Haemodynamic Instability in STEMI

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Dr. Dyah Siswanti E, SpJP, FIHA, 3rd Pekanbaru Cardiology Update, August 25th 2013. Pangeran Hotel Pekanbaru. Learn more at PerkiPekanbaru.com

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Haemodynamic Instability in STEMI

  1. 1. Haemodynamic instability in STEMI Dyah Siswanti 3rd PCU August 25th,2013,Pekanbaru
  2. 2. CHARACTERISTICS OF TYPICAL ANGINAL CHEST PAIN (ADAPTED FROM ROSEN’S, EMERGENCY MEDICINE) CHARACTERISTIC SUGGESTIVE OF ANGINA LESS SUGGESTIVE OF ANGINA TYPE OF PAIN DULL PRESSURE/CRUSHING PAIN SHARP/STABBING DURATION 2-5 MIN, <20 MIN SECONDSTO HOURS/CONTINUOUS ONSET GRADUAL RAPID LOCATION/CHEST WALL TENDERNESS SUBSTERNAL, NOT TENDER TO PALP. LATERAL CHEST WALL/TENDER TO PALP. REPRODUCIBALITY WITH EXERTION/ACTIVITY WITH BREATHING/MOVING AUTONOMIC SYMPTOMS PRESENT USUALLY ABSENT
  3. 3. Canadian Cardiovascular Association Classification of Angina CLASS 1 NO PAIN WITH ORDINARY PHYSICAL ACTIVITY CLASS 2 SLIGHT LIMITATION OF PHYSICAL ACTIVITY – PAIN OCCURS WITH WALKING, CLIMBING STAIRS,STRESS CLASS 3 SEVERE LIMITATION OF DAILY ACTIVITY – PAIN OCCURS ON MINIMAL EXERTION CLASS 4 UNABLE TO CONDUCT ANY ACTIVITY WITHOUT PAIN, PAIN AT REST
  4. 4. Overview of ACS Acute CoronaryAcute CoronaryAcute CoronaryAcute Coronary Syndromes*Syndromes*Syndromes*Syndromes* 1.57 Million Hospital Admissions - ACS UA/NSTEMIUA/NSTEMIUA/NSTEMIUA/NSTEMI† STEMISTEMISTEMISTEMI 1.24 million Admissions per year 0.33 million Admissions per year *Primary and secondary diagnoses. †About 0.57 million NSTEMI and 0.67 million UA. Heart Disease and Stroke Statistics – 2007 Update. Circulation 2007; 115:69–171.
  5. 5. Decreased O2 Supply •Flow- limiting stenosis •Anemia •Plaque rupture/clot Increased O2 Demand O2 supply/demand mismatch→Ischemia Myocardial ischemia→necrosis Pathophysiology ACS Asymptomatic Angina Pathophysiology of Stable Angina and ACS
  6. 6. Unstable Angina STEMINSTEMI Non occlusive thrombus Non specific ECG Normal cardiac enzymes Non-occlusive thrombus sufficient to cause tissue damage & mild myocardial necrosis ST depression +/- T wave inversion on ECG Elevated cardiac enzymes Complete thrombus occlusion ST elevations on ECG or new LBBB Elevated cardiac enzymes More severe symptoms
  7. 7. Early Invasive Conservative
  8. 8. Early Hospital Care Anti-Ischemic Therapy • Class I – Bed/Chair rest and Telemetry – Oxygen (maintain saturation >90%) – Nitrates (SLx3 Oral/topical. IV for ongoing iscemia, heart failure, hypertension) – Oral B-blockers in First 24-hours if no contraindications. (IV B-blockers class IIa indication) – Non-dihydropyridine Ca-channel blockers for those with contraindication fo B-blockers – ACE inhibitors in first 24-hours for heart failure or EF<40% (Class IIa for all other pts) (ARBs for those intolerant) – Statins
  9. 9. Early Hospital Care Anti-Platelet Therapy • Class I – Aspirin (162-325 mg), non enteric coated – Clopidogrel for those with Aspirin allergy/intolerance (300-600 mg load and 75 mg/d) – GI prophylaxis if a Hx of GI bleed – GP IIb/IIIa inhibitors should be evaluated based on whether an invasive or conservative strategy is used – GP IIb/IIIa inhibitors recommended for all diabetics and all patient in early invasive arm
