Cardiology Flashcards

1
Q

describe S1

A

closure of the mitral and tricuspid valves

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2
Q

describe S2

A

closure of the aortic and pulmonary valves

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3
Q

describe the Levin scale for grading cardiac murmurs

A
1; very faint
2; heard by a non-expert in optimum conditions
3; easily audible
4; thrill present
5; very loud and heard over a wide area
6; heard without a stethoscope
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4
Q

what are the features of aortic stenosis?

A

ejection systolic murmur (heard shortly after S1) in the aortic region
commonly radiates to carotid arteries
loudest on expiration and when sitting forward
slow rising pulse
narrow pulse pressure
heaving apex beat
reduced, absent or splitting S2

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5
Q

what are the causes of aortic stenosis?

A

calcification of the aortic valve
congenital disorder
rheumatic heart disease

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6
Q

what are the features of mitral regurgitation?

A
pan systolic murmur in the mitral region
radiating to the carotid arteries
loudest using the bell
loudest during expiration
displaced, hyperdynamic apex beat
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7
Q

what is the definition and causes of a pansystolic murmur?

A

heart throughout systole

mitral regurgitation
tricuspid regurgitation
ventricular septal defects

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8
Q

what are the causes of aortic regurgitation?

A
congenital
rheumatic heart disease
infective endocarditis
aortic dissection
CT disorders
aortitis
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9
Q

what are the features of aortic regurgitation?

A
early diastolic murmur
loudest at aortic area
loudest during expiration
Austin-Flint murmur
displaced apex beat
collapsing pulse
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10
Q

what are the causes of mitral stenosis?

A
rheumatic heart disease
congenital
left atrial myxoma
CT disorders
Mucopolysaccharidosis
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11
Q

what are the features of mitral stenosis?

A

low pitched, rumbling, mid-diastolic murmur
loudest over the apex
loudest on expiration
low volume, irregularly irregular pulse (AF)
loud S1 with tapping apex beat
malar flush

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12
Q

define heart failure

A

the inability of the heart to maintain cardiac output to meet the metabolic demands of the body

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13
Q

define cardiac output

A

the volume of blood pumped from each ventricle per minute

SV x HR

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14
Q

define stroke volume

A

the amount blood ejected with each heart beat ml/beat

EDV - ESV

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15
Q

define ejection fraction

A

SV/EDV x 100

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16
Q

define preload

A

maximum cardiomyocyte stretch at EDV

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17
Q

define afterload

A

pressure against which the ventricle contracts

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18
Q

define the Frank Starling curve

A

as preload increases, SV increases
until a maximum
higher is increased inotropy and lower is reduced inotropy

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19
Q

define HFrEF

A

the left ventricle is filled with blood but is only able to pump up to 40% before refilling
LVEF <40%

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20
Q

define HFpEF

A

the left ventricle has stiff and thick walls
even though it pumps all of its volume it is not enough to meet the body’s needs
loss of active diastolic relaxation
LVEF >50%

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21
Q

what are the causes of HFrEF?

A
IHD
old MI
alcohol/toxins
chemotherapy
dilated CMP
valvular HD
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22
Q

what are the causes of HFpEF?

A

HTN
hypertrophic CMP
restrictive CMP

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23
Q

what are the causes of high output HF?

A
anaemia
thyrotoxicosis; increased T4
sepsis
AV fistula
liver disease
Paget's disease
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24
Q

what are the signs and symptoms of heart failure?

A
raised JVP
rales
bilateral ankle oedema
murmur
laterally displaced apex beat
orthopnoea/PND
increased BNP
weight loss; high levels of interleukins
poor mood
fatigue
3rd HS
gallop rhythm
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25
Q

what are the signs specific to LSHF?

A
pulmonary oedema
crackles
cough
wheeze
blood-tinged sputum
tachypnoea
PND
elevated pulmonary capillary wedge pressure
restlessness
confusion
orthopnoea
tachycardia
exertional dyspnoea
fatigue
cyanosis
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26
Q

what are the signs specific to RSHF?

A
fatigue
increased peripheral venous pressure
ascites
hepatomegaly and splenomegaly
distended jugular veins
anorexia
GI distress
weight gain
dependent oedema
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27
Q

what are the causes of BNP increase?

A
LV dysfunction
previous CHF
age
renal dysfunction
ACS
pulmonary disease
PE
high output
AF
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28
Q

what is the management of HF?

