Monday, 13 November 2017

Respiratory Sepsis in Advanced Dementia 

Case study submission for the  College of Paramedics Carol Furber Award 2017

Respiratory Sepsis in Advanced Dementia
 

Patient details changed to maintain confidentiality 
Written March 2017, published online November 2017

Case

An ambulance was called to a residential nursing home for a 78-year-old male with difficulty in breathing. `Stanley` was found curled in the foetal position in his bed with obvious respiratory distress. 

The patient’s wife and daughter were with him and, in conjunction with the nursing home staff, explained Stanley had poor baseline health and recurrent chest infections. On this occasion, his breathing had deteriorated over several days before the out-of-hours GP had recommended an ambulance be called.

Initial assessment revealed

Airway Patent, dry
Breathing Respiratory rate = 28 Oxygen saturations = 85% on air, Increased work of breathing with accessory muscle use, Coarse rales, especially on the left sided lobes,Feeble but productive cough; yellow sputum
Circulation Heart rate = 122 in sinus tachycardia, Blood pressure = 98/50, Regular radial pulse, Warm peripheries
Disability Glasgow Coma Score = 8/15 (2,2,4); this was not acutely worsened from Stanley’s baseline Blood sugar = 8.3, Moaning and grimacing in apparent pain
Examination o Temperature = 38.80C, Dry skin and mucosa
Allergies None stated
Medications Morphine and midazolam (in `just in case` box; never previously used), Ventolin 
Past Medical History Dementia, Frailty
Social History Permanent resident in nursing home. Dependent on carers for all daily activities, including feeding and personal care. No ability to meaningfully interact with other people, Clinical frailty score = 8 Wife and daughter live nearby and share valid Lasting Power of Attorney. Another daughter lived in another county. 

The patient was diagnosed with respiratory sepsis in the context of advanced dementia. After reviewing the situation with the ambulance crew, Stanley’s family did not feel admission was in his best interests. He was given a total of 7.5mg of subcutaneous morphine which reduced respiratory distress and alleviated the patient’s pained moans. The patient was also referred by telephone to a palliative care team, who agreed to visit the next day.

Several weeks later, a letter was received by the ambulance trust’s patient experience department which stated the patient lived for a further week, before dying in the nursing home surrounded by his family. They were grateful he had not been taken to hospital by the ambulance crew.

Discussion

The UK Sepsis Trust highlight there are 150,000 cases of sepsis each year, causing 44,000 deaths1. To reduce mortality and morbidity, both the mainstream media2 and professional literature3 endorse aggressive management of sepsis by healthcare professionals, including paramedics4. Standard treatment includes early recognition, supplemental oxygen, intravenous fluids, antibiotics, lactate analysis and urine measurement; collectively known as the `Sepsis Six`5. Some Sepsis Six procedures are commonly implemented by ambulance clinicians, whereas others are undertaken in the emergency department or ward. Additional treatments may include intensive care unit admission, renal filtration, and inotrope administration6. 

It is argued that by better treating sepsis, a medium sized general hospital could prevent 100 deaths and save £1.25million annually7. However, some of the interventions are known to be painful8, with significant side effects and limited efficacy in patients with severe co-morbidities where death due to terminal disease is inevitable. Overall, their use might not be in the patient’s best interests9.

The National Institute for Health and Care Excellence’s `guideline 51` has advice for recognising acute changes in mental status caused by infection, even when the patient has underlying dementia. The guideline recommends sepsis is actively treated, and a 999 ambulance “usually” called when diagnosed outside of the acute hospital setting10. 

Dementia itself is a terminal illness11. There are 850,000 people living with the condition in the UK12, and their symptoms progressively worsen until they are completely dependent carers for all activities of daily living and unable to interact with other people; a state known as `advanced dementia`13. From the onset of symptoms, survival rarely exceeds 10 years14 and many articles argue that dementia-related decline is undignified and unpleasant for the patient’s friends and family to experience15. 

The most common precipitating cause of dementia-related death is overwhelming respiratory infection, which is reported in 66% of fatalities. Studies have shown that it is possible to successfully treat respiratory infection in patients with advanced dementia, where the primary outcome measure is short-term extended lifespan, but treatment does not improve the patient’s quality of life, levels of comfort or long-term survival17. 

It is therefore argued in some end of life care literature that people with advanced dementia and severe respiratory infection may be best cared for with the alleviation of symptoms and a focus on comfort, rather than be admitted to hospital9. 

The UK Ambulance Services Clinical Practice Guidelines 2016 have a chapter on end of life care which endorse ambulance clinicians to “consider” alternative pathways and seek multidisciplinary advice to avoid unnecessary admission to the emergency department. Where interventions are required by the ambulance clinician, there is advice on a range of techniques to reduce suffering and appropriately facilitate natural death18. 

Stanley received morphine from the ambulance crew, which apparently reduced suffering and made his family less fearful for his welfare. A clinician discussed the situation was a local palliative care team, made an initial referral and developed an appropriate plan for further care that respected his family’s wishes and resulted in a more satisfactory experience of death. 

