CVS Week 2 Flashcards
1
Q
describe the impact of fixed vessel narrowing in the setting of stable coronary artery disease
A
in the presence of mild to moderate atherosclerosis, there is still preservation of coronary blood flow
however, in extensive narrowing, there is a pressure drop across the stenosis, leading to limited vessel flow
2
Q
what are 3 factors that determines the hemodynamic significance of stenotic lesions
A
length of lesion and extent of narrowing
degree of compensatory vasodilation
myocardial O2 demand
3
Q
how does endothelial dysfunction contribute to, and exacerbate, myocardial ischemia
A
impaired release of vasodilators, leading to a net vasoconstrictive effect
decline in antithrombotic properties of vasodilators such as NO and prostacyclins
4
Q
describe the impact of metabolic disruption during ischemia
A
normally, the healthy myocardium uses fatty acids as the predominant substrate
however, when there is restricted O2 supply during ischemia, there is limited oxidative phosphorylation, resulting in increased rate of glycolysis and a shift from net lactate uptake to lactate production
5
Q
what are 4 non-atherosclerotic factors that can result in ischemia
A
rapid elevation of myocardial O2 demand e.g rapid tachycardia
decreased blood O2 carrying capacity (anemia)
coronary vasospasm
congenital abnormalities or trauma to coronary arteries
6
Q
what is coronary artery disease (CAD)
A
pathological process characterised by atherosclerotic plaque accumulation in the epicardial arteries, whether obstructive or non-obstructive
7
Q
what are two types of stable CAD/chronic coronary syndrome (CSS)
A
fixed obstructive CAD
ischemia w non-obstructive coronary arteries (INOCA)
8
Q
what are 3 types of angina
A
chronic stable
unstable
prinzmetal’s variant
9
Q
describe chronic stable angina
A
demand ischemia
coronary flow impaired under conditions of high O2 demand leading to ischemia
10
Q
describe unstable angina / prinzmetal angina
A
supply ischemia
coronary flow impaired under resting conditions leading to ischemia
11
Q
what are the 3 characteristics/criteria of angina
A
constricting discomfort in the front of the chest or in the neck, jaw, shoulder, arm
precipitated by physical exertion
relieved by rest or nitrates within 5 min
12
Q
typical angina meets how many things in the angina criteria
A
all 3
13
Q
atypical angina meets how many things in the angina criteria
A
2 of the 3
14
Q
non-anginal chest pain meets how many things in the angina criteria
A
one or none
15
Q
describe grade 1 angina
A
angina only with strenuous exertion
presence of angina during strenuous, rapid, or prolonged ordinary activity (walking or climbing the stairs)
16
Q
describe grade 2 angina
A
angina w moderate exertion
slight limitation of ordinary activities when performed rapidly, after meals, in cold, in wind, walking uphill etc.
17
Q
describe grade 3 angina
A
angina w mild exertion
having difficulties walking one or two blocks, or climbing one flight of stairs at normal pace and conditions
18
Q
describe grade 4 angina
A
angina at rest
no exertion needed to trigger angina
19
Q
what are the 2 contemporary types of acute coronary syndrome (ACS)
A
non-ST elevatin myocardial infarction (NSTEMI)
ST-elevation myocardial infarction (STEMI)
20
Q
traditionally, unstable angina also used to be considered as a type of ACS. why is this not the case anymore?
A
traditionally, UA was defined by absence of an elevated biomarker (troponin) level.
