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4 - Med > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is atherosclerosis ?

A

chronic inflam + activation of immune system => lipid deposition in artery walls => fibrous atheromatous plaques => stiffening, stenosis + rupture

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2
Q

what size vessels does atherosclerosis affect ?

A

medium and large

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3
Q

what is a thrombus in fast flowing arteries mainly made of ?

A

mainly formed of platelets

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4
Q

name modifiable CVD RF ? (8)

A
  • high cholesterol
  • smoking
  • alcohol
  • poor diet
  • poor sleep
  • sedentary lifestyle
  • stress
  • obesity
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5
Q

name non-mod CVD RF ? (3)

A
  • increasing age
  • FHx
  • Male
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6
Q

what is primary prevention for cardiovascular disease ?

A

QRISK > 10% => statin (atorvastatin 20mg at night)

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7
Q

How do statins work ?

A

reduce cholesterol produced by liver by inhibiting HMG CoA reductase

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8
Q

statin SE ? (4)

A
  • myopathy
  • rhabdomyolysis
  • T2DM
  • haemorrhagic stroke
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9
Q

secondary prevention for CVD ?

A

4As
- Antiplatelet (aspirin, clopidogrel)
- Atorvastatin
- atenolol/bisoprolol
- ACEI

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10
Q

stable angina pathophys ?

A

caused by atherosclerosis affecting coronary arteries => insufficient supply of blood to meet demand => chest pain

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11
Q

how to differentiate between stable and unstable angina ? (2)

A

stable when: sx only come with exertion + always relieved by GTN

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12
Q

what is the definitive Ix for stable angina ?

A

cardiac stress testing (with ECG)

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13
Q

stable angina Mx ? (3)

A

3 steps
- immediate sx relief (GTN spray)
- long term sx relief (BB or CCB - verapamil, diltiazem)
- secondary prevention (4As)

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14
Q

what would you consider revascularisation in a patient with stable angina ?

A

(PCI or CABG plus DAPT for 1 yr - clopi and aspirin)
- when optimal med therapy proves inadequate or if ERR bad

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15
Q

what are the 3 types of ACS ? what tissue affected? ischaemia or infarction ? troponin levels

A
  • unstable angina (sub endo ischaemia): trop -ve
  • NSTEMI (sub endo infarct): trop +ve
  • STEMI (transmural infarct): trop +ve
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16
Q

what do all ACS have in common ?

A

all share plaque rupture, thrombosis and inflammation

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17
Q

describe ECG changes in STEMI ? (4)

A
  • ST elevation
  • Tall T waves
  • New LBBB
  • Pathological Q walves
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18
Q

describe ECG changes in NSTEMI/unstable angina ?

A
  • ST depression
  • T wave inversion
  • non-specific
  • Normal !
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19
Q

what blood test would you specifically get in suspected ACS ?

A

troponin
- get 2 samples few hrs apart to see increase (or trend)

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20
Q

what could cause a raised troponin ? (5)

A

(released when myocardial cell damage)
- Myocarditis
- Pericarditis
- MI
- ventricular strain
- PE
more

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21
Q

What is immediate Mx of ACS ?

A

CPAIN
- call ambulance
- perform ECG
- aspirin 300mg
- IV morphine (+antiemetic - metaclopromide)
- Nitrate
(give oxy if sats < 95%)

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22
Q

STEMI Mx ? (after initial Mx) time frames ?

A
  • PCI within 2 hrs of presenting
  • thrombolysis > 2 hrs (streptokinase, alteplase)
    (or CABG)
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23
Q

ongoing mx of ACS ? generally (3)

A
  • echo to assess LVF
  • cardiac rehab
  • secondary prevention
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24
Q

what is secondary prevention after ACS ?

