have failed to control symptoms. Only about 50% of patients with normal sinus rhythm (usually those with documented systolic dysfunction) will have relief of heart failure from digitalis. Better results are obtained in patients with atrial fibrillation. If the decision is made to use a cardiac glycoside, digoxin is the one chosen in most cases (and the only one available in the USA). When symptoms are mild, slow loading (digitalization) with 0.125-0.25 mg per day is safer and just as effective as the rapid method (0.5-0.75 mg every 8 hours for three doses, followed by 0.125-0.25 mg per day). 

Patients with normal sinus rhythm and a wide QRS interval, eg, greater than 120 ms, have impaired synchronization of ventricular contraction. Poor synchronization of left ventricular contraction results in diminished cardiac output. Resynchronization, with left ventricular or biventricular pacing, has been shown to reduce mortality in patients with chronic heart failure who were already receiving optimal medical therapy. 

Abnormal impulse generation. The normal automatic rhythm of the cardiac pacemaker cells has been disrupted. Injury and disease may directly render the SA and AV cells incapable of maintaining normal rhythm. Also, cells that do not normally control cardiac rhythm may begin to compete with pacemaker cells, thus creating multiple areas of automaticity. 

Quinidine is used for the maintenance of normal sinus rhythm in patients with atrial flutter or fibrillation. It is also used occasionally to treat patients with ventricular tachycardia. Because of its cardiac and extracardiac side effects, its use has decreased considerably in recent years and is now largely restricted to patients with normal (but arrhythmic) hearts. In randomized, controlled clinical trials, quinidine-treated patients are twice as likely to remain in normal sinus rhythm compared with controls. However, drug treatment was associated with a twofold to threefold increase in mortality. 

Tikosyn Dofetilide 125, 250, 500 (jig Capsule Maintenance of normal sinus rhythm and conversion of atrial fibrillation/ flutter Cardiac ion channel blocker/ antiarrhythmic drug MCC, corn starch, silicon dioxide, magnesium stearate Pfizer... 

Intravenous lidocaine has been used to treat severe chronic daily headache in 19 patients (three men, median age 37 years) (9). There were adverse effects during four infusions of lidocaine hyperkalemia (6.4 mmol/1), which did not resolve after withdrawal of lidocaine transient hypotension (75/50 mmHg), which was attributed to concomitant droperidol an unspecified abnormality of cardiac rhythm and on another occasion a transient bradycardia and chest pain with a normal electrocardiogram, fever, and intractable nausea. The study was neither randomized nor placebo-controlled, and in no case was the adverse event strongly associated with the administration of lidocaine. 

A 65-year-old woman, who had had normal preoperative serum electrolytes and a normal QT interval with sinus rhythm, received hydroxyzine and atropine premedication followed by thiopental and vecuronium for anesthetic induction. Endotracheal intubation was difficult and precipitated atrial fibrillation, which was refractory to disopyramide 100 mg. Anesthesia was then maintained with sevoflurane 2% and nitrous oxide 50%. Ten minutes later ventricular tachycardia ensued, refractory to intravenous lidocaine, disopyramide, and magnesium. DC cardioversion resulted in a change to a supraventricular tachycardia, which then deteriorated to torsade de pointes. External cardiac massage and further DC cardioversion were initially unsuccessful, but the cardiac rhythm reverted to atrial fibrillation 10 minutes after the sevoflurane was switched off. Two weeks later she had her operation under combined epidural and general anesthesia, with no changes in cardiac rhythm. 

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