UNIT 6 Nursing Management of patients with cardiovascular problems
๐ซ Anatomy & Physiology of the Cardiovascular System.
๐งฉ 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:
โค๏ธ Heart
๐ฉธ Blood vessels (arteries, veins, capillaries)
๐ Blood
๐ซ II. ANATOMY OF THE CARDIOVASCULAR SYSTEM
1๏ธโฃ โค๏ธ The Heart
๐ธ Location: Center of chest in mediastinum, tilted slightly left. ๐ธ Size: About the size of a fist. ๐ธ Weight: ~250โ350g
๐ท A. Structure of the Heart
Part
Description
๐น Chambers
4 chambers โ Right Atrium (RA), Right Ventricle (RV), Left Atrium (LA), Left Ventricle (LV)
๐น Valves
Ensure one-way blood flow:
โข Tricuspid (RAโRV)
โข Pulmonary (RVโPulmonary Artery)
โข Mitral/Bicuspid (LAโLV)
โข Aortic (LVโAorta)
๐น Layers of Heart Wall
โข Endocardium โ Inner layer
โข Myocardium โ Thick muscular middle layer
โข Epicardium โ Outer layer (also called visceral pericardium)
๐น Pericardium
A double-walled sac that surrounds & protects the heart. Contains lubricating pericardial fluid.
2๏ธโฃ ๐ฉธ Blood Vessels
There are three main types:
Type
Function
Feature
๐ฅ Arteries
Carry blood away from heart
Thick, muscular walls (high pressure)
๐ฆ Veins
Carry blood to the heart
Have valves, less pressure
๐จ Capillaries
Connect arteries and veins
Site of exchange (Oโ, COโ, nutrients, waste)
3๏ธโฃ ๐ Circulations of Blood
Circulation
Path
Function
๐ฌ๏ธ Pulmonary
Heart โ Lungs โ Heart
Exchanges COโ for Oโ
๐ Systemic
Heart โ Body โ Heart
Supplies oxygenated blood to tissues
โค๏ธ Coronary
Heart โ Heart muscle โ Heart
Feeds oxygen to myocardium itself
โ๏ธ III. PHYSIOLOGY OF THE CARDIOVASCULAR SYSTEM
๐น 1. ๐ Cardiac Cycle
The complete heartbeat from start to finish.
Phase
Activity
โค๏ธ Systole
Contraction โ Blood ejected
๐ Diastole
Relaxation โ Chambers refill with blood
โฑ Normal Heart Rate: 60โ100 bpm ๐ซ One cycle = ~0.8 seconds
๐น 2. โก Conduction System of the Heart (Electrical Impulse Pathway)
Node
Function
๐ธ SA Node (Sinoatrial)
Pacemaker of the heart (initiates impulse)
๐ธ AV Node
Delays impulse for atrial contraction
๐ธ Bundle of His
Conducts signal to ventricles
๐ธ Purkinje Fibers
Stimulate ventricular contraction
๐ ECG waves: P wave โ Atrial depolarization QRS complex โ Ventricular depolarization T wave โ Ventricular repolarization
๐น 3. ๐ Pathway of Blood Flow
๐ Systemic & Pulmonary Circulation Combined:
cssCopyEditBody โ ๐ฆ Superior/Inferior Vena Cava
โ โค๏ธ Right Atrium โ Tricuspid Valve โ Right Ventricle
โ Pulmonary Valve โ ๐ฅ Pulmonary Artery โ Lungs
โ ๐ฉ Pulmonary Veins โ Left Atrium โ Mitral Valve
โ Left Ventricle โ Aortic Valve โ Aorta โ Body
๐น 4. ๐ฉธ Cardiac Output (CO)
๐ Definition: Volume of blood pumped by heart per minute.
Assist with fall precautions if on antihypertensives causing dizziness
๐ 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
๐ SAMPLE NURSING CARE PLAN (Short Format)
๐งพ Nursing Diagnosis
Risk for Noncompliance related to lack of knowledge
๐ฏ Goal
Patient will verbalize understanding of HTN management in 2 days
๐ฉบ Interventions
1. Educate on meds, diet, exercise
Assess barriers to adherence
Involve family in care plan | | ๐ Evaluation | Patient correctly explains meds and demonstrates BP log |
โ I. COMPLICATIONS OF HYPERTENSION
Uncontrolled hypertension leads to target organ damage โ affecting the heart, brain, kidneys, eyes, and blood vessels.
๐ซ 1. Cardiovascular Complications
Complication
Description
โค๏ธ Left Ventricular Hypertrophy (LVH)
Thickening of heart muscle due to increased workload
๐ฅ Heart Failure
Heart becomes too weak to pump effectively
๐ข Myocardial Infarction (Heart Attack)
Due to coronary artery disease
๐ฉธ Aneurysm
Weakening and ballooning of artery walls
๐งฑ Peripheral Artery Disease (PAD)
Narrowing of peripheral arteries causing leg pain
๐ง 2. Cerebrovascular Complications
Complication
Description
๐ง Stroke (CVA)
Rupture or blockage of blood vessels in the brain
๐ช๏ธ Transient Ischemic Attack (TIA)
Mini-stroke; warning sign of a full stroke
๐ตโ๐ซ Cognitive Impairment
Memory loss, confusion due to poor brain perfusion
๐งฝ 3. Renal (Kidney) Complications
Complication
Description
๐งช Chronic Kidney Disease (CKD)
Damage to nephrons due to high pressure
๐ง Proteinuria
Protein leaks into urine (early sign of kidney damage)
๐ End-stage Renal Disease (ESRD)
May require dialysis or kidney transplant
๐๏ธ 4. Ocular Complications
Complication
Description
๐๏ธ Hypertensive Retinopathy
Damage to retinal blood vessels
๐ Blurred Vision or Vision Loss
Due to hemorrhage or swelling in retina
๐ II. KEY POINTS โ QUICK RECAP FOR STUDENTS
โ Definition: BP โฅ140/90 mmHg on 2 separate occasions โ Causes: Primary (90โ95%) or Secondary (5โ10%) โ Risk Factors: Genetics, obesity, high salt intake, stress, smoking โ Symptoms: Often silent; may present with headache, vision changes, dizziness โ Diagnosis: BP measurement, lab tests (renal, lipid), ECG, fundoscopy โ Management:
๐ง 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)
๐ 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
Monckebergโs
Medium arteries
Calcium in media, no obstruction
Aging, incidental finding
๐งฌ 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.
๐ Step-by-Step Mechanism (Especially in Atherosclerosis type)
Endothelial Injury โฎ Caused by hypertension, smoking, diabetes, or high cholesterol โฎ Leads to inflammation and damage of the inner lining (intima)
Foam Cell Formation โฎ Macrophages engulf oxidized LDL โ become foam cells โฎ Forms fatty streaks along artery walls
Plaque Development โฎ Smooth muscle cells migrate and multiply โฎ Collagen + lipids + cells = fibrous plaque forms โฎ Narrows artery, stiffens wall
Plaque Rupture & Clot Formation โฎ Plaque may rupture โ triggers platelet aggregation & thrombus (clot) โฎ Can cause sudden occlusion of blood flow โ heart attack or stroke
๐ In arteriolosclerosis (small vessels): wall thickens due to hyaline deposits or smooth muscle overgrowth ๐ In Monckebergโs sclerosis: calcium deposits in the media โ arteries harden but lumen stays open
๐จ II. SIGNS AND SYMPTOMS
โ Arteriosclerosis is often asymptomatic until significant narrowing or acute blockage occurs.
Raynaudโs Disease (also called Raynaudโs 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.
๐ก 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 Raynaudโs
๐ Systemic Lupus Erythematosus (SLE)
๐ฆด Rheumatoid Arthritis
๐ Scleroderma
๐ฆ Sjรถgrenโs Syndrome
๐ง Occupational trauma (vibration tools)
โ๏ธ Repeated cold exposure
๐ Certain medications (beta-blockers, chemotherapy)
๐ฌ Smoking
๐งช Thyroid disorders
๐น III. TYPES OF RAYNAUDโS
Type
Features
Notes
Primary Raynaudโs (Disease)
No identifiable cause
More common, less severe, symmetrical
Secondary Raynaudโs (Phenomenon/Syndrome)
Associated with other diseases
More severe, may cause ulcers, tissue damage
๐ Triggering Factors for Both Types:
Exposure to cold temperature
Emotional stress or anxiety
Use of vibrating tools
Smoking or caffeine use
๐งฌ I. PATHOPHYSIOLOGY OF RAYNAUDโS DISEASE
Raynaudโs 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 โฎ Reduces blood flow to fingers or toes โฎ Causes ischemia (lack of oxygen)
Triphasic Color Change:
Pallor (white) โ due to lack of blood flow
Cyanosis (blue) โ due to deoxygenated blood pooling
Rubor (red) โ reactive hyperemia when blood flow returns
Reperfusion โฎ When the vasospasm resolves, blood rushes back, leading to redness, burning, and throbbing pain
๐ In Secondary Raynaudโs, 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.
๐จ II. SIGNS AND SYMPTOMS
Symptom
Description
๐จ Color changes in fingers/toes
White (pallor) โ Blue (cyanosis) โ Red (hyperemia)
๐ง Cold sensation in fingers/toes
Especially with exposure to cold air/water
๐ช๏ธ Numbness or tingling
Due to reduced blood supply
๐ฅ Burning or throbbing pain
During the rewarming or reperfusion phase
๐ฆถ Stiffness or discomfort
In affected digits
โ ๏ธ Ulcers or sores (secondary type)
In severe or long-standing cases
โ Symmetrical involvement
Often seen in primary type
๐ฉ Asymmetrical + skin/tissue damage
Suggests secondary Raynaudโs
๐งช III. DIAGNOSIS OF RAYNAUDโS DISEASE
๐งพ 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)
๐งช B. Nailfold Capillaroscopy
Microscopic exam of capillaries at the base of the fingernail
Normal in primary Raynaudโs
Abnormal/damaged capillaries in secondary Raynaudโs (e.g., scleroderma)
๐ C. Blood Tests (for Secondary Raynaudโs)
Test
Purpose
๐งช ANA (Antinuclear Antibody)
Detect autoimmune diseases like lupus, scleroderma
๐งช ESR/CRP
Inflammation markers
๐งช Rheumatoid factor (RF)
For rheumatoid arthritis
๐งช CBC
To rule out anemia or infection
๐งช Thyroid function tests
Rule out hypothyroidism
๐ D. Cold Stimulation Test(Rarely used)
Measures how long it takes fingers to return to normal temperature after cold exposure
๐ I. MEDICAL MANAGEMENT
๐ฏ Goals:
Reduce the frequency and severity of attacks
Prevent tissue damage (especially in secondary cases)
Improve quality of life
๐น A. Lifestyle & Preventive Measures(First-line for ALL patients)
Intervention
Purpose
๐งค Keep warm
Wear gloves, socks, warm clothing in cold weather
โ๏ธ Avoid cold exposure
Use heated water, avoid AC, cold rooms
๐ฌ Stop smoking
Nicotine causes vasoconstriction
โ Avoid caffeine
Caffeine also triggers vasospasm
๐ Stress management
Relaxation techniques to prevent stress-induced attacks
๐ Regular exercise
Improves circulation and vascular health
๐ซ Avoid vibration tools
Can worsen symptoms (e.g., jackhammers, drills)
๐น B. Pharmacological Treatment
Used when lifestyle changes are not enough or in moderate to severe cases
1๏ธโฃ 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
2๏ธโฃ 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 Raynaudโs
Phosphodiesterase inhibitors
Sildenafil
Promote vasodilation in refractory cases
โ ๏ธ In Secondary Raynaudโs:
Also manage the underlying condition:
Scleroderma, SLE, RA, etc.
๐ฉบ II. SURGICAL / INTERVENTIONAL MANAGEMENT
๐ง Used in severe or treatment-resistant cases with risk of gangrene or ulceration
๐น A. Sympathectomy
๐ง Procedure:
Surgical interruption of sympathetic nerves that cause vasospasm
Can be digital (finger) or lumbar (lower limb)
๐ Indicated for:
Severe, disabling Raynaudโs
Tissue damage not responding to medications
Ulcers or risk of gangrene
๐ง Can be done:
Surgically (cutting nerves)
Chemically (nerve block)
Endoscopically (minimally invasive)
๐น B. Digital Artery Reconstruction or Bypass
For patients with severely narrowed vessels
Restores blood flow to affected digits
Rare and highly specialized
๐น C. Amputation
Last resort
In cases of irreversible tissue death (gangrene) in fingers or toes
๐ SUMMARY TABLE: MANAGEMENT OF RAYNAUDโS
Management
Examples
Used When
๐งค Lifestyle
Warm clothing, no smoking
Mild cases
๐ Medications
CCBs, alpha-blockers, SSRIs
Moderate cases
๐ IV prostacyclins
Iloprost
Severe secondary Raynaudโs
๐ฉป Surgery
Sympathectomy, arterial bypass
Refractory or gangrene
๐ฉโโ๏ธ NURSING MANAGEMENT OF RAYNAUDโS DISEASE
(For Clinical Care, Student Notes, and Exams)
๐ฏ 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
๐งโโ๏ธ I. NURSING ASSESSMENT
Assessment Area
Key Points
๐ง History
Onset, duration, frequency of attacks, triggers (cold/stress)
๐ฌ Symptoms
Pallor, cyanosis, redness in fingers/toes; pain, numbness
๐ Vital Signs
Especially temperature of affected extremities
๐ฉบ Circulation
Check peripheral pulses, capillary refill, color, temperature
๐ฆถ Skin
Look for ulcers, cracks, gangrene in fingers or toes
๐ง Psychosocial
Assess stress levels, anxiety, coping mechanisms
๐งพ II. COMMON NURSING DIAGNOSES
โ๏ธ Ineffective Peripheral Tissue Perfusion related to vasospasm
๐ฃ Acute Pain related to decreased oxygen supply during vasospasm
โ Knowledge Deficit related to disease process and self-care
โ ๏ธ Risk for Impaired Skin Integrity due to prolonged ischemia
๐ญ Risk for Noncompliance related to lack of motivation for lifestyle changes
๐ฉบ III. NURSING INTERVENTIONS
๐น 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
๐น 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
๐น 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
๐น D. Health Education
Topic
Content
โ๏ธ Cold Avoidance
Dress warmly, use hand warmers, avoid cold exposure
๐ซ Avoid triggers
No smoking, limit caffeine, manage stress
๐ Medication adherence
Explain purpose and side effects of vasodilators
๐ง Stress control
Deep breathing, yoga, meditation
๐ Exercise
Gentle aerobic activity improves circulation
๐ When to seek help
Worsening attacks, ulcers, or blackened fingertips
โ IV. EVALUATION CRITERIA
Goal
Expected Outcome
๐ฉธ Improve circulation
Warm, pink extremities with intact pulses
โ Reduce pain
Patient reports decreased frequency and intensity of attacks
๐ก๏ธ Prevent skin damage
No ulcers, intact skin, no gangrene
๐ Increase knowledge
Patient demonstrates understanding of self-care
โ๏ธ Ensure compliance
Patient adheres to medication and preventive care
๐ 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 |
โ I. COMPLICATIONS OF RAYNAUDโS DISEASE
Although often mild and manageable, severe or untreated cases, especially in secondary Raynaudโs, can lead to serious complications due to prolonged reduced blood flow (ischemia) to the extremities.
