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CARDIAC CYCLE
DR : SAIDALAVI
Carl John Wiggers
Otto Frank
Sir Thomas Lewis
Ernest H Starling
Introduction
Principal function of cardiovascular system is to deliver oxygen and
nutrients to and remove carbon dioxide and wastes from metabolizing
tissues.
It is by two specialized circulations in series
1. low resistance pulmonary driven by right heart
2. high resistance systemic driven by left heart
Systolic pressure in the vascular system refers to the peak pressure
reached during the systole, not the mean pressure.
The diastolic pressure refers to the lowest pressure during diastole.
WIGGERS DIAGRAM
EVENTS IN CARDIAC CYCLE
PRESSURE VOLUME LOOP
The Lewis or wiggers cycle, Guyton & Hall. Textbook of Medical Physiology, 11th Edition
WIGGERS DIAGRAM
EVENTS IN CARDIAC CYCLE
PRESSURE VOLUME LOOP
Cardiac cycle
The cardiac cycle describes pressure, volume and flow
phenomena in the ventricles as a function of time.
Similar for both LV and RV except for the timing, levels of
pressure.
It yields important information on
the temporal sequence of events in
the cardiac cycle.
The three basic events are
(1)LV contraction
(2) LV relaxation
(3) LV filling
Phases of cardiac cycle
LV Contraction
Isovolumetric contraction (b)
Maximal ejection (c)
LV Relaxation
Start of relaxation and reduced ejection (d)
Isovolumetric relaxation (e)
LV Filling
Rapid phase (f)
Slow filling (diastasis) (g)
Atrial systole or booster (a)
Time Intervals
Total ventricular systole
0.3 sec
Isovolumic contraction (b) 0.05 sec (0.015sec
for RV)
Maximal ejection (c)
0.1 sec
Reduced ejection (d)
0.15 sec
Total ventricular diastole
0.5 sec
Isovolumic relaxation (e)
0.1 sec
Rapid filling phase (f)
0.1 sec
Slow filling (diastasis) (g) 0.2 sec
Atrial systole or booster (a) 0.1 sec
GRAND TOTAL (Syst+Diast) = 0.8 sec
Description of Cardiac cycle
phases
1.
Pressure & Volume events
2.
ECG correlation
3.
Heart sounds
LV
RELAXATION
• Isovolumic
contraction(b)
• Maximal
Ejection( c)
LV
CONTRACTION
• Isovolumic
relaxation(e)
• Start of relaxation and
reduced ejection (d)
• Rapid phase(f)
• Slow filling
(diastasis)(g)
• Atrial systole or
booster(a)
LV FILLING
The letters are arbitrarily allocated so that atrial systole(a) coinicides with the a wave and (c ) with the c wave of JVP.
LV contraction.
LV pressure starts to build up
when the arrival of calcium ions
at the contractile proteins starts
to
trigger
actin-myosin
interaction.
On
the
electrocardiogram
(ECG), the advance of the
wave
of
depolarization
is
indicated by the peak of the R
wave .
Soon after, LV pressure in the
early contraction phase builds
up and exceeds that in the left
atrium . (normally, 10 to 15 mm
Hg).
about 20 milliseconds later M1,
the mitral component of the first
heart sound occurs.
Mitral valve closure is often thought to coincide with the crossover
point at which the LV pressure starts to exceed the left atrial pressure.
In reality mitral valve closure is delayed because the valve is kept
open by the inertia of the blood flow.
Shortly thereafter, pressure changes in the right ventricle, similar in
pattern but lesser in magnitude to those in the left ventricle, cause the
tricuspid valve to close. there by creating T1, the second component
of the first heart sound.
When the pressure in the left ventricle exceeds that in the
aorta, the aortic valve opens, usually a clinically silent event.
Opening of the aortic valve is followed by the phase of rapid
ejection.
The rate of ejection is determined not only by the pressure
gradient across the aortic valve, but also by the elastic
properties of the aorta and the arterial tree, which undergoes
systolic expansion.
