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Abnormalities of cardiac conduction and cardiac rhythm
Introduction
The development of the modern-day electrocardiogram (ECG) started with the recognition by scientists that the electric currents regulating the heart could be detected at the surface of the skin. In the late 1800s Willem Einthoven built a machine called a string galvanometer that recorded a tracing representing the direction of cell depolarization through the heart as a series of positive and negative deflections around an isoelectric baseline. He called it an electrocardiogram. Now, over 100 years later, ECGs remain a mainstay of diagnostic cardiac evaluation.
All perioperative clinicians, whether anesthesiologists, intensivists, or pain specialists, must be proficient in recognizing normal and abnormal ECG findings. The ECG is considered the single most important clinical test to diagnose cardiac dysrhythmias, ischemia, and infarction. In preoperative risk stratification, a resting 12-lead ECG is a helpful tool to evaluate symptoms suggestive of arrhythmia or for detection of more covert problems such as silent ischemia in diabetics. Also, a preoperative ECG is a helpful baseline to determine the seriousness of ST or rhythm changes detected intraoperatively or postoperatively.
In the operating room, it is rare that we can monitor 12 leads during an anesthetic procedure. Most commonly, a 5-lead continuous ECG is used, and leads II and V 5 are monitored to assess heart rhythm, rate, and ST trending. This choice of leads has been shown to detect 80% of ischemic changes. Lead II monitors the heart in the distribution of the right ventricle and the inferior wall of the left ventricle, which is perfused by the right coronary artery (RCA). Lead V 5 represents the lateral wall of the left ventricle, which is perfused by the left circumflex artery (Lcx).
Conduction system of the heart overview
The human body is composed of approximately 37 trillion cells. Cellular arrangement into organ systems allows the cells to perform unique functions supporting the life and health of the body. The heart and its associated vasculature form a complex and dynamic organ system. The heart’s pumping function is accomplished by the coordinated contraction of 2 to 3 billion cardiac muscle cells (myocytes) within the heart. Stimulation of the myocytes comes from electrical signals generated in specialized tracts of cardiac tissue called the myocardial conduction system. The conduction system includes the sinoatrial (SA) node, atrioventricular (AV) node, bundle of His, right and left interventricular bundles, and Purkinje fibers ( Fig. 8.1 ). Cells of the conduction system communicate with the myocytes by various specialized ion channels such as gap junctions, sodium potassium pumps, and calcium channels.
At rest, myocytes are polarized with a resting membrane potential of −80 to −90 mV. This means that the intracellular charge is more negative in comparison to the extracellular charge. The polarized state is maintained by a specific membrane-bound sodium-potassium adenosine triphosphatase (Na + -K + ATPase) that concentrates potassium intracellularly and extrudes sodium into the extracellular milieu.
Ion fluctuations in neighboring cells cause the sodium and calcium channels to open temporarily to allow positive ion entry. This alters the charge on the membrane of the myocyte from negative to positive. If the intracellular charge reaches +20 mV, an action potential (or depolarization) occurs. When an action potential occurs, the myocyte shortens (contracts). In summary, electrical stimulation from conduction system tissue causes the cell membranes of the myocytes to go from a resting (negative) polarized state to a contracted (positive) depolarized state.
A properly functioning conduction system produces a wave of depolarization resulting in perfectly coordinated contraction of the atria and ventricles ( Fig. 8.2 ). After depolarization, myocytes are refractory to immediate electrical stimulation that might result in additional action potentials. The myocardial action potential can be broken down into five phases: phase 0, rapid depolarization by sodium influx; phase 1, rapid repolarization by potassium efflux out of the cell; phase 2, plateau from calcium (positive ions) influx starting to balance the potassium (positive ion) efflux; phase 3, continued repolarization by potassium concentration within the cell; and phase 4, the resting polarized state of the relaxed myocardial cell.
Myocyte contraction stimulated by an action potential involves thick and thin contractile myofilaments that slide past each other by forming repetitive cross bridges. The interaction of the conduction system and the contractile apparatus is termed excitation-contraction (E-C) coupling . The contractile process is highly calcium dependent. Calcium sources for this process come from intracellular (sarcoplasmic reticulum) and extracellular (sodium-calcium pump) sources. The E-C coupling provides a critical balance of inotropy (speed and strength of cardiac muscle contraction), a function critical to systole, and lusitropy (ability to relax and allow ventricular chamber filling), a function critical to diastole. Stroke volume is dependent on inotropy and lusitropy. A person may be affected with systolic, diastolic, or both systolic and diastolic dysfunction. Loss of inotropy leads to systolic heart failure, also termed heart failure with reduced ejection fraction , while loss of lusitropy leads to diastolic heart failure or heart failure with preserved ejection fraction.
A wide variety of physiologic states (acquired, inherited, iatrogenic) can affect E-C coupling. Certain drugs the patient may be using or abusing, medically directed or illegally, can precipitate systolic and diastolic dysfunction or ischemia particularly when combined with anesthetic agents. Some examples are street drugs such as cocaine, fentanyl, heroin, and prescription narcotic analgesics. Many of the drugs used in anesthesia temporarily alter or influence cardiac contractility, and some of the commonly used drugs for cardiac rhythm and blood pressure regulation affect the E-C coupling system. This includes cardiac glycosides, phosphodiesterase inhibitors, and angiotensin-converting inhibitors.
Digitalis, a cardiac glycoside, is thought to increase the intracellular availability of calcium by inhibiting the Na/Ca exchanger pump, which decreases the amount of Ca extruded from the cell. Phosphodiesterase type 3 inhibitors, such as milrinone, are used as inotropes in clinical medicine. They inhibit the breakdown of cyclic adenosine monophosphate (cAMP). Increasing levels of available cAMP serve to increase intracellular calcium, which increases the force of myocardial contraction. Angiotensin II is a potent vasoconstrictor that acts on the myocardium through specific receptors that over time can cause left ventricular hypertrophy (LVH) in patients with hypertension. The angiotensin receptors are stimulated by a cAMP-mediated mechanism. Angiotensin-converting enzyme (ACE) inhibiting drugs such as lisinopril block this stimulation, lower blood pressure, and help prevent LVH by a vasodilatory action.
Normally, the SA node is the primary pacemaker of the heart. The SA node is a tract of cells located at the junction of the superior vena cava and the right atrium. The impulse generated by the SA node propagates across the right and left atria, causing them to contract. After passing through the atria, the electrical impulse travels to the AV node. The AV node is located in the right atrium above the insertion of the septal leaflet of the tricuspid valve and anterior to the coronary sinus. The AV node can function as a secondary pacemaker for the heart if the SA node fails. Both the SA and AV nodes are richly innervated by the sympathetic and parasympathetic nervous systems. As such, it is influenced by endogenous hormones such as epinephrine and exogenous substances such as β blockers and other therapeutic drugs.
When the electrical impulse reaches the AV node, it slows down due to the long refractory period characteristic of this tissue. This so-called AV delay serves to prevent overstimulation of the ventricles in the event of abnormally rapid atrial impulses. A good example of this protective effect is seen in atrial flutter, where the atrial rate can be greater than 200 beats per minute (bpm), but due to the AV delay the impulses are conducted through to the ventricle at a 3:1 or 4:1 ratio.
