Cardiac Output & Starling's Law of the Heart Lecture 32 PDF

Cardiac output and Starling’s Law of the Heart Lecture 32  Cardiodynamics Refers to movements and forces generated during cardiac contractions Important terms: – End-diastolic volume (EDV) – The amount of blood in each ventricle at the end of ventricula...

Cardiac output and Starling’s Law of the Heart Lecture 32  Cardiodynamics Refers to movements and forces generated during cardiac contractions Important terms: – End-diastolic volume (EDV) – The amount of blood in each ventricle at the end of ventricular diastole (start of ventricular systole) – how full the ventricle is before contraction – End-systolic volume (ESV) - The amount of blood remaining in each ventricle at the end of ventricular systole (after contraction) (start of ventricular diastole) – Stroke volume (SV): The amount of blood pumped out of each ventricle during a single beat; can be expressed as: SV = EDV — ESV – Ejection fraction: The % of EDV represented by SV Figure 20-19 A Simple Model of Stroke Volume. Filling Start When the pump handle is raised, pressure within the cylinder decreases, and water enters through a one-way valve. This corresponds to passive filling during ventricular At the start of the pumping diastole. cycle, the amount of water in the cylinder corresponds to the amount of blood in a ventricle at the end of ventricular diastole. This amount is known as the end- diastolic volume (EDV). Ventricular diastole End-systolic volume (ESV) End-diastolic volume (EDV) Stroke volume Pumping When the handle is depressed as far as it will go, some water will remain in the cylinder. That amount corresponds to the end-systolic volume (ESV) remaining in the ventricle at the end of ventricular systole. The amount of water pumped out As the pump handle is corresponds to the stroke pushed down, water is volume of the heart; the stroke forced out of the cylinder. volume is the difference This corresponds to the between the EDV and the ESV. Ventricular period of ventricular ejection. systole  Cardiodynamics Cardiac output (CO): Volume of blood ejected from left ventricle in one minute Cardiac output is an indicator of blood flow through peripheral tissues CO is indication of ventricular efficiency over time CO can be adjusted by changes in Either Heart rate (HR) – number of heartbeats per minutes or Stroke volume (SV) - amount of blood pumped out of each ventricle during each contraction  Calculating Cardiac Output CO = HR × SV CO = cardiac output (mL/min) HR = heart rate (beats/min) SV = stroke volume (mL/beat) Example – If HR is 75 beats/min and SV is 80 mL/beat – CO = 75 beats/min × 80 mL/beat = 6000 mL/min CO is highly regulated to ensure adequate blood supply to peripheral tissues  Factors Affecting Cardiac Output – Cardiac output Can be adjusted by changes in heart rate or stroke volume – Heart rate Can be adjusted by autonomic nervous system or hormones that make homeostatic changes to heart rate as cardiovascular demand changes Factors act by modifying the autorhythmicity of the heart – Stroke volume Adjusted by changing EDV or ESV SV peaks when EDV is highest and ESV lowest Figure 20-20 Factors Affecting Cardiac Output. Factors Affecting Factors Affecting Heart Rate (HR) Stroke Volume (SV) Autonomic End-diastolic End-systolic innervation Hormones volume volume HEART RATE (HR) STROKE VOLUME (SV) = EDV − ESV CARDIAC OUTPUT (CO) = HR × SV Figure 20–20 (Navigator)  Factors affecting Heart rate Autonomic Innervation – Heart has dual innervation Parasympathetic & sympathetic – by means of nerve network = Cardiac plexus Both divisions innervate SA and AV nodes Parasympathetic innervation – Vagus nerves (CN X) carry parasympathetic preganglionic fibers to small ganglia in cardiac plexus Sympathetic innervation – Postganglionic neurons are located in the cervical and upper thoracic ganglia from where postganglionic fibers extend Autonomic Innervation Figure 20–21 (Navigator)  Cardiac centers of medulla oblongata – Has autonomic headquarters for cardiac control – Cardioacceleratory center controls sympathetic neurons that increase heart rate – Cardioinhibitory center controls parasympathetic neurons that slow heart rate Reflex pathways regulate the cardiac centers and receive input from ANS headquarters in hypothalamus  Autonomic Innervation – Cardiac reflexes Cardiac centers monitor and respond to changes in: – Blood pressure - monitored by baroreceptors – Arterial concentrations of O2 and CO2 – monitored by chemoreceptors Cardiac centers adjust cardiac activity according to information received – Autonomic tone Dual innervation maintains resting tone by releasing ACh and NE at the nodes and into myocardium Fine