B P7 C67 Ventricular Arrhythmias Flashcards
(152 cards)
1
Q
Ventricular arrhythmias originate in the _____. These include premature ventricular complexes (PVCs), nonsustained and sustained ventricular tachycardias (VT), and ventricular fibrillation (VF)
A
Ventricular myocardium or His-Purkinje system
2
Q
Ventricular arrhythmias that occur in the absence of structural heart disease and a defined ion channel abnormality are referred to as _____ and are usually benign.
A
Idiopathic
3
Q
PVCs are due to _____, producing a depolarization wavefront that propagates through the ventricles independent of activation from the atrium and AV node
A
Abnormal impulse formation (automaticity, triggered activity)
or
Reentry in the ventricular myocardium or Purkinje system
4
Q
A PVC is characterized by the _____.
A
(1) Premature occurrence of an abnormal QRS complex that usually has a duration exceeding 120 msec
(2) Corresponding T wave is typically broad and in the opposite direction of the major QRS deflection
(3) Typically not preceded by a P-wave
5
Q
PVCs can also fall between sinus beats without disturbing AV conduction and without producing a pause, defined as _____ PVCs
A
Interpolated
6
Q
If PVCs are relatively late in the cardiac cycle the PVC activation wavefront may collide with a sinus wavefront that has already reached the ventricles, producing _____.
A
Fusion beats
7
Q
The ventricular activation sequence is largely determined by the site of initial ventricular activation and hence the _____ morphology is an indication of the location of the ventricular arrhythmia origin
A
QRS
8
Q
Those that have a dominant S wave in V1 are termed left bundle branch block (LBBB)—like and generally originate in the _____.Those with a dominant R wave in V1 are termed right bundle branch block (RBBB)—like and generally originate in the _____ in the morphologically normal heart.
A
Dominant S wave in V1: LBBB - RV or IVS
Dominant R wave in V1: RBBB - LV
9
Q
Analysis of the frontal plane axis and precordial lead patterns further refine prediction of the likely origin. Initial depolarization of the inferior wall produces a _____ frontal plane axisaxis, and depolarization of the anterior wall produces an _____ frontal plane axis.
Exceptions occur and predicting the arrhythmia origin from the QRS morphology is less reliable when structural heart disease with scar that changes ventricular activation is present
A
Inferior wall: superior frontal plane axis
Anterior wall: Inferiorly directed frontal plane axis
10
Q
PVCs with a single QRS morphology are referred to as _____. The presence of PVCs with different QRS morphologies is referred to as _____ and usually indicates more than one PVC focus, although variable conduction away from a single focus is also a possible cause.
A
Unifocal: Single QRS morphology
Multifocal or multiform: Different QRS morphologies
11
Q
Frequent multifocal PVCs are more often associated with _____.
A
Structural heart disease
12
Q
PVCs may occur in repetitive patterns. Every conducted sinus beat followed by a PVC is _____. Every two sinus beats followed by a PVC is _____.
A
Bigeminy: each beat ff by a PVC
Trigeminy: Every 2 sinus beats ff by a PVC
13
Q
A _____ coupling interval is consistent with reentry or triggered activity as the mechanism
A
Fixed
14
Q
_____ coupling with a common interval between PVCs suggests abnormal automaticity from a parasystolic focus that is relatively protected from ventricular activation from conducted sinus beats.
A
Variable
14
Q
Two consecutive PVCs are referred to as a PVC _____. Three consecutive beats is a triplet
A
Couplet: 2 consecutive PVCs
Triplet: 3 consecutive PVCs
15
Q
Nonsustained VT is defined as a run of consecutive ventricular beats persisting for ____.
A
3 beats to 30 seconds
16
Q
VT is also characterized by its QRS morphology. _____ VT has the same QRS morphology from beat to beat, consistent with a single origin for each beat. _____ VT has a continually changing QRS morphology. The initial beats of a run of monomorphic VT may have a variable QRS morphology.
A
Monomorphic: Same QRS morphology from beat to beat
Polymorphic: Changing QRS morphology
17
Q
PVC frequency is associated with _____ during long-term follow-up.
A
Mortality and heart failure
18
Q
On ambulatory monitoring PVCs increase with _____.
A
Age
CV risk factors: HTN and smoking
19
Q
The 15-year risk of heart failure increased from 19.3% for those with _____% PVCs/day to 30.8% for those who had _____% (approximately 1000 PVCs) per day at baseline.
A
0.01% PVCs/d = 19.3% HF risk
1% PVCs/d or 1000PVCs/d: 30.8% HF risk
20
Q
Runs of VT that are _____ raise concern for risk of rapid sustained arrhythmias causing syncope or sudden death
A
(1) Polymorphic
(2) Faster than 220 beats/min
(3) Start near the peak of the T-wave of the preceding sinus beat
21
Q
During exercise testing _____ or more PVCs/minute occur at some stage (before, during exertion, or during recovery) in fewer than 10% of patients without a history of heart disease.
A
7 or more
22
Q
Nonsustained VT occurs in fewer than 5%,is typically _____ beats in duration or shorter, and slower than ____ beats/ minute
A
5 beats in duration or shorter
<200 bpm
23
Q
Benign idiopathic arrhythmias often originate from the _____.
