Exam #1 N222

Cardiac Rhythms and Heart Failure

Basic ECG Rhythm interpretation

Basic ECG Rhythm Interpretation

• Electrical Conduction Pathway: Depolarization and repolarization generate electrical changes across cell membranes1. The impulse originates in the Sinoatrial (SA) node, travels across internodal pathways to the Atrioventricular (AV) node, moves through the Bundle of His and bundle branches, and spreads through the Purkinje fibers.

• Waveforms & Normal Intervals:

  • P Wave: Represents atrial depolarization; P waves should look uniform and precede every QRS complex1.

  • QRS Complex: Represents ventricular depolarization; normal duration is less than 0.12 seconds. A widened QRS complex signifies a conduction delay or bundle branch block.

  • T Wave: Represents ventricular repolarization1.

  • PR Interval: Represents the time taken for impulse transmission from the SA node through the AV node to the ventricles (beginning of P wave to beginning of QRS complex)1. Normal duration is 0.12 to 0.20 seconds1. An interval $>0.20$ seconds indicates an AV conduction delay (AV heart block).

  • QT Interval: Represents total ventricular depolarization and repolarization time (beginning of Q wave to end of T wave)1. Normal is less than half the R-R interval at heart rates of 60–100 bpm1. Duration $>0.50$ seconds is considered dangerously prolonged.

  • R-R Interval: Used to assess ventricular rate and regularity; equal distances represent a regular rhythm1.

• Eight Steps for ECG Analysis: (1) Measure heart rate, (2) Examine R-R regularity, (3) Examine P wave morphology, (4) Measure PR interval, (5) Verify P wave precedes every QRS, (6) Measure QRS width, (7) Measure QT interval, (8) Interpret overall rhythm1.

• Triggers in High-Acuity Patients: Patients with electrolyte imbalances, hypoxemia, fluid volume shifts, or extreme temperature variations are highly vulnerable to dysrhythmias.

Telemetry Electrode Placement

What do you tell the patient when putting them on electrodes? There are no electrical, it just takes a picture of your heart and hold still

Purpose of Telemetry

Telemetry allows continuous ECG monitoring while giving patients freedom of movement within a certain area without losing transmission of the ECG signal. The ECG cable attaches to a battery-operated transmitter held in a pouch, and the signal transmits to a remote monitor via antennae (usually in the ceiling).

Electrode Placement Location

For continuous ECG monitoring, electrodes are placed on the trunk rather than the limbs. Movement of the extremities causes "noise" or motion artifact on the ECG signal, so trunk placement on a more stable area minimizes artifacts and provides a clearer signal.

Five-Electrode System Placement

If the monitoring system provides five electrode cables, this placement allows the monitor lead-select control to be changed to provide lead I, II, III, aVR, aVL, aVF, or one chest lead. The monitor automatically alters the polarity of the electrodes to provide the lead selected.

• Memory trick to help memorize Five-Electrode System Placement

  • Right upper is white and right lower is green because snow always lays on top of green. Think of RIGHT and WHITE and how they sound similar

    • WHITE ON RIGHT

    • WHITE OVER GREEN (SNOW OVER GRASS)

  • Left upper is black and left lower is red because smoke always rises from the fire

    • BLACK OVER RED (SMOKE OVER FIRE)

  • Brown is like chocolate and is on the center of the chest by the heart (more towards right side)

    • I HEART CHOCLATE

Proper Skin Preparation

To ensure best signal transmission and decrease skin impedance:

• Clean the skin and clip hairs if needed

• Ensure the area for electrode placement is dry

• Verify the gel on each electrode is moist and fresh

• Contact site should be free of lotion or other substances that increase skin impedance

• Electrodes cannot be placed on irritated skin or over scar tissue

Application Technique

Attach the electrode to the lead cable first, then to the contact site.

Roles and Responsibilities

• Assistive personnel (AP) may apply the electrodes

• The nurse determines which lead to select and checks for correct electrode placement

• The nurse is responsible for accurate patient assessment and management

Monitoring Systems

Most acute care facilities have monitor technicians educated in ECG rhythm interpretation who provide technical support. This is particularly helpful on telemetry units without bedside monitors. However, nursing assessment remains critical to initiate appropriate interventions

Left-sided vs. right-sided heart failure

Left-Sided Heart Failure (LHF): The left ventricle cannot pump effectively, resulting in decreased systemic tissue perfusion and blood backing up into the lungs. The left ventricle is responsible for pumping oxygenated blood out to the body. When the left ventricle cannot pump effectively, blood backs up into the left atrium and then into the pulmnonary veins and LUNGS.

• Clinical Findings: Dyspnea, shortness of breath, orthopnea, paroxysmal nocturnal dyspnea, weakness, fatigue, dizziness, acute confusion, oliguria (low urine output), bilateral crackles, wheezes, elevated pulmonary capillary wedge pressure, pulmonary congestion pink-tinged or blood-tinged sputum, and high risk for acute pulmonary edema.

  • Might be in a tripod position to help breathe better

Right-Sided Heart Failure (RHF): The right ventricle cannot pump effectively, causing blood to back up into the systemic venous circulation.

• Clinical Findings: Jugular venous distension (JVD), peripheral/dependent edema, swollen hands and feet, increased abdominal girth, ascites, hepatomegaly, splenomegaly, and fluid retention. Daily weight is the most reliable indicator of fluid gain or loss.

Heart failure assessment findings

• Laboratory Testing: Electrolytes (low sodium and potassium), CBC (low Hgb/Hct), Urinalysis (revealing proteinuria and high specific gravity), elevated B-type Natriuretic Peptide (BNP), and Arterial Blood Gases (ABGs).

• Imaging & Diagnostics: Chest X-ray (CXR showing cardiomegaly or pulmonary congestion), ECG, and Echocardiography (identified as the best diagnostic tool) to evaluate structure and Ejection Fraction (EF)

Left-Sided Heart Failure

Cardiovascular Signs:

• Tachycardia or pulsus alternans (pulse alternating in strength)

• Irregular heart rhythms: premature atrial contractions (PACs), premature ventricular contractions (PVCs), or atrial fibrillation

• Decreased cardiac output leading to impaired tissue perfusion

Respiratory Signs:

• Dyspnea - described as "trouble catching my breath," "breathlessness," or "difficulty breathing"

• Respiratory rate typically exceeds 20 breaths/min

• Orthopnea (dyspnea when lying flat) - ask how many pillows used for sleeping

• Paroxysmal nocturnal dyspnea3

• Cough - initially irritating, nocturnal, usually nonproductive in early HF

• Cough with frothy sputum in pulmonary edema

• Inspiratory crackles and pleural effusions on exam

• Cyanosis and signs of hypoxia from impaired gas exchange

Other Signs:

• Fatigue and weakness with activity or heaviness in arms/legs

• Activity intolerance - inability to perform ADLs or climb stairs without symptoms

• Chest pain from impaired myocardial perfusion

• Palpitations or fast heartbeat

• Nocturia when at rest

• Renal dysfunction from decreased blood flow to organs

• S3 gallop on cardiac exam

Right-Sided Heart Failure

Fluid Accumulation:

• Jugular venous distention (JVD)

• Dependent edema: ankles/legs in ambulatory patients; sacrum in bedridden patients

• Hepatomegaly (liver engorgement)

• Hepatojugular reflux

• Ascites - abdominal fluid can exceed 10 L

• Increased abdominal girth

GI Effects:

• Early satiety from abdominal pressure on stomach/intestines

• Malnutrition, anorexia, GI distress

Heart failure interventions and symptom management

• Priority Nursing Problems: Impaired gas exchange, decreased cardiac output, fatigue/weakness, and potential for pulmonary edema.

• Priority Nursing Interventions:

• Promote Gas Exchange: Position patient in high Fowler's if short of breath. Monitor respiratory rate every 1 to 4 hours and auscultate breath sounds every 4 to 8 hours. Maintain target oxygen saturation via oxygen therapy or ventilation assistance.

• Improving Cardiac Output: Improved/increased cardiac pump effectiveness, hemodynamic regulation, and medications

• Manage Output & Balance: Administer prescribed diuretics and cardiac medications, enforce fluid restrictions, manage energy conservation, and monitor daily weight.

• Acute vs. Chronic Compensatory Mechanisms: Acute HF has a sudden onset where compensatory mechanisms do not have time to activate. Chronic HF activates compensatory mechanisms (Sympathetic Nervous System, Renin-Angiotensin-Aldosterone System, and ventricular remodeling) that initially help but ultimately worsen cardiac performance.

Acute Heart Failure Management

Immediate Goals: Interrupt the cycle of decreasing contractility, increasing preload, and increasing afterload.

Pharmacological Interventions:

• Oxygen, nitrates, and morphine: Improve myocardial oxygenation, relieve coronary spasm, and lower preload through systemic venodilation

• Diuretics: Reduce preload

• Inotropic drugs (dopamine, dobutamine, milrinone): Increase contractility and raise blood pressure in hypotensive patients

• ACE inhibitors, ARBs, aldosterone blockers: Reduce preload and afterload by decreasing aldosterone levels and peripheral vascular resistance

Advanced Support: Patients with severe HFrEF may benefit from intraaortic balloon pump (IABP) or left ventricular assist devices (LVADs) until surgery can be performed.

Chronic Heart Failure Management

Management is based on four clinical stages:

• Stage A (at risk): Lifestyle modification, reduced sodium intake, increased physical activity, weight loss, blood pressure and glucose management

• Stages B-D: Progression to advanced therapies

Current Drug Therapy Guidelines:

• First-line drugs: ACE inhibitors (lisinopril, enalapril, captopril), ARBs (valsartan, candesartan, losartan), or valsartan/sacubitril (Entresto), and beta blockers (metoprolol, carvedilol, bisoprolol)

• Additional drugs: Loop diuretics (furosemide), SGLT2 inhibitors (dapagliflozin, empagliflozin), hydralazine/isosorbide dinitrate, spironolactone, and ivabradine

• Digoxin: Only added after other drugs are utilized

HFpEF-Specific Treatment: Spironolactone, dual angiotensin-neprilysin inhibitors, SGLT inhibitors, ARBs, exercise training, and management of comorbidities.

