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Part 1 > cardio > Flashcards

cardio Flashcards

1
Q

You are a CT1 in Acute Medicine covering the hospital at night. You are called to the surgical ward to see a 35-year-old patient who is reporting palpitations. She is known to have Wolff-Parkinson-White syndrome. Her ECG shows fast atrial fibrillation. On examination, there is no evidence of haemodynamic instability. What is the most appropriate pharmacological management option for this patient?

A

Verapamil

Avoid AV node blockade (dig or bisop) in accessory pathways

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2
Q

What does troponin T bind to?

A

Tropomyosin is a protein which regulates actin. It associates with actin in muscle fibres and regulates muscle contraction by regulating the binding of myosin.

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3
Q

Features suggesting VT rather than SVT with aberrant conduction

A 
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms
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4
Q

Major bleeding on warfarin

A

stop warfarin, give intravenous vitamin K 5mg, prothrombin complex concentrate

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5
Q

Hypokalaemia ECG

A 
U waves
small or absent T waves (occasionally inversion)
prolong PR interval
ST depression
long QT
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6
Q

Second heart sound (S2)

A

loud: hypertension
soft: AS
fixed split: ASD
reversed split: LBBB

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7
Q

Irregular Cannon A waves vs Regular

A

Caused by the right atrium contracting against a closed tricuspid valve. May be subdivided into regular or intermittent

Regular cannon waves
ventricular tachycardia (with 1:1 ventricular-atrial conduction)
atrio-ventricular nodal re-entry tachycardia (AVNRT)

Irregular cannon waves
complete heart block

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8
Q

Strep viridians vegetation eradication

A

IV benpen

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9
Q

fusion and capture beats

A

suggest VT

Amiodarone first line

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10
Q

Hypertrophic obstructive cardiomyopathy Mx

A 
Management
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

Drugs to avoid
nitrates
ACE-inhibitors
inotropes

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11
Q

Strep viridians vegetation eradication

A

IV benpen

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12
Q

fusion and capture beats

A

suggest VT

Amiodarone first line

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13
Q

Hypertrophic obstructive cardiomyopathy Mx

A 
Management
Amiodarone
Beta-blockers or verapamil for symptoms
Cardioverter defibrillator
Dual chamber pacemaker
Endocarditis prophylaxis*

Drugs to avoid
nitrates
ACE-inhibitors
inotropes

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14
Q

poor prognostic in ACS

A 
age
development (or history) of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class*
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation

*Killip class - system used to stratify risk post myocardial infarction

Killip class	Features	30 day mortality
I	No clinical signs heart failure	6%
II	Lung crackles, S3	17%
III	Frank pulmonary oedema	38%
IV	Cardiogenic shock	81%
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15
Q

Eisenmenger’s syndrome

A

Eisenmenger’s syndrome describes the reversal of a left-to-right shunt in a congenital heart defect due to pulmonary hypertension. This occurs when an uncorrected left-to-right leads to remodeling of the pulmonary microvasculature, eventually causing obstruction to pulmonary blood and pulmonary hypertension.

Associated with
ventricular septal defect
atrial septal defect
patent ductus arteriosus

Features
original murmur may disappear
cyanosis
clubbing
right ventricular failure
haemoptysis, embolism

Management
heart-lung transplantation is required

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16
Q

brugada syndrome

A

Pathophysiology
a large number of variants exist
around 20-40% of cases are caused by a mutation in the SCN5A gene which encodes the myocardial sodium ion channel protein

ECG changes
convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
partial right bundle branch block
the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome

Management
implantable cardioverter-defibrillator

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17
Q

poor prognostic in ACS

A 
age
development (or history) of heart failure
peripheral vascular disease
reduced systolic blood pressure
Killip class*
initial serum creatinine concentration
elevated initial cardiac markers
cardiac arrest on admission
ST segment deviation

*Killip class - system used to stratify risk post myocardial infarction

Killip class	Features	30 day mortality
I	No clinical signs heart failure	6%
II	Lung crackles, S3	17%
III	Frank pulmonary oedema	38%
IV	Cardiogenic shock	81%
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18
Q

Pulmonary arterial HTN

Management

A

Management should first involve treating any underlying conditions, for example with anticoagulants or oxygen. Following this, it has now been shown that acute vasodilator testing is central to deciding on the appropriate management strategy. Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide.

