Complex cardioversion?

[brock8024]

Well this is very interesting on many different levels. First off how can anyone just say well I am doing this and if you do not want me too say so now because I am doing it, well that is just wrong. I always try to explain to my patients what I am about to do to them. I do not care what their GCS is I still explain, just for the reason it is professional and they are a HUMAN. I think it is sad when we stop treating people like they are humans. In my classes we are taught that if someone calls you for a stubbed toe take them and treat them like they have a million dollars. We got into this not for the money but to help people. I have been told that if you are only in this for the trauma or the "good" calls where people are near dead or what ever then you are in this for the wrong reason. I mean some places run anywhere from 1 to 12 calls a shift but it is what we went to school for, so that is my rant on that. I think that every patient should have the treatments explained to them no matter what the mental state is.

As far as what to do to the pt it seems that we are damned if we do damned if we do not. One thing I did not notice was what a ECG showed, this can change things greatly. I would not give this patient adenocard just for the fact that I can not tell if it is A-fib or what ever. If I remember right it is a big no no to give adenocard to a patient in A-fib. Please correct me if I am wrong. I would start off with my ABC's and start either a NRB or explain that I am going to apply a BVM and assist his breathing. Again if I remember right you can assist ventilations on a consiouse patient, you just have to corridnate the breaths with them. Then I would figure out intubate or not to intubate. Yes the rate is a problem but we can think about two things at once, and if we ever get stumped ABC. As far as treating the rate I would run a ECG and try to figure out what is going on. I know there is a setting on the Lifepak 12 where you can speed the paper up making the tracing easier to interpret. I would for sure start a IV and NS tko for meds. I would start off with lasix if he could tolerate it, then MONA as long as the BP held up. As far as the rate I would let my ER doctor help me with that. I would call medical control and see what he wanted me to do. I do not know what protocols say about cardioverting but I would call the ER and let them know because there may be a better answer. Remember sometimes two heads or three heads are better than one. Plus if something happens I know have documentation that med control gave me the order. Takes some of the liability off me, which may be a good thing if the patient dies after you cardiovert them. I know one of my instructors said it looks bad if your patient has a pulse and loses it because of the treatment espicially if they could have made it to the ER with out the treatment. Remember ACLS guidelines are not set is stone they are just that GUIDELINES

Yes if they need cardioverting then why waste the time in giving pain meds or versed. Who cares they needed it. Well if you put 100J or 360J through me, I think my BP and anxiety is going to go through the roof and if it did not work with the fisrt 100J and then you tell me you have to go higher hell no. That is why you explain stuff to your patient. And it may take a few mins for the meds to work but if you shock them while it is working they may know what you are doing right then, but they might not remember after the meds take affect. I have seen doctors give a med not wait for it to work and re-set a bone or what ever and the patient wakes up later not remembering. Why because the med had time to do its job.

Ok enough with my rant and what I think. I am just a paramedic student that is all. I do not know anything but it is fun to pretend. LOL

Sorry for any spelling mistakes.

[firefighter523]

Guess what, If you see a supraventricular rhythm, and you cant tell if it is SVT or AFib, I don't think you would give a CCB before you would give adenosine!!! Adenosine is a natural occuring agent that will chemically convert PSVT to NSR. In the event that it doesn't, it will slow the Afib down so you can see it. Then you will treat accordingly!!!

[firefighter523]

Brock.................

Oh my God, I cant even think strait after reading the rest of your post. I hope you just started class!! Please don't come to PA!!!!

[brock8024]

Brock.................

Oh my God, I cant even think strait after reading the rest of your post. I hope you just started class!! Please don't come to PA!!!!

Umm I graduate in May. Is there something wrong with my post? Please tell me why I should not come to PA?

[brock8024]

http://www.blackwell-synergy.com/doi/abs/1....2000.tb00662.x

An 86-year-old female developed supraventricular tachycardia 36 hours after a myocardial infarction (MI). She developed atrial fibrillation and polymorphic ventricular tachycardia (PVT) following administration of 12 mg ofadenosine. The PVT caused hemodynamic instability with no response to cardioversion, but termination with procainamide. The heart is vulnerable to hemodynamically unstable, possibly lethal, PVT early after MI under some circumstances. This vulnerability may be exposed following administration of adenosine. Extra caution is warranted when using adenosine in the post-Mi period.

