DOCUMENTATION

Nursing Notes vs. Charting

Charting is a nursing process that includes all the documentation required from nurses. This might
include legal, professional, and institution-specific requirements.

Some examples of charting include documenting medications administered, vital signs, physical
assessments, and interventions provided.

Nursing notes
•are a narrative written summary of a given nursing care encounter. This might include a description of a
nursing visit, a specific care event, or a summary of care. A nurse’s note is a form of charting that describes
the nurse’s decision-making process regarding the nursing care provided.
•an important part of high-quality nursing documentation because they provide an opportunity for nurses
to demonstrate their nursing knowledge and communicate the nursing process to other team members of
the patient’s interprofessional care team.

How Are Nursing Notes Used?

•A clear and comprehensive nursing note serves several purposes in nursing practice, both in patient care
and to provide legal protection to the nurse writing the note.

Reasons to write high-quality nursing notes include:

•1.Contributing to continuity of care for patients. Continuous care requires that the care provided to
the patient is well-organized and that there is cooperative communication between nurses and other
interdisciplinary team members. Continuous care contributes to patient-centered and safe care. Nursing
notes allow all people on the care team to understand the patterns of patient care
•2. Communicating care goals. Nursing notes are one place where the nurse can share the plan of care
with team members. Nursing notes also allow others to see what interventions have been performed so far
and what the outcome of those interventions were.

•3. Demonstrating the nurse’s knowledge as required by professional regulators. Nursing notes are
useful for demonstrating the knowledge, skill, and judgment required by the nurse’s professional
regulators, such as their college. In addition, if there is ever a concern about a nurse’s license, nursing notes
can be used as evidence of competent and safe practice in line with professional standards of practice

•4. Contribute to quality improvement. Quality improvement projects across nursing settings may
include a review of charts to understand the care process. Nursing notes that accurately and
comprehensively reflect care delivered allow for more precise quality improvement initiatives.
•5. Contribute to nursing research. Nursing research projects may include a review of the chart. Similar
to quality improvement initiatives, nursing notes that accurately reflect the care provided allow accurate
research data to be collected.
•6. Legal protection. Nursing notes are included in the patient/client’s permanent medical record. In the
case of legal action related to care that a nurse provided or was involved in, nursing notes demonstrating
that ethical and competent nursing care was delivered provide legal protection to the nurse.
•7. Reimbursing insurance claims. In some jurisdictions, insurance or other healthcare payers may
directly reimburse nursing care. The nursing note may describe the rationale for reimbursable nursing
activities in this case.
•These are just a few key reasons nurses should spend time and effort writing high-quality nursing notes.

How to Write Good Nursing Notes (What’s included)

•Different work settings may have an expected format or even templates for nursing notes. However, all
nursing notes should include evidence of the nursing process. There are different templates for what
should be included in a nursing note.
•Institutional or hospital policies may be in place on what should be included in the nursing note.
However, it is the individual nurse’s responsibility and a demonstration of nursing knowledge and
judgment to decide what information is relevant or irrelevant for the nursing note.
How to Write Good Nursing Notes (What’s included
•Nurses’ notes usually include subjective (what the patient tells you) and objective (assessment/analysis)
data. However, the nurse should be careful not to include judgements or their own opinion in nursing notes.
It is important to include subjective data. However, subjective data should be written in quotation
marks as statements made by the patient rather than objective facts.

•Two common templates for nursing notes use the mnemonics DAR and SOAPIE. Rather than absolute
rules that describe how a nursing note should be structured, these two mnemonics are to be used as
guidelines and to help the nurse remember what information should be included in their note.

SOAPIE:
•Subjective (what the patient tells you), Objective(the nurse’s assessment), Analysis (interpretation of
data), Plan (what the nurse plans to do), Implementation (what was done) and Evaluation(how did the
intervention work?)

DAR( FDAR)
•DAR: Data (both subjective and objective), Action (what was done), Response (how did the patient
respond?
•There are other acceptable templates for nursing notes. The nurse should check with their institution if
there is a preferred or institution-specific policy regarding what should be included in the nursing note.
• Overall, what must be included in the nursing note is the nurse’s own name, the name of the
patient/client, the date and time of the note, and a demonstration of the appropriate nursing process.
•Nursing notes should also be made in chronological order.

•When writing a nursing note regarding a consultation with another healthcare provider, the nurse
should include the name and designation of the other healthcare provider in addition to other
components of the nursing note.

Nursing Note Examples

•Patient: Jane Doe
Date: January 30, 2023 ( SOAPIE )
•13:17: Patient reports pain to lower abdomen, rates pain at 7/10. She states that the pain has been
increasing over the past half hour after her return from PACU. Mrs. Doe describes the pain as a “dull
ache.” (Subjective) Abdominal dressing is dry and intact. Bowel sounds are hypoactive X4. Most recent
vital signs BP 114/82, HR 88, respiration 18, Sp02 94% on room air. (Objective) Patient experiencing
post-operative pain related to recent hernia operation. (Analysis) Writer will offer patient education
regarding PCA usage. (Plan)
•13:26: Writer reminded the patient about how to use the button on her PCA to control her pain. Writer
educated patient on the importance of managing post-surgical pain early to maintain comfort.
(Intervention)
•13:57 Reassessed patient pain after PCA education. Patient now describes that her pain is “subsiding.”
When rating her pain on the pain scale, patient now describes her pain as 2/10 which is acceptable to her.
(Evaluation)
•This note includes all elements of the SOAPIE note and also is written at the time in which the activity
was performed so there is a clear sequence of events.

