Cardiopulmonary resuscitation (CPR) in special circumstances includes the emergency intervention for special causes, special environments and special patients. Special causes cover the potential reversible causes of cardiac arrest that must be identified or excluded during any resuscitation, divided into two groups, 4Hs and 4Ts: hypoxia, hypo-/hyperkalaemia and other electrolyte disorders, hypo-/hyperthermia, hypervolemia, tension pneumothorax, tamponade (cardiac), thrombosis (coronary or pulmonary) and toxins. The special environments section includes recommendations for the treatment of cardiac arrest occurring in specific locations: cardiac surgery, catheterisation laboratory, dialysis unit, dental surgery, commercial airplanes or air ambulances, field of play, difficult environment (e.g. drowning, high altitude, avalanche and electrical injuries) or mass casualty incident. CPR for special patients gives guidance for the patients with severe comorbidities (asthma, heart failure with ventricular assist devices, neurological disease and obesity) and pregnancy women or elderly people.
- cardiopulmonary resuscitation
- special causes
- special patients
- special environment
According to the actual guidelines for cardiopulmonary resuscitation (CPR), early recognition and calling for help, early defibrillation, high-quality resuscitation with minimal interruption of chest compressions and treatment of reversible causes are the most important interventions that can improve the outcomes after cardiac arrest [1–4].
The 2015 Guidelines for resuscitation published by European Resuscitation Council divide the resuscitation in special circumstances into three parts: special causes, special environments and special patients .
The first part covers treatment of potentially reversible causes of cardiac arrest, for which specific treatment exists and which are divided into two groups of four, called ‘the 4Hs and 4Ts’: hypoxia; hypo-/hyperkalaemia and other electrolyte disorders; hypo-/hyperthermia; hypovolaemia; tension pneumothorax; tamponade (cardiac tamponade); thrombosis (coronary and pulmonary) and toxins (poisoning) [1, 4].
The third part contains the recommendation for the patients with specific conditions and those with certain long-term comorbidities, where a modified approach and different treatment decisions may be necessary .
2. Special causes
The effective ventilation with supplementary oxygen during the early moment of resuscitation is essential during CPR. Also, it is recommended to monitor the efficacy of ventilation via capnometry which measures end-tidal CO2. CPR is indicated to monitor the effectiveness of manoeuvres by obtaining a value between 10 and 20 mmHg. An abrupt increase of end-tidal CO2 values indicates return of spontaneous circulation (ROSC). If after oro-tracheal intubation, there is no waveform during CPR, but a flat line, this should alert for misplacement of endotracheal tube [1, 4, 6].
Hypothermia decreases oxygen consumption at cellular level, so the heart and the brain can tolerate for a longer period of time cardiac arrest. This is the basic concept of the protective effect of hypothermia in cardiac arrest. Sometimes complete neurological recovery can be found even after prolonged cardiac arrest, but only if hypothermia was installed before respiratory arrest [1, 4, 6–9].
The first measure is to remove the patient from cold environment, remove clothes which are usually wet or cold and try to prevent any other heat loss. Quick mobilisation of patient with hypothermia can induce arrhythmias [1, 4, 6].
Hypothermia need to be treated with gradual rewarming using normal or electric blankets and warm IV fluids. The goal is to achieve an increase of temperature with a rate of 1–1.5°C per hour. It should be used IV fluid (normal saline, for example) heated at approx. 40°C and also gastric lavage, peritoneal lavage, bladder lavage, using fluids heated at approx. 40°C.
Monitor electrolytes disorder hourly, especially hyperkalaemia, which can appear during heating manoeuvres. Oxygen should be delivered also heated and humidified at 40°C, using a mechanical ventilator, after oro-tracheal intubation [1, 4–6].
Regarding CPR manoeuvres, in case of hypothermia-associated thoracic stiffness is present. Thus, chest compressions are harder to perform, and ventilation will require higher pressures than in normal situation [1, 4, 5, 7–9].
