Transcript Slide 1

Cardiogenic shock
Kasia Hryniewicz, M.D.
Greater Twin Cities Area Chapter of AACN
Fall Symposium
November 8, 2013
Minneapolis Heart Institute, Abbott Northwestern Hospital,
Minneapolis, MN
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 CS
1. 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
Tamponade
2%
Other
7%
1.4%
Shock - pathophysiology
Hochman J:Circulation 107:2998, 2003
Risk factors
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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 class
were major predictors of CS accounting
for over 95 percent of the predictive
information.
Killip acute HF class
Class 1
Class 2
Class 3
Class 4
Absence of rales over
the lung fields and
absence of S3.
Rales over 50% or less
of the lung fields or
the presence of an S3.
Rales over more than
50% of the lung fields.
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.
Onset
Based 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-shock
COMMIT 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!
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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 elevated
3. A clinically evident systemic inflammatory
response 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 cont
Pharmacologic 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.
Results
1. 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
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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
H&P, ECG, echo (TEE)
IABP?/MCS (ECMO)?
Acute MI
Mechanical complications
Cath lab
Severely depressed EF, STE
Revascularization
Surgery
PCI
MCS (ECMO?)
Thank you!