FARMAKOLOGI :

MEDICAMENTOSA / OBAT-2AN
 JANTUNG & HEMODINAMIK

• SULANTO SALEH-DANU R.,

• BAGIAN FARMAKOLOGI & TERAPI
• FAKULTAS KEDOKTERAN - UGM.
• BAGIAN FARMAKOLOGI
• FAKULTAS KEDOKTERAN – UKDW.
KOMPONEN JANTUNG :
 OTOT / MUSCLE :
MYOCARDIUM;
 SYSTEM KONDUKSI IMPULS
(sifat OTONOM);
 VASA : ARTERIA DAN VENA.
THE HEART
-DISTRIBUTION :
OXYGEN, NUTRIENT,
WATER, ELEKTROLIT, HEART PUMPING : OXYGEN and
MUSCLE NUTRIEN to whole organ
VITAMIN, HORMON,
and tissues
MEDICINES etc, etc.
to the organ and tissues.

CARDIOVASCULAR VESSELS
‘ROAD’ / pipe for distribution
-CARRYING and
Oxygen and Nutrient to all
-TRANSPORTING : Carbon
organs and tissues
dioxyde; metabolism
production, metabolism
residual BLOOD CARRYING MATERIAL-
- CONTRIBUTOR : immune sys NUTRIENT to the body
- TERMOREGULATION & “GARBAGES” from
the body to out side .

4
 As a PUMP: pumping the blood
HEART to whole body
Blood vessels : limited capacity

ELECTRICAL CONDUCTION SYST.:

to maintain the heart rate
and rhythm

HEART MUSCLE (MYOCARDIUM) :

need OXYGEN and other “food”
for the activity

Control & Coordintion :

AUTONOMIC NERVOUS
SYSTEM
5
KELAINAN AKTIFITAS GEJALA /
JANTUNG FISIK SIMPTOM
FATIQUE
DYSPNEU
CHEST PAIN
OEDEMA, dll
NEW YORKHEART ASSOCIATION ( NYHA ) :
CLASS I : TIDAK ADA PEMBATASAN AKTIFITAS
FISIK; PADA AKTIFITAS FISIK RUTIN
TIDAK ADA GEJALA !
CLASS II : AKTIFITAS RUTINE TIMBUL GEJALA
RINGAN, TIDAK MEMBERATKAN.
CLASS III : AKTIFITAS FISIK TIMBUL GEJALA/SIMPTOM
YANG NYATA; TETAPI UTUK ISTIRAHAT
SIMPTOM MEREDA.
CLASS IV : TANPA AKTIFITAS (ISTIRAHAT) GEJALA
SIMPTOM SUDAH TAMPAK
( CLASS V : TIDAK ADA KAITAN / ATYPICAL )
KELAINAN PADA JANTUNG dapat terjadi :
OTOT (MYOCARDIUM) :
GAGAL JANTUNG; MYOCARDITIS; NEOPLASMA dll

