Supraventricular & Ventricular Arrhythmias
Sections
Atrial Flutter
Description:
Rapid, regular P waves give ECG "sawtooth" appearance.
Atria beat ~300 beats/minute. Only ½ - 1/3 of the electrical impulses make it through the AV node and reach the ventricles, so heart rate is increased ~150 beats per minute.
Symptoms & Signs:
May be none. Or, may cause palpitations, and reduced CO, difficulty breathing, weakness, chest discomfort, syncope.
Treatment:
Rate control with drugs: beta-blockers, calcium channel blockers (verapamil, diltiazem). Rhythm control with cardioversion, drugs (antiarrhythmics), possibly ablation. Anticoagulants (warfarin) are used to prevent thromboembolism).
Risk Factors:
Commonly occurs in healthy people, but risk increases with other cardiac conditions, binge alcohol consumption, diabetes.
Clinical Concerns:
When coupled with other cardiac complications, can lead to stroke, makes heart work more difficult, ventricular weakening, and coagulation is more likely. Patients may have periods of atrial fibrillation.
Atrial Fibrillation
Description:
Rapid, irregular and indiscrete P waves on ECG. Atria do not contract in coordinated fashion, but send fast and irregular signals to ventricles increase heart rate.
Symptoms & Signs:
May be asymptomatic. Or, may experience lack of energy, fast, irregular pulse, difficulty breathing, palpitations, chest discomfort, dizziness.
Treatment:
Rate control with beta blockers and nondihydropyridine calcium channel blockers. AV node blockers possible (but rule out Wolff-Parkinson-White Syndrome with accessory pathway; look for wide QRS). Anticoagulation before cardioversion therapy to prevent thromboembolism.
Risk Factors:
Other cardiac problems, hyperthyroidism, obesity, diabetes, lung disease, binge alcohol consumption.
Clinical Concerns:
Stroke, systemic emboli. Echocardiography to check for structural defects, thyroid function tests. Must rule out Wolff-Parkinson-White Syndrome before prescribing AV-node blocking drugs, which are fatal to affected individuals.
Asystole
Often described as "Flat-lining" on ECG.
Cessation of electrical and mechanical cardiac activity, associated with decompensation of ventricular fibrillation.
Pulseless Electrical Activity
Cardiac electrical activity is present, but no pulse is present due to inactivity of cardiac muscle.
Both asystole and pulseless electrical activity can lead to cardiac arrest.
Premature Beats (Atrial & Ventricular)
Description:
Early atrial or ventricular contractions, visible on ECG. Caused by ectopic pacemaker activity.
Symptoms & Signs:
Palpitations, "skipped" beats.
Treatments:
Asymptomatic, if no other problems. Beware of antiarrhythmias, which can cause more serious arrhythmias.
Risk Factors:
Stress, caffeine, alcohol, hypoxia, electrolyte imbalances. Heart disease, pulmonary disease, and scarring can also interfere with normal electrical activity.
Clinical Concerns:
Can develop flutter/fibrillation.
Wolff-Parkinson-White Syndrome
Accessory electrical pathway that predisposes to Supraventricular tachycardia
Description:
Short PR interval and positive delta wave at beginning of broad QRS complex; delta wave reflects early depolarization. Occurs as result of AV node bypass, called bundle of Kent.
Symptoms & Signs:
May be asymptomatic. May have episodes of increased heart rate, chest pain, dizziness, palpitations, difficulty breathing.
Treatments:
Direct-current cardioversion therapy is preferred; long term treatment may require catheter ablation. Beware digoxin/nondihydropyridine calcium channel blockers to WPW patients, as they may trigger ventricular fibrillation (fatal).
Risk Factors:
Congenital form (mutation on Chromosome 7), or acquired.
Clinical Concerns:
Associated with Ebstein anomaly, displaced tricuspid valve). Atrial fibrillation can develop (depends on presence of antegrade conduction through accessory connection).
Ventricular Tachycardia
Description:
3+ consecutive beats 120+ beats/minute; abnormal ventricular automacy.
Symptoms & Signs:
May be asymptomatic if duration is short (aka, paroxysmal) or rate is not excessive; If sustained, palpitations, difficulty breathing, chest pain, dizziness, fainting, death.
