CCRN Pediatric Exam Overview

CCRN Pediatric Course Outline

• The CCRN Pediatric exam contains 150 multiple-choice questions, with 125 being scored, and allows 3 hours for completion.
• The exam is pass/fail, and answers can be changed during the test.

Exam Components by Percentage

• Clinical Judgment comprises 80% of the exam, covering various systems and conditions.
  • CV: 15%
  • Pulmonary: 16%
  • Neuro: 12%
  • Multisystem: 14%
  • Endocrine: 4%
  • Hematology/Immunology: 4%
  • GI: 5%
  • Renal/GU: 4%
  • Integumentary: 2%
  • Musculoskeletal: 2%
  • Behavioral/psych: 2%
• Professional Caring and Ethical Practice accounts for 20% of the exam.

Professional Caring and Ethical Practice Breakdown

• Advocacy/moral agency: 3%
• Caring practices: 3%
• Response to diversity: 4%
• Facilitation of learning: 2%
• Collaboration: 2%
• Systems thinking: 3%
• Clinical inquiry: 2%

Renewal Requirements

• Certification must be renewed every 3 years.
• 432 hours of bedside care within the past 3 years, with 144 hours in the last 12 months is required.
• 100 Synergy Continuing Education Recognition Points (CERPs) earned over past 3 years is also needed
• Synergy CERPs categories: 60 Category A, 10 Category B, 10 Category C.
• Retaking the test every 3 years is an alternative renewal method.

Application Process

• Complete the exam application and verify clinical practice requirements.
• The AACN Certification Corporation notifies Applied Measurement Professional (AMP) of eligibility.
• AMP sends a postcard, after receipt, schedule the test ASAP via phone or online (www.goamp.com).
• Pass the test.

Preparation Tips

• Identify and focus on areas of weakness.
• AACN offers assessment questions to pinpoint weak areas.

Test Day Strategies

• Aim to answer at least 50 questions in the first hour.
• Allocate no more than 2 minutes per question.
• There's no penalty for guessing.
• Base answers on TYPICAL patients, not atypical cases.

Question Strategy Guide

• Broader Focus: Select the most comprehensive answer.
• Qualifying Words: Pay attention to words like "first," "most," and "highest priority."
• Negative Words: Proceed carefully with questions containing "not," "except," etc.
• Avoid Absolute Words: Be cautious of answers with "always," "all," "never," or "none."
• When Unsure: Opt for the most logical nursing care option.
• Jeopardy Questions: Identify the core question at the end of lengthy, detailed scenarios.

Cardiovascular Lecture #1

• Cardiac Topics relevant to the CCRN: Acute pulmonary edema, cardiac surgery, cardiogenic shock, cardiomyopathy, dysrhythmias, heart failure, hypertensive crisis, cardiac/vascular catheterization, myocardial conduction system defects, pulmonary hypertension, structural heart defects.
• Testable Nursing Actions: Applying leads for CV monitoring, identifying and monitoring rhythms, assessing hemodynamic status, and managing patients requiring various interventions like ECGs, arterial catheters, cardiac caths, cardioversion, CVP monitoring, defibrillation, invasive hemodynamic monitoring, and vascular stenting.

Cardiovascular Anatomy and Physiology Overview

• A strong grasp of normal anatomy is crucial for recognizing abnormalities.
• Cardiac Output (CO) is the volume of blood ejected from the LV in 1 minute.
• CO = Heart rate x Stroke volume.
• Factors Influencing CO: Preload, afterload, compliance, and contractility.
• Cardiac Index (CI) = Cardiac output / BSA.
• Stroke Volume (SV) is the volume of blood ejected from the LV with each contraction.
• SV influencers: Preload, contractility, compliance, afterload.

