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CCRN®
Exam Review
Sixth Edition
Presented by:
Mary Ann “Cammy” Christie,
MSN, APRN, CCRN-CSC-CMC, PCCN
www.MedEdSeminars.net
CCRN Exam Review | Mary Ann “Cammy” Christie, MSN, APRN, CCRN-CSC-CMC, PCCN
Table of Contents
Program Description and Learning Outcomes i
Introduction and Synergy 1
Hematology/Immunology/Integumentary 4
Cardiovascular 14
Endocrine 30
Gastrointestinal 37
Neurology 48
Behavioral and Psychosocial 54
Renal 64
Respiratory 71
Musculoskeletal and Multisystem 92
MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

Copyright 2020 MED-ED, Inc., All Rights Reserved
CCRN Exam Review | Mary Ann “Cammy” Christie, MSN, APRN, CCRN-CSC-CMC, PCCN
Program Description
This two-day course provides the critical care nurse with a review of AACN’s 2020 core curriculum.
The agenda combines central knowledge-based lectures for nurses working in the ICU with an
essential review of nursing care and interventions according to the AACN exam blueprint for the
critical care provider. This review is not an introduction to the ICU, but a comprehensive update for
the professional at the bedside and preparing for the certification examination.
Program Learning Outcomes

This program prepares the learner to:
1. Discuss and practice test-taking skills.

2. Review critical anatomy, physiology and pathophysiology of each system.
3. Discuss significant assessment and diagnostic findings relevant to the critical care
environment.
4. Discuss clinical presentation as well as specific patient management of commonly seen critical
care conditions.

i
Course Objectives Requirements
• Prepare you to take the • Current unrestricted RN license
CCRN Examination in the United States
• Clinical practice in critical care
• Not what’s new in critical
1,750 hours in 2-year period
care with 875 hours in last year or
• Not an update Current clinical practice for
• A review of the essentials of at least 5 years with
critical care nursing minimum of 2,000 hours
(with 144 hours in past year)
• BSN not a requirement
1 2
Application Exam
• Obtain application: American • Details:
Association of Critical-Care
Nurses (AACN) – 150 questions
• 800-899-2226 or www.aacn.org – 3 hours to complete
• Apply
• Receive “Authorization to Test” • READ ALL INSTRUCTIONS!
letter – No pencil, calipers, calculator
• Schedule Test: H&R Block, PSI
• 90-day window to take exam
• Passing: 71% overall
3 4

1
CCRN Blueprint Blueprint
Clinical 80% Professional 20% Professional: Synergy Model
• Cardiovascular 17% • Advocacy/Moral 3% Patient-centered care
• Respiratory 15% • Caring Practice 4% Needs of the patient matched
• Multisystem 14% • Collaboration 4% with the nurse’s ability
• Endocrine, GI, • System Thinking 2% 1999
Renal, Hematology • Diversity 2%
Integumentary 20%
New concept: whole patient
• Clinical Inquiry 2% and resources that patient
• Musculoskeletal • Learning 3% needs for successful outcome
Neurology
Psychosocial 14%
5 6
Recertification/Renewal Recertification/Renewal
• Maintaining CCRN: • Clinical
Category A • Min: 60, Max: 80
certification 3 years
• Recertification:
• Safety, Mental Illness, Caring
– Retaking exam
Category B • End of Life, Diversity, HIPAA
– Continuing Education Units • Min: 10, Max: 30
(CEUs)
• CEUs by synergy model • Collaboration, Precepting,
Category C Communication, Teamwork
• Min: 10, Max: 30
7 8

2
A patient’s family expresses anxiety regarding When teaching a family member to perform an
the meaning of numbers on the patient’s aspect of patient care, the nurse realizes that
monitor and asks the nurse for clarification. The family members:
nurse’s most appropriate response would be:
a. are affected by timing of teaching
a. “The numbers indicate the patient is having
problems.” b. learn best if they perceive a need to learn
b. “The numbers help us to determine the best
treatment.” c. learn best if shown a complex procedure all
c. “Which numbers on the monitor concern at once
you?”
d. “What don’t you understand about the d. learn unrelated tasks first
monitor?”
9 10
A patient with cerebral edema after a subarachnoid

hemorrhage has been ordered nifedipine 10 mg by
mouth every 4 hours. The patient’s blood pressure
(BP) is 150/85 mm Hg. How should the nurse
respond to this order?
a. Ask the pharmacist to clarify the order.

b. Discuss the purpose of the order with the
physician.
c. Research the indications and safety of
nifedipine.
d. Administer the medication to control the BP.
ESSENTIALS
11 12

3
Stress Response and
Essentials of Critical Care Immunosuppression
• Heart rate (HR), respiratory rate (RR),
temperature
• Blood pressure (BP): systolic and diastolic • Stress response
• Acute vs. chronic stress: total body response
• Tissue oxygenation
• HR, BP, RR, temp. and blood sugar changes
• Supply and demand • Impaired gag, cough or swallow
• Changed gastric pH, colonization, volume
• GOAL: enhance O2 delivery and aspiration
decrease O2 demand • Acute phase stress reactions = catabolism,
decreased healing, inhibit immune response
• Sequential infections
13 14
Hematology
Immunology Platelets
• ETOH
• Hemostasis: • Aspirin/clopidogrel • Thrombocytopenia
• Termination of bleeding (Plavix)/prasugrel • Heparin-induced
• Vascular response (Effient) thrombocytopenia
• Vasospasm
• GP IIb, IIIa inhibitors (HITT)
• Thromboxane A2
• Platelet response • NSAIDs • production
• Coagulation • destruction
• Dilutional
15 16

4
Disseminated Intravascular
Coagulopathy (DIC): Definition DIC
• A syndrome characterized by • Factors triggering DIC

thrombus formation and hemorrhage • Tissue factors: tissue breakdown
secondary to overstimulation of the • Platelet aggregation: stimulation
normal coagulation process, with (sepsis)
resultant decrease in clotting factors • Injury to vascular endothelium and
and platelets exposure to collagen
• DIC may be chronic or acute. • Shock, endotoxin, acidosis or hypoxia
• Thrombosis, then hemorrhage. • SIRS activated
17 18
DIC DIC: Etiology
• Etiology: always secondary • Infection and sepsis

• Vascular disorders • Hematological/immunological
• Anaphylaxis
• Shock • Hemolytic blood transfusion reaction
• Vasculitis • Massive blood transfusion
• Giant hemangioma • Prolonged cardiopulmonary bypass
• Sickle-cell crisis
• Dissecting aneurysm • Transplant reaction
19 20

5
DIC DIC: Clinical Presentation
• Trauma • Cancers • Abnormal bleeding

• Multitrauma • OB complications • Signs of thrombosis
• Burns • Embolism • Change in level of consciousness
(LOC)
• Acute anoxia • GI complications • Chest pain, ST-T wave changes,
• Heat stroke • Pulmonary systolic BP
• Crush injury complications • Dyspnea, hypoxemia
• Head injury • Toxins • Urine output, proteinuria,
electrolyte imbalance
• Surgery
• Abdominal pain, diarrhea
21 22
Clinical Indications of
Platelet Dysfunction Labs: DIC
• Petechiae (first indication of DIC)

• Decreased • Increased
• Ecchymosis
• Platelets (< 100,000) • PT (> 15 seconds)
• Purpura
• Fibrinogen (< 200 • PTT (> 60-90
mg/ seconds)
100 mL) • FDP/FSP (> 10 g/mL
• Antithrombin III bur < 100)
(<70%) • D-dimer (> 2 mg/L)
• Specific to fibrin
23 24

6
Medical Management Blood Products
• Maintain ABCs. • Risks of transfusion

• Stop bleeding, fluid resuscitation.
• Noninfectious
• Treat stimuli.
• Infectious
• Correct hypovolemia, hypotension,
hypoxia, and acidosis. • Immunologic
• Stop microclotting to maintain perfusion. • Aged blood
25 26
Blood Products
• Red blood cells (RBCs)

• Action: increase O2 carrying capacity
• Indications:
• Significant H&H with normal volume
• Slow blood loss
• Avoid fluid and circulatory overload
• Administration: blood filter, 2-4 hours
• Complications: transfusion reaction,
hepatitis
27 28

7
Blood Replacement Blood Replacement
• Coagulation components: platelets • Fresh frozen plasma (FFP)

• Action: platelet count, aides clotting • Action: clotting factors, water and
electrolytes
• Indications: platelet count
• No platelets
• Administration: component filter, rapid
• Indications: coagulant deficiencies,
infusion viable Factors V and VIII
• Complications: transfusion reaction, • Administration: filter, rapidly, thaw
mismatching, hepatitis, allergic • Complications: same as platelets
reactions, febrile reaction
29 30
Blood Replacement Blood Replacement
• Cryoprecipitate • Adverse reactions

• Action: raises Factors VIII + XIII • Hyperkalemia, hypocalcemia
• Prevents and controls bleeding • Decreased 2,3-Diphosphoglycerate
fibrinogen and anti III (2,3-DPG), ammonia intoxication
• Indications: Hemophilia A, von • Hypothermia, hepatitis, HIV
Willebrand factor, DIC • Cytomegalovirus, acute respiratory
• Administration: filter rapidly distress syndrome (ARDS),
• Complications: hepatitis transfusion- related acute lung injury
(TRALI)
31 32

8
Complications of DIC Anemias
• Mortality: 40%-60% • Deficiency of hemoglobin

• Hypovolemic shock • Most common causes
• Acute renal failure • Excessive blood loss
• Excessive blood cell destruction (hemolysis)
• Infection
• Deficient RBC production (ineffective
• ARDS
hematopoiesis)
• Stroke
• GI dysfunction
33 34
Classifications Complications
• Production vs. destruction of loss • Decreased exercise tolerance

• RBC Size
• Hypoxemia
• Microcytic anemia: iron deficiency,
thalassemia • Cold intolerance
• Macrocytic anemia: megaloblastic,
deficiency of B12, folate, hypothyroidism,
• Fatigue
ETOH abuse, drugs
• Normocytic anemia: acute blood loss, aplastic
• Dimorphic anemia: Two causes act together.
• Heinz body anemia: cytoplasm of RBCs has
dark spots, dietary
35 36

9
Treatments Cancer
• Depends on cause • Immunosuppression

• Due to drugs, cancer itself
• Iron deficiency, vitamin
• Nutritional concerns
supplementation, epoetin alfa
• Organ dysfunction
• Blood transfusion • Stress response
• Hypercoagulable: increased risk of DVT
• Cancer cells
• Stress hormones
• Bed rest, volume status
37 38
Oncological Complications Wounds
• Tumor lysis syndrome • Pressure ulcers

