11. FAAL KARDIOVASKULER
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Transcript of 11. FAAL KARDIOVASKULER
KardiovaskularKardiovaskular
Oleh:Oleh:M. Rasjad IndraM. Rasjad Indra
Fungsi Umum Kardiovaskuler Fungsi Umum Kardiovaskuler
Melayani kebutuhan jaringan:Melayani kebutuhan jaringan:– Mengangkut nutrisi & oksigen ke jaringanMengangkut nutrisi & oksigen ke jaringan– Mengangkut sisa metabolisme dari jaringanMengangkut sisa metabolisme dari jaringan– Mengangkut hormon ke sel targetMengangkut hormon ke sel target
Memelihara lingkungan internal untuk Memelihara lingkungan internal untuk kehidupan & fungsi optimal sel.kehidupan & fungsi optimal sel.
Bagaimana pengendalian kerja Sistem Kardiovaskuler agar dapat melayani kebutuhan jaringan seluruh tubuh???
Aliran Darah
Tekanan Darah
Memenuhi Kebutuhan Perfusi Jaringan
Pompa Jantung
Tahanan Pembuluh Darah Lokal
Tahanan Pembuluh Darah Total
Kontraksi Otot jantung
Potensial Aksi
Sistem Konduksi & Otot Jantung
Ruang & Katub jantung
Kontraksi Otot Pembuluh Darah
Otot Pembuluh Darah
Siklus jantung
PengendalianParameter:
1. Curah jantung2. Tekanan darah [P]3. Aliran darah [Q]4. Tahanan pembuluh darah [R]
Curah jantung = Volume sekuncup x frekuensi jantung
RPQ
Hukum Ohm:l
Q
8
Pr 4Hukum Poiseuille:
r = jari-jari pembuluh darahŋ= viskositas darahl = panjang pembuluh darah
Fungsi Bagian KardiovaskulerFungsi Bagian KardiovaskulerJantungJantung: : – Memompa darahMemompa darahArteriArteri: : – Transpor darah di bawah tekanan tinggi ke jaringan.Transpor darah di bawah tekanan tinggi ke jaringan.AteriolAteriol: : – Mengatur aliran darah yg menuju kapilerMengatur aliran darah yg menuju kapilerKapilerKapiler: : – Pertukaran cairan, nutrisi elektrolit hormon antara Pertukaran cairan, nutrisi elektrolit hormon antara
darah dan cairan interstisialdarah dan cairan interstisialVenulaVenula: : – Mengalirkan darah dari kapiler ke vena sedangMengalirkan darah dari kapiler ke vena sedangVenaVena: : – Mengalirkan darah dari jaringan ke jantungMengalirkan darah dari jaringan ke jantung– Reservoir darah terkendaliReservoir darah terkendali..
Volume Darah di Sistem Volume Darah di Sistem KardiovaskularKardiovaskular
84 % di sirkulasi sistemik:84 % di sirkulasi sistemik:– 64 % di vena64 % di vena– 13 % di arteri13 % di arteri– 7 % di arteriole dan kapiler sistemik7 % di arteriole dan kapiler sistemik
16 % di sirkulasi paru dan jantung:16 % di sirkulasi paru dan jantung:– 7 % di jantung7 % di jantung– 9 % di paru9 % di paru
Penampang pembuluh darahPenampang pembuluh darah
Pembuluh darahPembuluh darah Penampang (cmPenampang (cm22))
AortaAorta 2,52,5Ateri kecilAteri kecil 2020
ArterioleArteriole 4040
KapilerKapiler 25002500
VenuleVenule 250250
Vena kecilVena kecil 8080
Vena cavaVena cava 88
Kecepatan Aliran DarahKecepatan Aliran Darah
Di aorta: 33 cm / detikDi aorta: 33 cm / detikDi kapiler: 0,3 mm / detikDi kapiler: 0,3 mm / detik
Oleh karena tekanan darah makin ke perifer makin turun, maka aliran darah:
• Panjang kapiler: 0,3 – 1 mm darah berada di kapiler 1 – 3 detik
• Waktu untuk pertukaran antara plasma dan interstisial sangat singkat!!!!
Tekanan DarahTekanan Darah
3 Prinsip Dasar Fungsi 3 Prinsip Dasar Fungsi KardiovaskulerKardiovaskuler
1.1. Aliran darah ke setiap jaringan Aliran darah ke setiap jaringan dikendalikan berdasarkan kebutuhan dikendalikan berdasarkan kebutuhan jaringan.jaringan.
