Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BDS2 bams > CV medicine > Flashcards

CV medicine Flashcards

1
Q

technical name for a heart attack

A

myocardial infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

ACS

A

angina (+PVD) - ischaemia

MI (+CVA) - infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

diagnosis of ACS

A

history
ECG: STEMI, NSTEMI
biomarkers: troponin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

atherosclerosis

A

build up of cholesterol/fats in artery walls
progressive
lose x8 in blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what happens if an atherosclerotic plaque ruptures?

A

occlusion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

stages of progression of atherosclerosis

A 
normal
fatty streak
plaque
increasing plaque
obstructive atherosclerotic plaque
plaque fissure erosion - thrombosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

why is CAD severe?

A

no anastomotic supply

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

angina definition

A

reversible heart muscle ischaemia

- coronary arteries narrow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

classical angina

A 
no pain at rest 
pain with certain level of exertion (lactic acidosis) - worse with cold weather/emotion
pain relieved by rest
pt lives within levels of tolerance
gradual deterioration
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

signs of classical angina

A

often no signs

occ hyperdynamic circulation - anaemia, hyperthyroidism, hypovolaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

unstable angina

A

symptoms at rest with no biomarkers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pain with angina

A

central crushing chest pain

  • radiation
  • same pain but varies between individuals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

angina investigations

A

ECG - ST segment elevation/depression
angiography
echocardiography
isotope studies

eliminate other disease - thyroid, anaemia, valve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

angina tx principles

A

reduce oxygen demands of heart

increase oxygen delivery to tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

angina tx - reduce oxygen demands of heart

A

reduce after load and preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

afterload

A

bp

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

preload

A

venous pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

effect of sitting up re angina

A

reduce venous return

reduce CO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

angina tx - increase oxygen delivery to tissues

A

angioplasty - dilate
CABG - bypass

blocked/narrowed vessels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

angina non-drug therapy

A

explain - live within limitations

modify risk factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

angina drug therapy

A

reduce MI risk - aspirin
hypertension - Ca channel blockers, diuretics, ACE inhibitors, B-blockers
reduce preload/dilate coronary vessels - nitrates
emergency - GTN spray/tab

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

angina surgery

A

CABG
angioplasty and stenting (PCI) - gold standard in HA

need anti platelets in both

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

CABG

A

bypass blockage in coronary artery that can’t be txed in any other way
can’t redo, mortality risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

PVD

A 
'angina' of the tissues - usually LL
atheroma in femoral/popliteal vessels
'claudication'
indicates 'arteriopath' - MI risk
limitation of fct
poor wound healing
men and smokers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

congestive heart failure

A

hypertrophy of myocyte but no increase in blood supply
heart weight x2-3 of normal
increased metabolic demands - ischaemia - apoptosis - HF
oedema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

cardiac tumours prevalence

A

rare

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

benign cardiac tumours

A

myxoma, lipoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

malignant cardiac tumours

A

angiosarcoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what other sources of cardiac tumour?

A

local extension of tumours from the thoracic cavity e.g. bronchogenic carcinoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

calcific aortic stenosis

A

commonest valvular condition
dystrophic calcium deposits due to tissue inflammation and hyperlipidaemia
narrowing of valvular orifice

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

rheumatic heart disease

A

complication of RF
host immune reaction against strep A antigens
T2 and T4 hypersensitivity reactions
fibrinoid necrosis
thickening and fusion, calcification of valves
risk for IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

why do L valves fail more commonly?

