This document provides an overview of cardiogenic shock, including its definition, pathophysiology, etiology, clinical presentation, diagnosis, and management. Cardiogenic shock is defined as inadequate tissue perfusion due to the heart's inability to pump an adequate amount of blood, despite adequate intravascular volume. It results from a severe reduction in cardiac output and stroke volume. The most common cause is severe left ventricular dysfunction following acute myocardial infarction, though right ventricular failure can also cause cardiogenic shock. Management involves general support measures, pharmacological therapy including inotropes and vasopressors, hemodynamic management, mechanical support such as IABP, and early reperfusion when possible. Early invasive management and avoidance of excessive fluids for right

1. CARDIOGENIC SHOCK
A RAPID REVIEW
MUHAMMAD ABDELMONEIM
FELLOW-ICU

3. OBJECTIVES
• Shock and cardiogenic shock definition
• Pathophysiology
• Etiology
• Management

4. Shock
• A significant reduction of systemic tissue perfusion, resulting in
decreased oxygen delivery to the tissues
• This creates an imbalance between oxygen delivery and oxygen
consumption
Rapid initial resuscitation (usefully driven by protocol) is fundamental for
improved outcome, since “time is tissue”

5. Stages of shock
incitingevent
Pre-Shock
Shock
End-organ dysfunction

6. Definition of Cardiogenic shock (CS)
• CS is a clinical condition of inadequate tissue (end-organ)
perfusion due to the inability of the heart to pump an adequate
amount of blood in the presence of adequate intravascular
volume
Simply
Pump failure to the point of tissue hypo perfusion

7. PATHOPHYSIOLOGY
• Systemic hypotension, which is present in most patients with
cardiogenic shock, is defined as a persistent systolic blood
pressure below 80 to 90 mmHg or a mean blood pressure 30
mmHg lower than the patient's baseline level
• In cardiogenic shock, hypotension results from a decrease in
stroke volume and a severe reduction in the cardiac index
(<1.8 L/ min per m2 without support or <2.0 to 2.2 L/min per
m2 with support)

8. PATHOPHYSIOLOGY
• The fall in blood pressure may in part be moderated by a marked
elevation in systemic vascular resistance (SVR)
• However, the combination of a low cardiac output and elevated
SVR may result in a marked reduction in tissue perfusion.
Not all patients fall into this hemodynamic profile

9. • Patients with confirmed cardiogenic shock developing within
36 hours of an acute MI, the mean left ventricular ejection
fraction on echocardiography was unexpectedly high at 31 %
• Furthermore, calculated systemic vascular resistance varied
widely and on average was not elevated despite vasopressor
use
• Thus, in some patients, post-MI shock is accompanied by
relative vasodilation rather than vasoconstriction
PATHOPHYSIOLOGY
SHOCK TRIAL

10. • The most likely explanation for vasodilation in the setting of
cardiogenic shock is the presence of a systemic inflammatory
state similar to that seen with sepsis
• Approximately half of all CS patients have small or normal LV
size, which represents failure of the adaptive mechanism of
acute dilation to maintain stroke volume in the early phase of MI
PATHOPHYSIOLOGY
SHOCK TRIAL

12. Etiology
• Severe dysfunction of the left ventricle (LV) is the most
common presentation of cardiogenic shock in the setting of
acute myocardial infarction
• The majority of patients have an acute ST elevation MI, but
cardiogenic shock also occurs in approximately 2.5 percent of
patients with a non-ST elevation MI

13. Etiology
• Severe right ventricular (RV) failure is a cause of, or a major
contributor to, cardiogenic shock in 5% of cases and is typically
seen with an inferior MI
Such patients do not develop pulmonary congestion unless there is
concurrent involvement of the LV

15. CLINICAL PRESENTATION

16. DIAGNOSIS
• Laboratory findings
• ECG
• Echocardiography
• Hemodynamic monitoring
• Coronary angiography

17. MANAGEMENT

18. • General Support Measures
• Antithrombotics
• Blood sugar control
• Treat hypoxemia
• We should have a low threshold to institute ventilatory support
whether noninvasive or invasive
MANAGEMENT

19. MANAGEMENT
• Pharmacological Treatment
• inotropic and vasopressor agents, which should be used in the
lowest possible doses
• Higher vasopressor doses are associated with poorer survival
• Inotropics has a central role , but it increase myocardial ATP
consumption such that short term hemodynamic improvement
occurs at the cost of increased oxygen demand when the heart is
already failing and supply is already limited

20. • Hemodynamic Management
• PA (Swan-Ganz) catheterization is frequently performed to
confirm the diagnosis of CS, to ensure that filling pressures are
adequate, and to guide changes in therapy
• There has been a decline in PA catheter use relating to
controversy sparked by a prospective observational study that
suggested that PA catheters were associated with poor
outcome
• No such association has been shown in CS
• Clinical assessment with echocardiography is a reasonable
alternative

21. • The American College of Cardiology/American Heart
Association (ACC/AHA) guidelines recommend norepinephrine
for more severe hypotension because of its high potency
• Although both dopamine and norepinephrine have inotropic
properties, dobutamine is often needed in addition
MANAGEMENT

22. • Mechanical Support: IABP
• Use of an IABP improves coronary and peripheral perfusion via
diastolic balloon inflation and augments LV performance via
systolic balloon deflation with an acute decrease in afterload
• Reperfusion
• The earlier the better
• Best benefit within 1st 3 Hrs
• But up to 48 Hrs post incident proved to have survival benefit
MANAGEMENT

23. Right Ventricle
• RV dysfunction may cause or contribute to CS.
• Predominant RV shock represents only 5% of cases of CS
complicating MI
• RV failure may limit LV filling via a decrease in CO, ventricular
interdependence, or both
• Patients with CS due to RV dysfunction have very high RV end-
diastolic pressure, often >20 mm Hg
• RV end-diastolic pressure of 10 to 15 mm Hg has been
associated with higher output than lower or higher pressures
• The common practice of aggressive fluid resuscitation for RV
dysfunction in shock may be misguided
MANAGEMENT

24. Treatment of CS Due to
Mechanical Complications
• It was previously thought that optimal timing involves a
balance of operating before the onset of multiorgan system
failure with delaying surgery to allow scarring of involved
myocardium for better stability of repair
• The unpredictability of rapid deterioration and death with VSR
and papillary muscle rupture makes early surgery necessary
even though there may be apparent hemodynamic
stabilization with IABP
MANAGEMENT

25. Management of Special Conditions
• LV outflow obstruction is critical in patients with hypotension,
because diuretics and inotropic agents exacerbate obstruction
• Treatment of CS with hypertrophic obstructive
cardiomyopathy includes volume resuscitation and β-blockade
• Pure α-agonists may also be used to increase afterload,
increasing cavity size and decreasing obstruction

26. To Conclude
• Recent evidence challenges the notion that patients with CS
are a “lost cause.” In fact, an early invasive approach can
increase short- and long-term survival and can result in
excellent quality of life.
• Rememnber
• Early perfusion
• Early surgery for mechanical complications even if apparantly
stable on IABP
• Low triger for MV
• Least needed vasopressors
• RV/CS >> traditional excessive fluids to preserve preload is not
optimal ( RVEDP 10 to 15 mmHg is optimal)