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2016.11.03. Related Learing objectives • 27. Cardiac muscle: structural and functional characterization, electromechanical coupling, cardiac metabolism, regulation of contractile force • 28. Cardiac cycle. Cardiac work. • 29. Factors determining the cardiac output. The Frank-Starling law of the heart. • 30. Cardiac muscle: cellular electrophysiology. Electrocardiography (ECG) • 31. The coronary circulation I. II. III. IV. V. VI. Anatomy Origin and spread of cardiac excitation Heart muscle Mechanical events of the cardiac cycle Integrated control of cardiac output ECG Heart 1 2016.11.03. Size and location • • • • • • • • 250-350 g 150 mm x 110 mm – about the size of a fist located anterior to the vertebral column and posterior to the sternum Pericardium Wall of the heart: endothel, myocardium, endocardium Septum cordis Heart valves between the chambers - Atrium, ventriculus Coronary circulation 2 2016.11.03. A heart valve normally allows blood flow in only one direction through the heart. The four valves determine the pathway of blood flow through the heart. A heart valve opens or closes incumbent upon differential blood pressure on each side. Heart innervation Automation Autonomous nervous system Vagal nerve (X.) Th1-4 chonotropic, dromotropic, inotropic, bathmotropic, lusytropic effects 3 2016.11.03. Cardiac muscle • is a type of involuntary striated muscle found in the walls and histological foundation of the heart, specifically the myocardium • Cardiomyocytes – 1-4 cell nuclei • Intercalated discs – gap junction – syncytium (AP generates local circuits) I. II. III. IV. V. VI. Anatomy Origin and spread of cardiac excitation Heart muscle Mechanical events of the cardiac cycle Integrated control of cardiac output ECG Heart 4 2016.11.03. Intrinsic conduction system of the heart Conduction rate in cardiac tissue tissue Conduction rate (m/s) SA node <0.01 Atrial pathway 1.0-1.2 AV node 0.02-0.05 Bundle of His 1.2-2.0 Purkinje system 2.0-4.0 Ventricular muscle 0.3-1.0 I. II. III. IV. V. VI. SA node discharge most rapidly, spontaneously (100/min) Latent pacemakers AV node – slow conduction rate – delay (0.1s) Anatomy Origin and spread of cardiac excitation Heart muscle Mechanical events of the cardiac cycle Integrated control of cardiac output ECG Heart 5 2016.11.03. SA- and AV-nodes (nodal tissue) • • • • Pacemaker potential, discharge spontaneously Fluctuating membrane potential (prepotential) Fast voltage-dependent sodium channels are inactive AP – – – – Atrial and ventricular fibers + bundle of His, Purkinje-system • AP – RAPID and sharp depolarization – vd Na+ and Ca2+ (L) channels; K+ channels – Plateau – High amplitude – Fast propagation SLOW depolarization If; vd. Ca2+ channels (T and L types); multile K+ channels Small amplitude Slowly propagation Dissection of the cardiac action potential. Top: The action potential of a cardiac muscle fiber can be broken down into several phases: 0, depolarization; 1, initial rapid repolarization; 2, plateau phase; 3, late rapid repolarization; 4, baseline. Bottom: Diagrammatic summary of Na+, Ca2+, and cumulative K+ currents during the action potential. As is convention, inward currents are downward, and outward currents are upward. 6 2016.11.03. Left: Anatomical depiction of the human heart with additional focus on areas of the conduction system. Right: Typical transmembrane action potentials for the SA and AV nodes, other parts of the conduction system, and the atrial and ventricular muscles are shown along with the correlation to the extracellularly recorded electrical activity, that is, the electrocardiogram (ECG). The action potentials and ECG are plotted on the same time axis but with different zero points on the vertical scale. LAF, left anterior fascicle. neuron Striated muscle Smooth muscle Resting potential (mV) -80-90 -80-90 -40-60 Myocardial fiber -80-90 Time of action potential 0.2-2 1-5 20-300 300 1-4 50 0 10-100 200-3000 300 Na+ influx Ca++ influx Na+ and Ca++ influx somatic autonomic autonomic Delay (ms) Time of contraction (ms) Mechanism of action potential innervation Na+ influx 7 2016.11.03. Skeletal muscle vs cardiac muscle In the absolute refractory period (ARP), the cardiac myocyte cannot be excited, whereas in the relative refractory period (RRP) minimal excitation can occur. 1. As with skeletal muscle, the action potential in a heart cell will initiate contraction of that cell. 2. action potential duration is much longer than in skeletal muscles. 8 2016.11.03. 3. the contraction in the heart muscle occurs during the action potential, as shown in figure A (while in skeletal muscles the contraction occurs after the action potential). 4. The refractory period of the cardiac action potential is much longer 5. Therefore, in the heart, the contraction is finished before a second action potential can be generated, as shown in figure B. 6. Thus, the contractions in the heart can not summate (as they can in skeletal muscles; temporal summation). 1. In skeletal muscle the resting length is quite close to the optimal length of muscle contraction 2. The passive tension in cardiac muscle rises more steeply than in skeletal muscle 3. The active length -tension curve of cardiac muscle shows that small changes in sarcomere length produces large changes in tension due to: a) better overlap between the myofilaments b) enhanced sensitivity of the myofilaments to Ca → At a longer muscle fibre length more troponin C molecules are bound to Ca resulting in greater crossbridge cycling. 4. cardiac muscle normally operates only on the ascending limb of the curve 9 2016.11.03. Regulation of contractile force 1. 2. Initial sarcomer length – Frank-Starling law of the heart – „heterometric” regulation SY nervous system – „homometric” regulation (β1) 1. 2. The increase of extracellular calcium concentration (Caffeine: SR Ca++ release) Na-K-pump inhibition (cardiac glycosides) 10 2016.11.03. I. II. III. IV. V. VI. VII. Anatomy Origin and spread of cardiac excitation Heart muscle Mechanical events of the cardiac cycle Integrated control of cardiac output ECG Coronary circulation Heart Divisions of the cardiac cycle: A) systole and B) diastole. The phases of the cycle are identical in both halves of the heart. The direction in which the pressure difference favors flow is denoted by an arrow; note, however, that flow will not actually occur if valve prevents it. 11 2016.11.03. Stages of the cardiac cycle DIASTOLE 530 ms Phases Time (ms) Semilunar valves Atrioventricular valves pressure volume Proto -diastole 40 Start to close closed ↓ No change Isovolumetric Relaxation 80 closed closed ↓ No change Rapid filling 100 closed opened No change ↑ Slow filling 210 closed opened No change ↑ Atrial systole 100 closed opened small ↑ ↑ 50 closed closed ↑ No change rapid ejection 90 opened closed small↑ ↓ Slow ejection 130 opened closed no change ↓ Isotonic relaxation SYSTOLE 270 ms Isovolumetric contraction ejection 12 2016.11.03. Volume-pressure curve of the left ventricle Vena pulse Right atria l pressure Atrial systole Closure of the AV valves Fast ventricular filling Upward movement of anlus fibrosus – atrial pressure increase 10-7. ábra . A jobb pitvari nyomásingadozások és a vena jugularis externa térfogatingadozásai a szívciklus alatt. Little, R. C., Little, W. C. (1989): Physiology of the Heart and Circulation. 4. kiadás, Year Book Medical Publ. Chicago ILL alapján. A felső (színes) görbén a v. jugularis externán regisztrált térfogatváltozás (vénapulzus), az alsó (fekete) görbén a jobb pitvar nyomásingadozásai láthatók. A függőleges szaggatott vonalak jelzik, hogy a vénapulzus később következik be, mint az azt létrehozó pitvari nyomásváltozás 13 2016.11.03. Heart sounds Stethoscope „lub” S1: vibration induced by the sudden closure of the atrioventricular valves at the start of the ventricular systole „dup” S2: shorter, high pitched, closure of the aortic and pulmonary valves just after the end of ventricular systole • • • Standard two-dimensional, three-dimensional, and Doppler ultrasound to create images of the heart Non-invasive Indications: – – – – Geometry of the heart Detection of volume-changes SV determination Valves Echocardiography 14 2016.11.03. • • • • • End-diastolic