Case of the Week: Shortness of Breath and Nausea
Author: Christian Gerhart, MD
Reviewer: Jessica Pelletier, DO
You are working a day shift in pod 2 of the emergency department (ED). The triage note is below:
“Patient to ED…[brought in by EMS] (BIBEMS). Patient arrives with shortness of breath and N/V. Which began 3 days ago. Patient states she was recently seen for the same reason. Patient has a PMHx of asthma and seizures. Patient 98% on room air. VSS”
Her vitals are:
RR: 18 BPM
HR: 117 BPM
T: 36.7 C
BP: 112/87 mmHg
O2 sat: 97% RA
She reports having worsening chest pain, upper abdominal pain, and shortness of breath over the past 2-3 days. The chest pain is midsternal, constant, and pleuritic. She also describes an episode of non-bloody, non-bilious vomiting yesterday. The patient says she was recently admitted to another hospital for breathing problems but never really felt better. She has a history of asthma with prior need for BIPAP but no history of intubation. The patient also has heart failure with preserved ejection fraction. You review her chart and see she was admitted to the ICU for an asthma exacerbation about a month ago. She had an outside ED visit for chest pain with a reassuring workup. Her CT PE at that time was negative for PE and showed a small pericardial effusion with mild cardiomegaly and dilation of the pulmonary trunk consistent with pulmonary hypertension.
On exam, the patient is awake, alert and speaking in full sentences but ill-appearing. Her extremities are warm with palpable peripheral pulses. She is tachypneic with mildly increased work of breathing, bilaterally diminished breath sounds and prominent expiratory wheezing. She has diminished but otherwise normal heart sounds. Her upper abdomen is tender. She has bilateral pitting edema to the mid shin.
What would your next steps be?
The patient is placed on the monitor and IV access is obtained. She is given albuterol, ipratropium and methylprednisolone for a possible asthma exacerbation. She receives IV hydromorphone for her upper abdominal pain. A chest x-ray, EKG, labs, and a CT PE + abdomen/pelvis with contrast is ordered to further evaluate her symptoms. The patient is reassessed and does not feel any better after the initial interventions. Her EKG and portable chest x-ray are shown below:
Figure 1 - EKG.
Figure 2 - Portable 1-view chest x-ray
What would your next move be?
The chest x-ray demonstrates significant cardiomegaly. No baseline is available for comparison. It is always challenging to interpret portable chest x-rays, but this is a clear finding. The patient’s EKG was notable for sinus tachycardia, poor R wave progression and borderline low voltage across the limb leads. If you look closely in the lead V1 rhythm strip there is an additional finding, which in retrospect gives another clue to the final diagnosis. Her repeat blood pressure was 99/61 mmHg and her heart rate was unchanged. Given the patient’s lack of improvement with additional interventions and chest x-ray findings, a bedside echocardiogram was performed (Fig. 3 and 4).
Figure 3 – Parasternal long axis view demonstrating a very large, circumferential, pericardial effusion.
Figure 4 – Representative IVC view demonstrating with a dilated, non-collapsible IVC. Image from Radiopedia.
Although it was challenging to assess for sonographic tamponade with the actual windows obtained, the suspicion was that she was experiencing early tamponade physiology because of her tachycardia and low blood pressure. Cardiology was emergently consulted for drainage. A 500 mL bolus of lactated ringers (LR) was given as a temporizing measure. The patient was transferred to the critical care pod in the ED and an arterial line was placed, at which time her BP was found to be 86/57 mmHg. Shortly afterwards, cardiology took the patient to the catheterization lab for pericardiocentesis and pericardial drain placement. There was 1.2 L of bloody output upon insertion. The patient was admitted to the cardiac ICU (CCU) and did well. At the time of discharge, the cause of her pericardial effusion was still unclear.
