Advanced life support

Sanjay  Sharma; Aneil  Malhotra

Advanced life support1

Key points

Cardiac arrest may occur as a result of several cardiac disorders including acute coronary syndrome, cardiomyopathy, congenital heart disease, ion channel diseases and valvular heart disease and cardiac tamponade
Effective chest compressions and early defibrillation when appropriate are crucial for optimal outcomes in a cardiac arrest
In the setting of a cardiac arrest, the expertise of a cardiologist is required for the delivery of prompt and safe revascularisation in the context of atherosclerotic coronary artery disease, or pericardiocentesis in the case of cardiac tamponade, as well as guidance for subsequent therapy in survivors of cardiac arrest from other cardiac diseases

Epidemiology

The majority of out-of-hospital cardiac arrests (OHCAs) in the UK occur at home, with only 20% of OHCA occurring in public places. In both OHCAs and in-hospital cardiac arrests (IHCAs), the initial rhythm is usually non-shockable (pulseless electrical activity or asystole), with only 20% of IHCAs initiated by a shockable rhythm (ventricular fibrillation/pulseless ventricular tachycardia).

Pathophysiology

The main causes of a cardiac arrest are the 4 H's and 4 T's: hypoxia, hypovolaemia, hypothermia, hypo- and hyperkalaemia, thromboembolic (pulmonary embolism/myocardial infarction), toxins, tension pneumothorax and tamponade.

This chapter focuses on atherosclerotic coronary artery disease and cardiac tamponade.

Atherosclerotic coronary artery disease

The acute coronary syndrome (ACS) incorporates unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI) and ST-segment elevation myocardial infarction (STEMI). Whilst the clinical presentation of each of these conditions differs, the underlying pathophysiological process remains similar – myocardial ischaemia due to mismatch between myocardial oxygen supply and demand and additionally, in myocardial infarction (MI), the presence of myocyte necrosis. The underlying cause of ACS is often atherosclerotic plaque rupture resulting in an acute reduction of the coronary lumen patency. Plaque rupture initiates a cascade of events including distal embolisation of the plaque into the coronary vessel, acute thrombosis within the coronary artery and also into the ruptured plaque, and also vasoconstriction of the smooth muscle cells surrounding the coronary artery. ACS may also occur in the presence of increased physiological stress, due to an increase in myocardial oxygen requirements. Disease conditions resulting in a demand–supply mismatch of myocardial oxygenation include anaemia, sepsis, tachy- and bradyarrhythmias, and respiratory failure.

Cardiac tamponade

During a cardiac arrest, particularly in the setting of trauma, postcardiac surgery, myocardial rupture or aortic dissection, there should be a high degree of suspicion for cardiac tamponade. Accumulation of fluid, gas or clot in the pericardial space results in increased pericardial pressure. When this pressure exceeds intracardiac pressure in the atria and ventricles, impaired cardiac filling ensues which can result in cardiac tamponade, and ultimately, cardiac arrest. Both the volume of fluid/gas/clot and the rate at which it accumulates in the pericardial space are important in the propensity for developing cardiac tamponade. A small volume of fluid/gas/clot that accumulates quickly can result in tamponade because of the rapid increase of pressure in the pericardial space.2

Clinical features

Atherosclerotic coronary artery disease

The clinical features of ACS are described in the atherosclerotic heart disease chapter; however, the main symptom of ACS is chest pain/tightness that may radiate to the arms, neck, back or upper abdomen. Breathlessness, a more atypical symptom of ACS, is seen particularly in women, the elderly and diabetic patients.

Cardiac tamponade

The pathognomonic signs of cardiac tamponade are referred to as ‘Beck's triad,’ comprising of muffled heart sounds, hypotension – pulsus paradoxus (>20 mmHg difference in systolic blood pressure between inspiration and expiration) and a raised jugular venous pressure; however, these clinical signs may not always be present in tamponade, e.g. in hypovolaemic states.

Investigations and diagnosis

Atherosclerotic coronary artery disease

The diagnosis of ACS is made in the setting of typical symptoms of chest pain and ECG changes involving the ST-segment and/or T wave, or the development of left bundle branch block (LBBB). The diagnosis of MI is made with a cardiac biomarker, e.g. high sensitivity troponin, elevated above the 99th centile, in combination with any one of the following: typical symptoms; ECG changes of the ST-segment or T wave, Q waves or LBBB; regional wall motion abnormality on imaging or loss of viable myocardium; or the presence of intracoronary thrombus on angiography or postmortem.

