This document discusses the current management of cardiogenic shock. It defines cardiogenic shock and describes its causes, predictors of mortality, and pathophysiology. Treatment involves hemodynamic support, volume management, inotropic drugs, and early revascularization, which significantly reduces mortality. Mechanical circulatory support devices like IABP, Tandem Heart, Impella, and ECMO can further improve hemodynamics and outcomes when used as adjuncts to optimal medical therapy. Timing of revascularization is critical, with survival benefits seen for up to 48 hours after myocardial infarction onset. Special considerations are discussed for managing shock in the elderly, from mechanical causes, and with specific device therapies.

1. DEPARTMENT OF CARDIOLOGY
CURRENT MANAGEMENT
ISSUES OF CARDIOGENIC SHOCK
Gopal C Ghosh
UNIT-1

2. DEFINITION
• Cardiogenic shock is a state of end-organ
hypoperfusion due to cardiac failure
• Pulmonary artery (PA) catheterization;
Doppler echocardiography used to confirm
elevation of LV filling pressures
Circulation. 2008;117:686-697

3. • Persistent hypotension (systolic blood pressure <80 to 90 mm
Hg or mean arterial pressure 30 mm Hg lower than baseline)
• Severe reduction in cardiac index (<1.8 L / min/m2
without support or <2.0 to 2.2 L/ min/m 2 with support)
• Adequate or elevated filling pressure (eg, left
ventricular [LV] end-diastolic pressure >18 mm Hg or right ventricular [RV] end-
diastolic pressure >10 to 15 mm Hg)
• Clinically by cool extremities, decreased urine output, and/or alteration in
mental status.
Circulation. 2008;117:686-697

4. 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

5. OTHER CAUSES
• Acute myopericarditis
• Tako-tsubo cardiomyopathy
• Acute valvular regurgitation (trauma, degenerative
disease)
• Aortic dissection
• Acute stress in the setting of aortic or mitral stenosis
• Massive pulmonary embolism

6. Incidence
• Complicate approximately 5% to 8% of
STEMI and 2.5% of non-STEMI cases
• Incidence is on the decline (Increasing
number of myocardial infarction diagnosed
due to use of troponin & increase use of
reperfusion therapy )
The Global Registry of Acute Coronary
Events (GRACE). Heart. 2007;93:177–182

8. • Historic mortality rate for CS complicating an acute
myocardial infarction (MI) was 80 to 90 percent
(1975 to 1988)
N Engl J Med 1991; 325:1117
• Shortterm mortality rates between 42-48 %
Circulation 2009; 119:1211
• Swiss registry (1997-2006): showing similar trends
Ann Intern Med 2008; 149:618

10. Predictors
• GUSTOI database identified the following
predictors of 30day survival (receive initial fibrinolysis)
o Increasing age (odds ratio 1.49 for each 10 year
increase)
o Prior MI
o Physical findings at the time of diagnosis (the
presence of altered sensorium and cold, clammy skin)
o Oliguria
Am Heart J 1999; 138:21

11. PATHOPHYSIOLOGY

13. IATROGENIC FACTORS
WORSENS CARDIOGENIC
SHOCK

15. Treatment
General measures
• Antithrombotic therapy with aspirin and
heparin
• Clopidogrel may be deferred until after
emergency angiography

16. Hemodynamic assessment
• Pulmonary artery catheterisation
• Non-invasive Doppler measurement:
Short mitral deceleration time (<140 ms) is
highly predictive of pulmonary capillary
wedge pressure >20 mm Hg in CS
Am Heart J. 2006;151:890 e9–e15

17. Volume management
• Intravenous fluid replacement:
PCWP, arterial oxygen saturation(SaO2),
systemic arterial pressure, and cardiac output
• The usual value in CS is between 18 and 25
mmHg
J Am Coll Cardiol 2000; 36:1071

18. Pharmacological Treatment
• Pharmacological support: inotropic and
vasopressor agents, lowest possible doses
• Higher vasopressor doses poorer survival
• ACC/AHA guidelines recommend
norepinephrine for more severe hypotension
because of its high potency
Circulation. 2004;110:588–636
Int J Cardiol. 2007;114:176–182

