Decision tree.
The initial assessment of the dysrhythmia patient should include pulse, blood pressure, peripheral perfusion demonstrated by capillary refill, and any indication of impaired organ perfusion, such as acute change in mental status. Acute cardiovascular collapse, indicated by loss of consciousness, pulselessness, or severe hypotension, necessitates immediate therapy. In a hemodynamically stable patient, establishing an etiology and treatment plan can be accomplished with less urgency.
Predisposing factors in the perioperative patient
Many predisposing factors result directly from recent surgery or anesthesia. Medical history and co-morbidities are important components in the initial work-up of patients with arrhythmia. Patients with diabetes, chronic obstructive pulmonary disease (COPD), and coronary artery disease (CAD) are more likely to have negative outcomes than those without.[3] Cardiac surgeries, craniotomies, and dental and ocular procedures have been correlated with increased incidences of arrhythmias. A recent medication history can be helpful in the differential diagnosis, as many chronic prescriptions are withheld prior to surgery, and many drugs new to the patient may be given on the day of surgery. Increased sympathetic outflow is common postoperatively and increases the risk of many dysrhythmias. Factors that contribute to the postoperative predisposition toward dysrhythmia can include:
Hypercarbia or hypoxia
Obstructive sleep apnea (OSA) is a particularly dangerous cause of hypercarbia and hypoxia. Postoperatively, OSA frequently leads to hypercapnic respiratory acidosis and failure.
Hyper/hypothermia
Anemia
Intravascular hypo/hypervolemia
Pre-existing disease
Coronary disease: CAD is an important predisposing factor toward arrhythmias in the perioperative period.[4]
Pre-existing congenital arrhythmia disorders such as Wolff Parkinson White (WPW) are exacerbated postoperatively.
Intracranial disease, especially subarachnoid hemorrhage, can commonly lead to ST-T-wave changes and may easily mimic myocardial ischemia and infarction.[5]
Myocardial infarction
Catecholamine levels (endogenous or iatrogenic) – catecholamine release increases cellular potassium uptake, leading to lower serum levels.
Electrolyte, acid–base, and metabolic derangements
Intraoperative fluid therapy may lead to derangements in electrolytes vital for appropriate cardiac depolarization and contraction. Hypomagnesemia, hypo or hyperkalemia, and hypocalcemia are common in the PACU.
Hyperventilation due to inadequately treated pain or mechanical ventilation can lead to alkalosis and decrease levels of serum potassium. This phenomenon may precipitate severe cardiac arrhythmias.[6]
Drug effects
Perioperative drugs that increase or potentiate endogenous catecholamines, such as ephedrine, cocaine, and ketamine, can facilitate the development of tachyarrhythmias.
Neuraxial anesthesia causes vasodilation and hypotension, leading to a compensatory tachycardia or to a bradycardia if the level of sympathectomy involves high thoracic cardiac accelerator nerves.
Intravascular injection or high total doses of infiltrated local anesthetics, particularly bupivacaine, may lead to asystole and cardiac arrest. This form of cardiac arrest can be very difficult to treat and requires prolonged CPR in many cases.[7]
– 20% intralipid is the treatment option of choice in this situation; however, the exact mechanism of action is unclear.[8]
Mechanical factors
Intravascular catheter or device placement
Surgical factors
Cardiac surgery: Cannulation of the major vessels of the heart, cross clamping of the aorta, and direct manipulation of the myocardium lead to higher incidences of arrhythmias following cardiac surgery.
Dental surgery leads to sympathetic and parasympathetic excitation and can be associated with generation of arrhythmias.[9] Junctional rhythms can be directly correlated to trigeminal nerve (CN V) irritation.
Eye surgery can induce the oculocardiac reflex, leading to severe bradycardia in response to traction on the rectus muscles of the orbit. The reflex arc comprises CN V stimulation and subsequent stimulation of the vagus nerve (CN X). Children and neonates following strabismus surgery may demonstrate an exaggerated response.
