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
Patient verbalizes understanding of illness, meds, and follow-up
⚠️ Prevent complications
No arrhythmias, heart failure, or embolic events occur
❗ I. COMPLICATIONS OF MYOCARDITIS
If not treated early, myocarditis can lead to serious and potentially life-threatening complications.
1. 💓 Heart Failure
Inflammation and damage to heart muscle weakens the pumping ability
Can lead to left-sided or biventricular failure
2. ⚡ Arrhythmias
Electrical conduction system may be disrupted by inflammation
Can cause:
Atrial fibrillation
Ventricular tachycardia or fibrillation (sudden death risk)
Heart block
3. ❤️🩹 Dilated Cardiomyopathy (DCM)
Chronic myocarditis → thinning and dilation of heart chambers
Results in progressive heart failure
4. 🧠 Thromboembolism / Stroke
Reduced heart function and chamber dilation may lead to clot formation
Can embolize to brain (stroke) or other organs
5. 🩸 Cardiogenic Shock
In fulminant myocarditis, cardiac output drops dramatically
May lead to multi-organ failure and death
6. 🫀 Sudden Cardiac Death
Due to ventricular arrhythmias or pump failure
Common in undiagnosed or untreated cases
📌 II. KEY POINTS – QUICK RECAP
🔑 Key Concept
Summary
🧠 Definition
Inflammation of the heart muscle (myocardium)
🦠 Most common cause
Viral infections (e.g., Coxsackievirus)
🩺 Key symptoms
Fatigue, chest pain, dyspnea, palpitations
📈 ECG finding
ST-T changes, arrhythmias
🧪 Lab finding
↑ Troponin, CRP, ESR, WBC
🧠 Gold standard imaging
Cardiac MRI
💊 First-line treatment
Supportive care + treatment of HF/arrhythmias
⚠️ Major risks
Heart failure, arrhythmias, DCM, sudden death
👩⚕️ Nursing care focus
Cardiac monitoring, rest, medication, education
🩺 Avoid in acute phase
Strenuous activity/exercise
💚 ENDOCARDITIS
Definition | Causes | Types
🧠 I. DEFINITION
Endocarditis is an inflammation or infection of the inner lining of the heart (endocardium), most commonly affecting the heart valves. It is usually caused by microorganisms (mainly bacteria) entering the bloodstream and adhering to damaged cardiac tissue or prosthetic valves.
🦠 It can lead to valve destruction, emboli, and life-threatening complications if not treated promptly.
⚠️ II. CAUSES
Endocarditis is caused when infectious agents enter the bloodstream and settle in the heart, especially on damaged valves or prosthetic devices.
Rapid onset, high fever, caused by virulent organisms (e.g., S. aureus)
Can affect normal valves
🐌 Subacute Infective Endocarditis
Slow onset, caused by less virulent organisms (e.g., S. viridans)
Usually affects damaged valves
🔁 Prosthetic Valve Endocarditis (PVE)
Occurs on mechanical or bioprosthetic valves after surgery
💉 IV Drug-Associated Endocarditis
Commonly involves tricuspid valve, caused by S. aureus
💢 Non-Infective Endocarditis (NBTE)
Sterile vegetations in malignancy, lupus, or hypercoagulable states
E.g., Libman–Sacks endocarditis in SLE
🧬 I. PATHOPHYSIOLOGY
Endocarditis typically begins when bacteria or fungi enter the bloodstream (bacteremia or fungemia) and adhere to the damaged endocardial surface or heart valves.
🔁 Step-by-Step Process:
Endothelial injury:
Can occur due to turbulent blood flow, prosthetic valves, or IV drug use.
Platelet and fibrin deposition:
A sterile thrombus (NBTE) forms at the site of injury.
Microorganism entry:
From sources like dental work, catheters, surgery, or infected skin.
Colonization of thrombus:
Bacteria or fungi adhere and multiply in the thrombus, forming vegetations (clumps of microorganisms + platelets + fibrin).
Vegetation formation:
These vegetations damage valves, interfere with function, and may break off → causing emboli.
Immune response + systemic effects:
Triggers inflammation, fever, and immune complex deposition (causing kidney or skin involvement).
🚨 II. SIGNS & SYMPTOMS
Signs depend on whether the condition is acute (sudden, severe) or subacute (gradual, milder).
🔷 General Symptoms:
Symptom
Explanation
🌡️ Fever and chills
Most common symptom; may be absent in elderly or immunocompromised
🛏️ Fatigue, weakness
Due to chronic infection and heart dysfunction
💓 Heart murmur
New or changed murmur due to valve damage
🦵 Night sweats, weight loss
Common in subacute form
💢 Arthralgia, myalgia
From immune complex deposition
😮💨 Dyspnea
Due to heart failure if valve is severely damaged
🔷 Classic Clinical Signs(more specific to infective endocarditis):
Sign
Description
🔴 Petechiae
Small red/purple spots on skin, conjunctiva, palate
🖐️ Osler’s nodes
Painful red nodules on fingers/toes (immune complex-mediated)
🖐️ Janeway lesions
Painless red spots on palms/soles (septic emboli)
👁️ Roth spots
Retinal hemorrhages with pale centers
💉 Splinter hemorrhages
Thin, red to brown lines under nails
⚠️ Complication Signs:
Sudden stroke (embolism to brain)
Hematuria (kidney infarcts)
Heart failure (valve destruction)
Sepsis or septic shock
🧪 III. DIAGNOSIS OF ENDOCARDITIS
📋 A. History and Physical Examination
What to Ask / Examine
Why
Recent dental work, surgery, IV drug use
Potential source of infection
New/changing heart murmur
Sign of valve involvement
Fever, fatigue, embolic signs
Common symptoms
🧬 B. Laboratory Tests
Test
Findings
💉 Blood cultures (×3)
Gold standard – positive for bacteria or fungi in multiple sets
🧪 CBC
↑ WBCs (infection), anemia (chronic disease)
🔥 ESR / CRP
Elevated (inflammatory markers)
🧫 Rheumatoid factor
May be positive due to immune activation
🩸 Urinalysis
Hematuria or proteinuria (renal involvement)
🧠 Procalcitonin
May be elevated in bacterial infection
📷 C. Imaging
Imaging
Purpose
🧠 Echocardiography (2D or TEE)
Confirms vegetations on valves
Transesophageal echo (TEE) is more sensitive than transthoracic (TTE)
🩻 Chest X-ray
May show cardiomegaly or pulmonary emboli
📈 ECG
May detect arrhythmias or conduction block (if abscess extends)
✅ Diagnostic Criteria: Modified Duke Criteria
Criteria
Includes
Major
Positive blood cultures, evidence of endocardial involvement on echo
Monitor for infection, cardiac changes, embolic signs, and patient education
🛡️ Prevention
Antibiotic prophylaxis for high-risk patients before dental/surgical procedures
💙 CARDIOMYOPATHIES
Definition | Causes | Types
🧠 I. DEFINITION
Cardiomyopathy refers to a group of diseases of the heart muscle (myocardium) that affect the heart’s size, shape, structure, and function, making it harder for the heart to pump blood efficiently.
🫀 Cardiomyopathies may lead to heart failure, arrhythmias, valve problems, or sudden cardiac death, even in previously healthy individuals.
⚠️ II. CAUSES OF CARDIOMYOPATHY
Cardiomyopathies can be genetic (inherited) or acquired (due to other diseases or external factors).
