Pulseless ventricular tachycardia is a life-threatening cardiac arrhythmia in which coordinated ventricular contractions are replaced by very rapid but ineffective contractions, leading to insufficient organ perfusion and heart failure. Pulseless ventricular tachycardia is a medical emergency.
Due to rapid ventricular contractions, the ventricular filling decreases markedly, leading to a dramatic decrease in cardiac output. As a result, a pulse is absent. Electrophysiology identifying factors for pulseless ventricular tachycardia include; tachycardia (>100 bpm), wide QRS complexes (> 120 milliseconds), atrioventricular (AV) dissociation, presence of fusion or capture beats and an electrical axis between -90 to -180. There are several scoring systems to differentiate ventricular tachycardia from a wide complex supraventricular tachycardia, but 90% of wide complex tachycardia cases will be ventricular tachycardia.
The ventricular arrhythmia can be characterized as either monomorphic (no variation of the QRS from beat to beat) or polymorphic (changing or multiform QRS from beat to beat). The most common cause of pulseless ventricular tachycardia is cardiac ischemia.
Pulseless ventricular tachycardia (VT) can result from a multitude of causes and predisposing conditions, including but not limited to, structural heart disease, electrolyte disturbances, drugs/medications, and congenital/inherited channelopathies. The most common cause of ventricular tachycardia (including pulseless VT) is concomitant structural heart disease.
Below are several examples organized into the following categories:
Structural Heart Disease:
Drugs/medications that cause QT prolongation:
Ventricular tachycardia (VT) remains a significant contributor to most sudden cardiac deaths in the U.S., at an estimated rate of approximately 300000 deaths per year. The majority of these deaths occur in adults greater than 35 years of age, with at least half attributable to ventricular arrhythmias. Estimates of its prevalence vary from 30% to 75% of out-of-hospital cardiac arrests despite recent increases in the incidence of pulseless electrical activity. However, the true incidence is unknown due to inevitable degeneration to asystole if unwitnessed. Despite the decline in coronary artery disease mortality and advancements in resuscitation services, survival from these events remains low, especially if occurring outside the hospital environment, with an associated survival rate of less than 10%.
Electrophysiological mechanisms of pulseless ventricular tachycardia are increased automaticity and triggered activity. Electrical impulses originating in ventricular myocardium spread through ischemic myocardium or scar tissue resulting in retrograde atria activation or AV dissociation.
In pulseless ventricular tachycardia, the ventricles contract at a rate too rapid to allow for an adequate filling time during diastole, subsequently resulting in hemodynamic collapse from a diminished cardiac output causing insufficient blood supply to end organs. Abnormal ventricular conduction and asynchrony further reduce the effectiveness of ventricular contractions and aggravate the hemodynamics, leading to sudden collapse. There are two main types of ventricular tachycardia with the morphology of the QRS complexes serving as clues to the cause responsible for the rhythm.
In monomorphic ventricular tachycardia, which is more common, the QRS complexes are identical because there is increased automaticity originating from a single focus in either of the ventricles or a re-entry circuit within the ventricle. The most common cause for monomorphic ventricular tachycardia is scarring of the myocardium from myocardial infarction, which promotes the development of an electrical circuit around the non-conducting fibrotic tissue resulting in the formation of multiple circuits that potentially can evolve into a re-entrant ventricular tachyarrhythmia.
In polymorphic ventricular tachycardia, the QRS complexes vary in morphology and usually result from inherent genetic mutations that disrupt the ion channel function of cardiac myocytes and cause electrophysiological abnormalities during ventricular repolarization. Congenital conditions predisposing to polymorphic ventricular tachycardia usually exhibit prolongation of the QT interval on the EKG. Acquired etiologies that may lead to the development of polymorphic ventricular tachycardia also include drug toxicity of antiarrhythmic drugs, antibiotics, and antipsychotic medications that prolong the QT interval.
Before the event, patients with pulseless ventricular tachycardia may complain of chest pain, palpitations, dyspnea, light-headedness, and syncope. On physical examination, there will be signs of impaired perfusion, hypotension, tachypnea, elevated jugular venous pressure, and S1 heart sound. Sudden collapse results from ineffective ventricular contractions and low cardiac output.
At the time of the event, patients with pulseless ventricular tachycardia are unconscious and unresponsive without a palpable pulse. Any delay in starting defibrillation dramatically reduces survival, and death may occur in a few minutes.
The diagnosis of pulseless VT is based on physical examination and ECG. Cardiopulmonary resuscitation, according to Advanced Cardiac Life Support guidelines, should be started immediately as far as the diagnosis is confirmed. ECG findings usually include regular R-R intervals, rapid ventricular rate with an undistinguishable atrial rate (absence of p-waves), AV dissociation, and a wide QRS complex (more than 0.12 sec).
Several ECG criteria have been created to help diagnose VT. These criteria include:
The Classical Criteria:
If any single one of the above Brugada criteria is present, then VT is diagnosed.
The Vereckei Criteria:
In general, per the AHA, basic criteria to support the diagnosis of VT includes :
Pulseless ventricular tachycardia is a medical emergency, and its management should follow advanced life support guidelines. Pulseless VT requires immediate electrical cardioversion with high-energy defibrillator (150-200 J on biphasic and 360 J on monophasic). Delaying defibrillation for 2 minutes or more decrease survival rate compared with patients received immediate defibrillation (39,3% vs. 22,2%).
In a series of shocks, each following shock should be higher in energy than the previous shock. After the first shock delivered, 5 cycles of CPR should be performed. Each CPR cycle should contain 30 chest compressions followed by 2 breaths. Cardiopulmonary resuscitation is performed only until the defibrillator is ready. Defibrillation requires fewer joules if it is done early. After every shock, chest compressions should be performed, along with oxygen delivery and intravenous injection of vasopressors and antiarrhythmic drugs.
