NLE Cardiovascular Nursing — Inflammatory, Valvular and Vascular DisordersDetailed Explanation

Infective Endocarditis

Infective endocarditis (IE) is an infection of the endocardium — the inner lining of the heart — and most commonly affects the heart valves. The most frequent causative organisms are Streptococcus viridans (associated with dental procedures and structural heart disease) and Staphylococcus aureus (associated with intravenous drug use and prosthetic valves). The pathophysiology begins with bacteremia: bacteria enter the bloodstream and adhere to already-damaged or abnormal valve surfaces. They proliferate and form vegetations — irregular clumps made of fibrin, platelets, red blood cells, and microorganisms. These vegetations are dangerous because they (1) destroy valve leaflets causing regurgitation, (2) can break off and embolize to the brain (stroke), kidneys, spleen, or lungs (pulmonary embolism). The tricuspid valve is classically involved in IV drug users because bacteria from the injection enter the venous system and reach the right heart first. The mitral and aortic valves are more commonly involved in non-drug users. Clinical manifestations follow two patterns: systemic infection signs (fever, chills, malaise, night sweats, weight loss) and peripheral embolic signs. The peripheral signs are high-yield NLE content: Janeway lesions are painless, flat, reddish macules on the palms and soles (mnemonic: 'J for Just painless'); Osler's nodes are painful, raised nodules on the fingertips and toes (mnemonic: 'O for Ouch!'); splinter hemorrhages appear as thin, dark lines under the fingernails from microemboli in nail-bed capillaries; Roth spots are oval retinal hemorrhages with pale centers visible on funduscopic exam; petechiae appear on the skin, conjunctiva, and mucous membranes. A new or changed heart murmur is a hallmark finding — the murmur results from turbulent flow through the vegetation-laden or damaged valve. Diagnosis uses the Duke Criteria and requires blood cultures (ideally three sets from different sites before starting antibiotics), echocardiography (transesophageal echo is more sensitive), and laboratory markers (elevated ESR, CRP, leukocytosis). Treatment is prolonged IV antibiotics — typically 4 to 6 weeks — based on organism and sensitivity. Surgical valve repair or replacement is needed for refractory infection, severe valve destruction, or recurrent embolization. Nursing management centers on the nursing process: Assessment includes monitoring temperature trends, new murmurs, and embolic signs. The priority NANDA nursing diagnosis is Risk for Decreased Cardiac Output related to valvular damage. Other diagnoses include Hyperthermia, Activity Intolerance, and Deficient Knowledge regarding antibiotic prophylaxis. The most critical nursing action before starting antibiotics is obtaining blood cultures — this preserves the ability to identify the causative organism and guide therapy. Nurses must also teach high-risk patients (those with prosthetic valves, prior IE, or structural heart disease) about antibiotic prophylaxis before dental procedures and invasive surgeries, as per the American Heart Association guidelines adopted in Philippine practice.

Pericarditis and Cardiac Tamponade

Pericarditis is inflammation of the pericardium — the two-layered fibroserous sac surrounding the heart. Causes include viral infections (most common, especially Coxsackievirus), bacterial infection, autoimmune diseases (lupus, rheumatoid arthritis), uremia (renal failure), post-MI (Dressler's syndrome), and radiation therapy. The cardinal clinical feature is chest pain that is distinctly pleuritic: sharp, stabbing, and worsens with inspiration (deep breathing) and when lying flat (supine). The pain characteristically IMPROVES when the patient sits up and leans forward — a classic NLE clue. This position reduces the pressure of the heart against the inflamed pericardium. A pericardial friction rub is the hallmark auscultatory finding: a high-pitched, scratchy, leather-on-leather sound best heard at the left sternal border with the patient sitting forward. It may have up to three components per cardiac cycle (corresponding to atrial systole, ventricular systole, and early diastole). ECG findings in pericarditis include diffuse (widespread) saddle-shaped ST elevation and PR depression in multiple leads — contrasting with the localized ST elevation of MI. Management includes NSAIDs (aspirin or ibuprofen) as first-line anti-inflammatory therapy, colchicine to prevent recurrence, and rest. Corticosteroids are used only for specific indications (refractory cases, autoimmune pericarditis). The most feared complication of pericarditis is cardiac tamponade — a life-threatening condition where fluid accumulates in the pericardial space, compressing the heart and preventing it from filling adequately. The key to remembering tamponade is Beck's Triad: (1) Hypotension (falling cardiac output), (2) Muffled or distant heart sounds (fluid muffles transmission), and (3) Jugular Venous Distention — JVD (blood backs up into the venous system because the heart cannot accept volume). An additional finding is pulsus paradoxus — an abnormal drop in systolic BP greater than 10 mmHg during inspiration (normally BP drops slightly with inspiration, but in tamponade this drop is exaggerated). The trachea remains midline (distinguishing it from tension pneumothorax, which deviates the trachea). Echocardiography is the gold standard for diagnosing tamponade. Emergency treatment is pericardiocentesis — needle aspiration of the pericardial fluid under ultrasound guidance. Nursing priorities: position the patient in Fowler's (upright, leaning forward), prepare for emergency pericardiocentesis, monitor for hemodynamic instability, administer IV fluids as ordered to temporarily maintain filling pressure, and have emergency equipment at bedside. NANDA nursing diagnoses include Decreased Cardiac Output related to pericardial compression (PRIORITY — Maslow: physiological need for circulation), Acute Pain related to pericardial inflammation, and Anxiety related to acute illness.