The link and article which I think is intersting.

http://www.aafp.org/afp/20020615/2479.html

Management of Common Arrhythmias: Part I. Supraventricular Arrhythmias

A. KESH HEBBAR, M.D., and WILLIAM J. HUESTON, M.D.

Medical University of South Carolina, Charleston, South Carolina

Family physicians frequently encounter patients with symptoms that could be related to cardiac arrhythmias, most commonly atrial fibrillation or supraventricular tachycardias. The initial management of atrial fibrillation includes ventricular rate control to provide adequate cardiac output. In patients with severely depressed cardiac output and recent-onset atrial fibrillation, immediate electrical cardioversion is the treatment of choice. Hemodynamically stable patients with atrial fibrillation for more than two days or for an unknown period should be assessed for the presence of atrial thrombi. If thrombi are detected on transesophageal echocardiography, anticoagulation with warfarin for a minimum of 21 days is recommended before electrical cardioversion is attempted. Patients with other supraventricular arrhythmias may be treated with adenosine, a calcium channel blocker, or a short-acting beta blocker to disrupt reentrant pathways. When initial medications are ineffective, radiofrequency ablation of ectopic sites is an increasingly popular treatment option. (Am Fam Physician 2002;65:2479-86. Copyright© 2002 American Academy of Family Physicians.)

A PDF version of this document is available. Download PDF now (8 pages / 129 KB). More information on using PDF files.

Heart palpitations and cardiac arrhythmias are common problems encountered by family physicians. Patients may present with acute cardiac rhythm abnormalities. Although these arrhythmias are usually benign, they can indicate significant underlying heart disease. More often, patients have chronic arrhythmias, such as atrial fibrillation, that may require treatment to reduce the risk of future complications. The challenges for the family physician are to determine which arrhythmias are benign and which indicate probable cardiac malfunction, and to manage recurrent or chronic rhythm abnormalities.

Atrial fibrillation is the most common cardiac arrhythmia family physicians are likely to encounter.

This two-part article reviews common atrial and ventricular arrhythmias, with a focus on initial management decisions. Part I discusses supraventricular arrhythmias. Part II discusses ventricular arrhythmias and the management of rhythm abnormalities in special populations, including pregnant women, athletes, and children.

Atrial Fibrillation

Atrial fibrillation is the most common cardiac arrhythmia family physicians are likely to encounter. This rhythm abnormality affects 3 to 5 percent of patients more than 60 years of age1 and becomes increasingly common with advancing age. The median age of patients with atrial fibrillation is 75 years, and the prevalence of the arrhythmia doubles every 10 years after the age of 55.2,3 In the United States, atrial fibrillation is estimated to affect almost 9 percent of patients more than 75 years of age.2

Most risk factors for atrial fibrillation are associated with structural or ischemic heart disease. Risk factors include hypertension, left ventricular hypertrophy, dilated and restrictive cardiomyopathies, coronary artery disease, chronic obstructive pulmonary disease, and diabetes in women.1

The annual risk of stroke in patients with atrial fibrillation and normal valve function has been reported to be 4.5 percent per year.4 Anticoagulation with warfarin (Coumadin) reduces the risk by about two thirds.4 The mortality rate for stroke in patients with atrial fibrillation is approximately twice as high as the rate in patients without this rhythm abnormality.5 Although anticoagulation is contraindicated in some elderly patients, a study in Great Britain6 found that about 60 percent of patients identified in community screenings as having atrial fibrillation were eligible for, and would benefit from, this treatment.

The annual risk of stroke in patients with atrial fibrillation and normal valve function has been reported to be 4.5 percent per year.

MANAGEMENT

The first step in managing a patient with atrial fibrillation is to decide whether there is a high likelihood of safe conversion to sinus rhythm or whether the patient should be allowed to remain in atrial fibrillation. A patient with recent onset of atrial fibrillation (within the previous 12 months) and no evidence of enlargement of the left atrium has a greater chance of achieving and maintaining sinus rhythm. If the arrhythmia is long-standing and the patient is not a suitable candidate for rate cardioversion, initial treatment should focus on ventricular rate control, with consideration given to long-term stroke prophylaxis.

Restoration of Sinus Rhythm. Patients who present within 48 hours of the onset of new atrial fibrillation are candidates for cardioversion with a low risk of embolism. Conversion to sinus rhythm can be attempted by electrical shock or with antiarrhythmic drugs. Patients who have been in atrial fibrillation for more than 48 hours or for an undetermined period are more likely to have atrial thrombi and may develop emboli with immediate electrical or medical (pharmacologic) cardioversion.