Nursing Interventions

Monitoring:

• Vital signs (blood pressure, heart rate, respirations)

• Daily weights

• Intake and output

• Heart and breath sounds

• Serum potassium and magnesium levels (before digoxin administration)

Safety Considerations:

• Use infusion pump for IV heart failure medications

• Monitor for hypokalemia

• Watch for syncope with hydralazine/isosorbide dinitrate

• Check drug compatibility for milrinone solutions

• Verify normal blood pressure, pulse, potassium, and creatinine before valsartan/sacubitril

BNP and Echocardiogram (EF)

B-Type Natriuretic Peptide (BNP)

What is BNP?

BNP is a hormone produced by the ventricles. It's released when tension in the left ventricular wall increases, commonly occurring with congestive heart failure, or when transmural atrial pressure or mean arterial pressure increases.

Function:

• Dilates arterioles

• Promotes kidney excretion of salt and water

• Acts as a natural antagonist to the renin-angiotensin-aldosterone system (RAAS)

• Causes vasodilation and increases renal sodium and water excretion, decreasing blood pressure

• Protects against deleterious effects of volume and pressure overload on the heart and kidneys

Clinical Use in Heart Failure:

• BNP levels are usually elevated in patients with heart failure

• Used to confirm diagnosis alongside clinical signs, symptoms, and echocardiography

• Normal range is around 100

• Elevated in both HFrEF and HFpEF

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Echocardiogram and Ejection Fraction (EF)

Echocardiography Role:

• Gold standard diagnostic tool for confirming heart failure

• Demonstrates ventricular filling patterns and ejection fraction

• In HFpEF: Shows poor ventricular filling with normal EFs

Ejection Fraction Values:

Normal EF: 50-70% (some sources cite 55-70%)

HFrEF (Systolic Heart Failure):

• EF <40%

• EF <30% qualifies for ICD placement due to sudden cardiac death risk

HFpEF (Diastolic Heart Failure):

• EF ≥50%

• Despite normal ejection fraction, symptoms and signs of heart failure are present

• Diagnosis confirmed by presence of HF signs/symptoms, normal left ventricular EF, AND evidence of diastolic dysfunction1

Clinical Correlation:

• EF measures percentage of blood ejected from the heart during systole3

• As EF decreases in HFrEF, tissue perfusion diminishes and blood accumulates in pulmonary vessels

• In HFpEF, the ventricle cannot relax/fill adequately despite preserved pumping ability

Systolic vs. diastolic heart failure

Which one has a higher ejection fraction? IT is diastolic

Differences

Systolic Heart Failure (HFrEF - Heart Failure with Reduced Ejection Fraction)

• Ejection Fraction: ≤40% (normal is 55-70%)

• Primary Problem: Inability to contract adequately - heart cannot pump blood effectively

• Mechanism: Decreased contractility from ventricular remodeling

• Also called: "Forward failure" because cardiac output is decreased

• Patient Population: More common in all demographics

• ICD Indication: EF <30% qualifies for implantable cardioverter/defibrillator

• Leads to dilated ventricle, weak contraction, and pumps less blood out

Diastolic Heart Failure (HFpEF - Heart Failure with Preserved Ejection Fraction)

• Ejection Fraction: ≥50%

• Primary Problem: Inability to relax adequately during diastole - ventricle cannot fill properly

• Mechanism: Decreased compliance and stiffening from inflammation, fibrosis, and remodeling

• Key Feature: Ventricle becomes less compliant; more pressure needed to move same volume

• Prevalence: Represents >50% of left heart failure cases; cited as 20-40% in another source

• Patient Population: Primarily older adults and females with chronic hypertension and undetected coronary artery disease

• Leads to stiff ventricle, impaired relaxation, and less filling but pumps out normal EF

Similarities

Risk Factors:

• Hypertension

• Aging

• Obesity

• Diabetes

• Myocardial ischemia

• Valvular heart disease

• Atrial fibrillation

• Cardiomyopathies

Clinical Manifestations:

• Dyspnea on exertion and fatigue

• Pulmonary congestion symptoms

• Signs and symptoms are similar between both types

Pathophysiology:

• Both involve neurohumoral changes (increased RAAS and SNS)

• Both result in ventricular remodeling

• Both can cause pulmonary edema and systemic congestion

Outcomes:

• Both associated with poor quality of life and significant mortality

Management: Treatment approaches are similar for both types

Prosthetic valve replacement aftercare

• If you have a valve replacement, what do you worry about? You worry about clotting because they are usually on blood thinners

• Patients with mechanical prosthetic heart valves require lifelong oral anticoagulation therapy (monitoring PT/INR) to prevent thromboembolism. Nursing care includes teaching bleeding precautions and enforcing prophylactic antibiotic therapy prior to dental or invasive procedures to prevent infective endocarditis.

Immediate Postoperative Care

Monitoring Priorities:

• Cardiac output (CO): Patients with valve replacements are at higher risk for significant CO reductions after surgery, especially those with aortic stenosis or left ventricular failure from mitral valve disease

• Heart failure signs: Report any indications of HF to the surgeon immediately

• Postoperative nursing interventions are similar to those for CABG patients

Anticoagulation Management

Mechanical Valves:

• Require lifelong anticoagulation therapy with warfarin to prevent thrombus formation

• Target INR: 3.0 to 4.0 (higher than standard anticoagulation)

• Frequent INR monitoring required

Biologic Valves (Xenografts):

• Long-term anticoagulation NOT indicated due to little risk for clot formation

• Includes porcine (pig) and bovine (cow) valves

• Must be replaced every 7-10 years; durability relates to patient age

Patient Education

Bleeding Precautions (for those on warfarin):

• Avoid foods high in vitamin K (especially dark green leafy vegetables)

• Use electric razor to avoid skin cuts

• Report any bleeding or excessive bruising to provider

Infection Prevention:

• Risk for infective endocarditis with defective or repaired valves

• Inform all health care providers of valve replacement history

• Require prophylactic antibiotics before all invasive dental procedures

Incision Care:

• Watch for and report fever, drainage, or redness/hyperpigmentation at sternal incision site

• Avoid heavy physical activity involving upper extremities for 3-6 months to allow healing

Activity Resumption:

• Most patients return to normal activity after 6 weeks

Preoperative Preparation

Dental clearance required before elective valve replacement:

• Dental caries or periodontal disease must be resolved first

• Stop oral anticoagulants at least 72 hours before surgery

Noninfectious Lower Respiratory Disorders

Oxygen Delivery Modalities

Low-Flow Oxygen Delivery Systems

Nasal Cannula:

• Flow rates: 1-6 L/min

• Oxygen concentrations: 24% (at 1 L/min) to 44% (at 6 L/min)

• Flow rates >6 L/min don't increase gas exchange and cause mucosal irritation

• Indication: Mild SOB, asthma, COPD, CF, pneumonia, to ease work of breahting

• Risks: Mucosal drying, skin breakdown at nares and ears

Face Masks:

• Simple face mask: Delivers variable oxygen concentrations

  • Flow rate: 6-10 L/min

  • Indication: If NC is insufficient and/or mild respiratory distress

  • Risks: Claustrophobia, CO2 buildup on low flow rates, cannot eat or drink while wearing, may not fit well

• Nonrebreather mask: Provides highest oxygen level of low-flow systems

  • Can deliver Fi O₂ >90% depending on breathing pattern

  • Flow rate: 10-15 L/min to keep reservoir bag inflated

  • Has one-way valve between mask and reservoir

  • Flaps prevent room air from entering through exhalation ports

  • Used for unstable respiratory status when intubation may be needed

  • Indication: If NC or simple mask are insufficient, traumatic injuries, after smoke inhalation

  • Risks: Uncomfortable on patient’s face, impedes patient’s ability to communicate, eat, and drink

High-Flow Oxygen Delivery Systems

High-Flow Nasal Cannula (HFNC):

• Flow rates: 30-60 L/min

• Oxygen concentrations: 24% to 100%

• Provides heat, humidity, and precise Fi O₂

• Better tolerated than other high-flow systems

• Less tissue breakdown risk than NPPV because it uses nasal cannula instead of tight-fitting mask

• Adjust Fi O₂ and flow rates independently using pulse oximetry

• Indication: Pneumonia, post-extubation, pre-oxygenation prior to intubation, DNI patients with respiratory failure

• Risks: Expensive, not typically available for home use due to high flow rates

Venturi Mask (Ventimask):

• Delivers most accurate oxygen concentration without intubation

• Works by pulling in proportional room air for each liter of oxygen

• Adapters with different-sized holes allow specific air-oxygen mixing

• Each adapter requires different flow rate

• Indication: Often used in persistent hypercarbia or moderate to severe hypoxemia (COPD)

• Risks: Only goes up to 60% FiO2, so not for patients who have significantly high oxygen demands, bulky; impedes communication, eating, and drinking

Other High-Flow Systems:

• Aerosol mask: Used when high humidity needed

• Face tent: Fits over chin, extends halfway across face; useful for facial trauma/burns

Noninvasive Positive-Pressure Ventilation (NPPV)

CPAP (Continuous Positive Airway Pressure):

• Delivers set positive airway pressure continuously during inhalation and exhalation

• Used primarily for obstructive sleep apnea

• Requires tight-fitting nasal-oral facemask, nasal mask, or nasal pillows

• Newer machines: quiet, humidified, smaller masks to improve adherence and maintain tissue integrity

• Can monitor parameters (O₂ saturation, apnea episodes, heart rate)

Big Valve Mask

-A face mask and reservoir bag that is positioned over the patient’s nose/mouth while forcing air into the lungs by squeezing the bag

-Delivers 12-15 L/min

-Indication: Emergent resuscitation, hypercapnic, respiratory failure, hypoxic respiratory failure, apnea, altered mental status with the inability to protect the airway

-Risks: Requires an effective seal, provider fatigue, used for short-term ventilation only

