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cardiovascular Flashcards

1
Q

how would you explain what is SBP and DBP

A

SBP measures the pressure in the arteries when the heart beats

DBP measures the pressure in the arteries in between heart beats

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2
Q

what are the factors to consider for ASCVD risk estimator

A

demographics
- age
- sex
- race

labs
- SBP
- DBP
- HDL-C
- total cholesterol

PMHx
- DM
- smoler
- HTN treatment

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3
Q

what are the risk factors of CVD

A
  • SBP and DBP
  • age (≥65yo for women; ≥55yo for male)
  • FHx of premature CVD
  • dyslipidemia
  • DM
  • obesity (BMI≥30)
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4
Q

what are the prognostic factors of CVD

A

cerebrovascular diseases
- stroke
- TIA

renal diseases
- albuminuria/ proteinuria
- CKD ≥stage 3

heart diseases
- CHF
- angina pectoris
- MI
- coronary revascularisation
- left ventricle hypertrophy

vascular diseases
- aortic aneurysm
- peripheral artery disease
- hypertensive retinopathy

atherosclerosis

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5
Q

what are the identifiable secondary causes of HTN

A
  1. drug-induced
  2. CKD
  3. renal artery stenosis
  4. thyroid or PTH diseases
  5. nephropathy from T1DM
  6. obstructive sleep apnea
  7. primary hyperaldosteronism
  8. hypercortisolism
  9. rare monogenic ion transport disorders
  10. pheochromocytoma
  11. coarctation of the aorta
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6
Q

what are the drugs that can induce HTN

A
  • illicit substances (cocaine, amphetamine, crystal meth, ecstasy)
  • corticosteroids, NSAIDs, coxibs
  • OCs with estrogen
  • diet pills
  • decongestants (pseudoephedrine, naphazoline)
  • immunosuppressants
  • herbal (ma huang)
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7
Q

what are the non-pharmacological management for HTN

A
  • limit alcohol intake to max 2u/day for men and 1u/day for women
  • smoking cessation
  • physical activity (≥150mins/w of moderate intensity where HR is elevated from baseline on ≥3d/w)
  • weight management to obtain BMI ≤23
  • diet modifications to include more fruits and vegetables and low-fat dairy products while reducing intake of total and saturated fats
  • limit salt intake to 5-6g/d (approx 1 teaspoon) –> choose homecooked meals, eat less gravy, sauces and soup when eating out, use herbs and spices to flavor food instead of salt and sauces
  • stress management through adopting meditation, deep breathing or massage techniques and ensuring adequate good quality sleep
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8
Q

how is BP classified

A

normal BP: SBP <130 and DBP <85
high-normal BP: SBP 130-139 or DBP 85-89
grade I HTN: SBP 140-159 or DBP 90-99
grade II HTN: SBP 160-179 or DBP 100-109
grade III HTN: SBP ≥180 or DBP ≥110
isolated systolic hypertension: SBP ≥140 and DBP <90

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9
Q

what are the target BP goals

A

120-130/70-80
as tolerated for >65yo

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10
Q

what are the general monitoring parameters and follow ups

A
  • BP q6-12m if low risk, q3-6m if moderate to very high risk
  • BMI, FBG, lipid, electrolytes q12m
  • others as indicated per individual profile
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11
Q

what are the key things to note regarding choice of antihypertensives

A
  • caution diuretic in DM –> increases risk of hyperglycemia
  • caution BB in DM –> masking of hypoglycemic symptoms
  • avoid ACEi/ARB in CKD –> can increase risk of hyperkalemia and renal failure and angioedema
  • avoid Spironolactone in CKD esp with ACEi/ARB –> can increase risk of hyperkalemia and renal failure
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12
Q

what are the drug-specific monitoring parameters and follow up upon initiation

A

ACEi/ARB
- renal panel in 1-2w
- presence of cough
- ADR cross reactivity (with other classes that target RAAS)

BB
- in 2-4w
- check PR control

CCB
- in 2-4w
- check PR control for NDHP-CCB

diuretic
- renal panel in 1-2w

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13
Q

what are the major factors influencing BP

A

Arterial BP = CO x Peripheral Resistance

components of CO
- HR
- contractility
- filling pressure (as determined by venous tone and blood volume)

components of peripheral resistance
- arteriolar tone

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14
Q

which of the components are part of preload vs which are part of afterload and define both these terms

A

preload is the stretching of cardiac muscles before contraction, associated with ventricular filling
- filling pressure as determined by blood volume and venous tone

afterload is the force against which the heart has to contract to eject the blood
- peripheral resistance as determined by arteriolar tone

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15
Q

elaborate on the RAAS system for when there is a drop in BP

A

short term
- drop in BP –> activation of sympathetic nervous system –> (i) activation of beta1 receptors in heart (ii) activation of beta1 receptors in smooth muscle –> (i) increases cardiac output (ii) increases peripheral resistance –> both (i) and (ii) lead to increase in BP

long term
- drop in BP –> decreased renal blood flow –> increases renin –> increased angiotensin II –> increases aldosterone –> increase Na+ and H2O retention –> increases blood volume –> increases BP
- drop in BP –> decreased renal blood flow –> decreases GFR –> increases Na+ and H2O retention –> increases in blood volume –> increase BP

