Cardiovascular/Heart (ch.18) Pt2

18.5 Electrical Events of the Heart

• Heart depolarizes and contracts without nervous system stimulation, although rhythm can be altered by AUTONOMIC NERVOUS SYSTEM 

• Coordinated heartbeat is a function of:

1. Presence of GAP JUNCTIONS

2. Intrinsic cardiac conduction system

• Network of noncontractile (autorhythmic) cells

• Initiate and distribute impulses to coordinate depolarization and contraction of heart

Action potential initiation by pacemaker cells

• Cardiac pacemaker cells have unstable resting membrane potentials called pacemaker potentials or prepotentials

• Three parts of action potential:

1. PACEMAKER POTENTIAL: K⁺ channels are closed, but slow Na⁺ channels are open, causing interior to become MORE POSITIVE (or less negative)

2. DEPOLARIZATION: Ca²⁺ channels open (around –40mV), allowing huge influx of Ca²⁺, leading to rising phase of action potential

3. REPOLARIZATION: K⁺ channels open, allowing efflux of K⁺, and cell becomes MORE NEGATIVE

   1. Setting the Basic Rhythm: The Intrinsic Conduction System - Sequence of excitation

      1. Cardiac pacemaker cells pass impulses, in following order, across heart in ~0.22 seconds

         1. Sinoatrial node →

         2. Atrioventricular node →

         3. Atrioventricular bundle →

         4. Right and left bundle branches →

         5. Subendocardial conducting network (Purkinje fibers)

1. SINOATRIAL (SA) NODE

   1. PACEMAKER of heart in right atrial wall

      1. Depolarizes faster than rest of myocardium

   2. Generates impulses about 75×/minute (sinus rhythm)

      1. Inherent rate of 100×/minute tempered by extrinsic factors

      2. Impulse spreads across atria, and to AV node

2. ATRIOVENTRICULAR (AV) NODE

   1. In inferior interatrial septum

   2. Delays impulses approximately 0.1 second

      1. Because fibers are smaller in diameter, have fewer gap junctions

      2. Allows atrial contraction prior to ventricular contractions

   3. Inherent rate of 50×/minute in absence of SA node input

3. ATRIOVENTRICULAR (AV) BUNDLE (bundle of HIS)

   1. In superior interventricular septum

   2. Only ELECTRICAL connection between atria and ventricles

      1. Atria and ventricles not connected via GAP JUNCTIONS

4. RIGHT & LEFT BUNDLE BRANCHES

   1. Two pathways in interventricular septum

   2. Carry impulses toward APEX of heart

5. SUBENDOCARDIAL CONDUCTING NETWORK

   1. Also referred to as PURKINJE FIBERS fibers

   2. Complete pathway through interventricular septum into apex and ventricular walls

   3. More elaborate on LEFT side of heart → PUMPS TO SYSTEMIC CIRCUIT

   4. AV bundle and subendocardial conducting network depolarize 30/minute in absence of AV node input

   5. Ventricular contraction immediately follows from apex toward atria

   6. Process from initiation at SA node to complete contraction takes ~0.22 seconds

Clinical – Homeostatic Imbalance 18.4

• Defects in intrinsic conduction system may cause:

  • ARRHYTHMIAS: irregular heart rhythms

    • Uncoordinated atrial and ventricular contractions

  • FIBRILLATION: rapid, irregular contractions

    • Heart becomes useless for pumping blood, causing circulation to cease; may result in brain death

    • Treatment: DEFIBRILLATION interrupts chaotic twitching, giving heart “clean slate” to start regular, normal depolarizations

• Defective SA node may cause ectopic focus, an abnormal pacemaker that takes over pacing

  • If AV node takes over, it sets junctional rhythm at 40-60 beats/min

  • EXTRASYSTOLE (premature contraction): ectopic focus of small region of heart that triggers impulse before SA node can, causing delay in next impulse

    • Heart has LONGER time to fill, so next contraction is felt as thud as larger volume of blood is being pushed out

    • Can be from excessive caffeine or nicotine

• To reach ventricles, impulse must pass through AV node

• If AV node is defective, may cause a heart block

  • Few impulses (partial block) or no impulses (total block) reach ventricles

  • Ventricles beat at their own intrinsic rate

    • Too slow to maintain adequate circulation

  • Treatment: ARTIFICIAL PACEMAKER, which recouples atria and ventricles

Modifying the Basic Rhythm: Extrinsic Innervation of the Heart

• Heartbeat modified by ANS (symp/parasymp) via cardiac centers in 

  • CARDIOACCELERATORY CENTER: sends signals through sympathetic trunk to increase both rate and force

    • Stimulates SA and AV nodes, heart muscle, and coronary arteries

  • CARDIOINHIBITORY CENTER: parasympathetic signals via VAGUS NERVE (X) to decrease rate

    • Inhibits SA and AV nodes via vagus nerves

Action Potentials of Contractile Cardiac Muscle Cells

• Contractile muscle fibers make up bulk of heart and are responsible for pumping action

  • Different from skeletal muscle contraction; cardiac muscle action potentials have plateau

Steps involved in AP:

1. Depolarization opens fast voltage-gated Na⁺ channels; Na⁺ enters cell

   1. POSITIVE feedback influx of Na⁺ causes rising phase of AP (from 90 mV to +30 mV)

2. Depolarization by Na⁺ also opens slow Ca²⁺ channels

   1. At +30 mV, Na⁺ channels close, but slow Ca²⁺ channels remain open, prolonging depolarization

      1. Seen as a PLATEAU

3. After about 200 ms, slow Ca²⁺ channels are closed, and voltage-gated K⁺ channels are open

   1. Rapid efflux of K⁺ repolarizes cell to RMP

   2. Ca²⁺ is pumped both back into SR and out of cell into extracellular space

Difference between contractile muscle fiber and skeletal muscle fiber contractions

• AP in skeletal muscle lasts 1-2 ms

  • Cardiac muscle it lasts 200 ms

• Contraction in skeletal muscle lasts 15–100 ms

  • Cardiac contraction lasts over 200 ms

• Benefit of longer AP and contraction:

  • Sustained contraction ensures efficient EJECTION of blood

  • Longer refractory period prevents TETANIC contractions

Electrocardiography

ELECTROCARDIOGRAM GRAPH → can detect electrical currents generated by heart

ELECTROCARDIOGRAM (ECG or EKG) is a graphic recording of electrical activity

• Composite of all action potentials at given time; not a tracing of a single AP

• Electrodes are placed at various points on body to measure voltage differences

  • 12—LEAD ECG is most typical

• Main features:

  • P WAVE: depolarization of SA node and atria

  • QRS COMPLEX: ventricular depolarization and atrial repolarization

  • T WAVE: ventricular repolarization

  • P–R INTERVAL: beginning of atrial excitation to beginning of ventricular excitation

  • S–T SEGMENT: entire ventricular myocardium DEPOLARIZED

  • Q–T INTERVAL: beginning of ventricular depolarization through ventricular repolarization

Problems that can be detected:

• Enlarged R waves may indicate ENLARGED VENTRICLES → (HCM hypertrophic cardiomyopathy)

• Elevated or depressed S-T segment indicates CARDIAC ISCHEMIA

Prolonged Q-T interval reveals a repolarization abnormality that increases risk of VENTRICULAR ARRHYTHMIAS