Pharmacology of Cardiovascular Medications
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Questions and Answers

Which receptor is primarily responsible for the vasoconstriction caused by phenylephrine?

  • Beta-2
  • Alpha-1 (correct)
  • Beta-1
  • Dopaminergic

    • A patient with aortic regurgitation is being treated with phenylephrine. Which of the following is a potential risk?

  • Decreased left ventricular afterload
  • Improved cardiac output
  • Increased coronary perfusion
  • Worsening of aortic regurgitation due to increased left ventricular afterload (correct)

    • What is the main mechanism of action of vasopressin?

  • Reducing cyclic AMP to enhance fluid loss.
  • Directly blocking alpha receptors to cause vasodilation.
  • Increasing cyclic AMP to enhance water reabsorption and direct vasoconstriction. (correct)
  • Stimulating beta receptors to increase heart rate.

    • Which vasopressin receptor is primarily responsible for vasoconstriction?

    <p>V1</p> Signup and view all the answers

    At low doses, dopamine's main effect is what?

    <p>Renal and mesenteric vasodilation</p> Signup and view all the answers

    At high doses (>10 mcg/kg/min), the primary effect of dopamine is:

    <p>Alpha-1 vasoconstriction</p> Signup and view all the answers

    What is the primary mechanism of action of dobutamine?

    <p>Beta-1 adrenergic agonism, increasing heart rate and contractility</p> Signup and view all the answers

    Besides its primary beta-1 effect, what secondary effect can dobutamine exhibit?

    <p>Weak Beta 2 vasodilation</p> Signup and view all the answers

    Which of the following best describes the primary effect of milrinone?

    <p>Promotes vasodilation and increases cardiac contractility.</p> Signup and view all the answers

    A patient with acidosis requires inotropic support. Which medication would have its effect diminished?

    <p>Milrinone</p> Signup and view all the answers

    Procainamide is classified as which type of antiarrhythmic?

    <p>Class 1a (Sodium channel blocker - Moderate)</p> Signup and view all the answers

    Which of the following best describes how procainamide affects the myocardium?

    <p>Prolongs repolarization, decreasing myocardial excitability and conduction velocity.</p> Signup and view all the answers

    What is the primary mechanism of action of lidocaine as an antiarrhythmic?

    <p>Blocks sodium channels, shortening repolarization.</p> Signup and view all the answers

    Which antiarrhythmic medication primarily affects potassium channels resulting in the lengthening of the action potential?

    <p>Amiodarone</p> Signup and view all the answers

    Which of the following medications may cause a widened QRS complex?

    <p>Procainamide</p> Signup and view all the answers

    Which of the following effects is not associated with amiodarone?

    <p>Increased contractility</p> Signup and view all the answers

    What is the primary mechanism by which Fentanyl reduces pain?

    <p>By increasing the pain threshold and impacting ascending pain pathways.</p> Signup and view all the answers

    Why does Midazolam have an inhibitory effect on neuron excitability?

    <p>It increases neuronal membrane permeability to chloride ions, causing hyperpolarization.</p> Signup and view all the answers

    How does Morphine primarily achieve its analgesic effects?

    <p>By inhibiting the ascending pain pathways and altering pain perception.</p> Signup and view all the answers

    Through which receptor does Etomidate primarily exert its sedative effects?

    <p>GABA receptor</p> Signup and view all the answers

    What is the mechanism of action of Succinylcholine at the myoneural junction?

    <p>It binds to acetylcholine receptor and causes flaccid muscle paralysis due to depolarization.</p> Signup and view all the answers

    What is a notable side effect of Succinylcholine related to electrolyte balance?

    <p>Transient hyperkalemia due to the opening of potassium channels.</p> Signup and view all the answers

    How does the lipid solubility of Fentanyl affect its action in the body?

    <p>It means some is sequestered in inactive lung sites leading to a more time to respiratory depression.</p> Signup and view all the answers

    What is a potential side effect of Etomidate that healthcare providers should be aware of?

    <p>It can cause adrenocortical suppression lasting 4-8 hours.</p> Signup and view all the answers

    Which of the following best describes the mechanism of action of diltiazem?