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16
Q

what are the determinants of vascular tone, outline the r/s

A
  1. ca2+ channel
    - Ca2+ ions forms a complex with calmodulin that activates MLCK to phosphorylate myosin-LC, leading to muscle contraction
  2. adenylyl cyclase
    - adenylyl cyclase converts ATP into cAMP that activates protein kinase A to increase reuptake of Ca2+, thus reducing formation of complex, subsequent activation of MLCK and phosphorylation of myosin-LC
  3. guanylyl cyclase
    - guanylyl cyclase converts GTP into cGMP which increases de-phosphorylation of myosin-LC, leading to muscle relaxation
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17
Q

what are the key functions of angiotensin II

A

angiotensin II causes vasoconstriction and stimulates secretion of aldosterone from adrenal cortex

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18
Q

what is the role of aldosterone

A

aldosterone is a hormone that acts on the kidneys to increase reabsorption of Na+ and H2O from the urine back into the bloodstream, leading to salt and water retention in the kidneys, leading to increased blood volume and BP

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19
Q

what is the moa of ACEi and list the drugs in this class

A

lisinopril, enalapril, captopril, ramipril
- ACE enzyme is involved in conversion of angiotensin I to angiotensin II, inhibition of this path reduces the ability of angiotensin II to induce vasoconstriction and aldosterone secretion, causing reduced peripheral vascular resistance and salt and water retention, leading to a drop in BP
- ACE enzyme is also involved in inactivation of bradykinin, thus inhibiting this path causes reduced inactivation of bradykinin which is the component largely responsible for dry cough s/e; bradykinin also activates NO and PG to further induce vasodilation and decrease BP

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20
Q

what are the available formulations and max dosing for each ACEi

A

lisinopril
- avail in 5, 10mg
- max 40mg/day

enalapril
- avail in 5, 10mg
- max 40mg/day

captopril
- avail in 12.5, 25mg
- max 150mg/day

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21
Q

what are the c/i and s/e of ACEi

A
  • c/i in pregnancy
  • s/e are severe hypotension, acute renal failure, hyperkalemia, dry cough, angioedema
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22
Q

what is the moa of ARB and list the drugs in this class

A

losartan, valsartan, telmisartan, candesartan, irbesartan, eprosartan
- works by direct antagonism of angiotensin II receptors and produce BP lowering effects by antagonising AT1-induced vasoconstriction, aldosterone release, catecholamine release, arginine vasopressin release, water intake and hypertrophic response

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23
Q

what are the c/i and s/e of ARBs

A
  • c/i in pregnancy
  • s/e include (less) dry cough, acute renal failure, hypotension, hyperkalemia, angioedema
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24
Q

what is the moa of BB and list the drugs in this class

A

non-selective
- propranolol
- pindolol
- carvedilol

selective
- atenolol
- bisoprolol
- metoprolol

  • BB competitively block beta adrenergic receptors to prevent epinephrine and norepinephrine from binding to the beta receptors
  • this blockade reduces activation of adenylyl cyclase that would have typically resulted from interaction of epinephrine and norepinephrine with beta receptors –> reduced formation of cAMP from ATP –> reduced activation of MLCK –> reduced phosphorylation of myosin-LC –> reduced muscle contraction
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25
Q

what are the c/i and s/e of BB

A
  • c/i in asthmatics (due to risk of bronchoconstriction upon blockade of beta2 receptors on bronchial smooth muscle)
  • caution in CCB+BB as risk of excessive suppression of sympathetic activity
  • s/e include bradycardia, hypotension, decreased exercise capacity and bronchoconstriction
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26
Q

what is the moa of CCB and list the drugs in this class

A

DHP CCB
- amlodipine
- nifedipine

NDHP CCB
- verapamil
- diltiazem

  • CCB primarily block L-type calcium channels in cardiac and smooth muscle cells which are responsible for allowing Ca2+ to enter the cells during depolarisation thus causing muscle contraction
  • intracellular calcium concentration is essential for activating MLCK which phosphorylates myosin-LC and initiate contraction process
  • by inhibiting calcium entry, CCB reduce the availability of Ca2+ available for MLCK activation, leading to decreased phosphorylation and ultimately allow for muscle relaxation
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27
Q

what are the c/i and s/e of CCBs

A
  • c/i in pre-existing depressed cardiac function (due negative inotropic effects, increased risk of hypotension)
  • s/e: edema, ankle swelling, HA, dizziness, sleepiness, palpitations, flushing, SOB, GI discomfort, muscle pain
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28
Q

compare the actions between DHP CCB and NDHP CCB

A

DHP CCB selectively block L-type calcium channels in the cardiac and smooth muscle cells

NDHP CCB in addition to blocking L-type calcium channels, they also have additional effects on cardiac conduction tissues specifically in SA and AV nodes, slowing the conduction through these nodes

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28
Q

what is the moa of diuretics and list the drugs in this class

A

loop diuretics
- furosemide
- bumetanide

thiazides
- hydrochlorothiazide
- indapamide

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29
Q

illustrate what occurs at the loop of henle

A
  • the thin descending limb is permeable to water but not to ions and water is extracted from it by osmotic forces because the surrounding interstitial fluid becomes increasingly hypertonic as it descends
  • the thick ascending limb is impermeable to water, has a basolateral Na/K/ATPase transporter that transports Na+ into the interstitium and K+ into the tubular epithelial cells –> energy from this transporter is used for Na/K/2Cl co transporter to transport Na+ K+ and Cl- from tubular fluid into tubular epithelial cells –> accumulation of K+ in tubular epithelial positive electrical potential –> facilitate paracellular reabsorption of Mg2+ and Ca2+ –> while Na+ and Cl- are reabsorbed into the interstitium via other transporters and pathway
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29
Q

what is the moa of loop diuretics and list the drugs in this class

A

furosemide, bumetanide

  • loop diuretics selectively inhibits the luminal Na/K/2Cl cotransporter –> increase excretion of Na+, Cl- and K+ –> thus also increase excretion of Mg2+ and Ca2+
  • loop diuretics also induce PG synthesis, esp PGE2 to induce vasodilating effect –> increases renal blood flow –> enhance delivery of filtered fluid to the tubules –> increasing urine output ie. diuresis
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30
Q

what are the c/i and s/e of loop diuretics

A
  • c/i are sulphonamide allergy, electrolyte deficiency, renal failure (CrCl <30), concomitant K supplement or K-sparing diuretic
  • s/e are hypoK, hypoNa, hypoMg, hypoCa, hyperuricemia, ototoxicity
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31
Q

what is the moa of thiazide diuretics and list the drugs in this class

A

hydrochlorothiazide, indapamide

  • at the DCT, Na+ and Cl- are reabsorbed into tubular epithelial cells via apical Na/Cl transporter, and Ca2+ are reabsorbed via apical Ca2+ channel and basolateral Na/Ca exchanger
  • thiazide diuretics block the Na/Cl transporter leading to decreased Na+ and Cl- reabsorption thus increasing excretion in the urine, along with water, and can lead to increased K+ excretion as well
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32
Q

what is the c/i and s/e of thiazide diuretics

A
  • c/i in sulphonamide allergy, renal failure (CrCl <30), hepatic encephalopathy (can cause worsening of neurological sx), DM, hypokalemia
  • s/e include hypokalemic metabolic alkalosis, hyponatremia, hyperglycemia, hyperlipidemia, hyperuricemia
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33
Q

what is the moa of vasodilators and list the drugs in this class

A
  • works by promoting the production or release of nitric oxide which is a potent vasodilator –> NO diffuses into nearby smooth muscle cells and activates guanylyl cyclase which converts GTP into cGMP –> dephosphorylation of myosin-LC –> muscle relaxation
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34
Q

what are the third line agents for add-ons to resistant hypertension or if additional compelling indications

A
  • mineralocorticoid receptor antagonist (spironolactone, eplerenone)
  • alpha antagonists (alpa1: terazosin, prazosin, doxazosin; alpha2: methyldopa, clonidine)
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35
Q

list the recommended, add-on and c/i drugs for the following comorbidities: HF, angina, hx of stroke/AF, AF (rate), DM, DM+albuminuria, recurrent stroke prevention, CKD 3, CKD 1/2 + albuminuria, CKD 5, BPH, heart block, ISH, asthma and COPD, gout

A

HF
- recommended beta1-BB, ACEi/ARB/ARNi
- add on diuretic/ aldosterone antagonist
- c/i NDHP CCB

angina
- recommended: DHP CCB, BB
- add on: ACEi/ARB/DHP CCB/ diuretic

hx of stroke/AF:
- recommended BB
- add on ACEi/ARB (ARB may prevent recurrence of AF)

AF (rate)
- recommended NDHP CCB, BB

DM
- recommended ACEi/ARB (any first line)

DM+Albuminuria
- recommended ACEi/ARB

recurrent stroke prevention
- recommended thiazide + ACEi

CKD 3 or CKD1/2+Albuminuria
- recommended ACEi/ARB

CKD 5
- recommended ACEi/ARB
- c/i spironolactone (aldosterone antagonist)

BPH
- alpha antaonist

heart block
- c/i NDHP CCB, BB

ISH
- recommended diuretic, DHP CCB

asthma and copd
- c/i BB

gout
- c/i diuretic

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36
Q

what is the definition of OH

A

a decrease in SBP of 20mmHg or a decrease in DBP of 10mmHg within 3 mins of standing when compared with BP from sitting/ supine

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37
Q

what is the management strategy for OH

A
  • avoid large carb rich meals
  • limit alcohol intake
  • ensure adequate hydration
  • investigate root cause
  • titrate antihypertensives slowly
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38
Q

how to counsel on home BP monitoring

A
  1. measure your BP two times a day, once in the morning before breakfast, medications and exercise and once in the evening, both at the same time each day
  2. avoid food, caffeine, alcohol 30 mins prior to the measurement
  3. sit quietly during monitoring, sit with legs and ankles uncrossed and back supported against a chair, stay calm and do not talk while measuring your BP
  4. position your arm at rest, at level of your heart on a table or a chair arm, use a pillow as needed to elevate (hand above heart level reduces BP vs below heart level increases BP)
  5. place cuff on bare skin and not over clothing, avoid rolling long sleeves up (ensure appropriate cuff size, measure circumference of upper arm midway between elbow and shoulder and choose a cuff size with this measurement; undersized cuff increases BP while oversized lowers BP)
  6. wait for at least one minute before repeating, write the two readings down in a BP log book and average them
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39
Q

how would you explain what is arrhythmia

A

abnormal heart rhythm due to defects in impulse generation, defects in impulse conduction or both

