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Cardiology Flashcards

1
Q

what is cardiovascular disease?

A

fatty deposits and stiffening of walls (Atherosclerosis) in medium and large arteries due to chronic inflammation and activation of the immune system

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2
Q

how can cardiovascular disease lead to a thrombus?

A

the stiffening leads to HTN and heart strain, the stenosis leads to reduced blood flow. The increased pressure leads to rupture and thrombus formation

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3
Q

what are the risk factors for cardiovascular disease?

A

older age, family history, male, smoking, obesity, sedentary lifestyle, stress, poor sleep, lack of exercise, antipsychotics, CKD, HTN, DM, immune conditions

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4
Q

what are the complications of CVD?

A

angina, MI, stroke, PVD, mesenteric ischaemia, TIA

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5
Q

how is CVD prevented?

A

primary - optimise RFs, QRisk>10% give statins
secondary - aspirin, antiplatelet, atenolol, atorvastatin, ACEi

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6
Q

how is statin prescribed?

A

usually 20mg OD atorvastatin taken at night
check LFTs at 3 months and 12 months then not again if normal - transient rise in ALT and AST but is <3x normal limit then is ok
check lipids at 3 months - aim for 40% reduction in non-HDL cholesterol - if not check compliance and then increase dose

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7
Q

what are the side effects of statins?

A

myopathy, T2DM, rare - haemorrhagic stroke

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8
Q

what is stable angina?

A

it is narrowing of the coronary arteries therefore when there is increased demand for blood supply there is chest pain - always relieved by GTN and not brought on at rest

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9
Q

what are the investigations for stable angina?

A

CT coronary angiography, H+E, ECG, bloods (baselines + lipid profile, fasting glucose, HbA1c, TFTs)o[aw d

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10
Q

what is the management of stable angina?

A

refer, advise, medical, surgical
medical - GTN
long term - BB, CCB, long acting nitrate etc
surgical - PCI with coronary angioplasty, CABG
secondary - aspirin, atorvastatin, ACEi

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11
Q

what is the pathophysiology of ACS?

A

thrombus blocks a CA - fast flowing artery so thrombus mostly made of platelets

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12
Q

what are the investigation and findings in ACS?

A

H+E, bloods, CXR, serial troponins, CT angiography, echo, ECG
STEMI - LBBB or ST elevation
NSTEMI - increased trop or ST depression, path Q wave or inverted T wave
UA - no raise in trop

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13
Q

what is the presentation of ACS?

A

central crushing chest pain, clamminess, sweating, N+V, SOB, palpitations, radiation to jaw and arm, feeling of impending doom, or silent

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14
Q

what are the ECG lead territories?

A

LCA - I, aVL and V3 - V6
RCA - II, III, aVF
circumflex - I, aVL, V5+6
LAD - V1-V4

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15
Q

what is the treatment for acs?

A

acute stemi - PCI if within 2 hours of presentation or thrombolysis if not, morphine, oxygen, nitrate, aspirin, clopidogrel
acute NSTEMI - beta blockers, aspirin, ticagrelor, morphine, anticoagulant, nitrates

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16
Q

what is the GRACE score?

A

it predicts the risk of a further MI or death 6m after PCI - <5% is low risk, 5-10% intermediate and >10% high risk

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17
Q

what are the complications of MI?

A

death, rupture of septum or papillary muscles, oedema, HF, arrhythmias, aneurysm, Dressler’s syndrome

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18
Q

what is the secondary prevention of ACS?

A

lifestyle, aspirin, antiplatelet, atorvastatin, ACEi, atenolol, aldosterone antagonist if in clinical HF

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19
Q

what is the pathophysiology of acute HF?

A

unable to move blood from LV to body - backs up into pulmonary veins - leaky - fluid in alveoli - breathlessness and PO

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20
Q

what are the causes of acute LVF?

A

iatrogenic, sepsis, MI, arrhythmias

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21
Q

what does BNP do?

A

released from the myocardium when overstretched - decreases SVR and increases urinary output of water therefore reducing strain on heart - sensitive but not specific to LVF

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22
Q

what are the investigations of acute LVF?