however, now that we have moved from sensitive tests to highly sensitive tests, the biomarker troponin can be seen to be present more often than before, meaning the diagnosis of UA under these conditions has now changed to NSTEMI
21
Q
what is cardiac troponin
A
specific and sensitive biomarker of cardiac injury
22
Q
what is the most common reason of ACS
A
obstruction of coronary artery blood flow by thrombus that develops as a result of underlying atherosclerotic plaque complication
23
Q
what are 4 less common causes of ACS
A
spontaneous coronary artery dissection (SCAD)
coronary artery spasm
coronary microvascular dysfunction
MI w non obstructed coronary arteries (MINOCA)
24
Q
describe plaque rupture
A
most frequent
develops in a lesion w a necrotic core and thin overlying fibrous cap
following disruption of fibrous cap, a luminal thrombus develops due to physical contact b/w platelets and thrombogenic necrotic core
25
describe plaque erosion
characterised by absence of endothelium rather than fibrous cap disruption
most eroded lesions lack a necrotic core and have a thick fibrous cap
lead to disturbance of flow resulting in toll-like receptor 2 activation, recruitment of neutrophils and subsequent promotion of de-endothelialisation. this allows blood to come in contact w plaque collagen to form neutrophil-rich thrombus
26
terms STEMI and NSTEMI correctly used in patients with...
clinical characteristics compatible w myocardial ischemia
AND
demonstrate elevated troponin
27
what 3 things must be taken into account to diagnose ACS
symptoms
ECG
serum troponin
28
describe symptoms patients with acute MI may present with
pain - chest (most common), abdomen, intrascapular, throat, jaw
dyspnea
diaphoresis (sweating)
nausea/vomiting
palpitations
weakness
29
the typical symptoms of an MI may not be present in...
women
diabetics
older individuals
30
an ECG allows initial categorisation of a suspected MI into one of three groups. what are the 3 groups
STEMI
NSTEMI
undifferentiated chest pain (non-diagnostic ECG)
31
describe ST elevation
result of transmural infarct
not often seen, but earliest change is dev of hyperacute or peaked T wave (localised hyperkalemia)
then, elevation of J point
then, ST elevation pronounced
then, ST segment may eventually become undistinguished from T wave
32
what other conditions can ST elevation be seen in
myocarditis
acute pericarditis
benign early repolarisation variant
33
describe STEMI
complete thrombotic occlusion of coronary vessel
transmural infarction ('full thickness')
34
describe NSTEMI
partial thrombotic occlusion of coronary vessel
subendocardial infarction (as blood can still be supplied to surrounding tissue in areas where the vessel isnt occluded)
35
describe non-ST elevation
result of subendocardial infarct
manifest by ST depression and/or T wave inversions without ST segment elevations
ST-T wave abnormalities may be diffuse in many leads or more commonly localised to leads associated w region of ischemic myocardium
36
describe non diagnostic ECG
initial ECG often not diagnostic in those ultimately diagnosed w acute MI
for any in whom suspicion of ACS remains high, repeat ECG in 20-30 min intervals
37
what is troponin
complex of 3 regulatory proteins (C, I and T) integral to skeletal and cardiac muscle contraction
cardiac troponin I and T are specific and sensitive biomarkers of cardiac injury
an elevation must be interpreted in context of history and ECG
rise and fall must be document in acute MI (change of 5 requires cardiology opinion)
38
what are 6 life threatening conditions
ACS
stress cardiomyopathy
aortic dissection
pulmonary embolism
tension pneumothorax
esophageal rupture
39
outline stress cardiomyopathy
transient regional systolic left ventricular dysfunction in setting of stress
substernal pain similar to acute MI
40
outline aortic dissection
acute chest and back pain
sharp pain
ripping or tearing quality
41
outline pulmonary embolism
dyspnoea, followed by pleuritic pain and cough
42
outline tension pneumothorax
sudden onset of pleuritic chest pain and dyspnea
43
outline esophageal rupture
associated w straining and vomiting
44
what are 3 non life threatening cardiac conditions
stable myocardial ischemia/angina
peri(myo)carditis
aortic stenosis
45
outline peri(myo)carditis
sharp pain
pleuritic
decreased by leaning forward
radiates to trapezius ridge
associated w fever
46
outline aortic stenosis
