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60 Cards in this Set

  • Front
  • Back
6 ddx's for acute severe chest pain
ACS
aortic dissection
pericarditis
pneumothorax, PE
herpes zoster

(musculoskeletal, GI reflux, trauma, bronchopneumonia)
immediate management of ACS
ABCDE! baseline SEWS + IV access
Morphine IV (+anti-emetic)
O2
Nitrate (GTN)
Aspirin & Clopidogrel (300mg)
what's the definitive management/ treatment for STEMI (ACS)
PCI reperfusion
PCI reperfusion
what Ix's is suspect ACS
ECG
troponin (12hrs after onset)
ECG
troponin (12hrs after onset)
what defines a STEMI on the ECG
ST-elevation:
- ≥1mm in 2+ limb leads
- ≥2mm in 2+ chest leads

new onset BBB (Remember: WiLLiaM & MaRRoW)
ST-elevation:
- ≥1mm in 2+ limb leads
- ≥2mm in 2+ chest leads

new onset BBB (Remember: WiLLiaM & MaRRoW)
for a STEMI, if PCI can't be delivered in 90mins, what do you do?
THROMBOLYSIS (e.g. tPA, streptokinase)
if no contraindications
what are the contraindications of thrombolysis for STEMI which can't receive PCI within 90mins
suspect aortic dissection
recent haemorrhage/ CVA/ trauma/ surgery
active peptic ulcer
uncontrolled HTN
aggresive CPR
warfarin therapy
a pt suffering an acute STEMI has a cardiac arrest in the ambulance for which he required aggressive CPR- how will this effect his type of treatment
thrombolysis is contraindicated!
2 main groups of complications following an MI
arrhythmic
mechanical (structural)
name some arrhythmic complications of an MI
AF, atrial flutter
VF/ VT
heart block
asystole
electromechanical dissociation
some mechanical (structural) complications of MI
LVF
ventricular aneurysm
cardiogenic shock
pericardial tamponade
VSD
MR
MI secondary prevention includes weight loss. How much is recommended for BMI 25-30
5-10% loss
MI secondary prevention includes weight loss. How much is recommended for BMI >30
15-20% loss
MI secondary prevention includes exercise. How much is recommended per day and to what intensity?
20-30 mins
slight breathlessness
post-MI secondary prevention: what diet is recommended
Mediterranean-styl
omega-3 (2-4 oily fish/wk)
low salt
low fat
fruit & veg
what ECG changes migth be seen in an NSTEMI / unstable angina
ST depression
T wave inversion
characterise cardiac chest pain
DULL central tight/ heavy/ crushing
radiate - jaw/ arm
nausea, sweating, dyspnoea, palpitations
DULL central tight/ heavy/ crushing
radiate - jaw/ arm
nausea, sweating, dyspnoea, palpitations
differentiate stable angina and ACS (incl unstable angina)
what might cause a rupture of an atherosclerotic plaque
iatrogenic (e.g. PCI)
twisting artery (heart beat)
⇈lipid content: thin cap
sudden pressure changes
2 important prothrombotic factors released by platelets (targeted by antiplatelet therapy)
ADP (ADP receptor antagonists- clopidogrel)
TXA2 (aspirin- blocks COX which sythesises it)
ADP (ADP receptor antagonists- clopidogrel)
TXA2 (aspirin- blocks COX which sythesises it)
what tPA
natural fibrinolytic
natural fibrinolytic
what's the heart's response to STEMI (occulsion of a vessel)

how does it heal
ischaemia --> INFARCT
inflam
necrosis
heal: scar tissue, dilatation
LV dilatation can occur after an MI-

What condition does LV dilatation ensue?
LVF
LVF
what's an ECG feature of an old MI
T wave inversion
Q waves
T wave inversion
Q waves
what 2 blood makers are suggestive on an MI
troponin T
CK (non-specific)
when does troponin T peak
how long is it raised for
12-24hrs
1 week
aspirin if given immediately for ACS
how does it work
irreversible blocks COX 
COX  ⇏ TXA2  ⇏ GPllb/llla receptors for fibrin  ⇏ platelet aggregation 

reduce PLATELET AGREGGATION
irreversible blocks COX
COX ⇏ TXA2 ⇏ GPllb/llla receptors for fibrin ⇏ platelet aggregation

reduce PLATELET AGREGGATION
clopidogrel is given immediately ACS
how does it work
ADP receptor antagonist (P2Y12 receptor)
 ⇏ GPllb/llla receptor  ⇏ fibrin  platelet aggregation
ADP receptor antagonist (P2Y12 receptor)
⇏ GPllb/llla receptor ⇏ fibrin platelet aggregation
prior to undergoing PCI, what drug must pt's take? eG?

how does it work?
GPllb/llla receptor antagonist (tirofiban)
prevents fibrin aggregating platelets
anti-platelet
GPllb/llla receptor antagonist (tirofiban)
prevents fibrin aggregating platelets
anti-platelet
what are the indications for IMMEDIATE reperfusion therapy (PCI via coronary angiography)
ST elevation: STEMI
- ≥1mm in 2+ limb leads
- ≥2mm in 2+ chest leads

new onset BBB (Remember: WiLLiaM & MaRRoW)
management of ACS NSTEMI (or unstable angina)

how long for
MONAC
1) aspirin long term
2) clopidogreal 3 months

3) high risk- coronary ANGIOGRAPHY & revascluarisation (PCI/ CABG)
what classifies high risk ACS unstable angina pt's - i.e for angiography & revascularisation
ischaemia
high GRACE score
what's the worst arrhythmic complication forseeable post-MI

how to treat
VF
DEFIB!!
VF
DEFIB!!
what's Dressler's syndrome?
when does it occur?
clinical signs?
post-MI/ heart surgery.
auto-ab against ❤
--> recurrent pericarditis, pleural effusion, fever, anaemia

chest pain, pleura/ pericardial rub
cardiac tamponade
treatment of Dressler's syndrome
steroids
anti-inflam
(autoimmune syndrome)
acute pericarditis is a complication post-MI
clinical signs
central chest pain- worse inspiration/ lying flat
relief SITTING FORWARDS!
pericardial friction rub