19. Mortality Rates
De Backer D et al. N Engl J Med 2010;362:779-789

20. Kaplan-Meier Curves for 28-Day Survival in the Intention-to-Treat Population
De Backer D et al. N Engl J Med 2010;362:779-789

21. Forest Plot for Predefined Subgroup Analysis According to Type of Shock
De Backer D et al. N Engl J Med 2010;362:779-789

22. Mechanical Support: IABP
• Not every patient has a hemodynamic response
to IABP
• Response predicts better outcome
Circulation. 2003;108(suppl I):I-672

24. The Lancet, Volume 382, Issue 9905, 16–22 November 2013, Pages

25. Figure 2. Time-to-event curves for all-cause mortality up to 12 months Event rates represent Kaplan-
Meier estimates. Two patients in the IABP group died at days 388 and 419 postrandomisation, which is
represented in the Kaplan-Meier curves.
Intra-aortic balloon counterpulsation in acute myocardial infarction complicated by cardiogenic
shock (IABP-SHOCK II): final 12 month results of a randomised, open-label trial
The Lancet, Volume 382, Issue 9905, 16–22 November 2013, Pages

26. EUROTRANSFER registry

27. EUROTRANSFER registry
Postepy Kardiol Interwencyjnej. 2014; 10(3): 175–180

28. Cochrane Database Syst Rev 2015; 3:CD007398

29. Circulation 2004; 110:588

30. ACC/AHA/ESC
RECOMENDATIONS
• ACC/AHA 2007 & 2013 update also
recomends same
• ESC 2008 & 2012: same recomendations

31. Reperfusion
• Survival benefit of early revascularization
• Thrombolysis
PCI is impossible
If a delay has occurred in transport for PCI and
when MI and CS onset were within 3 hours

32. REVASCULARISATION
• Early revascularization decreases mortality
rates
− SMASH (Urban P et al. Eur Heart J
1999;20:1030-8)
− SHOCK (Hochman JS et al. N Engl J Med
1999;34:625 -34)
− ACC/AHA guidelines on acute myocardial
infarction (Ryan TJ et al. Circulation
1999;100;1016-30)

34. Emergency revascularisation - SHOCK
Trial
47%
50%
53%
56%
63%
66%
0%
10%
20%
30%
40%
50%
60%
70%
30 days (n=302) 6 months (n=301) 12 months (n=299)
Mortality(%)
ERV
IMS
p=0.11
p=0.03
85% of survivors NYHA Class I/II at 12 months
Hochman JAMA 2000;285:190

36. Emergency revascularisation in the
Elderly- SHOCK Trial
41%
75%
57%
53%
0%
10%
20%
30%
40%
50%
60%
70%
80%
<75 years (n=246) >75 years (n=56)
30-dayMortality(%)
ERV
IMS

37. Elderly - SHOCK & other registry
data
48% 47% 46%
81%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
SHOCK Registry Mayo Clinic Northern New
England
30-dayMortality(%)
ERV
IMS

38. Circulation 2004; 110:588

39. Timing of PCI
• Presentation 0 to 6 hours after symptom onset
was associated with the lowest mortality
[ ALKK registry(German). door-to-angiography times were <90 minutes in
approximately three fourths of patients. ]
• SHOCK trial: increasing long-term mortality
as time to revascularization increased from 0
to 8 hours
• Survival benefit as long as 48 hours after MI
and 18 hours after shock onset

40. Stenting and Glycoprotein
IIb/IIIa Inhibition
• Stenting and glycoprotein IIb/IIIa inhibitors
were independently associated with improved
outcomes
ADMIRAL. N Engl J Med. 2001;344:1895–1903

41. ACC/ AHA guidelines

42. Treatment of CS Due to Mechanical
Complications
• Mechanical complications of MI, including
rupture of the ventricular septum, free wall, or
papillary muscles, cause 12% of CS cases
• Ventricular septal rupture has the highest
mortality, 87%
• Strongly suspected in patients with small
infarct size and shock

