268 CHAPTER 5 Coronary artery disease STEMI: reperfusion by primary PCI Time is of the essence for reperfusion, and each institut ion should have its recommended protocol. It is imperative that there are no delays in eith er the decision-making or implementation processes for reperfusion. If primary PCI is chose n, one telephone call should ensure a rapid response. Primary PCI \200 Primary PCI is the current gold standard reperfusion strategy for treatment of STEMI. Primary PCI requires signi \201 cant co-ordination between the emergency services, communi ty hospitals, and invasive centers. It must only be performed if: (1) a primary PCI program is available; (2) the patient presents to an invasive center and can undergo catheterizati on without delay. Indication for primary PCI \200 All patients with chest pain and ST-segment elevation or new LBBB ful \201 l primary PCI criteria (compare with indications for thrombolysis). \200 This w ill include a group of patients where ST-segment elevation may not ful \201 l thrombolysis criteria. In general, patients in whom thrombolysis is contraindicated should be managed by primary P CI. Cases where there is signi \201 cant risk of bleeding must be managed individually. Outcome in primary PCI \200 Data from over 10 large randomized trials demonstrate a super ior outcome in patients with STEMI who are treated with primary PCI in comparison to thrombolys is. There is a signi \201 cant short-term, as well as long-term reduction in mortality and major adverse cardiac events (MACE) (death, non-fatal reinfarction and non-fa tal stroke) in STEMI patients treated with primary PCI. Furthermore, primary PCI patients h ave overall better LV function, a higher vessel patency rate, and less recurrent myocardial ischaemia. Multiple studies (including PRAGUE-2 (PRimary Angioplasty in patients transferred from Gene ral community hospitals to specialized PTCA Units with or without Emergency thrombolysis) a nd DANAMI-2 (Danish Acute Myocardial Infarction)) have also demonstrated that interhospital transportation for primary PCI (community hospital to invasive center) is safe, and primar y PCI continues to remain superior to thrombolysis despite the time delays involved. Complications \200 Complications bleeding from the arterial puncture site, stroke, recurrent infarction, need for emergency CABG, and death, which are similar to high-risk PC I cases (71 % ). The best results are obtained from high-volume centers with experience of primary PCI. SURGERY FOR ACUTE STEMI 269 Each primary PCI center will have its own policy for management of cases, including the use of low molecular weight heparin/unfractionated heparin (LMWH/UFH), antiplatelet agents (e.g. GPIIb/IIIa), etc. It is generally accepted that in the acute pha se only the \200\230culprit \200\231 lesion(s)/ vessel(s) will be treated. The pattern of disease in the remainder of the vessels will determine whether total revascularization shou ld be performed as an inpatient or an elective case in the future. STEMI patients treated with primary PCI can be discharged safely within 72 hours of admissi on, without the need for further risk strati \201 cation. Primary PCI is more cost-effective in the long-term, with signi \201 cant savings from fewer days in hospital, less need for readmission, and less heart failure. Post-discharge care, secondary prevention, and rehabilitation remain identical to other MI cases. Rescue PCI As an adjunct to thrombolysis, this should be reserved for patients who remain s ymptomatic post thrombolysis (failure to reperfuse), or develop cardiogenic shock (see b Ca rdiogenic shock, p. 288). We recommend all patients who do not settle post-thrombolysis (on going symptoms and ongoing ST-elevation with/without symptoms) to be discussed with the loc al cardiac center, for urgent catheterization and revascularization. Surgery for acute STEMI Emergency surgical revascularization (CABG) cannot be widely applie d to patients who suffer a MI outside of the hospital. CABG in uncompli- cated STEMI patien ts after 6 hours from presentation is contraindicated, secondary to signi \201 cant hemorr hage into areas of infarction. Unstable patients have a very high perioperative mortality. CABG in the context of an acute STEMI is of value in the following situations: \200 persistent or recurrent chest pain despite thrombolysis/primary PCI \200 high-risk coronary anatomy on catheterization (left main stem coronary artery (LMS), left anterior descending coronary artery (LAD) ostial disease) complicated STEMI (acute MR, ventricular septal defect (VSD)) \200 patients who have unde rgone successful thrombolysis but with surgical coronary anatomy on catheterization patients known to have surgical coronary anatomy on catheterization performed prior to admission with STEMI. 