VASKULARISASI JANTUNG :
AMI; ANGINA PECTORIS; dll

KONDUKSI IMPULS  GANGGAUN IRAMA dan

FREKWENSI KONTRAKSI JANTUNG :
BRADYCARDI; TACHYCARDI; ARYTHMIA dll
 CORONARY HEART DISEASES :
KELAINAN (ATHEROSCLEROTIC CAD;
JANTUNG ISCHEMIC HEART DISEASES)
 CHRONIC STABLE ANGINA PECTORIS
 CORONARY VASOSPASM & ANGINA
with NORMAL CORONARY ARTERIO-
CONGENITAL :
GRAMS
-STENOSIS PIULMONARIS
 ACUTE CORONARY SYNDROMES
-COARTACTION AORTA
without ST-SEGMENT ELEVATION.
-ATRIAL SEPTAL DEFECT
 ACUTE MYOCARDIAL INFARCTION
-SEPTATAL/FORAMEN OVALE
with ST-SEGMENT ELEVATION
-VENTRICULAR SEOTAL DEFECT
-TETRALOGI FALLOT
-PATENT DUCTUS AETERIOSUS VALVULAR HEART DISEASES :
MITRAL STENOSIS
MITRAL REGURGITATION
CONGESTIVE HEART FAILURE AORTA STENOSIS
(DECOMPENSASIO CORDIS) AORTA REGURGITATION
 ACUTE HEART FAILURE & TRICUSPIDAL STENOSIS
PULMONARY EDEMA TRICUSPIDAL REGURGITATION
OULMONIC REGURGITATION
PROLAPS : MITRAL VALVE
DISTURBANCE OF RATE & RHYTHM :
-ATRIAL PREMATURE BEATS MYOCARDITIS &
(Atrial Extrasystole)
-PAROXYSMAL SUPRAVENTRICULAR
THE CARDIOMYOPATHIES :
INFECTIOUS MYOCARDITIS
TACHYCARDIA
DRUG INDUCED & TOXIC
-SUPRAVENTRICULAR TACHYCARDIAS
MYOCARDITIS
(Preexcitation Syndromes)
DILATED CARDIOMYOPATHY
-ATRIAL FIBRILLATION
TAKO-TSUBO CARDIOMYOPATHY
-ATRIAL FLUTTER
HYPERTROPHIC CARDIO-
-MULTIFOCAL(Chaotic) ATRIAL TACHYCARDIA
MYOPAHTY
-AV JUNCTIONAL RHYTHM
RESTRICTIVE CARDIOMYOPATHY
-VENTRICULAR PREMATURE BEAT
(Ventricular Extrasystoles)
-VENTRICULAR TACHYCARDIA

MISCELLANEOUS DISORDERS OF THE HEART:

ACUTE RHEUMATIC FEVER & RHEUMATIC HEART DISEASES.
DISEASES OF PERICARDIUM : Acute Inflammatory Percarditis;
Pericardial Effusion & Tamponade; Constrictive Percarditis
PULMONARY HYPERTENSION & PULMONARY HEART DISEASES
NEOPLASTIC DISEASES OF THE HEART
 HEART DISEASES

 CONGESTIVE HEART FAILURE

or DECOMPENSATIO CORDIS;

ANGINA PECTORIS
( CHEST-PAIN 
ACUTE MYOCARDIAC INFARCTION);

 CARDIAC ARRHYTMIAS.

10
CONGESTIVE HEART FAILURE
(CHF)

DECOMPENSATIO CORDIS

GAGAL JANTUNG

13
CONGESTIVE HEART FAILURE /
DECOMPENSATIO CORDIS /
GAGAL JANTUNG
Left Ventricle FAILURE :
exertional dyspnea; cugh; fatigue; orthopnea;
paroxysmal nocturnal dyspnea; cardiac enlargement;
rales; gallop rhythm; and pulmonary venous congestion

Right Ventricle FAILURE :

elevated venous pressure; hepatomgaly; dependent
edema; usually due to LV Failure.
CONGESTIVE HEART FAILURE /
DECOMPENSATIO CORDIS /
GAGAL JANTUNG

Cardiac output is inadequate to provide

the oxygen needed by the body

SYSTOLIC FAILURE : the mechanical pumping

(contractility) and the ejection fraction of the reduced.

DIASTOLIC FAILURE : stiffening and loss of

adequate relaxation plays a mayor role
reducing the cardiac output .
15
CONGESTIVE HEART FAILURE
(CHF)/
DECOMPENSATIO CORDIS /
GAGAL JANTUNG

CONGESTIVE / CHRONIC
Increased exertion
Emotion
Salt in diet
Noncompliance
etc.

