PR2!53 Cardi0vascular System Flashcards
1
Q
Define blood pressure in words and equation
A
Aerial pressure in systemic circulation between aortic valve and arterioles
BP = CO x TPR
2
Q
Define cardiac output
A
CO = SV x HR
3
Q
Differentiate systolic and diastolic BP
A
Systolic pressure refers to the blood pressure in the arteries that results when your heart contracts or beats, pushing blood out.
Diastolic pressure refers to the blood pressure (which falls) when your heart relaxes between beats.
Diastolic blood pressure can increase with age as a result of stiffening arteries.
4
Q
Define postural hypotension and how the change in BP is detected
Define the BP
A
Fall in BP due to change in posture (from sitting to standing) → Gravity / Compliance of veins → decreased venous return → decreased stroke volume → mean arterial pressure
Detected by baroreceptors (eg. aortic, carotid)
Decrease in SBP by 20mmHg or DBP by 10mmHg within 3 minutes of standing when compared to BP from sitting/supine position
Possible etiologies:
Age-related, severe volume depletion, baroreflex dysfunction, autonomic insufficiency (eg. Diabetes), certain antihypertensives, antidepressants
5
Q
Describe the short term regulation of blood pressure
Via what?
A
Via autonomic regulation upon detection any baroreceptors
- Decreased parasympathetic efferent output –> increase HR and hence CO
- Increased sympathetic efferent output –> increase activation of a1 receptor in arterioles (increase TPR) + increase venous return (increase SV) + increase activation of B1 receptor in heart (increase contractibility of heart hence SV)
6
Q
Describe the long term regulation of BP? Via what?
A
Via renin angiotensin aldosterone system upon detection by kidney (Justaglomerular apparatus: senses pressure in afferent arteriole and Cl- transport)
1. High BP detected by kidneys which releases renin
2. Renin convert angiotensinogen (produced by liver) into AG1
3. AG1 is converted to AG2 by ACE
4. AG2 –> causes vasoconstriction + stimulate release of aldosterone by adrenal glands
5. Aldosterone stimulate Na and H20 reabsorption
7
Q
Role of AG2 in RAAS
A
- Stimulate arteriole constriction –> increase TPR
- Act on adrenal cortex for release of aldosterone
- Acts on hypothalamus to release ADH –> increases thirst, reabsorption of water and increases vasoconstriction
8
Q
List down the different ranges of BP under MOH guidelines
A
HTN:
- >/= 140/90mmHg
Normal: </= 130/85mmHg
High-normal: 130-139/85-90mmHg
G1: 140-159/90-99mmHg
G2: 160-179/100-109mmHg
G3: >/=180/110mmHg
9
Q
Define the BP for isolated systolic hypertension
A
> /- 140mmHg/ <90mmHg
Difference between SBP and DBP >80mmHg
10
Q
Potential causes of HTN
(clue: list the diff organs and what might have gone wrong)
A
Heart: sympathetic overdrive
Increased resistance of arteries and arterioles
Sympathetic overdrive
Dysregulation of vascular smooth muscle tone (eg. smoking, ageing)
Smooth muscle hypertrophy due to insulin resistance
Kidneys
Sympathetic overdrive
Insensitivity of the RAAS
Obesity
Angiotensin released from adipocytes
Increased blood volume
Increased blood viscosity (dysregulation of clotting)
11
Q
List out causes of secondary HTN (different categories: Medications, Diseases, Food)
A
Diseases:
- CKD
- Cushings syndrome
- Parathyroid/Thyroid diseases
- Obstructive sleep apnoea
Medications
- Corticosteroids
- Calcineurin inhibitors
- Decongestants (psuedoephedrine)
- Estrogen containing contraceptives
- Erythropoiesis stimulating agents
- NSAIDs
Others:
- St Johns Wort
- Ergot containing herbal products
- Liquorice
- Sodium
- Ethanol
12
Q
Non-pharm/Lifestyle changes for HTN patients
A
- Healthy BMI: 18.5-22.9kg/m2
- Sufficient sleep: 7-8h
- Exercise: 150min moderate intensity exercise/week OR 10 000 steps/day
- Diet
- Low sodium (5-6g of salt/day OR <1.5mg Na/day)
- Increase K intake (aim for 3.5-5mg K/day)
- Eat more veg, fruits, poultry, nuts
- Reduce intake of dairy, red meat, sweets - Quit smoking
- Reduce alcohol and caffeine consumption
- Reduce stress
13
Q
When to initiate treatment for HTN patients (in terms of different stages of HTN and varying CV risk)
A
From High-normal onwards, all need lifestyle intervention.
Grade 2-3: Regardless of CV risk –> Start/intensify therapy
Grade 1:
- CV risk >20% or 3 CV risk factor –> Start/intensify therapy
- CV risk <20% or 0-2 CV risk factor –> Consider pharmacotherapy if BP poorly controlled in next TCU in 3-6mths
High-normal:
- CV risk<20%: Don’t start tx
- CV risk>20%: Consider pharmacotherapy if BP poorly controlled in next TCU in 3-6mths
14
Q
List out the CVD risk factors (total of 7)
A
- Age
- M55, W65 - HTN
- Obesity
- Smoking
- Family history of premature cardiovascular disease
- Dyslipidaemia
- DM
15
Q
List of cases of target organ damage
A
Heart
- Congestive HF
- Angina pectoris
- Myocardial infarction
- Left ventricular hypertrophy
- Coronary revascularisation
Renal
- CKD S3 (eGFR<30ml/min)
- Albuminuria (ACR?30mg/mmol)
Cerebrovascular
- Stroke (ischemic/haemorrhagic)
Vascular
- Peripheral arterial disease
- Aortic aneurysm
- Hypertensive retinopathy
Atherosclerosis
16
Q
Differentiate HTN emergency and urgency
A
Urgency:
- Not associated with acute or immediately progressing end-organ injury
- Does not require admission
Emergency:
- Associated with end-organ injury
Defined as: Severe HTN (grade 3, BP>180/110mmHg) associated with acute end-organ damage which is often life-threatening and requires immediate but careful intervention to lower BP (usually IV)
Red flags:
Headache
Visual disturbances
Chest pain
Dyspnea
Dizziness
Neurological deficits
17
Q
List the classes of antihypertensives and their MOA
A
- ACE inhibitors/ARBs
- ACEi: inhibit ACE which is responsible for conversion of AG1 to AG2 + prevents inactivation of bradykinin to allow vasodilation
