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CARDIAC CYCLE. DR RAKESH JAIN SR Cardiology Govt. Medical College, Calicut. 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.

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cardiac cycle

CARDIAC CYCLE

DR RAKESH JAIN

SR Cardiology

Govt. Medical College, Calicut.

cardiac cycle1
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
slide3
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)
electrical system brief
Electrical System: Brief
  • Action potentials originating
  • in the sinus node travel to
  • AV node (1m/s) in 0.03 sec.
slide5

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.
delay in av node 0 13sec
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

slide7
Rapid Transmission in the Purkinje System (1.5 to 4.0 m/sec)

i.e.

• About 6x that in ventricular muscle

• About 150x that in A-V nodal fibers

allowing almost instantaneous transmission of the cardiac impulse throughout the ventricular muscle

  • (B/c of very high level of permeability of the gap junctions)
slide10
Cardiac cycle – basically describes…
  • Pressure
  • Volume, and
  • Flow phenomenon

in ventricles as a function of time

basics
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

phases of cardiac cycle
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)

time intervals
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

slide15
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

description of cardiac cycle phases
Description of Cardiac cycle phases
  • Pressure & Volume events
  • ECG correlation
  • Heart sounds
  • Clinical significance
atrial systole a v valves open semilunar valves closed
Atrial SystoleA-V Valves Open; Semilunar Valves Closed
  • Blood normally flows continually from great veins into atria
  • 80% flows directly thr atria into ventricle before the atria contracts.
  • 20% of filling of ventricles – atrial contraction
  • Atrial contraction is completed before the ventricle begins to contract.
slide18
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
Atrial SystolePressures & Volumes
  • ‘ a ‘ wave – atrial contraction, when atrial pressure rises.
  • Atrial pressure drops when the atria stop contracting.
slide20
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)
abnormalities of a wave
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 standstillAtrial flutter

why blood does not flow back in to svc pv while atria contracting even though no valve in between
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.
atrial systole ecg
Atrial SystoleECG
  • 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
Atrial SystoleHeart 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
causes of s4
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.

clinical facts about s4
Clinical Facts about S4
  • In contrast to S3, which may mean ventricular failure, the presence of S4 does not indicates heart failure. It only signify “hardworking ventricle”.
  • The presence of S4 correlate with a gradient of at least 50mmHg across LVOT in suspected LVOT obstruction.

(This correlation is not applicable in HCM)

slide27
In setting of MI, an audible S4 indicates that at least 10% of myocardium is at jeopardy.
  • In presence of Shock, S4 indicates that hypovolemia is unlikely as PCWP will be >18mmHg.
  • S4 can be heard when RVEDP >12mmHg on Rt or LVEDP > 15mmHg on Lt side. If EDP is very high i.e. >25 mmHg, S4 may be absent b/c of insufficient atrial functions.
jvp x descent
JVP: x descent
  • Prominent x descent

1    Cardiac tamponade2    Constrictive pericarditis3    Right ventricular ischemia with preservation of atrial

contractility

  • Blunted x descent

1    Atrial fibrillation2    Right atrial ischemia

isovolumetric contraction pressure volume changes
Isovolumetric ContractionPressure & 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.
slide31
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

lv torsion
LV Torsion

left-handed helix in subepicardium

right-handed helix in subendocardium

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 Cardiol Img 2009;2:648–55)

isovolumetric contraction ecg
Isovolumetric ContractionECG
  • The QRS complex is due to ventricular depolarization, and it marks the beginning of ventricular systole.
isovolumetric contraction heart sounds
Isovolumetric ContractionHeart 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)

s1 heart sound
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
some clinical facts about s1
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.
slide37
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

ejection aortic and pulmonic valves open av valves remain closed
EjectionAortic 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
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.
rapid ejection ecg heart sounds
Rapid EjectionECG & Heart Sounds
  • In rapid ejection part of the ejection phase there no specific ECG changes / heart sounds heard.
slow ejection aortic and pulmonic valves open av valves remain closed
Slow EjectionAortic 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.
slow ejection ecg heart sounds
Slow EjectionECG & Heart Sounds
  • T wave – slightly before the end of ventricular contraction
  • it is d/t ventricular repolarization
  • heart sounds : none
beginning of diastole isovolumetric relaxation all valves closed
Beginning of DiastoleIsovolumetric relaxationAll 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
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 .
isovolumetric relaxation1
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 .
isovolumetric relaxation ecg heart sounds
Isovolumetric relaxationECG & 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.
why a2 occurs prior to p2
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.
s2 heart sound
S2 heart sound
  • Appears in the terminal period of the T wave
  • lasts 0.08 – 0.12s
some clinical facts about s2
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.
slide52
Fixed split: two components fails to move with respiration.
  • Reverse split: Inaudible split during inspiration and audible split during expiration.(recognized by wider split in expiration)
common causes of wide split s2
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
common causes of wide fixed split s2
Common causes of wide fixed split S2
  • ASD
  • All causes of wide split with associated severe right ventricular failure.
common causes of single s2
Common causes of single S2
  • Truncus arteriosus
  • Pulmonary atresia
  • Aortic atresia
  • TGA
  • AS, PS
  • Single loud P2 in extreme PAH
causes of reverse split s2
Causes of reverse split S2
  • LBBB
  • RV pacing
  • RV ectopy
  • Severe AS
  • Acute MI
  • WPW type B
  • Severe TR
  • Aneurysm of ascending aorta
  • Severe systemic hypertension
jvp v wave
JVP: V wave
  • Elevated v wave