• Metabolic abnormalities that can occur as a • An area of skin that breaks down
complication of cancer treatment when an irritant has occurred
• Analogous to rhabdomyolysis • Risk factors
• Wheelchair, cannot move, malnutrition
• Pericardial effusion
• Decreased blood flow
• Alzheimer’s disease, fragile skin
• Urinary incontinence or bowel incontinence
39 40

10
Symptoms of Pressure Ulcer Pressure Ulcer
• Red skin that gets worse over time, blister • Stages

then opens • Stage I: reddened area, when pressed
• Commonly occurs on: does not turn white
• Buttocks, elbow, hips, heels, ankles • Stage II: Skin blisters or forms open sore.
• Shoulders, back, back of head • Stage III: Skin now develops an open,
sunken crater.
• Stage IV: Pressure ulcer becomes so
deep that there is damage to the muscle,
bone, tendons and joints.
41 42
Skin Complications Peripheral IV Review
Cellulitis Necrotizing Fasciitis
• Complications: phlebitis, extravasation of

IV fluids and/or medications, hematoma
formation
• Thrombophlebitis 15%
• Minimize catheter movement, upper
extremity only, smallest suitable catheter,
less than 3 days
43 44

11
Extravasation Extravasation
• Stop injection; leave catheter in place. • Observe the region for pain, induration or
• Slowly aspirate; apply pressure. necrosis.
• Remove IV access. • Continue warm/cold therapy for 48-72
• Inform MD and obtain orders. hours.
• Elevate area 48 hours, warm/cold • Advise patient to resume activity with
compress. affected limb as tolerated.
• Initiate substance-specific antidote. • Consider surgical evaluation for persistent
or worsening symptoms.
• Phentolamine (OraVerse), sodium
thiosulfate, hyaluronidase (Amphadase)
45 46
Hematology Pearls
• DIC = high PT/PTT, low fibrinogen, low

platelets, high FSP (FDP), high D-dimer
• Give heparin in DIC accelerates
formation of antithrombin III, inactivates
thrombin and prevents conversion of
fibrinogen into fibrin.
47 48

12
Question Question
A primary chemical mediator in anaphylactic Which of the following lab diagnostic findings
reaction is: will most likely be seen in DIC?
A. myocardial depressant factor A. PT & PTT prolonged

B. histamine B. fibrinogen increased
C. complement C. platelet count increased
D. interferon D. D-dimer normal
– The pathophysiology of anaphylaxis includes:
• Bronchospasm, hemolysis and rapid DIC, increased
vascular permeability and third spacing
49 50
Question
The clinical presentation of DIC includes: • Today is a gift, and every day, miracles are scattered about
if only we have eyes to see them.
A. signs of thrombus formation
B. excessive bleeding
C. decrease in platelet count
D. all the above
51 52

13
Cardiac
To drive hemoglobin
to the cell
53
53 54
55 56

14
• Cardiac cycle
• Aortic pressure
• Coronary artery perfusion pressure (CAPP)
– CAPP = diastolic BP - pulmonary artery wedge
pressure (PAWP)
– Normal: 60-80 mm Hg
57 58
DETERMINATES OF VENTRICULAR
CARDIAC CYCLE
FUNCTION
59 60

15
Use
Assessment of Function
61
61 62
• SVO2
–Cardiac output/cardiac input
–Hemoglobin & hematocrit
–Oxygenation
–Metabolic demand
63 64

16
• Hypokalemia: ventricular irritability
– Flat T with prominent U wave
– T wave + U wave same amplitude
– ST-segment flattening
– Prolongation of QT interval (K+ < 2.0)
– ST-segment depression
65 66
• Hyperkalemia; asystole
• Hyperkalemia
– > 5.5 tall, narrow, peaked T
waves – Treatment:
– QRS widens • Remove potassium: Kayexalate or dialysis
– P wave widens • Shift potassium: insulin and dextrose, NaHCO3-
– > 6.5 QRS widens • Calcium: to protect the heart
– > 8.0 wide QRS
– P wave
barely visible
67 68

17
• Hypocalcemia: torsades de pointes • Hypomagnesemia: torsades de pointes
– Prolonged QT – Prolonged QT
– Prolonged ST seg – Broad, flattened T wave
• Hypercalcemia: agonal or asystole – Dysrhythmias
– Shortened QT • Hypermagnesemia: agonal to asystole
– PR, QT prolonged
– Shortened ST seg
– Prolonged QRS
69 70
• CAD
– Definition
– Pathophysiology
– Etiology
– Risk factors
– Clinical manifestations
• Heart failure (HF), angina, unstable angina, acute
coronary syndrome (ACS), acute myocardial infarction
(AMI), sudden death
71 72

18
• Clinical presentation
• ECG presentation normal; enzymes normal
• Treatment modalities
• Rest, NTG, ASA
73 74
• Antiplatelet therapy: dual therapy • Clinical presentation, ECG, enzymes

• Vasodilator • Pathophysiology: blood clot
– Nitroglycerin: patch, sublingual, longer-acting isosorbide
mononitrate (Imdur) • New terminology
• Beta blocker
– Decreases MVO2
• ACS
– Regulates BP, HR & rhythm
• ACE inhibitor
– BP control, reduces remodeling
• Statin
75 76

19
• Biochemical markers • Treatment management
– Troponin +, CPK - • MVO2 supply MVO2 demand
– Diagnosis: unstable angina, minimal myocardial
damage – ASA
• Prognosis: high risk – Beta blockers
– Heparin
– NTG
– Morphine
– GP IIb-IIIa inhibitor drugs
77 78
• Management • Two functions

• Assistance for the ventricle – Decrease afterload
• Medications – Increase coronary perfusion
• Mechanical assist • Absolute contraindication:
• Intra-aortic balloon pump (IABP) aortic insufficiency
• Additional diagnostics: catheterization • Monitor for:
– Vascular exam
– Timing
79 80

20
• Interventional • Preprocedure
– Percutaneous transluminal coronary angioplasty – NPO, consent
(PTCA) – Labs, ECG, insulin orders, oral medications
– Stent placement for patient with diabetes, prehydrate,
acetylcysteine (Mucomyst) for renal
– Directional coronary atherectomy (DCA) insufficiency patients.
– Vascular exam, allergies
– On-call meds: ASA, clopidogrel (Plavix),
etc.
81 82
• Monitor ECG Six P’s

• Vascular assessment • Pain
• Labs, heparin protocol, IIb, IIIa infusion • Pulse
• Activity restrictions, progression • Pallor
• Sheath removal • Polar
• Medications • Paresthesia
• Paralysis
83 84

21
• Time = Muscle, Muscle = Life
• Etiology: totally occlusive clot
• Pathophysiology
• Labs: troponin, LDH, CPK, MB band
• ECG, echo, chest X-ray
85 86
Posterior
Right side
87 88

22
• VOMIT: 12-Lead, enzymes: MONA • Assess for clinical indications of right-ventricle MI
– ECG, vital signs, BLS, ACLS – ECG changes V4R, V5R, V6R
– Hemodynamic parameters – ↓ RAP, ↓ PAWP
• Manage and monitor. – ↓ CO, CI, MAP, ↑ SVR
• Reduce size of infarct. – Clinical indications of right-ventricle failure
– Door to diagnosis and treatment – Minimal to absent pulmonary congestion
– Catheterization laboratory
– Open the artery.
89 90
• Maintain adequate filling pressures.

• Administer volume.
• Avoid diuretics and/or venodilators.
• Maintain contractility.
91 92

23
• Medical and surgical revascularization
• Medications: antiplatelet, vasodilator,
beta blockers, ACE inhibitors, statin
• CABG
• Preop, postop care
• Atrial fibrillation (AF)
93 94
• Think HF.
– Median sternotomy • Progressive disease
– Right or left thoracotomy • Malperfusion
– Valve types • Cardiomyopathy
– Anticoagulation
95 96

24
Left-Ventricular Failure Right-Ventricular Failure
• CAD/LV infarct • CAD/RV infarct • Tachycardia • Weakness,
• Dysrhythmias • Dysrhythmias • Tachypnea, fatigue
• Volume overload • Volume overload dyspnea, • Mental confusion
• Valvular disease • Valvular disease orthopnea, PND • Murmur MR
• VSD • VSD • Left-sided S3 • ABGs
• CMP • CMP
• Displaced MPI • Chest X-ray
• Coarctation of aorta • Myocardial contusion
• Tamponade • Pulmonary • Cough, pulsus • ECG: atrial
hypertension alternans arrhythmia, LAE,
• Oliguria LVH
97 98
• JVD • Nocturia • Treat the cause, improve oxygenation.

• Hepto-jugular reflux • Weakness, fatigue • Decrease MVO2, decrease preload.
(HJR) • Weight gain • Monitor volume status: low-sodium diet.
• Dependent edema • Murmur TR
• Diuretics
• Heave at sternum • Right-sided S3
• CVP
• NTG, pulmonary vasodilators (oxygen)
• Hepatomegaly
• Abnormal liver • Decrease afterload.
• Anorexia, nausea, functions
vomiting, – Beta blockers, carvedilol (Coreg)
• ECG: RAE, RVH,
abdominal pain atrial arrhythmia • Control dysrhythmias.
• Ascites
99 100

25
• Increase contractility: IABP
– SNS stimulants: dobutamine
– Phosphodiesterase inhibitors: milrinone
– Dopamine
– Digoxin
101 102
103 104

26
• Control BP.
• Repair: stent or surgical
• Postoperative care: pain control, BP control,
pulmonary concerns, renal concerns, spinal cord
ischemia
• Postoperative complications: pulmonary, BP, renal
• Ambulate, incentive spirometer, ambulate
105 106
• ABCs
• ST-segment depression = ischemia
• Cardiac output/input:
preservation of perfusion • ST-segment elevation = current injury
• Maintaining HR X SV • IABP = increase coronary perfusion, decrease
afterload: so it increases myocardial oxygen supply
• PRELOAD
and decreases demand
• AFTERLOAD
• CONTRACTILITY
107 108

27
• ST elevation in II, III + aVF = inferior You are caring for a patient recently
infarction admitted with an inferior-wall MI. Which of
• ST elevation in I, aVL, V1-6 = anterior the following 12-lead ECG findings would
infarction you anticipate?
A. T-wave inversion I and aVL

B. Q-wave formation and ST-segment
elevation in II, III and aVF
C. QRS duration > 0.10 in all 12 leads
D. R wave taller in V6
109 110
Your patient with an inferior-wall MI also The most common complication of an MI is:
has a right ventricular infarction. He soon
develops right ventricular failure. Which of A. an arrhythmia
the following data obtained would correlate
this? B. HF
C. cardiogenic shock
A. PAP 23/8 PCWP 19 CVP 20 D. pulmonary edema
B. PAP 54/28 PCWP 14 CVP 14
C. PAP 28/10 PCWP 10 CVP 20
D. PAP 12/4 PCWP 24 CVP 18
111 112

