CV medicine Flashcards
technical name for a heart attack
myocardial infarction
ACS
angina (+PVD) - ischaemia
MI (+CVA) - infarction
diagnosis of ACS
history
ECG: STEMI, NSTEMI
biomarkers: troponin
atherosclerosis
build up of cholesterol/fats in artery walls
progressive
lose x8 in blood flow
what happens if an atherosclerotic plaque ruptures?
occlusion
stages of progression of atherosclerosis
normal fatty streak plaque increasing plaque obstructive atherosclerotic plaque plaque fissure erosion - thrombosis
why is CAD severe?
no anastomotic supply
angina definition
reversible heart muscle ischaemia
- coronary arteries narrow
classical angina
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
signs of classical angina
often no signs
occ hyperdynamic circulation - anaemia, hyperthyroidism, hypovolaemia
unstable angina
symptoms at rest with no biomarkers
pain with angina
central crushing chest pain
- radiation
- same pain but varies between individuals
angina investigations
ECG - ST segment elevation/depression
angiography
echocardiography
isotope studies
eliminate other disease - thyroid, anaemia, valve
angina tx principles
reduce oxygen demands of heart
increase oxygen delivery to tissues
angina tx - reduce oxygen demands of heart
reduce after load and preload
afterload
bp
preload
venous pressure
effect of sitting up re angina
reduce venous return
reduce CO
angina tx - increase oxygen delivery to tissues
angioplasty - dilate
CABG - bypass
blocked/narrowed vessels
angina non-drug therapy
explain - live within limitations
modify risk factors
angina drug therapy
reduce MI risk - aspirin
hypertension - Ca channel blockers, diuretics, ACE inhibitors, B-blockers
reduce preload/dilate coronary vessels - nitrates
emergency - GTN spray/tab
angina surgery
CABG
angioplasty and stenting (PCI) - gold standard in HA
need anti platelets in both
CABG
bypass blockage in coronary artery that can’t be txed in any other way
can’t redo, mortality risk
PVD
'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
congestive heart failure
hypertrophy of myocyte but no increase in blood supply
heart weight x2-3 of normal
increased metabolic demands - ischaemia - apoptosis - HF
oedema
cardiac tumours prevalence
rare
benign cardiac tumours
myxoma, lipoma
malignant cardiac tumours
angiosarcoma
what other sources of cardiac tumour?
local extension of tumours from the thoracic cavity e.g. bronchogenic carcinoma
calcific aortic stenosis
commonest valvular condition
dystrophic calcium deposits due to tissue inflammation and hyperlipidaemia
narrowing of valvular orifice
rheumatic heart disease
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
why do L valves fail more commonly?
higher pressure
valve stenosis
narrowed opening
types of stenosis and importance
aortic stenosis can lead to heart failure
mitral stenosis not as important
valve incompetence
don’t close properly - backflow
consequence of valvular disease
reduce efficiency of heart as pump - heart failure
symptoms of valvular disease
rarely any symptoms - undiagnosed
valvular issues
stenosis
incompetence
insufficiency
vegetations
causes of valvular disease
common in elderly and Downs congenital MI - papillary muscle rupture RF dilatation of aortic root - syphilis, aneurysm formation
valvular disease investigation
Ultrasound
types of valve replacement
mechanical - metal
porcine
mechanical valve replacement
last longer
anticoagulants
middle age
porcine valve replacement
only last around 10yrs
don’t need anticoagulants
v young - outgrow it, falls
elderly
important principle when choosing valve replacement
few changes as possible - mortality risk
what is there a risk of after valve replacements?
IE
why are CHDs often undetected?
asymptomatic
cyanosis
central
peripheral - cold env
when 5g/dl or more deoxygenated Hb in blood
CHDs investigation
US
types of CHD
ASD (hypertrophy)
VSD
coarctation of aorta (narrowed)
PDA (connects pulmonary artery to aorta)
potential risk of CHDs
IE risk?
IE
microbial infection of endocardium (usually valves)
what is the biggest risk factor for IE?
prev IE
pathogenesis of IE
surface abnormalities haemodynamic changes bacteraemia turbulence platelet/fibrin deposition vegetation microbial attachment and multiplication enlargement
is IE easy to recognise?
no
ABP drug regime
amoxicillin 3g 1hr before
clindamycin 1.5g (higher ADA risk - only use if penicillin allergic)
primary prevention
stop from getting disease
secondary prevention
detect early and prevent progression
aspects of secondary prevention
lifestyle changes
control cholesterol - statin
control hypertension
anti-platelet drugs - aspirin
when should aspirin be used as secondary prevention?
when identified CV disease
when high risk with no identified disease
anticoagulants broad use
if in heart
antiplatelets broad use
if peripheral bvs
irreversible risk factors
- age
- sex
- FH
reversible risk factors
SMOKING
obesity
diet
exercise
reversible genetic risk factors
hypertension
hyperlipidaemia
diabetes
stress?
