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PHRM 5001 > 7. Cardiotonics > Flashcards

7. Cardiotonics Flashcards

1
Q
  1. What are cardiotonic drugs used for?

2. Why is the heart one of the body’s most active organs? (3 things it increases)

A
  1. Restore blood flow to organs and prevent ischemia

2. ↑ oxygen demand, ↑ energy needs, ↑ CO2 production

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2
Q
  1. Cardiotonic agents are administered to ….? (2 things)
  2. What factors affect HR?
  3. What factors affect SV?
A
  1. Restore CO, ↓ cardiac workload
  2. SNS impulses, PNS impulses, catecholamines, chronotropic drugs
  3. Preload (ventricular distensibility, venous return), myocardial contractility, afterload (SVR), inotropic drugs
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3
Q

Define:

  1. Chronotropic drug
  2. Inotropic drug
  3. Dromotropic drug
A
  1. Agent affecting the rate of contraction of the heart
  2. Agent affecting the strength of muscular contraction
  3. Agent that influences the conduction of electrical impulses
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4
Q

What are the characteristics of CHF? (4 things)

A

↓ cardiac output, florid edema, ↑ ventricular preload and afterload, cardiomegaly

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5
Q
  1. What does increased preload lead to, and what value will this reflect in on the R side of the heart? L side?
  2. What does ↑ pressures in the pulm. circulation lead to? (4 things)
A
  1. Leads to elevated ventricular filling pressures, R side reflected in ↑ CVP, L side reflected in ↑ PCWP
  2. Leaky capillaries, pulmonary edema, impaired alveolar gas exchange, dyspnea
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6
Q
  1. What does cardiomegaly lead to in the heart, and what does this negatively effect/do?
  2. Due to what happened in Q1, widespread edema occurs. What does this cause in the LV? What about RV?
A
  1. Ventricular wall rigidity, negatively effects Frank-Starling mechanism (↓ ventricular pumping action)
  2. ↑ afterload in LV (↑ SVR), ↑ afterload in RV (PVR)
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7
Q
  1. How does your body compensate in CHF to maintain CO?
    & More specifically…
  2. SNS _________ which stimulates ______ to ______.
  3. Activation of _______ causes an ↑ in _______ to maintain _______. This causes an ↑ ____ on an already ____ heart.
A
  1. ↑ HR
  2. SNS ↑ circulating catecholamines to stimulate SA node to ↑ HR
  3. Activation of RAAS pathway causes an ↑ in sodium retention to maintain systemic BP, and this causes an ↑ load on an already weakened heart.
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8
Q
  1. How is CHF initially treated?

2. If these fail, what is introduced, and what are the goals? (Hint: 3 goals)

A
  1. Lifestyle changes (weight loss, restricted sodium, control of HTN)
  2. Drug therapy is introduced, and the goals are ↑ myocardial contractility, ↓ cardiac preload, ↓ cardiac afterload
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9
Q

What are the 3 classes of positive inotropes used to treat CHF?

A

Cardiac glycosides, catecholamines, cAMP phosphodiesterase (PDE) inhibitors

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10
Q

What are cardiac glycosides derived from? What is the parent drug?

A

Derived from Digitalis genus of flowering plants, parent drug is Digitalis (dried leaves of purple foxglove plant)

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11
Q
  1. Digoxin (Lanoxin) differs from Digitalis in terms of what 2 things?
  2. What is the MOA? (3 steps)
  3. What does this ↑ intracellular Ca2+ do to improve cardiac contractility?
  4. What category of drugs does Digoxin belong?
A
  1. Potency and duration of action
  2. Same as Digitalis…
    a) inhibits Na2+, K+ - ATPase pump
    b) this ↑ intracellular Na2+
    c) activates Na2+ - Ca 2+ active transport mechanism
  3. Positive inotropic action
  4. Cardiac glycosides
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12
Q
  1. Digoxin has ___ dromotropic effects causing…? And has ___ chronotropic effects causing…..?
  2. What clearance mechanism does Digoxin rely on?
A
  1. Negative dromotropic effect, inhibitory effect on vagus nerve, slows AV node conduction (each beat more effective!)
    Negative chronotropic effect, ↑ CO which ↓ SNS stimulation of SA node, ↓ HR (reduces work)
  2. Renal clearance
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13
Q
  1. What are the precautions when using Digoxin?
  2. How is the therapeutic index? What can Digoxin worsen?
  3. What other type of medication should you not take while on Digoxin and why?
A
  1. Pre-existing bradycardia, myocardial infarction, avoid concurrent administration of Ca2+, anti-arrhythmic therapy
  2. Very small, can worsen arrhythmias
  3. Diuretics, can cause K+ and Mg+ depletion
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14
Q

