Checked by Dr. Smith
Cardio #86
Fri, 01/29/03, 11am
Dr. Smith
Jennifer Uxer for Jaclyn Levan
Page 1 of 4
Cardiac Cycle
I.
II.
Introduction
 Practice questions will be posted for Monday’s workshop. Another set will then
be posted to help with the week’s studies.
 Note that the last to ppt slides will not be addressed on this exam.
 Be able to construct elements of the Wigger’s Diagram because you understand
the physiology.
 Refer to the Wigger’s Diagram as you’re studying Dr. Downey’s lectures.
 Learn how things relate to each other: know what’s going on in the contractile
phase, how things relate in the P/V loop.
 Note that both Wigger’s Diagrams in the notes are from different sources. The
1st was used because it fits nicely on a slide and is the same as the one in our
text. The second is helpful because it has things broken out for the left side of
the heart and the right side of the heart.
 Be able to answer questions on differences in pressures.
 Pulmonary artery vs aorta pressure
 Right ventricular pressure vs left ventricular pressure. These pressures are
the same in the chambers during diastole. There’s a problem if they’re not
the same.
 Preload = end diastolic volume = the increase in the stretch in the chamber
Wigger’s Digram (fig 23 – 10, p. 369)
A. Overview
1. Systole and Diastole—think of these in terms of the electrical event or
mechanical events
2. Mechanical vs Electrical
 ECG shows the electrical activation/inactivation
 Mechanical events are associated with the heart as a pump—
contraction/relaxation. Compare the atrium and ventricle.
 If it’s not said explicity, the reference is to the left ventricle.
 Is the onset of atrial systole at the same time as ventricular systole?
No. The electrical event precedes the mechanical event. The
electrical simulation begins in the atrium, so it contracts (P wave)
before the ventricle.
B. Normal Valve Function
1. Pressure gradient determines if they are opened or closed.
2. Passive vs active: Valves are passive.
 Their opening and closing is dictated by the pressure gradient, a
‘swinging door’ effect.
 Leaflets prevent valves from swinging the wrong direction.
 Series of events: high pressure builds up, the valve opens, high pressure
builds on the other side, and the valve closes.
 If the valves don’t work properly, there’s pathology (lecture in 2 weeks)
Checked by Dr. Smith
Cardio #86
Fri, 01/29/03, 11am
Dr. Smith
Jennifer Uxer for Jaclyn Levan
Page 2 of 4
3. Papillary muscles are on the inside of the chamber, are tethered to the valves
via the chordae tendineae, and keep the valves from prolapsing back.
 They’re needed on the AV valves. In the atrium there’s about 5 – 10
mmHg; in the ventricle there’s about 120 – 200 mmHg (upper end is
hypertensive).
 A large pressure gradient is established between the 2 chambers and
causes lots of strain on the valves. The papillary muscles are activated
to keep the valve from flopping back.
4. Heart sounds aren’t really the sound of the valves closing. They’re due to
the turbulence created in the blood flow and involve vibrations in the
chamber walls.
C. Atrial Systole
1. Ventricles fill just before systole.
2. Electric signal is generated from the SA node, and the electrical wave
travels through the atria. (P wave on the ECG precedes atrial contraction)
3. The atrial contraction precedes the ventricular contraction generating a
pressure wave. (Atria contract while the ventricle is relaxed.) Venous flow
still continues into the atria, so if the AV valve is open, the atria is a conduit
to the ventricle.
4. a wave (atrial pressure)—Dr. Smith’s not real concerned with this.
5. Volume increases in the atrium and the pressure slowly increases due to the
additional volume.
6. Electrical event is started turning on contraction. The atrium squeezes and
increases the pressure. When the valve opens, the atrium and ventricle are
essentially the same chamber and their pressures are the same (changes track
together).
7. When the atrium squeezes, the pressure increases and pushes a little extra
blood into the ventricle. This “tops off” the ventricular filling. Most filling
doesn’t happen during atrial contraction. At rest, this “topping off” atrial
contribution is about 10% (CHANGE TO THE POWERPOINTS!!).
During exercise, it can contribute up to 20-25%.
 Atrial fibrillation is a discoordinated sequence of activation. If this
occurs, you lose the topping off of the ventricle. At rest, this is not a
profound effect on preload. During exercise, it limits the cardiac output.
8. 4th heart sound (normal due to atrial contraction—uncommon) Heard in
people with think chest and is associated with pressure and little extra flow.
D. Ventricular Systole
1. Electrical activation starts with the QRS before contraction.
2. Contraction starts:
 Ventricular pressure increases because blood’s virtually incompressible
and is rapidly greater than atrial pressure.
