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Cardiovascular System. Functional Organization of Cardiovascular system CARDIOVASCULAR SYSTEM HEART (PUMP) VESSELS (DISTRIBUTION SYSTEM) Blood.

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Presentation on theme: "Cardiovascular System. Functional Organization of Cardiovascular system CARDIOVASCULAR SYSTEM HEART (PUMP) VESSELS (DISTRIBUTION SYSTEM) Blood."— Presentation transcript:

1 Cardiovascular System

2 Functional Organization of Cardiovascular system CARDIOVASCULAR SYSTEM HEART (PUMP) VESSELS (DISTRIBUTION SYSTEM) Blood

3 Functions of Cardiovascular System: I. Primary (main) function of the heart: ♥ Acts as a muscular pump: ♥ Acts as a muscular pump: in order to maintain adequate level of blood flow in order to maintain adequate level of blood flow throughout CVS by pumping blood under press into throughout CVS by pumping blood under press into vascular system. vascular system. ♥ Responsible for the mass movement of fluid in ♥ Responsible for the mass movement of fluid in body. body.

4 Functions of Cardiovascular System (continued) II. Secondary functions: 1. Transportation: 1. Transportation:  delivers O 2 to tissues, & brings back CO 2 to lungs.  delivers O 2 to tissues, & brings back CO 2 to lungs.  carries absorbed digestion products to liver & tissues.  carries absorbed digestion products to liver & tissues.  carries metabolic wastes to kidneys to be excreted.  carries metabolic wastes to kidneys to be excreted.  distribution of body fluids.  distribution of body fluids. 2. Regulation: 2. Regulation:  Hormonal: carries hormones to target tissues to produce their effects.  Hormonal: carries hormones to target tissues to produce their effects.  Immune: carries antibodies, leukocytes (WBCs), cytokines, & complement  Immune: carries antibodies, leukocytes (WBCs), cytokines, & complement to aid body defense mechanism against pathogens. to aid body defense mechanism against pathogens.  Protection: carries platelets, & clotting factors to aid protection of the body  Protection: carries platelets, & clotting factors to aid protection of the body in blood clotting mechanism. in blood clotting mechanism.  Temperature: helps in regulation of body temperature, by diverting blood to cool or warm the body.  Temperature: helps in regulation of body temperature, by diverting blood to cool or warm the body.

5 Anatomy of the heart: Positioned between two bony structures – sternum and vertebrae (CPR) Hollow, muscular organ. Hollow, muscular organ.

6 Atrium: weak primer pump for the ventricle Ventricle: the main pumping force     Rt. Ventricle Lt. ventricle Rt. Ventricle Lt. ventricle Pulmonary circulation Systemic circulation Pulmonary circulation Systemic circulation

7 Valves of the heart: ♥ 2 atrioventricular (AV) valves: ■ One way valves. ■ Allow blood to flow from atria into ventricles. ■ Tricuspid (Rt) & Mitral (Lt). ♥ 2 semilunar valves : ■ One way valves. ■ At origin of pulmonary artery & aorta. ■ Pulmonary (Rt) & Aortic (Lt). ■ Open during ventricular contraction.

8 Heart Valves One way flow in heart is ensured by heart valves One way flow in heart is ensured by heart valves Valves open & close passively Valves open & close passively - open  by forward P by blood - open  by forward P by blood - close  by backward P by blood - close  by backward P by blood

9 Atrioventricular Valve Function

10 Semilunar Valve Function

11 No valves between atria and veins No valves between atria and veins Reasons Reasons Atrial pressures usually are not much higher than venous pressures Atrial pressures usually are not much higher than venous pressures Sites where venae cavae enter atria are partially compressed during atrial contraction Sites where venae cavae enter atria are partially compressed during atrial contraction

12 The fibrous skeleton of the heart Serves 3 roles: A mechanical base: atria anchored above and ventricles below A mechanical base: atria anchored above and ventricles below Perforated by 4 apertures, each containing a valve Perforated by 4 apertures, each containing a valve Insulates the ventricles Insulates the ventricles

13 Blood Flow Through and Pump Action of the Heart

14 Pulmonary circulation systemic circulation Starts at right ventricle Ends at left atrium Receives blood from right side of heart Carries blood between heart and lungs Blood perfusing the lungs is partially deoxygenated All blood flows through lungs Low pressure, low resistance Starts at left ventricle Ends at right atrium Receives blood from left side of heart Carries blood between heart and other organ systems Blood perfusing the organ systems is oxygenated Part of the blood go to different organ systems High pressure, high resistance

15 Vascular Tree Closed system of vessels Closed system of vessels Consists of Consists of Arteries Arteries Carry blood away from heart to tissues Carry blood away from heart to tissues Arterioles Arterioles Smaller branches of arteries Smaller branches of arteries Capillaries Capillaries Smaller branches of arterioles Smaller branches of arterioles Smallest of vessels across which all exchanges are made with surrounding cells Smallest of vessels across which all exchanges are made with surrounding cells Venules Venules Formed when capillaries rejoin Formed when capillaries rejoin Return blood to heart Return blood to heart Veins Veins Formed when venules merge Formed when venules merge Return blood to heart Return blood to heart

16 Arteries Structure of arterial wall  Plentiful of elastic fibers….high compliance Function:  Rapid transit passage-ways for blood from heart to tissues  Pressure reservoir

17 Arteries as a Pressure Reservoir

18 Arterioles (resistance vessels) Arterioles (resistance vessels)  Very small arteries that delivers blood to capillaries  Structure  Very little elastic tissue but thick layer of smooth muscle  Function Regulating blood flow from arteries to capillaries by regulating resistance according to tissue metabolic needs.

19 Capillaries Microscopic vessels that connects arterioles to venules Microscopic vessels that connects arterioles to venules Structure Structure  Single wall layered vessels (endothelial cells)  Undergoes extensive branching Maximized surface area and minimized diffusion distance Maximized surface area and minimized diffusion distance Velocity of blood flow through capillaries is relatively slow Velocity of blood flow through capillaries is relatively slow Provides adequate exchange time Provides adequate exchange time Function: Function:  Exchange of nutrients and wastes between blood and tissue cells

20 Capillaries cont. Under resting conditions many capillaries are not open Under resting conditions many capillaries are not open Capillaries surrounded by precapillary sphincters Capillaries surrounded by precapillary sphincters Contraction of sphincters reduces blood flowing into capillaries in an organ Contraction of sphincters reduces blood flowing into capillaries in an organ Relaxation of sphincters has opposite effect Relaxation of sphincters has opposite effect

21 Veins Carry blood from tissues to heart Carry blood from tissues to heart Structure: Structure:  Thin wall  Less smooth muscle and considerable amount of collagen  Less elastic fibers Function: Function:  Passage ways back to heart  Blood reservoir (capacitance vessels)

22 Properties of Cardiac Muscle 22

23 Heart Composed of Three Layers 23

24 Properties of Cardiac Muscle Fibers 24

25 Exhibit branching Adjacent cardiac cells are joined end to end by specialized structures known as intercalated discs Within intercalated discs there are two types of junctions Desmosomes Gap junctions..allow action potential to spread from one cell to adjacent cells. Heart function as syncytium when one cardiac cell undergoes an action potential, the electrical impulse spreads to all other cells that are joined by gap junctions so they become excited and contract as a single functional syncytium. Atrial syncytium and ventricular syncytium Histological Properties of Cardiac Muscle Fibers 25

26 THE CARDIAC MUSCLE Contractile muscle fibres (myocardium 99%) Atrial muscle fibres & Ventricular muscle fibres - Both contract same as in sk. Muscle - Duration of contraction much longer Excitatory & conductive muscle fibres (autorhythmic 1%) - Few contractile fibrils (v.weak contraction) - Exhibit either automatic rhythmic discharge(AP) OR Conduction of the AP through heart 26

27 Properties of Cardiac Muscle Fibers 1. 1. Autorhythmicity: The ability to initiate a heart beat continuously and regularly without external stimulation 2. 2. Excitability: The ability to respond to a stimulus of adequate strength and duration (i.e. threshold or more) by generating a propagated action potential 3. 3. Conductivity: The ability to conduct excitation through the cardiac tissue 4. 4. Contractility: The ability to contract in response to stimulation 27

