Discuss the ethology and management of various cardiac arrhythmia occurring during anaesthesia ?
Arrhythmias are common during and after surgery and the initiating factor for an arrhythmia after surgery is usually a transient insult such as hypoxemia, cardiac ischemia, catecholamine excess, or electrolyte abnormality.
Common intraoperative arrhythmias are
Sinus Bradycardia
Sinus bradycardia is diagnosed when
1. Heart rate: Slower than 60 beats/min. In patients maintained on chronic β-blocker therapy, it is defined as a heart rate of less than 50 beats/min.
2. Rhythm: Regular
3. P/QRS: Ratio of 1 : 1.
4. QRS complex: Normal morphology.
5. Significance:Treatment is recommended if hypotension, ventricular arrhythmias, or signs of poor peripheral perfusion are observed.
6. Treatment: Usually none is necessary. (1) atropine, 0.5 to 1.0 mg by intravenous bolus repeated every 3 to 5 minutes, up to 0.04 mg/kg or approximately a 3.0-mg total dose for the average 75-kg male patient; (2) ephedrine, 5 to 25 mg by intravenous bolus; (3) dopamine or dobutamine (if blood pressure is adequate), 5 to 20 µg/kg/min by intravenous infusion; (4) epinephrine, 2 to 10 µg/min by intravenous infusion; (5) isoproterenol, 2 to 10 µg/min by intravenous infusion. Temporary transcutaneous or transvenous pacing if drug refractory bradycardia persists.
Sinus Tachycardia
Sinus tachycardia is the most common arrhythmia in the perioperative period,Common causes include pain, inadequate anesthesia, hypovolemia, fever, hypoxia, hypercapnia, heart failure, and drug effects.
1. Heart rate: Faster than 100 beats/min in adult patients and may be as high as 170 beats/min.
2. Rhythm: Regular.
3. P/QRS: Ratio of 1 : 1.
4. QRS complex: Normal
5. Significance: Prolonged tachycardia in patients with underlying heart disease can precipitate MI and congestive heart failure (CHF)
6. Treatment: Hypovolemia and light anesthesia are the most common causes. In patients with ischemic heart disease in whom tachycardia develops, Hypovolemia or other causes should also be addressed in these patients.
Atrial Premature Beats
Helpful points in differentiating APBs with aberrant ventricular conduction from VPBs include (1) the presence of a preceding P wave, usually abnormally shaped; (2) an RBBB configuration of the QRS complex; (3) the presence of an rsR′ ventricular complex in V1;
1. Heart rate: Variable, depending on the frequency of the APBs.
2. Rhythm: Irregular.
3. P/QRS: Usually 1 : 1. The P waves have various shapes and may even be lost in the QRS or T waves.
4. QRS complex: Usually normal unless ventricular aberration is present.
5. Significance: APBs represented around 10% of all intraoperative arrhythmias.
6. Treatment: Rarely necessary.
Paroxysmal Supraventricular Tachycardia
1. Heart rate: 130 to 270 beats/min.
2. Rhythm: Usually regular unless the impulse originates from multiple atrial foci.
3. P/QRS: 1 : 1 relationship, although the P wave may often be hidden in the QRS complex or T wave.
4. QRS complex: Generally normal,
5. Significance: During anesthesia, PSVT accounts for up to 2.5% of all arrhythmias,PSVT can be precipitated by changes in autonomic nervous system tone, by drug effects, or by intravascular volume shifts and can produce severe hemodynamic deterioration.
Treatment: Even though this arrhythmia is not usually associated with hemodynamic deterioration, the following can be undertaken to treat it:
a. Vagal maneuvers such as carotid sinus massage should be applied only to one side.
b. Adenosine, which is the drug of choice, is given by 6-mg rapid (2 seconds) intravenous bolus, preferably through an antecubital or central vein. If no response is elicited, second and third doses of 12 to 18 mg of adenosine may be administered by rapid intravenous bolus.
c. Verapamil (2.5 to 10 mg given intravenously) terminates AV nodal reentry successfully
d. Amiodarone (150-mg infusion over a 10-minute period for the loading dose) is a recent addition.
