Cardio Mod 2 Flashcards
4 terms associated with conducting system of the heart
- Syncytium
a. Cardiac muscle fiber arrangement allows rapid spread of electrical activity - Automaticity
a. Ability to spontaneously depolarize to action potential threshold - Rhythmicity
a. Regular generation of action potential by heart - NSR (normal sinus rhythm)
a. Healthy heart, heart beat originates from SA node approximately 70 bpm at rest
SA Node (sinoatrial): “pacemaker” of the heart
a. Depolarization initiated at SA node in healthy heart
b. Located in right atria at junction of SVC as it enters right atria
c. Rate of SA node
• “Normal” adult rate = 75 action potentials per minute
SA node is increased by:
(i) increase temp (thus tachycardia w/fever)
(ii) various drugs (effect all nodal tissue)
(iii) Inspiration
1. briefly decreases vagus tone to heart thus increase HR
2. Respiratory sinus arrhythmia – is normal occurrence and occurs as result of inspiration/vagus reflex
SA node is decreased by:
(i) Increase parasympathetic (vagus) influence
(ii) decrease sympathetic influence
(iii) meds: ex - digitalis (effects all nodal tissue)
Internodal atrial pathway
a. Depolarization spreads rapidly throughout atria
b. Approximately 0.1 second to spread complete atrial depolarization
c. Three named bundles travel throughout atria
• Anterior, middle and posterior nodal pathways
• Anterior pathway (Bachmann bundle) transmits directly to left atria
• Posterior pathway conducts SA node to AV node
AV Node (atrioventricular)
a. Depolarization “delayed” at AV node (0.05 - 0.1 seconds) due to slower conduction rate of the node tissue
• Sympathetic nervous system will shorten this delay
• Parasympathetic (vagus) will lengthen the delay
b. The delay allows mechanical contraction of atria (atrial kick)
c. AV node is located in right posterior portion of the interatrial septum
• just superior to tricuspid valve & anterior to ostium of coronary sinus
d. “Normal” adult rate = 50 action potentials per minute
Bundle of His and associated R/L bundle branches
a. “Continuation” of AV node located in posterior border of interventricular septum
b. Serves as origin of right/left bundle branches
c. Electrical AP wave transmits quickly down the septum through the bundle branches
R / L Bundle Branches
a. The Bundle of His splits into a pair of conductive pathways called the right and left bundle branches that run down the interventricular septum and continue toward ventricular apices.
b. Right Bundle Branch (RBB)
• Minimal branches as travels to right ventricular apex
c. Left Bundle Branch (LBB)
• May divide into two more branches
(i) Left Anterior Bundle Branch (LABB)
(ii) Left Posterior Bundle Branch (LPBB)
Purkinje fibers
a. Terminal branches of the R/L Bundle Branches Descend to ventricle apices
b. RAPIDLY transmits depolarization throughout ventricles
• Spread from apex back to fibrous ring
c. Approximately 0.1 seconds to spread complete ventricular depolarization
d. Intrinsic rate 20 – 40 action potentials per second
P wave
a. SA node is depolarized and sends AP throughout atria
b. Action potential travels throughout atria via internodal atrial pathways
c. Approximately 1/10 second to spread complete atrial depolarization
AP arrives at AV Node is delayed due to slow conduction
a. Slow conduction causes 1/10 second delay
b. Conductivity of AV nodal fibers will be influenced by ANS and drugs
PR or PQ interval
a. Represents duration from start of atrial activation to start of ventricular activation
b. Measured from beginning of P wave to beginning of Q or R wave (beginning of QRS complex)
QRS complex
a. Represents ventricular depolarization
• Q wave - septal depolarization
• R wave - ventricular depolarization
• S wave - depolarization of the Purkinje fibers
b. May not always see a Q or S wave on ECG
ST segment
a. As ventricles reach full depolarization there is brief period of no electrical activity
T wave
a. Represents ventricular repolarization
U wave
a. Not always seen, represent repolarization of the papillary muscles or Purkinje fibers.
