Module #2 - Electrical Activity of the Heart Flashcards
What is syncytium?
Cardiac muscle fiber arrangement that allows rapid spread of electrical activity
What is automaticity?
Ability to spontaneously depolarize to action potential threshold
What is rhythmicity?
Regular generation of action potential by heart
What is NSR (normal sinus rhythm)?
Healthy heart –> heart beat originates from SA node @ ~ 70 bpm (resting)
What is bradycardia?
slowed HR
What is tachycardia?
elevated HR
Where does the spontaneous electrical activity of the heart originate?
SA node
Why does the electrical activity occur in the SA node?
Constant leakage of Na+ during diastole
What happens after the SA node reaches a certain threshold (d/t Na+ influx)?
Depolarization occurs –> spreads throughout atria –> systole (atrial contraction)
How fast does electrical depolarization need to occur?
Rapidly to allow for repolarization
How long is the electrical conduction time for atrial and ventricular depolarization?
0.2 seconds (will vary as HR changes)
Where is the SA node located?
R atria @ junction of SVC
What is the normal adult rate of action potentials in the SA node?
75 action potentials/minute
What is the rate of the SA node increased by?
Increased temp –> tachycardia w/ fever
Drugs –> effect nodal tissue
Inspiration
How does inspiration change the SA node rate?
Breifly decreases vagus tone to heart –> increase HR
What is respiratory sinus arrhythmia?
Normal occurrence –> result of inspiration/vagus reflex
What is the rate of the SA node decreased by?
Increased parasympathetic (vagus) influence
Decreased sympathetic influence
Meds –> digitalis (effects all nodal tissue)
After depolarization of the SA node, where does the depolarization spread?
Rapidly throughout atria
** ~ 0.1 s to spread complete atrial depolarization
What are the nodal pathways that travel throughout the atria?
Anterior
Middle
Posterior
What is the name of the anterior pathway and where does it transmit directly?
Bachmann bundle
Directly to left atria
Where does the posterior atrial pathway conduct?
SA node –> AV node
How long is the depolarization delayed at the AV node?
0.05 - 0.1 second
**slower conductivity of the node tissue
Which nervous system will shorten depolarization delay at the AV node?
Sympathetic nervous system
Which nervous system will prolong the depolarization delay at the AV node?
Parasympathetic (vagus) nervous system
Why is the depolarization delayed at the AV node?
Allows mechanical contraction of atria (atrial kick)
Where is the AV node located?
Right posterior portion of the intertribal septum
**just superior to tricuspid valve and anterior to osmium of coronary sinus
What is the normal adult rate of action potentials per minute @ the AV node?
50 action potentials per minute
What is the Bundle of His?
Continuation of AV node
Origin of right/left bundle branches
Where is the bundle of His located?
Posterior border of inter ventricular septum
How do the electrical Ap waves transmit through the Bundle of His?
Transmit quickly through bundle branches
Where does the Right Bundle Branch (RBB) go and is it branched?
Travels to right ventricular apex
Minimal branches
How is the Left Bundle Branch (LBB) branched?
2+ branches:
Left Anterior Bundle Branch (LABB)
Left Posterior Bundle Branch (LPBB)
What are the Purkinje fibers?
Terminal branches of the R/L Bundle Branches
Where doe the Purkinje fibers travel?
To ventricle apices
What do the Purkinje fibers do?
Rapidly transmit depolarization throughout ventricles
**spread from apex back to fibrous ring
How long does it take to spread complete ventricular depolarization?
~ 0.1 seconds
What is the intrinsic rate of action potentials per second of Purkinje fibers?
20 - 40 action potentials per second
Describe what is happening when you see a P wave on an ECG
SA node is depolarized and sends AP throughout atria
Action potential travels throughout atria via internal atrial pathways
~ 1/10 second to spread complete atrial depolarization
Describe what is happening when the AP arrives @ AV node
Slow conduction causes 1/10 second delay
**conductivity of AV nodal fibres influenced by ANS and drugs
What is the PR or PQ interval (not PR or PQ segment)?
Duration from start of atrial activation to start of ventricular activation
**Measured from beginning of P wave to beginning of Q or R wave (beginning of QRS complex)
What is the QRS complex
Ventricular depolarization
**may not always see a Q or S wave
What does the Q wave represent in the QRS complex?
Septal depolarization
What does the R wave represent in the QRS complex?
Ventricular depolarization
What does the S wave represent in the QRS complex?
Depolarization of the Purkinje fibrs
What is the ST segment (not St interval)?