After exiting the AV node, the impulse passes between the fibrous AV rings of the tricuspid and mitral valves and continues down the proximal ventricular conduction system within the interventricular septum. This part of the conduction system, the bundle of His, splits into right and left portions called bundle branches. The right and left bundle branches terminate as an interlacing network of small fibers called the His-Purkinje system. As the impulse travels through the bundle branches, the first portion of the ventricles to depolarize is the septum. It is followed by depolarization of the apex and most of the ventricular free walls. The last area to be depolarized is the superior portion of the left ventricular free wall and the right ventricular outflow tract.
While the sinus node portion of the conduction system is responsible for being the dominant pacemaker of the heart, any myocyte can generate an action potential and become an ectopic pacemaker in certain circumstances. The location of the group of cells acting as the dominant pacemaker affects the resultant heart rate and waveform morphology. In general, the further away from the SA node the dominant pacemaker is, the slower the heart rate generated.
The average rate of impulse generation by the SA node is 60 to 100 bpm. If the AV node takes over as the dominant pacemaker due to SA node dysfunction, then the so-called nodal or junctional rhythm generates an average rate of 40 to 60 bpm. Impulses below the AV node such as ventricular cells generate an extremely slow heart rate in the range of 30 to 45 bpm in the absence of a faster sinus or AV node dominant rhythm.
Interruptions or abnormalities in the blood supply to the heart can significantly impair the conduction system. The RCA supplies the SA and AV nodes in 60% to 85% of people. The remaining population get blood supply to these major pacemakers from the left circumflex coronary. This explains why patients suffering from an inferior myocardial infarction (MI; occlusion of the RCA) often present with conduction disturbances such as bradyarrhythmia or heart block as slower ectopic foci take over rate dominance due to the ischemic insult and dysfunction of the SA and AV nodes. Prompt restoration of blood flow to the ischemic tissue can correct the bradyarrhythmia, but temporary transcutaneous or transvenous pacing may be necessary in the interim.
Physiologic actions represented in the ECG
As clinicians we rely on measurable data from tests and personal observations to guide our therapeutics. The ECG is one of the most important diagnostic tests to corroborate and define clinical signs and symptoms of rhythm disturbances and ischemic heart disease. The ECG machine apparatus processes, filters, and translates weak electrical signals detected on the skin surface into a tracing. For clinical use, it can be a continuous active trace as used in intensive care units (ICUs) or the operating room, or a single snapshot of cardiac rate rhythm captured in a resting 12-lead ECG.
The ECG components that we examine, the PQRST complex, reflect physiologic actions within the heart ( Fig. 8.3 ). The P wave coincides with spread of action potentials across the right and left atria, causing them to contract. The PR interval is normally 120 to 200 ms. Existence of a P wave on ECG indicates that the impulse was generated by the SA node. Electrical impulse movement through the bundle branches coincides with the isoelectric PR interval on the ECG tracing. After the electrical impulse exits the AV node and travels through the bundle branches, the first portion of the ventricles to depolarize is the septum. This causes a minor ECG deflection called the Q wave. It is followed by depolarization of the apex and the bulk of the ventricular free walls, as reflected in the R wave of the ECG. The last area to be depolarized is the superior portion of the left ventricular free wall and the right ventricular outflow tract. Depending on the bulk of the left ventricular free wall, this vector may show up as a negative deflection, the S wave. The interval from the Q wave through the R wave to the end of the S wave is called the QRS complex. Normal QRS duration varies depending on age and gender. Abnormal intraventricular conduction is suggested by a QRS complex that exceeds 110 ms in adults. The portion of the ECG between the S and T waves (ST segment) is normally isoelectric and represents the time between ventricular depolarization and the start of ventricular repolarization.
ST segments that are not isoelectric can indicate ischemia, electrolyte abnormalities, or other pathologic states. Acute ST segment changes trending down (ST depression) or up (ST elevation) should be considered myocardial ischemia until proven otherwise. The pattern of ECG leads reflecting the ST changes gives a clinical indication of which area of myocardium is ischemic or damaged. Inferior wall ischemia will show up in leads II, III, and aVF. Anterior ischemia is often seen in the precordial leads V 1 through V 6 . Left ventricular septal ischemia is seen in V 1 to V 3 and lateral wall abnormalities in V 4 to V 6 .
Other causes of ST-segment elevation considered in a differential of acute ST elevation include acute inflammatory states (myocarditis and pericarditis), hyperkalemia, acute myocarditis, nonischemic vasospasm, LVH, ventricular aneurysms, cardiac tumors, hypothermia (Osborne waves), and early repolarization (ER) .
ER is a notching or slurring at the terminal part of the QRS complex giving the appearance of ST elevation. Most literature defines ER as being present on the ECG when there is J-point elevation of 0.1 mV or greater in two adjacent leads with either a slurred or notched morphology. Patients with early repolarization are more often young, athletic, with black ancestry, and male. Early repolarization on ECG has been thought to represent exercise-induced interventricular septal thickening although there are studies suggesting an increased risk of arrhythmia, particularly idiopathic ventricular fibrillation, in these patients.
Hyperkalemia may have peaked T waves, PR interval and QRS duration increases, atrial standstill, ST elevation in V 1 to V 2 , or sine wave. Osborne waves are characteristically seen in hypothermia (typically body temperature <34°C and appear as a J-point elevation in the precordial leads).
ST-segment depression is often seen in LVH (LV strain), with certain cardioactive drugs (digoxin), and hypokalemia. Digitalis toxicity may lead to both tachyarrhythmia and bradyarrhythmia. Hypokalemia may cause ST-segment depression, decrease in T-wave amplitude or T-wave inversion, increase in U-wave amplitude, merging of the T and U waves, increase in P-wave size and duration, PR interval prolongation, and widening of the QRS complex.
Ventricular repolarization is represented by the T wave. After the T wave there is another isoelectric period until the depolarization process begins again. The T-wave deflection should be in the same direction as the QRS complex and should not exceed 5 mm in amplitude in standard limb leads or 15 mm in precordial leads. T waves should be upright in all leads except aVR and V 1 .
The QT interval is the time from the start of the Q wave to the end of the T wave. It represents the time taken for full ventricular depolarization and repolarization. The QT shortens at faster heart rates and lengthens at slower heart rates. Normal values for the QT interval should be corrected for the heart rate (QTc) because the QT interval varies inversely with heart rate. Typically, women have longer QT intervals than men do. This difference is more pronounced at slower heart rates.
The prolongation of repolarization in LQTS results in a dispersion of refractory periods throughout the myocardium. This abnormality in repolarization allows afterdepolarizations to trigger premature ventricular contractions (PVCs). These PVCs can degenerate into a form of pulseless ventricular tachycardia called torsades de pointes (TdP). TdP, also called polymorphic ventricular tachycardia, is a distinct form of reentrant ventricular tachycardia initiated by a PVC in the setting of abnormal ventricular repolarization (prolongation of the QT interval). TdP is a lethal arrhythmia characterized by a twisting of the peaks or rotation around the ECG baseline. In other words, there is a constantly changing cycle length, axis, and morphology of the QRS complexes around the isoelectric baseline during TdP (see Fig. 8.7 , later). This dysrhythmia may be repetitive, episodic, or sustained and may degenerate into ventricular fibrillation.
