Arrhythmias

The patient with unstable angina or a NSTEMI can have a delayed angiogram within 48 hours of admission.

While the ECG is most important, serial cardiac markers are also important. The main cardiac enzyme involved is the CK-MB enzyme, while markers of cell contents of myocardial cells include troponin I, myoglobin, and troponin T. These are seen at different times but the troponins are far more sensitive and are seen earlier in the bloodstream compared to the cardiac enzymes. In some case, the test is too sensitive and the chance of false positivity does exist. For this reason, the results seen must be balanced with the symptoms, risk factors, and ECG findings.

The coronary angiography is both diagnostic and therapeutic if combined with percutaneous coronary intervention. If done soon after an MI, it can effectively abort the process so that the amount of coronary damage will be minimized. Besides being able to resolve the ischemia, the angiography can assess the other coronary arteries as well as things like ejection fraction. Other imaging techniques, like echocardiography or radionuclide scanning, will not generally be helpful.

The treatment starts in the prehospital setting with aspirin, oxygen, nitrates and possible ECG to expedite diagnosis and further management. An IV is started and continuous cardiac monitoring is accomplished. Morphine was once suggested but there are adverse outcomes associated with it. Drug therapy can involve antiplatelet drugs like aspirin or clopidogrel, anticoagulant drugs, or fibrinolytics, such as tissue plasminogen activator. Many patients will have percutaneous coronary angiography, while a few will not be candidates for this and will require a coronary artery bypass graft or CABG.

ARRHYTHMIAS

Cardiac arrhythmias can happen for a variety of reasons, including ischemic heart disease, congenital diseases of the heart, electrolyte abnormalities, toxins or drugs, and hormonal imbalances, such as low thyroid conditions and hyperthyroidism. Among drugs or toxins, both caffeine and alcohol are contributors to cardiac arrhythmias.

Cardiac tissues can be called fast-channel or slow-channel tissues. The fast-channel tissues are the working myocytes and the cells of the His-Purkinje system, which are

poor pacemakers but fast conductors of electricity. The slow-channel tissues are those of the SA or AV node, which are the traditional pacemaker cells that do not conduct electricity very well themselves. The SA node has the fastest rate of spontaneous depolarization so it will set itself up to be the pacemaker of the heart.

You should be familiar with the different types of arrhythmia you may encounter when evaluating the patient. Arrhythmias can be divided in different ways. For example, there are tachyarrhythmias, bradyarrhythmias, and rhythm disturbances that have no abnormalities in the overall rate. There are also wide-complex arrhythmias and narrowcomplex arrhythmias. Those that are more narrow-complex in appearance tend to originate prior to the AV node and tend to be faster, while wide-complex arrhythmias are secondary to an initiated rhythm below the AV node. These can be slow or fast. Ventricular fibrillation and asystole are agonal rhythms that usually end in death unless a rhythm can be reestablished through defibrillation.

An atrioventricular nodal reentry tachycardia usually involves a premature P wave originating from somewhere in the atrium that gets propagated down the normal pathways but also cycles back to reenter the AV node much faster than a normal SA nodal impulse. This is generally a tachyarrhythmia made worse by sympathetic stimulation of the heart that shortens the refractoriness of the tissue.

The main symptom seen is palpitations, although if the rate is too fast, there will be chest discomfort, dyspnea, syncope, or presyncope. If prolonged, the patient will have a release of atrial natriuretic peptide and polyuria. You may see cannon waves, which are large jugular venous pulsations.

In any tachyarrhythmia, if the QRS is narrow, the origin of the disturbance is above the bifurcation of the His bundle branch. If the QRS is wide, the origin of the disturbance is ventricular. An alternative might be a supraventricular origin with some type of intraventricular conduction defect or a situation where there is ventricular preexcitation, such as is seen in Wolff-Parkinson-White or WPW syndrome. Figure 3 shows a typical ECG tracing in WPW syndrome:

Figure 3.

Bradyarrhythmias happen when the heart rate is less than 60 beats per minute. We will talk further about the different types of heart block that can cause this. If there is no relationship between the P wave and QRS complex, this is a complete heart block. It leads to some type of escape rhythm. If the AV node is normal, the escape rhythm will be seen as a narrow QRS complex. If the escape rhythm is junctional and the AV node is not normal, the QRS will be wide. The QRS will be wide as well if the escape rhythm comes from below the AV node and is ventricular.

There are essentially four types of tachyarrhythmia that depend on four different issues. These include regular rhythms versus irregular rhythms as well as narrow versus wide QRS complexes. Irregular, narrow QRS arrhythmias with a fast rhythm include the following:

• Atrial fibrillation involves a narrow complex tachyarrhythmia in the absence of any discrete P waves. • Atrial flutter involves the presence of sawtooth uniform P waves with variable conduction of these P waves but with a rate that is also usually too fast.

• Atrial tachycardia involves regular but abnormal P waves and variable conduction so that the QRS complexes will not be regular and the rate is usually less than 250 beats per minute. • Multifocal atrial tachycardia involves discrete P waves that come from different places in the atria so the P waves themselves will be different from beat to beat.

If the QRS complex is wide and the rhythm is irregular, it could mean that there is a bundle branch block or a situation of ventricular preexcitation. The more common thing seen, however, is polymorphic ventricular tachycardia.

When it comes to regular rhythms and narrow QRS complexes seen in tachyarrhythmias, you have four choices to consider, including the following:

• Sinus tachycardia, which involves P waves and normal QRS complexes but a rate that is greater than 100 beats per minute. • Atrial tachycardia is similar but the rate is faster and the AV conduction is consistent from beat to beat. • Atrial flutter can be present but, if the AV conduction ratio is the same from beat to beat, the rhythm will be regular. • In SVT or supraventricular tachycardia, there is a circular pathway that continually stimulates the AV node so the rate is rapid and regular. Figure 4 shows what paroxysmal SVT looks like:

Figure 4.

Any of these tachyarrhythmias will have a regular rhythm but a wide QRS complex if there is a bundle branch block. In addition, if there is monomorphic ventricular tachycardia, as is seen in figure 5, the QRS complex will be wide but the rate will be regular:

Figure 5.

Atrial fibrillation is worth looking at further because it is so common and because it is something you will help patients deal with on a chronic basis. Some patients will have no symptoms, while others will have weakness, palpitations, exercise intolerance, presyncope, and dyspnea at rest. The acute rhythm disturbance is far less dangerous to the patient than the long-term complication of thromboembolism, often leading to a high risk of stroke unless this risk is reduced.

In atrial fibrillation, the atria do not contract at all but, in most cases, the QRS complex will still be narrow. The rate is generally irregular and may or may not be fast. Atrial fibrillation affects more than 2 million people in the United States with an increasing prevalence with advancing age. The major complication is the formation of a thrombus inside the atria, which causes a risk of stroke that is about 7 percent per year. There is also the possibility of systemic emboli, such as those affecting the GI tract, kidneys, heart, and eyes. Cardiac output will decrease by 10 percent just because the atria do not contract. If the rate is too fast in addition, the cardiac output will further diminish.

In considering the etiology of atrial fibrillation, you need to consider that it can be caused by coronary artery disease, hypertension, cardiomyopathy, valvular disorders involving the mitral or tricuspid valve, binge drinking, or hyperthyroidism. There are rare causes of atrial fibrillation, including pericarditis, myocarditis, COPD, and pulmonary embolism. Atrial fibrillation can start with atrial flutter that degenerates to involve a fibrillating atrium.

Atrial fibrillation can come in different forms. In paroxysmal atrial fibrillation, the duration is less than a week and the person spontaneously converts to sinus rhythm. In persistent atrial fibrillation, the duration is greater than a week and it does not convert itself. In long-lasting persistent atrial fibrillation, the duration is a year or more but restoration of normal rhythm can still occur. In permanent atrial fibrillation, restoration of normal rhythm is not possible.

In diagnosing atrial fibrillation, an ECG will detect the rhythm, while an echocardiogram can best show the presence of a thrombus in the atrial cavity. Thyroid function studies should also be done. The ECG will show a complete absence of P waves, usually associated with a narrow complex QRS pattern that is generally irregular.

Your treatment will be different, depending on what you want to achieve. In some cases, the goal is rate control only, which will control symptoms and reduce the risk of cardiomyopathy and hemodynamic instability. AV node blockers like any of the beta blockers or calcium channel blockers can be used. Digoxin is less effective but will help heart failure. Amiodarone will also be necessary as an anti-arrhythmic drug.

Another option is rhythm control, which involves synchronized cardioversion or antiarrhythmic drugs. Prior to doing this, you’ll need to prevent thromboembolism because cardioversion is associated with an increased risk of throwing off an embolism at the time of cardioversion. Anticoagulation should happen for 3 weeks before and 4 weeks after cardioversion. Class Ia and class III antiarrhythmic drugs can also be used instead of cardioversion but these are only effective about half the time.

Ablation procedures also work for atrial fibrillation. In such cases, the AV node can be ablated in order to precipitate complete heart block. In such cases, you must put in a pacemaker unless you ablate just one AV nodal pathway. There are advanced techniques that can be done, such as pulmonary vein isolation.

Long-term prevention of thromboembolism can involve warfarin or Coumadin therapy, which works well but requires frequent coagulation studies to be tested of the blood. Other choices include apixaban, edoxaban, or rivaroxaban, which are also oral anticoagulants that do not require blood testing to be effective. Some patients can have a filter placed that will prevent passage of any clot beyond the filter.

Atrioventricular block or AV block involves some type of separation between the atrial impulse and the ventricular impulse. Most commonly, this is caused by fibrosis of the conduction system of the heart but can be caused by ischemic heart disease. Other, less common causes, are drugs like beta blockers or calcium channel blockers, increased vagal tone, congenital heart disease, and valvular heart disease.

There are four different types of AV block, most of which involve some type of bradycardia. In first-degree AV block, no beats are skipped but the PR interval is too long. This can be normal in athletes. Second-degree AV block comes in two types. In Mobitz type I or Wenckebach phenomenon, the PR interval lengthens over a few beats until the P wave is dropped altogether. This is less likely to indicate heart disease than Mobitz II phenomenon, which involves a consent PR interval with intermittent dropping of QRS complexes in a relatively consistent pattern, such as 3:1 block or 4:1 block. This is often so symptomatic that a pacemaker is required. Figure 6 shows what a second degree Mobitz II heart block looks like:

Figure 6.