exertional pain
dyspnea
presyncope/syncope
47
what are 5 non life threatening pulmonary conditions
pneumothorax
pneumonia
malignancy
asthma/COPD exacerbation
pleuritis
48
what are 4 non life threatening GI conditions
GORD
peptic ulcer disease
esophageal motility disorders
esophagitis
49
when should troponin be measured to diagnose MI
for high sensitivity troponin-T, negative test taken after 2 hrs after symptom onset is reliable for ruling out MI
if first test is negative within 2 hrs, do another test within 3 hrs
for standard sensitive troponin test, need to get negative troponin at least 6-8 hrs after symptom onset
50
which leads of ECG correspond with the lateral region of the heart
l, aVL, V5, V6
51
which leads of ECG correspond with the anterior region of the heart
V1, V2
52
which leads of ECG correspond with the inferior region of the heart
ll, lll, aVF
53
which leads of ECG correspond with the septal region of the heart
V3, V4
54
leads V1-V4 are correlated with which artery/s
LAD
55
leads l, aVL, V5, V6 are correlated with which artery/s
LCx
diagonal branch of LAD
56
leads ll, lll, aVF are correlated with which artery/s
RCA or dominant LCx
57
what are the 3 general stages of acute STEMI management
pre hospital
in hospital (ED, cath lab, CCU)
post hospital discharge
58
what is involved in the pre hospital stage of STEMI management
make diagnosis
assess risk
ensure stability
aim for early reperfusion
59
what is involved in the in hospital stage of STEMI management
establish reperfusion
prevent re-thrombosis
avoid, recognise, and manage acute complications
educate and initiate secondary prevention
60
what is involved in the post hospital stage of STEMI management
maintain secondary prevention
monitor compliance and risk factor targets
diagnose recurrences
61
outline immediate management of STEMI
early ECG
insert cannula
selection of reperfusion strategy (less than 30 mins for thrombolytics and less than 90 mins for PCI)
300mg aspirin
analgesia (nitrates, morphine, and oxygen if SaO2 less than 90)
occasionally IV metoprolol
maintain patient at rest
treat bradycardia and hTN
62
what is the importance of early intervention to reestablish reperfusion (through either thrombolytics or PCI)
time = myocardium
the longer the patient goes untreated, the more of the myocardium becomes damaged and hence the risk of death increases largely
early intervention allows for prevention of extensive damage
63
what is PCI
percutaneous coronary intervention
method of establishing reperfusion
gold standard treatment in patients with STEMI or MI w new LBBB who present within 12 hr of symptom onset
64
what is thrombolysis
method of establishing reperfusion
uses thrombolytics for STEMI patients if Sxs <12hr
use if patient not have access to PCI or capability to transfer for PCI in 90min
aim for needle time within 30 min
65
what should you do after successful thrombolysis
aim for routine early coronary angiography within 3-24 hr after successful thrombolysis
initiate preparatory anticoagulant + antiplatelet regimen before and during transfer to PCI hospital
66
what are some notable early complications of acute STEMI
LV impairment w many consequences e.g acute pulmonary oedema, cardiogenic shock, long term HF, LV thrombus
arrhythmias
mechanical: papillary muscle rupture, ventricular septal defect, free wall rupture causing tamponade
pericarditis
67
outline the use of echocardiogram after an acute STEMI
usually performed after 24-48 hr, then repeated at 3-6 months
gives assessment of LV function and regional wall motion and can look for pre existing complications from MI e.g valve dysfunction or septal rupture
68
outline the use of cardiac MRI after an acute STEMI
less commonly done than echo, unless there is ambiguity abt the diagnosis of MI or if need to assess myocardial viability and scar formation
69
describe the management of NSTEMI/UA
timeline for NSTEMI angiography is described as urgent, rather than an emergency
angiography within 24hr of admission
prior to angio: IV access, aspirin, sublingual GTN, therapeutic parenteral anticoagulation, admission to cardiac monitored bed, commencement of statin and possible ACE inhibitor/beta blocker
70
what can be done for post MI care according to the australian guidelines
dual antiplatelet therapy for 12 months
statins
ACE inhibitors
beta blockers
71
what is the LDL goal for secondary prevention of CHD
<1.8mmol
72
