Cardiovascular Anatomy and Physiology Slide

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• Weight : 200-425 gram

• Heart rate : 100.000 x/ day

• Blood pump: 2.000 galon (7.571 ltr) / menit

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Anatomy of the Heart Anatomy of the Heart

• Right AtriumRight Atrium

– 2-3mm muscle thickness2-3mm muscle thickness

– Systemic drain through SVC, Systemic drain through SVC, IVC and Coronary Sinus

IVC and Coronary Sinus – Tricuspid valve: anterior, Tricuspid valve: anterior,

posterior and medial posterior and medial

• Papillary muscles and Papillary muscles and chordae tendineae

chordae tendineae

• Right VentricleRight Ventricle

– 3 – 5 mm muscle thickness3 – 5 mm muscle thickness – 1/3 LV1/3 LV

– Anterosuperior outflow to the Anterosuperior outflow to the pulmonary circulation

pulmonary circulation

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• Pulmonary CirculationPulmonary Circulation

– Pulmonary valve: right, left and anteriorPulmonary valve: right, left and anterior

– Pulmonary branchPulmonary brancharteriolesarteriolescapillariescapillaries

• Left AtriumLeft Atrium

– 3mm muscle thickness3mm muscle thickness – Larger than RALarger than RA

– Mitral valve: anterior and posteriorMitral valve: anterior and posterior

• Left VentricleLeft Ventricle

– 8-15 mm thick and 4.5-5.5 cm diameter8-15 mm thick and 4.5-5.5 cm diameter

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Right Atrium

Right Atrium = = 2 - 8 mmHg2 - 8 mmHg

■■ Right VentricleRight Ventricle == 25 - 30 systolic press 25 - 30 systolic press 2 - 8 diastolic press 2 - 8 diastolic press

■ ■ Pulmonary artery Pulmonary artery = = 115 - 30 systolic press5 - 30 systolic press

4 - 12 end diastolic press4 - 12 end diastolic press 9 - 18 9 - 18 MPAPMPAP

■■ Left AtriumLeft Atrium == 2 - 10 mmHg (Pul. Wedge) 2 - 10 mmHg (Pul. Wedge)

■ ■ Left VentricleLeft Ventricle = 100 - 120 peak systolic= 100 - 120 peak systolic

3 - 12 end diastolic 3 - 12 end diastolic

■■ AortaAorta == 120/80 mmHg 120/80 mmHg

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Coronary circulation Coronary circulation

• Left main BranchLeft main Branch

– Left Anterior DecendingLeft Anterior Decending

• Anterior left ventricle wall, V3-Anterior left ventricle wall, V3- V5V5

– Circumflex branchesCircumflex branches

• Posterior LV and part of RV, Posterior LV and part of RV, lead I and VL

lead I and VL

• Right Coronary ArteryRight Coronary Artery

– AV node and common Bundle of AV node and common Bundle of HisHis

– II, V and VF, conduction II, V and VF, conduction abnormalities

abnormalities

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ECG and Coronary Anatomy

Anatomic Site ECG Leads Artery

Inferior II, III, aVF Right

Lateral I, aVL, V5, V6 L Circumflex Anterior V3-V4 (I, aVL) Left

Anteroseptal V1-V2 LAD

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Cardiac Conduction system Cardiac Conduction system

• Sinoatrial (SA) nodeSinoatrial (SA) node

– Junction of the SVC with RAJunction of the SVC with RA – 100-110 beats / minute 100-110 beats / minute

– Anterior, middle and posterior Anterior, middle and posterior internodal

internodal

• Atrioventricular (AV) nodeAtrioventricular (AV) node

– Near the ostium of coronary sinusNear the ostium of coronary sinus

• Bundle of HisBundle of His

– Membranous interventricular to Membranous interventricular to the apex of the septum

the apex of the septum

• Right and Left bundle branchRight and Left bundle branch – Endocadium of the ventricleEndocadium of the ventricle

• Purkinje systemPurkinje system

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Cardiac

Cardiac E E lectrophysilogy lectrophysilogy

• SA node SA node

– spontaneous generation of spontaneous generation of action potentials

action potentials

– 100-110 action potentials 100-110 action potentials ("beats") per minute.

("beats") per minute.

– ““vagal tone" brings the vagal tone" brings the resting heart rate down to resting heart rate down to 60-80 beats/minute.

60-80 beats/minute.

– The normal range for sinus The normal range for sinus rhythm is 60-100

rhythm is 60-100 beats/minute.

beats/minute.

