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Cardiac arrest 

Cardiac arrest
Chapter:
Cardiac arrest
Source:
Focused Intensive Care Ultrasound
Author(s):

Gajen Sunthar Kanaganayagam

, Andrew Constantine

, and Susanna Price

DOI:
10.1093/med/9780198749080.003.0021

Introduction

Survival of in-hospital cardiac arrest in adults is approximately 24%, and 45% of these events occur in ICU. All resuscitation guidelines suggest that identifying and treating the underlying cause of arrest are vital. FoCUS is the only way to diagnose many of the potentially treatable causes of cardiac arrest at the bedside. When cardiovascular pathology is severe enough to cause cardiac arrest, FoCUS findings are frequently obvious, and information gained within this time can fundamentally change patient management.

FoCUS is now recommended as part of advanced life support (ALS) algorithms, provided that appropriately trained practitioners are available and that the images are acquired during the 5-s pulse/rhythm check without compromising high-quality cardiopulmonary resuscitation (CPR). Subsequently, formal echocardiography is valuable to guide ongoing management in the post-cardiac arrest setting.

This chapter will present how ALS-compliant FoCUS can help confirm the cardiac rhythm, diagnose reversible causes, and predict favourable outcomes during CPR. It will describe how to recognize severe hypovolaemia, cardiac tamponade, coronary artery thrombosis, massive PE, and tension pneumothorax, and when to intervene. It will conclude by introducing how echo can assist clinical management during post-resuscitation care.

Practicalities of FoCUS within advanced life support

Although seemingly simple, appropriate performance of FoCUS during resuscitation requires specific training and that the practitioner and team must respect the paramount importance of high-quality CPR, with regard to timing, interpretation, and communication of findings. Performing FoCUS during chest compressions is challenging, and therefore, imaging is recommended during the 5-s pulse/rhythm check. However, this imposes a strict time frame for image acquisition. Whereas some diagnoses may be readily apparent, it is likely that repeated acquisitions (and potentially different views) might be required in successive pulse/rhythm checks. Loops should be acquired prospectively and stored for review, allowing interpretation while high-quality CPR is ongoing. Echo modalities are limited to 2D (no Doppler), using qualitative estimation of cardiac function/chamber dimensions. Initially, a subcostal view is recommended, as this is the easiest, most reproducible to obtain and does not interfere with chest compressions or defibrillation pads. Where images are not achievable, the A4C and then parasternal views should be attempted. As with any imaging in the acute setting, FoCUS must be interpreted within the clinical context, taking into account resuscitative measures that have already occurred. Interpretation and communication are in line with other decision-making in ALS, with a binary rule-in/rule-out approach.

FoCUS and cardiac rhythm

In certain circumstances, FoCUS can be useful in determining the cardiac rhythm:

  • Where the ECG suggests asystole, echo may demonstrate coordinated cardiac activity, thus promoting ongoing resuscitative efforts. Whether ECG or echo is the gold standard for diagnosis of asytole in cardiac arrest remains to be determined.

  • Ventricular fibrillation (VF) appears on echocardiography as diffuse, asynchronous contractile myocardial activity. Although each minute of delay to defibrillation reduces the probability of survival to hospital discharge by 10%, whether defibrillating non-ECG detectable (fine) VF is as beneficial remains unclear. Focused echocardiography has been used to identify VF in rare cases of cardiac arrest where there are barriers to effective rhythm analysis.

  • Detection of output during arrest is generally performed by palpating central pulses; however, this is inaccurate in profound hypotension, and up to 45% of trained healthcare professionals are unable to perform an accurate assessment during cardiac arrest. Pulseless electrical activity (PEA) encompasses ‘true PEA’ (electromechanical dissociation: organized electrical activity associated with cardiac standstill) and ‘pseudo-PEA’ (no palpable pulse despite coordinated cardiac electrical and mechanical activity). Demonstration of pseudo-PEA can be used to support/encourage ongoing resuscitative efforts, as the outcome is likely to be better, in particular where a reversible cause is demonstrated (Figure 21.1).