28
A normal wedge pressure, increased pulmonary artery Medical management of valvular disease includes:
pressures and evidence of right ventricular (RV) failure
would most likely indicate:
A. prevention of infection
A. cardiac tamponade B. treatment of HF
B. left ventricular (LV) failure C. treatment of dysrhythmias
C. an MI D. all of the above
D. pulmonary embolism (PE)
113 114
Symptoms to evaluate for the diagnosis of HF may • Failure needn’t be a negative thing.
include:
• Rather, we learn from our mistakes and fail
A. dyspnea at rest
smarter the next time.
B. orthopnea
C. nocturnal cough
D. all of the above
115 116

29
Diabetes Insipidus (DI)
• Definition: clinical condition characterized
by impaired renal conservation of water,
resulting in polyuria, low urine specific
gravity, dehydration, ↑ serum Na+
• Caused by deficiency of antidiuretic
hormone (ADH) from the pituitary or
decreased renal responsiveness to ADH
• Etiology: neurogenic, nephrogenic
(lithium), psychogenic (polydipsia)
117 118
Pathophysiology Clinical Presentation

• Deficiency of ADH or • Urine specific gravity: < 1.005
inadequate renal tubule • Serum sodium >145 mEq/liter
response to ADH • Elevated blood urea nitrogen (BUN)
• Diuresis of large volumes of • Increased serum osmolality
hypotonic urine
• Increased H+H
• Dehydration and hypernatremia
• Shock and/or neuro effects,
confusion to seizures
• Permanent vs. temporary
119 120

30
Treatment
• Management: detect clinical indication of
DI
– Monitor urine output, weight, serum
labs, hypovolemia • (DI) = Dehydration and
– Correct fluid deficit
High-Serum Na+
– Administer exogenous ADH, aqueous
vasopressin, desmopressin (DDAVP),
Diapid (intranasal)
121 122
Syndrome of Inappropriate
SIADH: Neurogenic
Antidiuretic Hormone (SIADH) • Neurogenic: Pituitary tumor, CNS trauma,
stroke, ICH, CNS infection, Guillain-Barré
• Definition: clinical condition syndrome, CVA, nonmalignant pulmonary
characterized by impaired renal disease
excretion of water, resulting in oliguria, • Ectopic SIADH: production of a substance
high urine-specific gravity, water indistinguishable from ADH by tissue
intoxication and hyponatremia – Oat-cell CA
• Nephrogenic SIADH: general anesthetics,
narcotics, tricyclics, acetaminophen (Tylenol),
anticonvulsants
• Hypoxia, stress, multifactorial in ICU patient
123 124

31
SIADH SIADH
• Oliguria: urine output less than • Headache, personality changes, altered
0.5 mL/kg/hour level of consciousness (LOC)
• Urine specific gravity: > 1.030 • Seizures
• Clinical indications of overhydration • Muscle weakness or cramps
• ↑ CVP, ↑ RAP, ↑ PAOP • Serum sodium < 120 mEq/liter
• Anorexia, nausea/vomiting, diarrhea • ↓ BUN
• Dyspnea and pulmonary edema • ↓ Serum osmolality
• ↓ H+H
125 126
SIADH Treatment SIADH

• Correct fluid volume excess
– NO free water
– Fluid restriction • Swimming in water:
– Diuretics Low-Serum NA+
• Correct electrolyte imbalance
– Increase dietary sodium
– Hypertonic saline: for Na+ <125 or if
experiencing seizures
• Institute seizure precautions
127 128

32
Diabetic Ketoacidosis DKA
• Diabetes mellitus (DM): a group of metabolic – Insufficient insulin = hyperglycemia =
diseases characterized by hyperglycemia that osmotic diuresis = glycosuria,
results from defects in insulin secretion, insulin dehydration, and electrolyte imbalance
action or both – Breakdown of glycogen is activated and
• Diabetic ketoacidosis (DKA): hyperglycemic its synthesis inhibited = impaired glucose
crisis associated with metabolic acidosis and uptake by adipose tissue causes impaired
elevated serum ketones, the most serious triglyceride synthesis and liberation of
metabolic disturbance of type 1 DM free fatty acids into the blood
• Hyperosmolar hyperglycemic state (HHS): – Excessive free fatty acids enter the liver =
hyperglycemic crisis associated with the ketoacidosis
absence of ketone formation, most serious
metabolic disturbance type 2 DM
129 130
DKA DKA Presentation

• Undiagnosed type 1 DM • Serum glucose > 300-800
• Known type 1 DM • Na+ = K+ ↑ then ↓↓
– Illness, infection, omission of insulin, • Ketones ↑, BUN/creatinine ↑
trauma, surgery, noncompliance
• Serum osmolality > 295-330
• Nondiabetic: Cushing’s syndrome,
hyperthyroidism, pancreatitis, drugs • ABGs = metabolic acidosis
(steroids, thiazide diuretics, phenytoin • Increased white blood cells
[Dilantin]), pregnancy (WBCs)
131 132

33
DKA Presentation DKA Treatment
• Nausea/vomiting, abdominal pain, • ABCs, monitor
polyphagia, polydipsia, polyuria • Identify and treat cause:
• Weakness, fatigue, weight loss infection: cultures.
• Clinical indications of dehydration • Correct fluid volume deficit.
• Tachycardia, orthostatic hypotension • Correct sugar.
• Kussmaul breathing
• Lethargy progressing to coma
133 134
DKA Treatment DKA Treatment

• Normalize serum glucose • Normalize serum glucose.
– Regular insulin 0.1-0.15 – Infusion decreased when blood glucose
units/kg followed by infusion < 250 mg/dL
– Serum glucose should drop no more – Subcutaneous insulin by sliding scale
than 75-100 mg/dL per hour to avoid started before IV infusion discontinued
hypoglycemia, hypokalemia, cerebral • Replace potassium, phosphate, magnesium.
edema. • Correct acid-base imbalance: fluids
• Maintain safety.
135 136

34
Complications HHS
• Definition: hyperglycemic crisis
Cardiovascular Neurologic • Etiology: usually seen in patients over 50,
Hypovolemic Seizures, cerebral with glucose intolerance (insulin
shock edema, coma insensitivity): may follow:
Renal – Pancreatitis, burns, hepatitis, trauma,
Dysrhythmias
Acute renal failure ETOH, hypertonic nutrition, drugs (beta
Embolism (RF) blockers, thiazide, phenytoin, steroids)
Myocardial Electrolyte • Dehydration
infarction (MI) imbalance
Pulmonary edema
137 138
HHS Presentation Treatment ABCs

• Glucose > 600-2,000 • ABCs, monitor, identify cause: infection
• Low serum Na+ (BS) • Correct fluid volume deficit.
• Low K+ • Normalize serum glucose level.
• BUN/creatinine ↑
• Correct electrolyte imbalance.
• Safety
• Serum osmolality ≈ 330-450
• Monitor for complications:
• ABGs: normal pH; acidosis
–Hypovolemic shock, dysrhythmias,
(if present) is lactic acidosis. acute renal failure, thromboembolism,
myocardial infarction, pulmonary
embolism, cerebral edema
139 140

35
Hypoglycemia Adrenal Insufficiency
• Females > males Adrenal Function
• More common in the elderly • Stress response
• Sympathetic nervous system (SNS)
• ETOH, infection
• Insufficiency: complication of critical
• Signs and symptoms of acute hypoglycemia illness
• Treatment: replace Signs and Symptoms
141 142
The Thyroid Endocrine Pearls

• Function: master gland • SIADH = low-sodium levels
• Regulates all metabolism – Fluid restriction, 3% NS
• Hypo: depression, dyslipidemia,
• DI = neurological injury
dysmenorrhea
• Hyper: metabolism: Graves disease, – High-serum sodium
thyroid storm, hashitoxicosis – Dehydration
• Vasopressin = ADH = Pitressin
• HHS = severe dehydration
143 144

36
Endocrine Pearls *
• Normal serum osmolarity = 275-295 The “cardinal sign” of SIADH is:
• Acidosis causes shift of cellular K+ to serum.
A. hyponatremia
SIADH is clinically manifested by: B. urinary output of 10 liters/day
C. hypotension
A. hyperosmolar state D. systemic edema
B. low output state
C. myxedema state
D. water intoxication state
145 146
* GI Hemorrhage
Which of the following is characteristic of
diabetes insipidus? • Introduction
– Loss of new or old blood from GI tract
A. low urine osmolarity – Emesis or stool
B. serum osmolarity increased – 85% of all GI hemorrhages are upper GI
C. serum sodium elevated tract
D. all of the above – Shock leading to multisystem failure and
death
– Prevention: admitting orders, PUD
prophylaxis
147 148

37
Pathophysiology
Management
• Most common causes of upper • Ensure ABCs
GI hemorrhage: • Restore circulating blood volume and
– Peptic ulcers control bleeding: await GI services
– Esophageal or gastric varices – IV, Foley, crystalloids, colloids
– Gastritis – Blood transfusion
– Mallory-Weiss tear • NG tube: gastric lavage, prepare for
• Lower GI hemorrhage: procedures and/or OR or IR, H2 blockers
– Diverticular disease, tumors, ulcerative or PPI—IV, NPO status
colitis • Serial and daily labs: amylase and lipase
149 150
Treatment: ABCs Esophageal Varices
• Therapy for H. pylori • Definition: dilation of the submucosal

• Maintain fluid and electrolytes esophageal veins
• Nutritional concerns • Etiology: cirrhosis, portal vein thrombosis,
• Complications: hepatic venous outflow obstruction,
congenital hepatic fibrosis
– Aspiration pneumonitis, recurrent
bleeding, perforation, acute pancreatitis,
MI, DIC, sepsis, shock
– Ammonia levels
151 152

38
Esophageal Varices
• Management:
– ABCs, restore circulating blood volume
– Endoscopy: sclerotherapy, ligation or
banding
– Vasopressin, administer sandostatin
(Octreotide)
– Tips: transjugular intrahepatic
portosystemic shunt
– All other complications: electrolyte,
coagulation, liver failure, ETOH withdrawal,
renal failure (RF), pneumonia
153 154
Hepatic Failure Hepatic Failure: Etiology—Acute

• Definition: inability of liver to perform • Viruses Trauma
organ functions – Fulminant viral hepatitis Reye’s syndrome
• Hepatic encephalopathy: neurologic failure – Herpes simplex Acute fatty liver of
as a result of hepatic failure – CMV pregnancy
• Hepatotoxic drugs Acute hepatic vein
• Ischemia occlusion
155 156