A

6As
- Aspirin
- Another antiplatelet (ticagrelor/clopi)
- Atorvastatin
- ACEI (ramipril)
- Atenolol (or other BB)
- Aldosterone antagonist

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25
Q

what are the complications of MI (STEMI/NSTEMI) ? (5) which most liekly in first 24 hrs *

A

DREAD
- Death
- Rupture syndromes
- oEdema (HF) *
- Arrhythmias *
- Dresslers

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26
Q

what is rupture syndromes ? name some, think about anatomy

A

(Complication of MI)
- LAD occlusion => intra-ventricular infarct => VSD => murmur + HF
- RCA occlusion => papillary muscle infarct => acute MR
- big LAD occlusion => free wall infarct => free all rupture => cardiac tamponade

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27
Q

how does MI cause HF ? Mx ?

A

HF/oEdema
- LAD occlusion => LV infarction => pulm oedema + reduced EF => reduced CO => hypotension => acute LVHF (+cardiogenic shock)
- Mx: oxy, diuretics, stop IV fluids

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28
Q

how does MI cause arrhythmias ? describe some

A
  • RCA occlusion => AV node desctruction => heart block => bradycardia
  • LAD/LCx occlusion => LV re-entrant circuit => VT => VF => cardiac arrest
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29
Q

what is dresslers syndrome ? complication of what ? how long after ?

A

14 days post MI
- pericarditis as a result of injury to pericardium
(localised immune response => inflam of pericardium)

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30
Q

dresslers syndrome Mx ?

A
  • ECG
  • NSAIDs (aspirin, ibuprofen)
  • or if more severe: steroids
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31
Q

name some indications for permanent pacemaker ? (4)

A
  • complete AV node block
  • mobitz type II
  • persistent AV block after anterior MI
  • symptomatic bradycardia
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32
Q

What is an arrhythmia ?

A

abnormal heart rhythms caused by interruptions to normal electrical signals that coordinate heart contraction

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33
Q

what can braqdyarrhythimas be split into ? what HR ?

A
  • sinus Brady
  • AV node block
    (HR <60)
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34
Q

sinus Brady pathophys ?

A

usually San dysfunction => reduce SA node firing => reduce electrical signals to atria and ventricles

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35
Q

causes of sinus bradycardia ? think drugs (4)

A
  • Beta blocker
  • CCB (verapamil, diltiazem)
  • digoxin
  • hyperkalaemia
    (increase vagal tone - PSNS)
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36
Q

what can cause AV node block ?

A

inferior MI => AV node ischaemia => A node destruction => reduced nodal conduction

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37
Q

describe the different types of Heart block ?

A
  • First degree (prolonged PR interval)
  • Second degree Mobitz I (wenkebach) (PR intervals gradually elongate until a P wave is completely blocked)
  • Second degree Mobitz II (PR interval is consistent but some P waves don’t conduct)
  • third degree (complete AV dissociation)
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38
Q

Mx of unstable patient presenting with arrhythmia at risk of asystole ? (3)

A
  • IV atropine
  • Inotropes
  • pacemaker
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39
Q

what is tachycardia ? what can it be broadly split into ?

A

HR > 100
- narrow complex tachy (QRS < 0.12s)
- Broad complex tachy (QRS > 0.12 s)

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40
Q

name some narrow complex tachycardias ? (4)

A
  • sinus tachycardia (not an arrhythmia)
  • SVT
  • A Fib
  • A flutter
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41
Q

what is SVT ? is it broad or narrow complex ?

A

supraventricular tachycardia: abnormal electrical signals from above ventricles
- electrical signals re-enter atria from ventricle => AVN => vent => self-perpetuating
(narrow complex tachycardia)

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42
Q

what two types does SVT include ?

A
  • AVRT (atrioventricular re-entrant tachycardia)
  • AVNRT (AV nodal re-entrant tachycardia)
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43
Q

SVT ECG changes ?

A

QRS followed by T then QRS then T (P waves buried in T)

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44
Q

what is WPW ? what kind of arrhythmia ?

A

congenital assessor conduction pathway (bundle of Kent) connecting A + V
- SVT - AVRT (narrow complex tachycardia)

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45
Q

What ECG changes does WPW cause ?