ACUTE H F/PULMONARY EDEMA

16
STRATEGY CHF

1. CORRECTION THE REVERSIBLE CAUSES;

2. INCREASING MYOCARDIAC CONTRACTILITY;

3. REDUCING CARDIAC PRELOAD

(blood volume filling heart ventricle
during diastolic phase);

4. REDUCING CARDIAC AFTERLOAD

( pressure needed for pumping the blood
to the circulation systems ;
Systolic phase)

NON-PHARMACOTHERAPY

PHARMACOTHERAPY
17
TREATMENT OF CHRONIC H F :

1. Reduce workload of the heart

a. Limit activity, put on bed rest
b. Reduce body weight
c. Control hypertension
2. Restrict sodium intake
3. Restrict water
4. Give diuretic
5. Give ACE inhibitor or ARB
6. Give digitalis
(if systokic dysfunction with 3rd heart soundor
atrial fibrillation present)
7. Give β-blocker
(to patients with stable class II-IV HF)
8. Give vasodilators
9. Cardiac resynchronization if
wide QRS interval is present in normal sinus
rhythm.
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PHARMACOTHERAPY

 DIURETICS
 ALDOSTERONE RECEPTOR ANTAGONIST
 ACE – inhibitors
 ANGIOTENSIN RECEPTOR BLOCKERS
 BETA – blockers
 CARDIAC GLYCOSIDES / CARDIOTONIC
 VASODILATORS
 BETA AGONISTS, dopamine
 BIPYRIDINES
 NATRIURETIC PEPTIDE
(Katzung,BG et al., 2007)

19
 MECHANISM and SITE OF ACTION
DRUGS USE IN CONGESTIVE HEART FAILURE

1. DIGOXIN (an alkaloid GLYCOSIDE / CARDIOTONIC)

 increase myocardium contractility by increasing calcium penetration to
myocardium
DOBUTAMINE ( SYMPATHOMIMETIC Group )
 increase myocardium contractility by increasing production cAMP in
bounding β1 -receptor.

2. DIURETICs Group;
 reducing afterload by reducing blood volume ( increase of urine excretion )

3. Angiotensin Converting Enzym (ACE) – Inhibitors / ARBs:

CAPTOPRIL; CANDESARTAN; dll.
 the effect dilatation peripheral blood vessels  cause decreasing
afterload

4. HYDRALAZINE  relaxation of arteriole  decreasing afterload

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HAL-HAL YANG PERLU DIPERHATIKAN PADA
PENDERITA GAGAL JANTUNG:

1. INTERAKSI DIGOKSIN dengan

- CALCIUM  POTENSIASI DIGOKSIN.
- QUINIDIN ( golongan ANTIARITMIA CORDIS )  kadar DIGOKSIN
meningkat ( ikatan dengan protein )

2. MAKANAN / NUTRISI : JANGAN diberikan yang memperberat

kerja jantung atau yang BERINTERAKSI dengan OBAT-OBAT yang
digunakan.

3. Untuk DIGOKSIN, salah satu sifat obat ini di akumulasi ditubuh, cara
pemakaian harus memperhatikan besar obat yang diekresikan dalam
24 jam. Waktu paruh panjang ( 40 - >160 jam ).
21
ANGINA PECTORIS/
CHEST PAIN /
NYERI DADA

22
 DRUGS USED IN THE TREATMENT
OF ANGINA PECTORIS.

 angina pectoris refers to a strangling or pressure-like pain

caused by cardiac ischemia.
The pain is usually located sub sternally but sometimes
perceived in the neck, shoulder, or epigastrium.

 ATHEROSCLEROTIC ANGINA
Type of ANGINA = CLASSIC ANGINA
= ANGINA OF EFFORT

 VASOSPASTIC ANGINA
= REST ANGINA
= VARIANT ANGINA
 UNSTABLE ANGINA = PRINZMETAL’S ANGINA
= CRESCENDO ANGINA
= ACUTE CORONARY SYNDROME
23
ANGINA PECTORIS
impairment oxygenation of the heart muscle

Imbalancing the supply to the need of oxygen

of the heart muscles (myocardium)

CHEST PAIN (left side) and/or

DYSPNEA,
EPIGASTRIC PAIN
24
25
... major determinant of coronary insufficiency :
myocardial fiber tension ( the higher the tension,
the greater the oxygen requirement ).................

