Ventricular Dysrhythmias Flashcards
Possible differences between Ventricle tachycardia (VT) and supraventricular tachycardia (SVT) with variance
VT
- age >50 years old
- has had a history of heart issues
- QRS >140 msec*
- AV dissociation (p waves have the same rate but dont match the rate of QRS)*
- arterial pulse various and is not constant
- presents with fusion and/or capture beats*
SVT w/ variance
- age is less than or equal to 35
- no past history of heart issues
- QRS <140 msec*
- arterial pulse is unaffected
- = diagnostic
Fusion beat vs capture beats
Both are specific for V tac
Fusion = impulses below and above the AV node are fused into one
- causes an odd looking beat that appears like a combination of a P wave and the QRS complex with a super narrow QRS
Capture beat = impulse comes above the AV node and through it immediately right after its repolarization and “captures” the ventricles
- causes very quick and noticeable spiking QRS complex usually in the opposite direction fo the other QRS complexes
- will also be narrow compared to the rest but may look widened
- note both beats can be found in monomorphic and polymorphic VT*
Management of V tach
If stable
- procainamide (1A) first to stabilize the membrane
- Amiodarone (3) 2nd
- Lidocaine (1b) similar to procainamide
Unstable
- shock
Should you ever give a patient with WPW CBBs digoxin, adenosine?
NO
It will kill them
Monomporhic V. Tach vs polymorphic V. Tach
Monomorphic:
-V tach in which all R waves look the same with the same amplitudes in all leads
Polymorphic:
- V tach in which R waves have beat-to-beat variation in amplitude and rate.
- can occur in any leads
- torsades is a type of this
Nonsustained vs sustained ventricular tachycardia
Non-sustained = 3 or more consecutive QRS complex of uniform configuration at a rate of 100bpm that lasts under 30 sec
sustained = 3 or more consecutive QRS complex of uniform configuration at a rate of 100bpm that lasts over 30 sec
Two most serious clinical presentations of Ventricular tachycardia
1) degenerates into Ventricular fibrilation and cardiac arrest
2) produces syncope
What is hemodynamically stable Ventricular tachycardia often misdiagnosed as on an ECG?
SVT w/ aberrant conduction
i.e SVT w/ RBBB or LBBB
Monomorphic V/ tach w/ underlying CAD
Most common form of V. Tach encountered clinically.
- the substrate for the tachycardia is ischemic tissue that provides a one way block reentry circuit
- produces a wide QRS complex w/ uniformed R waves
- the QRS patterns often does not produce an RBBB or LBBB variant (but still can)
- if it shows an RBBB pattern, the substrate is located in the left ventricle (and vise versa for RBBB)
QRS complex deflections in monomorphic V. Tach w/ associated CAD that help show where the substrate is located
Positive QRS in lead aVR and a negative lead in V4 suggests apex as site of ischemic tissue
Positive QRS in leads 2/3/aVF suggest anterior wall of the either ventricle as site of ischemic tissue
Negative QRS in leads 2/3/aVF suggest inferior wall of either ventricle as site of ischemic tissue
Positive QRS in leads 1/aVL suggest septum as the site of ischemic tissue
Direct management acute of monomorphic V. Tach
If patient is unstable
- direct current cardioversion (shock)
If patient is stable
- IV doses of amiodarone is 1st line unless acute MI is present as the substrate
- IV doses of lidocaine can work in situations where acute MI is present
- IV procainamide can also work also, however not 1st line due to ADR of hypotension
DONT use CBBs unless SVT is present
Management of Monomorphic V tach long term.
Focus is on prevention therapy
- combination of drugs are used, however their use should not ever be encouraged long term due to ADRs
- if using drugs, class 3 agents (amiodarone and sortalol) are most promising
- implantable cardioverter defibrillators (ICDs) is best non-pharmacological treatment if patient consents
- radiofrequency cathator ablation is the best choice of non-pharmacological treatment after ICD if the tachycardia can not be tamed.