๐น 1. Digital Ulcers
Painful sores on fingertips or toes
Occur due to chronic ischemia
Difficult to heal and may become infected
๐น 2. Skin Infection (Cellulitis)
Occurs when ulcers or cracks allow bacteria entry
Can spread to deeper tissues
๐น 3. Gangrene
Tissue death due to prolonged lack of oxygen
May require amputation of affected finger or toe
More common in secondary Raynaudโs
๐น 4. Loss of Fingertip or Toe Tissue
Due to recurring or untreated episodes
Permanent damage from repeated ischemia
๐น 5. Decreased Hand Function
Due to stiffness, pain, or tissue loss
Affects activities of daily living (ADLs)
๐น 6. Psychological Impact
Anxiety about attacks
Embarrassment about hand appearance
Stress can worsen condition
โ II. KEY POINTS โ QUICK RECAP FOR NURSING STUDENTS
๐ Topic
๐ Key Point
โ Definition
Raynaudโs is a vasospastic disorder causing episodic constriction of small arteries in fingers/toes
โ๏ธ Triggers
Cold exposure, emotional stress
๐ Phases
White (pallor) โ Blue (cyanosis) โ Red (hyperemia)
๐ฉโโ๏ธ Types
Primary (idiopathic, mild) and Secondary (due to diseases like SLE, scleroderma)
๐งช Diagnosis
Based on history, nailfold capillaroscopy, and autoimmune blood tests
Keep extremities warm, prevent triggers, educate on self-care and ulcer prevention
โ ๏ธ Complications
Ulcers, infections, gangrene, amputation, decreased hand function
๐ฅ ANEURYSM
(Definition, Causes, and Types โ )
๐ง 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.
๐ก If left untreated, an aneurysm may enlarge and rupture, causing life-threatening internal bleeding.
Often silent โ may cause pain, pulsating mass, or neuro signs
๐งช Diagnosis
Ultrasound, CT angiography, MRI
๐ Medical management
BP control, statins, surveillance for small aneurysms
๐ ๏ธ Surgical options
Open repair, EVAR, clipping/coiling for cerebral aneurysms
๐ฉโโ๏ธ Nursing care
Monitor vitals, perfusion, bleeding; educate on lifestyle & warning signs
๐จ Major complication
Rupture โ shock โ death if untreated urgently
๐ฆต PERIPHERAL VASCULAR DISORDERS (PVDs)
(Definition, Causes, and Types โ )
๐ง 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.
๐ก PVDs impair blood circulation due to narrowing, blockage, or spasm of peripheral vessels.
๐ II. CAUSES / RISK FACTORS
Category
Common Causes
๐งฌ Non-Modifiable
โข Aging
โข Family history of vascular disease
โข Male gender
๐ ๏ธ Modifiable
โข Smoking ๐ฌ
โข Diabetes mellitus ๐
โข Hypertension ๐ข
โข High cholesterol ๐ณ
โข Obesity โ๏ธ
โข Sedentary lifestyle ๐
โข Stress ๐ฅ
๐ฆ Others
โข Infections (e.g., vasculitis)
โข Autoimmune diseases
โข Blood clotting disorders
๐ข III. TYPES OF PERIPHERAL VASCULAR DISORDERS
PVDs are broadly classified into two categories: ๐น Peripheral Arterial Disorders ๐น Peripheral Venous Disorders
๐ท 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
โ ๏ธ Complications
Gangrene, amputation, ulcers, PE, severe pain, limb loss
โค๏ธ CORONARY ARTERY DISEASES (CAD)
A Full Clinical & Nursing Overview
๐ง 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).
๐ด Reduced blood flow to the heart muscle โ chest pain (angina), heart attack (MI), or heart failure.
โ ๏ธ II. CAUSES / RISK FACTORS
๐น Modifiable Risk Factors:
๐ฌ Smoking
๐ Hypertension (HTN)
๐ High cholesterol (โ LDL, โ HDL)
โ๏ธ Obesity
๐ Physical inactivity
๐ท Alcohol use
๐ง Diabetes mellitus
๐ฅ Stress
๐น Non-Modifiable Risk Factors:
๐ด Age (men >45, women >55)
๐งฌ Family history of CAD
๐จ Male gender (higher early risk)
๐ข 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 โ heart muscle damage
Silent Ischemia
No symptoms; detected on ECG
Variant (Prinzmetalโs) Angina
Spasm of coronary artery causing temporary obstruction
๐งฌ IV. PATHOPHYSIOLOGY OF CAD
Endothelial injury (due to HTN, smoking, diabetes, etc.)
โ CAD = Blockage of coronary arteries due to atherosclerosis โ Risk factors include: smoking, HTN, diabetes, cholesterol, obesity โ Symptoms: chest pain, SOB, fatigue, sweating โ Diagnosis: ECG, cardiac enzymes, angiography โ Treatment: lifestyle + meds + PCI or CABG โ Nurses play a key role in monitoring, education, emotional support, and complication prevention
โค๏ธโ๐ฉน CORONARY ATHEROSCLEROSIS
(Definition, Causes, and Types โ Full Details)
๐ง 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.
๐งฌ Plaque is made up of cholesterol, fat, calcium, and cellular debris.
๐ 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)
๐ข III. TYPES OF ATHEROSCLEROTIC LESIONS IN CORONARY ARTERIES
Coronary atherosclerosis can vary by severity and stability of the plaque:
1๏ธโฃ Stable Plaque (Fixed Atherosclerosis)
Slowly growing, thick fibrous cap
Leads to stable angina
Less likely to rupture, but restricts blood flow
2๏ธโฃ Unstable Plaque (Vulnerable Plaque)
Thin fibrous cap, large lipid core
Prone to rupture โ triggers clot formation
Can cause acute coronary syndromes (e.g., MI, unstable angina)
3๏ธโฃ Calcified Plaque
Hard, brittle deposits of calcium
Reduces elasticity of arteries
Common in elderly patients
4๏ธโฃ Non-obstructive Atherosclerosis
Narrowing <50%, may be asymptomatic
Still carries risk of rupture and thrombus formation
๐งฌ 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.
๐ 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 โ become foam cells
Fatty Streak Formation
Early stage of plaque development
Foam cells accumulate โ form yellowish streaks in vessel wall
Fibrous Plaque Formation
Smooth muscle cells migrate and secrete collagen
A fibrous cap forms over the lipid core โ partial blockage of artery
Plaque Rupture & Thrombus Formation
Unstable plaques may rupture
Triggers platelet aggregation and clot formation (thrombus)
Can acutely block the artery โ Myocardial Infarction (MI)
๐ The gradual narrowing causes chronic ischemia, leading to angina. A sudden rupture causes acute coronary syndrome (e.g., unstable angina, MI).
๐จ II. SIGNS AND SYMPTOMS
Symptoms depend on degree of blockage, rate of progression, and presence of complications.
๐น Common Symptoms:
Symptom
Description
๐ข Chest pain (angina)
Squeezing, pressure, or heaviness, often radiating to jaw, arm, or back
๐ซ Shortness of breath
Especially on exertion
๐ Fatigue
Due to reduced oxygen to the myocardium
๐ Palpitations
Irregular or rapid heartbeat
๐ฆ Sweating (diaphoresis)
Often with angina or MI
๐คข Nausea or vomiting
Especially in MI
๐ฐ Anxiety
Common during angina or ischemia episodes
โ Asymptomatic
Common in diabetics or elderly (silent ischemia)
๐งช 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
๐ฉโโ๏ธ NURSING MANAGEMENT OF CORONARY ATHEROSCLEROSIS
(Clinical, Educational & Exam-Oriented)
๐ฏ 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
๐งพ I. NURSING ASSESSMENT
Area
What to Assess
๐ฉบ Vital Signs
BP, HR, RR, Oโ saturation
๐ Chest pain
Use PQRST:
P: Provocation
Q: Quality
R: Radiation
S: Severity
T: Time
๐ ECG Monitoring
Look for ST changes, arrhythmias
๐งช Lab values
Troponin, CK-MB, lipid profile
๐ง Psychosocial status
Anxiety, fear, stress level
๐ง Activity tolerance
Monitor for SOB or fatigue during ambulation
๐ฉบ II. NURSING DIAGNOSES
โ Ineffective Tissue Perfusion (cardiac) related to reduced coronary blood flow
๐ข Acute Pain related to myocardial ischemia
๐ Anxiety related to fear of death or unfamiliar environment
โ Deficient Knowledge related to disease condition and treatment
โ ๏ธ Risk for Decreased Cardiac Output related to electrical conduction changes or ischemia
๐ฉน III. NURSING INTERVENTIONS
๐ท A. Managing Chest Pain (Angina)
Action
Rationale
๐๏ธ Bed rest during pain
Reduces cardiac workload
๐ Administer nitrates (e.g., Nitroglycerin)
Vasodilation relieves ischemia
๐ Monitor ECG continuously
Detect arrhythmias or ischemic changes
๐ง Oxygen therapy if prescribed
Improves myocardial oxygenation
๐ฌ Stay with patient, reduce anxiety
Emotional support lowers Oโ demand
๐ท 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
๐ท C. Education for Lifestyle & Medication
Topic
Teaching Points
๐ฝ๏ธ Diet
Low saturated fat, low salt, high fiber
๐ Exercise
Daily walking, avoid overexertion
๐ญ Smoking
Strongly advise cessation
๐ Medications
Importance of daily use, side effects, and timing
๐ง Stress control
Relaxation techniques, counseling if needed
๐ Follow-up
Regular monitoring of BP, lipids, ECG
๐ท 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
โ IV. EVALUATION CRITERIA
Goal
Expected Outcome
๐ Relieve pain
Pain score โ, patient verbalizes relief
๐ซ Maintain perfusion
Stable vitals, no ECG changes, warm extremities
๐ง Reduce anxiety
Patient appears calm, understands plan
๐ Improve knowledge
Patient explains medications, lifestyle changes
๐ซ Prevent complications
No MI, arrhythmias, or readmission
๐ 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 0โ1 pain level, no ECG changes |
โ 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.
๐ด 1. Angina Pectoris
Stable angina: Predictable chest pain on exertion
Unstable angina: Occurs at rest; may precede heart attack (MI)
โค๏ธ 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
โก 3. Arrhythmias (Irregular Heart Rhythms)
Due to ischemia or infarction
Can include ventricular tachycardia or fibrillation (life-threatening)
๐ซ 4. Heart Failure
Chronic ischemia weakens the heart muscle
Results in reduced cardiac output, pulmonary congestion, and edema
๐ง 5. Stroke
A clot or plaque debris can travel to the brain
Causes ischemic stroke
๐ 6. Sudden Cardiac Death
Often due to fatal arrhythmia (e.g., ventricular fibrillation)
May occur without warning, especially in undiagnosed patients
๐ II. KEY POINTS โ QUICK RECAP
๐ Topic
Key Information
โ Definition
Plaque buildup in coronary arteries โ narrowed blood flow
โ Primary cause of CAD
Coronary atherosclerosis is the most common cause
๐ Main risk factors
Smoking, diabetes, HTN, high cholesterol, obesity, sedentary life
Monitor vitals, chest pain, ECG, provide medication, patient teaching
๐จ Complications
MI, arrhythmias, stroke, heart failure, sudden death
๐ ANGINA PECTORIS
(Definition, Causes, and Types)
๐ง 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.
๐ก Angina is a warning sign of underlying coronary artery disease (CAD).