39
Hepatic Failure: Chronic Portal Hypertension
• Chronic liver failure: • Esophageal varices

– Cirrhosis • Splenomegaly: thrombocytopenia, vitamin
K deficiency
– Wilson’s disease
• Inability to produce adequate bile
– Primary or metastatic tumor of the liver
• Impaired carbohydrate (CHO), fat, protein
metabolism (hypoglycemia)
• Inability to store vitamins and manufacture
clotting factors
157 158
Portal Hypertension Clinical Presentation
• Inability to detoxify toxins and drugs and • Fulminant hepatic failure

remove bacteria – Jaundice, tachycardia, hypotension, fluid
retention, ascites, ↓ urine output, spider nevi,
– Drug or toxin intoxication palmar erythema, bleeding, electrolyte
– Hepatic encephalopathy imbalance, asterixis, hyperventilation,
increased ICP, sepsis, portal hypertension
• Ammonia: protein metabolism
• Cirrhosis
• Convert ammonia to urea – Azotemia, bruising, bleeding, nutritional
abnormalities, fatigue, weight loss, impaired
bilirubin metabolism, respiratory alkalosis
159 160

40
Management
• Identify and treat cause of liver failure
– Avoid hepatotoxic drugs.
– Avoid ETOH.
– Monitor liver function tests.
• Airway, etc.
• Aspiration: safety
• Electrolytes: ↓K+, ↓Ca+
• Renal insufficiency
161 162
Complications Pancreatitis
• Malnutrition ARDS • Definition: acute inflammation of the

– Immunosuppression Peritonitis pancreas, forms include:
– Poor wound healing Sepsis – Interstitial: edematous pancreas,
hypovolemia
– Edema, ascites Hepatorenal syndrome
– Hemorrhagic: extensive necrosis of
• Hemorrhage Gradual loss of function.
Associated with cirrhosis
pancreas and peripancreatic tissue and
– Esophageal varices Oliguria and ↑ urine Na+ fat, erosion into blood vessels,
– Coagulopathy, DIC ATN hemorrhage, often SIRS
• Hypoglycemia Cerebral edema
– Acute vs. severe acute pancreatitis
• Electrolyte imbalance
(SAP)
163 164

41
Etiology Pathophysiology
• Alcoholism  Trauma, surgical • Etiologic factor triggers activation of pancreatic
• Obstruction of common bile  Radiation enzymes and pancreatic cell injury =
duct  Pregnancy autodigestion of pancreas = damage to acinar
– Cholelithiasis  Ovarian cyst cells = erosion into vessels = inflammatory
– Post ERCP  Hypercalcemia process = necrosis of fat and exudates with high
– Hypertriglyceridemia  Lupus albumin content = hypoalbuminemia and ascites
Thiazide  Infections • Hypocalcemia
– Lasix, estrogen  Ischemia, post-CPB
• Peptic ulcer w/perforation
• Release of necrotic toxins (cascade) may
 Idiopathic (20%) cause sepsis and SIRS.
165 166
Clinically Clinically
• Acutely ill, hyperthermic • ↓ Ca++, ↓ K+, hyperglycemia
• PAIN • Elevated serum amylase and lipase
• Nausea & vomiting, dyspepsia, flatulence,
• Elevated urine amylase
weight loss, weakness
• Look like AMI • Elevated liver function tests
– Tachycardia, fever, hypotension, jaundice, • CT, MRI = pancreatic swelling, edema or
Grey Turner’s sign, abdominal distention, necrosis
ascites, ↓ BS, steatorrhea, respiratory
findings
• Shock
167 168

42
Treatment: ABCs Prevent Complications
• Decrease release of and destruction by • Hypoglycemia DIC

pancreatic enzymes • Hypocalcemia Perforation
– Pain management • Pseudocysts Bleeding
– Nutritional care, TPN, lipids, • Pancreatic abscess ETOH withdrawal
electrolytes • Pancreatic fistula Immobilization
– Prevent infection, ETOH withdrawal • Hypovolemic shock SIRS
• ARDS
169 170
Intestinal Infarction Clinical Presentation

• Definition: necrosis of intestinal wall resulting • Clinical: anorexia, pallor, abdominal pain,
from ischemia severe cramping or nonspecific diffuse
• Etiology – Abdominal tenderness, urgent bowel
– Arteriosclerosis, vasculitis, mural thrombus, movements
emboli (atrial fibrillation [AF]), • Objective: tachycardia, hypotension, tachypnea,
hypercoagulability, surgical procedures (aorta fever, dehydration, vomiting (persistent and/or
clamp), vasopressors, strangulated intestinal bloody), abdominal guarding and rigidity
obstruction, intra-abdominal infection,
cirrhosis
171 172

43
Management Intra-Abdominal Hypertension
• Management: ABCs • Renal dysfunction
• Maintain adequate circulating volume • Respiratory compromise
– D/C vasopressors with bowel ischemia • Intra-abdominal pressure greater than
• Prevent and treat pain (morphine)
18 mm Hg
• Prevent perforation (bowel rest)
– NG tube, elevate head of bed (HOB)
• Prepare for surgical intervention
173 174
GI Infections C. difficile
• Diarrhea • Species of gram-positive bacteria

– Viral infections • Most serious cause of antibiotic-
– Parasites associated diarrhea and leads to
– Bacterial toxins pseudomembraneous colitis
– Consequence of critical illness • Diagnosis: more than 3 days of watery,
• Types: secretory, osmotic, motility, foul- smelling stool, with history of
inflammatory, dysentery antibiotic therapy and colitis
(abdominal pain)
175 176

44
Treatment Prevention
• When diagnosis is made, treatment • Proper antibiotic use

should be started ASAP. • Infection control measures
• Metronidazole (Flagyl) 500 mg 3X daily
• Oral vancomycin (Vancocin) 125 mg 4X
daily
• Both for 10-14 days
177 178
Remember: The Gut GI Surgery
• Nutritional support • Obstruction: fluid balance, most common

• Electrolytes cause is adhesions, hernias, tumors,
ulcers, infections, postop patient
– Most frequent indication for GI surgery
– X-ray, CT
– Treatment: fluids, lytes, nitroglycerin, prepare
OR
179 180

45
Perforation of the Esophagus
• Perforation: sudden onset abdominal pain, • Esophageal perforation is a challenge

very ill – Diagnostic and therapeutic due to the rarity of the
– Most common appendicitis, ruptured tic condition and the variability of the presentation
– Basic principles are applied to the management
– Presentation: hypovolemia, abd signs
of esophageal perforation
– Diagnosis: WBCs, lytes, X-ray, CT • Rapid diagnosis
– Treatment: surgical repair • Appropriate hemodynamic monitoring and support
• Antibiotic therapy
• Restoration of luminal integrity
• Control of extra-luminal contamination
181 182
Nursing Care
Postoperative Management
• Nutritional support: NPO for 7 days + Jejunal tube • NPO — nutrition
feedings started on POD 2 (unless ileus occurs).
• TPN is usually not started, unless the patient has • NGT
extreme nutrition deficit. • Chest-tube management
• Maintained on broad spectrum antibiotics for 7-10
days • Pulmonary care
• Contrast esophagram is obtained on POD 7 if the • Fluid status
patient is clinically stable. If there is no evidence of an
esophageal leak or postoperative ileus, the NGT is • Infection and antibiotics
removed and oral feeding may begin. • Post-operative care: lungs, kidneys, lungs,
• Drains remain in place until patients are tolerating oral
feedings and without clinical evidence of a leak.
nutrition, ambulation, DVT proph., PUD
proph.
183 184

46
GI Pearls GI Pearls
• Arterial perfusion of small intestine • Cullen’s sign: ecchymosis around

– Superior mesenteric artery umbilicus in hemorrhagic pancreatitis
• Complications of pancreatitis = bilateral • Kehr’s sign: splenic rupture = left shoulder
rales, atelectasis of left base, pleural pain due to diaphragmatic irritation.
effusion and ARDS, HHS, low Ca+ • GI assessment: inspection, auscultation,
palpation, labs
185 186
Question Question
The administration of vasopressin should be The inability of the liver to conjugate what
most carefully monitored in patients who substance is a primary contributor to hepatic
have: coma?
A. diabetes insipidus A. ammonia

B. CAD B. urea
C. hypotension secondary to GI bleed C. fatty acids
D. DM D. bilirubin
187 188

47
Question Question
Cimetidine, or rantidine, acts to reduce Which of the following laboratory findings is

stress ulcers by inhibiting the production of MOST specific for pancreatitis?
which substances?
A. leukocytosis
A. histamine B. elevated serum and urine amylase
B. gastrin C. hyperglycemia and hypokalemia
C. acetylcholine D. decreased serum albumin and total
D. calcium protein
189 190
Cerebral Metabolism
Courage: • Oxygen requirements

Cartwheeling past our comfort zones – 2% of body weight, 20% of cardiac output
– Cerebral cortex most sensitive to O2 delivery
and trying something a little bit scary
– Anoxia caused cerebral edema + neuron death.
every day.
• Nutrient
To stretch … – High metabolic rate, glucose (ATP)
– Brain does not require insulin to use glucose.
– ↓ BS, ↑ BS (dehydration)
191 192

48
Cerebral Perfusion Pressure (CPP)
• CPP = mean arterial pressure (MAP) -

mean intracranial pressure (ICP)
– Changes in MAP or ICP affect CPP.
– Normal MAP 70-105 mm Hg
– Normal ICP 5 - 15 mm Hg
– Normal CPP 60 - 100 mm Hg
Intracranial HTN:
Monro-Kellie Doctrine
193 194
CPP Assessment
Increase Cerebral Decreased Cerebral

Blood Flow Blood Flow
• Neuro exam
 Hypercapnia  Hypocapnia –Mental status
 Hypoxemia  Hyperoxemia –Motor function
 Blood viscosity  Blood viscosity –Sensory function
 Hyperthermia  Hypothermia –Cranial nerves
 Drugs: vasodilators  Drugs: anesthetics, –Deep tendon reflexes
 barbiturates
195 196

49
Additional Assessment Additional Assessment
– Blood pressure (BP) and heart rate (HR) • Temperature

– Respiratory rate (RR) and rhythm • Central fever: injury to hypothalamus
• Bradypnea: central nervous system
(CNS) depression
– Does not respond to antipyretics
• Cheyne-Stokes: cerebral • Peripheral fever
hemisphere – Caused by infection
• Hyperventilation: lower midbrain or
upper pons – Does respond to antipyretics
• Apneustic: mid to lower pons
• Ataxic: medulla
197 198
Clinical Picture
Nursing Care
ABCs Infection
Aspiration Complications of
ICP/CPP/MAP bed rest
Volume status DVT/PE
Nutrition Rehab potential
Bowel and bladder Function
Psychosocial
199 200

50
Primary Types of Brain Injury Closed Head Injury
• Trauma: concussion, contusion, sheer injury • Etiology: blunt trauma, cell injury
• Ischemia: global, regional • Pathophysiology:
• Inflammatory/infection: meningitis: viral vs. – Focal injury: contusion
bacterial • Partial or complete dysfunction for
– Glucose levels of cerebrospinal fluid less than 24 hours, bruising, petechial
(CSF) hemorrhages, possible laceration,
• Compression tumor, edema, hematoma possible areas of infarction and
• Metabolic: encephalopathies: anoxic, necrosis = edema, intracranial
hypoxic-ischemic, metabolic, infectious hypertension
201 202
Closed Head Injury Closed Head Injury
• Concussion: transient state of partial or • Diffuse injury: loss of consciousness > 24

complete paralysis of cerebral functioning hours, axonal disruption
with complete recovery within 12 hours, – Amnesia, residual deficits in memory
headache • Diffuse axonal injury: severe mechanical
– Mild: no loss of consciousness (LOC) or disruption of axons and neuronal
memory loss pathways in both cerebral hemispheres,
diencephalon and brain stem
– Classic: LOC or memory loss
203 204

51
Management Brain Death
ABCs Maintain CPP > 70 • Cardinal finding in brain death

Assess for additional Prepare for OR or – Coma or unresponsiveness
injuries IR – Absence of cerebral motor responses to
Prevent/detect Institute seizure pain in all extremities
intracranial HTN and precautions – Absence of brain-stem reflexes
secondary brain – Apnea
injury
205 206
Brain Death
• Cerebral angiography: no intracerebral filling at

level of carotid bifurcation
• EEG: no electrical activity during a period of at
least 30 minutes
• Transcranial doppler: no diastolic or
reverberating flow
• Somatosensory and brain-stem auditory evoked
potentials
• Technetium Tc 99m brain scan: no uptake
207 208

52
Intracranial Hematomas
• Subdural hematoma (SDH):

– Spontaneously, older, ETOH
– Usually venous bleed, accumulated
below dura mater, classification
• Acute SDH: clinical indications
occur within 24 hours
• Subacute: within 2 weeks
• Chronic: weeks to months
209 210
Intracranial Hematomas Stroke: Ischemic
• Epidural Hematoma (EDH): BRAIN ATTACK

– Linear skull fracture, usually arterial bleeding
associated with tearing of arteries,
accumulates above the dura mater
• Sudden, severe disruption of cerebral
– History of precipitating event, history of short
circulation with a subsequent loss of
period of unconsciousness followed by lucid neurologic function caused by
interval and then rapid deterioration, thrombus or embolus
headache and increasing irritability
211 212

53
Stroke: Ischemic Risk Factors
• Etiology: atrial fibrillation (AF), • Family history • Substance abuse

atherosclerosis, HTN, • Hypertension • Oral contraceptives
hypercoagulability • Smoking • Dysrhythmias
• Clinical: sudden onset • Hyperlipidema • Hypercoagulability
• Diagnosis: CT, MRI, cerebral • Obesity • Sedentary lifestyle
angiogram
213 214
Management Stroke: Hemorrhagic
• VOMIT • Definition: neurologic deficit caused by

• ABCs, oxygenation and blood sugar interruption of blood flow to the brain
caused by vessel rupture
• Essential care: timing of symptoms • ICH: trauma, HTN, tumor, thrombolytic,
• Identify type: ischemic or hemorrhagic anticoagulants, bleeding disorders
– CT scan • Subarachnoid hemorrhage (SAH):
• Time of onset of symptoms, blood sugar hemorrhage into the subarachnoid
and pulse oxygenation space
• Aneurysms, AV malformations
215 216

54
Subarachnoid Treatment
• WHERE: intracranial blood into the CSF-filled Maintain airway, ventilation, oxygenation,
space between the arachnoid and pia mater VOMIT.
membranes on the surface of the brain and Prevent/monitor clinical indications of
basal cisterns, bleeding into ventricular system intracranial hypertension.
Prevent/monitor for delayed ischemia
• Most frequent cause of SAH: aneurysm following SAH.
formation with leak, HTN
Identify vasospasm by worsening of
– Severe trauma neurologic status: occurs anytime from
– Symptoms: result of irritation of blood in brain 3-21 days.
tissue
217 218
Treatment: Vasospasm Procedures
• Administer calcium channel blockers. • Aneurysm

• Triple H therapy: hypertension, – Surgical: clipping, wrapping, ligation
hypervolemia, hemodilution – Endovascular: coiling (embolization coils),
intravascular balloon placement
• Minimize potential for rebleed and
• Arteriovenous malformation
to promote stability.
– Surgical excision, embolization
• Fluid stent
• Intracranial hemorrhage
– Surgical removal of clot
• Monitor: problems post
219 220

55
Overall Stroke Care, Overall Stroke Care,
Goals of Treatment Goals of Treatment
• Minimize damage and maximize recovery. • Cardiovascular function
• Essential initial care – Dysrhythmias, acute myocardial infarction (MI),
• Stabilize patient airway and breathing. 20% of stroke patients have change in CPK-MB
– Monitor breathing patterns, swallowing, – Hypotension and ↓ cardiac output
aspiration, intubate. • Elevated ICP, pulmonary hygiene
• Optimization of cardiovascular function: • Seizures, hyperglycemia, nutrition, bowel function,
– BP management: < 185/110, labetalol or DVT, pressure sores, fever (33%), depression
calcium channel blocker
221 222
Poststroke: First 24 Hours Status Epilepticus
• Care of the ABCs • Definition: sudden, paroxysmal episode of

• Swallow evaluation exaggerated activity
• Assessment of aspiration
• Pneumonia • Etiology: withdrawal, toxic levels of drugs,
• Urinary retention CNS infection, stroke, brain tumors,
cerebral edema, metabolic disorders
223 224

56
Treatment Neuromuscular Disorders
• Airway and ventilation • Respiratory compromise
• Assess causes or contributing factors. • Muscular dystrophy
• Protect patient from injury.
• Guillain-Barré syndrome
• Stop seizure activity.
• Myasthenia
• Monitor and prevent complications.
• Monitor and document duration of seizure
activity.
• Fluid and electrolytes
225 226
Neuro Pearls Neuro Pearls
• Multisystem effects of ICP • Temperature = hypothalamus

1. Airway issues: pulmonary compromise • NO hypotonic solutions in patient with ↑
2. ECG abnormalities: hemodynamic ICP
3. GI bleeding • Aminocaproic acid (Amicar) prevents a
4. Effects of bed rest rebleed, acts as an antifibrinolytic agent.
227 228

57
Question Question
The patient suddenly becomes unresponsive as you are
speaking to him, and he develops trembling of all extremities.
Your priority is:
The most common cause of SAH is:
A. Notify MD. A. aneurysms

B. Administer diazepam IV. B. coagulopathies
C. Establish an airway. C. trauma from falls
D. Perform a rapid neuro check.
D. ischemia
229 230
Question Question
In a patient with increased intracranial The single most important index of the
pressure (ICP), cerebral perfusion pressure neurologic state is the:
(CPP) should be maintained at:
A. level of consciousness (LOC)
A. 40 mm Hg B. pupillary reaction
B. 50 mm Hg C. extremity movement
C. 60 mm Hg D. vital signs
D. 70 mm Hg
231 232

58
Question Question
A patient is admitted to the ICU after sustaining a knife Which of the following is a necessary
wound to the back. Assessment findings include loss of pain
and temperature on the right side and loss of motor function
immediate assessment for an injury of C3-
on the left. Vital signs are stable, and he is alert and C4?
oriented. No other injuries are noted. Based on the
preceding information, which type of neurologic syndrome is
likely to be developing? A. motor ability
A. Central cord B. heart rate (HR)
B. Brown-Séquard C. temperature
C. Anterior cord
D. ventilation
D. Horner
233 234
Question Behavioral/Psychosocial
Which vital sign changes (due to loss of • Antisocial behavior, aggression, violence
sympathetic nervous stimulation) would • Pain, agitation, delirium (PAD)
occur after a spinal cord lesion about T5? • Delirium and dementia
• Medical nonadherence
A. bradycardia and hypotension • Substance abuse
• Suicidal or risk-taking behaviors
B. bradycardia and hypertension
• Post-traumatic stress disorder (PTSD)
C. tachycardia and hypotension
D. hypertension and bradycardia
235 236

59
PAD Agitation
• Pain • Identify agitation in the ICU patient

• Agitation • Scales:
• Delirium o Richmond Agitation-Sedation Scale (RASS)
o Sedation-Agitation Scale (SAS)
• Scales for assessment
• Excessive restlessness, nonpurposeful mental
• Treatment: Identify risk factors, environmental risk factors, and physical activity due to tension and
“ICU psychosis.” anxiety. No clear universally accepted
• Daily activities: ABCDEF guidelines for those intubated on definition. Continual movement, pulling at
mechanical ventilation
dressings, disoriented and does not follow
commands
237 238
Delirium Delirium
• What is delirium? • Imbalance of neurotransmitters

– Acute onset of mental status changes • Who is at risk? Anyone
• Facts:
– And inattention
– 66%-90% of ICU patients
– And/or disorganized thinking/altered
– Onset ICU Day 2
level of consciousness (LOC)
– How long? 4 days
– 10% remain delirious at the time of discharge
• Overall 7 out of 10 patients will have delirium.
239 240

60
Delirium Treatment
• Associated with: • Identify the etiology: assessments

– Increased length of stay • Modify risk factors.
– Increased time of ventilator • Haldol: 2-10 mg IV every 20-30 minutes,
– Higher costs then 25% of loading dose every 6 hours
– Increased mortality • Effects on heart: prolonged QT interval
– 3-fold increase risk of death at 6
months
241 242
Treatment Dementia
• Develop a protocol. • Loss of mental functions, such as

• Assess and perform rapid treatment. thinking, memory and/or reasoning
• Look at current medications. • Not a disease: group of symptoms
• Do not oversedate. – Substance abuse, severe depression,
• Use aspiration precautions. medications, stroke, vitamin B12
deficiency, AIDS-associated dementia
• Alzheimer’s: most common cause of
dementia
243 244

61
Depression: A Complex Matter Treatment of Depression
• Depressive disorder: a syndrome that • SSRIs: medications that increase amount

reflects a sad and/or irritable mood of neurochemical serotonin in brain
• Negative thoughts, moods and behaviors • Fewer side effects than tricyclic
antidepressant and MAOIs
• First-line drug of treatment
• Paroxetine (Paxil), sertraline (Zoloft),
citalopram (Celexa), fluvoxamine (Luvox)
and escitalopram (Lexapro)
245 246
Treatment of Depression Depression
• Dual-acting antidepressants • Afflicts 1 in 6 Americans

