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Questions and Answers
What is the primary function of the atria in the heart?
What is the primary function of the atria in the heart?
Which component of the heart is responsible for the automatic rhythmic electrical discharge?
Which component of the heart is responsible for the automatic rhythmic electrical discharge?
What type of muscle fiber arrangement is found in cardiac muscle?
What type of muscle fiber arrangement is found in cardiac muscle?
How do the durations of contraction in cardiac muscle compare to those in skeletal muscle?
How do the durations of contraction in cardiac muscle compare to those in skeletal muscle?
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What is the function of intercalated discs in cardiac muscle?
What is the function of intercalated discs in cardiac muscle?
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Which part of the heart supplies the main pumping force for peripheral circulation?
Which part of the heart supplies the main pumping force for peripheral circulation?
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Which statement is true about cardiac muscle fibers?
Which statement is true about cardiac muscle fibers?
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What causes the semilunar valves to close at the end of systole?
What causes the semilunar valves to close at the end of systole?
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Which of the following contributes to the greater velocity of blood ejection through the aortic and pulmonary valves compared to A-V valves?
Which of the following contributes to the greater velocity of blood ejection through the aortic and pulmonary valves compared to A-V valves?
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What anatomical feature differentiates the A-V valves from the semilunar valves?
What anatomical feature differentiates the A-V valves from the semilunar valves?
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What occurs at the point of closure of the aortic valve according to the aortic pressure curve?
What occurs at the point of closure of the aortic valve according to the aortic pressure curve?
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What is the diastolic pressure typically recorded in the aorta before the next ventricular contraction?
What is the diastolic pressure typically recorded in the aorta before the next ventricular contraction?
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What is the normal refractory period of the ventricles?
What is the normal refractory period of the ventricles?
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What role does the sinus node play in the cardiac cycle?
What role does the sinus node play in the cardiac cycle?
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During which phase of the cardiac cycle do the ventricles fill with blood?
During which phase of the cardiac cycle do the ventricles fill with blood?
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How is the duration of the cardiac cycle related to heart rate?
How is the duration of the cardiac cycle related to heart rate?
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What happens during the relative refractory period?
What happens during the relative refractory period?
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Why is there a delay during the passage of the cardiac impulse from the atria to the ventricles?
Why is there a delay during the passage of the cardiac impulse from the atria to the ventricles?
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What is the approximate duration of a cardiac cycle at a heart rate of 72 beats per minute?
What is the approximate duration of a cardiac cycle at a heart rate of 72 beats per minute?
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Which statement about the refractory period of atrial muscle is true?
Which statement about the refractory period of atrial muscle is true?
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What effect does an increased heart rate have on the duration of systole?
What effect does an increased heart rate have on the duration of systole?
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What primarily initiates the action potential in skeletal muscle?
What primarily initiates the action potential in skeletal muscle?
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What causes the plateau in the action potential of cardiac muscle?
What causes the plateau in the action potential of cardiac muscle?
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How do calcium ions affect cardiac muscle contraction compared to skeletal muscle?
How do calcium ions affect cardiac muscle contraction compared to skeletal muscle?
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What happens to potassium permeability after the onset of the action potential in cardiac muscle?
What happens to potassium permeability after the onset of the action potential in cardiac muscle?
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What is the duration of the slow calcium-sodium channels opening during the cardiac action potential?
What is the duration of the slow calcium-sodium channels opening during the cardiac action potential?
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What occurs right after the calcium and sodium influx ceases in cardiac muscle?
What occurs right after the calcium and sodium influx ceases in cardiac muscle?
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Which of the following is a characteristic of fast sodium channels?
Which of the following is a characteristic of fast sodium channels?
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What causes the rapid return of the membrane potential to its resting level in cardiac muscle?
What causes the rapid return of the membrane potential to its resting level in cardiac muscle?
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Which statement about action potentials in cardiac muscle is true?
Which statement about action potentials in cardiac muscle is true?
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What is the primary function of the atria during the last third of diastole?
What is the primary function of the atria during the last third of diastole?
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What is true about the period of isovolumic (or isometric) contraction?
What is true about the period of isovolumic (or isometric) contraction?
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At what pressure does the left ventricular pressure need to rise to push the semilunar valves open?
At what pressure does the left ventricular pressure need to rise to push the semilunar valves open?
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Which phase accounts for the majority of blood ejection from the ventricles?
Which phase accounts for the majority of blood ejection from the ventricles?
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What happens immediately after ventricular contraction begins?
What happens immediately after ventricular contraction begins?
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What characterizes the period of isovolumic relaxation?
What characterizes the period of isovolumic relaxation?
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What is the consequence of elevated pressures in the large arteries following ventricular contraction?
What is the consequence of elevated pressures in the large arteries following ventricular contraction?
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The final phase of ventricular pumping is characterized by what event?
