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Chapter 18 --The Heart

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Chapter 18 --The Heart Use the video clip, CH 18 Heart Anatomy for a review of the gross anatomy of the heart J.F. Thompson, Ph.D. & J.R. Schiller, Ph.D. & G.R. Pitts ... – PowerPoint PPT presentation

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Title: Chapter 18 --The Heart


1
Chapter 18 --The Heart
  • Use the video clip, CH 18 Heart Anatomy for a
    review of the gross anatomy of the heart
  • J.F. Thompson, Ph.D. J.R. Schiller, Ph.D.
    G.R. Pitts, Ph.D.

2
Pericardium
The sac containing the heart
3
3 Layers Form the Hearts Wall -
  • Epicardium (outer)
  • Myocardium (middle)
  • Endocardium (inner)

4
Pericarditis
  • inflammation of the pericardium
  • painful
  • may damage the lining tissues
  • may damage myocardium

fibrinous pericarditis
5
Cardiac Tamponade
  • a buildup of pericardial fluid, or
  • bleeding into the pericardial cavity
  • may result in cardiac failure
  • Elizabeth, Empress of Austria (d. 1898) by
    assassination with a hat pin

6

Chambers of the Heart
  • Internally - 4 compartments
  • R/L atria with auricles
  • R/L ventricles
  • Interatrial septum separates atria
  • Interventricular septum separates ventricles
  • Left ventricular wall is much thicker because it
    must pump blood throughout the body and against
    gravity

LA
RA
LV
RV
7
Blood Flow through the Heart
  • Right atrium (RA) - receives deoxygenated blood
    from three sources
  • superior vena cava (SVC)
  • inferior vena cava (IVC)
  • coronary sinus (CS)

SVC
(CS
RA
IVC
8
Blood Flow through the Heart
  • Right ventricle (RV)
  • receives blood from RA
  • pumps to lungs via Pulmonary Trunk (PT)
  • Pulmonary Trunk (PT) - from RV branches into the
    pulmonary arteries (PA)
  • Pulmonary arteries
  • deoxygenated blood from the heart to the lungs
    for gas exchange
  • right and left branches for each lung
  • blood gives up CO2 and picks up O2 in the lungs
  • Pulmonary veins (PV) - oxygenated blood from the
    lungs to the heart

PA
PA
PT
RA
RV
9
Pulmonary Circulation
10
Blood Flow through the Heart
  • Left atria
  • receives blood from PV
  • pumps to left ventricle
  • Left ventricle (LV)
  • sends oxygenated blood to the body via the
    ascending aorta
  • aortic arch
  • curls over heart
  • three branches off of it feed superior portion of
    body
  • thoracic aorta
  • abdominal aorta

Aortic arch
LA
PV
PV
LV
11
Schematic of Circulation
Know the names of the valves indicated here.
12
Schematic of Circulation
Review Routes
13
Myocardial Blood Supply
  • Myocardium has its own blood supply
  • coronary vessels
  • simple diffusion of nutrients and O2 into the
    myocardium is impossible due to its thickness
  • Collateral circulation duplication of supply
    routes and anastomoses (crosslinked connections)
  • Heart can survive on 10-15 of normal arterial
    blood flow

14
Myocardial Blood Supply
  • Arteries
  • first branches off the aorta
  • blood moves more easily into the myocardium when
    it is relaxed between beats ? during diastole
  • blood enters coronary capillary beds
  • note the collateral circulation

15
Myocardial Blood Supply
  • Coronary veins
  • deoxygenated blood from cardiac muscle is
    collected in the coronary veins and then drains
    into the coronary sinus
  • deoxygenated blood is returned to the right
    atrium

16
Coronary Circulation Pathologies
  • Compromised coronary circulation due to
  • emboli blood clots, air, amniotic fluid, tumor
    fragments
  • fatty atherosclerotic plaques
  • smooth muscle spasms in coronary arteries
  • Problems
  • ischemia (decreased blood supply)
  • hypoxia (low supply of O2)
  • infarct (cell death)

17
Pathologies (cont.)
  • Angina pectoris - classic chest pain
  • pain is due to myocardial ischemia oxygen
    starvation of the tissues
  • tight/squeezing sensation in chest
  • labored breathing, weakness, dizziness,
    perspiration, foreboding
  • often during exertion - climbing stairs, etc.
  • pain may be referred to arms, back, abdomen, even
    neck or teeth
  • silent myocardial ischemia can exist

