Đang tải... (xem toàn văn)
(BQ) Part 2 book Tarascon pocket cardiology presents the following contents: Cardiovascular therapeutics (coronary revascularization, pacemaker therapy, cardiac resynchronization for heart failure, implantable defibrillator therapy,...), supplement - bedside procedures (central venous catheterization, arterial line placement, right heart catheterization,...).
Section III Cardiovascular Therapeutics 15161_CH27_Final.indd 232 02/12/11 2:32 PM 27 ■ Coronary Revascularization60 Introduction Coronary revascularization is the process of restoring blood flow (oxygen and nutrients) to the essential myocardium The method of and indications for coronary revascularization are complex and often debated topics The basic goals of coronary revascularization include the following three items: (1) Improve clinical symptoms (2) Improve long-term survival (3) Attempt to decrease the incidence of nonfatal outcomes such as myocardial infarction, congestive heart failure, and malignant arrhythmias There are three common methods for approaching coronary revascularization: • Percutaneous coronary intervention (PCI) is a generic term referring to any therapeutic procedure directed at treating the narrowed (stenotic) segments in coronary arteries using a combination of balloon angioplasty and stent implantation, coronary atherectomy, or thrombectomy • Coronary artery bypass surgery (CABG) is a surgical procedure directed at bypassing the stenotic coronary artery segments using vessels harvested from other places in the body (lower extremity veins or thoracic/ abdominal arterial grafts) • Fibrinolysis in the setting of ST-Elevation myocardial infarction (STEMI) Percutaneous Coronary Intervention • PCI involves repair of the artery by advancing equipment over a coronary guide wire that has been advanced past a blockage in the artery • PTCA (percutanous transluminal coronary intervention) angioplasty is when balloon inflation crushes the coronary plaque against the walls of the vessel, restoring blood flow to the downstream myocardium • Advanced adjunctive techniques are utilized for specific clinical scenarios and lesions subsets Such devices include: •• Rotational (diamond tipped drill) or laser atherectomy for calcified, noncompliant vessels •• Manual or mechanical thrombectomy for large thrombus burden •• Protection devices, utilized in saphenous vein grafts, to capture debris liberated during PCI, avoiding embolization downstream ❍❍ No benefit demonstrated in native coronary arteries 233 15161_CH27_Final.indd 233 02/12/11 2:32 PM 234Coronary Revascularization • PTCA is now almost always accompanied by the implantation of a coronary stent •• Coronary stents are small (2.0–5.0 mm) metallic tubes that are mounted on balloons and advanced to the blockage over the coronary guidewire •• When the balloon is inflated, the stent is expanded and deployed against the wall of the vessel •• The stent creates a larger lumen, avoids abrupt closure related to vessel dissection and acts as a mechanical scaffold to prop open the vessel •• Compared with angioplasty alone, stents reduce restenosis, recurrent narrowing of the artery, abrupt closure, and early thrombosis of the vessel due to vessel dissection after angioplasty •• Restenosis still occurs with stents and is due to slow neointimal proliferation causing reblockage with scar tissue •• Stent thrombosis is an entity distinct from restenosis where there is abrupt clot formation within the stent The latter most often presents as a recurrence of chest pain without infarction, while the stent thrombosis is generally an acute infarction with significant morbidity and associated mortality • Uncoated bare-metal stents (BMS) were the first stents •• Restenosis rates were 10–30% or more with these • Stents coated with antiproliferative drugs (everolimus, sirolimus, paclitaxel, biolimus A9, and zotarolimus) were developed and reduced restenosis by approximately 60% or more •• Drug-eluting stents (DES) suppress restenosis by retarding neointimal proliferation by locally modulating healing, immune, and inflammatory responses to the stent •• Though DES have reduced restenosis and the need for repeat revascularization, one drawback has been the infrequent occurrence (≈1/400) of “late stent thrombosis” occurring 12 months or more after initial stent implantation • Plaque characterization and angiographically obscured or intermediate lesions can be characterized with intravascular ultrasound (IVUS) or optical coherence tomography (OCT) • The hemodynamic significance of angiographically obscured or intermediate lesions can be assessed by measuring the fractional flow reserve (FFR) •• FFR is assessed using a special wire with a pressure transducer on the end ❍❍ After the wire is advanced past the lesion of interest, induction of maximal hyperemia with adenosine administration is performed, and the pressure distal to the stenosis is compared to aortic pressure ❍❍ Hyperemia with adenosine induces coronary steal in hemodynamically significant lesions by redirecting blood flow away from arteries 15161_CH27_Final.indd 234 02/12/11 2:32 PM Recommended Guidelines for Revascularization 235 where maximal vasodilation is present at baseline to areas where vasodilation is not maximal at baseline •• FFR–guided revascularization compared with angiographically guided revascularization has been associated with improved outcomes •• An FFR of < 0.75–0.80 is deemed hemodynamically significant Recommended Guidelines for Revascularization Unstable ischemic disease: • PCI has been shown to improve clinical outcomes during STEMI (death, recurrent myocardial infarction) and moderate- and high-risk UA/ NSTEMI (death, myocardial infarction, urgent revascularization) • Controversy and outcomes are mixed for: •• STEMI patients presenting > 12 hours post-symptom onset without ongoing symptoms of ischemic/clinical instability •• Revascularization of non-culprit arteries before hospital discharge in patients who are clinically stable, without recurrent or provocable ischemia, and normal LVEF •• After successful treatment of the culprit artery by PCI/fibrinolysis, if the risk of revascularization exceeds the estimated risk of the infarction or if significant comorbid conditions make survival unlikely despite revascularization Stable ischemic disease in patients without prior CABG: • See Chapter 11, Ischemic Heart Disease and Stable Angina, pp 73 • For stable angina, revascularization is indicated to improve symptoms if there is failure of maximal anti-ischemic medical therapy •• Failure is defined as at least two classes of therapies to reduce anginal symptoms •• Patients with intermediate- or high-risk stress test