This case positively demonstrates the modern face of paramedic practice, where reasoned decisions and evidence-based care is provided by skilled and autonomous professionals in complex situations with competing treatment paradigms, rather than simply transporting patients approaching the end of their life to an emergency department at great inconvenience and discomfort, and at avoidable expense to the wider NHS.  

With high-profile campaigns relating to both dementia and sepsis raising public recognition and expectation, associated demands on NHS services may grow. The ambulance services may see ever more frequent calls to people like Stanley, and paramedics must continue to be appropriately supported to make complex medical decisions in situations where death is a real possibility, while alleviating pressure on busy emergency departments, but ultimately act in the patient’s best interests.

References

1. UK Sepsis Trust, Homepage, 2016, http://sepsistrust.org/
2. Daily Mail, 2015, http://www.dailymail.co.uk/news/article-3046312/Hospitals-failing-spotsilent-killer-Treating-sepsis-early-save-12-500-lives-year.html
3. Langley, M. & Langley, C., Journal of Paramedic Practice volume 4, issue 5, 2012, http://www.paramedicpractice.com/cgi-bin/go.pl/library/article.cgi?uid=91457
4. Ambulance Today, Doing the Best for Sepsis Patients, 2014, http://www.ambulancetoday.co.uk/news-item/doing-the-best-for-sepsis-patients/
5. UK Sepsis Trust, Sepsis Six, 2017, http://sepsistrust.org/wpcontent/uploads/2016/04/Black-Sepsis-6-Poster-Medical-2.jpg
6. Rhodes A et al., Surviving Sepsis Campaign: International Guidelines for Management for Sepsis and Septic Shock: 2016, Critical Care Medicine, 2016 http://journals.lww.com/ccmjournal/Fulltext/2017/03000/Surviving_Sepsis_Campaign___Int ernational.15.aspx
7. UK Sepsis Trust, Key recommendations, 2013, http://sepsistrust.org/wpcontent/uploads/2013/10/briefing.pdf
8. Bledsoe, B., Porter, R. & Cherry, R. Paramedic Care Principles and Practice Introduction to Advanced Prehospital Care, Intravenous Access and Medication Administration, 2006, Brady
9. Watson, M., Lucas, C., Hoy, A., Back, I. & Armstrong, P. Palliative Adult Network Guidelines, 2011, Mount Vernon Cancer Network
10. National Institute for Health and Care Excellence, NG51: Sepsis: recognition, diagnosis and early management, 2016, https://www.nice.org.uk/guidance/NG51
11. Alzheimer’s Society, End of life care, 2017, https://www.alzheimers.org.uk/info/20046/help_with_dementia_care/80/end_of_life_care/3
12. Alzheimer’s Society, Dementia UK report, 2017, https://www.alzheimers.org.uk/info/20025/policy_and_influencing/251/dementia_uk
13. Mitchell, S.L. Advanced Dementia, New England Journal of Medicine, 2015, http://www.nejm.org/doi/full/10.1056/NEJMcp1412652
14. Alzheimer’s Society, The later stages of dementia, 2017, https://www.alzheimers.org.uk/info/20073/how_dementia_progresses/103/the_later_stages _of_dementia/4
15. The Guardian, The raw horror of Alzheimer’s, 2010, https://www.theguardian.com/lifeandstyle/2010/jun/01/andrea-gillies-mother-in-lawalzheimers
16. Alzheimer’s Society, The later stages of dementia, 2017, https://www.alzheimers.org.uk/info/20073/how_dementia_progresses/103/the_later_stages _of_dementia/4
17. Givens, J. et al. Survival and Comfort After Treatment of Pneumonia in Advanced Dementia, Archives of Internal Medicine, 2012, https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2914628/
18. UK Ambulance Services Clinical Practice Guidelines 2016, Association of Ambulance Chief Executives


Tuesday, 26 September 2017

My clinical documentation template


My clinical documentation template
Matt Green @MLG1611, September 2017

[Consider your name, role and time/date; especially if adding to someone else’s paperwork]. This format assumes lots of data has been captured elsewhere on the patient report form.

On arrival: ABC [tick is present, cross if absent]/where the patient is/other important people on scene/any ongoing treatment.

Presenting complaint: 1-2 words and duration

History of presenting complaint: 1-3 short sentences, culminating in trigger for ambulance call/dispatch

On examination:

Central nervous system [As appropriate GCS, capacity assessment, FAST, seizure details, head injury, loss of consciousness, nausea/vomiting etc]

                Respiratory system [Auscultation, cough, sputum, smoking history, pleuritic pain etc]

Cardiovascular system [Central and peripheral perfusion, comments on heart rate/blood pressure, ECG analysis, description of pain and other relevant symptoms, total external blood loss]

Gastrointestinal system [Inspection, auscultation, palpation, percussion, last vomiting, bowels last opened]

                Genitourinary system [Normal/abnormal with description, urine analysis]

                Musculoskeletal system [Injuries, trauma, mobility, spinal assessment]