A

higher pressure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

valve stenosis

A

narrowed opening

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

types of stenosis and importance

A

aortic stenosis can lead to heart failure

mitral stenosis not as important

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

valve incompetence

A

don’t close properly - backflow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

consequence of valvular disease

A

reduce efficiency of heart as pump - heart failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

symptoms of valvular disease

A

rarely any symptoms - undiagnosed

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

valvular issues

A

stenosis
incompetence
insufficiency
vegetations

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

causes of valvular disease

A 
common in elderly and Downs
congenital 
MI - papillary muscle rupture
RF
dilatation of aortic root - syphilis, aneurysm formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

valvular disease investigation

A

Ultrasound

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

types of valve replacement

A

mechanical - metal

porcine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

mechanical valve replacement

A

last longer
anticoagulants
middle age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

porcine valve replacement

A

only last around 10yrs
don’t need anticoagulants
v young - outgrow it, falls
elderly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

important principle when choosing valve replacement

A

few changes as possible - mortality risk

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what is there a risk of after valve replacements?

A

IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

why are CHDs often undetected?

A

asymptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

cyanosis

A

central
peripheral - cold env
when 5g/dl or more deoxygenated Hb in blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

CHDs investigation

A

US

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

types of CHD

A

ASD (hypertrophy)
VSD
coarctation of aorta (narrowed)
PDA (connects pulmonary artery to aorta)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

potential risk of CHDs

A

IE risk?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

IE

A

microbial infection of endocardium (usually valves)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

what is the biggest risk factor for IE?

A

prev IE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

pathogenesis of IE

A 
surface abnormalities
haemodynamic changes
bacteraemia
turbulence
platelet/fibrin deposition
vegetation
microbial attachment and multiplication 
enlargement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

is IE easy to recognise?

A

no

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

ABP drug regime

A

amoxicillin 3g 1hr before

clindamycin 1.5g (higher ADA risk - only use if penicillin allergic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

primary prevention

A

stop from getting disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

secondary prevention

A

detect early and prevent progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

aspects of secondary prevention

A

lifestyle changes
control cholesterol - statin
control hypertension
anti-platelet drugs - aspirin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

when should aspirin be used as secondary prevention?

A

when identified CV disease

when high risk with no identified disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

anticoagulants broad use

A

if in heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

antiplatelets broad use

A

if peripheral bvs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

irreversible risk factors

A
  • age
  • sex
  • FH
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

reversible risk factors

A

SMOKING
obesity
diet
exercise

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

reversible genetic risk factors

A

hypertension
hyperlipidaemia
diabetes
stress?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

risk modification

A

info
belief
motivation
behavioural change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

ACE inhibitors - name

A

-pril

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

ACE inhibitors - mechanism of action

A

reduce excess water and salt retention
reduce bp

inhibit AT1 to AT2 (vasoconstrictor) so reduce aldosterone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

ACE inhibitors - SEs

A

cough
hypotension
angio-oedema
lichenoid reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

AT2 blockers name

A

-artan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

B-blockers - name

A

-olol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

atenolol

A

selective (B1 only)

only on B-receptors in CV system

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

B-blockers - action

A

reduce heart muscle excitability
stop arrhythmias
reduce bp
prevent increase in hr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

negative effects of B blockers

A

postural hypotension
make HF worse (reduce heart efficiency)
non-selective can make asthma worse

74
Q

diuretics indication

A

for heart failure

75
Q

diuretics mechanism of action

A

reduce bp

increase salt and water loss - reduce plasma volume so reduce cardiac workload

76
Q

types of diuretics

A

thiazide - bendroflumethiazide

loop - frusemide

77
Q

side effects of diuretics

A 
Na+/K+ imbalance if not monitored
dry mouth (elderly)
78
Q

types of nitrates

A

short-acting - GTN

long-acting - isosorbide mononitrate

79
Q

GTN

A

short acting nitrate for emergency tx of angina

80
Q

isosorbide mononitrate

A

long acting nitrate for prevention of angina

81
Q

mechanism of action of nitrates

A

vasodilators

  • dilate veins so reduce preload
  • dilate resistance arteries so reduce afterload
  • dilate colateral coronary artery supply so reduce anginal pain
82
Q

administration of nitrates

A

inactivated by FPM so sublingual, transdermal, IV

short-shelf life

83
Q

side effect of nitrates

A

headache

84
Q

Ca channel blockers mechanism of action

A

reduce bp

block Ca channels in smooth muscle

85
Q

Ca channel blockers in peripheral bv’s

A

relaxation and vasodilation

-pine

86
Q

Ca channel blockers in heart muscle

A

slow conduction of pacing impulses

Verapamil

87
Q

side effect of Ca blockers

A

gingival hyperplasia

88
Q

Warfarin mechanism of action

A

coumarin
inhibits synthesis of vitK dependent CFs
- 2,7,9,10 (slow)
- protein C and S (quick) ACs

89
Q

why do you need to use heparin when starting warfarin?

