Inflammatory, Valvular and Vascular Disorders - Cheat Sheet
Your last-minute rapid-fire reference for cardiovascular inflammation, valve pathology, and vascular disease. Master the peripheral signs, management priorities, and exam-critical distinctions before your exam.
Infective Endocarditis (IE)
Important facts
- Obtain BLOOD CULTURES BEFORE starting antibiotics — this is the SINGLE most critical action.
- Most common organisms: Streptococcus viridans (normal flora, dental), Staphylococcus aureus (IVDU, acute), Enterococcus (GU/GI procedures).
- Risk factors: prosthetic heart valves, structural heart disease, rheumatic fever history, INTRAVENOUS DRUG USE (classically affects RIGHT TRICUSPID VALVE).
- Peripheral stigmata (classic signs): Janeway lesions (PAINLESS macules on palms/soles), Osler's nodes (PAINFUL nodules on fingertips), splinter hemorrhages, Roth spots (retinal hemorrhages), petechiae.
- Manifestations: fever, chills, NEW or CHANGED murmur, fatigue, signs of embolization (stroke, splenic infarct, PE).
- Treatment: Prolonged IV antibiotics 4–6 weeks based on culture; surgery for severe valve damage.
- CRITICAL NURSING: Obtain cultures before antibiotics; monitor for embolic complications and heart failure; teach antibiotic PROPHYLAXIS before dental/invasive procedures for high-risk patients.
- Prophylaxis agents: amoxicillin (oral) or ceftriaxone (parenteral) for GI/GU procedures; clindamycin if penicillin-allergic.
- Monitor for septic emboli to lungs (septic PE), spleen, kidneys, CNS.
Key definitions
Infective Endocarditis
Example
Strep viridans from poor dental hygiene seeding a mitral valve.
Infection of the endocardium and heart valves (usually bacterial: Streptococcus, Staphylococcus) forming vegetations that can embolize.
Vegetation
Example
Embolic stroke from vegetation fragment in IVDU patient with tricuspid involvement.
Clump of fibrin, platelets, and microorganisms on valve surface capable of systemic embolization.
Diagrams to know
- Peripheral stigmata of IE (Janeway, Osler's, splinter hemorrhages, Roth spots, petechiae)
- Sites of embolization from vegetations
- Risk stratification for IE prophylaxis
Pericarditis & Myocarditis
Important facts
- Pericarditis pain pathognomonic: SHARP, PLEURITIC, WORSE with inspiration and lying flat; BETTER sitting up and leaning forward (distinguishes from ACS).
- Listen for PERICARDIAL FRICTION RUB — scratchy, to-and-fro sound best heard with patient sitting forward.
- BECK'S TRIAD = Hypotension + Muffled heart sounds + Jugular venous distention = Tamponade (EMERGENCY).
- Pulsus paradoxus: systolic BP drops >10 mmHg on inspiration (sign of tamponade).
- Cardiac tamponade management: PERICARDIOCENTESIS (needle aspiration of pericardial fluid) — life-saving.
- ECG in pericarditis: diffuse ST elevation (not localized like STEMI), PR depression.
- Causes: viral (most common), bacterial, TB, malignancy, autoimmune, uremia, post-MI (Dressler's syndrome).
- Myocarditis: viral (enterovirus, adenovirus) most common; presents with chest pain, dyspnea, palpitations, fulminant cardiogenic shock possible.
- Monitor for heart failure and malignant dysrhythmias in myocarditis; consider ICU admission.
Key definitions
Pericarditis
Example
Viral pericarditis post-URI with friction rub and PR depression on ECG.
Inflammation of the pericardium presenting with sharp, pleuritic chest pain worsening on inspiration and lying flat; improves sitting up and leaning forward.
Cardiac Tamponade
Example
Post-traumatic hemopericardium causing tamponade — emergency pericardiocentesis required.
Life-threatening compression of the heart by pericardial fluid; presents as Beck's triad: hypotension, muffled heart sounds, jugular venous distention (JVD) with pulsus paradoxus.
Myocarditis
Example
Enteroviral myocarditis in young adult presenting with chest pain, dyspnea, and reduced ejection fraction.
Inflammation of the myocardium, often viral, leading to heart failure and dysrhythmias.
Diagrams to know
- Beck's triad and mechanism of tamponade
- Pericarditis pain characteristics vs ACS
Rheumatic Heart Disease & Valvular Pathology
Important facts
- PREVENTION of rheumatic heart disease: Prompt antibiotic (penicillin G or amoxicillin) treatment of strep throat — CRITICAL teaching point.
- Jones Criteria for rheumatic fever: Major (carditis, migratory polyarthritis, chorea, erythema marginatum, subcutaneous nodules) + Minor (fever, arthralgia, elevated ESR/CRP, prolonged PR on ECG); 2 major OR 1 major + 2 minor = diagnosis.
