Cardio Cardiac cycle

THE CARDIAC

CYCLE

Physiology Department

• 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.

Objectives

Preload• Preload is regulated by venous 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

End-Diastolic Volume

StrokeVolume

Normal Range: SV increases with EDV

Maximum CapacityTo Produce SV

Mechanism: Length-Force Relations of Muscle Contraction

Family of Frank-Starling Curves

Stroke Volume

Preload (End-Diastolic Volume)

Increase inCardiacContractility

At a given EDV, SV increases With cardiac contractility

Low

High

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.

Objectives

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

• 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.

Objectives

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

• 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.

Objectives

Pressure-volume loop

Ventricular filling

Isovolumic contraction

Ejection

Isovolumic relaxation

LV Pressure-volume loop

LV Pressure-Volume Loop andFrank-Starling’s Law

LVPressure

LV Volume

Systolic Curve

Diastolic Curve

SV2

EDV2EDV1

SV1

ESV

EDV2 > EDV1

SV2 > SV1

LV Pressure-Volume Loop andAfterload

LVPressure

LV Volume

Systolic Curve

Diastolic Curve

SV2

EDV1

SV1

ESV

EDV2 = EDV1

SV2 < SV1

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 2 > P in chamber 3?

•Valve A is open, and volume moves from 2 into 3

•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 3 > P in chamber 2?

•P in chamber 1 increases

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

•No fluid will move when the valve is closed

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

•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 RegurgitationLow diastolic aortic pressure

Normal systolic aortic pressure

High diastolic ventricular pressure

High ventricular volume

Diastolic, and early systolic murmur

Acute Aortic valve regurgitation

LV AORTA

dotted line, normal ventricle; dashed line, acute AI; full line, chronic AI


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

Illustration copyright 2002, 2003 Nucleus Communications, Inc. All rights reserved. http://www.nucleusinc.com


• 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.

• 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).

Aortic Stenosis

Systolic ventricular pressure > Aortic Pressure

Rate of ejection reduced (see volume trace)

Systolic murmur (wedge shaped)

• 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

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

High systolic atrial pressure (see v curve)

Causes volume loading of the left ventricle

Systolic murmur

Mitral insufficiency or

regurgitation

6

There is no isovolumetric contraction phase (line B/C), because of the ejection of blood into the left atrium at the begining of ventricular 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 insuficiency or regurgitation

Mitral stenosis

Atrial pressure is high throughout cycle

Diastolic murmur (filling murmur)

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 mitral valve stenosis

LeftVentricularPressure

Left ventricular volume (Preload)

Acute Aortic valve stenosis

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



Left ventricular volume or Preload

Acute mitral valve regurgitation


Left ventricular volume (Preload)

Acute mitral valve stenosis


Cardio Cardiac cycle

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