28 1. Autorhythmicity  myogenic (independent of nerve supply)  due to the specialized excitatory & conductive system of the heart  intrinsic ability of self-excitation intrinsic ability of self-excitation (waves of depolarization) (waves of depolarization)  cardiac impulses cardiac impulses Definition: the ability of the heart to initiate its beat continuously and regularly without external stimulation 28

29 Have two important functions 1. Act as a pacemaker (set the rhythm of electrical excitation) 2. Form the conductive system (network of specialized cardiac muscle fibers that provide a path for each cycle of cardiac excitation to progress through the heart) Autorythmic fibers Forms 1% of the cardiac muscle fibers 29

30  Sinoatrial node (SA node) Specialized region in right atrial wall near opening of superior vena cava.  Atrioventricular node (AV node) Small bundle of pecialized cardiac cells located at base of right atrium near septum  Bundle of His (atrioventricular bundle) Cells originate at AV node and enters interventricular septum Divides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer walls  Purkinje fibers Small, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium Locations of autorythmic cells 30

31 Mechanism of Autorythmicity Autorythmic cells do not have stable resting membrane potential (RMP) Natural leakiness to Na & Ca  spontaneous and gradual depolarization Unstable resting membrane potential (= pacemaker potential) Gradual depolarization reaches threshold (-40 mv)  spontaneous AP generation 31

32 Rate of generation of AP at different sites of the heart RATE(Times/min)SITE 100 SA node 40 - 60 AV node 20 - 35 AV bundle, bundle branches,& Purkinje fibres  SA node acts as heart pacemaker because it has the fastest rate of generating action potential  Nerve impulses from autonomic nervous system and hormones modify the timing and strength of each heart beat but do not establish the fundamental rhythm. 32

33 Pacemaker sets HR SA node firing rates set HR Why? If SA node defective? AV node: 50 bpm ventricular cells: 35 bpm  Implant mechanical pacemaker! 33

34 2. Excitability Definition: The ability of cardiac muscle to respond to a stimulus of adequate strength & duration by generating an AP AP initiated by SA node  travels along conductive pathway  excites atrial & ventricular muscle fibres 34

35 Action potential in contractile fibers 35

36 Refractory period Long refractory period (250 msec) compared to skeletal muscle (3msec) Long refractory period (250 msec) compared to skeletal muscle (3msec) During this period membrane is refractory to further stimulation until contraction is over. During this period membrane is refractory to further stimulation until contraction is over. It lasts longer than muscle contraction, prevents tetanus It lasts longer than muscle contraction, prevents tetanus Gives time to heart to relax after each contraction, prevent fatigue Gives time to heart to relax after each contraction, prevent fatigue It allows time for the heart chambers to fill during diastole before next contraction It allows time for the heart chambers to fill during diastole before next contraction AP in skeletal muscle : 1-5 msec AP in cardiac muscle :200 -300 msec 36

37 3. Contractility Definition: ability of cardiac muscle to contract in response to stimulation 37

38 Excitation-Contraction Coupling in Cardiac Contractile Cells Similar to that in skeletal muscles 38

39 4. Conductivity Definition: property by which excitation is conducted through the cardiac tissue 39

40 Criteria for spread of excitation & efficient cardiac function 1. Atrial excitation and contraction should be complete before onset of ventricular contraction - ensures complete filling of the ventricles during diastole 2. Excitation of cardiac muscle fibres should be coordinated  ensure each heart chamber contracts as a unit  accomplish efficient pumping - smooth uniform contraction essential to squeeze out blood 3. Pair of atria & pair of ventricles should be functionally co- ordinated  both members contract simultaneously - permits synchronized pumping of blood into pulmonary & systemic circulation 40

41 TissueConduction rate (m/s) Atrial muscle 0.3 Atrial pathways 1 AV node0.05 Bundle of His 1 Purkinje system 4 Ventricular muscle 0.3-0.5 41

