Ineffective Tissue Perfusion and Hypertension Study Notes

Peripheral Vascular Disease (PVD): Overview, Causes, and Risk Factors

• Definition of Peripheral Vascular Disease (PVD): Refers to any disease state affecting the blood vessels located within the extremities.

• Primary Etiology: The most common cause is atherosclerosis, which is defined as the buildup of cholesterol and lipids that create "fat" deposits along the vessel walls.

• Secondary Etiologies:

  • Formation of blood clots.

  • Inflammation of the arteries.

  • Infections.

  • Physical injury.

  • Diabetes.

  • Arteriosclerosis.

• Risk Factors for PVD:

  • Family history of vascular disease.

  • Obesity.

  • Sedentary lifestyle.

  • Smoking (tobacco use).

  • Diabetes.

  • High cholesterol levels.

  • Hypertension ($HTN$).

Peripheral Arterial Disease (PAD)

• Alternative Name: Also known as Peripheral Arterial Occlusive Disease.

• Description: This is a specific form of $PVD$ involving the narrowing of the arteries, which leads to reduced blood flow to distal extremities.

• Etiology: Usually caused by atherosclerosis.

• Clinical Presentation:

  • The Hallmark/Early Sign: Intermittent Claudication. This is defined as reproducible ischemic muscle pain. It occurs specifically during activity and is relieved when the patient rests. It is often the first symptom a patient notes.

• The Six P’s of PAD:

  1. Pain.

  2. Paresthesia (numbness or tingling).

  3. Pallor (paleness).

  4. Pulselessness.

  5. Paralysis.

  6. Poikilothermia (the extremity feels cold).

Chronic Venous Insufficiency

• Pathophysiology: This condition occurs when the venous wall and/or the valves in the leg veins are not functioning effectively. This makes it difficult for blood to return to the heart from the lower extremities.

• Manifestations:

  • Edema: Swelling in the lower extremities.

  • Venous Stasis Ulcers: Wounds caused by poor venous return.

  • Altered Pigmentation: Known as "vascular discoloration." Skin may appear reddish or bluish with brown pigmentation.

  • Temperature: The skin is typically warm to the touch.

  • Pulses: Pulses remain palpable in venous insufficiency.

  • Skin Texture: Dry, cracking skin.

  • Sensation: Aching and cramping pain.

  • Structural Changes: Presence of varicose veins.

Comparison: Arterial vs. Venous Characteristics

• Arterial Characteristics:

  • Pain Characteristics: Intermittent claudication. The pain gets better if the patient dangles their foot off the bed; however, elevating the feet makes the pain worse.

  • Edema: Generally absent.

  • Pulses: The pulse is either absent or weak.

  • Ulcer Drainage: No drainage from sores.

  • Ulcer Appearance: Sores are round and smooth.

  • Necrosis: Presence of black eschar.

  • Skin Temperature: The foot is cool to the touch.

  • Location of Sores: Typically found on the toes and feet.

  • Treatment ($TX$): Antiplatelets such as clopidogrel and surgical treatments like Fempop (femoral-popliteal) bypass.

• Venous Characteristics:

  • Pain Characteristics: Dull, achy pain.

  • Edema: Present in the lower legs.

  • Pulses: Pulse is present/palpable.

  • Ulcer Drainage: Drainage is present.

  • Ulcer Appearance: Sores have irregular borders.

  • Skin Condition: Presence of yellow slough or ruddy skin.

  • Location of Sores: Typically found on the ankles.

Diagnostics and Nursing Management for PVD

• Diagnostic Tools:

  • Ultrasound: Used to identify blockages or restrictions.

  • Ankle Brachial Index ($ABI$): Used specifically for $PAD$.

  • $CT$ angiography ($CTA$).

  • Angiography: Involves the femoral or radial arteries.

  • $MR$ angiography ($MRA$).

  • Contrast phlebography (venography).

• Laboratory Testing:

  • D-Dimer.

  • $PT/INR$.

  • $PTT$.

  • Lipid panel.

• Nursing Assessment:

  • Palpation of pulses. Use of a Doppler is required if pulses are unpalpable.