Atrial thrombi are not evident on transthoracic echocardiograms, but they can been seen on transesophageal echocardiograms.7 If the transesophageal echocardiogram reveals thrombi, anticoagulation is recommended before cardioversion is attempted. Anticoagulation can be accomplished using warfarin, with the dosage adjusted to achieve an International Normalized Ratio (INR) between 2.0 and 3.0 for a minimum of 21 days.8

If the transesophageal echocardiogram does not show thrombi on multiplane views, cardioversion can be attempted. Short-term anticoagulation with heparin should be started before the procedure, and warfarin therapy should be initiated after cardioversion.8

When rhythm conversion is indicated, it can be accomplished using direct-current cardioversion or pharmacologic therapy. Synchronized cardioversion is currently considered the treatment of choice for the restoration of sinus rhythm and, in appropriately selected patients, has a success rate of at least 80 percent.4 Cardioversion is also indicated in patients with hypotension, angina, heart failure, or other evidence of severe compromise caused by atrial fibrillation.5

Medical cardioversion of atrial fibrillation may be achieved with class IA drugs (quinidine, disopyramide [Norpace], procainamide [Procanbid]) or with amiodarone (Cordarone). In the past, quinidine was frequently used for both cardioversion and maintenance of sinus rhythm in patients who had undergone electrical cardioversion. However, because of the proarrhythmic action of class IA agents and their detrimental effects on left ventricular function, these drugs are now used less often than amiodarone for primary therapy of atrial fibrillation.4

Amiodarone therapy is successful in 86 percent of patients who have had atrial fibrillation for less than two years.4,9 Treatment is also effective in 40 to 60 percent of patients with long-standing atrial fibrillation that has been resistant to other agents and to electrical cardioversion.4 Amiodarone can be given in a dosage of 200 mg a day, which is lower than the dosages that have been associated with thyroid abnormalities and pulmonary fibrosis. Although there is little risk of toxicity when amiodarone is given in a low dosage, it is prudent to monitor patients for the development of thyroid, pulmonary, hepatic, and cardiac side effects.

Findings on the usefulness of various agents for the conversion of atrial fibrillation, based on the evidence-based practice program of the Agency for Healthcare Research and Quality, are summarized in Table 1.10 Although drugs such as digitalis preparations and sotalol (Betapace) are sometimes used for rate control, they are not effective for converting atrial fibrillation to sinus rhythm.10,11

TABLE 1

Medications for Converting Atrial Fibrillation to Sinus Rhythm

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Drug and class Usual oral dosing Odds ratio for conversion compared with placebo (95% CI)*

Flecainide (Tambocor): class IC 50 mg every 12 hours; increase by 50 mg per day every 4 days to maximum of 300 mg per day. 24.7 (CI: 9.0 to 68.3)

Ibutilide (Corvert) given IV, followed by dofetilide (Tikosyn) given orally: both class III Ibutilide: 0.01 mg per kg IV over 10 minutes; if first dose is not effective, give second infusion 10 minutes later (maximum dose: 1 mg).

Dofetilide: 0.1 to 0.5 mg every 12 hours 29.1 (CI: 9.8 to 86.1)

Disopyramide (Norpace): class IA 100 to 200 mg every 6 to 8 hours 7.0 (CI: 0.3 to 153)

Amiodarone (Cordarone): class III 800 to 1,600 mg per day for 7 to 14 days; then 200 to 400 mg per day as maintenance 5.7 (CI: 1.0 to 33.4)

Propafenone (Rythmol): class IC 150 mg every 12 hours; if needed, increase dose every 3 to 4 days to maximum of 300 mg every 12 hours. 4.6 (CI: 2.6 to 8.2)

Quinidines: class IA Quinidine sulfate (Quinidex): 400 mg every 6 hours

Quinidine gluconate (Quinaglute): 648 mg every 8 to 12 hours 2.9 (CI: 1.2 to 7.0)

--------------------------------------------------------------------------------

CI = confidence interval; IV = intravenous.

*--Odds ratio is expressed as the number of times conversion is more likely with drug compared with placebo.

Information from Management of new onset atrial fibrillation. Summary, evidence report/technology assessment: no. 12. Rockville, Md.: Agency for Healthcare Research and Quality, May 2000; AHRQ publication no. 00-E006. Retrieved April 23, 2002, from www.ahcpr. gov/clinic/epcsums/atrialsum.htm.

If external electrical cardioversion is unsuccessful and antiarrhythmic drug therapy fails, other measures can be used. However, these approaches are usually reserved for use in patients who cannot tolerate atrial fibrillation and patients who have associated systolic dysfunction. Techniques include internal electrical cardioversion through the application of electrical current to pulmonary veins via a transcatheter cathode4 and radiofrequency ablation of the atrioventricular node with insertion of a ventricular pacemaker.12 In addition, an implantable atrial defibrillator can be used to provide rapid cardioversion in patients with atrial fibrillation that cannot be controlled with medications.13

Rate Control in Chronic Atrial Fibrillation. In patients in whom rhythm conversion is not indicated or those who have new-onset atrial fibrillation with a rapid ventricular response, treatment may be needed to control the ventricular rhythm. Excessive ventricular rates may result in diminished cardiac output because of poor filling time, and in ischemia because of increased myocardial oxygen demand. Medications used for ventricular rate control in patients with atrial fibrillation are listed in Table 2.14

