Acute Coronary Syndrome Management RRT

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Made by Ranjith R Thampi. This was a powerpoint I had made for a Cardiology Seminar during internship. Got it checked by cardiologists, all approved. Covers management of UA, NSTEMI and STEMI. This was my favorite topic. I think the flowcharts will be clear to the point. Kindly comment and let me know.

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  • Exclude secondary causes- Anemia, Arrhythmias', Heart Failure, Hypoxemia, Infection, Uncontrolled HPT,Stress, ThyrotoxicosisThose with chest pain >20mins with h/o syncope, presyncope are admitted in ED where a battery of tests and procedures will be followed.
  • NSTEMI accounts for Greater % of mortality <1yr as compared to STEMI patients
  • Stress Tests:Exercise tolerance test (stress test or treadmill test)Nuclear stress testStress echocardiogramDischarge on upgraded therapy with urgent cardiology follow-up.
  • -Respiratory Depression with Morphine >10mgAvoid Nitrates in Hypotension-Pain Persisting?IV Nitrates GTN 50mg in 50 mL NS @ 2-10mL/hr titrate dose and maintain BP >100mm Hg--Beta Blocker Contraindicated in Asthma, COPD, LVF, Bradycardia, Coronary Artery Spasm-CCB- *Avoid using Verapamil and a Beta blocker together Asystole. Instead,Diltiazem 60-120 mg/8hr PO(Dilzem 30mg 1-1-1)
  • -Add GPIs before going for Invasive procedures
  • H- Haemodynamic compromiseE- ECG ( persistent ST-depression, new T-wave depression >2mm, Transient ST-elevation in > 2 contiguous leads)A- Arrhythmia (Sustained VT)R- Renal( CRF with GFR<60ml/minT- Troponin riseD- DMO- Ongoing Chest Discomfort >10minsC- Coronary Revascularization of any type within 6 months
  • Low Risk Patients(<3 TIMI)- Discharge if repeat Troponin(>12hr) is negative Further Investigation Stress Test, Angiogram
  • High Risk Patients(>4 TIMI)- Optimize Drugs BBs, CCBs, ACE-i, Nitrates, STATINS No improvement? Angiography with or without PCI or CABG/ Cardiac Catheterisation
  • -IABP Device placed in DTA connected to ECG gated pump tunes to diastole(Twave to Rwave)
  • Works by increasing DBP and Thence, MEAN ARTERIAL PRESSURE~~ Perfusion Pressure
  • Nitrates: Best for Unstable Angina. Directly dilates coronary stenoses and increases oxygen delivery to the ischemic regionPrefers Coronary Vessels in contrast to other vasodilatorsSulfhydryl-donating compounds are necessary for this activity, and their rapid depletion leads to haemodynamic disturbance and decreased effect
  • -Both Asp And Clopi together help in Plaque stabilization and thrombus arrest-Prasugrel in combination with aspirin is an option for the prevention of atherothrombotic events in patients with acute coronary syndromes and undergoing percutaneous coronary intervention if immediate primary PCI is necessary, stent thrombosis occurs during treatment with clopidogrel, or the patient has diabetes mellitus.
  • Best limited to High Risk PatientsAbciximabpreffered in UA patients in whom PCI is planned within the following 24 hrs(Expensive!)*When Aspirin + UFH are used with GP inhibitors, dose of heparin should be conservative during coronary procedures, and heparin should be discontinued after procedure if it is uncomplicated.
  • -ANTICOAGULANT PERIOD- Monitor APTT 6hrly Alter IVI to maintain APTT at 1.5-2.5 times controlstop injection when pain-free for 24hrs, give 3-5 day therapy
  • LMWH contains fragments of UFH but has better efficacy than UFH… more expensive though-Fondaparinux- Factor Xa Inhibitor-Bivalirudin- Direct thrombin Inhibitor-Dose of UFHshould be reduced during coronary angioplasty when aspirin and GPIIb-IIIa inhibitors are being administered concomitantly, and heparin should be discontinued after an uncomplicated procedure
  • *Best for patients with Unstable Angina or NSTEMILonger Half life… can be given od or BdCauses Less BleedingHigher ratio (3:1) of anti-Xa to anti-IIa activity
  • ACE inhibitors more preffered than ARBs in MIFetopathies- Fetal GR, Hypoplasia of organs, Fetal DeathACE inhibitors. Drugs that reduce vascular resistance (of the arteries) and relieve some of the strain on the heart, allowing the heart to pump more efficiently. Because they help the left ventricle to pump out oxygen-rich blood, they are often prescribed if the left ventricle was damaged during the heart attack and is no longer functioning normally. The drugs will continue to be taken for life.