e. Esmolol (1 mg/kg by bolus and 50 to 200 mg/kg/min by infusion) has been shown to be effective
f. Edrophonium or neostigmine can be given by intravenous bolus.
g. Phenylephrine (100 µg by intravenous bolus) is administered if the patient is hypotensive.
h. Intravenous digitalization is performed with one of the short-acting digitalis preparations: ouabain (0.25 to 0.5 mg given intravenously) or digoxin (0.5 to 1.0 mg given intravenously).
i. Rapid overdrive pacing may be done in an effort to capture the ectopic focus.
j. Synchronized cardioversion may be performed with incremental doses of energy of 100, 200, 300, and 360 J, preferably after light sedative premedication.Electrode catheter ablation with radiofrequency energy has evolved as the definitive, long-term treatment of most persistent AV reentrant or focal atrial SVTs.
Atrial Flutter
Atrial flutter most commonly represents a macro-reentrant arrhythmia that circulates in a specific manner in the right atrium Because it is associated with very fast heart rates, it is generally accompanied by AV block. Classic sawtooth flutter waves (F waves) are usually present The characteristics of atrial flutter are as follows:
1. Heart rate: The atrial heart rate is 250 to 350 beats/min with a ventricular rate of about 150 beats/min (2 : 1 or varying AV conduction block).
2. Rhythm: The atrial rhythm is regular. The ventricular rhythm may be regular if a fixed AV block is present or irregular if a variable block exists.
3. P/QRS: Usually there is a 2 : 1 block with an atrial rate of 300 beats/min and a ventricular rate of 150 beats/min, but it may vary between 2 : 1 and 8 : 1. F waves are best seen in leads V1 and II and the esophageal lead.
4. QRS complex: Normal. T waves are lost in the f waves.
5. Significance: Atrial flutter does not always indicate severe heart disease. It can be seen in patients with CAD, mitral valve disease, pulmonary embolism, hyperthyroidism, cardiac trauma, cancer of the heart, and myocarditis.
6. Treatment: Pharmacologic or synchronized DC cardioversion, when indicated, should be performed only after careful consideration or evaluation of a possible thromboembolic event. Initial treatment should consist of control of the ventricular response rate with drugs that slow AV node conduction:
a. β-Blockers such as esmolol (1 mg/kg by intravenous bolus) or propranolol.
b. Calcium channel blockers such as verapamil (5 to 10 mg given intravenously) or diltiazem
If the ventricular response is excessively rapid or hemodynamic instability is present, or both, the following guidelines should be used:
c. Synchronized DC cardioversion starting at a relatively high energy of 100 J and gradually increasing to 360 J is indicated.
d. The class III antiarrhythmic agent ibutilide (Corvert, 1 mg in 10 mL saline or 5% dextrose in water [D5W] infused slowly intravenously over a 10-minute period) has been documented to convert atrial flutter to sinus rhythm in most patients with relatively new-onset atrial flutter. This may be repeated once, and although it is highly effective, life-threatening torsades de pointes ,may occur hours after ibutilide administration, thus making 4- to 8-hour monitoring after treatment highly desirable.
e. Procainamide (5 to 10 mg/kg for the intravenous loading dose, infused no faster than 0.5 mg/kg/min)
f. Amiodarone (150-mg intravenous loading dose infused over a 10-minute period, followed by 1 mg/min intravenously for 6 hours, a 0.5-mg/min intravenous infusion for 18 hours, and then a reduced intravenous dose or switching to an oral dose) has recently been shown to be effective.
Atrial Fibrillation
Atrial fibrillation is an excessively rapid and irregular atrial focus with no P waves appearing on the ECG; instead, fine fibrillatory activity is seen,most commonly encountered irregular rhythm. It is often described as irregularly irregular and may be associated with a pulse deficit. Its characteristics are as follows:
1. Heart rate: The atrial rate is 350 to 500 beats/min, and the ventricular rate is 60 to 170 beats/min.
2. Rhythm: Irregularly irregular.
3. P:QRS: The P wave is absent and replaced by f waves or no obvious atrial activity at all.
4. QRS complex: Normal.
5. Significance:idiopathic, paroxysmal atrial fibrillation has become increasingly recognized.The loss of atrial “kick” from inefficient contraction of the atria may reduce ventricular filling and significantly compromise cardiac output.
may be associated with the development of atrial thrombi, possibly resulting in pulmonary or systemic embolization.