TABLE 2

Medications for Ventricular Rate Control in Atrial Fibrillation

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Drug Dosing Side effects and complications

Calcium channel blockers

Diltiazem (Cardizem) Acute IV: 0.25 mg per kg over 2 minutes; then 0.35 mg per kg after 15 minutes if needed; then 10 mg per hour in drip if needed Acute: heart block, CHF, hypotension (~3%)

Long-term: constipation

Oral maintenance: 180 to 240 mg per day

Verapamil (Calan) Acute IV: bolus of 5 to 10 mg over 2 minutes; may repeat 10 mg in 15 to 30 minutes Acute: heart block, CHF, hypotension (~5% to 10%)

Oral maintenance: 240 to 320 mg per day Long-term: constipation

Beta blockers Acute IV: 1 to 3 mg at 1 mg per minute; repeat in 2 minutes if needed. Acute: heart block, bronchospasm, CHF

Propranolol (Inderal) Oral maintenance: 10 to 30 mg every 6 to 8 hours Long-term: fatigue, depression

Esmolol (Brevibloc) Acute IV: 0.5 mg per kg over 1 minute; then 0.05 mg per kg per minute by IV drip for 4 minutes Acute: hypotension (20% to 50%), heart block, CHF

Digoxin (Lanoxin) Acute IV: 0.25 to 0.50 mg; then 0.25 mg every 4 to 6 hours to total of 1.0 mg Heart click, visual disturbances, delirium, hallucinations

Oral maintenance: 0.125 to 0.25 mg per day

--------------------------------------------------------------------------------

CHF = congestive heart failure.

Information on side effects and complications from Physicians' desk reference. 56th ed. Montvale, N.J.: Medical Economics, 2002.

Acute management of ventricular rates can usually be achieved with intravenously administered diltiazem (Cardizem), given in an initial bolus of 15 to 20 mg (0.25 mg per kg) over two minutes, or with an intravenously administered beta blocker such as propranolol (Inderal), given in a dose of 0.5 to 1 mg (up to 3 to 5 mg if needed).

A number of medications, including calcium channel blockers, beta blockers, and digoxin (Lanoxin), are effective for maintaining ventricular rates within acceptable ranges. Because calcium channel blockers are associated with better exercise tolerance, they may be preferable to beta blockers.15 Digoxin is associated with a high degree of exercise intolerance; therefore, it should be reserved for use in patients who are relatively immobile, who cannot tolerate other treatment options, or who have significant ventricular dysfunction.

Paroxysmal Supraventricular Tachycardias

Based on duration, supraventricular tachycardias are usually categorized as paroxysmal, persistent, or chronic. Paroxysmal supraventricular tachycardia (PSVT) is the most common of these arrhythmias and the one that is most often encountered in the primary care setting. Longer-duration supraventricular tachycardias can be treated similarly to PSVT, but cardiology consultation is often required to identify the electrophysiologic mechanism responsible for sustaining the arrhythmia. In contrast to ventricular tachycardias (discussed in part II of this article) and atrial fibrillation, PSVT is usually a narrow-complex tachycardia with a regular rate.

MECHANISMS

Atrioventricular Nodal Reentry Causing PSVT. Atrioventricular nodal reentry, the most common mechanism of PSVT, occurs when two pathways exist with different conduction rates. A premature atrial complex that is blocked in the fast pathway and redirected through the slow pathway usually triggers the tachycardia (Figure 1). The electrical signal proceeds down the slow pathway and then reenters the fast pathway in a retrograde direction. By the time the signal has propagated down the slow pathway and back around on the fast pathway, the slow pathway is no longer refractory and is ready to conduct the signal again, completing a continuous circuit.

Reentry Paroxysmal Supraventricular Tachycardia

FIGURE 1. Mechanism for reentrant paroxysmal supraventricular tachycardia. (A) A premature atrial complex (PAC) occurs and is blocked in a fast pathway, but it can propagate down the slower pathway. ( By the time the electrical signal reaches the end of the slow pathway, the fast pathway has repolarized, and retrograde conduction of the wave occurs. © The wave then returns down the slow pathway, setting up a closed circuit that is self-sustaining.

FIGURE 2. Atrial tachycardia from reentry (lead II), with negatively conducted P waves (arrows) buried in the ST segment.

Reentrant tachycardias usually produce a narrow-complex tachycardia with no discernible P wave. The rate is usually between 160 and 190 beats per minute. In a less common form of atrioventricular nodal reentrant tachycardia, the circulating wavefront proceeds in an antegrade fashion down the fast pathway and in a retrograde fashion up the slow pathway. In this form, inverted P waves (Figure 2) are clearly visible in lead II of the electrocardiogram (ECG).

It is important to note that atrioventricular nodal reentrant tachycardia can result in a wide-complex tachycardia if the patient has preexisting bundle branch block.