🔹 A. Primary (Genetic / Idiopathic)
Cause
Explanation
🧬 Familial inheritance
Often autosomal dominant; linked to structural or electrical abnormalities
Thickened heart muscle (especially interventricular septum); often genetic
Diastolic dysfunction, risk of sudden cardiac death, especially in young athletes
📏 Restrictive Cardiomyopathy (RCM)
Stiff myocardium restricts filling; often due to infiltrative diseases like amyloidosis or hemochromatosis
Normal size but impaired diastolic function
🤰 Peripartum Cardiomyopathy
Occurs in late pregnancy or postpartum period
Mimics dilated cardiomyopathy
🩸 Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Fatty/fibrous replacement of right ventricular muscle; often genetic
Palpitations, syncope, risk of ventricular arrhythmias
🧬 I. PATHOPHYSIOLOGY
The pathophysiology of cardiomyopathy depends on the type, but all forms impair the heart’s ability to pump blood effectively, leading to heart failure, arrhythmias, and organ hypoperfusion.
🔹 A. Dilated Cardiomyopathy (DCM)
Heart chambers (especially LV) become enlarged and weak
Risk of ventricular arrhythmias and sudden cardiac death
🔹 C. Restrictive Cardiomyopathy (RCM)
Ventricular walls become stiff due to fibrosis or infiltration (e.g., amyloidosis)
Normal systolic function, but impaired diastolic filling
Leads to pulmonary congestion, edema, and right-sided heart failure
🔹 D. Peripartum Cardiomyopathy
Similar to DCM, but occurs late in pregnancy or postpartum
Reduced ejection fraction, often reversible with early treatment
🔹 E. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Fatty/fibrous tissue replaces right ventricular muscle
↓ Contractility and ↑ arrhythmogenic risk → VT, sudden death
🚨 II. SIGNS AND SYMPTOMS
Symptoms may vary by type, but most forms share features of heart failure and reduced cardiac output.
✅ General Symptoms of Cardiomyopathy:
Symptom
Cause
😮💨 Dyspnea on exertion
Pulmonary congestion
🛌 Fatigue and weakness
↓ Cardiac output
🦵 Peripheral edema
Right heart failure
💓 Palpitations / Arrhythmias
Electrical instability
🧍 Orthopnea, PND
Fluid accumulation when lying down
🧠 Syncope or dizziness
Poor perfusion or arrhythmia
💢 Chest pain
Especially in HCM due to ischemia
⚰️ Sudden cardiac arrest
Risk in HCM and ARVC
🔷 Specific Signs by Type:
Type
Distinct Features
DCM
S3 gallop, enlarged heart, LV dysfunction
HCM
Harsh systolic murmur (↑ with Valsalva), strong apical beat
RCM
Signs of right-sided HF: JVD, hepatomegaly, ascites
ARVC
Frequent ventricular arrhythmias, syncope
Peripartum
Appears in last trimester or postpartum, resembles DCM
🧪 III. DIAGNOSIS OF CARDIOMYOPATHY
📋 A. History and Physical Exam
Ask about family history, recent pregnancy, alcohol/drug use, or viral illness
Check for murmurs, edema, lung crackles, hepatomegaly
🧠 B. Diagnostic Tests
Test
Purpose/Findings
📈 ECG
May show arrhythmias, LVH, ST-T changes
🧠 Echocardiogram (2D/3D)
Primary diagnostic tool:
Wall thickness, chamber size
EF %, valve function
Obstruction (in HCM) | | 💡 Cardiac MRI | Detailed images of heart structure and scarring | | 🩻 Chest X-ray | Cardiomegaly, pulmonary congestion | | 🧪 BNP / NT-proBNP | ↑ in heart failure (DCM, RCM) | | 💉 Genetic testing | In familial cases (HCM, ARVC) | | 🧪 Cardiac enzymes | Rule out MI if chest pain is present | | 📉 Cardiac catheterization | Rule out ischemic cardiomyopathy | | 🔬 Endomyocardial biopsy | In suspected myocarditis or infiltrative causes
💊 I. MEDICAL MANAGEMENT
Treatment focuses on: ✅ Managing symptoms (especially heart failure) ✅ Preventing complications (arrhythmias, thromboembolism, sudden cardiac death) ✅ Addressing the underlying cause or type
🔹 A. General Medications (All Cardiomyopathies)
Drug Class
Examples
Purpose
💓 ACE inhibitors / ARBs
Enalapril, Losartan
Reduce afterload, improve heart function
💊 Beta-blockers
Metoprolol, Carvedilol
Slow heart rate, reduce oxygen demand, control arrhythmias
💧 Diuretics
Furosemide, Spironolactone
Relieve fluid overload and pulmonary congestion
💉 Anticoagulants
Warfarin, DOACs
Prevent emboli in A-fib or severe LV dysfunction
💢 Antiarrhythmics
Amiodarone, Digoxin
Used for arrhythmias (ventricular or atrial)
🔷 B. Type-Specific Medical Management
1. Dilated Cardiomyopathy (DCM)
Standard heart failure medications (ACEIs, BBs, diuretics)
Anticoagulants if low EF or atrial fibrillation
Aldosterone antagonists (e.g., spironolactone) for advanced HF
2. Hypertrophic Cardiomyopathy (HCM)
Beta-blockers or Calcium channel blockers to slow heart rate and improve filling
Avoid drugs that reduce preload/afterload too much (e.g., nitrates, diuretics in excess)
Antiarrhythmics if symptomatic VT or AF
3. Restrictive Cardiomyopathy (RCM)
Diuretics to relieve congestion
Treat underlying cause (e.g., amyloidosis, sarcoidosis)
Rate control for atrial fibrillation
Anticoagulation if thrombus risk
4. Peripartum Cardiomyopathy
Similar to DCM, but avoid ACEIs in pregnancy
May use beta-blockers, diuretics cautiously
Often improves postpartum with proper management
5. ARVC (Arrhythmogenic Right Ventricular Cardiomyopathy)
Focus on arrhythmia control
Beta-blockers, antiarrhythmics, and ICD if needed
Restriction of intense physical activity
🛠️ II. SURGICAL / INTERVENTIONAL MANAGEMENT
Surgical treatment is considered in severe or unresponsive cases, or to prevent sudden cardiac death.
🔄 A. Implantable Cardioverter Defibrillator (ICD)
Use
When Indicated
Prevent sudden cardiac death from arrhythmias
– EF <35% in DCM or post-MI
HCM or ARVC with VT/VF history
Family history of sudden cardiac death |
🔧 B. Pacemaker (PPM)
For bradycardia, heart block, or synchronization in heart failure (CRT: Cardiac Resynchronization Therapy)
🫀 C. Surgical Myectomy(HCM)
Description
Indication
Resection of thickened septum
For patients with severe LVOT obstruction and refractory symptoms despite meds
💉 D. Septal Alcohol Ablation(HCM)
Description
Indication
Alcohol injected into septal artery to shrink thickened septal tissue
Alternative to surgery in high-risk or older patients
♻️ E. Left Ventricular Assist Device (LVAD)
Use
Purpose
End-stage DCM or other cardiomyopathy
Used as a bridge to transplant or destination therapy
🫀 F. Heart Transplant
Indication
Notes
Severe end-stage heart failure unresponsive to all other treatments
Especially in younger patients or non-ischemic cardiomyopathy
Common in HCM & ARVC – screen first-degree relatives
❤️🩹 CARDIAC DYSRHYTHMIAS
(Also known as Cardiac Arrhythmias)
🧠 1. DEFINITION
Cardiac dysrhythmia is an abnormality in the heart’s rhythm, rate, or conduction pattern caused by disturbance in the generation or transmission of electrical impulses.
It may be too fast (tachycardia), too slow (bradycardia), or irregular, and can originate from atria, AV node, or ventricles.
⚠️ 2. CAUSES
Category
Examples
🧠 Electrolyte imbalance
↓ K⁺, ↓ Mg²⁺, ↑ Ca²⁺
❤️ Myocardial ischemia or infarction
Scarred or oxygen-deprived tissue disrupts conduction
💊 Drug toxicity
Digoxin, beta-blockers, antiarrhythmics
⚡ Conduction abnormalities
Bundle branch block, AV block
📉 Hypoxia or acidosis
From COPD, sleep apnea, etc.
