PEMBEKALAN

FARMAKOTERAPI
ROTASI KLINIK
ANESTESI

TIM FARMAKOLOGI
FK UNISSULA
NO DAFTAR PENYAKIT MENURUT LoC
SKDI
OBSTETRI GINEKOLOGI
1 REAKSI ANAFILAKSIS 4A
2 SYOK SEPTIK 3B
3 SYOK HIPOVOLEMIK 3B
4 SYOK KARDIOGENIK 3B
5 SYOK NEUROGENIK 3B
6 CARDIORESPIRATORY ARREST 3B
7 FIBRILASI VENTRIKULAR 3B
8 BENDA ASING 2
 SHOCK SYNDROME
Kumar and Parrillo (1995) The state in which profound and
widespread reduction of effective tissue perfusion leads first
to reversible, and then if prolonged, to irreversible cellular
injury.
Shock is a condition in which the cardiovascular system fails
to perfuse tissues adequately.
An impaired cardiac pump, circulatory system, and/or
volume can lead to compromised blood flow to tissues.
Inadequate tissue perfusion can result in :
generalized cellular hypoxia (starvation)
widespread impairment of cellular metabolism
tissue damage organ failure
death
 PATHOPHYSIOLOGY
Cells switch from aerobic to anaerobic metabolism

lactic acid production

Cell function ceases & swells

membrane becomes more permeable

electrolytes & fluids seep in & out of cell

Na+/K+ pump impaired

mitochondria damage

cell death
 COMPENSATORY MECHANISMS

Sympathetic Nervous System (SNS)-Adrenal

Response
1. SNS - Neurohormonal response, stimulated by
baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (SVR-Afterload)
Increased Preload
 COMPENSATORY MECHANISMS

2. SNS Hormonal : Renin-angiotension system

Decrease renal perfusion
Releases renin angiotension I
angiotension II potent vasoconstriction
& releases aldosterone adrenal cortex
sodium & water retention
 COMPENSATORY MECHANISMS

3. SNS Hormonal : Antidiuretic Hormone

Osmoreceptors in hypothalamus
stimulated
ADH released by Posterior pituitary gland
Vasopressor effect to increase BP
Acts on renal tubules to retain water
 COMPENSATORY MECHANISMS

