Chapter 3. Perioperative Rhythm Abnormalities

• The transesophageal echocardiography (TEE) machine records the electrocardiogram (ECG) simultaneously with all TEE imagery. This is done so that echocardiographers can correlate echo images throughout systole and diastole. Alterations in rhythm can have sweeping and at times ultimately fatal hemodynamic consequences. Thus, the rapid interpretation of abnormal rhythms and their correction is critical in cardiac anesthesia practice.

The ECG remains one of the main monitors used by anesthesiologists. It is primarily employed in anesthesia practice to detect heart rate and rhythm changes, and perioperative myocardial ischemia. The ECG detects electrical currents flowing through the body generated by the electrical activity of the heart. ECG leads are positioned throughout the body and provide various perspectives (depending upon where the lead is placed) of the electrical activity of the heart. Examining the ECG in multiple leads provides the anesthesiologist the ability to discern if perceived changes in ECG pattern are widespread (found in multiple leads) or are perhaps less significant (motion artifact). At the end of diastole, the atria contract providing the atrial contribution to the patient's cardiac output generating the "P" wave. Following atrial contraction, the ventricle is loaded awaiting systole. Systole commences at the QRS beginning with isovolumetric contraction following a 120 to 200 milliseconds conduction delay at the AV node. Subsequently, intracavitary pressure builds, the atrioventricular valves (eg, mitral or tricuspid) close, and the arterioventricular valves (eg, aortic, pulmonic) open resulting in ventricular ejection of the stroke volume (SV). The QRS represents the electrical activity generated by the depolarization of the left and the right ventricles. Depolarization proceeds from the AV node through the interventricular septum via the His-Purkinje fibers. The QRS segment lasts approximately 120 milliseconds. Repolarization of the ventricles produces the ST segment and the T wave. Electrolyte abnormalities (eg, hypocalcemia) and drug effects (eg, droperidol) can delay repolarization leading to a prolonged QT interval. This can result in potentially life-threatening ventricular arrhythmias.

Electrolyte disorders, heart structure abnormalities, and myocardial ischemia can cause aberrations in the patient's baseline ECG without producing an arrhythmia per se (Figure 3–1). Electrolyte abnormalities occur with some frequency perioperatively. Hyperkalemia can present following cardioplegia administration during cardiopulmonary bypass (CPB), following iatrogenic administration, or associated with metabolic acidosis. As the potassium concentration increases, the T wave becomes progressively peaked. Hyperkalemia can ultimately produce broad, complex ventricular activity and asystole. Treatment is with immediate administration of calcium chloride. Glucose and regular insulin are given to lower the potassium concentration.

Hypokalemia lengthens the QT interval placing the patient at risk for les torsades de pointes type of sinusoidal ventricular fibrillation.

Hypocalcemia and hypomagnesemia likewise can prolong the QT interval placing the patient at risk for ventricular fibrillation. Hypermagnesemia is associated with various conduction abnormalities and is seen from time to time in the obstetrical patient being treated for preeclampsia. Hypercalcemia can also cause T-wave abnormalities.

Ventricular hypertrophy, cardiomyopathies, and inherent conduction disorders can all alter the baseline ECG. Increased QRS size in the left precordial leads (eg, V5, V6) may indicate the presence of left ventricular hypertrophy associated with increased afterload and/or obstruction to left ventricular outflow tract (LVOT) ejection. Conversely, tall QRS waves in the right precordial leads (eg, V1, V2) might indicate right ventricular hypertrophy secondary to pulmonary hypertension.

Right and left bundle branch blocks in addition to various prolongations in the QRS are evidence of impaired cardiac conduction and often herald the presence of cardiac disease.

ST-segment elevations and depressions are associated with transmural and subendocardial ischemia, respectively. Pathologic (wide and deep) Q waves suggest myocardial infarction. TEE imagery demonstrating poorly contractile myocardium can be compared with ECG tracings to identify and to confirm the presence of ischemic myocardium.

