How can a patient with S1 radiculopathy, diastolic dysfunction, iron deficiency anemia, and peripheral hypoperfusion have normal Ankle-Brachial Index (ABI) and venous return flow test results despite compromised extremity perfusion due to low stroke volume index (SVI) and preferential perfusion to the heart and lungs?

Understanding Normal ABI and Venous Studies Despite Peripheral Hypoperfusion in Low Cardiac Output States

The Paradox Explained

Normal ABI and venous return tests do not exclude peripheral hypoperfusion in patients with severely reduced stroke volume index (SVI) because these tests measure large vessel patency and pressure gradients, not tissue-level perfusion or microcirculatory flow. 1, 2

The key distinction is between macrovascular versus microvascular perfusion:

• ABI measures large artery occlusive disease (atherosclerotic stenosis or occlusion), not the adequacy of tissue perfusion or cardiac output distribution. 1
• A normal ABI (0.91-1.40) indicates that there is no significant stenosis in the major arteries from the aorta to the ankle, but it provides no information about forward flow volume, microcirculatory perfusion, or tissue oxygen delivery. 1, 2
• Similarly, venous return flow tests assess venous valve competence and patency, not arterial perfusion adequacy. 1

Why This Occurs in Low Stroke Volume States

In patients with severely reduced SVI and diastolic dysfunction, several mechanisms explain normal vascular testing despite tissue hypoperfusion:

Preserved Arterial Patency with Reduced Flow Volume

• The arterial "pipes" remain open (normal ABI), but the volume of blood flowing through them is critically reduced due to low cardiac output from diastolic dysfunction and reduced SVI. 1
• ABI only detects pressure gradients caused by stenotic lesions; it cannot measure absolute flow volume or cardiac output distribution. 1, 2
• In low-flow states with normal ejection fraction but reduced stroke volume (as seen in diastolic dysfunction with small, thick-walled ventricles), the ABI remains normal because there is no arterial obstruction. 1

Compensatory Redistribution of Cardiac Output

• Preferential perfusion to vital organs (heart, brain, lungs) occurs through neurohormonal vasoconstriction of peripheral vascular beds, reducing extremity perfusion despite patent arteries. 1
• This compensatory mechanism maintains blood pressure (and thus ABI) while sacrificing peripheral tissue perfusion. 1
• The body prioritizes central circulation over peripheral circulation when cardiac output is insufficient to meet total body demands. 1

Microcirculatory Dysfunction Not Detected by ABI

• Tissue hypoperfusion in low cardiac output states occurs at the capillary and microcirculatory level, which ABI cannot assess. 1, 2
• Reduced capillary perfusion pressure, increased interstitial edema (from venous congestion in diastolic dysfunction), and impaired oxygen extraction all contribute to tissue ischemia despite normal large vessel patency. 1, 3

Additional Contributing Factors in This Clinical Context

Iron Deficiency Anemia

• Iron deficiency anemia reduces oxygen-carrying capacity, compounding tissue hypoxia even when blood flow is adequate. 4, 5
• Severe anemia can cause systemic hypoperfusion and has been documented to cause ischemic events even without vascular occlusion. 4
• The combination of reduced cardiac output and reduced hemoglobin creates a "double hit" to tissue oxygen delivery. 4, 6

Diastolic Dysfunction with Low-Flow State

• Patients with severe aortic stenosis or diastolic dysfunction can present with low-flow, low-gradient physiology despite normal ejection fraction, characterized by stroke volume index <35 mL/m², small LV cavity, thick walls, and normal LVEF ≥50%. 1
• This creates a paradoxical situation where systemic perfusion is inadequate despite preserved ejection fraction and patent peripheral arteries. 1

S1 Radiculopathy Confounding Clinical Assessment

• Neurologic symptoms from radiculopathy may mask or be confused with vascular claudication symptoms, making clinical assessment of perfusion adequacy more challenging. 1

What Tests Would Actually Detect This Problem

To assess tissue-level perfusion in low cardiac output states, consider:

• Toe-brachial index (TBI) with waveform analysis provides better assessment of distal perfusion than ABI, particularly when microcirculatory dysfunction is suspected. 1, 2, 7
• Transcutaneous oxygen pressure (TcPO2) directly measures tissue oxygenation; values <30 mm Hg indicate severe ischemia. 1
• Skin perfusion pressure (SPP) assesses microcirculatory perfusion; values <40 mm Hg predict poor wound healing. 1
• Echocardiographic assessment of stroke volume index directly quantifies cardiac output and can identify low-flow states. 1
• Lactate levels may be elevated in severe systemic hypoperfusion despite normal peripheral pulses and ABI. 1

Clinical Implications and Management

The presence of normal ABI should not provide false reassurance in patients with clinical signs of peripheral hypoperfusion and known low cardiac output states. 1, 2

• Address the underlying cardiac dysfunction (diastolic heart failure, low SVI) as the primary cause of peripheral hypoperfusion. 1, 3
• Treat iron deficiency anemia aggressively to improve oxygen-carrying capacity. 5, 6
• Consider advanced perfusion assessment (TBI, TcPO2, SPP) if tissue ischemia is suspected despite normal ABI. 1, 2
• Recognize that peripheral hypoperfusion in this context is a manifestation of inadequate cardiac output, not peripheral arterial disease. 1

Critical Pitfall to Avoid

Never assume adequate peripheral perfusion based solely on normal ABI in patients with known low cardiac output, diastolic dysfunction, or severe anemia. 1, 2 ABI is a screening tool for peripheral arterial occlusive disease, not a measure of tissue perfusion adequacy or cardiac output distribution. 1