Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

344 > STABLE ISCHEMIC HEART DISEASE 2.0 > Flashcards

STABLE ISCHEMIC HEART DISEASE 2.0 Flashcards

1
Q

Vascular Protection

Angiotensin Converting Enzyme Inhibitors (ACEI)

Rationale?

A

• Rationale:

  • ↓ progression of atherosclerosis
  • plaque stabilization
  • ↓ neo-intimal formation
  • ventricular remodeling
  • endothelial function
  • fibrinolysis

• properties thought to be independent of blood
pressure lowering effects
- controversial

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Vascular Protection

Angiotensin Converting Enzyme Inhibitors (ACEI)

Place in therapy?

A

• Meta-analysis of 6 trials (n = 33,500)

  • Follow-up x 4.4 yr
    • High risk patients (CAD with preserved LV function)
    • 16% RRR in nonfatal MI
    • 17% RRR in CV mortality
    • 13% RRR in all-cause mortality

• Place in therapy

  • Consider in all patients with IHD in the absence of CI
  • Especially in those with other indications:
    • Post-MI
    • Systolic heart failure (HFrEF)
    • DM nephropathy / CKD
  • ARBs are a reasonable alternative (ONTARGET trial)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Vascular Protection

Angiotensin Converting Enzyme Inhibitors (ACEI)

Adverse Effects?

A

CNS Lightheadedness, dizziness, fatigue BP, postural BP
ENT Angioedema (rare, but life threatening) symptoms
CVS Hypotension +/- orthostasis BP
RESP Dry cough (20%) symptoms
GI Nausea/vomiting, taste disturbance symptoms
GU Renal dysfunction (expect up to 30%↑Scr) SCr, BUN
DERM Rash symptoms
Lytes Hyperkalemia K

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Vascular Protection

Angiotensin Converting Enzyme Inhibitors (ACEI)

Contraindications?

A
  • History of angioedema
  • Bilateral renal artery stenosis
  • Hypersensitivity
  • Pregnancy
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Medical Therapy - Symptom Control

Needs Assessment

A

Does my patient need symptons control?

  • frequency of attacks
  • sSeverity of attacks
  • impact on exercise tolerance
  • impact of ADL
  • impact on QOL
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Medical Therapy - Symptom Control

What are the goals?

A 
Goals:
  • Frequency of symptoms
  • Intensity of symptoms
  • Functional capacity
  • Improve quality of life
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Medical Therapy - Symptom Control

Options?

A

Options:

• First line:
- β-blockers

• Second line:

- Calcium channel blockers (CCB)
- Long acting Nitrates

• Third line:
- Ranolazine ( New to Canada 2021 – refractory
angina)
- Ivabradine (Not indicated in Canada for SIHD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Medical Management of IHD

Summary

A

see slide 14

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Beta-blockers:

anti-ischemic effects

HR, cardiac contractility, myocardial tension = oxygen demand

regional flow distibution, O2 extraction, coronary blood flow = supply

A

• Reduction in HR and contractility = lowering MvO2

• Slight decrease in BP (through reduction in CO,
inhibition of renin) = reduced afterload, lowering
myocardial wall stress and MvO2

• Does not generally improve oxygen supply, although
increased diastolic time may improve coronary
perfusion

• Note: unopposed alpha stimulation may lead to
worsening vasoconstriction in vasospastic angina

(see slide 15 for reference)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Beta-blockers:

anti-ischemic effects

Cardiac effects?

A

Cardiac effects:
B1-receptors in cardiac nodal tissue, conducting system and contracting myocytes

• ↓Cardiac sympathetic tone:

  • Chronotropy (heart rate)
  • Inotropy (contractility)
  • Dromotropy (electrical conduction)
  • Lusitropy (relaxation)

• Vascular effects (minor):
- Mild vasoconstriction (unopposed alpha effects)
- Blocking beta-2 receptors removes vasodilatory
influence that normally opposes the alpha
mediated vasoconstriction

(see slide 16 for reference)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Beta-blockers:

Clinical effects?

A

• Delays or eliminates angina during exercise
- limits in HR & BP during exercise

  • Decreases the needs for short acting NTG
  • Decrease frequency of angina

• No specific agent has proven to be superior
- avoid those acebutolol with intrinsic sympathomimetic
activity (ISA) and sotalol (anti-arrhythmic)
- may worsen vasospastic angina
* Unopposed alpha-blockade

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Beta-blockers:

Why high dose beta-blockers should never be stopped abruptly?

