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Coverage - Major Topic Areas

• Cell structure, membrane organization, organelles (ER, Golgi, mitochondria, lysosomes)
• Homeostasis and control systems, negative/positive feedback

• Ion transport, action potentials, neuromuscular junction
• Skeletal, smooth, and cardiac muscle physiology

• Cardiac muscle, rhythmical excitation, ECG, cardiac output, cardiac failure

• Blood pressure regulation, microcirculation, lymphatic system, local/humoral control

• RBCs, hemoglobin, WBCs, immunity, blood groups, hemostasis/coagulation

• Pulmonary ventilation, gas exchange, transport of O2/CO2, regulation of respiration

• Renal function, urine formation, acid-base balance, diuretics

• Sensory processing, motor control, cerebellum, basal ganglia, cerebral cortex, sleep, autonomic nervous system

• Vision, hearing, taste, smell, somatic sensation, pain

• Pituitary, thyroid, adrenal, pancreas/insulin, parathyroid, reproductive hormones

• Motility, secretion, digestion, absorption, GI blood flow

• Carbohydrate, fat, protein metabolism; body temperature regulation; nutrition

• Exercise physiology, performance limits

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Cardiac Muscle, Action Potentials, the Heart as a Pump, Cardiac Cycle, Regulation, and Heart Valves

Guyton and Hall Textbook of Medical Physiology

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TOPIC 1: Cardiac Muscle

Three Types of Cardiac Muscle

1. Atrial muscle
2. Ventricular muscle
3. Specialized excitatory and conductive fibers (e.g., SA node, AV node, Purkinje fibers)

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Cardiac Muscle Anatomy

• The subepicardial (outer) layer spirals leftward; the subendocardial (inner) layer spirals rightward - a double helix arrangement.
• During systole (contraction), the apex rotates counterclockwise and the base rotates clockwise (viewed apex-to-base), creating a wringing/twisting motion that pulls the base downward toward the apex.
• At end-systole, the ventricle acts like a loaded spring - it recoils/untwists during diastole, rapidly drawing blood in.

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Cardiac Muscle Is a Syncytium

• When one cardiac cell is excited, the action potential spreads to all other cells
• The entire atrial mass contracts as a single unit (atrial syncytium)
• The entire ventricular mass contracts as a single unit (ventricular syncytium)
• The atrial and ventricular syncytia are electrically insulated from each other by the fibrous AV ring - the only pathway between them is the AV bundle (bundle of His)

This "all-or-nothing" behavior of the heart syncytia is fundamental - either the whole atria contract together, or none of it contracts.

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TOPIC 2: Action Potentials in Cardiac Muscle

The Cardiac Action Potential vs. Skeletal Muscle

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Phases of the Cardiac Action Potential

• Fast voltage-gated Na⁺ channels open suddenly
• Na⁺ rushes in, membrane potential shoots from -90 mV to about +20 mV
• These channels are almost identical to those in skeletal muscle

• Fast Na⁺ channels close
• Brief, small repolarization

1. Slow ("L-type") Ca²⁺ channels open - Ca²⁺ flows in from extracellular fluid (slow inward current)
2. K⁺ permeability decreases - unlike skeletal muscle, K⁺ channels partially close after depolarization

• Slow Ca²⁺ channels close
• K⁺ channels reopen, K⁺ rushes out
• Membrane repolarizes rapidly back to resting potential

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Why the Plateau Matters: Ca²⁺ and Contraction

• Drugs that block Ca²⁺ channels (e.g., verapamil) reduce cardiac contractility
• High extracellular Ca²⁺ strengthens contraction
• Low extracellular Ca²⁺ weakens or stops the heart

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The Absolute Refractory Period

"Duration of contraction of cardiac muscle is mainly a function of the duration of the action potential, including the plateau - about 0.2 second in atrial muscle and 0.3 second in ventricular muscle." - Guyton & Hall

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TOPIC 3: The Heart as a Pump

