Departemen Kardiologi FK USU

RSUP. H. Adam Malik

Medan
 SA node
Sumber impuls normal/
alamiah , 60 – 100

AV node
Bisa mengeluarkan
impuls 40-60x/menit

Berkas His
Serabut Purkinje

Ventrikel
Bisa mengeluarkan impuls
20-40 x/menit
4
CAUSE OF CARDIAC ARRHYTHMIAS :

• Disturbances in automaticity : bertambah cepat

atau bertambah lambatnya suatu daerah otomatisitas.
Misal di sinus node, AV node, abnormal beats/
depolarisasi atrium, AV junction, ventrikel, VT, dll.

• Disturbances in conduction : konduksi terlalu cepat

(WPW) atau terlalu lambat (blok AV).

• Combinations of altered automaticity and

conduction.
Tachyarrhythmia Bradyarrhytmia
(rate >100 x/min) (rate < 60 X/min)

• QRS sempit (<0.12 ms) • AV blok derajat 1, 2 & 3

• QRS lebar (>0.12 ms) • RBBB & LBBB
 Underlying cardiac disease
- Ischemic heart disease
- Valvular heart disease
- Hypertensive heart disease
- Congenital heart disease
- Pre excitation (short of PR interval)
- Long QT (congenital or acquired)
 Drugs
- anti-arrhytmia

- sympathomimetic.

- B2 agonis, cocaine, anti depresants

(tricyclic), Aminophylline, caffeine.

- alcohol.
 Metabolic abnormalities.
- Electrolyte (low  K, Na, Ca, Mg )

- Hypoximia, Hypercarbia.

- Acidosis

0 Endocrine abnormalities
-Thyrotoxicosis, Phaeochrocytoma.
 Miscellaneous.
- Febrile illness
- Emotional stress
- Smoking
- Fatigue.
 Symptoms
Palpitations: nontachycardiac; rapid and regular; rapid and
irregular (regularly irregular or irregularly irregular).
Abrupt or accelerating onset and termination?

Dyspnea
Chest discomfort
Syncope; “nearly blacked out”; syncope with spell
Polyuria
Cardiac arrest
Signs
Heart rate and pulses: regularity; amplitude; deficit
Hypotension
Hypoperfusion
 Lebar gel. QRS

 Keteraturan gel. QRS

P wave ??
 QRS sempit

Irama
Irama Teratur
Tidak teratur

Supraventricular
Sinus Tachycardia Atrial Fibrillation
Tachycardia

Atrial Flutter
SVT :
-due to re-entry mechanism
-narrow QRS complex
-regular
-retrograde atrial depolarization
-P wave ?
Atrial Fibrillation :

-from multiple area of re-entry within atria

-or from multiple ectopic foci
-irregular, narrow QRS complex
-very rapid atrial electrical activity
(400-700 x/min).
-no uniform atrial depolarization
Atrial Flutter :
-The result of a re-entry circuit within
the atria
-Irregular / regular QRS rate
-Narrow QRS complex
-Rapid P waves (300x/min), “sawtooth”
 QRS lebar

Irama
Irama Teratur
tidak teratur

Ventricular Ventricular
Tachycardia Fibrillation
Ventricular Tachycardia
VT
VT
Torsade de Pointes
Ventricular Fibrillation
 VENTRIKEL EXTRA SYSTOLE

SR

VES
 Sinus rhythm
with
Multifocal VES

VES VES

SR SR
SR SR SR SR
Sinus rhythm with VES couplet
Sinus Rhythm with VES, R on T
  Atrial Fibrillation.
- Rate control :
1. Digoxin.
Digitalization dose : 0,03 mg x BW (Kg)
Maintenance dose : 0,125 – 0,25 mg /day,
depends on – renal function.
Route :oral tablet 0,25 mg or
Injection ampule 0,5 mg
- Propranolol
- Metoprolol
- Atenolol
- Bisoplrolol
- Carvedilol
 Amiodaron
Tablet : 200 mg.
Injection : 150 mg
Loading dose : 3 x 200 mg ( 5 days)
Maintenance dose : 100 – 200 mg / day.
Contraindication : Thyroid and Lung
(fibrotic) dysfunction.
1. ATP injection ( 8 mg – 20 mg )
2. Verapamil injection ( 2,5 – 10 mg)

