THE

CARDIAC
CYCLE

Physiology
Department
 Objectives
• 01. Define the term cardiac cycle.
• Define preload and explain why ventricular end-diastolic
pressure, atrial pressure, and venous pressure are all good
estimates of ventricular preload in a normal heart.

• Define afterload and explain why arterial pressure is a good

estimate of afterload in a normal heart. Predict the consequence
of an increase or decrease in arterial pressure on the cardiac
workload.

• Define the difference between cardiac performance and cardiac

contractility. Describe the impact of changes in preload,
afterload, and contractility in determining cardiac performance.
• Preload is regulated by venous Preload
return to the heart
• Preload is the load (stretch,
filling) on the ventricle before
ejection

• Measures of Preload: End-

diastolic volume, end-diastolic
pressure, right atrial pressure
• Frank-Starling’s Law: An
increase in preload leads to an
increase in stroke volume
EDV = End Diastolic Volume
ESV = End Systolic Volume
SV = Stroke Volume
 Afterload
• Definition: The load
against which the
LV ejects after the
opening of the aortic
valve
• Simple measure of
afterload: mean
arterial pressure
 Cardiac Contractility
• Definition: Contractile
capability of the heart
• Simple measure of
cardiac contractility:
Ejection Fraction
• EF = SV/EDV
• Cardiac contractility is
increased by
sympathetic stimulation
• Family of different Frank-Starling curves for

different cardiac contractility

Frank-Starling’s Law of the Heart

Maximum Capacity
Stroke To Produce SV
Volume

Normal Range:
SV increases with EDV

End-Diastolic Volume

Mechanism: Length-Force Relations of Muscle Contraction

 Family of Frank-Starling Curves

At a given EDV, SV increases

With cardiac contractility
High

Stroke
Volume
Increase in
Cardiac
Contractility
Low

Preload (End-Diastolic Volume)

 Objectives
02. Know the various phases of ventricular systole and
ventricular diastole. Contrast the relationship between pressure
and flow into and out of the left and right ventricles during each
phase of the cardiac cycle.

• Draw, in correct temporal relationship, the pressure, volume,

heart sound, and ECG changes in the cardiac cycle. Identify the
intervals of isovolumic contraction, rapid ejection, reduced
ejection, isovolumic relaxation, rapid ventricle filling, reduced
ventricular filling and atrial contraction.

• Understand the basic functional anatomy of the

atrioventricular and semilunar valves, and explain how they
operate.

• Understand how and why left sided and right sided events
differ in their timing.
Single cardiac cycle
Phase 1    Atrial contraction

Phase 2    Isovolumetric

contraction

Phase 3    Rapid ejection

Phase 4    Reduced ejection

Phase 5    Isovolumetric

relaxation

Phase 6    Rapid ventricular

filling

Phase 7    Reduced

ventricular
filling
 Objectives
•  03. Draw and describe the length-tension
relationship in a single cardiac cell. Correlate the
cellular characteristics of length, tension, and velocity
of shortening with the intact ventricle, characteristics
of end diastolic volume, pressure, and dP/dt.

• Define contractility and explain why dP/dt is a useful

index of contractility. Explain the cellular basis for the
effects of Ca2+ on cardiac muscle, but not skeletal
muscle, contractility.

 
Isotonic and isometric contraction
Isotonic and isometric contraction
 Effect of Sympathetic stimulation on contractility

1. Increased dp/dt – increased slope, thus increased rate of pressure development

2. Increased peak LVP due to more forceful contraction
3. Increased rate of relaxation due to increased rate of calcium sequestration
4. Decreased systolic interval due to effects #1 and #2
 Objectives
• 04. Draw a ventricular pressure-volume loop and on it labels
the phases and events of the cardiac cycle (ECG, valve
movement).

• Differentiate between stroke volume and stroke work. Identify

stroke volume and stroke work from a pressure-volume loop.

• Draw the change in pressure-volume loops that would result

from changes in a) afterload, b) preload, or c) contractility, for
one cycle and the new steady state that is reached after 20 or
more cycles.

• 05. Ejection fraction.

Define ejection fraction and be able to calculate it from end
diastolic volume, end systolic volume, and/or stroke volume.
Predict the change in ejection fraction that would result from a
change in a) preload, b) afterload, and c) contractility.
 Pressure-volume loop
Ejection

Isovolumic Isovolumic
relaxation contraction

Ventricular
filling
LV Pressure-volume loop
 LV Pressure-Volume Loop and
Frank-Starling’s Law

Systolic Curve
LV
Pressure EDV2 > EDV1
SV2 > SV1
SV2

SV1 Diastolic Curve

LV Volume
ESV EDV1 EDV2
 LV Pressure-Volume Loop and
Afterload

Systolic Curve
LV
Pressure EDV2 = EDV1
SV2 < SV1
SV2

SV1 Diastolic Curve

LV Volume
ESV EDV1
 Objectives
06. Understand the properties of sound and auditory
perception that form the basis of auscultation.

Describe the timing and causes of the four heart sounds.