2.2. Curah jantung dikontrol terutama oleh Curah jantung dikontrol terutama oleh keseluruhan kebutuhan jaringan.keseluruhan kebutuhan jaringan.
3.3. Tekanan darah dikontrol oleh pengendali Tekanan darah dikontrol oleh pengendali aliran darah lokal maupun oleh aliran darah lokal maupun oleh pengendali curah jantung.pengendali curah jantung.
ELEKTROKARDIOGRAFIELEKTROKARDIOGRAFI
BIPOLAR STANDARD LEADS
UNIPOLAR AUGMENTED EXTRIMITY LEADS
UNIPOLAR PRECORDIAL LEADS
KURVA EKG
Gelombang EKGGelombang EKG
P: dihasilkan dari depol atriumP: dihasilkan dari depol atriumQ (q): Defleksi negatif pertama, hasil dari depol Q (q): Defleksi negatif pertama, hasil dari depol ventrikelventrikelR (r): Defleksi positif pertama selama R (r): Defleksi positif pertama selama depolarisasi ventrikel.depolarisasi ventrikel.S (s): Defleksi negatif pertama setelah RS (s): Defleksi negatif pertama setelah RR’ (r’): Defleksi positif kedua setelah S (s)R’ (r’): Defleksi positif kedua setelah S (s)T: Defleksi hasil repolarisasi ventrikelT: Defleksi hasil repolarisasi ventrikelU: Defleksi positif setelah T hasil repolarisasi U: Defleksi positif setelah T hasil repolarisasi lambat septum interventrikularis.lambat septum interventrikularis.
Interval EKGInterval EKG
R-R: interval antara dua puncak RR-R: interval antara dua puncak RPP: interval antara dua permulaan PPP: interval antara dua permulaan PP-R: interval awal P sampai awal QRS (0,12-0,20)P-R: interval awal P sampai awal QRS (0,12-0,20)– Depolarisasi atriumDepolarisasi atrium– Keterlambatan di AV nodeKeterlambatan di AV node– Perjalanan impuls ke bundle of HisPerjalanan impuls ke bundle of His
QRS: interval dari awal Q sampai akhir S (<0,10)QRS: interval dari awal Q sampai akhir S (<0,10)VAT: interval dari awal Q sampai puncak R(<0,05)VAT: interval dari awal Q sampai puncak R(<0,05)Q-T: Interval dari awal Q sampai akhir T(<0,43)Q-T: Interval dari awal Q sampai akhir T(<0,43)
Segmen EKGSegmen EKG
PR segment: dari akhir P s/d awal QRSPR segment: dari akhir P s/d awal QRS– Keterlambatan impuls di AV NodeKeterlambatan impuls di AV Node
ST segment: akhir QRS (J point) s/d awal TST segment: akhir QRS (J point) s/d awal T– Keterlambatan repolarisasi ventrikel setelah Keterlambatan repolarisasi ventrikel setelah
depolarisasi ventrikel tuntasdepolarisasi ventrikel tuntas
Injury current: menyebabkan ST segemnt Injury current: menyebabkan ST segemnt elevasi atau depresielevasi atau depresi
Local Control of Blood Local Control of Blood FlowFlow
IntroductionIntroduction
The greater the metabolism The greater the metabolism the greater the greater its blood flowits blood flow– Liver: 95 ml/min/100 g of liver tissue.Liver: 95 ml/min/100 g of liver tissue.– Kidneys: 1100 ml/min Kidneys: 1100 ml/min cleansing the blood. cleansing the blood.
The importance of blood flow control The importance of blood flow control effective & efficienteffective & efficient– Serving metabolic needServing metabolic need– Efficient heart workload.Efficient heart workload.
Mechanism of Blood Flow ControlMechanism of Blood Flow ControlAcute control (rapid changes in local vasodilatation / Acute control (rapid changes in local vasodilatation / vasoconstriction):vasoconstriction):– Effect of tissue metabolismEffect of tissue metabolism– The availability of oxygen changes.The availability of oxygen changes.– Two basic theories:Two basic theories:
Vasodilator theory: Vasodilator theory: adenosine; COadenosine; CO22; histamine; K; histamine; K++ & H & H++
Oxygen lack theory: Oxygen lack theory: vasomotion in metarterioles & precapillary vasomotion in metarterioles & precapillary sphincters.sphincters.