A

H+E, ECG, ABG, CXR, bloods including trop and BNP, echo

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23
Q

what will a CXR of acute LVF show?

A

cardiomegaly, upper lobe diversion, bilateral pleural effusions, fluid in interlobar fissures and septal lines

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24
Q

what is the point of an echo?

A

shows if there is reduced EF - >50% is normal

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25
what is the presentation of acute LVF?
breathlessness, look unwell, pink frothy sputum, cough, increased RR and HR, decreased sats, 3rd HS, bilateral basal crackles, hypotension from shock, raised JVP, oedema
26
what is the management of PO?
position, oxygen, diuretic, morphine, antiemetic, nitrates
27
what is chronic heart failure?
impaired LV contraction or relaxation leading to chronic back pressure of blood
28
what are the symptoms of chronic heart failure?
breathlessness, cough, PND, orthopnoea, oedema
29
how is CHF diagnosed?
clinical presentation, BNP, echo, ECG
30
what are the causes of CHF?
IHD, valvular HD, HTN, arrhythmias
31
what is the management of CHF?
refer if BNP>2000 urgently, annual pneumococcal and flu vaccine, optimise RFs, surgery if valvular and severe, ACEi, BB, aldosterone antagonist, loop diuretic, monitor U+Es
32
what is the pathophysiology of cor pulmonale?
right sided HF due to respiratory disease - pressure in the PA increases - ventricles unable to pump so it backs up into venous system
33
what are the causes of cor pulmonale?
COPD, PE, ILD, CF, pulmonary HTN
34
what is the presentation of cor pulmonale?
asymptomatic or SOB, syncope, peripheral oedema, hypoxia, cyanosis, increased JVP murmurs, 3rd HS, hepatomegaly
35
what is the management of cor pulmonale?
symptomatic and treat cause and LTOT
36
what are the four cardiac arrest rhythmas?
shockable - VT and VF non shockable - PEA and asystole
37
what is atrial flutter?
re-entrant - saw tooth baselines, atria beat at about 300bpm but only half go through so ventricular at 150bpm - associated with thyrotoxicosis, IHD, cardiomyopathy and HTN - rate control with BB or cardioversion, treat cause, anticoagulation, radiofrequency ablation
38
what is torsades de pointes?
it is prolonged repolarisation meaning that you get random contractions - self limiting or can progress to arrest causes - long QT, medication, electrolyte disturbance treatment - cause, Mg infusion, defib if VT, long term BB (except sotalol), ICD or pacemaker
39
what is SVT?
it is a reentry - narrow complex tachy treatment - valsalva manoeuvre or carotid sinus massage, IV adenosine in fast IV bolus, verapamil, DC cardioversion long term - radiofrequency ablation, BB, CCB, amiodarone
40
what are ventricular ectopics?
premature ventricular beats - brief palpitations random, abnormal broad QRS on otherwise normal ECG mx - check for anaemia, electrolytes, thyroid and reassure
41
describe the heart blocks?
1st degree - long PR 2nd degree - Mobitz type 1/Wenchebach - progressive increase in PR until QRS dropped or type 2 - regular dropping of QRS 2:1 block - 2 P waves for each QRS 3rd degree - complete - no relationship between P and QRS
42
what is the management of brady/AVNB?
IV atropine 500mcg x6 if required inotropes transcutaneous cardiac pacing if stable just observe
43
what is atropine?
it is an antimuscarinic - inhibits the PNS - can give dry eyes, constipation, urinary retention, pupil dilatation
44
what is AF?
disorganised electrical activity - absence of P waves - irregularly irregular ventricles - tachycardia, HF, and risk of stroke associated
45
what is the presentation of AF?
palpations, SOB, symptoms of associated conditions, syncope
46
what is a DDx for AF?
ventricular ectopic this will regulate during exercise though
47
what are the causes of AF?
valvular or non valvular - sepsis, mitral valve pathology, IHD, thyrotoxicosis, HTN,
48
what is the first line treatment in majority of patients?