  • Pacing devices continue to deliver energy during cardiac arrest until deactivated and will therefore potentially produce an electrical rhythm on a monitor without leading to coordinated cardiac contraction. This can be easily misinterpreted. Differentiating true PEA from pseudo-PEA remains important and is a potential role for FoCUS.


Figure 21.1 Diagnosis of pulseless electrical activity (PEA) using echocardiography. PLAX view using M-mode, demonstrating no cardiac motion despite the presence of coordinated electrical activity. The diagnosis is true PEA, or electromechanical dissociation (EMD).

Figure 21.1 Diagnosis of pulseless electrical activity (PEA) using echocardiography. PLAX view using M-mode, demonstrating no cardiac motion despite the presence of coordinated electrical activity. The diagnosis is true PEA, or electromechanical dissociation (EMD).

Differential diagnoses

The major use of FoCUS in cardiac arrest is to provide diagnostic information to guide management, including potentially lifesaving procedures such as pericardiocentesis, thrombolysis, volume resuscitation, or transfer for PCI. It is then used to guide post-resuscitation care.

Hypovolaemia

Hypovolaemia causing cardiac arrest is likely to be severe, and presence of any of the following echocardiographic parameters should raise suspicion of the diagnosis:

  • Hyperdynamic biventricular function

  • LVEDA <5.5 cm2/m2 of body surface area (BSA)

  • Small IVC at end-expiration (<1 cm spontaneously ventilating, <1.5 cm positive pressure ventilation), with variable respiratory change.

In the absence of ventricular pathology, a significant reduction in preload will result in hyperdynamic biventricular function, with low EDVs. However, there are other causes for these appearances. LVH and/or right ventricular failure/PHT may also result in the appearance of an unloaded LV with a low LVEDA. Here, left ventricular size does not correlate with potential volume responsiveness. IVC dimensions are affected by changes in intrathoracic pressure, and a number of parameters have been used to estimate potential volume responsiveness by determining changes in dimension in response to ventilation. Thus, a small/collapsed IVC may represent hypovolaemia, whereas a dilated IVC may have no predictive value for RAP, in particular in the context of cardiorespiratory disease. Here, causes other than hypovolaemia should be considered, including PE, tamponade, or acute myocardial infarction. However, volume resuscitation may still be indicated. Where hypovolaemia is suspected, US can be used as an extension to clinical examination to search for potential causes, including examination of the thorax (haemothorax) and abdomen (aortic aneurysm/visceral injury). Figure 21.2 describes some of the potential pitfalls when assessing volaemic status with echo.


Figure 21.2 Determination of volaemic status using echo—potential pitfalls. (a) Subcostal view, TTE showing a dilated, non-collapsing IVC in a patient with tamponade. This patient may respond to volume loading acutely. (b) PSAX view in a patient with right ventricular infarction (note the dilated right heart, compared with the left heart). This patient had a dilated, non-collapsing IVC but had been volume-loaded as the LV was small and non-dilated. However, they did not respond to volume loading. (c) A4C view in a patient with cardiogenic shock. The LV is dilated, with regional wall thinning (basal septum, arrow) and apical thrombus (asterisk). Despite the dilated LV, the patient was profoundly hypovolaemic and responded well to volume resuscitation. (d) Short-axis view (TOE) of the LV in a patient resuscitated from cardiac arrest. The patient was hypovolaemic, but the LV remained small, as it was encased in tumour (T). IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; T, tumour.

Figure 21.2 Determination of volaemic status using echo—potential pitfalls. (a) Subcostal view, TTE showing a dilated, non-collapsing IVC in a patient with tamponade. This patient may respond to volume loading acutely. (b) PSAX view in a patient with right ventricular infarction (note the dilated right heart, compared with the left heart). This patient had a dilated, non-collapsing IVC but had been volume-loaded as the LV was small and non-dilated. However, they did not respond to volume loading. (c) A4C view in a patient with cardiogenic shock. The LV is dilated, with regional wall thinning (basal septum, arrow) and apical thrombus (asterisk). Despite the dilated LV, the patient was profoundly hypovolaemic and responded well to volume resuscitation. (d) Short-axis view (TOE) of the LV in a patient resuscitated from cardiac arrest. The patient was hypovolaemic, but the LV remained small, as it was encased in tumour (T). IVC, inferior vena cava; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; T, tumour.

