UNIT 6 Nursing Management of patients with cardiovascular problems
🫀 Anatomy & Physiology of the Cardiovascular System.
🧩 I. INTRODUCTION
The Cardiovascular System (CVS) is also called the Circulatory System. It is a transport system that delivers oxygen, nutrients, hormones and removes wastes from body tissues. It comprises the:
❤️ Heart
🩸 Blood vessels (arteries, veins, capillaries)
💉 Blood
🫀 II. ANATOMY OF THE CARDIOVASCULAR SYSTEM
1️⃣ ❤️ The Heart
🔸 Location: Center of chest in mediastinum, tilted slightly left. 🔸 Size: About the size of a fist. 🔸 Weight: ~250–350g
🔷 A. Structure of the Heart
Part
Description
🔹 Chambers
4 chambers – Right Atrium (RA), Right Ventricle (RV), Left Atrium (LA), Left Ventricle (LV)
🔹 Valves
Ensure one-way blood flow:
• Tricuspid (RA→RV)
• Pulmonary (RV→Pulmonary Artery)
• Mitral/Bicuspid (LA→LV)
• Aortic (LV→Aorta)
🔹 Layers of Heart Wall
• Endocardium – Inner layer
• Myocardium – Thick muscular middle layer
• Epicardium – Outer layer (also called visceral pericardium)
🔹 Pericardium
A double-walled sac that surrounds & protects the heart. Contains lubricating pericardial fluid.
2️⃣ 🩸 Blood Vessels
There are three main types:
Type
Function
Feature
🟥 Arteries
Carry blood away from heart
Thick, muscular walls (high pressure)
🟦 Veins
Carry blood to the heart
Have valves, less pressure
🟨 Capillaries
Connect arteries and veins
Site of exchange (O₂, CO₂, nutrients, waste)
3️⃣ 💓 Circulations of Blood
Circulation
Path
Function
🌬️ Pulmonary
Heart → Lungs → Heart
Exchanges CO₂ for O₂
🔄 Systemic
Heart → Body → Heart
Supplies oxygenated blood to tissues
❤️ Coronary
Heart → Heart muscle → Heart
Feeds oxygen to myocardium itself
⚙️ III. PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM
🔹 1. 🔁 Cardiac Cycle
The complete heartbeat from start to finish.
Phase
Activity
❤️ Systole
Contraction → Blood ejected
💗 Diastole
Relaxation → Chambers refill with blood
⏱ Normal Heart Rate: 60–100 bpm 🫀 One cycle = ~0.8 seconds
🔹 2. ⚡ Conduction System of the Heart (Electrical Impulse Pathway)
Node
Function
🔸 SA Node (Sinoatrial)
Pacemaker of the heart (initiates impulse)
🔸 AV Node
Delays impulse for atrial contraction
🔸 Bundle of His
Conducts signal to ventricles
🔸 Purkinje Fibers
Stimulate ventricular contraction
📊 ECG waves: P wave – Atrial depolarization QRS complex – Ventricular depolarization T wave – Ventricular repolarization
🔹 3. 🔄 Pathway of Blood Flow
🔁 Systemic & Pulmonary Circulation Combined:
cssCopyEditBody → 🟦 Superior/Inferior Vena Cava
→ ❤️ Right Atrium → Tricuspid Valve → Right Ventricle
→ Pulmonary Valve → 🟥 Pulmonary Artery → Lungs
→ 🟩 Pulmonary Veins → Left Atrium → Mitral Valve
→ Left Ventricle → Aortic Valve → Aorta → Body
🔹 4. 🩸 Cardiac Output (CO)
📌 Definition: Volume of blood pumped by heart per minute.
⛔ Ineffective Health Maintenance related to knowledge deficit
💢 Risk for Decreased Cardiac Output related to increased afterload
💬 Knowledge Deficit regarding disease process and management
❓ Risk for Noncompliance with medication or lifestyle changes
💦 Fluid Volume Excess related to sodium and water retention
🩺 III. NURSING INTERVENTIONS
🔹 A. Monitoring & Observation
Monitor BP at regular intervals (lying, sitting, standing)
Record intake/output, daily weight
Assess for organ damage signs: chest pain, SOB, visual changes, confusion
Monitor lab reports: electrolytes, kidney function
🔹 B. Medication Administration
Administer prescribed antihypertensives (e.g., ACE inhibitors, beta-blockers)
Monitor for side effects: dizziness, orthostatic hypotension, dry cough (ACEIs)
Check pulse and BP before giving meds
Educate about medication adherence and not to stop suddenly
🔹 C. Patient Education
Topic
Teaching Points
🧂 Diet
Reduce salt (<5g/day), avoid fried & processed food
🏃 Exercise
Encourage 30 mins/day – walking, yoga, aerobics
🍷 Habits
Stop smoking, limit alcohol
🧘 Stress Management
Meditation, breathing exercises
📈 BP Monitoring
Teach home BP monitoring and when to seek help
💊 Medications
Name, timing, purpose, side effects
🔹 D. Lifestyle Support
Encourage weight reduction
Refer to dietitian or counselor as needed
Help set realistic goals for behavior change
🔹 E. Preventing Complications
Monitor for signs of:
🧠 Stroke: slurred speech, weakness, facial droop
❤️ MI: chest pain, SOB
🧽 Kidney failure: reduced urine output, swelling
Assist with fall precautions if on antihypertensives causing dizziness
📌 IV. EVALUATION CRITERIA
BP maintained within target range
Patient demonstrates correct medication use
Patient verbalizes understanding of diet and lifestyle modifications
No signs of complications (stroke, MI, kidney failure)
Improved compliance and coping
📋 SAMPLE NURSING CARE PLAN (Short Format)
🧾 Nursing Diagnosis
Risk for Noncompliance related to lack of knowledge
🎯 Goal
Patient will verbalize understanding of HTN management in 2 days
🩺 Interventions
1. Educate on meds, diet, exercise
Assess barriers to adherence
Involve family in care plan | | 📊 Evaluation | Patient correctly explains meds and demonstrates BP log |
❗ I. COMPLICATIONS OF HYPERTENSION
Uncontrolled hypertension leads to target organ damage – affecting the heart, brain, kidneys, eyes, and blood vessels.
🫀 1. Cardiovascular Complications
Complication
Description
❤️ Left Ventricular Hypertrophy (LVH)
Thickening of heart muscle due to increased workload
💥 Heart Failure
Heart becomes too weak to pump effectively
💢 Myocardial Infarction (Heart Attack)
Due to coronary artery disease
🩸 Aneurysm
Weakening and ballooning of artery walls
🧱 Peripheral Artery Disease (PAD)
Narrowing of peripheral arteries causing leg pain
🧠 2. Cerebrovascular Complications
Complication
Description
🧠 Stroke (CVA)
Rupture or blockage of blood vessels in the brain
🌪️ Transient Ischemic Attack (TIA)
Mini-stroke; warning sign of a full stroke
😵💫 Cognitive Impairment
Memory loss, confusion due to poor brain perfusion
🧽 3. Renal (Kidney) Complications
Complication
Description
🧪 Chronic Kidney Disease (CKD)
Damage to nephrons due to high pressure
💧 Proteinuria
Protein leaks into urine (early sign of kidney damage)
🔚 End-stage Renal Disease (ESRD)
May require dialysis or kidney transplant
👁️ 4. Ocular Complications
Complication
Description
👁️ Hypertensive Retinopathy
Damage to retinal blood vessels
👀 Blurred Vision or Vision Loss
Due to hemorrhage or swelling in retina
📌 II. KEY POINTS – QUICK RECAP FOR STUDENTS
✅ Definition: BP ≥140/90 mmHg on 2 separate occasions ✅ Causes: Primary (90–95%) or Secondary (5–10%) ✅ Risk Factors: Genetics, obesity, high salt intake, stress, smoking ✅ Symptoms: Often silent; may present with headache, vision changes, dizziness ✅ Diagnosis: BP measurement, lab tests (renal, lipid), ECG, fundoscopy ✅ Management:
🧘 Lifestyle changes (DASH diet, weight loss, no smoking)
Calcium deposits in the media (middle layer) of medium-sized arteries
Arteries remain patent (not narrowed), but become stiff
Common in older adults
Usually asymptomatic and discovered incidentally on X-ray (visible as calcification)
📌 SUMMARY TABLE: TYPES OF ARTERIOSCLEROSIS
Type
Affected Vessels
Key Feature
Common Association
Atherosclerosis
Large & medium arteries
Fatty plaque in intima
Coronary artery disease, stroke
Arteriolosclerosis
Small arteries/arterioles
Wall thickening & lumen narrowing
Hypertension, diabetes
Monckeberg’s
Medium arteries
Calcium in media, no obstruction
Aging, incidental finding
🧬 I. PATHOPHYSIOLOGY OF ARTERIOSCLEROSIS
Arteriosclerosis primarily affects arterial blood flow by causing hardening and thickening of the artery walls, leading to narrowing of the vessel lumen and reduced tissue perfusion.
🔄 Step-by-Step Mechanism (Especially in Atherosclerosis type)
Endothelial Injury ⮕ Caused by hypertension, smoking, diabetes, or high cholesterol ⮕ Leads to inflammation and damage of the inner lining (intima)
Foam Cell Formation ⮕ Macrophages engulf oxidized LDL → become foam cells ⮕ Forms fatty streaks along artery walls
Plaque Development ⮕ Smooth muscle cells migrate and multiply ⮕ Collagen + lipids + cells = fibrous plaque forms ⮕ Narrows artery, stiffens wall
Plaque Rupture & Clot Formation ⮕ Plaque may rupture → triggers platelet aggregation & thrombus (clot) ⮕ Can cause sudden occlusion of blood flow → heart attack or stroke
📌 In arteriolosclerosis (small vessels): wall thickens due to hyaline deposits or smooth muscle overgrowth 📌 In Monckeberg’s sclerosis: calcium deposits in the media → arteries harden but lumen stays open
🚨 II. SIGNS AND SYMPTOMS
❗ Arteriosclerosis is often asymptomatic until significant narrowing or acute blockage occurs.
🩺 Depends on the organ system affected:
🫀 Coronary Arteries (Heart) – Atherosclerosis
💓 Chest pain (angina)
🫁 Shortness of breath
💢 Palpitations
🚨 Myocardial infarction (if complete blockage)
🧠 Carotid Arteries (Brain)
🧠 Dizziness or confusion
👄 Slurred speech
😵💫 Sudden weakness or numbness (especially on one side)
🧠 Stroke or transient ischemic attack (TIA)
🦵 Peripheral Arteries (Legs) – PAD
🦵 Leg pain during walking (intermittent claudication)
🧊 Cold, pale, or bluish extremities
🦶 Non-healing ulcers or gangrene
👁️ Retinal Arteries (Eyes)
👀 Blurred vision
🔍 Retinal hemorrhages on fundoscopy
🧪 III. DIAGNOSIS OF ARTERIOSCLEROSIS
Diagnosis depends on location and severity, often combining history, examination, and diagnostic tests.
