1. 1 Topics to be addressed: Blood Anatomy of Blood Vessels Anatomy of the Heart The Conduction System The Cardiac Cycle Cardiodynamics Blood Flow and its Regulation Adaptation and Disorders of the Cardiovascular System Overview of the Cardiovascular System

2. 2 Cardiodynamics: Control of Cardiac Output Cardiac Output = the volume of blood pumped by the left ventricle in one minute = number of beats/minute X volume pumped with each beat = Heart Rate X Stroke Volume CO = HR X SV Determines oxygen available to tissues Typically measured in ml/min or L/min At rest, CO~5 liters/min; can rise to 30 liters/min during strenuous activity

3. 3 Cardiodynamics : Control of Cardiac Output Some basic terms to know End-diastolic volume (EDV): the amount of blood in the left ventricle just before contraction End-systolic volume (ESV): the amount of blood left in the left ventricle after contraction (it doesn’t all get pumped) Stroke volume (SV) : the amount pumped out of the left ventricle during systole SV=EDV-ESV

4. 4 Cardiodynamics: Factors that affect Cardiac Output Cardiac output can be adjusted with changes to one or more variables Heart rate (speeding up or slowing down) End diastolic volume (how much blood fills ventricle between beats) End systolic volume (how much ventricle pumps out each beat) CO = HR X SV SV = EDV-ESV CO = HR X (EDV – ESV) CO = HR X SV HR = heart rate (beats/min) SV = stroke volume (milliliters pumped out/beat)

5. 5 CO = HR X SV Factors Affecting Cardiac Output: control of heart rate Autonomic innervation is the primary factor affecting HR Cardiovascular center of medulla oblongata in the brainstem drives the autonomic nervous system: one part of this, the Cardiac Center, regulates heart activity cardioacceleratory center controls sympathetic neurons, causes them to release more norepinephrine at SA node (increases heart rate); NE binds to Beta-1 adrenergic receptors on SA node cells. cardioinhibitory center controls parasympathetic neurons of vagus nerve, leading to acetylcholine release at SA node (slows heart rate); ACh binds to muscarinic receptors on SA node cells. Medulla

6. 6 Autonomic Innervation of the Heart Note that parasympathetic fibers innervate the SA and AV nodes Sympathetic fibers innervate both nodes, atrial muscle and ventricular muscle Drug Target: Circulating epinephrine mimics this sympathetic nervous system effect

7. 7 HOW is heart rate controlled? Autonomic axons adjust heart rate by slowing down or speeding up the rate of spontaneous depolarization of pacemaker cells Parasympathetic Sympathetic (and hormones) Chronotropic drugs are used to alter heart rate

8. 8 CO = HR X SV Factors Affecting Cardiac Output: control of stroke volume CO = HR X SV CO = HR X (EDV – ESV) Stroke volume can be adjusted by changing the EDV, the ESV, or both

9. 9 Two main factors influence the End Diastolic Volume: Factors that cause more blood to return to heart result in larger fill volume (the EDV) Filling time: duration of ventricular diastole Longer fill time results in larger fill volume Related to heart rate Venous return: rate of blood flow during ventricular diastole Vasoconstriction is a critical factor affecting venous return SV = EDV - ESV CO = HR X SV Factors Affecting Cardiac Output: control of stroke volume

10. Seeley, Stevens, Tate, Anatomy & Physiology 8 th ed, McGraw Hill, 2008 The Sympathetic Nervous System Innervates Blood Vessels and Controls Vessel Diameter Sympathetic fibers are always “talking” to the smooth muscle in the walls of blood vessels… this is called sympathetic “tone”. This continuous rate of action potential firing leads to continuous release of transmitter and sustained low level of contraction of the smooth muscle, and thus partial vasoconstriction of the vessel. Increased sympathetic activity increases the degree of constriction to reduce blood flow = Vasoconstriction Decreased sympathetic activity decreases the degree of constriction, dilating the vessel to increase blood flow = Vasodilation Sympathetic Transmitter: Norepinephrine Receptor Type : Alpha-1 adrenergic Usually, vasodilation of blood vessels occurs because local chemicals in active tissues (eg. skeletal muscle) trigger the smooth muscle cells to relax, increasing blood flow and providing more oxygen and nutrients to the tissue.

11. 11 How does vasoconstriction increase venous return? Vasoconstriction mobilizes blood in the capacitance vessels

12. 12 Clinical treatments to Improve Venous Return Compression cuffs

13. 13 Three main factors influence the End Systolic Volume: Factors that cause more blood to be pumped from ventricle affect volume left in ventricle after systole (the EDV) Preload :Ventricular stretching during diastole Contractility: Force produced during contraction, at a given preload Afterload: Tension the ventricle needs to produce to open the aortic valve and eject blood SV = EDV - ESV CO = HR X SV Factors Affecting Cardiac Output: control of stroke volume

14. 14 Preload is the degree of ventricular stretching during diastole Directly proportional to EDV : more blood in ventricle = more stretch Stretch affects the ability of muscle cells to produce tension Preload affects stroke volume ANPS 19 Skeletal Muscle Mechanics lecture The amount of stretch on a sarcomere influences its ability to develop tension. This is especially true for contractile cells of the heart, and is called the Frank-Starling Law of the Heart The more blood in the ventricle, the greater the stretch on the ventricle wall and the stronger the contraction

15. 15 Contractility – how hard the ventricle contracts is affected by factors that adjust calcium levels in the muscle cells Sympathetic nervous system activity affects contraction strength Stimulation of the sympathetic nerves causes release of norepinephrine on the heart cells, leading the ventricles to contract with more force, and pump out more blood ( Increasing stroke volume and thus decreasing ESV) Hormones from the bloodstream (epinephrine, norepinephrine, thyroid hormone) affect contraction strength Note two ways that heart function is controlled clinically: BETA BLOCKERS : Contractile cells have Beta-1 adrenergic receptors to respond to epinephrine and norepinephrine CALCIUM CHANNEL BLOCKERS : decrease calcium entry or release in contractile cells; less calcium=less actin/myosin interaction=less tension Contractility affects stroke volume

16. 16 Afterload affects stroke volume Afterload – the aortic pressure that must be overcome in order for the ventricle to eject blood Any factor that restricts arterial blood flow increases peripheral resistance, and affects the heart as afterload (valve stenosis, high blood pressure, atherosclerosis, etc.) As afterload increases, stroke volume decreases, and therefore ESV increases

17. 17 the percentage of EDV represented by SV: a weak heart pumps out less Typical Ejection Fraction Numbers: 50-75%Heart's pumping ability is Normal 36-49%Heart's pumping ability is Below Normal 35% and BelowHeart's pumping ability is Low Ejection Fraction an important clinical measure of heart function Example: left ventricle volume at end of diastole (EDV): 100 ml left ventricle volume at end of systole (ESV) : 40 ml stroke volume (EDV-ESV) : 60 ml ejection volume (SV/EDV) : 60%

18. 18 Review: Main Factors Affecting Cardiac Output CO = HR X SV CO=HR X (EDV-ESV) 1.Heart Rate Control Factors Autonomic nervous system (sympathetic + parasympathetic) Circulating hormones 2. Stroke Volume Control Factors EDV- end diastolic volume filling time rate of venous return ESV- end systolic volume preload (stretch on ventricle wall) contractility (calcium availability within muscle cell) afterload (downstream resistance)

19. 19 Review: Main Factors Affecting Cardiac Output

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