Brief period of no electrical activity
**ventricles reach full depolarization
What does the T wave represent?
Ventricular depolarization
What does the U wave represent?
Repolarization of the papillary muscles or Purkinje fibers
Remnants of ventricular depolarization
Pathology (electrolyte disruption)
**not always seen
What is the QRS duration?
Ventricular depolarization
Atrial repolarization
What is the QT interval?
Ventricular depolarization
VEntricular repolarization
What is the ST interval (NOT ST segment)?
Ventricular depolarization
= QT interval - QRS duration
What is the difference between segments and intervals?
Segments = between waves
Intervals = include one or both waves
What is the normal P - R interval length?
0.12 - 0.20 seconds
When would you see lengthening of the P - R interval?
1° AV Block
What does an enlarged QRS represent?
Increase in duration
**Normal = 0.08 - 0.12 seconds
When would you see an enlarged QRS?
V-fib
Hyperkalemia
Bundle Branch Block
When would you see an enlarged QT interval?
Potential MI
Other pathologies
**Normal duration = 0.35 - 0.42 seconds
What are the causes of an elevated S - T segment?
Potential acute MI
Ischemia
Other pathologies
What are the causes of a depressed S - T segment?
Potential ischemia (myocardium receiving insufficient O2)
Acute posterior MI
Other Pathologies
What are the causes of a flat or inverted T-wave?
Potential ischemia ischemia
Hypokalemia
What are the causes of an elevated or tall T- wave?
Potential Hyperkalemia
What are the causes of a prominent U-wave?
Hypokalemia
What are examples of abnormal rhythms?
Heart Blocks
Ectopic Foci
Tachycardia
Ventricular Tachycardia
What is a heart block?
Complete/partial interruption of conduction between atria/ventricles
What is considered a complete heart block?
3rd degree heart block
What is considered an incomplete heart block?
1st and 2nd degree heart blcoks
What happens to the pacemaker during a 3rd degree heart block?
Ventricles become pacemaker
35 - 45 bpm (atria beating @ rapid rate)
What will the ECG pattern of a 3rd degree heart block look like?
The P waves occur at a faster rate that isn’t coordinated with the QRS waves.
What happens during 1st degree heart block?
All atrial impulses reach ventricles but takes “long time”
What does the ECG pattern of a 1st degree heart block look like?
This results in a longer, flatter line between the P and the R waves
What happens during 2nd degree heart block?
Some but not all atrial impulses reach the ventricles –> won’t have ventricular depolarization for every atrial depolarization
What will the ECG pattern of a 2nd degree heart block look like?
Pattern of QRS waves doesn’t follow each P wave as it normally would
What is an example of an ectopic foci?
PVC = preventricular contraction
What happens during PVC?
Myocardium in ventricle spontaneously depolarizes
What will the ECG pattern of PVC look like?
Unexpected QRS between normal sinus rhythm
What is atrial tachycardia?
Form of supra ventricular tachycardia (SVT)
Rapid heart rate originating in atria
Which is more deadly, ventricular tachycardia/fibrillation or atrial ventricular tachycardia/fibrillation?
Ventricular tachycardia/fibrillation
What happens to the heart during atrial tachycardia (besides pumping faster)?
Loses ability to pump efficiently
**Stasis of blood increases risk of clots
What is atrial flutter?
Atria contract 200 - 350 action potential (HR) per minute
** AV node/ventricles can’t keep up and “max out” around 200 bpm
What will pts w/ atrial flutter feel?
Characteristic sensations of regular palpitations
What is atrial fibrillation (A-fib)?
Chaotic, uncoordinated depolarization
Atria “contract” > 300 - 350 action potentials (HR) per minute
**most common arrhythmia encountered in clinical practice
What is ventricular tachycardia (V - tach)?
Rapid HR originating in ventricles
> 100 bpm and > 3 irregular beats (PVCs) in a row)
What can V - tach lead to?
Ventricular fibrillation
What is the treatment of Ventricular tachycardia?
Varies:
Can be acute emergency or may not require immediate intervention
What is ventricular fibrillation (VF or V - fib)?
Rapid, chaotic, uncoordinated ventricular contractions
Functionally heart can’t act as a pump
Is ventricular fibrillation an emergency?
YES!
Need BLS/ACLS interventions
Anything longer than few minutes = fatal
MC cause of death in MI = V-Fib
What are the 2 types of cardiac action potentials (AP’s)?