  10. 10. Early Hospital Care Anticoagulant Therapy • Class I – Unfractionated Heparin – Enoxaparin – Bivalarudin – Fondaparinux – Relative choice depends on invasive vs conservative strategy and bleeding risk
  11. 11. FIBRINOLYTICS • STREPTOKINASE – 1.5mu infusion over 30min (1hour – ACLS) • rtPA – accelerated infusion over 1.5hrs • 15mg IV bolus, 0.75mg/kg over 30 min, 0.5mg/kg over 1hr • ANISTREPLASE – 30 U IV over 5 min • TENECTEPLASE – 30 TO 50 MG • RETEPLASE – 10 U IV bolus, ffd. 10U IV after 30 min
  12. 12. Brief Review of Thrombolytic Trials GISSI-1: Streptokinase 18% reduction in mortality at 21 d GUSTO-1: tPA. 15% reduction in 30-day mortality compared to Streptokinase GUSTO-3: Reteplase had no benefit over tPA but is easier to use (double bolus) ASSENT: TNKase is similar to tPA but with less non-cerebral bleeding and better mortality with symptoms>4 hrs: Single bolus, fibrin selective, resistance to PAI-1 *Overall risk of ICH is 0.7%; Strokes occurred in 1.4%
  13. 13. Secondary Prevention Class I Indications • Aspirin • Beta-blockers: (all pts, slow titration with moderate to severe failure • ACE-Inhibitors: CHF, EF<40%, HTN, DM (All pts-Class IIa) ARB when intolerant to ACE. (Class IIa as alternative to ACEI) Aldosterone blockade: An ACEI, CHF with either EF<40% or DM and if CrCl>30 ml/min and K<5.0 mEq/L • Statins • Standard Risk Factor Management
  14. 14. SHOCK Trial 70 63 56 47 50 55 0 20 40 60 80 30 days 6 months 12 months Mortality(%) Medical stabilization Emergency revascularization 302 pts with cardiogenic shock within 36°°°° of AMI & ST↑↑↑↑/new LBBB randomized to emergency revasc. (n=152) or initial medical care (n=150) p=NS P<0.05 P<0.05 Hochman J et al. NEJM
  15. 15. 26% 41% 60%57% 0% 20% 40% 60% 80% 100% STOPAMI-I STOPAMI-2 Myocardialsalvage (%LVmyocardium) t-PA +- Abcx Stent/Abcx The STOPAMI Trials Schomig A et al. NEJM and Lancet STOPAMI-I: 140 pts with AMI rand. to acc t-PA v. stent/abcx STOPAMI-II: 162 AMI pts rand. to acc t-PA/abcx v. stent/abcx P<0.001 P=0.001
  16. 16. Complications of Myocardial Infarction • ArrhythmiasArrhythmiasArrhythmiasArrhythmias • Ventricular Septal PerforationVentricular Septal PerforationVentricular Septal PerforationVentricular Septal Perforation • Ischemic Mitral Regurgitation, PapillaryIschemic Mitral Regurgitation, PapillaryIschemic Mitral Regurgitation, PapillaryIschemic Mitral Regurgitation, Papillary Muscle RuptureMuscle RuptureMuscle RuptureMuscle Rupture • Ventricular Free Wall RuptureVentricular Free Wall RuptureVentricular Free Wall RuptureVentricular Free Wall Rupture • Systemic EmbolismSystemic EmbolismSystemic EmbolismSystemic Embolism • Ventricular AneurysmVentricular AneurysmVentricular AneurysmVentricular Aneurysm • PericarditisPericarditisPericarditisPericarditis • Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)
  17. 17. Ventricular Arrhythmias •60-110 BPM; Up to 20% STEMI patients have this •Usually a result of reperfusion; no specific therapy needed if HD stable. Otherwise, atropine or even atrial pacing may increase sinus rate to overdrive pace the AIVR •Routine post-MI management with B-blockers, ACE, etc.