ABG interpretation

Normal ABG Values

• pH: 7.35-7.45

• PaCO₂: 35-45 mmHg

• HCO₃⁻: 21-28 mEq/L

Step-by-Step Interpretation

Step 1: Determine pH Status

• pH <7.35 = Acidosis

• pH >7.45 = Alkalosis

Step 2: Identify the Primary Cause

• Respiratory: Look at PaCO₂

  • High CO₂ (>45) with low pH = Respiratory Acidosis

  • Low CO₂ (<35) with high pH = Respiratory Alkalosis

• Metabolic: Look at HCO₃⁻

  • Low HCO₃⁻ with low pH = Metabolic Acidosis

  • High HCO₃⁻ with high pH = Metabolic Alkalosis

Step 3: Check for Compensation

• Body attempts to normalize pH by adjusting the opposite system

• Partial compensation: pH still abnormal but moving toward normal

• Full compensation: pH returns to 7.35-7.45

Clinical Conditions

Respiratory Acidosis:

• Excessive CO₂ buildup combines with water to produce carbonic acid, decreasing blood pH

• Causes: Hypoventilation, COPD, respiratory muscle fatigue

Respiratory Alkalosis:

• Triggered by hyperventilation from hypoxia and pain

• Shows low PaCO₂ on ABG analysis

• Example: Early pulmonary embolism

COPD-Specific Pattern:

• Chronic respiratory acidosis (increased PaCO₂)

• Metabolic alkalosis as compensation (kidneys retain bicarbonate, elevating HCO₃⁻)

• pH remains lower than normal despite elevated bicarbonate

• Not all COPD patients retain CO₂; hypercapnia more common in advanced emphysema than bronchitis

Metabolic Acidosis:

• Develops from lactic acid buildup due to tissue hypoxia

• Seen in late-stage pulmonary embolism after initial respiratory alkalosis

Clinical Application

Monitoring:

• Obtain baseline ABGs, then use pulse oximetry to gauge treatment response

• Compare repeated ABG values to assess changes in respiratory status

Critical Signs:

• Severe dyspnea with respiratory muscle fatigue

• Unresponsive hypoxemia

• Respiratory acidosis

• These indicate impending respiratory failure

Asthma (Triggers, Assessment findings, Peak flow zones, and Interventions)

• Pathophysiology & Triggers: Chronic condition involving reversible bronchial obstruction, airway inflammation, and hyperresponsiveness. Triggers include allergens, exercise, cold air, respiratory infections, and environmental pollutants.

• Assessment & Diagnostic Findings: Dyspnea, wheezing, coughing, use of accessory muscles, chest tightness, and decreased expiratory airflow. Pulmonary function tests show decreased FEV1 or PEFR (15%–20% below expected). An increase of 12% in FEV1 after bronchodilator administration confirms an asthma diagnosis.

• Peak Flow Meter Zones & Priorities:

  • Green Zone: Equal to or greater than 80% of personal best (good control).

  • Yellow Zone: 50%–80% of personal best (caution; take quick-relief medication).

  • Red Zone: Less than 50% of personal best (severe medical alert)1.

  • Priority Action in Red Zone: Administer rescue drugs (Short-Acting Beta-Agonists / SABAs) immediately.

• Interventions: Oxygen therapy during acute attacks, exercise as tolerated to balance ventilation-perfusion matching, inhaled corticosteroids, and mucolytics

Asthma vs. COPD

• Asthma: Reversible airway obstruction driven by acute spasms and inflammation.

• COPD: Irreversible, progressive tissue destruction combining Emphysema (alveolar destruction and air trapping) and Chronic Bronchitis (chronic airway inflammation and hypersecretion).

• Oxygen Safety in Chronic Hypercarbia: COPD patients with chronic elevated CO2 rely on a hypoxic drive to breathe. Administer low-flow oxygen (1–2 L/min via nasal cannula) to avoid blunting their respiratory drive.

• COPD Interventions: Monitor respiratory status at least every 2 hours; teach controlled coughing, energy conservation, chest physiotherapy, diaphragmatic breathing, and pursed-lip breathing

Key Differences

Feature	Asthma	COPD
Reversibility	Variable and reversible airflow limitation	Not fully reversible; pathologic changes are permanent
Age of Onset	All ages; 6.5% of children, 8% of adults	Typically develops after prolonged exposure (smoking history)
Airflow Obstruction	Increases ≥12% after bronchodilator	Progressive and unresponsive to bronchodilators
Primary Problem	Chronic airway inflammation causing hyperresponsiveness	Chronic obstruction from structural damage (bronchitis/emphysema)
Symptom Pattern	Intermittent episodes varying in time and intensity	Progressive dyspnea; chronic bronchitis has persistent productive cough
Physical Exam (Between Episodes)	Often normal	Barrel chest, tripod position, pursed-lip breathing, use of accessory muscles
Cough	Variable, increases with inflammation	Chronic bronchitis: persistent productive cough; Emphysema: productive only during exacerbations

Lung cancer (Risk factors, Assessment findings, and Symptom management)

• Risk Factors: Cigarette smoking (primary cause; e.g., 40+ pack-year history), occupational exposure to asbestos or radon, and genetics.

• Assessment Findings: Persistent cough, hemoptysis, chest pain, dyspnea, wheezing, hoarseness, and unexplained weight loss.

• Symptom Management: Palliative radiation therapy, chemotherapy, pain management, and thoracentesis to relieve pleural effusion

Risk Factors

Primary Risk Factor:

• Cigarette smoking: Accounts for 80-90% of primary lung cancers

• Tobacco smoke contains >7000 chemicals, 69 classified as carcinogens

• Risk greatest in individuals who start young and continue throughout life

Other Risk Factors:

• Aging

• Secondhand (environmental) smoke

• Radon gas exposure

• Occupational exposures: Asbestos and other workplace toxins

• Radiation

• Indoor and outdoor air pollution

• Genetic mutations (growth factor receptors, DNA repair mechanisms)

Assessment Findings

History:

• Pack-year smoking history

• Workplace hazards

• Warning signals: hoarseness, cough, sputum production, hemoptysis, shortness of breath, change in endurance

• Recent symptom changes or position-related symptoms

Pain Patterns:

• Chest pain/discomfort: Can occur at any stage; may be localized or one-sided, ranging from mild to severe

• Fullness, tightness, or pressure: Suggests obstruction

• Piercing/pleuritic pain: Occurs on inspiration

• Pain radiating to arm: Indicates nerve plexus invasion in advanced disease

Pulmonary Symptoms:

• Often nonspecific and appear late in disease

• Chills, fever, cough: Related to pneumonitis/bronchitis from obstruction

• Blood-tinged sputum: May occur with tumor bleeding

• Hemoptysis: Later finding

• Purulent, copious sputum: Indicates infection/necrosis

• Breathing patterns: Labored, painful, obstructive (prolonged exhalation alternating with shallow breathing), or rapid/shallow with pleuritic pain

• Dyspnea and wheezing: With airway obstruction

Physical Exam:

• Abnormal retractions

• Accessory muscle use

• Flared nares, stridor

• Asymmetric diaphragmatic movement

• Fremitus changes: Increased where air spaces replaced by tumor/fluid; decreased/absent with bronchial obstruction

Symptom Management

Dyspnea:

• Positioning: Semi-Fowler's or lounge/reclining chair

• Oxygen therapy: Relieves dyspnea and anxiety when hypoxemic

• Continuous morphine infusion

Hemoptysis & Obstruction:

• Radiation therapy: Relieves hemoptysis, bronchial/vein obstruction (superior vena cava syndrome), esophageal compression, bone metastasis pain

Pleural Effusion:

• Thoracentesis: Removes fluid via needle/catheter; may connect to gravity drainage for large volume

Chest tube management

• Purpose is to drain air or fluid from the pleural space to re-expand the lungs.

• Nursing Priorities: Keep drainage unit upright and below chest level; monitor water seal chamber (tidaling with respiration is normal; continuous bubbling indicates an air leak); measure drainage volume/color; maintain occlusive dressing over insertion site; keep sterile water and occlusive dressing at bedside

Purpose & Components

Chest tubes drain air and blood from the pleural space after thoracotomy, allowing lung reexpansion. The system consists of:

• One or more chest tubes

• Collection container below chest level

• Water seal preventing air from entering chest

Three-Chamber System:

1. Drainage collection chamber: Connects to patient; measure fluid hourly in first 24 hours; fluid must never contact tubes (prevents drainage, risks tension pneumothorax)

2. Water-seal chamber: Contains ≥2 cm water; acts as one-way valve preventing air return to patient

3. Suction control chamber: Wet or dry type; set per surgeon order

Nursing Priorities

Main goals: Ensure system integrity, promote comfort, ensure patency, prevent complications

Hourly Checks:

• Sterility and patency of system

• Keep sterile gauze at bedside (cover site if tube dislodges)

• Keep padded clamps at bedside (use if system interrupted)

Water-Seal Assessment

Normal Findings :

• Bubbling: Normal during forceful expiration/coughing (air expelled from chest)

• Tidaling: Water rises 2-4 inches on inhalation, falls on exhalation

Abnormal Findings:

• Continuous bubbling: Indicates air leak; notify surgeon

• No bubbling: May indicate lung reexpanded OR tube blocked/kinked

• Absent tidaling: Lung fully reexpanded OR obstruction present

• Excessive bubbling: May indicate air leak

Tube Placement

Two insertion sites:

• Air drainage tube: Third intercostal space (lateral to scapula)

• Blood drainage tube: Sixth intercostal space

Removal

Performed when drainage minimal and lung expansion stable. Post-removal care:

• Site dressed with occlusive dressing

• Observe for drainage

• Assess hourly for respiratory distress for first few hours

Portable Systems

"Dry" systems use dynamic flutter valve instead of water seal; lighter weight allows ambulation and home discharge with tubes in place

Inflammation, Hematology & HIV

Inflammation vs. Infection

• Inflammation: Non-specific, immediate innate tissue response to injury or foreign invasion characterized by five cardinal signs: redness, warmth, swelling, pain, and reduced function.

