112 Acute coronary syndrome Definitions Acute coronary syndrome (ACS) includes unstable angina and evolving MI, which share a common underlying pathology \200\224plaque rupture, thrombos is, and inflammation. However, ACS may rarely be due to emboli or coronary spasm in normal coronary arteries or vasculitis (p. 416). Usually divided into ACS with ST-segment elevatio n or new-onset LBBB \200\224what most of us mean by acute MI \200\224and ACS without ST-seg ment elevation \200\224the ECG may show ST-depression, T-wave inversion, nonspecific chang es, or be normal (includes non-Q wave or subendocardial MI). The degree of irreversible myo cyte death varies, and significant necrosis can occur without ST-elevation. Cardiac troponi ns (T and I) are the most sensi- tive and specific markers of myocardial necrosis and have become the test of choice in patients with ACS (see below). Risk factors Nonmodifiable: Age , \231\202 sex, family history of IHD (MI in first-degree relative <55 yrs). Modifiable: S moking, hypertension, DM, hyperlipidemia, obesity, sedentary lifestyle. Controversial risk factors include stress, type A personality, LVH, apoprotein A ^ , fibrinogen ^ , hyperinsul ine- mia, homocysteine levels ^ , ACE genotype, and cocaine use. Diagnosis is based on the presence of at least two out of three of: Typical history, ECG changes, and cardiac enzyme rise (World Health Organization [WHO] criteria). Symptoms Acute central chest pain, lasting >20 min, often associated with nausea, diaphoresis, dyspnea, palpitations. May present wit hout chest pain ( \200\234silent \200\235 infarct) or with atypical chest pain (e.g., in el derly or diabetic patients). In such patients, presentations may include syncope, pulmonary edema, epigastric pain and vomiting, postoperative hypotension or oliguria, acute confusio nal state, stroke, diabetic hyperglycemic states. Signs Distress, anxiety, pallor, sweatine ss, pulse or ^ , BP ^ or , fourth heart sound. There may be signs of heart failure (J VP ^ , third heart sound, and bibasilar crackles) or a pansystolic murmur (papillary muscle dysfunc- tion/rupture; ventral septal defect [VSD]). A low-grade fever may be pres- ent. L ater, a pericardial friction rub or peripheral edema may develop. Tests ECG: Classically, h yperacute (tall) T waves, ST elevation or new LBBB occur within hours of acute Q wave (tran smural infarction). T wave inversion and the development of pathological Q waves follow ove r hours to days (p. 95). In other ACS : ST-depression, T-wave inversion, nonspecific change s, or normal. In 20% of MIS, the ECG may be normal initially. CXR: Look for cardiomegaly, p ulmonary edema, or a widened mediastinum (?aortic dissection). Don \200\231t routinely dela y treatment while waiting for a CXR. Blood: CBC, electrolytes, renal function, glucose ^ , lipids , cardiac enzymes ^ (CK, troponin); CK is found in myocardial and skeletal muscle . It is raised in MI, after trauma (falls, seizures) or prolonged exercise, and in myositis , hypothermia, and hypothyroidism. Check CK-MB isoenzyme levels if there is doubt as to the source (normal CK-MB/CK ratio <5%). Troponin T bet- ter reflects myocardial damage (peaks at 12 \200\22324 h; elevated for >1 wk). If normal \211 6 h after onset of pain, and ECG normal, risk of missing MI is tiny (0.3%). Peak post-MI levels also help risk stratificatio n. Differential diagnosis (p. 90) Angina, pericarditis, myocarditis, aortic dis- section, p ulmonary embolism, and esophageal reflux/spasm Management See emergencies (p. 749). The man agement of ACS with and without ST-segment elevation varies. Likewise, if there is no ST-el evation, and symptoms settle without a rise in cardiac troponin, then no myocardial damage has occurred, the prognosis is good, and patients can be discharged. e n i c i d e m r a l u c s a v o d r a C i 113 Therefore, the two key questions are: Is there ST-segment elevation? And, is there a rise i n troponin? Mortality 50% of deaths occur within 2 h of onset of symptom. Figure 5.15 Enzyme changes following acute MI Cardiac enzymes \227 50 Trop CK CK \200\223MB AST LDH Trop Creatine kinase CK cardiac isoenzyme Aspartate transaminase Lactate dehydrogenase Cardiac t roponin CK \227 5 l e v e CK \200\223MB \227 4 l e m y z n e m u r e S \227 3 LDH \227 2 AST \227 1 0 1 2 3 4 6 5 Days 7 8 9 10 114 Figure 5.16 Sequential ECG changes following acute MI Management of ACS Prehospital Arrange emergency ambulance. Aspirin 325 mg chewed (if no abs olute CI) and NTG sublingual. Analgesia, such as morphine 5 \200\22310 mg IV (not IM becaus e of risk of bleeding with thrombolysis). Ask if the patient took a PDE 5 inhibitor (silden afil, vardenafil, tadalafil) since nitrates are contraindicated in that situation. In the h ospital O 2 , morphine, aspirin (p. 751). Then the key question for subsequent management o f ACS is whether there is ST-segment elevation (includes new-onset LBBB or a true posterior MI). ST-segment elevation \212Primary angioplasty or thrombolysis, if no contraindication \212 \222 -blocker , e.g., atenolol 5 mg iv, unless contraindicated \212ACE-inhibitor : Consider starting ace-inhibitor (e.g., lisinopril 2.5 mg) in all normotensive patients with in 24 h of acute MI, especially if there is clinical evidence of heart failure or echo evid ence of LV dysfunction. ACS without st-segment elevation \212 \222 -blocker , e.g., atenolol 5 mg iv, unless contr aindicated \212Low-molecular-weight heparin (LMWH) (e.g., enoxaparin) \212Nitrates , unle ss contraindication (usually given IV) \212 e n i c i d e m High-risk patients (persistent or recurrent ischemia, ST-depression, DM, troponin ^ ) requi re infusion of a GPIIb/IIIa antagonist (e.g., tirofiban), and, ideally, urgent angiography. Clopidogrel may be useful in addition to aspirin. Low-risk patients (no further pain, flat or inverted T waves, or normal ECG, and negative troponin) can be discharged if a repeat t roponin is negative. Treat medically and arrange further investigation (e.g., stress test, angiogram). r a l u c s a v o d r a C \212 i Subsequent management Bed rest for 48 h; continuous ECG monitoring. \212 \212 Daily examination of heart, lungs, and legs for complications ( Daily 12-lead ECG, electrol ytes and renal function, cardiac enzymes for 2 \200\2233 d The length of time to give antic oagulant therapy and the type of antico- agulant therapy (heparin or LMWH, direct thrombin inhibitors, IIb/IIIa antagonists) is an area of active research. p. 116) \212 \212Prophylaxis against thromboembolism: E.g., LMWH SC until fully mobile. If large anteri or MI, consider warfarin anticoagulation for 3 months as pro- phylaxis against systemic emb olism from LV mural thrombus. Continue daily low-dose aspirin (e.g., 81 mg) indefinitely. A spirin reduces vascular events (MI, stroke, or vascular death) by 29%. \212Start oral - blocker (e.g., metoprolol 50 mg/6 h, enough to lower the pulse to 60 ; continue for at least 1 yr). Long-term \222 -blockade reduces mortality from all causes by 25% in patients who have had a previous MI. If contraindicated, consider verapamil or d iltiazem as an alternative. 115 \212Continue ACE-inhibitor in all patients: ACE-inhibitor in those with evidence of heart failure reduces 2-yr mortality by 25 \200\22330%. \212Start a statin : Cholesterol reduction post-MI has been shown to be of benefit in pati ents with both elevated and normal cholesterol levels. Some treat all patients, others only if total cholesterol >200 mg/dL or LDL >130 mg/dL. \212Address modifiable risk factors: Discourage smoking (p. 89). Encourage exercise. Identify and treat DM, hypertension, and hyperlipidemia. \212Exercise ECG: May be useful in risk stratification post-MI and in sub- jects without S T-segment elevation or a troponin rise. Not necessary in patients who received a cardiac ca th and appropriate intervention. \212General advice: If uncomplicated, discharge after 5 \200\2237 d. Work: Return to work after 4 \200\22312 wks. A few occupations should not be restarted post-MI: airline pilots, air traffic controllers, divers. Drivers of public service or heavy goods vehicles may be p ermitted to return to work if they meet certain criteria. Patients undertaking heavy manual labor should be advised to seek a lighter job. Diet: A diet high in fish, fruit, vegetable s, and fiber, and low in saturated fats should be encouraged. Exercise: Encourage regular d aily exercise. Sex: Intercourse is best avoided for 1 month. Travel: Avoid air travel for 2 months. Review symptoms at 5 wks post-MI: Angina? Dyspnea? Palpitations? \212 Review at 3 months \212Check fasting lipids: Does the dose of statin need to be raised to reach If angina recurs, treat conventionally, and consider coronary angiography. goal levels? Figure 5.17 Acute posterolateral MI 116 Complications of MI \212Cardiac arrest (p. 736); cardiogenic shock (p. 757) \212Unstable angina: Manage along standard lines (p. 752) and refer to a car- diologist for urgent investigation. \212Bradycardias or heart block: Sinus bradycardia : Treat with atropine 0.6 \200\2231.2 m g IV. Consider temporary cardiac pacing if no response, or poorly tol- erated by the patien t. First-degree AV block : Observe closely as approxi- mately 40% develop higher degrees of AV block. Wenckebach (Mobitz type I) block : Does not require pacing unless poorly tolerat ed. Mobitz type II block : Carries a high risk of developing complete AV block; should be p aced. Complete AV block : Insert pacemaker; may not be necessary after inferior MI if narro w QRS and reasonably