Outcome in primary PCI \200 Data from over 10 large randomized trials demonstrate a superior outcome in patients with S TEMI who are treated with primary PCI in comparison to outcomes with thrombolysis. There is a signi \201 cant short-term, as well as long-term, reduction in mortality and major adve rse cardiac events (MACE) (death, nonfatal reinfarction, and nonfatal stroke) in STEMI pati ents treated with primary PCI. Furthermore, primary PCI patients have overall better LV fun ction, a higher vessel patency rate, and less recurrent myocardial ischemia. Multiple studi es (including PRAGUE-2 and DANAMI-2) have also demonstrated that interhospital transportati on for primary PCI (community hospital to invasive center) is safe, and primary PCI remains superior to thrombolysis despite the time delays involved. Complications \200 Bleeding from arterial puncture site, stroke, recurrent infarction, need for emergency coro nary artery bypass grafting (CABG), and death are similar in frequency to that in nonemerge nt high-risk PCI cases ( 1%). The best results are obtained from high-volume centers with s igni \201 cant experience in primary PCI. Each primary PCI center will have its own policy for management of cases, including the use of low-molecular-weight (LMW) or unfractionated (UF) heparin, antiplatelet agents (e.g., gpIIb/IIIa inhibitors), etc. It is generally acce pted that in the acute phase only CHAPTER 2 Coronary artery disease 102 the \200\234culprit \200\235 lesion(s) and vessel(s) will be treated. The pattern of disea se in the remainder of the vessels will determine whether further revascularization should be performed as an inpatient or an elective case in the future. STEMI patients treated with uncomplicated primary PCI can often be discharged safely within 72 hours of admission with out the need for further risk strati \201 cation. Primary PCI is more cost-effective in th e long term than thrombolysis with signi \201 cant savings from fewer days in the hospital , less need for readmission, and less heart failure. Post-discharge care, secondary prevent ion, and rehabilitation remain identical to that for other MI cases. Rescue PCI Rescue PCI may be performed as an adjunct to thrombolysis but should be reserved for patients who remain symptomatic post-thrombolysis (failure to reperfuse) or develop ca rdiogenic shock. We recommend that all patients who continue to have post-thrombolysis symp toms and/or ongoing ST-elevation with or without symptoms be discussed with the local invas ive cardiac center for urgent catheterization and revascularization. SURGERY FOR ACUTE STEMI 103 Surgery for acute STEMI Emergency surgical revascularization (CABG) cannot be widely applie d to patients who suffer an MI outside the hospital. CABG in uncomplicated STEMI patients a fter 6 hours from presentation is contraindicated second- ary to signi \201 cant hemorrhag e into areas of infarction. Unstable patients have a very high rate of perioperative mortal ity. CABG in the context of an acute STEMI is of value in the following situations: \200 High-risk coronary anatomy on catheterization (left main stenosis, left anterior descending [LAD] ostial disease). Complicated STEMI (acute mitral regurgitation, or ventricular ruptu re) STEMI patients (with or without successful thrombolysis) with additional coronary lesio ns whose anatomy is best served by CABG on prior or subsequent catheterization \200 CHAPTER 2 Coronary artery disease 104 STEMI: additional measures Low-molecular-weight and unfractionated heparin UFH \200 \200 There is no indication for \200\234routine \200\235 IV heparin following SK. IV heparin (4 000 U/max IV bolus followed by 1000 U/hr max adjusted for an aPTT ratio of 1.5 \200\2232.0 times control) should be used routinely following rtPA and its derivatives for 24 \200\2234 8 hours. LMWH \200 There is clinical trial data supporting the use of LMWH and thrombolysis (e.g., enoxaparin 30 mg IV bolus, then 1 mg/kg SC q12h). As an alternative to UFH, LMWH can be used at a prop hylactic dose to prevent thromboembolic events in high-risk patients. Clopidogrel \200 This should be administered to all patients undergoing primary PCI (loading dose 300 \200 \223600 mg po followed by 75 mg qd). The length of therapy is determined by the type of ste nt used. Drug- eluting stents require longer term use of clopidogrel than bare-metal stents (current guidelines for ACS is 1 year of Plavix). Glycoprotein (gp) IIb/IIIa inhibitors \200 There are multiple ongoing trials to evaluate the role of these agents in combination with thrombolysis and/or LMWH. These are recommended routinely in the context of STEMI patients treated with primary PCI. Lower doses of LMWH/UFH should be used (consult manufacturers inf ormation sheet for individual agents). They can also be used in the context of rescue PCI s ubsequent to failed thrombolysis, although