Tachycardia
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Introduction
Tachycardia, or a heart rate above 100 in adults, is a physiologic response to increased metabolic demand or reduced oxygen delivery. Sinus tachycardia can occur normally due to changes in the body outside the heart, during exercise or stress, after administration of various drugs, or following a host of pathological processes.
Tachycardia may also result directly from abnormal heart function, mediated by aberrant electrical activity in the atria, ventricles, or the electrical conducting system.
Sinus tachycardia normally resolves following removal of the precipitating cause. Arrhythmias may also spontaneously resolve, though they may also lead to increasingly chaotic rhythm of the heart and result in pulseless ventricular tachycardia and/or ventricular fibrillation. These signify cardiac arrest, and death will rapidly follow if defibrillation and other treatments are not provided.
The Case of Hector R.
Hector is a 66 year-old man who has noticed his heart 'thumping in his chest' off and on for the past two days. He is a bit worried, as his father died from a heart attack at the same age. He therefore comes to his doctors office for assessment.
- Q: what further questions do you ask?
- Q: how do you examine Hector?
- Q: what tiests do you consider?
Narrow Complex Tachycardias
- sinus
tachycardia - premature atrial
contractions - multifocal atrial
tachycardia - atrial
flutter - atrial
fibrillation
Sinus Tachycardia or Supraventricular Tachycardia
Sinus tachycardia is a physiologic response, with increased sympathetic tone, following a variety of conditions. These can include:
- exercise
- stress or anxiety
- pain
- sleep deprivation
- anemia
- fever
- hypoxia
- hypovolemia
- pregnancy
Medications that can lead to a sinus tachycardia can include:
- caffeine, nicotine, or other stimulants
- sympathetic drugs
- vasodilators
- anticholinergic drugs
- beta blocker withdrawal
Metabolic causes include:
- hypoglycemia
- hyperthyroidism
- phaeochromocytoma
ECG findings include:
- normal P waves and QRS complexes
Supraventricular tachycardias can include: AV nodal re-entry, WPW with orthodromic conduction, or accelerated junctional tachycardia.
SVT is the most common sustained dysrrhythmia in children. It is not life-threatening, but can be symptomatic.
Treatment includes carotid massage, valsava maneuver, medications, or cardioversion if unstable. Catheter ablation can be used to destroy distinct rentry foci, mapped using electrophysiologic techniques.
Premature Atrial Contractions
Premature atrial contractions (PACs) are common in healthy and diseased hearts. They can be exacerbated by:
- sympathetic stimulation
- caffeine, nicotine, cocaine, or other stimulants
- alcohol
- stress
They originate from automaticity or reentry in an atrial site.
They are usually asymptomatic but can cause palpitations.
ECG findings can include:
- abnormal P waves and are followed by normal QRS complexes, unless it falls during the refractory period.
Beta blockers are the preferred treatment if needed.
Multifocal Atrial Tachycardia
Multifocal atrial tachycardias can result in regular or irregular rhythms...
Atrial Flutter
Atrial flutter is characterized by regular atrial activity at a rate of 180-350 bpm. Many of these beats fall during the ventricular refractory period, resulting in a much slower ventricular heart rate. A fixed block can result in a ventricular rate of 300, 150, 100, 75, or 60.
Atrial flutter is typically caused by a large rentry circuit. It generally occurs following heart disease, and can can be transient, persistent, or permanent.
ECG findings includes:
- P waves with a sinusoidal or sawtooth appearance.
Flutter can be treated with cardioversion, implantable pacing, catheter ablation, or medications. However, some antiarrythmics can worsen the tachycardia by slowing the atria enough to allow 1:1 ventricular contraction, speeding up the ventricles.
Atrial Fibrillation
main article: atrial fibrillation
Atrial fibrillation is a very common atrial arrhythmia in which the atria contract chaotically and often very rapidly. As many of these beats are conducted through the heart, the ventricular rhythm can also be quite fast, often up to 140-160.
Cardiac output can decrease with the increased ventricular rate, and cardiac ischemia can also result due to the increased metabolic demand. Atrial fibrillation can also lead to blood clots forming in the poorly contracting atria. These clots can leave the heart and cause strokes and other types of ischemic disease in the body.
Atrial fibrillation is frequently seen with increased age, hypertension, and in heart disease. There are many other known risk factors, described on it's dedicated page listed above.
Wide Complex Tachycardias
- premature ventricular
contractions - ventricular tachycardia
- Torsades
de Pointes - ventricular
fibrillation
Premature Ventricular Contractions
Premature ventricular contractions (PVCs) arise when an ectopic ventricular focus spontaneously fires an action potential. This appears as a widened QRS complex, as the impulse travels in an altered path. If every alternating beat is a PVC, it is called bigeminy. Consecutive PVCs are called couplets, and three are triplets.
PVCs are common in healthy people, particularly adolescents. Benign PVCs are single, uniform, disappear with exercise, and have no structural abnormalities present.