If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers

If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil

Patients with progressive symptoms should be considered for a heart-lung transplant.
Search
Search textbook…

Links
European Society of Cardiology42
2015 Guidelines for the diagnosis and treatment of pulmonary hypertension

Respiratory Medicine journal36
Pulmonary vasodilator testing and use of calcium channel blockers in pulmonary arterial hypertension

 Suggest linkReport broken link
Media
YouTube
Pulmonary hypertension
Osmosis - YouTube263
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19
Q

Intravenous glycoprotein IIb/IIIa receptor antagonists

A

should be given to patients who have an intermediate or higher risk of adverse cardiovascular events (predicted 6-month mortality above 3.0%), and who are scheduled to undergo angiography within 96 hours of hospital admission.

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20
Q

Pulmonary arterial hypertension

features

A

progressive exertional dyspnoea is the classical presentation
other possible features include exertional syncope, exertional chest pain and peripheral oedema
cyanosis
right ventricular heave, loud P2, raised JVP with prominent ‘a’ waves, tricuspid regurgitation

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21
Q

Pulmonary arterial HTN

Management

A

Management should first involve treating any underlying conditions, for example with anticoagulants or oxygen. Following this, it has now been shown that acute vasodilator testing is central to deciding on the appropriate management strategy. Acute vasodilator testing aims to decide which patients show a significant fall in pulmonary arterial pressure following the administration of vasodilators such as intravenous epoprostenol or inhaled nitric oxide.

If there is a positive response to acute vasodilator testing (a minority of patients)
oral calcium channel blockers

If there is a negative response to acute vasodilator testing (the vast majority of patients)
prostacyclin analogues: treprostinil, iloprost
endothelin receptor antagonists: bosentan, ambrisentan
phosphodiesterase inhibitors: sildenafil

Patients with progressive symptoms should be considered for a heart-lung transplant.
Search
Search textbook…

Links
European Society of Cardiology42
2015 Guidelines for the diagnosis and treatment of pulmonary hypertension

Respiratory Medicine journal36
Pulmonary vasodilator testing and use of calcium channel blockers in pulmonary arterial hypertension

 Suggest linkReport broken link
Media
YouTube
Pulmonary hypertension
Osmosis - YouTube263
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22
Q

Infective endocarditis - indications for surgery:

A

severe valvular incompetence
aortic abscess (often indicated by a lengthening PR interval)
infections resistant to antibiotics/fungal infections
cardiac failure refractory to standard medical treatment
recurrent emboli after antibiotic therapy

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23
Q

ECG features of Digoxin

A

down-sloping ST depression (‘reverse tick’)
flattened/inverted T waves
short QT interval
arrhythmias e.g. AV block, bradycardia

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24
Q

ECG changes - territories

A

Anteroseptal V1-V4 Left anterior descending
Inferior II, III, aVF Right coronary
Anterolateral V4-6, I, aVL Left anterior descending or left circumflex
Lateral I, aVL +/- V5-6 Left circumflex
Posterior Tall R waves V1-2 Usually left circumflex, also right coronary

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25
Q

Percutaneous coronary intervention

main complications

A

Two main complications may occur
stent thrombosis: due to platelet aggregation as above. Occurs in 1-2% of patients, most commonly in the first month. Usually presents with acute myocardial infarction
restenosis: due to excessive tissue proliferation around stent. Occurs in around 5-20% of patients, most commonly in the first 3-6 months. Usually presents with the recurrence of angina symptoms. Risk factors include diabetes, renal impairment and stents in venous bypass grafts

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26
Q

Angina first line

A

A beta-blocker or a calcium channel blocker is used first-line to prevent angina attacks

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27
Q

ACEI for HTN develops angio-oedema and dry cough

A

Angiotensin-receptor blockers should be used where ACE inhibitors are not tolerated

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28
Q

HTN Mx

A

insert photo

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29
Q

Most common cause of endocarditis:

A

Staphylococcus aureus

Staphylococcus epidermidis if < 2 months post valve surgery

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30
Q

4th Heart sound in Aortic Stenosis

A

A fourth heart sound is sometimes noted during atrial contraction. In aortic stenosis, this is caused by vigorous left atrial contraction against a stiff, non-compliant ventricle.

