Arrythmia And Atrial Fibrillation Flashcards
1
Q
What is the normal length of the PR interval?
A
0.12 to 0.20 seconds
2
Q
What is the normal length of the QRS complex?
A
0.08 to 0.12 seconds (3 squares)
3
Q
What is the normal length of the QT interval?
A
0.35 to 0.43 seconds
4
Q
What defines a narrow complex QRS?
A
Less than 0.1 m/s (less than 2.5 squares)
5
Q
What defines a broad complex QRS?
A
Over 0.1 m/s (more than 2.5 squares)
6
Q
What does a peaked P wave indicate?
A
Right atrial enlargement (P.pulmonale)
7
Q
What does a bifid P wave indicate?
A
Left atrial enlargement
8
Q
What is a Q wave?
A
A negative deflection before the R wave
9
Q
When is a Q wave considered pathological?
A
If seen in V1-V3, indicates current or prior MI.
10
Q
What does more than 3 different P wave shapes on rhythm strip indicate?
A
mutlifocal atrial rhythm
11
Q
What does ST elevation indicate?
A
Ischaemic heart disease if downsloping in 2 leads
12
Q
What are De Winter T waves?
A
Upsloping ST depression with symmetrical tall peaked T waves caused by occlusion of LAD.
13
Q
What does ST elevation in anterior leads indicate?
A
LAD blockage
14
Q
What does ST elevation in inferior leads typically indicate?
A
RCA blockage but can be PLV blockage
15
Q
What is the blood supply to the lateral leads?
A
left circumflex artery
16
Q
Wha is the blood supply to the inferior leads?
A
Right coronary artery, and sometimes PLV
17
Q
What is the blood supply to the posterior region of the heart?
A
posterolateral artery, a branch of the left ventircle
18
Q
What does ST elevation on mutiple leads in more than one orientation (anterior + inferior) indicate?
A
pericarditis with a saddle shape.
19
Q
What is the effect of digoxin on the ECG?
A
Down-sloping P wave with flattened T waves, called a inverted tick, which indicates that it is working due to increasing contractility with increased myocardial oxygen demand.
20
Q
What causes giant T waves inversions on chest leads?
A
Cerebral waves- due to raised ICP.
21
Q
What is the effect of hypothermia on ECG?
A
Hypothermia causes a J/Osborn wave, that resembles a retrograde delta wave on the chest leads.
22
Q
What does hyperkalemia cause on an ECG?
A
Tall, peaked T waves and bradycardia
->Hyperkalemia causes increased rate of repolarisation, reducing myocardial excitability which suppresses impulses from SA node causing tall tended/peaked T wave and bradycardia that can progress to cardiac
23
Q
What is the effect of chronic hyperkalemia on the ECG?
A
In chronic hyperkalemia, there is a widening of the QRS in a bizarre shape sometimes, flattening of P wave , prolonged PR interval and conduction blocks.
It can progress to ventircular fibrillaiton
24
Q
What is the effect of hypokalemia on ECG?
A
ECG changes occur with 2.5-2.9mmol/l causes reduced rate of repolarisation, with T wave inversion and ST depression on many leads. There is risk of progression t o life threatening ventricular arrythmias such as ventricular tachycardia, ventricular fibrillation and Torsades de pointes.
Hypokalemia is associated with hypomagnesaemia so treatment is with IV replacement of both
25
What is the Sokolow criteria?
Describes criteria for left ventricular hypertrophy:
S wave depth in V1 + tallest R wave height in V5 or V6 > 35 mm
26
What is Cornell’s criteria?
Used to assess for left ventricular hypertrophy: R wave in avL and S wave in V3 is greater than 29mm indicates left ventricular hypertrophy
27
What is junctional escape rhythm?
QRS complex before a P wave, which can occur with heart block or sick sinus syndrome as ventricular area is where electrical signal starts.
28
What is atrial escape rhythm?
Impulse originates from a different part of the atria, known as enhanced automaticity, which may be from lower part of right atria towards upper right atria.
29
What is the primary location of the sinoatrial node?
Right atrium
30
How is the polarity of the ECG determined?
inferior wall leads such as Lead II, Lead III and avF.
31
What is a typical cause of tachycardia in neonates?
In a foetus and neonata, AVRT and atrial flutter are a typical cause of tachycardia which typically resolves spontaneously in utero or by one year of age. However if persistent, hydrops fetalis may occur
32
What is indeterminate axis?
Indeterminate axis is where there is extreme axis deviation to -150 degrees, where all leads are negative apart from avR.
33
What are the causes of indeterminate axis?
It typically occurs due to extreme hyperkalemia, chronic lung disease such as extreme COPD/Emphysema, ventiruclar pacing in apex.
34
What is appropriate discordance?
Abnormal depolarisaiton causes abnormal repolarisation, known as appropriate discordance, this means abnormal QRS complex will typically mean abnromal T wave.
35
What are the causes of right bundle branch block?
RVH
-> associated with cor pulmonale from pulmonary embolus, or ischaemic heart disease, rheumatic heart disease, congenital heart disease, myocarditis.
36
How does left anterior fasicular block affect ECG?
Left anterior fasicular block will cause left axis deviation on ECG. This is more common than Left anterior fasicular block.