- ARBs: selectively + competitively blocks AG2 type 1 receptor - ## BB
- CCB
- Diuretics
18
Q
Main clinical difference between ACEi and ARB
A
ACEi causes more dry cough and angioedema SE
- Increased bradykinin concentration
- Bradykinin and prostaglandin idiosyncratic reactions, increased sensitivity of bradykinin-dependent airway sensory nerve fibres
- Bradykinin and substance P induce inflammatory like reactions which causes vasodilation, plasma extravasation –> angioedema
ARB does not interfere with bradykinin/NO concentration –> no dry cough SE
19
Q
Common AE of ACEi and ARB
A
Severe hypotension
- dizziness, faintness, lightheadedness
Hyperkalemia
- Increase aldosterone –> increase Na excretion = Increase K retention
Acute renal failure
- Less AG2 effect–> vasodilation = reduce renal perfusion –> impairs GFR
Dry cough + Angioedema (More in ACEi)
20
Q
Contraindications of ACEi and ARB
1 Absolute CI
+ Others
A
Pregnancy
Hyponatremia
Hyperkalemia
Hx of angioedema
Volume depletion
Bilateral renal artery stenosis
21
Q
List the different types of BB (in terms of the receptors they act on) + examples
A
Cardioselective BB (Selectively inhibits B1 receptors)
- Bisoprolol
- Atenolol
- Metoprolol
Non selective BB (Inhibits B1 and B2 receptors)
- Propranolol
- Timolol
BB with intrinsic sympathomimetic activitity (stimulates B receptors partially)
- Pindolol
- Penbutolol
BB that inhibits alpha1 and beta receptors
- Carvedilol
- Labetalol
22
Q
Clinical significance of BB with intrinsic sympathomimetic activitity
A
Can be used when patients require BB but experience severe bradycardia from other BB
23
Q
Clinical significance of BB that inhibits alpha 1 and beta receptors
A
Less effects on HR and CO than pure BB
24
Q
How exactly does BB help lower BP
A
Beta-1 adrenoreceptor blockade inhibits adenylyl cyclase from conversion of ATP to cAMP hence reduce PKA activation from activating Ca2+ channel –> reduce Ca2+ influx = reduced contractibility of heart
25
AE of BB
Hypotension
Bronchospasm/bronchoconstriction
Heart block
Bradycardia
Insomnia/vivd dreams
Depression
Fatigue
Impotence
25
How does BB cause bronchospasm as a SE?
B2 blockade on smooth muscle of blood vessels in the bronchus causes bronchoconstriction
26
Contraindications of BB
Asthma
2nd/3rd degree heart block
Systolic HF
27
Mechanism of CCB + Difference between DHP and non-DHP CCB
Calcium ion influx inhibitors
- Reduction in Ca ion influx = reduce release of Ca from internal stores, less Ca binds to troponin C -->
1. At cardiac muscles reduces cardiac contractibility (lowered CO)
2. At vascular smooth muscles --> allows vasodilation (reduce TPR)
Non-DHP CCB: more on cardiac contractibility
DHP CCB: more on vascular muscle tone + cardiac
28
Examples of DHP and non-DHP CCB + Which is used for:
1. Anti-arrhythmia
2. Anti-angina
3. Anti-hypertension
DHP CCB: nifedipine, amlodipine, felodipine
nonDHP CCB: diltiazem SR, verapamil SR
1. Anti-arrhythmia: nDHP
2. Anti-angina: DHP
3. Anti-hypertension: DHP
29
Common SE of CCB (across both classes)
Hypotension
- Dizziness, lightheadedness
Flushing
Peripheral edema
- More in DHP CCB
Headache
30
SE unique to DHPCCB
Tachycardia
Gingival hyperplasia (Nifedipine)
30
SE unique to nDHPCCB
Bradycardia
Constipation (Verapamil)
AV block
Systolic HF
31
Important DDI to look out for in nDHP CCB
Digoxin interaction
32
CI for CCB (for the 2 different classes)
DHPCCB
- Severe hypotension
nDHPCCB
- Systolic HF
- 2nd/3rd degree AV block
- Sick sinus syndrome
- Severe hypotension
33
Formulation preferred for DHP CCB
Long acting/Sustained release
34
Important administration counselling point for CCB
Swallow whole
35
List the different classes of diuretics + examples
1. Thiazide / Thiazide-like
- Chlorthalidone
- Hydrochlorothiazide
- Metolazone
- Indapamide
2. Loop
- Frusemide
- Bumetanide
- Torsemide
3. Potassium sparing
- Mineralcorticoid receptor antagonist: Spiranolactone
- Eplerenone
4. Osmotic
- Mannitol
36
Which classes of diuretics causes
1. Hyperkalemia
Potassium sparing diuretics (including MRA like spiranolactone)
37
Which classes of diuretics causes
1. Hypokalemia
Loop diuretics and Thiazide/thiazide-like diuretics
38
SE of diuretics --> can we look at this together (the electrolyte changes)
Changes in K levels (Hypo/hyper)
Hyperuricemia (diuretic causes lower fluid volume so higher conc of uric acid)
Increased urination
Hyperglycaemia
Hyponatremia
39
Unique SE to spiranolactone, eplerenone
Gynaecosmastia
Hirsutism
Menstrual irregularities
40
CI of thiazide diuretics
Persistent anuria/oliguria
Advanced kidney failure
41
In what situation is loop diuretic more effective/suitable than thiazide
In severe CKD/failure
- where thiazide is CI but loop is not (can still be used)
Loop is diuretic of choice if pt has severe CKD
42
Special populations to monitor during use of diuretics
DM
Gout
43
Which class of diuretics are considered weaker diuretics, often used in combination with others and why?
Potassium sparing
- Use with Thiazide to minimise K+ lowering effects
44
What antihypertensive class should be avoided when pt has concomitant congestive HF
CCB (more on nDHP CCB because of negative inotropic effects)
45
What antihypertensive class should be avoided when pt has concomitant asthma?
BB
46
What antihypertensive class should be used with caution when pt has concomitant renal diseases
ACEi/ARB
Some Diuretics
47
What antihypertensive class should be avoided/used with caution when pt has concomitant DM
BB
(heart beat slower, hard to tell when there is hypoglycemias --> dangerous)
48
What antihypertensive class should be avoided when pt is pregnant
ACEi/ARB
49
Choice of therapy anti-hypertensive for congestive HF
BB + ACEi/ARB
+/-diuretics
AVOID nonDHPCCB
50
Choice of therapy anti-hypertensive for AFib/post MI
BB
2nd line: ACEi/ARB
51
Choice of therapy anti-hypertensive for DM patient (if proteinic?)
