cardio Flashcards
(564 cards)
1
Q
atherosclerosis is the principal cause of what?
A
heart attack
stroke
gangrene of the extremities
2
Q
what are the major cell types involved in atherogenesis?
A
endothelium
macrophages
smooth muscle cells
platelets
3
Q
what is the critical bit of atherosclerotic plaque life?
A
inflammation
4
Q
what is the most successful treatment for atherosclerotic plaques?
A
stents + medical therapies
5
Q
what kinda consistency do plaques have?
A
oatmeal like at first - then gets really hard (like drainpipes)
6
Q
when does atherosclerosis become a problem?
A
when the plaque ruptures, leading to thrombus formation and ultimately death
7
Q
list some risk factors for atherosclerosis
A
FH (v strong predictor) age tobacco smoking high serum cholesterol obesity diabetes hypertension
8
Q
where are atherosclerotic plaques found?
A
within peripheral and coronary arteries
9
Q
distribution of atherosclerotic plaques is governed by what?
A
haemodynamic factors
10
Q
what are the haemodynamic factors that govern plaque distribution? (3)
A
- changes in flow/turbulence (eg at bifurcations) cause artery to alter endothelial cell function
- wall thickness also changes leading to neointima
- altered gene expression in key cell types is vital
11
Q
changes in flow/turbulence can cause arteries to alter endothelial cell function - possibly leading to plaques. where is this most likely to happen?
A
at bifurcations
12
Q
an atherosclerotic plaque is a complex lesion consisting of: (4)
A
lipid
nectrotic core
connective tissue
fibrous “cap”
13
Q
define angina
A
chest pain or pressure, usually due to not enough blood flow to the heart
14
Q
what are the 2 consequences of plaques?
A
- occlusion - of vessel lumen resulting in angina
OR - rupture - thrombus formation - death
15
Q
name some examples of good inflammation
A
pathogens
parasites
tumours
wound healing
16
Q
name some examples of bad inflammation
A
myocardial repercussion injury atherosclerosis ischaemic heart disease rheumatoid arthiritis asthma inflammatory bowel disease shock excessive wound healing
17
Q
neutrophils have an important role in cleaning up dead/injured cells in wound healing but can also what?
A
extend area of injury beyond that originally cut off blood supply (this is known as ischaemia-reperfusion injury)
18
Q
in septic/traumatic shock, large number of _______ are mobilised from bone marrow n recruited to tissues to fight potential infection
A
neutrophils
19
Q
what helps ignite inflammation in arterial wall?
A
modified/oxidated LDL (normal too big to enter)
endothelial dysfunction
20
Q
what is the stimulant for adhesion of leukocytes?
A
chemoattractants (chemicals that attract leukocytes)
21
Q
how do chemoattractants work?
A
once inflammation is initiated, chemoattractants are released from endothelium and send signals to leukocytes
chemoattractants are released from site of injury and a conc gradient is produced
22
Q
what is a non-specific indicator of inflammation?
A
CRP
c reactive protein
23
Q
list some inflammatory cytokines found in plaques?
A
IL-1 IL-6 IL-6 IFN-gamma TGF-ß MCP-1 CRP
24
Q
leukocyte recruitment to vessel walls is mediated by what?
A
selectins
25
transmigration in inflammation is controlled by what?
interns n chemoattractants
26
what are the 5 steps in progression of atherosclerosis
1. fatty streaks
2. intermediate lesions
3. fibrous plaques/advanced lesions
4. plaque rupture
5. plaque erosion
27
describe (1) fatty streaks (in the progression of atherosclerosis)
plaque constantly grows and recedes
fibrous cap has to be resorbed and redeposited in order to be maintained
if balance shifts eg in favour of inflammatory conditions, cap becomes weak n plaque ruptures
basement membrane, collagen n nectrotic tissue exposure
- thrombus (clot) formation and vessel occlusion
28
what is a thrombus aka
clot
29
how can we detect plaque rupture
by ECG
30
describe (5) plaque erosion (in the progression of atherosclerosis)
2nd most prevalent cause of coronary thrombosis
lesions tend to be small 'early lesions'
fibrous cap does not disrupt
luminal surface underneath clot may not have endothelium but is smooth muscle rich
v difficult to detect w imaging
31
describe (2) intermediate lesions (in the progression of atherosclerosis)
composed of layers of:
- foam cells (lipid laden macrophages)
- vascular smooth muscle cells
- t lymphocytes
- adhesion n aggregation of platelets to vessel wall
32
describe (3) fibrous plaques/advanced lesions (in the progression of atherosclerosis)
implodes blood flow
prone to rupture
covered by dense fibrous cap made of collagen, elastin etc
may be calcified
contains: smooth muscle cells, macrophages, foam cells, t lymphocytes
33
describe (4) plaque rupture (in the progression of atherosclerosis)
plaque constantly growing receding
fibrous cap has to resorbed and redeposited in order to be maintained
if balance shifted eg in favour of inflammatory conditions, the cap becomes weak and plaque ruptures
clot formation and vessel occlusion
34
how do u treat CAD
PCI
35
what does PCI stand for?
percutaneous coronary intervention aka a stent
36
5-10y ago, restenosis was a MAJOR limitation but no longer is. why?
drug eluting stents!
37
how do drug eluting stents work?
by reducing smooth cell proliferation and this in turn reduces regrowth after placement of the stent
38
what is a major adverse reaction of aspirin/clopidogrel/ticagrelor?
excessive bleeding
39
what is myocarditis aka
inflammatory cardiomyopathy (inflammation of the heart muscle)
40
what is inflammatory cardiomyopathy aka
myocarditis (inflammation of the heart muscle)
41
what is the normal weight of the heart
230-280g for females
| 280-340g for males
42
what is contraction of the heart initiated by?
depolarisation
| changes to Ca concentration
43
what is normal systolic EF (ejection fraction)?
60-65%
44
failure to transport blood out of the heart is WHAT?
cardiac failure
45
cariogenic shock = what?
severe failure
46
myocardial hypertrophy can be an adaptive/physiological response when?
athletes
| pregnancy
47
if u exceed stretch capability of sarcomeres, what happens to cardiac contraction force?
it diminishes
48
hypertrophic response can be triggered by what?
```
angiotensin 2
ET-1
insulin like growth factor 1
TGF-ß
(these activate mitogen-activated protein kinase)
```
49
what happens w left sided cardiac failure?
pulmonary congestion
| then overload of right side
50
what happens w right sided cardiac failure?
venous hypertension n congestion
51
diastolic cardiac failure results in what?
a stiffer heart
52
the heart comprises a single chamber until which week of gestation?
5th
53
congenital heart disease results from what?
faulty embryonic development
54
what are some single genes associated with heart disease?
trisomy 21 (downs)
turners (XO)
di-George syndrome
55
which drugs can influence heart disease?
```
thalidomide
alcohol
phenytoin
amphetamines
lithium
oestrogenic steroids
```
56
what is PDA?
patent ductus arteriosus
| - persistent opening between the 2 major blood vessels leading from the heart
57
what is VSD?
ventricular septal defect
| - hole in the wall separating the two ventricles of the heart
58
what is ASD?
atrial septal defect
| - hole in the septum of the 2 atria
59
what is truncus arteriosus?
rare type of heart disease
in which a single blood vessel (truncus arteriosus)
comes out of the R&L ventricles, instead of pulmonary artery & aorta
60
what is total anomalous pulmonary venous return (TAPVR)?
heart disease in which the 4 veins that take blood from the lungs to the heart do not attach normally to the left atrium
61
what is hypo plastic left heart syndrome (HLHS)?
birth defect that affects normal blood flow through the heart.
as the baby develops during pregnancy, the left side of the heart does not form correctly
62
what does tetralogy of fallot result in?
low oxygenation of blood
due to the mixing of oxygenated and deoxygenated blood in the LV via the VSD
and preferential flow of the mixed blood from both ventricles through the aorta
bc of the obstruction to flow through the pulmonary valve
63
what are the 4 components of tetralogy of fallout?