• sinus bradycardia , sinus sinus bradycardia , sinus tachycardia.

tachycardia.

• Controls both atrial and Controls both atrial and ventricular rhythm.

ventricular rhythm.

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• SA node causing atrial contraction. SA node causing atrial contraction.

• The impulse travels into the ventricles via The impulse travels into the ventricles via the atrioventricular node (AV node).

the atrioventricular node (AV node).

• Specialized conduction pathways (bundle Specialized conduction pathways (bundle branches and Purkinje fibers) within the branches and Purkinje fibers) within the

ventricle rapidly conduct the wave of ventricle rapidly conduct the wave of

depolarization throughout the ventricles to depolarization throughout the ventricles to

elicit ventricular contraction.

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Cardiac and

Cardiac and V V ascular Nerves ascular Nerves

• Sympathetic system Sympathetic system

• Parasympathetic system Parasympathetic system

• Cerebral vasomotor system Cerebral vasomotor system

• Cardiac receptor Cardiac receptor

• Neural supply of the peripheral Neural supply of the peripheral vasculature

vasculature

• Pericardium Pericardium

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Extrinsic Innervation of the Heart

• Heart is

stimulated by the sympathetic

cardioaccelerator y center

• Heart is inhibited by the

parasympathetic cardioinhibitory center

Figure 18.15

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Autonomic Control

• Inhibitory pathway (parasympathetic).Inhibitory pathway (parasympathetic).

– Cardio-inhibitory centre (medulla oblongata)Cardio-inhibitory centre (medulla oblongata) – Vagus nerve.Vagus nerve.

– Ganglia within heart wall.Ganglia within heart wall.

– SA & AV nodes.SA & AV nodes.

• Acceleratory pathway (sympathetic).Acceleratory pathway (sympathetic).

– Cardio-acceleratory centre (medulla Cardio-acceleratory centre (medulla oblongata)

oblongata)

– Thoracic spinal cord.Thoracic spinal cord.

– Sympathetic ganglion.Sympathetic ganglion.

– Sympathetic cardiac nerve.Sympathetic cardiac nerve.

– SA & AV nodesSA & AV nodes

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Autonomic Control

• Inhibitory pathway (parasympathetic).Inhibitory pathway (parasympathetic).

– Cardio-inhibitory centre (medulla oblongata)Cardio-inhibitory centre (medulla oblongata) – Vagus nerve.Vagus nerve.

– Ganglia within heart wall.Ganglia within heart wall.

– SA & AV nodes.SA & AV nodes.

• Acceleratory pathway (sympathetic).Acceleratory pathway (sympathetic).

– Cardio-acceleratory centre (medulla Cardio-acceleratory centre (medulla oblongata)

oblongata)

– Thoracic spinal cord.Thoracic spinal cord.

– Sympathetic ganglion.Sympathetic ganglion.

– Sympathetic cardiac nerve.Sympathetic cardiac nerve.

– SA & AV nodesSA & AV nodes

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Efek Stimulasi Simpatis pada Jantung

• SA node : norepinefrin menyebabkan penurunan permeabilitas thd K+  K+ keluar sedikit 

depolarisasi cepat  potensial aksi cepat

• AV node dan pacemaker yang lain :

meningkatkan kecepatan transmisi impuls

• Sel-sel kontraktil atrium & ventrikel :

peningkatan permeabilitas Ca shg influks Ca

meningkat  kontraksi atrium dan ventrikel lebih kuat

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Effect of Parasimpathetic stimulation on the heart

• SA node : acetylcholine increases permeability of SA node to K+  more K+ out of cell

hyperpolarization  action potential lama tercapai

• AV node : decreases excitability prolonging transmission impulses to the ventricle

• Atrial contraction cells : shortens action potential by reduction slow inward Ca2+  plateau phase reduced  atrial contraction weakened

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Sympathetic Parasympathetic

Vagus nerve

Heart rate  Myocardial contractility  Heart rate 

Myocardial contractility  Peripheral resistance  Catecholamines 

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Cardiac cycle Cardiac cycle

• RA and LA filling RA and LA filling

– TV and MV are closedTV and MV are closed

• Isovolumetric relaxation of the Isovolumetric relaxation of the LVLV

– AV has close but LV AV has close but LV

pressure still higher than LA pressure still higher than LA

• Open of the AV valvesOpen of the AV valves

– LV and RV relaxation, rapid LV and RV relaxation, rapid filling

filling

– Atrial contraction, P waveAtrial contraction, P wave

• AV valves closeAV valves close – Atrial fillingAtrial filling

– CVP and PA catheterCVP and PA catheter

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Electrocardiograph (ECG) Electrocardiograph (ECG)