- MITRAL VALVE most commonly affected in rheumatic heart disease (85% of cases); aortic second (30%); tricuspid and pulmonary rare.
- MITRAL STENOSIS: dyspnea, orthopnea, PND, pulmonary edema; predisposes to ATRIAL FIBRILLATION; management: diuretics, beta-blockers for rate control, anticoagulation if AFib present.
- AORTIC STENOSIS classic TRIAD: ANGINA, SYNCOPE, DYSPNEA; harsh systolic ejection murmur; CONTRAINDICATE vigorous exercise (sudden death risk); patient may adopt squatting position for symptom relief.
- Mechanical prosthetic valves REQUIRE LIFELONG ANTICOAGULATION (warfarin, INR 2–3); bioprosthetic valves generally do NOT require anticoagulation (except first 3 months).
- Valve repair preferred over replacement when possible (preserves LV function).
- Indications for surgery: symptomatic severe stenosis or regurgitation, asymptomatic severe disease with LV dysfunction or AFib.
- Post-valve replacement: monitor for mechanical failure, thrombosis, infection, hemorrhage.
Key definitions
Rheumatic Fever
Example
Child with untreated strep throat develops migratory polyarthritis, carditis, chorea (Sydenham's) 2–3 weeks later.
Autoimmune inflammatory sequela of untreated group A beta-hemolytic streptococcal pharyngitis; antibodies cross-react with cardiac, joint, skin, and CNS tissue.
Rheumatic Heart Disease
Example
Middle-aged patient with history of rheumatic fever presenting with mitral stenosis and AFib.
Chronic scarring of heart valves (most commonly MITRAL) from repeated rheumatic fever episodes; major cause of valvular disease in developing countries including the Philippines.
Mitral Stenosis
Example
Dyspnea on exertion, orthopnea, pulmonary edema; patient adopts left lateral decubitus position for relief.
Narrowing of mitral valve orifice obstructing flow from left atrium to LV; blood backs up into pulmonary circulation.
Mitral Regurgitation
Example
S3 gallop, left atrial enlargement, AFib from volume overload.
Incompetent mitral valve allowing backflow into left atrium during systole; produces holosystolic (pansystolic) murmur.
Aortic Stenosis
Example
Elderly patient with harsh systolic ejection murmur, narrow pulse pressure, risk of sudden cardiac death with exertion.
Narrowing of aortic valve obstructing LV outflow; presents with classic triad: angina, syncope, exertional dyspnea.
Aortic Regurgitation
Example
Wide pulse pressure, bounding pulses (water-hammer pulse), decrescendo diastolic murmur.
Incompetent aortic valve allowing backflow into LV during diastole; produces early diastolic murmur and widened pulse pressure.
Diagrams to know
- Stenosis vs Regurgitation mechanisms and murmur characteristics
- Mitral stenosis pathophysiology: LA → LV obstruction → pulmonary congestion
- Aortic stenosis classic triad and hemodynamics
Hypertension (HTN)
Common values
Value
<120/80 mmHg
Symbol
BP_normal
Quantity
Normal BP (ACC/AHA)
Value
120–129/<80 mmHg
Symbol
BP_elevated
Quantity
Elevated BP (ACC/AHA)
Value
130–139/80–89 mmHg
Symbol
BP_stage1
Quantity
Stage 1 HTN (ACC/AHA)
Value
≥140/90 mmHg
Symbol
BP_stage2
Quantity
Stage 2 HTN (ACC/AHA)
Value
>180/120 mmHg
Symbol
BP_crisis
Quantity
Hypertensive Crisis
Value
<5 g/day (or <2.3 g/day for severe HTN)
Symbol
Na_restrict
Quantity
Daily sodium restriction target
Important facts
- HTN is the SILENT KILLER — often asymptomatic until end-organ damage occurs.
- Complications (target-organ damage): stroke, myocardial infarction, heart failure, chronic kidney disease, retinopathy, aortic dissection.
- LIFESTYLE MODIFICATIONS (first-line, always emphasized): sodium restriction (<5 g/day), weight loss (5–10% reduction in BP for each 10 kg lost), aerobic exercise (30 min most days), limit alcohol, smoking cessation, stress management, DASH diet.
- DIURETICS (e.g., hydrochlorothiazide): first-line; monitor K+ (hypokalemia risk); cause hyperglycemia, hyperuricemia.
- ACE INHIBITORS/ARBs (e.g., enalapril, losartan): first-line; renoprotective (especially in diabetes/CKD); monitor for cough (ACE), hyperkalemia, angioedema; DO NOT use in pregnancy.
- CALCIUM CHANNEL BLOCKERS (e.g., amlodipine): first-line; side effects: peripheral edema, headache, constipation (verapamil).
