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Cardiovascular Block > Antianginals > Flashcards

Antianginals Flashcards

1
Q

Causes of Angina/Ischemia

A

Decreased oxygen supply:
Atherosclerosis
Fixed stenosis/stable plaque
Unstable plaque – Acute coronary syndrome
Vasospasm
Hypotension (decreased perfusion)
Anemia/Lung disease/Hypoxia (decreased blood O2 content)

Increased oxygen demand:
Tachycardia
Hypertension
Aortic stenosis

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2
Q

Relationship Between Degree of Stenosis and Coronary Flow

A

At 70% stenosis at maximal flow (not at rest) the flow starts to drop off because cannot dilate anymore to compensate

At 90% at rest, we see decrease because autoregulation can’t take care of providing enough coronary flow to the heart

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3
Q

Ischemic Progression

A

As duration of ischemia occurs see perfusion abnormalities first (stress test or nuclear imaging)
Then diastolic dysfunction, then systolic dysfunction (stress echo to see wall abnormalities)
EKG will start to change (exercise treadmill)
Development of angina – last stage so have already had the other changes

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4
Q

Physical Exam: Possible Abnormalities

A

Vitals can be normal
Transient murmur from mitral regurgitation. Mitral valve is supplied by anterior and posterior papillary muscle and if R coronary artery is occluded then the muscles may become damaged
S3 if heart failure, and ventricular relaxation is an active process and if ischemia is occurring the compliance decreases due to stiffness thus causing the S4
Femoral arteries and abdomen bruits
Can have asymptomatic exam

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5
Q

Treatment for Stable Angina

A

Nitrates
Beta Blockers
Calcium Channel Blockers
Ranolazine

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6
Q

Nitrates

A

SL = sublingual
Spray instead of sublingual for those with dry mouth
Patches on for 12 hours and off for 12 hours to prevent nitrate tolerance
If trouble getting rid of chest pain give IV

Does not require an intact endothelium (endothelial independent vasdoilation)
After entering the vessel wall, nitrates are converted to nitric oxide (NO), this requires sulfydryl groups (SH)
NO stimulates guanylate cyclase to produce cGMP
cGMP lowers calcium in the vascular smooth muscle cell resulting in vasodilation

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7
Q

Effects of Nitrates

A

Dilation of venous (largely) and arterial vascular smooth muscle
Effect of venodilation = diminished venous return AND reduced ventricular end-diastolic volume and pressure
Effect of arterial dilation = decreased blood pressure AND reduction in aortic impedance to left ventricular ejection
Total coronary flow is increased in normal individuals, but the ability to dilate atherosclerotic epicardial coronary arteries is more modest

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8
Q

Detrimental Effects of Nitrates

A

Nitrates sometimes cause reflex tachycardia to increase the HR and this is detrimental
By decreasing BP it also causes decreases in diastolic pressure which causes decrease in perfusion pressure which is detrimental

Nitrate Tolerance: over time have little effects; use of smallest effective dose and frequency will help with this

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9
Q

Effects of Nitrates on Other Areas of the Body

A

Nitrates can relax smooth muscles in the other areas of the body, so not all pain relieved is heart pain
If treat patient with nitrate, must think that their pain could have been from other sources other than the heart because of the other effects it causes

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10
Q

Types of Beta Receptors

A

B1 = heart in myocytes to cause positive inotropic effect; on SA/AV nodes it increases chronotropic effect

B2 = lung and small amount in the myocardium; bronchodilation; if blocked, then constriction occurs and wheezing especially in asthma patients

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11
Q

Beta Receptors Mechanism of Action

A

Beta receptor is situated on cardiac sarcolema
The G-protein system links the beta receptor to adenyl cyclase system
When beta receptor activated, adenyl cyclase produces cAMP from ATP

cAMP has the following actions:
Opening of Calcium channels – increased inotropy
Increases rate of reuptake of cytosolic calcium into the sarcoplasmic reticulum (SR) – increased rate of relaxation
Increased chronotropy

Beta blockers inhibit this process

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12
Q

Cardioselective Beta Blockers

A 
Atenolol
Esmolol
Metoprolol
Bisoprolol
Nebivolol
Acebutolol
Celiprolol

*only work on B1 receptor

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13
Q

Vasodilatory Noncardioselective Beta Blockers

A

Have some alpha blockade = vasodilatory
Labetolol
Carvedilol

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14
Q

ISA Activity Beta Blockers

A

Intrinsic sympathomimetic activity (ISA), where at baseline there is partial stimulation of beta receptor, but at normal or increased levels it causes beta blockade

