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216 SECTION 4: Resuscitative Procedures  CENTRAL VENOUS OXYGEN SATURATION Venous oxygen saturation monitoring assesses the relationship between tissue oxygen extraction, oxygen delivery, and oxygen consumption, with low values reflecting inadequate delivery and/or excessive con sumption. It is ideally measured in the pulmonary artery as a mixed venous sample (Sm vo 2); however, this is impractical in the ED, and central venous oxygen saturation (S cvo 2) measured from the internal jugular or subclavian veins acts as a surrogate. A normal oxygen extraction ratio of 25% to 35% results in a venous oxygen delivery (reflected in venous oxygen saturation) of approximately 70% of arterial oxygen delivery. In healthy individuals, S cvo 2 is 2% to 3% less than Smvo 2; in shock states, S cvo 2 is typically 5% to 10% higher than Sm vo2 as blood flow is redistributed from the abdominal vascular beds to the cerebral and coronary circulation. 39 Although absolute values of S cvo 2 and Sm vo2 may be different, low values of either measurement reflect an imbal ance in oxygen transport and portend worse outcomes. Most important, the two measures typically change in parallel and thus trends in S cvo closely reflect trends in Smvo 2.40 Clinical Use of Central Venous Oxygen Saturation The principal value of Scvo 2 is to detect occult inadequate oxygen delivery. Regardless of the underlying pathophysiologic state (e.g., heart failure, septic shock, trauma), a low S cvo 2 value represents inadequate oxygen delivery rela tive to oxygen consumption, which can be due to inadequate delivery due to hypoxemia, anemia, or impaired CO (low contractility, hypo volemia, or tamponade) and/or increased oxygen consumption due to increased metabolic demand (Table 32-3). Normal (approximately 70%) or high Scvo 2 values do not necessarily mean that the patient is well. Scvo 2 is a global measure of oxygen transport, and regional areas of tissue hypoperfusion can exist with normal Scvo 2 values, particularly in the lower half of the body. In several disease states (e.g., hypothermia, terminal shock, cyanide poisoning), tissues oxygen extraction from the blood is impaired, leading to “arterialization” of the venous blood with high S cvo 2. Routine measuring of S cvo 2 in sepsis is not recommended, but if a central venous catheter is in place, obtaining a single S cvo 2 measurement is reasonable. A low S cvo 2 is always abnormal.  LACTATE In critical illness, an oxygen debt develops when oxygen delivery is inadequate to meet tissue demand and compensatory mechanisms are exhausted. This results in global tissue hypoxia, anaerobic metabolism, and lactate production. High lactate is a prognostic marker in critically ill patients with various forms of shock, known since the 1800s. 41 This type of acidosis due to anaerobic metabolism is called type A lactic acidosis. In addition to shock, other causes of elevated lactate include seizure, diabetic ketoacidosis, malignancy, thiamine deficiency, malaria, human immunodeficiency virus infection, carbon monoxide or cyanide poi soning, and mitochondrial myopathies. Commonly used drugs, such as albuterol, propofol, metformin, simvastatin, lactulose, antiretrovirals, niacin, isoniazid, and linezolid, can also cause a lactate elevation. This type of acidosis is called type B lactic acidosis and is not due to hypoperfusion.

