Is cardiology high yield on the PEBC exam?

Yes. Cardiovascular therapeutics is one of the largest areas of pharmacotherapy, so conditions like hypertension, atrial fibrillation, heart failure, anticoagulation, and acute coronary syndrome come up often. The exact mix is randomized from one sitting to the next, but cardiology is consistently worth strong preparation.

What cardiology topics should I focus on for the PEBC?

The core areas are hypertension, heart failure, atrial fibrillation and stroke prevention, anticoagulation (warfarin and the DOACs), venous thromboembolism, acute coronary syndrome, and dyslipidemia. Knowing first-line versus second-line therapy and the major contraindications matters more than memorizing trial names.

Does the PEBC test anticoagulation and warfarin dosing?

Anticoagulation is a core area, so it is worth knowing how to choose between warfarin and a DOAC, the INR target and monitoring for warfarin, the duration of therapy for VTE, and the major drug and food interactions. These show up across both standalone questions and full cases.

How should I study cardiology for the PEBC?

Work from the Canadian guidelines, because the PEBC expects the Canadian standard of care. The main ones for cardiology are Hypertension Canada, the Canadian Cardiovascular Society (CCS) guidelines for heart failure, atrial fibrillation, acute coronary syndrome, and dyslipidemia, and Thrombosis Canada for anticoagulation and venous thromboembolism. Focus on drug selection and monitoring rather than trial names, and practice reading a vignette for the comorbidity that rules a drug in or out.

PEBC Cardiology Practice Questions

Cardiology is one of the biggest therapeutic areas on the PEBC exam. Hypertension, atrial fibrillation, heart failure, anticoagulation, acute coronary syndrome, and venous thromboembolism all show up, and most of them turn on choosing the right drug for a specific patient rather than recalling a fact.

The questions below are a sample across those areas. Each one explains why the correct answer is correct and why every other option is wrong, so you can see the comorbidity or the monitoring detail that decided the answer.

Written and reviewed against current Canadian guidelines and references.

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How to approach a PEBC cardiology question

1Read the whole vignette for the one detail that rules a drug in or out: pregnancy, asthma, renal function, a recent bleed, an allergy. The best answer often changes with a single comorbidity.
2Anchor on the Canadian guidelines (Hypertension Canada, the Canadian Cardiovascular Society). The PEBC expects the Canadian first-line choice, which is not always what you remember from school or a US source.
3Separate first-line from also-works. Most cardiology questions hand you two reasonable drugs and ask for the preferred one, so know the preferred agent and the reason it is preferred.
4Watch the monitoring and the numbers: INR targets, potassium on an ACE inhibitor or a diuretic, heart rate goals in atrial fibrillation. Many questions hinge on the follow-up, not the first dose.
5For anticoagulation, settle the indication first, then the agent, then the duration. Mixing up those three is the most common trap in this area.

Practice questions

Tap an answer to see why each option is right or wrong.

Question 1Cardio Drug Review

Which statement about ACE inhibitors is FALSE?

Incorrect · Answer: B

PEBC Yield: Highadr-recognitioncontraindication-checkmonitoringdrug-selection

ACE inhibitors can increase potassium by reducing aldosterone-mediated potassium excretion.

B) (Correct)

Correct. ACE inhibitor cough is not usually dose-dependent; it can occur even at low doses and typically requires switching to an ARB if persistent.

ACE inhibitors may rarely cause angioedema through bradykinin accumulation.

A modest GFR drop after initiation can be expected; the concerning threshold is a larger rise in creatinine or GFR fall that suggests renal hypoperfusion or renovascular disease.

Question 2Hypertension

JK is a 34 year old female presenting to the pharmacy concerned about elevated blood pressure readings at home (average 142/88 mmHg over one week). She takes an oral contraceptive pill containing ethinyl estradiol, a daily multivitamin, and naproxen 250 mg occasionally for menstrual cramps. She drinks 2 cups of coffee daily and exercises 3 times per week. Which of the following is the most likely drug-related cause of her elevated blood pressure?

Incorrect · Answer: B

PEBC Yield: HighADR-recognitiondrug-interactionoral-contraceptive

Standard daily multivitamins are not a recognized cause of hypertension. They contain vitamins and minerals at recommended daily allowances that do not significantly affect blood pressure.

