Chapter 20 The Cardiovascular System
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Transcript Chapter 20 The Cardiovascular System
Chapter 20 - The Heart
Location and Size of Heart
Located in thoracic
cavity in mediastinum
About same size as
closed fist
base is the wider
anterior portion
apex is tip or point
Pericardium: Heart Covering
Fibrous Pericardium
Rests on and is
attached to diaphragm
Tough, inelastic sac of
fibrous connective
tissue
Continuous with blood
vessels entering,
leaving heart at base
Protects, anchors
heart, prevents
overstretching
Parietal (Outer) Serous Pericardium
Thin layer adhered to
inside of fibrous
pericardium
Secretes serous
(watery) lubricating
fluid
Pericardial Cavity
Contains pericardial
(serous) fluid
lubricates surface of
parietal and visceral
serous pericardium
decreases friction
Visceral (Inner) Serous Pericardium
Adheres to Heart
Forms epicardium
Secretes watery
(serous) lubricating
fluid
Pericardium
Homeostatic Imbalances
Pericarditis
inflammation of pericardium
painful, rubbing of tissues
can damage myocardium
Cardiac tamponade
a buildup of pericardial fluid
bleeding into pericardial cavity
may result in cardiac failure
Heart wall - Three layers
Epicardium (outer)
visceral layer of
pericardium
thin, transparent
smooth, slippery
Myocardium (middle) cardiac muscle
Endocardium (inner)
endothelium over connective
tissue
smooth lining for inside of
heart, valves
continuous w/ endothelium
of vessels
Chambers of the Heart
External landmarks
coronary sulcus
separates
atria/ventricles
anterior/posterior
interventricular sulcus
separates right/left
ventricles
Internally - 4
compartments
R/L atrium w/ auricles
R/L ventricles
Interatrial septum
separates atria
Interventricular
septum separates
ventricles
Ventricular thickness varies depending on
function
Right – pumps to lungs (pulmonary circulation)
Left – pumps to the body (systemic circulation)
Valves of the Heart
Function to prevent
backflow of blood
into/through heart
Open, close in response
to changes in pressure
in heart
Four valves
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 ventricular
contraction, pressure
increases
papillary muscles
contract, prevent valves
from pushing back into
atria
Atrioventricular (AV) valves
Separate atria,
ventricles
tricuspid valve -
right
bicuspid (mitral)
valve - left
Semilunar valves
In arteries that exit
heart to prevent blood
from re-entering heart
pulmonary semilunar
valves
aortic semilunar valves
Pathologies
incompetent – do not
close
stenosis – stiff and do
not close
Blood Flow Through Heart
Right atrium (RA) receives deoxygenated
blood from three
sources
superior vena cava
(SVC)
inferior vena cava (IVC)
coronary sinus
Right ventricle (RV)
receives blood from RA
pumps to lungs
Pulmonary trunk - from RV
branches into pulmonary
arteries (PA)
Pulmonary arteries
from heart to lungs for gas
exchange
right and left branches for
each lung
blood gives up CO2 and picks
up O2
Pulmonary veins (PV) oxygenated blood from
lungs to heart
Pulmonary Circulation
Left atria
receives blood from PV
pumps to left ventricle
Left ventricle (LV)
sends blood to body via
ascending aorta
aortic arch
curls over heart
three branches off of it
that feed superior
portion of body
thoracic aorta
abdominal aorta
Myocardial Blood Supply
Myocardium has own
blood supply
coronary vessels
diffusion into tissue
impossible due to
thickness
much overlap of vessels
and anastomoses (art-art
connections)
Heart can survive on 1015% of normal arterial
blood flow
Arteries
left coronary artery divides
into anterior interventricular
artery and circumflex arteries
anterior interventricular
artery supplies walls of both
ventricles and septum
circumflex supplies LV and LA
right coronary artery small
branches to RA, divides into
posterior interventricular and
marginal artery
posterior interventricular
supplies walls of both
ventricles
marginal branch supplies RV
Coronary veins
blood into muscle then
drains into coronary sinus
supplied by great cardiac
vein (drains anterior of
heart) and middle cardiac
vein (drains posterior)
Coronary Circulation Pathologies
Faulty coronary
circulation due to:
blood clots
fatty atherosclerotic
plaques
smooth muscle spasms in
coronary arteries
Problems
ischemia
hypoxia
Pathologies (cont.)
Angina pectoris - "strangled chest"
pain w/ myocardial ischemia - referred pain!
tight/squeezing sensation in chest
labored breathing, weakness, dizziness,
perspiration, foreboding
often during exertion - climbing stairs, etc
silent myocardial ischemia
Pathologies (cont.)
