Untitled Quiz

AV Conduction Blocks

• Delay or interruption in the transmission of the impulse from the atria to the ventricles
• Can be caused by medications
• Usually asymptomatic
• No treatment required

First Degree AV Heart Block

• Delayed conduction from atrium to ventricle (but no interruption)
• Prolonged PR interval (> 200 msec)
• All PR intervals are equal
• Usually asymptomatic
• Can be caused by medications
• No treatment required

Second Degree AV Block: Mobitz Type I (Wenckebach)

• The PR interval progressively increases until one p-wave is blocked and isn’t transmitted to the ventricles
• Notable PR interval lengthening with a P-wave not followed by a QRS complex
• The cycle starts all over again after that drop (regularly irregular)
• Treatment is usually not indicated as this rhythm usually is asymptomatic

Second Degree AV Block: Mobitz Type II

• Dropped QRS complex that is NOT preceded by a lengthening of the PR interval
• The PR interval is consistent (either normal or prolonged), until one p-wave is blocked and isn’t transmitted to the ventricles
• Symptoms may be present and are more common than Mobitz Type I and include presyncope, syncope, fatigue, or SOB
• More serious than type I second-degree AV block
• May progress to third degree (complete) AV block
• Often treated with a pacemaker

Third Degree (Complete) Heart Block

• The atria and ventricles beat independently of each other
• P-waves are not associated with QRS complexes
• Atrial pacing is greater than ventricular pacing
• ECG will show equal RR intervals and equal PP intervals but no association
• May be caused by MI, degeneration of the conductive tissue, and Lyme Disease
• Treated with a Pacemaker

Left Bundle Branch Block (LBBB)

• Normally, the septum is activated from left to right
• In LBBB, septal depolarization is reversed
• Leads to QRS duration > 120ms
  • Produces tall R waves in the lateral leads (I, V5-6) and deep S waves in the right precordial leads (V1-3)
• Produces a broad or notched (‘M’-shaped) R wave in the lateral leads (V5, V6) and (‘W’-shaped) dominant deep S waves in V1

Right Bundle Branch Block (RBBB)

• QRS duration is greater than 120 msec
• QRS in V1-V2 displays rSR’ pattern “bunny ears” or the letter “M”
• Lateral leads (I, V6) broad deep S-wave that is greater than R-wave duration.

Bundle Branch Block “Turn Signal Theory”

• Criteria: QRS complex > 120 msec, reference lead V1
• LBBB: ‘W’-shaped in V1
• RBBB: ‘M’-shaped in V1

Hyperkalemia

• Potassium (K+): 3.5-5.0 mEq/L
• ECG changes depend on serum level and how rapid of a change
• K+ = 5.5 - 6.5 mEq/L
  • Tall, peaked, narrow based T waves
  • QT interval shortening
• K+ = 6.5 - 7.5 mEq/L
  • First-degree AV block
  • QRS widening
• K+ > 7.5 mEq/L
  • Disappearance of P waves

Hypokalemia (HypUkalemia)

• Severe or symptomatic hypokalemia
  • Depression of the ST segment, decrease in the amplitude of the T-wave, and an increase in the amplitude of U waves
  • U-waves are often seen in the lateral precordial leads V4 to V6
  • Prolongs the QT interval
  • Increased amplitude and width of the P-wave

Hypercalcemia

• Calcium, serum (total): 8.5-10.2 mg/dL
• QT interval shortening (usually due to shortening of the ST segment)
• Note: Little if any effect on P, QRS, or T wave

Hypocalcemia

• Prolonged QT interval (earliest and most common finding) due to ST segment prolongation
• No change in the duration of the T wave (seen only with hypocalcemia or hypothermia)

Hypothermia: Osborne “J” Waves

• Hypothermia results in sinus bradycardia with widening of the QRS
• Prolongation of PR and QT intervals
• Osborne (“J”) waves, which are late upright terminal deflections of the QRS complex (“camel hump” sign)

Summary

• Hyperkalemia: tall peaked T-waves, QT interval shortening
• Hypokalemia: ST segment depression, shallow T-waves, U-waves
• Hypercalcemia: QT interval shortening
• Hypocalcemia: Prolonged QT interval
• Hypothermia: Osborne “J” waves

Left Ventricular Hypertrophy (LVH)

• Response to pressure overload states
• Increase in size of the myocardial fibers
  • Parallel addition of sarcomeres
• Causes
  • Hypertension (most common cause)
  • Aortic stenosis
  • Aortic regurgitation
  • Mitral regurgitation
  • Coarctation of the aorta
  • Hypertrophic cardiomyopathy

Sick Sinus Syndrome

• When the SA node is damaged and no longer generates normal heartbeats at a normal rate
  • Another cause of Pathologic Bradycardia
• Most common caused is gradual loss of SA node function that comes with age
• Sx: Dizziness, Pre-syncope, Syncope, SOB, Fatigue
• Tx: Pacemaker