    <p>It inhibits calcium ions from entering smooth vascular muscle, causing vasodilation and decreased heart rate.</p> Signup and view all the answers

    Why might nicardipine be preferred over diltiazem in the ICU setting?

    <p>Nicardipine is a stronger vasodilator with a different effect on heart rate.</p> Signup and view all the answers

    What is the primary mechanism of action for rocuronium?

    <p>Preventing acetylcholine from binding to receptors</p> Signup and view all the answers

    What is a primary effect of propofol’s mechanism of action?

    <p>Global CNS depression through GABA-A potentiation and NMDA receptor blockade.</p> Signup and view all the answers

    Which of the following best describes the mechanism of action of vecuronium?

    <p>Inhibits depolarization by blocking acetylcholine receptors at the motor end plate.</p> Signup and view all the answers

    How does dexmedetomidine function to reduce blood pressure and heart rate?

    <p>Through activation of alpha-2a receptors, which inhibits the release of norepinephrine.</p> Signup and view all the answers

    Cisatracurium (Nimbex) is preferred over atracurium in patients who are cardiovascularly unstable because cisatracurium:

    <p>Does not produce histamine release.</p> Signup and view all the answers

    How does atropine exert its effects on the heart?

    <p>Blocks acetylcholine at parasympathetic sites to increase heart rate.</p> Signup and view all the answers

    Which of the following most accurately describes the effects of diltiazem?

    <p>Negative inotropic, chronotropic, and dromotropic effects.</p> Signup and view all the answers

    What is the primary mechanism by which fentanyl exerts its analgesic effect?

    <p>By binding to the MU 1 and MU 2 receptors.</p> Signup and view all the answers

    What is the result of adenosine activating A1 purinergic receptors in the cardiomyocytes?

    <p>Negative inotropic and chronotropic effects.</p> Signup and view all the answers

    A patient with liver disease is given rocuronium, what effect will it likely have?

    <p>Prolonged duration of action</p> Signup and view all the answers

    What is a significant contraindication for the use of nicardipine?

    <p>Hepatorenal impairment and CHF.</p> Signup and view all the answers

    What receptor type does Atropine interact with?

    <p>Muscarinic</p> Signup and view all the answers

    What is the primary mechanism of action of an alpha-2 receptor agonist?

    <p>Inhibit the release of norepinephrine.</p> Signup and view all the answers

    Which drug is a reversal agent for Rocuronium?

    <p>Sugammadex</p> Signup and view all the answers

    What is the primary mechanism by which an antiarrhythmic medication slows conduction time through the SA and AV nodes?

    <p>By hyperpolarizing the SA node.</p> Signup and view all the answers

    Which of the following best describes nitric oxide's role when introduced by nitroglycerin?

    <p>It forms free radicals that induce vasodilation by acting on peripheral arteries and veins.</p> Signup and view all the answers

    How does nitroprusside reduce cardiac afterload?

    <p>By directly acting on smooth muscle in both veins and arteries to cause vasodilation of the peripheral vasculature.</p> Signup and view all the answers

    Besides vasodilation, what is a significant consideration when administering nitroprusside?

    <p>Risk of cyanide poisoning.</p> Signup and view all the answers

    Which of the following best explains why an antiarrhythmic medication would be used to interrupt re-entry pathways through the AV node?

    <p>To slow conduction through the AV Node, thereby disrupting errant electrical circuits.</p> Signup and view all the answers

    Study Notes

    ICU Medications

    • Vasopressors: Medications used to increase blood pressure.

    • Positive Inotrope: Increases heart contractility.

    • Positive Chronotrope: Increases heart rate.

    • Positive Dromotrope: Increases electrical signals and automaticity in the heart.

    Alpha-1 Stimulation

    • Results: Vasoconstriction (increased blood pressure (BP)).

    Alpha-2 Stimulation

    • Results: Inhibits the release of norepinephrine, acetylcholine, and insulin.

    Beta-1 Stimulation

    • Results: Positive chronotrope (increased heart rate (HR)), positive inotrope (increased contractility), and increased release of renin.