A

lifestyle changes (salt, diet, exercise, rehabilitation)

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29
Q

what is the GDMT of HFrEF?

A
RAAS inhibition (ACEi, ARB, ARNI)
MRA inhibitors (spironolactone, eplerenone)
SNS inhibition (beta blockers)
SGLT2 (dapagliflozin, empagliflozin)
CRT
IHD
LVAD
transplant
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30
Q

define cardiac tamponade

A

quick accumulation of pericardial fluid causing cardiac compression which impedes diastolic filling

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31
Q

define constrictive pericarditis

A

recurrent pericarditis or effusions that cause marked thickening of the pericardium

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32
Q

what are the features of acute pericarditis?

A
sharp, sudden onset, pleuritic, retrosternal chest pain
worse lying back
younger
male
recent viral infection
recent MI
previous cardiothoracic surgery
autoimmune disease
uraemia
dialysis
diaphoretic
tachycardia
pericardial rub
diffuse ST elevation
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33
Q

what are the features of pericardial effusion/tamponade?

A
pulses paradoxus
hypotension
increased JVP
muffled heart sounds
peripheral oedema
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34
Q

what are the features of constrictive pericarditis?

A

increased JVP
Kussmaul’s sign
pericardial knock (loud S3)

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35
Q

what is the management of acute pericarditis?

A

NSAIDs
PPI for gastric protection
colchicine
steroids in severe cases

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36
Q

what is the management of pericardial effusion?

A
NSAIDs
PPI for gastric protection
colchicine
steroids in severe cases
pericardiocentesis or ECHO of evidence of tamponade
surgical pericardectomy
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37
Q

define aortic dissection

A

a tear in the intimal layer of the aorta causing blood to enter the medial layer

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38
Q

name the types of aortic aneursym

A

saccular
fusiform
false

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39
Q

what are the causes of aortic aneursym?

A
bicuspid aortic valve
Marfan's syndrome
Ehlers-Danlos syndrome
osteogenesis imperfecta
turner's syndrome
noonan's syndrome
hypertension
trauma
pregnancy
cocaine
surgical procedures (iatrogenic)
vascular inflammatory diseases
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40
Q

describe Marfan’s syndrome

A
mutations in the FBN1 gene
autosomal dominant
long, long bones
upwards lens dislocation and myopia
high arched palate
long fingers and toes
Pectus excavatum
scoliosis
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41
Q

describe Turner’s syndrome

A
45,X
coarctation of aorta
bicuspid aortic valve
streak ovaries, amenorrhoea and infertility
horseshoe kidney
broad chest and widely spaced nipples
webbed neck
low hairline
narrow, high arched palate
low-set ears
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42
Q

describe Noonan’s syndrome

A
associated with PTPN11, KRAS, SOS1
short stature
pulmonary stenosis
webbed neck
superior or inferior Pectus excavatum
cryptorchidism
coagulation defects
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43
Q

what are the symptoms and signs of aortic dissection?

A
abrupt onset, sharp chest pain
interscapular or radiates to the back
collapse
cold legs
paraesthesia of lower limbs
hypo/hypertension
pulse deficit in arms
new murmur (aortic regurgitation)
focal neurological deficit
ST elevation
widened mediastinum
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44
Q

what are the complications of aortic dissection?

A
aortic rupture
end-organ ischaemia
continuing pain and hypertension
early false lumen expansion
large single entry
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45
Q

what is the management of aortic dissection?

A

urgent surgery (A)
medical therapy, TEVAR (uncomplicated B)
surgery (complicated B)

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46
Q

describe cardiac syncope

A

rapid onset
short duration
spontaneous and prompt recovery
may be associated with a prodrome

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47
Q

describe presyncope

A

prodrome without syncope

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48
Q

what is the cause of cardiac syncope?

A

cerebral hypo perfusion secondary to fall in MAP

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49
Q

describe a carotid sinus massage

A
>40 years
pressure applied to carotid sinus for >5s
positive if pause >5s
used to terminate SVT
avoided in previous stroke, TIA
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50
Q

describe reflex syncope

A
typically younger patient
prolonged standing
crowding
hot places
prodrome of autonomic innervation (pallor, sweating)
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51
Q

what is the management of reflex syncope?