volume (EDV): 110-160 ml End-systolic vloume (ESV): 40-80 ml Stoke volume (SV): 70 ml (physical exercise: 140 ml) Ejection fraction=SV/EDV (0.5-0.7) Left ventricle: – Systole: 110 mmHg diastole: 6-8 mmHg • Left atrium: 6-8 mmHg • Right ventricle: – Systole: 24 mmHg diastole: 0-2 mmHg • • • • I. II. III. IV. V. VI. Right atrium: 0-2 mmHg Heart rate: 70/min (physical exercise: 180) Cardiac output: 5.5 L/min (Physical exercise: 24 L/min) cardiac index=CO/body surface area 3,2 l/minxm2 Anatomy Origin and spread of cardiac excitation Heart muscle Mechanical events of the cardiac cycle Integrated control of cardiac output ECG Heart 15 2016.11.03. • CO=Heart rate x SV • SV=EDV-ESV • Cardiac index: Cardiac output CO/body surface area (male, at rest, lying: 3.2 L/m2) Effect of sympathetic (noradrenergic) and vagal (cholinergic) stimulation on the membrane potential of the SA node. Note the reduced slope of the prepotential after vagal stimulation and the increased spontaneous discharge after sympathetic stimulation. 16 2016.11.03. PRELOAD AFTERLOAD • • The degree to which the myocardium is stretched before it contracts (venous return) Resistance against which blood is expelled (contraction or dilatation) – Blood volume – Venous resistance – decrease the venous reservoires – Intrathoracic pressure „respiratory pump” – Skeletal muscle contraction (muscular actvity) – „muscle pump” – Sucktion force of the heart • Direct flow into the ventricle during diastolic filling • Anulus fibrosus moves downward during systole, thus decreases atrial pressure Peripheral resistance Starling heart-lung preparation to determine cardiac output (CO) CO meas. Intact pulmonary circulation LV-RA connection with a tube No innervation Change periheral resistance (afterload) Change venous return (preload) Intact coronary circulation Venous return (tank) Volume register 17 2016.11.03. Interactions between the components that regulate cardiac output and arterial pressure. Solid arrows indicate increases, and the dashed arrow indicates a decrease. Frank-Starling law „Energy of contraction is proportional to the initial length of the cardiac muscle fiber” Length – extent of the preload proportional to the EDV Heterometric regulation of cardiac output (vs homeometric SY regulaion) reason: calcium sensitivity of the contractile filaments of myocytes depends on the initial length of the fiber 18 2016.11.03. „Frank-Starling –law” and volume-pressure loop 10-14. ábra . Consequencies of Increased preload. 10-15. ábra . Consequencies of increased afterload. The effect of the autonomic nervous system on the heart Sympathetic (SY) Parasympathetic (PSY) • positive chronotropic (Firing rate) – – • negative chronotropic – Β1 receptor – cAMP – Ica increase Speeds If – • Positive inotropic (Contraction force) and lusitropic – – • NA- Β1 receptor – cAMP – Ica increase SR Ca-pump activity increase Positive dromotropic (conductivity rate) – – • Ca++-channel phosphorilation, ICa++-increase Delay in the AV node is shortened Negative dromotropic – – • ACh – M2 - cAMP level decrease – decreases If and slows the opening of the Ca++ channels ACh-sensitive K+-channel (M2) – slope of prepotential is decreased because of hyperpolarization Positive bathmotropic (excitability) • ACh-sensitive K+-channel (M2) – slope of prepotential is decreased because of hyperpolarization Delay in the AV node is lengthened Negative bathmotropic 19 2016.11.03. Hormonal effects on heart Thyroid gland (permissive role): Insulin, glucagon, growth hormone: I. II. III. IV. V. VI. positiv inotropic and chronotropic effect Increased number and sensitivity of 1 receptors positiv inotropic effect Anatomy Origin and spread of cardiac excitation Heart muscle Mechanical events of the cardiac cycle Integrated control of cardiac output ECG Heart 20 2016.11.03. ECG - electrocardiogram • • interpretation of the electrical activity of the heart over a period of time, as detected by electrodes attached to the outer surface of the skin and recorded by a device external to the body ECG is used to measure – – – – • the rate and regularity of heartbeats (tachy/bradycardia; arrhythmias) the