SCAI CHAP 5 Vasocative Drugs Flashcards
(26 cards)
Q1: How are coronary vasodilators generally classified based on their mode of action?
Q2: How do endothelium-dependent vasodilators cause vasodilation?
Q3: What molecule is converted from L-arginine in the action of endothelium-dependent drugs?
Q4: How do endothelium-independent vasodilators act on vascular smooth muscle cells (VSMCs)?
Q5: What molecule is converted into cyclic GMP (induces vasodilation) in the action of endothelium-independent vasodilators?
Q6: What is nitroglycerin metabolized into within VSMCs?
Q7: What does S-nitrosothiol activate to produce cyclic GMP (induces vasodilatation) ?
Q8: Does nitroglycerin have a more pronounced effect on venous or arterial circulation?
Q9: How does nitroglycerin’s venodilatation affect myocardial oxygen demand?
Q10: Does nitroglycerin dilate normal, diseased, or both types of coronary arteries?
Q11: What is the clinical importance of nitroglycerin’s coronary artery dilation ?
Q12: What are the routes of administration for nitroglycerin?
Q13: What is nitroglycerin commonly used for in the catheterization laboratory?
Q14: Name two purposes of nitroglycerin use during coronary angiography or PCI.
Q15: How does nitroglycerin help patients with elevated filling pressures?
A1: Endothelium dependent (Arginine) and endothelium independent (GTP)
A2: By converting L-arginine into nitric oxide in a healthy endothelium
A3: Nitric oxide
A4: They act directly on VSMCs, *bypassing the endothelium
A5: Guanosine triphosphate or GTP
A6: *Nitric oxide ( which is in turn converted to S-nitrosothiol )
A7: *Guanylate cyclase enzyme
A8: Venous circulation
A9: It reduces myocardial wall stress, decreasing oxygen demand
A10: *Both normal and diseased coronary arteries
A11: It is important in patients with vasospastic angina
A12: Sublingual, intra-arterial (IA), intravenous (IV), and intracoronary (IC)
A13: To prevent or treat arterial spasm
A14: Improve coronary *flow and *provoke myocardial bridging
A15: By reducing preload
Q1: What is the typical bolus dose range for intracoronary (IC) nitroglycerin administration?
Q2: What adverse effects can higher doses of IC nitroglycerin cause?
Q3: Nitroglycerin should not be administered to patients with systolic blood pressure below what value?
Q4: How long should patients wait after taking phosphodiesterase-5 inhibitors before receiving nitroglycerin?
Q5: Name the phosphodiesterase-5 inhibitors mentioned that require *48-hour wait before nitroglycerin administration.
Q6: Why should nitroglycerin be administered cautiously in patients with severe aortic stenosis?
Q7: What other cardiac conditions warrant caution when administering nitroglycerin?
Q8: Why is there an increased risk of hypotension in volume-dependent pathologies when nitroglycerin is administered?
Q9: What are two treatments for hypotension caused by nitroglycerin administration?
Q10: What is the effect of nitroglycerin on coronary vasodilation beyond a certain dose?
Q11: How does reflex tachycardia relate to nitroglycerin dosing?
Q12: What specific volume-dependent pathology is mentioned that requires caution with nitroglycerin?
A1: 50 to 400 micrograms (µg)
A2: Hypotension and reflex tachycardia without further coronary vasodilation
A3: 90 mm Hg
A4: 24 ( Vardenafil, Avanafil, Sildenafil) to 48 hours
A5: Tadalafil (Cialis or Adcirca)
A6: Due to increased risk of exaggerated and deleterious hypotensive response
A7: Hypertrophic cardiomyopathy, severe left main disease, right ventricular infarction
A8: Because of volume depletion or volume-dependent pathology leading to exaggerated hypotension
A9: Intravenous fluids and vasopressors
A10: No further augmentation in coronary vasodilation occurs
A11: Reflex tachycardia can occur with higher doses of nitroglycerin
A12: Restrictive cardiomyopathy
Q1: What type of molecule is nitroprusside?
Q2: What enzyme does nitroprusside activate?
Q3: What molecule is generated by guanylate cyclase activation?
Q4: What is the effect of cyclic GMP on smooth muscle?
Q5: Does nitroprusside have a more potent effect on arterial or venous beds?
Q6: Name two clinical conditions nitroprusside can be used to treat.
Q7: What is the starting IV dose range of nitroprusside?
Q8: By how much can the nitroprusside dose be titrated?
Q9: What is the maximum IV dose of nitroprusside?
Q10: How is nitroprusside administered during PCI to treat **slow or no-reflow?