Overview of Blood Flow Through the Heart

• Right heart - pumps deoxygenated blood through the pulmonary circulation (low pressure, ~8 mm Hg)
• Left heart - pumps oxygenated blood through the systemic circulation (high pressure, ~80 mm Hg)

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Atria as Primer Pumps

1. Reservoir phase - Blood flows from great veins/pulmonary veins into the atria
2. Conduit phase (early diastole) - ~70-80% of blood flows directly through the atria into ventricles before the atria even contract
3. Contractile phase - Atrial contraction provides the remaining 20-30% ventricular filling, acting as a "booster pump"

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Left Ventricular Torsion (Wringing) Aids Ejection

• Enhances ejection of blood by squeezing the ventricle from multiple angles
• Stores elastic energy (like a spring)
• Causes rapid untwisting in diastole, which actively sucks blood into the ventricle (diastolic suction)

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TOPIC 4: The Cardiac Cycle

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Phases of the Cardiac Cycle

DIASTOLE (Ventricular Filling)

• AV valves (mitral and tricuspid) open
• Atrial pressure > ventricular pressure, so blood rushes in rapidly
• Left ventricular volume rises steeply on the volume curve

• Blood continues flowing from veins → atria → ventricles (passive)
• Only a small additional amount enters

• Atria contract, giving a final thrust of blood into the ventricles
• Adds 20-30% to ventricular end-diastolic volume (EDV)
• Represented on ECG as the P wave

Note: With aging, hypertension, or cardiac fibrosis, ventricles stiffen - they rely more on atrial contraction to achieve adequate filling.

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SYSTOLE (Ventricular Contraction & Ejection)

• Ventricles begin contracting (QRS complex on ECG)
• Ventricular pressure rises sharply
• AV valves snap shut (produces first heart sound, S1)
• Semilunar valves (aortic, pulmonary) are still closed - no blood ejected yet
• Ventricular volume is unchanged (isovolumic = no volume change)

• Left ventricular pressure exceeds ~80 mm Hg → aortic valve opens
• Right ventricular pressure exceeds ~8 mm Hg → pulmonary valve opens
• Rapid ejection (first 1/3): ~70% of ejected volume leaves
• Slow ejection (last 2/3): remaining ~30% of ejected volume leaves
• Ejection Fraction (EF) = ~60% of end-diastolic volume is ejected

• Ventricular relaxation begins suddenly (T wave on ECG)
• Arterial pressures push blood back toward ventricles
• Semilunar valves snap shut (produces second heart sound, S2)
• AV valves still closed - pressure falls rapidly with no volume change
• Cycle then begins again with ventricular filling

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Atrial Pressure Waves: a, c, and v

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Heart Rate Effects on Cardiac Cycle

• Total cycle duration decreases
• Diastole is shortened more than systole
• At 3x normal heart rate, systole = 65% of the cycle (vs. 40% at rest)
• Very rapid rates don't allow adequate ventricular filling before the next contraction

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TOPIC 5: Regulation of Heart Pumping

Intrinsic Regulation: The Frank-Starling Law

"The heart automatically pumps into the arterial system all the blood that comes to it from the veins."

• More venous return → more ventricular filling → cardiac muscle stretched to longer initial length
• Overstretched actin-myosin filaments have more cross-bridge formation potential
• Result: stronger contraction and greater stroke volume

• If the right ventricle pumps slightly more blood into the lungs, the left ventricle automatically receives more blood, stretches more, and pumps out more - keeping outputs of both sides balanced second by second.

