Local Control of Blood Flow

Introduction

The greater the metabolism the greater its blood flow– Liver: 95 ml/min/100 g of liver tissue.– Kidneys: 1100 ml/min cleansing the

blood. The importance of blood flow control

effective & efficient– Serving metabolic need– Efficient heart workload.

Mechanism of Blood Flow Control

Acute control (rapid changes in local vasodilatation / vasoconstriction):– Effect of tissue metabolism– The availability of oxygen changes.– Two basic theories:

Vasodilator theory: adenosine; CO2; histamine; K+ & H+

Oxygen lack theory: vasomotion in metarterioles & precapillary sphincters.

– Other nutrients besides Oxygen:– Lack of glucose vasodilatation– Vitamin B deficiency vasodilatation

The examples of acute metabolic control of local blood

flow1. Reactive hyperemia

• Blocked (seconds – hours) unblocked• Blood flow increases to 4 – 7 times

normal• Depend on how long it is blocked.

2. Active hyperemia• Tissue activity lack of nutrient &

release vasodilator substances.• Local blood flow increases 20 times in

muscle during heavy exercise.

Blood flow control & The arterial pressure changes

Acute autoregulation theory:1. The metabolic theory2. The myogenic theory (still doubtful !!)

Endothelial-Derived Relaxing Factor “EDRF” (NO):

– Rapid flow of blood shear stress NO release relaxes the local arterial wall.

Long Term Blood Flow Regulation

1. Change in Tissue Vascularity– Reconstruction to meet the needs of

the tissues– Role of Oxygen in Long-Term

Regulation.– Vascular Endothelial Growth Factors:

1. VEGF2. FGF3. Angiogenin

2. Collateral Circulation:

Humoral Regulation of The Circulation

1. Vasoconstrictor Agents:1. Norepinephrine & Epinephrine2. Angiotensin3. Vasopressin4. Endothelin

2. Vasodilator Agents:1. Bradikynin2. Histamin

3. Effects of Ion & Other Chemical Factors1. Calcium vasoconstriction2. Potasium Vasodilatation3. Magnesium powerful vasodilatation4. Hydrogen vasodilatation5. Acetate & Citrate mild degree

vasodilatation

Rapid Control of Arterial Pressure by

Nervous System

TIM BLOK CARDIOVASKULER

Pengendalian sirkulasi oleh sistem saraf

Peran sistem saraf dalam pengendalian aliran darah lokal sangat kecil.

Sistem saraf lebih berperan pada fungsi global dalam hal:

1. Pendistribusian darah ke area tubuh tertentu

2. Kekuatan pompa jantung3. Pengendalian cepat tekanan darah

Three Major Changes

If sympathetic nervous system are stimulated

1. Almost all arterioles are constricted• Increases the total peripheral resistance

2. The veins especially & other large vessels are strongly constricted• Increases venous return increase cardiac out

put (Starling Law)

3. The heart enhancing cardiac pumping• Increases heart rate• Increases cardiac contractility

Anestesi spinal menyebabkan penurunan tekanan darah akibat hilangnya tonus vasomotor

Reflex Mechanism for Maintaining Normal Arterial Pressure

Baroreceptor Reflexes:– The receptors: Baroreceptors or

Pressoreceptors Located in the wall of several of large systemic

arteries Sinus caroticus n. Hering n.

Glossopharyngeus tr. Solitarius Med. Oblongata.

Arcus aortae n. Vagus– The Response: Feedback signals to reduce

arterial pressure Vasodilatation of the veins and arterioles Decreased heart rate & the strength of heart

contraction

Efek perubahan tekanan arteri (ΔP) terhadap perubahan transmisi impuls n. Hering dari sinus Caroticus (ΔI)

Baroreseptor lebih merespons perubahan tekanan daripada tekanan stasioner

Penjepitan a. carotis communis menyebabkan peningkatan tekanan arteri (MAP), pelepasan jepitan menurunkan tekanan arteri

Function of Baroreceptor Reflex

During changes in Body Posture– To maintain relatively constant arterial

pressure in the upper body Pressure Buffer Function

– Opposes either increases or decreases in arterial pressure.