    Beta-2 Stimulation

    • Results: Vasodilation (decreased blood pressure (BP)), and bronchodilation.

    Beta-1 Cell Location

    • Location: Cardiac myocytes.

    Beta-2 Cell Location

    • Location: Smooth vascular muscle, mainly in the lungs.

    Norepinephrine Mechanism of Action

    • Mechanism: Stimulates Beta-1 and Alpha-1 receptors, mostly Alpha-1 receptors stronger than Beta.

    Epinephrine Mechanism of Action

    • Mechanism: Stimulates Alpha, Beta-1, and Beta-2 receptors; Beta-1 effect stronger than in norepinephrine. Alpha activation causes vasoconstriction, beta-1 causes positive inotropic, chronotropic and dromotropic effects, and beta-2 causes bronchodilation.

    Phenylephrine Mechanism of Action

    • Mechanism: Direct alpha-adrenergic agonist with virtually no beta effect, producing systemic vasoconstriction, increasing coronary perfusion without raising heart rate (HR). Good for CAD or aortic stenosis.
    • Concerns: May cause reflex bradycardia when used with patients with aortic regurgitation, worsening the problem because of LV afterload increase.

    Vasopressin Mechanism of Action

    • Mechanism: Produced in the hypothalamus and stored in the posterior pituitary gland, increases cyclic adenosine monophosphate (cAMP), increasing water permeability in renal tubules to decrease urine output, increasing blood pressure. Acts as a direct vasoconstrictor. V1 receptor responsible for vasoconstriction, V2 for fluid reabsorption and increased blood volume.

    Dopamine Mechanism of Action

    • Mechanism: Stimulates alpha, beta, and dopaminergic receptors; dose dependent. Low doses mainly affect D1 and D2 receptors, causing renal and mesenteric vasodilation. Higher doses affect Beta-1 receptors, leading to increased heart rate (HR), increased contractility (inotropic), renal vasodilation. Even higher doses (>10 mcg/kg/min) predominantly cause Alpha-1 effects leading to vasoconstriction.

    Dobutamine Mechanism of Action

    • Mechanism: Potent Beta-1 agonist with weaker Beta-2 effects; Beta-1 stimulation causes increases in heart rate (HR) and contractility (inotropic). Increases cardiac output. Moderate Beta-2 effect causes vasodilation and higher doses affect alpha receptors.

    Milrinone Mechanism of Action

    • Mechanism: Phosphodiesterase 3 inhibitor, causing vasodilation with some inotropic effect (increased contractility) and little chronotropic effect (increased HR). Increases inotropy (contractility) and pulmonary and peripheral vascular dilation that leads to improved cardiac output. Decreases systemic vascular resistance (SVR). Less tachycardia than dobutamine. Effect decreases in acidodic patients.

    Procainamide Mechanism of Action

    • Mechanism: Class 1A antiarrhythmic, blocking sodium channels, prolongs repolarization. Decreases myocardial excitability and conduction velocity, increases effective refractory period. Causes myocardial depression and can widen QRS which causes hypotension. Useful for broad spectrum of tachyarrhythmias.

    Lidocaine Mechanism of Action

    • Mechanism: Class 1B antiarrhythmic; blocks sodium channel permeability on neuronal membrane. Shortens repolarization in myocardial cells, suppresses automaticity of ectopic foci and treats ventricular arrhythmias.

    Amiodarone Mechanism of Action

    • Mechanism: Class III antiarrhythmic (potassium channel blocker); affects sodium and calcium channels. Prolongs action potential and refractory period in myocardial tissue, which decreases AV conduction and inhibits abnormal automaticity, decreasing SVR. Much less cardiac depressing than Procainamide.

    Diltiazem Mechanism of Action

    • Mechanism: Calcium channel blocker; inhibits calcium entry into channels of smooth vascular muscle, resulting in negative inotropic (decreased contractility), negative chronotropic (decreased heart rate), and negative dromotropic effects. Relaxes coronary smooth muscle, causing vasodilation, increasing myocardial oxygen delivery, and slower heart rate.

