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Shock Kardiogenik
CARDIAC CENTER
REGIONAL CARDI0VASCULAR CENTER
RS. DR. M DJAMIL, PADANG
Dr. MUHAMMAD SYUKRI, Sp JP(K), FIHA, FSCAI, FAPSIC
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FAKTOR PENENTU FUNGSI JANTUNG
STROKE
VOLUME
PRELOAD
Kontraktilitas
CARDIAC OUTPUT
HEART RATE
AFTERLOAD
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HEMODINAMIK
• Ilmu yang mempelajari
– Fungsi jantung sebagai pompa
– Sistem sirkulasi darah
– Autoregulasi sistem kardiovaskuler
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PEREDARAN DARAH TEPI
• DITENTUKAN OLEH :
• Ukuran( Size )
• Panjang pembuluh darah
• Tahanan
• Viskositas
Prinsip fisika aliran : Hukum Poiseulle’s
SVR = 8 length X Viscosity
π R4
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KORELASI KLINIK GANGGUAN
HEMODINAMIK DAN KONTROL SISTEM
KARDIOVASKULER
•
SHOK ( GAGAL SIRKULASI )• HIPERTENSI
• HIPOTENSI
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KONTROL SISTEM KARDIOVASKULER
• Kontrol jangka pendek
– Baroreseptor
– Sistem Simpatik/Para simpatik
– Jantung dan Pembuluh darah
• Kontrol jangka panjang – Juxta Glomerulus Renal
– Renin – Angiotensin- Aldosteron
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Shock
• Suatu keadaan dimana perfusi jaringan tidakadekuat menyebabkan kekurangan oksigen danpengkutan bahan bahan metabolik terganggu.
• Gangguan produksi dan pemanfaatan energi,perubahan metabolisme sel, asidosis, cedera sel,rusaknya integritas sel, disfungsi jaringan danorgan dan akhirnya kematian bila tidak di atasisecara cepat dan agresif.
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Gambaran Klinis
A. Tanda Vital
B. Kulit C. Volume Urine
D. Status Mental
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Tanda Vital
• Pulsa Nadi : Takikardia
• Tekanan Darah :
– TDS < 90 mmHg
• Shock Index : HRTD
N = 0.5 – 0.7
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Kulit
• Dingin
• Clammy (lembab dan basah)
• Diaphoretic
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Volume Urine
• Pekat
• Jumlah urine menurun
• Oliguria < 0.5 cc/kg/jam
• Anuria
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Status Mental
• Confuse
• Agitasi
• Lethargi
• Coma
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Triad kardiovaskular
1. Problem irama atau frekuensi jantung.
2. Problem pompa Jantung.
3. Problem volume atau tahanan
vaskular
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Problem Irama Atau Frekuensi
Jantung
• Irama cepat
– SVT
– AF
– VT
• Irama Lambat
– Sinus bradikardia
– Junctional Rhythm
– AV block
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Problem pompa Jantung
• Primer
– Myokardial Infark
– Cardiomyopathy
– Myocarditis
– IVS rupture
– Disfungsi katup akut
• Sekunder
– Myxoma atrium
– Tamponadde jantung
– Emboli Paru
– Tension Pneumothorak
– Obstruksi vena kava
– Obat yang dapat mendepresi myocard
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Problem volume atau
tahanan vaskular
• Volume cairan berkurang
– Perdarahan
– Muntah/diare
–
Luka bakar – Diabetes Insipidus
– dll
• Ukuran vaskular yang bertambah
– Anaphylaxis
– CNS injury – Toxin
– Obat-obtan
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Pasien Monitor• Monitor ketat
– Tanda Vital
– Irama Jantung
– Saturasi Oksigen ( Pulse Oximetry)
– Volume Urine – Penilaian pasien
• Monitor Invasif
– Artery Line
–
Central venous Pressure – Pulmonary artery catheterization ( Swan-Ganz )
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Perawatan Pasien Shock
a. Nilai, amankan dan atasi jalan nafas dan sirkulasi
sesuai dengan indikasi
b. Secara bersamaan berikan 02, pasang IV line,
monitor kontinu Sat o2 dan irama jantung
c. Segera dapatkan data tanda vital, ECG, BGA,
Riwayat penyakit
d. Segera kerjakan Chest X- Ray, Laboratorium yang
relevan.
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Cardiogenic Shock and
Hemodynamics
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Outline
Cardiogenic Shock
– Etiologies
– Pathophysiology
– Clinical Findings
– Treatment
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Shock Kardiogenik
Definition
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SHOCK Registry JACC Sept. 2000, Supp. A
Spectrum of Clinical Presentations
MortalityRespiratory
DistressHypotension Hypoperfusion
21%
22%
70%
60%
5.6%
28%
65%
1.4%
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SHOCK= Inadequate Tissue Perfusion
Mechanisms:
– Inadequate oxygen delivery
–Release of inflammatory mediators
– Further microvascular changes,compromised blood flow and furthercellular hypoperfusion
Clinical Manifestations:
– Multiple organ failure
–
Hypotension
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Schematic
LVEDP elevation
Hypotension
Decreased coronaryperfusion
Ischemia
Further myocardial
dysfunction
Neurohormonal
activation
Vasoconstriction
Endorgan hypoperfusion
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Hemodynamic Parameters
Systemic Vascular Resistance (SVR)
Cardiac Output (CO)
Mixed Venous Oxygen Saturation
(SvO2)
Pulmonary Capillary Wedge Pressure
(PCWP)
Central Venous Pressure (CVP)
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Normal Values
Right Atrial
Pressure, CVP
Mean 0-6mmHg
PulmonaryArtery Pressure
SystolicEnd-diastolic
mean
15-30mmHg4-12mmHg
9-19mmHg
PCWP Mean 4-12mmHg
Cardiac Output 4-8 L/min
Mixed Venous
O2 Sat
>70%
SVR 800-1200
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Differentiating Types of Shock
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Clinical Findings
Physical Exam: elevated JVP, +S3, rales, oliguria,acute pulmonary edema
Hemodynamics: dec CO, inc SVR, dec SvO2
Initial evaluation: hemodynamics (PA catheter),echocardiography, angiography
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4 Potential Therapies
Pressors
Intra-aortic Balloon Pump (IABP)
Fibrinolytics
Revascularization: CABG/PCI
Refractory shock: ventricular assist
device, cardiac transplantation
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Pressors do not change outcome
• Dopamine –
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IABP is a temporizing measure
Augments coronary blood flow in diastole
Balloon collapse in systole creates a vacuum effect
decreases afterload
Decrease myocardial oxygen demand
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IABP
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Indication for IABP
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Contraindications to IABP
Significant aortic regurgitation or significant
arteriovenous shunting
Abdominal aortic aneurysm or aortic dissection
Uncontrolled sepsis
Uncontrolled bleeding disorder
Severe bilateral peripheral vascular disease
Bilateral femoral popliteal bypass grafts for severeperipheral vascular disease.
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Complications of IABP
Cholesterol Embolization
CVA
Sepsis
Balloon rupture
Thrombocytopenia
Hemolysis
Groin Infection
Peripheral Neuropathy
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Revascularization – SHOCK
trial
Overall 30-Day Survival in the Study
Hochman J et al. N Engl J Med 1999;341:625-634
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SHOCK trial
Hochman J et al. N Engl J Med 1999;341:625-634
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Copyright restrictions may apply.
Hochman J. S. et al. JAMA 2006;295:2511-2515.
Kaplan-Meier Long-term Survival of All Patients and Those Discharged Alive
Following Hospitalization
SHOCK 6 years later
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