A
RVOT
24
In competitive athletes without evidence of heart disease, 7% have PVCs during exercise testing, usually fewer than ___, and these were associated with a benign prognosis in one study.
<10
24
PVCs can be produced by direct mechanical, electrical, or chemical stimulation of the myocardium and are often noted during _____. Management is directed at correcting the underlying illness.
Acute coronary syndromes
Myocarditis
Hypoxia
Electrolyte abnormalities, particularly hypokalemia
25
Palpitations are often perceived as a “thump” or strong beat from the sinus beat terminating a _____ after the PVC
Longer period of ventricular filling
26
_____waves may be present in the venous pulse when the atria contract during ventricular systole of the PVC.
Cannon A waves
26
Although the stroke volume of the PVC is often _____ to produce a palpable pulse, premature heart sounds are commonly audible. Frequent PVCs may effectively produce bradycardia.
Insufficient
27
Idiopathic PVCs most often originate from a single site in the _____.
RVOT/VLOT
Valve annuli
Papillary muscle
28
_____ PVCs are more often associated with underlying structural heart disease
Multifocal PVCs
29
Very rarely closely coupled PVCs that start near the ____ wave of the preceding sinus beat initiate rapid polymorphic VT/VF that causes cardiac arrest
peak of the T wave
30
_____ PVCs do not require therapy unless they are occurring with sufficient frequency to depress ventricular function. Symptoms often wax and wane over long periods of time and may resolve in over a third of patients.
Asymptomatic
31
Mild symptoms are often sufficiently managed by _____ Removal of provocative factors, such as caffeine, is reasonable.
If treatment is required, chronic administration of a _____ is a reasonable first therapy, particularly if PVCs are increased with activity or emotion.
Efficacy is relatively low, but symptoms can be improved despite lack of a major impact on PVC frequency.
Mild: Reassurance
If treatment is required: beta- blocker - first line
Others:
NDHP CCBs verapamil or diltiazem
Class IC drugs Flecainide or propafenone
Amiodarone
32
Catheter ablation should be considered in Idiopathic PVCs/NSVT (With no structural heart disease/Electrical heart disease) when _____.
Therapy is warranted and beta-blockers are ineffective or not desired, particularly when a single dominant PVC morphology is identified
33
The likelihood of successful ablation depends on whether the PVCs are present at the time of the procedure to allow localization of its origin, and whether the focus is accessible.
Success rates are greatest for the _____, and lower for _____.
Greatest: **RV outflow tract**
Lower: **Papillary muscles** and those that arise from the **basal LV septum**
34
Catheter ablation effectively reduced RV outflow tract PVCs in ___% of patients and was more effective than chronic metoprolol or propafenone therapy
81%
35
Treatment with the _____ increased mortality in post-infarct patients, possibly due to proarrhythmic effects.
Class IC drug flecainide
Class III drug D-sotalol
36
In patients with depressed ventricular function and PVCs in the background of structural heart disease , _____ is a therapeutic option, but long-term toxicities are an important consideration
Amiodarone
37
Catheter ablation can be considered if a dominant PVC morphology is present that can be targeted for ablation. During ____, routine attempts to suppress PVCs with antiarrhythmic medications do not improve outcome and are not warranted.
PVCs that trigger recurrent episodes of VF, may respond to _____
Acute myocardial infarction
Quinidine
38
Very frequent PVCs can cause _____ of ventricular function
Reversible depression
38
In PVC induced CMP, most have more than ____% PVCs as assessed from at least 24 hours of ambulatory recording, but PVC frequency during any 24-hour period can vary substantially and ventricular dysfunction has been seen in patients with only ___% PVCs during a single monitoring period. Multiday ECG monitoring may provide a better assessment of PVC burden.
> 15% PCVs/d - CMP
5% - ventricular dysfunction
39
When depressed ventricular function is encountered in a patient with frequent PVCs there are four major possibilities:
(1) cardiac contractility may be normal, but the frequent PVCs are impairing measurement of ventricular function;
(2) PVCs are depressing cardiac contractility;
(3) an underlying cardiomyopathic process is present and causing the PVCs;
(4) An underlying cardiomyopathy is present and the PVCs are further depressing ventricular function.
40
_____ suggest underlying cardiomyopathy in patients with PVCs
(1) Sinus QRS duration **>130 msec**
(2) PVC burden **< 17%**
(3) Substantial **LV dilation**
(4) **Multifocal** PVCs
(5) Areas of **LGE** on MR imaging
41
If PVCs are suspected to cause or contribute to cardiomyopathy, suppression of PVCs and reassessment of ventricular function is warranted. _____ are the major pharmacologic options.
Catheter ablation is recommended if there is a _____.
Beta-adrenergic blockers and amiodarone
(1) Dominant PVC morphology that can be targeted
(2) Antiarrhythmic drug therapy is ineffective, not tolerated, or not preferred for longterm therapy
42
Patients with very frequent PVCs and normal ventricular function warrant follow-up. Optimal risk assessment and surveillance is not defined but annual ambulatory recording and echocardiogram is reasonable for subjects with more than _____% PVCs.
15% to 20% PVCs
43
The ventricular rate in accelerated idioventricular rhythm is typically _____. Conduction of sinus beats to the ventricle producing fusion beats and capture beats is common
60 to 100 beats/minute, often only slightly exceeding the sinus rate, producing interference AV dissociation
44
Ventricular tachycardia can be due to _____.
