Obat-Obatan Resusitasi

Terapi obat direkomendasikan

setelah resusitasi jantung paru yang
efektif dan defibrilasi pada henti
jantung.
Beberapa obat memiliki manfaat
jangka pendek, yaitu peningkatan
survival rate ke rumah sakit, seperti
vasopressor dan antiaritmia.
Definition of Cardiac arrest:
It is loss of cardiac function, breathing
and loss of consciousness.

Diagnosis of cardiac arrest (TRIAD):

1) Loss of consciousness.
2) Loss of apical & central pulsations
(carotid, femoral).
3) Apnea.
Types (forms) of
cardiac arrest:
1) Asystole
(Isoelectric line).
2) Ventricular
fibrillation
(VF).
3) Pulseless
Ventricular
tachycardia
(VT).
4) PEA: pulseless
 Epinephrine
WHY?
Natural catecholamine with and -adrenergic agonist
activity
Results in:
flow to heart and brain
SVR, SBP, DBP
electrical activity in the myocardium & automaticity (
success with defibrillation)
myocardial contraction (for refractory circulatory shock
(CABG))
increases myocardial oxygen requirements

Primary benefit: -vasoconstriction

-adrenergic activity controversial b/c myocardial work
Standar dose : 1 mg/IV
ETT dose : 2-2,5 mg

WHEN?
VF/VT, asystole, PEA, bradycardias
 Vasopressin
WHEN?
Alternative to epinephrine for shock-refractory VT/VF
WHY?
Natural antidiuretic hormone
Potent vasoconstrictor by stimulation of SM -V 1 receptors
:
BP & SVR; CO, HR, myocardial O2 consumption and
contractility
Does not myocardial oxygen consumption
Not affected by severe acidosis
Class IIb for shock-refractory VF
Class Indeterminate for PEA, asystole
Half life = 10-20 minutes
Dose?
40 Units IVP - one time only!!!
 Why Vasopressin?
During CPR, plasma ADH levels are higher in patients
with return of spontaneous circulation (ROSC)
During CPR patients may be severely acidotic
Epinephrine compared to vasopressin pre-hospital
CPR (20 patients/study group)
Multiple animal studies showing ROSC

EPI (n=20) VP (n=20)

Survival to hospital35% 70%
(p=0.06)
24 hour survival 20% 60% (p=0.02)
Discharge alive 15% 40%
(p=0.16)
 VFib/Pulseless VT Algorithm
Please Shock-Shock-Shock, EVerybody Shock, And Let's Make
Patients Better
Please - Precordial Thump If pulse-less with no defibrillator
Shock 200J*
Shock 200-300J*
Shock 360J* (*only consecutive, if persistent)
EVerybody - Epinephrine 1 mg IV q3-5 min or Vasopressin 40 U
IVP
If VF/PVT persists, "CONSIDER" antiarrhythmics and sodium bicarb. NOTE:
always "max out" one agent before proceeding to the next in order to limit pro-
arrhythmic drug-drug interactions
Shock 360J
And - Amiodarone (First Choice) 300mg IV push. May repeat once
at 150mg in 3-5 min. (max. cumulative dose: 2.2g IV/24hrs)
Drugs Used for Heart Rhythm and Rate
Amiodarone
WHY?
Class III antiarrhythmic (characteristics of all classes)
Na, K and Ca channel blocker & & -adrenergic
blocker
Prolongs AP and RP
Decreases AV conduction velocity & SN function

New Recommendations (WHEN?):

pulseless VT or VF (IIb)
hemodynamically stable VT (IIb), polymorphic VT
(IIb), wide-complex tachycardia uncertain origin (IIb)
refractory PSVT (preserved function, IIa; impaired
function IIb)
atrial tachycardia (IIb)
cardioversion of AF (IIa)
 Amiodarone
HOW?
Cardiac arrest (PVT/VF) - 300mg IVP diluted
in 20-30ml, may repeat with 150mg in 10
minutes, or start infusion (max=2..2 g/24h)
Atrial & ventricular arrhythmias in
impaired hearts
150mg IVP over 10 min
May repeat q10-15 min, or start gtt 1mg/min x 6
hours, then 0.5mg/min x 18 h
WHAT?
Hypotension, bradycardia (slow rate,
fluids)
 Why Amiodarone?
ARREST Trial

Objective:
Efficacy of IV amiodarone in out-of-
hospital cardiac arrest due to ventricular
fibrillation or pulseless ventricular
tachycardia
Endpoints:
Hospital admission with perfusing rhythm
Survival to discharge
Functional neurologic status at discharge
*Insufficiently powered to detect survival to discharge and
functional neurologic status*
Drugs Used for Heart Rhythm and Rate
Magnesium Sulfate