Any firstline
- Opt for ACEi if proteinuric
52
Antihypertensive for Pregnant patients (3)
Labetalol
Nifedipine
Methyldopa
53
Choice of therapy anti-hypertensive for pt with BPH
alpha blockers
54
Usual choice of antihypertensive for elderly
CCB/Diuretics
55
BP targets to titrate against for elderly
65-80yo:
Aim <150mmHg --> then aim for <140mmHg --> then aim for 130mmHg if tolerated
56
When do we start antihypertensive tx for elderly >80yo
When BP>160/90mmHg
56
BP treatment target for normal adults and for pt with comorbidities
normal: <120-130 / 70-80mmHg
comorbidities: <130/80mmHg
57
Number of drugs to start HTN patients on
G1: 1 drug
G2-3: 2 drugs
58
Safety monitoring parameters for various antihypertensive classes + TCU intervals
ACEi/ARB --> TCU:1-2wk
- Renal Panel (SCr, K, urea)
- Presence of dry cough/angioedema
BB --> TCU: 2-4wk
- PR
CCB --> TCU: 2-4wk
- PR
Diuretics --> TCU1-2 wk
- Renal panel (SCr, K, urea, +/-Na)
59
Causes of resistant HTN
Inadequate dosing
Non-adherence
Obesity, OSA
Diet: excessive Na, alcohol intake
Volume overload (heart/kidney disease)
Insufficient diuretic tx
Improper BP measurement
60
Definition of heart failure
Failure to pump at sufficient rate
OR
Ability to pump at elevated filling pressure (after compensation)
61
3 main factors that affect cardiac output + examples
1. Preload (Volume)
- Eg. Haemorrhage
2. Heart (Contractibility, HR)
- Myocardial infarction
- Bradycardia
3. Afterload (Resistance)
- Hypertension
62
Acute presentation of heart failure
Sympathetic activation + Parasympathetic inactivation
- Increase HR
- Increase strength of contractions
- Sweating
- Chest pain
63
Long term presentation of heart failure
RAAS activation
- Oliguria
- Increased fluid accumulation --> oedema, breathlessness (pulmonary oedema)
- Remodelling of heart and blood vessels --> worsens HF
64
Why RAAS activation in HF is maladaptive?
1. Fluid reabsorption by kidney
- Can only help to increase CO to a certain limit
- Beyond that will just be causing edema, breathlessness
2. AG2
- Causes remodelling of heart --> inflammation, fibrosis, hypertrophy
- Increases vasoconstriction and stiffening of material walls --> increase workload heart
65
Types of heart failure and the respective ejection fraction + Normal ejection fraction
Normal EF: >60%
HFrEF
- EF/= 50%
66
Equation of Ejection Fraction
SV/End Diastolic Volume x 100%
- % of blood pumped out over the total amount of blood in ventricle right before systole
67
What role does the natriuretic peptide system play in HF
Counteract RAAS to reduce heart workload
- Natriuretic peptides (ANP and BNP) released from ventricle helps to increase GFR, increase vasodilation and decrease renin --> decrease AG2 & aldosterone --> reduce BP
68
Which three drug classes commonly used to counteract RAAS in HF
ACEi
Diuretics
ARNi (Angiotensin Receptor Neprilysin inhibitor)
- Utilises the natriuretic peptide system
69
MOA of ARNi
(Clue: add in the cons + which drug should also be used in combination)
Inhibit neprilysin from breaking down natriuretic peptides --> promote diuresis and vasodilation
BUT also inhibits breakdown AG2 --> should be used in combination with ARB
70
Should ARNi be used in combination with ACEi? Why?
No.
Both ARNI and ACEi increase concentration of bradykinin --> causes cough + massive vasodilation (BP drops)
71
List the 4 stages of HF
Stage A: At risk
- At risk for HF but w/o current or previous s/sx of HF and w/o structural or functional heart diseases or abnormal biomarkers
Example: HTN, CVD, DM, obesity, exposure to cardiotoxic agents, genetic variant for cardiac myopathy, family Hx of cardiomyopathy
Stage B: Pre-heart Failure
- W/o current or previous s/sx of HF
AND 1 of the following:
Structural heart disease
Increased filling pressure (eg. reduced ejection fraction)
Increased natriuretic peptide levels
Increased cardiac troponin levels
Stage C: Symptomatic Heart Failure
- Current or previous s/sx of HF
Stage D: Advanced Heart Failure
- Marked HF sx that interfere with failure life + recurrent hospitalisations despite attempts to optimise guideline-directed medical therapy
72
How is HF diagnosed? (Labs, Clinical presentation, Diagnostic tool)
S/Sx
- Dyspnoea
- Orthopnoea
- Ascites (loss of appetite, swelling/discomfort in abdomen)
- Confusion/hallucination
- Swelling of peripheral lower limbs --> Observed in sudden 2-3kg weight gain in a week
Labs
- Natriuretic peptide levels: NT-proBNP>125pg/ml; BNP ≥ 35pg/ml
ECG
Transthoracic echocardiography
73
New York Heart association classification of HF (Class 1-4)
Class 1: No s/sx
Class 2: Comfortable at rest; slight limitation of physical activity (ordinary physical activity cause fatigue, palpitation, dyspnoea)
Class 3: Comfortable at rest; marked limitation of physical activity (less ordinary physical activity cause fatigue, palpitation, dyspnoea)
Class 4: S/sx at rest
74
HFrEF Pharmacotherapy Choice of Drugs Classes + Examples
Fantastic 4
1. ACEi/ARB/ARNi
2. BB (Bisoprolol, Carvedilol, Metoprolol XL)
3. SGLT2i (Empaglifozin, Dapagliflozin)
4. Mineralcorticoid Receptor Antagonist (Spiranolactone)
+/- Diuretics (eg. frusemide, bumetanide, metolazone)
75
Which class of diuretic is preferred in HFrEF
Loop diuretics
76
Target HR for HFrEF patient
50-70bpm
77
What to do if HFrEF patient 's BP is already quite low, but HR still >70bpm?
Since patient is on maximally tolerated BB, add on ivabradine to lower HR to target without furthering lowering BP
78
MOA of ivabradine + what indication is it used for
Slows down SA node firing --> Lowers HR for HFrEF patient, angina
79
AE of ivabradine
Bradycardia
HTN
AFib
80
What should be done if a HFrEF patient on Fantastic 4 + Ivabradine develops AFib as well?
Stop Ivabradine (worsens AFib)
81
CI of ivabradine
Sick Sinus Syndrome
Acute decompensated HF
Sinoatrial block
Third degree AV block
Bradycardia (<70bpm)
Severe hepatic impairment
Concomitant strong CYP 3A4i
82
For a HF patient, when can ivabradine be initiated?
Upon compensation.
HF patient who are symptomatic + fluid overload --> Do not initiate
83
For HFrEF patient, when should SGLT2i be initiated? Under what conditions/what should we check before initiating?