๐ Pain typically occurs when the oxygen demand of the heart exceeds the supply, especially during exertion or stress.
โ ๏ธ II. CAUSES / RISK FACTORS
๐น Direct Causes:
Cause
Description
๐ฉธ Coronary Atherosclerosis
Narrowing of coronary arteries due to plaque buildup
๐ฅ Coronary artery spasm
Sudden temporary tightening of the artery wall
๐ฉบ Severe anemia
Less oxygen-carrying capacity of blood
๐ Tachycardia/arrhythmias
Increased heart demand, less coronary perfusion
๐ Aortic stenosis or hypertrophy
Increased workload on the heart
๐ง Emotional stress or cold exposure
Triggers increased heart demand
๐น Risk Factors (Same as CAD):
๐ฌ Smoking
๐ High cholesterol
โ๏ธ Obesity
๐ Diabetes mellitus
๐ข Hypertension
๐งฌ Family history of heart disease
๐ Sedentary lifestyle
๐ด Age (older adults more at risk)
๐ข III. TYPES OF ANGINA PECTORIS
1๏ธโฃ Stable Angina (Exertional Angina)
Most common type
Occurs predictably during exertion, stress, or excitement
Relieved by rest or nitroglycerin
Lasts a few minutes
2๏ธโฃ Unstable Angina
Occurs at rest or with minimal exertion
Unpredictable, more severe, lasts longer
Medical emergency โ precursor to myocardial infarction
Not relieved easily by rest or usual medications
3๏ธโฃ Variant Angina (Prinzmetalโs 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
4๏ธโฃ 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
5๏ธโฃ Silent Ischemia
No symptoms despite ischemia
Detected on ECG or stress tests
Common in diabetics and elderly
๐งฌ 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.
๐ 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 โ triggers nerve endings
Chest Pain/Discomfort Occurs
Usually relieved by rest or vasodilators (e.g., nitroglycerin)
๐ Important: Angina causes reversible myocardial changes; no permanent damage occurs unless ischemia progresses to infarction.
๐จ II. SIGNS & SYMPTOMS OF ANGINA PECTORIS
Symptom
Description
๐ข Chest pain
Pressure, squeezing, heaviness, or tightness in the chest
๐ Radiating pain
To jaw, neck, back, shoulders, or left arm
๐ง Cold sweat (diaphoresis)
Common during anginal episodes
๐ซ Shortness of breath
Especially with exertion
๐ซค Fatigue
Feeling of tiredness even with mild activity
๐คข Nausea or indigestion-like symptoms
More common in women
๐ฐ Anxiety or sense of doom
Often occurs with chest discomfort
โฐ Typical Angina Episode:
Duration: 2 to 10 minutes
Triggered by exercise, emotion, cold
Relieved by rest or nitroglycerin
๐ Unstable angina lasts longer, is more intense, and may occur at rest โ emergency!
๐งช III. DIAGNOSIS OF ANGINA PECTORIS
๐งพ A. History & Physical Exam
PQRST of pain
Risk factors (HTN, diabetes, smoking, etc.)
Assess vital signs and general condition
๐ฉบ 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
๐ C. Blood Tests
Test
Purpose
Troponin I/T, CK-MB
Normal in angina (โ only if MI occurs)
Lipid profile
Detects dyslipidemia
Blood sugar, HbA1c
Screen for diabetes
๐งช D. Stress Testing
Treadmill Test (TMT) โ provokes ischemia during exercise
Used to detect exercise-induced angina
๐ฅ๏ธ E. Imaging Studies
Test
Purpose
๐ง Echocardiography
Evaluates wall motion abnormalities
๐งช Myocardial Perfusion Scan
Visualizes blood flow to heart muscle
๐ฉบ Coronary Angiography
Gold standard for identifying blockages
๐ I. MEDICAL MANAGEMENT OF ANGINA
๐ฏ Goals:
Relieve chest pain
Improve coronary blood flow
Prevent progression to myocardial infarction (MI)
Reduce cardiac workload
Modify risk factors
๐น A. Lifestyle Modifications (Essential for all patients)
MI, arrhythmia, heart failure, stroke, sudden death
โค๏ธโ๐ฅ MYOCARDIAL INFARCTION (MI)
(Definition, Causes, and Types)
๐ง 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.
๐ด Caused by occlusion (usually by a blood clot) in one or more coronary arteries.
โ ๏ธ II. CAUSES / RISK FACTORS
๐น A. Immediate/Direct Causes
Cause
Description
๐ฉธ Atherosclerotic plaque rupture
Most common โ triggers thrombus formation
๐ฅ Thrombus formation
Clot blocks coronary artery
๐ Coronary artery spasm
Sudden, temporary tightening of the vessel
๐ซ Severe hypoxia/anemia
Decreases oxygen supply to the heart
โก High oxygen demand
In situations like fever, tachycardia, hyperthyroidism
๐น B. Predisposing Risk Factors
Modifiable
Non-Modifiable
๐ฌ Smoking
๐ด Age (men >45, women >55)
๐ Diabetes
๐งฌ Family history of CAD/MI
๐ข Hypertension
๐จ Male gender
๐ High cholesterol
โ
โ๏ธ Obesity
โ
๐ Sedentary lifestyle
โ
๐ท Alcohol, stress
โ
๐ข III. TYPES OF MYOCARDIAL INFARCTION
MI is classified based on ECG changes, location, and pathological features:
๐ท A. Based on ECG Changes
Type
Description
๐ฅ ST-Elevation MI (STEMI)
Complete blockage of a coronary artery
ST segment elevated on ECG
More severe, emergency
๐จ Non-ST Elevation MI (NSTEMI)
Partial blockage, less severe
No ST elevation, but elevated troponin
Still serious, requires urgent care
๐ท B. Based on Anatomic Location (seen on ECG & angiography)
Type
Infarct Location
Affected Artery
๐ซ Anterior MI
Front wall of left ventricle
Left Anterior Descending (LAD) artery
๐ซ Inferior MI
Lower wall of heart
Right Coronary Artery (RCA)
๐ซ Lateral MI
Lateral wall of LV
Circumflex artery
๐ซ Posterior MI
Back wall of heart
RCA or circumflex
๐ท C. Other MI Classifications
Type
Description
๐งช Silent MI
No obvious symptoms; seen in diabetics and elderly
๐ Type 1 MI
Due to plaque rupture and thrombus (classic heart attack)
๐ฅ Type 2 MI
Due to increased demand or decreased supply without clot (e.g., severe anemia, sepsis)
๐ฅ Type 4 & 5 MI
Related to PCI (Type 4) or CABG surgery (Type 5)
๐งฌ 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.
๐ Step-by-Step Pathophysiology:
Coronary Artery Narrowing (Atherosclerosis)
Fatty plaques develop in artery walls over time
Plaque Rupture or Erosion
The plaque surface breaks โ 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 โ pain
If untreated > 20โ30 min, necrosis (cell death) starts
Infarction and Loss of Function
Irreversible damage occurs in affected area
May lead to impaired contraction and arrhythmias
๐ The location and size of infarction depend on which artery is blocked and how long the blockage lasts.
๐จ II. SIGNS & SYMPTOMS OF MI
Symptoms may vary by age, gender, and comorbid conditions.
๐ด Classic Symptoms (Especially in STEMI):
Symptom
Description
๐ข Severe chest pain
Pressure/squeezing in chest >20 min, not relieved by rest
๐ Pain radiation
To jaw, neck, back, left arm, or shoulder
๐ฆ Sweating (diaphoresis)
Cold, clammy skin
๐ซ Shortness of breath
Due to decreased cardiac output or pulmonary congestion
๐คข Nausea/vomiting
Common, especially in inferior MI
๐ฐ Anxiety, fear, restlessness
“Impending doom” feeling
๐ง Cool, pale extremities
Due to vasoconstriction and poor perfusion
๐ Low BP and weak pulse
In cases of cardiogenic shock or heart failure
๐ง Atypical Presentations
Especially in elderly, women, and diabetics:
Fatigue
Indigestion
Dizziness
No chest pain (Silent MI)
๐งช III. DIAGNOSIS OF MYOCARDIAL INFARCTION
Diagnosis is based on clinical symptoms + ECG changes + cardiac biomarkers.
๐น A. Electrocardiogram (ECG)
Finding
Meaning
โฌ๏ธ ST elevation
Indicates STEMI
โฌ๏ธ ST depression/T wave inversion
Suggests NSTEMI or ischemia
โ Q waves
Sign of old MI (after 24โ48 hrs)
โ ECG should be done within 10 minutes of suspected MI.
๐น B. Cardiac Biomarkers
Test
Purpose
Timeline
๐งช Troponin I or T
Most sensitive & specific marker of MI
Rises in 3โ6 hrs, peaks at 12โ24 hrs, remains elevated for 7โ10 days
๐งช CK-MB
Useful in re-infarction monitoring
Rises in 4โ6 hrs, normal in 48โ72 hrs
๐งช Myoglobin
Earliest marker, but not specific
Rises in 1โ2 hrs, peaks at 6 hrs
๐น C. Other Diagnostic Tools
Tool
Use
๐ง Echocardiography
Assesses wall motion, pumping function, valve status
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 โ leading to impaired blood flow, pressure overload, or regurgitation.
Especially with atrial fibrillation or prosthetic valves
๐ฆ Infective endocarditis
Infection risk especially post-surgery
๐ฉธ Bleeding
From anticoagulant use
๐ Sudden cardiac death
Rare but possible with severe stenosis
๐ XI. KEY POINTS โ QUICK RECAP
โ Valvular disorders may be congenital or acquired โ Involve stenosis (narrowing) or regurgitation (leaking) โ Common causes: rheumatic fever, aging, infection, congenital anomalies โ Symptoms: murmurs, dyspnea, fatigue, edema, palpitations โ Diagnosis: echocardiography is key โ Treatment: medications, valve repair or replacement โ Nursing care focuses on fluid balance, symptom monitoring, education
โค๏ธโ๐ฉน MITRAL STENOSIS (MS)
Full Nursing and Clinical Overview
๐ง 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.
๐ฉบ Normally, the mitral valve orifice is 4โ6 cmยฒ. In MS, it may shrink to <2 cmยฒ.
โ ๏ธ II. CAUSES
๐น A. Most Common Cause:
๐ฆ Rheumatic fever (post-streptococcal infection) โ accounts for 90% of cases globally
๐น B. Other Causes:
Cause
Description
๐งฌ Congenital MS
Rare, valve malformation from birth
๐ฆ Infective endocarditis
Damages valve leaflets
๐ Radiation therapy
Fibrosis of valve
๐งช Autoimmune disorders
(e.g., SLE, rheumatoid arthritis) cause inflammation & thickening
๐ ๏ธ Calcification with aging
In elderly, less common than aortic stenosis
๐ข III. TYPES OF MITRAL STENOSIS
Type
Description
๐ฉบ Mild MS
Valve area > 1.5 cmยฒ โ usually asymptomatic
๐ฉบ Moderate MS
Valve area 1.0โ1.5 cmยฒ โ symptomatic with exertion
๐ฉบ Severe MS
Valve area < 1.0 cmยฒ โ 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
โ X. COMPLICATIONS
Complication
Description
๐ข Atrial fibrillation
Common in MS due to LA enlargement
๐ง Stroke
From emboli originating in fibrillating atrium
๐ซ Pulmonary edema
Due to back pressure from LA
๐ซ Right-sided heart failure
From long-standing pulmonary hypertension
๐ฆ Infective endocarditis
Risk due to damaged valve
๐ Bleeding
From anticoagulation therapy if not well monitored
๐ XI. KEY POINTS โ QUICK SUMMARY
โ Mitral stenosis = narrowing of mitral valve โ obstructed LA to LV flow โ Most commonly caused by rheumatic fever โ Symptoms: dyspnea, fatigue, A-fib, murmur, hemoptysis โ Diagnosed by echo, ECG, auscultation โ Treated with diuretics, beta-blockers, anticoagulants, and surgery (PBMV, MVR) โ Nurses should monitor for HF, A-fib, embolism, ensure medication adherence, and provide education
๐ MITRAL REGURGITATION (MR)
Comprehensive Clinical & Nursing Overview
๐ง 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).
๐ This causes volume overload in the left atrium and ventricle, leading to dilation, pulmonary congestion, and eventually heart failure.