A

because you get initial hypercoagulation

as warfarin quickly inhibits proteins C and S which are anticoagulants

90
Q

what should INR on warfarin be?

A

2-4

91
Q

why should you monitor pt on warfarin closely?

A

food and drug interaction

unpredictable bioavailability

92
Q

Warfarin and IDBs

A

avoid if can but not contraindicated

93
Q

mechanism of action of statins

A

lipid lowering
HMG coA reductase inhibitors
inhibit cholesterol synthesis in liver

94
Q

side effects of statins

A

myositis with interaction with antifungals

muscle pain - reduce dose or take before bed

95
Q

statins and antifungals

A

fluconazole

omit statin - fine as makes difference over years not days

96
Q

antiplatelets

A 
aspirin
clopidogrel
dipyridamole 
Prasugrel
Ticagrelor
97
Q

aspirin mechanism of action

A

inhibits platelet aggregation
- alters TA2 and prostacyclin balance
irreversible for life of platelet

98
Q

clopidogrel mechanism of action

A

inhibits ADP induced platelet aggregation

99
Q

dipyridamole mechanism of action

A

inhibits platelet phosphodiesterase

100
Q

new antiplatelets

A

Prasugrel, Ticagrelor

only prescribe in conjunction with aspirin

101
Q

advantage of antiplatelets

A

can have more atherosclerosis without the severe consequences
- platelets don’t stick on platelets as much

102
Q

NOACs

A

rivaroxaban
apixaban
dabigatran

103
Q

rivaroxaban mechanism of action

A

inhibit FXa

104
Q

apixaban mechanism of action

A

inhibit FXa

105
Q

dabigatran mechanism of action

A

direct thrombin inhibitor

106
Q

NOACs pros and cons

A

short 1/2 life
fewer interactions
£
less testing

107
Q

what should you avoid on NOACs?

A

NSAIDs, erythromycin, clarithromycin

108
Q

atherosclerosis

A

fat deposits in walls of mostly large and medium blood vessels
multifactorial

109
Q

atherosclerosis risk factors

A 
HYPERLIPIDAEMIA
age
gender
genes: familial hypercholesterolaemia (mutation of LDL receptor gene)
diabetes/hypertension
lifestyle
110
Q

atheroma formation

A

chronic endothelial cell injury - hypertension etc
permeability increases. lipid deposited in initial layers
macrophages in - foam cells, fatty streaks, may regress
smooth muscle proliferation
healing phase - fibrous tissue over lipid. Plaque

111
Q

effects of atherosclerosis

A 
ischaemia
infarction
thrombosis
embolism
CV effects - angina, MI, CVA
112
Q

thick atherosclerotic plaques

A

stable

113
Q

thin atherosclerotic plaques

A

platelets can hit against endothelium - thrombosis

114
Q

what stage of atherosclerosis is reversible?

A

fatty streaks

115
Q

aneurysms

A

abnormal dilatation

may be fatal

116
Q

causes of aneurysms

A

developmental
degenerative
traumatic

117
Q

most common aneurysms

A

AAAs - atherosclerosis

118
Q

factors influencing hypertension

A

gene

env

119
Q

hypertension boundaries

A

systolic >140mmHg
- >160 in isolated systolic hypertension
diastolic >90mmHg

120
Q

diastolic bp

A

resting arterial pressure

important one - spend more time in this pressure

121
Q

diagnosing hypertension

A

3 separate measurements, sitting

- diff days, a week apart

122
Q

hypertension risk factors

A 
FH
drugs - OCP, NSAIDs, steroids
age
obesity
pregnancy
etc
123
Q

outcome of hypertension

A

accelerated atherosclerosis

renal failure

124
Q

mechanism of hypertension

A 
none usually found
essential hypertension: no obvious cause, probably related to control mechanism within arterial walls
rare triggers
 - renal artery stenosis
 - endocrine tumours
125
Q