Preload Explained

• Preload is the volume of blood in the ventricles at the end of diastole and before contraction.
• It is determined by cardiac fiber length/strength and the volume of blood returned to circulation.
• Measurement: RA line and CVP estimate preload; PA artery capillary wedge pressure is an exact measurement.
• Frank-Starling Law: The force of contraction is proportional to initial muscle fiber length.
• Myocardial Failure: Volume can worsen a patient’s clinical status.
• Factors Affecting Preload: Variations in volume, systemic/pulmonary HTN, excessive PEEP, dysrhythmias, vasopressors/inotropes.
• Interventions to Increase Preload: Volume administration (crystalloids, colloids, blood products), compensatory mechanisms (renin-angiotensin, ADH, aldosterone, catecholamines).
• Interventions to Decrease Preload: Diuretics, ANP/BNP, vasodilators, afterload reduction (milrinone).

Afterload Explained

• Afterload is the workload ventricles must overcome to pump; systemic BP estimates afterload.
• Measured by SVR and PVR.
• SVR = (MAP – CVP) / CO.
• High afterload can decrease CO in a sick heart.
• Increase Afterload: Systemic/pulmonary HTN, polycythemia, outflow obstructions, vasoconstrictors, heart failure.
• Decrease Afterload: Sepsis, vasodilators (cardene, nipride), anaphylaxis.

Compliance Explained

• Compliance is the ability of ventricles to relax and distend during diastole.
• Compliance = change in V / change in P.
• "Good” compliance means a large volume of fluid creates only a small change in ventricular pressure.
• “Poor” compliance means a small fluid volume can produce a large pressure change.
• Decreased Compliance: Myocardial hypoxemia/acidosis, CHF, ventricular hypertrophy, pericardial tamponade, high PEEP, positive inotropic medications.
• Enhanced Compliance: Afterload reducers - milrinone!

Contractility Explained

• Contractility is the squeeze generated by the myocardial muscle.
• Measurement: Echocardiography estimates contractility; cardiac cath directly measures it.
• Atrial contraction accounts for 10-40% of LV filling, depending on HR (atrial kick).
• Shortening and Ejection Fraction are measures.
• Factors Affecting Contractility: Electrolyte imbalances (Ca), sympathetic stimulation, physiological depressants, pharmacological agents.
• Increase Contractility: Positive inotropes, sympathetic stimulators, hypercalcemia.
• Decrease Contractility: Pharmacology, negative inotropes, hypoxemia/hypercapnia, long-term CHF, parasympathetic stimulators, acidosis, hypo/hypercalcemia, hypo/hyperglycemia/magnesemia/natremia/kalemia.

Autonomic Nervous System Explained

• Sympathetic Stimulation: Releases norepinephrine (NE), increases HR, contractility, and conduction time.
• Parasympathetic Stimulation: Releases acetylcholine, decreases HR and conduction time via vagus nerve stimulation.
• Alpha (α) Adrenergic (norepi, phenylephrine, dopamine at higher doses): Arterial vasoconstriction, increases intracellular calcium.
• Beta (β) Adrenergic: Increases SA node discharge, increasing inotropy, chronotropy, and AV conduction time.
• B1 (epi, dopamine at lower doses): Acts on heart, agonists increase inotropy, chronotropy, and rennin secretion.
• B2 (dobutamine): Acts on lungs, agonists prompt smooth muscle relaxation, bronchodilation.
• Vasopressors: Typically raise BP.
• Inotropic: Act through alpha and beta receptors to vasodilate/vasoconstrict/enhance contractility.
• Chronotropic: Change HR by affecting nerves controlling the heart or rhythm from the SA node.

Disorders of the Heart: Cardiac Failure

• Cardiac Failure: Heart's inability to maintain sufficient cardiac output to meet the body’s needs.
• Left Heart Failure: LV unable to completely empty during systole.
• Pathophysiology: Decreased CO from decreased contractility, backflow of blood from LV to LA, increased PAP, PCWP, and CVP.
• Causes: LV infarction, valvular disease (pediatrics).
• Clinical Manifestations: Respiratory (pulmonary venous congestion/edema, dyspnea, tachypnea, rales, frothy sputum, decreased SaO2/PaO2), Cardiac (cardiomegaly, poor perfusion, tachycardia, hypotension, S3 sound).
• Late Signs: Right Heart Failure, acidosis, decreased GFR, decreased mentation.