18
Pathologies (cont.)
  • Myocardial infarction (MI) - heart attack
  • thrombus/embolus in coronary artery
  • some or all tissue distal to the blockage dies
  • if pt. survives, muscle is replaced by scar
    tissue
  • Long term results
  • size of infarct, position
  • pumping efficiency?
  • conduction efficiency, heart rhythm

19
Pathologies (cont.)
  • Treatments
  • clot-dissolving agents
  • angioplasty (bypass surgery)
  • Reperfusion damage
  • re-establishing blood flow may damage tissue
  • oxygen free radicals - electrically charged
    oxygen atoms with an unpaired electron
  • radicals indiscriminately attack molecules
    proteins (enzymes), neurotransmitters, nucleic
    acids, plasma membrane molecules
  • further damage to previously undamaged tissue or
    to the already damaged tissue

20
Valve Structure
  • Dense connective tissue covered by endocardium
  • AV valves
  • chordae tendineae - thin fibrous cords
  • connect valves to papillary muscles

21
Valve Function
  • Opening and closing a passive process
  • when pressure low, valves open, flow occurs
  • with contraction, pressure increases
  • papillary muscles contract pull valves together

22
Valves of the Heart
  • Function to prevent backflow of blood
    into/through heart
  • Open and close in response to changes in pressure
    in heart
  • Four key valves tri- and bi-cuspid (mitral)
    valves between the atria and ventricles and
    semi-lunar valves between ventricles and main
    arteries
  • Valves also close the entry points to the atria

Tricuspid
Bicuspid (Mitral)
Semi-lunar
23
Atrioventricular (AV) valves
  • Separate the atria from the ventricles
  • bicuspid (mitral) valve left side
  • tricuspid valve right side
  • note the feathery edges to the cusps

anterior
bicuspid
tricuspid
24
Semilunar valves
  • in the arteries that exit the heart to prevent
    back flow of blood to the ventricles
  • pulmonary semilunar valves
  • aortic semilunar valves
  • Pathologies
  • Incompetent does not close correctly
  • Stenosis hardened, even calcified, and does not
    open correctly

25
Normal Action Potential
Review in Chapter 11
26
Cardiac Muscle Action Potential
  • Contractile cells
  • near instantaneous depolarization is necessary
    for efficient pumping
  • much longer refractory period ensures no
    summation or tetany under normal circumstances

27
Cardiac Muscle Action Potential
electrochemical events
28
Cardiac Muscle Action Potential
sarcolemmas ion permeabilities
  • opening fast Na channels initiates
    depolarization near instantaneously
  • opening CA channels while closing K channels
    sustains depolarization and contributes to
    sustaining the refractory period
  • closing Na and Ca channels while opening K
    channels restores the resting state

repolarization
29
Cardiac Muscle Action Potential
  • long absolute refractory period permits forceful
    contraction followed by adequate time for
    relaxation and refilling of the chambers
  • inhibits summation and tetany

30
Pacemaker Potentials
  • leaky membranes
  • spontaneously depolarize
  • creates autorhythmicity
  • the fact that the membrane is more permeable to
    K and Ca ions helps explain why concentration
    changes in those ions affect cardiac rhythm

31
Conduction System and Pacemakers
  • Autorhythmic cells
  • cardiac cells repeatedly fire spontaneous action
    potentials
  • Autorhythmic cells the conduction system
  • pacemakers
  • SA node
  • origin of cardiac excitation
  • fires 60-100/min
  • AV node
  • conduction system
  • AV bundle (Bundle of His)
  • R and L bundle branches
  • Purkinje fibers

Its as if the heart had only two motor units
the atria and the ventricles!
32
Conduction System and Pacemakers
  • Arrhythmias
  • irregular rhythms slow (brady-) fast
    (tachycardia)
  • abnormal atrial and ventricular contractions
  • Fibrillation
  • rapid, fluttering, out of phase contractions no
    pumping
  • heart resembles a squirming bag of worms
  • Ectopic pacemakers (ectopic focus)
  • abnormal pacemaker controlling the heart
  • SA node damage, caffeine, nicotine, electrolyte
    imbalances, hypoxia, toxic reactions to drugs,
    etc.
  • Heart block
  • AV node damage - severity determines outcome
  • may slow conduction or block it

33
Conduction System and Pacemakers
  • SA node damage (e.g., from an MI)
  • AV node can run things (40-50 beats/min)
  • if the AV node is out, the AV bundle, bundle
    branch and conduction fibers fire at 20-40
    beats/min
  • Artificial pacemakers - can be activity dependent

