Ventricular Muscle Action Potential, Conducting System of Heart, Type 216 Heart Block, List the factors affecting venous return.

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This Comparison Chart illustrates the electrocardiographic (ECG) characteristics of Atrioventricular (AV) blocks. It features three stacked rhythm strips categorized as First, Second, and Third-degree heart blocks, emphasizing the relationship between P waves (atrial depolarization) and QRS complexes (ventricular depolarization). The 'First degree heart block' panel demonstrates a consistent 1:1 P-to-QRS ratio with a fixed, prolonged PR interval. The 'Second degree heart block' panel shows intermittent conduction failure, where specific P waves are not followed by a QRS complex. The 'Third degree heart block' panel depicts complete AV dissociation, where P waves and QRS complexes occur independently and at different rates, indicating a total interruption of impulse transmission and the presence of a ventricular escape rhythm. This diagnostic illustration is designed for cardiovascular education to help students and clinicians distinguish between different stages of cardiac conduction system disease and their associated clinical significance.

This diagnostic image consists of a series of four electrocardiogram (ECG) rhythm strips demonstrating the rapid clinical progression of atrioventricular (AV) conduction abnormalities over a period of 4.5 hours. The top panel, labeled 'Time point 0', shows an ectopic atrial rhythm with organized P-wave activity and narrow QRS complexes. The second strip, recorded 2.5 hours later, displays a second-degree Mobitz type II AV block, characterized by intermittently dropped QRS complexes without preceding PR interval lengthening. The third strip, 30 minutes later, indicates a first-degree AV delay (prolonged PR interval) and intraventricular conduction delay (widened QRS). The final rhythm strip at 4.5 hours shows third-degree (complete) AV block, characterized by complete AV dissociation and a slow, wide QRS complex ventricular escape rhythm. This progression illustrates acute cardiac conduction system failure, typically associated with myocardial infiltration or severe injury, as seen in patients with leukemic infiltration of the heart.

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1. Ventricular Muscle Action Potential

(Guyton and Hall Textbook of Medical Physiology)

The action potential recorded in a ventricular muscle fiber averages about 105 millivolts - the intracellular potential rises from approximately -85 mV (resting) to about +20 mV at peak, before repolarizing.

The hallmark feature is a prolonged plateau lasting ~0.2-0.3 second, which makes ventricular contraction last up to 15 times longer than skeletal muscle contraction.

Phases of the Ventricular Action Potential

Ventricular action potential phases with ionic currents

Figure 9.5 - Phases of action potential of cardiac ventricular muscle cell and associated ionic currents (Na+, Ca2+, K+). Guyton & Hall.

Phase	Name	Key Ion Events
Phase 0	Rapid Depolarization	Voltage-gated fast Na+ channels open → rapid Na+ influx → membrane potential rises to +20 mV
Phase 1	Initial Repolarization	Fast Na+ channels close; K+ leaves through open K+ channels
Phase 2	Plateau	L-type Ca2+ channels (slow Ca2+ channels) open → Ca2+ and Na2+ influx; K+ channels close → prolonged depolarization
Phase 3	Rapid Repolarization	Ca2+ channels close; slow K+ channels open → rapid K+ efflux → return to resting potential
Phase 4	Resting Membrane Potential	Stable at -80 to -90 mV; no spontaneous depolarization (unlike SA/AV nodal cells)

Why is There a Plateau? (Two Key Mechanisms)

L-type Ca2+ channels (slow channels): In cardiac muscle, the AP is sustained by both fast Na+ channels AND slow Ca2+ channels. The slow Ca2+ channels remain open for several tenths of a second, maintaining depolarization.
Decreased K+ permeability: Immediately after AP onset, K+ permeability drops ~5-fold (unlike skeletal muscle). This prevents early K+ efflux, sustaining the plateau.

When slow Ca2+ channels finally close at the end of 0.2-0.3 s, K+ permeability rapidly increases, K+ rushes out, and repolarization is complete.

Note: Healthy ventricular muscle has no If current (funny current) and therefore shows no pacemaker activity. The resting potential is stable at -80 mV between beats.

