Heart Anatomy and Function Quiz

Heart Anatomy

• The heart is about the size of a closed fist.
• It is located between the lungs in the thoracic cavity, behind and slightly to the left of the sternum (in the mediastinum).
• Shaped like a cone lying on its side, with an apex and base.

The Pericardium

• Definition: A membrane that surrounds and protects the heart.
• Structure: Composed of fibrous pericardium and serous pericardium.
• Function: Confines the heart within the mediastinum while allowing freedom of movement for contractions.

The Heart Wall

• Components: Epicardium, Myocardium, and Endocardium.

Chambers of the Heart

• Two superior chambers: Atria.
  • Separated by the interatrial septum.
  • Receive blood from veins.
• Two inferior chambers: Ventricles.
  • Separated by the interventricular septum.
  • Eject blood into arteries.
  • Right Ventricle, Left Ventricle, Right Atrium and Left Atrium

Heart Valves

• Blood is propelled into a ventricle or out of the heart into an artery as heart chambers contract.
• Valves open and close in response to pressure changes.
• Each valve ensures one-way blood flow, opening / closing to prevent backflow.
• No valves are present on the venous entry to atria.

Chambers and Valves: Atria

• Right Atrium: Receives blood from the Superior and Inferior vena cava and Coronary sinus. Blood passes through the Tricuspid Valve (right atrioventricular valve) into the right ventricle.
• Left Atrium: Receives blood from the lungs through pulmonary veins. Blood passes through the Bicuspid (Mitral) Valve to the left ventricle.

Chambers and Valves: Ventricles

• Right Ventricle: Receives blood from the right atrium via the tricuspid valve. Pumps blood through the pulmonary valve (pulmonary semilunar valve) to the pulmonary trunk (dividing into right and left pulmonary arteries)
• Left Ventricle: Receives blood from the left atrium via the bicuspid valve. Pumps blood through the aortic valve (aortic semilunar valve) to the ascending aorta.

Atrioventricular Valves

• Situated between the atria and ventricles.
• Include the bicuspid (mitral) and tricuspid valves.
  • Bicuspid valve cusps: open/closed, chordae tendineae: slack/taut, papillary muscles: relaxed/contracted.

Semilunar Valves

• The aortic and pulmonary valves.
• Allow blood ejection from the heart into arteries (pulmonary trunk and ascending aorta) when ventricles contract and prevent backflow when ventricles relax.

Innervation and Blood Supply

• Supplied by autonomic fibers.
• Sympathetic increases heart rate and contractile force.
• Parasympathetic decreases heart rate.

Innervation and Blood Supply

• Blood moving through the chambers doesn't exchange nutrients with myocardial cells.
• Myocardial cells receive blood supply from coronary arteries branching from the aorta.
• Most coronary veins drain to the coronary sinus, emptying into the right atrium.

Electrical Activity of the Heart

• Cardiac Muscle Cells, Intrinsic Conduction System, Pacemaker Potentials, Cardiac Muscle Action Potentials.

B- Cardiac Muscle Cells

• Cardiac muscle is striated and branching.
• Cells are connected by intercalated discs containing desmosomes (mechanical) and gap junctions (electrical)
• Gap junctions allow action potentials to spread rapidly.

Heart Characteristics

• Atomicity: Spontaneously depolarizes, triggers action potentials that spread, inducing further heart muscle contraction.

Cardiac Muscle Cells

• Cardiac muscle is striated and contains branching fibers.
• Adjacent cardiac cells are joined by intercalated discs (desmosomes and gap junctions) to hold them together during heart contraction.
  • Gap junctions allow action potentials to quickly spread to adjacent cells.

Cellular Structure

• Like skeletal muscles, cardiac muscle cells are striated, containing myofibrils, sarcomeres, T-tubules, troponin, and tropomyosin.
• Unlike skeletal muscles, cardiac cells are usually uninucleated, smaller, and branched (joined by intercalated discs with desmosomes and gap junctions). They have more mitochondria and larger T-tubules compare to their skeletal counterparts. Ca2+ for contraction comes from both the SR and ECF.

The Heart Muscle

• The heart muscle is made up of a network of cardiac cells.
• The sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, right and left bundle branches, and Purkinji Fibers are part of the specialized conduction system for the heartbeat and contraction.