In case of ROSC, pulse in patients with hypothermia is very weak due to peripheral vasoconstriction, so is needed to consider Doppler examination to assess correctly the presence or absence of circulation.
Hypothermic patients without signs of cardiac instability (systolic blood pressure ≥90 mmHg, absence of ventricular arrhythmias or core temperature ≥28°C) can be rewarmed externally using minimally invasive techniques (warm air and warm intravenous fluid). Patients with signs of cardiac instability should be resuscitated in the field and transferred directly to a centre capable of extracorporeal life support (ECLS) [1, 4–9].
History of fluid or blood loss may be available. Rectal examination can identify massive lower GI bleeding; nasogastric intubation can identify massive upper GI bleeding, and bedside FAST can diagnose massive intraperitoneal bleeding. Treatment is with fluids (crystalloids, colloids), administered rapidly IV and blood products. If colloids are administered, blood samples are necessary before of this, to work compatibility cross-match blood test, because colloids can interfere with the results [1, 4, 6].
The new treatment algorithm for traumatic cardiac arrest was developed to prioritise the sequence of life-saving measures. Chest compressions should not delay the treatment of reversible causes.
Suspect of tension pneumothorax during cardiac resuscitation if breath sounds are unequal on chest auscultation after verifying correct endotracheal tube placement. Other useful clinical sign for diagnosis are one immobile, distended hemi thorax; hyper resonance with percussion over the chest wall; trachea deviation to opposite side of tension pneumothorax and jugular veins distention. Treatment is immediate needle decompression or other technique to decompress the chest in TCA—to perform unilateral or bilateral thoracotomies in the 4th intercostal space. In the presence of positive pressure ventilation, thoracotomies are likely to be more effective than needle thoracentesis and quicker than inserting a chest tube [1, 5, 11–14].
Acute coronary thrombosis or acute myocardial infarction is one of the most common causes of cardiac arrest. Risk factors are a history of coronary artery disease and initial rhythm of VF/VT. Cardiac catheterisation after resuscitation is an underused procedure. A 12-lead ECG in the immediate postcardiac arrest state can identify an ST-elevation acute myocardial infarction and allows for arrangements of immediate coronary angiography. Myocardial and neurologic function can improve after percutaneous coronary intervention following cardiac arrest. Therefore, after ROSC, especially in the face of post-ROSC, ECG evidence of acute myocardial infarction, cardiac catheterisation and percutaneous coronary revascularisation is recommended, if available and appropriate [1, 4, 5].
Acute pulmonary embolism will be suspected by clinical symptoms such as dyspnoea, chest pain and syncope, either only one of this or in combination. Most frequent patient-related predisposing factors for developing pulmonary embolism include age, history of previous deep vein thrombosis, active cancer, neurological disease with extremity paresis, medical condition causing prolonged bed rest, such as heart or acute respiratory failure or post-surgery, congenital or acquired thrombophilia, hormone replacement therapy and oral contraceptive therapy [1, 4, 5, 15–17].
Electrocardiographic signs of RV strain, such as inversion of T waves in leads V1–V4, a QR pattern in lead V1, the classic pattern of S1Q3T3 ECG type and incomplete or complete right bundle-branch block, may be helpful also to raise the suspicion for pulmonary embolism.
The administration of fibrinolytic when pulmonary embolism is the suspected cause of cardiac arrest remains the actual recommendation. Pulmonary embolism causing cardiac arrest requires fibrinolysis or embolectomy. However, the diagnosis is rarely made at time of collapse, and even then, most systems are not geared to make such prompt diagnosis and initiate the necessary procedures for embolectomy [1, 4, 5, 15, 16, 19].
Fibrinolytic agents could be considered during cardiac arrest from suspected pulmonary embolism on a case-by-case basis. Factors suggestive of pulmonary embolism causing cardiac arrest include two of three signs/symptoms (prearrest respiratory distress, altered mental status or shock); arrest witnessed by a physician or emergency medical technician and PEA as the first or primary arrest rhythm. Ongoing CPR is not a contraindication to fibrinolysis, and after fibrinolytic drug is administered, CPR should be continued for at least 60–90 min before terminating resuscitation attempts [1, 4, 15–18, 20].