🧬 Congenital defects
Long QT syndrome, WPW
📈 Stress or stimulants
Caffeine, anxiety, smoking
🛠️ Post cardiac surgery
Trauma to conduction pathways
🔢 3. TYPES OF CARDIAC DYSRHYTHMIAS
🔹 A. Bradyarrhythmias (Slow HR <60 bpm)
Sinus bradycardia
AV blocks (1st, 2nd, 3rd degree)
Junctional rhythm
🔹 B. Tachyarrhythmias (HR >100 bpm)
Supraventricular Tachycardia (SVT)
Atrial Fibrillation (AF)
Atrial Flutter
Ventricular Tachycardia (VT)
Ventricular Fibrillation (VF)
🔹 C. Irregular Rhythms
Premature Atrial Contractions (PACs)
Premature Ventricular Contractions (PVCs)
Atrial/Ventricular Bigeminy or Trigeminy
🧬 4. PATHOPHYSIOLOGY
Cardiac rhythm is generated by the SA node, conducted through the AV node, Bundle of His, and Purkinje fibers. Dysrhythmias occur due to:
Abnormal automaticity – SA node not firing correctly
Ectopic pacemakers – Other cells generate impulses
Re-entry circuits – Impulses circle through tissue (e.g., SVT)
Conduction block – Delay or loss of signal (e.g., AV block)
Sinus bradycardia is a type of cardiac arrhythmia characterized by a sinus rhythm with a heart rate less than 60 beats per minute (bpm), originating from the sinoatrial (SA) node.
📌 It may be normal (physiological) in athletes and during sleep, or abnormal (pathological) when it leads to symptoms like dizziness, fatigue, or syncope.
⚠️ 2. CAUSES
Category
Examples
🧘 Physiological
Athletes, during sleep, meditation
💊 Medications
Beta-blockers, digoxin, calcium channel blockers
⚡ Electrolyte imbalances
Hyperkalemia, hypothermia
💔 Cardiac conditions
MI (especially inferior wall), sick sinus syndrome, myocarditis
Sinus Tachycardia is a sinus rhythm with a heart rate greater than 100 beats per minute (bpm), originating from the SA (sinoatrial) node, maintaining a normal P wave, PR interval, and QRS complex.
📌 It is usually a physiological response to stress, exercise, pain, fever, or anemia, but can also be pathological if persistent or symptomatic.
⚠️ 2. CAUSES
Category
Examples
🧘 Physiological
Exercise, anxiety, fever, pregnancy
🧃 Hypovolemia
Blood loss, dehydration
💊 Medications
Atropine, caffeine, epinephrine
🧠 Stress & pain
Physical or emotional
🦠 Infections
Sepsis, fever, systemic inflammation
❤️ Cardiac conditions
MI, CHF, pericarditis, PE
🩸 Anemia or hypoxia
Low O₂-carrying capacity
🩺 Endocrine
Hyperthyroidism, pheochromocytoma
🔢 3. TYPES OF SINUS TACHYCARDIA
Type
Description
✅ Physiological
Normal response (e.g., exercise, fever)
⚠️ Pathological
Due to disease (e.g., shock, anemia, sepsis)
🔄 Inappropriate Sinus Tachycardia (IST)
Persistent high HR without clear cause and often symptomatic
Atrial Flutter is a type of supraventricular tachycardia characterized by rapid, regular atrial contractions (250–350 beats/min) due to a re-entry circuit in the right atrium.
⚡ Although the atrial rate is very fast, not all impulses pass through the AV node, resulting in ventricular rates that are often regular and slower (e.g., 2:1, 3:1 conduction).
Supraventricular Tachycardia (SVT) is a rapid heart rhythm (>150 bpm) that originates above the ventricles, usually in the atria or AV node, and results in narrow QRS complexes.
📌 It is often sudden in onset and termination (paroxysmal), leading to palpitations, dizziness, and sometimes chest pain or syncope.
VF begins with multiple ectopic impulses in the ventricular myocardium.
These impulses cause rapid, erratic electrical activity, leading to:
No organized depolarization
No effective ventricular contraction
Zero cardiac output → no perfusion to brain and organs
Within seconds → loss of consciousness Within minutes → death unless treated rapidly with defibrillation.
🚨 4. SIGNS & SYMPTOMS
Symptom
Characteristics
❌ No pulse
Ventricles not contracting effectively
❌ No blood pressure
Complete pump failure
🧠 Loss of consciousness
Within seconds
🛑 No respiration
Agonal or absent breathing
🔉 No heart sounds
Silent on auscultation
📉 Sudden cardiac arrest
Collapse, cyanosis, death if untreated
🧪 5. DIAGNOSIS
Tool
Findings
📈 ECG
No P wave, no QRS complex
Irregular, chaotic waveform
Fibrillatory baseline with no identifiable rhythm | | 🧪 Cardiac enzymes | May be done post-resuscitation to detect MI | | 🧠 ABG | Severe acidosis if prolonged arrest | | 🧬 Electrolytes & drug levels | Evaluate for underlying cause |
🆘 6. EMERGENCY MANAGEMENT (ACLS)
VF is a shockable rhythm. Immediate action is critical.
Administer slowly IV; monitor Mg²⁺, reflexes, respiratory rate
Epinephrine
Sympathomimetic
↑ HR, contractility & vasoconstriction
VF, VT (pulseless), asystole, severe bradycardia
Tachycardia, hypertension, arrhythmias
Give per ACLS; monitor ECG/BP; central line preferred if continuous infusion
Dopamine
Inotrope / Vasopressor
Stimulates β1 receptors → ↑ HR & contractility
Bradycardia, hypotension, shock
Tachycardia, arrhythmias, angina
IV pump only; monitor HR, BP; use central line to prevent tissue necrosis
Procainamide
Antiarrhythmic (Class Ia)
Slows conduction & prolongs repolarization
AF, VT, WPW Syndrome
Lupus-like syndrome, hypotension, QT prolongation
Monitor ECG (QRS/QT), BP, CBC regularly
Sotalol
Beta-blocker + Class III
Slows HR & prolongs repolarization
AF, VT
Bradycardia, torsades, QT prolongation
Monitor QTc interval; adjust dose in renal impairment
✅ Nursing Summary Points:
Nursing Role
Key Actions
🔍 Monitor ECG
Watch for bradycardia, QT prolongation, block progression
🩺 Monitor vitals
HR, BP, SpO₂ before and after administration
💉 Administer IV safely
Use appropriate technique (e.g., fast push for adenosine, slow for amiodarone)
❌ Hold medications if needed
If HR < 50–60 bpm or BP < 90/60 mmHg
🧪 Check labs
Electrolytes, digoxin level, renal/liver panels
🗣️ Patient education
Purpose of medication, how to check pulse, signs of toxicity
📋 Documentation
Drug name, dose, time, rhythm pre/post, patient response
👩⚕️ COMMON NURSING MANAGEMENT OF CARDIAC DYSRHYTHMIAS PATIENT
🎯 Goals of Nursing Care:
Restore and maintain effective cardiac rhythm
Ensure adequate cardiac output and perfusion
Prevent complications such as stroke or cardiac arrest
Educate the patient for long-term self-care and compliance
Provide psychological support
🧾 I. NURSING ASSESSMENT
Focus Area
What to Monitor
💓 Cardiac rhythm
ECG strip/telemetry: rate, rhythm, PQRST patterns
📈 Vital signs
HR, BP, RR, SpO₂, temperature
🧠 Neurological status
LOC, confusion, stroke symptoms (especially in AF)
🫁 Respiratory status
Dyspnea, crackles, signs of HF
💧 Fluid balance
I&O, edema, daily weight
🧍 Activity tolerance
Fatigue, dizziness, syncope
🩺 II. COMMON NURSING DIAGNOSES
🫀 Decreased cardiac output related to abnormal heart rhythm
⚡ Risk for decreased perfusion related to ineffective circulation
🧠 Risk for injury (e.g., falls, syncope, stroke)
😰 Anxiety related to palpitations or fear of sudden death
❓ Deficient knowledge regarding disease, medications, and lifestyle
🩸 Risk for bleeding related to anticoagulant therapy (e.g., in AF)
🩹 III. NURSING INTERVENTIONS
🔷 A. Monitoring & Early Detection
Continuous ECG/telemetry monitoring
Monitor for:
Worsening rhythm (e.g., from SVT to VF)
