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Phase 3 > Week 5 > Flashcards

Week 5 Flashcards

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1
Q

In what situations is ECG first line?

A

for patients with chest pain, palpitations or blackouts

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2
Q

Which are the unipolar ECG leads?

A

Limb leads - aVR, aVL, aVF

chest leads V1-V6

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3
Q

Which are the bipolar leads?

A

Leads I, II and III

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4
Q

What does lead I measure?

A

RA-LA

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5
Q

What does lead II measure?

A

RA-LL

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6
Q

What does lead III measure?

A

LA-LL

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7
Q

Why can atrial depolarisation not be seen in ECG?

A

lost in QRS complex

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8
Q

What is the P wave?

A

atrial depolarisation

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9
Q

What does the QRS complex represent?

A

ventricular depolarisation

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10
Q

What is the ST segment?

A

plateau phase of repolarisation

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11
Q

What is the T wave?

A

Final rapid repolarisation

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12
Q

What is the Q wave?

A

conduction through perkinje fibres

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13
Q

Describe the systemic approach to any ECG

A 
clinical context
date, time, patient details 
assess technical quality 
Identify P /QRS /T
measure heart rate
check ECG intervals
Determine QRS axis
Look at P/QRS /T morphology 
Do not rely on automatic interpretation
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14
Q

How can you quickly determine heart rate from an ECG?

A

300 divided by the number of large squares between each QRS complex
or number of QRS complexes across 10 seconds X 6

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15
Q

What is the normal range for a PR interval?

A

<1 large square

<200ms

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16
Q

What does a prolonged PR interval suggest?

A

heart block

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17
Q

What us the normal range for QRS?

A

<3 small squares

<120ms

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18
Q

What does a prolonged QRS complex mean?

A

bundle branch block

or life threatening hypokalaemia - dehydration, renal impairment

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19
Q

What is the normal QT interval

A

<11 small squares

<440ms

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20
Q

What does a prolonged QT internal suggest?

A

Associated with ventricular tachycardia

can go into VF. young patient with syncope

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21
Q

What is meant by the QRS axis?

A

direction of average depolarisation in the heart - dominated by left ventricular depolarisation

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22
Q

How is the QRS axis determined?

A

from limb leads
relative to lead I
normal is -30 to +90 degress
axis is approximated by dissing the lead with the most +ve QRS

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23
Q

IN a normal axis, where is the QRS positive?

