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ADV DX ECG's

WilliamWallace Adv DX chapt 10 ECG's

QuestionAnswer
What is an ECG an indirect measurement of the electrical activity within the heart
What do ECG's not measure pumping ability, abnormalities of cardiac structure, probability of MI
Chief complaint suggestive of ECG chest pain, exert ional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, pedal edema, fainting, palpations, nausea and indigestion in high risk pts
Past medical hx suggestive of ECG hx of heart disease, hx of cardiac surgery
physical exam suggestive of ECG unexplained tachycardia at rest, hypotension, <capillary refill, abnormal heart sounds, pedal edema, cool cyanotic extremities, abnormal heave or lift of pericardium, diaphoresis, JVD, abnormal sensorium, hepatojugular reflex, bilateral insp crackles
*SA Node normally is pacemaker, has greatest automaticity, causes depolarization (60-100bpm)
*AV Node normally acts as back up pacemaker (40-60 bpm)
electrical conduction system of the atria SA node to the 3 internodal atrial conduction tracts leading to AV node and 1 intranodal conduction tract to left atrium (Bachman’s bundle)
Atrioventricular Junction AV Node and bundle of His (.05 second delay)
electrical conduction of the ventricles from bundle of his in AV junction to bundle branches (30-40 bpm) to purkinje network (30-40 bpm)
Systole ventrical contraction
Diastole ventrical relax
atrial kick contraction of the atria (at latter end of systole) just before ventrical contraction-aids in ventrical filling and accounts for 10-20% of CO in healthy person
AV Node delay .05 seconds, delay before passing into bundle of his, allows for complete filling of ventricals before contraction (also protects vents from fast rates)
automaticity cells that have the ability to generate electrical activity spontaneously
pacemaker cells cells w/high degree of automaticity that provide electrical power to heart
myocardial cells contract in response to elec stimuli and pump blood
ectopic impulse impulse originating outside the SA Node
SA Node is stimulated by the sympathetic nervous system, what kinds of things can increase SA Node rate (fight or flight) stress, anxiety, exercise, medication. CHF, hyperthyroidism
what can slow the SA node rate (or stop it) vagal stimulation (parasympathetic), also drugs disease etc
coronary arteries supply 02 and nutrients to heart, arise from descending aorta and branches to coronary vessels
Infarctions blockage of one or more coronary vessels leading to regionalized tissue ischemia and tissue death
MI and ischemia cause what dysrrhythmias and <CO
Hypoxia and ischemia of myocardium causes <PaO2, <HB, <perfusion
how can sympathetic stimulus cause ischemia >workload w/o concurrent blood flow (blocked coronary arteries)
what electrolyte imbalance cause dysrrhythmias potassium, magnesium and calcium are most common
poor cardiac output and HR to slow causes <output, HR to fast vents, not enough time to full so less blood pumping <CO
causes of dysrrhythmias hypoxia, ischemia, sympathetic stimulation, drugs, electrolyte imbalance
acetycholine neurotransmitter of the parasympathetic NS, aka cholinergic, <HR
norepinephrine neurotransmitter of the sympathetic NS, aka adrenergic, >HR, >contractility
alpha and beta adrenergic receptor sites alpha are in blood vessels through out body and B receptor are in heart and lung only
receptor site mnemonic ABCD alpha constrict-beta dilate
heart receptor alpha and B1
lung receptor B2
blood vessel receptor alpha and B2
*4 major characteristics of cardiac cells automaticity, excitability/irritability, conductivity, contractility/rhythmical
action potential electrical charge passing through cell and propagating to other cells (all in one fashion)
polarized resting state
depolarization muscle contraction(loss of negative charge)
