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USMLE® Step 1 flashcards
1
Q

What are the surface tracings in an electrogram?

A

Leads I, II, and V1 = surface tracings recorded at a speed of 100 mm/sec (faster than speed of surface ECG which is 25 mm/sec)

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2
Q

What is HRAd on an electrogram?

A

HRA d –> High RA placement

  • represents electrical activity as it traverses the distal electrodes of the catheter placed in the high RA (HRA)
  • corresponds to P wave on surface electrograms
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3
Q

What are the HISp and HISm on the intracardiac electrogram?

A
  • HIS p and HIS m
  • obtained from electrodes located at proximal and mid portion of the HIS bundle catheter
  • first/largest deflection of HIS p represents atrial activity at the distal portion of the atria
  • low amplitude, broad signal = ventricular activation, corresponds with QRS on surface tracing
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4
Q

What is HISd on the intracardiac electrogram?

What does it represent?

A
  • HIS d = distal HIS electrode position
  • 3 electrograms for each P-QRS complex
    • first = largest and corresponds to P wave
    • second = sharp signal, represents HIS bundle activation
    • third = ventricular activation in the septum occurring just below tricuspid valve
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5
Q

What is RVa tracing on the intracardiac electrogram?

A

RVa = electrical activity traversing the RV apex

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6
Q

Which electrogram tracing can measure conduction across the AV node?

A

HIS bundle catheter (HIS p, m, d)

-AH time can be measured from the low RA recording (HIS p) and the bundle electrogram (HIS m, d)

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7
Q

What is normal AH interval?

What is AH interval?

A
  • 45-140 msec
  • Conduction time through the AV Node.
  • measurement is obtained by evaluating the time between the Atrial and His bundle electrograms on one of the His catheter recordings.
  • dependent on patient’s age and autonomic state
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8
Q

When is a short AH interval seen?

What does it suggest?

A
  • children and adults “juvenile AV node”
  • brisk AV nodal conduction
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9
Q

When is a long AH interval seen?

What does it suggest?

A
  • slow AV nodal conduction
  • Causes:
    • fibrosis due to CAD or senile degeneration
    • AV nodal blockade (BB, non-dihydrpyridine CCB’s)
    • High Vagal Tone
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10
Q

How is the HV interval measured?

A

measured from the beginning of the HIS bundle electrogram recording (second deflection on the HIS bundle catheter during sinus rhythm) to the first ventricular electrogram either on:

  • the HIS bundle recording (the third deflection in sinus rhythm)

or

  • RV electrogram

or

  • even on any of the surface QRS recordings.
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11
Q

What does HV measure?

A
  • represents distal conduction activation
  • conduction time from the His bundle (located just below the AV node) –> first identifiable onset of ventricular activation.
  • the time it takes for an electric impulse to traverse the HIS bundle, the bundle branches, and the Purkinje network in order to activate the ventricles
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12
Q

Describe the measurement

A
  • measurement of HV interval
    • from beginning of His bundle recording to the first ventricular electrogram
  • HV = 90 msec –> prolonged
    • normal HV = 25-55 msec
  • Patient with first-degree AV block and RBBB on surface ECG
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13
Q

What is a normal HV interval?

Describe the HV interval?

A
  • 25-55 msec
  • conduction time from the His bundle (located just below the AV node) –> first identifiable onset of ventricular activation.
  • normal HV interval is not affected by autonomic state or pharmacologic agents
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14
Q

What does a short/negative HV interval suggest?

A
  • ventricular activation occurs before HIS bundle activation
    • Accessory pathway (WPW)
    • VT
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15
Q

The site of AV block may be determined by this?

A
  • His bundle electrogram
    • determines AV node vs. distal conducting system blocks
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16
Q

What does a prolonged HV interval suggest?

A
  • abnormal conduction in the distal cardiac conduction
  • portends a higher likelihood of conduction failure –> heart block
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17
Q

What two medications can be used to reduce the risk for ICD shocks in VT?

What trials demonstrated this?

A
  • Sotalol and Amiodarone
  • OPTIC - 2005 (Optimal Pharmacological Therapy in Cardioverter Defibrillator Patients) study.
  • Amiodarone (+ BB) superior to Sotalol
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18
Q

Sotalol:

  • MOA
  • Major side effect
  • Elimination
A
  • MOA:
    • IKr blockade - delayed-potassium rectifier channel
    • Beta receptor blockade (predominant action at doses < 160 mg daily)
  • Side effects
    • Torsades de pointes < 2%
      • increases in setting of bradycardia, female gender, pre-excisting QT prolongation, history of heart failure, VF, VT, hypokalemia
      • Avoid in combination with QT prolonging agents
  • Elimination:
    • Kidney 100%
    • No pharmacologic interaction with warfarin, digoxin HCTZ
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19
Q

What is the difference in survival, in refractory VF patients comparing Lidocaine and Amiodarone?

