Case 7: Palpitations Flashcards
what are the inner, middle and outer layers of the heart called
inner= endocardium
middle= myocardium
outer= epicardium
function of cardiomyocytes
contract in unison to provide and effective pump action to ensure adequate blood perfusion of the organs and tissues
what cells make up the bulk volume of the heart
cardiomyocytes
what % of the bodies total cell volume is cardiomyocytes
30-40%
which gender have a lower risk of sudden death and AF
female
important Qs when taking history for palpitations
recent viral illness
history of anxiety
weight loss, diarrhoea (thyroid symptoms)
diet (vegetarian?), heavy menstruation, any other bleeding (possibly anaemia)
high tea/coffee/alcohol intake
family history of sudden death
illicit drug use (amphetamines)
smoker
hypertension
are you pregnant (higher output)
anything else- chest pain, sweating, nausea
what to ask about the palpitations specifically
what do you mean by heart beating fast
tap it out
are there beats missing
regular/irregular
is it constant
how long does it last
any precipitating features (on exertion/ at rest)
anything making better/worse
what could be the cause of palpitations
normal physiological response- to pain, temperature, hormone response
sinus tachycardia
excess thyroid hormone can cause arrythmias/sinus tachycardia
what is the process of an action potential (ion channels opening and closing)
voltage gated Na+ open
Na+ inflow depolarises the membrane and triggers opening of more Na+, creates a positive feedback cycle and rapidly rising membrane voltage
Na+ channels close when cell depolarises and voltage peaks at nearly +30mV
Ca2+ entering slow Ca channels prolongs depolarisation of the membrane (creates plateau)- this falls slightly due to K+ leakage (most K+ stay closed until end of plateau)
Ca2+ close and Ca2+ is transported out of cell, K+ opens and rapid K+ outflow returns membrane to its resting potential
the cardiac conduction cycle
the SA node and rest of the conduction system are at rest
SA node initiates AP which sweeps across the atria
after reached AV there is 100 ms delay allowing the atria to complete pumping blood before impulse is transmitted to AV bundle
after delay, impulse travels through AV bundle and bundle branches to purkinje fibres and reaches right papillary muscle via moderator band
impulse spreads to contractile fibres of ventricle
ventricular contraction begins
lead I detects electrical activity from which aspect of the heart
left lateral
lead aVR detects electrical activity from which aspect of the heart
right atrium
lead V6 detects electrical activity from which aspect of the heart
left ventricle
what are the two main classifications of arrhythmias
narrow complex and broad complex tachycardias
red flag symptoms with palpitations
SOB
chest pain
syncope
heart failure
if patient presents with palpitations what are you looking for
HR and rhythm and BP (if signs of haemodynamic instability admit the patient)
check for murmurs suggestive of valvular disease
assess for signs of heart failure (raised JVP, lung crepitations, peripheral oedema)
signs of thyrotoxicosis (as can cause arrhythmia)
anaemia (can result in sinus tachycardia as physiological response to low Hb the heart pumps faster to ensure more O2 reaches organs)
infection and sepsis
signs of thyrotoxicosis
goitre
tremor
exophthalmos
signs of anaemia
pallor of creases
conjuctivae
signs of infection
temperature
flushing
what may be causing a short-lived fast palpitation in someone young
sinus tachycardia due to anxiety/stress
intermittent arrythmia such as SVT
cause of flip flopping palpitations
extra systoles such as supra ventricular or ventricular premature contractions
there is a pause then forceful contraction and the sensation that the heart has stopped results from the pause
cause of rapid fluttering palpitations
sustained supra ventricular arrhythmias
the sudden cessation of this arrhythmia can suggest paroxysmal supra ventricular tachycardia
this is further supported if the patient can stop the palpitations by using Valsalva manoeuvre
what may irregularly irregular palpitations indicate
AF
what may an irregular pounding sensation in the neck suggest
atrioventricular dissociation (atria are contracting against closed tricuspid and mitral valves, therefore producing cannon A waves)
