Week Seven - Case One Flashcards
1
Q
what are arrhythmias
A
abnormal heart rhythms
2
Q
what are the shockable cardiac arrest rhythms
A
ventricular tachycardia
ventricular fibrillation
3
Q
what are the non shockable cardiac arrest rhythms
A
pulseless electrical activity (all electrical activity except VF/VT, including sinus rhythm without a pulse)
asystole (no significant electrical activity)
4
Q
what does narrow complex tachycardia refer to
A
a fast heart rate with a QRS complex duration of less than 0.12 seconds
5
Q
on a normal 25mm/sec ECG, 0.12 seconds equals how many small squares?
A
3 small squares
therefore the QRS complex will fit within 3 small squares in narrow complex tachycardia
6
Q
what are the four main differentials of a narrow complex tachycardia
A
Sinus tachycardia (treatment focuses on the underlying cause)
Supraventricular tachycardia (treated with vagal manoeuvres and adenosine)
Atrial fibrillation (treated with rate control or rhythm control)
Atrial flutter (treated with rate control or rhythm control, similar to atrial fibrillation)
7
Q
what are patients with syncope, heart muscle ischaemia (chest pain), shock or severe heart failure treated with
A
synchronised DC cardioversion under sedation or general anaesthesia
8
Q
what is added if initial DC shocks are unsuccessful
A
intravenous amiodarone
9
Q
what does broad complex tachycardia refer to
A
a fast heart rate with a QRS. complex duration of more than 0.12 seconds or 3 small squares on a ECG
10
Q
what are the broad complex tachycardias
A
Ventricular tachycardia or unclear cause (treated with IV amiodarone)
Polymorphic ventricular tachycardia, such as torsades de pointes (treated with IV magnesium)
Atrial fibrillation with bundle branch block (treated as AF)
Supraventricular tachycardia with bundle branch block (treated as SVT)
11
Q
what is atrial fuller caused by
A
a re-entrant rhythm in either atrium
12
Q
how does the electrical signal re-circulate in atrial flutter
A
in a self-perpetuating loop due to an extra electrical pathway in the atriaw
13
Q
what is the usual atrial rate in atrial flutter
A
300 beats per minute
14
Q
why does the signal not usually enter the ventricles on every lap
A
due to the long refractory period of the AV node
15
Q
what does this result In, in terms of ratio of atrial and ventricular contractions
A
this often results in two atrial contractions for every one ventricular contraction (2:1 conduction), giving a ventricular rate of 150 beats per minute
there may be a 3:1 or a 4:1 variable conduction ratio
16
Q
what is the appearance of atrial flutter on an ECG
A
sawtooth appearance on the ECG with repeated P wave occurring at around 300 per minute, with a narrow complex tachycardia
17
Q
what is the treatment for atrial flutter
A
similar to AF, including anticoagulation based on the CHA2DS2-VASc score
radiofrequency ablation of the re-entrant rhythm can be a permanent solution
18
Q
what is the QT interval
A
from the start of the QRS complex to the end of the. T wave
19
Q
what does the QTc estimate the QT internal is if the heart rate was 60BPM
A
prolonged at:
More than 440 milliseconds in men
More than 460 milliseconds in women
20
Q
what does a prolonged QT interval represent
A
represented prolonged repolarisation of the heart muscle cells (myocytes) after a contraction
21
Q
what is depolarisation
A
the electrical process that leads to heart contraction
22
Q
what is repolarisation
A
is a recovery period before the muscle cells are ready to depolarise again
23
Q
what can waiting a long time for repolarisation result in
A
spontaneous depolarisation in some muscle cells
24
Q
what are these abnormal spontaneous depolarisations before repolarisation known as
A
afterdepolarisations
25
what do these afterdepolarisations do
spread throughout the ventricles, causing a contraction before proper repolarisation.