there is a greater risk of bleeding. Current cli nical use is determined on a case-by-case basis in most centers. Calcium antagonists \200 \200 These are best avoided, especially in the presence of LV impairment. Diltiazem and verapami l started after day 4 \200\2235 in post-MI patients with normal LV function may have a smal l bene \201 cial effect. Amlodipine is safe to use in patients with poor LV function post- MI. Nifedipine has been shown to increase mortality and should be avoided. \200 RIGHT VENTRICULAR (RV) INFARCTION 105 Right ventricular (RV) infarction RV infarction results in elevated right-sided pressures ( RA and RVEDP) and low left-sided pressures (resulting in low BP and cardiac output [CO]). I t is common in inferior STEMI. Diagnosis \200 Clinical: Kussmaul \200\231s sign, and pulsus paradoxus) with absence of p ulmonary edema in the context of a low output state (dBP, cold extremities) ECG: in patient s with inferior STEMI a 0.1 mV (>1 mm) ST-segment elevation in any one of leads V4R \200 \223V6R is highly sensitive and speci \201 c for RV infarction. See Figure 2.3 for differe nt ECG patterns identi \201 ed in right-sided precordial leads. Changes may be transient a nd present in the early stages only. ECHO: signs of right heart failure (elevated jugular venous pulsations, look for RV dilation and wall motion abnormalities. Management \200 Aim to maintain a high RV preload. \200 \200 Initially give 1 \200\2232 L of IV \202 uids rapidly. Avoid use of nitrates and diuretics as they reduce preload and can worsen hypotension. In patients requiring pacing, AV synchr ony must be maintained to ensure maximal CO (requires atrial and ventricular wires). Cardio vert any arrhythmias (e.g., AF/ \202 utter or ventricular rhythms). Reduce afterload. \200 \200 \200 This is particularly important if there is concomitant LV dysfunction. Insert intra-aortic balloon pump (IABP) Arterial vasodilators can be used with caution (Na nitroprusside, hydra lazine) or ACE inhibitors. Inotropic support should ideally be avoided and used only if all other measures fail to res tore hemodynamic status. Reperfusion of the right coronary artery (RCA) (PCI and thrombolys is) has been demonstrated to improve RV function and reduce mortality. In extreme cases, su rgically implantable right ventricular assist devices (RVAD) may be used. CHAPTER 2 Coronary artery disease 106 ST-segment elevation \211 1 mm and positive T wave Proximal occlusion of right coronary artery Distal occlusion of right coronary artery No ST-segment elevation and positive T wave ST-segment depression \211 1 mm and negative T wave Occlusion of circumflex coronary artery Figure 2.3 ST-elevation and T-wave con \201 guration in lead V4R in inferoposterior acute MI. Proximal occlusion of the RCA produces ST elevation >1 mm and a positive T wave. Distal occlusion is characterized by a positive T wave but no ST elevation. Occlusion of the circ um \202 ex artery produces a negative T wave and ST depression of at least 1 mm. Reproduce d with permission from Wellens HJ (1999). N Engl J Med 340(5):381 \200\223383. Copyright 1999 Massachusetts Medical Society. All rights reserved. STEMI: PREDISCHARGE RISK STRATIFICATION 107 STEMI: predischarge risk strati \201 cation It is important to identify the subgroup of pa tients who have a high risk of reinfarction or sudden death. These patients may require fur ther revascu- larization or placement of an automatic implantable cardioverter de \201 bri l- lator (AICD) prior to discharge. Primary PCI group STEMI patients treated with primary PCI are at a much lower risk of devel oping post-MI complications than those without treatment or with thrombolytic therapy. There is ongoing debate as to whether patients treated with primary PCI who are found to ha ve additional high-grade coronary lesions at the time of angiography should have total reva scularization as an inpatient or whether this can be achieved after functional testing on a n outpatient basis. Patients who should have electrophysiological assessment prior to dis- charge are listed below. Thrombolysis group Patients treated with thrombolysis should be risk strati \201 ed prior to dis- charge, and high-risk patients should have inpatient (or early outpatient) angiogra phy (Fig. 2.4). High-risk patients are indicated by the following: \200 \200 Signi \201 cant post-infarct angina or unstable angina Positive exercise test (modi \201 ed Bruce protocol) with angina, >1 mm ST depression or fall in BP Cardiomegaly on CXR, poor LV function on ECHO (EF <40%) Documented episodes of ventricular ectopy or VT >24 hours po st- infarction Frequent episodes of silent ischemia on Holter monitoring \200 Electrophysiological evaluation All STEMI patients with 1) nonsustained VT and/or documente d ejec- tion fraction (EF) <40% or 2) sustained/pulseless VT/VF (regardless of EF) should b e considered