Phys Lab M10

Heart

Four-chambered muscular pump that circulates blood through the pulmonary and systemic circuits. The right side pumps deoxygenated blood to the lungs, while the left side pumps oxygenated blood to the body.

Blood Flow Through the Heart

Body → Superior/Inferior Vena Cava → Right Atrium → Tricuspid Valve → Right Ventricle → Pulmonary Valve → Pulmonary Trunk → Pulmonary Arteries → Lungs → Pulmonary Veins → Left Atrium → Mitral (Bicuspid) Valve → Left Ventricle → Aortic Valve → Aorta → Body.

Heart Wall Layers

Endocardium lines the heart chambers; myocardium is the thick muscular layer responsible for contraction; epicardium is the thin outer layer covering the heart.

Major Internal Heart Structures

Tricuspid valve (RA→RV), Mitral/Bicuspid valve (LA→LV), Pulmonary valve (RV→Pulmonary trunk), Aortic valve (LV→Aorta), chordae tendineae, papillary muscles, trabeculae carneae, and interventricular septum all contribute to efficient one-way blood flow.

Chordae Tendineae & Papillary Muscles

Papillary muscles contract during ventricular systole to tighten the chordae tendineae, preventing the AV valves from prolapsing back into the atria.

Trabeculae Carneae

Irregular muscular ridges inside the ventricles that improve contraction efficiency and prevent the ventricular walls from sticking together during contraction.

Interventricular Septum

Thick muscular wall separating the right and left ventricles; contains portions of the cardiac conduction system including the bundle branches.

Coronary Circulation

The myocardium receives oxygenated blood from the coronary arteries and returns deoxygenated blood through the cardiac veins into the coronary sinus before entering the right atrium.

Cardiac Conduction System

Specialized cardiac muscle tissue that initiates and distributes electrical impulses, allowing the heart to beat rhythmically without nervous stimulation (automaticity).

Automaticity

The intrinsic ability of pacemaker cells, primarily in the SA node, to spontaneously depolarize and generate action potentials without external stimulation.

Cardiac Conduction Pathway

SA Node → AV Node (brief delay) → Bundle of His → Right & Left Bundle Branches → Purkinje Fibers → Ventricular contraction.

Sinoatrial (SA) Node

The heart's natural pacemaker located in the superior right atrium; initiates each heartbeat through spontaneous depolarization.

Atrioventricular (AV) Node

Located at the bottom of the right atrium; delays the electrical impulse so the atria completely contract and fill the ventricles before ventricular contraction begins.

Bundle of His, Bundle Branches & Purkinje Fibers

The Bundle of His carries impulses from the AV node into the interventricular septum, where it divides into right and left bundle branches before spreading rapidly through Purkinje fibers to produce coordinated ventricular contraction.

Pacemaker Cell Action Potential

Depolarization occurs as sodium and calcium enter pacemaker cells; repolarization occurs as potassium leaves. The delay between action potentials allows the heart to relax during diastole before the next beat.

Electrical vs Mechanical Activity

Electrical depolarization always precedes mechanical contraction. The conduction system creates the electrical signal, while the myocardium produces the pumping action.

Purpose of the AV Node Delay

The brief pause at the AV node ensures the ventricles have enough time to fill with blood before they contract, maximizing cardiac output.Electrocardiogram (ECG)

ECG Components

P wave = atrial depolarization; PR interval = conduction from the SA node through the AV node; QRS complex = ventricular depolarization (atrial repolarization is hidden); ST segment = ventricles fully depolarized and contracting; T wave = ventricular repolarization; QT interval = total time for ventricular depolarization and repolarization.

P Wave, QRS Complex & T Wave

P wave represents atrial depolarization initiated by the SA node; QRS complex represents ventricular depolarization as the impulse travels through the Bundle of His, bundle branches, and Purkinje fibers; T wave represents ventricular repolarization. :contentReference[oaicite:0]{index=0}

PR Interval, ST Segment & QT Interval

PR interval reflects the AV node delay that allows ventricular filling; ST segment represents ventricular contraction with no net electrical movement; QT interval measures the total duration of ventricular depolarization and repolarization. :contentReference[oaicite:1]{index=1}

Heart Rate Regulation

Heart rate is primarily controlled by the autonomic nervous system and circulating hormones, which alter SA node firing rate, AV node conduction, and myocardial contractility.