  • Beta Blockers- Not preferred in the first 24 hrs as per current guidelines <24 hrs Indicated only when there are recurrent arrythmiasCCBs- Also not preferred, only when there is severe AnginaBeta blockers. Drugs that reduce pulse rate, lower blood pressure and allow the heart to pump less vigorously while still meeting the body’s needs. Research suggests that they can help maintain a normal heart rhythm and reduce the risk of further cardiac events or sudden cardiac death. Once prescribed, the drugs are taken for life. They might not be prescribed for patients who have a history of asthma, insulin-dependent diabetes, severe peripheral vascular disease or very slow heart rate (bradycardia). There has been concern that prolonged use of beta blockers may impair sexual function and bring on symptoms of depression. However, studies have found no greater incidence of sexual dysfunction and depression in people taking beta blockers when compared to people given an inactive pill, or placebo.
  • Inferior STEMI
  • About 33% of patients with ACS and normal CK (and no ECG changes of infarction) have elevated cTn. Such patients with elevated cTn are, however, four times more likely to suffer further infarction or death in the next 30 days.
  • -Best preferred upto 12 hrs-Indicated even after 12hrs ONLY when there is persistent Angina or Preserved R-waveAvoid Thrombolysis when ST-depression alone, T-wave inversion alone, or normal ECG-PCI can be done beyond 12 hours in all cases and is the preferred treatment WHEN AVAILABLE for all STEMI cases as per current guidelines
  • SK- Do not repeat unless within day 4 of 1st dose
  • Usually appear in 1 hr after thrombolysis in ECG
  • Angina- MC in NSTEMI 25%, Reinfarction- MC in DM Medical OR Intervention5-20% Cases go for Cardiogenic Shock, Use IABP, Assess PCWP, EF < 40%, Aldosterone Antagonist(Eplerenone)Rupture Urgent Surgical RepairArrhythmias- Asystole(Atropine), VF/VT(Defib, i/v Adr, i/v Amiodarone), Bradycardia(Atropine, Dopamine)DVT/PE  LMWHPericarditis- MC following Anterior Infarction, ST elevation in all leads with no reciprocal ST depression NSAIDS+AnalgesiaDressler’s Syndrome- 1-8weeks Post MI, C/F- Febrile Illness+ Pericardial Effusion + Pleural EffusionCause- Autoimmune Mechanism, Treatment- NSAIDs+ Aspiration+ Steroids(Severe)
  • Investigations- ECG, U&E, cardiac enzymes/troponins, ABG, CXR, Echocardiogram. If indicated, CT thorax(aortic dissection/PE)Monitor- CVP, BP, ABG, ECG, Urine Output,
  • Investigations- ECG, U&E, cardiac enzymes/troponins, ABG, CXR, Echocardiogram. If indicated, CT thorax(aortic dissection/PE)Monitor- CVP, BP, ABG, ECG, Urine Output,
  • Acute Coronary Syndrome Management RRT

    1. 1. Treatment ofAcute Coronary Syndrome Ranjith R Thampi
    2. 2. OBJECTIVES I. Initial evaluation & stabilization II. Optimized Anti-ischaemic & Anti-platelet therapy III. Focused cardiac care
    3. 3. Chest pain suggestive of ischemia Immediate assessment within 10 Minutes Initial labs Emergent History & and tests care Physical 12 lead ECG  IV access  Establish Obtain Initial  Cardiac diagnosis cardiac enzymes monitoring  Read ECG FBC, Electrolytes,  Oxygen  Identify Urea, Creatinine,  Nitrates complications Coagulation  Aspirin  Assess for Studies reperfusion CXR
    4. 4. ECG assessmentNon-specific ECGUnstable Angina ST Depression or dynamic T wave inversions NSTEMI ST Elevation or new LBBB STEMI
    5. 5. UNSTABLE ANGINA NSTEMI
    6. 6. General Measures Oxygen and ECG monitoring Oxygen 2-4 L/min Pain Relief 5-10mg Morphine iv + 10mg Metoclopramide iv Control Ischaemia  Nitrates- GTN spray or Sublingual Tabs 0.3-0.6 mg/5 mins i/v Nitroglycerin 10 g/min  -blockers/CCB’s
    7. 7. Therapeutic Goals PREVENT Re-thrombosis & Downstream Embolization  Anti-platelettherapy  Aspirin upto 300 mg stat + 75 mg OD  Clopidogrel 300-600 mg 75 mg OD  Glycoprotein IIB/IIIA inhibitors  Anti-coagulant therapy  UFH or LMWH LMWH- Inj. Heparin s/c 1mg/kg 12hrly UFH- Inj. Heparin 5000U i/v bolus + IVI