A
  • short PR (<0.12)
  • narrow QRS complex (>0.12)
  • delta wave
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46
Q

SVT Mx ? (4)

A
  • vagal manoeuvres
  • adenosine
  • verapamil or BB
  • DCC
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47
Q

name some vagal manoeuvres ? (2)

A
  • valsalva manœuvre
  • carotid sinus massage
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48
Q

how do you manage narrow or broad complex tachycardia with life threatening features ?

A

synchronised DC cardio version under GA/sedation
- IV amiodarone if unsuccessful

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49
Q

what is broad complex tachycardia ?

A

HR >100
QRIS > 0.12s

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50
Q

Name some types of broad complex tachycardia ? most common ?

A
  • Ventricular tachycardia (commonest cause)
  • polymorphic ventricle tachycardia
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51
Q

what is prolonged QTc ? give reference ranges and explain pathophys ?
what does it increase the risk of ?

A

prolonged QTc: >440 men, >40 women
- prolonged repolarisiotn after heart muscle contraction => spontaneous depolarisation in some muscles => TdP (polymorphic vent tachycardia) => ventricular tach (=> cardiac arrest) or revert to sinus

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52
Q

causes of prolonged QTc ?

A
  • long QT syndrome
  • APs
  • citalopram
  • flecanide
  • sotalol
  • amiodarone
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53
Q

briefly explain Mx for narrow context tachycardias:
- sinus tachycardia ?
- Atrial flutter ?
- Atrial fibrillation ?
- SVT ?

A
  • sinus tachycardia: treat underlying cause (stress, infection)
  • AF/Aflut: Rate + rhythm control
  • SVT: vagal manœuvre + adenosine
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54
Q

briefly explain Mx for broad complex tachycardias:
- ventricular tachycardia ?
- polymorphic ventricular tachycardia ?

A
  • vent tachycardia: IV amiodarone
  • polymorphic vent tachycardia (TdP): IV magnesium
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55
Q

there is a pulseless patient (cardiac arrest): what are the shockable rhythms ? (2)

A
  • VT
  • V Fib
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56
Q

there is a pulseless patient (cardiac arrest): what are the non-shockable rhythms ? (2)

A
  • asystole
  • pulseless electrical activity
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57
Q

what is atrial fibrillation ? and what arrhythmia category is it in ?

A

chaotic irregular atrial rhythm
- SVT (originates in atria)

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58
Q

and what bpm is af usually ?

A

300-600 bpm

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59
Q

name some of the cardiac and non cardiac causes of af ?

A
  • cardiac causes: increase LA pressure (due to CHF, mitral stenosis or ischaemia - seen in 22% of MI patients)
  • non-cardiac: hypoxia, electrical disturbances
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60
Q

how does increases LA pressure cause AF ?

A

increased LA pressure => atrial dilatation => atrial remodelling => re-entry circuits

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61
Q

what are the different types of AF ? (3) describe a bit

A
  • paroxysmal (cardiac remodelling not complete): ep 30s - 48 hrs that self resolve
  • persistent
  • chronic: 7 days - 1 yr
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62
Q

paroxysmal AF Mx ?

A

pill in pocket approach (flecanide)

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63
Q

name and explain some complications of AF ?

A
  • thromboembolisi: blood pools (usually atrial appendage) => stasis => thrombus => VTE/stroke/TIA/mesenteric ischaemia
  • Acute HF: increase HR => reduce diastolic time => reduce CO => shock
  • chronic tachycardia => dilated cardiomyopathy
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64
Q

what investigations for AF ?seen on ECG for AF ?

A
  • irregularly irregular ventricular contraction
  • absent P waves
  • narrow QRS complex tachycardia (SVT)
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65
Q

what could be seen on echo in patient with AF ? (2)

A
  • LA thrombus
  • valvular disease
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66
Q

what are the 4 parts to AF control ?

