Acknowledgement This training package was created by Joseph Schar and Chantelle Skinner. Please direct any questions to your CSO or Team Leader.

Post-ROSC Management Acknowledgement This training package was created by Joseph Schar and Chantelle Skinner. Please direct any questions to your CSO or Team Leader. Offline Reading Download as PDF Welcome Introduction Post-Cardiac Arrest Syndrome Post-ROSC Management Paediatric Post-ROSC Management References

Summative Assessment Details Download PDF for of ine reading

Section 1 of 8 Welcome Welcome to the Post-ROSC Management clinical development package. This package will provide an overview of the key principles and priorities following return of circulation that are reflected in the new paramedic Post-ROSC Management CPG. It will outline a stepwise ABCDE approach to the post- ROSC patient and provide evidence summaries and best practice principles regarding optimal management following ROSC. References are provided should you wish to expand your knowledge. Overview and learning outcomes: Review the pathophysiology of the post-cardiac arrest syndrome. Review the key principles of post-rosc management in a stepwise ABCDE approach. Introduce the new changes to paramedic practice, including treating adults with hypotension and an altered conscious state; and Code STEMI activation. A summative assessment. Objective Successful completion of the online package will require at least 80% correct responses to the 12 MCQ. Once issued with an authority to practice (ATP) following this online package AND completion

of the paramedic 2-day conference you will be able to use the Post-ROSC Management CPG. The package will take approximately 45 minutes to complete.

Section 2 of 8 Introduction Post-return of spontaneous circulation (ROSC) management is an important step in the continuum of resuscitation. The quality of treatment provided in the post-cardiac arrest period the final ring in the Chain of Survival significantly influences the patient s ultimate outcome. [1] Resuscitation councils, including ANZCOR, have separate post-rosc guidelines from cardiac arrest guidelines. This recognises the distinct importance of management in this period. While there is a paucity of robust post-rosc literature, particularly pre-hospitally, studies have indicated negative outcomes associated with sub-optimal ROSC management.2 Therefore, up to date guidance that supports our delivery of optimal post-rosc management is the motivation for the development of a CPG. While tailoring our post-rosc care to the individual patient needs takes precedence, general principles in the CPG will standardise the management and expectations across clinical levels and articulate what is considered best practice. A difficult, but essential, skill is to be able to adapt our thinking once ROSC is achieved. We should be expecting ROSC in our cardiac arrest patients and have a clear plan to manage the patient when it occurs. The post-rosc patient is now a very different patient with different needs and priorities to the one that was in cardiac arrest. As such, we need to have the ability to mentally re-dispatch ourselves to this new critically unwell patient who may now also be affected by the post-cardiac arrest syndrome. This e-learning package provides a background, evidence summaries and practical recommendations relevant to every dot point in the new Post-ROSC Management CPG. The CPG details are displayed in text boxes, followed by the rationale for their inclusion in this new guideline.

CPG-120-P - Post-ROSC Management (Paramedic) CPG

Section 3 of 8 Post-Cardiac Arrest Syndrome The International Liaison Committee on Resuscitation (ILCOR) in 2008 published a consensus statement detailing the post-cardiac arrest syndrome. The syndrome has 4 key components: 1 Post-cardiac arrest brain injury 2 Post-cardiac arrest myocardial dysfunction 3 Systemic ischaemia / reperfusion response, and 4 Persistent precipitating pathology. Patients who achieve ROSC following cardiac arrest have a high mortality rate that can be attributed to a unique pathophysiological process that involves multiple organs. These are often superimposed on the disease or injury that caused the cardiac arrest as well as underlying co-morbidities. Injury caused by global ischaemia during the cardiac arrest is compounded by additional damage that occurs during and after reperfusion. The severity of the post-cardiac arrest syndrome will vary between patients and depend on the time in cardiac arrest, the cause of the arrest and pre-morbid health. It may not occur at all if the cardiac arrest is brief. [3]

Table 1 illustrates the components of the post-cardiac arrest syndrome and their pathophysiology, clinical manifestations and potential treatments. Note: the potential treatments that are highlighted are what we can offer prior to hospital arrival.