1    Tricuspid regurgitation2    Right ventricular heart failure3    Reduced atrial compliance (restrictive myopathy)

  • a wave equal to v wave

1    Tamponade2    Constrictive pericardial disease3    Hypervolemia

rapid inflow rapid ven filling a v valves open
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.
rapid inflow volume changes
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.
rapid inflow rapid ven filling ecg heart sounds
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.
clinical facts about s3
Clinical facts about S3
  • In presence of HF, S3 correlates well with ventricular end diastolic pressure and is usually >25mmHg on left side.
  • Right sided S3 correlate well with rapid y descend in neck veins.
  • Normal A2-S3 interval is between 120-160 msec.
gallop rhythm
Gallop rhythm

A gallop rhythm is a grouping of three heart sounds that together sound like hoofs of a galloping horse.

  • Protodiastolic gallop or ventricular gallop or S3 gallop

addition of an S3 to the physiological S1 and S2 creates a three-sound sequence, S1-S2-S3.

  • Presystolic galloprhythm or atrial gallop

addition of an S4 to the physiological S1 and S2 creates a three-sound sequence, S4-S1-S2.

(during tachycardia S4-S1 can fuse, producing a summation gallop )

causes of s3
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

jvp y descent
JVP: y descent
  • Prominent y descent

1    Constrictive pericarditis2    Restrictive myopathies3    Tricuspid regurgitation

  • Blunted y descent

1    Tamponade2    Right ventricular ischemia3    Tricuspid stenosis

diastasis a v valves open
DiastasisA-V Valves Open
  • remaining blood which has accumulated in atria slowly flows into the ventricle.
diastasis volume changes
DiastasisVolume changes
  • Ventricular volume increases more slowly now. The ventricles continue to fill with blood until they are nearly full.
diastasis ecg heart sounds
DiastasisECG & Heart Sounds
  • ECG : no deflections
  • Heart Sounds : none
volumes
Volumes
  • End diastolic vol : During diastole, filling of ventricle increases vol of each ventricle to

~ 110 -120 ml

  • StrokeVol :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
slide71

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

rv v s lv
RV v/s LV
  • Rt Ventricular
  • Pressure wave 1/5th
  • dp/dt is less
  • Isovolumic contraction &
  • relaxation phases are short.
timing of cardiac events
Timing of Cardiac EVENTS
  • RA start contracting before LA
  • LV start contracting before RV
  • TV open before MV,
  • so RV filling start before LV.
  • RV peak pressure 1/5th of LV.
  • RV outflow velocity smooth
  • rise & fall, while Lt side initial
  • peak followed by quick fall.
the first cardiac catheterization
The First cardiac catheterization

Cardiac catheterization was first attempted by Dr Werner Forssmann in 1929, at the age of 25 yrs only, when he was a resident in a hospital at Eberswalde, near Berlin. He was his own subject. A fellow resident who agreed to pass the catheter, got scared and abandoned the effort by the time the catheter reached the axilla. Forssmann completed the task himself with radiographer holding the mirror infront of screen. Forssmann catheterize his heart safely nine times till he had no more peripheral veins left to try. But this was not enough to convince the medical world about the safety of the procedure. After being banished from academics, frustrated Forssmann settled for medical practice in a small town.

It was extensive studies with catheterization by Dr Andre Cournand & Dr Dickinson Richard Jr. and eventually the novel prize for physiology & medicine was awarded jointly to Forssmann, Cournand & Richard in 1956.