stable pulse \211 40 \200\22350. Bundle branch block : MI complicate d by trifascicular block or nonadjacent bifas- cicular disease should be paced. \212Tachyarrhythmias: NB: K + , hypoxia, and acidosis all predispose to arrhythmias and should be corrected. Regular wide complex tachycardia after MI is almost always VT. If hem odynamically stable, give lidocaine or amiodarone. If this fails, can repeat at a lower dos e. Would review ACLS protocols. Consider maintenance antidysrhythmic therapy. Early VT (<24 h) : Give lidocaine by infusion for 12 \200\22324 h or amiodarone. Late VT (>24 h) amiodar one and start oral therapy (amiodarone or sotalol). SVT. AF or flutter : If compromised, DC cardioversion. Otherwise, control rate with digoxin, -blockers, or calcium channel bloc kers. In atrial flutter or intermittent AF, try amiodarone or sotalol. \212Left ventricular failure (LVF) (p. 754) \212Right ventricular failure (RVF)/infarctio n: Presents with low cardiac output and JVP ^ . Insert a Swan \200\223Ganz catheter to meas ure right-sided pressures and guide fluid replacement. If BP remains low after fluid replacement, give inotropes. e n i c i d e m \212Pericarditis: Central chest pain, relieved by sitting forwards. ECG : Saddle-shaped ST elevation. Treatment : NSAIDs. Echo to check for effusion. \212DVT and PE: Patients are at risk of developing DVT and PE and should be prophylactically heparinized until fully mobile. r a l u c s a v o d r a C \212Systemic embolism: May arise from an LV mural thrombus. After large anterior MIs, consider anticoagulation with warfarin for 3 months. \212Cardiac tamponade (p. 755): Presents with low cardiac output, pulsus para- doxus, JVP ^ , muffled heart sounds. Diagnosis : Echo. Treatment : Pericardial aspiration (provides te mporary relief [p. 730]), surgery i \212Mitral regurgitation: May be mild (minor papillary muscle dysfunction) or severe (chor dal or papillary muscle rupture or ischemia). Presentation : Pulmonary edema. Diagnosis : E cho. Treat LVF (p. 754) and consider valve replacement. \212Ventricular septal defect: Presents with pansystolic murmur, JVP ^ , cardiac failure. Diagnosis : Echo. Treatment : Surgery. 50% mortality in first week \212Late malignant vent ricular arrhythmias: Occur 1 \200\2233 wks post-MI and are the cardiologist \200\231s night mare. Avoid hypokalemia, the most easily avoid- able cause. \212Dressler \200\231s syndrome: Recurrent pericarditis, pleural effusions, fever, anemia and ESR ^ 1 \200\2233 wks post-MI. Treatment : NSAIDs; steroids if severe \212Left ventricular aneurysm: This occurs late (4 \200\2236 wks post-MI) and presents wit h LVF, angina, recurrent VT, or systemic embolism. ECG : Persistent ST segment elevation. T reatment : Anticoagulate, consider excision. 117 Angina pectoris This is due to myocardial ischemia and presents as a central chest tightnes s or heaviness that is brought on by exertion and relieved by rest. It may radi- ate to one or both arms, the neck, jaw, or teeth. Other precipitants: Exercise, emotion, cold weather , and heavy meals. Associated symptoms: Dyspnea, nausea, diaphoresis, lightheadedness. Caus es Mostly atheroma; rarely, anemia, AS, tachyarrhythmias, HOCM, arteritis/small vessel dise ase. Types of angina Stable angina : Induced by effort, relieved by rest. Unstable (crescen do) angina : Angina of increasing frequency or severity; occurs on minimal exertion or at r est; associated with highly increased risk of MI. Decubitus angina : Precipitated by lying flat. Variant (Prinzmetal \200\231s) angina : Caused by coronary artery spasm (rare; may co exist with fixed stenoses). Tests ECG : Usually normal, but may show ST depression; flat or inverted T waves; signs of past MI. If resting ECG normal, consider exercise ECG (p. 99), thallium scan (p. 107), or coronary angiography. Management Alteration of lifestyle : Stop smoking, encourage exercise, weight loss. Modify risk factors : Hypertension, DM, etc. (p. 89). \212 Aspirin (81 mg/24 h) reduces mortality by 34%. \222 \212 -blockers: E.g., aten olol 50 \200\223100 mg/24 h PO, unless contraindications (asthma, COPD, LVF, bradycardia, coronary artery spasm). \212Nitrates: For symptoms, give NTG spray or sublingual tabs, up to every half hour. Prop hylaxis: Give regular oral nitrate, e.g., isosorbide mononi- trate 10 \200\22330 mg PO (e.g ., bid; an 8 h nitrate-free period to prevent tol- erance) or slow-release nitrate (e.g., I mdur 60 mg/24 h). Alternatives : Adhesive nitrate skin patches. SE : Headaches, BP . \212Calcium antagonists: Amlodipine 5 \200\22310 mg/24 h; diltiazem 90 \200\223180 mg/12 h PO. \212 \212 If total cholesterol >200 mg/dL, give a statin ( Unstable angina requires admission and urg ent treatment: See (p. 752). p. 111). Emergencies Indications for