Accessory Pathways Causing PSVT. Accessory pathways (Wolff-Parkinson-White syndrome) and other bypass tracts can cause PSVT. In patients with Wolff-Parkinson-White syndrome, a shortened PR interval and a slurred upstrike to the QRS complex "delta wave" on the resting ECG indicate the presence of an accessory pathway (Figure 3).

It should be noted that the resting ECG may be normal in some patients with Wolff-Parkinson-White syndrome, because of the inability of the accessory pathway to conduct in the antegrade direction. The usual mechanism of PSVT in this setting is antegrade conduction down the normal pathways through the atrioventricular node and retrograde conduction through the accessory pathway.

The ECG in an atrial arrhythmia with an accessory pathway usually shows a narrow-complex tachycardia at rates of 160 to 240 beats per minute. Delta waves are absent because the normal pathways are used for ventricular activation. Inverted P waves may be seen in the inferior leads. In a much less common form of PSVT, antegrade conduction is down the bypass tract and results in a wide-complex tachycardia.

Increased Automaticity Causing PSVT. Increased automaticity usually occurs when the atrium is enlarged, as in patients with chronic lung disease, congestive heart failure, or electrolyte and acid-base disturbances. Usually, the stretched atria fire irregularly, producing multiple premature beats that emanate from different areas of the atria. Because the foci for the ectopic beats are in multiple sites, the P waves vary in morphology, giving rise to the term "multifocal atrial tachycardia."

FIGURE 3. Patient with Wolff-Parkinson-White syndrome. Note the short PR interval and slurred upstrike (arrows), termed a "delta wave."

FIGURE 4. Blocked premature atrial complex. In the complex preceding the pause, note the altered morphology of the T wave (arrow), caused by superimposition of a P wave on the T wave.

The diagnosis of multifocal atrial tachycardia depends on the identification of an irregular rhythm with three or more different P-wave morphologies. The rate is usually between 130 and 180 beats per minute. Treatment is directed at correcting the underlying cause. Antiarrhythmic drugs are usually not helpful.

MANAGEMENT

In most patients, PSVT is benign and self-limited. However, some patients can have angina, hypotension, and intense anxiety. The first step in the management of PSVT is to determine whether the patient is hemodynamically stable. If PSVT is sustained and there is any indication of instability (i.e., angina, shortness of breath, decreased level of consciousness, hypotension, or congestive heart failure), electrical cardioversion should be performed urgently.

If the symptoms are restricted to discomfort (e.g., palpitations and anxiety), conservative measures should be applied. Conservative management of PSVT can include both nonpharmacologic and pharmacologic measures (Table 3).16

Vagal maneuvers to increase parasympathetic tone and slow conduction through the atrioventricular node should be the first approach. Patients should be taught some of these maneuvers for use in future episodes. They should also be instructed to avoid inciting factors, such as caffeine, tobacco, alcohol, pseudoephedrine, and stress. Carotid sinus massage can be attempted, but its role has become more limited because of the effectiveness of drug therapy and the risk of embolism from carotid pressure in some patients.

The goal of pharmacologic management is to slow or block atrioventricular nodal conduction. Agents used for this purpose include adenosine (Adenocard), calcium channel blockers (verapamil [Calan] or diltiazem), and beta blockers (e.g., esmolol [brevibloc]).

Adenosine is an ultra­short-acting agent that is cleared quickly (half-life of 1 to 6 seconds). This agent is given intravenously in an initial dose of 6 mg, which is followed by one or two 12-mg boluses. Adenosine works by reducing conductance along the slow antegrade pathway. Side effects include flushing, dyspnea, and chest pain. Because of the short half-life of adenosine, these effects are usually very brief and do not ordinarily result in complications.

One advantage of adenosine is that it lacks the negative inotropic effects of calcium channel blockers. Adenosine can also decrease the sinus rate transiently and produce a "rebound" sinus tachycardia. Adenosine should not be used in patients with heart transplants, because such patients may be too sensitive to its effects.17

Calcium channel blockers can also be used to disrupt a reentrant pathway. Verapamil can be given in a 5- to 10-mg bolus over 2 minutes, followed by 10 mg in 15 to 30 minutes if the initial dose does not convert the arrhythmia.18 Verapamil and other calcium channel blockers should not be used in patients with an undiagnosed wide-complex tachycardia, because of the risk of fatal hypotension or ventricular fibrillation if the arrhythmia is actually ventricular tachycardia and not PSVT.19

Intravenously administered diltiazem is also effective.20 Initial treatment consists of a bolus of 0.25 mg per kg administered over two minutes. A repeat bolus of 0.35 mg per kg given over two minutes can be administered 15 minutes later.

