Triage: This is where he arrested. Arriving by private vehicle, his family carried him into the waiting room where he would soon take his last few breaths. The nurse glanced at a diaphoretic, stuporous, bradypneic, and pale young man, and called back to the main ED that she was wheeling in a critical. By the time they had him in a wheelchair, he stopped breathing and had no pulse.
Bed one: This is where he was resuscitated. A few seconds later, he was hoisted onto a gurney, chest compressions and bag mask ventilation initiated. Intubation was uneventful, and breath sounds were equal with full chest rise. He was not difficult to bag. Resistance to airflow from the tracheobronchial tree, alveoli, or surrounding pleural space was not the cause of arrest. Cardiac rhythm was wide and slow. Ventilation and epinephrine brought return of a narrow-complex tachycardia and a measurable blood pressure.
Hypotension. His pulses were bounding as his MAP read 40. IV fluids and norepinephrine were ordered. Conversations across the bed were about whether he had a PE or a massive MI, cardiac, tamponade, or sepsis.
Physical exam. The patient is a well developed young man with no trauma or inflammation to his head or neck. His suprasternal notch and carotid pulsations were bounding and hyperdynamic. Point of maximal cardiac- impulse was vigorous but not displaced. No murmur or rub could be detected. His abdomen was soft, and his GU area was normal. His back was unremarkable. Although he was diaphoretic, he was cool, not warm. A notable finding, his left upper extremity was edematous, from the dorsum of his hand all the way to his mid-upper arm. Minimal pitting. No warmth. No induration. No skin changes.
Upper extremity DVT? “Pulmonary embolus” was thrown around by the doctors, and the nurses were nodding their heads in agreement. The idea was to get him to CT, and prepare thrombolytics if his blood pressure did not respond to volume and vasopressors.
Traditional ultrasound. We noted dynamic myocardium, no pericardial effusion, and a flat IVC. We pushed for more fluids, and the family was called back to get a history.
They claimed he had been active and well until two days earlier. He had been complaining of pain in his left hand. It was a little swollen, but it didn't stop him from continuing to work construction or from performing any of his daily activities. That afternoon, he had noticeable trouble breathing. He became difficult to arouse so his family drove him to the ED.
I suppose this sounds like a pulmonary embolus. The history fits. The extremity exam fits. But one thing does not fit.
Bounding pul-ses. Immediately post-resurrection, at a MAP of 40, his pulses were bounding. Not weak, feeble, or thready as in a cardiogenic or obstructive form of shock. Bounding. Rechecking his pulses now, while at a MAP of 70 on 20 micrograms/minute of norepinephrine, they were less impressive. But that brief moment post-resuscitation carries a clue to his hypotension. The more marked the hypotension, the more meaningful this clue becomes.
In the absence of unstable tachy- or bradyarrythmia, all known causes of hypo-tension should fall to one of only a few categories.
Decreased volume in the left ventricle at end diastole (LVEDV). The left ventricle has little to work with at the start of systole, little to pump forward. Low left-ventricle volume could be from an impediment to blood flow somewhere upstream. Obstruction at the confluence of the great veins and right atrium arises from strangulation by cardiac tamponade or kinking by mediastinal shift with increased pleural pressures. Primary right ventricle pump failure or a proximal or widespread obstruction to pulmonary arteries will also deprive the left ventricle of end-diastolic volume. More commonly, low LVEDV is from low volume in the entire body, venous system and intracellular space, where there has been blood loss or dehydration.
Decreased left ventricle contractility. If volume is not the issue, left ventricle function can be so poor that it does not pump what it is given because of myocardial ischemia, infarction, or inflammation. Alternatively, acute valvular incompetence negates forward flow despite a vigorously contracting myocardium.
Arteriolar relaxation. If volume and left ventricle contractile function are not the main culprits, then blood makes it through the left ventricle outflow tract and into the aorta. Poor tone within the brachial artery in this case is not from a hypovolemic, cardiogenic, or obstructive cause. The only other locale to focus on now is the arteriole distally. Widespread loss of arteriolar tone means red blood cells stream through the lumen of the vascular tree, with little in the way of lateral forces against the vessel wall. The result is an easily compressible brachial artery when a blood pressure cuff is applied. Pulses in this last case can be feeble, normal, or bounding.
Our ultrasound showed no tamponade strangulating inflow to the right heart, no distension of the IVC characteristic of failure of the right heart or obstruction to pulmonary blood flow as the sole cause of hypotension, and a dynamic left ventricle myocardium whose cavity in systole is completely obliterated in a patient without a murmur to indicate regurgitant flow. In this case, whatever central volume the patient has, it must be flowing forward through the thoracic circuit and out into the aortic root. We are left following it out to arterioles.
Distributive shock. Despite adequate volume, transthoracic flow, and cardiac function, the inadequate distribution of nutrients is such that red blood cells released into the aortic lumen cannot bring oxygen to mitochondrial membranes. Mitochondria themselves may not be prepared to use that oxygen.
Loss of arteriolar tone redirects blood away from vital organs and to the peripheral circuit. Systemic loss of sympathetic tone from a cervical or high thoracic cord lesion should always be considered. But the majority of cases fall to inflammatory mediators of sepsis. Many patients are concomitantly hypovolemic, and accompanying arteriolar dilation in these instances is a loss of venous tone with peripheralization of whatever venous volume remains. The combination is visible to us as a flat IVC on ultrasound.
Distributive shock, our patient has this. Despite his history of present illness and a swollen limb, his pulses and ultrasound findings do not support obstructive shock from the type of massive pulmonary thromboembolus required to produce a mean brachial artery tone of 40.
Less traditional ultrasound. At the bedside, we see compressible axillary and brachial veins in his edematous limb. Nothing to support upper extremity DVT. Traveling down the arm, we notice something: The extensor muscle compartments of his forearm are not normal. Fiber architecture is distorted, there seem to be hyper- and hypoechoic areas within the muscle, and the compartment is much larger when compared with ultrasound images from the other side.
Myonecrosis as a source for septic shock? We called our surgical consultants who made a lateral skin incision at the bedside, exposing the extensors. Opening the fascia revealed the muscle to be necrotic. He went immediately to the operating room where, despite debridement and thereafter amputation, he expired on hospital day 2.
He did not have a necrotizing fasciitis but rather a necrotizing myositis. It was contained for whatever reason by intact fascia; there were no skin findings. Quite commonly fatal, the inflammatory cascade that follows results in diffuse arteriolar dilation, redirection of arterial blood flow away from vital areas, peripheralization of venous volume, and a poisoning of mitochondrial membranes, impairing their use of whatever oxygen happens to percolate their way.
The severe acidosis that follows means a further loss of vascular tone, cardiac conduction, and contractility. Skin warm or cold, pulses bounding or feeble, the patient is now hypotensive. Eventually mentation declines and a depressed ventilatory drive adds a respiratory component to the marked metabolic acidosis. Cardiac and vascular function acutely decline from the now combined acidosis, and the patient turns pulseless. With intubation and correction of the respiratory component, he has return of spontaneous circulation, and is back to the state of hypotension dictated by his metabolic derangement alone. Unfortunately, in this case, he lived only long enough for us to find the cause.
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