6.2 Dysrhythmias: Bradycardias and High-Grade AV Blocks

Dysrhythmias: Bradycardias and High-Grade AV Blocks

Bradyarrhythmias represent a common and potentially life-threatening clinical challenge in critical care transport. Symptomatic bradycardia is defined as a heart rate less than 50 beats per minute (bpm) that results in signs or symptoms of inadequate systemic tissue perfusion. Pathophysiologically, bradycardia arises from either sinus node dysfunction (decreased automaticity or sinoatrial exit block) or atrioventricular (AV) conduction blocks. Common etiologies include acute myocardial infarction (particularly inferior MI affecting the RCA, which supplies the AV node in 90% of patients), electrolyte derangements (severe hyperkalemia), hypothermia, elevated vagal tone, and drug toxicities from beta-adrenergic antagonists, calcium channel blockers, or cardiac glycosides (digoxin).

When evaluating bradycardia in the transport environment, the clinician must quickly assess for hemodynamic instability. Signs of instability include hypotension, altered mental status, signs of systemic shock, ongoing ischemic chest pain, and acute congestive heart failure.

Classification and Electrocardiographic Identification of AV Blocks

Atrioventricular blocks represent a delay or interruption in the transmission of electrical impulses from the atria to the ventricles. They are classified based on their ECG characteristics and the anatomical site of the block:

First-Degree AV Block

First-Degree AV block is characterized by a delayed but successful conduction of all atrial impulses to the ventricles. On the ECG, this is represented by a prolonged PR interval (> 0.20 seconds, or 5 small boxes) that remains constant from beat to beat. Every P wave is followed by a QRS complex, and the R-R interval is typically regular. This block is located within the AV node itself and is generally benign, requiring no active treatment unless drug-induced.

Second-Degree AV Block Type I (Mobitz I / Wenckebach)

Second-Degree Type I AV block is characterized by a progressive delay in AV nodal conduction until an impulse is completely blocked. On the ECG, the PR interval progressively prolongs with each subsequent beat until a P wave occurs without a corresponding QRS complex. Following this dropped beat, the PR interval resets to its shortest duration, and the cycle repeats. The R-R intervals are irregular, and the rhythm is characterized by 'grouped beating'. This block is typically located within the AV node, is often transient (e.g., associated with inferior wall MI or high vagal tone), and usually responds well to vagolytic therapy if symptomatic.

Second-Degree AV Block Type II (Mobitz II)

Second-Degree Type II AV block is a severe conduction system disorder characterized by intermittent failure of impulse conduction below the AV node, typically within the Bundle of His or bilateral bundle branches (infranodal). On the ECG, the PR intervals of all conducted beats are constant and may be normal or prolonged. However, some P waves are suddenly blocked, resulting in dropped QRS complexes without warning or PR interval changes. This rhythm carries a high risk of progressing to complete heart block or ventricular standstill. Because the site of the block is infranodal, atropine is typically ineffective and can be hazardous; accelerating the atrial rate without improving AV conduction can increase the block ratio (e.g., from 2:1 to 3:1), further reducing ventricular rate.

Third-Degree (Complete) AV Block

Third-Degree AV block is characterized by a complete failure of conduction between the atria and the ventricles. The atria and ventricles beat independently under the control of their respective pacemakers (AV dissociation). On the ECG, the P-P intervals are regular and the R-R intervals are regular, but there is no relationship between P waves and QRS complexes. P waves may be buried within QRS complexes or T waves. The QRS morphology and ventricular rate depend on the location of the escape pacemaker:

• Junctional Escape: If the block is at the AV node or Bundle of His, a junctional pacemaker takes over, producing a narrow QRS complex (< 0.12 seconds) at a rate of 40-60 bpm. This is relatively stable.
• Ventricular Escape: If the block is lower in the conduction system, a ventricular pacemaker takes over, producing a wide, bizarre QRS complex (>= 0.12 seconds) at a slow rate of 20-40 bpm. This is highly unstable and associated with profound hypoperfusion.

