- SUSHILKUMAR S GUPTA.PGY2 INTERNAL MEDICINE.

MAIMONIDES MEDICAL CENTER.BROOKLYN, NY, 11219.

Ventricular Tachycardia and Management. Case Based

approach.

Chief Complaint.

77 y/o MaleChief complaint: Found on street,

unconscious, brought in by EMS to the hospital.

Past Medical History

Atrial Fibrillation from past 15 years s/p Pacemaker in May 2014. Echo done in July 2015 -45% (outpatient).

HypertensionHyperlipidemiaDiabetes MellitusBPH

HPI

The patient was brought in by EMS, while he was found unconscious on street, duration unknown.

He had a rapid Heart rate – 250beats per minute.On detailed evaluation later after he was

conscious, patient states that while he was riding his bike he had chest pain, felt dizzy and had headache after which he became unconscious and when woke up was found to be in hospital.

On baseline, Patient is ambulatory, ADL independent, AOO x 3.

Social Hx Non smoker Non alcoholic No illicit drug use described Married, lives with wife.

Family Hx No family history of Arrhythmia or Cardiovascular

disorder.Surgical Hx

Pacemaker insertion in May 2014.

Review of Systems

General: -fever, -chillsNeuro: +generalized weakness, -confusion, +dizziness,

+loss of consciousnessSkin: -lesions, -rashNose, Mouth, Throat: -nasal discharge, -epistaxisRespiratory: -cough, +dyspnea, -hemoptysis, -pleuritic -

wheezingCardiovascular: +chest pain, +palpitationsGI: -constipation, +abdominal pain, -diarrhea, -nausea, -

vomiting, -hematochezia, -black stoolsExtremities: +bilateral LE swelling.GU – No hematuria or dysuria.

Physical Exam

Vitals: Temp 100.7F, HR 285bpm, RR 26bpm, BP 92/65mmhg, O2 sat 100% on 2L NC

General: Lying in stretcher, unconsciousPsych: unable to assessNeuro: unconscious, Pupils bilateral equal size and

reacting.Skin: No rashes observed, dry skinHEENT: NC/AT, dry oral mucosaRespiratory: Left side healed scar from pacemaker

insertion, clear breath sounds bilaterally, no wheezing, rales or crackles auscultated

Cardiac: tachycardia, normal S1/S2, no murmurs appreciated

Abdominal: Soft, non-distended, active BS, RUQ tenderness.Extremities: 2+ pitting edema, 1+ dorsalis pedis.

Medication List

Warfarin 3mg OD.Tamsulosin 0.4mg QHSSimvastatin 20mg QHS.Metformin 1gm BIDLosartan 25mg ODAtenolol 50mg BID

Baseline EKG

Initial Lab Workup

16.512.2

37.8394

135

4.3

100

21

19

0.9303

PT – 94.6INR – 8.5Ca – 8.5AG - 14BNP – 488Mg -1.4

Cardiac Enzymes:Myoglobin – 57, 58,39CKMB – 3.1, 2.7Troponin I - <0.03, 0.03, 0.03

EKG strip recorded by EMS staff

In Emergency Department

Pt received 150mg of Iv Amiodarone Bolus in the field which did not break the rhythm, was brought to MMC ER. EKG strip – shows monomorphic VT.

He received 100 Joules Synchronized Cardio version and Iv Amiodarone drip was initiated.

IVF NS was started. Aspirin 325mg.CT head – negative for any acute intracranial

disease.CXR – Left side pacemaker, enlarged Cardiac

Silhouette. Mild Pulmonary vascular congestion.Labs and Blood culture were sent. IV Ab were

initiated.USG abdomen – significant for cholecystitis.

New ECHO study in the hospital

1. Severely decreased left ventricular systolic function. 2. Left ventricular ejection fraction, by visual estimation,

is 20 - 25%. 3. Severely dilated right atrium. 4. Moderately dilated left atrium. 5. Moderately dilated LV cavity size. 6. Moderately enlarged right ventricle. 7. Mild thickening of the anterior and posterior mitral

valve leaflets. 8. Moderate aortic valve sclerosis without stenosis. 9. Moderately reduced RV systolic function.10. Trivial pericardial effusion.

Next day

Next morning at 9.20 AM, patient CODED. Polymorphic Vtach on monitor. QTC was prolonged, so Amiodarone drip was discontinued.

CPR was initiated under the ACLS protocol, 3 shocks were given, patient was resuscitated and Lidocaine drip was initiated.