A
adequate fluid/solute intake
avoiding situations
counterpressure maneouvres
physical activity
fludrocortisone
midodrine
stop/reduce hypotensive drugs
pacing
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52
Q

describe the mechanism of fludrocortisone and midodrine

A

increases renal sodium reabsorption
expands plasma volume

alpha agonist
frequent dosing

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53
Q

describe POTS

A

rise in heart rate associated with change in posture
sustained increase
no significant reduction in BP

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54
Q

what is the management of POTS?

A

adequate fluid/solute intake
encourage physical activity
beta blockers/ivabradine

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55
Q

what are the causes of regular rhythm on an ECG?

A
sinus
atrial flutter
SVT
VT
complete heart block
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56
Q

what are the causes of irregular rhythm on an ECG?

A
sinus arrhythmia
Mobitz T1
Mobitz T2
AF
ectopics
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57
Q

describe LBBB

A

RBB is still functioning and depolarises first
wave of depolarisation spreads across to LV
ventricular depolarisation is overall slower

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58
Q

what are the causes of LBBB?

A
IHD
cardiomyopathy
LVH
aortic dysfunction
conduction system fibrosis
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59
Q

what are the causes of RBBB?

A
relatively common in normal hearts
cor pulmonale
PE
IHD
ASD
conduction system fibrosis
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60
Q

name the pathological tachycardias

A

AF
atrial flutter
supraventricular tachycardias (AVNRT, AVRT)

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61
Q

what is the management of AF?

A

anticoagulant

rate vs rhythm control

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62
Q

what is the management of adult tachycardia with adverse features (shock, MI, HF, syncope)?

A
3x synchronised DC shock
seek expert help
amiodarone 300mg IV 10-20min
repeat shock
amiodarone 900mg/24hr
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63
Q

what is the treatment of VT?

A

amiodarone 300mg IV/20-60min

then 900mg/24hr

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64
Q

what are the risk factors for asystole?

A

recent asystole
Mobitz T2 AV block
complete heart block with broad QRS
ventricular pause >3s

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65
Q

what is the treatment of asystole?

A

atropine 500mcg IV repeat to a max of 3mg
or
transcutaneous pacing

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66
Q

what are the risk factors for atherosclerosis?

A
CVD
smoking
HTN
dyslipidaemia
DM
FHx premature CVD
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67
Q

what are the complications of HTN?

A
LVH
microalbuminuria
declining GFR
retinal disease
atherosclerosis
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68
Q

what are the secondary causes of HTN?

A
primary hyperaldosteronism
Cushing's syndrome
pheochromocytoma
renal artery stenosis
intrinsic renal disease
coarctation of the aorta
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69
Q

what is the management of HTN for those with diabetes or caucasians <55 yrs

A

ACEi or ARB
CCB
thiazide-like diuretic

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70
Q

what is the management of HTN for those who are black African or caucasians >55 yrs

A

CCB

ACEi or ARB or thiazide-like diuretic

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71
Q

define familial hypercholesterolaemia

A

LDL disorder that increases the risk of premature cardiovascular disease

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72
Q

describe the mechanism of FH

A

faulty LDL-receptor (majority)
faulty Apo-B100
gain of function PCSK9
less LDL taken into cells and increased cell production of LDL

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73
Q

what are the signs of FH?

A

corneal arcus
tendon xanthoma
total cholesterol >7.5mmol/L
personal/family Hx of premature CAD

74
Q

what is the treatment of familial hypercholesterolaemia?

A

lifestyle changes
statin
ezetimibe
PCSK9 inhibitor

75
Q

what are the causes of cardiac decompensation?

A
myocardial ischaemia/infarction
arrhythmia (AF, heart block)
valve dysfunction
respiratory tract infection
alcohol
cardiomyopathy
fluid retention secondary to other organ failure
non-adherence to medication
76
Q

what is the management of heart failure?

A
sit up to relieve dyspnoea
oxygen therapy if hypoxic
loop diuretic (furosemide)
ACEi or ARB
cardioselective beta blocker (nebivolol)
MRA (spironolactone or eplerenone)
ivabradine and sacubitril valsartan
SGLT2 inhibitors
dietary salt restriction
alcohol reduction
smoking cessation
fluid restriction
exercise
77
Q

define hypertension

A

SBP > 140mmHg or DBP > 90mmHg

78
Q

what are the signs of end-organ hypertensive damage?

