Ventricular Arrhythmias Flashcards
Premature Ventricular Complexes (PVCs)
Asymptomatic or causes mild palpitations
warning arrhythmias
Can occur in patients with or without structural heart disease
non life threating
CAST trial (Cardiac Arrhythmia Suppression Trial):Empiric pharmacologic therapy (Class IC agents) is NOT effective and is associated with INCREASED mortality and death due to arrhythmias–>but stops symptoms
In normal healthy patients (no heart disease) little prognostic implications
In patients with history of MI (or other structural disease) some forms of PVCs are associated with a higher risk of sudden cardiac death (SCD) and may be predictive of future risk of ventricular fibrillation
Ventricular Tachycardia (VT)
Duration of VT
Wide QRS tachycardia that is ≥ 3 or more consecutive PVCs occurring at a rate > 100 beats/minute
Asymptomatic (VT with a pulse) or life-threatening (pulseless VT) associated with pulseless, hemodynamic collapse*
Torsades de Pointes (TdP)
≥ 3 consecutive PVCs occurring at a rate >100 beats/ minute
Can either be asymptomatic (i.e. asymptomatic VT with a pulse) or can result in hemodynamic collapse (i.e. pulseless VT)
Ventricular Fibrillation (VF)
Acute medical emergency resulting in hemodynamic collapse*, syncope, and cardiac arrest
Results in hemodynamic collapse, syncope, and cardiac arrest. Cardiac output and BP are not recordable
Considered a medical emergency requiring CPR
Cardiac Arrest
Unexpected loss of cardiac function
Loss of pulse and blood pressure resulting in a loss of oxygen delivery to vital organs, including the heart and brain
If not treated IMMEDIATELY can lead to Sudden Cardiac Death (SCD)
Sudden Cardiac Death (SCD)
Unexpected cardiac death occurring in a patient within one hour of experiencing symptoms
Hemodynamic collapse of hemodynamic instability
BP (SBP
Acute Episode of VT Treatment
Hemodynamically stable
Amiodarone IV
β- blockers IV (if associated with MI)
Always have DCC available
Acute VT and hemodynamic significance
Hemodynamically unstable
Direct cardiac cardioversion (DCC)
ACLS algorithm
Can add IV amiodarone
Acute Episode of VT Treatment
48 hours
If VT occurs during the first 48 hours of an acute MI, it will probably not reappear on a chronic basis after the infarcted area has been reperfused or healed with scar formation
Acute Episode of VT Treatment
correction
Correction of the underlying precipitating factors will usually prevent further recurrences of VT
i.e. electrolyte abnormalities (hypomagnesemia, hypokalemia), digoxin toxicity, ischemia (MI)
VT Chronic Treatment
Non-pharmacologic Management
Correct acute episode
Depends on risk factors (i.e. LV function, s/p MI, ECG findings)
Implantable Cardioverter Defibrillator (ICD):( musst wait 40 days post-MI
Recurrent or inducible VT on EP study
High-risk characteristics (i.e. EF
VT Chronic Treatment
pharmacologic Management
Prevention with β-blockers only or addition of antiarrhythmic therapy (i.e. amiodarone
Torsades de Pointes (TdP)
Torsade de Pointes (TdP) is a polymorphic rhythm which is a form of ventricular tachycardia (VT)
Associated with prolonged QT interval or QTc interval and prolonged repolarization
Electrolyte disturbances (hypomagnesemia, hypokalemia)**
Female gender (have prolonged QT interval)z***
Medications**
Myocardial Ischemia
HF
Bradycardia
Torsades de Pointes (TdP)
Drug induced
methadone, haloperidol, trimethoprim/sulfamethaxazole, voriconazole, amiodarone)
Antiarrhythmic agents (Type IA (quinidine, procainamide), Type III (sotalol, dofetilide, ibutilide)
Treatment of TdP
ALL
TdP and hemodynamic significance
and
First line agent
Resolve underlying cause
- Remove and correct underlying causes (i.e. medications which increasing QT interval)
- Treat electrolyte abnormalities (i.e. magnesium
Treatment of TdP
TdP and patient is hemodynamically stable
Magnesium sulfate IV
Magnesium Sulfate IV- Drug of Choice (DOC)
At least 1-2 grams IV
or
IV push
Dilute in 10 mL of D5W and give over 5- 20 minutes
Can give IV push in an emergent situation
1st line
- only give when patient has TdP or if patient is hypomagnesemic
Treatment of TdP
TdP and patient is hemodynamically unstable
Direct cardiac cardioversion
Magnesium sulfate IV
Magnesium Sulfate IV- Drug of Choice (DOC)
At least 1-2 grams IV
or
IV push
Dilute in 10 mL of D5W and give over 5- 20 minutes
Can give IV push in an emergent situation
Direct current cardioversion- 1st line therapy
If the patient is significantly hemodynamically compromised
Frequently associated with ventricular rate > 150 beats/minute and unconscious
Chronic Treatment of TdP:
Unnecessary in most patients
Avoid medications which can prolong QT interval
Ventricular Fibrillation (VF)
VT can also cause the heart to beat irregularly, causing the ventricles to “quiver.”