Pericardial Tamponade
When discussing tamponade, we should distinguish between traumatic and atraumatic tamponade. In trauma patients (typically) penetrating trauma) a small amount of blood in the pericardial sac collecting over a short period of time can lead to hypotension and death. The treatment of traumatic pericardial tamponade is surgical. Pericardiocentesis is not preferred (unless perhaps you are somewhere without a surgeon) since this does not address the underlying injury and it is likely that the blood will reaccumulate shortly. Additionally, if there is clotted blood, it is often ineffective to attempt drainage with pericardiocentesis.
Atraumatic pericardial effusions have a number of different potential etiologies. The most common is malignancy, followed by infectious/inflammatory, and hemorrhagic. A few key causes to consider in the ED are acute myocardial infarction with wall rupture and ascending aortic dissection extending into the pericardial space. A special case is post-surgical tamponade. In patients with recent cardiac surgery the transthoracic echocardiogram is unreliable, as there may be focal clotted blood pushing on the heart. Even a small amount of blood can be clinically significant. These patients may need a transesophageal echocardiogram and certainly need a discussion with their surgeon if there is any suspicion for tamponade.
Pericardial effusions exist on a spectrum from a small, inconsequential effusion to a large effusion with hemodynamic consequences. However, it is not always easy to make this distinction. Patients often have other medical conditions that cloud the picture such as pulmonary hypertension, infection, and hypo- or hypervolemia. Additionally, there are many patients in whom a pericardial effusion is a bystander to the underlying problem causing their acute symptoms. All this being said, there are a few characteristics that should make us concerned that a pericardial effusion is causing tamponade, or at least contributing to the patient’s clinical picture. First, rapid accumulation of fluid can lead to rapid progression of tamponade. In the acute setting (such as trauma) as little as 50 mL of blood can lead to hemodynamic collapse. A key concept to remember is that it is the pressure, not the volume, that leads to tamponade physiology. When an effusion accumulates over days to weeks, as in our patient’s case, an enormous amount of pericardial fluid can accumulate with minimal hemodynamic effects. Larger amounts of pericardial fluid place patients at risk for tamponade. If we see a circumferential pericardial effusion on ultrasound, especially if the diameter is >2 cm measured at end-diastole, this should make us seriously question if the patient has or is at risk of progressing to tamponade. Have a low threshold for discussion with cardiology in any patient with a large pericardial effusion if there is any concern for clinical or sonographic tamponade.
The presentation of pericardial tamponade can be vague and non-specific. However, the most common symptom is dyspnea. In retrospect, this patient’s EKG with low voltage and electrical alternans was classic for tamponade. Chest x-ray can show cardiomegaly (as in this case), though this is not sensitive or specific. Most patients with tamponade will have either tachycardia or tachypnea. Caution should be taken in patients on beta blockers as they may not mount a tachycardic response to tamponade. Hypotension is a late finding.
This case of pericardial tamponade is an excellent illustration of the power of bedside ultrasound. Unless the etiology is immediately clear, any patient with dyspnea who is ill-appearing needs a bedside ultrasound sooner than later! The diagnosis of tamponade can be made in seconds. Recall that we need to distinguish between clinical tamponade and sonographic tamponade. It can be challenging to decide who is in clinical tamponade as there are no clear diagnostic criteria and we must use our gestalt and take into account the entire clinical picture. Clinical tamponade is evidenced by signs of hypoperfusion, such as hypotension, elevated lactate, and cool extremities. You may see evidence of pulsus paradoxus on the pulse oximetry or arterial line tracing. Sonographic tamponade will be discussed below.
Ultrasound Findings in Pericardial Tamponade
As previously mentioned, larger effusions are associated with a higher risk of tamponade. Circumferential pericardial effusions are more concerning. One of the earliest findings in tamponade is right atrial systolic collapse. This is best visualized on the apical four chamber view. The specificity is unclear but the sensitivity when signs of clinical tamponade is present is thought to approach 100%. Right ventricular diastolic collapse is thought to have a lower sensitivity (around 50%) but a higher specificity (approximately 80%) for identifying tamponade as compared with right atrial systolic collapse. Evaluation for right ventricular diastolic collapse is best accomplished in the apical four chamber view, though any view in which the AV valves and RV free wall can be visualized may be adequate. Finally, a dilated, minimally collapsible IVC is almost always seen in patients with tamponade, and the sensitivity is estimated to be approximately 95%.
