Acute Coronary Syndromes (ACS) Management in the ED - University of Adelaide PDF

UNOFFICIAL Deb Wright MNSc Nurse Consultant Acute Cardiac Assessment Service CALHN ED QEH/RAH deborah.wright@sa...

UNOFFICIAL Deb Wright MNSc Nurse Consultant Acute Cardiac Assessment Service CALHN ED QEH/RAH [email protected] Acute Coronary Syndromes(ACS)- management in the ED & beyond University of Adelaide 2 Key concepts Pathophysiology of ACS Goal of treatment Evidence base for treatment Aims to: o Maximise oxygen delivery to the tissues o Reduce the area of ischaemia o Revascularise o Control symptoms o Preserve ventricular function o Reduce morbidity and mortality Sex differences in ACS, both biological and physiological Novel concepts in diagnosis University of Adelaide 3 Epidemiology Global perspective An estimated 17.9 million people died from cardiovascular diseases (CVD) in 2016, representing 32% of all global deaths. Of these deaths, an estimated 7.4 million were due to coronary artery disease (CAD) Over three quarters of CVD deaths take place in low- and middle-income countries By 2030 more than 23 million people will die annually from CVD (WHO 2019) University of Adelaide 4 Epidemiology Regional perspective CAD Acute myocardial infarction (AMI) o More than 2% of people report o Almost 2% of people experience living with CAD, accounting for AMI sometime in their life – over 590,000 people 430,000 Australians o Kills one Australian every 30 o Responsible for causing almost minutes, on average 50 people a one in 25 deaths - one person day, 2x males dying of AMI every 80 minutes - average 19 people a day o Remains the leading cause of death for Aboriginal & Torres o Over 150 people are hospitalised Strait Islander (A&TSI) peoples, due to AMI every day - one death rates 2.5 x the rest of the person every nine minutes population o Prevalence, deaths & o Over 400 people are hospitalisations from AMI have hospitalised for CAD every day, been decreasing over past 10 one person every three to four years minutes (NHFA 2024) University of Adelaide 5 Epidemiology Regional perspective Presentations to Emergency Departments (ED) o 75,900 presentations to Australian EDs with a principal diagnosis of CAD in 2020-21 o Rate of 295 presentations per 100,000 population o Of these ▪ 58,200 (77%) were admitted to the presenting hospital ▪ 9,600 (13%) departed without being admitted or referred ▪ 7,300 (10%) were referred to another hospital for admission (AIHW 2023) University of Adelaide 6 Epidemiology Females & CVD Australian data o CVD is a leading cause of illness o A&TSI women and death among Australian ▪ estimated 12,500 A&TSI women women had a form of heart, ▪ estimated 510,000 (4.8%) stroke or vascular disease in Australian women reported 1 or 2012–13 more heart, stroke and vascular diseases in 2017–18 ▪ 7,100 had CAD ▪ 22,200 women had an acute coronary event (AMI or UA) in 2016 ▪ Indigenous women are up to ▪ 12% of the total burden of twice as likely as non- disease among Australian Indigenous women to have women in 2015 CVD, and to die from CAD or ▪ caused 22,200 female deaths in stroke 2016—more than any other (AIHW 2019) disease group University of Adelaide 7 Epidemiology Young women ( 5 mm in a lead with a negative QRS If in doubt perform serial ECGs University of Adelaide 12 Comparison Normal LBBB STEACS in LBBB STE II, III, aVF, V6 STD V2-V4 (concordance) (concordance) University of Adelaide 13 Non ST- elevation ACS Collectively referred to as NSTEACS Includes UA & NSTEMI Due to a partial occlusion of the coronary artery ECG features include T wave inversion &/or ST depression Differentiation of UA & NSTEMI is determined by the troponin Emergency reperfusion therapy not indicated University of Adelaide 14 Pathophysiology of ACS Plaque rupture The most common cause of fatal AMI in 76% of men & 55% of women Typically seen as a large necrotic core with a disrupted fibrous cap infiltrated by macrophages & lymphocytes Platelet activation & aggregation Thrombus formation Coronary spasm (Mehta et al, 2016) (Werns, 2008 p 593) University of Adelaide 15  (Werns, 2008 p 592) University of Adelaide 16 Pathophysiology of ACS in women Obstructive atherosclerotic disease of the epicardial coronary arteries remains the basic cause of AMI in both sexes, however findings from the WISE study (2006) reveal plaque characteristics differ for women o younger women have a tendency towards plaque erosion where a fibrous cap is absent at the plaque erosion site & the exposed intima consists predominantly of smooth muscle, with only scant lipid cores & little inflammation data has suggested a greater role