b. May represent
• Repolarization of the papillary muscles or Purkinje fibers
• Remnants of ventricular repolarization
• Pathology (electrolyte disruption)
Summary of ECG Intervals
- PR Interval – atrial depolarization and conduction through AV node
- QRS duration – ventricular depolarization and atrial repolarization
- QT interval – ventricular depolarization and ventricular repolarization
- ST interval (not ST segment) – ventricular repolarization
a. ST Interval = QT interval minus QRS duration
P-R interval lengthening
- 1° AV Block
* Normal PR interval duration = 0.12 - 0.20 sec
Enlarged QRS
- Duration increased (normal QRS duration = 0.08-0.12 sec)
* V-fib, hyperkalemia, bundle branch block
Enlarged QT interval
- Normal duration = 0.35-0.43 sec
* potential myocardial infarction and many other pathologies
S-T segment elevation/depression
• Represents the time between the end of the spread of the impulse through the ventricles and repolarization of the ventricles.
• ELEVATED S-T segment
(i) Potential acute myocardial infarction (MI), ischemia, and many other pathologies
• DEPRESSED S-T segment
(i) Potential ischemia (myocardium receives insufficient oxygen), acute posterior MI and many other pathologies
T Wave flat or elevated
• Flat/inverted T-wave
(i) potential ischemia (myocardium receives insufficient oxygen), hypokalemia
• Elevated/tall T-wave
(i) potential hyperkalemia
Prominent U Wave
• Hypokalemia
Incomplete Heart Block– 1st and 2nd degree
(i) 1st degree block
1. all atrial impulses reach ventricle but takes “a long time”
(ii) 2nd degree block
1. Some but not all atrial impulses reach ventricles
2. therefore will not have ventricular depolarization for every atrial depolarization
Complete Heart block 3rd degree
• Complete block: 3rd degree heart block
(i) Complete disruption of conduction between atria and ventricles
(ii) Ventricles become pacemaker….usually at 35 – 45 bpm while atrial beating a rapid rate
Ectopic foci
• Example: PVC (preventricular contraction)
(i) Myocardium in ventricle spontaneously depolarizes
(ii) Result is unexpected QRS between normal sinus rhythm on ECG
Atrial Tachycardia
(i) Form of supraventricular tachycardia (SVT)
(ii) Rapid heart rate originating in atria
(iii) Less deadly than ventricular tachycardia/fibrillation
(iv) Heart losses ability to pump efficiently
1. stasis of blood increase risk clots
Atrial Flutter
- atria “contract” 200-350 action potential (HR) per minute
- characteristic sensations of regular palpitations
- NOTE: AV node and ventricles can’t keep up and “max out” around 200 bpm
Atrial Fibrillation
- atria “contract” > 300-350 action potentials (HR) per minute
- really chaotic, uncoordinated depolarization
- most common arrhythmia encountered in clinical practice
- NOTE: AV node and ventricles can’t keep up and “max out” around 200 bpm
Ventricular Tachycardia
- rapid HR originating in ventricles
- > 100 bpm and > 3 irregular beats (PVCs) in a row
- may lead to more lethal V-fib
- Treatment varies: acute emergency or may not require immediate intervention
Ventricular Fibrillation
- rapid, chaotic, uncoordinated ventricular contractions
- functionally heart can’t act as a pump
- MEDICAL EMERGENCY to activate BLS (basic life support)/ACLS (advanced cardiac life support) interventions
- Anything longer than few minutes – fatal
- MC cause of death in MI is V Fib
2 Types of Action Potentials in the Heart
• Slow response AP’s – occur in nodal tissue (SA and AV nodes)
• Fast response AP’s – occur in Purkinje fibers and myocardial cells of atria & ventricles
b. These AP’s essentially determine HR, contractility and conduction of heart
Intrinsic and Extrinsic Factors Influences on Cardiac Cell AP’s
a. Autonomic nervous system • Parasympathetic • Sympathetic b. Pharmaceuticals (WV classifications) • Anti-arrhythmic medications c. ECF ion concentration • Sodium (Na+) • Potassium (K+) • Calcium (Ca2+)
Slow Response Action Potential
a. Characteristic of SA and AV nodal cells
b. “Leaky membrane potential” or “drifting resting membrane potential” and lack of plateau are distinguishing characteristics of this AP