Start after compensation with chronic loop diuretics
Ensure no:
- Diabetic ketoacidosis
- IV inotrope/vasodilator within 2 days
- IV diuretics
- SBP>100mmHg
84
What labs/clinical presentation should be monitored/looked out for when HFrEF pt is on F4? + General TCU period
ACEi/ARB/ARNI: Renal panel (K, SCr, urea), BP --> 1 wk after initiation
BB: BP, PR, clinical status (SE of BB)
SGLT2i: Renal panel, BP, Genitourinary tract infections, euglycemia ketoacidosis --> TCU 2-4 wks
MRA: RP (SCr, K, urea), BP, Gynaecosmastia (TCU 1 week)
Diuretics:
- Renal panel (SCr, K, urea), body weight
85
When should BB be initiated and adjusted for HFrEF pt
After compensation, when stable.
DO NOT UPTITRATE IF OVERLOADED
86
What to note when patient is switching from ACEi to ARNI?
36h washout period
87
What to note/add to patient's tx plan when patient is on loop diuretic?
KCl replacement if necessary
88
Patient counselling points for HFrEF
1. Fluid restriction (1.5-2L)
2. Reduced sodium intake 2–3 g/d (5–7.5 g/d salt)
3. Increase K intake if necessarily (food rich in K: spinach, chickpeas, broccoli, banana etc.)
3. Weigh themselves in the morning after peeing, record in daily weight chart
Be alarmed if >2kg increase overnight or over a few days
4. Managing expectations
- Time taken to feel Bette
- AE of medications
89
Important pt counselling point for BB
Takes up to 3-6mths for maximal benefits + Paradoxical worsening of sx initially
90
What is observed on the ECG for AFib vs Atrial Flutter?
AFib:
- Regularly irregular rhythm
- Irregular RR intervals
- No P wave
Atrial flutter
- Sawtooth appearance
- Regular RR intervals
91
Diseases commonly associated with AFib
HF
Longstanding poorly controlled HTN
Disorder of heart valves
92
What is Torsades de Pointes?
A type of life-threatening ventricular tachycardia as a result of QTc prolongation
93
Common drugs associated with QTc prolongation
Class 1a and 3 antiarrhythmic drugs
Antimicrobials
Antipsychotics
Antidepressants
94
One of the most prominent sequelae of AFib
Stroke
- Irregular rhythm leads to turbulent flow and blood accumulation causing clot formation and embolisation
95
What are the 2 main ways to manage AFib?
How to decide which way to manage?
Rate control and Rhythm control
1. Usually opt for rate control first
- If symptomatic despite well-controlled HR --> Rhythm control
2. Opt for Rhythm control if:
- Young (<65yo)
- High likelihood of maintaining sinus rhythm: 1st AF ep, AF precipitated by temporary event (acute illness), recent onset of AF
96
What is the target HR in rate control for AFib patients?
97
Apart from rate/rhythm control for AFib patients, what else should be considered for the care plan?
Stroke prevention using anticoagulant
98
How does rate control in AFib works? (Rate of what?)
Slows down the rate of AV node conduction
- Prevents multiple stimuli from being conducted through AV node and reaching ventricles
99
What are the 4 main classes of drugs used in AFib treatment for rate control?
(ABCD)
Amiodarone
Beta-blockers
CCB (Non-DHP)
Digoxin
100
Amongst the classes of drugs used in Afib, what cannot be used for patients with concomitant HFrEF?
Non-DHP CCB
101
Amongst the classes of drugs used in Afib, what cannot be used for patients with concomitant thyroid diseases?
Amiodarone
- Similar structure to thyroid hormones
102
Firstline tx for AFib with no comorbidities + Decided on rate control
Beta-blocker / Non-DHP CCB
103
Firstline tx for AFib with asthma/severe COPD + Decided on rate control
Non-DHP CCB
104
Firstline tx for AFib with HFrEF + Decided on rate control
Beta-blocker
105
What can be added on for a AF patient on BB for rate control but HR still above target?
(What is target HR? + 2nd line, 3rd line drug)
Target: 80bpm
Add on Digoxin (2nd line), or Amiodarone (3rd line)
AVOID using BB with NonDHP CCB
106
Target HR for patient with HFrEF + AFib
Target the lower number (which is HFrEF target)
<70bpm
107
If new AF onset patient is going for rhythm control, what drugs can be given?
- Given that patient has no structural heart disease
Class 1C and 3 Anti-arrhythmic drug
(Safe People Die First)
- Sotalol
- Propafenone
- Dronedarone
- Flecainde
108
If new AF onset patient is going for rhythm control, what drugs can be given?
- Given that patient has structural heart disease (eg. HFpEF, CAD, significant valvular disease)
Only class 3 Anti-arrhythmic drug
(SAD)
- Sotalol
- Amiodarone
- Dronedarone
109
If new AF onset patient is going for rhythm control, what drugs can be given?
- Given that patient has HFrEF
Only Amiodarone
110
MOA of Class 1 AAD
Na channel blockers
- Decreases rate of depolarisation --> decreases slope in phase 0
111
MOA of Class 3 AAD
K channel blockers
112
Examples of class 1c AADs
Flecainide
Propafenone
113
AE of Flecainide (What class is flecainide?)
Class 1C AAD
(Fleas Are Very Gross)
- Giddiness
- Visual disturbance
- Acute decompensated heart failure
114
AE of Propafenone (What class is propafenone?)
Class 1C AAD
(Pope Has A Dainty Magical BB)
- Dizziness
- Metallic taste --> N/V
- Bradycardia
- Heart block
- Bronchospasm
- Acute decompensated heart failure
115
DDI of Flecainide
Amiodarone
Digoxin
116
DDI of Propafenone
Digoxin
Warfarin
CYP interactions
117
Which class of AAD cannot be given to AF patient with valvular heart disease/HFrEF? Why?
Class 1C
- Increases mortality and pro-arrhythmic after MI
118
What BB are used in AFib patients (PO and IV)
IV: Esmolol, Metoprolol
PO: Atenolol, Bisoprolol, Metoprolol, Carvedilol
119
MOA of amiodarone
K channel blocker
120
Why is amiodarone used very cautiously as only 3rd/4th line?
Extensive extra cardiac SE profiles + High potential for DDI (CYP inhibition)
121
What CYP are inhibited by amiodarone?
1A2, 1C9, 2D6, 3A4
122
Monitoring parameters when AFib patient is on amiodarone?
