The Intensive Care Manual - part 6 pot

8 / Cardiac Arrhythmias 195 FIGURE 8–4 Twelve-lead ECG from a patient with atrial fibrillation and a controlled ven- tricular response. Note the chaotic baseline without defined atrial activity. There is a sugges- tion of a more organized pattern in the V 1 lead, but this is not seen in other leads. The ventricular response is characteristically “irregularly irregular.” ch08.qxd 11/7/01 4:14 PM Page 195 Atrial flutter has also been extensively studied electrophysiologically. Unlike the disorderly atrial activities in fibrillation, it is now well-accepted that for most instances of clinically encountered atrial flutter, the electrical impulse circulates around in the right atrium in one large loop. Because atrial flutter is more orga- nized than atrial fibrillation, it displays more organized atrial activities of larger amplitude on ECG. Atrial flutter usually has an associated “sawtooth” pattern, which represents revolving atrial activities and is best appreciated in the inferior limb leads 2, 3, and aVF (Figure 8–5). In typical atrial flutter, the reentrant circuit usually has a well-defined cycle length at about 300 beats/min. Often, there is a 2:1 AV conduction pattern during atrial flutter, leading to a consistently regular ventricular response of 150 beats/min. Many of the impulses of a SVT can be transmitted down to the ventricle via the AV junction, especially when AV conduction is enhanced by release of cate- cholamines. The rapid ventricular rate is usually the main problem associated with atrial arrhythmias in the ICU. The fast rates are especially troublesome for patients who have underlying CAD or ventricular hypertrophy, because ischemia and significant hemodynamic compromise can occur rapidly. The goal of ther- apy in the care of patients with atrial arrhythmia is stabilization of hemodynam- ics and ventricular rate control. During sustained atrial arrhythmias in a patient with stable blood pressure, AV nodal blocking agents, such as beta blockers, cal- cium channel blockers, and digoxin, are all effective agents in slowing the ven- tricular response. Diltiazem can be given intravenously as a bolus at a dose of 5 to 20 mg, which may be followed by an infusion of the same drug at rates of 5 to 20 mg/hr. This allows for rapid control of heart rate and subsequent conversion to oral long-term therapy. Digoxin is also effective, but the onset of action is some- what longer than that of diltiazem. Digoxin is typically given as a loading dose of 1 mg over the course of 24 hours. We typically give 0.5 mg initially, followed by another 0.25 mg in 4 to 6 hours and a second 0.25 mg in yet another 4 to 6 hours. If there is hemodynamic compromise, then urgent restoration of sinus rhythm with direct-current (DC) energy-synchronized cardioversion is imperative. In addition, if the rapid ventricular response rate during atrial arrhythmia is making conditions such as myocardial ischemia, infarction or congestive heart failure worse, early cardioversion is also indicated. Pharmacologic antiarrhythmic agents are usually used for chemical cardiover- sion and maintenance of sinus rhythm, if the patient’s blood pressure permits their use. Oral antiarrhythmic agents for atrial fibrillation include class 1a drugs, such as quinidine and procainamide; class 1c drugs, such as propafenone and flecainide; and class 3 drugs, such as sotalol and amiodarone. Procainamide has been the first- line intravenous antiarrhythmic that is traditionally used. More recently, intra- venous amiodarone has also been used with success. Intravenous procainamide is typically given as a bolus of 10 to 15 mg/kg of body weight over 20 to 30 minutes, followed by a maintenance infusion at a rate of 1 to 6 mg/min. Care must be taken when administering procainamide intravenously because it may cause significant prolongation of the QT interval and the QRS duration; if given rapidly, it may also 196 The Intensive Care Manual ch08.qxd 11/7/01 4:14 PM Page 196 8 / Cardiac Arrhythmias 197 FIGURE 8–5 Twelve-lead ECG from the same patient in Figure 8–4, now showing a charac- teristic “sawtooth” pattern that is especially apparent in inferior leads. This patient alternates between atrial fibrillation and “typical” atrial flutter. The rate of the flutter waves is some- what slower than is usually seen (230/min) as a result of antiarrhythmic therapy. ch08.qxd 11/7/01 4:14 PM Page 197 cause hypotension. Procainamide should not be given at a rate faster than 50 mg/min. Intravenous amiodarone is usually given in a 150-mg bolus over 10 min- utes and may be repeated if ineffective. Then a maintenance