1) large VSD
2) pulmonary stenosis
3) overriding of the aorta above VSD
4) bc of these, RV becomes hypertrophied (thickened)
64
what is tricuspid atresia?
when tricuspid valve is missing or abnormally developed.
the defect blocks blood flow from RA to RV
65
what are some examples of left-right shunts?
```
VSD
ASD
PDA
truncus arteriosus
TAPVR
hypoplastic left heart syndrome
```
66
what are some examples of right-left shunts?
tetralogy of fallot
| tricuspid atresia
67
which heart conditions result in no shunts?
```
complete transposition of great vessels
coarctation
pulmonary stenosis
aortic stenosis
coronary artery origin from pulmonary artery
```
68
what is Eisenmenger's syndrome?
process in which a long-standing L-R cardiac shunt caused by a congenital heart defect
causes pulmonary hypertension & eventual reversal of the shunt into a cyanotic R-L shunt
69
how can a PDA be solveD?
can be closed:
- surgically
- by catheters
- or by prostaglandin inhibitors (indomethacin)
70
what is the characteristic shape of tetralogy of Fallot on radiology?
boot-shape
71
what is complete transposition of the great arteries?
aorta coming off RV and pulmonary trunk off LV
72
what are some risk factors of complete transposition of great arteries (when aorta comes off RV and pulmonary trunk off LV)
male bias
| associated w diabetes
73
coarctation of the aorta usually happens where?
just after the arch
with excessive blood flow being diverted through carotid/subclavian vessels into systemic vascular shunts to supply the rest of the body
74
coarctation of the aorta is particularly associated with which syndrome?
turner's
| also an association w berry aneurysms of the brain
75
what is endocardial fibroelastosis?
thickening within the muscular lining of the heart chambers
due to an increase in the amount of supporting connective tissue (inelastic collagen) and elastic fibers.
76
what is a frequent complication of congenital aortic stenosis and coarctation?
secondary endocardial fibroelastosis (thickening within muscular lining of heart)
can lead to stiffening of heart n cardiac failure
77
primary endocardial fibroelastosis follows what kinda pattern?
familiar
78
what is dextrocardia?
when ur heart points to right side rather than left
| usually associated w CV abnormalities but can be normal
79
name 4 risk factors for ischaemic heart disease
1. systemic hypertension
2. cigarettes
3. DM
4. elevated cholesterol
(also obesity, age, male, FH, sedentary lifestyle habit)
80
remember: coronary heart disease = ischaemic heart disease
IHD is what it used to be called
81
list some reasons for imperfect blood supply to heart
atherosclerosis
thrombosis
thromboembolism
artery spasm
82
healthy individual has coronary reserve ___ of resting blood flow
4-8x
83
what is an aneurysm
dilation of part of the myocardial wall (usually associated w fibrosis and myocyte atrophy)
84
what is pericarditis?
a delayed pericarditic reaction following infarction (2-10w)
inflammation of the pericardium
85
whats the WHO classification for hypertension?
>140/90 mmHg
86
what is hypertensive heart disease?
reflects cardiac enlargement due to hypertension and in absence of other cause
87
compensatory hypertrophy of the heart initially starts with what....
increased myocyte size
squaring of nuclei
slight increase of interstitial fibrous tissue
88
what is cor pulmonale?
condition that most commonly arises out of complications from pulmonary hypertension
aka right-sided heart failure (RV)
89
what happens in cor pulmonale?
RV hypertrophy
| dilation due to pulmonary hypertension
90
what is acute rheumatic fever? and why is in the cardio flashcards?
group A ß-haemolytic streptococcus infection
usually upper RI
remains a major factor with regard to heart disease in developing world
91
what are some clinical features of acute rheumatic fever
carditis (cardiomegaly, murmurs, pericarditis, cardiac failure)
92
what is cardiomegaly?
abnormal enlargement of the heart
93
what is infective endocarditis?
an infective process involving cardiac valves. usually caused by bacteria
94
what are some consequences of (rheumatic) infection?
rapidly increasing cardiac valve distortion and disruption with acute cardiac dysfunction
95
calcific aortic stenosis may reflect what?
rheumatic aortic valve disease or degenerative processes
96
calcific aortic stenosis is accelerated where?
in bicuspid aortic valves
97
calcification of the mitral valve results is usually what?
asymptomatic and of no significance
| only of significance following rheumatic valvular disease/previous vulvitis
98
what is mitral valve prolapse?
when the 2 flaps do not close evenly
degeneration of the mitral valves such that
the inner fibrous layer becomes more loose and fragmentary with accumulation of mucopolysaccharide material
99
what are the main problems that affect mitral valve?
prolapse
regurgitation
stenosis
100
what sound do u get on auscultation when the mitral valve prolapses?
S3
101
what is the most common form of myocarditis?
viral
102
list some infectious causes of myocarditis
```
viruses (coxsackie, echo, influenza)
rickettsia
bacteria (diphtheria, streptococcal)
fungi and protozoa parasites
metazoa
```
103
what are some non-infectious causes of myocarditis?
hypersensitivity/immune related diseases (rheumatic fever, rheumatoid arthritis)
radiation
miscellaneous - sarcoid, uraemia
104
myocarditis can often have an association with what?
an upper RI preceding
105
how can drug reactions influence myocarditis?
causes inflammatory infiltrate particularly around blood vessels within the myocardium - predominance of eosinophils
106
what is DCM?
dilated cardiomyopathy - heart becomes enlarged, can't pump blood effectively
(poorly generated contractile force leads to dilation of heart)
107
is DCM (dilated cardiomyopathy) genetic?
one third familiar
| mostly autosomal dominant
108
what is secondary dilated cardiomyopathy?
enlargement of the heart caused by a med cond
eg alcohol, catecholamines, cocaine, pregnancy
109
what is HCM?
hypertrophic cardiomyopathy - thickened heart
110
what is the diff btwn dilated and hypertrophic cardiomyopathy?
dilated - swollen, enlarged
hypertrophic - thickened
therefore, harder for the heart to pump blood
111
mutations associated with troponin T are associated with what?
risk of sudden death
112
what is an amyloid?
a protein that is deposited in the liver, kidney, spleen or other tissues in certain diseases
113
what is a cardiac myxoma?
noncancerous tumour in the upper LHS/RHS
| mostly grows in the septum
114
what are blood vessels lined by to maintain vascular integrity?
endothelial cells
115
blood coagulation occurs when fibrinogen is converted to what?
fibrin
116
clot lysis involves what?
plasminogen being converted to plasmin which then acts on fibrin to produce fibrin degradation products
117
what is the racial bias for hypertensive vascular disease?
afro-caribbean
118
what is the main function of ANP?
to lower BP
| balances RAAS system
119
what is vasculitis?
group of disorders that destroy blood vessels by inflammation (primarily caused by leukocyte damage)
120
what is abdominal aortic aneurysm?
localised enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal diameter
usually cause no symptoms except when ruptured
121
what is a berry aneurysm?
small aneurysm that looks like a berry and classically occurs at the point at which a cerebral artery departs from the circular artery (the circle of Willis) at the base of the brain
122
what is syphilis?
an STI - inflammatory disease affecting vasa vasorum
123
what's vasa vasorum?
network of small blood vessels that supply the walls of large blood vessels, such as elastic arteries and large veins
124
what is a varicose vein?
enlarged and torturous vein, mostly affecting superficial leg veins
125
what is angiosarcoma?
highly aggressive malignant neoplasm of endothelial cells
126
what is kaposi's sarcoma linked to?