4. SNS Hormonal : Adrenal Cortex

Anterior pituitary releases
adrenocorticotropic hormone (ACTH)
Stimulates adrenal Cx to release
glucorticoids
Blood sugar increases to meet increased
metabolic needs
 FAILURE OF COMPENSATORY
RESPONSE
Decreased blood flow to the tissues causes
cellular hypoxia
Anaerobic metabolism begins
Cell swelling, mitochondrial disruption, and
eventual cell death
If Low Perfusion States persists : IRREVERSIBLE
DEATH IMMINENT
 STAGES OF SHOCK
1. Initial stage - tissues are under perfused, decreased
CO, increased anaerobic metabolism, lactic acid is
building.
2. Compensatory stage - Reversible. SNS activated by
low CO, attempting to compensate for the decrease
tissue perfusion.
3. Progressive stage - Failing compensatory mechanisms
: profound vasoconstriction from the SNS
ISCHEMIA. Lactic acid production is high metabolic
acidosis. Irreversible or refractory stage - Cellular
necrosis and Multiple Organ Dysfunction Syndrome
may occur DEATH IS IMMINENT!!!!
 NET RESULTS OF CELLULAR SHOCK
1. Systemic lactic acidosis
2. Decreased myocardial contractility
3. Decreased vascular tone
4. Decrease blood pressure, preload, and cardiac
output
 SHOCK : CLASSIFICATION
1. Hypovolemic shock - due to decreased circulating
blood volume in relation to the total vascular
capacity and characterized by a reduction of diastolic
filling pressures.
2. Cardiogenic shock - due to cardiac pump failure
related to loss of myocardial contractility/functional
myocardium or structural/mechanical failure of the
cardiac anatomy and characterized by elevations of
diastolic filling pressures and volumes.
 SHOCK : CLASSIFICATION
3. Extra-cardiac obstructive shock - due to obstruction
to flow in the cardiovascular circuit and
characterized by either impairment of diastolic filling
or excessive afterload.
4. Distributive shock - caused by loss of vasomotor
control resulting in arteriolar/venular dilatation and
characterized (after fluid resuscitation) by increased
cardiac output and decreased SVR.
Classification of Circulatory Shock
A. HYPOVOLEMIC SHOCK
1. Hemorrhagic
Trauma
Gastrointestinal
Retroperitoneal
2. Fluid depletion (nonhemorrhagic)
External fluid loss
Dehydration
Vomiting
Diarrhea
Polyuria
Classification of Circulatory Shock
Interstitial fluid redistribution
Thermal injury
Trauma
Anaphylaxis
3. Increased vascular capacitance (venodilatation)
Sepsis
Anaphylaxis
T oxins / drugs
Classification of Circulatory Shock
B. CARDIOGENIC SHOCK
1. Myopathic
Myocardial infarction (hibernating myocardium)
Left ventricle
2. Right ventricle
3. Blunt Cardiac Injury (trauma)
4. Myocarditis
5. Cardiomyopathy
6. Post-ischemic myocardial stunning
7. Septic myocardial depression
Classification of Circulatory Shock
8. Pharmacologic
Anthracycline cardiotoxicity
Calcium channel blocker
9. Mechanical
Valvular failure (stenotic or regurgitant)
Hypertropic cardiomyopathy
Ventricular septal defect
10. Arrhythmic
Bradycardia
Classification of Circulatory Shock
C. EXTRACARDIAC OBSTRUCTIVE
1. Impaired diastolic filling (decreased ventricular
preload)
Direct venous obstruction (vena cava)
Intrathoracic obstructive tumors
Increased intrathoracic pressure
Tension pneumothorax
Mechanical ventilation (with excessive pressure
or volume depletion)
Asthma
Classification of Circulatory Shock
Decreased cardiac compliance
Constrictive pericarditis
Cardiac tamponade
2. Impaired systolic contraction (increased ventricular
afterload)
Right ventricle
Pulmonary embolus (massive)
Acute pulmonary hypertension
Left ventricle
Embolus
Aortic dissection
 Classification of Circulatory Shock
D. DISTRIBUTIVE SHOCK
1. Septic (bacterial, fungal, viral, rickettsial)
2. Toxic shock syndrome
3. Anaphylactic, anaphylactoid
4. Neurogenic (spinal shock)
5. Endocrinologic
Adrenal crisis
Thyroid storm
6. Toxic (e.g., nitroprusside, bretylium)
 PATHOPHYSIOLOGY OF
HYPOVOLEMIC SHOCK
Decreased intravascular volume leads to :
Decreased venous return
Decreased ventricular filling
Decreased stroke volume
Decreased CO
Inadequate tissue perfusion!!!!
 PATHOPHYSIOLOGY OF
CARDIOGENIC SHOCK
1. Impaired pumping ability of LV leads to :
Decreased stroke volume
Decreased CO
Decreased BP
Compensatory mechanism
Decreased tissue perfusion
2. Impaired pumping ability of LV leads to :
Inadequate systolic emptying
Left ventricular filling pressures (preload)
Left atrial pressures
Pulmonary capillary pressure
Pulmonary interstitial & intraalveolar edema !!!!
 PATHOPHYSIOLOGY OF
DISTRIBUTIVE SHOCK