270 CHAPTER 5 Coronary artery disease STEMI: additional measures Low molecular weight and unfractionated heparin UFH \200 There is no indication for \200\230routine \200\231 IV heparin following SK. \200 IV heparin (4000 U max IV bolus followed by 1000 U/h max adjusted for an aPTT (activated partial throm boplastin time) ratio of 1.5 \200\2232.0 times control) should be used routinely following rt-PA and its derivatives for 24 \200\22348 hours. LMWH \200 There are trial data for the use of LMWH and thrombolysis (e.g. enoxaparin 30 m g IV bolus, then 1 mg/kg SC q12h). LMWH can be used at a prophylactic dose to prevent thromboembolic events in patients who ar e slow to mobilize, as an alternative to UFH. Clopidogrel \200 Should be administered to all patients undergoing primary PCI (loading dose 300 mg PO followed by 75 mg od). If coronary stents are used, patients should remain on clopidogrel for at least 1 month in bare-metal stents and 12 months in coated stents. \200 More data are required to see whet her longer-term treatment may be of bene \201 t following thrombolysis alone. Glycoprotein IIb/IIIa inhibitors \200 There are multiple ongoing trials to evaluate their role in combination with thrombolysis and/or LMWH. Are recommended routinely in the context of STEMI patients treated with primary PCI. Lower doses of LMWH/UFH should be used (consult manufacturer \200\231s in formation sheet for individual agents). \200 They can also be used in the context of resc ue PCI subsequent to failed thrombolysis, although there is a greater risk of bleeding. Each case must be judged on its merits. Magnesium \200 Earlier trials giving Mg 2 + before or with thrombolytic agents showed som e bene \201 t in mortality. ISIS-4 showed no bene \201 t from the routine use of IV magne sium post-MI. However Mg 2 + was given late (6 hours) after thrombolysis, by which time the protective effect of Mg 2 + on reperfusion injury may have been lost. Trials are ongoing. Current accepted role for Mg 2 + is con \201 ned to Mg 2 + deplete patients and patients with reperfusion, supraventricular, and ventricular arrhythmias. Dose: 8 mmol in 20 mL 5 % dextrose over 20 minutes followed by 65 mmol in 100 mL 5 % dextro se over 24 hours. (Contraindications: serum Cr > 00 mol/L, 3 AV block.) STEMI: ADDITIONAL MEASURES 271 Calcium antagonists \200 Best avoided, especially in the presence of LV impairment. \200 Diltiazem and verapamil started after day 4 \200\2235 in post-MI patients with normal LV function have a small bene \201 cial effect. Amlodipine is safe to be used in patients with poor LV post-MI. \200 Nifedipine has been shown to increase mortality and should be avoided. 272 CHAPTER 5 Coronary artery disease Right ventricular infarction \200 RV infarction results in elevated right-sided pressures (RA, right ventricular end-diastolic pressure (RVEDP)) and low left-sided pressures (BP, C O). It is common in inferior STEMI. Diagnosis \200 Clinical : signs of right heart failure (iJVP (jugular venous pressure), Kussmaul \200\231s sign, pulsus paradoxus) with absence of pulmonary oedema in the context of a low-output state (dBP, cold peripheries). ECG : in patients with inferior STEMI, a 0.1 mV ( > 1 mm) ST segment elevation in any one o f leads V 4R \200\223V 6R is highly sensitive and speci \201 c for RV infarction. See Fig . 5.14 for different ECG patterns identi \201 ed in right-sided precordial leads. Changes may be transient and present in the early stages only. ECHO : looking for RV dilation and wall motion abnormalities. Management \200 Aim to maintain a high RV preload: initially give 1 \200\2232 L of colloid rapidly \200 avoid use of nitrates and diuretics as they reduce pre-load and can worsen hypotension in patients requiring pacing, AV synchrony must be maintained to ensure maximal CO (atrial and ventricular wires) cardiovert any arrhythmias (supraventricular tachycardia (SVT), AF/ \202 utter or ventricular rhythms). Reduce afterload: this is particularly important if there is concomitant LV dysfunction \200 insert intra-a ortic balloon pump (IABP) \200 arterial vasodilators can be used with caution (Na nitropr usside, hydralazine), or ACE-Is. Inotropic support should ideally be avoided and used if all other measures fail to restore haemodynamic status. Reperfusion of the right coronary artery (RCA) (PCI and thrombolysis) has been demonstrated to improve RV function and reduce mortality. RIGHT VENTRICULAR INFARCTION 273 Fig. 5.14 ST-elevation and T-wave con \201 guration in lead V 4R in inferoposterior AMI. P roximal occlusion of the RCA produces ST elevation > 1 mm and a positive T wave. Distal occ lusion is characterized by a positive T wave but no ST elevation. Occlusion of the circum \202 ex artery produces a negative T wave and ST depression of at least 1 mm. Adapted with permission from Wellens HJ (1999). N Engl J Med 340 : 1383. 