A

I and II

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24
Q

Describe left axis deviation

A

-30 to -90 degrees

positive QRS in I, negative in II and aVF

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25
What does left axis deviation suggest?
left ventricular hypertrophy
26
Describe right axis deviation
+90 to +180 degrees | (negative QRS in I, positive in aVF
27
What does right axis deviation suggest?
hypertrophy of the right ventricle - pulmonary hypertension
28
Describe extreme axis deviation
+180 to -90 degrees | (negative QRS in I and II, positive in aVR
29
What does extreme axis deviation suggest?
ventricular tachycardia | paced ryhthm, all impulses could be in ventricle if pace maker is there
30
Describe normal P/QRS/T morphology
P wave is upright in the inferior leads Normal ST segment is flat T wave has the same polarity as the QRS
31
How can P waves be described?
positive, negative or biphasic
32
How are QRS complexes described if the first deflection is negative?
Q wave
33
What is the name for a positive deflection in QRS complex?
R wave
34
Wha t is the name for any negative deflection after R?
S wave
35
How can the ST segment be described?
isoelectric, elated or depressed
36
How can any further positive deflection after R be described in the QRS complex?
R'
37
How can T waves be described?
upright, inverted or flat | - also concordant or discordant vs QRS
38
Describe left bundle branch block
``` broadening of QRS complex characteristic negative QRS complex in VI positive in V6 T waves are discordant notching of V6 ```
39
Describe right bundle branch block
inverted T waves in VI V6- no discordant T waves Left ventricular repolarisation
40
How do you recognise an arryhtmia?
``` What is the QRS rate are the QRS complexes regular? is the QRS board or narrow? Are there P waves What is the P:QRS relation? ```
41
What types of bradyarrythmias are there?
sinus bradycardia junctional bradicardia atrioventricular block - first degree, second degree, Mobitz I/II, third degree
42
Describe sinus bradycardia
rate <60bpm regular, narrow QRS P waves present P:QRS is 1:1
43
Describe junctional bradycardia
rate <60bpm regular, narrow QRS No P waves present
44
Describe second degree AV block - mobitz type 1
slowest rate <60bpm irregular narrow QRS P:QRS not 1:1 regularly irregular
45
Describe second degree AV block - mobitz type II
slowest rate <60bpm irregular narrow QRS P:QRS not !:! often indication for pace maker
46
Describe complete AV block
rate <60bpm regular broad QRS no relation between P and QRS
47
What drug may be used to treat bradyrhythmias?
atropine | anticholinergic - decreases vagal tone
48
What appearance does a pacemaker have on ECG?
looks like left bundle branch block
49
Give examples of regular narrow complex tachycardias
sinus/junctional | SVT
50
Give examples of irregular narrow tachycardias
AF
51
Give examples of broad complex regular tachycardias
monomorphic VT | SVT with BBB
52
Give examples of broad complex irregular tachycardias
polymorphic VT AF with BBB pre-excited AF
53
Describe sinus tachycarida
rate >100 bpm regular, narrow QRS P waves present P:QRS is I:I
54
Describe atrial fibrillation
rate variable - fast irregular, narrow QRS no P waves
55
Describe atrial flutter
macro-reentrant atrial tachycardia regular narrow QRS sawtooth atrial activity - about 300bpm may get variable AV block
56
Describe supraventricular tachycardia
``` rate - more than 150bpm regular, narrow QRS P waves present P:QRS is 1:1 AVRT, AVNRT or atrial tachycardia ```
57
Describe broad complex tachycardia
``` regular borad QRS P waves may still be seen ventricular tachycardia SVT with BBB SVT over an accessory pathway ```
58
How can VT and SVT be differentiated?
fusion beats, capture beats, AV dissociation, extreme rightward or NW axis, or QRS concordance more likely to be VT if in doubt always treat as VT
59
What does ST elevation in the anterior leads suggest?
MI in left anterior descending artery
60
What does ST elevation in lateral leads suggest?
MI is distal, left anterior descending artery or circumflex artery
61
What does ST elevation in the inferior leads suggest?
MI in right coronary artery or circumflex
62
What is heart failure?
failure of the heart to pump blood at a rate sufficient to meet the metabolic requirements of the tissues - caused by an abnormality of any aspect of cardiac function and with adequate cardiac filling pressure
63
How is heart failure characterised?
by typical haemodynamic changes (systemic vasoconstriction) and neurohumoral activation
64
What does heart failure cause clinically?
breathlessness, effort tolerance, fluid retention, and is associated with frequent hospital admission and poor survival
65
What are common causes of heart failure in the UK?
``` coronary artery disease hypertension idiopathic toxins genetic ```
66
What are the less common causes of heart failure in the UK?
``` valve disease infections congenital heart disease metabolic pericardial disease (e.g. TB) endocardial disease ```
67
Describe HF-REF
systolic HF younger more often male coronary aetiology
68
Describe HF-PEF
diastolic HF older more often female hypertensive aetiology
69
Describe chronic (congestive) heart failure
present for a period of time | may have been acute or become acute
70
Describe acute (decompensated) heart failure
usually admitted to hospital worsening of chronic new onset
71
Describe the pathophysiology of heart failure
myocardial injury left ventricular systolic dysfucntion perceived reduction in circulating volume and pressure neurohumoral activation systemic vasoconstriction renal sodium and water retention which leads to further left ventricular systolic dysfuction
72
What hormones are related in response to heart failure?
SNS RAAS ET, AVP etc natriuretic peptides
73
What are the symptoms of heart failure?
dyspnoea and cough ankle swelling fatigue/ tiredness
74
What are the signs of heart failure?
``` peripheral oedema elevated JVP third heart sound displaced apex beat pulmonary oedema pleural effusion ```
75
Describe NYHA class I
no symptoms and no limitation in ordinary physical activty
76
Describe NYHA class II
mild symptoms (shortness of breath or angina) and slight limitation during normal activity
77
Describe NYHA class III?
marked limitation in activity due to symptoms, even less than ordinary activity - walking short distances only comfortable at rest
78
Describe class IV NYHA
severe limitations | experience symptoms even while at rest. mostly bedbound
79
What investigations will all patients receive for heart failure?
``` ECG CXR echocardiogram blood chemistry haematology natriuertic peptides ```
80
What investigations will selected patients get for heart failure?
``` coronary angiography exercise test adulatory ECG monitoring myocardial biopsy genetic testing ```
81
Describe the treatment of heart failure
``` Beta blocker and ACE inhibitor (or ARB) MRA sacubitril/valsartan ICD or CRTP/CRTD, ivabradine digoxin consider transplant ```
82
What affect does angiotensin II have on the blood vessels?
``` vasoconstriction SMC hypertrophy superoxide generation enodthelin secretion monocyte activation inflammatory cytokines reduced fibrinolysis ```
83
What affect does angiotensin II have on the kidneys?
sodium and water retention efferent arterial vasoconstriction globular and interstitial fibrosis
84
What affect does angiotensin II have on the heart?
``` cellular hypertrophy myocyte apoptosis myocardial fibrosis inflammatory cytokines coronary vasoconstriction positive isotropy proarrythmia ```
85
What affect does angiotensin II have on the adrenal gland?
aldosterone secretion
86
What affect does angiotensin II have on the brain?
vasopressin secretion | sympathetic activation
87
What do natriuretic peptides do?
vasodilation natriuresis diuresis inhibition of pathologic growth/fibrosis
88
What does neprilysin do?
breaks down natriuretic peptides
89
What can be seen in chest X-ray in stage I heart failure?
redistribution pulmonary vessels | cardiomegaly
90
What can be seen on chest X-ray in stage 2 heart failure?
kerely lines peribronchial cuffing hazy contours of vessels thickened interlobar fissures
91
What can be seen on chest x-ray in stage 3 heart failure?
consolidation air bronchogram cottonwool appearance pleural effusions
92
Describe redistribution of pulmonary vessles
in the normal chest x-ray vessels in lower zones are larger than equivalent vessels in upper zones if vessels in upper zones are enlarged them elevated pulmonary venous pressure should be considered
93
What are kerley B lines?
spatial lines - fid leakage into interlobular septa seen at bases perpendicular to the pleural surface if transient or rapidly developing virtually diagnostic of pulmonary oedema
94
What are kerly A lines?
caused by distension of the anastomotic channels between the peripheral and central sympathetic oblique
95
What are kerly c lines?
reticular opacities at the lung bases
96
What are the signs of interstitial oedema?
peribronchial cuffing | hazy contour of vessles
97
Describe peribronchial cuffing
normally walls of bronchi are invisible | when fluid collects in peribronchial interstitial space the bronchial walls become visible
98
Describe hazy contour of vessels
not only enlarged but lose their defined margin due to surrounding oedema requires previous examinations
99
Describe subpleural pulmonary oedema
fluid can accumulate in the loose connective tissue beneath the visceral pleura seen as a sharply defined band on increased density
100
Describe alveolar oedema
represents spill of fluid from interstitial into alveolar spaces resulting in airspace opacity bilateral usually butterfly distribution rapid change - infection slower than HF
101
Describe pleural effusions
fluid within potential space between parietal and visceral layers divided into transudates and exudates
102
When are transudates found in pleural effusions?
LVF, cirrhosis, nephrotic syndrom | myxoedema, PE, sarcoidois
103
When are exudates found in pleural effusions?
PE, bacterial infection, bronchial ca | fungal/viral infection. lymphoma
104
What is the appearance of pleural effusions on chest X-ray?
homogenous lower zone opacity with a curvilinear upper border large effusions obscure heart border and displace mediastinum, airways and diaphragm
105
Describe subpolmonic effusion
fluid can accumulate in a subpulmonic location can be difficult to detect as upper edge of fluid mimics contour of diaphragm principle sign is apparent elevation of hemidiaphragm
106
What is a valve?
a device for controlling the passage of fluid thorough a pipe or duct, especially an automatic device allowing movement in one direction only
107
What can go wrong with valve leaflets?
``` calcification thickening degeneration infection prolapse ```
108
What can go wrong with the valve apparatus or annulus?
annular dilitation annular calcification apparatus tethering/thickeing/ rupture regional wall motion abnormality
109
What does stenosis cause?
pressure overload increased pressure in LV hypertrophy
110
What does regurgitation cause?
volume overload | ventricles start to dilate due to increased volume
111
Describe rheumatic valve disease
acute rheumatic fever mainly strep pyrogens throat infections antibody cross reactivity affecting connective tissue cardiac injury generated by recurrent inflammation and fibrinous repair and scarring less prevalent in antibiotic age
112
Describe the aortic valve
lies between LV and aorta 3 cusps right, less, non coronary
113
What can cause aortic stenosis?
thickening calcification rheumatic valve disease congenital
114
What are the symptoms of aortic stenosis?
shortness of breath pre syncope chest pain reduced exercise capacity
115
What can cause aortic regurgitation?
``` degeneration rheumatic valvular disease aortic root dilatation systemic disease endocarditis ```
116
Which systemic diseases can cause aortic regurgitation?
marfan's syndrome ehlers danlos syndrome ankylosing spondyltis SLE
117
What are the symptoms of aortic regurgitation?
shortness of breath | reduced exercise capacity
118
Describe bicuspid aortic valves
prone to premture dysfunction associated with aortic abnormalities genetic component
119
Describe the mitral valve
lies between LA and LV 2 leaflets anterior and posterior
120
Describe mitral stenosis
``` rheumatic valve disease pressure overload dilated LA atrial fibrilation pulomary hypertension secondary right heart dilatation ```
121
What are the symptoms of mitral stenosis?
``` shortness of breath palpitation chest pain haemoptysis right heart failure symptoms ```
122
Describe mitral regurgitation?
``` volume overload - LA/LV LV and LA dilatation pulomary hypertension secondary right heart dilatation atrial fibrillation ```
123
What are the symptoms of mitral valve regurgitation?
shortness of breath palpitation right heart failure symptoms
124
Describe the pulmonic valve
3 leaflets | lies between RV and pulmonary artery
125
Describe the tricuspid valve
3 leaflets | lies between RA and RV
126
How are valve defects assessed?
``` history examination blood pressure ECG echo CT MRI exercise tolerance tesr CPET stress echo catheterisation ```
127
What is infective endocarditis?
infection of the endocardium and/or intra-cardiac devices | can lead to formation of vegetation and destruction of cardiac tissue
128
What are the cardiac risk factors for infective endocarditis?
``` existing valvular heart disease congenital heart disease prosthetic heart valves indwelling cardiac devices `past history of IE ```
129
What are the non-cardiac risk factors for infective endocarditis?
``` immunodeficiency diabetes alchohol dependency indwelling IV lines IV drug use (mostly right sides IE) ```
130
How do people get IE?
``` dental manipulation dental disease extra-cardiac infection invasive procedure cardiac surgery IV drug use no clear cause ```
131
Describe staphylococci in endocarditis
aureas - 26.6% - IVDU | coagulase negative staph - epidermis, device/line related or early PVE
132
Describe streptococci and enterococci in IE
oral stereo - 18.7% non-oral - associated with colorectal cancer enterococci - 10.5%
133
What does HACEK stand or?
haemophilus, aggregatibacter, cardiobacterium, eikenella corrodens, kingella
134
how does IE develop?