findings (because a large amount of myocardium is in jeopardy and/or LM or 3-vessel coronary disease may be present) should be referred for angiography and/or revascularization (see Chapter 5, ECG Exercise Stress Testing, pp 30): ❍❍ Low-risk stress test findings: estimated cardiac mortality 3% per year • Variable appropriateness guidelines (appropriate/uncertain or inappropriate) exist for numerous combinations of CAD vessel involvement, angina severity, and extent of medical therapy •• This section focuses on generally appropriate criteria as outlined in the guidelines for selected, common scenarios 15161_CH27_Final.indd 235 02/12/11 2:32 PM 236Coronary Revascularization • Revascularization is appropriate in patients who have 1-, 2-, or, 3-vessel disease with or without involvement of the proximal left anterior descending (without left main stenosis), CCS III/IV angina, and lowrisk stress test findings • Revascularization is appropriate in asymptomatic patients with 1- or 2-vessel disease with proximal LAD involvement (without left main stenosis) on appropriate medical therapy; patients with-3 vessel disease with no proximal LAD involvement and intermediate -or high-risk stress test findings are also candidates for revascularization • Revascularization is appropriate in patients with intermediate stress test findings who have CCS I–IV on maximal medical therapy with 1-, 2-, or 3-vessel disease, with or without proximal LAD involvement; patients with CCS III–IV symptoms with 1-, 2-, or 3-vessel disease with or without proximal LAD involvement and the intermediate-risk stress test findings are also candidates • Revascularization is appropriate in patients with high risk stress test findings and CCS I-IV symptoms on no/minimum/maximal medical therapy with 1/2/3 vessel with or without proximal LAD involvement Among patients with advanced coronary artery disease, appropriateness for PCI and CABG are illustrated by the guidelines presented in Table 27-1: • For patients where revascularization is necessary, CABG is appropriate in all of the advanced CAD clinical scenarios shown in Table 27-1 • PCI is appropriate only in those patients with 2-vessel CAD and proximal LAD involvement and uncertain in patients with 3-vessel disease or those who are not candidates for CABG • CABG is clearly indicated in those patients with left main stenosis and/ or LM stenosis with multi-vessel CAD • The revascularization guidelines in Table 27-1 are a topic of much debate and paradigms continue to evolve For example, many patients with isolated left main coronary artery disease can be safely treated with PCI table 27-1. Acute Coronary Syndromes CABG No DM, nl EF DM vessel CAD + prox LAD A A vessel CAD A A Isolated LM A A LM stenosis + more CAD A A Low EF A A A A PCI No DM, nl EF A U I I DM A U I I Low EF A U I I A – appropriate, U – uncertain, I – Inappropriate Source: Elsevier Adapted from ACCF/AHA Coronary Revascularization guidelines J Am Coll Cardiol 2009;53(6):530-553 15161_CH27_Final.indd 236 02/12/11 2:32 PM Recommended Guidelines for Revascularization 237 • Randomized trials of PCI with DES vs CABG suggest improved outcomes with CABG for patients with multi-vessel disease who have intermediateor high-risk anatomy PCI may be acceptable for those with low-risk anatomy (SYNTAX Trial61) • Decisions are individualized based on individual patient circumstance (e.g., surgical risk and feasibility, anatomic risk for PCI, comorbid conditions, patient preference) 15161_CH27_Final.indd 237 02/12/11 2:32 PM 28 ■ Pacemaker Therapy62 Introduction The pacemaker is an artificial device that augments heart rate by electrical stimulation of the myocardium in response to bradycardia Bradycardia requiring pacemaker therapy is usually symptomatic and due to sinus node dysfunction and/or advanced pathology of the conduction system, such as complete heart block The pacemaker does not directly treat tachycardia—patients often have this misconception—and care must be taken to distinguish pacemakers from implanted cardioverter-defibrillators (ICDs), which primarily treat ventricular tachyarrhythmias The fact that all ICDs possess pacemaker functionality in the event of bradycardia may be a source of such confusion Also, in the inpatient setting, pacemakers are either temporary or permanent, whereas in the outpatient setting, all pacemakers are permanent This chapter covers both types of pacemakers Indications for Permanent Pacemaker (PPM) Table 28-1 describes how the guidelines list indications for a therapy such as pacemakers • Sinus node dysfunction (SND) refers to abnormalities in atrial impulse generation from the sinus node SND associated with symptoms, such as fatigue, lightheadedness, or syncope, constitutes a strong indication for PPM implantation Symptomatic SND requiring a PPM should reflect one or more of the following characteristics: •• Sinus rhythm with pauses ≥ seconds •• Awake heart rate < 40 bpm Table 28-1. Classes of Indication Used by the ACC/AHA/HRS 2008 Guidelines for Device Based Therapy ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy (1) used most up to date clinical data to stratify a comprehensive set of indications for PPM implantation: • Class I: PPM should be implanted, as benefit greatly outweighs risk • Class IIa: PPM is reasonable, as benefit outweighs risk • Class IIb: PPM may be considered, as benefit is at least greater than or perhaps equal to risk • Class III: PPM should not be implanted, as benefit is less than or at best equal to risk For the sake of brevity, this section will focus on the most common indications for PPM implantation based on these guidelines 238 15161_CH28_Final.indd 238 02/12/11 2:32 PM Indications for Temporary Pacing 239 •• Chronotropic incompetence—inability to intrinsically increase heart rate in response to physical stress or exertion •• Sinus bradycardia with the concomitant necessity for drugs which lower heart rate, such as beta-blockers in patients with paroxysmal tachycardias (e.g., rapid atrial fibrillation, atrial flutter) •• Postoperative or post-myocardial infarction SND which remains persistent and fails to show reasonable recovery • Acquired AV node or conduction system dysfunction—3rd-degree or advanced 2nd-degree block regardless of anatomic level—also warrants a PPM in any one of the following circumstances: •• Associated symptoms, such as fatigue, lightheadedness, or syncope •• Sinus rhythm with pauses ≥ seconds •• Atrial fibrillation with pauses ≥ 5.0 seconds •• 3rd-degree AV block or advanced 2nd-degree AV block at any anatomic level and arrhythmias requiring medications which themselves cause symptomatic bradycardia •• Ventricular arrhythmias induced by AV node dysfunction •• Advanced AV node or conduction system dysfunction with the concomitant need for drugs which may worsen conduction, such as beta-blockers in CAD •• Postoperative or post-myocardial infarction 3rd-degree or advanced 2nd-degree AV block which remains persistent and fails to show reasonable recovery • Carotid sinus hypersensitivity syndrome consists of recurrent syncope caused by stimulation of the carotid body, which lies in the carotid sinus at the bifurcation of the carotid artery Such stimulation may occur with tight neckwear, head turning, or shaving If carotid massage produces a pause of ≥ seconds in the context of this syndrome, then a PPM is indicated • Cardiac resynchronization therapy (CRT) (see chapter 29) is pacing the free wall of the left ventricle in order to overcome delayed activation of a portion of the left ventricle (dyssynchrony) Dyssynchrony can be seen by imaging techniques such as echocardiography; however prolonged QRS duration (typically with left bundle branch block) is also indicative of ventricular conduction delay Pacing from the septal side of the LV and free wall reduces dyssynchrony, increases ventricular efficiency, and reduces congestive heart failure •• CRT is indicated in patients with an LVEF ≤ 35% and QRS ≥ 120 ms and New York Heart Association Class III or IV congestive heart failure Indications for Temporary Pacing • Profound bradycardia (or asystole) causing acute hemodynamic instability •• Frequently used as a “bridge” to permanent pacemaker therapy (unless the cause of bradycardia is transient or reversible) ❍❍ Awaiting resolution of issues preventing permanent pacemaker implantation, such as anticoagulation, infectious processes 15161_CH28_Final.indd 239 02/12/11 2:32 PM 240 Pacemaker Therapy Pacemaker Basics • Permanent implantable pacemakers Pacemakers consist of the pulse generator (“generator”), which contains circuitry, and a battery, and leads The generator has sockets to receive the leads and set screws to secure the lead(s) The leads are insulated wires with exposed electrodes designed to contact the myocardium for sensing and pacing Leads may be unipolar or bipolar for sensing and pacing (Unipolar lead pacing requires that the case of the generator act as the second electrode.) •• Transvenous permanent pacemaker ❍❍ Leads are implanted via an accessed vein (typically the subclavian, axillary, or cephalic vein) ❍❍ The generator is connected to the lead(s) and placed in a subcutaneous (or submuscular) pocket •• Epicardial permanent pacemaker ❍❍ Leads are secured to the epicardium and tunneled to the generator pocket ❍❍ The generator is connected to the leads and placed in a pocket, which may be abdominal or pectoral • Temporary pacing •• Transcutaneous (external) pacing utilizes large pad-electrodes (which can also be used for defibrillation) ❍❍ Noninvasive and can be initiated quickly ❍❍ Pacing impulses capture skeletal muscle as well as the heart; very painful •• Epicardial temporary pacing leads are frequently placed during cardiac surgery The leads can be connected to a temporary generator; programming is readily adjustable Leads can be removed many days after surgery •• Percutaneous, transvenous pacing requires a lead to be positioned from a venous access site (femoral, subclavian, or internal jugular vein) and a temporary generator is used ❍❍ For longer term temporary pacing, a lead designed to be permanent can be implanted percutaneously, connected to a generator remaining outside the body (which can be taped to the skin) • Pacing sites: Endocardial leads are usually placed in venous (rightsided) chambers to minimize the risk of thromboembolism •• Single-chamber pacing usually utilizes a lead placed in the right ventricle ❍❍ Ventricular-only pacemakers are used in patients with permanent atrial fibrillation with no plans for return to sinus rhythm ❍❍ Single chamber atrial pacing can be used for patients with sinus node dysfunction, but there is a risk of bradycardia/asystole if the patient subsequently develops heart block 15161_CH28_Final.indd 240 02/12/11 2:32 PM Classification of Most Common PPM Modes 241 •• Dual chamber: Leads are placed in the right atrium (RA) and right ventricle (RV) ❍❍ Classically RV leads are placed in the RV apex, though active fixation (screw-type) leads may be implanted along the RV septum and in the RV outflow tract ❍❍ RA leads are conventionally placed in the RA appendage, though the appendage is usually amputated in cardiac surgery cases requiring cardiopulmonary bypass Other RA sites can be effective and can be chosen by checking pacing parameters at other RA sites ❍❍ Biventricular (resynchronization) pacing requires an additional lead to pace the left ventricle Transvenous leads are guided to a left ventricular site via the coronary sinus and the left ventricular veins Classification of Most Common PPM Modes The NASPE/BPEG (North American Society for Pacing and Electrophysiology/ British Pacing and Electrophysiology Group) established a code in 1987 to describe pacing modes (Table 28-2): • First letter: Pacing which chambers—that is, A = right atrium, V = R ventricle, D = both R atrium and R ventricle • Second letter: Sensing from which chambers—that is, A, V, and D • Third letter: Manner of responding to sensing—that is, = none, T = triggered (a sensed event triggers a pacing stimulus), I = inhibited (a sensed event inhibits a pacing stimulus), and D = dual (an event in one chamber inhibits stimulus in that chamber but triggers a stimulus in the other chamber, after an appropriate delay, and if not inhibited) • Fourth letter (optional): signifies additional features For practical purposes, the only letter seen here is “R” for rate responsiveness (the lower rate limit rises when a device sensor perceives activity) If rate responsiveness is not used, the fourth position is usually blank Table 28-2. The NASPE/BPEG Pacing Code Sensed Response to Paced chamber Chamber Sensed Events A (Atrial) A (Atrial) I (Inhibited) V (Ventricular) V (Ventricular) T (Triggered) D (Dual) D (Dual) D (Inhibited and O (No pacing) O (No sensing) Triggered by event in the other chamber) O (No response to sensed events) 15161_CH28_Final.indd 241 Rate Responsiveness R (Rate responsiveness on; if no rate responsiveness, this position usually left blank) 02/12/11 2:32 PM 372 shock—Continued right heart catheterization for, 308, 309 shock therapy direct current See direct current (DC) cardioversion ICDs for See implantable cardioverterdefibrillators (ICDs) shunts/shunting, in congenital heart disease cardiac catheterization of, 49, 308 cardiac magnetic resonance imaging of, 47 cyanotic, 186 left-to-right, 183, 184, 308 restrictive vs nonrestrictive VSDs