TFT, LFT, Chestxray, ECG, Annual eye checkups
123
AE of amiodarone
Pulmonary fibrosis
Hypo/Hyperthyroidism
Optic neuritis/neuropathy
Hepatic toxicity
Bradycardia
Ataxia/Peripheral neuropathy
Photosensitivity
124
DDI of amiodarone
Digoxin
Warfarin
125
Examples of Class 3 AAD
Sotalol
Dronedarone
Amiodarone
126
SE of sotalol (think of BB)
Sota Breeds Artistic Hearts But Quitepainful
Bradycardia
ADHF
Heart block
Bronchospasm
QTc prolongation
127
What condition (non-CVD) to take note of when patient has angina? What to be cautious of when giving medication for this condition?
Erectile dysfunction.
Concomitant administration of PDE5i for ED may cause life threatening hypotension --> Space apart
24h: sildenafil, vardenafil
48h: tadalafil
128
Which BB to avoid in patients with active liver disease?
Propanolol
Metoprolol
129
Which BB to avoid in pt with CKD?
Atenolol
Sotalol
130
Describe the various kinds of lipoproteins in our body (4 kinds: how is it synthesised)
1. VLDL
- Synthesised by hepatocytes (endogenously)
2. IDL
- VLDL loses TG to form IDL and fatty acids
- Fatty acids is taken up by peripheral adipocytes and muscles for ATP production
- IDL can be re-taken up by hepatocytes for reprocessing or loses further TG to form LDL
3. LDL
4. HDL
- Produced in liver
131
Roles of LDL and HDL
LDL
- bad cholesterol
- In high amount, deposits around smooth muscle fibres in arteries resulting in plaque that may rupture --> increasing risk of CAD
HDL
- Removes excess cholesterol from blood and body cells and transport them to liver for elimination
- Prevents accumulation of cholesterol in the blood
132
2 sources of cholesterol in body
1. Endogenous (synthesised by liver)
2. Exogenous (absorbed through diet)
133
What is the cause of Familial Hyperchylomicronemia (Class 1)?
- What levels are high?
Deficiency of lipoprotein lipase
- High chylomicrons + TG levels (+++)
- Cholesterol (+)
134
What is the cause of Familial Hypercholesterolemia (Class 2A)?
- What levels are high?
Decreased number of normal LDL receptors
- High LDL
- Cholesterol (++)
- TG (NIL)
135
What is the cause of Familial Combined Hyperlipidemia (Class 2B)?
- What levels are high?
Overproduction of VLDL in liver
- High LDL and VLDL
- Cholesterol (++)
- TG (++)
136
What is the cause of Familial dysbetalipoproteinemia (Class 3)?
- What levels are high?
Overproduction/Underutilisation of IDL
- High B-VLDL
- Cholesterol and TG (++)
137
What is the cause of Familial Triglyceridemia (Class 4)?
- What levels are high?
Overproduction/decreased removal of VLDL
- High VLDL
- TG (++)
- Cholesterol (+)
138
What is the cause of Familial mixed hypertriglyceridemia (Class 5)?
- What levels are high?
Increased production/decreased clearance of VLDL and chylomicrons
- High VLDL, Chylomicrons
- Cholesterol (+)
- TG )++)
139
Which types of dyslipidemia causes high ASCVD risk?
Class 2a Familial Hypercholesterolemia
Class 2b Familial combined hyperlipidemia
140
What are some drugs that may cause high TG?
Estrogen contraceptive
Systemic glucocorticord
Non selective BB
Loop/thiazide diuretics
Antiretroviral protease inhibitors
Atypical antipsychotics (clozapine, risperidone)
141
MOA of statins + what kinds of hyperlipidemia is it effective for
HMG-CoA Reductase inhibitor
- inhibit HMG-CoA Reductase which is responsible for cholesterol synthesis in liver --> reduces cholesterol synthesis
- low intracellular C --> upregulates LDL receptor to uptake LDL into cell
Effective for all hyperlipidemia
142
List the drug classes used for hyperlipidemia
Statins
Ezetimibe
PCSK9i
Fibrates
Bile acid binding resins
Omega 3 acid ethyl esters
Niacin
143
Range of LDL reduction (%) possible by statin
21-63%
144
Range of LDL reduction (%) possible by ezetimibe as
1. Monotx
2. On top of statin
3. On top of cholestyramine
1. 15-22%
2. 21-27%
3. 10-20%
145
Range of LDL reduction (%) possible by PCSK9i as
1. Monotx
2. On top of statin + ezetimibe
1. 46-73%
2. Additional 30%
146
Range of LDL reduction (%) possible by cholestyramine
18-25%
147
Range of LDL reduction (%) possible by Niacin
5-25%
148
Range of LDL reduction (%) possible by fenofibrate
30-31%
149
Range of TG reduction (%) possible by statin
10-20%
150
Range of TG reduction (%) possible by Niacin
20-50%
151
Range of TG reduction (%) possible by fenofibrate
30-50%
152
Range of TG reduction (%) possible by omega-3 FA
20-61%
153
Amongst the drug classes for hyperlipidemia, which are effective in LDL reduction?
Statin
Ezetimibe
PCSK9i
Cholestyramine
Fenofibrate
154
Amongst the drug classes for hyperlipidemia, which are effective in TG reduction?
Statin
Fenofibrate
Niacin
Omega3 FA
155
Baseline monitoring parameters upon initiation of a lipid lowering agent (eg. statin) + Threshold to allow initiation
Lipid panel
ALT (Within 3x ULN)
CK (Within 4x ULN)
156
When do you need to repeat monitoring labs after initiation of lipid lowering agent
Lipid panel (4-8 weeks after initiation) then annually
ALT 8-12 weeks then no need routine monitoring
CK no need routine monitoring; check when patient presents with SAMS
157
When are statins usually administered? Why? (any exceptions?)
ON -->
because HMG-CoA reductase in endogenous pathway is most active (since no food taken, so less exogenous pathway)
Except Atorvastatin and Rosuvastatin which can be taken OM due to long t1/2
158
Where are statins eliminated?
Metabolised mainly in liver
159
AE of Statins
Myalgia (muscle pain with normal CK)
Myositis (CK>ULN)
Rhabdomyolysis (CK>10xULN + renal injury)
Myoglobinuria (redrawn urine colouration)
New onset DM
Hepatic failure (ALT>3xULN)
Memory and cognition
160
Risk factors for Statin Associated Muscle Symptoms
>75yo
Female
Low BMI
Asian
Genetic factors (CYP450 mutation)
DDI
High level of physical activity
Impaired kidney function
Liver impairment
Hypothyroidism (under/untreated)
Diet (grapefruit juice, alcohol, drug abuse)
Acute infection
161
Under what circumstance do you need to stop statins tx?
1. S/sx of muscle injury: regardless of CK levels
2. S/sx of malaise fatigue nausea
3. CK>5xULN
4. ALT>3x ULN
5. AST>5xULN
162
CI of statin
Pregnant
Lactation
Teenagers/children (lack of cholesterol affects neurodevelopment)
Active liver disease
Persistence increase in transaminases
163
What should be done if a female patient on statin intends to try conceiving?