onoxide or cyanide poi soning, and mitochondrial myopathies. Commonly used drugs, such as albuterol, propofol, metformin, simvastatin, lactulose, antiretrovirals, niacin, isoniazid, and linezolid, can also cause a lactate elevation. This type of acidosis is called type B lactic acidosis and is not due to hypoperfusion. 37 However, all lactic acidosis is associated with poor outcome, and types A and B lactic acidosis can both be present. It is key TABLE 32-3 Contributors to Abnormal Central Venous Oxygen Saturation (S cvo 2) Low Scvo 2 (<70%) High Scvo 2 (>70%) Low Do2 High ˙Vo2 High Do2 Low ˙Vo2 Hypoxia, suctioning (low Sao2) Exercise Hyperoxia (high Fio2) Hypothermia Anemia, hemorrhage (low Hgb) Pain Erythrocytosis (high Hgb) Anesthesia, pharmacologic paralysis Cardiac dysfunction, hypovolemia, shock, arrhythmia (low CO) Hyperthermia, shivering, seizure Hyperdynamic state (high CO) Arteriovenous shunting, mitochondria defect, terminal shock Note: Determining the causes of and treating a low or high S cvo 2 clinical state involves troubleshooting for conditions resulting in abnormal oxygen delivery (D o2) and oxygen consumption ( ˙Vo2). Abbreviations: CO = cardiac output; Fio2 = fraction of inspired oxygen; Hgb = hemoglobin; Sa o2 = arterial oxygen saturation. to understand that not all lactic acidosis is due to hypoperfusion, and fluid administration is based on the global assessment, not just lactate value. Blood lactate concentrations also reflect the interaction between its production and elimination. During critical illness, a patient with hepatic dysfunction may have a higher lactate level compared with another patient without liver disease due to impaired hepatic clearance. Lactate elevation in a patient with chronic liver disease still portends a poor prognosis, because patients with liver disease do not have a high lactate level in the absence of shock. Hyperlactatemia is not always accompanied by hypotension or a low bicarbonate level and/or elevated anion gap. Most recently, a blood lactate level ≥2 mmol/L became part of the new definition of septic shock, 44 and an elevated lactate level in a normotensive patient requires further attention because a continued increase in lactate levels is associated with increased mortality.45 Lactate clearance (a drop of at least 25% within 6 hours of an initial elevated level) in patients with septic shock is associated with increased 60-day survival. 46 When lactic acidosis accompanies low-flow disease states such as sepsis, mortality increases by almost threefold; 47 thus, all lactic acidosis should be alarming to the emergency physician. REFERENCES The complete reference list is available online at www.TintinalliEM.com. Cardiac Pacing and Implanted Defibrillation Swee Han Lim Wee Siong Teo Venkataraman Anantharaman PURPOSE OF PROCEDURE Cardiac pacing serves to maintain or restore myocardial depolarization and thus ensure adequate cardiac output. In the ED, pacing corrects rhythm disturbances or starts in anticipation of a conduction problem with hemodynamic impact. Indications for emergency pacing are provided in Table 33-1. GENERAL EQUIPMENT Cardiac pacemakers deliver an electrical stimulus to the heart through electrodes, causing depolarization and subsequent cardiac contraction. The modern implanted pacemaker only stimulates the heart chamber if it does not recognize (sense) intrinsic electrical activity from that chamber after a selected time interval. Impulses go to the atria, ventricles, or both. CHAPTER Tintinalli_Sec04_p0143-0228.indd 216 7/31/19 1:45 PM

nd subsequent cardiac contraction. The modern implanted pacemaker only stimulates the heart chamber if it does not recognize (sense) intrinsic electrical activity from that chamber after a selected time interval. Impulses go to the atria, ventricles, or both. CHAPTER Tintinalli_Sec04_p0143-0228.indd 216 7/31/19 1:45 PM CHAPTER 33: Cardiac Pacing and Implanted Defibrillation 217 large-amplitude pacing spikes. Most of the newer transcutaneous pacing units have a monitor that filters pacing spikes, allowing simultaneous monitoring.  RISKS AND PRECAUTIONS There is little risk of electrical injury to healthcare providers during transcutaneous pacing. The electrode insulation allows contact with the patient, including closed chest compressions, while pacing.  EQUIPMENT Table 33-3 lists the equipment needed to perform transcutaneous pacing.  TECHNIQUE If time and conditions allow, explain the procedure to the patient and administer IV sedation and analgesia before pacing. Vital signs and ECG monitoring are mandatory during the procedure. Place the pacing pads on the patient’s chest either in the anterolateral or anterior-posterior position (Figure 33-1). The anterior-posterior position minimizes transthoracic electrical impedance by sandwiching the heart between the two pads. The same pads and electrodes allow pacing, cardioversion, and defibrillation in most of the newer defibril lator units. In bradyasystolic arrest or with depressed sensorium, turn the stimulating current to maximum output; after restoring pulses, you may titrate energy downward to a level just above loss of capture. In a still-conscious patient with a hemodynamically compromising bradycardia, slowly increase the output from the minimum setting until capture—usually between 50 and 100 mA. Continue pacing at about 1.25 times the threshold of initial electrical capture. Transcutaneous pacing may be fixed rate (asynchronous) or demand (synchronous). Asynchronous pacing delivers an electrical impulse at a regular interval without regard to intrinsic cardiac pacemaker activity. This creates the potential risk of precipitating a dysrhythmia if the pac ing stimulus occurs during the vulnerable period of ventricular repolarization. Although many state a preference for synchronous pacing, there are little outcome or safety data to support that preference.  OUTCOMES ASSESSMENT Assess capture using the ECG on the filtered monitor of the pacing unit. Look for the presence of a consistent ST segment and T wave after each pacer spike. Palpate for carotid and femoral pulses with each such waveform. Bedside cardiac US can assess external pacer mechanical contraction, identifying capture. If these appear favorable, assess blood pressure by cuff or arterial catheter. Failure to capture with transcutaneous pacing may be related to faulty electrical contact, inadequate current, poor pacing pad placement, or the underlying pathology. Recheck the lead connections, skin–electrode contact, and electrode placement. On occasion, pneumothorax, pericardial effusion or tamponade, severe myocardial ischemia, and metabolic derangements limit capture. Unless an easily resolved trigger exists, arrange for transvenous pacing as soon as possible. TRANSVENOUS PACING The indications for transvenous pacing are the same as for other methods of cardiac pacing. Transvenous pacing is an urgent rather than emergent intervention, with transcutaneous pacing serving as the bridge. TABLE 33-1 Indications for Emergency Pacing Indication Comments Symptomatic or hemodynamically unstable bradycardia/AV block Symptoms include hypotension, change in mental status, angina, and pulmonary edema. Pharmacologic therapy may be used to temporize while preparing to pace.

