Facts read from aanpcert.org and 2 more · last checked Nov 7, 2026
Blood pressure, cholesterol and chest pain fill much of a family practice schedule. This page follows them the way a visit runs: measure, classify, treat, recheck, for adults only.
Practice questions
60 questions written to the FNP-C outline; each choice is explained once you pick.
Tap an option: why each one is right or wrong appears under it.
Adult cardiovascular care
A 45-year-old has a soft systolic murmur at the left lower sternal border. Which finding on dynamic auscultation confirms that the murmur is right-sided (tricuspid)?
Expiration increases return to the left heart, so murmurs that grow louder in expiration are usually left-sided; this is the reverse of the sign being asked for.
Inspiration increases venous return to the right ventricle, so a tricuspid regurgitation murmur becomes louder (Carvallo sign).
Standing lowers preload and makes most murmurs softer; the murmurs that grow louder on standing are those of hypertrophic cardiomyopathy and mitral valve prolapse.
No change with breathing is nonspecific and does not localize the murmur to either side of the heart.
A 60-year-old man is scheduled for elective inguinal hernia repair. He has well-controlled hypertension, no history of heart disease, and climbs two flights of stairs without chest pain or dyspnea. His ECG last year was normal. Which is the most appropriate preoperative recommendation?
Stress testing is not indicated when the procedure is low risk and the patient can do 4 or more METs; testing would not change management and may lead to unnecessary procedures.
Starting a beta-blocker on the day of surgery increases the risk of stroke and death; patients already taking one continue it, but new starts are not done this way.
An echocardiogram is ordered for unexplained dyspnea, a new murmur, or suspected heart failure, none of which he has.
A low-risk operation in a patient who climbs two flights of stairs without symptoms needs no further cardiac testing under the ACC/AHA perioperative approach.
A 68-year-old man with dyspnea has elevated jugular venous pressure. Which additional finding best supports right-sided heart failure?
A laterally displaced apical impulse indicates left ventricular enlargement.
Bibasilar crackles reflect pulmonary venous congestion from left-sided heart failure, not systemic venous congestion.
A sustained rise in jugular venous pressure with abdominal pressure (hepatojugular reflux) shows that the right ventricle cannot handle extra venous return, which supports right-sided failure.
Pulsus paradoxus (an inspiratory systolic drop over 10 mm Hg) suggests cardiac tamponade or severe asthma/COPD.
A 30-year-old man has sharp, pleuritic chest pain that improves when he leans forward, one week after a viral illness. Which examination finding is most characteristic of his likely diagnosis?
Pulsus alternans (alternating strong and weak beats) is a sign of severe left ventricular systolic dysfunction.
Pleuritic pain that eases when leaning forward after a viral illness is acute pericarditis, and a scratchy friction rub heard with the patient leaning forward is its characteristic sign.
A fixed split S2 is the auscultatory sign of an atrial septal defect.
An S3 gallop reflects rapid filling of a failing or volume-overloaded ventricle, not pericardial inflammation.
A 62-year-old woman with peripheral arterial disease reports reproducible calf cramping after walking one block, relieved by rest. She smokes and takes a statin and aspirin. What is the most appropriate management plan?
Revascularization is reserved for lifestyle-limiting claudication that persists despite exercise and medical therapy, or for limb-threatening ischemia.
Supervised exercise therapy plus smoking cessation is first-line for claudication (with her statin and aspirin); continued smoking speeds PAD progression, and cilostazol can be added later if she has no heart failure.
Full-dose oral anticoagulation adds bleeding risk without improving claudication in stable PAD.
Avoiding walking worsens conditioning and claudication distance; walking to near-maximal pain with rest breaks is the treatment.
A 57-year-old woman with varicose veins has 3 days of a tender, red, firm cord along the medial thigh following the great saphenous vein. There is no leg swelling, and she is afebrile. What is the most appropriate next step?
Superficial vein thrombosis of the thigh can extend toward the saphenofemoral junction and coexists with DVT in up to a quarter of cases, so duplex ultrasound defines its extent and decides on anticoagulation (ACCP/CHEST).
A tender cord along a vein is thrombosis with inflammation, not bacterial cellulitis; antibiotics do not treat it.
Warm compresses and an NSAID suit a small below-knee superficial thrombosis after it has been imaged; treating a thigh cord without imaging can miss extension toward the deep system.
A D-dimer is nonspecific and is often raised by the superficial clot itself, so it cannot define extent or exclude DVT here.
A 71-year-old man with atrial fibrillation who stopped his apixaban 2 weeks ago has 3 hours of severe pain and numbness in the left foot. The foot is pale and cold with absent popliteal and pedal pulses, reduced sensation in the toes, and mild weakness of toe dorsiflexion. What is the most appropriate next step?
An ABI is a test for chronic PAD; scheduling it as an outpatient wastes the hours before muscle and nerve damage become irreversible.
Cilostazol and exercise treat chronic intermittent claudication, not an acute arterial occlusion.
