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Non-specific ECG changes are common after surgery and anesthesia.
Mild QT-interval prolongation is commonly observed after surgery and anesthesia.
ST-segment depression or elevation should raise suspicion for possible cardiac ischemia.
Just as general anesthesia is considered the greatest medical discovery of the nineteenth century, electrocardiography (ECG) may be considered one of the greatest discoveries of the twentieth century.[1] First invented in 1901 by William Einthoven, the ECG still aids today in clinical cardiac diagnosis and therapy.[2] The consultants and American Society of Anesthesiology (ASA) members surveyed for the ASA practice advisory on post-anesthetic care recommend using pulse rate, blood pressure, and ECG (in selected patients) for monitoring circulation along with attention to oxygenation, ventilation, level of consciousness and temperature in the Post-Anesthesia Care Unit (PACU).[3] There are many ECG changes that occur commonly in the PACU. Some ECG changes could represent a normal variant within the population requiring no intervention, while others can signal life-threatening conditions that require immediate intervention. ECG interpretation consists of specific findings such as the heart rate, the rhythm, the axis, evidence of hypertrophy, and any evidence of ischemia or infarction. Combining these specific findings with the patient’s presenting signs and symptoms can lead to a final diagnosis and management plan.
Tachycardia
The normal QRS complex lasts from 0.06 to 0.12 seconds. Tachycardia can be classified as either narrow or widened QRS complex tachycardia. Narrow QRS complex tachycardia reflects rapid activation of the ventricles. Widened QRS complex tachycardia reflects abnormally slow ventricular activation. One of the most common ECG changes found in the PACU is sinus tachycardia.[4] A normal heart rate ranges from 60 to 100 beats per minute (bpm). Tachycardia increases myocardial oxygen consumption, decreases myocardial oxygen supply, and decreases cardiac output by shortening ventricular filling time, which could be detrimental to a patient with an already compromised myocardium. Patients with underlying coronary disease are at an increased risk for myocardial infarction (MI), when tachycardic.
Symptoms: The symptoms of tachycardia are broad. Patients could complain of acute chest pain, shortness of breath, a feeling of impending doom, or palpitations could be the lone symptom. Tachycardia is frequently the result of incisional pain, hypotension secondary to hypovolemia, hemorrhage, or fever.
Diagnosis: Narrow QRS complex tachycardia is characterized by QRS complex <120 ms. Sinus tachycardia, atrial fibrillation, and paroxysmal supraventricular tachycardias (PSVTs) are examples of frequently encountered narrow complex tachycardias in the PACU. Sinus tachycardia can be easily diagnosed with an ECG tracing showing a heart rate >100 bpm and sinus rhythm. Sinus tachycardia has a broad differential diagnosis. It is important to rule out the life-threatening causes initially. Widened QRS complex tachycardias are characterized by QRS complex >120 ms, such as ventricular tachycardia.
Management: Management of most tachycardias involves treating the inciting disorder. If the patient is unstable, with hypotension, impaired vital organ function, or imminent cardiac arrest: immediate intervention is required.[5] Unstable wide complex tachycardia should be treated by the ACLS algorithm immediately. Synchronized cardioversion should be performed with sedation if the patient is still stable and conscious. For stable PSVT, vagal maneuvers such as bearing down to increase abdominal pressure will terminate up to 25% of cases.[6] Intravenous adenosine can be used when vagal maneuvers fail, as an alternative to electrical cardioversion. For all tachycardic patients, the preload should be optimized with intravenous fluids or blood transfusion when anemic, pain should be controlled, patient body temperature should be corrected with antipyretics or warming blankets, and acidosis, electrolyte abnormalities, or respiratory disorders should be corrected. Reduction of the heart rate while correcting the underlying cause can be initially accomplished with β-blockers or calcium channel blockers in most patients with narrow complex tachycardia, including atrial fibrillation.
Bradycardia and AV block
Bradycardia may be seen as a normal variant in the absence of heart disease in well-conditioned athletes, some elderly, and in otherwise healthy patients. In the postoperative period, bradycardias are common secondary to anesthetics and analgesics given in the operating room and PACU. Increased vagal tone due to heightened central parasympathetic activity and sympathetic withdrawal on the sinoatrial node can be associated with profound bradycardia. The normal PR interval is 0.12 to 0.20 seconds. This represents the amount of time an impulse travels from the beginning of atrial depolarization to the beginning of ventricular depolarization. These impulses become delayed or interrupted in atrioventricular (AV) block. AV blocks are classified as first, second, or third degree. These blocks may be caused by medications, electrolyte disturbances, and anatomical or structural problems.
Symptoms: Patients can have asymptomatic bradycardia with or without AV block. Bradycardia may be an incidental finding on ECG or present with symptoms such as fatigue, syncope, decreased mental status, or nausea and vomiting.
Diagnosis: Sinus bradycardia is classified as sinus rhythm with a rate below 60. First degree AV block is characterized on ECG by a prolonged PR interval >0.20 seconds, infrequently causes symptoms, and may be a side effect of β-blockers and many other medications. Second degree AV block: Mobitz type I (Wenckebach) consists of a progressive prolongation of the PR interval with successive beats followed by a dropped QRS complex. Second degree AV block: Mobitz type II is characterized on ECG by a non-conducted P wave, or “dropped QRS” not preceded by PR prolongation. Third degree AV block is characterized on ECG by complete dissociation between the atria and ventricles, with P waves and QRS complexes showing complete independence from one another. Along with ECG interpretation, the patient should be evaluated for signs and symptoms. Some causes of bradycardia could be exaggerated vagal activity from vomiting, coughing, or even from a tight collar with pressure on the carotid sinus, increased intracranial pressure, MI, obstructive sleep apnea, and medications. The Trendelenburg position following spinal anesthesia has been associated with severe bradycardia.[5]
Management: Asymptomatic or minimally symptomatic bradycardia requires no intervention. First degree AV block is generally benign and found incidentally on ECG. Second degree AV block: Mobitz type I (Wenckebach) is a block at the AV node and is usually transient, asymptomatic, and generally does not require immediate intervention, but may be the only sign of an underlying disorder. Second degree AV block: Mobitz type II is usually caused by pathology below the AV node, usually symptomatic, and may progress to third degree AV block. Management of symptomatic bradycardia depends on the severity. If the patient is unstable – hypotensive, showing signs of impaired vital organ function or imminent cardiac arrest – then ACLS should be initiated.[6] The initial treatment for symptomatic bradycardia is atropine. Atropine is an anticholinergic drug that increases the heart rate by blocking the effects of acetylcholine on the SA node.[7] The recommended dose is 0.5 mg IV every 3 to 5 minutes with a maximum dose of 3 mg.[6] Medication may be a temporary measure and transcutaneous pacing should be considered. Immediate pacing should be considered with third degree AV block and unstable patients unresponsive to atropine. Alternative medications to consider are catecholamines such as dopamine, epinephrine, isoproterenol, and dobutamine. Dopamine and epinephrine have α– and β-adrenergic actions, and infusions of either can be started at 2 to 10 mcg/kg/min. Isoproterenol is a β-adrenergic agent with a recommended dose of 2 to 10 mcg/min by infusion titrated to effect.[6] Dobutamine is another commonly used β-adrenergic agent, started at 2 to 10 mcg/kg/min. While both of these β-agonists are effective at increasing the heart rate, they can be associated with hypotension secondary to vasodilation.
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