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Preload and Afterload

• Increased by: increased venous return, increased blood volume
• More preload → more stretching → stronger contraction (Frank-Starling)

• Increased afterload → requires more force → if the heart cannot compensate, stroke volume falls

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Extrinsic Regulation: Autonomic Nervous System

Sympathetic Stimulation

• Increases heart rate (chronotropy): From 70 to 180-200 beats/min (up to 250 in rare cases)
• Increases force of contraction (inotropy): Can double the force
• Net effect: Cardiac output can increase 2-3 fold
• Mechanism: Norepinephrine released → β₁ receptors → increased Ca²⁺ entry and faster Ca²⁺ cycling

Parasympathetic (Vagal) Stimulation

• Decreases heart rate dramatically: Strong vagal stimulation can briefly stop the heart; the heart then "escapes" and beats at 20-40 beats/min
• Decreases contraction strength by 20-30%
• Vagal fibers are distributed mainly to the atria, not the ventricles
• Therefore, vagal effect is primarily on heart rate rather than contraction force
• Combined effect can reduce ventricular pumping by 50% or more

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Cardiac Function Curve (Starling Curve)

• Normal curve: As right atrial pressure rises, cardiac output rises
• Sympathetic stimulation: Shifts curve upward and to the left (more output at any given filling pressure)
• Parasympathetic stimulation / heart failure: Shifts curve downward and to the right

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TOPIC 6: Function of the Heart Valves

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Atrioventricular (AV) Valves: Mitral and Tricuspid

• Consist of fibrous leaflets attached to the fibrous ring of the heart
• Connected to chordae tendineae (tendinous cords)
• Chordae tendineae attach to papillary muscles on the inner ventricular walls

• When ventricular pressure rises and exceeds atrial pressure, leaflets swing upward to close
• The chordae tendineae and papillary muscles prevent the leaflets from everting (popping back into the atrium under high pressure)
• Papillary muscles contract simultaneously with the ventricle, keeping the chordae taut
• If chordae rupture or papillary muscles fail → valve prolapses into atrium → mitral/tricuspid regurgitation

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Semilunar Valves: Aortic and Pulmonary

• Each valve has three cup-shaped cusps (semilunar = half-moon shape)
• No chordae tendineae needed - their cup shape allows them to self-seal

• When ventricular pressure drops at end of systole, blood starts flowing backward from the arteries
• This backflow fills the cups of each cusp, causing the three cusps to come together in the midline and seal tightly
• The valve snaps shut - producing S2 (second heart sound)
• The cusps are extremely thin and can open/close with almost no resistance to forward flow and no regurgitation backward

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Heart Sounds and Valves

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Valve Dysfunction: Key Concepts

• Mitral regurgitation: blood leaks into left atrium during systole
• Aortic regurgitation: blood leaks back into left ventricle during diastole

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SUMMARY: The Big Picture

SA Node fires
      ↓
Atria depolarize (P wave) → Atria contract (atrial kick)
      ↓
AV Node delay (0.1 sec) → allows atrial filling of ventricles
      ↓
Bundle of His → Purkinje fibers → Ventricles depolarize (QRS)
      ↓
Isovolumic contraction → AV valves close (S1)
      ↓
Semilunar valves open → Ejection (stroke volume ~70 mL, EF ~60%)
      ↓
Isovolumic relaxation → Semilunar valves close (S2)
      ↓
AV valves open → Rapid filling → Slow filling → Atrial kick
      ↓
Next cycle begins

• Frank-Starling mechanism (intrinsic) - adjusts beat-by-beat based on filling
• Sympathetic nerves - can boost output 2-3x
• Parasympathetic (vagal) nerves - can reduce output by 50%+

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1. Cardiac Muscle - Three types, striated anatomy, intercalated discs, gap junctions, syncytium concept, and the unique double-helix torsion of the left ventricle
2. Action Potentials - The 4 phases, the critical plateau (Phase 2) caused by slow Ca²⁺ channels + reduced K⁺ permeability, why the long refractory period prevents tetany
3. Heart as a Pump - Right vs. left heart, atria as primer pumps (3 phases of filling), the 300-400% cardiac reserve
4. Cardiac Cycle - All phases of diastole and systole with exact pressures, volumes, and timing; the a/c/v atrial waves; ECG correlation
5. Regulation - Frank-Starling law (intrinsic), preload vs. afterload, sympathetic (2-3x boost) and parasympathetic (50%+ reduction) control
6. Heart Valves - Structure and mechanism of AV valves (with chordae/papillary muscles) and semilunar valves, heart sounds S1-S4, stenosis vs. regurgitation

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Cardiac Muscle Is a Syncytium

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What Is a Syncytium?

