cardio Flashcards
what is prinzmetals angina
non exertional chest pain due to coronary artery vasospasm
seen w brief st elevation and no raised biomarkers
seen in younger px esp w cocaine use
what is decubitus angina
chest pain brought on by lying flat
what is stable angina
central crushing chest pain (or to jaw, neck, l shoulder) brought on by exertion and relieved by rest <5min ir glyceryl trinitrate spray (GTN spray) mostly due to atheromous plaque
modifyable risk factors stable angina
obesity
smoking
poor diet
t2dm
hyperlipidaemia
sedentary lifestyle
htn
non-modifiable risk factors stable angina
FHX
male
ethnicity - south asian, afro-caribbean
incr age
signs and symptoms stable angina
central crushing chest pain due to exertion- relieved by stress
exertional dyspnoea
incr sweating
nausea
diagnosis stable angia
ecg- normal, may show st depression
normal biomarkers/ troponin
ct angiogram to show luminal narrowing
symptomatic treatment stable angina
glyceryl trinirate spray
long term treatment stable angina 1-3rd line
CCB or BB
ccb + bb
ccb+bb+ antianginal med eg long acting nitrate
non-pharmacological management stable angina
lose wt, incr exercise, stop smoking, better diet, control other co-morbidities
ddx for stable angina
acute coronary syndrom, heart failure pericarditis
ccb needed for stable angina + example
non rate limiting eg amylodipine not verapamil
can cause excessive brdycardia
tx if medicine isnt successful for stable agina
revascularisation
- pci (percutaneous intervention)
- cabg (coronary artery bypass grafting)
+/- cabg
- more invasive, incr risk of stroke, long recovery time
+ better outcome/ prognosis
-/+ pci
+ less invasive, short recovery time
- risk of stent thrombosis
what is pci
percutaneous intervention
- inflating a ballon in an atheromous vessel to dilate to help blood flow
what is cabg
coronary artery bypass grafting
- left internal mammary artery used to bypass left anterior descending artery to bypass occlusion/ atheroma
conditions of acute coronary syndrome
unstable angina
non stemi
stemi
general pathogenesis of acs
- atheroma formation
endothelial damage causes the entery of LDL into intima layer of artery - this oxidises causing inflam response -> macrophages
1. FATTY streak- 10yrs <
- lipid laden marcophages and t cells
- INTERMEDIATE LESIONS
- layers of smooth muscle, foam cells and t cells
- FIBROUS ADVANCED LESIONS
- lipid core w necrotic debis
- fibrous cap w smooth muscle, collagen and elastin
- tough fibrous cap - more stable - less chance of rupture
- protrudes into lumen -> stenosis can cause ischaemia and reduced perfusion
- PLAQUE RUPTURE
- cap needs to be maintained by reabsorption and redeposition of smooth muscle
- thins with damage eg enzymic activity causing it to haemorrhage and rupture
- contrnts released into lumen causing thrombus formation , which can cause ischaemia and infarction
- cap needs to be maintained by reabsorption and redeposition of smooth muscle
- INTERMEDIATE LESIONS
what % vessel occlusion does sx start to occur in stable angina
approx 70%
what is unstable angina
crushing central chest pain occurs spontanteously/ not due to exertion and not relieved by rest or gtn spray
due to partial occlusion of vessel
what is nonstemi
partial occlusion of a vessel leading to tissue necrosis and release of biomarkers eg troponin but not seen w st elevation
what is a stemi
st elevation myocardial infarct
complete occlusion of a coronary vessel causing cardiac tissue necrosis with raised biomarkers and ecg changes
are ecg changes seen in unstable angina
not commonly
- may see t wave inversion or st depression
what are the ecg changes seen in a nonstemi
st depression
t wave inversion
ecg changes in stemi
st elevation
pathological q waves after a few days (indicated previous MI)
new left bundle branch block
t wave inversion
what are 2 biomarkers raised in MI
troponin - specific - rise seen after 3 hrs of MI
creatinine kinase MB - non specific also seen in bone pathology