LV pressure rises to a peak and then starts to fall.
Pressure & Volume Changes
The AV valves close when
the pressure in the ventricles
(red) exceeds the pressure in
the atria (yellow).
As the ventricles contract
isovolumetrically -- their
volume does not change
(white) -- the pressure inside
increases, approaching the
pressure in the aorta and
pulmonary arteries (green).
JVP: c wave- d/t Right
ventricular contraction
pushes the tricuspid valve
into the atrium and increases
atrial pressure, creating a
small wave into the jugular
vein. It is normally
simultaneous with the carotid
pulse.
Ventricular chamber geometry changes
considerably as the heart becomes more spheroid
in shape; circumference increases and atrial baseto-apex length decreases.
Early in this phase, the rate of pressure development
becomes maximal. This is referred to as maximal
dP/dt.
Ventricular pressure increases rapidly
LV ~10mmHg to ~ 80mmHg (~Aortic pressure)
RV ~4 mmHg to ~15mmHg (~Pulmonary A pressure)
At this point, semilunar (aortic and pulmonary) valves open
against the pressures in the aorta and pulmonary artery
Isovolumetric Contraction
ECG
The QRS complex is due to ventricular
depolarization, and it marks the
beginning of ventricular systole.
Isovolumetric Contraction
Heart Sounds
S1 is d/t closure and after
vibrations of AV Valves. (M1
occurs with a definite albeit
20 msec delay after the LVLA pressure crossover.)
S1 is normally split (~0.04 sec)
because mitral valve closure
precedes tricuspid closure.
(Heard in only 40% of normal
individuals)
Ejection
Aortic and Pulmonic Valves Open; AV Valves Remain Closed
The Semilunar valves ( aortic ,
pulmonary ) open at the
beginning of this phase.
Two Phases
• Rapid ejection - 70% of the blood
ejected during the first 1/3 of
ejection
• Slow ejection - remaining 30% of
the blood emptying occurs during
the latter 2/3 of ejection
Rapid Ejection
Pressure & Volume Changes
When ventricles
continue to contract ,
pressure in ventricles
exceed that of in aorta
& pul arteries & then
semilunar valves open,
blood is pumped out of
ventricles & Ventricular
vol decreases rapidly.
Slow Ejection
Aortic and Pulmonic Valves Open; AV Valves
Remain Closed
Blood flow from the
left ventricle to the
aorta rapidly
diminishes but is
maintained by aortic
recoil, the
“Windkessel effect “
At the end of
ejection, the
semilunar valves
close. This marks the
end of ventricular
systole mechanically.
As the cytosolic calcium ion concentration starts to decline
because of uptake of calcium into the SR under the influence
of activated phospholamban, more and more myofibers enter
the state of relaxation and the rate of ejection of blood from
the left ventricle into the aorta falls. ( phase of reduced
ejection)
During this phase, blood flow from the left ventricle to the aorta
rapidly diminishes but is maintained by aortic recoil—the
Windkessel effect.
†WINDKESSEL in German AIRCHAMBER or elastic reservoir
Slow Ejection
ECG & Heart Sounds
T wave – slightly
before the end of
ventricular
contraction
it is d/t ventricular
repolarization
heart sounds :
none
LEFT VENTRICULAR RELAXATION.
The pressure in the aorta exceeds the falling pressure in the left
ventricle.
The aortic valve closes, creating the first component of the
second sound, A2 (the second component, P2, results from
closure of the pulmonary valve as the pulmonary artery
pressure exceeds that in the right ventricle).
There after, the ventricle continues to relax. Because the mitral
valve is closed during this phase, the LV volume cannot
change (isovolumic relaxation).