Long QT syndrome can be congenital or acquired and predisposes the affected patient to TdP. The incidence of congenital and acquired prolonged QT syndromes is higher in women. The strongest predictor of the risk of syncope or sudden death in patients with congenital prolonged QT syndrome is a QTc exceeding 500 ms. A preoperative ECG to rule out long QT syndrome (LQTS) is useful in a patient with a history of unexplained syncope, a family history of sudden death, and prior to initiating treatment with a drug that has potential to prolong the QT interval.
Common drugs that might be encountered in the perioperative period that are associated with QT prolongation include propofol; chloral hydrate; β 2 agonists (albuterol); methadone; antiarrhythmic drugs; antiemetics such as ondansetron and granisetron; many antipsychotics such as chlorpromazine, serotonin reuptake inhibitors, trazodone, fluroquinolone, and macrolide antibiotics; HIV antiretrovirals; cocaine; herbs such as licorice extract; and toxic exposure to organophosphate insecticides. Isoflurane and sevoflurane have both been shown to prolong the QTc in otherwise healthy children and adults. However, there is insufficient information to favor one volatile anesthetic over another.
Preoperative treatment of LQTS includes correction of electrolyte abnormalities, particularly magnesium or potassium, and discontinuation of drugs associated with QT prolongation if possible. These patients are often on β blockers for PVC suppression. Cardiac pacing is also a treatment option in LQTS because TdP is often preceded by bradycardia. Pacing is usually employed in combination with β-blocker therapy. Implantable cardioverter-defibrillators (ICDs) with pacing capability have emerged as lifesaving therapy for patients with recurrent symptoms and recalcitrant TdP despite PVC suppression therapy with β blockers. Temporary or permanent pacing at a higher backup rate than usual can prevent the bradycardia that precedes TdP and abort the arrhythmia. In addition, left cervicothoracic sympathetic ganglionectomy may reduce dysrhythmogenic syncope in patients with congenital LQTS who cannot take β blockers or have recurrent syncope despite ICD and β-blocker therapy.
Short QT syndrome (SQTS) is an inherited electrical disease of the heart associated with paroxysmal atrial fibrillation, ventricular tachycardia, ventricular fibrillation, syncope, and sudden cardiac death (SCD). In contrast to long QT syndrome, ion channel defects associated with SQTS lead to abnormal shortening of repolarization, predisposing affected individuals to a risk of atrial and ventricular arrhythmias. The corrected QT interval (QTc) in this syndrome is 0.30 seconds or less. SQTS, first reported in 2000, is a rare inherited disorder that affects the movement of ions through channels within the cell membrane associated with marked shortened QT intervals and an increased risk of SCD in individuals with a structurally normal heart.
Cardiac conduction disturbances
An intact cardiac conduction system normally ensures conduction of each sinus node impulse from the atria to the ventricles. Inherited abnormalities of the conduction system, certain drugs, iatrogenic trauma, and disease processes can disrupt normal conduction and result in heart block. The classification of conduction block is by the site of disruption and the degree of blockade.
Acute and chronic ischemia account for about 40% of cases of AV block. New heart block in the setting of acute MI occurs on the order of 10% to 20%. The most common conduction disturbances associated with ischemia and acute MI are left bundle branch block (LBBB) and right bundle branch block (RBBB) with left anterior fascicular block (LAFB). In this situation, restoration of blood flow can improve or correct the conduction block. Chronic AV blockade present prior to an ischemic episode is not usually reversible with reperfusion.
Cardiomyopathies, including hypertrophic obstructive cardiomyopathy and infiltrative processes such as amyloidosis, sarcoidosis, and cardiac tumors, can contribute to the development of heart block. Inflammation of the heart tissue from infections or autoimmune diseases, such as rheumatic fever, Lyme disease, thyroid disorders, neuromuscular degenerative diseases, diphtheria, viruses, systemic lupus erythematosus, dermatomyositis toxoplasmosis, bacterial endocarditis, and syphilis can contribute to myocarditis associated with heart block. Congenital heart defects with associated structural abnormalities such as atrial septal defect (ASD) and ventricular septal defect (VSD) can also cause heart block. Physiologic states associated with hyperkalemia such as end-stage renal disease with potassium greater than 6.0 mEq/L can also precipitate AV block.
Any procedure with the potential to cause edema, impingement, or interruption of the tissues that surround the conduction system can precipitate periprocedural episodes of AV block. Surgeries such as aortic or mitral valve replacement, transcatheter procedures, and catheter ablations have AV block as a known risk. Transcatheter aortic valve implantation (TAVI) risk of AV block is 2% to 8%; transcatheter closure of patent foramen ovale (PFO), ASD and VSD, and catheter ablations for arrhythmia (supraventricular tachycardia, atrial fibrillation, or aberrant pathways as with Wolff-Parkinson-White syndrome) AV block risk is approximately 1%. Septal ablation for hypertrophic obstructive cardiomyopathy (HOCM), a procedure where alcohol is injected into the septal branch of the left anterior descending artery to cause septal shrinkage and relief of left ventricular outflow obstruction, has a high incidence of AV block at 8% to 10%. In all these situations, the block may be a transient or permanent conduction abnormality requiring temporary pacemaker support or a permanent pacemaker implantation.
Quite a few medications can cause AV block particularly in patients with underlying conduction system disease. The list of drugs includes β blockers, calcium channel blockers (especially verapamil and diltiazem), digoxin, amiodarone, procainamide, and quinidine, to name a few. In most cases, the resulting AV block is at least partially reversible following withdrawal of the offending medication(s).
First-degree atrioventricular heart block
A delay in passage of the cardiac impulse through the AV node resulting in a PR interval of greater than 200 ms is called first-degree AV block. A normal PR interval is 120 to 200 ms. Higher heart rates tend to slightly shorten the PR interval. This condition only impacts the PR interval, so the corresponding QRS complex is of normal duration.
The PR interval measures the speed of conduction between the atria and the ventricles. It is the time it takes for atrial depolarization, conduction through the AV node, His bundle, bundle branches, and terminal Purkinje fibers. The conduction delay resulting in a first-degree heart block is most frequently in the AV node but may also be in the His-Purkinje system. In first-degree heart block, every P wave has a corresponding QRS; all other types of heart block present with some dyssynchrony or absence of QRS following a P wave.
Patients with first-degree heart block are usually asymptomatic and seldom need treatment for this condition. First-degree AV block can be found in patients with and without structural heart disease. This type of conduction disturbance occurs in males twice as often as in females. Most commonly it is seen in highly conditioned athletes or in patients taking medications that slow conduction through the AV node such as digoxin, β blockers, and calcium channel blockers. It can be associated with pathologic states such as ischemia, infiltrative diseases, muscular dystrophies, myocarditis, Lev disease, and Lenègre disease. Lev disease is a calcification of the aortic and mitral rings adjacent to the conduction system in patients over 70 years of age. Lenègre disease a progressive, fibrosis/sclerosis of the conduction system in younger (age <60 years) individuals.