– Other nutrients besides Oxygen:Other nutrients besides Oxygen:– Lack of glucose Lack of glucose vasodilatation vasodilatation– Vitamin B deficiency Vitamin B deficiency vasodilatation vasodilatation
The examples of acute metabolic The examples of acute metabolic control of local blood flowcontrol of local blood flow
1.1. Reactive hyperemiaReactive hyperemia• Blocked (seconds – hours) Blocked (seconds – hours) unblocked unblocked• Blood flow increases to 4 – 7 times normalBlood flow increases to 4 – 7 times normal• Depends on how long it is blocked.Depends on how long it is blocked.
2.2. Active hyperemiaActive hyperemia• Tissue activity Tissue activity lack of nutrient & release lack of nutrient & release
vasodilator substances.vasodilator substances.• Local blood flow increases 20 times in Local blood flow increases 20 times in
muscle during heavy exercise.muscle during heavy exercise.
Blood flow control & The arterial Blood flow control & The arterial pressure changespressure changes
Acute autoregulation theory:Acute autoregulation theory:1.1. The metabolic theoryThe metabolic theory2.2. The myogenic theory (still doubtful !!)The myogenic theory (still doubtful !!)
Endothelial-Derived Relaxing Factor Endothelial-Derived Relaxing Factor “EDRF” (NO):“EDRF” (NO):
– Rapid flow of blood Rapid flow of blood shear stress shear stress NO NO release release relaxes the local arterial wall. relaxes the local arterial wall.
Long Term Blood Flow RegulationLong Term Blood Flow Regulation
1.1. Change in Tissue VascularityChange in Tissue Vascularity– Reconstruction to meet the needs of the Reconstruction to meet the needs of the
tissuestissues– Role of Oxygen in Long-Term Regulation.Role of Oxygen in Long-Term Regulation.– Vascular Endothelial Growth Factors:Vascular Endothelial Growth Factors:
1.1. VEGFVEGF2.2. FGFFGF3.3. AngiogeninAngiogenin
2.2. Collateral Circulation:Collateral Circulation:
Humoral Regulation of The CirculationHumoral Regulation of The Circulation1.1. Vasoconstrictor Agents:Vasoconstrictor Agents:
1.1. Norepinephrine & EpinephrineNorepinephrine & Epinephrine2.2. AngiotensinAngiotensin3.3. VasopressinVasopressin4.4. EndothelinEndothelin
2.2. Vasodilator Agents:Vasodilator Agents:1.1. BradikyninBradikynin2.2. HistaminHistamin
3.3. Effects of Ion & Other Chemical FactorsEffects of Ion & Other Chemical Factors1.1. Calcium Calcium vasoconstriction vasoconstriction2.2. Potasium Potasium Vasodilatation Vasodilatation3.3. Magnesium Magnesium powerful vasodilatation powerful vasodilatation4.4. Hydrogen Hydrogen vasodilatation vasodilatation5.5. Acetate & Citrate Acetate & Citrate mild degree vasodilatation mild degree vasodilatation
Rapid Control of Arterial Rapid Control of Arterial Pressure by Nervous Pressure by Nervous
SystemSystem
Pengendalian sirkulasi oleh sistem Pengendalian sirkulasi oleh sistem sarafsaraf
Peran sistem saraf dalam pengendalian Peran sistem saraf dalam pengendalian aliran darah lokal aliran darah lokal sangat kecil.sangat kecil.Sistem saraf lebih berperan pada fungsi Sistem saraf lebih berperan pada fungsi global dalam hal:global dalam hal:
1.1. Pendistribusian darah ke area tubuh tertentuPendistribusian darah ke area tubuh tertentu2.2. Kekuatan pompa jantungKekuatan pompa jantung3.3. Pengendalian cepat tekanan darah Pengendalian cepat tekanan darah
Three Major Changes Three Major Changes If sympathetic nervous system are stimulatedIf sympathetic nervous system are stimulated1.1. Almost all arterioles are constrictedAlmost all arterioles are constricted
• Increases the total peripheral resistanceIncreases the total peripheral resistance2.2. The veins especially & other large vessels are The veins especially & other large vessels are