• Infection: Multiplication of microorganisms (bacteria, viruses, fungi) within body tissues. Infection triggers inflammation, but inflammation can occur without infection

Key Differences

Feature	Inflammation	Infection
Definition	Nonspecific body response to tissue injury or invasion	Invasion of pathogens that multiply and cause disease
Relationship	Can occur without infection	Usually triggers inflammation and is accompanied by it
Causes	Tissue injury, infections, allergic reactions, noninfectious invasions	Pathogens (bacteria, viruses, fungi, parasites)

Inflammation Without Infection

Tissue Injury Examples:

• Joint sprains

• Myocardial infarction

• Blister formation

Noninfectious Invasion Examples:

• Allergic rhinitis

• Contact dermatitis

• Other allergic reactions

Important: Inflammation does not always mean infection is present

Inflammation With Infection

Common Examples:

• Otitis media

• Appendicitis

• Viral hepatitis

• Cholecystitis

Vascular Response

Normal state: Minimal lymphocytes and macrophages in tissue

Inflamed state:

• Arteriole and venule dilation

• Capillary bed expansion

• Neutrophil emigration into tissues

• Plasma protein leakage causing edema

Types of Inflammation

Acute:

• Short duration (hours to days, typically 8-10 days)

• Self-limiting; continues only until threat eliminated

• Can be localized or systemic

Chronic:

• Lasts weeks, months, or years

• Often systemic

• Develops when acute response inadequate or doesn't resolve

• Associated with persistent bacterial contamination, foreign objects, resistant microorganisms

• Examples: ulcerative colitis, rheumatoid arthritis

Clinical Application

Key Nursing Consideration: Always assess for source of inflammation—differentiate between infectious causes requiring antimicrobial therapy versus non-infectious causes requiring different interventions

Active immunity vs. Passive immunity

• Innate Physical/Physiological Barriers: Skin, mucous membranes, cilia, body temperature, and pH.

• Active Immunity: Body produces its own antibodies against an antigen.

• Natural Active: Direct exposure to an infectious pathogen.

• Artificial Active: Vaccination/immunization.

• Passive Immunity: Pre-formed antibodies are transferred from an outside source (temporary protection).

• Natural Passive: Placental transfer or breast milk.

• Artificial Passive: Exogenous antibody injection (e.g., IVIG)

Key Differences

Feature	Active Immunity	Passive Immunity
Definition	Body actively makes its own antibodies against antigens	Antibodies transferred from another human or animal
Duration	Long-lasting	Short-term only
Body's Role	Takes active part in antibody production	Receives preformed antibodies; no active participation
Antibody Source	Self-produced	Foreign (recognized as non-self, eliminated quickly)

Active Immunity

Natural Active Immunity:

• Antigen enters body naturally (e.g., influenza A virus)

• Body responds by making antibodies

• Most effective and longest lasting type of adaptive immunity

• Usually causes disease initially but provides protection against reinfection

Artificial Active Immunity (Vaccine-Induced):

• Occurs through immunization/vaccination

• Attenuated antigens placed into body (oral or injection)

• Body actively produces antibodies

• Usually doesn't cause disease due to processed antigens

• Lasts many years; requires booster doses to maintain protection

• Examples: tetanus, diphtheria, polio vaccines

Passive Immunity

Natural Passive Immunity:

• Antibodies passed mother to fetus via placenta

• Antibodies passed to infant via colostrum and breast milk

Artificial Passive Immunity:

• Injection of antibodies created in another person or animal

• Provides immediate protection but short-lived

• Used to prevent disease/death when patient has little/no active immunity

• Examples: rabies exposure, tetanus exposure, poisonous snake bites

• COVID-19 convalescent plasma: High concentration of antibodies from recovered patients; most effective within 72 hours of symptom onset

Clinical Example

Tetanus wound management:

1. First: Inject antitetanus antibodies (passive immunity for immediate protection)

2. Later: Administer tetanus toxoid vaccine (active immunity for long-term protection)

Important Note

Antibody-mediated immunity works with inflammation and is most effective when combined with cell-mediated immunity

CBC Interpretation (WBC, RBC, Hgb/Hct, Platelets)

Complete Blood Count Components

What's Included:

• RBC count, WBC count, hematocrit, hemoglobin, red blood cell indices, platelet count

• CBC with differential also measures percentages of neutrophils, lymphocytes, monocytes, eosinophils, basophils

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White Blood Cell (WBC) Count

Measures: All leukocytes in 1 μL (or 1 L) of blood

Normal Range: 5,000–10,000 cells/mm³ (or 5–10 × 10⁹/L)

Interpretation:

• Elevated: Indicates infection, inflammation, or leukemia

• Decreased: Suggests bone marrow suppression, overwhelming infection, or immunosuppression

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Red Blood Cell (RBC) Count & Indices

RBC Count: Measures circulating RBCs in 1 mm³ (or 1 L) of blood

Adult/Older Adult Normal Range:

• Males: 4.2–6.2 million cells/mm³ [3]

• Females: 4.2–6.2 million cells/mm³ [3]

Hematocrit (Hct): Percentage of RBCs in total blood volume

• Normal range: 37%-52%

• Evaluates anemia and polycythemia

Hemoglobin (Hgb): Total amount of hemoglobin measured in g/dL

• Anemia indicators: Men <14 g/dL; Women <12 g/dL

RBC Indices Help Classify Anemia:

• MCV (Mean Corpuscular Volume): Average RBC size

  • Elevated = macrocytic (megaloblastic anemia)

  • Decreased = microcytic (iron deficiency anemia)

• MCH (Mean Corpuscular Hemoglobin): Average hemoglobin weight per RBC

• MCHC (Mean Corpuscular Hemoglobin Concentration): Average hemoglobin percentage per RBC

  • Decreased = hypochromic (lighter color; iron deficiency anemia)

• RDW (Red Cell Distribution Width): Variation in RBC size

Reticulocyte Count: Immature RBCs with nucleus

• Normal: ~2% of circulating RBCs

• Elevated in anemia/hemorrhage: Indicates bone marrow responding appropriately

• Low without cause: Suggests aplastic, iron-deficient, or pernicious anemia; malignancy; marrow failure

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Platelet Count

Normal Range: 150,000-400,000/mm³

Clinical Significance of Thrombocytopenia:

• 40,000-80,000/mm³: Prolonged bleeding from trauma, dental work, surgery

• <20,000/mm³: Critical value—risk of spontaneous, difficult-to-control bleeding

Lupus manifestations and complications

• Cutaneous Lupus (CLE): Skin-limited lesions; skin biopsy is the definitive diagnostic test.

• Systemic Lupus Erythematosus (SLE): Chronic, progressive autoimmune connective tissue disorder causing vasculitis and organ damage.

• Clinical Manifestations: Butterfly rash across face, photosensitivity, alopecia, oral ulcers, joint pain (arthralgia), muscle atrophy, and chronic fatigue. Fever is the classic indicator of an acute flare. Chronic steroid therapy risks osteonecrosis (bone death from avascularity, usually in the hip)

Overview

Systemic Lupus Erythematosus (SLE) is a chronic autoimmune disorder that can affect any organ in the body. It occurs more often in females (ages 20-40) and affects Black individuals more frequently than White individuals.

Pathophysiology

SLE produces autoantibodies against self-antigens, forming circulating immune complexes (type III hypersensitivity) that deposit in tissues 15. The most characteristic antibodies are antinuclear antibody (ANA) and anti-double-stranded DNA (anti-dsDNA) 15.

Key Manifestations by System

Skin:

• Malar (butterfly) rash: Dry, scaly, raised rash on cheeks/nose; appears in ~50% of patients

• Worsens with sun exposure (photosensitivity)

• Facial darkening (cheeks, nose, chin)

• Alopecia

• Oral/throat ulcers

• Non-scarring initially; may fluctuate with flares/remissions

Musculoskeletal:

• Arthritis and arthralgias (feet, ankles, knees, wrists, fingers)

• Bilateral joint involvement

• Painful, red, swollen joints with inflamed synovium

• No joint deformities (unlike rheumatoid arthritis—bone/cartilage not eroded)

• Myositis (muscle inflammation)

• Osteonecrosis/avascular necrosis: Especially after ≥5 years steroid treatment

Renal:

• Lupus nephritis: Common; high risk for end-stage renal failure

• Proteinuria

Hematologic:

• Anemia (type II hypersensitivity—RBC destruction)

• Lymphopenia (lymphocyte destruction)

• Thrombocytopenia (platelet destruction)

Other Systems:

• Serositis, pleuritis (visceral lining inflammation)

• Cardiovascular disease (major cause of death)

• Neurologic: Seizures, psychosis

• GI: Abdominal pain, vasculitis, hepatobiliary disease

• Eyes: Keratoconjunctivitis, retinopathy

Constitutional Symptoms:

• Chronic fatigue: Debilitating during flares; caused by stress, depression, inflammation, insomnia, infection

• Intermittent low-grade fever from chronic inflammation

Major Complications

• Organ failure (especially renal)

• Infection (leading cause of death)

• Cardiovascular disease (leading cause of death)

Lupus nephritis and renal monitoring

• Immune complexes deposit in glomeruli, leading to kidney involvement.

• Nursing Action: Monitor BUN, serum creatinine, proteinuria, hematuria, and severe hypertension.

• Drug Therapy: Corticosteroids (Prednisone for flares), Hydroxychloroquine (Plaquenil to reduce flare frequency), and DMARDs/immunosuppressants

Pathophysiology of Lupus Nephritis

Mechanism: Autoantibodies (especially anti-dsDNA) form circulating immune complexes that deposit in:

• Glomerular capillaries

• Kidney tubule basement membranes

This causes loss of tissue integrity and chronic inflammation.

