CRIT BIT CORNER

Case Study

Patient Overview

An 80-year-old male with:

• Idiopathic pulmonary fibrosis (baseline O₂ 2–3L, recently ↑ to 8L)
• Non-small cell lung cancer on radiation
• CAD with prior MIs s/p CABG
• Hypertension
• Hyperlipidemia

Presented with acute on chronic hypoxic respiratory failure, initially attributed to:

• Radiation pneumonitis
• Viral infection (Coronavirus positive)

Initial Hospital Course

• Treated with steroids for pneumonitis
• Persistently high oxygen requirements (8–9L NC)
• Intermittent hypertension
• Developed 2:1 AV block → concern for high-grade conduction disease → taken for pacemaker placement

Acute Decompensation

During pacemaker placement:

• Developed right-sided pneumothorax →  Initially decompressed with chest tube

Then rapidly deteriorated:

• Severe hypoxia
• PEA arrest → VF arrest → ROSC after ~10–15 minutes

Required:

• 3L crystalloid
• Multiple vasopressors (epinephrine, norepinephrine, vasopressin)

What Is SAM?

Systolic anterior motion (SAM) occurs when the anterior leaflet of the mitral valve is pulled into the left ventricular outflow tract (LVOT) during systole, partially obstructing blood flow leaving the ventricle . This creates two major problems simultaneously:

• Dynamic LV outflow obstruction → decreased forward cardiac output
• Mitral regurgitation → blood leaking backward into the left atrium

The result is a form of functional cardiogenic shock, but one that behaves very differently than typical pump failure. What makes SAM especially dangerous is that it is dynamic and physiology-dependent. It can appear suddenly, worsen rapidly, and respond paradoxically to standard ICU therapies.

The Physiology

SAM is not just anatomy—it is flow physics in motion. During systole, blood is rapidly ejected through the LVOT. As velocity increases, two key forces act on the mitral valve:

1. Venturi Effect (Pressure Drop)

• High-velocity flow creates a local drop in pressure, which “pulls” the leaflet toward the LVOT.

2. Drag Forces (Dominant Mechanism)

• Blood flow physically pushes and drags the leaflet anteriorly, pulling it into the outflow tract.

These forces act on a valve that is already anatomically vulnerable, creating a self-reinforcing cycle:

• Valve moves anteriorly
• LVOT narrows
• Flow velocity increases
• More drag → more obstruction

This is why SAM is dynamic and can rapidly worsen in real time .

Normal Treatments Make SAM Worse

This is where SAM becomes clinically dangerous—because our reflex interventions often worsen the physiology.

Inotropes (e.g., dobutamine)

• Increase contractility
• Increase ejection velocity
• Increase drag forces → Worsens LVOT obstruction

Vasodilators

• Reduce afterload
• Increase flow velocity across LVOT → Worsens obstruction

Diuretics

• Decrease preload
• Shrink LV cavity → Brings mitral valve closer to LVOT

Result:

The more we “treat shock,” the worse the obstruction becomes. This explains why the patient deteriorated despite appropriate initial management.

Helpful Mental Model

Think of SAM like trying to drink through a straw that collapses when suction increases.

• The harder you pull (inotropes), the more it collapses
• The less fluid in the system (low preload), the easier it collapses
• The narrower the straw (small LVOT), the worse it gets

The solution isn’t more suction. The solution is:

• Widen the straw (increase preload)
• Reduce suction force (beta blockade)
• Stabilize the system (increase afterload)