BIOL 2314 Chapter 20- The Heart Conduction 03

Cardiac Muscle Contraction

• Autorhythmic – generates its own action potentials without external nerves.
• Requires continual ATP supply for cross-bridge cycling.
• Contraction is longer and more prolonged than in skeletal muscle (≈3–5× duration).
• Structural features:
• Intercalated disks – gap junctions & desmosomes → electrical synctium; rapid AP spread.
• Smaller sarcoplasmic reticulum (↓ SR) than skeletal → must import extracellular $Ca^{2+}$ .
• Longer T-tubules extend to Z-lines → aid in uniform Ca^{2+} delivery.
• Excitation–contraction coupling is dominated by extracellular Ca^{2+}-induced Ca^{2+} release (CICR):

Voltage-gated L-type $Ca^{2+}$ channels open in T-tubule membrane.
Influx of extracellular $Ca^{2+}$ triggers ryanodine receptors on SR.
Massive SR release ↑ cytosolic $Ca^{2+}$ → binds troponin → contraction.
Removal: $Ca^{2+}$ -ATPase pumps (SERCA) + $Na^+$ / $Ca^{2+}$ exchanger return Ca^{2+} to SR/exterior.

Cardiac vs. Skeletal Action Potentials

• Cardiac contractile AP timeline (Fig. 20.15):

Rapid depolarization – fast $Na^+$ channels open (influx); $K^+$ channels close.
Early repolarization halted by opening of slow L-type $Ca^{2+}$ channels (influx) → Plateau (~175 ms).
Plateau ends when $Ca^{2+}$ channels close, slow $K^+$ channels fully open (efflux) → Repolarization back to $-90\,\text{mV}$ .
• Skeletal AP has no plateau; lasts ~2 ms.
• Functional consequences:
• Cardiac AP ≈250–300 ms → extended refractory period (prevents tetanus).
• Skeletal muscle can tetanize because refractory (<5 ms) ends long before peak tension.

Refractory Periods & Tension Development

• Absolute refractory period – membrane completely insensitive to new APs; spans the entire plateau and early repolarization.
• Relative refractory period – some $Na^+$ channels reset; only suprathreshold stimuli elicit AP.
• In cardiac muscle, peak mechanical tension develops during absolute refractory period ⇒ another contraction cannot start until relaxation begins.
• Graphical comparison (Page 4/5):
• Cardiac tension curve overlaps AP.
• Skeletal tension peaks after refractory ends, permitting summation/tetanus.

Sinoatrial (SA) Node Action Potential & Heart-Rate Hierarchy

• SA node = primary pacemaker (70–80 bpm at rest).
• Autorhythmic cell ion events (Fig. 20.13):

Pacemaker potential (prepotential): slow $Na^+$ & $Ca^{2+}$ leak in, $K^+$ channels gradually close → slow depolarization toward threshold (≈ $-40\,\text{mV}$ ).
Depolarization spike: T-type then L-type $Ca^{2+}$ channels open (influx); $K^+$ channels closed.
Repolarization: $Ca^{2+}$ channels close; $K^+$ channels open (efflux) → returns to $-60\,\text{mV}$ .
• Secondary pacemakers (ectopic foci):
• AV node: 40–60 bpm – drives rhythm if SA fails.
• Purkinje system / bundle branches: 15–40 bpm if higher centers fail.

Cardiac Conduction System (Fig. 20.12)

• Structural pathway:

SA node (roof of right atrium).
Internodal pathways → both atria; atria contract top-down.
Atrioventricular (AV) node – only electrical bridge between atria & ventricles; inherent delay (~0.09 s) allows ventricular filling.
AV bundle (Bundle of His) → left & right bundle branches in interventricular septum.
Purkinje fibers → subendocardium → ventricular myocardium; depolarize apex first, contraction proceeds apex → base (efficient ejection).
• Heart at rest: sequence 1 ↠ 5 produces one heartbeat.