Atrial fibrillation is the most common postoperative arrhythmia,It is typically a transient, reversible phenomenon that may develop in patients who possess an electrophysiologic substrate for the arrhythmia that is present before or as a result of surgery. β-blockers are efficacious in the prevention of postoperative atrial fibrillation. Perioperative administration of amiodarone, sotalol, nondihydropyridine calcium channel blockers, and magnesium sulfate has also been associated with a reduction in the occurrence of atrial fibrillation
Treatment:
Treatment of acute atrial fibrillation is by focussing on controlling the ventricular response, especially with the administration of diltiazem or esmolol intravenously. Ibut Synchronized DC cardioversion should be relied on in patients with pronounced hemodynamic instability. However, if fibrillation is present for longer than 48 hours, attempts to restore sinus rhythm may be associated with a heightened risk for thromboembolism. In a patient with a normal coagulation profile, adequate anticoagulation for 3 to 4 weeks should be considered before attempting to restore sinus rhythm. Alternatively, transesophageal echocardiographic examination to rule out atrial thrombi may be substituted. New developments in electrophysiologic techniques for ventricular defibrillation consisting of biphasic current shocks have shown superiority to the conventional monophasic
Junctional Rhythms
The AV node itself and sites just above and below it can act as pacemakers. It makes sense to consider this ectopic activity as arrhythmias of the AV junction. The resultant P wave is abnormal and, depending on the position of the ectopic pacemaker, may be very close to, buried in, or after the QRS complex. Depending on the rate of fire of the ectopic pacemaker, the resultant rhythm is nodal premature; nodal quadrigeminy, trigeminy, or bigeminy; nodal rhythm; or nodal tachycardia.
1. Heart rate: Variable, 40 to 180 beats/min (i.e., nodal bradycardia to junctional tachycardia).
2. Rhythm: Regular.
3. P/QRS: 1 : 1, but there are three varieties:
a. High nodal rhythm: The impulse reaches the atrium before the ventricle; the P wave therefore precedes the QRS but has a shortened PR interval (0.1 second).
b. Mid nodal rhythm: The impulse reaches the atrium and the ventricle at the same time. The P wave is lost in the QRS.
c. Low nodal rhythm: The impulse reaches the ventricle first and then the atrium, so the P wave follows the QRS complex.
4. QRS complex: Normal, unless altered by the P wave.
5. Significance: Junctional rhythms are common in patients under anesthesia (about 20%), especially with halogenated anesthetic agents. Junctional rhythms frequently decrease blood pressure and cardiac output by about 15%, but they can decrease it up to 30% in patients with heart disease.
6. Treatment: Usually, no treatment is required, and the rhythm reverts spontaneously. If hypotension and poor perfusion are associated with the rhythm, treatment is indicated. Atropine, ephedrine, or isoproterenol can be used in an effort to increase the activity of the SA node so that it will take over as the pacemaker. Dual-chamber electrical pacing at a rate faster than a slow nodal rhythm is another option.
Ventricular Premature Beats
VPBs result from ectopic pacemaker activity arising below the AV junction. The VPB originates in and spreads through the myocardium or ventricular conducting system, thereby resulting in a wide (>0.12-second), bizarre QRS complex. The ST segment usually slopes in the direction opposite the main deflection of the QRS complex. There is no P wave associated with a VPB, but retrograde depolarization of the atria or blocked sinus beats may obscure the diagnosis.
Although an APB normally reaches the SA node and resets the sinus rhythm, such an occurrence is rare when the ectopic pacemaker is in the ventricle. A VPB often blocks the next depolarization from the SA node, but the following sinus beat occurs on time. The result is a fully compensatory pause consisting of the interval from the VPB to the expected normal QRS, which is blocked at the AV node, plus a normal sinus interval.
VPBs are common during anesthesia, where they account for 15% of observed arrhythmias. They are much more common in anesthetized patients with preexisting cardiac disease. Other than heart disease, known etiologic factors include electrolyte and blood gas abnormalities, drug interactions, brainstem stimulation, and trauma to the heart.