  • Collection of health history and risk factors.

  • Calculation of the $CHAD-VAS$ Score.

  • Assessment of skin color, texture, and capillary refill.

  • Assessment of edema and identification of underlying causes.

  • Monitoring Hemoglobin and Hematocrit ($H\&H$) and Pulse Oximetry.

  • Identification of lesions or wounds.

• Nursing Interventions:

  • Positioning: For arterial issues, do not elevate legs above the level of the heart.

  • Activity: Encourage Range of Motion ($ROM$).

  • Thermoregulation: Keep the patient warm, but do not apply direct heat.

  • Pharmacology: Administer antiplatelet medications, anticoagulants, and peripheral vasodilators.

  • Care: Closely monitor pulses and perform diligent wound and foot/leg care.

• Collaborative Management:

  • Address lifestyle changes and risk factors.

  • Medication Administration:

    • Antiplatelets: Clopidogrel and Aspirin.

    • Antihyperlipidemic: "Statin" medications.

    • Antihypertensive: Cilostazol (a vasodilator that also inhibits platelet aggregation).

  • Surgical Options: Stenting and Vascular bypass.

Raynaud’s Phenomenon

• Description: Characterized by intermittent arterial constriction of small blood vessels, typically occurring on both sides of the body.

• Affected Areas: Primarily the fingers, but can also affect the toes, tip of the nose, earlobe, skin over the kneecap, or the nipples.

• Manifestations: Sudden vasoconstriction causes color changes, numbness, tingling, and burning pain.

• Triggers: Episodes are usually brought on by cold exposure or emotional stress.

• Care Instructions: Protect the patient from cold and known triggers. Prevent injury to the hands and fingers.

Ischemia Events and Thrombosis

• Two Main Causes of Ischemia:

  • Embolism: A blood clot formed elsewhere that travels to a vessel.

  • Thrombosis: A blood clot that forms directly within a vessel, often involving atherosclerosis plaque.

• Deep Vein Thrombosis ($DVT$):

  • Definition: The formation of a blood clot within a deep vein of an extremity (typically legs, sometimes arms).

  • Manifestations: Localized pain, redness, and swelling. May cause decreased distal pulses if swelling compresses an adjacent artery. Signs of decreased perfusion to distal tissue.

  • Virchow’s Triad (High Risk Factors):

    1. Endothelial damage.

    2. Venous stasis.

    3. Altered coagulation.

• Arterial Thrombosis: Emboli typically form within cardiac chambers and lodge in an artery, causing cessation of distal blood flow and organ-specific failure symptoms.

• Pulmonary Embolism ($PE$): Emboli travel to the pulmonary vasculature, causing chest pain and shortness of breath.

• DVT Preventative Measures:

  1. $TED$ stockings.

  2. Sequential Compression Devices ($SCD$).

  3. Positioning: Periodic elevation of lower extremities.

  4. Exercises and $ROM$ exercises.

  5. $CHADVASC$ Scoring.

  6. Medication: Subcutaneous heparin, subcutaneous low molecular weight heparin (e.g., Lovenox), $PO$ Warfarin, and antiplatelets (Aspirin/$ASA$; clopidogrel).

Pharmacologic Management: Heparin and Warfarin

• Heparin:

  • Administered as a continuous $IV$ infusion during the acute phase.

  • Requires monitoring of $aPTT$ levels with titration of the drip per hospital policy.

• Warfarin:

  • Administered $PO$ during the heparin infusion (known as the "heparin to warfarin bridge").

  • Requires several days to reach a therapeutic level.

  • Monitor $INR$ for $PO$ dosage adjustments.

  • Therapeutic $INR$ Range: $2-3$.

• Warfarin Patient Teaching:

  • Wear a medic alert bracelet.

  • Take the medication at the same time every day (am or pm); do not stop abruptly.

  • Regularly monitor $INR$ levels.

  • Consult a provider before starting any other medications.

  • Avoid alcohol.

  • Review signs and symptoms of bleeding and follow bleeding precautions.

  • Notify a physician if surgery is needed.