Distributive shock = vasogenic shock

Defining feature : loss of peripheral resistance
Dominantly septic shock, anaphylactic and neurogenic
shock less common
 PATHOPHYSIOLOGY OF
DISTRIBUTIVE SHOCK
1. Anaphylactic shock :
Immediate hypersensitivity reaction mediated by the
interaction of IgE on mast cells and basophils with the
appropriate antigen resulting in mediator cascade.
Anaphylactoid reactions involve similar release of
mediators via non-immunologic mechanisms.
Primary mediators include histamine, serotonin,
eosinophil chemotactic factor, and proteolytic
enzymes.
Secondary mediators include PAF, bradykinin,
prostaglandins, and leukotrienes.
 Pathophysiology Anaphylactic Shock
Antigen exposure body stimulated to produce IgE
antibodies specific to antigen : drugs, bites,
contrast, blood, foods, vaccines
Reexposure to antigen : IgE binds to mast cells
and basophils Anaphylactic response
 PATHOPHYSIOLOGY OF
DISTRIBUTIVE SHOCK
2. Septic Shock
Syndrome of profound hypotension due to release
of endotoxins / TNF / vasoactive peptides following
bacterial destruction
Usually associated with normal blood volume, high /
low CO, and low SVR
Re-distribution of blood to splanchnic vessels, with
resultant poor skin perfusion
 PATHOPHYSIOLOGY OF
DISTRIBUTIVE SHOCK
2. Septic Shock
Sepsis is considered present if an infection is
suspected or proven and 2 or more of the following
criteria are met : tachycardia (>90x/min), tachypnea
(>20x/min), fever (>38,3oC) or temperature
<35,6oC, leucocytosis (>12.000/mm3) or leucopenia
(<4000/mm3). Severe sepsis is defined as sepsis
associated with organ dysfunction, hypoperfusion,
or hypotension. Septic shock is diagnosed when
hypotension persist despite adequate fluid
resuscitation or when perfusion abnormalities occur.
 Pathophysiology of Septic Shock :
Initiated by gram-negative (most common) or gram
positive bacteria, fungi, or viruses

Cell walls of organisms contain Endotoxins

Endotoxins release inflammatory mediators (systemic
inflammatory response)

Vasodilation & increase capillary permeability

Shock due to alteration in peripheral circulation &
massive dilation
 PATHOPHYSIOLOGY OF
DISTRIBUTIVE SHOCK
3. Neurogenic Shock
A type of distributive shock that results from the
lossor suppression of sympathetic tone
Causes massive vasodilatation in the venous
vasculature, venous return to heart, cardiac output.
Most common etiology : Spinal cord injury above T6
Neurogenic is the rarest form of shock!
 Pathophysiology of Neurogenic Shock :

Distruption of sympathetic nervous system

Loss of sympathetic tone

Venous and arterial vasodilation

Decreased venous return

Decreased stroke volume

Decreased cardiac output

Decreased cellular oxygen supply

Impaired tissue perfusion

Impaired cellular metabolism
 MANAGEMENT

USE THE ABCDE APPROACH TO RECOGNISE :

AIRWAY PROBLEMS
BREATHING PROBLEMS
CIRCULATION PROBLEMS
DISABILITY PROBLEMS
EXPOSURE PROBLEMS
 THERAPY OF HYPOVOLEMIC SHOCK
Airway / breathing / C-spine control
Stop all obvious haemorrhage
Insert I.v. lines, take blood for X-match
Give rapid bolus of fluid, then assess
response
Decide on need for surgery vs. decision to
investigate
 THERAPY OF CARDIOGENIC SHOCK
Limiting/reducing myocardial damage during Myocardial Infarction :
1. Increased pumping action & decrease workload of the heart
Inotropic agents
Vasoactive drugs
Intra-aortic balloon pump
Cautious administration of fluids
Transplantation
2. Consider thrombolytics, angioplasty in specific cases
3. Optimizing pump function : aggresive airway management,
judicious fluid management, vasoactive agents, morphine as
needed, vasodilators as needed for afterload reduction, short
acting beta blocker, esmolol, for refractory tachycardia
THERAPY OF ANAPHYLAXIS SHOCK
 THERAPY OF SEPTIC SHOCK
Find and kill the source of the infection broad spectrum
antibiotics urgently. Intravenous antibiotic therapy should be
initiated within the first six hours after obtaining appropiate
cultures. When the potential pathogen or infection source is
not immediately obvious, we favor broad-spectrum antibiotic
coverage directed against both gram-positive and gram-
negative bacteria.
A judicious choice of antimicrobial therapy should be based
on the host characteristics, the site of infection, the local
ecology and the pharmacokinetics and pharmacodynamics of
the antibiotics.
In practise, if Pseudomonas is an unlikely pathogen :
combining vancomycin with one of the following :
 THERAPY OF SEPTIC SHOCK
Cephalosporin 3rd generation (ceftriaxone or cefotaxime),
4th generation (cefepime)
Beta-lactam / beta lactamase inhibitor (piperacillin-
tazobactam)
Carbapenem (imipenem or meropenem)
If Pseudomonas is a possible pathogen : combining vancomycin
with two of the following :
Antipseudomonalcephalosporin (ceftaidime, cefepime)
Antipseudomonal carbapenem (imipenem, meropenem)
Antipseudomonal beta-lactam (piperacillin-tazobactam)
Fluoroquinolone with good anti-pseudomonal activity
(ciprofloxacin)
 THERAPY OF SEPTIC SHOCK