Myocardial infarction
(MI) - heart attack
thrombus/embolus in
coronary artery
tissue distal to
blockage dies
if survival, muscle
replaced by scar tissue
Long term results
size of infarct, position
pumping efficiency?
conduction efficiency,
heart rhythm
Pathologies (cont.)
Treatment
clot-dissolving agents
angioplasty
Reperfusion damage
re-establishing blood flow may damage tissue
oxygen free radicals - electrically charged molecules
w/ unpaired electron
radicals attack proteins (enzymes),
neurotransmitters, nucleic acids, plasma membranes
further damage to previously undamaged tissue
or already damaged tissue
Myocardium (Cardiac Muscle)
Cells are involuntary, striated, branched
Fibers connected to others by intercalated discs
gap junctions allow AP's to pass from fiber to fiber
desmosomes
“spot welds”
prevent cardiac fibers from separating
Intercalated Discs
Normal Action Potential
Cardiac Muscle Action Potential
Long absolute
refractory period
Pacemaker potentials
Leaky membranes
Spontaneously depolarize
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 of His
R and L bundle branches
Purkinje fibers
Conduction System and Pacemakers
Arrhythmias
irregular rhythm
abnormal atrial and ventricular contractions
Fibrillation
rapid, out of phase contractions
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
Heart block
AV node damage - severity determines outcome
may slow conduction or block it
Conduction System and Pacemakers
SA node damage (MI)
AV node can run things (40-50 bts/min)
if AV node out AV bundle, bundle
branch/conduction fibers fire at 20-40
bts/min
Artificial pacemakers - can be activity
dependent
Atrial,Ventricular Excitation Timing
SA node to AV node - small delay
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 better
fill the ventricles
once to AV bundle, conduction rapid to rest
of ventricle
Extrinsic Control of Heart Rate
Basic rhythm of heart set
by pacemaker system
Central control from medulla
sympathetic input
parasympathetic input
Electrocardiogram
Electrical activity
of the heart
P wave
QRS complex
T wave
Cardiac Cycle
Connection between
electrical and
mechanical events
Systole
Diastole
Isovolumetric
contraction
Isovolumetric
relaxation
Quiz!!!!!
1. Superior vena cava
2. Right atrium
3. Tricuspid valve
4. Right ventricle
5. Papillary muscle
6. Aorta (aortic
arch)
7. Pulmonary trunk
8. Left atrium
9. Bicuspid valve
10. Interventricular
septum
Cardiac Output
Amount of blood pumped by each
ventricle in 1 minute
CO = HR x SV
HR
heart rate
70 bts/min
SV
stroke volume
70 ml/min
CO 5 L/min (70 bts x 70 ml)
Regulation of Stroke Volume
SV = EDV – ESV
EDV
End Diastolic Volume
volume of blood in the heart after it fills
(following diastole)
120 ml
ESV
End Systolic Volume
volume of blood in the heart after contraction
(after systole)
50 ml
each beat ejects about 60% of blood in
ventricle
Most important factors in regulating SV:
preload, contractility and afterload
Preload
degree of stretch of cardiac muscle cells before
contraction
determined by EDV
Contractility
increase in contractile strength separate from
stretch and EDV
determined by changes in Ca++ availability
Afterload
pressure that must be overcome for ventricles to
eject blood from heart
determined by TPR
Preload
Muscle mechanics
length-tension relationship?
fiber length determines # of cross bridges
cross bridge # determines force
increase/decrease fiber length increase/decrease
force generation
Cardiac muscle
how is cardiac fiber length determined/regulated?
fiber length determined by filling of heart – EDV
factors that effect EDV (anything that effects
blood return to heart) increase/decrease filling
increase/decrease SV
Preload – Frank-Starling Law of the
Heart
length tension relationship of heart
length = EDV
tension = SV
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?
Increase the number
of cross bridges by
increasing amount of
Ca++ inside the cell –
positive inotrope
Sympathetic nervous
system opens channels
to allow Ca++ to enter
the cell
Increase force of contraction without
changing fiber length
Afterload
Flow = P/R
If blood pressure is high (TPR), difficult
for heart to eject blood
More blood remains in ventricle with
each beat
Heart has to work harder to eject blood,
change the length/tension of the heart
Regulation of Heart Rate
Intrinsic regulators
pacemakers
Bainbridge effect
increase in EDV increases HR
filling stretches SA node increasing depolarization and HR
Extrinsic regulators
autonomic nervous system
sympathetic
parasympathetic
hormones – epinephrine, thyroxine
ions – Na+, K+, Ca++
body temperature
age
gender
exercise