Septic Cardiomyopathy (SCM)

Definition

Septic cardiomyopathy is a reversible myocardial dysfunction occurring in patients with sepsis or septic shock, characterized by global (biventricular) systolic and/or diastolic dysfunction, ventricular dilatation, and reduced myocardial contractility, not explained by coronary artery disease, and typically resolving within 7–10 days in survivors.

Key hallmark:
Reversible myocardial depression in sepsis


Epidemiology

  • Occurs in 30–60% of patients with septic shock
  • Associated with:
    • Higher vasopressor requirements
    • Prolonged ICU stay
    • Increased mortality (especially when persistent or RV involved)


Historical Perspective 

  • First described by Parker et al., 1984
  • Demonstrated:
    • ↓ Ejection fraction
    • ↑ LV end-diastolic volume
    • Reversibility in survivors


Pathophysiology 

Septic cardiomyopathy is not due to ischemia, but due to cellular, metabolic, and inflammatory myocardial stunning.

1. Cytokine-Mediated Myocardial Depression

  • TNF-α
  • IL-1β
  • IL-6
    → Direct negative inotropic effect

2. Nitric Oxide (NO) Excess

  • iNOS upregulation → ↑ NO
  • Causes:
    • ↓ Myofilament calcium sensitivity
    • Mitochondrial dysfunction
    • Vasoplegia + myocardial depression

3. Mitochondrial Dysfunction

  • Impaired oxidative phosphorylation
  • ↓ ATP generation
  • “Cytopathic hypoxia” (oxygen present but unusable)

4. Calcium Handling Abnormalities

  • Impaired sarcoplasmic reticulum Ca²⁺ cycling
  • ↓ Excitation–contraction coupling

5. Autonomic Dysregulation

  • ↓ β-adrenergic receptor density
  • Desensitization to catecholamines
  • Explains poor response to inotropes

6. Microcirculatory Dysfunction

  • Endothelial injury
  • Capillary shunting
  • Patchy myocardial hypoperfusion

7. Apoptosis & Myocardial Edema

  • Increased cardiomyocyte apoptosis
  • Interstitial edema → diastolic dysfunction


Hemodynamic Characteristics

Parameter

Septic Cardiomyopathy

Cardiac output

Normal / ↓

SVR

↓↓↓ (septic vasodilation)

LVEDV

↑ (ventricular dilatation)

EF

↓

Filling pressures

Normal / low

Response to fluids

Limited

Response to inotropes

Variable / reduced


Left vs Right Ventricular Dysfunction

Left Ventricular Dysfunction

  • Most common
  • Global hypokinesia
  • Dilated LV
  • Reduced EF

Right Ventricular Dysfunction (Poor Prognosis)

  • Due to:
    • Sepsis-induced pulmonary vasoconstriction
    • ARDS
    • Mechanical ventilation (high PEEP)
  • Leads to:
    • Reduced LV preload
    • Hypotension refractory to vasopressors


Diastolic Dysfunction (Often Missed)

  • Common even when EF preserved
  • Caused by:
    • Myocardial edema
    • Fibrosis
  • Strong predictor of mortality


Clinical Features

  • Persistent hypotension despite fluids
  • High vasopressor requirement
  • Poor lactate clearance
  • Low cardiac output state in late sepsis
  • Signs overlap with septic shock → echo is essential


Diagnosis

No Single Diagnostic Test 

Diagnosis is clinical + echocardiographic.


Echocardiography 

Typical Findings

  • Global hypokinesia (not regional)
  • ↓ LVEF
  • LV dilatation
  • RV dysfunction
  • Diastolic dysfunction (E/e′ ↑)

Important exam point:
Regional wall motion abnormality → think ACS, not septic cardiomyopathy


Biomarkers

Marker

Interpretation

Troponin

Often elevated (membrane leak, not MI)

BNP / NT-proBNP

Elevated (stretch, volume overload)

Lactate

Reflects severity, not specific


Hemodynamic Monitoring

  • PAC / Echo / Pulse contour analysis may show:
    • Low CI
    • Normal or low PAOP
    • Reduced stroke volume


Differential Diagnosis

Condition

Key Difference

Acute MI

Regional wall motion abnormality

Stress (Takotsubo) cardiomyopathy

Apical ballooning

Viral myocarditis

Persistent dysfunction

Hypovolemia

Improves with fluids

Pulmonary embolism

Acute RV strain, echo signs


Management 

No specific therapy reverses SCM — management is supportive


1. Source Control

  • Early antibiotics
  • Drain abscess, remove infected devices


2. Fluid Management

  • Avoid both under- and over-resuscitation
  • Dynamic indices preferred
  • Overloading worsens myocardial edema


3. Vasopressors (First Line)

  • Norepinephrine = drug of choice
  • Maintain MAP ≥ 65 mmHg


4. Inotropes

Used when:

  • Persistent hypoperfusion
  • Low cardiac output on echo

Options

Drug

Comment

Dobutamine

First-line inotrope

Epinephrine

Inotrope + vasopressor

Milrinone

Rarely used (hypotension risk)

SSC: Add dobutamine if myocardial dysfunction with hypoperfusion persists


5. Vasopressin

  • Reduces NE requirement
  • No direct inotropic effect


6. Mechanical Ventilation Strategy

  • Avoid excessive PEEP (RV strain)
  • Lung protective ventilation


7. Steroids

  • Hydrocortisone may:
    • Improve catecholamine responsiveness
    • Reduce vasopressor requirement
  • No direct myocardial recovery effect


8. Mechanical Circulatory Support (Rare)

  • VA-ECMO:
    • Refractory septic cardiogenic shock
    • Selected young patients
    • Controversial, resource-intensive


Prognosis

Key Points

  • Reversible in survivors
  • Recovery usually within 7–10 days
  • Worse prognosis with:
    • Persistent LV dysfunction
    • RV dysfunction
    • Diastolic dysfunction
    • High troponin levels


Key Exam Points

  • Septic cardiomyopathy is reversible
  • Caused by cytokines, NO, mitochondrial dysfunction
  • Global, not regional, hypokinesia
  • EF ↓ but LV dilates → stroke volume may be preserved early
  • Echo is diagnostic
  • Treat sepsis, not heart failure per se