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Exam (elaborations) NUR-634

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Connecting the Dots: The Role of Peer Support in Achieving 3P Exam Success

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Cardiovascular System
Topic 1: Anticoagulant and Antiplatelet Therapy

Clinical Vignette
A 68-year-old male with hypertension and hyperlipidemia presents for follow-
up three weeks after a new diagnosis of atrial fibrillation. He has no history
of stroke or bleeding. His current medications include lisinopril 20 mg daily
and simvastatin 20 mg nightly. Renal function today: eGFR 55 mL/min. He
asks why he can’t “just take a baby aspirin instead of those stronger blood
thinners.”

Rationales / Answers

 Pathophysiology: Atrial fibrillation causes chaotic atrial activity →
blood stasis → thrombus formation, usually in the left atrial appendage.
Platelet inhibitors work mainly on arterial clots (platelet-rich), whereas
atrial thrombi are fibrin-rich and require anticoagulation.
 Assessment: Obtain CBC, PT/INR, aPTT (baseline), serum creatinine,
LFTs. Assess CHA₂DS₂-VASc and HAS-BLED scores. Bleeding risk rises
with age > 75, prior bleed, alcohol use, uncontrolled hypertension.
eGFR 55 → DOACs acceptable.
 Pharmacology:
o Apixaban 5 mg BID preferred (safe down to eGFR 15); no routine
INR monitoring; re-check renal function q6–12 months.
o Warfarin alternative if cost or drug interactions matter; maintain
INR 2–3; consistent vitamin K intake.
o Avoid dual therapy unless recent stent/ACS.
 Teaching Pearls: Emphasize medication adherence, bleeding
precautions (soft toothbrush, electric razor, limit alcohol), avoid
NSAIDs. Encourage consistent follow-up.



Topic 2: Aortic Regurgitation

Clinical Vignette
A 56-year-old male presents with increasing shortness of breath when
climbing stairs and occasional palpitations. He notes a “pounding” heartbeat
when lying on his left side. On exam you detect a high-pitched, blowing
diastolic murmur best heard along the left sternal border with the patient
leaning forward. His blood pressure is 150/50 mmHg; you also note a
bounding carotid pulse.

,  Pathophysiology: Incomplete closure of the aortic valve during
diastole causes blood to flow back into the LV → volume overload →
eccentric hypertrophy → progressive LV dilation and eventual systolic
dysfunction. Wide pulse pressure results from increased stroke volume
(elevated systolic) and rapid diastolic runoff (low diastolic).
 Assessment:
o History: exertional dyspnea, orthopnea, palpitations, awareness
of heartbeat.
o Physical exam: “water-hammer” (Corrigan) pulse, de Musset’s
head bob, Quincke’s pulse, high-pitched diastolic murmur at LSB,
Austin Flint murmur (functional mid-diastolic rumble).
o Diagnostics: transthoracic echocardiogram (quantifies
regurgitant fraction, LV dimensions); CXR may show
cardiomegaly.
 Pharmacology / Treatment:
o Afterload reduction with ACE inhibitors, ARBs, or nifedipine to
reduce regurgitant volume.
o Diuretics if volume overload symptoms present.
o Avoid beta-blockers in severe AR —they prolong diastole and
worsen regurgitation.
o Surgery (valve replacement) indicated for symptomatic patients
or LV EF < 55 % / end-systolic dimension > 50 mm.
o Monitoring: BP and renal function for those on ACE/ARB; watch
for hypotension.
 Teaching Pearls: Encourage regular cardiology follow-up; advise
patients to report new dyspnea or decreased exercise tolerance
promptly; avoid heavy isometric exercise.



Topic 3: Atrial Fibrillation

Clinical Vignette
A 74-year-old female presents with fatigue and mild shortness of breath for
two days. She denies chest pain. Her pulse is irregularly irregular at 118
bpm, blood pressure 134/78 mmHg, and she has trace bilateral ankle edema.
ECG confirms atrial fibrillation with a ventricular rate of 120 bpm. She is not
currently on anticoagulation.

 Pathophysiology: Disorganized atrial electrical activity (>350
impulses/min) leads to loss of coordinated atrial contraction, decreased
preload, and potential thrombus formation due to stasis in the left
atrial appendage. Cardiac output may drop by 10–30%.
 Assessment:
o Irregularly irregular pulse and heart sounds (variable S1).
o ECG: no distinct P waves, irregularly spaced QRS complexes.