referral Diagnostic uncertainty; new angina of sudden onset; recurrent angi na if past MI or CABG; angina uncontrolled by drugs; unstable angina. Percutaneous translum inal coronary angioplasty (PTCA) involves balloon dila- tation of the stenotic vessel(s). I ndications: Poor response or intolerance to medical therapy; refractory angina in patients not suitable for CABG; previ- ous CABG; post-thrombolysis in patients with severe stenoses, symptoms, or positive stress tests. Comparisons of PTCA versus drugs alone show that PTCA may control symptoms better but with more frequent cardiac events (e.g., MI and need for CA BG) and little effect on overall mortal- ity. Complications: Restenosis (20 \200\22330% wit hin 6 months); emergency CABG (<3%); MI (<2%); death (<0.5%). Stenting reduces restenosis r ates and the need for bail-out CABG. NICE recommends that >70% of angioplasties should be a ccompanied by stenting. Drug-coated stents reduce restenosis. Antiplatelet agents (e.g., cl opidogrel) reduce the risk of stent thrombo- sis. IV platelet glycoprotein IIb/IIIa-inhibit ors (e.g., eptifibatide) can reduce procedure-related ischemic events. CABG: Indications: L eft main disease, multivessel disease, multiple severe stenoses, distal vessel disease, pat ient unsuitable for angioplasty, failed angioplasty, refractory angina, MI, pre-operatively (valve or vascular sur- gery). Comparisons of CABG versus PTCA have found that CABG result s in better symptom control and lower re-intervention rate but longer recovery time and len gth of inpatient stay. Studies also show that CABG improves long-term survival compared to medical therapy. 118 Arrhythmias Disturbances of cardiac rhythm or arrhythmias are: \212 \212 \212 \212 Caus es Cardiac : MI, coronary artery disease, LV aneurysm, mitral valve disease, cardiomyopathy , pericarditis, myocarditis, aberrant conduc- tion pathways. Noncardiac : Caffeine, smoking , alcohol, pneumonia, drugs ( 2 -agonists, digoxin, tricyclics, Adriamycin, doxorubicin) , metabolic imbal- ance (K + , Ca 2+ , Mg 2+ , hypoxia, hypercapnia, metabolic acidosis, th yroid disease, pheochromocytoma). Presentation is with palpitation, chest pain, presyncope/ syncope, hypotension, or pulmonary edema. Some arrhythmias may be asymptomatic and incident al (e.g., AF). History Take a detailed history of palpitations. Ask about precipitating fac - tors, onset, nature (fast or slow, regular or irregular) duration, associated symptoms (c hest pain, dyspnea, light headedness). Review drug history. Ask about past medical history or family history of cardiac disease. Tests CBC, electrolytes, glucose, Ca 2+ , Mg 2+ , thy roid-stimulating hormone (TSH). ECG : Look for signs of IHD, AF, short P \200\223R interval (WPW syn- drome), long QT interval (metabolic imbalance, drugs, congenital), U waves (hypo kalemia). Undertake 24 h ECG monitoring; several recordings may be needed. May need a conti nuous monitor. Echo : To look for structural heart disease (e.g., mitral stenosis). Provoca tion tests : Exercise ECG, cardiac cath- eterization, and electrophysiological studies may be required. Treatment If the ECG is normal during palpitations, reassure the patient. Othe rwise, treatment depends on the type of arrhythmia. Common Often benign (but may reflect underlying heart disease) Often intermittent, causing diagnostic difficulty Occasionally severe, causing cardiac compromise Bradycardia (p. 120): If asymptomatic and rate is >40 bpm, no treatment is required. Look f or a cause (drugs, sick sinus syndrome, hypothyroidism) and stop any drugs that may be cont ributing ( -blocker, digoxin). If rate is <40 bpm or patient is symptomatic, give atropi ne 0.5 \200\2231.0 mg IV (up to maximum of 3 mg). If no response, insert a temporary pacing wire (p. 732). If necessary, start an isoproterenol infusion or use external cardiac pacin g. Sick sinus syndrome: Sinus node dysfunction causes bradycardia arrest, sinoatrial blo ck or SVT alternating with bradycardia/asystole (tachy \200\223brady syndrome). AF and thro mboembolism may occur. Pace if symptomatic. SVT (p. 121): Narrow complex tachycardia (rate >100 bpm, QRS width <120 ms). Acute management : Vagotonic maneuvers followed by IV ade- no sine or verapamil (if not on -blocker); DC shock if compromised. Maintenance therapy : -blockers or verapamil. af/flutter (p. 123): May be incidental finding. Control ventricul ar rate with -blockers, calcium channel blockers, or digoxin. Use flecainide for preex- cited AF. DC shock if compromised (p. 731). VT (p. 125): Broad complex tachycardia (rate >1 00 bpm, QRS duration >120 ms). Acute management : IV lidocaine or amiodarone, if no respons e or if compromised DC shock. Oral therapy : Amiodarone loading dose (400 mg/8 h PO for 7 d , then 400 mg/12h for 