Def: The cardiac events that occur from beginning of one heart beat to the beginning of the next. ■ first assembled by Lewis in 1920 but first conceived by Wiggers in 1915 Atria act as PRIMER PUMPS for ventricles & ventricles provide major source of power for moving the blood through the vascular system. ■ Initiated by spontaneous generation of AP in SA node (located in the superior lateral wall of the right atrium near the opening of the superior vena cava)

1. CARDIAC CYCLE
DR MOHD IDREES
SR2 Cardiology
LPSIC KANPUR

2. Cardiac Cycle
■ Def: The cardiac events that occur from
beginning of one heart beat to the beginning of
the next.
■ first assembled by Lewis in 1920 but first
conceived by Wiggers in 1915

3. ■ Atria act as PRIMER PUMPS for
ventricles & ventricles provide major
source of power for moving the blood
through the vascular system.
■ Initiated by spontaneous generation of
AP in SA node (located in the superior lateral wall of
the right atrium near the opening of the superior vena cava)

4. Electrical System: Brief
Action potentials originating
in the sinus node travel to
AV node (1m/s) in 0.03 sec.

5. 1. AV nodal delay of 0.09 sec before the impulse
enters the penetrating portion of the A-V bundle
2. A final delay of another 0.04 sec occurs mainly in
this penetrating A-V bundle
total delay in the A-V nodal and A-V bundle
system is about 0.13 sec
A total delay of 0.16 sec occurs before the excitatory
signal finally reaches the contracting muscle of the
ventricles from its origin in sinus node.

6. Delay in AV node (0.13sec)
■ Why delay?
Diminished numbers of gap junctions Between
successive cells in the conducting pathways.
■ Significance?
Delay allows time for the atria to empty their blood
into the ventricles before ventricular contraction
begins

7. ■ Rapid Transmission in the Purkinje
System (1.5 to 4.0 m/sec)
allowing almost instantaneous
transmission of the cardiac impulse
throughout the ventricular muscle
■ (B/c of very high level of permeability of the gap
junctions)

8. Summary of Cardiac Impulse
Transmission

9. Mechanical Phase

10. Cardiac cycle – basically
describes…
1. Pressure
2. Volume, and
3. Flow phenomenon
in ventricles as a function of time

11. Basics
■ 1 Beat = 0.8 sec (800 msec)
■ Systole = 0.3 sec
■ Diastole = 0.5 sec
In tachycardia, Diastolic phase decreases more
than systolic phase

12. Phases of cardiac cycle
LV Contraction
Isovolumic contraction (b)
Maximal ejection (c)
LV Relaxation
Start of relaxation and reduced ejection (d)
Isovolumic relaxation (e)
LV Filling
Rapid phase (f)
Slow filling (diastasis) (g)
Atrial systole or booster (a)

13. Time Intervals
Total ventricular systole 0.3 sec
■ Isovolumic contraction (b) 0.05 sec
■ 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

14. Physiologic Versus Cardiologic Systole
and Diastole
PHYSIOLOGIC
SYSTOLE
CARDIOLOGIC
SYSTOLE
Isovolumic
contraction
Maximal
ejection
From M1 to A2,
including:
Major part of isovolumic
contraction
Maximal ejection
Reduced ejection
PHYSIOLOGIC
DIASTOLE
CARDIOLOGIC
DIASTOLE
Reduced
ejection
Isovolumic
relaxation
Filling phases
A2-M1 interval
(filling phases included)
20msec
Physiological systole

15. 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

16. Description of Cardiac cycle
phases
1. Pressure & Volume events
2. ECG correlation
3. Heart sounds
4. Clinical significance

17. Atrial Systole
A-V Valves Open; Semilunar Valves Closed
➢ Blood normally flows
continually from great
veins into atria
➢ 80% flows directly
through atria into
ventricle before the atria
contracts.
➢ 20% of filling of
ventricles – atrial
contraction
➢ Atrial contraction is
completed before the
ventricle begins to
contract.

18. ■ 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

19. Atrial Systole
Pressures & Volumes
■ ‘ a ‘ wave – atrial
contraction, when atrial
pressure rises.
■ Atrial pressure drops
when the atria stop
contracting.

20. ■ After atrial contraction is complete
LVEDV typically about 120 ml (preload)
End-diastolic pressures of
LV = 8-12 mmHg and
RV = 3-6 mmHg
■ AV valves floats upward (pre-
position)

21. Abnormalities of “a” wave
■ Elevated a wave
Tricuspid stenosis
Decreased ventricular compliance (ventricular failure, pulmonic
valve stenosis, or pulmonary hypertension)
■ Cannon a wave
Atrial-ventricular asynchrony (atria contract against a closed tricuspid valve)
complete heart block, following premature ventricular contraction,
during ventricular tachycardia, with ventricular pacemaker
■ Absent a wave
Atrial fibrillation or atrial standstill
Atrial flutter

22. Why blood does not flow back in to SVC/PV
while atria contracting, even though no valve
in between?
■ Wave of contraction through the atria
moves toward the AV valve thereby
having a "milking effect."
■ Inertial effects of the venous return.