what may palpitations induced by exercise represent
cardiomyopathy
ischemia
channelopathies
excess of what during stress and exercise may cause palpitations
catecholamines
secondary advice to reduce palpitations
smoking cessation
weight reduction
reduced caffeine
anxiety management
what tests would you do on a young patient presenting with short lived intermittent palpitations
FBC- to rule out anaemia
TFTs- even if no symptoms as thyroid disease can present with intermittent palpitations only
pathophysiology of bradycardias
depolarisation fails to initiate or conduct properly
in SA node disease or heart block (AV node, His-bundle)
pathophysiology of tachycardias
abnormal depolarisation occurring in the heart
in enhanced automaticity or reentry
what is seen on ECG with sinus bradycardia
normal upright P wave preceding every QRS with a ventricular rate of less than 60BMP
normal causes of sinus bradycardia
seen in athletes or when asleep
when would you need to consider treatment for sinus bradycardia
if symptomatic- SOB, syncope, fatigue, haemodynamical instability
what may be needed for sinus bradycardia
pacemaker
what is sinus pause
is a bradycardia
SA node fails to generate electrical impulse for what is generally a brief period of time
symptoms of sinus pause
missed/skipped beats
flutters
palpitations
hard beats
presyncope
dizzy/lightheaded
syncope
pathophysiology of sinus pause
if the heart misses a beat blood does not flow during that time period resulting in a lack of O2 perfusion throughout body
treatment for sinus pause
may involve medication
possible temporary/permanent pacemaker
what us sinoatrial exit block (heart block)
the depolarisations that occur in the sinus node cannot leave the node towards the atria- they are blocked
what is seen on ECG with sinoatrial exit block (heart block)
seen as a pause
SA exit block can be distinguished from sinus arrest because the pause in SA exit block is a multiple of the P-P interval that preceded the pause
types of heart block
1st degree
2nd degree (wenckeback or mobitz type I)
2nd degree (mobitz type II)
3rd degree
what is automaticity in terms of tachycardias
an area of myocardial cells depolarise faster than the SA node
may be atrial or ventricular tissue
most occur at a single focal site
what is reentry in terms of tachycardias
an electrical pathway which is not supposed to be there connecting two areas which should not be connected
these connections can be congenital or because of heart disease
if this connection exists it can form an electrical circuit
what is a supraventicular tachycardia (SVT)
heart condition where the heart suddenly beats much faster than normal
this originates from faulty electrical impulses in upper part of the heart (atria/nodes) rather than from the ventricles
what is a venticular tachycardia (VT)
sequence of 3 or more ventricular beats
frequency must be higher than 100BMP (mostly 110-250BMP)
types of SVT
AF
atrial flutter
AVNRT
AVRT
atrial tachycardia
types of VT
ventricular tachycardia
ventricular fibrillation
wolff Parkinson white syndrome is a form of which SVT
AVNRT
pathophysiology of Wolff Parkinson white
SVT which uses an AV accessory tract
this accessory pathway may also allow conduction during other supra ventricular arrhythmias such as AF or flutter
how are the types of Wolff Parkinson white classified
based off ecg findings
what is type A Wolff Parkinson white
delta wave and QRS predominantly upright in precordial leads
dominant R wave in lead V1 may be misinterpreted as right bundle branch block
what is type B Wolff Parkinson white
delta wave and QRS complex predominantly negative in leads V1 and V2 and positive in other precordial leads, resembling left bundle branch block
how common is Wolff Parkinson white
found in 1-3 people per 1000
found in all ages but most common in young previously healthy people
what complication has Wolff Parkinson white been linked to
sudden cardiac death in children and young adults
how can vagal manoeuvres help with tachycardias
vagal manœuvres make your vagus nerve act on the hearts natural pacemaker slowing down its electrical impulses
the vagus nerve (goes from brainstem to abdomen) plays major role in parasympathetic nervous system which controls a number of things including HR
diagnostic uses of vagal manoeuvres
