cardiogenic shock BY DR.Mohammad Abdeljawad.pptx About shock (cardiogenic shock) IcU

1. CARDIOGENIC SHOCK
Done by: Mohammad Abdeljawad
12/3/2022
1

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Definition
Cardiogenic shock is a syndrome due to primary cardiac dysfunction
resulting in an inadequate cardiac output, comprising a lifethreatening
state of tissue hypoperfusion, which can result in multiorgan failure and
death.
Contemporary Management of Cardiogenic Shock: A Scientific Statement from the American Heart Association. Circulation
2017,

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The definition includes the following hemodynamic parameters:
 persistent hypotension (systolic blood pressure <80 to 90 mmHg
or mean arterial pressure 30 mmHg lower than baseline)
 severe reduction in the cardiac index (<1.8 L/min per m2 without
support or <2 to 2.2 L/min per m2 with support)
 adequate or elevated filling pressures
eg, left ventricular [LV] end-diastolic pressure >18 mm Hg or right ventricular [RV] end-diastolic pressure >10 to
15 mm Hg)
Reynolds HR, Hochman JS. Cardiogenic shock: current concepts and improving outcomes. Circulation 2008;
117:686.

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Mortality rates for patients with cardiogenic shock remain
frustratingly high, ranging from 50% to 80%. (1)
( 1 ) Hochman JS, Boland J, Sleeper LA, Porway M, Brinker J, Col J, et al.
Current spectrum of cardiogenic shock and effect of early revascularization on mortality. Results of an International Registry. SHOCK
Registry Investigators. Circulation. 1995;91:873-81

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causes of cardiogenic shock

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Acute myocardial infarction (MI) is the most common cause of
cardiogenic shock .
Fox KA, Steg PG, Eagle KA, et al. Decline in rates of death and heart failure in acute coronary
syndromes, 1999-2006. JAMA 2007; 297:1892.

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A total of 219 patients were included in the study. Patients were recruited from emergency departments, cardiac
and intensive care units, The study enrolled consecutive patients aged over 18 years within 6 h from identification
of cardiogenic shock. Mean age was 67 (12) years, and 74% were men. The main co-morbidities were
hypertension (60%), CAD (35%), and diabetes (28%), while a history of previous MI (25%) or heart failure (16%)
was less common

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 Acute
myocardial
infarction (MI)
accounts for 81%
of patient in CS
Non-ACS causes consisted mainly of worsening of chronic heart failure
ST-segment–elevation myocardial
infarction (STEMI) is associated
with a 2-fold increased risk for
development of CS compared with
non–ST-segment–elevation
myocardial infarction (NSTEMI).

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ACS was independently
associated with worse
prognosis
suggesting clearly better
survival in patients with other
causes of cardiogenic shock

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Risk factors for development of CS in the context of MI include
older age, anterior MI, hypertension, diabetes mellitus, multivessel
coronary artery disease, prior MI or angina, prior diagnosis of heart
failure, STEMI, and left bundle-branch block. A long duration of
symptoms before treatment and Higher incidences of CS are observed
in women,
Lindholm MG, Kober L, Boesgaard S, Torp-Pedersen C, Aldershvile J. Cardiogenic shock complicating acute myocardial
infarction: prognostic impact of early and late shock development. Eur Heart J. 2003; 24: 258–265.

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Clinical Presentation and Physical Examination

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Signs and symptoms of cardiogenic shock usually develop after hospital
admission (median,6.2 hours ) and the majority of patients develop shock
within first 24 hours of AMI
Regarding time as a factor of occurrence of CS, it is worth mentioning that only
20.0% of post-infarction shocks are present at hospital admission
Sakai K, Nakagawa Y, Soga Y, Ando K, Yokoi H, Iwabuchi M, Yasumoto H. et al. Comparison of 30-day outcomes in patients <75 years of age versus
>or=75 years of age with acute myocardial infarction treated by primary coronary angioplasty. Am J Cardiol. 2006;98(8):1018–1021
Therefore, during the hospitalization continuous observation of the patient should be kept, aiming at the early
recognition of clinical signs and laboratory indicators of shock

