Andrew Stephen, MD
Background, pathophysiology
There are no industry funded trials of any significance on critically ill patients that suffer MI and none at all that we know of on SICU patients. The population of patients in the SICU that suffers MI is very heterogeneous and often have contraindications to anticoagulation or antiplatelet therapy. In the SICU Type 2 Demand MI is much more common than Type I. Key features below:
Type 1
Result from plaque rupture and occlusion. Present from outside the hospital to ER acutely. May benefit from anticoagulation, antiplatelet therapy, PCI, CABG. More often ST elevations. ECHO may show a new focal wall motion abnormality.
Type 2
Myocardial oxygen demand exceeds supply. More often occur as a result of physiologic stress-sepsis, hemorrhage, hypotension, tachycardia, hypoxia, pressors, inotropes. Do not benefit from anticoagulation, antiplatelets. Treat and reverse the underlying cause. Patients are more likely to have a demand MI if there is some degree of preexisting CAD but it is not required. ECHO more likely to show a hyperdynamic underfilled heart or a global decline in function.
A couple of our cases(among likely many) to illustrate the confusion and delay in diagnosis that can occur
Case 1: A 67 year old man presents to the ER in December 2015 shortly after playing tennis with a chief complaint of diffuse abdominal pain and lightheadedness. His abdomen is distended and moderately tender on exam. His EKG shows some ST depressions and his CT scan shows a moderate to large amount of free fluid without solid organ injury. He has no history of cirrhosis. The patient goes to the catheterization lab and has a coronary stent placed. His abdominal pain continues and he develops worsening hemodynamics going onto two vasopressors in the CCU. He is rescanned and there is even more abdominal fluid. He is taken to the OR by the Surgery 3 team and several liters of blood are found in the abdomen and he is packed. The trauma/SCC team assumes care of the patient. On subsequent trips to the OR he is repacked and a mesenteric tear is noted. Differential diagnosis is limited, question segmental arterial mediolysis. The patient eventually recovers but needs a vicryl mesh, skin graft, develops an ECF that is taken down in July 2017.
Commentary-The key to this case is the chief complaint, abdominal physical exam, and CT findings that need to be explained before proceeding to catheterization. Most likely this patient’s bleeding and physiologic stress led to the ST depressions and the hemodynamic instability. The patient likely did not need urgent coronary revascularization but rather control of hemorrhage and restoration of intravascular volume with blood products. The delay in control of hemorrhage may have contributed to a much longer SICU, hospital stay, and multiple complications.
Case 2: A 65 year old man presents to an outside medical center with a chief complaint of right upper quadrant pain, vomiting, and malaise. Similar to Case 1 he undergoes a cardiac workup and has a catheterization but continues to feel terrible and have hemodynamic decline. He is transferred to RIH and his scan and labs are revisited. A diagnosis of acute gangrenous cholecystitis is made and he has an emergency open subtotal cholecystectomy. He has a significant fluid requirement and remains on vasopressors from more than 24 hours postoperatively and suffers AKI with creatinine 2-3 times above baseline. He also has a cystic duct leak requiring two ERCPs.
Commentary-This patient’s surgical source control was significantly delayed by pursuing the cardiac pathway. This likely contributed to the development of AKI and duration of his pressor requirement and ICU stay. It is unclear whether it made any difference in the occurrence of the bile leak. The gallbladder was likely quite gangrenous on his arrival to the outside center.
Approach to patient with Type 2 MI
Optimize hemodynamics and intravascular volume status.
Control hemorrhage, septic sources.
Consider low dose, frequent beta blocker dosing-5mg IV q4 hours and transition to PO.
Use hold parameters for beta blocker. They increase risk of death, CVA if they create hypotension.
+/- Aspirin.
Usually can stop checking troponin early on.
Hemoglobin goal uncertain, >7 or >8 g/dL is reasonable.
Issues with troponin
The clinical history and EKG are more useful and guide decisions about Type 1 vs 2 MI and then all the subsequent plans.
As assay sensitivity has increased specificity has decreased.
There are multiple non-coronary ischemia sources of elevated troponin-sepsis, AKI, CRI, CHF, PE, CVA. “Troponin leak” is an arguable term but may exist after all. About 40% of ICU patients develop an elevated troponin, see below reference.
Carroll I, Mount T, Atkinson D. Myocardial infarction in intensive care units: A systematic review of diagnosis and treatment. J Intensive Care Soc. 2016;17(4):314-325.