Sympathetic Nervous System

Increases heart rate, conduction velocity, and contractility during exercise, stress, or excitement by releasing norepinephrine and epinephrine that bind β-adrenergic receptors on the SA node, AV node, and myocardium. :contentReference[oaicite:2]{index=2}

Parasympathetic Nervous System

Primarily carried by the vagus nerve; decreases heart rate during rest by slowing SA node firing and AV node conduction, allowing the heart to conserve energy. :contentReference[oaicite:3]{index=3}

Hormonal Regulation of the Heart

Epinephrine and norepinephrine from the adrenal medulla increase heart rate and force of contraction during stress or exercise, while thyroid hormone (T4) increases the heart's sensitivity to sympathetic stimulation and raises cardiac output. :contentReference[oaicite:4]{index=4}

Cardiac Output (CO)

The amount of blood pumped by one ventricle each minute; calculated using the formula CO = Heart Rate × Stroke Volume (CO = HR × SV).

Heart Rate (HR)

Number of heartbeats per minute; increased by sympathetic stimulation and hormones, decreased by parasympathetic stimulation.

Stroke Volume (SV)

Amount of blood ejected from one ventricle with each heartbeat; determined primarily by preload, afterload, and myocardial contractility.

Factors Affecting Cardiac Output

Cardiac output is influenced by heart rate, stroke volume, venous return, end-diastolic volume, end-systolic volume, filling time, sympathetic/parasympathetic activity, blood pressure, oxygen availability, and circulating hormones. :contentReference[oaicite:5]{index=5}

How Cardiac Output Changes

Cardiac output increases when heart rate or stroke volume increases; decreases when either heart rate or stroke volume falls significantly.

Electrical vs Mechanical Events

Depolarization (electrical event seen on the ECG) occurs before myocardial contraction (mechanical event), allowing electrical activity to coordinate effective pumping.

Clinical ECG Associations

P wave = atrial activity; QRS = ventricular contraction; T wave = ventricular recovery. Remember that atrial repolarization occurs during the QRS complex and is not normally visible on the ECG.Cardiac Cycle

Systole vs. Diastole

Systole is the contraction phase when blood is ejected from the chambers; diastole is the relaxation phase when the chambers fill with blood. The heart spends most of the cardiac cycle in diastole.

Preload vs. Afterload

Preload is the amount of ventricular stretch at the end of diastole (related to end-diastolic volume); afterload is the pressure or resistance the ventricles must overcome to eject blood. Increased preload generally increases stroke volume, while increased afterload makes the heart work harder. :contentReference[oaicite:1]{index=1}

Frank-Starling Law

The more the ventricular walls are stretched by incoming blood during filling (greater preload), the stronger the ventricular contraction and the greater the stroke volume—up to a physiological limit. :contentReference[oaicite:2]{index=2}

End-Diastolic Volume (EDV)

The volume of blood present in a ventricle just before contraction; a major determinant of preload.

End-Systolic Volume (ESV)

The volume of blood remaining in a ventricle after contraction; lower ESV generally indicates more complete ventricular emptying.

Stroke Volume (SV)

The amount of blood ejected from one ventricle during each heartbeat; calculated as SV = EDV − ESV.

Relationship Between Preload, Stroke Volume & Cardiac Output

Increased venous return raises EDV (preload), which increases stroke volume through the Frank-Starling mechanism and can increase cardiac output if heart rate remains constant.

Mean Arterial Pressure (MAP)

Represents the average pressure in the arteries throughout one cardiac cycle and is the best indicator of tissue perfusion because it reflects the pressure actually driving blood to organs. :contentReference[oaicite:3]{index=3}

Heart Sounds

Heart sounds are produced by valve closure rather than blood flowing through the heart; they correspond to specific events in the cardiac cycle. :contentReference[oaicite:4]{index=4}

S1 vs. S2 Heart Sounds

S1 ("lub") occurs when the tricuspid and mitral (AV) valves close at the beginning of ventricular systole; S2 ("dub") occurs when the pulmonary and aortic (semilunar) valves close at the beginning of ventricular diastole. :contentReference[oaicite:5]{index=5}

Cardiac Cycle Sequence

Atrial depolarization (P wave) → atrial contraction → ventricular depolarization (QRS complex) → ventricular contraction and blood ejection → ventricular repolarization (T wave) → ventricular relaxation and filling before the next heartbeat.

Electrical Events vs. Heart Sounds

Electrical activity always occurs first (seen on the ECG), followed by the mechanical contraction of the heart and then the closure of valves that produces the audible heart sounds.

Putting It All Together

The SA node initiates the heartbeat, the conduction system coordinates contraction, the ECG records electrical activity, valves ensure one-way blood flow, preload and afterload influence stroke volume, and cardiac output determines how much blood reaches the body's tissues each minute.

Lab Review Concepts

Know the cardiac conduction pathway, identify each ECG wave and interval, distinguish sympathetic vs. parasympathetic effects, understand the Frank-Starling Law, differentiate preload from afterload, identify S1 and S2 heart sounds, calculate cardiac output (CO = HR × SV), and explain why MAP is a better indicator of tissue perfusion than systolic blood pressure alone.