Signs of low perfusion (cold extremities, low urine output)
Sudden changes in LOC or BP
🔷 B. Medication Management
Administer prescribed antiarrhythmics, rate/rhythm control, or anticoagulants
Watch for side effects: bradycardia, hypotension, QT prolongation, bleeding
Monitor INR if on warfarin
Educate on drug compliance and timing
🔷 C. Emergency Preparedness
Keep emergency equipment ready:
Defibrillator, crash cart, oxygen, suction
Be prepared for:
ACLS protocol if pulseless rhythm (VF, VT)
Synchronized cardioversion if unstable but with pulse
🔷 D. Oxygenation & Positioning
Administer oxygen if SpO₂ < 94%
Keep patient in semi-Fowler’s position to ease breathing
🔷 E. Patient Safety
Implement fall precautions (especially in bradycardia, dizziness, syncope)
Provide calm environment to reduce anxiety
Restrict activity during acute episodes
🔷 F. Patient & Family Education
Teach:
How to monitor pulse
Importance of medication adherence
Signs to report (palpitations, chest pain, fainting)
Dietary considerations (e.g., vitamin K and warfarin)
Use of vagal maneuvers (in SVT)
Educate about ICD or pacemaker care if applicable
📋 IV. EVALUATION CRITERIA
Goal
Expected Outcome
❤️ Rhythm stability
Normal sinus rhythm or controlled arrhythmia
🩸 Perfusion adequate
Stable vitals, good LOC, warm extremities
📉 No complications
No stroke, HF, bleeding, or arrest
📚 Knowledge improved
Verbalizes understanding of condition & meds
🧍 Safety maintained
No falls or injuries from syncope
✅ V. KEY REMINDERS FOR NURSES
Always assess the patient first, not just the monitor!
Be vigilant in post-cardioversion or post-defibrillation care
Understand drug indications and interactions
Support emotional needs — arrhythmias can be terrifying for patients
Encourage follow-up with cardiology and regular ECG monitoring
🫀 HEART BLOCK (ATRIOVENTRICULAR BLOCK)
Full Clinical Overview for Nursing and Medical Learning
🧠 1. DEFINITION
Heart block (also called atrioventricular block or AV block) refers to a delay or complete interruption in the conduction of electrical impulses from the atria to the ventricles via the AV node, bundle of His, or bundle branches.
🛑 This causes the atria and ventricles to beat out of sync, resulting in bradycardia, decreased cardiac output, or even asystole.
⚠️ 2. CAUSES
Category
Examples
💔 Cardiac diseases
MI (especially inferior/posterior), ischemic heart disease, cardiomyopathy, myocarditis
First-degree AV block is the mildest form of heart block, characterized by a delay (not a block) in the conduction of electrical impulses from the atria to the ventricles through the AV node, resulting in a prolonged PR interval on the ECG.
📏 PR interval > 0.20 seconds (5 small boxes on ECG) ⚠️ Every impulse still reaches the ventricles, but slower than normal.
ECG monitoring, educate patient, assess for progression
❌ No pacemaker needed
Unless part of a more complex conduction abnormality
🫀 SECOND-DEGREE HEART BLOCK
Type I (Wenckebach) & Type II (Mobitz II) (Definition | Causes | Types | Pathophysiology | ECG | Symptoms | Management | Nursing Care | Complications | Key Points)
🧠 1. DEFINITION
Second-degree AV block is a type of heart block in which some atrial impulses are not conducted to the ventricles, resulting in intermittently dropped QRS complexes.
⚠️ There are two types:
Type I (Wenckebach or Mobitz I) – progressive delay until one beat is dropped
Type II (Mobitz II) – sudden dropped beats with no warning
🔢 2. TYPES & ECG DIFFERENCES
Type
Description
ECG Features
Stability
Type I (Wenckebach)
Progressive PR interval lengthening until a QRS is dropped
Grouped beating, regularly irregular rhythm
Usually benign and transient
Type II (Mobitz II)
Fixed PR interval with sudden dropped QRS
Constant PR, intermittent non-conducted P waves
Serious – may progress to complete heart block
⚠️ 3. CAUSES
Type I
Type II
– Inferior MI
Vagal tone
Digoxin, beta-blockers
Sleep, athletes | – Anterior MI
Ischemia or fibrosis of conduction system
Post cardiac surgery
Autoimmune disorders (e.g., lupus) |
🧬 4. PATHOPHYSIOLOGY
Type I (Wenckebach):
Delay in AV node conduction → PR interval lengthens
Eventually, one atrial impulse fails to conduct → dropped QRS
After the dropped beat, the cycle repeats
Type II (Mobitz II):
Sudden failure of conduction without prior PR lengthening
Usually indicates damage below AV node (in His-Purkinje system)
High risk of progression to third-degree (complete) block
🚨 5. SIGNS & SYMPTOMS
Type I (Wenckebach)
Type II (Mobitz II)
Often asymptomatic
Dizziness, syncope
Mild bradycardia
Sudden fainting spells (Stokes-Adams attacks)
Fatigue, SOB
Severe bradycardia
Irregular pulse
May cause decreased cardiac output
🧪 6. DIAGNOSIS
Test
Findings
📈 ECG
Type I: Progressive PR prolongation → dropped QRS
Type II: Constant PR with dropped QRS without warning | | 📊 Holter monitor | For intermittent blocks | | 🧪 Blood tests | Electrolytes, TSH, digoxin levels | | 💉 Drug history | Identify AV-blocking meds (beta-blockers, CCBs, digoxin) | | 🧠 Echocardiography | To assess for structural heart disease or wall motion defects |
💊 7. MEDICAL MANAGEMENT
Type
Management
Type I (Wenckebach)
Often does not require treatment
Remove AV node-blocking drugs
Atropine IV if bradycardia is symptomatic
Observe and monitor | | Type II (Mobitz II) |
High risk → requires urgent intervention
Temporary pacing if symptomatic
Prepare for permanent pacemaker
Avoid AV node blockers |
🛠️ 8. SURGICAL / DEVICE MANAGEMENT
Procedure
Indication
🔋 Temporary pacing
For unstable Mobitz II or severe bradycardia
🫀 Permanent pacemaker
Always indicated in Mobitz II or symptomatic high-grade block
🚫 Avoid
AV-nodal blockers (e.g., beta-blockers, CCBs, digoxin) in Mobitz II
👩⚕️ 9. NURSING MANAGEMENT
🔷 A. Assessment & Monitoring
Continuous cardiac monitoring (ECG/telemetry)
Check vital signs, especially for bradycardia, hypotension
Assess for signs of syncope, confusion, poor perfusion
🔷 B. Emergency Preparedness
Keep defibrillator and temporary pacemaker ready
Administer atropine IV or dopamine infusion as per protocol
Prepare for cardiologist consultation or pacemaker insertion
🔷 C. Medication Safety
Hold AV-nodal depressants (digoxin, beta-blockers, CCBs)
Administer oxygen, fluids, or pressors if needed
Monitor electrolyte levels and correct imbalances
🔷 D. Patient Education
Teach about pacemaker (if placed)
Instruct on symptom reporting (lightheadedness, syncope)
Encourage regular follow-up and ECG monitoring
❗ 10. COMPLICATIONS
Complication
Description
⚠️ Progression to 3rd-degree block
Especially in Mobitz II
🧠 Syncope or falls
Due to sudden dropped beats
💀 Sudden cardiac arrest
If conduction stops completely
🔋 Pacemaker dependency
Post-implantation in Mobitz II
🩸 Complications from bradycardia
Heart failure, hypotension, fatigue
✅ 11. KEY POINTS – QUICK SUMMARY
🔑 Topic
Summary
📚 Definition
Intermittent failure of AV conduction (some P waves not followed by QRS)
🔢 Type I
PR interval gradually lengthens, then QRS dropped (usually benign)
❗ Type II
Fixed PR with sudden dropped QRS — dangerous!