for implantation of an AICD for secondary preven- tions (AVID, CIDS trial). Pa tients post-MI with decreased LVEF (<35%) 4 \200\2236 weeks after index event should be con sidered for AICD implantation for primary prevention (MADIT and MUSTT trials). Discharge and secondary prevention \200 : because the thrombolysis Length of hospital stay in uncomplicated patients group needs to undergo risk strati \201 cation prior to discharge, they tend to have a mean hospital sta y of 5 \200\2237 days. The primary PCI group generally has shorter hospital stay, between 3 and 4 days. Prior to discharge, an agreed-upon plan between the patient (patient \200\231s family) and physician is necessary to address modi \201 able risk factors, bene \201 cia l medication, and rehabilitation program. Modi \201 able risk factors include the followin g: \200 Management of lipids and use of statins \200 Detection and treatment of diabete s \200 Ensuring blood pressure is adequately controlled CHAPTER 2 Coronary artery disease 108 \200 It is vital that patients understand their prescribed medical regimen and, in partic ular, the importance of long-term treatment. Unless there are contraindications, all patien ts should be on a minimum of \200 \200 \200 \200 All patients should undergo a card iac rehabilitation program. Counseling to discontinue smoking Advice on a healthy diet and weight loss Aspirin 325 mg qd (if true allergy, use clopidogrel 75 mg qd) ACE inhibitor at the recommen ded dosage Statin at the recommended dosage The role of long-term formal anticoagulation is controversial. STEMI Complications \200 Heart failure \200 Shock \200 Post-MI rest or low- threshold angin a \200 Non-sustained or sustained VT \211 24 hours post MI No complications Assess LV function EF \211 45% EF \211 45% Functional test \200 Sub-maximal exercise ECG test \200 Dobutamine stress echocardiogra phy \200 Other Inpatient angiography followed by electrophysiological study Positive for ischemia Negative for ischemia Outpatient angiography Figure 2.4 Suggested strategy post-STEMI in patients who have undergone thrombolysis to det ermine the need for inpatient angiography or electrophysiological study. This \201 gure w as published in Antman EM (2000). Cardiovascular Therapeutics, 2nd edition. Copyright Elsev ier 2000. STEMI: COMPLICATIONS 109 STEMI: complications Complications \200 \200 \200 Continuing chest pain Fever A new systolic murmur may suggest ventricular septal defect (VS D), acute MR, or pericarditis. Dysrrhythmia (VT, AV block, ectopy, and bradycardia) Pump fa ilure \200\224hypotension, cardiac failure, and cardiogenic shock \200 Complications are encountered more commonly in patients post-STEMI, but can also be found i n NSTEMI patients. In NSTEMI patients, complica- tions are more common when multiple cardia c events have occurred. Further chest pain Chest pain post-MI is not necessarily angina. Careful history is needed to characterize the pain. If there is doubt about the etiology of pain in the absence of EC G changes, a stress test or thallium imaging may aid diagnosis. A bruised sensation and musculoskeletal pains are common in the \201 rst 24 \200\22348 ho urs, especially in patients who have received CPR or repeated DC shock. Use topical agents for skin burns. Recurrent infarction is an umbrella term including extension of infarction in the original territory or new infarct in a second territory. \200 \200 It is usually associated with recurrent ST elevation. If cardiac enzymes are not yet back t o normal, a signi \201 cant change is a twofold rise above the previous nadir. Patients sh ould ideally undergo immediate PCI. Thrombolysis is an alternative but a less attractive ap proach. Standard thrombolysis criteria must be met. Bleeding is a risk (Note: SK should not be used in patients whose original STEMI was treated with SK). Post-infarction angina (angina developing within 10 days of MI) should be treated with stan dard medical therapy. All patients with angina prior to discharge should undergo cardiac ca theterization and revascularization as an inpatient. Pericarditis presents as sharp, pleuritic, and positional chest pain, usually 1 \200\2233 d ays post-infarct. It is more common with STEMI. A pericardial friction rub may be audible. ECG changes are rarely seen. Treat with high-dose aspirin (600 mg qid po) covering with a proton pump inhibitor (e.g., l ansoprazole 30 mg qd po). Other nonsteroidal anti- in \202 ammatory drugs (NSAIDs) have be en associated with higher incidence of LV rupture and increased coronary vascular resistanc e and are probably best avoided. Pericardial effusion is more common with anterior MI especially if compli- cated by cardiac failure. Detection is with a combination of clinical features and echocardiography. Most r esolve gradually over a few months with no active intervention. Tamponade is rare and may b e