• the leaky/drifting resting membrane potential makes the SA node the “pacemaker”…automaticity
3 Phases of slow response action potential
• Phase 4 (slow depolarization)
(i) this phase is responsible for automaticity
(ii) “leaky” membrane potential (“funny” current = “If”)
1. ↑ Na+ into cell that depolarizes the membrane via “slow Na+ channels”
(iii) Once membrane potential reaches -50mV signals ↑ Ca2+ into cell via “transient calcium channels”
(iv) Net total influx of Na+ and Ca2+ eventually reach threshold (-40 to -30 mV) to trigger action potential
• Phase 0 (upstroke)
(i) ↑↑ Ca2+ into cell via “slow long lasting calcium channels” that causes depolarization of the membrane during action potential
• Phase 3 (repolarization)
(i) ↑↑ K+ out of cell is responsible for repolarization of the membrane back down to the resting membrane potential
Fast Response Action Potential
a. Characteristic of myocardial cells of atria/ventricle & Purkinje fibers
b. Requires action potential from adjacent cell
c. Five phases (phases 0-4)
• Phase 0 (upstroke)
• Phase 1 (initial repolarization)
• Phase 2 (plateau)
• Phase 3 (repolarization)
• Phase 4 (resting membrane potential)
Phase 0 (upstroke) of Fast Response AC
(i) Action potential from adjacent cardiac cell depolarizes membrane to threshold voltage (approximately -70 mV)
(ii) Rapid ↑↑ Na+ into cell via fast Na+ channels that depolarizes the membrane
Phase 1 (initial repolarization) of Fast Response AC
(i) Initial ↑ K+ out of cell via transient K+ channels begins to repolarize the membrane
Phase 2 (plateau) of Fast Response AC
(i) ↑ Ca2+ into cell via “slow long lasting calcium channels” that causes a plateau in the repolarization
1. this essential prolongs mechanical contraction which allows for adequate ejection for ventricles
Phase 3 (repolarization) of Fast Response AC
(i) ↑↑ K+ out of cell combined with inactivation of “slow long lasting calcium channels” repolarizes the membrane back down to the resting membrane potential
Phase 4 (resting membrane potential) of Fast Response AC
(i) Inward and outward currents of K+ maintain resting membrane potential
(ii) ↑ Ca2+ and Na+ channels closed
Parasympathetic and Sympathetic innervations
- Parasympathetic
a. Innervates SA/AV and atria only (sparse innervation in ventricles)
↓ HR, ↓ conduction velocity and small effect on ↓ contractility of atria - Sympathetic
a. Innervates atria and ventricles (including nodes)
↑ HR, ↑contractility, ↑ relaxation rate (aka…less relaxation time)
Parasympathetic stimulation will effect the Atria and Ventricles how?
a. Atria:
• Promote/prolong K+ efflux out and inhibit Na+ and Ca2+ influx into pacemaker cells
• Primary effect – hyperpolarizes cell membrane and decreases slope/ increases duration of Phase 4
(i) Phase 3 - Hyperpolarize due increased K+ efflux out
(ii) Phase 4 - Decreased slope/ increased duration due to inhibited Na+ and Ca2+ influx into pacemaker cells
b. Ventricles:
• parasympathetic does not innervate ventricles
Sympathetic (NE) stimulation will
a. Promote/prolong Ca2+ influx into pacemaker and cardiac muscles cells in both atria and ventricles
• Cardiac muscle cells
(i) Primary effect – increase amplitude of Phase 2
(ii) Increase contractility, decrease relaxation time
• Pacemaker cells
(i) Primary effect – increased slope/decrease duration of Phase 4
(ii) Increase rate and conduction velocity
Class I agents (Sodium channel blockers)
Vaughan Williams classification of antiarrhythmic agents
a. Inhibits sodium (Na+) channel = ↓ HR
• Myocardial cells of atria/ventricle slows rate of depolarization (Phase 0)
• Nodal cells – slows rate of “leaky membrane” depolarization (Phase 4)
b. Class Ia agents include quinidine, procainamide and disopyramide.
c. Class Ib agents include lidocaine, mexiletine, tocainide, and phenytoin.
d. Class Ic agents include encainide, flecainide, moricizine, and propafenone.
Class II agents (beta blockers)
Vaughan Williams classification of antiarrhythmic agents
a. Anti-sympathetic nervous system agents (beta-blockers)
b. Inhibit sympathetic activity on nodal cells/myocardial cells = ↓ HR and ↓ contractility of heart
c. Examples of Class II agents include esmolol, propranolol, and metoprolol.