• The word syncytium means a mass of cells that are so interconnected that they behave as one single unit
• Cardiac muscle is called a syncytium because when one cell gets excited, the action potential rapidly spreads to ALL other cells
• Think of it like a row of dominoes - one falls, and they all fall together

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The Building Blocks: Intercalated Discs

• Under a microscope, you can see dark bands crossing across cardiac muscle fibers - these are called intercalated discs
• Intercalated discs are actually the cell membranes that separate one individual cardiac muscle cell from the next
• So cardiac muscle fibers are made up of many individual cells connected in series and in parallel with one another - not one giant cell

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The Key Structure: Gap Junctions

• At each intercalated disc, the cell membranes fuse together to form special structures called gap junctions
• Gap junctions are permeable communicating junctions - meaning ions can pass freely through them
• Ions move with ease along the longitudinal axes (lengthwise direction) of the cardiac muscle fibers
• Because ions flow freely → action potentials travel easily from one cardiac cell to the next, straight across the intercalated discs

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The Two Syncytia of the Heart

• Atrial syncytium - makes up the walls of the two atria (right and left atrium)
• Ventricular syncytium - makes up the walls of the two ventricles (right and left ventricle)

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How Are the Two Syncytia Separated?

• The atria and ventricles are separated by a fibrous tissue that surrounds the atrioventricular (AV) valvular openings
• This fibrous tissue is electrically non-conductive - action potentials cannot pass directly through it
• So the atrial syncytium cannot directly excite the ventricular syncytium
• The ONLY pathway for electrical conduction from atria to ventricles is through a specialized structure called the AV bundle (bundle of His) - a bundle of conductive fibers a few millimeters in diameter

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Why Does This Division Matter? (The Functional Significance)

• Because the atria and ventricles are electrically isolated from each other (except through the AV bundle), the atria can contract first and the ventricles contract slightly after
• This sequential contraction - atria first, then ventricles - allows the atria to act as primer pumps, filling the ventricles with blood before the ventricles contract
• If the two syncytia were not separate, both atria and ventricles would contract simultaneously - the atrial "boost" of blood would be lost

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Summary in One Line

"Cardiac muscle is a syncytium of many heart muscle cells in which the cardiac cells are so interconnected that when one cell becomes excited, the action potential rapidly spreads to all of them." - Guyton & Hall

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How the AV Bundle Delay Ensures Proper Atrial-to-Ventricular Timing

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The Core Purpose - Why a Delay Is Needed

• The cardiac impulse must NOT travel from the atria into the ventricles too rapidly
• A deliberate delay is built into the system to give the atria time to empty their blood into the ventricles before ventricular contraction begins
• The atria act as primer pumps - they must finish contracting and pushing blood into the ventricles first, and only then should the ventricles contract
• Without this delay, the atria and ventricles would contract almost simultaneously - the atrial "boost" of blood would be lost

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Step 1: Impulse Originates at the SA Node (Time = 0)

• Every heartbeat begins with a spontaneous action potential generated in the sinoatrial (SA) node, located in the superior lateral wall of the right atrium near the opening of the superior vena cava
• From here, the impulse spreads rapidly through both atria via internodal pathways
• The atria depolarize and contract - this is the atrial kick
• The impulse reaches the AV node about 0.03 second after leaving the SA node

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Step 2: The AV Node - The Major Site of Delay

• The AV node is located in the posterior wall of the right atrium, immediately behind the tricuspid valve
• Once the impulse arrives at the AV node, it is held up (delayed) for about 0.09 second within the AV node itself before it can pass into the penetrating portion of the AV bundle
• This is the single largest source of delay in the entire conduction system

• The AV nodal fibers and transitional fibers have diminished numbers of gap junctions between successive cells
• Fewer gap junctions = greater resistance to the flow of excitatory ions from one cell to the next
• Therefore, each successive cell is slow to be excited, creating the delay