re-polarization return to resting state (negative charge returns)
*Pwave (.11 seconds) depolarization of the atria, impulse spreads across atria and triggers atrial contractions
*QRS complex (<.12) impulse spreads to ventricals, triggers ventrical contraction, (depolarization)
T-Wave ventricals returning to resting state
*PRI PR interval, .12-.20, measures time from onset of atrial contraction to onset of vent contraction, aka time for elec impulse to spread through and AV node (3-5 small squares)
short PRI indicates progression of elec impulse is outside normal path
*long PRI indicates delay in conduction or AV block
normal QRS <.12
wide QRS indicates originates in ventricular if supraventricular it has deviated from normal course
narrow QRS normal, supraventricular
ST Segment begins at end of QRS and ends at beginning of Twave, normally flat
*elevated or depressed ST segment depressed ischemia, elevated MI
U-wave follows Twave, may be seen or unseen, final phase of ventrical re-polarization
QT interval from beginning of Q to end of T, should be ½ of R-R
long QT interval >1/2 of R-R (if HR is <80bpm), hypokalemia, hypocacemia, side effect of meds like quinidine
R-prime a QRS complex that has a second positive deflection, the first is the R, the second is R-prime
S-prime second S wave in QRS
normal mean axis between 0 and 90 degrees
Right axis deviation right vent is enlarged
Left axis deviation left vent is enlarged
S&S of dysrrhythmias chest pain, dyspnea, fine crackles, palpations, pale cool skin, dizziness/syncope, sense of impending doom, low BP-<90systolic, <LOC
interpreting dysrrhythmias can be accomplished in 3 levels 1ventrical response (abnormal conduction), 2 categorize based on origin, 3 electro-physiology (pathway of conduction disturbance)
how is ventrical response determined QRS complexes and pulse strength (to fast/slow, irritability, lethal, absent)
categories of origin are atrial, junctional, ventricular
electrophysiology of dysrrhythmias ectopic beat/rhythm, escape beats/rhythms, AV block, bundle branch block
*bradycardia rate <60
*tachycardia rate >100
irregular rhythms may be random or in patterns, ectopic beat, escape beat, second degree AV block, atrial Fib, sinus dysrrhythmias
*evaluate Pwave positive, round, <.10, <2.5 mm tall, all should look alike
*odd shaped Pwaves are indicative of atrial enlargement
*more than one Pwave may indicative of atrial flutter (Pwaves look alike), atrial fib (Pwaves don't look alike), 2nd or 3rd degree heart block
*evaluating PR interval norm .12-.20 seconds, >.20 is possible heart block (delayed AV node)
*evaluating QRS norm <.12, wide w/bundle branch block, ectopic beat in vent (PVC's), ventrical dysrrhythmias (vtach, idioventricular rhythm or premature ventricular complex), 3rd degree heart block
*evaluating ST segment norm is isoelectric(flat), elevated is myocardial injury, depressed is ischemia
cases of right axis deviation left vent infarction, rt vent hypertrophy, COPD, pulm emboli, normal in infants,
causes of left axis deviation rt vent infarction, left vent hypertrophy, abdominal obesity, ascites, or ab tumor, pregnancy
*evaluating the Qwave norm is <.04 and less than 1/3 amplitude of R, greater than 1/3 R is pathologic, indicative of new or old MI
*Right atrium enlargement is seen in pts chronic pulm hypertension (as with COPD)
*Right atrium enlargement is diagnosed by rt deviation of Pwave, tall Pwave or prominent or negative Pwave
*cor pulmonale (rt atrium enlargement) shifts axis how to the right
*absolute bradycardia <60 bpm w/no problems to pt (athlete)
*relative bradycardia <60 bpm not tolerated well by pt, pts with compromised cardiac function may cause hypotension, syncope, <CO, CHF or shock
transient bradycardia may be caused by >vagal tone from carotid massage, manipulation of tubes, suctioning, valsalva maneuver