Beginning of Diastole
Isovolumetric relaxation All Valves Closed
At the end of systole, ventricular relaxation
begins, allowing intraventricular pressures to
decrease rapidly (LV from 100mmHg to
20mmHg & RV from 15mmHg to 0mmHg),
aortic and pulmonic valves abruptly close
(aortic precedes pulmonic) causing the
second heart sound (S2)
Valve closure is associated with a small
backflow of blood into the ventricles and a
characteristic notch (incisura or dicrotic
notch) in the aortic and pulmonary artery
pressure tracings
After valve closure, the aortic and pulmonary
artery pressures rise slightly (dicrotic wave)
following by a slow decline in pressure
Isovolumetric relaxation
Throughout this and the
previous two phases, the
atrium in diastole has
been filling with blood on
top of the closed AV
valve, causing atrial
pressure to rise gradually
JVP - "v" wave occurs
toward end of
ventricular contraction –
results from slow flow of
blood into atria from
veins while AV valves are
closed .
LEFT VENTRICULAR RELAXATION.
When the LV pressure falls
to below that in the left
atrium, the mitral valve
opens (normally silent) and
the filling phase of the
cardiac cycle restarts.
Isovolumetric relaxation
ECG & Heart Sounds
ECG : no deflections
Heart Sounds : S2 is
heard when the
semilunar valves
close.
A2 is heard prior to
P2 as Aortic valve
closes prior to
pulmonary valve.
LEFT VENTRICULAR FILLING PHASES.
As LV pressure drops below that in the left atrium, just after
mitral valve opening, the phase of rapid or early filling occurs,
which accounts for most of the ventricular filling.
Active diastolic relaxation of the ventricle may also contribute
to early filling ( “Ventricular Suction During Diastole”).
Such rapid filling may cause the physiological third heart
sound (S3), particularly when there is a hyperkinetic
circulation.
LV FILLING PHASES.
As pressures in the atrium and ventricle equalize,
LV filling virtually stops (diastasis).
This is achieved by atrial systole (or the left atrial
booster), which is especially important when a
high cardiac output is required, as during
exercise, or when the LV fails to relax normally, as
in left ventricular hypertrophy.
Diastasis
A-V Valves Open
blood which has
accumulated in
atria slowly flows
into the ventricle.
Rapid Inflow ( Rapid Ven. Filling)
ECG & Heart Sounds
ECG : no deflections
Heart sounds : S3 is heard,
lasts 0.02-0.04 sec
(represent tensing of chordae
tendineae and AV ring during
ventricular relaxation and filling)
Whatever the mechanism, a
sudden inherent limitation in
the long axis filling
movement of the LV is
consistently observed.
Protodiastole
Proto –means original, first
The period of start of ventricular relaxation.
Lasts until the semilunar valves are closed.
It is 0.04 sec.
Atrial Systole
A-V Valves Open; Semilunar Valves Closed
Blood normally flows
continually from great
veins into atria
80% flows directly thro
atria into ventricle
before the atria
contracts.
20% of filling of
ventricles – atrial
contraction
Atrial contraction is
completed before
the ventricle begins to
contract.
Atrial contraction normally
accounts for about 10%-15% of LV
filling at rest, however, At higher
heart rates, atrial contraction may
account for up to 40% of LV filling
referred to as the "atrial kick”
The atrial contribution to ventricular
filling varies inversely with duration
of ventricular diastole and directly
with atrial contractility
Atrial Systole
Pressures & Volumes
‘ a ‘ wave – atrial
contraction, when atrial
pressure rises.
Atrial pressure drops when
the atria stop contracting.
Atrial Systole
ECG
p wave – atrial depolarization
impulse from SA node results in depolarization &
contraction of atria ( Rt before Lt )
PR segment – isoelectric line as depolarization
proceeds to AV node.
This brief pause before contraction allows the
ventricles to fill completely with blood.
Atrial Systole
ECG
p wave – atrial depolarization
impulse from SA node results in depolarization &
contraction of atria ( Rt before Lt )
PR segment – isoelectric line as depolarization
proceeds to AV node.
