Human Physiology Textbook PDF

KIN 101 Human Physiology, textbook Instructor: Michael Scarlett Office: VVC 4-409 reading Email: [email protected] Office Hours: By appointment Phone: 780 492 2213...

KIN 101 Human Physiology, textbook Instructor: Michael Scarlett Office: VVC 4-409 reading Email: [email protected] Office Hours: By appointment Phone: 780 492 2213 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Notes Regarded as the most information dense section of the course Requires attending lectures and reviewing the notes Don’t be scared of the number of slides (e.g. step slides, hidden slides) Math: Yes there will be math you will need a calculator during the final exam Highly recommend Road Maps to keep things straight. Memorization without context will be more confusing. Final Exam usually 110-120 questions in 3 hours. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Human Physiology, An Integrated Approach KEY QUESTIONS Bigpicture CHP 14. How does blood leave the heart? CHP 15. Where does blood go after leaving the heart?* How does it return? CHP 16. What is the make up of blood? What can it do? CHP 17 The lung is an air filled sac in our body, how does it move air? CHP 18 Where does blood go after leaving the heart?* Why is their air in our lungs? CHP 19 Wait a minute how does all that water get from my stomach into my pee? Why is it yellow? CHP 20 Whoa… you are telling me my blood organ (heart), air organ (lungs), and my pee organs (kidneys) all work together. How does that work? Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Human Physiology, An Integrated Approach Eighth Edition Overview of the Cardiovascular System 1. The Heart (CHP 14) Structure, Chambers, Valves, and Blood Supply. Unique Features of Cardiac Muscle. Pressure and volume 2. Blood vessels (CHP 15) Comprised of: Arteries, arterioles, capillaries, venules, and veins. Blood pressure and Homeostasis 3. Blood (CHP 16) Components and Function Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Human Physiology, An Integrated Approach Eighth Edition Chapter 14 Cardiovascular Physiology 14.1 to 14.7 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.5(g)-(h) The Heart cardiacmuggs Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  against fights r Figure 14.5(a)-(b) The Heart to gravity o Close brain farfrom toes to are systemic 8 pumans it Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.5d The Heart top of musclecells mm how an wrapped around 0 reduces friction limits fly Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Figure 14.5(e)-(f) The Heart Strong membranous sac that encases and protects the heart. Fused to the diaphragm. imitchhood pumpedin Within the sac is permin pericardial fluid that C lubricates and allows the heart (myocardium) to anchored 2 operate in a friction free diagram environment. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Looking Outside the Heart Corinary artery supplying blood to the Normal circulation. Restricted circulation. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Looking Inside the Heart Echocardiogram Provides information on: blood should flow one ▫ The size and shape of the only be a heart, was ▫ Its pumping strength, and ▫ The location and extent of any damage. It is especially useful for assessing diseases of the heart valves and cardiac hypertrophy. http://www.youtube.com/watch?v=7TWu0_Gklzo&feature=related Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Looking Inside the Heart Ventricular Wall highpressure Immisfictive Thickness Right vs. Left. iii iii blood 10W PTR pump pulemary WHY THE DIFFERENCE? Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  aiiiiiiIFA.am 1 oxygenated µ an blood age H 55 values septum Jonnie come musere in the powers wholebody transports lotsofessentials wroughout the body high lowpressuregradient cares arteriescarryblood pa EFÉÉI away from the 8 bloodtowards then carry pulmonary veins Gotta exceptiontoartensive run monoxygen I R ffifffffiiiiiit.ae L bact bloodcoming to thebody bigger systemicflow side i i f iiÉ ÉÉÉÉÉÉ EEEEE e.EE iiff YÉ fifii Y ventricles É t myocardium pericardium forstudying septum iii in for oinereeacnpargoestos ignite.ms whereeach i partgetsblood sendsbloodto immansans sustemic veumonary fitiI u aareu e arm wenn aorta Human Plumbing: PUMP Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.8b Figure 14.7(a)-(b) Heart valves create one- way flow through the heart Mitral Valve is another name for the BICUSPID valve on the left side of the heart nowmany that leaves birdseyeview Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.7(c)-(d) Heart valves create one- way flow through the heart Semilunar valves open and close in response to pressure differences drops pressure gives own blood Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.8 The coronary circulation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved https://ufhealth.org/uf-health-aortic- disease-center/aorta-anatomy V cornam v Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.1 The cardiovascular system SE The Systemic circulation toviscera blood Includes: blood2 191m ARTERIES that carry oxygenated blood from the left ventricle to the tissues. VEINS that carry deoxygenated blood back to the right atrium. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.1 The cardiovascular system The Pulmonary circulation Includes blood vessels that go: From the right ventricle to the lungs. ▫ Pulmonary Arteries. From the lungs to the left atrium. ▫ Pulmonary Veins. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  MATH… Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  b da.meter now Pressure and Blood Flow diameter low pre How does blood flow? Ohm’s Law Flow = Δ Pressure / Resistance a in thebody The Physiological Equivalent Q = MAP / TPR nowMY'dpumping Q = Cardiac Output (CO) (Heart Function)bloodflowoutof min MAP = Mean Arterial Pressure (Blood Pressure) TPR = Total Peripheral Resistance (Blood Vessels and their diameter) all branchesyouarefeeding Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Q = Cardiac Output l important beats/min x mlblood/beat Ex'S BPM Heart Rate x Stoke Volume ML min The amount of blood leaving the Ventricles every Minute! (usually the Left ventricle and Right ventricle are matched) if 12 leaves R L 1Lneeds to be replenished Yressure surfume Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.8b  MAP = Mean Arterial Pressure Outward Pressure exerted on the walls of blood vessels (arteries, arterioles) outwardpush against blofssel stretch canchange side MAP α cardiac output x resistance Homeostasis = physiological equilibrium Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.8b  diameter how Total Peripheral Resistance Total resistance of all the blood vessels Most impacted by the ARTERIOLES typicalMAP rest 51PM peripheral 1 pressure Nance further frompump pressure decreases Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  my chambers Yessir alcauria lift.fi Feasts isii R ii L systemic evil Rode flow 4  Resistance The radius (r) of the blood vessels determines resistance and is physiologically regulated. VASODILATION VASOCONSTRICTION ▫ r increases. ▫ r decreases. narrowing of the tube ▫ R decreases. ▫ R increases. resistance radius ▫ Blood flow increases* ▫ Blood flow decreases* pressure to balanceflow *Assuming pressure is constant. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Resistance Flow through a tube is inversely proportional to resistance. Resistance (R) Opposes Flow. –If resistance increases, flow decreases. –If resistance decreases, flow increases. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Resistance no Resistance opposes flow due to friction. Resistance (R) depends on: – Length of the tube (L):  R∝L – Radius of the tube (r):  R ∝ 1/r4 diamgres.is factor 4 now – Viscosity (η) of the fluid:  R∝η R increases as L and η increase, and r decreases. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  MAP refers to NET driving pressure = ΔP = P1-P2 Q refers to flow due to central factors = (HR x SV) R refers to resistance due to peripheral factors = diameter or r4 Tightly regulated Adjusted to maintain homeostasis MAP = Q x R total peripheral howthe body functions Q = MAP R = MAP R total peripheral Q  flow 4 more 0.5 flow flow whenresistance less 14 0.25 flow ΔP 0.5 7  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.5(g)-(h) The Heart Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.14 Electrical conduction in myocardial cells special action potentials SAnode tons peno Etcetera Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.9 Cardiac muscle Iiii c Organised in a spiral arrangement to produce a “wringing” motion when the atria or ventricles contract Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.9 Cardiac muscle  Desmosomes siemens  Gap Junctions it r ie  Strong protein that surrounds  Provide electrical connection. sarcomeres and bind  Electrical signals are rapidly neighbouring sarcomeres. transmitted via these protein  Allow force to be transferred. pores providing the basis for SYNCHRONOUS CONTRACTION. Intercalated Disk Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.9 Cardiac muscle 1. Single nucleus per fiber. 2. Distinctive short rectangular shape. Are smaller compared to skeletal muscle 3. Spontaneously Contract Pacemaker cells within the sinoatrial (SA) node control rate 4. Branch and join neighboring cardiac cells through intercalated disks, which are comprised of Desmosomes hold cells together Gap Junctions move ions Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.9 Cardiac muscle 6. Ca2+ is sequestered in the sarcoplasmic reticulum (SR) as in skeletal muscle but SR is less voluminous. Cardiac muscle depends partly on extracellular Ca2+. 7. t-tubular network is more extensive than skeletal muscle Allows rapid, synchronous excitation-contraction coupling. 8. Large volume of mitochondria (~ 1/3rd of volume). This feature is due to the dependence of the heart on aerobic ATP production. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.14 Electrical conduction in myocardial cells Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.11 Action potential of a cardiac contractile cell Study Yain Note the m duration of the i siiiiiii Differences EE Action Potential iiiiiiiii.im Phase* Membrane channels 0 Na+ channels open 1 Na+ channels close + 2 Ca2+ channels open; fast K channels close 3 Ca2+ channels close; slow K + channels open 4 Resting Potential *The phase numbers are a convention. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.12(a)-(b) Refractory periods and summation Force generated in heart muscle is proportional to number of active crossbridges calcium dependant calcium release Determined by how much calcium is bound to troponin hoynes Years Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.12(c)-(d) Refractory periods and summation Force generated in skeletal muscle is proportional to number and frequency of stimulations (somatic AP’s) wayshorter Pushes hard Tetanus and fused tetanus build tension. Summation determines level of tension. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Excitation-Contraction Coupling in Cardiac Muscle This figure shows the cellular events leading to contraction and relaxation in a cardiac contractile cell. Action potential enters from adjacent cell. Ca2+ ECF Voltage-gated Ca2+ ICF channels open. Ca2+ enters cell. RyR Ca2+ induces Ca2+ release camaraderie through ryanodine SR L-type Sarcoplamsic receptor-channels (RyR). Ca2+ reticulum (SR) Ca2+ Ca2+ stores Local release causes channel Ca2+ spark. Summed Ca2+ sparks T-tubule create a Ca2+ signal. Ca2+ sparks Ca2+ signal DrawI Ca2+ -induced Ca2+ release Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.9 Excitation-Contraction Coupling in Cardiac Muscle This figure shows the cellular events leading to contraction and relaxation in a cardiac contractile cell. Action potential enters from adjacent cell. Ca2+ ECF Voltage-gated Ca2+ ICF channels open. Ca2+ enters cell. RyR Ca2+ induces Ca2+ release through ryanodine SR L-type Sarcoplamsic receptor-channels (RyR). Ca2+ reticulum (SR) Ca2+ Ca2+ stores Local release causes channel Ca2+ spark. Summed Ca2+ sparks T-tubule create a Ca2+ signal. Ca2+ sparks Ca2+ ions bind to troponin to initiate contraction. Ca2+ signal Ca2+ Ca2+ Relaxation occurs when Actin Ca2+ unbinds from troponin. Contraction Relaxation Myosin Calcium binds to troponin, Crossbridge cycle as in skeletal muscle Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.9  Excitation-Contraction Coupling in Cardiac Muscle This figure shows the cellular events leading to contraction and relaxation in a cardiac contractile cell. Action potential enters from adjacent cell. Ca2+ 2 K+ 3 Na+ Ca2+ ECF Voltage-gated Ca2+ ATP NCX ICF channels open. Ca2+ 3 Na+ enters cell. RyR Ca2+ Ca2+ induces Ca2+ release through ryanodine SR L-type Sarcoplamsic receptor-channels (RyR). Ca2+ reticulum (SR) Ca2+ Ca2+ stores Local release causes channel Ca2+ spark. ATP Summed Ca2+ sparks T-tubule create a Ca2+ signal. Ca2+ sparks Ca2+ ions bind to troponin to initiate contraction. Ca2+ signal Ca2+ Ca2+ Relaxation occurs when Actin Ca2+ unbinds from troponin. Ca2+ is pumped back into the sarcoplasmic reticulum for storage. Myosin Contraction Relaxation Ca2+ is exchanged with Na+. Relaxation calcium removed from cytoplasm Na+ gradient is maintained Figure 14.9 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Na by the Rights Reserved +-K+-ATPase. Figure 14.10 EC coupling in cardiac muscle Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Cardiac Muscle Contraction Can Be Graded Force generated is proportional to number of active crossbridges –Determined by how much CALCIUM is bound to troponin Sarcomere length affects force of contraction Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.14 Electrical conduction in myocardial cells instringatemaker outputof Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved REVIEW: The Resting Potential is the Transmembrane Potential of an Undisturbed Cell EXTRACELLULAR FLUID Cl– –30 –70 0 +30 mV 3 Na+ Na+ leak K+ leak channel channel Sodium– Plasma potassium membrane exchange pump CYTOSOL Protein 2 K+ Protein Protein Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Figure 14.13 Action potentials in cardiac autorhythmic cells fast castchannels Characterized by an unstable membrane potential. Since the membrane potential never “rests” at a constant value, it is called a “Pacemaker potential”. leakysodium Channels Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.13 Action potentials in cardiac autorhythmic cells i reauncey shower Ion Movement During an Autorhythmic Cell Depolar repolar Action Potential Na+ and Ca++ contribute to depolarization Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved flow 4 0.5 decreased flow d double resistance 0.25 to radius is the biggest thing that effets flow Figure 14.13 Action potentials in cardiac autorhythmic cells Ea Yore leakychanney If channels are called funny current channels. I = current f = funny cilanners If are specalized Channels found in pacemaker more active in SAnodes than Avnodes Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.13 Action potentials in cardiac autorhythmic cells Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved End Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Copyright This work is protected by United States copyright laws and is provided solely for the use of instructors in teaching their courses and assessing student learning. Dissemination or sale of any part of this work (including on the World Wide Web) will destroy the integrity of the work and is not permitted. The work and materials from it should never be made available to students except by instructors using the accompanying text in their classes. All recipients of this work are expected to abide by these restrictions and to honor the intended pedagogical purposes and the needs of other instructors who rely on these materials. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Additional Notes for self study… Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Table 14.2 The Heart and Major Blood Vessels Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Table 14.3 Comparison of Action Potentials in Cardiac and Skeletal Muscle Autorhythmic Blank Skeletal Muscle Contractile Myocardium Myocardium UNSTABLE pacemaker Membrane Potential Stable at – 70-80 mV Stable at –90 mV potential; usually starts at –60 mV + + Net Na entry through lf Events Leading to Net Na entry through ACh- Depolarization enters via gap channels; reinforced by Ca2+ Threshold Potential operated channels junctions entry Rising Phase of Na+ entry Na+ entry Ca2+ entry Action Potential Extended plateau caused by Ca+ Repolarization + Rapid; caused by K + efflux entry; rapid phase caused by K + Rapid; caused by K efflux Phase efflux Normally none; when Due to excessive K + efflux at repolarization hits –60 mV, high K + permeability. When K + None; resting potential is –90 Hyperpolarization + the lf channels open again. channels close, leak of K + and Na mV, the equilibrium potential for K+ Ach can hyperpolarize the restores potential to resting state cell Duration of Action Variable; generally 150+ Short: 1–2 msec Extended: 200+ msec Potential msec + Long because resetting of Na Not significant in normal Refractory Period Generally brief Na+ channel gates delayed until end function of action potential Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Summary 1 The primary function of the cardiovascular system is the transport of nutrients, water, gases, wastes, and chemical signals to and from all parts of the body. (p. 434; Tbl. 14.1) The human cardiovascular system consists of a heart that pumps blood through a closed system of blood vessels. (p. 435; Fig. 14.1) 473 Blood vessels that carry blood away from the heart are called arteries. Blood vessels that return blood to the heart are called veins. The heart has four chambers: two atria and two ventricles. (p. 435; Fig. 14.1) The pulmonary circulation goes from the right side of the heart to the lungs and back to the heart. The systemic circulation goes from the left side of the heart to the tissues and back to the heart. (p. 435; Fig. 14.1) Dee Unglaub Silverthorn. (2018) Human Physiology : An Integrated Approach (8th Edition) [2.5.8484.0] Retrieved from http://texidium.com Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Summary 2 Blood flows down a pressure gradient (ΔP), from the highest pressure in the aorta and arteries to the lowest pressure in the venae cavae and pulmonary veins. (p. 436; Fig. 14.2) In a system in which fluid is flowing, pressure decreases over distance. (p. 437; Fig. 14.3) The pressure created when the ventricles contract is called the driving pressure for blood flow. (p. 436) Resistance of a fluid flowing through a tube increases as the length of the tube and the viscosity (thickness) of the fluid increase, and as the radius of the tube decreases. Of these three factors, radius has the greatest effect on resistance. (p. 438) If resistance increases, flow rate decreases. If resistance decreases, flow rate increases. (p. 437; Fig. 14.3) Fluid flow through a tube is proportional to the pressure gradient (ΔP), A pressure gradient is not the same thing as the absolute pressure in the system. (p. 437; Fig. 14.3) Flow rate is the volume of blood that passes one point in the system per unit time. (p. 439) Dee Unglaub Silverthorn. (2018) Human Physiology : An Integrated Approach (8th Edition) [2.5.8484.0] Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Retrieved from http://texidium.com Summary 3 The heart is composed mostly of cardiac muscle, or myocardium. Most cardiac muscle is typical striated muscle. (p. 442; Fig. 14.5h) Contractile cells contain striated fibers organized into sarcomeres The signal for contraction originates in autorhythmic cells in the heart. Autorhythmic cells are noncontractile myocardium. (p. 445) Myocardial cells are linked to one another by intercalated disks that contain gap junctions. The junctions allow depolarization to spread rapidly from cell to cell. (p. 446; Fig. 14.9) Valves in the heart and veins ensure unidirectional blood flow. (p. 435; Fig. 14.1) The coronary circulation that supplies blood to the heart muscle originates at the beginning of the aorta and drains directly back into the chambers of the heart. (p. 445; Fig. 14.8) Dee Unglaub Silverthorn. (2018) Human Copyright © Physiology 2019, 2016,: An Integrated 2013 Pearson Approach Education,(8th Inc.Edition) All Rights Reserved [2.5.8484.0] Retrieved from http://texidium.com Summary 4 In contractile cell excitation-contraction coupling, an action potential opens Ca2+ channels. Ca2+ entry into the cell triggers the release of additional Ca2+ from the sarcoplasmic reticulum through calcium-induced calcium release. (p. 448; Fig. 14.10) The force of cardiac muscle contraction can be graded according to how much Ca2+ enters the cell. (p. 447) The action potentials of myocardial contractile cells have a rapid depolarization phase created by Na+ influx, and a steep repolarization phase due to K+ efflux. The action potential also has a plateau phase created by Ca2+ influx. (p. 449; Fig. 14.11) Autorhythmic myocardial cells have an unstable membrane potential called a pacemaker potential. The pacemaker potential is due to If channels that allow net influx of positive charge. (p. 451; Fig. 14.13) The steep depolarization phase of the autorhythmic cell action potential is caused by Ca2+ influx. The repolarization phase is due to K+ efflux. (p. 451; Fig. 14.13) Dee Unglaub Silverthorn. (2018) Human Physiology : An Integrated Approach (8th Edition) [2.5.8484.0] Retrieved from http://texidium.com Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Human Physiology, An Integrated Approach KEY QUESTIONS CHP 14. How does blood leave the heart? CHP 15. Where does blood go after leaving the heart?