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Quizzes > Health & Medicine > Human Anatomy & Medicine

Paramedic Quiz: Master Negative Chronotropic Effect Medications

Ready to tackle negative chronotropic effect drugs? Dive into this Paramedic Chapter 7 quiz!

Difficulty: Moderate
2-5mins
Learning OutcomesCheat Sheet
Paper art illustration for paramedic quiz on negative chronotropic effect medications on coral background

This quiz helps you identify negative chronotropic medications and decide when they slow heart rate in EMS care. You'll practice scenario-based questions with instant feedback to spot gaps before an exam or shift. For extra practice, check the cardiac med guide and a quick paramedic quiz .

What does a negative chronotropic effect refer to in cardiac pharmacology?
Increase in contractility
Increase in heart rate
Decrease in conduction velocity
Decrease in heart rate
A negative chronotropic effect specifically means a reduction in heart rate by slowing the sinoatrial node. This is distinct from inotropic effects, which alter contractility. Many beta-blockers and certain calcium channel blockers exhibit this property.
Which of the following is a selective beta-1 adrenergic receptor blocker?
Propranolol
Metoprolol
Nadolol
Carvedilol
Metoprolol preferentially blocks beta-1 receptors in the heart, reducing heart rate without significant bronchial beta-2 effects at standard doses. Nonselective agents like propranolol block both beta-1 and beta-2. This selectivity makes metoprolol safer in patients with reactive airway disease.
Which beta-blocker is considered non-selective?
Nadolol
Atenolol
Metoprolol
Esmolol
Nadolol blocks both beta-1 and beta-2 receptors equally, reducing heart rate and affecting bronchial smooth muscle. Atenolol and metoprolol are cardioselective at lower doses. Non-selectivity increases risk of bronchospasm in susceptible patients.
Which calcium channel blocker most significantly slows AV nodal conduction?
Amlodipine
Nifedipine
Diltiazem
Felodipine
Diltiazem has significant negative chronotropic and dromotropic effects on the AV node. Dihydropyridines like nifedipine and amlodipine primarily affect vascular smooth muscle. This property makes diltiazem useful for rate control in atrial fibrillation.
What heart rate defines bradycardia?
Between 60 and 100 beats per minute
Less than 60 beats per minute
Exactly 60 beats per minute
Greater than 100 beats per minute
Bradycardia is defined as a resting heart rate below 60 beats per minute. It may be physiologic in athletes or pathologic in conduction disease. Negative chronotropic drugs can induce bradycardia therapeutically or as a side effect.
Which of the following drugs is commonly used to control ventricular rate in atrial fibrillation through negative chronotropic action?
Amiodarone
Furosemide
Hydralazine
Diltiazem
Diltiazem reduces AV nodal conduction and slows ventricular rate in atrial fibrillation. Hydralazine and furosemide do not affect AV nodal conduction directly. Amiodarone has rate control properties but is used for rhythm conversion and maintenance rather than acute rate control.
Which side effect is most likely with non-selective beta-blockers?
Tinnitus
Hyperglycemia
Bronchospasm
Constipation
Non-selective beta-blockers block beta-2 receptors in bronchial smooth muscle, leading to bronchoconstriction. This makes them relatively contraindicated in asthma or COPD. Hyperglycemia is less directly linked, and tinnitus and constipation are uncommon.
Which beta-blocker has intrinsic sympathomimetic activity?
Pindolol
Atenolol
Esmolol
Metoprolol
Pindolol is a partial agonist with intrinsic sympathomimetic activity, causing less resting bradycardia. Atenolol, esmolol, and metoprolol are pure antagonists. ISA may limit maximal bradycardia but could be beneficial in patients with baseline low heart rate.
Which ultra-short-acting beta-blocker is administered intravenously for acute rate control?
Metoprolol
Nadolol
Propranolol
Esmolol
Esmolol has a very short half-life (~9 minutes) and is given IV for acute heart rate control. Propranolol and metoprolol have longer durations, making them less suitable for rapid titration. Nadolol is oral and long-acting.