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Step 3: Further Delay in the Penetrating AV Bundle

• After the AV node, the impulse enters the penetrating portion of the AV bundle - a bundle of small conductive fascicles that pass through the fibrous tissue separating the atria from the ventricles
• An additional delay of 0.04 second occurs here as the impulse travels through this fibrous barrier

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The Total Delay: 0.16 Second

• This 0.16 second delay is enough time for the atria to contract completely and push blood into the ventricles before ventricular contraction even begins

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Step 4: Rapid Transmission Through the Ventricular Purkinje System

• Once the impulse clears the AV bundle and enters the ventricular Purkinje system, everything reverses - conduction becomes extremely fast
• Purkinje fibers transmit action potentials at 1.5 to 4.0 m/sec - about 6 times the speed of normal ventricular muscle fibers, and 150 times the speed of some AV nodal fibers
• Why so fast? Purkinje fibers have a very high level of permeability of gap junctions at their intercalated discs - ions pass from cell to cell with almost no resistance
• The impulse travels from the bundle branches through the entire ventricular Purkinje network in just 0.03 second
• Transmission through the ventricular muscle mass itself takes another 0.03 second
• Total ventricular activation time = only 0.06 second - the entire ventricular muscle contracts almost simultaneously

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The AV Bundle Is a One-Way Street

• The AV bundle normally conducts only forward - from atria to ventricles
• Action potentials cannot travel backward from ventricles to atria through the AV bundle
• This prevents reentry of impulses from the ventricles back into the atria, which would cause dangerous arrhythmias
• Everywhere except at the AV bundle, the atrial and ventricular muscles are separated by the continuous fibrous barrier - a complete electrical insulator

Exception: In rare cases, an abnormal accessory pathway (as in Wolff-Parkinson-White syndrome) penetrates the fibrous barrier at a point other than the AV bundle. This allows impulses to travel backward from ventricles to atria, causing serious cardiac arrhythmias.

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The Big Picture: Timing Summary

SA Node fires (0.00 sec)
        ↓  [0.03 sec - fast, through atria]
AV Node arrives (0.03 sec) → ATRIA CONTRACT HERE
        ↓  [0.09 sec delay - slow, AV node]
Penetrating AV Bundle (0.12 sec)
        ↓  [0.04 sec delay - AV bundle fascicles]
Ventricular Purkinje system entered (0.16 sec)
        ↓  [0.03 sec - lightning fast, Purkinje fibers]
Entire ventricular muscle activated (0.19 sec) → VENTRICLES CONTRACT

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Why This Design Is So Elegant

"This delay allows the atria to contract ahead of ventricular contraction, thereby pumping blood into the ventricles before the strong ventricular contraction begins. Thus, the atria act as primer pumps for the ventricles." - Guyton & Hall

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Chapter 9: Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves

Guyton and Hall Textbook of Medical Physiology - Complete Key Points

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SECTION 1: Cardiac Muscle Physiology - Three Types

• The heart has 3 types of cardiac muscle:
  1. Atrial muscle - contracts to push blood into ventricles
  2. Ventricular muscle - contracts to push blood into arteries
  3. Specialized excitatory and conductive fibers (SA node, AV node, Purkinje fibers) - these contract weakly but their real job is generating and conducting electrical signals
• Atrial and ventricular muscle contract much like skeletal muscle, but for a much longer duration

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SECTION 2: Cardiac Muscle Anatomy

• Striated like skeletal muscle - has actin and myosin filaments that slide during contraction (same sliding filament mechanism)
• Fibers are arranged in a latticework - they divide, recombine, and spread, forming an interlocking network
• Left ventricular torsion: The LV muscle is arranged in a double helix (outer layer spirals left, inner layer spirals right). This causes a wringing/twisting motion during systole
  • The apex rotates counterclockwise, base rotates clockwise - like squeezing a wet towel
  • At end-systole the ventricle is like a loaded spring - it recoils during diastole, actively sucking blood in