Cardiac tamponade

Cardiac tamponade arises from an increase in intrapericardial pressure, causing impaired chamber filling and/or emptying, thus negatively impacting cardiac function. As pressure (rather than volume) is important, development of tamponade relates to the rate of accumulation, rather than size of the collection per se. Although tamponade is a clinical diagnosis, the classical features of Beck’s triad are rarely obvious during resuscitation. The use of echocardiography to demonstrate the presence of a pericardial collection and study its haemodynamic significance is well described in the cardiological literature. Features of tamponade include a swinging heart, right ventricular diastolic collapse, right atrial systolic collapse, pseudo-SAM, an enlarged and non-pulsatile IVC, and exaggerated respiratory variation of cardiac chamber size and transvalvular flows.

In non-arrested patients, abnormal flows correlate well with clinical features. However, these are affected by interventions, including positive pressure ventilation, and may not be present at all in certain circumstances such as post-cardiac surgery. Demonstration of a pericardial collection in a patient with cardiac arrest (unless it is very small and/or another cause for arrest is immediately apparent) should lead to consideration of immediate pericardiocentesis. Intravascular volume resuscitation should be undertaken as a temporizing measure, even in the presence of a dilated and non-collapsing IVC.

Pericardiocentesis can be performed using echocardiographic guidance to determine the optimal approach, depth of the collection, and presence of the pericardiocentesis cannula in the pericardial space, confirmed with agitated saline (Figure 21.3). Finally, full aspiration of the collection can be monitored. Echocardiographic guidance is associated with fewer complications, although a major complication rate of 1.2% remains, including perforation of abdominal organs, coronary arteries, or cardiac chambers, pneumothorax, and death.


Figure 21.3 Echocardiography in tamponade. (a) Pericardial collection (P) compressing the whole heart, but in particular the RV which is slit-like. There are fibrinous strands seen within the collection, but when seen to this extent (minimal), they do not preclude attempted pericardiocentesis, in particular when associated with cardiac arrest. (b) Pericardiocentesis. A pericardial drain (arrowed) is seen in the pericardial collection (P), through which agitated saline has been injected (asterisk, *), confirming correct placement within the pericardial space. (c) TTE (A4C view) in a patient 12 hours post-mitral valve replacement. The mitral prosthesis is not clearly seen, and the right heart border is impossible to define. No echo features of tamponade were demonstrated using Doppler. TOE was performed to exclude a collection (see d). (d) TOE in the same patient as (c). A huge haematoma in the pericardial space (P) is seen compressing the right atrium and ventricle, so it becomes slit-like with functional tricuspid stenosis. Only a small amount of blood is seen passing into the right ventricle on colour Doppler (arrowed). LA, left atrium; LV, left ventricle; RV, right ventricle.

Figure 21.3 Echocardiography in tamponade. (a) Pericardial collection (P) compressing the whole heart, but in particular the RV which is slit-like. There are fibrinous strands seen within the collection, but when seen to this extent (minimal), they do not preclude attempted pericardiocentesis, in particular when associated with cardiac arrest. (b) Pericardiocentesis. A pericardial drain (arrowed) is seen in the pericardial collection (P), through which agitated saline has been injected (asterisk, *), confirming correct placement within the pericardial space. (c) TTE (A4C view) in a patient 12 hours post-mitral valve replacement. The mitral prosthesis is not clearly seen, and the right heart border is impossible to define. No echo features of tamponade were demonstrated using Doppler. TOE was performed to exclude a collection (see d). (d) TOE in the same patient as (c). A huge haematoma in the pericardial space (P) is seen compressing the right atrium and ventricle, so it becomes slit-like with functional tricuspid stenosis. Only a small amount of blood is seen passing into the right ventricle on colour Doppler (arrowed). LA, left atrium; LV, left ventricle; RV, right ventricle.