A

hypertensive retinopathy on fundoscopy (silver wiring, arteriovenous nipping, haemorrhages, papilloedema)

79
Q

what are the signs of atherosclerotic changes?

A

arterial bruits (carotid, groin, abdomen, aorta, renal)

80
Q

what are the signs of ECF volume depletion?

A
thirst
tachycardia
hypotension (postural)
reduced CRT
dry mucous membranes
decreased skin turgor
decreased urine output
81
Q

what are the causes of cardiogenic shock?

A

severe dysfunction of LV due to ischaemia
papillary muscle rupture
intraventricular septum rupture
LV wall rupture (causing tamponade)

82
Q

why do patients develop hypoxia in cardiogenic shock?

A

normally the LV contracts with more force but it cannot because it is severely ischaemic and dysfunctional
blood does not get pumped out of the left side of the heart and it pools in the pulmonary circulation
= pulmonary oedema and hypoxia

83
Q

what are the risk factors for ischaemic heart disease?

A

FHx
smoking
HTN
hyperlipiaemia
DM (long-term corticosteroid therapy increases risk of DM)
CKD
highly calcified blood vessels (due to abnormal bone mineral metabolism in CKD)

84
Q

what are the features of Buerger’s disease

A

symptoms similar to critical limb ischaemia
young
male
upper limb involvement

85
Q

what are the features that distinguish Buerger’s disease and critical limb ischaemia?

A

CLI; unlikely to affect anyone <40yrs
uncommon to affect upper limbs
vascular risk factors; DM, HTN
chronic condition that presents as intermittent claudication, worsening over time

86
Q

what is the differential diagnosis of Buerger’s disease?

A

critical limb ischaemia
scleroderma
raynaud’s
SLE

87
Q

what are the ECG features of digoxin toxicity?

A
down-sloping ST depression
flattened/inverted T waves
short QT interval
arrhythmias; AV block
bradycardia
88
Q

define nephrotic syndrome

A

proteinuria (>3.5g/24hr)
hypoalbuminaemia (25g/L)
oedema

often see hypercholesterolaemia

89
Q

what is the difference between nephrotic and nephritic syndrome?

A

nephritic syndrome has red blood cells in the urine

90
Q

what are the primary causes of nephrotic syndrome?

A

mesangiocapillary GN
minimal change disease
membranous nephropathy
focal segmental glomerulosclerosis

91
Q

what are the secondary causes of nephrotic syndrome?

A
hep B and C
amyloidosis
SLE
diabetic neuropathy
paraneoplastic
NSAIDs
penicillamine
92
Q

what are the symptoms and signs of nephrotic syndrome?

A
lethargy
foamy urine
anasarca
periorbital oedema
pleural effusion
ascites
anaemia
dyspnoea
93
Q

what is the treatment of nephrotic syndrome?

A
dietary water/salt restriction
loop diuretics
ACEi/ARB
anticoagulants
manage BP
immunosuppression; cyclophosphamide, corticosteroids
94
Q

describe the clinical presentation of nephrotic syndrome

A
severe, rapidly progressing pitting oedema
in areas of low tissue resistance
characteristically in the morning
positive protein urine dip
hypoalbuminaemia
BP normal/increased
eGFR normal/mildly impaired
95
Q

what is the management of nephrotic syndrome?

A

children; mostly minimal change disease, steroids

adults; biopsy

96
Q

what are the complications of nephrotic syndrome?

A

susceptibility to infections
thromboembolism
hyperlipidaemia
growth retardation

97
Q

what are the causes and consequences of RSHF?

A

intrinsic lung disease causing pulmonary hypertension
right sided cardiomyopathy

hepatomegaly
raised JVP
bilateral limb oedema
ascites

98
Q

describe CCF

A

fluid overload caused by LV dysfunction

RV failure due to pulmonary hypertension

99
Q

what are the CXR signs of heart failure?

A
alveolar oedema (bat’s wing)
kerley B lines
cardiomegaly
dilated prominent upper lobe vessels
pleural effusion
100
Q

what is the treatment of heart failure?

A
diuretics
ACEi/ARB
beta blockers
amlodipine
digoxin
cardiac rehab
cardiac transplant
biventricular pacing
palliatve care in ESHF
101
Q

what are the causes of acute heart failure?