The management and prognosis depend on the specific type of VT and underlying heart disease.
Reentry
Triggered activity
Automaticity
44
The mechanism in AIVR is likely _____. This arrhythmia is usually seen in patients with structural heart disease, particularly during _____. It lasts for seconds to minutes and does not usually have an important hemodynamic effect.
Automaticity
* Reperfusion of AMI
* Myocarditis
44
Suppressive therapy for AIVR is rarely necessary but may be needed if loss of AV synchrony and acceleration of heart rate produces _____. Accelerating the atrial rate with administration of _____ can suppress the rhythm.
Symptoms or a fall in blood pressure in a compromised patient
Atropine or atrial pacing
44
Monomorphic VT is a wide QRS tachycardia that has the same ____ indicating a stable ventricular depolarization sequence for each beat. The QRS duration typically exceeds _____ msec, but is occasionally shorter for VTs originating in the septum or that utilize a portion of the Purkinje system.
It is usually regular, but ___ msec variation in cycle length is not uncommon, and occasionally marked cycle length variation is encountered in the presence of antiarrhythmic medications, or at the onset and prior to spontaneous termination.
Rates can range from slower than _____ to faster than _____/min.
The same QRS configuration from beat to beat
QRS > 120 msec
Variation: 20 msec
<100 bpm to > 270 bpm
45
Vagotonic maneuvers or administration of adenosine may increase AV block exposing a _____, or if 1:1 VA conduction is present in VT, may cause transient _____, confirming VT.
It is important to recognize that a 1:1 relation between atrium and ventricle does not exclude VT because _____ may occur such that each QRS is followed by a retrograde p-wave.
In many cases P-waves are difficult to discern and the relation between P-waves and QRS complexes cannot be determined with certainty.
Supraventricular arrhythmia with aberration
VA dissociation
Retrograde VA conduction
45
AV dissociation may be evident from the presence of _____ beats
Fusion beats or capture beats
45
Sustained monomorphic VT is usually regular. The atrium is not involved in the tachycardia.
The presence of _____ between ventricular and atrial activity strongly favors VT over supraventricular tachycardia, the exception being _____, which is rare in adults, and some rare forms of AV nodal reentry
Dissociation
Junctional ectopic tachycardia with aberrancy
46
The same wide QRS morphology during sinus rhythm and the tachycardia suggests _____; this can also occur, however, in patients with _____.
SVT with aberrancy
Bundle branch reentry VT
47
The majority of sustained monomorphic VT associated with structural heart disease are due to _____ through regions of myocardial scar, consisting of fibrosis and surviving myocyte bundles.
Reentry
48
Diminished coupling between myocyte bundles and complex anatomic arrangement of the bundles contributes to slow conduction and facilitates conduction block needed for reentry.The slow conduction occurs during propagation through the scar, which is typically a small mass of myocardium that does not contribute to the surface ECG.The QRS is inscribed when the VT wavefront reaches the border of the scar and propagates across the ventricles.
The QRS configuration reflects the “exit” of the reentry circuit from the scar. Hence the location of the scar can often be inferred from the VT ____ morphology, which is then an indication of the infarct or scar location.
QRS
49
Cardiac imaging will often show the area of scar as a _____. Small areas of scar, however, particularly in the RV may escape detection with imaging. In the electrophysiology laboratory scars are evident as areas of _____ due to replacement of myocardium by fibrosis and abnormal electrograms.
Cardiac Imaging:
Region of LGE
Absence of perfusion
Abnormal wall motion
EPS:
Low electrogram voltage
50
In the presence of disease of the Purkinje system and surrounding myocardium VT can be due to reentry circuits that utilize the bundle branches or fascicles.
The VT has a QRS morphology consistent with activation of the ventricles from the Purkinje system, resembling _____. These VTs are uncommon, occurring in fewer than 10% of patients with recurrent VT referred for catheter ablation, but are important to recognize because they can mimic _____ and most are well treated with ablation.
Bundle branch block
Mimic: SVT with aberrancy
51
_____ is the most common form of VT from the Purkinje system.
The circulating wavefront usually propagates down the right bundle branch, through the septum and up the left bundle branch to complete the circuit. VT has a typical _____ configuration. Rarely the circuit revolves in the reverse direction giving rise to an RBBB configuration. The VT is often rapid, faster than _____/min. It is associated with disease of the Purkinje system and often with severe LV dysfunction.
Most patients have an ____ during sinus rhythm, despite the ability of the left bundle to sustain repetitive retrograde conduction during VT.
Bundle branch reentry
LBBB
>200 bpm
IVCD or even a pattern of complete LBBB
52
VT can originate from a small focus of triggered activity or reentry.The mechanism can usually not be established with certainty. These are most often encountered in patients who do not have structural heart disease, often associated with PVCs of the same QRS morphology. Common locations of origin are in the _____.
Papillary muscles
Outflow tracts (Including sleeves of myocardium that extend along the aorta or pulmonary artery)
Valve annuli
53
Focal VTs tend to be enhanced by _____ stimulation
Beta-adrenergic
54
Rapid monomorphic VT, faster than _____ beats/min, usually causes hypotension that may present as syncope, or cardiac arrest. VT can degenerate to VF, which may then be the initial rhythm detected by emergency medical responders; this is rare in patients without structural heart disease
>200 bpm
55
_____ should be performed in case of impaired consciousness, hypotension, or pulmonary edema, after sedation if possible if the patient is conscious.