A1: Direct nitric oxide *donor
A2: Guanylate cyclase
A3: Cyclic GMP (induces vasodilation)
A4: Smooth muscle relaxation and vasodilation
A5: ++Arterial beds
A6: Hypertensive crisis and acute heart failure (particularly due to acute mitral regurgitation)
A7: 0.25 to 0.3 µg/kg/min
A8: 0.5 µg/kg/min every few minutes
A9: 10 µg/kg/min
A10: **In 25- to 200-µg intracoronary (IC) boluses with a quick saline flush up to *1000 µg
Q1: What type of calcium channel do calcium channel blockers inhibit?
Q2: What are the two main classes of calcium channel blockers?
Q3: Name three examples of *dihydropyridine ( d for direct vasodilators ) calcium channel blockers.
Q4: Name two examples of *nondihydropyridine (non direct vasodilators) calcium channel blockers.
Q5: What is the predominant effect of dihydropyridine calcium channel blockers?
Q6: How do nondihydropyridines affect cardiac contractility and AV nodal conduction?
Q7: What general effects do calcium channel blockers have on peripheral vascular resistance and blood pressure?
Q8: How do calcium channel blockers affect *coronary blood flow?
Q9: For what types of arrhythmias are nondihydropyridines used in the catheterization laboratory?
Q10: Which calcium channel blocker is used to treat hypertensive crisis?
Q11: What conditions can calcium channel blockers treat related to vascular spasm?
Q12: What is a common side effect of dihydropyridine calcium channel blockers?
Q13: What negative cardiac effect is more pronounced with nondihydropyridines?
Q14: What conduction disturbances can nondihydropyridines cause?
Q15: Why are nondihydropyridines generally *contraindicated in patients with * right or left ventricular dysfunction?
A1: L-type calcium channel present on VSMC and slow responding myocardial cells
A2: Dihydropyridines and nondihydropyridines
A3: Amlodipine, felodipine, isradipine, nicardipine, nifedipine
A4: Verapamil and diltiazem
A5: *Predominant vasodilator effect with little or no effect on cardiac contractility or conduction
A6: They have a more pronounced effect on *reducing cardiac contractility and *AV nodal conduction
A7: Decrease peripheral vascular resistance and blood pressure
A8: *Increase coronary blood flow
A9: Supraventricular and atrial arrhythmias
A10: *Nicardipine
A11: *Radial or coronary spasm, slow flow or no-reflow
A12: Hypotension and reflex tachycardia
A13: Negative inotropy
A14: AV nodal blocks or *sinus arrest
A15: Because of their negative inotropic effects, which can *worsen ventricular dysfunction ( more verapamil than diltiazem )
Q1: What is the initial IV bolus dose of diltiazem for supraventricular tachycardia (SVT) or atrial tachycardias?
Q2: What is the maintenance infusion rate of diltiazem for SVT or atrial tachycardias?
Q3: What is the intra-arterial (IA) dose range of diltiazem for *radial artery spasm?
Q4: What is the intracoronary (IC) bolus dose range of diltiazem for *slow flow or no-reflow?
Q5: What is the initial IV bolus dose of verapamil for SVT or atrial tachycardias?
Q6: When can a second IV dose of verapamil be given, and what is the dose range?
Q7: What is the IA dose range of verapamil for radial artery spasm?
Q8: What is the typical IC bolus dose range of verapamil for slow flow or no-reflow ( 60-100 % success rate)?
Q9: How many IC boluses of verapamil may be given for slow flow or no-reflow?
Q10: What is the success rate range of verapamil IC boluses for slow flow or no-reflow?
Q11: Which dihydropyridine calcium channel blocker can be given IV or IA?
Q12: What is the IV infusion dose of nicardipine for treating hypertension?
Q13: What is the maximum IV infusion dose of nicardipine?
Q14: What is the IC bolus dose of nicardipine for slow flow or no-reflow treatment ( 99% success rates +++++) ?
Q15: For what procedures is IA nicardipine used prophylactically to prevent no-reflow?
A1: 0.25 mg/kg (15-20 mg) over 2 minutes
A2: 5 to 20 mg/h
A3: *2.5 to 5 mg IA
A4: *0.5 to 2 mg IC
A5: 2.5 to 5 mg over 2 minutes
A6: *15 to 30 minutes later; 5 to 10 mg (~0.15 mg/kg)
A7: 2.5 to 5 mg IA
A8: 50 to 200 µg
A9: 2 to 4 boluses
A10: 60% to 100% success rates
A11: *Nicardipine
A12: 5 mg/h
A13: 15 to 20 mg/h
A14: *200 µg
A15: Saphenous vein graft (SVG) PCIs and rotational atherectomy
** Nicardipine dose is 2.5 to 5 mg IA for prophylactic treatment or treatment of radial artery spasm during transradial procedures.
Q1: What type of receptor agonist is adenosine?
Q2: To which receptor does adenosine bind on *arteriolar smooth muscle cells?
Q3: What molecule’s production is increased by adenosine binding to A2A receptors?