    8. 8. Therapeutic Goals Relieve Obstruction  Cardiac catheterization  Percutaneous Coronary Interventions  Coronary Artery Bypass Graft
    9. 9. Unstable Angina/NSTEMI Focused Cardiac Care Based on Risk: (ACS Guidelines 2006) Low Risk: <2 % chance MI or Death within next 6 months High Risk: >10 % chance of Mortality in 6 months High Risk: H E A R T D O C
    10. 10. Low Risk
    11. 11. UA/NSTEMI High Risk- Very Unstable -Consider adding GP IIb/IIIa inhibitors (along with aspirin, clopidogrel and heparin) -Urgent/ Immediate Cardiac Catheterization (<24 hrs) after starting UFH i/v -Consider use of Intra-Aortic Balloon Pump to stabilize patient prior to coronary angiography
    12. 12. Low & High Risk Longterm Therapy Aspirin 75 mg Daily Clopidogrel 75 mg Daily Atorvastatin 80 mg Ramipril 10 mg Beta Blockade- Metoprolol/Atenolol Glycemic Control Life-style modification
    13. 13. NITRATES NITRATES Low dose- Venodilator High dose- Arteriolar dilator Reduces Preload/Afterload + MOD MOA- Acts by releasing NO in vascular smooth muscle Inhibits Platelet Aggregation ADR- Throbbing Headache, Nausea, Dizziness, Hypotension, Reflex Tachycardia, Tolerance develops over longterm use C/I- Hypotension, Sildenafil Use(Viagra)
    14. 14. ANTIPLATELETS ASPIRIN COX inhibitor- TXA2 synthesis by platelets fall  Irreversible inhibition of platelet aggregation  Stabilize plaque and arrest thrombus CLOPIDOGREL  Irreversible inhibition of platelet aggregation via inhibition of ADP and fibrinogen by altering surface receptors  Used in support of cath / PCI intervention or if unable to take aspirin  Course of 3-12 month duration depending on scenario *NEWER ANTIPLATELETS Ticagrelor 50,100,200 mg Prasugrel 60 mg bolus + 10 mg (C/I: prior TIA, >75 yrs) i/v Cangrelor 180 mg loading + 90 mg BD
    15. 15. Platelet GP IIb/IIIa Receptor Inhibitors -Inhibition of platelet aggregation at final common pathway -Best for PCI, reduces ischemic complications ADR- Hemorrhage, Thrombocytopenia, Arrhythmias, Constipation Abciximab..pci Only through Eptifibatide..acs Parenteral Infusion Tirofiban..acs
    16. 16. ANTICOAGULANTSHEPARIN MOA- Inhibition of Factor Xa and Thrombin IIa mediated conversion of fibrinogen to fibrin ADR- Bleeding, Hypersensitivity reactions, Thrombocytopenia(HIT), Osteoporosis, Skin necrosis, Alopecia, Hypoaldosteronism C/I- Bleeding disorders, SBE, Ocular & Neurosurgery, Chronic alcoholics, Cirrhosis, Renal Failure
    17. 17. Heparin Types- UFH, LMWH UFH 60 U/Kg iv bolus + M 16 U/Kg/hr LMWH Enox- 1 mg/Kg s/c BD Dalte- 120 IU/Kg Fondaparinux (Apixaban, Rivaroxaban) Bivalirudin
    18. 18. Thrombus Formation and Agents Acting
    19. 19. ACE-inhibitors Captopril, Lisinopril , Ramipril, Perindopril MOA- Inhibits A1 pressor action, Reduced Aldosterone, Reduced vasoconstriction, reduced sodium retention Improves LV Dysfunction ADR- Hypotension, Hyperkalemia, Dry Cough, Angioedema, Fetopathies, ARF C/I- Renal Failure, Renal Artery Stenosis Start early and aim for highest doses Captopril - 50mg TDS, Lisinopril 20mg D, Ramipril 10mg D
    20. 20. Angiotensin Receptor Blockers Losartan, Temisartan, Candesartan, Olmesartan, Valsartan ARB as substitute for patients unable to use ACE-I MOA- AT2 receptor blockade Prevents: Vasoconstriction, sympathetic stimulation, Aldosterone and Adr release from adrenals, Salt & Water reabsorption ADR- Hypotension, Hyperkalemia, FetopathiesSTATINS- Atorvastatin, Simvastatin, Rosuvastatin MOA- HMG CoA inhibition, blocks hepatic cholesterol synthesis, Increased LDL, VLDL blood clearance ADR- GI disturbances, Myopathies, Myalgia, Headache C/I- Liver Disease, Renal Impairment