and, 184 right-to-left, 181, 187, 197 single ventricle and, 194, 195 Tetralogy of Fallot and, 187, 188f transposition of the great arteries and, 189, 190f, 191, 193 sick sinus syndrome (SSS), 146, 149, 270 signs and symptoms See also clinical presentations of acute coronary syndromes, 82 of acute decompensated heart failure, 107 of aortic regurgitation, 128–129 of cardiovascular disease, 5–6, of chronic stable angina, 76 of coarctation of the aorta, 186 of constrictive pericarditis, 207 of infectious endocarditis, 141–142 15161_IDXX_Final.indd 372 Index of mitral regurgitation, 135–136, 137 of mitral stenosis, 131, 132 of pericarditis, 203 of tricuspid regurgitation, 138 of valvular heart disease, 123–124 single coronary artery, 200 single ventricle, 194–197 clinical presentations of, 195 definitions for, 194–195 Fontan surgery for, 195, 196–197 Glenn shunt for, 194, 195 management of, 196–197 Norwood procedure for, 194–195 physical examination for, 195–196 single-chamber pacing, 240 single-photon emission computed tomography myocardial perfusion imaging, 42–45 sinoatrial conduction time (SACT), 55 sinus node electrophysiology studies of, 53, 55, 57 sinus node dysfunction (SND), 19, 146 pacemakers for, 238–239, 240 syncope related to, 170 sinus node recovery time (SNRT), 55 corrected, 55 sinus of Valsalva (SOV) anomalies of, 199, 200 ruptured aneurysm of, sinus rhythm, 21 atrial fibrillation restoration to, 265–266, 270 in AV reentrant tachycardia, 155–156, 156f sinus tachycardia caused by pulmonary embolism, 29 situs inversus, 13, 29 6-minute walk test for pulmonary hypertension, 229 smoking risk assessment of, 65–66 smoking cessation drug therapies for, 71–72 general principles of, 70–71 sodium channel blockade atrial fibrillation and, 267 sodium nitroprusside, 106t for acute decompensated heart failure, 109 for aortic dissection, 218 for chronic heart failure, 113 for mitral regurgitation, 136 soft tissue structure attenuation in cardiac radionuclide imaging, 44–45 sotalol, 106t, 161t, 166–167 for atrial fibrillation, 267, 268 spinal cord stimulation for chronic stable angina, 79 spironolactone, 67, 114 “split His,” 56 “square root” sign, 207, 310 SSS (sick sinus syndrome), 146, 149, 270 ST elevation myocardial infarction (STEMI), 82 ACE inhibitors and, 68 angiography for, 86–87 antiplatelet therapy for, 84–85 antithrombotic therapy for, 86 chest pain relief for, 84 diagnostic testing for, 48, 82–83 general therapeutic measures for, 84 ischemic heart disease risk for, 75 parenteral medication guidelines for, 99t–106t 02/12/11 3:09 PM Index post-hospital discharge care for, 88 revascularization for, 86–87, 87f, 233, 235 thrombolytic therapy for, 96t, 97t, 98t treatment goals for, 84 treatment of, 84–86 ST segment, 11f, 12 in acute coronary syndromes, 82–83 conformations of, 24 pericarditis impact on, 28 in rhythm interpretation, 21 in stable angina, 77, 80 widened QRS complex and, 24 ST segment depression, 24, 28 in exercise stress testing protocol, 34 ST segment elevation, 24, 28 in exercise stress testing protocol, 34 stable angina See chronic stable angina Stanford classification of aortic dissection, 216 staphylococci causing infectious endocarditis, 140, 142, 143, 144 causing post-pacemaker implantation infections, 246 STAR plan for smoking cessation, 71 stasis of blood atrial fibrillation and, 264 statins for carotid disease, 225 for lipid management, 69–70 steal phenomenon coronary, in coronary revascularization, 234–235 coronary-subclavian, 211 subclavian, 211 15161_IDXX_Final.indd 373 373 stenosis aortic valve, 124–127 of carotid artery, 224, 224t of coronary arteries See coronary stenosis heart sound abnormalities with, 8, 9, 9t, 10t of mesenteric artery, 222 mitral valve, 130–132 pulmonic valve, 8, 138 of renal artery, 213, 214, 215 of subclavian artery, 211 syncope related to, 170, 171 tricuspid valve, 9, 138 in valvular heart disease, 123 stents/stenting for carotid disease, 226 for coarctation of the aorta, 186 for coronary artery disease, 46, 85, 88, 234 for peripheral arterial disease, 210 for renal artery disease, 215 steroids for pericarditis, 204–205 stimulus artifacts in paced rhythms, 28 stool softeners, 231 streptococci causing infectious endocarditis, 140, 142, 143 streptokinase, 106t absolute contraindications to, 98t for STEMI, 96t, 97t, 98t stress testing exercise See exercise stress testing pharmacologic See pharmacologic stress testing stroke cardiac disease and, 223 carotid disease and, 223–224, 225, 226 ischemic, 325 prevention of, stroke risk, with atrial fibrillation anticoagulation therapy for, 264–266, 265t CHA2DS2-VASc scoring of, 265, 266t CHADS2 scoring of, 264–265, 265t sinus rhythm and, 265–266 stroke volume (SV), 307 in valvular heart disease, 127, 134 subarachnoid hemorrhage, 326 subclavian arteries catheterization and angiography of, 52 peripheral arterial disease of, 211 subclavian steal phenomenon, 211 subclavian vein catheterization infraclavicular approach to, 296, 297f supraclavicular approach to, 297 subcutaneous devices for implantable cardioverterdefibrillators, 253 substrate in sudden cardiac death, 176–177 substrate mapping with ablation therapies, 159, 160, 272 in electrophysiology studies, 53, 54, 56, 57 subxiphoid approach to pericardiocentesis, 317, 318f sudden cardiac arrest (SCA), 6, 176, 178 sudden cardiac death (SCD), 176–180 conditions contributing to, 75, 81, 122, 189 epidemiology of, 176 with hypertrophic cardiomyopathy, 119–120 02/12/11 3:09 PM 374 sudden cardiac death (SCD)—Continued implantable cardioverterdefibrillators for, 253, 254, 257 introduction to, 6, 176 prevention of, 159, 160, 179–180 substrate and, 176–177 therapy for, 178 triggers of, 178 with ventricular tachyarrhythmias, 159, 160, 169, 176 sudden death syncope causing, 168, 172, 174 superior sinus venosus atrial septal defect, 181, 182f superior vena cava (SVC) obstruction of, in single ventricle physiology, 194, 195 supportive therapies for acute decompensated heart failure, 108 supraventricular tachycardias (SVTs), 151–156 atrial, 151–156, 151f, 152f ECG interpretation of, 5, 20, 157–159, 158f implantable cardioverterdefibrillator detection of, 259, 261, 262f paroxysmal See paroxysmal supraventricular tachycardias (PSVTs) syncope related to, 169 therapies for, 4, 159 wide complex tachycardia vs., 330, 331 surgery for abdominal aortic aneurysm, 220 for aortic dissection, 218, 219 for atrial fibrillation, 268, 269 15161_IDXX_Final.indd 374 Index bacterial endocarditis prophylaxis for, 201 emergency, perioperative evaluation for, 62, 63f implantable cardioverterdefibrillators management during, 263 risk stratification for See preoperative risk stratification for thoracic aortic