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Guyton & Hall - UGA Final Exam Study Guide

Chapters 9, 10, 11, 14, 15, 16

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CHAPTER 9 - Cardiac Muscle; The Heart as a Pump and Function of the Heart Valves

1. Structure of Cardiac Muscle

• The heart has two functional syncytia: the atrial syncytium and the ventricular syncytium, separated by fibrous tissue around the A-V valves.
• Cardiac cells are connected by intercalated discs - cell membranes that fuse into permeable gap junctions, allowing ions to flow freely between cells. This makes cardiac muscle act as one unit ("syncytium").
• Cardiac muscle is striated like skeletal muscle with actin and myosin filaments, but contracts ~15x longer.
• The left ventricle has helical fiber layers (subepicardial spirals leftward, subendocardial spirals rightward) producing a twisting/wringing motion during systole that aids ejection and a spring-like recoil during diastole.

2. Cardiac Action Potential Phases

• Key difference from skeletal muscle: Phase 2 plateau caused by L-type Ca2+ channels (slow calcium channels / calcium-sodium channels). This prolongs contraction 15x longer than skeletal muscle.
• Conduction velocity: 0.3-0.5 m/sec in atrial/ventricular muscle; up to 4 m/sec in Purkinje fibers.

3. Refractory Period

• Absolute refractory period: ~0.25-0.3 seconds (nearly as long as the contraction itself) - prevents tetanus in cardiac muscle.
• Relative refractory period: follows the absolute; a stronger-than-normal stimulus can cause an early (premature) contraction.

4. Excitation-Contraction Coupling

1. Action potential spreads along T tubules.
2. Voltage-dependent L-type Ca2+ channels in T tubule membrane open.
3. Ca2+ entering the cell triggers ryanodine receptor channels (calcium-release channels) in the sarcoplasmic reticulum.
4. Massive Ca2+ release into sarcoplasm - "calcium-induced calcium release."
5. Ca2+ binds troponin → cross-bridge formation → contraction (sliding filament mechanism).
6. Relaxation: Ca2+ pumped back into SR by Ca2+-ATPase; excess removed by Na+/Ca2+ exchanger.

5. Heart Valves

• A-V valves (tricuspid = right; mitral/bicuspid = left): prevent backflow from ventricles to atria during systole. Supported by chordae tendineae attached to papillary muscles.
• Semilunar valves (aortic and pulmonary): prevent backflow from arteries into ventricles during diastole. No chordae - must be strong fibrous tissue.
• Valves open and close passively based on pressure gradients.
• Mitral valve prolapse can result from papillary muscle paralysis (e.g., myocardial infarction).

6. Cardiac Cycle - Key Pressures & Volumes

• End-diastolic volume (EDV): ~110-120 mL normally; can reach 150-180 mL.
• End-systolic volume (ESV): ~40-50 mL normally; can decrease to 10-20 mL with strong contraction.
• Stroke volume (SV) = EDV - ESV ≈ 70 mL normally.
• Atrial pressure: right ~0 mm Hg, left ~7 mm Hg (both during contraction).
• Systolic aortic pressure: ~120 mm Hg. Diastolic: ~80 mm Hg.
• Incisura (dicrotic notch): brief pressure blip when aortic valve snaps closed.

7. Frank-Starling Law of the Heart

• "The heart pumps all the blood that comes into it" - the more the heart is filled during diastole, the more forcefully it contracts.
• Mechanism: increased stretch → optimal overlap of actin/myosin → greater force.
• Allows the heart to automatically match cardiac output to venous return.

8. Work Output of the Heart

• Stroke work output = stroke volume × pressure against which blood is pumped.
• Left ventricle pumps ~6x more pressure work than right (systemic vs. pulmonary pressures).
• Cardiac reserve: the maximum percentage increase in cardiac output above normal (~300-400% in trained athletes; ~100-200% in untrained; <0% in severe heart failure).

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CHAPTER 10 - Rhythmical Excitation of the Heart

1. SA Node - The Pacemaker

• Located at the junction of the superior vena cava and right atrium.
• Has an intrinsic self-excitation rate of ~70-80 beats/min (under autonomic tone; inherent rate ~100/min).
• Slow diastolic depolarization (pacemaker potential): resting membrane potential is never stable - drifts from -55 to -40 mV, then fires.
• Caused by: progressive decrease in K+ permeability + "funny current" (If - slow Na+/K+ inward current) + T-type Ca2+ channels.