of microvascular disease in the pathophysiology of coronary events amongst women o greater frequency of distal microvascular embolisation in the setting of a fatal epicardial thrombosis as compared to men (Merz et al 2006) University of Adelaide 17 University of Adelaide 18  Consequences of myocardial ischaemia Arrhythmia Cell death Pump failure Ionic & biochemical alterations > acidosis Apoptosis  extracellular K+ & intracellular Ca++ overload Occurs in early phase Late response to prolonged myocardial Creating unstable electrical substrate In response to oxidative stress & proinflammatory ischaemia cytokines Sustained ventricular tachyarrhythmias Necrosis Impairment of myocardial contraction (VT,VF) (systole) Cell damage so severe that it is unable to May be associated with circulatory collapse & function  CO & SV > HT >  coronary perfusion > require immediate treatment Damaged cell swells > metabolic failure > rapid worsening ischaemia > progressive myocardial depletion ATP > failure of ion pumps & Ca++ dysfunction > death overload Plasma membrane ruptures with spillage of Atrial fibrillation intracellular contents into surrounding areas > May warrant urgent treatment when a fast activating inflammation >  tissue damage ventricular response rate is associated with Impairment of myocardial relaxation haemodynamic deterioration (diastole) LVEDP > pulmonary congestion > hypoxaemia > worsening ischaemia > progressive myocardial dysfunction > death University of Adelaide 19 Fourth universal definition of AMI Published 2018 by the European Society of Cardiology (ESC) Redefining New concepts in the differentiation of AMI from myocardial injury Updated concepts in relation to clinical classification of MI o Criteria for AMI (types 1, 2 and 3) o Criteria for coronary procedure-related MI (types 4 and 5) New information related to other mechanisms causing MI, such as Takotsubo cardiomyopathy (TTCM) & MI with non-obstructive coronary arteries (MINOCA) University of Adelaide (ESC 2019) 20 Type 1 MI Criteria for type 1 MI Detection of a rise and/or fall of cardiac troponin (cTn) with at least one value above the 99th percentile URL and with at least one of the following: o Symptoms of AMI o New ischaemic ECG changes o Development of pathological Q waves o Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality in a pattern consistent with an ischaemic aetiology o Identification of a coronary thrombus by angiography including intracoronary imaging or by autopsy (ESC 2019) University of Adelaide 21  Non-ACS causes of cTn elevation Life threatening non coronary conditions Acute neurological Critically ill patients, Burns, especially if disease, including stroke especially with Aortic dissection Pulmonary embolism Hypoxia affecting >30% of or subarachnoid respiratory failure or body surface area haemorrhage sepsis University of Adelaide 22 Non-ACS causes of cTn elevation Cardiac contusion, or other trauma including Rhabdomyolysis with surgery, ablation, Renal failure cardiac injury pacing, frequent defibrillation shocks Infiltrative diseases, e.g. amyloidosis, Congestive heart failure TTCM haemochromatosis, – acute & chronic sarcoidosis, & scleroderma Coronary vasculitis e.g. Inflammatory diseases, Tachy- or False positives: Cross Systemic Lupus e.g. myocarditis or bradyarrhythmias, or reacting heterophile Erythematosus, myocardial extension of heart block antibodies Kawasaki syndrome endo-/pericarditis Drug toxicity or toxins, e.g. anthracyclines, Aortic valve disease Hypertrophic CM Extreme exertion carbon monoxide poisoning (Chew et al, 2016) University of Adelaide 23 Presentation Chest pain & dyspnoea are the most common complaints Areas where pain is experienced in AMI, showing common (dark red) and less common (light red) areas on the chest and back University of Adelaide 24 Characteristic symptoms in presentation with AMI Chest pain/discomfort (pressure, tightness, squeezing) Additional symptoms with chest pain Radiation of pain to jaw, neck, shoulders, arm, back, epigastrium Associated symptoms: dyspnoea, nausea, vomiting, light headedness, diaphoresis University of Adelaide 25 Sex specific symptoms in females presenting with AMI Chest pain: sharp, pleuritic, burning, aching, soreness, reproducible Other symptoms excluding chest pain Unusual fatigue Unusual shortness of breath Upper back/chest pain, neck, jaw, shoulder, back, epigastric pain Flu-like symptoms Dizziness Generalized scared/anxiety feeling Generalized weakness Indigestion Palpitations (Mehta et al, 2016) University of Adelaide 26 Silent ischaemia Episodes of ischemia in the absence of chest pain Present with