• P P wave represents atrial depolarisation wave represents atrial depolarisation

• Q wave Q wave represents depolarisation at represents depolarisation at the bundle of His

the bundle of His

• R wave R wave represents the main spread of represents the main spread of depolarisation, from the inside out,

depolarisation, from the inside out, through the base of the ventricles through the base of the ventricles

• S waveS wave shows the subsequent shows the subsequent depolarisation of the rest of the depolarisation of the rest of the

ventricles upwards from the base of the ventricles upwards from the base of the

ventricles ventricles

• T wave T wave represents repolarisation of the represents repolarisation of the myocardium after systole is complete myocardium after systole is complete

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• Gel P : depolarisasi atrium

• Gel Q : depolarisasi diberkas HIS

• Gel R : depolarisasi dari bagian dalam ke bagian luar dasar ventrikel

• Segmen PR : waktu yang dibutuhkan oleh impuls dari SA node ke AV node,

terjadi perlambatan AV node

• Gel S : depolarisasi ventrikel menyebar naik dari bagian dasar ventrikel

• Kompleks QRS : depolarisasi ventrikel

Electrocardiograph (ECG)

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• Segmen ST : waktu sejak akhir

depolarisasi ventrikel sebelum terjadi repolarisasi (fase plateu). Saat terjadi kontraksi dan pengosongan ventrikel

• Gel T : repolarisasi atrium

• Interval TP : waktu saat terjadinya repolarisasi dan pengisian ventrikel

Electrocardiograph (ECG)

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Coronary autoregulation Coronary autoregulation

• Coronary perfusion constant at BP 50- Coronary perfusion constant at BP 50- 120 mmHg

120 mmHg

• Coronary arteriole (diameter <150um) Coronary arteriole (diameter <150um) dilatation

dilatation

• Oxygen demand alter the autoregulation Oxygen demand alter the autoregulation (Myocardial oxygen tension )

(Myocardial oxygen tension )

• Most important regulator Most important regulator   metabolic metabolic

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Cardiac output Cardiac output

• Volume of blood pumped by Volume of blood pumped by the heart each minute

the heart each minute

• CO = HR x SVCO = HR x SV

– SV ratio = EF = (EDV-SV ratio = EF = (EDV- ESV) / EDV (Normal 0.6- ESV) / EDV (Normal 0.6- 0.7)0.7)

– Preload, afterload, Preload, afterload,

contractility, heart rate and contractility, heart rate and ventricular compliance

ventricular compliance

• CI = CO / BSACI = CO / BSA

– Normal 2,5-3,5 ltr/minute Normal 2,5-3,5 ltr/minute m2m2

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Kesanggupan intrinsik jantung untuk penyesuaian diri terhadap beban yang berbeda

Dalam batas fisiologis  jantung akan memompakan semua darah yang masuk kedalam jantung tanpa menimbulkan

penumpukan darah berlebihan. Ini disebabkan oleh

peregangan yang ditimbulkan volume darah yang masuk  menyebabkan kekuatan kontraksi bertambah.

Dengan perkataan lain:

Kontraksi jantung sewaktu sistolis akan bertambah kuat bila pengisian darah lebih

banyak pada masa diastolik.

Frank Starling’S LAW

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THE HEART AS A PUMP

• REGULATION OF CARDIAC OUTPUT

– Heart Rate via sympathetic &

parasympathetic nerves – Stroke Volume

• Frank-Starling “Law of the Heart”

• Changes in Contractility

• MYOCARDIAL CELLS (FIBERS)

– Regulation of Contractility – Length-Tension and Volume-

Pressure Curves

– The Cardiac Function Curve

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Preload

Kontraktilitas

Afterload

Ukuran ventrikel kiri

Pemendekan serabut

miokard

Stroke volume

Heart rate

Cardiac output

Tekanan Darah Resistensi

perifer

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Contractility of the heart Contractility of the heart

• Contractility

– inotropic state independent of changes in preload, afterload, or heart rate

• Compliance

– nonlinear change in ventricular end-

diastolic volume/change in end-diastolic

pressure

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Myocardial metabolism Myocardial metabolism

• Energy source: lactate and fatty acidEnergy source: lactate and fatty acid – Linier uptake of fatty acidLinier uptake of fatty acid

