Cardiac L 14 Flashcards
cardiac muscle is regulated by the
autonomic nervous system
is cardiac muscle striated or non striated
striated
Myosin and actin filaments form
sarcomeres
Contraction occurs by means of sliding
thin filaments
cardiac muscle is connected via
via gap
junctions called intercalated discs (electrical
synapses that permit impulses to be
conducted cell to cell).
is cardiac muscle multinucleated?
NO
define myocardium
a mass of cardiac muscle cells connected to
each other via gap junctions.
do action potentials have to occur at all cells in myocardium to simulate ALL the cells in myocardium?
no, Action potentials that occur at any cell in a myocardium can
stimulate all the cells in the myocardium
-behaves as single functional unit
what is pacemaker potential?
Cardiac muscle producing action potentials automatically
(without innervation)
what is heart rate influenced by?
autonomic innervation and
hormones.
are voltage-gated calcium
channels directly connected to calcium
channels in the SR?
NO,
instead:calcium acts as a second messenger to open
SR channels: called calcium induced calcium release
what is cardiac output?
Cardiac output – the volume of blood
pumped each minute by each ventricle:
cardiac output = stroke volume X heart rate
(ml/minute) (ml/beat) (beats/min)
a. Average heart rate = 70 bpm
b. Average stroke volume = 70 to 80 ml/beat
c. Average cardiac output = 5,000-5,500 ml/minute
how is cardiac rate regulated?
Spontaneous depolarization occurs at SA node
when HCN channels open, allowing Na+ in.
a. Open due to hyperpolarization at the end of the
preceding action potential
b. Sympathetic norepinephrine and adrenal
epinephrine keep HCN channels open, increasing
heart rate.
c. Parasympathetic acetylcholine opens K+ channels,
slowing heart rate.
d. Controlled by cardiac center of medulla oblongata
that is affected by higher brain centers
what antagonistic influence increases cardiac rate?
Positive chronotropic effect
Tachycardia >100 bpm
what antagonistic influence decreases cardiac rate?
Negative chronotropic effect
Bradycardia < 60 bpm
what are the sympathetic and parasympathetic effects of the SA node?
sympathetic:Increased rate of diastolic
depolarization; increased
cardiac rate
parasym:Decreased rate of diastolic
depolarization; decreased
cardiac rate
what are the sympathetic and parasympathetic effects of the AV node?
sym:Increased conduction rate
para:Decreased conduction
rate
what are the sympathetic and parasympathetic effects of the atrial muscle?
sym: Increased strength of
contraction
para:No significant effect
what are the sympathetic and parasympathetic effects of the ventricular muscle?
sym: Increased strength of
contraction
para: No significant effect
what 3 variables is stroke volume regulated by?
- End diastolic volume (EDV): volume of blood in the
ventricles at the end of diastole
a) Sometimes called preload
b) SV increases with increased EDV. - Total peripheral resistance: Frictional resistance in
the arteries
a) Called afterload
b) Inversely related to SV - Contractility: strength of ventricular contraction
a) SV increases with increased contractility.
normally, about how much % of the end diastolic volume (EDV) is ejected?
60%,
aka the ejection fraction: amount of blood pumped out of the ventricle/total amount of blood in ventricle
what is the frank starling law?
increased end diastolic volume (EDV) results in increased contractility and thus increased stroke volume
what is Intrinsic Control of Contraction Strength due to?
1) Due to myocardial stretch
a) Increased EDV stretches the myocardium,
which increases contraction strength.
b) Due to increased myosin and actin overlap and
increased sensitivity to Ca2+ in cardiac muscle
cells
what is the Adjustment for rise in peripheral resistance?(Intrinsic Control of Contraction Strength.)
a) Increased peripheral resistance will
decrease stroke volume
b) More blood remains in the ventricles, so
EDV increases
c) Ventricles are stretched more, so they
contract more strongly
Extrinsic Control of Contractility
1) Contractility – strength of contraction at any
given fiber length
2) Sympathetic norepinephrine and adrenal
epinephrine (positive inotropic effect) can
increase contractility by making more Ca2+
available to sarcomeres. Also increases
heart rate.
3) Parasympathetic acetylcholine (negative
chronotropic effect) will decrease heart rate
which will increase EDV →increases
contraction strength →increases stroke
volume, but not enough to compensate for
slower rate, so cardiac output decreases
regulation of cardiac output equation
cardiac output=cardiac rate x stroke volume(total peripheral resistance and mean arterial pressure)
what is the distribution of blood at rest?
-small veins and venules, systemic veins, large veins
- capillaries
-systemic arteries
-heart
-lungs`
- 60-70%
- 4-5%
-10-12%
-8-11%
-10-12%