Adult Health Study Guide
Module 4
Cardiovascular & Vascular Module
Hypertension • Heart Failure • Vascular Disorders
NUR 3215
Built from instructor lecture slides & transcripts (Harding et al., 2023 used only to clarify mechanism)
1. Hypertension (HTN)
Hypertension is the most important modifiable risk factor for cardiovascular disease. It is often called the “silent killer” because most patients are asymptomatic — about 108 million U.S. adults are affected, ~71% are uncontrolled, and ~49% are untreated.
Pathophysiology — the mechanism
Everything in HTN comes back to one equation: BP = CO × SVR. To lower BP, you must lower cardiac output (CO), systemic vascular resistance (SVR), or both. Every antihypertensive drug works by turning down one side of this equation.
Cardiac output (the volume/pump side): CO = SV × HR. If a patient is fluid overloaded, CO rises and BP rises.
Systemic vascular resistance (the container side): the force opposing blood flow. The principal factor is the radius of the small arteries and arterioles — controlled by smooth muscle in the tunica media. Vasoconstriction raises SVR and BP.
Short-term regulation (sympathetic nervous system — acts in seconds): baroreceptors in the carotid sinus and aortic arch sense a BP drop and signal the brainstem.
Beta-1 receptors (heart): ↑ heart rate and contractility → ↑ CO.
Alpha-1 receptors (vascular smooth muscle): vasoconstriction → ↑ SVR.
Beta-2 receptors (lungs, coronary arteries): vasodilation and bronchodilation. Non-selective beta-blockers (e.g., propranolol) block beta-1 AND beta-2, so they can cause bronchoconstriction — avoid in asthma.
Key pathology: in chronic HTN the baroreceptors “reset” to a higher normal, so the body actually fights efforts to lower the pressure.
Long-term regulation (RAAS — Renin-Angiotensin-Aldosterone System): a domino chain. Low renal blood flow → kidney releases renin → angiotensinogen converts to angiotensin I → ACE (the catalyst) converts it to angiotensin II.
Angiotensin II is a potent vasoconstrictor → ↑ SVR.
Angiotensin II also triggers aldosterone → kidneys retain sodium and water → ↑ blood volume → ↑ CO.
Primary (essential) HTN = 95% of patients: multifactorial (genetics + lifestyle). Continuous BP elevation causes medial hyperplasia (thickening of the arteriole wall) → the lumen narrows → perfusion drops → organ damage. Chronic and incurable, but controllable.
Secondary HTN = 5%: caused by a specific underlying condition or drug — renal/kidney disease (most common), renal artery stenosis, primary aldosteronism, pheochromocytoma, Cushing syndrome, or medications (estrogen-containing oral contraceptives, glucocorticoids). Treat the underlying cause and the HTN often resolves. Red flags: sudden severe BP elevation or an abdominal bruit over the renal arteries.
Risk factors
Modifiable: diet high in saturated fat and salt, physical inactivity, stress, excessive alcohol, smoking, obesity, coexisting diabetes/kidney disease.
Non-modifiable: aging, family history, African American race.
Clinical presentation & symptoms
Usually asymptomatic. “Absence of symptoms ≠ absence of disease.” Silent vascular damage occurs while the patient feels fine.
Late signs (severe — organs already struggling): fatigue, dizziness, angina, dyspnea. These are NOT early warnings.
Diagnostic tests & findings
Accurate technique: correct cuff size (too small = falsely high reading) and arm supported at heart level.
Ambulatory BP monitoring (24 hr): rules out white-coat HTN and assesses diurnal variability. Normal “dippers” drop ~10% at night; non-dippers / reverse dippers are at much higher cardiovascular risk.
Home readings predict CVD risk better than office readings — take morning (before meds) and evening.
Treatment & nursing interventions
First line — lifestyle changes
Physical activity: ≥150 min moderate exercise/week → SBP ↓ 4–9 mmHg.
Weight loss: ~1 mmHg BP drop per kilogram lost; also slows atherosclerosis.
Sodium reduction: <2300 mg/day for healthy adults, <1500 mg for greater reduction. Teach the “Salty Six”: bread products, deli/cured meats, pizza, soup, sandwiches, poultry.
Diet additions: ↑ potassium and calcium from food (not supplements — calcium supplements are NOT recommended for BP). Limit alcohol/sugary drinks; quit smoking.
