he is cool and clammy, with evidence of peripheral cyanosis and prominent jugular venous distension. Anesthesia has successfully placed an arterial line and initiated several fluid boluses while awaiting your arrival; however, there has been no significant improvement in his hemodynamics. You note that his systolic blood pressure on the arterial line appears to decrease by at least 10 mmHg during respiration. While you prepare the appropriate intervention, what would be the best next step to help confirm the likely diagnosis?Chest X‐rayCT angiogramCBCEKGTransthoracic echocardiogramThis patient is exhibiting signs of cardiac tamponade, with evidence of pulsus paradoxus, jugular venous distension, and hypotension. The primary tool for diagnosis of cardiac tamponade is Doppler echocardiography, which in the presence of tamponade typically shows a circumferential pericardial fluid layer and compressed chambers with high ventricular ejection fractions. On inspiration, both the ventricular and atrial septa move leftward and reverse on expiration, due to the fixed pericardial volume. Right ventricular collapse is typically less sensitive but more specific for tamponade. The inferior vena cava is typically dilated with minimal respiratory variation. CT angiogram may demonstrate pericardial effusion, distension of the superior and inferior vena cavae, and reflux of contrast material into the azygos vein and inferior vena cava. However, these represent static images rather than the dynamic information presented by echocardiography. Chest x‐ray may demonstrate an enlarged cardiac silhouette but is particularly unreliable in early/acute tamponade (choice A). Additionally, obtaining a CT scan is typically not portable, requiring transporting a hemodynamically unstable patient to obtain the study (choice B). A CBC would be of little use to obtaining this diagnosis (choice C). EKG may show evidence of pericarditis or electrical alternans but is unreliable in the diagnosis of tamponade (choice D).Answer: ESpodick DH . Acute cardiac tamponade. N Engl J Med. 2003; 349 (7): 684–90. doi: https://doi.org/10.1056/NEJMra022643. PMID: 12917306.12 A 27‐year‐old man presents after jumping from a diving board and striking the bottom of a pool with his upper body. On presentation, he has no sensation or motor strength of his lower extremities. On examination, he appears flaccid and you cannot elicit spinal reflexes. His heart rate is 54 beats/min, blood pressure 90/54, and respiratory rate 18. Despite appropriate fluid resuscitation, he remains hypotensive, though you identify no evidence of ongoing hemorrhage. What type of shock does this likely represent?ObstructiveDistributiveCardiogenicHypovolemicAnaphylactic This patient demonstrates bradycardia, hypotension, and neurologic deficits in the setting of possible cervical or high thoracic spine trauma, suggesting he may have a component of neurogenic shock. This shock is a result of spinal cord injury with sudden loss of sympathetic tone with preserved parasympathetic activity and autonomic instability, leading to bradycardia and hypotension. These changes are typically seen with an injury to the spinal cord above T6. Disruption of the sympathetic division of the autonomic nervous system affects three areas of the cardiovascular system: coronary blood flow, cardiac contractility, and heart rate. There is systemic hypotension due to a decrease in sympathetic fiber‐mediated arterial and venous vascular resistance, along with venous pooling and loss of preload, with or without bradycardia. The bradycardia is often exacerbated by suctioning, defecation, turning, and hypoxia. The hypotension places patients at increased risk of secondary spinal cord ischemia due to impairment of autoregulation. With preserved parasympathetic activity, this translates clinically into bradycardia (and possibly other cardiac arrhythmias) in the setting of profound hypotension. Trauma patients are hypotensive as a result of blood loss or intravascular hypovolemia but will mount an appropriate tachycardic response. Blood loss must be ruled out and treated appropriately before assuming that hypotension is due solely to spinal cord injury. It is common to have both blood loss and spinal cord injury. Initial management is composed of volume resuscitation to account for the increased intravascular space secondary to increased vasodilation, as well as vasopressors for blood pressure control. In addition to pressor support, chronotropic and inotropic support may be necessary. Norepinephrine is started initially but in refractory cases, epinephrine and vasopressin infusions may be required. Bradycardia usually responds to atropine and glycopyrrolate but in severe cases, dopamine infusion is required. When blood loss is a part of the presentation, volume resuscitation should be with blood products and not crystalloids. Spinal shock is often confused with neurogenic shock. Spinal shock, on the other hand, refers to loss of all sensation below the level of injury and is not circulatory in nature. Both may, however, coexist in a patient.Answer: BStein DM, Knight WA . Emergency neurological life support: traumatic spine injury. Neurocrit Care. 2017; 27 (Suppl 1): 170–180.Phillips AA, Krassioukov AV . Contemporary cardiovascular concerns after spinal cord injury: mechanisms, maladaptations, and management. J Neurotrauma. 2015; 32 (24): 1927–42. doi: https://doi.org/10.1089/neu.2015.3903. Epub 2015 Sep 1. PMID: 25962761.
13 Shock is defined as:Blood pressure less than 90 mm Hg.Heart rate greater than 140 beats/min.Urine output less than 0.5 ml/kg/hr.Inadequate perfusion to meet end organ metabolic needs.All of the above.Shock is defined by some as inadequate perfusion to meet end organ metabolic needs. Tissue and cellular hypoxia can be due to inadequate delivery, increased consumption, inadequate utilization, or a combination of these states. Although this is often reflected in hemodynamic changes such as hypotension, tachycardia, or oliguria, these are not sufficient criteria alone to diagnosis a patient as being in shock. A patient may present hypertensive, normotensive, or hypotensive. Conditions such as neurogenic shock may result in a patient with bradycardia despite inadequate perfusion. Shock can be further differentiated into hypovolemic, cardiogenic, obstructive, or restrictive (vasodilatory/distributive). Causes of obstructive shock include pulmonary embolism, tension pneumothorax, and pericardial tamponade. Causes of obstructive shock typically lead to decreased cardiac output and are sometimes included into the cardiogenic shock category. Identification of these sub categories of shock is crucial to guiding therapeutic intervention.Answer: DKislitsina ON, Rich JD, Wilcox JE et al. Shock ‐ classification and pathophysiological principles of therapeutics. Curr Cardiol Rev. 2019; 15 (2): 102–113. doi: https://doi.org/10.2174/1573403X15666181212125024. PMID: 30543176; PMCID: PMC6520577.Vincent JL, De Backer D . Circulatory shock. N Engl J Med. 2013; 369: 1726.
14 A 53‐year‐old woman with a history of ulcerative colitis controlled with 50 mg of oral prednisone daily undergoes a laparoscopic converted to open colectomy. Intra‐operatively there are no complications noted and she receives appropriate fluid resuscitation. However, post‐operatively she is noted to be febrile and hypotensive. This hypotension is refractory to additional fluid boluses or multiple vasopressors. On physical examination, her abdomen does not appear distended and she is appropriately tender. What would be the best next step in management of this patient?Additional fluid boluses.Adding on an additional vasopressor.Return to the operating room for exploration.Administer stress dose hydrocortisone.Begin broad‐spectrum antibiotics.This patient with a history of chronic adrenal suppression due to daily prednisone use presents with signs and symptoms consistent with an adrenal crisis. These events are typically brought on by an inability for the body to mount an appropriate response to an insult by generating endogenous cortisol secondary to chronic adrenal suppression. Unless administered appropriate exogenous glucocorticoids, they may exhibit evidence of hypotension refractory to typical interventions, abdominal pain, nausea/vomiting, and confusion. Additional fluid boluses or adding an additional vasopressor would not address the underlying pathology and has already been described as unsuccessful in this vignette (choices A, B). Initiating broad‐spectrum antibiotics similarly does not address the underlying issue and would have no impact on this patient’s hemodynamics (choice E). Septic shock would most likely develop later and not immediately. While a hypotensive patient post‐operatively may be due to blood loss and ultimately require return to the operating room for exploration, in this case, failure to recognize the underlying adrenal crisis would result in unnecessary re‐exploration (choice C).Answer: DRushworth RL, Torpy DJ, Falhammar H . Adrenal Crisis. N Engl J Med. 2019; 381 (9): 852–861. doi: https://doi.org/10.1056/NEJMra1807486. PMID: 31461595.
15 A 71‐year‐old patient has acute, non‐perforated appendicitis. His BMI is 27 and otherwise
