CV Drugs 2 Flashcards
PATHOPHYSIOLOGY OF AF
i) what is it?
ii) what can happen to the atrial muscle? name three things this may be related to?
iii) name four risk factors? what sign on echo means the AF is unlikely to resolve
iv) name two things that may be seen on ECG
i) chaotic electrical activity - impulses generated from all over the atria
ii) fibrosis and loss of atrial muscle mass
- related to ageing, chamber dilation, inflammation and genetic predis
iii) RF are HTN, age, cardiac disorders, lung disease, hyperthyroid, electrolyte disorders, diabetes
- unlikely to resolve if there is atrial dilation on echo
iv) no P waves and irregular QRS
CLASSIFICATION OF AF
i) what is lone AF?
ii) what type of AF is present for less than 7 days? what is present for more than 7 days?
iii) what is permanent AF?
iv) what same risk do all types of AF carry?
v) name four clinical features
i) lone = AF in a patient that doesnt have echo changes, may be due to genetic predis
ii) <7 days = paroxysms (patients spont cardiovert in 7 days)
>7 days = persistent
iii) permanent - over 7 days with failed cardioversion
iv) all types of AF carry the same thromboembolic risk
v) asymp, palpitations, SOB, chest pain, syncope, HF
AF TREATMENT
i) what are the three main approaches to treatment?
ii) what two categories can patients be in with recent onset AF? what are the treatments for each category?
iii) after what duration is risk of VTE increased? after what length of time should rate control be used to trear?
iv) what increases the risk of a clot disloging?
v) is rate or rhythm control better for mortality? which is usually used in elderly?
vi) give three instances when rhythm control is preferred? what is the time limit for this?
i) rate control, rhythm control and anticoagulation
ii) recent onset > are they compromised or not?
- compromised - BP <90 = dont have time for drugs to work therefore need to cardiovert/DC shock
- not compromised - good BP and or asymp > time for medication to work > therefore pharma therapy eg rate/rhythm control
iii) after 48hrs risk of VTE is increased
- >48hrs use rate control to slow HR
- <48hrs attempt back to sinus rhythm using rhythm control
iv) switching from AF to sinus rhythm
v) research shows rhythm control is slightly better but not sig diff
- usually use rate control as it decreases risk of VTE
vi) rhythm control if asymp, younger patient, adequate rate control or there is HF
- 48hr rule
AF - RATE CONTROL TREATMENT
i) what is used first and second line in acute AF without HF?
ii) what is used first and second line in acute with HF? what drugs should not be given in HF?
iii) what is given first and second line in permanent AF?
iv) what is given in paroxysmal AF? who is this most commonly used in? when is it contrainidcated?
i) without HF > beta blocker or CCB or dig (if sedentary)
second line - add dig
ii) with HF > dig or amiodarone first line
- add amiodarone second line
- dont use a beta blocker or CCB
iii) permanent > if you have tried to cardiovert but cant
- beta blocker to CCB
- add dig second line or amiodarone third line
iv) paroxysmal > give pull in a pocket (flecanide)
- most commonly used in younger patients (they can tell when its coming on and take it)
- contraindicated if there are ischaemic changes eg in BBB
- amiodarone can be used but only as a last resort as it takes a long time to get to steady state and has lots of SEs
AF - RHYTHM CONTROL TX
what should be given when:
i) acute cardioversion and normal heart
ii) acute cardioversion and abnormal heart
iii) main sinus rhythm and normal heart
iv) maint sinus rhythm but abnormal heart
v) what is the 48hr rule
i) flecainide
ii) amiodarone
iii) flecainide
iv) amiodarone
v) if AF is present for longer than 48hrs > need anticoag and elective cardioversion
DRUGS USED IN RATE CONTROL
i) name three cardio selective beta blockers? which one is renally cleared and good in liver disease? which two are contraindicated in liver disease?
ii) name two non cardioselective?
iii) name two mixed beta blockers (vasodilatory)
iv) name two rate limiting CCBs? name two non rate limiting CCBs
i) cardioselective = atenolol (renally cleared so good in liver disease)
- bisoprolol and metoprolol (liver contrainidcated)
ii) non cardioselec - propanolol, cavedilol and sotalol
iii) mixed = labetalol (treats HTN) and carvedilol
iv) rate limiting CCB > verpamil and diltiazem
- non rate limiting = amlodipine, nifedipine
BLEEDING RISK AND AF
i) what CHAD VASC score should a patient be on warfarin or DOAC?