26
when this leads to recurrent contractions without normal repolarisation, what is this called
torsades de pointes
27
what is tornadoes de pointes a type of
polymorphic ventricular tachycardia
28
what does torsades de pointes look like on an ECG
it looks like standard ventricular tachycardia but with the appearance that the QRS complex is twisting around the baseline. the height of the QRS complex gets progressively smaller, then larger, then smaller and so on
29
how does torsades de pointes terminate and what does the lead to
terminates spontaneously and will revert to sinus rhythm or progress to ventricular tachycardia
30
what can this ventricular tachycardia lead to
cardiac arrest
31
what are the causes of prolonged QT
Long QT syndrome (an inherited condition)
Medications,
Electrolyte imbalances, such as hypokalaemia, hypomagnesaemia and hypocalcaemia
32
what medications can cause a prolonged QT
such as antipsychotics, citalopram, flecainide, sotalol, amiodarone and macrolide antibiotics
33
what is the management of a prolonged QT internal include
stopping and avoiding medications that prolong the QT interval
correcting electrolyte disturbances
beta blockers
pacemakers or implantable cardioverter defibrillations
34
what beta blocker is not used in the management of a prolonged QT internal
sotalol
35
what is the acute management of torsades de pointes
correcting the underlying cause
magnesium infusion (even if they have a normal serum magnesium)
defibrillation if ventricular tachycardia occurs
36
what are ventricular ecoptics
premature ventricular beats caused by random electrical discharges outside the atria
37
how do ventricular ectopics appear on an ECG
as isolated, random, abnormal, broad QRS complexes on an otherwise normal ECG
38
what does bigeminy refer to
when every other beat is a ventricular ectopic.
39
what would the ECG show in bigeminy
a normal beat, followed immediately by an ectopic beat, then a normal beat, then an ectopic and so on
40
what is the management of bigeminy
Reassurance and no treatment in otherwise healthy people with infrequent ectopics
Seeking specialist advice in patients with underlying heart disease, frequent or concerning symptoms (e.g., chest pain or syncope), or a family history of heart disease or sudden death
41
what medication is sometimes used to manage symptoms of bigeminy
beta blockers
42
when does first degree heart block occur
where there is delayed conduction through the AV node.
43
what does first degree heart block look like on an ECG
despite the delated conduction, every atrial impulse leads to a ventricular contraction, meaning every P wave is followed by a QRS complex.
on an ECG , first degree heart block present as a PR interval greater than 0.2 seconds
44
what is second degree heart block
is where some atrial impulses do not make it through the AV node to the ventricles
45
what else are there instances of in second degree heart block
where P waves are not followed by QRS complexes.
46
what are the two types of second degree heart block
Mobitz type 1 (Wenckebach phenomenon)
Morbitz type 2
47
what is Mobitz type One
when the conduction through the AV node takes progressively longer until it finally fails, after which it resets and the cycle restarts
48
what is shown on an ECG in Mobitz type One
there is an increasing PR interval until a P wave is not followed by a QRS complex.
the PR interval then returns to normal, and the cycle repeats itself
49
what is Mobitz type 2
where there is intermittent failure of conduction through the AV node, with an absence of QRS complexes following P was vested
50
usually, what is there with Mobitz type two
usually a set ratio of P waves to QRS complexes
for example, three P waves for each QRS complex
the PR interval remains normal
51
what is there a risk of in Mobitz type two
asystole
52
what is a 2:1 block
is where there are two P waves for each QRS complex
every other P wave does not stimulate. a QRS complex.