HIV and AIDS
| cancer that causes patches of cancer to grow under the skin
127
what are some risk factors for DVT
```
venous flow stasis from any cause eg cardiac falure
injury
hypercoagulability
advanced age
sickle cell disease
```
128
what is hypercoagulability?
thrombophilia/prothrombotic stage - abnormality of blood coagulation that increases thrombosis risk
129
what is type A behaviour pattern characterised by?
competitiveness, impatience and hostility
130
what are some unmodifiable risk factors for CHD?
age
sex
ethnicity
genetic
131
what are some lifestyle risk factors for CHD?
smoking
diet
physical inactivity
132
what are some clinical risk factors for CHD?
hypertension
lipids
diabetes
133
what are some psychosocial risk factors for CHD?
```
modifiable:
behaviour traits
depression/anxiety
work
social support
```
134
what is type A?
coronary prone behaviour pattern
competitive, hostile, impatient
135
how can u assess behaviour?
questionnaires eg self-report (poor), Minnesota multiphase personality index (MMPI)
structured clinical interview eg speech, answer content
136
what are the 3 aspects of recurrent coronary prevention?
cognitive - reconstructing thoughts to positive
behavioural - relaxation, walk at a steady pace
emotional - learn to relax in response to early signs of anxiety or anger
137
discuss psychosocial work characteristics
there are sig associates btwn psychosocial job characteristics and MI
those working 11h+ a day, 67% more likely to have an MI
138
how is social support linked to CHD?
both quality and quantity of social relationships are related to morbidity/mortality
139
what are epicardial vessels?
L & R CA's lie on the surface of the heart - distribute blood to diff regions of the heart
140
what is angina?
a symptom which occurs as a consequence of restricted coronary blood flow
141
what is angina always almost exclusively secondary to?
atherosclerosis
142
why does angina happen?
bc there's a mismatch btwn oxygen demand and supply
143
remember: atherosclerosis develops over time....
stable angina tends to be at approx a 4 (on a scale of 1-7 where 1 is a normal blood vessel)
144
what is SCAD?
spontaneous coronary artery dissection - uncommon emergency condition that occurs when a tear forms in 1 of the BV in the heart
145
what does myogenic control ensure?
*insert graph*
that flow (Q) remains constant in a physiological range of BP (P)
so for any given BP, heart is able to maintain blood flow!
146
when can there be a oxygen supply and demand mismatch? (3)
1. impairment of blood flow by proximal arterial stenosis
2. increased distal resistance eg LVH
3. reduced oxygen-carrying capacity of blood eg anaemia
147
remember pouiselle's law, why?
diameter of ?arteries has to fall below 75% before symptoms occur
148
in the healthy system, the resistance of the epicardial artery is negligible and so the flow through the system is determined by what?
the resistance (tone) of the microvascular vessels
149
discuss healthy rest (in the electro-hydraulic analogy)
in the health system, the resistance of the epicardial artery is negligible and so the flow through the system is determined by the resistance (tone) of the microvascular vessels
total flow is 3ML/S
150
discuss healthy exercise (in the electro-hydraulic analogy)
under exercise conditions, more flow is needed to meet metabolic demand
the microvascular resistance falls so that flow can increase
total flow can increase up to around 5x (15ml/s)
151
discuss diseased rest (in the electro-hydraulic analogy)
epicardial disease causes the resistance of the epicardial vessel to increase
to compensate, the microvascular resistance falls
so that flow can be maintained at 3ml/s
152
discuss diseased exercise (in the electro-hydraulic analogy)
epicardial resistance is high due to the stenosis
during exercise, the microvascular resistance falls to try and increase flow
but there comes a point where minimising microvascular resistance is 'maxed out' and can fall no more
at this pt, flow cannot meat metabolic demand
myocardium becomes ischaemic and pain is typically experienced
only way to reverse this is to rest, thus reducing demand for flow
153
name some other anginas
```
printzmetal's angina (coronary spasm)
microvascular angina (syndrome x)
crescendo angina and unstable angina... ACS
```
154
what are some non-modifiable risk factors for angina?
gender
FH
personal history
age
155
what are some modifiable risk factors for angina?
smoking
diabetes
hypertension
sedentary lifestyle
156
what are some signs of ischaemic heart disease?
```
male
middle aged
transverse ear cases
midline sternotomy
tar stained fingers
corneal arcus
```
157
what is the presentation of angina like? (3)
1. heavy, central, tight, radiation to arms, jaw, neck
2. precipitated by exertion
3, relieved by rest/SL GTN
158
what does GTN do?
dilate arteries
159
what is the presentation of chest pain like?
v subjective
160
the scale of 3 for NICE diagnostic pathways
```
3/3 = typical angina
2/3 = atypical pain
≤1/3 = non-anginas pain
```
161
what is OPQRRRSTT?
```
O - onset
P - position (site)
Q - quality (nature/character)
R - relationship (with exertion, posture, meals, breathing and with other symptoms)
R - radiation
R - relieving or aggravating factors
S - severity
T - timing
T - treatment
```
162
what is the presentation of angina like?
```
differential diagnosis
pericarditis
pulmonary embolism/pleurisy
chest infection
dissection of the aorta
```
163
what is a differential diagnosis?
```
the process of differentiating between 2+ conditions which share similar signs or symptoms
pericarditis/myocarditis
pulmonary embolism/pleurisy
dissection of the aorta
MSK
psychological
```
164
what is the presentation of angina on examination?
often normal or near normal
165
what is Htn short for?
hypertension
166
does ECG have direct markers of angina?
no, it is often normal
but Q waves, T-wave inversion, BBB are some sign of IHD
167
why might u do an echo for angina?
to check for LV function
there are no direct markers of angina
but there may be signs of:
previous infarcts (Q waves, T wave inversion, BBB)
168
list some anatomical investigations for angina
```
CT angiography (non-invasive)
invasive angiography
```
169
what are some physiological investigations of angina?
```
all non-invasive:
what is
exercise stress treadmill
stress echo
SPECT (nuclear perfusion)
perfusion
```
170
what is the treadmill test?
induces ischaemia while walking uphill, incrementally fast
look for ST segment depression
detects a 'later' stage of ischaemia so not used that much anymore (also bc so many patients are unsuitable - can't walk, v unfit, BBB)
171
whats the diff btwn sensitivity and specificity
sensitivity - if u have it, how likely is the measurement to pick it up
specificity - looking at PPV, so if u have a positive result, how likely is it that u have the disease?
172
what does the invasive angiogram involve?
its purely anatomical
for a long time was the "gold standard" for CAD patients
u pass wire, n measure the pressure before n after the clot
173
what is the main primary prevention of CAD?
```
reducing risk and complications!!
eg hypertension - antihypertensives
hypercholesterolaemia - statins n lipid modulating therapies
T2DM - diabetic therapy
smoking - smoking cessation
diet - general advice
```
174
what are the 3 major arms of therapy?
1. lifestyle changes
2. pharmacological
3. interventional (PCI and sometimes surgery)
175
what is the are some 1st line antianginals?
beta blockers
nitrates
calcium channel antagonists
176
what are some ß1 specific beta blockers?
bisoprolol and atenolol
177
what do beta blockers do?
antagonise sympathetic nervous activation
- reduce HR (negative chronotrope)
- reduce contractility (negative inotrope)
so, reduce work of heart. oxygen demand
178
why is coronary blood flow unique?
it occurs in diastole. if u lower HR, u naturally spend more time in diastole thus increasing time to fill arteries
179
do patients tolerate beta blockers well?
a lot don't
180
what are some side effects of beta blockers?
tiredness, nightmares
bradycardia
erectile dysfunction
cold hands n feet
181
what are some contraindications for beta blockers?
severe bronchospasm; asthma
| prinzmetal's angina
182
what are nitrates?
1st line antagonists
primary VENOdilators
diates systemic veins (reduces venous return to RHS of the heart)
SO reduces preload
therefore (via F-S mechanism) reduces work of heart and oxygen demand
(also dilate coronary arteries - antagonise spasm)
183
what are calcium channel antagonists?