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40
Q

how can arrhythmias be classified

A
  1. by speed of HR
    - tachy-arrhythmias (HR >100) includes AF/flutter, ventricular fibrillation/ tachycardia, supraventricular tachycardia
    - brady-arrhythmias (HR<60) includes conduction blockas
  2. by origin in the heart
    - atrial
    - ventricular
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41
Q

what is the pathophysiology of AF

A

AF arises when depolarization signals fires off from abnormal areas in the atria instead of from the sinus nodes –> stimuli bombards the AV node with multiple signals instead of a single signal from the sinus node –> atrial quivers and results in the loss of meaningful contraction

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42
Q

what are the typical conditions that AF is associated with

A

AF is commonly associated with underlying heart disorders leading to atrial distension (stretching of the atria)
- HFrEF, HFpEF
- HTN
- disorders of the heart valves

but also associated with
- ischemia/ infarction (IHD)
- pulmonary embolism
- chronic lung disease resulting in pulmonary HTN
- states of high adrenergic tone (alcohol withdrawal, sepsis, viral illness)
- drug-induced states
- cardiac surgery

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43
Q

what comorbidity is AF commonly associated with

A

HF
- close pathophysiological r/s and share many predisposing risk factors

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44
Q

what is the major consequence of AF

A

AF increases the risk of stroke

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45
Q

what are the goals of therapy for AF

A
  • relieving symptoms through rate (slow down AF) or rhythm control (revert back to normal rhythm)
  • stroke prevention
  • addressing risk factors and triggers
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46
Q

what is the key pharmacological approach for AF

A

ABC

Anticoagulation (Avoid stroke)
Better symptom control through rate or rhythm control
CV risk factors and concomitant diseases

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47
Q

what are the drugs for AF pharmacological management

A
  1. class IC - flecainide, propafenone
  2. class II - BB (esmolol IV, metoprolol IV, bisoprolol PO, atenolol PO, carvedilol PO, metoprolol PO)
  3. class III - amiodarone, sotalol
  4. class IV - NDHP CCB (verapamil IV/PO, diltiazem IV/PO)
  5. digoxin (cardiac glycoside)
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48
Q

which classes are for rate control vs which are for rhythm control

A

class I for rhythm
class II and IV for rate
class III for both rate and rhythm

49
Q

what is the first line for AF management and what is it

A

first line is rate control as it is often sufficient to improve AF-related sx, which refers to the slowing of AV nodal conduction to prevent the multiple stimuli from being conducted through the AV node to reach the ventricles

50
Q

what is the target HR for rate control

A

<80 at rest, <110 during exercise

51
Q

what is the rough treatment algorithm for AF

A

first line is BB or NDHP CCB
- if HFrEF, choose BB (evidence of benefit and cardioprotective effect and inhibition of sympathetic system vs NDHP CCB has negative inotropic effect)
- if c/i to BB (asthma, copd, severe hypotension, conduction block), choose NDHP CCB

second line is either class that has not yet been trialed
- if HFrEF, consider adding digoxin to BB
- if c/i to BB then add digoxin to NDHP CCB

third/ forth line is amiodarone

52
Q

what is the moa of digoxin and what class is it

A

digoxin is a cardiac glycoside that works by directly suppressing SA and AV nodal conduction to increase refractory period and decrease conduction velocity to decrease rate

and indirectly enhances vagal tone to increase parasympathetic activity and thus slowing AV node conduction –> decrease rate

53
Q

what are the pk characteristics of Digoxin, any dose adjustments required

A
  • digoxin has a large Vd and distributes extensively to peripheral tissues thus it has a longer onset
  • long half life and is renally cleared thus requires dose adjustments for R impairment
  • also has NTI
  • monitoring of ECG and electrolytes as digoxin can be pro-arryhthmic, higher risk in elderly and R impairment
54
Q

how might digoxin be pro-arrhythmic

A
  • blocks Na/K/ATPase pump in cardiac cells which increases intracellular Na+, causing an influx of Ca2+ leading to positive inotropic actions
55
Q

when is rhythm control used

A
  • patients who are likely to benefit most being in sinus rhythm ie. younger patients
  • patients who are still symptomatic despite rate-controlled
  • high likelihood of maintaining sinus rhythm (first AF episode, short hx, precipitated by temporary event)
56
Q

what are the criterias to be assessed when determining the appropriate anti-arrhythmics for

A

if none or minimal signs of structural heart disease –> class IC and III

if CAD, HFpEF, significant valvular disease (eg. mitral/ arterial stenosis) –> class III

if HFrEF –> amiodarone only

57
Q

what are the c/i for class IC drugs

A

c/i in IHD, HF, valvular diseases (severe liver diseases in propafenone)