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31
Q

acute pericarditis ECG changes

A

Investigations
ECG changes
the changes in pericarditis are often global/widespread, as opposed to the ‘territories’ seen in ischaemic events
‘saddle-shaped’ ST elevation
PR depression: most specific ECG marker for pericarditis
all patients with suspected acute pericarditis should have transthoracic echocardiography

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32
Q

Acute pericarditis Features and Causes

A

Features
chest pain: may be pleuritic. Is often relieved by sitting forwards
other symptoms include non-productive cough, dyspnoea and flu-like symptoms
pericardial rub
tachypnoea
tachycardia

Causes
viral infections (Coxsackie)
tuberculosis
uraemia (causes 'fibrinous' pericarditis)
trauma
post-myocardial infarction, Dressler's syndrome
connective tissue disease
hypothyroidism
malignancy
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33
Q

hypothermia ECG

A 
bradycardia
'J' wave - small hump at the end of the QRS complex
first degree heart block
long QT interval
atrial and ventricular arrhythmias
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34
Q

first line Ix for stable chest pain

A

Contrast-enhanced CT coronary angiogram is the first line investigation for stable chest pain of suspected coronary artery disease aetiology

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35
Q

cholesterol embolisation

A

Overview
cholesterol emboli may break off causing renal disease
the majority of cases are secondary to vascular surgery or angiography. Other causes include severe atherosclerosis, particularly in large arteries such as the aorta

Features
eosinophilia
purpura
renal failure
livedo reticularis
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36
Q

cha2ds2-vasc score

A 
Risk factor	Points
C	Congestive heart failure	1
H	Hypertension (or treated hypertension)	1
A2	Age >= 75 years	2
Age 65-74 years	1
D	Diabetes	1
S2	Prior Stroke or TIA	2
V	Vascular disease (including ischaemic heart disease and peripheral arterial disease)	1
S	Sex (female)
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37
Q

Takayasu’s arteritis

A

Features
systemic features of a vasculitis e.g. malaise, headache
unequal blood pressure in the upper limbs
carotid bruit
intermittent claudication
aortic regurgitation (around 20%)

Associations
renal artery stenosis

Management
steroids

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38
Q

The recommended antibiotic treatment in a patient with a prosthetic valve, no penicillin allergy and staphylococcal endocarditis

A

flucloxacillin, gentamicin, rifampicin

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39
Q

Pulsus alternans

A

regular alternations in force of arterial pulse

severe LV dysfunction

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40
Q

ramipril first dose

A

ramipril can cause first dose hypotension

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41
Q

aortic valve endocarditis worrying ECG change

A

prolonged PR interval - arotic root abscess

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42
Q

prolonged PR interval

A 
idiopathic
ischaemic heart disease
digoxin toxicity
hypokalaemia*
rheumatic fever
aortic root pathology e.g. abscess secondary to endocarditis
Lyme disease
sarcoidosis
myotonic dystrophy
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43
Q

AV heart block in what type of MI

A

inferior MI

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44
Q

coarctation of the aorta features

A 
Features
infancy: heart failure
adult: hypertension
radio-femoral delay
mid systolic murmur, maximal over back
apical click from the aortic valve
notching of the inferior border of the ribs (due to collateral vessels) is not seen in young children
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45
Q

inferior MI which artery?