53
what is third degree heart block also called
complete heart block
54
what sort of relationship between the P waves and QRS complexes is seen in third degree heart block
no observable relationship
55
what is there a significant risk of in third degree heart block
significant risk of asystole
56
what does bradycardia refer to
a slow heart rate, typically less than 60 beats per minute
57
what are the three main causes of bradycardia
medications
heart block
sick sinus syndrome
58
what medications can cause bradycardia
beta blockers
59
what does sick sinus syndrome encompass
many conditions that cause dysfunction in the SA node
60
what is sick sinus syndrome often caused by
idiopathic degenerative fibrosis of the SA node
61
what can sick sinus syndrome result in
sinus bradycardia, sinus arrhythmias, and prolonged pauses
62
what does asystole refer to
the absence of electrical activity in the heart - resulting in cardiac arrest
63
there is a risk of asystole in what conditions
Mobitz type 2
Third-degree heart block (complete heart block)
Previous asystole
Ventricular pauses longer than 3 seconds
64
what is the management of unstable patients and those at risk of asystole
Intravenous atropine (first line)
Inotropes (e.g., isoprenaline or adrenaline)
Temporary cardiac pacing
Permanent implantable pacemaker, when available
65
what are the two options for temporary cardiac pacing
Transcutaneous pacing, using pads on the patient’s chest
Transvenous pacing, using a catheter, fed through the venous system to stimulate the heart directly
66
what is atropine
an antimuscarinic medication
67
how does atropine work
by inhibiting the parasympathetic nervous system, inhibiting the PNS leads to side effecting of pupil dilation, dry mouth, urinary retention and constipation
68
what is Wolff-Parkinson-White Syndrome
a genetic disorder that allows abnormal conduction to occur in the heart, via an accessory pathway
69
what is WPW sometimes called
a pre-excitation syndrome
70
what are the other types of pre-excitation syndromes
Others include Lown-Ganong-Levine syndrome, and Mahaim-type pre-excitation.
71
what can WPW lead to
atrial fibrillation, atrial flutter and a type of SVT known as Atrioventircular re-entry tachycardia (AVRT)
72
what is V node re-entry tachycardia (AVNRT).
the tachycardia excite due to aberrant conduction through the AV node itself, and occurs in structurally normal hearts
73
what is Atrioventricular re-entry tachycardia (AVRT)
the abnormal conduction occurs though an accessory pathway which is an anatomical abnormality
74
what can AVRT pre-dispose to
VF and cardiac arrest
75
what do all pre-excitation syndromes result in
faster conduction of impulses through an accessory pathway
76
what does faster conduction of impulses through an accessory pathway lead to
a shorter PR interval on ECG. once this impulse reaches the ventricles, conduction does not occur via the normal conducting system route, which causes an altered QRS complex
77
what is the altered QRS complex seen in WPW
sloping R wave - known as a delta wave
78
what are the defining ECG changes of WPW
short PR interval
delta wave
non-specific t wave change
79
what is the epidemiology and aetiology of WPW
incidence 0.3 per 1000
prevalence 0.1-0.3%
more common in men
congenital structural heart abnormality, although most often does not present until teenage years or early adulthood
80
what is the presentation of WPW often
often asymptomatic and may be discovered incidentally on an ECG
81
what do acute episodes of SVT present with
SOB, palpitations, dizziness, chest pain and syncope
may also present with AF or atrial flutter
82
what may acute episodes be followed by
polyuria - SVT causes dilation of the atria, which releases atrial natuertic factor
83
what can happen in severe cases of WPW
VF and cardiac arrest
84
what does the accessory pathway allow for in most individuals and what is the exception
in most, the accessory pathway allows conduction in both directions, in 15% of cases, it allows only retrograde conduction
85
what is orthodermic conduction
the accessory pathway allows the electrical signal to return to the atria from the ventricles. (usually the only route by which this ca occur is the AV node, and in a healthy individual the AV node only allows conduction in one direction, and thus this cannot occur
86
what is the accessory pathway sometimes referred to as in WPW
Bundle of Kent
87
in what percentage of patients with WPW does atrial flutter occur in
up to 7%
88
in what percentage of patients with WPW does atrial fibrillation occur in
20%
89
what can atrial flutter and atrial fibrillation lead to
VF or VT as the rapid atrial rate can be transferred directly to the ventricles via the accessory pathway without passing through the moderating effect of the AV node
90
when is pre-excitation
not during an acute episod e
91
what is a classical WPW sign which may be seen outside of the acute episode in an otherwise normal asymptomatic patient
delta wave
92
what does the delta wave refer to
a slurred upstroke of the QRS complex, often in association with a short PR interval
93
what may the delta wave do to the QRS complex
make the base of the QRS complex broad
94
what are the usual ST changes seen in pre-excitation
usually discordant changes occur in the opposite direction to the QRS complex
95
what are the two types of WPW
Type A
Type B
96
what is Type A WPW
positive delta wave and QRS throughout. can look like right bundle branch block
97
what is Type B WPW
negative delta wave in V1 and V2, positive in other precordial leads. can look like left bundle branch block
98
what is orthodermic conduction
retrograde conduction through the accessory pathway
99
what are the features of orthodermic conduction
Rate 200-300
Absent p waves (not visible behind fast QRS complexes)
Narrow QRS (<120ms) unless other abnormalities (e.g. Bundle branch block) are present
T wave inversion
wST segment depression
100
what are the features of antidromic conduction
rate 200-300
wide QRS due to abnormal ventricular depolarisation through accessory pathway
101
what are the features of atrial fibrillation
ratem>200
irregular
wide QRS complex as an abnormal ventricular conduction and depolarisation as signal bypasses AV node
102
what is used to aid diagnosis of WPW
May involve the use of 24-hour Holter monitors to try to capture episodes of arrhythmia
Stress testing can help elicit arrhythmias
Routine bloods will likely be normal, but can rule out other causes of arrhythmias
Echo may be performed to rule out other visible structural heart abnormalities
Electrophysiology studies can show where the accessory pathway is to mark a site for ablation
103
what is the treatment of choice for AVRT episodes / haemodynamically unstable patients
DC cardio version is the treatment of choice
104
if haemodynamically stable:
Attempt vagal manoeuvres (e.g. ask patient to blow on 50ml syringe, carotid sinus massage)
If unsuccessful, give adenosine (6mg initially, followed by 12mg if required. Further 12mg dose can also be given)
Consider synchronised DC cardioversion if above unsuccessful
Avoid adenosine in AF as can paradoxically increase ventricular rate
105
what do you treat as if there is any doubt as to the diagnosis
treat as VT
106
what is the treatment for asymptomatic patients
may just have regular follow ups
Can have radio-frequency (RF) ablation therapy to destroy the accessory pathway
- 95% successful
- Usually done after electrophysiology studies have confirmed the site of the accessory pathway
- Has now largely replaced surgical ablation. Surgical may still be used in those in which RF ablation has failed, or who have other structural heart abnormalities
Drug treatment may be used in those unsuitable or unwilling to undergo ablation therapy
107
after resolution of the acute episode, what is the treatment of symptomatic patients
May require drug therapy to prevent further episodes. Often amiodarone, flecainide or sotalol are used
An anti-arrythmic (usually calss IC or III) plus an AV node blocker should be used. AV node blocker alone is not enough to control the rapid rates seen in WPW involving the accessory pathway
108
what is contraindicated in WPW
digoxin and is associated with increased risk of death
109
what is the prognosis for WPW
prognosis is generally very good. radio frequency ablation is often curative
sudden death can occur but is rare - around 0.1%
110
what does the risk of death correlate with
risk correlates with short R-R interval <250ms indicates highest risk
111
what are the 3 features of heart failure
basal crepitations, ankle oedema, JVP
112
what can anaemia result in as a physiological response to low haemoglobin
results in sinus tachycardia, the heart pumps faster to ensure oxygen reaches the organs
113
what is the definition of palipitations
rapid pulsations or abnormal rapid or irregular beating of the heart.