B) (Correct)

Correct. Oral contraceptives containing estrogen (sex hormones) are a recognized drug-related cause of hypertension. Estrogen promotes sodium and water retention and can increase angiotensinogen levels, leading to BP elevation. This is particularly relevant in younger women with otherwise unexplained hypertension.

While caffeine can acutely elevate BP, moderate regular coffee consumption (2 cups daily) typically does not cause sustained hypertension. The body develops tolerance to caffeine's pressor effects with regular use. Caffeine is listed as an appetite suppressant/stimulant cause but moderate intake is less likely than OCP.

Regular exercise is a protective factor against hypertension, not a cause. Physical activity is one of the recommended non-pharmacological measures for both prevention and management of HTN.

Question 3Cardio Drug Review

KS is pregnant and taking lovastatin for primary prevention. Which statement is NOT appropriate?

Incorrect · Answer: B

PEBC Yield: Highcontraindication-checkcounsellingadr-recognitionmonitoring

Reviewing discontinuation during pregnancy is appropriate (statins are contraindicated).

B) (Correct)

Correct. Continuing lovastatin as 'preferred pregnancy lipid therapy' is NOT appropriate — statins (including lovastatin) are contraindicated in pregnancy. Primary-prevention lipid therapy is generally deferred during pregnancy.

Assessing for active liver disease (another statin contraindication) is appropriate.

Counselling about myalgia and rare rhabdomyolysis is appropriate statin adverse-effect counselling.

Question 4DVT & PE

How long must parenteral anticoagulation precede dabigatran for acute VTE treatment?

Incorrect · Answer: D

PEBC Yield: Highmonitoringdrug-selectionduration-of-therapytherapeutic-substitution

Tempting because some anticoagulant switches happen quickly. Wrong here because dabigatran requires a longer initial parenteral lead-in. Would be correct for selected same-day transition scenarios, not dabigatran initiation.

Tempting because it sounds like a short bridge. Wrong here because the required lead-in is longer. Would be correct only for a different local transition protocol.

Tempting because warfarin overlap is at least 5 days. Wrong here because dabigatran requires 5 to 10 days of parenteral anticoagulation before initiation. Would be correct for the minimum overlap concept in warfarin bridging.

D) (Correct)

Correct. Dabigatran and edoxaban require 5 to 10 days of parenteral anticoagulation before oral VTE treatment begins.

Question 5DVT & PE

A 72-year-old with a history of upper GI bleeding requires anticoagulation for new VTE. Which DOAC is preferred?

Incorrect · Answer: A

PEBC Yield: Highdrug-selectiongi-bleed-riskanticoagulationcomorbidity-considerations

A) (Correct)

Correct. Apixaban demonstrates a lower rate of major and clinically relevant non-major GI bleeding than the other DOACs and is preferred in patients with prior GI bleeding.

Tempting because rivaroxaban is a widely used DOAC. Wrong here because once-daily peak exposure increases GI bleed risk relative to apixaban. Would be correct if no GI bleeding history.

Tempting because dabigatran also avoids vitamin K interactions. Wrong here because dabigatran has the highest GI bleeding signal among DOACs and is the worst choice for prior GI bleed. Would be correct if GI bleeding were not a concern.

Tempting because edoxaban is once-daily and renally adjusted. Wrong here because its GI bleeding profile does not match apixaban's safety advantage. Would be correct if asking about a once-daily option in a non-GI-bleed patient.

Question 6Hypertension

Which daily sodium intake target is recommended as part of lifestyle management for hypertension?

Question 7Warfarin Dosing

During warfarin initiation with LMWH overlap, what minimum overlap duration is used before stopping LMWH?

Incorrect · Answer: C

PEBC Yield: Highswitching-therapymonitoring

Tempting because warfarin effects begin after a delay. Wrong here because the overlap minimum is 5 days.

Tempting because it is close to the minimum. Wrong here because LMWH overlap is not stopped at day 4 by this rule.

C) (Correct)

Correct. LMWH is continued for at least 5 days and until the INR is therapeutic on two days.

Tempting because some patients require longer overlap. Wrong here because 10 days is not the minimum overlap rule.

