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Phase 2b > Cardiovascular revision > Flashcards

Cardiovascular revision Flashcards

1
Q

what ECG leads show the right coronary artery

A

aVF, 2, 3

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2
Q

what side of the heart do leads aVF, 2, and 3 represent

A

inferior

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3
Q

what ECG leads represent the left anterior descending artery

A

V1-V4

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4
Q

what side of the heart do leads V1-V4 show

A

anterior and septal

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5
Q

what ECG leads represent the left circumflex artery

A

V5, V6, aVL, 1

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6
Q

what side of the heart do leads V5, V6, aVL and 1 show

A

lateral

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7
Q

what makes the S1 heart sound

A

mitral and tricuspid closure

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8
Q

what makes the second heart sound

A

aortic and pulmonary valve closure

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9
Q

What does S3 heart sound show

A

rapid ventricular filling in early diastole

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10
Q

when is the S3 heart sound normal

A

young/pregnant people

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11
Q

What pathology does the S3 heart sound mean

A

mitral regurg and heart failure

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12
Q

What is the S4 heart sound

A

pathological gallop

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13
Q

what causes the pathological gallop (S4)

A

due to blood forced into stiff hypertrophic ventricle (LVH + aortic stenosis)

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14
Q

what are the two broad categories of ischaemic heart disease

A

angina and MI

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15
Q

what causes central crushing chest pain

A

myocardial ischaemia as a result of reduced flow in the coronary arteries

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16
Q

what are the three categories of angina pain

A

1) central crushing chest pain +/- radiating to neck/jaw
2) brought on by exertion
3) relieved with 5 mins rest or GTN spray

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17
Q

what are the three acute coronary syndromes

A

unstable
NSTEMI
STEMI

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18
Q

what are the levels of ischaemia/infarction in the three types of ACS

A

unstable - severe ischaemia
NSTEMI - partial infarction
STEMI - transmural infarct

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19
Q

what is the QRISK score

A

predicts risk of CVD in 10 upcoming years
(score of 10+ = 10% + risk in next 10 years)

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20
Q

what should be started with a 10+ score in QRISK

A

lipid lowering therapy - statins = primary prevention

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21
Q

what are the 4 types of angina

A

stable
unstable
prinzmetals
decubitus

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22
Q

what is stable and unstable angina

A

stable - normal 3 part definition
unstable - pain at rest, not relieved with GTN or inactivity

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23
Q

what is prinzmetals angina

A

due to coronary vasospasm (not CV vessel atherogenesis)

24
Q

who might have prinzmetals angina

A

cocaine users

25
Q

what would an ECG show in prinzmetals angina

A

ST elevation

26
Q

what is decubitus angina

A

induced when patient lies flat

27
Q

risk factors for ischaemic heart disease

A

obesity
T2DM
HTN
smoking
age (older)
male
FHx
cocaine use

28
Q

what are the three steps of atherogenesis

A

fatty streaks
intermediate lesions
fibrous plaques (advanced)

29
Q

where does the fatty streak form and in what age group and how does it occur

A

appears in internal wall
less than 10 y/o
T-cells and lipid laden macrophages (foam cells)

30
Q

what occurs in the intermediate lesions

A

foam cells (bigger, taken up lipids), T-cells + vascular smooth muscle cells

platelets also aggregate and adhere to site, inside vessel lumen

31
Q

what occurs in the fibrous plaques

A

large lesions (foam cells, T-cells, smooth muscle, fibroblasts, lipids with a necrotic core) develop fibrosis cap over top of lesion

32
Q

at what percent of lumen occlusion does symptoms of stable angina begin to occur

A

70-80%

33
Q

symptoms of ischaemic heart disease

A

central crushing chest pain +/- radiate to jaw/neck
nausea
sweating
fatigue
dyspnoeic weak breathing

34
Q

diagnosis for stable angina

A

1st line -ECG - resting = normal, exercise induced (ischaemic) results in change
GS - CT angiography = stenosed atherosclerotic arteries

35
Q

treatment for symptoms of stable angina

A

GTN sublingual spray

36
Q

lifestyle modifications to treat stable angina

A

decrease weight
stop smoking
healthy diet

37
Q

pharmacological treatment for angina

A

1) CCB (amlodipine) (heart failure = CI) or beta-blocker (bisoprolol)(astham = CI)

2)CCB + Beta-blocker

3) CCB + BB + antianginal - ivabradine or long-acting nitrates

38
Q

what CCB are not appropriate for angina and why

A

non-rate limiting; can cause excessive bradycardia

-not verapamil or diltiazem

39
Q

surgical options for angina (ischaemic heart disease)

A

revascularisation
PCI - balloon stent coronary artery
CABG - bypass graft (LAD bypassed by LMA)

40
Q

pros and cons of PCI and CABG

A

PCI + less invasive, - risk of stenosis

CABG + better prognosis, - more invasive

41
Q

what are the two types of MI and what causes them

A

type 1 - IHD
type 2 - increase demand or cavasospasm

42
Q

what are the three categories for ACS

A

unstable angina
NSTEMI
STEMI

43
Q

what are the ECG changes seen after an MI

A

hyperacute T waves
pathologically deep Q waves
LBBB

44
Q

What is the occlusion, infarction, ECG and trop and creatine kinase status in unstable angina

A

partial occlusion of minor coronary artery
no infarction, ischaemia only
normal ECG - maybe some ST depression / T wave inversion
No trop/CK change

45
Q

What is the occlusion, infarction, ECG and trop and creatine kinase status in NSTEMI

A

major / partial occlusion of total minor coronary artery
sub-endothelial infarction (area far away from CA occlusion dies)
ECG shows ST depression and T wave inversion and no Q waves
Elevated trop

46
Q

What is the occlusion, infarction, ECG and trop and creatine kinase status in STEMI

A

total occlusion of major CA
there is transmural infarction
ST segment elevation in local leads + Q waves
elevated trop and CK due to infarction

47
Q

is trop or CK a better marker for ACS

A

trop has a shorter half-life and may be better a few days after event

48
Q

symptoms of ACS

A

same as stable angina, but pain is at rest and not relievable
palpitations and may be more severe

49
Q

diagnosis of ACS

A

ECG
biomarkers
CT angiogram - shows extent of occlusion

50
Q

acute treatment of ACS episode

A

morphine
O2 (if sats <94%)
GTN
aspirin (300mg)
clopidogrel (75mg)

51
Q

what is the GRACE score

A

mortality risk of patients with ACS from MI (w/in 6 months-3years)

52
Q

what to do in a NSTEMI/unstable angina with a high risk GRACE score

A

immediate angiogram + consider PCI

53
Q

STEMI treatment

A

PCI - w/in 12 hours of symptom onset / <2 hours of first medical contact
thrombolysis if >12hours with alteplase

54
Q

what can be used in long term prevention for ACS

A

beta-blocker (life)
aspirin (300mg, then 75mg for life)
atorvastatin (80mg life)
ACE-i (life)
clopidogrel (75mg for 12mnths)

55
Q

complications of ACS

A

short term - HF due to vent fibrillation, mitral incompetence, LV free wall rupture, cardiogenic shock

longer than 2 wks - dressler syndrome (autoimmune pericarditis), HF, LV aneurysm, heart literally becomes saggy

56
Q
A

Phase 2b (16 decks)

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