CCRN Review Course 2015

PROSPECTUS: This lecture series is designed to provide the critical care health care
provider with a review of AACN’s core curriculum. Provided in a lecture format, the
instructor will review anatomy and physiology, physical assessment (including
hemodynamics and utilization of invasive assessment tools), and pathophysiology in a
systems approach. Topics that are discussed include: Cardiac, Pulmonary,
Neurological, Renal, Endocrine, Hematological, Gastrointestinal, and Psychological and
Legal aspects of care. This review is not an introduction to the environment of the
Critical Care area, but a comprehensive update for the professional already in practice
at the critical care bedside and preparing for the CCRN Certification Examination.

OBJECTIVES: At the completion of this lecture, the participant will be able 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.

AGENDA: Day One 8 am to 4:30 pm Day Two 8 am to 4 pm

Day One: Introduction, Hematology, Cardiovascular, Endocrine, and Gastrointestinal

Day Two: Neurologic, Renal, Pulmonary, Multisystem Failure and Summary

Cammy House-Fancher, ACNP, MSN, CCRN-CSC, PCCN

Cammy is a nationally known speaker with over 40 years of Critical Care

experience. Cammy has taught the CCRN Review as well as Critical Care Updates with
an emphasis on the critical thinking skills of the bedside practitioner. As well as
lecturing across the country, Cammy is a reviewer for several revered nursing journals,
has numerous publications in the area of critical care, and continues to have an active
practice as an Acute Care Nurse Practitioner at the University of Florida, Division of
Cardiothoracic Surgery. As a critical care nurse practitioner, Cammy brings much
clinical practice skill to the lectures as well providing clinical pearls for bedside care.

1
Table of Contents

I. Introduction to the TEST

II. Hematology/Immunology
Physiology, Stress Response, Homeostasis, Bleeding, Pathophysiology,
DIC and Blood Products

III. Cardiovascular
Anatomy and Physiology, Cardiac Output, Hemodynamics, Assessment,
Coronary Artery Disease and Heart Failure

IV. Endocrine
Stress Response, DI, SIADH, Diabetes: DKA and HHNK

V. Gastrointestinal
Anatomy and Physiology, GI bleeding, Esophageal Varices, Hepatic Failure,
Pancreatitis, Intestinal Infarction, and GI Surgery

VI. Neurology
Anatomy and Physiology, Cerebral Perfusion Pressure, Assessment,
Increased Intracranial Pressure, Neurological Problems, Neuro-Muscular
Problems, Head Injury, Stroke, and Spinal Cord Injury
Behavioral

VII. Renal
Anatomy and Physiology, Renal Assessment, Acute Renal Failure, and
Chronic Renal Failure

VIII. Pulmonary
Anatomy and Physiology, Assessment, Pathophysiology, Acute Respiratory
Failure, Mechanical Ventilation, ARDS, Pneumonia, Aspiration, Status
Asthmaticus, Pulmonary Embolism, and Chest Trauma

IX. Multisystem Organ Failure

General Definitions, Classifications, Clinical Presentations, Treatment
Protocols, and Management

X. Additional Reference Material

Electrolytes
Test Taking Strategies
Reference List

House-Fancher 2
Introduction

Requirements for the CCRN Exam:

 Current, unrestricted RN license in US
 Clinical practice in Critical Care: 1750 hours in the last 2-year period

 BSN not required

Obtaining application:
 AACN (800) 899-2226 or www.aacn.org (go to certification, then CCRN)

 Apply; receive authorization to test (takes between 2-4 days to 2-3 weeks)

 Schedule: Make appointment at nearest testing site – H&R Block

 You have 90 days to take the exam

Blue Print of Exam:

Clinical 80% Synergy 20%

Cardiac 20
Pulmonary 18 Advocacy and Moral Agency 3
Multisystem 8 Caring Practice 4
Neurology 12 Collaboration 4
Gastrointestinal 6 Systems Thinking 2
Renal 6 Response to Diversity 2
Endocrine 5 Facilitation of Learning 3
Hematology/ Clinical Injury 2
Immunology 2
Behavioral 4

Professional: Synergy Model 1999

 Synergy Model: Patient Centered Care
 Looks at the whole patient and resources that the patient requires for successful
outcome
 Needs of the patient matched with the nurse’s ability

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A patient’s family expresses anxiety regarding the meaning of numbers on the patient’s
monitor and asks the nurse for clarification. The nurse’s most appropriate response
would be:

a. The numbers indicate the patient is having problems

b. The numbers help us to determine the best treatment
c. Which numbers on the monitor concern you?
d. What don’t you understand about the monitor?

