1
Q
what is retrograde conduction in the cardiac conduction cycle?
A
impulses that begin below the AV node can be transmitted backward toward the atria.
usually takes longer than normal conduction
causes atria and ventricles to beat out of sync
2
Q
what is an escape beat?
A
a compensatory beat generated by a lower pacemaker site (ie not SA node)
3
Q
what are the intrinsic firing rates of the different pacemaker cells of the heart?
A
SA node - 60 -100 bpm
AV junction - 40 to 60 bpm
Purkinje fibres - 20 to 40 bpm
4
Q
what are leads I, II, III of the ECG representing?
A
5
Q
on an ECG, how many large blocks = 1 second??
A
five large blocks
6
Q
A biphasic deflection will occur on an ECG if the electrical current is traveling in a direction ___
A
perpendicular to the positive electrode
7
Q
what does p wave represent?
A
atrial depolarization - conduction of electrical impulse through the atria
8
Q
peaked, notched or enlarged P waves represent?
A
atrial hypertrophy or enlargement
9
Q
inverted P waves represent? (ie. when upright sinus p waves -> becomes inverted)
A
may signify retrograde or reverse conduction from AV junction toward atria
10
Q
absent p waves represent?
A
may signify conduction by a route other than the SA node, as with junctional or atrial fibrillation rhythm
11
Q
varying p waves represent?
A
impulse may be coming from different sites, as with wandering pacemaker rhythm, irritable atrial tissue or damage near SA node
12
Q
which part of the cardiac conduction cycle does the PR interval represent?
A
tracks the atrial impulse from atria through AV node, bundle of His, and right/left bundle branches
-> long PR interval = conduction delay as seen in AV block
12
Q
what does the QRS complex represent?
A
depolarization of the ventricles (after which, they contract)
*so if broad QRS -> increased intraventricular conduction time -> may signify ventricular conduction delay
13
Q
normal deflection of QRS complexes?
A
positive in leads I, II, III, aVL, aVF, and V4 to V6
negative in leads aVR and V1 to V3
14
Q
missing QRS complex after p wave may signify?
A
AV block or ventricular standstill
15
Q
what does the ST segment represent?
A
end of ventricular conduction or depolarization and the beginning of ventricular recovery or repolarization
16
Q
1 small box on ECG is how much voltage?
A
0.1mV (1mm)
16
Q
ST segment depression significant if ?
A
> 0.5mm below baseline (ie 1/2 small box)
17
Q
ST segment considered elevated if?
A
1mm or more above baseline (ie. one small box)
18
Q
what does the T wave represent?
A
ventricular recovery or repolarization
19
Q
QT interval measures?
A
ventricular depolarisation and repolarisation
- extends from beginning of QRS complex to end of T wave
20
Q
prolonged QT increases risk of which arrhythmia?
A
torsades de pointes
20
Q
what is the U wave?
A
represents the recovery period of the purkinje or ventricular conduction fibres. not always present
prominent U wave may be 2’ hyperCa, hypoK, digoxin toxicity
21
Q
a standard 12 lead ECG strip captures how many seconds of data?
A
10 seconds
22
what supplies blood to the SA node?
either the right coronary artery or the left circumflex
23
SA node nerve supply?
affected by vagus nerve and several sympathetic nerves
24
why does sinus arrhythmia occur in response to respiration?
during inspiration, increase in blood flow back to heart -> reduces vagal tone -> HR increases
during expiration, venous return decreases -> increased vagal tone -> HR slows
24
sinus arrhythmia may occur with?
may occur naturally in athletes and children, relating to respiration
or
inferior wall MI, advanced age, digoxin use, morphine use, conditions involving increased intracranial pressure
25
if sinus arrhythmia develops suddenly in patient taking digoxin, what to be aware of?
digoxin toxicity
26
why may sinus bradycardia occur naturally during sleep?
reduced metabolic demands
27
potential causes of sinus bradycardia?
- post MI in which SA node affected
- drugs
28
symptomatic sinus bradycardia may occur because?
pt with underlying cardiac disease may not be able to compensate for drop in rate by increasing its stroke volume
->
drop in cardiac output
-> hypotension/ dizziness
29
clinical significance of sinus bradycardia depends on?
symptomatic or not?
how low is the rate? -> usually most adults can tolerate HR 45 and above
30
what cardiac diseases may result in sinus bradycardia?
- SA node disease
- cardiomyopathy
- myocarditis
- myocardial ischaemia
- post inferior wall MI
31
what conditions may produce excess vagal nerve stimulation and thus sinus bradycardia?
sleep, deep relaxation, valsalva manoeuvre, carotid sinus massage, vomiting
32
what drugs may cause sinus bradycardia?