MYOCARDIAL OXYGEN REQUIREMENT

INTRAMYOCARDIAL FIBER TENSION

+
EJECTION
TIME
+ + + + +
HEART
PERIPHERAL HEART FORCE
BLOOD VOLUME VENOUS TONE RESISTANCE RATE

DIASTOLIC FACTORS SYSTOLIC FACTORS

26
 MANAGEMENT UNSTABLE ANGINA

This CONDITION : is a MEDICAL EMERGENCY

AGGRESIVE REVASCULARIZATION :
PHARMACOTHERAPY PTCA or CABG

27
 MANAGEMENT (PHARMACOTHERAPY)
OF STABLE ANGINA)

Relieve / prevent pain

Slow progression of atherosclerosis
Improve prognosis

ACUTE ATTACK : WARNING.

-STOP ACTIVITIES
-GLYCERYL TRINITRATE spray
400 microgram metered dose
sublingually, repeat once after
5’ if pain persists (max of 2 meter
dose); OR
-GLYCERYL TRINITRATE tablt
300 to 600 microgram s.l. repeat
every 3 to 5 minute (max.1800 µg);
OR
-ISOSORBIDE DINITRATE tablt
5 mg s.l., repeat every 5’ (max.
3 tablt)
AVOID NITRATES if the patient has used
sildenafil (Viagra) in the previous 24 hours OR
tadalafil (Cialis) in the previous 5 days
CONTINUING THERAPY:
-ASPIRIN 75 to 300 mg p.o. daily OR if intolerant:
-CLOPIDOGREL 75 mg daily PLUS EITHER:
-ATENOLOL 25 – 100 mg p.o.daily OR
-METOPROLOL 25-100 mg p.o. daily
28
 DRUGS THERAPY FAILS
and/or
HIGH RISK MI

REVASCULARIZATION:

PTCA ( PercutaneusTransCoronary Angioplasty )

CABG (Coronary Artery Bypass Grafting)

29
 STABLE ANGINA

Vasospasm may
reduce supply

Effort
increases
demand

Symptoms: Diagnosis
Crushing sensation  Possible resting ECG changes
in chest or neighbouring areas during exercise stress test :
 Associated with effort - ST segment elevated or depressed
- arrhythmias
 Relieved by rest or - decreased BP
nitroglycerin - ischaemic myocardium revealed by
thallium-201 or MIBI imaging
 Angiography shows
coronary artery disease 30
 VARIANT ANGINA = vasospastic angina
= Prinzmetal’s angina

Symptoms
-- angina pain at rest
-- angina not effort-related
-- often occurs on early morning
-- exacerbated by smoking
Diagnosis
-- ST segment elevation during
pain
-- angina induced by ergonovine
-- angoigraphy may not reveal
coronary artery diseases
-- exercise stress test of little value

Variant angina, in which vasospasms is the primary cause of coronary insufficiency,

is must less common than stable angina. However, vasospasms is often a
contributing factor in both stable and unstable angina.
31
 Drugs used in angina pectoris

Vasodilators Cardiac depressants

Nitrates Calcium blockers Beta-blockers

Long duration

Intermediate

Short duration
(Trevor,AJ; Katzung,BG; Masters,SB; 2011)
32
 OBAT-OBAT YANG DIGUNAKAN
PADA SERANGAN ANGINA (ANGINA PECTORIS)
AIMS :  mengatasi nyeri dada atau mencegah timbulnya nyeri dada
 menghambat progresi dari atherosclerosis
 memperbaiki prognosis

SERANGAN AKUT :
 NON-FARMAKOTERAPI : segera diistirahatkan begitu serangan
nyeri muncul, baringkan pada tempat yang aliran udara baik.
 FARMAKOTERAPI :
- GLYSERIL TRINITRAT spray 400 mcg/metered dose, sublingual,
diulang tiap 5 menit sampai nyeri hilang/berkurang atau
- GLYSERIL TRINITRATE tablet 300 – 600 mcg s.l. diulang tiap
3-5 menit sampai mencapai dosis max 1.800 mcg atau
- ISOSORBIDE DINITRATE tablet 5 mg, diberikan s.l.. Diulang
tiap 5 menit. Maksimum 3 tablet.