  • Maintain consistency with Vitamin $K$ rich food intake.

  • Note: Patients may occasionally be on both $ASA$ and Warfarin simultaneously.

Aortic Disorders

• Aneurysm: A weak point in the arterial wall, typically caused by atherosclerosis.

  • Thoracic Aneurysm: Can be asymptomatic; symptoms include pain when lying supine and shortness of breath.

  • Abdominal Aneurysm: Patients describe a "heart beating" in the stomach or abdominal throbbing.

  • Emergency Symptoms: Severe back or abdominal pain.

  • Treatment: Strict blood pressure ($BP$) control and vascular surgery.

• Dissection: A tear or rip in the aortic wall.

  • Symptoms: Sudden onset of severe pain, sweating (diaphoresis), tachycardia, and pale skin.

  • Management: Urgent vascular surgery.

Hypertension (HTN)

• Definition: Elevation of blood pressure greater than the limits defined as "normal" by the $AHA$.

• Variations:

  • Essential $HTN$.

  • Secondary $HTN$.

  • White Coat $HTN$.

  • Malignant $HTN$.

  • Pregnancy-induced $HTN$.

• Pathophysiology:

  • Alteration in the body's ability to regulate pressure.

  • Over time, $HTN$ damages vessels, causing arterial walls to thicken for protection.

  • Injured vessels become inflamed, leading to increased vascular permeability and further wall thickening, which in turn increases $BP$ in a detrimental cycle.

• Physiological Definitions:

  • Systolic Pressure: Measured when the heart contracts.

  • Diastolic Pressure: Measured when the heart relaxes between beats.

• Risk Factors:

  • Age, Race, and Gender.

  • Family history.

  • Obesity and High Cholesterol.

  • Inactivity and Stress.

  • Tobacco use, Alcohol intake, and high Sodium intake.

• The "Silent Killer": Often asymptomatic until end-organ damage occurs (Stroke, $MI$, Renal failure, Heart failure, Retinal damage). Retinal damage is commonly caught at the eye doctor.

• The 4 C’s (Complications):

  1. Coronary Artery Disease ($CAD$).

  2. Congestive Heart Failure ($CHF$).

  3. Cerebral Vascular Accident ($CVA$).

  4. Chronic Renal Failure ($CRF$) or Chronic Kidney Disease ($CKD$).

HTN: Assessment and Diagnostics

• Diagnostic Criteria: Diagnosis requires an average taken of $2$ or more blood pressure measurements across different encounters.

• Assessment Tools:

  • Urinalysis ($UA$).

  • Basic Metabolic Panel ($BMP$) to check $BUN$, Creatinine ($CRT$), and electrolytes.

  • Blood Glucose ($BG$).

  • Lipid panel.

  • $EKG$ and Chest X-ray.

• Nursing Priorities:

  • BP screening and monitoring vital signs.

  • Maintaining perfusion.

  • Strict intake and output ($I\&O$) to assess for fluid retention and renal damage.

  • Assess the efficacy of diuretics.

  • Assess cardiovascular, renal, neurologic, and peripheral status.

• Patient Education:

  • DASH Diet: Low sodium diet.

  • Limit caffeine and alcohol.

  • Smoking cessation and physical activity.

  • Orthostatic Hypotension: Warn patients to move slowly; avoid hot baths and strenuous activity immediately after medication administration.

  • Importance of medication compliance.

HTN: Pharmacologic Therapy

• Hypertensive Urgency vs. Emergency:

  • Urgency: SBP > 180 with no current evidence of secondary organ damage. Goal: Decrease $BP$ soon.

  • Emergency: SBP > 180 with evidence of target organ injury. Goal: Decrease $BP$ immediately.

• Initial Therapy: Typically starts with a Thiazide diuretic.

Diuretics for HTN

• Mechanism: Promoting diuresis of fluid and electrolytes reduces blood volume and blood pressure.

• Loop Diuretics (e.g., Furosemide):

  • Most potent.

  • Prevents reabsorption of sodium, chloride, and fluid in the kidneys; potassium is excreted.