274 CHAPTER 5 Coronary artery disease 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. They should undergo coronary a ngio graphy with view to revascularzation prior to discharge (if not treated with primary P CI) and/or electrophysiological investigations as necessary. Primary PCI group \200 STEMI patients treated with primary PCI are at a much lower risk o f developing post-MI complications. There is ongoing debate whether patients treated with primary PCI should have total revascularization as an inpatient or whether this can be achieved after f unctional testing on an outpatient basis. Follow your local policy. Patients who should have electrophysiological assessment prior to discharge are listed below. Thrombolysis group \200 Patients treated with thrombolysis should be risk strati \201 ed prior to discharge, and high-risk patients should have inpatient (or early outpatient) ang iography. High-risk patients include: \200 signi \201 cant post-infarct angina or unstab le angina \200 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 (ejection fraction (EF)<40 % ) documented episodes of regular venous embolisms (VEs) and VT 24 h post infarction frequent episodes of silent ischaemia on Holter monitoring. Electrophysiological study All STEMI patients with (1) non-sustained VT and documented EF<4 0 % or (2) sustained/pulseless ventricular tachycardia/ \201 brillation (VT/VF) (regard- l ess of EF) should undergo electrophysiological testing prior to discharge (MADIT (Multicent er Automatic De \201 brillator Implantation trial) and MUSTT (Multicenter Unsustained Tach ycardia Trial) trials), with a view to de \201 brillator implantation. Discharge and secondary prevention \200 Length of hospital stay in uncomplicated patients : the thrombolysis group need to undergo risk strati \201 cation prior to discharge and t end to have a mean hospital stay of 5 \200\2237 days. The primary PCI group have shorter ho spital stay, between 3 \200\2234 days. Prior to discharge, an agreed plan between the patient (patient \200\231s family) and physi cian is necessary to address modi \201 able risk factors, bene \201 cial medication, and a rehabilitation program. Modi \201 able risk factors include: management of lipids and use of statins \200 detection and treatment of diabetes \200 e nsuring blood pressure is adequately controlled \200 counseling to discontinue smoking \200 advice on a healthy diet and weight loss. STEMI: PREDISCHARGE RISK STRATIFICATION 275 It is vital patients understand the medical regime, and in particular the importance of lon g-term \200\230prognostic medication \200\231. Unless there are contraindications, all pat ients should be on a minimum of: \200 aspirin 75 mg od (if true allergy, use clopidogrel 75 mg od) \200 ACE-I at the recommended dosage \200 statin at the recommended dosage The role of long term formal anticoagulation is controversial. \200 All patients must be plugged into a rehabilitation program. STEMI No complications 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 Assess LV function EF \211 45% EF \211 45% Functional test \200 Submaximal exercise ECG test \200 Dobutamine stress echocardiograp hy \200 Other Inpatient angiography followed by electrophysiological study Negative for ischaemia Positive for ischaemia Outpatient angiography Fig. 5.15 Suggested strategy post-STEMI in patients who have undergone thrombolysis to dete rmine the need for inpatient angiography/electrophysiological study. Adapted from Antman EM (2000). Cardiovascular Therapeutics 2nd edition. Saunders, Philadelphia. 276 CHAPTER 5 Coronary artery disease STEMI: complications Complications These include: \200 continuing chest pain \200 fever \200 a new systolic murmur \200\224 VSD, acute MR, or pericarditis \200 dysrrhythmia (VT, AV block ectopics, and bradycardia) \200 pump failure \200\224 hypotension, cardiac failure, and cardiogenic shock. Complications are encountered more commonly in patients po st-STEMI, but can also be found in NSTEMI patients. In NSTEMI patients, complica- tions are more common where multiple cardiac events have occurred. Further chest pain \200 Chest pain post-MI is not necessarily angina. Careful history is needed to characterize pain. If there is doubt about the etiology of pain in the absence of ECG changes, stress/thallium imaging may aid diagnosis. \200 A bruised sensation and mus culoskeletal pains are common in the \201 rst 24 \200\22348 hours, especially in patients who have received cardiopulmonary resuscitation (CPR) or repeated DC shock. Use topical ag ents for skin burns. Recurrent infarction is an umbrella term including both extension of infarction in the orig inal territory, or repeated infarct in a second territory: \200 usually associated with r ecurrent ST elevation \200 if cardiac enzymes are not yet back to normal, a signi \201 c ant change is a twofold rise above the previous nadir patients should ideally undergo immediate PCI. Thrombolysis is an alternative, but a less a ttractive approach. Standard thrombolysis criteria must be met. Bleeding is a risk (NB: SK should not be used on a second occasion). 