A 
High dose beta-blockers should never be stopped abruptly because:
    A) rebound tachycardia
    B) rebound hypotension
    C) rebound broncospasm
    D) A and B

A) rebound tachycardia
(beta blockers cause hypotension)
- Upregulate beta receptors, when you take them away, you have too mmuch receptors and there is too much stimulaion
Never abruptly stop in the community

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Beta-blockers:

Place in therapy?

A

Place in therapy:

• BB are the initial choice in the absence of CI in all
patients
- post-MI patients = ↓ death and recurrent MI
- extrapolate data to patients without MI

• Initiation
- Baseline:
* BP(SBP >100), HR (>60 bpm), euvolemic (HF), no
contraindications
- Titration:
* to HR (55-60 or lower if no symptoms of
bradycardia) or symptom relief
* Avoid abruptly stopping therapy, especially high
doses
> Rebound tachycardia secondary to upregulation of
beta receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Beta-blockers:

Contraindications

A

• Reactive airway disease (e.g., asthma)
- Caution in COPD (use β1 selective)

  • 2° or 3° heart block
  • Decompensated HF
  • Severe PAD

• Pheochromocytoma (without αlpha blockade)
neuroendocrine tumor that grows from cells called chromaffin cells

• Hypersensitivity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Beta-blockers:

Adverse Effects

A

see slide 21

CNS Fatigue, insomnia, vivid dreams,
depression symptoms
CVS Bradycardia, hypotension, decreased
exercise tolerance, heart block BP, HR, ECG
RESP Bronchospasm (> non-selective agents) symptoms
ENDO Mask hypoglycemia, increase blood
glucose and triglycerides, lower HDL-C symptoms
Other Impotence, decreased libido, cold
extremities symptoms

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Beta-blockers:

Benefits of Cardio-Selectivity

A

• What you can minimize by using cardio-selective
agents:
- Beta-2 blockade in:
* lungs: bronchospasm
* pancreas: potential hyperglycemia (transient, little
clinical significance)
* liver: blunt the recovery from hypoglycemia
* vascular smooth muscle: potential aggravation of
intermittent claudication or Raynaud’s phenomenon

• Cardio-selectivity is dose-dependent; at higher doses,
cardio-selective agents lose their relative selectivity for
beta-1 receptors and can block beta-2 receptors as
effectively.

• The dose at which cardio-selectivity is lost varies from
patient to patient.

17
Q

Is metoprolol a good choice for Mr. Smythe?

A

Is metoprolol a good choice for Mr. Smythe?

A) Yes
B) No
C) Maybe

Is metoprolol a good choice for Mr. Smythe?
Yes, he doesnt have contraindications

18
Q

Calcium Channel Blockers (CCB):

Anti-Ischemic Effects

A

• Non-DHP: ↓HR and contractility = ↓MvO2

• DHP: ↓ arterial resistance and afterload = ↓ lowering
myocardial wall stress and MvO2.
Coronary artery dilation, improving oxygen supply
(mainly in vasospastic angina)

• Competitive antagonist of L-type calcium channels
- vascular smooth muscle, cardiac myocytes, nodal
tissue (SA and AV node)
- decreased calcium available for contractile elements,
smooth muscle relaxation and vasodilation

• Depending on the agent may have:
- ↓ inotropy (demand)
- ↓ chronotrophy (supply and demand)
- ↓ dromotropy, conduction velocity (supply and
demand)
- vasodilation, coronary and systemic (supply and
demand)

(see slide 25 for reference)

19
Q

Calcium Channel Blockers (CCB):

Properties

A

see slide 27

NDHP CCB: Verapamil, Diltiazem
DHP CCB: Nifedipine, Amlodipine, Felopidine

dilt and verapamil will slow the heart rate. affect cardiac specifically

DHP affect peripheral vasodilation, no effects on heart rate (sig vasodilation that can cause reflex tachcardia by nifedipine)

20
Q

Calcium Channel Blockers (CCB):

Cardiac vs Vascular Selectivity

A

• Non-DHPs:
- higher selectivity for L-type calcium channels in heart
contractile cells (verapamil > diltiazem), as they prefer
channels undergoing increased frequency of
depolarization.

