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, Ph.D.

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Pericardium
The sac containing the heart
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3 Layers Form the Hearts Wall -

• Epicardium (outer)
• Myocardium (middle)
• Endocardium (inner)

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Pericarditis

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

fibrinous pericarditis
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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

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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
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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
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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
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Pulmonary Circulation
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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
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Schematic of Circulation
Know the names of the valves indicated here.
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Schematic of Circulation
Review Routes
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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

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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

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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

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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)

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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

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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

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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

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Valve Structure

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

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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

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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
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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
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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

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Normal Action Potential
Review in Chapter 11
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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

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Cardiac Muscle Action Potential
electrochemical events
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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
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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

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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

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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!
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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

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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

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Atrial,Ventricular Excitation Timing
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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

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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

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Electrocardiogram

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

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Electrocardiogram
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Cardiac Cycle

• Relationship between electrical and mechanical
  events
• Systole
• Diastole
• Isovolumetric
• contraction
• Ventricular
• ejection
• Isovolumetric
• relaxation

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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
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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

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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

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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

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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

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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
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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?

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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

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Positive Inotropic Effect

• increase the force of contraction without
  changing the length of the cardiac muscle cells

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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

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Regulation of Heart Rate

• Intrinsic
• Pacemakers
• Bainbridge effect
• Increase in EDV increases HR
• Filling the atria stretches the SA node
  increasing depolarization and HR

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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

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Regulation of Heart Rate
Overview
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End Chapter 18