infusion of 1 g of amio- darone every 24 hours may be given. A central venous line is recommended with the use of intravenous amiodarone to avoid phlebitis. Intravenous amiodarone has not yet been officially approved as a therapy for supraventricular arrhythmias. Both of these agents can further lower a patient’s blood pressure; therefore, close monitoring of patients is mandatory when these agents are used. Intravenous ibu- tilide has also been reported to be an effective agent for cardioversion, although its conversion rate for atrial flutter is much higher than for atrial fibrillation. Ibutilide may lead to significant QT prolongation and should be avoided in patients with electrolyte imbalance or who are already on agents that can prolong QT intervals, such as phenothiazines. Caution and continuous ECG monitoring must be exer- cised with the use of ibutilide, because dramatic QT prolongation can lead to tor- sades de pointes, and potentially convert a nonemergent arrhythmia to one that causes immediate hemodynamic collapse. Intracardiac thrombi and systemic em- boli may form in patients with atrial fibrillation or atrial flutter sustained for more than 48 hours. Therefore, if anticoagulant therapy is not contraindicated by con- current medical problems, it should be initiated for these patients. Precipitating factors that may lead to atrial fibrillation and atrial flutter should be sought if clinical conditions warrant such concerns. For example, it is well- documented that pulmonary embolism can lead to atrial arrhythmias, especially atrial fibrillation. This may be important in postoperative patients or patients with hypercoagulable states. Other factors that can lead to atrial fibrillation or atrial flutter include hypertensive heart disease, valvular disease, pericarditis, myocarditis, hyperthyroidism, and even fever. Another supraventricular rhythm disturbance that is seen frequently in the critically ill patient is multifocal atrial tachycardia (MAT), which is a rapid irreg- ular rhythm that is characterized by a rate that exceeds 100 beats/min and has at least three distinct P-wave morphologies. This is most frequently seen in patients with severe underlying lung disease, particularly those receiving inhaled bron- chodilators or theophylline preparations. Treatment is difficult and should be aimed primarily toward improving the pulmonary condition. There are several reports on the use of both intravenous metoprolol and intravenous verapamil to control the rate. Caution must be used when giving beta blockers, such as meto- prolol, to patients with reactive lung disease; our experience with this agent in this situation has not been successful. Reentrant SVTs, including AV nodal reentrant tachycardia and AV reentrant tachycardia using a bypass tract, are characterized by regular, narrow complex tachycardia on the surface ECG. It may be possible to identify a retrograde P wave after the QRS complex, particularly in the case where a bypass tract is in- volved, but if the retrograde conduction is sufficiently rapid, it may not be visi- ble. It may also be difficult to detect a P wave in cases of rapid sinus tachycardia. In these cases, we advise the use of adenosine injections or carotid sinus massage 198 The Intensive Care Manual ch08.qxd 11/7/01 4:14 PM Page 198 as therapeutic intervention and for diagnostic purposes. The initial dose of adenosine is 6 mg, given as a rapid intravenous injection. If there is no response, a dose of 12 mg may be given. In cases of reentrant SVTs or some atrial tachycar- dias, the response to adenosine is usually prompt termination of the tachycardia. In the case of sinus tachycardia, however, a brief slowing of the sinus rate is seen, which usually allows identification of distinct P waves. WIDE COMPLEX TACHYCARDIA A wide complex tachycardia may lead to serious consequences or it may be a rel- atively benign occurrence. The correct diagnosis of such a tachycardia is impera- tive, especially in the critical care setting. A wide complex tachycardia usually arises from a ventricular origin; however, an SVT with aberrant conduction can also manifest as a wide complex tachycardia. Other than ventricular fibrillation, ventricular tachycardia is the most ominous tachyarrhythmia involved in the care of patients in the ICU. Because it may lead to rapid hemodynamic collapse, prompt intervention is necessary. SVT often is better tolerated, although signifi- cant hemodynamic compromise can occur quickly as well. Hemodynamic stabil- ity in conjunction with a wide complex tachycardia does not rule out ventricular tachycardia. Equally important is an understanding of