Intro to EKG Interpretation-AH ch. 27

12-Lead ECG

*used to diagnose dysrhythmias, conduction abnormalities, chamber enlargement, and myocardial ischemia, injury, or infarction* -can also suggest cardiac effects of electrolyte disturbances (high or low Ca++ & K+ levels) and the effects of antiarrhythmic meds -has 10 electrodes for 12 leads (6 precordial & 4 limbs) *primary focus: left ventricle bc this is the part of the heart needed to pump blood out to the body* -additional leads can be added -this is an ECG machine that is placed at the pt's side for an immediate recording

Ventricular Tachycardia (VT/V-Tach) Overview

-3 or more PVCs in a row, occurring at a rate exceeding 100 bpm -causes are similar to those causing PVCs -pts with larger MIs & lower EFs are at higher risk of lethal V-Tach -2 Forms: 1. Pulseless 2. Unstable with Pulse

Sinus Rhythms

-ALL originate in the SA node -P waves all look alike -vary according to rate: 1. Normal Sinus Rhythm (NSR) 2. Sinus Bradycardia 3. Sinus Tachycardia (Sinus Tach) -remember that CO is affected by rates too slow or too fast bc CO= HR x SV

Interpreting ECG Rhythm: Step 3

-EXAMINE THE P WAVES -look at similarities bw size, shape, and appearance-may be assumed to originate from SA node -different shapes mean different foci (a signal may be coming from somewhere other than the SA node)

Interpreting ECG Rhythm: Step 4

-EXAMINE THE P to QRS RATIO -every P wave should be followed by a QRS complex -every QRS complex should be preceded by a P wave

Interpreting ECG Rhythm: Step 6

-EXAMINE THE QRS COMPLEX -size & shape should be similar (nice & skinny) *width should be <0.12 sec* -wider: likely ventricular issue -narrower: SA or AV node issue -QT interval measurement should also be examined-is it getting longer?

Interpreting ECG Rhythm: Step 2

-HEART RATE -count the number of R waves in a 6 sec strip & multiply by 10 -ex. 7 R waves in a 6 sec strip, the HR is 70

Interpreting ECG Rhythm: Step 7

-INTERPRET THE RHYTHM -look for signs of hemodynamic compromise: cool, clammy, diaphoretic, dizzy, anxious, decreased LOC, decreased BP -remember: check the pt

Interpreting ECG Rhythm: Step 5

-MEASURE THE PR INTERVAL -normal: 0.12-0.20 sec -longer PR interval: AV Blocks -ex. first degree AV block PR >0.20

Overview of Atrial Fibrillation- AF/A-Fib

-MOST common sustained cardiac arrhythmia -affects nearly 15% of those >85 -loss of atrial kick decreases CO (20-30%) -increased risk of emboli due to pooled, clotted blood in the atria (INCREASED RISK FOR STROKE) -due to many areas/cells in the atria are firing on their own -high risk of coagulation bc blood just sits there (COPD can cause this) -it's rapid, disorganized & uncoordinated twitching of the atrial musculature -loss of atrial kick may lead to symptoms of HF like SOB, fatigue, exercise intolerance, and malaise

If a person has atrial fibrillation, will they go into cardiac arrest?

-No, not normally bc the ventricles are working fine -many ppl are walking around with A-Fib & are fine

Interpreting ECG Rhythm: Step 1

-RHYTHM: Is it regular (drumbeat rhythm) or irregular? -plot out the R-R intervals -plot out the P-P intervals -for irregular rhythms (spaces bw QRS complexes will change): determine if it's essentially regular with some irregularity or if it's irregularly irregular

Sinus Tachycardia

-Rate: 100-200 bpm -Rhythm: Regular -P Waves: Uniform & Upright -P to QRS Ratio: 1:1 -PR Interval: 0.12-0.20 sec -QRS Complex: <0.12 sec

Normal Sinus Rhythm

-Rate: 60-100 bpm -Rhythm: Regular -P waves: uniform & upright -P to QRS ratio: 1:1 -PR Interval: 0.12-0.20 sec -QRS Complex: <0.12 sec

Sinus Bradycardia

-Rate: <60 bpm -Rhythm: Regular -P waves: uniform & upright -P to QRS ratio: 1:1 -PR Interval: 0.12-0.20 sec -QRS Complex: <0.12 sec *basically, it's exactly the same as sinus rhythm, except </= 59 bpm

Atrial Flutter (A-Flutter)

-Rate: Atrial (250-350); Ventricular is variable -Rhythm: Usually regular -P Waves: *sawtooth/shark teeth* pattern (can get identifiable P waves) -P to QRS Ratio: typically 3:1 or 4:1 -PR Interval: Unable to determine -QRS Complex: Usually narrow

Atrial Fibrillation-AF/A-Fib

-Rate: Atrial 350-600 bpm; ventricular=variable -Rhythm: Irregularly irregular -P Waves: NONE; fibrillatory waves -P to QRS Ratio: NO identifiable P waves -PR Interval: Unable to measure -QRS Complex: usually narrow *T Waves will disappear* -pulse usually jumps around (e.g. 80 to 100 to 70); probably bc not all signals are getting to the ventricles bc AV node blocks some

Premature Ventricular Contractions (PVCs)

-Rate: Depends on underlying rhythm -Rhythm: looks normal (PQRST to wide & bizarre) -P Waves: NONE -PR Interval: NONE -P to QRS Ratio: 0:1 or 1:1 (if P wave is there) -QRS Complex: >/= 0.12 sec (WIDE & BIZARRE) *T wave is usually opposite QRS direction*

Premature Atrial Complex (PAC)

-Rate: Normal; depends on underlying rhythm -Rhythm: Irregular due to early P waves, creating a PP interval that is shorter than others -P Waves: an early & different P wave may be seen or may be hidden in the T wave; other P waves in the strip are consistent -P to QRS Ratio: usually 1:1 -PR Interval: the early P Wave has a shorter-than-normal PR Interval, but still bw 0.12-0.20 sec -QRS Complex: QRS that follows the early P Wave is usually normal, but it may be abnormal or even absent

Ventricular Fibrillation (VF/V-Fib)

-Rate: Ventricular >300/min -Rhythm: Ventricular is extremely irregular -P Wave: NONE -PR Interval: NONE; *no atrial activity is seen on ECG* -QRS Complex: irregular, undulating waves without recognizable QRS omplexes

Ventricular Tachycardia (VT/V-Tach)

-Rate: typically 150-250 bpm; may be faster or slower -Rhythm: usually regular; may be slightly irregular -P Waves: NONE -PR Interval: NONE or very irregular if P waves are seen -P to QRS Ratio: 0:1 -QRS Complex: >/= 0.12 sec (WIDE & BIZARRE) *>/= 3 PVCs in a row= V-Tach*

Ventricular Fibrillation (VF-V-Fib) Treatment

-SHOCK: depolarize heart & give SA node chance to start over (basically stops the heart to allow SA node to recapture) -start immediate CPR until defibrillation is available -if arrest not witnessed or there was more than a 4 min delay in EMS response, 5 cycles of CPR may be given prior to defib. -after initial defib., 5 addtl cycles of CPR (about 2 min of continuous chest compressions in intubated pt), beginning with chest compression & alternating with a rhythm check & defib., are used to convert VF to an electrical rhythm that produces a pulse -Epi should be given ASAP after the 2nd rhythm check (immediately before or after 2nd defib) & then every 3-5 min.

If both the SA node and AV node fail, are there any other homeostatic mechanisms that can depolarize the ventricles?

-Yes, the Purkinje fibers can depolarize the ventricles; however, they generally cannot support the heart bc their intrinsic rate is 20-40 bpm which is not enough to maintain oxygenation of the tissues -known as the ventricular pacemaker

Ambulatory ECG Monitoring or a Holter Monitor

-a small, lightweight tape recorder-like machine that the pt wears & that continuously records the ECG on a tap, which is later viewed an analyzed with a scanner -for pts to take home & sends ECG info to physician so they can download this info to see how this pts heart is working at home (some pts heart rhythm will be fine in the hospital & then change at home)

15-Lead ECG

-adds 3 additional chest leads across the right precordium & is used for early diagnosis of right ventricular & left posterior (ventricular) infarction

18-Lead ECG

-adds 3 posterior leads to the 15-lead ECG & is useful for early detection of myocardial ischemia & injury

Ventricular Asystole

-aka flatline -absent QRS complexes in 2 different leads, although P waves may be apparent for a short duration -no heartbeat, no palpable pulse, & no respirations -without immediate treatment=fatal -rapid assessment to determine cause (e.g. hypoxia, drug OD, severe electrolyte imbalance, hypovolemia, cardiac tamponade, tension pneumothorax, trauma, hypothermia, coronary or pulmonary thrombosis) -start CPR & intubate, establish IV line -after 2 min. or 5 cycles of CPR, a bolus of IV Epi is given & repeated at 3-5 min. intervals -CAN'T SHOCK -not very survivable; <1% chance

Why is the P wave smaller than the QRS wave? What would it signify if the P wave becomes larger?

-bc the ventricles are a larger muscle mass & they generate a larger amplitude -representing by a higher voltage on ECG paper -if the P wave becomes larger, it would signify atrial hypertrophy (if QRS complex starts getting big, it could mean ventricular hypertrophy)

ST Segment

-bw QRS complex & T wave -should be at same level (baseline) as segment bw T & P waves -represents early ventricular repolarization -normally isoelectric=when no electric activity is detected, the line on the graph remains flat -it's analyzed to identify whether it's above or below the isoelectric line

Causes of Premature Atrial Complex (PAC)

-caffeine, alcohol, nicotine -stretched atrial myocardium (e.g. hypervolemia) -anxiety -hypokalemia -hypermetabolic states (pregnancy) -atrial ischemia, injury, or infarction

Atrial Flutter (A-Flutter) Signs & Symptoms

-can cause serious S&S -chest pain -SOB -low BP

Causes of Premature Ventricular Contractions (PVCs)

-can occur in health ppl with intake of caffeine, alcohol, nicotine -cardiac ischemia or infarction -increased workload on heart (HF or tachycardia) -digitalis toxicity -hypoxia -acidosis -electrolyte imbalances (hypokalemia, hypomagnesemia

Rapid Ventricular Response

-can occur when a person is in A-Fib & the AV node starts letting more signals reach the ventricles -this leads to an increased ventricular rate, which means the ventricles won't be able to fill & SV gets messed up

Hardwire Monitoring

-cardiac monitor at pt's bedside for continuous reading -used in ICUs -can monitor O2 stat, respirations, many leads

1-Minute ECG Strip

-contains 300 large boxes & 1500 small boxes -an easy & accurate way of determining HR with a regular rhythm is to count the number of small boxes within an RR interval & divide 1500 by that number -ex. if 10 small boxes bw 2 R waves, the HR= 1500/10= 150 bpm -25 small boxes=1500/25=60 bpm

What is another way to determine heart rate that is used usually when the rhythm is irregular and based on a 1-minute ECG strip?

-count the number of RR intervals in 6 sec & multiply that number by 10 -top of ECG paper is usually marked at 3 sec intervals (one 3 sec interval=15 large boxes horizontally) -you would count the RR intervals & not the QRS complexes bc a computed HR based on the other would be inaccurately high

Monophasic Defibrillators

-deliver current in only one direction -require increased energy loads

Biphasic Defibrillators

-deliver electrical charge to the positive paddle, which then reverses back to the originating paddle -this system allows for lower, possibly nonprogressive energy levels, with potentially less myocardial damage

Electrical Cardioversion

-delivery of a "timed" electrical current to terminate a tachydysrhythmia -defib. is set to synchronize with the ECG so that the electrical impulse discharges during ventricular depolarization (QRS) -synchronization prevents discharge from occurring during ventricular repolarization, which could result in VT or V-Fib. -pt is NPO for at least 4 hrs before -place gel-covered paddles or conductor pads on front & back -before cardioversion, pt gets moderate sedation IV & analgesic med or anesthesia -supplemental O2 needed during procedure

QT Interval

-don't have to know much about; just be aware of it -goes from beginning of QRS complex to end of T wave -represents total time for ventricular dp & rp -ALOT of drugs prolong QT interval; varies with HR, gender & age -if QT interval becomes prolonged, pt may be at risk for a lethal ventricular dysrhythmia called torsades de pointes

Conduction of Heart

-electric impulse from SA node through the atria to the AV node -then, the electrical impulse travels very quickly through Bachmann's bundle & bundle of His to the R & L bundle branches & the Purkinje fibers, located in the ventricular muscle -the electrical stimulation of the muscle cells of the ventricles in turn causes the mechanical contraction of the ventricles (systole); the cells repolarize & the ventricles relax (diastole)

P Waves

-electrical impulse starting in the sinus node & spreading through the atria; atrial depolarization -normally 2.5 mm or less in height and 0.11 sec or less in duration -energy travels through RA to LA via Bachman's Bundle *normally, P wave is small, rounded & upright in lead II*

Normal Electrical Conduction

-electrical impulse that stimulates & paces the cardiac muscle originates in the SA node (located near the SVC & right atrium) -electrical impulse occurs at a rate of 60-100 bpm in adult

Electrophysiology (EP) Study

-electrodes placed inside the heart in order to obtain an intracardiac ECG -used to determine the most effective treatment plan & to diagnose the dysrhythmia -bc it's invasive, it's performed in the hospital & may require that the pt be admitted

ECG Paper

-graph paper -horizontal axis=time; vertical axis=voltage -based on horizontal axis (time): each "big" square=0.2 sec; so 5 "big" squares= 1 sec -based on vertical axis (voltage): each "big" square=5 mm (5 mm by 0.2 sec) -in hospital, usually they will print them out in 6 sec strips (30 big squares) -small square=1 mm by 0.04 sec

Electrocardiography (ECG)

-graphic representation of the electrical impulses of the heart -obtained by placing electrodes in standard positions on the skin of the chest wall & extremities -recordings of the electrical current flowing bw two electrodes is made on graph paper or displayed on a monitor

Atrioventricular (AV) Node

-intrinsic rate=40-60 bpm -when the SA node fails, the AV node can take over but it's slower -stimulates muscle cells of the atria to contract -major job: slows the electrical impulse, giving the atria time to contract & fill the ventricles with blood (atrial kick= accounts for nearly 1/3 of the volume ejected during ventricular contraction)

What does it mean when atrial fibrillation is defined as paroxysmal dysrhythmia?

-it means that A-Fib is transient, starting & stopping suddenly and occurring for a very short time

What does it mean if the QRS complex starts becoming wider?

-it's taking longer for the ventricles to depolarize -representing by a longer time on the horizontal axis of the ECG paper

Causes of Sinus Bradycardia

-lower metabolic needs (sleep, athletic training, hypothyroidism) -vagal stimulation -meds: calcium channel blockers, amiodarone, and BBs -increased ICP; MI -Hs & Ts: hypovolemia, hypoxia, H+ ion (acidosis), hypo/hyperkalemia, hypoglycemia, hypothermia, toxins, tamponade (cardiac), tension pneumothorax, thrombosis (cardiac or pulmonary), and trauma (hypovolemia, increased ICP)

What if you are interpreting lead II of an ECG strip, an the P wave is upside down?

-may be due to wrong placement OR it could mean that the electricity is traveling in the wrong direction -it could mean that there's a group of cells near the AV node that is actually depolarizing the heart & sending the signal backwards

Premature Ventricular Contractions (PVCs) Overview

-not that serious; some ppl have them every week r/t caffeine, nutritional deficiencies (low Mg++ or low K+) -if PVCs become more common & irregular, let HC provider know -an impulse that starts in a ventricle & is conducted through the ventricles before the next normal sinus impulse -if PVCs look the same then they are originating in the same place in ventricles; if they look different then the signal is coming from other areas/cells in ventricles -bigeminy=every other complex is PVC; trigeminy=every 3rd complex is PVC; quadrigeminy=every 4th complex is PVC -very common in heart attack

Overview of Atrial Flutter (A-Flutter)

-occurs bc of a conduction defect in the atrium & causes a rapid, regular atrial rate, usually bw 250-400 times/min -bc the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node (if AV node let all of them in, it would cause V-Fib) -often occurs in pts with COPD, valvular disease, thyrotoxicosis & in ppl after open heart surgery & repair of congenital cardiac defects

Causes of Atrial Fibrillation-AF/A-Fib

-occurs in ppl of advanced age with structural heart disease, such as valvular heart disease (most often mitral or tricuspid) -CAD, HTN -Diastolic/systolic HF -diabetes, obesity -hyperthyroidism -pheochromocytoma -pulmonary HTN & embolism -obstructive sleep apnea -acute moderate to heavy ingestion of alcohol

Leads

-on an ECG, several different recordings can be obtained of the heart by using a variety of electrode combinations, called leads -lead= specific view of the electrical activity of the heart; imaginary lines formed bw 2 electrodes -provide a "snapshot" of electrical activity of the heart -each lead provides a different view -appearance of ECG varies with lead placement (ex. in some leads, the QRS is inverted) -standard ECG has 12 leads or 12 different views *for this class, we will only interpret lead II*

Causes of Sinus Tachycardia

-physiologic or psychological stress (acute blood loss, anemia, shock, hypo/hyper volemia, heart failure, pain, hypermetabolic states, fever, exercise, anxiety) -meds: catecholamines, aminophylline, atropine, caffeine, alcohol, nicotine, amphetamines, cocaine, ecstasy -enhanced automaticity of the SA node and/or excessive sympathetic tone with reduced PS tone (known as inappropriate sinus tachycardia) -autonomic dysfunction, causing postural orthostatic tachycardia syndrome (POTS)

Torsades de Pointes

-polymorphic ventricular tachycardia preceded by a prolonged QT interval -common causes: CNS disease, certain meds, low levels of Mg++, Ca++, or K+ -bc this rhythm is likely to cause the pt to deteriorate & become pulseless, immediate treatment is required: correction of any electrolyte imbalance, administration of isoproterenol (Isuprel) IV, or initiation of ventricular pacing

Interpreting the ECG

-printed on graph paper that is divided by light & dark vertical & horizontal lines at standard intervals -time & rate=horizontal axis -amplitude or voltage=vertical axis -positive deflection: when ECG wave moves toward the top of the paper; negative deflection=when it moves toward the bottom -composed of waveforms (PQRST & maybe U) and of segments & intervals (PR interval, ST segment, QR interval) *waves=deflections, segments=flat lines, intervals=combo of waves & lines*

Electrical Interference ECG

-pt has fever or there is shaking in their muscles that interfere with ECG tracing

To enhance the interpretation of the ECG, what additional information should be obtained?

-pt's age -gender -BP -height -weight -symptoms -meds (esp. digitalis & antiarrythmic agents)

Ventricular Fibrillation (VF/V-Fib) Overview

-severe electrical chaos in ventricles -multiple foci fire in erratic & disorganized manner -most common dysrhythmia in pts with cardiac arrest -NO VENTRICULAR CONTRACTION=NO PERFUSION TO VITAL ORGANS -No pulse, no respirations, no audible heartbeat -cardiac arrest & death are imminent if the dysrhythmia is not corrected -CPR doesn't solve it; it only buys you time

Ventricular Rhythms

-these are dysrhythmias in which the ventricles become the pacemaker 1. Premature Ventricular Contractions (PVCs) 2. Ventricular Tachycardia (VT) 3. Ventricular Fibrillation (VF) *know basic treatments for VT & VF*

U Wave

-thought to represent repolarization of the Purkinje fibers -rare wave -sometimes appears in pts with hypokalemia, HTN or heart disease -if present, it follows the T wave & is usually smaller than the P wave -if it's tall, it may be mistaken for an extra P wave

PR Interval

-time it takes impulse to travel through atria & to ventricles -measured from beginning of P wave to first deflection after PR segment (aka to beginning of QRS complex); basically time it takes for the signal to reach the ventricles *prlonged in heart block bc problem bw communication bw atria & ventricles* -represents time needed for sinus node stimulation, atrial depolarization, & conduction through AV node before ventricular depolarization *Need to memorize: usually 0.12-0.20 sec (3-5 small boxes)*

Telemetry

-transmission of radiowaves from a battery-operated transmitter to a central bank of monitors -primary benefit: wireless system, which allows pts to ambulate while one or two ECG leads are monitored -transmitter can be placed in a disposable puch & worn around the neck or simply secured to the pt's clothing; MONITOR STAYS WITH PT *cardiac telemetry does NOT diagnose dysrhythmia, it only monitors dysrhythmia* -most transmitter batteries are changed every 24-48 hrs

What cells control the heart rate?

-under normal conditions, the cells of the SA node control the HR bc these are the pacemaker cells with the fastest intrinsic depolarization -all tissue around the SA node is connective tissue, so it's nonconductile; however, you can develop conduction tissue or scar tissue in other places of the heart that can interfere with the SA node

Defibrillation

-used in emergency situations as treatment of choice for *VF & pulseless VT* -NOT USED FOR PTS WHO ARE CONSCIOUS OR HAVE A PULSE -depolarizes a critical mass of myocardial cells all at once; when they repolarize, the SA node usually recaptures its role as the pacemaker -2 types: monophasic (send electricity through one pad) or biphasic (in most hospitals) -goal: allow SA node to resume control -if unsuccessful, CPR is immediately initiated & other ALS treatments are begun -Epi or vasopressin is administered after defib. to make it easier to convert the dysrhythmia to a normal rhythm with the next defib.

To prevent interference from the electrical activity of skeletal muscle, where are the limb electrodes usually placed?

-usually placed on areas that are not bony & do not have significant movement

QRS Complex

-ventricular depolarization -measured from first deflection following PR segment to beginning of ST segment -should be tall & skinny -normal length: <0.12 sec (<3 small boxes); remember that 1 small box=0.04 sec

T Wave

-ventricular repolarization -if T wave is peaked= hyperkalemia -nice, rounded upright deflection; usually somewhat bigger than the P wave -one of the first things that you will see with heart attacks is T wave inversion (ischemia= T wave will flip upside down) -T wave will start flattening out with hypokalemia

Overview of Premature Atrial Complex (PAC)

-very benign; known as "when the heart skips a beat" -occurs when a group of cells in the atria decide to depolarize the heart before the SA node can reset itself (electrical impulse occurs inside atria, but outside SA node; it's an ectopic beat) -impulse is faster than SA node & causes an early beat that leads to an early contraction -often seen with sinus tachycardia -if PACs are infrequent, no treatment is necessary; they're common in healthy ppl & often don't need treatment -if they are frequent (>6/min), then this may mean A-Fib

The beginning of the P wave to the start of the Q wave should be less than _____________ seconds.

0.2

Atrial Rhythms

1. Atrial Fibrillation (AF/A-Fib) 2. Atrial Flutter (A-Flutter) 3. Premature Atrial Complex (PAC)

Electrical Stimulation vs Electrical Relaxation

1. Electrical Stimulation= depolarization -mechanical contraction= systole 2. Electrical Relaxation= repolarization -mechanical relaxation= diastole

ECG Rhythm Strip Interpretation

1. Irregular/Regular Rhythm 2. Fast/Slow HR 3. Locate P wave. Is there a P wave for every QRS? 4. Determine the PR interval (Normal= 0.12-0.20 sec/3-5 very small boxes) 5. Identify the QRS (Normal= <0.12 sec/ <3 very small boxes) 6. Identify the ST segment. Is it at baseline? 7. Identify the T wave. Upright? Peaked? Flattened?

Defibrillator Steps

1. Self-adhesive pads are applied to pt's chest (remove hair PRN) 2. Protect pt from burns 3. Defibrillator charged & "all clear" (keep O2 away from pads) 4. Shock is delivered 5. If normal rhythm resumes, do 5 cycles of CPR then CHECK PULSE 6. If no pulse, CPR resumes

Cardiac Rhythm Classification

1. Sinus Rhythms -NSR -sinus tachycardia/bradycardia 2. Atrial Rhythms (issue created in atria; a group of cells is depolarizing faster than the SA node) -PACs -A-Fib/A-Flutter 3. Junctional Rhythms (just have a general idea of; atria is depolarizing backwards; hard to recognize) -premature junctional complex -nonparoxysmal junctional tachycardia -AV nodal reentry tachycardia 4. Ventricular Rhythms (originate in ventricles) -PVCs -V-Tach/V-Fib

Ventricular Tachycardia (VT/V-Tach) Treatment

1. Unstable with Pulse -sedate pt if they're hemodynamically stable enough -if they're awake with low BP, don't sedate them -synchronized cardioversion=shock them; set defibrillator to their HR 2. Pulseless -CALL A CODE & BEGIN CPR -defibrillate; treat just like V-Fib -follow ACLS protocol

What is the most common cause of ventricular fibrillation? a. atrial fibrillation b. hypertension c. coronary artery disease (CAD) d. nicotine

c. coronary artery disease (CAD) & resulting acute MI

The appearance of the ECG will vary based on _______________ placement.

electrode -Note: it's important for the nurse to know the correct placement of electrodes bc if it's in the wrong place, you will get the wrong picture of the heart, resulting in a wrong diagnosis.

A standard 12-lead ECG reflects electrical activity primarily in the _______________ ventricle.

left

ST segment elevation suggests _____________________________________.

myocardial injury; or myocardial cellular death -such as heart attack (aka STEMI= ST segment elevation myocardial infarction)

ST segment depression suggests ________________________________.

myocardial ischemia