Q4: What effect does increased cyclic AMP have on smooth muscle cells?
Q5: What physiological effect does adenosine produce in coronary arteries?
Q6: For what diagnostic evaluations is adenosine used in the catheterization laboratory?
Q7: What is the typical intracoronary (IC) bolus dose of adenosine for the *right coronary artery (RCA)?
Q8: What is the typical IC bolus dose of adenosine for the *left coronary artery (LCA)?
Q9: What is the intravenous (IV) infusion dose of adenosine for FFR or CFR evaluation?
Q10: How soon is maximal hyperemia achieved after *IC adenosine bolus administration?
Q11: How long does the *plateau of hyperemia last after IC adenosine bolus?
Q12: How long does it take for peak hyperemic effect to be reached after *IV adenosine administration?
Q13: How long does the hyperemic effect last after stopping IV adenosine?
Q14: Which produces *more hyperemia, IV or IC adenosine?
Q15: In pulmonary hypertension vasodilator challenge testing, what is the starting IV adenosine infusion dose?
Q16: By how much is the IV adenosine dose increased every 2 minutes during pulmonary hypertension testing?
Q17: What is the maximum IV adenosine dose during pulmonary hypertension testing?
Q18: What IC adenosine bolus doses are used to treat **slow or no-reflow during coronary and SVG PCI ( 90% success rate ++++ )?
Q19: What is the success rate of IC adenosine in treating slow or no-reflow?
Q20: What is the purpose of the quick saline flush after IC adenosine bolus?
A1: *Nonselective adenosine receptor *agonist
A2: A2A receptors
A3: Cyclic adenosine monophosphate (cAMP)
A4: Smooth muscle cell relaxation and vasodilation
A5: Coronary hyperemia
A6: Fractional flow reserve (FFR), coronary flow reserve (CFR), and microvascular resistance assessment
A7: 50-100 µg
A8: 100-200 µg
A9: *140 µg/kg/min over 2 to 3 minutes
A10: Within a few *seconds
A11: Around 5 seconds
A12: Within 2 minutes
A13: Less than 30 seconds
A14: IV adenosine +++++ ( IV adenosine permits measurement of pullback FFR ) ++++
A15: 50 µg/kg/min
A16: 50 µg/kg/min every 2 minutes
A17: 250 µg/kg/min
A18: 24 to 60 µg
A19: 90% ( looks like best is nicardipine then adenosine )
A20: To quickly clear the adenosine from the artery
Q1: What type of receptor agonist is regadenoson?
Q2: How is regadenoson administered?
Q3: For what imaging technique is regadenoson used as a stress agent?
Q4: How quickly is peak hyperemia reached after regadenoson administration?
Q5: How long does the hyperemia last after regadenoson administration?
Q6: What IV adenosine infusion dose was regadenoson compared to in FFR evaluation?
Q7: How does regadenoson’s effectiveness in measuring FFR compare to adenosine?
Q8: Name two advantages of regadenoson over adenosine.
Q9: List three common side effects of adenosine.
Q10: What drug can reverse severe and prolonged side effects of adenosine?
Q11: In which patients is adenosine contraindicated?
Q12: Why should adenosine be used cautiously in patients with bronchospastic lung disorders?
A1: Selective adenosine A2A receptor agonist
A2: Single 0.4-mg intravenous (IV) bolus
A3: Nuclear myocardial perfusion imaging
A4: Within seconds
A5: Around 2 minutes
A6: 140 µg/kg/min ++++
A7: It is *as effective as adenosine with a strong linear correlation
A8: More *rapid hyperemia and ease of use
A9: Bronchospasm, chest pain, dyspnea
A10: 50 to 100 mg of IV aminophylline
A11: Patients with heart transplantation++++ ( due to denervation, adenosine can cause asystole and response is unpredictable ) or second- or third-degree heart block without a pacemaker
A12: Risk of adenosine-induced bronchoconstriction
Q1: What is papaverine primarily used for in cardiology?
Q2: What is the proposed mechanism of action of papaverine?
Q3: How does papaverine affect smooth muscle cells (SMCs)?
Q4: What coronary assessments is intracoronary (IC) papaverine used for?
Q5: What is the *onset of action time for IC papaverine?
Q6: How long does the effect of IC papaverine typically last?
Q7: What are the commonly used IC bolus doses of papaverine for the right coronary artery (RCA) and left coronary artery (LCA)?
Q8: What cardiac electrical interval can papaverine prolong?
Q9: What potentially serious arrhythmia can papaverine cause?
Q10: What adverse effect can papaverine have when combined with some ionic contrast agents?
A1: Papaverine is used as a potent arterial vasodilator to induce coronary hyperemia for assessment of coronary flow reserve (CFR) or fractional flow reserve (FFR).
