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cardio Flashcards

1
Q

what is prinzmetals angina

A

non exertional chest pain due to coronary artery vasospasm
seen w brief st elevation and no raised biomarkers
seen in younger px esp w cocaine use

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2
Q

what is decubitus angina

A

chest pain brought on by lying flat

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3
Q

what is stable angina

A

central crushing chest pain (or to jaw, neck, l shoulder) brought on by exertion and relieved by rest <5min ir glyceryl trinitrate spray (GTN spray) mostly due to atheromous plaque

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4
Q

modifyable risk factors stable angina

A

obesity
smoking
poor diet
t2dm
hyperlipidaemia
sedentary lifestyle
htn

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5
Q

non-modifiable risk factors stable angina

A

FHX
male
ethnicity - south asian, afro-caribbean
incr age

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6
Q

signs and symptoms stable angina

A

central crushing chest pain due to exertion- relieved by stress
exertional dyspnoea
incr sweating
nausea

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7
Q

diagnosis stable angia

A

ecg- normal, may show st depression
normal biomarkers/ troponin
ct angiogram to show luminal narrowing

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8
Q

symptomatic treatment stable angina

A

glyceryl trinirate spray

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9
Q

long term treatment stable angina 1-3rd line

A

CCB or BB
ccb + bb
ccb+bb+ antianginal med eg long acting nitrate

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10
Q

non-pharmacological management stable angina

A

lose wt, incr exercise, stop smoking, better diet, control other co-morbidities

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11
Q

ddx for stable angina

A

acute coronary syndrom, heart failure pericarditis

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12
Q

ccb needed for stable angina + example

A

non rate limiting eg amylodipine not verapamil
can cause excessive brdycardia

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13
Q

tx if medicine isnt successful for stable agina

A

revascularisation
- pci (percutaneous intervention)
- cabg (coronary artery bypass grafting)

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14
Q

+/- cabg

A
  • more invasive, incr risk of stroke, long recovery time
    + better outcome/ prognosis
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15
Q

-/+ pci

A

+ less invasive, short recovery time
- risk of stent thrombosis

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16
Q

what is pci

A

percutaneous intervention
- inflating a ballon in an atheromous vessel to dilate to help blood flow

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17
Q

what is cabg

A

coronary artery bypass grafting
- left internal mammary artery used to bypass left anterior descending artery to bypass occlusion/ atheroma

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18
Q

conditions of acute coronary syndrome

A

unstable angina
non stemi
stemi

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19
Q

general pathogenesis of acs

A
  • atheroma formation
    endothelial damage causes the entery of LDL into intima layer of artery
  • this oxidises causing inflam response -> macrophages
    1. FATTY streak
    • 10yrs <
    • lipid laden marcophages and t cells
      1. INTERMEDIATE LESIONS
        • layers of smooth muscle, foam cells and t cells
      2. FIBROUS ADVANCED LESIONS
        • lipid core w necrotic debis
        • fibrous cap w smooth muscle, collagen and elastin
        • tough fibrous cap - more stable - less chance of rupture
        • protrudes into lumen -> stenosis can cause ischaemia and reduced perfusion
      3. PLAQUE RUPTURE
        • cap needs to be maintained by reabsorption and redeposition of smooth muscle
          - thins with damage eg enzymic activity causing it to haemorrhage and rupture
          - contrnts released into lumen causing thrombus formation , which can cause ischaemia and infarction
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20
Q

what % vessel occlusion does sx start to occur in stable angina

A

approx 70%

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21
Q

what is unstable angina

A

crushing central chest pain occurs spontanteously/ not due to exertion and not relieved by rest or gtn spray
due to partial occlusion of vessel

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22
Q

what is nonstemi

A

partial occlusion of a vessel leading to tissue necrosis and release of biomarkers eg troponin but not seen w st elevation

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23
Q

what is a stemi

A

st elevation myocardial infarct
complete occlusion of a coronary vessel causing cardiac tissue necrosis with raised biomarkers and ecg changes

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24
Q

are ecg changes seen in unstable angina

A

not commonly
- may see t wave inversion or st depression

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25
Q

what are the ecg changes seen in a nonstemi

A

st depression
t wave inversion

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26
Q

ecg changes in stemi

A

st elevation
pathological q waves after a few days (indicated previous MI)
new left bundle branch block
t wave inversion

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27
Q

what are 2 biomarkers raised in MI

A

troponin - specific - rise seen after 3 hrs of MI
creatinine kinase MB - non specific also seen in bone pathology