QRS synchronous electrical cardioversion
56
For hemodynamically stable wide QRS tachycardia a 12-lead ECG should be obtained. If the diagnosis is uncertain, an intravenous bolus of _____ may be administered during ECG monitoring, as this may transiently interrupt AV or VA conduction, clarifying the diagnosis
Adenosine
57
For acute pharmacologic termination of sustained VT, intravenous _____ was more effective for termination than amiodarone in one trial. Both are vasodilators that induce _____ in up to 30% of patients.
It should not be given to patients with ESRD due to the risks of accumulation of its metabolite _____ that can cause _____.
Procainamide
Hypotension
QT prolongation and polymorphic VT
58
If the patient is known to have an **idiopathic VT without structural heart disease**, acute management is dependent on the specific VT. Intravenous administration of _____ can often terminate these VTs.
If the diagnosis of **idiopathic left ventricular fascicular reentrant tachycardia** is certain, intravenous_____ will usually terminate the arrhythmia.
Idiopathic VT w/o Structural HD: IV beta-blockers
Idiopathic LV fascicular reentrant tachycardia: IV verapamil or diltiazem
-----------
Administration of calcium channel blockers is **contraindicated for acute management of other sustained VTs due to the risk of inducing hemodynamic instability**.
59
Reversible conditions contributing to the initiation and perpetuation of VT should be sought and corrected including factors that _____.
Increase sympathetic tone, often related to other acute illness
Hypokalemia
Hypoxia
Acidosis
60
VT that occurs 3 or more times within 24 hours has been defined as an “_____” and is associated with difficult to control VT and increased mortality
Electrical storm
61
Ongoing electrical storm with VT that recurs frequently after cardioversion or is incessant despite termination attempts is a life-threatening emergency. Precipitating factors, most commonly _____, should be addressed. Very wide sinusoidal tachycardia should prompt immediate consideration and treatment for _____.
Elevated sympathetic tone
Hyperkalemia
62
Treatment of electrical storm involves:
(1) **IV amiodarone** and measures to **reduce sympathetic tone** should be initiated.
(2) The **nonselective beta-blocker propranolol** was more effective than metoprolol in one study, suggesting a role for potent nonselective beta-blockade.
(3) **Sedation** escalating to general anesthesia is often effective.
(4) Other means of reducing cardiac sympathetic stimulation include **percutaneous stellate ganglion block** and **high thoracic epidural anesthesia**.
(5) Assessment of **appropriate ICD function** and possible **proarrhythmic effects from antiarrhythmic medications** should be considered.
(6) If initial measures are ineffective, **emergent catheter ablation** should be considered
63
After the initial presentation of sustained VT, underlying heart disease should be characterized and consideration given to therapy to reduce the risk of arrhythmia recurrence and sudden death. Most patients will be found to have an area of ventricular scar as the cause, most commonly _____.
Prior myocardial infarction
64
_____ are especially important considerations for patients with RV origin VTs.
Other important causes include prior myocarditis, and ventricular scars from prior cardiac surgery, such as repaired tetralogy of Fallot.
In the absence of structural heart disease VT is referred to as idiopathic.
ARVC and cardiac sarcoidosis
65
Patients with scar-related sustained monomorphic VT are at risk for cardiac arrest from VT recurrence, which varies with the type and severity of the underlying disease.
Placement of an ICD that will terminate VT should it recur is usually warranted provided the patient has a reasonable expectation for _____.
Survival with acceptable quality of life for the next year and desires the protection of the ICD
----------
ICDs reduce arrhythmic death in patients with **depressed ventricular function who have had sustained hypotensive or syncopal VT that is not related to a reversible cause (secondary prevention)**, and also in patients who are at **increased risk for a 1st episode of sustained VT (primary prevention of SCD)**
66
ICDs reduce arrhythmic death in patients with _____
(1) Increased risk for a first episode of sustainedVT (primary prevention of sudden death)
(2) Depressed ventricular function who have had sustained hypotensive or syncopal VT that is not related to a reversible cause (secondary prevention)
67
ICDs terminate VT by _____, but do not prevent VT occurrences
Antitachycardia pacing (ATP)
or
Delivery of a cardioversion shock if ATP is not effective
68
Idiopathic VT in the absence of structural heart disease rarely causes sudden death and an ICD is ____. Beta-adrenergic blockers or catheter ablation are often effective.
Not usually warranted
69
Sustained monomorphic VT may present any time after myocardial infarction, but often more than _____ years after the acute infarction.