Right Heart Failure Explained

• Right Heart Failure: Often a progression of left heart failure.
• Causes: Pulmonary HTN, RV infarct, cardiomyopathy.
• Pathophysiology: Increased myocardial oxygen demand/HR/PA pressures, decreased CO, pulmonary vasculature resistance.
• Clinical Manifestations: JVD, hepatojugular reflux, dependent pitting edema, hepatomegaly, anorexia, nausea, failure to thrive, weight gain, increased CVP/PVR.
• Diagnosis of Congestive Heart Failure: History, PE, labs, CXR.
• Split heart sounds/murmurs.
• Decreased peripheral pulses
• Increased liver size.
• ECG/ECHO changes.
• Lab Findings: Dilutional anemia/hyponatremia, decreased UOP, albumin in urine, hypoglycemia, increased WBCs, polycythemia, iron deficiency anemia.

Treatment of Congestive Heart Failure

• Goals: Maximize cardiac performance and reduce myocardial oxygen demand.
• Inotropic Agents: Digoxin, milrinone, VADs--promote increased contractility to increase CO.
• Decrease Myocardial Oxygen Demand: Dobutamine, bedrest, anxiolytics, beta blockers, dysrhythmia/pain management
• Optimize (Reduce) Preload: Diuretics, restrict sodium/fluids, venous dilation with nitroglycerin.
• Decrease Afterload: Nipride (nitroprusside), ACE inhibitors (captopril), milrinone, IABP in extreme cases.

Cardiomyopathies Explained

• Cardiomyopathies: Disease of the heart muscle.
• Types: Dilated, hypertrophic, restrictive.
• Dilated (“the big”): Most common in children, massive cardiomegaly/LV dilation, decreased SV/EF on echo.
• Management: Positive inotropic agents, diuretics, vasodilators, afterload reduction (milrinone).
• Hypertrophic (“the bad”): Increased myocardial mass, decreased ventricular cavity size, blood flow obstruction (LVOTO).
• Management: Beta adrenergic agonists, calcium channel blockers, diuretics/inotropes with caution, pacing, surgical resection.
• Restrictive (“the ugly”): Defect of the endocardium itself due to fibrosis/scarring, normal systolic function but decreased diastolic function.
• Management: None specific, CHF, symptomatic treatment (diuretics, digoxin, vasodilators, antiarrhythmics), lifestyle changes.
• Clinical Manifestations of Cardiomyopathy: Cardiomegaly, poor perfusion, CHF, low CO, decreased UOP/LOC, syncope, thromboembolic events, arrhythmias, shock.
• Diagnosis: CXR, ECG, Echo, viral titers, cardiac cath.
• General Management Principles: Decrease cardiac workload (fluid/sodium restriction, supplemental oxygen, intubation/ventilation), DVT prophylaxis, VADs, transplant.

Cardiogenic Shock Explained

• Cardiogenic Shock: Myocardial dysfunction leading to inadequate tissue BF, decreased coronary perfusion, and myocardial ischemia (bad cycle!).
• Causes: CHD/repair sequelae, cardiomyopathy, myocardial ischemia, Kawasaki disease, hypoxemia, anomalous coronary arteries, severe tachycardia, high-dose beta agonists, "itis-es" (myocarditis, endocarditis, pericarditis), valvular disease, hypoglycemia, hypothermia, altered electrolytes, dysrhythmias, myocardial depressant factors.
• Management: Minimize oxygen demands (intubation/ventilation, normothermia, sedation, pain management, correct anemia).
• Maximize Myocardial Performance: Correct arrhythmias, optimize preload/contractility, reduce afterload.
• Exclude congenital/traumatic heart disease, surgical/other therapies.

