PATHOGENESIS
The main reason for heart failure is reduced
RISK FACTORS
1. High blood pressure
2. Diabetes
3. Family history
4. Age
5. Lifestyle factors
ETIOLOGY
Coronary artery disease (CAD)
Myocardial infarction (heart
attack)
Cardiomyopathies
Valvular heart disease
Congenital heart defects
HEART FAILURE
TREATMENT/MANAGEMENT
MEDICAL MANAGEMENT:
1. Medications: Diuretics, ARBs,
Beta-blockers and other
medications.
2. Implant devices: Pacemakers,
Defibrillators, CRT, VADs.
3. Surgical Procedures: Valve
surgery, CABG, heart transplant
NURSING MANAGEMENT:
1. Assessment and Monitor
2. Education and Empowerment
3. Symptom Management
4. Psychosocial Support
5. Continuity of Care
cardiac output but various mechanisms
contribute to its development. In myocardial
injury is one of the form foundation of most cases.
An injury to the heart muscle can occur due to
various factors like coronary artery disease (CAD),
myocardial infarction, heart valve disease,
cardiomyopathies and infection, this injury
weakens the heart muscle, reducing its
contractility and pumping efficiency, So in
response to decreased cardiac output, the body
activates compensatory mechanisms to maintain
blood pressure and organ perfusion. This involves
the release of hormones like epinephrine,
norepinephrine, and aldosterone in which this
hormones increases heart rate, constrict blood
vessels, and retain salt and water initially helping
to maintain BP. However, over time, this
prolonged neurohumoral activation can further
stress the heart, leading to progressive ventricular
remodeling and worsening heart failure. In
response to the stress and injury, the heart
undergoes structural changes in an attempt to
compensate for the decreased pumping function.
DIAGNOSIS CLINICAL
MANIFESTATION
1. Medical History and Physical
Dyspnea (shortness of breath)
examination
Fatigue and Weakness
2. blood test
Cough and Wheezing
3. Electrocardiogram (ECG)
Edema (swelling)
4. Chest X-ray
Jugular Venous Distention
5. Echocardiogram
(JVD)
Cold and Clammy Skin
 RISK FACTORS PATHOGENESIS
The journey begins with Group A
1. Genetic Predisposition
streptococcal (GAS) infection, usually a
2. Environmental Factors
seemingly ordinary strep throat. However,
3. Repeated GAS Infections
certain strains of GAS possess a protein called
4. Age
M protein with remarkable mimicry to human
heart tissues. This molecular mimicry triggers
an abnormal immune response. The body's
ETIOLOGY defense system, trained to fight GAS,
mistakenly attacks self-tissues, particularly
heart valves, due to the structural similarities
Group A Streptococcal (GAS) in which this phenomenon, called cross-
Infection reactivity, leads to inflammation and immune
Molecular Mimicry and Immune cell infiltration in the heart valves. Activated
Dysregulation immune cells release inflammatory mediators,
Inflammatory Cascade and causing endothelial cell activation in the valve
Valve Damage linings. This activation facilitates the adhesion
Fibrotic scarring
Thickening and narrowing RHEUMATIC HEART and migration of other immune cells, further
amplifying the inflammatory response. The

DISEASE inflammatory milieu promotes tissue damage,

resulting in scar tissue formation and
TREATMENT/MANAGEMENT thickening of the heart valves. The thickened
and scarred valves become stiff and lose their
flexibility.
MEDICAL MANAGEMENT:
1. Antibiotic Prophylaxis
2. Medication for symptoms:
Diuretics, Beta blockers, ACE
inhibitors and ARBs,
Anticoagulant
3. Surgical: Mitral Stenosis, Mitral
DIAGNOSIS CLINICAL
regurgitation, Aortic stenosis,
MANIFESTATION
1. Clinical Suspicion:
Tricuspid valve regurgitation
Symptoms
NURSING MANAGEMENT: Medical History Heart murmur
1. Assessment and Monitor 2. Physical Examination Fatigue and Exertional Dyspnea
2. Education and Empowerment Auscultation Palpitations
3. Symptom Management Other Findings: Edema, JVD, Chest pain
4. Psychosocial Support Abnormal lung sounds Edema
5. Continuity of Care 3. Diagnostic Tests: ECG,
Echocardiogram, Chest X-ray, Blood
test
 RISK FACTORS PATHOGENESIS
Certain gene variants influence factors like salt
1. Family History
handling, sodium-potassium pumps, and
2. Age
endothelial function, increasing susceptibility.
3. Ethnicity
Also, High dietary salt intake, obesity, chronic
4. Sex: Men are more prone to
stress, smoking, and excessive alcohol
developing hypertension than
consumption all contribute to the
women before menopause.
hypertensive pathway. Increased activity of
5. Pre-existing Medical Conditions
the sympathetic nervous system leads to
Lifestyle Habits
vasoconstriction and elevated heart rate,
raising blood pressure. Renin release from the
kidneys triggers a cascade leading to
ETIOLOGY angiotensin II production. This potent
vasoconstrictor narrows blood vessels and
Genetic Predisposition promotes aldosterone release, further
Neurohormonal Dysregulation increasing salt and water retention, elevating
Environmental Factors blood pressure. The protective lining of blood
Endothelial Dysfunction vessels becomes impaired, losing its ability to
Kidney Involvement HYPERTENSION dilate and relax properly which leads to
vasoconstriction, inflammation, and oxidative
involvement. Additionally, Chronic high blood
TREATMENT/MANAGEMENT pressure damages the kidneys, impairing their
ability to regulate blood pressure through
sodium and water excretion. This, in turn,
MEDICAL MANAGEMENT: perpetuates the hypertensive cycle.
1. Lifestyle Modifications: Dietary
changes, Weight management,
Exercise, Alcohol moderation,
Smoking cessation, Stress
management.
2. Medication for symptoms:
DIAGNOSIS CLINICAL
Diuretics, Beta blockers, ACE
MANIFESTATION
1. Clinical Suspicion:
inhibitors and ARBs, CCB.
Symptoms
NURSING MANAGEMENT: Medical History Headache
1. Assessment and Monitor 2. Blood Pressure Monitoring Fatigue and Difficulty
2. Education and Empowerment 3. Laboratory Tests: Concentrating
3. Symptom Management Basic metabolic panel Dizziness and Lightheadedness
4. Psychosocial Support Lipid profile Palpitations and Irregular
5. Continuity of Care Uri
Heartbeat
 RISK FACTORS PATHOGENESIS
1. Personal History
2. Demographic In Virchow’s Triad, there are three key element
3. Medical Conditions that favor clot formation such as the venous stasi
4. Surgery and Immobilization in which Slow blood flow in deep veins, often du
5. Pregnancy and hormones to prolonged sitting, leg injuries, or medica
6. Lifestyles conditions, allows blood cells to stagnate and
clump together. Next is the endothelial injury thi
damage to the inner lining of veins, caused b
trauma, surgery, inflammation, or certai
medications, disrupts the smooth flow and
ETIOLOGY triggers clot formation. Lastly
hypercoagulability in which an increased
i