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A total of 219 patients were included in the study. Twenty-four per cent of
them had shock at presentation to hospital, whereas 62% developed shock
within the first 24 h from admission. Only 14% developed shock after 24 h
from admission
. Clinical picture and risk prediction of short‐term mortality in cardiogenic
shock: clinical picture and outcome of cardiogenic shock. Eur J Heart
Fail. 2015; 17:501–509.
Harjola V‐P, Lassus J, Sionis A, Køber L, Tarvasmäki T, Spinar J, Parissis J, Banaszewski M,
Silva‐Cardoso J, Carubelli V, Di Somma S, Tolppanen H, Zeymer U, Thiele H, Nieminen MS,
Mebazaa A; for the CardShock study investigators and the GREAT network

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The presenting symptoms of cardiogenic shock are variable
. The most common clinical manifestations of shock, such as
hypotension, altered mental status, oliguria, and cold, clammy skin,
can be seen in patients with cardiogenic shock.

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Patients with CS most commonly present with cool extremities and signs of
pulmonary congestion
This presentation is termed “cold and wet” and reflects a reduced
cardiac index (CI), increased systemic vascular resistance, and
increased PCWP
Cardiogenic Shock Cyrus Vahdatpour, MD; David Collins, MD; Sheldon
Goldberg, MD, FACC

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Patients may also present euvolemic or “dry and cold”, which
indicates a reduced CI, increased systemic vascular resistance, and
normal PCWP.
Cardiogenic Shock Cyrus Vahdatpour, MD; David Collins, MD; Sheldon
Goldberg, MD, FACC

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An under-recognized presentation of CS is the “wet and
warm” subtype. This represents a systemic inflammatory
response syndrome reaction in conjunction with an MI and is
associated with a higher incidence of sepsis and mortality.
These patients have a reduced CI, low-to-normal
systemic vascular resistance, and an elevated PCWP
Kohsaka S, Menon V, Lowe AM, Lange M, Dzavik V, Sleeper LA, Hochman JS; SHOCK Investigators . Systemic
inflammatory response syndrome after acute myocardial infarction complicated by cardiogenic shock. Arch Intern
Med. 2005; 165:1643–1650.

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Clinically significant signs
of SIRS leading to a
diagnosis of suspected
sepsis were noted in 54
(18%) of 297 patients
Of these 54 patients, 40
(74%) had positive
culture results and 14
(26%) did not

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Conclusions:
Almost one fifth of patients with
acute myocardial
infarction complicated by CS
showed clinical signs
of severe systemic inflammation,
and those who were culture-
positive for sepsis had twice the
risk of death.
ACS-associated CS patients with culture-positive
sepsis have 2 times the risk of mortality

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It should be noted that a subset of cardiogenic shock patients who
present with poor cardiac output and evidence of systemic hypo
perfusion but with out frank hypotension has been described
They have a lower mortality than their hypotensive counterparts

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Investigations

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Routine Initial Investigations
Complete blood counts , renal function, blood glucose, coagulogram
metabolic panels should be obtained every 12 to 24 hours as they offer
valuable information about oxygenation, electrolyte status, and end-organ
damage

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Type 1 MI is caused by an acute atherothrombosis as result of plaque rupture
or erosion. Frequent monitoring of troponins may reflect extent of injury that is
time-dependent from the initial insult.
 In the setting of CS, as in STEMI, it is not recommended to wait for the
presence of elevated cardiac enzymes before emergent catheterization.

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CS causes reduced oxygenation to peripheral tissues that
results in lower pO2 levels and elevated pCO2 levels. Higher
levels of lactic acid can be associated with increased mortality
Predictors of in‐hospital mortality after percutaneous coronary intervention for cardiogenic
shock. Int J Cardiol. 2007;

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Conclusions: Hyperlactatemia,
hyperglycemia and increased
levels of uric acid on CCU
admission are univariate
predictors of in-hospital
death. Moreover, at multivariate
analysis, hyperlactatemia (>6.5
mmol/l) is an independent
indicator of in-hospital death in
CS patients
complicating STEMI
In 45 consecutive patients (71 years) with CS complicating STEMI treated with primary percutaneous coronary intervention (PCI)
serum levels of lactate, glucose and uric acid on coronary care unit (CCU) admission were measured. The end-point was in-
hospital death.