Cardiogenic/Obstructive Shock Explained

• Cardiogenic/Obstructive Shock: Caused by obstruction to cardiac output, affecting systemic perfusion.
• Examples: Pulmonary embolism, thrombus, valvular stenosis, aortic coarctation, great vessel trauma/abnormality.

Hypertensive Crisis Explained

• Hypertension: BP > 95th percentile for age, sex, and height on 3+ occasions.
• Hypertensive Crisis: Acute, life-threatening elevation in BP, causing end-organ abnormalities or death.
• Causes: Renal parenchymal/vascular disease, renal secreting tumors, polycystic kidney disease, Wilm’s tumor, neurologic causes (increased ICP, Guillain-Barre, dysautonomia, intraventricular hemorrhage, obstructive hydrocephalus), family patterns of HTN, obesity, hyperlipidemia, insulin resistance, pheochromocytoma, pituitary tumors, coarctation, Cushing syndrome, polycythemia, Williams syndrome, Turner’s syndrome.
• Management: Pharmacologic interventions (alpha/beta blockers, diuretics, vasodilators, pain management, anxiolysis).
• Lifestyle Changes: Low salt/cholesterol/fat diet, exercise program.

Cardiovascular Lecture #2

• Topics Overview: Structural heart disease, general principles of cardiac surgery, cardiac assist devices.
• Fetal Circulation: Gas exchange in the placenta.
• No intracardiac shunts!
• Neonatal Circulation: High PVR, low SVR, low CO.
• Birth Transitions: Low PVR, high SVR, high CO.
• FO and DA should close.
• Gas exchange shifts from placenta to lungs.
• PVR decreases rapidly.

Shunting Explained

• Ductus Arteriosus: Should constrict at birth in response to increase in SaO2 and loss of maternal prostaglandins.
• Functional Closure: Occurs 12-24 hours after birth.
• Anatomic Closure: Occurs in approximately 2 weeks.
• Open DA: L to R shunting, resulting in pulmonary overcirculation.
• Foramen Ovale: Opening in midatrial wall.
• Fetus: R to L shunt.
• Neonate: L to R shunt (SVR > PVR).
• Functional Closure: Very soon after birth (first breath).
• Anatomic Closure: Days to weeks later.
• Intermittent PFO: Due to changes in SVR.

Shunt Classifications

• Left to Right Shunt: Oxygenated blood from systemic to pulmonic circulation.
• Body receives oxygenated blood
• Acyanotic.
• Right to Left Shunt: Deoxygenated blood from pulmonic to systemic circulation.
• Body receives deoxygenated blood
• Cyanotic.

Vascular Resistance and Flow

• Pulmonary Vascular Resistance
• Systemic Vascular Resistance

Congenital Heart Disease (CHD)

• Suspect CHD when: Murmur & cyanosis, crying worsens cyanosis, failed hyperoxia test, abnormal weight loss, poor feeding with tachypnea, discordant upper/lower pulses and pressures, "septic appearing" infant, diagnosed with a syndrome.
• Trisomy 21: Atrioventricular septal defect (AVSD), VSD, ASD (any/all septal defects).
• Trisomy 18 (Edward’s): VSD, HLHS.
• 45X (Turner’s): VSD, coarc, aortic stenosis (AS), HLHS.
• Williams: supravalvular stenosis.
• DiGeorge: interrupted aortic arch, TOF.
• Noonan: pulmonary valve stenosis.

CHD Classifications

• Acyanotic with Increased Pulmonary Blood Flow
• L to R shunting
• VSD: Can result in pulmonary hypertension and complicated post-op course, arrhythmias common (JET is common).
• Amount of shunting depends on the pressures of SVR and PVR
• Repair depends on size with monitoring for symptom progression.
• Delayed Repair
• ASD: L to R shunting via communication between L and R atria, determined by compliance of L and R ventricles and size of the defect.
• Indications for closure: RV volume overload (too much L to R shunting), arrhythmias, emboli, significant increases in PVR related to L to R shunting.
• AVSD: Commonly associated with T21.
• 3 major issues: Common AV valve, ASD, and VSD
• Management: Surgical repair in infancy - VSD patched, ASD patched, and mitral valve repaired Complications for surgery