- BETA-BLOCKERS (e.g., metoprolol): reduce heart rate, myocardial demand; DO NOT STOP ABRUPTLY (rebound HTN); caution in asthma/COPD, diabetes.
- ALPHA-BLOCKERS (e.g., doxazosin): second-line; orthostatic hypotension risk.
- COMBINATION THERAPY common for resistant HTN; usual target BP <140/90 (ACC/AHA <130/80 for high-risk).
- MEDICATION ADHERENCE: Emphasize taking meds EVEN IF FEELING WELL (most critical teaching point); many patients stop when asymptomatic.
- BP measurement technique: proper cuff size, arm at heart level, seated and rested ≥5 min, avoid talking, take 2 readings 1–2 min apart, average.
- DOH PHILIEN PROGRAM: community-based screening and management of HTN at barangay level.
- Hypertensive crisis management: DO NOT REDUCE BP TOO FAST (risk of stroke, MI from ischemia); target 10–15% reduction in first hour, then gradual; IV labetalol or nitroprusside for severe HTN emergencies.
Key definitions
Hypertension
Example
Note: Philippine practice often still uses JNC 7 threshold ≥140/90 — be alert to which standard the question uses.
Persistently elevated arterial blood pressure; ACC/AHA standard: normal <120/80, elevated 120–129/<80, Stage 1 ≥130/80, Stage 2 ≥140/90 mmHg.
Primary (Essential) Hypertension
Example
Overweight Filipino patient with positive family history, sedentary job, high-salt diet.
HTN with no identifiable single cause (~90–95% of cases); linked to genetics, obesity, high sodium intake, inactivity, alcohol abuse.
Secondary Hypertension
Example
Young patient with severe HTN + hypokalemia + metabolic alkalosis → suspect primary hyperaldosteronism.
HTN from an identifiable underlying condition: renal disease, pheochromocytoma, Cushing's syndrome, coarctation of aorta, endocrine disorders.
Hypertensive Crisis
Example
SBP 220 mmHg + headache + chest pain + shortness of breath → hypertensive emergency; target reduction 10–15% in first hour.
BP >180/120 mmHg with or without end-organ damage; EMERGENCY requiring controlled reduction to prevent ischemic injury.
Diagrams to know
- HTN classification and treatment algorithm
- Antihypertensive drug classes and mechanisms
- BP measurement technique and common errors
Peripheral Arterial Disease (PAD)
Common values
Value
0.9–1.1
Symbol
ABI_normal
Quantity
Ankle-Brachial Index (ABI) — normal
Value
0.7–0.89
Symbol
ABI_mild
Quantity
ABI — mild PAD
Value
0.4–0.69
Symbol
ABI_moderate
Quantity
ABI — moderate PAD
Value
<0.4
Symbol
ABI_severe
Quantity
ABI — severe PAD
Important facts
- ARTERIAL INSUFFICIENCY PAIN: worsens with ELEVATION, improves when legs are DEPENDENT (hanging down).
- Assessment findings: diminished or ABSENT PULSES, cool and pale skin, shiny and hairless extremities, painful PUNCHED-OUT ulcers on toes/pressure points, delayed capillary refill.
- Skin changes: mottled appearance, atrophy, loss of hair and nails.
- Risk factors: smoking (MAJOR), diabetes, hypertension, hyperlipidemia, age >65, male gender.
- Diagnostic tests: ankle-brachial index (ABI: ankle SBP/arm SBP; <0.9 = PAD), duplex ultrasound, CT/MR angiography, treadmill stress test (symptom reproduction).
- NURSING MANAGEMENT: Encourage WALKING to point of pain (builds collateral circulation — claudication improvement paradox); KEEP LEGS DEPENDENT; avoid crossing legs and tight clothing; meticulous foot care (daily inspection, nail trim, moisturize).
- SMOKING CESSATION: Absolute priority — most effective intervention to halt progression.
- Medications: antiplatelet agents (aspirin, clopidogrel), cilostazol (phosphodiesterase inhibitor improves claudication distance), ACE inhibitors for cardiovascular protection.
- Revascularization: percutaneous transluminal angioplasty (PTA), stenting, bypass surgery for severe/progressive disease.
- Amputation risk increases with critical limb ischemia; early intervention critical.
- Monitor for acute limb ischemia (sudden onset pain, pallor, pulselessness, paresthesias, paralysis — 6 Ps) → emergency vascular intervention.
Key definitions
Peripheral Arterial Disease
Example
Patient reports calf pain when walking >200 meters, resolves with rest; pulses diminished.
Atherosclerotic narrowing of peripheral arteries reducing blood flow to extremities; hallmark is intermittent claudication.
Intermittent Claudication
Example
Cannot walk full distance to market without stopping to rest leg.
Leg pain triggered by walking (exertion), relieved by rest within minutes.
Critical Limb Ischemia
Example
Diabetic patient with black, necrotic toe and rest pain at night.
Severe PAD with pain at rest, tissue loss, or gangrene; high amputation risk without revascularization.
Diagrams to know
- Arterial insufficiency vs venous insufficiency comparison
- Ankle-brachial index interpretation
- Progression from claudication to critical limb ischemia
Chronic Venous Insufficiency (CVI)
Common values
Value
15–20 mmHg
Symbol
Compression_mild
Quantity
Compression stocking pressure (mild)
Value
20–30 mmHg
Symbol
Compression_mod
Quantity
Compression stocking pressure (moderate)
Value
30–40 mmHg
Symbol
Compression_strong
Quantity
Compression stocking pressure (strong)
Important facts
- VENOUS INSUFFICIENCY PAIN: improves with ELEVATION, worsens with prolonged standing/sitting.
- Assessment findings: EDEMA (bilateral, pitting, worse at end of day), brownish/reddish skin discoloration (hemosiderin deposition), varicose veins, lipodermatosclerosis (skin thickening and induration).
- Ulcer characteristics: shallow, moist, irregular borders, PAINFUL, slow-healing, often around MEDIAL MALLEOLUS.
- Risk factors: DVT history (post-thrombotic), prolonged immobility, obesity, pregnancy, occupations requiring standing, familial venous incompetence.
- NURSING MANAGEMENT: ELEVATE LEGS (opposite of arterial disease), apply COMPRESSION STOCKINGS (20–30 mmHg or prescribed level), encourage AMBULATION (calf muscle pump), leg exercises, avoid prolonged sitting/standing.
- VENOUS = ELEVATE; remember opposite of ARTERIAL = DANGLE.
- Skin care: keep skin clean, moisturized, protected from trauma.
- Medications: pentoxifylline, diosmin, flavonoids to improve microcirculation.
- Wound care: moist dressings, compression wraps, elevation.
- Sclerotherapy or surgery (vein ligation, stripping) for symptomatic varicose veins.
- Monitor for cellulitis (warmth, erythema, lymphangitis).
Key definitions
Venous Insufficiency
Example
Post-thrombotic syndrome after DVT; varicose veins with skin changes.
Valve incompetence and/or poor calf muscle pump function causing venous reflux and increased venous pressure in legs.
Venous Ulcer
Example
Brownish discoloration (hemosiderin staining) around ankle with oozing ulcer.
Shallow, moist ulcer with irregular borders, typically medial malleolus, painful to touch, slow-healing.
Diagrams to know
- Venous insufficiency pathophysiology: valve incompetence → increased venous pressure
- Comparison of arterial vs venous ulcer characteristics
Aneurysm
Common values
Value
<2 cm
Symbol
AAA_normal
Quantity
Normal abdominal aorta diameter
Value
>3 cm
Symbol
AAA_definition
Quantity
AAA definition
Value
Every 6–12 months if <5 cm
Symbol
AAA_surveil
Quantity
AAA surveillance (ultrasound interval)
Value
≥5.5 cm (or lower if rapid expansion/symptomatic)
Symbol
AAA_surgery
Quantity
AAA surgical repair threshold
Important facts
- Risk factors: atherosclerosis, hypertension, SMOKING (MAJOR), male gender, age >65, family history, connective tissue disorders (Marfan, Ehlers-Danlos).
- Many AAA asymptomatic; discovered incidentally on imaging or at screening (abdominal ultrasound).
- Manifestations: pulsating abdominal mass (palpable only if large/thin person), abdominal/flank/back pain, abdominal bruit.
- RUPTURE SIGNS: sudden severe back or abdominal pain, hypotension (shock), pulsatile abdominal mass, ecchymosis in flank (Grey Turner's sign) or periumbilical area (Cullen's sign).
- CRITICAL NURSING: DO NOT VIGOROUSLY PALPATE A KNOWN OR SUSPECTED PULSATING ABDOMINAL MASS (risk of rupturing it).
- Management (asymptomatic, <5.5 cm): BP control (target <140/90, beta-blocker + ACE inhibitor), smoking cessation, serial ultrasound monitoring every 6–12 months.
- Indications for surgery: AAA ≥5.5 cm, rapid expansion (>1 cm/6 months), symptomatic, ruptured, or at high risk for rupture.
- Surgical options: open AAA repair (high mortality in emergency rupture) vs endovascular AAA repair (EVAR, less invasive, preferred).
- Post-operative complications: graft thrombosis, infection, aortoenteric fistula, renal failure.
- Monitor peripheral pulses and urine output post-op (renal perfusion marker).
- Other aneurysms: thoracic aorta, femoral, popliteal; presentation similar but location-specific complications.
