Cardiogenic shockKasia Hryniewicz, M.D.

Minneapolis Heart Institute, Abbott Northwestern Hospital, Minneapolis, MN

Greater Twin Cities Area Chapter of AACN Fall Symposium

November 8, 2013

Definition• Cardiogenic shock (CS) is a clinical

condition of inadequate tissue perfusion due to cardiac dysfunction.

Definition cont• persistent hypotension (systolic blood

pressure <80 to 90 mmHg or mean arterial pressure 30 mmHg lower than baseline)

• severe reduction in cardiac index (<1.8 L/ min per m2 without support or <2.0 to 2.2 L/ min per m2 with support)• adequate or elevated filling pressures

Etiology

Cardiogenic shock

Acute Chronic- End stage

cardiomyopathy, inotrope dependent

Etiology – Acute CS1. Acute myocardial infarction

– Large infarct, reinfarction– Mechanical complications MR, VSD, free wall

rupture– Right ventricular infarction

2. Non-infarct related- acute myocarditis- acute MR – chordal rupture/endcarditis- acute AI – dissection, endocarditis- stress induced cardiomyopathy- myocardial contusion

Incidence- SHOCK registry• 1190 pts- overall

incidence – 5%• The majority of

patients have a STEMI, but CS occurs in 2.5% (NSTEMI)

LV failure 79%

Severe MR 7%

VSD 4%

Isolated RV infarct

2%

Tamponade 1.4%

Other 7%

Shock - pathophysiology

Hochman J:Circulation 107:2998, 2003

Risk factors• Older age• Anterior MI• Hypertension• diabetes mellitus• multivessel coronary artery disease• Prior MI or diagnosis of heart failure• STEMI• Left bundle branch block on the

electrocardiogram (ECG)

Risk factors continue• In the GUSTO-I and GUSTO-III trials of

fibrinolytic therapy in acute STEMI- Age- systolic blood pressure- heart rate- Killip classwere major predictors of CS accounting

for over 95 percent of the predictive information.

Killip acute HF classClass 1 Absence of rales over

the lung fields and absence of S3.

Class 2 Rales over 50% or less of the lung fields or the presence of an S3.

Class 3 Rales over more than 50% of the lung fields.

Class 4 Cardiogenic shock

Symptoms• severe systemic hypotension• signs of systemic hypoperfusion (eg, cool

extremities, oliguria, and/or alteration in mental status)

• respiratory distress due to pulmonary congestion.

Not all patients present with this syndrome. In

particular, most patients develop shock after presentation.

OnsetBased on GUSTO trials• Shock was present on admission in 0.8 % at hospital

presentation and an additional 5.3 % developed shock after admission, either as a sudden event or as a gradual fall in blood pressure.

• Approximately 50 percent of patients who developed shock after admission did so within the first 24 hours after the infarct.

In SHOCK trial: the median time from MI to onset of cardiogenic shock was 5.5 hours and 75 % of patients developed shock within 24 hours.

Onset cont• Shock developed significantly later

among patients with a NSTEMI (median 76 to 94 hours versus 9.6 hours for those with STEMI).

Pre-shockCOMMIT trial randomization to early beta

blockade was associated with a 30% higher occurrence of CS in patients:

- > 70 years of age- SBP < 120 mm Hg- HR >110 beats per minute- Killip Class > 1

Commit trial.

Diagnosis is key!• H&P• ECG• Echo (TTE/TEE)• S-G catheter• Coronary angiogram

Treatment

Shock trial• Inclusion criterion: shock due to LV

failure complicating myocardial infarction

• 302 pts randomly assigned to emergency revascularization (n=152) or initial medical stabilization (n=150).

Shock trial• IABP was performed in 86 percent of

the patients in both groups. • The primary end point mortality from

all causes at 30 days.• Secondary end point six-month

survival

Shock trial results

- No difference in mortality at 30 days (46.7% vs 56%, p=0.11)

- Significant decrease in all cause mortality at 6 months (50.3% vs. 63.1% p=0.027).

Shock trial – what have we learned?

1. Average LV ejection fraction (EF) is only moderately severely depressed (30%), with a wide range of EFs and LV sizes noted.

2. SVR on vasopressors is not elevated3. A clinically evident systemic inflammatoryresponse syndrome is often present in patients

with CS.4. Most survivors have NYHA class I status.

Predictors of outcome• Coronary anatomy - Higher mortality in pts with a LM

SVG lesion than in those with LCX, LAD or RCA (79 and 70 % vs 37and 42%). RCA culprit lesions were associated with the best prognosis

• Echocardiographic predictors - (LVEF) and severity of mitral regurgitation (MR). LVEF <28 percent survival at one year was

24% vs 56% Moderate or severe MR survival at one year was 31 % vs 58% However, there was benefit of early revascularization at all levels of LVEF and MR grade.

• Symptom onset to reperfusion time - mortality only 6.2 percent in patients reperfused within two hours of symptom onset

Methods• Randomized, prospective, open-label,

multicenter trial• 600 patients with CS complicating acute

myocardial infarction, randomly assigned to - IABP, (301 pts) or - no IABP (299 pts)

plus early revascularization• The primary end point 30-day all-cause

mortality. • Safety assessments - major bleeding,

peripheral ischemic complications, sepsis, and stroke.

Results

Results

Results• At 30 days –

119 patients in the IABP group (39.7%)

and 123 patients in the

control group (41.3%) had died (P = 0.69).

- At 6 months – no difference in mortality.

Conclusions…• The use of IABP did not significantly

reduce 30-day or 6 month mortality in patients with cardiogenic shock complicating acute MI for whom an early revascularization strategy was planned.

Conclusions…The IABP-SHOCK II trial could have affirmed contemporary clinical practice and guidelines,“ "Instead, it revealed surprising results. . . . We must now move forward with the understanding that a cardiovascular condition with 40% mortality at 30 days remains unacceptable

CS-Management• General measures- ventilation support to correct hypoxemia

and, in part, acidosis- Optimize intravascular volume- Sodium bicarbonate only for severe

metabolic acidosis (arterial pH less than 7.10 to 7.15)

- Aspirin- Intravenous heparin- insertion of pulmonary artery catheter

Management contPharmacologic support- Vasopressors and inotropes

(norepinephrine, vasopressin, dopamine, neosinephrine, dobutamine, milrinone)

Mechanical support- IABP???- Full mechanical support (ECMO?)

Which pressor is best?

Results• 1679 pts, 858 dopamine and 821

norepinephrine. • Primary outcome – rate of death at 28

days• Secondary endpoint – number of days

without need for organ support and occurrence of adverse events.

Results1. No difference in primary outcome(52.5% vs 48.5%)2. Less AE in norepinephrine group(24.1% vs 12.4%, p<0.001)3. In CS subgroup analysis Dopamine was associated with

significantly higher mortality comparing with norepinephrine.

What about mechanical support?

ExtraCorporeal Membrane Oxygenation

• VV (veno-venous) respiratory failure• VA (veno-arterial) full hemodynamic

support for refractory cardiogenic shock

• Relatively easy placement• Temporary stabilization, bridge to

recovery/permanent VAD• Requires anticoagulation

ECMO at ANWH• 46 pts between 2012-2013• Percutanously placed in the cath lab• Survival to discharge 70%• Major complications – bleeding • Patients managed by HF

cardiologists/RNs/perfusionists in CT ICU

Approach to a pt with CS

Acute MIMechanical complications

Surgery

H&P, ECG, echo (TEE)

Cath lab

Revascularization

IABP?/MCS (ECMO)?

Severely depressed EF, STE

PCIMCS (ECMO?)

Thank you!