Principle 1: The Four Interfaces of the Circulatory System
It is tempting to think about the heart and vascular system as a pump connected to a series of pipes throughout the system. But doing so leads to several physiologic inconsistencies.
Sylvester J et al. Clin Chest Med. 1983 May;4(2):111-26
There are several models of varying complexity which imperfectly describe the interplay between the heart, lungs, and vasculature of the human body. In clinical medicine, utilizing a model simple enough to rationalize, but complex enough to describe major interactions in the body, especially as they pertain to hemodynamic states of shock, is important. One such model is the 4-interface model.
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The four principle interfaces of the circulatory system include the:
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1. Left Ventricle → Arterial System (Interface I)
This interface reflects the heart's ability to generate forward flow in the context of vascular resistance, captured by the concept of ventriculo-arterial coupling (VAC). An imbalance between cardiac contractility (Ees) and arterial load (Ea) impairs stroke volume (SV) and cardiac output (CO). Bedside echo parameters like LVEF and LVOT-VTI can offer insight into this coupling. Recognizing uncoupling here helps tailor the use of inotropes and vasopressors more effectively.
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2. Arterioles → Capillaries (Interface II)
This is where macro meets microcirculation. Excessive vasoconstriction or inappropriate vasopressor use can raise critical closing pressure (Pcc) and reduce perfusion pressure to tissues, even if MAP appears normal. This interface explains why “not all MAPs are created equal.” Clinical surrogates like capillary refill time (CRT) and skin mottling score have emerged as useful, low-cost indicators of microvascular status and macro to microcirculatory coupling.
3. Capillaries → Right Atrium (Interface III)
This interface reflects the efficiency of venous drainage from the microcirculation. Once blood passes through the capillaries, its exit into the venous system depends on the pressure gradient between the post-capillary space and central venous pressure (CVP). When CVP rises—due to fluid overload, mechanical ventilation, RV dysfunction, or increased venous tone; this gradient narrows, impairing flow and promoting venous congestion.
Importantly, elevated CVP functions not just as a cardiac preload marker, but as tissue afterload, directly impeding microvascular clearance and promoting interstitial edema. This can lead to capillary compression, reduced capillary density, and ultimately tissue hypoperfusion, even when macro-hemodynamic parameters appear stable.
4. Right Ventricle → Pulmonary Artery (Interface IV)
The final interface evaluates RV-PA coupling, critical for maintaining venous return and preventing backward failure. Acute or chronic pulmonary hypertension can elevate RV afterload (Ea), leading to right heart strain and subsequent congestion. Parameters like TAPSE/PASP, RV S', and RVOT Doppler patterns help assess coupling at this level and guide fluid and vasoactive management.