BBs, digoxin, calcium channel blockers, lithium, and antiarrhythmics, eg sotalol, amiodarone, propafenone, and quinidine.
33
what non cardiac disorders may cause sinus bradycardia?
hyperK, increased intracranial pressure, hypothyroidism, hypothermia, glaucoma
34
what symptoms may u get with sinus bradycardia?
- hypotension -> dizziness/ LOC/ confusion/ syncope
- palpitations / pulse irregularities if experiencing more ectopic beats e.g. premature atrial, junctional or ventricular contractions
35
tx of sinus bradycardia if symptomatic?
- identify and correct underlying cause e.g. remove drug cause
- transcutaneous/ transvenous pacing
- permanent pacemaker insertion
- atropine/ adrenaline/ dopamine
36
Medications for symptomatic sinus bradycardia?
1st line: Atropine
-> dose 0.5mg, can be repeated every 3-5 mins to maximum of 3mg total
2nd line: Adrenaline infusion 2-10 mcg/min
3rd: dopamine infusion 2-10 mcg/kg/min
37
sinus tachycardia may be detrimental because?
- myocardial demands for oxygen are higher -> tachycardia can bring on an episode of chest pain in patients with CAD
- can be detrimental for patients with obstructive types of heart conditions such as HOCM, aortic stenosis
38
how can tachycardia lower cardiac output?
- reduces ventricular filling time and thus the amt of blood pumped each contraction
39
treatment of sinus tachycardia?
treat underlying cause
maintain adequate cardiac output and tissue perfusion
40
if tachycardia leads to cardiac ischaemia, what treatment can be given?
BBs, CCBs such as verapamil
41
what symptoms to check for in patients with sinus tachycardia?
- ask for chest pain/ angina (as tachycardia can -> myocardial ischaemia)
- check for signs / symptoms of HF
- intake / output
- evaluate for underlying cause e.g. pain, PE
42
what is sinus pause/arrest?
lack of electrical activity in the atrium, atrial standstill
-> entire PQRST complex will be missing from ECG strip
43
sinus pause vs sinus arrest
sinus pause: one or two beats not formed
sinus arrest: 3 or more beats not formed
44
conditions that can cause sinus arrest?
* sinus node disease, such as fibrosis and idiopathic degeneration
* increased vagal
tone: Valsalva maneuver, carotid sinus massage, and vomiting
* drugs: beta blockers, digoxin, quinidine, procainamide and salicylates
* cardiac disorders: chronic CAD, acute myocarditis, car- diomyopathy, and hyper- tensive heart disease
* acute inferior wall MI
* sick sinus syndrome
* acute infection
45
emergent treatment of patient with sinus pause and symptomatic?
- temporary pacing
- administration of atropine/ adrenaline
- stop offending drug if any!
- long term mx -> PPM
46
what symptoms to evaluate for if patient has recurrent sinus pauses?
- evidence of decreased cardiac output e.g. altered mental status, low BP, cool/clammy skin
- dizzy/lightheaded/ blurred vision/ syncope
47
what activities increase vagal stimulation and increase likelihood of sinus pauses?
valsalva manœuvre, vomiting
48
what is sick sinus syndrome aka sinus node dysfunction?
wide spectrum of SA node abnormalities: disturbances in the way impulses are generated or inability to conduct impulses to the atrium
49
how does sick sinus syndrome usually present?
one or a combination of:
* sinus bradycardia
* SA block
* sinus arrest
* sinus bradycardia alternating with sinus tachycardia
* episodes of atrial tachyarrhythmias, such as atrial fibrillation and atrial flutter
* failure of the sinus node to increase heart rate with exercise
50
why does sick sinus syndrome develop?
usually dysfunction of sinus node's automaticity or abnormal conduction or blockages of impulses coming out of the nodal region.
-> stem from a degeneration of the area's autonomic nervous system and partial destruction of the sinus node
51
causes of sick sinus syndrome?
- conditions leading
to fibrosis of the SA node, ie increased age, atherosclerotic heart disease, HTN, and cardiomyopathy
- trauma to SA node caused by open heart surgery, pericarditis, or rheumatic heart disease
* autonomic disturbances ie hypervagatonia and degeneration of the autonomic nervous system
* drugs e.g. digoxin, BB
52
what is considered a significant sinus pause?
2-3 seconds or more
53
sick sinus syndrome: what happens when you monitor the patient's heart rate during exercise or exertion?
may have an inappropriate response to exercise e.g. failure of the HR to increase
54
treatment in symptomatic sick sinus syndrome?