Pharmacology — mapped to BP = CO × SVR
Drug class
Action on the equation
Examples / nursing notes
Thiazide diuretics
↓ CO (↓ volume) — first choice for HTN alone
Hydrochlorothiazide; take early in day
Loop / K-sparing diuretics
↓ CO (↓ volume)
Loop: furosemide, bumetanide
K-sparing: spironolactone, eplerenone
ACE inhibitors
↓ SVR — block ACE (Ang I→II)
Lisinopril, enalapril (“-pril”)
SE: dry cough, angioedema; first-line for RAAS
ARBs
↓ SVR — block Ang II receptors
Losartan, valsartan (“-sartan”); used if ACE cough
Calcium channel blockers
↓ SVR — relax vessel smooth muscle
Amlodipine
Beta blockers
↓ CO — block beta-1
Metoprolol, atenolol
Alpha agonists / blockers
↓ SVR — block alpha-1/SNS
Clonidine
Aldosterone antagonists
↓ volume + block RAAS
Spironolactone, eplerenone (also K-sparing)
Hyperkalemia watch: ACE inhibitors, ARBs, and aldosterone antagonists all reduce aldosterone → monitor potassium. Combination therapy (e.g., a diuretic + a CCB) lets each drug be used at a lower dose.
Managing side effects & the “adherence gap”
The disease is silent but the cure can make patients feel worse, so they stop their meds. Nursing focus is on managing side effects and adherence.
Orthostatic hypotension (a fall risk): rise slowly, dangle legs before standing; sit down if dizzy.
Xerostomia (dry mouth): sugarless gum or hard candy.
Nocturia: take diuretics early in the day.
Sexual dysfunction: encourage reporting to the HCP for a medication change rather than stopping abruptly.
Hypertensive crisis (sneak peek — >180/120)
Urgency: very high BP, NO target organ damage → oral meds (captopril, labetalol), lower gradually over hours/days.
Emergency: high BP PLUS acute target organ damage (chest pain, stroke signs, acute renal failure) → ICU + IV meds.
Safety rule: decrease MAP by no more than 25% in the first hour — dropping pressure too fast can cause an ischemic stroke.
Older adults (>65)
Physiology: loss of arterial elasticity (arteriosclerosis), myocardial stiffness, blunted baroreceptor reflexes → high orthostatic hypotension risk.
Goals: community-dwelling target SBP <130; institutionalized/comorbid patients use clinical judgment (strict control raises fall risk). “Start low, go slow.”
Complications — target organ damage
Cerebrovascular disease: stroke / TIA (4× risk increase).
Retinopathy: retinal hemorrhage, vision loss.
Left ventricular hypertrophy: → coronary artery disease and heart failure.
Nephrosclerosis: → chronic kidney disease / renal failure.
⭐ Clinical Pearl / NCLEX
Orthostatic hypotension is defined as a drop of ≥20 mmHg systolic OR ≥10 mmHg diastolic on standing — a classic exam value and a major fall risk in older adults on antihypertensives.
Red flag: In a hypertensive emergency, do NOT normalize BP rapidly — reduce MAP by ≤25% in the first hour to avoid cerebral ischemia.
2. Heart Failure (HF)
Heart failure is the inability of the heart to provide sufficient cardiac output to meet the body’s metabolic needs. The heart hasn’t stopped — its pumping capacity is reduced, so perfusion is inadequate, especially during exertion. The brain, kidneys, and muscles suffer most.
Pathophysiology — the mechanism
Start with CO = SV × HR (normal 4–8 L/min at rest). Stroke volume depends on three factors:
Preload (the stretch): volume in the ventricle at end of diastole. Frank-Starling law — more stretch (within reason) = stronger contraction.
Afterload (the resistance): what the ventricle pumps against. ↑ SVR (high BP) wears out the left side; pulmonary hypertension wears out the right side. High afterload ↑ O₂ demand.
Contractility (the squeeze): muscle strength, ↑ by the sympathetic nervous system (epinephrine) and positive inotropes.
The vicious cycle of HF: low CO → body senses crisis → SNS + RAAS activate → ↑ HR and massive vasoconstriction to keep BP up → this ↑ afterload → the exhausted heart works harder and O₂ demand climbs → chronic strain causes
Ventricular remodeling: the ventricles dilate (stretch out) or undergo hypertrophy (thicken) → progressive failure.
The body’s “emergency brake” — BNP: B-type natriuretic peptide is released by the ventricles in response to excessive stretch. It promotes diuresis and vasodilation to offload the heart, and is used clinically as a diagnostic marker of fluid overload.