📉 Symptoms
Fatigue, bradycardia, syncope, low BP
⚡ Management
Type I → observe; Type II → pacemaker
👩⚕️ Nursing care
ECG monitoring, hold AV-blockers, pacing readiness
Third-degree AV block, also called complete heart block, is a complete failure of electrical conduction between the atria and ventricles.
🔌 Atria and ventricles beat independently, with no relationship between P waves and QRS complexes. ❗ It is a life-threatening bradyarrhythmia and often leads to syncope, heart failure, or cardiac arrest.
⚠️ 2. CAUSES
Category
Common Causes
💔 Cardiac
Myocardial infarction (esp. inferior or anterior wall), cardiomyopathy, myocarditis
Patient verbalizes knowledge of meds and pacemaker care
✅ No complications
No arrest, stroke, or worsening block occurs
❗ IV. KEY NURSING TIPS
🧠 Always treat the patient, not just the monitor
⚠️ Watch for progression from 1st → 2nd → 3rd degree block
⛑️ Be pacing-ready in Mobitz II and 3rd-degree blocks
❌ Avoid AV nodal blockers in higher-degree blocks
💬 Keep communication open with physician if symptoms or ECG worsen
🫀 Congestive Heart Failure (CHF)
Definition | Causes | Types
✅ 1. DEFINITION
Congestive Heart Failure (CHF) is a clinical syndrome in which the heart is unable to pump blood effectively to meet the metabolic demands of the body, resulting in inadequate tissue perfusion and fluid accumulation (congestion) in the lungs and/or peripheral tissues.
💡 It may involve failure of the left ventricle, right ventricle, or both, and leads to shortness of breath, fatigue, edema, and exercise intolerance.
⚠️ 2. CAUSES OF CHF
🔹 A. Cardiac Causes
Condition
Description
Coronary artery disease (CAD)
Most common cause; reduces oxygen supply to heart muscle
Myocardial infarction (MI)
Causes damage to the heart muscle
Hypertension (HTN)
Increases workload of the heart, leading to hypertrophy and dysfunction
Valvular heart diseases
Stenosis or regurgitation increases pressure and volume load
Arrhythmias (AF, VT)
Affect cardiac output
Cardiomyopathy
Dilated, hypertrophic, or restrictive heart disease
Often caused by left-sided failure or pulmonary conditions
Peripheral edema, ascites, hepatomegaly, JVD
B. Based on Ejection Fraction (EF)
Type
Description
EF (%)
Heart Failure with Reduced Ejection Fraction (HFrEF)
Systolic dysfunction – heart can’t pump
EF < 40%
Heart Failure with Preserved Ejection Fraction (HFpEF)
Diastolic dysfunction – heart can’t fill
EF ≥ 50%
Heart Failure with Mid-Range EF (HFmrEF)
Intermediate group
EF 41–49%
C. Based on Duration
Type
Description
Acute Heart Failure
Sudden onset of symptoms, often medical emergency
Chronic Heart Failure
Long-standing, gradually progressive condition
Acute-on-Chronic
Sudden worsening of chronic heart failure
🔬 4. PATHOPHYSIOLOGY OF CHF
🧠 Basic Mechanism:
When the heart fails to pump blood efficiently, the body activates compensatory mechanisms that initially maintain perfusion but eventually worsen heart failure.
🌀 Step-by-Step Pathophysiology:
🫀 Decreased Cardiac Output → due to ventricular dysfunction (systolic or diastolic)
🧠 Neurohormonal Activation:
↑ Sympathetic nervous system (SNS) → ↑ HR & vasoconstriction
↑ Renin-Angiotensin-Aldosterone System (RAAS) → sodium & water retention → ↑ blood volume
↑ Antidiuretic hormone (ADH) → fluid retention
💧 Fluid Accumulation:
Left-sided HF → pulmonary congestion
Right-sided HF → systemic venous congestion
🏋️ Ventricular Remodeling:
Hypertrophy & dilation of ventricles → worsens cardiac function over time
🫁 Resulting Problems:
Pulmonary congestion
Edema
Reduced organ perfusion
Progressive decline in cardiac output
🚨 5. SIGNS AND SYMPTOMS
🔹 A. Left-Sided Heart Failure (LHF)
System Affected
Symptoms
🫁 Respiratory
Dyspnea on exertion, orthopnea (difficulty breathing lying down), paroxysmal nocturnal dyspnea (PND), cough with frothy sputum, crackles
🫀 Cardiac
Fatigue, tachycardia, S3 gallop
🧠 Cerebral
Confusion, restlessness (due to ↓ perfusion)
🧍 General
Weakness, exercise intolerance
🔹 B. Right-Sided Heart Failure (RHF)
System Affected
Symptoms
🦵 Peripheral
Dependent edema (legs, ankles)
🧍 Abdominal
Hepatomegaly, ascites, anorexia, nausea
🧠 Systemic
Jugular venous distension (JVD), weight gain
💩 GI symptoms
Abdominal fullness, bloating
💡 RHF is often secondary to LHF due to backup of blood into the lungs.
🧪 6. DIAGNOSTIC EVALUATION
Test
Purpose / Findings
📈 ECG (Electrocardiogram)
Detect arrhythmias, MI, or left ventricular hypertrophy
🧪 BNP / NT-proBNP
Elevated in heart failure (>100 pg/mL); marker of severity
🧪 Serum Electrolytes
Check for Na⁺, K⁺ imbalances (due to diuretics or RAAS activation)
🧪 Renal Function (BUN, Creatinine)
Evaluates kidney perfusion & side effects of medications
Lifelong meds, lifestyle changes, regular monitoring, possible devices
🫁🫀 COR PULMONALE
(Definition | Causes | Types)
✅ 1. DEFINITION
Cor Pulmonale is a condition characterized by enlargement and failure of the right ventricle of the heart due to pulmonary hypertension caused by chronic diseases of the lungs or pulmonary vasculature.
Cor Pulmonale is caused by chronic lung diseases or pulmonary vascular conditions that lead to increased resistance in the pulmonary arteries (pulmonary hypertension), making the right side of the heart work harder.
