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Home , Cardiac output, Dromotropic, Endocardium, Fossa ovalis (heart)

Cardiovascular System – Point of maximum Heart: intensity

• Roughly size of human fist (~ 250 – 350 grams)

Cardiovascular System: • Located in the mediastinum (medial cavity of thorax) Heart • “Double pump” composed of

2/3 of heart mass lies left of mid-sternal line

Base

Coronary sulcus

Anterior Apex intraventricular sulcus Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figures 18.1 / 18.4

Cardiovascular System – Heart Cardiovascular System – Heart : Compression of heart due Heart: to fluid / build up Heart: • Anchors cardiac fibers Pericardial sac: Double-walled sac enclosing the heart in pericardial cavity Heart layers: • Reinforces heart structures • Directs electrical signals

Fibrous Pulmonary • Protects heart Pulmonary trunk trunk • Anchors heart • Prevents overfilling

Parietal pericardium Epicardium • Often infiltrated with fat Pericardial cavity • Contains serous fluid Myocardium (friction-free environment) • Contains fibrous skeleton Visceral pericardium Left Left atrium

Pericarditis: Inflammation of the pericardial sac Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.2 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figures 18.2 / 18.3

Cardiovascular System – Heart Atria: Cardiovascular System – Heart Heart – Chambers, Vessels & Valves • Receiving chambers Heart – Chambers, Vessels & Valves • Small, thin-walled Ligamentum arteriosum: (largest in body) Ligamentum Remnant of fetal duct between arteriosum Aorta and pulmonary truck () Carries blood to body

Pectinate muscles: Superior Pulmonary (4) Muscle bundles; assist Left vena cava in atrial contraction Returns blood atrium Returns blood from lungs Right Auricles: (‘little ears’) above diaphragm atrium Increase atrial volume

Fossa ovalis: Pulmonary trunk Shallow depression; : Left Carries blood to lungs remnants of hole between Cone-like muscle; assists Inferior atria in fetal heart in valve closure Right vena cava ventricle Returns blood : below diaphragm Ventricles: Muscle ridges; assist • Discharging chambers in maintaining momentum • Large, thick-walled Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.4 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.4

1 Cardiovascular System – Heart Cardiovascular System – Heart Side-by-side pumps of the heart Heart – Chambers, Vessels & Valves serve separate circuits Heart – Chambers, Vessels & Valves Blood in the atria / ventricles provides little nourishment to heart tissue

How does the heart itself get nourishment? O2-rich; CO2-poor Pulmonary circuit Answer: (Heart attack) (short, low pressure loop) pectoris: Myocardial : O2-poor; Thoracic pain caused by fleeting Myocardial death resulting from CO2-rich deficiency in blood delivery prolonged coronary blockage (long, high pressure loop) Left Systemic circuit Right coronary coronary artery artery Circumflex 1/200 body’s Right mass; 1/20 body’s O -poor; O -rich; artery 2 2 marginal blood supply CO -rich CO -poor 2 2 artery (feeds left atrium and posterior wall (feeds right lateral of left ventricle) ventricular wall)

In steady state, Posterior Workload Anterior from each ventricle must be interventricular not interventricular equal as well as the venous artery equal Anastomosis artery return to each atrium (feeds posterior (junction of vessels) (feeds interventricular ventricular walls) septum and anterior ventricular walls) Right side Left side Costanzo (Physiology, 4th ed.) – Figure 4.1 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.7

Cardiovascular System – Heart Cardiovascular System – Heart

Heart – Chambers, Vessels & Valves Blood in the atria / ventricles provides Heart – Chambers, Vessels & Valves Blood flows through the heart in a single little nourishment to heart tissue direction due to the presence of valves

How does the heart itself get nourishment? Cusp: Flap of endocardium reinforced Answer: Coronary circulation by connective tissue core

Coronary circulation delivery limited to when heart is relaxed… Aortic Pulmonary semilunar (empties blood back Coronary semilunar valve into right atrium) sinus valve

