The Vicious Circles that Lead to the .

EXAMPLES OF VICIOUS CIRCLE CONCEPT

Massive Myocardial Infarction

CI

GUT Integrity RES Compromise

4 - Response VR 3rd Space Sequestration ECFV

Capacitane Bed Pooling

. Final Common Pathway of Circulatory Failure and death Myocardial Depression

Release of Bacteria & Their Products

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)

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

Infark ventrikel kanan

SYOK

Gangguan mekanik - ruptura : + septum + dinding ventrikel + m. papillaris - disfungsi m. papillaris

Gb. 1. Penyebab syok kardiogenik pada infark miokard ( Schreiber, T.L. et al; Am Heart J, 117 : 436, 1989 )

Arterioles Interstitial fluid (the buffering sea in which cells reside)

Blood flow

Capillary bed

Oxygen Carbon dioxide Nutrients

Venules

THE CAPILLARY EXCHANGER

THE CELL (metabolic factory)

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.

Impaired cellular Oxygen 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 hypoxic sequence of cellular events in shock

Inadequate myocardial perfusion

Reduction in coronary perfusion pressure and coronary blood flow

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

Critical decrease in stroke volume, decreased arterial pressure The self-perpetuating vicious cycle of progressive myocardial damage and dysfunction in AMI shock.

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 Respons hemodinamik Respons sirkulasi perifer - Takhikardi - Kontraktilitas - Preload ventrikel - Tekanan pengisian ventrikel - Tahanan perifer - Tonus vena perifer - Volume intra vaskuler - Perfusi organ vital

Tekanan darah

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)

Respons kompensasi Takhikardi Kontraktilitas Volume end-diastolik Tekanan diastolik ventrikel kiri

Efek sampingan Kebutuhan O2 Perfusi miokardium

Kebutuhan O2
Kebutuhan O2 Perfusi subendokard Kongesti pulmonal Hipoksemia

Tahanan perifer sistemik

Afterload dan cardiac output Kebutuhan O2

TABEL 3. EFEK SAMPINGAN PADA JARINGAN AKIBAT RESPONS KOMPENSASI GAGAL JANTUNG ( Chatterjee, K. : Crit Care Clin, 1: 569, 1985 )

CLINICAL

SYST. ART. PRESS

CI*

PERI

PCWPP**

VASC. RES.
N/ N USUALLY /

I. II.

UNCOMP MILD CHF

N/ USUALLY N

III. SEVERE CHF IV. SHOCK : CARDIOGENIC HYPOVOLEMIC

* CI :

N/

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 NORMAL = 10 12 mmHg OPT WITH AMI = 14 18 mmHg

** PCWPP :

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

DIAGNOSIS
KLINIK

- 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 DINI 2. KOREKSI FAKTOR-FAKTOR PRESIPITASI 3. PEMANTAUAN HEMODINAMIK 4. PENGOBATAN MEDIKAMENTOSA 5. IABC 6. PTCA 7. TINDAKAN BEDAH

PENGELOLAAN LOW CARDIAC OUTPUT SYNDROME

1. 2. 3. 4. ADAKAH KOMPLIKASI PERDARAHAN, TAMPONADE, INFARK MIOKARD. KOREKSI FAKTOR NON KARDIAK RESPIRASI, ASAMBASA, ELEKTROLIT. OPTIMASI HR/IRAMA ( 90 100 / men ) OPTIMASI PRELOAD ( PCWP 15 18 mmHg ) - CAIRAN - TRANSFUSI BILA Ht < 30 % HITUNG CARDIAC OUTPUT BILA CI < 2 l/m2/min INOTROPIK - DOPAMINE DOBUTAMINE - CaCl2 - EPINEFRIN + CaCl2 - DIGOXIN HITUNG SVR IABP

5.

6. 7.