Access to the chest is limited during cardiac surgical procedures. Since ECG interpretation is critical throughout the procedure it is very important that the leads be securely fixed to the patient to avoid having to replace them during the operation. ECG tracings should be clear at the start of the case so to facilitate rhythm interpretation intra-operatively.

Bradycardia and bradyarrhythmias routinely complicate the perioperative management of the cardiac surgery patient. Hyperkalemia, myocardial ischemia, vagal effects, intrinsic cardiac disease, hypoxemia, loss of sympathetic tone can all contribute to the development of varying degrees of heart block and/or sinus bradycardia at any time during heart surgery.

Sinus bradycardia (sinus rate less than 60 bpm) frequently is associated with anesthesia induction, narcotic administration, a reflex response to systemic hypertension, and beta blockade. Sinus bradycardia is of little consequence assuming cardiac output is sufficiently preserved to maintain an acceptable blood pressure and tissue perfusion.

Recall,

Blood pressure = Cardiac output × Systemic vascular resistance

Cardiac output = Stroke volume × Heart rate

Therefore, if the heart rate falls—even if sinus rhythm is maintained—the patient may become hemodynamically unstable. Too slow a sinus rhythm provides other pacemaker cells in the heart the opportunity to emerge resulting in various other nodal or ventricular arrhythmias. Additionally, too slow a heart rate increases the diastolic filling time resulting in a prolonged filling of the left ventricle, increased left ventricular end-diastolic volume, and depending upon left ventricular compliance, increased left ventricular end-diastolic pressure (LVEDP). Reduced endocardial perfusion may occur.

Recall,

Coronary perfusion pressure (CPP) = Diastolic blood pressure (DBP) − LVEDP

Treatment for sinus bradycardia must be determined on a case-by-case basis depending upon the patient's hemodynamic performance. Bradycardia in response to systemic hypertension is corrected by lowering the blood pressure. Sinus bradycardias resulting from anesthesia induction may need to be treated if they result in hypotension and low cardiac output. Atropine (IV) 0.4 to 2.0 mg can be administered to correct the heart rate. The causes of sinus bradycardia should be sought and corrected. A slowing heart rate in the setting of hypoxemia is immediately worrisome and may indicate impending circulatory arrest. Ephedrine (5-10 mg IV) can be judiciously administered to the heart surgery patient experiencing hypotension and sinus bradycardia as a consequence of anesthesia induction. However, ephedrine's reliance upon release of native catecholamine reserves may make it a poor choice in the catecholamine-depleted patient. Likewise, various inotropic infusions (eg, epinephrine [2 μg/min IV] infusion and upward, dobutamine [2-10 μg/kg/min] etc) can be administered to increase the patient's heart rate. Of course, administration of catecholamines as well as atropine might lead to the development of accelerated nodal or ventricular rhythms. Temporary pacing (see later) can be used where available and when indicated to provide atrial, ventricular, or atrial-ventricular pacing as needed.

At times, patients will present with competing atrial pacemaker cells each resulting in an atrial driven rhythm albeit at different rates and with differing "P"-wave morphologies. Nodal rhythms emanate from the AV node and result in inadequate filling of the left ventricle due to the absence of a coordinated atrial contraction. The contribution of the atrial beat to effectively load the left ventricle at the end of diastole varies from patient to patient depending upon age and left ventricular compliance and atrial elastance. The less compliant the left ventricle the more dependent it becomes upon the contribution of the atrial contraction. When nodal rhythms emerge hemodynamic consequences may be nil or great depending upon the individual patient and their degree of diastolic dysfunction. Patients with a slow nodal rhythm may respond to administration of atropine and inotropic agents in a manner similar to the treatment of sinus bradycardia. On the other hand, some nodal rhythms develop into AV junctional tachycardia and require treatment as described below for supraventricular tachycardias.

Varying degrees of heart block are also quite common in the cardiac surgery patient. Impairment of the conduction system occurs frequently perioperatively secondary to ischemia, electrolyte disorders, and iatrogenic, surgically mediated injury to the heart's conduction system as it passes through the intraventricular septum. First-degree heart block occurs when there is a prolongation in the AV interval. Second-degree heart block occurs when not all of the atrial beats are conducted through the AV node to the ventricle. Mobitz type 1 block or Wenckebach block is associated with a gradual prolongation of the AV interval until a ventricular beat fails to occur. Often Mobitz type 1 block requires no direct therapy. Conversely Mobitz type 2 block has a propensity to deteriorate to third-degree heart block. In this form of second-degree atrioventricular block the atrial pacemaker beat is not always conducted through to the ventricle. Sporadically, atrial contractions can occur without a ventricular beat. In third-degree heart block no atrial beats are conducted through to the ventricle. A slow ventricular pacemaker may emerge leading to the atria and ventricles contracting in a discordant fashion. The "P" waves can be seen marching through the ECG tracing without an associated QRS immediately thereafter. Hemodynamic instability often becomes manifest and temporary pacing is frequently required perioperatively.

Left and right bundle branch blocks are very common in heart surgery patients as they can portend the presence of intrinsic cardiac disease. In patients with a left bundle branch block pulmonary artery catheterization can result in a mechanically induced concomitant right bundle branch block producing complete heart block and hemodynamic instability. A temporary pacing ability (eg, external cutaneous pacing) should be available whenever right heart catheterization is planned in the left bundle branch block patient.

The ability to provide temporary pacing is essential in cardiac anesthesia practice. Bradyarrhythmias as described earlier can present at any point in the patient's perioperative course. Many patients require some form of pacing to separate from cardiopulmonary bypass even if only for a few minutes until the heart is reperfused and/or the potassium concentration reduced. Transient perioperative ischemia can also produce varying degrees of heart block necessitating some form of emergent pacing. Temporary pacing must be distinguished from permanent pacing. Permanent pacemakers are increasingly being implanted in patients for the treatment of heart failure.1 Permanent biventricular pacing provides a more effective myocardial contraction in the heart failure patient by reducing the width of the QRS complex. Additionally, many permanent pacemakers contain the ability to sense an increase in respiratory rate and thus are able to increase the pacing rate in response to exercise. Finally, with an ever-increasing number of patients at risk for sudden cardiac death (SCD), these devices contain a defibrillation or anti-tachycardia function permitting electrical conversion of malignant rhythms (ICDs). Permanent pacemaker/defibrillators are discussed in Chapter 15.

Temporary pacemakers in general are designated by a three-letter code relating to their function: The first letter identifies the chamber or chambers of the heart paced (A for atrium, V for ventricle, D for dual [both A+V] and O for none). The second letter identifies which, if any, of the chambers are sensed. The third letter indicates the response of the device to a sensed beat (I for inhibited, D for both inhibition and triggering). Thus, a temporary VVI pacemaker would pace the ventricle, sense the ventricle, and be inhibited if a ventricle beat was detected. Likewise a DDD temporary pacemaker would pace both the atrium and the ventricle, sense both chambers, and either be inhibited or deliver a beat depending upon what the device senses.

There are many different modes of temporary pacing available to anesthesiologists perioperatively. Transcutaneous pacing is usually available as a part of most modern cardioverter/defibrillator devices. Pacing/defibrillation patches are applied to the chest and ventricular pacing initiated by setting the pacing rate and the output from the device until the heart is captured and a beat generated. Transcutaneous pacing is ventricular pacing and as such the atrial contribution to the cardiac output is lost. Often pacing patches are placed prophylactically in cardiac surgery patients in order to provide for a quick pacing capability should the rhythm be lost before the heart is exposed and epicardial pacing wires placed. In reoperative heart surgery patients, access to the heart may be difficult thus preventing rapid sternal opening and application of epicardial pacing wires. Placement of transcutaneous pacing pads perioperatively is especially suggested in these cases to provide for a temporary ventricular beat.

Temporary esophageal pacing systems can be used to pace the atrium. They have limited application in the heart surgery patient since this atrial pacing modality (AOO) does not provide for ventricular capture. Moreover, a TEE probe frequently occupies the esophagus during cardiac surgical procedures.

Temporary epicardial pacing has been used in cardiac surgery since the 1960s.2 Surgeons routinely place epicardial pacing wires to provide for both atrial and ventricular pacing. These wires are passed from the surgical field to the anesthesiologist and attached to a pulse generator. The anesthesiologist next chooses the pacemaker mode and settings. Generally, the DDD mode is chosen to provide for temporary pacing. To set the pacemaker the anesthesiologist selects:

1. Heart rate: The rate can be set lower than the patient's own rate to provide an emergency backup pacing function or can be set at any rate desirable. Often rates of between 80 and 100 bpm are selected.

2. Output: The electrical output (up to 20 mA) of both the atrial and ventricular pacing components is set so to establish capture of the signal by the heart to generate a beat.

3. Sensitivity: The sensitivity of the device is set to determine which signals will result in inhibition of the pacemaker function. For example, A sensitivity of 0.5 mV, V sensitivity of 2.0 mV.

4. Pulse width duration: Generally of short duration 1 millisecond.

5. AV interval: 150 to 200 millisecond.

Pacemaker settings are adjusted to achieve the best possible hemodynamics. Usually this occurs when the atrial and ventricular contractions are timed to provide for sufficient loading of the left ventricle during diastole. As with all pacing functions, inappropriate delivery of a paced beat during repolarization of the heart can initiate ventricular fibrillation. Consequently, asynchronous ventricular pacing modes (VOO) are best avoided. Recently, cardiac resynchronization therapy (CRT) through biventricular epicardial pacing perioperatively has been suggested to improve ventricular function when separating from cardiopulmonary bypass.3 Biventricular pacing provides for a reduced width of the QRS resulting in better coordination of left ventricular contraction and improved hemodynamics.

From time to time, anesthesiologists may place either a temporary transvenous pacing catheter or a pulmonary artery catheter with pacing capabilities. A balloon-tipped pacing wire can be placed in the right heart following central venous access. The output of the pulse generator is adjusted until beat capture is achieved.

Various pulmonary artery catheter designs have either electrodes built into them or additional channels by which transvenous pacing wires can be placed. These leads are attached to a temporary pulse generator and pacing can be initiated as appropriate. However, in the overwhelming majority of instances, the anesthesiologist will employ temporary epicardial pacing to wean from CPB or emergent transcutaneous pacing during resuscitative efforts. From time to time patients with heart block will appear to the operating room with a temporary pacer wire in place for surgery previously placed by the cardiology staff. Placement of a pulmonary artery flotation catheter can readily dislodge both temporary transvenous pacemakers as well as recently placed permanent transvenous wires.

Both sinus tachycardias and various supraventricular arrhythmias are common in the perioperative cardiac surgery patient. Rapid heart rates can have profound hemodynamic consequences perioperatively resulting from inadequate ventricular filling secondary to the loss of atrioventricular synchrony and/or reduced diastolic filling time. The causes of perioperative sinus tachycardia are legion including: hyperthermia, hypovolemia, anemia, light anesthesia, vasoactive infusions, and sympathetic stimulation to name a few. Correction of the underlying initiating mechanism of sinus tachycardia will generally resolve the issue perioperativley. Often in the cardiac surgery patient, the intense surgical stimulation of sternal opening can lead to both a hypertensive and tachycardic response necessitating administration of additional narcotics and increased concentrations of inhalational agents.

Supraventricular tachycardias (SVTs) also frequently occur perioperatively. Very fast sinus tachycardias can be difficult to distinguish from SVTs perioperatively. SVTs, of course, lack the "P" wave that would be found in a sinus tachycardia. SVTs are generally produced through re-entrant mechanisms. Re-entrant arrhythmias occur when conduction tissues in the heart (either within the AV node or through accessory conduction pathways) depolarize and repolarize at varying rates.4 In this way a self-perpetuating loop of repolarization and depolarization within the AV node can occur resulting in the development of SVT. SVTs occur frequently during both cardiac and noncardiac surgery. SVTs producing ischemia or hemodynamic collapse are routinely treated in the cardiac surgery patient with synchronized cardioversion. Adenosine 6 to 12 mg IV can be given to slow AV node conduction potentially disrupting the re-entrant loop. Attention should be paid as adenosine can result in a third-degree atrioventricular block in heart transplant patients. Various beta-blockers and calcium antagonists can also be employed in patients with SVT with the exception of the SVTs as a manifestation of Wolff-Parkinson-White syndrome. Occasionally an SVT can appear as wide QRS complex tachycardia similar in appearance to ventricular tachycardia (VT) and should be treated as VT until otherwise proven.5

Atrial fibrillation/flutter (AF) can likewise complicate the perioperative management of the cardiac surgery patient. The incidence of new postoperative atrial fibrillation (AF) ranges from 17% to 35% following cardiac surgery.5 Moreover, many patients with impaired ventricular function and/or valvular disease present to cardiac surgery already in AF as a baseline. Such patients tend to have very dilated atria (Video 3–1) and must be screened for the presence of intra-atrial clot if they have been in AF without having been anticoagulated (TEE Videos 3–2 and 3–3). Prophylaxis against postoperative AF is usually undertaken perioperatively with beta-blockers in those patients without contraindications. Amiodarone (IV and PO) can be given in combination with beta-blockers to further reduce the new onset of AF postoperatively. Sotalol can likewise be employed to reduce the incidence of perioperative AF.

Patients brought to surgery with long-standing AF associated with valvular heart disease (eg, mitral stenosis) may undergo the "maze" procedure at the time of surgery to disrupt conduction pathways in the atria and so eliminate atrial fibrillation. Amiodarone by infusion is also started (150 mg IV load followed by infusion 1 mg/min for 6 h and 0.5 mg/min for 18 h) followed by oral therapy.

AF can also appear unexpectedly during cardiac surgical procedures secondary to manipulation of the heart, the inflammatory response, and changing autonomic tone. The irregular ventricular response can become rapid >150 bpm leading to hemodynamic collapse necessitating internal synchronized cardioversion. Surgeons can place internal paddles on the heart and effectively restore sinus rhythm with relatively low energy of 10 to 20 J. External cardioversion often requires 50 to 200 J depending upon patient factors (eg, size); however, newer biphasic devices require less energy delivery in order to be effective.

The American Heart Association/American College of Cardiology (AHA/ACC) have produced voluminous guidelines on the management of all aspects of atrial fibrillation.6 These guidelines include suggestions for the management of postoperative atrial fibrillation. Class I (benefits far outweigh risks) guidelines suggest the use of beta-blockers to prevent AF development in cardiac surgery patients if not contraindicated. Additionally, amiodarone is suggested in cardiac surgery patients thought at risk for perioperative AF development (Class IIa benefit is greater than risk). Additionally, the guidelines suggest that it is reasonable to administer antiarrhythmic medications to maintain sinus rhythm in those patients with recurrent or refractory AF. Lastly, anticoagulation therapy and attempts at cardioversion should be applied as in nonsurgical patients assuming no contraindications exist.

The perioperative development of ventricular fibrillation (VF) represents an immediate threat to the patient's life and requires the simultaneous generation of a differential diagnosis, defibrillation, and therapy to prevent VF recurrence. Ventricular arrhythmias are associated with myocardial ischemia, heart failure, hypoxemia, various cardiomyopathies, electrolyte abnormalities, prolonged QT syndrome, inotrope administration, and mechanical manipulation of the heart. The AHA/ACC have developed extensive guidelines for the management of ventricular arrhythmias.7 Both VF and pulseless ventricular tachycardia (VT) require immediate resuscitative efforts as systemic blood flow ceases during these arrhythmias. Defibrillation should be undertaken immediately for VF and cardioversion for VT. In the operative setting the open sternum permits the delivery of defibrillation current through the use of internal paddles. Additionally, should the rhythm fail to be restored open chest cardiac massage can be initiated. Also, immediate institution of CPB can be undertaken to preserve tissue perfusion while efforts are made to restore cardiac function.

