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NU 170 Exam 1 | Maternal-Child Nursing | (2026) Study Guide PDF | Galen Nursing

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INSTANT PDF DOWNLOAD — This NU 170 Exam 1 Study Guide is tailored for Maternal-Child Nursing students at Galen College of Nursing. It covers the foundational concepts typically assessed in Exam 1, helping students build a strong understanding of maternal and pediatric nursing principles early in the course. The study guide is structured for clarity and efficiency, focusing on core nursing concepts, safety priorities, patient care considerations, and exam-relevant material essential for success in maternal-child nursing. NU 170 exam 1, NU170 study guide, maternal child nursing exam, Galen nursing exam, maternal child nursing PDF, nursing exam prep PDF, Galen College nursing, nursing school exam guide, maternal nursing study guide, pediatric nursing exam prep, maternal child exam review, nursing fundamentals maternal, Galen nursing PDF, nursing student notes, maternal child nursing notes, nursing exam 1 review, Galen nursing study guide, nursing school PDF

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Subido en
13 de enero de 2026
Número de páginas
25
Escrito en
2025/2026
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NU 170
EXAM 1 STUDY GUIDE
Maternal-Child Nursing
Galen College of Nursing

,CARE OF PATIENTS WITH COMPLEX RESPIRATORY PROBLEMS

Structures of the lungs

- Trachea, left/right bronchus, segmental bronchus, subsegmental bronchus, alveoli
- Visceral pleura/parietal pleura lubrication
- Right side of lung (3 lobes)
o Usually aspirate on this side r/t longer/straighter airway

Gas Exchange Structures

- Bronchiole, terminal bronchiole, respiratory bronchioles, alveoli

The Alveoli

- Have about 290 million
- Type 2 pneumocytes secrete surfactant (fatty protein) to keep the alveoli open and keep fluid
away from alveoli

Gas Exchange

- Breath O2 in O2 goes into blood stream CO2 releases from blood stream blow CO2 out

COPD: effect on lungs

- Healthy alveoli expand and contract giving adequate perfusion
- COPD alveoli have lost elasticity and rely on the impulse from the brain when the CO2 in their
blood is too high causing their drive to breath to happen automatically (like kussmaul respirations)
o COPD consists of Emphysema and Chronic Bronchitis
Causing bronchial spasms and dyspnea

Bronchitis and Emphysema

- Chronic Bronchitis
o Caused by smoking, characterized by inflammation and structural changes
o Causes excessive secretions (mucous plug)
- Emphysema
o Elastic fibers destroyed leading to hyperinflation

Acute Respiratory Failure
- Progressive or sudden
- Deterioration of gas exchange function in the lungs
o Hypoxemia – PaO2 of less than 50 mmHg (normal 80-100)
o Hypercapnia – PaCO2 greater than 50 mmHg
Decreased LOC if this happens call the Doc to get blood gas
o Acidosis – pH less than 7.35 (normal 7.35 – 7.45)
- Ventilatory failure – Can’t get O2 in
o Asthma, sleep apnea, myasthemia gravis
- Oxygen failure – O2 getting in but it isn’t getting picked up
o Pneumonia, ARDS, PE, shock

Blood Gas Values

- pH = 7.35 – 7.45, pCO2 = 35 – 45 (respiratory), HCO3 = 22 – 28 (metabolic)
- Increased CO2 = acid build-up, acidosis; Increased HCO3 = alkaline build-up, alkalosis
- ROME (Respiratory Opposite, Metabolic Equal)

1

, Pathophysiology of Respiration

- Occurs at the alveolar capillary units exchange of oxygen and carbon dioxide oxygen
attaches to the circulating hemoglobin molecules 2 processes occur, ventilation and perfusion
- V/Q scan measures how well the alveoli are being ventilated and perfused
o Radioactive dye used to find PE
o Ventilation – perfusion mismatch = PE

Causes of Acute Respiratory Failure

- Decreased respiratory drive (narcotics, COPD w/ too much O2)
- Obstruction of the airways (Bronchitis, sleep apnea, asthma)
- Trauma (Injury to the lung tissue or chest wall)
- Dysfunction of the chest wall (spinal cord injury, any condition that affects breathing)
- Disorders (sleep apnea, PE, overdose of opiods/alcohol)

Clinical Manifestations of Acute Respiratory Failure

- Early: Impaired O2 (give O2), restlessness, fatigue (promote rest), headache, dyspnea, air
hunger, tachycardia, increased BP
o Use interventions
- Progressive: Confusion, lethargy, tachycardia, tachypnea, central cyanosis, diaphoresis,
respiratory arrest
o Call rapid response
- Intervention Rapid response ICU

Medical Management

- Increased oxygenation, intubation, mechanical ventilation, ICU, bronchodilators, antibiotics, anti-
inflammatories

Nursing Management

- Anticipate and assist with intubation
- Monitor (assess): LOC, RR, O2, ABGs continuous pulse oximetry
- Prevent ventilator associated pneumonia

Acute Respiratory Distress Syndrome (ARDS)
- Severe form of acute lung injury, usually results in death
- Starts with Acute Respiratory Failure sudden, progressive pulmonary edema with
increasing bilateral infiltrates in lungs
- Refractory hypoxemia – giving pt 100% FiO2 but it isn’t making a difference in O2 stat
- Reduced lung compliance

Causes of Acute Respiratory Distress Syndrome (ARDS)

- Aspiration – acid destroys alveoli/surfactant leads to inflammation
- Drug ingestion and overdose
- Hematologic disorders (DIC massive transfusions)
o TRALI – Transfusion related acute lung injury
- Prolonged inhalation of smoke or corrosive substances, near drowning
- Infection (pneumonia)
- Metabolic disorders
- Shock, trauma, major surgery


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