Great cardiac Right atrioventricular Left valve atrioventricular () valve (bicuspid valve) Small cardiac () vein Middle cardiac vein Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.7 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.4

Cardiovascular System – Heart Cardiovascular System – Heart

Heart – Chambers, Vessels & Valves Valves open / close based on Heart – Chambers, Vessels & Valves pressure differences

Atrioventricular valves Semilunar valves Pathophysiology: (prevent backflow into atria) (prevent backflow into ventricles)

Valvular Regurgitation: Valvular stenosis: (collagen cords) Aortic semilunar valve (pig) Chordae Valve does not close properly; Valve flaps become stiff; Papillary tendineae blood regurgitated opening constricted muscle Causes: • Congenially deformed valve • Post-inflammatory scarring • Infective • Rupture of cord / muscle

Causes: • Congenially deformed valve • Post-inflammatory scarring Treatment = Valve replacement (papillary muscles tighten) • Calcification of valve Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figures 18.9 / 18.10

2 Cardiovascular System – Heart Cardiovascular System – Heart Functional syncytium: The entire myocardium behaves Heart – Chambers, Vessels & Valves Muscle Fiber Anatomy Gap junction as a single coordinated unit • Striated, branched cells (~ 85 – 100 m) Heart designed to create complex flow patterns • Single nucleus (sometimes two…) (direct / maintain blood momentum) • Large [mitochondria] (~ 15x skeletal muscle) • High fatigue resistance • Electrical synapses (intercalated discs) 1) Chambers arranged in loop pattern Desmosome 2) Delivery vessels curved Contractile cell: 3) Grooves / ridges within chambers

Less elaborate T-tubule system and sarcoplasmic reticulum compared to skeletal muscle

Randall et al. (Animal Physiology, 5th ed.) – Figures 12.4 / 12.10 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure18.11

Cardiovascular System – Heart Cardiovascular System – Heart Conducting cells: Cardiac Electrophysiology Cardiac cells specialized to quickly spread Cardiac Electrophysiology action potentials across myocardium • Weak force generators The concepts applied to cardiac APs are the same concepts System allows for orderly, as applied to APs in / skeletal muscle sequential depolarization and Intrinsic Conduction System: contraction of heart Normal sinus rhythm: Review:

1) AP originates at SA node • Membrane potential determined by 2) SA node fires at 60 – 100 beats / min relative conductances / concentrations Atrial internodal tracts of permeable ions : (SA node) 3) Correct myocardial activation sequence • Located in right atrial wall • Ions flow down electrochemical gradient toward equilibrium potential (Nernst equation) • Initiates action potentials (APs) • Pacemaker (~ 80 beats / min) • Membrane potential expressed in mV; inside cell expressed relative to outside • Resting membrane potential determined primarily by K+ ions (leaky K+ gates at rest) Bundle • Na+ / K+ pumps maintain [gradients] across branches membranes : (AV Node) • Connects atria to ventricles • Changes in membrane potential caused by flow of ions into / out of cell • Slowed conduction velocity • Ventricular filling • Threshold potential represents the point at Purkinje which a depolarization even becomes fibers self-sustaining (voltage-gated channels)

Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.14 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 11.14

Cardiovascular System – Heart Cardiovascular System – Heart gX = conductance

Cardiac Electrophysiology Cardiac Electrophysiology VG = voltage-gated APs of Atria, Ventricles & Purkinje System: APs of Atria, Ventricles & Purkinje System: Phases of the Action Potential: Long duration AP (150 – 300 ms) Long refractory period Phase 0 – Upstroke

Plateau: Sustained period of depolarization Maximum : • Period of rapid depolarization ~ 240 beats / min + • Na enters via VG channels ( gNa)

Phase 1 – Initial repolarization

• Brief period of repolarization (mV) • Na+ channels close ( g ) Na

(g) + • K exits via VG channels ( gK)

Steep electrochemical gradient Tension Tension

Membrane potential potential Membrane Phase 2 – Plateau • Stable, depolarized membrane potential + • K exits via VG channels ( gK) (L-type) • Ca++ enters via VG channels ( g ) Stable RMP Ca

Ca2+ entry initiates release of more Ca2+ Time (ms) Net current = 0 from intracellular stores (excitation-contraction coupling) Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.12 Costanzo (Physiology, 4th ed.) – Figure 4.12 Costanzo (Physiology, 4th ed.) – Figure 4.13

3 Cardiovascular System – Heart Cardiovascular System – Heart gX = conductance

Cardiac Electrophysiology VG = voltage-gated Cardiac Electrophysiology APs of Atria, Ventricles & Purkinje System: APs of Atria, Ventricles & Purkinje System: Phases of the Action Potential:

Phase 3 – Repolarization Refractory Periods: • Period of rapid repolarization 2+ • Ca cannels close ( gCa) Absolute refractory period (ARP) + • K exits via VG channels ( gK) • Na+ channels closed (reset at ~ -50 mV) Rate slows due to Rate slows due to decrease in K+ decrease in K+ electrochemical Phase 4 – Resting membrane potential electrochemical Relative refractory period (RRP) gradient gradient • Membrane potential stabilizes • Greater than normal stimulus required • All VG channels closed to generate AP (some Na+ channels recovered) • K+ exits via “leaky” channels • Na+ / K+ pumps restore [gradients] Supranormal period (SNP) • Cell is more excitable than normal due • Full Na+ channel recovery Changes in RMP (due to [gradient] issues) directly affect responsiveness of heart • Potential closer to threshold than at rest # of VG Na+ channels available to Effective refractory period (ERP) respond decreases as RMP (not enough Na+ channels have recovered) becomes more (+) Net current = 0 Cardiac dysrhythmia = irregular heartbeat Costanzo (Physiology, 4th ed.) – Figure 4.13 Costanzo (Physiology, 4th ed.) – Figure 4.15

Cardiovascular System – Heart Cardiovascular System – Heart

Cardiac Electrophysiology Pacemaker of the Heart: Cardiac Electrophysiology APs of the Sinoatrial Node: 1) Exhibits automaticity (spontaneous AP generation) 2) Unstable resting membrane potential Other myocardial cells also have the capacity for spontaneous phase 4 depolarization; these are called latent pacemakers 3) No sustained plateau

Phase 0 – Upstroke Location Intrinsic firing rate (impulses / min) • Slower than other cardiac tissue ++ (T-type) • Ca enters via VG channels ( gCa) Sinoatrial node 70 – 80 Atrioventricular node 40 – 60 The pacemaker with the Phase 1 / Phase 2 fastest rate controls the heart rate Absent Bundle of His 40 15 – 20 Phase 3 – Repolarization • Similar to other cardiac cells Overdrive suppression: Latent pacemakers own capacity to spontaneously Phase 4 – Spontaneous depolarization depolarize is suppressed by the SA node. • Accounts for automaticity of SA node + • Na enters via VG channels ( gNa) Ectopic pacemaker: Latent pacemaker takes over and becomes the pacemaker • Open via repolarization event 1) SA node firing rate decreases (e.g., damage / drug suppression) Once threshold reached, VG Ca2+ 2) Intrinsic rate of latent pacemakers increases channels open (return to Phase 0) 3) Blockage in normal conduction pathway (e.g., disease) • Rate of depolarization sets heart rate Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.13 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.14

Cardiovascular System – Heart Cardiovascular System – Heart Allows for proper timing Cardiac Electrophysiology of heart events Cardiac Electrophysiology Electrocardiogram (ECG or EKG): Conduction velocity (speed at which APs propagate in tissues) Correlates with conduction time Graphical recording of electrical currents differs among myocardial tissues through AV node Correlates with the plateau generated and transmitted through heart PR interval of the ventricular AP

QT interval R

~ 1 m / s Repolarization of atria ~ 0.05 m / s Duration corresponds to atrial conduction rate (hidden)

T Only connection: P atria  ventricles ~ 1 m / s ~ 4 m / s P wave Depolarization of Q Repolarization of the atria the ventricles S

QRS wave Depolarization of the ventricles Costanzo (Physiology, 4th ed.) – Figure 4.14 Randall et al. (Animal Physiology, 5th ed.) – Figure12.8

4 Cardiovascular System – Heart Cycle length: Cardiovascular System – Heart Time between one R wave Cardiac Electrophysiology and the next Cardiac Electrophysiology

Heart rate = 60 / cycle length The autonomic nervous system can directly affect the heart rate; Cycle length (beats / min) these effects are called effects

Recall: spontaneous depolarization = VG Na+ channels Positive chronotrophic effects: (increase heart rate) • Under sympathetic control

Leads to  g ; cells SA Na NE node reach threshold more rapidly Sinoatrial node Pharmacology:

β1 receptors β-blockers (e.g., propanolol)

Negative chronotrophic effects: (decrease heart rate) • Under parasympathetic control : : Leads to  gNa; cells SA node nonfunctional Poor conduction at AV node reach threshold SA less rapidly ACh node

Leads to  gK; cells hyperpolarized during : Muscarinic receptors repolarization stage Out-of-phase contractions (further from threshold) Costanzo (Physiology, 4th ed.) – Figure 4.16

Cardiovascular System – Heart Cardiovascular System – Heart Contraction occurs according Cardiac Electrophysiology Cardiac Muscle Contraction to sliding filament model

The autonomic nervous system can also directly conduction velocity at The basic contractile machinery between cardiac and smooth muscle is similar the AV node; these effects are called effects

Positive dromotropic effects: (increase conduction velocity) Recall: AV node slow point in intrinsic conduction pathway • Under sympathetic control

Leads to  g ; cells AV Ca NE node depolarize more rapidly following threshold ~ 0.05 m / s

β1 receptors

Negative dromotropic effects: (decrease conduction velocity) • Under parasympathetic control

AV Leads to  gCa &  gK; cells ACh node depolarize more slowly following threshold

Heart block: Muscarinic receptors Signals fail to be conducted at AV node Costanzo (Physiology, 4th ed.) – Figure 4.14 Costanzo (Physiology, 4th ed.) – Figures 1.21 / 1.22

Cardiovascular System – Heart Cardiovascular System – Heart Inotropism: Intrinsic ability of myocardial cells Cardiac Muscle Contraction Cardiac Muscle Contraction to develop force at a given length

Excitation-contraction coupling translates the action potential The autonomic nervous system can directly affect heart contractility; into the production of tension these effects are called inotropic effects

Dihydropyridine 1) Faster tension receptors Positive inotropic effects: 2)  peak tension Cardiac AP initiated in membrane development (increase contractility)

• Spreads to cell interior via T-tubules • Under sympathetic control 2+ Ryanodine 2+ • Triggers L-type Ca channels in membrane 1) Ca reaccumulated in SR receptors 3) Faster recovery 2+ • Ca ATPase Ca2+ enters cell (plateau phase) 2) Ca2+ extruded from cell NE Cardiac • Ca2+ ATPase tissue • Triggers Ca2+-induced Ca2+ release from SR (E) • Ca2+ / Na+ exchanger • Also triggered by circulating Mechanisms for changing Ca2+ floods cytoplasm catecholamines β receptors tension production: 1

2+ 2+ 1)  Ca in SR =  Ca release to cytoplasm Mechanisms of action: 2)  Ca2+ inward current =  Ca2+ in cytoplasm 1) Phosphorylation of Ca2+ channels in sarcolemma Cross-bridging cycling initiated Relaxation •  Ca2+ enters during plateau / released from SR

2+ • Ca2+ binds to troponin C; cross-bridging occurs 2) Phosphorylation of phospholamban (regulates Ca ATPase activity) •  uptake / storage of Ca2+ in SR • Shorter twitch time allows for more time for ventricle to fill The magnitude of the tension • Faster relaxation time Tension developed is proportional to the • Increased peak tension during subsequent ‘beats’ • Increased tension generation intracellular [Ca2+] equals stronger contraction Similar to Costanzo (Physiology, 4th ed.) – Figure 4.18 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.12

5 Cardiovascular System – Heart Inotropism: Cardiovascular System – Heart Inotropism: Intrinsic ability of myocardial cells Intrinsic ability of myocardial cells Cardiac Muscle Contraction to develop force at a given length Cardiac Muscle Contraction to develop force at a given length

The autonomic nervous system can directly affect heart contractility; The autonomic nervous system can directly affect heart contractility; these effects are called inotropic effects these effects are called inotropic effects Only affect Positive inotropic effects: myocardium Negative inotropic effects: (increase contractility) in atria (decrease contractility)

• Under parasympathetic control

Cardiac ACh tissue Digoxin (atria) Digitoxin

Ouabain Muscarinic receptors

• ACh decreases inward Ca2+ current during plateau • ACh increases outward K+ current (shorten plateau phase) Digitalis purpurea 1) Cardiac glycosides inhibit Na+-K+ ATPase 2) Intracellular [Na+] increases Both  Ca2+ entering cell and thus the amount Cardiac glycosides are a class of drugs 3) Change in Na+ gradient slows down of Ca2+ available for tension development that act as positive inotropic agents Ca2+-Na+ exchanger Used extensively for the treatment 4) Intracellular [Ca2+] increases of congestive 5)  [Ca2+] =  tension development

Costanzo (Physiology, 4th ed.) – Figure 4.20 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.12

Cardiovascular System – Heart Cardiovascular System – Heart

Cardiac Muscle Contraction Cardiac Muscle Contraction

Changes in heart rate also produce changes in cardiac contractility The maximum tension that can be developed by a myocardial cell depends on its resting length (similar to skeletal muscle) Example: Sarcomere length of ~ 2.2 m = L for cardiac muscle Increase in heart rate = Increase in cardiac contractility max Overlap of actin / myosin optimal for cross-bridge formation 1)  heart rate =  APs per unit time =  total amount of Ca2+ entering cell per unit time

AND

2)  Ca2+ entering cell per unit time =  accumulation of Ca2+ in SR for future release

Myocardium cells maintain a ‘working length’ of ~ 1.9 m Positive staircase effect 1.9 m 2.2 m As heart rate increases, the tension developed on each beat increases stepwise to a maximal value Additional Length-dependent Mechanisms: 1) Increasing muscle length increases Ca2+-sensitivity of troponin C 2) Increasing muscle length increases Ca2+ release from SR * Sympathetic input will enhance response Costanzo (Physiology, 4th ed.) – Figure 4.19 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 9.22

Cardiovascular System – Heart Cardiovascular System – Heart = Contraction of heart Cardiac Muscle Contraction = Relaxation of heart Cardiac Muscle Contraction

Ventricular function is described by several parameters: Frank-Starling Law of the Heart: The volume of blood ejected by the ventricle depends on the volume 1) Cardiac Output: Total volume of blood ejected by each ventricle per unit time (usually one minute) Stronger present in the ventricle at the end of diastole tension Cardiac output = Heart rate x volume generated (ml / min) (beats / min) (ml / beat) optimal overlap = optimal tension

2) : Volume of blood ejected by each ventricle per heart beat *

Stroke volume = End diastolic volume - End systolic volume (ml) (ml) (ml)

3) : Fraction of the end diastolic volume ejected in each stroke volume Sarcomere length = ~1.9 m Sarcomere length = ~ 2.2 m

Stroke volume (ml) Ejection fraction = : End diastolic volume (ml) 120 ml 150 ml Preload The resting length from which cardiac muscle contracts Stroke volume: 70 ml Heart rate = 75 beats / min (end diastolic cardiac fiber length) Calculate: Ejection fraction: 0.50 End diastolic volume = 140 ml The more blood that collects in the ventricle, Cardiac output: 5250 ml / min the more the cardiac cells are stretched Cardiac muscle normally ‘held’ on the ascending limb of End systolic volume = 70 ml * the length-tension curve; much ‘stiffer’ than skeletal muscle Costanzo (Physiology, 4th ed.) – Figure 4.21

6 Cardiovascular System – Heart Cardiovascular System – Heart

Cardiac Muscle Contraction Cardiac Muscle Contraction

Frank-Starling Law of the Heart: A ventricular pressure-volume loop allows for the function of a The volume of blood ejected by the ventricle depends on the volume ventricle to be observed for a single heart beat present in the ventricle at the end of diastole Left ventricle

optimal overlap = optimal tension Isovolumetric contraction (1  2) Systolic pressure-volume • Ventricle activates (systole) curve Physiologic range no change (~ linear relationship)  space + in blood =  pressure volume opens 0.64 90 ml • Aortic / mitral valves closed Sarcomere length = ~1.9 m Sarcomere length = ~ 2.2 m Stroke volume Paorta > Pventricle > Patrium 0.50 70 ml Ventricular ejection (2  3) At high levels, This relationship ensures that the volume the • Aortic valve opens 0.39 55 ml ventricles heart ejects in systole equals the volume reach a limit Pventricle > Paorta (line levels out) it receives in venous return • Blood rapidly ejected ( volume) Positive inotropic effect =  ejection fraction 140 ml Negative inotropic effect =  ejection fraction • Atrium ‘tops off’ blood in ventricle • Ventricle relaxed (late diastole) Costanzo (Physiology, 4th ed.) – Figure 4.22 Costanzo (Physiology, 4th ed.) – Figure 4.23

Cardiovascular System – Heart Cardiovascular System – Heart

Cardiac Muscle Contraction Cardiac Muscle Contraction

A ventricular pressure-volume loop allows for the function of a A ventricular pressure-volume loop allows for the function of a ventricle to be observed for a single heart beat ventricle to be observed for a single heart beat

Left ventricle Increased preload Increased Increased contractility Isovolumetric relaxation (3  4)

Systolic • Ventricle relaxes (early diastole) pressure-volume curve no change  space + in blood =  pressure volume

Aortic • Aortic / mitral valves closed valve opens Paorta > Pventricle > Patrium

Mitral Stroke volume valve opens Ventricular filling (4  1)

• Mitral valve opens • Increased end diastolic volume Afterload: • Increased tension / pressure

Patrium > Pventricle • Increased stroke volume Pressure in the vessel leaving • Decreased end systolic volume (Frank-Starling Law) the heart (e.g., aorta) that must • Ventricle refills be overcome to eject blood • Increased stroke volume

Slight pressure increase due to • Increased internal pressure passive filling of compliant • Decreased stroke volume • Atrium ‘tops off’ blood in ventricle ventricle • Ventricle relaxed (diastole) Costanzo (Physiology, 4th ed.) – Figure 4.23 Costanzo (Physiology, 4th ed.) – Figure 4.24

Cardiovascular System – Heart Cardiovascular System – Heart Force = results in greatly Cardiac Muscle Contraction Distance = stroke volume Cardiac Muscle Contraction increased O2 consumption, even though cardiac output reduced The stroke work is defined as the work the heart performs on each beat The myocardial O2 consumption rate correlates directly with the cardiac minute work Work = force x distance  cardiac minute work =  O2 consumption Left ventricle Cardiac minute work: HOWEVER (aortic pressure) Work performed by the heart during The largest percentage of O consumption is for pressure work a unit time (e.g., minute) 2

Force = aortic pressure (pressure work) Mean aortic pressure = 100 mm Hg THUS Distance = cardiac output (volume work) Law of Laplace: Work Mean pulmonary pressure = 15 mm Hg (area inside In a sphere (e.g., heart), pressure correlates curve) Increases in cardiac output or increases in directly with tension and wall thickness and aortic pressure will increase work of the heart correlates inversely with radius

