EKG-Electrocardiogram

Steps to read the EKG

1. Determine Rate (300/#big boxes ~ 60-100bpm)
2. Determine Rhythm (P:QRS ratio)
   
3. P waves
   
4. PR interval (0.12-0.2)
   
5. QRS Complex (0.06-0.12)

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  P wave: atrial depolarization (atrial contraction/systole)
  (0.7-0.12)

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  QRS complex: ventricular depolarization (contraction/systole) and hidden atrial repolarization (diastole)
  (0.05-0.10)

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  T wave: ventricular repolarization and relaxation

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  PR interval: line from the end of the p wave to the onset of the QRS complex
  AV node delay
  (0.12-0.2 –> 3-5mm)

• Def:
  • a sudden stop in heartbeat (ventricular standstill).

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  Causes:
  • hypovolemia, hypoxia, acidosis, tension pneumothorax, cardiac tamponade, acute MI, overdose of tricyclic antidepressants (SSRI) selective serotonin reuptake inhibitor, severe electrolyte disturbances.

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  Presentation:
  • Patient will not have a pulse or blood pressure, a code blue!

• Presentation:
  • 1) ASx
  • 2) SOB
  • 3) Chest Pain
  • 4) palpitations
  • 5) irregularly irregular pulse

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  EKG:
  • no P waves, with variable and irregular QRS response

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  Acute:  PIRATES
  
  • 1) Pulmonary disease
  • 2) Ischemia
  • 3) Rheumatic heart disease
  • 4) Anemia/Atrial myxoma
  • 5) Thyrotoxicosis
  • 6) Ethanol
  • 7) Sepsis

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  Chronic:
  
  • 1) HTN
  • 2) CHF

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  Management:
  • If unstable
    – synchornized electrical cardioversion starting at 100J
  • If stable
    – control rate w/ diltiazem or B-blockers and anticoagulate if duration is >48hrs
    – Elective cardioversion may be performed if <48hrs; or need to anticoagulate and perform TEE prior to conversion
  • Do not give nodal blockers if there is evidence of WPW syndrome on EKG

• Calculators:
  • MDCalc CHADS2-VASc Score
  • MDCalc CHADS2 Score

• Presentation:
  • 1) Asymptomatic
  • 2) palpitations
  • 3) Syncope
  • 4) lightheadedness

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  EKG:
  • regular rhythm;
  • “sawtooth” appearance of P waves;
  • rate 240-320bpm w/ varying degrees of blockade

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  Management:
  • If unstable
    – synchronized electrical cardioversion starting at 100J
  • If stable
    – control rate w/ diltiazem or B-blockers and anticoagulate if duration is >48hrs
    – Elective cardioversion may be performed if <48hrs; or need to anticoagulate and perform TEE prior to conversion
  • Do not give nodal blockers if there is evidence of WPW syndrome on EKG
  • anticoagulation and rate control, cardiovert like Afib

• Types:
  • First degree AV block
  • Second degree AV block
  • Third degree AV block

• Causes:
  • 1) none
  • 2) increased vagal tone
  • 3) B-blocker/CCB use

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  EKG:
  • PR interval > 200 msec

• EKG:
  • progressive PR lengthening until a dropped beat occurs;
  • PR interval then resets

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  Causes:
  • 1) drug effects (digoxin, B-blockers, CCBs)
  • 2) increased vagal tone
  • 3) sinoatrial conduction disease
  • 4) R coronary ischemia or infarction

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  Treatments:
  • 1) stop offending drug
  • 2) Atropine
  • 3) pacemaker placement

• EKG:
  • unexpected dropped beat(s) w/o a change in PR interval

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  Presentation:
  • 1) occasionally syncope
  • 2) frequent progression to third-degree AV block

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  Causes:
  • 1) fibrotic disease of conduction system
    2) acute/subacute/prior MI

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  Treatments:
  • pacemaker placement

• EKG:
  • no relationship btw P and QRS waves

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  Presentation:
  • 1) syncope
  • 2) dizziness
  • 3) acute heart failure
  • 4) hypotension
  • 5) cannon A waves

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  Treatments:
  • pacemaker pacemaker

• EKG:
  • Rate 150-250bpm
  • P wave buried in QRS or shortly after

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  Presentation:
  • palpitations
  • SOB
  • angina
  • syncope
  • lightheadedness

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  Management:
  • carotid massage; Valsalva; adenosine can stop the arrhythmia
  • cardiovert if hemodynamically unstable

• EKG:
  • the retrograde P wave is often seen after a normal QRS

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  Presentation:
  • palpitations
  • SOB
  • angina
  • syncope
  • lightheadedness

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  Management:
  • carotid massage, Valsalva, or adenosine can stop the arrhythmia.
  • cardiovert if hemodynamically unstable

• Etiology:
  • Mutation in the cardiac sodium channel gene (sodium channelopathy)
    
  • – 60 diff mutations identified.
    