>10 years
69
Most patients with ICMP have LV ejection fraction of less than __%.Wide complex tachycardia, syncope, and cardiac arrest are common presentations. Multiple QRS morphologies ofVT are common due to multiple potential reentry circuits within the infarct scar
<40%
70
The QRS morphology reflects the infarct scar location and its border zone with healthy myocardium. _____ infarcts often give rise to VTs that have a superiorly directed frontal plane axis. Anteroseptal infarcts often give rise to LBBB-like VTs when the exit is on the _____ and RBBB-like VTs when the VT exit is at the
_____ infarct border.
Superior direction: Inferior wall
LBBB like: Septum
RBBB like: Lateral
71
An episode of sustained VT late after myocardial infarction usually warrants placement of an _____. Recurrent VT terminated by the ICD is detected in up to 70% of patients over the following 2 to 3 years
ICD
72
ICDs are also recommended for infarct survivors who are at risk for a first episode of VT based on LV ejection fraction of 35% or less with symptoms of heart failure or less than 30% even in the absence of symptoms provided that they are: _____
(1) at least 40 days from acute infarction
(2) are more than 90 days from a revascularization procedure
73
Catheter ablation abolishes VT in about 50% of patients, and reduces the frequency of recurrences in an additional 20% to 30%. Procedure-related mortality is 1% to 3% with patients who have severe ventricular dysfunction and comorbidities at greatest risk. Complications occur in 5% to 8%, most commonly _____, but stroke, tamponade, and vascular injury can occur.
Femoral bleeding
74
_____ after catheter ablation is a marker for increased long-term mortality.
Recurrent VT
75
Areas of late gadolinium enhancement consistent with ventricular scar are detected by cardiac MR imaging in approximately a third of patients with nonischemic dilated cardiomyopathy (NICM) and are associated with increased risk of sudden death.A genetic mutation is identifiable in approximately __% of patients and is associated with worse long-term mortality, occurrence of VT, and sudden death than those without an identifiable genetic cause of cardiomyopathy.
40%
76
Sustained monomorphic VT in NICM is most commonly due to _____ in regions of scar often near the base of the hear
rRentry
77
ICDs are also recommended for patients with NICM who have _____.
(1) LV ejection fraction of 35% or less despite medical therapy for ventricular dysfunction
(2) patients with high-risk genetic cardiomyopathies, including many with lamin A/C mutations
78
ARVC is an inherited disorder characterized by fibrofatty replacement of the _____ creating the substrate for PVCs and sustained monomorphic VT and less commonly polymorphic VT/VF.
RV free wall that typically extends from the TVA and RV outflow region toward the apex
78
Heart block from ablation of VT originating from the basal septum can occur and warrants _____ pacing.
Biverntricular
78
A common presentation in ARVC is sustained monomorphic VT with an _____ configuration in V1
LBBB
78
_____ favors ARVC.
LBBB VT with a superior axis or multiple VTs
78
A _____ are found in ARVC.
Prolonged terminal activation duration (nadir of the S wave to QRS offset >55 msec in V1), or less commonly epsilon waves
79
Arrhythmias in ARVC are commonly provoked by exertion. Chronic therapy with a _____ is recommended.
An ICD is recommended for those who have had sustained arrhythmias, syncope, or RV or LV dysfunction with ejection fraction of 35% or less, and is considered for patients with less severe manifestations of disease because the initial symptomatic event can be sudden death
Beta blocker
79
.Approximately half of the patients with ARVC have an identifiable mutation involving a desmosomal protein, most commonly _____, followed by other desmosomal and non-desmosomal proteins.
Desmosome:
Plakophilin-2
Desmoplakin
Desmoglein
80
With _____, unaffected gene carriers of ARVC appear to have an excellent outcome without therapy.
Avoidance of exercise
81
If ARVC VT recurrences require suppression,_____ have been used. Catheter ablation, which often requires an epicardial approach, reduces episodes
Sotalol
Amiodarone
Flecainide
82
In contrast, sustained monomorphic VT is usually due to reentry facilitated by scar areas that are often associated with prior surgical repair, most commonly in _____
Tetralogy of Fallot
83
Areas of dense fibrosis owing to _____ form regions of conduction block that define reentry circuit borders and create anatomically defined isthmuses with slow conduction that allow macroreentrant VTs.These isthmuses can be identified during stable rhythm and be ablated with very low rates of VT recurrence if conduction block in the isthmus can be achieved.
Surgical incisions
Patch material
Valve annuli
84
VT may be associated with _____ late after repair such that percutaneous or surgical pulmonary valve replacement is warranted. It is important to consider ablation for VT prior to or combined with these procedures as placement of a valved conduit does not abolish VT and may prevent future access to the isthmus causing VT.
Pulmonary regurgitation and RV enlargement
85
Sudden death occurs at a rate of 1% per year in patients with genetic hypertrophic cardiomyopathy. _____ are the most common rhythms identified at sudden death
Polymorphic VT (PMVT) and VF
85
_____ are likely arrhythmogenic factors in HOCM.
Sustained monomorphic VT is uncommon but can occur due to scar-related reentry, most commonly in patients who have a fibrotic _____, which occurs in fewer than 5% of patients
Ventricular myocyte disarray
Interstitial fibrosis
Susceptibility to myocardial ischemia
86
Sarcoidosis is characterized by noncaseating granulomas that can involve any organ. Cardiac involvement can cause atrial and ven- tricular arrhythmias, heart block, and heart failure. VT is the presenting event in one-third of patients. The granulomas heal, leaving areas of fibrosis that can be the substrate for scar-related reentrant _____ VT that persists after active inflammation resolves.
Sustained monomorphic VT
87
ICDs are also considered in sarcoidosis for primary prevention of sudden death, particularly if there is evidence of depressed LV function, scar on cardiac MR imaging, or inducible VT at electrophysiologic testing. _____ may prevent or slow active disease progression and may improve AV block and PVCs but is unlikely to prevent recurrences of sustained VT once the fibrotic substrate is present.