A2: It inhibits a phosphodiesterase enzyme, increasing cyclic AMP in smooth muscle cells ( coronary dilatation ) .
A3: It causes smooth muscle relaxation and arterial vasodilatation.
A4: Coronary flow reserve (CFR) and fractional flow reserve (FFR) assessment.
A5: Within 10 to 30 seconds ( a little bit delayed )
A6: 45 to 60 seconds from the time of administration ( also delayed or prolonged )
A7: 8 mg for the right coronary artery (RCA) and 12 mg for the left coronary artery (LCA).
A8: QT interval ++++++
A9: Torsades de pointes +++++
A10: Crystallization ++++ when combined with some ionic contrast agents ( it can increase coronary venous lactate production, which may cause myocardial ischemia )
Q1: What type of neurotransmitter is acetylcholine?
Q2: What receptors does acetylcholine stimulate on endothelial cells?
Q3: What does acetylcholine cause in a **healthy endothelium?
Q4: How does acetylcholine cause vasoconstriction?
Q5: What determines the net effect of acetylcholine on coronary arteries?
Q6: What is the typical response to acetylcholine in *normal coronary arteries ( healthy endothelium)?
Q7: What effect does acetylcholine have in patients with endothelial dysfunction?
Q8: For what condition is acetylcholine used diagnostically?
Q9: Besides vasospastic angina, what vasomotor responses can acetylcholine assess?
Q10: In a study of stable angina patients with *minimal coronary disease, what percentage had *epicardial spasm ( in this study it is defined as >75% coronary narrowing with symptom production) ?
Q11: What percentage of patients had *microvascular spasm (symptom reproduction with ischemic electrocardiogram [ECG] changes and no epicardial spasm) in the same study ?
Q12: What are the usual intracoronary *incremental doses of acetylcholine injected into the *right coronary artery (RCA)?
Q13: What are the usual intracoronary **incremental doses of acetylcholine injected into the *left coronary artery (LCA)?
Q14: How is spasm *defined after acetylcholine administration?
Q15: What medication can reverse acetylcholine-induced coronary spasm?
A1: An endogenous neurotransmitter
A2: Muscarinic receptors
A3: Endothelial-dependent vasodilatation via release of nitric oxide and other vasoactive substances
A4: By direct activation of receptors on smooth muscle cells (SMCs)
A5: The *balance between endothelial-dependent vasodilation and direct SMC activation (constriction)
A6: Mild vasodilation or no change in vessel caliber
A7: Vasoconstriction or *coronary spasm
A8: Vasospastic angina
A9: Epicardial and microvascular *vasomotor responses ( abnormal vasomotor response can lead to ischemia in patients with normal cornaries or stable angina)
A10: 45% ( almost half )
A11: 55% ( more than a half )
A12: 20, 50, and 80 µg
A13: 20, 50, 100, and 200 µg
A14: ≥90% coronary narrowing with clinical evidence of ischemia
A15: Intracoronary nitroglycerin
*** Spasm caused by *low doses of acetylcholine is usually more *proximal and focal. Spasm caused by *higher acetylcholine doses is associated with more *distal and diffuse spasm.
Q1: How is acetylcholine metabolized in the body?
Q2: What are the typical continuous infusion doses of acetylcholine used to assess normal endothelial coronary artery function?
Q3: What physiological effect does acetylcholine have on *normal coronary arteries?
Q4: Name three potential side effects of acetylcholine administration.
Q5: What *precaution is recommended during acetylcholine administration in the right coronary artery (RCA)?
Q6: What was the incidence of major complications associated with intracoronary acetylcholine in a large meta-analysis?
Q7: What type of drug is ergonovine?
Q8: What is ergonovine commonly used for outside of cardiology?
Q9: How is ergonovine used in the coronary arteries?
Q10: What is the intracoronary (IC) infusion dose of ergonovine for the RCA?
Q11: What is the IC infusion dose of ergonovine for the left coronary artery (LCA)?
Q12: Describe the alternative method of ergonovine administration via slow IC injections.
Q13: What is the maximum cumulative dose of ergonovine when given by slow IC injections?
Q14: What monitoring is performed during ergonovine administration?
Q15: What symptom prompts ECG monitoring during ergonovine testing?
A1: Acetylcholine is very short acting and rapidly inactivated.
A2: 0.02 to 2.2 µg (10⁻⁸, 10⁻⁷, 10⁻⁶ M)
A3: Mild vasodilatation and augmentation of coronary blood flow.
A4: Marked bradycardia, heart block, and profound vasospasm.
A5: Temporary pacing is recommended during administration in the RCA.
A6: 0.5% incidence of major complications, with no deaths reported.
A7: An ergot derivative.
A8: To induce uterine contractions to treat or prevent postpartum hemorrhage.
A9: To provoke coronary spasm and evaluate patients with angina and normal or minimal coronary artery disease.