signs and symptoms of acs
- severe crushing central chest pain radiating to neck, jaw, shoulder
- dyspnoea
- sweating
- palpitations
- anxiety - feeling of impending doom
- nausea
- hypotension and tachycardia
1st line investigations of acs
ecg withing 10 min/ immediately
troponin bloodtest
2nd line investigations of acs
ct angiogram - identify occluded vessel
what leads of an ecg show a lad occluson
V1-4
which leads shows a left circumflex occlusion
I, aVL, V5, V6
which leads show a right coronary artery occlusion
II, III, aVF
which leads show a septal view of LAD
V1-2
which leads show and anterior view of LAD
V3-4
what is acute management for acs
MONAC
Morphine
Oxygen (if low oxy sat)
Nitrates (short acting)
Aspirin (300mg)
Clopidgrel (75mg)
secondary acute management for unstable angina and nonstemi
after MONAC
- GRACE score - 6mmth mortality risk
- if low risk - monitor
- if high risk - urgent angiogram and consider pci
what is the management of stemi
after MONAC
- urgert pci within 2hrs of sx
- thrombolysis w allopase after 12 hrs sx
long term prevention of acs
aspirin 75mg daily
bb eg propanolol
clopidogrel - 12mnth
acei
atrovstatin
complications of MI
DARTHVADER
death
aneurysms
rupture
tamponade
heart failure
valvular disease
arrhythmias
dresslers syndrome
embolism
recurrance regurgitation
what is dresslers syndrome
autoimmune pericarditis occuring 2 wks after MI
what is htn
clinical bp reading >=140/90mmHg
ambulatory bp >=135/85mmHg
what are the 2 types of htn
primary ‘essential’ htn
secondary htn
what is essential htn
primary htn that has no underlying cause
95% cases
what are causes of secondary htn
renal: ckd, glomerulonephropathy
endo: cushings, phaeochromocytoma, hypertension
risk facctors htn -non/modifiable
non:
- ethnicity- afro-caribbean
- incr age
- fhx
- men
modifiable:
- high salt intake
- obesity
- sedentary lifestyle
- smoking
symptoms htn
ASx may have pulsatile headache
secondary condition sx
what is malignant htn
stage 3 htn classed as >= 180/120 mmHg
start immediate treatment
symptoms of maligant htn
hypertensive retinopathy - papilloedema, blurred vision
cardiac signs eg chest pain
polyuria , oligouria
investigations for htn
1st. clincal bp reading on each arm - record lowest value
2nd. if >140/90 do ambulatory bp for 24 hrs or home bp monitoring
(should have an average of 135/85mmHg)
what secondary investigations should bedone for htn
secondary organ damage
- fundoscopy for retinopathy
- urinalysis for kidney function
- Hba1c`
htn tx for afro-caribbean woman age 60 (1st-3rd line)
> = 55yrs or afro-caribbean
1st CCB
2nd CCB + ACEi (or ARB if CI) or thiazide like diuretic
3rd CCB + ACEi (or ARB) + thiazide like diuretic
htn tx for 30yr old w t2dm
<55 or w t2dm
1st ACEi (or ARB)
2nd ACEi (or ARB) + CCB
3rd ACE (or ARB) + CCB + thiazide like diuretic
htn tx for 58yr old afro-caribbean w t2dm
with DM follow ACEi path but use ARB instead
If not afro caribbean >55 w t2dm follow ACE i path
what is stage 1 htn
home/ ambulatory bp >135/85mmHg
clincal bp >140/90mmHg
what is stage 2 htn
ambulatory bp 150/95mmHg
clinical bp 160/100mmHg
what is pericarditis
inflammation of the pericardium- mostly acute
can either be dry (fibrinous) or effusive (purulent, haemorrhagic or serous)
- effusion is secondary to inflammation + can cause further complications
2 main causes of percarditis
idiopathic
viral - coxsakkie
name 5 other causes of pericarditis
idiopathic
viral: coxsakkie, EBV, VZV, HIV
TB
Autoimmune: SLE, RA, sjogren
dresslers syndroms: autoimmune following after mi
Hypothyroidism
typical px of pericarditis
male, 20-50s w recent viral infection
describe pericardial chest pain
severe sharp pleuritic chest pain that radiates to trapezius, neck, jaw
worse when lying down and relieved by sitting foward
signs and symptoms for pericarditis
severe sharp pleurtic chest pain
-worse lying down
- better sitting foward
pericardial friction rub on ascultation
- to and fro high pitch/ leathery extra heart beat