Nursing Note Examples

•Patient: Jill Doe
Date: January 30, 2023 ( DAR)
•0927: On assessment patient described increased shortness of breath related to her chronic asthma.
Patient stated that she “uses her inhaler at home when I get short of breath.” Patient respiration rate 22,
Sa02 92% on room air, wheeze audible on auscultation of lungs. (Data) Writer administered 2 puffs (34
mcg) of patient’s Ipratropium PRN inhaler. (Action) Patient states that shortness of breath now resolved.
(Response)

General Advice on Writing Nursing Notes

 •Writing high-quality nursing notes is a skill like any other nursing skill that takes time and focused effort
to improve. With practice, nursing notes will become second nature as one pillar of safe and effective
clinical practice. Here are a few quick practice pointers to improve your nursing notes.
•If you are using paper charting, ensure that the writing is legible. Illegible charting does not
accomplish the goal of communicating care to the team and will not legally protect the nurse.

PATIENT F.A. ADMITTED TO MEDICAL WARD @ 9:15 AM WITH DATA GATHERED AS GCS 13 E3 V4 M6
WITH O2 SUPPORT VIA NASAL CANNULA REGULATED AS 6L/MIN, DIAPHORETIC, COLD CLAMMY SKIN,
RESTLESS, INCOHERENT, ECTOMORPHIC BODY PHYSIQUE, WITH IVF OF PNSS1L X 8HRS, VITAL IGNS
TAKEN AS BP 78/ 53mmHg, CR 100 BPM, PR 96 RAPID THREADY, RR30 CPM LABORED BREATHING TEMP
37.2, O2 SAT 91%

AT 11:40 AM VITAL SIGNS TAKEN AS TEMP 38.7, FLUSHED FACE, STILL WITH EPISODES OF DIFFICULTY OF
BREATHING, STILL RESTLESS BP 98/70mmHg CR 96BPM, RR24CPM O2 SAT 93%

CHF- CONGESTIVE HEART FAILURE

What is Congestive Heart Failure (CHF)?
Congestive Heart Failure (CHF) is a clinical syndrome characterized by the heart's inability to pump blood
effectively, leading to inadequate tissue perfusion and fluid retention. It can involve the left, right, or both
ventricles and may be systolic (impaired contraction) or diastolic (impaired relaxation) in nature.

Etiology
• Cardiac - Myocardial infarction, coronary artery disease (CAD), cardiomyopathy, valvular disorders
• Vascular - Hypertension
• Metabolic - Diabetes mellitus, thyroid disorders
• Lifestyle - Alcohol abuse, smoking, physical inactivity
• Others - Anemia, renal failure, infection

Pathophysiology
1. Primary insult (e.g., MI, valve disease, hypertension) Leads to reduced cardiac output.
2. Body compensates via:
o Sympathetic Nervous System (SNS) activation → increased HR & contractility
Renin- Angiotensin-Aldosterone System (RAAS) → vasoconstriction, sodium and water retention
• Antidiuretic Hormone (ADH) release → water retention
3. These compensatory mechanisms cause:
o Increased preload and afterload
o Cardiac remodeling (hypertrophy and dilation)
o Progressive myocardial dysfunction
4. Result: fluid accumulation (congestion) in lungs, legs, abdomen; impaired perfusion of vital organs.

Types of Congestive Heart Failure

Left-Sided Heart Failure

This is the most common type.
Two subtypes:
• Systolic Heart Failure (Heart can't pump well
The heart muscle is weak and can't squeeze enough blood out to the body.
Blood backs up into the lungs → causes shortness of breath.
• Diastolic Heart Failure (Heart can't relax well).
The heart is stiff and can't fill with enough blood.
Less blood gets pumped out → causes fatigue and swelling.

Right-Sided Heart Failure

• The right side of the heart can't pump blood properly to the lungs.
• Blood backs up into the veins → causing swelling in the legs, feet, belly.
 • Often caused by left-sided heart failure or lung problems (like COPD).

Congestive Heart Failure

(Both )
• Both the left and right sides of the heart are not working well.
• Symptoms: Breathing problems, swelling, tiredness, and weight gain from fluid.
Signs & Symptoms

Left-sided CHF:
o Dyspnea on exertion
o Orthopnea (needs pillows to sleep)
o Paroxysmal nocturnal dyspnea (PND)
o Fatigue
o Pulmonary crackles
o Cough with frothy sputum

Right-sided CHF:
o Peripheral edema
o Ascites
o Jugular venous distention
(JVD)
o Hepatomegaly
o Weight gain

Diagnostic Investigations

o BNP/NT -proBNP - Confirms HE (elevated levels)

o Echocardiography - Measures EF, wall motion, valve status
o ECG - Detects MI, arrhythmias, hypertrophy
o Chest X-ray - Cardiomegaly, pulmonary congestion
o CBC, Electrolytes, LIFTs, RFTs - Assess comorbidities, fluid/electrolyte statu

NURSING MANAGEMENT

Assessment
o Monitor vital signs (BP, HR, RR,
SpO,)
o Assess lung sounds (crackles), heart sounds (S3)
o Monitor for edema (legs, sacrum), weight gain
o Observe for fatigue, dyspnea, decreased activity tolerance
 o Monitor urine output, I&0
charting
o Evaluate mental status (early sign of hypoxia)

Interventions
o Position patient in high Fowler's to ease breathing
o Administer oxygen as prescribed
o Give medications as ordered and monitor for effects
o Daily weight monitoring
o Restrict fluids and sodium intake if prescribed
o Encourage small frequent meals
o Promote rest and conserve energy
o Educate patient and family

NURSING CONSIDERATIONS

HEALTH EDUCATION

o Daily weight monitoring - Report >2 kg in 2 days

o Low-sodium diet - <2g/day
o Fluid restriction - Usually 1.5-2 L/day
o Medication adherence - Take as prescribed
o Recognize warning signs:
o Worsening dyspnea
o Edema increase
Rapid weight gain
o Decreased urination
o Avoid smoking, alcohol, NSAIDs
o Enroll in cardiac rehabilitation if eligible

SHOCK
INTRODUCTION
• Cells need two things to function: oxygen and glucose. This allows the cells to generate energy and do
their specific jobs. When cells don't receive either of them or both, they stop functioning.

