The document discusses the characteristics of anginal chest pain and classifies various levels of angina according to severity. It details the pathophysiology and management of acute coronary syndromes (ACS) including non-ST elevation myocardial infarction (NSTEMI) and ST elevation myocardial infarction (STEMI), covering both acute treatments and secondary prevention strategies. Additionally, it highlights complications of myocardial infarction such as arrhythmias and acute mitral regurgitation, emphasizing the importance of appropriate medical management and revascularization.

1. Haemodynamic instability in
STEMI
Dyah Siswanti
3rd PCU
August 25th,2013,Pekanbaru

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. 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. 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. 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. 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

8. Early Invasive
Conservative

9. 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

10. 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

11. Early Hospital Care
Anticoagulant Therapy
• Class I
– Unfractionated Heparin
– Enoxaparin
– Bivalarudin
– Fondaparinux
– Relative choice depends on invasive vs
conservative strategy and bleeding risk

12. 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

13. 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%

14. 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

15. 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

16. 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

17. 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)

18. 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.

19. 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

20. 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

21. 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

22. 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

23. 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

24. 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)

25. 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

26. 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

27. 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

28. 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

29. 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)

30. 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

31. 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

32. 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

33. 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

34. 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

35. Thank you