Increased vagal tone in any fashion can be pro-arrhythmic. Profound sinus bradycardias, ventricular escape beats, heart block, and asystole have been observed following actions that increase vagal tone. Traction of peritoneum and abdominal mesentery, direct pressure on the vagus nerve during carotid surgery, jugular vein cannulation, and carotid sinus palpation are all possible causes of increased vagal tone.[1] It seems appropriate that an initial goal in postoperative dysrhythmia therapy should be to identify and remove causative and correctable predisposing factors in the recovery room. The stress response and derangements in normal physiology resulting from surgery continue past the recovery phase, and therefore, appropriate post-recovery therapy, consultation, level of care, and monitoring should be considered prior to discharge from the PACU.
Bradyarrhythmias
Bradycardia is defined as a heart rate <60 bpm. Bradycardia can occur frequently in healthy patients and is often of little clinical consequence. However, heart rates <40 bpm are poorly tolerated in most individuals and can lead to hemodynamic compromise. Transient bradycardias are frequent in the PACU, but therapy is not indicated unless bradycardia recurs or is symptomatic. As described previously, increased vagal tone can be an etiology for bradyarrhythmias. Sustained symptomatic bradycardias should be treated initially with intravenous (IV) atropine 0.5 to 1 mg, while an external pacing system is retrieved.[10] The total dose of atropine should not exceed 3 mg.[11] Beta-agonists such as epinephrine or dopamine may be useful if the bradycardia is refractory to anticholinergic therapy. Percutaneous or transvenous pacing should follow if pharmacological intervention is not successful.
Tachycardias
A QRS segment is either described as narrow complex (<0.12 seconds) or wide complex (>0.12 seconds). Narrow complex arrhythmias usually demonstrate supraventricular tachycardia (SVT), and wide complex arrhythmias originate in the ventricle or represent SVT with a pre-existing bundle branch block (BBB) or other intraventricular conduction delay.
Supraventricular tachycardias
Supraventricular tachycardias usually are narrow QRS complex, unless the patient has a concurrent BBB, have a heart rate >100 bpm, and they may or may not contain P waves. Supraventricular indicates an atrial or nodal origin for the tachycardia. Estimated incidence following non-cardiac surgery is about 3–4% and even as high as 37% following total pneumonectomy.[12]
Sinus tachycardia
Sinus tachycardia is common postoperatively. Causes can include anxiety, pain, fever, hypovolemia, anemia, hypoxemia, hypercarbia, and perioperative medications. There is no conduction abnormality in sinus tachycardia, and treatment consists of improving the underlying cause. Rate control with β-blockers or calcium channel blockers is reasonable, especially in patients with coronary or stenotic valvular heart disease.
Atrial tachycardia
Atrial tachycardias often originate from a separate ectopic pacer focus than the SA node, or they are caused by reentrant pathways. Atrial tachycardias are more common in children than in adults, but they comprise about 8% of paroxysmal SVTs in adults. These tachycardias can be identified by P-wave morphologies that are different than that of sinus rhythm.
Multifocal atrial tachycardia (MFAT)
This atrial tachycardia is usually seen in acutely ill, elderly patients. It is also seen in patients with significant pulmonary disease.[13] In MFAT, there are three or more different P-wave morphologies, and the rhythm is irregularly irregular. Predisposing factors include hypoxia, hypercapnia, myocardial infarction, congestive heart failure, and electrolyte disturbances. Beta-blockers, calcium channel blockers, and amiodarone are mainstays in therapy.[14]
AV nodal reentry tachycardia
AV nodal reentry is the most common SVT, accounting for 60% of SVTs.[15] Accessory pathways from the atria to ventricle lead to multiple depolarizations of the ventricle. P waves are usually absent, or unusually shaped. Simultaneous forward and reverse signal conduction across the AV node and accessory pathway cause the aberrant P-wave morphology. Management can consist of maneuvers designed to increase vagal tone and obliterate the reentrant signal propagation. These include Valsalva maneuvers and carotid massage among others. Adenosine (6–12 mg IV) can also break the reentry process, and owing to its short half-life, it has few side effects. Adenosine has some diagnostic usefulness as well. If significant cardiovascular compromise exists, electrical cardioversion may be indicated. Calcium channel blockers and digoxin can inhibit AV nodal conduction and allow for unopposed accessory pathway conduction and rapid atrial fibrillation (AF) in susceptible patients, such as those with WPW.[10]
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