Physiology of Venous Return Cardiac Output

Guyton Model

Rumaisah Satyawati
Guyton Physiology = Right Heart Physiology
 PENDAHULUAN
JANTUNG KIRI VS JANTUNG KANAN

PRELOAD

KONTRAKTILITAS

AFTERLOAD

Penyakit jantung iskemik Syok hipovolemik

Penyakit jantung kongestif Syok kardiogenik
Syok distributif
Syok obstruktif
INTENSIVIST
???
Funk, Duane J, Eric Jacobsohn. The Role of Venous Return in Critical Illness and
Shock—Part I: Physiology. Critical Care Medicine 2013
 PENDAHULUAN
Jantung hanya dapat memompa ke arteri dari apa yang jantung terima

INPUT OUTPUT
(VR) (CO)

Jantung kanan Stroke Volume

Sirkulasi perifer Heart rate

 PRINSIPNYA JANTUNG KANAN

• Perpanjangan system vena,

• Tidak bisa mengikuti hukum frank starling,
karena komplians nya sangat besar ,
• Tidak mudah berkontraksi, namun masih bisa
mengalirkan darah, karena fungsi utama ,
mengalirkan dari atrium kanan ke arteri
pulmonalis.
 KARAKTERISTIK SISTEM VENA
1
DISTENSIBILITAS

(penambahan volume pada

setiap peningkatan 1 mmHg Distensibilitas sistemik vena 8x dibanding arteri
tekanan)
Distensibilitas pulmonal vena 6x dibanding arteri

2
KOMPLIANS

(total darah yang dapat Komplians vena 24x dibanding arteri

disimpan dalam sirkulasi
untuk setiap peningkatan
tekanan 1 mmHg) Vena adalah penampung darah
IDEAL
Guyton, Arthur C, John E. Textbook of Medical Physiology. 11 th ed. Vascular Distensibility and Functions of the
Arterial and Venous Systems. 2006.
FUNCTION OF THE VENOUS SYSTEM
Distribution Of Blood In The Various Components Of The
Circulatory System

64%
 FRANK-STARLING LAW OF THE HEART

“AN INCREASE IN THE VOLUME OF BLOOD FILLING THE HEART STRETCHES

THE VENTRICULAR WALL, CAUSING CARDIAC MUSCLE TO CONTRACT
MORE FORCEFULLY AND STROKE VOLUME TO INCREASE.”
 FRANK STARLING CURVE IN CRITICALLY
ILL FLUID MANAGEMENT
flat
CVP 8-12 mmHg
GEDVI >800 Preload-Independence =
Wedge pressure Artinya, setiap peningkatan preload pada
SVV/PPV area ini TIDAK akan meningkatkan stroke
PLR Will increase the stroke volume volume, bahkan dapat menurunkan stroke
FluidVolume
Stroke Responsive, SV >10% steep volume yg akan menyebabkan “low cardiac
output”

Preload-dependence =
Artinya, setiap peningkatan preload by volume
loading pada area ini akan meningkatkan stroke
volume, sehingga cardiac output akan meningkat

Every increasing preload by volume loading

Preload
 THE IMPACT OF STARLING’S PRELOAD
DEPENDENCY TO FLUID MANAGEMENT
PHYSIOLOGY OF VOLUME
FLUID BOLUS RESUSCITATTION IN CRITICALL ILL
OR FLUID
RESPONSIVENESS
Glycocalix damage - Increased
CYSTALLOID permeability/gap
INFUSION

Leakage


Interstitial
INCREASE FILLING
hypovolemia

Fluid shift
Plasma

PRESSURE  ATRIAL
NATRIURETIC
PEPTIDE (ANP)
LAUNCHED Lymph

In critical illness 
Urine output leakage >> lymph flow
decrease  STILL
HYPOPERFUSION  tissue edema
 WHAT ABOUT SEPSIS
PROTOCOL?

CRITIQUES OF EGDT
(RIVERS STUDY)
 EGDT IN THE TREATMENT OF SEVERE SEPSIS
AND SEPTIC SHOCK

Aggressive fluid resuscitation

achieving CVP 8-12 mmHg
using crystalloid then colloid

Rivers. NEJM 2001

OVERLOAD
 EVIDENCE SUPPORTING THE DELETERIOUS
EFFECTS OF AGGRESSIVE FLUID
RESUSCITATION IN SEPSIS

Marik, Bellomo. A rational approach to fluid therapy in sepsis. Review article. British Journal of Anaesthesia, 2015
• Studi against EGDT Rivers yaitu ARISE, PROMISE & Jenssen
menunjukkan pasien2 sepsis yang diloading cairan tanpa target CVP 8-
12 mempunyai angka kematian yang jauh lebih kecil dari angka
kematian pada studi EGDT Rivers.