  • – Autosomal dominance has been demonstrated

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  Brugada Sign in TYPE 1 (EKG):
  • Coved ST segment elevation >2mm in greater than 1 of V1-V3 followed by a NEGATIVE T-wave

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  Type 1 Brugada Must be Assoc. w/ clinical Criteria to make the dx:
  • 1) Documented VF or polymorphic ventricular tachycardia (VT)
    
  • 2) Family hx sudden cardiac death < 45 years old
    
  • 3) Coved-type ECG in family members
    
  • 4) Inducibility of VT with programmed electrical stimulation
    
  • 5) Syncope
    
  • 6) Nocturnal agonal Respiration

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  Brugada Type II ECG:
  • Greater than 2 mm of saddleback shaped ST elevation

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  Management Goal of Treatment:
  • Prevention of sudden cardiac arrest and the termination of any ventricular tachyarrhythmias with an implantable cardioverter-defibrillator

• EKG:
  • three or more unique P-wave morphologies and rate >100bpm

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  Causes:
  • multiple atrial pacemakers
  • reentrant pathways
  • COPD
  • hypoxemia

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  Management:
  • 1) treat the underlying disorder
  • 2) verapamil or B-blockers for rate control and suppression of atrial pacemakers (not very effective)

• EKG:
  • early, wide QRS no preceded by a P wave. PVCs are usually followed by a compensatory pause

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  Causes:
  • ectopic beats arise from ventricular foci; hypoxia; electrolyte abnormalities; hyperthyroidism

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  Management:
  • treat underlying cause;
  • if symptomatic give B-blockers or occasionally other antiarrhythmics

• Causes:
  • 5Hs and 5Ts
  • Hypovolemia
  • Hypoxia
  • Hydrogen ion: acidosis
  • Hyper/HypoK other metabolic
  • Hypothermia
  • Tablets: Drug OD, ingestion
  • Tamponade: cardiac
  • Tension pneumothorax
  • Thrombosis: coronary
  • Thrombosis: PE

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  Management:
  • epinephrine or vasopressin; simultaneously search for the underlying cause and provide empiric tx
  • bradycardic PEA only – Give atropine

• Presentation:
  • 1) Asymptomatic
  • 2) lightheadedness
  • 3) syncope
  • 4) chest pain
  • 5) hypotension

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  Management:
  • If symptomatic
    
    • – give atropine (to increase HR) and consider dopamine, epinephrine, and glucagon
  • If Mobitz II or third-degree heart block is present
    
    • – place transcutaneous pacemaker pads, and have atropine at the bedside
  • If hemodynamically unstable pts
    
    • – A temp transvenous pacemaker may be required

• Presentation:
  • 1) palpitations
  • 2) shortness of breath

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  Conditions Suggest:
  • 1) fear
  • 2) pain
  • 3) exercise
  • 4) hyperthyroidism
  • 5) volume contraction
  • 6) infection
  • 7) pulmonary embolism

• Management:
  • If unstable
    
    • – perform synchronized electrical cardioversion
  • If stable
    
    • – control rate w/ vagal maneuvers (Valsalva maneuver, carotid sinus massage, or cold stimulus)
  • If resistant to maneuvers
    
    • – give up three doses of adenosine followed by other AV nodal blocking agents (CCBs or B-blockers)

• Causes:
  • associated with
  • long QT syndrome
  • proarrhythmic response to meds
  • hypokalemia
  • congenital deafness

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  Management:
  • Correct hypokalemia,
  • withdraw offending agent,
  • give Mag initially and
  • cardiovert if unstable

• Management:
  • immediate electrical cardioversion and ACLS protocol
  • unsynchronized shock w/ 360J–>360-J shock–>epinephrine–>360-J shock–>amiodarone or lidocaine–>360-J shock–>epinephrine
  • Vasopressin can be given in place of the 1st or 2nd dose of epinephrine
  • – amiodarone, lidocaine, procainamide, or sotalol may be used for stable Vtach

• Management:
  • Cardioversion
  • unsynchronized shock w/ 360J–>360-J shock–>epinephrine–>360-J shock–>amiodarone or lidocaine–>360-J shock–>epinephrine
  • Vasopressin can be given in place of the 1st or 2nd dose of epinephrine
  • – amiodarone, lidocaine, procainamide, or sotalol may be used for stable Vtach

• Causes: 
  • “Skippy route” for conduction fibres to follow = accessory route

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  Presentation:
  • Often asymptomatic, but be wary of sudden death

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  ECG:
  • Shortened P-R interval;
    
  • Widened QRS with slurred onset (delta wave)

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  Management:
  • Monitor if asymptomatic and risk of death small;
    
  • RF ablation if symptomatic,
  • medical therapy if unsuccessful.

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  Cause of death:
  • If ventricles contract twice from input from two routes