114
what are the causes of high output state palpitations
anaemia or pregnancy
115
what are the structural cardiac causes of palpitations
valvular heart disease, ischaemic heart disease, hypertension
116
what is Bradycardia
slow heartbeat
the resting heart rate is less than 60 beats in a minute in an adult
117
what is tachycardia
fast heartbeat
the resting heart rate is greater than 100 beats a minute in an adult
118
what is the pathophysiology of bradycardia
occur when depolarisation fails to initiate or conduct properly
119
what are some examples of bradycardias
SA node disease
heart block (AV node, His bundle)
120
what is the pathophysiology of tachycardias
occur when there is abnormal depolarisation occurring in the heart;
- enhanced automaticity
- reentry
121
what is the pacemaker of the heart
the SA node
122
what does sinus bradycardia look like on an ECG
when there is a normal upright P wave in lead II - sinus P wave - preceding every QRS complex with a ventricular rate of less than 60 beats per minute
123
what is needed for treatment of permanent pathologic bradycardia
pacemaker
124
what is sinus pause
describes a condition where the SA node fails to generate an electrical impulse for what is generally a brief period of time
125
if a patient has sinus pause, what may they complain of
missed or skipped beats, flutters, palpitations, hard beats or may feel faint, dizzy or lightheaded or experience a synopal episode (passing out)
frequent pauses would heighten these symptoms. this is a result of the patient actually missing or dropping beats
126
what is the treatment for sinus pause
may involve the use of medications or the use of a temporary to permanent pacemaker
127
what happens during Sino-atrial exit block
the depolarisations that occur in the sinus node cannot leave the node towards the atria. they are blocked
128
what is sinaltrial exit block (heart block) expressed as on ECG
a pause.
129
how can SA exit block be distinguished from sinus arrest
because the pause in SA exit block is a multiple of the P-P interval that preceded the pause
130
what is first degree heart block
slow conduction through the AV node
131
what is 2nd degree heart block - Wenckebach or Morbitz type I
AV conduction becomes slower and slower until it misses a beat
132
what is 2nd degree heart block - Mobitz type II
fixed block usually 2:!
133
what is third degree heart block
complete heart block - no conduction to the ventricles
an escape pacemaker takes over from the His-bundle / bundle branch
134
what is automaticity
an area of myocardial cells that depolarise faster than the SA node. this may be atrial or ventricular tissue
most occur at a single focal sight
135
what is reentry
an electrical pathway that is not supposed to be there, connecting two areas that should not be connected
abnormal electrical connections can be congenital, or they can form because of heart disease.
if such a connection exists, it can form an electrical circuit
136
what is supra ventricular tachycardia
is a heart condition where the heart suddenly beats much faster than normal.
137
where does SVT originate from
faulty electrical impulses in the upper part of the heart, rather than from the ventricles
138
what is ventricular tachycardia
defined as a sequence of three or more ventricular beats
the frequency must be higher than 100bpm
139
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
in atrial fibrillation
- grossly irregular
- 400-600 bpm
- 75-175 bpm
- absent
- slows down rate; irregularity remains
140
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
in atrial flutter
- regular (sometimes alternating block)
- 250-350 bpm
- 75-150bpm
- negative sawtooth in lead II
- temporary reduced conduction
141
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
AVNRT
- regular
-180-250 bpm
- 180-250 bpm
- in QRS complex (R')
- stops
142
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
atrial tachycardia
- regular
- 120-250bpm
- 75-200 bpm
- preceded QRS, p wave differs from sinus-p
- temporary AV block
143
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
atrio-ventriclar reentry tachycardia (AVNT)
- regular
- 150-250bpm
- 150-250bpm
- RP
144
what are the two types of VT
ventricular tachycardia
ventricular fibrillation
145
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
Ventricular tachycardia
- regular (mostly)
- 60-100 bpm
- 110-250bpm
- AV dissociation
- no rate reduction (sometimes accelerates)
146
what is the
- regularity
- atrial frequency
- ventricular frequency
- P wave
- effect of adenosine
ventricular fibrillation
- irregular
- 60-100 bpm
- 400-600 bpm
- AV dissociation
- none
147
what type of SVT is WPW syndrome an example of
AVRT
148
what is the pattern of pre-excitation on an ECG
sinus rhythm with a short PR interval and clear delta waves
149
what does pre-excitation indicate
conduction via an accessory pathway
150
what is the trio used to diagnose WPW syndrome
The presence of pre-excitation on a 12 lead ECG, symptoms and SVT is called Wollf-Parkinson-White (WPW) syndrome.