A10: 10 µg/min over 4 minutes for a maximal dose of 40 µg.
A11: 16 µg/min over 4 minutes for a total dose of 64 µg.
A12: Slow IC injections over 1 minute each of sequential doses of 1, 5, 10, and 30 µg at 3- to 5-minute intervals.
A13: 50 µg maximum cumulative dose.
A14: ECG obtained at the end of each interval or if angina symptoms develop.
A15: Development of angina symptoms.
Q1: When should angiography of the right and left coronary arteries be promptly performed?
Q2: What is the typical PHYSIOLOGIC coronary response to ergonovine?
Q3: What degree of focal coronary narrowing indicates coronary spasm?
Q4: What additional findings must accompany severe focal narrowing to diagnose coronary spasm?
Q5: How can ergonovine-induced spasm be reversed?
Q6: How many patients were included in the study comparing IC acetylcholine-induced spasm to IC ergonovine ?
Q8: Which agent was more likely to provoke spasm in patients without fixed stenosis?
Q9: What was the percentage of spasm provoked by acetylcholine in patients without fixed stenosis?
Q10: What was the percentage of spasm provoked by ergonovine in patients without fixed stenosis?
Q11: What was the complication rate with the acetylcholine test?
Q12: What was the complication rate with the ergonovine test?
Q13: Were any myocardial infarctions reported as complications in either test?
Q14: Were there any deaths reported as complications in either test?
Q15: What does this data suggest about the safety of acetylcholine and ergonovine testing?
A1: When angina symptoms occur
A2: *Diffuse coronary narrowing
A3: Greater than 75% or 90% focal coronary narrowing
A4: Ischemic ECG changes or typical symptoms
A5: Administration of intracoronary nitroglycerine
A6: 873 patients AcH and ergonovine 635 patients
A8: Acetylcholine
A9: 36.2%
A10: 25.5%
A11: 1.4%
A12: 0.2%
A13: No
A14: No
A15: Both tests are generally safe with low complication rates
Q1: What effect do vasopressor drugs generally have on systemic vascular resistance (SVR) and mean arterial pressure (MAP)?
Q2: What do inotropic drugs increase in the heart?
Q3: Can some vasopressor drugs have both vasopressor and inotropic effects?
Q4: What effect does stimulation of *peripheral α1 receptors cause?
Q5: What effect does stimulation of *cardiac α1 receptors have?
Q6: What do *β1 receptors mainly affect?
Q7: What effect does stimulation of *β2 receptors have on vasculature?
Q8: What is the effect of stimulating dopaminergic DA1 receptors?
Q9: In which vascular beds does *DA1 receptor stimulation cause vasodilation?
Q10: What type of receptor agonist is *phenylephrine?
Q11: What is the main effect of phenylephrine?
Q12: How does phenylephrine affect cardiac inotropy and cardiac output?
Q13: In what clinical situations is phenylephrine commonly used?
Q14: What are the typical doses of phenylephrine for rapid bolus administration?
Q15: What are some adverse effects of phenylephrine?
Q16: Why can phenylephrine cause a marked increase in blood pressure in patients on nonselective β blockers?
Q17: What *reflex response can phenylephrine induce?
Q18: What types of vasoconstriction can phenylephrine cause?
Q19: How is phenylephrine administered in the catheterization laboratory to correct hypotension?
Q20: For which cardiac conditions is phenylephrine used when hypotension develops?
A1: They cause an increase in systemic vascular resistance (SVR) and mean arterial pressure (MAP).
A2: Cardiac contractility and chronotropy.
A3: Yes, depending on the receptors they stimulate.
A4: Vasoconstriction.
A5: Augments inotropy ( from AI : Alpha-1 adrenergic receptors are present in the smooth muscle cells of coronary arteries. Activation of these receptors causes vasoconstriction of the coronary vessels. However, under normal physiological conditions, the coronary circulation is primarily regulated by metabolic and endothelial factors, and sympathetic alpha-mediated vasoconstriction plays a minor role. In certain pathological or pharmacological states (e.g., high sympathetic tone, use of alpha-agonists), alpha receptor-mediated coronary vasoconstriction can become significant, potentially contributing to coronary spasm or ischemia )
A6: Inotropy and chronotropy ( beta 1 are MAINLY located in myocytes )
A7: *Vasodilation ( located MAINLY in vessels )
A8: *Vasodilation.
A9: *Renal, splanchnic, cerebral, and coronary beds.
A10: Pure α receptor agonist ++++
A11: Peripheral vasoconstriction ( peripheral alpha 1)
A12: Minimal effect on cardiac inotropy and cardiac output ( cardiac alpha 1)
A13: Hypotension with low SVR, such as sepsis, neurologic disorders, anesthesia- or medication-induced hypotension, and during *carotid stenting.
