7. Cardiotonics Flashcards
1
Q
- What are cardiotonic drugs used for?
2. Why is the heart one of the body’s most active organs? (3 things it increases)
A
- Restore blood flow to organs and prevent ischemia
2. ↑ oxygen demand, ↑ energy needs, ↑ CO2 production
2
Q
- Cardiotonic agents are administered to ….? (2 things)
- What factors affect HR?
- What factors affect SV?
A
- Restore CO, ↓ cardiac workload
- SNS impulses, PNS impulses, catecholamines, chronotropic drugs
- Preload (ventricular distensibility, venous return), myocardial contractility, afterload (SVR), inotropic drugs
3
Q
Define:
- Chronotropic drug
- Inotropic drug
- Dromotropic drug
A
- Agent affecting the rate of contraction of the heart
- Agent affecting the strength of muscular contraction
- Agent that influences the conduction of electrical impulses
4
Q
What are the characteristics of CHF? (4 things)
A
↓ cardiac output, florid edema, ↑ ventricular preload and afterload, cardiomegaly
5
Q
- What does increased preload lead to, and what value will this reflect in on the R side of the heart? L side?
- What does ↑ pressures in the pulm. circulation lead to? (4 things)
A
- Leads to elevated ventricular filling pressures, R side reflected in ↑ CVP, L side reflected in ↑ PCWP
- Leaky capillaries, pulmonary edema, impaired alveolar gas exchange, dyspnea
6
Q
- What does cardiomegaly lead to in the heart, and what does this negatively effect/do?
- Due to what happened in Q1, widespread edema occurs. What does this cause in the LV? What about RV?
A
- Ventricular wall rigidity, negatively effects Frank-Starling mechanism (↓ ventricular pumping action)
- ↑ afterload in LV (↑ SVR), ↑ afterload in RV (PVR)
7
Q
- How does your body compensate in CHF to maintain CO?
& More specifically… - SNS _________ which stimulates ______ to ______.
- Activation of _______ causes an ↑ in _______ to maintain _______. This causes an ↑ ____ on an already ____ heart.
A
- ↑ HR
- SNS ↑ circulating catecholamines to stimulate SA node to ↑ HR
- Activation of RAAS pathway causes an ↑ in sodium retention to maintain systemic BP, and this causes an ↑ load on an already weakened heart.
8
Q
- How is CHF initially treated?
2. If these fail, what is introduced, and what are the goals? (Hint: 3 goals)
A
- Lifestyle changes (weight loss, restricted sodium, control of HTN)
- Drug therapy is introduced, and the goals are ↑ myocardial contractility, ↓ cardiac preload, ↓ cardiac afterload
9
Q
What are the 3 classes of positive inotropes used to treat CHF?
A
Cardiac glycosides, catecholamines, cAMP phosphodiesterase (PDE) inhibitors
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)
11
Q
- Digoxin (Lanoxin) differs from Digitalis in terms of what 2 things?
- What is the MOA? (3 steps)
- What does this ↑ intracellular Ca2+ do to improve cardiac contractility?
- What category of drugs does Digoxin belong?
A
- Potency and duration of action
- Same as Digitalis…
a) inhibits Na2+, K+ - ATPase pump
b) this ↑ intracellular Na2+
c) activates Na2+ - Ca 2+ active transport mechanism - Positive inotropic action
- Cardiac glycosides
12
Q
- Digoxin has ___ dromotropic effects causing…? And has ___ chronotropic effects causing…..?
- What clearance mechanism does Digoxin rely on?
A
- 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) - Renal clearance
13
Q
- What are the precautions when using Digoxin?
- How is the therapeutic index? What can Digoxin worsen?
- What other type of medication should you not take while on Digoxin and why?
A
- Pre-existing bradycardia, myocardial infarction, avoid concurrent administration of Ca2+, anti-arrhythmic therapy
- Very small, can worsen arrhythmias
- Diuretics, can cause K+ and Mg+ depletion
14
Q
What can Digoxin cause at……
- Low doses?
- High doses?