🔍 A. History & Physical Examination
Risk factors: HTN, smoking, DM, hyperlipidemia
Absent or weak pulses
Bruits (vascular sounds) on auscultation
Skin changes (cold, shiny, hair loss in legs)
🧪 B. Laboratory Tests
Test
Purpose
💉 Lipid profile
Check cholesterol (LDL ↑, HDL ↓)
🧪 Blood sugar, HbA1c
Check for diabetes
🧪 CRP (C-reactive protein)
Inflammatory marker
🩸 Renal function tests
If kidneys involved
🖥️ C. Imaging & Diagnostic Tools
Test
Use
🫀 ECG & Echocardiogram
Assess cardiac damage or ischemia
📈 Doppler Ultrasound
Check blood flow in limbs and carotids
💉 Angiography (CT/MR/Coronary)
Visualizes narrowed or blocked arteries
👟 Ankle-Brachial Index (ABI)
Compare BP in leg and arm to detect PAD
👁️ Fundoscopy
Identify retinal artery changes
📌 Diagnosis is confirmed when imaging shows narrowed, calcified, or blocked arteries with clinical symptoms.
🩺 I. MEDICAL MANAGEMENT OF ARTERIOSCLEROSIS
🎯 Goals of Treatment:
Slow or stop plaque progression
Prevent rupture or clot formation
Restore and maintain blood flow
Prevent complications (MI, stroke, PAD)
🔹 A. Lifestyle Modifications (First-line for all patients)
Raynaud’s Disease (also called Raynaud’s Phenomenon) is a vascular disorder characterized by episodic vasospasm of the small arteries and arterioles, usually in the fingers and toes, in response to cold or stress.
💡 It leads to reduced blood flow, causing color changes, numbness, pain, and tingling in the affected areas.
Occurs due to underlying medical conditions, especially autoimmune or connective tissue diseases.
Common Causes of Secondary Raynaud’s
💉 Systemic Lupus Erythematosus (SLE)
🦴 Rheumatoid Arthritis
💠 Scleroderma
🦠 Sjögren’s Syndrome
🔧 Occupational trauma (vibration tools)
❄️ Repeated cold exposure
💊 Certain medications (beta-blockers, chemotherapy)
🚬 Smoking
🧪 Thyroid disorders
🔹 III. TYPES OF RAYNAUD’S
Type
Features
Notes
Primary Raynaud’s (Disease)
No identifiable cause
More common, less severe, symmetrical
Secondary Raynaud’s (Phenomenon/Syndrome)
Associated with other diseases
More severe, may cause ulcers, tissue damage
📌 Triggering Factors for Both Types:
Exposure to cold temperature
Emotional stress or anxiety
Use of vibrating tools
Smoking or caffeine use
🧬 I. PATHOPHYSIOLOGY OF RAYNAUD’S DISEASE
Raynaud’s is a disorder involving vasospasm (sudden narrowing) of small arteries and arterioles, primarily affecting the fingers and toes, triggered by cold or emotional stress.
Vasospasm of Arterioles ⮕ Reduces blood flow to fingers or toes ⮕ Causes ischemia (lack of oxygen)
Triphasic Color Change:
Pallor (white) – due to lack of blood flow
Cyanosis (blue) – due to deoxygenated blood pooling
Rubor (red) – reactive hyperemia when blood flow returns
Reperfusion ⮕ When the vasospasm resolves, blood rushes back, leading to redness, burning, and throbbing pain
📌 In Secondary Raynaud’s, the vessels are already damaged or inflamed due to another disease (like SLE or scleroderma), leading to more severe and prolonged attacks with possible ulcers or gangrene.
🚨 II. SIGNS AND SYMPTOMS
Symptom
Description
🎨 Color changes in fingers/toes
White (pallor) → Blue (cyanosis) → Red (hyperemia)
🧊 Cold sensation in fingers/toes
Especially with exposure to cold air/water
🌪️ Numbness or tingling
Due to reduced blood supply
🔥 Burning or throbbing pain
During the rewarming or reperfusion phase
🦶 Stiffness or discomfort
In affected digits
⚠️ Ulcers or sores (secondary type)
In severe or long-standing cases
❗ Symmetrical involvement
Often seen in primary type
🚩 Asymmetrical + skin/tissue damage
Suggests secondary Raynaud’s
🧪 III. DIAGNOSIS OF RAYNAUD’S DISEASE
🧾 A. Clinical History & Physical Exam
Recurrent episodes of color change in extremities
Triggered by cold or emotional stress
No other systemic symptoms (primary) OR associated with autoimmune signs (secondary)
🧪 B. Nailfold Capillaroscopy
Microscopic exam of capillaries at the base of the fingernail
Normal in primary Raynaud’s
Abnormal/damaged capillaries in secondary Raynaud’s (e.g., scleroderma)
💉 C. Blood Tests (for Secondary Raynaud’s)
Test
Purpose
🧪 ANA (Antinuclear Antibody)
Detect autoimmune diseases like lupus, scleroderma
🧪 ESR/CRP
Inflammation markers
🧪 Rheumatoid factor (RF)
For rheumatoid arthritis
🧪 CBC
To rule out anemia or infection
🧪 Thyroid function tests
Rule out hypothyroidism
📊 D. Cold Stimulation Test(Rarely used)
Measures how long it takes fingers to return to normal temperature after cold exposure
💊 I. MEDICAL MANAGEMENT
🎯 Goals:
Reduce the frequency and severity of attacks
Prevent tissue damage (especially in secondary cases)
Improve quality of life
🔹 A. Lifestyle & Preventive Measures(First-line for ALL patients)
Intervention
Purpose
🧤 Keep warm
Wear gloves, socks, warm clothing in cold weather
❄️ Avoid cold exposure
Use heated water, avoid AC, cold rooms
🚬 Stop smoking
Nicotine causes vasoconstriction
☕ Avoid caffeine
Caffeine also triggers vasospasm
😌 Stress management
Relaxation techniques to prevent stress-induced attacks
🏃 Regular exercise
Improves circulation and vascular health
🚫 Avoid vibration tools
Can worsen symptoms (e.g., jackhammers, drills)
🔹 B. Pharmacological Treatment
Used when lifestyle changes are not enough or in moderate to severe cases
1️⃣ Vasodilators(First-line drug therapy)
Drug Class
Example
Action
Calcium Channel Blockers (CCBs)
Amlodipine, Nifedipine
Relax and widen blood vessels, reduce frequency/severity of attacks
2️⃣ Other Medications (as needed)
Drug Type
Examples
Purpose
Alpha blockers
Prazosin
Prevent blood vessel constriction
Topical nitroglycerin
For digital ulcers
Improves local blood flow
Selective serotonin reuptake inhibitors (SSRIs)
Fluoxetine
Useful if stress is a trigger
Prostacyclin analogs (e.g., Iloprost)
IV therapy in severe cases
Potent vasodilation; used in secondary Raynaud’s
Phosphodiesterase inhibitors
Sildenafil
Promote vasodilation in refractory cases
⚠️ In Secondary Raynaud’s:
Also manage the underlying condition:
Scleroderma, SLE, RA, etc.
🩺 II. SURGICAL / INTERVENTIONAL MANAGEMENT
🔧 Used in severe or treatment-resistant cases with risk of gangrene or ulceration
🔹 A. Sympathectomy
🧠 Procedure:
Surgical interruption of sympathetic nerves that cause vasospasm
Can be digital (finger) or lumbar (lower limb)
📌 Indicated for:
Severe, disabling Raynaud’s
Tissue damage not responding to medications
Ulcers or risk of gangrene
🔧 Can be done:
Surgically (cutting nerves)
Chemically (nerve block)
Endoscopically (minimally invasive)
🔹 B. Digital Artery Reconstruction or Bypass
For patients with severely narrowed vessels
Restores blood flow to affected digits
Rare and highly specialized
🔹 C. Amputation
Last resort
In cases of irreversible tissue death (gangrene) in fingers or toes
📝 SUMMARY TABLE: MANAGEMENT OF RAYNAUD’S
Management
Examples
Used When
🧤 Lifestyle
Warm clothing, no smoking
Mild cases
💊 Medications
CCBs, alpha-blockers, SSRIs
Moderate cases
💉 IV prostacyclins
Iloprost
Severe secondary Raynaud’s
🩻 Surgery
Sympathectomy, arterial bypass
Refractory or gangrene
👩⚕️ NURSING MANAGEMENT OF RAYNAUD’S DISEASE
(For Clinical Care, Student Notes, and Exams)
🎯 OBJECTIVES OF NURSING CARE
Improve peripheral circulation
Prevent triggering factors (cold/stress)
Manage pain/discomfort during attacks
Prevent tissue damage and complications
Educate for self-care and lifestyle modifications
🧑⚕️ I. NURSING ASSESSMENT
Assessment Area
Key Points
🧠 History
Onset, duration, frequency of attacks, triggers (cold/stress)
💬 Symptoms
Pallor, cyanosis, redness in fingers/toes; pain, numbness
📏 Vital Signs
Especially temperature of affected extremities
🩺 Circulation
Check peripheral pulses, capillary refill, color, temperature
🦶 Skin
Look for ulcers, cracks, gangrene in fingers or toes
🧘 Psychosocial
Assess stress levels, anxiety, coping mechanisms
🧾 II. COMMON NURSING DIAGNOSES
❄️ Ineffective Peripheral Tissue Perfusion related to vasospasm
😣 Acute Pain related to decreased oxygen supply during vasospasm
❓ Knowledge Deficit related to disease process and self-care
⚠️ Risk for Impaired Skin Integrity due to prolonged ischemia
🚭 Risk for Noncompliance related to lack of motivation for lifestyle changes
🩺 III. NURSING INTERVENTIONS
🔹 A. Improve Peripheral Circulation
Keep the patient warm (blankets, warm water bottles near hands/feet)
Encourage wearing wool gloves, socks, and layers of clothing in cold weather
Avoid exposure to cold environments, cold drinks, and air-conditioned rooms
Teach the patient to wiggle fingers/toes regularly to promote circulation
🔹 B. Pain and Discomfort Management
Administer prescribed vasodilators (e.g., calcium channel blockers)
Apply warm compresses during or after an attack (not hot)
Encourage relaxation techniques to reduce anxiety-triggered vasospasm
🔹 C. Prevent Skin Breakdown
Inspect fingers and toes daily for ulcers, blisters, cracks
Maintain skin hydration with emollients
Teach proper nail care to avoid injury
Avoid trauma: use gloves during chores, avoid tight rings/shoes
🔹 D. Health Education
Topic
Content
❄️ Cold Avoidance
Dress warmly, use hand warmers, avoid cold exposure
🚫 Avoid triggers
No smoking, limit caffeine, manage stress
💊 Medication adherence
Explain purpose and side effects of vasodilators
🧘 Stress control
Deep breathing, yoga, meditation
🏃 Exercise
Gentle aerobic activity improves circulation
📞 When to seek help
Worsening attacks, ulcers, or blackened fingertips
✅ IV. EVALUATION CRITERIA
Goal
Expected Outcome
🩸 Improve circulation
Warm, pink extremities with intact pulses
❌ Reduce pain
Patient reports decreased frequency and intensity of attacks
🛡️ Prevent skin damage
No ulcers, intact skin, no gangrene
📚 Increase knowledge
Patient demonstrates understanding of self-care
✔️ Ensure compliance
Patient adheres to medication and preventive care
📝 SAMPLE NURSING CARE PLAN (Short Format)
Component
Description
Diagnosis
Ineffective Peripheral Tissue Perfusion related to vasospasm
Goal
Improve circulation and prevent tissue damage
Interventions
1. Keep extremities warm
Educate on avoiding cold exposure
Monitor skin integrity and pulses | | Evaluation | Patient has fewer attacks, warm skin, no skin breakdown |
❗ I. COMPLICATIONS OF RAYNAUD’S DISEASE
Although often mild and manageable, severe or untreated cases, especially in secondary Raynaud’s, can lead to serious complications due to prolonged reduced blood flow (ischemia) to the extremities.