Types of heart failure
Left vs. right (a backward-failure problem)
Left-sided HF (“Left = Lungs”)
Right-sided HF (“Right = Rest of body”)
Mechanism
LV fails → blood backs up into the left atrium and pulmonary veins → fluid into the alveoli
RV fails → blood backs up into the venous system. Most common cause = left-sided HF (cor pulmonale)
Key signs
Dyspnea, orthopnea, PND
Crackles/rales; pink frothy sputum
S3/S4; pale/mottled skin, fatigue
Restlessness = early hypoxia sign
Jugular venous distention (JVD)
Hepatomegaly → RUQ pain, nausea, anorexia
Ascites; dependent peripheral edema
Weight gain (most reliable fluid sign); S3/S4
Systolic vs. diastolic (by ejection fraction)
HFrEF — Systolic (“pumping problem”)
HFpEF — Diastolic (“filling problem”)
Mechanism
Ventricle is thin-walled and weakened — loses the squeeze needed to eject blood
Ventricle is thick and stiff — can’t relax and fill during diastole
Ejection fraction
LVEF < 40%
LVEF preserved (55–65%): normal % of a low volume
Ejection fraction (EF) = ejected volume ÷ end-diastolic volume × 100 (e.g., 70 mL ÷ 120 mL ≈ 58%). For this class remember: normal 50–70%, borderline 41–49%, and <40% = HFrEF. Treat the patient’s symptoms, not just the number.
Risk factors & etiology
Primary: hypertension (most common cause — treating HTN ↓ HF incidence by 50%), coronary artery disease/MI (damages muscle), structural/valvular disease (aortic or pulmonic stenosis).
Contributing: diabetes, metabolic syndrome, advanced age, tobacco, obesity/inactivity, vascular disease.
Other causes: congenital defects (septal defects), cardiomyopathies, viral myocarditis, dysrhythmias, toxins (alcohol, illicit drugs, chemotherapy).
Precipitating (acute decompensation): infection, anemia, thyroid disorders, and — very commonly — medication nonadherence.
Diagnostic tests & findings
Echocardiogram = gold standard: measures LVEF, chamber size, wall motion, and valve function.
Transesophageal echo (TEE): invasive probe swallowed under sedation; keep NPO until the gag reflex returns (~1–2 hr).
BNP: the diagnostic tiebreaker — differentiates cardiac vs. respiratory dyspnea. High = cardiac/fluid overload.
Chemistries: K⁺, Na⁺, and BUN/creatinine for cardiorenal monitoring.
12-lead ECG: detects dysrhythmias. Chest X-ray: cardiomegaly and pulmonary congestion (white cloudiness). Cardiac catheterization/angiogram: assesses CAD.
Classification: NYHA (functional, Classes I–IV, numbers) vs. AHA/ACC (structural + risk, Stages A–D, letters). Higher numbers/letters = worse.
Treatment & nursing interventions
Mortality benefit — slow remodeling in HFrEF
ACE inhibitors / ARBs: block RAAS → ↓ afterload and ↓ remodeling. Watch for dry cough/angioedema (ACE) and hyperkalemia (both). Examples: lisinopril, valsartan.
Beta blockers (metoprolol succinate, carvedilol): block chronic SNS overstimulation → ↓ HR and O₂ demand. Start low, go slow; monitor for bradycardia and hypotension.
ARNI — Entresto (sacubitril/valsartan): an ARB combined with a neprilysin inhibitor; boosts beneficial BNP effects and is more effective than ACE inhibitors alone at reducing hospitalizations.
Aldosterone antagonists (spironolactone): block aldosterone’s fibrotic effects on the heart; K-sparing → monitor renal function and potassium closely.
Mechanism note (textbook): neprilysin is the enzyme that breaks down natriuretic peptides (ANP/BNP). Inhibiting it raises BNP levels, enhancing diuresis, natriuresis, and vasodilation while inhibiting aldosterone and renin — which is why an ARNI amplifies the heart’s own “emergency brake.”
Symptom management — fluid control (no mortality benefit)
Diuretics: loop (furosemide/Lasix) acts at the loop of Henle, removing large fluid volumes; thiazides are milder, often combined. Monitor for hypokalemia; risk of ototoxicity (hearing changes) with rapid IV Lasix.
Positive inotropes — digoxin: ↑ contractility, ↓ HR. Narrow therapeutic range — early toxicity signs are nausea and visual changes (yellow halos).
Vasodilators — BiDil (hydralazine + isosorbide dinitrate): improves outcomes specifically in Black/African American patients with HFrEF.
Nutrition, lifestyle & safety
Sodium restriction ≤2 g/day; avoid the “Salty Six.”
Fluid restriction: reserved for Stage D or persistent retention (not routine for mild HF); hospitalized severe cases often 1000–1500 mL.