• DHPs:
- higher selectivity for the more inactivated L-type
calcium channel in vascular smooth muscle

• All bind to different areas of the alpha 1 subunit in the
L-type calcium channel

21
Q

Calcium Channel Blockers (CCB):

Which CCB would be the best choice to combine with metoprolol in the symptom treatment of SIHD?

A

Which CCB would be the best choice to combine with metoprolol in the symptom treatment of SIHD?

A) diltiazem
B) amlodipine
C) verapamil
D) A and C

Avoid diltiazem and verapamil in combo with metoprolol
Additive effects on HR, cause bradycardia
amlodipine

22
Q

Calcium Channel Blockers (CCB):

Place in therapy

A

Place in therapy:
• second-line agent ( but equally as effective as BB in
symptoms)
• combination treatment
• useful for coronary spasms (Prinzmental’s or variant)

Short-acting dihydropyridine CCB may ↑ risk of adverse CV events (MI/CVA) from rapid BP drops

Long-acting CCB are effective at relieving symptoms

Initiation:
• Baseline:
- BP(SBP >100), HR (>60 bpm), no contraindications
• Titration:
- to HR (55-60 or lower if no symptoms of
bradycardia) or symptom relief
- NB: only verapamil and diltiazem significantly effect
HR

23
Q

Calcium Channel Blockers (CCB):

Adverse Effects

A

see slide 32

CNS Dizziness, fatigue, headache symptoms
CVS Hypotension, brady-/tachycardia,
heart block, decreased exercise tolerance BP, HR, ECG
GI Constipation (verapamil) symptoms
DERM Rash (diltiazem), flushing (DHP) symptoms
Other Peripheral edema (DHP) (Dose related,
20%) symptoms

24
Q

Calcium Channel Blockers (CCB):

Contraindications

A

• 2nd or 3rd degree heart block or sick sinus syndrome
without a pacemaker (NDHP)

  • Hypotension
  • Bradycardia (NDHP)

• Heart failure with reduced ejection fraction [HFrEF]
(except amlodipine)

25
Q

Calcium Channel Blockers (CCB):

Drug Interactions

A

see slide 34

see slide 35

Digoxin ↓HR, ↑digoxin (verapamil/diltiazem)
Monitor HR, monitor digoxin
β-blockers ↓HR (verapamil, diltiazem), ↓BP
Avoid use, monitor HR, BP

Diltiazem 3A4 substrate and
inhibitor Potential for multiple drug interactions

Verapamil 3A4 substrate and inhibitor, 1A2 and 2C substrate, Pglycoprotein

Felodipine 3A4 inhibitor

26
Q

Nitrates:

Anti-Ischemic Effects

A

• Venous dilation -> ↓ preload -> ↓ myocardial wall
tension -> ↓ MvO2 (Myocardial oxygen consumption )

• Lower preload -> ↓ diastolic wall stress -> improved
subendocardial blood flow -> improved regional flow
distribution

  • Mild coronary vasodilation -> may improve O2 supply
  • Mild afterload reduction

(see slide 36 for reference)

27
Q

Nitrates:

MOA?

Clinical effects?

A

MOA:
• Vasodilation:
- Converted to nitric oxide by vascular endothelium
- Activates cGMP -> ↓ cellular calcium -> smooth
muscle relaxation and vasodilation

Clinical effects:
• improve exercise tolerance
• time to onset of angina
• ischemic threshold

28
Q

Nitrates:

Place in therapy

A

Place in therapy:

• rescue treatment (rapid-acting)
- all patients with angina should have rapid-acting
NTG

• prophylaxis (long acting)

- econd line 
- combination treatment
- may be useful in vasospasm
29
Q

Nitrates:

Tolerance

A
  • MOA unknown
  • tolerance to anti-anginal and hemodynamic effects

• require a “nitrate-free” period
- 8-12 hours

• counseling required
- Always inquiry about patch use

30
Q

Nitrates:

Use of rapid acting NTG

Instructions?

Other use?

A

Instructions:
• Stop and sit down (avoids presyncope/ syncope)
• After one dose, if NO relief or gets worse → call 911
• If improves, but does not resolves wait 5 minutes,
take a second dose, if NOT resolved in 5 minutes →
call 911 and take another dose
• Can continue to take q5min until EMS arrives

Other use:
• prophylactic use prior to activities known to cause
angina in individual patients

31
Q

Nitrates:

Adverse Effects

A

see slide 42

CNS Headache, dizziness symptoms
CVS Hypotension, reflex tachycardia,
palpitations, syncope BP, HR
GI Nausea, vomiting, diarrhea symptoms
MSK Weakness symptoms
DERM Flushing, rash symptoms
32
Q

Nitrates:

Contraindications?