23. 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.

24. 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

25. Causes of S4
■ Physiological;
>60yrs (Recordable, not audible)
■ Pathological;
All causes of concentric LV/RV hypertrophy
Coronary artery disease
Acute regurgitant lesions
An easily audible S4 at any age is generally
abnormal.

26. JVP: x descent
■ Prominent x descent
1 Cardiac tamponade
2 Constrictive pericarditis
3 Right ventricular ischemia with preservation of atrial
contractility
■ Blunted x descent
1 Atrial fibrillation
2 Right atrial ischemia

27. Beginning of VenTRICULAR Systole
Isovolumetric Contraction
All Valves Closed

28. Isovolumetric Contraction
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.

29. ■ Ventricular chamber geometry changes considerably as the
heart becomes more spheroid in shape; circumference
increases and atrial base-to-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

30. Isovolumetric Contraction
ECG
■ The QRS complex is due to ventricular
depolarization, and it marks the
beginning of ventricular systole.

31. 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 LV-
LA pressure crossover.)
■ S1 is normally split (~0.04
sec) because mitral valve
closure precedes tricuspid
closure.
(Heard in only 40% of normal
individuals)

32. S1 heart sound
■ low pitch and relatively long-lasting
■ lasts ~ 0.12-0.15 sec
■ frequency ~ 30-100 Hz
■ appears 0.02 – 0.04 sec after the
beginning of the QRS complex

33. Some Clinical facts about S1
■ S1 is a relatively prolonged, low
frequency sound, best heard at apex.
■ Normally split of S1 (~40%)is heard
only at tricuspid area.(As tricuspid
component is heard only here.)
■ If S1 is equal to or higher in intensity
than S2 at base, S1 is considered
accentuated.

34. ■ Variable intensity of S1 and jugular venous
pulse are highly specific and sensitive in the
diagnosis of ventriculoatrial dissociation during
VT, and is helpful in distinguishing it from
supraventricular tachycardia with aberration.
Value of physical signs in the diagnosis of ventricular tachycardia. C J
Garratt, M J Griffith, G Young, N Curzen, S Brecker, A F Rickards and A J Camm,
Circulation. 1994;90:3103-3107

35. 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

36. 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.

37. Rapid Ejection
ECG & Heart Sounds
■ In rapid ejection part of
the ejection phase there
no specific ECG changes /
heart sounds heard.

38. Slow Ejection
Aortic and Pulmonic Valves Open; AV Valves
Remain Closed
■ Approx. 200msec after the QRS
vent. repolarisation occurs as
shown by T wave, which leads to
decline in ventricular active
tension & pressure generation, so
rate of ejection falls. Ventricular
pressure falls slightly below
outflow tract pressure, however
outflow still occurs due to kinetic
energy of blood and elastic recoil
of aorta(Windkessel effect)
■ At the end of ejection, the
semilunar valves close. This marks
the end of ventricular systole
mechanically.

39. Slow Ejection
ECG & Heart Sounds
■ T wave – slightly
before the end of
ventricular
contraction
■ heart sounds :
none

40. Beginning of Diastole
■ 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

41. Isovolumetric relaxation
■ Volumes remain constant because all
valves are closed
■ volume of blood that remains in a
ventricle is called the end-systolic
volume (LV ~50ml).
■ pressure & volume of ventricle are low
in this phase .

42. 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 .

43. Isovolumetric relaxation
ECG & Heart Sounds
■ ECG : no deflections
■ Heart Sounds : S2
is heard when the
semilunar vlaves
close.
■ A2 is heard prior to
P2 as Aortic valve
closes prior to
pulmonary valve.

44. Why A2 occurs prior to P2 ?
■ “Hangout interval” is longer for pulmonary
side (~80msec),compared to aortic side
(~30msec).
Hangout interval is the time interval from crossover
of pressures (ventricle with their respective vessel) to
the actual occurrence of sound.
■ Due to lower pressure and higher
distensibility, pulmonary artery having longer
hangout interval causing delayed PV closure
and P2.

45. S2 heart sound
■ Appears in the terminal period of
the T wave
■ lasts 0.08 – 0.12s

46. Some clinical facts about S2
■ Normal split: Two components heard during
inspiration and is single sound during expiration.
(A2-P2 ~20- 50 msec in inspiration)
■ Clinically split is defined as wide, if it is heard
well in standing position, in expiration (normally
not heard as the split is 15 msec, which can not be heard
by human ears)
■ Single S2: absence of audible split in either
phase of respiration.

47. Common causes of wide split S2
■ RBBB
■ Sev PAH
■ ASD
■ Idiopathic dilatation of pul artery
■ Sev right heart failure
■ Moderate to severe PS
■ Severe MR
■ Normal variant

48. Common causes of wide fixed split
S2
■ ASD
■ All causes of wide split with
associated severe right ventricular
failure.

49. JVP: V wave
■ Elevated v wave
1 Tricuspid regurgitation
2 Right ventricular heart failure
3 Reduced atrial compliance (restrictive myopathy)
■ a wave equal to v wave
1 Tamponade
2 Constrictive pericardial disease
3 Hypervolemia

50. Rapid Inflow ( Rapid Ven. Filling)
A-V Valves Open
■ Once AV valves are open
the blood that has
accumulated in atria flows
into the ventricle.

51. Rapid Inflow
Volume changes
■ Despite the inflow of blood
from the atria,
intraventricular pressure
continues to briefly fall
because the ventricles are
still undergoing relaxation
■ JVP: Seen as y-descent.

52. 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)

53. Causes of S3
■ Physiological: Childrens & young adults <40 yrs
(nearly 25%)
(Not heard in normal infants & adult
>40 yrs.)
■ Pathological:
Ventricular failure
Hyperkinetic state (anemia, thyrotoxicosis, beri-beri)
MR, TR
AR, PR
Systemic AV fistula

54. JVP: y descent
■ Prominent y descent
1 Constrictive pericarditis
2 Restrictive myopathies
3 Tricuspid regurgitation
■ Blunted y descent
1 Tamponade
2 Right ventricular ischemia
3 Tricuspid stenosis

55. Diastasis OR REDUCED FILLING
A-V Valves Open
■ remaining blood
which has
accumulated in
atria slowly flows
into the ventricle.

56. Diastasis
Volume changes
■ Ventricular volume
increases more slowly
now. The ventricles
continue to fill with blood
until they are nearly full.

57. Diastasis
ECG & Heart Sounds
■ ECG : no deflections
■ Heart Sounds : none

58. The Lewis or wiggers cycle

59. 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

60. RV v/s LV
Rt Ventricular
• Pressure wave 1/5th
• dp/dt is less
• Isovolumic
contraction &
relaxation phases
are short.

61. 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
rise & fall, while Lt side
initial
peak followed by quick
fall.

62. PRESSURE VOLUME LOOP

63. Pressure-Volume Loop
Pressure-volume loop of RV
is same as that of LV,
however the area is only
1/5th
of LV because pressures
are so much lower on right

68. ■ Maximal pressure that can be developed by
LV at any given LV volume is defined by end
systolic PV relationship (ESPVR)
■ ESPVR line is representative of contractility of
heart
■ When contractility ↑ slope of ESPVR is higher
■ ↓ slope of ESPVR is s/o ↓ contractility
■ Slope of EDPVR is reciprocal of vent.
compliance

69. PRELOAD, AFTERLOAD & STROKE VOLUME

70. ABNORMAL PRESSURE VOLUME LOOP

71. CHANGES IN PRELOAD AND STROKE
VOLUME

72. CHANGES IN AFTERLOAD AND STROKE VOLUME

73. SYSTOLIC DYSFUNCTION

74. DIASTOLIC DYSFUNCTION

75. CARDIAC TAMPONADE

76. ■ Increased
stroke volume
■ Increased EF
■ Decreased
ESV

78. AORTIC STENOSIS

79. PV Loop in MS

80. PV loop in MR
■ EDV will ↑↑, ESV↓
■ Total SV↑(apparent
SV↓)
■ No true
isovolumetric
contraction or isovol.
relaxation
■ Afterload ↓-height↓

81. PV Loop in AR
■ No true isovol.
Contraction or
isovol. Relaxation
■ EDV ↑↑, ESV↑
■ Total SV ↑
■ Vol.↑, afterload↑,
height↑

82. Uses of PV loop
■ Work done by heart(stroke work)= total
area under curve
■ Width indicated SV=EDV-ESV
■ Height indicates afterload, ventricular
Activity
■ EF= SV/EDV X100

83. SYSTOLIC TIME
INTERVALS
■ Systole has 2 distinct time periods-pre-
ejection period(PEP) & left ventricular
ejection time(LVET)
■ PEP is defined as time between the onset
of electrocardiographic systole & the
opening of aortic valve
■ LVET begins with the AoV opening &
terminates at its closure-marked by the
onset of S2

84. ■ QS2(Electromechanical
systole)=PEP+LVET
■ QS2 is constant over a wide variety
of cardiac disorders
■ Increased inotropic state is reflected
by ↓ in QS2 & a decreased
inotropic state prolongs QS2.

85. THANK YOU

86. ATRIAL PV LOOP