43. Survival from mechanical causes
94%
71%
47%
39%
28%
0%
10%
20%
30%
40%
50%
60%
70%
80%
90%
100%
VSD Acute Severe MR
In-hospitalMortality(%)
No Surgery
Surgery
Percutaneous closure
Shock Registry JACC 2000;36:1104 & 36: 1110
GUSTO 1 Circulation 2000;101:27
Holzer R CCI 2004;61:196

44. Management of Special Conditions
• Treatment of CS with hypertrophic
obstructive cardiomyopathy: volume
resuscitation and betablockade. Pure alpha-
agonists may be used to increase afterload,
increasing cavity size and decreasing
obstruction
• Outflow obstruction: seen in tako-tsubo
cardiomyopathy

45. Other mechanical devices
• Left ventricular and biventricular assist device
: surgically placed, bridge to therapy & bridge to
transplantation
• Percutaneous left atrialto-
femoral arterial ventricular assist device(Tand
em heart)
• ECMO
• Percutaneous transvalvular left ventricular ass
ist device (LVAD)[Impella]

47. Clinical spectrum of Cardiogenic Shock
Biswajit Kar et al. Circulation. 2012;125:1809-1817
Copyright © American Heart Association, Inc. All rights reserved.

48. •Left atrial-to-femoral arterial
LVAD
•Low speed centrifugal continuous
flow pump
•21F venous transeptal cannula
•17F arterial cannula
•Maximum flow 4L/minute
Tandem Heart pLVAD

49. Tandem Heart Outcome Data
42%
47%
45%
36%
0%
5%
10%
15%
20%
25%
30%
35%
40%
45%
50%
Thiele (n=41) Burkhoff (n=33)
30daymortality(%)
Tandem Heart
IABP
Improved haemodynamic parameters
Increase in bleeding, limb ischaemia, and sepsis
Thiele EHJ 2005;26:1276. Burkhoff AHJ 2006;152:e1

50. Impella
Axial flow pump
Much simpler to use
Increases cardiac output & unloads LV
LP 2.5
12 F percutaneous approach; Maximum
2.5 L flow
LP 5.0
21 F surgical cutdown; Maximum 5L
flow

51. Impella outcome data
• 1 RCT of Impella 2.5 in AMI Cardiogenic Shock
• ISAR-SHOCK
– 26 patient RCT Impella vs IABP
–  Cardiac Index,  MAP (by 10mmHg) vs IABP
– Complications ≤ IABP
– No difference in mortality

54. Percutaneous ECMO
• CARDIOHELP & LIFEBRIDGE-B2T
system (FDA approved)
• Advantage: over other modern PVADs is the
lack of need for transseptal puncture or
transfer to a cardiac catheterization laboratory

55. Indications
• Short-term cardiopulmonary support in
patients with postcardiotomy CS
Doll N et al. Ann Thorac Surg. 2004; 77: 151–157
• Bridge-to-recovery device in patients with
fulminant myocarditis
Asaumi Y et al. Eur Heart J. 2005; 26: 2185–2192
• Improves 30-day outcomes when used for
hemodynamic support during primary PCI in
patients presenting with STEMI and profound
CS
Sheu JJ et al. Crit Care Med. 2010; 38: 1810–1817

56. Timing of Implantation
• Rather than continued escalation of medical
therapy, early institution of mechanical
circulatory support via IABP and/or PVAD-
mediated circulatory support should strongly be
considered

57. Goals of Support and Weaning
• Maintain mean arterial pressure >60 mm Hg
and a mixed venous oxygen saturation of
>70%
• Minimal/no pressor requirement and
improving end-organ function.
• Average duration was 5.8±4.75 days
Tallaj JA et al. J Am Coll Cardiol. 2011; 57: 697–699

58. What we should do about STEMI
Cardiogenic Shock
• Emergency angiography and revascularisation: Primary PCI preferably
– All patients <75 years
– Selected patients ≥75 years
• On-table echo to rule out mechanical defects
• Stabilise the patient in the lab before revascularisation
– IABP
– Pressors if required (Norepinephrine/dopamine)
– Anaesthetic support
• Consider calling the surgeon for true surgical disease
• PCI culprit artery. Other vessels if shock persists
• Use abciximab for PCI
• Consider percutaneous LVAD if shock persists with IABP + multi-vessel
revascularisation