โ ๏ธ II. CAUSES
๐น A. Primary MR (Structural Abnormality of Valve)
Cause
Description
๐ฆ Rheumatic heart disease
Causes thickening or retraction of valve leaflets
๐งฌ Mitral valve prolapse (MVP)
Leaflets bulge into LA during systole
๐ฆ Infective endocarditis
Destroys valve tissue
๐ง Degenerative changes (aging)
Leads to leaflet or chordae rupture
๐งช Congenital defects
Malformed leaflets or chordae
๐น B. Secondary MR (Functional)
Cause
Description
โค๏ธ Dilated cardiomyopathy
Stretches annulus, preventing proper closure
๐ Ischemic heart disease / MI
Damages papillary muscles or chordae tendineae
๐ข Hypertension
Long-standing pressure overload enlarges LV
๐ข III. TYPES OF MITRAL REGURGITATION
Type
Description
๐ Acute MR
Sudden onset, often due to chordae rupture or MI
โ Pulmonary edema, severe symptoms
๐ Chronic MR
Gradual onset due to progressive valve degeneration
โ May be asymptomatic for years
๐งฌ IV. PATHOPHYSIOLOGY
Mitral valve fails to close during systole
Blood leaks from LV โ LA
โ LA volume & pressure โ LA dilation
Backflow of blood โ pulmonary congestion
LV compensates by dilating to maintain output
Over time โ LV dysfunction, decreased cardiac output, and heart failure
๐จ V. SIGNS AND SYMPTOMS
Symptom
Explanation
๐ซ Dyspnea, orthopnea
Due to pulmonary congestion
๐ข Fatigue, weakness
Reduced cardiac output
๐ Palpitations
Due to atrial fibrillation or compensatory tachycardia
๐ Holosystolic murmur
Heard best at apex, radiates to axilla
๐จ Shortness of breath on exertion
Early sign of pulmonary involvement
๐ฆถ Peripheral edema, ascites
In late stages with right-sided HF
๐ Atrial fibrillation
Due to LA enlargement
๐ซ S3 heart sound
Indicates volume overload in LV
๐งช VI. DIAGNOSIS
Test
Purpose
๐ฉบ Auscultation
Systolic murmur at apex, may radiate to axilla
๐ง Echocardiography (2D/Doppler)
Gold standard โ shows regurgitant flow, LV/LA size
๐ ECG
Atrial fibrillation, LA enlargement, LV hypertrophy
๐ฉป Chest X-ray
LA and LV enlargement, pulmonary congestion
๐งช Cardiac catheterization
Pre-surgery assessment and to check coronary arteries
๐ VII. MEDICAL MANAGEMENT
Drug Class
Use
๐ง Diuretics
Reduce pulmonary congestion and edema
๐ ACE inhibitors / ARBs
โ Afterload and prevent remodeling
๐ Beta-blockers
Control heart rate, reduce myocardial oxygen demand
๐ Anticoagulants (Warfarin)
For atrial fibrillation to prevent emboli
๐ง Digoxin
Improves contractility in HF with A-fib
๐ฉธ Vasodilators
Reduce afterload and regurgitant volume
๐ ๏ธ VIII. SURGICAL MANAGEMENT
Procedure
Indications
๐ง Mitral valve repair
Preferred when feasible, preserves native valve
๐ Mitral valve replacement (MVR)
Indicated in severely damaged valves
โ Mechanical: lifelong anticoagulants
โ Bioprosthetic: fewer meds but limited durability
๐ Transcatheter repair (MitraClip)
Minimally invasive for high-risk surgical patients
๐ซ Treatment of underlying cause
CABG if ischemic cause, control of HTN or HF
๐ฉโโ๏ธ IX. NURSING MANAGEMENT
๐ Assessment:
Monitor VS, lung sounds, heart rhythm
Watch for signs of HF, A-fib, embolic events
๐ฉบ 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
โ X. COMPLICATIONS
Complication
Explanation
๐ข Heart failure
From chronic volume overload
โก Atrial fibrillation
Increases embolic stroke risk
๐ง Thromboembolism
Especially with A-fib
๐ซ Pulmonary hypertension
From backpressure into lungs
๐ Sudden cardiac death
Rare, but possible in severe MR
๐ฆ Infective endocarditis
Especially in damaged/prosthetic valves
๐ XI. KEY POINTS โ QUICK RECAP
โ Mitral regurgitation = backward flow from LV to LA due to valve incompetence โ Causes: MVP, rheumatic disease, ischemia, cardiomyopathy โ Symptoms: dyspnea, fatigue, murmur, A-fib โ Diagnosis: echocardiogram is gold standard โ Managed with diuretics, ACEIs, anticoagulants, valve repair/replacement โ Nurses monitor for HF, arrhythmias, embolism, and educate on meds and lifestyle
๐ TRICUSPID STENOSIS (TS)
Full Clinical & Nursing Overview
๐ง 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.
๐ฉบ It is less common than mitral or aortic valve disease and often occurs with mitral stenosis.
โ ๏ธ II. CAUSES
๐น A. Most Common Cause
๐ฆ Rheumatic heart disease (especially in combination with mitral valve disease)
๐น B. Other Causes
Cause
Explanation
๐ฆ Infective endocarditis
Especially in IV drug users
๐งฌ Congenital tricuspid atresia or stenosis
Rare birth defects
๐ Carcinoid syndrome
Tumor-secreted substances damage valve
โ ๏ธ Radiation therapy
Causes fibrosis of valve
๐ฉธ Pacemaker/ICD lead injury
Mechanical trauma to the tricuspid valve
๐ข III. TYPES OF TRICUSPID STENOSIS
Type
Description
๐ Isolated TS
Very rare; most often seen with other valve lesions
๐ Combined TS with TR
Tricuspid stenosis may progress to regurgitation due to valve fibrosis and annular dilation
๐งฌ IV. PATHOPHYSIOLOGY
Tricuspid valve narrows โ obstructs blood flow from RA to RV
Right atrial pressure increases โ RA dilation
Systemic venous congestion โฎ Blood backs up into veins โ hepatomegaly, ascites, peripheral edema
Assess for fatigue, decreased exercise tolerance, and fluid overload
Check daily weight, intake & output
๐ฉบ 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
๐ 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
โ X. COMPLICATIONS
Complication
Explanation
๐ข Right-sided heart failure
Due to prolonged RA pressure and systemic backup
โก Atrial fibrillation
From RA enlargement
๐ง Thromboembolism
Especially with A-fib and blood stasis in RA
๐ซ Pulmonary embolism
From venous thrombus
๐ฆ Infective endocarditis
Especially in IV drug users or with prosthetic valves
๐งช Liver congestion / cirrhosis
Chronic hepatic venous congestion
๐ XI. KEY POINTS โ QUICK SUMMARY
โ Tricuspid stenosis = narrowed tricuspid valve โ obstructed flow from RA to RV โ Most common cause: Rheumatic fever, often with mitral valve disease โ Key symptoms: edema, ascites, hepatomegaly, fatigue, diastolic murmur โ Diagnosis: Echo + auscultation + ECG/X-ray findings โ Treated with diuretics, salt restriction, and surgery if severe โ Nursing care: monitor fluid balance, hepatomegaly, heart rate, and provide education
๐ TRICUSPID REGURGITATION (TR)
Full Clinical & Nursing Overview
๐ง 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.
๐ This leads to right atrial volume overload, systemic venous congestion, and eventually right-sided heart failure.
โ ๏ธ II. CAUSES
๐น A. Primary TR (Structural Valve Abnormality)
Cause
Description
๐ฆ Rheumatic heart disease
Causes scarring and valve distortion
๐ฆ Infective endocarditis
Especially in IV drug users
๐งฌ Congenital malformations
Ebsteinโs anomaly
๐ฅ Trauma
Injury to chordae or papillary muscles
๐ Carcinoid syndrome
Causes fibrotic changes in valve leaflets
๐น B. Secondary (Functional) TR โ Most Common Type
Cause
Description
โค๏ธ Right ventricular dilation
Due to left-sided heart failure, pulmonary hypertension
๐ซ Dilated cardiomyopathy
Enlarged heart stretches tricuspid annulus
๐ RV infarction
Damages tricuspid valve support structures
๐ฉบ Pacing leads / ICD wires
Mechanical disruption of valve function
๐ข III. TYPES OF TRICUSPID REGURGITATION
Type
Description
๐ Acute TR
Sudden onset due to trauma, infective endocarditis, or RV infarction
๐ Chronic TR
Progressive annular dilation from RV overload (more common)
๐ Primary TR
Structural damage to valve leaflets or chordae
๐ Secondary TR
Functional valve incompetence due to annular dilation (common)
๐งฌ IV. PATHOPHYSIOLOGY
Tricuspid valve fails to close completely during systole
Assess for dyspnea, fatigue, RUQ pain, daily weight changes
๐ฉบ 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
๐ Patient Education:
Avoid excess salt/fluid intake
Importance of daily weight monitoring
Report signs of worsening HF (e.g., โ edema, breathlessness)
Dental hygiene and infection prevention (risk of endocarditis)
Lifelong cardiologist follow-up if prosthetic valve
โ X. COMPLICATIONS
Complication
Description
๐ข Right-sided heart failure
From chronic volume overload
โก Atrial fibrillation
Secondary to RA enlargement
๐ง Thromboembolism / stroke
From A-fib
๐งช Hepatic congestion / cirrhosis
From chronic liver venous congestion
๐ฆ Infective endocarditis
Especially in IV drug users or prosthetic valves
๐ซ Pulmonary hypertension
In long-standing cases or with left heart failure
๐ XI. KEY POINTS โ QUICK RECAP
โ Tricuspid regurgitation = backflow of blood from RV to RA during systole โ Most common cause: RV dilation (functional TR) โ Symptoms: edema, JVD, ascites, murmur, hepatomegaly โ Diagnosis: Echocardiogram, clinical signs, chest X-ray โ Management: Diuretics, salt restriction, valve repair/replacement โ Nurses monitor fluid balance, A-fib, liver function, and educate on compliance and follow-up
โค๏ธโ๐ฉบ AORTIC STENOSIS (AS)
Complete Clinical & Nursing Overview
๐ง 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.
๐ Normally, the aortic valve area is 2.5โ3.5 cmยฒ. In severe AS, it’s <1.0 cmยฒ.
โ ๏ธ II. CAUSES
๐น A. Congenital Causes
Bicuspid aortic valve (2 leaflets instead of 3)
Valvular dysplasia in infants/children
๐น B. Acquired Causes
Cause
Description
๐ง Degenerative (senile) calcification
Most common in elderly due to aging
๐ฆ Rheumatic heart disease
Causes commissural fusion and valve thickening
๐งฌ Radiation-induced fibrosis
Rare
๐ข III. TYPES OF AORTIC STENOSIS
Type
Description
๐ง Congenital AS
Often presents earlier in life
๐ด Degenerative AS
Calcification-related; common in older adults
๐ฆ Rheumatic AS
From post-streptococcal damage; often with mitral involvement
Minimally invasive, used in high-risk surgical patients
๐ Balloon Valvuloplasty
Temporary relief; used in children or bridging to TAVR/AVR
๐งฉ Ross procedure(young patients)
Pulmonary valve replaces aortic valve (autograft)
๐ฉโโ๏ธ IX. NURSING MANAGEMENT
๐ Assessment:
Monitor for dyspnea, chest pain, syncope
Check heart sounds, pulse quality, lung sounds
Monitor BP, HR, ECG, fluid balance
๐ฉบ Interventions:
Administer medications as prescribed
Keep patient in semi-Fowlerโs 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
๐ 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)
โ X. COMPLICATIONS
Complication
Description
๐ข Heart failure
Due to prolonged pressure overload
๐ง Syncope/injury
From decreased cerebral perfusion
โก Arrhythmias (A-fib, VT)
From hypertrophied or ischemic myocardium
๐งช Sudden cardiac death
Risk increases if untreated
๐ฆ Infective endocarditis
Particularly with calcified valves
๐ซ Pulmonary edema
Late-stage due to LV failure
๐ XI. KEY POINTS โ QUICK SUMMARY
โ Aortic stenosis = narrowed valve obstructs LV outflow โ Most common in elderly (degenerative) or congenital (bicuspid valve) โ Symptoms: angina, syncope, dyspnea โ Diagnosis: Echocardiogram = gold standard โ Treatment: Surgical replacement (AVR/TAVR) if severe/symptomatic โ Nurses monitor for HF, low output signs, safety, and pre/post-op care
โค๏ธโ๐ฉบ AORTIC REGURGITATION (AR)
Complete Clinical & Nursing Overview
๐ง 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).
๐ This leads to volume overload of the LV, causing dilation, hypertrophy, and eventually left-sided heart failure.
โ ๏ธ II. CAUSES
๐น A. Primary (Valvular) Causes
Cause
Description
๐ฆ Rheumatic heart disease
Post-streptococcal infection damaging valve
๐ฆ Infective endocarditis
Destroys valve leaflets
๐งฌ Congenital bicuspid aortic valve
Leads to early degeneration
๐ฅ Trauma or aortic dissection
Tears the valve or annulus
๐ง Senile calcification
Degeneration with aging
๐น B. Secondary (Aortic Root Disease) Causes
Condition
Description
๐ข Marfan syndrome, Ehlers-Danlos
Connective tissue disorders dilating aortic root
๐ฅ Ankylosing spondylitis, syphilis
Inflammatory or infectious aortitis
๐ Hypertension
Can dilate the aortic root and valve annulus
๐ข III. TYPES OF AORTIC REGURGITATION
Type
Description
๐ Acute AR
Sudden onset due to trauma, dissection, or endocarditis โ emergency
๐ Chronic AR
Gradual progression from degenerative or rheumatic disease
๐งฌ IV. PATHOPHYSIOLOGY
Aortic valve fails to close during diastole
Blood leaks from aorta โ LV
LV receives excess volume โ dilates and hypertrophies to maintain output
Over time, LV decompensation occurs โ โ ejection fraction, heart failure symptoms
Educate on low-sodium diet, activity restriction, and fluid balance
๐ 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
โ X. COMPLICATIONS
Complication
Description
๐ข Heart failure
Due to progressive LV dilation and dysfunction
โก Arrhythmias
Atrial fibrillation or ventricular arrhythmias
๐ง Embolic events
From LV thrombus or A-fib
๐ Sudden cardiac death
Especially in severe untreated cases
๐ฆ Infective endocarditis
Risk in damaged valves
๐ XI. KEY POINTS โ QUICK SUMMARY
โ Aortic regurgitation = backward flow from aorta to LV during diastole โ Causes: rheumatic disease, infective endocarditis, congenital defects, aortic root disease โ Symptoms: dyspnea, fatigue, wide pulse pressure, bounding pulse, diastolic murmur โ Diagnosis: Echo = gold standard โ Treatment: Vasodilators, surgery (AVR) if severe/symptomatic โ Nurses monitor fluid status, cardiac output, heart failure, and educate on meds, follow-up, and prevention
๐ PULMONARY STENOSIS (PS)
Complete Clinical & Nursing Overview
๐ง 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.
๐ The narrowing increases right ventricular pressure, leading to RV hypertrophy, and, if severe, right-sided heart failure.
