Atrioventricular Heart Blocks, Bradycardia, Sinus Sick Syndrome Flashcards
What is the defining ECG feature of first-degree AV block?
Prolonged PR interval (>200 ms = 5 small boxes on an ECG) with all P waves followed by QRS complexes.
What is the management of first-degree AV block?
Reassurance, as it is usually asymptomatic and benign.
What is the defining ECG feature of Mobitz Type I AV block?
Progressive prolongation of the PR interval until a P wave is not followed by a QRS complex.
What is a pseudonym for Mobitz Type I?
Wenckebach
What are the symptoms of Mobitz Type I AV block?
Usually asymptomatic but may cause mild fatigue or lightheadedness in rare cases.
What is the management of Mobitz Type I AV block?
Observation and reassurance in asymptomatic patients.
What is the defining ECG feature of Mobitz Type II AV block?
Intermittent non-conducted P waves without progressive prolongation of the PR interval. The diagnosis of Mobitz type II AV block is made by ECG showing intermittent nonconducted P waves and a regular PR interval; it differs from Mobitz type I AV block, which shows nonconducted P waves following progressive elongation of the PR interval.
What can lead to Mobitz Type II AV block?
Ischemia, electrolyte abnormalities, medications (eg, beta blockers, nondihydropyridine calcium channel blockers), infiltrative disease (eg, sarcoidosis, or age-related fibrosis can lead to impaired electrical conduction across the AV node.
What medication that is commonly used in heart failure can lead to heart blocks?
Beta-blockers. This is especially true for beta blockers that are renally cleared like atenolol in the setting of kidney disease.
What is the mechanism of beta blocker toxicity?
The cardiac effects of beta blockers are mediated by the inhibition of beta-1 receptor activity resulting in reduced intracellular cAMP. In contractile myocytes, reduced CAMP levels decrease the release of calcium, which decreases contractility. In the pacemaker cells, reduced cAMP levels decrease the slope of phase 4 depolarization (due to impaired activity of the HCN “funny” channels). The result is sinoatrial node dysfunction and decreased atrioventricular node conduction. Clinical manifestations include bradyarrhythmia (eg, sinus bradycardia, sinus arrest, atrioventricular block) with hypotension and signs of poor organ and tissue perfusion (eg, confusion). Hypotension should be treated with intravenous fluids, and symptomatic bradycardia causing hemodynamic instability should be treated with atropine. In addition, glucagon is useful in counteracting beta blocker toxicity. It acts by directly increasing cAMP via activation of glucagon receptors, bypassing the blocked adrenergic receptors to increase heart rate and contractility (and improve bronchospasm and glucose metabolism when needed). Calcium gluconate sometimes given to increase blood pressure.
What is the range of symptoms associated with Mobitz Type II AV block?
Patients may be asymptomatic or may have symptoms of poor cardiac output (eg, dyspnea, lightheadedness, syncope).
In Mobitz Type II AV blocks, the dropped beats are … ?
Random
Why is Mobitz Type II AV block considered more serious?
Unlike Mobitz type I AV block (usually asymptomatic and benign), Mobitz type II AV block has a high rate of progression to complete (third-degree) AV block and potentially devastating outcomes (eg, sudden cardiac death). Therefore, in the absence of a reversible cause (eg, pharmacologic AV nodal blockade, hyperkalemia, myocardial ischemia), Mobitz type II AV block necessitates the placement of a permanent pacemaker.
What is the management of Mobitz Type II AV block?
Pacemaker placement due to the risk of progression to complete heart block.
Can patients with Mobitz Type II AV block undergo stress testing?
Because Mobitz type II AV block often progresses to potentially fatal (complete) AV block, stress testing should not be performed without a pacemaker in place. If there is high suspicion for ischemia as a reversible cause, a temporary, rather than a permanent, pacemaker can be inserted prior to testing. Lack of chronotropic competence (an appropriate increase in heart rate with exertion) is expected in patients with advanced AV block, so testing for it is generally not useful.
Is Mobitz Type II AV block managed with atropine?
Per advanced cardiac life support protocol, unstable patients (eg, those with hypotension, confusion, or chest pain) with Mobitz type II AV block or another bradycardia should be treated with intravenous atropine (0.5 mg every 3-5 minutes). However, atropine can sometimes worsen bradycardia due to Mobitz type II AV block and is not recommended in stable patients.
What is the defining ECG feature of third-degree AV block?
Complete dissociation between atrial (P waves) and ventricular (QRS complexes) activity.
What is the typical ventricular rate in third-degree AV block?
30–40 beats per minute, due to a junctional or ventricular escape rhythm.
This patient has symptoms of reduced cardiac output (eg, lightheadedness, syncope), and his ECG shows bradycardia. What is this rhythm?
junctional escape rhythm.
How is the HR estimated from an EKG?
Method 1:
300 / “no. of boxes between QRS intervals”
Method 2:
“no. of QRS complexes in 10 sec.” x 6
What is the first-line treatment for symptomatic sinus bradycardia?
Atropine (first-line medication).
What is the management for atropine-refractory bradycardia?
Transcutaneous pacing, dopamine infusion, or epinephrine infusion.