Myocardial infarction

Echocardiography is used in the diagnosis, monitoring, and risk stratification of coronary artery disease and its complications. With respect to cardiac arrest, certain situations warrant particular consideration. FoCUS may reveal RWMAs in the territory of one or more coronary arteries, suggesting new ischaemia (normal left ventricular wall thickness with hypokinesia, akinesia, or dyskinesia) or indicating prior myocardial infarction (left ventricular wall thinning, akinesia, or dyskinesia). Chest pain prior to arrest lasting >45 minutes with no RWMAs is unlikely to be of cardiac origin. By contrast, short episodes of ischaemia may not be associated with any RWMAs, and here echo cannot be used to exclude important coronary artery disease. Subtle RMWAs and advanced echo techniques (contrast/strain echo) are not the realm of FoCUS. However, obvious areas of non-functioning muscle within a suitable clinical context should raise the possibility of coronary artery thrombosis and consideration of urgent therapies such as PCI and avoidance of medications that increase cardiac oxygen demand. Important non-ischaemic conditions that may also be associated with RWMAs include dilated cardiomyopathy, pacing-induced dyskinesia, and Takotsubo cardiomyopathy.

Demonstration of a hyperdynamic LV in the context of a low output state raises the suspicion of a mechanical complication of acute myocardial infarction. Ventricular free wall rupture is a relatively rare complication, occurring in 0.2–2% of cases (Figure 21.4). However, it remains a catastrophic event, with a high mortality rate. Echo is the diagnostic tool of choice, but only a pericardial collection may be seen in up to 30%. Here careful scanning of the left ventricular free wall is indicated. Severe acute MR may result from acute myocardial infarction with PM rupture/dysfunction. The presence of a hyperdynamic LV in the context of cardiogenic shock and pulmonary oedema, together with a structurally abnormal MV (with the head of the PM visible prolapsing into the LA in systole), is diagnostic. Ventricular septal rupture may also complicate acute myocardial infarction. It is occasionally apparent using 2D echo, and colour Doppler is diagnostic. Isolated right ventricular infarction is uncommon, and features demonstrated using FoCUS are non-specific. Findings of a dyskinetic/akinetic RV with/without dilatation suggest the diagnosis. However, more advanced echo techniques are needed, and differentiation from other causes of right ventricular dysfunction can be challenging.


Figure 21.4 Cardiac rupture post-myocardial infarction. (a) Acute ventricular septal rupture (arrowed) in a patient post-cardiac arrest. (b) Ventricular free wall rupture in a patient post-acute myocardial infarction. The left ventricular wall (distal septum) is thinned and dyskinetic (arrowed). There is a small amount of fluid in the pericardial space. An incidental finding was a left atrial myxoma (asterisk) seen prolapsing across the mitral valve. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; VSR, ventricular septal rupture.

Figure 21.4 Cardiac rupture post-myocardial infarction. (a) Acute ventricular septal rupture (arrowed) in a patient post-cardiac arrest. (b) Ventricular free wall rupture in a patient post-acute myocardial infarction. The left ventricular wall (distal septum) is thinned and dyskinetic (arrowed). There is a small amount of fluid in the pericardial space. An incidental finding was a left atrial myxoma (asterisk) seen prolapsing across the mitral valve. LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; VSR, ventricular septal rupture.

