“Modern means of providing the airway patency and artificial lung ventilation for adults”
“Circulation and respiration arrest. Technology for EMC provision for adults”
Primary examination
Approach the injured, if possible, from the side of his/her head. First of all, visually assess patient’s general condition (age, sex, morphology of the body, language, skin colour, posture, availability of the movements (thorax, limbs), mimicry, eyes condition, visible injury made by traumatizing factor). Make initial resolution of its degree and further algorithm of help. Figure out the condition of consciousness according to the algorithm AVPU:
A – Alert (conscious, gives adequate answers to the questions, is able to perform conscious actions when asked by the medical rescuer);
V – Responds to Verbal stimuli (to a loud sound near the ear);
P– Responds to Pain (responds to pinch in the area of left thoracic muscle at the turn of 180 degrees);
U – Unresponsive. If there is a suspicion of simulation of unconsciousness, open patient’s eyelids, using 1st and 2nd fingers. The conscious patient will strain his/her eyelids muscles and they will open with tension.
Let’s make a priori assumption that cerebral trauma occurs at transport accidents, sports accidents, falling from high places, traumas in water and children’s traumas.
Fix with your hands a neck part of the spine in the position which you found the injured in. (medical assistant 1) If that position does not promote breathing, carefully turn the injured on his/her back or to the position, which is close to a stable (on his/her side) (medical assistant 1 + medical assistant 2). Start initial examination according to the A, B, C technique (optimal term of performance – 10 sec) (doctor).
Step A Provide patency of airways support (medical assistant 1):
Evaluate if there is a need to examine oral cavity. In case of secretion available (blood, vomitive mass, outside objects (depending on the mechanism of an injury), it is necessary to open oral cavity (between molar teeth you should put a spreader to prevent accidental pressing of fingers), take out outside objects with a clutch and tampon, provide the cleaning of oral cavity and pharynx, clean them from secretion (if there are several injured, the priority is to arrange them, according to the relief of the area, head down); throw the patient’s head back and raise his/her chin; in case of suspicion of cerebral trauma, it is prohibited to throw patient’s head back, you should raise only his/her chin.
Provide patency of airways support, find out if there are signs of life:
• Patient’s response
• Provide patency of airways support
• Check respiration and pulse (not more than 10 sec)
…to confirm or oppose the circulatory arrest.
Patency of airways support
Portable set of respiratory equipment
Primary examination
Step B. Make sure if the patient is breathing. Count the frequency of respiration during 10 sec.
Indications for carrying out trachea intubation apnoea;
risk of aspiration;
danger or presence of respiratory disorder (damage of respiratory tracts, maxillary-facial trauma);
closed craniocerebral injury;
hypoxemia, in spite of carrying out oxygen therapy;
frequency of respiration less than 10 or more than 30 per minute (for adults) danger of respiratory standstill (sepsis, major burns).
If the breathing is pathological but not agonal (deep and noisy), and also in case of shallow breathing, a patient should be given oxygen therapy (10-15 liters per minute).
Objective criteria is the data of pulsoximetria:
saturation <92 % – indication to oxygenotherapy;
saturation <90 % – indication to intubation.
Simultaneously with making decision concerning necessity of artificial ventilation and providing oxygen, put a neck collar (a doctor, medical assistant or a driver can do it) and continue initial examination.
Step C.
At the same time find out if there is pulse in the carotid (during 10 sec) (in case the patient is unconscious) (doctor). If there is not – start doing closed chest-cardiac massage (doctor, while medical assistant 2 is preparing cardiomonitor and defibrillator) with frequency of 100 times per minute – 30 pressures on the chest and 2 ventilations (medical assistant 1). Simultaneously, connect electrodes of cardiomonitor, link it up and find out the reason of cardiac arrest (medical assistant 2).
“Quick evaluation ”
Taking electrodes, classic, self-adhesive electrodes.
Examine if there is any external haemorrhage (doctor). In case of its availability stop the haemorrhage – press the wound with your hand using sterile tissue. If the haemorrhage stops, put the clutch, bandage. If you found a patient with an amputated limb, stop hemorrhage while evaluating the breathing and pulse condition. Pay attention to the skin temperature (using the back of your hand), skin colour, time of colour return after pressure on the nail, skin moisture (doctor). This information will indicate the development of the shock. Paleness, skin moisture, skin cooling and also increase of the time of nail skin colour renewal after pressing for more than 2 sec indicates a development of a shock. In case of shock development, external hemorrhage, suspicion of internal hemorrhage, organize transfusion of the blood substitutes (medical assistant 2).
Check if the patient has trinkets, bracelets, or badges – medical markers, which may hold information about patient’s condition, allergy, need for certain medication (for example, when a patient suffers from diabetes, epilepsy, etc), especially, when the patient is unconscious. While examining the patient give priority to:
dangerous mechanism of the trauma;
decrease in the level of consciousness;
respiratory failure;
abnormalities at initial examination;
considerable aberrations at general examination (it is possible to make immediate conclusion of patient’s condition, his/her viability, tactics of examination and medical treatment);
Algorithm of providing help and examination for the patient
Category “Load and Go“after primary examination
This category includes patients, who have very serious mechanism of the trauma (fall from the top, severe sports injury, car accident, etc) or negative impression of the patient at initial examination (amputation of the limb, severe defects, etc);
at initial examination decrease in the level of consciousness is found;
malfunction of respiratory tracts or respiratory failure;
malfunction of cardiovascular activity (shock or uncontrolled hemorrhage);
injured children and pregnant women.
Recognition of the Critically
Ill Patient and Prevention
of Cardiorespiratory Arrest
Objectives
To understand:
The importance of early recognition of the critically ill patient
The causes of cardiorespiratory arrest in adults
The ABCDE approach to identify and treat patients at risk of cardiorespiratory arrest
Introduction scores (EWS) or calling criteria. The score of one or more vital sign observations, or the total EWS, gives the level of intervention required, which might be that vital signs need to be monitored more frequently, or that ward doctors or a resuscitation team should be called to the patient. Alternatively, systems incorporating ‘calling criteria’ are based on routine observations, which activate a response when one or more observations reach an extremely abnormal value. It is not clear which of these two systems is better.
Even when doctors are alerted to a patient’s abnormal physiology, there is often delay in attending the patient or calling for more senior help.
Most people who have a cardiorespiratory arrest die. Survivors from in-hospital cardiac arrest usually have a witnessed and monitored VF arrest, caused by primary myocardial ischaemia, and receive immediate and successful defibrillation (e.g., on the coronary care unit).
Most in-hospital cardiac arrests are not sudden or unpredictable events. In approximately 80% of cases clinical signs deteriorate over the few hours before arrest. These patients often have slow, progressive physiological deterioration; often hypoxia and hypotension are either not noticed by staff, or are recognised but treated poorly. The cardiac arrest rhythm in these patients is usually non-shockable (PEA or asystole) and very few of them survive and leave hospital.
Early recognition and effective treatment of critically ill patients might prevent some cardiac arrests, deaths, and unanticipated intensive care unit (ICU) admissions. Early recognition also helps to identify individuals for whom cardiorespiratory resuscitation is not appropriate or who do not wish to be resuscitated.
Much of this chapter is based on critically ill patients in the hospital setting. The same basic principles however apply to the care of critically ill patient in the out-of-hospital setting.
