Term
|
Definition
| voltage difference between interior & exterior of cell; established by eletrochemical gradients of Na, K, Ca, & Cl ions |
|
|
Term
| resting membrane potential (RMP) |
|
Definition
|
|
Term
|
Definition
| occurs when transmembrane potential changes and becomes LESS NEGATIVE |
|
|
Term
|
Definition
| occurs when transmembrane potential RETURNS to negative RMP |
|
|
Term
|
Definition
| transient alteration of transmembrane potential & is the impulse responsible for cardiac conduction |
|
|
Term
|
Definition
| ability of cardiac cells to spontaneously depolarize to generate action potentials |
|
|
Term
|
Definition
| time during which a cell cannot be stimulated by another action potential |
|
|
Term
|
Definition
rapid depolarization (upstroke) due to:
- rapid influx of Na;
- influx of Ca starts at -60 mV; |
|
|
Term
|
Definition
initial repolarization due to:
- transient active eflux of K; |
|
|
Term
|
Definition
plateau due to:
- K efflux (repolarization) balanced by Ca influx (depolarization) |
|
|
Term
|
Definition
rapid repolarization due to:
- K efflux increases while Ca influx decreases; |
|
|
Term
|
Definition
resting membrane potential (diastole) due to:
- established by active transporters (Na/K ATPase, Na/Ca exchanger); |
|
|
Term
|
Definition
| normal pacemaker, has the fastest inherent rate: 60-100 bpm |
|
|
Term
|
Definition
impulses from fastest pacemaker prevent spontaneous firing of slower, downstream pacemakers;
- failure/blockage of upstream pacemakers means downstream pacemakers take over & result in a HR that is in range of inherent rate of new pacemaker |
|
|
Term
|
Definition
slower pacemaker;
40-60 bpm |
|
|
Term
|
Definition
slowest pacemaker;
20-40 bpm; |
|
|
Term
|
Definition
| ECG component that represents atrial depolarization & contraction |
|
|
Term
|
Definition
| ECG component that represents AV nodal conduction duration |
|
|
Term
|
Definition
| ECG component that represents ventricular depolarization & contraction |
|
|
Term
|
Definition
| ECG component that represents ventricular repolarization |
|
|
Term
|
Definition
| ECG component that represents period when ventricles are depolarized |
|
|
Term
|
Definition
| ECG component that represents ventricular action potential duration & represents beginning of QRS complex to end of T wave |
|
|
Term
|
Definition
| tachycardia causes this to occur to QT interval |
|
|
Term
|
Definition
| this occurs to QT interval in bradycardia |
|
|
Term
|
Definition
MoA:
- failure of impulse initiation;
- decreased automaticity; |
|
|
Term
|
Definition
MoA:
- failure of impulse propagation from atrium to ventricles; |
|
|
Term
|
Definition
MoA:
1) enhanced automaticity;
2) triggered automaticity;
3) re-entry |
|
|
Term
|
Definition
| caused by increased rate, due to adrenergic stimulation, hypokalemia, mechanical stretch, ischemia |
|
|
Term
| decreased phase 4 slope, hyperpolarization |
|
Definition
| caused by decreased rate that can occur with ACh, or parasympathetic stimulation |
|
|
Term
| Delayed Afterdepolarizations (DADs) |
|
Definition
| follows a normal AP & is due to increased intracellular Ca (ischemia, adrenergic stress, digitalis, HF) & usually occurs with underlying rapid HRs |
|
|
Term
| Early Afterdepolarizations (EADs) |
|
Definition
| interrupts Phase 3 repolarization & is often due to hypokalemia, drugs that prolong AP, and usually occurs with underlying SLOW HRs |
|
|
Term
|
Definition
occurs when impulse re-enters & depolarizes an area more than once;
Requires:
- 2 pathways for conduction;
- area of unidirectional block in one pathway;
- slowed conduction in unblocked pathway; |
|
|
Term
| Normal Sinus Rhythm (NSR) |
|
Definition
regular rate & rhythm of healthy heart;
HR: 60-100 bpm, all ECG components are NORMAL; |
|
|
Term
|
Definition
