Cardiogenic Shock

Subijakto Sjarif SpJP.FIHA

Definition
The term shock is used to describe
complex pathophysiologic syndrome(s)
arising from any multitude of causes.
Shock usually results from a critical
impairment of blood flow to vital organs
and tissues and/or the ability of those
tissues to utilize essential nutrients. The
common denominator in all forms of shock
is microcirculatory insufficiency
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 Common Causes of
Shock
Cardiogenic shock
 Myocardial failure
 Left ventricular (e.g. ischemia, infarction,
cardiomyopathy)
 Right ventricular (e.g. infarction, pulmonary
hypertension, cor pulmonale)
 Arrhythmiák
 Valvular regurgitation or stenosis
 Ventricular septal rupture or free-wall rupture
 Obstructive lesions
 myxoma, pulmonary embolism, pricardial
tamponade
 Cardiogenic Shock

Impaired Pump Valvular regurgitation

Function or stenosis
Myocardial Infarction Septal Rupture
Asthma cardiale Pericardial
Severe Acidosis tamponade
Barbiturat intoxication Pneumothorax
Toxins of Septic Embolism
Shock
 Cardigenic shock

Cardiac Output

Preload
 Decreased Cardiac Output

Decreased arterial pressure

Decreased systemic blood flow

Decreased cardiac Decreased nutrition Intravascular clotting

nutrition of tissues

Decreased nutrition Decreased nutrition

of vascular system Tissue ischemia
Of brain

Decreased vasomotor Increased capillary Release of

activity permeability toxins

Vascular
dilatatio Decreased
n Blood volume
Venous pooling

Cardiac depression Decreased venous return

 Pathophysiology of
Shock
Tissue hypoxia
Activation of protective mechanisms
 Negative feed back mechanisms
Failure of the protective mechanisms
 Positive feed back mechanisms
 Over activation of the immune system

Multiple Organ Failure

 Major Hemodynamic
Determinants of Tissue
Perfusion
Systemic arterial pressure
Arterial Pressure=Cardiac Output x Total Vascular
Resistance

Organ vascular resistance

Nutritional microcirculatory patency
 Major Hemodynamic
Determinants of Tissue
Perfusion
Systemic arterial pressure
 Total vascular resistance
 Total arteriolar resistance, vascular muscle
tone
 tissue metabolites
 neurohumoral factors
 toxins
 Blood viscosity
 Cardiac output
 Heart rate (brady- and tachyarrhythmias)
 Stroke volume
 preload (cardiac filling pressure and volume)

 total circulating blood volume

 distribution of blood volume

 atrial contraction

 diastolic filling time (heart rate)

 Inotropic state
 total functioning ventricular muscle mass

 intrinsic (myocardial) control mechanism

 extrinsic (noncardial) neurocirculatory control mechanisms

 myocardial perfusion

 myocardial oxygen demand

 physiologic/pharmacologic depressant

 humoral agents

 Afterload
 Aortic diastolic pressure

 Ventricular size
Organ vascular resistance
 Occlusive vascular disease
 Local arteriolar and venular resistance
 Neurogenic factors
 Humoral factors
 Local autoregulation
Nutritional microcirculatory patency
 Precapillary sphincter tone
 Postcapillary venular tone
 Intracapillary aggregation of blood components
 Capillary endothelial integrity
 Stages of Shock

Compensatory Stage (Non-Progressive

Shock)
Progressive Shock
 Non-Progressive Shock
Blood pressure falls  Baroreceptors are stimulated
Sympathetic tone increases and parasynpathetic
decreases  Adrenal medulla releases EP, NEP
1-receptor stimulation  HR and Cardiac output
increase, 2-receptor stimulation  vasoconstriction,
bronchodilatation, metabolism, -receptor
stimulation centralization
AII/aldosteron, generalized vasoconstriction, fluid
retention, Increased CO, pulmonary blood flow
decreases  ventillation/perfusion mismatch
Chemoreceptors stimulated  hyperventillation 
alkalosis with hypoxemia
 Progressive Shock
Compensatory mechanisms are no longer able to keep CO and BP.
If not corrected, massive cellular injury will result.

Hypotension and arteriolar vasoconstriction 

tissue hypoxia
Lactic acidosis, low intracellular ATP  cell
dysfunction, arrhytmias and conduction
disturbances
Acidosis  arterial vasodilatation, fluid filtration 
decreased venous return  CO decreases
Cardiac contractility decreases  CO decreases
Membrane injury, increased permeability, bacterial
toxins, DIC
 Pathophysiology of shock
Stage I. Stage II. Stage III.

Cellular membrane
Microcirculatory Injury
Failure
Decreased perfusion Endothelial Damage
Low Cardiac Major End-Organ
Output or Vasodilatation Dysfunction
Pathogenesis

Compensated Decompensated Cellular

hypotension hypotension
? Death

Potentially reversibile
shock Irreverzibile shock
 Preload
Contractile state Stroke volume
Afterload

Total circulating blood volume Aortic root diastolic pressure

Distribution of blood volume systemic vascular resistance
body position arterial viscoelasticity
intrapericardial pressure aortic root blood volume
intrathorachal pressure

AD
venous tone

AF
LO

TE
E
Impedance
PR

RL
Atrial Cotraction

OA
D
Ventricular size
CONTRACTILE STATE

Functioning ventricular Intrinsic/extrinsic neurohumoral Depressants

hypoxia
muscle mass mechanisms acidosis
absolute mass sympathetic nervous system alkalosis
oxygenisation sympathoadrenal axis drugs
circulating catecholamines other circulating myocardial
parasympathetic nervous system depressant factors
 Therapy
Early diagnosis
Monitoring:
 (EKG, AP, PV, Hrt, CVP, blood gas, pH,
diuresis)
 electrolytes, glucose, plasma proteins, amino
acids, lactic acid
Elimination of primary problem
Normal tissue oxygenazation (60-70 mmHg
 almost normal pO2
Antibiotics
Steroids
 SYOK KARDIOGENIK
PADA
INFARK MIOKARD AKUT
Kematian di rumah sakit pada pasien
infark miokard akut menurut ada
tidaknya syok tahun 1975-1997
Syok Non-syok

80

60

40

20

0
1975 1978 1981 1984 1986 1988 1990 1991 1993 1995 1997

Golberg. N Engl J Med 1999;340:1162-8

 DEFINISI
SHOCK Trial:
Kriteria klinis:
- TDS < 90 mm Hg, > 30 menit sebelum
inotropik
- perlu PBIA/inotropik utk TDS > 90 mm
Hg
- hipoperfusi organ: oliguri, ekstremitas
dingin/lembab
- laju jantung > 60x/mnt (t’msk pacu jantung)
 DEFINISI

Kriteria hemodinamik:
- tekanan baji kapiler paru > 15 mm Hg
- indeks curah jantung < 2.2 lt/mnt/mm2
 PENELITIAN KLINIS
GISSI (1986): 11.806 pasien, 280 Killip IV
GUSTO-I (1993): 40.176 pasien, 2814 syok
GUSTO-III (1997): 15.058 pasien, 643 syok
(S)MASH (1999): 55 pasien
SHOCK (1999): 302 pasien. 900 ps tidak
memenuhi kriteria: SHOCK Trial Registry
 Presentasi klinis pasien infark miokard akut dengan
kecurigaan syok kardiogenik karena gagal ventrikel kiri

tanpa kongesti dan hipoperfusi kongesti, tanpa hipoperfusi

hipoperfusi, tanpa kongesti kongesti dan hipoperfusi
6% 3%

28%

63%

Menon. SHOCK Trial Registry. JACC 2000;36:1071-6

Angka kematian pasien infark miokard
akut berdasarkan ada tidaknya
hipotensi dan hipoperfusi

hipotensi tanpa
hipoperfusi

hipoperfusi
tanpa hipotensi

hipotensi dan
hipoperfusi

0 20 40 60 80

Menon. SHOCK Trial Registry. Am J Med 2000;108:374-80

 PRESENTASI KLINIS
SHOCK Trial Registry: 20% pasien syok
kardiogenik adalah NSTEMI. Angka kematian
sama dengan kelompok STEMI
GUSTO Trials: dari 5% pasien syok, hanya
0.5%-1% yang datang dengan syok, sisanya
syok terjadi di rumah sakit. Perlu mengetahui
prediktor terjadinya syok setelah trombolitik.
 Sistem skoring untuk memprediksi
terjadinya syok kardiogenik setelah
pemberian trombolitik
Umur Laju jantung TD sistolik Berat badan
thn skor X/mnt skor mmHg skor Kg skor
20 6 40 3 80 59 40 19
30 12 60 0 100 49 60 17
40 19 80 8 120 39 80 15
50 25 100 14 140 32 100 12
60 31 120 17 160 27 120 10
70 37 140 19 180 23 140 8
80 43 160 22 200 18 160 6
90 49 180 24 220 14 180 4
200 27 240 9 200 2
220 29 260 5
240 32 280 0
260 34
Sistem skoring untuk memprediksi terjadinya
syok kardiogenik setelah pemberian trombolitik
Trombolitik Killip Lokasi infark Faktor resiko lain
obat skor klas skor lokasi skor Faktor skor
TPA 0 I 0 Anterior 8 Riwayat infark sebelumnya 5
SK-IV 5 II 9 Inferior 1 Riwayat BPK sebelumnya 6
Combo 3 III 17 lainnya 0 Tanpa riwayat angioplasti 6
SK-SQ 6 Perempuan 3
Hipertensi 2
Sistem skoring untuk memprediksi terjadinya
syok kardiogenik setelah pemberian
trombolitik
 skor Kemungkinan terjadinya syok
kardiogenik di rumah sakit
92 1%
103 2%
110 3%
114 4%
118 5%
130 10%
137 15%
142 20%
146 25%
149 30%
152 35% Hasdai.
155 40% JACC 2000;
158 45% 35:136-43
159 50%
Patofisiologi syok kardiogenik pada
infark miokard akut

Califf. N Engl J Med 1994;330:1724-30

 TROMBOLITIK
GISSI: trombolitik vs tidak – 69.9% vs 70.1%
Fibrinolytic Therapi Trialist (FTT)
Collaborative Group: manfaat trombolitik
pada hipotensi
SHOCK Trial registry: trombolitik, trombolitik
+ PBIA, tanpa trombolitik – 62.9%, 46.5% vs
76.5%
Hanya 40%-50% pembuluh penyebab infark
yang mengalami reperfusi
 TROMBOLITIK

Nampaknya terapi trombolitik saja tidak

cukup untuk memperbaiki angka
harapan hidup pasien syok kardiogenik
Perlu kriteria untuk menentukan mana
pasien yang ditrombolitik, mana yang
langsung intervensi invasif
Pompa Balon Intra Aortik
(PBIA)
AHA: klas I
1970-an: satu-satunya modalitas terapi
– hasil tak jelas
GUSTO-I: kecenderungan penurunan
angka kematian 30 hari
SHOCK Trial Registry: keuntungan
pemakaian PBIA
Angka kematian di rumah sakit pada
pasien syok kardiogenik berdasarkan
pemakaian PBIA dan trombolitik
80
70
60
50
40
30
20
10
0
PBIA + Trombolitik
trombolitik

Sanborn. JACC 2000;36:1123-9

Trombolitik vs PBIA ?
TACTICS: Thrombolysis and
Counterpulsation to Improve
Cardiogenic Shock Survival Trial
HEROICS: How Effective are
Revascularization Options in
Cardiogenic Shock Trial
 ANGIOPLASTI
Edep dkk: setelah analisa multivariat,
revaskularisasi dini tetap merupakan
faktor penentu meningkatnya harapan
hidup
GUSTO-I: revaskularisasi dini
dihubungkan dengan penurunan angka
kematian 30 hari dan 1 tahun
(S)MASH dan SHOCK
(S)MASH (The Swiss Multicenter Evaluation
of Early Angioplasty for Shock Following
Myocardial Infarction) (1992-1996): 55 pasien

IMA
< 48 jam

Syok kardiogenik

< 24 jam

Randomisasi
28 ps 22 ps

Revaskularisasi dini Stabilisasi medis awal

SHOCK (Should We Emergently Revascularize
Occluded Coronaries for Cardiogenic Shock) (1993-1998):
302 pasien.

IMA
<36 jam

Syok kardiogenik

< 12 jam

Randomisasi
152 ps 150 ps

Revaskularisasi dini Stabilisasi medis awal

< 6 jam >54 jam
 Angka kematian pasien syok
kardiogenik berdasarkan strategi
penanganan: Hasil SHOCK Trial
Revaskularisasi dini Stabilisasi medis awal

70
60
50
40
30
20
10
0
30 hari 6 bulan 12 bulan

Hochman. N Engl J Med 1999;341:625-34

 BEDAH PINTAS
KORONER
SHOCK Trial: dilakukan pada penyakit arteri
koroner yang lebih berat. Angka kematian 1
tahun sebanding dengan angioplasti
(52%vs51%). Pada SHOCK Trial Registry:
28%vs 46%.
Revaskularisasi daerah iskemik non-infark:
penting ! Bedah pintas koroner merupakan
pilihan strategi yang optimal.
AHA klas IIa
KEBERHASILAN TERAPI
1960-an: pemulihan dari syok dan
bebas suport presor > 24 jam
1970-an: pasien dapat meninggalkan
rumah sakit dalam keadaan cukup baik
Saat ini: meningkatnya harapan hidup
dan kualitas hidup jangka panjang
 Perbandingan mortalitas strategi
agresif dan konservatif pada kelompok
usia > 75 tahun

80
70
60
50
40 agresif
30 konservatif
20
10
0
30 hari 1 tahun

White. Eur Heart J 2000;21:1897-1901

 Strategi penanganan pasien syok
kardiogenik pada infark miokard
akut
Infark miokard akut
hipotensi - hipoperfusi
Non-syok Syok

Trombolitik/
angioplasti Non-usila Usila

Skor Hasdai I Skor Hasdai II

Resiko syok Resiko syok Prognosis Prognosis Konservatif

tinggi rendah baik buruk

Agresif Konservatif Agresif Konservatif

MATUR NUHUN