โ ๏ธ II. CAUSES
๐น A. Congenital (Most Common)
Cause
Description
๐ถ Isolated congenital PS
Most common, due to malformed or fused valve leaflets
In very severe obstruction (especially in infants)
๐ฅ Palpitations
Due to RV strain or arrhythmias
๐ Harsh systolic ejection murmur
Best heard at left upper sternal border
Often accompanied by thrill and click
๐ง Jugular vein distention (JVD)
Sign of right-sided heart failure
๐ฆต Peripheral edema, hepatomegaly
From venous congestion
๐งช VI. DIAGNOSIS
Test
Findings
๐ง Echocardiography (2D & Doppler)
Gold standard โ shows valve anatomy, gradient, RV size
๐ฉบ Auscultation
Systolic murmur, ejection click
๐ ECG
Right ventricular hypertrophy, right axis deviation
๐ฉป Chest X-ray
Enlarged RV, post-stenotic dilation of pulmonary artery
๐ Cardiac catheterization
Confirms pressure gradient and evaluates for intervention
๐ VII. MEDICAL MANAGEMENT
Medical treatment is supportive, especially in mild cases.
Drug
Purpose
๐ง Diuretics (e.g., Furosemide)
For right heart failure symptoms
๐ Beta-blockers
May help reduce RV pressure and control rate
๐ Prophylactic antibiotics
For prevention of infective endocarditis (in some cases)
๐ฉธ Oxygen therapy
For cyanotic infants (if hypoxemia present)
๐ ๏ธ VIII. SURGICAL / INTERVENTIONAL MANAGEMENT
Procedure
Indication
๐ Balloon Valvuloplasty
First-line treatment in moderate to severe valvular PS
Minimally invasive, often curative
๐ง Surgical Valvotomy / Commissurotomy
For complex anatomy or failed balloon procedure
๐ Valve replacement
Rarely needed; in cases with severely deformed valves
๐งฉ Repair of associated defects
If PS is part of complex congenital heart disease
๐ฉโโ๏ธ IX. NURSING MANAGEMENT
๐ Assessment:
Monitor vital signs, heart and lung sounds, oxygen saturation
Assess for exercise intolerance, edema, cyanosis, fatigue
๐ฉบ 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)
๐ 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)
โ X. COMPLICATIONS
Complication
Description
๐ข Right ventricular hypertrophy and failure
From long-standing pressure overload
๐ง Arrhythmias
Due to RV strain
๐ Sudden cardiac death
Rare, but possible in untreated severe PS
๐ Cyanosis
From poor pulmonary circulation in infants
๐ฆ Infective endocarditis
If valve is damaged
๐ Pulmonary regurgitation
Post-balloon dilation or surgery
๐ XI. KEY POINTS โ QUICK SUMMARY
โ Pulmonary stenosis = narrowing of pulmonary valve โ obstructs blood flow from RV to lungs โ Most commonly congenital โ Symptoms: dyspnea, fatigue, murmur, cyanosis, right-sided HF signs โ Diagnosis: Echo is gold standard โ Treatment: Balloon valvuloplasty is first-line in moderate-severe cases โ Nursing role: Monitor symptoms, meds, educate parents/patient, prepare for interventions
๐ PULMONARY REGURGITATION (PR)
Full Clinical & Nursing Overview
๐ง 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).
๐ Leads to right ventricular volume overload, progressive RV dilation, and right-sided heart failure if severe and untreated.
โ ๏ธ II. CAUSES
๐น A. Primary (Valvular) Causes
Cause
Description
๐งฌ Congenital heart defects
e.g., Tetralogy of Fallot (post-repair), pulmonary valve dysplasia
๐ฆ Infective endocarditis
Valve destruction from infection
๐งฌ Carcinoid syndrome
Causes fibrotic deposits on valve leaflets
๐ Rheumatic heart disease
Less commonly affects pulmonary valve
๐น B. Secondary (Functional) Causes
Cause
Description
๐ Pulmonary hypertension
Causes annular dilation of the pulmonary valve
๐งช Post-balloon valvuloplasty
Over-dilation can damage valve
๐ง Connective tissue disorders
e.g., Marfan syndrome
๐งผ Iatrogenic causes
From surgical or catheter-based procedures
๐ข III. TYPES OF PULMONARY REGURGITATION
Type
Description
๐ Congenital PR
Associated with other defects like Tetralogy of Fallot
๐ Acquired PR
Due to conditions like pulmonary HTN, infections, or surgery
๐ Functional PR
Valve is structurally normal but doesn’t close due to annular dilation
Most patients with mild PR are asymptomatic and donโt require specific treatment. Moderate-to-severe PR may require medical or surgical intervention.
Treatment
Purpose
๐ง Diuretics (e.g., Furosemide)
Reduce preload and congestion
๐ ACE inhibitors / Beta-blockers
Used in RV dysfunction or HF
๐งช Treat underlying cause
Control pulmonary hypertension, infections
๐ฆ Prophylactic antibiotics
May be needed post-valve surgery or for certain congenital conditions
๐งฌ Oxygen therapy
In case of cyanosis or hypoxemia
๐ ๏ธ VIII. SURGICAL / INTERVENTIONAL MANAGEMENT
Procedure
Indications
๐ Pulmonary Valve Replacement (PVR)
For severe symptomatic PR or progressive RV dilation
Watch for signs of right-sided heart failure (e.g., JVD, hepatomegaly, ascites)
๐ฉบ 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
๐ 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
โ X. COMPLICATIONS
Complication
Description
๐ข Right ventricular failure
Due to chronic volume overload
โก Arrhythmias
e.g., atrial flutter, ventricular tachycardia
๐ง Thromboembolism
Due to atrial fibrillation or sluggish flow
๐ Sudden cardiac death
Rare, but possible in severe untreated cases
๐ฆ Infective endocarditis
Risk in damaged or prosthetic valves
๐ XI. KEY POINTS โ QUICK SUMMARY
โ Pulmonary regurgitation = backflow of blood from pulmonary artery to RV during diastole โ Most often caused by congenital defects or pulmonary hypertension โ Symptoms: fatigue, JVD, edema, hepatomegaly, murmur โ Diagnosed by echocardiography (Doppler), ECG, chest X-ray โ Treatment: diuretics, valve replacement, management of underlying cause โ Nursing care includes fluid monitoring, medication administration, patient education
๐ฉโโ๏ธ COMMON NURSING MANAGEMENT OF VALVULAR HEART DISEASES
(Applies to Mitral, Aortic, Tricuspid, and Pulmonary Valve Disorders)
Stable HR/BP, good capillary refill, strong pulses
๐ง Enhance activity tolerance
Performs ADLs without fatigue
๐๏ธ Manage fluid volume
No edema, weight stable, normal I&O
๐ Adhere to therapy
Takes meds, reports for INR testing
๐ Understand condition
Verbalizes knowledge about disease and care plan
โ V. COMPLICATIONS TO MONITOR FOR
Heart failure
Atrial fibrillation
Embolic events (stroke, MI)
Infective endocarditis
Sudden cardiac death
Bleeding from anticoagulants
๐ KEY POINTS SUMMARY
โ Valvular diseases โ disrupt forward blood flow, leading to heart failure โ Assessment, medication adherence, and education are cornerstones of care โ Echocardiogram is the key diagnostic tool โ Nurses play a vital role in early detection of complications, symptom control, and patient empowerment
โค๏ธโ๐ฅ RHEUMATIC HEART DISEASE (RHD)
Definition, Causes, and Types
๐ง 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.
๐ฆ It primarily affects the mitral and aortic valves, causing stenosis, regurgitation, or both.
โ ๏ธ II. CAUSES
๐ท Primary Cause
Untreated or inadequately treated Group A beta-hemolytic Streptococcal (GAS) pharyngitis (strep throat) โ Leads to autoimmune response โ Causes inflammation of heart, joints, skin, and brain โ Repeated attacks cause progressive scarring and deformity of heart valves
๐น Risk Factors
Factor
Explanation
๐ง Children aged 5โ15 years
Most vulnerable age group
๐งซ Poorly treated strep throat
No or inadequate antibiotics
๐ง Overcrowded living conditions
Increases risk of GAS infection
๐ฐ Low socioeconomic status
Limited access to healthcare
๐ Recurrent streptococcal infections
Increases risk of rheumatic fever and RHD
๐ข III. TYPES OF RHEUMATIC HEART DISEASE
Type
Description
๐ Valvular RHD(most common)
Damage and deformation of heart valves, especially:
Mitral valve โ stenosis and/or regurgitation
Aortic valve โ less commonly involved | | ๐ซ Myocardial RHD | Inflammation of heart muscle (myocarditis) during rheumatic fever; may lead to cardiomegaly | | ๐ฉบ Pericardial RHD | Inflammation of the pericardium (pericarditis) โ rare, may cause pericardial effusion | | โป๏ธ Mixed RHD | Involvement of more than one valve or cardiac layer (pancarditis) in severe cases |
๐งก Most Common Type
Mitral Stenosis (narrowing of mitral valve due to chronic inflammation and scarring)
โค๏ธโ๐ฅ RHEUMATIC HEART DISEASE (RHD)
Part 2: Pathophysiology, Signs & Symptoms, Diagnosis
๐งฌ 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).
๐ 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 bodyโs own tissues, especially the:
Heart (valves, myocardium, pericardium)
Joints
Skin
Central nervous system
Leads to inflammation (pancarditis) and damage:
Valve inflammation (valvulitis) โ leaflet thickening, fibrosis, and scarring
Chordae tendineae shorten โ 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).
๐ It can be acute, subacute, or chronic, and may lead to constrictive pericarditis if not managed properly.
โ ๏ธ II. CAUSES
Pericarditis can be idiopathic (unknown cause) or secondary to various infections, injuries, or systemic diseases.
๐น A. Infectious Causes
Type
Examples
๐ฆ Viral (most common)
Coxsackievirus, echovirus, HIV, influenza
๐งซ Bacterial
Tuberculosis (TB), staphylococcus, streptococcus
๐ Fungal
Histoplasmosis, aspergillosis
๐ชฑ Parasitic
Rare, e.g., toxoplasmosis
๐น B. Non-Infectious Causes
Type
Examples
๐ Myocardial infarction
Post-MI pericarditis (early) or Dresslerโs syndrome (late, autoimmune)
Blood in pericardial sac (e.g., TB, malignancy, trauma)
๐งฌ I. PATHOPHYSIOLOGY
The pericardium is a double-layered sac (parietal and visceral) that surrounds the heart. It normally contains a small amount (~15โ50 mL) of lubricating fluid.
๐ Pathological Process in Pericarditis:
Trigger (infection, injury, autoimmune, etc.) โฎ Initiates inflammation of the pericardial layers
Vascular permeability increases โฎ Leads to exudation of fluid, proteins, and inflammatory cells
Depending on the cause:
Fibrin deposits โ “Dry” or fibrinous pericarditis
Fluid accumulation โ pericardial effusion
Pus โ purulent pericarditis
Blood โ hemorrhagic pericarditis
Persistent inflammation โ pericardial thickening, scarring, and adhesions
In chronic or severe cases: โฎ Pericardium becomes rigid โ restricts diastolic filling of heart โฎ Leads to constrictive pericarditis
๐จ II. SIGNS AND SYMPTOMS
Symptoms can vary based on type, cause, and severity.
๐ท Common Symptoms of Acute Pericarditis:
Symptom
Description
๐ข Sharp, pleuritic chest pain
Sudden onset, worsens with deep breathing, coughing, or lying flat
Improves when sitting up and leaning forward
๐ฉบ Pericardial friction rub
Scratchy, high-pitched sound heard with stethoscope at LLSB (lower left sternal border)
โ Remember: Pericarditis may appear similar to myocardial infarction, but the ECG, pain pattern, and patient position help differentiate them!
โค๏ธโ๐ฅ MYOCARDITIS
Definition, Causes, and Types
๐ง I. DEFINITION
Myocarditis is an inflammation of the myocardium, the muscular middle layer of the heart wall, which can impair the heartโs ability to pump blood effectively and cause arrhythmias, heart failure, or even sudden cardiac death.
๐ฉบ 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.
โ ๏ธ II. CAUSES OF MYOCARDITIS
Myocarditis can have infectious, non-infectious, and autoimmune causes.
Allergic reaction to drugs (eosinophils present in biopsy)
๐ Chagas myocarditis
Caused by Trypanosoma cruzi parasite in endemic areas (Latin America)
๐งฌ 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.
๐ 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:
โ Contractility = โ 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
๐จ II. SIGNS AND SYMPTOMS
Symptoms of myocarditis can range from mild to life-threatening, and may mimic other cardiac conditions like acute coronary syndrome.
