2/ High-output failure = elevated cardiac output, but a circulation that still fails. The failure is clinical: pulmonary oedema and venous congestion, or hypotension with organ hypoperfusion.

3/ Mechanism 1 — volume overload Excess stressed volume → ↑mean systemic pressure → ↑venous return → ↑CO. The heart becomes full, loses reserve, and filling pressures rise. Common causes: renal failure, fluid overload.

4/ When filling pressures rise too far: • Pulmonary oedema • Systemic venous congestion → impaired organ perfusion Occasionally, severe overload also raises afterload enough to trigger LV failure — especially if baseline function is poor. This is the classical high-output

5/ Arteriovenous shunts magnify this. They bypass: Arteriolar resistance Venular compliance → Big increases in venous return and CO. But this bypass means pressures rise → congestion and failure. Examples: large dialysis fistulae (esp. with volume overload), thyrotoxicosis,

6/ Mechanism 2 — vasodilated hyperdynamic states Here, SVR is very low. If fluids or pressors restore Pms, venous return and CO become high. But MAP stays low because SVR is inadequate.

7/ This isn’t pulmonary oedema/congestion. Instead: organ hypoperfusion from low MAP — despite high CO. Examples: resuscitated septic shock, advanced cirrhosis with splanchnic vasodilation

8/ In practice, many conditions combine these mechanisms. Cirrhosis → fluid retention, portosystemic shunting, and vasodilation. Dialysis fistula → shunt effect, but decompensation often needs volume overload (eg missed dialysis) That’s why real patients rarely fit neatly into

9/ You’ll often read: “CO is still too low to meet demand.” This is misleading in thyrotoxicosis and cirrhosis — the problem isn’t infinite demand, it’s abnormal pressures and distribution. (Severe anaemia is different: here the limit is O₂ content, not CO.)

10/ Think about exercise: demand increases far more than in thyrotoxicosis, cirrhosis, or AV shunts — yet perfusion is fine. Failure here is about congestion (pressures too high) or hypotension (pressures too low), not inadequate litres/min.

11/ Take-home: High-output ≠ healthy. • Too much volume → ↑pressures → pulmonary oedema/venous congestion (high BP). • Too little resistance → hypotension → organ hypoperfusion (low BP). Two different faces of a “high-output” circulation — both pathological.

@icmteaching In hemodynamics, LV end-diastolic volume is key to estimate preload. But remember : that same volume must be compressed to generate force and open the aortic valve → afterload. When preload rises beyond the efficient range, instead of helping, it raises afterload → more

@icmteaching 👌👌