Activity: cardiac rehab reduces mortality; teach energy conservation (balance rest/activity); avoid extremes of heat and cold.
Avoid NSAIDs (ibuprofen/Advil/Motrin, naproxen/Aleve) — cause sodium/water retention; Tylenol is generally preferred. Avoid decongestants (stimulants ↑ workload).
Infection prevention: annual flu and pneumonia vaccines are essential — infection ↑ metabolic O₂ demand and triggers decompensation.
Home management (patient teaching)
Daily weights — the “3 S’s”: same time (morning), same scale, same clothing. Call the provider for weight gain >3 lb in 2 days OR 3–5 lb in a week (fluid, not fat).
Pulse check: radial pulse for 1 full minute; call if <50 or >100 (or per provider limits).
Report worsening symptoms: waking breathless (PND) or needing more pillows to sleep → call the provider.
Complications & advanced therapies
Complications: pleural effusion, dysrhythmias (atrial fibrillation → high thrombus risk), cardiorenal syndrome (kidney failure from low perfusion).
Advanced (Stage D): ICD for sudden cardiac death prevention if EF <35%; VAD (bridge-to-transplant or destination therapy); heart transplant (gold standard for end-stage); palliative care when NYHA Class IV symptoms persist.
⭐ Clinical Pearl / NCLEX
Sudden weight gain >3 lb in 2 days or 3–5 lb in a week is the earliest, most reliable sign of fluid retention and worsening HF — teach patients to call the provider even when they still feel fine.
Two high-yield red flags: (1) digoxin toxicity = nausea + yellow halos around lights; (2) new restlessness/confusion in left-sided HF = early hypoxia — check pulse ox and lung sounds immediately.
3. Vascular Disorders
Foundations — the two roads
Arterial system (supply road): high-pressure, carries oxygenated blood away from the heart; thick muscular walls. The problem in arterial disease is a delivery failure.
Venous system (return road): low-pressure/high-volume, carries deoxygenated blood toward the heart; relies on one-way (semilunar) valves and the skeletal muscle (calf) pump to fight gravity.
The endothelium: innermost lining that maintains hemostasis. Disruption (by HTN, smoking, high cholesterol) triggers the coagulation cascade → fibrin clots and blockages.
Diagnostic visualization & screening
Doppler ultrasound: maps blood flow when pulses are hard to palpate.
Ankle-Brachial Index (ABI): ankle systolic BP ÷ higher brachial systolic BP. Normal 1.0–1.3; mild PAD 0.71–0.90; severe PAD / critical ischemia ≤0.40.
Segmental BP (thigh, below knee, ankle): a drop >30 mmHg between segments localizes the blockage.
Angiography = gold standard for exact location/severity: contrast dye + X-ray. Radial approach (more comfortable, less bleeding) vs. femoral approach (larger-vessel access, strict flat bedrest afterward). IVUS gives a 360° cross-section of the arterial wall.
Angiography patient safety
Pre-procedure: verify contrast dye allergy (shellfish/iodine link is a myth — ask about contrast); baseline vitals + neurovascular check (mark distal pulses); labs (cardiac biomarkers, creatinine — kidneys must clear the dye); NPO 6 hr; give ordered sedatives; teach the flushing/fluttering sensation.
Post-procedure: compare to baseline; strict bedrest if femoral; check the insertion site for hematoma/bleeding every 15 min for the first hour; recheck distal pulses (a colder extremity suggests occlusion); monitor ECG for dysrhythmias/ST changes; push fluids to flush the dye.
Peripheral Artery Disease (PAD) — “the blockade”
Pathophysiology: progressive narrowing from thickening of the intima/media layers; a marker of advanced systemic atherosclerosis (the heart and brain vessels are likely affected too).
Risk profile: tobacco use (the single most important risk factor — it accelerates PAD), diabetes (earlier onset; high sugar roughens arterial walls), hypertension, high cholesterol, age >60.
Clinical signs
Intermittent claudication (hallmark): ischemic muscle pain triggered by exercise (lactic acid buildup — “angina of the legs”), resolving within ~10 min of rest.
Skin/perfusion changes: thin, shiny, taut skin; hair loss; paresthesia in the toes; diminished or absent pedal and popliteal pulses.
Arterial ulcers: “punched out,” on bony prominences/tips of toes, minimal drainage.
Positional test: elevation pallor (pale when raised) → dependent rubor (dusky red when hanging down).
Critical Limb Ischemia (CLI) — the danger zone
Definition: chronic ischemic rest pain >2 weeks, nonhealing ulcers, or gangrene.
Rest pain: worse at night when lying flat (limbs level with the heart lose gravity assistance). Patients sleep in chairs or dangle their legs.
