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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