The final phase of ventricular pumping is characterized by what event?
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Which statement correctly describes the flow of blood during the heart cycle?
Which statement correctly describes the flow of blood during the heart cycle?
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Study Notes
Cardiac Muscle, Cardiac Cycle, and Function of Atria, Ventricles, and Valves
- The heart functions as two separate pumps: a right heart pumping blood through the lungs, and a left heart pumping blood through the peripheral organs.
- Each heart is a pulsatile two-chamber pump composed of an atrium and a ventricle.
- The atrium acts as a weak primer pump, assisting in moving blood into the ventricle.
- Ventricles provide the primary pumping force, propelling blood through pulmonary and peripheral circulations.
- Specialized mechanisms in the heart, called cardiac rhythmicity, ensure a continuous succession of heart contractions by transmitting action potentials throughout the cardiac muscle.
Physiology of Cardiac Muscle
- The heart comprises three major types of cardiac muscle: atrial muscle, ventricular muscle, and specialized excitatory and conductive fibers.
- Atrial and ventricular muscles contract similarly to skeletal muscles, but contraction duration is longer in cardiac muscles.
- Specialized excitatory and conductive fibers contract weakly due to fewer contractile fibrils. They exhibit either automatic rhythmic electrical discharges in the form of action potentials or conduct action potentials through the heart.
- Cardiac muscle fibers are arranged in a latticework, where they connect and spread.
- Cardiac muscle is striated, similar to skeletal muscle.
- Cardiac muscle fibers contain actin and myosin filaments similar to skeletal muscle, which slide past each other.
- Intercalated discs are the dark areas that cross cardiac muscle fibers, being cell membranes separating individual cardiac muscle cells from each other.
- Cardiac muscle fibers consist of interconnected cells.
Physiology Of Cardiac Muscle (continued)
- Intercalated discs fuse cells, creating permeable communicating junctions (gap junctions) allowing ion diffusion.
- Ions move easily in the intracellular fluid through the longitudinal axes of the cardiac muscle cells.
- Action potentials transmit across cardiac muscle cells with ease, meaning that action potentials quickly spread throughout the heart.
- The heart is composed of two syncytiums: the atrial syncytium, which forms the walls of the two atria, and the ventricular syncytium, forming the walls of the two ventricles.
- Atrioventricular (A-V) valves are surrounded by fibrous tissue that separates the atria from the ventricles.
- Action potentials are not conveyed directly from the atrial syncytium to the ventricular syncytium. They are transmitted only through a specialized conductive system (A-V bundle).
- The division into syncytiums enables atria to contract slightly before ventricles, enhancing blood pumping effectiveness.
Physiology of Cardiac Muscle (continued)
- Ventricular muscle fiber action potentials average about 105 mV, indicating a significant rise in intracellular potential between beats.
- After the initial spike, the membrane remains depolarized for about 0.2 seconds, demonstrating a plateau before abrupt repolarization.
- The plateau phase extends ventricular contraction by a factor of 15, compared to skeletal muscle.
What Causes the Long Action Potential and the Plateau?
- Cardiac and skeletal muscle differ in membrane properties, causing prolonged action potentials and plateaus.
- Skeletal muscle action potentials arise primarily from the rapid opening of numerous fast sodium channels, which allow sodium ions to enter. These channels remain open for a brief period and then close, leading to repolarization.
- Cardiac muscle action potentials involve two types of channels: fast sodium channels (similar to skeletal muscle) and slow calcium channels, also known as calcium-sodium channels. The latter open slower but remain open for longer periods.
- Calcium and sodium ions flow into the cardiac muscle fiber during this prolonged period, maintaining depolarization and creating the plateau in the action potential.
- Calcium ions entering during the plateau phase trigger muscle contraction, while calcium ions causing skeletal muscle contraction are released from internal stores.
- A faster decrease in cardiac muscle membrane permeability for potassium ions after the action potential onset contributes to the plateau phase.
What Causes the Long Action Potential and Plateau? (continued)
- The decreased potassium permeability drastically reduces potassium ion outflow, preventing early action potential voltage return to its resting level.
- When slow calcium-sodium channels close, and calcium/sodium ion influx ceases, rapid potassium ion loss raises the membrane potential back to its resting value. This results in the end of the action potential.
Physiology of Cardiac Muscle (continued)
- Cardiac muscle, like other excitable tissues, is refractory to restimulation. This refractory period represents the time interval during which a normal cardiac impulse cannot re-excite a previously excited area of the heart.
- The ventricular normal refractory period spans from 0.25 to 0.30 seconds, about the same as the prolonged plateau action potential's duration.
- There is an additional relative refractory period, lasting approximately 0.05 seconds, where the muscle is more challenging to excite but potentially excitable by a sufficiently strong stimulus.
- Atrial muscle has a much shorter refractory period compared to ventricles.