Cardiac Muscle Is a Syncytium

• Intercalated discs = dark bands seen in histology - these are cell membranes separating individual cardiac cells
• At each intercalated disc, membranes fuse to form gap junctions - pores that let ions flow freely between cells
• Result: when one cell is excited, the action potential spreads instantly to ALL cells - the entire atrial or ventricular mass contracts as one unit
• The heart has TWO syncytia:
  • Atrial syncytium = all atrial cells connected
  • Ventricular syncytium = all ventricular cells connected
• The two syncytia are electrically separated by a fibrous ring - the ONLY bridge between them is the AV bundle (bundle of His)
• This separation means atria contract first → then ventricles contract (the correct pumping sequence)

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SECTION 3: Action Potentials in Cardiac Muscle

• Resting membrane potential = -85 mV; peaks at +20 mV during action potential
• Total amplitude = 105 mV
• The most important feature: there is a long PLATEAU lasting ~0.2 sec (atrial) to 0.3 sec (ventricular) - this makes cardiac contraction 15x longer than skeletal muscle

Why does the plateau exist? (Two reasons)

1. Slow L-type Ca²⁺ channels (slow calcium channels) open during depolarization and stay open for several tenths of a second - Ca²⁺ and Na⁺ keep flowing in, maintaining depolarization
2. K⁺ permeability decreases ~5-fold right after depolarization begins - K⁺ cannot rush out to repolarize the cell (this is the opposite of skeletal muscle)

• Both effects together hold the membrane near 0 mV for a prolonged time = the plateau

Velocity of Conduction

• Action potentials conduct through cardiac muscle at 0.3 to 0.5 m/sec - much slower than skeletal muscle

The Refractory Period

• Cardiac muscle has a very long absolute refractory period (~0.2-0.25 sec) - the entire duration of contraction
• This means cardiac muscle cannot be tetanized (cannot be re-stimulated while it's contracting)
• This is essential - if the heart tetanized like skeletal muscle, it would never relax to fill with blood, and death would follow

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SECTION 4: Excitation-Contraction Coupling - Ca²⁺ and T-Tubules

• The process by which the action potential triggers contraction is called excitation-contraction coupling
• When an action potential passes over the cardiac membrane, it spreads into the interior via transverse (T) tubules
• T-tubule action potential → triggers Ca²⁺ release from sarcoplasmic reticulum (SR)
• BUT cardiac muscle also gets extra Ca²⁺ from outside the cell through the T-tubule walls themselves (via voltage-dependent Ca²⁺ channels)
• This extracellular Ca²⁺ then triggers more Ca²⁺ release from SR via ryanodine receptor channels (calcium-induced calcium release)
• Final step: Ca²⁺ in sarcoplasm → binds troponin → cross-bridge formation → contraction

Why cardiac muscle depends on extracellular Ca²⁺:

• The SR of cardiac muscle is less well developed than in skeletal muscle - it cannot store enough Ca²⁺ by itself for full contraction
• So cardiac muscle must have extracellular Ca²⁺ to contract normally
• The T-tubules in cardiac muscle are 5x wider (25x greater volume) than skeletal muscle T-tubules, and are coated with electronegative mucopolysaccharides that bind and store Ca²⁺ right next to the cell
• A heart placed in calcium-free solution will quickly stop beating
• More extracellular Ca²⁺ = stronger contraction; less Ca²⁺ = weaker contraction

Duration of Contraction

• Cardiac muscle contraction lasts about 0.2 sec (atrial) and 0.3 sec (ventricular) - directly tied to the action potential plateau duration

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SECTION 5: The Cardiac Cycle

• The cardiac cycle = all events from one heartbeat to the beginning of the next
• At 72 beats/min → each cycle = 0.833 seconds
• Every cycle starts with an action potential from the SA node → spreads through atria → delayed at AV node → into ventricles

Systole vs. Diastole

• Systole = ventricular contraction (~0.4 of cycle at rest)
• Diastole = ventricular relaxation and filling (~0.6 of cycle at rest)
• At high heart rates: diastole is shortened more than systole → ventricles don't fill completely

