Lecture 4

Phases of the Cardiac Cycle

• The cardiac cycle consists of systole and diastole.

  • Systole: ventricular contraction and ejection of blood.

  • Diastole: ventricular relaxation and filling of the ventricles with blood.

• The cardiac cycle length spans from the beginning of one heartbeat to the start of the next.

  • Each heartbeat includes one ventricular systole and one ventricular diastole.

  • The heart spends more time in diastole, which is crucial for ventricular filling since ventricles fill with blood when relaxed.

Systole

• Ventricular systole is divided into:

  • Isovolumetric ventricular contraction.

  • Ventricular ejection.

• Ventricular contraction squeezes blood, generating pressure to create blood flow.

• Isovolumetric ventricular contraction:

  • All heart valves (AV and semilunar) are closed.

  • Blood volume in ventricles remains constant.

  • Pressure rises as muscle develops tension but cannot shorten.

  • Blood cannot enter or exit ventricles.

• During this phase, ventricular walls develop tension, raising blood pressure, but the blood's incompressibility prevents flow.

• Ventricular myocardium squeezes against incompressible blood; ventricular muscle fibers cannot shorten.

• Ventricular ejection phase:

  • Ventricular pressure exceeds artery pressure.

  • The forward pressure gradient opens semilunar valves, enabling ventricular muscle fibers to shorten and eject blood into arteries.

  • AV valve remains closed, held by chordae tendineae and papillary muscles.

• Ventricular muscle fibers shorten as blood is ejected.

• Stroke volume: the volume of blood ejected from each ventricle during systole.

  • SV = EDV - ESV

  • Both ventricles eject the same volume, but the left ventricle generates more pressure.

  • Ventricles do not eject their entire blood volume when contracting.

Diastole

• Ventricular diastole is divided into:

  • Isovolumetric ventricular relaxation.

  • Ventricular filling.

• Ventricles fill with blood only when the ventricular myocardium (muscle layer) is relaxed.

• Isovolumetric ventricular relaxation:

  • All heart valves are closed.

  • Blood volume remains constant.

  • Pressure drops as the myocardium relaxes.

  • AV and semilunar valves are closed. Myocardium is relaxing.

• Ventricular filling:

  • AV valves open, allowing blood flow from atria to ventricles.

  • Ventricles receive blood passively while atria are relaxed.

  • Atria receive blood from veins when in diastole.

  • Once atria are full and ventricles are relaxed, atrial pressure exceeds ventricular pressure, creating a forward pressure gradient.

  • This gradient opens AV valves, allowing blood to flow from atria to ventricles.

• Two phases of ventricular filling:

  • Passive ventricular filling.

  • Atrial contraction (atrial kick).

• Passive ventricular filling:

  • Ventricles receive about 70% of their blood volume.

  • Both atria and ventricles are relaxed.

  • Atrial pressure is greater than ventricular pressure.

• Atrial contraction (atrial kick):

  • Completes ventricular filling, ventricles still relaxed.

Cardiac Cycle

• Cardiac cycle: rhythmical contraction and relaxation of heart chambers coordinated by electrical activity.

• Represents events in heart chambers during one heartbeat.

• The same events occur simultaneously on both sides of the heart.

• The left ventricle contracts with more force due to a thicker myocardium (muscle layer).

Pressure-Volume Curve (Wiggers Diagram)

• Pressure is key to understanding blood flow patterns and valve behavior.

• Pressure is generated by muscle contraction and chamber filling.

• Blood flows from high to low pressure areas.

• Valves open and close due to pressure gradients.

  • Forward pressure gradient opens valves.

  • Backward pressure gradient closes valves.

• End-diastolic volume (EDV):

  • The volume of blood in each ventricle at the end of diastole, measured in mL.

• End-systolic volume (ESV):

  • The volume of blood in each ventricle at the end of systole, measured in mL.

• Ventricles do not eject their entire blood volume during contraction.

• Stroke volume (SV):

  • The volume of blood pumped out of each ventricle during systole.

  • Calculated as: SV = EDV - ESV

  • Typical value at rest: ~70-75 mL.

Wiggers Diagram

• Wigger’s diagram shows pressure and volume changes in the heart.

• Events occur simultaneously on both sides of the heart.

• During ventricular filling:

  • Semilunar valves are closed.

  • Atrioventricular (AV) valves are presumed open, allowing blood to flow from the atria to the ventricles aided by a pressure decrease in the ventricles.

• During ventricular ejection:

  • The AV valves are closed, and the semilunar valves are open, allowing blood to flow out of the ventricles.

The Right Heart

• The right ventricle develops lower pressures than the left ventricle during systole.

• It undergoes the same sequence of events as the left ventricle.

Heart Sounds

• First heart sound (lub):

  • Caused by the closure of the AV valves at the beginning of isovolumetric ventricular contraction.

  • Signifies the onset of ventricular systole.

• Second heart sound (dub):

  • Caused by the closure of the semilunar valves.

  • Signifies the onset of ventricular diastole.

• Heart sounds reflect turbulence as valves close due to pressure changes.

• Valves on the left and right sides of the heart close simultaneously.

  • Lub and dub sounds represent valve closures on both sides of the heart.