A
  • Rate control (first line)
  • Rhythm control
  • anticoagulate
  • Ablation (if rate/ryhthm control not effective)
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67
Q

describe rate control in AF ? options (3)

A
  • BB (bisoprolol)
  • CCB (verapamil, diltiazem)
  • digoxin (only in sedentary ppl as stops HR increasing even when exercising)
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68
Q

describe rhythm control in AF ? time frames

A
  • if haemodynamically unstable or <48 hrs or anti coagulated for 3-4 weeks + TTE: DCC, then antiocoagulate for 4 weeks
  • pharma cardioversion: amiodarone, flecanide (but can increase risk of TdP
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69
Q

describe the anticoagulation in AF Mx ?

A

CHA2DS2-VASc score >/=2 : anticoagulant

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70
Q

how does ablation work in AF Mx ? when consider ?

A

when rate/rhythm control not tolerated
- creates scar tissue to prevent re-entry

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71
Q

what is atrial flutter ? arrhythmia type ?

A

(SVT - narrow complex tachycardia)
- regularly occurring atria activity (>240 flutter waves/min)

72
Q

describe he relevance of cavotircuspid isthmus to A flutter ?

A

in some patients electrical impulses cross isthmus slowly compared to rest of atrial tissue => develop re-entrance circuit

73
Q

what is the classification of A flutter ? most common ? describe a bit

A
  • isthmus dependant (most common): flutter circuit travels through CTI)
  • isthmus indepedant
74
Q

describe typical ECG findings in Atrial flutter ? (4)

A
  • narrow complex tachycardia
  • regular atrial activity at 300bpm
  • low of isoelectric baseline
  • saw tooth waves
75
Q

A fib presentaiton ? (4)

A
  • palpitations
  • sob
  • dizziness
  • syncope
76
Q

Atrial flutter Px ?

A
  • worsening HF + pulmonary symptoms
  • palpitations
  • fatigue
77
Q

overview of atrial flutter Mx ?

A
  • haemodynamically unstable: emergency electrical cardioversion
  • stable: same as AF (rate + rhythm control + anticoagulation)
78
Q

What is Heart Failure ?

A

inability o heart to meet tissues demands

79
Q

how does excessive preload affect ventricle ?

A

=> vent dilatation

80
Q

how does excessive afterload affect ventricle ?

A

=> vent hypertrophy

81
Q

what is systolic HF ?

A

inability of ventricle to contract normally

82
Q

what is diastolic HF ?

A

inability of ventricles to relax + fill normally

83
Q

LHF Sx ? (5)

A
  • dyspnoea
  • poor exercise toarence
  • orthopnea
  • PND
  • fatigue
84
Q

how do you distinguish systolic and diastolic HF ? explain this pathophys

A

ejection fraction
- Systolic HF: due to drop in LV contractility => reduced LVEF (<40%) => reduce CO
- Diastolic HF: due to increased afterload => hypertrophic LV => reduce CO with preserved LVEF (HFpEF)

85
Q

name some causes of systolic LHF ? (3)

A

(things that drop LV contractility)
- MI
- cardiomyopathy (often dilated)
- IHD

86
Q

name some causes of diastolic LHF ? (4)

A

(things that cause increased afterload)
- chronic HTN
- aortic stenosis
- ventricular hypertrophy
- tamponade

87
Q

explain pathphys of RHF ? cause ?

A

due to reduced contractility => dilated RV => reduced RV EF
- caused by MI

88
Q

explain pathophys of diastolic RHF ?

A
  • anything that increased afterload (pulmonary hypertension) => RV hypertrophy
89
Q

complications of LHF ?

A
  • pulm congestion
  • cariogenic shock
90
Q

explain how LHF causes pulmonary congestion ?

A

blood congests back form LV to LA => pulm veins => increase pulm wedge pressure => fluid leak + pulm oedema => dyspnoea (PND + orthopnoea)

91
Q

explain how LHF causes cariogenic shock ?

