Management of Anterior Myocardial Infarction with Shock

in a Non PCI center

What is shock?

• Shock is the clinical syndrome that results from inadequate

tissue perfusion ,leading to impaired oxygen delivery –

cellular dysfunction.

• Clinically accompanied by hypotension (i.e MAP <60mm

Hg in previously normotensive individual).

Harrison’s Principles of Internal Medicine ,18th ed ,2215.

Non cardiac cause of shock

Hypovolemia Excess use of diuretics

Blood loss Post fibrinolysis

Dehydration Diabetics,elderly,acute pancreatitis

Vasodilation excess use of nitrates

Septicemia Infection secondary to indwelling urinary catheter

Anaphylaxis During thrombolysis

Renal failure Diabetics,elderly,previous CKD

They should ruled out in a MI patient with shock,as the management is different and some are reversible. though they add to the mortality risk.

Cardiogenic Shock• One of the most common causes of death after an MI.

• Mostly occurs < 48 hrs after hospitalization, rather at presentation

(90% vs 4.5%).

• About 6% of STEMI, 3% of NSTEACS patients.

• Mortality is 6 times more(within index hospitalization).

• 90% mortality (pre thrombolytic era), 40-50% presently.

• Survival at 3yrs and 6 yrs – 40% and 30% respectively.

• Early recognition, prompt revascularization helps in improved

survival. 1.SHOCK registry, Circulation 1995;91:873-881.2.MILIS Study group, JACC;1989;14:40-6..3.Goldberg RJ et al,NEJM 1991;325:1117-1122.4.Goldberg et al ,Circulation 2009 ; 119(9):1211-9.

Definition Characterized by

• Marked and persistent (>30 min) hypotension

• SBP < 90 mmHg, or

• Drop in SBP by 30 mm Hg below basal levels, or

• Supportive pharmacotherapy required to maintain SBP > 90 mm Hg.

• Reduced cardiac index (<2.2 liters/min/m2)

• signs of impaired organ perfusion (altered mental status,cold

extremeties,oliguria)

• elevated left ventricular filling pressure (PCWP >18 mmHg).

About 40% of left ventricular mass to be affected. Braunwald’s HEART DISEASE,10th ed. Pg:1123.

Causes of Cardiogenic Shock

Predominant LV Failure

74.5%

Acute Severe MR

8.3%

VSD

4.6%

Isolated RV Shock

3.4%

Tamponade/rupture

1.7%Other

7.5%

Shock Registry

JACC 2000 35:1063

Killip – Kimball Classification

Am J Cardiol. 1967 Oct;20(4):457-64

APPROACH

Approach to patient in shock

Predictive indicators of Cardiogenic shockHistorical Features

Age > 65 yrs Lab FindingsFemale gender Hyperglycemia (>180mg/dl)

Previous infarction Increased blood lactate

Diabetes mellitus CK-MB >160 IU/L

History of angina,stroke or PVD Peak LDH > 4normal

Physical examinationSinus tachycardia Cardiac

Clinical hemodynamic class III - IV ECG – new ST elevation,LBBB

Agitation,abnormal mental status CXR – pulmonary edema

Clinical events ECHO LVEF < 0.35

Reinfarction Remote Asynergy

Hypotension Wall motion index

CAD patients at risk…

• Extensive Anterior wall STEMI

• LMCA stenosis + previous LVDysfunction.

• Osteoproximal LAD total occlusion.

• LAD + Previous h/o CAD.

• TVD + Diabetes.

Cardiac biomarkers• Established markers - CPK-MB, Quantitative troponins.

• NT Pro BNP – reflect LV dysfunction, effects of therapy (Normal

<400pg/ml).

• ST -2 - new biomarker( IL2 family) - marker of cardiac stress and

myocardial fibrosis.

• High levels post AMI - higher incidence of HF, readmission at 30

days ,higher mortality at 30 days.

Circulation ,2004;109(18):2186-90.

Preliminary • Back rest

• Oxygen supplementation (O2 Sat < 90%)

• Early mechanical ventilation if O2 supplementation not effective.

• ABG analysis for acid-base status.

• CVP monitoring after insertion of a jugular venous line.

• Hourly monitoring of urine.

• Anxiolytics

• Loading dose of Soluble aspirin,clopidogrel (if not given).

• Subcutaneous heparin – 60U/kg bolus – 10-12 U/hr

Rule out reversible causes.

• Correct acidosis (MC neglected).

• Hyperglycemia with insulin.(strict control of blood sugars not

advised) . NICE study.

• Bradyarrhythmias – transvenous pacing.

• Recurrent VT,AF - DC shock,overdrive pacing .

Medical management

• Vasopressors/Inotropic support (double edged swords)

– Dopamine

– Noradrenaline

– Dobutamine

– Levosimendan

– Milrinone

• Vasodilators

• Diuretics

Aim:Maintaining adequate systemic and coronary perfusion by ↑ SBP with pressors, optimal LV filling pressure - adjusting volume status.

Recommended is SBP 90mm Hg or Mean BP >60mmHgPCWP >20 mmHg

Dopamine• Initial drug of choice in hypotension.• and receptor and DA receptor stimulator.• ↑ HR,BP,CO,SVR,PCWP• Higher mortality when compared to NE in maintaining an effective

MAP. SOAP NEJM2010;362:779-789

Dosage Effect

0.5 -4 µg/kg/min Renal arteriolar vasodilation(DA receptor)Increase in urinary output.

4 -6 µg/kg/min Renal beneficial effects lost.Vasoconstriction (1 and NE)

Increased HR,CO,BP.

> 15 µg/kg/min Marked vasconstriction occurs.Seldom advised in Cardiogenic Shock.

Management of Cardiogenic Shock,Chirstopher.P.Cannon

Combination with dobutamine

• Dopamine (6-10µg/kg/min) and dobutamine

(2-10µg/kg/min) has several merits.

• If SBP&DBP low, PCWP >24 mmHg - Norepinephrine to

be tried in combination with dobutamine.

Circulation,1983;67:620-626.

Norepinephrine • When SBP<70mm Hg with signs of shock.

• When SVR is not elevated (<1,800dyne-s/cm5).

• Temporary manuever (2-4µg/min).

• If SBP >90 mmHg not attained with a dose of 15ug/min, further

increase not beneficial.Action of NE

Alpha receptor vasoconstriction Increase in SBP,DBP

Adv - Coronaries are adequately perfused

Adverse effect on renal tissue

Causes necrosis.

Management of Cardiogenic Shock,Chirstopher.P.Cannon

Milrinone

• Positive inotropic and significant vasodilator actions.

• ↑CO, LV filling pressures.

• Effective in RV dysfunction.

• Minimal effect on myocardial oxygen demand.

• Long half life.

• 50µg/kg bolus over 10 min – 0.0375 to 0.75 µg/kg/min.

Goodman & Gilman’s The Pharmacological basis of Therapeutics

Nitroprusside

• Very low dose (0.4 ug/kg/min).

• Reduces afterload .

• Useful in patients with severe MR or ventricular septal rupture.

• Causes coronary steal.

• Deleterious effect (If given <8 hrs of onset of pain).

• Combined with dopamine/dobutamine when afterload is to be

reduced without fall in BP.

Goodman & Gilman’s The Pharmacological basis of Therapeutics

Levosimendan

• Inotropic action by binding cardiac troponin C.

• Sensitizes myofilaments to calcium.

• 6 to 12 µg/kg loading dose over 10 minutes ----- 0.05 to 0.2

µg/kg/min as a continuous infusion.

• Effective in acute HF post MI - RUSSLAN trial.

• Risk of hypokalemia, frequent VPCs.

Murphy ,Mayo Clinic Cardiology Concise Textbook,4th Ed

Eur Heart J. 2002 Sep;23(18):1422-32.

Tilarginine

• Excess NO contributes to hypotension.,plays a role in

pathophysiology of cardiogenic shock.

Dzavik et al. 2007.

Alexander et al.2007.

• Isoform – nonselective NOS inhibitor.

• Despite establishment of an open infarct artery ,it revealed no

effect on mortality.

• An increase in blood pressure noted. Khan,Encylopedia of Cardiac Diseases,2nd ED

Unproven benefit

• Oxygen radical scavangers

• Adenosine

• Neutrophil inhibitors

• Substrate infusions of glutamate/aspartate

• Glucose – insulin – potassium infusion

• Coenzyme Q10

• Intravenous L- Carnitine.

Semin Thoracic Cardiovascul Surg 1993;5:151-161.

SHOCK trial

• Median time to onset of shock was 5.6 hrs.

• Most infarcts were Anterior in location.

• At 30 days - no significant overall benefit of early revascularization

for patients with STEMI or new LBBB who had cardiogenic shock

due to LV dysfunction. (46.7 % and 56.0 %; P= 0.11).

• lower mortality from all causes at 6 months. (50.3 % vs. 63.1 %,

P=0.027).

• Early revascularization be strongly considered for patients with

Acute Myocardial Infarction complicated by cardiogenic shock.N Engl J Med 1999; 341:625-634

Thrombolysis • Does reduce the incidence of cardiogenic shock.

[ASSET trial (5.1% vs 3.8%,p<0.05),APSAC multicenter trial (9.5 % to

3.2%,p=0.03) ].

• In established cardiogenic shock --- UNCERTAIN.

• No benefit on hospital survival - on STK use in GISSI trial.(n=280 pts,

STK 69.9% vs 70.1% untreated,p=NS).

• FTT analysis – absolute benefits of thrombolysis in patients with

evidence of hypotension and tachycardia (73 lives saved/1000 pts).

• Reperfusion rate was 44% in 44 Cardiogenic shock patients with STK

(SCAR registry).ASSET trial ,Lancet 1988;2:525-530.

APSAC ,Am J Cardiol 1988;62:347-351.GISSI trial,Lancet 1986;1:397-402.

FTT,Lancet 1994;343:311-322SCAR registry ,Am J Cardiol 1985;55:871-877.

Why thrombolysis not effective?

• Limited evidence.

• Complex mechanical, hemodynamic ,metabolic factors.

• Acidosis - impaired transformation of plasminogen to plasmin

- decreased efficacy

Becker et al.A Heart J 1993;125:919-929.

• coronary perfusion pressure – delivery of plasminogen

activators to thrombus impaired. Zidansek et al,Thromb Hemostat,1991.

Pressure dependent thrombolysis

• Successful thrombolysis with tPA in patients with cardiogenic

shock after infusion of dopamine or NE (MAP>100mmHg).

Garber et al,Can J Cardiol;1995;11:30-6.

• Combine therapy more beneficial than either therapy alone .

Chest 1994;105:997-1002.

• Imp. Role in hospitals without revascularization facilities by

stabilizing patients and facilitating their transfer to teritiary

centers.

IABP assisted Thrombolysis

• Patients in cardiogenic shock

– TT had lower in-hospital mortality rates (54% vs 64%),

– IABP counterpulsation had lower in-hospital mortality rates

(50% vs 72%).

• Revascularization influenced in-hospital mortality rates

significantly (39% vs 78%).

SHOCK registry

Which thrombolytic agent is effective?

• Use of accelerated tPA better than STK in reducing cardiogenic

shock (5.5% vs 6.9%)(GUSTO1).

• Cardiogenic shock after treatment - STK,Heparin better than tPA

(51% vs 57%,p=0.061).

• Advantage of STK – prolonged systemic fibrinolytic state with

decreased viscosity produced by streptokinase.

Mechanical and other causes

• MR – Nitroprusside ,NTG.

• VSR – Surgical referral.

• Percardial tamponade – Pericardiocentesis.

• AF – Cardioversion.

• VT – Cardioversion.

• VT storm – Magnesium infusion, Esmolol, Overdrive pacing.

• Pneumothorax secondary to CPR – ICD.

Treatment of Cardiogenic Shock

Emergency revascularization with either PCI or CABG is

recommended in suitable patients with cardiogenic shock

due to pump failure after STEMI irrespective of the time

delay from MI onset.

In the absence of contraindications, fibrinolytic therapy

should be administered to patients with STEMI and

cardiogenic shock who are unsuitable candidates for

either PCI or CABG.

I IIaIIbIII

I IIaIIbIII

ACC/AHA STEMI GUIDELINES 2013;Circulation.2013; 127: 529-555

Treatment of Cardiogenic Shock

The use of intra-aortic balloon pump counterpulsation

can be useful for patients with cardiogenic shock after

STEMI who do not quickly stabilize with

pharmacological.

Alternative LV assist devices for circulatory support

may be considered in patients with refractory

cardiogenic shock.

I IIaIIbIII

I IIaIIbIII

ACC/AHA STEMI GUIDELINES 2013;Circulation.2013; 127: 529-555

Conclusion • Cardiogenic shock main cause of death in AMI patients.

• Immediate diagnosis & management required.

• Rule out Noncardiac causes of shock .

• Gold standard - Invasive approach.

• In Non PCI center, fibrinolytic therapy and IABP should be used

while provisions are made for invasive treatment.

• Newer therapies may help in decreasing the significant mortality

of cardiogenic shock in the future.

An ounce of prevention is

worth a pound of care Benjamin Franklin