🔹 1. Digital Ulcers
Painful sores on fingertips or toes
Occur due to chronic ischemia
Difficult to heal and may become infected
🔹 2. Skin Infection (Cellulitis)
Occurs when ulcers or cracks allow bacteria entry
Can spread to deeper tissues
🔹 3. Gangrene
Tissue death due to prolonged lack of oxygen
May require amputation of affected finger or toe
More common in secondary Raynaud’s
🔹 4. Loss of Fingertip or Toe Tissue
Due to recurring or untreated episodes
Permanent damage from repeated ischemia
🔹 5. Decreased Hand Function
Due to stiffness, pain, or tissue loss
Affects activities of daily living (ADLs)
🔹 6. Psychological Impact
Anxiety about attacks
Embarrassment about hand appearance
Stress can worsen condition
✅ II. KEY POINTS – QUICK RECAP FOR NURSING STUDENTS
🔑 Topic
📝 Key Point
✅ Definition
Raynaud’s is a vasospastic disorder causing episodic constriction of small arteries in fingers/toes
❄️ Triggers
Cold exposure, emotional stress
🔁 Phases
White (pallor) → Blue (cyanosis) → Red (hyperemia)
👩⚕️ Types
Primary (idiopathic, mild) and Secondary (due to diseases like SLE, scleroderma)
🧪 Diagnosis
Based on history, nailfold capillaroscopy, and autoimmune blood tests
Keep extremities warm, prevent triggers, educate on self-care and ulcer prevention
⚠️ Complications
Ulcers, infections, gangrene, amputation, decreased hand function
💥 ANEURYSM
(Definition, Causes, and Types – )
🧠 I. DEFINITION
An aneurysm is a localized, abnormal dilation or ballooning of an artery due to a weakened arterial wall. It can occur in any artery but is most common in the aorta, brain, and peripheral arteries.
💡 If left untreated, an aneurysm may enlarge and rupture, causing life-threatening internal bleeding.
Often silent → may cause pain, pulsating mass, or neuro signs
🧪 Diagnosis
Ultrasound, CT angiography, MRI
💊 Medical management
BP control, statins, surveillance for small aneurysms
🛠️ Surgical options
Open repair, EVAR, clipping/coiling for cerebral aneurysms
👩⚕️ Nursing care
Monitor vitals, perfusion, bleeding; educate on lifestyle & warning signs
🚨 Major complication
Rupture → shock → death if untreated urgently
🦵 PERIPHERAL VASCULAR DISORDERS (PVDs)
(Definition, Causes, and Types – )
🧠 I. DEFINITION
Peripheral Vascular Disorders (PVDs) refer to a group of diseases that affect the blood vessels outside the heart and brain, primarily the arteries and veins of the limbs, especially the legs.
💡 PVDs impair blood circulation due to narrowing, blockage, or spasm of peripheral vessels.
🔍 II. CAUSES / RISK FACTORS
Category
Common Causes
🧬 Non-Modifiable
• Aging
• Family history of vascular disease
• Male gender
🛠️ Modifiable
• Smoking 🚬
• Diabetes mellitus 💉
• Hypertension 💢
• High cholesterol 🍳
• Obesity ⚖️
• Sedentary lifestyle 🛌
• Stress 😥
🦠 Others
• Infections (e.g., vasculitis)
• Autoimmune diseases
• Blood clotting disorders
🔢 III. TYPES OF PERIPHERAL VASCULAR DISORDERS
PVDs are broadly classified into two categories: 🔹 Peripheral Arterial Disorders 🔹 Peripheral Venous Disorders
🔷 A. Peripheral Arterial Disorders (PAD)
Involves narrowing or blockage of arteries that carry oxygen-rich blood to limbs.
Pulse checks, foot care, leg elevation or dependency, patient education
⚠️ Complications
Gangrene, amputation, ulcers, PE, severe pain, limb loss
❤️ CORONARY ARTERY DISEASES (CAD)
A Full Clinical & Nursing Overview
🧠 I. DEFINITION
Coronary Artery Disease (CAD) is a condition where the coronary arteries, which supply oxygen-rich blood to the heart muscle, become narrowed or blocked due to atherosclerosis (plaque buildup).
🔴 Reduced blood flow to the heart muscle → chest pain (angina), heart attack (MI), or heart failure.
⚠️ II. CAUSES / RISK FACTORS
🔹 Modifiable Risk Factors:
🚬 Smoking
💉 Hypertension (HTN)
🍔 High cholesterol (↑ LDL, ↓ HDL)
⚖️ Obesity
🛌 Physical inactivity
🍷 Alcohol use
🧁 Diabetes mellitus
😥 Stress
🔹 Non-Modifiable Risk Factors:
👴 Age (men >45, women >55)
🧬 Family history of CAD
👨 Male gender (higher early risk)
🔢 III. TYPES OF CORONARY ARTERY DISEASE
Type
Description
Stable Angina
Predictable chest pain during exertion, relieved by rest
Unstable Angina
Sudden chest pain at rest; a medical emergency
Myocardial Infarction (MI)
Complete blockage → heart muscle damage
Silent Ischemia
No symptoms; detected on ECG
Variant (Prinzmetal’s) Angina
Spasm of coronary artery causing temporary obstruction
🧬 IV. PATHOPHYSIOLOGY OF CAD
Endothelial injury (due to HTN, smoking, diabetes, etc.)
✅ CAD = Blockage of coronary arteries due to atherosclerosis ✅ Risk factors include: smoking, HTN, diabetes, cholesterol, obesity ✅ Symptoms: chest pain, SOB, fatigue, sweating ✅ Diagnosis: ECG, cardiac enzymes, angiography ✅ Treatment: lifestyle + meds + PCI or CABG ✅ Nurses play a key role in monitoring, education, emotional support, and complication prevention
❤️🩹 CORONARY ATHEROSCLEROSIS
(Definition, Causes, and Types – Full Details)
🧠 I. DEFINITION
Coronary Atherosclerosis is a type of arteriosclerosis that involves the buildup of plaque (fatty deposits) inside the walls of the coronary arteries, leading to narrowing, hardening, and reduced blood flow to the heart muscle.
🧬 Plaque is made up of cholesterol, fat, calcium, and cellular debris.
📌 This is the most common cause of Coronary Artery Disease (CAD) and can lead to angina, myocardial infarction (MI), heart failure, or sudden death.
Males at higher early risk (females risk increases after menopause)
🔢 III. TYPES OF ATHEROSCLEROTIC LESIONS IN CORONARY ARTERIES
Coronary atherosclerosis can vary by severity and stability of the plaque:
1️⃣ Stable Plaque (Fixed Atherosclerosis)
Slowly growing, thick fibrous cap
Leads to stable angina
Less likely to rupture, but restricts blood flow
2️⃣ Unstable Plaque (Vulnerable Plaque)
Thin fibrous cap, large lipid core
Prone to rupture → triggers clot formation
Can cause acute coronary syndromes (e.g., MI, unstable angina)
3️⃣ Calcified Plaque
Hard, brittle deposits of calcium
Reduces elasticity of arteries
Common in elderly patients
4️⃣ Non-obstructive Atherosclerosis
Narrowing <50%, may be asymptomatic
Still carries risk of rupture and thrombus formation
🧬 I. PATHOPHYSIOLOGY OF CORONARY ATHEROSCLEROSIS
Coronary atherosclerosis is a chronic, progressive disease involving the buildup of plaques in the coronary arteries. It leads to narrowing of the arteries, restricting oxygen-rich blood flow to the heart muscle.
🔄 Step-by-Step Pathophysiology:
Endothelial Injury
Due to HTN, smoking, high cholesterol, diabetes
Damaged endothelium allows LDL cholesterol to infiltrate the artery wall
Lipid Infiltration & Inflammation
LDL becomes oxidized
Attracts macrophages which ingest LDL → become foam cells
Fatty Streak Formation
Early stage of plaque development
Foam cells accumulate → form yellowish streaks in vessel wall
Fibrous Plaque Formation
Smooth muscle cells migrate and secrete collagen
A fibrous cap forms over the lipid core → partial blockage of artery
Plaque Rupture & Thrombus Formation
Unstable plaques may rupture
Triggers platelet aggregation and clot formation (thrombus)
Can acutely block the artery → Myocardial Infarction (MI)
📌 The gradual narrowing causes chronic ischemia, leading to angina. A sudden rupture causes acute coronary syndrome (e.g., unstable angina, MI).
🚨 II. SIGNS AND SYMPTOMS
Symptoms depend on degree of blockage, rate of progression, and presence of complications.
🔹 Common Symptoms:
Symptom
Description
💢 Chest pain (angina)
Squeezing, pressure, or heaviness, often radiating to jaw, arm, or back
🫁 Shortness of breath
Especially on exertion
🛌 Fatigue
Due to reduced oxygen to the myocardium
💓 Palpitations
Irregular or rapid heartbeat
💦 Sweating (diaphoresis)
Often with angina or MI
🤢 Nausea or vomiting
Especially in MI
😰 Anxiety
Common during angina or ischemia episodes
❗ Asymptomatic
Common in diabetics or elderly (silent ischemia)
🧪 III. DIAGNOSIS OF CORONARY ATHEROSCLEROSIS
Diagnosis is based on clinical symptoms, risk assessment, blood tests, and imaging.