AMI indicates acute myocardial infarction; ACS, acute coronary syndrome; IABP, intraaortic balloon pump; LVAD, left ventricular assist device; EMCO, extracorporeal membrane oxygenation; COPD, chronic obstructive pulmonary disease; CNS, central nervous system; CVA, cerebrovascular accident; PE, pulmonary embolism; and PCAS, post cardiac arrest syndrome. 1. Post-cardiac arrest brain injury A common cause of morbidity and mortality following cardiac arrest is brain injury. The brain has little tolerance to ischaemia and a unique response to reperfusion. The mechanisms of brain injury following cardiac arrest are complex and can continue for hours to days. It has been shown that an initial period of hyperaemia occurs in the first few minutes following ROSC due to elevated cerebral perfusion pressures and impaired cerebrovascular autoregulation, followed by vasospasm and hypoperfusion.3 Post-cardiac arrest brain injury may be exacerbated by hypotension, hypo/hypercarbia, hypo/hyperoxaemia, pyrexia, hypo/hyperglycaemia, and seizures. [1] These factors can be minimised, addressed or prevented by our meticulous attention to optimal post- ROSC management. 2. Post-cardiac arrest myocardial dysfunction Significant myocardial dysfunction is common after cardiac arrest, is usually responsive to treatment and is usually reversible. Transient increases in circulating catecholamine (e.g. adrenaline, noradrenaline) concentrations immediately following ROSC often result in increased HR and BP. Myocardial dysfunction can occur early in the post-rosc phase and is characterised by alterations in HR, rhythm and hypotension. It can occur despite preserved coronary blood flow, indicating a stunning phenomenon as opposed to infarction or permanent injury. 3. Systemic ischaemia / reperfusion syndrome The whole-body ischaemia that occurs during cardiac arrest and the reperfusion that occurs post- ROSC results in a number of processes that contribute to multiple organ failure. Thus, the post-

cardiac arrest syndrome has many similar pathophysiological processes to that of severe sepsis. Consequently, it shares many clinical manifestations such as intravascular volume depletion, vasodilation and impaired vasoregulation, impaired oxygen delivery and utilisation, and increased susceptibility to infection. [3] 4. Persistent precipitating pathology The precipitating pathology that caused / contributed to the cardiac arrest can complicate, and be complicated by, the simultaneous pathophysiology of the post-cardiac arrest syndrome. This needs to be rapidly identified and addressed. Having a high suspicion of the cause of the arrest can influence your management approach to the post-rosc patient. The most common pathology causing out of hospital cardiac arrest is acute coronary syndrome. Other common non-cardiac causes include pulmonary disease, CNS disease, PE, overdose/poisoning, sepsis, and trauma. Consider and correct where possible the reversible causes of cardiac arrest: Hypoxia Hypovolaemia Hyper / hypokalaemia / metabolic disorders Hypothermia / hyperthermia Tension pneumothorax Tamponade Toxins Thrombosis (pulmonary / coronary) Practice Question

Potential treatments to minimise and address components of the postcardiac arrest syndrome include: Airway protection and mechanical ventilation Early haemodynamic optimisation Seizure control Glucose control All of the other answers SUBMIT

Section 4 of 8 Post-ROSC Management Post cardiac arrest management can be defined in several phases: the immediate (0-20 mins) and early (20 min 6-12 hrs) phases, when early interventions may be most effective the intermediate (6-12 hrs 72 hrs) phase, when injury pathways are still active and aggressive treatment is often required the recovery (>72 hrs) phase, when prognostication is more reliable and the patient outcomes become more predictable. Click on the button to the right of this page to work through this section.