DEFINITION
• Shock is defined as a condition where the tissues in the body don't receive enough oxygen and nutrients
to allow the cells to function.

CLASSIFICATION
1. Cardiogenic shock- It occurs due to systolic or diastolic dysfunction.
2. Hypovolemic shock- It occurs due to intravascular fluid volume.
3. Obstructive shock- It occurs when there is physical obstruction in blood flow.
4. Distributive shock- (neurogenic, anaphylactic & septic)
 o Neurogenic shock- It occurs from trauma that leads to spinal cord injuries.
o Anaphylactic shock- It is acute life threatening hypersensitivity reaction to a sensitizing substance
like drug, chemical, vaccine, food etc.
o Septic shock- Also known as blood poisoning, is a condition caused by infections that lead to
bacteria entering blood

ETIOLOGY
o Severe allergic reaction
o Significant blood loss
o Heart failure
o Blood infections
o Dehydration
o Poisoning
o Burns

CLINICAL MANIFESTATIONS
o Extremely low blood pressure
o Weakness
o Chest pain
o Weak pulse
o Excessive sweating
o Dizziness
o Moist, clammy skin
o Unconsciousness
o Rapid, shallow breathing
o Feeling anxious, agitated or confused

COMPLICATIONS
o Loss of consciousness
o Respiratory failure
o Coagulation disorder
o Multi organ damage
o Coma
o Death

MANAGEMENT
1. MEDICAL MANAGEMENT
A. PHARMACOLOGICAL MANAGEMENT
o Crystalloids: ringer's solution and normal saline
o Inotropic agents: like dopamine, dobutamine and epinephrine
o Vasodilators: nitroglycerine
o Diuretics: lasilactone, furosemide
o Antibiotics: ciprofloxacin, amoxicillin and clavulanic acid
o Antihistamines: epinephrine used in anaphylactic shock.
o Corticosteroids: dexamethasone
o Sodium bicarbonate: used to treat metabolic acidosis
o Broncodilators: like atropine, aminophylline etc.

B. NON- PHARMACOLOGICAL MANAGEMENT

o Modified trendelenberg position
o Assessment of vital signs
o Oxygen administration
o Parenteral nutrition support

II. SURGICAL MANAGEMENT

o Wound debridement- in case of chronic infected wound, burns wound debridement to be done for
fast healing
o Angioplasty-in case of myocardial infarction angioplasty can be performed
 o Tracheostomy

III. NURSING MANAGEMENT ASSESSMENT

o Continuous monitoring of vital signs should be done.
o Assess Airway, breathing & circulation of the patient.
o Check for urine output of the client.

NURSING DIAGNOSIS
o Impaired tissue perfusion related to decrease cardiac output, decreased venous return
o In effective breathing pattern related to hypoxia, bronchospasm
o Fluid volume deficit related to vomiting hemorrhage
o Acute pain related to myocardial infarction
o Imbalanced nutrition less then body requirement related to vomiting, low intake of food

Chronic Kidney Disease ( CKD )

Chronic kidney disease (CKD and chronic renal disease) means that there’s damage to your kidneys
and they aren’t working as well as they should. Your kidneys are like a filter in your body — filtering out
wastes, toxins and extra water from your blood. They also help with other functions like bone and red blood
cell. When your kidneys begin to lose their function, they can’t filter waste, which means the waste builds
up in your blood.

Kidney disease is called “chronic” because kidney function slowly decreases over time. CKD can lead to
kidney failure, which is also called end-stage kidney disease.

There’s no cure for chronic kidney disease. But there are steps you can take to slow kidney damage.
Treatments like dialysis and transplantation are options for kidney failure (end-stage kidney disease).

What do your kidneys do?

Your kidneys have many jobs, but their main job is to clean your blood, getting rid of toxins, waste and
excess water as urine (pee). Your kidneys also balance the amount of electrolytes (such as salt and
potassium) and minerals in your body, make hormones that control blood pressure, make red blood cells
and keep your bones strong.

What are the 5 stages of chronic kidney disease?

● Stage 1
GFR (mL/min)
90 and higher
Means: Your kidneys are working well but you have signs of mild kidney damage

● Stage 2
GFR (mL/min)
60 to 89
Means: Your kidneys are working well but you have more signs of mild kidney damage

● Stage 3a
GFR (mL/min)
45 to 59
Means:Your kidneys aren’t working as well as they should and show mild to moderate damage. This is the
most common stage. You may notice symptoms at this stage.

●Stage 3b
GFR (mL/min)
30 to 44
Means: Your kidneys show moderate damage and don’t work as well as they should. With the right
treatment, many people can stay in this stage and never advance to stage 4.

Stage 4
GFR (mL/min) 15 to 29
Means: You have very poor kidney function; your kidneys are severely damaged and close to not working.
●Stage 5
GFR (mL/min)
Less than 15
Your kidneys are very close to failing or have stopped working. You may need kidney dialysis or a kidney
transplant at this stage.

How common is this condition

About 15% of adults in the United States have chronic kidney disease. Some 37 million people in the U.S.
are living with chronic kidney disease.