Unimportance of Baroreceptor System for Long Regulation– The resetting of baroreceptor systems

Pencatatan tekanan darah selama 2 jam pada kondisi NORMAL (gambar atas) dan pada beberapa minggu setelah DENERVASI sinus caroticus dan Sinus aorticus

Frekuensi distribusi MAP selama 24 jam pada anjing NORMAL dan beberapa minggu setelah denervasi baroreseptor

Chemoreceptors Reflex:– The receptors sensitive to:

Lack of oxygens; CO2 excess and H+ excess. Located in the wall of small arteries; Carotid Bodies &

Aortic Bodies.– Not a powerful control in a normal arterial

pressure range Important in below 80 mmHg

Low-pressure Receptors:– Stretch receptors– Located in the wall of: Pulmonary arteries &

Atrium– Role: to minimize arterial pressure changes in

response to changes in blood volume.

Reflex Mechanism for Maintaining Normal Arterial Pressure (Cont.)

Volume Reflex (Atrial Reflex that Activate the Kidney)– Stimulation: Stretch of the atria– Response:

1.Dilatation of the afferent arteriole in the kidney2.To Hypothalamus Decrease ADH secretion 3.Release of Atrial Natriuretic Peptide (ANP)

The Bainbridge Reflex– Stimulation: Stretch of the atria– Response: n. Vagus Med. Oblongata Increase

the heart rate & strength of the heart contraction

Reflex Mechanism for Maintaining Normal Arterial Pressure (Cont.)

CA

CI

HIGHER CENTER

VASOMOTORCENTERCI CA

JANTUNG

SV Hr

C.O.PX

TPR

“Blood Pressure”O2

H

CO2

PH

CHEMORECEPTOR

+

VCVD

+

“Baroreceptor”

-

BARORESEPTORCONTROL “Blood Pressure”

TEKANAN DARAH

C.O.P T.P.R

S.V Hr

EDV

IVFP

VR

VC

BV

VD

ESV

MC

SK

CPM

S

PS

PEGVMC

LVMC

VK/VD

NEUROHUMO-RAL CONTROL

BHN LOKALO2,CO2,H,K

EMP

B.VISC.

HT

FAKTOR YG MEMPENGARUHI “BP”

KONTROL TEK. DARAH SISTIM SARAF:

CNS : VASOMOTORCENTER ( CA & CI ) LUAR CNS: “BR” & “CR”

SISTIM HUMORAL / KIMIA / HORMON: RENIN-ANGIOTENSIN, ALDOSETRON, VASOPRESIN ADRENALIN, NOR ADRENALIN, ACETYLKOLIN K, Mg, H, Ca, Na, CO2,CO, ROS, LAKTAT,

PYRUVAT. SISTIM HEMODINAMIK:

VOLUME DARAH & TEK. OSMOTIK/HIDROSTATIK Pada sistim ini lebih banyak dipengaruhi oleh

perubahan-2 tek hidrostatik, osmotik & oncotik yg terdapat diluar dan didalam sistim vaskuler

Mekanismenya berjalan secara simultan & saling melengkapi & Tujuannya: menunjang “homeostatics”

BRAINSTRESS STRESS PSIKOLOGIFISIKSUHUTOXIN

HIPOTHALAMUS

REAKSI HORMONAL REAKSI NEURAL

VASOPRESIN CRF

RETENSI Na & H2O

VMC SIMPATIS

HEART VASKULER

INOTROPIK, EDVVENT.DIST,FILLING P

CPM

SV X Hr

COP “R”X

“BP”

BV

VASOKONS-TRIKSI

JGA

RENINANGIOTENSINOGEN+ ANGIOTENSIN I

CONVERTING ENZYM

ANGIOTENSIN II PARU

LIVER

ADRENAL CORTEX

ALDOSTERON BRAINVMC

Intake H2O

“S”retensi Na

& H2O

BV JANTUNG

ARTERI

GLOMERULUS

VASOKONSTRIKSI

RCOP

“BP”

SVHr

RBF

RENIN-ANGIOTENSINCONTROL”BP”

x

CA

CI

HIGHER CENTER

VASOMOTORCENTERCI CA

JANTUNG

SV Hr

C.O.PX

TPR

“BP”O2

H

CO2

PH

CHEMORECEPTOR

+

VKVD

+“BR”

-

BARORESEPTORCONTROL “BP”

SHORTTERM CONTROL “BP” VIA BARORECEPTOR REFLEX

F:CARDIACPHYSIOLOGY/CHAP.18B/IBNU/NEW/PAPI/CARDIOVASKULERPHYSIOLOGY/2004

KELAINAN TEK. DARAH HIPERTENSI: Tek.darah melebihi nilai nor-

malnya. N Bp: 120/80 & MAP=93,33 mmHg misalnya : 130/95 mmHg atau lebih besar.

HIPOTENSI : Tek. Darah kurang dari nilai nor- malnya.Biasanya ada hub.nya dengan shock! Misalnya: 80-90/60- 55 mmHg atau lebih kecil.

KLASIFIKASI HIGH BLOOD PRESSURE : Hipertensi essensiil: penyebab tak jelas, mungkin

karena kacaunya sistim kontrolnya (saraf,hemodinamik,humoral)

Hipertensi skunder: penyebab jelas, ada kelainan organ seperti peny. ginjal; tumor cortex adrenalis;toximia gravidarum;obat

Klasifikasi lain: Hipertensi ringan, Hipertensi sedang dan Hipertensi berat

HIPERTENSI ESSENSIILFAKTOR

Genetik,makanan;minumanEmosi & stress psikosial; obat; merokok; olah raga

Pemicu fisiogenesis:

Kacau sistim kontrol“Bp” (neural,hemodinamik

& humoral)

Ht .Ess

Ubah “life style”

Cara mengatasi

Tdk merokok

Tdk minum alkohol

Kurangi makan garam

OR Hilangkan stress

Tidur cukup

Health Wellness

Stop obat

Obat anti hipertensi2

1

HIPERTENSI SKUNDERHt.skunder: suatu Ht dengan

penyebab yg dapat di identifikasikanPenyebab:1. peny. Ginjal;2.hiper

sekresi aldos- teron krn kelainan cortex adrenalis; 3.tumor kel medulla adrenalis (feokromositoma); 4.toxae- mia gravidarum; 5.grave`s disease?; 6.peny. Kardiovaskuler.

Gejala: Tek.drh > normal (S/D ) & jika D > 120 mmHg dikenal Ht. Maligna dng gejala se- perti papil edema, stroke,gagal jantung &ginjal.

PENYEBAB HYPERTENSION

HYPER-TENSION

Tu.med Adr

Tu cortex

ald

Renin-Agt

Retensi Na &H2O

KVS defect:

CNS

Cushing

COR

Head injury,tu-Mor,psychiatricdisturbances

Stenosis Ao

atherosclerosis

hipertiroidism

Ht renal

Spasme

Constr.renal

Hidronefrosis,pyelonefritis,GNA/C

Toxaemia,

KOMPLIKASI HIPERTENSI JANTUNG:

Ht. Menyebabkan beban kerja jantung & merusak pembuluh darah sehingga “TPR” meningkat.

Hipertropi ventrikel kiri left heart failure Ht. Meningkatkan faktor “after load” O2D > O2S SEHINGGA TERJADI INSUFISIENSI

KORONER OTAK:

Stroke ( transient cerebral ischemia attack/bleeding)

Hypertensive encephalopathy (gejala prodromalnya mual-muntah,insomnia, sulit konsentrasi, akhirnya coma & kejang2.

ARTERI: proses sklerosis, trombosis dan pembuluh drh mudah pecah (jantung,ginjal,otak dll).

140

130

115

90

155

N

Border line

95S

D

Area

Area

peningkatan

190

60

Area

Abnormal

VARIASI

BLOOD PRESSURE

OBAT ANTI HIPERTENSI TUJUAN: MENGEMBALIKAN “PERAN SISTIM

CONTROL Bp” AGAR DAPAT BERFUNGSI & MENGHINDARI KOMPLIKASINYA

OBAT : BETA BLOKERS: PROPANOLOL, ATENOLOL,

OXYPRENOLOL,NADOLOL,CARTEOLOL. DIURETIKA: HCT; FUROSEMIDE, DIAMOX.,

SPIRONOLACTON,ALDACTON,C.THALIDONE. VASODILATATOR: KALSIUM ANTAGONIST

MISALNYA: DILTIAZEM, NIFEDIPINE, VERAPAMIL, AMIODIPINE.

ANTICONVERTING ENZYM/ACE INHIBITORS: CAPTOPRIL ( CAPOTEN,CAPTENSIN)

GABA : HEXAMOTHONIUM. ANXIOLYTIC:MENCEGAH STIMULASI HIGHCENTER.