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33 Cards in this Set

  • Front
  • Back
heart murmur
sound of blood leaking through a narrow (stenosed) valve or a valve that fails to close properly; caused by a leaky valve
special features of cardiac muscle
myogenic - nerves not needed to stimulate contraction

generate own action potential for contraction

pacemaker cells have the highest rate of action potentials

stimulate the other cells at the pacemaker rate (intact heart)
syncytium
electrical coupling (gap junctions) and tight membranous connections (intercalated disks) in cardiac muscles allow for many cells to contract as a single unit
what is ischemia?
give an example
absence of blood flow (low O2 levels)
causes cell death and acute pain

Ex: myocardial infarction (heart attack)
what happens to O2 starved cardiac cells?
ATP deficiency would lead to inability to pump Ca++ out of muscle cells

lactic acid + HIGH Ca++ causes:
->gap junctions close
->no transfer of ions b/w cells
->no contraction
how does Ca++ enter cardiac muscle cells?
Ca++ enters cell from the plasma by an action potential that opens voltage gated Ca++ channels. This triggers Ca++ ions from the sarcoplasmic reticulum (SR) to enter the cardiac muscle
how does Ca++ leave cardiac muscle cells?
2 pumps are used:
(1)Na/Ca exchanger linked to Na/K ATPase
->moves Ca++ into extracellular fluid
(2)Ca ATPase
->moves Ca++ into SR
what's the difference between skeletal and cardiac muscle contraction?
skeletal - force of a single twitch is ALL or NONE

cardiac - contraction is graded
->HIGH concentration of Ca++
->INCREASE in cross bridges
->MORE forceful contraction
what is cardiac glycosides as digitalis?
substance that prevents removal of Ca++ back into the plasma

causes INCREASE Ca++ levels -> MORE forceful contraction of the heart
effect of catecholamines on cardiac muscle
binds to beta 1 receptors in cardiac muscle
->INCREASES force of contraction
->DECREASES duration of contraction
effect of catecholamines on pacemaker cells
bind to beta 1 receptors on pacemaker cells
->INCREASES the frequency of action potentials
->INCREASES the rate of contraction
special features of action potential in ventricular cells
1)rapid depolarization due to Na+ entry
2)influx of Ca++ causes a long plateau
3)long refractory period prevents muscle tetany
special features of action potential in pacemaker cells
1)resting membrane potential unstable
2)slow depolarization begins spontaneously after repolarization
->ion flow in I_f channels (funny-current channels)
3)Ca++ influx causes depolarization
4)K+ efflux causes repolarization
electrical activity pathway for heart
-SA node (Pacemaker) sends electrical signal
->travels to Left/Right Atria through internodal fibers (atria contract)
->AV node and AV bundle
->Left/Right Ventricles through bundle branches
->Perkinje Fibers
->ventricular muscles (causes ventricle to contract)
important function of AV node
1)prevents action potentials from moving directly from atria to top of the ventricles

2)delays conduction of action potentials from atria to ventricles
=>allows time for the atria to complete contraction before the ventricles contract
If abnormal pacemaker function, then...?
-next fastest cells set the pace of action potentials
-heart rate will be too slow
-mechanical pacemaker correct the problem.
what is heart block?
list 2 types of heart block
abnormal pacemaker function
->poor conduction from the atria to ventricles

complete hb
-atria generates HIGHER action
potentials then ventricles
-mechanical pacemaker corrects problem

partial hb
-slows conduction from atria to ventricles
what is ECG?
represents the electrical activity of the heart recorded from electrodes placed on the surface of the skin

measures net charge moving towards and away the recording electrodes

voltage measured b/w 2 electrodes (lead)

does NOT record action potentials
what is einthoven's triangle?
represents minimal # of leads to give an ECG

lead I - left/right arms
lead II - right arm/left leg
lead III - left leg/left arm
what are the following:
p wave
qrs complex
t wave
pr interval
qt interval
P wave - atrial depolarization (atrial contraction)
QRS complex - ventricular depolarization (ventricular contraction)
T wave - ventricular repolarization (ventricles recharging for next contraction)
PR interval - time of electrical conduction from atria to ventricles
QT interval - time required for depolarization and repolarization of the ventricles.
factors changing the recording of an ECG
1)dial on the ECG is placed on lead II
->taller peaks than lead I or III

2)reverse position of electrodes
->waves inverted (neg rather than positive)

3)patient sitting vs lying down
determining heart rate on ECG
count number of R waves over a few seconds then # of waves in 60 seconds

Ex) 4 R Waves over 3 seconds
4/3sec = HR/60sec
HR = 80 waves/sec = bpm
abnormalities of heart from ECG
3rd degree block
atrial fibrillation
ventricular fibrillation
prolonged PR interval
prolonged QT interval (QT Syndrome)
what is 3rd degree block?
more than 1 P Wave before QRS complex

causes complete heart block

more P Waves (atria) than R Waves (ventricles) = HIGHER action potential in atria then ventricles
what does a prolonged PR interval cause?
partial heart block
-slows conduction b/w atria and ventricles
steps of the cardiac cycle
1)diastole (ventricles fill w/ blood)
2)atrial systole (blood -> ventricles)
3)EDV (end ventricle relaxation)
4)isovolumetric ventricular contraction
-all valves closed
5)ventricular ejection (opens semilunar valve/blood ejected)
6)ESV
7)isovolumetric ventricular relaxation
closure of which valve causes a particular heart sound
S1(first) - closure of AV valves
S2(second) - closure of semilunar valves
what are types of AV and semilunar valves?
AV valve
-tricuspid (right)
-bicuspid (mitral) (left)
semilunar valves
-aortic
-pulmonary
when in the cardiac cycle is the volume of blood in the left ventricle maximal and minimal?
maximal - EDV (ventricle filled)
minimal - ESV (ventricles empty)
what's stroke volume and cardiac output?
SV
=volume pumped/beat (ml/min)
=EDV - ESV

CO = HR x SV
INCREASE HR, INCREASE CO
(beats/min X ml/min)
what modulates Heart Rate?
autonomic neurons
-tonic parasympathetic signals (DECREASE HR)
-sympathetic neurons from medulla oblangata (INCREASE HR)
what conditions decrease cardiac output?
tachycardia
-very FAST HR that decreases the filling time

ventricular fibrillation
what affects stroke volume?
1)contractility
-Ca++, Norepinephrine

2)stretch of fibers (prop to venus return)

-venous return (HIGH)
=>inspiration (blood -> heart)
=>exercise leg muscles (one-way valve)
=>constriction (blood -> heart)

-venous return (LOW)
=>gravity