• More severe depression • Life-time incidence
• Act on both the serotonin and norepinephrine systems – 20% women
• Venlafaxine (Effexor), duloxetine (Cymbalta) – 12% men
• More common in people with medical
illness
247 248

62
Substance Abuse Suicide
• ETOH • “Are you thinking of killing yourself?”

• Drugs • “Do you have a plan?”
• Withdrawal: stages • “Do you have a gun?”
• Benzodiazepines • “When are you going to do this?”
• Needs help
• Suicide prevention: nursing interventions
249 250
PTSD PTSD
• PTSD is a mental health condition that is • Prevention

triggered by a terrifying event, either – Support systems
experiencing it or witnessing it. Symptoms – Ability to discuss the event(s)
may include flashbacks, nightmares and
– Do not self-medicate.
severe anxiety, uncontrollable thoughts
about the event. – Hospital post-ICU conferences, roundtable
discussions, support group
• Treatment: main is psychotherapy, may
include medications: antidepressants,
antianxiety medications, prazosin
251 252

63
• Nonadherence to medical/surgical advice,
treatments, mainly medications, diet and
exercise
253 254
Renal Renal Blood Flow
• Regulation of homeostasis • Kidneys receive 20%-25% of cardiac output

• Extracellular volume and osmolality • Autoregulation: maintains constant in
• Electrolytes glomerular filtration rate (GFR)
• Excretion of metabolic wastes
• Mean arterial pressure (MAP) 80-180 mm Hg
• Regulation of acid-base balance
prevents changes in GFR
• Production and release of hormones – Afferent arteriole’s ability to dilate or constrict
• Aldosterone and ADH
• Filtration ceases if MAP is 40 to 60 mm Hg.
• Erythropoietin
• Bone mineralization
255 256

64
Renal Assessment Pathophysiology
• Weight and fluid changes • Hypovolemia:

• Serum osmolality: 275-295 mOm/liter – Tachycardia, orthostatic hypotension, ↓ CVP,
• BUN:creatinine ratio: 10:1 RAP, PCWP, CO/CI, > SVR, flat jugular
– If BUN is elevated disproportionate to creatinine: veins, weakness, lethargy, anorexia, poor
• Dehydration (prerenal) skin turgor, thirst, low-grade fever, syncope,
• Catabolism oliguria, >> BUN with normal creatinine, >>
• Blood in gut
H+H, > serum osmolality
257 258
Management Pathophysiology
• Hypervolemia
– Excessive fluid intake
• Monitor intake + output, weight.
– Retention of Na+ and water
• Replace fluid with similar fluids. • Steroid therapy, heart failure (HF), liver failure,
stress response, nephrotic syndrome, acute or
• Provide frequent oral and skin care. chronic renal failure (RF)
• Tachycardia, ↑ BP, ↑ CVP, RAP, ↑ PWCP, weight
gain, JVD, tachypnea, dyspnea, lethargy, apathy,
disorientation, indications of pulmonary or cerebral
edema, ↓ serum osmolality, ↓ BUN, ↓ H+H
259 260

65
Treatment Acute Renal Failure (ARF)
• Monitor I+O, daily weight, labs
– Decrease excess volume • Definition: any sudden severe impairment or
• Restrict fluid intake and Na+ intake cessation of kidney function: characterized by
• Administer diuretics accumulation of nitrogenous wastes and fluid
• Hemodialysis and electrolyte imbalances:
– Prevent complications: skin and mouth • Prerenal: disrupted blood flow to the kidney
care – Low intravascular volume, ↓ CO, vasodilation,
renovascular disease: most common in floor patient
261 262
ARF ARF
–Cortical: intrarenal damage to renal • Medullary: acute tubular necrosis (ATN)

tissue – Nephrotoxic drugs, prolonged ischemic injury, any
causes of prerenal failure that is prolonged:
• Glomerulonephritis, vasculitis, interstitial prolonged ischemia destroys tubular basement
nephritis (renal capillary swelling) membrane: most common in ICU patient
• Postrenal: obstruction to urine outflow
– Mechanical obstruction, functional obstruction:
neurogenic bladder, diabetic neuropathy
263 264

66
Stages of ARF
• Onset: period from the precipitating event to

beginning of oliguria or anuria
• Duration: hours to days
• BUN/creatinine: normal or slightly
decreased
• Mortality: 5%
265 266
Stages of ARF Stages of ARF
• Oliguric-anuric: when urine output is less than 400 • Diuretic: urine output is > 400 mL/24 h until
mL in 24 hours
• Duration: 1-2 weeks
lab values stabilize
• BUN/creatinine: increases • Duration: 1-2 weeks
• Mortality: 50%-60% • Urine output: may be > 3 L/24 h
• Other: metabolic acidosis, water gain with dilutional • Mortality: 25%
hyponatremia, hyperkalemia, hyperphosphatemia,
hypocalcemia, hypermagnesemia, azotemia • Other: metabolic acidosis, Na+ may be
normal or low, high K+ continues
267 268

67
Stages of ARF Treatment
• Recovery: period between when the lab • Support renal perfusion and improve
values stabilize until they are normal GFR
• Duration: 3-12 months – Volume
• BUN/creatinine: back to 100% normal – Inotropes (dopamine), vasopressors
– Administer diuretic challenge
• Mortality: 10%-15%
• Maintain fluid, electrolyte and acid-base
• Other: uremia, acid-base imbalances, and
electrolyte imbalances gradually resolve balanced
– Na+, K+, phosphorus, magnesium
• Diminish accumulation of nitrogenous
wastes
– Protein restriction dialysis
269 270
Treatment Management: Complications
• RF increases mortality overall.

• Prevent further damage to kidney
• Renal: chronic RF in 25-30% of acute RF
– Eliminate nephrotoxic agents
• Cardiovascular: dysrhythmias,
• Monitor peak and trough levels of drugs hypertension, pericarditis, pulmonary
– Nutrition edema, HF
– Prevent infection • Neurologic: coma, seizures
– Monitor and treat anemia (Epogen). • Metabolic: electrolyte imbalance
• GI: peptic ulcer disease, hemorrhage,
anorexia, nausea & vomiting, abdominal
distention, pancreatitis, ileus
271 272

68
Management: Complications Renal Replacement Therapies
• Hematologic: anemia, uremic • Dialysis

coagulopathies, ↑ WBC, platelet dysfunction – Semipermeable membrane; blood/dialysate
– Principles
• Infection: pneumonia, immunosuppressed
• Types
• Pulmonary: pulmonary edema,
– Peritoneal
hyperventilation, acid-base imbalance
– Hemodialysis
• Nutrition – Continuous renal replacement therapy (CRRT)
273 274
ARF Question
Prerenal ATN Mr. J., 24, boxes on the weekends. He has

Urine Na+ < 20 > 40-100 sustained blunt trauma to the left kidney
BUN: Creatinine >20:1 10:1 during a boxing match. Which of the
Furosemide (Lasix) No urine following indicates renal trauma?
or fluids + urine A. severe flank pain and diaphoresis
B. hematuria and flank tenderness
C. urethral bleeding
D. side pain and hemoptysis
275 276

69
Question Question
A patient with chronic RF asks why he is The primary etiology of hyperphosphatemia

anemic. The nurse explains that this is due is:
to: A. over-replacement
A. blood loss via the urine B. hypercalcemia
B. renal insensitivity to vitamin A C. RF
C. inadequate production of D. hypoalbuminemia
erythropoietin
D. inadequate retention of serum iron
277 278
Question Question
Bradycardia, tremors and twitching muscles Hyponatremia is usually associated with:

are associated with which electrolyte A. fluid overload
disorder? B. dehydration
A. hypokalemia C. diuresis
B. hyperkalemia D. overadministration of normal saline
C. hypophosphatemia
D. hyperphosphatemia
279 280

70
Renal Pearls
• Know the electrolytes!!!!!

• Know the electrolytes for all systems!!!
281 282
The Lungs
• Oxygenation + ventilation
• Brain: neural control, pH cerebrospinal fluid
(CSF), peripheral control
• Bellows
• Alveolar/capillary bed
283 284

71
Ventilation/Perfusion (V/Q) Goal
• To have V/Q match

• Recruitment: IS and PEEP
– Volume status
– Good right ventricular (RV) function
– Pulmonary artery pressures
285 286
Pulmonary Assessment: VOMIT
• Respiratory rate (RR) and rhythm

• Oxygen saturations
• Tracheal deviation
• Breath sounds
287 288

72
Tracheal Deviation Assessment: VOMIT
• Pulmonary exam
• Arterial blood gas (ABG)
• Chest X-ray
289 290
ABG CO2 Monitoring
• pH 7.55 7.21 • Capnography

• CO2 28 28 – Used to measure
• O2 88 97 CO2 levels while
• Bicarb 24 14 patients are under
anesthesia: to
monitor any patient
with respiratory
concerns
291 292

73
Pulmonary Hypertension Primary Pulmonary Arterial Hypertension
• Primary: rare lung disorder, pressure in the lung • Symptoms

circulation is high for no apparent reason. – Fatigue or tiredness, dizziness, swelling of
– Mean PAP greater than 25 mm Hg at rest and 30 mm Hg ankles, advanced to severe pulmonary failure
during exercise • Treatment: cath, response to oxygen
– Causes: Raynaud’s, appetite suppressants, cocaine and – Calcium channel blockers
HIV
– IV prostacyclin, endothelin receptor
antagonists: bosentan (Tracleer)
– Transplantation
293 294
Secondary Pulmonary Arterial Hypertension Lung Abnormalities
• Other reasons for pulmonary pressure RESTRICTIVE OBSTRUCTIVE

increases • Atelectasis • Asthma
• Pneumonia • Chronic bronchitis
• Pulmonary emboli, heart failure (HF), • Pneumothorax • Emphysema
obstructive sleep apnea, any condition that • Pulmonary edema
causes hypoxemia, HIV infection, lung • Pulmonary fibrosis
disease, valve disease • Acute respiratory
• Treatment: underlying disease distress syndrome
(ARDS)
• Obesity
295 296

74
Acute Respiratory Failure (ARF) Hypoxemia
• Pulmonary system is no longer able to meet • V/Q mismatch primary cause

the metabolic demands of the body. • Shunt effect
– Hypoxemic: PaO2 < 50 torr – Blood is not oxygenated as it travels through
– Hypercapnic: PaCO2 > 50 torr the lungs.
• Acute or chronic – Treatment: removing the obstruction,
reopening (recruiting) atelectatic zones,
preventing closure (derecruitment) of affected
lung units
297 298
Assessment ARF
• Clinical indications of hypoxemia/hypoxia • Hypercapnia

