Cardio Flashcards

1
Q

Raised JVP, PR depression and ST elevation suggests..

A

pericarditis

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2
Q

a pansystolic murmur is affecting the ____ or _____ valves?

if the lungs are clear where must the problem be?

A

mitral or tricuspid

clear lungs - must be tricuspid

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3
Q

the left coronary artery divides into which two arteries?

A

left anterior descending

circumflex

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4
Q

what area of the heart does the circumflex artery supply?

A

lateral
left atrium
posterior left ventricle

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5
Q

what parts of the heart does the left anterior descending artery supply?

A

anterior

anterior left ventricle
anterior septum

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6
Q

what parts of the heart does the right coronary artery supply?

A

posterior

right atrium and ventricle
inferior left ventricle
posterior septum

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7
Q

symptoms of a heart attack?

A
central crushing chest pain
radiating to jaw/arms 
palpitations 
sweating
nausea 
anxiety / feeling of impending doom
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8
Q

ST elevation or _______ is classsified as a STEMI

A

new left bundle branch block

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9
Q

ECG changes seen in an NSTEMI?

A

ST depression
Deep T wave inversion
pathological Q wave

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10
Q

troponin is a non specific marker. give 2 situations other than MI when it might be raised:

A
Chronic renal failure
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism
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11
Q

2 acute treatment for STEMI?

A

primary PCI if within 2 hrs

thrombolysis if after 2hrs

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12
Q

how does alteplase work?

A

it is a fibrinolytic

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13
Q

treatment of an NSTEMI?

A

B – Beta-blockers unless contraindicated
A – Aspirin 300mg stat dose
T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)
M – Morphine titrated to control pain
A – Anticoagulant: Fondaparinux (unless high bleeding risk)
N – Nitrates (e.g. GTN) to relieve coronary artery spasm

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14
Q

what score is used in NSTEMI to assess whether you need to do PCI?

A

GRACE

if more than 5% / medium risk, do it

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15
Q

presentation of dresslers syndrome?

A

2-3 weeks after MI
pericarditis
pericardial rub
pleuritic chest pain

ECG shows global ST elevation and T wave inversion

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16
Q

treatment for dresslers sydndrome?

A

aspirin
prednisolone
pericardiocentesis

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17
Q

what ECG change in 1st degree heart block?

A

PR interval is longer than 0.2 seconds

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18
Q

If the QRS waves do not always follow P but the PR interval is constant what is this?

A

2nd degree heart block

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19
Q

define 3rd degree heart block?

A

P waves unrelated to QRS

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20
Q

what causes Prinzmetals angina and how does it present?

A

coronary artery spasm

presents w sudden cardiac pain at rest

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21
Q

treatment/management of prinzmetals angina?

A
avoid triggers eg smoking, cocaine, hypomagnesium 
calcium channel blockers (amlodipine)
long acting nitrates (ivabradine)
GTN 
avoid beta blockers and aspirin
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22
Q

angina is a mismatch of oxygen demand and supply. give 4 situations when demand is increased?

A
exercise
stress
cold
hyperthyroid
hypertrophy
hyper or hypo volaemia 
tachycardia 
eating
anaemia
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23
Q

gold standard investigation for angina?

A

CT coronary angiography

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24
Q

side effect of GTN?

A

headache

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25
Q

1st line prophylactic treatment for angina?

A

atenolol / propanolol

verapamil

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26
Q

what is ‘dual antiplatelet therapy’?

A

aspirin

P2Y12 inhibitor eg ticagrelor, clopidogrel

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27
Q

what are the two categories of heart failure?

A
  • reduced ejection fraction (systolic failure) - problem with muscle contraction
  • without reduced ejection fraction (diastolic failure) - problem with filling, poor compliance
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28
Q

5 aetiology of heart failure?

A
ischaemic heart disease 
hypertension 
alcohol
cardiomyopathy 
valve disease 
endocarditis 
pericarditis 
respiratory disease 
drugs that cause arrythmias
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29
Q

what happens in the ‘transition to failure’ when heart failure is developing?

A

poor CO = low bp
vasopressin – renin – vasoconstriction – hypertension
sodium and fluid retention, because of vasopressin/renin
endothelin released from damaged vessels
= aldsosterone
= sympathetic activation
= apoptosis of myocytes
left sided failure – fluid backs up – right sided failur

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30
Q

clinical presentation of heart failure?

A
breathless esp when lying 
tired
oedema esp legs 
cold peripheries 
hepatomegaly 
ascites 

tachycardia
displaced apex beat
raised JVP
murmur

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31
Q

3 investigations you might do in ?heart failure?