The preferred method of gastrointestinal decontamination in patients with protected airways is activated charcoal but is most effective only if given within first hour from ingestion. Drug overdose is rarely identified as a cause of cardiac arrest during the resuscitation process. In the event of antidepressant overdose, administer IV sodium bicarbonate. Lipid emulsion infusion may be useful in cardiac arrest associated with cyclic antidepressants or local anaesthetics.
Opioid poisoning causes respiratory depression followed by respiratory insufficiency or respiratory arrest. The use of naloxone can prevent the need for intubation. The initial doses of naloxone are 0.4–2 mg IV, IO, IM or SC and may be repeated every 2–3 min. Additional doses may be needed every 20–60 min. Titrate the dose until the victim is breathing adequately and has protective airway reflexes [4, 5, 21].
3. Special environment
The special environments include cardiac arrest in specific locations: operating theatre, cardiac surgery, catheterisation laboratory, dialysis unit, dental surgery, commercial airplanes or medical helicopters, field of play, outside environment (e.g. drowning, remote area, high altitude, avalanche, lightning strike and electrical injuries) or the scene of a mass casualty incident.
Cardiac arrest following major
The management of perioperative cardiac arrest starts with advanced life support (ALS) algorithm, but with appropriate modifications depending on the cause identified. Key to successful resuscitation is recognition of the need to perform emergency re-sternotomy, especially in the context of tamponade or haemorrhage, where external chest compressions may be ineffective. Re-sternotomy should be performed within 5 min if other interventions have failed.
Cardiac arrest may occur during percutaneous coronary intervention (PCI) for ST-elevation myocardial infarction (STEMI) or non-STEMI, or it may be a complication during angiography as air or thrombus embolism in the coronary artery, artery intima dissection or pericardial tamponade. A defibrillator must be available in the angiography room, and self-adhesive defibrillation pads may already be placed at the beginning of the procedure in high-risk patients.
Cardiac arrest from shockable rhythms (ventricular fibrillation or pulseless ventricular tachycardia) during
Most of the standard reversible causes (4Hs and 4Ts) apply to
During cardiopulmonary resuscitation, it follows the universal ALS algorithm, and the dialysis access open for drug administration A shockable rhythm (VF/pulseless VT) is more common in patients undergoing haemodialysis than in the general population [25–29]. So the delay in delivering defibrillation must be minimised.
The patient will not be moved from the dental chair to start CPR, the dental chair will be reclined into a horizontal position or a stool will be placed under the head to increase its stability during CPR. Consider the over-the-head technique of CPR, if access of the chest is limited [30–32].
If the CPR equipment is available, attach oxygen to the facemask or self-inflating bag. Request immediate flight diversion to the nearest appropriate airport. The in-flight use of AEDs aboard commercial airplanes can result in up to 50% survival to hospital discharge . AEDs and appropriate CPR equipment should be mandatory on board of all commercial aircraft in Europe, including regional and low-cost carriers .
The incidence of cardiac arrest on board of
Sudden and unexpected collapse of a sportsman
Rescue breaths/ventilation will continue until an ALS team arrives and is ready to intubate the victim. Palpation of the pulse is not always reliable. As soon as possible, use information from monitoring modalities such as the ECG, end-tidal CO2, and echocardiography to confirm the diagnosis of cardiac arrest. If the drowning victim is hypothermic or hypovolaemic, modify the ALS approach in accordance with the treatment of hypothermia and give IV warm fluid.
The chances of good outcome from cardiac arrest in
Safety measures are essential for providing CPR to the victim of an
Ensure that any power source is switched off and approach the casualty only if it is safe and start standard BLS and ALS without delay. Airway management may be difficult, and early tracheal intubation is needed if there are electrical burns around the face and neck. Head and spine trauma can occur after electrocution, and the spine immobilisation must be performed.