151
what is WPW syndrome
SVT that uses an AV accessory tract
the accessory pathway may also allow conduction during other supra ventricular arrhythmias such as atrial fibrillation or flutter
152
what is type A WPW syndrome
the delta wave and QRS complex are predominantly upright in the precordial leads
the dominant R wave in lead V1 may be misinterpreted as right bundle branch block
153
what is type B WPW syndrome
the delta wave and the QRS complex are predominantly negative in leads V1 and V2 and positive in the other precordial leads, resembling left bundle branch block
154
how common is WPW syndrome
relatively common, and found in 1-3 per 1000 of the population
155
what are vagal manoeuvres
physical actions that make your vagus nerve act on your hearts natural pacemaker, slowing down its electrical impulses
156
what is the most common Vagal manoeuvre
valsalva maneourve
157
how are vagal manoeuvres used diagnostically
can be used to distinguish between ventricular tachycardia and supraventircular tachycardia by slowing down the rate of conduction at the SA or AV nodes
158
how are vagal maneouvres used therapeutically
Therapeutic: Vagal manoeuvres are the first-line treatment of hemodynamically stable supraventricular tachycardia, serving to slow down or terminate the arrhythmia. Vagal manoeuvres have a reported success rate of conversion to sinus rhythm for SVT around 20-40%, possibly being higher for AVNRT (an SVT associated with a bypass tract). Whereas the modified Valsalva manoeuvre is most effective in adults, cold water immersion may be preferred as a safe, effective, and non-invasive treatment for paediatric SVT.
159
what is the Valsalva manoeuvre
While lying on your back, take a deep breath and act like you’re exhaling but with your nose and mouth closed for 10 to 30 seconds. It should feel like trying to breathe air out into a blocked straw.
160
what is the Diving reflex
While sitting, take several deep breaths, hold your breath and then quickly put your whole face into a container of ice water. Keep your face submerged as long as you can. The alternative approach is putting a bag of ice water or an ice-cold, wet towel against your face.
161
what is the carotid sinus massage
Carotid sinus massage - Lie on your back with your head turned to one side. The doctor will use their fingers to push on your carotid sinus for five to 10 seconds. If it doesn’t work, they can try again after a minute or try the other side of your neck.
162
when should you not do vagal manoeuvres
- Low blood pressure
- Chest pain
- Shortness of breath
- A shortage of oxygen in their body
- An inability to get enough blood to their organs
163
if concerned about an arrhythmia, what steps should you take?
request a 24-48 hour ECG
164
what are the DVLA guidelines regarding arrhythmias for Group One - cars and motorcycles
Group 1 (car or motorcycle):
- Must stop driving if the arrhythmia has caused or is likely to cause incapacity.
- Driving may be permitted when the underlying cause has been identified and the arrhythmia has been controlled for at least four weeks.
165
what does the DVLA say regarding arrhythmias for Group 2: lorry or bus
Group 2 (lorry or bus):
- Disqualifies from driving if the arrhythmia has caused or is likely to cause incapacity. DVLA must be informed.
- Driving may be permitted when:
-- The underlying cause has been identified.
-- The arrhythmia is controlled for at least three months.
-- The LV ejection fraction is ≥40%.
-- There is no other disqualifying condition.
166
if you are getting sinus tachycardia as a result of anxiety or stress, what can be prescribed
a beta blocker such as propranolol
167