P = Pressure H = Thickness (height) 2HT T = Tension P = R = Radius r

Left ventricle What are the ramifications thicker than if a person exhibits (e.g., preload) right ventricle systemic ? Costanzo (Physiology, 4th ed.) – Figures 4.23 / 4.24

7 Cardiovascular System – Heart Cardiovascular System – Heart Recall: Cardiac Muscle Contraction Cardiac output equals the total volume of also applicable to measuring blood ejected by a ventricle per unit time blood flow to individual organs

The cardiac output can also be measured using the Fick principle A man has a resting O2 consumption of (conservation of mass) 250 mL O / min, a femoral arterial O All measurable 2 2 qualities content of 0.20 mL O2 / mL blood, and a pulmonary arterial O content of 0.15 In the steady state, the rate of O consumed by the body 2 2 mL O / mL blood. must equal the amount of O2 leaving the lungs (pulmonary veins) minus 2 the amount of O2 returning to the lungs () What is his cardiac output?

O2 consumption = COleft ventricle x [O2]pulmonary vein – COright ventricle x [O2]pulmonary artery

O2 consumption equal Cardiac Output = [O2]pulmonary vein – [O2]pulmonary artery Solve for cardiac output: 250 mL O2 / min Cardiac Output = 0.20 mL O / mL blood – 0.15 mL O / mL blood O2 consumption 2 2 Cardiac Output = [O2]pulmonary vein – [O2]pulmonary artery Cardiac Output = 5000 mL / min

Cardiovascular System – Heart Cardiovascular System – Heart

Mechanical / Electrical Overview: Mechanical / Electrical Overview:

Cardiac Cycle: Mechanical and electrical events during single heart beat : Mechanical and electrical events during single heart beat

Phases of the cardiac cycle: Aortic valve A B C Phases of the cardiac cycle: Aortic valve A B C D E F opens opens Ventricle Atrial Systole: (A) Reduced Ventricular Ejection: (D) ‘topped off’ Aortic valve • Preceded by P wave on ECG (20%) • Ventricles begin to repolarize (start of T wave) closes • Increased tension in left atrium • Ventricular / atrial pressure falls (blood still moving out) • Ventricular volume / pressure increases • Atrium continues to fill (pressure rising)

Isovolumetric Ventricular Contraction: (B) Isovolumic Ventricular Relaxation: (E) • Begins during QRS wave on ECG • Ventricles fully repolarize (T wave complete) • Ventricular pressure increases (systole) • Left ventricular pressure drops rapidly (diastole) (1st heart sound – ‘Lub’) • Aortic valve closes (2nd heart sound – ‘Dub’) • Mitral valve closes Mitral valve Mitral valve • NO VOLUME CHANGE closes • NO VOLUME CHANGE closes

Rapid Ventricular Ejection: (C) Rapid Ventricular Filling: (F) Mitral valve opens • Aortic valve opens (Pventricle > Paorta) • Mitral valve opens (Patrium > Pventricle) • Majority of stroke volume ejected • Ventricular volume increases rapidly • Aorta pressure increases • Little change in ventricular pressure (compliance) • Atrial filling begins • Aortic pressure decreases (blood carried away) Left pump Left pump

Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.20 Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.20

Cardiovascular System – Heart

Mechanical / Electrical Overview:

Cardiac Cycle: Mechanical and electrical events during single heart beat

Phases of the cardiac cycle: Aortic valve A B C D E F G opens Reduced Ventricular filling: (G) Aortic valve • Longest phase of cardiac cycle closes • Final portion of ventricular filling

Increase in heart rate reduces G phase interval; if heart rate too high, ventricular filling compromised

Mitral valve closes

Mitral valve opens

http://www.youtube.com/watch?feature=endscreen&NR=1&v=xS5twGT-epo Left pump

Marieb & Hoehn (Human Anatomy and Physiology, 8th ed.) – Figure 18.20

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