CENTRAL VENOUS PRESSURE–GUIDED DE-

RESUSCITATION IN MANAGING
OVERLOAD IN ICU

CHANGING PARADIGM IN FLUID

MANAGEMENT

Yohanes George
 TARGET DERESUSITASI
PROTOKOL DERESUSITASI FARMAKOLOGI YANG AMAN DENGAN
MENGUNAKAN:
A. TARGET ENDPOINT PHYSIOLOGY
1. target klinis (resolusi edema, perbaikan oksigenasi paru)
2. Target fluid balans 24 jam – 1 Liter (20%)
B. TARGET SAFETY PERFUSION.
1. Lactate darah <1 mmol/L
2. Target fungsi ginjal, peningkatan ureum dan creatinin <25% dan
3. Target perubahan Na < 4 mmol/L.

S. Goldstein, S. Bagshaw, M. Cecconi, M. Okusa, H. Wang, J. Kellum, M. Mythen and A. D. Shaw for the ADQI XII Investigators Group.
Pharmacological management of fluid overload. British Journal of Anaesthesia 113 (5): 756–63 (2014).
Target balance negatif belum tercapai, Lasik  RRT
masih edema, oksigenasi masih buruk

Lactate > 1, Creatinin naik >25%,

Na naik > 4 mmol/L
Stop lasik 
fluid terapi?
• Rationale for using diuretics:
– to ameliorate AKI includes prevention of tubular obstruction,
– reduction in medullary oxygen consumption and increase in renal
blood flow
– reducing fluid overload and venous congestion
• Surrogate Parameter for fluid overload;
– Increased CVP
– peripheral edema
– increased intra-abdominal pressure
• Diuresis responsiveness; urinary output of at least 100 ml/h
following a test dose of 1.0–1.5 mg furosemide/kg BW predicted
reduced progression to a higher stage of AKI in oliguric patients
CENTRAL VENOUS PRESSURE AND TOTAL FLUID

Marik, Bellomo. A rational approach to fluid therapy in sepsis. Review article. British Journal of Anaesthesia, 2015
CENTRAL VENOUS PRESSURE AND TOTAL
FLUID OF RESUSCITATION
CENTRAL VENOUS PRESSURE AND TOTAL
FLUID OF RESUSCITATION
CENTRAL VENOUS PRESSURE AND TOTAL
FLUID OF RESUSCITATION
 GUYTON’S THEORY

CARDIAC OUTPUT
RETURN FUNCTION CARDIAC FUNCTION

CVP  CONTRACTILITY

 GRADIENT
PRESSURE
CVP-Pms

Pms

Circulatory Physiology: Cardiac Output And Its Regulation. A.C. Guyton.W.B. Saunders
Co. Philadelphia 1963
 YANG MENENTUKAN CARDIAC OUTPUT
MENURUT GUYTON
CARDIAC OUTPUT
RETURN FUNCTION CARDIAC FUNCTION
CONTRACTILITY

CVP = 0
CENTRAL VENOUS
PRESSURE 1
RVR 3
RESISTANCE TO VENOUS RETURN
DIAMETER VEIN CAVA AND BLOOD
VISCOSITY
2
GRADIENT PRESSURE
MCFP-CVP

MCFP = 8
MEAN SYSTEMIC FILLING PRESSURE
 STRESSED VOLUME (NON-SPLANCHNIC
CIRCULATION)

Circulatory Physiology: Cardiac Output And Its Regulation. A.C. Guyton.W.B. Saunders
Co. Philadelphia 1963
 HUBUNGAN ANTARA PENINGKATAN CVP
DAN KEJADIAN AKI
VENOUS RETURN = CARDIAC OUTPUT

RETURN FUNCTION CARDIAC FUNCTION

FLUID LOADING, HEART

FAILURE  CVP 

 GRADIENT PRESSURE Transmitted backward pressure

 Kidney venous pressure.
CVP - Pms

CONGESTIVE
MCFP KIDNEY FAILURE

Circulatory Physiology: Cardiac Output And Its Regulation. A.C. Guyton.W.B. Saunders
Co. Philadelphia 1963
CVP AND AKI AND MORTALITY IN
HEART FAILURE
CVP AND AKI AND MORTALITY
CENTRAL VENOUS PRESSURE AND
ACUTE KIDNEY INJURY IN SEPSIS
CENTRAL VENOUS PRESSURE AND GUIDING FLUID
DE-RESUSCITATION
MONITORING HEMODYNAMIC DURING FLUID
REMOVAL
Total blood volume No
Change post furosemide
Furosemide significant
decreased PAOP

Furosemide significant
decreased CVP
ICU RSPI – PRE-ELIMINARY
De-Resuscitation Strategy Targeting Low Central Venous Pressure
in Post Laparoscopic Appendectomy With Severe Sepsis and Fluid
Overload

• Forty six-years old patient admitted to the Emergency Department with severe
sepsis ec intra abdominal infection due to acute appendicitis complicated with
acute kidney injury and disseminated intravascular coagulopathy (DIC). After
receiving significant fluid resuscitation and antibiotic (meropenem 3x2 gram and
metronidazole 2x1 gram), he underwent laparoscopic appendectomy and admitted
to ICU.
• On arrival, he was sedated and ventilated, with signs of tissue hypoperfusion
(anuria, lactate was 8.3 mmol/l). Circulation was supported by noradrenaline (0.12
μg/kg/minute) and dobutamine (5 μg/kg/minute). The patient had a low dynamic
compliance of the respiratory system (CRS value) 28 ml/cmH2O with a PaO2/FIO2
ratio up to 160, dilated IVC and significant B-lines. His cumulative fluid balance
prior to ICU admission was positive, up to 2700 ml.
• Furosemide infusion was started 2 hours later, aiming to achieve a negative fluid
balance of up to 1000-2000 ml/24 h and CVP 0-2mmHg. Sustained low-efficiency
dialysis (SLED) was also initiated due to increasing sCr and Ur. SLED and furosemide
infusion continued up to full stabilization of the renal function in the patient. The
patient was discharged to the ward on 5th day
14

0-2
 ICU RSPI – PRE-ELIMINARY
“CVP-driven de-resuscitation prevents acute kidney
Case series: 3 septic + 1 DSSinjury”
1. Pasien A, laki laki 46 tahun paska prosedur appendektomi
laparoskopi dengan sepsis intraabdominal berat.
2. Pasien B, laki-laki berusia 58 tahun sepsis pneumonia paska syok
kardiogenik disebabkan oleh infark miokardium anterior luas.
3. Pasien C, anak 12 tahun paska laparotomi eksplorasi karena
peritonitis generalisata.
4. Pasien D, anak 10 tahun dengan sindroma syok dengue, efusi
pleura dan sepsis pneumonia.
Conclusion
 Conclusion

• High CVP is a surrogate marker of fluid overload

• High CVP is harmfull and correlate with AKI
• Furosemide de-resuscitation decreased CVP and
decreased risk of AKI
• Continuous drip furosemide didn’t affect hemodynamic
Terima kasih