Page 1 of 17 Phases of post-cardiac arrest syndrome. Figure 1: Phases of post-cardiac arrest syndrome. [3] The immediate and early phases of post-rosc management aim to prevent cardiac arrest recurrence, provide organ support, and limit ongoing injury. Management priorities include requesting clinical support, treating precipitating causes, and preparing for rapid transport. For simplicity and consistency, the patient should be treated following the ABCDE approach. A full set of observations should be taken to establish a baseline condition and identify abnormalities that need to be addressed. Where the cause of the cardiac arrest is known, tailor your post-rosc management to the patient s particular dysfunction or disease by referring to relevant CPGs. This includes following a traumatic cardiac arrest, where management and treatment priorities may be determined by the patient s injuries.

Page 2 of 17 Airway Once ROSC is achieved, re-assessment of the airway should occur. If a supraglottic airway (SGA) is in place then this needs to be reviewed to ensure it is optimally positioned. After any movements, such as extrication, airway re-assessment should always be a priority to ensure the SGA remains optimally placed and with a good seal. Suctioning should occur as required. If a patient has neurological recovery post-rosc where they are gagging on the SGA or becoming significantly agitated because of its placement, it is reasonable to remove the SGA, consider another airway adjunct if tolerated, and continue oxygenation. Gagging and agitation will increase the patient s plasma catecholamine concentrations, which may provoke raised intracranial pressures, hypertension, or arrhythmias. [1]

Page 3 of 17 Breathing Clinical Practice Guideline Avoid hyperventilation. Start at 10 breaths / min and consider ventilation strategy. Continue waveform capnography monitoring. Avoid excessive ventilation volumes. Some patients will regain spontaneous respirations following ROSC. If these patients have an advanced airway in place and/or the bag-valve mask is being held over their face then gentle assistance with ventilations should occur. This is particularly important for paediatrics and patients with reduced ventilatory function. Following cardiac arrest, sub-optimal respiratory management has been associated with worse outcomes. [2] Post-ROSC, patients blood carbon dioxide levels and ph are controlled by ventilations. Ventilation strategy refers to the rate, volume and pressures delivered during IPPV. Optimal ventilation of the post-rosc patient balances the need to reverse hypoxia and acidosis with the potential deleterious effects of hyperventilation, hypocapnia and hyperoxia. [4] We will explore these individually.

Page 4 of 17 Breathing - Hyperventilation Figure 2: Cerebral Blood flow dependence on PCO 2 [20] Hyperventilation (from excessive respiratory rates, tidal volumes, or both) is common and can have adverse effects on haemodynamics and carbon dioxide levels in the blood (PaC0 2 ). Hyperventilating a patient post- ROSC can cause increases in intrathoracic pressure, which can decrease preload and result in reduced cardiac output and coronary perfusion pressure. [4] This could be deleterious in patients with haemodynamic compromise. Hyperventilation can also expel high concentration of carbon dioxide. This can lead to low carbon dioxide levels in the blood (hypocapnia). Hyperventilation causing hypocapnia can result in cerebral vasoconstriction, which can markedly reduce cerebral blood flow and lead to harmful cerebral ischaemia. Figure 2 shows the relationship between arterial PC0 2 and changes in cerebral blood flow. Note the significant percentage reduction of cerebral blood flow as blood carbon dioxide levels drop. An association between hypocapnia and poor neurological outcome is commonly reported in the literature. [1] Therefore, avoiding hypocapnia, and hyperventilation, is important.

While hyperventilation can cause hypocapnia, hypoventilation can result in further increases in a patient s blood carbon dioxide levels (hypercapnia). Hypercapnia can also contribute to secondary brain injury and may increase the likelihood of a further cardiac arrest.

