CARDIOGENIC SHOCKA RAPID REVIEW

MUHAMMAD ABDELMONEIMFELLOW-ICU

OBJECTIVES

• Shock and cardiogenic shock definition• Pathophysiology • Etiology• Management

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”

Stages of shock

inciting event

Pre-Shock

Shock

End-organ dysfunction 

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

SimplyPump failure to the point of tissue hypo perfusion

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)

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

• 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

• 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

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

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

CLINICAL PRESENTATION

DIAGNOSIS

• Laboratory findings• ECG• Echocardiography• Hemodynamic monitoring• Coronary angiography

MANAGEMENT

• General Support Measures

• Antithrombotics• Blood sugar control• Treat hypoxemia• We should have a low threshold to institute ventilatory support

whether noninvasive or invasive

MANAGEMENT

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

• 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

• 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

• 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

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

Treatment of CS Due toMechanical 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

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

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)