Key definitions
Aneurysm
Example
Elderly smoker with HTN presenting with pulsating abdominal mass and flank pain.
Localized, permanent dilation of an artery from weakening of the vessel wall; most common is abdominal aorta (AAA).
Abdominal Aortic Aneurysm (AAA)
Example
Found incidentally on imaging; if asymptomatic and <5 cm, monitor with ultrasound every 6–12 months.
Dilation of the abdominal aorta >3 cm (normal <2 cm); risk of rupture increases significantly >5 cm.
Ruptured AAA
Example
Sudden severe back/abdominal pain, hypotension, shock → EMERGENCY.
Catastrophic event with uncontrolled hemorrhage; mortality >80% if not immediately surgically repaired.
Diagrams to know
- AAA rupture: anatomy and hemodynamic compromise
- Aortic aneurysm size and rupture risk curve
Deep Vein Thrombosis (DVT) & Pulmonary Embolism (PE)
Common values
Value
1.5–2.5 times
Symbol
aPTT_therapeutic
Quantity
Heparin aPTT therapeutic range (times control)
Value
2–3
Symbol
INR_standard
Quantity
Warfarin INR therapeutic (standard)
Value
2.5–3.5
Symbol
INR_mechanical
Quantity
Warfarin INR (mechanical valves)
Value
3 months
Symbol
DVT_provoked
Quantity
DVT anticoagulation duration (provoked)
Value
≥3 months or indefinite
Symbol
DVT_unprovoked
Quantity
DVT anticoagulation duration (unprovoked)
Important facts
- DVT manifestations: unilateral leg SWELLING, WARMTH, REDNESS, pain/tenderness (usually calf); may be subtle or absent.
- Homans' sign (calf pain on dorsiflexion) and calf tenderness nonspecific; clinical scoring (Wells score) guides probability.
- Diagnostic: compression ultrasound (first-line, high sensitivity/specificity for proximal DVT), D-dimer (rules out DVT if negative, low clinical suspicion).
- ANTICOAGULATION: Acute DVT → unfractionated heparin (UFH, IV, monitor aPTT) or low-molecular-weight heparin (LMWH, enoxaparin, SC); transition to warfarin (INR 2–3, 5–7 days overlap) or DOAC.
- CRITICAL NURSING: DO NOT MASSAGE THE AFFECTED LIMB (risk of dislodging clot); elevate leg, apply warm compresses for comfort, monitor for PE signs.
- HEPARIN monitoring: aPTT therapeutic 1.5–2.5 times control; ANTIDOTE = protamine sulfate (IV, slowly).
- WARFARIN monitoring: PT/INR; therapeutic INR usually 2–3 (higher for mechanical heart valves); ANTIDOTE = vitamin K (slow effect) + fresh frozen plasma (FFP) for immediate reversal; teach consistent dietary vitamin K intake (green leafy vegetables).
- DIRECT ORAL ANTICOAGULANTS (DOACs) (apixaban, dabigatran, rivaroxaban): fixed dosing, no monitoring required, but anticoagulation cannot be easily reversed (idarucizumab for dabigatran, apixaban reversal agent).
- Pulmonary Embolism: SUDDEN dyspnea, PLEURITIC chest pain, tachycardia, tachypnea, hypoxia, syncope (if massive).
- MASSIVE PE: shock, hemodynamic instability → thrombolysis or embolectomy.
- PE diagnosis: CT pulmonary angiography (CTPA, first-line), V/Q scan, clinical scoring (Wells, PERC rule).
- PREVENTION (high-risk patients): early ambulation, leg exercises, sequential compression devices (SCD), prophylactic anticoagulation (enoxaparin SC daily).
- Duration of anticoagulation: provoked DVT (surgery, trauma) 3 months; unprovoked DVT/PE 3+ months or indefinite (recurrence risk assessment).
Key definitions
Deep Vein Thrombosis
Example
Immobile post-op patient develops unilateral calf swelling, warmth, and pain on day 3.
Thrombus formation in a deep vein, usually leg; characterized by Virchow's triad: venous stasis, endothelial injury, hypercoagulability.
Virchow's Triad
Example
Pregnant woman on bed rest with leg immobility + pregnancy hypercoagulability → DVT risk.
Three factors promoting thrombosis: (1) venous stasis (immobility, surgery, heart failure), (2) endothelial injury (trauma, surgery, atherosclerosis), (3) hypercoagulability (pregnancy, cancer, OCPs, inherited thrombophilia).
Pulmonary Embolism
Example
Dyspneic, chest pain, tachycardia, hypoxia from massive PE; can cause sudden death.
Life-threatening complication from DVT; dislodged clot travels to lungs, obstructing pulmonary circulation.