endothelial injury caused by valve sclerosis, rheumatic valvulitis or direct bacterial activty development of non-infected platelet thrombus bacterial adherence to thrombus and colonisation further cycles of endothelial injury and thumbs deposition leads to formation of bacterial vegetation
135
Describe acute IE
acute and aggressive onset of symptoms often due to staph areas progressive valve destruction and metastatic infection
136
Describe subacute IE
insidious, non specific presentation strep viridian's most commonly metastatic infection uncommon
137
What are the symptoms of IE?
``` fever fatigue anorexia weight loss night sweats dyspnoea ```
138
What are the symptoms of embolic phenomena in IE?
stroke, meningitis, lung assess, emboli abdominal pain back pain - osteomyelitis
139
When should IE be considered?
fever in presence of risk factors sepsis of unknown origin evidence of embolic phenomena history,
140
What are the vascular phenomena in IE?
``` septic embolism - stroke, digital gangrene spilnter haemorrhages laneway lesions conjunctival haemorrhages pulmonary , renal or splenic infarcts petechial rash ```
141
What are the immunological phenomena in IE?
glomerulonephritis oslers nodes roth spots
142
What are some other sign's of IE?
murmur splenomegaly neurological signs nail clubbing
143
What are osier's nodes?
painful, eryhtmetous nodular lesions, necrotising vasculitis
144
What are janeway lesions?
non painful, erythematous, blanching macule , embolic microabscesses
145
What are splinter haemorrhages?
non-blanching, linear, reddish-brown lesions - not full length of nail
146
Describe roth spots
retinal haemorrhages with pale centres
147
What can cause nail clubbing?
atrial myxoma, cyanotic congenital heart disease, bronchietactis, interstitial lung disease and lung cancer
148
What are the major clinical criteria in modified duke diagnosis of IE?
blood cultures positive for infective endocarditis | evidence of endocardial involvement - echo / valvular regurgitation
149
what are the minor clinical criteria in the diagnosis of IE?
``` predisposition fever vascular phenomena immunological phenomena microbiological eveidence ```
150
When is IE diagnosis definite ?
two major criteria one major and three minor criteria 5 minor criteria
151
What antibiotics are used fro NVE?
amoxicillin / flucloxacilin/ gent
152
What antibiotics are used for PVE?
vancomycin/gentamycin/rifampicin
153
What are the indications for cardiac surgery in IE?
valve dysfunction leading to heart failure uncontrolled infection prevention of embolism
154
What are the symptoms of MI?
``` chest pain back pain jaw pain indigestion sweetness/claminess shortness of breath none (diabetes / dementia) death ```
155
What are the signs of MI?
``` tachycardia distressed patient heart failure(crackles, raised JVP) shock arrhythmia none ```
156
What is troponin?
part of cardiac myocyte | release in blood stream is a marker of cardiac necrosis
157
What is the universal definition of MI?
any elevation in troponin in clinical setting consistent with MI
158
What is type 1 MI?
spontaneous MI due to primary coronary event
159
What is type 2 MI?
increased oxygen demand /decreased supply - heart failure, sepsis, anaemia, arryhtmias, hypertension or hypotension
160
What is type 3 MI?
sudden cardiac death
161
What is type 4a MI?
MI associated with PCI
162
What is type 4b MI?
Stent thrombosis documented by angiography or PM
163
What is type 5 MI?
MI associated with CABG
164
What are cases of type 2 MIs?
``` congestive heart failure tachyarrythmias PE sepsis apical ballooning syndrome anything that stresses the heart ```
165
What can cause chronic troponin elevation (not MI)
renal failure chronic heart failure infiltrative cardiomyopathies
166
What is unstable angina?
an acute coronary event without rise in tropnin
167
how can a stem in posterior wall be detected in ECG?
anterior ST depression
168
what is the immediate management of a STEMI?
``` ABCD ambulance, defib aspirin 300mg PO UF heparin morphine anti-emetics clopidogrel ticagrelor (in hospital) activate PPCI team ```
169
How does primary PCI compare to thrombolysis?
``` improves survival reduced strokes reduces repeated MI reduces further angina speeds up reconvery shortens time in hospital ```
170
What is the subsequent management of a STEMI?
coronary care unit drugs for secondary prevention echo for LV function and cardiac structure cardiac rehab
171
What drugs are used for secondary prevention of MI?
ACE inhibitors BB statins eplerenone (diabetes / clinical heart failure)
172
When would an ICD be considered following an MI?
if LVSD > 9 months
173
What are the complications of an MI?
``` arrthymias heart failure cariogenic shock myocardial rupture psychological ```
174
What is the definition of hypertension?