After the conversion to sinus rhythm, the patient should be monitored continuously. Metabolic acidosis quickly follows cardiovascular collapse. If the arrhythmia is terminated within 30 to 60 seconds, significant acidosis does not occur. If a patient is unresponsive after return to a normal rhythm or the event happened out-of-hospital, hypothermia cooling to 32-34 degrees Celcius for 24 hours should be initiated for possible neurologic recovery.
In every case of pulseless VT acute myocardial infarction should be suspected and urgent coronary angiography and PCI should be considered if feasible. Fibrinolytic therapy during CPR for pulseless VT is not recommended.
Medical treatment of pulseless VT usually is carried out along with defibrillation and includes intravenous vasopressors and antiarrhythmic drugs. 1 mg of epinephrine IV should be given every 3 to 5 minutes. Epinephrine can be replaced by vasopressin given 40 units IV once. Amiodarone is the most studied drug and is used for the prevention of sudden cardiac death (SCD). Sotalol is the most widely used alternative but is associated with an increased risk of SCD due to decreasing defibrillation threshold. Patients on beta-blockers reported having lower mortality rates.
For primary prevention of SCD in patients from the high-risk group, as well as for secondary prevention in patients who already have a prior history of sustained VT or VF, ICD implantation is recommended. Implantable cardiac defibrillators (ICDs) have benefits in terms of mortality and survival rates compared to medical treatment.
The following signs speak in favor of ventricular tachycardia: QRS complex greater than 0.14 seconds with right bundle branch morphology or greater than 0.16 seconds with left bundle branch morphology, RS interval > 100 ms in a precordial lead, AV dissociation, negative QRS concordance in the precordial leads and ventricular fusion beats.
If the patient’s condition allows, differential diagnosis of a wide-complex tachycardia should be made between ventricular tachycardia (80% of wide-QRS tachycardia cases), supraventricular tachycardia (SVT) with aberrant conduction (15% to 20%) and SVT with pre-excitation and antidromic atrioventricular reentrant tachycardia (AVRT) (1% to 5%). Every wide complex tachycardia should be considered as VT until proven otherwise.
Prognosis of pulseless ventricular tachycardia heavily depends on the time from the onset of tachycardia to defibrillation and restoration of sinus rhythm and efficient perfusion. Shorter delays in defibrillation associated with higher survival rates, up to 50%. Delays in treatment up to 15 minutes decrease the survival rates to as low as 5%. The prognosis also depends on a patient's cardiac status, including underlying ischemic or structural heart disease, as well as other comorbidities.
Pusless ventricular tachycardia can lead to cardiac arrest and insufficient organ perfusion, which is the main cause of most complications. Anoxic brain injury and lifelong neurological complications can result from tachycardia that lasts for greater than 3 minutes. Anoxic brain injury is one of the multiple pathophysiological conditions that can occur in post-cardiac arrest syndrome.
Other complications of the post-cardiac arrest syndrome include post-cardiac arrest myocardial dysfunction and systemic ischemia/reperfusion response. Myocardial dysfunction from ischemia can lead to transient global dysfunction and is a common cause of early mortality after cardiac arrest. Reperfusion after ischemia causes activation of immunologic and coagulation pathways, which increases the risk of multiple organ failure and infections. The ischemic-reperfusion injury also depletes intravascular volume and impairs vasoregulation and oxygen delivery to organ tissues. Treatment for post-cardiac arrest syndrome includes multiple areas of treatment measures, including hemodynamic monitoring, airway management, and neurological assessments.
Pulseless ventricular tachycardia is most commonly due to cardiac ischemia. Patients with ischemic heart disease should be educated on lifestyle changes such as low cholesterol and low salt diet and regular exercise. Patients who smoke should be encouraged to quit smoking. Patients should be sure to establish with a cardiologist for follow up and for proper medical management to ensure the underlying cause is being properly treated and to prevent reoccurrence. In patients where the cause of ventricular tachycardia was due to medication side effects, proper medication education for all patients is essential.
Pearls and Key Issues
Pulseless ventricular tachycardia is a life-threatening arrhythmia. Early recognition and prompt cardiopulmonary resuscitation with defibrillation can be life-saving and may also prevent lifelong complications. Interprofessional healthcare teams usually include nurses, physicians, mid-level providers, anesthesia, respiratory therapists and pharmacists. Effective communication between all members of the healthcare team is essential for early initiation of life-saving measures in patients who develop pulseless ventricular tachycardia. Each minute in treatment delay decreases the chance of survival by approximately 10%. Continuing medical education keeps providers and medical staff up to date on The American Heart Association ACLS protocol, and all healthcare team members need to be certified and remain current. In persons who recover, prompt evaluation by a cardiologist is essential for the prevention of recurrent arrhythmias and complications. [Level 1]
A board-certified cardiology pharmacist will play a vital role in these cases, given the nature of the drugs involved. They will consult with the cardiology team on agent selection, appropriate dosing, check for interactions, and provide direction to nursing staff on adverse events. Nursing will monitor the patient after assisting in the emergency procedures upon arrival at the healthcare facility. These interprofessional actions will increase survival in cases of pulseless VT. [Level 5]
Bystander CPR and public access to a defibrillator have helped increase the survival rate of out of hospital cardiac arrest, although survival remains under 10%. Once the patient has arrived at the hospital, temperature control, and cardio-cerebral resuscitation measure further improve overall survival. [Level 1]
Regardless of the location, early recognition and prompt initiation of advanced cardiac life support protocol are crucial elements to survival.
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