Title
Not All Shock is Created Equal
Introduction
Despite increasing rates of revascularization and advances in percutaneous mechanical circulatory support, cardiogenic shock (CS) carries a mortality rate of greater than 40% with its incidence increasing annually. Early recognition remains one of the most crucial yet challenging facets of the disease process due to phenotypic variation. SCAI classification has aided in early identification, risk stratification of patients, and in directing triage efforts, but patient presentations and therapeutic response remain heterogeneous and dynamic. We present a case of CS that highlights the potential for expeditious deterioration of even early-stage CS and required a dynamic approach with rapid device escalation.
Clinical Case
A 76-year-old male with non-ischemic cardiomyopathy (LVEF 10%) presented with dyspnea. Initial vital signs noted blood pressure 126/79 mmHg, heart rate 90 bpm, oxygen saturation 100% on ambient air, and normothermia. Initial physical exam noted cool lower but warm upper extremities, 1+ pitting edema, and jugular venous distention to the mandible. Initial labs showed mild acute kidney injury (AKI), lactate of 4 mmol/L, brain natriuretic peptide >5000 pg/mL, and no acute ischemic changes on electrocardiogram. The patient received diuresis, but abruptly became hypertensive, tachycardic, hypoxic, and cool in extremities. Repeat labs noted progression of AKI, lactate of 10 mmol/L, and new acute liver injury. Due to concern for worsening CS and to define hemodynamics, right heart catheterization (RHC) was performed (Table 1) and resulted in placement of right percutaneous axillary Impella (Abiomed, Danvers, MA). Femoral access was precluded due to bilateral iliac artery complete total occlusions and significant vascular disease. Despite diuresis and afterload reduction, his CS remained refractory, and the patient was upgraded to an Impella 5.5 via surgical cutdown. Over time, he was successfully weaned off inotrope and Impella support with normalization of renal and liver function. Repeat RHC showed significant improvement in biventricular filling pressures. Goal directed medical therapy and volume status were optimized as seen on repeat RHC (Table 1). The patient ultimately received an Optimizer (Impulse Dynamics, Marlton, NJ) for cardiac contractility modulation due to preclusion of advanced therapies given his severe peripheral vascular disease and patient preference.
Discussion
While all CS is intrinsically characterized by end organ dysfunction secondary to cardiac functionality, clinical presentations exist across a spectrum of severity and must be approached individually and frequently reassessed to do potential for rapid decline. This case highlights the dynamic nature of CS clinical course and therapeutic response and exemplifies how frequent clinical reassessment required rapid device escalation and led to myocardial recovery.
Table 1: RHC Hemodynamic Data – Initial and Post-Impella Removal
| RHC Hemodynamics | Initial RHC | Post-Impella RHC |
| Right Atrium Pressure (mmHg) | 28 | 7 |
| Right Ventricle Pressure (mmHg) | 60/30 | 55/10 |
| Pulmonary Artery Pressure (mmHg) | 70/40 (45) | 55/20 (31) |
| Pulmonary Capillary Wedge Pressure (mmHg) | 38 | 15 |
| Right Atrium Oxygen Saturation (%) | 17.9 | 62 |
| Pulmonary Artery Oxygen Saturation (%) | 19.5 | 70 |
| Aorta Oxygen Saturation (%) | 87 | 99 |
| Cardiac Output (L/min) / Cardiac Index (L/min/min2) | 2.39 / 1.18 | 7.8 / 3.7 |
| Systemic Vascular Resistance (dynes-sec-cm-5) | 2581 | 685 |
| Pulmonary Vascular Resistance (dynes-sec-cm-5) | 268 | 164 |