Haemodynamic instability in

STEMI

Dyah Siswanti

3rd PCU

August 25th,2013,Pekanbaru

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

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

Overview of ACS

Acute Coronary Acute Coronary Acute Coronary Acute Coronary

Syndromes*Syndromes*Syndromes*Syndromes*

1.57 Million Hospital Admissions - ACS

UA/NSTEMIUA/NSTEMIUA/NSTEMIUA/NSTEMI† STEMISTEMISTEMISTEMI

1.24 millionAdmissions per year

0.33 millionAdmissions 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.

Decreased O2 Supply

•Flow- limiting stenosis

•Anemia

•Plaque rupture/clot

Increased O2 Demand

O2 supply/demand mismatch→Ischemia

Myocardial ischemia→necrosis

Pathophysiology ACS

Asy

mpt

omat

ic

Ang

ina

Pathophysiology of Stable Angina and ACS

Unstable

AnginaSTEMINSTEMI

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

Early Invasive

Conservative

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

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

Early Hospital Care

Anticoagulant Therapy

• Class I

– Unfractionated Heparin

– Enoxaparin

– Bivalarudin

– Fondaparinux

– Relative choice depends on invasive vs

conservative strategy and bleeding risk

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

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%

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

SHOCK Trial

7063

5647 50 55

0

20

40

60

80

30 days 6 months 12 months

Mo

rtal

ity

(%)

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

26%41%

60%57%

0%

20%

40%

60%

80%

100%

STOPAMI-I STOPAMI-2

Myo

card

ial s

alva

ge

(% L

V m

yoca

rdiu

m)

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

Complications of Myocardial Infarction

• ArrhythmiasArrhythmiasArrhythmiasArrhythmias

• Ventricular Septal PerforationVentricular Septal PerforationVentricular Septal PerforationVentricular Septal Perforation

• Ischemic Mitral Regurgitation, Papillary Ischemic Mitral Regurgitation, Papillary Ischemic Mitral Regurgitation, Papillary Ischemic Mitral Regurgitation, Papillary Muscle RuptureMuscle RuptureMuscle RuptureMuscle Rupture

• Ventricular Free Wall RuptureVentricular Free Wall RuptureVentricular Free Wall RuptureVentricular Free Wall Rupture

• Systemic Embolism Systemic Embolism Systemic Embolism Systemic Embolism

• Ventricular AneurysmVentricular AneurysmVentricular AneurysmVentricular Aneurysm

• PericarditisPericarditisPericarditisPericarditis

• Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)Cardiogenic Shock (another lecture)

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.

PVC’s

• Extremely common, along with short runs of Extremely common, along with short runs of Extremely common, along with short runs of Extremely common, along with short runs of

NSVTNSVTNSVTNSVT

• Amiodarone won’t increase mortality, other Amiodarone won’t increase mortality, other Amiodarone won’t increase mortality, other Amiodarone 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

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

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

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

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 be Often induced by vagal reaction that may be Often induced by vagal reaction that may be Often induced by vagal reaction that may be protectiveprotectiveprotectiveprotective

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)

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

Symptoms, Exam, and Diagnosis

• Chest pain, dyspneaChest pain, dyspneaChest pain, dyspneaChest pain, dyspnea

• PE: Harsh, holosystolic murmur PE: Harsh, holosystolic murmur PE: Harsh, holosystolic murmur PE: Harsh, holosystolic murmur along sternal border radiating to along sternal border radiating to along sternal border radiating to along sternal border radiating to base/apex/R parasternum; thrill in base/apex/R parasternum; thrill in base/apex/R parasternum; thrill in base/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 is Compared to acute MR, murmur is Compared to acute MR, murmur is Compared to acute MR, murmur is loud. Up to 20% of patients may loud. Up to 20% of patients may loud. Up to 20% of patients may loud. Up to 20% of patients may have MR as well thoughhave MR as well thoughhave MR as well thoughhave MR as well though

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 status TIMING is questionable but clinical status TIMING is questionable but clinical status TIMING is questionable but clinical status should not preclude thisshould not preclude thisshould not preclude thisshould not preclude this

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 essentially Rupture is usually partial since total is essentially Rupture is usually partial since total is essentially Rupture is usually partial since total is essentially incompatible with lifeincompatible with lifeincompatible with lifeincompatible with life

• Usually in setting of inferior MI involving the posteromedial Usually in setting of inferior MI involving the posteromedial Usually in setting of inferior MI involving the posteromedial Usually in setting of inferior MI involving the posteromedial papillary muscle (single PDA blood supply as opposed to papillary muscle (single PDA blood supply as opposed to papillary muscle (single PDA blood supply as opposed to papillary 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’s MI and in 1% of MI’s MI and in 1% of MI’s MI and in 1% of MI’s and requires emergent operative repair (50% mortality in 24 and requires emergent operative repair (50% mortality in 24 and requires emergent operative repair (50% mortality in 24 and requires emergent operative repair (50% mortality in 24 hrs)hrs)hrs)hrs)

• Accounts for 7% of cardiogenic shock and 5% of mortality Accounts for 7% of cardiogenic shock and 5% of mortality Accounts for 7% of cardiogenic shock and 5% of mortality Accounts 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

Symptoms, Exam, Diagnosis

• Symptoms: Those of heart Symptoms: Those of heart Symptoms: Those of heart Symptoms: Those of heart failurefailurefailurefailure

• PE: May or may not hear loud PE: May or may not hear loud PE: May or may not hear loud PE: May or may not hear loud systolic murmur (need a systolic murmur (need a systolic murmur (need a systolic murmur (need a gradient)gradient)gradient)gradient)

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) to Afterload reduction (nitroprusside if possible) to Afterload reduction (nitroprusside if possible) to Afterload 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

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 3 Most commonly between 1 and 4 days (up to 3 Most commonly between 1 and 4 days (up to 3 Most 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 previous More common in patients without previous More common in patients without previous More common in patients without previous infarctioninfarctioninfarctioninfarction

Symptoms, Exam, Diagnosis

• Acute symptoms include sudden chest pain (esp with Acute symptoms include sudden chest pain (esp with Acute symptoms include sudden chest pain (esp with Acute 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 (chest like symptoms (chest like symptoms (chest like 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

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

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 and Arrhythmias are most common complication and Arrhythmias are most common complication and Arrhythmias 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 wall VSD’s, papillary muscle rupture, and free wall VSD’s, papillary muscle rupture, and free wall VSD’s, papillary muscle rupture, and free wall

ruptures carry a VERY high mortality and require ruptures carry a VERY high mortality and require ruptures carry a VERY high mortality and require ruptures 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

Thank you