🔹 A. Pulmonary (Lung) Causes
Disease
Description
Chronic Obstructive Pulmonary Disease (COPD)
Most common cause — includes emphysema, chronic bronchitis
Bronchiectasis
Chronic airway dilation and infection
Pulmonary fibrosis
Scarring of lung tissue
Chronic asthma
Long-standing uncontrolled asthma can lead to pulmonary pressure overload
Obstructive Sleep Apnea (OSA)
Causes hypoxia and pulmonary vasoconstriction
Tuberculosis (TB)
Advanced pulmonary TB damages lung vasculature
🔹 B. Pulmonary Vascular Causes
Condition
Description
Pulmonary embolism (PE)
Acute block in pulmonary arteries → sudden right heart strain
Primary pulmonary hypertension
Rare, progressive ↑ pressure in lung vessels
Recurrent thromboembolism
Chronic PE leads to persistent pulmonary hypertension
🔹 C. Chest Wall / Neuromuscular Disorders
Condition
Description
Kyphoscoliosis
Deforms thoracic cage, restricts lung expansion
Obesity Hypoventilation Syndrome
Hypoventilation due to excess weight
Neuromuscular diseases
E.g., muscular dystrophy impairing respiratory function
🔢 3. TYPES OF COR PULMONALE
Type
Description
Acute Cor Pulmonale
Sudden strain on the right ventricle, usually due to massive pulmonary embolism
Chronic Cor Pulmonale
Gradual onset due to long-standing lung disease like COPD; more common form
🔬 4. PATHOPHYSIOLOGY OF COR PULMONALE
🧠 Step-by-Step Mechanism:
Chronic lung disease (e.g., COPD) causes:
Alveolar hypoxia (↓ O₂)
Chronic inflammation and destruction of pulmonary capillaries
This leads to pulmonary vasoconstriction and loss of vascular bed
Resulting in increased pulmonary vascular resistance (PVR) → pulmonary hypertension
The right ventricle (RV) must work harder to pump blood into stiff pulmonary arteries
Over time, RV undergoes hypertrophy (muscle thickens) → then dilates and fails
Leads to systemic venous congestion (right-sided heart failure symptoms)
Oxygen therapy, bronchodilators, diuretics, steroids, treat underlying cause
🛠️ Advanced options
Long-term oxygen therapy, anticoagulants, transplant in end-stage
👩⚕️ Nursing role
Oxygen monitoring, fluid balance, medication administration, education on lifestyle changes
🚨 Emergency risk
Pulmonary embolism in acute cases or respiratory failure if decompensated
🫁 PULMONARY EDEMA
(Definition | Causes | Types)
✅ 1. DEFINITION
Pulmonary edema is a medical condition characterized by accumulation of fluid in the alveoli and interstitial spaces of the lungs, leading to impaired gas exchange and respiratory distress.
💡 It is often a life-threatening emergency if not treated promptly, especially in its acute form.
⚠️ 2. CAUSES OF PULMONARY EDEMA
Pulmonary edema can result from both cardiac (heart-related) and non-cardiac causes:
🔹 A. Cardiogenic Causes (due to increased pulmonary capillary pressure)
Cause
Description
Left-sided heart failure
Most common cause — LV fails to pump blood → backup in lungs
Head trauma, seizures increasing sympathetic activity
🔢 3. TYPES OF PULMONARY EDEMA
Type
Description
Common Causes
Cardiogenic Pulmonary Edema
Due to increased hydrostatic pressure in pulmonary capillaries from heart failure
LV failure, MI, hypertension, valve disease
Non-Cardiogenic Pulmonary Edema
Due to alveolar-capillary membrane damage or increased permeability
ARDS, sepsis, trauma, high altitude
Acute Pulmonary Edema
Sudden and severe form of fluid accumulation in lungs
Flash pulmonary edema in MI, hypertensive crisis
Chronic Pulmonary Edema
Develops gradually in chronic heart or kidney disease
CHF, renal failure
🔬 4. PATHOPHYSIOLOGY
Pulmonary edema occurs when fluid shifts from the pulmonary capillaries into the interstitial tissue and then into the alveoli, disrupting gas exchange.
📈 Step-by-Step Mechanism:
🔹 A. Cardiogenic Pulmonary Edema
Left ventricular dysfunction → blood backs up into the left atrium
↑ Pressure in pulmonary veins & capillaries
↑ Hydrostatic pressure forces fluid from capillaries into alveoli
Alveolar flooding → impaired oxygen diffusion
Leads to hypoxemia, dyspnea, and respiratory failure
Cardiogenic = ↑ PCWP & BNP; Non-cardiogenic = normal heart function
🚨 Emergency
Acute pulmonary edema is a life-threatening condition needing urgent care
📉 Prevention
Manage CHF, avoid fluid overload, treat infections early
🫀⚡ CARDIOGENIC SHOCK
(Definition | Causes | Types – With Visual Symbols & Full Explanation)
✅ 1. DEFINITION
🔴 Cardiogenic Shock is a life-threatening condition in which the heart fails to pump enough blood to meet the body’s demands, leading to inadequate tissue perfusion, cellular hypoxia, and multi-organ dysfunction.
🧠 It is most commonly a result of severe left ventricular failure, often due to acute myocardial infarction (AMI).
💥 2. CAUSES OF CARDIOGENIC SHOCK
🔹 A. 🫀 Cardiac Causes (Most Common)
🔍 Condition
🧠 Description
💔 Acute Myocardial Infarction (AMI)
🚨 Most common cause → massive damage to LV reduces contractility
💢 Severe Heart Failure (CHF)
Chronic weak heart becomes unable to maintain output
🩺 Arrhythmias
Tachycardia or bradycardia reduces effective cardiac output
🫀 Valvular Disease
Aortic or mitral stenosis/regurgitation leads to output obstruction or backflow
💉 Cardiomyopathy
Dilated or hypertrophic → poor contractility or restricted filling
🔩 Post-cardiac surgery
Temporary shock state post open-heart surgery
💔 Mechanical Complications of MI
Papillary muscle rupture → mitral regurgitation
Ventricular septal rupture → left-to-right shunt
Free wall rupture → pericardial tamponade
🔹 B. 🧬 Non-Cardiac Contributing Factors
💡 Factor
📌 Effect
🚫 Hypoxia
↓ Myocardial oxygen supply worsens pump failure
🧂 Electrolyte Imbalance
(K⁺, Ca²⁺) alters electrical and mechanical heart function
💥 The failing heart can’t handle the volume, causing:
Pulmonary congestion (backward failure)
Systemic hypoperfusion (forward failure)
🔄 Leads to vicious cycle of worsening hypoxia, ischemia, and multi-organ failure
🔄 Visual Chain:
MI or LV Failure ⬇ ↓ CO → ↓ BP ⬇ ↓ Organ Perfusion ⬇ Tissue Hypoxia & Acidosis ⬇ Further Myocardial Dysfunction ⬇ ⚠️ Shock Spiral → Multi-Organ Failure
Monitor vitals, oxygenation, urine output, mental status, prepare for ICU support
⚠️ Mortality
High without timely intervention (30–60%) — needs rapid action
📉 Goals
Restore CO, maintain perfusion, prevent organ failure, treat cause
🛡️ Prevention
Early MI treatment, CHF management, regular cardiac checkups
🫀💧 CARDIAC TAMPONADE
(Definition | Causes | Types)
✅ 1. DEFINITION
Cardiac Tamponade is a life-threatening medical emergency in which fluid (usually blood or effusion) accumulates in the pericardial sac, creating pressure that compresses the heart and prevents it from filling and pumping effectively.
🔁 Leads to ↓ Cardiac output, hypotension, and shock.
🧠 It’s not just about fluid — it’s about how fast it accumulates.
Slower accumulation over days or weeks → body compensates initially
Chronic Tamponade 🧍♂️
Long-standing effusion with signs of right heart compression
Regional Tamponade 📍
Localized fluid compressing only part of the heart
📌 Remember
Even a small amount of fluid (as little as 100 mL) can cause tamponade if it accumulates quickly, but the pericardium can stretch to hold >1000 mL if the fluid builds up slowly.