    21. 21. Beta Blockers Atenolol, Carvedilol, Esmolol, Metoprolol, Pindolol MOA- Decreases HR, Force of contraction, Cardiac Output, Prolongs Systole, Antiarrhythmic ADR- Ppts CHF, Carbohydrate Intolerance, Altered Lipid Profile C/I- Bradycardia, Reactive airway disease, Sinus Node Dysfunction/AV block, Severe Heart failure *Diltiazem insteadCalcium Channel BlockersAmlodipine, Diltiazem, Nifedipine, Nimodipine, Verapamil MOA- Smooth muscle relaxation & vasodilation Slows HR, Reduces: afterload, myocardial contractility, MOD ADR- Accentuates AV Block, CHF *Nifedipine causes abrupt changes in BP and HR occur without appropriate Beta Blockade C/I- LV Dysfunction, Cardiogenic Shock, Sick Sinus Syndrome, Hepatic impairment
    22. 22. ECG assessmentNon-specific ECGUnstable Angina ST Depression or dynamic T wave inversions NSTEMI ST Elevation or new LBBB STEMI
    23. 23. STEMI
    24. 24. STEMI 2 situations when it becomes difficult to diagnose STEMI  Chronic or Rate Dependent LBBB  Paced Rhythm
    25. 25. ACS Clinical Diagnosis MONA: Morphine + antiemetic Oxygen Nitrates Aspirin 300 mg stat Clopidogrel 600 mg statBlood Tests:Troponin at 12 hours afteronset of pain, U&E, cholesterol,FBC, coagulationAdmission or subsequent ECG
    26. 26. Immediate ECG criteria Triage-1 mm ST elevation inat least 2 limb leads-2 mm ST elevation in atleast 2 precordial leads 12 Lead ECG Showing thrombolyseable criteria Ix on admission-LBBB with typicalclinical presentation U&E, FBC, Cholest, coagulation Repeat Definite STEMI 12 hrs Troponin, ECG Extra ECG Control RBS requirementsInferior ST elevation Primary PCI Tenectoplase (TKN-tPA)Do Rpt ECG Drug of choice with LMWH forPosterior changes Thrombolysis pts <75 yrs independent of siteDeep ST-elevation + (if PCI unavailable immediately) of infarct Target < 30 mintall R waves in V1- V3 Streptokinase (SK) Door-needle time in > 75% patients Consider for pts > 75 yrs due to lower incidence of ICH Repeat ECG 90 min from comencement of lytic Aim: > 50% reduction in peak ST segment elevation
    27. 27. REASSESS Risk assessment & secondary preventionAspirinStatinEarly beta blockadeAce- inhibitorsAngiogram Pre dischargeRehablitationConsider patient’s pre morbid state & suitabilityfor revascularisation Failed Reperfusion Haemodynamics compromise Continuing pain Discuss suitability for rescue PCI
    28. 28. THROMBOLYSIS Lyses fibrin thrombi and reduces clot-caused infarct size allowing reperfusion D2N Time- <30 mins Best Time- Upto 12 hrs from Onset of symptoms Primary PCI Usually done under anticoagulant cover Coronary recanalization is done with Angioplasty and commonly Stenting Best D2B Time- <90 mins
    29. 29. THROMBOLYSIS Streptokinase & Urokinase[1.5 MU in 100 ml NS ivi/1 hr] S/E: Nausea, Vomiting, Haemorrhage, Stroke Tenectaplase [0.5 mg/Kg over 10 seconds] Bolus Injection best for paramedics Indication: Ant. Wall MI, Previous SK use SBP< 100 mm Hg, New LBBB Alteplase Reteplase[2 iv boluses 2hrs apart] [10 MU bolus/2mins + 10 MU bolus after 30 mins] *Patients with STEMI who have not received reperfusion therapy should be treated with fondaparinux immediately
    30. 30. Thrombus Formation and Agents Acting
    31. 31. THROMBOLYSISECG is done after 1 hr and assessed: Successful Thrombolysis -Reperfusion Arrhythmias (Accelerated idioventricular rhythm) -Persistent Ventricular ectopics -Alleviation of chest pain Failed Thrombolysis - Uncontrolled pain(Persistent Angina) - Continuing ST- elevation - Absent VTc, Absent Idioventricular arrhythmias Consider re-thrombolysis with rt-PA, Tenecteplase, Rescue PCI
    32. 32. Contraindications to thrombolysis ABSOLUTE  RELATIVE Active GI Bleed  Traumatic CPR Aortic Dissection  Surgery<10 days Previous ICH  Arterial Puncture<24 hrs Stroke<2 months  SBP>180 Intracranial aneurysm/  Bleeding Tendency neoplasm  Trauma Head injury<2 months  Pregnancy Pericarditis  Bacterial Endocarditis Pancreatitis Warfarin/INR>3 Contraindications vary slightly between thrombolytics
    33. 33. Primary PCI Current primary PCI strategy: Initiate Glycoprotein IIb/IIIa inhibitor in ED, together with Aspirin+Heparin, followed by rapid application of coronary angioplasty with stenting Operator and institutional experience is an issue more important to outcomes with primary PCI than fibrinolysis.
