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01
ECG BASICS
Waveforms, intervals, measurement -- Thaler Ch.1
Thaler (9e, Ch.1): The P wave represents atrial depolarization, the QRS complex represents ventricular depolarization, and the T wave represents ventricular repolarization. Each wave can be described by a single mean vector of given direction and magnitude.
02
P WAVES & ATRIAL ACTIVITY
SA node, atrial depolarization, PR interval -- Thaler Ch.1-3
Thaler (9e, Ch.1): The vector of atrial depolarization points leftward and inferiorly -- P waves are upright in leads I, II, aVF, and V5-V6. Lead aVR records a purely negative P wave because it sees the current moving away. P wave amplitude must not exceed 2.5mm (0.25 mV) in any lead.
03
QRS COMPLEX
Ventricular depolarization, bundle branches, axis -- Thaler Ch.1-4
Thaler (9e, Ch.1): The first part of the QRS reflects septal depolarization (left to right), which creates small septal Q waves in lateral leads. The remainder reflects the dominant left ventricle swinging the mean vector leftward. R wave progression: V1 smallest R, V5 largest. Normal QRS axis: 0 to +90 degrees (extended to -30 degrees by most cardiologists).
04
ST SEGMENT & T WAVES
Ischemia, injury, infarction patterns -- Thaler Ch.6
Thaler (9e, Ch.6): ST elevation in two or more contiguous leads defines a STEMI. Symmetric T wave inversions are characteristic of ischemia; asymmetric inversions (gradual down, abrupt up) are typical of secondary repolarization abnormalities from LVH. These two patterns must be distinguished clinically.
05
HEART BLOCKS
AV blocks, bundle branch blocks, hemiblocks -- Thaler Ch.4
Thaler (9e, Ch.4): "What is a conduction block? Think of it as an interruption somewhere in the normal conduction pathway." Mobitz II and third-degree blocks have a significant risk of progressing to complete cardiac standstill. Mobitz I (Wenckebach) is usually benign. RBBB + left anterior fascicular block = bifascicular block -- high risk in acute anterior MI.
06
SVT, AFIB & ATRIAL RHYTHMS
AVNRT, atrial flutter, atrial fibrillation, MAT -- Thaler Ch.3
Thaler (9e, Ch.3): AVNRT uses a reentrant circuit within the AV node -- onset and termination are abrupt, rate 150-250 bpm, QRS is usually narrow. Atrial flutter produces sawtooth F-waves at 250-350/min with AV block. Atrial fibrillation is the most common sustained arrhythmia -- irregularly irregular, no true P waves, multiple tiny reentrant circuits whirling in unpredictable fashion.
07
VTACH, VFIB & VENTRICULAR RHYTHMS
PVCs, VTach, VFib, Torsades, AIVR -- Thaler Ch.3
Thaler (9e, Ch.3): Ventricular tachycardia has a rate of 100-250 bpm with wide, bizarre QRS complexes. AV dissociation (P waves marching through independently), fusion beats, and capture beats are the most reliable criteria for VTach vs SVT with aberrancy. Ventricular fibrillation is a totally disorganized rhythm that is immediately life-threatening -- the only treatment is defibrillation.
08
12-LEAD INTERPRETATION
Lead groups, STEMI localization, coronary territories -- Thaler Ch.6
Thaler (9e, Ch.6): "Localizing the infarct: inferior STEMI = II, III, aVF (RCA); anterior STEMI = V1-V4 (LAD); lateral STEMI = I, aVL, V5-V6 (LCx). Posterior MI appears as a mirror image on standard leads -- dominant R in V1, horizontal ST depression V1-V3."
09
ELECTROLYTE DISTURBANCES
Hyperkalemia, hypokalemia, calcium, Thaler Ch.7
Thaler (9e, Ch.7): Hyperkalemia produces a predictable sequence of ECG changes as potassium rises: peaked T waves, PR prolongation, P wave flattening and disappearance, QRS widening, and finally a sine wave pattern preceding ventricular standstill. Each stage must be recognized urgently.
10
PULMONARY EMBOLISM
Right heart strain, S1Q3T3, ECG patterns, ALS management
Clinical Pearl: Sinus tachycardia is the most common ECG finding in PE (40-70% of cases). S1Q3T3 is classic but present in only about 20%. A completely normal ECG is seen in up to 30% of confirmed PE cases -- a normal ECG never rules it out.
11
CLINICAL APPLICATION & ALS
ACLS algorithms, prehospital decision-making, AHA 2025
AHA 2025 / NREMT: Stable vs. unstable is the first branch point in every tachycardia and bradycardia algorithm. Unstable = hypotension, AMS, ischemic chest pain, pulmonary edema, or signs of shock caused by the rhythm. Unstable = immediate electrical therapy.
12
TREATMENT PROTOCOLS
Stable vs. Unstable -- Drugs, Doses, AHA 2025 Algorithms
Sources: AHA 2025 Guidelines for CPR and ECC, ACLS algorithms, NREMT Paramedic Examination Specifications 2024, National EMS Education Standards. Always follow your local medical director protocols (ICEMA/REMSA/local) which may differ.
STABLE vs. UNSTABLE