Conduction velocity in ventricular muscle: 0.3-0.5 m/sec. In Purkinje fibers: up to 4 m/sec.

2. Conducting System of the Heart

(Color Atlas of Human Anatomy Vol. 2 + Guyton & Hall)

The conducting system consists of specialized cardiac muscle cells that generate and propagate impulses to coordinate cardiac contraction.

Components (in Sequence of Impulse Transmission)

Structure	Location	Rate (impulses/min)	Notes
Sinoatrial (SA) Node (Keith-Flack node)	Posterior wall of right atrium, near SVC opening, in sulcus terminalis cordis	60-80	Primary pacemaker; spindle-shaped, ~10 mm long; lies beneath the epicardium
Atrioventricular (AV) Node (Aschoff-Tawara node)	Atrioventricular septum, interatrial septum; between coronary sinus opening and septal cusp of tricuspid valve	50-60	~5 mm long; only normal electrical bridge from atria to ventricles; introduces physiological conduction delay
Bundle of His (AV bundle)	Penetrates cardiac skeleton toward ventricles; reaches superior margin of muscular interventricular septum	-	Trunk divides into right and left bundle branches
Right Bundle Branch	Curves down; enters septomarginal trabecula; reaches anterior papillary muscle	-	Ends in subendocardial plexus at apex
Left Bundle Branch	Fans out in flat bundles along interventricular septum; usually divides into two major fascicles	-	Reaches base of papillary muscles; subendocardial networks
Purkinje Fibers	Subendocardial networks throughout ventricles	25-45	Fastest conduction (up to 4 m/sec); distribute impulse to working myocardium

Key Functional Principles

Hierarchy of pacemakers: The SA node fires fastest so it drives the others. If SA fails, AV node takes over; if AV node fails, the ventricles (Purkinje system) take over at 25-45/min.
AV delay: The AV node introduces a conduction delay (~0.12 s) to allow atrial contraction to complete before ventricular systole begins.
One-way conduction: The AV node is the only normal electrical pathway from atria to ventricles. There is no other route.
ECG correlation: SA node activity → P wave; AV delay → PR interval; Bundle branch/ventricular activation → QRS complex.

3. Heart Block (Type 2:1 / "Type 216" context)

(Braunwald's Heart Disease + Guyton & Hall)

Heart block is a disturbance of impulse conduction - it must be distinguished from interference, which is physiologic refractoriness from a preceding impulse.

Classification of AV Block

First-Degree AV Block

Every atrial impulse is conducted to the ventricles (1:1 relationship preserved).
PR interval > 0.20 second (normal ≤ 0.20 s). Prolongation up to 1.0 second has been recorded.
No dropped beats; regular ventricular rate.
PR interval seldom exceeds 0.35-0.45 s (beyond that, conduction ceases entirely).
Usually caused by AV node delay; QRS is typically normal.
ECG finding: Prolonged PR interval with normal QRS.
Clinical: Often benign; used to gauge severity in rheumatic carditis.

Figure 13.5 - Prolonged P-R interval caused by first-degree AV heart block (lead II). Guyton & Hall.

Second-Degree AV Block (with 2:1 Block = "Type 216")

Some atrial impulses are NOT conducted to the ventricles - there are "dropped beats" (P waves without QRS complexes).

Mobitz Type I (Wenckebach):

Progressive lengthening of PR interval until one P wave is not conducted (dropped beat), then the cycle resets.
Almost always caused by abnormality in the AV node.
Generally benign; usually no pacemaker required.

Mobitz Type II:

Sudden block of conduction without prior PR prolongation - the PR interval is fixed before the dropped beat.
Typically caused by abnormality of the His-Purkinje system.
May show 2:1, 3:1, or 3:2 ratios (e.g., 2:1 = two P waves for every one QRS complex - the "Type 216" pattern).
More dangerous - risk of progression to complete heart block; pacemaker implantation often required.