This brief pause before contraction allows the
ventricles to fill completely with blood.
Atrial Systole
Heart Sounds
S4 (atrial or presystolic gallop) - atrial emptying after
forcible atrial contraction.
appears at 0.04 s after the P wave (late diastolic)
lasts 0.04-0.10 s
Caused by vibration of ventricular wall during rapid
atrium emptying into non compliant ventricle
Physiologic Versus Cardiologic Systole
and Diastole
cardiologic systole, demarcated by heart
sounds rather than by physiologic events,
starts fractionally later than physiologic
systole and ends significantly later.
Cardiologic systole> physiologic systole
Physiological systole –start of isovolumic contraction to the
peak of ejection phase.
Physiological diastole – commences as pressure falls.
Fits well in pressure volume curve
ECHO cardiac cycle
Rapid filling phase of diastole
Atrial systole
Left ventricular rotation: a
neglected aspect of the cardiac
cycle
Rotation of the left ventricle around its longitudinal axis is an
important but thus far neglected aspect of the cardiac cycle.
LV rotation during systole maximizes intracavitary pressures,
increases stroke volume, and minimizes myocardial oxygen
demand.
LV Torsion
left-handed helix in subepicardium right-handed helix in sub endocardium
Figure: Schematic Drawing of LV Torsion
The image on the left shows the myofiber directions. Solid lines epicardial region;
dashed lines endocardial region. The image on the right shows untwisting.
ED end-diastole; ES end-systole; LV left ventricle.
(J Am Coll Cardio Img 2009;2:648–55)
Shearing and restoring forces accumulated during systolic
twisting are released during early diastole and result in
diastolic LV untwisting or recoil promoting early LV filling.
LV twist and untwist are disturbed in a number of cardiac
diseases and can be influenced by several therapeutic
interventions by altering preload, afterload, contractility, heart
rate, and/or sympathetic tone,
Phonocardiogram
A graphic recording of cardiac
sound
A specially designed
microphone on the chest wall.
Sound waves amplified,
filtered and recorded.
Doppler Echocardiography has
replaced the
phonocardiography
Hemodynamic Correlates
of S1
The first high-frequency component of M1
coincides with the downstroke of the left atrial c
wave and is delayed from the LV–left atrial
pressure crossover by 30 ms.
Forward flow continues for a short period following
LV–left atrial pressure crossover as a result of the
inertia of mitral flow, with M1 occurring 20 to 40 ms
later.
An even greater delay between the occurrence
of T1 and RV–right atrial pressure crossover has
been shown.
T1 coincides with the downstroke of the right atrial
c wave.
These hemodynamic data confirm the prime role
played by the AV valves in the genesis of S1
The Second Heart Sound
RV ejection begins prior to LV ejection, has a longer duration,
and terminates after LV ejection, resulting in P2 normally
occurring after A2.
the pulmonary artery incisura is delayed relative to the aortic
incisura, primarily a result of a larger interval separating the
pulmonary artery incisura from the RV pressure compared with
the same left-sided event.
This interval has been called the hangout interval,
a purely descriptive term coined in Shaver et al
more than 40 years ago.
Its duration is felt to be a reflection of the
impedance of the vascular bed into which the
blood is being received.
Normally, it is less than 15 ms in the systemic
circulation and only slightly prolongs the LV
ejection time.
Circulation, Volume 51, January 1975
EDWARD I. CURTISS, M.D., ROBERT G. MATTHEWS, M.D.,
AND JAMES A. SHAVER, M.D.
In the low-resistance, high-capacitance
pulmonary bed, however, this interval is normally
much greater than on the left, varying between
43 and 86 ms.
Hangout interval contributes significantly to the
duration of ejection.
Normal Physiologic
Splitting
Normally during expiration, A2 and P2 are
separated by an interval of less than 30 ms and
are heard by the clinician as a single sound
During inspiration, both components become
distinctly audible as the splitting interval widens,
primarily caused by a delayed P2, although an
earlier A2 contributes to a lesser degree .
