Cardiology Flashcards
MOA of ACEi
Prevent the conversion of angiotensin I to II in the lungs
No aldosterone secreted from the adrenal glands
side effects of ACEi
cough
angioedema
hyperkalaemia
first dose hypotension (more common in patients taking diuretics)
monitoring required for ACEi
U&Es before initiating treatment & after increasing the dose
acceptable rise of creatinine up to 30% from baseline, and potassium up to 5.5mmol/L
when starting ACEi, significant renal impairment may be a sign of what
bilateral renal artery stenosis
interaction of ACEi
high dose diuretic therapy e.g 80mg of furosemide
increases risk of hypotension
cautions & contraindications of ACEi
pregnancy and breastfeeding
aortic stenosis (hypotension)
renovascular disease (renal impairment)
hereditary angioedema
potassium >5 mmol/L before initiating treatment
role of anticoagulation in AF
preventing a stroke
what is the CHA2DS2-VASc mneumonic?
C – Congestive heart failure
H – Hypertension (including treated HTN)
A2 – Age >75 (Scores 2)
D – Diabetes
S2 – Stroke or TIA previously (Scores 2)
V – Vascular disease (ischaemic heart disease, peripheral vascular disease)
A – Age 65-74
S – Sex (female)
what happens if CHA2DS2-VASc score shows no need for anticoagulation
need to do a transthoracic echocardiogram to exclude valvular heart disease
valvular heart disease + AF = absolute indication for anticoagulation
how to formalise the risk of anticoagulation therapy?
ORBIT score
Haemoglobin <130 g/L for males and < 120 g/L for females, or haemtocrit < 40% for males and < 36% for females = 2
> 74 years = 1
previous bleeding event = 2
renal impairment <60ml/min = 1
antiplatelet therapy = 1
anticoagulation used in AF
first line = DOACs
then warfarin
advantages of DOACs
no monitoring required
no major interactions
shorter half life than warfarin
reversal agents of DOACs & warfarin
apixaban & rivaroxaban = Andexanet alfa
dabigatran = Idarucizumab
warfarin = vitamin K
what is the target INR for AF
2-3
MOA of warfarin
inhibits epoxide reductase, preventing the reduction of vitamin K to its active hydroquinone form
prevents carboxylation of clotting factor II, VII, IX and X (mnemonic = 1972) and protein C.
what is warfarin
a vitamin K antagonist
Vitamin K is essential for the functioning of several clotting factors, warfarin blocks vitamin K and prolongs the prothrombin time
has a long half life, can take several days to achieve a stable INR (international normalised ratio)
inducers of P450 system
decrease INR
rifampicin
smoking
chronic alcohol intake
antiepileptics: phenytoin, carbamazepine
barbiturates: phenobarbitone
inhibitors of P450 system
increase INR
antibiotics e.g. ciprofloxacin, erythromycin, clarithromycin
isoniazid
omeprazole
amiodarone
SSRIs
fluconazole, ketoconazole
allopurinol
what can potentiate warfarin
warfarin is affected by the cytochrome P450 system in the liver, where this system is normally involved in the metabolism of warfarin
general potentiators:
liver disease
cranberry juice
P450 enzyme inhibitors
NSAIDs
green leafy vegetables containing vitamin K
what to do if BP is >180/20mmHg
admit for specialist assessment if signs of retinal haemorrhage/papilloedema or life threatening symptoms e.g. heart failure, AKI, new onset confusion
referral if phaechromocytoma suspected
if none of the above, arrange urgent end organ damage investigations e.g. urine dipstick & ACR, bloods (HbA1c, lipids, U&Es), ECG
lifestyle advice for lowering BP
reduce caffeine
lower salt intake <6g a day
lose weight
exercise
stop smoking & drinking alcohol
MOA of thiazide diuretics
work by inhibiting sodium reabsorption at the beginning of the distal convoluted tubule (DCT) by blocking the thiazide-sensitive Na+-Cl− symporter
side effects of thiazide diuretics
hypotension
dehydration
hyponatremia, hypokalaemia, hypercalcemia
gout
impotence
rare:
thrombocytopenia
pancreatitis
agranulocytosis
what do thiazide diuretics decrease the incidence of
kidney stones due to hypocalciuria
MI secondary prevention
dual antiplatelet therapy
statin
ACEi
beta blocker
post ACS = ticagrelor + aspirin, stop ticagrelor after 12 months
post PCI = prasugrel/ticagrelor to aspirin, stop 2nd antiplatelet after 12 months
*** this period of time can be altered
if signs of heart failure e.g. reduced ejection fraction and physical signs, start eplerenone 3-14 days after
