Low cardiac output or shock or circulatory failure was the terminal state of any disease including cardiovascular problem. It is consist distributive, volume, obstructive and cardiogenic circulatory failure leading multi organ failure and mortality. Hemodynamic monitoring is important evaluation to guide the medication and treatment.

1. Workshop
Low Cardiac Output Management
ASMIHA 2018
Isman Firdaus, MD
FIHA, FAsCC, FAPSIC, FESC, FSCAI

2. FACULTY
Instructor Qualification and Institution
Dr. Isman Firdaus, SpJP(K), FIHA, FAsCC, FAPSIC,
FESC, FSCAI
Cardiovascular Intensivist-Intervensionist
ICVCU Harapan Kita Hospital
Dr. Dafsah A Juzar, SpJP(K), FIHA, FAsCC, FAPSIC,
FESC
Cardiovascular Intensivist-Intervensionist
ICVCU Harapan Kita Hospital
Dr. Rita Zahara, SpJP(K), FIHA Cardiovascular Intensivist
ICU Post Cardiac Surgery Harapan Kita
Hospital
Dr. M. Fadhil, SpJP(K), FIHA Cardiovascular Intensivist-Intervensionist
RSUP M Djamil Padang
Dr. Siska Suridanda, SpJP(K), FIHA Cardiovascular Intensivist-Intervensionist
ICVCU Harapan Kita Hospital
Dr. Akhtar, SpJP(K), FIHA Cardiovascular Intensivist-Intervensionist
ICVCU RS Wahidin Makassar

3. The Objectives
1. Definition, pathophysiology and clinical diagnosis of LCO
2. Volemic, distributive, obstructive and cardiogenic shock
3. Hemodynamic assessment of LCO invasive and non
Invasively: Preload assessment, Afterload, Contractility
4. vasoactive drugs, such as vasopressor (noradrenaline,
adrenaline, and vasopressin)
5. Hemodynamic interpretation with simulation cases and
how to intervene
6. knowledge and Skill of CVC line insertion
7. Skills on hemodynamic assessment using non invasive
device

4. Time Topics Instructor
07.30 – 08.00 Re-registration
08.00 – 08.30 Opening Isman Firdaus, MD
Pretest All Instructors
08.30 – 09.00 Definition, and Clinical Diagnosis of LCO + Care Plane in ICVCU Isman Firdaus, MD
09.00 – 09.30 Introduction of Hemodynamic Monitoring Rita Zahara, MD
09.30 – 10.00 ABC of Acute Heart Failure M. Fadhil , MD
10.00 – 10.30 Coffee Break
10.30 – 11.15 Preload Assessment and Fluid Management in ICCU Dafsah A Juzar, MD
11.15 – 12.00 Cardiac Output and Afterload problem in ICCU: Non-Invasive and
Invasive Measurement
Isman Firdaus, MD
12.00 – 13.30 Lunch
13.30 – 14.00 Pressor vs Inotropic Support in Low Cardiac Output State: Tips and
Tricks
Retno Widowati, MD
14.00 – 14.30 Device in ICCU: Management and Complication Akhtar F Muzakkir, MD
14.30 – 15.00 Case discussion:
Cardiogenic Shock Case
Device Case
Preload Case
All Instructors
15.00 – 15.30 Post Test
Closing
All Instructors
Isman Firdaus, MD
Workshop on Acute Cardiovascular Care: Low Cardiac Output Management in ICCU
Day, date : Thursday, April 19, 2018
Venue : Mutiara 10, Ritz-Carlton Hotel, Jakarta
Time : 07.30 – 16.00

5. Definition and Clinical Diagnosis of Low Cardiac Output
(Volume, Distributif, Obstructive, and Cardiogenic)
Isman Firdaus, MD
FIHA, FAsCC, FAPSIC, FESC, FSCAI
Intensive Cardiovascular Care Unit, National Heart Center, Harapan Kita Hospital/
Departement of Cardiology and Vascular Medicine,
Faculty of Medicine, University of Indonesia

6. TERMINOLOGY
Circulatory Failure
Shock
Low Cardiac Output State

7. • Low cardiac output syndrome as the requirement
for MCS or inotropic support for longer than 30
minutes in intensive care unit to maintain the
systolic blood pressure higher than 90 mm Hg
and the cardiac index greater than 2.2 L/min per
square meter (Rao et all)

8. What is Circulatory Failure?
• circulatory failure
Etymology: L, circulatio + fallere, to deceive
“inability of the cardiovascular system to supply the cells
of the body with enough oxygenated blood to meet their
metabolic demands. The condition may result from
abnormal cardiac function, as in myocardial infarction;
from an inadequate circulating volume of blood, as
occurs in hemorrhage; or from mass systemic
vasodilation, as may occur in gram-negative septicemia”.
See also shock.
Mosby's Medical Dictionary, 8th edition. © 2009, Elsevier.