If underlying cardiac or metabolic conditions are present, PVCs can represent dangerous precursours to severe dysrhythmias or sudden death.
Ventricular Tachycardia
Ventricular tachycardia (VT) is a run of three or more PVCs. Sustained VT lasts linger than 30 seconds, can induce syncope, or requires termination by drugs or cardioversion.
Ventricular tachycardia is commonly seen in patients with structural heart disease, including myocardial infarction, heart failure, hypertrophy, electrical diseases, valvular heart diseases, and congenital heart diseases. Reentry circuits are most commonly old scars.
ECG findings
QRS complexes are wide, and occur at rates of 100-200, or sometimes faster. These wide QRS complexes distinguish ventricular tachycardia from supraventricular causes.
Idiopathic VT exists and is rarely life-threatening. However, new-onset, VT is an emergency, as it can quickly deteriorate into ventricular fibrillation. Cardioversion is normally done, or drugs such as amiodarone, procainamide, or lidocaine can be used to medically convert the rhythm. Underlying risk factors should be identified and addressed, and pacemakers are very useful for future episodes.
Torsades de Pointes
Torsades de pointes is a form of ventricular tachycardia with varying amplitudes of QRS waves. It is commonly caused by drugs, electrolyte imbalances (hypokalemia or hypomagnesemia), on top of prolonged QT intervals. It is usually symptomatic but frequently self-limiting.
Ventricular Fibrillation
main article: cardiac arrest
Ventricular fibrillation is rhythm that signifies cardiac arrest - the cessation of a heart beat sufficient to perfuse the body. Clearly this is a life-threatening emergency, requiring rapid, high-quality resuscitation in the form of CPR and defibrillation.
VF often is a terminal rhythm that follows other arrhythmias, especially ventricular tachycardia and Torsades de Pointes, described previously.
History and Physical Exam
A tachycardia may represent an unstable, life-threatening condition. Ensure the patient's ABC's (airway, breathing, and circulation) are being managed, as described under 'basic life support'.
- history
- physical exam
History
When interviewing a patient with undiagnosed tachycardia, inquire into the following:
- when did it begin?
- has this ever happened before? (get details)
- is there chest pain or shortness of breath?
- have they passed out?
- is there fever, chills, or other evidence of infection?
A review of systems is also warranted.
Past medical history should include:
- heart disease
- thyroid disease
Social history should include:
- sleep patterns
- alcohol use
- drug use
- cigarette smoking
- caffeine intake
- stress levels
Physical Exam
Examine the patient's overall state, including:
- level of consciousness
- vital signs
- colour
Specific attention should be paid to:
- cardiac exam
- respiratory exam
Investigations
- lab investigations
- diagnostic imaging
Lab Investigations
If investigations are warranted, bloodwork should include:
- CBC
- electrolytes
- creatinine
- troponin
- TSH
- calcium, magnesium
Diagnostic Imaging
ECG is the mainstay of imaging. Other tests to investgate a tachycardia can include:
- chest X-ray (investigate for heart failure)
- echocardiogram
Management
Treatment of tachyarrhythmias is meant to stabilize the patient, protect against lethal consequences, and mitigate the underlying cause(s) of the arrhythmia.
As described, it is paramount to assess and address the ABC's when managing a patient with tachycardia. This can include:
- Opening the airway
- Providing supplemental oxygen, postive pressure ventilation, and/or intubation
- IV access x2 and fluid administration
- Chest compressions
- Defibrillation
Medications that may be used to slow the heart and maintain it in normal rhythm include:
- beta blockers
- calcium channel blockers
- digoxin
- amiodarone
- adenosine
Antiarrhythmics must be used with caution due to the high risk of further arrhythmic complications and death.
Electrical cardioversion and defibrillation can be used to depolarize the bulk of myocardial tissue, interrupting rentry and allow the sinus node to regain pacemaker control. Implantable cardioverters can be used to automatically cardiovert or defibrillate a heart.
Pathophysiology
main article: electrical control of the heart
There are many underlying processes that can lead to tachycardias:
Ectopic Rhythms
If an area of tissue develops an intrinsic rate of firing faster than that of the SA node, ectopic (premature) beats can occur. They can occur due to high catecholamine concentrations, hypoxemia, ischemia, electrolyte disturbances, and drugs such as digitalis.
Abnormal Automaticity
Injured cardiomyocytes can acquire automaticity and spontaneously depolarize, though means not fully understood, but likely involving a slow calcium current.
Triggered Activity
Under certain conditions, action potentials can trigger abnormal depolarizations that result in extra heart beats or rapid arrhythmias. Afterdepolarizations appear as oscillations and can be early, during repolarization, or delayed. Early afterdepoloarizations are most common during conditions that prolong APs, such as long GT syndrome.
Reentry
Reentry occurs when impulses circuluate around a unidirectional conduction block, recurrently depolarizing a region of cardiac tissue. Reentry around distinct anatomic pathways usually appears as monomorphic tachycardia on an ECG, while fibrillation is likely caused by multiple circulation reentry wave fronts.
Resources and References
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