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Semester 1 ( 3rd Year) > Case 7: Palpitations > Flashcards

Case 7: Palpitations Flashcards

1
Q

what are the inner, middle and outer layers of the heart called

A

inner= endocardium
middle= myocardium
outer= epicardium

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2
Q

function of cardiomyocytes

A

contract in unison to provide and effective pump action to ensure adequate blood perfusion of the organs and tissues

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3
Q

what cells make up the bulk volume of the heart

A

cardiomyocytes

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4
Q

what % of the bodies total cell volume is cardiomyocytes

A

30-40%

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5
Q

which gender have a lower risk of sudden death and AF

A

female

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6
Q

important Qs when taking history for palpitations

A

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

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7
Q

what to ask about the palpitations specifically

A

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

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8
Q

what could be the cause of palpitations

A

normal physiological response- to pain, temperature, hormone response

sinus tachycardia

excess thyroid hormone can cause arrythmias/sinus tachycardia

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9
Q

what is the process of an action potential (ion channels opening and closing)

A

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

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10
Q

the cardiac conduction cycle

A

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

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11
Q

lead I detects electrical activity from which aspect of the heart

A

left lateral

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12
Q

lead aVR detects electrical activity from which aspect of the heart

A

right atrium

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13
Q

lead V6 detects electrical activity from which aspect of the heart

A

left ventricle

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14
Q

what are the two main classifications of arrhythmias

A

narrow complex and broad complex tachycardias

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15
Q

red flag symptoms with palpitations

A

SOB
chest pain
syncope
heart failure

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16
Q

if patient presents with palpitations what are you looking for

A

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

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17
Q

signs of thyrotoxicosis

A

goitre
tremor
exophthalmos

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18
Q

signs of anaemia

A

pallor of creases
conjuctivae

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19
Q

signs of infection

A

temperature
flushing

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20
Q

what may be causing a short-lived fast palpitation in someone young

A

sinus tachycardia due to anxiety/stress

intermittent arrythmia such as SVT

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21
Q

cause of flip flopping palpitations

A

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

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22
Q

cause of rapid fluttering palpitations

A

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

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23
Q

what may irregularly irregular palpitations indicate

A

AF

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24
Q

what may an irregular pounding sensation in the neck suggest

A

atrioventricular dissociation (atria are contracting against closed tricuspid and mitral valves, therefore producing cannon A waves)

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25
Q

what may palpitations induced by exercise represent

A

cardiomyopathy
ischemia
channelopathies

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26
Q

excess of what during stress and exercise may cause palpitations

A

catecholamines

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27
Q

secondary advice to reduce palpitations

A

smoking cessation
weight reduction
reduced caffeine
anxiety management

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28
Q

what tests would you do on a young patient presenting with short lived intermittent palpitations

A

FBC- to rule out anaemia
TFTs- even if no symptoms as thyroid disease can present with intermittent palpitations only

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29
Q

pathophysiology of bradycardias

A

depolarisation fails to initiate or conduct properly
in SA node disease or heart block (AV node, His-bundle)

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30
Q

pathophysiology of tachycardias

A

abnormal depolarisation occurring in the heart
in enhanced automaticity or reentry

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31
Q

what is seen on ECG with sinus bradycardia

A

normal upright P wave preceding every QRS with a ventricular rate of less than 60BMP

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32
Q

normal causes of sinus bradycardia

A

seen in athletes or when asleep

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33
Q

when would you need to consider treatment for sinus bradycardia

A

if symptomatic- SOB, syncope, fatigue, haemodynamical instability

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34
Q

what may be needed for sinus bradycardia

A

pacemaker

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35
Q

what is sinus pause

A

is a bradycardia
SA node fails to generate electrical impulse for what is generally a brief period of time

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36
Q

symptoms of sinus pause

A

missed/skipped beats
flutters
palpitations
hard beats
presyncope
dizzy/lightheaded
syncope

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37
Q

pathophysiology of sinus pause

A

if the heart misses a beat blood does not flow during that time period resulting in a lack of O2 perfusion throughout body

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38
Q

treatment for sinus pause

A

may involve medication
possible temporary/permanent pacemaker

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39
Q

what us sinoatrial exit block (heart block)

A

the depolarisations that occur in the sinus node cannot leave the node towards the atria- they are blocked

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40
Q

what is seen on ECG with sinoatrial exit block (heart block)

A

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

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41
Q

types of heart block

A

1st degree
2nd degree (wenckeback or mobitz type I)
2nd degree (mobitz type II)
3rd degree

