Cardiovascular Medicine Flashcards
1
Q
2 main processes in ACS
A
- blood vessel narrowing
- blood vessel occlusion (much more dramatic)
2
Q
3 main arteries supplying the heart
A
- right coronary
- left anterior descending coronary
- circumflex coronary
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
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
5
Q
3 main causes of ACS
A
- atherosclerosis itself can proceed gradually causing ischaemia which can be reversed if oxygen demand is reduced
- build up of clot on atherosclerosis - can happen quickly. this is what happens in many cases of MI
- spasm of arteries can narrow artery and cause prinzmetal angina
6
Q
stable angina
A
demand ischaemia, vessel unable to dilate enough, pain on exertion, no infarct, ECG is normal, troponin is normal
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
8
Q
is stable and unstable angina reversible
A
yes
9
Q
NSTEMI
A
type of MI. subendocardial infarct. ECG inverted T waves or potential ST segment depression but no elevation. troponin elevated.
10
Q
STEMI
A
type of MI. complete occlusion of vessel - transmural infarct. ST elevation. elevated troponin.
11
Q
ACS diagnosis
A
- history
- ECG findings - STEMI = ST elevation, NSTEMI = non ST elevation
- biomarkers - raised troponin
ptx will present with central crushing chest pain
12
Q
what is angina
A
reversible ischaemia of the heart muscle i.e. narrowing of one or more coronary arteries
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
14
Q
stable angina signs
A
often non occasional hyperdynamic circulation i.e. anaemia/hyperthyroidism/hypervolemic
15
Q
angina investigations
A
ECG - resting AND exercise
eliminate other disease e.g. thyroid/valve
angiography
echocardiography
isotope studies
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
17
Q
2 main forms of angina treatment
A
- reducing oxygen demands of heart
- increasing oxygen delivery to tissues
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
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
20
Q
CABG
A
coronary artery bypass grafting
21
Q
risk factors of acs
A
smoking
diet
exercise
cholesterol
22
Q
to reduce MI risk give
A
aspirin
23
Q
what drugs reduce hypertension
A
diuretics, Ca channel antagonists, ACE inhibitors, beta blockers
24
Q
emergency treatment of angina attack
A
GTN (glyceryl trinitride). short shelf life. reduces preload. give sublingually due to FPM.
25
options for surgical therapy for ACS
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
26
what is pvd
peripheral vascular disease
'angina' of lower limb
atheroma in femoral/popliteal vessels
intermittent claudication during exercise
27
how does ischaemia become infarction
- 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
28
tissue death if infarcted for how long
>20 mins
29
where infarction happens (3)
heart - coronary artery atheroma
limb - femoral & popliteal arteries
brain - carotid arteries (aka embolic stroke)
30
immediate action for an infarction
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
31
to prevent further MI
risk factor management
aspirin
32
transient ischaemic attacks are known as
stroke
33
how does a stroke happen
blood clot from diseased carotid artery breaks off and travels to cerebral artery where it lodges and causes a stroke
34
signs and symptoms of MI
chest pain which travels from left arm to neck, nausea, sweating, shortness of breath, anxiety, fatigue, weakness, abnormal heartbeat
35
to diagnose MI
- 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
36
primary care of MI
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
37
MI treatment up to 3hrs from onset
primary PCI - acute angioplasty & stenting if available
38
MI treatment up to 6hrs from onset
thrombolysis - will dissolve blood clot that has blocked arteries
39
further MI treatment
drug treatment to improve penumbra (tissue surrounding infarction) which will make final damage on cardiac less
40
contraindications for thrombolysis
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
41
complications of MI
1. death
2. post MI arrythmias
3. heart failure
4. ventricular hypofunction & mural thrombosis
5. DVT & pulmonary embolism
42
long term medical management of MI
1. prevent next MI - risk modification/aspirin/beta blocker/ACE inhibitor
2. treat complications - heart failure/arrhythmias/psychological distress
43
what are cardiac arrhythmias
disorders of heart rate
44
2 types of cardiac arrhythmias
1, tachyarrhythmia - FAST
atrial fibrillation / ventricular tachycardia
2. bradyarrhythmia - SLOW
heart block / drug induced ! via beta blocker or digoxin
45
heart block
- 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
different classifications of heart block
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
most common way to treat heart block
external pacemaker used to pace ventricles
48
what does tachyarrhythima do
impairs cardiac function by reducing diastolic filling time and reduced output leads to heart failure
49
2 types of tachyarrhythmia
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
atrial fibrillation
irregularly irregular pulse
51
when to use cardiac pacemakers
used to treat BRADYarrhythmias
52
why use cardiac pacemakers
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
when would there be electrical interference with pacemaker
dental equipment - theoretical risk only
pulp testers are okay
avoid induction scalers though
54
p wave
atrial depolarisation
55
qrs complex
ventricular depolarisation
56
t wave
ventricular repolarisation
57
