An air medical team is enroute to the emergency room of a community-based hospital for a 55-year-old male who presented with hypotension and severe (10 on a scale of 0 to 10) “tearing” back pain. He had been discharged a short time earlier from the same facility with a diagnosis of “lumbar strain.” Further evaluation and workup reveals a Stanford “Type A” (see “Emergencies of the Aortic Kind”) aortic dissection. Flight time to the referral center will be approximately 15 minutes.
Upon arrival of the transport team, the patient appears to be in extremis. He is dyspneic with dusky nail beds and circumoral cyanosis. His current vital signs include a heart rate of 124 beats per minute, respiratory rate of 22 breaths per minute and labored; a blood pressure of 82/66 and an oxygen saturation of 91 percent by face mask. A bedside ultrasound performed by the referring physician reveals excess fluid within the pericardial sac.
Clinical examination of this patient alone suggests shock. He is in need of immediate stabilization prior to packaging for transport.
Most clinicians would agree upon the treatment needed but what if there were no one available to perform the procedure? What if the referring physician’s specialty was family medicine instead of emergency medicine and is not comfortable, or capable of appropriately stabilize this patient prior to transport? If no one is able to accomplish “plan A,” are you as an air medical provider able to formulate and implement an effective “plan B?”
A different type of “cardiogenic” shock: Diagnosis and the pathophysiology
Depending on the textbook one decides to reference, this particular patient’s shock state could be classified as “obstructive” or “cardiogenic.” It is safe to say that neither classification is wrong. What is important at this particular point in time is recognizing what is occurring and why, and performing appropriate management in order to move this patient to definitive care.
One potential complication of an aortic dissection involving the proximal aorta is the movement of blood in a retrograde fashion. This can eventually fill the pericardial sac and cause impingement on ventricular filling and ejection.
Clinical manifestations of this phenomenon are in response to autonomic nervous system (ANS) compensation attempting to overcome decreased stroke volume and cardiac output related to the obstructive process.
The most well known set of clinical signs are referred to as “Beck’s Triad,” and include:
1. Jugular venous distention
2. Muffled heart tones
3. Narrowing pulse pressure
Additionally, ANS response will include tachypnea, tachycardia and decreased peripheral perfusion in an attempt to increase oxygen delivery to vital tissues6. Pulsus “Paradoxus” (changes in the strength of peripheral pulses secondary to the patient’s respiratory cycle) and “Alterans” (changes or alteration in ECG amplitude or voltage) may occur as a result of excess strain on the myocardium1. The patient may also present with altered mental status and widened mediastinum on chest x-ray3.
Laboratory values may reveal a patient in respiratory alkalosis secondary to tachypnea or metabolic acidosis with increased base deficits secondary to reduced perfusion and cellular oxygenation.
If the latter is the case, expect an increased serum lactate level and reduced central venous oxygenation (ScvO2). The patient may also present with electrolyte derangements such as hyperkalemia and hypocalcemia as well as alterations in blood counts and coagulopathies (a distinct possibility secondary to the original diagnosis of aortic dissection).
If invasive monitoring is in place, expect a dampened arterial waveform and visual verification of pulsus paradoxus. Central venous pressure (CVP) and pulmonary capillary wedge pressure (PCWP) will increase as chamber pressures within the heart begin to equilibrate1. Systemic vascular resistance (SVR) will rise in response to decreased stroke volume and cardiac output.
Management
Most sources would agree that immediate management and stabilization of this type of shock (“plan A” in our scenario above) is to remove some excess fluid from the pericardial sac, thus relieving pressure on the left ventricle.
The fastest and easiest method to accomplish this is to do a pericardiocentesis5,7. Oftentimes, as little as 10 to 20 ml of fluid aspiration is all that is needed to relieve shock secondary to tamponade.
This procedure is not without risk (e.g., embolism, infection, laceration of other organs or coronary circulation, inducing lethal cardiac arrhythmias to name several6). Additionally, not all air medical transport programs are credentialed to perform this procedure.
While often done in the past as a blind procedure, many advocate the use of ultrasound or 2-D echocardiogram-guided pericardiocentesis7. The ready availability of bedside ultrasound has shifted the standard of care from pericardiocentesis and bedside pericardial windows from a blind to and imaging guided procedure.