A
- Anorexia, bradycardia, nausea and vomiting, PVC’s
2. Ventricular tachycardia, V-fib, visual disturbances/hallucinations
15
Q
- What drug class does Dopamine (Intropin) belong to?
- What is Dopamine a precursor of? Where is it synthesized? (Hint: 2 places)
- Does it cross the BBB? What does this mean?
- How long is the DOA? What is Dopamine degraded by?
A
- Catecholamines
- Norepinephrine, synthesized in adrenergic neurone and adrenal medulla
- NO! therefore the CV effects are maximized, and CNS effects are minimized
- 10 min DOA, degraded by endogenous COMT
16
Q
- What do low doses of dopamine stimulate and what does this cause?
- What about intermediate doses?
- High doses?
A
- Stimulate dopaminergic receptors, ↑ renal blood flow (vasodilation)
- Stimulate cardiac B1-adrenergic receptors, powerful inotropic effects
- Stimulate alpha 1-adrenoceptors, powerful vasoconstrictor
17
Q
What are Dopamine’s MOA? (3 things)
A
- Direct stimulation of receptors
- Indirect stimulation of adrenergic nerve fibres to release NE
- ↑ renal blood flow facilitates diuresis, therefore ↓ circulating volume and cardiac workload
18
Q
- Dopamine indications? (3)
- Contraindications? (2)
- Precautions? (2)
- Adverse rxn? (4)
A
- CHF, cardiogenic shock secondary to MI, hypotension
- Pre-existing tachyarrhythmias, pheochromocytoma (worsens HTN)
- Can reverse effects of beta blockers, MI can ↑ myocardial O2 demand
- Tachycardia, anginal pain, palpitations, headache
19
Q
- What drug class does Dobutamine (Dobutrex) belong to?
- What is it indicated for?
- Natural or synthetic? What is it similar to?
- Why do you use it in the absence of hypotension?
- What components determine the pharmacologic effect?
A
- Catecholamines
- Treatment of severe CHF in absence of hypotension
- Synthetic catecholamine similar to dopamine
- B/c does not stimulate dopamine receptors, not metabolized to NE
- Racemic components
20
Q
- What receptors does Dobutamine’s R-isomer act on? What effects does this cause?
- What receptors does Dobutamine’s S-isomer act on? What effects does this cause?
A
- B-receptors, positive inotropic and chronotropic effects, along with vasodilation
- Alpha receptors, vasoconstriction is overcome by dominant B activity
21
Q
- Contraindications to Dobutamine? (2)
- Precautions? (3)
- Adverse effects? (4)
A
- Cardiogenic shock with severe hypotension, pre-existing arrhythmias
- Can lead to tachyphylaxis when used > 72 hrs, can aggravate pre-existing ischemia d/t ↑ O2 demand, sulphite sensitivities
- Tachycardia, anginal pain, hypotension, headache
22
Q
- What is the newest class of inotropic agent? 2. What 3 features makes these meds valuable?
A
- cAMP phosphodiesterase inhibitors
- Cause less cardiac irritation than digoxin, fewer effects on HR than catecholamines, valuable in long-term treatment of refractory CHF
23
Q
- What class of drugs does Amrinone (Inocor) belong to? What does this drug directly do?
- What is the MOA?
- What does this med cause to the periphery, improving what 2 things?
A
- cAMP phosphodiesterase inhibitors, directly improves myocardial contractility to ↑ CO
- Enzyme inhibition ↑ cAMP levels within myocardial cells —> ↑ rate of Ca2+ influx, improving force of contraction
- Peripheral vasodilation, can improve cardiac preload and afterload
24
Q
What are the adverse effects of Amrinone (Inocor)? (5 of them)
A
- Hepatotoxicity
- Arrhythmias
- Hypotension
- Fever
- Nausea
25
Q
- What class of drugs does Milrinone (Primacor) belong to?
- What does this drug do to the body, and which drug is it more potent than?
- When is this drug indicated? (4 possibilities)
A
- cAMP phosphodiesterase inhibitors
- Inotropic vasodilator; more potent than amrinone
- 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