Should first-degree heart block develop during clinical care, identification of drugs or situations that increase vagal tone or decrease AV conduction should be sought. The clinical evaluation for any heart block that develops during an anesthetic should include evaluation and treatment of ischemia and electrolyte abnormalities and ensuring adequate oxygenation and blood pressure. Digoxin levels should be checked before surgery, and serum potassium should be maintained at normal levels. Usually removing the offending vagal stimulation or drug is all that is needed to restore normal conduction in these patients. Atropine, a centrally acting vagolytic medication, can be employed to increase heart rate and speed conduction of cardiac impulses through the AV node if necessary.
Second-degree atrioventricular heart block
Second-degree AV block can be suspected when a P wave is present without a corresponding QRS complex. There are two types of second-degree heart block: Mobitz type I (Wenckebach) and Mobitz type II. Mobitz type I is characterized by a sequence of progressive prolongation of the PR interval until a QRS is dropped. It is thought to occur because each successive depolarization produces a prolongation of the refractory period of the AV node. This process continues until an atrial impulse reaches the AV node during its absolute refractory period and conduction of that impulse is blocked completely. A pause allows the AV node to recover, and then the process resumes. This type of block is often transient, asymptomatic, and rarely progresses to third-degree heart block since secondary pacemakers in the AV node usually take over pacing duties and maintain adequate cardiac output.
Mobitz type I block can be the result of myocardial ischemia or infarction, myocardial fibrosis or calcification, or infiltrative or inflammatory diseases of the myocardium, or it can occur after cardiothoracic surgery. It can also be associated with the use of certain drugs such as calcium channel blockers, β blockers, digoxin, and sympatholytic drugs. Mobitz type I block does not usually require treatment unless the decreased ventricular rate results in signs of hemodynamic compromise. Symptomatic patients may be treated with atropine as needed. If atropine is unsuccessful, pacing may be indicated.
Mobitz type II heart block is characterized by a sudden and complete interruption of conduction with loss of the QRS following the P wave. Patients are usually symptomatic, with palpitations and near-syncope being common complaints. Mobitz type II block is considered more serious and the conduction interruption is usually at a point below the AV node in the bundle of His or in a bundle branch. This type of second-degree heart block is much more likely to be associated with permanent damage to the conduction system and is more likely to progress to third-degree heart block.
Treatment of a Mobitz type I or II second-degree heart block that develops during an anesthetic depends on the ventricular response and the patient’s symptoms. In the presence of an acceptable ventricular rate and an adequate cardiac output, no acute treatment is needed. All safety parameters should be checked and maximized ensuring adequate oxygenation, hemodynamic parameters, and blood chemistries. Plans should be for pacemaker support if the block should progress or the patient becomes unstable. Temporizing treatment for Mobitz type II block includes transcutaneous or transvenous cardiac pacing until a permanent pacemaker is in place. Atropine is unlikely to improve bradycardia in this situation, but an isoproterenol infusion acting as a so-called chemical pacemaker may be helpful as a temporizing measure prior to pacemaker placement.
Third-degree atrioventricular heart block
Third-degree AV heart block, also known as complete heart block, is complete interruption of AV conduction and is characterized by AV dissociation. There is no conduction of cardiac impulses from the atria to the ventricles. Third-degree heart block can manifest as a slow escape rhythm insufficient to sustain an acceptable cardiac output. Continued activity of the ventricles is due to impulses from an ectopic pacemaker distal to the site of the conduction block. If the conduction block is near the AV node, the heart rate is usually 45 to 55 bpm and the QRS complex is narrow. When the conduction block is below the AV node (infranodal), the heart rate is usually 30 to 40 bpm and the QRS complex is wide.
Third-degree heart block is usually symptomatic with the bradycardia induced reduction in cardiac output contributing to congestive heart failure (CHF) with symptoms such as weakness and dyspnea. Onset of third-degree AV block in an awake patient may be signaled by near syncope or syncope. Syncope attributed to third-degree heart block is called an Adams-Stokes attack. The most common cause of third-degree AV block in adults is fibrotic degeneration of the distal conduction system associated with aging (Lenègre disease).
In anesthetized patients, third-degree heart block can be due to cardiac ischemia, metabolic or electrolyte abnormalities, infection or inflammation near the conduction system, reperfusion injury, or stunned myocardium after cardiac surgery. Treatment of third-degree AV block occurring during anesthesia consists of transcutaneous or transvenous cardiac pacing. An intravenous (IV) isoproterenol infusion may also be helpful in maintaining an acceptable heart rate by acting as a chemical pacemaker. Caution must be exercised when administering antidysrhythmic drugs to patients with third-degree AV block before permanent pacemaker placement. Such drugs may suppress the only remaining functioning ectopic pacemaker responsible for maintaining the heart rate. Preoperative placement of a transvenous pacemaker or the availability of transcutaneous cardiac pacing is necessary before an anesthetic is administered for insertion of a permanent cardiac pacemaker.
In patients with isolated chronic RBBB, the progression to complete AV block is rare. Patients with bifascicular block (RBBB and left anterior or posterior fascicular block) or complete LBBB have a 6% incidence of progression to complete heart block. Approximately 8% of patients with acute inferior wall MI develop complete heart block. It is usually transient, although it may last for several days. Development of new bifascicular block plus first-degree AV block is associated with a very high risk (40%) of progression to complete heart block. ECG evidence of alternating bundle branch blocks, even if asymptomatic, is a sign of advanced conduction system disease and is an indication for permanent pacing.
Intraventricular conduction disturbances
Intraventricular conduction disturbances are abnormalities in conduction occurring past the AV node involving the His-Purkinje system of the myocardium. Two major branches emerge from the singular bundle of His, the left and the right bundle branches. The LBB divides into two fascicles: the left anterior superior fascicle and the left posterior inferior fascicle. The RBB is a relatively thin bundle of fibers that courses down the right ventricle and then branches late in its course near the right ventricular apex. The right and left bundle branches terminate in an interlacing network of small fibers (i.e., His-Purkinje system).
Normal, rapid conduction of the depolarization signal results in near simultaneous contraction of the left and right ventricles, which optimizes the myocardial pump function. Intraventricular conduction disturbances can be due to structural changes or disease processes, acquired or inherited, affecting the ventricular myocardium. The wide range of causes includes necrosis, fibrosis, calcification, infiltrative lesions, or impaired vascular supply. This subset of disorders includes incomplete and complete RBBB, LAFB, left posterior fascicular block (LPFB), and complete LBBB. These abnormalities change the shape and/or duration of the QRS complex. They may be fixed and present at all heart rates, or they may be intermittent and occur only with tachycardia or bradycardia.
Right bundle branch block
The left and right ventricles should depolarize virtually simultaneously. When the RBB is interrupted (complete RBBB), electrical stimuli from the AV node conducts to the bundle of His and down the LBB. In the absence of conduction down the right bundle, the left ventricle depolarizes first while the right ventricle polarized later, causing the characteristic ECG findings. RBBB is recognized by a widened QRS complex (≥120 ms in adults) and a rSR′ configuration in leads V 1 and V 2 . There is also a deep S wave (>40 ms) in leads I and V 6 . Some patients exhibit an incomplete RBBB where the QRS is prolonged between 110 and 120 ms, and the other criteria for RBBB is fulfilled. Interpretation of ST segments for diagnosis of ischemia and MI in the presence of RBBB is not altered. By contrast, the presence of a LBBB renders the ST segments of the ECG difficult to interpret and unreliable for diagnosis of ischemia and MI.