A 2022 study in revealed that CKD cases in the Philippines have risen to 35.94%, far above the global
average of 9.1-13.4%.

What are the symptoms of chronic kidney disease?

• A need to pee more often.
• Tiredness, weakness, low energy level.
• Loss of appetite.
• Swelling of your hands, feet and ankles.
• Shortness of breath.
• Foamy or bubbly pee.
• Puffy eyes.
• Dry and itchy skin.
• Trouble concentrating.
• Trouble sleeping.
• Numbness.
• Nausea or vomiting.
• Muscle cramps.
• High blood pressure.
• Darkening of your skin.

What are common causes of kidney disease?

● HIGH BLOOD PRESSURE ( HYPERTENSION )
● DIABETES

Is kidney disease hereditary?

Yes, kidney disease can run in biological families. Risk factors for CKD, like diabetes, also tend to run in
families.

Who is at risk for chronic kidney disease?

• Have diabetes.
• Have high blood pressure.
• Have heart disease.
• Have a family history of kidney disease.
• Have a long history of taking NSAID (nonsteroidal anti-inflammatory drugs) pain relievers.

What are the complications of chronic kidney disease?

• Low red blood cell count (anemia).
• Weak and brittle bones.
• Gout.
• Metabolic acidosis. This is a chemical imbalance (acid-base) in your blood caused by a decrease in
kidney function.
• High blood pressure.
• Heart disease and blood vessel disease, including increased risk of stroke and heart attack.
• Nerve damage.
• High potassium (hyperkalemia), which affects your heart’s ability to function correctly.
• High phosphorus (hyperphosphatemia).
• High risk of infection due to a weak immune system.
• Fluid buildup, leading to swelling in your feet, ankles and hands.
Diagnosis and Tests
• Blood Test
• Urine Test
• Ultrasound
• MRI
• CT Scan
• Biopsy

Management and Treatment

• Make and keep your regular healthcare provider/nephrologist (kidney specialist) visits. These
providers monitor your kidney health.
• Manage your blood glucose (sugar) if you have diabetes.
• Avoid taking painkillers and other medications that may make your kidney disease worse.
• Manage your blood pressure levels.
• Follow a kidney-friendly diet.
• Don’t smoke.
• Exercise/be active on most days of the week.
• Stay at a weight that’s healthy for you.

Medications for kidney disease

• An angiotensin-converting enzyme (ACE) inhibitor or an angiotensin receptor blocker (ARB) to lower
your blood pressure.
• Phosphate binder if your kidneys can’t eliminate phosphate.
• A diuretic to help your body eliminate extra fluid.
• Medications to lower cholesterol levels.
• Erythropoietin to build red blood cells if you’re anemic.
• Vitamin D and calcitriol to prevent bone loss.

SEPTICEMIA
Septicemia is a serious bloodstream infection that occurs when bacteria (or other pathogens) enter the
blood and spread throughout the body, triggering a systemic inflammatory response. It is often a precursor
to sepsis, a life-threatening condition.

Source of Infection
• Pneumonia
• Urinary tract infections (UTIs)
• Skin or soft tissue infections
• Abdominal infections
• Surgical wounds or invasive procedures

Common Causes
• Bacterial infections (most common: E. coli, Klebsiella, Staphylococcus aureus, and Streptococcus
species)
• Fungal infections (e.g. Candida species)
• Viral infections (less common)

Risk Factors
• Weakened immune system (e.g., HIV, cancer, transplant)
• Elderly or infants
• Chronic diseases (e.g., diabetes, kidney disease)
• Use of invasive devices (e.g., IV catheters, urinary catheters)
• Recent surgery or trauma
Signs And Symptoms

• High fever or hypothermia

• Chills and rigors
• Rapid breathing (tachypnea)
• Rapid heart rate (tachycardia)
• Low blood pressure (hypotension)
• Confusion or altered mental status
• Nausea, vomiting, or diarrhea
• Cold, clammy, or discolored skin

Pathophysiology

• Entry of Pathogens: Bacteria from an infection (e.g., UTI, pneumonia, wound infection) enter the
bloodstream.
• Systemic Spread: The bacteria and their toxins spread throughout the body via blood.
• Immune Response: The immune system responds by releasing inflammatory mediators.
• Inflammatory Cascade: This causes vasodilation, increased capillary permeability, and clot
formation.
• Organ Dysfunction: Reduced oxygen delivery to tissues can cause multi-organ failure, progressing
to sepsis or septic shock.

Diagnostic Test

• Blood cultures (to identify the microorganism)

• CBC (increased WBC or decreased in severe cases)
• Procalcitonin or CRP (markers of infection)
• Lactate level (indicator of sepsis severity)
• Urinalysis, wound, or sputum cultures
• Imaging (e.g., chest X-ray, CT scan) to find the source

Medical Management

Antibiotic Therapy

• Start broad-spectrum antibiotics immediately (within 1 hour of suspicion)

• Adjust based on culture results

Supportive Therapy

• IV fluids (to correct hypotension)

• Vasopressors (e.g., norepinephrine) if fluid resuscitation fails
• Oxygen therapy or mechanical ventilation if needed

Surgical Intervention

• Drain abscesses or remove infected tissue if applicable

Nursing Management

• Monitor vital signs closely (esp. temp, BP, HR, RR)

• Assess for mental status changes
• Monitor urine output (renal perfusion)
• Monitor response to antibiotics
Interventions
• Administer medications as prescribed
• Ensure timely collection of blood cultures
• Provide fluid resuscitation
• Maintain aseptic technique to prevent infection
• Educate patient and family about sepsis risks

Complications
• Sepsis
• Septic shock
• Organ failure (kidneys, lungs, heart)
• Death if not treated rapidly

CIRHOSIS OF THE LIVER

Cirrhosis of the liver is a chronic, progressive liver disease characterized by the replacement of normal liver
tissue with fibrous scar tissue and regenerative nodules. This process leads to the deterioration of liver
function, which can result in life-threatening complications. Cirrhosis is the final common pathway of various
liver injuries from a multitude of causes.

