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:
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
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
10. Joint Royal Collages Ambulance Liaison
Committee (JRCALC). (2016). UK Ambulance Services Clinical Practice Guidelines.
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
17. Resuscitation Council (UK). (2015).
Peri-arrest arrhythmias. https://www.resus.org.uk/resuscitation-guidelines/peri-arrest-arrhythmias/#bradycardia
