Physiology SECTON IV CIRCULATION Chapter 9~11. 2009-09 SECTON VI CIRCULATION Chapter 9~112...

Physiology

SECTON IV

CIRCULATION

Chapter 9~11

2009-09SECTON VI CIRCULATION Chapter 9~11 2

Introduction

Definition of circulationCirculatory system is made up of the heart and vessels in which blood is flowing in certain direction, going round and begin again

Function of circulationCardiovascular system transport the blood flow circulating the whole body, maintain the homeostasis ►Heart---- as a blood pump►Vessels---- distributing and collecting the blood flow


Introduction

Pulmonary circulation Gases exchange in the

lungsSystemic circulations

Metabolic substances exchange in every well of the body


Introduction

Non-circulation functionThe heart and vessels as the endocrine organs►Atrial natriuretic peptide (ANP)…►Endothelin (ET)…


Content of the course

CHAP 9 ELECTRICAL PROPERTIES OF THE CARDIAC MUSCLE

CHAP 10 THE ELECTROCARDIOGRAM

CHAP 11 THE HEART AS A PUMP

CHAP 12 DYNAMICS OF BLOOD AND LYMPH FLOW

CHAP 13 CARDIOVASCULAR REGULATORY MECHANISMS

CHAP 14 CIRCULATION THROUGH SPECIAL REGIONS



9.1 INTRODUCTION

9.2 RESTING MEMBRANE POTENTIAL AND ACTION POTENTIAL

9.3 ORIGIN AND SPREAD OF CARDIAC EXCITATION

9.4 EFFECT OF CARDIAC INNERVATION STIMULATION



9.1 INTRODUCTION

Physiologic properties ►Electrophysiological properties

Excitability AutorhythmicityConductivity

►Mechanical propertyContractility

Conducting system


9.1 INTRODUCTION

Cardiac myocyte►Contractile myocardium

Atrial muscles, ventricular muscles►Autorhythmic myocardium

S-A node, A-V node, bundle of His and its branches, Purkinje fibers

Electrical activity of myocardium



9.2.1 Resting membrane potential EK ＝ 61.5·log [K+]o/ [K+]i

＝ 61.5·log [4]o/ [135]I

＝－ 90mv



9.2.2 The ion currents responsible for the action potential

Ventricular action potential►Depolarizing phase

Phase 0 : INa, IK , ICa(L)►Repolarizing phase

Phase 1 : ItoPhase 2 : ICa (L) , IKPhase 3 : IKPhase 4 :resting state, active ion exchange



Factors affecting excitability of myocardium►Relationship of resting potential and threshold level►Characters of Na+ channel

Resting:Active: Inactive: effective refractory period



9.2.3 The pacemaker potentialsS-A node action potential►Auto-depolarizing phase—4: IK, ICa(T), INa(F),

Ca2+ sparks ►Depolarizing phase—0: ICa(L)

►Repolarizing phase—3: IK

Purkinje fibers►4: INa(F), IK



Factors affecting autorhythmicity of myocardium►Maximum diastolic potential►Spontaneous depolarization►Threshold potential



9.3.1 Anatomic consideration ►Spetial conductive system in heart►SA node: normal pacemaker►Autonomic innervations

Right vagus and sympathetic nerve→ SA nodeLeft vagus and sympathetic nerve→ A-V node



9.3.2 Spread of cardiac excitation►Sequence of cardiac excitation

Normal pacemaker: S-A node function as the pacemaker for the entire heartLatent or sub ordinary pacemaker Ectopic pacemaker

►Factors affecting conductivitySpeed and amplitude of depolarizationExcitability of neighbor cell


9.4 EFFECT OF CARDIAC INNERVATIONS STIMULATION

9.4.1 Effect of vagal cardiac nerves stimulation ►The parasympathetic postganglionic fibers release

primarily acetylcholine (ACh), which binds to M2-receptors →G(γ)►Inhibiting the heart actions

9.4.2 Effect of sympathetic cardiac nerves stimulation►The sympathetic postganglionic fibers release prim

arily norepinephrine (NE), which binds mainly to 2-receptors →Gs►Exciting the heart actions



10.1 RECORDING LEADS OF ECG

10.2 NORMAL ECG (EKG)




Basic principle ►Body is a volume conductor►The heart is a current source in the center of a volu

me conductor (Einthoven's triangle)►The ECG may be recorded by using an exploring electrod►Depolarization moving toward an active electrode in a volume conductor produces a positive deflection, whereas depolarization moving in the opposite direction produces a negative deflection



Recording lead►Bipolar recording

Standard limb leadsleads I, II, and III

Augmented limb leadsaVL, aVR, aVF

►Unipolar recording Precordial leads

Waves of the ECG►P, Q R S, T (,U)