Stop statin 4 weeks prior to cessation of contraceptives
164
How many % of LDL reduction can doubling of statin dose achieve?
6-7%
165
How many % of LDL reduction can 40mg atorvastatin achieve?
~50%
165
Rank the statins according to decreasing potency
Rosuvastatin
Atorvastatin
Simvastatin
Lovastatin; Pravastatin; Fluvastatin
166
Patient counselling points on statin initiation
Potential SAMS SE
- May cause muscle pain, tenderness, weakness
- Risk of these SE increases with low thyroid function, poor kidney function, if you take with other drugs or if you are >65yo.
Severity of SE
- Sometimes, severe muscle problem may lead to kidney problems (rhabdo)
- Rarely, deaths have happened
Contract patient
- Contact doctor right away in case of any abnormal muscle discomfort and if these symptoms persists even after your doctor has asked you to stop
Potential Liver Injury
- Very bad and sometimes deadly liver problems have occured BUT this is very rare
- Look out for symptoms like: reddish brown urine, light coloured stools, yellow skin/eyes, malaise, throwing up, not hungry, upset stomach or stomach pain --> pls contact your dr right away
167
Which statin is not affect by CYP3A4 inhibition/DDI?
Rosuvastatin
168
What are the DDI (Category X or D) with statins?
Amiodarone
Gemfibrozil
169
What is a Class C DDI with statins?
Colchicine
170
How much LDL reduction can High Intensity Statin achieve?
List the High Intensity Statins
>50%
- Atorvastatin 40-80mg
- Rosuvastatin 20-40mg
171
How much LDL reduction can Moderate Intensity Statin achieve?
List the Moderate Intensity Statins
30-49%
- Atorvastatin 10–20 mg, Lovastatin 40–80 mg, Pitavastatin 1–4 mg, Pravastatin 40–80 mg, Rosuvastatin 5–10 mg, Simvastatin 20–40 mg
172
MOA of PCSK9i
Inhibits PCSK9 enzyme which is involved in LDL receptor degradation
- Hence more LDL receptors can uptake and internalise circulation LDL
173
What kinds of hyperlipidemia is PCSK9i useful for?
Type 2A and 2B
174
Disadvantage of using PCSK9i?
Biologic requires administration via injection
175
Examples of PCSK9i
Evolucumab, Alirocumab
176
MOA of fibrates
Ligand of PPAR-a which increases activity of lipoprotein lipase --> increase TG breakdown to reduce TG levels
- Can also decrease VLDL secretion by liver and hence lower LDL
- Moderate HDL increase
177
Given that a patient is currently on statin and has a TG>5.6mmol/L, what should be added to his tx?
Fibrates
- Opt for Fenofibrate
Avoid gemfibrozil due to DDI
178
Compare the 2 types of Fibrates in terms of:
- Administration timing
- CV outcomes
- CV mortality
- Renal CI threshold
Fenofibrate:
- With meals
- No improved CV outcome
- No improved CV mortality rate
- CrCl<30ml/min
Gemfibrozil
- 30min before meal
- Improved CV outcome
- No improved CV mortality rate
- CrCl<10ml/min
179
Compare and contrast angina and MI (similarities and differences)
Similarities: they happen when there is a mismatch between demand and supply of oxygen (blood flow) to the cardiac muscles.
Differences:
- Angina is reversible → can be relieved with rest or when exercise stops VS MI is Irreversible → no oxygen to cardiac muscles, muscle will die
- In angina, the blood vessel not completely blocked VS in MI, Blood vessel completely blocked → no blood flow
180
Monitoring parameters for fibrate
LFT (routine testing)
SCr
181
CI of fibrates
Liver impairment
182
MOA of omega 3 FA in hyperlipidemia
Reduce hepatic TG production
- EPA and DHA are poor substrates for enzyme involved in TG biosynthesis
Increase TG clearance from VLDL
183
How is omega-3 FA eliminated
Metabolised in liver
184
Example of omega-3 FA
Omacor (460mg EPA, 380mg DHA)
185
Symptoms of myocardial ischaemia
- Pressure, burning sensation in chest (may radiate to neck, shoulder, jaw, back, upper abdomen, either arm)
- Dyspnea
- Diaphoresis (sweating)
- Nausea
- Decreased exercise tolerance
- Pain scale usually >5
186
When should omega 3 be taken?
Take with food for increased bioavailability
187
DDI of omega3
Blood thinners
- Reduces thromboxane A2 production --> Increases risk of bleeding
188
Counselling of AE for omega 3
Fishy taste
Burping
Diarrhoea
Nausea
189
Which of the lipid lowering agent has the most potent HDL increasing effect?
Niacin
190
MOA of niacin
Strongly inhibit lipolysis in adipose tissue hence lower TG in VLDL and cholesterol (in VLDL and LDL)
Also decreases circulating fibrinogen and increasing tissue plasminogen activator → reverse thrombosis a/w hypercholesterolemia and atherosclerosis
Potent increase in HDL
191
What are examples of chronic coronary syndrome?
- stable angina
- stable ischaemic heart disease
192
What are examples of acute coronary syndrome?
- ST elevated MI (STEMI)
- Non ST elevated MI
- Unstable angina
193
What types of hyperlipidemia can Niacin be used for?
Type 2b and 4
194
AE of Niacin
Flushing
Pruritus
Hyperurecemia
Gout
Niacinamide Good For Pimple
195
Types of angina + their characteristics
- stable angina (triggered by physical activity or strong emotions, usually lasts <5 min, relieved by s/l GTN)
- unstable angina (blood clots that may partially dissolve and form again --> blocking blood flow, requires PCI procedure)
- microvascular angina (spasms within walls of very small arterial blood vessels, can last 10-30min)
- vasospastic or variant angina (spasm in coronary* arteries, can occur at rest, relieved by medications)
196
MOA of cholestyramine + what is the class of drug
Bile acid binding resins
- Binds to (-) bile acids and salts in small intestine
- Hepatocytes increases conversion of cholesterol into bile acid hence reducing intracellular cholesterol concentration
- LDL uptake into hepatocytes increases hence reduces plasma LDL
197
Important patient counselling points for cholestyramine
Space apart 1-2h before or 4-6h after taking other medications
198
Which type of hyperlipidemia is cholestyramine useful for?
Type 2A
199
What is the main issue with usage of cholestyramine?
It increase TG levels
200
MOA of ezetimibe
Selectively inhibits cholesterol transport protein in small intestines and hepatocytes
201
Main symptoms for typical angina
1. discomfort in the front chest or nexk, jaw, shoulder, arm
2. precipitated by physical action
3. relieved by rest or nitrates within 5 min
202
Which lipid level is reduced with ezetimibe?