ETIOLOGY AND RISK FACTOR

Cirrhosis can develop due to numerous underlying conditions, including:
- Chronic Alcohol Consumption: The most common cause worldwide; alcohol-related liver disease
(ALD).
- Viral Hepatitis: Chronic hepatitis B (HBV) and hepatitis C (HCV) infections are significant
contributors.
- Non-Alcoholic Fatty Liver Disease (NAFLD): Often associated with obesity, diabetes, and
metabolic syndrome.
- Chronic Cholestatic Diseases: Such as primary biliary cholangitis and primary sclerosing
cholangitis.
- Genetic Disorders: Such as hemochromatosis, Wilson’s disease, and alpha-1 antitrypsin
deficiency.
- Drug-Induced Liver Injury: including long-term use of certain medications and toxins.
- Other Causes: Including autoimmune hepatitis and infiltrative disease.

PATHOPHYSIOLOGY

1. Liver Injury: Chronic injury leads to hepatocyte death.

2. Fibrosis Formation: Activated hepatic stellate cells produce excessive extracellular matrix.
3. Architectural Distortion: Fibrous tissue replaces normal liver architecture, disrupting blood
flow and liver function
4. Nodule Formation: Regeneration attempts lead to regenerative nodules, further impairing
liver architecture.
5. Functional Decline: Consequences include impaired metabolism, detoxification, synthesis,
and immune functions.

CLINICAL FEATURES

General symptoms:
• Fatigue
• Weakness
• Anorexia
• Weight loss

Signs of Liver Dysfunction:

o Jaundice
o Spider angiomata
 o Palmar erythema
o Gynecomastia in men
o Testicular atrophy
o Ascites
o Hepatic encephalopathy (confusion, altered consciousness)
o Bleeding tendencies (easy bruising, petechiae, bleeding gums)

Complications
o Variceal bleeding
o Spontaneous bacterial peritonitis
o Hepatorenal syndrome
o Hepatocellular carcinoma

DIAGNOSIS
Diagnosis involves a combination of clinical, laboratory, imaging, and histopathological assessments:

•Laboratory Tests:

• Elevated liver enzymes (ALT, AST)

• Elevated bilirubin
• Decreased albumin
• Prolonged prothrombin time (PT/INR)
• Thrombocytopenia
• Elevated serum ammonia (in encephalopathy)

IMAGING STUDIES

- Ultrasound: Detects liver surface irregularities, ascites, splenomegaly, varices.

- Elastography (FibroScan): Measures liver stiffness, indicating fibrosis severity.

- CT/MRI: Further evaluation of complications and tumors.

HISTOLOGY
Liver biopsy remains the gold standard for definitive diagnosis, revealing fibrosis, nodule formation, and
architectural distortion.

SEROLOGICAL TESTS
- Viral serologies (HBV, HCV)
- Autoantibodies (for autoimmune causes)
- Iron studies, ceruloplasmin, alpha-1 antitrypsin levels (for genetic causes)

STAGING

Several scoring systems assist in staging:

- Child-Pugh Score: Assesses severity based on bilirubin, albumin, INR, ascites, and
encephalopathy.
- Model for End-Stage Liver Disease (MELD): Uses bilirubin, INR, and creatinine to predict
prognosis and prioritize transplantation.

MANAGEMENT

General Principles:

- Treat Underlying Cause: Abstinence from alcohol, antiviral therapy, or removal of

hepatotoxic agents.
 - Nutritional Support: Adequate caloric intake, protein intake balanced to prevent
encephalopathy.
- Vaccinations: Hepatitis A and B vaccines, pneumococcal vaccine, annual influenza vaccine.
- Monitoring and Screening: Regular surveillance for hepatocellular carcinoma (ultrasound
and alpha-fetoprotein every 6 months).

SPECIFIC TREATMENTS

- Ascites and Edema:

- Sodium restriction
- Diuretics (spironolactone, furosemide)
- Paracentesis for refractory ascites
- Variceal Bleeding:
- Endoscopic band ligation
- Non-selective beta-blockers (e.g., propranolol)
- Vasoconstrictors (octreotide) during acute bleeding
- Hepatic Encephalopathy:
- Lactulose to reduce ammonia absorptiom
- Rifaximin as adjunct
- Hepatorenal Syndrome:
- Vasoconstrictors (terlipressin)
- Albumin infusion
- Liver Transplantation: The definitive treatment for advanced cirrhosis and iTs complications.

PREVENTIONS

- Lifestyle modifications: Abstain from alcohol, maintain healthy weight.

- Vaccination and screening: For viral hepatitis.
- Management of risk factors: Control of metabolic syndrome.

Cirrhosis of the liver is a complex, multifactorial disease that requires early detection and comprehensive
management to prevent severe complications. Advances in antiviral therapies, better understanding of
disease mechanisms, and liver transplantation have improved outcomes, but prevention remains
paramount
Acute Coronary Syndrome (ACS)
1. Introduction
Acute Coronary Syndrome (ACS) is an umbrella term for a group of conditions that result from a
sudden, reduced blood flow to the heart. This reduction in blood flow, known as ischemia, is
typically caused by a rupture of an atherosclerotic plaque in a coronary artery, leading to
thrombus (blood clot) formation that partially or completely obstructs blood flow. ACS is a
medical emergency that requires immediate diagnosis and treatment to prevent or limit damage
to the heart muscle.