๐ท General Symptoms:
Symptom
Explanation
๐ก๏ธ Fever, fatigue, malaise
Often early, due to viral/inflammatory origin
๐ General weakness
Due to reduced cardiac output
๐ซ Shortness of breath (dyspnea)
Especially on exertion or lying flat (orthopnea)
๐ข Chest pain
May be sharp, pleuritic (inflammation-related) or mimic angina
Gold standard for visualizing inflammation, edema, and scarring of myocardium
๐ท Chest X-ray
May show cardiomegaly, pulmonary congestion
๐งช D. Definitive Diagnosis:
Endomyocardial biopsy (rarely done)
To detect inflammatory cell infiltrates, viral particles
Reserved for severe or unexplained cardiomyopathy
๐ I. MEDICAL MANAGEMENT OF MYOCARDITIS
The primary goals are to: โ Treat the underlying cause โ Support cardiac function โ Prevent or manage complications (e.g., heart failure, arrhythmias)
๐น A. General Measures
Measure
Purpose
๐ Bed rest
Decrease myocardial oxygen demand and reduce risk of arrhythmias
โณ Activity restriction
Especially important for athletes (for at least 3โ6 months)
๐ฅ Nutritional support
Heart-healthy diet, fluid restriction if needed
๐น B. Pharmacologic Therapy
Drug Class
Example
Purpose
๐ง Diuretics
Furosemide
Reduce pulmonary congestion and fluid overload
๐ ACE inhibitors / ARBs
Enalapril, Losartan
Improve cardiac output and reduce afterload
๐ Beta-blockers
Metoprolol, Carvedilol
Control heart rate and reduce myocardial workload
๐ข Antiarrhythmics
Amiodarone (if indicated)
For serious arrhythmias (PVCs, VT)
๐ Anticoagulants
Warfarin, Heparin
If patient develops atrial fibrillation or LV thrombus
๐งฌ Immunosuppressive therapy
Prednisone, Azathioprine
In autoimmune or giant cell myocarditis (under specialist care only)
๐ฆ Antivirals / Antibiotics
If specific infectious cause is identified (rarely effective in viral myocarditis)
๐น C. Advanced Therapies for Severe Cases
Therapy
Indication
๐ฉธ IV inotropes (e.g., Dobutamine, Milrinone)
Acute heart failure with poor perfusion
๐ IVIG (Intravenous Immunoglobulin)
Used in pediatric or autoimmune myocarditis (controversial in adults)
๐ก๏ธ Corticosteroids
In autoimmune or hypersensitivity myocarditis
๐ ๏ธ II. SURGICAL / INTERVENTIONAL MANAGEMENT
Reserved for severe, refractory, or end-stage myocarditis when medical management fails.
๐ A. Implantable Cardioverter Defibrillator (ICD)
Purpose
Use
Prevent sudden cardiac death due to ventricular arrhythmias
In patients with life-threatening arrhythmias or low EF <35% after 3 months of treatment
โก B. Temporary Pacing or Permanent Pacemaker
For heart block or bradyarrhythmias not responsive to medical therapy
Especially in conduction system involvement
๐ซ C. Mechanical Circulatory Support (MCS)
Device
Use
Intra-aortic balloon pump (IABP)
Supports cardiac output temporarily
Ventricular Assist Devices (VADs)
Bridge to recovery or transplant in end-stage heart failure
๐ซ D. Heart Transplant
Indication
Notes
End-stage heart failure unresponsive to all treatments
Last resort in fulminant or chronic myocarditis causing irreversible cardiomyopathy
Patient verbalizes understanding of illness, meds, and follow-up
โ ๏ธ Prevent complications
No arrhythmias, heart failure, or embolic events occur
โ I. COMPLICATIONS OF MYOCARDITIS
If not treated early, myocarditis can lead to serious and potentially life-threatening complications.
1. ๐ Heart Failure
Inflammation and damage to heart muscle weakens the pumping ability
Can lead to left-sided or biventricular failure
2. โก Arrhythmias
Electrical conduction system may be disrupted by inflammation
Can cause:
Atrial fibrillation
Ventricular tachycardia or fibrillation (sudden death risk)
Heart block
3. โค๏ธโ๐ฉน Dilated Cardiomyopathy (DCM)
Chronic myocarditis โ thinning and dilation of heart chambers
Results in progressive heart failure
4. ๐ง Thromboembolism / Stroke
Reduced heart function and chamber dilation may lead to clot formation
Can embolize to brain (stroke) or other organs
5. ๐ฉธ Cardiogenic Shock
In fulminant myocarditis, cardiac output drops dramatically
May lead to multi-organ failure and death
6. ๐ซ Sudden Cardiac Death
Due to ventricular arrhythmias or pump failure
Common in undiagnosed or untreated cases
๐ II. KEY POINTS โ QUICK RECAP
๐ Key Concept
Summary
๐ง Definition
Inflammation of the heart muscle (myocardium)
๐ฆ Most common cause
Viral infections (e.g., Coxsackievirus)
๐ฉบ Key symptoms
Fatigue, chest pain, dyspnea, palpitations
๐ ECG finding
ST-T changes, arrhythmias
๐งช Lab finding
โ Troponin, CRP, ESR, WBC
๐ง Gold standard imaging
Cardiac MRI
๐ First-line treatment
Supportive care + treatment of HF/arrhythmias
โ ๏ธ Major risks
Heart failure, arrhythmias, DCM, sudden death
๐ฉโโ๏ธ Nursing care focus
Cardiac monitoring, rest, medication, education
๐ฉบ Avoid in acute phase
Strenuous activity/exercise
๐ ENDOCARDITIS
Definition | Causes | Types
๐ง 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.
๐ฆ It can lead to valve destruction, emboli, and life-threatening complications if not treated promptly.
โ ๏ธ 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
๐ Subacute Infective Endocarditis
Slow onset, caused by less virulent organisms (e.g., S. viridans)
Usually affects damaged valves
๐ Prosthetic Valve Endocarditis (PVE)
Occurs on mechanical or bioprosthetic valves after surgery
๐ IV Drug-Associated Endocarditis
Commonly involves tricuspid valve, caused by S. aureus
๐ข Non-Infective Endocarditis (NBTE)
Sterile vegetations in malignancy, lupus, or hypercoagulable states
E.g., LibmanโSacks endocarditis in SLE
๐งฌ 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.
๐ 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 โ causing emboli.
Immune response + systemic effects:
Triggers inflammation, fever, and immune complex deposition (causing kidney or skin involvement).
๐จ II. SIGNS & SYMPTOMS
Signs depend on whether the condition is acute (sudden, severe) or subacute (gradual, milder).
๐ท General Symptoms:
Symptom
Explanation
๐ก๏ธ Fever and chills
Most common symptom; may be absent in elderly or immunocompromised
๐๏ธ Fatigue, weakness
Due to chronic infection and heart dysfunction
๐ Heart murmur
New or changed murmur due to valve damage
๐ฆต Night sweats, weight loss
Common in subacute form
๐ข Arthralgia, myalgia
From immune complex deposition
๐ฎโ๐จ Dyspnea
Due to heart failure if valve is severely damaged
๐ท Classic Clinical Signs(more specific to infective endocarditis):
Sign
Description
๐ด Petechiae
Small red/purple spots on skin, conjunctiva, palate
๐๏ธ Oslerโs nodes
Painful red nodules on fingers/toes (immune complex-mediated)
๐๏ธ Janeway lesions
Painless red spots on palms/soles (septic emboli)
๐๏ธ Roth spots
Retinal hemorrhages with pale centers
๐ Splinter hemorrhages
Thin, red to brown lines under nails
โ ๏ธ Complication Signs:
Sudden stroke (embolism to brain)
Hematuria (kidney infarcts)
Heart failure (valve destruction)
Sepsis or septic shock
๐งช III. DIAGNOSIS OF ENDOCARDITIS
๐ 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
๐งฌ B. Laboratory Tests
Test
Findings
๐ Blood cultures (ร3)
Gold standard โ positive for bacteria or fungi in multiple sets
๐งช CBC
โ WBCs (infection), anemia (chronic disease)
๐ฅ ESR / CRP
Elevated (inflammatory markers)
๐งซ Rheumatoid factor
May be positive due to immune activation
๐ฉธ Urinalysis
Hematuria or proteinuria (renal involvement)
๐ง Procalcitonin
May be elevated in bacterial infection
๐ท C. Imaging
Imaging
Purpose
๐ง Echocardiography (2D or TEE)
Confirms vegetations on valves
Transesophageal echo (TEE) is more sensitive than transthoracic (TTE)
๐ฉป Chest X-ray
May show cardiomegaly or pulmonary emboli
๐ ECG
May detect arrhythmias or conduction block (if abscess extends)
โ 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
๐ก๏ธ Prevention
Antibiotic prophylaxis for high-risk patients before dental/surgical procedures
๐ CARDIOMYOPATHIES
Definition | Causes | Types
๐ง I. DEFINITION
Cardiomyopathy refers to a group of diseases of the heart muscle (myocardium) that affect the heartโs size, shape, structure, and function, making it harder for the heart to pump blood efficiently.
๐ซ Cardiomyopathies may lead to heart failure, arrhythmias, valve problems, or sudden cardiac death, even in previously healthy individuals.
โ ๏ธ II. CAUSES OF CARDIOMYOPATHY
Cardiomyopathies can be genetic (inherited) or acquired (due to other diseases or external factors).
๐น A. Primary (Genetic / Idiopathic)
Cause
Explanation
๐งฌ 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
๐ Restrictive Cardiomyopathy (RCM)
Stiff myocardium restricts filling; often due to infiltrative diseases like amyloidosis or hemochromatosis
Normal size but impaired diastolic function
๐คฐ Peripartum Cardiomyopathy
Occurs in late pregnancy or postpartum period
Mimics dilated cardiomyopathy
๐ฉธ Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Fatty/fibrous replacement of right ventricular muscle; often genetic
Palpitations, syncope, risk of ventricular arrhythmias
๐งฌ 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.
๐น A. Dilated Cardiomyopathy (DCM)
Heart chambers (especially LV) become enlarged and weak
Risk of ventricular arrhythmias and sudden cardiac death
๐น 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
๐น D. Peripartum Cardiomyopathy
Similar to DCM, but occurs late in pregnancy or postpartum
Reduced ejection fraction, often reversible with early treatment
๐น E. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
Fatty/fibrous tissue replaces right ventricular muscle
โ Contractility and โ arrhythmogenic risk โ VT, sudden death
๐จ II. SIGNS AND SYMPTOMS
Symptoms may vary by type, but most forms share features of heart failure and reduced cardiac output.
โ General Symptoms of Cardiomyopathy:
Symptom
Cause
๐ฎโ๐จ Dyspnea on exertion
Pulmonary congestion
๐ Fatigue and weakness
โ Cardiac output
๐ฆต Peripheral edema
Right heart failure
๐ Palpitations / Arrhythmias
Electrical instability
๐ง Orthopnea, PND
Fluid accumulation when lying down
๐ง Syncope or dizziness
Poor perfusion or arrhythmia
๐ข Chest pain
Especially in HCM due to ischemia
โฐ๏ธ Sudden cardiac arrest
Risk in HCM and ARVC
๐ท Specific Signs by Type:
Type
Distinct Features
DCM
S3 gallop, enlarged heart, LV dysfunction
HCM
Harsh systolic murmur (โ 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
๐งช III. DIAGNOSIS OF CARDIOMYOPATHY
๐ A. History and Physical Exam
Ask about family history, recent pregnancy, alcohol/drug use, or viral illness
Check for murmurs, edema, lung crackles, hepatomegaly
๐ง B. Diagnostic Tests
Test
Purpose/Findings
๐ ECG
May show arrhythmias, LVH, ST-T changes
๐ง Echocardiogram (2D/3D)
Primary diagnostic tool:
Wall thickness, chamber size
EF %, valve function
Obstruction (in HCM) | | ๐ก Cardiac MRI | Detailed images of heart structure and scarring | | ๐ฉป Chest X-ray | Cardiomegaly, pulmonary congestion | | ๐งช BNP / NT-proBNP | โ in heart failure (DCM, RCM) | | ๐ Genetic testing | In familial cases (HCM, ARVC) | | ๐งช Cardiac enzymes | Rule out MI if chest pain is present | | ๐ Cardiac catheterization | Rule out ischemic cardiomyopathy | | ๐ฌ Endomyocardial biopsy | In suspected myocarditis or infiltrative causes
๐ I. MEDICAL MANAGEMENT
Treatment focuses on: โ Managing symptoms (especially heart failure) โ Preventing complications (arrhythmias, thromboembolism, sudden cardiac death) โ Addressing the underlying cause or type
๐น A. General Medications (All Cardiomyopathies)
Drug Class
Examples
Purpose
๐ ACE inhibitors / ARBs
Enalapril, Losartan
Reduce afterload, improve heart function
๐ Beta-blockers
Metoprolol, Carvedilol
Slow heart rate, reduce oxygen demand, control arrhythmias
๐ง Diuretics
Furosemide, Spironolactone
Relieve fluid overload and pulmonary congestion
๐ Anticoagulants
Warfarin, DOACs
Prevent emboli in A-fib or severe LV dysfunction
๐ข Antiarrhythmics
Amiodarone, Digoxin
Used for arrhythmias (ventricular or atrial)
๐ท 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
๐ ๏ธ II. SURGICAL / INTERVENTIONAL MANAGEMENT
Surgical treatment is considered in severe or unresponsive cases, or to prevent sudden cardiac death.
๐ 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 |
๐ง B. Pacemaker (PPM)
For bradycardia, heart block, or synchronization in heart failure (CRT: Cardiac Resynchronization Therapy)
๐ซ C. Surgical Myectomy(HCM)
Description
Indication
Resection of thickened septum
For patients with severe LVOT obstruction and refractory symptoms despite meds
๐ 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
โป๏ธ E. Left Ventricular Assist Device (LVAD)
Use
Purpose
End-stage DCM or other cardiomyopathy
Used as a bridge to transplant or destination therapy
๐ซ F. Heart Transplant
Indication
Notes
Severe end-stage heart failure unresponsive to all other treatments
Especially in younger patients or non-ischemic cardiomyopathy
๐ SUMMARY TABLE
Type
Medical Rx
Surgical Rx
DCM
HF meds + anticoagulants
ICD, LVAD, transplant
HCM
BBs, CCBs, antiarrhythmics
Myectomy, septal ablation, ICD
RCM
Diuretics, treat cause
Rarely surgical; transplant in advanced cases
ARVC
BBs, antiarrhythmics
ICD, ablation if needed
Peripartum
HF meds (safe in pregnancy)
Rarely transplant if severe
๐ฉโโ๏ธ NURSING MANAGEMENT OF CARDIOMYOPATHIES
Common in HCM & ARVC โ screen first-degree relatives
โค๏ธโ๐ฉน CARDIAC DYSRHYTHMIAS
(Also known as Cardiac Arrhythmias)
๐ง 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.