A
  • ALIVE trial - 2001 (Amiodarone vs. Lidocaine in Prehospital VF Evaluation) compared the two in treatment of Cardioversion refractory VF in the field.
  • Amiodarone demonstrated improved survival (2:1) to hospital admission
  • No difference in survival to hospital discharge
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20
Q

What arrhythmia most likely in a patient with Ebstein’s anomaly? How would it manifest?

A
  • AVRT
  • likely related to bypass tract –> manifests as pre-excitation
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21
Q

What did the AVID trial show?

What population of patients were included and benefit from ICD over antiarrhythmics?

A
  • AVID - 1997 (Antiarrhythmics Versus Implantable Defibrillators) in patients with history of Ventricular Arrhythmia
  • Secondary prevention (class I indications)
  • VF arrest (resuscitation)
  • Sustained VT with syncope
  • Sustained VT with an LVEF < 40% associated with severe symptoms (HF, angina)
22
Q

What is the treatment for inappropriate ICD shock that occurs due to a supraventricular arrhythmia?

A
  • Elimination of VT zone (170 bpm) –> single-zone program strategy (VT/VF = 200 bpm) led to reduction in inappropriate therapies and improved survival
  • MADIT-RIT (Multicenter Automatic Defibrillator Implantation Trial - Reduce Innappropriate Therapy)
23
Q

What are the Class I indications for ICD?

A
  1. Survivors of cardiac arrest due to sustained VT or VF, not due to a reversible cause
  2. Spontaneous sustained VT in the setting of structural heart disease.
  3. Syncope of unknown cause with induction of sustained VT (or VF) that is hemodynamically significant.
  4. Prior MI ( > 40 days earlier) with LVEF < 35% and NYHA functional class II-III heart failure.
  5. NICM with LVEF < 35% and NYHA functional class II-III heart failure.
  6. Prior MI ( > 40 days earlier) with LVEF < 30% and NYHA functional class I heart failure.
  7. Spontaneous nonsustained VT, prior MI with LVEF < 40%, inducible sustained VT (or VF).
24
Q

What are complications of CIED placement?

A
  • Infection
  • Hematoma (pocket)
  • Hemothorax
  • Pneumothorax
  • Pericardial effusion/tamponade from lead perforation
  • Lead dislodgement
  • Extracardiac stimulation (phrenic, diaphragmatic, other)
  • Thromboembolism
  • Arrhythmias (including inability to convert induced VF)
  • Anesthetic risks
  • Death
25
Q

What clinical circumstances preclude use of a S-ICD?

A
  • CRT
  • Antitachycardia pacing support
  • Bradycardia pacing support
26
Q

What subset of patients require S-ICD?

A
  • Vascular access limitations
    • HD pateints
    • Prior lead extraction
27
Q

What are Class IIa indications for ICD?

A
  1. Syncope of unknown origin in the setting of NICM with significant LV dysfunction
  2. Spontaneous sustained VT in the setting of normal or near normal LV function (excludes VT amenable to ablation with structurally normal heart)
  3. Hypertrophic cardiomyopathy with > 1 risk factor for sudden death in that disease state.
  4. Arrhythmogenic right ventricular cardiomyopathy/dysplasia with > 1 risk factor for sudden death in that disease state.
  5. Long QT syndrome with syncope (or polymorphic VT) despite beta-blockers.
  6. Patients awaiting cardiac transplantation as an outpatient.
  7. Brugada syndrome and syncope.
  8. Brugada syndrome and documented VT.
  9. Catecholaminergic VT and syncope or VT.
  10. Cardiac sarcoidosis, giant cell myocarditis, or Chagas disease.
28
Q

What are Class IIb indications for ICD?

A
  1. NICM with LVEF < 35%, and NYHA functional class I heart failure.
  2. Long QT syndrome with established high-risk features.
  3. Syncope of unknown origin in the setting of significant structural heart disease.
  4. Familial cadiomyopathy associated with sudden cardiac death.
  5. Patients with noncompaction cardiomyopathy.
29
Q

What does SNRT measure?

A
  • Sinus Node Recovery Time
  • measures spontaneous recovery of the sinus node after overdrive suppression
  • Normal uncorrected SNRT < 1400 ms
  • Nromal corrected SNRT < 550 ms

-

30
Q

What are the criteria for Left Anterior Fascicular Block (LAFB)?