Pain, pallor, pulselessness, sensory loss, and early weakness after stopping anticoagulation mean acute embolic limb ischemia with a threatened limb; heparin and emergency vascular surgery are needed within hours.
Waiting a week for a duplex scan means likely limb loss; acute ischemia with motor or sensory deficits is an emergency.
A 72-year-old man with exertional dyspnea and near-syncope has a systolic murmur. Which auscultatory finding would most support aortic stenosis?
Aortic stenosis gives a harsh crescendo-decrescendo ejection murmur at the right upper sternal border that radiates to the carotids; exertional dyspnea and near-syncope are part of its classic presentation.
A continuous 'machinery' murmur below the left clavicle is a patent ductus arteriosus.
A low-pitched mid-diastolic rumble at the apex is mitral stenosis, a diastolic lesion.
A holosystolic murmur at the apex radiating to the axilla is mitral regurgitation.
A 55-year-old man describes substernal chest tightness that occurs reliably after climbing two flights of stairs and resolves within minutes of rest. His resting ECG is normal, and he walks 2 miles daily apart from these episodes. Which initial evaluation is most appropriate?
Invasive angiography is for high-risk noninvasive findings, unstable symptoms, or angina that persists despite therapy, not as the first test in stable angina.
Troponins detect myocardial injury in acute coronary syndrome; they are normal in stable exertional angina and do not test for inducible ischemia.
With typical exertional angina, a normal resting ECG, and the ability to exercise, an exercise treadmill test is a reasonable first test for inducible ischemia.
A calcium score refines risk in people without symptoms; it does not test whether exertional chest tightness is ischemic.
A 61-year-old man with diabetes reports two episodes of chest pressure while watching television in the past 2 days, each lasting about 20 minutes. He is pain-free in the office, and his resting ECG is unchanged from last year. What is the most appropriate next step?
Stress testing is not done until acute coronary syndrome has been excluded, and a week's delay risks myocardial infarction.
New chest pressure at rest lasting 20 minutes is unstable angina, an acute coronary syndrome; same-day emergency evaluation with serial troponins is needed even when the office ECG is unchanged.
Attributing new rest chest pressure in a diabetic man to reflux, without first excluding acute coronary syndrome, is the dangerous anchoring error.
Giving nitroglycerin for home use and following up in a month leaves an active acute coronary syndrome unevaluated.
A 72-year-old woman has 2 months of progressive exertional dyspnea, orthopnea, and ankle swelling. Examination shows elevated jugular venous pressure and bibasilar crackles, and NT-proBNP is elevated. Which test is most important to establish the type of heart failure and guide therapy?
A chest radiograph shows congestion and cardiomegaly but not the ejection fraction, so it cannot classify the heart failure.
Repeating NT-proBNP adds nothing; the level supports the diagnosis but does not show ventricular function or the type of heart failure.
Catheterization looks for coronary disease or measures pressures in selected cases; it is not the first test to define heart failure type, and nothing here makes it urgent.
Every patient with suspected heart failure needs a transthoracic echocardiogram; the ejection fraction separates HFrEF, HFmrEF, and HFpEF, which determines the guideline-directed medications.
A 60-year-old man on a statin reports new muscle pain. Which finding indicates the need for dose adjustment or hold?
Brief morning joint stiffness suggests osteoarthritis; joint stiffness is not a statin muscle effect.
Tension-type headaches are not a statin adverse effect that changes therapy.
Fatigue after poor sleep has an obvious other cause and does not indicate statin myopathy.
Muscle symptoms with an elevated CK indicate statin-associated myopathy; the statin is held or reduced, and very high CK or dark urine calls for rhabdomyolysis testing.
A 68-year-old presents with new atrial fibrillation. Which history element is most important to identify a reversible trigger?
Family history raises lifetime risk but does not identify a cause that can be corrected now.
Hypertension is the most common chronic risk factor for AF, but it is a substrate, not an acute trigger that can be removed.
Infection, heavy alcohol use ('holiday heart'), and thyrotoxicosis are common reversible triggers of new atrial fibrillation; treating them can restore sinus rhythm.
Earlier self-terminating palpitations suggest paroxysmal AF that was already present; they are not a reversible trigger.
A 45-year-old man with known mitral valve prolapse has 3 weeks of low-grade fever, night sweats, and fatigue that began 2 weeks after a dental extraction. He has a new holosystolic murmur at the apex, painless hemorrhagic macules on his palms, and tender nodules on two finger pads. What is the most likely diagnosis?
Acute rheumatic fever follows streptococcal pharyngitis, mostly in children, with migratory arthritis and carditis rather than embolic skin lesions.
Libman–Sacks endocarditis is a sterile valve lesion in lupus and does not cause fever with Osler nodes and Janeway lesions.
Polyarteritis nodosa causes livedo, neuropathy, and renal involvement, not a new murmur after dental work.
Weeks of fever and a new regurgitant murmur after a dental procedure in someone with a valve lesion, plus Janeway lesions and Osler nodes, indicate subacute infective endocarditis; three sets of blood cultures come before antibiotics.