Virchow's Triad tendency of blood to clot can arise from inherited

Genetic predisposition conditions, pregnancy, hormonal changes, certai
Medical conditions: Chronic medications, or medical conditions like cancer. i
kidney disease, thyroid Endothelial injury exposes collagen, a protei
disorders, inflammatory bowel
disease.
Lifestyle factors
DEEP VEIN that activates platelets and initiates the clottin
cascade. Then the Platelets stick to the injured

TREATMENT/MANAGEMENT
THROMBOSIS site and attract other platelets, forming an initia
clump. The Clotting factors in the blood conver
fibrinogen into fibrin, a mesh-like protein tha
traps red blood cells, solidifying the clot and
MEDICAL MANAGEMENT: potentially obstructing the vein.
1. Prevent Clot Growth and Extension:
Anticoagulants, Compression Stockings
2. Thrombolytic Therapy
3. Catheter -directed interventions
4. Lifestyle modification
5. Long-term anticoagulation
DIAGNOSIS CLINICAL
NURSING MANAGEMENT:
MANIFESTATION
1. Medical Hiistory
1. Vigilantly monitoring vital signs
2. Physical Examination: Palpitation,
2. Assessing pain and limb symptoms homan’s sign, inspection Pain
3. Monitoring for bleeding risks 3. D-dimer blood test Swelling
4. Lifestyle modification coaching 4. MRI or CT Scan Warmth and Tenderness
5. Doppler ultrasound Skin Changes
Fatigue and Malaise
Fever
Homan's Sign
 RISK FACTORS PATHOGENESIS
1. Personal history
2. Age: Risk increases with age, particularly after An aneurysm is primarily caused by a weakenin
50 for brain aneurysms and 65 for abdominal in the walls of an artery. This weakening can b
aortic aneurysms. due to various factors such as high blood pressur
3. Sex: Men are more prone to abdominal aortic (hypertension), atherosclerosis (buildup of plaqu
aneurysms, while women are more susceptible in the arteries), genetic predisposition, trauma
to brain aneurysms before menopause. infections, or certain diseases affecting the blood
4. Lifestyle Habits vessels. The arterial walls, when weakened, los
ETIOLOGY their elasticity and become susceptible t
bulging or ballooning. The constant pressur
from the blood flowing through the weakened
Weakened Arterial Wall area puts stress on the arterial wall, causing it t
High blood pressure widen and form an outpouching called a
Turbulent blood flow aneurysm. In response to the structural weakness
Atherosclerosis the body's inflammatory processes might b
Trauma activated. Inflammation can further weaken th
Genetic Predisposition
ANEURYSM arterial wall and contribute to the expansion o
the aneurysm.

TREATMENT/MANAGEMENT
MEDICAL MANAGEMENT:
1. Blood Pressure Control
2. Cholesterol Management
3. Smoking Cessation
CLINICAL
4. Genetic Counseling and Screening MANIFESTATION
5. Lifestyle Modifications
NURSING MANAGEMENT: 1. Brain aneurysms
1. Educate patients and families about
aneurysms, treatments, and lifestyle
DIAGNOSIS Headache
Nausea and vomiting
changes Vision changes
1. Physical Examination
2. Make measures to prevent falls and 2. CT Scan Neck pain and stiffness
pressure on aneurysm sites. 3. Ultrasound Seizures and focal neurological
3. Regularly assess vital signs, symptoms, and 4. MRI deficits
medication responses 5. Angiography 2. Abdominal aortic aneurysms:
6. Screening Test Pain
4. Monitor for complications and report
7. Genetic Testing Pulsating mass
changes promptly.
5. Prepare patients for surgery and provide fatigue; loss of appetite
postoperative care.