7 d) followed by maintenance therapy (200 \200\223400 mg/24 h). SE : Corneal deposits, photosensitivity, hepatitis, pneumonitis, lung fibrosis, nightmares, INR ^ (warfarin potentiation), T4 ^ , T3 . Monitor LFT and thyroid function tests (TFT). Fin ally, pacing may be used to overdrive tachyarrhythmias, to treat bra- dyarrhythmias, or pro phylactically in conduction disturbances (p. 127). Implanted automatic defibrillators can s ave lives and are indicated for patients with an ejection fraction <35% and New York Heart Association (NYHA) class II \200\223III heart failure symptoms. e n i c i d e m r a l u c s a v o d r a C i 119 Figure 5.18 Diagnosis of bradycardias and AV block (a) 120 (b) Narrow complex tachycardia ECG shows rate of >100 bpm and QRS complex duration of <120 ms. Differential diagnosis \212Sinus tachycardia : Normal P wave followed by normal QRS \212S VT : P wave absent or inverted after QRS \212AF : Absent P wave, irregular QRS complexes \212Atrial flutter : Atrial rate usually 300 bpm giving \200\234flutter waves \200\235 or \200\234saw- tooth \200\235 baseline (p. 120), ventricular rate often 150 bpm (2:1 block). See Table 5.6. e n i c i d e m r a l u c s a v o d r a C \212Atrial tachycardia : Abnormally shaped P waves, may outnumber QRS \212Multifocal atri al tachycardia : Three or more P wave morphologies, irregu- i lar QRS complexes \212Junctional tachycardia : Rate 150 \200\223250 bpm, P wave either buried in QRS complex or occurring after QRS complex Principles of management See algorithm (Figure 5.19) . \212 If the patient is compromised, use DC cardioversion ( \212 Otherwise, identify the underlying rhythm and treat according ly. \212 Vagal maneuvers (carotid sinus massage, Valsalva maneuver) transiently increase A V block, and may unmask an underlying atrial rhythm. If unsuccessful, give adenosine, which causes transient AV block. It has a short half-life (10 \200\22315 sec) and works in two w ays: By transiently slowing ventricles to show the underlying atrial rhythm and by cardiove rting a junctional tachycardia to sinus rhythm. p. 731). \212 Give 6 mg IV bolus into a large vein; follow by saline flush, while recording a rhythm stri p; if unsuccessful, give 12 mg, then 12 mg again at 2 min inter- vals, unless on dipyridamo le or post cardiac transplantation. Warn of SE : Transient chest tightness, dyspnea, headac he, flushing. CI : Asthma, second-/ third-degree AV block, or sinoatrial disease (unless pa cemaker). Drug inter- actions: Potentiated by dipyridamole, antagonized by theophylline. Sp ecific management Sinus tachycardia Identify and treat the cause. SVT: If adenosine fails, use verapamil 5 \200\22310 mg IV over 2 min, or over 3 min if elderly (not if already on -blocker). If no response, give further dose of 5 mg IV after 5 \200\22310 min. Alternativ es : Atenolol 2.5 mg IV at 1 mg/min repeated at 5 min intervals to a maximum of 10 mg or so talol. If no good, use DC cardioversion. AF/flutter: Manage along standard lines (p. 123). Atrial tachycardia: Rare. If due to digoxin toxicity, stop digoxin; consider digoxin-specif ic antibody fragments (p. 789). Maintain K + at 4 \200\2235 mmol/L. Multifocal atrial tachy cardia: Most commonly occurs in COPD. Correct hypoxia and hypercapnia. Consider verapamil i f rate remains >110 bpm. Junctional tachycardia: There are three types of junctional tachyc ardia: AV nodal reentry tachycardia (AVNRT), AV reentry tachycardia (AVRT), and His bundle tachycardia. Where anterograde conduction through the AV node occurs, vagal maneuvers are w orth trying. Adenosine will usually cardiovert a junctional rhythm to sinus rhythm. If it r ecurs, treat with a -blocker or amiodarone. Radiofrequency ablation is increasingly bein g used in AVRT and in some patients with AVNRT. WPW syndrome (ECG, p. 124) Caused by congen ital accessory con- duction pathway between atria and ventricles. Resting ECG shows short P \200\223R interval and widened QRS complex due to slurred upstroke or \200\234delta wave. \200\235 Two types: WPW type A (+ve wave in V 1 ), WPW type B ( \200\223ve wave in V 1 ). Patients present with SVT, which may be due to an AVRT, preexcited AF, or preexcited atrial flutter. Refer to cardiologist for electro- physiology and ablation of the accessory pathway. 