VF is considered a MEDICAL EMERGENCY
No cardiac output (no blood flow)
Cardiovascular collapse= sudden cardiac death (SCD)
Occurs most commonly in patients with ischemic heart disease, coronary artery disease, or LV dysfunction
ACUTE management of VF (ACLS algorithm)
PROMPT and EFFECTIVE cardiopulmonary resuscitation (CPR)
Delivery of defibrillation (for shockable rhythms
Diagnosis of VF
Palpitations
Syncope
Hemodynamic instability
ECG
Electrical disorganization in ventricular myocardium
No distinct wave forms
Acute VF Treatment
Advanced cardiac life support (ACLS)
Chronic VF Treatment
Assessment
Assess underlying cause if reversible (i.e. s/p MI within 48 hours of VF arrest) long term treatment is NOT necessary
Implantable Cardioverter Defibrillator (ICD) for all survivors of VF arrest (if no reversible causes are found)
Chronic VF Treatment
Antiarrhythmic therapy
If patient refuses an ICD
If patient experiences frequent shocks with ICD
Drug of choice: AMIODARONE IV
–>Convert to PO therapy when possible
–>May require higher maintenance dose compared to atrial fibrillation (400- 600 mg PO daily)
Sustained VT (SuVT)
Lasts > 30 seconds
May require intervention to restore a stable rhythm because of hemodynamic compromise
Can degenerate into Pulseless VT/ Ventricular Fibrillation (VF)
TdP is a form of polymorphic VT
Hemodynamically stable
(Magnesium Sulfate IV)
Hemodynamically unstable
(Direct Cardiac Cardioversion)
(Magnesium Sulfate IV)
Non- Sustained VT (NSVT)
Spontaneously self terminates after short duration
VT with a pulse
Pulseless VT (cardiac arrest)
Premature Ventricular Complexes
Healthy patients without structural heart disease
No treatment is necessary
Premature Ventricular Complexes
Symptomatic patients without structural heart disease
β- blockers can be used in patients to suppress symptomatic PVCs
Premature Ventricular Complexes
Patients with MI
or other structural heart disease
Antiarrhythmic empiric therapy is NOT recommended
*ONLY β- blockers have been proven to prevent arrhythmias and overall mortality in patients s/p MI
CAST trial (Cardiac Arrhythmia Suppression Trial)
Trial ended early due to excess mortality in the encainide and flecainide arm
PVCs during MI are not predictive of VF
PVCs after MI infarction increase risk of sudden death
Empiric pharmacologic therapy (Class IC agents) is NOT
effective and is associated with INCREASED mortality and death due to arrhythmias
VT Assessment
FIRST assess patient status and symptoms to determine hemodynamic stability
–>Mental Status
==>Blood pressure
Assess and treat underlying causes
Ischemia (i.e. Myocardial Infarction)
Drug-induced (i.e. digoxin toxicity, antiarrhythmics)
Electrolyte abnormalities (i.e. hypomagnesemia, hypokalemia)
Electrocardiogram Evaluation
Holter Monitoring Continuous Electrocardiogram (ECG or EKG) monitoring (Ambulatory setting)
or
Invasive electrophysiology study (EP study)
If arrhythmia can be reproduced it is called “Inducible”
Patient elgible for inplantable cardiac device.
Must D/C all meds antiarrhythmic
Ventricular Tachycardia (VT)
Etiology
Myocardial scarring from a previous myocardial infarction (MI)
—=> Can occur within 48 hours of an acute MI
Metabolic or electrolyte abnormalities (i.e. hypoxemia, hypomagnesemia, hypokalemia)
Medications (i.e. digoxin toxicity) + Amiodoarine