S and S of hypertension

A

usually none
headaches
TIAs

126
Q

hypertension indications for further investigations

A

young pt
resistant
accelerated
‘unusual’ history

127
Q

hypertension investigations

A 
urinalysis
serum biochemistry
serum lipids
ECG
renal US
128
Q

hypertension tx

A

modify risk factors

drugs

129
Q

heart failure

A

pump failure

tissue hypoxia - failure of circulation

130
Q

high output heart failure

A

system works but can’t provide enough as demand has increased
rare
anaemia, thyrotoxicosis

131
Q

low output heart failure

A

more common = pump failure

132
Q

causes of low output heart failure

A

heart muscle disease - MI, myocarditis
pressure overload - hypertension, aortic stenosis
vol overload - mitral/aortic incompetence
prolonged low level ischaemia
arrhythmias - AF, heart block
drugs - B-blockers, CS, anticancer drugs

133
Q

left side failure S and S

A 
dyspnoea
pulmonary oedema
frothy cough
tachycardia
low bp
low vol pulse
hypo perfusion - systemic
134
Q

right side failure S and S

A

ascites, ankle oedema - systemic venous hypertension
raised JVP
tender enlarged liver
pulmonary hypoperfusion

135
Q

general heart failure symptoms

A

SOB
swelling of feet and legs
chronic lack of energy
cough - frothy sputum

136
Q

acute heart failure tx

A

hospital

O2, morphine, frusemide

137
Q

chromic heart failure tx

A 
community based
improve fct
reduce compensation effects e.g. reduce bp, fix valves, reduce compensatory increase in fluid
where possible tx the cause
 - high bp
 - AF
 - valve disease
 - anaemia
 - thyroid disease
138
Q

drug therapy in chronic heart failure

A

diuretics
ACE inhibitors
nitrates
digoxin

stop negative inotropes - B blockers

139
Q

digoxin

A

inotrope
increase force of contraction
RS HF - reduce symptoms but not problem

140
Q

shockable arrhythmias

A

VF and pVT

141
Q

non-shockable arrhythmias

A

asystole and PEA

142
Q

tachy

A

AF

V tachycardia

143
Q

brady

A 
heart block
drug induced (B-blocker, digoxin)
144
Q

cardiac pacemakers

A

treat bradyarrhythmias
keep hr at minimum level
theoretical risk of electrical interference

145
Q

sinus rhythm stages

A

P - atrial depolarisation
QRS - ventricular depolarisation
T - ventricular repolarisation

146
Q

regular hr

A

60-100 bpm

147
Q

VF

A

disorganised, v irregular, 300-600bpm
unstable heart electrical activity
no CO - death
defibrillate

148
Q

asystole appearance

A

slight waves as still some electrical activity in body

149
Q

AF

A

common in IHD
irregular rhythm
P wave fibrillatory (fine to course)

150
Q

infarction

A

thrombosis on atheroma plaque

may detach and travel to block vessels

151
Q

limb infarction

A

blocked femoral and popliteal arteries

thrombolysis, salvage surgery

152
Q

heart infarction

A

MI

coronary artery atheroma

153
Q

brain infarction

A 
carotid arteries
'stroke'
 - usually embolism from atheroma
 - occ a cerebral bleed
 - rarely vessel thrombosis (good collateral blood supply`)
loss of fct
154
Q

TIAs

A

platelets removed naturally so fct returns

risk of a big stroke

155
Q

types of MI

A 
spontaneous - primary coronary event
 - plaque fissure/rupture
MI secondary to ischaemia
sudden death with symptoms of ischaemia and evidence of ST elevation or thrombus (PCI/autopsy)
MI from PCI
MI from CABG
156
Q