Open-heart surgery for severe/multi-vessel disease
Thrombolysis
Used in acute MI if PCI is not immediately available
👩⚕️ NURSING MANAGEMENT OF CORONARY ATHEROSCLEROSIS
(Clinical, Educational & Exam-Oriented)
🎯 GOALS OF NURSING CARE
Maintain adequate myocardial perfusion
Relieve and prevent chest pain
Promote lifestyle modifications
Prevent complications like MI or arrhythmias
Educate the patient for long-term self-care
🧾 I. NURSING ASSESSMENT
Area
What to Assess
🩺 Vital Signs
BP, HR, RR, O₂ saturation
💓 Chest pain
Use PQRST:
P: Provocation
Q: Quality
R: Radiation
S: Severity
T: Time
📈 ECG Monitoring
Look for ST changes, arrhythmias
🧪 Lab values
Troponin, CK-MB, lipid profile
🧘 Psychosocial status
Anxiety, fear, stress level
🧍 Activity tolerance
Monitor for SOB or fatigue during ambulation
🩺 II. NURSING DIAGNOSES
❌ Ineffective Tissue Perfusion (cardiac) related to reduced coronary blood flow
💢 Acute Pain related to myocardial ischemia
😟 Anxiety related to fear of death or unfamiliar environment
❓ Deficient Knowledge related to disease condition and treatment
⚠️ Risk for Decreased Cardiac Output related to electrical conduction changes or ischemia
🩹 III. NURSING INTERVENTIONS
🔷 A. Managing Chest Pain (Angina)
Action
Rationale
🛏️ Bed rest during pain
Reduces cardiac workload
💊 Administer nitrates (e.g., Nitroglycerin)
Vasodilation relieves ischemia
📈 Monitor ECG continuously
Detect arrhythmias or ischemic changes
💧 Oxygen therapy if prescribed
Improves myocardial oxygenation
💬 Stay with patient, reduce anxiety
Emotional support lowers O₂ demand
🔷 B. Promoting Circulation & Preventing MI
Monitor for new or worsening chest pain
Assess peripheral pulses and capillary refill
Administer antiplatelets, beta-blockers, statins as prescribed
Report ST elevation or rising troponin promptly
🔷 C. Education for Lifestyle & Medication
Topic
Teaching Points
🍽️ Diet
Low saturated fat, low salt, high fiber
🏃 Exercise
Daily walking, avoid overexertion
🚭 Smoking
Strongly advise cessation
💊 Medications
Importance of daily use, side effects, and timing
🧘 Stress control
Relaxation techniques, counseling if needed
📅 Follow-up
Regular monitoring of BP, lipids, ECG
🔷 D. Post-Angioplasty or Post-CABG Care (if applicable)
Monitor puncture site (PCI) for bleeding or hematoma
Assess graft patency and chest tube drainage (CABG)
Encourage early ambulation and breathing exercises
Provide emotional reassurance and rehabilitation support
✅ IV. EVALUATION CRITERIA
Goal
Expected Outcome
💓 Relieve pain
Pain score ↓, patient verbalizes relief
🫀 Maintain perfusion
Stable vitals, no ECG changes, warm extremities
🧠 Reduce anxiety
Patient appears calm, understands plan
📚 Improve knowledge
Patient explains medications, lifestyle changes
🚫 Prevent complications
No MI, arrhythmias, or readmission
📝 SAMPLE NURSING CARE PLAN (Short Format)
Component
Example
Diagnosis
Acute Pain related to decreased coronary perfusion
Goal
Patient will report pain relief within 15 minutes
Interventions
1. Administer nitroglycerin
Monitor ECG
Provide calm environment | | Evaluation | Patient reports 0–1 pain level, no ECG changes |
❗ I. COMPLICATIONS OF CORONARY ATHEROSCLEROSIS
If untreated or poorly managed, coronary atherosclerosis can lead to serious, life-threatening complications due to reduced oxygen supply to the heart muscle.
🔴 1. Angina Pectoris
Stable angina: Predictable chest pain on exertion
Unstable angina: Occurs at rest; may precede heart attack (MI)
❤️ 2. Myocardial Infarction (MI)
Complete blockage of a coronary artery
Leads to heart muscle death if not treated immediately
Presents with severe chest pain, sweating, nausea
⚡ 3. Arrhythmias (Irregular Heart Rhythms)
Due to ischemia or infarction
Can include ventricular tachycardia or fibrillation (life-threatening)
🫀 4. Heart Failure
Chronic ischemia weakens the heart muscle
Results in reduced cardiac output, pulmonary congestion, and edema
🧠 5. Stroke
A clot or plaque debris can travel to the brain
Causes ischemic stroke
💀 6. Sudden Cardiac Death
Often due to fatal arrhythmia (e.g., ventricular fibrillation)
May occur without warning, especially in undiagnosed patients
📌 II. KEY POINTS – QUICK RECAP
🔑 Topic
Key Information
✅ Definition
Plaque buildup in coronary arteries → narrowed blood flow
❗ Primary cause of CAD
Coronary atherosclerosis is the most common cause
🔎 Main risk factors
Smoking, diabetes, HTN, high cholesterol, obesity, sedentary life
Monitor vitals, chest pain, ECG, provide medication, patient teaching
🚨 Complications
MI, arrhythmias, stroke, heart failure, sudden death
💓 ANGINA PECTORIS
(Definition, Causes, and Types)
🧠 I. DEFINITION
Angina pectoris is a clinical symptom characterized by chest pain or discomfort caused by transient myocardial ischemia (i.e., reduced blood supply to the heart muscle) without actual heart muscle death.
💡 Angina is a warning sign of underlying coronary artery disease (CAD).
📌 Pain typically occurs when the oxygen demand of the heart exceeds the supply, especially during exertion or stress.
⚠️ II. CAUSES / RISK FACTORS
🔹 Direct Causes:
Cause
Description
🩸 Coronary Atherosclerosis
Narrowing of coronary arteries due to plaque buildup
💥 Coronary artery spasm
Sudden temporary tightening of the artery wall
🩺 Severe anemia
Less oxygen-carrying capacity of blood
💓 Tachycardia/arrhythmias
Increased heart demand, less coronary perfusion
🔁 Aortic stenosis or hypertrophy
Increased workload on the heart
🧠 Emotional stress or cold exposure
Triggers increased heart demand
🔹 Risk Factors (Same as CAD):
🚬 Smoking
🍟 High cholesterol
⚖️ Obesity
💉 Diabetes mellitus
💢 Hypertension
🧬 Family history of heart disease
🛌 Sedentary lifestyle
👴 Age (older adults more at risk)
🔢 III. TYPES OF ANGINA PECTORIS
1️⃣ Stable Angina (Exertional Angina)
Most common type
Occurs predictably during exertion, stress, or excitement
Relieved by rest or nitroglycerin
Lasts a few minutes
2️⃣ Unstable Angina
Occurs at rest or with minimal exertion
Unpredictable, more severe, lasts longer
Medical emergency – precursor to myocardial infarction
Not relieved easily by rest or usual medications
3️⃣ Variant Angina (Prinzmetal’s Angina)
Caused by coronary artery spasm, not plaque
Occurs at rest, usually at night or early morning
Often seen in younger patients or those with vasospasm history
Relieved by calcium channel blockers and nitrates
4️⃣ Microvascular Angina
Chest pain with normal coronary arteries
Due to poor perfusion in tiny coronary vessels
More common in women, often misunderstood
May not respond well to nitrates
5️⃣ Silent Ischemia
No symptoms despite ischemia
Detected on ECG or stress tests
Common in diabetics and elderly
🧬 I. PATHOPHYSIOLOGY OF ANGINA PECTORIS
Angina pectoris occurs when there is a temporary imbalance between oxygen supply and demand of the myocardium (heart muscle), leading to ischemia, but not infarction.
🔄 Step-by-Step Mechanism:
Reduced Coronary Blood Flow
Due to atherosclerotic plaque, vasospasm, or thrombus
Increased Myocardial Oxygen Demand
During physical activity, emotional stress, fever, tachycardia
Myocardial Ischemia
When demand exceeds supply
Heart muscle gets insufficient oxygen and nutrients
Anaerobic Metabolism Begins
Leads to lactic acid buildup → triggers nerve endings
Chest Pain/Discomfort Occurs
Usually relieved by rest or vasodilators (e.g., nitroglycerin)
📌 Important: Angina causes reversible myocardial changes; no permanent damage occurs unless ischemia progresses to infarction.
🚨 II. SIGNS & SYMPTOMS OF ANGINA PECTORIS
Symptom
Description
💢 Chest pain
Pressure, squeezing, heaviness, or tightness in the chest
🔁 Radiating pain
To jaw, neck, back, shoulders, or left arm
🧊 Cold sweat (diaphoresis)
Common during anginal episodes
🫁 Shortness of breath
Especially with exertion
🫤 Fatigue
Feeling of tiredness even with mild activity
🤢 Nausea or indigestion-like symptoms
More common in women
😰 Anxiety or sense of doom
Often occurs with chest discomfort
⏰ Typical Angina Episode:
Duration: 2 to 10 minutes
Triggered by exercise, emotion, cold
Relieved by rest or nitroglycerin
📌 Unstable angina lasts longer, is more intense, and may occur at rest — emergency!
🧪 III. DIAGNOSIS OF ANGINA PECTORIS
🧾 A. History & Physical Exam
PQRST of pain
Risk factors (HTN, diabetes, smoking, etc.)
Assess vital signs and general condition
🩺 B. Electrocardiogram (ECG)
Use
Finding
Detects ischemia
ST depression, T wave inversion during pain
In Prinzmetal’s angina
May show ST elevation during spasm, but resolves afterward
💉 C. Blood Tests
Test
Purpose
Troponin I/T, CK-MB
Normal in angina (↑ only if MI occurs)
Lipid profile
Detects dyslipidemia
Blood sugar, HbA1c
Screen for diabetes
🧪 D. Stress Testing
Treadmill Test (TMT) – provokes ischemia during exercise
Used to detect exercise-induced angina
🖥️ E. Imaging Studies
Test
Purpose
🧠 Echocardiography
Evaluates wall motion abnormalities
🧪 Myocardial Perfusion Scan
Visualizes blood flow to heart muscle
🩺 Coronary Angiography
Gold standard for identifying blockages
💊 I. MEDICAL MANAGEMENT OF ANGINA
🎯 Goals:
Relieve chest pain
Improve coronary blood flow
Prevent progression to myocardial infarction (MI)
Reduce cardiac workload
Modify risk factors
🔹 A. Lifestyle Modifications (Essential for all patients)
MI, arrhythmia, heart failure, stroke, sudden death
❤️🔥 MYOCARDIAL INFARCTION (MI)
(Definition, Causes, and Types)
🧠 I. DEFINITION
Myocardial Infarction (MI), commonly known as a heart attack, is a life-threatening condition in which there is complete or prolonged blockage of blood flow to a part of the heart muscle, causing irreversible damage or death of myocardial tissue due to ischemia.
🔴 Caused by occlusion (usually by a blood clot) in one or more coronary arteries.
⚠️ II. CAUSES / RISK FACTORS
🔹 A. Immediate/Direct Causes
Cause
Description
🩸 Atherosclerotic plaque rupture
Most common — triggers thrombus formation
💥 Thrombus formation
Clot blocks coronary artery
🔁 Coronary artery spasm
Sudden, temporary tightening of the vessel
🫁 Severe hypoxia/anemia
Decreases oxygen supply to the heart
⚡ High oxygen demand
In situations like fever, tachycardia, hyperthyroidism
🔹 B. Predisposing Risk Factors
Modifiable
Non-Modifiable
🚬 Smoking
👴 Age (men >45, women >55)
💉 Diabetes
🧬 Family history of CAD/MI
💢 Hypertension
👨 Male gender
🍟 High cholesterol
–
⚖️ Obesity
–
🛌 Sedentary lifestyle
–
🍷 Alcohol, stress
–
🔢 III. TYPES OF MYOCARDIAL INFARCTION
MI is classified based on ECG changes, location, and pathological features:
🔷 A. Based on ECG Changes
Type
Description
🟥 ST-Elevation MI (STEMI)
Complete blockage of a coronary artery
ST segment elevated on ECG
More severe, emergency
🟨 Non-ST Elevation MI (NSTEMI)
Partial blockage, less severe
No ST elevation, but elevated troponin
Still serious, requires urgent care
🔷 B. Based on Anatomic Location (seen on ECG & angiography)
Type
Infarct Location
Affected Artery
🫀 Anterior MI
Front wall of left ventricle
Left Anterior Descending (LAD) artery
🫀 Inferior MI
Lower wall of heart
Right Coronary Artery (RCA)
🫀 Lateral MI
Lateral wall of LV
Circumflex artery
🫀 Posterior MI
Back wall of heart
RCA or circumflex
🔷 C. Other MI Classifications
Type
Description
🧪 Silent MI
No obvious symptoms; seen in diabetics and elderly
💉 Type 1 MI
Due to plaque rupture and thrombus (classic heart attack)
💥 Type 2 MI
Due to increased demand or decreased supply without clot (e.g., severe anemia, sepsis)
🏥 Type 4 & 5 MI
Related to PCI (Type 4) or CABG surgery (Type 5)
🧬 I. PATHOPHYSIOLOGY OF MI
A myocardial infarction occurs when blood flow through a coronary artery is suddenly blocked, cutting off oxygen supply to part of the heart muscle, causing irreversible tissue damage.