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28
Q

signs and symptoms of acs

A
  • severe crushing central chest pain radiating to neck, jaw, shoulder
  • dyspnoea
  • sweating
  • palpitations
  • anxiety - feeling of impending doom
  • nausea
  • hypotension and tachycardia
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29
Q

1st line investigations of acs

A

ecg withing 10 min/ immediately
troponin bloodtest

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30
Q

2nd line investigations of acs

A

ct angiogram - identify occluded vessel

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31
Q

what leads of an ecg show a lad occluson

A

V1-4

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32
Q

which leads shows a left circumflex occlusion

A

I, aVL, V5, V6

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33
Q

which leads show a right coronary artery occlusion

A

II, III, aVF

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34
Q

which leads show a septal view of LAD

A

V1-2

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35
Q

which leads show and anterior view of LAD

A

V3-4

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36
Q

what is acute management for acs

A

MONAC
Morphine
Oxygen (if low oxy sat)
Nitrates (short acting)
Aspirin (300mg)
Clopidgrel (75mg)

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37
Q

secondary acute management for unstable angina and nonstemi

A

after MONAC
- GRACE score - 6mmth mortality risk
- if low risk - monitor
- if high risk - urgent angiogram and consider pci

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38
Q

what is the management of stemi

A

after MONAC
- urgert pci within 2hrs of sx
- thrombolysis w allopase after 12 hrs sx

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39
Q

long term prevention of acs

A

aspirin 75mg daily
bb eg propanolol
clopidogrel - 12mnth
acei
atrovstatin

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40
Q

complications of MI

A

DARTHVADER
death
aneurysms
rupture
tamponade
heart failure
valvular disease
arrhythmias
dresslers syndrome
embolism
recurrance regurgitation

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41
Q

what is dresslers syndrome

A

autoimmune pericarditis occuring 2 wks after MI

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42
Q

what is htn

A

clinical bp reading >=140/90mmHg
ambulatory bp >=135/85mmHg

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43
Q

what are the 2 types of htn

A

primary ‘essential’ htn
secondary htn

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44
Q

what is essential htn

A

primary htn that has no underlying cause
95% cases

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45
Q

what are causes of secondary htn

A

renal: ckd, glomerulonephropathy
endo: cushings, phaeochromocytoma, hypertension

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46
Q

risk facctors htn -non/modifiable

A

non:
- ethnicity- afro-caribbean
- incr age
- fhx
- men

modifiable:
- high salt intake
- obesity
- sedentary lifestyle
- smoking

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47
Q

symptoms htn

A

ASx may have pulsatile headache
secondary condition sx

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48
Q

what is malignant htn

A

stage 3 htn classed as >= 180/120 mmHg
start immediate treatment

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49
Q

symptoms of maligant htn

A

hypertensive retinopathy - papilloedema, blurred vision
cardiac signs eg chest pain
polyuria , oligouria

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50
Q

investigations for htn

A

1st. clincal bp reading on each arm - record lowest value
2nd. if >140/90 do ambulatory bp for 24 hrs or home bp monitoring
(should have an average of 135/85mmHg)

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51
Q

what secondary investigations should bedone for htn

A

secondary organ damage
- fundoscopy for retinopathy
- urinalysis for kidney function
- Hba1c`

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52
Q

htn tx for afro-caribbean woman age 60 (1st-3rd line)

A

> = 55yrs or afro-caribbean
1st CCB
2nd CCB + ACEi (or ARB if CI) or thiazide like diuretic
3rd CCB + ACEi (or ARB) + thiazide like diuretic

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53
Q

htn tx for 30yr old w t2dm

A

<55 or w t2dm
1st ACEi (or ARB)
2nd ACEi (or ARB) + CCB
3rd ACE (or ARB) + CCB + thiazide like diuretic

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54
Q

htn tx for 58yr old afro-caribbean w t2dm

A

with DM follow ACEi path but use ARB instead
If not afro caribbean >55 w t2dm follow ACE i path

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55
Q

what is stage 1 htn

A

home/ ambulatory bp >135/85mmHg
clincal bp >140/90mmHg

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56
Q

what is stage 2 htn

A

ambulatory bp 150/95mmHg
clinical bp 160/100mmHg

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57
Q

what is pericarditis

A

inflammation of the pericardium- mostly acute
can either be dry (fibrinous) or effusive (purulent, haemorrhagic or serous)
- effusion is secondary to inflammation + can cause further complications

