Dr. Simon Parlow is part of the CAPITAL Research Group, University of Ottawa Heart Institute, Ottawa, Ontario, Canada. In this video Dr. Parlow discusses an Unusual Case of Obstructive Shock.
Link to Abstract-
A 54-year-old guy was admitted to the hospital with severe obstructive shock. A right atrial tumor was discovered to be the source of severe right ventricular inflow blockage and inadequate cardiac output. To alleviate the obstruction, the patient was treated with an emergency balloon catheter intervention, which resulted in hemodynamic stabilization. A positive result for diffuse large B-cell lymphoma was later found on the pathology report. (Intermediate level of difficulty.)
A 54-year-old male with dyspnea, limb edema, stomach bloating, and exhaustion reported to a peripheral hospital with a 2-week history of symptoms. The patient had increased hypotension and drowsiness over the next 1 to 2 hours, necessitating intubation and the start of vasopressor therapy. He was then transported to our quaternary care cardiac intensive care unit at the University of Ottawa Heart Institute in Ottawa, Ontario, Canada, for additional evaluation and management.
To be able to come up with a differential diagnosis for a patient who has obstructive shock.
To gain a better understanding of the function of hemodynamics in the treatment of obstructive shock caused by an intracardiac mass
He was severely hemodynamically unstable when he arrived. To keep his blood pressure at 75/58 mm Hg, he needed three vasopressors. He was bradycardic, with a sinus rhythm heart rate of 47 beats per minute. He was drugged and ventilated during his physical examination. With thready peripheral pulses and chilly extremities, he was mottled. His neck and face were reddish and swelled, and his veins were distended. On precordial auscultation, his heart sounds were hardly audible, with no murmurs or additional heart sounds detected. His lungs were both clean on auscultation. He had a somewhat enlarged abdomen but was not peritonitic. He'd had a Foley catheter put, but he hadn't peed in several hours. Despite ventilation with 100% inhaled proportion of inspired oxygen, he was hypoxemic, with an arterial Po2 of 75 mm Hg. With an arterial pH of 6.85 and a blood bicarbonate level of 4 mmol/L, his serum lactate level was 21.2 mmol/L.
Previous Medical Experience
During a visit to a peripheral emergency department two weeks before to his presentation, he was diagnosed with pericarditis and prescribed colchicine and ibuprofen. His previous medical history was basically unremarkable, save for cigarette smoking, and he had never taken any home remedies. He had no allergies or a history of illicit drug usage.
Differential Diagnosis is a term used to describe the process of distinguishing between two
The clinical examination and biochemical results of the patient are consistent with deep shock, as evidenced by hypotension and obvious signs of end-organ hypoperfusion (decreased level of consciousness, anuria, and elevated lactate). Several clinical symptoms can be seen at the bedside to assist in determining the subtype of shock. Symptoms of poor cardiac output, such as chilly extremities and thready pulses, as well as signs of high left ventricular (LV) or right ventricular (RV) filling pressures, such as pulmonary edema, peripheral edema, and jugular venous distention, are common in both cardiogenic and obstructive shock (1). Other types of shock, such as hypovolemic and distributive shock, as well as septic shock, are ruled out by the combination of these clinical symptoms. Furthermore, no clear symptoms of infection were present. The differential diagnosis based on our patient's clinical exam includes obstructive shock due to cardiac tamponade, large pulmonary embolism or an obstructive mass, or cardiogenic shock due to significant LV or RV dysfunction.
We started with an immediate point-of-care ultrasound to figure out what was causing the patient's shock. We found a big tumor in the right atrium with expansion across the tricuspid valve (TV). The right ventricle was underfilled and RV inflow was limited, resulting in decreased LV preload and cardiac output. The inferior vena cava (IVC) was a plethora of veins that were noncollapsible. The patient was transferred to the catheterization laboratory on an emergency basis for additional care after receiving a fast bolus of intravenous crystalloid fluid.
By navigating past the obstructive mass and into the pulmonary artery, we were able to get pressure tracings in each chamber and do a right-sided heart catheterization for hemodynamic assessment. The superior vena cava (SVC) pressure was found to be significantly higher than the right atrial (RA) pressure, with a gradient of 11 mm Hg. In addition, the RV diastolic pressure was 33 mm Hg higher than the RA pressure. The hemodynamic data taken during right-sided heart catheterization are shown in Table 1, and the diagnostic angiography and percutaneous intervention are shown in Figures 1A to 1D, as well as Videos 1, 2, and 3.