Cardiovascular System III: The Heart Overview of Cardiovascular System Purpose of Cardiovascular System: Transport and Delivery Heart

art = PUMP General Anatomy Arteries carry blood AWAY (from heart) Veins return blood to heart Two Circuits: Systemic Pulmonary Fig 12.51 V is your roadmap for this unit**** How maintain blood pressure; mean pressure (93) Increase mean pressure, increase cardiac output

Introduction: The Heart Heart is a DOUBLE PUMP but one pump feeds the other
blood in left heart different from blood from right heart

Thus each heart pumps the same amount- to keep balance Gross Anatomy: Overview
Heart in thoracic cavity Know anatomical terms (base- where ventricles originate, apex- point, etc) Right vs. left ventricles (brings oxygenated blood to rest of body) Right atrium gets blood from vena cava-big vein (used blood from body)

Pericardial Sac = Example of a Serous Membrane (connective tissues membrane, two layers, with fluid in between) Fibrous Pericardium dense CT; outer sac

Serous Pericardium Parietal - lines fibrous pericardium (surrounding, around) In between: Pericardial Fluid
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 Visceral-organs (AKA epicardium) covers myocardium; surrounds heart itself Note relationship of heart, lungs, and their serous membranes Function? - Lubrication to prevent heat build up and damage Pericarditis Inflammation of pericardium Increased fluid (secreted) Increased thickness + viscosity (as opposed to thin, thus decreases lubrication) Increased Adhesions Increased resistance due to friction (can hear friction rub) Causes: Trauma, chemo, radiation May be up to 2 L of fluid Pericardial Tamponade Large build-up of fluid in pericardial sac affects cardiac function Compresses heart Pericardiocentesis: process of withdrawing fluid with catheterway to take care of pericardial tamponade Wall of the Heart Epicardium (visceral pericardium: squamous epithelium, areolar CT and fat)-outer most layer Myocardium (cardiac muscle) Endocardium (areolar CT and endothelium) Muscle attaches to fibrous skeleton of the heart
- dont attach by tendons, but by intercalculated disks

Myocardium (cardiac muscle) note arrangement of muscle bundle (diagonal arrangement) ALLOWS WRINGING CONTRACTIONsqueeze blood out
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Chambers and Great Vessels External anatomy: atria and ventricles Which ventricle has thicker wall? Left ventricle. Why? Pumps to whole body, because left ventricle through the entire systemic circuit Left ventricle generates more pressure than right Left ventricle ejects same amount of blood as right

Chambers and Great Vessels Atria receive blood Right atrium from: Superior vena cava Inferior vena cava Coronary sinus- last large vein returning blood to heart itself Left atrium from: Pulmonary veins (4)

Ventricles pump blood away from heart (to arteries) Right ventricle pulmonary trunk (divides into two pulmonary arteries) Left ventricle Aorta Heart valves ensure one-way flow AV valves (open during relaxation phase) Tricuspid (Right AV valve)-three cusps between right and left atrium Bicuspid (Left AV valve; mitral valve)
Valves prevent back-flow from ventricle to atria**

Chordae Tendinae anchor AV valves to papillary muscles; attaching valve to muscle Function: Prevent eversion (opening backwards) of AV valves Semilunar Valves Aortic SL Pulmonary SL

- prevent backflow from great arteries aorta and pulmonary trunk

General Circulatory Plan Fig. 12.6, 12.8V; Table 22.3 M

From tissuesright atrium (superior/inferior vena cava, coronary sinus)

Coronary Circulation Coronary Arteries (part of systemic circulation!)

- feed heart muscles

Cardiac Veins and Coronary Sinus (veins collect here; one of 3 openings in arteries) Disorders: Angina Pectoris vasospasm of coronary arteries pain Myocardial Infarction (Heart Attack) cell death cardiac muscle death

Histology of Cardiac Muscle

Fig. 22.5 M

Atrial and Ventricular Syncytia (contractile)-myocytes that contract Syncytium = acts as one Gap junctions communicating functions- electrical synapses
Ions (carry currents) can flow from cell to cell through gap junction

Conducting System Similarities to Skeletal Muscle include*: Striated- occur because actin/myosin arrangement etc Contraction mechanism-depolarize, Ca2+ go thru T-tubules,

Differences from Skeletal Muscle include*: Muscle dont wrap around Bifurcations -forks

Anastomoses muscle cells connected together thru intercalated disks Intercalated Disks Desmosomes spot rivet (mechanical junction) Gap Junctions communicating junctions
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- allow action potential to spread (conduct) from cell to cell

Have T-tubules (holes)

Conducting System Specialized cardiac cells Non-contractile (only conduct) Autorhythmic self exciting; myogenic (set own contraction, no nerve has to tell them) Set heart rate (SA node) - in right atrium
(AV node)bundle of Hisright/left bundle branchapex of heartmany Purkinje fibers

Transmit excitation so that heart contracts in proper sequence Energy Requirements for Cardiac Muscle Lots of mitochondria oxidative phosphorylation to make ATP NEED for O2! cannot do anaerobic metabolism Fuel: Glucose Fatty acids Lactate Others Cardiac Electrophysiology Open Na+ channels and close K+ channels Na+ high outside K+ high inside Ca2+ high outside Inward current = positive in Selected Channels K channels Inward rectifiers- KIR; not directly voltage gated; open at negative potentials Delayed rectifiers (voltage gated)- open at positive potentials

