12.1 Lecture Cardiac Cycle Phases

Cardiac Cycle Phases

• Divided into four distinct phases: two for systole and two for diastole.

Diastolic Filling (Phase One)

• Passive process in early and middle phase one, blood drains from atria to ventricles.
• Atria contract at the end of phase one, before the mitral and tricuspid valves close.
• Contraction occurs immediately after the P-wave on ECG.
• Slight pressure jump in all four chambers with increased ventricular volume.
• Closing of mitral and tricuspid valves corresponds to the S1 heart sound.

Isovolumetric Contraction (Phase Two)

• Ventricles depolarize, causing the QRS complex on the ECG.
• Short period where all four valves are closed as ventricles contract.
• Rapidly increases pressure inside the ventricles.

Ejection Phase (Phase Three)

• Aortic and pulmonary valves open when ventricular pressures exceed those of the aorta and pulmonary artery.
• Blood rushes out from the ventricles.
• Ventricular volume drops sharply, then slows.
• Ventricles re-polarize, causing the T wave on the ECG.

Isovolumetric Relaxation (Phase Four)

• Aortic and pulmonary valves close, causing the S2 heart sound.
• All four valves are closed as ventricles relax.
• Pressure in the ventricles dips below atrial pressure, mitral and tricuspid valves open.
• Start of phase one, ventricles begin refilling rapidly, slowing as phase one continues.

Cardiac Muscle Characteristics

• Striated similarly to skeletal muscle, but with key differences.
• Left ventricle has sub-epicardio (outer) and sub-endocardio (inner) muscle layers.
• Layers are striated in different directions, enabling a twisting motion during systole.

Intercalated Discs

• Cell membranes between muscle fibers.
• Allow ions to move easily, facilitating action potential travel from cell to cell.
• Cardiac muscle cells are interconnected; excitation spreads to all cells.
• Fibrous tissue around AV openings separates atria and ventricle muscles, preventing direct action potential conduction.

Cardiac Muscle Action Potential

• Different from skeletal muscle due to a plateau phase.
• Ventricular contraction lasts up to 15 times longer than in skeletal muscle.
• Large number of fast sodium channels open briefly, creating the initial action potential, then close abruptly.
• Slow calcium channels open more slowly and remain open longer, allowing calcium and sodium influx.
• Potassium permeability decreases about fivefold.
• Closure of calcium channels and increased potassium permeability restores membrane potential to resting level.
• Plateau created by slow calcium channels and decreased potassium permeability.
• During the plateau, cardiac muscle is refractory to stimulation.
• Refractory period of ventricle is 0.25 to 0.3 seconds.

Excitation-Contraction Coupling

• Action potential spreads along T-tubule membranes to the interior of cardiac muscle.
• This triggers the sarcoplasmic reticulum to release calcium into the muscle.
• Calcium interacts with troponin, causing actin-myosin interaction and contraction (similar to skeletal muscle).
• Calcium ions also diffuse into the cell from the T tubules via calcium channels.
• Extracellular calcium diffusion increases the strength of cardiac muscle contraction.
• Contraction strength depends on calcium ion concentration in extracellular fluid.
• At the end of the action potential plateau, calcium influx is cut off.
• Calcium is transported back into sarcoplasmic reticulum and out of the cell.

Conducting System

• Cardiac cycle begins with spontaneous action potential generation in the SA node.
• Action potential travels through both atria, then through the AV bundle into the ventricles.
• Arrangement causes a 0.1-second delay between atrial and ventricular contraction.
• This delay allows the atria to act as a primer for the ventricles.
• Ventricles become the major power source for moving blood.

Waveforms

• Aortic pressure (dotted line), ventricular pressure (red line), ventricular volume (blue line), and ECG (gold line).
• "a" wave is caused by atrial contraction.
• "c" wave is caused by bulging of the AV valves backward during ventricular contraction.

Atrial Contraction

• Accounts for 20% of ventricular filling.
• Loss has minimal effect under most conditions.
• During systole, the atrium fills with blood (AV valves are closed).
• Blood is dumped into the ventricle during the first third of diastole.
• Small amount of blood flows into ventricles during the middle third of diastole.
• Atrial contraction gives a final thrust of blood to the ventricles during the final third.

Ventricular Contraction

• Isovolumetric contraction causes AV valves to close and opens aortic and pulmonary valves.
• Semilunar valves open when pressure rises above 80 mmHg (left ventricle) and 8 mmHg (right ventricle).
• Blood is ejected into the aorta and pulmonary artery.
• The rapid ejection period (first third of systole) ejects about 70% of the blood.
• As the ventricle relaxes, blood fills the large arteries, increasing pressure and closing the aortic and pulmonary valves.
• Isovolumetric relaxation occurs as ventricular pressure falls.

Ventricular Volume

• Normal ventricular filling (including atrial contraction) results in 110-120 mL of blood at the end of diastole.
• Contraction ejects about 70 mL, leaving 40-50 mL in the ventricle at the end of systole.
• Ejection fraction (amount of blood ejected) is typically about 60%.
• In an excitatory state, end-diastolic volume can be 150-180 mL, and end-systolic volume can be 10-20 mL.
• This can more than double cardiac output.

Pressure-Volume Diagram

• Demonstrates changes in ventricular volume and pressure during cardiac cycles.
• Pressure in a non-contracting ventricle does not increase much until after 150 mL.
• During systole, peak systolic pressure occurs when ventricular volume is between 110-150 mL.
• Systolic pressure can decrease with volumes exceeding this range due to overstretching of cardiac muscle fibers.

Valves

• AV valves prevent backflow into the atria.
• Semilunar valves prevent backflow into the ventricles.
• Valves open and close passively based on pressure gradients.
• High pressure in the arteries at the end of systole causes semilunar valves to close.
• Small openings for aortic and pulmonary valves lead to higher blood ejection velocity.

Ventricular Volume Graph Analysis

• End-systolic volume: ~50 mL.
• End-diastolic volume: ~120 mL.
• Little pressure change until volume approaches 120 mL.
• Isovolumetric contraction: pressure increases, but volume remains constant.
• Aortic valve opens, volume decreases, and pressure continues to rise due to contraction.
• Aortic valve closes, ventricle relaxes, and pressure decreases back to the beginning.
• Stroke volume increase widens loop due to increased volume, and loop gets taller from pressure increase, indicating heart pumping large blood volumes.

Preload and Afterload

• Preload: Tension on the muscle when it begins to contract.
• Afterload: Load against which the muscle exerts its contractile force.

Blood Flow Regulation

• Regulated by local tissue control.
• The heart pumps the blood that is returned to it.
• Increased preload equals increased contraction and cardiac output.

Frank-Starling Mechanism

• The more the heart muscle is stretched during filling, the greater the force of contraction and the quantity of blood pumped.
• Stretching cardiac muscle causes actin and myosin filaments to align for optimal overlap.

Vagal Fibers

• Vagal fibers are mainly distributed to the atria, not ventricles.
• Explains parasympathetic system's ability to change rate but not strength of contraction.
• Sympathetic system can stimulate and increase heart rate and contractile force.
• Sympathetic inhibition only decreases to a moderate extent.

Ion Changes

• Large quantities of potassium can block conduction of cardiac impulses from atria to ventricles.
• Calcium deficiency can cause cardiac weakness.
• Increased calcium levels can cause increased contractility.
• Hypocalcemia can cause spastic contraction.