valsalva can be used to distinguish between ventricular tachycardia and suparventricular tachycardias by slowing the rate of conduction at SA or AV nodes
carotid sinus massage are used to diagnose carotid sinus hypersensitivity
therapeutic uses of vagal manoeuvres
they are first line treatment of haemodynamically stable supraventricular tachycardia (slows down arrhythmia)
they have reported a success rate of conversion to sinus rhythm for SVT around 20-40% possibly higher for AVNRT (an SVT associated with a bypass tract)
examples of vagal manoeuvres
valsalva- lying on back take deep breath and act like you’re exhaling but with nose and mouth closed for 10-30 seconds- should feel like you’re trying to breath out air into a blocked straw
diving reflex- while sitting take several deep breaths, hold breath then quickly but whole face into a container of ice water, keep face submerged as long as you can
carotid sinus massage- lie on back with head turned to one side, doctor will use fingers to push down on your carotid sinus for 5-10secs
gag reflex
cough
handstand for 30 seconds
applied abdominal pressure- lie on back and fold lower body toward face until feet are past head, take breath and strain for 20-30 secs
what would mean patient is unstable and not suitable for vagal manoeuvres
low BP
chest pain
SOB
hypoxia
poor perfusion to organs
what are the DVLA rules regarding arrhythmias
group 1- must stop driving if arrhythmia has caused or is likely to cause incapacity, driving may be permitted if underlying cause has been identified and has been controlled for at least 4 weeks
group 2- disqualifies from driving if arrhythmia has caused or is likely to cause incapacity, DVLA must be informed
are atrial ectopic beats worrying
no they are normal findings and do not require treatment
what are one of the most common causes of palpitations
atrial (supraventricular) or ventricular ectopics
what are atrial (supraventricular) or ventricular ectopics usually described as
skipped/missed beats
the often occur in clusters (hour of frequent ectopics occurring once a month)
what may women describe a link with their atrial (supraventricular) or ventricular ectopics with
their menstrual cycle
are ventricular ectopics worrying
no can be a normal finding
usually associated with good long-term prognosis in patients with structurally normal hearts
in those with structural heart disease they should be evaluated more carefully (can give rise to LV dysfunction- tachycardiomyopathy/ tachycardia induced cardiomyopathy)
what can be used to treat sinus tachycardia induced by stress/anxiety
propanolol
what is seen on ECG with AF
absent/ abnormal P waves
irregularly irregular QRS complexes (R interval)
ventricular rate is usually fast
how to calculate ventricular rate on an ECG with AF
count number of QRS complexes on the rhythm strip and multiply by 6
what is heart rate like in AF with rapid ventricular response
over 180 BMP
what do you need to assess for before administering IV fluids
signs of heart failure
why might you do a FBC
look for raised WCC (infection)
why might you do Us and Es
check for dehydration
why might you do LFTs
baseline is required before administering medication
why might you do troponin
due to ischaemic changes on ECG
to exclude cardiac event
however, troponin is often raised with AF and rapid ventricular response
why might you do CRP
marker of inflammation and infection if raised
why might you do MSU (mid stream urine)
look for infection
why might you do chest X-Ray
to exclude pneumonia
why might you do blood culture
if patient has temperature (infection)
why might you do and ABG
if patient is hypoxia/hypercapnic
can get lactate as well to assess for sepsis
if palpitations last seconds what may it be
ectopy
if palpitations last minutes-hours what may it be
SVT
AF
atrial flutter
VT
if palpitations come on suddenly what may it be
SVT
paroxysmal AF
if palpitations come on gradually what may it be
sinus tachycardia
atrial tachycardia
what can palpitations result in
cardiac arrest
increased risk of sudden death
heart failure
haemodynamic instability resulting in dizziness/syncope
hospitalisation
how many patients have been diagnosed with AF in the UK
1.5 million
what is the most common sustained arrhythmia
AF
AF is most common at what age
1 in 3 have it over 65
what is the atrial beat like in AF
over 300 BMP