EP team and Heart Failure team were also involved.In evening patient again coded, he received shocks and was

resuscitated but this time he was also Intubated, Central and arterial line were inserted.

Electrolytes were replaced. Mg and K were monitored, although he was persistently found to be hypomagnesemic..

Pt was also placed on Levophed for short period for hypotension.

Hospital course

Pt continued to receive Iv Ab as per ID, however all the cultures remain negative during the hospitalization.

He also received multiple units of FFP to bring his INR in therapeutic range, to optimize for Cardiac cath.

After his INR -1.9, cath was done – which revealed clean CORONARIES, and he was diagnosed with Non Ischemic Cardiomyopathy.

Pt was extubated, maintained SPO2 -97% on NC, hemodynamically stable.

2 days later he DDD pacemaker was upgraded to DDD –ICD, and anticoagulation with Warfarin was initiated which was later on changed to Apixaban.

Now the Question is WHY AICD???????

Current status

Pt is still in hospital, afebrile, hemodynamically stable, accepting orally, ambulatory, no chest pain or sob.

AICD wound is clean with no signs of Pocket hematoma. Currently on Apixaban 5m Q12.

Pt still has repeated events of Afib with RVR, due to which dose of Toprol was increased to 100mg daily and Digoxin 0.25mg added to the regimen.

He is also on Lisinopril 2.5mg daily and Aldactone 25mg daily.

PO Mexilitine 150mg Q8. Lasix 40mg PO dailyNephrology is following for Hypomagnesemia. On Oral

supplementation.

SUSHILKUMAR S GUPTA.PGY2 IM.

Ventricular tachycardia and management.

Definition

Wide complex rhythm QRS>0.12sec

Rate > 100 (or 120) bpm

Origin: from one of the Ventricles i.e., distal to the bundle of His.

Three or more consecutive beats on a ECG.

Classification is based on:

1. Duration of Episodes

2. Morphology

3. Symptoms

1. Duration of Episodes

Three or More beats on an ECG at a rate >100bpm originating from Ventricles

Non Sustained VT: If rhythm self-terminates spontaneously in less than 30seconds

Sustained VT : If rhythm lasts > 30seconds (Even if it self-terminates spontaneously after 30s)

2. Morphology

1. Monomorphic VT : same configuration beat to beat. This is the most common VT; and the most common reason is ischemia.

2. Polymorphic VT : Continually changing QRS morphology. Causes – Ischemia, electrolyte disturbance, drug toxicity and familial.Torsade de pointes (twisting of points)Waxing and waning QRS amplitude during tachycardia associated with prolonged QT interval

3. Sinusoidal VT :sinusoidal appearance of rhythm. Electrolyte dist.4. Accelerated idioventricular rhythm (AIVR) – m/c cause - reperfusion arrythmia in first 12hrs after acute MI or during periods of elevated sympathetic tone. No treatment necessary, self terminates.

Prolonged QT interval

What is the difference between prolonged QT interval and Polymorphic VT??????

Acquired : K Channel blocking medication : Quinidine,

Erythromycin, Clarithromycin, Haloperidol, Droperidol, Ondensetron.

Type 1A antiarrhythmic : sotalol, Amiodarone,Congenital :

Brugada syndrome Congenital long and short QT syndromes Catecholamingeric polymorphic VT

Symptoms

Chest PainLight headednessPalpitationsSyncopeSudden Cardiac Death (SCD) :Ambulatory

ECG records at SCD have shown 50-60% at sustained monomorphic VT as the initial event.

Differentials

SVT with aberrant intraventricular conductionPreexcited Tachycardia (associated with or mediated

by accessory pathway)BBBVentricular paced rhythms

Treatment depends on hemodynamics: Stable Vs Unstable.

Management Algorithm:

Antiarrhythmic agents

Amiodarone (Class 3)

Large volume of distribution & long half lifeContraindications

Iodine sensitivity Sinus bradycardia Heart block

Precautions Incompatible with NS. Preferred with D5W. Preferable via CVC. Monitor TFT, PFT, LFT

Adverse effects Short term : Prolongation of QT interval, Skin reactions,

Brady, hypotension, corneal micro-deposits.

Pioneers of ICD.

Martin Mower

Michel Mirowski

Primary and Secondary indications of AICD use.

Primary Prevention - Patients at high risk for cardiac arrest due to a defined pre-existing disease state but without clinical expression of potentially fatal arrhythmias.

Secondary Prevention- Patients surviving cardiac arrests due to ventricular tachyarrhythmia's.

Thank you!