aneurysm, 221 surgery-specific risk in perioperative evaluation, 48, 60–64, 61t, 62f, 63f surgical ablation for atrial fibrillation, 269 electrocautery, effect on pacemakers, 243 surgical repair of atrial septal defects, 183 of atrioventricular septal defects, 185 of coarctation of the aorta, 186 of Ebstein’s anomaly, 198 of Eisenmenger physiology, 197, 198 of single ventricle, 194–195 of Tetralogy of Fallot, 187, 189 of transposition of the great arteries, 191, 192f, 193 of ventricular septal defects, 184 surgical revascularization for coronary artery disease See coronary artery bypass grafts (CABG) for renal artery disease, 215 surveillance for abdominal aortic aneurysm, 220 SV See stroke volume (SV) Swan-Ganz catheter, 229 See also right heart catheterization S-wave, 11f, 12 in paced rhythms, 28 pseudo, in AV node reentrant tachycardia, 154f in rhythm interpretation, 22, 25, 29 in wide complex tachycardia, 331 sympathomimetic crisis, drug-induced, 326 symptoms of cardiovascular disease, 4–5 disease-specific See signs and symptoms synchronized cardioversion, 159, 314–315 by implantable cardioverterdefibrillators, 260 for ventricular tachycardias, 159 syncope, 168–175 with aortic stenosis, 125 as cardiac disease sign, cardiac radionuclide imaging for, 43 cardiovascular disease causing, 169–171 in carotid sinus hypersensitivity syndrome, 239 definition of, 168 diagnostic problems of, 168 evaluation of, 171–175 implantable cardioverterdefibrillators for, 254, 257 incidence of, 168 neurocardiogenic, 169 neurologic disease causing, 171 orthostatic, 169, 171–172, 174, 175 possible causes of, 168–171 treatment of, 175 02/12/11 3:09 PM Index syndromes of cardiovascular disease, 5–6 systemic circulation in transposition of the great arteries, 189, 190f, 191 systemic vascular resistance (SVR), 306t, 307 in chronic heart failure, 110 in shock, 329t systolic anterior motion (SAM) in hypertrophic cardiomyopathy, 119 systolic blood pressure (SBP) in aortic dissection, 217, 218, 219 aortic regurgitation effect on, 128–129, 130 mitral regurgitation effect on, 133, 135 risk assessment of, 65–66 systolic dysfunction exercise stress testing for, 33, 34 left ventricular See left ventricular dysfunction systolic ejection murmur in aortic regurgitation, 129 systolic murmurs, 9, 9t systolic outflow murmur in hypertrophic cardiomyopathy, 119–120 tachy-brady arrhythmias, 146, 172, 176 tachycardia, 150–167 antiarrhythmic drugs for, 160, 161t, 162–167 atrial See atrial tachycardia cardiac computerized tomography and, 46 classification of, 151 15161_IDXX_Final.indd 375 375 in ECG interpretation, 19–20, 29, 157–159, 158f electrophysiology studies of, 53, 54, 56–57 mechanisms of, 150–151 with mitral regurgitation, 135, 136 with mitral stenosis, 131, 132 narrow complex, 157–158 supraventricular See supraventricular tachycardias (SVTs) syncope related to, 169–170, 172, 173 ventricular See ventricular tachycardia (VT) wide complex, 158–159, 158f tamponade See cardiac tamponade; pericardial tamponade TAVI (transcatheter aortic valve implantation) for aortic stenosis, 126 TCPC (total cavopulmonary connection) for single ventricle, 195 technetium in myocardial perfusion imaging, 42 in stress testing, 35 TEE See transesophageal echocardiography (TEE) telemetry ECG recording standards for, 16 temporary pacing, 240 for bradyarrhythmias, 149 indications for, 238, 239 urgent, 312–313 tenecteplase, 106t for STEMI, 96t, 97t, 98t Tetralogy of Fallot (ToF) clinical presentations of, 187 definitions for, 187, 188f management of, 189 TGA See transposition of the great arteries (TGA) thallium in myocardial perfusion imaging, 42 in stress testing, 35 theophylline for bradyarrhythmias, 149 therapy(ies) goals of, 3–4 introduction to, 3, thermodilution method for hemodynamic measurements, 306 thiazide diuretics, 68–69, 114 thienopyridines for acute coronary syndromes, 84–85 third-degree AV block mechanisms of, 148, 149, 149f pacemakers for, 239 thoracic aortic aneurysm, 221 thoracic outlet syndrome, 213 3-D maps in electrophysiology studies, 54 thrombectomy with percutaneous coronary intervention, 233 thrombin inhibitors, direct for acute coronary syndromes, 86 for atrial fibrillation, 86 thromboangiitis obliterans, 211–212 thrombocytopenia transesophageal echocardiography and, 42 thromboembolism atrial fibrillation risk for, 264, 264–266, 269–270 atrial flutter risk for, 270 peripartum cardiomyopathy and, 122 single ventricle and, 197 02/12/11 3:09 PM 376 thromboendarterectomy for pulmonary hypertension, 230 thrombolysis in myocardial infarction (TIMI) risk score for acute coronary syndromes, 83, 93t thrombolytic therapy, for acute coronary syndromes, 86–87, 87f See also fibrinolysis absolute contraindications to, 98t for myocardial infarction, 98t STEMI, 96t, 97t, 98t thrombosis/thrombus in acute coronary syndromes, 83, 86 congenital heart disease and, 198, 200 in coronary stents, 85, 88, 234 in infectious endocarditis, 139 left atrial, with atrial fibrillation, 266, 269 in peripheral arterial disease, 211 ticagrelor, 85, 100t tilt table testing, 174 tirofiban, 106t for acute coronary syndromes, 89f, 93t, 96t ToF See Tetralogy of Fallot (ToF) torsades de pointes, 27, 150, 157, 170, 178 total cavopulmonary connection (TCPC) for single ventricle, 195 transcatheter aortic valve implantation (TAVI) for aortic stenosis, 126 transcutaneous (external) pacing, 240 for myocardial infarction, 99t urgent, 312–313 15161_IDXX_Final.indd 376 Index transcutaneous patches for myocardial infarction, 99t transesophageal echocardiography (TEE), 40–42 for infectious endocarditis, 141, 142 for left atrial thrombus, with atrial fibrillation, 266, 269 limitations of, 41–42 utility of, 41 transischemic attack (TIA), 223, 225 transmembrane electrolyte imbalances tachyarrhythmias associated with, 150, 177 transmembrane phenomenon, 11 trans-myocardial laser revascularization (TMR), 79 transplantations See heart transplantation; lung transplantation transposition of the great arteries (TGA), 189 clinical presentations of, 193 complete, 189, 190f, 191 congenitally corrected, 191 management of, 193–194 therapeutic procedures for, 191–194 transthoracic echocardiography (TTE), 37–40 for infectious endocarditis, 141 limitations of, 40 standard views of, 37–40 utility of, 37–40 transvenous implantation of implantable cardioverterdefibrillators, 257–258 of pacemakers, permanent vs temporary, 240, 244–245 Traube’s sign, 129 treprostinil, 231 triangle of Koch in AV node reentrant tachycardia, 153 tricuspid atresia, 194 tricuspid regurgitation (TR), 137–138 in dilated cardiomyopathy, 118 heart murmurs with, 9, 9t jugular venous pulsation with, tricuspid stenosis (TS), 9, 138 tricuspid valve in atrial