Septic cardiomyopathy is a condition characterized by myocardial dysfunction occurring in the context of sepsis. It is a significant complication that can lead to increased morbidity and mortality in critically ill patients. Understanding the pathophysiology, clinical implications, and management of septic cardiomyopathy is essential for improving patient outcomes.
Primary myocardial cellular dysfunction in sepsis can manifest in multiple ways, including left and/or right ventricular impairment during systole or diastole, and with or without inadequate cardiac output (CO) and oxygen delivery.
Endothelial and inducible nitric oxide (NO)- synthase plays important roles in myocardial dysfunction. NO can alter preload and afterload, promote down-regulation of beta-adrenergic receptors, reduce response of myofilaments to calcium (Ca 2 + ), and increase mitochondrial permeability.
Mitochondrial dysfunction is multifactorial in sepsis, and can manifest with ultrastructural abnormalities. Secondary to impairment of the antioxidant capacity of mitochondria, oxidative stress interferes with signalling pathways, and also increases mitochondrial calcium and free fatty acid levels. Calcium dysregulation can also contribute to myocardial dysfunction.
Sympathetic hyperactivation in sepsis can lead to myocardial dysfunction through tachycardia, shortened diastole, and left ventricle (LV) filling. Beta-adrenergic receptor down-regulation could explain refractory response to catecholamines.
Finally, septic endothelial dysfunction, through glycocalyx degradation, can lead to microcirculatory hypoperfusion and capillary leaks, resulting in myocardial edema.
Although there is no consensus clear definition of SCM, most review articles and expert opinions agree on a few fundamental features of this unique form of cardiac dysfunction.
These features include acute uni- or bi-ventricular systolic or diastolic dysfunction with reduced contractility not due to coronary disease.
The first characteristic of septic cardiomyopathy is that it is acute and reversible, providing the patient recovers.
The second characteristic, is that depressed LV systolic function is associated with normal or low LV filling pressure, unlike the “classic” pattern of cardiogenic shock where LV pressures are elevated. This probably occurs due to an increase in the left ventricular compliance. Parker et al. Reported that end-diastolic and systolic ventricular volumes were increased but with normal or elevated stroke volume and cardiac index in septic shock survivors. In this study, although the number of patients is less, these results suggest that decreased ejection fraction may be caused by ventricular dilatation and not by decreased stroke volume.
The incidence of LV and/or RV dysfunction varies depending on evaluation methods and diagnostic criteria. This heterogeneity of incidence depends also on the timing of echocardiographic evaluation, and timing factors include evaluation before or after resuscitation, correction for preload and afterload, within the first 24 h, or within 72 h.
In a study by Boissier et al., LV dysfunction was diagnosed in 22% of patients assessed using echocardiography within 24 h, but also in an additional 9.8% of patients assessed between 25 h and 72 h. Vieillard-Baron et al. showed an incidence of LV dysfunction in 18% of patients assessed within 6 h, and 60% within 72 h. Therefore, as most echo parameters are dependent on loading conditions, the echo assessment should be repeated at multiple time points.
Sepsis also triggers takotsubo cardiomyopathy, also known as stress cardiomyopathy, apical ballooning syndrome, or broken-heart syndrome, which is different from sepsis-induced cardiomyopathy. Takotsubo cardiomyopathy typically occurs when the contractile function of the mid-to-apical segments of the left ventricle is depressed and there is hyperkinesis of basal walls, producing a balloon-like appearance of the distal ventricle.
Several tools can be used to evaluate LV ejection fraction (LVEF). Echocardiography is the most useful technique for bedside evaluation, but mag- netic resonance imaging (MRI) or ventriculography can also be used. Intrinsic myocardial contractility can be accurately measured by pressure-volume loop analysis using multicrystal sonomicrometry, a conductance catheter, MRI, or radionuclide techniques, but these techniques cannot be used during routine bedside care, particularly in critically ill patients.
Echocardiographic findings:
The first studies assessing SCM reported a lower mortality rate in patients with decreased LVEF and cardiac index. Increased LVEF and hyperkinesia might be associated with a higher mortality rate because this may reflect persistent pro- found vasoplegia.
Some studies have shown that isolated RV dysfunction was associated with worse survival. A recent database study suggested that echocardiographic assessment of myocardial function influenced hemodynamic management of patients with sepsis, which resulted in earlier discontinuation of vasopressor administration, and decreased 28-day mortality.
The Surviving Sepsis Campaign 2016–2018 strongly recommends norepinephrine as the first line vasopressor for treatment of septic shock, although evidence for this treatment is based on moderate quality evidence. Dobutamine can be added in cases with persistent hypoperfusion despite adequate fluid loading and administration of vasopressors, although this is not strongly recommended, and is based on low quality evidence.
Alterations in myocardial adrenergic responsiveness have been reported in patients with septic shock. However, catecholamines can cause many adverse effects, including cardiotoxicity, which has prompted additional scrutiny on whether use of catecholamine administration should be limited. Levosimendan is a calcium sensitizer that acts in a catecholamine-independent manner to minimize effects on oxygen demand, arrhythmias, and catecholamine resistance resulting from sepsis. Preliminary trials of levosimendan reported reduced mortality in patients with septic shock patients, but no benefit was found in a subsequent larger study. Therefore, the Surviving Sepsis campaign does not recommend use of levosimendan for treatment of septic shock owing to little evidence for therapeu-tic value, poor safety profile, cost, and limited availability of the drug.
LV diastolic dysfunction – Tachycardia and tachyarrhythmias in septic shock can worsen LV systolic and diastolic dysfunctions, and some studies have evaluated the use of short- acting beta-blockers, such as esmolol or landiolol to treat tachyarrhythmias with the goal of improving the prognoses of patients with septic shock.
Ivabradine, a selective inhibitor of If channels in the sinoatrial node, can lower heart rate without inducing negative inotropy, which is associated with beta blockers.
Septic myocardial dysfunction is common in septic shock, but definitions vary (LV and/or RV, systolic and/or diastolic dysfunction). Further studies are needed to improve our under- standing of the pathophysiology of SCM, to discriminate adaptive mechanisms to intrinsic myocardial decrease leading to hypoperfusion and organ failure, and to evaluate treatments.
Dr Vetriselvan P, MBBS, MD, DM Associate Consultant Critical Care Consultant Kauvery Hospital, Chennai
Dr Ramapriya S, MBBS, MD, DrNB Critical Care Postgraduate Kauvery Hospital, Chennai
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