Rheumatic Fever and Rheumatic Heart Disease

Rheumatic fever (RF) is an acute inflammatory, autoimmune complication of an untreated or inadequately treated upper respiratory tract infection by Group A beta-hemolytic Streptococcus (GAS), specifically Streptococcus pyogenes. It most commonly occurs in children and adolescents (5–15 years old) and remains endemic in the Philippines and other developing nations. The pathophysiology is molecular mimicry: antibodies produced against the streptococcal M protein cross-react with antigens in the heart, joints, skin, and central nervous system (the basal ganglia). This autoimmune attack causes pancarditis (inflammation of all heart layers), arthritis, skin manifestations, and neurological symptoms. Diagnosis of RF uses the revised Jones Criteria, which requires evidence of preceding GAS infection (positive throat culture, elevated ASO titer, or rapid strep test) PLUS either two major criteria OR one major and two minor criteria. Major criteria (mnemonic: JONES): Joints (migratory polyarthritis — moves from joint to joint), Oh (carditis — including valvulitis, pericarditis, myocarditis), Nodules (subcutaneous nodules — painless, firm, over bony prominences), Erythema marginatum (ring-shaped, non-pruritic rash on trunk and proximal limbs — spares the face), Sydenham's chorea (involuntary, purposeless movements of the hands and face — 'dancing disease'). Minor criteria include fever, elevated ESR/CRP, prolonged PR interval on ECG, and history of prior RF or RHD. The most dangerous consequence of RF is rheumatic heart disease (RHD) — permanent scarring and deformity of the heart valves caused by repeated episodes of RF. The mitral valve is most frequently affected (mitral stenosis in 65–70% of RHD cases), followed by the aortic valve. Fibrous thickening and fusion of valve leaflets leads to stenosis, regurgitation, or a combination. Each episode of GAS pharyngitis in a patient with prior RF risks another episode of carditis and further valve damage — this is why secondary prophylaxis is critical. Treatment of acute RF: (1) Eradicate GAS with penicillin G or amoxicillin (erythromycin for penicillin allergy); (2) Anti-inflammatory therapy — aspirin for arthritis, corticosteroids for severe carditis; (3) Rest during acute phase; (4) Prophylaxis begins immediately after treatment. Secondary prophylaxis — long-term monthly benzathine penicillin G injections (or daily oral penicillin) to prevent recurrent strep infections and further valve damage. Duration depends on the presence and severity of RHD: those without RHD take prophylaxis for 5 years or until age 21 (whichever is longer); those with persistent RHD may require prophylaxis until age 40 or lifelong. In Philippine public health, rheumatic fever and RHD are targeted through the DOH's cardiovascular disease prevention program, with barangay health workers educating families on the importance of treating sore throat with antibiotics. Nursing diagnoses: Decreased Cardiac Output (carditis — PRIORITY), Acute Pain (arthritis), Hyperthermia, Activity Intolerance, and Deficient Knowledge (prophylaxis and prevention).