As many air medical programs are discovering the benefits of sonography, this technology may be beneficial in assisting with this infrequent and sometimes precarious procedure. Further study may shed light on this idea. Other surgical procedures (such as tamponade relief via thoracotomy) are generally reserved for patients suffering from penetrating chest trauma4.
“Plan B,” while merely palliative may be effective in buying time in order to get to a surgeon (remembering that this patient is suffering from a dissection of his ascending aorta).
This plan would involve measures that would improve preload and thus, stroke volume as well as cardiac contractility. While this therapy definitely has limits with respect to the pathophysiology of cardiac tamponade, it may stabilize the patient enough to allow him to be safely transported.
Volume resuscitation with isotonic crystalloid is mainstay treatment for increasing preload7,9. Invasive monitoring (such as CVP) may help to guide therapy, although it is important to recognize that central pressures will be rise precipitously, reflecting the degree of tamponade.
These high values should not preclude judicious volume infusion, especially when other parameters, such as mean arterial pressure (MAP) or urine output, suggest hypoperfusion. One study suggests that the use of a hypertonic saline-dextran solution may be of some value over a traditional isotonic crystalloid in improving end-organ perfusion in patients suffering from tamponade8.
Improved intravascular volume expansion, increased preload and a reduction in afterload secondary to vasodilatation of mesenteric resistance vessels were all reported as a result of this therapy. While showing promise, this study was unfortunately limited to animal models. Further research is needed in order to validate its efficacy in humans.
Additionally, medications that provide cardiac contractility and reduced SVR may temporarily assist the failing heart secondary to obstruction. While controversial, a continuous infusion of a medication such as dobutamine may offer improved stroke volume and afterload reduction. Caution should be exercised as this medication could exacerbate hypotension7. Again, if it looks and smells like cardiogenic shock, you should treat it as such until you can get the patient to surgical intervention2.
Patient disposition
The patient in our above scenario initially responded to 500 ml of isotonic crystalloid. His systolic blood pressure rose and stabilized to the mid-90’s for transport. He acutely decompensated upon arrival to the intensive care unit at the referral center. An emergent pericardial window was performed and the patient was taken several hours later to surgery. Unfortunately, he died in the operating room.
Conclusion
Pericardial tamponade is an emergent, life-threatening type of cardiogenic shock. It manifests as a result of numerous etiologies (an extension of an aortic dissection is merely one). It requires a keen clinical eye and quick decision making in order to appropriately stabilize and transport.
While most authors agree that relief of obstruction is the primary management goal, not all transport providers are able to perform this life-saving procedure. More often than not, those that are allowed to perform this procedure are only allowed to do so in response to impending or actual cardiac arrest. Understanding what is happening and how to provide palliation until definitive care can be established is crucial.
References
1. Darovic GO. Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application (3rd Ed.). 2002. Saunders. pp. 627-633.
2. Ellender TJ and Skinner JC. The Use of Vasopressors and Inotropes in the Emergency Medical Treatment of Shock. Emergency Medicine Clinics of North America (26). 2008. 759-786.
3. Gilon D (et. al). Characteristics and In-Hospital Outcomes of Patients with Cardiac Tamponade Complicating Type A Acute Aortic Dissection. American Journal of Cardiology (103). 2009. 1029-1031.
4. Keogh SP and Wilson AW. Survival Following Pre-hospital Arrest with on-scene Thoracotomy for a Stabbed Heart. Injury 27(7). 1996. 525-527.
5. Marx JA, Hockenberger RS and Walls RM (Eds.). Rosen’s Emergency Medicine: Concepts and Clinical Practice (7th ed.). 2010. Mosby-Elsevier. pp. 404-406.
6. Pollak AN, Murphy M, Lenk Stathers C, Pecora D, McEvoy MT and Rabrich JS (Eds.). AAOS: Critical Care Transport. 2010. Jones and Bartlett. pp. 331-333.
7. Seferovic PM (et. al). Management Strategies in Pericardial Emergencies. HERZ (31). 2006. 891-900.
8. Terajima K, Aneman A and Haljamae H. Haemodynamic Effects of Volume Resuscitation by Hypertonic Saline-Dextran (HSD) in Porcine Acute Cardiac Tamponade. ACTA Anaaesthesiologica Scandinavica (48). 2004. 46-54.
9. Thattakkat K and Zbaeda M. Life-Threatening Aortic Dissection with Cardiac Tamponade in a Healthy 15 Year-Old Male. Pediatric Cardiology (27). 2006. 624-627.
