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Examen

Exam (elaborations) NUR-634

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Vista previa 4 fuera de 95 páginas

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

Información del documento

Subido en
17 de agosto de 2026
Número de páginas
95
Escrito en
2026/2027
Tipo
Examen
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