The RBB receives most of its blood supply from septal branches of the left anterior descending coronary artery. In most patients, it also receives some collateral supply from either the right or circumflex coronary systems depending on the dominance of the coronary system. Most of the population has a right dominant (coronary) system. Because of its superficial position as it courses down the interventricular septum and its less robust size, the right bundle is vulnerable to stretch as might occur with increased right heart pressures seen in acute situations such as pulmonary embolism, pulmonary edema, and chronic conditions such as pulmonary hypertension, chronic obstructive pulmonary disease (COPD)/emphysema/pulmonary fibrosis, and left-sided conditions transmitting pressure back to the right side such as mitral insufficiency and diastolic or systolic heart failure.
The incidence of RBBB typically increases with age, with up to 11.3% of people by age 80. It has an occurrence of between 1% and 2% in patients with no known structural or ischemic heart disease. In the absence of structural or functional heart disease, it is of no clinical significance in the perioperative period. With aging, the occurrence of RBBB is a representation of an idiopathic slowly progressive degenerative disease of the conduction system (Lev or Lenègre disease) in the absence of other causative factors. Isolated RBBB has no significant association with cardiac disease, ischemic heart disease, or cardiac risk factors.
A patient with RBBB is usually asymptomatic, and it is frequently discovered incidentally on ECG. On cardiac auscultation, the patient may have a split-second heart sound. In terms of prognosis, the conduction delay from RBBB rarely progresses to advanced AV block. Generally, the isolated presence of a RBBB does not require further evaluation or treatment. In patients without significant heart disease, RBBB has no additional risk. In patients with cardiovascular disease, including ischemia, infarction, inflammation (myocarditis), cardiomyopathies, or congenital heart disease, RBBB is an independent risk factor for all-cause mortality. In the setting of heart failure with a low ventricular ejection fraction in combination with RBBB, cardiac resynchronization therapy (CRT) is indicated.
RBBB is more common than LBBB. RBBB can exist in combination with block of either fascicle of the left bundle. Block of one of the two fascicles of the left bundle is called hemiblock. Although hemiblock is a form of intraventricular heart block, the duration of the QRS complex is normal or only minimally prolonged. RBBB in association with block of the left anterior fascicle, called left anterior hemiblock, is seen in 1% of all adults. RBBB with block of the left posterior fascicle, left posterior fascicular block, is called left posterior hemiblock and occurs much less frequently and is associated with a 1% to 2% risk of progression to third-degree heart block. The term bifascicular block is used when RBBB exists with either LAFB or LPFB.
Perioperative assessment and treatment of RBBB or RBBB with left anterior hemiblock consists of observation and awareness of drugs or clinical factors that may contribute to conduction disturbances. If contributing factors can safely be eliminated, this should be done. As with all anesthetics, maintenance of adequate blood pressure, arterial oxygenation, and normal serum electrolyte concentrations should be a priority to minimize potential compromise to the remaining fascicle due to ischemia, arrhythmia, or ventricular dysfunction. Regardless of the anesthetic technique chosen, there is no evidence to prefer one technique over the other if the abovementioned concerns are met. Surgery performed with either general or regional anesthesia does not predispose patients with preexisting bifascicular heart block to develop third-degree heart block. Preparation for care of patients with bifascicular block should include availability of pacing capability with staff trained in this technique if possible. Pacing in this situation can be instituted by transcutaneous or transvenous pacing should it be needed. Prophylactic placement of a temporary or permanent cardiac pacemaker is not necessary.
Brugada syndrome, an autosomal dominant genetic disorder with variable expression, has an ECG resembling RBBB. The majority of affected individuals are middle-aged males of Asian descent, with the highest prevalence in Southeast Asia. There is also increased incidence of Brugada syndrome in patients with schizophrenia. The ECG in these patients includes a pseudo-RBBB and persistent ST-segment elevation in leads V 1 to V 2 . These patients have an increased risk of ventricular tachyarrhythmias and SCD.
Left bundle branch block
The left bundle component of the bundle of His is composed of two components: the left anterior fascicle and the left posterior fascicle. A complete LBBB is recognized as a QRS complex of longer than 120 ms in duration in the absence of Q waves in leads I, V 5 , and V 6 , and a broad notched or slurred R wave in leads I, aVL, V 5 , and V 6 . The S and T waves are usually opposite in direction to the QRS. The appearance of LBBB on ECG is often an indication of serious heart disease (e.g., hypertension, coronary artery disease, aortic valve disease, cardiomyopathy). Isolated LBBB is often asymptomatic, and some patients do not exhibit LBBB until a critical heart rate is achieved.
The left and right bundles both receive blood supply from branches of the left anterior descending coronary artery (LAD). The LBB is more richly perfused than the RBB. Ischemia or infarction involving the LAD can affect the left or right bundle. The left posterior fascicle is usually spared because it receives additional blood supply from the posterior descending coronary artery, a branch of the right coronary artery. This is due to the redundant blood supply to the LBB and the fact that it branches early and widely into anterior and posterior fascicles during its course down the left ventricular septum.
This redundant blood supply to the LBB explains why complete disruption of the LBB, as indicated by LBBB on ECG, usually indicates more extensive cardiac disease or damage than RBBB.
As mentioned earlier, if one of the two fascicles of the LBB fails to conduct for whatever reason, this is called a hemiblock (HB). Block of the left anterior fascicle (LAHB) is the most common hemiblock. Left posterior hemiblock (LPHB) is uncommon because the posterior fascicle of the LBB is larger and better perfused than the anterior fascicle.
Development of LBBB during anesthesia should be taken seriously and may be a sign of myocardial ischemia. Taking care to treat hypertensive or tachycardic episodes, maximize oxygenation, and treat electrolyte abnormalities should be instituted immediately. ST-segment and T-wave changes (repolarization abnormalities) in the presence of LBBB cannot be relied on to diagnose ischemia as they are already abnormal due to the bundle branch block pattern. Additionally, a narrow complex tachycardia such as SVT may look like ventricular tachycardia (wide complex tachycardia) in a patient with LBBB because the QRS is widened from the LBBB. Another common perioperative scenario that can be mistaken for LBBB is ventricular pacing and biventricular pacing. Ventricular pacing electrodes pace from the right ventricle and result in a QRS that is typically widened. The presence of pacing spikes on ECG can help differentiate a V-paced patient from an ECG widened due to LBBB.
If a patient has a complete LBBB, special care needs to be taken when undergoing a right heart catheterization or other procedures that introduce a wire or catheter into the right ventricle such as placement of a pulmonary artery catheter or even a central line where the guidewire may pass into the right ventricle. The superficial course of the right bundle makes it vulnerable to disruption by trauma or inflammation. In these situations there is an increased risk of complete (third-degree) heart block due to the increased risk of catheter-induced RBBB in the setting of complete LBBB. RBBB (usually transient) occurs in approximately 2% to 5% of patients undergoing insertion of a pulmonary artery catheter.
