Ventricular Tachycardia & Ventricular Fibrillation
Introduction
Ventricular tachycardia (VT) is a broad complex (> 120ms) tachycardia ( >110bpm) originating in the ventricles and over riding the normal cardiac conduction.
VT can be sustained or unsustained and monomorphic or polymorphic
Sustained = duration > 30 seconds or requiring intervention due to haemodynamic compromise.
Non - sustained = Three or more consecutive ventricular complexes terminating spontaneously in < 30 seconds.
Monomorphic = QRS morphology is the same for all complexes. It is more common in structural or ischaemic heart disease
Polymorphic = VT with continuously varying morphology. More common in electrolyte abnormalities and secondary to drugs.
It requires a huge effort for the heart to remain in persistent VT. When the heart tires it becomes unable to maintain sufficient cardiac output to produce a palpable pulse and a cardiac arrest ensues. This is pulseless VT, which can transform into Ventricular Fibrillation (VF).
Ventricular Fibrillation is characterised by rapid, chaotic, disorganised electrical activity with no identifiable P waves or QRS complexes. The ventricles are quivering rapidly, resulting in ineffective pumping of blood out of the heart. This leads to cardiac arrest, which is fatal if not treated urgently with defibrillation
Ventricular tachycardia - broad complex regular tachycardia.
Ventricular Fibrillation - rapid chaotic disorganised electrical activity
Risk Factors for VT/VF
Increasing age
Ischaemic heart disease
Structural heart disease
LV failure, cardiomyopathy, HOCM
Prolonged QT interval
electrolytes - hypomagnesaemia, hypocalcaemia
drugs - TCA’s, quinolones, older antipsychotics,
FHx of sudden cardiac death
Clinical Features
Symptoms
Systemic
Fatigue, impending sense of doom, pre-syncope
Cardiovascular
chest pain, palpitations, diaphoresis,
Respiratory
SOB, cough productive of pink frothy sputum.
Signs
Signs of shock
Tachycardia, hypotension, pallor, hypoxia, delayed CRT,
Signs of heart failure
Tachypnoea, bilateral crackles, gallop rhythm, raised JVP, peripheral oedema
Differential Diagnosis
Broad Complex Tachy-arrhythmia
HR > 100 + Regular Broad Complex
Ventricular Tachycardia (VT) - rate > 110bpm
Sinus tachycardia with aberrancy
SVT with aberrancy
Accelerated intra-ventricular rhythm - HR 40–110
HR > 100 + Irregular Broad Complex
Polymorphic VT i.e. Torsades de Pointes
AF with aberrancy
AF with WPW
Clinical Investigations
Ventricular Tachycardia (with or without a pulse) and Ventricular Fibrillation are life threatening cardiac emergencies and are common causes of cardiac arrest and death if not treated urgently.
A rhythm strip on a defibrillator +/- an ECG are sufficient to make the diagnosis. No further investigations are necessary and treatment should not be delayed.
Once a safe perfusing rhythm has been restored, investigations should be performed to ascertain the cause of the VT/VF and to outrule any complications resulting from same.
Bedside
ECG
Ventricular tachycardia
Rate > 110bpm. QRS > 160 ms
Concordance of V1 - V6 (all QRS complexes pointing same direction)
Absence of typical LBBB/RBBB morphology
May see AV dissociation, Capture beats, Fusion beats
Post cardioversion
look for signs of ischaemia
look for evidence of conduction abnormality e.g. Brugada syndrome
assess for presence of prolonged QT interval - common cause of polymorphic VT
VBG
Poorly perfusing rhythm —> High lactate, low pH
Assess for Hypokolaemia
Laboratory
FBC, CRP
elevated acute phase reactants
Troponin
elevated troponin can occur secondary to primary ischaemic event causing the arrhythmia, or may be as a result of rate related troponin leak or secondary to CPR/Cardioversion
Magnesium, Calcium, Potassium
low Ca2+, low K+, low Mg2+ can all cause prolong QT interval
Radiology
Trans thoracic echo
? regional wall motion abnormality, ? cardiomyopathy
CXR
signs of heart failure
CT Brain
if prolonged cardiac arrest ? hypoxic brain injury.
Coronary angiogram
urgent PCI if STEMI on post cardioversion ECG
Management and Disposition
Initial Resuscitation
VT is a life threatening time critical emergency with the potential to deteriorate to VF and cardiac arrest. In the immediate setting there are 2 questions you need to ask yourself.
Does the patient have a pulse?
If they do have a pulse are they stable or unstable?
Pulseless VT/VF
Call for help
Commence CPR
Task someone to manage the airway. Apply O2
Attach defib/AED as soon as possible
VT + VF are shockable rhythms
if patient is on the defib and VT/VF arrest is witnessed shock them immediately otherwise analyse the rhythm and shock if inidcated as soon as the defib is available
Early defibrillation is recognised as a priority in the chain of survival. The likelihood of success decreases with time until initiation
Follow the shockable rhythm ACLS cardiac arrest algorithm opposite.
(courtesy of https://www.aclsmedicaltraining.com/adult-cardiac-arrest-vtach-and-vfib/)
Unstable VT
Should be managed in resus with full non invasive monitoring
Instability is implied if the patient is hypotensive, has a decreased level of consciousness, has signs of heart failure or chest pain.
Call for help
Task someone to manage the airway. Apply O2
Establish IV access
Synchronised DC cardioversion with 100J in the first instance.
Stable VT
Should be managed in resus with full non invasive monitoring.
Stability is implied if the patient is awake and alert with a perfusing blood pressure. The stable patient with VT is at high risk of becoming unstable and suffering a cardiac arrest.
Initial treatment involves loading with antiarrhythmic
IV amiodarone 150mg over 10 mins. Can be repeated x 1. Then commence amiodarone infusion
IV lignocaine or Sotalol are alternatives
Replace electrolytes if Torsades de Pointes/Polymorphic VT
IV MgSO4, IV KCl, IV Calcium as indicated
If patient becomes unstable at any time proceed to urgent synchronised DC cardioversion
Specific Treatment
Once sinus rhythm is restored seek and treat underlying cause
e.g. ischaemia, structural heart disease, electrolytes, drugs
Post cardiac arrest care
optimise airway, respiratory and haemodynamic parameters
Disposition
If evidence of acute ischaemic cause (i.e. STEMI) urgent transfer to cath lab for primary PCI
If conscious = Admission to a high acuity monitored area (e.g. CCU/HDU) under Cardiology service for further work up and ongoing management.
Unconscious patients requiring advanced airway management +/- other organ support will need to be admitted to ICU for ongoing care
References.
Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care
Dunn. R. Cardiac arrhythmias. The emergency medicine manual 5th edition. Vol 1.
This blog was written by Dr Gillian Cotter and was last updated in January 2021