🔄 Step-by-Step Pathophysiology:
Coronary Artery Narrowing (Atherosclerosis)
Fatty plaques develop in artery walls over time
Plaque Rupture or Erosion
The plaque surface breaks → triggers platelet activation
Thrombus (Blood Clot) Formation
Clot occludes the artery (partially or completely)
Ischemia of Heart Muscle Begins
Myocardial cells become oxygen-deprived within minutes
Anaerobic Metabolism & Cell Injury
Lactic acid accumulates → pain
If untreated > 20–30 min, necrosis (cell death) starts
Infarction and Loss of Function
Irreversible damage occurs in affected area
May lead to impaired contraction and arrhythmias
📌 The location and size of infarction depend on which artery is blocked and how long the blockage lasts.
🚨 II. SIGNS & SYMPTOMS OF MI
Symptoms may vary by age, gender, and comorbid conditions.
🔴 Classic Symptoms (Especially in STEMI):
Symptom
Description
💢 Severe chest pain
Pressure/squeezing in chest >20 min, not relieved by rest
🔁 Pain radiation
To jaw, neck, back, left arm, or shoulder
💦 Sweating (diaphoresis)
Cold, clammy skin
🫁 Shortness of breath
Due to decreased cardiac output or pulmonary congestion
🤢 Nausea/vomiting
Common, especially in inferior MI
😰 Anxiety, fear, restlessness
“Impending doom” feeling
🧊 Cool, pale extremities
Due to vasoconstriction and poor perfusion
📉 Low BP and weak pulse
In cases of cardiogenic shock or heart failure
🧓 Atypical Presentations
Especially in elderly, women, and diabetics:
Fatigue
Indigestion
Dizziness
No chest pain (Silent MI)
🧪 III. DIAGNOSIS OF MYOCARDIAL INFARCTION
Diagnosis is based on clinical symptoms + ECG changes + cardiac biomarkers.
🔹 A. Electrocardiogram (ECG)
Finding
Meaning
⬆️ ST elevation
Indicates STEMI
⬇️ ST depression/T wave inversion
Suggests NSTEMI or ischemia
❗ Q waves
Sign of old MI (after 24–48 hrs)
✅ ECG should be done within 10 minutes of suspected MI.
🔹 B. Cardiac Biomarkers
Test
Purpose
Timeline
🧪 Troponin I or T
Most sensitive & specific marker of MI
Rises in 3–6 hrs, peaks at 12–24 hrs, remains elevated for 7–10 days
🧪 CK-MB
Useful in re-infarction monitoring
Rises in 4–6 hrs, normal in 48–72 hrs
🧪 Myoglobin
Earliest marker, but not specific
Rises in 1–2 hrs, peaks at 6 hrs
🔹 C. Other Diagnostic Tools
Tool
Use
🧠 Echocardiography
Assesses wall motion, pumping function, valve status
May cause chest pain that worsens with inspiration or lying flat
🔷 5. Ventricular Aneurysm
Bulging or rupture of weakened heart wall post-infarction
Can cause thrombus formation, stroke, or heart failure
🔷 6. Papillary Muscle Rupture
Leads to acute mitral valve regurgitation
Results in sudden pulmonary edema and heart failure
🔷 7. Recurrent MI (Re-infarction)
Repeat MI within days or weeks
Usually due to incomplete revascularization or poor compliance
🔷 8. Death
May occur due to massive infarction or lethal arrhythmias
📌 II. KEY POINTS – QUICK RECAP
✅ Key Topic
🔍 Summary
💔 Definition
Irreversible death of heart muscle due to prolonged ischemia
🧬 Cause
Usually due to plaque rupture + thrombus in coronary artery
📊 Types
STEMI (complete block), NSTEMI (partial block)
💢 Classic symptom
Chest pain > 20 min, radiating, unrelieved by rest
🩺 Diagnosis
ECG + elevated troponin, CK-MB
💊 Emergency meds
MONA: Morphine, Oxygen, Nitrates, Aspirin
🛠️ Interventions
PCI (angioplasty), CABG (bypass), thrombolysis
👩⚕️ Nursing role
Monitor pain, ECG, O₂, vitals, anxiety, education
⚠️ Complications
Arrhythmias, HF, shock, pericarditis, death
❤️🩹 VALVULAR HEART DISORDERS
(Congenital & Acquired – Full Clinical Review)
🧠 I. DEFINITION
Valvular heart disorders refer to abnormalities or damage to one or more of the four heart valves (mitral, aortic, tricuspid, pulmonary), affecting their ability to open or close properly — leading to impaired blood flow, pressure overload, or regurgitation.
⚠️ II. CAUSES
🔹 A. Congenital Causes (from birth):
Bicuspid aortic valve (instead of 3 leaflets)
Pulmonary valve stenosis
Ebstein’s anomaly (tricuspid valve malformation)
Tetralogy of Fallot (includes pulmonary stenosis)
🔹 B. Acquired Causes:
Cause
Description
🦠 Rheumatic fever
Common cause of mitral stenosis (from untreated strep throat)
🧬 Degenerative changes
Age-related calcification (esp. aortic stenosis)
🦠 Infective endocarditis
Infection damaging valve tissue
💉 MI or ischemia
Affects papillary muscles supporting valves
🫀 Cardiomyopathy
Enlargement can cause valve leakage
🩺 Radiation or trauma
Rare but possible causes of valve injury
🔢 III. TYPES OF VALVULAR DISORDERS
Each valve may be affected by stenosis (narrowing) or regurgitation/incompetence (leakage):
Valve
Stenosis
Regurgitation
Mitral
Mitral stenosis (MS)
Mitral regurgitation (MR)
Aortic
Aortic stenosis (AS)
Aortic regurgitation (AR)
Tricuspid
Tricuspid stenosis (TS)
Tricuspid regurgitation (TR)
Pulmonary
Pulmonary stenosis (PS)
Pulmonary regurgitation (PR)
📌 Mixed lesions (stenosis + regurgitation) can also occur.
🧬 IV. PATHOPHYSIOLOGY
Disorder
Effect on Heart
🔒 Stenosis
Valve doesn’t fully open → blood flow is restricted → ↑ pressure behind the valve
Especially with atrial fibrillation or prosthetic valves
🦠 Infective endocarditis
Infection risk especially post-surgery
🩸 Bleeding
From anticoagulant use
💀 Sudden cardiac death
Rare but possible with severe stenosis
📌 XI. KEY POINTS – QUICK RECAP
✅ Valvular disorders may be congenital or acquired ✅ Involve stenosis (narrowing) or regurgitation (leaking) ✅ Common causes: rheumatic fever, aging, infection, congenital anomalies ✅ Symptoms: murmurs, dyspnea, fatigue, edema, palpitations ✅ Diagnosis: echocardiography is key ✅ Treatment: medications, valve repair or replacement ✅ Nursing care focuses on fluid balance, symptom monitoring, education
❤️🩹 MITRAL STENOSIS (MS)
Full Nursing and Clinical Overview
🧠 I. DEFINITION
Mitral Stenosis is a narrowing of the mitral valve opening, which impedes blood flow from the left atrium to the left ventricle, causing increased pressure in the left atrium, pulmonary vessels, and eventually the right heart.
🩺 Normally, the mitral valve orifice is 4–6 cm². In MS, it may shrink to <2 cm².
⚠️ II. CAUSES
🔹 A. Most Common Cause:
🦠 Rheumatic fever (post-streptococcal infection) – accounts for 90% of cases globally
🔹 B. Other Causes:
Cause
Description
🧬 Congenital MS
Rare, valve malformation from birth
🦠 Infective endocarditis
Damages valve leaflets
💊 Radiation therapy
Fibrosis of valve
🧪 Autoimmune disorders
(e.g., SLE, rheumatoid arthritis) cause inflammation & thickening
🛠️ Calcification with aging
In elderly, less common than aortic stenosis
🔢 III. TYPES OF MITRAL STENOSIS
Type
Description
🩺 Mild MS
Valve area > 1.5 cm² – usually asymptomatic
🩺 Moderate MS
Valve area 1.0–1.5 cm² – symptomatic with exertion
🩺 Severe MS
Valve area < 1.0 cm² – symptoms at rest, high risk of complications
Watch for signs of A-fib, embolism (e.g., stroke), pulmonary edema
Interventions:
Administer prescribed medications (diuretics, anticoagulants, beta-blockers)
Monitor INR for warfarin therapy
Maintain fluid restriction and low-sodium diet if heart failure present
Encourage rest, avoid exertion
Prepare patient for valvotomy or valve replacement as needed
Education:
Importance of medication compliance
Avoid infections (good dental care, hygiene)
Regular INR checks if on warfarin
Signs of stroke, HF, or worsening symptoms
Avoid high-altitude activities or pregnancy in severe MS
❗ X. COMPLICATIONS
Complication
Description
💢 Atrial fibrillation
Common in MS due to LA enlargement
🧠 Stroke
From emboli originating in fibrillating atrium
🫁 Pulmonary edema
Due to back pressure from LA
🫀 Right-sided heart failure
From long-standing pulmonary hypertension
🦠 Infective endocarditis
Risk due to damaged valve
💉 Bleeding
From anticoagulation therapy if not well monitored
📌 XI. KEY POINTS – QUICK SUMMARY
✅ Mitral stenosis = narrowing of mitral valve → obstructed LA to LV flow ✅ Most commonly caused by rheumatic fever ✅ Symptoms: dyspnea, fatigue, A-fib, murmur, hemoptysis ✅ Diagnosed by echo, ECG, auscultation ✅ Treated with diuretics, beta-blockers, anticoagulants, and surgery (PBMV, MVR) ✅ Nurses should monitor for HF, A-fib, embolism, ensure medication adherence, and provide education
💓 MITRAL REGURGITATION (MR)
Comprehensive Clinical & Nursing Overview
🧠 I. DEFINITION
Mitral Regurgitation is a condition in which the mitral valve does not close completely, allowing blood to flow backward from the left ventricle (LV) into the left atrium (LA) during systole (heart contraction).
🔁 This causes volume overload in the left atrium and ventricle, leading to dilation, pulmonary congestion, and eventually heart failure.