Further CHD Classifications

• PDA: Higher incidence in premature infants, L to R shunting, causing pulmonary overcirculation.
• Closure: Indomethacin or surgical ligation.
• Acyanotic with Ventricular Outflow Obstruction: Something is preventing the blood from leaving the L or V ventricle.
• Aortic Stenosis: Aortic valve commissures are fused together; leaflets are fused together, therefore valve movement is affected.
• Intervention: Balloon valvotomy or surgical incision of leaflets.
• Critical Aortic Stenosis: Patients are dependent on PDA for systemic flow.
• Coarctation of Aorta: Constriction of descending aorta.
• Discordant upper/lower extremities pulses and pressures.
• Intervention: PGE to maintain patency of PDA until surgical repair until surgical repair.
• Aimed at opening pulmonary valve, Balloon valvuloplasty or Surgical intervention

Cyanotic CHD Classifications

• Cyanotic with Decreased Pulmonary Blood Flow; Increased PVR and pulmonary pressures
• Tetralogy of Fallot: Underdevelopment of RV infundibulum.
• Determined by severity of PS/RVOTO
• Tet Spells: Caused by spasm of infundibulum muscle or sudden drop in SVR.
• Begin with irritability and hyperpnea.
• Followed by prolong period of intense cyanosis, leading to syncope.
• Tricuspid Atresia: Tricuspid valve atretic.
• PFO and/or ASD required for blood flow through the heart, usually have hypoplastic RV and/or RVOTO.
• Cyanotic with Increased Pulmonary Volume.
• Transposition of the Great Arteries (TGA): Aorta comes from RV; pulmonary artery comes from LV, parallel pulmonary and systemic circulations.
• Depend on PDA and/or PFO for survival for oxygenated and deoxygenated blood to mix from right to left side of the heart.
• Interventions: Require PGE or balloon septostomy.
• Surgical repair is ASO – lengthy and complicated repair

Further Cyanotic CHD Classifications

• Truncus Arteriosus: Conotruncal septation fails to happen during fetal development.
• Pulmonary artery and aorta fail to split, creating a single-valved vessel located above a VSD.
• Total Anomalous Pulmonary Venous Return (TAPVR): Drainage of the pulmonary veins into the systemic veins or into the right atrium.
• Hypoplastic Left Heart Syndrome (HLHS): Hypoplastic LV
• Management: PGE required to maintain PDA patency (ductal dependent) for systemic flow.
• Norwood with Neo Aorta with Shunt: Created from pulmonary artery to create an aorta, atrial septectomy to ensure adequate blood mixing.
• Glenn: Superior vena cava anastomosed to pulmonary artery, removes shunt taken down.
• Fontan: Inferior vena cava anastomosed via baffle to pulmonary artery

The Patient: Surgical Repair Considerations of CHD

• Multi-disciplinary team effort
• "Fragile” child, especially in post op phase
• Multiple surgeries and long term follow up
• Medications can be complicated
• Education on newborn care, pre and post surgery
• Perioperative Interventions
• Provides tissue perfusion and oxygenation during surgery
• Hemorrhage Potential Post Operatively

Post Operative Care Principles, Goals and Considerations

• Goals: Maintain CO / BP & control bleeding: >3 mL/kg/hr x3 hrs OR 5-10 mL/kg/hr = surgical team needs to know
• Assess BP / EKG trends
• Monitor Tamponnade: Acute increase in RAP/LAP OR equalization of RA and LA pressures or distention
• Look at arterial / venous measures
• Watch Tidal Volumes & Breathing
• Monitor CO and Perfusion Trends
• Potential need for mechanical ventilation
• Consider iNO with ventilation to help recruit flow
• ECMO if unable to maintain perfusion with normal ventilation