cutaneous pacing serving as the bridge. TABLE 33-1 Indications for Emergency Pacing Indication Comments Symptomatic or hemodynamically unstable bradycardia/AV block Symptoms include hypotension, change in mental status, angina, and pulmonary edema. Pharmacologic therapy may be used to temporize while preparing to pace. Severe sick sinus syndrome with prolonged asystole (generally >3 s) and syncope — Ventricular standstill due to complete heart block or Mobitz type II AV block — Torsades de pointes Overdrive pacing. Recurrent monomorphic ventricular tachycardia Overdrive pacing. The technique is limited by: Maximum pacing rate of the pacing device (usually 180 beats/min). Potential of accelerating the ventricular tachycardia and inducing ventricular fibrillation. Unstable supraventricular tachycardia Overdrive pacing should be used only after pharmacologic intervention and cardioversion have failed. Abbreviation: AV = atrioventricular. TABLE 33-2 Pacemaker Component Details Pacemaker Type Pulse Generator Location Electrode Location Transcutaneous External Skin of anterior chest wall and back or Anterior chest wall below right clavicle and apex Transvenous External Venous catheter with tip in right ventricle and/or right atrium Transesophageal External Esophagus Epicardial External or Internal Epicardium Electrodes are usually placed on heart’s surface during surgery Permanent Internal (subcutaneous in the prepectoral region) Venous or epicardial TABLE 33-3 Transcutaneous Pacing Equipment •   Pulse generator and monitor (usually a combination defibrillator/cardioversion/ pacemaker unit) •   Pacemaker pads with pacing cables •   ECG monitor and cables with ECG electrode pads Components of a cardiac pacemaker include: • Pulse generator • Electronic circuitry for sensing and pacing • Lead system that connects the pulse generator to the electrode(s) and stimulates the myocardium Relevant clinical details of these components are provided in Table 33-2. TRANSCUTANEOUS PACING Transcutaneous pacing is an emergency technique frequently chosen in patients presenting with hemodynamically significant bradycardia because of its easy application. It uses externally (chest wall) applied electrodes to deliver an electric impulse to stimulate the myocardium. Transcutaneous pacers differ from standard pulse generators: The pulse duration of the externally stimulating impulse is longer and the current output higher than in internal pacing. Muscle contraction (usually the chest wall or diaphragm) is notable during external pacing, especially at high outputs, and may be painful. The muscle twitching makes pal pation of the radial, carotid, or femoral pulse difficult. Finally, cardiac monitoring with standard ECG monitors is difficult during external pacing due to interference from the large current outputs that create Tintinalli_Sec04_p0143-0228.indd 217 7/31/19 1:45 PM

ts, and may be painful. The muscle twitching makes pal pation of the radial, carotid, or femoral pulse difficult. Finally, cardiac monitoring with standard ECG monitors is difficult during external pacing due to interference from the large current outputs that create Tintinalli_Sec04_p0143-0228.indd 217 7/31/19 1:45 PM 218 SECTION 4: Resuscitative Procedures Gather all equipment needed, including that to insert a central venous catheter (see Chapter 31, “Vascular Access”). Resuscitation equipment and drugs and the pacing needs are listed in Table 33-4.  TECHNIQUE Y ou should know the equipment and have practiced or done the procedure before starting. If conditions permit, explain the procedure to the patient and obtain informed consent. Next, identify the access site and approach and position the patient. The primary sites of catheter insertion in the ED are the right internal jugular vein (preferred) and the left subclavian vein. The right internal jugular vein allows a relatively straight line of access through the superior vena cava and right atrium into the right ventricle. The steps for transvenous pacemaker insertion are listed in Table 33-5. The most commonly encountered difficulties with transvenous pacing are securing venous access and obtaining proper placement of the stimulating electrode in the right ventricle, both of which can be time-consuming. When patients have decreased or no forward blood flow, positioning of the pacer tip within the right ventricle is difficult. Balloon-tipped catheters do not aid during low- or no-flow states. In an emergency, connect the pacemaker electrodes to the power source and advance the catheter until the tip encounters the endocardium of the right ventricle and creates capture. Set the initial rate between 80 and 100 beats/min, using the asynchronous mode (sensitivity off) initially in patients requiring emergency pacing for hemodynamically unstable bradycardias. Follow the ECG to determine the presence or absence of capture ( Figure 33-2). Adjust subsequent rate and sensitivity settings as clinically indicated by the response and underlying rhythm disturbance.  