the result of ventricu- lar rupture and/or hemorrhagic effusion. CHAPTER 2 Coronary artery disease 110 Pulmonary thromboembolism can occur in patients with heart failure and prolonged bed rest. Routine use of prophylactic LMWH and UFH com- bined with early mobilization has reduced the incidence of PE. Sources include lower limb veins and/or RV. Fever \200 \200 Often seen and peaks 3 \200\2234 days post-MI. Associated with elevated white blood cell co unt (WBC) and raised C-reactive protein (CRP). Other causes of fever should be considered ( infection, thrombophlebitis, venous thrombosis, drug reaction, and pericarditis). VENTRICULAR SEPTAL DEFECT POST-MI 111 Ventricular septal defect post-MI VSD is classically seen 24 hours (highest risk) to 10 day s post-MI and affects 2% \200\2234% of cases. Clinical features Features include rapid deterioration with a harsh pan-systolic murmur (ma ximal at the lower left sternal edge), poor perfusion, and pulmonary edema. The absence of a murmur in the context of a low-output state does not rule out a VSD. Diagnosis \200 Echocardiography \200\224the defect may be visualized on 2-D ECHO, and color- \202 ow Dopp ler shows the presence of left-to-right shunt. Anterior infarction is associated with apica l VSD and inferior MI with basal VSD. Failure to demonstrate a shunt on ECHO does not exclu de a VSD. Pulmonary artery (PA) catheter (especially in the absence of ECHO or inconclusive ECHO results) \200\224a step-up in oxygen saturation from radial artery (RA) to right vent ricle (RV) con \201 rms the presence of a shunt, which may be calculated by (Art sat \200\223 RA sat) Qp = pulmonary blood \202 ow Qp:Qs = where (Art sat \200\223 PA sat) Qs = systemic blood \202 ow Management Stabilization measures are all temporizing until de \201 nitive repair can take place. Hypotension and pulmonary edema should be managed as described elsewhere. Important principles are the following: \200 Invasive monitoring (PA catheter and arterial line) to dictate hemodynamic management. RA a nd pulmonary capillary wedge pressure (PCWP) dictate \202 uid administration or diuretic use. Cardiac output, mean arterial pressure, and arterial resistance determine the need for vasodilator therapy. If SBP >100 mmHg, cautious use of vasodilator therapy, generally with nitroprusside, will lower the systemic vascular resistance and reduce the magnitude of the shunt (not be used with renal impairment.). Nitrates will cause venodilatation and increas e the shunt and should be avoided. Give inotropes if severely hypotensive (initially dobuta mine but epinephrine may be required depending on hemodynamic response). Increasing systemi c pressure will worsen the shunt. In most cases, an intra-aortic balloon pump (IABP) should be inserted rapidly for counter-pulsation. Consult with surgeons early for possible repair . Operative mortality is high (20% \200\22370%), especially in the context of perioperative shock, inferoposterior MI, and RV infarction. Current recommendations are for high-risk ea rly surgical repair combined with CABG mitral valve (MV) repair or replacement. CHAPTER 2 Coronary artery disease 112 If the patient has been weaned off pharmacological and/or mechanical support, it may be pos sible to postpone surgery for 2 \200\2234 weeks to allow for some level of infarct healing. Patients should ideally undergo catheterization prior to surgical repair to ensure the cul prit vessel(s) are grafted. Closure of the VSD with catheter placement of an umbrella-shape d device has been reported to stabilize critically ill patients until de \201 nitive repai r is possible. ACUTE MITRAL REGURGITATION POST-MI 113 Acute mitral regurgitation post-MI Mitral regurgitation (MR) due to ischemic papillary musc le dysfunction or partial rupture is seen 2 \200\22310 days post-MI. Complete rupture cause s severe MR and is usually fatal. It is more commonly associated with inferior MI (which ma y affect the posteromedial papillary muscle) than anterior MI (anterolateral papillary musc le). \200\234Silent MR \200\235 is quite frequent and must be suspected in any post-MI patient with unexplained hemodynamic deterioration. Diagnosis is by ECHO. In severe MR, PA catheterization will show a raised pressure with a large v wave. Management (see p. 18) \200 Treatment with vasodilators, generally nitroprusside, should be started as early as possibl e once hemodynamic monitoring is available. Mechanical ventilation may be necessary. Consul t with surgeons early for possible repair. \200 CHAPTER 2 Coronary artery disease 114 Pseudoaneurysm and free wall rupture \200 This is demonstrated in up to 6% of STEMI patie nts and leads to sudden death in two-third. A proportion is present subacutely with cardiog enic shock, allowing time for intervention. Diagnosis of subacute cases can be made on a co mbination of clinical features of pericardial