Drug interactions?

A

Contraindications:
• Severe aortic stenosis (pre-load dependent)

Drug interactions:
• sildenafil (Viagra®, Revatio®), vardenafil (Levitra®),
tadalafil (Cialis®)
- Inhibits the breakdown of NO by PDE5 inhibitor
- coadmin = ↑ risk of life-threatening hypotension
(↑ ↑NO)
- Contraindicated
* At least 24h: sildenafil, vardenafil
* At least 3-4 days: tadalafil
- ALWAYS ask before prescribing NTG

33
Q

RANOLAZINE (Corzyna®)

A

• Approved second line anti-anginal (available in Canada,
$260/mo)

• Inhibits late sodium channel influx during repolarization
in myocytes
-> reduces intracellular sodium concentrations -> lowers
calcium influx -> lowers ventricular diastolic wall
tension -> lowers MvO2

  • Does not impact HR or BP (ideal add-on agent)
  • Can prolong QTC at higher doses

• Dosing: ranolazine ER 500 mg po BID, increased to
1000 mg BID in 2-4 weeks based on symptoms

34
Q

RANOLAZINE (Corzyna®)

Adverse Effect?

Contraindications?

Drug interaction?

A

ADverse Effects:
• constipation, nausea, dizziness, headache, prolong
QTc

Use with caution in CrCl < 50ml/min, contraindicated
in hepatic cirrhosis

Drug interaction:
• Avoid with concomitant QTc-prolonging agents:
antipsychotics, class 1a and III antiarrhythmic
(other than amiodarone), quinolones, macrolides,
azole antifungals
• Substrate of CYP 3A4 (major) and p-glycoprotein
(minor)
- Contraindicated with strong CYP 3A4 inducers:
phenytoin, carbamazepine, rifampin
- Contraindicated with strong CYP 3A4 inhibitors:
ketoconazole, clarithromycin, antitertovirals
• Inhibitor CYP 3A4 (weak) and p-glycoprotein:
dabigatran, simvastatin, cyclosporine, sirolimus

35
Q

IVABRADINE (Lancora®)

A

• Off-label, second line anti-anginal (available in
Canada, $50/mo)

• Inhibits sinus node HCN channel -> slower
generation of ‘funny’ current (spontaneous electrical
activity) -> reduction in HR -> reduction in MvO2

• Does not impact contractility

• Of note, increase death/nonfatal MI in CCS class 2-4
  angina (SIGNIFY trial subgroup analysis)

• Dosing: 2.5-7.5mg BID

36
Q

IVABRADINE (Lancora®)

Adverse Effect?

Contraindications?

Drug interaction?

A

Adverse Effect:
• visual disturbances (reversible), headache, dizziness,
bradycardia, afib, heart block

Contraindication:
• HR <70, severe hepatic disease

Drug interaction:
• Avoid with concomitant QTc-prolonging agents:
antipsychotics, class 1a and III antiarrhythmic (other
than amiodarone), quinolones, macrolides, azole
antifungals)
• Metabolized by CYP 3A4 (major)
- Contraindicated with strong CYP 3A4 inducers:
phenytoin, carbamazepine, rifampin
- Contraindicated with strong CYP 3A4 inhibitors:
ketoconazole, clarithromycin, anti-retrovirals,
diltiazem, verapamil,

37
Q

Treatment Approach

Summary

A

see slide 49

see slide 50

38
Q 
• Mr. Smythe comes to the pharmacy 1 week later after
  getting his new prescriptions:
  - EC ASA 81mg daily
  - Metoprolol 25mg BID
  - Nitroglycerin spray prn

• He reports that he is feeling better on his new
medications. He notices that he is only getting the
chest pressure weekly (was 2-3x per week) and only if
he ‘over does it’

• He reports his BP at 110 ∕ 70 and his HR = 70

• He states that he is feeling a little sluggish when he
walks and wonders if it is from the medications. He
states he is sleeping fine and has no other symptoms.

Mr. Smythe’s sluggishness could be from?

A

Mr. Smythe’s sluggishness could be from?

A) hypotension

B) bradycardia

C) exercise intolerance

D) All of the above

344 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions