Kardiovaskular

Oleh: M. Rasjad Indra

Fungsi Umum Kardiovaskuler

Melayani kebutuhan jaringan:
Mengangkut nutrisi & oksigen ke jaringan Mengangkut sisa metabolisme dari jaringan Mengangkut hormon ke sel target

Memelihara lingkungan internal untuk kehidupan & fungsi optimal sel.

Bagaimana pengendalian kerja Sistem Kardiovaskuler agar dapat melayani kebutuhan jaringan seluruh tubuh???

Memenuhi Kebutuhan Perfusi Jaringan

Tahanan Pembuluh Darah Lokal

Tahanan Pembuluh Darah Total

Aliran Darah Tekanan Darah Pompa Jantung

Kontraksi Otot Pembuluh Darah

Ruang & Katub jantung

Siklus jantung

Kontraksi Otot jantung Sistem Konduksi & Otot Jantung

Otot Pembuluh Darah Potensial Aksi

Pengendalian
Parameter:
1. 2. 3. 4. Curah jantung Tekanan darah [P] Aliran darah [Q] Tahanan pembuluh darah [R]

Curah jantung = Volume sekuncup x frekuensi jantung

Hukum Ohm:

P Q R

Hukum Poiseuille:

Pr 4 Q 8l

r = jari-jari pembuluh darah = viskositas darah l = panjang pembuluh darah

Fungsi Bagian Kardiovaskuler

Jantung:
Memompa darah

Arteri:
Transpor darah di bawah tekanan tinggi ke jaringan.

Ateriol:
Mengatur aliran darah yg menuju kapiler

Kapiler:
Pertukaran cairan, nutrisi elektrolit hormon antara darah dan cairan interstisial

Venula:
Mengalirkan darah dari kapiler ke vena sedang

Vena:
Mengalirkan darah dari jaringan ke jantung Reservoir darah terkendali.

Volume Darah di Sistem Kardiovaskular

84 % di sirkulasi sistemik:
64 % di vena 13 % di arteri 7 % di arteriole dan kapiler sistemik

16 % di sirkulasi paru dan jantung:

7 % di jantung 9 % di paru

Penampang pembuluh darah

Pembuluh darah Aorta Ateri kecil Arteriole Kapiler Venule Vena kecil Vena cava Penampang (cm2) 2,5 20 40 2500 250 80 8

Kecepatan Aliran Darah

Oleh karena tekanan darah makin ke perifer makin turun, maka aliran darah:

Di aorta: 33 cm / detik Di kapiler: 0,3 mm / detik

Panjang kapiler: 0,3 1 mm darah berada di kapiler 1 3 detik Waktu untuk pertukaran antara plasma dan interstisial sangat singkat!!!!

Tekanan Darah

3 Prinsip Dasar Fungsi Kardiovaskuler

1. Aliran darah ke setiap jaringan

dikendalikan berdasarkan kebutuhan jaringan. 2. Curah jantung dikontrol terutama oleh keseluruhan kebutuhan jaringan. 3. Tekanan darah dikontrol oleh pengendali aliran darah lokal maupun oleh pengendali curah jantung.

ELEKTROKARDIOGRAFI

BIPOLAR STANDARD LEADS

UNIPOLAR AUGMENTED EXTRIMITY LEADS

UNIPOLAR PRECORDIAL LEADS

KURVA EKG

Gelombang EKG
P: dihasilkan dari depol atrium Q (q): Defleksi negatif pertama, hasil dari depol ventrikel R (r): Defleksi positif pertama selama depolarisasi ventrikel. S (s): Defleksi negatif pertama setelah R R (r): Defleksi positif kedua setelah S (s) T: Defleksi hasil repolarisasi ventrikel U: Defleksi positif setelah T hasil repolarisasi lambat septum interventrikularis.

Interval EKG
R-R: interval antara dua puncak R PP: interval antara dua permulaan P P-R: interval awal P sampai awal QRS (0,12-0,20)
Depolarisasi atrium Keterlambatan di AV node Perjalanan impuls ke bundle of His

QRS: interval dari awal Q sampai akhir S (<0,10) VAT: interval dari awal Q sampai puncak R(<0,05) Q-T: Interval dari awal Q sampai akhir T(<0,43)

Segmen EKG
PR segment: dari akhir P s/d awal QRS
Keterlambatan impuls di AV Node

ST segment: akhir QRS (J point) s/d awal T

Keterlambatan repolarisasi ventrikel setelah depolarisasi ventrikel tuntas

Injury current: menyebabkan ST segemnt elevasi atau depresi

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 flow

1. Reactive hyperemia Blocked (seconds hours) unblocked Blood flow increases to 4 7 times normal Depends 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 theory 2. 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. VEGF 2. FGF

3. Angiogenin

2. Collateral Circulation:

Humoral Regulation of The Circulation

1.

