Physiology 1d: Cardiac Excitation

1) Atrial and ventricular myocytes 2) Purkinje fibers of the heart

1) SA node 2) AV node

Sinoatrial node

Interval from the beginning of the AP until the fiver is able to conduct another AP

Another AP cannot be generated

1) Another AP can be generated 2) Requires larger than normal depolarization membrane voltage

1/6 of a second ahead of ventricular contraction

All portions of the ventricles contract almost simultaneously

1) SA node initiates spread of AP thru atria 2) AP reaches AV node 3) Conduction slowed so atrial contraction occurs while ventricles fill before contraction 4) Excitation spreads rapidly thru ventricles via Purkinje fibers 5) Ventricular myocytes contract in coordinated fashion

1) Ability of heart to initiate own beat 2) Cardiac function does not require intact innervation; perfused heart can beat outside of body

Regularity of pacemaking activity

1) -55 to -60 mV 2) Cell membrane of sinus fibers naturally leaky to Na and Ca 3) Positive charges neutralize some intracellular negativity 4) Less negative membrane potential inactivates fast Na channels

1) More positive resting membrane potential 2) Cell gradually depolarizes during phase 4 due to inward flow of Na through slow channel (I_f) 3) When potential reaches threshold, Ca channels activate, generating AP 4) Repolarizes due to inactivation of Ca channels and opening of voltage-gated K channels that permit efflux of K

1) -40 mV 2) Activates Ca channels

Less rapid than cells of ventricular myocardium

Posterior wall of right atrium immediately behind tricuspid valve

1) Only direct electrical connection between atrial and ventricular chambers 2) Conduction delayed as electrical impulse reaches AV node

One way conduction of electrical impulse from AV node through the: 1) Bundle of His 2) Left and Right bundle branches 3) Ends in Purkinje fibers

Penetrate about 1/3 of the way into the muscle mass and finally become continuous with the cardiac muscle fibers

1) Divide into left and right bundle branches 2) Receive electrical impulse from Bundle of His 3) Progressively divide into smaller branches of Purkinje fibers

1) AV bundle 2) Receive electrical impulse from AV node 3) Divide into left and right bundle branches

.06 seconds

1) .3 to .5 m/s 2) 1/6 of the velocity in the Purkinje fibers

Once the impulse reaches the ends of the Purkinje fibers, it is transmitted thru the ventricular muscle by the ventricular muscle fibers themselves

1) Rate of phase 4 spontaneous depolarization 2) Maximum negative diastolic potential (MDP) 3) Threshold potential (TP)

The steeper the slope of phase 4, the faster the cell depolarizes

1) MDP 2) The more negative maximum diastolic potential, the slower the cell depolarizes

1) TP 2) The less negative threshold potential, the slower the cell depolarizes

1) Sympathetic Nervous System 2) Parasympathetic Nervous System

1) Sympathetic nerves are distributed to all parts of heart 2) Increase SNS activity raises HR mainly by increasing rate of diastolic depolarization

1) PNS nerves are distributed: A)
Mainly to SA and AV nodes B) Lesser extent to atrial muscle C) Little direct contact to ventricular muscle 2) Increased PNS activity diminishes HR by: A) Hyperpolarizing cell membrane B) Reducing rate of diastolic depolarization

1) AV node 2) Purkinje fibers 2) Impulse from the SA node discharges both the AV node and Purkinje fibers before self-excitation can occur in either of these 3) Latent pacemakers may initiate impulses and take over pacemaker function if: A) SA node slows B) Fails to fire C) Conduction abnormalities block the normal wave of depolarization from reaching them

1) 70 to 80 times per minute 2) Fastest pacemaker

1) 40 to 60 time per minute 2) Intermediate pacemaker

1) 15 to 40 times per minute 2) Slowest pacemaker

1) SA node suppress automaticity of latent pacemakers by hyperpolarizing the cells 2) When a cell is forced to fire faster than its intrinsic discharge rate, it stimulates the Na-K-ATPase to expell more Na from cell; resulting in their hyperpolarization