A

massive CO reduction => reduced systemic perfusion => increase SVR (to compensate for low BP) => vasocontrciton + cold peripheries

92
Q

complications of RHF ?

A

increases CVP => raised JVP + raised peripheral oedema + ascites + hepatomegaly

93
Q

HF investigations (4)

A
  • CXR
  • NT-pro BNP
  • Echo: systolic (HFrEF), diastolic (HFpEF)
  • NYHA classification
94
Q

how does BNP affect Hf Mx ?

A

determines when seen
>2000mg/l => wishing 2 weeks
- also measure of prognosis

95
Q

what are the CXR changes seen in patient with HF ?

A

ABCDE
- Alveolar oedema
- Kerley B lines
- Cardiomegaly
- Dilated upper lobe vessels
- Pleural Effusions

96
Q

Acute HF Mx ?

A

Pour SOD
- Pour away (stop) IV fluids
- Sit up
- Oxygen
- Diuretics (furosemide)

97
Q

long term HF Mx ? step wise (4)

A
  • ACEI (ramipril) or ARB
  • Add BB (bisoprolol) or SGLT-2 inhibitor
  • add aldosterone antagonist (spironolactone)
  • furosemide for oedema

(procedural: surgical procedure for valvular disease)

98
Q

What counts as high blood pressure ?

A

> 140/90 in clinic or >135/85 with ambulatory or home readings

99
Q

what is most common cause of hypertension ?

A

95 % primary hypertension (essential hypertension)
- developed on its own

100
Q

list the secondary causes of hypertension ? which most common

A

ROPE
- Renal disease (most common), like glomerulonephritis
- Obesity
- Pregnancy
- Endocrine (Cushings/conns)

101
Q

what is malignant hypertension ? what value ? px ? prognosis ?

A

> 200/130
- px: headache, visual disturbance, papilloedema
- untreated 90% die in 1 yr

102
Q

what is HTN a big RF for ? what else ?

A

biggest CVD RF
- IHD, CVA, hypertensive retinopathy, nephropathy

103
Q

how is HTN diagnosed ?

A

if clinic reading between 140/90-180/120 then ambulatory BP or home readings to confirm diagnosis

104
Q

describe the HTN staging ? systolic and diastolic

A
  • stage 1 (>140/90)
  • stage 2 (>160/100)
  • stage 3 (>180/120)
105
Q

describe stepwise HTN Mx ?

A

Step 1: <55 and not black: ACEI or ARB (if ACEI intolerant)
- >55 or black: CCB (amlodipine)
Step 2: A/ARB + CCB
Step 3: A/ARB + CCB + Diuretic (indapamide)
Step 4: A/ARB + CCB + D + additional (Sprinolactone, BB)

106
Q

describe blood flow in mitral regurgitation ? during which heart phase ?

A

back flow of blood form LV => LA (during systole)

107
Q

what are the causes of mitral regurgitation ? (5)

A
  • annular calcification (elderly)
  • rheumatic fever
  • IE
  • MV prolapse
  • EDS
108
Q

what can mitral regurgitation cause ? describe pathophys ?

A

LV volume overload => dilatation => progressive HF
- compensatory mechanisms (LA enlargement, LV increase contractility)

109
Q

mitral regurgitation Px ? (5)

A
  • dyspnoea
  • fatigue
  • palpitations
  • asymptomatic
  • sx of causative factor (infection, EDS)
110
Q

what is the most important Ix for heart murmurs ?

A

do an echo for all of em

111
Q

what would be seen on these Ix in mitral regurg
- CXR
- Echo

A
  • CXR: LA enlargement, central pulmonary artery enlargement
  • Echo: estimation of LA, LV size + function
112
Q

what heart on auscultation of mitral regurgitation ? heard loudest where ?

A
  • pan systolic murmur
  • heard loudest in mitral area (5th ICS, L MCL)
113
Q

Mitral regurgitation Mx ?