long term bradycardia can be caused by damage to SA node by MI
disease states that cause bradycardia hypothyroidism, hypothermia, hyperkalemia, meds
*sinus tachycardia 100-150 BPM with SA node as pacemaker, most often caused by fever, pain, hypoxemia, hypovelemia, hypotension, sepsis, heart failure and suctioning
*respiratory meds that cause sinus tachycardia methylxanthines (phosphodiesterase inhibitors) and B agonist
evaluating sinus dysrrhythmias usually benign, everything is normal except rhythm, rhythm will be off (space between the R-R)
what is paroxysmal atrial tachycardia 160-240 bpm, ectopic foci in the atrium takes over as pacemaker, sudden onset and ending, may cause hypotension, CHF, or ischemic episode, or recent/pre existing MI
danger of PAT (paroxysmal atrial tachycardia) >myocardial O2 demand but pump is ineffective because of rate, especially dangerous in pt with bad heart
Pt complaint with PAT light headed, palpations, possible fainting
causes of PAT stress, mitral valve disease, rheumatic heart disease, digitalis toxicity, alcohol, caffeine or nicotine
evaluating PAT rate 160-240 bpm, rhythm normal, Pwave abnormalities-hidden in QRS or if before QRS it appears pointed, can combine with Twave, PRI is usually not measurable
*atrial flutter pattern on ECG strip is caused by rapid firing of ectopic foci, sawtooth Pwave with normal QRS
*F-waves flutter waves, caused by rapid contractions of atria upon stimulation by re-entry or accelerated automaticity
atrial flutter reduces CO how reducing atrial kick
mural thrombi thrombi that form along the atrial walls (stagnated blood) during atrial flutter, migration may cause emboli
atrial flutter usually resolves how deteriorates to atrial Fib or spontaneously returns to normal
caused of atrial flutter valvular heart disease, MI, hypertension, cardiomyopathy, myocarditis and pericarditis
evaluating atrial flutter rate 180-400, rhythm is regular, Pwave is sawtooth can be 2:1, 3:1 etc, PRI not measurable (to many Pwave), QRS is normal <.12 sec
Atrial Fibrillation quivering of the atrials caused by multiple ectopic beats, causes complete loss of atrial pumping ability and increased risk of mural thrombi and emboli
caused of A Fib same as a-flutter plus hyperthyroidism, pulm diseases and congenital heart diseases
evaluating for A-Fib rate can be as high as 400bpm, rhythm is irregular irregular, Pwave is chaotic and irregular, PRI is unmeasurable, QRS <.12
PVC ectopic beat originating in ventrical, can occur in normal or diseased heart
common causes of PVC's anxiety, caffeine, alcohol, tobacco and meds. Also seen in pts with HX of MI, heart disease, acidosis, electrolyte imbalance, CHF, and hypoxia
when are PVC's dangerous multiple PVC's in less than 1 minute (indicates irritable vent area), couplets (2in a row), salvos (3 in a row), or R on T phenomenon
Salvos 3 PVC's in a row, also known as a run of Vtach
R on T phenomenon PVC's occur during Twave of preceding beat, can cause PVC's to turn into Vtach (when it happens Vtach QRS wave looks more rounded)
evaluating for PVC's rate is underlying, rhythm is regular, Pwave is not associated with PVC (others are normal), PRI not measurable (others are norm), QRS norm except with PVC>.12 abnormal look and premature, Twave is opposite direction of PVC (PVC up Twave down)
All PVC's are followed by what compensatory pause (because they are premature)
Ventricular Tachycardia run of 5 or more PVC's, looks like a series of wide QRS's w/no Pwave, tombstones or fireman hats
*what causes Vtach hypoxic heart, as with severe myocardial ischemia
evaluating Vtach rate 140-300 bpm, rhythm is regular, no Pwave with PVC, no PTI with PVC, wide QRS
Ventricular Fibrillation chaotic unorganized ventrical activity, wavy irregular pattern, no QRS, no rate, rhythm, Pwave or PRI
Asystole cardiac standstill-flatline-no pulse, dead