37
How does left posterior fasicular block affect ECG?
Left posterior fasicular block causes right axis deviation on ECG. It can only be made after excluding other causes of ROADright ventricular hypertrophy. Typically occurs with RBBB and rarely occurs in isolation.
38
How does right bundle branch block affect ECG?
No effective on deviation of ECG, but will show M shape on V1-V6.
39
What is the cause of Right bundle branch with right axis deviation?
Left posterior fasicular block
40
What is the cause of left bundle branch block?
Left bundle branch block typically occurs because of aortic stenosis, hypertension, dilated cardiomyopathy and ischaemic heart disease. QRS complex on V6 may be normal and characteristic or show broad tall R wave that is notched in an M wave.
41
What is Wolf-Parkinson-White syndrome associated with?
Atrial fibrillation
42
What is the ORBIT bleeding risk score used for?
To evaluate bleeding risk before starting anticoagulant therapy
43
What does the CHADS-2 VASCULAR score assess?
Stroke risk in patients with atrial fibrillation
44
Name one direct-acting oral anticoagulant (DOAC).
Apixaban, dabigatran, edoxaban, or rivaroxaban
45
What is a common cause of left axis deviation on ECG?
Left anterior fascicular block
46
What ECG change is associated with left bundle branch block?
Deep S waves in right chest leads and tall R waves in lateral leads
47
What is the most common type of cardiac arrhythmia?
Atrial fibrillation where there is chaotic abnormal electrical activity in the heart, that creates an irregular narrow complex tachycardia 350-450.
There are no P waves and irregular baseline which causes blood flow to become turbulent and increases the risk of a thrombus blood clot forming which can cause a stroke.
48
What is a typical presentation of atrial fibrillation?
Dyspnoea, palpitations, chest pain, dizziness, and fatigue
49
What are some risk factors for atrial fibrillation?
* Advanced age
* High blood pressure
*Haemodynamic stress from underlying heart disease
* Valvular disease
* Congenital heart disease
* Excessive alcohol consumption
50
What is the aetiology of atrial fibrillation?
cardiac modelling of the atria results in structural and electrical changes That shorten the refractory period.
*Hypertension
*Caffeine and electrolyte imbalances
*Fibrosis associatd with Sarcoidosis/amyloidosi due to left atrial dilation that triggers RAAS activation
*Obstructive apnoea due to vasoconstriction of blood vessels which increases peripheral resistance and causes cardiac damage over time
51
What are the patterns of atrial fibrillation?
paroxysmal atrial fibrillation
Persistent atrial fibrillation
Long-standing atrial fibrillation
52
What is paroxysmal atrial fibrillation?
Paroxysmal atrial fibrillation which reverts spontaneously in seven days, initiated in the myocardial tissue of the pulmonary veins. Occurs due to hypertension, structural or ischaemic disease.
53
What is persistent atrial fibrillation?
Rapid and uncontrolled ventricular rate lasting more than seven days, which results in electrical remodelling of the cardiac myocytes and requires pharmacological or electrical cardioversion.
54
What is long-standing persistent atrial fibrillation?
Present more than 12 months which requires pharmacological or cardioversion intervention
55
What is a trigger?
A trigger is typically related to underlying focus, and creates an ectopic focus of abnormal electrical charge, commonly around the pulmonary veins which creates unsynchonrised irregular firing of the electrical impulses.
56
What can cause trigger in Afib?
* Atrial ischaemia
* Inflammation
* Alcohol/illicit drugs
* Haemodynamic stress
* Neurological and endocrine disorders
* Older age
* Genetics
57
What is the clinical presentation of atrial fibrillation?
Presentation of atrial fibrillation is dyspnoea, palpitations, chest pain, dizziness and fatigue. Tachycardia and irregularly irregular pulse are typically present.
58
What are the investigations for atrial fibrillation?
*12 lead ECG-> shows irregularly irregular pattern and a ventricular rate between 80 and 180/min
*FBC to rule out infection, electrolyte abnormalities and metabolic disorders such as thyroid function
*Assessment of stroke risk with CHADS2-VASCULAR score, including for those with atrial flutter, continuing risk of arrythmia
Transthracic echocardiogram to assess for valvular and cardiomyopathies
59
What is the ORBIT score used for?
Prior to starting anti-coagulant therapy, ORBIT bleeding risk score for atrial fibrillation should be used
60
What are the components of the ORBIT bleeding score?
sex
recent bleeding history including internal
low GFR
administration with anti-platelet agents.
61
What are the components of the CHADS-2 Vascular score?
CHADS-2 VASCULAR score calculates stroke risk and includes
Congestive heart failure
Hypertension
Age over 75
Diabetes mellitus
Stroke/TIA/Thromboembolism
Vascular disease
Age 65 or over
Sex (Female)
62
How should CHADS-2 Vascular score be used?
Only consider anticoaugltion in someone with 1 point if they are male.
Points of 2 or more should receive full anticoagulation with warfarin or a DOAC due to increased risk.
63
When should warfarin be used for anticoagulation instead of DOACs?
DOACs are reccomended over warfarin except for patients with mitral stenosis and a mechanical heart valve.
64
Which drugs should be avoided with anticoagulants?