– Tachycardia = dysrhythmias – Abnormality of alveolar minute ventilation
– Tachypnea – Tidal volume (Vt)
– Dyspnea – Dead space (DS)
– Restlessness-confusion-lethargy-coma – Frequency (f)
– Accessory muscle use
– Cyanosis
299 300

75
ARF Assessment
• Hypercapnic respiratory failure, patient has: • Clinical indications of hypercapnia

– Central (depressed respiratory drive) – Tachycardia = dysrhythmias
– Neuromuscular – Bradypnea
– Abnormalities of the chest wall (restrictive) – Irritability, confusion
– Abnormalities of gas flow in airways – Inability to concentrate, somnolence, coma
(obstructive)
– Hypotension
– Increased dead space (Air sees no blood.)
– Facial rubor, headache
– Increased CO2 production
301 302
Assessment of ARF Management
• Altered mental status: agitation, • Oxygen supplementation

somnolence • Tracheal intubation and mechanical ventilation
(MV)
• Increased work of breathing: nasal flaring, • Pharmacologic adjuncts
tachypnea, dyssynchronous breathing – Beta2 agonists, anticholinergic agents
• Cyanosis – Corticosteroids, antibiotics
• Diaphoresis, tachycardia, hypertension,

signs of stress-catecholamine release
303 304

76
Review O2 Indications for MV
• Airways • Numerous indications for ETT and MV

– 1. Cannula: <40% – 1. Clinical or laboratory signs that the
– 2. Simple mask: 40%-60% patient cannot maintain an airway or
– 3. Partial rebreather mask: 60%-80% – 2. Adequate oxygenation or ventilation
– 4. Nonrebreather mask: 80%-100% • RR greater than 30 breaths/minute
• Maintain arterial O2 saturation > 90% with FiO2 >
– 5. Noninvasive positive-pressure 60%
ventilation • Increased CO2 > 50 mm Hg with pH < 7.25
305 306
MV MV
• Indications • Prove beneficial

– Acute ventilatory failure (AVF) with – Decrease systemic or MVO2
acidosis – Permit sedation
– Hypoxemia despite adequate O2 therapy – Reduce intracranial pressure (ICP)
– CO2 retention – Prevent atelectasis
– Apnea – Secure airway
307 308

77
MV Goal
• Types of ventilators • Most important goals of MV are:

– Positive pressure – Reduction in work of breathing
• Inspiration created by positive pressure – Assurance of patient comfort
• Expiration passive – Synchrony with ventilator
• Classifications: pressure-cycled, volume-cycled – Adequacy of ventilation and oxygenation
– Airway protection
309 310
MV Strategies: Lung-Protective Ventilation Improve Oxygenation
• Lung-protective ventilation • PEEP: Physiologic 5 cm

– Protect the lung: low Vt • Actions: improves the PaO2 without
increasing FiO2, ↓ surface tension, ↓
– Recruit the lung: PEEP intrapulmonary shunt
– Perfuse the lung: RV is filled and • Uses: ARDS, ARF
contracting. • Adverse effects: hemodynamic changes,
barotrauma, ↑ ICP
• Contraindications: untreated hypovolemia,
hypovolemic-neurogenic-anaphylactic or
septic shock
311 312

78
Removal CO2 Guidelines
• Alveolar ventilation 1. Ventilator mode: goals

• Frequency 2. Initial FiO2 = 100%, then wean to keep
sats > preset %
• Tidal volume
3. Initial Vt 5-10 mL/kg: ARF may require
• Dead space more to satisfy air hunger, ARDS less
4. RR = target pH and PaCO2
5. Add PEEP: diffuse lung injury and reduce
FiO2
313 314
Assessment of MV Patient Assessment of MV Patient
• Physical assessment: chest excursion, • System review

breath sounds, type of airway, ventilatory • Cardiovascular
mechanics – Heart rate (HR), rhythm, heart sounds,
• Pulse oximetry, ETCO2, ABG, CXR blood pressure (BP), hemodynamic
response
• Neurologic, renal, metabolic, GI (bowel
sounds, abdominal distention), nutritional,
immunologic, psychological
315 316

79
Complications ABCDE Bundle Components
• ↓ cardiac output • Aspiration

(CO) • GI effects
• Fluid retention • Infection
• Baro-biotrauma • Asynchrony
• Atelectasis • Anxiety
• Hypercapnia-hypo • Inability to wean
• Oxygen toxicity
317 318
New ABCDEF Bundle ARDS
A = Assess, prevent, and manage pain • Definition: syndrome of ARF

B = Both SAT and SBT
characterized by noncardiac
C = Choice of analgesia and sedation
D = Delerium: assess, prevent and manage pulmonary edema and manifested by
E = Early mobility and exercise refractory hypoxemia caused by
F = Family engagement and empowerment intrapulmonary shunt
319 320

80
ARDS Clinical Presentation
• Severe oxygenation defect

• Chest X-ray: diffuse bilateral infiltrates:
ground glass appearance
• Static compliance: stiff lung
• PCWP: < 18 mm Hg
• ↑ PAP
• ABGs: refractory hypoxemia
• Lung volumes are ↓ Vt, FVC
321 322
Treatment: Restore Oxygenation
• Improve delivery and reduce consumption

• With MV
– Low Vt
– High PEEP
• Decrease intra-alveolar fluid
– CPAP/PEEP, diuretics
– Avoid overhydration.
323 324

81
Treatment Pneumonia
• Hemodynamic monitoring • Definition: acute infection of the lung

• Inotropes as indicated by cardiac input parenchyma, including alveolar spaces
(CI) and interstitial tissue
• Decrease oxygen consumption and • Etiology
increase supply
• Predisposing factors
• Decrease pulmonary hypertension
• General support
325 326
Pneumonia Treatment
• Diagnostic • Prevention
– Fever • Maintain airway and ventilation
– WBCs – Positioning
– Sputum – Organism-specific antibiotics
– Chest X-ray
– Hydration
– Increased RR
– Bronchial hygiene
– Bronchoscopy
– Intubation
327 328

82
Complications Aspiration Pneumonia
• Monitor • Definition: lung injury related to the

– ARF inhalation of stomach contents, saliva,
– Pleural effusion food or other foreign material into the
– Empyema tracheobronchial tree
– Lung abscess • Pathophysiology: Oropharyngeal
secretions are most common.
– Septic shock
329 330
Risk Factors Status Asthmaticus
Altered consciousness and/or gag reflex • Definition: a recurrent, reversible airway

– Anesthesia, CNS disorder, altered disease characterized by increased airway
anatomy, GI conditions (hiatal hernia, responsiveness to a variety of stimuli that
vomiting), prolonged intubation, AO produce airway narrowing
surgery • Status asthmaticus: exacerbation of acute
– Enteral nutritional support asthma not relieved after 24 hours of
• NG tube maximal therapy
• Position
• Residual content
331 332

83
Management Pulmonary Embolism
• ABCs • Definition: obstruction of blood flow to one

• Maintain airway and ventilation. or more arteries of the lung by a thrombus
lodged in a pulmonary vessel: fat, air,
• Bronchodilators (short-acting) amniotic fluid, tumor, foreign body
• Anticholinergic • Etiology: hypercoagulability, alteration
• Mechanical ventilation in vessel wall, venous stasis
• Steroids – Fat emboli: osteomyelitis, sickle-cell
anemia, multiple long-bone fractures,
burns
333 334
Clinical Presentation Hemodynamics
• Most common symptoms • ↑ CVP + RAP

– Dyspnea: 73% • ↑ PAP with normal PCWP
– Pleuritic pain: 66% • ↑ PVR
– Cough: 37%
• ↓ CO/CI in massive PE
• Most common signs
• Hypoxemia (??)
– Tachycardia: 70%
– Rales: 51%
335 336

84
ECG Diagnostics
• Dysrhythmias: tachycardia, atrial fibrillation • ABGs

(AF) • Chest X-ray
• Blocks • ECG
• Tall, peaked P waves (P pulmonale) • Echo
• New bundle branch block • V/Q scan
• Right axis deviation • CT scan with PE protocol
• RV strain pattern • Pulmonary angiography
337 338
Treatment Complications
• Prevention • Pulmonary infarction • Pulmonary abscess

• Maintain airway and ventilation • Cerebral infarction • Acute respiratory
• Arrest thrombus: baseline clotting profile, • Myocardial infarction failure (ARF)
fibrinolytic therapy (MI) • Disseminated
• Heparin therapy • RV failure intravascular
• Oral anticoagulants: warfarin (Coumadin) 3-6 • Hepatic congestion coagulation (DIC)
months • Pneumonia • Shock
• Pulmonary embolectomy • Empyema • Bleeding secondary
• Surgical interruption of inferior vena cava: filter to therapy
339 340

85
341 342
Tension Pneumothorax Traumatic Pneumothorax
343 344

86
Thoracic Surgery
• Pulmonary care
• Aging population
• Risk factors: Identify high-risk patients
345 346
347 348

87
349 350
Indications for Surgery Postoperative
• Cardiac • Hyperinflation • Chest-tube

• Vascular • Atelectasis Management
• Esophageal • Mobilization of • Cardiovascular
• Tumors/infections secretions • Parameters
• Resection: rib/chest wall • Early ambulation – Pulse oximetry
• Cough – ABG/CXR/labs
• Pain – Chest tubes
351 352

88
Strategies: Nursing Care Strategies: Nursing Care
• Pulmonary assessment • Lung compliance

– Oxygenation – Cough
– Ventilation – IS
– Chest tubes – Suction
• Hemodynamic response – Bronchodilators
– AF – Position
– Volume status: renal function
353 354
Pulmonary Pearls Pearls
• Asthma: ominous signs = absence of • IV magnesium

wheezing, ↑ CO2 – Acts as bronchodilator
• ↓ CO2 and ↓ O2 with ARDS does not – Decrease inflammation
improve with oxygen therapy due to – 2 gm IV
shunting, treatment = PEEP, ↓ Vt, fluid – Effective with respiratory failure (RF)
restriction
• Oxygenate and ventilate
355 356

89
Question Question
The hallmark of ARDS is: The most common ECG changes that occur
A. refractory hypercapnia during pulmonary embolus are:
B. refractory hypoxemia A. Q waves in aVR and Lead I
C. low functional residual capacity B. tachycardia and AF
D. increased compliance C. bradycardia and ST-segment depression
D. high-degree AV blocks
357 358
Question Question
The principal contributing factors to venous Which of the features of pleural drainage
thrombosis include all of the following system indicates an active pleural leak?
except: A. bubbling in the water-seal chamber
A. AF B bubbling in the suction-control chamber
B. stasis of blood flow
C. fluctuation of water level in the water-seal
C. endothelial injury or vessel wall
chamber with respiration
abnormality
D. hypercoagulability D. no fluctuation of water level in the water-
seal chamber with respiration
359 360