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The CardShock risk Score for prediction of in-hospital mortality
low (scores 0–3)
8.7%
intermediate (scores 4–5)
36%
high (scores 6–9)
77%

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ECG
The ECG should be ordered within 10 minutes of presentation
The presence of ST-segment elevation in
≥2 contiguous leads is an indication for urgent reperfusion(1)
(1) Makki N, Brennan TM, Girotra S. Acute coronary syndrome. J Intensive Care Med. 2015; 30:186–
200.
Transient ST-segment elevation, ST-segment depression, and/
or T-wave inversions should raise clinical suspicion of
ACS

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Obtaining rapid echocardiography is imperative and should be
performed as soon as possible to assess for LV or right ventricular (RV)
dysfunction,valvular pathology,and to exclude AMI-related mechanical
complication (papillary muscle rupture, ventricular wall rupture,and
ventricular septal defect ) or cardiac tamponade.

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Cardiac catheterization is both the definitive diagnostic investigation
and guides therapeutic intervention in CS
complicating acute MI
Cardiac catheterization is typically preceded by several initial investigations and non-interventional management
strategies.
CS is a clinical diagnosis and no investigation should delay emergent cardiac catheterization.

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Rapid diagnosis with prompt initiation of pharmacological therapy to
maintain blood pressure and to maintain respiratory support along with a
reversal of underlying cause plays a vital role in the prognosis of patients
with cardiogenic shock
Ginwalla M,Tofovic DS, Current Status of Inotropes in Heart Failure. Heart failure clinics. 2018 Oct
Treatment

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Stabilization and Resuscitation Strategy
Intravenous Fluids
Fluid resuscitation strategy is a clinical challenge in the early
management of CS as it is often difficult to assess and can vary over
time
.
Jung C, Lauten A, Ferrari M. Microcirculation in cardiogenic shock: from scientific bystander to therapy target. Crit Care.

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lactated ringer solution greater than 200 ml per 15 to 30 minutes is
indicated in patients with no signs of fluid overload.
Patients are commonly diaphoretic, and relative hypovolemia may be present
in as many as 20% of patients with cardiogenic shock, so fluid boluses, titrated
to clinical endpoints of heart rate, urine output, and blood pressure, should be
considered as an initial measure unless frank pulmonary edema is present
Cardiogenic Shock
Cyrus Vahdatpour, MD; David Collins, MD; Sheldon Goldberg, MD, FACC

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Oxygenation and Ventilation
Oxygen goals vary depending on patient co morbidities, but in the acute
care setting blood oxygen saturations of >90% are acceptable
Cardiogenic Shock
Cyrus Vahdatpour, MD; David Collins, MD; Sheldon Goldberg, MD, FACC

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Non-invasive positive pressure ventilation, , improves respiratory failure,
increases oxygenation and pH, and decreases the partial
pressure of carbon dioxide (pCO2) and work of breathing.
Although a large randomized trial had neutral results, meta-analyses suggest it may improve dyspnoea and reduce the need for
intubation and mortality, compared with traditional oxygen
Weng CL, Zhao YT, Liu QH, Fu CJ, Sun F, Ma YL, Chen YW, He QY. Metaanalysis: noninvasive ventilation in acute cardiogenic pulmonary
edema. Ann Intern Med 2010;152:590600.

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When non-invasive forms of oxygenation and ventilation
are inadequate, invasive ventilation is required.
Low tidal volumes (5–7 mL/kg of ideal body weight) optimize blood flow
between the pulmonary and parenchymal vasculature. The decreased
resistance in the pulmonary circuit lowers stress on the RV, compared
withhigher tidal volumes.
Therefore, a low tidal volume strategy is
recommended when mechanically ventilating patients in CS.(1)
(1) Pulmonary vascular and right ventricular dysfunction in adult critical care: current and emerging options for management: a
systematic literature review.