A 70-year-old man reports that yesterday he lost vision in his right eye for 10 minutes, 'like a curtain coming down,' and it fully recovered. He has hypertension and smokes. He has no headache or jaw pain. Which test is most appropriate?
Transient monocular vision loss like a curtain is a retinal TIA, usually from carotid embolism; stroke risk is highest in the first days, so urgent carotid imaging is part of a same-day stroke workup.
Full recovery does not lower the risk; a TIA is a warning of an impending stroke and needs urgent evaluation.
Orbital MRI looks at the optic nerve and orbit, not at the embolic source in the carotid artery.
Temporal artery biopsy is for suspected giant cell arteritis, which brings headache, jaw claudication, or a high ESR; he has none.
A 68-year-old woman with long-standing hypertension has left ventricular hypertrophy on echocardiogram. With the bell held lightly at the apex and the patient turned onto her left side, you hear a soft, low-pitched sound just before S1 that fades when the bell is pressed firmly. Which finding is this?
A low-pitched sound just before S1 is an S4: atrial contraction pushing blood into a stiff, hypertrophied ventricle. It is common with long-standing hypertension and is absent in atrial fibrillation.
An S3 is also low-pitched and heard at the apex, but it comes just after S2, in early diastole, from rapid filling of a volume-overloaded ventricle.
An opening snap is a sharp, high-pitched sound shortly after S2 in mitral stenosis, not a soft sound just before S1.
A split S1 is two crisp, higher-pitched components heard best with the diaphragm at the lower left sternal border; it does not fade with firm pressure.
A 34-year-old man has a fasting LDL cholesterol of 212 mg/dL on two occasions. TSH, liver tests, urinalysis, and his medication list show no secondary cause. He has no cardiovascular disease. Which is the most appropriate management?
Risk calculators underestimate risk in severe hypercholesterolemia and do not apply to young adults with an LDL of 190 or higher; treatment does not wait for a risk score.
An LDL of 190 mg/dL or higher is severe hypercholesterolemia: a high-intensity statin is started without a risk calculation, because lifetime exposure, often from familial hypercholesterolemia, drives the risk.
Ezetimibe lowers LDL less than a statin and is an add-on when LDL stays high on a maximally tolerated statin, not first-line monotherapy.
Diet and exercise lower LDL by a modest amount and cannot bring 212 mg/dL to goal; withholding a statin prolongs exposure.
A 24-year-old man had a febrile viral illness 10 days ago. He now has chest discomfort, dyspnea on exertion, and palpitations. ECG shows diffuse nonspecific ST changes and frequent PVCs, troponin is markedly elevated, and echocardiography shows global left ventricular hypokinesis with an EF of 38% and no effusion. What is the most likely diagnosis?
Chest discomfort, palpitations, a high troponin, and new global LV dysfunction after a viral illness in a young adult indicate acute myocarditis; cardiac MRI supports it, and competitive sport is avoided for 3 to 6 months.
Acute pericarditis causes positional pleuritic pain and diffuse ST elevation, without global systolic dysfunction.
STEMI causes regional ST elevation and regional wall motion loss, not diffuse nonspecific changes with global hypokinesis in a 24-year-old after a viral illness.
Hypertrophic cardiomyopathy causes a thick ventricle with preserved or high ejection fraction, not new global hypokinesis.
A running total sits here; it fills in after your last pick.
3
Where cardiovascular answers go wrong
Two drugs on the same pathway. An ACE inhibitor plus an ARB (or a direct renin inhibitor) adds hyperkalemia and kidney injury without added benefit; ACC/AHA advises against the combination.
ACE inhibitors and ARBs in someone who could become pregnant. Both carry an FDA boxed warning for fetal toxicity, so the plan includes contraception; hypertension in pregnancy is taught on WHNP-BC pregnancy complications.
AV-nodal blockers in pre-excited AF. In atrial fibrillation with Wolff-Parkinson-White pre-excitation, beta-blockers, calcium channel blockers and digoxin are avoided, because they can speed conduction down the accessory pathway (ACC/AHA/ACCP/HRS, 2023).
Diltiazem or verapamil in reduced ejection fraction. Non-dihydropyridine calcium channel blockers are avoided in HFrEF (AHA/ACC/HFSA, 2022).
Diuretics as the whole heart failure plan. Loop diuretics relieve congestion but do not lower mortality. For HFrEF that 2022 guideline rests on four classes: renin-angiotensin blockade (an ARNI first, otherwise an ACE inhibitor or ARB), one of the three beta-blockers proven in HFrEF, an MRA such as spironolactone, and an SGLT2 inhibitor.
Does the FNP-C follow the 2025 ACC/AHA blood pressure guideline?
NPCB does not say which editions its items use. The 2025 guideline kept the 130/80 mm Hg threshold for stage 1 and moved risk estimation to the AHA PREVENT equations, so learn the current version and know the earlier one existed.
Does this page cover high blood pressure in pregnancy?