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Transcript
Marieb’s Human Anatomy and Physiology Ninth Edition Marieb w Hoehn Chapter 18 Heart Lecture 3 Lecture Overview • Physiology of cardiac muscle contraction • The electrocardiogram • Cardiac Output • Regulation of the cardiac cycle and cardiac output 2 Comparison of Skeletal and Cardiac Muscle Cardiac and skeletal muscle differ in: 1. Nature of action potential Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001 2. Source of Ca2+ 3. Duration of contraction Let’s look at this more closely 3 The Cardiac Muscle Action Potential Ca2+ ions enter from 1. Extracellular fluid (20%) 2. Sarcoplasmic reticulum (80%) ** Cardiac muscle is very sensitive to Ca2+ changes in extracellular fluid Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001 Recall that tetanic contractions usually cannot occur in a normal cardiac muscle cell 4 Electrocardiogram • recording of electrical changes that occur in the myocardium during the cardiac cycle • used to assess heart’s ability to conduct impulses, heart enlargement, and myocardial damage Important points to remember: - Depolarization precedes contraction - Repolarization precedes relaxation Three waves per heartbeat P wave – atrial depolarization QRS wave – ventricular depolarization T wave – ventricular repolarization 5 Electrocardiogram PR Interval: 0.12 – 0.20 sec QT Interval: 0.20 – 0.40 sec QRS Interval: < 0.10 sec Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001 6 Review of Events of the Cardiac Cycle Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2004 S2 1. Atrial contraction begins 2. Atria eject blood into ventricles 3. Atrial systole ends; AV valves close (S1) 4. Isovolumetric ventricular contraction 5. Ventricular ejection occurs 6. Semilunar valves close (S2) 7. Isovolumetric relaxation occurs 8. AV valves open; passive atrial filling S1 12 Cardiodynamics – Important terms • End-diastolic volume (EDV) – amount of blood present in the ventricles at end of ventricular diastole (~ 120 ml) • End-systolic volume (ESV) – amount of blood left in ventricles at end of ventricular systole (~ 50 ml) • Stroke volume (SV) – amount of blood pumped out of each ventricle during a single beat (SV = EDV – ESV) (~ 70 ml) • Ejection fraction – Percentage of EDV represented by the SV (SV/EDV) (~ 55%) 13 Cardiac Output (CO) • The volume of blood pumped by each ventricle in one minute CO ml/min = heart rate (HR) beats/min x stroke volume (SV) ml/beat Example: CO = 72 bpm x 75ml/beat 5,500 ml/min Normal CO 5-6 liters (5,000-6,000 ml) per minute 14 Regulation of Cardiac Output CO = heart rate (HR) x stroke volume (SV) Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001 • physical exercise • body temperature • concentration of various ions SV = EDV – ESV • calcium • potassium • parasympathetic impulses (vagus nerves) decrease heart action • sympathetic impulses increase heart action; epinephrine 15 Regulation of Cardiac Rate Autonomic nerve impulses alter the activities of the S-A and A-V nodes Rising blood pressure stimulates baroreceptors to reduce cardiac output via parasympathetic stimulation Stretching of vena cava near right atrium leads to increased cardiac output via sympathetic stimulation 16 Figure from: Hole’s Human A&P, 12th edition, 2010 Regulation of Cardiac Rate Tachycardia > 100 bpm Bradycardia < 60 bpm Parasympathetic impulses reduce CO, sympathetic impulses increase CO **ANS activity does not ‘make’ the heart beat, it only regulates its beat Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2004 17 Additional Terms to Know… • Preload – Degree of tension on heart muscle before it contracts (i.e., length of sarcomeres) – The end diastolic pressure (EDP) • Afterload – Load against which the cardiac muscle exerts its contractile force – Pressure in the artery leading from the ventricle 18 The Frank-Starling Mechanism • Amount of blood pumped by the heart each minute (CO) is almost entirely determined by the venous return • Frank-Starling mechanism – Intrinsic ability of the heart to adapt to increasing volumes of inflowing blood – Cardiac muscle reacts to increased stretching (venous filling) by contracting more forcefully – Increased stretch of cardiac muscle causes optimum overlap of cardiac muscle (length-tension relationship) Figure from: Understanding Pathophysiology, Heuther & McCance, 5th ed, Elsevier, 2011. 19 Factors Affecting Cardiac Output Figure adapted from: Aaronson & Ward, The Cardiovascular System at a Glance, Blackwell Publishing, 2007 ANS Parasympathetic HR Contractility CO = HR x SV SV Sympathetic ESV Afterload = EDV - ESV EDV CVP CO – Cardiac Output (~5L/min). Dependent upon Stroke Volume (SV; ~70 ml) and Heart Rate (HR) CVP – Central Venous Pressure; Pressure in vena cava near the right atrium (affects preload; Starling mechanism) Contractility – Increase in force of muscle contraction without a change in starting length of sarcomeres Afterload – Load against which the heart must pump, i.e., pressure in pulmonary artery or aorta ESV – End Systolic Volume; Volume of blood left in heart after it has ejected blood (~50 ml) EDV – End Diastolic Volume; Volume of blood in the ventricle before contraction (~120-140 ml) 20 Regulation of Cardiac Output Recall: SV = EDV - ESV Figure from: Martini, Anatomy & Physiology, Prentice Hall, 2001 CO = heart rate (HR) x stroke volume (SV) 21 Be sure to review, and be able to use, this summary chart Summary of Factors Influencing Cardiac Output Factor Effect on HR and/or SV Effect on Cardiac Output DECREASE HR K+ (hyperkalemia) HR and SV (weak, irreg. beats) K+ (hypokalemia) Irritability Ca2+ (hypocalcemia) SV (flaccidity) Decreased temperature HR Sympathetic activity HR and SV Epinephrine HR and SV Norepinephrine HR Thyroid hormone HR SV (spastic contraction) HR HR and SV Parasympathetic activity (vagus nerves) INCREASE Ca2+ (hypercalcemia) Rising temperature Increased venous return 22 Life-Span Changes • deposition of cholesterol in blood vessels • cardiac muscle cells die • heart enlarges • fibrous connective tissue of heart increases • adipose tissue of heart increases • blood pressure increases • resting heart rate decreases 24 Review • Cardiac muscle contraction differs in several important ways from skeletal muscle contraction – Duration of the action potential is longer – Ca2+ for contraction is derived from the extracellular fluid as well as the sacroplasmic reticulum – Length of contraction is longer – Tetany cannot develop due to length of the absolute refractory period • The electrocardiogram – Measures the electrical changes occurring in the heart – Is used to assess heart’s ability to conduct impulses, heart enlargement, and myocardial damage – Depolarization -> contraction, repolarization -> relaxation 25 Review • There are three major events (waves) in the ECG – P wave = atrial depolarization – QRS complex = ventricular depolarization – T wave = ventricular repolarization • The different leads of an ECG can be used to localize heart muscle abnormalities • Abnormalities in ECG presentation can be indicative of heart damage • Several common cardiac abnormalities – Arrhythmia – Tachycardia (and bradycardia) – Atrial flutter 26 Review • Important cardiodynamic terminology – End-diastolic volume (EDV) – amount of blood left in ventricles at end of ventricular diastole – End-systolic volume (ESV) – amount of blood left in ventricles at end of ventricular systole – Stroke volume (SV) – amount of blood pumped out of each ventricle during a single beat (EDV – ESV = SV) – Ejection fraction – Percentage of EDV represented by the SV 27 Review • Cardiac output (CO) – Amount of blood pumped by the heart in one minute – CO = stroke volume x heart rate – Normal (resting) CO 5-6 L/min • Factors Affecting CO – – – – Autonomic activity Hormones K+, Ca2+ Venous return 28 Review • Regulation of Cardiac Output – Heart Rate • Autonomic tone • Hormones • Venous return – Stroke Volume • • • • Autonomic tone Hormones Venous return Afterload 29