90
Question Question
Which type of condition can lead to a • You are helping another nurse to move a patient
up in bed when the low-pressure alarm on the
tension pneumothorax? ventilator goes off. It also indicates a low tidal
A. closed pneumothorax volume. The patient is becoming short of breath,
and his SpO2 has dropped from 0.95 to 0.84.
B. open pneumothorax The PETCO2 waveform is absent. The
C. subcutaneous emphysema endotracheal tube appears to be in place, and
there is no obvious disconnection from the
D. pneumomediastinum ventilator. The other nurse goes to call the
respiratory therapist. What should you do?
361 362
Question Question
A. Increase the Vt on the ventilator while The major signs and symptoms of ARF include:
instructing the patient to remain calm. A. increased RR, tachycardia, change in mental
B. Increase the FiO2 on the ventilator while status
instructing the patient to remain calm.
B. no change in RR, tachycardia
C. Remove the ventilator and begin manual
respiration (ambu). C. The major sign is the complaint of shortness
D. Increase the ventilator RR and peak flow. of breath (SOB).
D. There are no early signs of respiratory
failure.
363 364

91
• And of all heroic pursuits large and small,
we believe there may be none greater
than a life well-loved.
365 366
Musculoskeletal Rhabdomyolysis
• Fractures • Breakdown of muscle tissue that leads to release
• Functional limitation of myoglobin and muscle fiber debris into the
– Immobility, falls, antibiotics bloodstream. Toxic to the kidney (acute kidney
injury [AKI])
• Osteomyelitis
– Trauma, drugs (cocaine, amphetamines, statins,
heroin or PCP), genetic muscle diseases, extremes
of body temperature, ischemia or necrosis of
muscle cells, seizures, severe exertion (marathon),
lengthy operative procedures, severe dehydration
367 368

92
Healthcare-Associated Infections (HAI) HAI
• CLABSI Bundle • CAUTI: Most common HAI

– Perform daily audits to assess need for central line.
– Catheter only when indicated
– Follow proper insertion practices.
• Hemodynamic instability
– Handle and maintain central lines.
• Nucleated thoracic/lumbar spines
• Hand hygiene
• Urologic or gynecologic surgery
• Scrub access port or hub: access with sterile
devices. • Deep sedation
• Replace dressings as needed. • Urinary retention
• Dressing changes under aseptic technique – Drainage bag is kept lower than bladder.
369 370
CAUTI VAP
• Secure catheter with leg strap or tube holder. • Head of bed (HOB) elevated 30 degrees
• Strict handwashing • Oral care every 2 hours
• Perform per-care daily and after each BM. • Turn patient every 2 hours.
• Sterile technique • Sedation vacation
• Always scan bladder prior to catheterization to determine • Peptic ulcer disease (PUD) prophylaxis
urine volume and necessity.
• Deep vein thrombosis (DVT) prophylaxis
371 372

93
Bariatric Considerations Other Problems
• Abdominal pain: postoperative • Sleep disruption

– Anastomosis leak: considerable pain, acute abdominal • Thermoregulation: dysregulation
– Gastric bleeding
– Persistent vomiting and abdominal pain • Toxic ingestion: drugs and alcohol overdose
• Pulmonary embolism is always in the differential. • Comorbidity in patients with transplant history
• Long-term postoperative complications – Medications
– Nutritional concerns
– Immunosuppressed
– 1/3 of patients develop gallstones
– 20% of all patients require follow-up surgeries to correct – The transplant patient: antirejection medications and
complications transplant coordinator
373 374
Multisystem Organ Failure (MSOF) MSOF/SIRS

• Shock • Systemic inflammatory response syndrome (SIRS): the
• Definition: condition of insufficient perfusion of cells and vital systemic response to a variety of insults that begin as local
organs, causing tissue hypoxia inflammation
• Perfusion is inadequate to sustain life: results in cellular, – Collection of immune-mediated responses to infections, foreign
metabolic and hemodynamic derangements materials, tissue ischemia and reperfusion injuries
• Malperfusion • The cascade
375 376

94
Clinical Presentation Old Definitions
• SIRS
• Fever + leukocytosis = SIRS
• Criteria (2 or more of the following):
– Tachycardia (> 90/min.) • SIRS + infection = sepsis
– Hyperpnea (RR > 20/min., • Sepsis + MODS = severe sepsis
PaCO2 < 32 mm Hg)
• Severe sepsis + refractory hypotension = septic
– Hyperthermia (Temp. > 38⁰ C) or hypothermia (< 36⁰ C)
– White blood cells (WBCs) > 12,000 or below 4,000
shock
377 378
New Definitions Classification
• Hypovolemic: caused by inadequate

• Fever + leukocytosis: SIRS intravascular volume, external losses, internal
• Sepsis: life-threatening organ dysfunction due losses
to a dysregulated host response to infection • Cardiogenic: caused by impaired ability of
• Septic shock: subset of sepsis in which heart to pump blood, contractility, filling,
particularly profound circulatory, cellular and emptying
metabolic abnormalities increase mortality • Distributive or vasogenic: caused by massive
vasodilation caused by release of mediators
• Absent is the term severe sepsis, since sepsis
of inflammatory process in response to
has a mortality rate of 10%+, making the condition overwhelming infection, septic, anaphylactic,
already severe (2016) neurogenic
379 380

95
Important to Remember Infectious Diseases
• Any infection that requires antibiotics

• Preload – Start and stop date, renal protection
• Afterload – Fluid administration
• Contractility • The flu

• Heart rate (HR) and rhythm • Multidrug-resistant organisms: MRSA, VRE,
CRE, ESBL
• Perfusion
– Carbapenem-resistant Enterobacteriaceae (CRE):
nightmare infection, carbapenem resistant
Enterobacteriacease
– Extended-spectrum beta-lactamases (ESBL): enzyme
produced by bacteria, disable the antibiotic
381 382
Life-Threatening
Maternal/Fetal Complications Shock: Cardiogenic Treatment
• Eclampsia: blood pressure (BP) and

magnesium • Fix the pump!
• HELLP: complication of pregnancy • Drugs
characterized by hemolysis, liver dysfunction,
thrombocytopenia
• Oxygen
– Disseminated intravascular coagulation (DIC) • Intra-aortic balloon pump (IABP)
picture
• Perfusion
– Placental abruption
– Renal failure (RF)
• Postpartum hemorrhage
• Amniotic embolism
383 384

96
Cardiogenic Hypovolemic Shock
• What does this person look like? • Classes of Shock

– I 750-1,500 cc loss ↑ HR, narrow pulse
• VOMIT pressure, cool skin,
• Treatment of cardiogenic shock ↓ urine output
– Decrease preload. – II 1,500-2,000 cc ↑ HR, ↑ RR, ↓ BP,
LOC change, ↓urine
– Decrease afterload.
– III 2,000 cc-more ↑ HR, shallow
– Increase contractility. respirations, obtunded,
anuria
– IV Exsanguination
385 386
Specific to Hypovolemic Shock Specific to Anaphylactic Shock
• ABCs • Remove the offending agent, antigen.

• Maintain a patent airway (ABCs).
• Volume resuscitation
• Volume resuscitation
• Treat the cause: Stop source of fluid • Modify or block the effects of biochemical
loss; restore intravascular volume. mediators
• Inotropes: after volume restored – Administer sympathomimetics.
• IV epinephrine + steroids
• Utilize mechanical support.
• Antihistamines, bronchodilators
387 388

97
Specific to Neurogenic Shock Specific to Septic Shock
• ABCs • Prevent infection.

• Spinal cord immobilization • Avoid NPO status.
• Warming measures • Antibiotic therapy: Treat infection and neutralize toxin.
• Maintain MAP, prevent venous stasis • Control hyperthermia.
• Volume replacement
• Volume status
• Monitor for complications of shock or other
reason for shock
389 390
Septic Shock Management
• Consideration of End of Life • Identify infection. • Minimize O2

• Maximize O2 consumption.
delivery. • Mechanical ventilation
– Fluids: cultures • Monitor SVO2.
– Antibiotics • Control temperature
– Vasopressors and electrolytes.
– Maintain • Nutritional status
Hct > 21% • Control pain and
– Inotropes anxiety
• Prevent complications
391 392

98
Question Question
One of the most effective therapies in the In the treatment of shock, the team should:
treatment of sepsis is:
A. early antibiotic therapy A. Promote oxygenation and ventilation.

B. early treatment with multiple cardiac B. Enhance oxygen delivery.
inotropes
C. early treatment with mechanical C. Decrease oxygen consumption.
ventricular assistance D. all of the above
D. No treatment has been shown to be
successful.
393 394
Final Thoughts
• Learn to love without condition.

Talk without bad intention. Give
without any reason. And most of
all, care for people without any
expectation.
There is power in passion!!
396
395 396

99

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CCRN®

Program Description and Learning Outcomes i

Introduction and Synergy 1

Behavioral and Psychosocial 54

Musculoskeletal and Multisystem 92

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

Program Learning Outcomes

1. Discuss and practice test-taking skills.

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

A patient with cerebral edema after a subarachnoid

a. Ask the pharmacist to clarify the order.

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• A syndrome characterized by • Factors triggering DIC

DIC DIC: Etiology

• Etiology: always secondary • Infection and sepsis

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Trauma • Cancers • Abnormal bleeding

• Petechiae (first indication of DIC)

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Maintain ABCs. • Risks of transfusion

• Red blood cells (RBCs)

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Coagulation components: platelets • Fresh frozen plasma (FFP)

Blood Replacement Blood Replacement

• Cryoprecipitate • Adverse reactions

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Mortality: 40%-60% • Deficiency of hemoglobin

• Production vs. destruction of loss • Decreased exercise tolerance

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Depends on cause • Immunosuppression

Oncological Complications Wounds

• Tumor lysis syndrome • Pressure ulcers

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Red skin that gets worse over time, blister • Stages

Skin Complications Peripheral IV Review

Cellulitis Necrotizing Fasciitis

• Complications: phlebitis, extravasation of

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• DIC = high PT/PTT, low fibrinogen, low

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

A. myocardial depressant factor A. PT & PTT prolonged

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Antiplatelet therapy: dual therapy • Clinical presentation, ECG, enzymes

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Management • Two functions

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Monitor ECG Six P’s

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• Maintain adequate filling pressures.

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

• JVD • Nocturia • Treat the cause, improve oxygenation.

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net

MED-ED, Inc. | 1911 Charlotte Dr. Charlotte, NC 28203 | 800-763-3332 | www.MedEdSeminars.net