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HOSPITAL COURSEAfter admission to the ICU, the patient received an intravenous infusion of unfractionated heparin drip and an intravenous infusion of norepinephrine at 5 micrograms/minute for hemodynamic support.A Foley catheter was placed with urine output remaining 2g/d L hemoglobin drop) developed.This technique requires placement of an intra-arterial catheter to the site of the embolus with bolus and infusion of a thrombolytic agent .
In patients with less severe hypotension and more severe cardiac dysfunction, inotropic agents may be considered as an adjunct or alternative to norepinephrine [6-11].
Newer inotropic agents, such as amrinone, which act as both inotropic agent and pulmonary vasodilator have shown promise in animal studies and case reports [12,13].
The trachea was urgently intubated and heparin was discontinued.
Interventional radiology was consulted for catheter thrombectomy and inferior vena caval (IVC) filter placement.
FIGURE 1: CT scan of the chest demonstrating pulmonary emboli in bilateral main pulmonary artery What distinguishes massive from submassive pulmonary embolism?
Anticoagulation was initiated and the patient was transferred to the intensive care unit (ICU) for further management.
A number of detrimental effects of intravenous fluids have been documented in animal studies, including decreased cardiac output and diminished right coronary artery blood flow due to increased right ventricular dilation [4-9].
In the face of diminished right coronary artery flow, worsening right ventricular ischemia can lead to diminished RV systolic function, establishing a vicious cycle of auto-aggravation.
One study in humans , however, suggested that a 500 ml fluid load may initially improve cardiac output among patients with massive PE, although the long-term effects of fluid administration on cardiac function and hemodynamics are unclear.
Most authors would agree that intravenous fluids must be used with caution in patients with massive PE [15-17].