58
Q

what are the key characteristics of amiodarone

A
  • predominant class III properties
  • high affinity to tissues, large Vd –> requires LD
  • long half life –> effects maintained for 1-3m after discontinuation
  • has a structure similar to THs –> source of iodine
  • c/i in IHD, HF, valvular disease
  • high potential for DDI (incl digoxin and warfarin; these have NTI)
  • extracardiac s/e profile
  • monitoring: LFTs, TFTs, ECG, chest x-ray, physical exam, labs (at baseline and q6m)
59
Q

what is the extracardiac s/e profile of amiodarone

A
  • corneal microdeposits (halos)
  • N/V, abdominal discomfort
  • photosensitivity
  • blue-grey skin discoloration
  • may cause thyroid function derangements
  • pulmonary toxicity that can be fatal
  • deranged LFTs
  • numbness, neuropathy, parasthesia
60
Q

what are the key properties of sotalol

A
  • L-isomer has II (NSBB) and III effects; D-isomer has III effects
  • s/e include bradycardia, heart block, bronchospasm, ADHF
  • caution in renal impairment and dose adjust as long half life and renally cleared
  • caution for risk of QTc prolongation and dose-related risk of TdP
  • monitor renal func, QTc prolongation, HR, BP
61
Q

what are the non-pharmacological management for AF

A
  • patient education on self-management and exacerbation management
  • smoking
  • alcohol
  • diet
  • physical activity
62
Q

what is cardiac output and what is it affected by

A

volume of blood pumped by LV into aorta per min

  • HR
  • stroke volume (volume of blood ejected during systole) that depends on preload, afterload (peripheral resistance) and function of the heart as a pump (contractility)
63
Q

how would you explain what HF is

A

failure of the heart to pump at sufficient rate to service the metabolic requirements of the tissue or only able to do so at an elevated filling pressure

64
Q

what are the types of HF

A

left-sided HF
- HFrEF (LV loses its ability to pump with enough force to push blood into the circulation)
- HFpEF (LV loses its ability to relax normally due to muscle stiffness, unable to fill up with blood in between contractions)

right-sided HF
- RV unable to pump blood efficiently to the lungs for oxygenation
- often a consequence of left-sided HF

congestive HF
- associated with fluid accumulation

65
Q

what are the stages in HF and the primary aim for each stage

A

stage A: at risk for HF –> identify and modify risk factors

stage B: pre-HF –> treat risk and structural heart diseases to prevent HF

stage C: symptomatic HF

stage D: advanced HF

–> for both C and D, reduce symptoms, morbidity and mortality

66
Q

who are patients classified under stage A and stage B

A

stage A
- patients w/o s/sx of HF and w/o structural or functional heart diseases or abnormal biomarkers (includes HTN, CVD, DM, obesity, metabolic syndrome, genetic variant or FMHx of cardiomyopathy, exposure to cardiotoxic agent)

stage B
- patients w/o sx of HF but one of the following: structural heart disease and prev MI, evidence of elevated filling pressure, increased natriuretic peptide levels or persistently elevated cardiac troponin levels

67
Q

what are the goals of therapy for each stage of HF

A

stage A
- heart healthy lifestyle
- prevent LV structural abnormalities
- prevent vascular, coronary diseases

stage B
- prevent HF symptoms
- prevent further cardiac remodelling

stage C
- control symptoms
- improve QoL
- prevent hospitalization
- reduce morbidity
- prevent mortality

stage D
- control symptoms
- improve QoL
- reduce hospital readmissions
- establish patient’s end of life goals

68
Q

what are the key management strategies for each stage of AF

A

stage A
- ACEi/ARB
- statins as appropriate

stage B
- ACEi/ARB as appropriate
- BB as appropriate
- ICD/ revascularisation in some

stage C
[HFpEF]
- diuretics
- follow indicated comorbidities guidelines (HTN, DM, AF, CAD)
- ICD/ revascularisation in some
[HFrEF]
- diuretics
- ACEi/ARB
- ARNi
- BB
- aldosterone antagonist
(in some)
- ivabradin
- digoxin
- hydralazine/ ISDN
- IC/revascularisation/ CRT in some

stage 4
- advanced care measures
- heart transplant
- chronic inotropes
- temporary or permanent MCS
- experimental surgery or drugs
- palliative care and hospice
- ICD deactivation

69
Q

what is NYHA functional classification for HF

A

I: no limitation of physical activity, ordinary physical activity does not cause fatigue, palpitation and dyspnea

II: slight limitation of physical activity, comfortable at rest, ordinary physical activity causes fatigue, dyspnea and palpitations

III: marked limitation of physical activity, comfortable at rest, less than ordinary physical activity causes fatigue, dyspnea and palpitations

IV: unable to carry on any physical activity without discomfort, HF sx present at rest, discomfort increases if any physical activity undertaken

70
Q

what is the classification of HF by LVEF

A

HFrEF if LVEF ≤40%, HFpEF if LVEF ≥50%, HFmrEF if LVEF 41-49%

71
Q

what is the diagnostic algorithm for HF

A

assessment of clinical hx, labs, ECG, physical exam –> optional to obtain natriuretic peptide and cardiac troponin levels –> transthoracic echocardiogram –> confirm diagnosis