9. Cardiogenic Shock:
• Sindrom klinis yang disebabkan oleh gagal perfusi
akibat gangguan fungsi jantung yang ditandai
dengan nadi lemah, penurunan MAP < 65 mmHg,
penurunan cardiac index, terdapat peningkatan
LVEDP (LVEDP > 18 mmHg), dan penurunan curah
jantung (CO < 3,2 L/mnt)
• Syok kardiogenik dapat disebabkan oleh sindrom
koroner akut, masalah valvular, dan gagal jantung
yang berat, komplikasi mekanik ACS seperti
chordae rupture, IVS rupture, dan free wall
rupture.

10. Anamnesis
– Gangguan kesadaran mulai dari kondisi ringan hingga berat
– Penurunan diuresis
– Dapat disertai keringat dingin
– Nadi lemah

11. Pemeriksaan Fisik
– Terdapat tanda tanda hipoperfusi seperti perabaan kulit
ekstremitas dingin, takikardi, nadi lemah, hipotensi, bising
usus berkurang, oliguria
– Terdapat tanda-tanda peningkatan preload seperti JVP
meningkat atau terdapat ronki basah di basal
– Profil hemodinamik Forrester: basah dan dingin (wet and
cold)

12. Kriteria Diagnosis:
– Memenuhi kriteria anamnesis
– CO < 3,2 L/mnt atau CI < 2,2
– SVR meningkat pada fase awal, normal atau menurun pada
kondisi lanjut
– Pre load cukup atau meningkat
– TAPSE < 1,5 cm dari pemeriksaan ekokardiografi
– Diuresis < 0,5 mL/KgBB/jam

13. Target Tatalaksana
• Subjektif : tidak ada keluhan
• Objektif :
– MAP > 65 tanpa support inotropic atau MCS, atau TDS
>90 mmHg
– Diuresis > 1 cc/kg/jam
– CI > 2,2 atau CO > 3,5
– Residu –
 CARE PLAN

14. Cardiac Output and Afterload
problem in ICCU: Non-Invasive and
Invasive Measurement
Isman Firdaus, MD
FIHA, FAsCC, FAPSIC, FESC, FSCAI

15. What Do You Need to Know When You
Resuscitate a Patient in Shock?
• Arterial blood pressure
• Urine output
• Systemic acid–base balance (pH, SBE, lactate)
• Clinical assessment of tissue perfusion
– “warm and well perfused” or “cold and shut down”
• Measurement of global blood flow and tissue
perfusion
– Cardiac output or cardiac index
• Arterial oxygen delivery, oxygen uptake index
• Mixed venous saturation and PvO2

16. Characteristics of circulatory shock
Complex clinical syndrome encompassing a group of
conditions with variable hemodynamic manifestations
Common denominator is generalised inadequacy of
blood flow through the body; hypoperfusion
compromises the delivery of oxygen and nutrients
and the removal of metabolites; tissue hypoxia shifts
metabolism to anaerobic pathways with production of
lactic acid
if shock is not corrected it leads to:
a) cell dysfunction
b) irreversible multiorgan insufficiency
d) death
Characteristics of circulatory shock

17. Etiology of circulatory shock
1. Hypovolemic - intravascular fluid volume loss
hemorrhage, fluid depletion or
sequestration
2. Cardiogenic - impairment of heart pump
myopathic lesions: myocardial
infarction, cardiomyopathies
dysrhythmias
obstructive and regurgitant lesions of
intracardial blood flow mechanics

18. 3. Obstructive - factors extrinsic to cardiac valves and
myocardium
v. cava obstruction, pericardial
tamponade,
pulmonary embolism,
coarctation of aorta
4. Distributive - pathologic redistribution of intravascular
fluid volume
septicaemia: endotoxic, secondary to
specific infection
anaphylactic

19. HYPOVOLEMIC
EXTRACARDIAC
Obstruction CARDIOGENIC DISTRIBUTIVE
Fluid loss,
hemorrhage
e.g., Pericardial
tamponade
Myocardial
injury or
necrosis
Decreased
systemic
vascular
resistance
Myocardiac
dysfunction
Reduced
systolic performance
Reduced
filling
Low cardiac
output
Reduced
preload
Decreased arterial
pressure
Shock
Multiple organ
system failure
High or normal
cardiac output
Maldistribution
of blood flow in
microcirculation

20. Main Goal of Tx
Tissue perfusion &
oxygenation

21. Diuretikc
Vasodilator
Inotropic drugs :
Dobutamine
Milrinone
Levosimendan
COLD
(MAP < 70)
WET
PCWP >18
WARM
(MAP>70)
DRY
PCWP < 18

22. GAGAL
JANTUNG AKUT
Resusitasi segera
Distres atau nyeri
Diagnosis
definitif
Normal HR dan irama
Saturasi O2 >95%
MAP > 70
Naikkan FiO2,
CPAP,NIPPV
BCLS/ACLS
Preload
adekuat
Monitoring invasif, kateter
swan gans bila perlu
Tdk
Ya
tdk
ya
tdk
ya
ya
Algoritma
diagnosis
CO cukup : perbaiki asidosis
metabolik, SvO2 > 65%, tanda
klinis perfusi adekuat
tdk
ya
tdk
Pacing, anti
aritmia
tdk
ya
Analgesia/sedasi
Vasodilator,
pertimbangkan diuresis
bila volume overload
Fluid challenge
Inotropik/
Vasopresor /
IABP
Evaluasi
Tatalaksana
definitif
Algoritme Tatalaksana Cepat GJA

23. Goals ofMonitors
To assure the adequacy of perfusion
Early detection of inadequacy of perfusion
To titrate therapy to specific hemodynamic end point
To differentiate among various organ system
dysfunctions
Hemodynamic monitoringforindividualpatientshouldbe
physiologicallybasedand goal oriented

25. Advance in haemodynamic assessment
• Modification of old equipment
• Echocardiogram and esophageal doppler
• Pulse contour analysis and transpulmonary thermodilution
• Partial carbon dioxide rebreathing with application of Fick
principle
• Electrical bioimpedance

26. Central Venous
Catheter
Injectate temperature
sensor housing
PULSIOCATH thermodilution catheter
Injectate temperature sensor cable
PULSION disposable pressure transducer
Temperature interface cable
Pressure cable
PiCCO2 Setup

27. ECHO VS INVASIVE

28. Transthoracic echo
• Assessment of
– cardiac structure
– ejection fraction
– cardiac output
• Based on 2D and doppler flow
technique

29. Physiological Principles
MAP = CO x SVR
CO = HR x SV
Preload Contractility Afterload
~ 1
r4

30. Basic principles - Vasopressors
MAP = CO x SVR
CO = HR x SV
Preload Contractility Afterload
~ 1
r4

31. Basic principles - Inotropes
MAP = CO x SVR
CO = HR x SV
Preload Contractility Afterload

32. How to measure CO and SVR
Direct measurement
• Echo bed side
• Continuous Hemodynamic Monitoring (PiCCO,
Vigileo etc)
• Impedance Physioflow
SVR : MAP – CVP x 80
HR x SV
SV : VTI x CSA

33. THANK YOU

34. KASUS 1
• Laki-laki 35 th dengan DCM datang ke IGD dengan
keluhan lemas
• EF 28 %
• Obat-obatan :Furosemide 3 x 1 tab, Captopril 2 x
25 mg, Bisoprolol 1 x 5 mg
• TD 80/20 HR 120 x/mnt
• IVC 12/2
• SVR 1800
• TAPSE 2,8

35. Kesan gambaran hemodinamik?
Intervensi yang harus dilakukan?

36. Kasus 2
• Wanita, 75 tahun, Riwayat CHF lama dalam
pengobatan
• Keluhan nafas cepat
• Riwayat demam 3 hari SMRS
• TD 75/40
• HR 112x/mnt
• T=38
• EF 35%, Global hipokinetik
• IVC 17/12
• SVR 400

37. Kesan gambaran hemodinamik?
Intervensi yang harus dilakukan?