A
  • vasodilators (ACEI)
  • BB
  • antiocoagulants
  • if valve badly destroyed then valve replacement + life long warfarin
114
Q

what is rheumatic heart disease ? caused by what pathogen ?

A

caused by group A beta haemolytic streptococcus infection (often in children) that affects + damages heart valves => MR

115
Q

what is mitral stenosis ? during which phase of cardiac cycle ?

A

obstruction of LV inflow during diastole

116
Q

what murmur associated with mitral stenosis ? what other sign ?

A
  • mid-diastolic murmur
  • malar flush (due to reduced CO)
117
Q

describe aortic stenosis ? and the compensatory mechanisms ? (pathophys)

A

(congenital or acquired, disease of the ageing)
- as borrowing increases => restricts blood flow between LV + aorta => initially compensated by hypertrophy (to maintain pressure for CO)
- when this fails: LV function declines + symptoms develop

118
Q

aortic stenosis px ?

A
  • exertion syncope
  • angina
  • dyspneoa
    (typically in an old person)
    (can cause sudden death !!)
119
Q

aortic stenosis murmur on auscultation ? where loudest ?
what signs associated ?

A
  • ejection systolic murmur (loudest aortic area) loudest 2nd ICS at right sternal border
  • slow rising carotid pulse (narrower so harder for blood to get through), decreased amplitude (takes longer for smaller amount of blood to get through)
120
Q

aortic stenosis mx ?

A
  • good dental hygienist (poor dental health increases risk of bacterial infection in blood stream)
  • IE prophylaxis
  • aortic valve replacement (if symptomatic prognosis is port without surgery)
121
Q

what is aortic regurgitation ? during which phase of cardiac cycle ?

A

leakage of blood from aorta => LV during diastole

122
Q

aortic regurgitation murmur on auscultation ?heard loudest where ? what sings ?

A
  • early diastolic murmur (2nd ICS, R sternal border)
  • signs: collapsing pulse + hyper dynamic apex beat
123
Q

what congenital conditions is pulmonary stenosis associated with ? (3) what murmur

A
  • Turner
  • ToF
  • Williams
    (ejection systolic murmur)
124
Q

patient presents with fever + new murmur. this is what until proven otherwise ?

A

endocarditis until proven otherwise

125
Q

what is infective endocarditis ?

A

infection of heart valves (or other endocardial lined structures - septal defect, pacemaker)
- like bad infection (shivers + sick) + showers of infectious maternal into blood stream

126
Q

what pathogen most likely in IE ? in drug users ? in prosthetic valves ?

A
  • viridens group step (dental)
  • s.aureus (IV drug users)
  • staph epidermis (prosthetic valves)
127
Q

IE Px ?

A

(depends on site and organism)
- systemic infection
- embolisation (=> stroke, MI, kidney dystfunction)
- valve dysfunction (HF, arrhythmia, murmur)

128
Q

what signs might you see in IE ?

A
  • splinter haemorrhages
  • jaenway lesions
  • oilers nodes
  • Roth spots
  • heart murmur
129
Q

what is used to diagnose IE (what tool) ? what investigations would you do ?

A

modified duke criteria
- blood cultures: 3 sets at different times form different sites)
- echo (TTE/TOE) may show vegetations
- FBC, U+E, CRP

130
Q

IE Mx ?

A
  • IV Abx (choose drug depending on bug) for 6 weeks !
  • surgery to get ride of infected lateral (not always)
  • prevention (good dental hygiene)
131
Q

describe the pathophysiology of dilated cardiomyopathy ? causes what in the end ?

A

reduced contractility => reduce CO => reduce BP => increase SVR (to compensate low BP) => increase preload => overloads the weak heart => dilates => HFrEF

132
Q

causes of dilated cardiomyopathy ? (5)

A

(all cause reduced contractility)
- alcohol
- cocaine
- chagras
- coxsackie B
- takotsubos

133
Q

what is takatsubo ?

