Defibrillation, ventilation, pacing and resuscitation are essential components of cardiac surgical care. The 2015 European Resuscitation Council (ERC) guidelines report the incidence of resuscitation as 0.7–8% after adult cardiac surgery. This wide range is almost certainly due to resuscitation interventions frequently being undertaken in house on many cardiac surgical ICUs, and therefore going under the radar of the clinical audit. Prompt and effective basic life support (BLS) and early defibrillation for shockable rhythms are the two most important interventions after cardiac arrest. Chest reopening and extracorporeal membrane oxygenation (ECMO) for patients with refractory cardiogenic shock are additional therapeutic options. As patients undergoing cardiac surgery become older and sicker, quality of resuscitation will continue to increase in importance.
Conventional basic and advanced life support guidelines provide a useful framework but require modification in the cardiac surgical ICU setting. The European Association of Cardiothoracic Surgery (EACTS) guidelines summarise the key modifications that must be considered for adult patients in cardiac arrest after cardiac surgery. Although current resuscitation algorithms typically divide arrests into two (shockable and non-shockable) limbs, EACTS subdivide the non-shockable category and utilise a three-limb approach. The EACTS three-limb model emphasises important initial differences in management of patients presenting with severe bradycardia or asystole compared to those presenting with pulseless electrical activity (see Figure 25A.1). Important changes in the revised 2015 European Resuscitation Council guidelines are discussed below.
Maintaining the circulation has been promoted ahead of airway management and breathing in recent adult basic life support (BLS) guidelines. The traditional Airway, Breathing, Circulation and Defibrillation (ABCD) algorithm described in previous guidelines has been replaced by Circulation, Airway and Breathing (i.e. CAB). In general, 30 chest compressions at a rate of 100–120 per minute should now be given before any attempt to deliver rescue breaths. The efficacy of chest compressions can usually be verified in the ICU by studying the arterial pressure waveform. Interruptions to chest compressions should be minimised and last less than 10 seconds.
In situations where BLS is undertaken, the recommended ratio of chest compressions to ventilations is now 30:2. More chest compressions and fewer interruptions are achieved with this ratio than with the previously recommended 15:2 ratio. In the presence of a patent airway, effective chest compressions are considered more important than ventilation in the first few minutes of resuscitation. It should be borne in mind that coronary perfusion pressure progressively rises during chest compressions and rapidly falls with each pause for ventilation. Following a witnessed collapse in a patient with oxygenated arterial blood, the initial emphasis should normally be on chest compressions.
Because chest compressions may be injurious immediately following cardiac surgery, external cardiac massage is frequently deferred in the cardiac ICU providing defibrillation or external pacing therapy can be delivered within 30–60 seconds. The rationale for this approach and modifications to the Advanced Life Support (ALS) algorithm are discussed later.
The new 2015 Advanced Life Support (ALS) algorithm for the management of cardiac arrest in adults retains the shockable and non-shockable limbs (Figure 25A.2). There are subtle but important differences in recommendations for defibrillation for shockable rhythms in cardiothoracic ICU and the catheter laboratory. The EACTS guidelines include important advice on how to expedite the decision making and actual chest reopening process (see Figure 25A.1).
Figure 25A.1 EACTS guideline for resuscitation of a postoperative cardiac surgical ICU (or recovery) patient. From Dunning et al. (2009).
Pulseless VT and VF account for the majority of underlying dysrhythmias in patients who survive cardiac arrest in hospitals. For every minute the chances of successful defibrillation decline by 7–10%. Specialist cardiothoracic units should be capable of early detection, rapid defibrillation and superior outcomes. In the setting of the cardiac ICU, when external cardiac massage may be injurious, immediate defibrillation (i.e. DCAB) should be the first line response for all monitored in-hospital VF arrests.
Since 2005, a single shock (>150 J biphasic or 360 J monophasic) has been recommended instead of three ‘stacked’ shocks, in general hospitals. Interruptions to CPR during delivery of three shocks and improved first shock efficacy of biphasic defibrillators were cited as reasons for the change. In practice, most cardiac surgical ICU and catheter laboratory staff were unconvinced by the evidence for single shocks and continued to deliver up to three stacked shocks in quick succession when treating VF. More recent EACTS and ERC guidelines recognised this and recommend three stacked shocks in quick succession for VF/VT arrests occurring in the cardiac catheter laboratory and cardiac surgical ICU. In addition, contrary to the latest guidelines, there is usually no need to commence chest compressions after a successful shock in invasively monitored cardiac surgical patients.
A heterogeneous group of conditions may present as non-VF/VT cardiac arrest (Table 25A.1). Outcome is generally poor unless a reversible cause can be found and treated effectively. In the cardiac surgical ICU – where bleeding, hypovolaemia and tamponade are all readily treatable, and where additional therapeutic options are available – outcomes are considerably better than in the general ICU population. Examination of trends in RA pressure, PAWP and airway pressure all provide useful pointers as to the likely aetiology. Cessation of drainage from mediastinal drains does not exclude haemorrhage or tamponade as the drains may have become blocked. Although TTE and TEE echocardiography is often very useful in the cardiac ICU, echocardiography may miss localised collections and thus delay reoperation. Patients with clinical signs suggestive of tamponade should be reopened even if echocardiography is inconclusive.
|The Four ‘Hs’||The Five ‘Ts’|
When faced with an arrest of this type, it is essential to:
confirm that VF is not being missed and that ECG leads or pads are correctly attached,
treat bradycardia with epicardial pacing if wires are present,
exclude tension pneumothorax,
exclude underlying VF in the presence of fixed rate pacing, and
consider chest reopening if closed chest CPR is unsuccessful.
Symptomatic bradycardia is extremely common in the cardiac surgical ICU. ALS guidelines no longer recommend atropine as first line treatment. In the cardiac surgical ICU, where tachycardia is equally undesirable, pacing (when possible) is the preferred option. If pacing is not an option (e.g. no wires in situ or failure to capture), isoproterenol or dopamine are often used. Management of asystole that fails to respond to pacing is an indication for prompt chest reopening.
Suggested modifications to the standard ALS algorithm are shown in Figure 25A.2.
Figure 25A.2 Algorithm for resuscitation after adult cardiac surgery. Six suggested modifications to the standard ALS algorithm are highlighted in the six bright yellow boxes to the sides and below. Therapeutic hypothermia may be considered after successful resuscitation. Adapted from the Resuscitation Council (UK) 2010 ALS algorithm.
Drugs in Advanced Cardiac Life Support
Although the use of vasopressors at cardiac arrests has become standard practice, proof of efficacy is limited. Epinephrine 1 mg is recommended every 3 minutes to improve coronary and cerebral perfusion. The American Heart Association has suggested that vasopressin may be used as an alternative to epinephrine. Clinical studies, however, have failed to demonstrate that either vasopressin or high dose epinephrine (5 mg) offers any additional benefit.
On the cardiac surgical ICU it is entirely appropriate to modify the recommended pharmacological management of a monitored cardiac arrest. An α-agonist or smaller initial dosages of epinephrine (0.1–0.2 mg) may be administered to minimise the risk of hypertension and tachycardia following successful resuscitation. For patients with VF/VT arrests, it is standard practice to attempt at least three shocks before giving any epinephrine.
The evidence supporting the use of antiarrhythmic drugs in VF/VT is surprisingly weak. Two studies of out-of-hospital VF/VT arrest demonstrated that the administration of amiodarone after three unsuccessful shocks increased the likelihood of survival to hospital admission. Significantly, neither study demonstrated that amiodarone improved survival to discharge. Despite this latter finding, amiodarone has now been promoted ahead of lidocaine in the pulseless VF/VT algorithm. A bolus of amiodarone 300 mg is recommended for VF/VT arrests that persist after three shocks but this should not delay surgical reopening (see below). A further dose (150 mg) may be given for recurrent or refractory VF/VT, followed by an infusion of 900 mg over 24 hours. Lidocaine can still be given for VF/VT if the patient has received amiodarone but the evidence supporting its efficacy is weak. Magnesium should also be considered if there is clinical suspicion of hypomagnesaemia. Administration of sodium bicarbonate should be considered if arterial or mixed venous pH < 7.1.
|Confirmation of tracheal intubation|
|Monitoring ventilation rate|
|Monitoring quality chest compressions|
|Identifying ROSC during CPR|
|Prognostication during CPR: failure to achieve CO2 value >1.33 kPa (10 mmHg) after 20 minutes CPR associated with poor outcome|
The Fourth National Audit Project (NAP4) of the Royal College of Anaesthetists reported that 61% (22 of 36) of airway events in the ICU led to death or persistent neurological injury. Major risk factors for adverse events included anaesthetic experience of doctors, out-of-hours airway interventions, patient obesity and failure to use (or correctly interpret) capnography. A recurrent finding was the failure to consider the possibility of oesophageal intubation when presented with a flat capnograph trace. As well as providing valuable information about endotracheal tube position and patency, and ventilation, capnography also provides invaluable additional information about return of spontaneous circulation and cardiac output (see Table 25A.2). The introduction of mandatory waveform capnography in the CICU has arguably made the single biggest contribution to improved patient safety on the CICU since the publication of the first edition of CTiCICU 1e nearly a decade ago.
Following surgery through a sternotomy, chest reopening is both a diagnostic and therapeutic option in the cardiac surgical ICU. In addition, chest reopening allows internal cardiac massage, which is considerably more effective than external chest compressions. Haemorrhage, tamponade, graft occlusion and graft avulsion are conditions likely to be remedied by this approach. Patients most likely to benefit are: those with a surgically remediable lesion, those who arrest within 24 hours of surgery and those in whom the chest is reopened within 10 minutes of arrest. Delayed reopening or the finding of a problem that is not amenable to surgery (e.g. global cardiac dysfunction) is associated with a poor prognosis. Recent resuscitation guidelines confirm that chest reopening should be triggered by:
three failed shocks in VF/VT arrests (i.e. one resuscitation cycle);
exclusion of reversible causes (e.g. tension pneumothorax) and failure of initial treatment for non-VF/VT arrest.
Chest reopening should not be used as a ‘last ditch’ manoeuvre after a prolonged period of unsuccessful resuscitation. Although some units advocate initially stopping all infusions and syringe drivers to exclude iatrogenic drug administration errors, the majority tend to continue infusions unless there is a clinical suspicion of inadvertent vasodilator flushing being responsible for loss of CO. Whichever policy is used, it is important to ensure that anaesthesia and analgesia are restored prior to chest reopening. The EACTS guidelines and Cardiac Advanced Life Support (CALS) courses recommend six key roles in the management of a cardiac surgical ICU arrest (Figure 25A.3).
Figure 25A.3 Six key roles in cardiac surgical ICU arrest. From Dunning et al. (2009).
Cardiopulmonary Bypass and ECMO
The reinstitution of cardiopulmonary bypass (CPB) following emergency chest reopening may allow the resuscitation of a patient who would otherwise die. Hypothermic CPB restores organ perfusion, decompresses the heart, and allows the surgeon to consider all possible options in a more controlled setting. Valve replacement, repair of bleeding cannulation sites, graft revision and additional grafting may be undertaken with often surprisingly successful clinical outcomes. Whenever possible the patient should be transferred to the operating room before emergency reinstitution of CPB.
Patients with greater preoperative surgical risk, adverse intraoperative events and poor physiological state at the time of ICU admission are less likely to survive to hospital discharge. Similarly, refractory multisystem organ failure and recurrent nosocomial infection have been shown to be important determinants of mortality. For some patients, there comes a point when aggressive resuscitation is inappropriate and cardiopulmonary arrest becomes a terminal event. It is the duty of a doctor to identify these patients and to ensure that they are spared the indignity of futile interventions.
DNAR directives should be instituted if it is believed that death is inevitable and that CPR is unlikely to be successful. Sensible guidelines on implementation of DNAR orders can be found on the UK Resuscitation Council’s website (www.resus.org.uk/dnacpr).
Resuscitation Outside the ICU
The management of a cardiac arrest outside the ICU differs little from a cardiac arrest on a general surgical or medical ward. Seemingly trivial symptoms and vague ‘early warning’ signs should be taken seriously as they may herald a more sinister event. Although some arrests are unheralded, the majority of patients who arrest in the general ward setting display signs of physiological deterioration long before the event.
Early intervention seems intuitive and may reduce the incidence of cardiac arrests in the surgical ward setting. Early warning scores (EWS) are used to ‘track’ patients’ physiological status and ‘trigger’ a response or intervention. Tracking the patient – the so-called ‘afferent limb’ – involves either a single or multiple parameter scoring system. Single parameter scoring systems have limitations. Many of the suggested criteria for triggering a response are actually relatively late markers of physiological deterioration (Table 25A.3). Aggregated weighted systems may provide earlier warning of deterioration and can be adapted for use in cardiothoracic wards (Table 25A.4).
The use of medical emergency teams (MET) has been shown to reduce both the incidence of and mortality from unexpected ward arrests in general hospitals. The effectiveness of the MET concept is significantly hampered by incomplete documentation of patient observations. Given the importance of respiratory rate and urinary output, recording of these values is often surprisingly poor.
|Neurology||Fall in Glasgow coma scale (GCS) score >2 points|
|Renal||Urine output <0.5 ml/kg/hr for 2 consecutive hours|
|Oximetry||SpO2 < 90% regardless of FiO2|
|Other||Patients giving cause for concern who do not meet above criteria|
|Score||Tem p( 0C)||Neuro AVPU or ACDU||Respiratory rate||pO2/FiO2 ratio||Heart rate||Systolic BP||Urine output catheter in situ No catheter|
** pO2/FiO2 ratio = (kPa).
PU = passed urine; NPU = not passed urine.
The relative success of chest reopening following cardiac arrest on the ICU cannot be reproduced when chest reopening is undertaken on the ward or surgical floor. The proportion of surgically remediable causes of cardiac arrest decreases exponentially after surgery. As time passes, thromboembolic phenomena and cardiac failure become more common than surgical bleeding or tamponade. A small number of patients who sustain a witnessed arrest on the ward or surgical floor may benefit from chest reopening either locally with appropriate facilities or in the operating room. The decision to reopen a ward patient either locally or after ‘scoop and run’ is usually more difficult than the decision to reopen on the cardiac ICU. Whereas there is level-one evidence to support chest reopening in the cardiac ICU, the latest ERC guidelines do not specifically address the role of chest reopening for patients who arrest outside the cardiac ICU. A scoop and run approach should be considered following:
1. A witnessed arrest;
2. Unexpected arrest in a patient who had initially been making good progress;
3. Tension pneumothorax considered and excluded;
4. Close proximity to operating theatres;
5. Non-VF/VT arrest with a high index of suspicion of hypovolaemia (major bleeding), tamponade, acute thromboembolism or air embolism;
6. VF/VT arrests unresponsive to DC shocks that may have acute graft occlusion.
A patient’s suitability for chest reopening and reinstitution of CPB should be considered after one cycle of CPR. The decision to scoop and run must be made early because time is of the essence. Good quality chest compressions and ventilation must be maintained during transfer. Epinephrine 1 mg (or an alternative vasopressor) should be given every 3–5 minutes as per standard ALS guidelines, rather than the reduced dosages recommended in cardiac surgical ICU for patients in the immediate postoperative period. It needs to be emphasised that scoop and run will only be successful if both the heart and brain are successfully restored to normal or near-normal function.
VF/VT arrests during elective procedures in the catheter laboratory are invariably iatrogenic, typically amenable to very early defibrillation and associated with return of spontaneous circulation in >90% of cases, and have >80% chance of survival to discharge. As discussed earlier, recent ERC guidelines recommend administration of three stacked shocks in quick succession for VF/VT arrests occurring in the cardiac catheter laboratory. In cases of coronary dissection or other surgically amenable conditions, early consideration of transfer to the operating room and institution of CPB should be considered.
Patients undergoing primary percutaneous intervention who require airway intervention present similar challenges to those on the ICU albeit in a remote environment with potentially limited immediate anaesthetic support. As with the ICU, skilled anaesthetic assistance and waveform capnography are both mandatory.
ECMO assisted CPR, so-called E-CPR, is an additional therapeutic option for selected patients in ECMO centres. The CHEER trial recently reported that 14 of 26 (54%) patients with refractory in-hospital and out-of-hospital arrests survived to hospital discharge with full neurological recovery. Running a 24/7 catheter laboratory ECMO service mandates funding of:
1. Resident (or very close proximity) consultant cardiologist, intensivist and perfusion cover;
2. ICU costs associated with potentially prolonged ICU lengths of stay awaiting neurological prognostication in comatose survivors.
Patients sustaining cardiac arrests in a cardiothoracic surgical unit are twice as likely to survive to hospital discharge as patients who arrest in a general hospital. The essential requirements for a good clinical outcome are early detection, effective BLS and early defibrillation.
ALS algorithms require modification in the cardiac surgical ICU.
Consider the possibility of underlying VF in ‘asystolic’ arrests and paced patients with apparent pulseless electrical activity.
Look for epicardial pacing wires in bradycardic arrests before giving atropine and epinephrine!
The majority of cardiac arrests after cardiac surgery are heralded by symptoms and signs.
1. Aetiology of arrests in the cardiac surgical ICU:
2. VF arrests in the cardiac surgical ICU:
Immediate BLS 30:2 always
Prepare to restart chest compressions after single shock
Amiodarone (300 mg) and adrenaline (1 mg) should be given within 3 minutes of arrest
May be due to problems with intracardiac air or graft malfunction
Chest compressions are required after successful shock to reduce LV distension
3. Chest reopening in the cardiac surgical ICU:
4. PEA arrests due to tamponade:
5. Capnography in the cardiac ICU:
Rarely provides useful information
Is desirable in spontaneously breathing patients
High ETCO2 is a hallmark of deteriorating cardiac function
Is mandatory in all cardiac arrests requiring airway intervention
Patients suffering from cardiac arrest in the community and surviving it are frequently transferred to a cardiothoracic centre where further investigations and treatment are possible. The majority of these patients have already been intubated and ventilated, and are transferred directly to an angiography laboratory where percutaneous interventions are performed. Once the investigations and treatment in the angiography laboratory are completed the patients are then transferred to the cardiothoracic intensive care unit for further management.
With the advent and increasing availability of mechanical circulatory support (MCS) devices (including mechanical chest compression devices (MCCD) and extracorporeal membrane oxygenation (ECMO)/extracorporeal CPR (ECPR)) there are likely to be increasing numbers of out-of-hospital cardiac arrest patients transported to hospitals whilst still in cardiac arrest. Critical care clinicians must be comfortable with continuing high quality CPR and ACLS and with the operation of MCS devices.
Survival after out-of-hospital cardiac arrest (OHCA) is increasing but remains low, and varies across geographic regions and institutions. Where outcomes have improved it appears to be in younger patients and in those who have an initial shockable rhythm. This has been attributed to a focused improvement in each of basic life support (BLS), advanced cardiac life support (ACLS) and post-resuscitation care (PRC) – the elements that form a continuum of links in the ‘chain of survival’ (Figure 25B.1) outlined by the International Liaison Committee on Resuscitation (ILCOR):
early recognition and call for help to prevent cardiac arrest;
early cardiopulmonary resuscitation (CPR) to buy time;
early defibrillation to restart the heart;
post-resuscitation care to restore quality of life.
Figure 25B.1 Chain of survival, courtesy of the Adult Basic Life Support Guidelines of the Resuscitation Council.
ILCOR publishes a five yearly update to the International Consensus on cardiopulmonary resuscitation (CPR) and emergency cardiovascular care (ECC) Science with Treatment Recommendations (CoSTR). This document forms the basis for guidelines that are subsequently produced and endorsed by member organisations. An in-depth discussion of basic and advanced life support is beyond the scope of this chapter.
Strategies that have led to increased survival in a variety of settings have included systematic community based projects to enhance first responder CPR training, increased numbers of public access automated external defibrillators (AEDs) and protocolised in-hospital care pathways.
Overall survival and long-term outcomes after OHCA are related to the underlying cause of the arrest, the hypoxaemic/ischaemic insult to the brain and other organs during the period of circulatory arrest, and to the severity of the post-cardiac arrest syndrome (PCAS) that occurs with reperfusion – in the setting of a return of spontaneous circulation (ROSC) or with institution of MCS.
Post-cardiac arrest care begins immediately on reinstitution of circulation. Some patients with a readily reversible cause and short duration of cardiac arrest will suffer very little, if any, systemic insult. Immediate goals of treatment having achieved restoration of circulation (ROSC or MCS) include the diagnosis and management of the underlying cause of the cardiac arrest in order to prevent recurrence, minimising ongoing injury from both the cardiac arrest itself and the insults from reperfusion injury, and multiple organ support.
Four key components of PCAS have been described:
Post-cardiac Arrest Brain Injury
The brain is particularly vulnerable to hypoxic ischaemic injury in the setting of circulatory arrest. Reperfusion is associated with an ongoing cascade of cerebral injury. Mechanisms are incompletely understood but are thought to include: disruptions to calcium homeostasis, excitotoxicity, alterations in membrane permeability with resultant cellular oedema, free radical generation, mitochondrial dysfunction and activation of apoptotic pathways. Cerebrovascular autoregulation may be impaired for an extended period of time following cardiac arrest.
Clinical findings in post-cardiac arrest brain injury include coma, seizures, myoclonus, neurocognitive dysfunction and in the most severe cases, brain death. Post-cardiac arrest brain injury is the leading cause of morbidity and mortality after cardiac arrest. The protracted pattern of neuronal cell death suggests a wide therapeutic window with multiple potential pharmacological and physiological interventions to optimise outcome. To date, only therapeutic temperature management has shown any likelihood of improved outcomes. Post-cardiac arrest brain injury may be compounded by the other features of PCAS (persistent cardiovascular instability, complications from systemic ischaemia-reperfusion (hypo/hypergycaemia, hyperthermia), and persistent precipitating pathology (hypoxaemia)) as well as potentially by therapeutic interventions (hypo/hypercarbia, hyperoxia).
Haemodynamics in the immediate post-ROSC setting can be extremely labile, reflecting circulating endogenous and exogenous catecholamines, and an ischaemia-reperfusion injury to the myocardium (regardless of the initial cause of arrest). Following cardiac arrest there is a period of myocardial ‘stunning’ that occurs despite evidence of preserved coronary blood flow (where coronary ischaemia was not the primary cause of cardiac arrest) characterised by global hypokinesis and elevated filling pressures. Observational data and animal studies suggest that this reversible period of myocardial stunning lasts for up to 72 hours.
Clinically this can manifest as dysrhythmia, hypotension and evidence of a low cardiac output state with systemic hypoperfusion. Treatment is supportive and can include judicious fluid administration, inotropes, vasopressors, temporary pacing and MCS (intra-aortic balloon counterpulsation pump (IABP), venoarterial ECMO or left ventricular assist device (LVAD)). Cardiovascular instability and complications remain a leading cause of death in patients who survive an initial cardiac arrest.
Circulatory arrest prevents tissue oxygen and nutrient delivery and metabolic waste removal. Even with continuous CPR there is an accumulated systemic oxygen debt that causes endothelial activation and cellular (and subsequently organ) dysfunction and results in generalised activation of the inflammatory and coagulation cascades. The endothelial glycocalyx appears to play a central role in these processes. Systemic hypoperfusion may self-propagate and progress even with reinstitution of circulation due to post-cardiac arrest myocardial dysfunction, vasodilatation and microcirculatory failure. This ‘systemic inflammatory response syndrome’ (SIRS) shares many features with sepsis and can result in the clinical appearance of relative hypovolaemia (with interstitial oedema and capillary leak), abnormal circulatory autoregulation, impaired oxygen delivery and uptake, and an increased susceptibility to infection. The severity of the syndrome and markers of inflammation are associated with a poorer prognosis.
Primary myocardial disease is the most common cause of OHCA. However, circulatory arrest can be the presenting feature or final common pathway in any number (if not all) pathologies. More common etiologies can include the following:
pulmonary embolus; pneumothorax; hypoxaemia – drowning, aspiration, asphyxiation; end-stage chronic obstructive airways disease (COAD), asthma
subarachnoid haemorrhage (SAH), cerebrovascular accident, prolonged seizures
including electrolyte abnormalities and temperature derangement
hypovolaemia (haemorrhage), tension pneumothorax, tamponade
envenomation and overdoses
Thrombosis – coronary or pulmonary
Tamponade – cardiac
Assessment of likely antecedent cause(s) for the cardiac arrest must occur contemporaneously with ACLS and post-resuscitation care. This involves collateral history from first responders, paramedics, family members and medical staff as well as a focused clinical examination and investigations where appropriate.
Persistent precipitating pathology can both confound and complicate management of the post-cardiac arrest patient. Asphyxiation is associated with more severe cerebral oedema and post-cardiac arrest brain injury than other causes of circulatory arrest. A SIRS response in the setting of sepsis may potentiate the haemodynamic instability and multiple organ dysfunction associated with systemic ischaemia-reperfusion. Acute coronary syndrome (ACS) as a cause for cardiac arrest will exacerbate post-arrest myocardial dysfunction, and early percutaneous coronary intervention has been associated with improved neurologically intact survival.
The intensive care management of OHCA patients involves the diagnosis and treatment of the underlying cause for the arrest, managing subsequent cardiovascular dysfunction, minimising and managing any further organ damage, and prognostication. Critical care physicians are increasingly involved in the very early management of cardiac arrest patients – as part of rapid response teams (RRTs) attending in-hospital cardiac arrest (IHCA) and as an integral part of protocolised in-hospital care pathways for OHCA patients.
Due to a relative paucity of high quality research in post-resuscitative care, there are only limited data to support specific interventions. However, several hospital level critical care interventions have consistently been associated with improved outcomes after OHCA (see Figure 25B.2):
Early percutaneous coronary intervention (PCI);
Targeted temperature management (TTM);
Delayed prognostication before withdrawal of cardiorespiratory supports.
Figure 25B.2 Post-resuscitation care algorithm. SBP systolic blood pressure; PCI percutaneous coronary intervention; CTPA computerised tomography pulmonary angiogram; ICU intensive care unit; MAP mean arterial pressure; ScvO2 central venous oxygenation; CO/CI cardiac output/cardiac index; EEG electroencephalography; ICD implanted cardioverter defibrillator.
Assessment and management of the post-ROSC OHCA patient should occur simultaneously, using a team-based approach with an initial focus on the airway, breathing and circulation. History, examination, investigations and treatment should occur contemporaneously.
Important investigations to aid diagnosis and subsequent management include the following:
12-lead electrocardiogram (ECG): to identify evidence of coronary ischaemia, abnormal conduction such as a prolonged QT interval, or right heart strain (suggestive of a pulmonary embolus).
Transthoracic echocardiography (TTE): ultrasound is playing an increasing role in emergency and critical care medicine and is now incorporated into ALS algorithms. Early focused and/or formal TTE may help to differentiate the aetiology of OHCA and guide treatment decisions.
Blood tests: these include a full blood count, a blood group and screen, electrolytes, urea and creatinine, troponin, and early arterial blood gas to help establish the cause of the arrest, assess the severity of insults and provide baseline information. Toxicology analysis may be considered.
Chest X-ray: evaluation of primary pulmonary pathology, potential injuries sustained during resuscitation and the correct position of an endotracheal tube and central vascular access.
Computerised tomography (CT) brain/chest: may reveal intracranial haemorrhage as the cause of the arrest, or cerebral oedema as a result of ischaemic-hypoxic injury. In selected patients a CT chest scan may reveal a pulmonary embolus or aortic pathology.
Treatment algorithms should include general management of the OHCA patient and specific interventions depending on the cause of the arrest.
In patients where there is not an obvious non-cardiac cause of arrest, early PCI is associated with improved overall survival, and improved neurological outcomes. This includes patients without obvious ST segment elevation myocardial infarction (STEMI).
However, routine PCI in OHCA involves significant resource utilisation and further randomised controlled trials are required to clearly define the optimum timing and role for PCI in this cohort (Table 25B.1).
|Emergency coronary angiography is reasonable for select (e.g. electrically or haemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin with ST elevation on ECGb|
|Emergency coronary angiography is reasonable for select (e.g. electrically or haemodynamically unstable) adult patients who are comatose after OHCA of suspected cardiac origin but without ST elevation on ECGd|
a Class I, Level of Evidence B – randomised studies.
b Class I, Level of Evidence B – non-randomised studies.
c Class I, Level of Evidence C – expert opinion.
d Class IIa, Level of Evidence B – non-randomised studies.
e Class IIa, Level of Evidence C – limited data.
f Class IIa, Level of Evidence C – expert opinion.
g Class IIb, Level of Evidence B – non-randomised studies.
h Class IIb, Level of Evidence C – expert opinion.
i Class III, Level of Evidence B – non-randomised studies.
j Class III, Level of Evidence C – limited data.
Invasive arterial monitoring is recommended for continuous assessment of blood pressure, titration of fluids/vasoactive agents and to facilitate blood sampling. Large bore peripheral access may be used for fluid administration to correct any hypovolaemia. Where vasoactive agents (inotropes/vasopressors) are being considered, a central venous line should be inserted.
There is no evidence that defines an optimal target for mean arterial pressure (MAP). The aim should be to deliver adequate coronary, cerebral and systemic organ perfusion that is balanced against increasing the metabolic demands of an already stressed heart through the use of fluids and vasoactive agents. A recent meta-analysis associated higher MAP with improved neurological outcome but it is not clear that improving MAP was responsible for the improved outcomes.
MCS theoretically offers improved systemic and coronary perfusion without necessarily increasing myocardial oxygen consumption. The role of the intra-aortic counterpulsation balloon pump (IABP) remains controversial; and newer devices including ECMO and left ventricular assist devices (LVADs) are being used in selected patients in some specialist centres.
Oxygenation and Ventilation
Oxygen therapy after OHCA is controversial. There are conflicting retrospective data regarding whether hyperoxia is associated with an increased mortality in post-cardiac arrest patients. A prospective, multicentre, randomised controlled trial of air versus supplemental oxygen in STEMI patients who were not hypoxaemic demonstrated an increase in myocardial infarction size assessed at 6 months. In this context, it would seem prudent to titrate inspired oxygen levels to achieve saturations of 94–98%. Both hypoxaemia and hyperoxia should be avoided, but adequate peripheral perfusion and accurate saturation monitoring are imperative before considering reducing inspired oxygen concentrations.