Aminogylcoside (gentamicin, amikacin)

Monobactam (aztreonam)
Fluid Resuscitation
Maximize O2 delivery support
Vasoconstrictors
Inotropic drugs
THERAPY OF NEUROGENIC SHOCK

Alpha agonist to augment tone if perfusion still

inadequate
Dopamine at alpha doses (> 10 mcg/kg per min)
Ephedrine (12.5-25 mg IV every 3-4 hour)
Treat bradycardia with atropine 0.5-1 mg doses to
maximum 3 mg
May need transcutaneous or transvenous pacing
temporarily
 CARDIORESPIRATORY ARREST
The cessation of cardiac mechanical activity, as
confirmed by the absence of signs of circulation.
Drug treatment :
1. Vasopressor
Epinephrine iv/io dose : 1 mg every 3 5 minutes.
Vasopressin iv / io dose : 40 units can replace
epinephrine.
2. Antiarrhytmic agent
Amiodarone iv/io : first dose : 300 mg bolus,
second dose : 150 mg bolus.
If it is unavailable, lidocaine may be considered,
dose : 1 1,5 mg/kg iv bolus.
 PHARMACOTHERAPY OF
EMERGENCY DRUGS :
INOTROPIC, VASOACTIVE,
ANTIARRHYTMIC AGENTS
 1. ADRENALINE / EPINEPHRINE

An endogenous catecholamine high affinity for 1-

, 2- & 1-adrenergic receptors present in cardiac
and vascular smooth muscle, with effects being
more pronounced at low doses and 1 effects at
higher doses. The net effect of administration is an
increase in arterial & venous pulmonary pressures.
Epinephrine increases coronary blood flow by
increasing the relative duration of diastole at higher
heart rates & stimulating myocytes to release local
vasodilators.
 1. ADRENALINE / EPINEPHRINE
The doses of epinephrine in clinical use are similar to
those of norepinephrine. In septic shock, international
guidelines recommend the combination of
dobutamine + norepinephrine over epinephrine.
The most important drug for the treatment of an
anaphylactic reaction logical treatment.
Alpha-receptor agonist reverses peripheral
vasodilation and reduces oedema.
Beta-receptor activity dilates the bronchial airways,
increases the force of myocardial contraction, and
suppresses histamine and leukotriene release.
 1. ADRENALINE / EPINEPHRINE