72
Q

what are the typical presenting symptoms of HF

A
  • breathlessness
  • reduced exercise tolerance (fatigue, tiredness and increased time to recover after exercising)
  • ankle swelling
  • orthopnea
  • paroxysmal nocturnal dyspnea
73
Q

what is the key concept of pharmacological management of HFrEF

A

ACEi/ARB/ARNi + BB + SGLT2i + MRA +/- Diuretics

74
Q

how to determine whether to use ACEi/ARB/ARNi

A

in HFrEF NYHA II/III, ARNi first choice f/b ACEi f/b ARB

75
Q

what are the c/i considerations regarding use of ARNi and ACEi

A
  • ARNi should not be used within 36hr from last dose of ACEi
  • ARNi not for angioedema
  • ACEi not for angioedema
76
Q

what is the moa of ARNi and list the drug in this class

A

ARNi comprises of an angiotensin receptor and neprilysin enzyme inhibitor (valsartan and sacubitril respectively)
- angiotensin II binds to AT1 receptor to lead to vasoconstrictive effects
- neprilysin enzyme breaksdown bradykinin, angiotensin II, natriuretic peptides and others into inactive fragments

leading to
- increased vasodilation
- decreased sympathetic activity
- increased parasympathetic activity
- increased diuresis
- decreased cardiac hypertrophy
- decreased risk of arrhythmias

77
Q

what are the considerations when wanting to initiate BB

A
  • pt is euvolemic and hemodynamically stable
  • start with low dose
  • double dose in intervals no less than 2w
  • aim for target dose or at least the higher tolerated dose
  • monitor HR, BP and clinical status (if HR <50, half dose of BB)
78
Q

list the BB that can be used in HF

A
  • metoprolol
  • bisoprolol
  • carvedilol
79
Q

what is the moa of MRAs and list the MRAs that can be used in HF

A

spironolactone, eplerenone
- works as antagonists of the mineralocorticoid receptors (non-selectively for spironolactone; selectively for eplerenone) to block the action of aldosterone, a hormone key in regulating potassium and sodium balance
- in HF, there is elevated levels of aldosterone thus leading to increased levels of sodium retention and increased potassium excretion, leading to water retention

80
Q

what are the key considerations for MRA

A

eGFR >30 and serum K <5.0 (≤5.5 when on treatment)

81
Q

what are the s/e, monitoring and key differences between spironolactone and eplerenone

A
  • hyperkalemia, renal insufficiency (monitor these, esp ensuring serum K ≤5.5 during treatment)
  • since eplerenone is more selective against aldosterone action, and less on other steroid hormone receptors, it has lesser risk of s/e like gynaecomastia and vaginal bleeding
82
Q

what is the place in therapy of SGLT2i for HF

A
  • given to all symptomatic chronic HFrEF patients, irregardless of presence of T2DM
  • not for eGFR <30, T1DM, SBP <95-100
  • caution for euglycemic ketoacidosis, genital and soft tissue infections, adjustment of diuretics dose to prevent volume depletion
83
Q

place in therapy of hydralazine, ISDN, ivabradine and digoxin

A
  • hydralazine and ISDN if patients cannot be given first-line agents
  • ivabradine in LVEF ≤35% + resting HR ≥70 and unable to tolerate or c/i to BB
  • digoxin in symptomatic HFrEF + ACEi/ARNi + BB + MRA
84
Q

what are the monitoring parameters and TCU frequency for each of the drug classes used for HF

A

ACEi/ARB
- renal panel, K, urea, BP
- TCU q4w

ARNi
- renal panel, K, urea, BP
- TCU q4w

BB
- BP, PR, clinical status
- TCU q2-4w

MRA
- renal panel, K, urea, BP
- gynaecomastia for spironolactone
- TCU at week 1, week 4 f/b q4-8w

loop diuretic
- renal panel, K, urea, BP, BMI
- TCU q2-4w

SGLT2i
- renal panel, BP
- genitourinary tract infections, euglycemic ketoacidosis
- TCU q2-4w

85
Q

what are the drugs that can worsen HF

A
  • NSAIDs, coxibs –> inhibit PG synthesis leading to sodium and water retention, increased systemic vascular resistance and blunted diuretic response
  • TZDs –> possible calcium channel blockade
  • class IC AAD (flecainide) –> negative inotropic effect, pro-arrhythmic
  • class III AAD (sotalol) –> pro-arrhythmic, beta blockade
  • alpha 1 blocker (doxazosin) –> beta1 receptor stimulation with increases in renin and aldosterone
  • diltiazem, verapamil –> negative inotropic effects
86
Q

what are the non-pharmacological management for HF

A

lifestyle modifications
- restriction on Na, K, fluid
(K rich food are bananas, oranges, melon, spinach, tomato, potatoes, nuts and seeds)
- weight management, measure daily
- physical activity (as much as tolerable)
- smoking cessation
- limit alcohol intake

immunisation
- pulmonary congestion can increase risk of lung infections
- pneumococcal and annual influenza

cardiac rehabilitation programmes
- useful to help improve lung capacity, exercise tolerance and QoL

