Cardiogenic shock

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