Which electrocardiographic finding might be precipitated by excessive negative chronotropic drug dosing?
Wolff-Parkinson-White pattern
ST-elevation
Left bundle branch block
Second-degree AV block
Excessive slowing of AV nodal conduction can produce second-degree AV block. Bundle branch blocks involve ventricular conduction, not directly linked to AV nodal rate control drugs. ST-elevation indicates ischemia, and WPW is a pre-excitation syndrome.
Which agent increases vagal tone and produces a negative chronotropic effect?
Lidocaine
Amiodarone
Dobutamine
Digoxin
Digoxin acts on the central vagal nuclei and increases parasympathetic tone, lowering heart rate. Amiodarone and lidocaine primarily affect myocardial action potentials. Dobutamine is a beta-agonist that increases heart rate.
Which drug is contraindicated in asthmatic patients due to its non-selective beta-blocking action?
Esmolol
Propranolol
Atenolol
Metoprolol
Propranolol blocks beta-2 receptors in bronchial smooth muscle, risking bronchospasm in asthmatics. Cardioselective agents like atenolol and metoprolol are preferred when beta-blockade is needed. Esmolol is selective and ultra-short acting.
Which of the following is NOT a negative chronotropic agent?
Metoprolol
Verapamil
Diltiazem
Isoproterenol
Isoproterenol is a beta-agonist that increases heart rate (positive chronotrope). Verapamil, metoprolol, and diltiazem all slow heart rate. Clinically, isoproterenol can treat bradyarrhythmias by increasing sinus rate.
Which lab finding is most likely when a patient is overdosed on digoxin?
Hyponatremia
Hypermagnesemia
Hypokalemia
Hypercalcemia
Digoxin toxicity often occurs in the setting of hypokalemia, which enhances binding to the Na+/K+ ATPase. Hypercalcemia can exacerbate toxicity but is less directly causal. Sodium and magnesium changes are less specific.
What is the primary site of action for calcium channel blockers that produce negative chronotropy?
Coronary endothelium
Atrial muscle only
Ventricular myocytes
SA and AV nodes
Non-dihydropyridine calcium channel blockers act primarily at the SA and AV nodes to slow depolarization. Dihydropyridines target vascular smooth muscle more selectively. This nodal action leads to negative chronotropic and dromotropic effects.
Which condition would most likely be exacerbated by a negative chronotropic medication?
Sick sinus syndrome
Hyperthyroidism
Hypertension
Hyperlipidemia
Sick sinus syndrome features intrinsic SA node dysfunction and bradycardia; further rate slowing can cause syncope. Negative chronotropes are used cautiously or avoided. They may benefit hyperthyroid-associated tachycardia or hypertension but worsen primary bradyarrhythmias.
Which beta-blocker has the shortest elimination half-life, requiring continuous infusion for sustained effect?
Atenolol
Propranolol
Metoprolol
Esmolol
Esmolol's half-life is about 9 minutes due to rapid hydrolysis by red blood cell esterases. It requires continuous IV infusion for consistent rate control. Other beta-blockers have much longer half-lives and can be given intermittently.
Which laboratory parameter would you monitor to reduce the risk of toxicity when a patient is started on digoxin and a diuretic?
Creatinine kinase
Thyroid stimulating hormone
Potassium levels
White blood cell count
Loop and thiazide diuretics can cause hypokalemia, increasing digoxin toxicity risk. Monitoring serum potassium helps guide supplementation. CK, WBC, and TSH are unrelated to digoxin toxicity in this context.
Which mechanism explains how beta-blockers reduce heart rate?
Direct sodium channel blockade
Activation of muscarinic receptors
Inhibition of renin release only
Blockade of beta-1 receptors at the SA node
Beta-1 blockade in the SA node decreases the slope of phase 4 depolarization, slowing rate. While beta-blockers also reduce renin release, this is not the direct chronotropic mechanism. They do not activate muscarinic receptors or block sodium channels primarily.