Bucindolol
Pindolol
Acebutolol
Celiprolol

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15
Q

Mechanism of Anginal Relief of Beta Blockers

A

Beneficial:
As you slow the HR down, the diastolic time to fill increases
Reduction of arterial blood pressure resulting in decreased afterload

We can see improvement in perfusion pressures
Increased ventricular EDV, which increases radius and wall stress which are detrimental but overall beta blockers decrease O2 demand as a whole to decrease angina, but little effect on O2 supply

By slowing the HR down, you increase EDV so that causes the radius and wall stress to increase = not beneficial

Beta blockers are not effective for and are not used in the management of vasospastic angina

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16
Q

Beta Blockers Adverse Effects

A 
Bronchoconstriction
Bradycardia
Depressed A-V node conduction
Impaired myocardial contractility
Acute withdrawal syndrome
CNS effects (fatigue, depression, insomnia, nightmares)
Erectile dysfunction
 *KNOW THESE
17
Q

Types of Calcium Channels

A

L-type (long-lasting)
Myocardial & vascular smooth muscle cells: Admits substantial amounts of calcium ions required for initiation of contraction via calcium induced calcium release from the SR. This causes myocardial and smooth muscle contraction.
Pacemaker and nodal cells: Responsible for Phase 0 of the action potential

T-type (transient)
Opens at more negative potentials than the L-type
Plays important role in initial deoplarization of sinus and AV node.

18
Q

Calcium Channel Blockers Mechanism of Action

A

Dihydropyridines (DHPs)
Exert a greater inhibitory effect on vascular smooth muscle than on the myocardium (vasodilation)
Minimal effect on SA & AV node, thus can cause some reflex tachycardia

Non-dihydropyridines (N-DHPs)
Decreases force of myocardial contraction (negative inotropy)
Acts on SA & AV node (negative chronotropy and dromotropy)
Less effect on vascular smooth muscle than DHPs

19
Q

Calcium Channel Blocker Medications

A 
DHPs:
Amlodipine
Felodipine
Isradipine
Nicardipine
Nifedipine

NDHPs:
Verapamil
Diltiazem

20
Q

Pros and Cons of Calcium Channel Blockers

A 
Beneficial actions:
Decreased heart rate (Non-DHPs)
Reduced myocardial contractility (Non-DHPs)
Coronary artery vasodilation
Decreased arterial blood pressure

Nonbeneficial actions:
Reflex tachycardia with DHPs

21
Q

Calcium Channel Blocker Effects on the Heart

A

Decrease transmural pressure by decreasing BP
Decrease HR and contractility by working on myocardial cells themselves
May decrease resistance of coronary artery by inducing vascular smooth muscle relaxation and increasing blood flow
Decrease “r” due to minimal venodilation

With DHP, you do get reflex tachycardia because not affecting the SA and AV nodes

Overall NET effect of calcium channel blockers in effort angina = a decrease in myocardial oxygen demand and supply
Decreased demand is the dominant effect

22
Q

Clinical Use of Calcium Channel Blockers

A

Vasospastic angina

Stable (effort-induced) angina -usually when intolerant to beta blockers

23
Q

DHP Adverse Effects

A 
Tachycardia: avoid short acting types
Flushing 
Hypotension
Headache 
Edema - most common
Constipation
24
Q

NDHP Adverse Effects

A

Bradycardia
Hypotension
CHF exacerbation
Constipation

25
Q

Ca2+ Channel Blockers vs. Beta Blockers

A

Beta Blocker Preferred:
Post-infarct (Post-MI)
Low EF

Calcium Channel Blocker Preferred:
Vasospastic angina

26
Q

Ranolazine: Mechanism of Action

A

In ischemia myocardium, there is too much sodium so this med blocks the late sodium current (Ina) to prevent sodium build up

Ranolazine reduces calcium overload, diastolic relaxation failure, increased diastolic tension, and increased consumption of ATP

Diastolic relaxation is an active process and get consumption of ATP when that is not occurring

27
Q

Effects of Calcium Overload After Ischemic Event

A

Too much sodium drives this exchanger and uses ATP and get Ca2+ overload and get inhibition of diastolic relaxation, electrical instability, and consumption of ATP

28
Q

Clinical Use and Effects of Ranolazine

A

Decrease diastolic wall tension and thus improves diastolic perfusion

Decrease of anginal episodes in chronic stable angina

29
Q

Adverse Effects of Ranolazine

A

Headaches and nausea are the two most common
Nitrates, beta blocker, and Ca2+ channel blockers affects HR and BP, but this med doesn’t affect this
This med helps patients that have been diagnosed with low HR and BP already

30
Q

Stable Angina: Revascularization

A

If exhausted therapy with meds = revascularize them by placing stent (PCI) to improve supply, or do CABG
Last step in tx of angina

Cardiovascular Block (28 decks)

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