Page 5 of 17 Breathing - Capnography Figure 3: Waveform capnography demonstrating loss of ROSC We are currently unable to measure a patient s blood carbon dioxide levels in the pre-hospital environment, as it requires arterial blood gas (ABG) testing. If the waveform capnography was attached during cardiac arrest then an end-tidal carbon dioxide (EtC0 2 ) number will be displayed. Capnography use for paramedics is outlined in the paramedic capnography e-learning package and will be further discussed at the paramedic conferences. The EtC0 2 number may give us an indication of a patient s blood carbon dioxide levels but there are many factors following cardiac arrest that cause alterations in EtC0 2 numbers that don t accurately correspond with blood carbon dioxide levels. Therefore, it is not recommended that paramedics use EtC0 2 numbers to guide ventilation strategy after cardiac arrest. Following ROSC, waveform capnography still has several important functions: Monitor ventilation rates. Monitor waveform trends. Display characteristic waveform patterns e.g. shark fin pattern indicating obstruction. A marker of cardiac output and loss of ROSC.

Figure 3 displays a waveform capnography pattern that occurs when a patient has a sudden loss in cardiac output eg. loss of ROSC. Any sudden change in waveform trend should be a prompt to re-check your patient s cardio-respiratory status.

Page 6 of 17 Breathing - Ventilation rates Following ROSC, ventilations should continue at a rate of 10 breaths / minute. This is considered a reasonable starting point (and may be continued thereafter if appropriate), which balances avoiding hyperventilation (and hypocapnia) and further increasing hypercapnia. For simplicity, one breath every 6 seconds will deliver a rate of 10 breaths / minute. This strategy has been recommended in guidelines5 and has been adopted by ambulance services in Australia and internationally. The optimal IPPV rate and volume following ROSC may differ between patients and many factors should be taken into consideration, including the cause of the arrest. For example, an asthmatic arrest who is now post- ROSC is likely to have a severely hyper-inflated chest and will require slow ventilation rates (and smaller tidal volumes) to allow for adequate chest deflation. This should occur according to the Asthma CPG.

Page 7 of 17 Breathing - Ventilation volumes Measuring and approximating ventilation volumes is difficult in our environment. The aim is to provide just enough volume to see rise and fall of the chest. Delivering high ventilation volumes, especially with an advanced airway in place, can cause lung injury as well as potentially effecting haemodynamics and carbon dioxide levels.

Page 8 of 17 Breathing - Oxygen Therapy Clinical Practice Guideline - Continue high-flow oxygen therapy: For patients requiring assisted ventilations, continue oxygen 15L/min. For patients not requiring assisted ventilations, re-assess and apply optimal oxygen to maintain Sp0 2 94-98%. If Sp0 2 is unreliable, maintain high-flow oxygen. The optimal Sp0 2 range following ROSC has not been firmly established. Observational studies have frequently and consistently reported increased mortality and worse outcomes associated with hypoxemia (low PaO 2 ) following cardiac arrest.6 Maintaining Sp0 2 94% at all times is currently recommended. The administration of prolonged periods of high flow oxygen after ROSC has long been standard practice. Maximising oxygen delivery for several hours has been on the premise that patients have been severely hypoxic during the cardiac arrest and therefore might benefit from lots of oxygen post-rosc. Avoiding hypoxia has been, and still is, the most significant priority. Until recently there has been little evidence to support a change in this approach. However, recent studies have identified possible harm associated with excessive oxygen administration (hyperoxia) leading to very high Pa0 2 (hyperoxaemia). [7-8] No well powered randomised control trials have yet tested the pre-hospital titration of oxygen following ROSC on outcomes. However, SAAS has been, and will be, participating in important research in this area. The reduction of oxygen After Cardiac arrest (EXACT) study is a multi-centre, randomised, controlled trial (RCT) that will assess whether titrating oxygen to target saturations following ROSC improves outcome at hospital discharge. This study period will supersede standard oxygen administration guidelines. Outside of this study enrolment period, the current SAAS position is to continue high flow oxygen therapy in the immediate post- ROSC period. For patients who require assisted ventilations with the BVM (with or without an advanced airway), oxygen flow should remain at 15L/min. Patients who have had a brief cardiac arrest and have responded immediately to appropriate treatment may achieve return of normal cerebral function. These patients may not require oxygenation and ventilation through a BVM or advanced airway. Once a reliable Sp0 2 measurement occurs, optimal oxygen should be applied to maintain Sp0 2 94-98%. The priority here is avoiding hypoxia, hence oxygen therapy must still be