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58
Q

2 main causes of percarditis

A

idiopathic
viral - coxsakkie

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59
Q

name 5 other causes of pericarditis

A

idiopathic
viral: coxsakkie, EBV, VZV, HIV
TB
Autoimmune: SLE, RA, sjogren
dresslers syndroms: autoimmune following after mi
Hypothyroidism

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60
Q

typical px of pericarditis

A

male, 20-50s w recent viral infection

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61
Q

describe pericardial chest pain

A

severe sharp pleuritic chest pain that radiates to trapezius, neck, jaw
worse when lying down and relieved by sitting foward

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62
Q

signs and symptoms for pericarditis

A

severe sharp pleurtic chest pain
-worse lying down
- better sitting foward

pericardial friction rub on ascultation
- to and fro high pitch/ leathery extra heart beat

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63
Q

innervation of pericardium

A

phrenic nerve- so paiin refers to shoulder, neck and jaw

64
Q

investigations for pericarditis

A

ECG - diagnostic
- wide saddle shaped ST elevation
- PR depression

CXR: if effusion will show cardiomegaly

troponin- exclude MI
ESR
CRP

65
Q

main important differential with pericarditis

A

MI - central chest pain - but not pleuritic or worse lying down

66
Q

treatment for pericarditis

A

NSAIDs eg aspirin
Colchicine

67
Q

complications pericarditis

A

constrictive pericarditis (chronic) granulmous tissue formation of pericardium causing reduced cardiac output and congestiev heart failure

effusion may occur - pericardial effusion and this may result in cardiac tamponade if it affects heart function due to compression

68
Q

what is cardiac tamponade

A

complication of pericardial effusion
where excessive collection of pericardial fluid results in inability of heart to maintain CO and contract-> chamber collapse

69
Q

what are the signs and symptoms of cardiac tamponade

A

becks triad- incr jugular venous pressure, hypotension and muffled heart sounds

pulsus paradoxus - during inspiration, systolic pressure drops by >10mmHg

tachy cardia

70
Q

investigations for cardiac tamponade

A

ECG- tachycardia and different qrs amplitudes (electrical altercans)

CXR- cardiomegaly with pleural effusions
ECHO - diagnostic

71
Q

treatment for pericarditis

A

urgent pericardiocentesis

72
Q

what is infective endocarditis

A

infection of the endocardium usually due to bacteria

73
Q

risk factors infective endocarditis

A

men
congential heart disease (young px)
prosthetic valves (older px)
rheumatic heart diesase
poor dental hygeine/ rectent dental proceedue
IVDU

74
Q

what is typically affected in infective endocarditis

A

valves - typically left (aortic and mitral) but righ (tricuspid in ivdu)

75
Q

pathophysiology fo infective endocarditis

A
  • abnormal endocardium have increased platelet and fibrin deposition, esp near the valves
  • this incr likelihood of bacteria colonising there and infecting endocardium formign bacteria vegetatitons causing valvular damage
    can cause regurgitation
76
Q

signs for infective endocarditis (5)

A

janeway lesions - red marks on hands
oslers nodes - nodules on fingers
roth spots - white centered retinal haemorrhages
splinter haemorrhages - under fingernails
new heart murmer - due to regurgitation

77
Q

symptoms for infective endocarditis

A

non-specific
- fever
- headache
- wt loss, malaise, night sweats
- arthalgia due to septic emboli

78
Q

causes of infective endocarditis

A

mc s. aureus
s. viridans - poor dental hygine associated

79
Q

common bacteria causing infective endocarditis w poor dental hygine

A

s. viridans

80
Q

ivdu is associated w infective endocarditis on which side of the heart

81
Q

ddx of fever and new heart murmur

A

infective endocarditis- important to rule out

82
Q

1st line investigations for infective endocarditis -

A
  • blood cultures - 3 done w a 1 hour internal - must be done before AB tx starts
83
Q

diagnostic investigation for infective endocarditis

A

TOE
- transoesophageal echogram - more invasive than transthoracic echocardiogram but better imagine
- endocardial vegitations
- valvular regurgitations

84
Q

criteria used for diagnosing infective endocarditis and its composition

A

dukes criteria
- 2 major
- 5 minor

85
Q

major points of dukes criteria
what is dukes criteria

A

for diagnosign infective endocarditis
- 2/3 positve blood cultures
- echogram - vegetations/ regurgitations

