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Gill Heart Institute. Strive to Revive. Case Study 1. Case Objectives. Discuss critical aspects of initial resuscitation that affected outcomes Discuss important aspects of post-resuscitation care: ECMO Management of VT. CASE DETAILS. CC: unconscious during MVA
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Gill Heart Institute Strive to Revive Case Study 1
Case Objectives • Discuss critical aspects of initial resuscitation that affected outcomes • Discuss important aspects of post-resuscitation care: • ECMO • Management of VT
CASE DETAILS • CC: unconscious during MVA • HPI: 58 yo female w/ PMHx notable for obesity s/p gastric bypass surgery, DM, HTN, hypothyroidism who presented as a trauma alert after a MVA. Patient reportedly had swerved off the road and slowed to a stop with minimal trauma. Bystanders noted that patient was unconscious, and called EMS.
EMS called – found patient to be pulseless. CPR initiated. Primary rhythm was PEA, and was given epinephrine and chest compression • Regained Pulse in the field and was found to be tachycardic • Patient was transferred to OSH
At OSH, patient was intubated for airway protection and hypoxic respiratory failure • Found to be in Atrial Fibrillation with Rapid ventricular response • Loaded on Amiodarone at OSH • Transferred to UK as a Trauma Alert
HISTORY • PMHx: • HTN • Hypothyroidism • DM • OA • Obesity • PSurgHx: • s/p Gastric Bypass Surgery >10 years ago • Hernia repair • Total Knee replacement • FamHx: • No history of SCD or ICD placement. Detailed family history unavailable • SocHx: • Significant EtOH abuse per family that was present. • No known illicit drug use. • Significant social stressors – Recent death of husband and premature birth of grandchildren • ROS: • Not obtainable
HISTORY • Medications: • Levothyroxine 200 mcg daily • Lisinopril 10 mg daily • Metformin 500 mg twice daily • MetoprololSuccinate 25 mg daily • Allergies: No known drug or food allergies
PHYSICAL EXAM • Vitals: HR: 169, BP: 97/63, RR: 39, SpO2 of 99% on 100% FiO2 • Gen: Obese, mechanically ventilated, cool to touch • Head: Atraumatic, plethoric and cool • Eyes: Left pupil is 5 mm and right is 3 mm, reactive • Nose: Nares patent, no discharge • Mouth: Endotracheal tube in place • Neck: Trachea midline • Respiratory: Distant breath sounds • CV: Irregularly irregular, tachycardic, 1+ central pulses • Abdomen: Soft nontender distended • Extremities: Cool, absent distal pulses • Neuro: She is intermittently flexing upper extremities with no purposeful movement, no response to pain • Psych: Unable to assess
Afib with RVR to the 170s • Concern that patient had inadequate perfusion with SBP<100 • DCCV at 200 J x 1 with conversion to sinus rhythm transiently then return to Afib with RVR • Trauma called – no significant trauma noted
Work-up • CT PE – negative • CT head and spine – no significant acute findings other than rib fractures • Thought to be related to CPR • Cardiology consulted for evaluation
Patient went emergently to cardiac cath lab given cardiovascular arrest and subsequent arrhythmia • RHC • RA: 26 mmHg • PA: 52/24, mean of 38 mmHg • PCWP: 30 mmHg • PA saturation: 24% • CO , CI: 3.8 L/min , 1.9 L/min/m2 • Selective coronary angiography • Non-obstructive CAD • Left ventriculography • Global Hypokinesisw/ EF<30% • Left Heart catheterization • LVEDP: 30 mmHg
Given inotropes in the cath lab, with minimal improvement • Placed emergently on VA ECMO • Transferred to the CVICU under the care of the CCU team
Polymorphic ventricular tachycardia noted soon after arrival to the CCU • Defibrillated X 1 with return of sinus rhythm
Initial Labs: • CBC unremarkable • Na: 138 • K: 6.3 • Cl: 106 • CO2: 11 • BUN/Cr: 14/1.14 • Mag: 1.3 • Ca: 7.9 • Phos: 6.1 • ABG: • pH: 7.32 • PaCO2: 22 • PaO2: 291 • Base Deficit: 13 • Albumin 2.3 • AG: 21 • TnI: 0.29
Initial Labs: • CBC unremarkable • Na: 138 • K: 6.3 • Cl: 106 • CO2: 11 • BUN/Cr: 14/1.14 • Mag: 1.3 • Ca: 7.9 • Phos: 6.1 • ABG: • pH: 7.32 • PaCO2: 22 • PaO2: 291 • Base Deficit: 13 • Albumin:2.3 • AG: 21 • TnI: 0.29
Initial assessment • Cardiogenic shock with new global LV dysfunction • Etiology non-ischemic • EtOHvs other non-ischemic etiology • Stunning from either CPR or initial arrest • Afibw/ RVR secondary to this? • AG metabolic acidosis w/ respiratory compensation • Profound hyperkalemia and hypomagnesemia • QT prolongation • Mg and QT prolonging agents
Was initially on dopamine, but went into polymorphic VT • Magnesium aggressively repleted • Amiodarone and other QT prolonging agents had been stopped • Started on isoproterenol to increase basal heart rate and decrease opportunity for myocytes to spontaneously depolarize
Did not require vasopressors • Was cautiously diuresed • Close monitoring of electrolytes • Added afterload reduction as a part of a CHF regimen • Lisinopril • Spironolactone • Metoprolol switched to Carvedilol
Repeat ECG showed QTc of 530. • Had an episode of Afib while on isoproterenol requiring DCCV • No more VT after improvement in QTc and correction of Mg • Weaned off ECMO with stable HD • Extubated and transferred to the floor • Neurologically intact
Final Assessment: • Cardiogenic shock 2/2 non-ischemic CM – resolved • LV dysfunction – not resolved • Polymorphic VT – resolved • Prolonged QTc – improved, but not resolved • Respiratory failure after arrest – resolved
Summary of Hospital Course • Timeline
Resuscitative Measures • CPR delayed until EMS arrived • Fortunately, no evidence of anoxic brain injury • Role of ECMO • Needs clearly defined end point • In this case, to allow time and interventions for resolution of cardiogenic shock and VT • Management of VT • Reversible causes • Important to understand etiology of VT
DM • Questions