                Skin [Wounds, pallor/flushed, poor turgor]

                [Optional] Mental health/obstetrics and gynaecology/ear nose and throat/nutrition

[Comment on known important baseline issues as appropriate]

Impression: Working diagnosis [may be very specific or more general where aspects are not yet fully explained]

Plan: History, observations, assessment, treatment given, referrals made

Advice [if discharged]: To keep safe, to rest, to eat and drink well, to see GP for review, to use medications as per label, to call 111 for medical help as required, to call 999 if very concerned or unwell. Left alone/in care of X

Past medical history

Medications

Allergies [name as suggested by patient, and how the allergy presents]

Immunisations [where appropriate]

Social history

[Line and initials to prevent further entries]

For example:

M. Green, Clinical Supervisor, 0845 10/9/17. OA: ABC. Sat on sofa. CFR and family OS. PC: SOB 6/24. HPC: MI 6/52 ago. Recent SOBOE; now SOB at rest today. Family visited; concerned. 999->Amb. sent. OE: CNS: GCS=15/15. Capacity. Nil pain. Pupils=5mm BL. Nausea. RS: RR24. SOB/SOBOE++. Productive cough with frothy sputum. Ex-smoker; 40 pk years. SP02=93%OA. Auscultation: BL coarse crepitations in mid and lower lobes; little change with cough. CV: Warm peripheries. Nil chest pain. HR/BP as recorded. Nil sweating. 12-lead ECG; LBBB; known in patient. BL ankles; new pitting oedema. GIT: Nil vomiting. SNT. Normal bowel sounds. BLO this am. Normal food intake. GUS: Denies complaint. MSS: Mobile, nil reported trauma. Ongoing lower back pain with nil acute change. Skin: Apyrexic. Nil acute change. IMP: Acute heart failure after recent MI. Plan: Hx, obs, assess, oxygen to 94-98% SP02, nebulise 5mg SLB, GTN, IV access, consider furosemide depending on response to other Tx. To ED. R/V on route. PMH: MI 6/52 (2xstent), angina, hypertension, high cholesterol, NIDDM. Medication: Aspirin, clopidogrel, metformin, simvastatin, bisoprolol
Allergies: Penicillin (rash on arms). SH: Lives with partner. Mobile, self caring. Part time work as bookkeeper.----MG

Wednesday, 24 May 2017

Bradycardia management and beta-blocker toxicity


Beta Blocker Bother
Matt Green @MLG1611
May 2017


Mid-way through the Sunday shift, the mobile data terminal alerts you and Paramedic Maureen to a `64 year old male Patient keeps falling and can’t get up`. Whilst calls for fallen patients are common (you’ve already done three that shift), Maureen comments this patient is a little younger than the normal tumbled client and may have an underlying reason they have fallen repeatedly. You’re simply wondering if patient report forms should a copy and paste function.

On arrival, you’re met by the patient’s family who explain `Ian` is visiting for Sunday lunch. They say he has looked pale all day and has fallen several times before struggling to stand again. The last time Ian fell they were very concerned so told him to stay on the floor until an ambulance arrived.

You and Maureen enter the dining room; the only danger is the delicious looking roast dinner displayed on the table; it would be easy to become distracted and tuck in!

Ian is still laid, almost supine, beside his seat at the dinner table propped up by a few pillows.

You completes a primary survey

Airway
Patent and self-maintained
Breathing
Respiratory rate: 18
Oxygen saturations: 97% on air
Chest sounds: clear
No obvious respiratory distress
Circulation
Absent radial pulse
Palpable central pulse
Heart rate: 33
Blood pressure: 77/35
No chest pain
12-lead ECG: sinus bradycardia with 1st degree heart block. Occasional ventricular escape beats with wide QRS complexes but no other changes
Capillary refill time: 5 seconds
Disability
Glasgow Coma Scale: 15/15
FAST negative
Orientated to time, place and person
No pain
Pupils equal and reactive, 5mm bilaterally
Blood glucose = 5.2mmol/l
Exposure/environment
No obvious injuries
Pale complexion
No apparent intoxication with alcohol or illicit drugs
Temperature: 36.40c
Nausea





What are you going to do: Give Ian oxygen or not give oxygen?

Give oxygen: You place Ian on 15lpm oxygen through a non-rebreathing mask. His saturations rapidly climb to 100% but he does not feel better and other observations do not improve. You find it harder to hear Ian over the whooshing noise while hoping not to need a lot of oxygen for hypoxic patients later on in the shift. Maureen quietly comments how studies have shown patients do not benefit, and may even do worse, when oxygen is given unnecessarily.

Not give oxygen: Ian’s saturations maintain at 97% on air, in line with British Thoracic Society guidelines and you and Maureen can concentrate on evidence based interventions to manage his condition.  

Maureen learns that Ian recently saw his GP regarding poorly controlled hypertension and the reading was 182/111, so his bisoprolol was increased from 5mg to 10mg daily. Since then, Ian says he has felt dizzy on exertion but was not very worried about it until today. In addition to high blood pressure, Ian has hyperlipidaemia. He also takes amlodopine, simvastatin and aspirin but not allergic to any medication.

Maureen reviews the situation to form a diagnosis of symptomatic bradycardia, which could be related to recent medication changes. She explains that in an adult, a heart rate under 60 is called bradycardia and can have causes including heart disease and toxicity from prescribed medications. Emergency treatment includes identification and management of the underlying cause, ensuring adequate oxygenation and medications such as atropine. Transcutaneous pacing may also be required.



An intravenous cannula is easily placed and a 600mcg atropine bolus is given. Maureen monitors Ian’s ECG and you see an almost instant increase in his heartrate and a reduction in pallor.

You reassess Ian; his heartrate is now 87, regular and the 12 lead ECG shows a sinus rhythm with no other abnormalities. Supine blood pressure is 110/75 and Ian has no dizziness so able to slowly stand up and sit on a chair. Ian is stable for the rest of contact with the ambulance crew.

You decide to convey Ian to hospital where it is later confirmed his bradycardia and hypotension was a side effect of bisoprolol, so the next dose was withheld and he remained systemically well. After discharge Ian will return to his GP for long-term re-adjustment to his anti-hypertensive medication.

Causes of falls

There are a range of potential causes of falls in adults including1:

·         Cognitive impairment

·         Continence problems

·         A history of falls and associated problems such as fear of falling and associated injuries

·         Unsuitable or missing footwear

·         Health problems that increase the risk of falling

·         Medication

·         Postural instability

·         Mobility problems/balance problems

·         Syncope syndromes

·         Visual impairment

It is important the ambulance clinician carefully assesses the patient and environment to reach a reasoned conclusion to why the fall has taken place and then take steps to reduce the likelihood of it happening again, which may involve routine, urgent or emergency referral to another professional. Understanding the exact circumstances of falling may help identify the mechanism of injury and guide further management.

In this situation, Ian’s falls are possibly related to hypotension caused by recent medication changes so these problems needs to be explored further and corrected. However, differential causes should not be ignored either.

Management of hypertension

High blood pressure, also known as hypertension, is generally defined as a manual or electronic sphygmamonomometer reading greater than 140/90mmHg taken on numerous occasions over an extended period of time2. Persistently high blood pressure puts excess strain on the cardiovascular system, which risks precipitating heart attack or stroke. There are also hypertension links to kidney disease and dementia3.

Excessive blood pressure can be controlled by regular exercise, low fat and unsalted diets and medications such as calcium channel blockers, angiotensin converting enzyme inhibitors and beta blockers4.

Beta-blockers and toxicity

Beta-blockers such as bisoprolol prevent the binding of adrenaline and noradrenaline to beta-adrenoceptors in certain parts of the body. This inhibits some stimulus for the heart to beat, lowering the heart rate and reducing the force of blood flowing through the body5.

Although currently widely used to manage hypertension, there is some controversy regarding beta-blockers’ efficacy and some researchers have argued for a review of their use in this role to evidence continued use6.  

Symptoms of beta-blocker toxicity include hypotension, bradycardia and reduced urine output due to the renal effects of shock. Beta-blockers are contraindicated in a variety of conditions, including severe asthma as their action disrupts natural bronchodilation7.

Bradycardia

In adults, bradycardia is arbitrarily said to be any heart rate below 60 beats per minute8 and may be associated with other arrhythmia such as compensatory ventricular escape beats9. Defining bradycardia in children is variable, depending on their age; the JRCALC Clinical Practice Guidelines’ age-per-page can be used as a rapid guide to identifying abnormal heart rates in paediatrics which may require different management10. 

ECGs have a major role in bradycardia identification and management, however simply feeling a patient’s pulse or listening to heart sounds are also valid methods of discovering abnormally slow heart rates and may be sufficient to initiate emergency treatment.

A high-quality 12-lead ECG has many advantages and can be diagnostic of a wide range of cardiac abnormalities, however bradycardic rhythms can be identified using a 3-lead ECG meaning that monitoring defibrillators and more basic ECG machines have a potential role in bradycardia care. It is still important to record a 12-lead ECG as early as possible and to be repeated at appropriate intervals during patient contact, including before and after any intervention.

Common bradycardic ECG presentations11

Sinus bradycardia is diagnosed in the adult patient where the heart rate is below 60 beats per minute and the ECG shows every QRS complex is preceded by an associated P wave. While often assumed to be abnormal, sinus bradycardia can be normal in athletes at rest.

1st degree heart block is identified on the ECG where a P wave precedes every QRS complex by more than 200ms but the P-R duration does not alter. These are rarely symptomatic in isolation.

2nd degree type 1 heart block occurs where the P-R interval gradually lengthens before a QRS complex. Eventually a QRS complex fails to occur, followed by a short P-R interval again. These heart blocks are rarely symptomatic.

2nd degree type 2 heart block is more serious, involving regular missed QRS complexes despite P wave activity. The P-R interval does not lengthen, but this rhythm suggests substantial atrioventricular node disease and, when present in bradycardia, a risk of asystole which requires urgent treatment.

3rd degree heart block is characterised by disassociation between P and QRS wave activity as both hemispheres of the heart are working independently without electronic link. This suggests severe atrioventricular node disease, which might be so stark atropine is bound to be ineffective yet still indicated. These heart blocks in the context of bradycardia and when the QRS is broad require very urgent treatment.

Atrioventricular junctional escape rhythms are a type of cardiac activity which form a `safety net` when sinoatrial node impulses are absent. Here, P waves are absent, QRS complexes narrow and the heart rate is around 40 beats per minute.

Ventricular escape rhythm are even slower at around 30-35 beats per minute with absent P waves and broad QRS complexes.

When assessing any cardiac rhythm, remember to consider if the patient has a pulse and not in cardiac arrest!

Risk of asystole

The JRCALC 2016 Adult Bradycardia Algorhythm10 promotes the use of atropine in bradycardic patients at risk of asystole such as those with recent asystole, 2nd degree type 2 hearts block, 3rd degree heart block with broad QRS complexes or a ventricular standstill over greater than 3 seconds.

Where there is currently no risk of asystole, the patient should be observed for changes and managed as indicated

Management of bradycardia10

ABCDE approach

Medically unwell patients are best cared for using a structured assessment and management of airway, breathing, circulation, disability and examination. This method may reveal differential causes of Ian’s falls and guide further management using a range of care pathways, for example if Ian was falling due to new-onset leg weakness or hypoglycaemia.

Monitor SP02 and give oxygen if appropriate

Extreme hypoxia can cause bradycardia but remember that cardiac rhythm disturbance falls within the JRCALC `green` criteria for oxygen therapy, so oxygen should be given only if the patient is believed hypoxaemic. Therefore, monitor oxygen saturations and consider giving titrated oxygen to maintain saturations of 94-98%. Excessive oxygenation of people with cardiac rhythm disturbance could be ineffective or even harmful, so may be best avoided.

Gain venous access

All perenteral medications used in standard pre-hospital bradycardia management are suitable for intravenous or intraosseous administration, so establishing access early allows clinicians to rapidly intervene where indicated.

Ensure defibrillator is available

Cardiac rhythm disturbance may quickly degenerate to cardiac arrest where good-quality CPR and appropriate defibrillation have been shown to offer the best chance of successful resuscitation. Therefore, rapid access to a defibrillator is essential in bradycardia management.

Monitor ECG and obtain a 12-lead ECG, before during and after any interventions where possible and ensure copies are passed to the hospital and archived

A detailed ECG helps identify the precise nature of arrhythmia and documents the impact of various treatments. ECGs obtained at intervals throughout pre-hospital patient contact form an essential part of the patient record and can aid in-hospital clinicians’ decisions regarding treatment. For example, evidence a patient was unstable with second degree type 2 heart block in the ambulance may help hospital-based cardiologists decide whether an implanted pacemaker is indicated, even if the heart is in a normal rhythm after pre-hospital treatment.

If the patient is not acutely ill, there may be time to obtain expert advice

In a relatively stable patient, management advice may be sought from another healthcare professional such as a cardiologist either over the phone, or by conveying the patient to the emergency department or cardiac care unit, where local arrangements allow.

Identify adverse features to indicate unstable patients

In patients who are bradycardic, JRCALC’s defined adverse features are:

Shock with a systolic blood pressure less than 90mmHg
Heart rate less than 40 beats per minute
Ventricular arrhythmias compromising blood pressure
Heart failure

Observe

Patients who are bradycardic, with no adverse features and no risk of asystole are suitable for continued observation and transfer to further care. The ambulance clinician would need to be confident in their ability to rapidly identify any deterioration, so ECG and other baseline observations need to be reviewed frequently. 

Atropine

Atropine is a naturally occurring compound found in plants such as deadly nightshade12. It has a long history of use in cardiac arrhythmia, including featuring in Advanced Life Support guidelines for pulseless electrical activity and asystole until removal in 2010 due to lack of evidence to support its routine use during CPR13.

While atropine in cardiac arrest is no longer common practice, it is a safe and effective treatment when given in pulsed bradycardia because it:

·         May reverse vagal overdrive

·         May increase heart rate by blocking vagal activity in sinus bradycardia, second or third degree heart block

·         Enhances atrio-ventricular conduction

Atropine is commonly presented as either a pre-filled syringe or ampule, but different concentrations and volumes are in use so check what your Trust commonly uses to ensure you’re prepared to use it in an emergency situation. Based on JRCALC guidelines atropine is given in 600mcg boluses; smaller doses (less than 100mcg) are said to risk causing iatrogenic bradycardia however research undertaken in elective paediatric anaesthesia settings refutes this14.

Indications for atropine include symptomatic bradycardia with any adverse signs:

·         Absolute bradycardia (where the pulse rate is less than 40 beats per minute)

·         Systolic blood pressure below expected for age

·         Paroxysmal ventricular arrhythmias requiring suppression

·         Inadequate perfusion causing confusion etc

Atropine should not be given to hypothermic patients.