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42
Q

what is automaticity in terms of tachycardias

A

an area of myocardial cells depolarise faster than the SA node
may be atrial or ventricular tissue
most occur at a single focal site

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43
Q

what is reentry in terms of tachycardias

A

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

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44
Q

what is a supraventicular tachycardia (SVT)

A

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

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45
Q

what is a venticular tachycardia (VT)

A

sequence of 3 or more ventricular beats
frequency must be higher than 100BMP (mostly 110-250BMP)

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46
Q

types of SVT

A

AF
atrial flutter
AVNRT
AVRT
atrial tachycardia

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47
Q

types of VT

A

ventricular tachycardia
ventricular fibrillation

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48
Q

wolff Parkinson white syndrome is a form of which SVT

A

AVNRT

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49
Q

pathophysiology of Wolff Parkinson white

A

SVT which uses an AV accessory tract
this accessory pathway may also allow conduction during other supra ventricular arrhythmias such as AF or flutter

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50
Q

how are the types of Wolff Parkinson white classified

A

based off ecg findings

51
Q

what is type A Wolff Parkinson white

A

delta wave and QRS predominantly upright in precordial leads
dominant R wave in lead V1 may be misinterpreted as right bundle branch block

52
Q

what is type B Wolff Parkinson white

A

delta wave and QRS complex predominantly negative in leads V1 and V2 and positive in other precordial leads, resembling left bundle branch block

53
Q

how common is Wolff Parkinson white

A

found in 1-3 people per 1000
found in all ages but most common in young previously healthy people

54
Q

what complication has Wolff Parkinson white been linked to

A

sudden cardiac death in children and young adults

55
Q

how can vagal manoeuvres help with tachycardias

A

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

56
Q

diagnostic uses of vagal manoeuvres

A

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

57
Q

therapeutic uses of vagal manoeuvres

A

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)

58
Q

examples of vagal manoeuvres

A

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

59
Q

what would mean patient is unstable and not suitable for vagal manoeuvres

A

low BP
chest pain
SOB
hypoxia
poor perfusion to organs

60
Q

what are the DVLA rules regarding arrhythmias

A

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

61
Q

are atrial ectopic beats worrying

A

no they are normal findings and do not require treatment

62
Q

what are one of the most common causes of palpitations

A

atrial (supraventricular) or ventricular ectopics

63
Q

what are atrial (supraventricular) or ventricular ectopics usually described as

A

skipped/missed beats
the often occur in clusters (hour of frequent ectopics occurring once a month)

64
Q

what may women describe a link with their atrial (supraventricular) or ventricular ectopics with

A

their menstrual cycle

65
Q

are ventricular ectopics worrying

A

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)

66
Q

what can be used to treat sinus tachycardia induced by stress/anxiety

A

propanolol

67
Q

what is seen on ECG with AF

A

absent/ abnormal P waves
irregularly irregular QRS complexes (R interval)
ventricular rate is usually fast

68
Q

how to calculate ventricular rate on an ECG with AF

A

count number of QRS complexes on the rhythm strip and multiply by 6

69
Q

what is heart rate like in AF with rapid ventricular response

A

over 180 BMP

70
Q

what do you need to assess for before administering IV fluids

A

signs of heart failure

71
Q

why might you do a FBC

A

look for raised WCC (infection)

72
Q

why might you do Us and Es

A

check for dehydration

73
Q

why might you do LFTs

A

baseline is required before administering medication

74
Q

why might you do troponin

A

due to ischaemic changes on ECG
to exclude cardiac event
however, troponin is often raised with AF and rapid ventricular response

75
Q

why might you do CRP

A

marker of inflammation and infection if raised

76
Q

why might you do MSU (mid stream urine)

A

look for infection

77
Q

why might you do chest X-Ray

A

to exclude pneumonia

78
Q

why might you do blood culture

A

if patient has temperature (infection)

79
Q

why might you do and ABG

A

if patient is hypoxia/hypercapnic
can get lactate as well to assess for sepsis

80
Q

if palpitations last seconds what may it be

A

ectopy

81
Q

if palpitations last minutes-hours what may it be

A

SVT
AF
atrial flutter
VT

82
Q

if palpitations come on suddenly what may it be

A

SVT
paroxysmal AF

83
Q

if palpitations come on gradually what may it be

A

sinus tachycardia
atrial tachycardia

84
Q

what can palpitations result in

A

cardiac arrest
increased risk of sudden death
heart failure
haemodynamic instability resulting in dizziness/syncope
hospitalisation

