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BDS2 BAMS > Cardiovascular Medicine > Flashcards

Cardiovascular Medicine Flashcards

1
Q

2 main processes in ACS

A
  1. blood vessel narrowing
  2. blood vessel occlusion (much more dramatic)
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2
Q

3 main arteries supplying the heart

A
  1. right coronary
  2. left anterior descending coronary
  3. circumflex coronary
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3
Q

blood flow to coronary tissue during systole

A

no blood flow to coronary tissue through right or left circumflex coronary it only flows when valve is shut during diastole

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4
Q

atherosclerosis

A

area of stress in artery and turbulent blood flow causes damage to interior wall of artery allowing accumulation of fat within surface thus narrowing vessel

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5
Q

3 main causes of ACS

A
  1. atherosclerosis itself can proceed gradually causing ischaemia which can be reversed if oxygen demand is reduced
  2. build up of clot on atherosclerosis - can happen quickly. this is what happens in many cases of MI
  3. spasm of arteries can narrow artery and cause prinzmetal angina
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6
Q

stable angina

A

demand ischaemia, vessel unable to dilate enough, pain on exertion, no infarct, ECG is normal, troponin is normal

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7
Q

unstable angina

A

supply ischaemia, no infarct, partial occlusion of vessel, pain at rest, ECG can be normal, inverted T waves or ST depression, troponins normal

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8
Q

is stable and unstable angina reversible

A

yes

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9
Q

NSTEMI

A

type of MI. subendocardial infarct. ECG inverted T waves or potential ST segment depression but no elevation. troponin elevated.

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10
Q

STEMI

A

type of MI. complete occlusion of vessel - transmural infarct. ST elevation. elevated troponin.

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11
Q

ACS diagnosis

A
  1. history
  2. ECG findings - STEMI = ST elevation, NSTEMI = non ST elevation
  3. biomarkers - raised troponin
    ptx will present with central crushing chest pain
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12
Q

what is angina

A

reversible ischaemia of the heart muscle i.e. narrowing of one or more coronary arteries

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13
Q

stable angina symptoms

A
  • no pain at rest
  • pain with certain level of exertion
  • pain relieved by rest
  • ptx lives within limits of tolerance
  • gradual deterioration
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14
Q

stable angina signs

A

often non occasional hyperdynamic circulation i.e. anaemia/hyperthyroidism/hypervolemic

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15
Q

angina investigations

A

ECG - resting AND exercise
eliminate other disease e.g. thyroid/valve
angiography
echocardiography
isotope studies

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16
Q

what would show in exercise ECG of someone with angina

A

ST segment depression (due to ischaemia increase)
ECG changes resolve when exercise stops

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17
Q

2 main forms of angina treatment

A
  1. reducing oxygen demands of heart
  2. increasing oxygen delivery to tissues
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18
Q

how to reduce oxygen demands of heart

A
  • reduce afterload i.e. bp
  • reduce preload i.e. venous filling pressure
  • correct mechanical issues i.e. failing heart valves, septal defects
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19
Q

how to increase oxygen delivery to tissues

A
  • dilate blocked/narrowed vessels through angioplasty (and/or stent)
    -bypass blocked/narrowed arteries through CABG
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20
Q

CABG

A

coronary artery bypass grafting

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21
Q

risk factors of acs

A

smoking
diet
exercise
cholesterol

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22
Q

to reduce MI risk give

A

aspirin

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23
Q

what drugs reduce hypertension

A

diuretics, Ca channel antagonists, ACE inhibitors, beta blockers

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24
Q

emergency treatment of angina attack

A

GTN (glyceryl trinitride). short shelf life. reduces preload. give sublingually due to FPM.

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25
Q

options for surgical therapy for ACS

A

CABG - limited benefit of 10yrs, major surgery

Angioplasty + stenting - lower risk but lower benefit, risk of vessel rupture during procedure, PCI (percutaneous intervention), needs dual anti-platelet therapy

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26
Q

what is pvd

A

peripheral vascular disease
‘angina’ of lower limb
atheroma in femoral/popliteal vessels
intermittent claudication during exercise

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27
Q

how does ischaemia become infarction

A
  • atheroma in vessels, thrombosis on surface
  • thrombosis can enlarge rapidly to block vessel
  • plaque surface/platelets detach, travel downstream and block vessels
  • no blood flow to the area causes infarction
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28
Q

tissue death if infarcted for how long

A

> 20 mins

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29
Q

where infarction happens (3)

A

heart - coronary artery atheroma
limb - femoral & popliteal arteries
brain - carotid arteries (aka embolic stroke)

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30
Q

immediate action for an infarction

A

reduce tissue loss from necrosis
1. open blood flow to ischaemic tissue i.e. thrombolysis / angioplasty
2. bypass obstruction i.e. fem/pop bypass, CABG

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31
Q

to prevent further MI

A

risk factor management
aspirin

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32
Q

transient ischaemic attacks are known as

A

stroke

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33
Q

how does a stroke happen

A

blood clot from diseased carotid artery breaks off and travels to cerebral artery where it lodges and causes a stroke