adjustments meet needs of other systems  Autonomic Innervation – Effects on the SA Node How does dual innervation alter heart rate? – By changing the ionic permeabilities of cells in the conducting system Sympathetic and parasympathetic stimulation/effect – Greatest at SA node which affects heart rate through changes in the rate at which impulses are generated  Autonomic Regulation of Pacemaker Function Normal (resting) Spontaneous +20 depolarization Membrane 0 potential (mV) −30 Threshold −60 Heart rate: 75 bpm 0.8 1.6 2.4 Pacemaker cells a Have membrane potentials closer to threshold than those of other cardiac muscle cells (–60 mV versus –90 mV). Their plasma membranes undergo spontaneous depolarization to threshold, producing action potentials at a frequency determined by: (1)the membrane potential and (2)the rate of depolarization Any factor changing the rate of spontaneous depolarization or duration of repolarization in nodal cells will alter heart rate by changing time required for these cells to reach threshold  Effects on the SA Node – Parasympathetic stimulation ACh released opens chemically gated K+ channels in membrane→ K+ leaves nodal cells and slows rate of depolarization and extend duration of repolarization ACh thus slows the heart rate – Sympathetic stimulation NE release opens Na+ channels and Ca2+ channels →influx of these ions increase rate of depolarization and shortens duration of repolarization Nodal cells reach threshold much quicker NE thus increased the heart rate  Parasympathetic stimulation +20 Membrane 0 potential (mV) −30 Threshold Hyperpolarization −60 Heart rate: 40 bpm Slower depolarization 0.8 1.6 2.4 b Parasympathetic stimulation releases ACh, which extends repolarization and decreases the rate of spontaneous depolarization. The heart rate slows. Sympathetic stimulation +20 Membrane potential 0 (mV) −30 Threshold Reduced repolarization −60 More rapid Heart rate: 120 bpm depolarization 0.8 1.6 2.4 Time (sec) c Sympathetic stimulation releases NE, which shortens repolarization and accelerates the rate of spontaneous depolarization. As a result, the heart  Autonomic Innervation – Atrial Reflex Also called Bainbridge reflex Adjusts heart rate in response to venous return – amount of blood returning to the heart through veins Indirect effect of venous return on heart rate Stretch receptors in right atrium –When right atrium are stretched the stretch receptors trigger increase in heart rate –Through stimulating sympathetic activity If venous return to heart increases → HR increases → CO increases  Hormonal Effects on Heart Rate – Epinephrine (E) – Norepinephrine (NE) – Thyroid hormone Increase heart rate by sympathetic stimulation of SA node Venous return – Directly affects pacemaker (nodal) cells If venous return increases the atria receive more blood and walls are stretched Stretching of cardiac pacemaker cells of SA node leads to more rapid depolarization and increase HR – Indirectly affect HR Atrial reflex: when atrium walls stretch, stretch receptors trigger increase in HR by stimulating sympathetic division  Factors Affecting the Stroke Volume SV= EDV-ESV EDV – Amount of blood a ventricle contains at the end of ventricular diastole (before contraction) – EDV affected by Filling time – Duration of ventricular diastole – depends on heart rate (e.g. faster HR faster filling) Venous return – Affected by factors affecting rate of blood flow back to the heart – E.g. Increased venous return →increased EDV  Preload – The degree of ventricular muscle cell stretching during ventricular diastole – Directly proportional to EDV (↑ EDV →↑ preload) – Importance: Affects ability of muscle cells to produce tension – Amount of preload and degree of myocardial stretching varies with demands of the heart – Standing at rest – EDV is low (little stretching of ventricular muscle cells, sarcomere length short) – During ventricular systole – contractile cells thus develop little power and ESV is high (cells only contracted short distance) – During exercise VR increases and EDV increase, myocardium stretches further, sarcomeres reach optimal length and allow for forceful contractions  The EDV and Stroke Volume: Frank-Starling principle – Stretching the cardiac muscle cells past optimal length would reduce force of contraction BUT – Physical Limits - Ventricular expansion is limited by: Myocardial connective tissue The cardiac (fibrous) skeleton The pericardial sac – At rest: EDV is low Myocardium stretches less Stroke volume is low – With exercise: EDV increases Myocardium stretches more Stroke volume increases  The Frank–Starling Principle (Starling’s law of the heart) As EDV increases, stroke volume increases –General rule: More in more out  