sinus node fires slower than normal, at a rate of <60 bpm; rhythm is still regular w/ normal complex & intervals;
Causes: vagal stimulation, hypoxia, medications (beta-blockers) |
|
|
Term
|
Definition
sinus node fires faster than normal, HR >100 bpm; rhythm is still regular w/ normal complex & intervals;
Causes:
- fever, anxiety, pulmonary embolism, MI, drugs (atropine, anticholinergics), many other drugs |
|
|
Term
|
Definition
due to 1 or more irritable foci in atrium;
- characterized by P wave changes |
|
|
Term
| Supraventricular Tachycardia (SVT) |
|
Definition
originates above ventricles but exact origin is unknown;
HR >= 130 bpm, rhythm is regular, P waves are NOT discernable;
Causes: medications (stimulants), hypoxia, heart dx |
|
|
Term
| Atrial Fibrillation (Afib) |
|
Definition
hundreds of atrial ectopic foci fire at once & atrium depolarizes in small sections & as a result of contraction of atria is impaired & AV node cannot conduct atrial impulses;
Atrial Rate: 350-700 bpm;
Rhythm: 'irregularly irregular';
NO P waves present; QRS complexes at irregular intervals;
Causes: MI, lung dx, valvular heart dx, stimulants, EtOH |
|
|
Term
|
Definition
one atrial ectopic focus fires at a rapid rate but AV node conducts only some impulses;
Atrial Rate: 250-350 bpm;
"Sawtooth" flutter waves replace P waves, & 2 or more flutter waves to each QRS complex;
Causes: underlying heart dx, lung dx |
|
|
Term
|
Definition
SA node fires normally but conduction of impulse is partially or completely interrupted in AV conduction pathway;
impairs or blocks transmission of impulse from atria to ventricles;
1) PR interval is prolonged (> 0.2 sec) OR
2) P waves not consistently followed by QRS complexes;
Causes: AV node ischemia, medications (digoxin, beta-blockers, CCBs), MI; |
|
|
Term
|
Definition
impulse is delayed from SA node to ventricles & site of block is AV node;
PR interval prolonged > 0.2 sec;
1 P wave to each QRS complex; |
|
|
Term
| 2nd degree AV block type 1 |
|
Definition
site of block is usually AV node but PR-interval is progressively prolonged until some P wave impulses are not conducted --> "dropped" QRS complexes;
Atrial Rate: 60-100 bpm;
Ventricular rate < atrial rate;
Rhythm is usually irregular |
|
|
Term
| 2nd degree AV block type 2 |
|
Definition
site of block is His-Purkinje system;
Atrial Rate: 60-100 bpm;
Ventricular rate = 0.12 sec) indicate bundle branch block (BBB) |
|
|
Term
|
Definition
complete heart block;
Atrial Rate: 60-100 bpm;
Ventricular rate: 20-60 bpm (slow);
Rhythm is regular;
P waves are NOT associated with QRS complexes;
QRS complexes are widened if BBB |
|
|
Term
|
Definition
due to 1 or more irritable foci in ventricles taht cause retrograde depolarization of atria;
more dangerous form; |
|
|
Term
| Premature Ventricular Complexes (PVCs) |
|
Definition
premature beat from irritated ventricular tissue that occur at any rate;
rhythm is regular but interruped;
Wide (>0.12 sec), shape is different from other QRS complexes NOT preceded by P wave;
Causes:
- heart dx, hypokalemia, hypoxia, hypomagnesemia, stimulants |
|
|
Term
| Ventricular Fibrillation (VF) |
|
Definition
many irritable foci in ventricles fire rapidly;
no discernable P waves or QRS complexes, very irregular rhythm;
No cardiac output, pt functionally dead & requires IMMEDIATE defibrillation;
Causes:
- heart dx, hypokalemia, hypoxia, hypomagnesemia, stimulants, drowning, electrical shock, drug overdose |
|
|
Term
| Reducing automaticity in ectopic foci |
|
Definition
alter discharge in spontaneous pacemakers by:
1) decrease phase 4 slope;
2) increase threshold potential;
3) increase max diastolic potential;
4) increase AP duration |
|
|
Term
| Modify conduction of refractoriness in reentry circuits |
|
Definition
Way to increase refractoriness:
1) increase voltage dependence of channel recovery, reducing available unblocked channels;
OR
2) prolong AP, also extending point at which channels recover from inactivation |
|
|
Term
|
Definition
quinidine, procainamide, disopyramide;
- blockade of Na & K --> slows conduction velocity, prolongs refractory period, decreases automaticity by increasing threshold potential;
broad-spectrum agents used for supraventricular (SVCs) arrhythmias & ventricular arrhythmias |
|
|
Term
|
Definition
Class IA anti-arrhythmic
MoA: vagolytic & alpha adrenergic blocking properties;
Forms: PO, IV, IM;
PK: hepatic metabolism & elimination;
- CYP3A4 > CYP2C0; Strong inhibitor of CYP2D6, CYP3A4;
ADRs:
- prolonged QTc & TdP, VT, HF exacerbation, diarrhea, cinchonism, thrombocytopenia, hemolytic anemia, hepatitis; |
|
|
Term
|
Definition
Class IA anti-arrhythmic;
Forms: IV, IM, PO;
PK: hepatic metabolism, renal elimination;
- forms NAPA (Class III anti-arrhythmic activity, accumulates in renal failure);
ADRs:
- hypotension, prolonged QTc & TdP, diarrhea, drug-induced lupus, rare agranulocytosis; |
|
|
Term
|
Definition
Class IA anti-arrhythmic;
Similar to quinidine but w/ greater anticholinergic activity;
Forms: PO only;
PK: hepatic metabolism (CYP3A4), renal elimination;
ADRs:
- anticholinergic: dry mouth, urinary retention, blurred vision, constipation; HF exacerbation, nausea, anorexia, prolonged QTc & TdP |
|
|
Term
| Class IB Anti-arrhythmics |
|
Definition
lidocaine, mexilitene;
MoA: fast on-off Na channel antagonism --> depressed conduction in ischemic (depolarized) tissue; AP is either unaffected or shortened --> decreased automaticity;
Uses: only for ventricular arrhythmias |
|
|
Term
|
Definition
Class IB anti-arrhythmic;
also used as local anesthetic;
Effective for post-MI arrhythmias;
Forms: IV only;
PK: hepatic metabolism;
ADRs: seizures, tremor, dizziness, sedation, paresthesias, nausea, slurred speech, hearing disturbances, Rare: sinus arrest, impaired conduction, ventricular arrhythmias; |
|
|
Term
|
Definition
Class IB anti-arrhythmic;
Forms: PO only;
PK: hepatic metabolism, inhibits CYP1A2;
ADRs: tremor, dizziness, sedation, seizures, nausea, paresthesias, slurred speech, hearing disturbances; |
|
|
Term
| Class IC Anti-arrhythmics |
|
Definition
flecainide, propafenone;
MoA:
- potent, slow-off Na channel blockers --> profound slowing of conduction, leaves refractory period unaltered; leads to decreased automaticity;
Uses:
- effective in both supraventricular AND ventricular arrhythmias BUT pro-arrhythmic effects limit use for ventricular arrhythmias; |
|
|
Term
|
Definition
Class IC anti-arrhythmic;
Only used in pts w/o structural heart dx;
Forms: PO only;
PK: hepatic metabolism, renal elimination, inhibits CYP2D6;
ADRs:
- pro-arrhythmic, HF exacerbation, blurred vision, dizziness, HA, tremor, nausea; |
|
|
Term
|
Definition
Class IC anti-arrhythmic;
similar to propanolol & has weak beta-adrenergic antagonism;
Forms: PO only;
PK: hepatic metabolism, 1st pass --> 5-hydroxypropafenone --> active as Na channel blocker, less beta effects; Inhibitor of CYP2D6;
ADRs:
- pro-arrhythmic, HF exacerbation, bradycardia, bronchospasm, fatigue, dizziness, metallic taste; |
|
|
Term
| Class II Anti-arrhythmics |
|
Definition
Beta-blockers: esmolol, metoprolol, atenolol;
Acts in SA & AV nodes --> decrease conduction velocity, prolong refractory period, decrease automaticity;
Most useful for:
- tachycardias involving abnormal nodal automaticities or part of re-entry circuit;
- decreasing ventricular response in atrial tachycardias;
- controlling arrhythmias due to high sympathetic activity;
Use caution or AVOID if:
- sinus or AV node dysfunction (blocks);
- acute decompensated HF;
- asthma;
- peripheral vascular dx;
- poorly controlled DM; |
|
|
Term
| Class III Anti-arrhythmics |
|
Definition
