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Pharmacology > Cardiac Pharmacology > Flashcards

Cardiac Pharmacology Flashcards

1
Q

Pre-load

A

Volume of blood in the ventricles before they contract

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2
Q

After-load

A

The force against which the heart has to push the blood.

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3
Q

Ischemia

A
  • warning that the blood supply to the myocardium is insufficient.
  • Normally due to a narrowed (artherosclerosed) coronary artery.
  • This narrowing may get completely blocked off, leading to no blood supply to the myocardium (infarction, heart attack)
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4
Q

Aims of drug therapy in ischemic heart disease and heart failure

A
  • reduce pre-load
  • reduce afterload
  • reduce myo-proliferative stimulus
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5
Q

Beta 2 receptors

A

Vascular smooth muscle relaxation causes Vasodilation

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6
Q

Alpha 1 receptors

A

Vascular smooth Muscle contraction

vasoconstriction

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7
Q

beta blockers

A

Reduce contractility
Reduce HR
Reduce O2 consumption in the heart
Increase myocardial viability

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8
Q

beta blocker 1

A

Decrease heart rate
Decrease contractility
Decrease arterial constriction

This decreases 02 demand

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9
Q

Beta blockers II

A

decrease contractility
decrease cardiac output
increase pre load
increase o2 demand

beta blocker II - beta blocker I = reduced o2 demand

this increases myocardial viability

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10
Q

myocardial viability

A

ability of heart muscle that has been damaged or weakened due to reduced blood flow to recover function if blood flow is restored.

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11
Q

non selective beta 1 + 2 blockers

A

Propanolol (first generation), Nodolol and Sotalol

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12
Q

beta 1 blockers meds

A

Atenolol, metoprolol, acebutolol,bisoprolol,

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13
Q

3rd generation beta blockers

A

are a class of beta-blockers that not only block beta-adrenergic receptors but also possess additional beneficial effects, such as vasodilation

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14
Q

common 3rd gen beta blockers :
Carvedilol:

A

Blocks beta-1 and beta-2 receptors (non-selective).
Has alpha-1 blocking activity, causing vasodilation.
Antioxidant and anti-inflammatory properties.
Commonly used in heart failure, hypertension, and after a heart attack.

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15
Q

common 3rd gen beta blockers :
Nebivolol

A

Selective for beta-1 receptors (cardioselective).
Stimulates nitric oxide (NO) release, causing vasodilation.
Reduces arterial stiffness and improves endothelial function.
Often prescribed for hypertension and chronic heart failure.

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16
Q

Choice of beta blockers

A

ardiac Selective
Bisoproplol

Mixed Effect cardiac selective
Carvidolol, Nebivolol
Beta 1 blockade + peripheral vasodilation

17
Q

Beta blockers adverse effects

A

Bradycardia
AV conduction blocks
Sinus rhythm problems
Rebound tachycardia, angina & possibly MI
Changes in Blood glucose levels Carvedilol<metoprolol.
Erectile dysfunction (not nebivolol)
Sleep disturbances

18
Q

Renin - Angiotensin system

A

A drop in BP causes the Kidney to secrete renin.

Renin then converts angiotensinogen into angiotensin I –> converted to angiotensin II in the lungs

this increases vasoconstriction and stimulates aldosterone which retains sodium and water which increases blood volume.

19
Q

effect of ACE inhibitors

A

Vasodilatation
(without effecting Cardiac Output)
Reduce Sodium reabsorption
(via aldosterone secretion)
Reduce thirst

Clinical effect
Reduce Blood Pressure

20
Q

Adverse and side effects of ACE inhibitors

A

Adverse effects:
Cough
Rash
Renal impairment
Headache

Side effects:
Hypotension
Hyperkalemia Too much Potassium in the blood (due to aldosterone inhibition)

21
Q

Clinical management of Pt on ACE inhibitors

A

BP

Renal function (output and urea and electrolytes)

Liver function
* Some ACE inhibitors are prodrugs (depend upon the liver to convert them into their active form e.g. enalapril).

Postural stability

22
Q

Angiotensin II receptor inhibitors

A

This inhibition reduces the effects of angiotensin II, which include vasoconstriction, sodium retention, and aldosterone release.

Common drug is called Candesartan

23
Q

Adverse effects and side effects of Angiotensin II receptor antagonist

A

Adverse Effects:
Back pain
Fatigue
Poor kidney function: Increased plasma creatinine levels

Side Effects:
Hyperkaleamia (increased potassium) in DB II with renal disease
Dizziness
Headache

24
Q

Organic nitrates

A

Relax arterial and venous smooth muscles via liberation of nitric oxide

25
Q

Nitrates used in angina

A

Nitrates are converted to Nitric Oxide (NO) which causes peripheral dilation.

Preload is reduced –> decreased Cardiac workload and reduces O2 consumption

26
Q

Nitrates: hemodynamic effects

A
  1. Venous dilation
    Decreased preload, decreased ventricular size, vent wall stress and O2 demand
  2. Coronary vasodilation
    Increased myocardial perfusion, redistributes blood flow.

3.Arterial vasodilation
Decreased afterload so increased cardiac output and decreased BP

27
Q

Adverse effects of nitrates

A

Vascular headache
Orthostatic hypotension
Syncope
Rash

Tolerance

28
Q

What is nitrate tolerance

A

decrease in the effect of a drug

Develops with all nitrates

Is dose-dependent

Disappears in 24 h. after stopping the drug

29
Q

Nitrate tolerance mechanisms

A

Increase Symp NT,
Increased intravascular volume,
Increased Vasopressin release

30
Q

Avoidance of tolerance

A
  • Intermittent administration
    • Use the lowest possible dose
    • Intersperse a nitrate-free interval
31
Q

Calcium channel blockers

A

medications that primarily affect the movement of calcium ions through calcium channels in the muscle cells of the heart and blood vessels. Calcium is essential for muscle contraction, and by blocking its entry into these cells, CCBs help to relax and dilate blood vessels and reduce the force of heart contractions.

32
Q

Effect of Ca++ channel blockers on the CVS

A

CHeck power point slide 44

33
Q

Adverse affects

A
  • Hypotension
  • Headaches
  • Peripheral oedema
  • Constipation
  • A-V block
34
Q

Dihydropyridine Pharmacokinetics
(Amlodopine)

A

Amlodipine:
Bioavailability: 64-90%
Plasma protein binding: 93%
Metabolism: Phase 1 mainly CYP 3A4
Half life: (30-50 hours)
Excretion: Renal

35
Q

Dihydropyridine Pharmacokinetics

lercanidipine

A

Lercanidipine:
Bioavailability: ~10% (high first pass effect)
Plasma protein binding: >98%
Metabolism: Phase 1 mainly CYP 3A4
Half life: (8-10 hours)
Excretion: 50% Renal

Pharmacology (18 decks)

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