High-Grade AV Block

High-grade AV block is defined as the non-conduction of two or more consecutive P waves (e.g., 3:1 or 4:1 block) with a constant PR interval for the conducted beats. It represents severe, infranodal conduction system disease and is managed identically to Mobitz II and third-degree blocks.

Pharmacological Management (ACLS Guidelines)

The primary pharmacological agent for symptomatic bradycardia is Atropine. Atropine is a competitive antagonist of acetylcholine at muscarinic receptors. By blocking parasympathetic (vagal) input, it increases SA node automaticity and AV node conduction velocity.

• Dosing: Administer 1.0 mg IV/IO push every 3-5 minutes, up to a maximum total dose of 3.0 mg.
• Clinical Caveats: Atropine is ineffective and should be bypassed in patients with Mobitz II or wide-complex third-degree AV blocks, as the conduction block in these cases is located below the AV node where muscarinic receptors do not modulate conduction. In these situations, transcutaneous pacing must be initiated immediately. Atropine is also contraindicated in hypothermic bradycardia (where bradycardia is a protective, physiological response, and atropine can precipitate refractory ventricular fibrillation) and in heart transplant patients (due to surgical denervation of the vagus nerve).

If atropine is ineffective or contraindicated, continuous chronotropic infusions should be initiated:

• Epinephrine Infusion: 2-10 mcg/min IV/IO, titrated to hemodynamic response.
• Dopamine Infusion: 5-20 mcg/kg/min IV/IO. At doses of 5-10 mcg/kg/min, dopamine exerts primary Beta-1 adrenergic effects to increase heart rate and contractility. At doses > 10 mcg/kg/min, Alpha-1 adrenergic vasoconstriction dominates, raising systemic vascular resistance.

Transcutaneous Pacing (TCP)

Transcutaneous pacing (TCP) is the definitive emergency treatment for unstable bradycardia refractory to atropine, or when atropine is contraindicated.

Electrode Pad Placement

For critical care transport, the anterior-posterior (AP) pad configuration is preferred. AP placement sandwiches the heart between the electrodes, reducing transthoracic impedance. This allows for lower pacing current (milliamperes, mA), which improves the likelihood of capture and reduces patient discomfort. The anterior pad is placed over the left precordium (cardiac apex), and the posterior pad is placed on the left upper back, directly behind the anterior pad.

Procedure and Capture Verification

1. Attach the pacing pads and connect them to the monitor/defibrillator.
2. Select the pacing mode (demand pacing is preferred to prevent pacing spikes from landing on the T wave of any intrinsic beats, which can trigger ventricular fibrillation; fixed rate is used if artifact interferes with sensing).
3. Set the pacing rate: typically 60-80 bpm.
4. Set the current (output) to 0 mA and increase it gradually (by 5-10 mA increments) until electrical capture is achieved. Electrical capture is recognized by a vertical pacing spike immediately followed by a wide, bizarre QRS complex and a tall, broad T wave. Pacing thresholds typically range from 50 to 100 mA.
5. Once electrical capture is achieved, the clinician must immediately verify mechanical capture. Electrical capture does not guarantee myocardial contraction or cardiac output. Mechanical capture is confirmed by palpating a strong femoral pulse (never a carotid pulse, as the muscle contraction caused by pacing can mimic a pulse) and verifying improvement in systemic perfusion (e.g., rising blood pressure, improving mental status, capnography stabilization).
6. Set the pacing output 5-10 mA above the threshold of capture as a safety margin.

Sedation and Analgesia

TCP is highly painful and causes distressing skeletal muscle contractions. Unless the patient is unconscious, the flight paramedic must administer intravenous analgesics (e.g., Fentanyl 1 mcg/kg IV) and sedatives (e.g., Midazolam 0.05 mg/kg IV or Ketamine 0.5 mg/kg IV) to ensure patient tolerance, while continuously monitoring respiratory and hemodynamic status.