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 qds PO) covering with a p roton pump inhibitor (e.g. lansoprazole 30 mg od PO). Other NSAIDs have been associated wit h higher incidence of LV rupture and increased coronary vascular resistance, and are probab ly best avoided. Pericardial effusion is more common with anterior MI, especially if complicated by cardiac failure. Tamponade is rare and the result of ventricular rupture and /or haemorrhagic effusions. Detection is with a combination of clinical features and echoca rdiography. Most resolve gradually over a few months with no active intervention. STEMI: COMPLICATIONS 277 Pulmonary thromboembolism can occur in patients with heart failure and prolonged bed rest. Routine use of prophylactic LMWH and UFH combined with early mobilization have reduced the incidence of PE. Sources include lower limb veins and/or RV (see b Pulmonary embolism: asse ssment, p. 742). Fever \200 Often seen and peaks 3 \200\2234 days post-MI \200 Associated with elevated white cell count (WCC) and raised CRP \200 Other causes of fever should be considered (in fection, thrombophlebitis, venous thrombosis, drug reaction, pericarditis). 278 CHAPTER 5 Coronary artery disease Ventricular septal defect post-MI \200 Classically seen 24 hours (highest risk) to 10 day s post-MI and affects 2 \200\2234 % of cases. Clinical features include rapid deterioration with a harsh pansystolic murmur (maximal at the lower left sternal edge), poor perfusion, and pulmonary oedema. The absence of a murmur in the context of a low output state does not rule out a VSD. Diagnosis : echocardiography \200\224 the defect may be visualized on 2D ECHO, and color \202 ow Doppler shows the presence of left-to-right shunt. Anterior infarction is associated with apical VSD, and inferior MI with basal VSD. Failure to demonstrate a shu nt on ECHO does not exclude a VSD. Pulmonary artery (PA) catheter (especially in absence of ECHO or inconclusive ECHO results) \200\224 a step-up in oxygen saturation from RA to RV con \201 rms the presence of a shu nt, which may be calculated by: ( ( ) at RA sat ) at PA sat = = Q 5Q = \210\222 \210\222 pulmonary brr lood fl owoo Art srr Art srr = p where sQ Q Q p systemic blood flow = and Art arterial and sat arterial and sat saturation Management Stabilization measures are all temporizing until de \201 nitive repair can take place. Hypotension and pulmonary oedema should be managed as described elsewhere. Importan t principles are: \200 invasive monitoring (PA catheter and arterial line) to dictate hae modynamic management. RA and PCWP dictate \202 uid administration or diuretic use. CO, me an 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. Nitrates will cause venodilatation and increase the shunt and should be avoided. Not be used with renal impairment. inotropes if severely hypotensive (initially dobutamine but adrenaline may be required depe nding on haemodynamic response). Increasing systemic pressure will worsen shunt. in most cases an intra-aortic balloon should be inserted rapidly for counter pulsation. liaise with surgeons early for possible repair. Operative mortality is high (20 \200\22370 % ), especially in the context of perioperative shock, inferoposterior MI, and RV infarctio n. Current recommendations are for high-risk early surgical repair combined with CABG mi tral valve (MV) repair/replacement. VENTRICULAR SEPTAL DEFECT POST-MI 279 if the patient has been weaned off pharmacological and/or mechanical support, it may be possible to postpone surgery for 2 \200\2234 weeks to allow for some lev el of infarct healing. patients should ideally undergo catheterization prior to surgical repair to ensure culprit vessel(s) are grafted. closure of the VSD with catheter placement of an umbrella-shaped device has been reported to stabilize critically ill patients until de \201 nitive repair is possible. 