121 Figure 5.19 \211 122 \211 \227 Atrial fibrillation and flutter AF is a chaotic, irregular atrial rhythm at 300 \200\223600 bpm. The AV node responds intermittently, hence the irregular ventricular rate. It is comm on in the elderly ( \211 9%). The main risk is of embolic stroke, which is prevent- able by warfarin (reducible to 1%/yr from 4%; higher risk if old, poor LV function, DM, past TIA or stroke, or large left atrium on echocardiogram). Common causes: Heart failure, hyperten sion, cardiac ischemia, MI (seen in 22%), mitral valve disease, pneumonia, hyperthyroidism, alcohol. Rare causes: Cardiomyopathy, constrictive pericarditis, sick sinus syndrome, bron chial carcinoma, atrial myxoma, endocarditis, hemochromatosis, sar- coidosis, or other caus es of atrial dilatation. \200\234Lone \200\235 AF means none of the above causes. Signs an d symptoms: It may be asymptomatic (found incidentally) or present with chest pain, palpita tions, dyspnea, or presyncope. On examination, the pulse is irregularly irregular , the api cal pulse rate is greater than the radial rate, and the first heart sound is of variable in tensity. Look for signs of mitral valve disease or hyperthyroidism. Tests: ECG shows absent P waves, irregular QRS complexes. Blood tests: Electrolytes, cardiac enzymes, thyroid func tion tests. Echo to look for LA enlargement, mitral valve disease, poor LV function, and ot her structural abnormalities. Acute af (e.g., \211 72 h): \212 \212 e n i c i d e m r a l u c s a v o d r a C i Treat any associated acute illness (e.g., MI, pneumonia). -blocker or a calcium channel Control ventricular rate with either a blocker \200\224intravenously if necessary. Digoxin can also be used but is not considered a first-line agent. If AF does not resolve, consider drug or electrical cardioversion. Drug cardioversion: Amiodarone IVI (5 mg/kg over 1 h the n 900 mg over 24 h via a central line max 1.2 g in 24 h) or PO (200 mg/8 h for 1 wk, 200 m g/12 h for 1 wk, 100 \200\223200 mg/24 h maintenance). Alternative (if hemody- namically st able and no known IHD): Flecainide 2 mg/kg IV over >25 min (max 150 mg) with ECG monitoring . 300 mg stat PO may also work. DC cardioversion is indicated: (1) electively, following a first attack of AF with an identifiable cause; (2) as an emergency, if the patient is com- promised. Protocol : 200 J \206\222 300 J \206\222 360 J (100 J may be tried first, but i s successful in <20%). Anticoagulation is not required if AF is of recent onset (<48 h) wit h a structurally normal heart on echo, but aspirin may be given. Otherwise, anticoagulate w ith warfarin for at least 3 wks before and 4 wks after DC cardioversion or perform TEE to l ook for left atrial thrombus. 123 \212 \212 \212 Chronic AF: \212 -blockers or calcium channel blockers. If the rate is Control rate with not controlled o n high doses of one, consider adding a second agent. Digoxin can be used but will not contr ol the rate during exercise. Alternative : amiodarone PO. Anticoagulate with warfarin if >6 0 unless contraindication. Aim for an INR of 2.0 \200\2233.0. For those with no other risk factors (CHADS2 score: Heart failure, hypertension, age >75, DM, previous stroke, TIA, or t hrom- boembolism), or those in whom warfarin is contraindicated, aspirin (325 mg PO) can be used. \212 Paroxysmal af: \212 Many antiarrhythmic agents can be used to try to maintain sinus rhythm. Be cautious to not use an agent contraindicated in a certain patient population (e.g., flecainide in ischemic heart disease). Anticoagulate with warfarin. Figure 5.20 Summary of treatment of AF \212 \212 \212 Treat any reversible cause. Control ventricular rate. Consider cardioversion to sinus rhyth m, if onset within last 12 months (do echo first; is heart structurally normal?). Prevent e mboli: Warfarin (or aspirin). \212 124 Table 5.6 Note on atrial flutter \212 ECG: Continuous atrial depolarization (e.g., 300/min, but very vari- able) produces a sawt ooth baseline with variable block 2:1 or 3:1 usually. Carotid sinus massage or IV adenosine transiently blocks the AV node and may unmask flutter waves. Treatment: Same as AF. Consid er cavotricuspid isthmus ablation (this \200\234flutter isthmus \200\235 is low in the rig ht atrium). \212 \212 Figure 5.21 Wolff \200\223Parkinson \200\223White syndrome ECG of WPW syndrome (p. 121) in first and fourth beats; compared with the other beats, it c an be seen how the delta wave both broadens the ventricular complex and shortens the PR int erval. Wide complex tachycardia ECG shows rate of >100 and QRS complexes >120 ms (>3 small squares [p. 93]). If no clear QRS complexes, it is VF or asystole (p. 126). Principles of manageme nt \212 \212 Differential diagnosis \212 \212 ( NB: Premature ventricular beats should not cause confusion when occur- ring singly; but if >3 together at rate of >120, this const itutes VT.) Identification of the underlying rhythm (see Figure 5.22 ) may be dif- ficult; seek expert help. Diagnosis is based on the history (IHD ^ the likeli- hood of a ventricula r arrhythmia), a 12-lead ECG, and the lack of response to IV adenosine (p. 140). ECG findin gs in favor of VT: \212 \212 \212 \212 \212 \212 Concordance means QRS complexes are all +ve or \200\223ve. A fusion beat is when a \200\234normal