SSRIs and NSAIDs due to their inhibitory effects
65
What is the management for atrial fibrillation with a CHADS-VASCULAR score of 2 or above?
Anticoagulation therapy with a direct-acting oral anticoagulant
66
Which DOAC is best for patinets with multiple cardiovascular risk factors?
Apixaban, which is ideal for patients with multiple risk factors such as hypertension, diabetes and symptomatic heart failure
67
Which DOAC is best for patients with heat failure with low left ventricular ejection fraction?
Dabigratran is ideal for patients with heart failure and low left ventricular ejection fraction
68
What is edoxaban best for?
Edoxoaban is ideal for patients with congestive heart failure, diabetes, hypertension and previous TIA.
69
Which DOAC is best for patients with Non-valvular atrial fibrillation?
Rivaroxaban is ideal for patients with non-valvular atrial fib and multiple risk factors like hypertension, diabetes and congestive heart failure.
70
What is the treatment for haemodynamically unstable patients with adult tachycardia?
Assessment with ABCDE approach (airways, breathing, circulation, Disability, exposure) life threatening features like shock, syncope, MI or severe heart failure should cause progression to use
Electrical cardioversion is best for haemodynamically unstable patients, synchronised to R wave.
71
What is the treatment for persistent atrial fibrillation?
Requires pharmacological or electrical cardioversion
72
What is the first line treatment for pharmacological cardioversion for AFib?
Beta blocker or rate-limiting CCB such as diltiazem//verapamil
73
What is the second line treatment for AFib?
dronedarone is a class III antiarrythmic for people wit cardiovascular risk factors like hypertension and diabetes
74
What is the long term treatment for atrial fibrillation?
Rate control with beta blocker or rate limiting CBB like diltiazem
Anti coagulation therapy should begin if duration is over 48 hours
75
Which treatment for AFib is best for those with heart failure?
> for patients with heart failure, digoxin or amiodarone should be initiated (amiodarone continued for several months)
76
Which treatment is best for those with AFib unresponsive to antiarrythmic agents?
Radiofrequency ablation is for those unresponsive to antiarrythmic agents using heat (radiofrequency) or cryotherapy (cold( with anti-arrrythmic drugs 3 months after starting
77
What does a J wave on an ECG indicate?
Hypothermia
78
What is the ECG finding in right bundle branch block?
Slurred S wave on Lead I and aVL
79
Define atrial tachycardia.
Atrial rhythm with a rate over 100 bpm
80
What is the significance of reciprocal changes in ECG?
Indicates myocardial infarction
81
What are the NICE guidelines for rate control in atrial fibrillation?
Assume narrow or broad complex irregular tachycardia is atrial fibrillation
## Footnote
Electrical cardioversion is best for haemodynamically unstable patients, synchronised to R wave.
82
What should be done for patients with atrial fibrillation lasting less than 48 hours?
Heparin and electrical cardioversion; further anticoagulation is unnecessary.
83
What is the recommended management for atrial fibrillation lasting over 48 hours?
Anticoagulation should be given for 3 weeks before cardioversion and continued for at least 4 weeks lifelong for those with risk factors.
84
What acute treatment should be initiated for patients with heart failure and atrial fibrillation?
Digoxin or amiodarone.
85
What is the pill-in-pocket strategy?
Used for people with infrequent paroxysms, few symptoms or known precipitates, without a history of cardiac pathology.
86
What characterizes sinus arrhythmias?
Changes in heart rate associated with respiration, commonly seen in young people.
87
What distinguishes supraventricular rhythms from ventricular arrhythmias?
Supraventricular rhythms have narrow QRS complexes less than 200 m/s; ventricular arrhythmias have wide QRS complexes over 200 m/s.
88
Which SVT causes broad complex?
atrial fibrillation with bundle branch block or WPW.
89
What is the cause of Narrow complex with HR of 160-220?
supraventricular tachycardia
90
What is the cause of narrow complex with HR of 140-160?
if regular, atrial flutter
91
What is an escape rhythm?
Depolarization initiated from elsewhere than the SA node, typically the AV node or ventricular muscle.
On ECG this is characterised by a sinus pause, followed by a single and wide QRS complexion, to allow the heart beat to restore.
92
How to distinguish from SVT and ventricular arrythmia?
Supraventricular and ventiruclar arrythmias can be distinguished through application of pressure to the carotid sinus and injection of adenosine, which blocks conduction through AV node.
93
What is the effect of carotid sinus pressure?
Carotid sinus pressure causes vagal stimulation of SA node and increases delay in conduction in the AV node, which has no effect on ventiruclar arrythmias.
94
What is the characteristic of junctional extrasystoles?
They will have no P wave.
95
What does an atrial extrasystole show on an ECG?
An abnormally shaped P wave.
96
What is the cause of automaticity in the heart?
Inward flow of positive ions during diastole.
97
Where is the sinoatrial node (SAN) located?
Just below the superior vena cava, composed of pacemaker P cells with intrinsic pacemaker function and transition T cells that propogate signals to the right atrium
98
Where is the AVN located?
AVN is located in the right atria superior to the septal leaflet of the tricuspid valve. It sits within an anatomical region called the triangle of Koch, bordered y the coronary sinus optimum and septum of trispid valve.