COMPLICATIONS Complications include perforation of the myocardium, cardiac dys rhythmias, air embolism, failure of the circuit, catheter dislodgement, and delayed infection, plus any complications possible with central venous access (see Chapter 31). PERMANENT PACING Permanent pacing is not performed in the ED. 1 Permanent pacemaker pulse generator (battery) placement is usually on the side of the patient’s nondominant hand (thus, usually in the left prepectoral region below the left clavicle). The endocardial transvenous leads insert into the right ventricle at the apex, septum, right ventricular outflow tract, or His Bundle region and, in the case of a dual-chamber device, also in the right atrium. A subclavian or cephalic vein approach is common. An epicar dial lead may be implanted during open heart surgery. Patients with heart failure may have a cardiac resynchronization therapy device and will have three wires, with one in the atrium, one in the right ventricle, and one in the coronary sinus pacing the left ventricle. Pacemaker leads are either bipolar or unipolar in configuration; uni polar leads are prone to oversensing myopotential and electromagnetic interference. A new form of pacing is the leadless pacemaker where insertion of a miniature device transvenously for right ventricle implantation occurs. There is no device noted externally.  PACEMAKER NOMENCLATURE A five-letter code describes the features of the pacemaker. 4 The first three code letters are most commonly used. The first letter refers to the chamber or chambers in which the pacing occurs: A = atrium, V = ventricle, and D = dual chamber or both A and V .

here is no device noted externally.  PACEMAKER NOMENCLATURE A five-letter code describes the features of the pacemaker. 4 The first three code letters are most commonly used. The first letter refers to the chamber or chambers in which the pacing occurs: A = atrium, V = ventricle, and D = dual chamber or both A and V . The second letter Front AB C Front Back Front Back FIGURE 33-1. Placement of the transcutaneous pacing electrodes. A. Anterior (negative) electrode position centered over the cardiac apex. B. Anterior (negative) electrode position centered over the V 3 lead position. C. Posterior (positive) electrode position. [Reproduced with permission from Doukky R, Rajanahally RS: Transcutaneous cardiac pacing, in Reichman EF, Simon RR (eds): Emergency Medicine Procedures. Figures 20-2 and 20-3. Copyright © 2004. The McGraw-Hill Companies, Inc. All rights reserved.] TABLE 33-4 Equipment Needed for Transvenous Pacing •   Central catheter kit—introducer sheath must be one size larger than the pacer catheter •   Flexible transvenous cardiac pacing catheter •   Pacemaker generator and battery (and spare battery) •   Cardiac monitor •   Insulated connecting wire with alligator clamps at both ends Tintinalli_Sec04_p0143-0228.indd 218 7/31/19 1:45 PM

atheter kit—introducer sheath must be one size larger than the pacer catheter •   Flexible transvenous cardiac pacing catheter •   Pacemaker generator and battery (and spare battery) •   Cardiac monitor •   Insulated connecting wire with alligator clamps at both ends Tintinalli_Sec04_p0143-0228.indd 218 7/31/19 1:45 PM CHAPTER 33: Cardiac Pacing and Implanted Defibrillation 219 TABLE 33-5 Transvenous Pacemaker Insertion Step Comments 1. Gown in standard sterile fashion. Use sterile gloves and gown. Wear mask and hair covering. 2. Identify vessel using US guidance. — 3. Prep and drape patient using standard sterile procedure. Prep a wide area in case initial attempts fail and an alternate site is needed. Prep the entire ipsilateral neck and upper chest when preparing to insert an internal jugular or subclavian catheter. 4. Open a central catheter kit that contains an introducer catheter. Inspect for content in a sterile fashion. Place kit close to bedside and operator. Maintain sterile conditions. The introducer catheter should be one size larger than the pacing catheter. 