What can Digoxin cause at……

  1. Low doses?
  2. High doses?
A
  1. Anorexia, bradycardia, nausea and vomiting, PVC’s

2. Ventricular tachycardia, V-fib, visual disturbances/hallucinations

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15
Q
  1. What drug class does Dopamine (Intropin) belong to?
  2. What is Dopamine a precursor of? Where is it synthesized? (Hint: 2 places)
  3. Does it cross the BBB? What does this mean?
  4. How long is the DOA? What is Dopamine degraded by?
A
  1. Catecholamines
  2. Norepinephrine, synthesized in adrenergic neurone and adrenal medulla
  3. NO! therefore the CV effects are maximized, and CNS effects are minimized
  4. 10 min DOA, degraded by endogenous COMT
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16
Q
  1. What do low doses of dopamine stimulate and what does this cause?
  2. What about intermediate doses?
  3. High doses?
A
  1. Stimulate dopaminergic receptors, ↑ renal blood flow (vasodilation)
  2. Stimulate cardiac B1-adrenergic receptors, powerful inotropic effects
  3. Stimulate alpha 1-adrenoceptors, powerful vasoconstrictor
17
Q

What are Dopamine’s MOA? (3 things)

A
  1. Direct stimulation of receptors
  2. Indirect stimulation of adrenergic nerve fibres to release NE
  3. ↑ renal blood flow facilitates diuresis, therefore ↓ circulating volume and cardiac workload
18
Q
  1. Dopamine indications? (3)
  2. Contraindications? (2)
  3. Precautions? (2)
  4. Adverse rxn? (4)
A
  1. CHF, cardiogenic shock secondary to MI, hypotension
  2. Pre-existing tachyarrhythmias, pheochromocytoma (worsens HTN)
  3. Can reverse effects of beta blockers, MI can ↑ myocardial O2 demand
  4. Tachycardia, anginal pain, palpitations, headache
19
Q
  1. What drug class does Dobutamine (Dobutrex) belong to?
  2. What is it indicated for?
  3. Natural or synthetic? What is it similar to?
  4. Why do you use it in the absence of hypotension?
  5. What components determine the pharmacologic effect?
A
  1. Catecholamines
  2. Treatment of severe CHF in absence of hypotension
  3. Synthetic catecholamine similar to dopamine
  4. B/c does not stimulate dopamine receptors, not metabolized to NE
  5. Racemic components
20
Q
  1. What receptors does Dobutamine’s R-isomer act on? What effects does this cause?
  2. What receptors does Dobutamine’s S-isomer act on? What effects does this cause?
A
  1. B-receptors, positive inotropic and chronotropic effects, along with vasodilation
  2. Alpha receptors, vasoconstriction is overcome by dominant B activity
21
Q
  1. Contraindications to Dobutamine? (2)
  2. Precautions? (3)
  3. Adverse effects? (4)
A
  1. Cardiogenic shock with severe hypotension, pre-existing arrhythmias
  2. Can lead to tachyphylaxis when used > 72 hrs, can aggravate pre-existing ischemia d/t ↑ O2 demand, sulphite sensitivities
  3. Tachycardia, anginal pain, hypotension, headache
22
Q
  1. What is the newest class of inotropic agent? 2. What 3 features makes these meds valuable?
A
  1. cAMP phosphodiesterase inhibitors
  2. Cause less cardiac irritation than digoxin, fewer effects on HR than catecholamines, valuable in long-term treatment of refractory CHF
23
Q
  1. What class of drugs does Amrinone (Inocor) belong to? What does this drug directly do?
  2. What is the MOA?
  3. What does this med cause to the periphery, improving what 2 things?
A
  1. cAMP phosphodiesterase inhibitors, directly improves myocardial contractility to ↑ CO
  2. Enzyme inhibition ↑ cAMP levels within myocardial cells —> ↑ rate of Ca2+ influx, improving force of contraction
  3. Peripheral vasodilation, can improve cardiac preload and afterload
24
Q

What are the adverse effects of Amrinone (Inocor)? (5 of them)

A
  1. Hepatotoxicity
  2. Arrhythmias
  3. Hypotension
  4. Fever
  5. Nausea
25
Q
  1. What class of drugs does Milrinone (Primacor) belong to?
  2. What does this drug do to the body, and which drug is it more potent than?
  3. When is this drug indicated? (4 possibilities)
A
  1. cAMP phosphodiesterase inhibitors
  2. Inotropic vasodilator; more potent than amrinone
  3. Indicated in acute heart failure associated with cardiac surgery (transplant or bypass), also pulmonary hypertension, pulmonary congestion, RV heart failure (cor pulmonate)
26
Q

Milrinone (Primacor) causes ____ effects to the heart. This results in acute improvements in what 3 things?

A

Local effects! Results in improvement in stroke volume, cardiac output, and peripheral vasodilation

PHRM 5001 (12 decks)

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