87
Q

what is the risk stratification and their LDL-C goals

A

RISK STRATIFICATION
if established CAD, PAD, atherosclerotic cerebrovascular disease, aortic aneurysm, very high risk

if DM wo established CAD, PAD, atherosclerotic cerebrovascular disease, aortic aneurysm, CKD, or if CKD moderate to severe (eGFR <60) –> high risk

if ASCVD >20% –> high risk
if ASCVD 10-20% –> intermediate risk
if ASCVD <10% –> low risk

LDL-C GOALS
if ASCVD high risk, DM, CKD –> <1.8

if not ASCVD high risk, DM or new DM –> <2.6

88
Q

overview of drug classes for management of hyperlipidemia

A

statins (HMG-CoA reductase inhibitor)
- increases peripheral clearance

fibrates
- increases peripheral clearance

ezetimibe
- decreases intestinal sterol absorption

niacin
- decreases lipoprotein secretion

resins
- decreases fat absorption

PCSK9i
- decreases LDL receptor degradation

omega3
- decreases TG synthesis

89
Q

classify the drugs in the statins class

A

high intensity (≥50%)
- 20/40 rosuvastatin
- 40/80 atorvastatin

moderate intensity (30-49%)
- 5/10 rosuvastatin
- 10/20 atorvastatin
- 20/40 simvastatin
- 40/80 pravastatin
- 40/80 lovastatin

low intensity (<30%)
- 10 simvastatin
- 20 lovastatin
- 10/20 pravastatin

90
Q

what is the moa of statins

A

statins are HMG-CoA reductase inhibitors that have strong affinity to this enzyme to inhibit the rate limiting step of cholesterol synthesis, decrease in intracellular cholesterol levels leads to an upregulation of LDL receptors on cell surfaces

91
Q

how much further reduction if dose of statins are doubled

A

6-7% more

92
Q

how much more reduction if add ezetimibe to statins

A

20% more

93
Q

pk, s/e, c/i of statins

A
  • significant first pass effect –> ddi with 3A4 (statins are 3A4 substrates)
  • taken in the evening as HMG-CoA enzyme found to be most active at night
  • c/i in pregnant, lactating, children and teens due to affects on neurodevelopment, also c/i in active liver disease
  • s/e include elevated transaminases (≤3x ULN, stop statin if >3xULN) and SAMS
94
Q

classify SAMS

A

myalgia: normal CK
myositis/ myopathy: CK >10xULN with concerning symptoms
rhabdomyolysis: CK >40x ULN with renal injury w/wp myoglobinuria

95
Q

what is the moa of PCSK9i and list the drugs in this class

A

evolocumab, alirocumab
- works by inhibiting PCSK9 enzyme to decrease degradation of LDL receptors –> increase number of LDL-receptors on cell surface to bind and internalise circulating LDLs

96
Q

how much is LDL-C further reduced if PCSK9i added to statins

A

50-60% more

97
Q

what are the s/e and pk considerations of PCSK9i

A
  • slow onset
  • dosed q2-4w
  • s/e include inj site rxn (swelling, erythema, pain or tenderness, itching)
98
Q

what is the moa of fibrates and list the drugs in this class

A

fenofibrate, gemfibrozil
- works as a ligand to PPAR-alpha protein which leads to increased activity of lipoprotein lipase to cause a decrease in plasma TG levels

99
Q

what are the s/e and c/i of fibrates

A
  • s/e include liver toxicity and myopathy (and SCr elevations w/wo nephropathy for fenofibrate)
  • c/i in CrCl <30 for fenofibrate (G can up to <10)
100
Q

what is the moa of ezetimibe

A
  • selective inhibitor of cholesterol transport protein (NPC1L1)
101
Q

how often to recheck lipids

A

at 8-12w after initiation and adjustments f/b q12w

102
Q

what are some CVD that indicates very high risk ASCVD and what should be the LDL-C goal

A

LDL-C goal of <1.6mmol/L

  • stable angina, ACS, ST-elevation or non MI, unstable angina, cerebrovascular accident, TIA, carotid artery disease, PAD
103
Q

what is metabolic syndrome

A

any three of the following
- FBG >5.6
- large waist circumference
- TG >1.7
- low HDL

104
Q

how is HTG managed

A
  • for patients high risk but on optimized statin –> start fibrate if TG >2.3
  • for primary prevention –> start statin if TG >2.3
  • if TG >4.5, fibrate first line then statin add on later on if indicated
105
Q

what are the non-pharmacological management of dyslipidemias (LDL, TG)

A
  • avoid dietary trans fat, reduce dietary saturated fat, increase dietary fibre
  • reduce excessive body weight
  • reduce alcohol intake

FOOD CHOICES
- wholegrains > white bread, white rice, pasta
- lentils, peas, soybeans, beans
- raw and cooked vegetables
- fresh or frozen fruits > dried fruits and fruit juices
- skimmed milk and yogurt > low-fat milk
- skinless poultry, lean and oily fish
- grilling, boiling, steaming > stir-frying, roasting and frying

106
Q

considerations for management of hyperlipidemia in pregnancy

A
  • no statins, ezetimibe, fibrates during pregnancy –> stop statin 4w prior to cessation of contraception
107
Q

how would you explain what CAD is

A

a pathological process characterized by atherosclerotic plaque accumulation in epicardial arteries, whether obstructive or non-obstructive