, o Evaluate for underlying causes—check TSH, electrolytes,
echocardiogram for structural disease.
o CHA₂DS₂-VASc scoring: CHF, HTN, Age ≥75 (2), DM, Stroke (2),
Vascular disease, Age 65–74, Sex (female = 1).
 Pharmacology / Treatment:
o Rate control: beta-blockers (metoprolol), non-DHP calcium
channel blockers (diltiazem, verapamil); digoxin in sedentary
patients.
o Rhythm control: amiodarone, flecainide, sotalol; consider
electrical cardioversion if new onset (<48h) and stable.
o Anticoagulation: DOAC (apixaban, rivaroxaban, dabigatran,
edoxaban) preferred for non-valvular AF; warfarin if mechanical
valve or CrCl <15.
o Monitor: renal function q6–12 months; ECG for QT prolongation
with antiarrhythmics; INR for warfarin.
 Teaching Pearls:
o Reinforce adherence to anticoagulant therapy.
o Educate on pulse checks and signs of bleeding.
o Discuss avoidance of stimulants and alcohol excess.
o Ensure follow-up for rate/rhythm monitoring and risk
reassessment yearly.



Topic 4: Congestive Heart Failure (CHF)

Clinical Vignette
A 68-year-old woman presents with worsening shortness of breath, difficulty
sleeping flat, and swelling in her ankles over the past month. She has a
history of hypertension and a myocardial infarction three years ago. Her
medications include lisinopril and hydrochlorothiazide. On exam, you note
bibasilar crackles, 2+ pitting edema, and an S3 heart sound. Blood pressure
is 152/88 mmHg, heart rate 94 bpm, and oxygen saturation 93% on room air.

 Pathophysiology: Post-MI, loss of myocardial contractility →
decreased stroke volume and cardiac output. The body compensates
via RAAS activation → sodium and water retention → volume overload.
Chronic sympathetic activation leads to remodeling and worsening
dysfunction.
o HFrEF (systolic): EF < 40%, due to impaired contraction.
o HFpEF (diastolic): preserved EF, due to stiff ventricle and
impaired filling.
 Assessment:
o Symptoms: dyspnea, orthopnea, paroxysmal nocturnal dyspnea,
fatigue.

, o Exam: S3 (volume overload), rales, elevated JVP, peripheral
edema, hepatomegaly.
o Diagnostics:
 BNP/NT-proBNP elevated in HF (distinguishes from non-
cardiac dyspnea).
 Echocardiogram—EF and wall motion abnormalities.
 CXR—cardiomegaly, pulmonary congestion.
 Pharmacology / Treatment:
o Core agents:
 ACE inhibitors / ARBs / ARNIs (sacubitril–valsartan): reduce
afterload, improve survival.
 Beta-blockers (carvedilol, metoprolol succinate): blunt
sympathetic activation.
 Aldosterone antagonists (spironolactone, eplerenone):
improve mortality, monitor K⁺/Cr.
 Loop diuretics (furosemide, torsemide): relieve congestion;
monitor for hypokalemia, dehydration.
 SGLT2 inhibitors (dapagliflozin, empagliflozin): reduce
hospitalization and mortality.
o Monitoring: renal function, potassium, blood pressure, daily
weight.
o Education: daily weight log, sodium restriction (<2 g/day), fluid
restriction if severe.
o Red Flags: rapid weight gain >2–3 lb/day, increasing SOB, new
orthopnea, swelling.
 Teaching Pearls: Emphasize medication adherence, fluid balance,
early symptom recognition, and follow-up every 1–3 months. Vaccinate
(flu, pneumococcal) and encourage moderate exercise once stable.



Topic 5: Endocarditis

Clinical Vignette
A 42-year-old man with a history of intravenous drug use presents with fever,
chills, and fatigue for five days. He notes shortness of breath and occasional
chest discomfort. On exam, temperature 38.8 °C, heart rate 110 bpm, new
systolic murmur at the left lower sternal border, and several small, painless
lesions on the palms and soles.

 Pathophysiology: Transient bacteremia → adherence of organisms to
damaged endocardial surface → platelet–fibrin thrombus forms
vegetations → persistent infection and potential embolization. In IV
drug users, direct injection of skin flora seeds tricuspid valve first.
 Assessment: Fever, new or changing murmur, petechiae, Janeway
lesions (painless), Osler nodes (tender), Roth spots (retinal), splinter

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