5. Open pacing catheter and pacing kit (if available). Pulmonary artery catheters with dedicated atrial and ventricular ports may also be used. Assess integrity of the pacing catheter balloon by inflating it with 1.5 mL of air and immersing it in sterile saline. Air bubbles indicate a leaky balloon. 6. Attach the pacemaker to any of the V leads and ensure it is recording. — 7. Anesthetize area in all conscious patients. Inject area with 1%–2% lidocaine. Anesthetize the periosteum of the clavicle if using the subclavian approach. Reorient to landmarks after injection. 8. Hold the 18-gauge introducer needle on a 10-mL syringe in the dominant hand and align the needle to the target. — 9. Advance the needle slowly though the skin and subcutaneous tissue until a flash of dark venous blood appears. Maintain steady constant aspiration of syringe. 10. Stabilize the needle with the nondominant hand. — 11. Check for continued free venous flow with aspiration. If no flow is noted, withdraw the needle slightly, as the needle may have breached the poste rior vessel wall. 12. Remove the syringe attached to the needle, and immediately occlude the catheter with a finger. This maneuver helps to prevent introducing air in the catheter and subsequent central system air embolism. 13. Insert the guidewire gently through the needle. Always maintain a firm grip on the wire—do not let go of the wire for any reason. The wire should advance with minimal resistance. Do not force the wire for any reason. If the wire does not pass easily, reattach the syringe and aspirate to confirm continued venous flow. Reposition the needle as needed. Premature ventricular contractions (PVCs) or dysrhythmias during wire advancement may indicate that the wire is in the right atrium or beyond. 14. Remove the needle over the wire when the guidewire is inserted at least 10 cm into the vessel. — 15. Incise the skin with a #11 blade scalpel at the entry site to accommodate the introducer. Do not cut the guidewire. 16. Advance the introducer over the guidewire into the vessel lumen with a gentle twisting motion. Maintain a grip on the guidewire during this procedure. 17. Remove the guidewire. — 18. Insert and advance the pacing catheter approximately 10 cm. This ensures that the balloon is past the introducer catheter and within the vascular system. Inflate the balloon with 1.5 mL of sterile saline. 19. Slowly advance the catheter into the right ventricle. Use fluoroscopy or bedside US to guide placement. The ECG tracing recorded from the electrode also helps localize the position of the catheter tip. Inflate the balloon after the catheter enters the superior vena cava.

e the balloon with 1.5 mL of sterile saline. 19. Slowly advance the catheter into the right ventricle. Use fluoroscopy or bedside US to guide placement. The ECG tracing recorded from the electrode also helps localize the position of the catheter tip. Inflate the balloon after the catheter enters the superior vena cava. Stop advancing when the pacing catheter is in the apex of the right ventricle. 20. Reassess balloon integrity. — 21. Connect the pacemaker generator to the catheter. — 22. Disconnect the negative terminal of the pacemaker catheter from the ECG lead. — 23. Connect the proximal pacemaker catheter terminals to the terminals of the pace maker generator. — 24. Set the pacemaker generator on demand mode with a rate of 80–100 beats/min. Start with 5 mA of energy on the output dial. 25. Turn on the pacemaker. With optimal tip position, capture should occur at <2 mA. Pacing spikes and a wide QRS complex in lead V 1 reflect capture. 26. After capture, decrease the pacemaker generator output to just below where pacing stops. Continue pacing at 1.5–2.0 times the threshold output required for capture. 27. Examine the chest radiograph for catheter tip placement and signs of complications. — 28. Secure catheter and apply a sterile transparent dressing. — Tintinalli_Sec04_p0143-0228.indd 219 7/31/19 1:45 PM

put to just below where pacing stops. Continue pacing at 1.5–2.0 times the threshold output required for capture. 27. Examine the chest radiograph for catheter tip placement and signs of complications. — 28. Secure catheter and apply a sterile transparent dressing. — Tintinalli_Sec04_p0143-0228.indd 219 7/31/19 1:45 PM 220 SECTION 4: Resuscitative Procedures refers to the chamber or chambers in which sensing occurs. The letters are the same as those for the first letter code. “ I” indicates that a sense event inhibits the output pulse and causes the pacemaker to recycle the timing cycles, “ T” means that an output pulse is triggered in response to a sensed event. “ D” means that both “ T” and “ I” responses can occur. The most common pacemakers are VVI and DDD . The fourth letter is used to indicate the presence or absence of an adaptive-rate mechanism (rate modulation). Pacemaker designations may be VVIR or DDDR. The fifth letter indicates whether multisite pacing is present and is rarely used. See Figures 33-3 and 33-4 for examples of ECGs with pacemaker spikes.  