Cardiovascular Flashcards
Risk factors for atherosclerosis
Male FHx Smoking DM Hyperlipidaemia HTN
Characteristics of STABLE angina
Onset with exercise (increased demand)
Relieved by rest
CCP radiating to arm & neck
Complications of angina
Thrombotic - clot enlarges, blood flow reduces, ischaemia increases - AMI
Embolic - downstream clot causing claudication/DVT or PE or TIA/CVA or gut ischaemia
Why are men at greater risk of angina?
oestrogen in premenopausal women is protective
Why does DM increase risk of angina?
DM causes endothelium damage (increasing risk of atherosclerotic plaques) AND DM causes microvascular disease (blocks small cardiac vessels - too small for stent or lysis)
Why does smoking increase risk of angina?
smoking increases endothelial damage - increasing risk of atherosclerosis
How does UNSTABLE angina differ from stable angina
Unstable angina occurs at rest or minimal exertion - is not exercise/demand induced - so it is less predictable.
What ECG changes are seen for angina (ACS)?
None - ECG is normal
Define HTN
BP > 140/90
SBP increments in 19
DBP increments in 10
140-159/90-99 etc
Name the complications of HTN
CVA
IHD & ICardioMyopathy
Coronary Artery Disease
Rx for HTN
Lifestyle modification PLUS ABCDE (based on Dx & SEs) A = ACEI or ARB B = beta blockers C = calcium channel blockers D = diuretics E = ezetimibe & everything else
Name FIVE lifestyle modifications to Rx HTN
Diet - low salt, low fat
Exercise
Quit smoking
Dx where ACEI are useful
DM - helps with GFR
CCF - improves EF (ejection fraction) & survival
post MI - improves survival
CT diseases (scleroderma) - protects kidneys
young people
Dx where beta blockers are useful?
CCF - improves survival (carvedilol, metoprolol best)
post MI - improves survival
young people
Dx where calcium channel blockers (CCBs) are useful
survival NOT demonstrated in any subtypes BUT good for elderly
Dx where diuretics are useful for HTN Rx
survival NOT demonstrated in any subtypes BUT good for elderly
SE of ACEI/ARB
Angioedema (swelling in tongue, face)
cough (30% of ACEI) - switch to ARB
hyper K
hypo Na
dec CrCl (esp c/ renal artery stenosis - CI where bilateral)
Inc Cr = ARF [paradoxical; used in CRF to protect function, esp in DM]
SE of beta blockers
bradycardia hypoTN dyslipidaemia depression (exacerbation) exacerbate asthma & COPD [bronchospasm] hyper K
SE of CCBs
DHPs: peripheral vasodilation - odema, constipation, HF [b/c of the decrease to contractility/inotrophy] HR same or increase [except amlodopine - dec HR, used in IHD] non-DHPs: dec inotropes (contractility) see HR decrease - good for AF; oedema constipation HF [negative inotrophy/contractility]
Name the TWO types of CCBs
DHP - dihydroperadines [all end in pines; nifed, amlodo, felo]
non-DHP - dihydroperadines
SE of thiazide diuretics
HYPO K HYPO Na Inc sCa Inc sCr Inc sUric Acid, slipids, sGlucose
Name the TWO major diuretic classes used for HTN
Hydochlorothiazide - ascending limb
Frusemide - loop
SE of loop diuretics
HYPO K
HYPO Na
Dec sCa [dumps Ca into urine, CI for Hx of renal stones]
Inc Cr
Alpha1 blockers in HTN:
what suffix identifies them?
How do they work?
‘osin’ [tamulosin]
Vasodilation by blocking the alpha receptors on the vessel - preventing vasoconstriction
What is a potential SE of alpha blockers?
First dose HYPOTN - can cause syncope, so should be given before bed time
Other than HTN, what other use do alpha blockers have?
Rx BPH - used to relax the smooth muscle of the urethra to aid urination (relieve prostatic SEs)
Alpha 2 agonists in HTN: How do they work? Where are the receptors? Name a common one. What other use do they have? What is a problem when using clonidine?
Stimulate brain A2 receptors to decrease PVR and CO to lower BP
Pre-synaptic A2 receptors in brain stem feedback to downplay SNS tone by reducing Ca in cleft, inhibiting release of NA, lowering the BP
Clonidine
Opiod wdl
Central action means that cessation needs to be weaned IOT avoid wdl
Nitrates in HTN (& IHD): How do nitrates work in HTN mngt? What nitrates are commonly used? When are nitrates absolutely CI? How often should there be a nitrate free interval?
By causing dilation [venodilation > vasodilation, to INC pressure in coronary arteries]
decreases PRELOAD by dilating the veins, reducing pressure in RA, making more flow to the myocardium
decrease AFTERLOAD
GTN (typically as a patch)
ISMN - isosorbide mononitrate
CI in RV failure (or AMI)
Nitrate interval should be every day (why patches come off)
Spironolactone in HTN: What type of drug is it? How does this act? When is it indicated? SE? What similar drug does not cause gynaecomastica?
K sparing diuretic that acts in the DCT by blocking aldosterone;
Indicated in CHF with EF < 35%
SE include:
HYPER K
inc Cr causing ARF
Gynaecomastica (blocking one steroid hormone - affecting others)
Eplerenone
What is ezetimibe?
What drug is it sometimes combined with?
A drug that lowers the absorption of cholesterol
Simvastatin