rate control with BB, CCB or digoxin (aim<100bpm) if not new onset, not reversible, if not causing HF and not symptomatic
49
what is the other first line treatment?
rhythm control - cardioversion (pharmacological or electrical) if new onset, reversible etc if unstable then immediate if stable then anticoagulate for three weeks and use rate control in this time then use amiodarone, flecanide, or cardioversion long term - flecanide, dronedarone or amiodarone
50
how is anticoagulation decided?
HASBLED/ORBIT score v CHA2DVAS2c warfarin or NOACs (less risk of bleeding, less monitoring, more effective, no major interactions)
51
what are S3 and S4?
S3 is due to rapid ventricular filling - if the CT are pulled and twang back and can be normal from age 15-40 S4 is always abnormal and is due to hypertrophied or stiff ventricle
52
where are S1 and S2 heard best?
Erb's point - 3rd ICS, LSE
53
what are the accentuation manoeuvres?
sat up, forward and exhaled - AR, left hand side - MS
54
what are the murmur grades?
v quiet, quiet, loud, loud and thrill, v loud near chest and v loud off chest
55
what are the causes of MS and what murmur?
IE, RHD mid diastolic, low pitched rumbling, loud S1
56
what are the causes of MR and what murmur?
IHD, IE, RHD, CT disorders, idiopathic pan-systolic high pitched radiating to left anxilla
57
what causes AR and what is the murmur?
idiopathic, CT disorders early diastolic soft murmur, collapsing pulse
58
what causes AR and what murmur?
idiopathy, RHD ejection systolic high pitched crescendo-decrescendo radiating to carotid
59
what do each of the above murmurs cause?
MR - LA dilatation AR - LV dilatation MS - RA hypertrophy AS - RV hypertrophy
60
what is the most common scar with a prosthetic heart valve?
midline sternotomy
61
what is transcatheter aortic valve implantation used for?
severe aortic stenosis
62
what are the complications of prosthetic heart valves?
thrombus, IE, haemolysis, clicking for S1 and S2
63
which has a longer lifespan, bioprosthetic or metal?
mechanical - 20 years whereas bioprosthetic 10 years need warfarin if mechanical
64
how common is IE with prosthetic heart valves and what causes it?
2.5% or 1.5% if TAVI mortality of around 15% caused by gram positive cocci - staph, strep, entero
65
what is the criteria for HTN?
clinic BP >140/90 or home 135/85
66
what are the causes of HTN?
primary - essential - idiopathic secondary - renal, obesity, endocrine, pregnancy
67
what are the complications of HTN?
IHD, CVA, hypertensive neuro/retinopathy, HF
68
how often is HF screened for?
every 5 years unless DM or other RF or on border - every year
69
what are the targets for BP with treatment?
<80 years: <140/90 >80 years: <150/90
70
what are the stages of HTN?
1. 140/90 or 135/85 2. 160/100 or 150/95 3. >180/120
71
how do you check for end organ damage in HTN?
urine albumin:creatinine radio bloods - HbA1c, renal function, lipids fundus ECG
72
how do you treat HTN?
first line is lifestyle, optimise RFs, end organ damage and advice medication - ACEi or if black or>55 CCB add in ACEi/CCB/ARB add in thiazide like diuretic add in additional - depends on K+ - >4.5 use alpha blocker and <4.5 spironolactone/other potassium sparing diuretic
73
what are the indications for pacemakers?
symptomatic bradycardia, T2AVNB, 3rd degree block, severe HF, hypertrophic obstructive cardiomyopathy
74
how do pacemakers work?
they deliver electrical impulses to areas to restore activity using pulse generator and tracing leads under skin
75
how long do pacemakers last?
batteries last 5 years removed prior to cremation
76
what are the ECG changes of pacemakers?
sharp, vertical line on all leads before P - atrial before QRS - ventricular before both - dual chamber
77
what do ICDs do?
continually monitor and shock if required to return to sinus rhythm
78
where are pacemakers put?
in a single chamber (RV or RV), dual (RA and RV) or triple (RA, RV and LV - to resynchronise)

Finals (16 decks)

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