99
What are common causes of bradycardia?
* Sinus bradycardia
* Heart block
* Sick sinus syndrome
100
What investigations are done for bradycardia?
12 lead ECG, FBC for biochemical markers, glucose, thyroid levels, and drug screen.
101
What triggers increased vagal tone causing sinus bradycardia?
Nausea, vomiting, vasovagal attack, or carotid sinus hypersensitivity.
102
What is the emergency management for haemodynamically unstable patients with bradycardia?
Oxygen therapy, nil by mouth, bolus dose of atropine, and IV isoprenaline.
Bolus dose of atropine to block parasympathetic stimulation of SAN every 3-5 mins
0.2mg of IV isoprenaline which is a non-selective beta-1 and beta-2 agonist to increase heart rate
103
What is the management of adult bradycardia?
ABCDE approach, oxygen if appropriate, OBS, FBC for electrolyte imbalances and Bp and SpO2
104
How is haemodynamically unstable patients with adult bradycardia managed?
emergency IV 0.mg atropine and progress to isoprenaline with no response or adrenaline.
105
How are haemodynamically stable patients with adult bradycardia managed?
Haemodynamically stable patients are managed with observation on continuous ECG and supportive.
Transcutaneous pacing may be used via an external defibrillator , which requires patient sedation with benzodiazepine due to thoracic muscular
106
What is the cause of symptomatic bradycardia?
Symptomatic bradycardia should be managed with a transcutaneous pacemaker, especially for those not responding to atropine or second-line drugs.
It is reccomended for type II second degree AV bock or 3rd degree.
107
What are the drugs for symptomatic bradycardia?
Drugs for symptomatic include adrenaline, dopamine and glucagon.
108
What is sick sinus syndrome?
Malfunction of the SAN diagnosed with ambulatory cardiac monitoring.
109
What is the cause of sick sinus syndrome?
*Infiltration with deposits due to sarcoidosis, amyloidosis, haemochromatosis, collagen vascular disease or metastatic cancer
* Damage from cardiothoracic surgeries such as valve replacement or heart transplant
* Infection from bacterial endocarditis and Chagas’ disease causing conduction issues in the AV node
* Metabolic derangement from hypothyroidism, hyperkalemia, hypoxia and hyperthermia
* age related degeneration
110
How do sick sinus syndrome cause?
SA exit block, where there is failure of the T cells to transmit the impulses.
* Sinus pause or arrest
* Tachybrady syndrome and cause atrial fibrillation, in association with degeneration of AV node
* There is sinus pause, CNS underperfusion that causes syncope as a clinical sign.
111
What is the treatment of sick sinus syndrome?
Treatment of sick sinus syndrome is with a permanent pacemaker with a dual chamber due to the icreased risk of AV block and investigating for metabolic electrolyte imbalances.
There is a low risk of sudden cardiac death and this syndrome typically occurs in the elderly
112
What is sinus bradycardia?
Sinus bradycardia is a rhythm from the SAN node less than 60 bpm with the majority of patients asymptomatic, and a minority presenting with fatigue, lightheadedness, dizziness, exercise intolerance, syncope, cognitive slowing and heart failure.
It is associated with congestive heart failure and ischaemic heart disease.
113
What is the clinical signs for bradycardia?
Physical examination may show cyanosis, peripheral oedema, crackles and rales, dizziness and alterd consciousness.
114
What are the symptoms of sinus bradycardia?
* Fatigue
* Lightheadedness
* Dizziness
* Exercise intolerance
* Syncope
* Cognitive slowing
* Heart failure
115
What is a significant sinus pause?
Pauses more than 3 seconds.
116
What is tachycardia-bradycardia syndrome?
Tachycardia-bradycardia syndrome is where there is rapid narrow QRS complexes in absence of P waves followed by a sinus pause, and then P waves with sinus bradycardia for 5 minutes. This occurs due to ineffective SAN so the AVN will compensate.
117
What is SAN Weckenbach arrythmia?
SAN Weckenbach arrythmia where PR intervals decrease prior to a pause, where there is an absence of P waves followed by.
118
What is SAN type 2.2 block caused by?
SAN type 2.2 block is where there are intermittent loss of P waves
-> KEY IS TO COUNT WHEN P WAVES APPEAR AFTER T wave
119
What is SAN type 3 block cause by?
SAN type 3 block is where there is a complete absence of P wave, where there is a long sinus pause or sinus arrest or junctional escape.
120
What characterizes AV block?
Persistent P waves with no QRS complex.
121
What is first-degree AV block?
Increased PR interval with normal QRS width.
122
What characterizes second-degree AV block type 1 (Wenckebach)?
Increasing PR interval with a dropped beat.
123
What is Weckenbach arrythmia?
Type 1/Weckenback increase PR interval with dropped beat and then subsequent PRQS complex must show SHORT P wave
124
What is Mobitz arrythmia?
Type 2/Mobitz: increased ratio of P waves to QRS complexes and normal PR interval. This block primarily affects the bundle of His
125
What is the management for third-degree AV block?
Permanent pacemaker.
126
What causes bundle branch blocks?