A

rapid onset (stress) induced LV dysfunction, mimic MI
- tends to resolve spontaneously with time

134
Q

what is HOCM ? what does it cause ?

A

(hypertrophic cardiomyopathy)
- genetic mutation (usually autosomal dominant) => inter-ventricular septum hypertrophy => LV outflow tract obstruction => HFpEF
(leading cause of sudden cardiac death in young!)

135
Q

HOCM complications ? (5)

A
  • HF
  • MI
  • arrhythmias (a fib)
  • sudden cardiac death
  • MR
136
Q

HOCM Px ? O/E ?

A
  • asymptomattic
  • sob
  • fatigue
  • dizziness
  • chest pain
  • palpitations
  • HF sx
    O/E: ejection systolic murmur at lower left sternal border (louder with valsalva)
137
Q

HOCM Mx ? (3)

A

aim to reduce ventricular contractility: BB or verapamil
- surgical myomectomy
- avoid intense exercise

138
Q

what is pathophys of hypertrophic cardiomyopathies ?

A

hypertrophy => thick interventiruclar septum => reduce atria + ventricle size => almost closing in on itself at end of systole => decrease cardiac output

139
Q

what is myocarditis ? causes ? (2)

A

inflam of myocardium, often associated with pericardial inflammation
- causes: idiopathic (about 50%), infective (viral, bacteria)

140
Q

myocarditis px ? similar to what ?

A
  • similar to ACS Px
  • HF
  • palpitations
  • tachycardia
141
Q

myocarditis Ix ? gold standard ?

A
  • ECG (ST changes and T wave invention, AV block)
  • end-myocardial biopsy (gold standard)
142
Q

myocarditis Mx ? risk of what ?

A

supportive, treat underlying cause
- risk of developing dilated cardiomyopathy

143
Q

what is pericarditis ? causes ? (3)

A

inflammation of the pericardium
- cause: viral (common), underlying systemic (SLE), traumatic/iatrogenic (increasingly important - caused by previous procedures)

144
Q

pericarditis clinical presentation ? (3) some strange ones too. what is important differential ?

A
  • severe and sharp chest pain: pleuritic (worse with inspiration, received by sitting forward, worse supine (this rarely seen in IHD))
  • pain in shoulder + hiccups (phrenic nerve)
  • hoarse voice (recurrent laryngeal)
    (usually flowing seven preceding illness: fever, rash, joint pain)
    (need to distinguish from ischaemic chest pain)
145
Q

describe how to diagnose pericarditis ? (4)

A

(2/4)
- chest pain
- pericardial effusion (seen on echo)
- ECG changes
- pericardial friction rub

146
Q

describe ECG changes in pericarditis ? (2)

A
  • widespread ST elevation, PR depression
147
Q

what causes pericardial rub ?

A

pericardium inflammation => friction => sand paper sound

148
Q

pericarditis Mx ? if tamponade ?

A
  • NSAID (ibuprofen) + colchicine + PPI (omeprazole)
  • if tamponade: urgent percardiocentesis
149
Q

What is pericardial effusion

A

where excess fluid collects within pericardial sac (acute or chronic)
- can fill entire pericardial cavity or localised section

150
Q

describe the contents of the two types of pericardial effusion ?

A
  • transudates (low protein)
  • exudates (high protein, associated with inflam, blood, pus)
151
Q

pericarditis pathophys ?

A

extra fluid in potential space (pericardial cavity) => inward pressure on heart => harder to expand during diastole

152
Q

describe pathophys of pericardial tamponade ?

A

pericardial effusion is large enough to increase intrapercardial pressure => squeeze heart => reduce filling during diastole => reduce CO during systole

153
Q

causes of pericardial effusion ?

A
  • (high venous pressure => reduced pericardial drainage): congestive HF, pulm HTN
  • pericarditis: infection (TB, HIV), autoimmune (SLE), injury (MI)
154
Q

pericardial effusion px ?

