High-Output CHF

• Sinus tachycardia (”bounding” Quincke/Corrigan pulse)
• ↑ Pulse pressure (> 60 mmHg)
• ↑ Cardiac index (≥ 4L/min)
• Dynamic LVOT obstruction (”new systolic murmur”)*

High-Output Pathophysiology❓

• The discovery of a high-output cardiovascular state inherently means that, despite the visualized ↑ in cardiac output, the patient is still experiencing tissue hypoperfusion

• The first reason for occult tissue hypoperfusion is that the arterial tree is either diffusely “wide open” due to profound vasodilation (e.g. cirrhosis, sepsis), or that the arterial system has a strategic AV shunt stealing nutritional blood flow from the rest of the body’s organs (e.g. AV fistula)

• The second reason for occult tissue hypoperfusion is that there is deranged tissue perfusion at the molecular level due to ↓ O₂ Extraction, which can be absolute (e.g. impaired ox. phos.) or relative (e.g. ↑ metabolic demand)

Diagnostic Armamentarium 🧰

• Fever work-up (BCx, UA w/ reflex, CXR → contrast-enhanced cross-sectional imaging)

• [Vitamin B1] → empiric IV thiamine

• [TSH], FT4, FT3 ⊕ b-hCG

• CBC ⊕ LFTs

• CTA torso ⊕ extremities

• Bone scan, alkaline phosphatase

• Co-oximetry

• Clinical manifestations, diagnosis, and management of high-output heart failure

• Deranged Physiology (LVOT graphic)