Cardiac Assist Devices

• ECMO: <2kg, Nonpulsatile flow ; L, R, or BiVAD support
• Centrifigal Pump: >2 kg, Nonpulsatile flow ; L, R, or BiVAD support
• Pnemoatic Pump: > 17 kg, Nonpulsatile Flow ; L, R, or BiVAD support
• IABP: >3 kg Nonpulsatile counterpulsation ; improves myocardial perfusion and decreases O2 demand; L heart support

Review Questions

• Poor CO is often manifested by cold, pale, and mottled extremities.
• Stimulation of the sympathetic nervous system increases stroke volume and HR.
• Dopamine improves hemodynamic function through inotropic and chronotropic actions.
• A patient with CHR would most likely not exhibit increased UOP.
• Vasodilators are ordered for a patient with a hypertensive crisis to improve cardiac function and decrease afterload.
• A 12 year old hitting their chest represents cardiogenic/obstructive shock
• Medications used in the management of a persistent PDA includes Indomethacin.

Review Question : Cont.

• CHDs that result in increased pulmonary blood flow place an infant at greatest risk for congestive heart failure.
• Two cardiac anomalies associated with TOF are VSD and PS
• In an infant with TOF, the goals of treating a TET spell are to increase pulmonary blood flow and relax the infundibulum.
• A newborn is admitted with TGA a BAS needs to be performed, administer patient Alprostadil.
• Emergent management of the patient with suspected cardiac tamponade should include Percardiocentesis

Pulmonary Lecture #1

• Topics Reviewed: Acute lung Injury, ARDS, Embolism, Hypoxemia, Failure, Infections, trauma, asthma, surgery, and BPD.
• Nursing Action: Manage and evaluate ABG and ventilation
• Pediatric Considerations: Patient are mini adults, airway differences make it easier to obstruct, chest walls are more compliant in children and CNS is sensitive.

Airway Differences

• Airways: Obligatory Breathiers with epiglottis making intubation difficult
• Thoracic Cavity: Weak with poor diaphrgam allowing chest to compress with breath

Gas Exchange

• Alveolus: Type 1 cells for gas exchange. Small and decreased surface area
• Type 2 Cells for surfactant
• Pulmonary: Lungs are stiffer needing to stretch to allow alveoli to open especially with surfactant
• Compliancy: Volume is low with increasing stiffness
• Resistance: Affected by ETT and airways size
• Hypoxia is vasoconstriction with smaller surface area

V/Q Matching

• Normal ratio = 0.8

• 0.8 vent > perfusion, such as cardiogenic shock, stenosis, tricuspid or embolism

• < 0.8 perfusion > vent, such as pneumonia, ARDS, airway obstruction

Intrapulmonary Shunting

• Normal Intrapulm P(A)O2 - PaO2 values should be between 5 - 15 mmHg
• Calculate P(A) = Fi02 * (760-47) - PaC02/0.8
• P/F ratio: Determines Dead Space for Oxygen
• PaCO2 remains constant until the shunt hits 50%
• PVR = Resistance in Pulmonary

Oxyhemoglobin Curve

• Impacted by pH, 2,3-DPG and PaC02
• Left shift includes decreased PaC02 and temp, increased pH or CO poisoning
• O2 binds but cannot be released at the tissue level
• Releases: Right shift releases O2 loading temp , acidity with elevated 2,3-DPG

Acute Respiratory Failure

• Results: Hypoxemic from tissue disorders, increased airway resistance from abnormalities
• Patient Management: Support and noninvasive interventions
• Monitor Complications: High PEEP and decreased CO from pressure on vessels, trauma from ventilation and oxygen toxicity

ARDS

• Occurs with ALI with Characterized by PaO2/FiO2

Acute Pneumonia

• Etiology: Virus and infection from fluid imbalance due to consolidation of lungs
• Risk Factors: Aspiration and decreased immunity, such as TEP
• Clincial Manifastations: Fever with distress and cyanosis
• Patient Management: Prevention, ventillation and Oxygen; treat with possible antimicrobials

Acute Laryngotracheobronchitis (Croup)

• Etiology: Viral and Baterial swelling of Glottis
• Clincial Manifastations: Worse at night with stridor and barking, with mild fever. Note, High Fever is Pneumonia.
• Patient Management: Racemic epinearine and or Helium
• Complications: Avoid secretions
• Epiglottis
• Epidemology: Progressvie inflimmations of epiglottis

Patient Management

• Antibiotics and ventillation. Avoid unplanned extubations

Bronchiolitis

• Epidemiology: Inflammation of airway via RSV and flu. High risk if previous BPD or CHD
• Risk Factors may include: Complications and low Immunity
• Patent Manaement: Monitor 02, nutrition and high risk for ARDS

Pulmonary Lecture #2

• Topics: Overview of pneumothorax, asthma, pulmonary embolism, PHTN, BPD,CDH, TEP.
• Pneumothorax: Air trapped between the lung and can lead to collasped lungs. Air blocks VQ mismatcing.
• Manifeststions: Increased RR, WOB, and Chest wall dissymetry

Additional Presentation

• Tension Pneumo: Increased agitation and shifted towards the unaffected area. EMERGENCY to reduce pressure in the lung.
• Open Pneumo: Airsucks into chest.
• Trachea Inury: Rare in Peds due to increased compliancy, subcutanous amphysemsa
• Management: Remove for risk and PIP setting during removal. CT to insert and control venting

Status Asthmaticus

• Etilogy: Severe asthma
• Pathophysiology: Airways effected by increased air trapping = increases RR
• Treatment: Restore breathig ability. Monitor with medication and ventillation

Acute Pulmonary Embolism (PE)

• Ratre in children: Caused by SCD with undiagnosed issues. Most are free floating
• VQ effects: Increased O2 demand leads to right and systemic heart issues
• Management: High oxygen and supportive care

Pulmonary Hypertension (PHTN)

• Chronic hypoxia and increase pulm resistance via vascular issues
• Patho: High pressure, shunt issues and hypoxemia
• Diagnosics: Look at PaO2
• Managment: Sustained DIlation
• Cons: High FiO2 can harm Avelior tissue.
• IV Vasodialators with Hyperventialtion

BPD

• Follows a long period of breathing, can cause scarring in infant lungs
• Risk Factors: prematurity and low B/W
• Treatment: Provide support that are needed

Congenital Diaphragmatic Hernia

• Results: A birth disorder where the diaphragm has hole
• Caused: Opening allows abdominal areas to flow.
• Management: ECMO

Teacheoesphogeal Fistual (TEF)

• Abnormal connection with esophagus and treache
• Monitor for infection

Neurological Lecture

• Reviewers: GCS, seizures, and menigitis

Basics and Structure

• CN: 12 nerves from brain; with 3 pathways running through
• The brain: with structure and lobes
• Spinal and Auto nerves

Diagnostics

• EEG
• CT
• ICP

GCS

• Basic Scale
• Intubation impacts it abilities

ICP

• ICP: Normal 5-10. Pressure that impatts the ability for Brain blood to circulate
• Causes: TBI, Mass, Infection
• Symptoms: High BP, Irregularities, and Change in LOC.
• Treatment: Monitor environment to maximize.

Hydrocephalus

• Increases Fluid: Causes issues
• Symptoms: N/V, lethargy with increased head size
• Treatment: shunt
• Interventions: Monitor pressure

Spinal Injury

• Complete: Loss of function via vertebrae, spinal and edema
• Causes: MVA with steriods

Encephalopathy

• Disorders: Non-infectious with headache and decreased LOC
• Treatment: Support functions

Meningitis

• Inflammation of mengines: via bacterial (increased WBC) and viral
• Symptoms: Fever, rig,idity and change in LOC.
• Treatment: Anitbiotics for bacterial for short term.