A
  • chest pain
  • sob (worse lying flat)
  • fullness feeling
  • hiccups (compression of phrenic nerve)
  • dysphagia (compression of oesophagus)
  • hoarse voice (compression of recurrent laryngeal)
155
Q

pericardial effusion Ix ?

A
  • ECG
  • fluid analysis (bacterial culture, viral PCR)
  • TTE
  • CXR (enlarged cardiac silhouette)
156
Q

pericardial effusion mx ?

A
  • treat underlying cause (infection) and drainage of effusion
  • if pericarditis: NSAID + colchicine + PPI
  • draining: needles pericardiocentiusis, surgical drainage
157
Q

explain pathophys of chronic pericardial effusions ?

A

chronic pericardial effusion allows adaptation of parietal pericardium (rubber stretches) => rarely causes tamponade (compression of the heart)

158
Q

what is AAA ? over what size ?

A

abdominal aortic aneurysm: dilation of the abdominal aorta (>50% of original diameter)
- usually become aware when it ruptures (life threatening bleeding - 80% mortality)

159
Q

describe AAA screening

A

all men at 65

160
Q

AAA px ?

A
  • asymptomatic
  • non-specific abdo pain
  • pulsatile mass
  • incidental finding
161
Q

AAA Dx ?

A
  • ultrasound
  • CT angiogram (more detailed)
162
Q

AAA Mx ?

A
  • treat reversible RF (smoking, HTN)
  • elective repair (if symptomatic or large)
  • screening and surveillance
163
Q

how does ruptured AAA present ? Mx ?

A

px: severe abdo pain radiating to back, haemodynamic instability, pulsatile + expansive mass, collapse, LOC
- Mx: surgical emergency

164
Q

What is aortic dissection ? between which layers

A

it is when a break of tea forms in the inner layer of aorta => blood flows between layers of th wall of aorta (between intima + media)

165
Q

what are the 2 types of aorta dissection ?

A

stanford system classification
- A (ascending aorta)
- B (descending) (ascending not involved)

166
Q

aortic dissection presentation ?

A
  • Ripping tearing chest pain (anterior => ascending, posterior => descending)
  • hypertension
  • radial pulse defecit
  • diastolic murmur
  • focal neurological defects
167
Q

aortic dissection Mx ? for which classification ?

A

surgical emergency (high mortality)
- analgesia (morphine)
- BP + HR control (BB, verapamil)
- surgical intervention: if standard type A of complicated type B

168
Q

what is peripheral arterial disease ?

A

borrowing of arteries applying limbs + peripheries => reduced blood supply
- common (>20% in over 80 yo)

169
Q

what is intermittent claudication ? describe pathophys

A

muscle pain due to lack of oxy - triggered by activity, relieved by rest
- lactic acid build up + anaerobic metabolism leads to K build up => leg pain (cramps, achey pain, usually calf, thigh, buttox)

170
Q

what is critical limb ischaemia ? px ? (6)

A

inadequate blood at rest (pain at rest, non-healing luvers, gangrene)
- 6Ps: Pain, Pallor, Pulseless, Paralysis, Paraesthesia, Perishing cold

171
Q

critical limb ischaemia Mx ?

A

emergency and may require open surgery of angioplasty

172
Q

what test can be done to elicit signs of PAD ?

A

buergers test
- supine, leg at 45 degrees: pallor of leg suggests PAD

173
Q

Ix for PAD ? first line ?

A
  • duplex US (first line)
  • ABPI
  • angiography
  • donation classification for PAD
174
Q

intermittent claudication Mx ? (4)

A
  • lifestyle changes (reduce risk factors, optimise med treatment)
  • exercise training
  • naftidrofuryl oxalate (peripheral vasodilator)
  • bypass surgery
175
Q

what is acute limb ischaemia ? Mx ? (3)

A

rapid onset of ischaemia in limb due to thrombus
- Mx: end-vascular thrombolysis, bypass surgery, amputation

4 - Med (12 decks)

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