Recall that Cardiac Output = Heart Rate x Stroke Volume. Remember that patients with tamponade have decreased preload due to compression of the RV by their effusion. They are extremely preload-dependent. We can increase their stroke volume by addressing their preload. Temporizing measures include judicious IV fluids and vasopressors. Another option for increasing cardiac output is optimizing their heart rate. In a patient without compensatory tachycardia, chronotropic therapy with isoproterenol or epinephrine can be considered. Positive pressure ventilation can be deadly in these patients, as it can drop their preload and thus cardiac output precipitously. Be very, very careful about intubating a patient with tamponade. Do whatever you can to attempt drainage of the effusion before intubation.
Pericardiocentesis
At our institution we have cardiology immediately available, and it is less common for us to need to perform this procedure. However, if we do need to do it, there are a few different approaches. For those who are facile with ultrasound, a parasternal long axis ultrasound-guided approach is generally preferred. This allows for needle guidance and active avoidance of key structures such as the lung, liver, and internal mammary arteries. A subcostal approach can be considered, especially in patients who are in cardiac arrest, though this has a higher risk of liver injury. This can be performed either with or without ultrasound guidance. Consider ketamine as your sedative agent and be generous with local anesthesia. Keeping the patient’s bed elevated to 30-45 degrees can help prevent posterior layering of the effusion. If you choose to use ultrasound, the linear or curvilinear probes are preferred for needle guidance compared to the phased-array probe. In the ED, we have a few options in terms of which materials to use. A triple lumen central line kit can be utilized if available. If the effusion is very deep relative to the skin on ultrasound, then a long spinal needle can be considered. Another option is a single lumen central line kit. If possible, it is probably ideal to leave a catheter in the pericardial space until the patient goes to the procedural suite for drainage. The utmost care should be taken to use sterility during the procedure and ensure that any catheter left in the pericardial space remains sterile!
Northwestern EM has an excellent post on the procedure itself: https://www.nuemblog.com/blog/pericardiocentesis#:~:text=An%20emergent%20pericardiocentesis%20may%20be,is%20known%20as%20cardiac%20tamponade.
Ultimately, patients will need a pericardial window, typically performed by a thoracic surgeon, to prevent recollection of the pericardial effusion and recurrent tamponade. This definitive treatment can be performed after emergent drainage of the effusion via pericardiocentesis.
Take-Home Points
● Patients with dyspnea but no immediately obvious cause should undergo bedside cardiac ultrasound
● Clinical pericardial tamponade presents with shortness of breath, hypotension, tachycardia, and tachypnea
● Tamponade develops when the pressure in the pericardial space impedes cardiac output (so rapidly-collecting pericardial effusions are higher risk)
● Avoid positive-pressure ventilation prior to drainage of the effusion
● Temporizing measures include IV fluids and vasopressors
● Patients need drainage of the effusion via pericardiocentesis emergently, ideally via ultrasound guidance
References:
1) Alerhand S, Adrian RJ, Long B, Avila J. Pericardial tamponade: A comprehensive emergency medicine and echocardiography review. Am J Emerg Med. 2022;58:159-174. doi:10.1016/j.ajem.2022.05.001
2) Farkas, Josh. Internet Book of Critical Care. Pericardial Tamponade. 2021.
3) Feiger, D. Ibiebele, A. (2021, Feb 8). Pericardiocentesis. [NUEM Blog. Expert Commentary by Schimmel, D]. Retrieved from http://www.nuemblog.com/blog/pericardiocentesis.