A

right coronary artery

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46
Q

bendroflumathiazide side effects

A 
Common adverse effects
dehydration
postural hypotension
hyponatraemia, hypokalaemia, hypercalcaemia*
gout
impaired glucose tolerance
impotence
Rare adverse effects
thrombocytopaenia
agranulocytosis
photosensitivity rash
pancreatitis
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47
Q

SVT + asthma

A

adenosine contraindicated in severe asthma

give verapamil

48
Q

U+Es check before amiodarone

A

for hypokalaemia

49
Q

Left axis deviation

A 
Causes of left axis deviation (LAD)
left anterior hemiblock
left bundle branch block
inferior myocardial infarction
Wolff-Parkinson-White syndrome* - right-sided accessory pathway
hyperkalaemia
congenital: ostium primum ASD, tricuspid atresia
minor LAD in obese people
50
Q

Right axis deviation

A 
Causes of right axis deviation (RAD)
right ventricular hypertrophy
left posterior hemiblock
lateral myocardial infarction
chronic lung disease → cor pulmonale
pulmonary embolism
ostium secundum ASD
Wolff-Parkinson-White syndrome* - left-sided accessory pathway
normal in infant < 1 years old
minor RAD in tall people
51
Q

canon A waves

A

atrial contraction against a closed tricuspid valve - VT there is no coordination of ventricular and atrial contraction

52
Q

which antihypertensive worsens glycaemic control

A

bendroflumathiazide

53
Q

aortic stenosis most common cause

A

most common cause:
younger patients < 65 years: bicuspid aortic valve
older patients > 65 years: calcification

54
Q

ACS Treatment, when do you give clopidogrel?

A

based on GRACE score and ?PCI or not

also clopidogrel is reduced in efficacy by omeprazole

55
Q

Severe Aortic Stenosis

A 
narrow pulse pressure
slow rising pulse
delayed ESM
soft/absent S2
S4
thrill
duration of murmur
left ventricular hypertrophy or failure
56
Q

Multifocal Atrial Tachycardia

A

Multifocal atrial tachycardia (MAT) may be defined as a irregular cardiac rhythm caused by at least three different sites in the atria, which may be demonstrated by morphologically distinctive P waves. It is more common in elderly patients with chronic lung disease, for example COPD

Management
correction of hypoxia and electrolyte disturbances
rate-limiting calcium channel blockers are often used first-line
cardioversion and digoxin are not useful in the management of MAT

57
Q

Cardiac enzymes post MI

A

Key points for the exam
myoglobin is the first to rise
CK-MB is useful to look for reinfarction as it returns to normal after 2-3 days (troponin T remains elevated for up to 10 days)

58
Q

PCI window in STEMI

A

120 minutes - if not immediate thrombolysis

59
Q

hypercalcaemia

A 
Features
'bones, stones, groans and psychic moans'
corneal calcification
shortened QT interval on ECG
hypertension
60
Q

hypotension
raised JVP
muffled heart sounds

A

Beck’s triad
Cardiac Tamponade

also features include
dyspnoea
tachycardia
an absent Y descent on the JVP - this is due to the limited right ventricular filling
pulsus paradoxus - an abnormally large drop in BP during inspiration
Kussmaul’s sign - much debate about this
ECG: electrical alternans

61
Q

selenium deficiency linked with which heart condition

A

dilated cardiomyopathy

62
Q

dilated cardiomyopathy features and pathophysiology

A

Pathophysiology
•dilated heart leading to predominately systolic dysfunction
•all 4 chambers are dilated, but the left ventricle more so than right ventricle
•eccentric hypertrophy (sarcomeres added in series) is seen

Features
•classic findings of heart failure
•systolic murmur: stretching of the valves may result in mitral and tricuspid regurgitation
•S3
•’balloon’ appearance of the heart on the chest x-ray

63
Q 
Features
•eosinophilia
•purpura
•renal failure
•livedo reticularis

after vascular surgery or angiography

A

cholesterol embolization

64
Q

AF in HF with reduced EF

A

digoxin or bisoprolol

avoid diltiazem or verapamil - CCBs have negative inotropic effects

65
Q

malignant hypertension features

A

Basics
•severe hypertension (e.g. >200/130 mmHg)
•occurs in both essential and secondary types
•fibrinoid necrosis of blood vessels, leading to retinal haemorrhages, exudates, and proteinuria, haematuria due to renal damage (benign nephrosclerosis).
•can lead to cerebral oedema → encephalopathy

Features
•classically: severe headaches, nausea/vomiting, visual disturbance
•however chest pain and dyspnoea common presenting symptoms
•papilloedema
•severe: encephalopathy (e.g. seizures)