Clinical Manifestations

Urinary Changes:

• Proteinuria: Persistent protein in urine; key indicator of reduced kidney function

• Cloudy urine

• Hematuria (blood in urine)

• Foamy urine appearance (caused by protein)

Systemic Signs:

• Edema (feet, ankles, shins, sacrum)

• Hypertension

• Risk progression to end-stage renal failure (common cause of death in SLE)

Kidney Function Assessment

Urinalysis:

• Check for protein, blood, cloudiness, foam

• Proteinuria typically <2 g/24 hours

• Fixed specific gravity (~1.010) despite variable fluid intake

• RBCs and casts may be present

Blood Tests:

• ↓ GFR (glomerular filtration rate)

• ↑ Serum creatinine: >6 mg/dL; may reach 30 mg/dL

• ↑ BUN: Often 100-200 mg/dL

• Electrolyte disturbances:

  • Sodium retention (may appear falsely normal from dilution)

  • Hyperkalemia when oliguria develops

  • Hyperphosphatemia

  • Low-normal or decreased calcium

• Metabolic acidosis from hydrogen retention and bicarbonate loss

Additional Testing:

• Antibody levels: ANA, anti-dsDNA

• Complement levels: Typically decreased during active disease

Nursing Monitoring Priorities

Cardiovascular Assessment:

• Blood pressure, heart rate, pulse quality

• Jugular venous distention

• Capillary refill, oxygen saturation

Fluid Status:

• Crackles on lung auscultation

• Edema (lower extremities, sacrum)

• Daily weights

Vascular integrity is compromised in lupus nephritis, leading to hypoxic injury and chronic kidney disease

Management Considerations

Treatment depends on severity and may include immunosuppressive therapy, ACE inhibitors (to reduce proteinuria), and careful monitoring of hydration status to prevent acute kidney injury

HIV (cART therapy)

What is cART?

Combination antiretroviral therapy (cART), also called HAART (Highly Active Antiretroviral Therapy), refers to combinations of antiretroviral drugs used to treat HIV infection. This is the standard treatment and is typically started immediately upon HIV diagnosis confirmation.

Drug Combinations

cART usually includes at least three medications. Common combinations include:

• Two or three NRTIs (nucleoside reverse transcriptase inhibitors)

• Two NRTIs plus one or two protease inhibitors

• An NRTI plus an NNRTI (non-nucleoside reverse transcriptase inhibitor) with one or two protease inhibitors

Drug Classes & Mechanisms

• Reverse transcriptase inhibitors: Block reverse transcriptase enzyme

• Protease inhibitors: Inhibit protease retroviral enzyme

• Fusion inhibitors: Inhibit viral fusion

• CCR5 antagonists: Block CCR5 coreceptors on CD4 cells, preventing viral entry

• Integrase inhibitors: Prevent integration of proviral genes into human DNA

Treatment Goals

Primary goal: Achieve undetectable viral load (<50 copies/mL)

When effective, cART leads to:

• Significant reduction in mortality

• Decreased opportunistic infections

• Improved physical performance

• Significantly increased T-cell counts

Important Considerations

Lifelong Treatment: cART is not curative—HIV persists in reservoirs (especially CNS) where drugs are less effective, requiring lifetime adherence.

Prophylactic Treatment: Opportunistic infection prophylaxis is commonly started when CD4 count falls below 200 cells/mm³.

Drug Resistance: HIV can mutate over time, becoming resistant to therapy, especially with prolonged use. Evidence includes falling CD4 count and/or increased viral load, requiring regimen changes.

Resistance Testing: Recommended before starting cART.

Immune Reconstitution Inflammatory Syndrome (IRIS)

Some patients develop IRIS within 1-12 weeks of starting cART. As CD4+ T-cells rise and HIV replication suppresses, T-cells hyperreact to previously unrecognized opportunistic infections, causing:

• Fever, night sweats, fatigue

• New or worsening disease symptoms

HIV (CD4 count and viral load)

CD4+ T-Cell Count

Normal Range: 800-1200 cells/mm³

Clinical Significance by Stage:

• Stage I: CD4 count >500 cells/mm³

• Stage II: CD4 count 200-499 cells/mm³

• Stage III (AIDS): CD4 count <200 cells/mm³

Why It Matters:

• CD4+ T-cells are the primary target of HIV infection

• As HIV progresses, more CD4+ T-cells become infected and dysfunctional

• Low CD4 count = weakened immunity and increased risk of opportunistic infections

• CD4 count <200 cells/mm³ triggers need for prophylactic treatment for opportunistic infections

Viral Load Testing

What It Measures: The actual amount of HIV viral RNA particles present in 1 mL of blood (also called HIV RNA quantification testing).

Normal Result: "Undetected" in uninfected individuals

Clinical Uses:

• Measure prognosis and disease progression

• Assess effectiveness of antiretroviral therapy

• Determine need for prophylactic therapy

• Most accurate test for determining disease course (even more than CD4 count)

Testing Schedule:

• Baseline: Two tests, 2-4 weeks apart after HIV exposure

• Ongoing monitoring: Every 3-4 months

• After starting/changing ART: Every 4-6 weeks to assess efficacy

Interpretation:

• Higher viral load (>30,000 copies/mL): Greater likelihood of progression to stage III; lower survival

• "Undetectable" viral load: Does NOT mean virus-free—test limitations simply cannot detect below certain thresholds; virus still present

Key Relationship

Viral load parallels disease progression:

• As viral load ↑ → CD4 count ↓ → immunity worsens → stage progression

Treatment Goal: Suppress viral load to undetectable levels while CD4 count recovers

HIV (Patient education)

Transmitted via blood, sexual contact, and perinatal exposure. Not transmitted by casual contact, linens, toilet seats, or mosquito bites

Transmission & Risk Reduction

Body Fluids Containing HIV:

• Blood, semen, vaginal secretions, breast milk, amniotic fluid, cerebrospinal fluid, synovial fluid, pleural fluid, peritoneal fluid, pericardial fluid

Safer Sex Practices:

• Use latex or polyurethane condoms for every sexual encounter

• Avoid natural membrane condoms (do not block HIV)

• Use water-based lubricants (oil-based degrade latex)

• Discuss sexual activity and partner status openly

Needle Safety:

• Participate in needle exchange programs

• Learn proper syringe cleaning techniques if exchanges unavailable

Treatment as Prevention (TasP)

Undetectable = Untransmittable (U=U): When viral load is consistently undetectable with effective ART, HIV cannot be sexually transmitted to others

Important clarification: "Undetectable" does NOT mean virus-free—test limitations simply cannot detect below certain thresholds. The patient still has HIV and must continue ART and safer practices

Medication Adherence

Discuss level of adherence to antiretroviral therapy, as inconsistent use leads to:

• Viral rebound

• Drug resistance

• Disease progression

Ongoing Monitoring

Review and update health history at every visit:

• Chronologic infection history

• Current treatments and problems

• New symptoms or concerns

Reinforce health teaching regularly about transmission modes, safer practices, and treatment adherence

Emotional & Social Support

Assessment needed:

• Mental and emotional status

• Psychologic impact on patient, family, significant others

• Value systems, social patterns, hobbies, support systems, spiritual beliefs

Referral considerations:

• Social services for financial needs/insurance issues

• Community resources

• Support groups

Special Considerations

Financial support: Many patients require referrals to social services due to lack of health insurance and financial resources, especially given lifelong treatment requirements.

Educational approach: Assess knowledge level, reading level, preferred learning style, and familiarity with community resources to create effective, individualized teaching.

HIV (PrEP)

What is PrEP?

Preexposure prophylaxis (PrEP) involves HIV-negative individuals who are at high risk for HIV taking antiretroviral drugs before sexual activity or drug injection to prevent infection.

Effectiveness

When taken as prescribed, PrEP:

• Reduces risk of contracting HIV from sex by about 99%

• Reduces risk from injection drug use by up to 90%

Key to effectiveness: Consistent adherence. PrEP is much less effective when not taken consistently.

FDA-Approved PrEP Medications

Oral Medications:

• Tenofovir disoproxil fumarate/emtricitabine (Truvada): Approved for all people

• Tenofovir alafenamide/emtricitabine: Approved for sexually active men and transgender women

Injectable Medication:

• Cabotegravir: Available as oral or injection form

Important Black Box Warning

Both tenofovir combination drugs have an FDA black box warning:

• Should NOT be used in patients infected with hepatitis B virus (HBV)2

• Severe acute exacerbations of hepatitis B have occurred when patients stopped using these drugs for PrEP

Who Should Consider PrEP?

People at very high risk for HIV infection, including:

• HIV-negative person with HIV-positive sexual partner

• HIV-negative person with partner who uses injection drugs

Patient Education Priorities

• Daily adherence is critical for effectiveness

• PrEP does NOT eliminate the need for safer sex practices (condoms, etc.)

• PrEP does NOT protect against other sexually transmitted infections

• Regular monitoring and follow-up required

Contrast with Other HIV Prevention Strategies

• PrEP: HIV-negative person takes medication to prevent infection

• TasP (Treatment as Prevention): HIV-positive person takes medication to prevent transmission to others

Sickle Cell Crisis Interventions

• Sickling of HbS RBCs causes microvascular occlusion, tissue hypoxia, and severe pain.

• Priority Crisis Triad:

  1. Oxygenation: Maintain SpO2 greater than 95% to prevent further sickling.

  2. Hydration: Administer IV fluids to reduce blood viscosity.

  3. Pain Management: Administer continuous opioids/analgesics

Pain Management

Assessment First:

• Ask if pain is typical of past episodes—if not, explore other causes or complications

• Have patient rate pain 0-10 and evaluate intervention effectiveness using this scale

• Target: Pain controlled to ≤3/10 or level acceptable to patient

Medication Approach:

Acute Crisis:

• Start with IV opioid analgesics (morphine, hydromorphone)

• Use scheduled dosing or PCA pump—avoid PRN schedules (inadequate relief)

• Once relief obtained, taper IV dose and transition to oral

Moderate Pain:

• Oral opioids or NSAIDs

Important Considerations:

• Base pain management on past pain history, previous drug use, complications, and current assessment1

• Address bias: Patients with SCD often face accusations of drug-seeking. Evidence shows opioid misuse has NOT increased with the opioid epidemic, and deaths relate to disease complications, not opioid misuse

• Patients with opioid addiction history still need opioids during acute crisis—incorporate addiction management into overall plan

Hydration & Oxygenation

Hydration:

• Administer IV fluids as ordered

• Encourage oral hydration

• Dehydration increases sickling and must be avoided

Oxygen Therapy:

• Give oxygen during crises (lack of oxygen causes sickling)

• Ensure oxygen is nebulized to prevent dehydration

• Monitor oxygen saturation; collaborate on ABGs/chest x-ray if low

Perfusion Support

• Remove restrictive clothing

• Avoid keeping knees/hips flexed (restricts circulation)

Infection Prevention

• Auscultate lungs every 8 hours for crackles, wheezes, reduced sounds

• Monitor vital signs every 4 hours for fever

• Assess urine for infection signs

• Ensure vaccinations current: pneumonia, annual influenza, COVID-19 with boosters

Disease-Modifying Therapy

Hydroxyurea: Stimulates fetal hemoglobin production, reducing sickling and vasoocclusive events. Requires CBC monitoring for bone marrow suppression.

