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LIU Chuan Yong Institute of Physiology Medical School of SDU Tel 88381175 (lab) 88382098 (office) Email: [email protected] Website: www.physiology.sdu. edu.cn

LIU Chuan Yong 刘传勇 Institute of Physiology Medical School of SDU Tel 88381175 (lab)

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LIU Chuan Yong 刘传勇 Institute of Physiology Medical School of SDU Tel 88381175 (lab) 88382098 (office) Email: [email protected] Website: www.physiology.sdu.edu.cn. CHAPTER 4 THE CARDIOVASCULAR SYSTEM. Weight of the heart 300g Work: 75/min, 10000 beats /day - PowerPoint PPT Presentation

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  • LIU Chuan Yong Institute of PhysiologyMedical School of SDUTel 88381175 (lab) 88382098 (office)Email: [email protected]: www.physiology.sdu.edu.cn

  • CHAPTER 4THE CARDIOVASCULAR SYSTEM

  • Weight of the heart 300gWork: 75/min, 10000 beats /day35 million beats /year, 2.5 billion beats/life70ml/beat, 7200 l/dayThe work of the heart in one life is equivalent to lifting 30 tons to the Mount EverestThe busy and hard working heart!

  • MAIN FUNCTIONS OF THE CIRCULATORY SYSTEMTransport and distribute essential substances to the tissues.Remove metabolic byproducts.Adjustment of oxygen and nutrient supply in different physiologic states.Regulation of body temperature.Humoral communication.

  • Systemic and Pulmonary Circulation

  • A. Heart location in the chest

  • B. Heart Chambers

  • B. Heart Chamberspumps blood to pulmonary circulation from right ventricle2. Left Heartreceives oxygenated blood from pulmonary circulationpumps blood into systemic circulation1. Right Heartreceives venous blood from systemic circulation via superior and inferior vena cava into right atrium

  • C. Heart Valves1. Atrioventriculartricuspid--between RA and RV; three leafletsmitral--between LA and LV; two leaflets2. Semilunar pulmonic--three leafletsaortic--three leaflets

  • Prevent backward regurgitation

    Provide low resistance to forward flowHeart Valves

  • Section 1 The Heart as a PumpI Cardiac Cycle The period from the end of one heart contraction to the end of the next

  • Cardiac Cycle

    Diastole is longer than systole

    The sequence of systole and diastole

  • Cardiac Cycle: diastole and systoleDiastoleSystole

  • 2 The Phases of the Cardiac CyclePeriod of isometric (isovolumetric or isovolumic) contractionEvents: ventricular contraction ventricular pressure rise atrioventricular valve close the ventricular pressure increase sharplyPeriod: 0.05 secImportance: enable the ventricular pressure to rise from 0 to the level of aortic pressure (after-load)

  • (2) Period of ejectionEvents: ventricular contraction continuously the ventricular pressure rise above the arterial pressure semilumar valves open blood pours out of the ventricles

  • Rapid ejection period (0.10s, 60% of the stroke volume)Reduced ejection period (0.15s, 40% of the stroke volume)

  • (3) Period of isometric (isovolumic) relaxationEvents: ventricular muscle relax the ventricular pressure fall lower than the aortic pressure aortic valve close the ventricular pressure fall sharply

  • Period: 0.06-0.08 sImportance: Enable the ventricular pressure fall to the level near the atrial pressure

  • (4) Period of filling of the ventriclesEvents: Ventricular muscle relax continuously the ventricular pressure is equal or lower than the atrial pressure atrioventricular valve open blood accumulated in the atria rushes into the ventricular chambers quickly from the atrium to the ventricle.

  • Period of rapid filling. (0.11s, amount of filling, 2/3)Period of reduced filling (0.22s, little blood fills into the ventricle)

  • (5) Atrial systoleSignificance, 30% of the filling Be of major importance in determining the final cardiac output during high output states or in the failing heart

  • LEFT VENTRICULAR PRESSURE/VOLUME P/V LOOPLEFT VENTRICULAR PRESSURE (mmHg)LEFT VENTRICULAR VOLUME (ml)ABCDEF1001505001204080

  • 2 Pressure changes in the atria, the a, c, and v waves.a wave, the atrial contractionc wave, bulging of the A-V valves when the ventricles begin to contract

  • v wave, at the end of ventricle contraction, caused by the accumulated blood in the atria while the A-V valves are closed

  • The sounds heard over the cardiac region produced by the functioning of the heart.

    Heart Sounds

  • Heart SoundsS1- first sound Atrioventricular valves and surrounding fluid vibrations as valves close at beginning of ventricular systole

  • S2- second sound closure of aortic and pulmonary semilunar valves at beginning of ventricular diastoleS3- third sound vibrations of the ventricular walls when suddenly distended by the rush of blood from the atria

  • CARDIAC CYCLEAtrial SystoleMitral ClosesIsovolumic contract.Aortic opensS1Rapid EjectionReduced EjectionIsovolumic Relax.AorticclosesRapid VentricularFillingMitralopensS2Reduced Ventricular FillingAtrial Systole:>O:>D

  • II Cardiac OutputStroke Volume The volume pumped by the heart with each beat, = end diastole volume end systole volume, about 70 ml Ejection Fraction Stroke volume accounts for the percentage of the end diastolic volume, = stroke volume / end diastole volume X 100%, normal range, 55-65%

