drug treatment of AF and HF

Question 1

why is a gallop rhythm indicative of HF

Answer 1

dilated heart

Question 2

post tussive inspiratory crackles ?

Answer 2

normally due to pulmonary oedema

Question 3

how to relieve acute HF

Answer 3

sit upright 
IV frusemide 
morphine 
nitrates
digoxin 
oxygen

Question 4

how to relieve acute HF

Answer 4

sit upright 
IV furosemide 
morphine 
nitrates
digoxin 
oxygen

Question 5

diuretics

Answer 5

ie furosemide, bumetanide, torsemide
>improve symptoms of pulmonary congestions and decrease body weight
>side effects: dizziness headaches gastrointestinal upset, hypernatremia , hypokalaemia and dehydration

Question 6

furosemide

Answer 6

primarily eliminated renally

oral bio-availability is erratic and less predictable compared

Question 7

vasodilators

Answer 7

reduce symptoms in HF and improve haemodynamics by reducing preload, after load or both
decreases BP PCWP (pulmonary capillary wedge pressure) SVR - to reduce dyspnoea and improve peripheral oxygen delivery

Question 8

morphine

Answer 8

should be considered for patients with severe symptoms of restlessness, dyspnea, anxiety or chest pain
>use with caution (especially with patients with altered mental status and impaired resp. drive, hypotension, bradycardia, advanced atrioventricular block or carbon dioxide retention)
>2.5-5mg IV bolus dose
>usually use with antiemitic

Question 9

nitroglycerin

Answer 9

-vasodilator
>produces venous vasodilations at lower doses and arterial vasodilation as dosages increase
>reduces preload (pcwp, central venous pressure) and arterial BP thus decreasing cardiac filling pressures and increasing CO
>nitroglycerin is useful in patients with acute HF and hypertension or angina due to coronary vasodilation
>rapid and short acting
>side effects: headache, hypotension, abdominal discomfort. reflex tachycardia , paradoxical bradycardia

Question 10

digoxin

Answer 10

> has beneficial haemodynamic effects
including vagomimetic effects and ability to decrease ventricular rates - in patients with AF, attenuation of the RAAS, reduced pcwp and svr, increased CO, and improved LVEF
side effects: arrhythmias, cardiac conduction disorder, cerebral impairment, diarrhoea, dizziness, eosinophilia, nausea, skin reactions, vision disorders, vomiting
>has many potential drug interactions

Question 11

treatment for chronic HF

Answer 11

• oral loop diuretics - (furosemide and bumetanide do not have any neurohormonal antagonism)
• holy trinity - ACEI or ARB, BB, spironolactone (have neurohormonal antagonism)
• ivabradine if BB not tolerated or contra-indicated
• salcubitril/valsartan

Question 12

ACE inhibitors

Answer 12

RAS blockade
>they prevent the conversion of angiotensin I to angiotension II and also inhibit bradykinin degradation
>have beneficial effects in both the treatment and the prevention of HF

Question 13

angiotensin II blockers (AT1 antagonists)

Answer 13

acts via a family of cell bound angiotensin receptors
AT1 receptor has been shown to mediate the detrimental effects of angiotensin in patients with HF
>angiotensin II antagonists block the AT1 receptor

Question 14

RASB side effects

Answer 14

dry cough
hypotension
renal dysfunction 
hyperkalaemia 
>contraindications of the use of ACE inhibitors include angio-oedema, anaphylaxis on prev exposure, pregnancy, bilateral renal artery stenosis

Question 15

spironolactone

Answer 15

aldosterone levels commonly remain elevated in patients on ACE inhibitors and may contribute to worsening HF
>is a potassium sparing diuretic, is a competitive antagonist of aldosterone and has been shown to have additional benefits

Question 16

SCD

Answer 16

sudden cardiac death

Question 17

ICD

Answer 17

implantable cardioverter-defibrillator

>effectively treats malignant ventricular arrhythmias

Question 18

how to manage AF

rhythm or rate control?