    Nicardipine Mechanism of Action

    • Mechanism: Calcium channel blocker; has stronger vasodilator effects than diltiazem, decreasing SVR without decreasing contractility or heart rate. Prolonged QT interval in some cases; contraindicated with hepatorenal and CHF.

    Propofol Mechanism of Action

    • Mechanism: Causes global CNS depression by potentiating GABA-A receptor activity and decreasing glutamatergic activity. Enhances inhibitory effects of GABA, producing sedation.

    Dexmedetomidine Mechanism of Action

    • Mechanism: Alpha-2 receptor agonist, acting via alpha-2a receptor and inhibiting norepinephrine release. Causes sympatholysis, reducing vasoconstriction response to epinephrine and norepinephrine, decreasing HR and BP.

    Fentanyl Mechanism of Action

    • Mechanism: Binds to Mu 1 and Mu 2 receptors, increasing pain threshold, altering pain reception, and inhibiting ascending pain pathways.

    Midazolam Mechanism of Action

    • Mechanism: Binds to benzodiazepine receptor on postsynaptic GABA neuron. Inhibits neuron excitability by increasing GABA's effect on neuronal membranes, leading to chloride ion shifts and hyperpolarization, reducing excitability, and providing stabilization.

    Morphine Mechanism of Action

    • Mechanism: Binds to Mu1 an Mu2 receptors in the CNS, inhibiting ascending pain pathways, affecting pain response, resulting in CNS depression.

    Etomidate Mechanism of Action

    • Mechanism: Works on GABA receptor, producing sedation; rapid induction of sedation and minimal cardiovascular effects. May cause adrenocortical suppression lasting 4-8 hours.

    Succinylcholine Mechanism of Action

    • Mechanism: Depolarizing neuromuscular agent acting similarly to acetylcholine, causing depolarization of motor endplates at the myoneural junction leading to flaccid muscle paralysis.

    Rocuronium Mechanism of Action

    • Mechanism: Non- depolarizing neuromuscular blocker, preventing acetylcholine binding to its receptors at the neuromuscular junction, inhibiting depolarization. Prolonged duration in patients with impaired Liver or Kidneys. Reversal agent needed : Sugammadex.

    Vecuronium Mechanism of Action

    • Mechanism: Non- depolarizing neuromuscular blocker that blocks acetylcholine binding to its receptors on the motor endplates, inhibiting depolarization, and leading to paralysis. Prolonged duration in patients with impaired Liver or Kidneys.

    Cisatracurium (Nimbex) Mechanism of action

    • Mechanism: Non- depolarizing neuromuscular blocker; blocks acetylcholine receptors in neuromuscular junction, preventing depolarization.

    Atropine Mechanism of Action

    • Mechanism: Muscarinic receptor antagonist; blocks acetylcholine binding at parasympathetic sites, reducing effects on smooth muscles, glands, and CNS. Acts as a positive chronotrope. Decreasing secretions.

    Adenosine Mechanism of Action

    • Mechanism: Acts on purinergic receptors (P1 and P2). P1 is subdivided into A1 impacting cardiomyocytes, A2 affecting endothelial and vascular smooth muscle, and A3 affecting mast cells in lungs). Leads to effects on SA and AV nodes, interrupting reentry pathways through the AV node and leading to the restoration of sinus rhythm.

    Nitroglycerin Mechanism of Action

    • Mechanism: Creates free radical nitric oxide, leading to vasodilation mainly of the veins and coronary arteries. Decreasing preload and afterload reduces cardiac oxygen demand.

    Nitroprusside Mechanism of Action

    • Mechanism: Directly acting on venous and arterial smooth muscles, causing peripheral vasodilation. Reduces peripheral resistance, increasing cardiac output due to decreased afterload. Note: Metabolized to cyanide ions requiring caution.

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    Description

    Test your knowledge on the pharmacological effects and mechanisms of various cardiovascular drugs, including vasopressin, dopamine, dobutamine, and procainamide. This quiz covers their actions, classifications, and clinical implications in managing cardiovascular conditions.

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