Immunosuppressive therapy
88
Active inflammation associated with myocarditis can cause _____.
Multifocal PVCs
Nonsustained VT
Accelerated idioventricular rhythms
Polymorphic VT/VF
89
In a series of patients with lymphocytic myocarditis, PVCs and nonsustained VT often originated from the inferior LV giving rise to _____ axis QRS morphologies.
RBBB superior axis
90
_____ can be early manifestations of Chagas disease followed over years by ventricular dysfunction, often with aneurysms, and VT .
_____ can be the first clinical manifestation of disease and can be from ventricular arrhythmias or heart block. Sustained monomorphic VT is due to scar-related reentry, most commonly from the inferolateral left ventricle giving rise to VT that has an _____ axis QRS configuration.
RBBB, left anterior hemiblock, and PVCs
Sudden death
RBBB right axis
91
The right and left ventricular outflow regions are the most common locations for idiopathic VT as well as PVCs. These most frequently arise in tissue along the _____
Pulmonary or aortic valve rings
92
The initiating mechanism of outflow tract VTs is likely _____. VT can be paroxysmal or exercise induced. It may occur as repetitive monomorphic VT with bursts of tachycardia separated by a variable number of sinus beats .The QRS morphology of the VT has an inferiorly directed frontal plane axis, with _____
Triggered activity
Tall monophasic R waves in leads II, III, AVF
93
Failure of ablationin outflow tract VTs is often due to _____.Serious complications are uncommon, but can include cardiac perforation, coronary injury, and femoral access site bleeding.
(1) inability to initiate the arrhythmia to allow mapping in the EP laboratory
(2) origin from an inaccessible location that may be deep in the IVS or subepicardial adjacent to a coronary artery where ablation is not performed
94
The crux of the heart encompasses the tissue in the inferior portion of the septum extending from the basal inferior septum near the coronary sinus apically and inferiorly. The QRS shows a _____ frontal plane axis with QS complexes in II, III, and an LBBB or RBBB morphology, often with a prominent R in V2
Left superior frontal plane axis
95
From the left ventricular papillary muscles the QRS has an RBBB configuration with either _____ axis (posteromedial papillary muscle origin) or _____ axis (anterolateral papillary muscle origin)
RBBB
Plus:
Posteromedial: superior axis and S waves in V4 to V6
Anterolateral: inferior rightward axis
96
Most are benign, but very frequent arrhythmias may depress ventricular function and rare cases of papillary muscle PVC-induced VF occur.The presence of_____ in the adjacent LV wall has been associated with more severe arrhythmias.
Mitral annular disjunction and myocardial fibrosis
97
Left fascicular reentrant tachycardia, also known as _____ is due to reentry involving one or more of the left ventricular fascicles and adjacent ventricular tissue in the septum or papillary muscles.
Verapamil-sensitive fascicular tachycardia
98
VSFT can often be terminated by intravenous administration of _____, while intravenous administration of class I agents such as procainamide slow the tachycardia without termination.
Termination: Verapamil
Slow without termination: Class I (Procainamide)
98
The most common form of VSFT involves the _____ giving rise to an RBBB – like tachycardia with a superior left axis
LV posterior fascicle
99
Polymorphic VT is characterized by a continually changing QRS morphology that indicates the changing ventricular activation sequence. _____ is a specific type of polymorphic VT that has a waxing and waning QRS amplitude and is often associated with QT prolongation prior to initiation. The tachycardia is unstable and either terminates spontaneously or degenerates to VF
Torsade de pointes
99
Polymorphic VT degenerating to VF occurs within the first _____ hours in up to ___% of patients under care for acute type I myocardial infarction and may occur before, during, or after reperfusion. It also occurs in up to ___% of non-ST elevation infarctions
24 to 48 hours
STEMI: 10%
NSTEMI: 8%
100
Recurrent PVT episodes suggest ongoing ______ warranting angiography for consideration of further intervention. Rarely recurrent episodes are due to automaticity from damaged cells in the infarct border region
Ischemia
101
PMVT/VF during hospitalization for acute myocardial infarction is associated with greater in-hospital mortality, likely related to larger infarct size and comorbidities. Mortality is greater for those with arrhythmia that occurs more than _____ hours after infarction
>48 hours
102
The polymorphic VT torsade de pointes associated with QT interval prolongation is due to prolonged repolarization that allows recovery of time-dependent inward currents with creation of _____ that cause PVCs as well as repolarization heterogeneity facilitating reentry. Episodes are usually initiated by heart rate slowing or a PVC-induced pause.
EADs
103
Prior to VT due to ALQTS, the QTc interval is typically prolonged greater than _____ sec. Following defibrillation, the QT may be shorter in response to tachycardia and catecholamine administration, obfuscating the initial cause.
>0.48s
104
Any cause of QT prolongation can cause torsade de pointes. Drugs that block the repolarizing potassium current IKr are the most common offenders (_____).
Dofetilide
Ibutilide
Sotalol
Quinidine
105
Sustained episodes require immediate defibrillation. Recurrent episodes can usually be suppressed by _____ administered by rapid intravenous infusion and repeated as needed to suppress PVCs and NSVT.