โ ๏ธ 2. CAUSES
Category
Examples
๐ง Electrolyte imbalance
โ Kโบ, โ Mgยฒโบ, โ Caยฒโบ
โค๏ธ Myocardial ischemia or infarction
Scarred or oxygen-deprived tissue disrupts conduction
๐ Drug toxicity
Digoxin, beta-blockers, antiarrhythmics
โก Conduction abnormalities
Bundle branch block, AV block
๐ Hypoxia or acidosis
From COPD, sleep apnea, etc.
๐งฌ Congenital defects
Long QT syndrome, WPW
๐ Stress or stimulants
Caffeine, anxiety, smoking
๐ ๏ธ Post cardiac surgery
Trauma to conduction pathways
๐ข 3. TYPES OF CARDIAC DYSRHYTHMIAS
๐น A. Bradyarrhythmias (Slow HR <60 bpm)
Sinus bradycardia
AV blocks (1st, 2nd, 3rd degree)
Junctional rhythm
๐น B. Tachyarrhythmias (HR >100 bpm)
Supraventricular Tachycardia (SVT)
Atrial Fibrillation (AF)
Atrial Flutter
Ventricular Tachycardia (VT)
Ventricular Fibrillation (VF)
๐น C. Irregular Rhythms
Premature Atrial Contractions (PACs)
Premature Ventricular Contractions (PVCs)
Atrial/Ventricular Bigeminy or Trigeminy
๐งฌ 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 โ SA node not firing correctly
Ectopic pacemakers โ Other cells generate impulses
Re-entry circuits โ Impulses circle through tissue (e.g., SVT)
Conduction block โ 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.
๐ It may be normal (physiological) in athletes and during sleep, or abnormal (pathological) when it leads to symptoms like dizziness, fatigue, or syncope.
โ ๏ธ 2. CAUSES
Category
Examples
๐ง Physiological
Athletes, during sleep, meditation
๐ Medications
Beta-blockers, digoxin, calcium channel blockers
โก Electrolyte imbalances
Hyperkalemia, hypothermia
๐ 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.
๐ It is usually a physiological response to stress, exercise, pain, fever, or anemia, but can also be pathological if persistent or symptomatic.
โ ๏ธ 2. CAUSES
Category
Examples
๐ง Physiological
Exercise, anxiety, fever, pregnancy
๐ง Hypovolemia
Blood loss, dehydration
๐ Medications
Atropine, caffeine, epinephrine
๐ง Stress & pain
Physical or emotional
๐ฆ Infections
Sepsis, fever, systemic inflammation
โค๏ธ Cardiac conditions
MI, CHF, pericarditis, PE
๐ฉธ Anemia or hypoxia
Low Oโ-carrying capacity
๐ฉบ Endocrine
Hyperthyroidism, pheochromocytoma
๐ข 3. TYPES OF SINUS TACHYCARDIA
Type
Description
โ Physiological
Normal response (e.g., exercise, fever)
โ ๏ธ Pathological
Due to disease (e.g., shock, anemia, sepsis)
๐ 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 (250โ350 beats/min) due to a re-entry circuit in the right atrium.
โก 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.
๐ 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 โ no perfusion to brain and organs
Within seconds โ loss of consciousness Within minutes โ death unless treated rapidly with defibrillation.
๐จ 4. SIGNS & SYMPTOMS
Symptom
Characteristics
โ No pulse
Ventricles not contracting effectively
โ No blood pressure
Complete pump failure
๐ง Loss of consciousness
Within seconds
๐ No respiration
Agonal or absent breathing
๐ No heart sounds
Silent on auscultation
๐ Sudden cardiac arrest
Collapse, cyanosis, death if untreated
๐งช 5. DIAGNOSIS
Tool
Findings
๐ ECG
No P wave, no QRS complex
Irregular, chaotic waveform
Fibrillatory baseline with no identifiable rhythm | | ๐งช Cardiac enzymes | May be done post-resuscitation to detect MI | | ๐ง ABG | Severe acidosis if prolonged arrest | | ๐งฌ Electrolytes & drug levels | Evaluate for underlying cause |
๐ 6. EMERGENCY MANAGEMENT (ACLS)
VF is a shockable rhythm. Immediate action is critical.
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
โ Nursing Summary Points:
Nursing Role
Key Actions
๐ Monitor ECG
Watch for bradycardia, QT prolongation, block progression
๐ฉบ Monitor vitals
HR, BP, SpOโ before and after administration
๐ Administer IV safely
Use appropriate technique (e.g., fast push for adenosine, slow for amiodarone)
โ Hold medications if needed
If HR < 50โ60 bpm or BP < 90/60 mmHg
๐งช Check labs
Electrolytes, digoxin level, renal/liver panels
๐ฃ๏ธ Patient education
Purpose of medication, how to check pulse, signs of toxicity
๐ Documentation
Drug name, dose, time, rhythm pre/post, patient response
๐ฉโโ๏ธ COMMON NURSING MANAGEMENT OF CARDIAC DYSRHYTHMIAS PATIENT
๐ฏ 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
๐งพ I. NURSING ASSESSMENT
Focus Area
What to Monitor
๐ Cardiac rhythm
ECG strip/telemetry: rate, rhythm, PQRST patterns
๐ Vital signs
HR, BP, RR, SpOโ, temperature
๐ง Neurological status
LOC, confusion, stroke symptoms (especially in AF)
๐ซ Respiratory status
Dyspnea, crackles, signs of HF
๐ง Fluid balance
I&O, edema, daily weight
๐ง Activity tolerance
Fatigue, dizziness, syncope
๐ฉบ II. COMMON NURSING DIAGNOSES
๐ซ Decreased cardiac output related to abnormal heart rhythm
โก Risk for decreased perfusion related to ineffective circulation
๐ง Risk for injury (e.g., falls, syncope, stroke)
๐ฐ Anxiety related to palpitations or fear of sudden death
โ Deficient knowledge regarding disease, medications, and lifestyle
๐ฉธ Risk for bleeding related to anticoagulant therapy (e.g., in AF)
๐ฉน III. NURSING INTERVENTIONS
๐ท 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
๐ท 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
๐ท 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
๐ท D. Oxygenation & Positioning
Administer oxygen if SpOโ < 94%
Keep patient in semi-Fowlerโs position to ease breathing
๐ท E. Patient Safety
Implement fall precautions (especially in bradycardia, dizziness, syncope)
Provide calm environment to reduce anxiety
Restrict activity during acute episodes
๐ท 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
๐ IV. EVALUATION CRITERIA
Goal
Expected Outcome
โค๏ธ Rhythm stability
Normal sinus rhythm or controlled arrhythmia
๐ฉธ Perfusion adequate
Stable vitals, good LOC, warm extremities
๐ No complications
No stroke, HF, bleeding, or arrest
๐ Knowledge improved
Verbalizes understanding of condition & meds
๐ง Safety maintained
No falls or injuries from syncope
โ 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 โ arrhythmias can be terrifying for patients
Encourage follow-up with cardiology and regular ECG monitoring
๐ซ HEART BLOCK (ATRIOVENTRICULAR BLOCK)
Full Clinical Overview for Nursing and Medical Learning
๐ง 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.
๐ This causes the atria and ventricles to beat out of sync, resulting in bradycardia, decreased cardiac output, or even asystole.
โ ๏ธ 2. CAUSES
Category
Examples
๐ Cardiac diseases
MI (especially inferior/posterior), ischemic heart disease, cardiomyopathy, myocarditis
โ ๏ธ Atropine (0.5 mg IV) may be used for bradycardia in early or symptomatic cases ๐ซ Avoid digoxin, beta-blockers, and CCBs in high-degree blocks
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.
๐ PR interval > 0.20 seconds (5 small boxes on ECG) โ ๏ธ Every impulse still reaches the ventricles, but slower than normal.
ECG monitoring, educate patient, assess for progression
โ No pacemaker needed
Unless part of a more complex conduction abnormality
๐ซ SECOND-DEGREE HEART BLOCK
Type I (Wenckebach) & Type II (Mobitz II) (Definition | Causes | Types | Pathophysiology | ECG | Symptoms | Management | Nursing Care | Complications | Key Points)
๐ง 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.
โ ๏ธ There are two types:
Type I (Wenckebach or Mobitz I) โ progressive delay until one beat is dropped
Type II (Mobitz II) โ sudden dropped beats with no warning
๐ข 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 โ may progress to complete heart block
โ ๏ธ 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) |
๐งฌ 4. PATHOPHYSIOLOGY
Type I (Wenckebach):
Delay in AV node conduction โ PR interval lengthens
Eventually, one atrial impulse fails to conduct โ 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
๐จ 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
๐งช 6. DIAGNOSIS
Test
Findings
๐ ECG
Type I: Progressive PR prolongation โ dropped QRS
Type II: Constant PR with dropped QRS without warning | | ๐ Holter monitor | For intermittent blocks | | ๐งช Blood tests | Electrolytes, TSH, digoxin levels | | ๐ Drug history | Identify AV-blocking meds (beta-blockers, CCBs, digoxin) | | ๐ง Echocardiography | To assess for structural heart disease or wall motion defects |
๐ 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 โ requires urgent intervention
Temporary pacing if symptomatic
Prepare for permanent pacemaker
Avoid AV node blockers |
๐ ๏ธ 8. SURGICAL / DEVICE MANAGEMENT
Procedure
Indication
๐ Temporary pacing
For unstable Mobitz II or severe bradycardia
๐ซ Permanent pacemaker
Always indicated in Mobitz II or symptomatic high-grade block
๐ซ Avoid
AV-nodal blockers (e.g., beta-blockers, CCBs, digoxin) in Mobitz II
๐ฉโโ๏ธ 9. NURSING MANAGEMENT
๐ท A. Assessment & Monitoring
Continuous cardiac monitoring (ECG/telemetry)
Check vital signs, especially for bradycardia, hypotension
Assess for signs of syncope, confusion, poor perfusion
๐ท 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
๐ท C. Medication Safety
Hold AV-nodal depressants (digoxin, beta-blockers, CCBs)
Administer oxygen, fluids, or pressors if needed
Monitor electrolyte levels and correct imbalances
๐ท D. Patient Education
Teach about pacemaker (if placed)
Instruct on symptom reporting (lightheadedness, syncope)
Encourage regular follow-up and ECG monitoring
โ 10. COMPLICATIONS
Complication
Description
โ ๏ธ Progression to 3rd-degree block
Especially in Mobitz II
๐ง Syncope or falls
Due to sudden dropped beats
๐ Sudden cardiac arrest
If conduction stops completely
๐ Pacemaker dependency
Post-implantation in Mobitz II
๐ฉธ Complications from bradycardia
Heart failure, hypotension, fatigue
โ 11. KEY POINTS โ QUICK SUMMARY
๐ Topic
Summary
๐ Definition
Intermittent failure of AV conduction (some P waves not followed by QRS)
๐ข Type I
PR interval gradually lengthens, then QRS dropped (usually benign)
โ Type II
Fixed PR with sudden dropped QRS โ dangerous!
๐ Symptoms
Fatigue, bradycardia, syncope, low BP
โก Management
Type I โ observe; Type II โ pacemaker
๐ฉโโ๏ธ 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.
๐ Atria and ventricles beat independently, with no relationship between P waves and QRS complexes. โ It is a life-threatening bradyarrhythmia and often leads to syncope, heart failure, or cardiac arrest.
โ ๏ธ 2. CAUSES
Category
Common Causes
๐ Cardiac
Myocardial infarction (esp. inferior or anterior wall), cardiomyopathy, myocarditis
Patient verbalizes knowledge of meds and pacemaker care
โ No complications
No arrest, stroke, or worsening block occurs
โ IV. KEY NURSING TIPS
๐ง Always treat the patient, not just the monitor
โ ๏ธ Watch for progression from 1st โ 2nd โ 3rd degree block
โ๏ธ Be pacing-ready in Mobitz II and 3rd-degree blocks
โ Avoid AV nodal blockers in higher-degree blocks
๐ฌ Keep communication open with physician if symptoms or ECG worsen
๐ซ Congestive Heart Failure (CHF)
Definition | Causes | Types
โ 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.
๐ก It may involve failure of the left ventricle, right ventricle, or both, and leads to shortness of breath, fatigue, edema, and exercise intolerance.
โ ๏ธ 2. CAUSES OF CHF
๐น 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 โ heart canโt pump
EF < 40%
Heart Failure with Preserved Ejection Fraction (HFpEF)
Diastolic dysfunction โ heart canโt fill
EF โฅ 50%
Heart Failure with Mid-Range EF (HFmrEF)
Intermediate group
EF 41โ49%
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
๐ฌ 4. PATHOPHYSIOLOGY OF CHF
๐ง Basic Mechanism:
When the heart fails to pump blood efficiently, the body activates compensatory mechanisms that initially maintain perfusion but eventually worsen heart failure.
๐ Step-by-Step Pathophysiology:
๐ซ Decreased Cardiac Output โ due to ventricular dysfunction (systolic or diastolic)
๐ง Neurohormonal Activation:
โ Sympathetic nervous system (SNS) โ โ HR & vasoconstriction
โ Renin-Angiotensin-Aldosterone System (RAAS) โ sodium & water retention โ โ blood volume
Lifelong meds, lifestyle changes, regular monitoring, possible devices
๐ซ๐ซ COR PULMONALE
(Definition | Causes | Types)
โ 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.
