This schematic drawing depicts an example of the concept of “vicious circles,” in which a primary event becomes complicated and reinforced by other factors. CI = cardiac index; VR = venous return; ECFV = effective circulating fluid volume; RES = reticuloendothelial system.

(King, E.G. & Chin, W.D.N.: Crit Care Clin 1985; 1: 550)

…. Final Common Pathway of Circulatory Failure and death

Capacitane Bed Pooling

Release of Bacteria & Their Products

Myocardial Depression

3rd Space Sequestration

4 - Response

Integrity Compromise

GUT RES

CI

VR

ECFV

Massive Myocardial Infarction

EXAMPLES OF VICIOUS CIRCLE CONCEPT

The Vicious Circles that Lead to the ….

CARDIOGENIC

DISTR

IBUTI

VE

HYPOVOLEMIC

OBSTRUCTIVE

Gb. 1. Penyebab syok kardiogenik pada infark miokard

( Schreiber, T.L. et al; Am Heart J, 117 : 436, 1989 )

• Gangguan mekanik - ruptura : + septum

+ dinding ventrikel+ m. papillaris

- disfungsi m. papillaris

SYOK• Infark ventrikel kanan

• Penambahan disfungsi sistolik ventrikel kiri : - IM dengan ekstensi - IM luas - IM ringan dengan lesi luas sebelumnya - IM dengan gangguan metabolik

The site of dysfunction in shock is the capillary-interstitial fluid-cell interface. Organs are highly complex aggregates of billions of specialized cells. Abnormalities at this critical junction ae

associated with the signs and symptoms of organ dysfunction observed in patients in shock.

THE CAPILLARY EXCHANGER THE CELL (metabolic factory)

Venules

Capillary bed

ArteriolesB

loo

d f

low

OxygenCarbon dioxideNutrients

Interstitial fluid (the buffering sea in which cells reside)

The hypoxic sequence of cellular events in shock

Impaired cellularOxygen uptake or utilization Impaired capillary perfusion

Cell hypoxia (anaerobic metabolism)

Lactic acidosis

Decreased ATP (energy) production

Failure of the Na-K pump

Cellular swelling

Lysosomal rupture

Cell death Organ failure

Death of the entire organism

The self-perpetuating vicious cycle of progressive myocardial damage and dysfunction in AMI shock.

Critical decrease in stroke volume, decreased arterial pressure

Reduction in coronary perfusion pressure and coronary blood flow

Ventricular wall motion abnormalities;- Ischemic paralysis- paradoxic wall motion

Inadequate myocardial perfusion

DEFINISI

KEADAAN HIPOPERFUSI BERAT

JARINGAN TUBUH YANG DISEBABKAN

DISFUNGSI POMPA JANTUNG

TEKANAN DARAH SISTOLIK < 90 mmHg

PERFUSI ORGAN < (URINE < 20 ml/Jam)

VASOKONSTRIKSI PERIFER

Cardiogenic Shock• In the past it has been reported to occur in up to

20% of patients with STEMI• After fibrinolytic therapy, the incidence rate is in

the range of 7%• About 10% cardiogenic shock present at

admission whereas 90% develop it during hospitalization

• The mortality rate has decreased from 70-80% in the 1970s to 50-60 % in the 1990s

• Cardiogenic shock is the cause of death in about 60% of patients dying after fibrinolysis for STEMI

SYOK KARDIOGENIK

MORTALITAS

- PEMANTAUAN HEMODINAMIK

- IABC

- PTCA

- TINDAKAN BEDAH

INSIDENSI

- PENGOBATAN REPERFUSI

Infark miokard

Fungsi jantung

Cardiac output Tekanan darah

Respons hemodinamik

- Takhikardi - Kontraktilitas - Preload ventrikel - Tekanan pengisian ventrikel

Respons sirkulasi perifer

- Tahanan perifer - Tonus vena perifer - Volume intra

vaskuler - Perfusi organ vital

Respons neuro-humoral

- aktivitas simpatis - Tonus vagus - Catecholamin endogen - sistem renin angiotensin

aldosteron - pembebasan vasopresin

• cardiac output • tekanan darah • perfusi jaringan

Tabel 2. Kompensasi tubuh terhadap syok kardiogenik.(Chatterjee, K. : Crit Care Clin, 1 : 569, 1985)