⚠️ II. CAUSES
🔹 A. Primary MR (Structural Abnormality of Valve)
Cause
Description
🦠 Rheumatic heart disease
Causes thickening or retraction of valve leaflets
🧬 Mitral valve prolapse (MVP)
Leaflets bulge into LA during systole
🦠 Infective endocarditis
Destroys valve tissue
🧓 Degenerative changes (aging)
Leads to leaflet or chordae rupture
🧪 Congenital defects
Malformed leaflets or chordae
🔹 B. Secondary MR (Functional)
Cause
Description
❤️ Dilated cardiomyopathy
Stretches annulus, preventing proper closure
💔 Ischemic heart disease / MI
Damages papillary muscles or chordae tendineae
💢 Hypertension
Long-standing pressure overload enlarges LV
🔢 III. TYPES OF MITRAL REGURGITATION
Type
Description
🔄 Acute MR
Sudden onset, often due to chordae rupture or MI
→ Pulmonary edema, severe symptoms
🔁 Chronic MR
Gradual onset due to progressive valve degeneration
→ May be asymptomatic for years
🧬 IV. PATHOPHYSIOLOGY
Mitral valve fails to close during systole
Blood leaks from LV → LA
↑ LA volume & pressure → LA dilation
Backflow of blood → pulmonary congestion
LV compensates by dilating to maintain output
Over time → LV dysfunction, decreased cardiac output, and heart failure
🚨 V. SIGNS AND SYMPTOMS
Symptom
Explanation
🫁 Dyspnea, orthopnea
Due to pulmonary congestion
💢 Fatigue, weakness
Reduced cardiac output
💓 Palpitations
Due to atrial fibrillation or compensatory tachycardia
🔈 Holosystolic murmur
Heard best at apex, radiates to axilla
💨 Shortness of breath on exertion
Early sign of pulmonary involvement
🦶 Peripheral edema, ascites
In late stages with right-sided HF
🔁 Atrial fibrillation
Due to LA enlargement
🫀 S3 heart sound
Indicates volume overload in LV
🧪 VI. DIAGNOSIS
Test
Purpose
🩺 Auscultation
Systolic murmur at apex, may radiate to axilla
🧠 Echocardiography (2D/Doppler)
Gold standard – shows regurgitant flow, LV/LA size
📈 ECG
Atrial fibrillation, LA enlargement, LV hypertrophy
🩻 Chest X-ray
LA and LV enlargement, pulmonary congestion
🧪 Cardiac catheterization
Pre-surgery assessment and to check coronary arteries
💊 VII. MEDICAL MANAGEMENT
Drug Class
Use
💧 Diuretics
Reduce pulmonary congestion and edema
💓 ACE inhibitors / ARBs
↓ Afterload and prevent remodeling
💊 Beta-blockers
Control heart rate, reduce myocardial oxygen demand
💉 Anticoagulants (Warfarin)
For atrial fibrillation to prevent emboli
🧘 Digoxin
Improves contractility in HF with A-fib
🩸 Vasodilators
Reduce afterload and regurgitant volume
🛠️ VIII. SURGICAL MANAGEMENT
Procedure
Indications
🔧 Mitral valve repair
Preferred when feasible, preserves native valve
🔄 Mitral valve replacement (MVR)
Indicated in severely damaged valves
– Mechanical: lifelong anticoagulants
– Bioprosthetic: fewer meds but limited durability
💉 Transcatheter repair (MitraClip)
Minimally invasive for high-risk surgical patients
🫀 Treatment of underlying cause
CABG if ischemic cause, control of HTN or HF
👩⚕️ IX. NURSING MANAGEMENT
🔍 Assessment:
Monitor VS, lung sounds, heart rhythm
Watch for signs of HF, A-fib, embolic events
🩺 Interventions:
Administer prescribed medications (diuretics, beta-blockers, anticoagulants)
Daily weight, I&O, monitor edema
Restrict sodium and fluids if needed
Elevate head of bed, encourage semi-Fowler’s position for dyspnea
Prepare for echo, surgery, or catheterization as indicated
Monitor INR levels if on warfarin
Encourage rest and low exertion during acute episodes
Emphasize need for prophylactic antibiotics for dental/invasive procedures
Promote regular follow-up with cardiologist
❗ X. COMPLICATIONS
Complication
Explanation
💢 Heart failure
From chronic volume overload
⚡ Atrial fibrillation
Increases embolic stroke risk
🧠 Thromboembolism
Especially with A-fib
🫁 Pulmonary hypertension
From backpressure into lungs
💀 Sudden cardiac death
Rare, but possible in severe MR
🦠 Infective endocarditis
Especially in damaged/prosthetic valves
📌 XI. KEY POINTS – QUICK RECAP
✅ Mitral regurgitation = backward flow from LV to LA due to valve incompetence ✅ Causes: MVP, rheumatic disease, ischemia, cardiomyopathy ✅ Symptoms: dyspnea, fatigue, murmur, A-fib ✅ Diagnosis: echocardiogram is gold standard ✅ Managed with diuretics, ACEIs, anticoagulants, valve repair/replacement ✅ Nurses monitor for HF, arrhythmias, embolism, and educate on meds and lifestyle
💓 TRICUSPID STENOSIS (TS)
Full Clinical & Nursing Overview
🧠 I. DEFINITION
Tricuspid Stenosis is a narrowing of the tricuspid valve opening, which impairs blood flow from the right atrium (RA) to the right ventricle (RV) during diastole. This leads to increased right atrial pressure, systemic venous congestion, and reduced cardiac output.
🩺 It is less common than mitral or aortic valve disease and often occurs with mitral stenosis.
⚠️ II. CAUSES
🔹 A. Most Common Cause
🦠 Rheumatic heart disease (especially in combination with mitral valve disease)
🔹 B. Other Causes
Cause
Explanation
🦠 Infective endocarditis
Especially in IV drug users
🧬 Congenital tricuspid atresia or stenosis
Rare birth defects
💉 Carcinoid syndrome
Tumor-secreted substances damage valve
⚠️ Radiation therapy
Causes fibrosis of valve
🩸 Pacemaker/ICD lead injury
Mechanical trauma to the tricuspid valve
🔢 III. TYPES OF TRICUSPID STENOSIS
Type
Description
🔁 Isolated TS
Very rare; most often seen with other valve lesions
🔄 Combined TS with TR
Tricuspid stenosis may progress to regurgitation due to valve fibrosis and annular dilation
🧬 IV. PATHOPHYSIOLOGY
Tricuspid valve narrows → obstructs blood flow from RA to RV
Right atrial pressure increases → RA dilation
Systemic venous congestion ⮕ Blood backs up into veins → hepatomegaly, ascites, peripheral edema
Assess for fatigue, decreased exercise tolerance, and fluid overload
Check daily weight, intake & output
🩺 Interventions:
Administer diuretics, beta-blockers, anticoagulants as prescribed
Elevate legs to reduce edema
Monitor for signs of liver congestion (RUQ tenderness, jaundice)
Educate patient on low-sodium diet, fluid restriction, and activity pacing
📚 Education:
Adherence to medications and fluid balance monitoring
Daily weights (report gain >2 kg in 2 days)
Need for INR monitoring if on warfarin
Avoid activities that increase venous pressure (heavy lifting, prolonged standing)
Watch for symptoms of embolism if in A-fib
❗ X. COMPLICATIONS
Complication
Explanation
💢 Right-sided heart failure
Due to prolonged RA pressure and systemic backup
⚡ Atrial fibrillation
From RA enlargement
🧠 Thromboembolism
Especially with A-fib and blood stasis in RA
🫁 Pulmonary embolism
From venous thrombus
🦠 Infective endocarditis
Especially in IV drug users or with prosthetic valves
🧪 Liver congestion / cirrhosis
Chronic hepatic venous congestion
📌 XI. KEY POINTS – QUICK SUMMARY
✅ Tricuspid stenosis = narrowed tricuspid valve → obstructed flow from RA to RV ✅ Most common cause: Rheumatic fever, often with mitral valve disease ✅ Key symptoms: edema, ascites, hepatomegaly, fatigue, diastolic murmur ✅ Diagnosis: Echo + auscultation + ECG/X-ray findings ✅ Treated with diuretics, salt restriction, and surgery if severe ✅ Nursing care: monitor fluid balance, hepatomegaly, heart rate, and provide education
💓 TRICUSPID REGURGITATION (TR)
Full Clinical & Nursing Overview
🧠 I. DEFINITION
Tricuspid Regurgitation is a condition in which the tricuspid valve does not close properly, allowing blood to flow backward from the right ventricle (RV) to the right atrium (RA) during systole.
🔁 This leads to right atrial volume overload, systemic venous congestion, and eventually right-sided heart failure.
⚠️ II. CAUSES
🔹 A. Primary TR (Structural Valve Abnormality)
Cause
Description
🦠 Rheumatic heart disease
Causes scarring and valve distortion
🦠 Infective endocarditis
Especially in IV drug users
🧬 Congenital malformations
Ebstein’s anomaly
💥 Trauma
Injury to chordae or papillary muscles
💉 Carcinoid syndrome
Causes fibrotic changes in valve leaflets
🔹 B. Secondary (Functional) TR – Most Common Type
Cause
Description
❤️ Right ventricular dilation
Due to left-sided heart failure, pulmonary hypertension
🫀 Dilated cardiomyopathy
Enlarged heart stretches tricuspid annulus
💔 RV infarction
Damages tricuspid valve support structures
🩺 Pacing leads / ICD wires
Mechanical disruption of valve function
🔢 III. TYPES OF TRICUSPID REGURGITATION
Type
Description
🔁 Acute TR
Sudden onset due to trauma, infective endocarditis, or RV infarction
🔄 Chronic TR
Progressive annular dilation from RV overload (more common)
🔂 Primary TR
Structural damage to valve leaflets or chordae
🔁 Secondary TR
Functional valve incompetence due to annular dilation (common)
🧬 IV. PATHOPHYSIOLOGY
Tricuspid valve fails to close completely during systole
Assess for dyspnea, fatigue, RUQ pain, daily weight changes
🩺 Interventions:
Administer diuretics, vasodilators, anticoagulants as prescribed
Maintain fluid and sodium restriction
Elevate legs to reduce edema
Monitor INR if on warfarin
Educate about medication adherence and symptom tracking
📚 Patient Education:
Avoid excess salt/fluid intake
Importance of daily weight monitoring
Report signs of worsening HF (e.g., ↑ edema, breathlessness)
Dental hygiene and infection prevention (risk of endocarditis)
Lifelong cardiologist follow-up if prosthetic valve
❗ X. COMPLICATIONS
Complication
Description
💢 Right-sided heart failure
From chronic volume overload
⚡ Atrial fibrillation
Secondary to RA enlargement
🧠 Thromboembolism / stroke
From A-fib
🧪 Hepatic congestion / cirrhosis
From chronic liver venous congestion
🦠 Infective endocarditis
Especially in IV drug users or prosthetic valves
🫁 Pulmonary hypertension
In long-standing cases or with left heart failure
📌 XI. KEY POINTS – QUICK RECAP
✅ Tricuspid regurgitation = backflow of blood from RV to RA during systole ✅ Most common cause: RV dilation (functional TR) ✅ Symptoms: edema, JVD, ascites, murmur, hepatomegaly ✅ Diagnosis: Echocardiogram, clinical signs, chest X-ray ✅ Management: Diuretics, salt restriction, valve repair/replacement ✅ Nurses monitor fluid balance, A-fib, liver function, and educate on compliance and follow-up
❤️🩺 AORTIC STENOSIS (AS)
Complete Clinical & Nursing Overview
🧠 I. DEFINITION
Aortic Stenosis is a narrowing of the aortic valve opening, which obstructs blood flow from the left ventricle (LV) into the aorta during systole (contraction). This causes increased LV pressure, LV hypertrophy, and eventually heart failure if untreated.
🔒 Normally, the aortic valve area is 2.5–3.5 cm². In severe AS, it’s <1.0 cm².
⚠️ II. CAUSES
🔹 A. Congenital Causes
Bicuspid aortic valve (2 leaflets instead of 3)
Valvular dysplasia in infants/children
🔹 B. Acquired Causes
Cause
Description
🧓 Degenerative (senile) calcification
Most common in elderly due to aging
🦠 Rheumatic heart disease
Causes commissural fusion and valve thickening
🧬 Radiation-induced fibrosis
Rare
🔢 III. TYPES OF AORTIC STENOSIS
Type
Description
🧒 Congenital AS
Often presents earlier in life
👴 Degenerative AS
Calcification-related; common in older adults
🦠 Rheumatic AS
From post-streptococcal damage; often with mitral involvement
Done before surgery; assesses gradient, coronary status
💊 VII. MEDICAL MANAGEMENT
No medication can cure AS — medical therapy is supportive until surgery is needed.