STABLE

STABLE
Signs
  • SBP greater than 90 mmHg
  • Alert and oriented, GCS intact
  • Skin warm, dry, normal color
  • No active ischemic chest pain
  • No pulmonary edema
ApproachMedical management first. Time permits IV access, 12-lead, assessment. Medications before electricity.

UNSTABLE

UNSTABLE
Signs
  • Hypotension (SBP less than 90)
  • AMS -- altered mental status
  • Ischemic chest pain from the rhythm
  • Acute pulmonary edema
  • Signs of shock (diaphoresis, weak pulse)
  • Syncope caused by the rhythm
ApproachIMMEDIATE electrical therapy. Sedate if conscious and time allows. Do NOT delay for medications.
BRADYCARDIA (less than 60 bpm with symptoms)

STABLE BRADYCARDIA

STABLE
RhythmsSinus bradycardia, 1st degree AV block, Mobitz I (Wenckebach), slow junctional with adequate perfusion
ATROPINE SULFATE
0.5mg IVP -- repeat q3-5 min -- max total 3mg
IO: same dose if no IV available
Anticholinergic -- blocks vagal input to SA and AV nodes. More effective for nodal blocks than infranodal blocks.
Thaler (Ch.4) + AHA 2025: Atropine is first line for symptomatic bradycardia at the AV node level. Less effective or ineffective for blocks below the AV node (Mobitz II, 3rd degree with wide QRS escape). Always prepare TCP for those patients.

UNSTABLE BRADYCARDIA

UNSTABLE
Algorithm
  1. Atropine 0.5mg IVP while preparing pacer
  2. Transcutaneous Pacing (TCP) -- priority for infranodal blocks
  3. Sedate conscious patient (midazolam, ketamine, fentanyl per protocol)
  4. Dopamine infusion 2-10 mcg/kg/min if TCP unavailable
  5. Epinephrine infusion 2-10 mcg/min as alternative
  6. Transport to pacing-capable facility
TRANSCUTANEOUS PACING
Rate: 60-80 bpm (set above intrinsic rate)
mA: Start at 0, increase until electrical capture (wide paced complex after each spike)
Confirm mechanical capture: palpable pulse matching set rate
Set mA 10 above capture threshold to maintain capture
Electrical capture does NOT equal mechanical capture. Always confirm pulse. Sedation is mandatory for conscious patients.
DOPAMINE INFUSION
2-10 mcg/kg/min IV -- chronotropic and inotropic (beta-1 dominant at this range)
Atropine for Mobitz II or 3rd degree block with wide QRS -- may be ineffective or paradoxically worsen the block. TCP is primary for these rhythms.
SVT / NARROW COMPLEX TACHYCARDIA

STABLE SVT

STABLE
RhythmsAVNRT, AVRT, atrial tachycardia -- narrow QRS, regular, rate 150-250 bpm
Algorithm
  1. 12-lead ECG, O2, IV access, monitor
  2. Vagal maneuvers: modified Valsalva or carotid massage
  3. Adenosine 6mg rapid IVP with immediate 20ml flush
  4. Adenosine 12mg rapid IVP if no response (may repeat 12mg once)
  5. Rate control with diltiazem or metoprolol if persistent
ADENOSINE
6mg rapid IVP -- then 12mg -- then 12mg (three-dose protocol)
Use antecubital or proximal vein -- immediate saline flush 20ml
Half-life approximately 10 seconds
Transiently blocks AV node. Warn patient of flushing, chest tightness, brief asystole (normal). Must be given FAST. Print rhythm strip during administration. Ineffective in atrial flutter (unmasks F-waves but rarely converts).
Adenosine, diltiazem, beta-blockers, verapamil in WPW with pre-excited AFib -- may accelerate conduction via accessory pathway and precipitate VFib.
Pearl: Rate of exactly 150 bpm = suspect atrial flutter 2:1 until proven otherwise. Look carefully for sawtooth waves in II, III, aVF, V1. Adenosine will slow and unmask flutter waves.