L-Glutamine (Endari): Reduces oxidative stress, decreasing sickling and extending RBC lifespan

Polycythemia vera: labs and complications

Polycythemia Vera

• Myeloproliferative RBC cancer marked by massive overproduction of RBCs (>6 million/ mm³), leukocytes, and platelets.

• Diagnostic Labs: Hgb >18 g/dL or Hct >55%.

• Complications & Treatments: Hyperviscosity, hypertension, thrombosis, MI, and stroke. Treated with therapeutic phlebotomy (2–5 times/week), hydration, and anticoagulants

Diagnostic Laboratory Findings

WHO Major Criteria:

Males:

• Hemoglobin >16.5 g/dL

• Hematocrit >49%

Females:

• Hemoglobin >16 g/dL

• Hematocrit >48%

• OR RBC mass >25% above mean

Bone Marrow Biopsy:

• Hypercellularity with panmyelosis (trilineage proliferation)

• Prominent erythroid, granulocytic, and megakaryocytic proliferation

• JAK2 V617F or JAK2 exon 12 mutation present

WHO Minor Criteria:

• Serum EPO level less than normal range

Key Lab Abnormalities

Hypercellularity in peripheral blood:

• Excessive RBC production (primary problem)

• Excessive leukocyte production

• Excessive platelet production

Complications

Thrombotic Events:

• Thrombosis is a major cause of morbidity and mortality

• Blood hyperviscosity promotes sluggish blood flow and decreased microvascular circulation

• JAK2V617F mutation has a direct role in thrombosis development

• Thromboembolic events can lead to mental status changes

Hemorrhagic Events:

• Thrombocytosis with abnormal platelets creates susceptibility to bleeding

• Mucosal bleeding

Hematocrit-Related Complications:

• Hematocrit >50% causes rapid increase in viscosity

• Hematocrit 50-80% increases viscosity threefold

• Results in tissue hypoperfusion and hypoxia

Visual and Neurologic Changes:

• Neurologic deficits

• Visual changes

• Mental status changes from hypoperfusion/hypoxia

Disease Progression:

• Myelofibrosis (MF): Estimated 25% progress to fibrosis after 20 years

• Leukemia: PV can progress to leukemia

Treatment Goal

Focus is to decrease thrombotic and hemorrhagic complications through:

• Low-dose aspirin (100 mg daily reduces cardiac embolic events and death by 60%)

• Phlebotomy to maintain hematocrit <45%

• Hydroxyurea (cytoreductive drug) to control blood cell count

Chronic leukemia: signs, symptoms, labs, complications

• Uncontrolled proliferation of immature white blood cells (blast cells) in bone marrow.

• Labs & Manifestations: Decreased Hgb/Hct, decreased platelets, abnormal WBC (often markedly elevated).

• Major Complication: Infection/sepsis is the primary cause of death.

• Interventions: Infection control (preventing autocontamination from patient flora and cross-contamination from staff/visitors), systemic chemotherapy, and Hematopoietic Stem Cell Transplantation (HSCT). (Note: Other hematologic disorders include Multiple Myeloma involving plasma cells treated with bisphosphonates for bone protection, and ITP involving autoimmune destruction of platelets treated with steroids and IVIG).

Pathophysiology

Chronic leukemia involves chromosomal abnormalities in stem cells producing more mature but abnormal cells that divide rapidly. Unlike acute leukemia with blast cells, chronic leukemia cells partially develop but don't function normally.

Types:

• CML (Chronic Myeloid Leukemia): Affects granulocytes; commonly involves Philadelphia chromosome translocation

• CLL (Chronic Lymphocytic Leukemia): Affects lymphocytes, typically B cells

Signs & Symptoms

Cardiovascular:

• Increased heart rate, decreased blood pressure

• Murmurs and bruits (from less viscous blood)

• With greatly elevated WBC: increased blood pressure and bounding pulse

Respiratory:

• Dyspnea, cough (if infection present)

• Abnormal breath sounds

Skin:

• Pallor/ash gray appearance, coolness

• Petechiae (especially legs/feet)

• Infections or non-healing wounds

• Gum bleeding

GI:

• Weight loss, nausea, anorexia

• Reduced bowel sounds, constipation (decreased intestinal blood flow)

• Liver and spleen enlargement, abdominal tenderness

CNS:

• Headache, cranial nerve problems

• Papilledema, seizures, coma possible

Musculoskeletal/Lymphatic:

• Bone and joint tenderness

• Enlarged lymph nodes

Laboratory Findings

Peripheral Blood:

• WBC count: Variable (low, normal, or elevated)

• Hemoglobin/hematocrit: Decreased

• Platelets: Low

Coagulation Studies:

• Prolonged clotting time and aPTT

• Reduced clotting factors

Definitive Tests:

• Bone marrow aspiration/biopsy

• Chromosome analysis (e.g., Philadelphia chromosome in CML)

Complications

Abnormal cells accumulate in blood and lymphoid organs, leading to anemia, thrombocytopenia, and leukopenia. Reduced perfusion and gas exchange affect all organ systems

Blood administration and transfusion reactions

Before Transfusion

Critical Safety Checks:

• Two registered nurses must verify blood type, compatibility, patient identification, health record number, and date of birth

• Check expiration date and inspect for discoloration, gas bubbles, or cloudiness (bacterial growth/hemolysis indicators)

• Ensure ABO and Rh compatibility

• Use blood filter (170 microns) to remove sediment

• Administer only with normal saline—never Ringer's lactate or dextrose (cause clotting/hemolysis)

• Never add or infuse other drugs with blood

During Transfusion

Initial Monitoring:

• Assess vital signs immediately before starting

• Begin infusion slowly

• Stay with patient first 15-30 minutes (most severe reactions occur with first 50 mL)

• Take vitals 15 minutes after starting; if no reaction, increase rate to transfuse 1 unit in 2-4 hours

• Continue vitals every hour during transfusion

Patient Education:

• Report unusual sensations: chills, shortness of breath, hives, itching, back pain3

Transfusion Reaction Signs & Symptoms

Acute reactions (within 24 hours) include:

• Apprehension, restlessness

• Flushed skin

• Increased pulse and respirations

• Dyspnea, rash

• Joint or lower back pain

• Swelling

• Fever and chills (febrile reaction: begins 1 hour after start, may last up to 10 hours)

• Nausea, weakness, jaundice

• Chest or abdominal pain

• Feeling unwell or uneasy

Immediate Interventions for Suspected Reaction

STOP the transfusion immediately:

1. Stop blood/product and remove tubing

2. Keep IV patent with normal saline at slow rate (do NOT flush blood tubing—prevents more reaction-causing blood from entering patient)

3. Initiate Rapid Response Team

4. Monitor patient and vital signs closely

5. Do NOT discard blood product or tubing—return to blood bank/laboratory

6. Report to prescriber immediately

7. Administer oxygen and diphenhydramine IV push as ordered

8. Provide fluid resuscitation and hemodynamic monitoring if shock present

Caring for Patients with Cancer

Benign vs. Malignant tumors

• Benign Tumors: Encapsulated, well-differentiated cells that resemble parent tissue, grow by expansion without invading surrounding tissue, do not metastasize, and have normal mitotic rates.

• Malignant Tumors: Unencapsulated, poorly differentiated (anaplastic) cells, display invasive local growth, metastasize via blood and lymphatics, and undergo rapid, uncontrolled division

Key Differences

Characteristic	Benign	Malignant
Growth rate	Slow	Rapid
Encapsulation	Encapsulated with connective tissue	Lack a capsule
Differentiation	Well-differentiated cells	Loss of differentiation (anaplasia)
Tissue structure	Well-organized, retain normal structure	Disorganized, absent normal organization
Cell appearance	Uniform	Pleomorphic (marked variability in size/shape), large darkly stained nuclei
Invasiveness	Do not invade beyond capsule	Invade nearby blood vessels, lymphatics, surrounding structures
Metastasis	Cannot spread to other tissues/organs	Can metastasize (spread to remote body parts)
Mitotic cells	Very rarely present	Common

Naming Conventions

Benign tumors: Named by tissue of origin + suffix -oma

• Leiomyoma (smooth muscle tumor)

• Lipoma (fat cell tumor)

• Fibroadenoma (benign breast tumor)

Malignant tumors: Named by cell type of origin

• Carcinomas: Epithelial tissue cancers

• Adenocarcinomas: Ductal/glandular structure cancers (e.g., mammary adenocarcinoma)

• Sarcomas: Mesenchymal tissue cancers—connective tissue, muscle, bone (e.g., rhabdomyosarcoma)

• Lymphomas: Lymphatic tissue cancers

• Leukemias: Blood-forming cell cancers

Clinical Significance

Benign tumors:

• Generally not harmful

• Can be life-threatening if they grow large enough to compress critical organs

• Example: Benign meningioma can compress brain tissue, causing increased intracranial pressure

• Some can progress to malignancy

Malignant tumors:

• Over time, bear no comparison to original cells

• Abnormal cell replication leads to invasion of healthy cells, tissues, and organs

• Metastasis is the most important and deadly characteristic

TNM Staging

• T (Primary Tumor): Tx (cannot be assessed), T0 (no evidence), Tis (carcinoma in situ), T1-T4 (increasing tumor size/extent).

• N (Regional Nodes): Nx (cannot be assessed), No (no node involvement), N1-N3 (increasing regional lymph node involvement).

• M (Distant Metastasis): Mx (cannot be assessed), Mo (no distant metastasis), M1 (distant metastasis present)

TNM Staging System

The TNM system is used to describe the anatomic extent of cancers and has specific prognostic value for each solid tumor type.