Drug Class
Use
💧 Diuretics (cautious use)
For pulmonary congestion
💓 Beta-blockers / CCBs
Used carefully to manage angina or arrhythmias
💉 Nitrates (caution)
May cause hypotension due to fixed obstruction
🧪 Avoid vasodilators
Can worsen hypotension in AS
📌 Only mild cases may be managed medically. Severe AS requires surgical intervention.
🛠️ VIII. SURGICAL / INTERVENTIONAL MANAGEMENT
Procedure
Indication
🛠️ Aortic Valve Replacement (AVR)
Gold standard for symptomatic severe AS
💉 Transcatheter Aortic Valve Replacement (TAVR)
Minimally invasive, used in high-risk surgical patients
🎈 Balloon Valvuloplasty
Temporary relief; used in children or bridging to TAVR/AVR
🧩 Ross procedure(young patients)
Pulmonary valve replaces aortic valve (autograft)
👩⚕️ IX. NURSING MANAGEMENT
🔍 Assessment:
Monitor for dyspnea, chest pain, syncope
Check heart sounds, pulse quality, lung sounds
Monitor BP, HR, ECG, fluid balance
🩺 Interventions:
Administer medications as prescribed
Keep patient in semi-Fowler’s position for comfort
Avoid overexertion; balance rest and activity
Monitor for signs of decreased cardiac output
Prepare patient for echo, TAVR/AVR surgery as needed
📚 Education:
Report new or worsening symptoms (dizziness, angina, SOB)
Medication adherence and dietary sodium restriction
Importance of follow-up echocardiograms
Infection prevention (e.g., good oral hygiene for endocarditis prevention)
❗ X. COMPLICATIONS
Complication
Description
💢 Heart failure
Due to prolonged pressure overload
🧠 Syncope/injury
From decreased cerebral perfusion
⚡ Arrhythmias (A-fib, VT)
From hypertrophied or ischemic myocardium
🧪 Sudden cardiac death
Risk increases if untreated
🦠 Infective endocarditis
Particularly with calcified valves
🫁 Pulmonary edema
Late-stage due to LV failure
📌 XI. KEY POINTS – QUICK SUMMARY
✅ Aortic stenosis = narrowed valve obstructs LV outflow ✅ Most common in elderly (degenerative) or congenital (bicuspid valve) ✅ Symptoms: angina, syncope, dyspnea ✅ Diagnosis: Echocardiogram = gold standard ✅ Treatment: Surgical replacement (AVR/TAVR) if severe/symptomatic ✅ Nurses monitor for HF, low output signs, safety, and pre/post-op care
❤️🩺 AORTIC REGURGITATION (AR)
Complete Clinical & Nursing Overview
🧠 I. DEFINITION
Aortic Regurgitation (AR) is a condition where the aortic valve does not close properly, allowing blood to flow back from the aorta into the left ventricle (LV) during diastole (relaxation).
🔁 This leads to volume overload of the LV, causing dilation, hypertrophy, and eventually left-sided heart failure.
⚠️ II. CAUSES
🔹 A. Primary (Valvular) Causes
Cause
Description
🦠 Rheumatic heart disease
Post-streptococcal infection damaging valve
🦠 Infective endocarditis
Destroys valve leaflets
🧬 Congenital bicuspid aortic valve
Leads to early degeneration
💥 Trauma or aortic dissection
Tears the valve or annulus
🧓 Senile calcification
Degeneration with aging
🔹 B. Secondary (Aortic Root Disease) Causes
Condition
Description
💢 Marfan syndrome, Ehlers-Danlos
Connective tissue disorders dilating aortic root
🔥 Ankylosing spondylitis, syphilis
Inflammatory or infectious aortitis
📉 Hypertension
Can dilate the aortic root and valve annulus
🔢 III. TYPES OF AORTIC REGURGITATION
Type
Description
🔄 Acute AR
Sudden onset due to trauma, dissection, or endocarditis → emergency
🔁 Chronic AR
Gradual progression from degenerative or rheumatic disease
🧬 IV. PATHOPHYSIOLOGY
Aortic valve fails to close during diastole
Blood leaks from aorta → LV
LV receives excess volume → dilates and hypertrophies to maintain output
Over time, LV decompensation occurs → ↓ ejection fraction, heart failure symptoms
Educate on low-sodium diet, activity restriction, and fluid balance
📚 Education:
Emphasize medication adherence and regular follow-ups
Teach signs of worsening heart failure (weight gain, dyspnea, swelling)
Importance of endocarditis prevention and oral hygiene
Educate about surgery (AVR) when appropriate
❗ X. COMPLICATIONS
Complication
Description
💢 Heart failure
Due to progressive LV dilation and dysfunction
⚡ Arrhythmias
Atrial fibrillation or ventricular arrhythmias
🧠 Embolic events
From LV thrombus or A-fib
💀 Sudden cardiac death
Especially in severe untreated cases
🦠 Infective endocarditis
Risk in damaged valves
📌 XI. KEY POINTS – QUICK SUMMARY
✅ Aortic regurgitation = backward flow from aorta to LV during diastole ✅ Causes: rheumatic disease, infective endocarditis, congenital defects, aortic root disease ✅ Symptoms: dyspnea, fatigue, wide pulse pressure, bounding pulse, diastolic murmur ✅ Diagnosis: Echo = gold standard ✅ Treatment: Vasodilators, surgery (AVR) if severe/symptomatic ✅ Nurses monitor fluid status, cardiac output, heart failure, and educate on meds, follow-up, and prevention
💙 PULMONARY STENOSIS (PS)
Complete Clinical & Nursing Overview
🧠 I. DEFINITION
Pulmonary Stenosis (PS) is a condition where the pulmonary valve is narrowed, obstructing the flow of blood from the right ventricle (RV) to the pulmonary artery, thereby reducing blood flow to the lungs.
🔒 The narrowing increases right ventricular pressure, leading to RV hypertrophy, and, if severe, right-sided heart failure.
⚠️ II. CAUSES
🔹 A. Congenital (Most Common)
Cause
Description
👶 Isolated congenital PS
Most common, due to malformed or fused valve leaflets
In very severe obstruction (especially in infants)
💥 Palpitations
Due to RV strain or arrhythmias
🔈 Harsh systolic ejection murmur
Best heard at left upper sternal border
Often accompanied by thrill and click
🧍 Jugular vein distention (JVD)
Sign of right-sided heart failure
🦵 Peripheral edema, hepatomegaly
From venous congestion
🧪 VI. DIAGNOSIS
Test
Findings
🧠 Echocardiography (2D & Doppler)
Gold standard — shows valve anatomy, gradient, RV size
🩺 Auscultation
Systolic murmur, ejection click
📈 ECG
Right ventricular hypertrophy, right axis deviation
🩻 Chest X-ray
Enlarged RV, post-stenotic dilation of pulmonary artery
💉 Cardiac catheterization
Confirms pressure gradient and evaluates for intervention
💊 VII. MEDICAL MANAGEMENT
Medical treatment is supportive, especially in mild cases.
Drug
Purpose
💧 Diuretics (e.g., Furosemide)
For right heart failure symptoms
💓 Beta-blockers
May help reduce RV pressure and control rate
💊 Prophylactic antibiotics
For prevention of infective endocarditis (in some cases)
🩸 Oxygen therapy
For cyanotic infants (if hypoxemia present)
🛠️ VIII. SURGICAL / INTERVENTIONAL MANAGEMENT
Procedure
Indication
🎈 Balloon Valvuloplasty
First-line treatment in moderate to severe valvular PS
Minimally invasive, often curative
🔧 Surgical Valvotomy / Commissurotomy
For complex anatomy or failed balloon procedure
🔄 Valve replacement
Rarely needed; in cases with severely deformed valves
🧩 Repair of associated defects
If PS is part of complex congenital heart disease
👩⚕️ IX. NURSING MANAGEMENT
🔍 Assessment:
Monitor vital signs, heart and lung sounds, oxygen saturation
Assess for exercise intolerance, edema, cyanosis, fatigue
🩺 Interventions:
Administer diuretics, oxygen, or beta-blockers as ordered
Position in semi-Fowler’s if dyspnea is present
Encourage rest and avoid exertion in severe cases
Monitor for post-intervention complications (e.g., arrhythmias, bleeding)
📚 Education:
Teach importance of follow-up with cardiologist
Advise on endocarditis prevention (dental hygiene, antibiotics before dental/surgical work if indicated)
Teach parents (in infants) to monitor for feeding difficulty, cyanosis, irritability
Educate about activity levels, signs of deterioration (e.g., fainting, worsening fatigue)
❗ X. COMPLICATIONS
Complication
Description
💢 Right ventricular hypertrophy and failure
From long-standing pressure overload
🧠 Arrhythmias
Due to RV strain
💀 Sudden cardiac death
Rare, but possible in untreated severe PS
💙 Cyanosis
From poor pulmonary circulation in infants
🦠 Infective endocarditis
If valve is damaged
🔁 Pulmonary regurgitation
Post-balloon dilation or surgery
📌 XI. KEY POINTS – QUICK SUMMARY
✅ Pulmonary stenosis = narrowing of pulmonary valve → obstructs blood flow from RV to lungs ✅ Most commonly congenital ✅ Symptoms: dyspnea, fatigue, murmur, cyanosis, right-sided HF signs ✅ Diagnosis: Echo is gold standard ✅ Treatment: Balloon valvuloplasty is first-line in moderate-severe cases ✅ Nursing role: Monitor symptoms, meds, educate parents/patient, prepare for interventions
💙 PULMONARY REGURGITATION (PR)
Full Clinical & Nursing Overview
🧠 I. DEFINITION
Pulmonary Regurgitation (PR) is a condition in which the pulmonary valve does not close properly, allowing backward flow of blood from the pulmonary artery into the right ventricle (RV) during diastole (relaxation phase of the heart).
🔁 Leads to right ventricular volume overload, progressive RV dilation, and right-sided heart failure if severe and untreated.