flutter, 270 in AV node reentrant tachycardia, 153 Ebstein’s anomaly of, 198, 199f heart sounds of, transesophageal echocardiography assessment of, 41 trifascicular blocks, 27, 170 trigeminy, 26 trigger event in sudden cardiac death, 176, 178 in tachyarrhythmias, 150, 156, 157, 272 triglyceride level risk assessment of, 66 risk management of, 69–70 troponins in acute coronary syndromes, 83, 87, 90t cardiac radionuclide imaging and, 42–43 in myocardial infarction, 90t in pericarditis, 204 troubleshooting of implantable cardioverterdefibrillators, 261–263 of pacemakers, 243–244 02/12/11 3:09 PM Index TTE See transthoracic echocardiography (TTE) T-wave, 11f, 12 conformations of, 24–25 implantable cardioverterdefibrillators sensing of, 258 in rhythm interpretation, 21, 24, 29 T-wave inversion, 24–25 2:1 AV block, 148–149, 148f UA See unstable angina (UA) ulcer, penetrating aortic, 219 ultrafiltration for acute decompensated heart failure, 109 ultrasound imaging for abdominal aortic aneurysm, 220 for carotid disease, 224–225, 224t duplex, for mesenteric arterial disease, 222 intravascular, for plaque characterization, 234 renal, for renal artery disease, 214 transesophageal, of heart, 40–42 transthoracic, of heart, 37–40 unipolar surface electrograms, 12–13 in electrophysiology studies, 55, 58f University of Washington criteria for carotid ultrasound assessment, 224 “unroofed coronary sinus,” 181, 182f unstable angina (UA), 76, 82 angiography for, 87, 88 anti-ischemic therapies for, based on ischemia classifications, 91t–92t 15161_IDXX_Final.indd 377 377 antiplatelet therapy for, 84–85 antithrombotic therapy for, 86 chest pain relief for, 84 conservative therapy for, 88, 89f, 91t–92t, 93t diagnostic testing for, 48, 83 general therapeutic measures for, 84 hypertensive emergency with, 326 parenteral medication guidelines for, 99t–106t as perioperative risk, 59, 61, 62, 63f, 64 post-hospital discharge care for, 88 revascularization for, 87–88, 87f, 235 risk stratification for, 83, 88 treatment goals for, 84 treatment of, 84–88, 93t urgent temporary pacing, 312–313 urgent therapy for atrial fibrillation, 269–270 for sudden cardiac death, 178, 179 V1-V6 leads, of ECG, 13, 15 in electrophysiology studies, 58f in rhythm interpretation, 19, 21–22, 24, 25, 29 in standard 12-lead format, 16, 17f, 18 for wide complex tachycardia, 331 V-A dissociation implantable cardioverterdefibrillators detection of, 260 QRS morphology in, 331 wide complex tachycardia vs., 330–331 Valsalva maneuver effect on 2:1 AV block, 149 valve implantation for aortic stenosis, 126 valve orifice area right heart catheterization calculation of, 308 valve replacement for aortic regurgitation, 130 for aortic stenosis, 125–126 bioprosthetic vs mechanical valves for, 125, 130, 138, 139, 144 complications of, syncope related to, 170 for infective endocarditis, 143 for mitral regurgitation, 135–136 for mitral stenosis, 131 for Tetralogy of Fallot, 189 for tricuspid regurgitation, 138 valvular heart disease, 123–138 aortic, 124–130 cardiac magnetic resonance imaging of, 47 chronic stable angina risk and, 78 exercise stress testing for, 32 heart murmurs with, 9, 9t–10t infectious endocarditis as, 139–145 jugular venous pulsation abnormalities with, 7–8 mitral, 130–137 as perioperative risk, 59, 60, 62, 63f, 64 pulmonary hypertension with, 227, 228, 229 regurgitation as, 123 signs and symptoms of, 123–124 specific valve pathologies, 124–138 stenosis as, 123 02/12/11 3:09 PM 378 valvular heart disease—Continued syncope related to, 170, 172 therapy for, 124 transesophageal echocardiography assessment of, 41, 42 transthoracic echocardiography assessment of, 38 tricuspid, 137–138 vancomycin, 143 varenicline for smoking cessation, 72 vascular access See arterial access; venous access vascular disease/lesions atherosclerotic See atherosclerosis with atrial septal defects, 183 in carotid disease, 223–224 in coronary arteries See coronary artery disease (CAD) in infectious endocarditis, 141–142, 143 in parenchymal lung disease, 228 in peripheral arterial disease, 209–211 syncope related to, 170, 173 vascular resistance, 306, 307–308 pulmonary, 227, 229, 230, 306t, 307 systemic, 110, 306t, 307, 329t vasodilators See also nitrates for aortic regurgitation, 130 for chronic heart failure, 112, 113 coronary, in stress testing, 35, 36, 46 for hypertension, 69 pulmonary, for Eisenmenger syndrome, 198 15161_IDXX_Final.indd 378 Index for pulmonary hypertension, 229, 230 responsiveness to, 229, 308, 309 vasopressin, 106t in chronic heart failure, 110 for shock, 329t vasoreactivity test for pulmonary hypertension, 229–230 right heart catheterization for, 308, 309 vasospasm in Prinzmetal’s variant angina, 80, 81 vasovagal syncope, 169, 174, 175 Vaughan-Williams classification of antiarrhythmic agents, 159, 160, 161t vena cavae catheterization and angiography of, 50 venous access central, 292–299 See also central venous catheterization for electrical devices/ therapies See transvenous implantation for electrophysiology studies, 53 for right heart catheterization, 50, 309 venous pressures in constrictive pericarditis, 207, 208t ventricles aneurysm of, jugular venous pulsation wtih, dilatation of, jugular venous pulsation with, single, as congenital defect, 194–197 ventricular assist devices for advanced management of heart failure, 115 ventricular depolarization ECG wave depicting, 11f, 12 widened QRS complex related to, 22, 23 ventricular discordance in constrictive pericarditis, 208 ventricular ectopy, 26 ventricular escape rhythms, 23 ventricular fibrillation (VF), 157, 159 direct current cardioversion for, 314, 315 implantable cardioverterdefibrillators for, 254, 257, 259–263, 262f sudden cardiac death caused by, 176, 177, 178 syncope related to, 169–170 ventricular function assessment indications for, 111, 117 cardiac radionuclide imaging for, 43, 44 computed tomography of, 46 magnetic resonance imaging of, 46–47 with mitral regurgitation, 133, 134, 135 prognosis of, with peripartum cardiomyopathy, 122 with single ventricle, 196 systemic, with transposition of the great arteries, 192f, 193, 194 transesophageal echocardiography assessment of, 41 transthoracic echocardiography assessment of, 37–38, 40 02/12/11 3:09 PM Index wtih tricuspid regurgitation, 137–138 ventricular hypertrophy See also left ventricular hypertrophy (LVH); right ventricular hypertrophy (RVH) ECG changes with, 24, 25 with hypertrophic cardiomyopathy, 119 jugular venous pulsation abnormalities with, ventricular pacing automatic reduction of, 242 in ECG interpretation, 23, 25, 28 lead placement for, 239, 241, 249–250 ventricular premature complexes (VPCs), 26 ventricular premature depolarizations (VPDs), 26 ventricular rate in atrial fibrillation, 264, 266–267, 269–270 in atrial flutter, 270, 271 in ECG interpretation, 18–19 ventricular repolarization ECG wave depicting, 11f, 12 ventricular septal defects (VSDs) acute, cardiogenic shock with, 327t clinical presentations of, 184 heart murmurs with, 9t inlet, 182f, 184 management of, 184 muscular, 182f, 183 perimembranous, 182f, 183 restrictive vs nonrestrictive, 184 supracristal/infundibular, 182f, 184 in Tetralogy of Fallot, 187, 188f 15161_IDXX_Final.indd 379 379 ventricular tachycardia (VT), 151, 157f ambulatory ECG monitoring for, 16 catheter ablation therapy for, 272 caused by digoxin toxicity, 27 direct current cardioversion for, 314, 315 ECG interpretation of, 19–20, 157–159, 158f electrophysiology studies of, 56–57 in exercise stress testing protocol, 34 implantable cardioverterdefibrillators for, 254, 257, 259–263, 262f monomorphic vs polymorphic, 156–157, 156f, 176 sudden cardiac death and, 176, 177, 178 syncope related to, 169–170, 173 with Tetralogy of Fallot, 189 therapies for, 159–160 wide complex tachycardia vs., 330–332 widened QRS complex related to, 23 ventriculography, radionuclide for dilated cardiomyopathy, 118 verapamil, 106t for aortic dissection, 218, 219 for atrial fibrillation, 266, 267, 270 for hypertension, 68 for STEMI, 95t, 97t for supraventricular tachycardias, 159 for wide complex tachycardia, 330 vernakalant, 106t vertebrobasilar insufficiency, 226 very low-density lipoproteins (VLDL), 70 Veterans Affairs Trial on carotid endarterectomy, 225 VF See ventricular fibrillation (VF) viruses peripartum cardiomyopathy related to, 121 vital signs abnormalities with cardiac disease, in cardiovascular examination, orthostatic, syncope related to, 169, 171–172, 174, 175 vitamin supplements for chronic stable angina, 79–80 voltage, in ECG, 15 volume depletion shock with, 328t syncope related to, 168, 172, 175 volume status Eisenmenger syndrome and, 198 transthoracic echocardiography assessment of, 38 VPCs (ventricular premature complexes), 26 VPDs (ventricular premature depolarizations), 26 VSDs See ventricular septal defects (VSDs) VT See ventricular tachycardia (VT) VVI/VVIR mode of pacemaker, 242 V-wave correspondence to cardiac cycle, 310 in jugular venous pulsation, walk test, 6-minute for pulmonary hypertension, 229 warfarin for carotid disease, 225 02/12/11 3:09 PM 380 warfarin—Continued for peripartum cardiomyopathy, 122 for thromboembolism, with atrial fibrillation, 264, 265, 265t, 269 Waterston shunt, 187 Watson’s water hammer pulse, 129 waveforms arterial pressure, in IABP pulsation, 322, 323f of ECG, 11–12, 11f, 18, 21–25 in right heart catheterization, corresponding to cardiac cycle, 306, 310–311 wedge pressure See pulmonary capillary wedge pressure (PCWP) weight loss for chronic heart failure, 111 Wenckebach block, 147, 147f 15161_IDXX_Final.indd 380 Index electrophysiology studies of, 55, 56 wide complex tachycardia, 158–159, 158f urgent diagnosing of, 330–332 Wilkins score for mitral stenosis, 131 Wilson’s central terminal, 12–13, 15, 29 in electrophysiology studies, 55 Wolff-Parkinson-White (WPW) Syndrome, 21, 23–24, 155, 156 catheter ablation therapy for, 272 electrophysiology studies of, 57 reading ECG for, 158, 159 wide complex tachycardia vs., 330 women cardiac resynchronization therapy for, 249 cardiovascular disease risk classification in, 66 World Health Organization (WHO) classification of pulmonary arterial hypertension, 227–228 x descent correspondence to cardiac cycle, 310 x-axis, of ECG, 11, 15, 16f, 18 y descent correspondence to cardiac cycle, 310 in jugular venous pulsation, Yamaguchi variant of hypertrophic cardiomyopathy, 119 y-axis, of ECG, 11, 15, 16f yeast causing infectious endocarditis, 140 02/12/11 3:09 PM Code Algorithms Basic Life Support for MEDICAL Professionals1 For unresponsive patients not breathing or not breathing normally Cardiac arrest in children and infants, usually asphyxiation requiring ventilations + compressions Consider foreign-body airway obstruction TABLE Adults Children Infants Get help; Get AED; Start CPR: Compression, Airway, Breathing sequence Compression Rate 100/min 100/min 100/min Compression Depth ≥ 5cm; allow ≥ anteroposterior ≥ anteroposterior 3 complete depth (~5 cm); allow depth (~4 cm); allow recoil complete recoil complete recoil Interruptions Minimize, < 10 sec; Rotate compressors q Airway Head tilt and chin lift; Possible trauma → jaw thrust Untrained rescuers Compressions-only, no ventilations Compressions: 30:2 30:2 single rescuer 30:2 single rescuer Ventilation 15:2 two rescuers 15:2 two rescuers (No airway device) Compressions: 8–10 breaths/min lasting ~1 sec, asynchronous with chest Ventilation compressions, visible chest rise (Airway device) Defibrillation AED/Defibrillator as soon as possible, minimize interruptions in compressions Resume CPR immediately after each shock Upon recognition Pulse checks allocated < 10 sec unless definite pulse identified Place in (lateral recumbent) recovery position after clearly normal breathing and effective circulation restored Drowning victims (unresponsive) should receive rescue breathing 381 15161_EMxx_Final.indd 381 02/12/11 3:09 PM 382Code Algorithms ADVANCED CARDIAC LIFE SUPPORT CPR Give oxygen Attach defibrillator Yes No Shockable Rhythm? Asystole or Pulseless Electrical Activity VF/VT? CPR Obtain IV/IO access Epinephrine q 3–5 Advanced airway? Capnography? Shock CPR Obtain IV/IO access No Shockable Rhythm? Yes Yes Shock CPR Epinephrine q 3–5 Advanced airway? Capnography? No Shockable Rhythm? Shockable Rhythm? Return of spontaneous circulation (ROSC) Evident pulse & BP PETCO2 suddenly ≥ 40 mm Hg Medications Epinephrine mg IV/IO q 3–5 Vasopressin 40 unit IV/IO may replace 1st or 2nd dose of epinephrine Amiodarone IV/IO First dose: 300 mg bolus Second dose: 150 mg bolus No or CPR Treat reversible causes Yes Shock CPR Amiodarone Treat reversible causes CPR Depth ≥ cm, Rate ≥ 100 bpm, Allow complete recoil Minimize interruption Change compressor q 30:2 Compression:Ventilation without advanced airway Capnography: PETCO2 ≤ 10 mm Hg inadequate Art-line diastolic ≤ 20 mm Hg inadequate Yes Shockable Rhythm? No Return of Spontaneous Circulation? Advanced airway Endotracheal intubation or aboveglottis advanced airway Waveform capnography to confirm and monitor ETT placement 8–10 breaths/min during chest compressions Reversible causes - Hypovolemia - Hypoxia - Hydrogen ion (acidosis) - Hypo/hyperkalemia - Hypothermia - Tension pneumothorax - Tamponade, cardiac No - Toxins - Thromboembolism, pulmonary - Thrombosis, coronary Post-Arrest Care Figure 1. Adult cardiac arrest Adapted from Neumar RW, et al Adult advanced cardiovascular life