- temporary pacing/ PPM
- tachyarrhythmias may be treated with anti arrhythmic meds
- anticoagulation if assoc AF
55
Tx of sinus arrhythmia?
- no treatment if asymptomatic
- correction of the underlying cause
56
what mechanisms cause atrial arrhythmias to occur?
- enhanced automaticity of atrial fibres - triggering abnormal impulses
- circuit reentry: ie. delayed impulse due to slow conduction may end up producing another impulse during repolarization. e.g. in CAD, CMP, MI
- afterdepolarization: repetitive ectopic firing due to injured cell being partly repolarized
57
causes of increased automaticity causing atrial arrhythmias?
hypoxia, acidosis, hypoCa/ hypoK, digoxin toxicity
conditions what diminish SA node activity like increased vagal tone or hypoK can increase refractory period of SA node -> allowing atrial fibres to fire impulses
58
what are premature atrial contractions?
impulse originating outside the SA node, usually from an irritable focus in the atria
59
what can trigger Premature atrial contractions (PACs)?
alcohol, nicotine, anxiety, fatigue, fever, infection
coronary or valvular heart disease, respiratory failure/hypoxia, digoxin toxicity, electrolyte imbalances
60
PACs in heart disease may signify?
PACs may lead to serious arrhythmias e.g. AF/A Flutter
61
PACs in normal people?
usually of no concern as does not usually cause symptoms
62
PACs may be an early sign of what after an acute MI?
heart failure or electrolyte imbalance
63
Tx of PACs?
- asymptomatic no need tx
- if symptomatic, tx underlying cause e.g stop caffeine/ ETOH/ nicotine
64
mx of PACs in patient with ischaemic heart or valvular heart disease?
monitor for sign/symptoms of HF, electrolyte imbalances and development of more severe atrial arrhythmias
65
what is atrial tachycardia?
a form of SVT.
- usually 150-250 bpm
- rapid rate shortens diastole, resulting in loss of atrial kick, reduced CO, reduced coronary perfusion and ischaemic myocardial changes
66
what are the 3 different types of atrial tachycardia?
atrial tachycardia with block
multifocal atrial tachycardia
paroxysmal atrial tachycardia (PAT)
67
what cardiac conditions may cause atrial tachycardia?
- MI
- cardiomyopathy
- congenital anomalies
- WPW syndorme
- valvular heart disease
- component of sick sinus syndrome
- cor pulmonale
- hyperthyroidism
- systemic HTN
- digoxin toxicity (most common cause)
68
when may atrial tachycardia occur in patients without cardiac conditions?
- excess caffeine/ stimulants
- marijuana use
- electrolyte imbalances
- hypoxia
- physical/ emotional stress
69
complications of atrial tachycardia?
- angina
- heart failure / reduced EF
- ischaemic myocardial changes/ MI
70
signs of digoxin toxicity?
* CNS: fatigue, general muscle weakness, agitation, hallucinations
* Eye: yellow-green halos around objects, blurred vision
* GI: anorexia, nausea, vomiting
* CV: arrhythmias (most commonly, conduction disturbances with or without AV block, PVCs, and supraventricular arrhythmias), increased severity of heart failure, hypotension
71
rhythm in atrial tachycardia?
atrial rhythm is always regular,
ventricular rhythm is regular when AV block is constant and irregular when it isn’t
72
Atrial tachycardia with block
73
multifocal atrial tachycardia
- whereby numerous atrial foci are firing intermittently
> commonly see p waves with different configurations throughout the rhythm strip
74
what condition is multifocal atrial tachycardia Assoc w?
commonly seen in COPD
75
Paroxysmal atrial tachycardia (PAT)
- brief periods of tachycardia that alternate with periods of normal sinus rhythm
- due to rapid firing of an ectopic focus.
- commonly follows PACs
76
tx of atrial tachycardia?
- tx cause: e.g. if digoxin toxicity
- valsalva manoevure/ carotid sinus massage (but avoid in older adults)
- drugs: e.g. digoxin, BB, CCB
- atrial overdrive pacing
- if clinically unstable, synchronised cardioversion
77
risks of valsalva manouvre/ carotid sinus massage?