Beta-2 adrenergic receptors on mast cells inhibit

activation.
Adrenaline attenuates the severity of IgE-mediated
allergic reactions.
A vasopressor can be given as soon as feasible with
the primary goal of increasing myocardial and
cerebral blood flow during CPR and achieving ROSC.
Preparate : inj 1 mg/mL.
 THE RISK OF ADRENALINE
Adrenaline is not without risk, particularly when given
intravenously.
Adverse effects are extremely rare with correct doses
injected intramuscularly (IM). Sometimes there has
been uncertainty about whether complications (e.g.,
myocardial ischaemia) have been caused by the
allergen itself or by the adrenaline given to treat it.
Prolonged administration at high doses can cause
myocyte apoptosis and damage the arterial walls,
causing focal regions of myocardial contraction band
necrosis not unlike MI in appearance.
Adrenaline 1 mg amp No. I
Spuit disposible 3cc No. I
S imm
 2. DOPAMINE
As an endogenous central neurotransmitter and immediate
precursor to norepinephrine, dopamine acts on
dopaminergic as well as adrenergic receptors, eliciting a
variety of dose-dependent effects. At low doses up to 3
g/kg/min, it stimulates dopaminergic D1 postsynaptic
receptors concentrated in the coronary, renal, mesenteric,
and cerebral beds, as well as D2 presynaptic receptors
present in the vasculature and renal tissues, causing
vasodilation and increasing blood flow to these tissues. At
doses between 3 and 10 g/kg/min, dopamine increases
cardiac contractility and chronotropy by means of a mild
effect on 1-adrenergic receptors, resulting in a release of
norepinephrine and reduction of reuptake in presynaptic
sympathetic nerve terminals.
 2. DOPAMINE
A mild peripheral vasoconstrictive effect is also observed
that, due to an effect on 1-adrenergic receptors,
becomes pronounced and predominant at infusion rates
beyond 10 g/kg/min.
Dopamine is recommended as the first-line
inotropic/vasopressor agent to be administered in true
hypotensive cardiogenic shock. The infusion should
begin at 5 g/kg/min and be rapidly up-titrated to
achieve the desired effect on blood pressure. Doses
beyond 12.515.0 g/kg/min should be avoided and
second-line inotropic/vasopressor therapy should be
initiated in case of inadequate response to dopamine.
 2. DOPAMINE

Dopamine receptor activation at low doses

splanchnic dilation (2-5 mcg/kg/min).
Beta receptor activation-increase cardiac output (5-
10 mcg/kg/min).
Alpha receptor activation-vasoconstriction (>10
mcg/kg/min).
Preparate : inj 20 mg/mL, 40 mg/mL.
Dopamine 200 mg amp No. I
Aquabidestilata steril 50 cc No. I
Spuit disposible 50cc No. I
S imm
 3. DOBUTAMINE

Acting via stimulation of 1 and 2 receptors,

dobutamine is the inotropic agent of reference, but has
limited effect on increasing arterial pressure. Quite to
the contrary, the -adrenergic effects of dobutamine
cause peripheral vasodilation, although the vasodilating
effects observed are usually smaller than those observed
with some alternative inotropic drugs. While the
decrease in afterload can further increase cardiac output,
a decrease in arterial blood pressure can result in
myocardial ischemia by reducing coronary perfusion
pressure.
 3. DOBUTAMINE
Dobutamine is the preferred inotropic agent for the acute
management of low output states due to systolic heart
failure. Because dobutamine does not usually raise the
arterial blood pressure, it is not indicated as monotherapy in
patients with cardiogenic shock.
Primarily a -1 receptor agonist (cardiac stimulation), but it
also has mild -2 effects (vasodilation).
Causes a dose-dependent increase in stroke volume.
Decrease in cardiac filling pressures.
Dose : 2-20 mcg/kg/min.
Preparate : inj 25 mg/mL, inj 50 mg/mL, inj 12,5 mg/mL
Dobutamine 250 mg amp No. I
Aquabidestilata steril 50 cc No. I
Spuit disposible 50 cc No. I
S imm
 4. NOREPINEPHRINE
Norepinephrine is the major endogenous neurotransmitter
released by postganglionic adrenergic nerves. It behaves
primarily as a vasoconstrictor but also as a mild inotrope,
due to its effect on 1-adrenergic receptors and to a lesser
extent on -receptors. -receptor agonist that promotes
widespread vasoconstriction.
Its major effect is to increase systolic, diastolic, and pulse
pressure, while its effect on cardiac output is negligible. As a
result of the elevated diastolic pressure and an indirect
effect on cardiac myocytes to release local vasodilators,
coronary flow is also increased. At least in the setting of
septic shock, it has a more favorable effect on splanchnic
circulation than epinephrine and may even exert a more
favorable action in this regard than dopamine.
 4. NOREPINEPHRINE
Whether it is utilized as a second-line agent to stabilize
patients in cardiogenic shock, as recommended by the
AHA/ACC guidelines, or as first-line therapy, norepinephrine
is administered as an infusion ranging from 0.01 to 3.0
g/kg/min. The median dose administered in patients with
persistent shock despite an open infarct artery and
vasopressor support in the Tilarginine Acetate Injection in a
Randomized International Study in Unstable MI Patients
With Cardiogenic Shock (TRIUMPH) was 0.2 g/kg/min.
Administration of any vasoconstrictor agent carries a risk of
hypoperfusion and ischemia involving any tissue bed or
vital organ.
Preparate : inj 1 mg/mL.
Norepinephrine 4 mg amp No. I
Aquabidestilata steril 50 cc No. I
Spuit disposible 50 cc No. I
S imm
 Rumus perhitungan dosis syringe pump :
1. Tentukan dosis obat
2. Tentukan sediaan obat yaitu 1 ampul mengandung
(..... mg dalam ...... mL).
3. Pengenceran menjadi 50 mL.
4. Flow syringe pump =
(dosis x bb x 60) : pengenceran = ...... mL/jam