3. Amiodaron injection.

Loading dose : 300 mg / 250 cc in 30 – 60

minutes.
Maintenance dose : 450 – 600 mg /day
4. Cardioversion : DC shock synchronize
5. Ablation : radiofrequency or laser.
 Amiodaron
oral or injection : depends on benign or
malignant extrasystole.
 Mechanisms
 Ventricular Fibrillation
 Pulseless Ventricular Tachycardia
 Asystole
 Pulseless Electrical Activity (PEA)
 A condition; Not an ECG rhythm
 Most common rhythms
 Adults: ventricular fibrillation
 Children: Asystole, Bradycardic PEA
 Pediatric V-fib suggests:
 Drug toxicity
 Electrolyte imbalance
 Congenital heart disease
 ABCs come first!
 Airway - unobstructed?  manually open
 Breathing - no or inadequate  ventilate
 Circulation - no pulse in 5 sec  chest
compressions
 Do NOT wait on equipment
 Assure effective BLS before going to ALS
 Rise and fall of chest
 Air movement in lung fields
 Pulse with compressions
 First ALS priority is defibrillation
 Only cure for v-fib is defib
 The quicker the better
 Probability of resuscitation decreases 7-10% with each
passing minute
 Vascular access
 Antecubital space
 Arm, EJ, Foot (last resort)
 IO in peds < 6 y/o
 14 or 16 gauge
 LR or NS
 30 sec - 60 sec of CPR to circulate drug
 Intubation as time allows
 Less emphasis today as compared to past
 Epi, atropine, lidocaine may be administered down
tube
 2x IV dose
 IV is preferred
 ABC’s
 Witnessed arrest: Precordial thump
 Little demonstrated value but worth a try
 CPR until defibrillator available
 Quick Look for VF or pulseless VT
 Treat pulseless VT as if it were VF
 Defibrillate
 200 J, 300 J, 360 J
 Quickly and in rapid succession
 Identify cause if possible
 If still in VF/VT arrest, continue CPR for 1
minute
 Establish IV access and Intubate
 If sufficient personnel, attempt both simultaneously
 If not, quick attempt at IV access then attempt ETT

 Vasopressor Medication
 Epinephrine
 1 mg 1:10,000 IVP
 Repeat every 3-5 mins as long as arrest persists
 Vasopressin (alternative to Epinephrine)
 40 units IVP one time only
 Shock @ 360 J after each medication given as long
as VF/VT arrest persists
 Alternate epi-shock & antidysrhythmic-shock sequence
 Antidysrhythmic Medication
 amiodarone 300 mg IVP single dose
 lidocaine 1-1.5 mg/kg IVP, q 5 min, max 3mg/kg total
 procainamide 100 mg IV, q 5 min, max 17 mg/kg total
 magnesium 10% 1-2 g IV
 if hypomagnesemic or prolonged QT
 Characteristics
 The ultimate unstable bradycardia
 A terminal rhythm
 poor prognosis for resuscitation
 best hope if ID & treat cause
 No significant positive or negative deflections
 Possible Causes
 Hypoxia: ventilate
 Preexisting metabolic acidosis: Bicarbonate 1
mEq/kg
 Hyperkalemia: Bicarbonate 1 mEq/kg, Calcium 1
g IV
 Hypokalemia: 10mEq KCl over 30 minutes
 Hypothermia: rewarm body core
 Possible Causes
 Drug overdose
 Tricyclics: Bicarbonate
 Digitalis: Digibind (Digitalis antibodies)
 Beta-blockers: Glucagon
 Ca-channel blockers: Calcium
 Primary ABCD
 Confirm Asystole in two leads
 Reasons to NOT continue?
 Secondary ABCD
 ECG monitor/ET/IV
 Differential Diagnosis (5Hs & 5Ts)
 TCP (if early)
 Epinephrine 1:10,000 1 mg IV q 3-5 min.
 Atropine 1 mg IV q 3-5 min, max 0.04
mg/kg
 Consider Termination
 Possibilities
 Massive pulmonary embolus
 Massive myocardial infarction
 Overdose:
 Tricyclics - Bicarbonate
 Digitalis - Digibind
 Beta-blockers - Glucagon
 Ca-channel blockers - Calcium
 Identify, correct underlying cause if possible
 Possibilities:
 Hypovolemia: volume
 Hypoxia: ventilate
 Tension pneumo: decompress
 Tamponade: pericardiocentesis
 Acute MI: vasopressor
 Hyperkalemia: Bicarbonate 1mEq/kg
 Preexisting metabolic acidosis: Bicarbonate
1mEq/kg
 Hypothermia: rewarm core
 ABCDs
 ETT/IV/ECG monitor
 Differential Diagnosis
 Find the cause and treat if possible
 Epinephrine 1:10,000 1 mg q 3-5 min.
 If bradycardic,
 Atropine 1 mg IV q 3-5 min, Max 0.04 mg/kg
 TCP
 In many systems, consider termination
of efforts
 Hypovolemia  Tablets (Drug
 Hypoxia OD)
 Tamponade
 Hydrogen ions
(Acidosis)  Tension
Pneumothorax
 Hyper/hypo-  Thrombosis,
kalemia Coronary
 Hypothermia  Thrombosis,
Pulmonary
Check pulse after any treatment
or rhythm change
 If pulse present:
 Assess breathing
 Present?
 Air moving adequately?
 Equal breath sounds?
 Possible flail chest?
 If pulse present:
 Protect airway
 Position to prevent aspiration
 Consider intubation
 100% Oxygen via BVM or NRB
 Vascular access
 Assess perfusion
 Evaluate
 Pulses
 Skin color
 Skin temperature
 Capillary refill
 BP
 Key is perfusion, not pressure
 Management of Decreased Perfusion
 Fluid challenge
 Catecholamine infusion
 Dopamine, or
 Norepinephrine
 Titrate to BP ~ 90 to 100 systolic
 The
Deadly
Rhythms

PEA
VT VF (Pulse less
Electrical
Activity)
A systole
Treat the patient,
not the monitor . . . . . . . . .!!!