280 CHAPTER 5 Coronary artery disease Acute mitral regurgitation post-MI \200 MR due to ischaemic papillary muscle dysfunction or partial rupture is seen 2 \200\22310 days post-MI. Complete rupture causes torrential MR and is usually fatal. More commonly associated with inferior MI (posteromedial papillary muscle) than anterior MI (anterolateral papillary muscle). \200\230Silent MR \200\231 is quite frequent and must be suspected in any post-MI patient with unexplained haemodynamic deterioration. Diagnosis is by ECHO. In severe MR, PA catheterization will show a raised pressure with a large v wave. Management (see b Acute mitral regurgitation, p. 736). \200 Treatment with vasodilators, generally nitroprusside, should be started as early as possible once haemodynamic monitoring is available. Mechanical ventilation may be necessary. \200 Liaise with surgeons early for possible rep air. PSEUDOANEURYSM AND FREE-WALL RUPTURE 281 Pseudoaneurysm and free-wall rupture \200 Demonstrated in up to 6 % of STEMI patients and leads to sudden death in two thirds. A proportion present subacutely with cardiogenic shock allowing time for intervention (see b Cardiogenic shock, p. 288). Diagnosis of subacute cases can be made on a combination of clinical features of pericardia l effusion, tamponade, and echocardiography. \200 Patients who have undergone early throm bolysis have a lower chance of wall rupture. Stabilization of the patient follows similar lines to cardiogenic shock (see b Cardiogenic shock, p. 288). The case must be discussed with surgeons immediately, with a view to repair . 282 CHAPTER 5 Coronary artery disease Cocaine-induced MI \200 The incidence of cocaine-induced MI, LV dysfunction, and arrhythm ias is on the increase. It has been estimated that 14 \200\22325 % of young patients presenting to urban emergency departments with non-traumatic chest pain may have detectable levels of coc aine and its metabolites in their circulation. Of this group, 6 % have enzymatic evidence o f MI ( \201 gures are from USA). \200 Most patients are young, non-white, male, cigarett e smokers without other risk factors for ischaemic heart disease. Diagnosis \200 Can be dif \201 cult and must be suspected in any young individual with c hest discomfort at low risk of developing ischaemic heart disease. \200 Chest pain : occu rs most commonly within 12 h of cocaine use. Effects can return up to 24 \200\22336 h later, secondary to long-lasting active metabolites. ECG : is abnormal with multiple non-speci \201 c repolarization changes in up to 80 % of cases, and approximately 40 % may have diagnostic changes of STEMI qualifying for reperfusion therapy (see b STEMI: diagnosis, p. 258). Biochemical markers of cardiac injury : can be misleading, as most patients will have eleva ted CK levels secondary to rhabdomyolysis. TnT and TnI are vital to con \201 rm myocardial injury. 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 75 mg od. GTN: to be given at high doses as IV infusion ( > 10 mg/h \201 nal levels) and dose titrated to symptoms and haemodynamic response (see b ST elevation myocardial infa rction (STEMI), p. 256). Benzodiazepines: to reduce anxiety. Second-line agents \200 Verapamil : is given in high doses and has the dual function of reducing cardiac work load and hence restoring oxygen su pply and demand, as well as reversing coronary vasoconstriction. Should be given cautiously as 1 \200\2232 mg IV bolus at a time (up to 10 mg total) with continuous haemodynamic moni toring. This should be followed by high-dose oral preparation to cover the 24 hour period f or at least 72 hours post last dose of cocaine (80 \200\223120 mg PO tds). Phentolamine : is an A-adrenergic antagonist and readily reverses cocaine-induced vasoconst riction (2 \200\2235 mg IV and repeated if necessary). It can be used in conjunction with v erapamil. Labetalol : has both A- and B-adrenergic activity and can be used after verapamil and phent olamine if the patient remains hypertensive. It is is effective in lowering cocaine-induced hypertension, but has no effect on coronary vasoconstriction. COCAINE-INDUCED MI 283 Reperfusion therapy : evidence for use of thrombolysis is limited and generally associated with poor outcome secondary to hypertension- induced haemorrhagic complications. If the pat ient fails to settle after implementing \201 rst-line measures, verapamil, and phentolami ne, they should undergo immediate coronary angiography followed by PCI if appropriate (evid ence of thrombus/vessel occlusion). In the event that angiography is not available, thrombo lytic therapy can be considered. CAUTION : B-blockers must be avoided (e.g. propanolol). They exacerbate coronary vasoconstriction by allowing unopposed action of the A \200\223adrenerg ic receptors. Teaching points: cocaine-induced MI Pathogenesis \200 The cause of myocardial