VF is the commonest initial arrhythmia after high-voltage AC shock, and prompt defibrillation is essential. Asystole is more common after DC shock with standard ALS protocols.
Unlike normal circumstances, CPR is not usually initiated in
A triage system should be used to prioritise treatment and, if the number of casualties overwhelms the prehospital medical resources, withhold CPR for the patients without signs of life [1, 5]. For triage, the START triage is used. The first step is that everyone able to walk is directed to clear the scene, and respiratory status of nonwalking patients is assessed. If the casualty does not breathe, open the airway using head tilt and chin lift or jaw thrust. Assess breathing for no more than 10 s and if a patient does not begin breathing is declared dead. If an unresponsive victim is breathing normally, turn them into the recovery position and label as red-highest priority for treatment. The same goes for the patient with sign of hemodynamic instability.
Perform life-saving interventions in patients triaged as red (highest priority) to prevent cardiac arrest: control major haemorrhage, open airway using basic techniques, perform chest decompression for tension pneumothorax, use antidotes and consider initial rescue breaths in a nonbreathing child .
4. Special patients
Special patients with special guidance for CPR are considered to be the patients with severe comorbidities: asthma, heart failure with ventricular assist devices, neurological disease, obesity and those with specific physiological conditions (pregnancy, elderly people).
Cardiac arrest in a patient with
severe bronchospasm and mucous plugging leading to asphyxia;
cardiac arrhythmias caused by hypoxia, by stimulant drugs (beta-adrenergic agonists, aminophylline) or electrolyte abnormalities;
dynamic hyperinflation, that is, auto positive end-expiratory pressure (auto-PEEP), can occur in mechanically ventilated asthmatics. Gradual build-up of pressure occurs and reduces venous return and blood pressure and determines heart failure;
tension pneumothorax uni/bilateral.
These high-risk patients should be treated to prevent deterioration with oxygen to achieve an SpO2 94–98%, inhaled beta-2 agonists (salbutamol 5 mg) or intravenous beta-2 agonists for those patients in whom inhaled therapy cannot be used reliably, nebulised anticholinergics (ipratropium, 0.5 mg 4–6 hourly), nebulised magnesium sulphate, intravenous corticosteroids, intravenous bronchodilators and aminophylline, a dose of 5 mg kg−1 over 20–30 min. In cases of severe asthma associated with dehydration and hypovolemia IV fluids are necessary.
In case of cardiac arrest BLS is performed according to standard guidelines. Ventilation could be difficult because of increased airway resistance.
Modifications to standard ALS guidelines include the need for early tracheal intubation. The peak airway pressures recorded during ventilation of patients with severe asthma are significantly higher than the normal lower oesophageal sphincter pressure (approximately 20 cm H2O) [43, 44].
Respiratory rates of 8–10 breaths/min and a tidal volume required for a normal chest rise during CPR should minimise dynamic hyperinflation of the lungs [air trapping].
Tidal volume depends on inspiratory time and inspiratory flow. Lung emptying depends on expiratory time and expiratory flow. In mechanically ventilated severe asthmatics, increasing the expiratory time (achieved by reducing the respiratory rate) provides only moderate gains in terms of reduced gas trapping when a minute volume of less than 10 L min−1 is used .
Dynamic hyperinflation increases transthoracic impedance  but modern impedance-compensated biphasic defibrillation waveforms are no less effective in patients with higher impedance. Consider increasing defibrillation energy if the first shock is unsuccessful, and a manual defibrillator is available .
There is no good evidence for the use of open-chest cardiac compressions in patients with asthma-associated cardiac arrest. Looking through the four H’s and four T’s will identify potentially reversible causes of asthma-related cardiac arrest, often tension pneumothorax. This pathologic situation may be indicated by unilateral expansion of the chest wall, shifting of the trachea and subcutaneous emphysema. If a pneumothorax is suspected, perform needle decompression using a large-gauge cannula, followed by insertion of a chest tube.