Recognising the critically ill patient
In general, the clinical signs of critical illness are similar whatever the underlying process because they reflect failing respiratory, cardiovascular, and neurological systems, i.e., ABCDE problems (see below). Abnormal physiology is common on general wards, but important physiological observations in acutely ill patients are not done as often as they should be. To help early detection of critical illness, many hospitals now use early warning.
Response to critical illness
The traditional response to cardiac arrest is reactive: the name ‘cardiac arrest team’ implies it will be called only after cardiac arrest has occurred. In some hospitals the cardiac arrest team has been replaced by other resuscitation teams. For example, the medical emergency team (MET) responds not only to patients in cardiac arrest, but also to those with acute physiological deterioration. The MET usually comprises medical and nursing staff from intensive care and general medicine and responds to specific calling criteria (Table 1.1). Any member of the healthcare team can initiate a MET call. Early involvement of the MET may reduce cardiac arrests, deaths, and unanticipated ICU admissions. MET interventions are often simple tasks such as starting oxygen therapy and intravenous fluids. The benefits of the MET system remain to be proved.
In the UK, a system of pre-emptive ward care known as critical care outreach has developed. There are many forms of outreach services, from a single nurse to a 24-hour, seven days per week multiprofessional team.
Critically ill patients should be admitted to a critical care area, e.g., ICU, high dependency unit (HDU), or resuscitation room. These areas should be staffed by doctors and nurses experienced in advanced resuscitation and critical care skills.
There are fewer hospital staff on duty during the night and at weekends. This influences patient monitoring, treatment and outcomes. Admission to general wards in the evening or to hospital at weekends is associated with increased mortality. Patients discharged from ICUs to general wards at night have an increased risk of in-hospital death compared with those discharged during the day and those discharged to HDUs.
Acute Change in Physiology:
Airway Threatened
Breathing
All respiratory arrests
Respiratory rate < 5 min’
Respiratory rate > 36 min1
|
Circulation |
All cardiac arrests
Pulse rate < 40 beats min’
Pulse rate > 140 beats min ‘
Systolic blood pressure < 90 mmHg
|
Neurology |
Sudden decrease in level of consciousness
Decrease in GCS of > 2 points
Repeated or prolonged seizures
|
Other |
Any patient causing concern who does not fit the above criteria
Table 1.1 Medical Emergency Team Calling Criteria
Causes of cardiorespiratory arrest
Cardiorespiratory arrest can be caused by an airway, breathing or circulation problem.
CAUSES OF AIRWAY OBSTRUCTION
•Central nervous system depression
•Blood
•Vomitus
•Foreign body (e.g., tooth, food)
•Direct trauma to face or throat
•Epiglottitis
•Pharyngeal swelling (e.g., infection, oedema)
•Laryngospasm
•Bronchospasm
•Bronchial secretions
Recognition
Assess airway patency in anyone at risk of obstruction. A conscious patient will complain of difficulty in breathing, may be choking, and will be distressed. With partial airway obstruction, efforts at breathing will be noisy. With complete airway obstruction, respiration will be silent and there will be no air movement at the patient’s mouth. Any respiratory movements are usually strenuous. The accessory muscles of respiration will be involved with a ‘see-saw’ or ‘rocking horse’ pattern of chest and abdominal movement: the chest is drawn in, sometimes with marked indrawing at the sternal notch, and the abdomen expands on inspiration, with the opposite seen on expiration.
Airway obstruction
Causes
Airway obstruction can be partial or complete. Partial obstruction often precedes complete obstruction, which rapidly leads to cardiac arrest. Partial airway obstruction may lead to cerebral or pulmonary oedema, exhaustion, secondary apnoea, and hypoxic brain damage, and eventually to cardiac arrest.
Central nervous system depression may cause loss of airway control. Causes include head injury, hypercapnia, metabolic disorders such as hypoglycemia in diabetic patients, and drugs such as alcohol, opioids and general anaesthetics. Laryngospasm can occur if the upper airway is stimulated in a semi-conscious patient whose airway reflexes remain intact.
Treatment
The priority is to ensure that the airway remains patent. Treat any problem that places the airway at risk, for example, remove blood and gastric contents by suction from the airway and, unless contraindicated, turn the patient on their side. Assume actual or impending airway obstruction in anyone with a depressed level of consciousness, regardless of cause. Take steps to safeguard the airway and prevent further complications such as aspiration of gastric contents. The patient may need to be nursed on their side or with a head-up tilt. Consider using simple airway opening manoeuvres (head tilt, chin lift or jaw thrust), an oropharyngeal or nasal airway, elective tracheal intubation, or tracheostomy, and consider inserting a nasogastric tube to empty the stomach. Finally, remember to always give oxygen to the patient as early as possible.
Breathing problems
Causes
Breathing inadequacy may be acute or chronic. It may be severe enough to cause the patient to stop breathing (apnoea).This will rapidly lead to a secondary cardiac arrest if not treated. Respiratory arrest often arises from a combination of factors. In a patient with chronic respiratory inadequacy, a chest infection, muscle weakness, or fractured ribs may lead to exhaustion, further depressing respiratory function. If breathing is insufficient to oxygenate the blood adequately, lack of oxygen to the vital organs will lead to loss of consciousness and cardiac arrest will eventually occur.
Respiratory drive
Central nervous system depression may decrease or abolish respiratory drive. The causes are the same as those for airway obstruction from central nervous system depression.
Respiratory effort
The main respiratory muscles are the diaphragm and intercostal muscles. The latter are innervated at the level of their respective ribs and may be paralyzed by a spinal cord lesion above this level. The innervation of the diaphragm is at the level of the third, fourth and fifth cervical (neck) vertebrae. Spontaneous breathing cannot occur with severe cervical cord damage above this level.
Inadequate respiratory effort, caused by muscle weakness or nerve damage, occurs with many diseases (e.g., myasthenia gravis, Guillain-Barre syndrome, and multiple sclerosis). Chronic malnourishment and severe illness may also contribute to generalized weakness.
Breathing can be impaired by restrictive chest wall abnormalities such as kyphoscoliosis. Pain from fractured ribs or sternum, or surgical wounds, will prevent deep breaths and coughing.
Lung disorders
Severe lung disease will impair gas exchange. Causes include infection, chronic obstructive pulmonary disease (COPD), asthma, pulmonary embolus, lung contusion, acute respiratory distress syndrome (ARDS) and pulmonary oedema. Lung function is also impaired by a pneumothorax or haemothorax. A tension pneumothorax causes a rapid failure of gas exchange, a reduction of venous return to the heart, and a fall in blood pressure.
Recognition
Conscious patients will complain of shortness of breath and be distressed. The history and examination will usually point to the underlying cause. Hypoxia and hypercapnia cause irritability, confusion, lethargy and depressed consciousness. Cyanosis is a late sign. A high respiratory rate (e.g., more than 30 min’) is a useful, simple indicator of breathing problems. Pulse oximetry is an easy, non-invasive measure of the adequacy of oxygenation, but it is not a monitor of ventilation. Arterial blood gas measurement is needed to assess adequate ventilation. A rising arterial carbon dioxide tension (PaCGV,) indicates hypoventilation.
Treatment
Give oxygen to all hypoxic patients and treat the underlying cause. Further treatment can include needle decompression of a tension pneumothorax or antibiotics for a chest infection. Patients who are having difficulty breathing or are becoming tired will need help with their breathing. Non-invasive ventilation using a face mask can be useful and avoid the need for tracheal intubation and mechanical ventilation, but these may be needed and it is best to call for expert help early for these patients.
Circulation problems
Causes
Circulation problems include primary or secondary heart problems. The heart may stop suddenly or there may be inadequate cardiac output for a while before arrest.
Primary heart problems
Sudden cardiac arrest is most commonly caused by an arrhythmia secondary to ischaemia or myocardial infarction. The commonest initial cardiac arrest rhythm is ventricular fibrillation (VF).
Acute Coronary Syndromes
The acute coronary syndromes (ACS) comprise unstable angina, non-ST segment elevation myocardial infarction (NSTEMI), and ST segment elevation myocardial infarction (STEMI). These syndromes result from the same disease process in which, usually, thrombosis of a coronary artery is triggered by Assuring of an atheromatous plaque. The extent to which myocardial blood flow decreases determines the syndrome.
CAUSES OF VENTRICULAR FIBRILLATION
•Acute coronary syndromes
•Hypertensive heart disease
•Valve disease
•Drugs (e.g., antiarrhythmic drugs, tricyclic antidepressants, digoxin)
•Hereditary cardiac diseases e.g., long QT syndromes
•Acidosis
•Abnormal electrolyte concentration (e.g., potassium, magnesium, calcium)
•Hypothermia
Secondary heart problems
The heart is affected by changes elsewhere in the body. For example, a primary respiratory arrest will result in a secondary cardiac arrest due to lack of oxygen to the heart. Severe anaemia, hypothermia, and severe septic shock will also impair cardiac function which can eventually lead to a cardiac arrest.
Recognition
The signs and symptoms of cardiac disease include chest pain, shortness of breath, tachycardia, bradycardia, tachypnoea (high respiratory rate), hypotension, poor peripheral perfusion (indicated by prolonged capillary refill time), altered mental state, syncope (e.g., fainting) and oliguria.
Most sudden cardiac deaths occur in people with pre-existing cardiac disease, which may have been unrecognized. Asymptomatic or silent cardiac disease includes hypertensive heart disease, aortic valve disease, myocarditis, fibrosis, and silent ischaemia.
A few sudden cardiac deaths occur in people without any previous history and with an apparently normal heart. Victims tend to be young, active and otherwise healthy. Risk factors for cardiac disease include increasing age, a strong family history, being male, smoking, diabetes mellitus, hyperlipidaemia and hypertension. An increasing number of cardiac conditions have a genetic origin, including hypertrophic cardiomyopathy, right ventricular cardiomyopathy, and prolongation of the QT-interval.
Acute myocardial infarction (AMI) typically presents with chest pain that is felt as a heaviness or tightness or indigestion-like discomfort in the chest. The pain or discomfort often radiates into the neck or throat, into one or both arms (more commonly the left), and into the back or into the epigastrium. Some patients experience the discomfort more in one of these areas than in the chest.
Sometimes it may be accompanied by belching, which may be misinterpreted as evidence of indigestion as the cause.
A history of sustained (i.e., 30 minutes or more) acute chest pain typical of AMI, with acute ST segment elevation on a 12-lead ECG is the basis for a diagnosis of STEMI.
Some patients present with chest pain suggestive of AMI and less specific ECG abnormalities, such as ST segment depression or T wave inversion. In a patient with a history suggestive of ACS and laboratory tests showing substantial release of troponin (with or without elevated plasma concentrations of cardiac enzymes) this indicates that myocardial damage has occurred. This is referred to as NSTEMI.
Unstable angina should be considered when there is an unprovoked and prolonged episode of chest pain, raising suspicion of AMI but without definite ECG or laboratory evidence of AMI.
Treatment
Immediate general treatment for an acute coronary syndrome is:
■ Oxygen, in a high concentration.
■ Aspirin 300 mg, orally, crushed or chewed, as early as possible.
■ Nitroglycerine, as sublingual glyceryl trinitrate (tablet or spray).
■ Morphine (or diamorphine) titrated intravenously to avoid sedation and respiratory depression.
Further treatment depends on the type of acute coronary syndrome. Options include thrombolytic therapy or percutaneous coronary intervention (e.g., coronary angiography and stenting).
Most patients with ischemic cardiac pain are more comfortable sitting up; lying flat may provoke or worsen the pain. Consider an anti-emetic, especially if nausea is present.
Patients resuscitated after VF arrest are likely to have a further VF arrest unless preventative treatment is given. These patients may need treatment with anti-arrhythmic agents. If the patient has had an acute coronary syndrome the patient may benefit from thrombolytic therapy or percutaneous coronary intervention. Patients at high risk of VF, recurrent VF or VF from an unknown cause can benefit from an implantable defibrillator.
Treating the underlying cause should prevent secondary cardiac arrests; for example, early goal-directed therapy using the ABCDE approach to optimise vital organ perfusion decreases the risk of death in severe sepsis. Cardiovascular support includes correction of underlying electrolyte or acid-base disturbances, and treatment to achieve a normal cardiac rate, rhythm and output. Advanced cardiovascular monitoring, e.g., pulmonary artery catheter and echocardiography may be indicated. Appropriate manipulation of cardiac filling may require fluid therapy and vasoactive drugs. Inotropic drugs and vasoconstrictors will support cardiac output and blood pressure. These interventions will require expert help.
The ABCDE approach
Underlying principles
Do a complete initial assessment and re-assess regularly.
During the initial assessment of breathing, it is vital to
diagnose and treat immediately life-threatening conditions,
e.g., acute severe asthma, pulmonary oedema, tension
pneumothorax, massive haemothorax.
2. Treat life-threatening problems before moving to the next part of assessment.
3. Assess the effects of treatment.
4. Call for help early.
5. Use all members of the team. This will allow interventions, e.g., assessment, attaching monitoring equipment, and intravenous access, to be undertaken simultaneously.
6. Communicate effectively.
7. The aim of the initial treatments is to keep the patient alive, and achieve some clinical improvement. This will buy time for further treatment and expert help.
8. Remember – it can take a few minutes for treatments to work.
9. The ABCDE approach can be used irrespective of your training and experience in clinical assessment or treatment. The detail of your assessment and what treatments you give will depend on your clinical knowledge and skills. If you recognize a problem or are unsure call for help.
First steps
1. Ensure personal safety.
2. First look at the patient in general to see if the patient ‘looks unwell’.
3. In an awake patient ask, “How are you?” If the patient appears unconscious, shake him and ask, “Are you all right?” If he responds normally, he has a patent airway, is breathing and has brain perfusion. If he speaks only in short sentences, he may have breathing problems. Failure of the patient to respond is a clear marker of critical illness.
4. Monitor the vital signs early. Attach a pulse oximeter, ECG monitor, and non-invasive blood pressure monitor to all critically ill patients, as soon as possible.
5. Insert an intravenous cannula as soon as possible. Take bloodsamples for investigation.
Airway obstruction is an emergency. Get expert help immediately.
1. Look for the signs of airway obstruction:
• Airway obstruction causes paradoxical chest and abdominal movements (‘see-saw’ respirations) and the use of the accessory muscles of respiration. Central cyanosis is a late sign of airway obstruction. In complete airway obstruction, there are no breath sounds at the mouth or nose. In partial obstruction, air entry is diminished and ofteoisy.
2. Treat airway obstruction as an emergency:
Airway (A)
In most cases, only simple methods of airway clearance are needed (e.g., airway opening manoeuvres, suction, insertion of an oropharyngeal or nasopharyngeal airway). Tracheal intubation may be needed if these fail.
3. Give oxygen at high concentration:
Give high concentration oxygen using a mask with an oxygen reservoir. Ensure high flow oxygen (usually greater than 10 I min ‘) to prevent collapse of the reservoir during inspiration. If the patient’s trachea is intubated, give high concentration oxygen with a self-inflating bag.
In acute respiratory failure, try to maintain the PaGV, as close to normal as possible (approximately 13 kPa or 100 mmHg). In the absence of arterial blood gas values use pulse oximetry to guide oxygen therapy. A normal oxygen saturation is 97-100%. In the sickest patients this is not always possible so you may have to aim for lower values, i.e., above 8 kPa (60 mmHg) or 90-92% oxygen saturation on a pulse oximeter.
Breathing (B)
In almost all medical and surgical emergencies, consider hypovolaemia as the likeliest cause of shock, until proved otherwise. Unless there are obvious signs of a cardiac cause (e.g., chest pain, heart failure), give intravenous fluid to any patient with cool peripheries and a high heart rate. In surgical patients, rapidly exclude bleeding (overt or hidden). Remember that breathing problems, such as a tension pneumothorax, can also compromise a patient’s circulatory state. This should have been treated earlier on in the breathing assessment. Look at the colour of the hands and fingers: are they blue, pink, pale or mottled? Assess the limb temperature by feeling the patient’s hands: are they cool or warm?
Measure the capillary refill time. Apply cutaneous pressure for 5 seconds on a fingertip held at heart level (or just above) with enough pressure to cause blanching. Time how long it takes for the skin to return to the colour of the surrounding skin after releasing the pressure. The normal refill time is less than 2 seconds. A prolonged time suggests poor peripheral perfusion. Other factors (e.g., cold surroundings, poor lighting, old age) can prolong the time.
4. Assess the state of the veins: they may be underfilled or collapsed when hypovolaemia is present.
5. Palpate peripheral and central pulses, assessing.
Immediate Life Support shift (e.g., pneumothorax, lung fibrosis or pleural fluid).
Feel the chest wall to detect surgical emphysema or crepitus (suggesting a pneumothorax until proven otherwise).
Percuss the chest if you are trained to do so: hyper-resonance suggests a pneumothorax; dullness suggests consolidation or pleural fluid.
Auscultate the chest with a stethoscope if you are trained to do so: bronchial breathing indicates lung consolidation; absent or reduced sounds suggest a pneumothorax or pleural fluid.
The specific treatment of respiratory disorders depends upon the cause. Nevertheless, all critically ill patients should be given oxygen. In some patients with COPD, high concentrations of oxygen may depress breathing. However, these patients will also sustain organ damage or cardiac arrest if their blood oxygen tensions are allowed to decrease. In this group it is important to aim for a lower thaormal PaO, and oxygen saturation. A suitable target is a PaO, of 8 kPa (60 mmHg) or 90-92% saturation (SpOJ on pulse oximetry.
If any patient’s depth or rate of breathing is inadequate or the patient has stopped breathing, use pocket mask or two person bag-mask ventilation while calling urgently for expert help.
Circulation (C) for presence, rate, quality, regularity and equality. Barely palpable central pulses suggest a poor cardiac output, whilst a bounding pulse may indicate sepsis.
6. Measure the patient’s blood pressure. Even in shock, the blood pressure may be normal, because compensatory mechanisms increase peripheral resistance in response to reduced cardiac output. A low diastolic blood pressure suggests arterial vasodilation (as in anaphylaxis or sepsis). A narrowed pulse pressure (difference between systolic and diastolic pressures: normally about 35-45 mmHg) suggests arterial vasoconstriction (cardiogenic shock or hypovolaemia).
7. Auscultate the heart with a stethoscope if you are trained to do so.
8. Look for other signs of a poor cardiac output, such as reduced conscious level and, if the patient has a urinary catheter, oliguria (urine volume less than 0.5 ml kg [1] hour ‘).
9. Look thoroughly for external bleeding from wounds or drains, or evidence of concealed bleeding (e.g., thoracic, intraperitoneal or into gut). Don’t assume that empty surgical drains mean that the patient is not bleeding into a body cavity.
10. The treatment of cardiovascular collapse depends on the cause, but should be directed at fluid replacement, control of bleeding and restoration of tissue perfusion. Seek out signs of conditions that are immediately life-threatening, e.g., cardiac tamponade, massive or continuing haemorrhage, or septicaemic shock, and treat them urgently.
11. Insert one or more large (14 or 16 G) intravenous cannulae. Use short, wide-bore cannulae, because they enable the highest flow.
12. Take blood from a cannula for routine haemato/ogical, biochemical, coagulation and microbiological investigations, and cross-matching, before infusing intravenous fluid.
13. Give a rapid fluid challenge of 500 ml of warmed crystalloid solution (e.g., Hartmann’s or 0.9% saline) in 5-10 minutes if the patient is normotensive, or one litre if the patient is hypotensive. Use smaller volumes (e.g., 250 ml) for patients with known cardiac failure and use closer monitoring (listen to the chest for crepitations after each bolus). The use of invasive monitoring, e.g., central venous pressure (CVP), can help to assess fluid resuscitation.
14. Reassess the pulse rate and blood pressure regularly (every 5 minutes), aiming for the patient’s normal blood pressure or, if this is unknown, a systolic blood pressure greater than 100 mmHg.
15. If the patient does not improve, repeat the fluid challenge.
16. If the patient develops heart failure slow or stop the fluid infusion. Signs and symptoms of heart failure include shortness of breath, increased heart rate and crackles on chest auscultation. The patient may not be able to lay flat because of shortness of breath (orthopnoea). In severe heart failure the patient may have pink frothy sputum due to pulmonary oedema. Ask for expert help as the patient may need diuretics, vasodilators or inotropes.
17. If the patient has primary chest pain and a suspected acute coronary syndrome, assess the ABCDEs, record a 12-lead ECG early, and treat initially with oxygen, aspirin, nitroglycerine and morphine.
Number of responders
The single responder must always ensure that help is coming. Usually, other staff are nearby and several actions can be undertaken simultaneously.
Why is in-hospital resuscitation different?
The exact sequence of actions after in-hospital cardiac arrest depends on several factors including:
■ location (clinical or non clinical area; monitored or unmonitored area);
■ skills of the first responders;
■ number of responders;
■ equipment available;
■ hospital response system to cardiac arrest and medical emergencies, e.g., medical emergency team (MET), cardiac arrest team.
Location
Patients who have monitored arrests are usually diagnosed quickly. Ward patients may have been deteriorating before an unwitnessed arrest. Ideally, all patients who are at high risk of cardiac arrest should be cared for in a monitored area where facilities for immediate resuscitation are available. Patients, visitors or staff may also suffer from cardiac arrest ion-clinical.
Equipment available
Staff in all clinical areas should have immediate access to resuscitation equipment and drugs to help with rapid resuscitation of the patient in cardiorespiratory arrest. Ideally, the equipment used for CPR, including defibrillators, the layout of equipment, and the drugs should be standardised throughout the hospital. You should be familiar with the resuscitation equipment used in your clinical area.
Resuscitation team
The resuscitation team might be a traditional cardiac arrest team, called only when cardiac arrest is recognised. Alternatively, there may be strategies to recognise patients at risk of cardiac arrest and summon a team (e.g., MET) before cardiac arrest occurs.
In-hospital resuscitation
Collapsed / sick patient
Shout for HELP and assess patient
Call Resuscitation Team Assess ABCDE Recognize and treat
Oxygen, monitoring, IV access
CPR 30:2
with oxygen and airway adjuncts Call Resuscitation Team if appropriate
Apply pads / monitor
Attempt defibrillation if appropriate Handover to Resuscitation Team
Advanced Life Support when Resuscitation Team arrives
Figure 2.1 In-hospital resuscitation
10 Immediate Life Support
Sequence for ‘collapsed’ patient in a hospital
3A If he responds
• Urgent medical assessment is needed, which may be from a resuscitation team (e.g., MET). While waiting for the team, assess the patient by the ABCDE approach, give oxygen, attach monitoring, and obtain venous access.
1 Ensure personal safety
There are very few reports of rescuers suffering ill effects from undertaking CPR.
• Your personal safety and that of resuscitation team members is the first priority during any resuscitation attempt.
• Check the patient’s surroundings are safe.
• Put on gloves as soon as possible. Other protective measures, such as eye protection, aprons and face masks, may be necessary.
• The risk of infection is much lower than perceived. There are isolated reports of infections such as tuberculosis (TB), and severe acute respiratory distress syndrome (SARS). Transmission of HIV during CPR has never been reported. Use a pocket mask with filter,
or a barrier device with one-way valve, to reduce infection risk during rescue breathing. The efficacy of face shields is unproved and they do not reliably prevent transmission of bacteria to the rescuer side of the shield.
• Wear full personal protective equipment when the patient has a serious infection such as TB or SARS.
• Be careful with sharps; a sharps box must be immediately available.
• Use safe handling techniques for moving patients during resuscitation.
• Take care with patients exposed to poisons. If the patient has been exposed to hydrogen cyanide or hydrogen sulphide gas, assisted ventilation must be by mask with a non-return system to avoid exhaled air. Corrosive chemicals (such as strong acids, alkalis, or paraquat) or substances such as organophosphates are easily absorbed through the skin or respiratory tract. In these circumstances, care must be taken when handling the patient’s clothes or any of their body fluids, especially vomit.
• There are no reports of infection acquired during CPR training. Nevertheless, take sensible precautions to avoid potential cross-infection from manikins. Clean manikins regularly and disinfect thoroughly after each use.
2 Check the patient for a response
If you see a patient collapse, or find a patient apparently unconscious in a clinical area, first shout for help, then assess if he is responsive (shake and shout). Gently shake his shoulders and ask loudly, “Are you all right?”(Figure 2.2).
• If other members of staff are nearby it will be possible to undertake actions simultaneously.
3B If he does not respond
• The exact sequence will depend on your training and experience in the assessment of breathing and circulation in sick patients. Agonal breathing (occasional gasps, or slow, laboured or noisy breathing) is common in the early stages of cardiac arrest and should not be mistaken for a sign of life.
• Shout for help (if not already).
• Turn the patient on to his back.
• Open the airway using head tilt and chin lift (Figure 2.3).
Look in the mouth. If there is a foreign body or debris, remove it with forceps or suction.
If there is a risk of cervical spine injury, establish a clear upper airway by using jaw thrust or chin lift in combination with manual in-line stabilisation (MILS) of the head and neck by an assistant (if enough people are available). If life-threatening airway obstruction persists despite effective application of jaw thrust or chin lift, add head tilt a small amount at a time until the airway is open; establishing a patent airway takes priority over concerns about a potential cervical spine injury.
Keeping the airway open, look, listen, and feel for no more than 10 seconds (Figure 2.4) to determine if the patient is breathing normally (an occasional gasp, or slow, laboured or noisy breathing is not normal):
Look for chest movement (breathing or coughing).
Look for any other movement or signs of life.
Listen at the victim’s mouth for breath sounds.
Feel for air on your cheek.
It can be difficult even for trained hospital staff to be certain that there is no pulse. If the patient shows no signs of life (based on lack of movement, breathing, or coughing), start CPR until more experienced help arrives or the patient does show signs of life.
If you are trained and experienced in the assessment of sick patients, check for breathing and signs of life as described above and also assess the carotid pulse at the same time (Figure 2.5). This should be for no more than 10 seconds.
If the patient shows no signs of life, no pulse, or if there is any doubt, start CPR immediately.
If unsure, do not delay starting CPR. The patient is more likely to die if there is delay diagnosing cardiac arrest and starting CPR. Starting CPR on a very sick patient with a low cardiac output is unlikely to harm and may help.
• Assess the patient to confirm cardiac arrest even if the patient is monitored in a critical care area.
4A If he has a pulse or signs of life
• Urgent medical assessment is required, which may be a resuscitation team. While waiting for the team, assess the patient by the ABCDE approach, give the patient oxygen, attach monitoring, and insert an intravenous cannula.
4B If there is no pulse or no signs of life
Remember – treat the patient not the ECG
Cardiac monitoring
Introduction
Planned monitoring
ECG monitoring enables identification of the cardiac rhythm in patients in cardiac arrest. Monitoring patients at risk of developing arrhythmias can enable treatment before cardiac arrest occurs. Patients at risk of cardiac arrest include those with chest pain, collapse or syncope, palpitations, or shock (e.g., due to bleeding or sepsis). Simple, single-lead ECG monitoring will not reliably detect cardiac ischaemia. Record serial 12-lead ECGs in patients experiencing chest pain suggestive of an acute coronary syndrome.
Accurate analysis of cardiac rhythm abnormalities requires experience, but by applying basic principles most rhythms can be interpreted sufficiently to allow selection of the appropriate treatment. The inability to reliably recognise ventricular fibrillation (VF) or other rhythms likely to respond to a shock is a major drawback in the use of manual defibrillators. Shock advisory defibrillators and automated external defibrillators (AEDs) overcome this problem by automatic analysis of the rhythm. For a shockable rhythm, the defibrillator charges to a predetermined energy and instructs the operator that a shock is required. The introduction of AEDs has meant that more people caow apply defibrillation safely. People who lack training or confidence in recognising cardiac rhythms should use AEDs.
It may be difficult to diagnose accurately an abnormal peri-arrest rhythm. Nevertheless, by following simple rules, any arrhythmia can be classified sufficiently accurately to enable recognition that the rhythm is abnormal, to assess the effect of the rhythm on the patient’s clinical condition, and thus to select appropriate and effective treatment. For example, a precise ECG classification of a bradycardia is usually less important than recognising that the heart rate is inappropriately slow for the patient and starting appropriate treatment with atropine or cardiac pacing. It is equally important to assess the haemodynamic effects of a tachycardia. In many cases the precise treatment for a tachycardia, and the urgency for it, depends greatly on the effects of the arrhythmia on cardiac output. In turn, these depend.
When there is time to plan ECG monitoring, attach self-adhesive ECG electrodes to the patient’s chest. The positions described will allow records that approximate to standard lead I, II, and III of the conventional ECG. Select the configuration that displays the most prominent P waves (if organised atrial activity is present) with sufficient QRS amplitude. This is usually lead II.
The ECG cables are usually colour coded. In one common pattern (Figure 5.1) the red electrode goes to the right shoulder (Red to the Right), the yellow electrode to the left shoulder (yeLLow to Left), and the green or leg electrode below the pectoral muscles or on the upper abdominal wall (‘Green for Spleen’). Placing the electrodes over bone rather than muscle reduces electrical interference. Leave the precordium unobstructed for chest compression and defibrillation. If possible, shave the areas where the electrodes are attached, and clean the skin with alcohol to dissolve skin oil. Most adhesive electrodes include an electrolyte gel to ensure good electrical contact. Some electrodes have a rough surface on the wrapping, which can be used to gently abrade the skin before the electrode is attached, improving contact. In co-operative patients, reduce movement artefact by keeping them warm and reassured.
Emergency monitoring
Monitor the cardiac rhythm continuously with proper ECG electrodes as soon as possible after cardiac arrest. There are two quick ways to monitor the cardiac arrest rhythm if a defibrillator is available:
Self-adhesive defibrillation electrodes (‘pads’)
Self-adhesive electrodes can be used both for monitoring and for hands free shock delivery (Figure 5.2).
The electrodes are applied in the conventional positions: one beneath the right clavicle and the other over the left lower chest in the mid-axillary line. Wheecessary, e.g., lateral chest trauma or a right-sided permanent pacemaker, use the anterior-posterior position. For more information on alternative positions for electrode placement see chapter 6.
‘Quick-look’ paddles
Most modern manual defibrillators enable the rhythm to be monitored through the paddles when they are applied to the chest wall (Figure 5.3) but they need to be held in position. Unless there is a long interruption to chest compression, this allows only a quick-look at the rhythm. If the paddles are not held absolutely still, movement artefacts make it difficult to interpret the rhythm. To improve electrical contact gel pads should be used between the paddles and the skin.
Diagnosis from cardiac monitors
The displays and printouts from cardiac monitors are suitable only for recognition of rhythms and not for more detailed ECG interpretation.
Basic electrocardiography
The normal adult heart rate is defined as 60-100 min ‘. A rate below 60 min 1 is a bradycardia and a rate of 100 min 1 or more is a tachycardia.
Under normal circumstances depolarisation is initiated from a group of specialised pacemaker cells, the sinoatrial (SA) node, in the right atrium (Figure 5.4). The wave of depolarisation spreads from the SA node into the atrial muscle; this is seen on the ECG as the P wave (Figure 5.5). Atrial contraction is the mechanical response to this electrical impulse.
Spread to the ventricular muscle is along specialised conducting tissue the atrioventricular (AV) node and His-Purkinje system. The bundle of His bifurcates to allow depolarisation to spread into the ventricular muscle along two specialised bundles of conducting tissue the right bundle branch to the right ventricle and the left bundle to the left ventricle.
Depolarisation of the ventricles is reflected in the QRS complex of the ECG. The normal sequence of cardiac depolarisation described above is known as sinus rhythm. The T wave that follows the QRS complex represents ventricular repolarisation.
The specialised cells of the conducting tissue (the AV node and His-Purkinje system) enable coordinated ventricular depolarisation, which is more rapid than uncoordinated depolarisation. With normal depolarization, the QRS complex is narrow, which is defined as less than 0.12 seconds. If one of the bundle branches is diseased, conduction delay causes a broad QRS complex, i.e., greater than 0.12 seconds (3 small squares on the ECG).
Cardiac arrest rhythms
Larger ECG rhythms are included at the end of this chapter.
Ventricular fibrillation (VF)
In VF the ventricular myocardium depolarises randomly. The ECG shows rapid, bizarre, irregular waves of widely varying frequency and amplitude (Figure 5.6).
VF is sometimes classified as coarse or fine depending on the amplitude (height) of the complexes. If there is doubt about whether a rhythm is asystole or very fine VF, do not attempt defibrillation; instead, continue chest compressions and ventilation. Very fine VF that is difficult to distinguish from asystole will not be shocked successfully into a perfusing rhythm. Continuing good quality CPR may improve the amplitude and frequency of the VF and improve the chances of successful defibrillation and a perfusing rhythm. If the rhythm is clearly VF, attempt defibrillation.
Ventricular tachycardia (VT)
Ventricular tachycardia, particularly at higher rates or when the left ventricle is compromised, may cause profound loss of cardiac output. Pulseless VT is managed in the same way as Vf.The ЈCG shows a bToad-comp\ex tachycardia. In monomorphic VT, the rhythm is regular (or almost regular) at a rate of 100-300 min 1 (Figure 5.7).
Asystole
Usually there is neither atrial nor ventricular activity, and the ECG is a more or less straight line (Figure 5.8). Deflections, which can be confused with fine VF, can be caused by baseline drift, electrical interference, respiratory movements, or cardiopulmonary resuscitation. A completely straight line usually means that a monitoring lead has disconnected.Whenever asystole is suspected, check that the gain on the monitor is set correctly (1 mV cm1) and that the leads are connected correctly.
Figure 5.8 Asystole
If the monitor has the facility, view another lead configuration. Atrial activity, i.e., P waves, may continue for a short time after the onset of ventricular asystole: there will be P waves on the ECG but no evidence of ventricular depolarisation (Figure 5.9). These patients may be suitable for cardiac pacing.
Figure 5.9 P waves Asystole
Pulseless electrical activity (PEA)
The term pulseless electrical activity, sometimes referred to as electromechanical dissociation (EMD), means normal (or near normal) electrical activity without effective cardiac output, and is treated as cardiac arrest. The diagnosis is made from clinically absent cardiac output but a rhythm that would normally be accompanied by a good cardiac output.
Bradycardia
The treatment of bradycardia (less than 60 min ‘) depends on its haemodynamic consequences. Bradycardia may mean imminent cardiac arrest.
Agonal rhythm
Agonal rhythm is characterised by slow, irregular, wide ventricular complexes of varying shape (Figure 5.10). It is usually seen during the late stages of unsuccessful resuscitation. The complexes slow inexorably becoming progressively broader until all recognisable electrical activity is lost.
Figure 5.10 Agonal rhythm
Monitor the ECG in all patients in cardiac arrest
Automated defibrillators will recognise shockable rhythms (VF/VT) and advise a shock
Key learning points
Rhythm strips
Rhythm Strip 3 Fine ventricular fibrillation
Rhythm Strip 4 Ventricular tachycardia
Rhythm Strip 5 Asystole
Rhythm Strip 6 P-wave asystole
Rhythm Strip 7 Sinus bradycardia
Rhythm Strip 8 Agonal rythm
DefibrillationCHAPTER
Objectives
To understand:
The mechanism of defibrillation.
The factors affecting defibrillation success.
How to deliver a shock safely using an automated external defibrillator (AED).
How to deliver a shock safely using a manual defibrillator.
There is no strict relationship between body size and the energy needed for defibrillation. Factors such as the patient’s metabolic state, degree of myocardial ischaemia, and previous drug therapy also affect the success of defibrillation attempts, although little can be done about these during cardiopulmonary resuscitation.
Factors affecting defibrillation success
Introduction
If cardiac output stops, cerebral hypoxic injury starts within 3 minutes. For complete neurological recovery, successful defibrillation must be accomplished rapidly. If there is any delay in obtaining a defibrillator, start chest compressions and ventilation immediately. CPR will buy time and increase the chance of successful defibrillation. The definitive treatment of ventricular fibrillation or pulseless ventricular tachycardia (VF/VT) is a shock. The shorter the interval between the onset of VF/VT and the shock, the greater the chance of successful defibrillation.
Mechanism of defibrillation
Defibrillation is defined as the termination of fibrillation or, more precisely, the absence of VF/VT 5 seconds after shock delivery. To accomplish this, an electrical current is passed across the myocardium for synchronous depolarisation of a critical mass of the cardiac muscle, which allows the natural pacemaking tissue to resume control. To achieve this, defibrillators all have: a power source capable of providing direct current; a capacitor that can be charged to a pre-determined energy level; and two electrodes placed on the patient’s chest through which the capacitor is discharged. Success depends on sufficient current (measured in amperes) being delivered to the myocardium, although the actual current needed is difficult to estimate. This is because it depends on transthoracic impedance, the position of electrodes, and the passage of the current along other pathways in the thorax away from the heart; consequently, as little as 4% of the current reaches the heart. The energy stored in the capacitor can be determined, and for a given thoracic impedance the current flow is proportional to the energy. Some defibrillators measure the transthoracic impedance and adjust their output accordingly, which is known as impedance compensation.
Transthoracic impedance
Transthoracic impedance is influenced by electrode or paddle size, the paddle-skin coupling material, electrode-to-skin contact, paddle force, and phase of ventilation. A transdermal drug patch on the patient’s chest may prevent good contact and may cause arcing and burns if paddles or electrodes are placed over it: remove and wipe the area dry before applying the electrodes and attempting defibrillation.
Shaving the chest
Hairy chests increase impedance and can reduce defibrillation success and cause burns to the patient’s chest. Shave hair from the area where the electrodes are placed. Defibrillation must not be delayed if a razor is not immediately to hand. To minimise interruptions to chest compressions, shave the chest while another rescuer continues CPR.
Electrode size
Larger electrodes have lower impedance, but excessively large electrodes reduce transmyocardial current flow too much. For adult defibrillation, both handheld paddle electrodes and self-adhesive pad electrodes 8-12 cm in diameter are used and work well.
Coupling agents
If using manual paddles, gel pads are better than pastes and gels, which can spread between the two paddles, short-circuiting them and increasing the risk of arcing. Do not use bare paddles without coupling material because the resulting high skin resistance increases the risk of cutaneous burns. Do not use medical gels (e.g., ultrasound gel) or pastes, which may have poor electrical conductivity.
Paddle force
If using paddles, apply them firmly to the chest wall: the optimal force is 8 kg for an adult. Firm pressure reduces transthoracic impedance by improving electrical contact at the electrode-skin interface and reducing thoracic volume.
Electrode position
The electrodes are positioned for greatest current flow through the myocardium. The standard positions are one electrode to the right of the upper sternum below the clavicle, and the other (apical) in the mid-axillary line, approximately level with the V6 ECG electrode and clear of breast tissue. The apical electrode must be sufficiently lateral (Figure 6.1). Although the electrodes are marked positive and negative, they can be placed in either position. Other acceptable positions include:
Use of single shocks
First shock success of biphasic defibrillators exceeds 90%. Failure suggests the need for a period of CPR. Thus, immediately after giving a single shock, and without reassessing the rhythm or feeling for a pulse, resume CPR (30 compressions: 2 ventilations) for 2 minutes before delivering another shock (if indicated) (see below). Even if defibrillation is successful in restoring a perfusing rhythm, it is very rare for a pulse to be palpable immediately after defibrillation and the delay feeling for a pulse risks damaging the myocardium if a perfusing rhythm has not been restored. If there is a perfusing rhythm, chest compressions do not increase the chance of VF recurring. In post-shock asystole, chest compressions may induce VF.
• The lateral chest walls, one on the right and the other on the left (bi-axillary).
• One electrode in the standard apical position and the other on the right or left upper back.
• One electrode anteriorly, over the left precordium, and the other electrode posterior to the heart just inferior to the left scapula.
• Orientate the long axis of the apical paddle in a cranio-caudal direction.
Shock energy and waveforms
Monophasic defibrillators
Monophasic defibrillators are no longer manufactured although many remain in use. These devices deliver a current that flows in one direction (Figure 6.2). Because a monophasic waveform is less effective than a biphasic waveform, the recommended energy for a monophasic defibrillator is 360 J. Although the higher energy risks more myocardial injury, the benefits of earlier conversion outweigh the risks.
Pads versus paddles
Self-adhesive defibrillation pads are safe and effective and are better than standard defibrillation paddles. Consider using self-adhesive pads in peri-arrest situations and in clinical situations where patient access is difficult. They have a similar transthoracic impedance (and therefore efficacy) to manual paddles and the operator can defibrillate from a safe distance rather than having to lean over the patient. When used for initial monitoring of a rhythm, pads or paddles enable quicker delivery of the first shock than standard ECG electrodes, and pads are quicker than paddles.
Biphasic defibrillators
Biphasic waveforms deliver current that flows first positively and theegatively (Figure 6.3). Some biphasic defibrillators automatically adjust for variation in transthoracic impedance by altering the amplitude and duration of the waveform.
Biphasic waveforms are recommended whenever possible: they are more effective, and first shock defibrillation for long duration VF/VT is more likely. Biphasic defibrillation requires less energy. The devices have smaller capacitors and need less battery power. Consequently they are smaller, lighter and easily portable.-10 -15 -20
It is recommended that the initial biphasic shock should be at least 150 J whatever the type of biphasic waveform.
If you are unaware of the effective dose range of a device, use 200 J for the first shock because 200 J is within the reported range of selected doses that are effective for first and subsequent biphasic shocks, and 200 J can be provided by every biphasic manual defibrillator currently available. If biphasic devices are clearly labelled and providers are familiar with the devices in their clinical areas, there will be no need for the default 200 J dose.
If the first shock is unsuccessful, second and subsequent shocks can be delivered using either fixed or escalating energies (150-360 J), depending on the device. If you are unaware of the effective dose range and the first shock was a default 200 J, use an equal or higher dose for second or subsequent shocks, depending on the capabilities of the device.
Recurrent ventricular fibrillation
If a shockable rhythm recurs after successful defibrillation (with or without a return of spontaneous circulation) give the next shock at the previously successful energy.
Safety
Do not put members of the resuscitation team at risk. Be wary of wet surroundings or clothing: wipe any liquid from the patient’s chest before attempting defibrillation. No part of any person should make direct or indirect contact with the patient. Do not hold intravenous infusion equipment or the patient’s trolley during shock delivery. The defibrillator operator must not touch any part of the electrode surface, and electrode gel must not spread across the chest. Gel-impregnated pads reduce this risk – use them whenever possible. The operator must ensure that everyone is clear of the patient before delivering a shock.
Safe use of oxygen during defibrillation
In an oxygen-enriched atmosphere, sparks from poorly applied defibrillator paddles can cause a fire. The risk of fire can be reduced by taking the following precautions:
Take off any oxygen mask or nasal cannulae and place them at least 1 m away from the patient’s chest (Figure 6.4). Leave the ventilation bag connected to the tracheal tube or other airway adjunct. There is no increase in the concentration of oxygen in the zone of defibrillation when the ventilation bag is left connected to the tracheal tube, even with an oxygen flow of 15 I min ‘. Alternatively, disconnect the ventilation bag from the tracheal tube or other airway adjunct such as the laryngeal mask airway, and remove it at least 1 m from the patient’s chest during defibrillation.