MI strategies

A

reduce tissue loss from necrosis

prevent further episode

157
Q

MI strategies - reduce tissue loss from necrosis

A

oedema blocks other tissues
open blood flow to ischaemic tissue - thrombolysis, angioplasty
bypass obstruction - CABG, fem/popliteal bypass

158
Q

MI strategies - prevent further episode

A

risk factor management

aspirin

159
Q

MI S+S

A

pain, nausea, pale, sweaty
‘going to die’
silent MIs

160
Q

effect of MI

A

death around 50%

fct limitation

161
Q

complications of MI

A 
death
arrhythmias
HF
ventricular hypofct and thrombosis
 - papillary muscle rupture - valve disease
DVT and pulmonary embolism
complications of thrombolysis
162
Q

MI investigations

A 
ECG
 - ST segment elevation/T wave abnormalities
 - may be normal
 - Q waves only indicate old MI
cardiac enzymes
 - troponin
 - creatinine kinase
 - LDH and AST increase - not specific
163
Q

MI tx primary care

A

get to hospital
analgesia, aspirin, reassurance
(BLS)

164
Q

MI tx hospital

A 
primary PCI
thrombolysis if indicated
drug tx to reduce tissue damage
prevent recurrence/complications
aspirin - secondary prevention
165
Q

thrombolysis

A

can do up to 6hrs - if can’t get to PCI centre in time

inject streptokinase, TPA

166
Q

contraindications to thrombolysis

A

injury/surgery/IM injections
severe hypertension, active PUD
diabetic eye disease, liver disease, pregnancy

167
Q

medical management of MI

A

prevent next MI
- risk modification and aspirin
- B-blocker, ACE inhibitor
tx complications: HF, arrhythmias, psychological distress

168
Q

haemangioma

A

hamartoma of blood vessels without CT capsule
rapid growth first few weeks, usually regress over 1st 10yrs
60% H+N

169
Q

vascular malformations

A

present at birth and persist
may become more noticeable in elderly - epithelium thinner, calcium deposits
can get intraosseous malformations
types - cavernous, capillary, Sturge Weber syndrome

can develop them IO and inside bone
tx pts in hospital if bleeding risk
can also get in meninges of brain - may have epilepsy

170
Q

kaposi sarcoma

A

HHV-8
multi-focal low grade sarcoma of lymphatics and bv’s
HIV
immune deficiency - role in carcinogenesis

171
Q

angiosarcoma

A

develops in cells of blood or lymph glands
rare, aggressive
malignant, surgery

172
Q

drugs to prevent further disease

A

antiplatelets
statins
B-blockers
anticoagulants

173
Q

drugs to reduce symptoms of current disease

A 
diuretics
B-blockers
nitrates
Ca channel blockers
ACE inhibitors
174
Q

advice about reducing IE risk

A

attendance for oral care
rapid management infection
max OH and prevention
avoiding risk activity - piercings

175
Q

CV pathology

A 
2 processes
1 - blood vessel narrowing
 - inadequate O2 delivery for tissue needs
 - 'cramp' in affected tissue/muscle
 - no residual deficit at first
2 - blood vessel occlusion
 - no O2 delivery - tissue death
 - more severe pain
 - loss of fct of tissue

both processes result in loss of heart muscle
1 - long-term
2 - short-term

176
Q

when can you get VF?

A

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

177
Q

coagulation necrosis

A

cells retain outline, can be identified
cytoplasm darker
remains of nuclei - small and dark staining or break up and disappear
striations disappear
always inflammation - neutrophils first then macrophages

178
Q

granulation tissue

A

don’t get replacement of myocardium by myocardium
leaves scar
will affect fct of heart

179
Q

STEMI

A

classic heart attack

180
Q

NSTEMI

A

may be unstable angina

181
Q

if had MI how long should you avoid complex tx for?

A

at least 6m

BDS2 bams (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions