Sample Lecture – Shock, DVT vs. A-Fib

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Next Step: Make Cards on the Automatic Key Concepts, and Vignettes

Remember, the more you automatically know what each sentence means on your test, the better you will do. There are 4 stages in making interpretation more automatic:

• Stage 1: Unable to Make Pathophysiologic Chronologies in Either Timed or Untimed setting
• Stage 2: Basic Pathophysiologic Chronologies, but with Significant Gaps
• Stage 3: Detailed Pathophysiologic Chronology Without Time, but Unable to Consistently Generate PC During Timed Setting
• Stage 4: Consistent Pathophysiologic Chronologies in Timed Setting

My goal with these vignettes is to help you reach Stage 4. How do you do so?

• With the Automatic Key Concept cards, you can master the underlying information to move past Stages 1 + 2.
• Then, with the Vignette/Pathophysiologic Chronology cards, you can teach yourself to make these connections on your exam.

Automatic Key Concepts:

Copy + paste these into your cards, to make these key concepts more automatic.

High- vs. low-output causes of shock – how warm/cool will the skin feel in each? Why?

High output shock: warm, because vasodilation → blood flow ↑ to skin → warm skin

Low output shock: cool, because high sympathetic tone → vasoconstriction → skin flow ↓

Of the NACHOS categorization, which are high- vs. low-output causes of shock?

High-output: neurogenic, anaphylactic, septic

Low-output: cardiogenic, hypovolemic, obstructive

DVT vs. A-fib – which is more likely to cause acute mesenteric ischemia? Why?

Atrial fibrillation. Acute mesenteric ischemia between DVT or a-fib would likely be due to embolization of a clot to one of the vessels supplying the GI tract. It is much more likely that a clot from the left atrium would reach the arterial system (vs. a venous clot, which is much more likely to get stuck in the lungs).

DVT vs. atrial fibrillation – which is most likely to cause an embolic stroke? Why?

Atrial fibrillation >> DVT as cause of stroke

First, recall that a stroke = restricted ARTERIAL flow. A DVT is in the venous system. DVT → right heart → pulmonary arteries.

Atrial fibrillation can be in either your right (venous) or left (arterial) heart. It’s the fibrillation of the LEFT atrium that matters so much for stroke.

(Left) atrial fibrillation → clot forms → ejection via L ventricle → arterial system → can occlude cerebral arteries → stroke

DVT – what has to happen for it to cause a stroke?

Remember, a DVT is in the venous system. Thus, not only would it have to cross into the arterial system, but it would have to make its way to the cerebral/vertebral arteries. You would need:

A connection between right and left heart (e.g., a patent foramen ovale), AND

Reversal of the typical shunt from right to left, which is the OPPOSITE of a typical shunt (typical shunts are left to right). However, there is only a weak association between the presence of PFO and crytogenic stroke (stroke with unclear etiology), which makes up ~30% of strokes.

A woman with both a DVT and atrial fibrillation comes in with syncope. Her pulse is 80/min. Between her DVT and a-fib, what is the most likely pathophysiologic chronology of her syncope? Why?

DVT. DVT → (large) pulmonary embolism → LA venous return ↓ → LV preload ↓ → SV ↓ → CO ↓ → MAP ↓ → CPP ↓ → cerebral hypoperfusion → syncope

A patient with history of IV drug abuse has stroke symptoms. Assuming infective endocarditis, would the mitral or tricuspid valve be most likely to be affected? Why?

Mitral valve

Recall, embolic stroke happens because of ARTERIAL blockage. Thus, the source of the emboli would have to be from the left heart, making the mitral valve much more likely.

Vignette/Pathophysiologic Chronologies:

Copy + paste these into your cards, to make the connections behind these vignettes more automatic.

A 65-year-old man is admitted to the hospital after stent placement for a complete occlusion of the proximal left anterior descending artery. On post-procedure day 5, he becomes acutely hypotensive. Jugular venous pressure is 20 cm H2O, and there are inspiratory crackles on lung auscultation. Pulsus paradoxus is present, and his extremities are cool and clammy.

What is the pathophysiologic chronology?

Summary:

Post-MI LV free wall rupture → tamponade → cardiogenic shock → sympathetic tone ↑↑ → skin perfusion ↓

Detailed:

LAD occlusion → LV free wall ischemia → weakening of wall before fibrosis can occur → 5 days post-MI rupture of free wall → tamponade → LV SV ↓ → CO ↓

Cool, clammy skin: MAP ↓ → sympathetic tone ↑ → α1 agonism → vasoconstriction → skin blood flow ↓ → cool skin

Left → right heart failure: backup of blood into lungs → pulmonary edema → inspiratory crackles / back-up of blood into jugular veins

Pulsus paradoxus: tamponade → on inspiration, RV preload ↑ → LV compression → LV preload ↓ → LV SV ↓ → pulse pressure/SBP ↓ on inspiration

A man has atrial fibrillation, and a deep vein thrombosis. He experiences sudden right-sided upper extremity weakness, and speech difficulties. His pulse is 80/min.

What is the pathophysiologic chronology?

Atrial fibrillation → left atrium blood stasis → LA thrombus → embolization to arterial system → stroke

Why not DVT?

Recall that for a DVT to become a paradoxical embolus, you would need:

A connection between venous/arterial circulations, AND

Reversal of the typical left to right shunt

While this does occur, embolic stroke via atrial fibrillation would be MUCH more likely