  18. 18. PVC’s • Extremely common, along with short runs ofExtremely common, along with short runs ofExtremely common, along with short runs ofExtremely common, along with short runs of NSVTNSVTNSVTNSVT • Amiodarone won’t increase mortality, otherAmiodarone won’t increase mortality, otherAmiodarone won’t increase mortality, otherAmiodarone won’t increase mortality, other antiarrhythmics (other than Bantiarrhythmics (other than Bantiarrhythmics (other than Bantiarrhythmics (other than B----blockers) do.blockers) do.blockers) do.blockers) do. • BBBB----blockers, electrolytesblockers, electrolytesblockers, electrolytesblockers, electrolytes • Best if no antiarrhythmics are usedBest if no antiarrhythmics are usedBest if no antiarrhythmics are usedBest if no antiarrhythmics are used
  19. 19. Not So Benign Rhythm •Ischemic VT is often polymorphic; HR>100-110 BPM •Higher risk with more LV damage and in first 2 days after MI •Treat: DCCV, cath lab (if needed), electrolyte correction, amiodarone, lidocaine, B-Blockers
  20. 20. If That Didn’t Make You Nervous… Primary VF: Sudden event with no warning--10% STEMI patients before lytics. MUCH MUCH less now Secondary VF: Occurring in setting HF or shock Late VF: >48 hrs after MI-->Increased risk with IVCD, anterior wall MI, persistent SVT early in course, and RV infarction requiring pacing ***Have to worry about structural complication (free wall rupture)/ischemia Treat: Non-synced DCCV, electrolyte correction
  21. 21. Why get worked up about electrolytes? Nordrehaug JE, van der Lippe G: Hypokalemia and ventricular fibrillation in acute myocardial infarction. Br Heart J 50:525, 1983. NOTE: Pre-lytic study
  22. 22. Sinus Bradycardia/Junctional Escape Rhythm • 4444----5% of STEMI patients have a bradyarrhythmia5% of STEMI patients have a bradyarrhythmia5% of STEMI patients have a bradyarrhythmia5% of STEMI patients have a bradyarrhythmia • Sinus node ischemiaSinus node ischemiaSinus node ischemiaSinus node ischemia--------Blood supply to SA node is:Blood supply to SA node is:Blood supply to SA node is:Blood supply to SA node is: 65% RCA, 25% LCX, 10% dual supply.65% RCA, 25% LCX, 10% dual supply.65% RCA, 25% LCX, 10% dual supply.65% RCA, 25% LCX, 10% dual supply. • Most commonly seen in Inferior/posterior MI’s.Most commonly seen in Inferior/posterior MI’s.Most commonly seen in Inferior/posterior MI’s.Most commonly seen in Inferior/posterior MI’s. • Often induced by vagal reaction that may beOften induced by vagal reaction that may beOften induced by vagal reaction that may beOften induced by vagal reaction that may be protectiveprotectiveprotectiveprotective
  23. 23. Atrioventricular Block • First-Degree: Usually the RCA and does not require treatment. Hold the B-blocker for PR>240 ms • Second-Degree: Usually RCA disease and does not require treatment unless HR less than 50 and arrhythmia or symptoms. Otherwise, atropine or pace • Third-Degree: Can be from any location of infarct. Can be preceded by Mobitz II Block – Pace for symptoms and for hemodynamic support. Usually not needed in inferior MI’s as block is transient (pace for HR<40-50)
  24. 24. Post-MI VSD • ~2% of acute MI’s prior to reperfusion era • ~0.2% in GUSTO-I streptokinase trial • Without reperfusion, usually occurs within first week – Day 1--Large intramural hematomas that dissect – Day 3-5--Coagulation necrosis • 24 hr or less if receive lysis--Lytics reduce infarct size but may promote hemorrhagic dissection of myocardium
  25. 25. Symptoms, Exam, and Diagnosis • Chest pain, dyspneaChest pain, dyspneaChest pain, dyspneaChest pain, dyspnea • PE: Harsh, holosystolic murmurPE: Harsh, holosystolic murmurPE: Harsh, holosystolic murmurPE: Harsh, holosystolic murmur along sternal border radiating toalong sternal border radiating toalong sternal border radiating toalong sternal border radiating to base/apex/R parasternum; thrill inbase/apex/R parasternum; thrill inbase/apex/R parasternum; thrill inbase/apex/R parasternum; thrill in 1/2 patients; S3; Loud P2; TR.1/2 patients; S3; Loud P2; TR.1/2 patients; S3; Loud P2; TR.1/2 patients; S3; Loud P2; TR. • Compared to acute MR, murmur isCompared to acute MR, murmur isCompared to acute MR, murmur isCompared to acute MR, murmur is loud. Up to 20% of patients mayloud. Up to 20% of patients mayloud. Up to 20% of patients mayloud. Up to 20% of patients may have MR as well thoughhave MR as well thoughhave MR as well thoughhave MR as well though