• Semakin banyak jumlah total cairan resusitasi pada hari ke 3 semakin

tinggi angka kematian.
• Semakin banyak total cairan yang diberikan semakin naik nilai CVP.

• Peningkatan CVP sebenarnya menggambarkan jumlah total cairan

tubuh bukan total intravascular volume atau cardiac preload.
• Studi2 terdahulu gagal membuktikan CVP sebagai parameter endpoint
resusitasi.

• Dengan catatan cairan resusitasi adalah kristaloid maka jelas penyebab

peningkatan kematian akibat terjadinya fluid overload.
 WHAT DETERMINES CARDIAC
OUTPUT?

CARDIAC OUTPUT
VENOUS RETURN

THE HEART CANNOT PUT OUT MORE

THAN WHAT IT GETS BACK FROM THE
LARGE RESERVOIR OF VOLUME IN THE
SYSTEMIC CIRCULATION

Circulatory Physiology: Cardiac Output And Its Regulation. A.C. Guyton.W.B. Saunders
Co. Philadelphia 1963
 WHAT DETERMINES CARDIAC
OUTPUT?
CARDIAC OUTPUT

RETURN FUNCTION CARDIAC FUNCTION

STROKE VOLUME X HR
AFTERLOAD
CVP
CENTRAL VENOUS
PRESSURE 1 PRELOAD
CONTRACTILITY

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

MCFP
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
WHY VENOUS RETURN?
 VENOUS RETURN
• The quantity of blood which returns to the heart from peripheral
circulatory system
• Three principal factors that affect venous return to the heart from
the systemic circulation:
– Right atrial pressure (RAP = CVP), which exerts a backward force on the
veins to impede flow of blood from the veins into the right atrium.
– Degree of filling of the systemic circulation (measured by the Mean
Circulatory Filling Pressure = MCFP), which forces the systemic blood
toward the heart (this is the pressure measured everywhere in the systemic
circulation when all flow of blood is stopped).
– Resistance to blood flow (RVR) between the peripheral vessels and the
right atrium.

1. Guyton AC: Determination of cardiac output by equating venous return curves with cardiac response curves. Physiol Rev
1955; 35:123–129
2. Guyton AC, Lindsey AW, Kaufmann BN: Effect of mean circulatory filling pressure and other peripheral circulatory factors on
cardiac out- put. Am J Physiol 1955; 180:463–468
GUYTON’S VENOUS RETURN CURVE
Recently dead dog:
TRANSFUSION a pump replacing the heart
INCREASE MCFP & RA  pump  Aorta
RAP/CVP MCFP changed by increasing or
VENOUS RETURN BECOMES
decreasing the total quantity of
ZERO WHEN THE RIGHT blood
ATRIAL PRESSURE RISES TO
EQUAL THE MEAN SYSTEMIC
FILLING PRESSURE

DETERMINANTS OF VENOUS RETURN:

• Right arterial ressure (Pra)
• Mean circulatory filling pressure
(MCFP)
MCFP SHOULD BE HIGHER THAN
RAP/CVP  GRADIENT PRESSURE 8
mmHg

AC Guyton. Determination of cardiac output by equating venous return curves with cardiac
response curves physiol Rev 1955; 35: 123-139
GUYTON COMBINED VENOUS RETURN CURVE WITH
STARLING’S CARDIAC FUNCTION CURVE

WORKING
POINT
VENOUS RETURN AND CARDIAC
liters/m2/min
OUTPUT

0
RIGHT ARTERIAL PRESSURE
mmHg
 KESIMPULAN

• Pendekatan terhadap fisiologi kardiovaskular yang menilai baik jantung

maupun elemen-elemen pembuluh darah berguna untuk seorang
intensivis untuk dapat memberi terapi yang tepat

• Arthur Guyton memperkenalkan perubahan paradigma cara kerja sistem

sirkulasi yang memungkinkan kita dapat menganalisa interaksi kompleks
yang terjadi antara fungsional jantung dan aliran balik vena

• Guyton menunjukkan bahwa aliran balik vena tergantung pada

 sirkulasi perifer (MCFP),
 tekanan atrium kanan (Pra/CVP)
 resistensi aliran balik vena (Rvr)