RESUSCITATION IN PATIENTS WITH A PERMANENT PACEMAKER If a patient who has a permanent pacemaker requires countershock, place the pads or paddles at least 8 cm from the pulse generator. The current normal positioning of the paddles—below the right clavicle and apex of the heart—is safe because most pulse generators are below the left clavicle. Alternatively, place adhesive electrodes in an anteroposte rior configuration. After countershock, interrogate the pacemaker to ensure that it is still functioning normally. Potential problems after defibrillation include: • Pacemaker inhibition due to reversion to noise mode • Deletion (reprogramming) • Circuit damage • Myocardial damage adjacent to the lead tip caused by current trans mission via the electrode to the myocardial interface Another reason that immediate return of pacing (capture) fails after defibrillation is that global myocardial ischemia increases pacing threshold. If this occurs, try transcutaneous pacing at higher delivered energy settings.  PACEMAKER COMPLICATIONS Complications for which a patient may seek care in the ED early after pacemaker insertion are listed in Table 33-6. Pacemaker Syndrome Atrioventricular synchrony and the presence of ventriculoatrial conduction are most common in the setting of VVI pacing but may occur with the DDI mode. With VVI pacing, the ven tricle stimulation results in ventricular contraction. If sinus node func tions are intact, the native sinus impulse causes contraction with closed tricuspid and mitral valves. This results in an increase in jugular and pulmonary venous pressures and may produce symptoms of congestive heart failure. Atrial distention can result in reflex vasodepressor effects mediated by the CNS. If the contribution of atrial contraction to late diastolic ventricular filling is important in maintaining an adequate cardiac output, orthostatic hypotension may occur. DDI pacing in a patient with atrioventricular block can result in pacemaker syndrome if the sinus node discharge rate exceeds the programmed rate of the pacemaker. In most instances, symptoms are mild and patients adapt to them. In about one third of these patients, symptoms are severe. Treatment usu ally requires upgrading a VVI pacemaker to a dual-chamber pacemaker or lowering the pacing rate of the VVI unit so that ventricular pacing does not occur provided intrinsic conduction occurs. If symptoms occur FIGURE 33-3. Single-lead pacemaker. Only the ventricle is paced. FIGURE 33-2. Pacing with intermittent capture. “P” indicates paced beats, and “A” indicates pacer artifact without capture. Tintinalli_Sec04_p0143-0228.indd 220 7/31/19 1:45 PM

pacing does not occur provided intrinsic conduction occurs. If symptoms occur FIGURE 33-3. Single-lead pacemaker. Only the ventricle is paced. FIGURE 33-2. Pacing with intermittent capture. “P” indicates paced beats, and “A” indicates pacer artifact without capture. Tintinalli_Sec04_p0143-0228.indd 220 7/31/19 1:45 PM CHAPTER 33: Cardiac Pacing and Implanted Defibrillation 221 in a patient paced in the DDI mode, optimizing the timing of atrial and ventricular pacing is best done by a consulting cardiologist.  PACEMAKER MALFUNCTION Pacemaker malfunction occurs in four ways: failure to sense, failure to pace, failure to capture, or overpacing or pacemaker-associated tachycardia. Failure to Sense (Undersensing) Undersensing occurs when the pacemaker cannot detect the intrinsic electrical cardiac activity. This results from lead placement in an area of the heart with poor or vari able conductivity, or if a lead is loose, dislodged, or physically broken. Sensing failure can occur if the programmed sensing threshold is set too high. With undersensing, if the pacer is set in an inhibit mode, it will fire at a set rate that is uncoordinated with the patient’s underlying cardiac cycle (Figure 33-5A). Failure to Pace (Oversensing) Oversensing occurs when the pacemaker experiences interference from electrical signals within the body (i.e., skeletal or smooth muscle myopotentials) that are not related to the normal cardiac cycle. Sources of interference may include skeletal mus cle, the diaphragm, nerve stimulators, broken pacer leads, and uncommonly, coarse atrial fibrillation. When oversensing, the pacemaker erroneously inhibits the pulse generator, and the patient may develop bradycardic rhythms (Figure 33-5B). Failure to Capture Failure to capture occurs when the pulse generator fires but the current delivered to the endocardium is too low to initiate depolarization and wavefront propagation. Dislodged or broken leads, poor cardiac conductivity due to myocardial disease (e.g., ischemia, acidosis, fibrosis), and programming problems are the most common reasons for this malfunction. Failure to capture can be intermittent (Figure 33-5C).  