A 65-year-old man with exertional chest pain and an abnormal exercise stress test comes to the hospital for elective cardiac catheterization. The patient has no resting chest pain or shortness of breath. He has no known allergies. Temperature is 37 C (98.6 F) , blood pressure is 130/78 mm Hg, pulse is 84/min, and respirations are 15/min. Pulse oximetry shows an oxygen saturation of 98% on room air. Examination shows normal jugular venous pressure, clear lungs without crackles, normal heart sounds, no murmurs, and a normal capillary refill time. Ten minutes after the first injection of iodinated contrast during cardiac catheterization, the patient reports chest pain, abdominal pain, and dizziness; then he suddenly becomes obtunded and flushed. Blood pressure is 70/36 mm Hg, pulse is 128/min, and respirations are 32/min. Pulse oximetry shows an oxygen saturation of 90% on 2 L of oxygen via nasal cannula. Which of the following hemodynamic changes are most likely present in this patient at this time?

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Explanation: 11ec25c8_d89c_951c_bc81_3b5f33759d0a_MD0003_00 After receiving iodinated contrast, this patient developed chest pain, abdominal pain, dizziness, obtundation, flushed skin, hypotension, and respiratory distress, findings concerning for anaphylaxis. A widespread IgE-mediated release of inflammatory mediators (eg, histamine) in response to an allergen (eg, food, insect sting) is a classic cause of anaphylaxis. In addition, some substances (eg, iodinated contrast, opioids) may stimulate direct mast cell activation (nonimmunologic process), leading to an anaphylaxis-like response that can be clinically indistinguishable from IgE-mediated anaphylaxis. cause of anaphylaxis The primary disturbance in anaphylactic shock is profound peripheral vasodilation (ie, distributive shock, as also seen with septic shock), which has the following effects: distributive shock Arteriolar vasodilation causes decreased systemic vascular resistance (SVR) and consequent hypotension. Venular vasodilation causes decreased central venous pressure (CVP) and reduces venous return to the right atrium. The vasculature becomes leaky, resulting in loss of intravascular volume that further contributes to both hypotension and decreased CVP. With reduced venous return to the right atrium, right ventricular output and blood delivery to the left atrium and left ventricle are reduced. This leads to decreased pulmonary capillary wedge pressure (PCWP), a reflection of left atrial pressure. Despite the reduced left ventricular preload, cardiac output is commonly normal or increased in early distributive shock due to both the large decrease in SVR and a baroreceptor reflex-mediated increase in heart rate (ie, tachycardia). (Choice B) Hypovolemic shock involves massive intravascular volume depletion, leading to decreased CVP and PCWP. SVR is reflexively increased in response to reduced cardiac output and hypotension. Hypovolemic shock (Choice C) Obstructive shock most commonly involves an obstruction to blood flow between the right atrium and the pulmonary capillaries (eg, pulmonary embolism). CVP is increased, PCWP is decreased, and there is a reflexive increase in SVR. Obstructive shock (Choice D) Cardiogenic shock results from left ventricular failure. CVP and PCWP are increased due to backward transmission of increased pressure, and there is a reflexive increase in SVR. Cardiogenic shock Educational objective: Anaphylaxis and anaphylaxis-like reactions can cause distributive shock due to the widespread release of inflammatory mediators (eg, histamine) that incites massive peripheral vasodilation. Arteriolar vasodilation decreases systemic vascular resistance to cause hypotension, and venular vasodilation decreases central venous pressure and pulmonary capillary wedge pressure. References: The nomenclature, definition and distinction of types of shock. (http://www.ncbi.nlm.nih.gov/pubmed/30573009)

A 65-Year-Old Man with Exertional Chest Pain and an Abnormal