initiated at high-flow and Sp02 measurements closely monitored. If a patient has a good neurological function, is maintaining their own airway, is self-ventilating with a reliable Sp0 2 > 98% on high flow oxygen, it is reasonable to titrate the oxygen to achieve a target saturation between 94-98%. This target saturation is recommended in ANZCOR Guideline 11.7.1. [9] If at any point the Sp0 2 reading is considered to be an unreliable reading (eg poor peripheral perfusion, anaemic patient) or the Sp0 2 does not have a reliable trace, maintain or increase oxygen therapy to high flow. Preventing hypoxic episodes is considered more important than avoiding any potential risk of hyperoxia. [5]

Page 9 of 17 Breathing - Posture Clinical Practice Guideline: Optimise posture Following ROSC, consider the most appropriate posture for your patient. Raising the patient s head up to 30 may help prevent aspiration, improve lung mechanics and lower intracranial pressure (ICP).[4] However, this may not be appropriate in hypotensive patients or where C-spine precautions are applied. Raising the head up may be difficult to achieve on scene but is a consideration once the patient is on the stretcher. Ensure this does not obstruct your view of the patient.

Page 10 of 17 Breathing - Examination Clinical Practice Guideline: Perform chest examination, including auscultation of the lungs. Look at the patient s chest for symmetrical chest movement. Auscultate to ensure equal breath sounds bilaterally. If ribs have been fractured during chest compression (documented in up to 70% of OHCA receiving CPR) be aware of a potential pneumothorax. [1] Listen also for evidence of pulmonary oedema or other abnormalities.

Page 11 of 17 Circulation - Blood Pressure Management Clinical Practice Guideline - For adults with hypotension and altered conscious state: Administer sodium chloride 0.9% IV in 250 ml aliquots until a radial pulse is achieved or SBP=100 mmhg, to a maximum of 10 ml/kg up to 1000 ml. Reassess patient after each 250 ml and cease IV fluids if patient shows signs of pulmonary oedema. Consult with a SAAS Medical Practitioner via the EOC Clinician if hypotension persists. Haemodynamic instability is common post-rosc. Post-cardiac arrest myocardial dysfunction, impaired vasoregulation, and intravascular volume depletion can result in hypotension and arrhythmias.1 When considering BP goals post-rosc there is a balance between providing adequate perfusion to a brain that may have lost its autoregulatory ability with the potential for overstressing a post-ischaemic heart. [4] Adequate blood pressure for optimal organ perfusion will vary between post-cardiac arrest patients and will be influenced by individual pre-morbid pathophysiology and factors associated with resuscitation. A common cause of morbidity and mortality following cardiac arrest is brain injury. The brain has little tolerance to ischaemia and a unique response to reperfusion. [3] Post-cardiac arrest brain injury may be exacerbated by hypotension. [1] Hypotension, defined as a systolic blood pressure (SBP) <90-100 mmhg, has been associated with higher mortality and diminished functional recovery following out of hospital cardiac arrest. [10-13] Additionally, hypoxic-ischaemic brain injury (HIBI) can occur immediately following ROSC and can result in cerebrovascular autoregulation dysfunction in some patients. In these patients, cerebral perfusion pressures become dependent on systemic blood pressure. [14] Paramedics do not currently have capacity in their guidelines to treat post-rosc hypotension, unless it is covered in other specific CPGs. This has been rectified within the new Paramedic Post-ROSC Management CPG. In patients who have an altered conscious state and are hypotensive, there is a risk that their cerebral perfusion is inadequate and not treating their hypotension could result in further cerebral ischaemia. Therefore, maintaining a minimum BP target is important. Patients who have a brief cardiac arrest and a return of a GCS=15 indicate that their cerebral perfusion is adequate, and treating to a higher BP is not currently recommended. It is extremely important to auscultate the patient s chest before commencing fluid therapy and after each

250ml aliquot. If the patient shows any sign of pulmonary oedema then fluid therapy must be ceased. This can be a sign of cardiac failure that will require additional treatment, and continuing fluid therapy in these patients can be harmful.

