Rhythmical Excitation of the Heart

Rhythmical Excitation of the Heart

Overview

The heart's rhythmic excitation is essential for its function and is driven by specialized cells known as pacemaker cells.

Membrane Potential and Cardiac Pacemaker Cells

Millivolts

  • The action potential (AP) of cardiac pacemaker cells undergoes specific voltage changes, as detailed below:

    • Maximum potential: +20 mV

    • Threshold for discharge: -40 mV

    • Resting potential: -80 mV

Graphical Representation

  • A graphical representation depicts the membrane potential over time in seconds, showing changes in cardiac pacemaker cells.

Components of Membrane Potential

  • Resting Potential

    • The resting potential is around -80 mV.

    • Maintenance of the resting potential is crucial for normal cardiac rhythm.

  • Pacemaker Potential

    • This slow depolarization occurs due to:

    • Opening of sodium (Na\+) channels

    • Closing of potassium (K\+) channels

    • The membrane potential displays continuous fluctuation and does not reach a flat line.

  • Depolarization

    • Initiated when the pacemaker potential reaches the threshold.

    • Primarily driven by the influx of calcium (Ca2+).

  • Repolarization

    • Caused by:

    • Inactivation of Ca2+ channels

    • Opening of K\+ channels, resulting in K\+ efflux and returning the membrane potential to its negative voltage.

Action Potential Phases

  1. Pacemaker Potential

  2. Depolarization

  3. Repolarization

Sinoatrial (SA) Node

  • The SA node is specialized cardiac muscle located in the wall of the right atrium.

    • Features:

    • Fibers contain almost no contractile muscle filaments

    • Capable of self-excitation

    • Directly connected to the atrial muscle

    • Functions as the heart's natural pacemaker, controlling the entire heart's beating rate.

Atrioventricular (AV) Node

  • Located in the posterior wall of the right atrium behind the tricuspid valve.

  • Function: Delays cardiac impulse to ensure coordinated contraction.

    • Key delays include:

    • AV node delay: 0.09 seconds

    • AV bundle delay: 0.04 seconds

  • Inquiry: What causes the slow conduction?

AV Bundles

  • Function as a one-way conduction pathway from the atria to the ventricles.

  • Structure: Divided into left and right bundles.

  • Transmission time from AV bundles to ventricular fibers is approximately 0.06 seconds (QRS time).

Purkinje System

  • Composed of fibers leading from the AV bundle into the ventricles.

  • Characterized by:

    • Large fibers transmitting action potentials at velocities of 1.5 to 4 m/sec.

    • Facilitates nearly instantaneous transmission of cardiac impulses through the ventricular muscle due to many gap junctions in intercalated disks.

Pathway of the Heartbeat

Sequence of Events

  1. Impulse Generation by the SA Node: Pacemaker initiates impulses.

  2. Pause at the AV Node: Impulses experience a 0.1-second pause.

  3. AV Bundle Connection: Connects atria to ventricles.

  4. Bundle Branches: Conduct impulses through the interventricular septum.

  5. Subendocardial Conducting Network: Depolarizes contractile cells of both ventricles, facilitated by Purkinje fibers.

Time of Arrival of Cardiac Impulse

A detailed timeline depicts the time of arrival of the cardiac impulse at each key point, demonstrating the conduction pathway and delay times related to each node and bundle.

Delay Times

  • SA Node: 0.07 seconds

  • A-V Node: 0.09 seconds

  • QRS Transmission: 0.06 seconds

Clinical Imbalance - Arrhythmias

  • Definition: Irregular heart rhythms characterized by uncoordinated atrial and ventricular contractions.

  • Causes include:

    • Abnormal rhythmicity of the pacemaker.

    • Shift of pacemaker from the sinus node.

    • Blocks in various points of cardiac impulse transmission.

    • Abnormal pathways of transmission.

    • Spontaneous generation of abnormal impulses from different heart regions.

Clinical Snapshots

Tachycardia

  • Defined as a fast heart rate, usually greater than 100 beats/minute.

Bradycardia

  • Defined as a slow heart rate, typically less than 60 beats/minute.

Frank-Starling Mechanism

  • Intrinsic cardiac regulation of pumping ability relative to blood volume flowing into the heart.

    • Within physiological limits, the heart pumps all incoming blood.

    • Increased preload causes:

    • Stretching of cardiac muscle fibers

    • Enhanced force of contraction due to optimal actin and myosin filament overlap in the muscle.

Ventricular Fibrillation

  • The most severe form of cardiac arrhythmia where ventricles quiver instead of properly contracting.

    • May lead to minimal blood outflow from the heart.

    • Causes include electrical shock or ischemia of the cardiac muscle.

Ventricular Defibrillation

  • A treatment method involving the application of 1000 volts DC for short durations (a few milliseconds).

    • Results in refractoriness across the heart, lasting 3-5 seconds, until a new pacemaker establishes.

    • If the procedure is delayed beyond one minute post-fibrillation, the heart may weaken and require CPR.

Ischemic Heart Disease

  • Known as the leading cause of death in Western culture, affecting approximately 35% of individuals aged 65 and older in the US.

  • Characterized by inadequate coronary blood flow, which can arise from acute coronary occlusion or gradual weakening of cardiac function over time.

Atherosclerosis

  • A frequent contributor to decreased coronary blood flow, which may manifest as:

    • Thrombus: Local blood clot occluding the artery.

    • Coronary Embolus: A thrombus occluding a vessel further downstream.

    • Secondary Thrombosis: Resulting from coronary artery muscular spasms.

Myocardial Infarction (Heart Attack)

  • Defined by cell death areas repaired with noncontractile scar tissue.

  • Coronary circulation involves:

    • Left and right coronary arteries originating from the aorta.

    • Cardiac veins that collect blood from capillary beds to the coronary sinus, which empties into the right atrium.

Cardiac Arrest vs. Heart Attack

Cardiac Arrest

  • Occurs due to a malfunction in heart rhythm, causing it to stop beating unexpectedly.

  • Triggered by electrical malfunctions, leading to arrhythmias.

  • Symptoms include unresponsiveness, lack of breathing, and potential death within minutes without treatment.

    • Immediate Action:

    • Call emergency services (9-1-1) immediately.

    • Start CPR promptly.

    • Utilize an Automated External Defibrillator (AED) as soon as possible.

Heart Attack

  • Defined as a circulation issue, resulting from blocked blood flow to heart tissue.

  • Symptoms may occur abruptly and include chest discomfort, shortness of breath, sweats, and nausea/vomiting.

  • In contrast, the heart typically continues to beat during a heart attack which causes delayed treatment damage over time.

    • Women may experience symptoms that differ from men, including shortness of breath, nausea, and pain in the back, neck, or jaw.