pathophysiology of AF
here is disorganised electrical activity within the atria
gives rise to abnormal/absent P waves (sometimes called fibrillation waves)
AV node is usually unable to conduct as such rapid rates so there is consequently a degree of AV block
ventricular conduction is random and hence gives rise to irregularity of ventricular beats (causes irregular RR interval)
what is a major trigger for AF
pulmonary vein ectopy (enters the left atrium and triggers AF)
is AF or ventricular tachycardia more likely to result in cardiac arrest
ventricular tachycardia
there is an increased risk of death by what in AF
stroke (five fold increase and usually more severe and disabling)
heart failure (reduced LV systolic function)
what two conditions can cause each other
AF can cause heart failure
heart failure can cause AF
what tool should be used for stroke prevention with AF
CHA2DS2VASc score
how is the CHA2DS2VASc score used to treat patients with AF
if high stroke risk offered anticoagulation (DOACs 1st line)
need to assess bleeding risk
what tool is used to assess bleeding risk
HASBLED score
(3 or more is high risk and requires close monitoring)
which DOAC is licensed for patients with chronic kidney disease
apixaban
what therapies may be used for symptom control in AF
for rate control beta blockers
to maintain sinus rhythm amiodarone/flecainide
catheter ablation to maintain sinus rhythm (pulmonary vein isolation ablation)
permeant pacemaker to allow use of medications +/- an AV node ablation (pace and ablate)
what risk factors/co morbidities may increase AF risk
overweight
alcohol excess
hypertension
diabetets
sleep apnoea
heart failure
what timeframe is non sustained AF
< 30 seconds
what timeframe is long standing persistent AF
> 1 year
what timeframe is paroxysmal AF
between 30 seconds - 1 week
common causes for sustained palpitations
AF
sinus tachycardia
SVT
less common causes for sustained palpitations
ventricular tachycardia
common causes for non-sustained palpitations
atrial ectopic
less common causes for non-sustained palpitations
ventricular ectopic
what may be the underlying cause to sinus tachycardia
pain
exercise
anaemia
anaemia
thyrotoxicosis
pheochromocytoma
anxiety
what is torsades de pointes
ventricular tachycardia characterised by sinusoidal waveforms on ECG
can progress to ventricular fibrillation
rare but potentially life threatening
what beta blocker is used fo AF commonly
bisoprosol 2.5mg OD
what are some reversible causes of AF
lower respiratory tract infection
hyperthyroidism
excess alcohol
heart failure/cardiomyopathy
ischaemic heart disease
PE
hypokalaemia
what other test can help assess bleeding risk in patients with AF
ORBIT score
what findings fit with a diagnosis of pneumonia
raised urea
raised WCC
raised CRP
raised lactate
consolidation on X-Ray
warfarin mechanism and dose
vitamin K antagonist
variable INR (target 2.5, range 2-3)
apixaban mechanism and dose
factor Xa inhibitor
5mg twice daily (reduced to 2.5mg twice daily)
dabigatran mechanism and dose
direct thrombin inhibitor
150mg twice daily (reduced to 110mg twice daily)
edoxaban mechanism and dose
factor Xa inhibitor
60mg once daily (reduced to 30mg once daily)
rivaroxaban mechanism and dose
factor Xa inhibitor
20mg once daily (reduced to 15mg once daily)
who would be offered warfarin instead of DOACs
patients with mechanical heart valves or moderate-severe rheumatic mitral stenosis
what is the significance of a dilated left atrium
it is common in patients with hypertension
indicates left atrial stretch due to high intra cardiac pressures
may predispose to AF and other atrial arrhythmias
what is first line for rate control in AF
beta blockers (bisoprolol)
use with caution in patients with acute heart failure or elderly due to risk of hypotension
what is second line for rate control in AF
calcium channel blockers (diltiazem/verapamil)
avoid in patients with left ventricular systolic dysfunction as has negative inotropic effect
why do you avoid using bisoprolol and rate limiting calcium channel blockers together
high risk of AV block
what is the most common drug used for rhythm control in AF
flecainide
avoid in patients with coronary artery disease and structural heart disease
beta blocker or calcium channel blocker should be taken at the time to reduce risk of atrial flutter