Management of torsades and QT syndrome. (polymorphic V tach w/ prolonged QT intervals)
Acute
- give magnesium and prescribe antiarrhythmic if magnesium does not solve it
- You have to distinguish if the anti arrhythmic agent your prescribing is enabling the torsades
- if so DONT increase, remove patient off it and give IV magnesium sulfate 1st, then Ca+ and K+
Long term (after acute is solved ONLY)
- BBs (propranolol or nadolol are most common)
- if BBs are contraindicated, use pacemakers
- DONT give drugs that prolong QT (class 1a agents or digoxin)
PAS on procainamide, amiodarone and Sotolol drugs since they prolong QT interval and increase chance of remission
Congenital long QT syndrome
Similar to torsades in that it is a polymorphic V tach w/ prolonged QT intervals, however it is genetically traced
- can occur with deafness (Jervell Nielsen syndrome) or not (Romano-ward syndrome)
is caused by mutant K+ and Na+ channels which make electrolyte currents not work properly
- disrupt repolarization and depolarization of ventricles
- produces episodes of torsades that are often triggered by adrenergic stimulation via physical mental or emotional stress
- QT interval > 450ms
Symptoms
- near syncope or syncope
- lightheadeness
- Hx of cardiac arrest
Management of polymorphic V tach w/out prolonged QTs or torsades
Acute
- exclude or confirm acute ischemia (coronary arteriogram, ECG and Hx of patient)
- if ischemia is present give the any of the following:
- BBs or CBBs
- lidocaine if MI was the culprit
Prolonged
- usually ICDs
What are cases when unstable patients DONT get electricity?
Sepsis
Blood loss
Hypothermia
Widespread toxins
fix these first, then give shock
cardinal Difference between supraventricular tachycardia w/ variance vs V tach
narrow QRS = SVT w/ variance
Widened QRS = VT
- 120ms is the baseline*
Most important diagnostic test for VT
Rhythm strip!!
- then ECG, if its not caught on the rhythm strip, it often goes to VF quick
Normal intervals ECG review
PR interval: 120-200ms
ST interval: 80-120ms and isoelectric
RR interval: 600-1200ms and there is no discernible
QRS complex 80-120ms
QTc <400ms
Rate = 60-100/min
Danger ECG intervals and parts review
ST interval elevation = MI
ST interval depression = ischemia or digitalis poisoning
Prolonged QTc (>500ms) = quinidine toxicity, hypocalcemia, torsades, QT syndrome, VT or VF
Prolonged PR interval (>200ms) = AV blocks and/or WPW
- monitor P waves and Q waves to determine degree
widened QRS (>120ms) = VT
Presence of U waves = hypokalemia
Prominent Q waves (greater than 40ms (1 small box)) = MI
Brugada criteria
Used to rule out VT when it is expected.
Note: the rhythm must be regular (monomorphic) and all criteria must be met in order to rule out VT
1) is the RS complex present in any lead?
- If no = automatically VT
2) is the RS duration >100ms?
- if yes = automatically VT
3) is AV dissociation, fashion or capture beats present?
- if yes = automatically VT
Is the rhythm similar to RBBB or LBBB?
- if no, =. Automatically VT
- if all criteria is met, it is SVT w/ variance*
ACLS protocol for ventricular fibrillation
CPR immediately and give 1 shock
- 5 cycle of CPR
- if VF is still present give epinephrine and shock again
What is hallmark of WPW w/ atrial fib
Irregular rhythm that appear like A fib. And the HR is >250ms
- delta waves are usually present but may not be so obvious
QRS maybe be wide or shorted, dont look at this
Management of WPW
1) If narrow complexes are present:
Treat similar to a standard SVT
- give adenosine and/or CCBs/BBs
- give procainamide if the rate is
2) If wide complex and regular rhythm:
Treat similar to VT
3) If irregular rhythm and wide complex:
- give procainamide if stable
- give cardioversion if unstable
- UNDER NO CIRCUMSTANCES SHOULD YOU GIVE CBBS, BBS, DIGOXIN AMIODARONE OR ADENOSINE TO #3*
- will kill patient
Agents that are commonly given that can prolong QT
Amiodarone
Clarithromycin
Erythromycin
Ibutilde
Quinidine
Sotalol
Procainamide
- also electrolyte imbalances Hypo versions*
Idioventricular rhythms
Will look similar to VT in that QRS is prolonged and AV dissociation may be present
- difference is rate is almost always under 60/min, unless it’s Accelerated in which case 60-100*
Brugada syndrome
Specific type of ventricular fibrillation that often induces SCD
- genentic cause is often a mutation in SCN5A (autosomal dominant)
- patients often appear healthy and will suddenly die
ECG Categorized by the following:
- ST elevation similar to MI
- ST elevation is followed by negative T wave
- possess RBBB appearance
In order to diagnosis must show the ECG abnormalities and one of the following Hx criteria
- documented VF or polymorphic VT
- family history of SCD <45yrs
- syncope episodes
- VT is induced with electrical stimulation
Management is only ICD implantation
