Cardiology Flashcards
EKG findings with right atrial enlargement (RAE)
- P wave peaked in V1 (> 1.5 mm) or lead II (> 2.5 mm)
- This is caused by RA depolarization lasting longer than normal and waveform extends to end of LA depolarization. RA amplitude remains the same, though overlap with LA depolarization leads to taller p-wave.
- Remember: P-wave is normal width.
EKG findings in left atrial enlargement (LAE)
- P-wave shaped like an “m” OR p-wave is > 3 mm in V1 OR lead II
- LA depolarization takes longer –> LA/RA waves do not overlap as much (leading to dip in middle of p-wave) and combined depolarization of atria takes longer (i.e. increased width of p-wave)
Premature atrial complexes
- Common in neonates
- Mostly benign
- If on DIGOXIN, PACs could be concerning (also look for N/V/D, anorexia, blurry vision, halos, palpitations, syncope, dyspnea, confusion, dizziness, delirium, fatigue)
Use of digoxin in children
- Used for various heart conditions, including arrythmias and CHF.
- Improves strength and efficiency of the heart and helps control the rate and rhythm of the heartbeat.
EKG changes with HYPOkalemia
- Prolonged QT
- Flattened T-waves
- ST segment depression
- U-waves (think of empty glass of potassium [sitting in ST segment depression and/or on top of T-waves])
- PVCs
EKG changes with HYPERkalemia
- Peaked T-waves (opposite of hypokalemia)
- Absent or flat P-waves
- Widened QRS
- VTach
Treatment of hyperkalemia
- Calcium gluconate (to stabilize the heart rhythm - hyperkalemia can cause V-Tach)
- Sodium polystyrene
- Insulin (+ glucose to avoid hypoglycemia)
EKG findings with HYPOcalcemia
- Prolonged QT
EKG findings with HYPERcalcemia
- Shortened ST segment –> shortened QT
- Widened T-wave
EKG findings with HYPOmagnesemia
- Prolonged QT
- Prolonged PR
EKG findings associated with sodium changes
NO EKG changes associated with hypo- or hypernatremia
Electrolyte disturbances associated with prolonged QT
- HYPOkalemia
- HYPOcalcemia
- HYPOmagnesemia
Causes of prolonged QT
- MELT PC’s:
- hypoMagnesemia
- Erythromycin
- Levofloxacin
- TCAs
- low Potassium
- hypoCalcemia
- *LOW electrolytes result in sLOW interval**
Intrinsic rates of SA node, AV node and ventricles
- SA node = 80 bpm
- AV node = 60 bpm
- Ventricular = 40 bpm
- Think 8A node, then subtract 20 bpm as you move down the heart
Brugada syndrome
- RBBB + ST elevation in V1 -> V3 (precordial leads)
- Usually found in adults, though can be found in children
- May result in SUDDEN DEATH
Supraventricular tachycardia
- HR usually > 240 bpm
- Typically diagnosed in children < 6 months old
EKG findings with SVT
- Regular, narrow complex tachycardia (usually > 240 bpm)
Treatment of SVT
- Vagal maneuvers for 20 seconds (i.e. water or ice to the face, Valsalva if patient can cooperate)
- If these tx do not work and patient stable, treat with ADENOSINE 0.1 mg/kg (may repeat x 1 @ 0.2 mg/kg - max 12 mg/dose)
- If unstable or becoming unstable, use SYNCHRONIZED DC electrical cardioversion
- If > 12 months, may also try diltizaem or verapamil - though DO NOT use these meds in children < 12 months!!!!
- After patient in sinus rhythm, repeat EKG to assess for WPW
- Maintenance therapy = beta blocker (propranolol) for 1 year to prevent recurrence. If resistant to tx, perform radiofrequency ablation.
Wolff-Parkinson-White Syndrome
- Accessory pathway bypasses AV node and connects atrium directly to ventricle
- Normal short delay between A and V depolarization provided by AV node is not present –> pre-excitation leading to wave of depolarization that bypasses AV node
- Most common form is forward through AV node, then retrograde through accessory pathway (orthodromic)
- EKG = short PR (< 0.12 s) and widened QRS (> 0.10 s)
- Prone to develop AV reetrant tachycardia (AVRT) NOT AVNRT
- Tx tachycardia with vagal maneuvers and adenosine and prepare for cardioversion (if needed).
- Generally avoid Ca channel and beta blockers, though DO NOT use if in Afib/flutter (do not affect refractory period of accessory pathways, which is typically shorter than AV node) –> may lead to Vfib and death!
- If Afib/flutter present, tx with ibutilide or procainamide (increase refractory period of accessory pathway)
AV node reentrant tachycardia (AVNRT)
- Tachycardia originates at or near the AV node
- Fast and slow conduction pathway around or in AV node
- Typical AVNRT = “slow-fast”
- EKG = (look at V1) retrograde or absent p-waves, R’ (bunny ears - similar to w/ RBBB, though with normal QRS duration).
- Common cause of SVT - will respond to tx with vagal maneuvers and adenosine
What effect do vagal maneuvers and adenosine have?
Increase refractory period (or temporarily block) AV node
Atrial tachycardias
- Includes atrial fibrillation or atrial flutter
- DO NOT respond to adenosine or vagal maneuvers (these methods effect refractory period of AV node - with atrial tachycardias, the problem is in the atria, so blocking AV node further down the pathway won’t help).
In which patients are atrial fibrillation and atrial flutter most likely to occur?
Patients with repaired structural heart disease
Causes of ventricular tachycardia
- Digoxin toxicity
- Hyperkalemia
- Prolonged QT interval
- Treat with amiodarone (ONLY if absence of prolonged QT). May also tx with lidocaine or cardioversion.
Why is prolonged QT concerning?
- Can lead to Torsades de Pointes (which may lead to Vfib!)
Prevention and treatment of Torsades de Pointes
- Prevention = beta-blocker or defibrillator
- Treat with magnesium sulfate
- May also consider overdrive pacing
When to consider prolonged QT
- Loss of consciousness
- Drowning
- Syncope
- Seizure
Treatment of Familial Prolonged QT Syndrome
Beta-blocker
Indications for pacemaker with complete heart block
- Persists >7 days after surgery
- Symptomatic
- CHD AND HR < 75 bpm
- WithOUT CHD + HR < 55 bpm
Common presentation of complete heart block on boards
Child with bradycardia except when crying
What maternal condition can predispose to complete heart block?
Systemic lupus erythematosis