amiodarone, dofetilide, ibutilide, sotalol;
MoA:
- K channel blockers --> prolongs AP & refractory period, NO effect on conduction velocity or automaticity;
Amiodarone, sotalol effective for both supraventricular & ventricular arrhythmias;
Ibutilide, dofetilide ONLY used for supraventricular arrhythmias; |
|
|
Term
|
Definition
Class III anti-arrhythmic & other anti-arrhythmic properties;
analog of thyroid hormone;
Broad-spectrum, widely used;
Forms: PO & IV;
PK: variable bioavailability, very large VD, hepatic metabolism & elimination (CYP3A4, CYP2C9), very long elimination T1/2 (15-100 days), give loading doses;
ADRs:
- IV: hypotension, phlebitis; prolonged QTc & TdP, hyper/hypothyroidism, photosensitivity, corneal microdeposits, optic neuropathy/neuritis, increased LFTs (hepatitis), pulmonary fibrosis, neurotoxicity; |
|
|
Term
| Monitoring Parameters for Amiodarone |
|
Definition
Pulmonary fibrosis: CXRY baseline then q12 months unless symptomatic;
Thyroid dysfunction: thyroid fcn tests baseline then q6 months;
Optic neuritis: ophthalmologic exam baseline then q12 months;
Hepatitis: LFTs baseline then q6 months;
Bradycardia/heart block: ECG baseline then q3-6 months |
|
|
Term
|
Definition
Class III anti-arrhythmic;
New agent, structural analog to amiodarone;
Shorter T1/2: 24 hrs;
1st drug to demonstrate reduction in mortality & hospitalizations for pts w/ Afib |
|
|
Term
|
Definition
Class III anti-arrhythmic;
Potent, pure blockade of K channels in heart;
Forms: PO only;
PK: 80-95% bioavailability, C/I if CrCL <20 ml/min;
ADRs:
- prolonged QTc & TdP (C/I if QTc >440 msec), HA, dizziness;
Drug Interactions:
- C/I: cimetidine, verapamil, trimethoprim, ketoconazole, prochlorperazine, megesterol, HCTZ, other QTc-prolonging drugs;
- other anti-arrhythmics should be stopped or held for at least 3 half-lives;
use caution if given w/ CYP3A4 inhibitors; |
|
|
Term
|
Definition
Class II & III anti-arrhythmic;
- inhibits K channels AND is a non-selective beta-antagonist;
Forms: PO only;
PK: no hepatic metabolism, renally eliminated;
ADRs:
- prolonged QTc & TdP, dizziness, weakness, fatigue, bradycardia, bronchospasm, HF exacerbation; |
|
|
Term
|
Definition
Class III anti-arrhythmic;
Prolongs AP by inhibiting K channels, activates slow inward Na current;
ONLY used for conversion of Afib/flutter;
Forms: IV only;
PK: extensive 1st pass metabolism orally, undergoes rapid hepatic metabolism;
ADRs: prolonged QTc & TdP, HA, hypotension; |
|
|
Term
| Class IV Anti-arrhythmics |
|
Definition
diltiazem, verapamil;
MoA:
- L-type Ca channel blocker --> works in SA/AV nodes to slow conduction, prolong refractoriness, decrease automaticity;
Decreases ventricular response to supraventricular arrhythmias;
Effective for exercise-induced or triggered-automaticity arrhythmias;
Use caution or avoid if:
- sinus or AV node dysfunction (blocks);
- HF;
- Wolff-Parkinson-White Syndrome; |
|
|
Term
|
Definition
MoA: increases intracellular Ca --> positive inotropic effect, increased automaticity;
vagotonic effects --> indirect electrophysiological effects --> hyperpolarization --> shortens atrial APs, increased AV node refractoriness;
Used to control ventricular response to Afib/flutter;
Narrow therapeutic index, complex PK; |
|
|
Term
|
Definition
naturally-occurring nucleoside --> activated ACh-sensitive K channels in sinus, AV nodes --> shortens AP --> hyperpolarizes myocardium --> decreases automaticity;
Eliminated in seconds by uptake into almost any cell type --> requires rapid bolus dose;
ADRs: dyspnea, chest fullness (short-lived);
causes characteristic pause of short flatline on ECG (lasts 5 sec); |
|
|
Term
|
Definition
administered acutely for termination /prevention of recurrence of TdP;
- effective even if serum blood level is normal;
- dose NOT shorten QTc interval but is still effective; |
|
|