TABEL 3. EFEK SAMPINGAN PADA JARINGAN AKIBAT RESPONS KOMPENSASI GAGAL JANTUNG

( Chatterjee, K. : Crit Care Clin, 1: 569, 1985 )

• Takhikardi

• Kontraktilitas

• Volume end-diastolik

• Tekanan diastolik ventrikel kiri

• Tahanan perifer sistemik

• Kebutuhan O2

• Perfusi miokardium

• Kebutuhan O2

• Kebutuhan O2

• Perfusi subendokard

• Kongesti pulmonal

• Hipoksemia

• Afterload dan cardiac output

• Kebutuhan O2

Respons kompensasi Efek sampingan

I. UNCOMP

II. MILD CHF

III. SEVERE CHF

IV. SHOCK :

N /

USUALLY N

N /

N

USUALLY

/

CARDIOGENIC

HYPOVOLEMIC

N /

CLINICAL SYST. ART.

PRESS

CI* PERI

VASC. RES.

PCWPP**

* CI : NORMAL = 2.5 – 3.6 lt/min/m2

REDUCED = 2.2 – 2.5 lt/min/m2

HYPOPERFUSION = 1.8 – 2.2 lt/min/m2

SHOCK = 1.8 lt/min/m2

** PCWPP : NORMAL = 10 – 12 mmHgOPT WITH AMI = 14 – 18 mmHg

Diagnosis of cardiogenic shock

• Marked and persistent (> 30 minutes) hypotension SBP<80 mmHg

• 30 mmHg below previous basal levels

• Cardiac index < 1,8 l/mm/m2

• LVFP > 18 mmHg

• Hypoperfusion urine output < 30 ml/hr

DIAGNOSISKLINIK

- TEKANAN SISTOLIK < 90 mmHg

- PERFUSI ORGAN < (URINE < 20 ml/Jam )

- VASOKONSTRIKSI PERIFER

HEMODINAMIK

- PCWP > 18 mmHg

- CI < 2.2 l/men/m2

KRITERIA BAIK- CI > 2.5 l/min/m2

- PCWP < 15 mmHg- HR < 100/min

INTERVENSI BILA- CI < 2 l/min/m2

- PCWP > 20 mmHg- SVR > 1500 dyne.sec.cm-5

PENGELOLAAN

1. DETEKSI DINI2. KOREKSI FAKTOR-FAKTOR

PRESIPITASI3. PEMANTAUAN HEMODINAMIK4. PENGOBATAN MEDIKAMENTOSA5. IABC6. PTCA7. TINDAKAN BEDAH

PENGELOLAAN LOW CARDIAC OUTPUT SYNDROME

1. ADAKAH KOMPLIKASI PERDARAHAN, TAMPONADE, INFARK MIOKARD.

2. KOREKSI FAKTOR NON – KARDIAK RESPIRASI, ASAM-BASA, ELEKTROLIT.

3. OPTIMASI HR/IRAMA ( 90 – 100 / men )

4. OPTIMASI PRELOAD ( PCWP 15 – 18 mmHg )

- CAIRAN

- TRANSFUSI BILA Ht < 30 %

5. HITUNG CARDIAC OUTPUT

BILA CI < 2 l/m2/min INOTROPIK

- DOPAMINE

DOBUTAMINE

- CaCl2

- EPINEFRIN + CaCl2

- DIGOXIN

6. HITUNG SVR

7. IABP

Tabel 1. Gambaran hemodinamik syok kardiogenik

• PCWP/tek. Pengisian ventrikel kiri > 18 mmHg

• Cardiac indeks < 2.2

L/men/m2

H I < 18 > 2.2

H II > 18 > 2.2

H III < 18 < 2.2

H IV > 18 < 2.2

PCWP CI

(mmHg) (L/men/m2)