Class III agents (potassium channel blockers)
Vaughan Williams classification of antiarrhythmic agents
a. Prolongs potassium (K+) efflux – prolongs repolarization period = ↓ HR
b. Examples of Class III agents include amiodarone, azimilide, bretylium, clofilium, dofetilide, tedisamil, ibutilide, sematilide, and sotalol.
Class IV agents (calcium channel blockers)
Vaughan Williams classification of antiarrhythmic agents
a. Calcium channel blockers – act on long lasting calcium channels
b. Slows rate of depolarization of nodal cells (Phase 0) and inhibits “plateau” (Phase 2) of cardiac muscle cells: net result ↓ HR and ↓ contractility of heart
c. Examples of Class IV agents include verapamil and diltiazem.
Class V agents
Vaughan Williams classification of antiarrhythmic agents
a. Meds work by other or unknown mechanisms.
b. Class V agents include digoxin (digitalis).
• Digitalis stimulates the CNS to increase parasympathetic activity on the AV node = ↓HR
Influence of ECF(extra cellular fluid) ion concentration on Cardiac Function—-Clinical correlation:
- important to recognize normal and abnormal lab values of ion concentrations
- recognize the role each ion plays in the action potentials of cardiac cells in order to understand the cardiac consequences of “hyper” or “hypo” ion concentrations.
Influence of ECF(extra cellular fluid) ion concentration on Cardiac Function– Sodium (Na+)
- Sodium changes in ECF will produce electrical changes of cardiac cells but it is not as severe as alterations in ECF potassium
Influence of ECF(extra cellular fluid) ion concentration on Cardiac Function– Potassium (K+)
alters repolarization
- Hyperkalemia
a. Result is bradycardia
b. Severe hyperkalemia can be rapidly fatal (heart stops!)
Influence of ECF(extra cellular fluid) ion concentration on Cardiac Function— calcium (Ca2+)
- Hypercalcemia
a. If an abnormally large amount of calcium was introduced to the cardiac muscle then it would be unable to relax (cardiac rigor)
• Plateau of AP’s is prolonged
• Ca2+ within cardiac muscle – cross-bridge cycling would not be able to “release”
b. NOTE: very rare that a clinical condition would elevate calcium high enough to result in cardiac rigor.
Hyperkalemia effect on cardiac cells
• Phase 0 (fast response – myocardium)
(i) Resting membrane potential “lessens” (more positive) as ECF potassium increases
1. At first glance it would appear the threshold for the AP would be reached quicker and heart rate would increase.
2. Instead HR actually slows due to a slower conduction velocity of the myocardial cell (thus prolonged P wave, PR interval and QRS)
a. as the cell membrane “lessens” (i.e. goes from -80 to -70 to -60) then the conduction velocity of the cardiac muscle slows
• Phase 2 and 3 (fast response – myocardium)
(i) Hyperkalemia causes an INCREASE in the efflux of potassium out of myocardium during repolarization phases. (peaked T wave, shorten QT interval, ST seg changes)
1. result = shortened repolarization
2. mechanism not clearly understood – potassium channels simply react this way to elevated ECF potassium.
Hypokalemia
a. Results is tachycardias/arrhythmias
b. Can be fatal due to effect on heart but often co-existing morbidities just as fatal
c. Hypokalemia in ECF will hyperpolarize cells (more difficult to excite)
• In most cells hyperpolarization results in decreased excitability
• OPPOSITE occurs in cardiac cells – they become hyperexcitable and lead to tachycardia/arrhythmias
• Phase 2 and 3 (fast response – myocardium)
(i) The increased ECF will prolong or slow repolarization which causes the membrane potential to be delayed leading to reentrant arrhythmias
Potential ECG changes
• Initial: sagging of the ST segment, depression of the T wave, elevation of the U wave
• With marked hypokalemia: the T wave becomes progressively smaller and the U wave becomes increasingly larger. Sometimes, a flat or positive T wave merges with a positive U wave, which may be confused with QT prolongation
• Hypokalemia may produce premature ventricular and atrial contractions, ventricular and atrial tachyarrhythmias, and 2nd- or 3rd-degree atrioventricular block – all leading to potential ventricular fibrillation.