42 Cardiac impulse originates at SA node Cardiac impulse originates at SA node Action potential spreads throughout right and left atria Action potential spreads throughout right and left atria Impulse passes from atria into ventricles through AV node (only point of electrical contact between chambers) Impulse passes from atria into ventricles through AV node (only point of electrical contact between chambers) Action potential briefly delayed at AV node (ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling) Action potential briefly delayed at AV node (ensures atrial contraction precedes ventricular contraction to allow complete ventricular filling) Impulse travels rapidly down interventricular septum by means of bundle of His Impulse travels rapidly down interventricular septum by means of bundle of His Impulse rapidly disperses throughout myocardium by means of Purkinje fibers Impulse rapidly disperses throughout myocardium by means of Purkinje fibers Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions Rest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions Spread of Cardiac Excitation 42

43 Normal conduction pathway: SA node -> atrial muscle -> AV node -> bundle of His -> Left and Right Bundle Branches -> Ventricular muscle

44 Electrocardiography A recording of the electrical activity of the heart over time Gold standard for diagnosis of cardiac arrhythmias Helps detect electrolyte disturbances (hyper- & hypokalemia) Allows for detection of conduction abnormalities Screening tool for ischemic heart disease during stress tests Helpful with non-cardiac diseases (e.g. pulmonary embolism or hypothermia

45 Electrocardiogram (ECG/EKG) Is a recording of electrical activity of heart conducted thru ions in body to surface Is a recording of electrical activity of heart conducted thru ions in body to surface Fig 13.22a 13-60

46 Recording of the ECG: Leads used: Limb leads are I, II, II. So called because at one time subjects had to literally place arms and legs in buckets of salt water. Each of the leads are bipolar; i.e., it requires two sensors on the skin to make a lead. If one connects a line between two sensors, one has a vector. There will be a positive end at one electrode and negative at the other. The positioning for leads I, II, and III were first given by Einthoven. Form the basis of Einthoven’s triangle.

47 Types of ECG Recordings Bipolar leads record voltage between electrodes placed on wrists & legs (right leg is ground) Bipolar leads record voltage between electrodes placed on wrists & legs (right leg is ground) Lead I records between right arm & left arm Lead I records between right arm & left arm Lead II: right arm & left leg Lead II: right arm & left leg Lead III: left arm & left leg Lead III: left arm & left leg Fig 13.23 13-61

48 Fig. 13.22b

49 3 distinct waves are produced during cardiac cycle 3 distinct waves are produced during cardiac cycle P wave caused by atrial depolarization P wave caused by atrial depolarization QRS complex caused by ventricular depolarization QRS complex caused by ventricular depolarization T wave results from ventricular repolarization T wave results from ventricular repolarization ECG Fig 13.24 13-63

50 Elements of the ECG

51

52 Fig. 13.24b

53 Fig. 13.24c

54 Fig. 13.24d

55 Elements of the ECG: P wave Depolarization of both atria; Relationship between P and QRS helps distinguish various cardiac arrhythmias Shape and duration of P may indicate atrial enlargement

56

57 QRS complex: Represents ventricular depolarization Larger than P wave because of greater muscle mass of ventricles Normal duration = 0.08-0.12 seconds Its duration, amplitude, and morphology are useful in diagnosing cardiac arrhythmias, ventricular hypertrophy, MI, electrolyte derangement, etc. Q wave greater than 1/3 the height of the R wave, greater than 0.04 sec are abnormal and may represent MI

58

59 PR interval : From onset of P wave to onset of QRS Normal duration = 0.12-2.0 sec (120- 200 ms) (3-4 horizontal boxes) Represents atria to ventricular conduction time (through His bundle) Prolonged PR interval may indicate a 1st degree heart block

60 Fig. 13.24g

61 T wave: Represents repolarization or recovery of ventricles Interval from beginning of QRS to apex of T is referred to as the absolute refractory period

62 ST segment: Connects the QRS complex and T wave Duration of 0.08-0.12 sec (80-120 msec QT Interval Measured from beginning of QRS to the end of the T wave Normal QT is usually about 0.40 sec QT interval varies based on heart rate

63 Ischemic Heart Disease Is most commonly due to atherosclerosis in coronary arteries Is most commonly due to atherosclerosis in coronary arteries Ischemia occurs when blood supply to tissue is deficient Ischemia occurs when blood supply to tissue is deficient Causes increased lactic acid from anaerobic metabolism Causes increased lactic acid from anaerobic metabolism Often accompanied by angina pectoris (chest pain) Often accompanied by angina pectoris (chest pain) 13-78

