Adult Health 2: EKGs Flashcards

Cardiac electrophysiology
Terms Definitions
Dysrhythmias
-An irregularity/disturbance of normal electrical activity of the heart. -ALL influence performance of heart (usually for the worse). -The seriousness depends on specific nature of dysrhythmia AND underlying condition of patient.
Cardiac Conduction
-SA Node: initiates rate (60-100bpm) -AV Node: relays atrial impulses to ventricles (40-60bpm) -Then pass thru Bundle of His at AV junction and continues thru interventricular septum thru the R/L bundle branches. -Then out to Purkinje fibers in the ventricular myocardium.
EKG Paper
-1mm in size every 25 squares (5 squares x 5 squares) 5mm x 5mm box -1mm = 0.04 secs -5mm = 0.20 -Paper is "pulled" by machine past stylus which deflects in response to electrical activity of heart (action potential) and "writes" on paper
Vertical axis of EKG paper
(height of waves) - measures voltage produced by heart. -voltage is NOT important to rhythm strip analysis (except in 12-lead EKG analysis)
12-Lead EKG
-Looks at heart from 12 different "angles" or "views" -Needed for diagnosis of heart muscle damage, enlargement of cardiac chamber, and interruption of some portion of cardiac conduction system. -Usually done at "single point in time" - like an x-ray.
Single Lead EKG
"rhythm strip" is a print out of a single lead or view. -Less cumbersome as patient does not need to be connected to as many electrodes or wires. **Used for constant 24-hr monitoring in intensive care situations. -Usually sufficient for identifying BASIC DYSRHYTHMIAS (much info lost compared to 12-leads)
Ectopic Beats
Interrupt the normal conduction sequence and may not initiate a normal muscle contraction.
Telemetry
*Put underneath clavicles -White on Right -Clouds over Grass -Smoke over Fire -Christmas Tree on Bottom *Brown lead = Cardiac lead (goes to sternum)
Determining Heart Rate
*Every 15 large blocks (3 secs) *Estimate of HR = # of "beats" in 2 of these 3 second intervals and multiply by 10. *There are 10 six-second intervals in one minute.
Dubin's Method determining HR
*Relies on using large blocks on EKG paper. *Find QRS complex that falls on start of large block --> Count number of large blocks to next QRS complex *This tells you how many "fifths of a second" btw QRS complexes (each large block = 0.20 secs)
When can Dubin's Method be used? Why?
*ONLY used when the heartbeat rhythm is REGULAR (each QRS complex is same distance apart). *Result you will get will vary depending on which 3 QRS complexes you choose to measure
What do the deflections seen on EKGs represent?
The electrical depolarization of the atria and ventricles via the cardiac conduction system
What is an isoelectric line?
When the heart is resting btw "beats" the EKG machine draws a straight line on the paper.
P Wave
-First deflection in the normal cardiac cycle; represents depolarization of atria. -Gently rounded rather than peaked or pointed. -Depolarization of SA node itself does not generate enough voltage to be seen on the EKG; If P wave is normal in rate and appearance we assume that SA node depolarized to initiate the cycle.
QRS Complex
-Represents depolarization of the ventricles; much larger than P wave bc mass of myocardium being depolarized is much greater than the atria. -Specific shape of QRS complex is important when looking at 12-lead EKG, but not single lead rhythm strips. *0.04-0.10 secs
What is the normal duration of the QRS complex from beginning to end?
Should not be more than 0.12 seconds (3 small blocks)
T wave
-Represents repolarization of the ventricles; usually rounded and a little larger than the P wave. -May be pointed upward, downward, or almost flat; important on exam of 12-lead EKG but not when analyzing dysrhythmias with single lead rhythm strip
Repolarization of atria
-Voltage is so low that resulting wave ordinarily can't be seen. -Therefore, atrial repolarization occurs about same time as QRS and gets "lost" or "swamped" in it.
PR Interval
*Distance from beginning of P wave to very beginning of QRS; atrial depolarization *Represents time needed for depolarization wave to originate in SA node, spread thru the atria, travel thru AV node, and be poised to enter ventricles. *Normally 0.12-0.20 secs (3-5 small blocks)
ST Segment
*Segment of line btw the end of QRS complex and beginning of T wave. *Not important to measure duration. *May lie on normal, above, or below the isoelectric line. *Important when analyzing 12 lead but not single lead rhythm strip for dysrhythmia detection; usually neutral
QT Duration
*Distance from very beginning of QRS complex to the very end of T wave; time for ventricular depolarization and recover *It is important but not for dysrhythmia detection; normal QT duration varies depending on heart rate
U wave
-After ventricular repolarization and before atrial depolarization, same deflection as T, but smaller (late recovery of Purkinje's). *Could represent an MI
How to diagnose?