- stimulation of vagus nerve which inhibits SA node firing and slows AV node conduction
-> decreased HR, vasodilation, ventricular arrhythmias, stroke, cardiac standstill
78
what is atrial overdrive pacing, how can it help in atrial tachycardia?
helps to suppress the depolarization of the ectopic pacemaker and permits the SA node to resume its normal role
79
risks of atrial flutter?
if rate is too fast (ie >150 bpm), cardiac output and coronary perfusion is compromised
-> angina, heart failure, pulmonary oedema, hypotension, syncope
80
how does atrial flutter occur?
originates from single atrial focus, results in circuit reentry and possibly increased automaticity
usually 300 bpm.
commonly Assoc with 2nd degree block -> ventricular rate 150 bpm
81
causes of atrial flutter?
conditions that enlarge atrial tissue and increases atrial pressures
- severe mitral valve disease
- hyperthyroidism
- pericardial disease
- primary myocardial disease
- post cardiac surgery
- post MI
- COPD
82
tx of atrial flutter, haemodynamically unstable
synchronised electrical cardioversion
83
tx of atrial flutter in haemodynamically stable patients?
- rate and rhythm control
+ depends on duration of arrhythmia (e.g. <48h or >), patient's cardiac function, whether preexcitation syndromes are involved
84
tx of patient with atrial flutter <48h duration + normal cardiac function?
Consider direct current (DC) cardioversion
85
Any second upward deflection is called
R’
Ie RSR pattern
86
If the entire QRS complex consists of one large downward deflection, then this is called a QS wave.
87
Pathophysiology of mitral stenosis
MS restricts flow between LA and LV
->
Elevated LA pressures
-> pulmonary congestion
Eventually may cause RV failure
Also reduced LV filling means lower cardiac output
88
what precordial leads correspond to the right ventricle?
V1, 2, 3
89
what precordial leads correspond to the basal septum?
V2 and V3
90
what precordial leads correspond to the anterior wall of the left ventricle?
V2, V3, V4
91
what precordial leads correspond to the lateral wall of the LV?
V5, 6
92
what precordial leads correspond to the posterior wall of the LV?
V7 and V8
93
V5, 6, 7, 8 ST Elevation?
Posterolateral STEMI
94
V4, 5, 6 ST elevation?
Anterolateral STEMI
95
what are the laws of the R/S ratio?
1. under normal circumstances (ie LV stronger and bigger than RV)
- leads with R/S ratio <1 correspond to RV
- leads with R/S ratio > 1 correspond to LV
- leads with R/S ratio = 1 correspond to transition zone between the RV and LV (ie. inter ventricular septum)
2. Under normal circumstances, the R/S ratio increases as you go from right to left
96
usually which lead has R/S ratio of 1 and corresponds to the transitional zone?
V4
97
what happens if you see R/S ratio of 1 earlier e.g. in V2?
usually means counterclockwise rotation of the heart, meaning the V2 now represents the transition zone
98
what happens if you see R/S ratio of 1 in V6?
usually means clockwise rotation of the heart, such that V6 represents the transition zone
99
when can you not use R/S ratio to assess rotation of the heart?
1. Bundle branch block
2. Q wave infarction
3. Wolff-Parkinson-White syndrome
100
which lead corresponds to the transition zone?
the lead with R/S ratio of 1
101
precordial leads: where do you usually see TWI?
V1
102
precordial leads: what does p wave normally look like in v1?
negative or biphasic
103
where might you see normal Q waves in precordial leads?
usually v6, or ever v4-5
(but not V1-3)
104
some causes of delayed conduction of ventricles
- dilated or hypertrophic ventricles
- bundle branch block
105
how to look for left bundle branch block on ECG
RSR pattern over V5-6, with notching
+ QRS >0.12s
-> delayed depolarisation of the LV
106
RBBB on ECG?
RSR pattern with QRS >0.12s over V2
107
what is incomplete bundle branch block?
QRS 0.10-0.12s
108
how to look for LVH on ECG?
V1/2 S wave and V5/6 R waves represent LV ventricular mass
-> add the deeper S wave in V1/2 with the taller R wave in V5/6
-> if >35mm then = LVH
109
how to look for RVH on ECG?
"RSS"
R V1: >/=5mm
S V1: R/S ratio >/=1
S V5: >/= 5mm
-> 1 positive: suggestive, 2 positive: likely, 3 positive: very likely
110
downsloping ST depression usually seen in ?
ventricular hypertrophy
111
very deep ST depressions?
usually severe ischaemia
112
horizontal ST depression usually associated w?
coronary heart disease
113
upsloping ST depressions?
sympathetic tone e.g exercise
non specific for coronary artery disease
114
sagging/ scooping ST depression?
digoxin toxicity
hypoK
coronary artery disease
115
when looking at inverted T waves, what does symmetry / asymmetry suggest?
asymmetry more likely hypertrophy
symmetry more suggestive of ischaemia
116
when may you see T wave inversions that are difficult to interpret ie may not be ischaemic?
if there is inter ventricular conduction delay
- bundle branch block
- premature ventricular beats
- wolff Parkinson white syndrome
117
Usual pattern of q waves from V4-6?