Question 8Stroke & TIA

Which alteplase dose is most appropriate for eligible acute ischemic stroke?

Incorrect · Answer: C

PEBC Yield: Highdose-adjustmentcalculation

Tempting because it is a lower fibrinolytic dose. Wrong here because the standard alteplase stroke dose is higher. Would be correct only for a different protocol not used here.

Tempting because it sits between common dose ranges. Wrong here because it is not the standard acute ischemic stroke alteplase dose. Would be correct only under a nonstandard local protocol.

C) (Correct)

Correct. Alteplase is dosed at 0.9 mg/kg IV to a maximum of 90 mg for eligible acute ischemic stroke.

Tempting because thrombolysis is urgent. Wrong here because this dose exceeds the standard stroke dose and may increase bleeding risk. Would be correct for neither alteplase nor tenecteplase stroke dosing.

Question 9Atrial Fibrillation

KR is a 71 year old female with atrial fibrillation secondary to moderate mitral stenosis, hypertension, and osteoarthritis. She is initiated on warfarin today with a target INR of 2.0-3.0. Which of the following best describes the mechanism by which warfarin produces its anticoagulant effect?

Incorrect · Answer: D

PEBC Yield: Highdrug-selectioncounselling

Tempting because thrombin inhibition is a mechanism of anticoagulation, but this describes direct thrombin inhibitors such as dabigatran. Would be correct if the question asked about dabigatran.

This describes the antiplatelet mechanism of ASA. Warfarin acts on the coagulation cascade, not on platelet aggregation pathways.

This describes the mechanism of unfractionated heparin and low molecular weight heparins, which bind antithrombin III. Not the mechanism of warfarin.

D) (Correct)

Correct -- warfarin inhibits vitamin K epoxide reductase (VKORC1), depleting functional vitamin K reserves needed for hepatic synthesis of clotting factors II, VII, IX, and X, as well as anticoagulant proteins C and S. This is why warfarin has a delayed onset of 24-72 hours - existing functional clotting factors must be cleared before the anticoagulant effect manifests.

Question 10ACS & Stable Angina

Which item is NOT a recognized drug-related contributor to ACS risk?

Incorrect · Answer: D

PEBC Yield: Highadr-recognitiondrug-interaction

NSAIDs at scheduled doses are recognized ACS contributors via prothrombotic and BP effects.

Cocaine is a sympathomimetic stimulant and a well-recognized ACS contributor.

Combined oral contraceptives — especially in smokers — are listed as a drug-related ACS contributor.

D) (Correct)

Correct. Low-dose ASA is a cardioprotective antiplatelet; it lowers — rather than raises — ACS risk.

Want the full bank?

These are a sample. The full bank adds full-length cases and timed mock exams.

Sample full case

One patient with several linked questions, the format the real exam uses for case clusters.

RK is a 47-year-old hairdresser being discharged after inpatient treatment for an acute right-leg proximal DVT confirmed by Doppler ultrasound. Her leg pain and swelling have improved on enoxaparin 80 mg SC every 12 hours, and the discharge plan is to continue the same regimen at home until the thrombosis clinic finalizes oral therapy. Her past medical history includes hypertension and chronic kidney disease (eGFR 48), managed with ramipril 10 mg PO daily and amlodipine 5 mg PO daily; she also takes atorvastatin 20 mg PO at bedtime. She walks her dog twice daily and recently completed a community first-aid certification. She is anxious about self-injection, has mild bruising from the inpatient doses, and asks to practise with the first pre-filled syringe before leaving. The syringe label and dose match the discharge prescription, the solution is clear, and she has no active bleeding or recent procedures.

Question 1DVT & PE

While inspecting the syringe, RK sees a small air bubble and asks whether to push it out before injection. Which counselling advice is most appropriate?

Incorrect · Answer: B

PEBC Yield: Highlmwh-administrationpre-filled-syringesubcutaneous-techniqueair-bubble-exception

Prefilled enoxaparin syringes are MANUFACTURED with a small air bubble — it is not a fault or air pocket. The bubble serves to ensure the FULL labelled dose is delivered subcutaneously (the bubble pushes the last drop out of the needle hub). Pushing it out before injection wastes medication and reduces the delivered dose by ~10%. Counsel patients explicitly NOT to expel the bubble.

