Why do patients with sepsis and septic shock develop bradycardia?

Bradycardia in Sepsis and Septic Shock

Bradycardia in sepsis and septic shock is associated with lower mortality compared to tachycardia, even after adjustment for confounding factors. 1

Mechanisms of Bradycardia in Sepsis

• Sepsis-induced cardiac dysfunction is a common manifestation characterized by decreased contractility, impaired ventricular response to fluid therapy, and in some patients, ventricular dilatation 2
• Myocardial depression in sepsis is caused by circulating depressant factors rather than myocardial hypoperfusion 3
• Key mediators of cardiac dysfunction include:
  • Inflammatory cytokines (TNF-alpha, IL-1beta) that directly inhibit myocyte contractility 2
  • Nitric oxide, which has both deleterious and positive effects on myocardial function 2
  • Mitochondrial dysfunction and apoptosis contributing to cardiac depression 2
• Endothelial activation and coagulation system induction also play significant roles in sepsis pathophysiology 4

Clinical Significance of Bradycardia in Sepsis

• Relative bradycardia (heart rate <80 beats/min) occurs in approximately 44% of patients with septic shock requiring vasopressors 1
• Patients with relative bradycardia tend to have:
  • Lower 28-day mortality (21% vs 34% in tachycardic patients) 1
  • Slightly lower illness severity scores (SOFA and APACHE II) 1
• The association between relative bradycardia and improved survival persists even after adjustment for confounding factors 1

Management Considerations for Septic Shock with Bradycardia

• Dopamine can be considered as an alternative vasopressor to norepinephrine in patients with absolute or relative bradycardia 5, 6
• When selecting vasopressors for septic patients with bradycardia:
  • Norepinephrine remains the first-line vasopressor for septic shock 5, 7, 6
  • Target a mean arterial pressure (MAP) of 65 mmHg initially 5
  • Consider dopamine only in highly selected patients with low risk of tachyarrhythmias and bradycardia 5
• Fluid resuscitation should precede or accompany vasopressor therapy 5, 6
• Arterial catheter placement is recommended as soon as practical for all patients requiring vasopressors 5, 6

Monitoring and Supportive Care

• Continuous monitoring of hemodynamic parameters is essential 5
• Clinical endpoints for monitoring should include:
  • Mean arterial pressure 5
  • Skin color and capillary refill 5
  • Mental status 5
  • Urinary output 5
  • Lactate clearance 5
• Ultrasound assessment can help determine fluid requirements and cardiac function 5

Pitfalls and Caveats

• While bradycardia in sepsis appears to be associated with better outcomes, this should not be artificially induced without further evidence 1
• Sepsis-induced cardiac dysfunction typically recovers within 7-10 days in survivors 3
• Patients with pre-existing coronary artery disease may experience regional myocardial ischemia during sepsis, which can contribute to bradycardia 4
• Monitoring for signs of inadequate tissue perfusion is crucial, regardless of heart rate 5