66
Q

malignant hypertension Rx

A

bed rest, oral therapy, if severe/encephalopathic - IV nitroprusside of labetalol

67
Q

swan ganz catheter

A

measures pulmonary capillary wedge pressure

  • left atrial pressure (coming out of lungs
68
Q

coronary sinus (venous) drains to where

A

right atrium

69
Q

arterial blood supply of heart

A

Arterial supply of the heart
•left aortic sinus → left coronary artery (LCA)
•right aortic sinus → right coronary artery (RCA)
•LCA → LAD + circumflex
•RCA → posterior descending
•RCA supplies SA node in 60%, AV node in 90%

70
Q

hypokalaemia ECG

A
  • U waves
  • small or absent T waves (occasionally inversion)
  • prolong PR interval
  • ST depression
  • long QT
71
Q

furosemide MOA

A

inhibits the Na-K-Cl cotransporter in the thick ascending limb of the loop of Henle

72
Q

mitral valve prolapse features

A

Features
•patients may complain of atypical chest pain or palpitations
•mid-systolic click (occurs later if patient squatting)
•late systolic murmur (longer if patient standing)
•complications: mitral regurgitation, arrhythmias (including long QT), emboli, sudden death

73
Q

mitral valve prolapse associations

A 
Associations
•congenital heart disease: PDA, ASD
•cardiomyopathy
•Turner's syndrome
•Marfan's syndrome, Fragile X
•osteogenesis imperfecta
•pseudoxanthoma elasticum
•Wolff-Parkinson White syndrome
•long-QT syndrome
•Ehlers-Danlos Syndrome
•polycystic kidney disease
74
Q

bendroflumathiazide moa

A

inhibits sodium reabsorption by blocking the Na+-Cl− symporter at the beginning of the distal convoluted tubule

75
Q

Angina first line

A

give aspirin and statin
GTN PRN
beta blockier or CCB - uptitrate one before switching or adding another

CCB - monotherapy use diltiazem or verapamil
- combination therapy use nifedipine

76
Q

Scans for heart

A 
MUGA scan - LV function EF 
CT angiograph (cardiac CT)
Cardiac MRI- structural assessment
77
Q

endocarditis in colorectal cancer

A

streptococcus bovis

78
Q

hypercalcaemia features

A 
Features
•'bones, stones, groans and psychic moans'
•corneal calcification
•shortened QT interval on ECG
•hypertension
79
Q

Takotsubo cardiomyopathy

A

‘Broken heart syndrome’ and ‘Takotsubo apical ballooning syndrome’ describes a cardiomyopathy induced by severe stressful triggers (e.g. emotional upset).

apical ballooning appearance occurs due to severe hypokinesis of the mid and apical segments with preservation of activity of the basal segments.

80
Q

electrolyte abn causing VT

A

hypokalaemia

hypomagnesaemia

81
Q

convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave
partial right bundle branch block

SCN5A gene which encodes the myocardial sodium ion channel protein

A

Autosomal dominant - Brugada syndrome.

ICD needed
sudden death

82
Q

atrial flutter curative Rx

A

radiofrequency ablation of the tricuspid valve isthmus is curative for most patients

83
Q

new onset AF within 48 hours

A

consider DC cardioversion

84
Q

anaphylaxis how long to monitor for

A

8 hours

biphasic reaction can occur 8 hours post

85
Q

Prognostic factors for HOCM

A

syncope
family history of sudden death
young age at presentation
non-sustained ventricular tachycardia on 24 or 48-hour Holter monitoring
abnormal blood pressure changes on exercise

86
Q

Dipyridamole is a

A

non-specific phosphodiesterase inhibitor and decreases cellular uptake of adenosine

87
Q

Aortic stenosis management:

A

AVR if symptomatic, otherwise cut-off is gradient of 40 mmHg

88
Q

pan-systolic murmur
prominent/giant V waves in JVP
pulsatile hepatomegaly
left parasternal heave

A

tricuspid regurgitation

89
Q 
Features
mid-late diastolic murmur (best heard in expiration)
loud S1, opening snap
low volume pulse
malar flush
atrial fibrillation

Features of severe MS
length of murmur increases
opening snap becomes closer to S2

A

Mitral regurgitation

Rx valvotomy

90
Q

Rheumatic heart fever histology

ASO titre indicates exposure to group A streptococcus bacteria.

