Week 30: Cardio Pt I, Syncope/Arrhythmia

Although the definition of abnormal ECG varies among the many studies examining their role in the diagnosis of syncope, particular attention should be paid to any non-sinus rhythm, signs of ischemia, or conduction abnormalities.

Red flags to look for include:
Any non-sinus rhythm
signs of ischemia (ST or T wave abnormalities)
conduction abnormalities
Delta waves for WPW
Prolong QT

First degree heartblock, and Mobitz type I are NOT associated with poor outcomes in syncope

The patient has ventricular tachycardia (heart rate > 100 beats/minute originating from an ectopic ventricular focus). Electrocardiographic hallmarks of monomorphic VT include a rapid, regular rhythm with a wide QRS complex > 120 milliseconds with consistent beat-to-beat morphology. P waves are not seen, other than an occasional dissociated P wave. VT can be nonsustained, occurring with a few ventricular beats at a time which terminate spontaneously, or can occur in a sustained fashion.

VT occurs most commonly in the setting of ischemic heart disease/MI, but can also be seen in cardiomyopathies, valvular heart disease, inherited ion channel disorders, and drug toxicity. Hypoxia and electrolyte disorders, such as hyperkalemia, increase the propensity for ventricular ectopy and VT. The clinical effects of VT vary widely. Pulseless VT, the most severe manifestation, requires immediate defibrillation/ACLS. Unstable patients in VT who have a pulse, as evidenced by hypotension, ischemic chest pain, or altered mental status, should undergo electrical cardioversion. This patient, who has a normal blood pressure and minimal symptoms, has stable VT. Pharmacologic agents are first-line therapy for stable VT. Treatment options include procainamide, amiodarone, and lidocaine. Elective cardioversion can be performed if the patient fails to convert with antiarrhythmics or becomes clinically unstable. Administration of intravenous adenosine (A) is the treatment for supraventricular tachycardia. Defibrillation (C) is indicated in pulseless ventricular tachycardia, a form of cardiac arrest. Electrical cardioversion (D) is the treatment for unstable ventricular tachycardia, or if he fails to convert with pharmacologic therapy.

The patient’s rhythm strip demonstrates torsades de pointes, a polymorphic ventricular tachycardia precipitated by QT interval prolongation. Torsades de pointes is french for “twisting of the points,” which refers to the undulating appearance of the QRS complex. If untreated, this rhythm can lead to ventricular fibrillation. An intravenous bolus of magnesium sulfate is considered the first-line treatment for torsades de pointes. QT interval prolongation can be congenital, acquired, or a combination of both. The QT interval represents the sum of the action potential duration of the ventricular cardiomyocytes. The cardiac action potential during depolarization is characterized by inward sodium and calcium currents. During repolarization, the inward calcium current decreases and an outward potassium current increases. Drugs can prolong the QT interval by blocking or prolonging these currents. Antiemetics such as prochlorperazine are among the many different medications that can cause QT interval prolongation. Defibrillation is indicated in ventricular fibrillation or pulseless ventricular tachycardia, it is not considered first line for torsades de pointes, but is indicated if patient is pulseless. Adenosine is the treatment for SVT. Synchronized cardioversion is not indicated here, however overdrive pacing is indicated in IV magnesium resistant torsades if the patient remains stable.
Drugs that prolong QT: phenothiazine, abx, cyclic antidepressants, class IA antiarrhythmics (procainamide, quinidine), class IC (flecanide), droperidol, methadone, cocaine

Electrolyte abnormalities that prolong QT: hypomag, hypoCa, hypoK

In this scenario, the ventricle is acting as the pacemaker for the heart, so this tissue is the last line of defense for the heart to provide any sort of electrical activity to maintain cardiac output. Lidocaine, which may abolish the ventricular rhythm completely, is contraindicated because it may cause cardiac standstill. Atropine, due to its vagolytic properties, enhances sinus node automaticity and AV nodal conduction. Isoproterenol, a beta-adrenergic agonist, has both inotropic and chronotropic effects. Isoproterenol increases myocardial oxygen demand and should be used with caution in ischemic myocardium. Glucagon has been shown to be useful in the treatment of bradyarrhythmias secondary to beta-adrenergic blocking agents and calcium antagonists. Glucagon stimulates the SA node directly giving some mild increase in heart rate. Glucagon also increases cardiac contractility.

Placement of a magnet over a pacemaker will cause synchronous pacing at model-specific rates, it does NOT turn off the pacemaker.

Of note, AICDs all have pacemaker capability (usually from the R ventricular lead), and magnets DISABLE the AICD shocking ability, but it DEFAULTS the device to a pacemaker mode. So a magnet never over an AICD turns off the defibrillator and converts it to a pacemaker mode (usually 60bpm)

The patient in this question is presenting with a story and electrocardiogram that is consistent with third-degree atrioventricular heart block. In a third-degree (complete) atrioventricular heart block, no atrial impulses reach the ventricle. More than half of cases are caused by idiopathic progressive cardiac conduction disease with myocardial fibrosis and sclerosis that affects the conduction system. Other causes include myocardial ischemia, myocarditis, endocarditis, and atrioventricular nodal blocking medications. Patients generally present with fatigue, dyspnea, chest pain, syncope, mental status changes, or cardiac arrest. It is important for the clinician to obtain a good history including a list of all medications to determine the most likely etiology of the complete heart block. Diagnosis is usually confirmed with an electrocardiogram. Initial management depends on whether the patient is hemodynamically stable or unstable. Signs of hemodynamic instability include chest pain, mental status changes, acute pulmonary edema, and hypotension. This patient has mental status changes and is hypotensive. Steps should immediately be taken to prepare for transcutaneous cardiac pacing, but in the meantime, the patient should be treated with atropine. Atropine may only be successful in approximately 30% of patients with third-degree heart block, so other medications may be required, but the most recent Advanced Cardiac Life Support guidelines recommend atropine 0.5 mg intravenously as initial therapy.