– 90% of myocardial oxygen comsumption90% of myocardial oxygen comsumption

• Fasting priod : FFAFasting priod : FFA

• Myocardial lactateMyocardial lactate

– Arterial lactate and pyruvate oxidationArterial lactate and pyruvate oxidation

– Glugose, pyruvate, acetate and triglycerideGlugose, pyruvate, acetate and triglyceride

• Myocardial Oxygen ConsumptionMyocardial Oxygen Consumption

– 8-10 ml O2 per 10 mg myocardium per minute8-10 ml O2 per 10 mg myocardium per minute – HR, wall tension, myocardial contractilityHR, wall tension, myocardial contractility

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METABOLISME ATP OTOT

ATP dibentuk melalui proses :

• Anaerobic Glikolisis

Glikogen  glikogenolisis  glukosa  glikolisis  asam PiruvatAsam Laktat  2 ATP

• Kreatin fosfat

Dibentuk saat otot relaksasi  ~p + ADP  ATP

• Pada Maraton :metabolisme aerobik

• Fosforilasi oksidatif(Mitokondria)

- sumber energi utama : gula darah dan free fatty acids.

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Myocardial Supply-Demand ratio Myocardial Supply-Demand ratio

• Supply-demand balance to avoid ischemiaSupply-demand balance to avoid ischemia

• Oxygen SupplyOxygen Supply

– Diameter of coronary artery, LV EDP, Aortic Diameter of coronary artery, LV EDP, Aortic Diastolic Pressure, Arterial Oxygen content Diastolic Pressure, Arterial Oxygen content

– Coronary perfusion pressure = ADP - LV EDPCoronary perfusion pressure = ADP - LV EDP – Oxygen contentOxygen content

• PaO2, Hb, 2-3 DPGPaO2, Hb, 2-3 DPG

• pH, PCO2 and temperature in oxygen pH, PCO2 and temperature in oxygen dissociation

dissociation

• Oxygen DemandOxygen Demand

– HR and diastolic ventricular volume HR and diastolic ventricular volume

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Increased PaCo2 Decreased PaCo2

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Distribution of Cardiac Output Distribution of Cardiac Output

• brain 12%, heart 4%, liver 24%, kidneys

20%, muscle 23%, skin 6%, and intestines 8%.

• About 15% of the blood volume remains in the heart and pulmonary circulation, with the remainder in the systemic circulation.

• Of the blood in the systemic circulation, about 64% is in the veins

 Volume management

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Distribusi Cardiac Output

Cardiac Output Konsumsi oksigen

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Blood Pressure Blood Pressure

• Mean arterial pressure is the product of the cardiac output and the systemic

vascular resistance.

• Arterial pressure varies with the respiratory cycle.

– decreases 6 mm Hg or less during

inspiration because pulmonary venous capacitance increases

  pericardial tamponade

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Tekanan Darah

TD = Cardiac Output (CO) X Resistensi Perifer (TPR)

Cardiac HR Kontraktilitas

SV

Volume cairan Na, mineral corticoid

Vasodilator prostaglandin, kinin

Vasokonstriktor

angiotensin, catechol Humoral

Syaraf simpatis • Konstriktor  • Dilator 

Local ionic autoregulaty

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Arterial Pulse Arterial Pulse

• wave of vascular distention

• the pulse wave depends on the elasticity of the vessel

– aortic arch, 3–5 m/sec – subclavian, 7–10 m/sec

– small nondistensible peripheral arterial

15–30 m/sec

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Pulmonary Circulation Pulmonary Circulation

• low-pressure, low-resistance

• Functions

– metabolic transport of humoral substances and drugs

– Transport of blood through the lungs

– reservoir for the left ventricle  PA catheter – filtration of venous drainage

– transport of gas, fluid, and solutes across the walls of exchanging vessels.

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THE SYSTEMIC CIRCULATION

CAPACITY VESSELS

NORMAL

THE PULMONARY CIRCULATION

1. LOW RESISTANCE 2. LOW PRESSURE

(25/10 mmHg) 1. HIGH RESISTANCE 2. HIGH PRESSURE

(120/80 mmHg)

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Physiology of the Venous System Physiology of the Venous System

• 60% of the systemic blood volume is in

small veins and venules (diameters 20 μm to 2 mm)

• Venous return (VR), the rate of flow of blood from the periphery to the heart

– ~ cardiac output is equal to venous

return

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