PACEMAKER-ASSOCIATED TACHYCARDIA Occasionally the patient with an implanted device may present with a rapid paced rhythm. This may be due to: • Rapid atrial arrhythmia triggering an upper rate response in a patient with complete heart block • Pacemaker-mediated tachycardia • Runaway pacemaker Unless preprogrammed to mode switch, pacemakers detect rapid atrial rhythms and track them, resulting in pacing at the upper rate limit. Pacemaker-mediated tachycardia can occur in a dual-chamber TABLE 33-6 Complications Seen After Pacemaker Insertion Complication Comment Infection Infection rate is <1%. Infections are more common in patients after pacemaker replacement or prolonged procedure. Early infections are most commonly caused by Staphylococcus aureus or Staphylococcus epidermidis. Pacemaker infection presents as: Local inflammation or abscess formation in the pacemaker pocket, as evidenced by pain, tenderness, or redness at the site. Skin adherence to the device, especially with discoloration of the skin over it, is highly indicative of localized infection. Do not aspirate the pocket because this can worsen the infection. If only a superficial infection is suspected, antibiotics and analgesics may be given with an early referral to the device implanter to review. Erosion of the device or lead through the skin result ing in the leads or pulse generator being exposed. Complete device and lead removal is almost always required. Cardiac device–related infective endocarditis involv ing the lead or valves. Patient may present with sepsis and positive blood culture without sign of local inflammation.

evice or lead through the skin result ing in the leads or pulse generator being exposed. Complete device and lead removal is almost always required. Cardiac device–related infective endocarditis involv ing the lead or valves. Patient may present with sepsis and positive blood culture without sign of local inflammation. Thrombophlebitis and venous obstruction Symptomatic thrombosis of the upper extremities and central veins is uncommon, possibly because of extensive venous collaterals (0.3%–3.0% of patients). Site of insertion does affect incidence. Symptoms include edema, pain, or venous engorgement of the arm ipsilateral to lead insertion. Treatment includes IV heparin therapy followed by long-term warfarin administration. Pneumothorax 1% of patients. More common with subclavian introducer technique. Hemothorax and pneumomediastinum are rare. Pacemaker syndrome 20% of patients. New or worsening of symptoms such as syncope or nearsyncope, orthostatic dizziness, exercise intolerance, dizziness, uncomfortable pulsation over the neck and abdomen, right upper quadrant pain, etc. FIGURE 33-4. Atrioventricular pacer spikes seen best in leads II and aVF. Tintinalli_Sec04_p0143-0228.indd 221 7/31/19 1:45 PM

worsening of symptoms such as syncope or nearsyncope, orthostatic dizziness, exercise intolerance, dizziness, uncomfortable pulsation over the neck and abdomen, right upper quadrant pain, etc. FIGURE 33-4. Atrioventricular pacer spikes seen best in leads II and aVF. Tintinalli_Sec04_p0143-0228.indd 221 7/31/19 1:45 PM 222 SECTION 4: Resuscitative Procedures pacemaker when a premature ventricular ectopic beat triggers a ret rogradely conducted atrial depolarization outside the atrial refractory period, then sensed by the pacemaker, initiating ventricular pacing. If this continues, it can cause an endless loop tachycardia. Rarely the pacemaker may malfunction with acceleration of pacing (runaway pacemaker). This occurs when the pulse generator discharges at a rapid rate above its preset upper limit and is most commonly associated with a battery failure or damage from external interference. Placing a magnet over the pacemaker may help in the pacemaker-mediated tachycardia or runaway pacemaker. However, interrogation of the device is usu ally required, and the device must be replaced if programming is not successful.  