  26. 26. CCU Management • IABPIABPIABPIABP • VentilationVentilationVentilationVentilation • Diuresis/HF ManagementDiuresis/HF ManagementDiuresis/HF ManagementDiuresis/HF Management • Inotropes (can increase shunt)Inotropes (can increase shunt)Inotropes (can increase shunt)Inotropes (can increase shunt) • Nitroprusside if tolerated (can cause hypotension)Nitroprusside if tolerated (can cause hypotension)Nitroprusside if tolerated (can cause hypotension)Nitroprusside if tolerated (can cause hypotension) • Mortality with conservative management is HIGH (24%,Mortality with conservative management is HIGH (24%,Mortality with conservative management is HIGH (24%,Mortality with conservative management is HIGH (24%, 46%,46%,46%,46%, 67676767----82%82%82%82% at 24 hrs, 1 wk, and 2 months,at 24 hrs, 1 wk, and 2 months,at 24 hrs, 1 wk, and 2 months,at 24 hrs, 1 wk, and 2 months, respectively)respectively)respectively)respectively) • Ultimately, mechanical closure needed (surgery vs.Ultimately, mechanical closure needed (surgery vs.Ultimately, mechanical closure needed (surgery vs.Ultimately, mechanical closure needed (surgery vs. percutaneous)percutaneous)percutaneous)percutaneous)----TIMING is questionable but clinical statusTIMING is questionable but clinical statusTIMING is questionable but clinical statusTIMING is questionable but clinical status should not preclude thisshould not preclude thisshould not preclude thisshould not preclude this
  27. 27. Acute Mitral Regurgitation • Caused by papillary muscle ischemia or rupture (less likely).Caused by papillary muscle ischemia or rupture (less likely).Caused by papillary muscle ischemia or rupture (less likely).Caused by papillary muscle ischemia or rupture (less likely). Rupture is usually partial since total is essentiallyRupture is usually partial since total is essentiallyRupture is usually partial since total is essentiallyRupture is usually partial since total is essentially incompatible with lifeincompatible with lifeincompatible with lifeincompatible with life • Usually in setting of inferior MI involving the posteromedialUsually in setting of inferior MI involving the posteromedialUsually in setting of inferior MI involving the posteromedialUsually in setting of inferior MI involving the posteromedial papillary muscle (single PDA blood supply as opposed topapillary muscle (single PDA blood supply as opposed topapillary muscle (single PDA blood supply as opposed topapillary muscle (single PDA blood supply as opposed to anterolateral)anterolateral)anterolateral)anterolateral) • Rupture usually occurs 3Rupture usually occurs 3Rupture usually occurs 3Rupture usually occurs 3----5 days post5 days post5 days post5 days post----MI and in 1% of MI’sMI and in 1% of MI’sMI and in 1% of MI’sMI and in 1% of MI’s and requires emergent operative repair (50% mortality in 24and requires emergent operative repair (50% mortality in 24and requires emergent operative repair (50% mortality in 24and requires emergent operative repair (50% mortality in 24 hrs)hrs)hrs)hrs) • Accounts for 7% of cardiogenic shock and 5% of mortalityAccounts for 7% of cardiogenic shock and 5% of mortalityAccounts for 7% of cardiogenic shock and 5% of mortalityAccounts for 7% of cardiogenic shock and 5% of mortality associated with acute MIassociated with acute MIassociated with acute MIassociated with acute MI • Area of infarction does NOT have to be largeArea of infarction does NOT have to be largeArea of infarction does NOT have to be largeArea of infarction does NOT have to be large
  28. 28. Symptoms, Exam, Diagnosis • Symptoms: Those of heartSymptoms: Those of heartSymptoms: Those of heartSymptoms: Those of heart failurefailurefailurefailure • PE: May or may not hear loudPE: May or may not hear loudPE: May or may not hear loudPE: May or may not hear loud systolic murmur (need asystolic murmur (need asystolic murmur (need asystolic murmur (need a gradient)gradient)gradient)gradient)