Pulmonary embolism

PE accounts for around 5% of cardiac arrests (13% of those from a non-cardiac cause). Diagnosis allows initiation of potentially lifesaving procedures but should only be utilized for the initial diagnosis where the patient is too unstable to transfer for CT. In the presence of severe haemodynamic compromise (including cardiac arrest), physicians may have to rely solely upon the findings of bedside echocardiography and proceed to thrombolytic treatment without further investigations. Signs indicating PE as a possible diagnosis include evidence of right ventricular strain (right ventricular dilatation/free wall hypokinesis) or pressure overload (‘D-shaped’ LV during systole with a dilated, non-collapsible IVC), in the absence of significant left-sided or pulmonary disease (Figure 21.5). Despite clear limitations of FoCUS and echocardiography in the diagnosis of suspected acute PE in stable patients, PE leading to cardiac arrest is likely to be massive, resulting from occlusion of more than two-thirds of the pulmonary bed. Demonstration of a normal-sized and functioning RV in the context of cardiac arrest virtually excludes massive PE as the cause of arrest.


Figure 21.5 Right-sided pathology associated with cardiac arrest. (a) PLAX view demonstrating a dilated RV in acute PE. (b) M-mode showing a dilated RV and paradoxical septal motion (arrowed) in acute PE. (c) PSAX view demonstrating significant right ventricular dilatation, with a D-shaped septum. This patient had chronic right ventricular disease secondary to congenital heart disease. (d) A4C view immediately post-cardiac arrest showing opacification of the right heart due to massive air embolism (arrowed). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Figure 21.5 Right-sided pathology associated with cardiac arrest. (a) PLAX view demonstrating a dilated RV in acute PE. (b) M-mode showing a dilated RV and paradoxical septal motion (arrowed) in acute PE. (c) PSAX view demonstrating significant right ventricular dilatation, with a D-shaped septum. This patient had chronic right ventricular disease secondary to congenital heart disease. (d) A4C view immediately post-cardiac arrest showing opacification of the right heart due to massive air embolism (arrowed). LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle.

Pneumothorax

The sensitivity and specificity for LUS in the diagnosis/exclusion of pneumothorax exceeds that of plain chest radiography. Although if tension pneumothorax is suspected as a cause of cardiac arrest, this should be treated immediately by thoracocentesis; where the diagnosis is uncertain, then LUS can be helpful. In addition, where central venous access has been obtained during cardiac arrest, LUS may be used to demonstrate/exclude the presence of an anterior pneumothorax after line insertion. Features that should be sought have been well described in published guidelines and are detailed in Chapter 15 and include demonstrating the presence/absence of pleural sliding, A-lines, B-lines, the lung pulse, and the lung point. As with any US, knowledge of the potential pitfalls is vital to avoid misinterpretation.

Echocardiography and lung ultrasound in post-resuscitation care

In addition to the use of echo and LUS to improve diagnostic accuracy in the ALS setting, these techniques can be used to guide therapy in the post-resuscitation setting. Here the techniques used will extend beyond those of FoCUS, to include the whole range of echocardiographic modalities. Echocardiography can be used to define not only the underlying cause of cardiac arrest (including myocardial ischaemia/infarction, underlying pre-excitation/predisposition to arrhythmia, and severe acute valvular, aortic, and/or pulmonary pathology) and guide catheter laboratory/operating theatre interventions, but also to determine the pathophysiological consequences of the primary pathology, as well as the post-cardiac arrest syndrome. This is characterized by a systemic inflammatory response, and the echo features that should be sought (in addition to the underlying cause) are outlined in Chapter 25. These include potential requirement/tolerance to volume loading, myocardial support (including requirement for inotropic agents/avoidance of beta agonists/heart rate optimization and/or extracorporeal support), as well as estimation of LAP, PAP, and pulmonary vascular resistance and demonstration of interstitial oedema and the response to any therapies/interventions. The applicability of these more advanced echocardiographic techniques to the hyper-acute setting is not well validated. Great care must be taken to interpret findings in the clinical and pharmacological context of the patient, while appreciating the limitations of the technique itself. Recommendations are therefore that all patients should undergo a comprehensive echocardiogram by an expert as soon as possible after successful resuscitation.

