May 10, 2025 • 31 mins
Let’s Get Updated is an audio learning series that brings to life the key topics from Update in Anaesthesia—one topic at a time.
Each episode guides you through a full reading of a selected topic, making it easy to listen and read along. Whether you’re preparing for exams or brushing up on essential concepts, this podcast is built for anaesthesia learners in all settings, especially low-resource environments.
This is an independent educational project not affiliated with the World Federation of Societies of Anaesthesiologists (WFSA). Content is drawn from publicly available issues of Update in Anaesthesia.
~~~~~~~~~~
This episode features a full reading of “Aspects of Myocardial Physiology” from Update in Anaesthesia, Volume 24, Number 2.
Read along with the original article or simply listen in for a clear, guided walkthrough.
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(00:01):
Updates in anaesthesia, volume 24 #2.
Aspects of myocardial Physiologyby AM Campbell and JA Hough.
Summary This article describes in more detail the Physiology of
(00:28):
the cardiac action potentials, that is, nodal and ponchinja
cell, the mechanics of the cardiac cycle, and the control
of coronary artery perfusion. Cardiac action potentials Action
(00:55):
potentials APS are sequential changes in trans membrane
potential that occur as a resultof activity of ion channels
resulting in the propagation of electrical impulses in excitable
cells. The heart has a multicellular
(01:19):
structure but behaves like a syncytium because the individual
muscle cells communicate with their neighbours through gap
junctions, which provide low resistance pathways for easy
movement of action potentials between cells.
(01:44):
The cardiac action potential that is approximately 250
milliseconds is much longer thandose of nerve or skeletal
muscle, which is approximately 1to 3 milliseconds.
This is due to a prolonged plateau phase caused by calcium
(02:10):
ion influx. Two types of action potential or
pour in the heart, the fast response found in heart muscle
are pokinge fibres and the slow response found in pacemaker
(02:32):
tissues such as the sinoatrial and atrioventricular nodes.
The fast response seen in Figure1, the resting potential of
cardiac muscle and Pokhenge fibres, is about -90 millivolts.
(03:03):
Interior negative to exterior and AP is initiated when the
membrane is depolarized to a threshold potential of about -65
millivolts. The initial depolarization
(03:26):
originates from transmission from an adjacent cell via gap
junctions. Let's talk about the phases.
In the first response phase zerorapid depolarization.
(03:51):
The inward current caused by opening of fast sodium channels
becomes large enough to overcomethe outward current through
potassium channels, resulting ina very rapid upstroke.
Phase One early incomplete repolarization due to
(04:20):
inactivation of fast sodium channels and efflux of potassium
ions. Phase 2, plateau.
Phase A period of slow decay mainly due to calcium entering
(04:47):
the cell via L type. That is, L is long lasting
calcium channels which are activated slowly when the
membrane potential is more positive than about -35
millivolts. This is balanced by potassium E
(05:12):
flux through various potassium channels.
Calcium entry during the plateauis essential for contraction.
Blockers of L type calcium channels, for example verapamil,
reduce the force of contraction.Phase three, rapid
(05:42):
repolarization. Calcium influx declines and the
potassium outward current becomes dominant with an
increased rate of repolarization.
Phase four electrical diasto resting membrane potential is
(06:08):
restored. Next we get to Figure 1, talking
about the fast response Pokinje fibre action potential.
Pause the recording and take a little while to go through this
the slow response seen in Figure2.
(06:35):
These cells spontaneously depolarize and are said to have
automaticity. Phases one and two are absent.
(06:57):
Phase 4 pre potential or pacemaker potential.
There is no depolarization plateau and the cells have an
unstable resting membrane potential.
During this phase, they gradually depolarize from -60
(07:21):
millivolts to a threshold of -40millivolts due to a slow
continuous influx of sodium ionsand a decreased efflux of
potassium ions. A calcium current due to the
(07:42):
opening T type that is transientT is equal to transient calcium
channels completes the pacemakerpotential Phase 0
depolarization. We are still talking about the
phases in the slow response whenthe membrane potential reaches
(08:09):
threshold potential, the L type calcium channels open causing
calcium influx and an action potential is generated.
