1/ SVR looks precise: (MAP – RAP)/CO. But this neat number hides traps. It’s not “afterload,” it’s not pure “tone,” and sometimes it’s not even valid. A thread on why systemic vascular resistance misleads — and when it still helps. 🧵 #MedX
2/ SVR isn’t measured. It’s calculated from MAP, right atrial pressure, and CO. That makes it a derived ratio — not a direct property of the circulation.
3/ Because it has “resistance” in the name, we imagine SVR = arteriolar tone. It doesn’t. It’s just arithmetic.
4/ Afterload is the total load on the LV. Best described by arterial elastance, which includes: – Resistance (arterioles) – Compliance (large arteries) – Characteristic impedance (proximal aorta) – Inertial forces / HR SVR only reflects the steady resistive part.
5/ SVR is a mean value that mostly reflects arteriolar resistance. In systole, the LV also faces compliance & pulsatile loads. In diastole, forward flow runs almost entirely against arteriolar resistance. That’s why SVR is often called the “diastolic” component of afterload.
6/ The vasopressor paradox: Give noradrenaline → tone ↑, venous return ↑, MAP ↑. But if CO rises more than MAP, the equation spits out a lower SVR. Calculated SVR ↓, even though arterioles are tighter.
7/ The high-output trap: Sepsis, pregnancy, cirrhosis → CO is high. That alone drives SVR “low” — arithmetic, not necessarily true vasodilation. 🔗 More here in my earlier high-output physiology thread 👇https://x.com/icmteaching/stat...
8/ The formula assumes RAP is the downstream pressure. But if a vascular waterfall exists, the true downstream is the critical closing pressure (CCP). Then (MAP – RAP)/CO is invalid.
9/ Once a waterfall appears, vessels collapse at CCP. The circulation splits: – Arterioles see MAP → CCP – Venules see CCP → RAP Two separate resistances in series. Lumping them into one “SVR” becomes invalid. 🔗 CCP covered in detail in previous threads
10/ Clinical consequence: You can see “normal” or “low” SVR while organs are underperfused — because flow is pressure-limited by CCP, not governed by RAP. This can happen even when MAP sits in the “autoregulation range” — if CCP is elevated or autoregulation is lost.
11/ Where SVR does help 👇 In distributive (septic) shock, SVR is usually low — reflecting vasodilation & venous pooling. With norepinephrine, SVR usually rises — α-constriction restores tone, raises MAP, and shifts venous volume to stressed (↑Pms). Useful as a trend marker — if
12/ Better than chasing SVR: – CO and its determinants (Pms, heart, impedance) – MAP relative to autoregulatory thresholds / CCP – Bedside signs (refill, urine, mentation, lactate) – Echo context
13/ SVR isn’t afterload. It can fall while tone rises. And in waterfall states, it’s not valid. But in vasodilated shock, it may still trend usefully. Key: understand the physiology — don’t treat the number.
14/ This SVR thread is part of a wider series on cardiovascular physiology. If you’re new here, check out my pinned tweet (updated periodically)
Start here ⬇️ https://x.com/icmteaching/stat...
@icmteaching @khaycock2 @ThinkingCC @EMNerd_ @IM_Crit_ Taken together and simplified: This paradox (a fall in SVRI under norepinephrine) only seen in volume-overloaded patients without cardiomyopathy in distributive shock?
@Nadannzeigmal @khaycock2 @ThinkingCC @EMNerd_ @IM_Crit_ Great Q. The paradox (SVR falling on NE) happens when CO rises more than MAP. That’s most likely in distributive shock with preserved cardiac function and enough venous volume to recruit. If the ventricle can’t use the preload, or volume is low, SVR rises instead. Overload not
@icmteaching @khaycock2 @ThinkingCC @EMNerd_ @IM_Crit_ SVR a much better concept than an actuality
@icmteaching @khaycock2 @ThinkingCC @EMNerd_ @IM_Crit_ Excellent. In pulmonary circulation it is specially misleading, and its use is more widely teached and used as a marker of PVR, which is pretty bizarre.