risk modification
info
belief
motivation
behavioural change
ACE inhibitors - name
-pril
ACE inhibitors - mechanism of action
reduce excess water and salt retention
reduce bp
inhibit AT1 to AT2 (vasoconstrictor) so reduce aldosterone
ACE inhibitors - SEs
cough
hypotension
angio-oedema
lichenoid reactions
AT2 blockers name
-artan
B-blockers - name
-olol
atenolol
selective (B1 only)
only on B-receptors in CV system
B-blockers - action
reduce heart muscle excitability
stop arrhythmias
reduce bp
prevent increase in hr
negative effects of B blockers
postural hypotension
make HF worse (reduce heart efficiency)
non-selective can make asthma worse
diuretics indication
for heart failure
diuretics mechanism of action
reduce bp
increase salt and water loss - reduce plasma volume so reduce cardiac workload
types of diuretics
thiazide - bendroflumethiazide
loop - frusemide
side effects of diuretics
Na+/K+ imbalance if not monitored dry mouth (elderly)
types of nitrates
short-acting - GTN
long-acting - isosorbide mononitrate
GTN
short acting nitrate for emergency tx of angina
isosorbide mononitrate
long acting nitrate for prevention of angina
mechanism of action of nitrates
vasodilators
- dilate veins so reduce preload
- dilate resistance arteries so reduce afterload
- dilate colateral coronary artery supply so reduce anginal pain
administration of nitrates
inactivated by FPM so sublingual, transdermal, IV
short-shelf life
side effect of nitrates
headache
Ca channel blockers mechanism of action
reduce bp
block Ca channels in smooth muscle
Ca channel blockers in peripheral bv’s
relaxation and vasodilation
-pine
Ca channel blockers in heart muscle
slow conduction of pacing impulses
Verapamil
side effect of Ca blockers
gingival hyperplasia
Warfarin mechanism of action
coumarin
inhibits synthesis of vitK dependent CFs
- 2,7,9,10 (slow)
- protein C and S (quick) ACs
why do you need to use heparin when starting warfarin?
because you get initial hypercoagulation
as warfarin quickly inhibits proteins C and S which are anticoagulants
what should INR on warfarin be?
2-4
why should you monitor pt on warfarin closely?
food and drug interaction
unpredictable bioavailability
Warfarin and IDBs
avoid if can but not contraindicated
mechanism of action of statins
lipid lowering
HMG coA reductase inhibitors
inhibit cholesterol synthesis in liver
side effects of statins
myositis with interaction with antifungals
muscle pain - reduce dose or take before bed
statins and antifungals
fluconazole
omit statin - fine as makes difference over years not days
antiplatelets
aspirin clopidogrel dipyridamole Prasugrel Ticagrelor
aspirin mechanism of action
inhibits platelet aggregation
- alters TA2 and prostacyclin balance
irreversible for life of platelet
clopidogrel mechanism of action
inhibits ADP induced platelet aggregation
dipyridamole mechanism of action
inhibits platelet phosphodiesterase
new antiplatelets
Prasugrel, Ticagrelor
only prescribe in conjunction with aspirin
advantage of antiplatelets
can have more atherosclerosis without the severe consequences
- platelets don’t stick on platelets as much
NOACs
rivaroxaban
apixaban
dabigatran
rivaroxaban mechanism of action
inhibit FXa
apixaban mechanism of action
inhibit FXa
dabigatran mechanism of action
direct thrombin inhibitor
NOACs pros and cons
short 1/2 life
fewer interactions
£
less testing
what should you avoid on NOACs?
NSAIDs, erythromycin, clarithromycin
atherosclerosis
fat deposits in walls of mostly large and medium blood vessels
multifactorial
atherosclerosis risk factors
HYPERLIPIDAEMIA age gender genes: familial hypercholesterolaemia (mutation of LDL receptor gene) diabetes/hypertension lifestyle
atheroma formation
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
effects of atherosclerosis
ischaemia infarction thrombosis embolism CV effects - angina, MI, CVA
thick atherosclerotic plaques
stable
thin atherosclerotic plaques
platelets can hit against endothelium - thrombosis
what stage of atherosclerosis is reversible?