Answer 18

rhythm control if HF is due to AF

rate control is a pragmatic option (sinus rhythm is difficult to achieve in patients with AF associated with HF)

Question 19

what anti-arrhythmic drugs are safe to use in HF and ischaemic heart disease

Answer 19

amiodarone - kind of safe (long term could be toxic and should not be prescribed with digoxin!)
sotalol can be used in HF but less effective than amiodarone - cam cause renal impairment
Na channels AADIs are

Question 20

what anti-arrhythmic drugs are safe to use in HF and ischaemic heart disease

Answer 20

amiodarone - kind of safe (long term could be toxic and should not be prescribed with digoxin!)
sotalol can be used in HF but less effective than amiodarone - cam cause renal impairment
Na channels AADIs are contraindicated in CAD

Question 21

optimal agent for rate control ?

Answer 21

BBs for HF
CCBs (diltiazem and verapamil can worsen LV systolic function and are associated with worse outcomes in HF)
digoxin can be used but has many potential drug interactions

Question 22

what anticoagulants can be used

Answer 22

NOAC and warfarin but antiplatelets (aspirin/clopidogrel) are not beneficial in AF

Question 23

what is LBBB

Answer 23

left bundle branch block

>

Question 24

LBBB + LVHF = ?

Answer 24

cardiac dyssynchrony which worsens LV function and has a worse prognosis

Question 25

treatment for advanced heart failure

Answer 25

replace frusemide with bumetanide 
if diuretic resistant then add thiazide diuretic to loop diuretic 
sacubitril valsartan 
CRT - cardiac resynchronisation therapy 
digoxin

Question 26

entresto

Answer 26

an anti HF drug
promising
>is comprised of sacubitril with valsartan - inhibits nprilysin and hence the breakdown of BNP is prevented (salcubitril)
valsartan is a blockage of the AT1 receptor
»combined leads to vasodilation… decreased BP , decreased sympathetic tone, and decreased aldosterone levels
and natriuresis / diuresis

Question 27

CRT

Answer 27

biventricular pace maker which has two leads (for each ventricle)

Question 28

urgent treatment of AF

Answer 28

warfarin (bc of high risk of thromboembolic stroke)
NOACs are contra-indicated
>efficacy has not been tested in clinical trials
>higher risk of thromboembolism and possibly different mechanism of thrombosis, clot extends beyond the left atrial appendage, into the roof and wall of the LA

Question 29

management of valvular AF

Answer 29

rate control is used 
BB 
digoxin 
rate limited Ca channels blockers
consider valve surgery 
>want stroke prevention, symptoms relief, treat the underlying valve disease with valve surgery disease before irreversibly deleterious structural change

Question 30

management of NVAF (nonvalvulare AF)

Answer 30

consider changing amlodipine to a rate modulating CCB for BP control and rate control

Question 31

management of paroxysmal af (PAF)

Answer 31

rhythm control in AF:
flecainide except in HF and CAD
amiodarone and sotalol safe in HF but have serious side effects
RFCA (radio frequency catheter ablation) is preferred especially if there is no structural abnormality

Question 32

NVAF and anti coag.

risk of stroke

Answer 32

there is a need for anti coagulation if CHA2DS2VASc = 2

stroke risk in NVAF by CHA2DS2VASc score

Question 33

exceptions to CHA2DS2VASc

Answer 33

oacs strongly indicated regardless of stroke score
>valvular HD
>thyrotoxicosis
>hypertrophic cardiomyopathy

Question 34

warfarin vs noac

Answer 34

warfarin = 
many indications 
individualised dosing and regular INR monitoring 
drug interactions
long half life 
antidote is Vit K 
NOAC =
limited indications 
multiple fixed doses and INR monitoring is not required 
fewer drug interactions 
less studied 
short half life
no antidote an no proven way to reverse anti coagulation effects if bleeding occurs

Question 35

NOAC adverse effects

Answer 35

dabigatran -
bleeding anaemia nausea dyspepsia gastritis abdominal pain
increased liver enzymes
allergic reactions
apixaban -
bleeding anaemia
dyspepsia GI bleeding
thrombocytopenia increased liver enzymes
allergic reactions
rivaroxaban -
bleeding anaemia peripheral oedema itch, skin blisters muscle spasms
increased liver enzymes and allergic reaction