2Functional Organization of Cardiovascular system HEART(PUMP)VESSELS(DISTRIBUTIONSYSTEM)Blood
3Functions of Cardiovascular System: I. Primary (main) function of the heart:♥ Acts as a muscular pump:in order to maintain adequate level of blood flowthroughout CVS by pumping blood under press intovascular system.♥ Responsible for the mass movement of fluid inbody.
4Functions of Cardiovascular System (continued) II. Secondary functions:1. Transportation: delivers O2 to tissues, & brings back CO2 to lungs. carries absorbed digestion products to liver & tissues. carries metabolic wastes to kidneys to be excreted. distribution of body fluids.2. Regulation: Hormonal: carries hormones to target tissues to produce their effects. Immune: carries antibodies, leukocytes (WBCs), cytokines, & complementto aid body defense mechanism against pathogens. Protection: carries platelets, & clotting factors to aid protection of the bodyin blood clotting mechanism. Temperature: helps in regulation of body temperature, by diverting blood to cool or warm the body.
5Anatomy of the heart:Positioned between two bony structures – sternum and vertebrae(CPR)Hollow, muscular organ.
6Atrium: weak primer pump for the ventricle Ventricle: the main pumping force Rt. Ventricle Lt. ventriclePulmonary circulation Systemic circulation
7Valves of the heart: ♥ 2 atrioventricular (AV) valves: ■ One way valves.■ Allow blood to flow fromatria into ventricles.■ Tricuspid (Rt) & Mitral(Lt).♥ 2 semilunar valves :■ One way valves.■ At origin of pulmonary artery& aorta.■ Pulmonary (Rt) & Aortic (Lt).■ Open during ventricularcontraction.
8Heart Valves One way flow in heart is ensured by heart valves Valves open & close passively- open by forward P by blood- close by backward P by blood
14Pulmonary circulation systemic circulationPulmonary circulationStarts at left ventricleEnds at right atriumReceives blood from left side of heartCarries blood between heart and other organ systemsBlood perfusing the organ systems is oxygenatedPart of the blood go to different organ systemsHigh pressure, high resistanceStarts at right ventricleEnds at left atriumReceives blood from right side of heartCarries blood between heart and lungsBlood perfusing the lungs is partially deoxygenatedAll blood flows through lungsLow pressure, low resistance
15Vascular Tree Closed system of vessels Consists of Arteries Carry blood away from heart to tissuesArteriolesSmaller branches of arteriesCapillariesSmaller branches of arteriolesSmallest of vessels across which all exchanges are made with surrounding cellsVenulesFormed when capillaries rejoinReturn blood to heartVeinsFormed when venules merge
16ArteriesFunction:Rapid transit passage-ways for blood from heart to tissuesPressure reservoirStructure of arterial wallPlentiful of elastic fibers….high compliance
18Arterioles (resistance vessels) Very small arteries that delivers blood to capillariesStructureVery little elastic tissue but thick layer of smooth muscleFunction Regulating blood flow from arteries to capillaries by regulating resistance according to tissue metabolic needs.
19Capillaries Microscopic vessels that connects arterioles to venules StructureSingle wall layered vessels (endothelial cells)Undergoes extensive branchingMaximized surface area and minimized diffusion distanceVelocity of blood flow through capillaries is relatively slowProvides adequate exchange timeFunction:Exchange of nutrients and wastes between blood and tissue cells
20Capillaries cont.Under resting conditions many capillaries are not openCapillaries surrounded by precapillary sphinctersContraction of sphincters reduces blood flowing into capillaries in an organRelaxation of sphincters has opposite effect
21Veins Carry blood from tissues to heart Structure: Thin wall Less smooth muscle and considerable amount of collagenLess elastic fibersFunction:Passage ways back to heartBlood reservoir (capacitance vessels)
25Histological Properties of Cardiac Muscle Fibers Exhibit branchingAdjacent cardiac cells are joined end to end by specialized structures known as intercalated discsWithin intercalated discs there are two types of junctionsDesmosomesGap junctions..allow action potential to spread from one cell to adjacent cells.Heart function as syncytiumwhen 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
26THE CARDIAC MUSCLE Contractile muscle fibres (myocardium 99%) Atrial muscle fibres & Ventricular muscle fibres- Both contract same as in sk. Muscle- Duration of contraction much longerExcitatory & conductive muscle fibres (autorhythmic 1%)- Few contractile fibrils (v.weak contraction)- Exhibit either automatic rhythmic discharge(AP)ORConduction of the AP through heart
27Properties of Cardiac Muscle Fibers Autorhythmicity: The ability to initiate a heart beat continuously and regularly without external stimulationExcitability: The ability to respond to a stimulus of adequate strength and duration (i.e. threshold or more) by generating a propagated action potentialConductivity: The ability to conduct excitation through the cardiac tissueContractility: The ability to contract in response to stimulation
281. AutorhythmicityDefinition: the ability of the heart to initiate its beat continuously and regularly without external stimulationmyogenic (independent of nerve supply)due to the specialized excitatory & conductive system of the heartintrinsic ability of self-excitation(waves of depolarization)cardiac impulses
29Autorythmic fibers Forms 1% of the cardiac muscle fibers Have two important functions1. 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)
30Locations of autorythmic cells Sinoatrial node (SA node)Specialized region in right atrial wall near opening of superior vena cava.Atrioventricular node (AV node)Small bundle of pecializedcardiac cells located at base of right atrium near septumBundle of His (atrioventricular bundle)Cells originate at AV node and enters interventricular septumDivides to form right and left bundle branches which travel down septum, curve around tip of ventricular chambers, travel back toward atria along outer wallsPurkinje fibersSmall, terminal fibers that extend from bundle of His and spread throughout ventricular myocardium
31Mechanism of Autorythmicity Autorythmic cells do not have stable resting membrane potential (RMP)Natural leakiness to Na & Ca spontaneous and gradual depolarizationUnstable resting membrane potential (= pacemaker potential)Gradual depolarization reaches threshold (-40 mv) spontaneous AP generation
32Rate of generation of AP at different sites of the heart (Times/min)SITE100SA nodeAV nodeAV bundle, bundle branches,& Purkinje fibresSA node acts as heart pacemaker because it has the fastest rate of generating action potentialNerve impulses from autonomic nervous system and hormones modify the timing and strength of each heart beat but do not establish the fundamental rhythm.
33Pacemaker sets HR Implant mechanical pacemaker! SA node firing rates set HRWhy?If SA node defective?AV node: 50 bpmventricular cells: 35 bpm Implantmechanicalpacemaker!
342. ExcitabilityDefinition: The ability of cardiac muscle to respond to a stimulus of adequate strength & duration by generating an APAP initiated by SA nodetravels along conductive pathway excites atrial & ventricular muscle fibres
36Refractory periodLong refractory period (250 msec) compared to skeletal muscle (3msec)During this period membrane is refractory to further stimulation until contraction is over.It lasts longer than muscle contraction, prevents tetanusGives time to heart to relax after each contraction, prevent fatigueIt allows time for the heart chambers to fill during diastole before next contractionAP in skeletal muscle : 1-5 msecAP in cardiac muscle : msec
373. ContractilityDefinition: ability of cardiac muscle to contract in response to stimulation
38Excitation-Contraction Coupling in Cardiac Contractile Cells Similar to that in skeletal muscles
394. ConductivityDefinition: property by which excitation is conducted through the cardiac tissue
40Criteria 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 diastole2. 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 blood3. Pair of atria & pair of ventricles should be functionally co-ordinated both members contract simultaneously- permits synchronized pumping of blood into pulmonary & systemic circulation
41TissueConduction rate (m/s)Atrial muscle0.3Atrial pathways1AV node0.05Bundle of HisPurkinje system4Ventricular muscle
42Spread of Cardiac Excitation Cardiac impulse originates at SA nodeAction potential spreads throughout right and left atriaImpulse 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)Impulse travels rapidly down interventricular septum by means of bundle of HisImpulse rapidly disperses throughout myocardium by means of Purkinje fibersRest of ventricular cells activated by cell-to-cell spread of impulse through gap junctions
43Normal conduction pathway: SA node -> atrial muscle -> AV node -> bundle of His -> Left and Right Bundle Branches -> Ventricular muscle
44ElectrocardiographyA recording of the electrical activity of the heart over timeGold standard for diagnosis of cardiac arrhythmiasHelps detect electrolyte disturbances (hyper- & hypokalemia)Allows for detection of conduction abnormalitiesScreening tool for ischemic heart disease during stress testsHelpful with non-cardiac diseases (e.g. pulmonary embolism or hypothermia
45Electrocardiogram (ECG/EKG) Is a recording of electrical activity of heart conducted thru ions in body to surfaceFig 13.22a13-60
46Recording 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.
47Types of ECG Recordings Bipolar leads record voltage between electrodes placed on wrists & legs (right leg is ground)Lead I records between right arm & left armLead II: right arm & left legLead III: left arm & left legFig 13.2313-61
49ECG 3 distinct waves are produced during cardiac cycle P wave caused by atrial depolarizationQRS complex caused by ventricular depolarizationT wave results from ventricular repolarizationFig 13.2413-63
57QRS complex: Represents ventricular depolarization Larger than P wave because of greater muscle mass of ventriclesNormal duration = secondsIts 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
59PR interval: From onset of P wave to onset of QRS Normal duration = sec ( ms) (3-4 horizontal boxes)Represents atria to ventricular conduction time (through His bundle)Prolonged PR interval may indicate a 1st degree heart block
61T wave: Represents repolarization or recovery of ventricles Interval from beginning of QRS to apex of T is referred to as the absolute refractory period
62ST segment: QT Interval Connects the QRS complex and T wave Duration of sec ( msecQT IntervalMeasured from beginning of QRS to the end of the T waveNormal QT is usually about 0.40 secQT interval varies based on heart rate
63Ischemic Heart Disease Is most commonly due to atherosclerosis in coronary arteriesIschemia occurs when blood supply to tissue is deficientCauses increased lactic acid from anaerobic metabolismOften accompanied by angina pectoris (chest pain)13-78
64Ischemic Heart Disease Detectable by changes in S-T segment of ECGMyocardial infarction (MI) is a heart attackDiagnosed by high levels of creatine phosphate (CPK) & lactate dehydrogenase (LDH)Fig 13.3413-79
65Arrhythmias Detected on ECG Arrhythmias are abnormal heart rhythmsHeart rate <60/min is bradycardia; >100/min is tachycardiaFig 13.3513-80
66Arrhythmias Detected on ECG continued In flutter contraction rates can be /minIn fibrillation contraction of myocardial cells is uncoordinated & pumping ineffectiveVentricular fibrillation is life-threateningElectrical defibrillation resynchronizes heart by depolarizing all cells at same timeFig 13.3513-81
67Arrhythmias Detected on ECG continued AV node block occur when node is damagedFirst–degree AV node block is when conduction through AV node > 0.2 secCauses long P-R intervalSecond-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventriclesCauses P waves with no QRSIn third-degree or complete AV node block no atrial activity passes to ventriclesVentricles driven slowly by bundle of His or Purkinjes13-82
68Arrhythmias Detected on ECG continued AV node block occurs when node is damagedFirst–degree AV node block is when conduction thru AV node > 0.2 secCauses long P-R intervalFig 13.3613-83
69Arrhythmias Detected on ECG continued Second-degree AV node block is when only 1 out of 2-4 atrial APs can pass to ventriclesCauses P waves with no QRSFig 13.3613-84
70Arrhythmias Detected on ECG continued In third-degree or complete AV node block, no atrial activity passes to ventriclesVentricles are driven slowly by bundle of His or PurkinjesFig 13.3613-85
72ISOVOLUMETRIC CONTRACTION The Beginning of systole
73ISOVOLUMETRIC 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).
82When the heart contracts Cardiac OutputWhen the heart contracts
83Cardiac Output CO = SV x HR Cardiac Output is the volume of blood pumped each minute, and is expressed by the following equation:CO = SV x HRWhere:CO is cardiac output expressed in L/min (normal ~5 L/min)SV is stroke volume per beatHR is the number of beats per minute
86Preload: 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.The most important determining factor for preload is venous return.