UNSTABLE SVT

UNSTABLE
TreatmentIMMEDIATE synchronized cardioversion
Algorithm
  1. Press SYNC -- verify sync markers on R waves on screen
  2. Sedate if conscious and time allows
  3. SVT: start at 50-100J biphasic
  4. Atrial flutter: 50-100J biphasic (often converts at low energy)
  5. Reassess pulse and rhythm -- escalate energy if no conversion
  6. Re-engage SYNC before each subsequent shock (device may auto-revert)
SYNCHRONIZED CARDIOVERSION
SVT (narrow, regular): 50-100J biphasic
Atrial flutter: 50-100J biphasic
AFib: 120-200J biphasic
Monomorphic VTach with pulse: 100J biphasic
SYNC must be engaged before every shock
SYNC prevents R-on-T phenomenon (which can trigger VFib). If SYNC cannot lock on a fast irregular rhythm, use unsynchronized defibrillation energy.
ATRIAL FIBRILLATION / FLUTTER

STABLE AFib / AFlutter

STABLE
Algorithm
  1. O2, IV access, 12-lead, monitor
  2. Determine: new onset (less than 48h) vs. chronic
  3. Rate control: diltiazem 0.25mg/kg IVP over 2 min
  4. Alternative: metoprolol 5mg slow IVP over 5 min
  5. Anticoagulation (ED -- not typically prehospital)
  6. New onset AFib less than 48h may be cardioverted in ED
DILTIAZEM (Class IV CCB)
0.25mg/kg IVP over 2 min (typical 15-20mg)
Repeat 0.35mg/kg after 15 min if needed
Maintenance infusion: 5-15mg/hr
Rate control via AV node calcium channel blockade. Monitor for hypotension and bradycardia. Do NOT use in WPW + AFib.
Pearl: AFib greater than 48h onset or unknown duration -- do NOT cardiovert without anticoagulation (clot risk = stroke). Rate control and transport only. New onset less than 48h: cardioversion safer but still requires MD order.

UNSTABLE AFib / WPW + AFib

UNSTABLE
TreatmentSynchronized cardioversion 120-200J biphasic. WPW + AFib: cardioversion is treatment of choice.
WPW + AFib (STABLE) -- PROCAINAMIDE
15-18mg/kg IV at 20-50mg/min loading rate
Maintenance: 1-4mg/min infusion (hospital)
Slows conduction in accessory pathway. Stop if hypotension, QRS widens more than 50%, or QT prolongs significantly. Requires physician order and close monitoring.
Adenosine, digoxin, diltiazem, verapamil, beta-blockers in WPW + AFib -- blocks AV node while leaving accessory pathway open, forcing all conduction via accessory pathway, potentially causing VFib.
VENTRICULAR TACHYCARDIA (with pulse)

STABLE MONOMORPHIC VTach

STABLE
Algorithm
  1. 12-lead ECG, O2, IV/IO, monitor -- document rhythm
  2. Treat as VTach -- never assume SVT with aberrancy
  3. Amiodarone 150mg IV over 10 min
  4. If no response or deteriorating: synchronized cardioversion 100J
  5. Lidocaine 1-1.5mg/kg IVP as alternative
AMIODARONE (Class III)
Stable VTach: 150mg IV over 10 min
Arrest dose: 300mg IVP, then 150mg IVP
Blocks Na, K, Ca channels + beta-adrenergic
Monitor for hypotension during infusion. Drug of choice for most sustained VTach with pulse.
LIDOCAINE (Class IB)
1-1.5mg/kg IVP -- repeat 0.5-0.75mg/kg q5-10 min -- max 3mg/kg total
IO: same dose
Alternative to amiodarone. Blocks fast sodium channels. CNS toxicity at high doses: slurred speech, seizures, AMS.
Thaler (Ch.3): AV dissociation, fusion beats, and capture beats are the most reliable distinguishing features of VTach from SVT with aberrancy. When in doubt -- treat as VTach.