Calcium gluconate (B) would be recommended in any patient suspected of having hyperkalemia leading to a cardiac dysrhythmia. This patient’s history does not suggest hyperkalemia, and typically bradycardia associated with hyperkalemia presents with a wide complex rhythm instead of a narrow complex rhythm on electrocardiogram. Dobutamine (C) is recommended for patients with complete heart block and congestive heart failure. However, other medications are usually recommended before using dobutamine. Metoprolol (D) is a beta blocker and would worsen the patient’s heart block

As per the 2010 AHA guidelines, CPR should only take place until the defibrillator is ready, and defibrillation at 200 J should be performed as soon as possible in VF arrest. Escalating doses of 50–100–150 J are no longer recommended and 200 J should be used for biphasic defibrillators. Though epinephrine is recommended as part of ACLS, it should not take precedence over defibrillation and has not shown long-term benefit in the treatment of cardiac arrest.

this ECG demonstrates a narrow complex irregular tachycardia that is consistent with atrial fibrillation with rapid ventricular response. Patients with atrial fibrillation with a rapid ventricular rate should have the rate controlled to prevent worsening symptoms such as dyspnea and chest pain and development of a cardiomyopathy. In the past, physicians preferred a rhythm control strategy when treating atrial fibrillation with rapid ventricular response. However, multiple studies have not shown a mortality benefit to rhythm control versus rate control, thus, a rate control treatment strategy is preferred. The clinician also needs to consider the urgency of therapy when choosing the appropriate treatment. In patients with clinical or hemodynamic compromise, immediate cardioversion may be required. The patient in this question has mild symptoms, but none currently, and she is not hypotensive. She is an appropriate candidate for pharmacologic treatment. There are several treatment options to control the ventricular rate in atrial fibrillation, but beta-blockers and calcium channel blockers remain superior to other options like digoxin. Anecdotally, emergency physicians prefer calcium channel blockers because they find them to be more effective in treating acute atrial fibrillation with rapid ventricular response, however, both beta-blockers and calcium channel blockers have been shown to be equally effective in the acute setting. Since this patient is already taking metoprolol for other reasons, it might be wise for the clinician to use intravenous metoprolol at this time.

Adenosine (A) is an atrioventricular nodal blocking agent that is indicated to convert paroxysmal supraventricular tachycardia to sinus rhythm. When a patient presents with a fast ventricular rhythm that is difficult to distinguish between atrial fibrillation and supraventricular tachycardia, adenosine may also be used to determine the underlying rhythm. The clinician should be able to recognize this patient’s rhythm as irregular, rather than a regular narrow complex tachycardia. Amiodarone (B) is an antidysrhythmic that can be used to slow the ventricular rate in atrial fibrillation with rapid ventricular response, and it causes less hypotension than calcium channel blockers, but due to its negative long-term side effects, it is not used as first-line therapy. It is used more often for a wide complex tachycardia suggestive of ventricular tachycardia. Intravenous fluid administration (C) would be indicated for patients with sinus tachycardia thought to be due to infection or dehydration. This patient’s rhythm is not regular and does not suggest sinus tachycardia.

Brief (usually less than 10 seconds) tonic–clonic seizure activity can accompany syncope of any etiology. This activity is not accompanied by postictal disorientation, and it does not represent true seizure activity. It is usually described as myoclonic jerking. For cerebrovascular disease to cause a loss of consciousness, either both cerebral hemispheres or the brainstem must be deprived of blood flow. Therefore transient ischemic attacks and stroke are rarely the cause of syncope. Screening laboratory studies have been shown to add little to establishing a cause of syncope. In most cases, hypoglycemia is clinically suspected and abnormal electrolytes rarely account for a loss of consciousness. Anemia from bleeding is usually clinically evident. In otherwise healthy individuals, syncope is most commonly idiopathic (50%).

The patient’s ECG shows atrial fibrillation (AF) and an especially rapid ventricular response (RVR). Its variable, bizarre, wide QRS complexes suggest the presence of preexcited – or the Wolff-Parkinson-White (WPW) syndrome-related – AF. In hemodynamically stable patients, the initial treatment of preexcited AF with RVR consists of rhythm control with an antidysrhythmic agent such as procainamide 100 mg IV. While rate control with AV nodal blocking agents (e.g. diltiazem, metoprolol) is generally the initial treatment for AF with RVR, these medications’ effects can be disastrous for patients with preexcited AF. In this condition, rapidly conducting accessory pathways exist that can carry atrial impulses to the ventricle at rates exceeding 250 beats per minute. AV nodal blocking agents cause both faster and preferential conduction through these accessory pathways, which can result in extremely rapid ventricular response rates and deterioration to ventricular fibrillation. For these reasons, AV nodal blocking agents are contraindicated in preexcited AF.

Adenosine (A) is a short-acting AV nodal blocking agent. While useful in the management of narrow-complex, regular tachydysrhythmias such as AV nodal reentrant tachycardia, it has no role in the management of AF with RVR. Furthermore, its use is contraindicated in preexcited AF. While the initial treatment for AF with RVR generally consists of rate control with IV calcium channel blockers, such as diltiazem (B), or beta blockers such as metoprolol, use of these medications is contraindicated in preexcited AF. Synchronized electrical cardioversion (D) is indicated in the management of a number of tachydysrhythmias, including hemodynamically unstable AF with RVR. However initial treatment with pharmacologic therapy is appropriate for hemodynamically stable AF with RVR.