Treatments:
Cardioversion, antiarrhythmic drugs, defibrillator implant.
Risk Factors:
Heart disease, electrolyte imbalances, medications.
Clinical Concerns:
Can lead to heart failure, unconsciousness, sudden death by cardiac arrest.
Torsades de Pointes
Special case of ventricular tachycardia, associated with Long QT Syndrome.
Description:
Rapid, irregular QRS complexes "spiral" around baseline, as ventricular rate varies from cycle to cycle.
Symptoms & Signs:
Recurrent palpitations, dizziness, fainting, difficulty breathing.
Treatments:
Magnesium.
Risk Factors:
Electrolyte imbalances (hypocalcemia, hypokalemia); Medications (antiarrhythmics, tricyclic antidepressants, anti-histamines when taken with erythromycin. In individuals with Long QT Syndrome, can be triggered by stress, fear, etc.
Clinical Correlations:
Can lead to ventricular fibrillation, which is fatal.
Long QT Syndrome
Form of ventricular tachycardia, increases risk for Torsades de pointes.
Description:
Long QT interval on ECG, reflects defective ion channels.
Risk Factors:
Often inherited, but can be acquired (electrolyte imbalances, antihistamines, decongestants, diuretics, antiarrhythmic drugs, antidepressants, etc.). Inherited types may also be triggered by these medications.
Inherited types include Romano-Ward Syndrome (Types 1-3) and Jervell and Lange-Nielsen Syndrome, which is also associated with congenital deafness.
Clinical Correlations:
Prone to torsades de pointes, which can cause syncope, ventricular fibrillation, and sudden death.
Ventricular Fibrillation
Description:
Uncoordinated ventricular activity.
Symptoms & Signs:
Loss of consciousness, chest pain, dizziness, tachycardia.
Treatments:
CPR & Defibrillation
Risk Factors:
Ischemic heart disease, hypertrophic/dilated myopathies, Brugada syndrome, arrhythmic right ventricular dysplasia.
Clinical Concerns:
Cardiac arrest, Death
Clinical Cases
Case 1: Arrhythmia Presentation
A 61-year-old female returns to your clinic today after being diagnosed three days ago with a urinary tract infection. You prescribed her levofloxacin 250 mg orally (PO) once daily for three days. Last night, the patient reports "fainting" while watching television with her husband. There were no reported associated signs or symptoms, and the event was self limiting. She has no history of similar episodes. Today, she has no complaints and reports feeling "fit as a fiddle".
On physical examination, her blood pressure is 130/80 mm Hg, pulse 75/min, and respiratory rate 18/min. Her cranial nerves II through XII appear to be intact on cursory examination. No carotid bruits are observed. Chest auscultation demonstrates clear lung fields bilaterally, and a normal cardiac assessment. Her remaining physical examination is unremarkable. You obtain an electrocardiogram (EKG) in clinic today, which demonstrates QT prolongation.
Based on her history and physical examination, and EKG, what is the most likely cause of her syncopal episode?
Answer
- Ventricular arrhythmia
Explanation
This patient has QT prolongation secondary to antibiotic therapy. The loss of consciousness she experienced was likely secondary to a ventricular arrhythmia. The QT interval reflects how the lower chambers (ventricles) are functioning electrically. Normally, in males the QT interval is between 350 and 450 milliseconds (ms), and in females between 360 and 460 ms. If the QT interval is prolonged, it takes longer than usual for the heart to recharge between beats and cardiac output is diminished.
A prolonged QT interval (Long QT Syndrome) is most commonly a genetic disorder, though as in this clinical scenario, there are also medications (antiarrhythmics and antibiotics) which are known to cause QT prolongation. The most commonly implicated antiarrhythmics are class III (potassium-channel blockers) including amiodarone, dofetilide, and sotalol. Class 1a antiarrhythmics (fast sodium-channel blockers) such as quinidine and procainamide, are also offending agents. Antibiotics associated with QT prolongation are macrolides (azithromycin, erythromycin, clarithromycin), and fluoroquinolones (levofloxacin, ciprofloxacin, moxifloxacin). Initially, a prolonged QT interval will destabilize the ventricles and lead to inverted and beat-to-beat alternations in T-wave morphology (T-wave alternans), which is seen on this patient's initial EKG. T-wave alternans is caused by a variety of conditions and is an important marker of increased risk for sudden cardiac death.