Bradycardia should be corrected by _____at a rate that suppresses PVCs and nonsustained PMVT.
1 to 2 g of magnesium sulfate
Isoproterenol infusion or implementation of pacing
106
Type 1 (LQTS1) causes over a third of congenital LQTS. It is due to a mutation that decreases the repolarizing current ___. Episodes of syncope are classically triggered by exertion, including swimming, or emotional stress.The ECG typically shows _____. Chronic therapy with beta-adrenergic blockers is highly effective in preventing episodes.
IKs
Broad symmetric T-wave
107
Type 2 (LQTS2) is due to a mutation that decreases the repolarizing current ___, which is the same current that is most commonly blocked by agents causing acquired LQTS. Episodes of arrhythmia are classically provoked by emotional stress or surprise, such as sudden noises and are pause dependent.The risk is increased for women during the 9-month post-partum period. The ECG classically shows _____. Chronic therapy with beta-adrenergic blockers is protective.
IKr
Notched or humped appearing T waves
108
Type 3 (LQTS3) is due to a mutation in SCN5A that increases ___. Episodes of arrhythmia or sudden death tend to occur during sleep and slow heart rates. The ECG typically shows a _____. Therapy with beta-blockers is recommended. The sodium channel blocker _____ significantly shortens the QT interval in some individuals.
INa
Flat ST segment with a peaked T-wave
Mexiletine
109
Management of recurrent acute episodes of polymorphic VT includes intravenous administration of magnesium sulfate and overdrive pac- ing to shorten the QT interval.
Long term, avoidance of QT prolonging medications is critical. Asymptomatic individuals with mild QTc prolongation may not warrant additional therapy.
Chronic beta-blocker therapy with _____ is often sufficient, particularly for type 1 and 2 LQTS; metoprolol is less effective.
ICDs are considered in patients who have had cardiac arrest or who continue to have symptoms despite therapy.
Specific therapeutic strategies for the type of LQTS are emerging, including _____ for type 2 and _____ for type 3 LQTS.
Surgical cardiac sympathectomy is an option when these therapies fail.When a proband is discovered, cascade genetic screening for other affected family members is important.
LQTS1 and 2: Propranolol, nadolol (metoprolol less effective)
Emerging:
LQTS2: K supplementation
LQTS3: Na channel blockers
110
The short QT syndrome is characterized by polymorphic VT and atrial fibrillation in patients with a structurally normal heart and a QTc _____ milliseconds.
< 340 to 360 ms
111
There is a male predominance in SQTS. An ICD is recommended for patients who have had symptomatic arrhythmias. _____ may be helpful in diminishing episodes of VT
Quinidine
112
Brugada syndrome (BrS) is characterized by transient or persistent coved type ST-segment elevation in at least one right pre-cordial ECG lead. BrS is associated with syncope and sudden death due to ventricular arrhythmias. Approximately 25% to 30% of affected patients have a mutation in the ____ gene.
SCN5A
113
A type-1 ECG—consisting of a ____, with the electrodes positioned in the 2nd, 3rd, or 4th intercostal space that is present either spontaneously or after provocative drug test with intravenous administration of sodium-channel blockers—is required for diagnosis of BrS.
Coved ST elevation 2 mm followed by a descending negative T wave in at least one right precordial lead
114
_____ can unmask the BrS pattern in some subjects who otherwise have a normal ECG
Enhanced vagal tone
Fever
Drugs (particularly sodium channel blocking antiarrhythmic and psychotropic drugs)
115
The type-2 and type-3 ECGs, defined by a _____rdial leads are not diagnostic and not, by themselves, associated with increased risk for sudden cardiac death (SCD).
Saddleback pattern with broad R' followed by ST elevation>2 mm (type-2) or less than 2 mm (type 3)
116
The ___ is the only established therapy to protect against SCD and is recommended for patients with a history of cardiac arrest or syncope consistent with an arrhythmia who have a type-1 ECG.
Life- style changes, including avoidance of drugs and intoxicating amounts of alcohol and immediate treatment of fever are important.
For patients with recurrent arrhythmias _____ can reduce or prevent recurrences, but long-term treatment is hampered by side effects.
Catheter ablation targeting areas of abnormal electrocardiograms in the ____ can normalize the ECG and prevent PMVT recurrences.
ICD
Hydroquinidine or quinidine
Subepicardial RVOT
117
Early repolarization (ER) syndrome is diagnosed in _____.
(1) a patient with an ER pattern who has been resuscitated from otherwise unexplained VF
(2) in an SCD victim with a negative autopsy and a previous ECG with the ER pattern.
118
An ER pattern is defined as a J-point elevation (or a J-wave producing slurring of the terminal QRS) ____ of the 12-lead ECG and a QRS____.
(1) >/=1 mm in at least 2 contiguous inferior and/or lateral leads
(2) QRS duration less than 120 mss in leads without J waves
119
Although the absolute arrhythmia risk is estimated to be very low (____%),ER patterns have been associated with VF initiated by Purkinje or myocardial triggers and sudden cardiac death.
0.07%
120
The pathophysiology of ER is uncertain. Heterogeneity of the transmural voltage gradient across the ventricular wall due to abnormal rapid repolarization or delayed depolarization have been suggested. In contrast to BrS, the abnormal areas may more commonly involve the ____ aspects of the ventricles
Inferior
121
Suspected arrhythmogenic syncope in ERS, in particular with a _____ appear to be associated with a higher risk.