effusion, tamponade, and echocardiography. Pa tients who have undergone early thrombolysis have a lower chance of wall rupture. Stabiliza tion of the patient is similar to that for cardiogenic shock. The case must be discussed wi th surgeons immediately to facilitate early repair COCAINE-INDUCED MI 115 Cocaine-induced MI The incidence of cocaine-induced MI, LV dysfunction, and arrhythmias is on the increase. It is estimated that 14% \200\22325% of young patients presenting to urban emergency departments with nontraumatic chest pain may have detectable levels of cocaine a nd its metabolites in their circulation (see Box 2.6). Of this group, 6% have enzymatic evi dence of MI. Diagnosis \200 Diagnosis can be dif \201 cult and must be suspected in any young individual with chest di scomfort and at low risk for ischemic heart disease. occurs most commonly within 12 hours o f cocaine use. Chest pain Effects can return up to 24 \200\22336 hours later secondary to l ong-lasting active metabolites. ECG is abnormal with multiple nonspeci \201 c repolarizati on changes in up to 80% of cases, and approximately 40% may have diagnostic changes of STEM I qualifying for reperfusion therapy. Biochemical markers of cardiac injury patients will h ave elevated CK levels secondary to rhabdomyolysis. TnI is vital to con \201 rm myocardial injury. can be misleading, as many Management General measures \200 These are the same as for anyone presenting with an MI: oxygen: high \202 ow 5 \200\22310 L unless there is a contraindication; analgesia; aspirin 325 mg qd. Nitroglycerin should b e given at high doses as IV infusion (>10 mg/hr \201 nal levels) and dose titrated to sym ptoms and hemodynamic response. Benzodiazepines:to reduce anxiety. Calcium channel blockers . \200 Second-line agents \200 Verapamil cardiac workload and hence restoring oxygen supply and demand, as well as reversi ng coronary vasoconstriction. It should be given cautiously as 1 \200\2232 mg IV bolus at a time (up to 10 mg total) with continuous hemodynamic monitoring. This should be followed b y high-dose oral preparation to cover the 24-hour period for at least 72 hours after the la st dose of cocaine (80 \200\223120 mg po tid). Phentolamine cocaine-induced vasoconstrictio n (2 \200\2235 mg IV and repeated if necessary). It can be used in conjunction with verapam il. has both B- and A-adrenergic activity and can be used after Labetalol verapamil and phe ntolamine if the patient remains hypertensive. It is effective in lowering cocaine-induced hypertension but has no effect on coronary vasoconstriction. Reperfusion therapy: generally associated with poor outcome secondary to hypertension- is given in high doses and has the dual function of reducing is an A-adrenergic antagonist and readily reverses evidence for use of thrombolysis is limited and CHAPTER 2 Coronary artery disease 116 induced hemorrhagic complications. If the patient fails to settle after implementing \201 rst-line measures, verapamil, and phentolamine, they should undergo immediate coronary ang iography followed by PCI if appropriate (evidence of thrombus/vessel occlusion). In the eve nt that angiography is not available, thrombolytic therapy can be considered. CAUTION: Othe r may exacerbate coronary vasoconstriction by allowing unopposed action of the A-adrenergic receptors. B-blockers must be avoided (e.g., propanolol). They Box 2.6 Teaching points: cocaine-induced MI Pathogenesis \200 The cause of myocardial injury is multifactorial, including an increase in oxygen demand (i ncreased HR, BP, and contractility) in the context of decreased supply caused by a combinat ion of inappropriate vasoconstriction (in areas of minor atheroma), enhanced platelet aggre gation, and thrombus formation. The effects can be delayed as the metabolites of cocaine ar e potent active vasoconstrictors and can remain in the circulation for up to 36 hours (or l onger), resulting in recurrent waves of symptoms. Other complications \200 Cocaine-induced myocardial dysfunction includes MI, chronic damage secondary to repetitive sympathetic stimulation (as in pheochromocytoma), myocarditis secondary to cocaine impuriti es/infection, and unfavorable changes in myocardial/ endothelial gene expression. Cocaine-i nduced arrhythmias include both atrial and ventricular tachyarrhythmias, as well as asystol e and heart block (see post-MI arrhythmias Aortic dissection is multifactorial and ATRIAL TACHYARRHYTHMIA POST-MI 117 Ventricular tachyarrhythmias post-MI Accelerated idioventricular rhythm \200 Common (up to 20%) in patients with early reperfusion in \201 rst 48 hours. Usually self- limiting and short lasting with no hemodynamic effects If symptomatic, accelerating sinus r ate with atrial pacing or atropine may be of value. \200 Ventricular premature beats (VPB) \200 \200 Common and not related to incidence of sustained VT/VF Generally treated conservatively by correcting acid \200\223base and electrolyte abnormalities (aim K+ >4.0 mmol/L and Mg2+ >1. 