Page 12 of 17 Circulation - Coronary Reperfusion Considerations Clinical Practice Guideline: If ST elevation diagnostic of STEMI persists on the 12 lead ECG, activate the receiving hospital PCI team using the Code STEMI line (refer to Ischaemic Chest Pain CPG) and notify the receiving hospital early. The majority of OHCA cases are reported to have a cardiac origin, with obstructive coronary artery disease being the most dominant aetiology. [15] As part of a comprehensive post-rosc plan, an emphasis of directing management toward the early treatment of the underlying cause of the arrest is important. Use of coronary angiography and percutaneous coronary intervention (PCI) following OHCA has been reportedly increasing over the last decade, with an associated trend in survival to discharge in patients with post-arrest ECG STsegment elevation (STE). [16] Approximately 70% of patients who do present with ST elevation following out-of-hospital cardiac arrest (OHCA) are found to have an acute coronary occlusion. [17] This is comparable to findings of acute coronary syndrome (ACS) patients (who have not had a cardiac arrest) who undergo coronary angiography. [18-19] Since 2016, paramedics can activate the receiving hospital PCI-team in stable patients with STEMI. Following cardiac arrest, these patients do not fit current paramedic criteria for calling a code STEMI. However, these patients are regarded as the highest risk patients who may require immediate angiography. Therefore, the new Post-ROSC Management CPG enables paramedics to call a code STEMI following a cardiac arrest if ST elevation diagnostic of STEMI persists on the 12 lead ECG. Caution needs to be taken when immediately analyzing a post-rosc ECG. A post-ischaemic heart that has potentially had large doses of adrenaline during the arrest may take some time to settle into a stable rhythm and morphology, and interpretation of the ECG for ST elevation should wait until this occurs. It is also important to note that patients commonly have a GCS=3 or similar following OHCA, and with the new CPG this is not a contraindication for Code STEMI notification. Post-cardiac arrest patients will be considered unstable at the receiving ED and will be required to go directly to the resus room. However, the Code STEMI notification will inform the receiving Interventional Cardiologist and preparations can begin prior to your arrival. By activating a Code STEMI we are not committing a patient

to a particular procedure but identifying a high-risk patient who meets criteria for consideration. Whether the patient is then directed to the catheterization lab will be a decision for the receiving Doctors and Cardiology team. A Code STEMI notification should not take priority over other critical post-rosc management interventions. If you are close proximity to hospital then it may be more appropriate to notify the receiving hospital with your observations.

Page 13 of 17 Disability and Exposure Assessing a patient s neurological function post-rosc will include a GCS and pupillary examination. Performing a rapid secondary survey ensures that nothing has been missed. To examine the patient properly full body exposure may be necessary. These actions may give insight as to the cause of the cardiac arrest.

Page 14 of 17 Other Considerations - Blood Glucose Control Clinical Practice Guideline - For adults with hypoglycaemia: Administer glucose (10%) IV titrated to achieve a BGL between 4-10 mmol/l. Sodium chloride 0.9% 100 ml IV flush must be given before and after glucose IV. Avoid hyperglycaemia. Hyperglycaemia is common after cardiac arrest. A strong association exists between high BGL after resuscitation and poor neurological outcome. [4,9] Additionally, in critically ill patients severe hypoglycaemia is associated with increased mortality. Comatose patients are at risk of unrecognised hypoglycaemia; recording a BGL should be included as one of the post-rosc observations. If treating hypoglycaemia, administer the minimum amount of IV glucose to achieve a BGL within normal values (4-10 mmol/l). [4,9]