Which electrolyte disturbance enhances the negative chronotropic effect of calcium channel blockers?
Hypermagnesemia
Hypokalemia
Hypernatremia
Hypocalcemia
Magnesium competes with calcium at L-type channels, and hypermagnesemia can potentiate the nodal slowing effect of calcium channel blockers. Hypokalemia and hypocalcemia affect cardiac excitability differently. Sodium levels have minimal direct impact on CCBs' chronotropy.
When initiating a beta-blocker in a patient with stable angina, what is the expected change in myocardial oxygen demand?
Increase due to elevated afterload
No change
Decrease due to lower heart rate and contractility
Increase due to reflex tachycardia
Beta-blockers reduce heart rate and contractility, thereby reducing myocardial oxygen demand. Afterload may modestly rise but not enough to offset the overall demand reduction. Reflex tachycardia is prevented by the blockade itself.
Which pharmacokinetic property of metoprolol can be altered by concomitant use of CYP2D6 inhibitors?
Volume of distribution decreases
Bioavailability decreases
Protein binding decreases
Elimination half-life increases
Metoprolol is metabolized by CYP2D6; inhibitors of this enzyme prolong its half-life. Volume of distribution, bioavailability, and protein binding are less affected by CYP2D6 activity. Clinicians monitor for enhanced effects when inhibitors are co-prescribed.
Which negative chronotropic drug must be used with caution in Wolff-Parkinson-White syndrome with atrial fibrillation?
Esmolol
Verapamil
Digoxin
Atenolol
Verapamil can preferentially block AV node conduction and force conduction through the accessory pathway, potentially increasing ventricular rate. Beta-blockers and digoxin also carry risk but verapamil is particularly cautioned. Guidelines often avoid AV nodal blockers in pre-excited AF.
Which drug interaction may potentiate bradycardia when combined with a calcium channel blocker?
Furosemide
Warfarin
Statins
Digoxin
Digoxin and nondihydropyridine calcium channel blockers both slow AV nodal conduction, leading to additive bradycardia. Diuretics, warfarin, and statins do not directly affect AV nodal conduction. Clinical monitoring is advised when co-administering digoxin and diltiazem or verapamil.
Which electrophysiological phase is most affected by beta-blockers to produce negative chronotropy?
Phase 4 of SA nodal action potential
Phase 0 of ventricular myocyte
Phase 1 of Purkinje fibers
Phase 2 of AV nodal action potential
Beta-blockers decrease the slope of phase 4 depolarization in the SA node, which slows pacemaker firing. They have minimal direct effects on phase 0 or phase 2 in ventricular tissue at therapeutic concentrations. This targeted action underlies their chronotropic effect.
Which calcium channel blocker requires dose adjustment in hepatic impairment to avoid increased chronotropic suppression?
Nifedipine
Verapamil
Felodipine
Amlodipine
Verapamil is extensively metabolized by the liver; impairment prolongs its half-life and exaggerates negative chronotropic effects. Amlodipine and felodipine also undergo hepatic metabolism but require less immediate adjustment. Nifedipine is less likely to cause bradycardia.
Which hemodynamic change is expected when a negative chronotropic drug is administered acutely?
Increased diastolic filling time
Sudden rise in cardiac output
Decreased end-diastolic volume
Increased stroke volume only
Slowing heart rate allows more diastolic filling time, often increasing stroke volume but not necessarily end-diastolic volume reduction. Cardiac output may decrease slightly due to rate drop. It does not acutely raise cardiac output.
In which patient scenario is esmolol preferred over metoprolol for rate control?
Chronic hypertension maintenance
Acute postoperative sinus tachycardia requiring short-term control
Outpatient rate control for atrial fibrillation
Long-term heart failure management
Esmolol's very short half-life allows rapid titration and quick discontinuation, ideal for acute perioperative tachycardia. Metoprolol is better for chronic therapy. Esmolol is less practical for outpatient or long-term management.
