2. Cardiovascular drugs 1 Flashcards

1
Q

Pathophysiology of AF

A

chaotic electrical activity in the atria

Fibrosis and loss of atrial muscle related to:

  • inflammation
  • aging
  • genetics
  • chamber dilatation
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2
Q

AF risk factors

A
hypertension
valvular heart disease, 
cardiomyopathy, 
previous cardiac surgery, 
congenital heart disease, coronary artery disease, 
pericarditis,
lung disease - PE, 
pneumonia, 
COPD, 
hyperthyroidism, 
alcohol
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3
Q

AF classification

A

Lone AF
Paroxysmal <7 days
Persistent >7 days
Permanent >7 days with our without cardioversion

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4
Q

AF clinical features

A
asymptomatic
palpitations
SOB
chest pain
syncope
pre-syncope (light-headedness/dizziness)
heart failure
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5
Q

Atrial fibrillation treatment

A

Rate control
rhythm control
anticoagulation

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6
Q

Question to ask when someone presents with AF? and Treatment?

A

Are they compromised? (has the arrhythmia caused hypotension?)

If compromised - DC shock

If uncompromised - pharmacotherapy

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7
Q

AF treatment

A

<48 hours duration
-> attempt rhythm control

> 48 hours duration then attempt rate control

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8
Q

When is rate control preferred?

A

If more than 48 hours after AF onset

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9
Q

When is rhythm control preferred?

A
If less than 48 hours after AF onset
for symptom improvement
in younger patients
Heart failure related to AF
Adequacy of rate control
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10
Q

Acute AF without heart failure

A

Rate control
1st line: beta blocker or CCB (diltiazem or verapramil)
2nd line: add digoxin

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11
Q

Acute AF with heart failure

A

Rate control
1st line: digoxin, amiodarone
2nd line: amiodarone

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12
Q

Permanent or paroxysmal AF

A

Rate control
1st line: beta blocker or CCB (diltiazem, verapamil)
2nd line: add digoxin

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13
Q

Acute cardioversion, normal heart

A

Rhythm control

Flecainide, sotalol

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14
Q

Acute cardioversion, abrnomal heart

A

rhythm control

amiodarone

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15
Q

Maintain sinus rhythm - normal heart

A

rhythm control

Flecainide, sotalol

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16
Q

Maintain sinus rhythm, abnormal heart

A

rhythm control

amiodarone

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17
Q

What do Beta-adrenergic agonists do?

A

Block B2 receptors leading to stimulation of Gi which inhibits AC which makes cAMP which phosphorylates Calcium channels and lets Ca2+ through Calcium receptors into the heart, causing contraction?? So basically causes this

Block B1,2 receptors, activating Gs which acts on AC to cause something to do with Calcium idk

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18
Q

Non-cardioselective Beta blockers

A

propanolol
Carvidelol
Sotalol

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19
Q

Cardioselective beta blockers

A
atenolol
Bisoprolol
Esmelol
Metaprolol
Nebivolol
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20
Q

Vasodilatory

A

Labetalol

Carvedilol

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21
Q

Rate-limiting calcium channel blockers

A

verapamil

Diltiazem

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22
Q

Dihydropyridine calcium channel blockers (dipines)

A
amlodipines
nifedipin
lercanidipine
nimodipine
felodipine
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23
Q

Anticoagulation: CHA2DS2 VaSC

A
C- congestive heart failure = 1
H - hypertension =1
A2 - age >75 years =2
D - diabetes =1
S2 - previous stroke, TIA or thromboembolism =2
V - vascular disease =1
A - age 65 - 74 years =1
Sc = sex category (female gender) = 1

If CHA2DS2 VaSC is 2 or more, give warfarin or direct oral anticoagulent

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24
Q

When to give warfarin/direct oral anticoagulant?