* Fibrosis of the conduction system
* Hypertensive heart disease
* Valve disease
* Cardiomyopathies
*Infective endocarditis
*Myocarditis
*Congenital heart disease
127
What is left bundle branch block characterized by?
Delayed depolarization of the left ventricle causing a wide QRS.
128
What is right bundle branch block?
Right bundle branch bloc: depolarisation of the right ventircle is delayed, resulting in a wideQRS complex.
129
What is the management for symptomatic heart block?
Pacemaker for advanced blocks such as bifascicular or trifascicular.
130
What defines tachyarrhythmia?
Heart rate over 120 beats per minute.
131
What do p waves absent with QRS complex?
P waves absent-> indicates supraventricular tachycardia, which may originate from atria so provide IV adenosine, which blocks A1 receptors to slow AV node conduction
132
What do P waves present indicate?
treat as sinus tachycardia so investigate underlying causes
133
What are emergency management steps for adult tachycardia In haemodynamically unstable patient?
*External correction of rhythm with defibrillator
-> exception is chronic atrial fibrillation where ventricular rate is uncontrolled, so first line treatment is managing the precipitating factors
*Patients should be sedated with midazolam, morphine and metoclapramide
*Ventricular tachycardia should be managed with direct cardioversion and IV amiodarone bolus
*Focal atrial tachycardia should be treated with verapamil or beta blocker
134
What are emergency management steps for adult tachycardia in haemodynamically stable patient?
Continuous ECG monitoring
Valsalva manoeuvres, where forced expiration against closed glottis decreases venous return to the heart, therefore reduces cardiac preload and cardiac output.
Carotid sinus massage for supraventricular tachycardia by directly stimulating the carotid baroreceptors to induce bradycardia, vasodilation and hypotension.
135
What distinguishes supraventricular tachycardia?
Atrial rates greater than 200/min with QRS complexes less than 200 m/s.
136
What is the purpose of the Valsalva maneuver in tachycardia management?
Decreases venous return to the heart, reducing cardiac preload and output.
137
What is the role of IV adenosine in treating tachycardia?
Slows AV node conduction.
138
What is the effect of increased venous return on cardiac preload and output?
It reduces cardiac preload and cardiac output.
139
What is the mechanism of carotid sinus massage in treating supraventricular tachycardia?
It directly stimulates the carotid baroreceptors to induce bradycardia, vasodilation, and hypotension.
140
List some causes of sinus tachycardia.
* Drugs (caffeine, cocaine, salbutamol)
* Hyperthyroidism
* Pain
* Hypoxia
* Pyrexia
* Hypovolemia
* Myocarditis
* Hypoglycaemia
* Pulmonary embolism
* Hyperkalemia
141
What causes atrial tachycardia?
* Re-entry of electrical signals in large areas of the left and right atria
* Enhanced automaticity from spontaneous phase 4 depolarization
142
What can atrial tachycardia cause?
focal atrial tachycardia
Atrial flutter
143
What is focal atrial tachycardia caused by?
Abnormal automaticity or micro-reentrant circuit; focus of atrial cells firing faster than the SA node, which is terminated with administration of IV adenosine.
144
Describe atrial flutter.
Caused by a macro-reentrant circuit in the right atrium, with an atrial rate of 300 bpm and absence of an isoelectric baseline between P wave deflections. It causes a sawtooth appearance and narrow complex regular tachycardia and tends to have an AV block.it has a risk of stroke
145
What is the most common cause of atrial flutter?
Anti-clockwise re-entry.
-> The sawtooth appearance is caused by the inverted waves, typically affecting in Lead II and the inferior leads. This can affect ventiruclar rate due to AV conduction, resulting in a ratio of 2:1 block. Atypical atrial flutter is caused by clockwise re-entry circuit with positive flutter waves on Lead II and inferior leads.
The length of the re-entry circuit corresponds to right atria size, resulting in a rate around 140-160 and a notched T wave may be present, indicating right atria hypertrophy.
146
What is the significance of the sawtooth appearance in atrial flutter?
It is caused by inverted waves typically affecting Lead II and inferior leads.
147
What is the criteria Class 1c drugs?
Class 1c drugs can be used however they may paradoxically increase ventricualr rate, so should only be used in atrial flutter in combination with AVN blocking agent, such as amiodarone.
148
What should be started for patients with a new diagnosis of atrial flutter?
Anticoagulation due to the risk of thrombus formation, but CHADS2-VASC score must be done.
Rhythm control can be done in stable patients with anti-arrhythmic drugs for pharmacological cardioversion like amiodarone, Class Ia drugs, beta blockers, CCBs like diltiazem and verapamil. Rate control through CCBs and beta blockers.
149
List the rhythm control options for stable patients with atrial flutter.
* Anti-arrhythmic drugs (amiodarone, Class Ia drugs, beta blockers)
* Calcium channel blockers (diltiazem, verapamil)
150
What is the most effective method for restoring sinus rhythm in atrial flutter?
Radiofrequency ablation.
151
What is persistent focal atrial tachycardia associated with?
Cardiomyopathy and symptoms like dyspnea, oedema, and chest pain.
Treatment is only required for symptomatic patients with beta blocker, calcium channel antagonists to slow atrial rate
or triggered activity and is common in individuals with structural heart disease.
