Notes from guy ton of extrinsic cardiac conduction with image

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Here are the complete notes on Extrinsic Control of Cardiac Conduction from Guyton and Hall:

Extrinsic Control of Cardiac Conduction

Guyton and Hall Textbook of Medical Physiology

Overview: The Cardiac Nerves

The heart receives both sympathetic and parasympathetic innervation, as shown in Figure 9.14 below:

Cardiac sympathetic and parasympathetic nerves - Fig. 9.14 from Guyton & Hall. The vagi (parasympathetic) descend from above to the SA and AV nodes; the sympathetic chain on either side sends nerves that spread across all cardiac muscle.

Figure 9.14 - Cardiac sympathetic and parasympathetic nerves. AV = atrioventricular; SA = sinoatrial.

Distribution:

Parasympathetic (Vagus nerves): Mainly to SA node and AV node; some to atrial muscle; very little to ventricular muscle
Sympathetic nerves: Distributed to ALL parts of the heart - strong representation in ventricular muscle as well as all other areas

1. Parasympathetic (Vagal) Stimulation - SLOWS Rhythm & Conduction

Neurotransmitter: Acetylcholine (ACh) released at vagal endings

Effects:

Effect	Detail
Decreases SA node rhythm	Slows heart rate
Decreases AV node excitability	Slows impulse transmission to ventricles
Weak-moderate stimulation	Reduces heart rate to ~half normal
Strong stimulation	Can completely stop SA node OR completely block AV conduction

Ventricular Escape

When strong vagal stimulation blocks the SA node or AV conduction, the ventricles stop for 5-20 seconds, after which Purkinje fibers in the ventricular septal portion of the AV bundle take over at 15-40 beats/min - this is called ventricular escape.

Mechanism (Why ACh Slows the Heart)

ACh increases membrane permeability to K+ → rapid K+ leakage out of conductive fibers → hyperpolarization (inside becomes more negative than usual).

In the SA node:

Resting membrane potential shifts from the normal -55 to -60 mV down to -65 to -75 mV
The spontaneous upward drift (pacemaker potential) takes longer to reach threshold
→ Rate of self-excitation is greatly slowed; strong stimulation can stop it entirely

In the AV node:

Hyperpolarization reduces the ability of small atrial fibers to generate enough current to excite nodal fibers
Safety factor for AV transmission decreases
Moderate decrease = delayed conduction; large decrease = complete block

2. Sympathetic Stimulation - INCREASES Rhythm & Conduction

Neurotransmitter: Norepinephrine, acting on beta-1 adrenergic receptors

Effects (opposite to vagal):

Increases rate of SA nodal discharge (positive chronotropy)
Increases rate of conduction and excitability in ALL parts of the heart
Increases force of contraction in both atria and ventricles (positive inotropy)

Key figures: Maximal sympathetic stimulation can nearly triple heart rate and increase contractile strength by up to 2-fold.

Mechanism (Why Norepinephrine Speeds the Heart)

Beta-1 receptor activation increases permeability to Na+ and Ca2+ → membrane becomes more positive (resting potential more positive).

In the SA node:

More positive resting potential + faster upward drift of diastolic potential toward threshold
→ Heart rate increases (accelerated self-excitation)

In the AV node & AV bundle:

Increased Na+/Ca2+ permeability makes it easier for the action potential to excite each successive fiber
→ Conduction time from atria to ventricles decreases

In the myocardium:

Increased Ca2+ permeability → stronger cross-bridge cycling
→ Increased contractile strength

Summary Comparison Table

Parameter	Parasympathetic (Vagal)	Sympathetic
Neurotransmitter	Acetylcholine	Norepinephrine
Receptor	Muscarinic (M2)	Beta-1 adrenergic
Ion channel change	↑ K+ permeability	↑ Na+/Ca2+ permeability
Membrane effect	Hyperpolarization	More positive resting potential
SA node rate	Decreases	Increases
AV conduction	Slows or blocks	Faster
Contractility	Minimal effect (little ventricular innervation)	Increases up to 2x
Main targets	SA node, AV node, atria	Entire heart (strong in ventricles)

Source: Guyton and Hall Textbook of Medical Physiology, Chapter 10, pp. 140-141

Parasympathetic av node explain in simple

Here's the simple explanation right away:

The vagus nerve releases ACh → K+ leaks out → AV node gets "too negative" (hyperpolarized) → harder for the electrical signal to pass through → conduction slows or blocks completely.

Parasympathetic Effect on the AV Node - Simply Explained

Think of it like a Security Checkpoint

The AV node is like a security gate between the atria (upper chambers) and ventricles (lower chambers). Every heartbeat signal must pass through this gate.

The vagus nerve is like a guard that can slow down or close that gate.

Step by Step - What Happens

Step 1: Vagus nerve fires

Releases acetylcholine (ACh) onto the AV node

Step 2: ACh opens K+ channels

Potassium ions rush OUT of the cell
The inside of the cell becomes more negative than usual
This is called hyperpolarization

Step 3: The cell is now "harder to excite"

Normal resting state = -65 mV (easy to fire) After vagal stimulation = even more negative (hard to fire)

Think of it like a spring that is already compressed - you need more force to compress it further. The signal coming from the atria no longer has enough "push" to fire the AV node easily.

Step 4: Result depends on how strong the stimulation is

Vagal Strength	What Happens
Mild	Slight delay in conduction (longer PR interval on ECG)
Moderate	Noticeably slower conduction to ventricles
Strong	Complete AV block - signal cannot pass at all

What Happens After Complete Block?

If the AV node is fully blocked, the ventricles don't just stop forever. The Purkinje fibers (lower down in the heart) act as a backup pacemaker:

Ventricles pause for 5-20 seconds → then Purkinje fibers fire on their own at 15-40 beats/min

This backup rhythm is called ventricular escape - the ventricles "escape" from the blocked signal and make their own slow rhythm to keep blood pumping.

One-Line Summary

Vagus nerve → ACh → K+ out → hyperpolarization → AV node hard to excite → slow or blocked conduction → if totally blocked, Purkinje fibers take over (ventricular escape at 15-40 bpm)

Source: Guyton and Hall Textbook of Medical Physiology, Ch. 10

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