B) (Correct)

Correct. The air bubble in a prefilled enoxaparin syringe is INTENTIONAL — leave it in place and inject the full contents subcutaneously. Standard technique: rotate injection sites between abdominal wall (left and right of umbilicus, ≥2 inches away), upper outer thigh, or upper outer arm; pinch a fold of skin to lift fat from muscle; insert needle at 90° angle; inject the full contents including the bubble; DO NOT aspirate; DO NOT rub afterward (rubbing increases bruising). Source: enoxaparin product monograph (Sanofi Lovenox; generic Inclunox).

Aspiration before subcutaneous injection is NOT recommended for any modern SC injection (insulin, LMWH, GLP-1 agonists, etc.) — there are no vascular structures in the subcutaneous space to draw back into. Aspirating also wastes preparation time and disrupts the bubble. Removing the bubble loses ~10% of the dose.

A small air bubble is EXPECTED in a prefilled enoxaparin syringe and does not require replacement. Discarding the syringe wastes a $25-50 dose of medication and delays care. The product is intact and correctly labelled per the case — proceed with injection.

Question 2DVT & PE

Several days later, RK's thrombosis clinic decides to use warfarin for ongoing DVT treatment. She is still receiving therapeutic enoxaparin and has had no bleeding. The team wants to avoid both a gap in anticoagulation and premature discontinuation of the injectable agent. Which transition strategy is most appropriate?

Incorrect · Answer: B

PEBC Yield: Highlmwh-warfarin-bridgingoverlap-durationtransition-protocolacute-dvt-treatment

INR criterion (≥2 for 24 hours) is correct but minimum duration is too short. The 5-day rule exists because of the half-lives of vitamin K-dependent factors: Factor VII (~6 hours, depletes fastest — why INR rises early before full anticoagulation), Factor IX (~24 hours), Factor X (~36 hours), and Factor II (prothrombin, ~60-72 hours, the slowest). The INR reflects mostly Factor VII early on; the FULL anticoagulant effect waits for Factor II to deplete. At 3 days, Factor II is only partially depleted — the patient is under-anticoagulated despite a 'therapeutic' INR.

B) (Correct)

Correct. Per CHEST 2016 antithrombotic guidelines and Thrombosis Canada: for acute VTE transition to warfarin, overlap therapeutic LMWH (or UFH) with warfarin for AT LEAST 5 days AND until INR ≥2 for at least 24 hours. Both criteria must be met. The 5-day floor reflects the time for Factor II (prothrombin) depletion (half-life ~60-72 hours; ~5 half-lives ≈ full depletion). The INR ≥2 × 24h criterion confirms the depletion has translated into effective anticoagulation. Practical bridge: continue LMWH at full therapeutic dose during overlap; stop LMWH the morning after the 24-hour confirmed therapeutic INR window. Source: CHEST 2016; Thrombosis Canada VTE Treatment Pathway.

The 5-day duration is correct but 12 hours of therapeutic INR is too short. A single supratherapeutic INR can drop the next morning, especially in the first days of warfarin when Factor II is still depleting. The 24-hour criterion ensures the INR has stabilized at therapeutic level, not just transiently crossed it. Some Canadian institutions use 'two INRs ≥2 measured 24 hours apart' as the operational equivalent.

Both parameters wrong: 7 days is longer than required (unnecessary LMWH cost — ~$10-20/day for outpatient enoxaparin — and prolonged bleeding-risk window), and an INR threshold of 1.8 does not meet the standard ≥2 cutoff for effective anticoagulation in non-valvular VTE. Source: CHEST 2016 (≥2 is the threshold; sub-therapeutic INRs are associated with recurrent thrombosis).

Question 3DVT & PE

Two weeks later, RK's INR is stable at 2.4 on warfarin 4 mg daily and she reports no bleeding. The clinic confirms her DVT presented 2 weeks after an outpatient knee arthroscopy when she was using crutches and largely sedentary. RK is otherwise active, on no antiplatelets or NSAIDs, and her current medication review shows ramipril, amlodipine, and atorvastatin alongside the warfarin. The team reviews the total intended duration of anticoagulation. Which plan best matches the minimum recommended total duration?