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34
Q

signs and symptoms of MI

A

chest pain which travels from left arm to neck, nausea, sweating, shortness of breath, anxiety, fatigue, weakness, abnormal heartbeat

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35
Q

to diagnose MI

A
  • history; this is key
  • ECG findings; NSTEMI/STEMI
  • biomarkers; troponin - must be checked on admission and 24hrs later
    key - MI can happen without a specific trigger
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36
Q

primary care of MI

A

get patient to hospital alive
analgesia, aspirin & reassurance
BLS if required

note - MI does not always cause cardiac arrest but may happen due to arrhythmia from altered electrical conduction in heart tissues

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37
Q

MI treatment up to 3hrs from onset

A

primary PCI - acute angioplasty & stenting if available

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38
Q

MI treatment up to 6hrs from onset

A

thrombolysis - will dissolve blood clot that has blocked arteries

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39
Q

further MI treatment

A

drug treatment to improve penumbra (tissue surrounding infarction) which will make final damage on cardiac less

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40
Q

contraindications for thrombolysis

A
  1. injury/surgery/IM injections - recent blood clots would be dissolved
  2. severe hypertension, active PUD - would exacerbate active bleeding
  3. diabetic eye disease, liver disease, pregnancy
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41
Q

complications of MI

A
  1. death
  2. post MI arrythmias
  3. heart failure
  4. ventricular hypofunction & mural thrombosis
  5. DVT & pulmonary embolism
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42
Q

long term medical management of MI

A
  1. prevent next MI - risk modification/aspirin/beta blocker/ACE inhibitor
  2. treat complications - heart failure/arrhythmias/psychological distress
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43
Q

what are cardiac arrhythmias

A

disorders of heart rate

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44
Q

2 types of cardiac arrhythmias

A

1, tachyarrhythmia - FAST
atrial fibrillation / ventricular tachycardia

  1. bradyarrhythmia - SLOW
    heart block / drug induced ! via beta blocker or digoxin
45
Q

heart block

A
  • slow / no conduction through AV node to ventricles of impulse from SA node
  • prolonged P-Q interval on ECG
  • different levels of block depending on length of signal delay
46
Q

different classifications of heart block

A

1st degree = split second delay
2nd degree = 2 types, in both the P wave is blocked from initiating QRS complex
3rd degree = 30bpm - known as complete heart block as no impulse passed to ventricles

47
Q

most common way to treat heart block

A

external pacemaker used to pace ventricles

48
Q

what does tachyarrhythima do

A

impairs cardiac function by reducing diastolic filling time and reduced output leads to heart failure

49
Q

2 types of tachyarrhythmia

A

atrial - rapid atrial impulses conducted to ventricles giving high HR. narrow QRS on ECG (ventricular depolarisation)
ventricular - broad QRS as time taken for signal to pass through all ventricular muscle is increased. can lead to ventricular fibrillation and death.

50
Q

atrial fibrillation

A

irregularly irregular pulse

51
Q

when to use cardiac pacemakers

A

used to treat BRADYarrhythmias

52
Q

why use cardiac pacemakers

A

keep HR at minimum level
don’t ‘pace’ if HR above certain level i.e. 50bpm
have a ‘sensing’ and ‘pacing’ circuit
box fitted in chest wall, wires passed through blood vessels in sequence

53
Q

when would there be electrical interference with pacemaker

A

dental equipment - theoretical risk only
pulp testers are okay
avoid induction scalers though

54
Q

p wave

A

atrial depolarisation

55
Q

qrs complex

A

ventricular depolarisation

56
Q

t wave

A

ventricular repolarisation

57
Q

normal PQRST is called

A

sinus rhythm

58
Q

when would you have ventricular fibrillation

A

heart attack
electrocution
long QT syndrome - drug induced
Wolf-Parkinson-White syndrome

59
Q

what is ventricular fibrillation

A

unstable heart electrical activity
no cardiac output
no emptying of ventricle
requires defib externally or internally
looks like a squiggle on ECG

60
Q

asystole

A

no cardiac output
no electrical activity
defib not possible
treated with adrenaline to try produce electrical activity
low chance of survival
almost flat line on ECG

61
Q

irreversible risk factors for cardiovascular disease

A

age
sex
family history

62
Q

reversible factors for cardiovascular disease

A

smoking
obesity
diet
exercise
hypertension
hyperlipidaemia
diabetes

63
Q

primary prevention of CVD

A

exercise, diet, smoking
assess total risk

64
Q

secondary prevention of CVD

A

same as primary with addition of medical treatment

65
Q

3 types of anti-platelet drugs

A

aspirin
clopidogrel
dipyridamole

66
Q

aspirin

A

inhibits platelet aggregation
alters balance between throboxane A2 and prostacyclin
irreversible for life of platelet (7days)

67
Q

aspirin dose

A

low dose
75mg daily

68
Q

clopidogrel

A

inhibits ADP induced platelet aggregation

69
Q

dipyridamole

A

inhibits platelet phosphodiesterase

70
Q

can you use different anti-platelet drugs together

A

yes, their effect is additive

71
Q

why use anti - platelet drugs

A

significantly reduce chance of heart attack or stroke but only in ‘at risk’ population