beat \200\235 fuses with a VT complex to create an unusual complex, and a capture beat is a normal QRS between abnorma l beats (see Figure 5.22 ). Management Connect to a cardiac monitor; have a defibrillator a t hand. \212 \212 \212 \212 e n i c i d e m Identify the underlying rhythm and treat accordingly. If in doubt, treat as VT (the commone st cause). r a l u c s a v o d r a C VT; includes Torsade de pointes (see below) SVT with aberrant conduction (e.g., AF, atrial flutter) i +ve QRS concordance in chest leads Marked LAD AV dissociation (occurs in 25%) or 2:1 or 3:1 AV block Fusion beats or capture beats RSR complex in V QS complex in V 1 (with +ve QRS in V 1 ) 6 (with \200\223ve QRS in V 1 ) 125 Give high-flow oxygen by face mask. Obtain IV access and take blood for electrolytes, cardi ac enzymes, Ca Obtain 12-lead ECG. Obtain ABG (if evidence of pulmonary edema, reduced cons cious level, sepsis). 2+ , Mg 2+ . VT: Hemodynamically stable. \212 \212 \212OR lidocaine 1 \200\2231.5 mg/kg over 2 min, r epeated every 5 min to 300 mg max. \212 \212 \212 Correct hypokalemia and hypomagnesemia. Amiodarone 150 mg IV over 10 min, then 1 mg/min IV \227 6 h. If this fails, or cardiac arrest occurs, use DC shock. After correction of VT, establish th e cause from history/investigations. Maintenance antiarrhythmic therapy may be required. If VT occurs <24 h after MI, give IV lidocaine or amiodarone IVI for 12 \200\22324 h. If VT o ccurs >24 h after MI, give IV lidocaine or amiodarone infusion and start oral antiarrhythmi c (e.g., amiodarone). Prevention of recurrent VT: Surgical isolation of the arrhythmogenic area or implantation of an automatic defibrillator may help. \212 VF: ECG (see Figure 5.23 ): Use asynchronized DC shock (p. 731). See also the American Hear t Association ACLS Guidelines (p. 737). Ventricular extrasystoles (PVCS) are the most commo n post-MI arrhythmia but they are also seen in healthy people ( \211 10/h). Post-MI, they suggest elec- trical instability, and there is a risk of VF if the \200\234R on T \200 \235 pattern (i.e., no gap before the T wave) is seen. Specific therapies to decrease PVCs have been shown to increase mortality so only treat with -blockers. Otherwise, just obse rve patient and replace electrolytes. Torsade de pointes: Looks like VF but is VT with vary ing axis (ECG, see Figure 5.23 ). It is due to ^ QT interval (congenital, drug-induced, or biochemical) and also occurs post MI. Treatment : Mg sulfate overdrive pacing. Figure 5.22 Fusion and capture beats 126 Figure 5.23 Specimen rhythm strips (a) VT with a rate of 235/min. (b) VF. (c) Torsade de pointes tachycardia. Pacemakers Pacemakers supply electrical initiation to myocardial contraction. The pace- mak er lies subcutaneously, where it may be programed through the skin as necessary. Pacemakers usually last 7 \200\22315 yrs. See Table 5.7 for pacemaker terminology. Indications for te mporary cardiac pacing \212 \212 e n i c i d e m r a l u c s a v o d r a C Symptomatic bradycardia, unresponsive to atropine Acute conduction disturbances following M I: \212 After acute \200\223 Complete AV block \200\223 Mobitz type II AV block \200\223 Nonadja cent bifascicular or trifascicular block (p. 95) \200\223 After inferior MI, pacing may no t be needed in complete AV block if reasonably stable, rate is >40 \200\22350, and QRS comp lexes are narrow. anterior MI, prophylactic pacing is required in: i \212 \212 Suppression of drug-resistant tachyarrhythmias (e.g., SVT, VT) Special situations: During g eneral anesthesia, during cardiac surgery, dur- ing electrophysiological studies, drug over dose (e.g., digoxin, -blockers, verapamil). Indications for a permanent pacemaker \212 Complete AV block (Stokes \200\223Adams attacks, asymptomatic, congeni- tal) or Mobitz type II AV block (p. 120) with symptoms or HR <40 or >3 sec asystole Persistent AV block after anterior MI Symptomatic bradycardias (e.g., sick sinus syndrome [ Drug-resistant tachyarrhy thmias \212 \212 \212 Some say persistent bifascicular block after MI requires a permanent syst em: This remains controversial. Preoperative assessment: CBC, PT/PTT. Insert IV cannula. Ob tain consent for procedure under local anesthetic. Consider premedication. Give antibi- oti c coverage 20 min before, and 1 and 6 h after. Postprocedure assessment: Prior to discharge , check wound for bleeding or hematoma, check position on CXR, check pacemaker function. Du ring first week, inspect for wound hematoma, dehiscence, or muscle twitching. Count apical rate (p. 71): If this is \211 6 bpm less than the rate quoted for the pacemaker, suspect malfunction. Other problems: Lead fracture, pacemaker interference (e.g., from patient \200 \231s muscles). Types of pacemakers: Three-letter pacemaker codes