anginal equivalents Specific population who present with silent ischemia include: Diabetics Women Women with heart failure Hypertension Chronic renal disease (CRD)/ End stage renal disease (ESRD) (Yiadom 2011, Metcalfe 2012) University of Adelaide 27 History When assessing chest pain remember the following: Treat all chest pain as ischaemic until proven otherwise Chest discomfort is subjective The location of pain may correlate poorly to its source The severity of pain correlates poorly to the gravity of the cause Patients may have more than one clinical problem A careful assessment is mandatory University of Adelaide 28 Obtaining a history Using the symptom/ pain PQRST mnemonic can be helpful P Precipitation / Palliation Q Quality R Region / Radiation S Severity T Time – onset, duration, frequency, time of day Non – characteristic chest pain or symptoms especially in females – continue to ask yourself ‘is this ischaemic?’ Associated symptoms Risk factors University of Adelaide 29 Risk factors Major Contributing factors Sedentary lifestyle Non modifiable Stress o Family history of CVD Depression o A&TSI o Biology - ^ platelet reactivity & pro-inflammatory markers o Increasing age (females) o Behavioural o Male sex CKD/ESRD Modifiable Obstetric history o Smoking Women are at higher risk of o Hypertension future CVD if experiencing the o Diabetes following during pregnancy: o Placental abruption o Dyslipidaemia o Stillbirth o Obesity (^BMI) o Hypertensive disorders o Gestational diabetes mellitus o Obstructive sleep apnoea o Preterm birth (Grandi et al, 2019) University of Adelaide 30 Differential diagnosis Ischaemic CV causes Non ischaemic CV ACS causes Stable angina Aortic dissection & expanding aortic Severe aortic stenosis aneurysm Tachyarrhythmia Pulmonary embolism Non-CV causes Peri/myocarditis Gastrointestinal Musculoskeletal Pulmonary Herpes zoster University of Adelaide 31  Australian guidelines for the management of ACS University of Adelaide 32 University of Adelaide 33 ED pathways for risk stratification University of Adelaide 34 Integrated Cardiovascular Clinical Network CHSA (Country Health South Australia) University of Adelaide 35 Acute management of chest pain Getting to hospital Chest pain at rest or for a prolonged period (>10 min not relieved by nitrates), recurrent chest pain or associated with syncope or acute shortness of breath → medical emergency Ideally transported by ambulance to hospital with percutaneous coronary intervention (PCI) capability Early access to a defibrillator prevents sudden cardiac death Aspirin (300mg) should be given early Where appropriate, a 12-lead ECG should be taken en route & transmitted to a medical facility. Where formal protocols are in place, prehospital treatment (including fibrinolysis in appropriate cases) should be facilitated Pre-hospital activation of the CODE STEMI – found to improve mortality rates (Bajaj et al, 2012) University of Adelaide 36 Acute management of chest pain On arrival to hospital ECG within 1o min assessed promptly by an ECG- experienced clinician - serial ECG’s +/- R) sided or posterior ECG Ongoing close surveillance Continuous ECG monitoring - ST monitoring desirable Venous access Aspirin 300mg (if not already administered) Pain relief with nitrates /fentanyl/morphine* o Morphine administration slows absorption of oral medications including ticagrelor Blood – cTn, full blood count (FBC), & electrolytes, urea and creatinine (EUC) Chest X-Ray (CXR) Oxygen therapy * SpO2 30/60 – Consider prehospital administration (Chew et al, 2011) University of Adelaide 59 Absolute contraindications Risk of intracranial Risk of bleeding haemorrhage Prior haemorrhagic Active bleeding stroke Significant closed head Ischaemic stroke within injury or facial trauma 3 months within 3 months Known cerebral vascular Suspected aortic lesion dissection Known intracranial neoplasm University of Adelaide 60 Relative contraindications Severe uncontrolled hypertension (HT) on presentation BP > 180/110 Current use of Risk of History of chronic, poorly anticoagulants in intracranial controlled HT therapeutic doses haemorrhage Ischaemic stroke > 3 months ago Dementia Non compressible Known intracranial abnormality vascular puncture Recent major surgery Risk of < 3 weeks bleeding Traumatic or prolonged resuscitation > 10 min Recent internal bleeding < 4 weeks Other Pregnancy Active peptic ulcer University of Adelaide 61 Tenecteplase (TNK)/ Metalyse Derived from native tissue-type plasminogen activator Naturally occurring protein secreted by vascular endothelium that lyses clots Clot specific - binds at the clot surface