support Circulation 2010;122:S729–S767 15161_EMxx_Final.indd 382 02/12/11 3:09 PM Advanced Cardiac Life Support 383 Additional Comments on Adult Cardiac Arrest Ventilation, CO2 detectors, and oximetry Use suction devices Colorimetric CO2 detectors may be misleading if contaminated with acidic gastric contents or drugs (e.g., epinephrine via ETT) CO2 may be low in lung hypoperfusion (cardiac arrest) or severe airflow obstruction Ominous prognosticators: • P ETCO2 < 10 mm Hg (persistently) via ETT • Central vein O2 saturation < 30% • Diastolic BP < 20 mm Hg during CP Avoid hyperventilation Drug delivery IV Access: central line unnecessary if large-bore peripheral access is obtained IV access should not delay CPR and defibrillation Remember intraosseous and endotracheal delivery option Think ahead: Prepare drugs before rhythm and pulse checks Flush drugs with 10–20 mL IV fluid bolus Drugs can be administered via ETT: epinephrine, atropine, lidocaine, vasopressin, naloxone; use 2–2.5 × usual dose diluted in 5–10 mL NS or D5W Do not pause compressions for ventilation with advanced airway Ventricular tachycardia or ventricular fibrillation Amiodarone is a first line drug that increases ROSC Lidocaine does not increase ROSC Magnesium IV is indicated only for Torsades related to prolonged QT (1–2 g in 10 mL) Echo may have value in identifying treatable causes of cardiac arrest especially after ROSC Consider differential diagnosis: H’s and T’s on algorithm Accelerated idioventricular rhythm: May not require treatment if associated with perfusion Epinephrine: High doses are generally ineffective, except possibly in β-blocker or Ca-blocker overdose Vasopressin: Intended to be administered only once Asystole or pulseless electrical activity 15161_EMxx_Final.indd 383 02/12/11 3:09 PM 384Code Algorithms Emergency echocardiography: May be useful when cardiac tamponade or myocardial mechanical complications (wall or papillary rupture, VSD) are suspected Pacing: No utility in arrest except selected events such as iatrogenic asystole Consider differential diagnosis of reversible etiologies (H’s and T’s on algorithm) Is bradycardia clinically appropriate? Identify and treat cause of bradycardia Maintain airway and assist breathing if needed Oxygen if needed Cardiac rhythm, blood pressure, oximetry monitor IV access 12-lead ECG if available, but don’t delay emergency treatment Is the bradycardia persistent and is it causing: Hypotension? Altered mental status? Evidence of shock? Ischemic chest pain? Acute heart failure? No Atropine IV bolus First dose: 0.5 mg Repeat q 3–5 Maximum 3.0 mg Dopamine IV infusion 2–10 mcg/kg/min Epinephrine IV infusion 2–10 mcg/min Monitor & observe Atropine If atropine ineffective, then use Transcutaneous (external) pacemaker, or Dopamine infusion, or Epinephrine infusion Consider Expert consultation Transvenous pacemaker Figure 2. Bradycardia Adapted from Neumar RW, et al Adult advanced cardiovascular life support Circulation 2010;122:S729–S767 15161_EMxx_Final.indd 384 02/12/11 3:09 PM Advanced Cardiac Life Support 385 Is tachycardia clinically appropriate? Identify and treat cause of tachycardia Maintain airway and assist breathing if needed Oxygen if needed Cardiac rhythm, blood pressure, oximetry monitor IV access 12-lead ECG if available, but don’t delay emergency treatment Unstable? Hypotension? Altered mental status? Evidence of shock? Ischemic chest discomfort? Acute heart failure? Yes No Wide QRS > 120 ms? Synchronized cardioversion Consider sedation If narrow QRS tachycardia consider adenosine Cardioversion (synchronized) Narrow QRS regular: 50–100J Narrow QRS irregular:120J biphasic or 200J monophasic Wide QRS regular: 100J Wide QRS irregular: defibrillation (not synchronized) Adenosine IV bolus First dose mg rapid IV bolus and NS flush Second dose 12 mg IV if needed Anti-arrhthmic drugs for stable wide-QRS tachycardia Vagal maneuvers Adenosine (if regular) β-blocker or calcium-channel blocker Consider expert consultation Consider adenosine only if regular, monomorphic, wide QRS Consider anti-arrhythmic drug infusion Consider expert consultation Procainamide IV 20–50 mg/min until rhythm suppressed or hypotension or QRS width increases 50% or maximum 17 mg/kg infused Maintenance 1–4 mg/min Avoid in prolonged QT or in CHF Amiodarone IV First dose: 150 mg over 10 Repeat as needed if VT recurs Maintenance mg/min IV x hr Sotalol IV 100 mg (1.5 mg/kg) over Avoid in prolonged QT Figure 3. Tachycardia Adapted from Neumar RW, et al Adult advanced cardiovascular life support Circulation 2010;122:S729–S767 15161_EMxx_Final.indd 385 02/12/11 3:09 PM 386Code Algorithms Return of Spontaneous Circulation (ROSC) Optimize ventilation and oxygenation Maintain oxygen saturation ≥ 94% Consider advanced airway & waveform capnography Do not hyperventilate Ventilation & Oxygenation Do not hyperventilate Start 10–12 bpm Titrate to PETCO2 ~ 35–40 mm Hg Titrate FiO2 to SpO2 ≥ 94% Treat hypotension (SBP < 90 mm Hg) IV/IO bolus isotonic fluid Vasopressor infusion Search for treatable causes of hypotension 12-lead ECG IV/IO bolus fluid 1–2L NS or LR If therapeutic hypothermia, use 4° fluid Consider therapeutic hypothermia No Able to Follow Commands? Yes STEMI or AMI? No Further critical care Dopamine IV infusion 5–10 mcg/kg/min Norepinephrine IV infusion 0.1–0.5 mcg/kg/min (7–35 mcg/min for 70 kg adult) Yes Coronary reperfusion therapy Epinephrine IV infusion 0.1–0.5 mcg/kg/min (7–35 mcg/min for 70 kg adult) Reversible causes - Hypovolemia - Hypoxia - Hydrogen ion (acidosis) - Hypo/hyperkalemia - Hypothermia - Tension pneumothorax - Tamponade, cardiac - Toxins - Thromboembolism, pulmonary - Thrombosis, coronary Figure 4. Immediate care after cardiac arrest Adapted from Peberdy MA, et al Post-cardiac arrest care: 2010 AHA Guidelines Circulation 2010; 122:S768–786 References (1) Adapted from Travers AH, et al CPR overview: 2010 AHA Guidelines Circulation 2010;122:S676–S684 and Berg MD, et al Pediatric basic life support: 2010 AHA Guidelines Circulation 2010;122:S862–S875 15161_EMxx_Final.indd 386 02/12/11 3:09 PM ... arteries 23 3 15161_CH27_Final.indd 23 3 02/ 12/ 11 2: 32 PM 23 4Coronary Revascularization • PTCA is now almost always accompanied by the implantation of a coronary stent •• Coronary stents are small (2. 0–5.0... selected, common scenarios 15161_CH27_Final.indd 23 5 02/ 12/ 11 2: 32 PM 23 6Coronary Revascularization • Revascularization is appropriate in patients who have 1-, 2- , or, 3-vessel disease with or... Revascularization guidelines J Am Coll Cardiol 20 09;53(6):530-553 15161_CH27_Final.indd 23 6 02/ 12/ 11 2: 32 PM Recommended Guidelines for Revascularization 23 7 • Randomized trials of PCI with DES vs