PERUBAHAN HEMODINAMIKA PADA AKUT MIOKARD INFARK

( FORRESTER DKK : N.ENGL J MED; 295: 1361, 1976

PAWP = pulmonary artery wedge pressure; PADP = pulmonary artery diastolic pressure.Source : From C. Makabali, M.H. Weil, and R.J. Henning, An update on therapy for shock : Current concepts of mechanisms and management of circulatory shock. Cardiovasc. Rev. Rep. 3:899, 1982, with permission.

< 12

< 16

> 16

> 7

< 3

>3<7

> 3

< 3

200 ml x 10 min

100 ml x 10 min

50 ml x 10 min

Stop

Continue infusion without interruption

Wait 10 min

Stop

Repeat fluid challenge

Observe PADP/PAWP for 10 min before challenge

During infusion (0-9 min)

Immediately following 10-min infusion

After 10-min wait

StepsPAWP/PADP

(mm Hg) Fluid Infusion Rate

Fluid Challenge : PAWP/PADP ( 7-3 Rule )

CVP = central venous pressureSource : From C. Makabali, M.H. Weil, and R.J. Henning, An update on therapy for shock : Current concepts of mechanisms and management of circulatory shock. Cardiovasc. Rev. Rep. 3:899, 1982, with permission.

< 8

< 14

> 14

> 5

< 2

>2<5

> 2

< 2

200 ml x 10 min

100 ml x 10 min

50 ml x 10 min

Stop

Continue infusion

Wait 10 min

Stop

Repeat fluid challenge

Observe CVP for 10 min before challenge

During infusion (0-9 min)

Immediately following 10-min infusion

After 10-min wait

StepsCVP

(cm H2O) Fluid Infusion Rate

Fluid Challenge : CVP ( 5-2 Rule )

Suggested Therapy According to the Severity of Left Ventricular Failure and Initial Hemodynamic Abnormalities*

* Adapted from Gunnar, R.M., Lanbrew, C. T., Abrams, W., et al.: Task force IV : Pharmacologic interventions. Am. J. Cardiol., 50:393-408, 1982.

+ CI = cardiac index; PCWP = pulmonary capillary wedge pressure; SAP = systolic arterial pressure.

Pulmonary congestion

Pulmonary congestion

Decreased perfusion

Shock

I

II

III

> 2.5

< 2.5

< 2.5

> 18

> 18

> 18

> 100

> 100

> 90

DiureticsNitroglycerinNitroprussidePhentolamine

DobutamineDopamineNorepinephrineIntraaortic ballon

counterpulsationVasodilators

SUGGESTEDTHERAPY

SAP(mm Hg)

PCWP(mm Hg)

CI+(L/min/m2)

CLINICALSIGNSSUBSET

PENGARUH OBAT-OBATAN PADA HEMODINAMIK DAN KEBUTUHAN O2 PADA IMA

- HR

- KONTRAKSI >

- TEK. DARAH

- COR <

- COR <

- HR

- KONTRAKSI

= /

= /

= /

=

INOTROPIK

VASODILATOR

DIURETIKA

BLOCKER

OBAT HEMODINAMIK KEBUTUHAN O2

CI PCWP EFEK MEKANISME

A suggested therapeutic approach in hypotensive patients is outlined. ( = increase; = decrease; CO = cardiac output; SVR = systemic vascular resistance; AP = arterial pressure; PCWP = pulmonary capillary wedge pressure; IABP = intra-aortic balloon counterpulsation. )