Functional Syncytium

• One cardiac cell depolarizes, initiating an action potential, and the electrical impulse quickly spreads to other cells connected by gap junctions.
• Atrial and ventricular syncytia allow the atria and ventricles to contract as coordinated units.
• Heart muscle contraction is all-or-none; graded contractions are absent (skeletal muscle recruitment is not present).

The Heart Muscle

• Cardiac muscle cells are arranged in layers.
• Contraction of a chamber compresses blood within it.
• About 1% of cardiac cells are non-contractile, forming the conducting (electrical) system required for heart excitation.

Cardiac Cells

• Non-contractile cells include the SA Node, AV Node, Bundle of His, and Purkinje Fibers.

SA Node

• Located in the upper right atrium.
• Fastest, setting heart rate (70-80 action potentials per resting minute).
• Action potential spreads to both atria and the AV node.

AV Node

• Located in the lower right atrium near the ventricular septum.
• Second fastest.
• Sets pace in case of SA node damage.
• (40-60 action potentials per resting minute).
• Initiates a slight delay before spreading signals to the Bundle of His. (100 ms delay).

Bundle of His & Purkinje Fibers

• Located in the interventricular septum, branching to the right and left bundle branches.
• Purkinje Fibers travel up the outer ventricles (slowest pace).
• (20-40 action potentials/resting minute)
• Electrical signal spreads quickly to ventricles.

Cardiac Muscle Cell Action Potentials

• Action potentials initiate EC coupling in cardiac cells (like skeletal muscle). However, these action potentials arise spontaneously.
• Pacemaker cells (SA node) initiate action potential, spreading via gap junctions to contractile cells.
• Calcium plays a critical role, unlike skeletal muscle and neurons which depend solely on sodium and potassium ions. Muscle cell resting potential is -90mV, peak potential +20 mV

Cardiac Muscle Cell Action Potentials

• The various action potential phases (Phase 4, Phase 0, Phase 1, Phase 2, Phase 3).
• The phases are distinguished by the changes in ion permeability (sodium, potassium, calcium).

Cardiac Muscle Cell Action Potentials (Continued)

• The longer refractory period (longer than the entire muscle twitch) prevents sustained contraction (tetanus) to allow ventricles to fill with blood

Cardiac Pacemaker Action Potentials

• Myocardial pacemaker cells spontaneously produce action potentials independent of nervous input.
• Unstable membrane potential (-60 mV to -40 mV) gradually increases, initiating pacemaker potential instead of a resting potential.
• Pacemaker potential depolarizing to threshold triggers an action potential that spreads and causes muscle depolarization and subsequently, muscle contraction.

Cardiac Pacemaker Action Potentials

• Detailed ion movements (calcium and potassium) during pacemaker action potential.

Cardiac Pacemaker Action Potentials

• Myocardial Pacemaker Cells; voltage-gated Ca2+ channels and their effect on depolarization and repolarization.
• The speed of pacemaker cell depolarization controls heart rate.
• Other conductive cells have their own pacemaker activity but are dependent on action potentials arising from the SA node to reach the threshold.

Heartbeat Coordination

• The SA node, the natural pacemaker, initially generates impulses to both atria.
• Impulses propagate through the internodal pathways and then to the AV node, where there's a delay.
• From the AV node, impulses pass to ventricles, via the Bundle of His and Purkinje fibers.
• The SA node firing rate ultimately determines the heart rate.

Sequence of Excitation

• The SA node in the upper right atrium as the primary pacemaker.
• Impulse propagation through the atria and to the AV node.
• Impulse propagation from the AV node down the Bundle of His and Purkinje fibers to ventricular contraction.

Sequence of Excitation (Continued)

• Detailed steps in contraction sequence.

The Electrocardiogram (ECG)

• P-Wave, QRS complex, PR interval, ST segment, T-wave; corresponding to atrial depolarization, ventricular depolarization, the delay in AV Node, and ventricular recovery period. The ECG trace directly reflects sequential stages of the depolarization-repolarization events that occur in the heart.