152
What is the first step in managing adult tachycardia?
ABCDE assessment, check 12 lead ECG, BP, and SpO2.
153
How should unstable patients with tachycardia be managed?
Cardioversion with IV amiodarone or procainamide.
154
What is indicated for narrow complex irregular tachycardia for stable manoeuvres?
Rate control with beta blockers or diltiazem and consider if they have heart failure providing digoxin or amiodarone and anticoagulants if it lasts over 48 hours
155
What should be avoided in patients with carotid bruits when performing carotid sinus massage?
Carotid sinus massage, should be avoided in patients with carotid bruits or history of TIA or stroke, older age (higher risk of carotid artery disease)
156
What should be avoided in patients with regular complex tachycardia?
Regular complex tachycardia, either broad or narrow in haemodynamically stable patients should begin Vagal manoeuvres such as carotid sinus massage and valsalva manoeuvre which increases arterial pressure in the carotid sinuses and aortic arch, triggering the baroreceptors reflex to increase vagal parasymapthetic tone. It should not be used in unstable VT.
157
What is the recommended administration method for adenosine?
Fast IV bolus in a proximal cannula.
158
Which patients should not have adenosine administration?
Should not be given to patients with VT, asthma, COPD, heart failure, and hypotension.
159
What is the alternative treatment for adenosine if ineffective for narrow complex?
provide CCB like verapamil, diltiazem or beta blocker, typically for general SVT causes
160
What is the alternative treatment for adenosine if ineffective for broad complex?
Procainamide and class 3 drug amiodarone
161
What is the purpose of vagal maneuvers?
To increase vagal parasympathetic tone and reduce heart rate.
162
What is AVNRT?
A common cause of narrow complex tachycardia, particularly in young adults and women.
163
What is the most common type of AVNRT?
The most common sub-type is the slow-fast AVNRT where the slow pathway has anterograde conduction and recovers quickly for retrograde conduction by the fast AV nodal pathway and this occurs close to or at the AV node.
164
What is the clinical presentation of AVNRT?
Patients present with sudden onset of rapid palpitations due to a rapid heart rate and may have syncope (due to reduced filling of ventircle which reduce the cardiac output) shortness of breath, chest or neck pain, severe palpitations and pounding in the neck but ECG will show heart rate above 170bpm and prognosis is benign. It will cause regular narrow complex tachycardia
165
How is AVNRT treated?
AVRT can be terminated by IV adenosine to block the AV node conduction or vagal manoeveres and long term control with beta blockers, verapamil and diltiazem.
->First line treatment for recurrent symptomatic episodes is radiofrequency ablation.
->Haemodynamically unstable patients are managed with urgent electrical cardioversion for 3 attempts and once stable, progression to vagal exercises. ECG will show a heart rate above 150 and a narrow QRS complex with no P waves or may be retrograde or short PR.
166
What characterizes junctional tachycardia?
Narrow complex tachycardia without P waves.
167
What is pre-excitation in the context of cardiac arrhythmias?
Early activation of ventricles due to an accessory pathway bypassing the AV node. is characterised by shortening of PR interval due to the accessory pathway causing early activation of myocardium and slurring of the QRS complex called a delta wave, which causes a wide QRS complex.
168
Which conditions cause pre-excitation?
It is associated with conditions that have accessory pathways like AVRT, atrial tachycardia, Atrial flutter and atrial fibrillation
169
What is AVRT?
AVRT is where there is abnormal anatomical re-entrant pathway in areas other than the AV node allows anterograde conduction to occur.
170
What are the ECG findings for AVRT?
ECG will show shortened PR interval and broad QRS complex and the accessory pathways can result in atrial arrythmias due to accelerated conductions.
171
What are the forms of AVRT?
Orthrodromic AVRT
Antidromic AVRT
Junctional AVRT
172
What is the most common subtype?
Orthrdromic AVRT is the most common subtype, where the impulse travels normally through the AV node but on moving past the his-purkinje system, moves back through the accessory pathway to the atria, causing retrograde transmission. This causes abnormal T waves and fast narrow complex regular tachycardia with P waves typically not visible.
173
What is the features of Antidromic AVRT?
Antidromic AVRT where the impulse travels through the accessory pathway which has retrograde transmission up the His bundle -> AV node-> SAN. P waves are typically not3 visible. And it is a VERY DANGEROUS ARRYTHMIA
174
What is junctional AVRT?
Junctional AVRT, typically occurring in infants and children where it originates from the AV node directly due to an AV disassociation.
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How are stable patients with AVRT managed?
Stable patients are managed with procinamide, a class 1a anti-arrhythmic that inhibits fast sodium channels
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How are unstable patients managed?
Unstable patients are managed with ICD
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What is Wolff-Parkinson-White syndrome?
A congenital abnormality causing abnormal electrical circuits between the atria and ventricles, via the Bundle of Kent, causing part of the ventircle to be depolarised earlier.
It is characterised by short PR intervals due to pre-excitation of ventricle and prolonged QRS and is a subtype of a AVRT. The bundle of Kent can also enable retrograde electrical flow and result in a circuit. there must also be symptoms with palpitations, chest pain, dyspnoea, dizziness and syncope.
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What are the ECG features of Wolff-Parkinson-White syndrome?
