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Block 31 Cardio-respiratory > palpations and arrythmias > Flashcards

palpations and arrythmias Flashcards

1
Q

what are ventricular extrasystoles?

A
  • premature contraction of heart ventricles
  • premature QRS complex on ECG, long duration
  • most common form of cardiac arrhythmia
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2
Q

what is ventricular tachycardia?

A

regular fast heart rate arising from improper electrical activity in ventricles

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3
Q

what is AV nodal reentrent tachycardia?

A

abnormal fast heart rhythm
type of supra ventricular tachycardia (originate above bundle of his)
most common regular supra ventricular tachycardia

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4
Q

what can arrhythmias cause?

A 
sudden death
syncope
heart failure
chest pain
dizziness
palpitations
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5
Q

what are the 2 main types of arrhythmia?

A

bradycardia (<60bpm)

tachycardia (>100bpm)

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6
Q

what can tachycardias be subdivided into?

A
  • supraventricular tachycardia (arise from atrium of AV junction)
  • ventricular tachycardias (arise from ventricles)
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7
Q

what is the normal cardiac pacemaker?

A

sinus node

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8
Q

describe the modulation of the sinus node?

A

depolarises spontaneously
modulated by ANS
parasympathetic NS usually predominates
reduction in parasympathetic or increase in sympathetic can cause tachycardia and vice versa

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9
Q

what is normal sinus rate?

A

60-100

slightly faster in women

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10
Q

what characterises sinus rate on ECG?

A

upright p waves in leads I and II but inverted in AVR and V1

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11
Q

describe sinus arrhythmia?

A
  • fluctuations in ANS cause phasic changes sinus discharge rate
  • inspiration-decrease parasympathetic and increase HR on expiration HR falls
  • normal variation
  • predictable irregularities of pulse
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12
Q

describe sinus bradycardia?

A

<60bpm in day or <50bpm night

  • usually asymptomatic
  • normal in athletes due to increased vagal tone
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13
Q

what can the causes of both bradycardia’s and tachycardias be split into?

A

systemic or cardiac

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14
Q

what is sinus tachycardia?

A

sinus rate >100

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15
Q

describe the normal mechanism of spontaneous cardiac rhythmicity?

A

slow depolarisation of transmembrane voltage during diastole until threshold potential is reached and action potential of pacemaker cells takes off

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16
Q

in what situations is the mechanism of cardiac rhythmicity increased?

A

increasing rate of diastolic deplarisation
changing the threshold potential
eg sympathetic activation -> adrenaline release-> enhanced automaticity-> sinus tachycardia / escape rhythms / accelerated AV nodal rhythms

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17
Q

how can myocardial damage produce an arrhythmia?

A

myocardial damage can result in oscillations (after depolarisations) of the transmembrane potential at the end of the action potential which can reach threshold potential and produce an arrhythmia.

  • early after depolarisations-occur before transmembrane potential reaches threshold
  • delayed after depolarisations-when they develop after transmembrane potential is completed
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18
Q

what can exaggerate ‘after depolarisations’?

A 
pacing
catecholamines
electrolyte disturbances
hypoxia
acidosis
some medications-atrial tachycardias produced by digoxin toxicity are due to triggered activity
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19
Q

what is the mechanism of re-entry?

A

‘ring’ of cardiac tissue surrounds an inexcitable core such as in a region of scarred myocardium

tachycardia initiation:
one branch of pukinje fibres is refractory and the other is excitable. causing a unidirectional block. if conduction in the excitable branch is slow enough then refractory limb will recover and allow retrograde activation to complete the loop. if time to conduct around loop Is longer than refractory periods of tissue within the ring then this will be maintained.
this is how most regular paroxysmal tachycardias are produced

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20
Q

what are the potential causes of bradycardia?

A

failure of impulse formation (sinus bradycardia) or failure of impulse conduction from atria to ventricles (AV block)

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21
Q

what factors can cause bradycardia?

A 
Intrinsic factors
Extrinsic factors (that affect a normal sinus node)
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22
Q

what are the extrinsic factors that can cause bradycardia?

A
  • hypothermia, hypothyroidism, cholestatic jaundice, raised intracranial pressure
  • drugs such as beta blockers, antiarrythmics
  • neurally mediated syndromes
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23
Q

what are the intrinsic factors that can cause bradycardia?

A
  • acute ischaemia and infarction of sinus node (complication of acute MI)
  • chronic degenerative changes such as fibrosis of atrium and sick sinus syndrome
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24
Q

what are neurally mediated syndromes?

A

due to reflex that can result in bradycardia and reflex peripheral vasodilation
present as syncope or presyncope

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25
Q

give examples of neurally mediated syndromes?

A 
carotid sinus syndrome
neurocardiogenic syncope (vagovagal  syndrome)
postural orthostatic tachycardia syndrome?
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26
Q

what is carotid sinus syndrome?

A

elderly
results in bradycardia
syncope

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27
Q

what is neurocardiogenic syncope?

A

presents in young adults
due to physical and emotional situations affecting ANS
efferent output predominantly bradycardia, vasodilatory or mixed

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28
Q

what is posturalorthostatic tachycardia syndrome?

A

-sudden and significant increase in heart rate associated with normal or mildly reduced BP caused by standing
failure of peripheral vasculature to appropriately constrict in response to orthostatic stress compensated by excessive increase in HR
antihypertensives, tricyclic antidepressants and neuroleptics can cause syncope in elderly

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29
Q

how is sinus bradycardia treated?

A

identify and remove any extrinsic causes
temporary pacing in patients with reversible causes until normal sinus rate restored and in patients with chronic degenerative conditions until permanent pacemaker is implanted

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30
Q

how is chronic symptomatic sick sinus syndrome managed?

A

requires permanent pacing with antiarrythmic drugs (or ablation therapy) to manage tachycardia
thromboembolism is common so patient should be anti coagulated unless contraindication

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31
Q

what treatment can patients with carotid sinus hypersensitivity benefit from?

A

pacemaker implantation

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32
Q

what are the treatment options in vasovagal attacks?

A

avoidance if possible of situations known to cause syncope
sitting/lying down and applying counter pressure manoeuvres
increased salt intake, compression of lower legs , drugs such as beta blockers, alpha agonists

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33
Q

what treatment could be used in patients with malignant neurocardiogenic syncope?

A

permanent pacemaker therapy is helpful
dual chamber pacemakers with rate drop response which paces the heart at fast rate for set period of time to prevent syncope

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34
Q

what are the 3 forms of AV block?

A

first degree
second degree
third degree

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35
Q

what is first degree AV block?

A

prolongation of the PR interval to >0.22s

early atrial depolarisation is followed by conduction to the ventricles but with delay

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36
Q

what is second degree AV block?

A

when some p waves conduct and others do not

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37
Q

give examples of second degree AV block?

A
  • mobitz I
  • mobitz II
  • 2:1 or 3:1 (advanced) block
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38
Q

what is mobitz I block?

A

wenckebach block phenomenon
progressive PR interval prolongation until a P wave fails to conduct
the PR interval before the blocked p wave is longer than the pr interval after blockers p wave
AV node block

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39
Q

what is mobitz II block?

A

occurs when a dropped QRS complex is not preceded by progressive PR interval prolongation, usually wide QRS
infra nodal block such as His bundle
more likely to Progresso complete heart block than mobitz I

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40
Q

what is 2:1 or 3:1 (advanced) block?

A

when every second or third p wave conducts to ventricles

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41
Q

what is third degree (complete) AV block?

A

all atrial activity fails to conduct to the ventricles
need to establish aetiology
life is maintained by spontaneous escape rhythm

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42
Q

what escape rhythms are seen in complete heart block?

A

narrow complex escape rhythm

broad complex escape rhythm

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43
Q

What is a narrow complex escape rhythm?

A

originates in His bundle
region of the block lies more proximally in AV node
escape rhythm occurs with adequate rate 50-60bpm and relatively reliable

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44
Q

what is the treatment for narrow complex escape rhythm?

A
  • depend on aetiology

- recent onset due to transient causes may respond to IV atropine

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45
Q

what is broad complex escape rhythm?

A

implies that the escape rhythm originates below the His bundle and the region of the block is more distally in the his parking system
slow rhythm (15-40bpm) and unreliable
dizziness and blackouts
caused by degenerative fibrosis and calcification of distal conduction system

46
Q

what is bundle branch conduction delay?

A

slight widening of QRS complex

incomplete bundle branch block

47
Q

what are the causes of complete heart block?