Incorrect · Answer: A

PEBC Yield: Highvte-durationprovoked-vs-unprovokedrecurrence-risk-assessment

A) (Correct)

Correct. RK had a first proximal DVT with a clearly TRANSIENT provoking factor — outpatient knee arthroscopy followed by crutches and reduced mobility — that has now resolved. Per CHEST 2016 and Thrombosis Canada VTE Treatment Pathway, a first proximal DVT with a transient major provoker is treated for a total of 3 months of therapeutic anticoagulation, then reassessed for extension based on residual risk and patient values. Recurrence risk after stopping for a clearly provoked first VTE is approximately 1 to 3 percent per year, compared with roughly 5 to 10 percent per year for unprovoked first VTE — low enough that the bleeding risk of extended anticoagulation typically outweighs further benefit.

Bleeding-risk assessment for RK using HAS-BLED:

Hypertension (on ramipril/amlodipine): +1
Abnormal renal/hepatic function: +1 if CKD with eGFR under 60; RK's eGFR around 48 puts her borderline
Stroke, Bleeding history, Labile INR, Elderly over 65, Drugs (antiplatelet/NSAID), Drinking: all 0 — INR stable at 2.4 on a low warfarin dose, no antiplatelet/NSAID, age 47
HAS-BLED roughly 1 to 2 = MODERATE, not unambiguously low. CKD specifically nudges her up.

Key point: the 3-month choice is driven by the clearly transient provoking factor (post-op immobility, now resolved, leading to low recurrence risk after stopping), NOT by bleeding risk being low. Bleeding-risk assessment matters when deciding whether to extend beyond 3 months. Source: CHEST 2016 antithrombotic guidelines; Thrombosis Canada.

D-dimer testing after stopping anticoagulation has a role in stratifying recurrence risk for UNPROVOKED VTE (the HERDOO2 and DASH scores incorporate D-dimer) — it is NOT the basis for extending therapy in a clearly provoked first DVT. This protocol over-treats a low-recurrence-risk patient by anchoring on the wrong decision tool.

Residual venous obstruction (RVO) on follow-up imaging IS associated with recurrence risk but is not the standard determinant of stopping therapy in provoked DVT (REVERSE study, evidence not strong enough to drive duration decisions in transient-provoker cases). Six months is also longer than the minimum needed for this scenario.

Indefinite anticoagulation is considered for: unprovoked VTE with high recurrence risk, persistent major risk factors (active cancer, antiphospholipid syndrome), recurrent VTE, or selected high-risk thrombophilias (homozygous Factor V Leiden, antithrombin deficiency). Provoked status with a now-resolved transient factor absolutely changes the duration calculus — lifelong is over-treatment here.

Full-length cases like this, across every PEBC domain, live in the question bank.

Frequently asked questions

Is cardiology high yield on the PEBC exam?: Yes. Cardiovascular therapeutics is one of the largest areas of pharmacotherapy, so conditions like hypertension, atrial fibrillation, heart failure, anticoagulation, and acute coronary syndrome come up often. The exact mix is randomized from one sitting to the next, but cardiology is consistently worth strong preparation.
What cardiology topics should I focus on for the PEBC?: The core areas are hypertension, heart failure, atrial fibrillation and stroke prevention, anticoagulation (warfarin and the DOACs), venous thromboembolism, acute coronary syndrome, and dyslipidemia. Knowing first-line versus second-line therapy and the major contraindications matters more than memorizing trial names.
Does the PEBC test anticoagulation and warfarin dosing?: Anticoagulation is a core area, so it is worth knowing how to choose between warfarin and a DOAC, the INR target and monitoring for warfarin, the duration of therapy for VTE, and the major drug and food interactions. These show up across both standalone questions and full cases.
How should I study cardiology for the PEBC?: Work from the Canadian guidelines, because the PEBC expects the Canadian standard of care. The main ones for cardiology are Hypertension Canada, the Canadian Cardiovascular Society (CCS) guidelines for heart failure, atrial fibrillation, acute coronary syndrome, and dyslipidemia, and Thrombosis Canada for anticoagulation and venous thromboembolism. Focus on drug selection and monitoring rather than trial names, and practice reading a vignette for the comorbidity that rules a drug in or out.