1. Heart rate: Depends on the underlying sinus rate and frequency of the VPBs.
2. Rhythm: Irregular.
3. P/QRS: No P wave with the VPB.
4. QRS complex: Wide and bizarre, with a width of more than 0.12 second. If it is of an RBBB nature, prominent R forces are present in V1. If it is an LBBB in appearance, notching of the S wave and less acute downward sloping of the ST segment are common.
5. Significance: The new onset of VPBs must be considered a potentially serious event because in certain clinical situations, the arrhythmia may progress to VT or ventricular fibrillation. Such situations include coronary artery insufficiency, MI, digitalis toxicity with hypokalemia, and hypoxemia. VPBs are more likely to precede ventricular fibrillation if they are multiple, multifocal, or bigeminal; occur near the vulnerable period of the preceding ventricular repolarization (i.e., R-on-T phenomenon)or appear in short-long-short coupling sequences. VPBs are markers, not the cause of more severe arrhythmias.
6. Treatment: In most patients, VPBs (occurring as single, bigeminy, or trigeminy but excluding nonsustained VT) do not need to be treated, particularly if the patient does not have an acute coronary syndrome, and treatment is generally dictated by the presence of symptoms attributable to the VPBs. The first step in treatment is to correct any underlying abnormalities such as decreased serum potassium or low arterial oxygen tension. If the arrhythmia is of hemodynamic significance. lidocaine is the treatment of choice, with an initial bolus dose of 1.5 mg/kg. Recurrent VPBs can be treated with a lidocaine infusion at 1 to 4 mg/min; additional therapy includes esmolol, propranolol, procainamide, quinidine, disopyramide, atropine, verapamil, or overdrive pacing.
Ventricular Tachycardia
The presence of three or more sequential VPBs defines VT. Diagnostic criteria include the presence of fusion beats, capture beats, and AV dissociation. The specific morphologic appearance of the QRS complex may also be helpful in distinguishing VT from other arrhythmias. VT is classified by its duration and morphology. In duration, nonsustained VT lasts three beats and up to 30 seconds, and sustained VT lasts 30 seconds or longer. With monomorphic morphology, all complexes have the same pattern, and with polymorphic morphology, complexes constantly change patterns. Polymorphic VT with a long QTc is also called “torsades de pointes.”
The characteristics of VT are as follows:
1. Heart rate: 100 to 200 beats/min.
2. Rhythm: Generally regular, but may be irregular if the VT is paroxysmal.
3. P/QRS: Usually there is no fixed relationship
4. QRS complex: Wide, more than 0.12 second in width, with similar morphologic criteria in lead V1 as for VPB.
5. Significance: Acute onset is life threatening and requires immediate treatment.
6. Treatment: If the patient is hemodynamically stable, amiodarone administered as one or more intravenous doses of 150 mg in 100 mL saline or D5W over a period of 10 minutes, followed by an intravenous infusion of 1 mg/min for 6 hours and 0.5 mg/min thereafter, is the recommended current treatment (maximum intravenous dose, 2.2 g/24 hr). Although amiodarone is associated with substantially less hypotension than bretylium is, hypotension and bradycardia are its main side effects. Amiodarone's pharmacologic effects persist for more than 45 days. Lidocaine and procainamide have been used in the past with varying degrees of success to treat VT. Synchronized cardioversion is the indicated nonpharmacologic intervention in any wide-complex tachycardia, whether monomorphic VT or a wide-complex SVT. Polymorphic VT with a normal QT interval is treated with amiodarone and cardioversion. Metabolic abnormalities and drug toxicity must be considered and treated. Polymorphic VT with a prolonged QT interval is a more serious rhythm disturbance, and the recommended current treatment is an intravenous infusion of 1 g of magnesium administered over a 2- to 3-minute period. Precipitating metabolic or toxic causes should be treated. Overdrive pacing may also be helpful in this setting
Ventricular Fibrillation
Ventricular fibrillation is an irregular rhythm that results from a rapid discharge of impulses from one or more ventricular foci or from multiple wandering reentrant circuits in the ventricles. The ventricular contractions are erratic and are represented on the ECG by bizarre patterns of various size and configuration. P waves are not seen. Important causes of ventricular fibrillation include myocardial ischemia, hypoxia, hypothermia, electric shock, electrolyte imbalance, and drug effects
Its characteristics are as follows:
1. Heart rate: Rapid and grossly disorganized.
2. Rhythm: Totally irregular.
3. P/QRS: None seen.
4. QRS complex: Not present.
5. Significance: There is no effective cardiac output, and life must be sustained by artificial means, such as external cardiac massage.
