Ch.20 ❤️

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Last updated 6:02 PM on 2/3/26
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23 Terms

1
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Heart circulation

Double cardiovascular system

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Congestive Heart failure

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<p>Layers of Heart</p>

Layers of Heart

in → out

  1. Endocardium (simple squamous & connective tissue)

  2. Myocardium

  3. Parietal Pericardium

  • Pericardial cavity = pericardial fluid

<p>in → out</p><ol><li><p>Endocardium (simple squamous &amp; connective tissue)</p></li><li><p>Myocardium</p></li><li><p>Parietal Pericardium</p></li></ol><ul><li><p>Pericardial cavity = pericardial fluid</p></li><li><p></p></li></ul><p></p>
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Where is the Heart?

b/t Lungs at MEDIASTINUM = b

<p>b/t Lungs at MEDIASTINUM = b</p>
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Why are the ventricles the same size?

to stop congestion = same volume → ventricles same size but the left has more myocardium

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Functions of Heart Skeleton - Passive 80% filling of ventricles & delay?

Vacuum - atria contracting 20% into ventricles rest is like a medicine dropper
1. Electrical insulator b/t atria & ventricles

  • delay → skeleton stops action potential from going straight to ventricles

  1. anchors myocardium → spiral structure alows most output

  2. Valve seat - memo

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how do we prevent congestion on RIGHT atria?

fibrous connective tissue - chordae tendineae f that attached to papillary muscles on the ventricles
- attatch to flap of atriventricular valve
when heart contaracts blood preasurre pushing up - papillary will keep it from inverting(prolapsing)

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<p>Heart skeleton</p>

Heart skeleton

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InterATRIAL septum

Foramen ovalis → Fossa ovalis after birth

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Heart sounds

LUB - AV valves CLOSIN
DUB - Semilunar Pulmonary & aortic valves CLOSING w/ more force

Left side Ventricular preassure - 10 torr which increases to 120?

Heart murmurs - Valve disease LESS CARDIAC OUTPUT → CONGESTIVE HR FAILURE

  1. Valvular STENOSIS
    - hardening & Narrowing
    Result - pump faster/harder

  2. Valvular incompetence/Regurgitation
    Closes weird - blood goes back → flaging sound

    CONGESTIVE HR FAILURE → Chronic disease on Cardiac Output that could lead to Respiratory problems etc all because of different pressure equlization

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Coronary Circulation

Blood supply to myocardium
coronary arteries taking blood to capillary muscle

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Cardiac Cycle

  1. Mid diastole - ventricles = relaxing & expanding
    - Passive filling 80%, 20% atria contraction

  2. End of systole/start of distole - ventricles relax and their preassure drops (L 120→80) when this occurs semiluar valves close
    - all 4 valves shut → isovolumetric relaxation and we have end systolic volume =70ml

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Stroke volume

SV- volume of blood pumped out Left Ventricle (& right V) EACH BEAT
SV= EDV(150ml)-ESV(70ml) = 80ml/stroke

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Cardiac Output

volume of blood pumped our of LV in 1min
CO= stroke volume x stroke rate
CO= 80ml/stroke x 70 stroke/mins = 5,600 ml/min AT REST

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Average Human has how much blood?

~5500ml of blood
avg human 165 lbs 5’8

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Can stroke volume and cardiac output change? look over this

Yes, increased or decrease

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<p>Action potentials</p>

Action potentials

Membrane resting potential = average cell potential energy = -70mv , inside = 12 Na+ , 155 K+ 155 protein-, Outside = 145 Na , 4 K+ , 0 protein

Na/k Pump = To keep them at the proper distribution to stop equalization through diffusion and maintain charge

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Cardiac Muscle (myocardium) consists of

  1. Single cells w/ nucleus

  2. connected by INTERCALATED DISCS

  3. Autorhythmic (myogenic contractions) '
    Generates OWN action potentials

  4. Fibers=branched

Intercalated discs → thanks to gap junctions myocardium → connects them as two big cells (atria/ventricles) because theres no membrane

  • adhesion fibers stronger than membrane

  • HIGHLY permeable

Skeletal muscle fiber - connected to neurons

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2 types of Myocardium

  1. Contractile cell→ pump

  2. Conductive cell→ specialized myocardium = generate & conduct AP

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<p>Pacemaker Sinoatrial node (SA)</p>

Pacemaker Sinoatrial node (SA)

  1. No resting potential

  2. NO NEED FOR EXTERNAL STIMULUS = no neuron connection

  3. Rate is 100-120bpm

Na continuously leaks gets to threshold +50
Ca++ chennels open & leaks → spike UP Depolarization (two charges make it quicker)
+20 Na channelscloses
K open K goes out cell → -60 → K channels close → K UP


<ol><li><p>No resting potential</p></li><li><p>NO NEED FOR EXTERNAL STIMULUS = no neuron connection</p></li><li><p>Rate is 100-120bpm</p></li></ol><p></p><p></p><p>Na continuously leaks gets to threshold <strong>+50</strong><br>Ca<sup>++</sup> chennels open &amp; leaks → spike UP Depolarization (two charges make it quicker)<br>+20 Na channelscloses<br>K open K goes out cell → -60 → K channels close → K UP </p><p><br></p>
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Contractile cells

Resting potential -90 → +20
If it wasn’t under ANS → 110 bpm
Long refractory period → avoids cramping, allows Contraction→ Relax

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Electrical flow

  1. SA node sets pace by generating PP (55-200bpm)

  2. intermodal fibers 1m/sec - conduct AP → ATRIA & AV node

AV node 0.1 m/sec

  • Delays AP

Cardio skeleton = electrical insulator so AP goes through AV bundle → bundle branches→ purkinje fibers
4-6 = 8-10 m/sec

  1. AV bundle in septum

  2. bundle branches each ventricle

  3. Purkinje fibers

  4. myocardium of ventricles

    moderate → slow→sonic speed

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Contractile cells

conducts pacemaker potentials and leads it to contractile cells