64 Ischemic Heart Disease Detectable by changes in S-T segment of ECG Detectable by changes in S-T segment of ECG Myocardial infarction (MI) is a heart attack Myocardial infarction (MI) is a heart attack Diagnosed by high levels of creatine phosphate (CPK) & lactate dehydrogenase (LDH) Diagnosed by high levels of creatine phosphate (CPK) & lactate dehydrogenase (LDH) Fig 13.34 13-79

65 Arrhythmias Detected on ECG Arrhythmias are abnormal heart rhythms Arrhythmias are abnormal heart rhythms Heart rate 100/min is tachycardia Heart rate 100/min is tachycardia Fig 13.35 13-80

66 Arrhythmias Detected on ECG continued In flutter contraction rates can be 200-300/min In flutter contraction rates can be 200-300/min In fibrillation contraction of myocardial cells is uncoordinated & pumping ineffective In fibrillation contraction of myocardial cells is uncoordinated & pumping ineffective Ventricular fibrillation is life-threatening Ventricular fibrillation is life-threatening Electrical defibrillation resynchronizes heart by depolarizing all cells at same time Electrical defibrillation resynchronizes heart by depolarizing all cells at same time Fig 13.35 13-81

67 AV node block occur when node is damaged AV node block occur when node is damaged First–degree AV node block is when conduction through AV node > 0.2 sec First–degree AV node block is when conduction through AV node > 0.2 sec Causes long P-R interval Causes long P-R interval Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventricles Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventricles Causes P waves with no QRS Causes P waves with no QRS In third-degree or complete AV node block no atrial activity passes to ventricles In third-degree or complete AV node block no atrial activity passes to ventricles Ventricles driven slowly by bundle of His or Purkinjes Ventricles driven slowly by bundle of His or Purkinjes Arrhythmias Detected on ECG continued 13-82

68 AV node block occurs when node is damaged AV node block occurs when node is damaged First–degree AV node block is when conduction thru AV node > 0.2 sec First–degree AV node block is when conduction thru AV node > 0.2 sec Causes long P-R interval Causes long P-R interval Arrhythmias Detected on ECG continued Fig 13.36 13-83

69 Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventricles Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventricles Causes P waves with no QRS Causes P waves with no QRS Arrhythmias Detected on ECG continued Fig 13.36 13-84

70 In third-degree or complete AV node block, no atrial activity passes to ventricles In third-degree or complete AV node block, no atrial activity passes to ventricles Ventricles are driven slowly by bundle of His or Purkinjes Ventricles are driven slowly by bundle of His or Purkinjes Arrhythmias Detected on ECG continued Fig 13.36 13-85

71 THE CARDIAC CYCLE

72 ISOVOLUMETRIC CONTRACTION The Beginning of systole

73 ISOVOLUMETRIC CONTRACTION Heart The atrioventricular (AV) valves close at the beginning of this phase. Electrically, ventricular systole is defined as the interval between the QRS complex and the end of the T wave (the Q-T interval). Mechanically, ventricular systole is defined as the interval between the closing of the AV valves and the opening of the semilunar valves (aortic and pulmonary valves).

74 RAPID EJECTION

75 RAPID EJECTION Heart The semilunar (aortic and pulmonary) valves open at the beginning of this phase.

76 REDUCED EJECTION The end of systole

77 REDUCED EJECTION Heart At the end of this phase the semilunar (aortic and pulmonary) valves close.

78 ISOVOLUMETRIC RELAXATION The beginning of Diastole

79 ISOVOLUMETRIC RELAXATION Heart At the beginning of this phase the AV valves are closed.

80 RAPID VENTRICULAR FILLING

81 REDUCED VENTRICULAR FILLING (Diastasis)

82 Cardiac Output When the heart contracts

83 Cardiac Output Cardiac Output is the volume of blood pumped each minute, and is expressed by the following equation: CO = SV x HR CO = SV x HR Where: Where: CO is cardiac output expressed in L/min (normal ~5 L/min) CO is cardiac output expressed in L/min (normal ~5 L/min) SV is stroke volume per beat SV is stroke volume per beat HR is the number of beats per minute HR is the number of beats per minute

84

85 Preload

86 Preload: Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume…EDV) Preload: Preload is the muscle length prior to contractility, and it is dependent of ventricular filling (or end diastolic volume…EDV) This value is related to right atrial pressure. This value is related to right atrial pressure. The most important determining factor for preload is venous return. The most important determining factor for preload is venous return.

