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67 Cards in this Set

  • Front
  • Back
Fast Response AP
1) Atrial and ventricular myocytes 2) Purkinje fibers of the heart
Slow Response AP
1) SA node 2) AV node
Natural Pacemaker of the Heart
Sinoatrial node
Refractory Period
Interval from the beginning of the AP until the fiver is able to conduct another AP
Effective Refractory Period
Another AP cannot be generated
Relative Refractory Period
1) Another AP can be generated 2) Requires larger than normal depolarization membrane voltage
Timing of Atrial Contraction
1/6 of a second ahead of ventricular contraction
Timing of Ventricular Contraction
All portions of the ventricles contract almost simultaneously
Cardiac Excitation Overview
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
Automaticity
1) Ability of heart to initiate own beat 2) Cardiac function does not require intact innervation; perfused heart can beat outside of body
Rhythmicity
Regularity of pacemaking activity
SA Resting Membrane Potential
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
SA Node
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
SA Node Threshold
1) -40 mV 2) Activates Ca channels
Rate of Rise of SA Node Action Potential
Less rapid than cells of ventricular myocardium
AV Node Location
Posterior wall of right atrium immediately behind tricuspid valve
AV Node
1) Only direct electrical connection between atrial and ventricular chambers 2) Conduction delayed as electrical impulse reaches AV node
Ventricular Purkinje System
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
Purkinje Fibers
Penetrate about 1/3 of the way into the muscle mass and finally become continuous with the cardiac muscle fibers
Bundle Branches
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
Bundle of His
1) AV bundle 2) Receive electrical impulse from AV node 3) Divide into left and right bundle branches
Total Time for Transmission of Cardiac Impulse from Initial Bundle Branches to Ventricular Muscle Fibers
.06 seconds
Ventricular Muscle Fiber Velocity of Transmission
1) .3 to .5 m/s 2) 1/6 of the velocity in the Purkinje fibers
Transmission of Cardiac Impulse in Ventricular Muscle
Once the impulse reaches the ends of the Purkinje fibers, it is transmitted thru the ventricular muscle by the ventricular muscle fibers themselves
Determinants of Cell Firing Rates of Pacemaker
1) Rate of phase 4 spontaneous depolarization 2) Maximum negative diastolic potential (MDP) 3) Threshold potential (TP)
Rate of Phase 4 Spontaneous Depolarization
The steeper the slope of phase 4, the faster the cell depolarizes
The Maximum Negative Diastolic Potential
1) MDP 2) The more negative maximum diastolic potential, the slower the cell depolarizes
The Threshold Potential
1) TP 2) The less negative threshold potential, the slower the cell depolarizes
Control of Heart Rhythmicity and Impulse Conduction by Cardiac Nerves
1) Sympathetic Nervous System 2) Parasympathetic Nervous System
Control of Heart Rhythmicity and Impulse Conduction by Cardiac Nerves: SNS
1) Sympathetic nerves are distributed to all parts of heart 2) Increase SNS activity raises HR mainly by increasing rate of diastolic depolarization
Control of Heart Rhythmicity and Impulse Conduction by Cardiac Nerves: PNS
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
Latent Pacemakers
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
Rate of SA Node Discharge
1) 70 to 80 times per minute 2) Fastest pacemaker
Rate of AV Node Discharge
1) 40 to 60 time per minute 2) Intermediate pacemaker
Rate of Purkinje Fiber Discharge
1) 15 to 40 times per minute 2) Slowest pacemaker
Overdrive Suppression
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
Altered Impulse Formation
If the SA node becomes suppressed, the site of impulse formation shifts to latent pacemaker
Escape Rhythm
Continued series of escape beat
Escape Beat
Impulse initiated by a latent pacemaker
Types of Escape Beats
1) Junctional escape 2) Ventricular escape
Junctional Escape
Arises from the AV node of proximal Bundle of His
Ventricular Escape
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
Enhanced Automaticity of Latent Pacemakers
1) Situation where a latent pacemaker develops an intrinsic rate of depolarization faster than SA node 2) Produces ectopic beat
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
Ectopic Rhythm
Sequence of similar ectopic beats
Circumstances of 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
Afterdepolarizations
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
Early Afterdepolarizations
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
Conditions that Prolong AP
1) Therapy with certain drugs 2) Inherited long-QT syndromes 2) More likely to develop early afterdepolarizations
Early Afterdepolarization-Triggered AP
Self-perpetuating and lead to series of depolarization
Torsades de Pointes
1) Polymorphic ventricular tachycardia 2) Thought to be initiated by early afterdepolarizations
Delayed 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
Types of Afterdepolarizations
1) Early 2) Delayed
Tachycardia
Faster than normal heartbeat
States of High Intracellular Ca
1) Digitalis intoxication 2) Marked catecholamine stimulation
Delayed Afterpolarization Tachycardias
Some idiopathic ventricular tachycardias that occur in otherwise normal hearts are likely due to delayed afterpolarizations
Conduction Block
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
Conduction Block within the AV node or His-Purkinje System
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
Reentry
1) Under certain conditions, a cardiac impulse may re-excite some region through which it has already passed 2) Important mechanism of tachycardia generation
Unidirectional Block
Impulses can travel retrograde but not orthograde
Critical Conditions for Reentry
1) Unidirectional block 2) Slowed conduction through reentry path
Global Reentry
1) Between atria and ventricles 2) Often involves accessory conduction pathways such as bundles of Kent
Wolff-Parkinson-White Syndrome
Involves global reentry between atria and ventricles by bundle of Kent
Local Reentry
Local sites of reentry within a small region of ventricles or atrium can precipitate ventricular or atrial tachyarrhythmias, respectively
Reentry around Distinct Anatomic Pathways and ECG
1) Usually appear as monomorphic tachycardia on ACG 2) E.g. ventricular tachycardia
Reentry that Does Not Require Stable, Fixed Path
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.
Mechanism of Reentry
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