🔬 4. PATHOPHYSIOLOGY
Cardiac tamponade = Pressure buildup in the pericardial sac compresses the heart, especially the right atrium & ventricle → ↓ cardiac output → shock
🧠 Step-by-Step Mechanism:
💧 Fluid accumulates in the pericardial space (effusion or blood)
🧱 The non-stretchable pericardium gets tense
🫀 Compression first affects the right atrium and right ventricle → impaired diastolic filling
⬇️ ↓ Stroke volume and ↓ cardiac output
📉 Leads to hypotension, reflex tachycardia, and poor organ perfusion
🔁 The body activates compensatory mechanisms (↑ HR, vasoconstriction)
💥 If not relieved → shock, cardiac arrest, death
💡 Key Feature:
Even 100–200 mL of rapid fluid can cause tamponade.
Chronic tamponade may involve >1 liter if fluid accumulates slowly.
🚨 5. SIGNS AND SYMPTOMS
🩺 Classic Triad (Beck’s Triad)
🔍 Description
💓 Hypotension
Due to ↓ cardiac output
💉 Elevated Jugular Venous Pressure (JVD)
Due to backup of blood into venous system
🔇 Muffled (distant) Heart Sounds
Fluid insulates the heart
💡 Other Clinical Signs:
Symptom
Explanation
Symbol
😮💨 Tachypnea
To compensate for hypoxia
🫁
❤️ Tachycardia
Reflex to maintain CO
💓
📈 Pulsus Paradoxus
↓ SBP >10 mmHg during inspiration
⚠️
🧠 Anxiety, restlessness
From hypoxia
😰
🧍♂️ Weak peripheral pulses, cold extremities
↓ perfusion
❄️🖐️
🚽 Oliguria
↓ kidney perfusion
💧⬇️
🩸 Shock or cardiac arrest (late)
Life-threatening progression
🔥🚨
🧪 6. DIAGNOSTIC EVALUATION
🧪 Test
🩺 Findings / Purpose
📈 ECG
– Low voltage QRS
Electrical alternans (alternating QRS height) – specific finding | | 🧪 Chest X-ray | – May show enlarged cardiac silhouette in chronic tamponade
Often normal in acute cases | | 🧠 Echocardiogram (2D Echo) | ✅ GOLD STANDARD
Shows pericardial effusion, diastolic collapse of RA/RV
Detects even small amounts of fluid | | 💉 Cardiac Tamponade Panel | – ↑ Central venous pressure (CVP)
↓ Cardiac output/index
↓ BP
May show ↑ lactate (hypoperfusion) | | 💉 Pericardiocentesis (diagnostic + therapeutic) | – Withdraws fluid
Fluid sent for cytology, TB, culture, malignancy markers |
🫀💧 CARDIAC TAMPONADE
Medical & Surgical Management
💊 MEDICAL MANAGEMENT(Immediate Stabilization)
Drug / Therapy
Purpose / Action
Examples
Nursing Considerations
Oxygen Therapy
Improves oxygen delivery during hypoxia
Nasal cannula, mask, high-flow O₂
Monitor SpO₂, RR, ABG; elevate head
IV Fluids (Cautiously)
Temporarily ↑ preload to maintain BP until fluid is drained
NS, RL
Use small boluses to avoid overload
Vasopressors / Inotropes
Support BP and cardiac output
Dopamine, Norepinephrine, Dobutamine
Titrate carefully; monitor ECG, MAP, urine output
Analgesics / Anti-anxiety agents
Reduce pain, anxiety, O₂ demand
Morphine (if needed)
Monitor for respiratory depression; reduce stress
💡 Medical treatment is supportive and temporary — definitive treatment = fluid drainage.
🛠️ SURGICAL / PROCEDURAL MANAGEMENT
Procedure
Purpose / Indication
Nursing Considerations
🪡 Pericardiocentesis (Emergency)
Gold standard: Needle aspiration of pericardial fluid under echo/ECG guidance
– Continuous ECG + BP monitoring
Position patient 45–60° semi-Fowler’s
Watch for arrhythmias, pneumothorax, or bleeding | | 🚨 Emergency Thoracotomy | For traumatic cardiac tamponade or when pericardiocentesis fails | – Done in OR or ER under crash conditions
Decreased cardiac output related to mechanical compression of the heart
Ineffective tissue perfusion related to impaired oxygen delivery
Impaired gas exchange related to pulmonary congestion or hypoxia
Anxiety related to acute respiratory distress and life-threatening condition
Risk for fluid volume imbalance related to drainage procedures or shock
Risk for infection related to invasive procedures (pericardiocentesis)
🎯 C. PLANNING / GOALS
The patient will:
Maintain adequate cardiac output and BP
Exhibit normal respiratory rate and SpO₂ ≥ 90%
Demonstrate improved mental status and urine output
Report reduced anxiety
Be free from complications such as arrhythmias or infection
👩⚕️ D. INTERVENTIONS
🔹 1. Ensure Hemodynamic Stability
Monitor BP, MAP, HR, SpO₂, and ECG continuously
Administer IV fluids cautiously to maintain preload (as ordered)
Administer vasopressors/inotropes as prescribed (e.g., norepinephrine, dobutamine)
Prepare for emergency pericardiocentesis or thoracotomy
🔹 2. Support Oxygenation and Breathing
Administer supplemental oxygen to maintain SpO₂ ≥ 94%
Position patient in semi-Fowler’s or high-Fowler’s to ease breathing
Monitor ABGs and observe for signs of respiratory distress
🔹 3. Prepare for and Assist with Pericardiocentesis
Set up emergency tray with sterile supplies and ECG monitoring
Ensure IV access and crash cart availability
Monitor patient during and after the procedure:
Heart sounds, BP, SpO₂, and pulse quality
Watch for complications: arrhythmias, pneumothorax, bleeding
Send pericardial fluid for lab analysis: culture, cytology, TB markers
🔹 4. Manage Anxiety
Stay with the patient during episodes of distress
Use calm, reassuring tone and provide clear explanations
Administer anti-anxiety meds as prescribed (e.g., low-dose morphine if allowed)
🔹 5. Prevent and Monitor for Complications
Monitor urine output and renal function for early signs of hypoperfusion
Watch for signs of infection at drainage or surgical sites
Educate on reporting chest pain, SOB, bleeding, or fever
✅ E. EVALUATION
Goal
Expected Outcome
Cardiac output restored
Stable HR/BP, warm extremities, good capillary refill
Respiratory function maintained
SpO₂ ≥ 94%, RR normal, no dyspnea
Mental status normal
Oriented, no confusion, less anxious
No complications present
No infection, bleeding, or arrhythmias
Patient education effective
Patient verbalizes understanding of condition and follow-up needs
🫀🫁⚡ CARDIOPULMONARY ARREST
(Definition | Causes | Types)
✅ 1. DEFINITION
Cardiopulmonary arrest (CPA) is a sudden and complete cessation of effective cardiac and respiratory activity, resulting in loss of consciousness, absence of pulse, breathing, and circulation, which leads to death if not immediately treated.
🛑 It is a medical emergency requiring immediate CPR and advanced cardiac life support (ACLS) to prevent irreversible brain damage or death.
💥 2. CAUSES OF CARDIOPULMONARY ARREST
The causes are best remembered using the ACLS mnemonic “Hs & Ts” — helps identify reversible conditions during resuscitation.