A
decompensation of chronic HF
ACS
hypertensive crisis
acute arrhythmia
valvular regurgitation
severe aortic stenosis
severe acute myocarditis
volume overload
sepsis
severe brain insult
drug/alcohol abuse
phaeochromocytoma
thyrotoxicosis
anaemia
102
Q

what is the treatment of acute heart failure?

A
loop diuretics
morphine
nitrates (normal BP and no contraindication)
oxygen therapy
position upright

inotropic support
CPAP
intubate and ventilate
mechanical assisted device

103
Q

describe fulminant hepatic failure

A

massive necrosis of liver cells leading to severe impairment of liver function

104
Q

what is the standard calibration of an ECG?

A

speed of 25 mm/s

gain of 10 mm/mV

105
Q

what is the amplitude of an ECG affected by?

A

myocardial mass
net vector of depolarisation
thickness and properties of intervening tissues
distance between electrode and myocardium

106
Q

what are the causes of sinus bradycardia?

A
acute MI
inferior MI
sleep (high vagal tone)
beta blockers
CCB
digoxin
amiodarone
hypothyroidism
hypothermia
sick sinus syndrome
jaundice
raised ICP
107
Q

what are the causes of sinus tachycardia?

A
stress
exercise
anxiety
fever
hypothyroidism
salbutamol
theophylline
108
Q

what should the normal axis of the heart fall between?

A

+90 and -30

109
Q

which ECG leads should be positive and which should be negative?

A

I, II and III should be positive and aVR should be negative

110
Q

what is seen in LAD?

A

leads II, III and aVF are negative

the axis falls between -30 and -90

111
Q

what is seen in RAD?

A

lead I is negative

the axis falls between +90 and +180

112
Q

describe P wave abnormalities

A
P pulmonale (RA enlargement) is P waves with a height >2.5 small squares
P mitrale (LA enlargement) is P waves with a width >3 small squares
113
Q

describe a pathological Q wave

A

> 1 small squares in width and >2 small squares in depth

114
Q

describe poor QRS complex progression

A

when the R wave does not progressively increase from V1 to V6

115
Q

describe RBBB on an ECG

A

wide, notched rSR pattern in V1 and V2

116
Q

describe LBBB on an ECG

A

negative complex on V1, wide notched QRS

117
Q

describe tombstone ST elevation

A

the QRS complex, ST segment and T wave all fuse together and form a tombstone-like complex

118
Q

describe pericarditis on an ECG

A

saddle-shaped ST elevation

119
Q

where does an inferior infarction occur?

A

RCA

120
Q

where does a lateral infarction occur?

A

left coronary or circumflex arteries

121
Q

where does an anterior or septal infarction occur?

A

LAD

122
Q

what are the signs of myocardial ischaemia on an ECG?

A

tall T waves
biphasic T waves
T wave inversion

123
Q

what are the causes of angina pectoris?

A
atherosclerotic coronary obstruction
anaemia
thyrotoxicosis
aortic stenosis
hypertrophic cardiomyopathy
124
Q

what are the features of typical angina?

A
heaviness, pressure, weight, squeezing
radiation to inner arm, jaw, neck, shoulder, epigastrium
predictable onset
lasts 3-15 minutes
relieved with rest/GTN
125
Q

what are the features of atypical angina?

A
sharp, pleuritic, choking, pulsating
radiates inframammary, chest wall
random onset
lasts seconds-days
variable relief
126
Q

what are the signs of angina?

A
smoking
hypercholesterolaemia
cardiac arrhythmia
carotid bruits
HTN
valvular disease
HF
127
Q

what is the treatment of angina?

A

non-pharmacological; stop smoking, exercise and weight control, dietary modifications
vascular protectors; aspirin, ACEi, clopidogrel, statins
anti-anginal medication; beta blockers, CCB, nitrates, nicorandil, ivabradine
PCI
CABG

128
Q

describe ACS

A

STEMI
NSTEMI
unstable angina

129
Q

what are the causes of chest pain?

A
ACS
PE
pneumothorax
PUD
pericarditis
valvular disease
aortic dissection
130
Q

what is the immediate treatment of ACS?

A
pain relief
oxygen
aspirin
clopidogrel
statin
LWMH
cardiac monitoring
fibrinolytic therapy (STEMI)
GP 2b/3a inhibitor for NSTEMI or UA
PCI
CABG
131
Q

what is the secondary prevention of ACS?