  29. 29. CCU Management • Mechanical ventilation if neededMechanical ventilation if neededMechanical ventilation if neededMechanical ventilation if needed • IABPIABPIABPIABP--------especially for hypotensionespecially for hypotensionespecially for hypotensionespecially for hypotension • PCI if papillary m. ischemia (not rupture)PCI if papillary m. ischemia (not rupture)PCI if papillary m. ischemia (not rupture)PCI if papillary m. ischemia (not rupture) • Afterload reduction (nitroprusside if possible) toAfterload reduction (nitroprusside if possible) toAfterload reduction (nitroprusside if possible) toAfterload reduction (nitroprusside if possible) to MAP of 70MAP of 70MAP of 70MAP of 70----80 mm Hg80 mm Hg80 mm Hg80 mm Hg • Since mortality is 90% with medical therapy alone,Since mortality is 90% with medical therapy alone,Since mortality is 90% with medical therapy alone,Since mortality is 90% with medical therapy alone, surgery is the major therapy of choicesurgery is the major therapy of choicesurgery is the major therapy of choicesurgery is the major therapy of choice – Perioperative mortality 20Perioperative mortality 20Perioperative mortality 20Perioperative mortality 20----25%25%25%25% – Overall surgical mortality is even higherOverall surgical mortality is even higherOverall surgical mortality is even higherOverall surgical mortality is even higher
  30. 30. Free Wall Rupture • ~10% of patients who die in hospital from~10% of patients who die in hospital from~10% of patients who die in hospital from~10% of patients who die in hospital from STEMISTEMISTEMISTEMI • Most commonly between 1 and 4 days (up to 3Most commonly between 1 and 4 days (up to 3Most commonly between 1 and 4 days (up to 3Most commonly between 1 and 4 days (up to 3 weeks)weeks)weeks)weeks) • Caused by tear or dissecting hematomaCaused by tear or dissecting hematomaCaused by tear or dissecting hematomaCaused by tear or dissecting hematoma • More common with fibrinolysis compared to PCIMore common with fibrinolysis compared to PCIMore common with fibrinolysis compared to PCIMore common with fibrinolysis compared to PCI • More common in patients without previousMore common in patients without previousMore common in patients without previousMore common in patients without previous infarctioninfarctioninfarctioninfarction
  31. 31. Symptoms, Exam, Diagnosis • Acute symptoms include sudden chest pain (esp withAcute symptoms include sudden chest pain (esp withAcute symptoms include sudden chest pain (esp withAcute symptoms include sudden chest pain (esp with cough, strain) and sudden deathcough, strain) and sudden deathcough, strain) and sudden deathcough, strain) and sudden death • Subacute symptoms: PericarditisSubacute symptoms: PericarditisSubacute symptoms: PericarditisSubacute symptoms: Pericarditis----like symptoms (chestlike symptoms (chestlike symptoms (chestlike symptoms (chest pain, nausea, vomiting)pain, nausea, vomiting)pain, nausea, vomiting)pain, nausea, vomiting) • Exam (think HF and tamponade): JVD, pulsus,Exam (think HF and tamponade): JVD, pulsus,Exam (think HF and tamponade): JVD, pulsus,Exam (think HF and tamponade): JVD, pulsus, diminished heart sounds, rub, possibly a new murmurdiminished heart sounds, rub, possibly a new murmurdiminished heart sounds, rub, possibly a new murmurdiminished heart sounds, rub, possibly a new murmur
  32. 32. Treatment • Pericardiocentesis if time • Surgical repair is the only treatment • Mortality is reasonable if patient gets to the OR in time • 90% mortality without surgery
  33. 33. Summary of Acute STEMI Complications • Much more rare in the reperfusion eraMuch more rare in the reperfusion eraMuch more rare in the reperfusion eraMuch more rare in the reperfusion era – Look for them especially in delayed presentationLook for them especially in delayed presentationLook for them especially in delayed presentationLook for them especially in delayed presentation • Arrhythmias are most common complication andArrhythmias are most common complication andArrhythmias are most common complication andArrhythmias are most common complication and may require emergent treatmentmay require emergent treatmentmay require emergent treatmentmay require emergent treatment • VSD’s, papillary muscle rupture, and free wallVSD’s, papillary muscle rupture, and free wallVSD’s, papillary muscle rupture, and free wallVSD’s, papillary muscle rupture, and free wall ruptures carry a VERY high mortality and requireruptures carry a VERY high mortality and requireruptures carry a VERY high mortality and requireruptures carry a VERY high mortality and require emergent surgical consultationemergent surgical consultationemergent surgical consultationemergent surgical consultation – Support mechanically until patient receives operationSupport mechanically until patient receives operationSupport mechanically until patient receives operationSupport mechanically until patient receives operation
  34. 34. Thank you

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