Cardiac tamponade

The diagnosis of cardiac tamponade is made by echocardiography. The most easily identifiable findings include atrial and then ventricular collapse during systole and diastole respectively. The lowest pressure chambers of the heart (right sided) are affected first.

During inspiration, there is a reduction in intrathoracic pressure. This accentuates venous return to the heart, and hence increases right ventricular (RV) filling. The increased pulmonary compliance that additionally occurs during inspiration also contributes to the increased blood pool in the lungs and reduces pulmonary venous return to the left ventricular (LV). The reduced LV filling results in reduced stroke volume, and hence reduced systolic blood pressure. Conversely in expiration, with an increase in intrathoracic pressure, LV filling is increased. In cardiac tamponade, this respiratory variation is more marked with >25% variation across the mitral valve (MV) and >40% variation across the tricuspid valve (TV) and can be visualised with pulsed wave Doppler measurements. Additional echocardiographic features include abnormal septal motion with respiration (septal movement towards the LV in inspiration and towards the RV in expiration); dilated inferior vena cava with <50% collapse with inspiration (due to increased RA pressure); increased flow reversal in expiration in the pulmonary veins and increased flow reversal in inspiration in the hepatic veins.

In the setting of a cardiac arrest, echocardiographic features of tamponade will be absent. Focussed ultrasonography identifying pericardial fluid should prompt consideration of pericardiocentesis. In the setting of postcardiac surgery or chest trauma, resuscitative thoracotomy should be considered. The Resuscitation Council UK recommend ultrasonography using a subxiphoid approach, during the 10 seconds when pulse check is being performed and when chest compressions are halted to avoid delaying the delivery of effective cardiopulmonary resuscitation (CPR).

Treatment

Cardiac arrest

The Resuscitation Council UK algorithm for delivering advanced life support focusses on providing effective and prompt CPR, with emphasis on delivering good quality chest compressions, and where appropriate, early defibrillation. The 2015 ALS guidelines state that during CPR with an unprotected airway, two ventilations should be given after each sequence of 30 chest compressions. Once a tracheal tube or supraglottis airway device has been inserted, the lungs should be ventilated 3at a rate of about 10 breaths per minute and chest compressions should continue without pausing during ventilation. Haemodynamic monitoring and treatment of reversible causes of the cardiac arrest are also important.

Atherosclerotic coronary artery disease

The management of a cardiac arrest secondary to an ACS event is similar to described in the ACS chapter of this book, with the aim of providing early revascularisation where appropriate.

Pericardiocentesis

When cardiac arrest is deemed secondary to a cardiac tamponade, the definitive treatment is pericardiocentesis. Needle pericardiocentesis can be performed in the apical, left parasternal, left sternocostal and subxiphoid approaches. In the emergency setting, when ultrasound guidance is unavailable, the subxiphoid or left sternocostal approaches are recommended. In a non-cardiac arrest scenario, lying the patient at 35–40 degrees brings the heart closer to the anterior chest wall, however, in a cardiac arrest situation, pericardiocentesis should be performed in the supine position. The pericardiocentesis/spinal needle should be inserted at 45 degrees to the chest wall, angled towards the patient's left shoulder. During advancement of the needle, it is important to maintain negative pressure on the syringe attached to the needle until fluid is aspirated into the syringe. Aspiration to dryness should be attempted, followed by insertion of a pericardial drain.

Complications

Pericardiocentesis

Complications associated with pericardiocentesis can occur both peri- and postprocedure. Awareness of structures surrounding the heart is important when performing pericardiocentesis. In addition to avoiding damage to the lungs and the liver, a number of key vessels lie between the myocardium and the thoracic cage that are prone to laceration. The left internal mammary artery lies approximately 1–2 cm from the border of the sternum which then forms the superior mesenteric artery at the level of the 6th intercostal space. The left anterior descending and the right coronary artery lie along the anterior pericardium. Puncture of the myocardium or coronaries can result in arrhythmia and a delayed onset haemopericardium. Patients may also often demonstrate a marked vasovagal response following periocardiocentesis.

Chapter Notes

Advanced life support1