Might see normal small q wave in v4-6 but should get larger from 4-6
(If large q waves in V4-5 compared to 6 think abt infarct in that area)
118
Q waves getting deeper w infarction
119
Example of loss of r wave as a sign of MI in leads w deep s
120
Another eg of how lead without q can develop q waves
In general leads w deep S waves should not have q waves
121
How do qrs complexes usually look like in v1-3
Usually starts w r wave
122
What happens to r wave as we move from v1-5/6
Gets larger
123
When are q waves considered abnormal
1) > 1 small box (0.04s)
2) >= 1/4 of R wave size
124
Inferior wall MI changes?
ST elevation in II, III and aVF
And reciprocal changes in V1,2,3
125
Which limb leads demonstrate the inferior portion of the heart
II III aVF
126
Which limb leads demonstrate lateral aspect of the heart
I and aVL
127
Inferior wall MI changes?
ST elevation in II, III and aVF
And reciprocal changes in V1,2,3
128
What is the Sgarbossa criteria for
Diagnosing STEMI in LBBB or ventricular paced rhythms
129
Smith modified sgarbossa criteria
1) Concordant ST elevation ≥ 1 mm in ≥ 1 lead
2) Concordant ST depression ≥ 1 mm in ≥ 1 lead of V1-V3
3) Proportionally excessive discordant STE in ≥ 1 lead anywhere with ≥ 1 mm STE, as defined by ≥ 25% of the depth of the preceding S-wave
130
Persistent ST elevation in the anterior leads?
Could be myocardial aneurysm
131
Normal axis on ecg
I and II positive
-30 to + 90
132
Left axis deviation on ecg
I positive
II negative
133
Right axis deviation on ecg
I negative
aVF positive
134
What is north west axis on ecg
I negative
aVF negative
135
Right axis deviation on ecg
I negative
aVF positive
136
What are your axes on ECG
137
RBBB + right axis deviation
RBBB. + Left posterior fascicular block
138
RBBB + left axis deviation
RBBB + left anterior fascicular block
139
normal P wave
usually upright in lead II, may be bifid in V1
140
what kind of p wave will u see with RA hypertrophy
p pulmonale
- large p in V1, II (or I, aVF)
141
p wave in left atrial hypertrophy?
p mitrale usually seen in II
more negative P wave in v1
142
Features of right atrial enlargement
P-wave height in the inferior lead ≥2.5 mm (2.5 small boxes)
143
Normal rate of a junctional rhythm
40-60
144
Junctional rhythm + Rate 61-99
Accelerated junctional rhythm
145
Junctional rhythm + rate >100
Junctional tachycardia
146
How to differentiate junctional from ventricular escape rhhythm
Junctional: usually 40-60bpm + narrow complex qrs (unless underlying BBB)
Ventricular escape: rate 30-40 + usually wide complex
147
Mobitz type 1 vs mobitz type 2 implications
Mobitz type 1 (prolonging PR interval then dropped beat) usually a benign finding - can be due to increased vagal tone
Mobitz type 2 (fixed PR interval until dropped beat): usually indicates structural disease in AV node or his-purkinje system and is an indication for Pacemaker implantation
148
DDX of STEMI
• Prinzmetal angina (variant angina), in which there is vasospasm of a coronary artery
• Cocaine-induced MI, in which there is vasospasm of a coronary artery, with or without additional thrombotic occlusion
• Takotsubo (stress) cardiomyopathy.
• Brugada syndrome
• Pericarditis, in which there is usually diffuse ST-segment elevation.
• Left ventricular aneurysm
• Left bundle branch block (LBBB).
• LVH with repolarization abnormalities.
• J-point elevation, which is felt to be due to “early repolarization.”
• Severe hyperkalemia
• Hypercalcemia
149
What is electrical alternans?
In the presence of large pericardial effusions, the heart may “swing” resulting in an alteration of the amplitude of the QRS complex
150
What are cerebral T waves
strikingly deep and inverted T waves, most prominently seen in the precordial leads
most notably with subarachnoid and intracerebral hemorrhages
due to prolonged and abnormal repolarization of the LV, presumably secondary to autonomic imbalance
151
How to differentiate VT from SVT with aberrancy
Brugada criteria:
More likely VT if 1 or more
• Concordance in precordial leads (all QRS complexes upright or downward in precordial leads).
• Initiation of R wave to peak of S-wave duration >100 milliseconds.
• AV dissociation (especially if more QRS complexes than P waves are present).
152
Wellens suggestive of
Prox LAD stenosis
Cardiology 101
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