Electrocardiogram (ECG/EKG)

• Composite recording of all heart electrical activity; detects depolarization & repolarization waves.
• Waves & intervals:
• P wave – atrial depolarization (atrial systole starts just after).
• PR interval – SA → AV conduction; prolonged in AV block.
• QRS complex – ventricular depolarization (ventricular systole begins); atrial repolarization hidden here.
• ST segment – ventricular plateau; elevated/depressed in ischemia/MI.
• T wave – ventricular repolarization (ventricular diastole begins).
• Relationship of electrical to mechanical:
• Depolarization precedes systole; repolarization precedes diastole.

Refractory Phases on ECG (Page 10)

• Absolute refractory period – spans QRS to mid-T.
• Relative refractory period – latter part of T wave.
• Supernormal period – brief period immediately after relative refractory; cells hyperexcitable.

Cardiac Arrhythmias Overview

• Any deviation from normal sinus rhythm (60–100 bpm, regular P→QRS→T, 1:1 conduction).

Rate-Related Arrhythmias

• Tachycardia (>100 bpm)
• Causes: ↑ sympathetic tone, fever, toxins, hypovolemia.
• Bradycardia (<60 bpm)
• Causes: ↑ stroke volume (athletes), ↑ vagal tone, medications, hypothermia.
• Sinus arrhythmia
• Respiratory-linked HR variation (5–30 %); accentuated in youth, can signal failure/inflammation/ischemia.

Ectopic Action Potential Arrhythmias

• Atrial flutter
• Rapid, regular atrial rate (≈250–350 bpm); 2–3 P waves per QRS.
• Atrial fibrillation
• Chaotic atrial activity, no discernible P waves, irregularly irregular ventricular rhythm; thrombosis risk.
• Ventricular fibrillation
• Rapid, chaotic ventricular depolarizations; no organized QRS; fatal without defibrillation.

Blockage Arrhythmias

• SA node block
• Etiology: ischemia, degenerative damage.
• ECG: absent P waves, overall ↓ HR; junctional escape may appear.
• AV node (heart block)
• 1st degree: prolonged PR.
• 2nd degree: some P not followed by QRS.
• 3rd degree: atria & ventricles dissociate; ectopic ventricular rate.
• Causes: inflammation, ischemia, ↑ vagal tone.
• Bundle branch block
• Damage/infection/MI; widened QRS (>0.12 s).
• Premature atrial contractions (PAC)
• Ectopic focus in atrium fires early; P wave may merge with previous T or superimpose on QRS.
• Triggers: caffeine, alcohol, lack of sleep, smoking.
• Premature ventricular contractions (PVC)
• Early ectopic beat from ventricle; wide, bizarre QRS, inverted T; risk of progressing to V-fib.
• Triggers: irritability, coronary thrombosis, stimulants, sleep loss.

Numerical & Statistical References

• Normal SA node rate: $70\text{–}80\,\text{bpm}$ .
• AV node intrinsic rate: $40\text{–}60\,\text{bpm}$ .
• Ventricular (Purkinje) intrinsic: $15\text{–}40\,\text{bpm}$ .
• Skeletal AP duration ≈ $2\,\text{ms}$ ; Cardiac ≈ $250\text{–}300\,\text{ms}$ .
• Plateau (cardiac) voltage ≈ $+30\,\text{mV}$ ; resting ≈ $-90\,\text{mV}$ .

Clinical / Practical Implications

• Long refractory period prevents tetanus – essential for rhythmic pumping.
• CICR means hypocalcemia reduces contractility; hypercalcemia can produce spastic contraction.
• ECG interpretation is cornerstone for diagnosing MI, electrolyte disorders, conduction blocks, arrhythmias.
• Arrhythmia etiology often multifactorial (autonomic, metabolic, structural), guiding pharmacologic or electrical therapy.
• Understanding conduction system enables targeted treatments: ablation of ectopic foci, pacemaker implantation, defibrillation.