References
Vasodilatory shock: a review of pathophysiology and vasopressor therapy
Abstract
Vasodilatory shock is characterised by a global loss of vasomotor tone, leading to maldistribution of blood volume, low systemic arterial pressure and hypoperfusion. This syndrome can be caused by sepsis, anaphylaxis and a wide range of other aetiologies. This review article explores the pathophysiology of vasodilatory shock, including well-understood mechanisms and emerging avenues of future investigation. Options for vasopressor therapy are reviewed, including evidence from preclinical canine models, small animal clinical research, large human clinical trials and the Surviving Sepsis Campaign. Recommendations for rational vasopressor choice are extrapolated from this evidence. Future directions include the development of novel vasoactive agents, clinical data comparing the safety and effectiveness of vasopressors in small animals and the development of a veterinary-specific consensus statement guiding best practices for the treatment of vasodilatory shock.
Circulatory shock is a syndrome characterised by inadequate tissue perfusion leading to insufficient oxygen and nutrient supply for cellular function. Systemic consequences of circulatory shock include endothelial dysfunction, vasoplegia, multiple organ dysfunction syndrome and eventual death if left untreated. Circulatory shock has been classically divided into four categories, each defined by the type of pathology leading to inadequate perfusion (Silverstein and Hopper, 2022). These categories are:
Other subcategories such as hypoxic shock (decreased oxygen content in arterial blood) and metabolic shock (inability to use delivered oxygen) are independent of circulatory dysfunction.
Vasodilatory shock caused by sepsis is the most common form of shock among critically ill human patients (De Backer et al, 2010; Gitz Holler et al, 2019). Although similar data do not exist in veterinary medicine, it remains a common cause of morbidity and mortality in critically ill small animals in the authors’ experience. Besides sepsis, vasodilatory shock may be caused by non-in-fectious aetiologies leading to systemic inflammation (ie systemic inflammatory response syndrome) such as burn injuries, acute pancreatitis or trauma. Other causes include, but are not limited to, anaphylaxis, toxicoses (eg nitrogen or carbon monoxide), liver failure and glucocorticoid deficiency (Landry and Oliver, 2001; Narayan and Petersen, 2022). Persistent, severe shock of any cause can also result in pathological vasodilation.
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