Cardiac resynchronization therapy
Any delays in conduction, particularly of the lateral wall of the left ventricle (as in LBBB), cause dyssynchrony between the ventricles and impaired efficiency. This can lead to heart failure secondary to decreased left ventricular function and elevated left heart pressures. CRT with biventricular pacing has been used in patients with chronic heart failure with reduced ejection fraction and bundle branch block to improve ventricular function, symptoms, and survival. CRT is now a mainstay of treatment in patients who have left ventricular dysfunction (ejection fraction ≤35%), QRS prolongation (≥120 ms), and moderate to severe heart failure symptoms (New York Heart Association [NYHA] functional class III or IV) while receiving optimal medical therapy. CRT with or without a defibrillator component has been shown to reduce hospitalizations and all-cause mortality in these patients. Since being approved by the US Food and Drug Administration (FDA) in 1985, there are more than 3 million Americans living with a pacemaker and over 300,000 living with an ICD with pacing capacity. There is continual work to improve cardiac implantable electronic device (CIED) technology with the most current developments in leadless pacemakers and subcutaneous ICDs.
Some CIEDs are only pacers and others pace and defibrillate. The three standard components of a CRT pacer/defibrillator are a right atrial lead and right and left ventricular leads. Pacing of the left ventricle is most frequently achieved by transvenous placement of an electrode into the coronary sinus. CRT is usually an adjunct to medical optimization. The evidence of benefit is greatest in patients with LBBB and a QRS duration greater than 150 ms. The three leads are tuned to simulate a normal functioning His-Purkinje complex. By adjusting the timing of each lead, AV synchrony is optimized. The goal is to restore normal coordination of contraction of the right and left sides of the heart. For defibrillation capability, a specialized right ventricular lead with a built-in shocking coil is implanted with a larger pulse generator to power this functionality. In addition to internal defibrillation, an ICD can deliver antitachycardia or antibradycardia pacing and synchronized cardioversion. Detailed diagnostic data concerning intracardiac electrograms and dysrhythmia event markers are stored in the memory of the device and are downloaded for analysis during device checks.
There is a standard defibrillator coding system to delineate its functionality. The first letter is the chamber shocked ( O, none; A, atrium; V, ventricle; D, dual). The second letter indicates the antitachycardia pacing chamber ( O, none; A, atrium; V, ventricle; D, dual). The third position indicates the tachycardia detection mechanism ( E, electrogram; H, hemodynamic). The fourth position denotes the antibradycardia pacing chamber ( O, none; A, atrium; V, ventricle; D, dual).
The pulse generator is usually implanted in the left pectoral region to maximize the defibrillation vector. Right-sided implantation is avoided if possible because it significantly increases the defibrillation threshold, which can result in premature battery depletion. If the device detects ventricular fibrillation, the capacitor charges, then a secondary algorithm confirms the rhythm prior to shock delivery. During the confirmatory process, which lasts approximately 10 to 15 seconds, the patient may experience presyncope or syncope prior to defibrillation. This process prevents inappropriate shocks in response to self-terminating events or spurious signals. There are also diagnostic recording devices called loop recorders or insertable cardiac monitors that monitor and record rhythm but deliver no therapy. They function as a leadless Holter monitor to record rhythm data to aid in evaluation of patients suspected to have conduction system disease or paroxysmal arrythmia.
Anesthesia for insertion of ICDs
Preparation of a patient for ICD placement is the same as that for pacemaker insertion. Some of these procedures are done under general anesthesia because of the increased risks associated with repeated defibrillation during threshold testing. The nature and severity of the patient’s coexisting medical conditions dictate the extent of monitoring and the necessary clinical preparations.
Surgery in patients with cardiac implantable electronic devices
The presence of any type of CIED—whether an artificial cardiac pacemaker or ICD for any indication; whether pacing, cardioversion, defibrillation, or resynchronization—in a patient scheduled for surgery unrelated to the device introduces special considerations for preoperative evaluation and subsequent management of anesthesia to ensure patient safety and preservation of proper device function. These CIED recommendations apply to all forms of anesthetic care, from conscious sedation and monitored anesthesia care to regional and general anesthesia; there are no clear data regarding the effect of anesthetic technique on CIED function.
Preoperative evaluation
A patient with a preexisting CIED coming for surgery has at least one of three underlying cardiac problems: sustained or intermittent bradydysrhythmia, tachydysrhythmia, and/or heart failure. Bradydysrhythmias require pacing and may involve a single or dual lead depending on the function of the AV node. Tachydysrhythmias and heart failure usually require pacing and cardioversion/defibrillation capability using a pacemaker/defibrillator. Pacing the ventricle at a rate slightly faster than the tachycardia or overdrive pacing (short bursts of rapid pacing) can terminate ventricular tachycardia. Regardless of the indication for the device, any patient with a CIED requiring anesthetic care must undergo a detailed systematic preoperative evaluation. This preoperative evaluation should include identification of the brand and type of device, the clinical indication for the device, degree of dependence on the device, and assessment of device function. A patient who is compliant with regular device follow-up will have these parameters followed regularly as part of routine device checks that are performed at least once a year. In the absence of this documentation, clinical signs indicating that a patient is CIED dependent include a history of bradycardia symptoms, a history of AV node ablation, and an ECG showing a majority of paced beats.
All implanted cardiac devices are designed to detect and respond to low-amplitude electrical signals. Extraneous signals produced by external electric or magnetic fields can influence the function of CIEDs. These signals are known as electromagnetic interference (EMI). EMI can be any strong external electrical or magnetic force in close proximity to a CIED. EMI signals enter device circuits primarily through the leads. Other factors influencing the susceptibility of a device to EMI include field strength, patient body mass, and the proximity and orientation of the implanted electronic device to the EMI field. Perioperative EMI may cause damage to the pulse generator or leads (circuitry), damage to the tissue around the device (burns, thermal changes affecting impedance), failure of the device to pace or defibrillate, and inappropriate pacing or defibrillation. The current return pad (grounding pad) of the electrocautery system should be placed so that the current path does not cross the chest or CIED system. The grounding electrode should be as far as possible from the pulse generator to minimize detection of the cautery current by the pulse generator.
The most common CIED-related problem encountered in the perioperative period is interference with device function resulting from EMI. Use of monopolar electrocautery and the EMI it generates remains the principal intraoperative concern in patients with CIEDs. The cautery device generating the EMI field need not actually touch the patient to adversely affect the CIED. Use of coagulation settings in monopolar electrocautery uses a higher voltage and causes more EMI problems than use of nonblended cutting settings. The cautery tool and return pad should be positioned so the current pathway does not pass near the CIED pulse generator or leads. It is recommended to avoid cautery of tissue near the pulse generator and leads if possible. It is beneficial to keep the electrocautery current as low as possible and to apply electrocautery in short bursts, especially if current is being applied close to the pulse generator. Use of bipolar electrocautery or the ultrasonic harmonic scalpel is associated with lower rates of EMI on the pulse generator and leads. Even with the utmost caution, problems can arise.
Monitoring of the patient with a CIED should always follow the American Society of Anesthesiologists (ASA) standards and should include continuous ECG monitoring and continuous monitoring of a peripheral pulse. This can be done with a pulse oximeter, manual palpation of a pulse, auscultation of heart sounds, or intraarterial catheterization. Verification of the presence of a pulse is necessary to confirm continued cardiac activity in the event of disruption of the ECG signal by EMI. Skeletal muscle contractions and fasciculation from succinylcholine could inhibit a normally functioning cardiac pacemaker by misinterpretation of the myopotentials for intrinsic R waves. Clinical experience suggests that succinylcholine is usually a safe drug for use in patients with cardiac pacemakers and that if myopotential inhibition does occur, it is generally transient.
Preoperative interrogation of loop recorder devices should be done as long as it does not delay urgent or emergent care. The presence of the loop recorder poses no threat to the patient as it does not deliver any therapy to the heart, but all data may be lost if it is exposed to EMI.
No special laboratory testing or radiographs are needed for CIED patients undergoing surgery unless otherwise clinically indicated. At times, a chest radiograph can be useful to evaluate the location and external condition of pacemaker electrodes. Most current CIEDs have an x-ray code that can be used to identify the manufacturer of the device. If the patient is known to have a biventricular pacemaker, a chest radiograph to confirm the position of the coronary sinus lead is helpful when insertion of a central line or pulmonary artery catheter is planned. There have been reports of coronary sinus and endocardial lead dislodgement in association with central venous catheterization; however, the danger of dislodgement is minimal after the first month postinsertion.
There are no known CIED concerns involving exposure to plain x-rays, ultrasonography, fluoroscopy, mammography, or electroconvulsive therapy (ECT). However, there are reports of EMI associated with electrocautery, radiofrequency ablation, magnetic resonance imaging (MRI), radiation therapy, and lithotripsy. MRI scanning of patients with CIEDs is controversial and is generally regarded as contraindicated. However, 50% to 75% of patients with cardiac devices will likely need to undergo MRI at some point in their lifetime, so this is becoming an important concern. There is insufficient evidence at present to standardize management of the patient with a CIED needing MRI scanning. If MRI must be performed, care should be coordinated among the ordering physician, radiologist, and pacemaker specialist or cardiologist.
Management of EMI associated with radiofrequency ablation includes keeping the radiofrequency current path, which runs from the electrode tip to the current return pad, as far away from the pulse generator as possible. Some suggest keeping the ablation electrode at least 5 cm away from the pacer leads. Recommendations for patients undergoing lithotripsy include keeping the focus of the lithotripsy beam away from the pulse generator. If the lithotripsy triggers on the R wave, it may be necessary to disable atrial pacing before the procedure. There is insufficient evidence to standardize care for CIED patients needing radiation therapy. It is preferable to keep the device out of the radiation field. Most manufacturers recommend verification of appropriate pulse generator function at the completion of radiation therapy. No clinical studies have reported EMI or permanent CIED malfunction in association with electroconvulsive therapy, but care should be coordinated with a cardiologist. The device should be interrogated and the antitachycardia functions suspended. ECT can be associated with considerable swings in blood pressure, heart rate, and vigorous skeletal muscle contraction from the seizure activity, so backup external defibrillator and temporary pacing capability is recommended. In pacemaker-dependent patients, programming to asynchronous mode is recommended, so there is no pacing inhibition due to the myopotentials produced by the seizure.
Temporary pacing and defibrillation equipment should be immediately available before, during, and after procedures in CIED patients. It has been suggested that before performing defibrillation or cardioversion in a patient with an ICD in a magnet-disabled treatment mode, all sources of EMI be eliminated and the magnet be removed to reactivate the antitachycardia capabilities of the device. The patient can then be observed for appropriate CIED function. If emergency defibrillation is necessary in a patient with a CIED (permanent cardiac pacemaker or ICD that is turned off), an effort should be made to keep the defibrillation current away from the pulse generator and lead system. The recommended position of the electrode pads is the anterior-posterior position. An acute increase in pacing threshold and loss of capture by the CIED may follow external defibrillation. If this occurs, transcutaneous cardiac pacing or temporary transvenous pacing may be required.
Cardiac rate and rhythm should be monitored throughout the immediate postoperative period, including during transport from the anesthetizing location to the recovery area. Backup cardioversion-defibrillation and pacing equipment should be immediately available. Postoperative management of the patient with a CIED consists of interrogating the device and restoring appropriate baseline settings, including antitachycardia therapy in patients with defibrillators. This should be done as soon as possible after the procedure, either in the postanesthesia care unit or ICU.
Postoperative CIED checks may not be needed if surgery did not include use of EMI-generating devices, no electronic preoperative device reprogramming was done, no blood transfusions were administered, and no intraoperative problems were identified that related to CIED function. Remote device checks have facilitated preprocedural and postprocedural interrogation of CIEDs, particularly in clinical situations where there is no immediate availability of a qualified device interrogator.
Cardiac dysrhythmia overview
Cardiac rhythms that have abnormalities in rate, interval length, or conduction path are referred to as dysrhythmias. Intraoperative arrythmias occur in approximately 11% of general anesthetics. Patients with cardiac disease are more likely to have serious dysrhythmias. The most common intraoperative arrhythmias are sinus tachycardia and sinus bradycardia. There are three basic causes of dysrhythmia in the anesthetized patient: patient physiology and existing abnormalities, stimulation or iatrogenic factors from the procedure, and effects of the anesthetic itself. Most of these arrythmias are insignificant and transient. Some arrhythmias may only require observation and others immediate intervention. During a surgical procedure, it is the anesthesiologist’s responsibility to make our surgical colleagues aware of the untoward effects their action may be having on the anesthetized patient, such as vagal stimulation causing bradycardia and hypotension during intraperitoneal insufflation or gut traction. Expert knowledge of the interaction of patient physiologic states, drug therapy, and the effect of surgical procedures is why anesthesiologists are known as patient safety advocates.
Sinus dysrhythmia is a normal variant encountered in patients who exhibit normal sinus rhythm with a normal sinus rate (>60 bpm and <100 bpm), normal PR interval, normal QRS length, and normal ST intervals but an irregular RR interval length. This variation in the RR interval is usually due to a physiologic phenomenon known as the Bainbridge reflex, which accelerates the heart rate when intrathoracic pressure is increased during inspiration and slows the heart rate when the intrathoracic pressure decreases during expiration. Sinus dysrhythmia carries no increased risk of deterioration into a dangerous rhythm. It is seen frequently in children and young people and tends to decrease with age.
Mechanisms of tachydysrhythmias
A cardiac rhythm greater than 100 bpm is considered a tachydysrhythmia. A tachydysrhythmia can be initiated from a pacemaker source above or below the bundle of His. Tachydysrhythmias originating in tissue above the bundle of His are SVTs, which usually have a narrow QRS complex. Narrow complex tachycardias include sinus tachycardia, atrial flutter, atrial fibrillation, junctional tachycardia, paroxysmal atrial tachycardia, and accessory pathway–mediated reentrant tachycardias.
Tachydysrhythmias generated from below the AV node have a wide QRS complex. Wide complex tachycardias include ventricular tachycardia, SVT with an intraventricular conduction defect or bundle branch block, SVT with aberrant conduction, SVT with wide QRS due to a metabolic or electrolyte disorder, and SVT with conduction over a preexcitation (accessory) pathway.