persistant elevevation in retrial blood pressure >140/90 a BP level that increases the vascular risk in patients sufficient to require intervention the threshold at which benefits of action exceed those of inaction
175
What is optimal BP?
<120/ <80
176
What is normal BP?
120-129 | 80-84
177
What is high normal BP?
130-139 | 85-89
178
What is grade 1 hypertension?
140-159 | 90-99
179
What is grade 2 hypertension?
160-179 | 100-109
180
What is grade 3 hypertension?
>180 | >110
181
What is isolated systolic hypertension?
>140 | <90
182
What are the non-modifiable risk factors for primary hypertension?
age gender ethnicity genetic factors
183
What are the modifiable risk factors for primary hypertension?
``` diet physical activity obesity alcohol excess stress ```
184
What are the causes of secondary hypertension?
``` hyperaldosteronism thyroid disorders phaeochromocytoma renal artery stenosis exogenous steroid use NSAIDs herbal remedies cocaine ```
185
What are the two out of office BP measurement techniques?
24 hour ambulatory blood pressure monitoring | home blood pressure monitoring
186
What initial investigations can be carried out in a patient with hypertension?
``` U&Es electrolytes glucose lipid profile TFTs LFTs urine dipstick 12 lead ECG ```
187
What additional tests can be used in the elevation of hypertension?
``` renin and aldosterone 25 hour urine catecholamines echo renal ultrasound MRA renal ```
188
How is the cardiovascular risk assessed in hypertension?
``` BP category presece of end organ damage presence of diabetes CV renal disease ```
189
How can hypertension be managed?
lifestyle measures pharmacological management renal denervation
190
What medications can be used to treat hypertension?
diuretics ACE inhibitor /ARBs vasodilators- calcium channel blockers, beta blockers, alpha blockers
191
IN a patient under the age of 55, what are the steps in the pharmacological management of hypertension?
ACE inhibits or ARB then add calcium channel blocker then add thiazide diuretic consider alpha or beta blocker
192
What are the stages in the pharmacological management of patients over 55 or black patients with hypertension?
calcium channel blocker then add ACEI then add thiazide diuretic then consider beta/alpha blocker s
193
How is AF diagnosed?
irregularly irregular rhythm no discernible P waves >30 seconds
194
What are the other key ECG changes in AF?
absence of isoelectric baseline | fibrillary waves may be present
195
What is atrial flutter?
caused by re-entry circuit within RA length of re-entry circuit corresponds to size of RA predictable atrial rate about 300bpm ventricular rate determined by AV conduction ratio i.e. if 2:1 then ventricular rate will be about 150bpm
196
What is meant by a type 1 flutter?
typical IVC and tricuspid isthmus in circuit anti-clockwise or clockwise
197
What is a type 2 flutter?
atypical does not fit typical criteria less amenable to ablation
198
How is AF classified?
paroxysmal (<48 hours) persistent (>7 days or requires CV) long standing (>1 year) permanent (accepted)
199
Describe the pathophysiology of AF
progressie remodelling of atrial structure and ion channel function provoked by numerous stressors structural remodelling usually develops before the onset of AF
200
What are the hallmarks of AF pathophysiology
activation of fibroblasts, enhanced connective tissue deposition, and fibrosis
201
What is theory A in the electrophysiological mechanism of AF?
a focal source in pulmonary veins can trigger AF heirarchic organisation of AF with rapidly activated areas driving the arrhythmia documented in paroxysmal AF, but less obvious in persistent
202
What is theory B in the electrophysiological mechanism of AF
perpetuated by continuous conduction of several independent wavelets propagating through atrial musculature in seemingly chaotic manner
203
What are the cardiac causes of AF?
``` coronary artery disease conduction disease structural heart disease cardiomyopathy heart failure valvular disease hypertension ```
204
What are the endogenous causes of AF?
``` thyroid dysfunction COPD PE sleep apnoea diabetes CKD electrolyte disturbances obesity acid base disturbances ```
205
What are the exogenous causes of AF?
infection alcohol - chronic excess/binges smoking caffeine
206
What investigations are needed in AF?
``` ECG TFTs echo LFTs electrolytes CRP/blood cultures ```
207
What are the symptoms of AF?
palpitations dyspnoea chest tightness pre-syncope
208
What are the major complications of AF?
thromboembolism | heart failure
209
What is used to assess whether AF patients need stroke prevention?
ChA2DS2VASc risk scores
210
What can be used as stroke prevention in AF?
``` vitamin K antagonists DOACs antiplatelet agents transcatheter therapy surgical therapy ```
211