Atrial Pressure Waves: a, c, and v

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SECTION 6: The Atria as Primer Pumps

• Atrial filling occurs in 3 phases:
  1. Reservoir phase - blood flows in from great veins/pulmonary veins
  2. Conduit phase - ~70-80% of blood flows directly through atria into ventricles (passive, before atrial contraction)
  3. Contractile phase - atrial contraction pushes final 20-30% into ventricles (the "atrial kick")
• Atria increase ventricular filling effectiveness by ~30%
• Without atrial contraction: the person is fine at rest (heart has 300-400% reserve), but may develop shortness of breath during exercise

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SECTION 7: Ventricles as Pumps

Diastole (Filling)

• AV valves open → blood rushes in rapidly (period of rapid filling = first 1/3 of diastole)
• Middle 1/3 = slow trickle from veins through atria
• Last 1/3 = atrial contraction adds final boost

Systole (Ejection)

Key Volume Numbers

• End-diastolic volume (EDV) = 110-120 mL (volume in ventricle at end of filling)
• Stroke volume = ~70 mL (blood ejected per beat)
• End-systolic volume (ESV) = ~40-50 mL (blood remaining after ejection)
• Ejection fraction (EF) = ~60% (stroke volume ÷ EDV) - normally ~60%, falls in heart failure

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SECTION 8: Heart Valves Prevent Backflow

AV Valves (Mitral and Tricuspid)

• Prevent backflow from ventricles into atria during systole
• Have chordae tendineae (string-like cords) attached to papillary muscles on the ventricular walls
• When ventricles contract, papillary muscles also contract → pull chordae taut → prevent valve leaflets from everting back into the atria
• If chordae rupture or papillary muscles fail → valve prolapses → regurgitation

Semilunar Valves (Aortic and Pulmonary)

• Each has 3 cup-shaped cusps - no chordae needed
• When ventricles relax and pressure drops, blood flows backward slightly from arteries → fills the cups → cusps push together and snap shut
• Extremely efficient - open with almost no resistance, close with no leakage

Heart Sounds

• Valves opening makes no sound (slow, gradual process)
• Sounds come from vibration of valve leaflets + surrounding blood when valves snap shut

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SECTION 9: Work Output of the Heart

• Stroke work output = energy converted to work each beat, pumping blood from low-pressure veins to high-pressure arteries
• Two components:
  1. Volume-pressure work (external work) - the major component; moving blood against pressure
  2. Kinetic energy - accelerating blood through valves; normally only ~1% of total work
  • Exception: in aortic stenosis, kinetic energy can be >50% of total work (blood forced through narrow valve at high velocity)
• Right ventricle does ~1/6 the work of the left ventricle (because pulmonary pressure is ~1/6 systemic pressure)

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SECTION 10: Ventricular Volume-Pressure Relationship

• Diastolic pressure curve = how ventricular pressure rises as volume increases during filling
  • Below 150 mL: pressure stays low → blood fills easily
  • Above 150 mL: pressure rises sharply (fibrous tissue + pericardium can stretch no more)
• Systolic pressure curve = pressure generated during contraction at each volume
  • Peaks at ~150-170 mL filling volume
  • If stretched beyond this, systolic pressure actually falls (actin-myosin filaments pulled too far apart, fewer cross-bridges form)
• Physiological limits of cardiac output:
  • Maximum pumping occurs at optimal filling volume
  • Overfilling or underfilling both reduce efficiency

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SECTION 11: Regulation of Heart Pumping

Intrinsic Regulation - The Frank-Starling Mechanism

• The heart automatically pumps all the blood that comes to it from the veins
• More blood in = heart muscle stretches more = contracts with greater force = pumps more out
• Mechanism: stretching brings actin-myosin filaments to a more optimal overlap for cross-bridge formation → greater force
• This keeps right and left ventricular outputs perfectly balanced - if one side pumps a little more, the other side gets more blood, stretches more, and catches up automatically
• Bainbridge reflex: Stretch of the right atrium also directly increases heart rate by 10-20% (minor additional boost)