In the comatose OHCA patient with ROSC an endotracheal tube (ETT) should be inserted if this was not done as part of the ALS resuscitation. Tube position should be confirmed with clinical examination, continuous (waveform) end-tidal carbon dioxide monitoring and imaging (CXR or on CT chest scan if this is performed).
Hyperventilation with subsequent hypocarbia has been associated with worse neurological outcome in observational studies of OHCA, presumably due to cerebral vasoconstriction. Where possible, patients should be ventilated to normocarbia with a PaCO2 of 35–45 mmHg. This may need to be individualised in the patient with coexistent pathology where more definitive evidence exists for an alternative ventilation strategy – for example, permissive hypercarbia in the setting of acute respiratory distress syndrome (ARDS).
Post-cardiac arrest brain injury (as outlined above) is the major cause of morbidity and mortality in comatose patients who are initially resuscitated from OHCA. Multiple trials have demonstrated improved neurological outcomes with targeted temperature management to 32–36 °C in an attempt to mitigate the cascading cellular effects thought to be responsible for propagating neuronal cell death following ischaemia and reperfusion (see Table 25B.2). Benefits were most pronounced in patients with an initial shockable rhythm (ventricular fibrillation (VF) or pulseless ventricular tachycardia (VT)).
|Comatose adult patients with ROSC after cardiac arrest should have TTM for VF/pulseless VT OHCAa; for non-VF/pulseless VT (i.e. ‘non-shockable’)c and in-hospitala cardiac arrest.|
|Select and maintain a constant temperature between 32 °C and 36 °C during TTM.a|
|It is reasonable that TTM be maintained for at least 24 hours after achieving target temperature.f|
|Whether certain subpopulations of cardiac arrest patients may benefit from lower (32–34 °C) or higher (36 °C) temperatures remains unknown, and further research may help elucidate this.|
For footnotes see Table 25B.1.
The practicalities of active TTM involve significant resource allocation – equipment, education and training – and are not without complexity and complications. Continuous temperature monitoring is required. Cooling strategies need to address the induction and maintenance of TTM, and rewarming. Options include infusion of ice cold fluid, simple surface cooling with ice packs, or more formal systems with fluid or air circulating blankets, vests and limb wraps that include integrated control from continuous temperature monitoring. More aggressive and invasive cooling strategies can include intravascular heat exchange catheters, body cavity lavage or the institution of MCS. The risk and benefit of each strategy need to be considered on an institutional and individual patient level.
Shivering occurs as an autonomic response to hypothermia and can limit the effectiveness of TTM. Strategies to mitigate shivering include the use of short-acting sedative agents, opioid agonists and alpha-agonists but adequate temperature management often requires the use of short-acting non-depolarising neuromuscular blocking agents.
Bradycardia is common and can result in a reduced cardiac output. At lower temperatures systemic metabolic rate and oxygen consumption fall and the bradycardia is thought to be associated with improvements in diastolic function. Systemic vascular resistance may be increased where vasoconstriction predominates, but may be reduced in the setting of a significant SIRS response to systemic ischaemia-reperfusion. The net effect of the alterations to the adequacy of tissue oxygen delivery should be assessed on an individual basis.
A cold diuresis from renal tubular dysfunction may cause a relative hypovolaemia and significant electrolyte disturbance.
Insulin sensitivity is reduced at lower temperatures and blood glucose should be measured regularly. Where insulin is used in hypothermia, it is important to closely monitor blood glucose during rewarming as hypoglycaemia may occur.
Coagulation is impaired at lower temperatures but this does not appear to be associated with a clinically significant increase in bleeding rates.
Drug clearance is significantly reduced at lower temperatures and this must be taken into account when prognostication is being considered.
The perceived benefits of TTM have been demonstrated in a time where a focus on bundles of post-OHCA care has been instituted. It is unclear which component of these treatment bundles has been responsible for the greatest improvements in outcome. Although TTM is thought to be integral to these improved outcomes, the optimum temperature, timing and duration of TTM remain to be elucidated.
Post-cardiac arrest brain injury is the major cause of mortality in OHCA patients but the mode of death in these patients is invariably withdrawal of cardiorespiratory supports (WCRS) following prognostication of a poor neurological outcome. Where OHCA patients can be identified as having no prospect of meaningful neurological recovery, inappropriate treatments can be avoided. However, the gravity of the WCRS decision is such that prognostic assessment must be accurate and appropriate.
The self-fulfilling nature of a prognosis of poor neurological outcome leading to WCRS and death means that biases are inherent in many of the earlier studies of prognostication. This may have been further compounded by the use of sedative medications to facilitate TTM, from the effects of TTM on the pharmacokinetic and pharmacodynamic properties of the medications, and potentially from the TTM itself.
|The earliest time for prognostication using clinical examination in patients treated with TTM, where sedation or paralysis could be a confounder, may be 72 hours after return to normothermia.h|
|The earliest time to prognosticate a poor neurological outcome using clinical examination in patients not treated with TTM is 72 hours after cardiac arrest.b|
|This time until prognostication can be even longer than 72 hours after cardiac arrest if the residual effect of sedation or paralysis confounds the clinical examination.e|
|In comatose patients who are not treated with TTM, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is a reasonable exam finding with which to predict poor neurological outcome (false positive rate (FPR), 0%; 95% CI, 0%–8%).d|
|In comatose patients who are treated with TTM, the absence of pupillary reflex to light at 72 hours or more after cardiac arrest is useful to predict poor neurological outcome (FPR, 1%; 95% CI, 0%–3%).b|
|The findings of either absent motor movements or extensor posturing should not be used alone for predicting a poor neurological outcome (FPR, 10%; 95% CI, 7%–15% to FPR, 15%; 95% CI, 5%–31%)i. The motor examination may be a reasonable means to identify the population who need further prognostic testing to predict poor outcome.g|
|The presence of myoclonus (as distinct from status myoclonus) should not be used to predict poor neurological outcomes because of the high FPR (FPR, 5%; 95% CI, 3%–8% to FPR, 11%; 95% CI, 3%–26%).i|
|In combination with other diagnostic tests at 72 or more hours after cardiac arrest, the presence of status myoclonus during the first 72 to 120 hours after cardiac arrest is a reasonable finding to help predict poor neurological outcomes (FPR, 0%; 95% CI, 0%–4%).d|
|In patients who are comatose after resuscitation from cardiac arrest regardless of treatment with TTM, it is reasonable to consider the bilateral absence of the N20 SSEP wave 24 to 72 hours after cardiac arrest or after rewarming a predictor of poor outcome (FPR, 1%; 95% CI, 0%–3%).d|
|The persistent absence of EEG reactivity to external stimuli at 72 hours after cardiac arrest, and persistent burst suppression on EEG after rewarming, may be reasonable to predict a poor outcome (FPR, 0%; 95% CI, 0%–3%).g|
|Intractable and persistent (more than 72 hours) status epilepticus in the absence of EEG reactivity to external stimuli may be reasonable to predict a poor outcome.g|
|In comatose post-cardiac arrest patients who are not treated with TTM, it may be reasonable to consider the presence of burst suppression on EEG at 72 hours or more after cardiac arrest, in combination with other predictors, to predict a poor neurological outcome (FPR, 0%; 95% CI, 0%–11%).g|
|Given the possibility of high FPRs, blood levels of NSE and S-100B should not be used alone to predict a poor neurological outcome.j|
|In patients who are comatose after resuscitation from cardiac arrest and not treated with TTM, it may be reasonable to use the presence of a marked reduction of the GWR on brain CT obtained within 2 hours after cardiac arrest to predict poor outcome.g|
|It may be reasonable to consider extensive restriction of diffusion on brain MRI at 2 to 6 days after cardiac arrest in combination with other established predictors to predict a poor neurological outcome.g|
For footnotes see Table 25B.1.
Figure 25B.3 Prognostication algorithm. EEG electroencephalography; NSE neuron-specific enolase; SSEP somatosensory evoked potentials; ROSC return of spontaneous circulation; FPR false positive rate; CI confidence interval.
There is insufficient evidence to support routine use of MCS – mechanical chest compression devices (MCCD) and/or ECPR – in OHCA.
MCCDs have not been associated with improved survival to hospital discharge nor with improved neurological outcomes, and manual chest compression remains the standard of care. The use of MCCDs requires capital outlay for purchase and ongoing costs associated with education, training and maintenance. However, the appropriate use of MCCDs during patient transfer can facilitate staff safety whilst also minimising interruptions to chest compressions. This includes transport in emergency vehicles between health care facilities, and within hospitals for intervention in the angiography suite. Critical care practitioners should be familiar with the operation of these devices where they may be used in their centres. In accordance with current guidelines the focus should remain on minimising interruptions to chest compression.
ECPR is an area of growing interest and research. Preliminary reports from specialist ECMO centres with early institution of ECPR in selected patients have shown promising results when compared with conventional CPR – particularly in the setting of witnessed, in-hospital cardiac arrest (IHCA) with a short interval from arrest to starting ECMO. Results for OHCA have been less promising and this is thought to be related to the prolonged time between onset of cardiac arrest and institution of ECMO. Solutions currently being explored include the more rapid transport of patients with OHCA to ECMO centres and the role of pre-hospital ECPR. Further economic and ethical evaluation is required to establish the role of ECPR in OHCA and how these patients should subsequently be managed.
Mortality rates in OHCA patients remain high even after survival to ICU admission. Where patients fulfil broader criteria for organ donation this should be discussed with their family members and organ donor coordinators in line with hospital and national guidelines. In the setting of severe post-cardiac arrest brain injury patients may progress to brain death. Where cardiorespiratory supports are to be withdrawn, donation after circulatory death should be discussed.
Coronary ischaemia remains the leading cause of OHCA. Where OHCA occurs in younger patients or where investigations reveal no evidence of ischaemia, alternative diagnoses must be considered – including accelerated atherosclerotic disease, structural heart disease, and primary arrhythmias. Structural heart disease should be identified with imaging studies, and electrophysiological studies can help identify primary arrhythmias. In the event of death, a post mortem examination should be conducted. Where a heritable condition is identified as the cause of OHCA, screening should be offered to family members – including clinical examination, electrophysiological studies, cardiac imaging and potential genetic testing and counselling.
Post-resuscitation care is one of the four essential links in the ‘chain of survival’ designed to improve survival in OHCA.