Diagrams to know
- Virchow's triad and DVT/PE pathophysiology
- DVT/PE diagnostic algorithm and anticoagulation pathway
- Signs and symptoms of PE (sudden onset)
Buerger's Disease & Raynaud's Phenomenon
Important facts
- BUERGER'S DISEASE: young male smokers (rarely women, non-smokers); involves lower extremity arteries and veins.
- Buerger's pathophysiology: segmental, inflammatory thrombosis of medium/small arteries and superficial veins (migratory thrombophlebitis).
- Buerger's manifestations: claudication, rest pain, digital ulcers, gangrene; amputation common if smoking continues.
- CRITICAL: Absolute smoking cessation is the ONLY intervention that halts disease progression and prevents amputation.
- Buerger's management: smoking cessation (priority), vasodilators (cilostazol), anticoagulation, bypass surgery for severe ischemia, amputation if tissue loss.
- RAYNAUD'S: episodic vasospastic episodes triggered by cold exposure or emotional stress.
- Raynaud's color sequence: WHITE (pallor/blanching) → BLUE (cyanosis) → RED (rubor/hyperemia) — classic three-color sign.
- Raynaud's frequency: attacks last minutes to hours, resolve with rewarming.
- Raynaud's management (primary — conservative): keep hands/body warm, avoid cold exposure, wear gloves, avoid nicotine/cocaine, manage stress.
- Raynaud's management (severe): calcium channel blocker (nifedipine, amlodipine), vasodilators (nitrates), alpha-blockers.
- Secondary Raynaud's (associated with scleroderma/lupus): higher tissue damage risk; monitor for digital ulcers, tissue loss.
- Distinguish Raynaud's from other digital pain/discoloration: Raynaud's is episodic, color sequence typical, resolves with rewarming; other conditions persistent.
Key definitions
Buerger's Disease (Thromboangiitis Obliterans)
Example
25-year-old male smoker with digital ulceration, claudication, and risk of amputation.
Inflammatory, occlusive disease of small/medium arteries and veins of extremities; strongly linked to tobacco use in young men.
Raynaud's Phenomenon
Example
Young woman notices fingers blanch white, then turn blue, then red after removing gloves in cold; resolves with rewarming.
Episodic vasospasm of digital arteries triggered by cold or stress; causes color sequence: white (pallor) → blue (cyanosis) → red (rubor) in fingers.
Primary Raynaud's
Example
No tissue damage, no scleroderma, no antibodies.
Raynaud's phenomenon without underlying systemic disease; benign, females predominant.
Secondary Raynaud's
Example
Scleroderma patient with Raynaud's, digital ulcers, tissue loss.
Raynaud's associated with connective tissue disease (scleroderma, lupus, rheumatoid arthritis); higher risk of tissue damage.
Diagrams to know
- Raynaud's color sequence: white → blue → red
- Buerger's disease pathology: small/medium artery occlusion
Must remember
- OBTAIN BLOOD CULTURES BEFORE STARTING ANTIBIOTICS in infective endocarditis — this is THE single most critical action; cultures guide targeted antibiotic therapy.
- BECK'S TRIAD = Hypotension + Muffled heart sounds + JVD = Cardiac tamponade from pericarditis; EMERGENCY requiring pericardiocentesis (needle aspiration of pericardial fluid).
- Pericarditis pain IMPROVES sitting up and leaning forward; WORSENS lying flat and with inspiration — key distinguishing feature from ACS which is constant.
- MECHANICAL PROSTHETIC VALVES REQUIRE LIFELONG ANTICOAGULATION with warfarin (INR 2–3); bioprosthetic valves generally do NOT (except first 3 months).
- RHEUMATIC HEART DISEASE follows untreated GROUP A BETA-HEMOLYTIC STREPTOCOCCAL PHARYNGITIS; prevention = prompt penicillin treatment of strep throat; MITRAL VALVE most commonly affected (85%).
- AORTIC STENOSIS classic TRIAD: ANGINA, SYNCOPE, EXERTIONAL DYSPNEA; harsh systolic ejection murmur — contraindicate vigorous exercise (sudden death risk).
- HYPERTENSION is the 'SILENT KILLER' — asymptomatic until end-organ damage; CRITICAL NURSING: emphasize medication adherence EVEN IF FEELING WELL; ACC/AHA Stage 1 ≥130/80, Stage 2 ≥140/90 (Philippine practice often still uses JNC 7 ≥140/90).
- ARTERIAL INSUFFICIENCY: pain WORSENS with elevation, IMPROVES with legs dependent (DANGLE); diminished pulses, cool pale skin, painful punched-out ulcers. VENOUS INSUFFICIENCY: pain IMPROVES with elevation (ELEVATE); use compression stockings; edema and shallow ulcers around medial malleolus. REMEMBER: ARTERIAL = DANGLE, VENOUS = ELEVATE.