A

NT - pro - BNP will be raised

Echo - ejection fraction
ECG shows AF
CXR shows pulmonary congestion

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32
Q

what are the 4 severity classes for heart failure?

A

1 - asymptomatic
2- slight limitation to exercise
3 - severe limitation to exercise
4 - symptoms at rest

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33
Q

what does the ejection fraction need to be to be HFREJ?

A

40% or less

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34
Q

what is the 1st, 2nd and 3rd line treatment for heart failure with reduced EF?

A

1st line = ace inhib (or arb) + beta blocker
eg ramipril + bisoprolol

2nd line = swab arb/acei for hydralazine or add spironolactone

3rd line = consider valsartan sacubitril / digoxin / amiodarone

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35
Q

what does ivabradine do?

A

acts at the SAN to decrease heart rate

sometimes used for heart failure

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36
Q

for heart failure with preserved ejection fraction what is first line?

A

diuretic

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37
Q

5 risk factors for hypertension?

A
CKD
male
age
family history
increased sympathetic nervous system activity
smoking
salt 
obesity
alcohol
sedentary lifestyle
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38
Q

4 causes of secondary hypertension?

A

Pregnancy
Endocrine (hyperaldosteronsim, cushigs)
Renal impairment
Medication - steroids, antipsychotics, contraceptives

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39
Q

at what BP is hypertension diagnosed?

A

140/90

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40
Q

what is stage 2 and stage 3 hypertension?

A
1 = 140/90
2 = 160/100
3 = 180/120
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41
Q

what BP do you aim for when you have treated it?

A

140/90 for under 80
130/90 if high risk eg CKD, DM
150/90 if 80 +

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42
Q

first line antihypertensive for caucasian under 65?

A

ACEi eg -pril

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43
Q

first line antihypertensive for 65+ or afro-carribean?

A

calcium channel blocker eg amlodipine

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44
Q

what is malignant hypertension?

A

180/120 +
risk of immediate end organ damage
emergency

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45
Q

what two substances build up as a result of anaerobic metabolism, causing pain?

A

lactic acid

potassium

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46
Q

apart from pain, give 3 presentations of intermittent claudication?

A

thin shiny skin
ulceration
temperature difference
hair loss

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47
Q

most common cause of pericarditis?

A
viral
coxsackie
HHV8 
EBV
CMV
48
Q

IVDU commonly get infective endocarditis from which bacteria?

A

staph epidermidis

49
Q

rheumatic fever is caused by what bacteria/illnesses?

A

group A strep
strep throat
scarlet fever

50
Q

staph aureus pericarditis usually affects who?

A

immunocompromised

51
Q

3 non infective causes of pericarditis?

A
dresslers
sjoren/RA
uraemia
hypothyroid
aortic dissection
chronic heart failure
amyloidosis
52
Q

what is tamponade?

A

a pericardial effusion that is large enough to affect the beating of the heart

53
Q

what is constrictive pericarditis?

A

develops from chronic pericardial effusion – fibrosis – heart hasnt got room to beat

54
Q

what is the pain like in pericarditis?

A
severe, sharp (not crushing)
pleuritic
worse when lying
best when sitting forward 
rapid onset 
left of chest -- upper epigastric//shoulder
55
Q

apart from pain 3 symptoms of pericarditis?

A
breathlessness
cough
hiccups
fever 
tachycardia
56
Q

in pericarditis what can you hear with the stethoscope?

A

pericardial rub

on left of sternum with the bell

57
Q

what 3 things comprise Becks triad and what does it indicate?

A

hypotension
quiet heart sounds
distended jugular veins

cardiac tamponade

58
Q

to be diagnosed with pericarditis you need 2 of what 4 features?

A

Chest pain
ECG changes
Pericardial rub
Pericardial effusion

59
Q

On the ECG what do you see in pericarditis?

A

ST elevation, saddle shaped
PR depression
high J point
symmetrical but strange T wave

60
Q

in pericarditis what will you see on the echo?

A

pulsus paradoxus

effusion

61
Q

treatment for pericarditis?

A
colchicine 
IV abx 
rest
may need to raise heart rate
pericardiocentesis
62
Q

which valve disease is most common?

A

aortic stenosis

63
Q

two things that can cause all valve diseases?

A

infective endocarditis

rheumatic fever

64
Q

wide pulse is most commonly associated with which valve disease?

A

aortic regurg

high at first bc LV very full and need high pressure to expell all blood
low at end bc all the blood has fallen down back into LV

65
Q

aortic regurg and mitral stenosis both produce diastolic murmurs but what is the difference in the murmur?

A

aortic regurg - ‘blowing’ murmur at Erb’s point when pt is leaning forward

Mitral stenosis - low pitched murmur at the apex when pt is on their side

They are different because in aortic regug the blood is moving backwards whereas in mitral stenosis the blood is moving forward but slowly

66
Q

in which valve disease are you most likely to see mitral facies & what are they?

A

pink-purple patches on the cheeks
mitral stenosis
because this causes the worst pulmonary hypertension

67
Q

how do you treat mitral stenosis?

A

beta blockers/digoxin/amiodarone to slow the heart
diuretics
balloon valvectomy or replacement

68
Q

3 risk factors for infective endocarditis?

A
abnormal valves
prosthetic valve 
IVDU
recent surgery esp heart 
rheumatic fever
septal defect
69
Q

presentation of infective endocarditis?

A
new murmur 
embolic 
fever 
sepsis 
arrythmia
heart failure

petechiae
splinter haemorrhage
oslers nodes
janeway lesions

roth spots on fundoscopy

70
Q

what classifying system is used for the likelihood of infective endocarditis?

A

Dukes

need 2 major + 1 minor or 1 major + 3 minor

71
Q

2 things that are in the major Dukes category for infective endocarditis?

A

pathogen isolated on blood culture
evidence on echo
new valve leak

72
Q

what are 3 examples of minor Dukes criteria?

A
IVDU
prosthetic valve
fever
embolic event 
immune response
equivocal blood culture
73
Q

2 types of echo, which is better?

A

transthoracic is safer

transoesophageal is more invasive but cleaer

74
Q

management of infective endocarditis?

A

IV abx for 6 weeks

75
Q

what scoring system is used to calculate the risk of developing stroke from AF and what does the score mean about treatment?

A
CHAD2
Congestive heart failure
Hypertension
Age over 75 
Diabetes 
S2 - prev stroke or TIA - worth 2 points 

score of 0 – aspirin
score of 1 – warfarin or aspirin
score of 2+ – warfarin

76
Q

if there is primary resistant hypertension, loin pain and haematuria what do you need to be considering?

A

polycystic kidney disease

77
Q

what is Kussmauls sign?

A

increased jugular distention on inspiration

constrictive pericarditis

78
Q

aetiology of hypertrophic cardiomyopathy?

A
  • primary (primary hypertrophic obstructive cardiomyopathy) - autosominal dominant inheritance eg of a faulty sarcomere gene
  • secondary: in response to hypertension or valve defects
79
Q

what do you see on ECG in hypertrophic cardiomyopathy?

A

large voltages
inverted T wave
arrythmia

may lead to ventricular tachycardia/VF

80
Q

treatment for hypertrophic cardiomyopathy? 3

A

beta blocker or calcium channel blocker to decrease heart rate
amiodarone to stop arrythmia
anticoagulants to stop clotting especially if there is some AF

81
Q

what is the presentation of dilated cardiomyopathy?

A
thin overstretched walls are rubbish at contraction so is similar to heart failure 
arrythmia
fatigue
dyspnoea 
tachycardia
82
Q

what is Naxos disease?

A

A type of arrythmogenic cardiomyopathy caused by mutation in the genes that make the desmosome

83
Q

presentation of arrythmogenic cardiomyopathy?

A

arrythmia
palpitation
syncope
heart failure like when sevvere

84
Q

what is the ECG like in arrythmogenic cardiomyopathy?

A

epsilon waves
inverted T
wide QRS in V1-V3

85
Q

give 2 types of shock caused by decreased cardiac output and what might cause them?

A

hypovolaemic - eg haemorrhage, burns, diarrhoea, vomiting

cardiogenic - eg MI, myocarditis

Obstructive - eg tamponade, tension pneumothorax

86
Q

give 2 types of shock caused by decreased systemic vascular resistance?

A

septic
anaphylactic
neurogenic (eg spinal cord lesion that means the body loses its ability to control BP)

87
Q

physiological changes in compensated vs decompensated shock?

A

compensated : increased heart rate, peripheral vasoconstriction and increased resp to maintain BP

decompensated: BP is not maintained and/or the body continues to lose blood and cannot maintain sufficient volume

88
Q

5 presentations of shock (caused by decreased CO)?

A
hypoxia
tachycardia -- bradycardia as it becomes decompensated 
Kussmaul breathing / increased resp 
cold pale peripheries 
decreased cap refill
hypotension
confusion
weak pulse
89
Q

signs of anaphylactic/septic shock?

A
warm 
flushed
pyrexia / rigors
vomitting
cyanosis
pulmonary oedema 
wheeze (esp anaphylactic)
90
Q

treatment of shock?

A
A - maintain airway eg intubate 
B  - give oxygen
C - raised legs, give fluid/blood 
maintain heart rate 
manage cause - abx / adrenaline / hydrocortisone
91
Q

the 4 features of tetralogy of fallot?

A
right ventricular hypertrophy 
over riding aorta
small pulmonary outflow tract 
ventricular septal defect 
(PASH - pulmonary aorta septum  hypertrophy)
92
Q

in tetralogy of fallot can you expect cyanosis?

A

yes
deoxygenated blood can get into the systemic circulation
because right ventricular hypertrophy and poor pulmonary outflow = higher pressure on the right than the left = blood moves right to left

‘fallots spells’ = periods of cyanosis, especially when crying etc

93
Q

what is the treatment and long term prognosis of tetralogy of fallot?

A

surgical repair of septa defect
incise pulmonary valve – pulm outflow tract will grow as it is used, no need fo r such hypertrophy of RV anymore, so aorta can move back over

at risk of pulmonary valve regurgitation or arrythmia later in life but generally life normally

94
Q

in a ventricular septal defect would you expect cyanosis?

A

only in a large hole

in a small hole the blood will generally move from left (high pressure) to right (low pressure), all this means is that oxygenated blood goes back to the lungs unncessarily

when the hole is large lots of oxygenated blood goes to the lungs, this results in pulmonary hypertension and raises the pressure backing up into the right ventricle, one RV pressure is as high as LV, the blood will flow the opposite way (Eisenmenger) = cyanosis and v bad

95
Q

prognosis/complications of a small VSD?

A

buzzing murmur

increased risk of valve defects or infective endocarditis but generally fine

96
Q

what is the plexiform reaction?

A

thickening, fibrosis, hypertrophy of pulmonary vessels in response to pulmonary hypertension

97
Q

treatment options for a large ventricular septal defect?

A

patch the hole

band the pulmonary artery to decrease the blood flow to the lungs

98
Q

symptoms & investigation findings (inc a murmur!) of an atrial septal defect?

A

short of breath on exertion (lungs are full of blood that they have already oxygenated)
pulmonary flow murmur
CXR shows enlarged atria and pulmonary arteries

99
Q

do you get cyanosis in atrial septal defect?

A

no, blood flows from left (higher pressure) to right (lower pressure). it would be very unusual for Eisenmengers to develop because the atria have much lower pressure altogether than the ventricles

100
Q

what is co-arctation of the aorta? how might it present?

A

narrowing of the aorta
hypotension and formation of collateral vessels in lower body
hypertension in right arm not in left
radio-femoral delay
activation of RAAS and sympathetic systems

101
Q

how can coarctation of the aorta be repaired? do you always have to repair them?

A

with a stent or subclavian flap

you need to repair else can cause vascular fragility

102
Q

what do you see in pulmonary stenosis?

A

RV hypertrophy
decreased pulmonary blood flow
tricuspid regurgitation

103
Q

When is JVP raised?

A

pericarditis
right sided heart failure (not left).
– right sided heart failure = blood cannot get out of the right side into lungs = blood builds up around body. increased systemic blood in veins = raised JVP

104
Q

would you expect right or left sided heart failure to present with dyspnoea?

A

left sided
as blood builds up in the left side of the heart
so the blood cannot move from the lungs into the left and instead builds up in the left

105
Q

NT-pro-BNP is a marker of heart failure but what is it and where does it come from?

A

brain natriuretic peptide

released from the ventricles when they are stretched

106
Q

5 signs of left heart failure of an x ray?

A
Alveolar oedema 
B Kerley B lines (intersitial oedema)
Cardiomegaly 
Dilated upper lobe vessels 
E pleural Effusion
107
Q

SOB thats worse on exertion or lying + coughing pink frothy sputum + fine crackles on ascultation could be?

A

left sided heart failure

108
Q

2 times when you would get ST depression and 2 times when you would get ST elevation?

A

ST depression: NSTEMI, unstable angina

ST elevation: STEMI, pericarditis, prinzmetal angina

109
Q

what is the difference physiologically between a STEMI and an NSTEMI?

A

NSTEMI: the infarction does not go all the way across the myocardium

110
Q

definition of atherosclerosis?

A

Accumulation of lipids, macrophages, and smooth muscle cells in the intima of large and medium
sized arteries.

111
Q

what valve do you hear best at the left 2nd intercostal space?

A

pulmonary

112
Q

what valve do you hear best at the left 4th intercostal space on the sternal edge?

A

tricuspid

113
Q

what valve do you hear best at the left 5th intercostal space on the midclavicular line?

A

mitral

114
Q

what drug is NOT a good choice for coronary artery spasm?

A

beta blockers

115
Q

an early diastolic decrescendo murmur indicates what?

A

aortic regurg

116
Q

side effect of GTN?

A

headache