This blog post was written by Matt Green, a paramedic for an NHS Trust. Follow him on Twitter @MLG1611
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:
National Institute for Health and Care Excellence. (2013). Falls in older people: assessing risk and prevention: CG161. https://www.nice.org.uk/Guidance/CG161
NHS Choices. (2014). Getting a blood pressure test. http://www.nhs.uk/Conditions/Blood-pressure-(high)/Pages/Diagnosis.aspx
NHS Choices. (2014). High blood pressure (introduction). http://www.nhs.uk/conditions/blood-pressure-(high)/pages/introduction.aspx
NHS Choices. (2015). Is your blood pressure to high?. http://www.nhs.uk/Livewell/hypertension/Pages/Keepbloodpressurehealthy.aspx
Klabunde, R. (2015). Beta-adrenoceptor Antagonists (Beta-Blockers). http://cvpharmacology.com/cardioinhibitory/beta-blockers
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
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American Heart Association. (2016). Bradycardia. http://www.heart.org/HEARTORG/Conditions/Arrhythmia/AboutArrhythmia/Bradycardia-Slow-Heart-Rate_UCM_302016_Article.jsp#.VwY_BmfmrIU
Arrhythmia Alliance. (2010). Bradycardia (Slow Heart Rhythm). http://www.nhs.uk/ipgmedia/national/arrhythmia%20alliance/assets/bradycardia(slowheartrhythm).pdf
Joint Royal Collages Ambulance Liaison Committee (JRCALC). (2016). UK Ambulance Services Clinical Practice Guidelines.
Practical Clinical Skills. (2016). Arrhythmia Reference Guide. http://www.practicalclinicalskills.com/ekg-reference-guide.aspx
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/
Resuscitation Council (UK). (2010). Resuscitation Guidelines. https://www.resus.org.uk/EasysiteWeb/getresource.axd?AssetID=814&type=Full&servicetype=Attachment
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
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
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
Resuscitation Council (UK). (2015). Peri-arrest arrhythmias. https://www.resus.org.uk/resuscitation-guidelines/peri-arrest-arrhythmias/#bradycardia