Which pattern on a Holter monitor suggests excessive negative chronotropic drug effect?
Short PR intervals
Prolonged pauses greater than 3 seconds
Multifocal PVCs
Frequent PACs
Excessive AV nodal suppression can cause significant pauses. PACs and PVCs reflect ectopic activity, not directly chronotropy. Short PR intervals indicate pre-excitation rather than drug effect.
Which genetic polymorphism affects metabolism of metoprolol leading to variable chronotropic response?
CYP1A2 slow acetylator variant
UGT1A1 polymorphism
CYP2D6 poor metabolizer variant
CYP3A4 ultrarapid metabolizer variant
CYP2D6 poor metabolizers clear metoprolol slowly, resulting in higher plasma levels and greater heart rate reduction. CYP3A4 and UGT1A1 are less involved in metoprolol clearance. Genetic testing can guide dosing in some cases.
Which of the following best describes the effect of verapamil on intracellular calcium in nodal tissue?
Activates sodium-calcium exchanger
Enhances ryanodine receptor release
Reduces L-type calcium channel influx during phase 0
Increases T-type calcium influx during phase 4
Verapamil blocks L-type calcium channels in nodal cells, particularly during depolarization, reducing heart rate. It does not increase T-type channel influx or ryanodine-mediated release. The Na-Ca exchanger is not directly activated by verapamil.
Which negative chronotropic agent undergoes enterohepatic recycling affecting its dosing interval?
Atenolol
Digoxin
Esmolol
Metoprolol
Digoxin is partially excreted in bile and undergoes enterohepatic recycling, prolonging its half-life. Beta-blockers like esmolol, atenolol, and metoprolol do not have significant enterohepatic circulation. This influences digoxin's dosing and potential toxicity.
Which advanced monitoring parameter is most useful for assessing effective chronotropic suppression in ICU patients on beta-blockers?
Pulmonary artery occlusion pressure
Holter-derived heart rate variability
Central venous pressure
Serum lactate
Heart rate variability from continuous monitoring reflects autonomic tone and beta-blocker effect. CVP and PAOP measure preload and SVR, not directly chronotropy. Serum lactate indicates tissue perfusion rather than nodal suppression.
In patients with cirrhosis, which negative chronotropic drug's clearance is most reduced, necessitating lower dosing?
Esmolol
Atenolol
Verapamil
Nadolol
Verapamil is extensively metabolized hepatically and reduced clearance in cirrhosis can cause profound bradycardia. Esmolol is metabolized by RBC esterases and unaffected by liver dysfunction. Atenolol and nadolol are renally excreted.
Which receptor subtype blockade contributes to bradycardia but not to bronchoconstriction?
M2 muscarinic blockade
Alpha-1 blockade
Beta-1 selective blockade
Beta-2 blockade
Beta-1 selective blockade reduces heart rate without significant beta-2 bronchial effects at therapeutic doses. Beta-2 blockade causes bronchoconstriction. Alpha-1 and muscarinic blockade do not mediate chronotropy in the SA node.
Which advanced ECG finding indicates effective negative chronotropic drug therapy without pathologic conduction block?
Prolonged QRS complex
Frequent multifocal PVCs
Second-degree AV block Mobitz II
Sinus bradycardia with normal PR interval
Sinus bradycardia with a normal PR interval shows slowed pacemaker activity without AV block. Mobitz II and QRS prolongation indicate pathologic conduction issues. PVCs represent ectopy, not chronotropic suppression.
Which signaling pathway is directly inhibited by beta-1 blockade in cardiac pacemaker cells?
RAS - MAPK pathway
Phospholipase C - IP3 pathway
Nitric oxide - cGMP pathway
cAMP-PKA mediated funny current activation
Beta-1 receptor activation increases cAMP, enhancing the funny (If) current via PKA phosphorylation in SA nodal cells. Blockade reduces this pathway and slows phase 4 depolarization. Other pathways are less relevant to chronotropic control.
Which clinical trial provided evidence for beta-blocker mortality benefit in heart failure with reduced ejection fraction?
ALLHAT (amlodipine)
HOPE (ramipril)
RALES (spironolactone)