A14: 50 to 200 µg rapid boluses.
A15: Marked increase in blood pressure, reflex-mediated *bradycardia, severe peripheral and visceral vasoconstriction.
A16: Because β blockers block vasodilation, leading to unopposed α-mediated vasoconstriction.
A17: Reflex-mediated bradycardia.
A18: Peripheral and *visceral vasoconstriction ( expect radial artery spasm with phenylephrine )
A19: As rapid boluses or intravenous drip.
A20: Severe aortic valve stenosis and hypertrophic obstructive cardiomyopathy ( board question )
Q1: Which receptors does *norepinephrine predominantly stimulate?
Q2: What is the primary effect of norepinephrine on blood vessels?
Q3: For what clinical conditions is norepinephrine commonly used?
Q4: What are two potential side effects of norepinephrine?
Q5: How does norepinephrine affect systemic vascular resistance (SVR) and blood pressure?
Q6: Which patients are especially sensitive to norepinephrine’s blood pressure effects?
Q7: How does *epinephrine’s effect on α1 and β1 receptors compare?
Q8: What is epinephrine’s effect on β2 receptors?
Q9: At *lower doses, what does epinephrine do to cardiac output and SVR?
Q10: At *higher doses, which receptor stimulation predominates with epinephrine?
Q11: For what emergency conditions is epinephrine the *first-line drug?
Q12: What is epinephrine’s role in treating *severe cardiogenic shock?
Q13: What are common side effects of epinephrine?
Q14: How can epinephrine-induced severe hypertension affect the brain?
Q15: In what postoperative setting is epinephrine commonly used to treat hypotension?
A1: α1 and β1 receptors ( some effects on beta 2 )
A2: Significant vasoconstriction and minimal inotropic/chronotropic effect ( pretty much like Neo , I think )
A3: Severe cardiogenic shock, *septic shock, or shock refractory to other pressors, especially in low-SVR states
A4: Peripheral ischemia and arrhythmias
A5: Increases SVR and blood pressure
A6: Patients on non-selective β blockers
A7: Equipotent effects on α1 and β1 receptors ( like NE )
A8: Modest effects on β2 receptors ( like NE )
A9: Increases cardiac output with minimal decrease in SVR ( equal stimulation of alpha 1 and beta 2 )
A10: α1 receptor stimulation predominates, causing vasoconstriction
A11: Cardiac arrest (asystole, pulseless electrical activity, ventricular fibrillation) and anaphylactic shock
A12: *Second-line drug
A13: Tachycardia, ventricular arrhythmias, increased oxygen demand, cardiac ischemia, increased SVR, severe hypertension
A14: Can cause cerebrovascular hemorrhage
A15: Following cardiac surgery
Q1: What type of receptors does dopamine stimulate at *low doses (1-2 µg/kg/min)?
Q2: What effect does low-dose dopamine have on renal blood flow?
Q3: Which circulations experience *vasodilation due to low-dose dopamine?
Q4: What receptors does medium-dose dopamine (2-7 µg/kg/min) stimulate?
Q5: How does *medium-dose dopamine affect systemic vascular resistance (SVR) and blood pressure?
Q6: What receptors are predominantly stimulated by high-dose dopamine (>7-10 µg/kg/min)?
Q7: What is the effect of high-dose dopamine on SVR and mean arterial pressure (MAP)?
Q8: For what clinical conditions is dopamine occasionally used?
Q9: In which patient population is dopamine particularly useful for treating symptomatic bradycardia?
Q10: What are some adverse effects of high-dose dopamine?
Q11: Can dopamine cause renal vasoconstriction?
Q12: What is the risk of tissue **ischemia associated with dopamine?
Q13: How does dopamine’s effect on cardiac output change with dose?
Q14: What is the role of peripheral DA2 receptors in dopamine’s action?
Q15: Why might dopamine be chosen in patients without central venous access?
A1: Dopamine receptors (renal DA1 and peripheral DA2 receptors)
A2: Augments renal blood flow
A3: Renal, splanchnic, *coronary, and cerebral circulations
A4: β1 receptors ( increases cardiac output )
A5: *Variable effects depending on balance of vasodilation and increased cardiac output
A6: α1 receptors
A7: Vasoconstriction and increases in SVR and MAP
A8: Hypotension due to **nonprofound septic or cardiogenic shock, poor tissue perfusion ( oliguria, confusion ), symptomatic bradycardia
A9: Patients *without central venous access
A10: Tachycardia, arrhythmias, renal vasoconstriction, tissue ischemia
A11: Yes, particularly at high doses
A12: Increased risk at *high doses ( alpha effect )
A13: Increases with medium doses due to β1 stimulation
A14: Mediate peripheral vasodilation ( low dose )
A15: Because it can be administered peripherally and does not require central access
Q1: What type of receptor does *dobutamine predominantly agonize?