Converts entrapped plasminogen to plasmin Causes local clot lyses Minimal systemic effects Single bolus dose administered over ~10 sec Dose is weight dependent - 0.5 mg/kg Easy administration reduces delays Half life 24 min University of Adelaide 62 Adjunctive therapies with TNK Clopidogrel 300mg loading & 75 mg per day LMWH in conjunction with fibrin-specific agents is recommended over UFH 30 mg IV enoxaparin/clexane followed by 1mg/kg BD subcutaneous (SC) Adjust dose in patient ≥ 75 or those with renal dysfunction GP IIb/IIIa inhibitors not recommneded University of Adelaide 63  Other fibrinolytic therapies Streptokinase (STK) Half-life: 18-23 min IV infusion Alteplase (rTPA) Short half-life (5mins) IV bolus + infusion Retaplase IV bolus x2 University of Adelaide 64 Complications of fibrinolytics Management of bleeding Bleeding Manual pressure, pressure Rate of major bleeds < 5% bandages, sandbags Patients requiring transfusion is If significant cease thrombolytic < 1% agents & heparin Reverse heparin with protamine Transfusions may be required RBC, FFP, platelets & cryoprecipitate Antifibrinolytic therapy - Risk of bleeding increased aminocaproic acid (orally) in the elderly, low body Gastric bleeds; fast, IVT, IV mass index (BMI), female omeprazole sex & those undergoing Surgical intervention may be invasive procedures required ~ 4% University of Adelaide 65 Complications of fibrinolytics Stroke Predominately occurs within the first day High mortality - 63% Severe disability in survivors High risk patients include o Advance age, low BMI, HT, use of TNK, women STK with SC LMWH has the lowest incidence of stroke University of Adelaide 66 Nursing care during administraton A staff member must be with patient Advanced life support equipment at bedside Atropine & IV fluids (Bezold-Jarisch reflex) Frequent observation of vital signs Be aware of & observe for potential side effects & complications of thrombolytic therapy Repeat ECG 1 hr & 3 hrs post completion of therapy Obtain cTn as required post thrombolytic therapy University of Adelaide 67 Reperfusion markers Resolution of chest pain Reperfusion arrhythmias Accelerated idioventricular rhythm (AIVR) and ventricular premature complexes (PVCs) are most common o Usually self limiting and require no intervention Non sustained ventricular tachycardia (VT) o May be self limiting o If recurring episodes, may be managed pharmacologically if no haemodynamic instability Sinus bradycardia and high degree atrioventricular blocks (more commonly seen in large zone infarcts) o May require permanent pacemaker insertion if haemodynamically unstable Underlying mechanism o Operate mainly through non-reentrant pathways o Result of abnormal or enhanced automaticity due to intracellular Ca++ overload ST-segment resolution of 50% or more T wave inversion cTn peak within 12 hours University of Adelaide 68  Failed reperfusion If reperfusion has not occurred within 60-90 minutes or patients re-occlude rescue PCI should be considered Ideally performed no later than 90min after fibrinolysis Associated with an increased risk of bleeding Alternatively, a further dose of fibrinolytics may be given GP IIb/IIIa inhibitors may also be considered University of Adelaide 69 Complications of STEACS Recurrent chest pain UA Re – infarction Pericarditis Sudden Cardiac Dressler’s syndrome Cardiogenic shock Death Mechanical Defects Mitral valve prolapse Ventricular septal defect Arrhythmia / Heart failure Left ventricular (LV) conduction blocks aneurysm Thromboembolism LV free wall rupture leading to tamponade University of Adelaide 70 Indicators of a poor prognosis post STEACS Poor LV function Severe CAD LV function is the strongest UA predictor of survival Reinfarction Late ventricular Presence of co-morbidities arrhythmia's Increasing age AV blocks & conduction Persistent ST depression at blocks rest University of Adelaide 71 6-month mortality with poor LV function University of Adelaide 72 Preparation for discharge Non-invasive evaluation Imaging o Echocardiogram to assess LV function & ejection fraction (EF) Invasive evaluation (post fibrinolytic only) Angiogram Revascularisation Recommended within 24 hours Referral to Cardiac Rehabilitation program (Chew et al, 2016) University of Adelaide 73 Recommendations for internal cardiac defibrillator (ICD) implantation post STEACS Path A Path B EF  30% EF 30-40% (asymptomatic) OR > 30 days post STEMI EF  35% and NYHA Class II or III heart Non-sustained VT failure (monitoring) > 6 weeks post STEMI Positive electrophysiology study Revascularised (EPS) University of Adelaide 74 Mortality Associated With STEACS 15% 5-15% 