A

Aschoff bodies are granulomatous nodules found in rheumatic heart fever

91
Q

which beta blocker causes long QT

A

sotalol

92
Q

bisferiens pulse

A

mixed aortic valve disease

93
Q

aortic dissection Rx

A

type A - ascending aorta - control BP(IV labetalol) + surgery
type B - descending aorta - control BP(IV labetalol)

94
Q

S3 (third heart sound)

A

caused by diastolic filling of the ventricle
considered normal if < 30 years old (may persist in women up to 50 years old)
heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation

95
Q

broad complex tachycardia signs

A 
AV dissociation
fusion or capture beats
positive QRS concordance in chest leads
marked left axis deviation
history of IHD
lack of response to adenosine or carotid sinus massage
QRS > 160 ms
96
Q

Fondaparinux

A

Activates antithrombin III, which in turn potentiates the inhibition of coagulation factors Xa

97
Q

uraemic pericarditis Rx

A

dialysis

98
Q

STEMI and then reduced ejection fraction

A

give aldosterone antagonist

99
Q

which drug reduces efficacy of adenosine

A

aminophylline

100
Q

AF cardioversion, failed what do

A

If high-risk of failure of cardioversion (previous failure), offer electrical cardioversion after at least 4 weeks treatment with amiodarone

101
Q

PE when to thrombolyse

A

Massive PE + hypotension - thrombolyse

102
Q

pregnant ?PE

A

look for DVT

103
Q

Heart failure when to do resynchronisation

A

LVEF <35% + LBBB (QRS duration greater than 120 ms)

echo - asynchronous contraction of LV + RV and subsequently reduced ejection fraction.

104
Q

Angiotensin II receptor blockers

A

block the effects of angiotensin 2 at the AT1 receptor

105
Q

examples of strep viridians

A

Streptococcus mitis and Streptococcus sanguinis.

DENTAL HYGIENE

106
Q

biscuspid aortic valve assw 6x incvrease in change of

A

aortic dissection

107
Q

MgSO4 monitor

A

urine output, reflexes, respiratory rate and oxygen saturations should be monitored during treatment
respiratory depression can occur: calcium gluconate is the first-line treatment for magnesium sulphate induced respiratory depression

108
Q

Ischaemic changes in leads I, aVL +/- V5-6

which artery?

A

left circumflex

109
Q

most common position of cardiac tumour in adults

A

atrial myxoma - left atrium

110
Q

MI secondary prevention

A

All patients should be offered the following drugs:
dual antiplatelet therapy (aspirin plus a second antiplatelet agent)
ACE inhibitor
beta-blocker
statin

clopidogrel for 1 month, consider 12 months

111
Q

angina

A

aspirin

+ either CCB or bblocker

112
Q

aortic regurgitation features

A 
de quinke's nail bed pulsation
late early murmur 
mid diastolic in severe 
de mussets head bobbing 
wide pulse pressure, collapsing pulse
113
Q

B-type natriuretic peptide is mainly secreted

A

by the ventricular myocardium in response to strain

114
Q

The notch at the end of the QRS complex is referred to as an epsilon wave.

A

Arrhythmogenic right ventricular cardiomyopathy

115
Q

Eruptive xanthoma are due to high triglyceride levels and present as multiple red/yellow vesicles on the extensor surfaces (e.g. elbows, knees)

A

Causes of eruptive xanthoma
familial hypertriglyceridaemia
lipoprotein lipase deficiency

116
Q

haemodynamically stable broad complex tachycardia

A

amiodarone

117
Q

Indications for a temporary pacemaker

A

symptomatic/haemodynamically unstable bradycardia, not responding to atropine
post-ANTERIOR MI: type 2 or complete heart block*
trifascicular block prior to surgery

*post-INFERIOR MI complete heart block is common and can be managed conservatively if asymptomatic and haemodynamically stable

Part 1 (10 decks)

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