Q2: Is dobutamine primarily an inotrope or a pressor drug?
Q3: What condition is dobutamine mainly used to treat?
Q4: What effects does dobutamine have on cardiac output and systemic vascular resistance (SVR)?
Q5: How does dobutamine affect mean arterial pressure (MAP)?
Q6: Name three potential side effects of dobutamine.
Q7: What type of receptors does *isoproterenol stimulate?
Q8: What is the predominant effect of isoproterenol?
Q9: In what clinical situations is isoproterenol mainly used?
Q10: What effect does *continuous IV isoproterenol infusion have on heart rate and inotropy?
Q11: How does isoproterenol affect diastolic blood pressure and SVR ?
Q12: What are possible adverse effects of continuous IV isoproterenol infusion ?
Q13: Can isoproterenol be used to treat bradycardia unresponsive to atropine?
Q14: Is isoproterenol used in patients after cardiac transplantation?
Q15: What is the main difference in receptor activity between dobutamine and isoproterenol?
A1: β1 receptor ( not much effect on beta 2)
A2: Inotrope
A3: Low cardiac output congestive heart failure (CHF)
A4: Increases cardiac output and decreases SVR ( decreases cardiac filling pressures )
A5: Minimal decrease or no effect on MAP
A6: Tachycardia, **ventricular arrhythmias, **cardiac ischemia
A7: β1 and β2 receptors
A8: Predominant **chronotropic effect ( lesser effect on Inotropy and vasodilatation )
A9: To induce tachycardia ( like in brugada or torsades ), stimulate sinus node in resistant bradycardia to atropine or dopamine, and treat hypotension *related++++++ to bradycardia or post-cardiac transplantation ( EP love it )
A10: Significant increase in heart rate and inotropy
A11: ***Decrease in diastolic blood pressure and SVR
A12: *Ventricular arrhythmias, cardiac ischemia, hypertension or hypotension
A13: Yes
A14: Yes
A15: Dobutamine predominantly stimulates β1 receptors; isoproterenol stimulates both β1 and β2 receptors
Q1: What type of enzyme do phosphodiesterase inhibitors like *milrinone inhibit?
Q2: How do phosphodiesterase inhibitors increase intracellular cyclic AMP?
Q3: Are the inotropic effects of milrinone dependent on β-adrenergic receptors?
Q4: Compared to dobutamine, how does milrinone’s vasodilator effect differ?
Q5: How does milrinone’s chronotropic effect compare to dobutamine?
Q6: What condition is milrinone primarily used to treat?
Q7: Name two potential cardiac side effects of milrinone.
Q8: What is vasopressin classified as?
Q9: Which receptors does vasopressin stimulate on vascular smooth muscle cells (VSMCs)?
Q10: Which receptors does vasopressin stimulate in the renal collecting duct system?
Q11: For what conditions is vasopressin used as a second-line drug?
Q12: When is vasopressin used as a first-line drug during cardiac arrest?
Q13: Name two cardiovascular side effects of vasopressin.
Q14: What serious peripheral complication can vasopressin cause at high doses?
Q15: How does vasopressin affect cardiac output at high doses?
A1: Phosphodiesterase III
A2: By inhibiting phosphodiesterase III, increasing cyclic AMP ( vasodilator ) *independent of β-adrenergic receptors
A3: No, it is independent of β-adrenergic receptors
A4: Milrinone has a more potent central and peripheral *vasodilator effect than dobutamine
A5: Milrinone has a *lesser chronotropic effect compared to dobutamine ( Milrinone does not give much tachycardia like dobutamine )
A6: Low cardiac output *heart failure
A7: *Ventricular arrhythmias and cardiac ischemia. Also torsades and hypotension.
A8: An antidiuretic hormone with vasopressor effects
A9: V1 receptors
A10: V2 receptors
A11: Catecholamine-refractory septic or anaphylactic shock
A12: As a first-line drug instead of epinephrine during cardiac arrest
A13: Arrhythmias and hypertension
A14: Severe peripheral ischemia ++++ leading to splanchnic and skin vasoconstriction
A15: It decreases cardiac output at high doses
This is left blank on purpose
Q1: What class of antiarrhythmic drug is *procainamide?
Q2: How do the electrophysiologic properties of procainamide compare to *quinidine?
Q3: What effect of procainamide accounts for some of the hypotension seen with IV administration?
Q4: What is the major metabolite of procainamide?
Q5: What channel does N-acetyl procainamide (NAPA) block?
Q6: How is procainamide metabolized and excreted?
Q7: Why is procainamide not used for long-term treatment?
Q8: For which arrhythmias is procainamide indicated?
Q9: What is the loading dose infusion rate of procainamide?
Q10: When should procainamide infusion be *stopped during loading?
Q11: What is the maintenance infusion rate of procainamide?