A

smoking cessation

exercise, diet and weight control

132
Q

what is occuring if there is no electrical activity on an ECG?

A

asystole

133
Q

what pathologies have an irregular rhythm?

A

atrial fibrillation
sinus rhythm with ectopics
sinus rhythm with 2nd degree heart block (Mobitz type 1)

134
Q

what pathologies have narrow QRS complexes?

A

atrial arrhythmias

nodal arrhythmias

135
Q

what pathologies have wide QRS complexes?

A

ventricular arrhythmias

atrial arrhythmias aberrantly conducted

136
Q

what pathologies have atrial activity?

A

sinus rhythm
atrial flutter
atrial tachycardia

137
Q

describe 1st degree AV block

A

prolonged PR interval

138
Q

describe mobitz type 1

A

PR intervals get progressively longer until one is not followed by a QRS complex and then the cycle starts again

139
Q

describe mobitz type 2

A

every 2nd P wave conducts through to the ventricle and is followed by a QRS complex

140
Q

describe 3rd degree AV block

A

no relationship between the P waves and the QRS complexes

141
Q

what are the causes of AF?

A
idiopathic
HTN heart disease
rheumatic heart disease
sick sinus syndrome
thyrotoxicosis
alcohol misuse
cardiomyopathy
post-cardiac surgery
chronic pulmonary disease
142
Q

define ventricular tachycardia

A

3+ ventricular extrasystoles in succession at a rate of more than 120bpm

143
Q

define torsades de pointes

A

the hallmark arrhythmia associated with delayed repolarisation (QT prolongation)

144
Q

describe ventricular fibrillation

A

chaotic appearance
very fast rate
always associated with cardiac arrest

145
Q

what are the types of AF?

A

paroxysmal
persistent
permanent

146
Q

what are the causes of AF?

A
HTN
IHD
hyperthyroidism
mitral valve disease
alcohol
cardiomyopathy
post-operative
pulmonary disease
HF
sinus node disease
lone
147
Q

what else involved in the management of AF?

A

long-term antithrombotic therapy

except in those with contraindications to warfarin and those with lone AF <60 (aspirin)

148
Q

what are the 1st line drugs for rate control?

A

digoxin
beta blockers
CCB

149
Q

what are the 1st line drugs for rhythm control?

A

amiodarone
flecainide
occasionally propafenone and sotalol

150
Q

what are the symptoms of aortic stenosis?

A

chest pain
dyspnoea
dizziness
blackouts

151
Q

what are the complications of aortic stenosis?

A

HF
blackouts/sudden death
infective endocarditis

152
Q

what is the treatment of aortic stenosis?

A
education
dental hygiene
surgical replacement
percutaneous artificial valve replacement
avoid vasodilators
153
Q

what are the causes of aortic incompetence?

A
HTN
Marfan’s syndrome
aortic dissection
syphilis
congenital
rheumatic
infective endocarditis
trauma
ankylosing spondylitis
annulaortic ectasia
154
Q

what are the symptoms of aortic incompetence?

A

mostly asymptomatic
irreversible LV dysfunction; fatigue, dyspnoea, exercise intolerance
angina

155
Q

what is the treatment of aortic incompetence?

A

surgical replacement
vasodilator therapy
dental hygiene
education

156
Q

what are the chronic causes of mitral regurgitation?

A

myxomatous mitral leaflet prolapse
annular dilatation (LV dysfunction)
rheumatic heart disease
papillary muscle dysfunction

157
Q

what are the acute causes of mitral regurgitation?

A

infective endocarditis

papillary muscle dysfunction

158
Q

what are the symptoms of acute mitral regurgitation?

A

cardiogenic shock

acute pulmonary oedema

159
Q

what are the complications of acute mitral regurgitation?

A
arrhythmias
LV enlargement (cardiomegaly)
infective endocarditis
pulmonary oedema
cardiogenic shock
160
Q

what is the treatment of mitral regurgitation?

A

treatment of pulmonary congestion; ACEi, loop diuretics, beta blockers, digoxin
dental hygiene
treatment of associated conditions
mitral valve replacement/repair (those with a mechanical valve require long-term warfarin therapy)

161
Q

what are the symptoms of mitral stenosis?