Cardiac Cycle
- Cardiac cycle events between one heartbeat's start and the next are called the cardiac cycle and depend on initiation in the sinus node.
- The sinus node, located in the right atrium near the superior vena cava opening, creates an action potential that rapidly spreads through both atria.
- The action potential then travels through the A-V bundle to reach the ventricles, enabling atria to contract just before the powerful ventricular contractions.
- Because of the conduction system's arrangement, there's a slight delay of over 0.1 seconds in conveying the impulse to the ventricles from the atria. This allows atria to contract ahead of ventricular contraction, facilitating efficient blood pumping.
- The cycle includes a period of relaxation called diastole during which the heart fills with blood, and a contraction period known as systole
- The total time of the cardiac cycle, comprising both diastole and systole, is the inverse of the heart rate.
- As the heart rate rises, the cardiac cycle duration diminishes, meaning less time for relaxation between contractions.
Cardiac Cycle (continued)
- At a normal heart rate (72 beats/minute) systole accounts for about 0.4 of the cardiac cycle; at a faster rate (three times faster) systole rises to 0.65 - reduced time for relaxation hampers complete filling of the cardiac chambers between beats.
Cardiac Cycle: Atria
- Blood usually flows from the great veins directly into atria, with approximately 80% of blood flowing directly into ventricles even before atrial contraction.
- Atrial contraction leads to an approximate 20% additional filling of ventricles.
- The heart's function depends on the additional 20%; however, the heart can function normally even without additional filling, as it can pump significantly more blood than resting needs.
- Atrial failure typically isn't noticed except during strenuous activities like exercise.
- Atrial pressure waves (a, c, and v waves) reflect atrial contraction.
Cardiac Cycle: Atria (continued)
- The "a" wave reflects atrial contraction, increasing right atrial pressure by 4-6 mmHg and left atrial pressure by about 7-8 mmHg.
- The "c" wave signifies ventricular contraction, causing slight backflow into the atria and backward pressure on A-V valves.
- The "v" wave occurs late in ventricular contraction, with slow blood flow into atria from veins while A-V valves remain closed.
Cardiac Cycle: Ventricles
- During ventricular systole, blood accumulates in the atria because of the closed A-V valves.
- Ventricular pressure falls upon the completion of systole, triggering A-V valve opening.
- Blood quickly flows into the ventricles, creating a rapid filling phase of diastole.
- In the middle third of diastole, a small amount of blood flows directly from veins to ventricles.
- The final third of diastole is marked by atrial contraction, further propelling blood into the ventricles (adds approximately 20% of the filling).
Cardiac Cycle: Ventricles (continued)
- Immediately following ventricular contraction, ventricular pressure abruptly increases, closing the A-V valves.
- A further 0.02-0.03 seconds are needed for ventricular pressure build-up.
- Semilunar valves open, permitting ventricular emptying while contraction continues
- This isotonic period involves muscle tension buildup without significant shortening.
- Left ventricular pressure surpasses 80 mmHg and right ventricular pressure surpasses 8 mmHg, thus opening semilunar valves.
- Blood rapidly ejects from ventricles, accounting for 70% during the first third of ejection and 30% during the two following thirds.
Cardiac Cycle: Ventricles (continued)
- Ventricular relaxation promptly begins at the end of systole, rapidly reducing intraventricular pressure.
- The elevated pressure in arteries pushes blood back into the ventricles, snapping semilunar valves closed.
- Ventricular muscle continues to relax (without change in volume) for 0.03–0.06 seconds, thus creating the isometric relaxation period, before the A-V valves open and initiate a new ventricular pumping cycle.
End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output
- During diastole, ventricles fill to approximately 110-120 ml (EDV).
- Ventricular emptying during systole reduces volume by approximately 70 ml, defining stroke volume (SV).
- End-systolic volume (ESV) is the remaining ventricle volume, approximately 40-50 ml.
- The ejection fraction, the percentage of EDV ejected, typically stands at about 60%.
End-Diastolic Volume, End-Systolic Volume, and Stroke Volume Output (continued)
- Stronger heart contractions decrease ESV to 10-20 ml.
- Increased blood flow during diastole can make EDV reach 150-180 ml in healthy hearts.
- Both increased EDV and reduced ESV contribute to higher stroke volume, often reaching double the normal output.
Atrioventricular Valves
- A-V valves prevent backflow from ventricles into atria during systole.
- Semilunar valves halt backflow from aorta and pulmonary arteries into ventricles during diastole and close/open passively.
- A-V valves' thin filmy structures require less backflow for closure, contrasting with semilunar valves' substantial structures that demand significant backflow.
- Papillary muscles attach to A-V valve cusps via chordae tendineae, preventing valve inversion during ventricular contraction.
- Rupture or paralysis of chordae tendineae or papillary muscles may cause significant A-V valve leakage, leading to severe cardiac conditions, sometimes fatal.