Initial therapy Dopamine or Norepinephrine

CO, SVR, PCWP, AP AP, CO, PCWP Add Dobutamineor Amrinone

Inadequate AP, CO, PCWP

IABP

AddSodium Nitroprusside

or Nitroglycerin

InadequateCO, PCWP

Inadequate CO, PCWP

Inadequate CO, PCWP

Evaluation forSurgical Therapy

Inadequate PCWP

Inadequate CO

Add IABP

Add Dobutamine or Amrinones or Nitroglycerin

Add Nitroglycerin

Add Dobutamine or Amrinone

Add Sodium Nitroprusside or Phentolamine

Hemodynamic Monitoring

The sequence of ballon inflation and defaltion timed with cardiac cycle Ballon inflation (A) occurs early in diastole and results in an increase in diastolic pressure and improvement in cerebral and coronary blood flows. Ballon deflation (B) prior to ventricular systole enhances left ventricular ejection. (Bolooki, H. (ed) in Clinical Application of Intra-Aortic Balloon Pump, 1977: p.14)

A B

Tabel 4. Perubahan hemodinamik pada berbagai penyebab penurunan cardiac output.

Keterangan : A.K. = atrium kananPCWP = pulmonary capillary wedge pressureTDAP = tekanan diastolik a. pulmonalisSIV = septum inter ventrikuler

( Chatterjee, K. : Crit Care Clin, 1 : 572, 1985 )

Syok hipovolemik

Syok kardiogenik

Infark ventrikel kanan

Mitral insufisiensi

Cardiac tamponade

Ruptura SIV

N /

/ N

TDAP = PCWP

TDAP = PCWP

TDAP = PCWP

TDAP < PCWP

TDAP = PCWP

TDAP = PCWP

N /

-

-

+

-

+

-

Tek. A.K. PCWP EkualisasiTek. Diast.

TDAP - PCWP

Predicted probability for the in-hospital development of cardiogenic shock according to the number of independent risk factors present. Risk factors include age > 65 years, left ventricular ejection on admission < 35%, peak MB CK > 160 IU/liter, history of diabetes mellitus and previous myocardial infarction. MB CK = MB fraction of creatine kinase.

0 1 2 3 4 5

No. of Independent Risk Factors Present

Pre

dic

ted

Pro

bab

ilit

y (%

)

60

50

40

30

20

10

0

The “double-edged sword” of compensatory changes in shock

• Systemic vasoconstriction maintains blood flow to vital organs

• Inflammatory mediator release facilitates phagocytosis and resolution of injury

• Less essential circulations sacrificed, massive tissue ischemia and lactic acidosis

• Prolonged and/or overwhelming mediator release leads to the systemic inflammator response syndrome (SIRS) and multiple organ failure.

The effects of cardiac output and systemic vascular resistance on blood pressure

SVR increased

Systemic vascular resistance (SVR)

SVR decreased

Blood pressure

CO decreased

Cardiac output(CO)

CO increased

Tabel 5. Perubahan hemodinamika kegagalan jantung kiri serta pengobatan yang dianjurkan.

( Gunnar, R.M. et al.: Task fprce IV. Am J Cardiol, 50: 393-408, 1982)

Gol

I

II

III

Manifestasi klinik

Kongesti pulmonal

Kongesti pulmonal

cardiac output perfusi

Syok

CI (L/min/m2)

> 2,5

< 2,5

< 2,5

PCWP

> 18

> 18

> 18

Tek. Sist.

> 100

> 100

< 90

Pengobatan

- Diuretika

- Nitrogliserin

- Nitroprusid

- Fentolamin

- Dobutamin

- Dopamin

- Norepinefrin

- IABC

- vasodilator

Schematic representation of ventricular performance changes during the acute and recovery periods of septic shock in humans. (With permission from Parrillo JE et al: Septic shock in humans : advances in the understanding of pathogenesis, cardiovascular dysfunction and therapy, Ann Intern Med 113:228, 1990)

From Knaus WA, Wagner DP : Multiple systems organ failure: epidemiology and prognosis, Crit Care Clin 5:223, 1989