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Diagnosis Deconstructed: Solving Hypotension in 30 Seconds

Morchi, Ravi MD

doi: 10.1097/01.EEM.0000462408.94790.ca
Diagnosis Deconstructed

Dr. Morchiis an associate professor of emergency medicine at UCLA's David Geffen School of Medicine. Read his past columns athttp://bit.ly/MorchiCollection.

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A and B. After addressing airway patency and full entry to each hemithorax, assess circulation. Noting easy compressibility of the brachial artery by an external cuff, we diagnose “hypotension.”

Is the heart rate (HR) the cause? Poor tone to the brachial artery can be the result of low cardiac output from bradycardia or non-sinus tachycardia. The result of the latter is shortened diastolic LV filling time and coronary perfusion time, producing decreased LV end-diastolic volume (LVEDV) and subendocardial myocyte ischemia, respectively. Forward flow and arterial pressure drop. The treatment of HR-mediated hypotension is generally electrical.

Venous volume. Once it is determined that HR is not the culprit, move on to volume. A collapsing or flat IVC by ultrasound is a convenient indicator of low volume at every point upstream: RA, RV, pulmonary circuit, LA, and LVEDV. Low LVEDV translates to low CO.

Collapsing IVCs in the non-trauma patient represent external loss of plasma volume or peripheral redistribution from venodilation and capillary leak in sepsis. Crystalloid can be initiated, but think about hemorrhage. Serial bedside Hgb measurements and looking into the peritoneal and pleural cavities allow us to diagnose hemoperitoneum or hemothorax. The origin could be an undiagnosed solid organ injury days prior or spontaneous bleeding from an arterial aneurysm, vascular malformation, varix, or malignancy. Bloody needle aspirate of a fluid pocket is diagnostic. The retroperitoneum is difficult to visualize, but confirming a normal-sized aorta decreases the likelihood of spontaneous hemoretroperitoneum. Without this approach, intraperitoneal and retroperitoneal bleeding in the medical patient end up as delayed diagnoses.

Continuity of the thoracic circuit? If IVC volume appears adequate, the next question should be: Is this volume actually becoming LVEDV? There are a number of causes to obstruction of the circuit. The first to consider should be cavoatrial kinking from a displaced mediastinum in tension pneumothorax. The second is cardiac tamponade strangulating the cavoatrial junctions, RA, and RV. Impaired luminal filling at these points makes the IVC plethoric while LVEDV remains low. Tamponade accumulates slowly in most medical conditions, but acutely from a ruptured ventricle post MI or a perforated aortic wall in type A dissection. The latter case usually has a widened aortic root accompanying the pericardial effusion on ultrasound.

If no tamponade shows on ultrasound and the RV fills in diastole, other entities that may dissociate IVC from LVEDV include RV infarction, massive PE, intense pulmonary arteriolar constriction, or overinflated alveoli engorged with air under positive pressure ventilation in a patient with bronchiolar outflow limitations. Distended alveoli smash weak-walled capillary beds on all sides of them, creating a physical obstruction to pulmonary blood flow distalto the arteriole and precapillary sphincter. RV:LV ratios and septal flattening allows us to see the effects of obstructive shock in the pulmonary circuit.

Contractility. Once we are assured that LVEDV correlates with the IVC, we inquire about LV function. Short axis parasternal views with minimal change in systolic diameter can diagnose cardiogenic shock. Corroborative pulmonary findings should be noted. If the LV cavity decreases nicely in systole, then volume is leaving its lumen. Listen to the cardiac apex and anterior axillary line to exclude mitral regurgitation. Listen over the parasternal area for an acute VSD from septal rupture. Only then can we assume that volume is going out the aorta, rather than backwards or across into the RV. Listen over the left lower parasternal border and right upper sternal border for signs of acute aortic regurgitation at the LV outflow tract and aortic root, respectively.

With adequate HR, LVEDV, contractility, and competent valves, blood must be flowing up to the aortic arch. Pause here and recognize that easy compressibility at one brachial artery could be from low flow in this vessel alone. Consider an embolus or occluding intimal flap. Check another limb. Provided it too is low, this is unlikely to be pseudohypotension, and we can presume that the brachial artery tone represents its true lumen, not a localized obstruction.

Proceed distal to the artery toward arterioles. Diffuse loss of arteriolar tone allows blood to stream forward and exert less lateral force on the inside of larger upstream arterial walls. The result is easy compressibility and hypotension. Low SVR is sometimes corroborated by warm extremities and bounding pules. Feel for them. Most commonly from sepsis, it can also be the result of systemic histamine release, overdose of a vasodilating agent, fulminant hepatic failure, or loss of all sympathetic neural tone in cervical myelopathy. Severe acidemia from any cause, including direct mitochondrial toxins, will also vasodilate.

Running the circuit reveals the primary etiology to hypotension in most circumstances. It is useful even in multifactorial scenarios like sepsis mediating arteriolar vasodilation, anaerobic myocyte metabolism with LV impairment, and low LVEDV from peripheral redistribution in a venodilated state accompanied by capillary leak.

But recognize one thing. The HPI and ROS are not part of the deconstruction. Low brachial artery tone is a physical derangement, and should be deciphered using physical principles. Put aside the chief complaint for 30 seconds and run the circuit from great veins to arterioles. What you find may surprise you.

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