Phase three re polarisation due to E flux of potassium, no
(08:40):
epinephrine and epinephrine thatis mediated via beta one
receptors increase the slope of phase four by increasing calcium
influx, therefore increasing theheart rate.
Calcium influx also increases the force of contraction.
(09:06):
Acetylcholine, which is mediatedvia M2 receptors, decreases the
slope of phase four by increasing potassium efflux and
causing hyperpolarization, that is, increased negativity within
the cells. This makes the conduction tissue
(09:31):
much less excitable, so it takeslonger to spontaneously reach
the threshold level. This results in a decrease in
heart rate. The intrinsic rate of the
sinoatrial node is 100 per minute.
(09:54):
However, vagal tone decreases this to about 70 bits per
minute. Next we get to figure 2 talking
about the slow response sinuatrial node action
potential. Pause the recording and take a
(10:18):
little while to go through this refractory periods.
During the absolute refractory period ARP scene in Figure 1,
the cardiac cell is totally inexcitable.
(10:42):
During the following relative refractory period RRP, there is
a gradual recovery of excitability.
A supra maximal stimulus can elicit an action potential in
(11:03):
the relative refractory period. This action potential, however,
has a slower rate of depolarization, a lower
amplitude, and shorter duration than normal, and therefore the
(11:24):
contraction produced is weaker. Peak muscle tension occurs just
before the end of the absolute refractory period, and the
muscle is halfway through its relaxation phase by the end of
(11:45):
the relative refractory period. The long refractory period
protects the ventricles from toorapid a RE excitation, which
would impair their ability to relax long enough to refill
(12:06):
sufficiently with blood. Unlike skeletal muscle, 2
contractions cannot submit and afused Titanic contraction cannot
occur. The cardiac cycle.
(12:32):
The cardiac cycle refers to the relationship between electrical,
mechanical, that is, pressure and volume, and vascular events
occurring during one complete heartbeat seen in Figure 3.
(12:56):
Next we get to Figure 3, explaining the full events of
the cardiac cycle. Very, very important figure.
Kindly pause the recording and take your time.
Take your time to go through this figure.
(13:17):
Isovolumetric ventricular contraction early systo the
action potential is conducted through the AV node down the
bundle of his across both ventricles and ventricular
(13:40):
depolarization occurs. This is the QRS complex of the
ECG. Ventricular contraction causes a
sharp rise in ventricular pressure and the AV valves
(14:00):
close. That is the first heart sound.
Once this exceeds atrial pressure, preventing back flow
into the Atria, ventricular pressure increases dramatically
with no change in ventricular volume.
(14:24):
During this initial phase of ventricular contraction,
pressure is less than in the pulmonary artery and aorta, so
the outflow valves remain closed.
The ventricular volume does not change.
(14:45):
The increasing pressure causes the AV valves to bulge into the
Atria resulting in the C wave ofthe central venous pressure
trace ejection, that is systo the semi lunar valves open.
(15:14):
As ventricular pressure exceeds aortic blood pressure,
approximately 2/3 of the blood in the ventricles is ejected
into the arteries. Flow into the arteries is
initially very rapid, that is rapid ejection phase, but
(15:38):
subsequently decreases, that is reduced ejection phase.
The stroke volume SV is the volume of blood ejected from
each ventricle in a single bit, and the ejection fraction is
stroke volume over end diastolicvolume.
(16:06):
Arterial blood pressure rises toits highest point, that is
systolic blood pressure during the last 2/3 of systole before
the AV valves open again. Atrial pressure rises as a
result of feeling from the veins, resulting in the V wave
(16:32):
of the central venous pressure trace.
Active contraction ceases duringthe second-half of ejection and
the ventricular muscle repolarizes.
This is the T wave of the ECG. Ventricular pressure during the
(17:00):
reduced ejection phase is slightly less than in the
artery, but blood continues to flow out of the ventricle
because of momentum called protodiastole.
Eventually the flow briefly reverses causing closure of the
(17:25):
outflow valve and a small increase in aortic pressure
called the diacortic notch isovolumetric relaxation that is
(17:45):
early diastole. The ventricles relax and the
ventricular pressure falls belowarterial blood pressure.
