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Ongoing CPR Evaluation: Nurse's Role in the Hospital Setting

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1. Initial Recognition and Team Activation

1. Recognition - assess for unresponsiveness, absence of normal breathing, gasping
2. Immediate activation of the emergency response system (Code Blue/Crash team call)
3. Immediate high-quality CPR
4. Rapid defibrillation
5. Advanced life support and post-arrest care

"Management of cardiac arrest occurs in an orchestrated effort by a health care team led by a clinician who can monitor the efficacy and response to therapeutic interventions."

• Rosen's Emergency Medicine, p. 79

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2. Evaluating the Quality of Ongoing Chest Compressions

High-Quality CPR Parameters (AHA/ACLS Standards)

"Important benchmarks of quality CPR include compression rate 100-120 compressions/min, compression depth 5-6 cm, compression fraction at least 80%, full chest recoil between compressions, and a ventilation rate of 10 breaths/min."

• Rosen's Emergency Medicine, p. 79

"Slow compression rates, inadequate depth of compression, and substantial pauses are the norm. An approach to push hard, push fast, minimize interruptions, allow full chest recoil, and don't overventilate can markedly improve myocardial, cerebral, and systemic perfusion."

• Miller's Anesthesia, 10th Edition, p. 11299

Nursing Actions for Quality Control:

• Switch compressors every 2 minutes (or when fatigued) to prevent degradation in quality
• Use CPR feedback devices (force sensors/accelerometers) when available - these provide real-time verbal feedback on rate and depth
• Call out deviations - if depth is inadequate, verbally cue: "Push harder"

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3. ECG/Rhythm Monitoring and 2-Minute Cycle Checks

• Step 3: Pulse check (healthcare provider only) - maximum 10 seconds - if no pulse, resume immediately
• Step 4: Continue 30:2 compression-to-ventilation ratio (until advanced airway placed)
• Step 5: Apply defibrillator as soon as available
• Step 6: Continue CPR between rhythm checks, restart compressions immediately after defibrillation

• VF/pVT - defibrillate immediately, then resume CPR for 2 minutes before next rhythm check
• PEA/Asystole - focus on CPR quality + reversible causes (H's and T's)

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4. End-Tidal CO₂ (PETCO₂) Monitoring - Key Evaluation Tool

What the Nurse Evaluates:

"A peak in PETCO2 is the earliest sign of return of spontaneous circulation (ROSC) and may occur before palpable or measurable hemodynamic signs (pulse or blood pressure). When the heart is restarted, the dramatic increase in cardiac output...leads to a rapid increase in PETCO2."

• Roberts and Hedges' Clinical Procedures in Emergency Medicine, p. 72

"PETCO2 levels of 10 mm Hg or lower measured 20 minutes after the initiation of advanced cardiac life support accurately predicted death."

• Roberts and Hedges', p. 73

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5. Monitoring for Return of Spontaneous Circulation (ROSC)

"Restoration of adequate cardiac function is the defining factor of ROSC. Restoration of good neurologic function is the defining metric of a successful resuscitation."

• Rosen's Emergency Medicine, p. 79

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6. Evaluating Reversible Causes - The H's and T's

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7. Airway and Ventilation Assessment

• Confirm ET tube placement via ETCO₂ waveform and bilateral breath sounds
• Once advanced airway secured: deliver 1 breath every 6 seconds (10/min) without pausing compressions
• Avoid hyperventilation - it reduces cardiac output during CPR
• O₂ saturation via pulse oximetry (note: unreliable during arrest due to low perfusion)

"Hyperventilation during CPR should be avoided, as it is associated with reduced cardiac output during CPR."

• Rosen's Emergency Medicine, p. 80

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8. Medications During CPR - Nurse's Documentation and Evaluation

• Epinephrine 1 mg IV/IO every 3-5 minutes (vasopressor for all rhythms)
• Amiodarone 300 mg IV for refractory VF/pVT (then 150 mg if needed)
• Sodium bicarbonate for documented severe acidosis or hyperkalemia

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9. Factors Affecting CPR Outcome (for Evaluation Framing)

1. Pre-existing condition of the patient
2. Environment (in-hospital vs. out-of-hospital)
3. Initial ECG rhythm detected
4. Duration of no-flow time (time without CPR or spontaneous circulation)
5. Quality of life-supporting therapies during resuscitation
6. Quality of post-resuscitation care

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10. Summary Evaluation Checklist (Professor-Acceptable Format)

1. Responsiveness level - unresponsive, no breathing, no pulse confirmed
2. Compression quality - rate 100-120/min, depth 5-6 cm, full recoil, fraction ≥80%
3. Rhythm - every 2-minute check (VF/pVT = shock; PEA/asystole = continue CPR + treat cause)
4. PETCO₂ - rising = good CPR; spike = ROSC; <10 mmHg at 20 min = poor prognosis
5. Airway - tube confirmed, ventilation rate 10/min, no hyperventilation
6. Medications - epinephrine timing, antiarrhythmics as indicated
7. Signs of ROSC - ETCO₂ spike, palpable pulse, BP, spontaneous movement
8. Reversible causes - H's and T's actively addressed
9. Time tracking - elapsed CPR time, drug times, shock times documented
10. Team fatigue - compressor switch every 2 minutes

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References (Textbook Citations for Professor):

1. Rosen's Emergency Medicine, 10th Ed. - Chapter 5: Cardiac Arrest
2. Tintinalli's Emergency Medicine, 9th Ed. - Chapter 22: CPR (Tables 22-1, 22-2, 22-3)
3. Roberts and Hedges' Clinical Procedures in Emergency Medicine, 7th Ed. - ETCO₂ Monitoring
4. Miller's Anesthesia, 10th Ed. - Chapters 31, 34: Cardiac Arrest and Resuscitation Quality

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Functions of Growth Hormone (GH / Somatotropin)

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1. What is Growth Hormone?