fatty streaks
aneurysms
abnormal dilatation
may be fatal
causes of aneurysms
developmental
degenerative
traumatic
most common aneurysms
AAAs - atherosclerosis
factors influencing hypertension
gene
env
hypertension boundaries
systolic >140mmHg
- >160 in isolated systolic hypertension
diastolic >90mmHg
diastolic bp
resting arterial pressure
important one - spend more time in this pressure
diagnosing hypertension
3 separate measurements, sitting
- diff days, a week apart
hypertension risk factors
FH drugs - OCP, NSAIDs, steroids age obesity pregnancy etc
outcome of hypertension
accelerated atherosclerosis
renal failure
mechanism of hypertension
none usually found essential hypertension: no obvious cause, probably related to control mechanism within arterial walls rare triggers - renal artery stenosis - endocrine tumours
S and S of hypertension
usually none
headaches
TIAs
hypertension indications for further investigations
young pt
resistant
accelerated
‘unusual’ history
hypertension investigations
urinalysis serum biochemistry serum lipids ECG renal US
hypertension tx
modify risk factors
drugs
heart failure
pump failure
tissue hypoxia - failure of circulation
high output heart failure
system works but can’t provide enough as demand has increased
rare
anaemia, thyrotoxicosis
low output heart failure
more common = pump failure
causes of low output heart failure
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
left side failure S and S
dyspnoea pulmonary oedema frothy cough tachycardia low bp low vol pulse hypo perfusion - systemic
right side failure S and S
ascites, ankle oedema - systemic venous hypertension
raised JVP
tender enlarged liver
pulmonary hypoperfusion
general heart failure symptoms
SOB
swelling of feet and legs
chronic lack of energy
cough - frothy sputum
acute heart failure tx
hospital
O2, morphine, frusemide
chromic heart failure tx
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
drug therapy in chronic heart failure
diuretics
ACE inhibitors
nitrates
digoxin
stop negative inotropes - B blockers
digoxin
inotrope
increase force of contraction
RS HF - reduce symptoms but not problem
shockable arrhythmias
VF and pVT
non-shockable arrhythmias
asystole and PEA
tachy
AF
V tachycardia
brady
heart block drug induced (B-blocker, digoxin)
cardiac pacemakers
treat bradyarrhythmias
keep hr at minimum level
theoretical risk of electrical interference
sinus rhythm stages
P - atrial depolarisation
QRS - ventricular depolarisation
T - ventricular repolarisation
regular hr
60-100 bpm
VF
disorganised, v irregular, 300-600bpm
unstable heart electrical activity
no CO - death
defibrillate
asystole appearance
slight waves as still some electrical activity in body
AF
common in IHD
irregular rhythm
P wave fibrillatory (fine to course)
infarction
thrombosis on atheroma plaque
may detach and travel to block vessels
limb infarction
blocked femoral and popliteal arteries
thrombolysis, salvage surgery
heart infarction
MI
coronary artery atheroma
brain infarction
carotid arteries 'stroke' - usually embolism from atheroma - occ a cerebral bleed - rarely vessel thrombosis (good collateral blood supply`) loss of fct
TIAs
platelets removed naturally so fct returns
risk of a big stroke
types of MI
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
MI strategies
reduce tissue loss from necrosis
prevent further episode
MI strategies - reduce tissue loss from necrosis
oedema blocks other tissues
open blood flow to ischaemic tissue - thrombolysis, angioplasty
bypass obstruction - CABG, fem/popliteal bypass
MI strategies - prevent further episode
risk factor management
aspirin
MI S+S
pain, nausea, pale, sweaty
‘going to die’
silent MIs
effect of MI
death around 50%
fct limitation
complications of MI
death arrhythmias HF ventricular hypofct and thrombosis - papillary muscle rupture - valve disease DVT and pulmonary embolism complications of thrombolysis
MI investigations
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
MI tx primary care
get to hospital
analgesia, aspirin, reassurance
(BLS)
MI tx hospital
primary PCI thrombolysis if indicated drug tx to reduce tissue damage prevent recurrence/complications aspirin - secondary prevention
thrombolysis
can do up to 6hrs - if can’t get to PCI centre in time
inject streptokinase, TPA
contraindications to thrombolysis
injury/surgery/IM injections
severe hypertension, active PUD
diabetic eye disease, liver disease, pregnancy
medical management of MI
prevent next MI
- risk modification and aspirin
- B-blocker, ACE inhibitor
tx complications: HF, arrhythmias, psychological distress
haemangioma
hamartoma of blood vessels without CT capsule
rapid growth first few weeks, usually regress over 1st 10yrs
60% H+N
vascular malformations
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
kaposi sarcoma
HHV-8
multi-focal low grade sarcoma of lymphatics and bv’s
HIV
immune deficiency - role in carcinogenesis
angiosarcoma
develops in cells of blood or lymph glands
rare, aggressive
malignant, surgery
drugs to prevent further disease
antiplatelets
statins
B-blockers
anticoagulants
drugs to reduce symptoms of current disease
diuretics B-blockers nitrates Ca channel blockers ACE inhibitors
advice about reducing IE risk
attendance for oral care
rapid management infection
max OH and prevention
avoiding risk activity - piercings
CV pathology
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
when can you get VF?
heart attack
electrocution
long QT syndrome
Wolf-Parkinson-White syndrome
coagulation necrosis
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
granulation tissue
don’t get replacement of myocardium by myocardium
leaves scar
will affect fct of heart
STEMI
classic heart attack
NSTEMI
may be unstable angina
if had MI how long should you avoid complex tx for?
at least 6m