This causes the semi lunar valves to close causing the
second heart sound dope. The ventricular pressure falls
(18:12):
with no change in ventricular volume.
When ventricular pressure falls below atrial pressure, the AV
valves open and the cycle beginsagain.
Passive filling that is early diastole.
(18:41):
The atrial and ventricles are relaxed and ventricular pressure
is close to 0. The atrial ventricular valves
are open and the semilunar valves are closed.
Blood flows from the great veinsinto the atrial and ventricles.
(19:04):
About 80% of ventricular feelingoccurs during this phase,
consisting of an initial rapid filling phase followed by a
slower filling phase, that is diastasis, atrial contraction,
(19:30):
that is late diastole. A wave of depolarization
beginning at the sinuatrial nodespreads across both Atria and
reaches the AV node. This is the P wave of the ECG.
(19:56):
The Atria contracts and atrial pressures increases, producing
the A wave of the central venouspressure.
Trace blood continues to flow into the ventricles and
ventricular pressure increases slightly.
(20:20):
The atrial contribution to ventricular feeling increases as
heart rate increases. And diastole shortens and there
is less time for passive feelingventricular volume, that is EDVN
diastolic volume is equals to volume of blood in the
(20:42):
ventricle. At the end of diastole, arterial
pressure is at its lowest. At this stage of the cycle,
we're still talking about late diastole.
The X descent of the central venous pressure trace results
(21:05):
from atrial relaxation and downward displacement of the
tricuspid valve during ventricular systo.
The Y descent of the CVP trace is due to the atrial emptying as
the tricuspid valve opens and blood enters the ventricle.
(21:33):
Next we get to Figure 4 talking about left ventricular pressure
volume loop during a single heart cycle in a normal adult at
rest. Kindly pause the recording and
go through this. After that we get to Figure 5
(21:57):
talking about how the pressure volume loop is affected by the
contractility and compliance of the ventricle and factors that
alter refilling or ejection. Please take some time to go
through this. Also the pressure volume loop
(22:23):
seen in figures 4:00 and 5:00. This represents the events of
the cardiac cycle. The cardiac cycle proceeds in an
anti clockwise direction. A end diastole.
(22:47):
B Aortic valve opening. C Aortic valve closure.
D Mitral valve opening. EDV and end systolic volume are
(23:11):
represented by points A and C, respectively.
The area enclosed by the loop represents the stroke work.
Since work is equals to pressuretimes volume, the pressure
(23:31):
volume curve in dire stool is initially quite flat, indicating
that large increases in volume can be accommodated by only
small increases in pressure. However, the ventricle becomes
less distensible with greater feeling, as evidenced by the
(23:55):
sharp rise of the diastole curveat large intraventricular
volumes. Control of the coronary
circulation. Myocardial blood supply is from
the right and left coronary arteries, which run over the
(24:20):
surface of the heart, giving branches to the endocardium that
is the inner layer of the myocardium.
Venous drainage is mostly via the coronary sinus into the
right atrium, but a small proportion of the blood flows
directly into the ventricles through the Fibesian veins,
(24:47):
delivering on oxygenated blood to the systemic circulation.
The heart at rest receives about5% of the cardiac output.
Coronary blood flow is approximately 250 miles per
(25:09):
minute. Oxygen extraction by the
myocardiomat rest is very high, that is 65%, compared to other
tissues, that is 35%. Therefore, the myocardium cannot
(25:30):
compensate for reductions in blood flow by extracting more
oxygen from haemoglobin. Any increases in myocardial
oxygen demand must be met by an increase in coronary blood flow.
The three main factors influencing coronary flow are
(25:55):
mechanical, mainly external compensation and perfusion,
pressure, metabolic and neural. Next we get to figure 6, the
anatomy of the coronary arteries.
(26:18):
Kindly take a while to go through this coronary artery
compensation. Sorry, Coronary artery
compression and blood flow. Left coronary artery blood flow
is unique in that there is interruption of flow during
(26:43):
systo, that is, mechanical compression of vessels by
myocardial contraction and flow occurs predominantly during
diasto when cardiac muscle relaxers and no longer obstructs
blood flow through ventricular vessels.
(27:05):
Conversely, right coronary arterial flow rate is highest
during cysto because the aortic pressure driving flow increases
more during cysto, that is from 80 to 120 millimetres of
(27:26):
mercury, than the right ventricular pressure which
opposes flow that is from zero to 25 millimetres of mercury.
As about 80% of the total coronary arterial flow occurs
(27:46):
during diastole, a pressure around the aortic diastolic
pressure becomes the primary determinant of the pressure
gradient for coronary flow. Coronary perfusion pressure is
the arterial diastolic pressure minus left ventricular end
(28:12):
diastolic pressure, that is, CPPis equals to ADP minus LVEDP.
Increases in heart rates that shorten diastole time for
coronary blood flow are likely to increase oxygen consumption
(28:37):
more than elevations in blood pressure, which are likely to
offset increased oxygen demands by enhanced pressure dependent
coronary blood flow. The myocardium regulates its own
(28:57):
blood flow, that is auto regulation, closely between
perfusion pressures of 50 and 150 millimetres of mercury.
Beyond this range, blood flow becomes increasingly pressure
(29:19):
dependent. This auto regulation is due to a
combination of myogenic and metabolic mechanisms.
Metabolic factors. The close relationship between
coronary blood flow and myocardial oxygen consumption
(29:43):
indicates that one or more of the products of metabolism cause
coronary vasodilation. Hypoxia and adenosine are potent
coronary vasodilators. Other factors suspected of
(30:03):
playing this role include PA, CO2, hydrogen, potassium
lactate, and prostaglandins. Under normal conditions, changes
in blood flow are entirely due to variations in coronary artery
(30:27):
tone, that is, resistance in response to metabolic demand.
Neural factors. The coronary arterioles contain
A1 adrenergic receptors, which mediates vasoconstriction, and
(30:53):
beta 2 adreneric receptors, which mediates vasodilation.
Sympathetic stimulation generally increases myocardial
blood flow because of metabolic factors and not because of beta
2 adrenergic stimulation. This is shown experimentally
(31:19):
when the ionotrophic and chronotrophic effects of
sympathetic discharge are blocked by beta one selective
blocker to reduce metabolic demand.
An injection of no epinephrine in all anesthesized animals
elicits coronary vasoconstriction.
(31:43):
Therefore, the direct effect of sympathetic stimulation is
constriction rather than dilation of the coronary vessels
and highlights the importance ofmetabolic control.
Updates in anaesthesia, volume 24 #2.
Aspects of myocardial Physiologyby AM Campbell and JA Hough.
Summary This article describes in more detail the Physiology of
(00:28):
the cardiac action potentials, that is, nodal and ponchinja
cell, the mechanics of the cardiac cycle, and the control
of coronary artery perfusion. Cardiac action potentials Action
(00:55):
potentials APS are sequential changes in trans membrane
potential that occur as a resultof activity of ion channels
resulting in the propagation of electrical impulses in excitable
cells. The heart has a multicellular
(01:19):
structure but behaves like a syncytium because the individual
muscle cells communicate with their neighbours through gap
junctions, which provide low resistance pathways for easy
movement of action potentials between cells.
(01:44):
The cardiac action potential that is approximately 250
milliseconds is much longer thandose of nerve or skeletal
muscle, which is approximately 1to 3 milliseconds.
This is due to a prolonged plateau phase caused by calcium
(02:10):
ion influx. Two types of action potential or
pour in the heart, the fast response found in heart muscle
are pokinge fibres and the slow response found in pacemaker
(02:32):
tissues such as the sinoatrial and atrioventricular nodes.
The fast response seen in Figure1, the resting potential of
cardiac muscle and Pokhenge fibres, is about -90 millivolts.
(03:03):
Interior negative to exterior and AP is initiated when the
membrane is depolarized to a threshold potential of about -65
millivolts. The initial depolarization
(03:26):
originates from transmission from an adjacent cell via gap
junctions. Let's talk about the phases.
In the first response phase zerorapid depolarization.
(03:51):
The inward current caused by opening of fast sodium channels
becomes large enough to overcomethe outward current through
potassium channels, resulting ina very rapid upstroke.
Phase One early incomplete repolarization due to
(04:20):
inactivation of fast sodium channels and efflux of potassium
ions. Phase 2, plateau.
Phase A period of slow decay mainly due to calcium entering
(04:47):
the cell via L type. That is, L is long lasting
calcium channels which are activated slowly when the
membrane potential is more positive than about -35
millivolts. This is balanced by potassium E
(05:12):
flux through various potassium channels.
Calcium entry during the plateauis essential for contraction.
Blockers of L type calcium channels, for example verapamil,
reduce the force of contraction.Phase three, rapid
(05:42):
repolarization. Calcium influx declines and the
potassium outward current becomes dominant with an
increased rate of repolarization.
Phase four electrical diasto resting membrane potential is
(06:08):
restored. Next we get to Figure 1, talking
about the fast response Pokinje fibre action potential.
Pause the recording and take a little while to go through this
the slow response seen in Figure2.
(06:35):
These cells spontaneously depolarize and are said to have
automaticity. Phases one and two are absent.
(06:57):
Phase 4 pre potential or pacemaker potential.
There is no depolarization plateau and the cells have an
unstable resting membrane potential.
During this phase, they gradually depolarize from -60
(07:21):
millivolts to a threshold of -40millivolts due to a slow
continuous influx of sodium ionsand a decreased efflux of
potassium ions. A calcium current due to the
(07:42):
opening T type that is transientT is equal to transient calcium
channels completes the pacemakerpotential Phase 0
depolarization. We are still talking about the
phases in the slow response whenthe membrane potential reaches
(08:09):
threshold potential, the L type calcium channels open causing
calcium influx and an action potential is generated.
Phase three re polarisation due to E flux of potassium, no
(08:40):
epinephrine and epinephrine thatis mediated via beta one
receptors increase the slope of phase four by increasing calcium
influx, therefore increasing theheart rate.
Calcium influx also increases the force of contraction.
(09:06):
Acetylcholine, which is mediatedvia M2 receptors, decreases the
slope of phase four by increasing potassium efflux and
causing hyperpolarization, that is, increased negativity within
the cells. This makes the conduction tissue
(09:31):
much less excitable, so it takeslonger to spontaneously reach
the threshold level. This results in a decrease in
heart rate. The intrinsic rate of the
sinoatrial node is 100 per minute.
(09:54):
However, vagal tone decreases this to about 70 bits per
minute. Next we get to figure 2 talking
about the slow response sinuatrial node action
potential. Pause the recording and take a
(10:18):
little while to go through this refractory periods.
During the absolute refractory period ARP scene in Figure 1,
the cardiac cell is totally inexcitable.
(10:42):
During the following relative refractory period RRP, there is
a gradual recovery of excitability.
A supra maximal stimulus can elicit an action potential in
(11:03):
the relative refractory period. This action potential, however,
has a slower rate of depolarization, a lower
amplitude, and shorter duration than normal, and therefore the
(11:24):
contraction produced is weaker. Peak muscle tension occurs just
before the end of the absolute refractory period, and the
muscle is halfway through its relaxation phase by the end of
(11:45):
the relative refractory period. The long refractory period
protects the ventricles from toorapid a RE excitation, which
would impair their ability to relax long enough to refill
(12:06):
sufficiently with blood. Unlike skeletal muscle, 2
contractions cannot submit and afused Titanic contraction cannot
occur. The cardiac cycle.
(12:32):
The cardiac cycle refers to the relationship between electrical,
mechanical, that is, pressure and volume, and vascular events
occurring during one complete heartbeat seen in Figure 3.
(12:56):
Next we get to Figure 3, explaining the full events of
the cardiac cycle. Very, very important figure.
Kindly pause the recording and take your time.
Take your time to go through this figure.
(13:17):
Isovolumetric ventricular contraction early systo the
action potential is conducted through the AV node down the
bundle of his across both ventricles and ventricular
(13:40):
depolarization occurs. This is the QRS complex of the
ECG. Ventricular contraction causes a
sharp rise in ventricular pressure and the AV valves
(14:00):
close. That is the first heart sound.