Which treatment strategy should be used in which AF patients?
offer rate control as 1st line strategy, except - new onset secondary reversible cause HF thought primarily due by AF
212
Give an example of a class 1 antiarrythmic drug
flecainide | sodium channel blocker
213
Give examples of class II anti arrhythmic drugs
beta blockers bisprolol carvedilol
214
Give examples of class III anti arrhythmic drugs
k+ channel blockers | amioderone
215
Give examples of class IV anti arrhythmic drugs
Ca2+ Channel blockers diltiazem verapamil
216
Give examples of class V anti arrhythmic drugs
amiodarone
217
What are the main rhythm control drugs?
flecainide | amioderone
218
What are the main rate control drugs?
beta blockers digoxin calcium channel blockers
219
What are the risks associated with flecainide?
hypotension atrial flutter QT prolongation avoid in patents with IHD or significant structural heart disease
220
What are the risks associates with amiodarone?
``` phlebitis hypotension bradycardia/AV block will slow ventricular rate delated conversion to sinus rhythm ```
221
For which patients in catheter ablation used in AF?
with paroxysmal or persistent AF who fail AAD
222
What are the surgical options in AF treatment?
maze procedure
223
Describe ablation of AV node
ablation results in iatrogenic 3rd degree heart block controls ventricular rate in AF when medications fail to do so patients pacemaker dependent for life
224
Describe the RA
sinoatrial node | broad appendage
225
Describe the LA
narrow, long appendage | pulmonary venous confluence
226
Describe the RV
trabeculated endocardium | insertion of chord to IVS, moderator band
227
Describe the LV
smooth endocardium, ellipsoid cavity
228
What are the categories of cyanotic CHD?
no shunt and shunt
229
Give examples of no shunt CHDs
``` correction of aorta abstain's anomaly pulmonary stenosis bicuspid aortic valve subaortic membrane ccTGA ```
230
Give example of shunt CHDs
``` atrial septal defect ventricular septal defect AVSD patent ductus arterioles aortopulmonary window partial anomalous pulmonary venous drainage ```
231
Give examples of cyanotic CHDs
``` Eisenmenger syndtome tetralogy of fallot transposition of the great arteries tricuspid atresia pulomary atresia combined lesions - ASD with severe pulmonary stenosis ```
232
What is ccTGA?
congenitally correction transposition of the great arteries | usually not in isolation
233
What are the special considerations in arrhythmia in CHD?
``` common scar related haemodynamic lesion related emergency if fontan ```
234
What are the special considerations in pregnancy in CHD?
``` higer risk volume shift arrhythmia dissection risk outflow obstruction - CO can't be increased ```
235
Describe secundum ASD
shunts left to right in isolation right heart volume loading pulmonary flow murmur fixed, split second heart sound
236
What can secundum ASD lead to?
``` RV failure tricuspid regurgitation atrial arrhythmias pulmonary hypetension Eisenmenger syndrome ```
237
Describe transposition of the great arteries
oxygenated blood from pulmonary veins is re-ciculated to lungs deoxygenated blood from the body is recirculated to the body duct dependent circulation
238
Describe foetal circulation
in-utero oxygenation is by the maternal placenta pulmonary circulation is minimal and at high resistaance oxygenated blood returns to RA bia IVS it bypasses the RV/PA bia the foramen ovale of the blood that is pumped to the PA, most passes to the aorta via the ductus arteriosus
239
What are the consequences on surgery to treat transposition of the great arteries?
atrial switch | systemic RV- dilatation, tricuspid regurgitation, heart failure, atrial arrhythmias
240
Describe tetralogy of fallot
ventricular septeal defect overriding arota RVOT obstruction right ventricular hypertrophy
241
How is tetralogy of ballot repaired?
pulmonary artery and right ventricle enlarged using a patch muscular obstruction removed VSD closed with patch
242
What is the repaired history of tetralogy of fallot?
significant pulmonary regurgitation intrinsic iatrogenic arryhmia risk residual VSD pulmonary arterial/branch PA stenoses
243
Describe fontal/TCPC
single ventricle supports systemic circulation systemic venous return is directed to pulmonary arteries, bypassing the ventricular mass pulmonary circulation relies on maintained systemic venous pressure and low pulmonary vascular resistance dehydration, arrhythmia, bleeding and pulmonary embolus all potentially catastrophic
244
Describe coarction of the aorta
age at presentation depends on position and severity pre-ductal may cause lower limb cyanosis upper body hypertension, berry aneurisms, claudication and renal insufficiency may ensure

Phase 3 (15 decks)

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