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The use of Vasopressor and inotropes in CS should be initiated in
patients with inadequate tissue perfusion and adequate volume

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Although the lowest dose needed to support organ perfusion
should be used as these agents can increase afterload and oxygen
demand for the failing myocardium

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Vasopressors should be titrated to a mean arterial pressure with a typical
goal of >65 mm Hg.

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For the European Society of Cardiology, Dobutamine is currently
the first-line inotropic agent in the presence of acute heart failure with
low systolic arterial blood pressure.
ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure 2021: the Task Force for the Diagnosis and
Treatment of Acute and Chronic Heart Failure 2021

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For the American Heart Association, Dobutamine and Dopamine are
both cited as inotropic agents
ACCF/AHA guideline for the management of heart failure: executive summary: a report of the American College of
Cardiology Foundation/American Heart Association Task Force on practice guidelines

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In very hypotensive patients, initially a vasopressor agent (dopamine or
noradrenaline) was used because the action of peripheral vasodilation of
dobutamine may worsen coronary perfusion
Fang X, Wang K, Han D, He X, Wei J, Zhao L, Imam MU. et al. Dietary magnesium intake and the risk of cardiovascular
disease, type 2 diabetes, and all-cause mortality: a dose-response meta-analysis of prospective cohort studies

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However, the use of dopamine is still a matter of debate.
In a study comparing dopamine and norepinephrine as the first-line vasopressor agent in the
treatment of shock, the use of dopamine was associated with a greater number of cardiac
arrhythmias.
In addition, in a predefined subgroup analysis, the authors reported that the use of
dopamine was associated with an increased risk of death in the subgroup of 280
patients with cardiogenic shock.
. Comparison of dopamine and norepinephrine in the treatment of shock. The New England journal of medicine

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The New England journal of medicine

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There was no significant between-group difference in the rate of death at 28 days (52.5% in the
dopamine group and 48.5% in the norepinephrine group

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the rate of death at 28 days was significantly higher among patients with
cardiogenic shock who were treated with dopamine than among those with
cardiogenic shock who were treated with norepinephrine (280 were in cardiogenic shock
(135 in the dopamine group and 145 in the norepinephrine group),

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Epinephrine was compared to the combination of norepinephrine
and dobutamine in patients -resistant cardiogenic shock—for example,
with a cardiac index of less than 2.2 L/min/m2 and
MAP of less than 60 mm Hg.
Epinephrine or norepinephrine-dobutamine
were titrated to obtain a MAP of greater than 65 mm Hg.
Epinephrine infusion was as effective as the combination of norepinephrine
and dobutamine to improve cardiac index and oxygen-derived parameters.
Nevertheless, epinephrine infusion induced arrhythmia,
increased blood lactate level, and impaired splanchnic circulation
Comparison of norepinephrine-dobutamine to epinephrine for hemodynamics, lactate metabolism, and organ function variables
in cardiogenic shock

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Vasopressin has less pulmonary vasoconstriction than norepinephrine; and
may be more beneficial as a first-line vasopressor in patients
with CS with acute RVF
Gordon AC, Wang N, Walley KR, Ashby D, Russell JA. The cardiopulmonary effects of vasopressin compared with norepinephrine in septic
shock. Chest. 2012; 142:593–605.

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Inhibitors of phosphodiesterase (milrinone) have inotropic effect similar to
dobutamine, but with associated vasodilator effect.

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Short-term Intravenous Milrinone for Acute Exacerbation of Chronic
Heart FailureA Randomized Controlled Trial
Michael S. Cuffe, MD; Robert M. Califf, MD; Kirkwood F. Adams, Jr, MD;
Participants A total of 951 patients
admitted with an exacerbation of systolic
heart failure not requiring intravenous
inotropic support (mean age, 65 years;
92% with baseline New York Heart
Association class III or IV; mean left
ventricular ejection fraction, 23%)

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Routine use of IV milrinone for decompensated heart failure was not
associated with a reduction in hospital-based resource utilization at 60 days
and was associated with increased risk of hypotension and atrial arrhythmias.