Seizures

• Alters behavior - Symptoms on other issues.
• Can be general/ focal with phases.
• Medication : Lorzepam
• Managment Support Airway to treat hypoxemia

Spinal Abnormalities

• Myelen: Roots and chords through spinal
• Treatment : Closure to treat hydropenia

Tumor

• Tumors: Mass with location effecting it functionality and management with increased ICP

AVM

• Direct Connection : Between A and V
• Treatment : Varies based on Size and Location with Laser or surgery

Review Answers

• CF : Choroid Plexis with Arachnoid villae
• Symptoms : Pupil Dilation
• Obstruction : Increase CSF
• Best leveling : Lateral VEntricle
• Bleed type : Arterial.
• Initial Action : Head Midline
• Positive result : Meningeal Irritation
• Care Included SC issues with medication
• Meninginties CSF : Elevated Protein and glucose
• Arriving patient : Administer oxygen

Endocrine System

• Hormone regulation, Water and Electrolytes: Electrolyte balance & energy Production,

1. ADH (Vasopressin) reabsorbed urine by creating H20 permeability

• Produced by the hypothalamus,
• vasoconstriction
• increased blood pressure, CO

2. Natriuretic Hormones, releases water with sodium
3. Mineralocorticoids such as Aldosterone - Na / H20 reabsorption + Potassium excretion
4. Adrenal hormones (Cortisol conserving sodium = water retention)
5. Insulin - increase cell intake glucose by lower sugar levels
6. Glucagon - the increase levels of sugar with glycogenesis

Disorder of Water: Regulation: SIADH vs DI

• SIADH: Water into Body with Low SODIUM
• DI: "Potty" in which patients are THIRSTY
• CAUSE: TBI, tumor with medication
• Manfestations: Hypoonentremia vs HYPERnatriemia with dehydration and neuro issues
• DIagnostic : High OsmOLality AND SG
• Patients Mangagement includes treatment
• DDAVP vs Hypotenication treatments.

Acid Base: Hypoglycemia, DKA & Error Metabolism

• Causes & Patho: Altered insulin leads to lack KETONES,
• DKA: with PH < 7.3, glucose levels.
• Errors include: increase ammonia and acid.
• Manfestaton : 7 P + KUSSMAL BREATHING with K
• Manage: HYDRATE with isotonic
• Medication: Insulin , and fluid and electrolytes
• Avoid : rapid BG control.

Complications and Key Facts

• Patients need insulin when BS is 250
• Low sodium causes: Hypo with Neuro issues.
• Water is absorbed.

Immune System: Basics

• Anemia: Is hematopoiesis and related with O2
• Thrombocyt : Platelets with Normal Rate of 150,000
• Lekcocites WBC range to monitor immunity

Therapy

• Blood types must be matched
• PRBCS: Increase oxygen and hemoglobin
• Platelet Transfusions are for bleeding

Thrombolytic and Issues

• Etiology/ path- Bleeding / Thrombotic
• DIC - D dimer : D disolve
• Management: Prevent Clotting - Treat primary
• Risks: Increased HIT

Innmunity Issues

• Immune issue- SCID, CVID: with Increased for Infections
• SC Issue : Neutropenia vs Leukopenia

Tumor

• Tumor : Mass with Location
• Causes: Pressure to areas
• Hyperleuko,TLS & Compression
• Treatment- Fluids with medication

Sickle Cell

• Genetic Mutation: Occlusions via decreased RBCs
• Complications: Acute Pain
• Management: Treat Pain.

Hematology / Immunology : Review Questions

• CSF is the choroid plexus.
• Sympathomimetic Drug is expected with bronchodilation.
• Hydrocephalus flow obstructed of CSF.
• ICP is leavel the lateral ventricle.
• Brain Bleeds for year 8 is arterial.

• initial Independent Nuirsng intervetion Is HEAD IN midline.
  

• A positive brudzindski sign indicates menigeal irritation.
• An uncontrolled injury causes Spinal COD protective measures.
• Untreatmened Bactierial is increased WBX with eleated Proteins .