Emergency Briefcase Fast Facts Sepsis Induced Myocardial Dysfunction

Stage 1 · Arrival

“She is still hypotensive.”

A 66-year-old woman with diabetes and hypertension presents with fever, cough, confusion, and dyspnea. She has already received 1 L of balanced crystalloid.

Temp39.1°C

HR124

BP78/46

RR30

SpO₂91%

Exam: warm extremities, delayed capillary refill, right basilar crackles, no focal neurologic deficit. Chest radiograph shows a right lower-lobe infiltrate.

1. Which action is the best immediate next step?Give furosemide because crackles indicate cardiogenic pulmonary edemaStart norepinephrine, continue infection treatment, and assess response to additional fluid dynamicallyWait for a formal echocardiogram before administering vasoactive medicationStart dobutamine as first-line vasopressor

Teaching pointSeptic shock requires prompt antimicrobial/source-control work plus hemodynamic support. Norepinephrine is the first-line vasopressor. Further fluid should be guided by dynamic response and repeated assessment—not by an automatic series of boluses.

Stage 2 · Early course

The pressure improves. Perfusion does not.

Antibiotics are administered after cultures. Norepinephrine is titrated to 0.18 mcg/kg/min. MAP is now 68 mm Hg, but she becomes cool and mottled. Urine output is minimal. Lactate rises from 4.1 to 5.6 mmol/L.

ECG: sinus tachycardia, no STEMI pattern
hs-troponin: mildly elevated
BNP: elevated
ScvO₂: 54%

2. What is the best interpretation?MAP ≥65 proves resuscitation is completeElevated troponin establishes acute coronary occlusionPersistent hypoperfusion remains; reassess flow, preload responsiveness, cardiac function, and alternative causesThe rising lactate mandates 30 mL/kg more fluid regardless of examination

Teaching pointPressure is not flow. A MAP target is a starting point; persistent oliguria, mottling, rising lactate, and low venous oxygen saturation require reassessment. Troponin and BNP are common and nonspecific in sepsis.

Stage 3 · Bedside ultrasound

Define the shock phenotype

LV: globally reduced systolic function; estimated EF 30–35%
RV: normal size, mildly reduced function
Pericardium: no effusion
LVOT VTI: 10 cm
Passive leg raise: VTI rises only 4%
Lung ultrasound: scattered B-lines plus focal right-base consolidation

3. Which conclusion is most appropriate?The findings support mixed vasoplegic and low-output shock; she is unlikely to benefit from another empiric bolusAn EF below 40% alone proves sepsis-induced myocardial dysfunctionA low EF means norepinephrine should be stopped immediatelyB-lines mandate diuresis despite ongoing shock

Teaching pointLVEF is load-dependent and cannot define the syndrome by itself. Integrate global LV/RV function, output (such as VTI), congestion, dynamic fluid responsiveness, the clinical trajectory, and competing diagnoses.

Echo reasoning, not EF worship

Question	Look for
Is there obstruction?	Tamponade, massive PE, dynamic LV obstruction
Is flow low?	VTI/output, perfusion markers, trend
Would fluid help?	PLR or other dynamic stroke-volume response
Is there congestion?	Lung, venous, RV and filling pattern

Repeat focused echo when physiology or treatment response changes—not automatically every day for every patient.

Stage 4 · Resuscitation

Choose the next hemodynamic move

MAP is 67 on norepinephrine. PLR is negative. She has persistent hypoperfusion and low-flow echo findings.

4. Which treatment strategy is best?Give repeated 1-L saline boluses until lactate normalizesStop norepinephrine and give nitroglycerinStart levosimendan routinely for septic cardiomyopathyMaintain adequate arterial pressure and add inotropic support for persistent low-output hypoperfusion

Teaching pointWhen cardiac dysfunction and persistent hypoperfusion remain despite adequate volume status and arterial pressure, guidelines suggest dobutamine added to norepinephrine or epinephrine alone. This is a selective, closely monitored intervention—not routine treatment for every low EF.

Stage 5 · Inotrope trial

Use a therapeutic trial with stop rules

Dobutamine is started at a low dose while norepinephrine maintains MAP. Thirty minutes later, VTI improves, capillary refill shortens, and ScvO₂ rises. Heart rate increases from 118 to 132.

5. What is the best next action?Titrate dobutamine to normalize EF regardless of adverse effectsContinue only if net perfusion benefit persists; monitor rhythm, ischemia, pressure, and flowAdd another inotrope because tachycardia proves inadequate dosingStop all vasopressors because VTI improved

Teaching pointThe target is tissue perfusion, not a normal ejection fraction. Inotropes can cause tachyarrhythmia, myocardial ischemia, and hypotension. Define the desired response and stop or reduce therapy when harms outweigh benefit.

Stage 6 · Reassessment

Diagnosis remains provisional

Over 24 hours, source control and hemodynamics improve. No regional wall-motion abnormality emerges and serial ECGs remain nonischemic.

Vasopressors and dobutamine are weaned. A repeat echo on day 6 shows recovered global LV function. This pattern supports sepsis-associated myocardial dysfunction, after competing causes were assessed.

Important mimics and alternatives

Diagnosis	Clues
Acute coronary syndrome	Ischemic symptoms/ECG, regional wall-motion abnormality, culprit lesion
Stress cardiomyopathy	Characteristic regional pattern extending beyond one coronary territory
Massive pulmonary embolism	Acute RV pressure overload, compatible clinical context
Myocarditis	Clinical context, MRI/biopsy selectively
Pre-existing cardiomyopathy	Prior imaging/history and lack of reversibility

Recap

Your case performance

0/5

Complete the five case decisions to generate your interpretation.

Critical actions

Recognize shock and treat the infectious source without waiting for perfect phenotyping.
Use norepinephrine as first-line vasopressor; individualize pressure targets.
Reassess persistent hypoperfusion even when MAP is acceptable.
Use focused echo to assess LV, RV, output, congestion, obstruction, and fluid responsiveness.
Consider inotropic support only for persistent low-output hypoperfusion after adequate volume and pressure.
Track benefit and harm; repeat imaging when the clinical state changes.
Exclude ischemia, stress cardiomyopathy, PE, tamponade, myocarditis, and chronic dysfunction.