LDL
203
Place in therapy of ezetimibe
Add on to statin or when statin is intolerable
204
AE of ezetimibe
URTI
Sinusitis
Arthralgia
Limb pain
Diarrhoea
205
Non-pharmacological advice for hyperlipidemia
Avoid dietary transfats
Reduce dietary saturated fats --> replace with mono-/polyunsaturated fats
Replace animal fats with vegetable sources
Reduce dietary cholesterol
Reduce intake of mono-/disaccharides
Reduce alcohol intake
Increase dietary fibre
Use red yeast rice (??)
Lose excessive body weight
Increase physical activity
Quit smoking
206
Differential diagnosis for chest pain
- Cardiac (MI, angina, pericarditis, aortic dissection)
- GI (oesophageal spasm, GERD, pancreatitis, esophageal rupture, mediastinitis)
- Respiratory (pulmonary embolism, pneumothorax, pneumonia)
- Musculoskeletal (trauma, costochondriasis)
207
Examples of food preferred for hyperlipidemia
Wholegrains
Raw/cooked vegetables
Soybean
Fresh/frozen fruits
Non caloric sweeteners
Lean, oily fish
Skinless poultry
Skimmed milk/yogurt
Vinegar, mustard, fat-free dressings
Use grilling, boiling, steaming
208
Risk factors for angina / IHD
- family history
- hyperlipidemia
- diabetes
- hypertension
- smoking
- lifestyle factors
209
Main sequelae of high LDL levels
ASCVD
- LDL deposit on vascular walls → can get inflamed (bc plaque attracts WBC) and the plaque may rupture → block blood vessel lumen → cause thrombus → may lead to heart attack, stroke, artery diseases etc.
210
Risk factors of hyperlipidemia patients who have VERY HIGH ASCVD risk + target LDL level
<1.4-1.8mmol/L
FH
ASCVD (established CAD, ASCVD, aortic aneurysm, PAD)
DM + CKD
211
What medications are used for standard treatment of angina?
1. BB or CCB
2. BB + DHP CCB
3. Add 2nd line drug
212
Risk factors of hyperlipidemia patients who have HIGH ASCVD risk + target LDL level + 10-year risk score
<1.4-1.8mmol/L
Risk score>20%
- DM (with other ASCVD RF, >10yrs, microalbuminuria, TOD)
213
What medications are used for angina treatment in a patient that has HR>80bpm?
1. BB or non-DHP CCB
2. BB + non-DHP CCB
3. Add Ivabradine
4. Ranolazine or trimetazidine
214
Risk factors of hyperlipidemia patients who have MODERATE ASCVD risk + target LDL level + 10-year risk score
<2.6mmol/L
Risk score10-20%
DM<10 yrs + no RF
215
What medications are used for angina treatment in a patient that has HR<50bpm?
1. DHP-CCB
2. Long-acting nitrates
3. DHP CCB + long-acting nitrates
4. Ranolazine or trimetazidine
216
What medications are used in a patient who has hx of heart failure and was recently diagnosed with angina?
1. BB
2. Add long-acting nitrates or Ivabradine
3. Add 2ndline drug
4. Ranolazine or trimetazidine
217
Target LDL for low ASCVD risk hyperlipidemia patient
<2.6mmol/L
218
Firstline tx for patient with TG 6mmol/L with low-moderate ASCVD risk
Lifestyle + fibrate
- Add on statin if needed
219
What medications are used for angina treatment in a patient who has low blood pressure?
1. Low dose BB or Low dose non-DHP CCB
2. Add low-dose long-acting nitrates
3. Add Ivabradine or Ranolazine or Trimetazidine
220
Target TG level in general for patients
<5.6mmol/L
221
Target TG levels for patients with high CV risk
<2.3 mmol/L
222
Tx plan for patient with TG 4mmol/L with HIGH CV risk if:
1. Not on statin
2. On Statin
Both lifestyle +
1. Start statin
2. Add on fibrate to statin
223
What lipid lowering agents are considered safe for pregnant women?
Cholestyramine (bile binding resins)
PCSK9i -->No data to support
Others are CI
224
MOA of nitrates for angina
biotransformation and release NO → cause vasodilation → increase oxygen supply + reduce oxygen demand (by reducing preload, myocardial wall tension and myocardial volume oxygen)
225
SE of nitrates for angina and how to mitigate them
- Hypotension
- Dizziness
- Headache (usually resolves in 2 weeks with continued therapy) → can treat with paracetamol
226
nitrates can be used for both prevention and relief of symptoms in angina, what is something to note in the frequent use of nitrates?
- Nitrate tachyphylaxis (decreased response to medication):
- Occurs with long-acting nitrates
- Can be managed by maintaining nitrate-free interval: 10-14h daily ( → preferably at night since angina usually occur in the day with physical activity)
227
List the types of nitrates used for angina and their doses
1. Short-acting glyceryl trinitrate (GTN), 0.5mg/tab
2. Short-acting GTN spray, 0.4mg/spray
3. Long-acting GTN patch, 0.2-0.4mh/hour
4. Long-acting isosorbide dinitrate IR tab, 10-60mg q4-6h
5. Long-acting isosorbide mononitrate SR tab, start 60mg, titrate to 30-120mg/day
228
Which nitrate formulation has the fastest onset?
Sublingual GTN, onset in 1-3 min
(GTN spray has onset in 2-4 min)
229
Counselling points for sublingual glyceryl trinitrate in angina treatment?
- Place tablet under your tongue and allow it to dissolve completely. You may chew the tablet to small pieces to facilitate absorption but do not swallow it
- If using for angina prevention, dissolve tablet under your tongue before engaging in activities that may cause an angina attack
- Take medication at 1st sign of angina attack (eg. chest heaviness/pain, dyspnea). Do not wait until severe pain develops. Take medication while seated (bc of hypotension) Do not swallow or eat while using.
- Spit out tablet if it does not dissolve within 5 minutes.
- Medicine usually provides relief in 5 minutes
- If you still have chest pain after 5 minutes, call 995 or go the A&E. Continue to use medication every 5 minutes while going the hospital
- Medication is light-sensitive → keep in brown glass container and close tight
- Store in cool dry place, do not refrigerate.
- Carry them in your bag everywhere you go. Do not keep in your pocket (temperature may affect)
- Write down the date when you opened the bottle. Discard 8 weeks after opening.
230
Does beta blocker selectivity affect the efficacy of BB in angina patients? Any preference in selection of BB?
No, B1 selectivity does not affect the efficacy of BB for angina.
BUT B1 selective preferred in COPD, DM, PAD, dyslipidemia
231
What to consider in the choice of beta blockers for angina treatment in patients with other comorbidities?