Post-cardiac arrest syndrome comprises:
Post-cardiac arrest brain injury;
Post-cardiac arrest myocardial dysfunction;
Systemic ischaemia-reperfusion response;
Persistent precipitating pathology.
The hospital interventions that have been consistently associated with improved outcomes after OHCA are:
Early percutaneous coronary intervention (PCI);
Targeted temperature management;
Delayed prognostication before withdrawal of cardiorespiratory supports.
Prognostication should involve multiple assessment strategies, including examination, neurophysiological testing and neuroimaging.
Mechanical support in cardiac arrest is an evolving area. Further clinical, economic and ethical evaluation is required to establish the role of ECPR in both IHCA and OHCA.
1. The chain of survival does NOT include:
2. Regarding OHCA patients:
Primary myocardial disease is an uncommon cause of arrest in this population
Hyperoxia post-ROSC is associated with improved neurological outcomes
Hypercarbia should never be allowed to occur in these patients
Invasive arterial monitoring is indicated in the post-resuscitation care phase
3. Current ALS guidelines suggest:
Defibrillation should be delayed until the airway is secured
Interruptions to chest compression should be minimised
E-CPR has shown particularly promising results in the OHCA population
The use of MCCDs (compared to manual chest compressions) is associated with improved neurological outcomes
4. Regarding the ICU management of OHCA patients:
Observational studies suggest that the reversible ‘myocardial stunning’ effect can last for up to 6 hours
Routine arrhythmia prophylaxis with amiodarone is recommended in all patients
Echocardiography may help to guide patient management
Early percutaneous coronary intervention (PCI) should only be considered in patients with ST elevation on their ECG
5. Regarding neurological prognostication in OHCA patients:
A Glasgow coma motor score of 1 or 2 is a good predictor of poor neurological outcome
Clinical neurological examination should be performed at least 36 hours after ROSC
Multiple assessment strategies should be used, including examination, neurophysiological testing and neuroimaging
The majority of patients admitted to an intensive care unit require mechanical ventilation and consequently they are vulnerable to a number of airway complications. In these circumstances, airway emergencies such as airway obstruction, failed airway instrumentation, airway device failure or postextubation problems are life threatening situations.
In general, the management of the airway in the intensive care unit is inherently more complex than in the operating theatre, and complications of airway management are disproportionately higher. There are multiple patient, staffing and environmental factors that contribute to the higher complication rate. These factors may include the following: (i) patients are physiologically compromised and frequently unstable; (ii) airway management is usually time critical; (iii) it often occurs out-of-hours; and (iv) it is initially managed by junior medical staff.
The recognition of a compromised airway is the crucial first step in managing an airway emergency. Clinical features of significant airway compromise often involve increased work of breathing, inspiratory stridor, obstructed breathing pattern, desaturation and agitation. Untreated, the rapid development of hypoxia, hypercapnia, acidosis and cardiovascular collapse may ensue.
Rapid assessment of the situation and prompt management is critical to achieve a successful outcome. Airway emergencies are dynamic and often complex situations. The initial treatment priorities are to seek help and establish adequate oxygenation, while preparation for deterioration or airway difficulty is being arranged. In this chapter we will overview the challenges associated with the instrumentation of the airway in critically ill patients, the prevention and management of their airway complications, and the organisational aspects of airway safety in intensive care.
Airway obstruction is a blockage of the airway resulting in reduced or impeded gas flow. The exact incidence of airway obstruction in the cardiothoracic ICU is unknown and it remains one of the most challenging clinical scenarios for anaesthetists and intensivists.
There are many causes of airway obstruction (see Table 26.1). Anatomically, the obstruction may be supraglottic, glottic or subglottic. The clinical presentation depends on both the location of the obstructing lesion and the time course of its development. Inspiratory stridor suggests a significant upper airway obstruction with a reduction in airway diameter of at least 50%, whilst an expiratory wheeze indicates lower airway pathology.
|Obstructive sleep apnoea|
|Vocal cord palsy|
Clinical Presentation and Assessment
A focused history and examination allows rapid assessment of the patient. Important indicators of imminent airway compromise include hypoxia, agitation, inability to lie flat, failure to manage airway secretions and nocturnal symptoms. Importantly, any distress experienced by the patient may exacerbate the severity of the airway obstruction.
After initial assessment, the suspected site of the airway obstruction, the severity of the airway obstruction and the overall condition of the patient will guide further investigations. Initial tests may include a full blood count, inflammatory markers, blood cultures and a chest X-ray. In cases of suspected upper airway obstruction, computed tomography is ideal to delineate the lesion. However, in patients unable to lie flat, nasendoscopy exploration is the procedure of choice. In those with suspected lower airway obstruction due to a mass lesion, computed tomography of the chest and neck is indicated.
Initial Management of the Obstructed Airway
Acute or severe airway obstruction is a critical emergency. Initial supportive measures must include supplemental oxygen, sitting the patient upright and establishing intravenous access and appropriate monitoring. Deteriorating patients and those in extremis will need their airway secured. The definitive treatment should focus directly on the cause of the airway obstruction and is tailored to the individual patient. Antibiotics, corticosteroids and nebulised adrenaline may be effective for the treatment of upper airway swelling and infections, including epiglottitis or croup. Anaphylaxis should be managed with intravenous or intramuscular adrenaline in accordance with local and national guidelines. Foreign bodies may be dislodged by coughing or postural changes. Some patients can require urgent surgical assistance that may include ear, nose and throat, thoracic or cardiac surgery.
Airway management in patients with severe obstruction is a complex and high-risk process. All management decisions should be formulated after consultation between a senior anaesthetist and surgeon. The procedure is ideally performed in theatre and it is critical that the airway plan is well prepared and communicated, with all team members ready and the appropriate equipment in the room.
However, there is no universal management plan for securing the obstructed airway. Patients with upper airway obstruction should be assessed as to whether intubation is possible or a tracheostomy under local anaesthetic is required.
In patients who are considered possible to intubate, the airway plan may include awake fibreoptic intubation or gas induction. Caution should be exercised when using awake fibreoptic intubation – the procedure is often difficult and complete airway obstruction may be caused by the fibreoptic scope or loss of airway tone due to sedation or local anaesthesia. Regardless, an experienced surgeon, tracheostomy tray and rigid bronchoscope should be immediately available in the event of failure to intubate.
In patients with subglottic airway obstruction, the exact site of obstruction should be identified prior to embarking on intubation, unless the patient suffers an acute deterioration. The most important considerations are whether a tracheal tube can be safely passed beyond the obstruction and identification of an appropriate rescue plan. An awake fibreoptic intubation may be an appropriate plan A, allowing placement of the endotracheal tube beyond the site of obstruction. More distal tracheal obstruction precludes the use of tracheostomy as a rescue technique and requires the use of rigid bronchoscopy. In significant tracheobronchial obstruction, venovenous extracorporeal membrane oxygenation may be considered prior to securing the airway.
Failed airway management is a leading cause of morbidity and mortality in intensive care. The Fourth National Audit Project (NAP4) identified ten events in 2009 of failed endotracheal intubation in the intensive care unit and five of these deteriorated into a ‘can’t intubate, can’t oxygenate’ (CICO) situation, requiring cricothyroidotomy or emergency tracheostomy.
The incidence of a ‘can’t intubate, can’t oxygenate’ scenario was estimated to be less than 1/10,000 in 1991, and has probably fallen since then due to the advent of laryngeal masks. A thorough airway assessment will identify most patients with difficult airway, however, the positive predictive value of these tests is poor.
Factors identified in NAP4 as associated with failed intubation include patient obesity, known or predictable difficult airways, trainees with limited advanced airway experience, poor judgement and lack of equipment.
Prevention of a ‘can’t intubate, can’t oxygenate’ scenario requires proper airway assessment and planning. Every intubation should have a plan A, B, C and D as per the Difficult Airway Society (DAS) guidelines, with appropriate equipment ready, the patient position optimised and experienced personnel present.
‘Can’t intubate, can’t oxygenate’ exists when there have been failed attempts at intubation, failed attempts at oxygenation (facemask and supraglottic airway device) and low or falling oxygen saturations. Identification of a CICO situation is imperative to good outcomes. Repeated failed attempts at endotracheal intubation risk further airway trauma whilst delaying appropriate management. The reluctance to perform a surgical airway has been identified as a contributor to mortality in CICO situations.
The Difficult Airway Society published guidelines for management of unanticipated difficult intubation, including CICO. Failure to intubate necessitates that oxygenation, rather than intubation or ventilation, becomes the priority. Rapid development of severe hypoxaemia, hypoxic brain injury and cardiovascular collapse ensues if oxygenation is not re-established. Help should be sought as soon as intubation is recognised as difficult or failed.
Oxygenation must be obtained emergently via front of neck access (FONA), usually through the cricothyroid membrane. The DAS guidelines recommend the scalpel-bougie technique as first-line approach for FONA. This technique uses a cricothyroid incision with a scalpel, insertion of a bougie and rail-roading of a small cuffed endotracheal tube. This technique has higher success rates than a cannula technique and may be more acceptable to anaesthetic and intensive care specialists.
Cannula cricothyroidotomy and surgical tracheostomy are alternative techniques for emergency tracheal access. Cannula cricothyroidotomy involves the insertion of a large-bore cannula through the cricothyroid membrane and use of a high pressure oxygen delivery device. This technique can provide rapid rescue oxygenation; however it is not appropriate for ventilation and clearance of CO2. Further, the technique has reported high rates of failure, and inability to obtain a cannula cricothyroidotomy within five attempts requires an alternative technique. The risks of the technique include cannula displacement with potential to create significant surgical emphysema, barotrauma and volutrauma. A cannula cricothyroidotomy is an emergency and temporary oxygenation technique that allows stabilisation of the patient. A definitive airway should be established as a matter of priority by percutaneous or surgical tracheostomy.
Emergency surgical tracheostomy is less familiar to intensive care and anaesthetic specialists and risks inadvertent endobronchial intubation. It may be performed by those with suitable expertise and experience, particularly in failed FONA.Percutaneous tracheostomy is a technique familiar to intensive care specialists, and presents a viable alternative to establishing an emergency surgical airway. The technique utilises a cannula cricothyroidotomy initially. A wire is then inserted into the trachea, followed by a dilator and then a tracheostomy tube. Various tracheostomy sets exist, including single dilation sets. Current guidelines recommend scalpel-bougie as the initial technique as it is fast, has few steps and it establishes a definitive airway. The alternative techniques may be considered when the scalpel-bougie approach has failed and suitable expertise is available.
Figure 26.1 www.das.uk.com/guidelines/icu_guidelines2017. Reproduced from Guidelines for the management of tracheal intubation in critically ill adults, Higgs et al. (2017).
A variety of oxygen delivery techniques are available, but a detailed discussion is included in Chapter 17. An established surgical airway utilising a cuffed endotracheal tube allows direct connection to most ventilators or bag-valve-mask devices via a 15 mm connector; however, the use of a cannula presents a number of limitations. In a CICO scenario, the upper airway is obstructed, and the main route of exhalation is via the cricothyroidotomy cannula. Many oxygen delivery techniques, including jet ventilation devices, fail to allow exhalation and continue to deliver oxygen to the patient, risking significant and rapid volutrauma. Specially designed devices have an adequate exhalation valve. In the absence of these devices, the oxygen delivery device should be disconnected whenever the patient is not actively ventilated through the cannula cricothyroidotomy. Regular training and familiarisation with local cricothyroidotomy equipment is essential to maintain high standards for the rescue of CICO patients.
Tracheostomy is commonly performed in the intensive care unit for prolonged mechanical ventilation, upper airway obstruction and management of respiratory tract secretions. It may also be performed for rescue airway management or electively in theatre for major airway surgery or laryngectomy. The EPIC study estimated approximately 16% of patients in UK intensive care units have a tracheostomy at any one time.
Tracheostomies accounted for 50% (18/36) airway events in the intensive care unit in NAP4. Fourteen patients had their tracheostomy dislodged, resulting in seven deaths and four hypoxicbrain injuries (see Table 26.2). In two-thirds of these cases, the dislodgement occurred on moving or turning. Two further patients had failure to place an elective tracheostomy in intensive care and two had major haemorrhage post decannulation. Obesity was identified as a significant risk factor for tracheostomy complications and capnography was used infrequently. The high morbidity of tracheostomy complications led to the development of current national guidelines.
|Cricoid cartilage damage|
|Misplacement of tracheostomy|
|Tracheal tube complications|
|Fistula to surrounding structure|
Tracheostomy dislodgement is the most commonly lethal tracheostomy complication. Displacement occurs with all types of securement devices; however patient turning and obesity were associated with dislodgement. The infrequent use of capnography can lead to a delay in detection and worse outcomes.
A dislodged tracheostomy tube is an emergency and early recognition is crucial. Help and expert airway assistance should be sought. Assessment must be made immediately for airway, breathing and circulation (see Figure 26.2). Supplemental oxygen must be applied to both the face and neck stoma.
In those patients who require airway instrumentation, initial airway manoeuvres should be directed at the oral route, such as bag-mask ventilation and supraglottic airways, whilst sealing the neck stoma. Oxygenation may also be attempted via the stoma, using a small paediatric mask. Failure to oxygenate should lead to an attempt at oral intubation and advancing the tracheal tube beyond the stoma, followed by attempted intubation via the stoma, careful not to intubate the bronchus. Ideally, this is undertaken using fibreoptic bronchoscopy guidance. The use of capnography for the confirmation of a secured airway is mandatory.
Laryngectomy patients, however, have altered anatomy with no upper airway connection to the trachea. All attempts at oxygenation and airway instrumentation in these patients should be directed to the tracheostomy site.
Tracheostomy tubes may become blocked at any stage due to blood, secretions, displacement or cuff herniation. Clinical presentation includes dyspnoea, increased work of breathing and desaturation.
Immediate assessment should be undertaken. The inner tube or speaking device can be removed, leaving the tracheostomy in situ. A suction catheter should be inserted to assess the patency of the tracheostomy. If a suction tube cannot be passed, the tracheostomy cuff should be deflated to relieve the obstruction. If the patient does not improve then the tracheostomy tube should be removed.
Figure 26.2 Management of tracheostomy and laryngectomy airway emergencies.
Airway bleeding most commonly presents early post-tracheostomy insertion, but may also present postdecannulation. Bleeding or infection complicates 5% of percutaneous tracheostomies.
Tracheoinnominate artery fistula, caused by breaching of the tracheal wall into the innominate artery, is a rare but frequently fatal cause of airway haemorrhage, occurring days to weeks post tracheostomy insertion. It presents as massive airway haemorrhage, which requires immediate airway support. A tracheal tube may be advanced into the airway and the cuff inflated to tamponade the fistula before emergency surgery is performed.
Extubation is an important but often neglected component of airway management. A stable airway is removed and remains unsecured until the patient is able to maintain airway patency and protective reflexes. Most complications post extubation are minor. However, airway emergencies may occur due either to airway obstruction or contamination.
The Difficult Airway Society published guidelines on extubation post anaesthesia, stratifying patients into ‘low-risk’ or ‘at-risk’ groups with corresponding extubation algorithms.
Inadvertent extubation is not uncommon, occurring at a rate of one per 100 ventilator days. However, only four cases were reported in the NAP4 audit. Three of these patients were obese, the fourth was a known difficult airway and two patients suffered aspiration as a result. Capnography was not utilised in any of these cases.
Accidental extubation typically occurred during patient movement, sedation breaks and minor airway manipulation. Risk factors for unplanned extubation include higher levels of arousal, agitation and less experienced nursing staff. Identification of inadvertent extubation is crucial to limit the risk of complications such as aspiration, hypotension, arrhythmias, airway injury and respiratory compromise.
Not all patients will require reintubation. Supplemental oxygen and supportive manoeuvres may be adequate. Reintubation is more likely to be required in patients with deeper levels of sedation, high oxygen requirements, high levels of pressure support or positive end-expiratory pressure and cardiovascular instability.
Airway obstruction post extubation may occur secondary to reduced airway tone, laryngospasm or contamination of the airway. It is characterised by inspiratory stridor, respiratory efforts with reduced airflow and desaturation. The treatment depends on the cause.
Initial efforts should be focused on oxygenation. Jaw thrust and chin lift will frequently relieve obstruction due to drowsiness. An oropharyngeal or nasopharyngeal airway may help and bag-mask ventilation may be required. If the patient does not improve quickly, a secure airway should be re-established.
Laryngospasm causes either partial or complete airway obstruction. It often occurs in response to stimulation when patients are emerging from anaesthesia. Airway blood or mucus causing irritation of the vocal cords can result in laryngospasm. Initial management is supportive, with bag-mask ventilation utilising positive end-expiratory pressure. A strong jaw lift, known as Larson’s manoeuvre, may break the spasm. If it continues, resedation and muscle relaxation will cause the laryngospasm to cease. The increased respiratory effort with the closed glottis may cause negative pressure pulmonary oedema.
Less common causes of airway obstruction postoperatively include recurrent laryngeal nerve injury and foreign body. Bilateral, rather than unilateral, recurrent laryngeal nerve injury will cause upper airway obstruction. Foreign bodies include swabs, teeth and dentures. Risk factors include surgery on the upper airway and traumatic intubation.
The airway may become contaminated with secretions, blood or foreign bodies. Airway contamination will present with coughing, gagging or airway obstruction. Initial management is supportive. The airway may need to be secured by intubation and plans for a difficult intubation need to be established. Care should be taken to suction out the airway prior to extubation.
Airway emergencies in the intensive care unit are associated with high morbidity and mortality. Recognition and diagnosis is often delayed, hindering effective management. They may occur at any time and are often managed by junior medical and nursing staff unfamiliar with airway equipment or management of complex airway emergencies. Numerous factors have been identified that may reduce the rate of these complications and improve outcomes.
Staff and Training
Intensive care skill-mix with variable experience in airway emergencies should be minimised. All junior medical staff should be familiar with basic airway management techniques and staff with experience in advanced airway support should be available at all hours.
Staff education should focus on identifying those with difficult airways, their assessment and management. Identification of potentially difficult airways allows a defined plan to be made in the event of an emergency, including seeking assistance early. Airway management education includes training in basic and advanced airway skills as well as management algorithms for difficult and failed airways. Maintenance of emergency airway skills, including ‘can’t intubate, can’t oxygenate’ scenarios, may be best achieved with simulation and skills sessions training.
All intensive care units should have access to a difficult airway trolley and fibreoptic bronchoscopy. As specialists, it is important that intensivists are familiar with the contents and use of airway equipment available in their unit. Additionally, medical staff should be familiar and confident using a variety of different equipment.
Capnography is a crucial monitor for intubated and ventilated patients. Its use is universal in anaesthesia but variable in the intensive care unit. Capnography should be utilised for every intubation to confirm endotracheal tube position as well as throughout the period the patient is intubated and dependent on a ventilator.
Planning and Preparation
The early identification of patients at risk for airway complications and the recognition of an airway emergency is important for best outcomes. Identification of patients with potential airway difficulty allows the formulation and communication of an appropriate plan should trouble strike.
However, not all airway emergencies can be predicted and early recognition of an emergency remains crucial. A clearly formed management plan is critical; however all plans can fail and the back-up plans (B, C and D) are as important as the initial strategy. This must be communicated clearly with the team, experienced staff must be available and equipment ready.
Airway emergencies in the intensive care unit are complex situations associated with high rates of morbidity and mortality. Early identification of those at risk allows thorough planning and management in a controlled and timely manner. The nature of airway emergencies and complications necessitates that back-up plans with appropriately qualified staff and equipment are immediately available.
Airway management in the intensive care unit is associated with disproportionately high rates of complications.
Early recognition of emergencies allows preparation and planning.
The initial airway management should focus on providing oxygenation.
Securing the airway can be a complex process. Experienced personnel should be present and plans A, B, C and D ready in case of initial failure.
All intubated and ventilator dependent patients should have continuous capnography monitoring.