PEA pulseless electrical activity, rare and usually follows an event like tension pneumo, cardiac trauma, severe electrolyte imbalance or acid-base disturbance
PEA rhythm any rhythm that does not produce a pulse except Vtach, Vfib and asystole
most common AV Heart block causes meds like digitalis, damage from MI
1st degree AV heart block (mildest) prolonged PRI >.20 second delay at AV node
1st degree AV heart block causes meds (digitalis), >vagal tone, hyperkalemia, myocarditis, and degenerative disease
evaluating for 1st degree heart block rate normal, rhythm regular, Pwave normal, PRI prolonged (>.20), QRS norm at <.12
Second degree AV Block Type 1, aka Mobitz 1 aka Wenkebach (intermediate block) PRI gets long each beat until QRS is dropped, same causes as type 1
2nd degree AV Block type 2 aka Mobitz type 2 rare and serious, many Pwaves with out QRS, PRI can be normal or prolonged, but is always constant
evaluating 2nd degree mobitz 2 rate varies but ventrical is always less than atrial, rhythm is regular regular or regular irregular, Pwave looks normal but no QRS follows some.PRI is norm or long but all look alike, QRS <.12
causes of 2nd degree heart block type 2 damaged bundle branch fallowing an MI or degenerative disease
3rd degree block most extreme and dangerous heart block. Conduction problem is in bundle of his (narrow QRS) or in bundled branches (wide QRS), complete block, no conduction atria and ventricals
causes of 3rd degree heart blocks inferior MI, increased vagal tone, myocarditis, digitalis toxicity, may be permanent condition following MI or degenerative disease
evaluating 3rd degree heart block rate <60, rhythm is regular, Pwave is normal but not always followed by QRS, PRI varies many with no relationship to QRS, QRS is usually wide but can also be normal
idoventricular rhythm normal pacemaker is not setting pace, trials norm but ventrical wave is irritable ectopic beat, looks like slow wide bizarre QRS, with brady, leads to rapid heart failure, (looks like row of slow moving PVC's)
accelerated idoventricular rhythm variation of idoventricular but rate is 60-100
evaluating idioventricular rhythm rate 30-40, rhythm is regular, Pwave is absent, PRI none, QRS >.12
Junctional rhythm area of AV junction assumes pacemaker
causes of junctional rhythm AV node damage, electrolyte disturbance, digitalis toxicity, heart failure, valve disease, rheumatic fever
evaluating junctional rhythm rate 40-60, accelerated 60-100, junctional tachycardia >100, rhythm is reg, Pwave is absent, inverted or short, can be befor or after QRS, PRI if present is short, QRS <.12
Pwave following QRS is what junctional rhythm, shows retrograde conduction (up), and will be inverted (looks like ST segment is dipped)
If Pwave appears befor QRS in junctional rythm Pwave is not responsible for QRS if PRI is less than .12
deviation of the ST segment up or down suggests what abnormal myocardial perfussion and oxygenation (due to hyperkalemia), cardiac ischemia but no perminant damage
COPD causes what kind of axis deviation hyperinflation rotates heart & causes R axis deviation.
Cor pulmonale (R vent enlargement) causes what kind of deviation R axis deviation
COPD dysrhythmias Tachycardia, Multifocal atrial tachycardia, ventricle ectopic beats are most common (from hypoxemia & meds) & worsen at night due to hypoxemia.
Calculating EKG HR Between R-R, add lg boxes at .20 each and sm boxes at .04 then divide into 60. 2lg + 3sm is 60/.2+.2+.04+.04+.04 equals 60/.52 is a HR of 115
Prolonged QRS .12-.10 causes R or L bundle branch block, IVCD or L anterior or posterior fascicular block.
QRS >.12 Complete RBBB or LBBB (3rd degree block), IVCD, or PVC’S (v-tach & pacemakers)
IVCD intraventricular conduction delay.
Sick sinus syndrome disturbance of SA node causing marked variable in rhythm – cycles of brady and tachy.