Third-Degree (Complete) AV Block

Complete dissociation between atrial and ventricular activity.
P waves and QRS-T complexes are totally independent of one another.
Atrial rate: ~100 beats/min; Ventricular (escape) rate: < 40 beats/min.
Ventricles "escape" and beat at their own intrinsic rate from a subsidiary pacemaker (usually distal AV node or His bundle).

Figure 13.7 - Complete AV block (lead II) - note independent P waves and QRS complexes. Guyton & Hall.

Comparison of first, second, and third-degree heart blocks on ECG.

Causes of AV Block (Guyton & Hall)

Ischemia of AV node or AV bundle fibers (coronary insufficiency)
Compression of the AV bundle by scar tissue or calcification
Inflammation (endocarditis/myocarditis from diphtheria, rheumatic fever)
Excessive vagal stimulation (e.g., carotid sinus syndrome - rare)
Degeneration of the AV conduction system (elderly patients)
Medications: Digitalis, beta-adrenergic antagonists

Stokes-Adams Syndrome

When complete block comes and goes (intermittent), the ventricles may fail to pick up their own rhythm for 5-30 seconds (overdrive suppression). During this period, no blood is pumped and the patient faints (syncope - "Stokes-Adams attacks"). These patients typically require an artificial pacemaker.

4. Factors Affecting Venous Return

(Guyton and Hall Textbook of Medical Physiology)

Venous return can be calculated by the formula:

VR = (Psf - PRA) / RVR

Where: VR = venous return, Psf = mean systemic filling pressure, PRA = right atrial pressure, RVR = resistance to venous return

Normal values: VR = 5 L/min, Psf = 7 mm Hg, PRA = 0 mm Hg, RVR = 1.4 mm Hg/L/min

The three principal factors affecting venous return are:

1. Right Atrial Pressure (Back-Pressure Effect)

Right atrial pressure (PRA) impedes the flow of blood from veins into the right atrium.
As PRA rises, venous return falls (backward force dams blood in the systemic circulation).
Venous return falls to zero when PRA rises to equal Psf (~7 mm Hg).
When PRA falls below atmospheric pressure (~-2 mm Hg), veins entering the chest collapse - creating a plateau (venous return cannot increase further even with more negative PRA).

2. Mean Systemic Filling Pressure (Psf) - "Driving Force"

This is the pressure throughout the systemic circulation when all blood flow stops - it represents the degree of filling of the systemic circulation.
Normal Psf = 7 mm Hg.
Psf is the force that pushes blood toward the heart.
Increased Psf (e.g., from increased blood volume, sympathetic vasoconstriction) shifts the venous return curve to the right → increases venous return.
Decreased Psf (e.g., hemorrhage, vasodilation) shifts the curve left → decreases venous return.

3. Resistance to Venous Return (RVR)

Most RVR occurs in the veins (~2/3), with the remainder in arterioles and small arteries (~1/3).
When venous resistance increases, blood dams in veins; but since veins are highly distensible, venous pressure rises very little - so resistance is poorly overcome.
When arteriolar resistance increases, blood dams in arteries (low capacitance = 1/30th that of veins), arterial pressure rises sharply, and this pressure overcomes resistance more effectively.
A decrease in RVR to half-normal doubles venous return (rotates the venous return curve upward).
An increase in RVR to twice normal halves venous return.

Additional / Secondary Factors Affecting Venous Return

Factor	Effect on Venous Return
Blood volume (increased)	Increases Psf → increases venous return
Skeletal muscle pump	Muscle contractions compress veins → propels blood toward heart
Respiratory pump	Inspiration → negative intrathoracic pressure → expands right atrium/great veins → increases venous return
Sympathetic venoconstriction	Compresses capacitance vessels → raises Psf → increases venous return
Gravity/Posture	Standing: venous pooling in legs → decreases venous return; Supine: increases venous return
Valves in peripheral veins	Prevent retrograde flow; essential for effectiveness of muscle pump
Cardiac pumping ability	More vigorous pumping lowers PRA → enhances venous return gradient

Sources:

Guyton and Hall Textbook of Medical Physiology - Chapters 9, 10, 13, 20
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine - Chapter 68
Color Atlas of Human Anatomy, Vol. 2: Internal Organs

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