1. Time to desaturation following the onset of apnoea is influenced by:
2. Regarding patients with tracheostomy, which of the following is true?
The use of capnography will prevent complications from tracheostomy displacement
In suspected airway blockage, the tracheostomy should be removed immediately
Oral endotracheal intubation is not possible in patients with tracheostomy
Capnography should be utilised in ventilator dependent tracheostomy patients
Laryngectomy patients may be oxygenated adequately by facemask oxygenation
3. Regarding ‘can’t inubate, can’t oxygenate’ scenarios, which of the following is true?
An emergency call for help should be made after failed intubation and inability to oxygenate with a supraglottic airway device
After three failed attempts at cannula cricothyroidotomy, emergency tracheostomy should be attempted
If a cannula cricothyroidotomy is successful and a laryngeal mask is in place, the laryngeal mask should be left in situ
Cannula cricothyroidotomy allows adequate exhalation
If rescue cannula cricothyroidotomy is successful, the patient should be woken up
4. In the intensive care unit, which of the following is true regarding emergency airway management?
Oesophageal injury is a recognised and unavoidable complication of airway management
Suxamethonium is the preferred muscle relaxant, due to its quick offset in case of a failed airway
Preoxygenation may be suboptimal
Capnography should be used if a difficult intubation is anticipated
Airway rescue with a laryngeal mask is not appropriate, as the patients are usually unfasted
5. In postoperative patients after extubation, which of the following is true?
Signs of airway obstruction require immediate attention and re-intubation
Laryngospasm may respond to positive end-expiratory pressure
A hoarse voice does not indicate an airway injury
Vomiting is unlikely to lead to pulmonary aspiration
Chest pain as a symptom can lead to over 400 eventual diagnoses. Up to one third of those patients admitted to an acute medical unit may have chest pain as a component of their presenting complaint. Chest pain is almost ubiquitous in patients admitted to the cardiothoracic intensive care unit (CICU). For example, the preoperative patient with ischaemic heart disease may experience the full range of associated symptoms from central crushing pain with radiation, to the silent myocardial infarction of a long-term diabetic with associated neuropathy. Once these same patients have undergone surgical revascularisation, this ischaemic pain will probably be substituted for the dull, central tenderness of a median sternotomy, or the pleuritic pain of a residual pneumothorax irritated by the intercostal chest drains. The evaluation and subsequent treatment of chest pain on the CICU is vital to enhance the clinical outcome of this patient population.
In this chapter we will endeavour to discuss the rapid yet thorough assessment of chest pain as a symptom, the initial examination and investigation strategy required, and outline the emergent therapeutic options required for each differential diagnosis.
As with all clinical encounters the greatest aid to formulation of an accurate differential diagnosis is a thorough clinical history. Several confounding factors exist in the ICU patient that make the history less reliable. The spectrum of confounders ranges from those patients that are sedated and ventilated, through the heavily narcotised and disorientated, to the patient with ‘distraction’ pains who may under-report symptomatic changes. These challenges can result in important delays in the detection of the pathology underlying chest pain.
Given the above issues a focused approach to history taking is required. The mainstays of site, character, radiation, onset, severity, exacerbating factors and timing all still apply although many of these will be very dependent on the preceding interventions and current therapy that the patient is undergoing. The new onset of a complaint of chest pain, therefore, requires a flexible approach to clinical assessment to rule out the most important and potentially life threatening causes in a systematic fashion.
The role of clinical examination in the CICU can often be overlooked. With all the intensive monitoring and real time data that are now available, including bedside transthoracic echocardiography and easy access computerised tomography, the stethoscope can become a vestigial appendage. However, this patient population with positive pressure ventilation and invasive procedures is particularly prone to complications such as tension pneumothorax that need to be rapidly assessed, diagnosed and treated to avoid unnecessary morbidity and potential mortality. Indeed, the CICU patient is at particular risk when transferred from the controlled environment of the unit to other departments for investigation, and the role of clinical assessment must not be forgotten.
The elective patient recovering on the CICU is likely to have been thoroughly investigated prior to admission. Many of the emergent admissions will also have a diagnosis underlying their chest pain by the time they arrive. However, these critically unwell and increasingly aged patients are prone to further, sometimes unrelated, pathologies. Thus a physician must have a widespread understanding of those conditions that most commonly occur in the CICU patient.
It is beyond the scope of this chapter to cover all of the differential diagnoses the CICU staff may encounter in the patient with chest pain. However, we will aim to discuss those that are most common, those that are less common but life threatening, and those that are rare but need highlighting to ensure they are not overlooked.
Most of the patients that arrive on the CICU are likely to have undergone some investigation into their coronary vasculature, be it an invasive coronary angiography or some form of non-invasive functional or anatomical test. In fact, the majority of such patients will be admitted to the CICU to recover from a procedure, performed either percutaneously or surgically, to improve the vascular supply of the myocardial bed. These patients are not, however, immune from further myocardial ischaemia.
Primary percutaneous coronary intervention is now the revascularisation method of choice for patients presenting with an ST elevation myocardial infarction. The admission rate to the CICU following this procedure is around 5% and has been rising steadily year on year. The majority of these patients are intubated and ventilated in the periarrest period in the community, although some will require ventilation during the PPCI procedure itself. If the cardiac arrest is prolonged then these patients will undergo a period of cooling, or at least avoidance of hyperthermia, to aid neurological recovery.
A particular challenge in the ventilated patient post PPCI is the administration and absorption of dual antiplatelet medication. The risk of acute stent thrombosis in this population is tenfold that of the spontaneously ventilating patient, with a mortality approaching 40%. It is, therefore, important to ensure that patients receive and are absorbing the dual antiplatelets as prescribed by the interventional cardiology team, and that premature cessation is avoided in all but life threatening bleeding. In those patients who are unable to absorb enterically, alternatives include administration per rectum or substitution for an intravenous agent, for example the glycoprotein IIb/IIIa inhibitors such as abciximab, eptifibatide and tirofiban.
Any chest pain with concomitant ECG changes in the post PCI cohort of patients should trigger an emergent cardiology consultation to rule out acute stent thrombosis requiring repeat intervention. The second most common cause of postprocedural chest pain in this group is a technical problem with the stent placement, either an inflow or outflow coronary artery dissection, or perhaps the obstruction of a side branch. Finally, the role of untreated bystander disease is important as lesions that remain in other vessels may well become symptomatic in the high catecholamine milieu that exists post PPCI.
The rate of postoperative myocardial infarction following coronary artery bypass grafting is estimated to be between 5 and 10%. The incidence of graft related ischaemia is thought to be approximately 3%. In the intubated patient the clues to infarction and ischaemia are persistent low cardiac output state, dysrhythmia, evolving ECG changes and new regional wall motion abnormalities on echocardiographic imaging. The routine use of biochemical markers of myocardial damage is unlikely to be useful in the diagnosis in this population. In the awake patient, the chest pain of myocardial ischaemia can be difficult to differentiate from the postoperative sternal wound pain although any patient describing their usual angina should be investigated further. Patients in whom early graft failure is suspected have a significant adverse outcome unless treated promptly.
A second form of postprocedural cardiac ischaemia is that induced by poor myocardial protection. This is difficult to diagnose and may present as a global reduction in left or right ventricular function with associated haemodynamic compromise requiring inotropic support.
Even in the patient with apparently unobstructed coronary arteries who undergoes cardiac surgery, for example for a valve replacement, there is a risk of both plaque rupture and importantly embolic obstruction of the coronaries. This is particularly prevalent in those patients with dilated atria and preoperative atrial fibrillation. One final consideration is the occlusion of the coronary ostia by the stent struts on a prosthetic aortic valve.
A further mechanism of potential coronary flow limitation is the phenomenon of coronary vasospasm. This is often difficult to diagnose and is particularly prevalent at the time of high catecholamine drive, such as during extubation. Intravenous vasodilators usually allow rapid resolution and prevent the lasting damage of infarction.
Acute aortic dissection is the most common life threatening pathology of the thoracic aorta and carries a mortality of 1% per hour in the early stages. In the simplest Stanford classification, type A aortic dissection involves the ascending aorta, whereas type B dissections are those that do not involve the ascending aorta. This classification is useful, as type A dissections benefit from emergent surgical repair, whereas type B aortic dissections are best managed medically unless they become complicated. Type A aortic dissections are more common in patients in their sixth and seventh decades, whereas type B dissections typically affect the elderly.
Although traditionally thought to be associated with the connective tissue disorders such as Marfan, Loeys–Dietz and Ehlers–Danlos syndromes, more common predisposing factors include hypertension and bicuspid aortic valve anatomy. In the CICU setting, the physician must always be cognisant of the postsurgical patient with sudden onset of intrascapular pain and haemodynamic instability. Any instrumentation of the ascending aorta, be that percutaneously with ostial coronary stent placement, or surgically during aortic cannulation for cardiopulmonary bypass or during aortic valve replacement, may subsequently cause separation of the layers of the aortic wall. Rarely, reports have been published of aortic dissection following cocaine use, during heavy lifting and during systemic inflammatory vasculopathy. Although perhaps the most feared complication of pregnancy, dissection during pregnancy is relatively uncommon.
The typical chest pain associated with aortic dissection is said to be a searing or tearing pain that starts in the chest and rapidly radiates to the intrascapular region. Immediate complications include right coronary artery occlusion and associated inferior ST elevation, cardiac tamponade, acute aortic valve insufficiency and neurological deficit. Atypical presentations include renal failure of uncertain aetiology due to loss of the renal arterial supply, and mesenteric ischaemia manifest by rising serum lactate, abdominal pain and frequently loose stools. The loss of a peripheral pulse was only present in 19% of patients recorded in the International Registry of Acute Aortic Dissection series. In 15% of patients with an acute aortic dissection the chest radiograph will fail to show the classic widened mediastinum, and contrast enhanced computed tomography has become the first line in investigation. In those centres with expertise in transoesophageal echocardiography, this imaging modality has the advantage of being both sensitive and specific, and also relatively rapidly performed.
Once diagnosed, type A aortic dissection is initially treated by stabilisation of the patient using intravenous beta blockade. Thereafter, emergent surgery to obliterate the false lumen and repair the ascending aorta using an interposition graft is required.
Postprocedural management requires tight blood pressure control with beta-blocker therapy providing the pharmacological mainstay. Various authors have reported survival rates of between 50 and 90% 1 year following acute type A aortic dissection.