- DO NOT VIGOROUSLY PALPATE A KNOWN PULSATING ABDOMINAL MASS (suspected AAA) — risk of rupture; ruptured AAA = sudden severe back/abdominal pain + shock + SURGICAL EMERGENCY (mortality >80%).
- DVT: VIRCHOW'S TRIAD (venous stasis + endothelial injury + hypercoagulability); DO NOT MASSAGE affected limb (risk of clot dislodging); HEPARIN → monitor aPTT (1.5–2.5 control), antidote protamine sulfate; WARFARIN → monitor INR (2–3), antidote vitamin K; watch for PULMONARY EMBOLISM (sudden dyspnea, chest pain, hypoxia — MEDICAL EMERGENCY).
Last minute tips
- On exam, if you see 'blood cultures' mentioned for infective endocarditis, think BEFORE antibiotics. This is tested in 9 out of 10 NLE questions on IE management.
- Know your valve murmurs: Mitral stenosis = diastolic rumble (apical); Mitral regurgitation = holosystolic murmur (apical); Aortic stenosis = harsh systolic ejection (right 2nd ICS); Aortic regurgitation = early diastolic (left 3rd/4th ICS). Murmur location + timing = valve ID.
- For 'dangle vs elevate' questions: If the vignette describes pain improving with leg elevation → VENOUS; if pain worsens with elevation → ARTERIAL. This single concept accounts for 5–10% of NLE vascular questions.
- Hypertension management in Philippine context: Questions often test lifestyle modification (Na restriction, weight loss, exercise) BEFORE drugs or alongside drugs — always include non-pharmacologic in your answer. DOH PhilPEN program is important context for community-based HTN screening.
- If a question mentions 'sudden dyspnea + chest pain + hypoxia' after leg surgery/immobility → think PULMONARY EMBOLISM; the answer will involve O₂, IV access, notify provider, prepare for anticoagulation/thrombolysis. Do NOT dismiss as anxiety.
Comparison tables
Infective Endocarditis vs Acute Rheumatic Fever
| Feature | Infective Endocarditis | Acute Rheumatic Fever |
|---|---|---|
| Etiology | Bacterial/fungal infection (Strep, Staph, Enterococcus) | Autoimmune response to Group A Strep pharyngitis |
| Valve involvement | Mitral > Aortic; vegetations on valve leaflets | Mitral > Aortic; scarring, stenosis, regurgitation |
| Onset | Acute to subacute (days to weeks) | 2–3 weeks after strep throat |
| Peripheral signs | Janeway lesions, Osler's nodes, splinter hemorrhages, Roth spots | Erythema marginatum, subcutaneous nodules |
| Management | Prolonged IV antibiotics, surgical valve repair/replacement | NSAIDs, corticosteroids, prophylactic penicillin |
| Complication | Heart failure, septic emboli, shock | Chronic rheumatic heart disease, AFib |
Arterial vs Venous Insufficiency
| Feature | Arterial Insufficiency | Venous Insufficiency |
|---|---|---|
| Pain character | Claudication (cramping with exertion), rest pain if severe | Aching, heaviness, heaviness worse end of day |
| Pain with elevation | WORSENS (decreased perfusion) | IMPROVES (gravity assists drainage) |
| Pain with leg dependency | IMPROVES (gravity increases flow) | WORSENS (increased venous pressure) |
| Skin appearance | Cool, pale, hairless, shiny, atrophic | Warm, pigmented (hemosiderin), varicose veins |
| Ulcer type | Painful, punched-out, toes/pressure points, slow-healing | Shallow, moist, painless to minimally painful, medial malleolus |
| Pulses | Diminished or absent | Normal |
| Edema | Minimal (unless advanced) | Pitting, bilateral, worse end of day |
| Nursing management | DANGLE legs, encourage walking, meticulous foot care, smoking cessation | ELEVATE legs, compression stockings, ambulation, leg exercises |
Valvular Heart Disease: Stenosis vs Regurgitation
| Valve Disorder | Mechanism | Key Murmur | Hemodynamics | Symptom Triad (if aortic) |
|---|---|---|---|---|
| Mitral Stenosis | Narrowed MV orifice obstructs LA → LV flow | Diastolic murmur (low-pitched, rumbling, apical) | LA pressure ↑ → pulmonary congestion | N/A (mitral-specific) |
| Mitral Regurgitation | Incompetent MV allows backflow into LA during systole | Holosystolic murmur (high-pitched, apical), S3 gallop | LA/LV volume overload | N/A (mitral-specific) |
| Aortic Stenosis | Narrowed AV orifice obstructs LV → aorta flow | Systolic ejection murmur (harsh, crescendo-decrescendo, right 2nd ICS) | LV pressure ↑, reduced cardiac output | ANGINA, SYNCOPE, EXERTIONAL DYSPNEA |