Ventricular Function Curves

• Plotting stroke work output vs. mean atrial pressure gives the ventricular function curve (Starling curve)
• As atrial pressure (filling pressure) rises → stroke work increases → demonstrates the Frank-Starling law graphically
• Left ventricle works at much higher pressures than the right ventricle

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SECTION 12: Nervous Control - Sympathetic and Parasympathetic

Sympathetic Stimulation

• Increases heart rate (chronotropy): 70 → 180-200 beats/min (up to 250 in extremes)
• Increases contractile force (inotropy): doubles force of contraction
• Net result: cardiac output can increase 2-3 fold
• At rest, sympathetic nerves fire continuously at a slow rate keeping output ~30% above zero-sympathetic baseline

Parasympathetic (Vagal) Stimulation

• Strong stimulation can briefly stop the heartbeat, then heart "escapes" at 20-40 beats/min
• Reduces contractile strength by 20-30%
• Vagal fibers go mainly to the atria, not ventricles → effect is mainly on heart rate, not contraction strength
• Combined effects can reduce ventricular pumping by 50% or more

Cardiac Function Curve (Whole Heart)

• Plots right atrial pressure vs. cardiac output
• Sympathetic stimulation shifts curve up and left (more output for same filling)
• Parasympathetic stimulation shifts curve down and right (less output for same filling)

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SECTION 13: Effect of Potassium Ions

• Excess K⁺ (hyperkalemia): Heart becomes dilated, flaccid, slow
  • High extracellular K⁺ depolarizes the resting membrane (less negative potential)
  • This reduces action potential intensity → weaker contraction
  • K⁺ of 8-12 mEq/L (2-3x normal) can cause severe weakness, arrhythmia, and death
  • Can also block conduction through the AV bundle

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SECTION 14: Effect of Calcium Ions

• Excess Ca²⁺ (hypercalcemia): Opposite of K⁺ - heart moves toward spastic contraction
  • Directly activates the contractile process
• Deficient Ca²⁺ (hypocalcemia): Cardiac weakness (similar to hyperkalemia)
• Clinically, Ca²⁺ is tightly regulated in the blood → cardiac effects of abnormal Ca²⁺ are rarely a clinical concern

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SECTION 15: Effect of Temperature

• Fever / high temperature: Greatly increases heart rate (can double it)
  • Heat increases membrane permeability to ions → speeds up the self-excitation process
  • Moderate temperature rise (e.g., exercise) temporarily enhances contractile strength
  • Prolonged high temperature exhausts cardiac metabolic systems → weakens the heart
• Hypothermia / low temperature: Greatly decreases heart rate → can fall to a few beats/min near death (60-70°F / 15-21°C)

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SECTION 16: Arterial Pressure Load vs. Cardiac Output

• Increasing aortic pressure does NOT reduce cardiac output - until arterial pressure rises above ~160 mmHg
• In the normal range (80-140 mmHg systolic), cardiac output is determined almost entirely by how easily blood flows through the peripheral tissues (venous return), not by how hard the heart has to push against arterial pressure
• The heart automatically compensates for increased pressure load via the Frank-Starling mechanism

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QUICK REVISION TABLE

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What's included in the PDF:

• Cover page with title and chapter details
• 16 color-coded sections covering every topic in Chapter 9:
  • Cardiac muscle types and anatomy
  • Syncytium and gap junctions
  • Action potentials and the plateau
  • Excitation-contraction coupling and Ca²⁺
  • The cardiac cycle (all phases)
  • Atria as primer pumps
  • Ventricular pumping phases with a full phase table
  • Heart valves and heart sounds
  • Work output, Frank-Starling, nervous control
  • Effects of K⁺, Ca²⁺, and temperature
• Formatted tables throughout for easy scanning
• Quick Reference table at the end - all 20 key numbers in one place (EDV, SV, EF, pressures, timing, rates)