108
Q

what is the pathophysiology of angina pectoris

A
  • often the result of an imbalance between myocardial oxygen demand and supply (demand increased in the setting of a fixed decrease in supply)
  • stable and well-developed atherosclerotic plaques
109
Q

what is the approach in assessing patient’s chest pain

A

PQRST

P recipitating factors
P alliative measures
Q uality of the pain
R egion
R adiation
S everity
T emporal pattern (timing)

110
Q

classify various types of angina

A

typical angina
- meets the following three: (i) constricting discomfort in front of chest or neck, jaw, shoulder, arm (ii) precipitated by physical exertion (iii) relieved by rest or nitrates within 5mins

atypical angina
- meets two of the above

non-anginal
- meets only one or none

111
Q

how is angina assesed and diagnosed

A

cardiac testing
- resting ECG
- stress test or stress echocardiogram
- myocardial perfusion imaging
- cardiac MRI
- CT angiography
- coronary angiography (gold standard)
- coronary calcium scoring using CT

basic biochemistry testing
- repeated measurements of troponin to rule out ACS
- FBC incl Hb
- Cr and estimation of renal function
- lipid incl LDL-C
- screening for DM using HbA1c/FBG else OGTT
- assess thyroid function

112
Q

what are the goals of therapy for angina and how would they be achieved

A
  • reduce angina symptoms and exercise-induced ischemia
  • prevent cardiovascular events and death (MI and death, acute thrombotic events, development of ventricular dysfunction)

by two complementary pathways aiming to
- slow progression of atherosclerosis and prevent complications
- reduce number of ischemic episodes as well as increasing the amount of exertion or exercise a patient can accomplish before chest pain occurs

113
Q

what is the non-pharmacological management for angina

A
  • healthy diet (mediterranean diet; high in vege and fruits, little to no trans fat, limit low fat dairy products, avoid sugar-sweetened soft drinks, ≤5-6g of salt per day, 1-2 servings of fish per week, limited lean meat and liquid vegetable oils)
  • smoking cessation (5As)
  • limit alcohol intake
  • physical activity
  • healthy weight
114
Q

what is the treatment algorithm for angina

A
  • first line is BB and/or CCB, second line is LAN
  • if low HR and low BP, first line can consider trimetazidine or ranolazine
  • if recent MI, BB/ACEi/ARB
  • if asymptomatic angina + T2DM, ACEi/SGLT2i/GLP1RA
  • statins for all patients (add ezetimibe if not at goal f/b add PCSK9i if not at goal still)
  • antiplatelet therapy with Aspirin or Clopidogrel
115
Q

what is the moa of ivabradine and what is its place in therapy and the s/e

A
  • ivabradine is a selective inhbitor of the funny receptor in the SA node to disrupt the If current to cause slowing of SA firing and lead to decrease in HR
  • add on to BB or NDHP CCB if HR not at goal but limited by BP, or as monotherapy if intolerant or c/i to BB or NDHP CCB
  • only for patients in sinus rhythm
  • s/e include phosphenes, HA, dizziness, AF
116
Q

what are the types of nitrates and list examples

A

short acting nitrates
- GTN sublingual
- GTN spray

long acting nitrates
- GTN patch
- ISDN tablet (IR/SR)

117
Q

what is the counseling points for short acting nitrates

A
  • place a sublingual tablet under your tongue and allow it to dissolve completely, can chew into small pieces to facilitate absorption
  • if using for an anticipated anginal activity, dissolve the tablet before engaging in the activity
  • else it should be used at first sign of angina attack, do not wait until you experience severe pain
  • the relief should be felt within 5 mins, if still experience pain, use a second tablet, if still experience pain once again, use a third tablet
  • if you still have chest pain after using 3 tablets in a 15min window, call 995 or go to the nearest ED

storage
- keep the tablets in the brown glass container and close tightly, do not transfer them to another container
- store in a cool dry place but not in the refrigerator
- carry the tablets with you wherever you go but in your bag or purse and not your pocket
- date the bottle once opened, discard any unused tablets after 8w and obtain a fresh supply

118
Q

what is the key consideration for long acting nitrates

A

chronic administration of LAN can lead to a state of oxidative stress –> dysfunction of mitochondrial aldehyde dehydrogenase –> unable to produce NO –> antianginal effect of nitrate agents is reduced or lost

managed by maintaining a nitrate free interval of ~ 10-14hrs at night

119
Q

what is the moa and place in therapy, and s/e and c/i of trimetazidine

A

trimetazidine works by inhibiting beta oxidation of free fatty acids and is a cytoprotective drug –> switches from FFA oxidation to glucose oxidation –> increases cardiac metabolic efficiency
- second or third line agent
- generally well tolerated
- c/i in CrCl <30, parkinson’s and motor disorders

120
Q

what is the key considerations of ranolazine

A
  • s/e are QTc prolongation, N, C, dizziness, HA
  • caution in concomitant QTc prolonging drugs (antipsychotics, antidepressants, AADs)
  • risk of ddi with metformin as both compete with each other for clearance –> increased risk of lactic acidosis
121
Q
A

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