what is the HDL goal for secondary prevention of CHD
>1.0mmol
73
what is the triglyceride goal for secondary prevention of CHD
<2.0mmol
74
describe use of beta blockers in MI patients
should be prescribed for most patients after an MI unless contraindicated
75
describe use of ACE inhibitors in MI patients
should be given early after an MI/UA event and their use reviewed later
76
describe BP management in CHD patients
achieve and maintain <130/80
77
what 7 pharmacological things can be used to prevent further ischemic events
antiplatelets and/or anticoagulants
lipid lowering therapy
RAAS antagonists
BP control
beta blockers
colchicine
vaccination
78
describe the use of antiplatelets/anticoagulants
ALL patients with an atherosclerotic vascular condition should be considered for some type of AP/AC treatment unless contraindicated or inappropriate
can include aspirin, anticoagulant or combination of both (dual antiplatelets, and/or w one anticoagulant)
79
what are 3 indications for deciding antiplatelet/anticoagulant therapy
evidence base in each vascular territory
presence of other indication e.g AF
risk of thrombosis
80
what are 2 contraindications for deciding antiplatelet/anticoagulant therapy
risk of bleeding including falls
treatment adherence issues
81
what are 4 principles of antiplatelet/anticoagulant use
decision based on patient circumstances then set and forget
more drugs combined = higher efficacy = higher risk of bleeding
need to use dual antiplatelet for a period of time and then single when patient has a stent
if patient has AF or thrombus, then need to combine w anticoagulant
82
describe the use of lipid lowering therapy
ALL patients w atherosclerotic vascular condition should be considered for lipid lowering therapy unless contraindicated or inappropriate
generally start w statin, then, if unsuccessful or have adverse effect, move to another LDL lowering agent
if have other issues, such as low HDL or high TG, then consider other agents like fibrates
83
why target the RAAS system (ie why use RAAS antagonists)
upregulation of RAAS associated w remodelling of arteries when ischemic events occcur
therefore, blocking RAAS helps prevent further remodelling such as arteriolar hypertrophy which drives further ischemia
84
who should get a RAAS blocker
recent MI
diabetics
renal disease
HTN w vascular disease
systolic HF or LV impairment
ie pretty much everyone w atherosclerotic vascular disease
85
who does not need RAAS blocker
no recent ischemic events
well controlled BP
no diabetes
no renal disease
no systolic HF and normal LV function
low risk groups e.g non smokers
86
what causes MI type 1
plaque rupture/erosion w occlusive thrombus
plaque rupture/erosion w non-occlusive thrombus
87
what causes MI type 2
atherosclerosis and O2 supply/demand imbalance
vasospasm or coronary microvascular dysfunction
non-atherosclerotic coronary dissection
O2 supply/demand imbalance alone
88
what are 4 non modifiable risk factors for ASCVD
increasing age
sex
genetic factors
race/ethnicity
89
what are 3 modifiable factors for ASCVD
diet
smoking
physical inactivity
90
how can smoking lead to ASCVD
damages blood vessels and promotes inflammation, accelerating atherosclerosis progression
91
how can physical inactivity lead to ASCVD
sedentary lifestyle promotes weight gain and reduced CV fitness
92
how can diet lead to ASCVD
poor dietary choices high in saturated fats can contribute to plaque buildup in arteries
93
how can age lead to ASCVD
arterial dmg accumulates overtime
94
how can family history lead to ASCVD
increase susceptibility
95
how can biological sex lead to ASCVD
men tend to have higher risk compared to premenopausal women
96
what is hyperlipidaemia
high levels of lipids, including cholesterol and triglycerides, in the blood
97
what is hypercholesterolaemia
high levels of cholesterol in the blood
98
how does fibre intake reduce CHD risk in terms of GI action
soluble fibre binds to cholesterol in the digestive tract and helps eliminate it from the body, leading to lower LDL
99
how does fibre intake reduce CHD risk in terms of sugar absorption
fibre slows down the absorption of sugar, promoting stable blood sugar levels and reducing the risk of diabetes
100
outline the benefits of food fortification with plant sterols and stanols
they are structurally very similar to cholesterol and can compete w dietary cholesterol for absorption in the digestive tract via competitive inhibition