Page 15 of 17 Other Considerations - Temperature Management Clinical Practice Guideline: Maintain temperature within normal range (36-37.5 C). Animal studies indicate that early cooling post-rosc results in improved outcomes but this has yet to be demonstrated in human trials. [1] Pre-hospital cooling has not demonstrated benefit despite large numbers of patients studied. [9] Post-ROSC patients usually have drops in temperature within the first hour and hospital admission temperatures following OHCA are usually between 35-36 C. Temperatures less than 36 C may not be desired in patients with significant shock, myocardial dysfunction, or excessive risk of bleeding. [1] Therefore, if a post-rosc patient is hypothermic, consider applying blankets and space blankets to prevent further heat loss. Although the effect of elevated temperature on outcome is not proven, hyperthermia may aggravate ischaemia-reperfusion injury and neuronal damage through raised metabolic activity. [3] Passive cooling is appropriate for these patients, removing blankets and clothes to manage the hyperthermia. The overall aim of pre-hospital temperature management is to attempt to maintain a temperature within normal range.

Page 16 of 17 Other Considerations - Seizure Control Seizures are common after cardiac arrest and occur in approximately 30% of patients who remain comatose after ROSC. [1] Myoclonus is the most common seizure type, but focal and generalised tonic-clonic can also occur. Seizures can increase the cerebral metabolic rate up to 3-fold and prolonged seizures can exacerbate brain injury caused by cardiac arrest. Be alert for any seizure activity following ROSC. Treatment of post-rosc seizures should occur following relevant CPGs.

Page 17 of 17 Other Considerations - History If a clear history has not been obtained it is important to gather a comprehensive history as quickly as possible. Those involved with the patient prior to the cardiac arrest may have valuable insight into symptoms reported or actions prior, as well as the patient s physiological baseline (before the cardiac arrest). This history can be significant when the patient arrives at hospital and decisions are being made regarding appropriate treatment for the patient. Valuable information relating to the cardiac arrest should also be obtained, including time of the cardiac arrest, whether it was a witnessed arrest, and whether CPR or defibrillation occurred prior to SAAS arrival.

Section 5 of 8 Paediatric Post-ROSC Management The principles of paediatric post-rosc care are based around minimization and management of the components of the post-cardiac arrest syndrome. While much of the post-rosc management for adults includes reasonably standardized targets, paediatric intervention strategies are unique and therefore dependent on individual age, weight and normal physiological ranges expected of the child. For timely management of the anticipated physiological abnormalities in a paediatric post-rosc patient, early clinical support from a SAAS Medical Practitioner, via the EOC clinician, must occur. Paediatric cardiac arrest and return of circulation form a particularly small percentage of total ROSC seen by SAAS each year. However, each of these patients is significant, and changes to our understanding and management of post-rosc paediatric care can have a significant impact on the final outcome. As always, reversible causes including the 4 Hs and 4 Ts must be considered and treated whenever possible. With an anticipated ease of extrication compared to adults, transport of post-rosc paediatric patients should not be delayed. Click on the button to the right of this page to work through this section.

Page 1 of 6 Airway Paediatric cardiac arrest is less likely to be precipitated by a cardiac cause and is most commonly secondary to prolonged global hypoxaemia and ischaemia. [21] For this reason, close attention to airway and oxygenation in these patients is paramount. Posturing a paediatric patient correctly can have an impact on your ability to ventilate effectively and is an important component of your airway re-evaluation. This is of particular importance after any movement, after extrication and again prior to transport. Hyperextension of the neck can cause airway obstruction in small infants and should be avoided.

