CARDIAC DYSFUNCTION IN SEPSIS

Dr CM ShevlinNovember 2013

PROBLEMS• Definition

• Systolic dysfunction? Diastolic? Left?

Right?

• Diagnosis

• CVP? PAC? Echo - TOE? TTE?

• Prognosis

• Frequency

INTRODUCTION• Understanding has evolved over decades -

historically, cardiovascular changes are

hallmark of septic shock

• Traditionally: “warm shock” vs “cold shock”:

different entities vs stages of same process

• Under conditions of adequate volume

resuscitation reduced SVR increased cardiac

index, and obscures myocardial dysfunction

Parker MM, Shelhamer JH, Bacharach SL, et al: Profound but reversible myocardial depression in patients with septic shock. Ann Intern Med

1984; 100:483–490

Parker MM, McCarthy KE, Ognibene FP, et al: Right ventricular dysfunction and dilatation,

similar to left ventricular changes, characterize the cardiac depression of septic shock in

humans. Chest 1990; 97:126–131

Calvin JE, Driedger AA, Sibbald WJ. An assessment of myocardial function in human

sepsis utilizing ECG gated cardiac scintigraphy. Chest. 1981; 80: 579–586

HOW WAS DYSFUNCTION DIAGNOSED?

• Concept of depressed myocardial function despite increased CO emerged from studies utilising ventriculography and thermodilution (Parker et al)

• Showed that LV dysfunction persisted despite a hyperdynamic state and increased CI

• Able to demonstrate significant depression of myocardial function - impaired intrinsic myocardial performance, decreased LVSWI

• Changes reflected in right heart

WHAT ELSE?• Survivors more likely to have decreased ejection

fractions with increased EDVI

• Non-survivors more likely to have preserved cardiac volumes with less significant decreases in ejection fraction

• Reversible changes 7-10 days

• Diastolic dysfunction & right heart dysfunction not clear

THE RIGHT HEART• Behaves differently:

• LV afterload is decreased due to low SVR

• RV afterload increased due to increased PVR

• Number of studies have documented RV systolic dysfunction independent of pulmonary vascular resistance

• General consensus that RV dysfunction parallels LV dysfunction in sepsis

AETIOLOGY

• Multiple circulating factors suggested as culprits

• Direct inhibitory effects on myocyte contractility

• cytokines (TNF-alpha, IL1-B)

• lysozyme c

• endothelin 1

• Nitric oxide: complex role

• Mitochondrial dysfunction and apoptosis

• Adrenergic receptor hypo-responsiveness

MECHANISMS• Circulatory and microvascular changes

• volume depletion and vasodilatation

• Capillary leakage and microcirculatory changes

• Autonomic dysregulation

• Metabolic changes

• Mitochondrial dysfunction and cell death

Circulation.2007; 116: 793-802

IS THERE A BENEFIT TO MYOCARDIAL DEPRESSION?

• Adaptive response? (Rudiger A., Singer M. 2007)

• Reduces energy expenditure in a situation when energy generation limited

• Prevents activation of cell death pathways allowing for recovery

• Pulido et al (2012) - Myocardial dysfunction - no effect mortality 30 day or long term

PROGNOSIS OF MYOCARDIAL DYSFUNCTION

• Dobutamine stress test (Kumar, Parillo et al, 2007)

• Biomarkers:

• Elevation Troponin T and I correlate with presence left ventricular systolic dysfunction

• Increased levels of BNP also correlate with severe sepsis and septic shock

• So far…not clinically useful

CONCLUSION• Cardiac dysfunction in sepsis characterised by:

• decreased contractility

• impaired ventricular response to fluid therapy

• ?ventricular dilatation

• Complex pathophysiology: multiple circulating factors

• Management: haemodynamic support and treatment of infectious focus…& modulation of host response