The history of cardiac catheterization illustrates what reckless idealism of youth can achieve and the long time (here 27 yrs) might take the world to realize the value of even something of great significance.

references
References
  • Guyton and Hall Textbook of Medical Physiology, 11th Ed. Arthur C. Guyton, John E. Hall.
  • Cardiovascular Physiology Concepts Second Edition,Lippincott Williams & Wilkins, 2011
  • Clinical Methods in Cardiology By Soma Raju, Second Edition, orient longman
  • Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, ninth edition
  • Harrison's Principles of Internal Medicine, 19th edition, McGraw-Hill Book Co
  • Understanding Medical Physiology: A Textbook for Medical Students: By R.L. Bijlani, M.D., RL Bijlani MD SM DSc (Hon Causa) FAMS, S. Manjunatha,4th edition
slide76
7. Medical Physiology E-Book: By Walter F. Boron, Emile L.Boulpaep, Second Edition

8. 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

9. Color Atlas of Physiology. Stefan Silbernagel, Agamemnon Despopoulos. 6th Edition.

10. Jacc: cardiovascular imaging, Vol.2 No. 5, 2009. May 2009: 648-55.

slide77
QUIZ

1. Which letter indicates the point in the cardiac cycle that the mitral valve opens?

A. AB. BC. CD. D

slide78
2.In a normal cardiac cycle , true is

A. RA ejection precedes LA ejection B. RV contraction starts before LV contraction C. LV ejection starts before RV ejection D. Pulmonary valve closes before aortic valve

slide79
3. Which letter in the image represents the isovolumic contraction of the left ventricle in the heart?

A. FB. BC. HD. D

2.

slide80
4. Which of the following pairs is INCORRECT?

A. P wave: atrial depolarizationB. QRS complex: ventricular depolarizationC. T wave: ventricular repolarizationD. QT interval: Measure of duration of atrial action

potential

slide81
5. Isovolumic contraction phase correspond to A. AV opening to AV Closure B. MV closure to MV openingC. MV closure to AV opening D. AV opening to MV opening
slide82
6. Left ventricular end-diastolic volume is: A. 30-50 mls B. 50-70 mls C. 70-120 mls D. 120-150 mls
slide83
7. Prominent y descent in JVP seen in all except

A.    Constrictive pericarditis  B.    Restrictive cardiomyopathies  C.    Tricuspid regurgitation

D. Cardiac temponade

slide84
8. All are true about S3 except

A. Right sided S3 correlate well with rapid y descend

in neck veins.

B. S3 normally heard in normal infants

C. S3 usually indicates systolic dysfunction

D. S3 correlates well with ventricular end diastolic

pressure usually >25mmHg on left side

slide85
9. Cardiac apex is palpable during which phase of cardiac cycle

A. Isovolumic contraction phase

B. Isovolumic relaxation phase

C. Rapid ejection phase

D. Atrial systole phase

slide86
10. Sensitive & specific sign of ventricularterial

dissociation in VT are

A. Variable intensity of S1

B. Variable jugular venous pulse

C. Both A & B

D. None of the above

answers
Answers

1. Which letter indicates the point in the cardiac cycle that the mitral valve opens?

A. AB. BC. CD. D

slide88
2.In a normal cardiac cycle , true is

A. RA ejection precedes LA ejectionB. RV contraction starts before LV contraction C. LV ejection starts before RV ejection D. Pulmonary valve closes before aortic valve

slide89
3. Which letter in the image represents the isovolumic contraction of the left ventricle in the heart?

A. FB. BC. HD. D

2.

slide90
4. Which of the following pairs is INCORRECT?

A. P wave: atrial depolarizationB. QRS complex: ventricular depolarizationC. T wave: ventricular repolarizationD. QT interval: Measure of duration of atrial action

potential

slide91
5. Isovolumic contraction phase correspond to A. AV opening to AV Closure B. MV closure to MV openingC. MV closure to AV openingD. AV opening to MV opening
slide92
6. Left ventricular end-diastolic volume is: A. 30-50 mls B. 50-70 mls C. 70-120 mls D. 120-150 mls
slide93
7. Prominent y descent in JVP seen in all except

A.    Constrictive pericarditis  B.    Restrictive cardiomyopathies  C.    Tricuspid regurgitation

D. Cardiac temponade

slide94
8. All are true about S3 except

A. Right sided S3 correlate well with rapid y descend

in neck veins.

B. S3 normally heard in normal infants

C. S3 usually indicates systolic dysfunction

D. S3 correlates well with ventricular end diastolic

pressure usually >25mmHg on left side

slide95
9. Cardiac apex is palpable during which phase of cardiac cycle

A. Isovolumic contraction phase

B. Isovolumic relaxation phase

C. Rapid ejection phase

D. Atrial systole phase

slide96
10. Sensitive & specific sign of ventricularterial

dissociation in VT are

A. Variable intensity of S1

B. Variable jugular venous pulse

C. Both A & B

D. None of the above