```
1st line antagonists
primary ARTEROdilators
dilate systemic arteries (lower BP)
reduce afterload on the heart
lower energy required to prod same CO
tf reduce work of heart n oxygen demand
```
184
what are some 2nd line antianginals?
nicorandil
| ivbridine
185
what does nicorandil do?
2nd line antianginal
| mixed veno and artero-dilatory properties
186
what does ivbridine do?
2nd line abtianginal
| only useful in sinus rhythm
187
what do anti platelets do? and whats an example?
reduce cardiovascular events
decrease prostaglandin synthesis
decrease platelet aggregation
aspirin
188
what is a caution for anti platelets?
gastric ulceration
189
what are some alternatives instead of anti platelets?
includes p2y12 inhibitors
| eg clopidogrel, prasugrel, ticagrelor
190
what are statins
hmgcoa reductase inhibitors
191
what do statins do?
reduce CV events
reduce LDL cholesterol
anti-atherosclerotic
192
why is a stent inserted?
to restore patent (open/unobstructed) coronary artery and increase flow reserve
193
when is a stent inserted?
either when med fails (mostly)
| when high risk disease identified (fewer)
194
how is a stent inserted?
PCI - percutaneous coronary intervention - stenting
| CABG - coronary artery bypass graft - surgery
195
what are the pros of PCI
less invasive than CABG
convenient
repeatable
acceptable
196
what are the pros of CABG
prognosis
| deals with complex disease
197
what are the cons of PCI
risk of stent thrombosis
risk of restenosis
can't deal w complex disease
dual anti platelet therapy
198
what are the cons of CABG
```
invasive
stroke risk, bleeding
can't do if frail, comorbid
1 time treatment
length of stay
time for recovery
```
199
do we tend to do more or less CABG?
less, more PCI done
200
*LOOK AT TABLE OF +++++S AND -----S OF PCI/CABG
*WB 7TH JAN
201
define ACS
acute coronary syndrome - includes unstable angina, NSTEMI, and STEMI
202
what does unstable angina and NSTEMI constitute?
NSTE-ACS
203
how is MI generally diagnosed
on the basis of symptoms of myocardial ischaemia associated with characteristic elevation in serum cardiac troponin levels and/or characteristic ECG changes
204
how can the extent of MI be classified
non-Q-wave
or Q-wave
depending on whether or not there is development of pathological Q waves on ECG, which is associated with transmural infarction
205
list risk factors for atherosclerosis
```
smoking
high plasma cholesterol level
hypertension
DM
old age
renal failure
FH
```
206
what is diagnosis of ACS based on
firstly, the recognition of symptoms of myocardial ischaemia (inc chest pain)
secondly, on investigations that support diagnosis
207
what does the likelihood of the diagnosis be determined by
assessment of clinical risk factors for CAD
| using a risk score eg GRACE, TIMI risk scores
208
what does anti platelet therapy usually involve
dual:
aspirin
platelet p2y12 receptor antagonist (ticagrelor,clopidogrel, prasugrel)
209
list some beta blockers
bisoprolol
metoprolol
atenolol
210
when are beta blockers used
following STEMI orphan indicated in NSTE-ACS
211
what is the clinical classification for ppl with unstable angina
cardiac chest pain at rest
cardiac chest pain with crescendo pattern (eg unstable angina)
new onset angina
212
what is crescendo angina aka
unstable angina
213
how does troponin change w unstable angina
no significant rise
214
how is a STEMI diagnosed
on ECG at presentation
215
how is a NSTEMI diagnosed
retrospectively, after troponin results n sometimes other investigation results are available
216
what proportion of MI's happen in bed?
a third
217
what symptoms is MI associated with?
sweating
breathlessness
nausea
vomiting
218
what is a higher risk of MI associated with?
higher age
diabetes
renal failure
left ventricular systolic dysfunction
219
what is the initial management for an MI?
get to hosp ASAP
for paramedics: if ST elevation, contact primary PCI centre for transfer
take 300mg aspirin immediately
pain relief
220
what is hosp management for MI?
```
make diagnosis
bed rest
oxygen therapy if hypoxic
pain relief - narcotics/nitrates
aspirin +/- P2y12 inhibitor
consider beta blockers
consider other abtianginal therapy
consider urgent coronary angiography
```
221
what is the cause of majority of ACS cases?
rupture uf atherosclerotic plaque
| and consequent arterial thrombosis
222
what are some minor causes of ACS?
coronary vasospasm without plaque rupture
| drug use eg amphetamines, cocaien
223
what is troponin?
protein complex that regulates actin:myosin contraction
224
what is troponin a highly sensitive marker for, and is it specific to ACS?
cardiac muscle injury
| no
225
when is troponin also positive, if not ACS?
gram neg sepsis
pulmonary embolism
heart failure
arrhythmias
226
when are p2y12 inhibitors used?
in combo w aspirin in management of ACS (dual anti platelet therapy)
227
what are oral p2y12 inhibitors?
clopidogrel
prasugrel
ticagrelor
228
what is a short-acting IV p2y12 inhibitor
cangrelor
229
what is the caution with p2y12 inhibitors in dual anti platelet therapy?
increased bleeding risk
| exclude serious bleeding prior to admin
230
what are GpIIb/IIIa antagonists?
only IV drugs available
| used in convo with aspirin/oral p2y12 inhibitors - for management of patients undergoing PCI for ACS
231
what are anticoagulants used in addition to?
antiplatelets
232
what do anticoagulants do?
inhibit fibrin formation and platelet activation
233
what is PCI?
percutaneous coronary intervention
234
what is PCI aka
angioplasty w stent
235
list 2 anticoagulants
fondaparinux
| heparin
236
what is the treatment of choice for STEMI?
primary PCI
237
what are some adverse effects of P2y12 inhibitors?
bleeding eg GI bleeds
rash
GI disturbance
238
summarise secondary prevention of MI
DAPT; high dose statin eg atorvastatin 40-80mg; ACEI; beta blocker; aldosterone antagonist if heart failure and K+ not high
239
what are symptoms/signs of DVT like?
non-specific
| clinical diagnosis unreliable
240
list 2 symptoms of DVT
pain
| swelling
241
list 4 signs of DVT
tenderness
swelling
warmth
discolouration
242
how can u investigate DVT?
d-dimer: pos doesn't confirm diagnosis, but normal excludes
| US compression test proximal veins
243
what is DVT treatment
LMW heparin SC OD for min 5d
oral warfarin, INR 2-3, for 6m
compression stockings
treat/seek underlying cause
244
list some risk factors for DVT
surgery, immobility, leg fracture
OC pill, HRT, pregnancy
long haul flights/travel
245
what are some mechanical prevention measures for DVT
hydration
early mobilisation
compression stockings
foot pumps
246
what is a chemical prevention of DVT?
LMW heparin
247
why is LMW heparin used for DVT prevention?
low molecular weight
prods a more predictable anticoagulant response
frequent monitoring not needed to adjust dose
248
what can cause pulmonary embolism?
hypotension
cyanois
severe dyspnoea
right heart strain/failure
249
what is a common presentation of PE?
differential diagnosis of chest pain n sob
| consider also MSK, infection, malignancy, cardia, gastro causes
250
what are some symptoms of PE?
breathlessness
pleuritic chest pain
may have signs/symptoms of DVT
no other diagnosis more likely
251
what are some signs of PE?
tachycardia
tachypnoea
pleural rub
252
what is the initial CXR of PE like?
usually normal
253
what is the ECG of PE patient like
tachy
254
what do blood gases of a patient w PE look like
t1 resp failure
| decreased o2 and co2
255
what are some further investigations of PE?
d-dimer
| v/q scan
256
what is the treatment of PE the same as?