Rumus perhitungan dosis mikro drip :

1. Tentukan dosis obat
2. Tentukan sediaan obat yaitu 1 ampul mengandung
(..... mg dalam ...... mL).
3. Pengenceran menjadi 100 mL.
4. Flow syringe pump =
(dosis x bb x 60) : pengenceran = ...... Tts (mikro)/mnt
 5. ANTIARRHYTMIC AGENT
1. Amiodarone
Amiodarone is the first-line AAA given during
cardiac arrest because it has been clinically
demonstrated to improve the rate of ROSC and
hospital admission in adults with refractory
VF/pulseless VT. Preparate : inj 150 mg/3 mL.
2. Lidocaine
Preparate : inj 100 mg vial, 40 mg/2 mL.
Amiodarone 150 mg amp No. I
Spuit disposible 20 cc No. I
S imm
OTHER DRUGS
 ANTIHISTAMINES
Antihistamines are a second line treatment for
anaphylaxis reaction.
Antihistamines (H1) may help counter histamine-
mediated vasodilation and bronchoconstriction.
Diphenhydramine : competitive pharmacologic block
of peripheral and CNS H1 receptors plus - and M-
receptor block. Anti-motion sickness effect.
Preparate : Diphenhydramine inj 10 mg/mL.
Dose : Adult : 50 mg iv or im every 6 h
Children : 5 mg/kgBB
Diphenhydramine 150mg vial No. I
Spuit disposible 5 cc No. I
Needle disposible no. 23 No. I
S imm
 STEROIDS