When teaching a family member to perform an aspect of patient care, the nurse realized
that family members:

a. Are affected by timing of teaching

b. Learn best if they perceive a need to learn
c. Learn best if shown a complex procedure all at once
d. Learn unrelated tasks first

A patient with cerebral edema after a subarachnoid hemorrhage has been ordered
Nifedipine 10mg by mouth every 4 hours. The patient’s blood pressure is 150/85 mmHg.
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 blood pressure

The Test: 150 Questions, 3 hours: NOT like NCLEX, you must answer each question.
o READ all instructions, will not need paper, pencil, calipers, or calculator
o Passing is 71% overall

Recertification

Maintaining CCRN credentials: recertify every 3 years

 Recertification by re-taking the exam every 3 years

 Recertification by maintaining 100 CEUs every 3 years

2009 Synergy CEUs

• Clinical
Category A
• Min 60 Max 80

• Leadership, Team Building, Caring

Category B
• Min 10 Max 30

• Collaboration, Precepting
Category C
• Min 10 Max 30

House-Fancher 4
Hematology/Immunology

Hematology: Provides a medium for transportation of O2, CO2 and nutrients,

maintains hemostasis, maintains internal environment – temperature/acid/base
Immunology: Protects from invading foreign materials
Stress and Immunosuppression
 Stress Response: acute stress vs. chronic stress: total body response
 Sympathetic nervous system stimulation: vital signs
 Skin barrier and/or irritated mucous membranes
 Impaired gag, cough or swallow
 Increased gastric pH, colonization, volume aspiration, pneumonitis
 Malnutrition
 Acute phase stress reaction—catabolism, decreased healing, inhibited immune
response
 Sequential infections

Hemostasis: Termination of bleeding

 Vascular Response: vasospasm, Thromboxane A2 secretion, platelet response,
coagulation—clot formation
 Platelets: what effects platelets? Antiplatelet agents
Everything Aspirin
 Thrombocytopenia: Plavix
o Heparin induced thrombocytopenia Effient
Persantine
o Sepsis
PY12 Inh.
o Disseminated intravascular
coagulopathy GP IIb/IIIa ReoPro
o Antiplatelet drugs Inhibitors Integrilin
Aggrastat
DIC: Disseminated Intravascular
Unfractionated Heparin
Coagulopathy Heparin (LMWH) Lovenox
Fragmin
Syndrome characterized by thrombus
formation and hemorrhage. Secondary to over Fibrinolytic agents Streptase
Reteplase
stimulation of the normal coagulation process,
Activase
with resultant decrease in clotting factors and
platelets—platelet dysfunction Direct Thrombin Arixtra
 DIC may be acute or chronic Inhibitor Angiomax

Thrombus, then hemorrhage

House-Fancher 5
Factors triggering DIC:
 Tissue factors: tissue-break down
 Platelet aggregation: sepsis
 Injury to vascular endothelium and exposure to collagen

Etiology: always secondary condition

 Vascular disorders
 Infection and sepsis
 Hematological and immune disorders
 Anaphylaxis---histamine release with fluid movement causing edema and
vasodilation
 Hemolytic blood transfusion reaction
 Massive blood transfusion—more than 6 units/24 Hours
 Prolonged cardiopulmonary bypass (CPB)
 Sickle Cell Crisis
 Transplant Reaction
 Trauma, burns, acute anoxia, crush injury, head injury, OB complications, cancer

Presentation:
 Abnormal bleeding,
 Signs of thrombosis,
 Change in level of consciousness (LOC),
 Chest pain, S-T, T wave changes,
 Dyspnea, hypoxia,
 Decreased urine output, proteinuria, electrolyte imbalance,
 Abdominal pain, diarrhea

Clinical Presentation: Petechiae, ecchymosis, purpura, and bleeding

Decreased Platelets (<100,000)

Decreased Fibrinogen (<200 mg/100
mL)
Decreased Antithrombin III (<70%)

Increased PTT (>60-90 seconds)

Increased PT (>15)
Increased FDP/FSP (>10g/mL bur <
100)
Increased D-dimer (>2mg/L)
—specific to fibrin degradation

House-Fancher 6
Medical Management: stop bleeding

Always maintain ABC’s

 Careful for oral and mucosal bleeding
 Treat stimuli
 Correct hypovolemia, hypotension, hypoxia, and acidosis
 Stop microclotting to maintain perfusion