1) Rate: tachycardia, bradycardia 2) Rhythm: regular, irregular 3) P wave: upright? One-focus SA or different? Precede QRS? 4) PR interval: >0.20 - conduction delay, do they vary? 5) QRS: should be < 0.10, is it wide, bizarre? 6) T wave: upright? Elevated? U wave?
Dysrhythmias and causes?
*Abnormal or ectopic focus that initiates a beat; may be one beat or sustained beats; if its rate is faster than the intrinsic rate (100 for SA) than it will take over. *Causes: HYPOXIA, ischemia, sympathetic stimulation (stress, trauma, CHF, hyperthyroidism), meds (antiarrhythmics, bronchodilators, cardiac glycosides), electrolyte disturbances (K, Ca, Mg), stretch or hypertrophy
Normal Sinus Rhythm
Normal heart rhythm, in which impulses originate in the SA node and travel thru all normal conduction pathways w/out delay; wave forms look alike and have consistent durations *Rate: 60-100 *Rhythm: regular. *PR: upright (0.16) *QRS: 0.06
Sinus Bradycardia
May be normal in athletes; also seen with pain, increased ICP, acute MI, hypothermia, acidosis *Rate: < 60 BPM, P wave present, upright *Rhythm: Regular *PR: 0.12 - 0.20 sec *QRS: 0.6 - 0.10 sec Treated only if symptomatic (decreased LOC, syncope, hypotension): Atropine (Isoproterenol), and/or pacemaker
Sinus Tachycardia
Has all characteristic of NSR except rate is > 100 BPM; may be early sign of cardiac dysfunction (heart failure). -Manifestations: rapid pulse rate, SOB, dizziness *Rate: 101-150 BPM *Rhythm: Regular, P's upright *PR: 0.12 - 0.20 *QRS: 0.06 - 0.10 Treat only if symptomatic, and treat underlying cause: Beta blockers or verapamil may be used
Premature Atrial Contraction (PAC)
An ectopic atrial beat that occurs earlier than the next expected sinus beat. *Rate: P wave comes early (varies) *Rhythm: irregular, with normal rhythm interrupted by early beats arising in atria *PR: 0.12 - 0.20, but may be prolonged *QRS: 0.6 - 0.10 sec *Treatment: usually none required - Beta blocker may be prescribed
Supraventricular Tachycardia (SVT)
Tachycardia of sudden onset and termination; repeated depolarization - affects ventricular filling and cardiac output, and decreases coronary artery perfusion. *Rate: 100 - 280 (usually 150-200) *Rhythm: regular (P waves differ in shape from sinus P wave) *PR: very short; < 0.12 *QRS: normal *Treatment: Adenosine/beta blocker, oxygen therapy, temp. pacemaker, cardioversion
Atrial Flutter
Rapid and regular atrial rhythm; Type 1 atrial flutter ( 240-340 BPM) --> type 2 (350 or > BPM); EKG looks like "sawtooth" which is labeled as flutter. *Rate: atrial 250-350 BPM; ventricle is variable depending on degree of AV block *Rhythm: usually regular *QRS: usually normal, may be wide *Treatment: meds to slow ventricular response such as beta blocker or CCB (followed by amiodarone)
Atrial Fibrillation
Very common dysrhythmia characterized by disorganized atrial activity w/out discrete atrial contractions; common association w/ heart failure, rheumatic heart disease, CHD, HTN, hyperthyroidism; more prone to clots and strokes *Rate: atrial (300-600 BPM; too rapid to count), ventricular (100-180 in untreated pts) *Rhythm: irregular (always) *Absence of identifiable P wave *QRS: 0.06-0.10 sec *Treatment: meds to reduce ventricular response rate - metoprolol, diltiazem, digoxin, anticoagulation therapy to reduce risk of clot formation and stroke
Conduction Dysturbances: 1st Degree AV Block
A benign conduction delay that generally causes no threat, has no symptoms, and requires no treatment; EKG shows NSR, but the PR interval is > 0.20 secs *Rate: regular *Rhythm: regular *PR: > 0.20 sec *QRS: 0.06 - 0.10 *No treatment required
Conduction Disturbances: Wenkebach (2nd degree heart block)
Repeating pattern of increasing AV conduction delays until an impulse fails to conduct to the ventricles; PR intervals progressively lengthen until one QRS complex is not conducted or dropped. *Rate: can be slow *Rhythm: irregular *PR: (short, long, longer, drop) occurs in pattern *QRS: 0.06-0.10; sudden absence of QRS complex *Treatment: monitor/observe (rarely needs treatment)
Conduction Disturbances: Mobitz type 2 (2nd degree heart block)