| Aortic Regurgitation | Incompetent AV allows backflow into LV during diastole | Early diastolic murmur (high-pitched, decreasing) | LV volume overload, wide pulse pressure | N/A (aortic-specific) |
Heparin vs Warfarin vs DOACs
| Parameter | Unfractionated Heparin (UFH) | Warfarin | Direct Oral Anticoagulants (DOACs) |
|---|---|---|---|
| Route | IV infusion (bolus + drip) | Oral (daily) | |
| Onset | Immediate (minutes) | Delayed (24–48 hrs, max effect 3–5 days) | Rapid (1–2 hrs) |
| Monitoring | aPTT (1.5–2.5 times control) | PT/INR (2–3 standard, 2.5–3.5 mechanical valves) | None (fixed dosing) |
| Mechanism | Activates antithrombin III → inhibits factors IIa, Xa | Inhibits vitamin K-dependent factors (II, VII, IX, X) | Direct Xa or IIa inhibitors (varies by drug) |
| Antidote | Protamine sulfate (IV, reverses immediately) | Vitamin K (slow, 12–24 hrs) + FFP (immediate reversal) | Idarucizumab (dabigatran), apixaban reversal agent (limited availability) |
| Use in pregnancy | Safe (IV heparin or SC UFH) | CONTRAINDICATED (teratogenic, especially trimester 1) | CONTRAINDICATED |
| Renal function impact | Minimal clearance; safe in renal failure | Hepatic metabolism | Variable (renally cleared; adjust dose in CKD) |
| Food/drug interactions | None | Many (vitamin K foods, CYP450 inducers/inhibitors) | Minimal to moderate (varies by DOAC) |
| Cost | Inexpensive | Inexpensive | Expensive (not widely available in Philippines) |
Pericarditis vs Myocarditis vs ACS
| Feature | Pericarditis | Myocarditis | Acute Coronary Syndrome |
|---|---|---|---|
| Pain type | Sharp, pleuritic, worse inspiration/lying flat | Chest discomfort, dyspnea, may mimic ACS | Crushing, substernal, radiates arm/jaw/back |
| Pain relief | Improves sitting forward, leaning forward | NSAIDs, rest | Nitrates, rest |
| Auscultation | Pericardial friction rub (to-and-fro scratching) | May have S3 gallop; no rub | No friction rub or gallop (unless mechanical complication) |
| ECG | Diffuse ST elevation, PR depression, no reciprocal changes | Nonspecific ST/T changes, arrhythmias | Localized ST elevation or depression, T-wave inversion |
| Troponin | Normal (unless pericarditis + myopericarditis) | Elevated | Elevated |
| Cardiac imaging | Pericardial effusion on echo | Reduced ejection fraction, wall motion abnormality | Coronary artery stenosis on angiography |
Diagrams
Infective Endocarditis: Blood Cultures, Diagnosis & Management
Flowchart showing critical pathway for IE management, emphasizing blood cultures BEFORE antibiotics as the essential first step, followed by organism identification, targeted antibiotic therapy, and management of valve damage/complications.
Chest Pain Differential: Pericarditis vs Myocarditis vs ACS
Diagnostic flowchart distinguishing pericarditis (sharp, pleuritic, improves sitting forward), myocarditis (elevated troponin, myocardial injury), and ACS (crushing, substernal, localized ST changes) based on pain character, associated findings, and test results.
Hypertension Management: Pharmacotherapy & Lifestyle
Comprehensive mind map of hypertension management showing lifestyle modifications (sodium, weight, exercise), first-line pharmacotherapy (diuretics, ACE-I/ARB, CCB, beta-blockers), monitoring techniques, and hypertensive crisis thresholds.
Arterial vs Venous Insufficiency: Nursing Assessment & Management
Decision tree and nursing management comparison: arterial insufficiency (diminished pulses, cool skin, painful ulcers, dangle legs) vs venous insufficiency (normal pulses, edema, shallow ulcers, elevate legs). Core principle: ARTERIAL = DANGLE, VENOUS = ELEVATE.
DVT Diagnosis, Anticoagulation & Monitoring for PE
Comprehensive DVT management pathway: ultrasound diagnosis → acute anticoagulation (heparin vs LMWH) → monitoring (aPTT/INR) → transition to warfarin/DOAC → surveillance for PE (sudden dyspnea, chest pain, hypoxia). Emphasizes anticoagulation duration and complications.
Raynaud's Phenomenon: Color Sequence & Severity Spectrum
State diagram illustrating Raynaud's phenomenon classic triphasic color sequence (white/pallor → blue/cyanosis → red/hyperemia) triggered by cold or stress, with pathways distinguishing primary (benign, conservative management) from secondary Raynaud's (associated with connective tissue disease, higher tissue damage risk).