Arterial Underfilling: Definition and Pathophysiology
Arterial underfilling, also termed "effective arterial underfilling," is a hemodynamic state where the arterial circulation is inadequately filled relative to its capacity, resulting from splanchnic and systemic vasodilation that triggers compensatory activation of vasoconstrictor and antidiuretic systems, despite often normal or even increased total blood volume. 1
Core Pathophysiologic Mechanism
The central event is splanchnic vasodilation leading to expansion of the vascular compartment, which creates a relative deficit in arterial filling pressure even when total plasma volume is normal or elevated 1, 2
This represents a mismatch between vascular capacity and blood volume - the arterial tree becomes "underfilled" not because blood volume is reduced, but because the vascular space has enlarged beyond the available volume to adequately fill it 2, 3
The underfilling is "effective" rather than absolute, meaning the body perceives inadequate arterial filling and responds accordingly, even though measured blood volume may be increased 1
Compensatory Response Cascade
Arterial underfilling triggers activation of vasoconstrictor systems including the renin-angiotensin-aldosterone system and sympathetic nervous system 1
Non-osmotic release of antidiuretic hormone (arginine vasopressin) occurs as part of the compensatory mechanism to restore effective arterial volume 1
These compensatory mechanisms lead to renal sodium and water retention, resulting in plasma volume expansion in an attempt to "refill" the underfilled arterial circulation 1, 2
Renal vasoconstriction develops, initially preserving sodium but eventually reducing renal blood flow sufficiently to impair glomerular filtration rate 1
Clinical Context in Cirrhosis
In compensated cirrhosis without ascites, compensatory mechanisms successfully maintain blood volume despite vascular underfilling, preventing ascites formation 2
In decompensated cirrhosis, the combination of maximal arterial vasodilation, reduced oncotic pressure, and severe portal hypertension overwhelms compensatory mechanisms, leading to ascites formation 2
Central blood volume is significantly reduced in cirrhosis (21 ml/kg versus 27 ml/kg in controls), with the lowest values occurring in patients with gross ascites and reduced systemic vascular resistance 3
The reduction in central blood volume represents 25% versus 33% of total blood volume in cirrhotic patients compared to controls, indicating blood sequestration away from the central circulation 3
Key Distinguishing Features
Arterial underfilling differs from true hypovolemia - total blood volume is often normal or increased, but the distribution is abnormal with inadequate central arterial filling 2, 3
The underfilling is inversely correlated with hepatic venous pressure gradient (r = -0.41), indicating worsening with increasing portal hypertension 3
Systemic vascular resistance is reduced in patients with arterial underfilling, confirming the vasodilatory mechanism 3
Clinical Implications
From a management perspective, arterial underfilling may be mitigated by albumin infusion to improve oncotic pressure and effective arterial volume 1
Portal decompressive procedures can address the underlying portal hypertension contributing to splanchnic vasodilation 1
Diuretics must be used cautiously as they can worsen arterial underfilling by reducing preload, potentially precipitating acute renal failure despite clinical fluid overload 1
Renal hypoperfusion from arterial underfilling predisposes patients to acute kidney injury, hepatorenal syndrome, and increased susceptibility to additional hemodynamic insults 1