Valvular Heart Disease

Heart valves ensure unidirectional blood flow through the cardiac chambers. Valvular disease results in two types of dysfunction: stenosis — the valve orifice narrows, obstructing forward flow; or regurgitation (insufficiency) — the valve fails to close completely, allowing backward (retrograde) flow. Understanding the hemodynamic consequences of each lesion is essential for the NLE. MITRAL STENOSIS (MS): The mitral valve normally opens to allow blood to flow from the left atrium (LA) into the left ventricle (LV) during diastole. In MS (most commonly from RHD), the valve leaflets fuse and thicken, creating a narrowed orifice. Blood backs up from the LA into the pulmonary veins, causing pulmonary congestion (dyspnea, orthopnea, paroxysmal nocturnal dyspnea). Chronically elevated LA pressure dilates the atrium, creating the substrate for atrial fibrillation (AFib) — which further impairs filling and can cause LA thrombus formation and systemic embolism. MS produces a low-pitched, rumbling diastolic murmur, best heard at the apex with the bell of the stethoscope with the patient in the left lateral decubitus position. MITRAL REGURGITATION (MR): The mitral valve fails to close, allowing blood to jet back from the LV into the LA during systole. This produces a high-pitched, holosystolic (pansystolic) murmur radiating to the axilla, best heard at the apex. The LA and LV become volume-overloaded and dilate. Causes include MI (ischemic MR from papillary muscle rupture), mitral valve prolapse, IE, and RHD. AORTIC STENOSIS (AS): Obstruction of outflow from the LV through a narrowed aortic valve during systole. Causes include congenital bicuspid aortic valve and calcific degeneration in the elderly. The classic triad of symptoms is Angina, Syncope, and Exertional dyspnea (use the mnemonic: 'A-S-D or Almost Suddenly Dies' — because once these symptoms appear, prognosis without intervention is poor: angina = 5 years, syncope = 3 years, dyspnea/heart failure = 2 years survival). The murmur is a harsh, crescendo-decrescendo (diamond-shaped) systolic ejection murmur, best heard at the second intercostal space, right sternal border (aortic area), radiating to the carotids. Pulsus parvus et tardus (weak and delayed carotid upstroke) is a classic physical finding. AORTIC REGURGITATION (AR): The aortic valve does not close completely, allowing backflow from the aorta into the LV during diastole. This causes a widened pulse pressure (high systolic from increased stroke volume, low diastolic from backflow) and a blowing, decrescendo diastolic murmur at the left sternal border. Classic signs: Corrigan's pulse (waterhammer pulse — bounding peripheral pulses), Quincke's sign (pulsatile capillary blush in nail beds), and Duroziez's sign. MANAGEMENT: Medical therapy manages symptoms (diuretics for congestion, beta-blockers or calcium channel blockers for rate control in AFib, anticoagulation with warfarin for AFib or mechanical valves). Definitive treatment for severe valvular disease is surgical valve repair or replacement. Two types of prosthetic valves: (1) Mechanical valves — very durable but require LIFELONG anticoagulation with warfarin (INR target usually 2.5–3.5) to prevent thromboembolism; (2) Bioprosthetic (tissue) valves — from pig (porcine) or cow (bovine) pericardium — do NOT generally require long-term anticoagulation but have a shorter lifespan (10–15 years). Transcatheter Aortic Valve Replacement (TAVR) is now available for high-risk surgical patients with severe AS. Nursing care addresses Activity Intolerance, Decreased Cardiac Output, Deficient Knowledge regarding anticoagulation, and Anxiety. For anticoagulated patients: teach bleeding precautions, consistent dietary vitamin K intake, and regular INR monitoring.

Hypertension

Hypertension (HTN) is a chronic condition of persistently elevated arterial blood pressure (BP), making it the most common cardiovascular risk factor worldwide and in the Philippines. It is called the 'silent killer' because it is typically asymptomatic for years while silently damaging end organs. BP classification under ACC/AHA 2017 guidelines: Normal = below 120/80 mmHg; Elevated = 120–129/<80 mmHg; Stage 1 HTN = 130–139/80–89 mmHg; Stage 2 HTN = ≥140/90 mmHg. Note that Philippine clinical practice (DOH, PhilPEN, Philippine Heart Association) historically has used the JNC 7 threshold of ≥140/90 mmHg as the diagnostic cut-off — both frameworks coexist, so read exam questions carefully to identify which standard is being used. Hypertensive crisis is defined as BP >180/120 mmHg and is divided into: Hypertensive urgency (no acute end-organ damage — can be managed with oral medications over hours to days) and Hypertensive emergency (WITH acute end-organ damage such as hypertensive encephalopathy, stroke, aortic dissection, STEMI, or pulmonary edema — requires IV antihypertensives with CONTROLLED, GRADUAL BP reduction — lowering too fast causes ischemia from loss of autoregulation). Target: reduce MAP by no more than 25% in the first hour. ETIOLOGY: Primary (essential) HTN accounts for 90–95% of cases — no single identifiable cause; linked to genetics, high dietary sodium intake, obesity, sedentary lifestyle, alcohol, and aging. Secondary HTN has an identifiable cause — renal parenchymal disease (most common secondary cause), renal artery stenosis, primary aldosteronism, pheochromocytoma (episodic hypertension with headache, diaphoresis, palpitations), Cushing's syndrome, and sleep apnea. COMPLICATIONS (target-organ damage): Brain (hypertensive encephalopathy, stroke, transient ischemic attack); Heart (MI, left ventricular hypertrophy, heart failure); Kidneys (hypertensive nephropathy → CKD); Eyes (hypertensive retinopathy — classified by Keith-Wagener criteria); Peripheral arteries (PAD, aortic aneurysm). PHARMACOLOGICAL MANAGEMENT: Thiazide diuretics (hydrochlorothiazide/HCTZ) — first-line for most uncomplicated HTN; monitor potassium (hypokalemia risk). ACE inhibitors (enalapril, captopril, lisinopril) — preferred in diabetics with proteinuria and in post-MI; side effects: dry cough (class effect, due to bradykinin accumulation), hyperkalemia, angioedema (rare but life-threatening — switch to ARB). ARBs (losartan, valsartan, candesartan) — similar to ACEi but NO cough; preferred if cough develops with ACEi. Calcium channel blockers (amlodipine, nifedipine) — side effects include peripheral edema and headache; safe in pregnancy (nifedipine) for acute BP control. Beta-blockers (metoprolol, atenolol, carvedilol) — preferred in post-MI and heart failure with HTN; DO NOT abruptly stop (rebound hypertension and angina risk); caution in asthma and COPD (bronchospasm). NON-PHARMACOLOGICAL MANAGEMENT (lifestyle modifications — the DASH approach): Dietary sodium restriction (less than 2.4 g/day or less than 1 teaspoon of salt); DASH diet (fruits, vegetables, low-fat dairy, reduced saturated fat); weight loss (each 1 kg weight loss lowers BP by ~1 mmHg); aerobic exercise (30 minutes, most days); limit alcohol; smoking cessation. NURSING MANAGEMENT: Correct BP measurement technique is essential: proper cuff size (bladder encircles 80% of arm), arm at heart level, patient seated and rested for 5 minutes, no smoking or caffeine 30 minutes before. For Filipino patients using BHC or RHU services under PhilPEN, nurses screen and manage HTN at the community level. Key teaching: 'Take your medication even if you feel well — HTN is usually asymptomatic but continuously damages organs if uncontrolled.' NANDA nursing diagnoses: Risk for Decreased Cardiac Output, Deficient Knowledge regarding HTN management (very common in Filipino patients due to medication non-adherence), Nonadherence, Activity Intolerance.

Peripheral Arterial Disease and Chronic Venous Insufficiency

Peripheral vascular diseases affect the arteries and veins outside the heart and brain. The two most important conditions are Peripheral Arterial Disease (PAD) and Chronic Venous Insufficiency (CVI) — and the NLE heavily tests the nurse's ability to DIFFERENTIATE between them, as their assessments and interventions are OPPOSITE. PERIPHERAL ARTERIAL DISEASE (PAD): PAD results from atherosclerotic plaque buildup in the peripheral arteries (most commonly the lower extremities), reducing arterial blood flow. It shares the same risk factors as coronary artery disease: smoking (most significant modifiable risk factor), hypertension, diabetes mellitus, hyperlipidemia, and advanced age. The hallmark symptom is intermittent claudication — cramping, aching, or burning pain in the calf (or buttock/thigh for aortoiliac disease) that is reliably produced by walking a specific distance and RELIEVED BY REST. In severe disease, rest pain occurs — constant burning pain in the foot/toes at rest, especially at night, that is relieved by dangling the leg (gravity-assisted blood flow). Critical limb ischemia presents with rest pain, ulcers, or gangrene. Assessment findings of ARTERIAL INSUFFICIENCY: Diminished or absent peripheral pulses (dorsalis pedis, posterior tibial); cool, pale, shiny, hairless, trophic skin changes; prolonged capillary refill (>3 seconds); pallor with leg elevation and rubor (dependent redness) when legs are dangled; 'punched out,' dry, well-demarcated ulcers on the toes, heels, or pressure points — typically PAINFUL. ABI (Ankle-Brachial Index) = ankle systolic BP / brachial systolic BP. Normal is 0.9–1.3; below 0.9 suggests PAD; below 0.4 is critical ischemia. NURSING MANAGEMENT of PAD: Walk therapy — encourage regular walking TO the point of claudication pain, then rest, then walk again — this builds collateral circulation; Do NOT advise against all activity. Leg positioning: DANGLE the legs (dependent position to promote arterial gravity flow — 'arterial = dangle'); do NOT elevate legs in arterial disease (elevation decreases already poor arterial perfusion). Avoid tight socks, crossing legs, or cold exposure. Meticulous foot care — inspect feet daily (especially in diabetics with PAD: high risk for non-healing wounds and amputation); Avoid heating pads (neuropathy may prevent feeling burns). Pharmacological: antiplatelets (aspirin, clopidogrel) to reduce thrombotic events; cilostazol (PDE3 inhibitor — reduces claudication, contraindicated in heart failure); statins for lipid control. Definitive: angioplasty, stenting, or bypass surgery for severe disease. SMOKING CESSATION is the single most important intervention — smoking accelerates PAD progression and is the main modifiable risk factor. CHRONIC VENOUS INSUFFICIENCY (CVI): CVI results from incompetent or damaged venous valves in the deep veins of the legs, allowing venous blood to pool (venous stasis) in the lower extremities. Causes include DVT (most common), varicose veins, and prolonged standing. Symptoms: bilateral leg aching, heaviness, and swelling that WORSEN with prolonged standing or sitting and IMPROVE WITH LEG ELEVATION. Assessment findings of VENOUS INSUFFICIENCY: Edema (pitting, bilateral, worse at the end of the day); brownish skin discoloration at the medial malleolus (hemosiderin deposition from RBC extravasation); lipodermatosclerosis (hardening of subcutaneous tissue); varicose veins; shallow, moist, irregular ulcers at the medial malleolus — typically LESS PAINFUL than arterial ulcers; pulses are PRESENT and normal. NURSING MANAGEMENT of CVI: ELEVATE legs above heart level (reverses venous stasis — 'venous = elevate'); Apply graduated compression stockings or bandages (put on BEFORE rising from bed in the morning, when edema is least); Encourage ambulation and calf muscle pump exercises; Wound care for venous stasis ulcers; Weight loss, sodium restriction for edema management. CRITICAL DISTINCTION: ARTERIAL: pain with elevation (worse), diminished pulses, pale/cool leg, painful punched-out toe ulcers → DANGLE; VENOUS: pain with elevation RELIEVES (improves), present pulses, edematous/pigmented skin, moist medial malleolus ulcers → ELEVATE.

Abdominal Aortic Aneurysm

An aneurysm is a localized, permanent, abnormal dilation (ballooning) of an artery to more than 1.5 times its normal diameter, caused by weakness of the arterial wall. The most clinically significant aneurysm is the abdominal aortic aneurysm (AAA) — dilation of the abdominal aorta, typically below the renal arteries. Risk factors include atherosclerosis (most important underlying cause — degrades the medial layer of the aortic wall), hypertension (increases wall stress — LaPlace's law: wall tension increases with radius and pressure), smoking, male sex, age over 65, and positive family history. AAAs are clinically classified by diameter: small (less than 4 cm) — observed; moderate (4–5.4 cm) — monitored every 6–12 months with ultrasound; large (5.5 cm or greater) — surgical/endovascular repair indicated due to high rupture risk. MANIFESTATIONS: Most AAAs are ASYMPTOMATIC and found incidentally on imaging (abdominal ultrasound, CT scan) ordered for other reasons. When symptomatic: a pulsating, expansile mass in the periumbilical region; a systolic bruit over the mass; vague abdominal or back pain. The catastrophic complication is RUPTURE — sudden onset of severe, tearing, or ripping abdominal or back (flank) pain, rapidly progressing to hemorrhagic shock (hypotension, tachycardia, pallor, diaphoresis, decreased urine output). Ruptured AAA mortality is very high — up to 50–80% even with emergency surgery. NURSING MANAGEMENT: Key nursing actions — (1) NEVER vigorously palpate or deeply massage a known pulsating abdominal mass — this can dislodge thrombus or precipitate rupture (this is a HIGH-YIELD NLE point); (2) Strict blood pressure control (systolic BP target usually below 130 mmHg) to reduce wall stress and slow expansion — antihypertensives (beta-blockers preferred to reduce cardiac contractility and HR); (3) Serial imaging to monitor size; (4) Smoking cessation — smoking is independently associated with faster AAA expansion; (5) Teach the patient to report any sudden severe abdominal, back, or flank pain — a surgical emergency. SURGICAL REPAIR: Open surgical repair (traditional — resect the aneurysmal segment and replace with a synthetic graft) or Endovascular Aneurysm Repair (EVAR) — a less invasive approach where a stent graft is deployed via femoral artery to line the aneurysm from the inside. Postoperative nursing care after AAA repair: Monitor peripheral pulses (femoral, popliteal, dorsalis pedis, posterior tibial) frequently to detect graft thrombosis or embolism; monitor urine output (renal arteries may be affected, risking acute kidney injury); monitor for paralytic ileus (bowel sounds, abdominal distension); assess for spinal cord ischemia after thoracoabdominal repairs; monitor for endoleak after EVAR. NANDA diagnoses: Ineffective Tissue Perfusion (Peripheral) related to reduced arterial flow, Acute Pain related to post-surgical incision, and Risk for Deficient Fluid Volume related to hemorrhage.

Deep Vein Thrombosis and Pulmonary Embolism

Deep Vein Thrombosis (DVT) is the formation of a thrombus (blood clot) within a deep vein, most commonly in the deep veins of the lower extremity (popliteal, femoral, iliofemoral veins). DVT is part of the broader spectrum of Venous Thromboembolism (VTE), which includes DVT and its most deadly complication — Pulmonary Embolism (PE). PATHOPHYSIOLOGY — VIRCHOW'S TRIAD: The classic triad of risk factors for thrombus formation, named after Rudolf Virchow: (1) Venous stasis — slowing of blood flow: immobility (bedrest, long-haul flights), surgical procedures, heart failure, paralysis; (2) Endothelial injury — damage to the vein wall: surgery, trauma, IV catheter insertion, IV drug use; (3) Hypercoagulability — increased clotting tendency: pregnancy, postpartum period, oral contraceptive pills (OCP), malignancy, inherited thrombophilia (Factor V Leiden), dehydration, obesity. CLINICAL MANIFESTATIONS OF DVT: Often subtle or even silent! When symptomatic: unilateral calf swelling (most common), warmth, redness (erythema), and tenderness or pain in the affected leg, especially with calf palpation. Homans' sign — calf pain on dorsiflexion of the foot — is classically described but is non-specific (low sensitivity and specificity) and is no longer recommended as a reliable diagnostic test, though it may appear on older Philippine NLE items. Diagnosis is confirmed by duplex ultrasonography (imaging of choice) and D-dimer (elevated in DVT/PE but non-specific). PULMONARY EMBOLISM (PE): When a DVT clot dislodges and travels through the venous system → right heart → pulmonary arteries → occludes pulmonary blood flow. Clinical manifestations of PE: Sudden onset dyspnea (most common), pleuritic chest pain (sharp, worse with inspiration), tachycardia, tachypnea, hemoptysis, hypoxia, anxiety, and in massive PE: hypotension and right heart failure (obstructive shock). ECG findings: sinus tachycardia (most common), S1Q3T3 pattern (classic but uncommon). Diagnosis: CT Pulmonary Angiography (CTPA) — gold standard; V/Q scan for those with contrast allergy or renal impairment. NURSING MANAGEMENT OF DVT: Prevention is paramount — apply Sequential Compression Devices (SCDs/pneumatic compression stockings) to all at-risk immobile patients; early ambulation post-surgery; leg exercises (dorsiflexion/plantar flexion); adequate hydration; prophylactic anticoagulation (enoxaparin SC for surgical/immobile high-risk patients). For established DVT: Initiate anticoagulation therapy — unfractionated heparin (IV drip) or low-molecular weight heparin (LMWH — enoxaparin SC) as bridge therapy, transitioning to warfarin or a Direct Oral Anticoagulant (DOAC — rivaroxaban, apixaban, dabigatran) for 3 months or longer; ELEVATE the affected extremity; apply warm compresses for comfort; DO NOT MASSAGE the affected leg (risk of dislodging the clot and causing PE — HIGH-YIELD NLE point); Bed rest during the initial acute phase (controversial in current practice — guidelines increasingly support early ambulation even with DVT if it is stable and below the knee, but in the NLE context, 'do not massage' remains the clearest answer); Monitor for signs of PE continuously — sudden dyspnea and chest pain require immediate action (oxygen, call physician, prepare for emergency management). ANTICOAGULATION MONITORING — CRITICAL DRUG KNOWLEDGE: Unfractionated Heparin (UFH): Mechanism — activates antithrombin III, which inactivates thrombin and factor Xa; Monitor: aPTT (activated partial thromboplastin time) — therapeutic range is 1.5–2.5 times the control (approximately 60–100 seconds); Antidote: Protamine sulfate (1 mg protamine neutralizes 100 units of heparin). LMWH (Enoxaparin, Dalteparin): Does not require routine aPTT monitoring in most patients; monitor anti-Xa levels in special populations (renal failure, obesity, pregnancy). Warfarin (Coumadin): Mechanism — inhibits vitamin K-dependent clotting factors (II, VII, IX, X — the 'PITT' or '2, 7, 9, 10' factors); Monitor: PT/INR — therapeutic INR for DVT/PE is 2.0–3.0; Antidote: Vitamin K (phytonadione) for non-emergency reversal; Fresh Frozen Plasma (FFP) or 4-Factor Prothrombin Complex Concentrate (4F-PCC) for emergency reversal; Teaching: consistent dietary vitamin K intake (green leafy vegetables — kale, spinach, malunggay) — do not eliminate but keep consistent; avoid significant alcohol; report bleeding signs. DOACs (rivaroxaban, apixaban): No routine INR monitoring needed; no specific antidote in Philippines for older DOACs (though andexanet alfa exists for apixaban/rivaroxaban; idarucizumab for dabigatran); monitor renal function. DVT PREVENTION IN THE PHILIPPINE CONTEXT: Post-operative patients in Philippine hospitals routinely receive SCD therapy and LMWH prophylaxis. Nurses educate patients on leg exercises, hydration, and early ambulation — especially after orthopaedic (knee/hip replacement), abdominal, and pelvic surgeries.

Buerger's Disease and Raynaud's Phenomenon

These two smaller vascular conditions frequently appear on the NLE and are important to distinguish from each other and from PAD. BUERGER'S DISEASE (Thromboangiitis Obliterans, TAO): Buerger's disease is a non-atherosclerotic, inflammatory, occlusive disease of the small and medium-sized arteries AND veins of the upper and lower extremities. It primarily affects young men (20–40 years old) who are HEAVY SMOKERS. Unlike PAD (which is atherosclerotic), Buerger's involves segmental thrombus formation within vessel walls with intense inflammatory infiltrate. The etiology is strongly linked to tobacco use — both smoking and smokeless tobacco — and there is no identifiable cause other than tobacco. Manifestations: claudication of the feet and hands (arch claudication in the feet is classic), digital ischemia (blue, cold, painful fingers and toes), ulceration, and gangrene of the digits if untreated. Migratory thrombophlebitis (superficial vein inflammation that moves from one location to another) is a characteristic finding. Unlike atherosclerotic PAD, there are typically NO major risk factors (no DM, no dyslipidemia, no hypertension) other than smoking. Diagnosis is clinical: young male smoker, limb ischemia, no atherosclerosis risk factors; confirmed by angiography (characteristic corkscrew collaterals, segmental occlusions with abrupt cutoffs). TREATMENT AND THE SINGLE MOST IMPORTANT INTERVENTION: Complete and permanent tobacco cessation is the ONLY intervention that can halt disease progression and prevent amputation. No medication replaces this. If the patient continues to smoke, disease progression is inevitable. Medications (prostaglandins, iloprost) and surgical revascularization are adjunctive but ineffective without smoking cessation. Nurses focus on smoking cessation counseling, wound care, and pain management. RAYNAUD'S PHENOMENON: Raynaud's is episodic vasospasm of the digital arteries (fingers, toes, occasionally ears and nose), triggered by cold exposure or emotional stress. Two types: Primary Raynaud's (Raynaud's disease) — idiopathic, more common in young women, benign; Secondary Raynaud's (Raynaud's syndrome) — associated with connective tissue diseases (systemic sclerosis/scleroderma, lupus, Sjögren's syndrome), thoracic outlet syndrome, or drug use (ergotamine, beta-blockers). Manifestations: CLASSIC THREE-PHASE COLOR CHANGE of the fingers upon cold or stress exposure: (1) White (Pallor) — vasospasm causes digital artery closure → no blood flow → white, cold, numb fingers; (2) Blue/Cyanosis — deoxygenated blood remains in the digit → cyanotic, painful; (3) Red (Rubor) — vasospasm resolves, hyperemic blood flow returns → red, warm, throbbing. This triphasic sequence (white → blue → red) is the hallmark. Diagnosis is clinical. Management: CONSERVATIVE (avoid triggers): keep hands and entire body warm (insulated gloves, layered clothing), avoid cold water and environments, avoid tobacco (nicotine causes digital vasospasm), manage stress. Pharmacological for severe/frequent attacks: calcium channel blockers (nifedipine) — first-line drug therapy — they reduce the frequency and severity of vasospastic episodes by causing peripheral vasodilation. Phosphodiesterase-5 inhibitors (sildenafil) for severe cases. Sympathectomy (surgical) for refractory severe Raynaud's. NLE DISTINCTION: Buerger's disease = young male heavy smoker, inflammatory, limb ischemia, ulcers/gangrene, migratory phlebitis, treatment = COMPLETE SMOKING CESSATION. Raynaud's = young woman, episodic cold/stress-triggered color change (white-blue-red), conservative management + nifedipine.

Using Maslow's hierarchy and the nursing process, the priority is obtaining blood cultures BEFORE starting antibiotics. Blood cultures must be taken first to identify the causative organism and guide targeted antibiotic therapy. Once the cultures are collected (ideally within 15–30 minutes), antibiotics are started promptly. Giving vancomycin first would sterilize the blood and render cultures falsely negative. The painful nodules on fingertips are Osler's nodes — a classic sign of infective endocarditis. This is right-sided endocarditis (tricuspid valve involvement) classic for IV drug users.

This patient exhibits Beck's Triad — Hypotension + Muffled heart sounds + Jugular Venous Distention — along with pulsus paradoxus (>10 mmHg systolic BP drop on inspiration). This is cardiac tamponade, a life-threatening emergency requiring immediate pericardiocentesis (needle aspiration of pericardial fluid). Notifying the physician and preparing the procedure is the priority (Maslow: physiological safety — circulation). NSAIDs are for uncomplicated pericarditis and are not appropriate for tamponade. The patient should be positioned upright (NOT supine) if hemodynamically possible.

This is the most complete, accurate, and therapeutically appropriate explanation. Secondary prophylaxis with monthly benzathine penicillin G prevents recurrent GAS pharyngitis, which triggers additional RF attacks, each causing more valvular damage. The duration depends on the presence of RHD: with RHD, prophylaxis may continue until age 40 or longer, not just to age 18. Option A is partially correct but incomplete. Option C is incorrect (does not prevent viral infections). Option D is dangerously insufficient. This question tests Deficient Knowledge nursing diagnosis and patient education competency under RA 9173.

Mitral stenosis causes left atrial enlargement due to blood backing up from the obstructed valve. The enlarged left atrium (especially the left atrial appendage) is prone to blood pooling and thrombus formation, particularly in the presence of atrial fibrillation (AFib — the irregularly irregular rhythm). These thrombi can embolize to the brain, causing stroke, or to other organs. Warfarin (target INR 2–3) prevents this by inhibiting vitamin K-dependent clotting factors. This is the most accurate and therapeutically relevant explanation for the patient.

The classic triad of AS (Angina, Syncope, Dyspnea — mnemonic ASD or 'Almost Suddenly Dies') signals advanced, hemodynamically significant aortic stenosis. Once the triad appears, average survival without valve intervention is limited (angina = ~5 years, syncope = ~3 years, dyspnea/HF = ~2 years). The nurse's priority is recognizing the severity of this finding and ensuring urgent cardiology referral for surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR). The harsh systolic ejection murmur at the right 2nd ICS radiating to the carotids is classic for AS — not a benign murmur.

Massaging a DVT-affected limb is STRICTLY CONTRAINDICATED. Mechanical pressure can dislodge the thrombus from the vein wall, propelling it into the pulmonary circulation and causing life-threatening pulmonary embolism. The nurse must immediately and calmly instruct the patient to stop, explain the danger, and document the intervention. This is one of the most critically tested nursing actions in DVT management. The nurse should also reinforce DVT precautions: do not massage, elevate the leg, apply warm compresses (not massage), and report any sudden dyspnea or chest pain immediately.

This patient has primary Raynaud's phenomenon (Raynaud's disease) — the classic cold-triggered, triphasic (white → blue → red) digital vasospasm in a young woman without underlying disease. Management is primarily conservative: avoid cold, wear insulated gloves, dress in layers, and avoid nicotine (vasoconstrictor). If episodes are frequent and disabling, the physician may prescribe nifedipine (calcium channel blocker) — the drug of choice. Direct heat (heating pads) should be avoided as patients with vasospastic conditions may have impaired sensation and risk burns. Compression gloves are not appropriate and may restrict already-impaired flow.

Vigorous or deep palpation of a known or suspected AAA is contraindicated because it can precipitate rupture of the aneurysmal wall or dislodge a mural thrombus. At 5.8 cm, this AAA already meets the surgical repair threshold (≥5.5 cm) and is at higher rupture risk. The registered nurse under RA 9173 has the duty to supervise student nurses and ensure patient safety. This question tests both clinical knowledge (AAA precautions) and the supervisory role of the RN in clinical practice.