A

When CHA2DS2 VaSC is 2 or more

25
What to consider when giving anticoagulation?
Risk vs benefits - bleeding risk via HAS-BLED score
26
HAS-BLED score?
``` Bleeding risk H- Hypertension =1 A- Abnormal renal/liver function = 1 point each S- Stroke in past = 1 B- Bleeding history =1 L- Labile INRs =1 E- Elderly =1 D- drugs/alcohol concomitantly =1 point each ```
27
AF other treatments
Radiofrequency catheter or cryo-ablation | Left atrial appendage occlusion (LAAO)
28
Stroke classification
Ischaemic (blocked up) | Haemorrhagic (bleed out)
29
Stroke treatment
``` Fibrinolysis Antithrombotics -aspirin -clopidogrel -warfarin or DOACs Lipid modification Treat hypertension ```
30
Lipid modification
For primary and secondary prevention Exclude secondary cause of increased lipids e.g. excess alcohol, uncontrolled diabetes, hypothyroidism, liver disease and nephrotic syndrome
31
When to refer to a lipid specialist?
Consider referral if: 1. Total serum cholesterol >7.5mmol/l + family history of premature coronry artery disease 2. Total serum cholesterol >9mmol/l
32
Healthy/normal cholesterol levels
``` Total 5 or below HDL 1 or above LDL 3 or below Non-HDL 4or below Triglycerides 2.3 or below ```
33
Lipid modification - when to offer medicine for primary prevention
Offer atorvastatin for primary prevention of CVD to people who have: - 10% or greater 10 year risk of developing CVD - T1DM - CKD
34
Lipid modification - secondary prevention of CVD
Atorvastatin for ANYONE who has had a stroke or MI regardless of cholesterol
35
Ezetimibe
Monotherapy treats primary (heterozygous familial or non familial) hypercholesterolaemia in adults in whom initial statin therapy is contraindicated or not tolerated Ezetimine coadministered w initial statin therapy might be appropriate
36
Stroke - drug treatment (lipid lowering)
Nicotinic acid - stops FFA formation Fibrates - oxidise DDas and stop VLDLs and promote formation of HDLs Statins - inhibit HMG-CoA making cholesterol, and promote uptake of cholesterol to liver Ezetimibe - inhibits dietary cholesterol absorption into blood Resins - promote fats into the bile to be excreted?
37
Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i)- Alirocumab, evolocumab
Alirocumab, evolocumab bind to PCSK9, inhibiting the receptor binding to LDLRs on hepatocytes and causing their degradation which leads to more blood LDL-C levels, so results in less LDL cholesterol in the blood
38
Heart failure pathophysiology
Poor ventricular function/myocardial damage (e.g. post MI or dilated cardiomyopathy) leads to decreased SV and CO leads to neurohormonal response leads to activation of sympathetic system and RAAS result in vasoconstriction, increased sympathetic tone, angiotensin II, endothelins, impaired NO release -> sodium and fluid retention, increased vasopressin and aldosterone leads to further stress on ventricular wall and dilatation (remodelling) leads to worsened ventricular functioning leads to further heart failure
39
Heart failure treatment aims
Relieve symptoms | Reduce mortality
40
Heart failure treatment
Lifestyle - exercise, decrease alcohol, smoking cessation Drugs Devices Surgery
41
Heart failure treatments
Diuretics (improve symptoms) ACEI (slightly improve symptoms, mostly reduce mortality) Beta-blockers (improve symptoms and massively improve mortality) Aldosterone antagonists (improve symptoms and reduce mortality) ARBs (improve symptoms and reduce mortality) Hydralazine/nitrates (improve symptoms and reduce mortality) Digoxin (improve symptoms)
42
Heart failure - diuretics
loop diuretics: -furosemide thiazides: - bendroflumethiazide - metolazone (thiazide-like) K+ sparing: - spironolactone (mineralocorticoid receptor antagonists) - amiloride
43
loop diuretics
Furosemide | act at Na/K/Cl symporter
44
Thiazides
bendroflumethiazide Metolazone (thiazide-like) act at Na/Cl symporter
45
K+ sparing
spironolactone and amiloride act at epithelial Na channel
46
heart failure - diuretics effect
provide symptom control reduce cardiac preload side effects
47
Heart failure - ACE inhibitors
increase life expectancy vs placebo Effect more marked in patients with more severe LV dysfunction Benefit for all NYHA classes Reduces risk of hospitalisation
48
Heart failure - ACE inhibitors/ARBs mechanisms
ACE inhibitors inhibit ACE forming Angiotensin II from Angiotensin I, and bradykinin's effect ARB inhibit angiotensin receptors Effects: vasoconstriction, salt and water retention, aldosterone secretion
49
Heart failure - ACE inhibitors (...prils)
``` Ramipril Lisinopril Enalapril Perindopril Captopril (not used as much due to short half-life) ```
50
Heart failure - ARBs (...sartans)
losartan, candersartan, valsartan Reduces mortality Some data on QOL, symptom control used in patients who can't tolerace ACE-I
51
Heart failure - beta blockers?
BB increase life expectancy vs placebo All NYHA classes Reduces hospitalisation Low dose, titrate up, monitor HR, BP, clinical progression
52
Heart failure - spironolactone
Patients w severe heart failure, NYHA III-IV Increases life expectancy Reduces hospital admission low dose (12.5-25mg)
53
Spironolactone mechanism
inhibits aldosterone secretion
54
Chronic heart failure - treatment
Diuretics ACE-i (ARBs) Beta blockers Spironolactone
55
Chronic heart failure - other drugs
Ivabradine - use with or instead of BB if HR >75bpm Hydralazine & nitrate - use if ACEi/ARB not tolerated or contraindicated or in people of African origin Sacubitril(neprilysin inhibitor)/valsartan (ARB) - with NYHA class II to IV, a left ventricular ejection fraction of 35% or less and, who are already taking a stable dose of an ACE inhibitor or angiotensin receptor antagonist
56
Chronic heart failure
inhibitors of sodium-glucose cotransporter 2 (SGLT2) - works at S1 segment proximal tubule - 90% of renal glucose reabsorption diabetes drug but treats heart failure as a second result
57
Acute heart failure - basic measures
Sit patient upright | High dose oxygen -> corrects hypoxia
58
Acute heart failure - initial drug treament
IV loop diuretics - venodilation and diuresis IV opiates/opioids (morphine) - reduce anxiety and preload (venodilatation) IV, buccal or sublingual nitrates - reduce preload& afterload, ischaemia and pulmonary artery pressures Continue beta blockers but DO NOT initiate!