strongly constrictedstrongly constricted• Increases venous return Increases venous return increase cardiac out put increase cardiac out put
(Starling Law)(Starling Law)3.3. The heart enhancing cardiac pumpingThe heart enhancing cardiac pumping
• Increases heart rateIncreases heart rate• Increases cardiac contractilityIncreases cardiac contractility
Anestesi spinal menyebabkan penurunan tekanan darah akibat hilangnya tonus vasomotor
Reflex Mechanism for Maintaining Reflex Mechanism for Maintaining Normal Arterial PressureNormal Arterial Pressure
Baroreceptor Reflexes:Baroreceptor Reflexes:– The receptors: Baroreceptors or PressoreceptorsThe receptors: Baroreceptors or Pressoreceptors
Located in the wall of several of large systemic Located in the wall of several of large systemic arteriesarteriesSinus caroticus Sinus caroticus n. Hering n. Hering n. Glossopharyngeus n. Glossopharyngeus tr. Solitarius tr. Solitarius Med. Oblongata.Med. Oblongata.Arcus aortae Arcus aortae n. Vagusn. Vagus
– The Response: Feedback signals to reduce The Response: Feedback signals to reduce arterial pressurearterial pressure
Vasodilatation of the veins and arteriolesVasodilatation of the veins and arteriolesDecreased heart rate & the strength of heart Decreased heart rate & the strength of heart contractioncontraction
Function of Baroreceptor ReflexFunction of Baroreceptor Reflex
During changes in Body PostureDuring changes in Body Posture– To maintain relatively constant arterial To maintain relatively constant arterial
pressure in the upper bodypressure in the upper bodyPressure BufferPressure Buffer Function Function– Opposes either Opposes either increasesincreases or or decreasesdecreases in in
arterial pressure.arterial pressure.Unimportance of Baroreceptor System for Unimportance of Baroreceptor System for Long RegulationLong Regulation– The resetting of baroreceptor systemsThe 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
Chemoreceptors Reflex:Chemoreceptors Reflex:– The receptors sensitive to:The receptors sensitive to:
Lack of oxygens; COLack of oxygens; CO22 excess and H excess and H++ excess. excess.
Located in the wall of small arteries; Carotid Bodies & Aortic Located in the wall of small arteries; Carotid Bodies & Aortic Bodies.Bodies.
– Not a powerful control in a normal arterial pressure Not a powerful control in a normal arterial pressure rangerange
Important in below 80 mmHgImportant in below 80 mmHg
Low-pressure Receptors:Low-pressure Receptors:– Stretch receptorsStretch receptors– Located in the wall of: Pulmonary arteries & AtriumLocated in the wall of: Pulmonary arteries & Atrium– Role: to minimize arterial pressure changes in Role: to minimize arterial pressure changes in
response to changes in blood volume.response to changes in blood volume.
Reflex Mechanism for Maintaining Normal Reflex Mechanism for Maintaining Normal Arterial Pressure (Cont.)Arterial Pressure (Cont.)
Volume Reflex (Volume Reflex (Atrial Reflex that Activate the KidneyAtrial Reflex that Activate the Kidney))– Stimulation: Stretch of the atriaStimulation: Stretch of the atria– Response: Response:
1.1. Dilatation of the afferent arteriole in the kidneyDilatation of the afferent arteriole in the kidney2.2. To Hypothalamus To Hypothalamus Decrease ADH secretion Decrease ADH secretion 3.3. Release of Atrial Natriuretic Peptide (ANP)Release of Atrial Natriuretic Peptide (ANP)
The Bainbridge ReflexThe Bainbridge Reflex– Stimulation: Stretch of the atriaStimulation: Stretch of the atria– Response: n. Vagus Response: n. Vagus Med. Oblongata Med. Oblongata Increase the Increase the
heart rate & strength of the heart contractionheart rate & strength of the heart contraction
Reflex Mechanism for Maintaining Reflex Mechanism for Maintaining Normal Arterial Pressure (Cont.)Normal Arterial Pressure (Cont.)