HINDARI PEMAKAIAN PREPARAT NITRATE BERSAMA-SAMA DENGAN

SILDENAFIL (dalam waktu 24 jam) atau TADALAFIL (dalam waktu 5-6 hari)

33
CALCIUM CHANNEL-BLOCKING MEDICINES

DIHYDROPYRIDINE : NON-DIHYDROPYRIDINE :

 amlodipine  bepridil
 felodipine  diltiazem
 nicardipine  verapamil
 nifedipine
 nimodipine
 nisoldipine, etc.

VASODILATATION
34
 β-ADRENOCEPTOR-BLOCKING AGENTS

 obat-obat yang bekerja menghambat

reseptor β serabut syaraf syaraf simpatis

Pada angina hal-hal yang menguntungkan :

- menurunkan heart rate
- tekanan darah turun
- kontraktilitas otot jantung turun.

kebutuhan oksigen otot jantung turun

35
β – BLOKER AGENTS :

- Atenolol
- Carvedilol
- Labetalol
- Metopolol
- Nadolol
- Pindolol
- Propranolol
- Timolol, etc.

36
 Adverse Drug Reaction

Impaired/
failure Multiple polypharmacy compliance
disease state
organ

Altered organ
response

Adverse Drug
Altered drug
concentration Reactions

Homeostatic
regulation

37
 OXYGEN CONSUMPTION

ANGINA ATTACK

LONGTERM / UNCONTROLED

MYOCARD INFARCTION

CARDIAC ARREST DEATH

DEATH

38
CARDIAC ARRHYTHMIAS
ARITMIA CORDIS

39
ARHYTHMIC CORDIS : malfunction
of the electrical impuls conduction
in the heart.
ARITMIA CORDIS :
1. DECREASING THE HEART RATE  SINUS BRADYCARDIA

2. INCREASE THE HEART RATE  SINUS or VENTRICULAR TACHYCARDIA;

ATRIAL or VENTRICULAR PREMATURE DEPOLARIZATION;
ATRIAL FLUTTER)

3. INCOORDINATION / AUTONOM OF THE IMPULS CONDUCTION (ATRIAL

FIBRILLATION; MULTIFOCAL ATRIAL TACHYCARDIA; VENTRICULAR
FIBRILLATION)

4. NEW PATHWAY OF THE ELECTRICAL CONDUCTION (A – V REENTRY;

W-P-W / Wolff-Parkinson-White SYNDROME)

40
ARRHYTHMIC CLASSIFICATION
ARITMIA CORDIS from ATRIUM :
 SINUS BRADYCARDIA
 SINUS TACHYCARDIA
 MULTIFOCAL ATRIAL TACHYCARDIA
 PREMATURE ATRIAL DEPOLARIZATION (PAT)
 ATRIAL FLUTTER
 ATRIAL FIBRILLATION

ARITMIA CORDIS from VENTRICLE :

 VENTRICULAR TACHYCARDIA
 VENTRICULAR FIBRILLATION
 VENTRICULAR PREMATURE DEPOLARIZATION

ARITMIA CORDIS conduction from Atrium  Ventricle:

 A – V REENTRY
 W-P-W SYNDROME

41
PHARMACODYNAMIC ANTIARRHYTHMIC DRUGs

CLASSIFICATION : I; II; III; IV dan Unclassified ) :

Ia : action prolong the action potential duration (APD) and dissociate from
the channel with intermediate kinetics;
Ib : action shorten the APD in some tissue of the heart and dissociate from
the channel with rapid kinetics;
Ic : action have minimal effect on the APD and dissociate from the channel
with slow kinetics;

II : action is sympatholytic. Drugs with this action reduce β-adrenergic

activity in the heart ;

III : action is manifest by prolongation of the APD. Most action block

the rapid component of the delayed rectifier potassium current ( IKr );

IV : action is blockade of the cardiac calcium current. This action slows

conduction in region where the action potential upstroke is calcium
dependent, eg the sinoatrial and atrioventricular nodes;

Others : the effect depress ectopic focal of the heart.

42
 INDICATION OF ANTIARRTHYMIC DRUGs

CLAS Ia : supraventricular tachycardia; ventricular

tachycadia; prevention ventricular fibrilation;
symptomatic ventricular premature beats
CLAS Ib : ventricular tachycardia; prevention of ventricular
fibrillation; symptomatic premature beats
CLAS Ic : Life-threatening ventricular tachycardia or fibrillation;
refractory supraventricular tachycardia
CLAS II : supraventricular tachycardia; may prevent ventricular
fibrilation
CLAS III: AMIODARONE: refractory ventricular tachycardia;
supraventricular tachycardia; prevention ventricular
tachycardia; atrial & ventricular fibrilation;
DOFETILIDE: atrial fibrillation & flutter;
SOTALOL: ventricular tachycardia; atrial fibrillation;
IBUTILIDE : conversion of atrial fibrillation and flutter
CLAS IV: supraventricular tachycardia
CLAS Ia : quinidine; procainamide; disopyramide
(norpace)

CLAS Ib : lidocaine (xylocaine); mexiletine; tocainide

CLAS Ic : flecainide; indecainide; propafenone

(rythmonorm); moricizine

CLAS II : propranolol; esmolol; metoprolol

CLAS III: amiodarone; dronedarone;bretylium;

dofetilide; ibutilide; sotalol

CLAS IV: verapamil; diltiazem

Others : adenosine; digoxin; magnesium sulfate

44
HAEMODYNAMIC
and
SHOCK

45
HEMODYNAMICS.
Is the study of the relationship between
PRESSURE, RESISTANCE and the FLOW of BLOOD
in the cardiovasluar system.
( Aaronson, PI. & Ward J P T., 2000)

Is the study of the movement of the blood and

the forces concerned there in.
( Doorland’s Illustrated Medical Dictionary, 27th ed., 1988).

Hemodynamic, pertaining to the movements

involved in the circulation of the blood.
( Doorland’s Illustrated Medical Dictionary, 27th ed.,1988)

46
 CO = (MABP-CVP)/ TPR

CO = cardiac output,
MABP = mean arterial
blood pressure,
TPR = total peripheral
resistance,
CVP = central venous
pressure

(copy from :
Aaronson,PI., Ward,J.P.T., 1999)

47
AO = aorta
Lg. arteries = large arteries
Sm.arteries = small arteries
ART = arterioles
CAP = capillaries
VEN = venule
SV = venous
Sm veins = small veins
Lg veins = large veins

48
HEMODYNAMIC EMERGENCY

PRESSURE : - hypertension
- hypotension

RESISTANCY : - obtruction of vessel

- peripheral vasoconstriction
- massive bleeding

FLOW OF THE BLOOD : - blood viscocity

- angina/O2 supply
49
HAEMODYNAMICS
- Stroke / CVA
- Vital organ
PRESSURE -Hypertension damages.

-Hypotension - Shock

RESISTANCE -Vasoconstriction.

-Obstruction
Thrombus
Emboli
FLOW OF BLOOD -Scleroting of areteries

-Increase of velocity Hematokrit

BLOOD PRESSURE
50
HYPOTENSION

SHOCK

51
52
BLOOD PRESSURE
EMERGENCY
HYPOTENSION
ACTION

SHOCK
organs perfusion

ORGANS / TISSUES
DAMAGES
53
BLOOD FLOW

ORGANS
PERFUSION

CRITICAL PERIODE
REVERSEIBLE

IRREVERSIBLE

CELLULAR / TISSUE / ORGAN INJURY

DEATH

54
55
Classification of shock
by mechanism and common causes.

Hypovolemic shock

Cardiogenic shock

Obstructive shock

Distributive shock

( Messina, L.M., et al., 2003 ) 56

Hypovolemic Cardiogenic Obstructive Distributive
shock shock shock shock

Reduced Severe Severe

Reduced Reduced Decrease in
Ability to Myocardial
preload Systolic Systemic
Fill ventricle depression
performance Vascular
In diastole
resistance

Decrease in
Stroke volume

Hypotension Maldistribution
Decrease in CO
Of blood flow
In microcircul.
Severe decrease in
Tissue & organ blood flow

Multiple organ system

( Parrillo, JE., 1991 ) failure
57
 Hypovolemic shock

1. Loss of blood (hemorrhagic shock)

- External hemorrhagic : trauma, gastrointestinal bleeding,
etc.
- Internal hemorrhagic : hematoma, hemothorax,
hemoperitoneum.