Blood Products: treatment of bleeding is giving blood and blood products

Risks of transfusion
 Noninfectious
 Infectious
 Immunologic
 Aged blood

Products
RBC’s:
Action: to increase O2 carrying capacity
Indications: significantly decreased hemoglobin & hematocrit
Blood loss—active bleeding
Avoid fluid overload: remember about heart failure and blood products
Administration: blood filter, 2-4 hours
Complications: transfusion reaction, infection, volume overload
Platelets:
Action: coagulation components
Indications: platelet count or decreased platelet function
Administration: component filter, rapid infusion
Fresh Frozen Plasma:
Action: increase clotting factors, water and electrolytes, no platelets
Indications: coagulation deficiencies, viable
Factor V and VIII
Administration: filter, rapid (can give over 2 hours)
Complications: viral, fluid overload
Cryoprecipitate:
Action: raises Factors VIII + XII, prevents and controls bleeding, contains
Fibrinogen and Antithrombin III
Indications: DIC, von Willebrands
Administration: filter, rapid
Complications: infection

Blood Replacement: Adverse Reactions:

 Hyperkalemia, hypocalcemia, decreased 23DPG, ammonia
intoxication
 Hypothermia, infections, TRALI—ALI, fluid overload

When to give blood?? Which products to give?? Remember PRBC’s have no

coagulation factors

House-Fancher 7
Complications of DIC:
 Mortality 40-60%
 Hypovolemic shock, acute renal failure, infection, ARDS, stroke, GI dysfunction
 Multisystem failure
 Hematology Pearls
 DIC = high PT/PTT, low fibrinogen, low platelets, high FDP/FSP, high D-dimer

Hematology Pearls

 DIC = high PT/PTT, Low fibrinogen, low platelets, high FSP (FDP), high D-dimer

 The pathophysiology of anaphylaxis includes: bronchospasm, hemolysis and

rapid DIC, increased vascular permeability and third spacing

QUESTIONS

A primary chemical mediator in anaphylactic reaction is:

A. Myocardial depressant factor

B. Histamine
C. Complement
D. Interferon

Which of the following lab diagnostic findings will most likely be seen in DIC?
A. PT + PTT prolonged
B. Fibrinogen increased
C. Platelet count increased
D. D-dimer normal

The clinical presentation of DIC includes:

A. Signs of thrombus formation

B. Excessive bleeding
C. Decrease in platelet count
D. All the above

House-Fancher 8
Cardiovascular

Essentials of Critical Care: Vital Signs

 Heart rate—tissue hypoxia
 Respiratory rate—tissue hypoxia and metabolic acidosis
 Temperature—oxygen requirements
 Blood Pressure:
 Systole
 Diastole
 Pulse pressure
 The principles of oxygen demand and supply

Goals of critical care:

1. Enhance oxygen delivery
2. Decrease oxygen demand

Cardiovascular: The purpose and function: to drive hemoglobin to the cell

Anatomy and Physiology Review

The Right and Left Ventricle

 The Right: low pressure,
Purpose: to drive blood through the pulmonary vault
Right Ventricular Failure:
 Physiology: right ventricle fails and dilates; blood backs up into right
atrium and to the superior vena cava and inferior vena cava; causing
jugular vein distention and hepatic congestion
 Causes: acute right ventricular infarction, pulmonary embolus,
elevated pulmonary pressure
 Treatment: volume

 Left Ventricular Failure:

 Physiology: left ventricle fails and dilates; blood backs up into the left
atrium and to the pulmonary veins causing increased pulmonary
pressures and pulmonary edema
 Causes: acute left ventricular infarction, cardiomyopathies
 Treatment: fluid restriction, diuresis

Coronary Arteries

 Right Coronary Artery (RCA): perfuses the right atrium and right ventricle
o 90% of people - the RCA is dominant: perfuses the inferior left ventricle
 Left Coronary Artery (LCA): left main
 Left Circumflex (Cx): perfuses the left atrium and lateral wall of the left ventricle
 Left Anterior Descending (LAD): perfuses the anterior and apex of the left ventricle,
as well as 2/3 of the ventricular septum

House-Fancher 9
  The coronaries fill during ventricular diastole (ventricular rest) and flow is
dependent on diastolic pressure

 Coronary Artery Perfusion Pressure (CAPP): Diastolic BP – PCWP (pulmonary

artery wedge pressure)
 Normal is 60-80 mmHg
 Watch the diastolic blood pressure

The heart utilizes approximately 85% of available O2 at rest, when the myocardium
requires more O2 for proper functioning, the coronary arteries dilate in response to
increased demand

Supply (of oxygen) must equal Demand (of oxygen)

Cardiac Output = Stroke Volume X Heart Rate

DETERMINATES OF
VENTRICULAR FUNCTION

I.
II.

 Definitions to remember:
 Cardiac output and cardiac Index indicate perfusion to the cells
 Stroke Volume (SV) = amount of blood (mL) ejected with each ventricular
contraction
 Stroke Volume = preload, afterload, and contractility