Once this exceeds atrial pressure, preventing back flow
into the Atria, ventricular pressure increases dramatically
with no change in ventricular volume.
(14:24):
During this initial phase of ventricular contraction,
pressure is less than in the pulmonary artery and aorta, so
the outflow valves remain closed.
The ventricular volume does not change.
(14:45):
The increasing pressure causes the AV valves to bulge into the
Atria resulting in the C wave ofthe central venous pressure
trace ejection, that is systo the semi lunar valves open.
(15:14):
As ventricular pressure exceeds aortic blood pressure,
approximately 2/3 of the blood in the ventricles is ejected
into the arteries. Flow into the arteries is
initially very rapid, that is rapid ejection phase, but
(15:38):
subsequently decreases, that is reduced ejection phase.
The stroke volume SV is the volume of blood ejected from
each ventricle in a single bit, and the ejection fraction is
stroke volume over end diastolicvolume.
(16:06):
Arterial blood pressure rises toits highest point, that is
systolic blood pressure during the last 2/3 of systole before
the AV valves open again. Atrial pressure rises as a
result of feeling from the veins, resulting in the V wave
(16:32):
of the central venous pressure trace.
Active contraction ceases duringthe second-half of ejection and
the ventricular muscle repolarizes.
This is the T wave of the ECG. Ventricular pressure during the
(17:00):
reduced ejection phase is slightly less than in the
artery, but blood continues to flow out of the ventricle
because of momentum called protodiastole.
Eventually the flow briefly reverses causing closure of the
(17:25):
outflow valve and a small increase in aortic pressure
called the diacortic notch isovolumetric relaxation that is
(17:45):
early diastole. The ventricles relax and the
ventricular pressure falls belowarterial blood pressure.
This causes the semi lunar valves to close causing the
second heart sound dope. The ventricular pressure falls
(18:12):
with no change in ventricular volume.
When ventricular pressure falls below atrial pressure, the AV
valves open and the cycle beginsagain.
Passive filling that is early diastole.
(18:41):
The atrial and ventricles are relaxed and ventricular pressure
is close to 0. The atrial ventricular valves
are open and the semilunar valves are closed.
Blood flows from the great veinsinto the atrial and ventricles.
(19:04):
About 80% of ventricular feelingoccurs during this phase,
consisting of an initial rapid filling phase followed by a
slower filling phase, that is diastasis, atrial contraction,
(19:30):
that is late diastole. A wave of depolarization
beginning at the sinuatrial nodespreads across both Atria and
reaches the AV node. This is the P wave of the ECG.
(19:56):
The Atria contracts and atrial pressures increases, producing
the A wave of the central venouspressure.
Trace blood continues to flow into the ventricles and
ventricular pressure increases slightly.
(20:20):
The atrial contribution to ventricular feeling increases as
heart rate increases. And diastole shortens and there
is less time for passive feelingventricular volume, that is EDVN
diastolic volume is equals to volume of blood in the
(20:42):
ventricle. At the end of diastole, arterial
pressure is at its lowest. At this stage of the cycle,
we're still talking about late diastole.
The X descent of the central venous pressure trace results
(21:05):
from atrial relaxation and downward displacement of the
tricuspid valve during ventricular systo.
The Y descent of the CVP trace is due to the atrial emptying as
the tricuspid valve opens and blood enters the ventricle.
(21:33):
Next we get to Figure 4 talking about left ventricular pressure
volume loop during a single heart cycle in a normal adult at
rest. Kindly pause the recording and
go through this. After that we get to Figure 5
(21:57):
talking about how the pressure volume loop is affected by the
contractility and compliance of the ventricle and factors that
alter refilling or ejection. Please take some time to go
through this. Also the pressure volume loop
(22:23):
seen in figures 4:00 and 5:00. This represents the events of
the cardiac cycle. The cardiac cycle proceeds in an
anti clockwise direction. A end diastole.
(22:47):
B Aortic valve opening. C Aortic valve closure.
D Mitral valve opening. EDV and end systolic volume are
(23:11):
represented by points A and C, respectively.
The area enclosed by the loop represents the stroke work.