Intermittent failure of AV node to conduct an impulse to the ventricles w/out preceding delays in conduction; usually bundle branch delay. *Rate: atrial (regular), ventricular ( <60) *Rhythm: atrial (regular), ventricular (irregular) *PR: remains constant, but not all P waves are followed by QRS complexes (may be 2 P waves before QRS) *QRS: may or may not be normal *Treatment: pacemaker may be required to maintain cardiac output
Conduction Disturbances: 3rd Degree Heart Block
"Complete" heart block; occurs when atrial impulses are completely blocked in AV node and fail to reach ventricles. Result in atria and ventricles being controlled by different independent pacemakers with separate rates and rhythms. *Rate: atrial (regular), ventricular (15-60 BPM) *Rhythm: regular *No relationship btw P wave and QRS complex (independent rhythms) *Treatment: Immediate pacemaker needed
Premature Ventricular Contractions (PVC)
Ectopic ventricular beats that occur before the next expected beat of the underlying rhythm; may be felt as a "skipped beat" (no significance in ppl w/out heart disease). *Rate: variable *Rhythm: irregular, with PVC interrupting underlying rhythm and followed by pause. *No P wave preceding PVC *QRS: wide and bizarre (> 0.12)
PVC: Couplets
When 2 PVCs occur in a row (or in pairs); no adequate cardiac output when this happens
Ventricular Tachycardia (VT; V Tach)
Rapid ventricular rhythm defined as 3 or more consecutive PVCs; may occur in short bursts or runs, or may persist for more than 30 secs. *Rate: 100 - 250 BPM *Rhythm: regular *P wave not identifiable, QRS is 0.12 or greater (bizarre shape) *Cardiac output decreases and is HUGE problem
Ventricular Fibrillation (V-Fib)
Extremely rapid, chaotic ventricular depolarization causing ventricles to quiver and cease contracting (no cardiac output); AKA cardiac arrest; no contraction of heart muscle, only twitching and no cardiac output (sudden death). *Rate: too rapid to count *Rhythm: grossly irregular *P wave not identifiable, QRS is bizarre with varying shape and direction
Idioventricular Rhythm
Slow rhythm originating in the ventricles; occurs right before patient dies (heart does not completely stop - DNRs) *No P wave *QRS is wide, very poor cardiac output
Causes/Treatment of Sinus Tachycardia
*Causes: stress, exercise, fever, pain, meds, metabolic demands, hypovolemia (can lead to decreased diastolic filling time), < SV and cardiac enlargement. *Treatment: treat underlying prob - beta blockers (metoprolol, labetolol), calcium channel blockers (inderal, verapamil); if rate continues to SVT --> give adenosine, then cardizem
Causes and Treatment for Sinus Bradycardia
*Causes: decreased automaticity of SA node, HB, digoxin toxicity, MI, hyperkalemia; decreased cardiac output, unable to maintain perfusion, if slows too much then allows other pacemaker cells to take over. *Treatment: Atropine, pacemaker (must do if 2nd or 2rd degree HB, otherwise treat pt); avoid any suctioning (gag reflex)
Causes and Treatment for SVT
*Causes: may have runs w/out probs, fever, stress, adrenergic meds, caffeine, hypertrophy of atrium, asthma --> leads to incr. workload, decreased coronary blood flow and cardiac output. *Treatment: adenosine (adenocard), verapamil, diltiazem (cardizem), carotid massage, cardioversion
Causes and Treatment for A-Fib/Flutters
*Causes: CHF, LV failure, injury to SA node, catecholamine secretion; flutter may be more dangerous and spontaneous (may lead to less filling, SV, and cardiac output; A-fib is more chronic in nature - assess need for treatment by pt response (BP, C.O.) *Treatment: Cardizem, Digoxin (slows HR), Amiodarone (only for emergent), cardioversion, anticoagulants (esp for a-fib)
Causes and Treatment for V-Tach
*Causes: myocardial irritability, MI, ischemia, plaque formation, toxic irritation from drugs and chemicals, mechanical irritation from leads, hypoxia and hypertrophy of ventricles; pt first has angina, apprehension, then lower BP and C.O., unresponsive *Treatment: shock/cardioversion, epinephrine, vasopressin (rare), amiodarone, lidocaine (rarely used), mag sulfate (GI esp)
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