enable the identification of the pacemaker: The first letter indicates the chamber paced (A = atria, V = ventricles, D = dual chamber); the second letter identifies the chamber sensed (A = atria, V = ventric les, D = dual chamber, 0 = none), and the third letter indicates the pacemaker response (T = triggered, I = inhibited, D = dual, R = reverse). DDD pacemakers are the only pacemakers that sense and pace both chambers. The fourth letter (if present) is for rate responsivenes s during motion. ECG of paced rhythm (ECG 7 [p. 99] and Figure 5.24 for rhythm strip): If t he system is on \200\234demand \200\235 of 60 bpm, a pacing spike will only be seen if the intrinsic heart rate is <60 bpm. If it is cutting in at a higher rate, its sensing mode is malfunctioning. If it is failing to cut in at slower rates, its pacing mode is malfunction ing(i.e., the lead may be dislodged, the pacing threshold is too high, or the lead [or insu lation] is faulty). If you see spikes but no capture (i.e., no systole), suspect dislodgmen t. p. 118]) 127 Table 5.7 Some confusing pacemaker terms Fusion beat: Union of native depolarization and pacemaker impulse. Pseudofusion: The pacema ker impulse occurs just after cardiac depolariza- tion, so it is ineffective, but it distor ts the QRS morphology. Pseudo pseudofusion beat: If a DVI pacemaker gives an atrial spike w ithin a native QRS complex, the atrial output is noncontributory. Pacemaker syndrome: In si ngle-chamber pacing, retrograde conduction to the atria, which then contract during ventric ular systole. This leads to retrograde flow in pulmonary veins and reduced cardiac output. Pacemaker tachycardia: In dual-chamber pacing, a short-circuit loop goes between the electr odes, causing an artificial WPW-like syndrome. Solution : Single-chamber pacing. Figure 5.24 ECG of paced rhythm. 128 Heart failure: Basic concepts Definition Heart failure occurs when the heart fails to maint ain the cardiac output and BP to meet the body \200\231s requirements. Prognosis is poor, w ith >50% of patients dying within 5 yrs of diagnosis. Classification LVF and RVF may occur independently, or together as con- gestive heart failure (CHF) . Low-output cardiac failure : The heart \200\231s output is inadequate (e.g., ejection fraction <0.35) or is only adequ ate with high filling pressures. Causes: Usually ischemia, hypertension, valve disorders, o r idiopathic. See Table 5.8 for the New York Heart Association (NYHA) clas- sification of h eart failure. \212Pump failure due to: \212Heart muscle disease: IHD, cardiomyopathy (p. 144). \212Restricted filling: Constrict ive pericarditis, tamponade, restrictive cardio- myopathy. This may be the mechanism of act ion of fluid overload: For constriction or tamponade, an expanding right heart impinges on the LV, so filling is restricted by the ungiving pericardium. For restriction, the heart is unable to expand properly because of intrinsic myocardial disease. \212Inadequate heart rate: -blockers, heart block, post MI \212Negative inotropic drug s: E.g., most antiarrhythmic agents \212Excessive preload: E.g., mitral regurgitation or fluid overload; fluid over- load may cause LVF in a normal heart if renal excretion is impaired or big volumes are involved (e.g ., IVI running too fast). More common if there is simultanous compromise of cardiac functio n and in the elderly. \212Chronic excessive afterload: E.g., AS, hypertension NB: High-output failure is rare. Here, output is normal or increased in the face of much in creased needs. Failure occurs when cardiac output fails to meet needs. It will occur with a normal heart, but even earlier if there is heart disease. Causes: Heart disease with anemi a or pregnancy, hyperthy- roidism, Paget \200\231s disease, arteriovenous malformation or f istulas, beriberi. Consequences : Initially features of RVF; later LVF becomes evident. Sym ptoms depend on which ventricle is more affected. LVF : Dyspnea, poor exercise tolerance, f atigue, orthopnea, paroxysmal nocturnal dys- pnea (PND), nocturnal cough ( pink frothy sp utum), wheeze (cardiac \200\234asthma \200\235), nocturia, cool peripheries, weight loss, muscle wasting. RVF : Peripheral edema (up to thighs, sacrum, abdominal wall), abdominal di s- tension (ascites), nausea, anorexia, facial engorgement, pulsation in neck and face (tri cuspid regurgitation), epistaxis. In addition, patients may be depressed or complain of dru g-related side effects. Signs The patient may look ill and exhausted, with cool peripher- i es and peripheral cyanosis. Pulse : Resting tachycardia, pulsus alternans. Systolic BP , narrow pulse pressure, JVP ^ . Precordium : Displaced apex (LV dilatation), RV heave (pulm onary hypertension). Auscultation : S 3 gallop (p. 51), murmurs of mitral or aortic valve d