ECG/EKG & ACS

normal conduction pathway

• SA node (pacemaker)

  • “sinus rhythm” = electrical impulse begins in the SA/sinus node (P wave should be present)

  • atrial depolarization → atrial contraction

• AV node (brief delay before transmitting impulse to ventricles)

  • allows time for atrial contraction/filling before ventricular contraction

• Bundle of His/AV bundle

• Right + left bundle branches

• Purkinje fibers

  • ventricular depolarization spreads form apex upward

  • ventricles contract and eject blood

bundle branch block

• delayed/blocked conduction through a right or left bundle branch

  • may produce “bunny ears” on ECG

junctional rhythm

• pacemaker activity originates around the AV junction rather than the SA node

• P wave may be absent or inverted

ECG

• measures summed electrical activity of the heart recorded from the body surface

• Lead II: rhythm monitoring (especially atrial rhythms → A-fib, PACs)

3-lead vs 5-lead vs 12-lead

• 3-lead: 3 electrodes, basic continuous rhythm/rate, cannot adequately diagnose MI

• 5-lead: 5 electrodes, continuous telemetry, limited ST-segment evaluation

  • Limb Leads I, II, III, aVR, aVL, aVF, one V-lead for the chest

• 12-lead: 10 electrodes → 12 views, diagnostic cardiac work up, not practical for continuous monitoring

  • ischemia/ACS/MI

  • Limb Leads I, II, III, aVR, aVL, aVF, and Chest Leads V1–V6

ECG paper basics

• one small box: 0.04 sec

• one large box: 0.20 sec

• standard strip: 6 seconds (30 large boxes)

• vertical axis: measures voltage (0.1 mV → small box; 0.5 mV large box)

PQRST

• P wave: atrial depolarization

• QRS complex: ventricular depolarization

• T wave: ventricular repolarization

• PR interval: atrial impulse → through AV node

• ST segment: indicates myocardial ischemia/injury

• QT interval: ventricular depolarization → repolarization

PQRST normal intervals

• P wave: 0.08-0.10 sec

• PR interval: 0.12-0.20 sec

• QRS: 0.06-0.10 sec

• QTc: ≤0.44 sec

rhythm analysis steps

• Calculate HR

  • count # of QRS/R waves in 6 sec or count boxes between R waves x 0.04 then 60 divided by that #

• Determine regular vs irregular

  • measure R-to-R intervals

• Look for P waves

• Measure PR interval

• Measure QRS

• Assess ST segment

• Examine T wave

  • peaked with hyperkalemia

• Measure QT interval

  • RATE → RHYTHM → P → PR → QRS → ST → T → QT

normal sinus rhythm

• 60-100 bpm

• NSR

• 1 P for every QRS (narrow)

dysrhythmias nursing priorities

• FIRST LOOK AT PATIENT

• then check lead placement

  • disconnected lead

  • artifact

  • actual arrest

cardiac dysrhythmias etiology & risk factors

etiology

• delayed after depolarization

• heart block

• abnormal pacemaker (ectopic foci)

• reentry circuit activity

risk factors

• excess caffeine, stress, tobacco use

• Digitalis (digoxin), Quinidine overdose

• high BP & CAD

• heart muscle damage after MI, valve disease

sinus bradycardia

• <60 bpm, NSR (1 P for every QRS)

• causes: athlete, vasovagal response, PSNS stimulation, MI/heart dz, hypothermia, ↑ ICP, low hormones

  • vasovagal triggers: straining during defecation, vomiting, intubation, mechanical ventilation

• sxs: (act on these) CHEST PRESSURE/pain, dyspnea, fatigue, low BP, dizziness, seizure, fainting (syncope)

• tx: fall precautions, reverse the cause, medications, stimulate SNS, suppress PSNS

  • IV ATROPINE every 3-5 min, do NOT exceed 3 mg

  • consider cardiac pacemaker to support perfusion

sinus tachycardia

• >100 bpm, regular rhythm, 1 P:1 QRS (may be hidden with T wave d/t speed)

• causes: normal physiological response (fever, exercise, anxiety, dehydration, pain), fluid volume loss/excess, MI, shock, hyperthyroidism, stress, hypoxia, anemia, hemorrhage, hypotension, heart dz, L-sided heart failure, cardiac tamponade, meds (atropine, catecholamines, theophylline, CNS stimulants, caffeine, nicotine)

• sxs: chest pressure/pain, dyspnea, palpitations, lightheadedness

• tx: (only if sxs)

  • stable: evaluate rhythm, consider O2, establish IV, ID/tx reversible causes (adenosine → SVT/BB)

  • unstable: 12-lead ECG, administer meds, synchronized cardioversion, consider cardiac ablation

cardioversion vs. defibrillation

• cardioversion: synchronized, shock synchronized with R WAVE, usually pulse

  • unstable tachyarrhythmias, A-fib/flutter

• defibrillation: unsynchronized, shock delivered immediately, no pulse

  • VF and pulseless VT

atrial dysrhythmias

• SA node dominates (HR > 150 bpm)

• causes: cardiac dz, electrolyte imbalance, emotions, exercise, COPD, meds, nicotine

• sxs: skipped beats, pulse deficit

• tx: adress underlying cause (K loss), meds, cardioversion, lifestyle mods

atrial fibrillation

• no distinct P waves (irregular R-R spacing), no PR, atrial rate = 300-600 bpm, ventricular rate (untx) = 100-180 bpm

• decrease CO d/t loss of atrial kick (20% ventricular filling)

• premature ventricular contraction (PVC) early, full pause after, no pulse (irregular rhythm)

• causes: HEART DISEASE (HF, constrictive pericarditis, ischemic/rheumatic heart disease, mitral stenosis, atrial irritation, complication of CABG/valve replacement), COPD, PE, HTN, DM, thyroid dz, sepsis

• risk factors: uncontrolled BG, hyperthyroidism, kidney dz, OSA, smoking, alcohol, sedentary lifestyle, over 60

• sxs: HEART PALPITATIONS, fatigue, dyspnea, lightheadedness, chest pain

• tx: synchronized cardioversion, meds (metoprolol, diltiazem/CCB, digoxin), anticoagulant (reduce CVA and MI risk)

atrial flutter

• SAWTOOTH, atrial rate 240-360 bpm, no PR, ventricular rate depends on degree AV block

• P:QRS (2:1, 4:1, 6:1, variable)

• causes: MI, comp. CABG/valve replacement, antiarrhythmic meds (BB, CCB, amiodorone, digoxin)

• risk factors (same as a-fib): uncontrolled BG, hyperthyroidism, kidney dz, OSA, smoking, alcohol, sedentary lifestyle, over 60

• sxs: heart palpitations, fatigue, dyspnea, lightheadedness, chest pain

• tx: synchronized cardioversion, meds (BB, CCB + sodium channel blocker or amiodorone → not for older)

heart blocks

• AV junction either slow or block signal from reaching ventricles

• 1st degree

• 2nd degree (Mobitz I/Wenckebach) & 2nd degree (Mobitz II)

• 3rd degree (Complete heart block) = most severe

• tx: monitor, consider meds pt taking, intervene IMMEDIATELY

first-degree heart block

• 60-100 bpm, regular rhythm, PR >0.20 sec

• AV conduction delayed → every impulse still reaches ventricles

• causes: MI, electrolye (hypokalemia, hypomagnesemia), infections, hypothyroidism, autoimmune (RA, lupus), male, age > 60

  • antiarrhythmic meds (sodium channel blockers, BB, CCB, potassium channel blockers, cardiac glycosides, magnesium)

  • athletes d/t higher resting vagal tone → lower HR

• sxs: none

• tx: none

second-degree heart block (Mobitz I/Wenckebach)

• PR interval progressively longer → QRS drops

• atrial regular, ventricular irregular

• causes: severe CAD, anterior wall MI, acute myocarditis, digoxin toxicity

• sxs: none

• tx: monitor/observe, atropine/isoproterenol

second-degree heart block (Mobitz II)

• PR interval constant, QRS suddenly dropped

• may progress to third-degree block

• causes: extensive anterior wall MI, degenerative changes in His-Purkinje system, massive calcification of mitral/aortic valve anulus

• sxs: none (rare: dizziness, lightheadedness, palpitations, syncope)

• tx: atropine/isoproterenol, pacemaker therapy

third-degree heart block (complete heart block)

• complete failure of comm. between atria and ventricles (severely impair CO/perfusion)

• atrial 60-100 bpm, ventricular 15-60 bpm, no PR

• causes: inferior or anterior wall MI, congenital abnormality, rheumatic fever

• sxs: fainting, dizziness, extreme fatigue, chest pain, dyspnea

• tx: IMMEDIATE PACEMAKER

ventricular dysrhythmias

• MOST SERIOUS d/t CO severely reduced

• QRS wide and bizarre, foci within ventricles cause them to contract

  • one or two beats ok → series can be fatal

• causes: cardiac dz, CHF, MI, atrial enlargement, caffeine, electrolyte imbalance (low K)

premature ventricular contraction (PVC)

• an early ventricular beat before the next expected normal sinus beat

• premature, wide/bizarre QRS, followed by compensatory pause, unifocal (look similar) or multifocal (shapes differ d/t K imbalance)

• couplet (2 PVCs in a row), triplet (3 PVCs in a row)

• causes: cardiac muscle injury, chronic lung dz, electrolyte imbalance, caffeine, alcohol

• sxs: palpitations (fluttering or skipped beats), chest pain, dyspnea, lightheaded, syncope

ventricular tachycardia

• 150-250 bpm, regular rhythm (varies), no P waves, QRS > 0.12 (distorted)

• causes: severe heart disease, MI, digoxin toxicity, prolonged QT, electrolyte imbalance, acidosis

• sxs: acute MI (angina/chest pain), no pulse, altered LOC, pupil dilation → can lead to cardiac arrest

• tx: pulse (cardioversion) or pulseless (CPR/defib/amiodarone), pacemaker/ICD, meds (lidocaine, pronestyl)

  • < 30 sec: nonsustained V-tach

  • > 30 sec: sustained V-tach

ventricular fibrillation

• LETHAL RHYTHM

• most common cause of death w/ CAD

• no P wave, PR interval R-R interval, QRS

  • multiple ectopic in Purkinje network

• no HR/pulse/BP/respirations

• tx: CPR, meds (epi, amiodarone → not for older); shock (only if rhythm to shock them out of)

PEA and asystole

• PEA: electrical rhythm appears on monitor → NO palpable pulse/CO

  • death of cells/mitochondria

  • reversible causes:

    • 5 H’s: hypovolemia, hypoxia, hydrogen ion (acidosis), hypo/hyperkalemia, hypothermia

    • 5 T’s: tension pneumothorax, tamponade, toxins, thrombosis (pulmonary/coronary)

• asystole: no effective cardiac electrical activity or CO

acute coronary syndrome

• group of disorders caused by reduced/blocked coronary blood flow

  • unstable angina, NSTEMI, STEMI

• patho: atherosclerotic plaque → plaque rupture → platelets + clot formation → coronary artery becomes narrowed → ↓ myocardial oxygen → ischemia → injury → infarction

ischemia, injury, infarction

• ischemia: decreased oxygen/blood supply to myocardium (ST depression)

• injury: more severe myocardial compromise (ST elevation)

• infarction: irreversible myocardial tissue death (pathologic Q wave)

MI patho

• primary: coronary artery occlusion

• causes: coronary atherosclerosis, vasospasm, platelet aggregation, emboli, A-fib, LV mural thrombus, infective endocarditis vegetations

• low O2 → anaerobic metabolism → angina

STEMI, NSTEMI, unstable angina

Condition	Main ECG/marker clue
STEMI	ST elevation
NSTEMI	ST depression or T-wave inversion + elevated cardiac markers
Unstable angina	ACS symptoms without elevated markers in slide algorithm

cardiac markers

• most sensitive: cardiac troponin (cTnI, cTnT)

• CK-MB: increases 4-6 hr after MI (less specific)

• myoglobin: rapid increases 1-3 hr (not cardiac-specific)

• BNP/NT-proBNP: heart failure

• hs-CRP: inflammation/LT CV risk

ACS emergency care (IMPORTANT)

• main goal: ACUTE REPERFUSION

• baseline cardiac rhythm + serial ECG, vital signs, IV access/labs, oxygen if <90%, chewable aspirin, nitrates, morphine/opiaye PRN, reperfusion therapy, IV heparin

  • other therapies after: BB, ACE-I, statins, clopidogrel/Plavix, aspirin, SGLT-2/GLP-1 for other comoboridities