Esmolol, a short-acting beta blocker, can be given in an intravenous bolus of 0.5 mg per kg over 1 minute or in an infusion at a rate of 0.5 mg per kg per minute after an initial loading dose of 0.5 mg per kg. An advantage of esmolol over other beta blockers is its short half-life (four to five minutes), compared with the much longer half-lives (three hours or more) of most other beta blockers. Because of a similar depressive effect on left ventricular contractility, esmolol should be used with caution if initial treatment with a calcium channel blocker is not successful.

Other antiarrhythmic drugs, including quinidine, procainamide, flecainide (Tambocor), and amiodarone, may be used in patients who do not respond to initial medications. However, selective radiofrequency ablation is rapidly becoming the treatment of choice in this situation.

Long-term control of recurrent PSVT caused by atrioventricular nodal reentry may be achieved with pharmacologic therapy or radiofrequency ablation. Patients who have infrequent, well-tolerated recurrences may manage these episodes with self-administered physiologic maneuvers.

Radiofrequency ablation is now used early in the management of patients with PSVT caused by an accessory pathway (Wolff-Parkinson-White syndrome), atrioventricular nodal reentrant tachycardia, or atrial tachycardia.21 The success rate for radiofrequency ablation is 95 percent in patients with an accessory pathway or atrioventricular nodal reentrant tachycardia, and approximately 80 percent in patients with atrial tachycardia.21

TABLE 3

Treatment Options for Supraventricular Tachycardias

--------------------------------------------------------------------------------

Physiologic interventions

Rest

Valsalva maneuvers: gag reflex, ice packs, etc.

Carotid massage*

Avoidance of inciting factors: caffeine, tobacco, alcohol, pseudoephedrine, stress, etc.

Medications

Drugs with direct effect on atrioventricular node or accessory pathway: amiodarone (Cordarone), sotalol (Betapace), class IC drugs (flecainide [Tambocor], propafenone [Rythmol], etc.)

Drugs that work primarily on atrioventricular node: adenosine (Adenocard), calcium channel blockers, beta blockers, digoxin (Lanoxin)

Drugs that work primarily on accessory pathway: class IA drugs (quinidine, disopyramide [Norpace], etc.)

Radiofrequency ablation

Electronic pacing

--------------------------------------------------------------------------------

*--Controversial because of risk of embolism.

Adapted with permission from Myerburg RJ, Kessler KM, Castellanos A. Recognition, clinical assessment, and management of arrhythmias and conduction disturbances. In: Alexander RW, Schlant RC, Fuster V, eds. Hurst's The heart, arteries and veins. 9th ed. New York: McGraw-Hill, Health Professions Division, 1998:873-942.

Other Atrial Arrhythmias

SINUS ARRYTHMIA

Sinus arrhythmia is usually a normal event in young persons and athletes. In fact, it occurs with such high frequency that it may considered a normal variant rather than a true arrhythmia.

There are two forms of sinus arrhythmia. In the "respiratory" form, the RR interval shortens during inspiration and slows during expiration. Breath-holding eliminates the variation. In the "nonrespiratory" form, the same phasic variation is seen in the RR interval but is not related to respirations. This form of sinus arrhythmia occurs in elderly patients, patients with digoxin overdose, and patients with increased intracranial pressure.

Sinus arrhythmia is usually asymptomatic. Sometimes, however, the long pauses can cause dizziness or syncope. Treatment is usually unnecessary.

WANDERING ATRIAL PACEMAKER

Patients with wandering atrial pacemaker are usually not symptomatic. The condition is most often an isolated finding on the ECG and requires no treatment. Sometimes it is noted on physical examination as an irregularly irregular rhythm.

With wandering atrial pacemaker, the ECG shows variable P-wave morphology and PR intervals. The atrial impulses conduct in a 1:1 fashion and usually control the rhythm for several beats before shifting to another focus. The normal heart rate in wandering atrial pacemaker differentiates this condition from multifocal atrial tachycardia.

PREMATURE ATRIAL COMPLEXES

A premature atrial complex is generated from an ectopic focus in the atria. Therefore, the P wave is usually different in morphology from the usual sinus P wave. The impulse conducts along the normal pathways, generating a narrow QRS complex followed by a pause. Sometimes the premature atrial complex is not conducted and can mimic heart block (Figure 4).

Premature atrial complexes are found in a variety of settings, including the excessive consumption of caffeine or alcohol and the use of sympathomimetic drugs. These complexes can also be present in patients with structural heart disease.

Patients with premature atrial complexes are usually asymptomatic and require no treatment. A beta blocker given in a low dosage can be tried in patients with uncomfortable symptoms, but no studies of efficacy have been reported. Patients should be counseled to decrease their intake of caffeine, tobacco, and alcohol, and their use of over-the-counter sympathomimetic substances, which are often present in cold medicines and weight-loss preparations.