Conclusion

Echo performed during cardiac arrest will be focused and must not interfere with delivery of high-quality resuscitation. Novices can learn FoCUS with excellent correlation to that seen by experienced practitioners in the arrest scenario. Training involves attendance at an appropriate course, followed by mentored practice and maintenance of a logbook. Of note, even experienced sonographers/echocardiographers need training in ALS-compliant imaging, in order to minimize interruptions to chest compressions and optimize communication with the resuscitation team. Nonetheless, this adjunct to resuscitation provides all personnel with the ability to rapidly change the focus and management of the cardiac arrest scenario. When more time is available, comprehensive echocardiography should be performed to help clarify uncertainties and look more specifically at cardiac physiology, in particular in the post-arrest setting.

Chapter 21

MCQs

Questions

1. The following echocardiographic findings raise suspicion of systemic hypovolaemia as the cause of haemodynamic collapse in a ventilated patient:

  1. A Hyperdynamic left ventricular systolic function

  2. B In the context of PPV, an IVC measuring 1.2 cm with variable respiratory change

  3. C Right atrial systolic collapse

  4. D A small, ‘D-shaped’ LV during systole

  5. E A large left ventricular cavity size in diastole

2. The following are true of the use of FoCUS during the delivery of ALS:

  1. A A 20-s pause of chest compressions is required to gather adequate information

  2. B The subcostal and suprasternal windows are equally useful

  3. C Spectral Doppler is utilized to characterize important valvular lesions

  4. D FoCUS provides prognostic information when differentiating between ‘true PEA’ and ‘pseudo-PEA’

  5. E FoCUS replaces the need for TTE in the post-arrest period

Answers

1. The following echocardiographic findings raise suspicion of systemic hypovolaemia as the cause of haemodynamic collapse in a ventilated patient:

  1. A TRUE. Hyperdynamic function of both ventricles is typical in hypovolaemia.

  2. B TRUE. An IVC measuring <1.5 cm with variable respiratory change is in keeping with hypovolaemia.

  3. C FALSE. This is a characteristic finding in pericardial effusion with cardiac tamponade.

  4. D FALSE. This is a feature of a pressure-loaded RV (e.g. PE). In systemic hypovolaemia, the LV will be small, but circular in shape.

  5. E FALSE. The cavity size in diastole can be due to other cardiac conditions and is not necessarily indicative of fluid status.

2. The following are true of the use of FoCUS during the delivery of ALS:

  1. A FALSE. Images are acquired in periods of <10 s, during the pulse/rhythm check, in order to prevent interference with high-quality resuscitation.

  2. B FALSE. The subcostal view is recommended as the initial view, as it is easily obtained and reproducible. The suprasternal view forms part of a comprehensive transthoracic study.

  3. C FALSE. FoCUS is limited to 2D imaging without spectral Doppler analysis.

  4. D TRUE. Less than 1% of patients with cardiac standstill (‘true PEA’) survive to hospital discharge.

  5. E FALSE. Post-arrest, a full echocardiographic study can be useful (e.g. in identifying ischaemic heart disease or primary cardiomyopathy as a cause of arrest).

Further reading

Breitkreutz R, Price S, Steiger HV, et al. Focused echocardiographic evaluation in life support and peri-resuscitation of emergency patients: a prospective trial. Resuscitation 2010;81:1527–33.Find this resource:

Lancellotti P, Price S, Edvardsen T, et al. The use of echocardiography in acute cardiovascular care: recommendations of the European Association of Cardiovascular Imaging and the Acute Cardiovascular Care Association. European Heart Journal: Acute Cardiovascular Care 2015;4:3–5.Find this resource:

Price S, Ilper H, Uddin S, et al. Peri-resuscitation echocardiography: training the novice practitioner. Resuscitation 2010;81:1534–9.Find this resource:

Soar J, Nolan JP, Böttiger BW, et al.; Adult advanced life support section Collaborators. European Resuscitation Council Guidelines for Resuscitation 2015: Section 3. Adult advanced life support. Resuscitation 2015;95:100–47.Find this resource:

Via G, Hussain A, Wells M, et al. International evidence-based recommendations for focused cardiac ultrasound. Journal of the American Society of Echocardiography 2014;27:683.e1–33. Find this resource:

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