Although originally described as occurring in conjunction with an infective cause, the most common cause of superior vena cava syndrome (SVCS) worldwide is now malignancy of the lung, breast or mediastinal nodes. Of particular concern to the patients under consideration in this chapter, is the increasing incidence of iatrogenic SVCS secondary to device insertion, be those permanent pacemakers, implantable cardiac defibrillators or vascular access catheters. Although most commonly diagnosed due to the presence of distended neck and chest wall veins, cough, dyspnoea and facial swelling, several authors report the presence of a dull chest ache, mimicking that of cardiac ischaemia. Treatment very much depends on the underlying aetiology, with external neoplastic compression being best treated with debulking therapies be those chemotherapeutic or surgical. Thrombosis can be successfully reversed with thrombolysis and anticoagulation, and some cases require stenting to secure long-term patency.
The CICU has evolved over the last few decades such that the average unit has a plethora of patients undergoing various stages of organ support. Wide-bore vascular access catheters can be connected to continuous venovenous haemofiltration machines, extracorporeal membranous oxygenators, rapid infusers and ventricular assist devices. All of these life support technologies have the potential to allow the accidental entrainment of air into the circulation. Clinically, this often manifests as chest pain, dysrhythmia, right sided heart failure and dyspnoea. A venous air embolus can sometimes manifest as an arterial issue, such as stroke or myocardial infarction due to the passage from the right atrium to the left atrium through a patent foramen ovale or atrial septal defect.
The immediate management of vascular air embolus is to identify the source and eliminate further entrainment. In the case of the patient in cardiac arrest then vigorous cardiopulmonary massage has been shown to be beneficial. As with all iatrogenic complications, vigilant prevention is always better than the cure.
Both myocarditis and pericarditis are usually caused by an acute inflammatory process that may be secondary to a viral infection, an autoimmune inflammation or the presence of a toxin, either exogenous or from the accumulation of a metabolite. They may occur synchronously or can be seen as separate diagnoses. In Western countries most cases of myocarditis in previously healthy individuals are caused by enteroviruses, especially Coxsackie B. Other less prevalent causes include Lyme disease, caused by Borrelia burgdorferi, Chagas’ disease, caused by Trypanosoma cruzi (common in South America), and Kawasaki disease.
The prevalence is difficult to determine, as many cases are mild and may be subclinical. Patients usually present with myalgia, malaise, cough or GI upset, and fever. The risk of fatal arrhythmia may persist for several weeks after the onset of symptoms, and appears to be linked to strenuous exercise. The chest pain of both myocarditis and pericarditis may mimic that of acute myocardial infarction, and in the early stages of the illness the ECG may also be suggestive of an ST elevation MI. The typically scooped ST segment elevation and PR depression classically reported in pericarditis may take several hours to develop. Both echocardiography (which may show a regional wall motion abnormality in focal myocarditis) and troponin levels (which are frequently raised) are also poor differentiators. Many of these patients who present to the cardiologist will, therefore, be investigated with an invasive coronary angiogram.
Once recognised, the treatment of both myocarditis and pericarditis is largely supportive. Complications of cardiac failure are relatively rare and bridging to recovery is seldom necessary. Even in cases of acute cardiac decompensation, the majority of patients make a full recovery and preserve their myocardial function long term.
Cardiac Tamponade and Myocardial Rupture
Cardiac tamponade is defined as the compression of the cardiac chambers due to the accumulation of fluid, pus, blood clots or gas in the pericardial space. In the CICU environment the most common causes are the accumulation of blood post cardiac surgery, following percutaneous coronary intervention complicated by coronary artery perforation or myocardial rupture. The triad of high venous pressure, low systemic arterial pressure and muffled heart sounds is often observed. The presence of pulsus paradoxus, defined as a fall in arterial pressure of greater than 10 mmHg during inspiration, can often be determined by observing the respiratory variation of the arterial line trace during the ventilatory cycle. However, this clinical sign is not pathognomonic, and can also be seen in haemorrhagic shock, massive pulmonary embolus and severe obstructive pulmonary disease.
The most useful and immediate bedside test in the CICU environment is the echocardiogram, which typically confirms a pericardial collection, diastolic compromise of the right ventricle, the loss of respiratory variation in the IVC diameter, and greater than 25% respiratory variation in the transmitral and transtricuspid Doppler parameters. The treatment of cardiac tamponade is drainage of the pericardial collection, either percutaneously using CT or echo guided pericardiocentesis, or by re-exploration of the median sternotomy post cardiac surgery.
Myocardial rupture is an infrequent complication of myocardial infarction, occurring in approximately 2% of patients who have had unsuccessful or delayed revascularisation, but carries a high mortality due to cardiac tamponade. Clinical features that aid the diagnosis are a sudden onset of cardiovascular collapse, chest pain and jugular venous distension. Surgical repair is often fraught with the difficulty of very friable tissues.
Pneumothorax is particularly common in the postoperative patient on the CICU. However, the onset of a tension pneumothorax may be insidious, and must be recognised and treated swiftly to avoid potentially fatal consequences. More details of its management will be discussed in Chapter 28.
There are several well-recognised gastrointestinal causes of chest pain that are often overlooked in the initial assessment of the patient on the CICU. In the postoperative period the presence of a ruptured oesophagus secondary to transoesophageal echocardiography may be difficult to differentiate from a pneumothorax caused by the inadvertent opening of the pleural space. The leakage of gastric contents into the thorax can be insidious, and the subsequent sepsis difficult to manage unless a high clinical suspicion is maintained.
Cholecystitis is another mimic of acute myocardial infarction, with right upper quadrant or epigastric pain, symptoms of sympathetic overdrive and even inferior ST elevation on the 12-lead ECG. A complication of a common bile duct stone, pancreatitis is also seen in the critically unwell patient and serum or urinary amylase assays can aid in the diagnosis. The stress response to critical illness also raises the acidity of the contents of the upper gastrointestinal tract and can lead to gastric ulceration and haemorrhage and the subsequent chest pain.
Wound Pain and Sternal Dehiscence
Although sternal wound dehiscence is a rare complication of cardiac surgery, it is associated with significant morbidity and mortality. Preoperative risk factors include diabetes mellitus, obesity, chronic obstructive pulmonary disease and smoking. Operative factors include a long cardiopulmonary bypass time, postoperative haemorrhage, re-exploration of the wound, prolonged ventilation and the need for tracheostomy. The conscious patient often complains of sternal pain, and CT scanning of the thorax can reveal the sternal dehiscence, even in patients with little evidence of skin breakdown. Treatment varies from intravenous antibiotics through to complete sternotomy and reconstruction.
Takotsubo cardiomyopathy was first described in the early 1990s and is a reversible left ventricular apical ballooning that may mimic acute myocardial infarction. It is typically precipitated by acute emotional distress, especially in postmenopausal female patients with unobstructed coronary arteries. The Japanese term takotsubo means octopus pot, as the shape of the left ventricle with the typical apical ballooning is said to resemble the pot used by fishermen for catching octopodes. The syndrome often presents with severe chest pain, anterior ST elevation and a raise in cardiac biomarkers. It can, on occasion, cause cardiac arrest. The course is usually self-limiting with supportive care, but it can recur in up to one third of cases. Various pathogenic mechanisms have been proposed including vasospasm of the coronary vasculature secondary to a high catecholamine drive, although a neurogenic mechanism of myocardial stunning, as seen during acute neurological events, has also been considered.
Chest pain as a symptom is almost ubiquitous amongst patients on the cardiothoracic ICU. Without a broad understanding of the myriad of underlying diagnoses the ICU clinician may not be able to rapidly identify those that are life threatening versus those that are benign. The role of clinical examination must not be forgotten in these days of sophisticated monitoring and the easy availability of diagnostic imaging.
A broad understanding of the differential diagnoses underlying chest pain as a symptom is vital to rapid assessment and diagnosis in the CICU.
The mortality of an intubated and ventilated patient post primary PCI is tenfold that of a spontaneously ventilating patient.
The survival following type A aortic dissection is directly related to the time taken to diagnosis and subsequent initiation of definitive treatment.
Several gastrointestinal causes of chest pain are commonly seen in patients on the CICU and these diagnoses can be easily overlooked by the unwary.
1. Following primary PCI, dual antiplatelet therapy can be:
Safely withheld for 48 hours post procedure
Substituted for a glycoprotein IIb/IIIa inhibitor in those patients who are not absorbing orally
Discontinued with signs of non-life-threatening bleeding
A significant cause of a low platelet count
Omitted until the patient is spontaneously ventilating
2. Type A aortic dissection:
3. Superior vena cava syndrome:
4. In the absence of a pathological communication between the right and left heart, an air embolus should not present with:
5. Takotsubo cardiomyopathy is uncommonly associated with:
Respiration is a complex process during which gas exchange occurs between the respiratory system of the patient and the surrounding atmosphere. The two major functions of the respiratory system are to oxygenate the blood and to clear carbon dioxide (CO2) through ventilation of the lungs. Appropriate respiration requires several intact physiological pathways including the central and peripheral nervous systems, the respiratory muscles, the cardiopulmonary system, and an appropriate oxygen carrying capability with red blood cells. Pathological disruption of any of these systems can result in respiratory dysfunction.
Dyspnoea (breathlessness) is a symptom and sign. It is described by patients as difficulty with either inspiration, expiration or both. As a sign dyspnoea presents with involvement of accessory respiratory muscles and general distress. Dyspnoea is frequently but not exclusively associated with respiratory failure. Dyspnoea can be caused by both physical and psychological stimuli.
Dyspnoea as a sign is frequently obvious and most often associated with tachypnoea. Use of accessory respiratory muscles is a common sign. Acute dyspnoea leads to fatigue due to increased work of breathing.
Acute respiratory failure (ARF) is defined as the inability to meet the metabolic requirements of the patient through a failure of either oxygenation or ventilation. ARF can therefore be divided into two distinct subtypes including hypoxaemic respiratory failure (type 1) resulting in low arterial oxygen (PaO2) or hypercarbic respiratory failure (type 2) resulting in elevated arterial CO2 (PaCO2).
ARF is a common indication for admission to the intensive care unit (ICU), and can account for 17–56% of all admissions.
The relationship between dyspnoea and acute respiratory failure is variable. Some patients suffer and display dyspnoea without respiratory failure, and vice versa, some patients can be hypoxic or hypercarbic without the symptoms and signs of dyspnoea. The match of the two entities can give a clue to the duration of the problem, adaptive mechanisms and homeostatic control of the patients.