 PCWP/tek. Pengisian ventrikel kiri Cardiac indeks

> 18 mmHg < 2.2 L/men/m2

Tabel 1. Gambaran hemodinamik syok kardiogenik

PCWP (mmHg) HI H II H III H IV < 18 > 18 < 18 > 18

CI (L/men/m2) > 2.2 > 2.2 < 2.2 < 2.2

PERUBAHAN HEMODINAMIKA PADA AKUT MIOKARD INFARK ( FORRESTER DKK : N.ENGL J MED; 295: 1361, 1976

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

Steps PAWP/PADP (mm Hg) Fluid Infusion Rate

Observe PADP/PAWP for 10 min before challenge During infusion (0-9 min) Immediately following 10-min infusion After 10-min wait

< 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

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.

Fluid Challenge : CVP ( 5-2 Rule )

Steps CVP (cm H2O) Fluid Infusion Rate

Observe CVP for 10 min before challenge During infusion (0-9 min) Immediately following 10-min infusion After 10-min wait

<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

CVP = central venous 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.

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

CLINICAL SIGNS
Pulmonary congestion Pulmonary congestion Decreased perfusion Shock

CI+ PCWP (L/min/m2) (mm Hg) > 2.5 < 2.5 > 18 > 18

SAP (mm Hg) > 100 > 100

SUGGESTED THERAPY Diuretics Nitroglycerin Nitroprusside Phentolamine

I
II

III

< 2.5

> 18

> 90

Dobutamine Dopamine Norepinephrine Intraaortic ballon counterpulsation Vasodilators

* 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.

OBAT

HEMODINAMIK CI PCWP =/

KEBUTUHAN O2 EFEK MEKANISME HR KONTRAKSI > TEK. DARAH COR < COR < HR KONTRAKSI

INOTROPIK

=/

VASODILATOR DIURETIKA BLOCKER

=/

PENGARUH OBAT-OBATAN PADA HEMODINAMIK DAN KEBUTUHAN O2 PADA IMA

Initial therapy

Dopamine or Norepinephrine

Hemodynamic Monitoring
Add Sodium Nitroprusside or Phentolamine CO, SVR, PCWP, AP

AP, CO, PCWP

Add Dobutamine or Amrinone

Add Dobutamine or Amrinone Add Nitroglycerin Add Dobutamine or Amrinones or Nitroglycerin

Inadequate CO

Inadequate PCWP
Inadequate CO, PCWP Inadequate AP, CO, PCWP IABP

Add IABP

Inadequate CO, PCWP

Inadequate CO, PCWP

Add Sodium Nitroprusside or Nitroglycerin

Evaluation for Surgical Therapy

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. )

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)

Tek. A.K.
N/ /N

PCWP
N/

Ekualisasi Tek. Diast. + + -

TDAP - PCWP

Syok hipovolemik Syok kardiogenik Infark ventrikel kanan Mitral insufisiensi Cardiac tamponade Ruptura SIV

TDAP = PCWP TDAP = PCWP TDAP = PCWP TDAP < PCWP TDAP = PCWP TDAP = PCWP

Tabel 4. Perubahan hemodinamik pada berbagai penyebab penurunan cardiac output. Keterangan A.K. = atrium kanan PCWP = pulmonary capillary wedge pressure TDAP = tekanan diastolik a. pulmonalis SIV = septum inter ventrikuler ( Chatterjee, K. : Crit Care Clin, 1 : 572, 1985 ) :

60 Predicted Probability (%) 50 40 30 20

10
0 0 1 2 3 4 5

No. of Independent Risk Factors Present

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.

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 double-edged sword of compensatory changes in shock

CO increased
SVR increased

Cardiac output (CO) Systemic vascular resistance (SVR)

CO decreased Blood pressure SVR decreased

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

Gol

Manifestasi klinik

CI (L/min/m2)

PCWP

Tek. Sist.

Pengobatan

Kongesti pulmonal

> 2,5

> 18

> 100

- Diuretika - Nitrogliserin

II

Kongesti pulmonal cardiac output perfusi

< 2,5

> 18

> 100

- Nitroprusid - Fentolamin

III

Syok

< 2,5

> 18

< 90

- Dobutamin

- Dopamin
- Norepinefrin - IABC - vasodilator 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)

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