It is important to note that premature atrial complexes sometimes precipitate supraventricular tachycardia, atrial flutter, or atrial fibrillation.

Patients with sustained paroxysmal supraventricular tachycardia who are unstable should undergo emergency cardioversion.

Sinus Nodal Arrhythmias

SINUS PAUSE AND SINOATRIAL EXIT BLOCK

Sinus pause or arrest occurs when the sinoatrial node fails to discharge. The ECG shows a pause in the sinus rhythm, with no preceding P wave. Patients usually have no symptoms, but if the pause is prolonged, they may have lightheadedness, palpitations, syncope, and falls. In sinus arrest, the length of the pause has no relationship to the PP interval. Sinoatrial exit block is recognized by the pauses being multiples of PP intervals.

Sinus node dysfunction is usually caused by drugs such as digoxin, quinidine, or procainamide. It can also be caused by ischemia, myocarditis, or fibrosis.

From a therapeutic standpoint, it is probably not important to distinguish between sinus arrest and sinoatrial exit block. Both can occur in well-trained athletes22 and can be a factor in sick sinus syndrome.23

SICK SINUS SYNDROME

The term "sick sinus syndrome" encompasses a number of abnormalities, including sinus bradycardia, sinus arrest or exit block, combinations of sinoatrial and atrioventricular nodal conduction disturbances, and atrial tachyarrhythmias. More than one of these arrhythmias may be recorded in the same patient (bradycardia-tachycardia syndrome).

The abnormalities in sick sinus syndrome are usually due to ischemia, fibrosis, or drug-induced or autonomic dysfunction. Signs and symptoms are related to cerebral hypoperfusion and reduced cardiac output.

Treatment of recurrent symptomatic bradycardia or prolonged pauses requires implantation of a permanent pacemaker.24

The authors indicate that they do not have any conflicts of interest. Sources of funding: none reported.

Members of various family practice departments develop articles for "Practical Therapeutics." This article is one in a series coordinated by the Department of Family Medicine at the Medical University of South Carolina, Charleston. Guest editor of the series is William J. Hueston, M.D.

This is part I of a two-part article on common arrhythmias. Part II, "Ventricular Arrhythmias and Arrhythmias in Special Populations," appears on page 2491 of this issue.

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The Authors

A. KESH HEBBAR, M.D., is assistant professor in the Department of Family Medicine at the Medical University of South Carolina, Charleston. He graduated from the University of Madras Medical School, India, and received postgraduate training in internal medicine and general practice in Great Britain. Dr. Hebbar completed a family practice residency at the Medical University of South Carolina, where he currently coordinates cardiology training for family practice residents.

WILLIAM J. HUESTON, M.D., is professor and chair of the Department of Family Medicine at the Medical University of South Carolina. Dr. Hueston received his medical degree from Case Western Reserve University School of Medicine, Cleveland, and completed a family practice residency at Riverside Methodist Hospital, Columbus, Ohio.

Address correspondence to William J. Hueston, M.D., Department of Family Medicine, Medical University of South Carolina, P.O. Box 250192, Charleston, SC 29425 (e-mail: huestowj@musc.edu). Reprints are not available from the authors.

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Ryder KM, Benjamin EJ. Epidemiology and significance of atrial fibrillation. Am J Cardiol 1999;84(9A):R131-8.

Benjamin EJ, Levy D, Vaziri SM, D'Agostino RB, Belanger AJ, Wolf PA. Independent risk factors for atrial fibrillation in a population-based cohort. The Framingham Heart Study. JAMA 1994;271:840-4.

Golzari H, Cebul RD, Bahler RC. Atrial fibrillation: restoration and maintenance of sinus rhythm and indications for anticoagulation therapy. Ann Intern Med 1996;125:311-23.

Pritchett EL. Management of atrial fibrillation. N Engl J Med 1992; 326:1264-71.

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[brock8024]

Brock.................

Oh my God, I cant even think strait after reading the rest of your post. I hope you just started class!! Please don't come to PA!!!!

thanks for ur opinion we are all allowed to think what we will. Hope you have a great day.

[Just Plain Ruff]

Let me put my two cents in and my two fists

If you cardiovert me without pain meds or sedation unless I'm unconscious, when I wake up I'm gonna clock you.

If you cardiovert me agains my wishes no matter how bad off I am I'm gonna come back and clock you

There is no reason why you should not tell me what you are gonna do and if I say NO you better not do it.

Granted, if I need cardioversion then I'm gonna want it but if you do this against the patients wishes, if they say no then NO Means NO.

As a patient I have total control over what you do to me, if I say I don't want and iv you better not give me one.

I had a patient one day that was a blue as NAVY blue and he refused. I tried and tried to get him to let me treat him but he said NO I want to die.