* Short PR interval
* Delta wave
* Wide QRS complex
Wolf-Parkinson white has a risk of sudden cardiac death due to ventiruclar fibrillation, due to an accessory pathway with rapid anterograde conduction.
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How is Wolf-Parkinson White syndrome treated?
vagal manoeuvres to massage carotid one at a time to provide vagal stimulation to reduce transmission to the SAN and AVN. Cold towel will have similar effects at stimulating vagus nerve and rubbing eye.
Class 1a (fast Na+ channel blockers like procinamide) and Class III (K+ channel blocker like amiodarone ) which block the accessory pathway.
Radiofrequency ablation
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What is a class 3 antiarrythmic for treatment of Wolff-Parkinson White syndrome?
Sotalol is a class 3 antiarrythmic which is also a non-selective cbeta blocker of B1 to slow repolarisation and conduction of action potentials through atrial.
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What does ventricular tachycardia produce on an ECG?
A broad complex tachycardia with identical QRS complexes. Each leads have identical QRS complex with a shape similar to a LBBB or RBBB and no identifiable with no identifiable T waves.
182
List some conditions that cause ventricular tachycardia.
* Ischaemic heart disease
* Dilated cardiomyopathy
* Hypertrophic cardiomyopathy
* Chaga’s disease
* Inherited conditions (Brugada, long QT)
* Electrolyte imbalances (hypokalemia, hypocalcemia, hypomagnesemia)
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What is the clinical presentation of ventricular tachycardia?
Patients may present with syncope, SOB due to pulmonary oedema and Haemodynamically unstable, with hypotension, and decreased conscious level. Clinical exam can show signs of heart failure and heart failure.
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Differentiate between sustained and non-sustained ventricular tachycardia.
* Sustained: longer than 30 seconds, requires intervention
* Non-sustained: less than 30 seconds, does not require intervention
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What is the aetiology Of ventricular tachycardia?
1)) re-entry circuit
2) Triggered activity from early or late after-depolarisation
3) enhanced automaticity with abnormal impulse generation in region of ventircle
There is a rapid ventiruclar rate in VT causing a low cardiac output
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What are the ECG findings for ventricualr tachycardia?
Compensatory phase is where an ectopic pause occurs, followed by a prolonged Pause in the next R wave, due to a reduced stroke volume. This creates a feeling of palpitation.
Ectopic beat every other beat causes bigeminy pulse.
Ectopic beat every 3rd beat is trigeminy pulse.
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What is sustained ventiruclar tchycardia?
Sustained ventricular tachycardia is longer than 30 seconds which requires intervention as it typically causes haemodynamic instability.
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What is non-sustained ventricular tachycardia?
Non-sustained ventiruclar tachycardia is less than 30 seconds doesn’t cause instability and doesn’t require intervention.
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What is the management of SVT in unstable patients?
Haemodynamically unstable patients: 3 attempts of synchronised shock
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What is the management of SVT in stable patients?
vagal manoeuvres, IV antiarrythmic agents like Class 1 procinamide/lidocaine and class 3 amiodarone and sotalol.
-> if secondary to ischaemia, provide beta blocker
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What is long term management of SVT?
Long term management is with an implantable cardiac defibrillator and if underlying ischaemia long term beta blocker.
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What is monomorphic VT?
Monomorphic VT typically causes ventirucalr tachycardia with cardiac myopathies like dilated chambers. Monomorphic VT has a single stable QRS with normal beat variation.
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What are common causes of Torsades de Pointes?
* Myocardial ischaemia
* Low magnesium
* Hypokalemia
* Antipsychotics
* Long-QT syndrome
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Which drugs are known to induce Torsades de pointes?
Class III antiarrhythmics, Class 1a antiarrhythmics, tricyclic antidepressants, antipsychotics, antifungals, and antimicrobials
## Footnote
Examples include amiodarone, sotalol, haloperidol, and olanzapine.
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What is the treatment for Torsades de pointes?
Torsades de pointes is treated with IV magnesium to shorten repolarisation and potassium supplements.
There is a risk of progression to ventricular fibrillation IV magnesium and potassium supplements.
## Footnote
This treatment helps shorten repolarization and stabilize cardiac membranes.
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What does a U wave on an ECG indicate?
Repolarization of Purkinje fibers
## Footnote
It occurs after depolarization.
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What characterizes the ECG findings of Torsades de pointes?
Amplitude in QRS complexes twisting around the isoelectric line and prolonged QRS intervals
## Footnote
This is linked to ectopic beats during prolonged repolarization.
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What is the most common form of ventricular tachycardia?
Right ventricular outflow tract tachycardia, which is caused by automatic firing of cells in the right ventircle outflow tract which is induced by exercise, and there is no association with structural heart disease, metabolic abnormalities or long WT syndrome.
## Footnote
It is typically induced by exercise and has no association with structural heart disease.
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What are the ECG findings for right ventricular outflow tract tachycardia?
it is characterised by absence of P wave and broad QRS complexes that are identical in a lead with no identifiable T waves, and may have left/right axis deviation. ECG will show left bundle branch block with inferior axis domination and can be typically treated acutely with IV adenosine or verapamil
199
What are the causes of right ventricular outflow tract tachycardia?
Typical causes include electrolyte imbalances, illicit drug use infiltrative cardiomyopathy and myocardial ischaemia or hypokalemia.
200
What is arrythmogenic right ventricular cardiomyopathy?
Arrythmogenic right ventricular cardiomyopathy is an autosomal dominant condition where there is progressive loss of the ventricular myocardium to be replaced by fibrofatty tissue.
201
What is the cause of arrythmogenic right ventricular cardiomyopathy?
It primarily affects the intercalated disc, that causes a loss of conduction velocity through the sodium/potassium ion channels and a loss structural integrity of cardiomocytes which worsens during mechanical stress, leading to ventricular arrythmias and progressive RV cardiomyopathy that becomes dilation with a reduced ejection fraction
202
What are the ECG findings for arrythmogenic right ventiruclar cardiomyoapthy?
ECG may show Broad QRS and T wave inversion and an Epsilon wave, a small positive deflection at the end of a QRS complex with S upstroke detected in V1-V3. It is managed.
203
What are the typical causes of long QT syndrome in younger individuals?
Congenital long QT syndrome
## Footnote
It is frequently misdiagnosed as epilepsy or vasovagal syncope.
204
What is the aetiology of ventircular tachycardia?
It is linked to ischaemic heart disease, dilated cardiomyopathy and hypertrophic cardiomyopathy. Re-entry occurs around areas of diseased myocardium which may suddenly progress to ventricular fibrillation and cause sudden cardiac death.
205
What is the management for congenital long QT syndrome?
Beta-blockade and may include intravenous cardioversion
## Footnote
Acquired long QT syndrome should be managed with magnesium replacement.
206
What is the role of IV adenosine in treating right ventricular outflow tract tachycardia?
It is used for acute treatment
## Footnote
It can also be treated with verapamil.
207
What are pacemakers used for?
Management of bradycardia and atrial/ventricular tachyarrhythmias.
## Footnote
They sense and manage electrical impulses in the heart.
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What are the acute complications of pacemaker?
Acute complications of pacemakers includes staphylococci infection. Therefore antibiotic prophylaxis is important with flucloxacillin. The alternative is macrolide antibiotics such as clarithromycin or clindamycin.
209
What does the first letter of a pacemaker code indicate?
The chamber paced
## Footnote
The second letter indicates the chamber sensed, and the third letter indicates how the device responds.
210
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What is pacemaker syndrome?
Electrical AV dyssynchrony caused by a single chamber device. Dyssynchrony of the atria results in mistimed atrial contractions, causing back pressure in venous circulation that leads to congestion and decreased cardiac output.
Dyssynchrony of ventircle results in mistiming of contractions opposing the ventiruclar walls,
## Footnote
It leads to mistimed atrial contractions and decreased cardiac output.
212
What is the typical presentation of ventricular fibrillation?
Ventricular fibrillation is a medical emergency and most common cause of cardiac arrest, where rate is typically over 350bpm, and there is complete loss of shape in PQRS complex due to AV disassociation, where there is increase automaticity and triggered activity (early and late after depolarisation overcomes refractory threshold) which triggers extrasystoles. Unconsciousness, unresponsive without a palpable pulse
## Footnote
It typically occurs at a rate over 350 bpm with complete loss of PQRS complex shape.
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What is unsynchronized cardioversion?
High energy shock delivered anywhere on the cardiac cycle
## Footnote
It is used for pulseless ventricular tachycardia or when defibrillator synchronization fails.
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When should defibrillator not be used?
Defibririllator should not be performed for pulseless electrical activity, where electrical activity of the heart persists but is not sufficient to produce a clinically detectable pulse.
This occurs due to due to electro-mechanical uncoupling, where cardiac muscle cannot contract with adequate force in response to electrical depolarisation.
which can occur with 4Hs and 4Ts.
215
What are the 5 H's that can cause pulseless electrical activity?
* Hypovolemia
* Hypoxia: Intubation
* Hydrogen ions (acidosis)
* Hypokalemia
* Hypothermia
## Footnote
These conditions need to be addressed in treatment.
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What are the 4 T's that can lead to pulseless electrical activity?
* Toxins
* Tamponade
* Tension pneumothorax
* Thrombosis
* Trauma
## Footnote
These conditions must also be managed.
217
What is the assessment for arrhythmias?
Palpitations, syncope, 12-lead ECG, echocardiogram, ambulatory BP monitoring
## Footnote
Investigations include FBC for anemia and tests for electrolyte imbalances.
218
What is the aetiology of Torsades de pointes?
Common causes of Torsades de pointes is:
-> caused by triggered activity during early and late depolarisation.
-> myocardial ischaemia
-> low magnesium/hypokalaemia/hypocalcaemia
-> antipsychotics which reduce the resting negative potential for the cell and long-QT syndrome.
219
What is unsynchronised cardioversion?
Unsynchronised cardioversion is where high energy shock is delivered at the push of the button, and can occur anywhere on cardiac cycle QRS complex.
It is used for where there is no coordination of intrinsic electrical activity with pulse less ventricular tachycardia/fibrillation or defibrillator fails to synchronise in an unstable patient. It is ideal for patients that lack a QRS complex.