Jugular Venous Pulse tracing
JUGULAR VENOUS PULSE
Reflects volume change in the internal jugular
vein and closely resembles the pressure
changes in the right atrium.
A wave atrial contraction.
C wave onset of ventricular contraction.
X descent atrial diastole.
V wave atrial filling before AV valves open.
Y descent AV valves open filling of the
ventricles.
PRESSURES (mm Hg)
Right atrium mean
Normalavalues
wave
v wave
0-5
1-7
1-7
Right ventricle peak systolic/end diastolic
17-32/1-7
Pulmonary artery peak systolic/end diastolic
17-32/1-7
mean
9-19
PCWP
4-12
LA mean
4-12
a wave
4-15
v wave
4-15
LV peak systolic/end diastolic
90-140/5-12
Aorta peak systolic/end diastolic
90-140 /60-90
mean
70-105
Resistance (dynes/cm2) SVR
900-1400
PVR
40-120
Oxygen consumption index (L-min/m2)
115-140
Cardiac index (L-min/m2)
2.8-4.2
WIGGERS DIAGRAM
EVENTS IN CARDIAC CYCLE
PRESSURE VOLUME LOOP
Pressure volume loop
Best of the current approaches to the assessment of the
contractile behaviour of the intact heart.
Es,the pressure – volume relationship .
Changes in the slope of this line joining the different Es
points are generally good load independent index of the
contractile performance of the heart.
Enhanced inotropic effect, Es shifted upward and to the left.
Lusitropic effect shifted Es downward and to right.
The P-V relationship is linear in smooth muscle,curvilinear
in cardiac muscle(exponential).
Volumes
End diastolic vol : During diastole, filling of
ventricle increases vol of each ventricle
to
~ 110 -120 ml
Stroke Vol : amount of blood pumped
out of ventricle during systole. ~ 70 ml
End systolic vol : the remaining amount of
blood in ventricle after the systole. ~40 -50
ml
Pressure volume loop in cardiac
cycle
Atrial Pressure Volume Loop
The atrium serves as a “conduit” for flow from the
venous circulation to the ventricle, especially in
early diastole when the atrium is not contracting.
In addition, elevations in ventricular diastolic
pressures will be reflected in elevated pressures in
the atrium.
Atrial Pressure Volume Loop
A small reversal of flow following atrial contraction (a-wave)
A systolic phase (which is effectively “diastole” for the atrium) when
blood flows from the superior and inferior venacavae into the atrium
A small reversal of flow at end-systole (v-wave)
A diastolic filling phase when the atrium serves as a conduit for flow
from the systemic venous return to the RV
These filling phases are reflected in the patterns of jugular venous
pulsation :
a-wave following atrial contraction,
x-descent corresponding to atrial filling during ventricular systole,
v-wave at end-systole
y-descent corresponding to atrial filling during ventricular diastole
WIGGERS DIAGRAM
EVENTS IN CARDIAC CYCLE
PRESSURE VOLUME LOOP
RV CARDIAC CYCLE
RV cycle
RV v/s LV
Rt Ventricular
• Pressure wave 1/5th
• dp/dt is less
• Isovolumic
contraction &
relaxation phases are
short.
Timing of Cardiac EVENTS
1. RA start contracting
before LA
2. LV start contracting before
RV
3. TV open before MV,
so RV filling start before LV.
4. RV peak pressure 1/5th of
LV.
5. RV outflow velocity
smooth
References
1.Ganong’s Review of Medical Physiology,24th Edition.
2.Guyton and Hall, Textbook of Medical Physiology.
3.Best and Taylor’s Physiological Basis of Medical
Practice,13th edition.
4.HURST’S,THE HEART ,13th edition
5.Braunwald’s Heart Disease,10th edition
6.Circulation Journal.
7.European Heart Journal.
Clinical Echo; Catherine . M. Otto, 5th edition