Physiology Unit 3

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Last updated 5:37 AM on 3/26/26
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61 Terms

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Intercalated Discs

interdigitating folds between cells; mechanical junction (desmosomes) + electrical junctions (gap junctions) = syncytium

gap junctions allow for low resistance 1/400 pathway for electrical signal to spread cell-to-cell

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Specialized Cells

“leading”

low contractility, no stable RMP = reach TH sans neuronal stimulus

located in: SA node, internodal bundles, AV node, bundle of His, bundle branches + purkinje fibers

<p>“leading”</p><p>low contractility, no stable RMP = reach TH sans neuronal stimulus</p><p>located in: SA node, internodal bundles, AV node, bundle of His, bundle branches + purkinje fibers</p>
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Contractile Cells

“following”

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Capillaries

greatest total cross-sectional area (6000cm2) so blood flow velocity is slowest + most efficient

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Veins

type of vessel where BP is lowest

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Arterioles

vessel where BP will drop the most

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Cardiac Output

HR x SV (mL/min)

proportional relationship to stroke volume and heart rate (SV + HR)

inverse relationship to total peripheral resistance (TPR)

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Total Peripheral Resistance TPR

force the heart must overcome to push blood thru systemic circulation; main sources are vessel diameter, blood viscosity + vessel length

inversely proportional to cardiac output CO

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Laminar Flow

blood cells in the center of a vessel flow faster; silent

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Pulse Pressure

systolic - diastolic

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Poiseuille’s Law

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Fibrous Insulator

collagenous skeleton; rigid framework for dense regular connective tissue between atria and ventricles

gives delay + produces sequential events — allows time for electrical signal to spread thru atria for contraction, then for signal to spread thru ventricles for contraction

<p>collagenous skeleton; rigid framework for dense regular connective tissue between atria and ventricles</p><p>gives delay + produces sequential events — allows time for electrical signal to spread thru atria for contraction, then for signal to spread thru ventricles for contraction</p>
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Sarcomeres

striated actin and myosin filaments

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<p>Pericardium</p>

Pericardium

fibrous + serous sac surrounding heart, cushions / prevents friction b/c fluid

  1. fibrous pericardium - outer, tough, dense connective tissue

    1. pericardial cavity filled w/ fluid

  2. serous pericardium - inner, thin, double layer

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Parietal Surface

lines inner surface of parietal pericardium; attached to diaphragm and base of heart

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Visceral Surface

surrounds heart surface (epicardium)

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External Epicardium

first heart wall layer, visceral pericardial layer

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Myocardium

middle heart wall layer, cardiac muscle tissue

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Endocardium

innermost heart wall layer; simple squamous epithelium, covers internal surfaces of the heart / external surface of heart valves

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Chordae Tendineae

“heart strings", collagen fibers attached to lower surfaces of AV valve cusps; prevent valve cusps from flipping into atria during ventricular contraction

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Papillary Muscles

muscular ridges anchoring chordae tendineae

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Right Atria

auricle, smooth wall (posterior), pectinate muscles (ridges), crista terminalis (muscular ridge), fossa ovalis, coronary sinus, IVS, SVC openings, right AV valve

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Left Atria

auricle, mostly smooth wall, pectinate muscle (anterior), left AV valve (chordae tendineae)

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Lub

(S1) closing of AV valves

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Dub

(S2) closing of semilunar valves

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Fossa Ovalis

fetal = foramen ovale (small valve on left side closes d/t higher BP on left atrium side)

hole in atrial septum, most blood goes thru here; right → left shunt in systemic circuit

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Ligamentum Venosum

fetal = ductus venosus (closes d/t increased pressure in portal vein forcing blood flow thru liver sinuses)

shunt: blood bypasses liver to heart

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Ligamentum Arteriosum

fetal = ductus arteriosus (closes d/t oxygen change after umbilical cord removed, vessel constricts and closes)

pulmonary artery to aorta shunt; right → left shunt to systemic circuit

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PDA Patent Ductus Arteriosus

ductus arteriosus fails to close after birth = blood repeatedly flows back to lungs

net CO decreases so blood volume increases to compensate (high EPO); L+R ventricular hypertrophy, murmur thru systole + diastole

cyanosis of left skull + upper limb

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Tetralogy of Fallot

4 heart defects —

  1. pulmonary valve stenosis = decreased outflow to lungs

  2. R ventricular hypertrophy = pumping lotta blood

  3. ventricular septal defect

  4. aorta displaced over ventricular septum

septal defect d/t right → left shunt, most blood bypasses lungs = majority aortic blood is deoxygenated

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AV Nodal Delay

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Specialized Fibers

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Contractile Fibers

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SA SinoAtrial Node

first to depolarize, no stable RMP (never at rest)

leaky Na+ channels open as soon as depolarize → repolarize → open Na+ → rise to threshold

dont’t need voltage, strategically open sodium channels

70-80 depol/min → steepest potential (highest intrinsic rythym)

ANS innervation most dense

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Purkinje Fibers

fast conduction d/t many gap junctions at intercalated discs

15-30 depol/minute → more gradual prepotentials

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Prepotential

AKA pacemaker potential, unique to hear cells, generate own AP without stimulus

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AV AtrioVentricular Node

delays depolarization b/c cells smaller in diameter, more resistance, slower movement of electrical signal to bundle branches

40-60 depol/min

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Chronotropy

decreased by parasympathetic: Ca++, Na+, K+

increased by sympathetic: Ca++, Na+, K+

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Inotropy

force / strength of contraction, muscle fiber tension development

sympathetic (NE) division affects in all fibers (specialized + contractile), parasympathetic has little affect

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Baroreceptor Reflux

detect stretch in aorta + carotid body, too much =

high BP → high frequency AP down sensory neurons to medulla oblongata → integration center for cardioinhibotory center → vagus nerve to effector SA node of heart → mAChR

low BP → low frequency AP to cardioaccelatory center →parasympathetic nerve fibers → (nor)epinephrine increases rate of depolarization

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Absolute Refractory Period

very long in heart cells to prevent summation + tetany; cardiac contractile cell begins relaxation

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Latent Period

need Ca++ out of sarcoplasmic reticulum first, contraction happens after

very short in cardiac cell, allows muscle to start contracting during AP

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SKELETAL MUSCLE Excitation Contraction Coupling

  1. AP moves along T-tubule,

  2. voltage change senses by Na+VCG,

  3. signal communicated to VOCC, contraction occurs,

  4. calcium pumped back into sarcoplasmic reticulum,

  5. Ca++ binds to calsequestrin to facilitate storage,

  6. contraction terminated

<ol><li><p>AP moves along T-tubule, </p></li><li><p>voltage change senses by Na+VCG, </p></li><li><p>signal communicated to VOCC, contraction occurs, </p></li><li><p>calcium pumped back into sarcoplasmic reticulum, </p></li><li><p>Ca++ binds to calsequestrin to facilitate storage, </p></li><li><p>contraction terminated</p></li></ol><p></p>
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CONTRACTILE CARDIOCYTE Excitation Contraction Coupling

  1. AP moves along large T-tubule

<ol><li><p>AP moves along large T-tubule</p></li><li><p></p></li></ol><p></p>
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EDV

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ESV

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Preload

degree of muscle tension when it begins to contract

frank-starling principle: more in, more out

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Afterload

contractile force needed for ejection; affected by peripheral vasculature

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Contractility of Ventricle

availability of calcium, positive and negative intropoy (rare)

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Diastis

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