๐น A. Pulmonary (Lung) Causes
Disease
Description
Chronic Obstructive Pulmonary Disease (COPD)
Most common cause โ 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
๐น B. Pulmonary Vascular Causes
Condition
Description
Pulmonary embolism (PE)
Acute block in pulmonary arteries โ sudden right heart strain
Primary pulmonary hypertension
Rare, progressive โ pressure in lung vessels
Recurrent thromboembolism
Chronic PE leads to persistent pulmonary hypertension
๐น 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
๐ข 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
๐ฌ 4. PATHOPHYSIOLOGY OF COR PULMONALE
๐ง Step-by-Step Mechanism:
Chronic lung disease (e.g., COPD) causes:
Alveolar hypoxia (โ Oโ)
Chronic inflammation and destruction of pulmonary capillaries
This leads to pulmonary vasoconstriction and loss of vascular bed
Resulting in increased pulmonary vascular resistance (PVR) โ pulmonary hypertension
The right ventricle (RV) must work harder to pump blood into stiff pulmonary arteries
Over time, RV undergoes hypertrophy (muscle thickens) โ then dilates and fails
Leads to systemic venous congestion (right-sided heart failure symptoms)
Oxygen therapy, bronchodilators, diuretics, steroids, treat underlying cause
๐ ๏ธ Advanced options
Long-term oxygen therapy, anticoagulants, transplant in end-stage
๐ฉโโ๏ธ Nursing role
Oxygen monitoring, fluid balance, medication administration, education on lifestyle changes
๐จ Emergency risk
Pulmonary embolism in acute cases or respiratory failure if decompensated
๐ซ PULMONARY EDEMA
(Definition | Causes | Types)
โ 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.
๐ก It is often a life-threatening emergency if not treated promptly, especially in its acute form.
โ ๏ธ 2. CAUSES OF PULMONARY EDEMA
Pulmonary edema can result from both cardiac (heart-related) and non-cardiac causes:
๐น A. Cardiogenic Causes (due to increased pulmonary capillary pressure)
Cause
Description
Left-sided heart failure
Most common cause โ LV fails to pump blood โ backup in lungs
Head trauma, seizures increasing sympathetic activity
๐ข 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
๐ฌ 4. PATHOPHYSIOLOGY
Pulmonary edema occurs when fluid shifts from the pulmonary capillaries into the interstitial tissue and then into the alveoli, disrupting gas exchange.
๐ Step-by-Step Mechanism:
๐น A. Cardiogenic Pulmonary Edema
Left ventricular dysfunction โ blood backs up into the left atrium
โ Pressure in pulmonary veins & capillaries
โ Hydrostatic pressure forces fluid from capillaries into alveoli
Alveolar flooding โ impaired oxygen diffusion
Leads to hypoxemia, dyspnea, and respiratory failure
Cardiogenic = โ PCWP & BNP; Non-cardiogenic = normal heart function
๐จ Emergency
Acute pulmonary edema is a life-threatening condition needing urgent care
๐ Prevention
Manage CHF, avoid fluid overload, treat infections early
๐ซโก CARDIOGENIC SHOCK
(Definition | Causes | Types โ With Visual Symbols & Full Explanation)
โ 1. DEFINITION
๐ด 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.
๐ง It is most commonly a result of severe left ventricular failure, often due to acute myocardial infarction (AMI).
๐ฅ 2. CAUSES OF CARDIOGENIC SHOCK
๐น A. ๐ซ Cardiac Causes (Most Common)
๐ Condition
๐ง Description
๐ Acute Myocardial Infarction (AMI)
๐จ Most common cause โ massive damage to LV reduces contractility
๐ข Severe Heart Failure (CHF)
Chronic weak heart becomes unable to maintain output
๐ฉบ Arrhythmias
Tachycardia or bradycardia reduces effective cardiac output
๐ซ Valvular Disease
Aortic or mitral stenosis/regurgitation leads to output obstruction or backflow
๐ Cardiomyopathy
Dilated or hypertrophic โ poor contractility or restricted filling
Monitor vitals, oxygenation, urine output, mental status, prepare for ICU support
โ ๏ธ Mortality
High without timely intervention (30โ60%) โ needs rapid action
๐ Goals
Restore CO, maintain perfusion, prevent organ failure, treat cause
๐ก๏ธ Prevention
Early MI treatment, CHF management, regular cardiac checkups
๐ซ๐ง CARDIAC TAMPONADE
(Definition | Causes | Types)
โ 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.
๐ Leads to โ Cardiac output, hypotension, and shock.
๐ง Itโs not just about fluid โ itโs about how fast it accumulates.
Slower accumulation over days or weeks โ body compensates initially
Chronic Tamponade ๐งโโ๏ธ
Long-standing effusion with signs of right heart compression
Regional Tamponade ๐
Localized fluid compressing only part of the heart
๐ 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.
๐ฌ 4. PATHOPHYSIOLOGY
Cardiac tamponade = Pressure buildup in the pericardial sac compresses the heart, especially the right atrium & ventricle โ โ cardiac output โ shock
๐ง Step-by-Step Mechanism:
๐ง Fluid accumulates in the pericardial space (effusion or blood)
๐งฑ The non-stretchable pericardium gets tense
๐ซ Compression first affects the right atrium and right ventricle โ impaired diastolic filling
โฌ๏ธ โ Stroke volume and โ cardiac output
๐ Leads to hypotension, reflex tachycardia, and poor organ perfusion
๐ The body activates compensatory mechanisms (โ HR, vasoconstriction)
๐ฅ If not relieved โ shock, cardiac arrest, death
๐ก Key Feature:
Even 100โ200 mL of rapid fluid can cause tamponade.
Chronic tamponade may involve >1 liter if fluid accumulates slowly.
Electrical alternans (alternating QRS height) โ specific finding | | ๐งช Chest X-ray | – May show enlarged cardiac silhouette in chronic tamponade
Often normal in acute cases | | ๐ง Echocardiogram (2D Echo) | โ GOLD STANDARD
Shows pericardial effusion, diastolic collapse of RA/RV
Detects even small amounts of fluid | | ๐ Cardiac Tamponade Panel | – โ Central venous pressure (CVP)
โ Cardiac output/index
โ BP
May show โ lactate (hypoperfusion) | | ๐ Pericardiocentesis (diagnostic + therapeutic) | – Withdraws fluid
Fluid sent for cytology, TB, culture, malignancy markers |
๐ซ๐ง CARDIAC TAMPONADE
Medical & Surgical Management
๐ MEDICAL MANAGEMENT(Immediate Stabilization)
Drug / Therapy
Purpose / Action
Examples
Nursing Considerations
Oxygen Therapy
Improves oxygen delivery during hypoxia
Nasal cannula, mask, high-flow Oโ
Monitor SpOโ, RR, ABG; elevate head
IV Fluids (Cautiously)
Temporarily โ 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, Oโ demand
Morphine (if needed)
Monitor for respiratory depression; reduce stress
๐ก Medical treatment is supportive and temporary โ definitive treatment = fluid drainage.
๐ ๏ธ SURGICAL / PROCEDURAL MANAGEMENT
Procedure
Purpose / Indication
Nursing Considerations
๐ชก Pericardiocentesis (Emergency)
Gold standard: Needle aspiration of pericardial fluid under echo/ECG guidance
– Continuous ECG + BP monitoring
Position patient 45โ60ยฐ semi-Fowlerโs
Watch for arrhythmias, pneumothorax, or bleeding | | ๐จ 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)
๐ฏ C. PLANNING / GOALS
The patient will:
Maintain adequate cardiac output and BP
Exhibit normal respiratory rate and SpOโ โฅ 90%
Demonstrate improved mental status and urine output
Report reduced anxiety
Be free from complications such as arrhythmias or infection
๐ฉโโ๏ธ D. INTERVENTIONS
๐น 1. Ensure Hemodynamic Stability
Monitor BP, MAP, HR, SpOโ, 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
๐น 2. Support Oxygenation and Breathing
Administer supplemental oxygen to maintain SpOโ โฅ 94%
Position patient in semi-Fowlerโs or high-Fowlerโs to ease breathing
Monitor ABGs and observe for signs of respiratory distress
๐น 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, SpOโ, and pulse quality
Watch for complications: arrhythmias, pneumothorax, bleeding
Send pericardial fluid for lab analysis: culture, cytology, TB markers
๐น 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)
๐น 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
โ E. EVALUATION
Goal
Expected Outcome
Cardiac output restored
Stable HR/BP, warm extremities, good capillary refill
Respiratory function maintained
SpOโ โฅ 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
๐ซ๐ซโก CARDIOPULMONARY ARREST
(Definition | Causes | Types)
โ 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.
๐ It is a medical emergency requiring immediate CPR and advanced cardiac life support (ACLS) to prevent irreversible brain damage or death.
๐ฅ 2. CAUSES OF CARDIOPULMONARY ARREST
The causes are best remembered using the ACLS mnemonic “Hs & Ts” โ helps identify reversible conditions during resuscitation.
๐ฉบ A. โHsโ โ 5 Reversible Causes
H ๐ค
Cause
Explanation
๐ฉธ Hypovolemia
Severe fluid or blood loss
๐ง Hypothermia
Core body temp < 30ยฐC
๐จ Hypoxia
Oxygen deficiency in lungs/tissues
๐งช Hydrogen ion (Acidosis)
Metabolic or respiratory acidosis
โก Hyper/Hypokalemia
Electrolyte imbalance affects heart rhythm
๐ B. โTsโ โ 5 Reversible Causes
T ๐ค
Cause
Explanation
๐ฉธ Tension pneumothorax
Air in pleural space compresses heart/lungs
๐ Tamponade (Cardiac)
Fluid in pericardial sac compresses heart
๐ Toxins
Drug overdose, poisonings (e.g., opioids, TCA)
๐ซ Thrombosis (Pulmonary)
Massive pulmonary embolism
โค๏ธ Thrombosis (Cardiac)
Acute myocardial infarction (MI)
๐ข 3. TYPES OF CARDIOPULMONARY ARREST
๐ท๏ธ Type
โก Rhythm / Description
๐ Management Strategy
๐ฅ Ventricular Fibrillation (VF)
Chaotic, ineffective heart rhythm
Shockable โ Immediate defibrillation
๐ง Pulseless Ventricular Tachycardia (VT)
Rapid wide QRS rhythm without pulse
Shockable โ Defibrillation + CPR
๐จ Asystole
Flatline ECG โ no electrical activity
Non-shockable โ CPR + Epinephrine
๐ฉ Pulseless Electrical Activity (PEA)
ECG shows rhythm but no pulse
Non-shockable โ CPR + identify cause
๐ฆ Respiratory Arrest only
Cessation of breathing, pulse still present
Support airway + rescue breathing (BLS)
๐ Remember:
๐ง Brain death begins within 4โ6 minutes of CPA without oxygen. Immediate CPR + defibrillation saves lives!
๐ฌ 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.
๐ง Step-by-Step Process:
๐ Cardiac function ceases โ No effective contraction โ No pulse
๐ซ Respiratory arrest follows (or precedes in some cases) โ No oxygen intake
๐ง โ Oxygen delivery to brain & vital organs
โฌ๏ธ Cerebral perfusion drops within seconds โ loss of consciousness
๐ Anaerobic metabolism starts โ lactic acidosis and cellular injury
๐ Brain damage begins within 4โ6 minutes
๐ง Irreversible brain death in 8โ10 minutes without CPR
๐ซ Heart tissue begins to deteriorate โ multi-organ failure โ death
๐ Chain Reaction Visual:
Cardiac/Respiratory Arrest โฌ No circulation + No oxygen โฌ Brain & organ hypoxia โฌ Acidosis, organ failure, death
๐จ 5. SIGNS & SYMPTOMS OF CARDIOPULMONARY ARREST
๐ง General Signs
๐ฌ Details
๐ข Sudden collapse
Often without warning
๐ง Unresponsiveness
No reaction to tapping or shouting
๐จ Absence of breathing (Apnea)
No chest movement; gasping = ineffective
๐ No pulse (Cardiac arrest)
Check carotid or femoral pulse
๐ป Skin changes
Pale, cold, cyanotic (bluish)
๐๏ธ Dilated pupils
Fixed and unreactive in later stages
๐ Flatline on monitor
Asystole or non-perfusing rhythm on ECG
๐งช 6. DIAGNOSTIC EVALUATION (in-hospital or post-resuscitation)
๐ฌ Test
๐ฉบ Purpose / Findings
๐ ECG / Cardiac monitor
Determines type of rhythm (VF, VT, PEA, Asystole)
๐ฉธ ABG (Arterial Blood Gas)
Reveals severe acidosis, hypoxia (โ PaOโ), โ COโ
๐งช Serum electrolytes
Check for hyperkalemia, hypokalemia, Caยฒโบ imbalances
๐ Cardiac enzymes (Troponin, CK-MB)
To rule out acute MI as the cause
๐ Chest X-ray
Detects pneumothorax, effusion, or trauma
๐ง CT Brain / EEG(post-resuscitation)
Evaluate brain injury / hypoxic encephalopathy
๐ฉบ Echo / Ultrasound (POCUS)
Rule out cardiac tamponade, PE, poor contractility
๐ง Toxicology screen
If drug overdose suspected
๐ฉธ Lactate level
Indicates severity of hypoperfusion
๐ฉบ Diagnosis is Clinical First!
If a person is unresponsive, not breathing, and has no pulse โ START CPR IMMEDIATELY. Donโt delay for equipment or tests.