What TNM Stands For

• T = Tumor spread

• N = Node involvement

• M = Metastasis (presence of distant metastasis)

How It Works

T (Tumor):

• T1: Lesion <2 cm in size (example: breast)

• T2: Lesion 2–5 cm in size

• T3: Lesion invades skin and/or chest wall

N (Nodes):

• N0: No lymph nodes involved

• N1: Mobile nodes involved

• N2: Fixed nodes involved

• Higher number = more nodes involved

M (Metastases):

• M0: No metastases

• M1: Demonstrable metastases (lesions confirmed in distant organs)

• M2: Suspected metastases

Types of Staging

Clinical staging:

• Estimates extent before treatment

• Based on physical examination, imaging, and biopsy

Surgical staging:

• Assesses tumor size, number, sites, and spread by direct inspection during surgery

Pathologic staging:

• Most definitive type

• Determines tumor size, number, sites, and lymph node spread through pathologic examination of tissues obtained at surgery

General Four-Stage System

While TNM provides detailed classification, cancers are often described in stages:

• Stage 1: Cancer confined to organ of origin

• Stage 2: Locally invasive cancer

• Stage 3: Spread to regional structures (e.g., lymph nodes)

• Stage 4: Spread to distant sites (e.g., liver cancer spread to lung)

Clinical Significance

• Prognosis generally worsens with increasing tumor size, lymph node involvement, and metastasis

• Staging alters therapy choice—more aggressive therapy is delivered to more invasive disease

• Used by the World Health Organization for standardizing cancer staging

• Other staging systems exist for specific cancers (e.g., Dukes system for colorectal cancer, Clark levels for skin cancer)

Chemotherapy (Side effects, nursing considerations, and patient teaching)

• Side Effects: Nausea, vomiting, mucositis, alopecia, severe fatigue, diarrhea/constipation, and myelosuppression.

• Nursing Care & Teaching: Administer prophylactic antiemetics before treatment; ensure line patency to prevent extravasation of vesicants; teach infection control and bleeding precautions; advise small, frequent high-calorie/high-protein meals

Side Effects of Chemotherapy

Hematopoietic (Blood) System:

• Anemia (decreased RBCs/hemoglobin)

• Neutropenia (decreased WBCs) → immunosuppression

• Thrombocytopenia (decreased platelets) → bleeding risk

• Nadir: Lowest point of bone marrow activity/WBC counts after treatment

Other Common Side Effects:

• Nausea/vomiting → dehydration and electrolyte disturbances

• Alopecia (hair loss) - begins 2–4 weeks after treatment starts; occurs all over body

• Cardiotoxicity (e.g., doxorubicin can cause cardiomyopathy)

• Bone density loss (with aromatase inhibitors)

• Cutaneous reactions (rash on hands/feet)

• Diarrhea (especially with topoisomerase I inhibitors)

Nursing Considerations

Monitoring:

• Monitor blood counts closely with every treatment

• Contact prescriber if ANC drops <500 cells/mm³

• Chemotherapy may be discontinued until ANC >1000 cells/mm³

• Watch for dyspnea, crackles, edema, abdominal distention

Safety Interventions:

• Minimize tissue trauma (avoid IM injections, rectal temperatures if possible)

• Prevent bleeding and infection

• Ensure IV site patency to prevent extravasation

• Treat extravasation immediately per facility protocol

Supportive Care:

• Establish therapeutic relationship with trust and empathy

• Provide individualized teaching appropriate to patient's education level

• Encourage relaxation techniques (music, meditation, guided imagery)

• Connect with support resources: social services, spiritual guidance, financial assistance

Patient Teaching

Nutrition Management:

• Eat small, frequent meals in odor-free, quiet environment

• Practice energy conservation with rest periods before/after meals

• Consider appetite stimulants (megestrol acetate, dronabinol)

Hair Loss:

• Expect hair loss 2–4 weeks after treatment starts

• May lose hair all over body (scalp, eyebrows, eyelashes, pubic)

• Hair regrows after treatment; may have different texture/color initially

Critical Reporting:

• Immediately report: nausea, vomiting, diarrhea, fever, signs of infection or bleeding

Radiation therapy teaching

• Gently wash irradiated skin daily with water or mild soap; pat dry.

• Do NOT wash off or erase skin markings/tattoos.

• Avoid applying unapproved lotions, powders, perfumes, heating pads, or ice packs to the site.

• Protect skin from direct sunlight and wear loose, soft cotton clothing

Key Teaching Points

Treatment Overview:

• Radiation uses high-energy radiation to kill cancer cells

• Effects seen only in tissues within the radiation field (local treatment)

• Example: Chest radiation causes skin changes/hair loss only on treated chest area

Preparation & Duration:

• Whole-breast radiation: Delivered over 5–6 weeks

• Partial breast radiation (PBI): Shorter time interval, eliminating need for weeks of treatment

Skin Care Protocol

Critical Instructions:

• Do NOT remove temporary ink markings when cleaning skin until therapy is completed

• Avoid skin irritation and friction from clothing

• Wash irradiated area with mild soap and water

• Avoid scrubbing the skin

Expected Skin Changes:

• Skin in radiation path becomes dry and itchy

• Radiation dermatitis is the most common side effect

• Can range from redness/hyperpigmentation and rash to skin desquamation (peeling)

Common Side Effects

Site-specific effects:

• Fatigue: May be debilitating and last for months

• Hair loss: May be permanent if radiation to the head

• Altered taste

• Bone marrow suppression: Reduced immunity regardless of treatment site

Long-term effects:

• Inflammatory responses → tissue fibrosis and scarring (may appear years later)

• Increased risk for second malignancies due to DNA damage

Site-Specific Symptoms to Report

If receiving pelvic/prostate radiation:

• Urinary frequency, diarrhea, acute cystitis (pain, blood in urine)

• Radiation proctitis: urgency, cramping, bloody diarrhea, rectal leakage

• Report these symptoms immediately

• Symptoms usually subside after treatment

Dietary modifications if proctitis occurs:

• Limit spicy/fatty foods, caffeine, dairy products

• Drink plenty of water and other fluids

Emotional Support

Patients and families are anxious about radiation and look to nurses for explanation of treatment specifics and side effects 1. Accurate information helps patients cope with treatment

Mucositis mangagement

Inspect oral cavity daily; use a soft-bristle toothbrush; perform frequent oral rinses with normal saline or sodium bicarbonate (avoid commercial alcohol-based mouthwashes); avoid spicy, acidic, or hard foods; apply prescribed magic mouthwash or topical analgesics prior to meals

Definition

Mucositis is an inflammatory process affecting the mucous membranes of the oral mucosa and GI tract. It's a dose-limiting side effect of cancer therapy—severe cases may stop or delay treatment. The rapidly dividing mucosal membranes are easily impacted by chemotherapy.

Prevention

Oral Cryotherapy:

• Use ice water or ice chips for prevention in some patients

• Instruct patients to suck on ice chips before, during, and after rapid infusions of specific mucositis-causing agents (e.g., fluorouracil/5-FU)

• Mechanism: Vasoconstriction from cold temperature decreases exposure of oral mucous membranes to mucositis-causing agents

Management Strategies

Oral Hygiene:

• Frequent mouth assessment and oral hygiene are key

• Gentle flossing

• Salt and baking soda rinse

• Non-alcohol-based mouth rinse at frequent intervals during day and night when awake

• Frequency guided by intensity of mucositis

What to Avoid:

• Avoid mouthwashes containing alcohol or drying agents that may further irritate the mucosa

Impact on Patient

Mouth sores cause pain and interfere with:

• Hydration

• Nutrition

• Quality of life

Nursing Role

Nurses must stress the importance of thorough and frequent oral hygiene to patients

Myelosuppression (Neutropenia)

Neutropenia (Low WBC / Neutrophils):

• Nursing Priority: High infection risk. A fever (temperature greater than or equal to 100.4 F) is a medical emergency. Enforce neutropenic precautions (hand hygiene, private room, no fresh flowers/plants, low-bacteria diet)

Definition & Pathophysiology

Neutropenia results from bone marrow suppression caused by chemotherapy drugs. It's the greatest dose-limiting side effect of chemotherapy and can lead to death if sepsis is not managed appropriately and in a timely manner.

Key Facts:

• Many chemotherapy drugs cause myelosuppression and decrease natural responses to infection

• Neutropenia is temporary—immunity usually recovers within weeks after chemotherapy completion

• Most infections result from overgrowth of the patient's own normal flora (autocontamination)

Infection Risk

Critical Threshold:

• ANC <1000/mm³: Severely immunocompromised, high infection risk

• Severe risk if less than 500/mm³

Common Infection Sources:

• Fungal, bacterial, or viral

• Reactivation of dormant viruses (e.g., varicella)

• Skin, respiratory tract, intestinal tract

Clinical Presentation

Unique Challenge:

• Patients may have severe infection WITHOUT typical signs/symptoms

• May not develop high fever or purulent drainage even with severe infection

• Even low-grade fever can indicate infection

Nursing Considerations

Assessment Every Shift:

• Monitor daily CBC with differential and ANC

• Inspect mouth for lesions/mucosa breakdown

• Assess lungs every 8 hours for crackles, wheezes, reduced breath sounds

• Check urine for odor, cloudiness; ask about urgency, burning, pain

• Obtain vital signs at least every 4 hours

Sepsis Protocol:

• Delay can result in sepsis and death

• Draw blood cultures BEFORE starting antibiotics (crucial)

• Standard protocols specify: cultures (blood, urine, sputum, central line, wound), diagnostic tests (chest x-ray), immediate antibiotics

Infection Prevention:

• Good handwashing before patient contact is essential

• Use aseptic technique with any invasive procedure

• No fresh flowers in room (carry fungal spores)

• Growth factors (e.g., filgrastim) may be used to stimulate bone marrow production

Patient Teaching

Report Immediately:

• Fever

• Signs/symptoms of infection

• Skin/mucous membrane changes or rash

• Cough, burning on urination

• Pain around venous access site

• New drainage from wound/body area

Home Care Focus:

• Handwashing is critical

• Keep own normal flora under control

• Prevent organism transmission from others

Myelosuppression (Anemia)

Anemia (Low RBC / Hgb / Hct):

• Manifestations: Fatigue, pallor, dyspnea, tachycardia. Provide rest periods, oxygen support, and administer erythropoietin or RBC transfusions

Definition & Pathophysiology

Anemia from chemotherapy results from bone marrow suppression, causing decreased numbers of red blood cells and hemoglobin. This reduces the blood's oxygen-carrying capacity.