  • II Cardiac Output3. Minute Volume, or Cardiac Output the volume of the blood pumped by one ventricle in one minute = stroke volume X heart rate. It varies with sex, age, and exercise4. Cardiac Index, the cardiac output per square meter of body surface area. the normalized data for different size individuals, the normal range is about 3.0 3.5 L/min/m2

  • Determinants of Cardiac Output (CO)PreloadHeart Rate AfterloadContractilityCardiac OutputStroke Volume

  • DefinitionsPreloadamount of stretch on the ventricular myocardium prior to contractionAfterloadthe arterial pressure that a ventricle must overcome while it contracts during ejectionimpedance to ventricular ejection

  • DefinitionsContractilitymyocardiums intrinsic ability to efficiently contract and empty the ventricle (independent of preload & afterload)

  • Determinants of Cardiac Output1. Preload

  • Preload = ventricular filling or volume Determinants of Cardiac Output- Preload

  • Preload approximated by measuring:1. Central venous pressure (CVP) = right atrial pressure.2. Pulmonary capillary diastolic wedge pressure (PCWP) = LVEDP Parameters:1. CVP3 mmHg (normal range 1 - 5)2. PCWP9 mmHg (normal range 2 - 13)Determinants of Cardiac Output - Preload

  • Frank-Starling Mechanism of the HeartThe intrinsic ability of the heart to adapt to changing volumes of inflowing blood

  • the Frank - Starling mechanism of the heart:Left ventricle (LV) function curve, or Frank - Starling curve (1914):Normal range of the LVEDP, 5-6 mmHgOptimal initial preload, 15-20 mmHg (Sarcomere, 2.0 2.2 m When the LVEDP > 20 mmHg, LV work is maintained at almost the same level, does not change with the increase of LVEDP MechanismConcept of heterometric regulation

  • Factors determining the preload (LVEDP)

    Period of the ventricle diastole (filling) heart rateSpeed of the venous return (difference between the venous pressure and atrial pressure)

  • Importance of the heterometeric regulation

    In general, heterometric regulation plays only a short-time role, such as during the body posture change artery pressure increaseunbalance of ventricular outputsIn other conditions, such as exercise, cardiac output is mainly regulated by homometric regulation.

  • Determinants of Cardiac Output - Afterload

  • Short time change of the arterial pressureTransit arterial pressure rise isovolumetric contraction phase become longer period of ejection shorter stroke volume less more blood left in the ventricle leftLVEDP increase through heterometeric regulation stroke volume return to normal in next beat.

  • Long time high arterial pressure through neural and humoral regulation the stroke volume is maintained at normal level pathogenesis of the cardiovascular system

  • Contractility (neural and humoral regulation)Sympathetic nerve (norepinephrine) or the epinephrine and norepinephrine (adrenal gland) enhance the strength and the velocity of the cardiac contraction. The change of myocardial property is independent of the preload. We call it the contractility.Importance: exert a long time influence on the cardiac output.

    Determinants of Cardiac Output - Contractility

  • DefinitionsContractilitymyocardiums intrinsic ability to efficiently contract and empty the ventricle (independent of preload & afterload)

  • Action of Sympathetic StimulationSympathetic nerve stimulation increases cardiac contractility. At rest the heart is under sympathetic tone.Noradrenaline enhances calcium entry into cardiac cells.Parasympathetic stimulation has little affect on contractility due to the innervation pattern of the heart.

  • PRESSURE/VOLUME RELATIONSHIPS UNDER DIFFERENT CONDITIONSPRELOADAFTERLOADCONTRACTILITY

  • Normal range of the heart rate 60 100 beats/minWithin physiological limit?, the higher the heart rate, the more blood that the heart pump.Determinants of Cardiac Output - The heart rate

  • 1, at rest (without any regulation)2, during exercise (with humoral and neural regulation)

  • IV Cardiac Output ReserveThe maximal cardiac output subtracts the normal value. It reflects the ability of the heart to adapt the change of environment (internal or external)

  • Maximal levelMaximal diastole volume 160 ml (reserve 15ml);Maximal systole residual volume 20 ml (reserve 55ml)Maximal heart rate (without the stroke volume decrease )180 beats/min (reserve 105 beats/min)Maximal cardiac output (160 20) X 180 = 25.2 L/minNormal rangeEnd diastole volume 145ml end systole volume 75ml = stroke volume 70 mlHeart rate 75 beats/minNormal cardiac output = 70 X 75 = 5.25 L /min

    Cardiac output is a function of the interplay of multiple physiologic parameters.

    Stroke volume is influenced in a predictable order:1. Preload first influences contractility. 2. The combined effect of preload and contractility then influences the afterload response. 3. Only after the stroke volume is established does the heart rate respond to adjust the final cardiac output. Preload can be simply stated as the volume stretching the ventricular muscle prior to ejection. Afterload is the resistance to flow from the circulatory system.Contractility has historically been the most difficult parameter to measure in the clinical setting. It clearly is the most important parameter that is affected by cardiac pathology and cardioactive medications.Contractility has historically been the most difficult parameter to measure in the clinical setting. It clearly is the most important parameter that is affected by cardiac pathology and cardioactive medications.