Page 2 of 6 Breathing Paediatric Drug Chart Clinical Practice Guideline: For paediatric patients, ventilate at a normal age-appropriate respiratory rate, refer to SAAS paediatric RDR chart. If gastric distension is impeding effective ventilations (e.g. in paediatrics), decompress the stomach via the SGA gastric drainage tube. Particular attention must be paid to ventilation rate and volume in paediatric patients, with careful consideration to avoid hyperventilation and subsequent hyperinflation of the lungs. Only deliver ventilation volumes that achieve normal visible chest movement. Gastric insufflation can be a risk in a non-intubated, ventilated patient, especially with a poorly sealed airway. If the abdomen becomes distended, ventilation and circulation may be impeded. With the new post-rosc guideline and the introduction of i-gels, comes the

ability to decompress the stomach with an orogastric tube via the i-gel gastric drainage tube. This will be expanded upon in the paramedic conferences. The SAAS paediatric RDR chart or drug dose chart must be used to help determine the age-appropriate respiratory rate.

Page 3 of 6 Breathing - Oxygenation Recall the OxyHaemoglobin Dissociation Curve Much of the evidence regarding oxygenation in a post-rosc paediatric patient is centred around in-hospital care, arterial blood gas analysis and the ability to adjust oxygenation to achieve a desired partial pressure of oxygen in arterial blood (PaO 2 ). In the prehospital environment, without ABG availability, it is appropriate to maintain high flow oxygen in patients who require assisted ventilations. Hypoxaemia and hyperoxaemia can both cause harm. Similar to the adult approach, in patients that do not require assisted ventilations, and the Sp0 2 reading is considered reliable, then it may be appropriate to titrate the concentration of inspired oxygen to achieve and maintain SpO 2 94-98%. An Sp0 2 of 90%, although only 10% below normal haemoglobin-oxygen saturation, represents a partial pressure of oxygen in arterial blood of 60mmHg which is 40mmHg below normal. ANZCOR 2016 Early clinical support must be sought with a SAAS Medical Practitioner via the EOC Clinician to discuss appropriate management of paediatric patients whose cardiac arrest may have been caused by a long-term cardiac condition. Examples of these may include chronic lung disease or cyanotic heart disease.

Page 4 of 6 Circulation Clinical Practice Guideline - For paediatrics with hypotension (refer to SAAS paediatric RDR chart): Consult with a SAAS Medical Practitioner via the EOC Clinician for sodium chloride 0.9% IV Peripheral circulatory failure is common after ROSC. Prior to any circulatory intervention in a paediatric post- ROSC patient, clinical support with a SAAS Medical Practitioner via the EOC Clinician must be sought. Consideration for sodium chloride 0.9% in hypotensive paediatric patients with an altered conscious state is based on maintenance of cerebral perfusion.

Page 5 of 6 Other Considerations - Blood Glucose Control Clinical Practice Guideline -For paediatrics with hypoglycaemia Consult with a SAAS Medical Practitioner via the EOC Clinician for glucose (10%) IV starting at 2 ml/kg titrated to achieve a BGL between 4-10 mmol/l. Sodium chloride 0.9% 1 ml/kg IV flush must be given before and after glucose IV. Post-ROSC paediatric patients are at increased risk of hypoglycaemia. If this is determined, it must be treated efficiently in order to maintain normal levels appropriate for age. Any management of paediatric post-rosc hypoglycaemia must be in consultation with a SAAS Medical Practitioner for use of glucose (10%) IV. When appropriate, reassessment of blood glucose levels, even if initial reading is within normal limits, must be done.

Page 6 of 6 Other Considerations - Temperature The recommendation of temperature management in paediatric post-rosc patients is maintenance of normothermia. The same strategies described with adult patients can be applied to paediatrics. Hyperthermia (>37.5 C) may be associated with worse neurological outcomes and must be avoided where possible.

Section 6 of 8 References Reference-Post-ROSC.pdf 46.1 KB

Section 7 of 8 Summative Assessment Details Successful completion of the online package will require at least 80% correct responses to the 12 MCQs. You are allowed three attempts for the quiz. Please speak to your team leader if you have used up all three attempts. Once you have passed the quiz, you can obtain your certificate of completion by returning to your portal. Go to quiz

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