CASE REPORT

VENTRICULAR ARRHYTHMIA

Hana Rutyana Putri Antonio, MD

Mentor : Panji Gugah Bhaskara, MD

Internist
Supervisor : Paul Jonatan, MD
Achmad Bestari, MD

CIMACAN REGIONAL HOSPITAL

FEBRUARY 2020
CASE
o PATIENT IDENTITY

Name : Sumyati
Sex : Female
Age : 55 yo
Address : Ciherang
Work : Housewife
Religion : Moslem
Race : Sundanese

o ANAMNESIS

• Chief Complaint: palpitation

• Present history of illness:
Patient came to the policlinics due to palpitation. Patient felt palpitation for about 6 months.
Patient has never experienced chest pain, dyspnea, or syncope before. At the ward patient
didn’t feel nausea, no vomiting, no chest pain, or syncope. No history of cardiac disease
before. Patient has never recorded her electrical cardiac activity using ECG or examined by
echo before
• Previous history of illness:
Patient had no history of hypertension, DM, allergies, or any other chronic diseases before
• Family history:
History of CAD-, HF-, arrhythmia -, HT -, DM -
• Lifestyle:
Smoking -, alcohol consumption-, patient is not an athlete, routine exercise -

o SYSTEMIC ANAMNESIS

• Cerebrospinal : syncope -
• Cardiovascular : palpitation +, chest pain -
• Respiration : dyspnea -
• Gastrointestinal : heart burn-, nausea-, vomit-
• Musculoskeletal : tremor -
• Integumentary : cyanosis -
• Urogenital : oliguria -, polyuria -

o PHYSICAL EXAMINATION

At the Policlinics
Vital sign : HR 120bpm irregular RR 22x/min BP 110/70mmHg T 36.5◦C
Head and neck : Jugular vein distension –
Thorax : cardio S1 S2 non split, murmur-, gallop –
lung ves -/- rales-/- crackles-/- wheezing -/-
Abdomen : distension -, bowel sound normal, pain on palpation -,
muscular guarding –
Extremity : clubbing finger -, cyanosis -, peripheral edema –
o INITIAL ASSESSMENT AND PLAN

From the Policlinic :

• Assessment : AF RVR, CHF
• Plan :
- if RVR repeat digoxin bolus, if NVR switch to digoxin tab 0,125mg
- ECG in the next 4h

o FOLLOW UP

Jan 8, 2019 19.30

Advice:
Bolus amiodarone 150mg then drip 360mg in the 1st 6h, 540mg in the 2nd 18h

Jan 9, 2019
S: palpitation -, chest pain -
O:
Vital sign : HR 88 regular RR 22x/min BP 110/70mmHg T 36.5◦C
Head and neck : Jugular vein distension –
Thorax : cardio S1 S2 non split, murmur-, gallop –
pulmo ves -/- rales-/- crackles-/- wheezing -/-
Abdomen : distension -, bowel sound normal, pain on palpation -, muscular guarding –
Extremity : clubbing finger -, cyanosis -,
peripheral edema -
A: VT, CHF, Frequent VES
P:
- Furosemide 3x40mg iv
- Drip amiodarone 540mg in the next 18h  continue amiodarone tab 3x200mg
- Aspilet tab 1x80mg
- Candesartan tab 1x4mg
- Paracetamol tab 3x500mg
- Spironolactone 1x25mg
- Bisoprolol 1x 2,5 mg
- Plan to be referred to Hasan Sadikin Hospital
 Jan 9, 2019 09.00

Jan 9, 2019 21.00

Advice:
- Do ECG tomorrow morning
- Continue amiodarone tab, if not available change to bisoprolol 2,5mg
- If experience chest pain give: CPG loading 300mg then 1x75mg; Bolus heparin 60 U/kg
then drip 12 U/kg/h
- Lactulac 4x15cc
- Aspilet 1x80mg
- Atorvastatin 1x40mg
- Put on urinary catether

Jan 10, 2019

S: palpitation -, chest pain -
O:
Vital sign : HR 80 regular RR 20x/min BP 100/80mmHg T 36.5◦C
Head and neck : Jugular vein distension –
Thorax : cardio S1 S2 non split, murmur-, gallop –
pulmo ves -/- rales-/- crackles-/- wheezing -/-
Abdomen : distension -, bowel sound normal, pain on palpation -, muscular guarding –
Extremity : clubbing finger -, cyanosis -,
peripheral edema -
A: VT, CHF, Frequent VES
P:
- amiodarone tab 3x200mg
- Aspilet 1x80mg
- Atorvastatin 1x40mg
- Candesartan 1x8mg
- Lactulac 4x15cc
- Paracetamol tab 3x500mg
- Spironolactone tab 1x 25mg
- Repeat ECG post amiodarone
 ECG post amiodarone

o IMAGING

o LABORATORY EXAMINATIONS
Jan 8, 2019

PARAMETER RESULT NORMAL UNIT

RANGE

Hemoglobin 12.8 12.0-16.0 g/dL

Hematocrit 35.0 35.0-47.0 %

Erythrocyte 4.2 3.8-5.2 10^6/uL

MCV 83.4 80.0-94.0 fL

MCH 30.4 26.0-34.0 pg

MCHC 36.4 32.0-36.0 g/dL

Thrombocytes 239 150-450 10^3/uL

Leukocyte 5.9 4.8-10.8 10^3/uL

 WBC count:

PARAMETER RESULT NORMAL UNIT

Lymphocytes 44.2 20.0-40.0 %
RANGE

Monocytes 6.6 2.0-8.0 %

Blood Glucose 85 <200 mg/dL

Granulocytes 49.2 50.0-70.0 %

AST 46.3 <35 U/L

Absolute count:
ALT 68.1 <36 U/L

Lymphocytes 2.6 1.0-4.3 10^3/uL

Ureum 22.0 15-50 mg/dL

Monocytes 0.4 0.1-0.9 10^3/uL

Creatinine 0.89 0.6-1.1 mg/dL

Granulocytes 2.9 2.4-7.6 10^3/uL

Natrium 148.1 135-148 mmol/L

Potassium 3.76 3.5-5.5 mmol/L

Chloride 115.7 97-108 mmol/L

DISCUSSION
o NORMAL ECG

- The P wave records atrial depolarization and contraction. The first part of the P wave
reflects right atrial activity; the second part reflects left atrial activity
- There is a brief pause when the electrical current reaches the AV node and the EKG falls
silent (the PR segment).
- Ventricular depolarization generates the QRS complex
- The T wave records ventricular repolarization.
- Various segments and intervals describe the time between these events:
a. The PR interval measures the time from the start of atrial depolarization to the start
of ventricular depolarization.
b. The PR segment measures the time from the end of atrial depolarization to the start of
ventricular depolarization.
c. The ST segment records the time from the end of ventricular depolarization to the
start of ventricular repolarization.
d. The QT interval measures the time from the start of ventricular depolarization to the
end of ventricular repolarization.

Normal 12 Lead ECG

- The P wave is small and usually positive in the left lateral and inferior leads.It is often
biphasic in leads III and V1. It is usually most positive in lead II
and most negative in lead aVR.
- The QRS complex is large, and tall R waves (positive deflections) are
usually seen in most left lateral and inferior leads. R-wave progression refers
to the sequential enlargement of R waves as one proceeds across the
precordial leads from V1 to V5. A small initial Q wave, representing septal
depolarization, can often be seen in one or several of the left lateral leads,
and sometimes in the inferior leads.
- The T wave is variable, but it is usually positive in leads with tall R waves.

o DEFINITION OF ARRHYTHMIA

any disturbance in the rate, regularity, site of origin, or conduction of the cardiac electrical
impulse

o CLINICAL MANIFESTATION OF ARRHYTHMIA

- Palpitation
- Light headedness and syncope
- Chest pain
- Sudden death

o ETIOLOGY OF ARRHYTHMIA

o TYPES OF ARRHYTHMIA

- Arrhythmias of sinus origin

- Ectopic arrhythmia
- Reentrant syndrome
- Conduction blocks
- Preexcitation syndrome

o HOW TO ASSESS THE RYHTHM

- Presence of normal P waves

- Whether the QRS complexes is narrow or wide
- The relationship between the P waves and the QRS complexes
- Whether the rhythm is regular or irregular

o VENTRICULAR ARRHYTHMIA

• Premature Ventricular Contraction

Rules of Malignancy for PVCs
- Frequent PVCs
- Consecutive PVCs (3 or more in a row)
- Multiform PVCs
- R-on-T phenomenon (becomes VT)
 - Any PVC occurring during an acute myocardial infarction (or in any patient
with underlying heart disease)
• Ventricular Tachycardia
3 or more consecutives PVCs  VT
Sustained VT  last >30s
Pulseless VT  cardiac arrest need CPR and defibrillation
 Ventricular Fibrilation
Pre terminal event that needs CPR and defibrilation
 Accelerated idioventricular rhythm
Benign rhythm that sometimes seen during acute infarction or during the early hours
following reperfusion. Beat is around 50-100bpm, if below 50bpm it’s called idioventricular
rhythm.
 Torsades de Pointes
Prolongation of QT interval is seen. It’s classified as polymorphic VT.

o PATHOPHYSIOLOGY OF VENTRICULAR ARRHYTHMIA

- Enhanced normal or Abnormal automaticity  partially depolarized membrane potential,

for example in acute phase MI or transient ischemia
- Triggered activity
 early after depolarization: action potential prolongation (increase inward current or decrease
K depolarization), for example in polymorphic VT
 Delayed after depolarization: occur after complete membrane repolarization due to
intracellular calcium overload, for example in digoxin toxicity, catecholaminergic
polymorphic VT, idiopathic outflow VA
- Reentry
 an excitable gap separate the excitation wave-front from its tail of refractoriness , for
example in structural heart disease (scar after MI, post surgically repaired congenital
heart disease)
 heterogeneity in ventricular repolarization, for example in Brugada Syndrome

o DIAGNOSTIC AND EVALUATION OF ARRHYTHMIA

- History taking of patient symptoms, medication, past medical history, and family history
- Physical examination to identify the underlying etiology of VA
- Evaluation:

Noninvasive
• 12 Lead ECG
- Criteria diagnosis for VT : AV dissociation, QRS complex >0.14s, monophasic R
wave in aVR , specific QRS morphologies, absence of RS complex in all precordial
lead, RS interval >100ms at least 1 precordial lead
- May indicate: structural heart disease, inherited arrhythmia disorders
• Exercise test
- To diagnose catecholaminergic polymorphic VT, exertion related arrhythmia (with long
term ECG monitoring)
• Ambulatory ECG
• Implanted cardiac monitor
• Noninvasive cardiac Imaging :
• - echocardiography  recommended in patients with known or suspected VA that may
be associated with underlying structural heart disease or a risk of SCA
- cardiac MRI or CT
• Biomarkers
BNP or NT pro BNP might be useful as the prognostic for predicting SCD or SCA
• Genetic Testing

Invasive
• CT Angiography or Cardiac Catheterization
 Recommended in patients who recovered from unexplained SCA to confirm the
presence/absence of ischemic heart disease and guide decisions for myocardial
revascularization
• Electrophysiological Study
 Recommended in patient with ischemic/non ischemic cardiomyopathy, adult
congenital heart disease with syncope or other VA symptoms who don’t meet the
criteria of primary prevention ICD (Implantable Cardioverter Defibrilator) to assess the
risk of sustained VT

o THERAPY

Antiarrhythmic Medication
• Sodium Channel Blockers
 Limited role in prevention of VT or sudden cardiac death
• Beta Blockers
 Considered as first line antiarrhythmic therapy
 Adrenergic receptor blockage on sympathetic mediated mechanism, ↓ sinus rate, inhibition
of calcium excess by ryanodine receptor
 Could enhance antiarrhythmic efficacy if combine with membrane stabilizing
antiarrhythmic medication
 but beta blockers could increase risk of shock in patients with MI and risk factors for shock
• Amiodarone
 Amiodarone blocks beta receptors and sodium, calcium and potassium currents
(multichannel blockers)
 As primary prevention in high risk patient ( LVEF <40% with or without coronary disease),
amiodarone ↓ risk of sudden cardiac death (SCD)
 amiodarone reduces risk of SCD and all cause of mortality compared to other anti
arrhythmia
 iv amiodarone reduce recurrent VT/VF during resuscitation
 Chronic use of amiodarone would increase its adverse effect as well
• Calcium Channel Blockers
 non dihydropyridine Ca channel blockers have no roles in most VA cases
 verapamil could cause hemodynamic collapse in sustained VT patients with prior MI
 Ca channel blockers shouldn’t be given in VT patients with HF reduced EF
 In VT patients with non structural heart disease verapamil/ diltiazem could be given to
suppress some outflow tract origin
 Non antiarrhythmic medication
• Electrolytes
 In hypokalemia and hypomagnesemia patients(common consequences of diuretic
therapy in HF patients)
• N-3 polyunsaturated Fatty acids and lipids
statin reduce risk of SCD especially in patients with atherosclerotic CVD and or
ischemia
 Some RCTs showed no benefit in giving n-3 polyunsaturated fatty acid but it’s not
harmful if given

Management of sustained Monomorphic VT

 Management of VA in patients with ischemic heart disease

- In patients with IHD and recurrent VA, amiodarone and sotalol are useful to prevent
recurrent VA
- In patients prior MI and recurrent episodes of sustained VT and failed amiodarone
or other antiarrhythmic medication, catheter ablation is recommended
- In patients with IHD or symptomatic sustained recurrent monomorphic VT,
catheter ablation is recommended to prevent recurrent VA
- In patients prior MI, flecainide and propafenone should not be used
 Management of ventricular arrhythmia in structurally normal heart
- Avoidance of aggravating factor such as caffeine and sympathomimetic agents might
be sufficient in mild symptoms
- Class I anti arrhythmia (fast Na channel blocker) can be effective but avoided due to
its adverse effect
- If anti arrhythmia is ineffective, catheter ablation can be highly effective

o SUMMARY

- We should know the normal ECG before identify arrhythmia

 - Anamnesis of patient symptoms, present and previous history of illness, family history,
and physical examination are important to evaluate the presence of structural heart
disease and etiology of ventricular arrhythmia
- 12 lead ECG is the first diagnostic tool for ventricular arrhythmia, then
echocardiography and cardiac MRI/CT
- Beta blocker can be used as the first anti arrhythmic medication but should be avoided in
acute MI/ HF settings
- Amiodarone is a multichannel blocker that could reduce risk of sudden cardiac death and
prevent recurrent VT/VF during resuscitation
- Think of idiopathic ventricular arrhythmia if the etiology of VA is unknown

o REFERENCES

- 2017 AHA/ACC/HRS Guideline for Management of Patients with Ventricular

Arrhythmias and the Prevention of Sudden Cardiac Death
- The only EKG Book You’ll Ever Needed