Atrial tachy Series of 3 or more PAC’s (includes PAT-paroxysmal atrial tach)
Atrial flutter rate according to Karol’s handout 250-350
A Fib Uncoordinated atrial depolarization’s
Junctional escape Rhythms Inverted or no p-wave, AV node rhythm of 40-60
AV block Conduction block w/in AV node (sometimes bundle of his)
1st degree block PRI >.20, caused by increased vagal tone, digitalis, beta- blockers, calcium channel blockers or ischemia damage.
2nd degree AV block slow conduction at AV node so some don’t get through. Ventricle rhythm is < atrial rhythm.
2nd degree Type 1 (wenkebach) AV node block. PRI it elongates then drops QRS – most often seen in sleeping pt with high vagal tone (rarely is pacing indicated)
3rd degree complete block, but escape rhythms cause QRS but they originate in AV node, bundle of his or vent region. No synchrony between Pwaves & QRS atrial rhythm can be normal, but vent will be 30-40
SVT most often caused by reentry currents in atria or from vent to atria. Rate 140-250
VPB (Ventricular premature beats) Wide QRS, caused by eptopic foci in ventricle.
V Tach Caused by aberrant vent automatically or intra-ventricular reentry, can be sustained or paroxysmal (short run) wide QRS 100-200 bpm.
V Flutter vent depolarizes >200/min
V Fib Uncoordinated vent depolarization’s
The 3 types of heart cells are pacemaker (automaticity), conducting (conduct electricity), and myocardial cells ( contract in response to electricity)
where is the greatest degree of of automaticity SA node-thus the pacemaker
what is the back up pacemaker AV junction
blocked coronary artery causes what ischemia and infarction leads to dysrrhythmias and <QT
what does the QRS reflect on ECG electrical activity of the ventricals
during depolarization what happens in the myocardial cells K- moves out and NA+ and CA+ moves in
during re-polarization what happens in the myocardial cells K- moves back inside and NA+ and CA+ move to the outside
isoelectric flat (no positive of negative charge)
normal ECG has how many leads 12, 6 limb (vertical plane) and 6 chest (horizontal plane)
what are the 6 limb leads I, II, III, aVR, aVL, aVF
bipolar leads leads I, II, and III, voltage is measured as a difference in between two electrodes
augmented leads leads aVR, aVL, aVF are augmented by the machine because they are unipolar
frontal plane vertical plane of the limb leads, measures up-down, right-left etc.
what are the chest leads V1-V6
where are V1 and V2 located 4th intercostal space V1 on the left and V2 on the right
where is V6 located 5th intercostal in the midaxillary line (mid axillary would be if you cut body in half from top down, so mid axillary is under armpit) V3, V4 and V5 are located in between V2 and V6
depressed ST ischemia
elevated ST infarction, greater the height-greater the damage
elevated T ischemia (usually seen with depressed ST
significant increase in Q wave (.04) is indicative of what infarction
ECG's are useful for assessing what impact of lung disease on heart, severity of infarction, heart rhythm, never pick pumping ability or QT
what clinical findings suggest the need for ECG's orthopnea and syncope
what is the normal intrinsic rate of primary pacemaker 60-100
what is the normal intrinsic rate of secondary pacemaker 60-80
what does P wave represent atrial depolarization
what does QRS represent ventrical depolarization
what does T wave represent ventrical re-polarization
normal PR interval .20
normal QRS <.12
QRS is equally spaced with 3 large boxes between, whats the rate 100 (300/3 is 100)
QRS is equally spaced with 4 large boxes between, whats the rate 75 (300/4 is 75)
prolonged PR interval AV block
acute infarction looks like what on ECG elevated ST segment
difference between fibrillate and flutter flutter you can count and fibrillation is a quiver-chaotic, Ventrical fib and flutter originate low in the heart, so no QRS as with atrial fib and flutter (they have a QRS)
must know ID these strips and how to treat including meds brady, sinus tach, PVC, fine and course VFib, asystol, depressed ST and elevated ST
1 small box on strip .04 seconds
1 large box on strip .20 seconds
calculating bpm add the large boxes between R waves and devide into 300 so 300/3 is 100 bpm
Created by: williamwallace