Clinical Manifestations

Key Signs/Symptoms:

• Fatigue

• Changes in skin and nail texture/color

• Brittle, misshapen nails

• Cracked lip angles with fissures

Assessment

Before Treatment:

• Assess past/present medical history and drug allergies

• Document baseline signs/symptoms of anemia

• Assess for contraindications before starting treatment

Treatment Options

Erythropoiesis-Stimulating Agents (ESAs):

• Examples: epoetin alfa, darbepoetin

• Used to treat anemia associated with chemotherapy and end-stage renal disease

• Assess adequate body iron stores and bone marrow function before administration

Critical Safety Considerations with ESAs:

• Black box warning: Risk of heart attack, stroke, and death when used inappropriately

• Use caution if hemoglobin >10 g/dL (cancer patients) or >11 g/dL (renal patients)

• Target hemoglobin: 10 g/dL for chronic kidney disease patients not on dialysis; 11 g/dL for dialysis patients

• Increases tumor growth risk in head/neck cancers

• Monitor blood pressure—may rise as hematocrit rises

Timeframe for Response:

• Therapeutic effects take 2-6 weeks to appear

• Monitor for increased energy, appetite, sense of well-being

Adverse Effects of ESAs:

• Hypertension, fever, headache, pruritus, rash

• Nausea, vomiting, arthralgia

• Injection site reactions

• Increased thrombosis risk

Iron Supplementation

May be needed alongside ESAs if iron stores are inadequate.

Therapeutic responses include:

• Improved nutritional status

• Increased weight and activity tolerance

• Absence of fatigue

Adverse effects:

• Nausea, constipation, epigastric pain

• Black tarry stools, vomiting

Myelosuppression (Thrombocytopenia)

Bleeding Precautions: Use electric razor and soft toothbrush; avoid IM injections, rectal temperatures, aspirin/NSAIDs; apply pressure to puncture sites for greater than or equal to 10 minutes; check skin for petechiae/ecchymosis and test stool/urine for occult blood

Definition & Pathophysiology

Thrombocytopenia is a platelet count less than 150,000/mm³. It results from bone marrow suppression as a side effect of chemotherapy. Normal platelet count is 150,000-400,000/mm³.

Bleeding Risk Thresholds

Critical Values :

• <50,000/mm³: Risk for bleeding with minor trauma

• <20,000/mm³: Spontaneous, uncontrollable bleeding may occur

• <10,000/mm³: Severe spontaneous bleeding risk; may see skin manifestations (petechiae, ecchymoses, purpura) or mucous membrane bleeding

Clinical Presentation

Signs of Bleeding:

• Petechiae, purpura, enlarging bruises

• Blood in stools, urine, drainage, vomit (test for occult blood)

• Increased abdominal girth (internal hemorrhage)

Nursing Considerations

Assessment:

• Assess for evidence of bleeding at least every 4 hours

• Measure blood loss accurately

• Measure abdominal girth daily

• Inspect all body fluids for obvious/occult blood

Bleeding Precautions:

• Priority: provide a safe environment

• Institute interventions to minimize bleeding chance

• Avoid trauma and sharp objects

• Apply pressure to wounds for 10 minutes

Recovery Timeline :

• Platelet recovery is slower than other blood cells

• Patient remains at bleeding risk for weeks after discharge

• Platelet count must remain >50,000/mm³ before discontinuing precaution Transfusion Support

Indications:

• Platelet count <10,000/mm³

• Active bleeding with thrombocytopenia

• Scheduled invasive procedure

Administration:

• Infuse immediately after bringing to room

• Infusion time: 15-30 minutes

• Take vital signs: before, 15 minutes after start, and at completion

• May premedicate with diphenhydramine and acetaminophen if prior reaction history

Patient Teaching

Report immediately:

• Petechiae

• Blood in stool/urine

• Headache not responding to acetaminophen

Myelosuppression (Associated Lab Values)

Normal Values

Platelets (Thrombocytes):

• Normal: 150,000-400,000/mm³ (150-400 × 10⁹/L)

• Critical value: <20,000/mm³

White Blood Cells (WBCs):

• Normal: 5,000-10,000/mm³ (5-10 × 10⁹/L)

Absolute Neutrophil Count (ANC):

• Normal: 2,500-6,000/mm³ (2.5-6 × 10⁹/L)

Red Blood Cells (RBCs):

• Males: 4.7-6.1 million/mm³ (4.7-6.1 × 10¹²/L)

• Females: 4.2-5.4 million/mm³ (4.2-5.4 × 10¹²/L)

Hemoglobin:

• Males: 14-18 g/dL (140-180 g/L)

• Females: 12-16 g/dL (120-160 g/L)

Hematocrit:

• Males: 42%-52% (0.42-0.52 volume fraction)

• Females: 37%-47% (0.37-0.47 volume fraction)

Nadir Timing

Nadir = lowest blood cell count after chemotherapy:

• Typically occurs 7-10 days after administration

• Can occur 10-28 days depending on specific drug/combination

• Timing guides prophylactic antibiotic and hematopoietic growth factor administration

Risk Categories

Neutropenia Severity:

• Mild: 1,000-1,500/mm³

• Moderate: 500-1,000/mm³

• Severe: <500/mm³ (high infection risk)

Thrombocytopenia Risk:

• 40,000-80,000/mm³: Prolonged bleeding from trauma/surgery

• <50,000/mm³: Bleeding risk with small trauma

• <20,000/mm³: Spontaneous bleeding may occur

• <10,000/mm³: Severe spontaneous bleeding

Clinical Significance

Bone marrow suppression causes:

• Anemia: Decreased RBCs/hemoglobin → hypoxia and fatigue

• Neutropenia: Decreased neutrophils → immunosuppression

• Thrombocytopenia: Decreased platelets → impaired clotting and bleeding

Other from notes

What is sinus rhythm?

Normal Sinus Rhythm (NSR)

Normal sinus rhythm is the rhythm that originates from the sinoatrial (SA) node, which is the heart's primary pacemaker. The SA node can spontaneously and rhythmically generate electrical impulses at a rate of 60 to 100 beats/min.

ECG Characteristics of NSR

To meet criteria for normal sinus rhythm, the ECG must show:

• Regular rhythm

• Rate: 60-100 beats/min

• Consistent P wave shape in a given lead (indicating impulses consistently generated from the SA node)

• One P wave before each QRS complex

• Normal PR interval

• Normal QRS complex

How It Works

1. Impulse generation: The SA node (located near the junction of the right atrium and superior vena cava) fires spontaneously

2. Atrial activation: Impulses move through atrial muscle, causing atrial depolarization → P wave on ECG

3. Conduction delay: Impulses slow down in the AV node

4. Ventricular activation: Impulses travel through the conduction system to activate ventricles → QRS complex

Nervous System Influence

The SA node is richly supplied by sympathetic and parasympathetic nervous systems, which:

• Sympathetic: Increases rate of SA node discharge

• Parasympathetic: Decreases rate of SA node discharge

This balance controls heart rate adjustments.

Sinus Arrhythmia (A Normal Variant)

Sinus arrhythmia is a variant of NSR that:

• Results from changes in intrathoracic pressure during breathing

• Heart rate increases slightly during inspiration, decreases during exhalation

• Has all characteristics of NSR except irregularity

• Shows PP and RR interval variation >0.12 second

• Is frequently observed in healthy adults

What is atrial flutter?

-Atrial rate greater than 250

-Ventricular rate regular or irregular

-Atrial oscillations appear as sawtooth or flutter waves

-Described by the number of atrial oscillations (f waves)

What is atrial fibrillation?

-Most common sustained arrhythmia

-Atria contracting very rapidly, unable to empty, discharging greater than 350 BPM

-Blood remaining in atria prone to form clots

-QRS complex normal, but irregular

-Absent P waves

If a patient is in v tach or V fib, what do you do?

-Call a code

-Check response/pulse and then do CPR

What is ventricular asystole?

-Represents complete cessation of electrical impulse

-Ventricular fibrillation can mimic asystole

-Asystole is a terminal rhythm

-Flat line

What is sinus tachycardia?

-Rate greater than 100 bpm and less than 150 bpm

-Complications include angina

-Symptomatic treatment strategies:

• Antianxiety measures

• Pain relief measures

• Antipyretics

• Oxygen

• Calcium Channel Blockers

• Beta-blocking agents

• Fluids

• Vagal nerve stimulus (cough/bear down)

• Carotid artery massage

What is ventricular tachycardia?

-Classified as three or more consecutive PVCs occurring at a rapid rate, usually greater than 100 bpm

-Support (ACLS) by trained interdisciplinary team members

-May deteriorate into ventricular fibrillation

-R-R interval usually regular, but can be irregular

-Absent P waves or P waves not associated with QRS complex

-Wide QRS but somewhat uniform

-Rate greater than 100 BPM

-May or may not have a pulse

-Treatment strategies:

• Amiodarone

• Lidocaine

• Magnesium

• Cardioversion

• No pulse: Same treatment strategy as ventricular fibrillation (cardiopulmonary resusication)

Treatment

Stable VT (with pulse):

• Elective cardioversion is recommended per ACLS guidelines

• Withhold digoxin for up to 48 hours before cardioversion (digoxin increases ventricular irritability and puts patient at risk for VF after countershock)

• Oral antidysrhythmic agent may be prescribed to prevent recurrence

• Radiofrequency catheter ablation may be needed for persistent episodes

Unstable VT (without pulse):

• Treated identically to ventricular fibrillation

• Immediate defibrillation

What is Peak Flow meter?

-Blow into mouthpiece three times and use the highest reading of the three times to determine the current peak flow rate

-Measures how fast air flows out of your lungs