shock cardiogenic kuliah s1

8/15/2019 Shock Cardiogenic Kuliah S1

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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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shock cardiogenic kuliah s1

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