Cardiac Arrest

BACKGROUND

Every year in the US, we see 350,000 out of hospital and 290,000 in-hospital cardiac arrests. Adult Cardiac Life Support (ACLS) guidelines standardize treatment across all patients and throughout care environments, but may not provide optimal resuscitation for each individual patient. Despite efforts to translate research as quickly as possible, like any publication, ACLS guidelines are based on an average of > 10 year-old evidence.

Point-of-care ultrasound (POCUS), as always, is used to answer focused questions. Should I continue chest compressions or call the code? Is there a reversible cause of arrest that I can intervene on? Are my chest compressions effective? Resucitative ultrasound provides specific prognostic and diagnostic information for your patient in arrest and can guide the quality of chest compressions delivered.

PROGNOSTIC USES

When we are managing a patient in cardiac arrest, a prominent constant thought is “should I continue chest compressions or call the code?” Sometimes this is easy. The patient with obvious signs of non-survivable death, with rigor mortis or dependent livido should not be submitted to chest compressions. AAA with rupture seen on point of care ultrasound, unless caught exceedingly early, is not survivable.

For patients without an obvious non-survivable condition, point of care ultrasound can differentiate true cardiac standstill from pseudo-pea — cardiac activity on ultrasound with no palpable pulse. (Blaivas 2001, Tayal 2004, Salen 2005, Paradis 1992, Prosen 2010).

Until a firm definition of cardiac activity in arrest was established by the REASON study, there was considerable variability in interpretation of cardiac standstill in arrest. (Bocka 1988, Gaspari 2016, Hu 2017) Cardiac Activity is defined as:

Any visible movement of the myocardium, excluding movement of blood within the cardiac chambers or isolated valve movement“

You can see in this clip that in standstill there truly is no cardiac activity as defined above noted.

Patients with pseudo-PEA with no pulse but cardiac activity on ultrasound can further be spread along a specrtum from strong/organized cardiac activity and those with weak/disorganized activity. All of these patients are essentially in a state of profound shock. Patients with stronger/organized cardiac activity, have better survival, especially with vasopressor use as demonstrated in the REASON 2 trial (Gaspari 2017).

Some of the pitfalls to look for are false positives of isolated valve movement and movement due to mechanical ventilation. False negatives can be seen with profound bradycardia and the weak / disorganized cardiac activity demonstrated above.

DIAGNOSTIC US IN ARREST

For patients with pseudo-PEA, ACLS asks us to consider the Hs and Ts of reversible etiologies of cardiac arrest. Several of these (in yellow below) are easily assessed for with ultrasound.

Fine Ventricular Fibrillation. Very fine VF may not be seen on monitor tracings (Amaya 1999). This can be seen on surface echo, and will be much more apparent using transesophageal echocardiography. Unfortunately the ultrasound of a patient in Ventricular Fibrillation is like the chest x-ray of a tension pneumothorax. Stop scanning. Defibrillate. Continue your resuscitation.

Cardiac Tamponade. One of the highest value findings in arrest is pericardial effusion suggesting cardiac tamponade.

This is one of the truly helpful uses of the IVC. If the IVC is collapsed, your patient is not in tamponade, it will almost always be plethoric.

Again, when a reversible cause of the arrest is identified, just like VF, stop. Drain the effusion. Continue resuscitation.

Massive Pulmonary Embolism. We are accustomed to looking for signs of acute right ventricular strain when we are concerned for massive or submassive pulmonary embolism (PE). However, in cardiac arrest, there is substantial evidence that the RV will dilate in all cardiac arrest patients, not solely in arrest due to PE. (Berg 2005, Aagard 2017)

Because of this, in arrest, we look for direct evidence of venous thromboembolism — DVT in the legs, peri-catheter thrombosis, thrombosis in the IVC or clot-in transit in the right heart.

CPR QUALITY

While it is helpful to identify a reversible cause of arrest, and to know when to stop and when to press on, if you are not delivering effective chest compressions, you are not delivering oxygenated blood to the brain and more importantly to the coronary arteries.

The ability of well trained clinicians to perform CPR adequately has been shown to inconsistent with ACLS guidelines. (Abella 2005). The recommendations of the AHA include:

• Hand placement two fingers above xiphoid process
• Push hard and fast (depth of > 2 inches at a rate of 100-120)
• Minimize interruptions to chest compressions
• Change compressor every two minutes
• Use a CPR coach to monitor and improve all of the above.

CPR Quality Devices. Feedback pads that return information on depth and rate of compressions can be helpful. Mechanical compression devices like LUCAS and AUTOPULSE can deliver set rates and depths of compression.

End-tidal CO2 can be used as a physiologic marker of CPR Quality. If EtCO2 rises suddenly, your patient may have ROSC. If it remains less than 10 mmHg, then a change in depth or rate or compressor may be necessary.

Resuscitative TEE in Arrest. To assess CPR Quality without relying on a surrogate, only resuscitative TEE will give you the information you are looking for.

Optimizing Depth with resuscitative TEE in the mid-esophageal long axis view, you can see whether adequate force is being applied. The left ventricular walls should be completely apposed to maximize cardiac output with compressions.

Area of Maximal Compression Another variable unaccounted for in the AHA guidance above, is where compressions are being delivered. Unfortunately when the AHA hand placement recommendation is followed, only about 30% of patients will have chest compression over the left ventricle. The bulk of these patients will receive chest compressions over the aortic root or left ventricular outflow tract. In addition, the AMC has been shown to migrate during CPR in cardiac arrest. Both of these findings have the unfortunate consequence of obstructing any cardiac output which your CPR intended to generate and has been shown to result in lower arterial blood pressures, end tidal co2 and survivability. (Hwang 2009, Zanatta 2015, Shin 2007, Nestaas 2016, Cha 2013, Anderson 2016)

Optimizing AMC When the AMC is noted to be compressing the base of the heart / LVOT / Aortic root, move your hands laterally and inferiorly to move a few centimeters toward the apex with the goal of compressing the LV directly. Iterative repositioning should get you to the desired AMC.

In the absence of resuscitative TEE, clinicians must rely on systems like mechanical compression devices, CPR feedback pads, or surrogates like end-tidal CO2 levels to attempt to optimize their chest compressions. Although inexact, one can make a change in hand positioning and observe the effect on EtCO2 to see if you believe that an improvement was made.

COMMUNITY HOSPITAL RESUSCITATIVE TEE

Resuscitative TEE in Emergency Departments was first performed in a community hospital in 2008 and later shown to be both feasible and clinically influential. (Blaivas 2008, Arntfield 2016) The majority of Emergency Medicine (EM) Resuscitative TEE programs are found at large urban academic medical centers with EM residency programs and ultrasound fellowships.

However, a survey in 2022 showed that 10% (N=16) of EM TEE programs were found in community hospitals with no EM residency program. (Teran 2024)

REFERENCES

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MORE RESOURCES

Core Ultrasound – Cardiac Arrest Part 1 & Part 2