CACI
HIGHER CENTER
VASOMOTORCENTERCI CA
JANTUNG
SV Hr
C.O.PX
TPR
“Blood Pressure”O2
HCO2
PH
CHEMORECEPTOR
+
VCVD
+“Baroreceptor”
-
BARORESEPTORCONTROL “Blood Pressure”
Role of the Kidney in Long Term Role of the Kidney in Long Term Regulation of Arterial PressureRegulation of Arterial Pressure
Renal-Body Fluid System for Renal-Body Fluid System for Arterial Pressure ControlArterial 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 How Does Increased Fluid Volume Elevate the Arterial Pressure?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 Importance of Salt in the Renal-Body Fluid Schema for Arterial Pressure RegulationSchema for Arterial Pressure Regulation
Excess salt in the body Excess salt in the body → The osmolality of the → The osmolality of the body fluid increases → Stimulate the thirst body fluid increases → Stimulate the thirst center → Drink extra amounts of water → center → Drink extra amounts of water → Increases the extra-cellular fluid volumeIncreases the extra-cellular fluid volumeThe increase in osmolality in the extracellular The increase in osmolality in the extracellular fluid → Stimulate hypothalamus to secrete ADH fluid → Stimulate hypothalamus to secrete ADH → The kidney reabsorb water from the renal → The kidney reabsorb water from the renal tubular fluid → Increasing the extracellular fluid tubular fluid → Increasing the extracellular fluid volume.volume.Increasing extracellular volume → Elevation of Increasing extracellular volume → Elevation of the arterial pressure.the arterial pressure.
Renin-Angiotensin SystemRenin-Angiotensin System
Renin:Renin:– Small protein EnzymeSmall protein Enzyme– Synthesized in the JG cellsSynthesized in the JG cells– Stored in an inactive form: Stored in an inactive form: ProreninProrenin– This secretion is stimulated by fall blood This secretion is stimulated by fall blood
pressurepressure– Catalyze reaction: Angiotensinogen Catalyze reaction: Angiotensinogen → →
Angiotensin I.Angiotensin I.– It persists in the blood for 30 – 60 minutes.It persists in the blood for 30 – 60 minutes.
Decreased arterial pressure
Kidney
Angiotensinogen
Renin
Angiotensin I
Liver
Converting enzyme
Lungs
Angiotensin II
Blood vessels
Vasoconstriction
Aldosteron secre.
Sodium reabsorption
H2O & Na reabsorption
ADH secretion
Renal retension H2O & Na
Normal effective arterial blood volume
Essential HypertensionEssential HypertensionAbout 90-95 % of hypertension casesAbout 90-95 % of hypertension casesUnknown origin & strong hereditary tendencyUnknown origin & strong hereditary tendencyCharacteristics of severe essential hypertension:Characteristics of severe essential hypertension:
1.1. MAP is increased 40 – 60 %.MAP is increased 40 – 60 %.2.2. In the late & more severe stages: RBF decreased 50 %In the late & more severe stages: RBF decreased 50 %3.3. The resistance to blood flow through the kidneys is The resistance to blood flow through the kidneys is
increased twofold to fourfold.increased twofold to fourfold.4.4. But, GFR is often near normal.But, GFR is often near normal.5.5. The cardiac output is about normal.The cardiac output is about normal.6.6. The TPR is increased about 40 – 60 % The TPR is increased about 40 – 60 % ~ elevation of ~ elevation of
arterial pressure.arterial pressure.7.7. The kidney will not excrete adequate amount of salt The kidney will not excrete adequate amount of salt
and water unless the arterial pressure is high.and water unless the arterial pressure is high.
Treatment of Essential HypertensionTreatment of Essential HypertensionTwo types of drugs:Two types of drugs:
1.1. Increase renal blood flow (vasodilator drug):Increase renal blood flow (vasodilator drug):1.1. Inhibiting sympathetic nervous signal to the Inhibiting sympathetic nervous signal to the
kidneys or blocking the action of the sympathetic kidneys or blocking the action of the sympathetic transmitter substance on the renal vasculaturetransmitter substance on the renal vasculature
2.2. Directly paralyzing the smooth muscle of the Directly paralyzing the smooth muscle of the renal vasculaturerenal vasculature
3.3. Blocking the action of the renin-angiotensin Blocking the action of the renin-angiotensin system on the renal vasculature or renal tubules.system on the renal vasculature or renal tubules.
2.2. Decrease tubular reabsorption of salt and Decrease tubular reabsorption of salt and water:water:
– NatriureticNatriuretic– DiureticDiuretic
0 30 1 2 4 8 16 32 1 2 4 8 16 1 2 4 8 16
Detik Menit Jam Hari
0
1
2
3
4
5
6
7
8
9
10
11
Baroreseptor
Kemoreseptor
CNS ischemic responseRenal-blood volume pressure control
Stress relaxation
Renin-angiotensin Capillary fluid shift
Aldosterone