Q12: In which conditions is procainamide contraindicated?
A1: Class IA antiarrhythmic drug
A2: Similar electrophysiologic properties but without vagolytic and α receptor effects
A3: Ganglionic blocker effect
A4: N-acetyl procainamide (NAPA)
A5: Potassium (K) channel
A6: Hepatically metabolized to NAPA; both parent compund and metabolite are excreted renally
A7: Significant side-effect profile
A8: Hemodynamically **stable *monomorphic ventricular tachycardia (VT) and preexcited atrial fibrillation ++++ ( board question )
A9: 20 to 50 mg/min or 100 mg every 5 minutes until arrhythmia control or side effects occur
A10: If arrhythmia is controlled, hypotension occurs, QRS widens by 50%, or total dose of 17 mg/kg is given
A11: 1 to 4 mg/min maintenance infusion
A12: Prolonged QT interval or congestive heart failure (CHF)
Q1: What class of antiarrhythmic drug is lidocaine?
Q2: How does lidocaine affect the QT interval compared to other class I drugs?
Q3: On what type of myocardium does lidocaine mainly exert its suppressive effects?
Q4: What is lidocaine primarily used to treat?
Q5: Where is lidocaine metabolized in the body?
Q6: How do the metabolites of lidocaine compare to the parent drug in terms of antiarrhythmic effects?
Q7: Why should lidocaine *levels be monitored closely?
Q8: What is the typical IV bolus dose of lidocaine before ventriculography?
Q9: For which arrhythmias is lidocaine indicated if amiodarone is not available?
Q10: What is the *initial IV bolus dose of lidocaine for refractory VF or pulseless VT?
Q11: How often can *repeat *boluses 0.5 to 0.75 mg/kg of lidocaine be given?
Q12: What is the maintenance infusion rate of lidocaine?
A1: Class IB antiarrhythmic drug
A2: *Minimal effect on the QT interval compared to other class I drugs
A3: *Depolarized myocardium
A4: *Ventricular arrhythmias induced by ischemia +++++
A5: Liver
A6: They have *less antiarrhythmic effects than the parent drug
A7: To prevent toxicities, especially in patients with CHF or liver dysfunction
A8: 50 to 100 mg IV bolus to suppress ventricular ectopy or to treat ischemia-induced ventricular arrhythmias during cardiac catheterization or PCI.
A9: Ventricular fibrillation (VF) or *pulseless ( unstable ) ventricular tachycardia (VT).
(and for hemodynamically stable VT )
A10: 1 to 1.5 mg/kg IV bolus
A11: Every 5 to 10 minutes (the maximum cumulative dose is 3 mg/kg) for refractory VF or pulseless VT
A12: 1 to 4 mg/min
Q1: What class of antiarrhythmic drug is amiodarone?
Q2: What additional class effects does amiodarone have besides class III?
Q3: What is the main metabolite of amiodarone and its effect?
Q4: What solvent is required for IV administration of amiodarone?
Q5: what causes a decrease in heart rate and blood pressure, especially during IV Amiodarone bolus?
Q7: How long is the elimination half-life of amiodarone?
Q8: Which drugs’ clearance can amiodarone decrease +++?
Q9: What risk is increased when amiodarone is used with other antiarrhythmic or psychiatric drugs?
Q10: How should warfarin and digoxin doses be adjusted when used with long-term amiodarone?
Q11: What is the *initial IV bolus dose of amiodarone for VF or pulseless VT?
Q12: What is the maintenance infusion protocol for amiodarone after return of spontaneous circulation?
A1: Class III antiarrhythmic drug
A2: Class I, II, and IV effects
A3: Desethylamiodarone, a potent *sodium channel blocker
A4: Polysorbate 80
A5: Both *solvent and amiodarone’s β and calcium channel blocking effects
A6: Metabolized in the liver with minimal renal elimination
A7: Mean elimination half-life of 54 days ++ very long
A8: Flecainide, procainamide, and quinidine
A9: Prolonged QT interval and risk of torsades de pointes ( concomittant use with mexiletine, propafenone, quinidine, disopyramide, procainamide, tricyclic antidepressants and some of the antipsychotic drugs )
A10: Reduce doses by half
A11: 300 mg IV bolus ( Amiodarone is indicated for VF or pulseless VT and is given as a 300-mg IV bolus, with a supplemental 150-mg IV bolus dose if VF or pulseless VT *continues after defibrillation, or if it recurs. Amiodarone is also indicated for *stable VT or for pharmacologic conversion or rate control of *supraventricular
or atrial arrhythmias. A 150-mg IV bolus is infused over 10 minutes, followed by a maintenance dose infused at 1 mg/min for 6 hours followed by 0.5 mg/min for 18 hours )
A12: Infused at 1 mg/min for 6 hours, then 0.5 mg/min for 18 hours