* How does it return? CHP 16. What is the make up of blood? What can it do? CHP 17 The lung is an air filled sac in our body, how does it move air? CHP 18 Where does blood go after leaving the heart?* Why is their air in our lungs? CHP 19 Wait a minute how does all that water get from my stomach into my pee? Why is it yellow? CHP 20 Whoa… you are telling me my blood organ (heart), air organ (lungs), and my pee organs (kidneys) all work together. How does that work? Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Human Physiology, An Integrated Approach Eighth Edition Overview of the Cardiovascular System 1. The Heart (CHP 14) Structure, Chambers, Valves, and Blood Supply. Unique Features of Cardiac Muscle. Pressure and volume 2. Blood vessels (CHP 15) Comprised of: Arteries, arterioles, capillaries, venules, and veins. Blood pressure and Homeostasis 3. Blood (CHP 16) Components and Function Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Human Physiology, An Integrated Approach Eighth Edition Chapter 14 Cardiovascular Physiology 14.8 to 14.13 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  MATH… Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Q = Cardiac Output l beats/min x mlblood/beat Heart Rate x Stoke Volume PhxMI MLm Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.8b Cardiac Output How do you calculate Cardiac Output?  Q or CO. CO = Heart Rate (HR) × Stroke Volume (SV) Example:  Calculate CO for a HR of 70 beats/min and a stroke volume of 70 ml/beat. CO = Heart Rate (HR) × Stroke Volume (SV) CO = 70 beats/min × 70 ml/beat CO = ? 4900MLIMIN Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Stroke Volume (SV) Amount of blood pumped by one ventricle during a single contraction. co bottom  Units = ml/beat. relaxed filmulloud SV = End Diastolic Volume (EDV) – End Systolic Volume (ESV) kiteofhugiyy.inifyeEnetene p.gecijpgggaggnggygg Example: q blood jggastq regain ftp.fggagggnqjjgavqy  Calculate SV when EDV is 135 ml and ESV is 65 ml. SV = EDV – ESV SV = 135 ml – 65 ml Heart Rate SV beat MLBlood SV = ? Beatstman Finned Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Stroke Volume = SV = EDV – ESV 135ml/beat – 65ml/beat = 70ml/beat Cardiac Output = Q = HR x SV 70beats/min x 70ml/beat = 4900ml/min OR 4.9 L/min pratestions If HR  to 100 bpm…what is CO? online sfindones Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Stroke Volume How can we increase stroke volume? 1) Increase End Diastolic Volume.  More blood in the ventricle to be ejected.  Preload. 2) Increase Ejection Fraction. efficiency of emptying the  More of the blood in the ventricle is ejected.  Contractility. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Ejection Fraction Ejection fraction is the percentage of EDV ejected with a single contraction.  Functional Index of Ventricular Performance. Ejection fraction (EF) = Stroke volume (SV)/End Diastolic Volume (EDV) × 100 Example:  Calculate the ejection fraction if SV is 70 ml/beat and EDV is 135 ml. EF = SV ÷ EDV × 100 EF = 70 ml/beat ÷ 135 ml × 100 = 0.52 × 100 EF = 52% Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.23 Stroke volume and heart rate determine cardiac output Studyslide aFro Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  What is the pulse rate? 6hpm Pulse rate: time between pressure waves in an artery Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Systole, Diastole, Pulse Pressure 93mmHg Systolic Pressure 11 man bloodcot isavaring ▫ Highest pressure in the ventricles and arteries. ▫ Occurs during ventricular systole. Eireaxingtof Diastolic Pressure t.ITthe chambers ▫ Lowest pressure in the ventricles and arteries. ▫ Occurs during ventricular diastole. Pulse Pressure ▫ Difference between the systolic & diastolic pressures. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  What about atrial diastole.... deponarization iñ class cmeenanyq.EE mostof non eigenite potential action leasance I went 7 contraction sizing g out c I aaediate when isn'tbeating qq.gg i Each wave (pointy part) or segment (flat part) on an ECG represents a corresponding electrical event in the cardiac cycle. Mechanical events lag behind electrical events: contraction follows action potential. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  What is the heart rate? Heart rate: time between two R waves or two P waves Eirinn at 3second delay Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  The electrical events precede the mechanical events Ventricular Contraction Atrial Contraction begins just after begins during the the Q wave and latter part of the P continues wave and through through the the PR segment T wave electrical 9 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 1  P-Q or P-R segment: conduction through AV node and AV bundle ELECTRICAL P EVENTS ATRIA CONTRACT OF THE CARDIAC CYCLE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.16 Insert Figure 14.16 (4 of 9) R wave R ELECTRICAL EVENTS P OF THE CARDIAC Q CYCLE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.16 T wave: VENTRICULAR Repolarization REPOLARIZATION R ELECTRICAL P T EVENTS QS OF THE CARDIAC CYCLE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.16 Figure 14.14 The conducting system of the heart Slide SA node depolarizes. P wave SA node Purple shading in steps 2–5 represents The SA node AV node depolarization. Electrical activity goes depolarizes rapidly to AV node via internodal pathways. and then the atria Depolarization spreads more slowly across atria. Conduction slows through AV node. THE CONDUCTING SYSTEM OF THE HEART Q wave Depolarization moves rapidly through ventricular The SA node SA node conducting system to the apex of the heart. depolarizes Internodal and then the pathways Depolarization wave spreads upward from the apex. bundle branches located in the AV Why does the node septum AV bundle action potential Bundle branches spread upward R wave Purkinje The Purkinge apartofelectrical fibers through the me fibers depolarize conductionpathway thatensurescourain ventricle? located in the contractionof the muscles apex and outer FIGURE QUESTION walls of the heart What would happen to conduction if the AV node malfunctioned and could no longer depolarize? © 2016 Pearson Education, Inc. A Normal ECG consists of: Waves: deflections above or below baseline. Segments: sections of baseline between waves. Intervals: combinations of waves and segments. EEE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.15f P Wave Atrial Depolarization QRS Complex Ventricular Depolarization T Wave Ventricular Repolarization Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.15f PR segment Time between end of atrial depolarization and onset of ventricular depolarization. Conduction through the AV node and continuing Atrial Contraction. ST Segment Time between end of ventricular depolarization and onset of ventricular repolarization. Continuing Ventricular Contraction Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.15f PR Interval Time between onset of Atrial depolarization and Ventricular depolarization.  AV blocks. QT Interval Time between onset of Ventricular depolarization and end of repolarization.  Long QT syndrome. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.15f paen.ME iipsnode AV antagonistic node control parasym Sympathexc Ach slowing NE 57 bpm y 65 sunode 1005pm Max 2006pm heart v8 tonic control withdrawl  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.20(a)-b Autonomic control of heart rate Sympathetic control Parasympathetic control Increases heart rate Decreases heart rate down slows bc itmakessunodemorenegative NE on SA β1-adrenergic receptors in node G Ach on Muscarinic receptor K+ permeability increases Na+ and Ca++ permeability increases Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Studypage 60 50mL 3000mL min 32 min HR SV amt of blood amoof leavingventricles bloodleaving per beat permin EDV ESV full emptied 80mL 50mL parasy 1006pm s sympathetic T Intrinsic does this b cofsanode Figure 14.20(d)-(e) Autonomic control of heart rate sodium permability changes rs hyperpolarization Parasympathetic (PNS) V8is sanude Sympathetic (SNS) greyintrinsic crest title Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.20c Autonomic control of heart rate Study page 3 its item Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Autonomic control of heart rate SNS Effects on Heart Rate Cardiovascular control center in medulla oblongata If Sympathetic neurons (NE) 1-receptors of autorhythmic cells  Na and Ca2 influx  Rate of depolarization  Heart rate Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  AUTORHYTHMIC HR HR HR At Rest Activity Parasympathetic Sympathetic SA node INTRINSIC REST firing rate = MAX EXERCISE SA node 100/min SA node Parasympathetic Sympathetic dominates, dominates, HR = 50-70 EST.HRmax beats/min = 220-age 23yrs = 197 beats/min 34my PARASYMPATHETIC VAGAL WITHDRAWAL is when the Vagus nerve sends LESS stimulation This form of TONIC control INCREASES HR VAGAL WITHDRAWL Copyright SYMPATHETIC INPUT © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Changes in Pressure During the Cardiac Cycle 1. CLOCK  3. INTEGRATED  pump'sHole diastole 2. PUMP  expaypages Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.18 Mechanical events of the cardiac cycle isovolumevolume mere fine Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Events of the Cardiac Cycle Late diastole - both sets of chambers are relaxed and ventricles fill passively. START blood flowing inpressure high low Atrial systole - atrial contraction forces a small amount of additional blood into ventricles. S1 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17a Events of the Cardiac Cycle Late diastole - both sets of chambers are relaxed and ventricles fill passively. START Atrial systole - atrial contraction forces a small amount of additional blood into ventricles. S1 S2 whenventricle contract wantsto pressure Ventricular ejection - Isovolumic ventricular as ventricular pressure Contraction - first phase of rises and exceeds ventricular contraction pushes pressure in the arteries, AV valves closed but does the semilunar valves not create enough pressure to open and blood is open semilunar valves. ejected. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17a Changes in Volume During the Cardiac Cycle vallens End Diastolic Volume pushedat blood End Systolic Volume the Isovolume relaxation Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.18  volume on rain opens Stu blood r g pressure igovolumetric ΔP V pressure haschanged putvolumehas pressure change valusareclosed diastolic 40 emptied µ _End change in volume 00 volume 30 stays the volume same endsystolic volume Pressure-Volume Changes During the Cardiac Cycle my Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Pressure-Volume Changes During the Cardiac Cycle 120 KEY Left ventricular pressure (mm Hg) EDV = End-diastoilc volume ESV = End-systolic volume 80 A→B 40 Ventricular Filling START Passive filling (A→ A’) & EDV A A B Atrial contraction (A’ →B) 0 65 100 135 Left ventricular volume (mL) Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17b  Pressure-Volume Changes During the Cardiac Cycle 120 B→C KEY Isovolumic Left ventricular pressure (mm Hg) EDV = End-diastoilc volume ESV = End-systolic volume contraction. 80 Aortic Valve C Opens 40 Mitral Valve Closes START EDV B A A 0 65 100 135 Left ventricular volume (mL) Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17b  Pressure-Volume Changes During the Cardiac Cycle Stroke volume 120 D KEY ESV Left ventricular pressure (mm Hg) EDV = End-diastoilc volume Aortic Valve ESV = End-systolic volume 80 Closes C 40 C→D START EDV B A A Ejection of 0 65 100 135 blood Left ventricular volume (mL) into aorta. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17b  Pressure-Volume Changes During the Cardiac Cycle EDV - ESV = SV 135mL – 65mL = 70mL Stroke volume 120 D KEY ESV Left ventricular pressure (mm Hg) EDV = End-diastoilc volume Aortic Valve ESV = End-systolic volume 80 Closes C 40 emptied C→D START EDV B A A Ejection of 0 0 65 100 Left ventricular volume (mL) 0ᵗʰ 135 blood into aorta. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17b  Pressure-Volume Changes During the Cardiac Cycle Stroke Volume Stroke Volume C to D SV = EDV – ESV 120 D KEY ESV Left ventricular pressure (mm Hg) EDV = End-diastoilc volume 80 C ESV = End-systolic volume ONE CARDIAC EDV dynamic CYCLE 40 START B EDV D→A A A 0 Mitral65Valve 100 135 Isovolumic Left ventricular volume (mL) Opens relaxation. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.17b  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Changes in Pressure During the Cardiac Cycle A Aortic Valve Opens. Blood leaves to ventricles B iiiii Aortic Valve Closes. Most of the blood has been ejected a drops pressure C Avvalve opens Bicuspid (Mitral) Valve Closes. Ventricles are full of blood D Bicuspid (Mitral) Valve Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Opens.  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  PAUSE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Factors that Effect Stroke Volume amtof blood leaving EsYmin one.IE 1) Preload 2) Contractility 3) Afterload Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  1) Preload the chambergetspreloaded mistreating Tintin Enddiastolicvolume “The longer (MORE STRETCH) the muscle fiber & sarcomere when contraction begins, the greater the tension (MORE FORCE) developed.” greaterEDV greaterpreload greatercontractility Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  What fills will be emptied! Frank-Starling law of the heart: Stroke volume is proportional to EDV fill more empty more Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  1) Preload con’t End Diastolic Volume How can we increase the blood volume in the ventricles? Increased Venous Return  The amount of blood that returns to the heart from venous circulation.  Venous return is affected by: 1. Skeletal Muscle Pump. biggest one 2. Respiratory Pump. flow high lowpres 3. Venous constriction. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  1) Preload con’t Skeletal Muscle Pump Respiratory Pump Contraction of skeletal muscle that Decreased pressure on Inferior compresses veins and pushes blood Vena Cava allowing it to draw in toward the heart. more blood from the abdomen = Enhanced venous return. Enhanced venous return. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 15.4  1) Preload con’t Venous Constriction Increased sympathetic activity causes veins to constrict.  Decrease in volume of the veins.  Result is more blood is ‘squeezed’ out of them. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved 2) Contractility 1001 death doesn't Et If emptiesmere NE Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  2) Contractility con’t SNS Effects on Contractility Increased sympathetic activity = Increased epinephrine release. Increases strength of contraction. Increases rate of both contraction and relaxation. ability 2  Decreased duration of Increased contractility relax contraction. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  2) Contractility con’t Studypage Figure 14.22 Catecholamines increase cardiac contraction a on Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  3) Afterload leftside Afterload onRside is failure Is the combined load of EDV and arterial resistance during ventricular contraction. “Ventricular force must exceed the resistance created by blood filling the arterial system.” Blood must be pushed through the semilunar valves and into circulation. If the afterload (i.e. resistance) is increased, the heart must work harder to maintain stroke volume.  Ventricles must increase force of contraction.  Metabolic demand increases (need more O2 & ATP). Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  3) Afterload con’t a Eeristme diff parts of During aerobic exercise, peripheral body need t vasodilation will decrease afterload. Several clinical conditions such as Hypertension are associated with an increased afterload. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.23 Stroke volume and heart rate determine cardiac output Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Regulation of Cardiac Output AFTERLOAD ↕ Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Figure 14.22 Cool Research “We investigated whether differences in cardiac and haematological variables exist, and to what extent, between endurance trained versus untrained , pre- and post-peak height velocity (PHV) children, and how these central factors relate to maximal oxygen consumption.” https://physoc.onlinelibrary.wiley.com/doi/10.1113/JP282282 Perkins, D.R., Talbot, J.S., Lord, R.N., Dawkins, T.G., Baggish, A.L., Zaidi, A., Uzun, O., Mackintosh, K.A., McNarry, M.A., Cooper, S.-M., Lloyd, R.S., Oliver, J.L., Shave, R.E. and Stembridge, M. (2022), The influence of maturation on exercise-induced cardiac remodelling and haematological adaptation. J Physiol, 600: 583-601. https://doi.org/10.1113/JP282282 Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved End Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Copyright This work is protected by United States copyright laws and is provided solely for the use of instructors in teaching their courses and assessing student learning. Dissemination or sale of any part of this work (including on the World Wide Web) will destroy the integrity of the work and is not permitted. The work and materials from it should never be made available to students except by instructors using the accompanying text in their classes. All recipients of this work are expected to abide by these restrictions and to honor the intended pedagogical purposes and the needs of other instructors who rely on these materials. Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Additional Notes for self study… Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Summary 1 Action potentials originate at the sinoatrial node (SA node) and spread rapidly from cell to cell in the heart. Action potentials are followed by a wave of contraction. (p. 454; Fig. 14.15) The electrical signal moves from the SA node through the internodal pathway to the atrioventricular node (AV node), then into the AV bundle, bundle branches, terminal Purkinje fibers, and myocardial contractile cells. (p. 454; Fig. 14.15) The SA node sets the pace of the heartbeat. If the SA node malfunctions, other autorhythmic cells in the AV node or ventricles take control of heart rate. (p. 453) An electrocardiogram (ECG) is a surface recording of the electrical activity of the heart. The P wave represents atrial depolarization. The QRS complex represents ventricular depolarization. The T wave represents ventricular repolarization. Atrial repolarization is incorporated in the QRS complex. (p. 456; Fig. 14.16) An ECG provides information on heart rate and rhythm, conduction velocity, and the condition of cardiac tissues. (p. 459) One cardiac cycle includes one cycle of contraction and relaxation. Systole is the contraction phase; diastole is the relaxation phase. (p. 460; Fig. 14.18) Dee Unglaub Silverthorn. (2018) Human Physiology : An Integrated Approach (8th Edition) [2.5.8484.0] Retrieved from http://texidium.com Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Summary 2 Parasympathetic activity slows heart rate; sympathetic activity speeds it up. Norepinephrine and epinephrine act on β1-receptors to speed up the rate of the pacemaker depolarization. Acetylcholine activates muscarinic receptors to hyperpolarize the pacemakers. (p. 465; Fig. 14.20) Dee Unglaub Silverthorn. (2018) Human Physiology : An Integrated Approach (8th Edition) [2.5.8484.0] Retrieved from http://texidium.com Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved  Summary 3 The volume of blood at the end of ventricular filling is called the end-diastolic volume (EDV). (p. 461) The AV valves prevent backflow of blood into the atria. Closure of the AV valves create the first heart sound. (pp. 458, 463; Figs. 14.7, 14.19) During isovolumic ventricular contraction, the ventricular blood volume does not change, but pressure rises. When ventricular pressure exceeds arterial pressure, the semilunar valves open, and blood is ejected into the arteries. (p. 463; Fig. 14.19) Dee Unglaub Silverthorn. (2018) Human Physiology : An Integrated Approach (8th Edition) [2.5.8484.0] Retrieved from http://texidium.com Copyright © 2019, 2016, 2013 Pearson Education, Inc. All Rights Reserved Summary 4 Most blood enters the ventricles while the atria are relaxed. Only 20% of ventricular filling at rest is due to atrial contraction. The volume of blood in the ventricles at the end of contraction is called