Sequelae: tissue necrosis, delayed healing, high amputation risk.
Medical management — restoring flow
Risk modification: tobacco cessation is essential (nicotine causes vasoconstriction); DASH or Mediterranean diet; exercise 30–45 min, 3×/week — push through claudication to moderate severity, rest, then resume → builds collateral circulation.
Antiplatelets: aspirin or clopidogrel (Plavix). Warning: omeprazole (Prilosec) reduces clopidogrel’s effect → ↑ MI risk. Anticoagulants like warfarin are NOT as effective for PAD.
Statins (e.g., simvastatin) lower cholesterol and stabilize plaque.
Claudication-specific drugs: cilostazol (vasodilator — contraindicated in heart failure); pentoxifylline (↑ RBC flexibility).
Surgical interventions
Radiologic: PTA & stenting (balloon compresses plaque, stent holds it open), atherectomy (plaque removal), cryoplasty (cold therapy to limit restenosis).
Bypass: femoral-popliteal (fem-pop) using an autogenous vein or synthetic graft to detour around the lesion.
Endarterectomy / amputation: manual plaque removal; amputation for uncontrolled infection or extensive necrosis.
Post-op vigilance: assess the operative extremity q15min, then hourly — color, temperature, cap refill, pulses, sensation. Loss of a palpable pulse or a changed Doppler sound = emergency, notify the surgeon. Avoid knee-flexed positions (kinks the graft); turn frequently keeping the limb straight; monitor the 6 Ps (pain, pressure, paresthesia, pallor, paralysis, pulselessness) and watch for bleeding, hematoma, thrombosis, and compartment syndrome.
Arterial outliers — spasm & inflammation
Buerger’s disease (thromboangiitis obliterans): inflammatory disorder of small arteries/veins; targets men <45 who are heavy tobacco/marijuana users. Treatment is complete cessation — nicotine replacement is contraindicated because nicotine itself drives the inflammation.
Raynaud’s phenomenon: episodic vasospasm triggered by cold, stress, or caffeine. Classic color change: White (ischemia) → Blue (cyanosis) → Red (hyperemia). Treat with calcium channel blockers (nifedipine) and warmth.
Peripheral / Chronic Venous Insufficiency (PVI / CVI) — “the backflow”
Varicose veins (PVI): incompetent valves → dilated, tortuous superficial veins as blood pools backward. Heavy, achy legs, worse after standing, relieved by walking/elevation. Treatment: sclerotherapy (vein ablation); post-op compression stockings, avoid long travel for 1 week (DVT risk). Teach: avoid prolonged sitting or standing.
Chronic venous insufficiency (CVI): long-term valve incompetence → serous fluid and RBCs leak into tissue; RBC breakdown releases hemosiderin. Look for leathery, brawny (brownish) skin discoloration, persistent edema, and venous stasis ulcers above the medial malleolus that are irregularly shaped and weepy. Pain is worse in a dependent position.
Management: compression therapy is the cornerstone (stockings, Velcro wraps, Unna boot). Critical safety check — assess arterial status first; do NOT apply compression if ABI ≤0.40. Moist wound care (hydrocolloid/foam); nutrition high in protein, vitamins A & C, and zinc; antibiotics only with clinical infection (purulence/odor); elevate the limbs.
Arterial vs. Venous — the master comparison
Feature
Arterial (PAD)
Venous (PVI/CVI)
Root cause
Atherosclerosis → blockage of supply
Incompetent valves + high pressure → backflow
Pain
Sharp intermittent claudication with exercise; relieved by dangling legs
Dull, heavy ache; relieved by elevating legs above heart
Skin/temp
Cool, thin, shiny; elevation pallor / dependent rubor
Warm, thick; bronze-brown pigmentation; varicose veins
Pulses
Decreased or absent
Present (may be hard to palpate if edema)
Edema
Generally absent
Common (lower leg)
Ulcers
Tips of toes / lateral malleolus; rounded, “punched out”; minimal drainage
Near medial malleolus; irregular; moderate–large drainage
Primary goals
Antiplatelets + supervised walking
Compression + wound care
⭐ Clinical Pearl / NCLEX
NEVER apply compression therapy if the ABI is ≤0.40 (severe PAD) — it can completely shut off already-limited arterial supply. Always assess arterial status before treating a venous ulcer.
Ulcer location is the giveaway: arterial ulcers sit on the toes/lateral malleolus (punched out, dry); venous ulcers sit above the medial malleolus (irregular, weepy). And in Buerger’s disease, nicotine replacement is contraindicated.
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