- HF: carvedilol, metoprolol XL, bisoprolol
- Atrial fibrillation: sotalol
- CKD: avoid Atenolol
- Obstructive lung disease, asthma: preferably B1 selective BB
232
What to note if beta blocker is discontinued in angina patients and rationale
- Discontinuation of BB is tapered over at least 2 weeks
- Because receptors are upregulated in myocardium during treatment → abrupt withdrawal can cause catecholamine stimulation of receptors → can increase myocardial volume oxygen demand → induce ischemia / MI
233
Which beta blockers to avoid in angina patients with CKD
- Atenolol
- Sotalol
234
List the beta blockers that are mainly eliminated via hepatic route
- Metoprolol IR or XL
- Propanolol
235
List the beta blockers with high lipophilicity and the disadvantage of this
- Carvedilol
- Nebivolol
- Propanolol
High lipophilicity BB easier to pass through blood brain barrier --> may result in more CNS side effects
236
What kind of CCB to avoid in treatment of angina and why?
Short-acting DHP CCB --> Can cause reflex tachycardia
237
When to use DHP CCB vs non-DHP CCB in treatment of angina
- If HR >80bpm or low BP → use non-DHP
- Otherwise → use DHP
238
Which medications for angina treatment should not be used together? but which group of patients is this combination still used in?
BB + non-DHP CCB (initiate at low dose + close monitoring)
This can be used in patients with angina and high heart rate.
239
Which CCB has significant DDIs? and with what?
Verapamil (non-DHP CCB)
- DDI with CYP3A4 and PGP inhibitor
240
Ivabradine DDI
CYP3A4 interactions
241
Ivabradine dose for angina tx
- Initiate at 5mg BD (if pt<75 yo), can be increased after 3-4 weeks of treatment
- Max dose: 7.5mg BD
242
Ranolazine MOA
Largely unknown. Possibly due to mechanisms that improve myocardial function / perfusion.
243
Ranolazine dose for angina tx
Initiate 500mg BD, increase to 1000mg BD within 1-2 weeks if tolerated.
244
Ranolazine AE
- Constipation
- Nausea
- Dizziness
- Headache
- QTc prolongation
(Granola) Quite Costly Nowadays Damn Headache
245
Which medication for angina may be beneficial if the patient also has diabetes?
Ranolazine (2nd line) can help reduce blood glucose (HbA1c by 0.6-0.7%)
246
What to take note of when choosing medication for angina treatment if the patient also has diabetes?
Check if the patient takes Metformin. DDI of Ranolazine with Metformin.
247
Ranolazine DDI + how to mitigate
- Metformin → competes for clearance, increased risk of lactic acidosis
- Ranolazine 1000mg BD → max 850mg BD Metformin
- Ranolzaine 500mg BD → no need to adjust Metformin dose
248
Trimetazidine MOA
unknown. Likely due to beta-oxidation of free fatty acids → switch from FFA oxidation to glucose oxidation → increase cardiac metabolic efficacy
249
Trimetazidine Dose
IR: 20mg TDS
MR: 30mg BD
250
What kind of comorbidities should Trimetazidine not be used in patients with?
- CrCl <30ml/min
- Parkinson’s disease
- Motion disorder
- Restless leg syndrome
- Muscle rigidity
- Walking disorder
251
Trimetazidine use in patients with CKD
CI if CrCl <30ml/min. Otherwise, dose adjustment required.
CrCl 30-60 ml/min: reduce frequency
- IR: 20mg BD
- MR: 30mg OD
252
Risk factor modification in patients with angina
- Smoking cessation, weight management, healthy diet (vegetables, fruit, whole grains), physical activity
- Annual Influenza vaccination: IHD or atherosclerosis have increased risk of influenza
253
BP target in patients with HTN and angina
120-130mmHg
254
Lipid target in patients with hyperlipidemia and angina
Target: LDL<1.4mmol/L + 50% reduction
255
Blood glucose target in patients with DM and angina
- If established ASCVD and/or severe TOD: target HbA1c <8%
- Otherwise, HbA1c<7%
256
What medications to consider if patient has DM and angina?
- Add-on anti-platelet therapy (Aspirin 75-100mg OD, Clopidogrel 75mg OD)
- Aspirin first-line for ACS/CCS
257
What to use for angina treatment if the patient has poorly controlled asthma, heart failure and high heart rate?
1. Ivabradine (pt may alr be on this medication due to HF and BB contraindicated) or LAN
2. Ranolazine or Trimetazidine
258
List the common ACEi used + its starting dose and usual dosage range
Benazepril: 10mg; 20-40mg QD-BD
Fosinopril: 10mg; 20-40mg QD
Lisinopril: 10mg; 20-40mg QD
Enalapril: 5mg; 10-40mg QD-BD
Captopril: 25mg; 50-100mg BD-TDS
259
List the common ARB used + its starting dose and usual dosage range
Losartan: 50mg; 50-100mg QD-BD
Valsartan: 80-160mg; 160-360mg QD
Candesartan: 16mg; 8-32mg QD-BD
260
List the common cardioselective BB + its usual dosage range
Atenolol: 25-100mg QD-BD
Bisoprolol: 2.5-10mg QD
Metoprolol: 50-100mg QD (XL) -BD
261
List the non selective BB (B1 and B2) + usual dosage range
Nadolol: 40-120mg QD
Propranolol: 40-180mg QD(XL)-BD
Timolol: 20-40mg BD
262
List the mixed a1 and beta blockers + usual dosage range
Carvedilol: 12.5-50mg BD
Labetalol: 200-800mg BD
263
List the common DHP CCB used + usual dosage range
Amlodipine 2.5-10mg QD
Nifedipine SR 30-90mg QD
Felodiprine 2.5-20mg QD
264
List the nDHP CCB + usual dosage range
Verapamil SR: 180-480mg QD-BD
Diltiazem SR: 120-360mg BD
265
List the thiazide and thiazide-like diuretics + usual dosing
Chlorthalidone 12.5-25mg QD
Hydrochlorothiazide: 12.5-25mg QD
Indapamide: 1.25-2.5mg QD
Metalozone: 2.5-5mg QD
266
List the loop diuretics + usual dosing
Bumetanide 0.5-4mg BD
Frusemide: 20-80mg BD
Torsemide: 5-10mg QD
267
Usual dosing of spironolactone
25-50mg QD-BD
268
MOA of methyldopa + dosing
Centrally acting A2 agonist
- Lower BP via reduction of sympathetic tone and norepinephrine release by peripheral sympathetic termination
250-1000mg BD
269
Usual dosing for ezetimibe
10mg QD
270
Usual dosing of gemfibrozil
300-600mg BD