injury is multifactorial, including an increase in oxygen demand (iHR, iBP, icontractility) in the context of decrease in supply caused by a combination of inappropriate vasoconstriction (in areas of minor atheroma), enhanced plat elet aggregation, and thrombus formation. The effects can be delayed, as the metabolites of cocaine are potent active vasoconstrictor s and can remain in the circulation for up to 36 hours (or longer), resulting in a recurren t wave of symptoms. Other complications \200 Cocaine-induced myocardial dysfunction is multifactorial and inc ludes MI, chronic damage secondary to repetitive sympathetic stimulation (as in pheochromoc ytoma), myocarditis secondary to cocaine impurities/infection, and unfavorable changes in m yocardial/ endothelial gene expression. Cocaine-induced dysrrhythmias include both atrial and ventricular tachyarrhythmias, as well as asystole and heart block (see post-MI arrhythmias (see b Ventr icular tachyarrhythmias post-MI; Atrial tachyarrhythmia post-MI; Bradyarrhythmias and indic ations for pacing; Bradyarrhythmias post-MI, pp. 284 \200\2235). and cardiopulmonary resusc itation (see b Adult advanced life support, p. 712). \200 Aortic dissection (see b Aortic dissection: assessment, p. 766). 284 CHAPTER 5 Coronary artery disease Ventricular tachyarrhythmias post-MI Accelerated idioventricular rhythm \200 Common (up t o 20 % ) in patients with early reperfusion in \201 rst 48 h. \200 Usually self-limitin g and short lasting with no haemodynamic effects. \200 If symptomatic, accelerating sinus rate with atrial pacing or atropine may be of value. Suppressive anti-arrhythmic therapy ( lidocaine, amiodarone) is only recommended with degeneration into malignant ventricular tac hyarrhythmias. Ventricular premature beats (VPB) \200 Common and not related to incidence of sustained V T/VF. \200 Generally treated conservatively with the aim to correct acid \200\223base and electrolyte abnormalities (aim K + > 4.0 mmol/L and Mg 2 + > 1.0 mmol/L). Peri-infarction B -blockade reduces VPB. Non-sustained and monomorphic ventricular tachycardia \200 Associated with a worse clinic al outcome. \200 Correct reversible features such as electrolyte abnormalities and acid \200\223base balance. DC cardioversion for haemodynamic instability. \200 Non-sustained VT and haemodynamically stable VT (slow HR<100 bpm) can be treated with amiodarone (300 mg bolus IV over 30 min, f ollowed by 1.2 g infusion over 24 h). Lidocaine is no longer recommended as \201 rst line . Procainamide is an effective alternative, but is arrhythmogenic. For incessant VT on amiodarone consider overdrive pacing. Ventricular \201 brillation and polymorphic VT \200 A medical emergency and requires im mediate de \201 brillation. \200 In refractory VF consider vasopressin 40 U IV bolus. \200 Amiodarone 300 mg IV bolus to be continued as an infusion (see above) if output restored. Atrial tachyarrhythmias post-MI \200 Includes SVT, AF, and atrial \202 utter. \200 If patient is haemodynamically unstable they must undergo immediate synchronized DC cardioversion. Haemodynamically stable patients can be treated with digoxin, B -blockers, and/or calcium-c hannel blockers (see b Treatment options in tachyarrhythmias, p. 721). Amiodarone can be used to restore sinus rhythm. However, it is not very effective in contro lling 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. BRADYARRHYTHMIAS POST-MI 285 Bradyarrhythmias and indications for pacing Alternating or isolated RBBB/LBBB do not need p acing (unless haemody- namically unstable or progression to higher levels of block). New bi fasic- ular block (RBBB with either LAD or RAD) or BBB with \201 rst-degree AV block may require prophylactic pacing depending on the clinical picture. Indications for pacing shoul d not delay reperfusion therapy. Venous access (femoral or internal jugular vein) should be obtained \201 rst, and a pacing wire inserted later. External temporary cardiac pacing, atropine (300 mcg to 3 mg IV bolus) and isoprenaline can be used to buy time. Bradyarrhythmias post-MI First-degree AV block \200 Common and no treatment required. \200 Signi \201 cant PR prolongation ( > 0.20 s) is a contraindication to B-blockade. Second-degree AV block This indicates a large infarction affecting conducting systems, and mortality is generally increased in this group of patients. \200 Mobitz type I is self-li miting with no symptoms. Generally, requires no speci \201 c treatment. If symptomatic or there is progression to complete heart block, will need temporary pacing. Mobitz type II, 2:1, 3:1 should be treated with temporary pacing, regardless of whether it progresses to complete heart block. Third-degree AV block \200 In the context of an inferior MI, can be transient and does no t require temporary pacing unless there is haemodynamic instability or an escape rhythm of <40 bpm. Temporary pacing is required with anterior MI and unstable inferior MI. 286 CHAPTER 5 Coronary artery disease Hypotension and shock post-MI (See b Cardiogenic shock, p. 288). The important principles in managing hypotensive patients with MI are: if the patient is well perfused peripherally, no pharmacological intervention is required try to correct any arrhythmia, hypoxia, or acidosis \200 arrange for an urgent ECHO to ex clude a mechanical cause for hypotension (e.g. mitral regurgitation, VSD, ventricular aneurysm) that may require urgent surgery. Subgroups Patients may be divided into two subgroups. 1. Hypotension with pulmonary oedema \200 Secure central venous access \200\224 internal jugular lines are preferable if the patient may have received thrombolytic therapy. \200 Commence inotropes (See b Cardio genic shock, p. 288). \200 Further invasive haemodynamic monitoring as available (PA pres sures and wedge pressure monitoring, arterial line). Ensure optimal \201 lling pressures, guided by physical signs and PA diastolic or wedge p ressure. Signi \201 cant mitral regurgitation will produce large v waves on the wedge trac e and give high estimates of LVEDP. Ensure rapid coronary reperfusion (if not already done), with either thrombolytic therapy or primary PCI where available. Intra-aortic balloon counter pulsation (See b Intra-aortic balloon coun- terpulsation, p. 8 22) may allow stabilization until PCI can be performed. 2. Hypotension without pulmonary oedema \200 This may be due to either RV infarction or h ypovolaemia. Diagnosis \200 Check the JVP and right atrial pressure. This will be low in hypovolaemia and high in RV infarction. RV infarction on ECG is seen in the setting of inferior MI and ST elevation in right-sided chest leads (V 3R \200\223V 4R ). Management \200 In either case, cardiac output will be improved by cautious plasma expansion. Give 100 \200\223200 mL of colloid over 10 minutes and reassess. \200 Repeat o nce if there is some improvement in blood pressure and the patient has not developed pulmonary oedema. Invasive haemodynamic monitoring with a PA catheter (Swan \200\223Ganz) is necessary to ens ure hypotension is not due to low left-sided \201 lling pressures. Aim to keep PCWP 12 \200\22315 mmHg. Start inotropes if BP remains low despite adequate \201 lling pressures. \200 Use IV ni trates and diuretics with caution, as venodilatation will compromise RV and LV \201 lling and exacerbate hypotension. See b p.272 for management of RV infarction. This page intentionally left blank 288 CHAPTER 5 Coronary artery disease Cardiogenic shock \200 Affects 5 \200\22320 % of patients, and up to 15 % of MI patients can present with cardiogenic shock. Management involves a complex interaction between many medical, surgical, and intensive car e teams, with multiple invasive and non- invasive measures. Despite signi \201 cant advanc es, prognosis remains poor. Therefore, the absolute wishes of the patient with regard to such an invasive strategy should be respected from the onset. Diagnosis A combination of clinical and physiological measures: \200 clinical: marked, pe rsistent ( > 30 min) hypotension with SBP<80 \200\22390 mmHg \200 physiological: low card iac index (<1.8 L/mm/m 2 ) with elevated LV \201 lling pressure (PCWP > 18 mmHg). Management \200 Complex and must be quick. \200 Correct reversible factors, including: arrhythmias and aim to restore sinus rhythm \200 acid \200\223base and electrolyte abnorm alities \200 ventilation abnormalities \200\224 intubate if necessary Rapid haemodynamic, echocardiographic, and angiographic evaluation: \200 haemodynamic: to ensure adequate monitoring and access, including central venous lines, Swan \200\223Ganz, arterial line insertion, urinary catheter echocardiographic: to assess ventricular systolic function and exclude mechanical lesions, which may need to dealed with, emergency cardiac surgery including mitr al regurgitation (NB: tall v waves on PCWP trace), VSD, and ventricular aneurysm/psuedoanue rysm. angiographic: with a view to PCI or CABG if appropriate \200 Aim to improve haemodynamic status achieving a SBP (cid:2) 90 mmHg guided by physical signs and LV \201 lling pressures. As a general guide: \200 PCWP<15 mmHg \200\224 cautious of IV \202 uids (colloids) in 100 \200\223200 mL aliquots PCWP > 15 mmHg \200\224 inotropic support diuretics (if pulmonary oedema). Inotropes should be avoided if at all possible in acutely ischaemic patients. The aim should be to rapidly restore/maximize coronary \202 ow and of \202 