  • Considerations: Use cautiously with liver disease. May cause hypotension, dry mouth, dehydration, metabolic acidosis, and hypokalemia. Monitor renal panel. Take in the morning.

• Thiazide Diuretics (e.g., Hydrochlorothiazide/HCTZ):

  • Most commonly prescribed.

  • Inhibit sodium-chloride transporter in the distal tubule and cause vessels to relax (vasodilation).

  • Considerations: May cause dizziness and various electrolyte deficiencies (hypokalemia, hyponatremia, hypophosphatemia, hypomagnesemia). Hypokalemia increases risk for digoxin toxicity. Monitor $I\&O$, $BP$, and electrolytes. Take in the morning.

• Potassium Sparing Diuretics (e.g., Spironolactone):

  • Blocks aldosterone in the distal tubule to retain potassium while promoting diuresis.

  • Considerations: Often used with other diuretics to counter potassium loss. Contraindicated in kidney disease or hyperkalemia. Avoid potassium-high foods and salt substitutes. Do not use during pregnancy/breastfeeding. Monitor for hyperkalemia signs.

RAAS Path and Associated Medications

• Renin-Angiotensin-Aldosterone System (RAAS): Renin (kidney) acts on Angiotensinogen (liver) to create Angiotensin I. The Lungs provide Angiotensin Converting Enzyme ($ACE$) to convert it to Angiotensin II, which causes vasoconstriction and triggers Aldosterone (adrenal gland) to reabsorb sodium ($NaCl$) and water ($H_2O$).

• ACE Inhibitors (-pril):

  • Mechanism: Inhibit $ACE$ to decrease Angiotensin II.

  • Side Effects: Cough, hyperkalemia, sun sensitivity, leukocytosis, and serious reactions like Angioedema and Liver Dysfunction.

• Angiotensin II Receptor Blockers (ARBS) (-sartan):

  • Mechanism: Prevent Angiotensin II from binding to muscle receptors on vessels, causing dilation.

  • Used when $ACE-I$ are not tolerated. Side effects: Dizziness, cough, headache, angioedema, liver failure.

Calcium Channel Blockers and Beta-Blockers

• Calcium Channel Blockers (CCB): "A Very Nice Drug" (Amlodipine, Verapamil, Nifedipine, Diltiazem).

  • Mechanism: Blocks calcium entry to reduce electrical conduction and contraction force, dilating arteries.

  • Side Effects: Hypotension, flushing, drowsiness, liver dysfunction.

  • Warning: Grapefruit juice may increase serum concentration.

• Beta-Adrenergic Blockers (-lol):

  • B1 receptors: Increase Heart Rate ($HR$), contractility, and $AV$ conduction (e.g., metoprolol).

  • B2 receptors: Vasodilation and Bronchodilation (e.g., carvedilol).

  • Mechanism: Prevents chemical messengers from binding; slows $HR$, relaxes vessels.

  • Side Effects: Bradycardia, heart block, heart failure, orthostatic hypotension. Note: Masks symptoms of hypoglycemia.

Other Agents and Crisis Management

• Clonidine: Last line agent; impacts the neurologic system. Side effects: Drowsiness, dry mouth, headaches.

• Hydralazine: Direct vasodilation. Side effects: Fluid retention, tachycardia, headache.

• Hypertensive Crisis Medications:

  • Labetalol: Alpha- and beta-blocking agent. Dose: $20\,mg$ $IV$ over $2$ minutes; then $40-80\,mg$ $IV$ every $10$ minutes ($max\,300\,mg$) or $1-2\,mg/min$ continuous. Watch for bradycardia and increased renal labs.

  • Sodium Nitroprusside: Vasodilator. Given $IV$ with $ICU$ monitoring. Max rate: $10\,mcg/kg/min$. Watch for hypotension, inadequate cerebral perfusion, and Cyanide Toxicity.

  • Nicardipine: Calcium Channel Blocker via central line. Start at $5\,mg/hour$ $IV$, increase by $2.5\,mg/hour$ every $5-15$ minutes (max $15\,mg/hour$). Goal achieved: decrease to $3\,mg/hour$.