2. Conduction System (in order of activation)

1. SA node → generates impulse
2. Internodal pathways (anterior, middle, posterior) → conduct to AV node
3. AV node (in the lower posterior right atrium) → delays signal ~0.09-0.13 sec (total AV delay ~0.16 sec)
4. Bundle of His → carries impulse through fibrous septum
5. Left and Right Bundle Branches → down interventricular septum
6. Purkinje fibers → rapidly spread impulse through ventricular myocardium (4 m/sec)

• AV nodal delay is physiologically important: allows atria to contract and fill the ventricles before ventricular contraction begins.

3. Autonomic Control of Heart Rate

• Parasympathetic excess: can briefly stop the heart; causes escape rhythms.
• Vagal tone normally keeps resting heart rate at ~70 beats/min.

4. Ectopic Pacemakers

• Any part of the heart can become a pacemaker if the SA node fails or if local tissue becomes hyper-excitable.
• AV nodal rate: ~40-60 beats/min. Purkinje rate: ~15-40 beats/min.
• Ectopic beats (premature contractions) can occur in atria or ventricles.

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CHAPTER 11 - The Normal Electrocardiogram (ECG)

1. ECG Basics

• The ECG records extracellular electrical currents generated by the spreading wave of depolarization/repolarization across the heart.
• Depolarization wave moving TOWARD a positive electrode → upward deflection.
• Repolarization wave moving AWAY from a positive electrode → upward deflection (ventricular T wave is positive because repolarization spreads in the opposite direction to depolarization in the ventricle).

2. Normal ECG Waves

• Atrial repolarization (atrial T wave) is hidden within the QRS complex.

3. Depolarization vs. Repolarization Waves

• Depolarization wave = caused by spread of positive charge.
• Repolarization is NOT simply the reverse of depolarization - it spreads in an opposite direction (from epicardium to endocardium in ventricles), which is why the T wave is in the same direction as the QRS.

4. Standard Leads

• Limb leads (I, II, III): bipolar leads forming Einthoven's triangle.
• Augmented limb leads (aVR, aVL, aVF): unipolar.
• Precordial leads (V1-V6): unipolar chest leads.
• Einthoven's law: Lead II = Lead I + Lead III (at any moment).

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CHAPTER 14 - Overview of the Circulation: Pressure, Flow, and Resistance

1. Ohm's Law of Circulation

F = ΔP / R

• F = blood flow; ΔP = pressure difference across a vessel; R = resistance.
• It is the pressure difference, not absolute pressure, that drives flow. Two ends at the same pressure = zero flow.

2. Vascular Resistance Principles

• Poiseuille's Law: R = (8ηL) / (πr⁴)
  • Radius is the most powerful determinant - doubling the radius decreases resistance by 16x (r⁴ relationship).
  • η = viscosity; L = vessel length.
• Series resistance: R_total = R1 + R2 + R3...
• Parallel resistance: 1/R_total = 1/R1 + 1/R2 + 1/R3... → parallel circuits greatly reduce total resistance.
• Arterioles are the primary site of resistance in the circulation.

3. Blood Viscosity

• Normal blood viscosity: ~3x that of water.
• Determined primarily by hematocrit (the fraction of blood that is red blood cells).
• Hematocrit 40-45% = normal viscosity.
• Polycythemia (high hematocrit) → greatly increased viscosity → increased resistance.
• Plasma viscosity is ~1.5x water (due to proteins).

4. Laminar vs. Turbulent Flow

• Laminar (streamline) flow: blood flows in concentric layers; central velocity fastest (parabolic profile).
• Turbulent flow: occurs when Reynolds number (Re) > 2000-3000.
  • Re = (v × d × ρ) / η
  • v = velocity; d = diameter; ρ = density; η = viscosity.
  • Turbulence occurs with high velocity, large diameter, low viscosity, or at sharp bends/obstructions.
  • Turbulence creates audible sounds (murmurs/bruits) and greatly increases resistance.

5. Blood Flow Measurement

• Electromagnetic flowmeter: based on the principle that a conductor (blood) moving through a magnetic field generates a voltage proportional to flow.
• Ultrasonic Doppler flowmeter: measures frequency shift of reflected ultrasound; can record pulsatile flow.

6. Autoregulation of Blood Flow

• Tissues maintain relatively constant blood flow over a wide range of arterial pressures (70-175 mm Hg).
• Mechanism: local metabolic control - increased metabolism → vasodilation → restores flow.
• Law of Laplace: T = P × r (wall tension = pressure × radius) - explains why large aneurysms are prone to rupture.

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CHAPTER 15 - Vascular Distensibility and the Arterial/Venous Systems

1. Vascular Compliance (Distensibility)

• Compliance (C) = ΔV / ΔP - the volume increase per unit pressure increase.
• Veins are ~8x more compliant than arteries - they act as capacitance vessels.
• Arteries are relatively stiff - they function as pressure reservoirs (Windkessel effect), maintaining diastolic pressure by elastic recoil.
• The venous system contains >60% of total blood volume.