0 mmol/L) Peri-infarction B-blockade reduces VPB. Nonsustained and monomorphic ventricular tachycardia (VT) \200 \200 Associated with worse clinical outcomes. Correct reversible features such as electrolyte ab normalities and acid \200\223base balance. DC cardioversion for hemodynamic instability. No nsustained VT and hemodynamically stable VT (slow HR <100 bpm) can be treated with amiodaro ne (300 mg bolus IV over 30 minutes, followed by 1.2 g infusion over 24 hours). Lidocaine i s no longer recommended as \201 rst-line but may be used second- or third-line treatment. Procainamide is an effective alternative but may be pro-arrhythmic. For incessant VT on am iodarone, consider overdrive pacing. \200 Ventricular \201 brillation (VF) and polymorphic VT \200 \200 \200 Requires immediate de \201 brillation. In refractory VF consider vasopressin 40U IV bolus. Amiodarone 300 mg IV bolus to be continued as an infusion (see above) if output restored. Atrial tachyarrhythmia post-MI \200 \200 Includes supraventricular tachycardia (SVT), AF, and atrial \202 utter If patient is hemo dynamically unstable they must undergo immediate synchronized DC cardioversion. Hemodynamic ally stable patients can be treated with digoxin, B-blockers and/or calcium channel blocker s. Amiodarone can be used to restore sinus rhythm. However, it is not very effective in con trolling rate. Class I agents should generally be avoided as they increase mortality. In AF and \202 utter, patients should undergo anticoagulation to reduce embolic complications if there are no contraindications. CHAPTER 2 Coronary artery disease 118 Bradyarrhythmias and indications for pacing Isolated RBBB/LBBB does not need pacing (unless hemodynamically unsta- ble or progression to higher levels of block). New bifasicular bloc k (RBBB with either LAD or RAD) or BBB with \201 rst-degree AV block may require prophyla ctic pacing depending on the clinical picture. Indications for pacing should not delay repe rfusion therapy. Venous access (femoral or internal jugular vein) should be obtained \201 rst and the pacing wire inserted later. External temporary cardiac pacing, atropine (300 g to 3 mg IV bolus), and isoproterenol can be used to temporarily stabilize patients. Bradyarrhythmias post-MI First-degree AV block This is common and no treatment is required. Second-degree AV block This generally indicates a large infarction affecting the conduction system. Mortality is increased in this group of patients. \200 Mobitz type I is self-limiting with no symptoms. Generally, it requires no speci \201 c tr eatment. If the patient is symptomatic or has progression to complete heart block they will need temporary pacing. Mobitz type II, 2:1, 3:1 should be treated with temporary pacing re gardless of whether it progresses to complete heart block. Third-degree AV block \200 In the context of an inferior MI this can be transient and generally does not require tempo rary pacing unless there is hemodynamic instability or an escape rhythm of <40 bpm. Tempora ry pacing is required with anterior MI and unstable inferior MI. HYPOTENSION AND SHOCK POST-MI 119 Hypotension and shock post-MI Important principles in managing hypotensive patients with MI are as follows: \200 If the patient is well perfused peripherally, no pharmacological intervention is required. Try to correct any arrhythmia, hypoxia, or acidosis. Arrange for an urgent ECHO to exclude a mechanical cause for hypotension (e.g., mitral regurgitation, VSD, ventricular aneurysm, tamponade) that may require urgent surgery. \200 Patients may be divided into two subgroups 1. Hypotension with pulmonary edema \200 Secure central venous access \200\224internal jugular lines are preferable if the patient i s treated with thrombolytic therapy. Begin inotropes. Use further invasive hemodynamic moni toring as available (PA pressures and wedge pressure monitoring, arterial line). Ensure opt imal \201 lling pressures, guided by physical signs and PA diastolic or wedge pressure. S igni \201 cant mitral regurgitation will produce large v waves on the wedge trace and give high estimates of left ventricular end diastolic pressure (LVEDP). Ensure rapid coronary r eperfusion (if not already done), either with thrombolytic therapy or primary PCI, where av ailable. IABP counter-pulsation may allow stabilization until PCI can be performed. \200 2. Hypotension without pulmonary edema \200 \200 This may be due to either RV infarction or hypovolemia. Check the jugular venous pressure ( JVP) and RA pressure. This will be low in hypovolemia and high in RV infarction. RV infarct ion on ECG is seen in the setting of inferior MI and ST elevation in right-sided chest lead s (V3R \200\223V4R). In either case, cardiac output will be improved by cautious plasma exp