 Preload: the amount of volume returned to the ventricle at the end of diastole,
consists of:
 Venous return
 Intrathoracic pressure
 Drugs:
o Preload--overloaded: diuretics and/or vasodilators
o Preload--low: give volume
House-Fancher 10
Afterload: impedance to ventricular emptying, resistance to ventricular ejection
OR: workload of the ventricle to pump blood out

 Right ventricle afterload: pulmonary vascular resistance

 Left ventricle afterload: systemic vascular resistance (SVR) and/or Aortic Stenosis
(AS)

 Drugs: left ventricular afterload

o Reduce afterload: vascular smooth muscle relaxers, decrease the workload
of the left ventricle
 A = Ace Inhibitors
 ARBs—angio-receptor blockers: Diovan
 Alpha Antagonists: hydralazine, clonidine
 B = all Beta Blockers
 C = Calcium Channel Blockers

o Increase afterload: increase arterial tone, vasoconstrictors

 Levophed
 Vasopressin
 Neosynephrine
 Dopamine

Contractility: the ability of the ventricular muscle to contract and eject blood
 Drugs: Improve contractility
o Digoxin
o Dobutamine
o Milrinone
o Dopamine

House-Fancher 11
Heart Sounds: know S3 and S4

S1: beginning of ventricular systole

S2: beginning of ventricular diastole
S3: always pathologic: fluid overload
S4: always pathologic: decreased compliance, only in sinus rhythm!

Hemodynamics: the flow of blood as it travels through the heart and great vessels

 Uses: measure intra-chamber pressures and oxygenation, pacing, blood

sampling

 Measurements:

CVP 3-5 mmHg CO-------4-8 liters/min

RV 25/3-5 mmHg CI--------2.4-4.2 liters/min/m2
PAP 25/8-12 mmHg CVP-----3-5
PCWP 8-12 mmHg PAP-----25/8-12 mmHg
LA 4-12 mmHg PVR-----37-250 dynes/sec/cm2
LV 20/4-12 mmHg SVR-----800-1200dynes/sec/cm2

House-Fancher 12
Right ventricle Left Ventricle

Preload Preload
 Venous return  Return from right
 Volume status ventricle
 Intrathoracic  Volume
Pressure  Intrathoracic
Afterload Pressure
 PVR Afterload
 SVR
 Aortic Stenosis

DaO2 = arterial
oxygen delivery—
100%

SvO2 = true
mixed venous
oxygen 60-80%

VO2 = venous
oxygen: oxygen
consumption

ScvO2 = venous
oxygen in the
right atrium
65-85%

House-Fancher 13
 Hemodynamics:
SvO2
Cardiac output/index
Hemoglobin/Hematocrit
Oxygenation
Metabolic Demand

SVO2:
 True mixed venous blood, normal is 60-80%
 This gives information about oxygen consumption normal is 70-75%
 There is a 75% reserve of oxygen in the blood
 The SvO2: 4 pieces of information
o CO/CI, H&H, Oxygenation, Metabolic Demand

Put it all together: cardiac assessment:

Heart rate and rhythm
Stroke Volume – preload, afterload, contractility

Electrolytes and the Heart:

The 12 Lead ECG: rhythm disturbances, conduction defects, electrolyte imbalances,
drug toxicity, chamber enlargement or hypertrophy, myocardial ischemia, injury, and/or
infarction
Electrolytes:
 Hypokalemia: ventricular irritability

o Flat T wave with prominent U wave (in all 12 leads)

o T wave and U wave same amplitude
o S-T segment flattening
o S-T segment depression
o Treatment: replacement

House-Fancher 14
  Hyperkalemia: ventricular depression, asystole

o Greater than 5.5: tall, peaked T waves (in all 12 leads)

o P wave widens
o Greater than 6.5: QRS widens, bradycardia
o Greater than 8.0: wide QRS
o P wave barely visible
o Treatment: no more potassium, Lasix, Kayexalate, D50 –insulin—
bicarb—calcium (dialysis)
 Hypocalcemia: Torsade’s de Pointes
o Prolonged QT, prolonged S-T segment
 Hypercalcemia: shortened QT, shortened S-T segment
 Hypomagnesemia: Torsade’s de Pointes
o Prolonged Q-T, broad-flattened T waves, dysrhythmias
 Hypermagnesemia: agonal to asystole
o P-R and Q-T prolonged
o Prolonged Q-T interval

Coronary Artery Disease: CAD, the leading cause of death in the U.S.
 Definition: flow limiting lesion
 Pathophysiology: inflammatory disease
 Risk Factors: Diabetes
 Clinical manifestations: Heart Failure (HF), sudden death, angina, unstable
angina (acute coronary syndrome—ACS), myocardial infarction

HONDA

VOMIT H = Hypertension
V = Vital Signs O = Obesity
O = Oxygen N = Non-Insulin
M = Monitor D = Dependent
I = IV access A = Atherosclerosis
T = Treatment S = Sleep Apnea

1. Stable Angina:

Clinical presentation
 ECG presentation: no S-T changes
 Treatment modalities: rest, NTG, and ASA
House-Fancher 15
 o Antiplatelet Therapy: ASA, Plavix, Effient
o Vasodilator Therapy: NTG
o Beta Blocker: decreases MVO2 (myocardial oxygen demand), regulates HR,
rhythm, and BP
o ACE-I: BP control and reduces remodeling

2. Unstable Angina (UA) and NSTEMI: ACS = UA/NSTEMI (non-ST elevation

myocardial infarction)

Clinical presentation
 ECG presentation: S–T, T wave depression
 Pathophysiology: clot formation
 Biochemical Markers: positive troponin
 Treatment Management: increase supply—decrease demand
o ASA, Beta Blockers, Heparin, NTG, Morphine, GP IIb IIIa inhibitors
o Assistance for the Ventricle: Unstable patient unresponsive to primary
treatment
o IABP: two functions: decrease afterload, increase coronary perfusion
 Diastolic Augmentation
o Interventional Treatment:
 PTCA, Stent Placement, catheterization laboratory
 Nursing Care of the Interventional Cardiology Patient
 NPO, consent, labs, insulin, kidney protection, medications
 Post-procedures: monitor ECG—ST-T wave segment, vascular
examine, heparin, activity, medications
o Arterial Assessment: 6 P’s: Pulse, Pain, Pallor, Polar, Paresthesia, Paralysis

3. Acute Myocardial Infarction (STEMI): TIME EQUALS MUSCLE = MUSCLE =LIFE

Etiology: occlusive clot in the coronary artery

Clinical Presentation, Enzymes, 12 Lead ECG

House-Fancher 16
12 Lead ECG: You need to know location
 ST segment elevation is always current of injury or infarction
 ST segment depression is always myocardial ischemia
 Two or more contiguous leads – leads that are associated, such as, inferior or
anterior leads
 Leads II, III, and AVF are inferior leads
 Leads I and AVL are anterior lateral leads
 V1-2 are anterior septal leads
 V3-4 are anterior leads
 V5-6 are lateral

House-Fancher 17
STEMI Acute Management:
 VOMIT: 12 lead ECG, enzymes, MONA
 Manage and monitor
 ACLS for rhythms
 Reduce size of infarct
o Door to diagnosis and treatment
o Diagnosis: clinical presentation, 12 lead ECG, and enzymes
o Treatment Paradigm: ABC’s, oxygen, pain management, ASA
 Reperfusion therapies
 Cath Lab (PCI)
 Fibrinolysis
 Coronary Artery Bypass Graft (CABG)
o Increase myocardial oxygen supply
 Open the artery
 Oxygen
 Maintain CAPP—diastolic blood pressure
 Control dysrhythmias
 Beta Blocker
 Fibrinolytic therapy if delay in treatment
 Antiplatelet therapy
o Decrease O2 demand: pain and anxiety relief, temperature control
 Oxygen, Beta Blockers, ACE-Inhibitor, rhythm control

House-Fancher 18
Right Ventricular Infarction: Assess for infarctions: 15-18 Lead ECG

V4R—definitive lead for assessing right ventricle

Increased CVP, normal to low PAP and PCWP
Clinical indications of right ventricle failure
Minimal to absent pulmonary congestion
Management: maintain adequate filling pressures, administer volume, avoid
diuretics, and venodilators, and maintain contractility

Right Ventricular Infarction Left Ventricular Infarction

CVP ↑ CVP normal or ↑
PAP normal or low PAP elevated
PCWP normal or low PCWP elevated
CI/CO low or normal CI/CO low
SVR high SVR high

Complications of Acute Myocardial Infarction

 Dysrhythmias, heart failure, cardiogenic shock, papillary muscle dysfunction, VSD,

cardiac rupture, ventricular aneurysm, pericarditis, Dressler’s Syndrome, sudden
death

Summary of Treatment of CAD

 Medical Treatment:
o Antiplatelet, vasodilator, Beta Blocker, ACE-inhibitor, statin
 Surgical: CABG: continue with medical therapy
o Post-op care: Atrial fibrillation
 Prevent post op complications: pneumonia, DVT with pulmonary emboli
 Alveolar recruitment, incentive spirometer, and ambulation (both
pneumonia prevention and prevention of DVT)

 Post-operative valve surgery: mitral or aortic valve repair/replacement

o Median sternotomy, right or left thoracotomy, valve types and anticoagulation

Heart Failure: Is a progressive disease that does not improve, compensatory response:
neurohormonal blockade
o Block sympathetic nervous system—Beta Blockers
o Block renin-angio-tension system—ACE-Inhibitors
 Inability of the heart to meet the needs of the body: malperfusion, evidence of organ
dysfunction
o Etiology of heart failure (HF): most common in U.S. is CAD
o Clinical Presentation of Left Ventricular Failure (LVF)
 Tachycardia, tachypnea, dyspnea, orthopnea, PND, pulses alternans,
cough, weakness, fatigue, mental confusion, murmurs, ECG—atrial
arrhythmias, atrial fibrillation, left atrial enlargement, left ventricular
hypertrophy, chest x-ray—fluid overload, ABG’s—hypoxemia
House-Fancher 19
 o Clinical Presentation of Right Ventricular Failure
 Jugular venous distention, hepato-jugular reflux, dependent edema,
hepatomegaly, anorexia, nausea, vomiting, abdominal pain, ascites,
nocturia, weakness, fatigue, wt. gain, abnormal liver functions, ECG—
RAE, RVH, atrial dysrhythmias
o Management: Treat the cause if possible: improve oxygenation
 Decrease Preload
 Monitor volume status: low sodium diet
 Diuretics, Natrecor, NTG, pulmonary vasodilators (oxygen)
 Decrease MVO2: Decrease Afterload
 Beta Blockers, ACE-I
 Control heart rate and rhythm
 Increase Contractility
 Digoxin, Dobutamine, Milrinone, Dopamine (dose dependent)
 Intra-aortic balloon pump

Cardiac Pearls

o ABC’s
o CI/CO – preservation of tissue perfusion
o Purpose is to drive hemoglobin to the cell
o CO = SV X HR
o S-T-segment depression = ischemia
o S-T-segment elevation = current of injury, infarction
o S-T elevation of II, III, and AVF = inferior infarction, STEMI
o S-T elevation of I, AVL, V1-6 = anterior infarction, STEMI
o IABP: increase coronary artery perfusion, decrease afterload

QUESTIONS

You are caring for a patient recently admitted with an inferior wall myocardial infarction.
Which of the 12 Lead ECG findings would 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 greater than 0.01 in all 12 leads
D. R wave taller in V6

Your patient with an inferior wall myocardial infarction also has a right ventricular
infarction. He soon develops right ventricular failure. Which of the following data
obtained would correlate this?

A. PAP 23/8 PCWP 19 CVP 20

B. PAP 54/28 PCWP 14 CVP 14
C. PAP 28/10 PCWP 10 CVP 20
D. PAP 12/4 PCWP 24 CVP 18

House-Fancher 20
The most common complication of a myocardial infarction is:

A. Arrhythmias
B. Heart Failure
C. Cardiogenic Shock
D. Pulmonary Edema

A normal wedge pressure, increased pulmonary artery pressures, and evidence of right
ventricular failure would most likely indicate:

A. Cardiac Tamponade
B. Left Ventricular Failure
C. Myocardial Infarction
D. Pulmonary Embolism

Medical management of valvular disease includes:

A. Prevention of infection
B. Treatment of heart failure
C. Treatment of dysrhythmias
D. All the above

Symptoms to evaluate for the diagnosis of heart failure may include:

A. Dyspnea at rest
B. Orthopnea
C. Nocturnal cough
D. All the above

House-Fancher 21
Endocrine System

Functions: regulates secretion of hormones that alter metabolic functions

Diabetes Insipidus: Clinical condition characterized by impaired renal conservation of

water, resulting in polyuria, low urine specific gravity, dehydration, high serum Na+

 Cause: Deficiency of antidiuretic hormone (ADH) -from the pituitary

 Etiology: neurogenic, nephrogenic, psychogenic
 Pathophysiology:
o Deficiency of ADH or inadequate renal tubule response to ADH
o Diuresis of large volumes of hypotonic urine
o Dehydration and hypernatremia
o Shock and/or neurological effects
o Permanent vs. temporary
 Clinical Presentation:
o Polyuria: 5 to 15 liters/day
o Thirst, fatigue
o Dehydration: weight loss, poor skin turgor, postural hypotension, low filling
pressures
o Neurologic: restlessness, confusion, irritability, seizures, lethargy, and
coma
o Urine specific gravity less than 1.005, Na+ greater than 145 mEq/liter, BUN
elevated, serum osmolality increased, serum ADH low
 Management: detect clinical indications of diabetes insipidus
o Monitor urine output
o Correct fluid deficit, hypotonic solutions
o Administer exogenous ADH: aqueous vasopressin, DDAVP, Diapid
(intranasal)

Diabetes Insipidus = dehydration and high serum sodium

Syndrome of Inappropriate Antidiuretic Hormone (SIADH): Clinical condition

characterized by impaired renal excretion of water, resulting in oliguria, high urine
specific gravity, water intoxication and hyponatremia.

 Etiology:
o Neurologic: pituitary tumor, CNS depression, stroke, intracranial hemorrhage,
infection, Guillain-Barre Syndrome, CVA, non-malignant pulmonary disease

House-Fancher 22
 o Ectopic: production of a substance indistinguishable from ADH by tissue: oat
cell cancer
o Nephrogenic: general anesthesia, narcotics, Tylenol, tricyclic’s,
anticonvulsants
o Hypoxia, stress, multifactorial in ICU patient

 Pathophysiology: excessive amounts of ADH secreted from the pituitary

 Clinical Presentation:
o Oliguria---urine output less than 0.5 ml/kg/hour
o Urine specific gravity greater than 1.030
o Clinical indications of fluid overload
o Anorexia, nausea/vomiting, diarrhea
o Dyspnea, and pulmonary edema
o Headache, personality and behavioral changes, altered level of consciousness
o Seizures, muscle weakness or cramps
o Serum sodium less than 120 mEq/liter
o BUN decreased, serum osmolality decreased, serum ADH level increased

 Treatment: Detect SIADH in high risk patients, monitor urine output and specific
gravity
o Treat cause, surgery to remove malignancy
o Decrease water intake
o Decrease or discontinue drugs that may cause SIADH
o Correct fluid overload: fluid restriction, diuretics
o Correct electrolyte imbalance: increase dietary sodium, hypertonic saline if Na+
less than 125 or if patient has seizures
o Institute seizure precautions

SIADH = swimming in water, low serum sodium

Diabetes: Types of disorders

 Diabetes mellitus (DM): a group of metabolic diseases characterized by

hyperglycemia which results from defects in insulin secretion, insulin action, or both

 Diabetic ketoacidosis (DKA): hyperglycemia crisis associated with metabolic

acidosis and elevated serum ketones, the most serious metabolic disturbance of type
I DM

House-Fancher 23
 Hyperglycemia Hyperosmolar Nonketotic Condition (HHNK): hyperglycemic crisis
 associated with the absence of ketone formation, most serious metabolic disturbance
type 2 DM

DKA: insufficient insulin, hyperglycemia, osmotic diuresis, glycosuria, dehydration, and

electrolyte imbalance. Excessive free fatty acids

 Who has DKA?

o Undiagnosed type I DM, known type I DM with illness or infection,
noncompliant patient, non-diabetic with Cushing’s syndrome, hyperthyroidism,
pancreatitis, drug induced
 Presentation:
o Glucose 300-600
o Sodium normal
o Potassium is elevated then decreases with insulin administration
o Ketones are present
o BUN/creatinine ratio is elevated
o WBC’s may be elevated
o Serum osmolality is elevated ≈ 295-330
o ABG’s indicate metabolic acidosis
o Nausea/vomiting, abdominal pain, polyphagia, polydipsia, polyuria
o Weakness, fatigue, weight loss
o Clinical indications of dehydration: tachycardia, orthostatic hypotension
o Kussmaul’s respirations
o Lethargy progressing to coma
 Treatment:
o ABC’s, monitor
o Identify and treat cause: infection—blood cultures
o Correct fluid volume deficit
o Normalize serum glucose
o Regular insulin 0.1 – 0.15 units/kg, followed by infusion
o Serum glucose should drop no more than 75-100mg/dL/hour to avoid
hypoglycemia, hypokalemia, and cerebral edema
o Replace electrolytes
o Correct acid-base balance
o Maintain safety

 Complications:
o Cardiovascular: hypovolemia, dysrhythmias, embolism, STEMI, pulmonary
edema
o Neurological: seizures, cerebral edema, and coma
o Renal: acute renal failure, electrolyte imbalance