2. Arterial Pulse Pressure

• Pulse pressure = Systolic - Diastolic pressure (normally ~40 mm Hg).
• Mean arterial pressure (MAP) ≈ Diastolic + 1/3 × Pulse Pressure (or ≈ 93 mm Hg normally).
• Pulse pressure is increased by: increased stroke volume, decreased arterial compliance (arteriosclerosis), hyperthyroidism.
• Pulse pressure is decreased by: decreased stroke volume (heart failure), aortic stenosis.

3. Venous Return and Venous Pressure

• Central venous pressure (CVP): normally ~0 mm Hg at the right atrium.
• Elevated CVP: right heart failure, blood volume overload.
• Venous valves prevent retrograde flow in peripheral veins.
• Muscle pump: skeletal muscle contraction compresses veins and pushes blood toward the heart.
• Respiratory pump: inspiration decreases intrathoracic pressure → increases venous return.
• Veins constrict in response to sympathetic stimulation (venomotor tone) - important for mobilizing blood volume.

4. Blood Pressure Measurement

• Korotkoff sounds (heard with a stethoscope over the brachial artery as cuff pressure is released):
  • First sound = systolic pressure.
  • Last sound (muffles/disappears) = diastolic pressure.

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CHAPTER 16 - The Microcirculation, Capillary Fluid Exchange, Interstitial Fluid, and Lymph Flow

1. Capillary Structure and Exchange

• Continuous capillaries: tight junctions; least permeable (brain - blood-brain barrier).
• Fenestrated capillaries: pores in endothelium; more permeable (kidneys, intestine, endocrine glands).
• Discontinuous (sinusoidal) capillaries: large gaps; most permeable (liver, bone marrow, spleen).
• Water and small solutes cross via intercellular cleft pores (6-7 nm). Lipid-soluble substances cross directly through membranes.

2. Starling Forces - Capillary Fluid Exchange

Net filtration = Kf × [(Pc - Pif) - σ(πp - πif)]

• Slightly more fluid is filtered than reabsorbed. The excess is drained by the lymphatics.

3. Edema Formation

1. Increased capillary hydrostatic pressure (right heart failure, venous obstruction).
2. Decreased plasma oncotic pressure (hypoalbuminemia - liver disease, nephrotic syndrome, malnutrition).
3. Increased capillary permeability (inflammation, burns, allergic reactions).
4. Lymphatic obstruction (lymphedema - cancer, filariasis).

4. Lymphatic System

• Lymph capillaries are blind-ended with large intercellular gaps and anchoring filaments that pull them open when interstitial pressure increases.
• Lymph flow is propelled by: intrinsic rhythmic contraction of lymph vessel walls, compression by skeletal muscle, respiratory pressure changes.
• Lymphatic valves prevent backflow.
• Thoracic duct drains most of body into left subclavian vein. Right lymphatic duct drains right side.
• After a fatty meal, chylomicrons (fat droplets) enter intestinal lymphatics (lacteals) → thoracic duct → bloodstream.
• Safety factor against edema: ~17 mmHg total (due to increased lymph flow, decreased interstitial oncotic pressure as protein dilutes, and slightly negative baseline Pif).

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High-Yield Quick-Reference

Key Numbers to Memorize

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Practice Questions

1. Why can't cardiac muscle undergo tetanus like skeletal muscle?
   • Because the absolute refractory period (~0.25-0.3 sec) lasts almost as long as the contraction itself, preventing summation.
2. What two types of ion channels cause the plateau of the cardiac action potential?
   • L-type (slow) Ca2+ channels AND fast Na+ channels (the plateau is mainly maintained by Ca2+ channels).
3. A patient has ischemia of the papillary muscles. What valve problem would you expect?
   • Mitral valve regurgitation due to prolapse - the chordae tendineae are no longer held properly.

• Heart rate increases because vagal (parasympathetic) tone normally keeps rate suppressed below the SA node's intrinsic rate.

1. Why is the AV nodal delay physiologically important?
   • It gives the atria time to contract and fill the ventricles with blood before ventricular contraction begins.

• Because ventricular repolarization spreads in the opposite direction (epicardium to endocardium) compared to depolarization, so the T wave is also a positive deflection toward the recording electrode.

• Resistance decreases by 16x (r⁴ relationship in Poiseuille's Law).

1. Why does turbulent flow create heart sounds (murmurs)?
   • Turbulence creates chaotic, cross-directional flow that vibrates vessel walls and produces audible sounds.

• Elastic recoil (Windkessel effect) - arteries stretch during systole and recoil during diastole, pushing blood forward and maintaining pressure.

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