34
Atrial,Ventricular Excitation Timing
35
Atrial,Ventricular Excitation Timing
  • Sinoatrial node to Atrioventricular node
  • about 0.05 sec from SA to AV, 0.1 sec to get
    through AV node conduction slows
  • allows atria time to finish contraction and to
    better fill the ventricles
  • once action potentials reach the AV bundle,
    conduction is rapid to rest of ventricles

36
Extrinsic Control of Heart Rate
  • basic rhythm of the heart is set by the internal
    pacemaker system
  • central control from the medulla is routed via
    the ANS to the pacemakers and myocardium
  • sympathetic input - norepinephrine
  • parasympathetic input acetylcholine

37
Electrocardiogram
  • measures the sum of all electro-chemical activity
    in the myocardium at any moment
  • P wave
  • QRS complex
  • T wave

38
Electrocardiogram
39
Cardiac Cycle
  • Relationship between electrical and mechanical
    events
  • Systole
  • Diastole
  • Isovolumetric
  • contraction
  • Ventricular
  • ejection
  • Isovolumetric
  • relaxation

40
Cardiac Output
  • Amount of blood pumped by each ventricle in 1
    minute
  • Cardiac Output (CO) Heart Rate x Stroke Volume
  • HR 70 beats/min
  • SV 70 ml/beat
  • CO 4.9 L/min

Average adult total body blood volume 4-6 L
41
Cardiac Reserve
  • Cardiac Output is variable
  • Cardiac Reserve maximal output (CO) resting
    output (CO)
  • average individuals have a cardiac reserve of 4X
    or 5X CO
  • trained athletes may have a cardiac reserve of 7X
    CO
  • heart rate does not increase to the same degree

42
Regulation of Stroke Volume
  • SV EDV ESV
  • EDV
  • End Diastolic Volume
  • Volume of blood in the heart after it fills
  • 120 ml
  • ESV
  • End Systolic Volume
  • Volume of blood in the heart after contraction
  • 50 ml
  • Each beat ejects about 60 of the blood in the
    ventricle

43
Regulation of Stroke Volume
  • Most important factors in regulating SV preload,
    contractility and afterload
  • Preload the degree of stretching of cardiac
    muscle cells before contraction
  • Contractility increase in contractile strength
    separate from stretch and EDV
  • Afterload pressure that must be overcome for
    ventricles to eject blood from heart

44
Preload
  • Muscle mechanics
  • Length-Tension relationship?
  • fiber length determines number of cross bridges
  • cross bridge number determines force
  • increasing/decreasing fiber length
    increases/decreases force generation
  • Cardiac muscle
  • How is fiber length determined/regulated?
  • Fiber length is determined by filling of heart
    EDV
  • Factors that effect EDV (anything that effects
    blood return to the heart) increases/decreases
    filling
  • Increases/decreases SV

45
Preload
  • Preload Frank-Starling Law of the Heart
  • Length tension relationship of heart
  • Length EDV
  • Tension SV

As the ventricles become overfilled, the heart
becomes inefficient and stroke volume declines.
cardiac reserve
46
Contractility
  • Increase in contractile strength separate from
    stretch and EDV
  • Do not change fiber length but increase
    contraction force?
  • What determines force?
  • How can we change this if we dont change length?

47
Sympathetic Stimulation
  • Increases the number of cross bridges by
    increasing amount of Ca inside the cell
  • Sympathetic nervous stimulation (NE) opens
    channels to allow Ca to enter the cell

48
Positive Inotropic Effect
  • increase the force of contraction without
    changing the length of the cardiac muscle cells

49
Afterload
  • if blood pressure is high, it is difficult for
    the heart to eject blood
  • more blood remains in the chambers after each
    beat
  • heart has to work harder to eject blood, because
    of the increase in the length/tension of the
    cardiac muscle cells

50
Regulation of Heart Rate
  • Intrinsic
  • Pacemakers
  • Bainbridge effect
  • Increase in EDV increases HR
  • Filling the atria stretches the SA node
    increasing depolarization and HR

51
Regulation of Heart Rate
  • Extrinsic
  • Autonomic Nervous System
  • Sympathetic - norepinephrine
  • Parasympathetic acetyl choline
  • hormones epinephrine, thyroxine
  • ions (especially K and Ca)
  • body temperature
  • age/gender
  • body mass/blood volume
  • exercise
  • stress/illness

52
Regulation of Heart Rate
Overview
53
End Chapter 18
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