normal PQRST is called
sinus rhythm
58
when would you have ventricular fibrillation
heart attack
electrocution
long QT syndrome - drug induced
Wolf-Parkinson-White syndrome
59
what is ventricular fibrillation
unstable heart electrical activity
no cardiac output
no emptying of ventricle
requires defib externally or internally
looks like a squiggle on ECG
60
asystole
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
irreversible risk factors for cardiovascular disease
age
sex
family history
62
reversible factors for cardiovascular disease
smoking
obesity
diet
exercise
hypertension
hyperlipidaemia
diabetes
63
primary prevention of CVD
exercise, diet, smoking
assess total risk
64
secondary prevention of CVD
same as primary with addition of medical treatment
65
3 types of anti-platelet drugs
aspirin
clopidogrel
dipyridamole
66
aspirin
inhibits platelet aggregation
alters balance between throboxane A2 and prostacyclin
irreversible for life of platelet (7days)
67
aspirin dose
low dose
75mg daily
68
clopidogrel
inhibits ADP induced platelet aggregation
69
dipyridamole
inhibits platelet phosphodiesterase
70
can you use different anti-platelet drugs together
yes, their effect is additive
71
why use anti - platelet drugs
significantly reduce chance of heart attack or stroke but only in 'at risk' population
72
issues with anti-platelets and dentistry
prolonged bleeding time
drug combinations increase risk
73
why take oral anticoagulants
taken to inhibit clotting cascade but do not affect platelets
74
why take oral anticoagulants
taken to inhibit clotting cascade but do not affect platelets. reduce fibrin formed and therefore clot stability
75
examples of oral anticoagulants
warfarin
rivaroxiban
apixaban
dabigatran
edoxaban
76
how do oral anticoagulants impact bleeding in dentistry
stop bleeding in normal time but clot will not stabilise and will break down after a few hours causing bleeding to start again
77
what is warfarin and what does it do
coumarin based anticoagulant
inhibits synthesis of Vitamin K dependent clotting factors i.e. 2, 7, 9, 10 and proteins C and S
78
initial hypercoagulation on warfarin
anticoagulation takes 2-3 days
so hypercoagulated until factors 2 7 9 10 removed
need heparin to get anticoagulated straight away
79
what is INR
international normalised ratio
80
how does inr work
ratio of conversion of prothrombin to thrombin in a normal individual and patient
81
inr of warfarinised patient
should aim for 2-4
82
why monitor INR regularly
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
what are local haemostatic measures (3)
fibrinogen activator
suture
LA with vasoconstrictor
84
can you do IDB if patient on warfarin
yes if INR is 2-4 but try to avoid if possible but not contraindicated like in haemophiliac patients
85
what happens if INR too high / too low
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
why are NOACs different to warfarin
they do not require the same monitoring as they are predictable in their bioavailability
short half life
no significant drug interactions in dentistry
87
what are statins and how do they work
they are lipid lowering drugs that work by inhibiting cholesterol synthesis in the liver thus reducing total cholesterol and LDL
88
key interactions of statins
with antifungals i.e. fluconazole so omit statin during antifungal treatment
89
possible side effect of statins
possible myositis if plasma level of drug gets too high
90
how do beta blockers work
reduce excitability of cardiac conduction + stop arrhythmias + important to take following MI to reduce chances of VF and death
91
difference in beta blockers
atenolol - selective - beta 1 receptors only
pronanolol - non selective - beta 1 and 2
92
beta blockers and asthma
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
3 limitations of beta blockers
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
2 types of diuretics
thiazide diuretics - bendroflumethiazide
loop diuretcis - frusemide
95
uses of diuretics
antihypertensive
heart failure
96
how do diuretics work
increase salt and water loss from plasma thus reducing plasma volume and cardiac workload
97
side effects of diuretics
can lead to Na+/K+ imbalance
dry mouth in elderly
98
2 types of nitrates
1. SA - GTN - emergency management of angina
2. LA - isosorbide mononitrate - prevention of angina
99
how should nitrates be administered
-sublingual
-transdermal
-intravenous
inactivated by FPM
100
how do nitrates work
1. dilate veins (preload)
2. dilate resistance arteries (afterload)
3. dilate collateral coronary artery supply
101
how do calcium channel blockers work
work via calcium channels and change smooth muscle action in blood vessel walls
102
what are calcium channel blockers used for
hypertension
migraine
103
eg of calcium channel blockers
nifedipine, amlodipine - more active on peripheral blood vessels
verapamil - more active on heart muscle
104
side effects of calcium channel blockers
gingival hyperplasia
105
what does ACE in ACE inhibitors stand for
angiotensin converting enzymes
106
examples of ACE inhibitors
enalapril
ramapril
lisinopril
107
how do ACE inhibitors work
inhibit conversion of angiotensin I to angiotensin II which prevents aldosterone dependent reabsorption of salt and water
108
how does angiotensin II work
potent vasoconstrictor as well as triggering aldosterone dependent water reabsorption
109
what happens when angiotensin II is inhibited
inhibition acts as a direct vasodilator on arteries and reduction in plasma volume by preventing salt and water reabsorption