size and position of the chambers (hypertrophy, atrophy) the presence of any damage to the heart (infarction) the effects of drugs or devices used to regulate the heart, such as a pacemaker Calibration (speed of recordings, amplitude) – 25 mm/s (1mm=0.04s); 10 mm=1 mV (1mm=0.1 mV) • • Unipolar vs bipolar electrodes Limb leads and precordial leads 21 2016.11.03. Depolarization moving toward an active electrode in a volume conductor (body) produces a positive deflection, whereas depolarization moving in the opposite direction produces a negative deflection. By convention, an upward deflection is written when the active electrode becomes positive relative to the indifferent electrode, and a downward deflection is written when the active electrode becomes negative. The correlation of the electrical activity of the heart and the ECG recordings Spread of cardiac excitation 22 2016.11.03. Limb leads and augmented limb leads Einthoven (standard) Limb leads Goldberger (augmented) Limb leads Precordial leads V1 In the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum (breastbone). V2 In the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum. V3 Between leads V2 and V4. V4 In the fifth intercostal space (between ribs 5 and 6) in the mid-clavicular line. V5 Horizontally even with V4, in the left anterior axillary line. V6 Horizontally even with V4 and V5 in the midaxillary line. 23 2016.11.03. Directions of ECG leads in 3 dimensions Horizontal and frontal plane 24 2016.11.03. P wave: atrial depolarization; <100ms PQ (PR) segment: atrial plateau phase PQ (PR) interval: Atrial depolarization and conduction through AV node; 120-200 ms QRS duration:80-120 ms; Ventricular depolarization and atrial repolarization QT interval: Ventricular depolarization plus ventricular repolarization; 320-390 ms (heart rate) ST segment: Ventricular plateau phase T wave: Ventricular repolarization 12 leads routine ECG • • • Limb leads (I, II and III) Augmented limb leads (aVR, aVL, aVF) Chest (Precordial) leads (V1-V6) 25 2016.11.03. Clinical relevance of ECG • The heart's electrical axis (cardiac vector) is the general direction of the ventricular depolarization wavefront (or mean electrical vector). The QRS axis can be determined by looking for the limb lead or augmented limb lead with the greatest positive amplitude of its R wave. Left: Einthoven's triangle. Perpendiculars dropped from the midpoints of the sides of the equilateral triangle intersect at the center of electrical activity. RA, right arm; LA, left arm; LL, left leg. Center: Calculation of mean QRS vector. In each lead, distances equal to the height of the R wave minus the height of the largest negative deflection in the QRS complex are measured off from the midpoint of the side of the triangle representing that lead. An arrow drawn from the center of electrical activity to the point of intersection of perpendiculars extended from the distances measured off on the sides represents the magnitude and direction of the mean QRS vector. Right: Reference axes for determining the direction of the vector. 26 2016.11.03. • • The normal QRS axis is generally down and to the left, following the anatomical orientation of the heart within the chest. An abnormal axis suggests – – a change in the physical shape and orientation of the heart, or a defect in its conduction system that causes the ventricles to depolarize in an abnormal way. Normal −30° to 90° Normal Left axis deviation −30° to −90° May indicate left ventricular hypertrophy, left anterior fascicular block Right axis deviation +90° to +180° May indicate right ventricular hypertrophy, left posterior fascicular block EC calcium level 2,5 mmol/L • • Increased: enhanced myocardial contractility, relaxes less during diastole, heart eventually stops in systole – calcium rigor Decreased: decreased contraction force EC kalium level 4 mmol/L • • hyperkalemia: heart stops in diastole(reason: resting membrane potential decreases=> muscle fiber becomes unexcitable – decreased poropagation and contraction => heart failure) hypokalemia: ventricular extrasystole => heart failure Ional effects on the ECG 27