86
Q

5 minor points of dukes criteria

A

vascular abnormalities eg septic emboli
pyrexia
immunological manifestations eg roth spots
predespositing heart conditon / ivdu
1 positve blood culture

87
Q

treatment for infective endocarditis

A

6 wk ABs
2 wk IV then 4 wk oral

88
Q

tx for infective endocarditis due to s. aureus

A

vancomycin and rifampicin

89
Q

complications of infective endocarditis

A

sepsis
valvular regurgitation
congestive heart failure

90
Q

what are the 3 types of AV heart blocks

A

1st, 2nd, 3rd heart block

91
Q

describe 1st heart block

A

consistent prolonged PR interval >0.2sec with no missed AV conductance (no dropped qrs complexes)- slow conduction

92
Q

causes of 1st degree heart block

A

hypokalaemia
drugs: BB, CCB, digoxin, amiodarone
Inferior MI
cardiomyopathies

93
Q

symptoms and treatment of 1st degree heart block

A

ASx so no tx- pretty common

94
Q

what are the 2 types of 2nd degree heart block

A

Mobitz type 1 and 2

95
Q

describe mobitz type 1 heart block

A

2nd degree heart block
- progressive prolongation of PR interval until failure of AV conduction causing 1 dropped QRS
- pr interval is normal following then progressively prolongs again

96
Q

causes of mobitz 1 heart block

A

inferior MI
drugs: ccb, bb, digoxin, amiodarone
cardiomyopathies

97
Q

treatment of mobitz 1 heart block

A

if symptomatic -> pacemaker
eg chest pain

98
Q

describe mobitz ii heart block

A

2nd degree heart block
- consistent prolonged PR interval w occasional failure of AV conductance (occasional dropped qrs complexes)

99
Q

treatment of mobitz ii heart block

100
Q

symptoms of mobitz ii heart block

A
  • chest pain, dyspnoea, syncope if severe
101
Q

causes of mobitz type ii heart block

A

ant MI
SLE
rheumatic fever

102
Q

what are the ratios for mobitz i, ii

A

MI = ratio of p waves to qrs complexes of full cycle (until qrs is dropped) eg 4:3

MII = ratio of how many qrs complexes conducted before a dropped one X:1

103
Q

what is a 3rd degree heart block

A

AVN dissociation. Failure of conductance between atria and ventricles. P and qrs wave independent of eachother

104
Q

how do ventricles contract in 3rd heart block

A

escaped rhythm giving a narrow qrs complex or broard depending on where block originated

105
Q

causes of 3rd heart block

A

lyme disease
acute MI
endocarditis
HTN

106
Q

treatment 3rd heart block

A

IV atropine

107
Q

what is afib

A

irregularly irregular contraction of the atria 300-600bpm causing rapid and ireg ventricle contraction

108
Q

causes of afib

A

PIRATE
Pulmonary- PE/COPD
Idipathic/ IHD
Rheumatic heart disease/ mitral valve disease
Alcohol
Thyroid- hyperthyroidism
Electrolyte imbalance - low Mg, high/low K

109
Q

risk factors for afib

A

htn , t2dm , incr age, male

110
Q

symptoms and signs of afib

A

palpitations
dyspnoea
chest pain
ASx

hypotension
signs of heart failure
irreg pulse

111
Q

ecg findings of afib

A

absent p waves
irregular qrs complex
tachycardia

112
Q

types of afib

A

paroxysmal: <7 days
persistent: >7days and reseolves
permenant: unresolving

113
Q

acute managment for afib

A
  • DC cardioversion - defibrillation
114
Q

chronic managment for afib, once stable 1

A
  1. rate control: BB (bisoprolol), CCB (verapamil), or digoxin if have heart failure + anticoagulants for all
  2. rhythm control: amiodarone or electrical
115
Q

what is atrial flutter

A

regular fast contractions of the atria 250-320bpm characterised by saw tooth waves due to reentry waves

116
Q

signs and symptoms of atrial flutter

A

syncope
dyspnoea
palpitations
fatigue

117
Q

ecg findings of atrial flutter

A

sawtooth atrial flutters between narrow qrs complexes

118
Q

causes of atrial flutter

A

idiopathic, IHD, alcohol, htn

119
Q

treatment of atrial flutter

A

acute- dc cardioversion
after stable - rate control

120
Q

what does avrt stand for

A

atrioventricular re entrent tachyarrhythmia

121
Q

give an example fo avrt

A

wolff parkinison white syndrome

122
Q

pathophysiology of WPWS

A

accessory pathway - bundle of kent - which causes pre-excitement of the ventricles
as SAN impulse is conducted via BoK and atria to the AVN

123
Q

ecg findings of WPWS

A

short pr interval
wide qrs complex
delta wave- inital sloping of qrs interval

124
Q

1st, 2nd, 3rd line treatment of WPWS

A

1st. carotid massage/ valsalva manouver
2nd. IV adenosine - causes complete heart block so px feels like they are dyign
3rd. radiotherapy of ablation of bundle of ken

125
Q

what is IV adenosin used for and how does it work

A

for wolff parkinson white syndrome
- causes complete heart block and restarts the heart

126
Q

what is heart failure

A

inability of the heart to pump enough blood, therefore O2 to supply the metabolic demands of tissue, causing a syndrome of signs and symptoms

127
Q

what is AAA

A

permenent dilation of aorta more than 50% (>3cm typically) mc infrarenal

128
Q

where is the most common place for aaa to occur

A

infra renal

129
Q

2 types of aaa

A

true aaa- 3 layers of the blood vessel
false aaa - 1/2 layers of the blood vessel

130
Q

whos more at risk of an inflammatory aaa

A

younger pxs w atherosclerosis

131
Q

additionl feature of px w inflammatory aaa

132
Q

risk factors aaa

A

smoking - mainly
incr age
men
connective tissue diseases eg ellos danlos and marfans
htn

133
Q

what is the main risk factor of aaa

134
Q

what is the signs and symptoms of an unruptured aaa

A

mostly asx

135
Q

signs and symptoms of ruptured aaa

A
  • pulsatile abdo mass
  • sudden severe epigastric pain
  • tachycardic and hypotensive
136
Q

investigations of aaa

A

abdo ultrasound `

137
Q

managment of unruptured aaa <5.5cm

A

monitor and conservative management eg stop smoking, better diet, exercise

138
Q

conditions of surgical management for unruptured aaa

A

> 5.5cm
4cm and fast progression - dilates more than 1cm annualy

139
Q

managment for high risk unruptured aaa

A

surgical repair- endovascular aortic repair or open repair

140
Q

managment for ruptured aaa

A

urgent endovascular aortic repair

141
Q

heart murmur for aortic regurgitation

A

early diastolic blowing murumur, heard best on expiration and when sitting up

142
Q

heart murmur for aortic stenosis

A

ejection systolic crescendo decrescendo murmur radiating to apex and carotids

143
Q

heart murmur for mitral regurgitation

A

pansystolic blowing murmur radiating to left axilla

144
Q

heart murmur for mitral stenosis

A

rumbling mid diastolic murmur with opening snap, best hear on expiration when lying on lhs

145
Q

causes for aortic stenosis

A
  • ageing calcification
  • congenital bicuspid valve
  • rheumatic heart disease
146
Q

causes for aortic regurgitation

A
  • rhuematic heart disease
  • infective endocarditis
  • ED / M
  • congenital bicuspid valve
147
Q

causes for mitral stenosis

A
  • rhemuatic heart disease
148
Q

causes of mitral regurgitation

A
  • rheumatic heart disease
  • ED/ M
  • infective endocarditis
  • post MI
149
Q

symptoms and signs of aortic stenosis

A
  • SAD
  • syncope, angina, dyspnoea
  • narrow pulse pressure
  • ## slow rising pulse
150
Q

signs and symptoms for aortic regurgitation

A
  • PAD
  • palpitatins, angina, dysnpoea
  • collapsing carrigan pulse
  • austin flint murmur
  • widened pulse pressure
151
Q

signs and symptoms for mitral stenosis

A
  • Afib, palpitations, malar flush, dyspnoea
  • loud first heart sounf
152
Q

signs and symptoms for mitral regurgitaiton

A
  • palpitations, dyspnoea, weakness, fatigues
  • soft 1st heart sound
153
Q

investigations for valvular heart disease

A
  • ecg, cxr
  • gold: echocardiogram - look for chamber and valve abnormality and size
154
Q

general tx for valvular heart disease

A
  • valve repair. replacement
155
Q

treatment for high risk aortic stenosis

A

TAVI
transmembrane aortic valve implant

156
Q

what does valve stenosis cause (pathophysiology)

A

valves are unable to open properly as are stiff causing poor blood flow to next chamber/ blood vessel.
this causes proximal vessl to contract more to maintain cardiac output causing hypertrophy

157
Q

what does valve regirgitation cause

A
  • backflow of blood

ICS (11 decks)

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