"Growth hormone has multiple metabolic actions on liver, muscle, adipose tissue, and bone, as well as growth-promoting actions in virtually every other organ."

• Costanzo Physiology, 7th Ed., p. 416

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2. Regulation of GH Secretion

Hypothalamic Control (Two-Pathway System):

Stimulatory vs. Inhibitory Factors (Costanzo Physiology, Table 9.4):

Secretion Pattern:

• Released in a pulsatile manner (~every 2 hours)
• Largest burst: within 1 hour of falling asleep (stage III/IV NREM sleep)
• Peaks during puberty (driven by estrogen in females, testosterone in males)
• Declines with aging (senescence)

Negative Feedback Loops (3 loops):

1. GHRH inhibits its own secretion (ultrashort-loop)
2. IGF-1 (somatomedin C) inhibits GH from anterior pituitary
3. GH + IGF-1 stimulate somatostatin from hypothalamus → inhibits GH

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3. Mechanism of Action

Direct Action (via GH Receptors):

• GH receptors are on skeletal muscle, liver, adipose tissue, and many other cells
• Receptor is a tyrosine kinase-associated receptor (Janus kinase / JAK-STAT pathway)
• Activates STAT transcription factors, MAP kinase pathway, and AKT pathway depending on tissue

Indirect Action (via IGF-1 / Somatomedins):

• GH stimulates the liver (primarily) to produce IGF-1 (Somatomedin C)
• IGF-1 acts on target tissues via receptors with intrinsic tyrosine kinase activity (similar to insulin receptor)
• Most growth-promoting effects of GH are mediated through IGF-1

"The growth-promoting effects of growth hormone are mediated largely through production of somatomedins."

• Costanzo Physiology, 7th Ed., p. 416

"GH...induces release of IGF-1 from the liver, which is responsible for subsequent GH-like actions. The half-life of GH is short (~25 minutes)."

• Lippincott Illustrated Reviews: Pharmacology, p. 770

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4. Functions of Growth Hormone

A. Linear Bone Growth (Most Striking Effect)

• Mediated via IGF-1/somatomedins
• Stimulates DNA, RNA, and protein synthesis in cartilage cells (chondrocytes)
• Widens epiphyseal plates of long bones
• Increases proliferation of chondrocytes
• Increases periosteal bone growth
• Only effective while epiphyseal plates are open (before puberty closes the growth plates)

B. Protein Synthesis and Organ Growth (Anabolic Effects)

• Increases amino acid uptake into virtually all cells
• Stimulates synthesis of DNA, RNA, and protein
• Increases lean body mass and organ size
• Causes positive nitrogen balance (diverts amino acids from oxidation to protein synthesis)
• In muscle: increased amino acid transport + increased nitrogen retention + increased fat-free tissue

"These actions are accompanied by a direct anabolic influence of GH on protein metabolism with a diversion of amino acids from oxidation to protein synthesis and a shift to a positive nitrogen balance."

• Basic Medical Biochemistry, 6th Ed., p. 1481

C. Diabetogenic / Anti-Insulin Effect on Carbohydrate Metabolism

• GH causes insulin resistance in peripheral tissues (muscle, adipose)
• Decreases glucose uptake and utilization by muscle and fat
• Raises blood glucose concentration (similar effect to lack of insulin)
• Consequently increases blood insulin levels as a compensatory response
• Called "diabetogenic" because it mimics a diabetic state

D. Fat Metabolism (Lipolysis)

• Increases lipolysis in adipose tissue
• Inhibits lipoprotein lipase (reduces fat storage)
• Stimulates hormone-sensitive lipase (promotes fat breakdown)
• Decreases lipogenesis (less fat synthesis)
• Decreases glucose transport into fat cells
• Net effect: mobilizes free fatty acids into the blood for energy use
• Leads to decreased body fat and redistribution of body composition

E. Other Metabolic and Organ Effects

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5. Summary of GH Functions (Quick Reference)

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6. Pathophysiology (Clinically Important)

"Before puberty, excessive levels of growth hormone cause gigantism...After puberty...excess levels cause increased periosteal bone growth, increased organ size...insulin resistance, and glucose intolerance."

• Costanzo Physiology, 7th Ed., p. 417

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Textbook References:

1. Costanzo Physiology, 7th Ed. - Chapter 9 (Endocrine Physiology), pp. 415-417
2. Basic Medical Biochemistry: A Clinical Approach, 6th Ed. - Chapter 41, pp. 1481-1482
3. Lippincott Illustrated Reviews: Pharmacology - Chapter 23, pp. 769-770
4. Tietz Textbook of Laboratory Medicine, 7th Ed. - Endocrine section