ESV – The amount of blood that remains in the ventricle at the end of ventricular systole (contraction) – Three Factors That Affect ESV 1. Preload –Ventricular stretching during diastole 2. Contractility –Force produced during contraction, at a given preload 3. Afterload –Tension the ventricle produces to open the semilunar valve and eject blood  Contractility – Amount of force produced during a contraction at a given preload – Is affected by Autonomic activity Hormones – Factors increasing contractility Factors that have positive inotropic action Stimulate Ca2+ entry into cardiac muscle cells and increase force and duration of ventricular contraction – Factors decreasing contractility Factors that have negative inotropic action May block Ca2+ entry and depress cardiac muscle metabolism  Positive and negative inotropic factors include – ANS activity – Hormones – Changes in extracellular ion concentrations Effects of Autonomic Activity on Contractility – Sympathetic stimulation: positive inotropic effect NE released by postganglionic fibers of cardiac nerves Epinephrine and NE released by adrenal medullae Increase cardiac muscle metabolism - causes ventricles to contract with more force Increases ejection fraction and decreases ESV  Effects of Autonomic Activity on Contractility – Parasympathetic activity: negative inotropic effect ACh released by vagus nerves Result in hyperpolarization and inhibition Reduces force of cardiac contractions Ventricles contract less forcefully Ejection fraction decreases and ESV is larger  Hormones affecting contractility – Many hormones affect heart contraction E.g. E, NE, glucagon, thyroid hormones have positive inotropic effects Glucose – positive inotropic effect – Pharmaceutical drugs mimic hormone actions Stimulate or block beta receptors Affect calcium ions E.g., calcium channel blockers have negative inotropic effect  Afterload – Amount of tension that contracting ventricle must produce to force open semilunar valve and eject blood – Increases with increased resistance to blood flow out of the ventricle – ↑ afterload → longer period of isovolumetric contraction and shorter duration of ventricular ejection and larger ESV – As afterload increases, stroke volume decreases – Is increased by any factor that restricts arterial blood flow  Factors Affecting Stroke Volume Factors Affecting Stroke Volume (SV) Venous return (VR) Filling time (FT) Increased by Decreased by Increased by E, NE, VR = EDV FT = EDV sympathetic parasympathetic glucagon, VR = EDV FT = EDV stimulation stimulation thyroid hormones Contractility (Cont) of muscle cells Preload Cont = ESV Increased by Decreased by Cont = ESV vasoconstriction vasodilation Afterload (AL) End-diastolic End-systolic AL = ESV volume (EDV) volume (ESV) AL = ESV STROKE VOLUME (SV) EDV = SV ESV = SV EDV = SV ESV = SV  Summary: The Control of Cardiac Output Heart rate control factors – Autonomic nervous system Sympathetic and parasympathetic – Circulating hormones – Venous return and stretch receptors Stroke volume control factors – EDV Filling time and rate of venous return – ESV Preload, contractility, afterload Cardiac Reserve – The difference between resting and maximal cardiac outputs A Summary of the Factors Affecting Cardiac Output Factors affecting Factors affecting heart rate (HR) stroke volume (SV) Skeletal Blood Changes in muscle volume peripheral activity circulation Atrial Venous Filling Autonomic Hormones reflex return time innervation Preload Contractility Vasodilation or vasoconstriction Autonomic Hormones End-diastolic End-systolic innervation volume volume Afterload HEART RATE (HR) STROKE VOLUME (SV) = EDV − ESV CARDIAC OUTPUT (CO) = HR × SV b Factors affecting cardiac output Figure 20-24a A Summary of the Factors Affecting Cardiac Output. Maximum for trained athletes 40 exercising at peak levels 35 30 Cardiac output (L/min) Normal range 25 of cardiac output during heavy exercise 20 15 10 Average resting cardiac output 5 Heart failure 0 a Cardiac output varies widely to meet metabolic demands  The Heart and Cardiovascular System Cardiovascular regulation – Ensures adequate circulation to body tissues Cardiovascular centers – Control heart and peripheral blood vessels Cardiovascular system responds to: – Changing activity patterns – Circulatory emergencies  References Martini et al. Fundamentals of Anatomy & Physiology. 9th and 10th ed. Pearson education. Marieb & Hoehn. Human Anatomy & Physiology. 8th ed. Pearson education. Seeley et al. Anatomy and Physiology. 6th ed. McGraw-Hill. Patton & Thibodeau. Anatomy & Physiology. 7th ed. Mosby Inc. Autonomic Innervation of the Heart Autonomic Regulation of Pacemaker Cell Function Factors Affecting Cardiac Output