Acute cardiac care & resuscitation
Pathophysiologic Vasodilation in Cardiogenic Shock and Its Impact on Mortality
Authors' conclusion
Pathophysiologic vasodilation is prevalent in CS and independently associated with an increased risk of death. CS vasodilation can be identified by SVR <800 dynes•s•cm-5, high doses of pressors, or a blunted SVR response to pressors.
Study context
- Population
- Patients hospitalised at a cardiogenic shock (CS) referral centre with CS stages B to E, without concurrent sepsis or recent cardiac surgery
- Participants
- 713 patients
- Exposure
- Vasodilation vs none
- Outcome
- Death (multivariable-adjusted Cox models)
- Follow-up
- 14 days of CS onset
Methodological detailssingle-centre, CS referral centre, multivariable-adjusted Cox models
- Single-centre
- CS referral centre
- Multivariable-adjusted Cox models
Main finding
As reported in the abstract
Each 100-dynes•s•cm-5 decrease in systemic vascular resistance (SVR) below 800: 20% higher mortality, adjusted HR
1.23
P=0.004
Each 0.1-µg/kg per minute increase in norepinephrine equivalent dose: 15% higher mortality, adjusted HR
1.12
P<0.001
Blunted pressor response: nearly 2-fold mortality increase, adjusted HR
1.74
P=0.003
14-day mortality (all patients)
28%
Observational data: associations, not effects.
Further findings
Prevalence and haemodynamic profile
- Vasodilated
- 38%
- Median SVR, dynes•s•cm-5 (IQR 870-1652)
- 1308
- Median norepinephrine equivalent, µg/kg per minute (IQR 0-0.2)
- 0.11
- Blunted pressor response
- 28%
Original publication
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