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Finals > Cardiology > Flashcards

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
Q

what is the presentation of acute LVF?

A

breathlessness, look unwell, pink frothy sputum, cough, increased RR and HR, decreased sats, 3rd HS, bilateral basal crackles, hypotension from shock, raised JVP, oedema

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26
Q

what is the management of PO?

A

position, oxygen, diuretic, morphine, antiemetic, nitrates

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27
Q

what is chronic heart failure?

A

impaired LV contraction or relaxation leading to chronic back pressure of blood

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28
Q

what are the symptoms of chronic heart failure?

A

breathlessness, cough, PND, orthopnoea, oedema

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29
Q

how is CHF diagnosed?

A

clinical presentation, BNP, echo, ECG

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30
Q

what are the causes of CHF?

A

IHD, valvular HD, HTN, arrhythmias

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31
Q

what is the management of CHF?

A

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

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32
Q

what is the pathophysiology of cor pulmonale?

A

right sided HF due to respiratory disease - pressure in the PA increases - ventricles unable to pump so it backs up into venous system

33
Q

what are the causes of cor pulmonale?

A

COPD, PE, ILD, CF, pulmonary HTN

34
Q

what is the presentation of cor pulmonale?

A

asymptomatic or SOB, syncope, peripheral oedema, hypoxia, cyanosis, increased JVP murmurs, 3rd HS, hepatomegaly

35
Q

what is the management of cor pulmonale?

A

symptomatic and treat cause and LTOT

36
Q

what are the four cardiac arrest rhythmas?

A

shockable - VT and VF
non shockable - PEA and asystole

37
Q

what is atrial flutter?

A

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
Q

what is torsades de pointes?

A

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
Q

what is SVT?

A

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
Q

what are ventricular ectopics?

A

premature ventricular beats - brief palpitations
random, abnormal broad QRS on otherwise normal ECG
mx - check for anaemia, electrolytes, thyroid and reassure

41
Q

describe the heart blocks?

A

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
Q

what is the management of brady/AVNB?

A

IV atropine 500mcg x6 if required
inotropes
transcutaneous cardiac pacing
if stable just observe

43
Q

what is atropine?

A

it is an antimuscarinic - inhibits the PNS - can give dry eyes, constipation, urinary retention, pupil dilatation

44
Q

what is AF?

A

disorganised electrical activity - absence of P waves - irregularly irregular ventricles - tachycardia, HF, and risk of stroke associated

45
Q

what is the presentation of AF?

A

palpations, SOB, symptoms of associated conditions, syncope

46
Q

what is a DDx for AF?

A

ventricular ectopic
this will regulate during exercise though

47
Q

what are the causes of AF?

A

valvular or non valvular - sepsis, mitral valve pathology, IHD, thyrotoxicosis, HTN,

48
Q

what is the first line treatment in majority of patients?

A

rate control with BB, CCB or digoxin (aim<100bpm) if not new onset, not reversible, if not causing HF and not symptomatic

49
Q

what is the other first line treatment?

A

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
Q

how is anticoagulation decided?

A

HASBLED/ORBIT score v CHA2DVAS2c
warfarin or NOACs (less risk of bleeding, less monitoring, more effective, no major interactions)

51
Q

what are S3 and S4?

A

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
Q

where are S1 and S2 heard best?

A

Erb’s point - 3rd ICS, LSE

53
Q

what are the accentuation manoeuvres?

A

sat up, forward and exhaled - AR, left hand side - MS

54
Q

what are the murmur grades?

A

v quiet, quiet, loud, loud and thrill, v loud near chest and v loud off chest

55
Q

what are the causes of MS and what murmur?

A

IE, RHD
mid diastolic, low pitched rumbling, loud S1

56
Q

what are the causes of MR and what murmur?

A

IHD, IE, RHD, CT disorders, idiopathic
pan-systolic high pitched radiating to left anxilla

57
Q

what causes AR and what is the murmur?

A

idiopathic, CT disorders
early diastolic soft murmur, collapsing pulse

58
Q

what causes AR and what murmur?

A

idiopathy, RHD
ejection systolic high pitched crescendo-decrescendo radiating to carotid

59
Q

what do each of the above murmurs cause?

A

MR - LA dilatation
AR - LV dilatation
MS - RA hypertrophy
AS - RV hypertrophy

60
Q

what is the most common scar with a prosthetic heart valve?

A

midline sternotomy

61
Q

what is transcatheter aortic valve implantation used for?

A

severe aortic stenosis

62
Q

what are the complications of prosthetic heart valves?

A

thrombus, IE, haemolysis, clicking for S1 and S2

63
Q

which has a longer lifespan, bioprosthetic or metal?

A

mechanical - 20 years whereas bioprosthetic 10 years
need warfarin if mechanical

64
Q

how common is IE with prosthetic heart valves and what causes it?

A

2.5% or 1.5% if TAVI
mortality of around 15%
caused by gram positive cocci - staph, strep, entero

65
Q

what is the criteria for HTN?

A

clinic BP >140/90 or home 135/85

66
Q

what are the causes of HTN?

A

primary - essential - idiopathic
secondary - renal, obesity, endocrine, pregnancy

67
Q

what are the complications of HTN?

A

IHD, CVA, hypertensive neuro/retinopathy, HF

68
Q

how often is HF screened for?

A

every 5 years unless DM or other RF or on border - every year

69
Q

what are the targets for BP with treatment?

A

<80 years: <140/90
>80 years: <150/90

70
Q

what are the stages of HTN?

A
  1. 140/90 or 135/85
  2. 160/100 or 150/95
  3. > 180/120
71
Q

how do you check for end organ damage in HTN?

A

urine albumin:creatinine radio
bloods - HbA1c, renal function, lipids
fundus
ECG

72
Q

how do you treat HTN?

A

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
Q

what are the indications for pacemakers?

A

symptomatic bradycardia, T2AVNB, 3rd degree block, severe HF, hypertrophic obstructive cardiomyopathy

74
Q

how do pacemakers work?

A

they deliver electrical impulses to areas to restore activity using pulse generator and tracing leads under skin

75
Q

how long do pacemakers last?

A

batteries last 5 years
removed prior to cremation

76
Q

what are the ECG changes of pacemakers?

A

sharp, vertical line on all leads
before P - atrial
before QRS - ventricular
before both - dual chamber

77
Q

what do ICDs do?

A

continually monitor and shock if required to return to sinus rhythm

78
Q

where are pacemakers put?

A

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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