UNSTABLE VTach (pulse present)

UNSTABLE
TreatmentIMMEDIATE synchronized cardioversion 100J biphasic
Algorithm
  1. Confirm pulse is present
  2. Sedate if conscious (midazolam, ketamine, fentanyl per protocol)
  3. SYNC ON -- synchronized cardioversion 100J biphasic
  4. Escalate: 150J, 200J if no conversion
  5. If patient loses pulse: switch to cardiac arrest protocol immediately
  6. Amiodarone 150mg IV after conversion to prevent recurrence
Pearl: If VTach patient loses their pulse during your care -- immediately begin CPR and switch to unsynchronized defibrillation protocol. Pulseless VTach = cardiac arrest.
CARDIAC ARREST -- PULSELESS (VFib / Pulseless VTach / PEA / Asystole)

VFib / Pulseless VTach

ARREST
Algorithm
  1. CPR -- 2-2.4 inches depth, 100-120/min, full recoil, compression fraction target greater than 60%
  2. Defibrillate 200J biphasic -- UNSYNCHRONIZED -- resume CPR immediately after shock
  3. IV/IO access during CPR -- do not stop compressions
  4. Epinephrine 1mg IVP/IO every 3-5 min (AHA 2025: give as soon as possible)
  5. Check rhythm every 2 min -- defibrillate if shockable persists
  6. Amiodarone 300mg IVP after 3rd shock -- 150mg after 5th shock
  7. Advanced airway -- waveform capnography EtCO2 target greater than 10 mmHg
  8. Treat reversible causes: Hs and Ts
EPINEPHRINE 1:10,000
Cardiac arrest: 1mg IVP/IO every 3-5 min (no max in arrest)
ET route (last resort): 2-2.5mg diluted in 10ml NS
AHA 2025: Administer epinephrine as soon as possible in non-shockable rhythms. In VFib/pVTach, give after first cycle of CPR and defibrillation (approximately after 3rd shock). Vasopressin removed from AHA guidelines -- same outcomes, less evidence.
AMIODARONE (Arrest Dose)
1st dose: 300mg IVP/IO (after 3rd shock)
2nd dose: 150mg IVP/IO (after 5th shock)
Alternative: Lidocaine 1-1.5mg/kg IVP/IO
AHA 2025: High-quality CPR is the most important intervention. EtCO2 less than 10 mmHg after 20 min = consider TOR. Vasopressin no longer recommended. Double sequential defibrillation may be considered for refractory VFib per some protocols.

PEA / Asystole

ARREST
PEAOrganized electrical activity with NO pulse. Do NOT defibrillate. CPR + epi + treat reversible cause.
AsystoleConfirm in 2 leads. CPR + epinephrine + treat reversible causes. No defibrillation.
Algorithm
  1. CPR immediately -- high quality, minimize interruptions
  2. IV/IO access -- epinephrine 1mg IVP q3-5 min
  3. Advanced airway -- waveform capnography
  4. Search and treat the Hs and Ts
  5. Check rhythm every 2 min -- if VFib develops, defibrillate
THE Hs and Ts
Hs: Hypovolemia (fluid bolus), Hypoxia (O2/ventilation), H+ acidosis (bicarb), Hypo/Hyperkalemia (calcium/bicarb/insulin+D50), Hypothermia (warm)

Ts: Tension pneumo (needle decompression), Tamponade (pericardiocentesis), Toxins (antidotes), Thrombosis-PE (thrombolytics), Thrombosis-coronary (cath lab)
Pearl: PEA clues -- narrow fast PEA = hypovolemia or tamponade. Wide slow PEA = hypoxia, hyperkalemia, drug toxicity. ROSC = sudden EtCO2 spike above 35 mmHg. Do NOT interrupt CPR to check pulse unless EtCO2 spikes.
TORSADES DE POINTES / POLYMORPHIC VTach

Torsades de Pointes

BOTH
DefinitionPolymorphic VTach where QRS complexes twist around the isoelectric baseline. Associated with prolonged QTc (greater than 500ms).
Algorithm
  1. Magnesium sulfate 1-2g IV over 5-10 min (even with normal Mg)
  2. Correct electrolytes: target K+ greater than 4.0, Mg greater than 2.0
  3. Discontinue all QT-prolonging drugs
  4. Unstable or pulseless: unsynchronized defibrillation 200J
  5. Do NOT give amiodarone -- it prolongs QT and worsens TdP
MAGNESIUM SULFATE
Torsades with pulse: 1-2g IV over 5-10 min (2 min if deteriorating)
Pulseless TdP: 1-2g IVP/IO
Mix: 2g in 100ml NS for infusion
Membrane stabilizer -- suppresses early afterdepolarizations that trigger TdP. Monitor for hypotension and respiratory depression at high doses. Calcium gluconate reverses magnesium toxicity.
Amiodarone, sotalol, quinidine in Torsades -- these all prolong the QTc and will worsen TdP.