6. Treatment:
a. Cardiopulmonary resuscitation must be initiated immediately, and then defibrillation must be performed as rapidly as possible. Asynchronous external defibrillation should be performed with a DC defibrillator using incremental energies in the range of 200 to 360 J. The introduction of biphasic (and rectilinear) transthoracic shocks has reduced the energy levels required and increased the efficacy of ventricular defibrillation. 120 J of biphasic current was superior to 200 J of monophasic current, especially in patients with increased chest wall impedance.
b. Early administration of 1 g of magnesium sulfate may facilitate defibrillation. In some instances, epinephrine has been used for coarsening the fibrillation to facilitate defibrillation. Vasopressin has been added as a drug for the treatment of ventricular fibrillation. The vasopressin dose is a single 40-unit intravenous bolus. Subsequent administration of epinephrine should be delayed for at least 5 minutes after vasopressin. Supportive pharmacologic therapy may include lidocaine, amiodarone, bretylium, procainamide, phenytoin, or esmolol.
c. Torsades de pointes, which may mimic ventricular fibrillation or VT, is a life-threatening arrhythmia that occurs in the presence of disturbed repolarization (hence its association with prolonged QT intervals)Discontinuation of drugs that predispose to prolongation of the QT interval and correction of electrolyte abnormalities are essential in the treatment of torsades de pointes. Acute therapy may include defibrillation, 1 to 2 g of intravenous magnesium sulfate, intravenous isoproterenol, and overdrive pacing.
Conduction Defects
Conduction defects are most often chronic, are present on the baseline preoperative ECG,However, conduction defects may be observed for the first time during surgery and anesthesia. They can occur as a result of simple manipulation, such as passage of a pulmonary artery catheter through the right ventricle, but they can also be a manifestation of myocardial ischemia. Because high-grade (second- and third-degree AV blocks) conduction defects often have deleterious effects on hemodynamic performance, intraoperative recognition is important.
Three types of conduction system blocks are possible: SA block, AV heart block, and intraventricular conduction block.In an SA block, the block occurs at the sinus node. Because atrial excitation is not initiated, P waves are not found on the ECG. The next beat can be a normal sinus beat, a nodal escape beat, or a ventricular escape beat.
The second type of heart block is an AV heart block, or AV block, which may be incomplete or complete. First- and second-degree AV blocks are generally considered incomplete, whereas a third-degree AV block is considered to be a complete heart block. First-degree AV block is often found in healthy hearts, but it is also associated with CAD or digitalis administration. It is characterized by a PR interval longer than 0.21 second. All atrial impulses progress through the AV node to the Purkinje system. This form of heart block ordinarily requires no treatment. Second-degree AV block is associated with the conduction of some of the atrial impulses to the AV node and into the Purkinje system. It is further subdivided into two specific types. A Mobitz type I block, or a Wenckebach block, is characterized by progressive lengthening of the PR interval until an impulse is not conducted and the beat is dropped This form of block is relatively benign and often reversible, and it does not require a pacemaker. It may be caused by digitalis toxicity or MI and is usually transient. A Mobitz type I block reflects disease of the AV node.
Third-degree AV block, also called a complete heart block, occurs when all electrical activity from the atria fails to progress into the Purkinje system. The atrial and ventricular contractions are regular and irrespective to each other.The ventricular rate is approximately 40 beats/min. The QRS complex may be normal if the pacemaker site is in the AV node, but it is usually widened to longer than 0.12 second when the pacemaker site is located in the ventricle The heart rate is usually too slow to maintain adequate cardiac output, and syncope or Adams-Stokes syndrome may occur, as well as heart failure. These patients generally require insertion of a transvenous endocardial or epicardial pacemaker to increase their heart rate and cardiac output.
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