Channels mediating ITO current- I = current; T= transient; O = outward

 Fast Na channels- voltage gated; 3 conformations (1) closed resting and responsive (2) activated (3) inactivated closed and locked; absolute refractory period

Ca++ channels (voltage gated) L: slow (long-lasting Ca2+ channels) T: transient (short-lived); fast and open briefly

HCN channels (mediate Funny current; F channels in Vander) Cation channels- mainly sodium Hyperpolarization activated Cyclic Nucleotide gated Correlate ion currents, channels and membrane potential changes: SEE SUPPLEMENTARY NOTES!
Pacemaker cells generate potential and myocyte (cardiac cells) receive potential from pacemaker (actually contracts)

Pacemaker Potential SA, AV nodes Correlate ion currents, channels and membrane potential changes: SEE SUPPLEMENTARY NOTES! Sequence of Excitation: Fig. 22.12 M
No questions on Exam on EKG

EKG Overview EKG monitors sequence of cardiac excitation (Fig 12.11 V) SA node (atrial depolarization and contraction) AV node (signal delayed at AV node to AV bundles (get smaller then bigger, make sure have time to contract) Bundle of HisBundle branches Perkinje fibers (ventricles contract, depolarize) apex to base Atrial depolarization = P wave
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 Signal arrives at AV node Some Disorders of Conduction System AV block (Heart Block) No electrical connection between atria and ventricles Ectopic Focus Abnormal Pacemaker (outside where suppose to be)

More EKGs fig. 12.16V SKIP Extrinsic Innervation of the Heart Cardioacceleratory Center controls Sympathetic innervation (increases contraction and heart rate) Cardioinhibitory Center controls Parasympathetic innervation (only decreases heart rate) via Vagus nerve (X)
Medulla (brainstem) Heart rate is less than would be if pacemaker depolarizing by itself Figure 12.9 V

Vagal tone predominates at rest!

Mechanisms for ANS Control of SA Node (see also fig. 12.22 V) Vagal Activity ****Slows rate of pacemaker depolarization via decreased cAMP acting on HCN channels****
Close HCN channels, less Na coming in

[SKIP]

Via PLC, increases GK to hyperpolarize pacemaker cells

********Sympathetic (NE transmitter, also EPI from adrenal medulla) Increased cAMP acts on HCN channels to increase rate of pacemaker depolarization************* ****Prolonged opening of L type Ca++ channels (affects rate + strength)

Excitation-Contraction Coupling (fig. 9.40 V) SA node depolarization throughout cardiac conduction system AP T tubules, activates L type Ca++ channels; influx of Ca++, which activates Ryanodine receptors (RyRs), intracellular ion channels on SR membrane, release Ca++ from SR Ca++ binds troponin, activates cross bridge cycling; sliding of filaments SR for skeletal muscle, cardiac muscle get it from elsewhere as well (two sources) get Ca++ from Mechanical Events: Cardiac Cycle (Fig. 12.18V; 22.11 M) Recall importance of long refractory period for cardiac AP! (to prevent tetanus; must contract and relax = pump)

Systole = contraction; Diastole = relaxation Ventricular Systole = contraction of ventricles Atrial systole occurs during late ventricular diastole

Heart Sounds Caused by closing of valves (lub/dup)

AV valves (lub), SL (dup)

Isovolumetric (= volume) - all four valves must be closed always o Contraction of ventricles o Relaxation of ventricles Cardiac Output = Heart Rate * Stroke Volume (CO; ml/min) (HR; beats/min) (SV; ml/beat) Cardiac Reserve: COmaximal COresting Stroke Volume (SV) = EDV ESV
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EDV (end diastolic volume) determined by:

Length of ventricular diastole (how long is diastole) If heart rate too high than inadequate filling Venous return

ESV (end systolic volume) determined by:

Arterial blood pressure (how high blood pressure) Contractility (is contracting at rest on own, or added hormone, etc to eject it?)

Ejection Fraction = (EDV ESV)/EDV or SV/EDV Normal = >55% Heart Rate: EPI sympathetic stimulation increases (depolarize fast, increases heart rate), parasympathetic decreases (opposite, so hyperpolarize)

Control of Stroke Volume Preload: Frank-Starling Law of the Heart Increase EDV increase force of contraction to pump out extra blood INTRINSIC to cardiac muscle (part of cardiac muscle) (graph) As increase EDV also increase stroke volume, due to length-tension properties of cardiac muscle No change in ESV Changes in Sympathetic input (and contractility): Sympathetic stimulation (and adrenal medulla EPI) increased contractility increased force of contraction (independent of EDV)
Regardless of length, increase EDV, increase length, increase force End systolic volume (ESV), if contract harder, going to decrease

Mechanisms of Sympathetic Effects on Cardiac Contractility Fig. 12.27 V Because have Ca2++ from outside as well, DHP receptor also
connected to L channels on outside Get increase in heart rate, also increase strength

Contrast Sympathetic and Parasympathetic Effects Control of Stroke Volume Afterload Refers to back-pressure exerted by arterial blood must be exceeded for ventricles to eject blood from heart.
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 HYPERTENSION: afterload is increased, affecting ESV (and lowering stroke volume) increase afterload (increase ESV) would tend to lead to increase ESV and decreased CO, but heart pumps harder to compensate Summary: Major Factors Controlling Cardiac Output

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