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Cardiogenic Shock & MechanicComplications of Myocard Infar

NADIAR DWI NUARISA

BAMBANG HERWANTO

Department of Cardiology & Vascular MedicineDr. Sutomo Hospital – Faculty of Medicine Airlangga Un

Surabaya

2015



Introduction

Definition

•Ventricular Septal Rupture (VSR)

•Acute Mitral Regurgitation

•LV Free Wall Rupture

Mechanical Complication of AMI

Management of Cardiogenic Shock in AMI

Prognosis

Summary



Introduction Worldwide, coronary artery disease (CAD) is the single most freq

of death. Over seven million people every year die from CAD

Cardiogenic shock is a serious complication of acute myocardia

(AMI). Mortality is about 50%.

The mechanical complications of AMI are responsible for approx

25,000 deaths per year in the US.

Since the introduction of PCI, the incidence of mechanical com

reduced significantly to < 1%

Surgical evaluation should be performed early whenever there is

of a mechanical complication



Definition (WHO)

The definition was based on patient symptoms and ECG

findings Combination of two of three characteristics:

1. typical symptoms (i.e. chest discomfort)

2. enzyme rise

3. typical ECG pattern involving the development of Q

waves

But still myocardial infarction was mainly an ECG baseddiagnosis



Definition of Cardiogenic Shock

Is a clinical condition of inadequate tissue (end-organ)perfusion due to cardiac dysfunction

- hypotension ( SBP<90mmHg for 30 min, or the need fosupportive measures to maintain SBP≥90mmHg), fall ofMAP 30mmHg from baseline

- end-organ hypoperfusion (cool extremities or an urineoutput<30 ml/h)

- a cardiac index (CI) < 1,8 l/m/m2 or < 2.2 l/min/m2with haemodynamic support, and a pulmonarycapillary wedge pressure (PCWP)> 18 mmHg



Mechanical Complication of MI

Ventricular Septal Rupture (VSR) VSR is lethal complication of acute myocardial infarctio

(AMI)

Expected to occur within 16 hours after AMI. Theoutcome are poor

Independent risk factors for VSR : hypertension, olderage, female gender, history of previous stroke, CKD, CHdiabetes, smoking, & previous MI.

VSR direct effect is the shunting of blood from LV to RV →cardiogenic shock



On physical examination we can found pansystolic loud m

sounds most clearly at the left edge of the sternum, palpaparasternal thrill

ECG recordings showed anterior or inferior STEMI with AV b

Doppler echocardiography is the gold standard for diagndistinguish between papillary muscle rupture and VSR, assLV function, identified size & site of rupture



Management of VSR (Jones et al, European Heart Journa



VSR Surgery



Acute MR Acute mitral regurgitation secondary to papillary muscle

rupture is a life-threatening complication with a poorprognosis

Usually diagnosed in 2 to 7 days post-AMI, the average

time is approximately 13 hours. Papillary muscle rupture can be partially (occurring at

one end of the muscle) or complete.

Differential diagnosis of VSR → distinguished by a site ofthe murmur & by Swan-Ganz catheter



Pansystolic murmur loudest at the apex, with diastoliccomponents, and spread to the axilla.

ECG describe myocardial infarction posterior or inferior

Doppler Echocardiography is a standard for thediagnosis, monitoring, and planning surgical therapy.

In an acute atmosphere, shock cardiogenic andpulmonary edema may occur → not enough time forthe LV to dilate or compensation



Mitral valve repair & Mitral vareplacement

Management of Acute MR



LV Free Wall Rupture (LVFWR) 50% patients with LVFWR is diagnosed in 5 days post-AM

where 20% of them within 2 weeks.

Risk factors : age, female gender, HT, first AMI, & poorcollateral coronary artery

Blow-out ruptures are manifested with cardiogenicshock (arterial pressure < 70 mmHg for at least 10minutes)



ECG might manifest with increase of ST elevation by atleast 1mV in affected leads, ST elevation in aVL, non-inversion of the T wave

Pericardial effusion is the most commonechocardiographic finding.

Doppler echocardiography may appear as adiscontinuity of the myocardium & bidirectional shunt



Management of LV(Hellenic Journal of 2002)



LVFWR Surgery



Management of Cardiogenic Shock in A

The aim of initial resuscitation is to stabilize oxygenation &perfusion while revascularization is contemplated

We should prepare :

1. DC shock

2. Drugs : inotropes & vasopressors

3. Reperfusion strategies : the trombolytic therapy,

percutaneous coronary intervention (PCI), surgical

(CABG)

4. Mechanical circulatory support : IABP (Intraaortic Balloon

Pump Counterpulsation), extracorporeal membraneoxygenation (ECMO), percutaneus Ventricular Assist

Devices/pVAD (Impella recover system, Tandem heart)



Algorism for the management of ischemic cardiogenic shock (Reynolds & Hoc



IABP



ECMO



TandemHeart



Impella recovery system



Prognosis

VSR

Patients treated medically have poor overall prognosis,with a mortality rate of 24% in 24 hours, 46% in 1 week,and 82% mortality within 2 months.

Mortality after surgery is 42,9%.

54,1% mortality patient underwent surgery within 7 daysafter MI higher than patients who underwent surgery atmore than 7 days (mortality rate 18,4%).

The highest mortality rate (> 60%) in patients whounderwent surgery in the first 24 hours



Acute MR

Only 25% patients survive acute MR 24 hours after therupture of papillary muscle.

The average survival of patients without surgery just thredays

In one study, 5126 patients who underwent surgicalintervention, the mortality rate was 26,9% with a 15-yearsurvival of 39%

LVFWR

Operative mortality of LVFWR between 12% to 30%.

Long-term outcome of these patients is the survival of 7years.



Summary

The 3 most often mechanical complications after IMAare ventricular septal rupture (VSR), acute mitralregurgitation, and LV Free Wall Rupture (LVFWR)

This resulted in cardiogenic shock and require surgicaltreatment.

The mortality rate of each complication is still high, aftersurgery or without surgery.



Guideline Recommendation of Assist Devices According to ESC & AHA



Algorism for Revascularization in cardiogenic shock (ACC/AHA Guideline



Definition of AMI (ESC 2012)

The term AMI should be used when there is evidence of

myocardial necrosis in a clinical setting consistent with

myocardial ischaemia.

Detection of rise and/or fall of cardiac biomarker values with

at least one of the following:

- Symptoms of ischaemia

- New or presumably new significant ST-T changes or new

LBBB

- Development of pathological Q waves in the ECG

- Imaging evidence of new loss of viable myocardium, or

new regional wall motion abnormality

- Identification of an intracoronary thrombus by angiograph

or autopsy

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