MERIT-HF (metoprolol)
MERIT-HF demonstrated reduced mortality and hospitalizations in HFrEF patients on metoprolol. ALLHAT focused on hypertension with a calcium channel blocker, HOPE on an ACE inhibitor, and RALES on aldosterone antagonism. MERIT-HF remains a landmark beta-blocker trial.
Which component of the action potential is primarily targeted by non-dihydropyridine calcium channel blockers in nodal tissue to reduce heart rate?
Phase 3 repolarization
Phase 1 notch
Phase 0 upstroke
Phase 2 plateau
In nodal cells, phase 0 is driven by L-type calcium channels. Non-dihydropyridines like verapamil and diltiazem reduce the rate of rise of phase 0, slowing conduction and heart rate. Other phases are less dependent on calcium currents in these cells.
Which molecular change in the ?1 receptor can reduce efficacy of beta-blockers leading to attenuated negative chronotropic response?
Increased Gs protein coupling
Receptor conformational shift to the inactive state
Enhanced arrestin-mediated internalization
Upregulation of Gi proteins
Mutations that stabilize the inactive conformation of ?1 receptors reduce antagonist binding efficacy. Upregulation of Gi actually enhances inhibitory signaling, and Gs coupling is what beta-blockers oppose. Arrestin-mediated internalization affects receptor density but not binding affinity directly.
In research models, which downstream effector is reduced by chronic beta-1 blockade leading to decreased pacemaker current density?
Ryanodine receptor 2
Hyperpolarization-activated cyclic nucleotide-gated channel subtype 4 (HCN4)
Phospholamban
Voltage-gated sodium channel Nav1.5
Chronic beta-1 blockade lowers cAMP, which reduces HCN4 channel activity responsible for the pacemaker If current. Nav1.5 is involved in phase 0 of myocytes, not the funny current. RyR2 and phospholamban regulate calcium cycling, not direct chronotropy.
Which advanced imaging modality can quantify the effects of negative chronotropic drugs on myocardial perfusion reserve with high spatial resolution?
SPECT with technetium-99m
Cardiac MRI T1 mapping
PET with rubidium-82
Echocardiographic strain imaging
Rubidium-82 PET provides high-resolution quantification of myocardial perfusion reserve and can assess drug-induced changes. Echocardiographic strain assesses mechanics, MRI T1 mapping assesses fibrosis, and SPECT is less quantitative. PET is gold standard for perfusion quantification.
In translational studies, what effect does beta-1 blockade have on sinoatrial node gene expression profile?
Increased expression of ryanodine receptors
Downregulation of HCN4 and upregulation of Kir3.1 channels
Upregulation of Nav1.5 and downregulation of Kir2.1
Decreased phospholamban phosphorylation
Chronic beta-1 blockade reduces HCN4 transcription, lowering pacemaker current, and may increase Kir3.1 (GIRK) channels, enhancing hyperpolarizing currents. Nav1.5 changes affect conduction not primary pacemaking. RyR and phospholamban are calcium handling proteins.
Which computational model output best predicts the chronotropic response to combined beta-blocker and calcium channel blocker therapy?
Intracellular sodium transient amplitude
Integrated nodal action potential duration and If current amplitude reduction
Myocyte action potential plateau lengthening
Endothelial nitric oxide production
Predicting chronotropic response requires modeling changes in nodal AP duration and funny current amplitude. Myocyte plateau, sodium transients, and endothelial NO do not directly reflect SA node rate. Integrative nodal parameters yield the best correlation.
Which novel negative chronotropic agent targets SK channels in the sinoatrial node to modulate heart rate?
Ivabradine
Ranexa (ranolazine)
Ivomec
Apamin analogues
Apamin is an SK channel blocker studied for modulating nodal pacemaking via small-conductance Ca2+-activated K+ channels. Ivabradine targets HCN channels; ranolazine affects late sodium current; Ivomec is an antiparasitic. SK channel modulation is an emerging negative chronotrope strategy.
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Study Outcomes