Any wide QRS complex tachycardia should be assumed to be VT even if a pulse is present. When VT provides an acceptable blood pressure, pharmacological therapy (eg, procainamide, amiodarone) can be employed. Most likely in the perioperative period the surgeon will attempt cardioversion should such a rhythm occur. Intravenous lidocaine may be useful in patients where ischemia is a causative factor in the etiology of the rhythm aberrancy. VT associated with a prolonged QT interval produces les torsadesde pointes. The sine wave appearing ECG with polymorphic VT indicates the presence of torsades. Correction of any electrolyte abnormalities and discontinuation of any drugs that promote QT interval prolongation is mandatory.

Other causes of perioperative VF include air embolism in the coronary vessels or bypass grafts, myocardial ischemia, heart failure, migration of the pulmonary artery catheter into the RV or RV outflow track, and pacemaker misfires (R on T phenomenon). Any cardiac surgery patient can fibrillate at any time perioperatively. Correction of metabolic derangements prior to separation from CPB is useful in reducing the occurrence of VF perioperatively. During periods of patient transfer it is critically important that the patient be monitored at all times and electrical modalities be available to treat compromising dysrhythmias. The loss of an arterial pressure trace concurrent with the disappearance of the ECG and a falling end-tidal carbon dioxide measurement should immediately suggest the possibility of a lethal arrhythmia. Should VF be refractory to defibrillation, CPR can be initiated and maintained until the patient can be placed on CPB. Administration of epinephrine and/or vasopressin may be needed to successfully defibrillate the patient. Often only surgical repair of the patient's underlying cardiac pathology and emergent institution of CPB will permit patient survival. Prolonged hypothermia should also be employed postoperatively to reduce the incidence of reperfusion injuries.

ECG is a vital part of any TEE examination and should be placed whenever any echo examination is planned. The ECG is correlated with TEE imagery to determine when the patient is in diastole and when in systole. It is important to remember that mechanical events in the heart slightly lag behind the appearance of their corresponding electrical signals on the ECG.

Patients with AF frequently have dilated atria which are readily apparent on TEE. Poor flow associated with a poorly contractile atrium can be seen as spontaneous echo contrast "smoke" swirling in the left atrium. Pulse wave Doppler can be used to determine the velocity of flow in the left atrial appendage (LAA). The left atrial appendage appears as a beak-like structure on TEE examination. Reduced velocity in the LAA <45cm/s increases the risk of clot developing in the LAA. Patients presenting for cardioversion who have not been placed on anticoagulation for more than 24 hours require TEE prior to cardioversion to minimize the risk of embolization of atrial thrombus following the restoration of sinus rhythm.

Although beyond the scope of basic TEE, tissue Doppler techniques can be employed to determine the varying velocities of different segments of the myocardium during each cardiac beat. Tissue Doppler examines the velocities of the myocardium by filtering out the velocities of the red blood cells. Therefore the various velocities and timing of different ventricular segments during systole can be compared. When patients develop heart failure, the effectiveness of their conduction system in the ventricle becomes impaired. In patients with heart failure, the septal wall often contracts before the lateral wall thus making contraction of the ventricle less effective. Cardiac resynchronization therapy attempts to restore efficiency of the ventricular contraction by concomitant pacing of the left and right ventricle with two separate ventricular pacing leads. Tissue Doppler can assist in selecting patients who would benefit from CRT.

Elective Cardioversion

A 65-year-old patient presents for elective cardioversion with anesthesia.

Case Questions

What constitutes the anesthesia preoperative examination?

Although elective cardioversion is a brief procedure, a full anesthesia history should be obtained. Particular attention should focus on the presence of valvular heart disease, systolic and diastolic heart failure, and the patient's anticoagulation status.

When should a TEE examination be completed prior to cardioversion?

In any patient with AF for more than 24-hour duration without initiation of anticoagulation, a TEE examination should be performed immediately prior to cardioversion.

Assuming relatively preserved cardiac function, what anesthetic approach should be used for the TEE and cardioversion?

Provided there are no contraindications, deep sedation with propofol can be employed along with topicalization of the oropharynx. Patients should be sufficiently awake to aid in the TEE examination by swallowing the probe following topicalization.

Looking at (Video 3–3), should the cardioversion be performed?

The left atrial appendage demonstrates the absence of clot. The cardioversion may be performed.