(pericardial effusion/ tamponade)
central chest pain- worse inspiration/ lying flat
relief SITTING FORWARDS!
pericardial friction rub

(pericardial effusion/ tamponade)
how do you observe/ Ix complications of AMI
S&Ss
heart sounds + murmurs
creps
ECG
CXR
fluid balance (U&Es, U/O)
Starling forces govern fluid movement across capillary wall.
Which 2 forces favour filtration (into interstitial fluid)

which end of capillary is this greatest?
capillary hydrostatic (MAIN)- arteriolar end!
interstitial osmotic
capillary hydrostatic (MAIN)- arteriolar end!
interstitial osmotic
Starling forces govern fluid movement across capillary wall.
Which 2 forces oppose filtration (movement back into capillaries?)

which end of capillary is this greatest?
capillary osmotic (MAIN) - venule end!
interstitial hydrostatic
capillary osmotic (MAIN) - venule end!
interstitial hydrostatic
how do you calculate the net filtration pressure (NFP) of fluid movement across a capillary wall
NFP = (forces favouring capillary HYDROSTATIC p) - (forces opposing capillary ONCOTIC p)

NFP = (cap HYDRO + ISF oncotic) - (cap ONCOTIC + ISF hydro)
which 3 starling forces of attraction across a capillary wall remain constant
- ONCOTIC p's (capillary & ISF)
- ISF hydrostatic

cap hydro fluctuates
fluid movement across a capillary wall is greatest at which end for:
- ultrafiltration
- reabsorption
FILT: arteriolar end

REABS: venular end
how does po oedema manifest (clinical signs)
SOB
bibasal creps 
didsplaced apex (LVF)
CXR: prehilar haziness, po oedema, ↑cardiothoracic ratio
SOB
bibasal creps
didsplaced apex (LVF)
CXR: prehilar haziness, po oedema, ↑cardiothoracic ratio
2 main physiological causes of systemic/ po oedema? e.gs?

(referring to starling's law of capillary fluid exchange)
- ↑capillary hydrostatic p (i.e due to RVF/LVF, varicose veins, VTE)

- ↓ capillary oncotic p (malnutrition, protein malabsorption, excess renal excretion, hepatic failure)
2 physiological causes systemic/ po oedema ?

other than:
- ↑capillary hydrostatic p
- ↓ capillary oncotic p
- lymphatic insufficiency (obstruction, lymph node damage, filariasis)

- change in capillary perm (inflam, histamine)= ↑protein leakage
- lymphatic insufficiency (obstruction, lymph node damage, filariasis)

- change in capillary perm (inflam, histamine)= ↑protein leakage
how would you clinically assess for lymphatic insufficiency
"NON-PITTING" oedema
"NON-PITTING" oedema
post-MI/ ACS medications
aspirin
statin
BB
ACEIs
(+GTN for angina)
What's HF
low CO
S&Ss due to fluid retention / accumulation
CCF/ LVF/ RVF
3 causes LVF / LHF
post-MI
cardiomyopathy (dilated, poorly contracting)
valvular disease
3 causes RVF/ RHF
cor pulmonale
secondary to LVF/ LHF
congenital (R more common than L)
Symps LVF/ LHF
dyspnoea, orthopnoea, PND
nocturnal cough +/- pink frothy sputum (po oedema)
wheeze
poor exercise tolerance
fatigue
cold peripheries
signs LVF/ LHF
tachycardia
fine bibasal creps
pleural effusion
S3 gallop (accelerated blood filling due to ↑back pressure)
LV heave/ displaced apex
CXR findings in LVF/ LHF
bat wing shadows
kerly B lines
po oedema
bat wing shadows
kerly B lines
po oedema
S&Ss RVF/ RHF
nausea, anorexia,
periperal oedema
ascites
hepatomegaly
JVP, epistaxis
RV heave
Ix's HF
1) BNP, FBC, U&Es
2) ECG

3) echo (LV dysfunction)
CXR
treatment of HF depends on cause.

what are the 6 standard pharmacological treatment2 for CCF in prev-MIs & cardiomyopathies (egs)
DIURETICS (loop- frusemide) +/- Spironolactone
ACEIs (lisinopril)
BBs- start low go slow (bisiprolol)
... further:
- Digoxin for AF: inotrope
- Vasodilators (isosorbide mononitrate)
If HF is due to valvular heart disease (normally LVF/ LHF) what's the treatment
surgery
If HF is due to cor pulmonale (RVF/ RHF), what's the treatment
O2
DIURETICS only!!!
lifestyle advice for CCF/ HF/ CHF
stop smoking
stop alcohol!
optimise weight
LOW SALT / ?fluid intake
low level reg exercise
Implantable devices & surgery for CCF/ CHF/ HF
ICD (implantable cardiac defibs)
CRT (cardiac resync therapy) - prolonged QRS

new VALVE/s- if that's the cause
TRANSPLANT- if young & fit