Ventricular and life-threatening arrhythmias Flashcards
What is a VE
A premature beat arising from an ectopic focus within the ventricles.
Bypasses the His-Purkinje system and depolarises the ventricle directly.
Consequent interventricular conduction delayproduces QRS complexes with prolonged duration and abnormal morphology.
Ventricular Ectopics - ECG criteria
ECG criteria
Bizarre/broad QRS (≥0.12 seconds).
Premature.
Compensatory pause.
ST segment and T wave changes. - discordance: the ST segment and T wave are directed opposite to the main vector of the QRS complex.
2 VEs = Couplet
3 VEs = Triplet
4 VEs = Salvo
5+ VEs = VT
Types of VEs
Unifocal VEs - VEs can be unifocal, where they arise from a single ectopic focus and every VE looks identical.
Multifocal VEs - Multifocal VEs arise from two or more different areas of the heart, giving rise to multiple QRS morphologies.
PVCs arising from the LV have a RBBB appearance and PVCs arising from the RV have a LBBB appearance.
Ventricular Bigeminy - every other beats is a VE.
Ventricular Trigeminy - Every third beat is a VE.
Ventricular tachycardia - 5+ VEs. Broad complex tachy originating from the ventricles.
Regular rate
No P wave association
Impaired cardiac output
Ventricular tachycardia may impair cardiac output with consequent hypotension, collapse, and acute cardiac failure. This is due to extreme heart rates and lack of coordinated atrial contraction (loss of “atrial kick”).
VT classification
Monomorphic/polymorphic.
Duration: sustained or non-sustained.
Haemodynamically stable or unstable (hypotension, chest pain, unconscious).
Sustained ventricular tachycardia is defined as tachycardia that continues for more than 30 seconds or leads to hemodynamic compromise within 30 seconds and requires intervention. On the other hand, non-sustained ventricular tachycardia lasts less than 30 seconds and does not cause hemodynamic instability.
Causes of VT
Acute MI or Ischaemia
Past MI
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy
Arrhythmogenic Right Ventricular Dysplasia
Myocarditis
Mitral Valve Prolapse
Valvular Heart Disease
Repair of Tetralogy of Fallot
Idiopathic
Anti-arrhythmic drugs (!)
How does CHD cause VT
Myocardial damage from infarction, occurs days, weeks or even years after MI. the worse the ventricular function that more susceptible the patient is to this arrhythmia. VT pt whose LVEF <40% lower the EF the worse the prognosis
Poor ventricular function
- most AA’s drugs negatively ionotropic (weakening of contraction, reduced rate) i.e. they may worsen ventricular function and are ‘proarrhythmia’
- i.e. cause or aggravate arrhythmias. Amiodarone is fairly safe and is widely used in this situation. Supress arrhythmia unlikely to improve prognosis. ICD.
- Some cases not cause by scar but ichaemia likely on exertion – coronary revascularization maybe effective and beta blocker may prevent this arrhythmia. Ischemia can trigger PVCs, which can trigger VT or when areas of conduction become ischaemic, they can become electrically instable triggering abnormal electrical activity
How does DCM cause VT
DCM is a disease of your heart muscle which enlarges your heart’s main pumping chamber (left ventricle), causing your heart’s muscle wall to stretch and become thin (dilate). This makes it harder for your heart to pump blood out of your heart and around your body.
Your left ventricle is almost always affected. Over time, it can affect your right ventricle (another chamber) too.
Negatively inotropic antiarrhythmia drugs should be avoided, beta blockers and/or amiodarone maybe required and defibrillator implantation considered
How does HCM cause VT
The thickening of the heart muscle, particularly in the left ventricle, can cause the heart to become stiffer and less compliant, making it harder for the heart to relax and fill with blood. This can lead to impaired diastolic function and increased pressure within the heart chambers
Hypertrophic cardiomyopathy (HCM) can lead to ventricular tachycardia (VT) due to structural changes in the heart, including muscle thickening (myocardial hypertrophy), abnormal fiber arrangement, and fibrosis, which disrupt electrical conduction and create a substrate for abnormal heart rhythms
Cardiomyopathy- in many patients asymptomatic and benign, however can cause sustained and non-sustained ventricular tachycardia and sudden death maybe the first manifestation of the condition.
Sustained VT – Beta Blockers, amiodarone, ICD. Non-sustained VT- has been shown to be an important risk factor for sudden death. Other risks factors- syncope, family history of sudden cardiac death, severe left ventricular hypertrophy and failure to increase BP on ETT. >1 present amiodarone or ICD
How does ARVD cause VT
fatty/fibrous infiltration of RV, sometimes localised. Impaired function demonstrated by angiography, MRI or Echo. Often some LV involvement too.
Familial inherited autosomal dominant gene both genders equally likely to inherit men more commonly affected by clinical manifestations- arrhythmia/heart failure. Tachy arise from RV has LBBB in SR T wave inversion in V1-V3 QRS duration slightly increased.
How do epsilon waves cause VT
Epsilon waves are small, low-amplitude signals that appear on an electrocardiogram (ECG) between the end of the QRS complex and the beginning of the T wave.
They are a hallmark feature of ARVC/D, a condition where the right ventricle is structurally abnormal and prone to arrhythmias.
They represent delayed depolarization of the right ventricular myocardium
Epsilon waves are thought to be caused by delayed excitation of islands of surviving cardiomyocytes within the right ventricle, which are embedded in a sea of fat and fibrosis.
Epsilon waves are a major diagnostic criterion for ARVC/D.
They can help identify patients at risk for VT and other arrhythmias.
The presence of epsilon waves during VT may indicate a more severe form of the disease and a poorer prognosis.
Low amplitude wave seen in terminal portion of QRS complex in V1 and V2.
Pts present 20-50yrs with palpitations, pre syncope and syncope. Arrhythmia provoked by effort. Disease progressive. Sudden death can occur and maybe first manifestation.
Avoid exertion. Beta blockers and/or amiodarone. Consider ICD due to risk and progression-in those presenting with VT.
Distinguishing VT from SVT
There are several electrocardiographic features that increase the likelihood of VT:
Absence of typical RBBB or LBBB morphology
Very broad complexes (>160ms)
AV dissociation(P and QRS complexes at different rates)
Capturebeats— occur when the sinoatrial node transiently ‘captures’ the ventricles, in the midst of AV dissociation, to produce a QRS complex of normal duration.
Fusionbeats— occur when a sinus and ventricular beat coincides to produce a hybrid complex.
Positive or negativeconcordancethroughout the chest leads, i.e. leads V1-6 show entirely positive (R) or entirely negative (QS) complexes, with no RS complexes seen.
Capture and Fusion Beats in VT
Capture beat: the sinus node “captures” the ventricles producing a narrow-complex beat.
Fusion: a sinus and ventricular beat coincide to produce a hybrid complex of intermediate morphology.
The likelihood of VT is increased with:
Age
Structural heart disease
Ischaemic heart disease
Previous MI
Congestive heart failure
Cardiomyopathy
Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or ARVD).
Ventricular Fibrillation
The ventricles suddenly contract at rates of up to 500 bpm.
This rapid and irregular electrical activity renders the ventricles unable to contract in a synchronised manner, resulting in immediate loss of cardiac output.
The heart is no longer an effective pump.
Unless advanced life support begins, this rhythm is fatal.
Prolonged VF results in decreasing waveform amplitude, from initial coarse VF to fine VF and ultimately degenerating into asystole
VF ECG criteria
Rapid, disorganized, Uncontrollable, chaotic contraction of the Ventricles.
No identifiable P waves, QRS complexes, or T waves.
Rate 150-500 bpm.
No Cardiac Output - Loss of Consciousness
Medical Emergency – Start life support!
Ventricular Fibrillation - causes
Myocardial ischemia/ infarction
Cardiomyopathy (dilated, hypertrophic, restrictive)
Channelopathies e.g. Long QT (acquired / congenital) and Brugada syndrome
Aortic stenosis/ dissection
Cardiac tamponade
Pulmonary embolism
Drug-induced QT prolongation
Treatments
If haemodynamically stable and in VT: treat with amiodarone 300 mg IV over 20–60 min, followed by an infusion of 900 mg over 24 h.
If not haemodynamically stable: Give a 150J shock.
CPR
Resus guidelines = 2mins CPR before another rhythm check - if VT/VF then give 150J shock up to 3 shocks, then seek help from resuscitation team.
ICD/CRT-D
Guidance regarding ICD and CRT implantation
NYHA 1 w or w/o LBBB, wide QRS = ICD. If over 150ms with or w/o LBBB CRT-D
Class IV - CRT-P
Sinus Pause / Sinus arrest
The SA node fails to fire an impulse, the heart stops beating until the SA node fires a new impulse
Ventricular Standstill
Complication of CHB.
SA node sends its impulse (atria continue to beat normally). However, the impulse is unable to pass through the AV node. The Bundle of His also fails to take over and so the ventricles fail to contract (standstill).
P waves present.
No proceeding QRS complex.
No cardiac output. Requires CPR.
Asystole
SA node fails to send out an impulse, therefore the cardiac conduction cycle fails to start.
No conduction in the heart.
No QRS or P waves.
No cardiac output.
Requires immediate CPR
Pulseless electrical activation(PEA)
In PEA, there will be a surface ECG present, but the heart will not be contracting and pumping blood around the body.
6 Hs:
Hypovolaemia, hypoxia, hydrogen ions (acidosis), hyper/hypokalaemia, hypoglycaemia and hypothermia.
6 Ts:
Toxins, cardiac tamponade, tension pneumothorax, thrombosis (MI/PE), tachycardia and trauma (blood loss/hypovolaemia).
CPR and treat underlying cause - low survival rate