ii) what HASBLED score does a patient have significant risk of bleeding?
iii) name an area that can be cryoablated in AF
i) >=2
ii) >=3
iii) ablate in pulmonary veins (where the abornmal impulses are generated from)
SUPRAVENTRICULAR TACHYCARDIA
i) what is it?
ii) what is first and second line acute treatment?
iii) name two things that can be given to maintain sinus rhythm
iv) which true drugs/types are contraindicated in asthma?
v) what is polymorphic VT? what is the treatment?
vi) which two drugs are given to patients in cardiac arrest but shockable rhythm?
i) fast heart rhythms originating from the upper chambers of the heart
ii) first line - vagal manouevres (carotid sinus massage/valsalva > stim psym to slow HR) or adenosine (slows HR)
second line - beta blocker or CCB (diltiazem, verapamil)
iii) maint SR with beta blocker or CCB
iv) adenosine can ppt bronchospasm and beta blockers eg bisoprolol
v) variable complexes eg TSP
- give magnesium sulphate > stabilises the cardiac membrane
vi) adrenaline and amiodarone
ACUTE CORONARY SYNDROME
i) name four things that are given as initial mx of a STEMI?
ii) what drugs may be given post MI?
i) morphine, anti emetic, oxygen, nitrates, aspirin, anti plat
ii) aspirin, clopid, atorvastatin, bisoprolol, ramipril
HEART FAILURE - PATHOPHYSIOLOGY
i) what causes it? how does HF affect SV and CO?
ii) which ANS system is activated? what does this cause?
iii) which other system is activated? how does this affect fluid balance?
iv) what does this all ultimately lead to?
v) what are the two main aims of tx in HF?
i) caused by poor ventric function/myocardial damage
- decreased SV and CO
ii) activate sympathetic NS > vconstriction
iii) activ RAAS > sodium and fluid retentin (inc VP and aldo)
iv) leads to further stress oon ventric wall and dilation (remod) > worsening ventricular func and worsening HF
v) to relieve symptoms and reduce mortality
HEART FAILURE TREATMENT
i) what should be reccomended first line?
ii) which drug class may be given to help symptoms but dont improve mortality?
iii) which two drug classes improve mortality?
iv) what may be used in place of a beta blocker if heart rate is too high?
v) what can be used if ACEi or ARB not tolerated
vi) which diabetic drug can be used as an add on if patients have chronic HF with reduced EF?
i) lifestyle > excercise, decreasing alcohol and smoking cessation
ii) diuretics
iii) beta blockers and aldo antagonists, ACEi
iv) ivabradine
v) hydralazine + nitrate
vi) dapagliflozin (SGLT2 inhibitor)
DIURETICS
i) name a loop diuretic? which channel does it work on?
ii) name a thiazide? which channel does it work on?
iii) name a K+ sparing? which channel does it work on?
iv) name two effects diuretics have in HF
i) loop = furosemide - works on Na/K/Cl symporter
ii) thiazide = bendroflumethiazide - works on Na/Cl symporter
iii) K+ sparing = spiro - works on epithelial Na channel
iv) provide symptom control and reduce cardiac pre load
HF AND ACEI
i) what do they improve?
ii) which patients do they have a more marked effect in? what do they reduce the risk of?
iii) what is used in patients that cant tolerate ACEi?
i) improve life expectancy vs placebo
ii) more marked in patients with severe LV dysfunc
- reduce risk of hospitalisation
iii) ARB eg losartan
BETA BLOCKERS AND HEART FAILURE
i) what do they do in HF?
ii) which three BB is there evidence for?
iii) what dose should be started? what should be monitored?
i) increase life expectancy vs placebo
ii) evidence for bisoprolol, carvediolol, metoprolol
iii) start low and titrate up > monitor heart rate and BP
HEART FAILURE - SPIRONOLACTONE
i) which patients should this be given to?
ii) what does it inc? what does it dec?
iii) what does it inhibit? what does this cause
i) patients with severe HF
ii) inc life expectancy and decreases hosp admission
iii) inhibits aldo secretion which therefore inhibits salt and water retention