the consequences of both pharmacologic and nonpharmacologic therapy for wide complex tachycardia to avoid potentially harmful interventions. Some of the drugs used for the manage- ment of SVT, such as calcium channel blockers, may lead to adverse conse- quences in a patient with ventricular tachycardia. Therefore, in the ICU, all wide complex tachycardia should be assumed to be ventricular in origin until it can be ruled out with a high degree of certainty, especially in patients with known car- diac disease. Distinguishing ventricular tachycardia from SVT with aberrant conduction on the basis of surface ECGs can be difficult, especially because recordings from only one or two leads are often all that is available. There are some findings that may be helpful in diagnosis of the origin of a wide complex tachycardia. “Atrioventricular dissociation,” or evidence of separate atrial and ventricular activities, should always be sought in the patient with a wide complex tachycardia tracing. This is manifested as P waves and QRS complexes that are temporally unrelated. The P waves, or atrial ECGs, are often difficult to discern and may be present in any part of the cardiac cycle, including parts of the QRS complex or T waves. Techniques to amplify the amplitude of the atrial activities, such as esophageal leads or even placement of a transvenous electrode, may be helpful. Although the presence of AV dissociation is not completely diagnostic for ven- tricular tachycardia, it does make a ventricular tachycardia highly likely. The presence of a 1:1 AV relationship is consistent with either SVT or ventricular tachycardia and cannot be used to distinguish one from the other. 8 / Cardiac Arrhythmias 199 ch08.qxd 11/7/01 4:14 PM Page 199 Another phenomenon to look for is the presence of a “fusion” beat, i.e., a combined QRS complex resulting from impulses originating from two different areas of the heart. A combination, or fused, QRS complex between a beat origi- nating in the ventricle and one from a supraventricular site is more reliable for the diagnosis of ventricular tachycardia (Figure 8–6). Typically, this is seen in ventricular tachycardia with relatively slower rates, allowing time for the supra- ventricular impulses to conduct down to the ventricle. When possible, a 12-lead ECG should be obtained for further information in differentiating the origin of the tachycardia. There are well-tested morphologic criteria for wide complex tachycardias of both right and left BBB–type patterns in patients in whom the origins of tachycardia were confirmed by invasive electro- physiology studies. If the QRS morphology in a wide complex tachycardia displays a right BBB–type pattern and, in lead V 1 , the initial R wave (the initial positive deflec- tion) is dominant, the tachycardia is likely to be of ventricular origin. This can be seen either as a monophasic R wave in V 1 or as the first initial positive deflection (R) being taller than the second positive deflection (r′). In a wide complex tachy- cardia with a right BBB–type pattern, an R wave amplitude of less than the S wave in lead V 6 suggests ventricular tachycardia. In tachycardias displaying a left BBB–type pattern delay in the initial forces with a broadened r wave (r > 0.04 sec), notches in the initial QRS downstroke in lead V 1 suggest ventricular tachy- cardia. Furthermore, during tachycardia with a left BBB–type pattern, a q wave present in lead V 6 makes it likely that the tachycardia is of ventricular origin. 5 Basic premises for these criteria are that the more fragmented the initial QRS forces are and the wider the QRS duration is, the more likely there is a ventricular origin of the tachycardia. This results from muscle-to-muscle conduction during ventricular tachycardia rather than conduction down to the ventricles through specialized His and Purkinje tissues during SVT. These criteria were tested in patients who did not have existing BBBs or Wolff-Parkinson-White syndrome. Furthermore, these criteria probably cannot be relied on for patients on antiarrhythmic therapy, because many of these drugs can alter cardiac conductiv- ity and thereby affect the initial forces of the QRS complex patterns and duration. Another criterion on 12-lead ECGs that suggests a ventricular origin of a wide complex tachycardia is concordance of the QRS pattern in the precordial leads (V 1 through V 6 ). 6 Both positive concordance (i.e., all QRS complexes in V 1 though V 6 display monophasic R waves) and negative concordance (i.e., all pre- cordial QRS complexes display monophasic QS patterns) are suggestive of ventricular tachycardia. Negative concordance is diagnostic for ventricular tachy- cardia, but positive concordance may, rarely, result from tachycardia involving an accessory AV bypass tract. Table 8–3 summarizes the criteria that are useful for distinguishing the cause of a wide complex tachycardia. Cycle length variability is not a useful diagnostic criterion for wide complex tachycardias. While it is true that atrial fibrillation conducted with aberration dis- plays an irregularly irregular pattern, the rate of a ventricular tachycardia can often 200 The Intensive Care Manual ch08.qxd 11/7/01 4:14 PM Page 200 8 / Cardiac Arrhythmias 201 FIGURE 8-6 Twelve-lead ECG demonstrating a wide complex tachycardia. P waves (P) can be seen dissociated from the QRS in what is termed AV dissociation. In addition, fusion beats can also be detected (F). The combination of AV dissociation and fusion beats is, in almost all cases, diagnostic of ventricular tachycardia. ch08.qxd 11/7/01 4:14 PM Page 201 be irregular as well. Similarly, it has been suggested that alternating cycle length may be a marker for certain forms of SVT, but alternating cycle length variations have been well described in patients proven to have ventricular tachycardia. Always compare a patient’s baseline ECG to the one obtained during wide complex tachycardia. If a BBB pattern is present during sinus rhythm and the tachycardia displays a BBB pattern of the alternate bundle, then the tachycardia is very likely to be ventricular. As mentioned, the wider the QRS duration, the more likely that the tachycardia is of ventricular origin. Interestingly, a wide complex tachycardia with QRS duration shorter than the conducted QRS is al- most always caused by ventricular tachycardia. These tachycardias often are orig- inating from a septal region, and the left and right ventricles are activated in a more simultaneous fashion than a supraventricular impulse conducted down to the ventricle with a bundle branch conduction block. Other than ECGs, clinical physical examination may also help in distinguish- ing ventricular tachycardia from SVT with aberrant conduction. The presence of “cannon A waves,” resulting from atrial contraction against closed AV valves, during inspection of the jugular pulse suggests the presence of AV dissociation and, therefore, ventricular origin of the tachycardia. Variations in the intensity of the first heart sound (S 1 ) and splitting of S 1 during auscultation as a result of ven- tricular dyssynchrony also suggest ventricular tachycardia. Characteristics of a wide complex tachycardia may provide important clues about the underlying cardiac pathology. Patients with transmural scars from in- farctions or cardiomyopathy from various causes have a substrate for reentrant monomorphic ventricular tachycardia, or a wide complex tachycardia displaying a consistent QRS morphology from beat to beat. On the other hand, insufficient myocardial arterial supply or increased myocardial demand may lead to electro- 202 The Intensive Care Manual TABLE 8–3 Criteria for diagnosis of etiology of wide complex tachycardia based on Qrs morphology. 8 Aberration VT RBBB QRS ≤ 0.12 sec QRS ≥ 0.14 sec Axis: Normal Axis: Superior V 1 : rsR' or rR' V 1 : R, Rr', RS V 6 : R/S > 1 V 6 : R/S < 1 LBBB QRS ≤ 0.14 sec QRS ≥ 0.16 sec Axis: normal or leftward Axis: rightward Lead V 1 or V 2 : R < 0.04 sec Lead V 1 or V 2 : r ≥ 0.04 sec Onset to nadir: < 0.07 sec Onset to nadir: ≥ 0.07 sec Smooth downstroke Notch on downstroke V 6 : No Q wave V 6 : Q wave ABBREVIATIONS: VT, ventricular tachycardia; RBBB, right bundle branch block; LBBB, left bundle branch block. ch08.qxd 11/7/01 4:14 PM Page 202 physiologic instability within the myocardium, resulting in ventricular fibrilla- tion or polymorphic ventricular tachycardia, a wide complex tachycardia with varying QRS morphologies. Therefore, recognition of the different ventricular arrhythmias as manifestations of the underlying cardiac pathophysiology can help in choosing the proper therapeutic and management interventions. Urgent intervention for a wide complex tachycardia is often needed as a result of the hemodynamic effects. If hemodynamic collapse is evident or if blood pres- sure is unstable, countershock with DC energy is required. There are other clini- cal indications for relatively urgent DC cardioversion as well. These include ischemia or infarction, angina, and severe heart failure. If a patient’s blood pres- sure is stable, then the various criteria may be applied to distinguish ventricular and supraventricular origin of the tachycardia and a decision for appropriate therapy may be applied. Traditionally, intravenous lidocaine is the first antiarrhythmic used for ven- tricular tachycardia. Under ischemic conditions, such as during the infarction period, ventricular arrhythmias often are manifested as polymorphic ventricular tachycardia (Figure 8–7) or ventricular fibrillation. Under these circumstances, intravenous lidocaine is reasonably effective and it should be considered as a first-line agent. For nonacute infarction or non–ischemia-related ventricular ar- rhythmias, typically manifested as a monomorphic ventricular tachycardia (with consistent beat-to-beat QRS morphology), several clinical reports have suggested that intravenous procainamide may be more effective for termination than lido- caine. 9 Intravenous amiodarone has become widely available over the past few years. Data are becoming available suggesting its effectiveness in terminating and suppressing ventricular arrhythmias. 10 Amiodarone probably is superior in com- parison to lidocaine or procainamide for ventricular arrhythmia management. However, it may have a profound blood pressure–lowering effect and its use should be accompanied by cautious hemodynamic monitoring. 8 / Cardiac Arrhythmias 203 FIGURE 8–7 Rhythm strip showing 6-beat run of polymorphic ventricular tachycardia. There is a variable morphology to the QRS complexes of the tachycardia. This is often seen in the patients with ischemia. ch08.qxd 11/7/01 4:14 PM Page 203 The use of adenosine has been advocated as a diagnostic tool for distinguish- ing ventricular origins from supraventricular origins in a wide complex tachycar- dia. Adenosine has vasodilator effects and a possible “steal” phenomenon in the coronary circulation; this may induce myocardial ischemia and lead to further hemodynamic compromise. Even though the half-life of adenosine is brief, its ef- fects in patients with severe CAD may trigger a cascade of hemodynamic effects that may become irreversible. Therefore, we recommend that the use of adeno- sine as a diagnostic measure for wide complex tachycardia must be taken with caution, especially in patients with known severe coronary disease. Unless it is absolutely certain that the diagnosis is SVT, calcium channel blockers, such as diltiazem or verapamil, should not be used to treat wide complex tachycardias because there are a multitude of reports detailing hemodynamic collapse in pa- tients with ventricular tachycardia who were treated with these agents. 7 TORSADES DE POINTES Torsades de pointes is a subtype of polymorphic ventricular tachycardia that should be recognized because it has distinct diagnostic and therapeutic implica- tions that differ from other types of wide complex tachycardia. A French term meaning “twisting of the points,” torsades de pointes has an appearance similar to rapid QRS axis shifting. It is usually characterized by prolonged QT intervals, and it is often initiated with a premature ventricular extrasystole occurring on or around the T wave of the preceding beat. Known causes of torsade de pointes typically include conditions that prolong the QT interval, such as congenital long QT interval syndrome; electrolyte imbalances, such as hypokalemia, hypomag- nesemia, or hypocalcemia. Drugs that prolong the QT interval are also known to lead to torsades de pointes; these include class Ia and III antiarrhythmic drugs and some antihistamines and psychotropic medications. Table 8–4 lists a number of causes of prolongation of the QT interval and torsades de pointes. Care should be paid to patients with decreased clearance of any of these suspect medications as well as any combinations that may compound the prolongation of the QT in- terval. Remember that bradycardia may prolong the repolarization process, and thus the QT interval. The effects of these precipitants are more pronounced and the risk of torsades de pointes is higher in patients with bradycardia. If sustained, the acute intervention for torsades de pointes, as with all wide com- plex tachycardia with hemodynamic instability, is countershock with DC energy. Once a stable rhythm has been restored, the major goal of the therapy is to shorten the QT interval as much as possible. This obviously includes removal of the of- fending agent or correcting the underlying conditions. Sometimes cardiac pacing or the use of an isoproterenol infusion may be necessary to further decrease the ventricular repolarization time, especially if bradycardia is present. If the episodes of torsades de pointes are not sustained, then, in addition to the above interven- tions, empiric intravenous magnesium therapy has been suggested. 204 The Intensive Care Manual ch08.qxd 11/7/01 4:14 PM Page 204 [...]