2. Loss of plasma : burns, exfoliative dermatitis.

3. Loss of fluid and electrolytes

- External : vomiting, diarrhea, excessive sweating,
hyperosmolar states (diabetic ketoacidosis, nonketotic coma)
- Internal ( “third spacing”) : Pancreatitis, Ascites,
Bowel obstruction.
58
59
 Cardiogenic shock

- Dysrhythmia :
- Tachyarrhythmia
- Bradyarrhythmia

- “Pump failure” : secondary to myocardial infarction or

other cardiomyopathy.

- Acute valvular dysfunction (especially regurgitant lesions )

- Rupture of ventricular septum or free ventricular wall

60
 Obstructive shock

- Tension pneumothorax

- Pericardial diseases ( tamponade, constriction)

- Diseases of pulmonary vasculature

(massive pulmonary emboli, pulmonary hypertension)

- Cardiac tumor ( atrial myxoma )

- Left atrial mural thrombus

- Obstructive valvular diseases (aortic or mitral stenosis)

61
 Distributive shock

- Septic shock

- Anaphylactic shock

- Neurogenic shock

- Vasodilator drugs

- Acute adrenal insufficiency

62
 TREATMENT and MANAGEMENT SHOCK

1. GENERAL MEASURE :
“ ABC “  VENTILATION  Oxygen supply
Advanced Cardiogenic Life Support (ACLS)
Folley Catheter  urinary output
Laboratory : blood count
electrolyt
glucose
blood gas analyse
coagulation parameter
blood group
bacterial cultur

2. CENTRAL VENOUS PRESSURE ( CVP ) or

PULMONARY CAPILLARY WEDGE PRESSURE (PCWP)
63
3. VOLUME REPLACEMENT.
 I.V. LINE ( better use TRANFUSION SET )
HEMORRHAGIC SHOCK :
 BLOOD SUBSTITUTES / WHOLE BLOOD /
PBRC (Packed Blood Red Cells)
+ isotonic solution preventing increase of Hmt.
HYPOVOLEMIC SHOCK :
 Rapid bolus ISOTONIC CRISTALLOID  1 L
CARDIOGENIC SHOCK :
 ISOTONIC CRISTALLOID ( smaller volume )
SEPTIC SHOCK :
 Large volume ISOTONIC CRISTALLOID.

SHOCK in TRAUMA CAPITIS  HYPERTONIC SALINE (7.5%)

plus DEXTRAN.
64
4. MEDICATIONS
4.1. VASOACTIVE THERAPY :  INOTROPIC agents
 VASOPRESSOR agents
- AFTER ADEQUATE FLUID RESUSCITATION
- DEPENDS ON CARDIAC OUTPUT
Agents : - Dobutamine
- Nor-adrenaline/Nor-epinephrine
- Adrenaline/Epinephrine
- Dopamine
- Vasopressin ( antidiuretic hormon /ADH )
 DISTRIBUTIVE/VASODILATOR SHOCK

4.2. CORTICOSTEROID  SEPTIC SHOCK

4.3. Activated Protein C  as antithrombotic, profibrinolytic
and Anti-inflamatory
( SEPTIC SHOCK)
4.4. ANTIBIOTIC  DEFINITIVE THERAPY in SEPTIC SHOCK
4.5. SODIUM BICARBONATE  SEPTIC SHOCK with
LACTIC ACIDOSIS
65
PRINCIPLES SHOCK MANAGEMENT :

1. ALLEVIATING THE PRECIPITATING CAUSE OF SHOCK;

2. TREATING THE HAEMODYNAMIC AND

METABOLIC CONSEQUENCES;

3. MANAGING THE SECONDARY MEDICAL

COMPLICATIONS ( renal failure; pulmonary oedema etc.)

(Benowitz, N.L., et al., 1997)

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