(1) Dynamic and high J wave amplitude recorded immediately after the event
(2) J waves greater than 2.0 mm in inferior leads with horizontal/descending ST segment (>/= 0.1 mV 100 msec after J-point)
(3) J waves in several leads
(4) Family history of SCD or ERS
(5) Coexistence of other ECG abnormalities (LQT, short QT, Brugada)
122
In ERS, ICD is recommended for patients ____. Oral ____ therapy can suppress recurrent episodes.
Ablation of areas with delayed abnormal fractionated electrograms involving particularly the RV epicardium appears to reduce VF recurrence in highly symptomatic patients and can abolish the ER pattern.
In patients with VF storm administration of _____ can often suppress the arrhythmia.
Ablation targeting the abnormal epicardial substrate or PVC triggers can be lifesaving.
ICD:
(1) Resuscitated from VT or VF
(2) Who have had syncope attributable to VT
Quinidine
VF storm: isoproterenol or quinidine
123
Catecholaminergic polymorphic VT (CPVT) is a rare disorder characterized by exercise- or stress-induced ventricular arrhythmias including PVCs, bidirectional VT, and polymorphic VT/VF.These arrhythmias are due to abnormal calcium handling with increased intracellular calcium during sympathetic stimulation causing ____ and triggered activity. Mutations in the gene coding for the ____ cause an autosomal dominant form
DAD
Cardiac ryanodine receptor (RYR2)
124
Monomorphic PVCs in CPVT consistent with an ____ origin in ~60% typically occur at HR of ~100 bpm, progressing to bigeminy, polymorphic PVCs, and VT or VF at higher rates.
Bidirectional VT, although not common, is considered pathognomonic in young individuals without structural heart disease. Bidirectional VT is also seen in _____
Outflow-tract
Myocarditis
Anderson-Tawil syndrome
Digoxin toxicity
125
Chronic therapy in CPVT with ____ are first-line treatments. The addition of ____ suppresses arrhythmias in some patients.
Those who continue to have symptoms often benefit from cardiac surgical left sympathectomy.
Implantable defibrillators are ___ if possible. Shocks from the device, including inappropriate shocks for SVT tachycardia, can elicit sympathetic activation and VT storms
1st line: beta-adrenergic blockers and limiting exercise
Addition: flecainide, propafenone, or verapamil
Avoided
126
_____ is a terminal arrhythmia followed by death or severe brain injury from lack of perfusion if not corrected within _____ minutes. It is characterized by irregular undulations of varying contour and amplitude without distinct QRS complexes
VF
3-5 mins
127
VF and rapid ventricular flutter are most commonly encountered in ____ and can follow from polymorphic VT or monomorphic VT of any cause.
Coronary artery disease with ongoing myocardial ischemia
128
In structurally normal hearts VF can be elicited by _____.
(1) Electrical shock
(2) Precordial impact that causes cardiac depolarization during the T-wave (commotio cordis)
(3) Very rapid ventricular rates during atrial fibrillation in patients with an accessory pathway in the Wolff-Parkinson-White syndrome (4) Early PVCs or unusually rapid idiopathic VT to cause idiopathic VF.
129
Management should follow basic life support and advanced cardiac life support guidelines.
Asynchronous DC cardioversion using ___ J is mandatory therapy for VF, ventricular flutter, and pulseless VT.
Cardiopulmonary resuscitation is performed until CV can be performed and resumed immediately after each shock. If the first shock is ineffective subsequent shocks should be delivered at maximum defibrillator output.
A bolus of intravenous ____ can be administered if initial shocks are unsuccessful while cardiopulmonary resuscitation is continued. Recurrent fibrillation is common after an initially successful shock
Close monitoring should be continued with immediate ability to defibrillate again as further evaluation seeks to identify and treat the underlying cause.
200 J to 400J
Amiodarone of 300 mg
130
_____ is a sinusoidal tachycardia during which it is not possible to separate the QRS from the ST-T wave with certainty. It has rates faster than ____ beats/minute and can be a rapid monomorphic VT for which the etiologies are the same as for slower monomorphic VT, but can also occur during acute myocardial infarction or severe metabolic derangements.
Ventricular flutter
>280 bpm
131
Immediate electrical cardioversion or defibrillation is required. Correct synchronization of the defibrillator shock to the QRS, rather than T-wave, is not possible and an ____ shock should be used, always being prepared to apply a following shock for VF.
Asynchronous
132
Relatively slow ventricular flutter is a wide QRS tachycardia due to slow conduction through the myocardium that can be due to _____.
Hyperkalemia
Drug toxicity - cardiac sodium channel blocking drugs
Global ischemia (Severe)
Metabolic derangements (Severe)
133
For suspected hyperkalemia administration of ______.
Toxicity from a sodium channel blocking antiarrhythmic drug including flecainide, propafenone, and procainamide may respond to administration of _____, which can be in the form of sodium bicarbonate. Tachycardia increases sodium channel blockade by these drugs. Measures to slow the underlying sinus rate are helpful.
HyperK:
IV calcium followed separately by NaHCO is warrante3d, followed by measures to lower serum potassium.
Na channel blocker toxicity:
Hypertonic saline
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