In addition to the location of origin of the arrhythmia, we must consider the mechanism by which the impulse is accelerated beyond the usual pacemaker control of the sinus node. Tachydysrhythmias can result from three mechanisms: (1) increased automaticity in normal conduction tissue or in an ectopic focus, (2) reentry of electrical potentials through abnormal pathways, and (3) triggering of abnormal cardiac potentials due to afterdepolarizations.
Increased automaticity
A sustained rhythm resulting from accelerated firing of a pacemaker other than the SA node is called an ectopic rhythm. Dysrhythmias resulting from an ectopic focus often have a gradual onset and termination. Automaticity is not confined to secondary pacemakers within the conduction system; virtually any myocardial cell can exhibit automaticity under certain circumstances and is therefore capable of initiating cardiac depolarization. The fastest pacemaker in the heart is normally the SA node. The SA node spontaneously discharges at a rate of 60 to 100 bpm. The sinus node can be accelerated or overridden by ectopic pacemakers due to increased endogenous catecholamines, disease states, or iatrogenic drug effects.
The automaticity of cardiac tissue changes when the slope of phase 4 depolarization shifts or the resting membrane potential changes. Sympathetic stimulation causes an increase in heart rate by increasing the slope of phase 4 of the action potential and by decreasing the resting membrane potential. Conversely, parasympathetic stimulation results in a decrease in the slope of phase 4 depolarization and an increase in resting membrane potential to slow the heart rate (see Fig. 8.2 ).
Reentry pathways
Reentry pathways account for most premature beats and tachydysrhythmias. Pharmacologic or physiologic events may alter the balance between conduction velocities and refractory periods of the dual pathways, resulting in the initiation or termination of reentrant dysrhythmias. Reentrant dysrhythmias tend to be paroxysmal with abrupt onset and termination.
Reentry or triggered dysrhythmias require two pathways over which cardiac impulses can be conducted at different velocities ( Fig. 8.4 ) In a reentry circuit there is anterograde (forward) conduction over the slower normal conduction pathway and retrograde (backward) conduction over a faster accessory pathway.
Triggering by afterdepolarizations
Afterdepolarizations are oscillations in membrane potential that occur during or after repolarization. Normally these membrane oscillations dissipate; however, under certain circumstances they can trigger a complete depolarization. Once triggered, the process may become self-sustaining and result in a dysrhythmia. Triggered dysrhythmias associated with early afterdepolarizations are enhanced by a slow heart rate and are treated by accelerating the heart rate with positive chronotropic drugs or pacing. Conversely, triggered dysrhythmias associated with delayed afterdepolarizations are enhanced by fast heart rates and can be suppressed with drugs that lower the heart rate.
Supraventricular dysrhythmias
Sinus tachycardia
Normal sinus rhythm in a patient at rest is under the control of the sinus node, which fires at a rate of 60 to 100 bpm. When sinus rhythm exceeds 100 bpm, it is considered sinus tachycardia. The ECG shows a normal P wave before every QRS complex. The PR interval is normal unless a coexisting conduction block exists. Sinus tachycardia is caused by acceleration of SA node discharge due to either sympathetic stimulation or parasympathetic suppression. Typically, it is a nonparoxysmal increase in heart rate that speeds up and slows down gradually. It is the most common supraventricular dysrhythmia seen during anesthesia in the operating room. Reasons for sinus tachycardia range from simple to complex. Sinus tachycardia without hemodynamic instability is not life threatening. Sinus tachycardia is usually well tolerated in young healthy patients. It can occur in an awake patient as part of the normal physiologic response to stimuli (e.g., fear, pain, anxiety) or as a pharmacologic response to medications such as atropine, ephedrine, or other vasopressors. Intake of stimulant substances such as caffeine or cocaine may also cause sinus tachycardia. Other potential intraoperative causes include sympathetic stimulation, pain, vagolytic drug administration, hypovolemia, light anesthesia, hypoxia, hypercarbia, heart failure, cardiac ischemia, fever, and infection. The likelihood of sinus tachycardia is reduced by avoidance of sympathomimetic agents/vagolytic drugs, ensuring adequate anesthetic depth, maintenance of euvolemia, correction of hypercarbia, avoidance of hypoxemia, antibiotic treatment of suspected infection, use of the lowest effective dose of inotropic support for heart failure (many inotropes increase heart rate), and prompt treatment of myocardial ischemia ( Table 8.1 ).
TABLE 8.1
Perioperative Causes of Sinus Tachycardia
| Physiologic Increase in Sympathetic Tone |
| Pain |
| Anxiety or fear |
| Light anesthesia |
| Hypovolemia or anemia |
| Arterial hypoxemia |
| Hypotension |
| Hypoglycemia |
| Fever or infection |
| Pathologic Increase in Sympathetic Tone |
| Myocardial ischemia or infarction |
| Congestive heart failure |
| Pulmonary embolus |
| Hyperthyroidism |
| Pericarditis |
| Pericardial tamponade |
| Malignant hyperthermia |
| Ethanol withdrawal |
| Drug-Induced Increase in Heart Rate |
| Atropine or glycopyrrolate |
| Sympathomimetic drugs |
| Caffeine |
| Nicotine |
| Cocaine or amphetamines |
In patients with ischemic heart disease, diastolic dysfunction, or CHF, the heart rate increase above normal sinus rhythm can lead to significant clinical deterioration because of increased oxygen demand, increased wall stress, and a decrease in coronary perfusion. Treatment may include IV administration of a β blocker to lower the heart rate and decrease myocardial oxygen demand. However, β blockers must be used with caution in patients susceptible to bronchospasm and in patients with impaired cardiac function. Patients with a low ejection fraction may be dependent on elevated heart rate to maintain adequate cardiac output. A decrease in heart rate in the setting of a fixed reduced stroke volume may cause an abrupt and dangerous decrease in blood pressure.
Premature atrial beats
Premature atrial contractions (PACs) are early (premature) ectopic beats. They appear as a P wave with a QRS complex earlier than expected given the preceding two sinus beats. The P wave of the PAC originates from an ectopic focus in the atria. The PR interval is variable. Most often, the corresponding QRS complex is narrow because activation of the ventricles following the ectopic P wave occurs through the normal conduction pathway. PACs with aberrant conduction of atrial impulses can occur, resulting in a widened QRS complex that may resemble a PVC. There is typically a slight pause after a PAC before the next sinus beat.
Symptoms of PACs in an awake patient are much like symptoms of PVCs and include an awareness of a fluttering in the chest or a heavy or prominent heartbeat. PACs are common in patients of all ages, with or without heart disease. They often occur at rest and become less frequent with exercise. Emotional stress, alcohol, stimulant substances such as caffeine, nicotine, and cocaine can increase the prevalence of PACs. Patients with chronic lung disease, ischemic heart disease, and hyperthyroidism and digitalis toxicity often experience PACs.
PACs are usually hemodynamically insignificant and do not require therapy unless they are associated with initiation of a tachydysrhythmia. If they are implicated in the generation of a tachydysrhythmia, PACs can be suppressed with calcium channel blockers or β blockers.
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