10% pre-hospital in hospital 1-year mortality mortality mortality University of Adelaide 75  UNOFFICIAL NSTEACS – NSTEMI and Unstable Angina University of Adelaide 76 NSTEACS Includes Unstable angina (UA) Non-ST segment elevation myocardial infarction (NSTEMI) University of Adelaide 77  Differentiating between UA & NSTEMI not critical initially Why? University of Adelaide 78 University of Adelaide 79 Management of NSTEACS First priority is to confirm the diagnosis of ACS Symptoms on presentation ECG Cardiac biomarkers Second objective is to risk stratify patients Short – term adverse outcomes Directs the management of the patient University of Adelaide 80 The role of cTn in NSTEACS A positive cTn Differentiates between NSTEMI & UA Identifies a high-risk group with an increased risk of death & STEACS These patients should not have an EST Require hospitalisation & aggressive management Benefit from GP IIb/IIIa inhibitors University of Adelaide 81 Early medical management of NSTEACS Low risk (UA) Intermediate to very high risk (NSTEMI) Aspirin Aspirin P2Y12 inhibitors Ticagrelor, prasugrel, clopidogrel Anticoagulant therapy UFH/ LMWH GP IIb/ IIIa inhibitors at time of PCI Tirofiban Direct thrombin inhibition Bivalirudin Instead of anticoagulant + GP 11b/111a inhibitors in ^ bleeding risk University of Adelaide 82 Invasive management Very high-risk patients Ongoing ischaemia, ECG criteria, arrhythmias, acute heart failure (HF) Recommended within 2 hours High risk patients ECG criteria Recommended within 24 hours Intermediate risk Recurrent symptoms, inducible ischaemia on provocative testing Recommended within 72 hours (Chew et al, 2016) University of Adelaide 83 Long-term management of ACS – recommended discharge medications Antiplatelet Statins therapy Indefinitely Aspirin indefinitely Reduce absolute 2-year In combination with vascular event rate by P2Y12 inhibitor at least 1.1% in (ticagrelor/clopidogrel) established CAD for up to 12 months Reduce recurrent ischaemic events Reduce incidence/absolute rates of death, recurrent MI or stroke at 12 months by 5.3% (Chew et al, 2016) University of Adelaide 84 Long-term management of ACS – recommended discharge medications Renin-angiotensin  blockers antagonists Previous research ACE-I & ARBs suggested benefits in limiting infarct size & Cardio protective in the reduction in mortality ability to limit infarct size after MI & reduce ventricular remodeling Research predates current practice If evidence of HF, LV systolic dysfunction, May be of most benefit for diabetes, anterior MI or first 12 months, especially co-existent HT in patients with reduced systolic dysfunction Reduction in CV mortality, nonfatal MI & stroke in context of long-term secondary prevention (Chew et al, 2016) University of Adelaide 85 Lifestyle advice Smoking cessation Increase physical activity 30 min moderate exercise 5 days or more per week Good nutrition Weight loss Moderate alcohol consumption 2 standard drinks/day for men & 1 for women University of Adelaide 86 Addressing psychosocial factors Depression & anxiety Social isolation Lack of social support Are all related to poor outcomes All patients with CAD should be assessed for comorbid depression and level of social support University of Adelaide 87 Secondary prevention Cardiac Rehabilitation Programs Proven effective intervention All patients with cardiovascular disease should have access, & be actively referred, to comprehensive ongoing prevention & cardiac rehabilitation services Specific guidelines are available for Indigenous populations University of Adelaide 88 Chest pain action plan All patients should be provided with a written action plan for chest pain All patients should be discharged with short-acting nitrates Rest & self-administration of short-acting nitrates Self-administration of aspirin (unless If patients develop pain contraindicated) Call ambulance if not relieved completely after 10 min Individualised clinician notification and action plan for those living in areas where an ambulance is not readily available. University of Adelaide 89  UNOFFICIAL MINOCA – a working diagnosis University of Adelaide 90 Myocardial infarction with non-obstructive coronary arteries (MINOCA) ESC working group position paper 2017 Diagnosis made following coronary angiography in the evaluation of a clinical presentation consistent with AMI AMI clinical criteria o ‘Fourth Universal Definition of Myocardial Infarction’ Angiographic criteria o Absence of obstructive CAD in any potential infarct-related artery o Normal coronary arteries (no stenosis >30%) o Mild coronary atheromatosis (stenosis >30% but