 Valve slams shut—a passive event with activated papillary muscles.
 During filling Patria = Pventricle and they track together. (Atrial pressure is
a tad higher than ventricular to establish the gradient for flow)
Checked by Dr. Smith

Cardio #86
Fri, 01/29/03, 11am
Dr. Smith
Jennifer Uxer for Jaclyn Levan
Page 3 of 4
Valve status at the beginning of contraction: miral valve—closed; aortic
valve—closed (Mitral valve prolapse is when you get a clicking sound.
It’s like a sail on a sailboat when you change directions. The sail pops.
The valve is the same idea.)
3. Ventricular systole has 3 components
4. Component 1: Isovolumetic (no change in volume) contraction
 begins at end-diastolic volume
 QRS wave (ECG) precedes contraction
 Pv>Pa --AV valves close (no blood movement)
 1st heart sound—blood slams against the valve creating turbulence
5. Component 2: Rapid ejection
 Pv>PA--aortic valve opens (rapid ejection of blood due to the large
pressure head)
 ventricular volume decreases fastest
 aortic blood flow is at peak
 atrial pressure rises slowly as venous return continues
6. Reduced ejection
 T wave results from ventricular repolarization—repolarization is NOT
complete until the T wave is finished
 Pv ≤ PA but aortic flow continues due to inertia of blood
 closure of aortic valve ends period
 completely depolarizing
E. Ventricular Diastole
1. What contributes to the relaxation of the muscle? Ca2+ When this is
sequestered back into the sarcoplasmic reticulum (SR) from the cytoplasm,
the contraction stops = relaxation
2. Systolic pressure implies peak pressure; this occurs a few msec after peak
aortic pressure.
3. In relaxation, ventricular pressure decreases. You still have blood flow due
to the force that was generated on the blood. Momentum keeps it moving.
Clarifying this:
The incisura is where aortic pressure can actually be slightly above LV
pressure during systole, yet flow continues and the valve remains open.
This is due to the inertia of ther blood generated by the forceful contrcation-this inertia of forward blood movement keeps the valve open despite the
possibility that aortic pressure is slightly greater than LVP.
4. Isovolumetric relaxation
 Pv < PA-- aortic valve closes (no blood movement)—both valves closed
 2nd heart sound
 atria are filling (atrial pressure v wave) ventricular pressure rapidly
decreasing
5. Rapid ventricular filling
 Pv < Pa-- AV valves open
 blood flows through atria to fill ventricles—acts as a conduit
Checked by Dr. Smith
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III.
Cardio #86
Fri, 01/29/03, 11am
Dr. Smith
Jennifer Uxer for Jaclyn Levan
Page 4 of 4
3rd heart sound (usually turbulence due to high flow)—not usually heard
Why’s there rapid filling at the beginning of diastole? 1. pressure has
built up. 2. valve opens and the ventricle hasn’t finished relaxing—it’s
extremely compliant and will accept blood. Therefore, pressure
CONTINUES to decrease after the valve opens during the first few
msec.
6. Reduced ventricular filling
 ventricular filling continues at a slower rate
 ventricular and atrial pressures slowly rise together
7. ECG in state of diastolic phase (T-P interval)
 All ventricular cells are at resting membrane potential
8. What’s the atrium doing wile the ventricle contracts? Filling because
venous return doesn’t stop.
9. Electrical status of cell membrane resting potential is the same: ~ - 85 to 90mV.
Things to play with and their effect on the cardiac cycle
1. Effect of heart rate
 Change in heart rate on a beat to beat basis
 How does slowing it down/speeding it up change the cardiac cycle duration?
 Slow HR, increase filling time, increase end diastolic volume, increase
preload, increase stroke volume (assuming all else is constant—Starling’s
Law)
2. Where’s preload on Wigger’s diagram? Think about changes in it.
3. Afterload
 Has different elements
 On the Wigger’s diagram, the effectiveness of systole is indicative of
afterload
 Essentially, it’s the load to lift in isolated muscle. The pressure to overcome
before the heart starts ejecting blood.
 Affected by changes in vascular resistance. Increase the resistance, must
increase the pressure, more energy is spent overcoming afterload, decreased
blood ejection (Ohm’s Law)
4. Contractility
 Increase the rate of ventricular pressure, increase the rate of increase in
pressure (think about that one for a minute)
 Increase for given preload and afterload
 Rate of relaxation—leucotropy, diastolic function.
 Stimulation of the sympathetic nervous system—augment contraction,
accelerate relaxation process.