If the SA node becomes suppressed, the site of impulse formation shifts to latent pacemaker

Continued series of escape beat

Impulse initiated by a latent pacemaker

1) Junctional escape 2) Ventricular escape

Arises from the AV node of proximal Bundle of His

1) Arises from a more distal point in the conduction system 2) Very strong PSN stimulation suppresses excitability at both the SA and AV nodes; allowing the Purkinje fibers to develop rhythm of its own

1) Situation where a latent pacemaker develops an intrinsic rate of depolarization faster than SA node 2) Produces ectopic beat

1) Impulse is premature relative to normal rhythm cause by enhanced automaticity of latent pacemakers 2) Develops in cells that do not usually possess automaticity, like myocytes

Sequence of similar ectopic beats

1) High catecholamine concentrations can enhance the automaticiy of latent pacemakers, and if the resulting rate of depolarization exceeds that of sinus node, then ectopic rhythm develops 2) Hypoxemia, ischemia, electrolyte disturbances, and certain drug toxicities 3) Injured myocytes' membranes become leaky and resting potential becomes less negative, allowing gradual phase 4 depolarization in nonpacemaking cells

1) Oscillations of the membrane voltage that follow the first AP that result in abnormal APs 2) Results in: A) Extra heart beats or B) Rapid arrhythmias

1) Occur during plateau of AP (phase 2) or during rapid repolarization (phase 3) 2) More likely to develop in conditions that prolong the AP 4) Appear to be initiating mechanism of torsades de pointes

1) Therapy with certain drugs 2) Inherited long-QT syndromes 2) More likely to develop early afterdepolarizations

Self-perpetuating and lead to series of depolarization

1) Polymorphic ventricular tachycardia 2) Thought to be initiated by early afterdepolarizations

1) Appear shortly after repolarization is complete 2) Develop in states of high intracellular Ca 3) If amplitude reaches threshold voltage, AP will be generated; such AP can be self-perpetuating and lead to tachyarrhythmias

1) Early 2) Delayed

Faster than normal heartbeat

1) Digitalis intoxication 2) Marked catecholamine stimulation

Some idiopathic ventricular tachycardias that occur in otherwise normal hearts are likely due to delayed afterpolarizations

1) Can be transient or permanent 2) Caused by ischemia, fibrosis, inflammation, and certain drugs 3) Conduction block within the specialized conduction system of AV node or His-Purkinje system prevents

Prevents normal propagation of cardiac impulse 2) Allows latent pacemakers to function, leading to escape beats/rhythms 3) AV block is common and major reason for implantation of permanent pacemaker

1) Under certain conditions, a cardiac impulse may re-excite some region through which it has already passed 2) Important mechanism of tachycardia generation

Impulses can travel retrograde but not orthograde

1) Unidirectional block 2) Slowed conduction through reentry path

1) Between atria and ventricles 2) Often involves accessory conduction pathways such as bundles of Kent

Involves global reentry between atria and ventricles by bundle of Kent

Local sites of reentry within a small region of ventricles or atrium can precipitate ventricular or atrial tachyarrhythmias, respectively

1) Usually appear as monomorphic tachycardia on ACG 2) E.g. ventricular tachycardia

1) Spiral waves 2) In the ventricles, resulting tachycardia has continually changing QRS appearance producing polymorphic ventricular tachycardia. If such activation is rapid and very disorganized no distinct QRS complexes will be discernable and rhythm is ventricular fibrillation.

A) When AP reaches branch in conduction pathway (x), impulse travels down both fibers (α and β) to excited distal tissue B) Forward passage of impulse is blocked in β pathway but proceeds down the α path, when impulse reaches point y, if retrograde conduction of β path is intact, the AP can enter β from below and conduct in retrograde fashion C) When point x is reached again, if α path has not had sufficient time to repolarize, then impulse stops D) However, if conduction thru retrograde path is slow, it reaches x after α path has recovered, allowing impulse to excite α path again and a reentrant loop is formed