If allowed to progress, a prolonged QT will develop into a distinctive form of polymorphic ventricular tachycardia (VT) characterized by gradual changes in the amplitude and "twisting" of the QRS complexes around the isoelectric line (see image) known as Torsades de Pointes. If no pulse is present, the patient should be defibrillated. Otherwise, intravenous (IV) magnesium (2 g) is the first-line pharmacologic therapy for Torsades de Pointes.
Case 2: Arrhythmia Management
A 58-year-old male presents to the emergency department complaining of chest pain that began suddenly and has been ongoing for the last 30 minutes. The patient reports that the pain is located in the center of his chest and is described as a crushing sensation. He also reports shortness of breath, nausea, and diaphoresis. The patient has a history of hypertension, hyperlipidemia and a past myocardial infarction. He is currently taking aspirin, atorvastatin, lisinopril, and metoprolol.
On physical examination, the patient is alert and oriented but appears uncomfortable. His blood pressure is 160/90 mm Hg, heart rate 110/min, respiratory rate 20/min, and oxygen saturation is 96 percent on room air. The patient's cardiac examination reveals tachycardia and the presence of a III/VI systolic murmur. You order an electrocardiogram which shows ST-segment elevation in leads II, III, and aVF, consistent with an acute myocardial infarction. Laboratory results show an elevated troponin level. You order the patient to be given morphine, nitroglycerin, and aspirin, and place him on oxygen via facemask and cardiac telemetry. Suddenly, the patient becomes unresponsive and you note acute changes in his cardiac telemetry (see image).
Which of the following interventions is the best next step in managing this patient?
Answer
- Shock the patient with 200 Joules
Explanation
The patient in this scenario is demonstrating ventricular fibrillation on the electrocardiogram. The definitive treatment for ventricular fibrillation is electrical defibrillation. Most current defibrillators utilize a biphasic waveform that allows for a lower energy level to be used to achieve effective cardioversion. Shocks should only be delivered for pulseless ventricular tachycardia (VT) and ventricular fibrillation (VF). Patients receiving prompt defibrillation have improved survival (39.3 percent) compared to patients in whom defibrillation was delayed by 2 minutes or more (22.2 percent). It is important to differentiate ventricular fibrillation from pulseless electrical activity (PEA)/asystole as both these conditions are managed differently as per ACLS protocol.
Case 3: Arrhythmia Management (2)
You respond to an overhead page concerning an unresponsive patient (code). On arrival at the bedside, you find a 73-year-old male unresponsive. He is not your patient and you know nothing about his medical history or current regimen. Staff advise you he was admitted yesterday for exacerbation of long-standing congestive heart failure (CHF), and they are in the process of retrieving his current medication list.
The patient is being monitored, and vital sign readings demonstrate blood pressure 90/50 mm Hg, heart rate 320/min, respiratory rate 10/min, and an oxygen saturation of 85 percent on 2L of oxygen via nasal cannula. The rhythm strip on the monitor reveals a rapid, irregular tracing with no clear P waves, T waves, or QRS complexes.
Suddenly, the alarm on the cardiac monitor begins to sound, and the rhythm tracing now appears as a flat line with no apparent electrical activity. You quickly auscultate the patient's chest and hear no heart sounds, which you confirm by palpating the radial artery in his wrist and feeling no pulsation. You immediately order cardiopulmonary resuscitation (CPR) chest compressions to be initiated. What is the next most appropriate step in the management of this patient?
Answer
- Epinephrine 1 mg IV
Explanation
This patient's heart has stopped and there is no discernable electrical activity (asystole). This is confirmed by auscultation of the heart and palpation of the radial artery. In addition to high-quality cardiopulmonary resuscitation (CPR) chest compressions, this patient should be given epinephrine (adrenaline) 1 mg intravenously (IV) immediately. The initial dose may be repeated at 3 to 5 minute intervals until a shockable or perfusing rhythm is established.
Additional Information
Review of Cardiac Cycle; Cardiac Muscle Cell; Wigger's Diagram