There is mixed evidence of atropine efficacy in patients who have undergone heart transplant with associated nerve destruction, but studies report some success in non-emergency situations15.

Side effects of atropine include dry mouth, visual blurring and pupil dilations. There can also be confusion, occasional hallucinations, tachycardia and urine retention in the elderly.

Myocardial ischemia and infarction

Heart muscle suffering infarction may additionally be bradycardic due to myocardial damage, especially if disrupted coronary perfusion is affecting the sinoatrial or atrioventricular nodes or bundle of His. It then becomes a clinical decision whether to use atropine in an attempt to increase the heart rate, and therefore oxygen demands of the myocardium, or whether to await reperfusion therapy.

JRCALC guidelines suggest that bradycardia in infarction is only treated if it is causing problems with perfusion, such as hypotension.
Transcutaneous pacing

2016’s JRCALC guidelines state that if there is an unsatisfactory response to 600mcg atropine, further boluses may be given to a total of 3mg or transcutaneous pacing may be used.

Pacing should be learnt formally in an appropriate training situation using procedures and equipment approved by an effective clinical governance structure, but the principle involves placing defibrillation-style pads onto the patient’s chest and using regulated electrical current to stimulate cardiac contraction at a designated rate, such as 60 beats per minute. Exact methods vary between pacing devices, but the clinician selects the current required to reliably produce a simultaneous `pacing spikes` and ventricular contraction visualised on the ECG (this is called `capture`), and then configures the required rate. Where the machine detects a spontaneous heart rate falling below the programmes beats per minute threshold, an electrical current is discharged and cardiac contraction should occur16.

One significant difference between implanted pacemakers which are fitted by a cardiologist using wires placed directly into the heart, and transcutaneous pacing used by ambulance clinicians for the emergency management of bradycardia, is that transcutaneous pacing can be very painful due to the unintended stimulation of thoracic skeletal muscle when the current passes through the chest. This has implications for analgesia and sedation which may require additional medical support on scene or in hospital.

Transfer to further care

Symptomatic bradycardia and possible beta-blocker toxicity is best investigated and managed in hospital, via the emergency department or local arrangements with acute cardiology services. It will be a clinical decision whether a pre-alert and a blue light transfer is justified or whether transfer under normal road conditions is more appropriate, based on patient condition, observations, differential diagnosis and response to pre-hospital interventions.

In Ian’s case, as the bradycardia has resolved rapidly after a single dose of atropine and he is now stable with satisfactory observations, a rapid transfer to hospital is probably not beneficial and routine admission via emergency department triage is safe. Constant monitoring and reassessment will help identify deterioration and inform appropriate changes in management required during transfer.

Differences between JRCALC and Resuscitation Council (UK) guidelines17

In 2015’s Resuscitation Council (UK)’s guidelines, adverse features are listed as shock, syncope, myocardial ischemia or heart failure.

Currently outside of paramedics’ ordinary scope of practice, but also advocated by the Resuscitation Council (UK), are medications such as adrenaline infused at 2-10mcg per minute for bradycardia unresponsive to atropine and as an alternative to transcutaneous pacing. Other suggested medications are aminophylline, dopamine, glucagon (in beta-blocker or calcium channel blocker toxicity) and glycopyrrolate.

Slightly smaller 500mcg boluses of atropine are recommended by the Resuscitation Council (UK) but the maximum cumulative dose is 3mg in both sources.

The Resuscitation Council (UK) state the initial management and treatment of bradycardia includes the identification and correction of electrolyte abnormalities, alongside other reversible causes.



Multiple choice questions:

JRCALC guidelines (2016) state that `adverse signs` in bradycardia are:

A: Systolic blood pressure <90 mmHg, ventricular rate <40 bpm, ventricular arrhythmias compromising BP, heart failure

B: Sweating, low blood sugar, oxygen saturations <88% on air, bronchospasm

C: Chest pain, systolic blood pressure <70mmHg, increased urination and active haemorrhage

D: Aching joints, visual disturbance, vomiting and fever

Bisoprolol is a medication classified as a:

            A: Statin

            B: Loop diuretic

            C: Analgesic

            D: Beta-blocker

Atropine can be administered:

            A: Topically and rectally

            B: Intravenously and intraosseously

            C: Orally and sublingually

            D: Intravenously and intranasally

Bradycardia can only be identified on a 12-lead ECG

            A: True because ST segment changes are needed for diagnosis

            B: False; a 3-lead ECG may give enough detail

            C: If the machine provides computerised interpretation

            D: In adults under the age of 70

During myocardial infarction and when the patient is bradycardic, atropine should be given:

            A: Via continuous infusion

            B: In double doses

            C: When there are problems with perfusion

            D: After aspirin but before GTN

Bradycardia can be caused by:

            A: Beta-blocker toxicity

            B: Hypoxia

            C: Excellent cardiovascular health in athletes

            D: All of the above

A 3-lead ECG with an irregular QRS rate of 47 per minute and where the PR interval gets progressively longer before a ventricular contraction is missed is showing:

            A: Normal sinus rhythm

            B: Second degree type 1 heart block and bradycardia

            C: Anterior ST elevated myocardial infarction

            D: Second degree type 2 heard block and bradycardia

Transcutaneous pacing means:

            A: Inserting wires directly into the patient’s myocardium

            B: Permanent surgical implantation of a control device

            C: Giving dopamine to maintain a normal heart rate

D: Using suitable defibrillation-type pads connected to a pacing device set to the appropriate rate and current

Beta-blockers mainly inhibit the actions of:

A: Adrenaline and noradrenaline

B: Insulin and testosterone

C: Cortisol and glomerular filtrate

D: Hormones that are not yet classified

When a patient is being paced, an effective electronic relationship between the pacemaker’s current and ventricular contraction is called:

            A: Termination

            B: Detention

            C: Narrowing

            D: Capture

Answers: A, D, B, B, C, D, B, D, A, D



References:

1.    National Institute for Health and Care Excellence. (2013). Falls in older people: assessing risk and prevention: CG161. https://www.nice.org.uk/Guidance/CG161

2.    NHS Choices. (2014). Getting a blood pressure test. http://www.nhs.uk/Conditions/Blood-pressure-(high)/Pages/Diagnosis.aspx

3.    NHS Choices. (2014). High blood pressure (introduction). http://www.nhs.uk/conditions/blood-pressure-(high)/pages/introduction.aspx

4.    NHS Choices. (2015). Is your blood pressure to high?. http://www.nhs.uk/Livewell/hypertension/Pages/Keepbloodpressurehealthy.aspx

5.    Klabunde, R. (2015). Beta-adrenoceptor Antagonists (Beta-Blockers). http://cvpharmacology.com/cardioinhibitory/beta-blockers

6.    Lindholm, L.H., Carlberg, B. & Samuelsson O. (2005). Should beta blockers remain first choice in the treatment of primary hypertension? A meta-analysis. The Lancet volume 366, number 9496 pages 1545-1553. http://www.ncbi.nlm.nih.gov/pubmed/16257341

7.    Electronic Medicines Compendium. (2013). Bisoprolol Fumarate 10mg Film-coated tablets. http://www.medicines.org.uk/EMC/medicine/24621/SPC/Bisoprolol+Fumarate+10+mg+Film-coated+Tablets/#CONTRAINDICATIONS

8.    American Heart Association. (2016). Bradycardia. http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/Bradycardia-Slow-Heart-Rate_UCM_302016_Article.jsp#.VwY_BmfmrIU

9.    Arrhythmia Alliance. (2010). Bradycardia (Slow Heart Rhythm). http://www.nhs.uk/ipgmedia/national/arrhythmia%20alliance/assets/bradycardia(slowheartrhythm).pdf

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11.  Practical Clinical Skills. (2016). Arrhythmia Reference Guide. http://www.practicalclinicalskills.com/ekg-reference-guide.aspx

12.   Berdai, M.A., Labib, S., Chetouani, K. & Harandou, M. Atropa (2012) Belladonna intoxication: a case report. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3361210/

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14.  Eisa, l., Lerman, J., Raczka, M. & Heard C. (2015). Do small doses of atropine (<0.1mg) cause bradycardia in young children? http://www.medscape.com/medline/abstract/25762533

15.  Kociolek, L.K., Bierig, S.M., Herrmann, S.C. & Labovitz, A.J. (2006). Efficacy of atropine as a chronotropic agent in heart transplant patients undergoing dobutamine stress echocardiography. http://www.ncbi.nlm.nih.gov/pubmed/16686620

16.  Craig, K. (2006). How to provide transcutaneous pacing. Nursing, volume 36, page 22-23. http://journals.lww.com/nursing/Fulltext/2006/04003/How_to_provide_transcutaneous_pacing.7.asp

17.  Resuscitation Council (UK). (2015). Peri-arrest arrhythmias. https://www.resus.org.uk/resuscitation-guidelines/peri-arrest-arrhythmias/#bradycardia

Thursday, 11 May 2017

College of Paramedics' National Conference 2017


The College of Paramedics’ 2017 national conference 
Matt Green, @MLG1611
May 2017

The College of Paramedics’ (@ParamedicsUK) national conference is now an annual fixture and growing rapidly.  From 140 delegates at last year’s event in York, 200 members attended the St Johns Hotel in Solihull, West Midlands on 9th and 10th May 2017.

The conference attracted visitors and speakers from across the UK, in addition to Canadians, Americans, New Zealanders and Norwegians with a passion for pre-hospital care. The main sponsors were Capita (@CapitaPLC), Zoll EMS and Fire (@Zollemsfire), Class Professional (@ClassProfession) and Critical Healthcare (@CriticalHealthC) whose stands explained a range of products appealing to paramedics.

For the first time there was several streams of presentations happening simultaneously; on the first day a Clinical Practice and Education stream were mirrored on day two with a Critical Care and International & Community Paramedicine stream. Delegates were welcome to move between sessions as they wished.