A
dyspnoea
exercise intolerance
orthopnoea, PND
fatigue
syncope
cough
haemoptysis
wheeze
hoarseness
162
Q

what are the complications of mitral stenosis?

A
arrhythmias (AF)
systemic embolism
acute pulmonary oedema
pulmonary HTN
RVH
tricuspid regurgitation
right HF
infective endocarditis
163
Q

what is the treatment of mitral stenosis?

A
treatment of pulmonary congestion - loop diuretics, digoxin, beta blockers, ACEi
antibiotic prophylaxis
treatment of arrhythmias
anticoagulation
mitral valve replacement/repair
catheter balloon commisurotomy
164
Q

what are the causes of aortic dissection?

A
atherosclerosis
HTN
trauma
iatrogenic
inflammatory diseases (syphilis, vasculitis, aortitis)
toxic
Marfan syndrome
Ehler-Danlos syndrome
165
Q

what are the symptoms and signs of aortic dissection?

A
sharp pain
dyspnoea
syncope
neurological symptoms/stroke
tachycardia
weak/uneven pulses
hyper/hypotension
diastolic murmur of aortic regurgitation
166
Q

what are the complications of aortic dissection?

A
acute renal failure
aortic regurgitation
acute HF
acute coronary occlusion
cardiac tamponade
ischaemic bowel
stroke
Leriche’s syndrome
aortic perforation (haemoptysis, haematemesis, haemothorax)
167
Q

describe the DeBakey classification of aortic dissection

A

type I - originates in the ascending aorta and beyond the aortic arch
type II - originates and confined to the ascending aorta
type III - originates and confined to the descending aorta

168
Q

describe the Stanford classification of aortic dissection

A

type A - involves the ascending aorta

type B - does not involve the ascending aorta

169
Q

what is the treatment of aortic dissection?

A

type A - surgery
type B - medical management, surgery in tractable chest pain, risk of rupture, end organ ischaemia, periaortic or mediastinal haematoma, percutaneous stenting

170
Q

what are the causes of HCM?

A

AD mutations of the beta-myosin heavy chain gene and the myosin-binding protein C gene

171
Q

what are the complications of HCM?

A
diastolic dysfunction
MI
LV outflow obstruction
arrhythmias
infective endocarditis
sudden cardiac death
172
Q

what are the symptoms of HCM?

A
mostly asymptomatic
exertional dyspnoea
angina
syncope
palpitations
173
Q

what are the signs of HCM?

A
prominent a wave in JVP
rapid upstroke carotid pulse
ejection systolic murmur heard across praecordium
ECG - LVH, LBBB, giant T wave inversion
asymmetrical septal hypertrophy
enlarged LA
LVOT obstruction
systolic anterior motion of mitral valve
mitral regurgitation or prolapse
174
Q

what is the treatment of HCM?

A
beta blockers
verapamil
disopyramide
surgical myectomy
non-surgical (alcohol) ablation
ICD
exercise (avoid intensive and burst exercise)
175
Q

define IE

A

a microbial infection of the endovascular wall of the heart

176
Q

what is the classification of endocarditis?

A

active/treated

diagnostic status - presumed/confirmed

177
Q

what are the causes of IE?

A
streptococcus viridans, bovis
staphylococcus aureus
enterococci
HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella)
fungi
178
Q

what are the risk factors for IE?

A
valve replacement
valvular heart disease
structural congenital heart disease
HCM
previous infective endocarditis
IV narcotic abuse
haemodialysis
IV devices
piercings/tattoos
179
Q

what are the symptoms of IE?

A
fever
malaise
weakness
weight loss
pale
myalgia and arthralgia
dyspnoea
cough
chest pain
heart failure
neurological symptoms
180
Q

what are the signs of IE?

A
Janeway lesions
Osler’s nodes
Roth spots
finger clubbing
splinter haemorrhages
splenomegaly
vasculitic rash
glomerulonephritis (urine test)
neurological
181
Q

what are the complications of IE?

A
valve (destruction, incompetence, chordae rupture)
heart failure
heart block
mycotic aneurysm
emboli
pulmonary infiltrates
pneumonia
abscesses
182
Q

what is the treatment of IE?

A

antibiotics (depending on micro-organism)
surgery (haemodynamic compromise, persistent fever, abscess/fistula development)
antibiotic prophylaxis (for those at-risk)
dental hygiene