Vasoconstrictor Agents:
1. 2. 3. 4. Norepinephrine & Epinephrine Angiotensin Vasopressin Endothelin

2.

Vasodilator Agents:
1. Bradikynin 2. Histamin

3.

Effects of Ion & Other Chemical Factors

1. 2. 3. 4. 5. Calcium vasoconstriction Potasium Vasodilatation Magnesium powerful vasodilatation Hydrogen vasodilatation Acetate & Citrate mild degree vasodilatation

Rapid Control of Arterial Pressure by Nervous System

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 jantung 3. 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

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

Reflex Mechanism for Maintaining Normal Arterial Pressure (Cont.) 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 kidney 2. 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

BARORESEPTOR CONTROL Blood Pressure

HIGHER CENTER CA CI +

Baroreceptor + -

VASOMOTOR CENTER CI CA JANTUNG SV Hr

VD

C.O.P X TPR Blood Pressure

CHEMORECEPTOR VC O2 H PH CO2

Role of the Kidney in Long Term Regulation of Arterial Pressure

Renal-Body Fluid System for Arterial Pressure Control

Too much extracellular fluid The blood volume & arterial pressure rise

The kidneys excrete thr excess extracellular fluid

The arterial pressure back toward normal

Pressure diuresis: An increase in arterial pressure only a few mm Hg can double the renal output of water
Pressure natriuresis: An increase in arterial pressure only a few mm Hg can double the renal output of salt

How Does Increased Fluid Volume Elevate the Arterial Pressure?

Extracellular fluid volume Blood Volume Mean circulatory Filling pressure Venous return Cardiac output Auto-regulation Total peripheral resistance Arterial pressure

Importance of Salt in the Renal-Body Fluid Schema for Arterial Pressure Regulation
Excess salt in the body The osmolality of the body fluid increases Stimulate the thirst center Drink extra amounts of water Increases the extra-cellular fluid volume The increase in osmolality in the extracellular fluid Stimulate hypothalamus to secrete ADH The kidney reabsorb water from the renal tubular fluid Increasing the extracellular fluid volume. Increasing extracellular volume Elevation of the arterial pressure.

Renin-Angiotensin System
Renin:
Small protein Enzyme Synthesized in the JG cells Stored in an inactive form: Prorenin This secretion is stimulated by fall blood pressure Catalyze reaction: Angiotensinogen Angiotensin I. It persists in the blood for 30 60 minutes.

Angiotensinogen Kidney Renin Angiotensin I Decreased arterial pressure

Liver

Lungs Converting enzyme

Angiotensin II

Blood vessels

Aldosteron secre.

ADH secretion

Vasoconstriction

Sodium reabsorption

H2O & Na reabsorption

Renal retension H2O & Na

Normal effective arterial blood volume

Essential Hypertension
About 90-95 % of hypertension cases Unknown origin & strong hereditary tendency Characteristics of severe essential hypertension:
1. MAP is increased 40 60 %. 2. In the late & more severe stages: RBF decreased 50 % 3. The resistance to blood flow through the kidneys is increased twofold to fourfold. 4. But, GFR is often near normal. 5. The cardiac output is about normal. 6. The TPR is increased about 40 60 % ~ elevation of arterial pressure. 7. The kidney will not excrete adequate amount of salt and water unless the arterial pressure is high.

Treatment of Essential Hypertension

Two types of drugs:
1. Increase renal blood flow (vasodilator drug):
1. Inhibiting sympathetic nervous signal to the

kidneys or blocking the action of the sympathetic transmitter substance on the renal vasculature 2. Directly paralyzing the smooth muscle of the renal vasculature 3. Blocking the action of the renin-angiotensin system on the renal vasculature or renal tubules.

2. Decrease tubular reabsorption of salt and water:

Natriuretic Diuretic

CNS ischemic response

11 10 9 8 7 6 5 4 3 2 1 0 0 Detik 30 1 2 4 Menit 8 16 32 1 2 4 Jam 8 16 Stress relaxation Kemoreseptor Renin-angiotensin Baroreseptor

Renal-blood volume pressure control

Capillary fluid shift

Aldosterone

4 Hari

16