87 afterload

88 Afterload: Afterload is the tension (or the arterial pressure) against which the ventricle must contract. Afterload: Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases, afterload also increases. If arterial pressure increases, afterload also increases. Afterload for the left ventricle is determined by aortic pressure Afterload for the left ventricle is determined by aortic pressure Afterload for the right ventricle is determined by pulmonary artery pressure. Afterload for the right ventricle is determined by pulmonary artery pressure.

89 Inotropic and chronotropic Homometric regulation Homometric regulation

90 Regulation of heart and blood vessels

91 Significance: To maintain normal blood pressure, To maintain normal blood pressure, blood flow to be relativity constant. blood flow to be relativity constant. To redistribute blood supply to To redistribute blood supply to different tissue and organs. different tissue and organs. To redistribute blood supply to To redistribute blood supply to different tissue and organs. different tissue and organs.

92 Copyright 2009, John Wiley & Sons, Inc. CV Center

93 A. Neural regulation 1. Innervation of the heart dual innervation (1) cardiac sympathetic nerve (2) cardiac parasympathetic nerve A. Neural regulation 1. Innervation of the heart dual innervation (1) cardiac sympathetic nerve (2) cardiac parasympathetic nerve

94 Cardiac Symp n Cardiac Vagal n IML1-5 Amgiguus N, Dorsal motor N of vagus Preganglionic f Preganglionic f ACh ACh Postganglionic N N receptor Postganglionic f Postganglionic f NE Effects Ach inotropic  receptor chronotropic M receptor dromotropic propranolol Blocker atropine

95 (1) Effects of vagal nerve Vagal nerve ending → ACh. → binds to M cholinergic receptor →↑permeability to K + results in: in: ↓automaticity of S-A node :

96 ↓contractility due to : ↓contractility due to : ↑K + efflux at phase 3 repolarization ↑K + efflux at phase 3 repolarization →↓AP duration → Ca 2+ influx ↓ →↓AP duration → Ca 2+ influx ↓ → [Ca 2+ ] i ↓; → [Ca 2+ ] i ↓; ACh inhibits Ca 2+ influx → [Ca 2+ ] i ACh inhibits Ca 2+ influx → [Ca 2+ ] i ↓→ ↓contractility. ↓→ ↓contractility. ↓conductivity ↓conductivity

97 The left Vagus n:↓conductivity in A-V node The right Vagus n: ↓automaticity in S-A node.

98 (2) Effects of cardiac sympathetic nerve: nerve: Cardiac sympathetic nerve ending Cardiac sympathetic nerve ending → noradrenaline → binds to β- → noradrenaline → binds to β- adrenergic receptor→↑permeability adrenergic receptor→↑permeability to Ca 2+ leads to: to Ca 2+ leads to:

99 ↑Automaticity ↑Automaticity ↑Conductivity ↑Conductivity ↑Contractility ↑Contractility

100 The left Symp n : ↑contractility. The right Symp n : ↑HR.

101 Sympathetic input - HEART ACTIONS Nerve fibers release NE Nerve fibers release NE SA, atria, and ventricles SA, atria, and ventricles ↑ HR and contractility ↑ HR and contractility R side SA node R side SA node L side contractility L side contractility MECHANISM ß1 receptors – pacemaker activity ß1 myocardium contraction

102 Parasympathetic input - HEART ACTIONS Vagus nerve releases ACH Vagus nerve releases ACH SA and myocardium SA and myocardium HR and conduction velocity HR and conduction velocity R side SA node (HR) R side SA node (HR) L side contractility (slight) L side contractility (slight) MECHANISM Muscarinic receptors (M2) ßγ subunit (HR) Nitric oxide (weak inotropic effect)