A
  • congenital
  • idiopathic fibrosis
  • lenegre’s disease
  • ischaemic heart disease
  • non ischamic heart
  • cardiac surgery
  • iatrogenic
  • drug induced
  • infections
48
Q

what is complete bundle branch block?

A

associated with wider QRS complex

the shape of the QRS depends on whether the right or left is blocked

49
Q

what is right bundle branch black?

A

late activation of the right ventricle
deep S waves in leads I and V6 and tall late R wave in lead V1 (late activation moving towards right and away from left sided leads)

50
Q

what is left bundle branch block?

A

produces opposite to right.
deep S wave in lead V1 and tall late R wave in leads I and V6
abnormal Q waves because left bundle branch conduction normally responsible for initial ventricular activation

51
Q

what is hemiblock?

A

delay or block in divisions of the left bundle branch produces swing in direction of depolarisation of the heart
when anterior divisions blocked, the left ventricle is activated from inferior to superior. this produces a superior ad leftwards movement of axis.
delay or block in poster-inferior division swings the QRS axis inferiorly to the right

52
Q

what is bifascicular block?

A

combination of a block of any 2 of the following; right bundle branch, left anterograde-superior division and left posters-inferior division
block of the remaining fascicle will result in complete AV block

53
Q

what are the clinical features of heart blocks?

A

usually asymptomatic
RBBB-wide physiological splitting of second heart sound
LBBB-may cause reverse splitting of second sound
syncope in patients with intraventricular conduction disturbances due to intermittent complete heart block or ventricular tachyarrythmias
ECG monitoring and electrophysiological studies needed to determine cause

54
Q

what are the causes of right bundle branch block?

A

congenital heart disease
pulmonary disease
myocardial disease

55
Q

what are the causes of left bundle branch block?

A

left ventricular outflow obstruction

coronary artery disease

56
Q

what are supraventricular tachycardias?

A

arise from atrium of AV junction
conduction via his-purkinje system therefore QRS shape during tachycardia s usually similar to that seen in same patient during baseline rhythm

57
Q

what is inappropriate sinus tachycardia?

A

persistent increase in resting heart rate unrelated to or out of proportion with the level of physical or emotional stress
common in young women

58
Q

what are AV junctional tachycardias?

A

AV nodal re-entry and AV re-entry tachycardias

  • paroxysmal SVTs
  • young patients with no or little structural heart disease
  • AV node is essential component of the re-entry circuit
59
Q

give examples of supra ventricular tachycardias (SVTs)?

A 
sinus tachycardia
AVNRT
AVRT
AF
atrial flutter
atrial tachycardia
multifocal atrial tachycardia
accelerated junctional tachycardia
60
Q

what are the ECG features of sinus tachycardia?

A

p wave morphology similar to sinus rhythm preceding QRS

61
Q

what are the ECG features of AVNRT?

A

no visible p waves or inverted p wave immediately before or after QRS complex

62
Q

what are the ECG features of AVRT?

A

p wave visible between QRS and T wave

63
Q

what are the ECG features of AF?

A

irregularly irregular RR intervals and absence of organised atrial activity

64
Q

what are the ECG features of atrial flutter?

A

visible flutter waves at 300/min

sawtooth appearance

65
Q

describe the features of AVNRT?

A
  • twice as common in women
  • no obvious provocation
  • may stop spontaneously
  • QRS complexes- 140-240/min
66
Q

describe the features of AVRT?

A
  • due to macroreentry circuit, each part of the pathway is activated sequentially
  • atrial activation occurs after ventricular activation and p waves between QRS and T wave
67
Q

what are the symptoms of SVTs?

A
  • rapid regular palpitations, abrupt onset and sudden termination, spontaneously or precipitated by movements
  • termination by valsalva manoeuvres
  • anxiety, dizziness, dyspnoea, neck pulsation, central chest pain and weakness
  • polyuria
  • syncope
68
Q

what is the acute management for SVTs?

A
  • difficult to distinguish between AVNRT and AVRT
  • if also haemodynamically unstable (hypotension, pulmonary oedema) require cardioversion
  • if haemodynamically stable
69
Q

what is the valsalva manoeuvre?

A

abrupt voluntary increase in intrathoracic and intra-abdominal pressure by straining-vagal manoeuvres, including right carotid massage and facial immersion in cold water, valsalva manoeuvre
-if not successful-IV adenosine or IV verapamil or IV diltiazem or beta blockers

70
Q

what is the long term management for SVTs?

A

refer to cardiologist for electrophysiological evaluation and long term management

  • ablation of accessory pathway
  • verapamil, diltiazem and beta blockers
  • sodium channel blockers, potassium depolarisation current blockers, multichannel blocker-amiorarone
71
Q

give examples of atrial tachyarrhytmias?

A 
AF
atrial flutter
atrial tachycardia
atrial ectopic beats
(all from atrial myocardium)
72
Q

what can cause AF?

A
  • any condition resulting in raised atrial pressure, increased atrial muscle mass, atrial fibrosis or inflammation and infiltration of the atrium may cause AF
  • genetic and systemic causes
  • rheumatic heart disease, alcohol intoxication, thyrotoxicosis, hypertension, heart failure, hyperthyroidism
73
Q

name some cardiac causes of atrial tachyarrhythmias?

A 
hypertension
congestive heart failure
CAD
MI
valvular heart disease
cardiomyopathy 
myocarditis/pericarditis
WPW syndrome
sick sinus syndrome 
cardiac tumours
cardiac surgery
familial tachyarrhythmia
genetics
74
Q

name some non-cardiac causes of atrial tachyarrythmias?

A 
thyrotoxicosis
pheochromocytoma
pulmonary disease
pulmonary vascular disease
electrolyte disturbances
increased sympathetic tone
increased parasympathetic tone
postprandial arrhythmia
alcohol misues
caffeine, smoking, drug use
myotonic dystrophy 
Chagas' disease
75
Q

what is lone atrial fibrillation?

A

no cause can be found

76
Q

what chromosomal gene defects are linked to familial AF?

A

gene defects linked to chromosomes 10, 6, 5 and 4

77
Q

describe AF?

A
  • maintained by continuous, rapid (300-600/min) atria activation by re-entry wavelets driven by rapidly depolarising automatic foci
  • only a proportion of these are conducted to the ventricles
78
Q

what are the symptoms of atrial fibrillation?

A
  • incidental finding 30% of the time
  • rapid palpitations, dyspnoea and/or chest pain
  • deterioration of exercise capacity
79
Q

what are the signs of AF?

A
  • irregular pulse
  • ECG-fine oscillations of baseline, no clear p waves, rapid and irregular QRS rhythm
  • ventricular rate 120/180 when uncontrolled
80
Q

describe the management of acute AF?

A
  • if possible treat underlying cause
  • ventricular rate control
  • cardioversion with anticoagulation (DC shock or medically with antiarrythmic
  • anticoagulate
81
Q

what drugs are used in the treatment of AF for minimising thromboembolism?

A 
IV
-flecainide
-propafenone
-vernakalant 
-amiodarone
oral 
-flecainide
-propafenone
82
Q

what are the 2 strategies used for the long term management of AF?

A
  • rate control (AV nodal slowing agents plus oral anticoagulation)
  • rhythm control (antiarrhythmic drugs plus DC cardioversion plus oral anticoagulation
83
Q

In what patients is rhythm control advocated in?

A

younger patients
symptomatic
physically active

84
Q

describe rhythm control in treatment of AF?

A
  • recurrent paroxysms prevented with oral medications
  • no significant heart disease - any class Ia, 1c, III antiarrythmic (only use amiodarone when other medication fail)
  • heart failure/left ventricular hypertrophy - only amiodarone
  • coronary heart disease - stall, amiodarone
  • paroxysmal AF, early persistent AF-treat with left ablation
85
Q

what patients is rate control for AF appropriate in?

A
  • permanent form of arrhthmia with symptoms, improved by slowing HR or patients older than 65 with recurrent atrial tachyarrhythmias
  • persistent tachyarrhythmias and failed cardioversion and serial prophylactic anti arrhythmic
86
Q

describe rate control in treatment of AF?

A

digoxin, beta blockers, nondihydropyridine calcium channel blockers (verapamil or diltiazem)

87
Q

when is anticoagulation indicated in patients with AF?

A
  • AF related to rheumatic mitral stenosis or presence of prosthetic heart valve
  • CHADS2 score (CHADS2VASC score of 2 needs anticoagulation)
88
Q

what anticoagulants can be used in patients with AF?

A 
aspirin
warfarin
dabigatran 
apixaban
rivaroxaban
89
Q

what is atrial flutter?

A

organised atrial rhythm with atrial rate 250-350
typically involves macro re-entrant right atrial circuit around tricuspid annulus
regular sawtooth (F waves) between QRS complex
symptoms related to degree of AV block

90
Q

what is the management of atrial flutter?

A

cardioversion
if been in atrial flutter for more than 1-2 days should be treated similar way to AF.
anticoagulated 3 weeks prior to cardioversion
-class III antiarrythmics
-recurrent atrial flutter - catheter ablation

91
Q

give examples of ventricular tachyarrhythmias?

A
  • life threatening ventricular tachyarrhythmias
  • torsades de pointes
  • normal heart ventricular tachycardia
  • non-sustained ventricular tachycardia
  • ventricular premature beats
92
Q

what is the management for AVNRT and AVRT?

A

AV node blocking agents
class 1c or class III
catheter ablation

93
Q

what is the management for Wolff-parkinson-white syndrome?

A 
class Ic or class III
catheter ablation
94
Q

what is the management for AF?

A

maintain sinus rhythm
class 1c or class III with cardioversion
catheter ablation of ectopic focus
rate control: AV node slowing agents, AV node ablation plus pacemaker, anticoagulation

95
Q

what is the management for atrial flutter?

A

class 1c or class III
Catheter ablation
AV node blocking agents
anticoagulation

96
Q

what is the management of atrial tachycardia?

A

class 1c or class III
catheter ablation
AV node blocking agents
anticoagulation

97
Q

what is the management for life threatening ventricular tachyarrhythmias?

A

implantable cardioverter defibrillator

beta blockers

98
Q

what is the management for congenital long QT?

A

beta blockers with pacemaker ICD
correct bradycardia
correct electrolytes

99
Q

what is the management for acquired long QT?

A

beta blockers, calcium channel blockers, catheter ablation

100
Q

what is the management for non sustained VT?

A

beta blockers
class 1C and class III
ICD in certain subgroups

101
Q

what are the options for the long term management of cardiac tachyarrhthmias?

A
  • antiarrhythmic drug therapy
  • ablation therapy
  • device therapy
102
Q

what are class I antiarrythmics?

A

membrane depressant drugs reducing rate of sodium into the cel
slow conduction
delay recovery
reduce spontaneous discharge rate of myocardial cells

103
Q

what do class Ia drugs do and give an example?

A

disopyramide

lengthen action potential

104
Q

what do class Ib drugs do?

A

lidocaine

shorten the action potential

105
Q

what do class Ic drugs do?

A

flecainide, propafenone

don’t affect duration of acton potential

106
Q

what are class II antiarrythmics?

A 
anti sympathetic drugs
prevent effects of catecholamines on action potential
suppress AV nodal conduction
most are beta blockers
atenolol, propanolol, esmolol
107
Q

what are class III antiarrythmics?

A

prolong action potential
amiodarone and sotalol (beta blocker)
potassium channel blockers

108
Q

what are class IV antiarrhthmics?

A

calcium channel blockers
verapamil
diltiazem

109
Q

what is catheter ablation?

A

radiofrequency catheter ablation used in management of symptomatic tachyarrhythmias
3 or 4 electrode catheters placed into the heart chambers in order to record and pace from various sites
pacing atria or ventricles is used to trigger the tachycardia and mechanism

110
Q

what tachyarrhythmias can be readily ablated?

A 
AVNRT
AVRT
normal heart VT 
atrial flutter
atrial tachycardia 
atrial fibrillation
111
Q

what are implantable cardioverter defibrillators (ICD)?

A

improve survival patients who have had an episode of life threatening ventricular tachyarrhythmia
implanted in a postural position
recognises ventricular tachycardia or fibrillation and automatically delivers pacing or shock to cause cardioversion to sinus rhythm.

112
Q

what patients may benefit from prophylactic ICD placement?

A
  • CAD, significant left ventricular function impairment
  • NYHA class III-IV heart failure
  • poor LV function post MI
  • dilated and hypertrophic cardiomyopathy

Block 31 Cardio-respiratory (15 decks)

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