oad LV. Early revascularization is vital and has been shown to decrease mortality. IABP will p artially help achieve the aforementioned goals. If haemodynamic status does not improve post revascularization and IABP insertion, inotrope s should be used. The choice of agent can be dif \201 cult and should partly be guided by local protocols and expertise. Generally accepted choices depend on the clinical picture an d include: \200 if patient is hypotensive ( pulmonary oedema) \200\224 start with dopamine (up to 15 mcg/kg/min) and if ineffective substitute to adrenaline (epinephrine) an d/or noradrenaline (norepinephrine) CARDIOGENIC SHOCK 289 if the patient has adequate blood pressure ( pulmonary oedema) \200\224 dobutamine to increase cardiac output (starting at 2.5 \200\2235 mcg/kg/m in and increasing to 20 mcg/kg/min) titrating to HR and haemodynamics. Phosphodiesterase in hibitors can be used as an alternative. If hypotension and tachycardia complicate dobutamin e/ PDI inhibitor treatment, (nor)adrenaline can be added as a second agent to achieve desir ed haemodynamic effect. Use of diuretics, thrombolysis, GPIIb/IIIa antagonists, LMWH/UFH should follow normal princ iples, and is based on the clinical picture. 290 CHAPTER 5 Coronary artery disease Non-ST elevation myocardial infarction (NSTEMI)/unstable angina (UA) UA and NSTEMI are clos ely related conditions with similar clinical presen- tation, treatment, and pathogenesis bu t of varying severity. If there is bio- chemical evidence of myocardial damage, the conditi on is termed NSTEMI and, in the absence of damage, UA. Unlike patients with a STEMI, where diagnosis is generally made on presentation in the emer gency department, diagnosis of NSTEMI/UA may not be de \201 nitive on presentation and evo lves over the subsequent hours to days. Therefore, management of patients with NSTEMI/UA is a progression through a number of risk-strati \201 cation processes dependent on history, clinical features, and investigative results, which in turn determine the choice and timin g of a number of medical and/or invasive treatment strategies. Fig. 5.16 is a summary of a recommended integrated care pathway illustrating a management p lan for diagnosis and risk-directed treatment of a patient with STEMI/UA. Clinical presentation There are three distinct presentations: \200 rest angina (angina wh en the patient is at rest) \200 new-onset severe angina \200 increasing angina (previou sly diagnosed angina which has become more frequent, longer in duration, or lower in threshold). General examination (as indicated for all ACS (see b Acute coronary syndromes, p. 254)) mus t beundertaken, in particular to rule out pulmo- nary oedema, and assess haemodynamic stabi lity, cardiac valve abnormali- ties, and diaphoresis. 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 (see also b Acute coronary syndromes, p. 254): \200 transfer the pa tient to an area with continuous ECG monitoring and de \201 brillator facility strict bed rest. \200 give oxygen, aspirin 300 mg PO, SL nitrate, and mild sedation if required if pain persists give diamorphine 2.5 \200\2235 mg IV prn with metoclopramide 10 mg IV. General investigations : similar to STEMI patients (see b STEMI: diagnosis, p. 258) includi ng blood for FBC, biochemical pro \201 le, and markers of myocardial injury, lipid pro \201 le as well as CRP and thyroid function tests (TFTs) (if persistent tachycardia). Arran ge portable CXR (rule out LVF, mediastinal abnormalities). NSTEMI/UA 291 Con \201 rm diagnosis (see b NSTEMI/UA: diagnosis, p. 292). \200 Risk strati \201 catio n (see b NSTEMI/UA: risk strati \201 cation, p. 294) in order to determine appropriate med ical and invasive treatment strategies. High-risk patients should be admitted to CCU and lo w/ intermediate patients to monitored beds in step-down unit. Treatment is based on the patient \200\231s risk and includes: medical : \200\224 anti-ischaemic (see b NSTEMI/UA: medical management, p. 298) \200\224 antiplatelet (see b NSTEMI/UA: medical management, p. 298) \200\224 antithrombot ic (see b NSTEMI/UA: medical management, p. 298) invasive strategies (see b NSTEMI: invasive vs. non-invasive strategies, p. 301) Secondary prevention and discharge Symptoms suggestive of ACS Non-cardiac diagnosis Chronic stable angina NSTEMI/UA STEMI Admit ASA, clopidogrel, LMWH (UFH), GTN infusion, -blocker, statin Admit to CCU Reperfusion therapy Early risk stratification in emergency room see b Table 5.7, p. 295 Low risk Intermediate risk High risk Admit monitored bed. On-going symptoms? Admit to CCU IIb/IIIa inhibitors Early invasive strategy No late risk stratification Yes Treat as high risk Inpatient angiography High risk Low risk