A 68-year-old woman is admitted to the neurologic intensive care unit (NeuroICU) after a fall that led to a subdural hematoma. Past medical history is remarkable for hypothyroidism, hypertension, and hyperlipidemia. Admission medications include levothyroxine, 75 μg daily; carvedilol, 6.25 mg twice daily; and aspirin, 81 mg daily. Vital signs on arrival include a heart rate of 30 bpm (beats per minute), blood pressure of 68/30 mm Hg, temperature of 98°F, respiratory rate of 18 per minute, and a pulse oximetry of 96% on room air. Physical examination reveals an elderly woman of average build who is mildly dyspneic and slow to respond to questions. Cardiac examination is remarkable for bradycardic S1 and S2 without any murmurs, rubs, or gallops. Lung examination reveals normal breath sounds with no rales or rhonchi. Extremities are cold to touch. Neurologic examination reveals no focal deficits.
This ECG demonstrates sinus bradycardia (Figure 36-1). The human heart usually beats between 60 and 100 bpm. Bradycardia is defined as a heart rate of less than 60 bpm. The sinoatrial node is usually the origin of electrical impulse, which then spreads to the rest of the heart through specialized conducting tissue including the atrioventricular node, His bundle, Bundle branches (right and left bundle) and the Purkinje network (Figure 36-2). The aforementioned tissues are all capable of generating electrical impulses independently but are usually suppressed by the higher rate of electrical firing by the sinus node which is the dominant pacemaker in the heart in normal conditions. Dysfunction of the sinus node or block in any part of the conducting tissue can lead to bradycardia.
Bradycardia may be due to cardiac or noncardiac causes. Differentiating between the two is critical for proper management. Asymptomatic bradycardia generally requires no treatment. Well-trained athletes frequently have heart rates in the upper 30s. During sleep the heart rate can go down to the 30s, but pauses of more than 3 seconds or a heart rate in the 30s while awake are pathological. Similarly, drugs like β-blockers and calcium channel blockers can lead to marked bradycardia, necessitating withdrawal of these agents. In the NeuroICU any condition that leads to high intracranial pressure can trigger Cushing’s reflex, resulting in bradycardia, increased blood pressure, and irregular breathing. Hypothyroidism, hypoxia, hypothermia, metabolic acidosis, and hyperkalemia are other well-known causes of bradycardia due to noncardiac causes. Pain, vomiting, or spinal injuries can also cause high vagal tone, leading to bradycardia.
Disorder of impulse formation or transmission in the sinus node is termed sino-atrial node dysfunction. This manifests as sinus arrest or pause manifested on ECG as random P-P intervals or sinoatrial exit block when the P-P intervals are exact multiples of baseline P-P intervals. A particular subtype of sinus node dysfunction is the “Tachy-Brady” syndrome, also known as sick sinus syndrome. This is characterized by high atrial rates especially during paroxysms of atrial fibrillation or atrial flutter followed by intermittent pauses (> 3 seconds) and/or marked bradycardia. The pauses typically occur at time of conversion from atrial fibrillation to sinus rhythm, so called “conversion pause.” The pause may lead to dizziness, lightheadedness, and occasionally syncope. Usually addition of rate-controlling medications such as β-blockers and implantation of a permanent pacemaker is needed to counter the tachy-brady episodes.
The atrioventricular (AV) node provides the electrical connection between the atrial and ventricular chambers. High vagal tone, ischemia (especially involving right coronary artery), drugs such as β-blockers, calcium channel blockers, class 1 and 3 antiarrhythmic medications (Table 36-1), and trauma from cardiac surgery in the region of aortic, mitral, or tricuspid valve, which lie close to AV node, leads to atrioventricular nodal dysfunction, leading to AV block. Neurologic causes of AV block are the neuromyopathies such as Duchenne and Becker muscular dystrophy, peroneal muscular dystrophy, Kearns-Sayre syndrome, Erb dystrophy, and myotonic muscular dystrophy frequently requiring a pacemaker. Infiltrative processes secondary to sarcoidosis, hemochromatosis, and amyloidosis can also cause AV block.
| Class | Action | Drugs |
|---|---|---|
| I | Sodium channel blocker | |
| Ia | (Moderate) | Quinidine, procainamide, disopyramide |
| Ib | (Weak) | Lidocaine, mexiletine, phenytoin |
| Ic | (Strong) | Flecainide, propafenone |
| II | β-Blocker | Propranolol, carvedilol, metoprolol, etc. |
| III | Potassium channel blocker | Amiodarone, dronedarone, dotalol, dofetilide, ibutilide |
| IV | Calcium channel blocker | Verapamil, diltiazem |
| V | Miscellaneous | Digoxin, adenosine |
First-degree AV block (Figure 36-3) exists when the PR interval is more than 200 ms and represents prolonged conduction time rather than a block as there are no dropped beats. Second-degree AV block may be Mobitz type 1 (Figure 36-4) or Mobitz type 2 (Figure 36-5) block. In Mobitz type 1 block, there is progressive prolongation of PR interval followed by a dropped ventricular beat. The R-R intervals typically shorten prior to the dropped beat and the QRS duration is usually less than 120 ms, although presence of a pre-existing bundle branch block can cause the QRS to be prolonged. This is usually benign as the block is within the AV node and requires no further treatment. In Mobitz type 2 block, P-P and PR intervals remain fixed, but there is an intermittent failure of atrioventricular conduction leading to dropped ventricular beat. This results in a fixed ratio between P and R of 2:1, 3:1, 4:1, and so forth. Third degree or complete AV block (Figure 36-6) is characterized by complete dissociation of atrial and ventricular beats, which fire at their own intrinsic rates, with the atrial rate usually being faster than the ventricular rate. QRS complex is more than 120 ms if the block is below the His bundle. Mobitz type 2 block and complete heart block usually require insertion of a permanent pacemaker.
Our patient shows symptoms and signs of hypoperfusion as exemplified by her slow response to questions, dyspnea, cold peripheries, and low blood pressure. Atropine (0.5 mg IV q3-5 min prn for a maximum of 3 mg total) or transcutaneous pacing is urgently indicated to increase her heart rate. Because transcutaneous pacing is painful, sedation is generally required. Holding carvedilol and checking her thyroid hormones is also indicated as well as ruling out acute coronary syndrome with serial troponins. Consideration for a permanent pacemaker is appropriate and should be deliberated. Indications for pacing in sinus node dysfunction, AV node dysfunction, and after myocardial infarction with associated bradycardia are provided in Tables 36-2, 36-3, and 36-4, respectively. Bradycardia is defined as heart rate less than 60 beats per minute. For symptomatic bradycardia pacing is indicated once reversible causes are excluded. Pacemaker implantation is a relatively low-risk procedure (risk of bleeding and infection < 1%).
Class 1
|
Class 2a
|
Class 2b
|
Class 3
|
Class 1
|
Class 2a
|
Class 2b
|
Class 3
|
Class 1
|
Class 2b Permanent ventricular pacing may be considered for persistent second- or third-degree AV block at the AV node level, even in the absence of symptoms. (Level of Evidence: B) |
Class 3
|
A 28-year-old woman who is postpartum is admitted to the Neuro ICU with the diagnosis of PRES (posterior reversible encephalopathy syndrome). She is noted to have a rapid heart rate on telemetry at a rate of 180 bpm, and an ECG is obtained (Figure 36-7).
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