⚠️ II. CAUSES
🔹 A. Primary (Valvular) Causes
Cause
Description
🧬 Congenital heart defects
e.g., Tetralogy of Fallot (post-repair), pulmonary valve dysplasia
🦠 Infective endocarditis
Valve destruction from infection
🧬 Carcinoid syndrome
Causes fibrotic deposits on valve leaflets
💉 Rheumatic heart disease
Less commonly affects pulmonary valve
🔹 B. Secondary (Functional) Causes
Cause
Description
📈 Pulmonary hypertension
Causes annular dilation of the pulmonary valve
🧪 Post-balloon valvuloplasty
Over-dilation can damage valve
🧠 Connective tissue disorders
e.g., Marfan syndrome
🧼 Iatrogenic causes
From surgical or catheter-based procedures
🔢 III. TYPES OF PULMONARY REGURGITATION
Type
Description
🔁 Congenital PR
Associated with other defects like Tetralogy of Fallot
🔄 Acquired PR
Due to conditions like pulmonary HTN, infections, or surgery
🔂 Functional PR
Valve is structurally normal but doesn’t close due to annular dilation
🧬 IV. PATHOPHYSIOLOGY
Pulmonary valve fails to close properly
Blood leaks back into RV during diastole
Leads to RV volume overload
RV dilates and hypertrophies over time
Reduced RV efficiency → right-sided heart failure
Decreased forward flow → hypoxemia in severe cases
🚨 V. SIGNS AND SYMPTOMS
Symptom
Explanation
🛌 Fatigue, weakness
↓ Cardiac output
🫁 Exertional dyspnea
Pulmonary congestion or RV dysfunction
🧍 Jugular vein distention (JVD)
Sign of systemic venous congestion
💦 Peripheral edema
Due to fluid overload from right-sided HF
🧪 Hepatomegaly / Ascites
From venous congestion
🔈 Early diastolic murmur
High-pitched, best heard at left upper sternal border, increases with inspiration
💙 Cyanosis (in severe cases)
From inadequate oxygenation
💓 Palpitations
Possible with RV strain or arrhythmia
🧪 VI. DIAGNOSIS
Test
Finding
🧠 Echocardiography (2D/Doppler)
Gold standard – shows regurgitant flow, RV size, function
🩺 Auscultation
Diastolic murmur, Graham-Steell murmur (if secondary to pulmonary HTN)
📈 ECG
Right ventricular hypertrophy, right axis deviation
🩻 Chest X-ray
Enlarged right heart border, pulmonary artery dilation
Watch for signs of right-sided heart failure (e.g., JVD, hepatomegaly, ascites)
🩺 Interventions:
Administer diuretics, oxygen, beta-blockers/ACE inhibitors as prescribed
Elevate head of bed or legs to reduce dyspnea and edema
Monitor daily weights, I&O, signs of worsening HF
Prepare patient for echo, valve assessment, or surgery
📚 Education:
Teach medication adherence
Encourage low-sodium diet, fluid control
Educate about prophylactic antibiotics (if post-valve repair or high risk)
Stress importance of routine cardiology follow-up
Teach to report signs of fluid overload or fatigue
❗ X. COMPLICATIONS
Complication
Description
💢 Right ventricular failure
Due to chronic volume overload
⚡ Arrhythmias
e.g., atrial flutter, ventricular tachycardia
🧠 Thromboembolism
Due to atrial fibrillation or sluggish flow
💀 Sudden cardiac death
Rare, but possible in severe untreated cases
🦠 Infective endocarditis
Risk in damaged or prosthetic valves
📌 XI. KEY POINTS – QUICK SUMMARY
✅ Pulmonary regurgitation = backflow of blood from pulmonary artery to RV during diastole ✅ Most often caused by congenital defects or pulmonary hypertension ✅ Symptoms: fatigue, JVD, edema, hepatomegaly, murmur ✅ Diagnosed by echocardiography (Doppler), ECG, chest X-ray ✅ Treatment: diuretics, valve replacement, management of underlying cause ✅ Nursing care includes fluid monitoring, medication administration, patient education
👩⚕️ COMMON NURSING MANAGEMENT OF VALVULAR HEART DISEASES
(Applies to Mitral, Aortic, Tricuspid, and Pulmonary Valve Disorders)
Stable HR/BP, good capillary refill, strong pulses
🧍 Enhance activity tolerance
Performs ADLs without fatigue
🛏️ Manage fluid volume
No edema, weight stable, normal I&O
💊 Adhere to therapy
Takes meds, reports for INR testing
📚 Understand condition
Verbalizes knowledge about disease and care plan
❗ V. COMPLICATIONS TO MONITOR FOR
Heart failure
Atrial fibrillation
Embolic events (stroke, MI)
Infective endocarditis
Sudden cardiac death
Bleeding from anticoagulants
📌 KEY POINTS SUMMARY
✅ Valvular diseases → disrupt forward blood flow, leading to heart failure ✅ Assessment, medication adherence, and education are cornerstones of care ✅ Echocardiogram is the key diagnostic tool ✅ Nurses play a vital role in early detection of complications, symptom control, and patient empowerment
❤️🔥 RHEUMATIC HEART DISEASE (RHD)
Definition, Causes, and Types
🧠 I. DEFINITION
Rheumatic Heart Disease (RHD) is a chronic, permanent damage to the heart valves that results from one or more attacks of acute rheumatic fever (ARF), which is a post-streptococcal inflammatory disease.
🦠 It primarily affects the mitral and aortic valves, causing stenosis, regurgitation, or both.
⚠️ II. CAUSES
🔷 Primary Cause
Untreated or inadequately treated Group A beta-hemolytic Streptococcal (GAS) pharyngitis (strep throat) → Leads to autoimmune response → Causes inflammation of heart, joints, skin, and brain → Repeated attacks cause progressive scarring and deformity of heart valves
🔹 Risk Factors
Factor
Explanation
🧒 Children aged 5–15 years
Most vulnerable age group
🧫 Poorly treated strep throat
No or inadequate antibiotics
🧍 Overcrowded living conditions
Increases risk of GAS infection
💰 Low socioeconomic status
Limited access to healthcare
🔄 Recurrent streptococcal infections
Increases risk of rheumatic fever and RHD
🔢 III. TYPES OF RHEUMATIC HEART DISEASE
Type
Description
💓 Valvular RHD(most common)
Damage and deformation of heart valves, especially:
Mitral valve → stenosis and/or regurgitation
Aortic valve → less commonly involved | | 🫀 Myocardial RHD | Inflammation of heart muscle (myocarditis) during rheumatic fever; may lead to cardiomegaly | | 🩺 Pericardial RHD | Inflammation of the pericardium (pericarditis) — rare, may cause pericardial effusion | | ♻️ Mixed RHD | Involvement of more than one valve or cardiac layer (pancarditis) in severe cases |
🧡 Most Common Type
Mitral Stenosis (narrowing of mitral valve due to chronic inflammation and scarring)
❤️🔥 RHEUMATIC HEART DISEASE (RHD)
Part 2: Pathophysiology, Signs & Symptoms, Diagnosis
🧬 I. PATHOPHYSIOLOGY
Rheumatic Heart Disease is the chronic result of acute rheumatic fever (ARF), which is a delayed autoimmune reaction to Group A Streptococcal infection (usually throat infection).
🔁 Step-by-Step Process:
Streptococcal pharyngitis occurs (untreated or inadequately treated)
Body’s immune system produces antibodies to fight the strep bacteria
Due to molecular mimicry, antibodies also attack body’s own tissues, especially the:
Heart (valves, myocardium, pericardium)
Joints
Skin
Central nervous system
Leads to inflammation (pancarditis) and damage:
Valve inflammation (valvulitis) → leaflet thickening, fibrosis, and scarring
Chordae tendineae shorten → valve regurgitation or stenosis
Repeated ARF episodes = progressive and permanent valve damage
Pericarditis is an inflammation of the pericardium, the two-layered sac that surrounds the heart. It may cause chest pain, fluid accumulation (pericardial effusion), and in severe cases, cardiac tamponade (compression of the heart due to fluid buildup).
🔍 It can be acute, subacute, or chronic, and may lead to constrictive pericarditis if not managed properly.
⚠️ II. CAUSES
Pericarditis can be idiopathic (unknown cause) or secondary to various infections, injuries, or systemic diseases.
🔹 A. Infectious Causes
Type
Examples
🦠 Viral (most common)
Coxsackievirus, echovirus, HIV, influenza
🧫 Bacterial
Tuberculosis (TB), staphylococcus, streptococcus
🍄 Fungal
Histoplasmosis, aspergillosis
🪱 Parasitic
Rare, e.g., toxoplasmosis
🔹 B. Non-Infectious Causes
Type
Examples
💔 Myocardial infarction
Post-MI pericarditis (early) or Dressler’s syndrome (late, autoimmune)
Blood in pericardial sac (e.g., TB, malignancy, trauma)
🧬 I. PATHOPHYSIOLOGY
The pericardium is a double-layered sac (parietal and visceral) that surrounds the heart. It normally contains a small amount (~15–50 mL) of lubricating fluid.
🔁 Pathological Process in Pericarditis:
Trigger (infection, injury, autoimmune, etc.) ⮕ Initiates inflammation of the pericardial layers
Vascular permeability increases ⮕ Leads to exudation of fluid, proteins, and inflammatory cells
Depending on the cause:
Fibrin deposits → “Dry” or fibrinous pericarditis
Fluid accumulation → pericardial effusion
Pus → purulent pericarditis
Blood → hemorrhagic pericarditis
Persistent inflammation → pericardial thickening, scarring, and adhesions
In chronic or severe cases: ⮕ Pericardium becomes rigid → restricts diastolic filling of heart ⮕ Leads to constrictive pericarditis
🚨 II. SIGNS AND SYMPTOMS
Symptoms can vary based on type, cause, and severity.
🔷 Common Symptoms of Acute Pericarditis:
Symptom
Description
💢 Sharp, pleuritic chest pain
Sudden onset, worsens with deep breathing, coughing, or lying flat
Improves when sitting up and leaning forward
🩺 Pericardial friction rub
Scratchy, high-pitched sound heard with stethoscope at LLSB (lower left sternal border)
✅ Remember: Pericarditis may appear similar to myocardial infarction, but the ECG, pain pattern, and patient position help differentiate them!
❤️🔥 MYOCARDITIS
Definition, Causes, and Types
🧠 I. DEFINITION
Myocarditis is an inflammation of the myocardium, the muscular middle layer of the heart wall, which can impair the heart’s ability to pump blood effectively and cause arrhythmias, heart failure, or even sudden cardiac death.
🩺 It may be acute, subacute, or chronic, and often follows a viral infection, but can also be triggered by bacteria, toxins, autoimmune diseases, or drugs.
⚠️ II. CAUSES OF MYOCARDITIS
Myocarditis can have infectious, non-infectious, and autoimmune causes.
Allergic reaction to drugs (eosinophils present in biopsy)
🐛 Chagas myocarditis
Caused by Trypanosoma cruzi parasite in endemic areas (Latin America)
🧬 I. PATHOPHYSIOLOGY OF MYOCARDITIS
Myocarditis begins with injury or infection of the myocardium, usually due to viral agents or an autoimmune response, leading to inflammation and damage to the heart muscle.
🔁 Step-by-Step Process:
Initial Trigger:
Usually a viral infection (e.g., Coxsackievirus B)
Or toxic, allergic, autoimmune exposure
Immune Response Activated:
White blood cells, cytokines, and antibodies infiltrate the myocardium
Inflammatory reaction damages heart muscle cells
Cellular Damage:
Inflammation leads to myocyte necrosis (cell death)
This impairs the heart’s ability to contract and relax properly
Myocardial Dysfunction:
↓ Contractility = ↓ cardiac output
Heart becomes dilated or flabby (especially in chronic cases)
Arrhythmias and Heart Failure:
Inflammation and scarring may disrupt electrical conduction pathways
Risk of ventricular arrhythmias, sudden death, or progression to dilated cardiomyopathy
🚨 II. SIGNS AND SYMPTOMS
Symptoms of myocarditis can range from mild to life-threatening, and may mimic other cardiac conditions like acute coronary syndrome.
🔷 General Symptoms:
Symptom
Explanation
🌡️ Fever, fatigue, malaise
Often early, due to viral/inflammatory origin
🛌 General weakness
Due to reduced cardiac output
🫁 Shortness of breath (dyspnea)
Especially on exertion or lying flat (orthopnea)
💢 Chest pain
May be sharp, pleuritic (inflammation-related) or mimic angina