Presented to the ED with acute onset dyspnea, new O2 requirement 6 L NC, minimal PMH
BP 95/70, HR ~ 100, afebrile
Hypoxemia worsened during ED stay requiring intubation
Now hypotensive
CT obtained with unilateral right sided pulm infiltrates, small pleural effusions, no PE
Labs 🧪
WBC 20k
Troponin mild elevation
Lactic acid 5.0
Cr mild elevation
U/A with > 50 WBC
Antibiotics, 2 L IVF given and admitted to ICU
🛌Arrival to ICU
B: 50% FiO2 PEEP 10
C: BP 80/60 HR 120s on
Norepi 40 mcg/min
Vasopressin .03 u/min
Epi 5 mcg/min
Distal extremities cool, oliguric, systolic heart murmur heard over vent (old per notes)
Middle of night POCUS 🫀
RV mildly dilated but systolic function looks ok
IVC 2.5 cm minimal variation
LVEF is normal
AS suspected on visual assessment
Comprehensive echo ordered for better valve assessment in AM
Must be pneumonia and sepsis, right?
Time, antibiotics, source control...
Echo next morning gives the diagnosis:
Severe AS
+
Acute chordae tendineae rupture with severe MR
📜Lessons:
✔️Not everything is septic shock
✅Normal LV/RV function does NOT rule cardiogenic cause of shock-low cardiac output from MR+AS despite normal EF in this case
☑️Severe MR can cause unilateral pulmonary edema
✔️Narrow pulse pressure (BP 80/60) hints at cardiac cause
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A patient presents with 7 days of dyspnea, LE edema and fatigue. They have run out of all meds 2 weeks ago #COVID. They had an MI with ishcemic cardiomyopathy EF ~30%, also has a-fib.
Mild confusion
JVD+
Mild resp distress, crackles BL
No murmur
Hands, legs COLD and mottled to knees, toes and fingers purple, cap refill delayed
Pitting LE edema
The Berlin criteria: Acute onset within one-week, bilateral opacities on CXR not explained by cardiogenic pulmonary edema, pleural effusion etc. and a PaO2/FiO2 ratio of <300 mm Hg with PEEP 5 cm H2O.
More simply in the ED or acute setting I consider anyone with bilateral infiltrates + inflammation (sepsis, pneumonia, trauma etc) + hypoxemia to be at risk for ARDS and if intubated manage them with lung protective ventilation. 3/
The problem is bronchospasm and secretions narrow the airways and lead to obstruction, limitations in exhalation and high airway resistance.
On the vent, this is seen as a high peak pressure (high resistance) and a prolonged expiratory flow or incomplete exhalation. 2/
The high peak pressure isn’t really a problem unless the plateau (obtained by an end insp hold) is also high. The delicate alveoli only feel the plateau pressure. Best to keep the plateau pressure < 30 cm H20 by minimizing auto-PEEP as the auto-PEEP contributes to plat press 3/