Slow Response Action Potential
Fast Response Action Potential
Where do slow response action potentials occur w/ in the heart?
Nodal Tissue –> SA node/AV node
Where do fast response action potentials occur w/ in the heart?
Purkinje Fibers
Myocardial Cells of Atria/Ventricles
What do the cardiac action potentials do?
Determine HR
Determine Contractility
Determine Conduction
What are the intrinsic and extrinsic factors that influence cardiac action potentials?
Autonomic Nervous System –> sympathetic, parasympathetic
Drugs –> Anti-arrhythmic meds
Extra Cellular Fluid Ion Concentrations –> Na+, K+, Ca2+
What are the distinguishing characteristics of slow response action potentials?
Leaky Membrane Potential
Drifting Resting Membrane Potential
Lack of Plateau
**all make SA node the pacemaker –> automaticity
What are the 3 phases of slow response action potentials?
Phase 4
Phase 0
Phase 3
** No Phase 1 or 2
What is Phase 4 of slow response action potential?
Slow depolarization
Which phase is responsible for automaticity during slow response action potential?
Phase 4
What happens during “leaky” membrane potential?
↑ Na+ into cell that depolarizes the membrane via “slow Na+ channels”
What happens during Phase 4 of slow response action potential once membrane potential reaches -50 mV?
signals ↑ Ca2+ into cell via “transient calcium channels”
When is an action potential triggered during Phase 4 of slow response action potential?
When Net total influx of Na+ and Ca2+ reach threshold (-40 to -30 mV)
What is Phase 0 of slow response action potential?
Upstroke
What happens during Phase 0 of slow response action potential?
↑↑ Ca2+ into cell via “slow long lasting calcium channels” –> depolarization of the membrane during action potential
What is Phase 3 of slow response action potentials?
Repolarization
What happens during Phase 3 of slow response action potentials?
↑↑ K+ out of cell = repolarization of the membrane back down to the resting membrane potential
What is required for fast response action potentials?
Action potential from adjacent cell
What are the phases of fast response action potential?
Phase 0
Phase 1
Phase 2
Phase 3
Phase 4
What is phase 0 of fast response action potential?
Upstroke
What happens during phase 0 of fast response action potential?
Action potential from adjacent cardiac cell depolarizes membrane to threshold voltage (approximately -70 mV)
Rapid ↑↑ Na+ into cell via fast Na+ channels that depolarizes the membrane
What is phase 1 of fast response action potential?
Initial repolarization
What happens during phase 1 of fast response action potential?
Initial ↑ K+ out of cell via transient K+ channels begins to repolarize the membrane
What is phase 2 of fast response action potential?
Plateau
What happens during phase 2 of fast response action potential?
↑ Ca2+ into cell via “slow long lasting calcium channels” that causes a plateau in the depolarization
** prolongs mechanical contraction, allows for adequate ejection for ventricles
What is phase 3 of fast response action potential?
Repolarization
What happens during phase 3 of fast response action potential?
↑↑ K+ out of cell combined with inactivation of “slow long lasting calcium channels” repolarizes the membrane back down to the resting membrane potential
What is phase 4 of fast response action potential?
Resting membrane potential
What happens during phase 4 of fast response action potential?
Inward/outward currents of K+ maintain resting membrane potential
↑ Ca2+ and Na+ channels closed (?)
Where does the parasympathetic nervous system innervate the heart?
SA/AV nodes
Atria
Where does the sympathetic nervous system innervate the heart?
Atria
Ventricles
Nodes
What is the parasympathetic action on the heart?
↓ HR
↓ Conduction velocity
↓ Contractility of atria (small effect)
How does the parasympathetic nervous system achieve its effects?
Promote/prolong K+ efflux out; Inhibit Na+ and Ca2+ influx into pacemaker cells
What is the primary effect of parasympathetic stimulation on the atria?
hyperpolarizes cell membrane and decreases slope/increases duration of phase 4
What is the parasympathetic effect on phase 3?
Hyperpolarize d/t ↑ K+ efflux out
What is the sympathetic action on the heart?
↑ HR
↑ Contractility
↑ Relaxation rate
** less relaxation time
How does the sympathetic nervous system achieve its effects?
Promote/prolong Ca2+ influx into pacemaker and cardiac muscles cells in both atria and ventricles
What is the sympathetic effect on cardiac muscle cells and what does that mean?
↑ amplitude of Phase 2 –> ↑ contractility/↓ relaxation time
What is the sympathetic effect on pacemaker cells and what does that mean?