Aortic and Pulmonary Artery Valves
- Aortic and pulmonary artery semilunar valves function differently from A-V valves.
- High pressures in arteries during systole slam semilunar valves shut, contrasting with the more gradual closing of A-V valves.
- The semilunar valves are of smaller openings leading to greater blood ejection velocity than A-V valves.
- The durable and pliable valve constructs endure the increased physical stresses on the aorta and pulmonary arteries.
Aortic Pressure Curve
- Ventricular contraction rapidly increases ventricular pressure until the aortic valve opens.
- Subsequent pressure increase in ventricle slows as blood quickly leaves the ventricle through the aorta and systemic arteries.
- Blood entry into arteries stretches their walls, increasing arterial pressure to ~120 mmHg.
- The aortic pressure curve shows an incisura, a brief backward blood flow period preceding aortic valve closure.
- After aortic valve closure, aortic pressure slowly descends through diastole as stored blood flows through peripheral vessels.
- Aortic pressure typically decreases to 80 mmHg (diastolic pressure), which is two-thirds of the maximal pressure during contraction.
Concepts of Preload and Afterload
- The preload reflects the muscle tension when contraction begins, while the afterload dictates the load against which the muscle exerts its force during contraction.
- Preload, in cardiac contraction, is usually measured as end-diastolic pressure, the pressure in the ventricle after filling.
- Afterload is the pressure in the aorta leading away from the ventricle and acts against ventricular contraction, representing the force required to eject blood from the heart.
Concepts of Preload and Afterload (continued)
- Critical functional states of the heart and circulatory system often display significant changes in preload and afterload.
- Understanding preload and afterload is crucial for diagnosing abnormal heart function.
Regulation of Heart Pumping
- At rest, the heart pumps 4-6 liters of blood per minute.
- During vigorous exercise, the heart can pump four to seven times this amount.
- Intrinsic cardiac regulation and autonomic nervous system control regulate heart output.
Regulation of Heart Pumping (continued)
- Venous return, the rate at which blood flows into the heart, influences cardiac output under most circumstances.
- Local blood flow in peripheral tissues is managed by their individual control systems; combined venous blood flows into the right atrium.
- The heart automatically pumps this blood into arteries, creating a new circulation loop. This intrinsic capability of the heart to adapt to increasing blood inflow is called the Frank-Starling mechanism.
Regulation of Heart Pumping (continued)
- Stretching cardiac muscles during filling generates greater contraction force and increased blood pumping into the aorta.
- This mechanism helps the heart pump all the blood that returns to it through the veins.
- Increased filling stretches the cardiac muscle, producing a stronger contraction with the same increase in pumping.
- The right atrium's stretched wall augments heart rate (by 10-20%), contributing to increased blood pumping, though less significantly than the Frank-Starling mechanism.
Control by the Sympathetic & Parasympathetic Nerves
- Heart rate and pumping effectiveness are regulated by the sympathetic and parasympathetic nerves.
- Sympathetic stimulation significantly increases cardiac output (cardiac output can increase by over 100% - given the same atrial pressure).
- Strong sympathetic stimulation can augment heart rate in young adults, from normal 70 to even 250 beats per minute. It also increases the force of heart contraction twofold or threefold, augmenting blood pumping and pressure.
Control by the Sympathetic & Parasympathetic Nerves (continued)
- Sympathetic nerve inhibition slightly reduces cardiac output by reducing heart rate and contraction strength, sometimes by up to 30%.
- Parasympathetic stimulation (vagus nerves) can halt heartbeats for a few seconds, causing a brief pause before the heart resumes beating at a rate of 20-40 beats per minute.
- Parasympathetic stimulation can reduce heart muscle contraction by 20-30%.
- Vagal fibers mainly affect atria, impacting heart rate adjustments more than strength of contraction.
Effect of Potassium Ions
- Extracellular potassium buildup dilates and relaxes the heart, reducing heart rate.
- High potassium also blocks A-V bundle conduction, obstructing impulse transmission.
- Potassium elevations of 8-12 mEq/L lead to heart weakening and arrhythmias, potentially fatal.
- High extracellular potassium reduces resting membrane potential, decreasing action potential intensity. This diminishes heart muscle contraction.
Effect of Calcium Ions
- Excess calcium has the opposite effect on the heart compared to potassium, leading to spastic contraction, caused by a direct effect of calcium ions on initiating the cardiac process.
- Deficient calcium causes cardiac flaccidity, remarkably similar to high potassium effects.
- Calcium levels in the blood are meticulously regulated, minimizing clinically concerning cardiac effects.
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Test your understanding of cardiac muscle structure and function with this quiz. Questions cover the roles of the atria, cardiac muscle fibers, and the mechanisms of heart valves. Perfect for students studying cardiac physiology!