 
07. Describe the expected auscultation sounds that define
mitral stenosis, mitral insufficiency, aortic stenosis, and
aortic insufficiency and how each affects the cardiac cycle,
left ventricular oxygen needs, and coronary blood flow.

Draw, in correct temporal relationship, the pressure,

volume, murmur of each of the valvular defects referred
above.
FIG. 1 Interactive exercise-physiology of a pump. Chamber
1, left atrium; chamber 2, left ventricle; chamber 3, aorta;
valve M, mitral valve; valve A, aortic valve.
•What happens if P in chamber 1 > P in chamber 2?

•Valve M is open, and volume moves from 1 into 2

•What happens if P in 2 is greater than P in chamber 1?

•Fluid starting to move from 2 into 1 will close valve M,

•No fluid will move when the valve is closed

•What happens if P in chamber 2 > P in chamber 3?

•Valve A is open, and volume moves from 2 into 3
•What happens if P in 3 > P in chamber 2?

•Fluid starting to move from 3 into 2 will close valve A

•No fluid will move when the valve is closed

•What happens to the P in chamber 1 when it is compressed from the

outside?

•P in chamber 1 increases
•What happens to the P in chamber 2 when it is
compressed from the outside?
•P in chamber 2 increases

•Assume P in 3 is higher than P in 1. What would happen

if both valves M and A were open at the same time?

•Fluid would flow from 3 through 2 into 1

Aortic
Insufficiency or
Regurgitation
Low diastolic aortic
pressure
Normal systolic aortic
pressure
High diastolic
ventricular pressure
High ventricular
volume
Diastolic, and early
systolic murmur
 Acute Aortic valve regurgitation

dotted line, normal

ventricle; dashed
line, acute AI; full LV AORTA
line, chronic AI
 Acute Aortic valve regurgitation

Illustration copyright 2002, 2003

Nucleus Communications, Inc.
All rights reserved.
http://www.nucleusinc.com

Volume loading depend on:

• size of the aortic opening
• pressure gradient between the aorta and the left ventricle
• duration of regurgitation which is determined by the duration of diastole
 Acute Aortic valve regurgitation
• Traumatic or degenerative aortic
dissections can dilate the aortic root
and spread the valve leaflets causing
aortic insufficiency.
• In acute aortic insufficiency, the heart
has no time to adapt to volume
overload, and heart failure rapidly
results (rapid surgical correction).

• For chronic aortic insufficiency, a very long symptom-free interval is

typical. During this period, the patients have good exercise tolerance
and some may practice intensive sports. After years symptoms of heart
failure slowly develop:* fatigue,* edema formation, dyspnea.
 Aortic valve stenosis

Illustration copyright 2002, 2003 Nucleus Communications, Inc. All rights reserved. http://www.nucleusinc.com
Aortic Stenosis
Systolic ventricular
pressure > Aortic
Pressure
Rate of ejection
reduced (see volume
trace)
Systolic murmur
(wedge shaped)
 Acute Aortic valve stenosis

• Normal aortic valve area is 2-3 cm2. If it is less than 1.5 cm2, it is
hemodynamically relevant
• Outflow obstruction requires high ventricular pressures to generate ejection,
cardiac work is increased (increase of the area of the pressure volume loop)
 Acute Aortic valve stenosis
• The heart adapts to the increased pressure work by
concentric hypertrophy, i.e., by an increase in LV muscle
mass at normal LV volumes
• The clinical symptoms of aortic stenosis are: angina,
cardiac failure, syncope, sudden death

Concentric: chronic pressure

overload; sarcomeres in parallel
are added
Excentric: volume overload,
sarcomeres in series are added
 Mitral
insufficiency or
regurgitation

High systolic atrial

pressure (see v
curve)
Causes volume
loading of the left
ventricle
Systolic murmur
  
Mitral insuficiency  or regurgitation
 
 
 
 
 
 
 
 
 
 
 
There is no isovolumetric contraction phase (line B/C), because of the
  left atrium at the begining of ventricular
ejection of blood into the
contraction.  
 
More than 50% of LV volume can be ejected into the left atrium before the
aortic valve opens. This  mechanism reduces LV afterload (only moderate
 
LV hypertrophy develops).
 Mitral
stenosis
Atrial pressure is
high throughout
cycle
Diastolic murmur
(filling murmur)
 Acute mitral valve stenosis

Main feature of mitral stenosis: reduced preload reserve and

impaired LV inflow.
20-30 years before the onset of the first symptoms (dyspnea).
The one year survival after the onset of symptoms is only 80%,
making surgical valve replacement necessary
 Acute Aortic valve stenosis

Left
Ventricular
Pressure

Left ventricular volume (Preload)

Acute responses with no change in heart rate,
inotropy, blood volume, or systemic vascular
resistance
 Acute mitral valve regurgitation

Left
Ventricular
Pressure

Left ventricular volume or Preload

Acute responses with no change in heart rate, inotropy,
blood volume, or systemic vascular resistance
 Acute mitral valve stenosis

Left
Ventricular
Pressure

Left ventricular volume (Preload)

Acute responses with no change in heart rate, inotropy,

blood volume, or systemic vascular resistance