2. Anatomy and Physiology of the Heart and Coronary Arteries

To understand ACS, it's crucial to grasp the basic anatomy and physiology of the heart and its
blood supply:
●​ Heart: A muscular organ responsible for pumping blood throughout the body. It has four
chambers: two atria (upper chambers) and two ventricles (lower chambers).
●​ Coronary Arteries: These are the blood vessels that supply oxygen-rich blood to the
heart muscle itself. The two main coronary arteries are the left main coronary artery
(which branches into the left anterior descending and circumflex arteries) and the right
coronary artery.
●​ Atherosclerosis: A condition where plaque (composed of cholesterol, fatty substances,
cellular waste products, calcium, and fibrin) builds up inside the arteries. This plaque
hardens and narrows the arteries, limiting blood flow.
●​ Ischemia: Insufficient blood flow to a tissue, leading to a lack of oxygen.
●​ Infarction: Tissue death due to lack of blood supply.

3. Classification of Acute Coronary Syndrome

ACS is broadly classified into three main types, primarily based on electrocardiogram (ECG)
findings and cardiac biomarker levels:

a. ST-Segment Elevation Myocardial Infarction (STEMI)

●​ Description: Characterized by complete or near-complete occlusion of a coronary artery,

leading to transmural (full-thickness) myocardial ischemia and necrosis.
●​ ECG Findings: Persistent ST-segment elevation in two or more contiguous leads.
●​ Cardiac Biomarkers: Elevated levels of cardiac troponins (I or T) and creatine
kinase-myocardial band (CK-MB), indicating myocardial damage.
●​ Severity: The most severe form of ACS, requiring immediate reperfusion therapy
(primary percutaneous coronary intervention or fibrinolysis).

b. Non-ST-Segment Elevation Myocardial Infarction (NSTEMI)

●​ Description: Involves partial or transient occlusion of a coronary artery, resulting in

subendocardial (partial-thickness) myocardial ischemia and necrosis.
●​ ECG Findings: ST-segment depression, T-wave inversion, or non-specific ST-T wave
 changes. No persistent ST-segment elevation.
●​ Cardiac Biomarkers: Elevated levels of cardiac troponins (I or T) and CK-MB.
●​ Severity: Less immediately life-threatening than STEMI, but still requires urgent
evaluation and management.

c. Unstable Angina (UA)

●​ Description: Results from a temporary and severe reduction in blood flow to the heart,
but without sufficient myocardial necrosis to cause a rise in cardiac biomarkers. It is
considered a precursor to myocardial infarction if left untreated.
●​ ECG Findings: May show transient ST-segment depression, T-wave inversion, or be
normal.
●​ Cardiac Biomarkers: Normal levels of cardiac troponins and CK-MB.
●​ Severity: A warning sign of impending MI, indicating a need for prompt medical
intervention.

4. Pathophysiology: The Underlying Mechanisms

The primary pathophysiological event in Acute Coronary Syndrome (ACS) is the rupture or
erosion of an atherosclerotic plaque within a coronary artery. This triggers a complex cascade of
events that ultimately lead to reduced blood flow to the heart muscle (myocardium).

1.​ Atherosclerotic Plaque Formation:

Over years, various risk factors (e.g., high cholesterol, hypertension, smoking, diabetes)
contribute to the development of atherosclerosis. This involves the accumulation of lipids,
inflammatory cells, and fibrous tissue within the arterial walls, forming plaques. These plaques
can be "stable" or "vulnerable." Vulnerable plaques have a thin fibrous cap and a large lipid
core, making them prone to rupture.

2.​ Plaque Rupture or Erosion:

The most common initiating event in ACS is the rupture of a vulnerable atherosclerotic plaque.
Less commonly, plaque erosion (where the endothelium is disrupted without a deep rupture) can
occur. When the fibrous cap of the plaque tears, the highly thrombogenic (clot-forming) contents
of the plaque (such as collagen and tissue factor) are exposed to the circulating blood.

3.​ Platelet Adhesion and Aggregation:

Upon exposure to the thrombogenic plaque contents, circulating platelets immediately adhere
to the exposed surface. These platelets become activated, changing shape and releasing
various pro-thrombotic and vasoconstrictive substances (e.g., adenosine diphosphate [ADP],
thromboxane A2, serotonin). These substances attract more platelets, leading to rapid platelet
aggregation and the formation of a primary platelet plug.

4.​ Activation of the Coagulation Cascade and Fibrin Formation:

Tissue factor, released from the ruptured plaque, initiates the extrinsic pathway of the
coagulation cascade. This complex enzymatic process culminates in the generation of thrombin.
Thrombin plays a crucial role by converting fibrinogen into insoluble fibrin strands. These fibrin
strands then form a meshwork that stabilizes the platelet plug, creating a more robust and
organized thrombus (blood clot) within the coronary artery lumen.
 5.​ Coronary Artery Occlusion and Myocardial Ischemia:
The formation and growth of this thrombus, often combined with local vasoconstriction
(narrowing of the blood vessel), lead to a critical reduction or complete cessation of blood flow
through the affected coronary artery. This imbalance between myocardial oxygen supply and
demand results in myocardial ischemia (insufficient oxygen to the heart muscle).

Progression to Myocardial Infarction or Unstable Angina (The Three Categories of ACS):

The extent and duration of the coronary artery occlusion determine the specific manifestation
of ACS:

Unstable Angina (UA):

In UA, there is a severe, but often transient or incomplete, reduction in blood flow due to
dynamic obstruction (e.g., a non-occlusive thrombus that may spontaneously lyse, or
intermittent vasospasm). This causes myocardial ischemia but is insufficiently prolonged or
severe to cause myocardial cell death. Therefore, cardiac biomarkers (like troponins) remain
normal. It signals a critical imbalance that places the heart at high risk for future infarction.