    34. 34. Primary PCI Facilitated PCI Facilitated PCI is the use of pharmacological reperfusion treatment delivered prior to a planned PCI. *There is no evidence of a significant clinical benefit and so facilitated PCI is currently not recommended.
    35. 35. Primary PCI Rescue PCI Performed on a coronary artery which remains occluded despite fibrinolytic therapy. *Associated with significant reduction in heart failure & reinfarction Indication: -Evidence of failed fibrinolysis based on clinical signs and insufficient ST-segment resolution -Clinical or ECG evidence of a large infarct -If can be performed <12 hours after the onset of symptoms.
    36. 36. Primary PCI Preferred When: -Diagnosis in doubt -Cardiogenic Shock -Increased Bleeding -Symptoms for 2-3 hrs, clot more mature, less chance for lysis DISADVANTAGES: -Cost -Trained Personnel -Facilities
    37. 37. COMPLICATIONS
    38. 38. Complications ISCHAEMIC- Angina, Reinfarction, Infarct Extension MECHANICAL- LVD, Cardiogenic Shock, CHF, MV Dysfunction, Aneurysm, Cardiac Rupture ARRHYTHMIAS- Atrial, Ventricular, SA/AV Node Dysfunction THROMBOSIS & EMBOLIC- CNS, Peripheral embolisation, Pericarditis PSYCHOSOCIAL- Depression *Dressler’s Syndrome
    39. 39. Admit to CCU & Monitor closely KILLIP Pulmonary edemaClass 3+4 O2 2-4 L, aim for SaO2 >95% +Treatment Cardiogenic Shock ANALGESIA 2.5-5mg Morphine iv+ 10mg Metoclopramide iv INVESTIGATIONS and close monitoring Correct arrhythmias, U&E abnormalities or acid-base disturbance Optimize filling pressure,if available, measure Pulmonary Capillary Wedge Pressure(PCWP)
    40. 40. PCWPPCWP <15 mm Hg PCWP >15 mm Hgfluid loadPlasma Expander 100mL every 15 mins iv Inotropic support Aim for PCWP of 15-20 mm Hg eg: Dobutamine 2.5-10 g/kg/min ivi Aim for SBP >80 mm Hg Consider ‘renal dose’ dopamine 2-5 g/kg/min iv initially(via central line only) Consider intra-aortic balloon pump if expecting condition to improve, or time is required while awaiting surgery Look for and treat any reversible cause: MI or PE- Consider Thrombolysis; Surgery for: a/c VSD, MR, AR
    41. 41. Why Thrombolyse only STEMI?UA/ NSTEMI- Plaque stabilization toprevent progression of disease isrequired. More risk of bleedingcomplications.In UA/NSTEMIObstruction is caused by plaque(platelet-rich)In STEMIObstruction is by Thrombus
    42. 42. Prevention
    43. 43. Secondary Prevention Comorbid Diseases  HTN, DM, Dyslipidemia Behavioral  smoking, diet, physical activity, weight redn Cognitive  Education, cardiac rehab program
    44. 44. Secondary PreventionComorbid Disease management Blood Pressure  Goals < 140/90 or <130/80 in DM /CKD  Maximize use of beta-blockers & ACE-I Lipids  LDL < 100 mg/dl ; TG < 200 mg/dl  Maximize use of statins; consider fibrates/niacin first line for TG>500; consider omega-3 fatty acids Diabetes  HbA1c < 7%
    45. 45. Secondary prevention Behavioral intervention Smoking cessation  Cessation-class, meds, counseling Physical Activity  Goal 30 - 60 minutes daily  Risk assessment prior to initiation Diet  Fiber diet, omega-3 fatty acids  <7% total calories from saturated fats
    46. 46. Medication Checklist after ACS Antiplatelet agent  Aspirin* and/or Clopidorgrel  GP Inhibitors* Lipid lowering agent  Statins*  Fibrate / Niacin / Omega-3 FAs Antischaemic & LV remodelling Prevention  Beta blocker*  ACE-I*/ARB  Aldactone (as appropriate)
    47. 47. Thank You

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