Heart Sounds and Murmurs

• Normal blood flow through valves and vessels is laminar and silent.

  • Laminar flow: smooth, concentric layers of blood moving parallel in a vessel.

• Highest velocity (V_{max}) at the center and lowest velocity (V = 0) along the vessel wall.

• Flow profile is parabolic in long, straight vessels under steady conditions.

• High flow conditions can result in turbulence.

• Turbulent flow produces sound called a murmur.

• Stenotic valve: a valve that doesn't open completely, often due to stiff leaflets from calcium deposits or scarring.

  • Blood flow through a stenotic valve becomes turbulent, creating a murmur.

• Insufficient valve: a valve that doesn't close completely due to widening or scarring.

  • Backward blood flow creates turbulence, producing a murmur.

Autonomic Innervation of the Heart

• The heart is innervated by sympathetic and parasympathetic fibers.

• Sympathetic innervation:

  • Thoracic spinal nerves.

  • Postganglionic fibers innervate the entire heart (atria, ventricles, SA node, and AV node).

  • Releases norepinephrine.

• Parasympathetic innervation:

  • Vagus nerve.

  • Postganglionic fibers innervate the atria, SA node, and AV node.

  • Releases acetylcholine.

• The ventricles receive little parasympathetic innervation, so parasympathetic activity has minimal effect on the ventricular myocardium.

Effects of the ANS on the Heart

• Parasympathetic stimulation:

  • Decreases heart rate by reducing the rate of depolarization of the pacemaker potential.

  • Decreases conduction through the AVN, increasing AV nodal delay.

  • Decreases contractility of the atrial myocardium.

• Sympathetic stimulation:

  • Increases heart rate by increasing the rate of depolarization of the pacemaker potential.

  • Increases conduction through the AVN, decreasing AV nodal delay.

  • Increases contractility of atrial and ventricular myocardium.

Cardiac Output

• Cardiac Output (CO): amount of blood pumped by each ventricle per minute.

  • CO = HR Imes SV

• Stroke Volume (SV): the amount of blood pumped out of each ventricle during systole.

  • Typical values: 70-75 mL.

• Cardiac output differs from stroke volume in that it is measured per unit time.

Factors Affecting Cardiac Output

• As CO = HR x SV, modifying heart rate (HR) or stroke volume (SV) will alter cardiac output (CO).

• Heart Rate (HR) is altered by modifying the activity of the SAN (heart’s pacemaker).

• Stroke Volume (SV) is altered by varying the strength of contraction of the ventricular myocardium.

  • Increased strength of contraction increases SV; decreased strength decreases SV.

Heart Rate Factors

• The heart has resting autonomic tone, where both sympathetic and parasympathetic systems are active.

• One ANS division dominates when its firing rate increases above tonic level, while the other decreases.

• Parasympathetic and sympathetic effects are antagonistic for heart rate.

  • Increased HR: sympathetic stimulation increases, parasympathetic decreases.

  • Decreased HR: parasympathetic stimulation increases, sympathetic decreases.

• Under resting conditions, parasympathetic effects dominate heart rate.

• To increase heart rate: increase sympathetic activity and decrease parasympathetic activity.

  • Increased epinephrine from the adrenal medulla will stimulate the SAN, increasing HR, and decreasing the parasympathetic activity.

• To decrease heart rate: increase parasympathetic activity and decrease sympathetic activity.

• Sympathetic and parasympathetic effects on the heart are extrinsic factors.

• The conducting myocytes in the heart are responsible for initiating the heart rate.

Effect of the ANS on Heart Rate

• Sympathetic stimulation of the SAN increases the slope of the pacemaker potential, causing faster depolarization to threshold, thereby increasing heart rate.

  • Sympathetic stimulation increases the slope of the pacemaker potential by increasing the permeability of the F-type and T-type channels.

  • The F-type channels allow Na^+ to enter the cell and T-type channels allow Ca^{2+} to enter the cell, bringing the cells to threshold more rapidly

• Parasympathetic stimulation of the SAN decreases the slope of the pacemaker potential, causing slower depolarization to threshold, thereby decreasing heart rate.

  • Parasympathetic stimulation decreases the slope of the pacemaker potential by: decreasing F-type channel permeability, reducing the movement of Na+ into the cells, and increasing K^+ channel permeability, causing more K+ to leave the cell, making the cell more negative inside the pacemaker potential.

Effect of the ANS on the Pacemaker Potential

• Sympathetic stimulation: pacemaker potential rises more quickly to threshold, increasing heart rate.

• Parasympathetic stimulation: pacemaker potential rises more slowly to threshold, decreasing heart rate.

Summary of Factors Affecting Heart Rate

• Epinephrine acts similarly to norepinephrine released by sympathetic nerves.

• To increase HR: increased plasma epinephrine, increased norepinephrine release from sympathetic nerves, and decreased acetylcholine release from parasympathetic nerves acts on the SAN to increase HR.

• Sympathetic and parasympathetic systems are antagonistic for heart rate.

• To decrease HR: increase parasympathetic activity and decrease sympathetic activity to the SAN, as well as reduce epinephrine release.

SAN stands for sinoatrial node, which is the heart's natural pacemaker. It's a group of conducting myocytes in the heart responsible for initiating the heart