I explained risks and benefits of refusing and I told him that he would be dead in less than an hour.

He still refused. AS a matter of fact I tried to reason with him till I was blue in the face but it didnt' work.

We left the scene and just waited around the area. We got called back when he coded and we coded him till we got to the hospital where he died.

I cannot believe that there are people on this forum that will come hell or high water do something to a patient even if they said no.

There are two posters on this thread that seem to believe that they can do whatever they want to a patient when they are critical as your posts sound like you would do that. You know who you are. If I misunderstood the two of you please correct me if I'm wrong. If I'm not wrong and you would treat a patient against their will after they expressly said NO then I do not want you anywhere near me when I'm sick.

[brock8024]

Let me put my two cents in and my two fists

If you cardiovert me without pain meds or sedation unless I'm unconscious, when I wake up I'm gonna clock you.

If you cardiovert me agains my wishes no matter how bad off I am I'm gonna come back and clock you

There is no reason why you should not tell me what you are gonna do and if I say NO you better not do it.

Granted, if I need cardioversion then I'm gonna want it but if you do this against the patients wishes, if they say no then NO Means NO.

As a patient I have total control over what you do to me, if I say I don't want and iv you better not give me one.

I had a patient one day that was a blue as NAVY blue and he refused. I tried and tried to get him to let me treat him but he said NO I want to die.

I explained risks and benefits of refusing and I told him that he would be dead in less than an hour.

He still refused. AS a matter of fact I tried to reason with him till I was blue in the face but it didnt' work.

We left the scene and just waited around the area. We got called back when he coded and we coded him till we got to the hospital where he died.

I cannot believe that there are people on this forum that will come hell or high water do something to a patient even if they said no.

There are two posters on this thread that seem to believe that they can do whatever they want to a patient when they are critical as your posts sound like you would do that. You know who you are. If I misunderstood the two of you please correct me if I'm wrong. If I'm not wrong and you would treat a patient against their will after they expressly said NO then I do not want you anywhere near me when I'm sick.

You are so right. I do not understand why we can not give the proper meds or at least explain what we are doing. I mean it does not take that long, or why we do not explain stuff to ouor older patients just because they have not responded to stimulus in years. Who cares they are still human.

[Just Plain Ruff]

People who have been unconscious or in a coma for years have reported after coming out that they heard everything that was said in the room.

Just because someone is unconscious or has an AMS it does not mean that they cannot hear you or know what is going on.

How many diabetic patients that had low sugar that you reversed came back and said, I could hear you guys but just couldn't respond.

I think that we need to explain what we are doing to everyone including the ones who we DON'T think can hear us.

let me tell a little story about an incident that happened to me

i took a phone call from an irate father of a patient. he wanted to talk to the doctor. I set up the transfer, dialed the doctor's sleep room and asked the doc if he would talk to this asshole of a father. The doctor said, sure. I concluded the transfer. the phone rang again and guess what, it was the father and he had heard everything I said. He was pissed. I hem hawed around the issue but in the end all I could do was say "IM Sorry". I asked for his forgiveness, he gave it and it was all good.

I had no idea that he could hear what we were saying but since then, I've known that someone can always hear what I'm saying.

So long story short guys and gals, explain to the patient what you are doin even if you don't think they can hear you. Because they might be able to hear you.

Give sedation and pain meds whenever possible and Gosh darn it, listen to your patient, if they say NO that means NO.

[firefighter523]

Ruff, wow, um was that a cyber-threat, with the whole fist thing!?? I'm over it..... Please refer to the BLS curriculum about implied concent!!! Let me help you understand this a little better. Watch this, we will do it in the 1-2-3 method just like in grade school. 1) If they are hemodynamically unstable, ie with or without pulmonary edema.

2) If they have a tachy arrythmia, wide or narrow.

3) If they don't have a DNR or living will present.

All of that equals, yes I know you hate to hear this.... Not telling them, and here is the worse part......CARDIOVERT!!!! PS, and possibly without sedation. This is the standard of care. OBVIOUSLY...........if someone is awake and ABLE to hear you, you would, like a good paramedic, tell them what you are doing, even down to "little stick" right before you jab them with your cath!!

Brock.... Learn a whole lot more before you start picking your battles with Rx... If someone has a tachy arrythmia, and is unstable with or without rales, you NEED to fix the dysrythmia FIRST. You, hopefully wouldn't hit someone with Lasix to rid them of the PE before you would correct what is causing his low cardiac output, hence the back pressure building up in his pulmonary vasculature. He or she is not in fluid overload, it is just in the wrong place because of the screen-door effect, in the vasculature. Increase the cardiac filling time, increase ejection fraction, fluid goes back to where it is supposed to be, and finally call your report in!!!!

This horse has been beat enough, keep your nose in the books!!!!