If the patient is connected to a ventilator, e.g., in the operating room or critical care unit, leave the ventilator tubing (breathing circuit) connected to the tracheal tube. If chest compressions prevent the ventilator from delivering adequate tidal volumes, use a manual ventilation bag, which can be left connected, or detached and removed to a distance of at least 1 m. If the ventilator tubing is disconnected, ensure it is kept at least 1 m from the patient or, better still, switch the ventilator off; modern ventilators generate massive oxygen flows when disconnected. During normal use, when connected to a tracheal tube, oxygen from a ventilator in the critical care unit will be vented from the main ventilator housing well away from the defibrillation zone. Reduce the risk of sparks during defibrillation: use self-adhesive defibrillation pads.
Safety when using defibrillator paddles
Charge a manual defibrillator only with the paddles on the patient’s chest, not held in the air. When the paddles are first placed, inform team members whether the paddles are to be charged or are simply monitoring heart rhythm. If the defibrillator is charged but a shock is no longer indicated, modern equipment can be discharged safely by asking a colleague to alter the energy setting to zero or to press the disarm button.
Automated external defibrillators
Automated external defibrillators (AEDs) are sophisticated, reliable computerised devices that use voice and visual prompts to guide lay rescuers and healthcare professionals to attempt safe defibrillation in cardiac arrest victims (Figure 6.5).
Automated rhythm analysis
It is almost impossible to shock inappropriately with an AED. Movement is usually sensed, so movement artefact is unlikely to be interpreted as a shockable rhythm. It is much easier to train for the use of AEDs than for manual defibrillators. Automated equipment has made attempted defibrillation possible for a much wider range of medical, nursing, and paramedical staff, and even for lay workers such as police and first aiders. New technology should enable AEDs to provide information about frequency and depth of chest compressions during CPR.
In-hospital use of AEDs
AEDs should be considered in hospital to facilitate early defibrillation, especially in areas where staff have no skills at recognising rhythms or where defibrillators are used infrequently. An effective system for training and retraining should be in place. Adequate numbers of staff should be trained to enable achievement of the goal of providing the first shock within 3 minutes of collapse anywhere in the hospital.
Healthcare professionals should be trained, equipped, and authorised to perform defibrillation. Attempted defibrillation by first responders is vital, as the delay to delivery of the first shock is the main determinant of survival in cardiac arrest.
Defibrillators can have just an AED mode, just a manual mode or a combination of both AED and manual modes. The type of defibrillator available in a clinical area should depend on the skills of the staff. Ideally defibrillators that combine both an AED and manual mode are best.
Importance of uninterrupted chest compressions. The importance of early uninterrupted external chest compression is emphasised throughout this manual. The rescuer providing chest compressions should interrupt chest compressions only for rhythm analysis and shock delivery, and should be prepared to resume chest compressions as soon as a shock is delivered. When two rescuers are present, the rescuer operating the AED should apply the electrodes during CPR (Figure 6.6). Interrupt CPR only when it is necessary to assess the rhythm and deliver a shock. The AED operator should be prepared to deliver a shock as soon as analysis is complete and the shock is advised, ensuring no rescuer is in contact with the victim. The single rescuer should practise coordination of CPR with efficient AED operation.
Public access defibrillation (PAD) programmes
Public access defibrillation (PAD) and first responder AED programmes may increase the number of victims who receive bystander CPR and early defibrillation, thus improving survival from out-of-hospital cardiac arrest. These programmes require an organised and practised response from rescuers trained and equipped to recognise emergencies, activate the emergency medical system, e.g., ambulance service, provide CPR, and use the AED. Lay rescuer AED programmes with rapid response times in airports, on aircraft, or in casinos, and studies in which police officers were first responders have achieved survival rates as high as 49-74%.
Recommended elements for PAD programmes include:
• a planned and practised response;
• training of rescuers in CPR and AED use;
• a link with the local EMS system (e.g., ambulance service);
• a programme of continuous audit (quality improvement).
Public access defibrillation programmes are most likely to improve survival from cardiac arrest if they are in locations where witnessed cardiac arrests are likely. Suitable sites might be those where the probability of a cardiac arrest is at least once every 2 years (e.g., airports, casinos, or sports facilities). Approximately 80% of out-of-hospital cardiac arrests occur in private or residential settings, which inevitably limits the overall effect that these programmes can have on survival rates.
The AED algorithm
The AED algorithm is shown in Figure 6.8. It is based on the lay rescuer in the community. Depending on their training and local policy, in addition to the use of the AED, healthcare professionals should consider:
Assessing for pulse and signs of life to diagnose cardiac arrest. . Calling for a resuscitation team after in-hospital cardiac arrest.
. Recognising and treating the reversible causes of cardiac arrest.
. Use of other interventions (e.g., tracheal intubation, intravenous access, drug administration).
The advanced life support algorithm (chapter 3) includes these extra interventions. Make sure you, the patient, and any bystanders are safe. If the victim is unresponsive and not breathing normally:
. Send someone for the AED and call for an ambulance or resuscitation team.
. If you are on your own do this yourself.
Start CPR according to the guidelines (chapter 2). As soon as the defibrillator arrives:
. Switch on the defibrillator and attach the electrode pads. If more than one rescuer is present, CPR should be continued whilst this is done.
. Follow the voice or visual prompts.
. Ensure that nobody touches the patient whilst the AED is analysing the rhythm.
5A If a shock IS indicated:
. Ensure that nobody touches the patient (Figure 6.7 – top).
. Push shock button as directed (fully automatic AEDs will deliver the shock automatically.)
. Continue as directed by the voice or visual prompts.
5B If NO shock indicated:
. Immediately resume CPR using a ratio of 30 compressions to 2 breaths (Figure 6.7 – bottom).
. Continue as directed by the voice or visual prompts.
6 Continue to follow the AED prompts until:
. Qualified help (e.g., ambulance or resuscitation team) arrives and takes over.
. The victim starts to breathe normally.
. You become exhausted.
∙ The carrying case for the AED must contain strong scissors for cutting through clothing and a disposable razor for shaving chest hair.
Sources of information:
1. American Heart Association in collaboration with the International Liaison Committee on Resuscitation (ILCOR)/ International Guidelines 2000 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. A Consensus on Science // Resuscitation. – 2000. – 46. – P. 103 – 252.
2. European Resuscitation Council. Immediate life support. 1- st Edition. Published by European Resuscitation Council Secretariat VZW, 2006.
3. Lattore F., Nolan J., Robertson C. et al. The ALS working group of the European Resuscitation Council. The European Resuscitation Council Guidelines 2000 for Adult Advanced Life Support Resuscitation. 2000. – 48. – P. 211 – 212.
4. Safar P, Bircher NG. Cardiopulmonary and cerebral resuscitation. 3rd ed. London: WB Saunders, 1988.
5. John Campbell. International Trauma Life Support. USA. New Jersey 2008. P. 289.
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18. http://zakon2.rada.gov.ua/laws/show/5081-17
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20. http://www.bibliofond.ru/view.aspx?id=492657.