Corticosteroids may help prevent or shorten

protracted reactions. In asthma, early corticosteroid
treatment is beneficial in adults and children.
Mechanism of action : corticosteroids reduce the
synthesis of arachidonic acid by phospholipase A2 and
inhibit the expression of COX-2, the inducible form of
cyclooxygenase. Corticosteroids increase the respon-
siveness of adrenoceptors in the airway and they
probably act by other mechanisms as well.
 STEROIDS
Glucocorticoids bind to intracellular receptors and
activate glucocorticoid response elements (GREs) in
the nucleus, resulting in synthesis of substances that
prevent the full expression of inflammation and
allergy.
Inject hydrocortisone slowly intravenously or
intramuscularly, taking care to avoid inducing further
hypotension.
Preparate :
Dexamethasone : inj 5 mg/mL
Methyl prednisolone : inj 125 mg/2 mL
Hydrocortisone : inj 100 mg/vial
Dexamethasone 5 mg amp No. I
Spuit disposible 3 cc No. I
S imm
 BRONCHODILATORS
1. Salbutamol (inhaled or IV)
Mechanism of action : reverse asthmatic
bronchoconstriction are the direct-acting 2-
selective agonists. Beta-adrenoceptor agonists
stimulate adenylyl cyclase (via the 2-adrenoceptor
Gs-coupling protein-adenyl cyclase pathway) and
increase cyclic adenosine monophosphate (cAMP) in
smooth muscle cells. The increase in cAMP results in
a powerful bronchodilator response.
Indikasi : bronkospasme yang menetap yang tidak
dapat diatasi dengan adrenalin.
Preparat : inj 50 mcg/mL.
inhalasi nebules vial 2,5 mg.
Salbutamol nebule 2,5 mg amp No. I
Adult nebulizer mask No. I
S imm
 BRONCHODILATORS
2. Ipratropium (inhaled)
Mechanism of action : ipratropium and tiotropium
competitively block muscarinic receptors in the
airways and effectively prevent
bronchoconstriction mediated by vagal discharge.
Muscarinic antagonists reverse bronchoconstriction
in some asthma patients (especially children) and
in many patients with COPD.
Preparat : inhalasi (kombinasi ipratropium bromida
0,5 mg + salbutamol 2,5 mg).
Combivent nebule amp No. I
Adult nebulizer mask No. I
S imm
 BRONCHODILATORS
3. Aminophylline (IV)
Menghambat kerja enzim fosfodiesterase sehingga
menghambat pemecahan cAMP menjadi 5-AMP
yang tidak aktif.
Loading dose 4 5 mg/kgbb diencerkan dgn NaCl
0,9% dan diberikan perlahan lahan dalam waktu
10 menit.
Dosis rumatan : 0,7 0,9 mg/kgbb/jam atau 5 6
mg/kgbb/8 jam.
Preparate : inj 24 mg/mL.
Aminophylline 240 mg amp No. I
Spuit disposible 20 cc No. I
S imm
 ATROPINE SULFAT
Atropine sulfate reverses cholinergic-mediated decrease heart
rate and atrioventricular nodal conduction.
Atropine is no longer recommended for routine use in the
management of PEA / asystole & has been removed from the
cardiac arrest algorithm.
Atropine is indicated for bradychardia.
Pada bradikardi diberikan 0,5 1 mg iv setiap 3 5 menit
sesuai kebutuhan tidak melebihi 0,04 mg/kgbb. Penggunaan
dengan interval jangka pendek (3 menit) dan dosis yang lebih
tinggi (0,04 mg/kgbb) diberikan pada kondisi klinis yang berat.
Pemberian melalui trakea dengan dosis 2 3 x dosis iv
diencerkan dalam 10 ml saline normal.
Preparate : inj 0,25 mg/mL
Sulfas atropin 0,25 mg amp No. I
Spuit disposible 3 cc No. I
S imm
FLUID RESUSCITATION
 Therapy : Resuscitation Fluids

Correct hypotension first (golden hour)

Decrease heart rate
Correct hypoperfusion abnormalities
Monitor for deterioration of oxygenation
Crystalloid vs colloid
20 mL/kg fluid challenge in hypovolemic or septic
shock with re-challenges of 5 - 10 mL/kg
100 - 200 mL challenges in cardiogenic
 Insert large-bore iv cannulae use short, wide-bore
cannulae highest flow. Intra osseous access in
children when iv access is difficult.
Give a rapid fluid challenge : Adults - 500 mL of
warmed crystalloid solution (Hartmanns or 0.9%
saline) if the patient is normotensive or 1000 mL if
the patient is hypotensive. Patients with cardiac
failure smaller volumes (250 mL and use closer
monitoring (listen to the chest for crepitations after
each bolus). For children give 20 mL/kg of warmed
crystalloid.
Reassess the pulse rate and BP regularly (every 5
min), aiming for the patients normal BP.
Fluid Composition
1. Normal Saline
154 meq sodium
154 meq chloride
308 mOsm
pH 5.6
2. Lactated Ringers
130 meq sodium
109 meq chloride
4 meq potassium
3 meq calcium
28 meq lactate
273 mOsms
pH 6.6
Cant use LR while infusing blood!
Ringer lactate inf 500 cc flab No. I
Abbocath no. 18 No. I
Cum infus set No. I
S imm
 TERIMA KASIH
SELAMAT BELAJAR
 REFERENCES
1. American Heart Association : Cardiogenic Shock.
2. European Journal of Anaesthesiology : Antibiotic
therapy in patients with septic shock.
3. Evaluation and management of severe sepsis and septic
shock in adults.
4. Shock : types, recognition and therapy.
5. Society of Critical Care Medicine Shock :
Pathophysiology, Classification, and Approach to
Management.
6. The Nebraska Medical Center : Sepsis : Empiric
Antibiotic Selection Pathway.