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(3) patients with long-term beta-blocker use, in whom short-term
intravenous milrinone may even be preferred to dobutamine.
Thus, the use of these agents is limited to few categories of
patients
(1) patients with advanced heart failure awaiting transplantation in whom
intravenous milrinone could be better tolerated than dobutamine and its use
may allow the continuation of beta-blocker therapy controlling arrhythmias
or myocardial ischemia
(2) patients with acute decompensation of chronic heart
failure unable to achieve stabilization with the standard treatment

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NO synthase inhibitors have been proposed to be used in patients
with cardiogenic shock
Topalian S, Ginsberg F, Parrillo JE. Cardiogenic shock. Critical care medicine 2008;36:S66-74.
.
Tilarginine was unable to improve the survival rate in patients with cardiogenic
shock at 3 months in comparison with placebo.
Investigators T, Alexander JH, Reynolds HR, et al. Effect of tilarginine acetate in patients with acute myocardial infarction and
cardiogenic shock: the TRIUMPH randomized controlled trial. JAMA
Tilarginine is a nonselective NO synthase inhibitor developed for
treating acute heart failure
These negative results have interrupted the clinical development of this
new drug.

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Following the initial stabilization and restoration of adequate blood
pressure, tissue perfusion should be assessed. If tissue perfusion is
adequate but significant pulmonary congestion remains, diuretics may
be employed.

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No difference in the primary efficacy outcome of patients’ symptoms global
assessment was shown with a high-dose regimen, compared with a low-
dose regimen,
308 patients with acute decompensated heart failure to receive furosemide administered intravenously by means of either a
bolus every 12 hours or continuous infusion and at either a low dose (equivalent to the patient’s previous oral dose) or a high
dose (2.5 times the previous oral dose).

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Always remembering that excessive diuresis can result in severe
intravascular depletion, maintaining hypotension, hypoperfusion, infarct
extension, and ischemia, and adding dysfunction to the already
compromised left ventricle.
Stevenson LW, Pagani FD, Young JB, Jessup M, Miller L, Kormos RL. et al. Interagency registry of mechanically assisted circulatory
support. J Heart Lung Transplant. 2009;28(6):535–541.

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A satisfactory diuretic response can be defined as a urine sodium
content >50_70 mEq/L at 2 h and/or by a urine output >100 -150mL/h
during the first 6 h.

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Dilate venous and arterial vessels leading to a reduction in venous return
to the heart, less congestion, lower afterload,
increased stroke volume and consequent relief of symptoms
Vasodilators
Intravenous vasodilators may be considered to relieve AHF symptoms
when SBP is >110 mmHg.
especially those of arterial and venous action, such as sodium nitroprusside
2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

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Because of their mechanisms of action, i.v. vasodilators may be more
effective than diuretics in those patients whose acute pulmonary oedema
is caused by increased afterload and fluid redistribution to the lungs in
the absence or with minimal fluid accumulation
2021 ESC Guidelines for the diagnosis and treatment of acute and chronic heart failure

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However, two recent randomized trials comparing usual care with early
intensive and sustained vasodilation failed to show a beneficial effect of
i.v. vasodilators vs. high-dose diuretics

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Conclusions
Among patients with AHF, a strategy of early intensive and sustained
vasodilation, compared with usual care, did not significantly
improve a composite outcome of all-cause mortality
and AHF re hospitalization at 180 days

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.
Treatment: Dobutamine or vasoconstrictor therapy, combined with
mechanical cardiac support.
Profile: High PAWP /Low CO/High SVR /Low BP

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Treatment: Vasodilator therapy, if tolerated, or inodilator therapy with
dobutamine, milrinone. Add diuretic therapy
with furosemide for volume overload, or for a persistent PAWP
above 20 mm Hg.
Profile: High PAWP /Low CO /High SVR /Normal BP

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Management: Vasodilator therapy with nitroglycerin, nitroprusside, or
nesiritide, followed by diuretic therapy with furosemide if
there is evidence of volume overload, or if the PAWP remains
above 20 mm Hg despite vasodilator therapy
Profile: High PAWP /Low CO /High SVR /High BP.

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Continuous Renal Replacement Therapy
Acute kidney injury occurs in 13% to 28% in patients with CS,
and 20% will require continuous renal replacement therapy.
Adler C, Reuter H, Seck C, Hellmich M, Zobel C. Fluid therapy and acute kidney injury in cardiogenic shock after cardiac
arrest. Resuscitation

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Reperfusion Therapy
Although fibrinolytic therapy reduces the likelihood of the subsequent
development of shock after the initial presentation, it is clearly less
effective in patients with cardiogenic shock than in those without (1).
and has not been shown to reduce mortality in patients with established
cardiogenic shock.(2)
(2) GUSTO Investigators. An international randomized trial comparing four thrombolytic strategies for acute myocardial infarction. N Engl J
Med 1993;329:673-82.
(1) Becker RC. Hemodynamic, mechanical, and metabolic determinants of thrombolytic efficacy: a theoretic framework for assessing the limitations
of thrombolysis in patients with cardiogenic shock. Am Heart J 1993;125:919-29

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Although fibrinolytic therapy
reduces the likelihood of the
subsequent development of shock
after the initial presentation, it is
clearly less effective in patients with
cardiogenic shock than in those
without (1). and has not been
shown to reduce mortality in
patients with established
cardiogenic shock.(2)

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To date, emergency percutaneous revascularization is the only
intervention that has been shown to reduce mortality rates
consistently in patients with cardiogenic shock
(1) Berger PB, Holmes DR, Jr., Stebbins AL, Bates ER, Califf RM, Topol EJ. Impact of an aggressive invasive catheterization and
revascularization strategy on mortality in patients with cardiogenic shock in the Global Utilization of Streptokinase and Tissue Plasminogen
Activator for Occluded Coronary Arteries (GUSTO-I) trial. An observational study. Circulation 1997;96: 122-7.
2) Rogers WJ, Canto JG, Lambrew CT, et al. Temporal trends in the treatment of over 1.5 million patients with myocardial infarction in the US
from 1990 through 1999: the National Registry of Myocardial Infarction 1, 2 and 3. J Am Coll Cardiol 2000;36:2056-63.

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CONCLUSIONS
In patients with cardiogenic shock,
emergency revascularization did not
significantly reduce overall mortality at
30 days. However, after six months
there was a significant survival benefit.
Early revascularization should be
strongly considered for patients with
acute myocardial infarction complicated
by cardiogenic shock.

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Mechanical Support in Cardiogenic Shock

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there are registry data indicating that early MCS device use is associated
with improved survival rates.
Basir MB, Schreiber TL, Grines CL, Dixon SR, Moses JW, Maini BS, Khandelwal AK, Ohman EM, O'Neill WW. Effect of early
initiation of mechanical circulatory support on survival in cardiogenic shock. Am J Cardiol. 2017;

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Effect of Early Initiation of Mechanical Circulatory Support on Survival
in Cardiogenic Shock
Mir B. Basir, DO, Theodore L. Schreiber, MD, Cindy L. Grines, MD, Simon F. Dixon, MD, Jeffrey W. Moses, MD, Brijeshwar S. Maini, MD,
Akshay K. Khandelwal, MD, E. Magnus Ohman, MD, William W. O’Neill, MD
287 consecutive unselected patients presenting with AMICS who
underwent percutaneous coronary intervention (PCI) were included in
this analysis.
All patients were supported with either the Impella 2.5 or Impella CP.
Mean patient age was 66±12.5 years, 76% were male, mean left
ventricular ejection fraction was 25 ±12 %.
Prior to receiving MCS, 80% of patients required inotropes or
vasopressors and 40% were supported with intraaortic
balloon pump. 9% of patients were under active cardiopulmonary
resuscitation at the time of MCS implantation.

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In a multivariate analysis early implantation of a MCS device prior to PCI and prior to requiring
inotropes and vasopressors was associated with increased survival. Survival was 66% when MCS
was initiated <1.25 hours from shock onset, 37% when initiated within 1.25-4.25 hours, and 26%
when initiated after 4.25 hours .Survival to discharge was 44%..
Conclusion:
MCS implantation
early after shock
onset, before initiation
of inotropes or
vasopressors and
prior
to PCI, is
independently
associated with
improved survival in
patients presenting
with AMICS

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The most important finding in our analysis is
the temporal relationship of early use of
percutaneous mechanical circulatory support
and improved clinical outcomes. Survival was
found to be significantly improved if MCS
implantation was initiated prior to PCI

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Intra-Aortic Balloon Counterpulsation
IABP
is believed to decrease myocardial oxygen consumption, increase
coronary artery perfusion, decrease afterload and modestly increase
cardiac output (0.8–1 L/min)

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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
Holger Thiele, Uwe Zeymer, Franz-Josef Neumann, Miroslaw Ferenc, Hans-Georg Olbrich, Jِ rg Hausleiter, Antoinette de Waha, Gert Richardt, Marcus Hennersdorf, Klaus
Empen, Georg Fuernau, Steff en Desch, Ingo Eitel, Rainer Hambrecht, Bernward Lauer, Michael Bِ hm, Henning Ebelt, Steff en Schneider, Karl Werdan*, Gerhard Schuler*, on
behalf of the Intraaortic Balloon Pump in cardiogenic shock II (IABP-SHOCK II) trial investigators†
Between June 16, 2009, and March 3, 2012, 600 patients
were assigned to IABP (n=301) or control (n=299). Of
595 patients completing 12 month follow-up, 155 (52%) of
299 patients in the IABP group and 152 (51%) of 296
patients
There were no signifi cant diff erences
in reinfarction , recurrent revascularisation or stroke .
For survivors, quality-of-life measures including
mobility, self-care, usual activities, pain or discomfort,
and anxiety or depression did not diff er signifi cantly
between study groups

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American and European guidelines recently
downgraded IABP use for cardiogenic shock from a
class I to a class I1a and IIb recommendation
In conclusion, this randomised, multicentre
trial showed that IABP support did not reduce
12 month mortality in patients with cardiogenic
shock complicating myocardial infarction
undergoing early revascularisation
For patients in whom mechanical complications (eg, acute mitral regurgitation or rupture of the ventricular septum) are not
present and for whom revascularization is planned, we recommend not routinely placing an intraaortic balloon pump (Grade
1B)

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LV-to-aorta devices,
The Impella devices are axial flow pumps that are advanced from the common
femoral artery and passed retrograde across the aortic valve into the LV and
eject blood into the ascending aorta. cardiac output of 2.5 to 4 L/min

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The Detroit Cardiogenic Shock Initiative proposed the use of
standardized protocols with emphasis on early Impella insertion before PCI.
The Detroit Cardiogenic Shock Initiative Pilot Study reported 76% survival to
discharge with this approach
Feasibility of early mechanical circulatory support in acute myocardial infarction complicated by cardiogenic shock: the Detroit cardiogenic
shock initiative

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ECMO has been used in 13 000 patients and its rate of survival-to-
discharge is 39% when used in cardiac support
Paden ML, Conrad SA, Rycus PT, Thiagarajan RR; ELSO Registry . Extracorporeal life support
organization registry report 2012. ASAIO J. 2013; 59:202–210.
ECMO
The absence of large randomized controlled trials of ECMO in patients
with CS consigns its use to refractory cases as a bridging therapy to
LVAD or emergent heart transplantation
Khan MH, Corbett BJ, Hollenberg SM. Mechanical circulatory support in acute cardiogenic shock