Mediterranean diet
exercise (20-30 mins a day until slightly breathless)
stop smoking
management of angina pectoris
aspirin & statin in the absence of any contraindication
beta-blocker or calcium channel blocker first line
CCB as monotherapy = use rate limiting one e.g. diltiazem, verapamil
**if used in combination use a long-acting dihydropyridine calcium-channel blocker (nifedipine)
if poor response, titrate drug up to maximum dose
then add CCB/beta-blocker
only add a 3rd drug whilst a patient is awaiting assessment for PCI or CABG
beta blockers should not be concurrently prescribed with what
rate limiting CBB e.g. verapamil, diltiazem
risk of complete heart block
surgical options for angina pectoris
Percutaneous coronary intervention with coronary angioplasty
coronary artery bypass graft with great saphenous vein
** used in severe stenosis
what to look for when examining a patient you think may have coronary artery disease
midline sternotomy scar
brachial/femoral scars
inner calves scar (great saphenous vein harvesting scar)
what are the secondary causes of HTN
ROPE
renal disease = renal artery stenosis
obesity
pregnancy induced hypertension/pre-eclampsia
endocrine e.g. hyperaldosteronism
investigations for stable chest pain
first line = CT coronary angiography
second line = non-invasive functional imaging (looking for reversible myocardial ischaemia)
e.g. myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT) OR stress echocardiography
3rd line = invasive coronary angiography
criteria for anginal chest pain
- constricting discomfort in the front of the chest, or in the neck, shoulders, jaw or arms
- precipitated by physical exertion
- relieved by rest or GTN in about 5 minutes
all 3 = typical angina
2 = atypical
1 = non-anginal chest pain
presentation of cor pulmonale
hypoxia
cyanosis
raised JVP
peripheral oedema
hepatomegaly
third heart sound
murmurs (pan-systolic in tricuspid regurgitation)
causes of cor pulmonale
COPD
interstitial lung disease
PE
CF
primary pulmonary hypertension
side effects of statins
myopathy: myalgia myositis, rhabdomyolysis, asymptomatic raised creatine kinase
** risk increased if advanced age, female, low BMI, multi-system disease e.g. DM
liver impairment: check baseline, 3 months, and 12 months
contraindications for statins
macrolide antibiotics
pregnancy
intracerebral haemorrhage history
MOA of statins
inhibit the action of HMG-CoA reductase, the rate-limiting enzyme in hepatic cholesterol synthesis
should be taken at night, as this is when majority of cholesterol synthesis occurs
who gets the primary & secondary prevention of statins
primary = 20mg
QRISK >10%
T1DM who were diagnosed >10 years ago OR >40 OR have established nephropathy
secondary = 80 mg
established CVD e.g. prior stroke, TIA, MI
peripheral vascular disease
what should you do with the dose with antihypertensive medication before adding another medication?
prescribe maximum dose
MOA of clopidogrel
antagonist of the P2Y12 adenosine diphosphate (ADP) receptor, inhibiting the activation of platelets
what concurrently prescribed with clopidogrel is a cause for concern
omeprazole & esomeprazole - might reduce the effectiveness of clopidogrel
lansoprazole should be okay
what are the reversible causes of cardiac arrest?
Hs & Ts
Hypoxia
Hypovolaemia
Hypothermia
Hypoglycaemia
Hyper/hypokalaemia
Acidosis
Tension pneumothorax
Tamponade
Toxins
Thrombosis (coronary/pulmonary)
causes of RBBB
normal variant - increasing age
PE
right ventricular hypertrophy
cor pulmonale
MI
cardiomyopathy/myositis
indications of warfarin
mechanical heart valves
second line after DOACs in VTE and AF
target INR for warfarin in VTE and AF
VTE: 2.5, recurrent 3.5
AF = 2.5
side effects of warfarin
haemorrhage
teratogenic
purple toes
skin necrosis
*** when warfarin first started protein C is reduced, putting the body into a procoagulant state
normally avoided by concurrent heparin administration
thrombosis may occur in venules leading to necrosis
causes of chronic heart failure
hypertension
ischaemic heart disease
valvular disease e.g. aortic stenosis
arrythmias e.g. AF
presentation of chronic heart failure
breathlessness on exertion
cough (frothy white/pink sputum)
orthopnoea
paroxysmal nocturnal dyspnoea
peripheral oedema
when do you offer ambulatory BP monitoring/home BP monitoring
when clinic BP is >140/90mmHg