POST-ROSC CARE

POST-ROSC
AHA 2025Systematic post-arrest care significantly improves neurologically intact survival. Begin immediately on ROSC.
Algorithm
  1. Airway: confirm with waveform capnography EtCO2 35-45 mmHg
  2. Breathing: 10 breaths/min -- avoid hyperventilation. Target SpO2 92-98% -- avoid hyperoxia.
  3. Circulation: target SBP greater than 90 (ideally greater than 100). Fluid bolus 250-500ml NS if hypotensive. Vasopressors if needed.
  4. 12-lead ECG immediately -- if STEMI: activate cath lab regardless of neuro status
  5. Temperature: prevent hyperthermia (avoid temp greater than 37.5 C). Active cooling per protocol if comatose.
  6. Blood glucose: target 140-180 mg/dL. Treat hypoglycemia with D50.
AHA 2025 Keys: Avoid hyperoxia (SpO2 92-98%). Avoid hyperventilation (EtCO2 35-45). STEMI post-arrest = immediate cath regardless of coma. Prevent fever in comatose survivors.
ELECTRICAL THERAPY QUICK REFERENCE

DEFIBRILLATION vs. CARDIOVERSION vs. PACING

REFERENCE
DEFIB
  • VFib: 200J biphasic -- UNSYNCHRONIZED -- no pulse present
  • Pulseless VTach: 200J biphasic -- UNSYNCHRONIZED
  • Pulseless TdP: 200J biphasic -- UNSYNCHRONIZED
  • Resume CPR immediately after every shock
CARDIO-VERSION
  • SVT (narrow, regular): 50-100J -- SYNC ON
  • Atrial flutter: 50-100J -- SYNC ON
  • AFib: 120-200J -- SYNC ON
  • Monomorphic VTach with pulse: 100J -- SYNC ON
  • Re-engage SYNC after each shock (device may auto-revert to unsynchronized)
PACING (TCP)
  • Rate: 60-80 bpm (above patient intrinsic rate)
  • Start mA at 0 -- increase until electrical capture (wide complex after each spike)
  • Confirm mechanical capture: palpable pulse at set rate
  • Set mA 10 above capture threshold
  • Sedate all conscious patients -- TCP is painful
CARDIAC DRUG QUICK REFERENCE

ANTIARRHYTHMICS

REFERENCE
ADENOSINE
6mg IVP -- 12mg -- 12mg rapid push + 20ml flush. Half-life 10 sec. Narrow SVT only.
AMIODARONE
Stable VTach: 150mg over 10 min. Arrest: 300mg then 150mg IVP. Class III.
LIDOCAINE
1-1.5mg/kg IVP -- repeat 0.5-0.75mg/kg q5-10 min -- max 3mg/kg. Class IB.
MAGNESIUM SULFATE
1-2g IV over 5-10 min. Torsades, refractory VFib, eclampsia, severe hypomagnesemia.
DILTIAZEM
0.25mg/kg IVP over 2 min. Rate control -- AFib, atrial flutter, SVT. Class IV CCB.
METOPROLOL
5mg slow IVP over 5 min -- repeat up to 3 doses (15mg max). Rate control. Class II beta-blocker.
PROCAINAMIDE
15-18mg/kg IV at 20-50mg/min. WPW + AFib (stable), stable VTach. Class IA.

VASOACTIVE / CHRONOTROPIC

REFERENCE
EPINEPHRINE 1:10,000
Arrest: 1mg IVP/IO q3-5 min. Infusion (post-ROSC/bradycardia): 2-10 mcg/min. Alpha + Beta agonist.
ATROPINE SULFATE
Bradycardia: 0.5mg IVP q3-5 min -- max 3mg total. Anticholinergic -- vagolytic.
DOPAMINE INFUSION
2-20 mcg/kg/min IV. Dose-dependent: low = renal, mid = beta-1 (chronotropic/inotropic), high = alpha-1 (vasopressor).
NOREPINEPHRINE
0.1-0.5 mcg/kg/min IV. Post-ROSC hypotension. Strong alpha-1 + moderate beta-1.
CALCIUM CHLORIDE 10%
1g (10ml) IVP over 2-5 min. Hyperkalemia ECG changes, CCB overdose, hypocalcemia. Membrane stabilizer -- does NOT lower K+.
SODIUM BICARBONATE
1mEq/kg IVP. Hyperkalemia, TCA overdose, prolonged arrest, severe metabolic acidosis.
D50W
25g (50ml) IVP. Hypoglycemia -- post-ROSC glucose less than 70 mg/dL or symptomatic hypoglycemia.