D- The Cardiac Cycle

• The cardiac cycle's processes that result from depolarization and include atrial/ventricular contraction and relaxation.
• The cycle is separated into two phases: systole (ventricle contraction and blood expulsion) and diastole (ventricle relaxation and blood filling).
• The approximate duration of a cardiac cycle for a typical heart rate (72 beats/min) is 0.8 seconds.

Systole

• Isovolumetric Contraction portion: All heart valves are closed, ventricles contract (generating tension, but not shortening in length). Ventricular ejection starts when pressure surpasses aortic pressure, opening the aortic valve. Stroke volume is the volume of blood ejected from each ventricle during systole.

Systole (Continued)

• Specific events during ventricular ejection.

Diastole

• Isovolumetric Ventricular Relaxation: Semilunar valves close, ventricles relax. Ventricular volume is not changing.
• Ventricular Filling: Blood flows into ventricles; atrial contraction occurs at the end of diastole before atrial contraction, filling 80% before ventricles contract.
• Specific events during ventricular filling.
• End Diastolic Volume.

Heart Sounds

• Blood flow through valves is normally smooth; valve closure causes turbulence, producing heart sounds (S1 and S2).
• Abnormal heart sounds, arising from abnormal blood flow, are called murmurs.

E- Cardiac Output

• Cardiac Output (CO): The amount of blood pumped by each ventricle per minute.
• CO correlates with Stroke Volume (SV) and Heart Rate (HR), (CO=SV X HR).
• Normal cardiac output is approximately 5 Liters per minute. An athlete's cardiac output during exercise can exceed 35 liters/minute.

Regulation of Cardiac Output

• Heart rate (HR) and Stroke Volume (SV) do not always change in the same direction (effects of heart rate and stroke volume on cardiac output are not always similar).
• Examples of opposing effect such as blood loss, which will decrease SV and increase HR.

1- Control of Heart Rate

• The inherent (autonomous) discharge rate of the SA node (pacemaker) is approximately 100 beats/min.
• The normal resting heart rate is lower due to parasympathetic influence, but hormones and nerves can increase heart rate independently.

Neural Control of Heart Rate

• Changes in heart rate regulated by chronotropic effects (sympathetic neurons increase heart rate, while parasympathetic slows it).
• Dromotropic effects are also involved in conduction velocity through the heart

Other Heart Rate Controls

• Factors other than cardiac nerves (e.g., hormones, temperature, electrolytes) also affect heart rate, though they are often less significant.

2- Control of Stroke Volume

• Ventricles don't fully empty during contraction, so more forceful contractions can lead to greater emptying, increasing stroke volume.
• Three dominant factors influence the force of ventricular ejection: preload (end-diastolic volume), contractility (sympathetic nervous system input), and afterload (arterial pressures).

Preload: Frank-Starling Mechanism

• Preload refers to venous return (blood entering the heart), which is directly linked to the end-diastolic volume.
• Greater venous return (filling) causes more stretching in myocardial cells, which increases the force of contraction (increasing stroke volume).

Contractility: Sympathetic Regulation

• Norepinephrine acts on beta-adrenergic receptors to increase ventricular contractility (increasing contractility increases force and speed).
• Contractility refers to the strength of contraction for a given preload.

Contractility: Sympathetic Regulation (Continued)

• Extrinsic factors impacting contractility are described using 'positive inotropic effects'. The 'ejection fraction' or EF is a measure of contractility. It is the ratio of stroke volume (SV) to end-diastolic volume (EDV), averaging between 50-75% in healthy individuals during resting states.

Afterload: Arterial Pressure

• Increased arterial pressure reduces stroke volume ('afterload') as the heart must work harder to overcome the pressure difference.
• Several internal mechanisms can counteract the effect of arterial pressure on stroke volume.

Regulation of Cardiac Output (Summary)

• Regulation of cardiac output.

F- Measurement of Cardiac Function

• Cardiac output and heart function are measured by echocardiography and cardiac angiography, the latter being an invasive measure.
• Echocardiography can identify problems with cardiac valves and walls and helps in the evaluation of ejection fraction.

Test your knowledge on heart anatomy, including its structure, chambers, valves, and surrounding membranes. This quiz covers essential concepts about how the heart functions and its components. Perfect for students studying biology or anatomy.