Among the sessions I attended:

Day one

Paramedics into action; using AHPs to transform health, care and wellbeing by Shelagh Morris (@ShelaghDCAHPO)

Interesting working definition of `Advanced Clinical Practice` offered by Shelagh Morris @Auntymelon

Mark Bloch Lecture - `Learn, Develop, Achieve, Inspire` by Paul Gowens (@SASCONSULTPARA)

“If you’re going to leave a legacy, be respected for what you do.” Paul Gowen at the Mark Bloch Lecture. @FloBach

Exploring factors increasing paramedics’ likelihood of administering Analgesia in pre-hospital pain: cross-sectional study by Professor Julia Williams

I’m guilty of often not putting ethnicity data on the patient report form. Julia Williams now showing how this obstructs audit. @MLG1611

The Welsh Ambulance Service experience of changing their clinical model and reducing demand by Greg Lloyd (@HocoWast)

Welsh Amb clinical response model. Great MDT working to manage 999 calls. Paras in police control rooms & in GP practices. @And_Hodge

Paediatric patients: Should we just take them all in? by Will Broughton (@WilBroughton)

To get respiratory rate in a crying child – count the gaps in between the crying. They have to breathe at some point! @LizHarrisMCPara

A service evaluation of a dedicated pre-hospital cardiac arrest response unit in the North East of England by Graham Mclelland (@mcclg)

NEAS cardiac arrest response unit…11% increase on ROSC and 50% increase on survival to discharge. @SimonStanden

Can paramedics perform and evaluate a focused echocardiogram during a simulated 10-second pulse check, after a one-day training course? By Paul Younger (@PaulYounger1)

Really enjoyed your talk, as a student it would be fascinating to learn ultrasound as well @BatleyMiriam

Does current pre-hospital analgesia effectively reduce pain in children caused by trauma, within a UK ambulance service? By Greg Whitley (@GregWhitley7)

Out of 7843 children who reported pain, 51.6% received analgesia @PhilDrummer64

Paramedic Independent Prescribing: What might the future look like for paramedics and patients – A panel discussion by Matt Green, Gerry Egan, Andy Collen and Graham Harris (@MLG1611, @Gerry_Egan, @andycollen)

Discussing paramedic prescribing. 7 years in the making, huge amount of work behind the doors to get this far. Bright future. @PaulElliott_

Day two

Emergent issues of pre-hospital trauma management by paramedics, by Professor Sir Keith Porter (@KeithPorter999)

“If you are a cervical collar manufacturer, perhaps it’s time to seek new employment” @dlbywater

Norwegian guidelines for pre-hospital management of adult trauma patient with potential spinal injury by Per Kristian Hyldmo (@PHyldmo)

Per Kristian Hyldmo, Consultant Anaesthesiologist, favouring lateral trauma position in non intubated unconscious trauma patient @KayHug1

Home or hospital for people with dementia and one or more other multi-morbidities: retrospective data analysis by Kim Kirby (@FrankAndErrol)

HOMEWARD study. Kim Kirby presenting findings that ~50% pt’s with dementia are not conveyed compared to ~60% non-dementia pt’s. @And_Hodge

ICE ICE Baby: Post-ROSC  care on the ICU by David Thom (@DaveParaACCP)

A stay in ICU is physically demanding on patients. @KimToonMCPara

HEMS Dispatch: A systematic review by Georgette Eaton (@Georgette_Eaton)

Getting the right info from the right people makes a difference in HEMS dispatch. @StefCormackStef

Factors associated with clinical outcome in patients undergoing direct transfer to a Heart Attack Centre after return of spontaneous circulation following out-of-hospital cardiac arrest by Tim Edwards

In patients post cardiac arrest with ST elevation, things that favour ROSC:
-Time to ROSC
- Shockable rhythm
-Younger age
@MLG1611

Experience of Attending Traumatic incidents and Post-incident Support by Jo Mildenhall (@Jojo_Research)

Fascinating presentation from Jo Mildenhall inc. compassion fatigue, empathy and coping with traumatic incident exposure. @StefCormackStef

Does the deployment of a leadership trained Ambulance Officer improve CPR Quality during an Out of Hospital Cardiac Arrest by Oliver Zorab @Ozabs

@Ozabs speaking about importance of non-technical skills & leadership training in enhancing management of cardiac arrest. @MrJamesDuncan

Speaking up at scene: Should I? Would I? Could I? by Gordon Ingram (@FirstResponseGB)

Speak up, stand up. @ShumelRahman

Physical and Chemical Restraint by Kirsty Lowery-Richardson and Tim Edwards (@Kirsty_LLR)

In conclusion with ABD chemical restraint is safe so long as robust training, skills maintained and best interest of the patient with robust clinical governance @MedicalAlexWalter

Wow still buzzing from last couple of days at #ParaCon17 Roll on planning for #ParaCon18 #BuildingTheProfession @DarhleneTough

A full list of conference tweets can be found by following the hashtag #ParaCon17