🩺 A. “Hs” – 5 Reversible Causes
H 🔤
Cause
Explanation
🩸 Hypovolemia
Severe fluid or blood loss
🧊 Hypothermia
Core body temp < 30°C
💨 Hypoxia
Oxygen deficiency in lungs/tissues
🧪 Hydrogen ion (Acidosis)
Metabolic or respiratory acidosis
⚡ Hyper/Hypokalemia
Electrolyte imbalance affects heart rhythm
💉 B. “Ts” – 5 Reversible Causes
T 🔤
Cause
Explanation
🩸 Tension pneumothorax
Air in pleural space compresses heart/lungs
💔 Tamponade (Cardiac)
Fluid in pericardial sac compresses heart
🚑 Toxins
Drug overdose, poisonings (e.g., opioids, TCA)
🫀 Thrombosis (Pulmonary)
Massive pulmonary embolism
❤️ Thrombosis (Cardiac)
Acute myocardial infarction (MI)
🔢 3. TYPES OF CARDIOPULMONARY ARREST
🏷️ Type
⚡ Rhythm / Description
📋 Management Strategy
🟥 Ventricular Fibrillation (VF)
Chaotic, ineffective heart rhythm
Shockable – Immediate defibrillation
🟧 Pulseless Ventricular Tachycardia (VT)
Rapid wide QRS rhythm without pulse
Shockable – Defibrillation + CPR
🟨 Asystole
Flatline ECG – no electrical activity
Non-shockable – CPR + Epinephrine
🟩 Pulseless Electrical Activity (PEA)
ECG shows rhythm but no pulse
Non-shockable – CPR + identify cause
🟦 Respiratory Arrest only
Cessation of breathing, pulse still present
Support airway + rescue breathing (BLS)
📌 Remember:
🧠 Brain death begins within 4–6 minutes of CPA without oxygen. Immediate CPR + defibrillation saves lives!
🔬 4. PATHOPHYSIOLOGY
Cardiopulmonary Arrest occurs when both the heart and lungs suddenly stop working, resulting in the complete halt of blood circulation and gas exchange.
🧠 Step-by-Step Process:
💔 Cardiac function ceases → No effective contraction → No pulse
🫁 Respiratory arrest follows (or precedes in some cases) → No oxygen intake
🧠 ↓ Oxygen delivery to brain & vital organs
⬇️ Cerebral perfusion drops within seconds → loss of consciousness
🔁 Anaerobic metabolism starts → lactic acidosis and cellular injury
🕐 Brain damage begins within 4–6 minutes
🧠 Irreversible brain death in 8–10 minutes without CPR
🫀 Heart tissue begins to deteriorate → multi-organ failure → death
🔄 Chain Reaction Visual:
Cardiac/Respiratory Arrest ⬇ No circulation + No oxygen ⬇ Brain & organ hypoxia ⬇ Acidosis, organ failure, death
🚨 5. SIGNS & SYMPTOMS OF CARDIOPULMONARY ARREST
🧍 General Signs
💬 Details
💢 Sudden collapse
Often without warning
🧠 Unresponsiveness
No reaction to tapping or shouting
💨 Absence of breathing (Apnea)
No chest movement; gasping = ineffective
💓 No pulse (Cardiac arrest)
Check carotid or femoral pulse
🔻 Skin changes
Pale, cold, cyanotic (bluish)
👁️ Dilated pupils
Fixed and unreactive in later stages
💀 Flatline on monitor
Asystole or non-perfusing rhythm on ECG
🧪 6. DIAGNOSTIC EVALUATION (in-hospital or post-resuscitation)
🔬 Test
🩺 Purpose / Findings
📈 ECG / Cardiac monitor
Determines type of rhythm (VF, VT, PEA, Asystole)
🩸 ABG (Arterial Blood Gas)
Reveals severe acidosis, hypoxia (↓ PaO₂), ↑ CO₂
🧪 Serum electrolytes
Check for hyperkalemia, hypokalemia, Ca²⁺ imbalances
💉 Cardiac enzymes (Troponin, CK-MB)
To rule out acute MI as the cause
📊 Chest X-ray
Detects pneumothorax, effusion, or trauma
🧠 CT Brain / EEG(post-resuscitation)
Evaluate brain injury / hypoxic encephalopathy
🩺 Echo / Ultrasound (POCUS)
Rule out cardiac tamponade, PE, poor contractility
💧 Toxicology screen
If drug overdose suspected
🩸 Lactate level
Indicates severity of hypoperfusion
🩺 Diagnosis is Clinical First!
If a person is unresponsive, not breathing, and has no pulse → START CPR IMMEDIATELY. Don’t delay for equipment or tests.
💊 EMERGENCY MEDICAL MANAGEMENT (ACLS PROTOCOL)
Intervention
Purpose / Action
Examples / Drugs
Nursing Considerations
🚨 CPR (Cardiopulmonary Resuscitation)
Maintain circulation & oxygen delivery
Chest compressions (100–120/min), 2″ depth
High-quality CPR is priority #1
💨 Airway Management
Open airway, support breathing
Jaw thrust, oropharyngeal airway, suction
Maintain patency, watch for aspiration
🫁 Ventilation
Deliver oxygen to lungs
Ambu bag with O₂, intubation if needed
SpO₂ >94%, avoid over-ventilation
⚡ Defibrillation
Restore normal rhythm in shockable rhythms
Biphasic: 120–200J for VF/pulseless VT
Charge quickly; clear the patient before shock
💉 Epinephrine (1 mg IV/IO every 3–5 min)
↑ Coronary/cerebral perfusion; stimulates heart
All rhythms (VF, VT, PEA, Asystole)
Flush with 20 mL saline; monitor rhythm
💊 Amiodarone / Lidocaine
Antiarrhythmic; stabilizes rhythm
VF or pulseless VT refractory to shocks
Give after 3rd shock; monitor ECG
🧪 Treat Reversible Causes (Hs & Ts)
Correct underlying problems
Fluids, calcium, bicarbonate, antidotes
Based on suspected cause (e.g., PE, acidosis)
🔄 Rhythm Recheck every 2 min
Assess for return of circulation (ROSC)
ECG monitor
Do not interrupt CPR >10 sec
📌 Drug Summary Table
Drug
Indication
Dose
Epinephrine
All rhythms
1 mg IV/IO every 3–5 mins
Amiodarone
VF / pulseless VT
1st dose: 300 mg IV bolus, 2nd: 150 mg
Lidocaine
Alternate to Amiodarone
1–1.5 mg/kg IV
Atropine
For bradycardia (not asystole)
0.5 mg IV every 3–5 min (max 3 mg)
Magnesium Sulfate
Torsades de pointes
1–2 g IV over 5–20 mins
Sodium Bicarbonate
Severe acidosis or drug OD
1 mEq/kg IV
🛠️ SURGICAL / ADVANCED INTERVENTIONAL MANAGEMENT
Procedure
Purpose / Indication
Nursing Role / Considerations
Endotracheal Intubation
Secure airway if not breathing
Assist, confirm placement (ETCO₂, chest rise)
Advanced Airway Suctioning
Prevent aspiration & clear obstruction
Prepare suction, monitor oxygenation
Cardioversion(non-arrest rhythms)
Synchronized shock for unstable tachycardia
Done in VT with a pulse (not cardiac arrest)
Emergency Thoracotomy
For penetrating trauma causing arrest
OR procedure; high mortality but may save life
ECMO (Extracorporeal Membrane Oxygenation)
For refractory cardiac arrest (E-CPR)
ICU-level support; used in specialized centers
Post-ROSC PCI / Angioplasty
If cause is MI → revascularization
Prepare for Cath lab if ROSC achieved
Therapeutic Hypothermia (TTM)
Protect brain after ROSC
Cool to 32–36°C for 24 hrs; monitor vitals, electrolytes
🎯 GOALS OF MANAGEMENT
✅ Restore circulation, oxygenation, and perfusion ✅ Reverse underlying causes (Hs & Ts) ✅ Prevent organ damage (especially brain) ✅ Stabilize rhythm and hemodynamics ✅ Ensure safe recovery post-ROSC
👩⚕️ Nurse’s Role in Code Blue / Arrest
Initiate CPR immediately
Call code and prepare defibrillator
Start IV/IO line, administer drugs per order
Document time of arrest, interventions, meds given
Monitor response to treatment
Assist with intubation, ECG monitoring, post-ROSC care
👩⚕️🫀 NURSING MANAGEMENT OF CARDIOPULMONARY ARREST