10.2 NORMAL ECG (EKG)

Duration of the ECG►PR interval: 0.18s

Atrial depolarization and conduction through AV node►QRS duration: 0.08s

Ventricular depolarization and atrial repolarization►QT interval: 0.40s

Ventricular depolarization plus ventricular repolarization

►ST interval: 0.32sVentricular repolarization ST segment



11.1 MECHANICAL PROPERTIES OF THE CARDIAC MUSCLE

11.2 MECHANICAL EVENTS OF THE CARDIAC CYCLE

11.3 CARDIAC OUTPUT

11.4 CARDIAC RESERVE




11.1.1 Contractile response Dependent upon [Ca2+]o

[Ca2+]i↑ triggered by Ca2+o

No tetanus ►Contractile response lasts about 1.5 times as long as the action potential►Long ERP: phase 0 →3(repolarization -50mv)

Contraction in synchronism



11.1.2 Relation between muscle fiber length and tension►Starling‘s law of the heart (Frank-Starling law )

Energy of contraction is proportional to the initial length of the cardiac muscle fiber.The length of the muscle fibers (ie, the extent of the preload) is proportionate to the end-diastolic volume

►Heterometric regulation: dependent on initial length of myocardium fibers



►Contractility— inotropic effectHomometric regulation: independent of initial lengthActive regulation by the organism



11.2.1 Cardiac cyclePumping function is periodicity action

Heart rate: 60~100 beats/minCardiac cycle: 0.8s (~72 beats/min)

Systole and diastole►Atria systole and diastole►Ventricular systole and diastole►Whole cardiac diastole



Mechanism events: filling and ejection: driving the blood flow from vein to artery in certain direction►Difference pressure between atria, ventricles and arteries►Valves status: opened or closed ►Change of volume in ventricular chambers►Direction of blood flow



11.2.2 Atria systoleEvents in late diastole►The mitralis and tricuspid are opened and t

he aortic and pulmonary valves are closed►Blood flows: into the heart from caval vein, f

illing the atria and ventricles►Pressure in the ventricles remains low



Atria systole ►Atrial systole starts after the P wave of the EC

G►Propels some additional blood into the ventri

cles►Vena cava and pulmonary veins narrowed►Vome regurgitation of blood into the veins du

ring atrial systole



11.2.3 Ventricular systoleVentricular systole starts near the end of the R

wave and ends just after the T wave of the ECG

Isovolumetric ventricular contraction►lasts about 0.05 s►Mitral and tricuspid (AV) valves all closed►Intraventricular pressure rises sharply as th

e myocardium presses on the blood►No blood into or out the ventricles



Ventricular ejection►the ventricular pressures exceed aorta (80

mm Hg; 10.6 kPa) and pulmonary artery (10 mm Hg) ►The aortic and pulmonary valves open►Propels blood into the large arteries more ra

pidly



11.2.4 Ventricular diastole Isovolumetric ventricular relaxation►Ventricular pressure continues to drop rapid

ly ► The aortic and pulmonary valves are closed

Ventricular filling►Pressure falls below the atrial pressure►the AV valves open, permitting the ventricle

s to fill



11.2.5 Heat sounds►1st sounds: 0.15 s, 25-45 Hz

Myocardium contractionFlow impacting the cardiac wall Vibration set up by closure of A-V valves

►2nd sounds: 0.12 s, 50 Hz. Vibrations associated with closure of arterial valvesArterial roots vibration


11.3 CARDIAC OUTPUT

11.3.1 Cardiac output in various conditions►Stroke volume & ejection fraction►Cardiac output (CO, minute cardiac output) CO=Stroke volume × Heart rate

CO=70mL/beat×72/min=5.0L/min

►Cardiac index=CO/m2


11.3 CARDIAC OUTPUT

11.3.2 Factors controlling cardiac output

Control of stroke volume ： the major factors influencing force of contraction ►Intrinsic regulation: the Frank-Starling mec

hanismVenous flow returned →changes in end-diastolic volume →heterometric autoregulation


11.3 CARDIAC OUTPUT

►Extrinsic regulation: sympathetic stimulation, epinephrineTo increase myocardial contractility (inotropic status)→ the force of contraction at any given end-diastolic volume → hotmometric regulation


11.3 CARDIAC OUTPUT

►Afterload: the arterial pressuresAgainst which the ventricles pumpIncreasing pressures decrease the strength of contraction


11.3 CARDIAC OUTPUT

Control of heart rate►Cardiac nerves

Parasympathetic nerves (Cardiac Vagus) : heart rateSympathetic nerves: heart rate

►Epinephrine heart rate


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Physiology SECTON IV CIRCULATION Chapter 9~11. 2009-09 SECTON VI CIRCULATION Chapter 9~112...

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