103 Cardiac reflexes

104 Bainbridge Reflex Infusion of volume causes an increase in heart rate due to activation of atrial stretch receptors which causes medullary center activation of sympathetic output to the SA node Infusion of volume causes an increase in heart rate due to activation of atrial stretch receptors which causes medullary center activation of sympathetic output to the SA node

105 Reflex from atria Reflex from atria Type A Type A Type B Type B Reflex from left ventricle Reflex from left ventricle Coronary chemo reflex Coronary chemo reflex Sino Aortic reflex Sino Aortic reflex Reflex from periphery Reflex from periphery Reflex from higher centers Reflex from higher centers

106 Arterial blood pressure Systolic pressure Systolic pressure Diastolic pressure Diastolic pressure Mean pressure Mean pressure MAP = DP + 1/3 (SP-DP)

107 REGULATION OF ARTERIAL BLOOD PRESSURE Regulation of Blood Pressure Nervous Mechanism Renal Mechanism Hormonal Mechanism Local Mechanism By Vasomotor Center and Impulses from Periphery By Regulation of ECF Volume and renin – angiotensin mechanism By Vasocons- -trictor and Vasodilator Hormones By Local Vasocons- -trictors and Vasodilators

108 REGULATION OF ARTERIAL BLOOD PRESSURE SHORT-TERM CONTROL SHORT-TERM CONTROL (IN SEC – MIN) INTERMEDIATE-TERM CONTROL INTERMEDIATE-TERM CONTROL (30 MIN – HOURS) LONG – TERM CONTROL LONG – TERM CONTROL

109 SHORT-TERM CONTROL OF AP CNS ISCHAEMIC RESPONSE CNS ISCHAEMIC RESPONSE BARORECEPTOR REFLEX BARORECEPTOR REFLEX CHEMORECEPTOR REFLEX CHEMORECEPTOR REFLEX

110 INTERMEDIATE CONTROL OF AP RENIN - ANGIOTENSIN – VASOCONSTRICTOR MECH. RENIN - ANGIOTENSIN – VASOCONSTRICTOR MECH. STRESS RELAXATION OF VASCULATURE STRESS RELAXATION OF VASCULATURE FLUID – SHIFT THROUGH THE CAPILLARY WALL FLUID – SHIFT THROUGH THE CAPILLARY WALL

111 LONG – TERM CONTROL OF AP RENAL FLUID SHIFT (THROUGH ADH / VOLUME RECEPTORS) RENAL FLUID SHIFT (THROUGH ADH / VOLUME RECEPTORS) RENIN – ANGIOTENSIN – ALDOSTERONE MECH. RENIN – ANGIOTENSIN – ALDOSTERONE MECH.

112 Sequential events by which increased salt intake increases the arterial pressure. Increased salt intake Increased extracellular volume Increased arterial pressure Decreased renin and angiotensin Decreased renal retention of salt and water Return of extracellular volume almost to normal Return of arterial pressure almost to normal

113 LOCAL MECH. FOR CONTROL OF AP A. Vasodilatos 1. EDRF 2. Bradykinin 3. Histamine 4. ANP 5. VIP 6. Substance P 7. Prostacyclin 8. Adenosine 9. K + 10. Acidosis [ CO 2 ] 11. Hypercapnia 12. Hypoxia 13. Temperature

114 B. Vasoconstrictors 1.Endothelin-1 2.Angiotensin II 3.Norepinephrine 4.ADH 5.Serotonin 6.Thromboxane A2 7.Neuropeptide-Y 8.Cold

115 HORMONAL MECH. FOR CONTROL OF AP HORMONES RAISING AP HORMONES RAISING AP ADRENALINE ADRENALINE NORADRENALINE NORADRENALINE THYROXINE THYROXINE ALDOSTERONE ALDOSTERONE VASOPRESSIN VASOPRESSIN ANGIOTENSIN ANGIOTENSIN SEROTONIN SEROTONIN

116 HORMONAL MECH. FOR CONTROL OF AP HORMONES DECREASING AP HORMONES DECREASING AP VIP VIP BRADY KININ BRADY KININ PROSTAGLANDIN PROSTAGLANDIN HISTAMINE HISTAMINE ACETYLCHOLINE ACETYLCHOLINE ANP ANP

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