... also on the chronicity of the elevation in serum potassium level Although a close correlation exists between the potassium level and ECG changes in ch08.qxd 11/7/01 2 06 4:14 PM Page 2 06 The Intensive Care Manual animal models, the relation is less clear in clinical cases Abnormal potassium levels affect P waves, the QRS complex, and T waves P-wave voltage decreases as a result of slow intra-atrial... delay between when the device is activated and when the shock is delivered, because the shock is delivered only on the QRS configuration Under most circumstances, the best positioning for the electrodes is to have one placed anteriorly under the right clavicle to the right of the sternum and the other at the level of the left nipple in the midaxillary line The recommended initial energy for various arrhythmias... direct result of the passage of electrical current through the heart The resistance of the chest wall determines the amount of current that reaches the heart It is imperative that material be used between the electrodes of the device and the chest wall to not only reduce the electrical resistance, but also to minimize the risk of chest wall burns The electrical shock can be delivered in either a synchronized... Twelve-lead ECG from a patient with hyperkalemia, demonstrating loss of atrial activity, prolongation of the QRS duration, and merging of the ST segment with a prominent, peaked T wave 207 ch08.qxd 11/7/01 208 4:14 PM Page 208 The Intensive Care Manual These are best seen as an upward deflection at the onset of the ST segment in leads II, III, aVF, V5 and V6 The QT interval is often prolonged These... arises from the isthmus toward the left side The thyroid gland weighs 15 to 20 g Thyroid blood flow is fairly high at 4 to 6 mL/min per gram of thyroid tissue Physiology The thyroid gland contains follicles, and it is the cells surrounding these follicles, or the follicular cells, that produce the thyroid hormones Thyroxine (T4) is a prohormone with one-half to one-quarter the activity of the active... low-amplitude atrial depolarization and the PR interval lengthens With severe widening and attenuation of the P wave, there may be no atrial depolarization seen on the surface ECG, so the erroneous diagnosis of a junctional rhythm may be made Type I or II second-degree AV block may also occur As the QRS complex widens, the normally sharp contour of the QRS becomes wider and eventually merges with the. .. attempted to review some of the most common abnormalities of cardiac rhythm that are likely to be encountered in the critical care setting The significance of cardiac rhythm disturbances in this setting must be understood because they may be life-threatening Careful analysis of the rhythm is essential in making the correct diagnosis and instituting the correct therapy While there are excellent pharmacologic... markers of cardiac injury, because of their higher sensitivity and specificity for myocardial damage The initial rise of troponin levels occurs approxi- ch09.qxd 11/7/01 2 16 4:15 PM Page 2 16 The Intensive Care Manual mately 3 hours after myocardial injury, but it may occur several hours later in many patients Therefore, it is essential that the use of troponin levels for the diagnosis of acute MI includes... 4:15 PM Page 218 The Intensive Care Manual TABLE 9–2 Thrombolytic Therapy Advantages Disadvantages • Widely available, no catheterization lab or CABG capabilities needed • Treats the underlying acute problem; dissolves the occluding thrombus • Significantly decreases 30-day mortality rates (large, well-controlled trials) • Significantly decreases 5-year mortality rates (large, well-controlled trials)... to the phase and severity of the patient’s illness The other two conditions, namely hypothyroidism and thyrotoxicosis, are familiar in the outpatient arena as well and, in their extremes, present to the ICU as myxedema coma and thyroid storm, respectively More commonly, however, other illnesses supersede hypothyroidism and thyrotoxicosis, making it difficult for all but the astute clinician to make the . may also 1 96 The Intensive Care Manual ch08.qxd 11/7/01 4:14 PM Page 1 96 8 / Cardiac Arrhythmias 197 FIGURE 8–5 Twelve-lead ECG from the same patient in Figure 8–4, now showing a charac- teristic. through the heart. The resistance of the chest wall de- termines the amount of current that reaches the heart. It is imperative that material be used between the electrodes of the device and the. to have one placed anteriorly under the right clavicle to the right of the sternum and the other at the level of the left nipple in the midaxillary line. The recommended initial energy for various