↑ slope/↓ duration of Phase 4 –> ↑ rate/conduction velocity
What are the 5 main classes in the Vaughan Williams classification of anti-arrhythmic agents?
Class I agents = Na+ channel blockers
Class II agents = Beta blockers
Class III agents = K+ channel blockers
Class IV agents = Ca2+ channel blockers
Class V agents = unknown mechanism
What do class I agents do?
Inhibit Na+ channels –> ↓ HR
How do class I agents ↓ HR?
Slows rate of depolarization of myocardial cells of atria/ventricles –> Phase 0
Slows rate of “leaky membrane” depolarization of nodal cells –> Phase 4
What are the Class Ia agents?
Quinidine
Procainamide
Disopyramie
What are the Class Ib agents?
Lidocaine
Mexiletine
Tocainide
Phenytoin
What are the Class Ic agents?
Encainide
Flecainide
Moricizine
Propafenone
What are the Class II agents (beta blockers) do?
↓ HR
↓ Contractility
How do Class II agents (beta blockers) work?
Inhibit sympathetic activity on nodal cells/myocardial cells
Name the Class II agents
Esmolol
Proranolol
Metoprolol
What do the class III agents do?
↓ HR
How do the class II agents ↓ HR?
Prolong K+ efflux –> prolong repolarization period
Name the class III agents
Amiodarone
Azimilide
Bretylium
Clofilium
Dofetilide
Tedisamil
Ibutilide
Sematilide
Sotalol
What do class IV agents do?
↓ HR
↓ contractility of heart
How do class IV agents ↓ HR and ↓ contractility of heart?
Slow rate of depolarization of nodal cells (phase 0)
Inhibit plateau (phase 2)
What are the 2 examples of class IV agents?
Verapamil
Diltiazem
What is the only drug he has listed for class V agents?
Digoxin (digitalis)
What does digoxin (digitalis) do?
↓ HR
How does digoxin (digitalis) ↓HR ?
Stimulates CNS to ↑ parasympathetic activity on AV node
What does [Na+] change in the ECF do to the heart?
Produces electrical changes of cardiac cells
**not as severe as alterations in ECF K+
What does [K+] change in the ECF do to the heart
Alters repolarization
What happens to the heart under hyperkalemic conditions?
Bradycardia
**severe hyperkalemia –> heart stopping
What happens to phase 0 (fast response) under hyperkalemic conditions?
Resting membrane potential “lessens” (more positive) as ECF K+ ↑
Why does the HR slow in response to hyperkalemic conditions?
D/t slower conduction velocity of the myocardial cell –> prolonged P wave, PR interval, QRS
**as cell membrane “lessens” (goes from -80 –> -70 –> -60) the conduction velocity slows
What happens to Phase 2 and 3 (fast response) under hyperkalemic conditions?
↑ efflux of K+ out of myocardium during depolarization phases –> peaked T wave, shorten QT interval, ST set changes
Shortened repolarization
What is the characteristic INITIAL ECG changes under hyperkalemic conditions?
Initial ↑ P-R interval
Shortening of QT interval
Tall/symmetric/peaked T waves
What is the characteristic PROGRESSION ECG changes under hyperkalemic conditions?
Widening of QRS interval
Disappearance of P wave
Nodal/escape ventricular arrhythmias
What are the characteristic TERMINAL ECG changes under hyperkalemic conditions?
QRS complex degenerates into sine wave pattern
Ventricular fibrillation/asystole “flatline”
What happens to the heart under hypokalemic conditions?
Tachycardias
Arrhythmias
**can be fatal but coexisting morbidities just as fatal
Why does hypokalemia cause tachycardias and arrhythmias?
Unlike other cells in the body cardiac cells become HYPERexcitable
What happens to phase 2 and 3 (fast response) under hypokalemic conditions?
↑ ECF will prolong/slow depolarization –> delayed membrane potential –> reentrant arrythmias
What is the INITIAL ECG change you would see under hypokalemic conditions?
Sagging of ST segment
T waves become progressively smaller
U wave becomes progressively larger
**don’t confuse this w/ QT prolongation
What can hypokalemia do to contractions?
May produce premature ventricular/atrial contraction/tachyarrhythmias; 2nd or 3rd degree atrioventricular block
All can lead to potential ventricular fibrillation
What happens to the heart under hypercalcemic conditions?
Cardiac rigor –> heart unable to relax
Plateau of APs is prolonged
Ca2+ w/in cardiac muscle-cross-bridge cycling would not be able to “release”
**super rare