ansion. Give 100 \200\223200 mL of IV \202 uids over 10 minutes and reassess. Repeat once if there is some improvement in blood pressure and the patient has not developed pulmonary edema. Invasive hemodynamic monitoring with a PA catheter (Swan \200\223Ganz) is necessary to ensure hypotension is not due to low left-sided \201 lling pressures. Aim to keep PCW P 12 \200\22315 mmHg. Start inotropes if BP remains low despite adequate \201 lling press ures. Use IV nitrates and diuretics with caution as venodilatation will compromise RV and L V \201 lling and exacerbate hypotension. See p. 105 for management of RV infarction. \200 CHAPTER 2 Coronary artery disease 120 Cardiogenic shock This affects between 5% and 20% of patients, and up to 15% of MI patients can present with cardiogenic shock. Management involves a complex interaction between many medical, surgical, intensive care te ams with multiple invasive and noninvasive meas- ures. Despite signi \201 cant advances, p rognosis remains poor. Therefore, the absolute wishes of the patient with regard to such an invasive strategy should be respected from the outset. Diagnosis A combination of clinical and physiological measures: \200 Clinical: <80 \200\22390 mmHg. Physiological: pressure (PCWP >18 mmHg). marked, persistent (>30 minutes) hypotension with SBP low cardiac index (<1.8 L/mm/m2) with elevated LV \201 lling Management \200 \200 Management is complex and must be quick. Correct reversible factors: \200 \200 \200 R apid hemodynamic, echocardiographic, and angiographic evaluation: \200 Arrhythmias and aim to restore sinus rhythm Acid \200\223base, electrolyte abnormalities Ve ntilation abnormalities \200\224intubate if necessary Hemodynamic: central venous lines, Swan \200\223Ganz, arterial line insertion, urinary cath eter Echocardiographic: exclude mechanical lesions, which may need to be dealed with; for e mergency cardiac surgery for mitral regurgitation, VSD, or ventricular aneurysm or pseudoan eurysm Angiographic: to ensure adequate monitoring and access including to assess ventricular systolic function and Aim to improve hemodynamic status, achieving a SBP (cid:116)90 mmHg, guided by physical sig ns and LV \201 lling pressures. As a general guide: \200 with view to PCI or CABG, if appropriate PCWP <15 mmHg in 100 \200\223200 mL aliquots. PCWP >15 mmHg edema). \200\224cautious administration of IV \202 uids (colloids) \200\224inotropic support diuretics (if pulmonary Inotropes should be avoided if at all possible in acutely ischemic patients. The aim should be to rapidly restore or maximize coronary \202 ow and off- load LV. Early revasculariza tion is vital and has been shown to decrease mortality. IABP will help to achieve these goa ls. If hemodynamic status does not improve after revascularization and IABP insertion, inotrope s should be used. The choice of agent can be dif \201 cult and should be guided in part by local protocols and expertise. Generally accepted choices depend on the clinical picture: \200 If the patient is hypotensive ( pulmonary edema) start with dopamine (up to 15 g/kg/min ), and if ineffective, one may substitute epinephrine and/or norepinephrine. CARDIOGENIC SHOCK 121 If the patient has adequate blood pressure ( pulmonary edema) give dobutamine to increase cardiac output (starting at 2.5 \200\2235 g/kg/min and increasing to 20 g/kg/min), tit rating to HR and hemodynamics. Phosphodiesterase inhibitors (PDIs) can be used as an altern ative. If hypotension and tachycardia complicate dobutamine/PDI treatment, norepinephrine c an be added as a second agent to achieve the desired hemodynamic effect. Use of diuretics, thrombolysis, gp IIb/IIIa antagonists, and LMWH/UFH should follow normal principles and are based on the clinical picture. CHAPTER 2 Coronary artery disease 122 Non-ST elevation myocardial infarction (NSTEMI)/unstable angina (UA) UA and NSTEMI are clos ely related conditions with similar clinical pres- entation, treatment, and pathogenesis bu t of varying severity. If there is biochemical evidence of myocardial damage, the condition is termed NSTEMI; in the absence of damage it is termed UA. Unlike patients with a STEMI, in whom diagnosis is generally made on presentation in the em ergency department, diagnosis of NSTEMI/UA may not be de \201 nitive on presentation and e volves over the subsequent hours to days. Therefore, management of patients with NSTEMI/UA is a pro- gression through a number of risk strati \201 cation processes dependent on hist ory, clinical features, and investigative results. These in turn determine the choice and t iming of a number of medical and/or invasive treatment strategies. Figure 2.5 is a summary of a recommended integrated care pathway illustrating a management plan for diagnosis and risk-directed treatment of a patient with STEMI/UA. Clinical presentation There are three distinct presentations: \200 \200 New-onset angina Rest angina prior stable, exertional angina) Increasing angina whom angina has become more frequent or longer in duration or requires a lower threshold to elicit) (in a patient without prior angina) (angina when patient is at rest; may occur in a patient with (in a patient with previously diagnosed angina for General examination must be undertaken to rule out pulmonary edema, assess hemodynamic stab ility, and look for cardiac valve abnormalities. Integrated management plan We recommend that all patients follow a local integrated care pa thway on presentation. The various stages are broadly outlined below. See relevant pages fo r further information. Initial stabilization \200 \200 \200 Transfer patient to an area with continuous ECG monitoring. Strict bed rest is required. Gi ve oxygen, aspirin 325 mg po, sublingual nitrates, and mild sedation if required. If pain p ersists, give morphine 2.5 \200\2235 mg IV prn with metoclopramide 10 mg IV for nausea. General investigations are similar to those for STEMI patients, including blood for CBC, bi ochemical pro \201 le, markers of myocardial injury, and lipid. Arrange portable CXR (rule out LVF and mediastinal abnormalities). NSTEMI/UA 123 Symptoms suggestive of ACS Noncardiac diagnosis Chronic stable angina NSTEMI/UA STEMI Admit ASA, Clopidogrel, LMWH (UFH), NTG infusion, B-blocker, statin Admit to CCU Reperfusion therapy Early risk stratification in emergency room see Table, 2.2 Low risk Intermediate risk High risk No Late risk stratification see pXX X Admit monitored bed. On-going symptoms? Admit to CCU IIb/IIIa Early invasive strategy Yes Treat as high risk Inpatient angiography Low risk High risk Outpatient angiography Figure 2.5 NSTEM/VA \200\224integrated care pathway. Reprinted with permission from ACC Pra ctice Guidelines, J Am Coll Cardiol, 2000; 36:970 \200\2231062. Con \201 rm diagnosis Risk strati \201 cation (see Fig. 2.5, above) to determine appropri ate medical and invasive treatment strategies. High-risk patients should be admitted to a c oronary care unit (CCU) and low- to intermediate-risk patients to monitored beds in a step- down unit. Treatment is based on the patient \200\231s risk and includes the following: \200 Medical treatment \200 Anti-ischemic \200 Antiplatelet \200 Antithrombic Invasive str ategies (p. 131) Secondary prevention and discharge CHAPTER 2 Coronary artery disease 124 NSTEMI/UA: diagnosis Diagnosis in NSTEMI/UA is an evolving process and may not be clear on presentation. A combination of history, serial changes in ECG, and biochemical markers of m yocardial injury (usually over a 24- to 48-hour period) determine the diagnosis. Once a pat ient has been designated as having a diagnosis of ACS with probable or possible NSTEMI/UA t hey will require treatment outlined below. 1. Serial ECGs Changes can be transient and/or \201 xed, especially if a diagnosis of NST EMI is made. \200 ST-segment depression of ischemia (unless isolated in V1 \200\223V3, suggesting a posterior STEMI). T-wave inversion is sensitive but nonspeci \201 c for acute ischemia unless very deep ((cid:116)0.3 mV). Rarely, Q waves may evolve or there may be transient or new LBBB. (cid:116)0.05 mV is highly speci \201 c of myocardial 2. Serial biochemical markers of cardiac injury These are used to differentiate between NST EMI and UA, as well as to determine prognosis. We recommend levels at 0, 6, and 12 hours af ter the last episode of pain. A positive biochemical marker (CK, CK-MB, or troponin) in the context of one or more of the ECG changes listed above is diagnostic of NSTEMI. If serial markers over a 24-hour period from the last episode of chest pain remain negative, UA is di agnosed. Cardiac troponin T and I Both of these are highly cardiac speci \201 c and sensitive, can detect \200\234micro- infarction \200\235 in the presence of normal CK-MB, are not affecte d by skeletal muscle injury, and convey prognostic information (worse prognosis if posi- ti ve). Troponins can be raised in nonatherosclerotic myocardial damage (cardiomyopathy, myoca rditis, pericarditis) and should thus be interpreted in the context of the clinical picture . Both TnT and TnI rise within 3 hours of infarction. TnT may persist up to 10 \200\22314 day s and TnI up to 7 \200\22310 days. Results must be interpreted with caution in patients wit h chronic renal failure (see Fig. 2.5). \200 CK levels do not always reach the diagnostic twice upper-limit of normal and generally have little value in diagnosis of NSTEMI. CK-MB has low sensitivity and speci \201 city. CK-MB isoforms improve sensitivity (CK-MB2>1 U/L or CK-MB2/CK-MB1 ratio >1.5), but isoform assay s are not widely available clinically. Myoglobin is non \200\223cardiac speci \201 c, but levels can be detected as early as 2 hours after onset of symptoms. A negative test is usef ul in ruling out myocardial necrosis.