PACEMAKER PROGRAMMING ERRORS Pacemakers are computer-controlled devices with complex software that requires adjustment and maintenance. Reprogramming is noninvasive through radio frequencies. Occasionally, settings are inadvertently altered, or software can fail. Software changes may occur in set rates, sensing thresholds, and current outputs. IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS Implantable cardioverter-defibrillators are the treatment of choice for sudden cardiac death, reducing mortality from approximately 30% to 45% per year to <2% per year. 5 This remarkable impact, coupled with the failure (and potentially prodysrhythmic effects) of pharmacologic therapy and the increasing sophistication and miniaturization of the devices, all add to implantable cardioverter-defibrillator use. The most common cause of death in patients with an implantable cardioverterdefibrillators is congestive heart failure. An implantable cardioverter-defibrillator consists of a pulse generator, a lead system with both sensing and shocking electrodes, circuitry to analyze the cardiac rhythm and trigger defibrillation, and a power supply. In the past, insertion of these devices generally was by thora cotomy or sternotomy, and defibrillation occurred through electrodes positioned inside or outside the pericardium. In newer implantable cardioverter-defibrillators, sensing-pacing-defibrillation electrodes are inserted transvenously, and the control device is placed subcutaneously in the subpectoral region or in an abdominal pocket. Newer implantable cardioverter-defibrillators are better at discriminating supraventricular tachycardia and are capable of a variety of responses to ventricular tachycardia and fibrillation. Most device programs follow a tiered approach to ventricular dysrhythmias: antitachycardia pacing, lowenergy cardioversion, and finally defibrillation. Depending on the frequency of discharge and whether the pacemaker function is used, the latest implantable cardioverter-defibrillators have a projected life span of approximately 6 to 9 years, depending on whether they are single- or dual-chamber devices. Some newer devices may be implanted subcutaneously. These devices do not have pacing function and reside in the left axillary region, with the lead tunneled to the left sternal region. In such patients, place the defibrillation pad in the anterior-posterior region.  ED EVALUATION The most common reason a patient with an implantable cardioverterdefibrillator comes to the ED is evaluation after a delivered shock. Causes of inappropriate shock delivery are listed in Table 33-7.

the left sternal region. In such patients, place the defibrillation pad in the anterior-posterior region.  ED EVALUATION The most common reason a patient with an implantable cardioverterdefibrillator comes to the ED is evaluation after a delivered shock. Causes of inappropriate shock delivery are listed in Table 33-7. Determine the number of shocks delivered, the activity of the patient at the time of shock, and any prodromal symptoms or postshock trauma. Ask about any recent changes in rhythm-directed drug therapy. Focus the physical examination on the vital signs, the cardiovascular status, the generator pocket, and evidence of incidental trauma. Place each patient on a continuous ECG monitor, and obtain a 12-lead ECG; any shockrelated ST-segment elevations or depressions should resolve within 15 minutes; ongoing changes suggest new ischemia. Examine a chest radiograph for electrode migration, displacement, or fracture. Obtain rhythm-related drug levels and serum electrolyte levels. 6,7 If the patient is receiving repeated inappropriate shocks for a nonlethal rhythm, temporarily deactivate the implantable cardioverterdefibrillator by placing a magnet over the device. Defibrillation can be reenabled by removing the magnet. Have a cardiologist evaluate all patients with implantable cardioverter-defibrillators after exposure to a magnet. FIGURE 33-5. Various pacemaker malfunctions. A. Undersensing. B. Oversensing. C. Failure to capture. TABLE 33-7 Potential Causes of Inappropriate Implantable Cardioverter- Defibrillator (ICD) Shock Delivery •  False  sensing •  Supraventricular  tachycardia with rapid ventricular response •  Muscular  activity (shivering, diaphragmatic contraction) •  Extraneous  source (tapping of chest wall, vibrations, pacer spikes) •  Sensing  T waves as QRS complex (double counting) •  Sensing  lead fracture or migration •  Unsustained  tachyarrhythmia •  ICD–pacemaker  interactions •  Component  failure Tintinalli_Sec04_p0143-0228.indd 222 7/31/19 1:45 PM