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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.
PericardiumThe sac containing the heart
3 Layers Form the Heart’s Wall -
Epicardium (outer)
Myocardium (middle)
Endocardium (inner)
Pericarditis inflammation of the
pericardium painful may damage the lining
tissues may damage
myocardium
fibrinous pericarditisfibrinous pericarditis
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
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
Chambers of the Heart
RALA
LVRV
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)
(CS
SVC
IVC
RA
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
Blood Flow through the Heart
RA
PT
PA PA
RV
Pulmonary Circulation
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
LA
LV
Aorticarch
PV PV
Blood Flow through the Heart
Schematic of Circulation
Know the namesof the valvesindicated here.
Schematic of Circulation
ReviewRoutes
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
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]
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
Myocardial Blood Supply
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)
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
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
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
Valve Structure
Dense connective tissue covered by endocardium
AV valves chordae tendineae -
thin fibrous cords connect valves to
papillary muscles
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
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
Separate the atria from the ventricles bicuspid (mitral)
valve – left side tricuspid valve –
right side note the
feathery edges to the cusps
Atrioventricular (AV) valves
bicuspidtricuspid
anterior
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
Semilunar valves
Normal Action Potential
Review in Chapter 11
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
Cardiac Muscle Action Potential
electrochemicalevents
Cardiac Muscle Action Potential
sarcolemma’s 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
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
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
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
It’s as if the heart had only two motor units: the atria and the ventricles!
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
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
Atrial,Ventricular Excitation Timing
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
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
Electrocardiogram measures the
sum of all electro-chemical activity in the myocardium at any moment P wave QRS complex T wave
Electrocardiogram
Cardiac Cycle Relationship between electrical and
mechanical events Systole Diastole Isovolumetric contraction Ventricular ejection Isovolumetric relaxation
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
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
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
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
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
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”
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 don’t
change length?
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
Positive Inotropic Effect
increase the force of contraction without changing the length of the cardiac muscle cells
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
Regulation of Heart Rate
Intrinsic
Pacemakers
Bainbridge effect Increase in EDV increases HR Filling the atria stretches the SA node
increasing depolarization and HR
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
Regulation of Heart Rate
Overview
End Chapter 18