DVT
| ensure normal Hb, platelets, renal function, baseline clotting
257
what is DOAC
direct oral anticoagulant
258
what is INR
intl normalised ratio AKA prothrombin time
259
what is the prevention of PE same as?
DVT
260
what is thrombosis?
blood coagulation inside a vessel
261
what is appropriate coagulation?
when blood escapes a vessel
| failure of coagulation here leads to bleeding
262
what is the diff btwn arterial/venous thrombosis?
arterial: high pressure so PLATELET RICH
venous: low pressure so FIBRIN RICH
263
an arterial thrombus in coronary circulation is called WHAT?
MI
264
an arterial thrombus in the cerebral circulation is called WHAT?
CVA (stroke)
265
what is CVA?
cerebrovascular incident aka stroke
266
what is an arterial thrombus in the peripheral circulation called?
peripheral vascular disease
267
how can an MI be diagnosed>?
history
ECG
cardiac enzyme
268
how can a stroke/cva be diagnosed?
history
exam
CT/MRI
269
how can PVD be diagnosed?
history
exam
ultrasound
angiogram
270
what are some risk factors for atherosclerosis
```
smoking
hypertension
diabetes
hyperlipidaemia
obesity/sedentary lifestyle
stress/type A personality
```
271
what is the major enzyme responsible for clot breakdown?
TPA - tissue plasminogen activator
found on endothelial cells
catalyses conversion of plasminogen to plasmin
272
what is plasmin?
important enzyme present in blood - degrades many blood plasma proteins, including fibrin clots. it 'dissolves' already formed clots by degrading fibrin.
273
what is the degradation of plasmin termed?
fibrinolysis
274
what is the major enzyme of the fibrinolytic system?
plasmin
275
what does it feel like to have DVT?
swollen, warm, tender leg
276
what does a PE feel like?
pleuritic chest pain, breathlessness, cyanosis, death
277
how would u treat venous thrombosis?
initially: LMW heparin SC OD
then: oral warfarin 3-6m
or DOAC for 2-6m
278
what does heparin do?
binds to antithrombin and increases its activity
| indirect thrombin inhibitor
279
what does aspirin do?
inhibits cyclo-oxygenase irreversibly (COX)
| so stops clotting
280
what are the enzymes that prod prostaglandins called?
COX1/2
281
what do cox1 n cox2 do? and what does cox1 specifically prod?????
produce prostaglandins that promote inflammation, pain, and fever;
however, only COX-1 produces prostaglandins that activate platelets and protect the stomach and intestinal lining
282
waaaait, what are prostaglandins?
a group of physiologically active lipid compounds that have diverse hormone-like effects in animals.
they are derived enzymatically from the fatty acid arachidonic acid
283
how does warfarin reduce clotting?
blocs the formation of vitamin K–dependent clotting factors (10, 9, 7, 2) think 1972
prolongs prothrombin time
284
what are the vit K dependent clotting factors?
10
9
7
2
285
what is warfarin an antagonist for?
vit K
286
which vit is involved in coagulant?
k
| (german - koagulation) !!!
287
what is PT?
Prothrombin time - blood test that measures how long it takes blood to clot
288
when is PT looked @?
- to check for bleeding problems.
| - also to check whether anticoagulants are working
289
what can a PT test aka?
INR - international normalised ratio, standardised measurement of the time it takes for blood to clot
290
what is hypertension a major risk factor for? (6)
```
stroke
MI
heart failure
chronic renal disease
cog decline
premature death
```
291
how is hypertension diagnosed?
clinical BP of 140/90 mmHg or higher
292
ppl w suspected hypertension are offered whaT?
ambulatory BP monitoring (ABPM) to confirm diagnosis
293
what are the main targets for BP control?
cardiac output n peripheral resistance
interplay between RAAS n SNS
local vascular vasoconstrictor/vasodilator mediators
294
what are some drug types that affect RAAS for BP control?
```
renin inhibitor (stops angiotensinogen --> angiotensin I)
ace inhibitor (stops angiotensin I --> angiotensin II)
```
295
what are some drug types that affect SNS (noradrenaline) for BP control?
alpha blocker
beta blocker
calcium channel blocker?
296
what are ACE inhibitors good for?
hypertension
heart failure
diabetic nephropathy
297
name some ace inhibitors
ramipril
trandolapril
perindopril
298
what are the main adverse effects of ace inhibitors?
- related to red. ang II formation (hypotension, acute renal failure, hyperkalaemia)
- related to incr. kinin prod (cough, rash)
299
how are ace inhibitors generally tolerateD?
pretty well!
300
what are the main reasons why calcium channel blockers (CCB) might be used?
hypertension
IHD - angina
arrhythmia (tachycarida, fast)
301
name some CCB's
amldipine
nifedipine
felodipine
verapamil
302
what are L type calcium channel blockers?
drugs used as cardiac antiarrhythmics or antihypertensives
depending on whether the drugs have higher affinity for the heart (the phenylalkylamines, like verapamil), or for the vessels (the dihydropyridines, like nifedipine).
303
what can L type calcium channel blockers be used as?
cardiac antiarrhythmics
or
cardiac antihypertensives
304
which type of L type CCB's have a high affinity for the heart? n an example?
phenylalkamines
eg verapamil
so used as an antiarrhythmic
305
which type of L type CCB's have a high affinity for the vessels? n an example?
dihydropyridines
eg nifedipine
so used as an antihypertensive
306
what are some adverse effects of CCB's?
mainly dihydropyridines/antihypertensives
- flushing, headache, oedema, palpitations
mainly phenylalkamines/antiarrhythmics
- bradycardia, AV block
307
when are beta-adrenoceptor blockers used?
IHD - angina
heart failure
arrhythmia
hypertension
308
list some beta-adrenoceptor blockers (BB)
bisoprolol
propranolol
metoprolol
atenolol
309
what are the main adverse effects of BB?
```
fatigue
headache
sleep disturbances/nightmares
bradycardia
hypotension
worsening of: asthma, PVD
```
310
when are diuretics used?
to treat several conditions in medicine including heart failure, high blood pressure, liver disease and some types of kidney disease.
311
what is a diuretic?
any substance that promotes diuresis
312
what is a BB (beta-adrenoceptor blocker)?
prevent stimulation of adrenergic receptors
predominantly used to manage abnormal heart rhythms, and to protect the heart from a second heart attack after a first heart attack
313
what are diuretics aka
water pills
314
what is diuresis?
increased(/excessive) urine prod
315
name the 4 classes of diuretics
thiazides n related drugs (distal tubule)
loop diuretics (LoH)
k-sparing diuretics
aldosterone antagonists
316
name a thiazide and related diuretics
bendroflumethiazide
317
name a loop diuretic
furosemide
318
name a k-sparing diuretic?
spironolactone
| eplerenone
319
what are the main adverse effects of diuretics?
```
hypovolaemia
hypotension
low serum K, Na, Mg, Ca
raised uric acid (gout?)
impaired gluc tolerance
```
320
what is hypovolaemia?
state of decreased blood volume; more specifically, decrease in volume of blood plasma
321
how do the treatment steps for hypertension differ if u are under vs over 55 yrs (or A-C of any age)?
under: ACE inhibitor/ang II blocker
over: calcium channel blocker
322
what is the next step if ace-inhibitors/CCB don't work in hypertension?
combine both
then add a diuretic
etccccc
323
what is the diff btwn ANP and BNP?
atrial natriuretic peptide
british national p-...... brain natriuretic peptide *
324
where is ANP found?
atria
325
where is BNP found?
ventricles
326
what does ANP do?
hormone - causes a reduction in expanded ECF vol by increasing renal sodium excretion
327
what does BNP do?
hormone - secreted by cardiomyctes in response to stretching caused by increased ventricular blood volume
328
when are ANP/BNP released?
stretching of atrial/ventricular muscle cells
329
what are the main effects of the cardiac natriuretic peptides (ANP/BNP)
increase renal Na/water excretion
relax vascular smooth muscle
increased vascular permeability
inhibit release of : aldosterone, ang II, endothelia, ADH
330
the cardiac natriuretic peptide system is counter regulatory to whattttt??????
RAAS
331
what are the symptoms of chronic stable angina?
```
anginas chest pain
predictable
exertional
infrequent
stable
```
332
what are the symptoms of unstable angina/acute coronarysyndrome (NSTEMI)
unpredictable
may be at rest
frequent
unstable
333
what are the symptoms of STEMI ??
unpredictable;e
resp pain
persistent
unstable
334
what are the treatment options for chronic stable angina?
anti platelet therapy (aspirin, clopidogrel if aspirin intolerant)
lipid lowering therapy eg statins
short acting nitrate eg GTN
335
what are the treatment options for ACS (nstemi/stemi)
```
pain relief (GTN, opiates)
DAPT (aspirin+ticagrelor/prasugrel/clopidogrel)
antithrombin therapy
lipid lowering therapy (statins)
etc
```
336
how is ABPM (ambulatory BP monitoring) used to confirm high BP diagnosis?
at least 2 measurements per hour during person's usual waking hours
avg at least 14 measurements to confirm diagnosis
337
how is HBPM (home BP monitoring) used to confirm high BP diagnosis?
2 consecutive seated measurements, min 1min apart
BP recorded 2x a day for at least 4d and preferably for 1w
measurements on d1 discarded - avg value for remaining used
338
if u suspect a patient is hypertensive, wwyd?
measure BP in both arms .... if diff is 20 mmHg+ repeat. use arm w higher BP as measurement!
339
what are the 3 main antihypertensive effects of ACE inhibitors?
1. reduced vascular resistance
2. reduced ECF volume
3. bradykinin elevated NO
340
what is bradykinin?
an inflammatory mediator.
a peptide that causes blood vessels to dilate so decr BP
ACE inhibitors increase bradykinin (by inhibiting its degradation), further lowering BP
341
what are some advantages of ACE inhibitors?
good with diuretics
no effect on insulin or glucose
increased quality of life
342
do CCB's inhibit calcium?
no
| they prevent opening of voltage gated calcium channels
343
what can fibrosis lead to?
arrhythmias
344
what is dilated cardiomyopathy?
when the muscle of the heart is abnormal (can be too thick or thin)
345
what is dilated cardiomyopathy often mistaken for?
asthma
346
what is SADS?
sudden arrhythmic death syndrome
347
what are u predisposed to with Marfan syndrome?
aneurysm of ascending aorta
348
males or females w familiar hypercholesterolaemia have 100x risk of MI compared to normal?
females
349
what does cardiomyopathy refer to?
primary heart muscle disease
350
unexplained primary cardiac hypertrophy is referred to as what?
HCM
351
what does DCM stand for?
dilated cardiomyopathy
352
what happens with DCM?
LV/RV or 4 chamber dilatation/dysfunction
353
what is the main feature of arrhythmogenic cardiomyopathy
arrhythmia
354
all cardiomyopathies carry an _______ risk
arrhythmogenic
355
what is channelopathy
inherited arrhythmia
356
what is inherited arrhythmia (channelopathy) caused by?
ion channel protein gene mutations (usually K, Na, Ca)
357
how may channelopathies present?
recurrent syncope
358
sudden cardiac death in young ppl is often due to what?
an inherited condition
359
an inherited abnormality of cholesterol is referred to as what?
familiar hypercholesterolaemia
360
ICCs are usually inherited how?
dominantly
361
how thick is the fibrous parietal layer
2mm
362
parietal layer has WHAT to fix the heart in the thorax?
fibrous attachments
363
LA is mainly outside what
pericardium
364
pericardium has similar properties to what? n how
rubber - initially stretchy but becomes stiff at higher tension
365
pericardial sac has big/small reserve vol?
small
366
what is tamponade physiology?
small amt of vol added to space has dramatic effects on filling but so does removal of a small amt
367
what is cardiac tamponade?
aka pericardial tamponade
when fluid in the pericardium builds up, resulting in compression of the heart - reduces CO
368
define acute pericarditis
an inflammatory pericardial syndrome with or without effusion
369
define effusion
accumulation of fluid in an anatomic space
370
what are some infectious causes of pericarditis?
viral (common)
bacterial
fungal (v rare)
parasitic (v rare)
371
what are some non-infectious causes of pericarditis?
```
autoimmune (common)
neoplastic
metabolic
traumatic and iatrogenic
drug-related (rare)
```
372
describe some features of chest pain in pericarditis
severe
sharp and pleuritic
rapid onset
radiates to arm or more specifically trapezius ridge
relieved by sitting forward, exacerbated by lying down
373
what is pleuritic chest pain
characterised by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling
374
what are some other symptoms of pericarditis?
dyspnoea (difficulty breathing)
cough
hiccups
375
what does qds mean?
once a day
376
what does qid mean?
4x a day
377
what is differential diagnosis?
differentiating between 2+ conditions which share similar signs or symptoms
378
what are some differential diagnoses compared to pericarditis?
```
pneumonia
pulmonary embolus
GORD
MI/ischaemia
pneumothorax
peritonitis
pancreatitis
```
379
how can u diagnose pericarditis?
```
pericardial rub
sinus tachycardia
fever
signs of effusion
beck's triad
ecg
bloods
car
```
380
what does beck's triad consist of?
hypotension
elevated JVP
quiet heart sounds
381
what is pericardial friction rub?
audible medical sign used in the diagnosis of pericarditis.
on auscultation, this sign is an extra heart sound of to-and-fro character
resembles the sound of squeaky leather and often is described as grating, scratching, or rasping
382
what is tamponade
when fluid in pericardium builds up
| resulting in compression of the heart
383
what is pulsus paradoxus
abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration.
fall in systolic BP > 10mmHg
384
what are blood tests like if u have pericarditis
fbc: modest WCC incr, mild lypmphocytosis
high ESR
high troponin
cxr often normal in idiopathic
385
what is the management of pericarditis usually like?
sedentary activity until resolution of symptoms
| NSAIDs or aspirin
386
patients w acute pericarditis, what is their LT prognosis like?
good
387
what is the commonest cause of pericarditis in developed world
viral
388
define heart failure
inability of the heart to deliver blood (and oxygen) at a rate commensurate with the requirements of metabolising tissues
despite normal/increased cardiac filling pressures
389
what is the commonest cause of myocardial dysfunction
heart failure
390
what is HFREF
heart failure w reduced ejection fraction
391
what is ejection fraction *eyes emoji*
% of blood u empty out of LW w/ each beat
392
what are the 3 cardinal symptoms of heart failure
SOB
fatigue
ankle swelling
393
what are some signs of HF
tachycardia
displaced apex beat
added heart sounds
ascites
394
what is the NYHA classification like
```
class I - asymptomatic (no limitation)
class II - mild HF (slight limitation)
class III - moderate HF (marked limitation)
class IV - severe HF (inability to carry out physical activity w/o discomfort)
```
395
what are some complications of heart failure
renal dysfunction
rhythm disturbances
DVT, PE's
neurologica and psych complications
396
ACEI are less effective in who?
black ppl
397
with aldosterone antagonists in HF, beware of what?
renal impairment
| hyperkalaemia
398
what % of all live births have some form of cardiac defect?
1%
399
what involves tetralogy of Fallot?
1. VSD
2. pulmonary stenosis
3. hypertrophy of RV
4. overriding aorta
400
what are some severe pregnancy risks in CVS?
pulmonary hypertension
marfan's
systemic ventricular impairment
401
what are some moderate pregnancy risks in CVS?
coarctation
moderate to severe aortic stenosis
mechanical heart valves
402
what is the physiology of tetralogy of Fallot like
stenosis of RV outflow --> RV at higher pressure than LV
blue blood passes from RV to LV
so patients are BLUE
403
what is VSD?
ventricular septal defects
abnormal connection btwn 2 ventricles
many close spontaneously during childhood
404
what % of all congenital heart defects is VSD?
20%
405
what is the physiology of VSD like?
high pressure LV
low pressure RV
blood flows from high pressure to low
therefore NOT BLUE
406
what are some clinical signs of VSD (large hole)
small, breathless, thin baby
increased response rate
big heart on CXR
murmur varies in intensity
407
what are some clinical signs of VSD (small hole)
loud systolic murmur
well grown
normal HR, heart size
408
discuss what happens in Eisenmenger's syndrome
```
high pressure pulmonary blood flow
damage to delicate pulmonary vasculature
RV pressure increases
shunt direction reverses
patient becomes BLUE
```
409
what is ASD?
atrial septal defect
abnormal connection btwn atria
often presents in adulthood
410
discuss what happens in ASD
slightly higher pressure in LA vs RA
shunt L-->R
patient NOT BLUE
411
what happens if u have a large hole in ASD
sig increased flow through RH/lungs during childhood
right heart dilatation
increased chest infections
412
what happens if u have a small hole in ASD
small increase in flow
no RH dilatation
no symptoms
413
what are some clinical signs of ASD
pulmonary flow murmur
| CXR: big pulmonary arteries/heart
414
how can ASDs be closed
surgical
| percutaneous (key hole)
415
AVSD (atrio-ventricular septal defects) tend to happen w what?
downs syndrome
416
what does AVSD involve
ventricular septum
atrial septum
mitral and tricuspid valves
417
what is the physiology of AVSD like (complete defect)
```
breathlessness as neonate
poor weight gain
poor feeding
torrential pulmonary blood flow
surgically challenging repair
```
418
what is the physiology of AVSD like (partial defect)
can present in late adulthood
presents like small VSD/ASD
may be left alone - there's no RH dilatation
419
what is PDA?
patent ductus arteriosus
when ductus arteriosus fails to close after
420
in the foetus, what is the ductus arteriosus?
BV connecting main pulmonary artery to the proximal descending aorta.
allows most of the blood from the right ventricle to bypass the foetus's fluid-filled non-functioning lungs.
421
what is the physiology of PDA like
```
large
torrential flow from aorta to pulmonary arteries
breathless
poor feeding
failure to thrive
more common in prem babies
```
422
what is the risk of complications from PDA like
low
423
define coarctation of the aorta
narrowing of the aorta at the site of insertion of ductus arteriosus
424
what is severe coarctation of the aorta like
complete/almost complete obstruction to aortic flow
collapse w heart failure
needs urgent repair
425
what is mild coarctation of the aorta like
presents w hypertension
incidental murmur
should be repaired to prevent LT problems
426
what are some clinical signs of coarctation of the aorta
right arm hypertension
| murmur
427
what are some LT problems of coarctation of the aorta
hypertension (early CAD/strokes)
re-coarctation - requires repeat intervention
aneurysm at site of repair
428
normal AV has how many cusps?
3
429
why is a bicuspid AV an issue?
degenerates quicker than normal valves
become regurgitant earlier than normal valves
associated with coarctation and dilatation of ascending aorta
430
what is pulmonary stenosis
narrowing of RV outflow (to pulmonary artery)
431
what happens w severe pulmonary tenosis
RV failure as neonate
collapse
poor pulmonary blood flow
432
list common structural heart defects
```
VSD
ASD
AVSD
PDA
coarctation of aorta
bicuspid aortic valve
pulmonary stenosis
tetralogy off allot
Eisenmenger syndrome
```
433
NICE guidelines say that the use of _____ may reduce misdiagnosis of hypertension
ABPM
434
list some drugs that cause hypertension (≈8)
```
NSAIDs
comb oral contraceptive
corticosteroids
ciclosporin
cold cures eg phenlephedrine
SNRI antidepressants
some recreational drugs etc cocaine n amphetamines
```
435
list some lifestyle causes of hypertension (3)
obesity
excessive salt
excessive alcohol
436
majority of calcium antagonists used for hypertension are what classed?
I - dihydropyridines
437
how do calcium antagonists work? (CCB)
inhibit opening of voltage-gated (L type) Ca channels in vascular smooth muscle this reduces calcium entry
so reduces calcium available for muscle contraction
this reduction in peripheral resistance reduces systemic BP
438
beta blockers reduce what?
plasma renin
439
what does angiotensin II do
vasoconstricts
stimulates aldosterone release
enhances reabsorption of sodium
440
ACE inhibitors may induce a persistent what?
dry cough
441
how do thiazide diuretics help hypertension
inhibit Na reabsorption by DCT
| reduce ECF which is elevated in hypertension
442
what is one of the most common SPECIFIC causes of BP?
hyperaldosteronism
| too much aldosterone - incr BP - bc too much salt in body (high K)
443
if a patient has vvvv high BP - what would u examine?
eyes
| can have damage to BV at back of eyes, haemorrhage, swelling of optic nerve
444
what is the clinical threshold to consider drug treatment for hypertension?
140/90
445
what is the home threshold to consider drug treatment for hypertension?
135/85
446
what is s1 hypertension
above 140/90
lower than 160/100
lifestyle changes. if high risk, treatment
447
what is s2 hypertension
above 160/100
448
what are the symptoms of high BP
NONE
449
treatment of high BP can reduce what?
headaches
450
why prevent high BP?
stroke
ischaemic heart disease
heart failure
451
what is NNT for paracetamol
5
452
what is NNT for lifelong antihypertensives
NNT 3/4
453
losing how much weight has same effect as taking a BP lowering tablet?
5-10kg
454
what is the most common valvular heart disease?
aortic stenosis
455
in aortic stenosis, symptoms occur when valve area is ___ of normal?
1/4th
456
what is the main type of aortic stenosis
valvular
457
what is the pathophysiology of aortic stenosis?
a pressure gradient develops btwn LV and aorta (incr after load)
LV function initially maintained by compensatory pressure hypertrophy
when comp. mechanisms exhausted, LV function declines
458
what are some presentations of aortic stenosis
syncope
angina
dyspnoea
sudden death
459
what are some indications for intervention in aortic stenosis?
any symptomatic patient with severe AS
any patient with decreasing EF
any patient undergoing CABG with moderate/severe AS
460
AS is a disease of whaT?
ageing
461
to assess severity of AS, wwyd?
echocardiogram
462
asymptomatic AS: wwyd?
medical management
| surveillenace
463
symptomatic AS: wwyd?
AoV replacement
| even in elderly/CHF
464
what is AoV
aortic valve
465
what is chronic mitral regurgitation?
back flow of blood from LV --> LA during systole
466
mild MR is seen in what % of normal individuals?
80%
467
what are some compensatory mechanisms of MR (mitral regurgitation)
LA enlargement
LVH
increased contractility
468
what does an ECG of MR show
LA enlargement
AF
LV hypertrophy
(With severe MR)
469
what does a CXR of MR show
LA enlargement
| central pulmonary artery enlargement
470
how can MR be managed?
medications - vasodilators (ACEi), rate control for AF (beta blockers, CCB)
anticoagulation in AF/fkutter
diuretics for fluid overload
471
define aortic regurgitation (AR)
leakage of blood into LV during diastole due to ineffective coaptation of aortic cusps
472
what are some causes of AR
bicuspid AoV
| infective nedocarditis
473
what are some compensatory mechanisms of AR?
LV dilation
LVH
progressive dilation leads to HF
474
AR tends to be asymptomatic until when?
4th/5th decade
475
what will CXR show if pt has AR
enlarged cardiac silhouette
| aortic root enlargement
476
define mitral stenosis
obstruction of LV inflow that prevents proper filling during diastole
477
what Is the predominant cause of mitral stenosis
rheumatic carditis
478
define carditis....
inflammation of the heart or its surroundings
479
what is HTN
hypertension
480
what is haemoptysis
coughing up blood that comes from lungs/bronchial tubes
can be small flecks to a lot of bleeding
481
management of mitral stenosis is dictated by what?
symptoms
| state of ventricular function
482
what is infective endocarditis?
infection of heart valve(s) or other endocardial linked structures within the heart
serious n largely preventable complication of bacteraemia, usually in a patient w structurally abnormal heart valve
483
what are some endocardial linked structures in the heart that aren't valves
septal defects
pacemaker leads
surgical patches
etc
484
which patients are predisposed to developing infective endocarditis?
abnormal, regurgitant or prosthetic valves
485
which type of patients are most commonly affected by infective endocarditis
elderly
IV drug users
young w/ congenital heart disease
486
a pt with infective endocarditis presents with signs of what?
```
systemic infection (fever, sweating, etc)
may also have signs of embolisation of infected material eg stroke, PE, etc
```
487
when is surgery required for infective endocarditis?
if infection cannot be cured with ABs ie recurs after treatment/CRP doesn't fall
to treat complications eg aortic root abscess, severe valve damage
to remove infected devices
to replace valve after infection hw
to remove large vegetations before they embolism
488
what is dukes criteria for infective endocarditis?
2 major criteria:
- bugs grown from blood cultures
- evidence of endocarditis on echo, or new valve leak
5 minor criteria:
- predisposing factors
- fever
- vascular phenomena
- immune phenomena
- equivocal blood cultures
489
raised ___ is almost always present in IE
CRP
490
how can IE be treated
antimicrobials
treat complications eg arrhythmia, HF etc
surgery
491
as an F1, if a pt has suspected IE what should u do?
do lots of blood cultures
always write ?IE on diff of its with sepsis, request an echo
do it even more in high risk patients
beware of pt whose INR has shot up; sometimes 1st sign of IE!
492
what is an ECG aka
EKG
493
define ecg
representation of the electrical events of the cardiac cycle
494
what can we identify with ecgs? (6)
arrhythmias
myocardial Ischaemia/infarction
pericarditis
chamber hypertrophy
electrolyte disturbances ie hyper/hypokalaemia
drug toxicity (ie digoxin/drugs which prolong QT interval)
495
contraction of any muscle is associated with electrical changes called what?
depolarisation
496
what is the dominant pacemaker in the heart? n what's its intrinsic rate?
SA node
| 60-100 bpm
497
what is a back-up pacemaker and what is its rate?
AV node
| 40-60 bpm
498
what is the standard calibration of an ECG?
25 mm/s
499
electrical impulse that travels TOWARDS the electrode produces a what?
upright/positive deflection
500
what is the path of an impulse conduction from SA node to purkinje fibres?
SA node > AV node > bundle of His > bundle branches > Purkinje fibres
501
P wave is WHAT
atrial depolarisation
502
QRS wave is WHAT
ventricular depolarisation
503
T wave is WHAT
ventricular repolarisation
504
what is the PR interval ?
atrial depolarisation and delay in AV junction
| delay allows time for atria to contract before ventricles contract
505
on ecg paper, 1 small box horizontally is how many seconds
0.04s
506
on ecg paper, 1 large box horizontally is how many seconds
0.20s
507
on ecg paper, 1 large box vertically is how many mV?
0.5mV
508
standard ecg has how many leads?
12
509
what are the 12 leads for ecg?
3 standard limb leads
3 augmented limb leads
6 precordial leads
510
PR interval should be 120-200ms, how many lil squares?
3-5
511
width of QRS complex should not exceed 110ms, less than how many lil squares?
3
512
QRS complex should be dominantly upload in which leads?
I and II
513
QRS and T waves tend to have what in the limb leads?
same general direction
514
all waves are what in lead aVR?
negative
515
R wave must grow from V1-?
V4
516
S wave must grow from V1-? and then disappear in V6
V1-3
517
ST segment should start isoelectric, except where, where it may be elevated?
V1/V2
518
P waves should be upright where?
I
II
V2-6
519
should be no Q wave/small Q wave (less than 0.04s in width) where?
I
II
V2-6
520
T wave must be upright in which leads?
I
II
V2-6
521
P wave is always negative where?
lead aVR
522
P wave should be less than how many small squares in duration (across)?
3
523
P wave should be less than how many small squares in amplitude (up)?
2.5
524
where is P wave best seen
lead II
525
how does right atrial enlargement impact P wave?
tall
526
how does left atrial enlargement impact p wave?
notched ('m') shaped
527
short PR interval happens in which syndrome?
wolff-parkinson-white syndrome
528
long PR interval occurs when?
1st degree heart block
529
what does isoelectric mean?
flat
530
normal T wave is what?
asymmetrical (1st half having gradual slope than 2nd)
531
what are abnormal t waves like
```
symmetrical
tall
peaked
biphasic
inverted
```
532
what is the QT interval
total duration of depolarisation and repolarisation
533
QT interval does WHAT when HR increases?
decreases
534
QT interval should be btwn what (time)
0.35-0.45s
535
U waves are related to what?
afterdepolarisations
536
U waves are more prominent in ppl w what?
slow heart rates
537
what is the rule of 300 for HR? (regular rhythm)
counter number of "big boxes" btwn 2 QRS complexes, and divide 300 by this (smaller boxes w 1500)
538
if there are 1 big boxes btwn 2 QRS complexes, what is the HR?
300 by 300/1
539
if there are 3 big boxes btwn 2 QRS complexes, what is the HR?
100 bc 300/3
540
if there are 4 big boxes btwn 2 QRS complexes, what is the HR?
75 bc 300/4
541
what rule is it for irregular rhythm?
10 second rule
542
what is the 10second rule
for irrregular rhythm
so, ecgs record 10secs of rhythm per page
COUNT no. of beats present on the ECG
multiply by 6
543
QRS axis represents what?
overall direction of the heart's electrical activity
544
what do abnormalities of QRS axis hint at?
ventricular enlargement
| conduction blocks
545
normal QRS axis is from what?
-30degrees to +90degrees
546
-30degree to +90degree QRS axis is referred to as what?
left axis deviation
547
what is right axis deviation on QRS axis range?
+90degrees to +180degrees
548
amplitude of ECG deflection is related to what?
mass of the myocardium
549
width of ECG deflection reflects what?
spread of conduction
550
low amplitude p wave can be linked to which conditions?
atrial fibrosis
obesity
hyperkalaemia
551
high amplitude (tall) p wave can be linked to what?
right atrial enlargement
552
broad noticed "bifid" p wave is linked to what?
left atrial enlargement
553
broad QRS complex is linked to what?
ventricular conduction delay/BBB
554
small QRS complex is linked to what?
obese patient
pericardial effusion
infiltrative cardiac disease
555
tall QRS complexes are linked to what?
LVH
| thin patient
556
when can ST segment be elevateD?
in early repolarisation
MI
pericarditis
myocarditis
557
excessively rapid/slow depolarisation can be arrhythmogenic. why may this be
congenital
drugs
electrolyte disturbances
558
list some causes of bradycardia
conduction tissue fibrosis
ischaemia
inflammation/infiltrative disease
559
in ischaemia/infarction what happens to ST segment?
depression
560
how does Hyperkalaemia affect ecg
tall T waves
flattened P wave
broadening of QRS
eventually sine pattern
561
how does hypokalaemia affect ECG
flattening of T wave
| QT prolongation
562
how does hypercalcaemia affect QT?
shortens
563
how does hypocalcaemia affect QT?
prolongation
564
when does rheumatic fever usually present?
2-3w after a pharyngitis episode from strep. pyogenes
