chp 18 power point Flashcards
the sac containing the heart
pericardium
3 layers that form the heart
epicardium
myocardium
endocardium
inflammation of the pericardium painful may damage the lining tissues may damage myocardium is what disease
pericarditis
a buildup of pericardial fluid, or
bleeding into the pericardial cavity
may result in cardiac failure
cardiac tamponade
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
Right atrium (RA) - receives what kind of blood
deoxygenated
Right atrium (RA) - receives deoxygenated blood from three sources
superior vena cava (SVC)
inferior vena cava (IVC)
coronary sinus (CS)
Right ventricle (RV) pumps to lungs via
Pulmonary Trunk (PT)
what sends 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 arteries
What send oxygenated blood from the lungs to the heart
Pulmonary veins (PV) -
what receives blood from PV
pumps to left ventricle
left atria
what sends oxygenated blood to the body via the ascending aorta
left ventricle
duplication of supply routes and anastomoses (crosslinked connections)
is what
Collateral circulation
Myocardium has its own
blood supply
simple diffusion of nutrients and O2 into the myocardium is impossible due to
its thickness
Heart can survive on how much of normal arterial blood flow
10-15%
first branches off the aorta
arteries
blood moves more easily into the myocardium when it is what between beats -> during diastole
relaxed
what 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
arteries
what carries 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
Coronary veins
Compromised coronary circulation due to
- emboli: blood clots, air, amniotic fluid, tumor fragments
- fatty atherosclerotic plaques
- smooth muscle spasms in coronary arteries
-ischemia (decreased blood supply)
-hypoxia (low supply of O2)
-infarct (cell death)
are due to
circulation
classic chest pain
is
Angina pectoris
pathology causes pain is due to myocardial ischemia – oxygen starvation of the tissues
tight/squeezing sensation in chest
labored breathing, weakness, dizziness, perspiration, foreboding
Angina pectoris
pathology often during exertion - climbing stairs, etc.
pain may be referred to arms, back, abdomen, even neck or teeth
silent myocardial ischemia can exist
angina pectoris
heart attack
Myocardial infarction (MI)
what pathology causes thrombus/embolus in coronary artery
some or all tissue distal to the blockage dies
if pt. survives, muscle is replaced by scar tissue
Myocardial infarction (MI)
Long term results
of myocardial infarction
size of infarct, position
pumping efficiency?
conduction efficiency, heart rhythm
electrically charged oxygen atoms with an unpaired electron
oxygen free radicals
indiscriminately attack molecules: proteins (enzymes), neurotransmitters, nucleic acids, plasma membrane molecules
radicals
- re-establishing blood flow may damage tissue
- further damage to previously undamaged tissue or to the already damaged tissue
Reperfusion damage
what has dense connective tissue covered by endocardium
valves
- thin fibrous cords
- connect valves to papillary muscles
AV valves
when pressure low do valves open or close
open
with contraction, pressure increases
papillary muscles contract and
pull valves together
Function to prevent backflow of blood into/through heart
valves
Open and close in response to changes in pressure in heart
valves
Four key valves
Four key valves: tri- and bi-cuspid (mitral) valves between the atria and ventricles and semi-lunar valves between ventricles and main arteries
also close the entry points to the atria
valves
Separate the atria from the ventricles
bicuspid (mitral) valve – left side
tricuspid valve – right side
valves with feathery edges
tricuspid and bicuspid
in the arteries that exit the heart to prevent back flow of blood to the ventricles
semilunar valves
a semilunar valve that does not close properly is called
incompetent
a semilunar valve that is hardened, even calcified, and does not open correctly is called
stenosis
-near instantaneous depolarization is necessary for efficient pumping
cardiac muscles Contractile cells
-much longer refractory period ensures no summation or tetany under normal circumstances
cardiac muscles Contractile cells
opening fast Na+ channels does what
initiates depolarization near instantaneously in cardiac action potential
opening CA++ channels while closing K+ channels does what
depolarizes and contributes to sustaining the refractory period
closing Na+ and Ca++ channels while opening K+ channels does what
restores the resting state
long absolute refractory period permits
forceful contraction followed by adequate time for relaxation and refilling of the chambers
inhibits summation and tetany
long absolute refractory period
what kind of membranes does the heart have
leaky
the fact that the membrane is more permeable to K+ and Ca++ ions helps explain
why concentration changes in those ions affect cardiac rhythm
- spontaneously depolarize
- creates autorhythmicity
pacemaker potentials
cardiac cells repeatedly fire spontaneous action potentials
Autorhythmic cells
the conduction system
Autorhythmic cells:
origin of cardiac excitation
fires 60-100/min
SA node
-AV bundle (Bundle of His)
-R and L bundle branches
-Purkinje fibers
make up
conduction system
It’s as if the heart had only two motor units
: the atria and the ventricles
- irregular rhythms: slow (brady-) & fast (tachycardia)
- abnormal atrial and ventricular contractions means
Arrhythmias
-rapid, fluttering, out of phase contractions – no pumping
-heart resembles a squirming bag of worms
means
Fibrillation
-abnormal pacemaker controlling the heart
-SA node damage, caffeine, nicotine, electrolyte imbalances, hypoxia, toxic reactions to drugs, etc.
means
Ectopic pacemakers (ectopic focus)
-AV node damage - severity determines outcome
-may slow conduction or block it
mean
Heart block
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
once action potentials reach the AV bundle, conduction is
rapid to rest of ventricles
conduction slows
allows atria time to
finish contraction and to better fill the ventricles
basic rhythm of the heart is set by the
internal pacemaker system
pathway of the internal pacemaker
central control from the medulla is routed via the ANS to the pacemakers and myocardium
parasympathetic input for extrinsic control of the heart
acetylcholine
sympathetic input - for extrinsic control of the heart
norepinephrine
measures the sum of all electro-chemical activity in the myocardium at any moment
Electrocardiogram
Cardiac Output =
= Heart Rate x Stroke Volume
Amount of blood pumped by each ventricle in 1 minute
Cardiac Output
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
stroke volume -
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 what percentage of the blood in the ventricle
60%
Most important factors in regulating SV:
preload, contractility and afterload
the degree of stretching of cardiac muscle cells before contraction
preload
increase in contractile strength separate from stretch and EDV
contractility
pressure that must be overcome for ventricles to eject blood from heart
Afterload
increasing/decreasing fiber length does what
increases/decreases force generation
Length-Tension relationship?
fiber length determines number of cross bridges
cross bridge number determines force
How is fiber length determined/regulated?
Fiber length is determined by filling of heart – EDV (End Diastolic Volume)
Factors that effect EDV (End Diastolic Volume)
anything that effects blood return to the heart) increases/decreases filling
Increases/decreases SV
Cardiac muscle
– Frank-Starling Law of the Heart
preload
Length tension relationship of heart
Length = EDV (End Diastolic Volume) Tension = SV (stroke volume)
Sympathetic Stimulation increases the number
of cross bridges by increasing amount of Ca++ inside the cell
Sympathetic nervous stimulation (NE) does what to the heart
opens channels to allow Ca++ to enter the cell
Positive Inotropic Effect increase
increase the force of contraction without changing the length of the cardiac muscle cells
if blood pressure is high, it is
difficult for the heart to eject blood
more blood remains in the chambers after each beat
Afterload
heart has to work harder to eject blood, because of
the increase in the length/tension of the cardiac muscle cells
Intrinsic Regulation of Heart Rate
Pacemakers
Bainbridge effect
Increase in EDV increases HR
Filling the atria stretches the SA node increasing depolarization and HR
Bainbridge effect
Extrinsic regulation of Heart Rate
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