A
  • LAD (usually between -45 and -90 degrees)
  • Small Q waves with tall R waves ( = ‘qR complexes’) in leads I and aVL
  • Small R waves and deep S waves ( = rS complexes) in leads II, III, aVF
  • QRS duration normal or slightly prolonged (80-110ms)
  • Prolonged R wave peak time in aVL > 45ms
  • Increased QRS voltage in the limb leads
31
Q
A
  • Atrial fibrillation
  • Left anterior fascicular block
    • LAD
    • qR in I and aVL
    • rS in II, III, aVF
    • QRS normal or slightly prolonged (80-110ms)
    • Prolonged R wave peak time in aVL > 45ms
    • Increased QRS voltage in limb leads
  • Nonspecific ST and/or T wave abnormalities
32
Q

What are common arrhythmias associated with Digoxin toxicity?

A
  • atrial tachycardia
  • atrial fibrillation with complete heart block
  • accelerated junctional rhythm
  • AV block (2nd or 3rd degree)
  • Bi-directional VT

**exacerbated by hypokalemia, hypomagnesemia, hypercalcemia

33
Q
A

Digoxin toxicity

  • atrial tachycardia
  • AV block 2:1
  • exacerbated by hypokalemia, hypomagnesemia, hypercalcemia
34
Q

What is functional (rate-related) aberrancy?

A
  • mean QRS duration greater than 120ms in the setting of rapid heart rates, but returns to normal duration at slower heart rates
35
Q

What is the mechanism of PAC’s?

A
  • typically will conduct back to the SA node –> resetting the node –> temproarary pause
  • if SA entrance block exists (preventing conduction back to the SA node) –> node will not reset and either:
    • interpolated beat (extra QRS complex between otherwise constant R-R intervals)
    • full compensatory pause
36
Q

Define RBBB

A
  • QRS > 120ms
  • RSR’ pattern in V1-V3
  • Wide slurred S wave in I, aVL, V6 (S wave greater duration than R wave or > 40 ms)
  • R wave peak time >50ms in V1
37
Q

A clinical diagnosis of HCM is confirmed when these features are identified.

A
  • Increased LV wall thickness ( 13-60mm, average 22mm)
  • Nondilated LV chamber
38
Q

What is the most common location for LV hypertrophy in HCM?

A

basal anterior septum in continuity with the anterior free wall

39
Q

What is the pathology for HCM?

What is the characteristic histopathologic finding?

A
  • Abnormal intramural coronary arterioles –> decreased luminal cross-sectional area and impaired vasodilatory capacity –> blunted myocardial blood flow during stress (small vessel ischemia) –> myocyte death –> fibrosis
  • Disorganized and chaotic pattern of Interstitial Fibrosis
40
Q

What are the noninvasive clinical risk markers that can help identify HCM patients at high-risk for SCD / indication for ICD?

A
  • Hypotensive or attenuated BP response to exercise
  • Extreme LV hypertrophy (wall thickness > 30 mm)
  • Family History of premature HCM-related death (particularly if sudden death in close relatives)
  • Unexplained Syncope judged non-neurocardiogenic, particularly if recent, in young patients
  • NSVT on serial ambulatory EKG’s, particularly when bursts are multiple, repetitive, or prolonged

Subgroups who should also be considered for ICD

**LV apical Aneurysm

**LVEF < 50%

***LGE > 15% of LV mass

***Cardiac arrest/sustained VT

41
Q

What does LGE identify in HCM?

What level indicates high-risk for SCD / ICD placement?

A
  • Degree of myocardial fibrosis
  • > 15%
42
Q

What is the only proven therapy to prevent SCD in HCM patients?

A

ICD

43
Q
A

Pre-excitation

  • indicating a bypass tract
44
Q

Describe use of “pill-in-the-pocket”

What medications are used for this?

A
  • Initial rate control to prevent rapid conduction of A-fib/flutter
    • BB or CCB
  • Followed by administration of a single bolus dose of a class I antiarrhythmic drug
    • Flecainide 200-300 mg
    • Propafenone 450-600 mg
45
Q

What are contraindications to “pill-in-the-pocket” (or class Ic antiarrhythmics) approach?

A
  • Structural heart disease
  • Conduction system disease (bundle branch block)
46
Q

Describe the findings

A

4:1 rate controlled atrial flutter

  • no additional intervention required prior to surgery
47
Q

Describe the findings

A

Delayed afterdepolarizations

  • PVC’s with left bundle morphology and inferior axis —> focus at the RV outflow tract
48
Q
A
49
Q

What is a cause of delayed afterdepolarizations:

  • young adult without structural heart disease
A

PVC’s arise from triggered activity due to catecholamine-induced delayed afterdepolarizations

50
Q

What percentage of patients are LAA thrombi found in patients with AF > 2 days?

A

5-14%

51
Q
A

Medical (69 decks)

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