Non-ST-Segment Elevation Myocardial Infarction (NSTEMI):

NSTEMI results from a partial or transient complete occlusion of a coronary artery by a
thrombus, leading to subendocardial (partial-thickness) myocardial necrosis. The reduction in
blood flow is significant enough to cause detectable myocardial cell damage, leading to the
release of cardiac biomarkers (elevated troponins) into the bloodstream. The ECG changes
typically include ST-segment depression or T-wave inversion, but no persistent ST-segment
elevation.

ST-Segment Elevation Myocardial Infarction (STEMI):

STEMI is characterized by complete and sustained occlusion of a coronary artery, usually by
a large, occlusive thrombus. This leads to transmural (full-thickness) myocardial ischemia and
extensive myocardial necrosis (heart muscle death). The complete and persistent block
manifests on the ECG as persistent ST-segment elevation. Due to the significant damage,
cardiac biomarkers (troponins) are markedly elevated. This is the most severe form of ACS,
requiring immediate reperfusion to salvage myocardial tissue.

In summary, the journey from stable atherosclerotic plaque to the acute clinical syndromes of
UA, NSTEMI, or STEMI involves a sequence of plaque disruption, platelet activation, thrombus
formation, and subsequent reduction in coronary blood flow, culminating in myocardial ischemia
and, often, infarction.

5. Risk Factors
Many risk factors contribute to the development of atherosclerosis and, consequently, ACS.
These can be broadly categorized as modifiable and non-modifiable:

a. Modifiable Risk Factors:

●​ High Blood Pressure (Hypertension): Damages artery walls, making them more
 susceptible to plaque formation.
●​ High Cholesterol (Dyslipidemia): High levels of LDL ("bad") cholesterol contribute to
plaque buildup.
●​ Diabetes Mellitus: Damages blood vessels and promotes inflammation, accelerating
atherosclerosis.
●​ Smoking: Damages endothelial cells, promotes inflammation, and increases blood clot
formation.
●​ Obesity: Contributes to hypertension, dyslipidemia, and diabetes.
●​ Physical Inactivity: Increases the risk of obesity, hypertension, and dyslipidemia.
●​ Unhealthy Diet: High intake of saturated and trans fats, cholesterol, and sodium.
●​ Stress: Can contribute to other risk factors and directly impact cardiovascular health.

b. Non-Modifiable Risk Factors:

●​ Age: The risk of ACS increases with age.

●​ Sex: Men generally have a higher risk at a younger age, while women's risk increases
after menopause.
●​ Family History: A strong family history of early-onset coronary artery disease (CAD)
increases individual risk.
●​ Race/Ethnicity: Certain racial and ethnic groups may have a higher prevalence of risk
factors.

6. Signs and Symptoms

The classic symptom of ACS is chest pain (angina), but its presentation can be variable.
●​ Typical Angina:
○​ Location: Substernal (behind the breastbone), may radiate to the left arm,
shoulder, neck, jaw, back, or epigastrium.
○​ Character: Heaviness, pressure, tightness, squeezing, burning, or aching.
○​ Duration: Typically lasts longer than a few minutes and is not relieved by rest or
nitroglycerin (in the case of MI).
○​ Associated Symptoms: Shortness of breath (dyspnea), sweating (diaphoresis),
nausea, vomiting, dizziness, lightheadedness, fatigue, feeling of impending doom.
●​ Atypical Symptoms: More common in women, older adults, and individuals with
diabetes. May include:
○​ Fatigue
○​ Dyspnea without chest pain
○​ Indigestion or heartburn-like symptoms
○​ Arm pain (without chest pain)
○​ Back pain
○​ Generalized weakness
○​ Syncope (fainting)

7. Diagnosis
Prompt and accurate diagnosis is critical for effective management of ACS. The diagnostic
process typically involves:
a. Clinical Assessment:

●​ Detailed History: Including symptom onset, duration, character, radiation,

aggravating/alleviating factors, and presence of risk factors.
●​ Physical Examination: Assessment of vital signs, heart sounds, lung sounds, and signs
of heart failure.

b. Electrocardiogram (ECG):

●​ A 12-lead ECG should be performed within 10 minutes of presentation.

●​ STEMI: Persistent ST-segment elevation (\ge 1 \, mm in \ge 2 contiguous leads, or new
left bundle branch block).
●​ NSTEMI/UA: ST-segment depression, T-wave inversion, or non-specific changes. May be
normal in some cases of UA.

c. Cardiac Biomarkers:

●​ Cardiac Troponins (I or T): Highly sensitive and specific markers of myocardial injury.
Levels rise within 3-6 hours of myocardial damage, peak at 12-24 hours, and can remain
elevated for several days. Serial measurements are often performed.
●​ Creatine Kinase-Myocardial Band (CK-MB): Less specific than troponins but can be
useful. Rises within 4-6 hours, peaks at 18-24 hours, and returns to normal within 2-3
days.

d. Other Diagnostic Tests:

●​ Echocardiography: To assess ventricular function, wall motion abnormalities, and rule

out other causes of chest pain.
●​ Coronary Angiography: Gold standard for visualizing coronary artery anatomy,
identifying blockages, and guiding revascularization. Typically performed urgently in
STEMI and selectively in NSTEMI/UA.
●​ Stress Testing (after stabilization): To assess for inducible ischemia in patients with
NSTEMI/UA who have been stabilized.