In patients with
Transthoracic/transesophageal echocardiography, capnography or Doppler flow in a major artery may assist in the cardiac arrest diagnosis. If cardiac arrest is confirmed, start CPR, check the rhythm and perform defibrillation for shockable rhythms (VF/VT), start pacing for asystole. If during the first 10 days of surgery, cardiac arrest does not respond to defibrillation, perform re-sternotomy immediately.
Cardiac arrest associated with
The mechanism of cardiac arrest in neurological disease is related to:
loss of consciousness, causing airway obstruction, hypoxemia and respiratory arrest followed by cardiac arrest, or an increased risk of aspiration of gastric contents into the lungs
respiratory and cardiac depression caused by compression of the brain stem
arrhythmias and myocardial dysfunction associated with acute neurological injury (e.g. sub-arachnoid haemorrhage)
Sudden unexpected death in epilepsy .
Patients with subarachnoid haemorrhage may have ECG changes that suggest an acute coronary syndrome. Whether a computed tomography brain scan is done before or after coronary angiography will depend on clinical judgement regarding the likelihood of a subarachnoid haemorrhage versus acute coronary syndrome.
For resuscitation of
Optimal defibrillation energy levels in obese patients are unknown . So the recommended energy remains the same (150–360 J). Unlike monophasic defibrillators, modern biphasic defibrillators are impedance compensated and adjust their output according to the patient’s impedance. Defibrillation protocols for obese patients should therefore follow those recommended for patients with a normal BMI and consider higher shock energies for defibrillation if initial defibrillation attempts fail.
Foetal survival usually depends on maternal survival and initial resuscitation efforts should focus on the pregnant mother.
From 20 weeks’ gestation, the uterus can compress the inferior vena cava (IVC) and aorta, impeding venous return and cardiac output and therefore can cause pre-arrest hypotension or shock and, in the critically ill patient, may precipitate cardiac arrest [47, ]. During cardiac arrest, the compromise in venous return and cardiac output by the gravid uterus limits the effectiveness of chest compressions. Manually displace the uterus to the left is recommended to reduce IVC compression.
During CPR, the hand position for chest compressions may need to be slightly higher on the sternum for patients with advanced pregnancy—third trimester .
During BLS and ALS, pregnant patients are at risk of aspiration and oxygenation and ventilation are the priority over aspiration prevention. Early tracheal intubation (using a tracheal tube 0.5–1 mm internal diameter smaller than that used for a non-pregnant woman) with mechanical ventilation will however make ventilation of the lungs easier in the presence of increased intra-abdominal pressure.
The 4Hs and 4Ts approach helps identify all the common causes of cardiac arrest in pregnancy. The most important causes are
Haemorrhage: postpartum haemorrhage, ectopic pregnancy, placental abruption, placenta praevia, placenta accrete, uterine rupture. The key steps for treatment are stop the bleeding, fluid resuscitation, including use of rapid transfusion system and cell salvage  and correction of coagulopathy including use of tranexamic acid and/or recombinant activated factor VII.
Cardiovascular disease: acute myocardial infarction and aneurysm or dissection of the aorta and peripartum cardiomyopathy, pulmonary embolism, amniotic fluid embolism cause most deaths from acquired cardiac disease.
Pre-eclampsia and eclampsia need magnesium sulphate infusion for the treatment in peri-arrest situation.
Consider the need for an emergency hysterectomy or Caesarean section as soon as a pregnant woman goes into cardiac arrest. Delivery will relieve IVC compression and may improve chances of maternal resuscitation. Seek for help and ask gynaecologist and neonatologist to start preparing for emergency caesarean section—the foetus will need to be delivered if initial resuscitation efforts fail. The caesarean delivery also enables access to the infant so that newborn resuscitation can begin .
Special circumstances in cardiac arrest need special interventions with an appropriate approach of guidelines for cardiopulmonary resuscitation.