Since work is equals to pressuretimes volume, the pressure
(23:31):
volume curve in dire stool is initially quite flat, indicating
that large increases in volume can be accommodated by only
small increases in pressure. However, the ventricle becomes
less distensible with greater feeling, as evidenced by the
(23:55):
sharp rise of the diastole curveat large intraventricular
volumes. Control of the coronary
circulation. Myocardial blood supply is from
the right and left coronary arteries, which run over the
(24:20):
surface of the heart, giving branches to the endocardium that
is the inner layer of the myocardium.
Venous drainage is mostly via the coronary sinus into the
right atrium, but a small proportion of the blood flows
directly into the ventricles through the Fibesian veins,
(24:47):
delivering on oxygenated blood to the systemic circulation.
The heart at rest receives about5% of the cardiac output.
Coronary blood flow is approximately 250 miles per
(25:09):
minute. Oxygen extraction by the
myocardiomat rest is very high, that is 65%, compared to other
tissues, that is 35%. Therefore, the myocardium cannot
(25:30):
compensate for reductions in blood flow by extracting more
oxygen from haemoglobin. Any increases in myocardial
oxygen demand must be met by an increase in coronary blood flow.
The three main factors influencing coronary flow are
(25:55):
mechanical, mainly external compensation and perfusion,
pressure, metabolic and neural. Next we get to figure 6, the
anatomy of the coronary arteries.
(26:18):
Kindly take a while to go through this coronary artery
compensation. Sorry, Coronary artery
compression and blood flow. Left coronary artery blood flow
is unique in that there is interruption of flow during
(26:43):
systo, that is, mechanical compression of vessels by
myocardial contraction and flow occurs predominantly during
diasto when cardiac muscle relaxers and no longer obstructs
blood flow through ventricular vessels.
(27:05):
Conversely, right coronary arterial flow rate is highest
during cysto because the aortic pressure driving flow increases
more during cysto, that is from 80 to 120 millimetres of
(27:26):
mercury, than the right ventricular pressure which
opposes flow that is from zero to 25 millimetres of mercury.
As about 80% of the total coronary arterial flow occurs
(27:46):
during diastole, a pressure around the aortic diastolic
pressure becomes the primary determinant of the pressure
gradient for coronary flow. Coronary perfusion pressure is
the arterial diastolic pressure minus left ventricular end
(28:12):
diastolic pressure, that is, CPPis equals to ADP minus LVEDP.
Increases in heart rates that shorten diastole time for
coronary blood flow are likely to increase oxygen consumption
(28:37):
more than elevations in blood pressure, which are likely to
offset increased oxygen demands by enhanced pressure dependent
coronary blood flow. The myocardium regulates its own
(28:57):
blood flow, that is auto regulation, closely between
perfusion pressures of 50 and 150 millimetres of mercury.
Beyond this range, blood flow becomes increasingly pressure
(29:19):
dependent. This auto regulation is due to a
combination of myogenic and metabolic mechanisms.
Metabolic factors. The close relationship between
coronary blood flow and myocardial oxygen consumption
(29:43):
indicates that one or more of the products of metabolism cause
coronary vasodilation. Hypoxia and adenosine are potent
coronary vasodilators. Other factors suspected of
(30:03):
playing this role include PA, CO2, hydrogen, potassium
lactate, and prostaglandins. Under normal conditions, changes
in blood flow are entirely due to variations in coronary artery
(30:27):
tone, that is, resistance in response to metabolic demand.
Neural factors. The coronary arterioles contain
A1 adrenergic receptors, which mediates vasoconstriction, and
(30:53):
beta 2 adreneric receptors, which mediates vasodilation.
Sympathetic stimulation generally increases myocardial
blood flow because of metabolic factors and not because of beta
2 adrenergic stimulation. This is shown experimentally
(31:19):
when the ionotrophic and chronotrophic effects of
sympathetic discharge are blocked by beta one selective
blocker to reduce metabolic demand.
An injection of no epinephrine in all anesthesized animals
elicits coronary vasoconstriction.
(31:43):
Therefore, the direct effect of sympathetic stimulation is
constriction rather than dilation of the coronary vessels
and highlights the importance ofmetabolic control.
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