this competition leads to reduced cholesterol absorption, resulting in lower LDL
101
what components does the DASH diet place an emphasis on and why
fruits and veg - primary source of nutrients that help lower BP
whole grains - sustained energy and additional fibre to diet
lean protein - helps reduce saturated fat intake
102
what components does the mediterranean diet place and emphasis on and why
plant-based foods - provides essential vitamins, minerals, fibre, antioxidants
healthy fats - provides monounsaturated fats and omega-3 fatty acids
moderate dairy - sources of calcium and protein but contain less fat
103
outline the australian dietary guidelines
encourages consumption of food from all 5 food groups
emphasises importance of maintaining healthy body weight
not directly related to dietrary, but also encourages physical activity
104
describe peripheral artery disease (PAD)
atherosclerotic affection of the peripheral arterial tree, rather than cerebrovascular, cardiac, or abdominal vasculature
it has a tendency towards lower limbs
105
what are the symptoms/signs of PAD
often asymptomatic
most common symptom is intermittent claudication
HTN
arcus cornealis
tar staining
106
outline the pathophysiology of PAD
atherosclerotic plaque > arterial stenosis > collateral blood supply > further stenosis in these too > reduced peripheral perfusion > peripheral arterial ischemia > claudication and other symptoms/signs
107
what is cerebrovascular atherosclerosis
condition characterised by the build-up of fatty deposits in the blood vessels that supply the brain
this can also cause clots which can occlude or stenose the arteries leading to ischemic stroke
108
what are the symptoms/signs of cerebrovascular atherosclerosis
unilateral weakness
confusion
unilateral vision loss
hemi-negligence
trouble speaking
dizziness/syncope
109
explain the mechanism of intermittent claudication
atherosclerotic plaque > arterial stenosis > reduced peripheral perfusion > increased O2 demand during exertion > insufficient perfusion > ischaemia > buildup of metabolites > intermittent claudication
110
what are pharmacological options to manage PAD and cerebrovascular atherosclerosis
dual antiplatelet therapy
statin therapy
ACE inhibitor
111
what are non pharmacological options to manage PAD and cerebrovascular atherosclerosis
smoking cessation
dietary modification
regular exercise
112
what is chronic limb ischemia
range of symptoms and signs of limb ischemia that have developed over time
ranges from asymptomatic to limb-threatening
113
what is chronic limb threatening ischemia
collection of symptoms and signs depicting a critical reduction in perfusion which is inadequate to maintain healthy tissues at their lowest metabolic demands ie at rest
114
what is acute limb ischemia
sudden decrease in limb perfusion leading to potential threat to limb viability
115
what are the 3 stages of acute limb ischemia
subcritical - doppler signal/no neurological deficit
critical - no doppler signal/neurological deficit
irreversible - complete neuro deficit/tense muscles/no cap. refill
116
what the 6 signs (6 p's) of acute limb ischemia
pain
pallor
pulseless
paraesthesia
paralysis
perishingly cold
117
what are 2 conservative interventions for PAD
exercise
analgesia
118
what are 4 pharmacological interventions for PAD
antiplatelets
statins
anticoagulants
thrombolytics
119
what are 4 endovascular interventions for PAD
balloon angioplasty
stents
thrombolysis
embolisation
120
what are 5 surgical interventions for PAD
amputation
thrombectomy
endarterectomy
patch plasty
grafts
121
aside from PAD, what are 3 differential diagnoses for leg pain
osteoarthritis
lumbar nerve root irritation
spinal canal stenosis
122
outline osteoarthritis for leg pain
pain w exercise
pain w sitting/lying down
not relieved by just standing still, need to sit down
123
outline lumbar nerve root irritation for leg pain
aching in calf
pain radiation from back of leg from buttock to ankle
need to sit or lie down for relief
spinal flexion may help
straight leg raise may precipitate the pain
124
outline spinal canal stenosis for leg pain
pain can be very similar to claudication
have to sit or lie down to relieve pain
pain can occur while just standing
often takes a long time to settle after walking
125
what are 4 investigations that can be used for carotid disease
duplex ultrasound
CT-angiography
MR-angiography
DSA