WHY? Magnesium deficiency causes arrhythmias

Facilitates ventricular repolarization by enhancing
intracellular potassium flux, dilates coronary
arteries

WHEN? Suspected hypomagnesemia, pulseless

VT/VF, torsade de pointes

HOW? Class IIa in suspected hypomagnesemia, TdP,

and Class IIb in VF/VT: 1 - 2gm slow IVP in 100ml

WHAT? Hypotension at large doses

Drugs Used for Heart Rhythm and Rate
Procainamide

WHY?
Suppresses both ventricular and atrial
arrhythmias
Type Ia antiarrhythmic, affects fast
Na+channels-slowing conduction velocity,
prolongs RP, and decreases automaticity
Phase IV depolarization
WHEN?
Refractory/recurrent VF/VT
Control of rapid ventricular response (IIb)
Conversion SVT (AF/Fl) (IIa)
Drugs Used for Heart Rhythm and Rate
Procainamide

HOW? VF: 20-30 mg/min slow infusion (max=17

mg/kg)
AF with rapid vent. response: 100 mg over 5
min then infuse@ 1 - 4 mg/min
1-2 gm/250ml D5W

WHAT? Stop infusion if patient hypotensive, widened

QRS >50%, arrhythmia suppression, or
dose=17mg/kg
Dose reduction in renal failure
SLE syndrome
Levels: PA=4-12 g/ml
NAPA=7-15 g/ml (active metabolite-Class
III)
Drugs Used for Heart Rhythm and Rate
Lidocaine
WHY?
Type IB antiarrhythmic
Affects fast Na+ channels, shortens refractory period
Suppresses spontaneous depolarization
Local anesthetic, increases fibrillation threshold
Suppresses ventricular ectopy post-MI
Without effecting myocardial contractility, BP or AV nodal conduction

WHEN?
SECOND-CHOICE agent
VT/VF refractory to electrical countershock and
epinephrine
(Indeterminate)
Control of PVCs (Indeterminate)
Hemodynamically stable VT (IIb)
Not for routine prophylaxis post-MI, however, accepted in high-
risk patients
(hypokalemia, myocardial ishchemia, LV dysfunction)
Drugs Used for Heart Rhythm and Rate
Lidocaine

HOW? Class IIa: 1 - 1.5 mg/kg IVP q5 - 10 min

(max=3mg/kg)
Infusion (with pulse): 1 - 4 mg/min (if pulse is
regained)
Therapeutic Levels: 1.5-6 g/ml
ET Dose: 2-2.5 times IV dose
Preparation: 1-2 gm/250 ml D5W or NS

WHAT? Hepatic metabolism, renal elimination

Bradycardia, cardiac arrest, seizures
Lidocaine toxicity/neurotoxicity - twitching, LOC,
seizures, coma
Lidocaine levels persist in low CO states
 Drugs Used to Improve Cardiac Output and
Blood Pressure
Sodium Bicarbonate
WHY? Enhances sodium shift intracellularly, buffers acidosis,
decreases toxicity of TCAs, increases clearance of acidic
drugs

WHEN? Class I - hyperkalemia

Class IIa - bicarbonate-responsive acidosis metabolic
acidosis secondary to loss of bicarb (renal/GI);
overdoses (TCAs, phenobarbital, aspirin)
Class IIb - protracted arrest in intubated patients
Class III - hypoxic lactic acidosis

HOW? 1 mEq/kg IVP, 0.5mEq/kg q10 min prn

WHAT? May worsen outcome if not intubated/ventilated.

Metabolic alkalosis, decreased O2 delivery to tissues,
hypokalemia, CNS acidosis, hypernatremia, hyperosmolarity
Incompatible with calcium, epinephrine, atropine, norepinephrine, isoproterenol
 Summary
V.Fib and Pulseless V.Tach
Changes:
Vasopressin added - Class IIb 40 U IVP x 1
Epinephrine - Class Indeterminate 1mg IVP q 3-
5 min
Amiodarone added - Class IIb
300mg IVP (cardiac arrest dose). May repeat 150mg x
1
Lidocaine - Class Indeterminate 1-1.5 mg/kg IVP
q 3-5 min (Max = 3mg/kg)
Procainamide is acceptable but not
recommended due to long administration times
Bretylium fell off algorithm due manufacturing
problems
Terima Kasih