  1. Understand Negative Chronotropic Mechanisms -

    Explain how a medication that possesses a negative chronotropic effect will slow atrioventricular nodal conduction and reduce heart rate.

  2. Identify Negative Chronotropic Effect Drugs -

    Recognize and list common negative chronotropic effect drugs used in EMS, including beta-blockers and calcium channel blockers.

  3. Interpret ECG Alterations -

    Analyze ECG tracings to detect bradycardia and AV blocks resulting from negative chronotropic effect drugs in emergency medicine.

  4. Apply Clinical Scenarios from Paramedic Chapter 7 Quiz -

    Select appropriate negative chronotropic interventions in real-world vignettes based on Nancy Caroline emergency medicine quiz principles.

  5. Evaluate Contraindications and Adverse Effects -

    Assess patient-specific risks, contraindications, and common adverse effects when administering negative chronotropic medications.

  6. Self-Assess with Instant Quiz Feedback -

    Use the free EMS medication quiz format to identify knowledge gaps and reinforce mastery of chronotropic effect emergency medicine concepts.

Cheat Sheet

  1. Mechanism of Negative Chronotropic Action -

    A medication that possesses a negative chronotropic effect will slow heart rate by reducing SA node automaticity and AV nodal conduction, as emphasized in Nancy Caroline emergency medicine quiz materials. This occurs via β1-receptor blockade or L-type calcium channel inhibition, per American Heart Association guidelines. Use the mnemonic "BB Ca time" to link beta-blockers and calcium channel blockers with chronotropic slowing.

  2. Key Drug Classes -

    Negative chronotropic effect drugs primarily include β-blockers (e.g., metoprolol, propranolol) and non-dihydropyridine calcium channel blockers (e.g., diltiazem, verapamil), as noted in paramedic chapter 7 quiz review. Metoprolol's typical IV dose is 5 mg over 2 minutes every 5 minutes (max 15 mg), while diltiazem is given as 0.25 mg/kg bolus. Remember "MVP" - Metoprolol, Verapamil, Propranolol - for speedy recall in EMS medication quiz prep.

  3. Clinical Indications -

    In chronotropic effect emergency medicine scenarios, these agents treat supraventricular tachycardias (SVT) and rate control in atrial fibrillation, per Journal of Emergency Nursing protocols. For narrow-complex SVT, administer adenosine first, then consider diltiazem or metoprolol if adenosine is contraindicated. Always confirm hemodynamic stability before giving negative chronotropic drugs in the field.

  4. Contraindications & Adverse Effects -

    Contraindications include acute heart failure, second- or third-degree AV block, and severe hypotension, underscored in Nancy Caroline's text. Common adverse effects are bradycardia, hypotension, and potential bronchospasm with nonselective β-blockers, as per American College of Cardiology guidelines. Monitor PR interval on ECG - avoid therapy if PR > 0.20 seconds.

  5. Monitoring & Titration -

    Effective use requires close monitoring of heart rate and blood pressure on continuous telemetry, a staple tip from paramedic chapter 7 quiz resources. Titrate doses to achieve a target rate of 60 - 80 bpm, using the formula "ΔDose = (Baseline HR - Target HR) × Sensitivity Factor," as taught in university EMS pharmacology courses. Always reassess patient response every 5 minutes to adjust infusion rates safely.

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