72
Q

issues with anti-platelets and dentistry

A

prolonged bleeding time
drug combinations increase risk

73
Q

why take oral anticoagulants

A

taken to inhibit clotting cascade but do not affect platelets

74
Q

why take oral anticoagulants

A

taken to inhibit clotting cascade but do not affect platelets. reduce fibrin formed and therefore clot stability

75
Q

examples of oral anticoagulants

A

warfarin
rivaroxiban
apixaban
dabigatran
edoxaban

76
Q

how do oral anticoagulants impact bleeding in dentistry

A

stop bleeding in normal time but clot will not stabilise and will break down after a few hours causing bleeding to start again

77
Q

what is warfarin and what does it do

A

coumarin based anticoagulant
inhibits synthesis of Vitamin K dependent clotting factors i.e. 2, 7, 9, 10 and proteins C and S

78
Q

initial hypercoagulation on warfarin

A

anticoagulation takes 2-3 days
so hypercoagulated until factors 2 7 9 10 removed
need heparin to get anticoagulated straight away

79
Q

what is INR

A

international normalised ratio

80
Q

how does inr work

A

ratio of conversion of prothrombin to thrombin in a normal individual and patient

81
Q

inr of warfarinised patient

A

should aim for 2-4

82
Q

why monitor INR regularly

A

degree of anti coagulation changes regularly due to interaction with food and other drugs. it binds to plasma proteins and is metabolised in the liver so any drugs that interact or affect this can interfere with warfarin action.

83
Q

what are local haemostatic measures (3)

A

fibrinogen activator
suture
LA with vasoconstrictor

84
Q

can you do IDB if patient on warfarin

A

yes if INR is 2-4 but try to avoid if possible but not contraindicated like in haemophiliac patients

85
Q

what happens if INR too high / too low

A

too low - will not have protection offered by drug and will produce too many clots
too high - puts patient at risk of internal bleeding

86
Q

why are NOACs different to warfarin

A

they do not require the same monitoring as they are predictable in their bioavailability
short half life
no significant drug interactions in dentistry

87
Q

what are statins and how do they work

A

they are lipid lowering drugs that work by inhibiting cholesterol synthesis in the liver thus reducing total cholesterol and LDL

88
Q

key interactions of statins

A

with antifungals i.e. fluconazole so omit statin during antifungal treatment

89
Q

possible side effect of statins

A

possible myositis if plasma level of drug gets too high

90
Q

how do beta blockers work

A

reduce excitability of cardiac conduction + stop arrhythmias + important to take following MI to reduce chances of VF and death

91
Q

difference in beta blockers

A

atenolol - selective - beta 1 receptors only
pronanolol - non selective - beta 1 and 2

92
Q

beta blockers and asthma

A

salbutamol is a beta 2 agonist and if patient takes beta 2 blocker it will prevent action of salbutamol in lungs if asthma attack occurs

93
Q

3 limitations of beta blockers

A
  1. prevent increase in HR causing postural hypotension
  2. reduce heart efficiency making heart failure worse (negative inotrope)
  3. block beta receptors in lungs
94
Q

2 types of diuretics

A

thiazide diuretics - bendroflumethiazide
loop diuretcis - frusemide

95
Q

uses of diuretics

A

antihypertensive
heart failure

96
Q

how do diuretics work

A

increase salt and water loss from plasma thus reducing plasma volume and cardiac workload

97
Q

side effects of diuretics

A

can lead to Na+/K+ imbalance
dry mouth in elderly

98
Q

2 types of nitrates

A
  1. SA - GTN - emergency management of angina
  2. LA - isosorbide mononitrate - prevention of angina
99
Q

how should nitrates be administered

A

-sublingual
-transdermal
-intravenous
inactivated by FPM

100
Q

how do nitrates work

A
  1. dilate veins (preload)
  2. dilate resistance arteries (afterload)
  3. dilate collateral coronary artery supply
101
Q

how do calcium channel blockers work

A

work via calcium channels and change smooth muscle action in blood vessel walls

102
Q

what are calcium channel blockers used for

A

hypertension
migraine

103
Q

eg of calcium channel blockers

A

nifedipine, amlodipine - more active on peripheral blood vessels
verapamil - more active on heart muscle

104
Q

side effects of calcium channel blockers

A

gingival hyperplasia

105
Q

what does ACE in ACE inhibitors stand for

A

angiotensin converting enzymes

106
Q

examples of ACE inhibitors

A

enalapril
ramapril
lisinopril

107
Q

how do ACE inhibitors work

A

inhibit conversion of angiotensin I to angiotensin II which prevents aldosterone dependent reabsorption of salt and water

108
Q

how does angiotensin II work

A

potent vasoconstrictor as well as triggering aldosterone dependent water reabsorption

109
Q

what happens when angiotensin II is inhibited

A

inhibition acts as a direct vasodilator on arteries and reduction in plasma volume by preventing salt and water reabsorption

BDS2 BAMS (3 decks)

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