88Afterload: Afterload is the tension (or the arterial pressure) against which the ventricle must contract. If arterial pressure increases, afterload also increases.Afterload for the left ventricle is determined by aortic pressureAfterload for the right ventricle is determined by pulmonary artery pressure.
89Inotropic and chronotropic Homometric regulation
91Significance:To maintain normal blood pressure,blood flow to be relativity constant.To redistribute blood supply todifferent tissue and organs.
92CV CenterCopyright 2009, John Wiley & Sons, Inc.
93A. Neural regulation 1. Innervation of the heart dual innervation (1) cardiac sympathetic nerve (2) cardiac parasympathetic nerve
94Cardiac Symp n Cardiac Vagal n IML 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+ resultsin:↓automaticity of S-A node:
96↓contractility due to : ↑K+ efflux at phase 3 repolarization→↓AP duration → Ca2+ influx ↓→ [Ca2+]i↓;ACh inhibits Ca2+ influx → [Ca2+]i↓→ ↓contractility.↓conductivity
97The left Vagus n:↓conductivity in A-V node The right Vagus n: ↓automaticity in S-A node.
98(2) Effects of cardiac sympathetic nerve: Cardiac sympathetic nerve ending→ noradrenaline → binds to β-adrenergic receptor→↑permeabilityto Ca2+ leads to:
100The left Symp n：↑contractility. The right Symp n：↑HR.
101Sympathetic input - HEART ACTIONSNerve fibers release NESA, atria, and ventricles↑ HR and contractilityR side SA nodeL side contractilityMECHANISMß1 receptors – pacemaker activityß1 myocardiumcontraction
102Parasympathetic input - HEART ACTIONSVagus nerve releases ACHSA and myocardiumHR and conduction velocityR side SA node (HR)L side contractility (slight)MECHANISMMuscarinic receptors (M2)ßγ subunit (HR)Nitric oxide (weak inotropic effect)
104Bainbridge ReflexInfusion 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
105Reflex from left ventricle Coronary chemo reflex Sino Aortic reflex Reflex from atriaType AType BReflex from left ventricleCoronary chemo reflexSino Aortic reflexReflex from peripheryReflex from higher centers
107REGULATION OF ARTERIAL BLOOD PRESSURE Regulation of Blood PressureNervousMechanismRenal MechanismHormonalMechanismLocalMechanismBy Vasomotor Center and Impulses from PeripheryBy Regulation of ECF Volume and renin – angiotensin mechanismBy Vasocons--trictor and Vasodilator HormonesBy Local Vasocons--trictors and Vasodilators
108REGULATION OF ARTERIAL BLOOD PRESSURE SHORT-TERM CONTROL(IN SEC – MIN)INTERMEDIATE-TERM CONTROL(30 MIN – HOURS)LONG – TERM CONTROL
109SHORT-TERM CONTROL OF AP CNS ISCHAEMIC RESPONSEBARORECEPTOR REFLEXCHEMORECEPTOR REFLEX
110INTERMEDIATE CONTROL OF AP RENIN - ANGIOTENSIN – VASOCONSTRICTOR MECH.STRESS RELAXATION OF VASCULATUREFLUID – SHIFT THROUGH THE CAPILLARY WALL
111LONG – TERM CONTROL OF AP RENAL FLUID SHIFT (THROUGH ADH / VOLUME RECEPTORS)RENIN – ANGIOTENSIN – ALDOSTERONE MECH.
112Sequential events by which increased salt intake increases the arterial pressure. Increased extracellular volumeIncreased arterial pressureDecreased renin and angiotensinDecreased renal retention of salt and waterReturn of extracellular volume almost to normalReturn of arterial pressure almost to normal
113LOCAL MECH. FOR CONTROL OF AP A. Vasodilatos1. EDRF2. Bradykinin3. Histamine4. ANP5. VIP6. Substance P7. Prostacyclin8. Adenosine9. K+10. Acidosis [ CO2]11. Hypercapnia12. Hypoxia13. Temperature