8. Management and Treatment

The management of ACS depends on the type of ACS (STEMI vs. NSTEMI/UA) and aims to
restore blood flow, limit myocardial damage, alleviate symptoms, and prevent future
cardiovascular events.

a. Immediate Management (Pre-hospital and Emergency Department):

●​ MONA (Morphine, Oxygen, Nitroglycerin, Aspirin): While historically a mnemonic, the

order and necessity of these interventions have evolved.
○​ Aspirin (ASA): Administer immediately to all suspected ACS patients (unless
contraindicated) to inhibit platelet aggregation.
○​ Nitroglycerin (NTG): Sublingual or IV, to reduce chest pain by causing
vasodilation.
 ○​ Oxygen: Administer if oxygen saturation is below 90% or if the patient is in
respiratory distress.
○​ Morphine: For severe pain not relieved by nitroglycerin.
●​ Antiplatelet Therapy:
○​ P2Y12 Inhibitors: Clopidogrel, Ticagrelor, Prasugrel (often given in conjunction
with aspirin). These further inhibit platelet aggregation.
●​ Anticoagulation:
○​ Heparin (unfractionated or low molecular weight) or Bivalirudin to prevent thrombus
propagation.

b. Reperfusion Strategy (for STEMI):

The goal is to open the blocked artery as quickly as possible.

●​ Primary Percutaneous Coronary Intervention (PCI): The preferred method if available
within a timely manner (door-to-balloon time < 90 minutes). Involves threading a catheter
to the blocked artery, inflating a balloon to open the vessel, and often placing a stent to
keep it open.
●​ Fibrinolysis (Thrombolysis): Administering clot-dissolving medications (e.g., alteplase,
tenecteplase) if PCI is not readily available (door-to-needle time < 30 minutes).

c. Management for NSTEMI/UA:

●​ Risk Stratification: Patients are stratified into low, intermediate, and high risk based on
clinical features, ECG changes, and biomarker levels.
●​ Pharmacological Management:
○​ Dual antiplatelet therapy (aspirin + P2Y12 inhibitor)
○​ Anticoagulation
○​ Beta-blockers: Reduce myocardial oxygen demand and improve outcomes.
○​ Statins: Lower cholesterol and stabilize plaque.
○​ ACE inhibitors/ARBs: For patients with left ventricular dysfunction or other
comorbidities.
●​ Invasive Strategy: Early coronary angiography with possible PCI or coronary artery
bypass grafting (CABG) is generally recommended for high-risk NSTEMI patients. A
delayed or selective invasive strategy may be considered for lower-risk patients.

d. Long-Term Management and Secondary Prevention:

After the acute phase, ongoing management is crucial to prevent recurrent events:
●​ Lifestyle Modifications:
○​ Smoking cessation
○​ Regular physical activity
○​ Heart-healthy diet (low in saturated/trans fats, cholesterol, sodium)
○​ Weight management
○​ Stress management
●​ Medication Adherence:
○​ Aspirin (indefinitely)
○​ P2Y12 inhibitor (for a specified duration, usually 6-12 months)
○​ Statins (high-intensity, indefinitely)
 ○​ Beta-blockers (for at least one year, longer if indicated)
○​ ACE inhibitors/ARBs (if indicated)
●​ Cardiac Rehabilitation: Structured exercise, education, and counseling program to
improve cardiovascular health and reduce risk.
●​ Regular Follow-up: With a cardiologist for ongoing monitoring and management of risk
factors.

9. Complications of ACS
ACS can lead to various complications, some of which are life-threatening:
●​ Arrhythmias (Dysrhythmias): Irregular heart rhythms, including ventricular fibrillation
(VF) and ventricular tachycardia (VT), which can lead to sudden cardiac death.
●​ Heart Failure: Weakening of the heart muscle, leading to fluid buildup in the lungs and
other parts of the body.
●​ Cardiogenic Shock: Severe form of heart failure where the heart cannot pump enough
blood to meet the body's demands, leading to organ dysfunction.
●​ Mechanical Complications:
○​ Ventricular Septal Rupture (VSR)
○​ Papillary Muscle Rupture (leading to severe mitral regurgitation)
○​ Free Wall Rupture (can cause cardiac tamponade)
●​ Pericarditis: Inflammation of the sac surrounding the heart.
●​ Recurrent Ischemia/Infarction: Further episodes of reduced blood flow or heart attack.
●​ Stroke: Due to emboli (blood clots) originating from the heart.

10. Prognosis
The prognosis of ACS has significantly improved with advancements in diagnosis and
treatment. However, it remains a serious condition. Factors influencing prognosis include:
●​ Extent of Myocardial Damage: Larger areas of infarction are associated with worse
outcomes.
●​ Timeliness of Reperfusion: Earlier reperfusion leads to better myocardial salvage and
outcomes.
●​ Presence of Complications: Development of heart failure, arrhythmias, or mechanical
complications worsens prognosis.
●​ Adherence to Secondary Prevention: Patients who diligently manage their risk factors
and adhere to medications have a better long-term outlook.

11. Conclusion
Acute Coronary Syndrome is a critical cardiovascular emergency stemming from abrupt
reduction in blood flow to the heart muscle. Early recognition of symptoms, rapid diagnosis
through ECG and cardiac biomarkers, and prompt implementation of reperfusion strategies
(especially for STEMI) are paramount to minimizing myocardial damage and improving patient
outcomes. Long-term management focusing on lifestyle modifications, medication adherence,
and cardiac rehabilitation is essential for preventing recurrent events and enhancing the quality
of life for individuals who have experienced ACS. Continued research and public awareness
campaigns are vital in the ongoing fight against this prevalent and potentially devastating
condition.