85
Q

how many patients have been diagnosed with AF in the UK

A

1.5 million

86
Q

what is the most common sustained arrhythmia

A

AF

87
Q

AF is most common at what age

A

1 in 3 have it over 65

88
Q

what is the atrial beat like in AF

A

over 300 BMP

89
Q

pathophysiology of AF

A

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)

90
Q

what is a major trigger for AF

A

pulmonary vein ectopy (enters the left atrium and triggers AF)

91
Q

is AF or ventricular tachycardia more likely to result in cardiac arrest

A

ventricular tachycardia

92
Q

there is an increased risk of death by what in AF

A

stroke (five fold increase and usually more severe and disabling)
heart failure (reduced LV systolic function)

93
Q

what two conditions can cause each other

A

AF can cause heart failure
heart failure can cause AF

94
Q

what tool should be used for stroke prevention with AF

A

CHA2DS2VASc score

95
Q

how is the CHA2DS2VASc score used to treat patients with AF

A

if high stroke risk offered anticoagulation (DOACs 1st line)
need to assess bleeding risk

96
Q

what tool is used to assess bleeding risk

A

HASBLED score
(3 or more is high risk and requires close monitoring)

97
Q

which DOAC is licensed for patients with chronic kidney disease

A

apixaban

98
Q

what therapies may be used for symptom control in AF

A

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)

99
Q

what risk factors/co morbidities may increase AF risk

A

overweight
alcohol excess
hypertension
diabetets
sleep apnoea
heart failure

100
Q

what timeframe is non sustained AF

A

< 30 seconds

101
Q

what timeframe is long standing persistent AF

A

> 1 year

102
Q

what timeframe is paroxysmal AF

A

between 30 seconds - 1 week

103
Q

common causes for sustained palpitations

A

AF
sinus tachycardia
SVT

104
Q

less common causes for sustained palpitations

A

ventricular tachycardia

105
Q

common causes for non-sustained palpitations

A

atrial ectopic

106
Q

less common causes for non-sustained palpitations

A

ventricular ectopic

107
Q

what may be the underlying cause to sinus tachycardia

A

pain
exercise
anaemia
anaemia
thyrotoxicosis
pheochromocytoma
anxiety

108
Q

what is torsades de pointes

A

ventricular tachycardia characterised by sinusoidal waveforms on ECG
can progress to ventricular fibrillation
rare but potentially life threatening

109
Q

what beta blocker is used fo AF commonly

A

bisoprosol 2.5mg OD

110
Q

what are some reversible causes of AF

A

lower respiratory tract infection
hyperthyroidism
excess alcohol
heart failure/cardiomyopathy
ischaemic heart disease
PE
hypokalaemia

111
Q

what other test can help assess bleeding risk in patients with AF

A

ORBIT score

112
Q

what findings fit with a diagnosis of pneumonia

A

raised urea
raised WCC
raised CRP
raised lactate
consolidation on X-Ray

113
Q

warfarin mechanism and dose

A

vitamin K antagonist
variable INR (target 2.5, range 2-3)

114
Q

apixaban mechanism and dose

A

factor Xa inhibitor
5mg twice daily (reduced to 2.5mg twice daily)

115
Q

dabigatran mechanism and dose

A

direct thrombin inhibitor
150mg twice daily (reduced to 110mg twice daily)

116
Q

edoxaban mechanism and dose

A

factor Xa inhibitor
60mg once daily (reduced to 30mg once daily)

117
Q

rivaroxaban mechanism and dose

A

factor Xa inhibitor
20mg once daily (reduced to 15mg once daily)

118
Q

who would be offered warfarin instead of DOACs

A

patients with mechanical heart valves or moderate-severe rheumatic mitral stenosis

119
Q

what is the significance of a dilated left atrium

A

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

120
Q

what is first line for rate control in AF

A

beta blockers (bisoprolol)
use with caution in patients with acute heart failure or elderly due to risk of hypotension

121
Q

what is second line for rate control in AF

A

calcium channel blockers (diltiazem/verapamil)
avoid in patients with left ventricular systolic dysfunction as has negative inotropic effect

122
Q

why do you avoid using bisoprolol and rate limiting calcium channel blockers together

A

high risk of AV block

123
Q

what is the most common drug used for rhythm control in AF

A

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

Semester 1 ( 3rd Year) (12 decks)

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