House-Fancher 24
HHNK: Hyperglycemic Hyperosmolar Non-ketotic Condition: Hyperglycemic
Crisis
 Etiology: usually seen in patients over 50 years of age with glucose intolerance:
may follow: pancreatitis, burns, hepatitis, trauma, ETOH abuse, hypertonic nutrition,
drugs
 Pathophysiology: relative insulin deficiency, hyperglycemia causing osmotic
diuresis with severe dehydration with decreased GFR, renal failure and neurologic
changes
 Clinical Presentation:
o Glucose 600-2000
o Na+ is low (secondary to elevated blood sugar)
o Potassium is low
o BUN/creatinine high
o Serum osmolality high ≈ 330-450
o ABG’s normal pH, if acidosis is present consider lactic acidosis
 Treatment: ABC’s, monitor
o Identify cause—infection—blood cultures
o Normalize serum glucose level
o Correct electrolyte imbalance
o Safety
o Monitor for complications
 Hypovolemic shock, dysrhythmias, acute renal failure, thromboembolism,
STEMI, pulmonary edema, cerebral edema

Hypoglycemia: females greater than males, more common in elderly, ETOH abuse, and
infection
 Signs and symptoms: sympathetic nervous system stimulation—tachycardia,
nausea/vomiting, headache, change in behavior, change in level of consciousness
 Treatment: replace glucose

Endocrine Pearls

Normal serum osmolality = 275-295

Acidosis causes shift of cellular K+ to serum

Know difference between DKA and HHNK

SIADH = low Na+: restrict fluid, 3% saline

DI = high Na+, dehydrated: Vasopressin = ADH = Pitressin: HHNK=Severe

Dehydration

House-Fancher 25
 DKA HHNK
Type I DM Type II DM
Lack of insulin Deficient or Insensitive to insulin

Glucose 300-800 600-2000

Sodium normal artificially low
Potassium high low
ABG metabolic acidosis normal pH

SIADH is clinically manifested by:

A. Hyperosmolar state
B. Low output state
C. Myxedema state
D. Water intoxication state

The “cardinal sign” of SIADH is:

A. Hyponatremia
B. Urinary output of 10 liters/day
C. Hypotension
D. Systemic edema

Which of the following is characteristic of DI?

A. Low urine osmolality
B. Serum osmolality increased
C. Serum sodium elevated
D. All the above

 DKA the patient is initially hyponatremic

 In HHNK the patient is initially hyponatremic
 Should you treat the hyponatremia in HHNK

House-Fancher 26
Gastrointestinal

Gastrointestinal Bleeding

o Loss of new or old blood from the GI tract

o Emesis or stool
o 85% of GI bleeding is upper GI tract
o Shock leading to multisystem failure and death

 Pathophysiology: injury to mucosal lining

o Most common upper GI hemorrhages
 Peptic ulcers
 Esophageal or gastric varices, gastritis
 Mallory-Weiss Tear
o Most common lower GI hemorrhages
 Diverticular disease, tumors, ulcerative colitis
 Management: ABCs, monitor
o Restore circulating volume, and control bleeding
o IV, Foley, volume replacement, blood transfusions, coagulation factors
o NGT, gastric lavage, prepare for procedures—OR or IR
(Interventional Radiology)
o Vasopressin – monitor ECG
o NGT: gastric lavage: prepare for procedures—IR or OR, PPI or H2 Blockers
o Serial and daily labs
o Therapy for ulcers
o Maintain fluid and electrolytes
o Nutritional support
 Complications:
o Aspiration pneumonitis, recurrent bleed, perforation, acute pancreatitis,
STEMI, DIC, sepsis, shock, monitor ammonia levels

Esophageal Varices: dilation of the submucosal esophageal veins

 Etiology: cirrhosis, portal vein thrombosis, hepatic venous outflow obstruction,

congenital hepatic fibrosis
 Pathophysiology: fibrotic liver changes and resistance to normal venous drainage
of the liver to the portal vein causing increased pressure and portal hypertension. This
pressure begins formation of collateral circulation and distention of submucosal veins
of the distal esophagus and stomach and the predisposition for bleeding
 Management:
ABCs, restore circulating volume, NGT placement, endoscopic exam, vasopressin,
Sandostatin (Octreotide), TIPS—Transjugular Intrahepatic Porto-Systemic Shunt
 Complications: electrolyte imbalance, coagulopathy, liver failure, ETOH withdrawal,
renal failure, pulmonary distress and pneumonia
 Treatment: decrease gastric production, local vasoconstriction,

House-Fancher 27
Hepatic Failure: inability of the liver to perform organ functions—over 200 functions

 Etiology:
o Acute hepatic failure: virus, herpes simplex, CMV, hepatotoxic drugs,
ischemia and trauma
o Chronic hepatic failure: cirrhosis, Wilson’s disease, primary or metastatic
tumor of the liver
 Pathophysiology:
o Cirrhosis: liver parenchymal cells are progressively destroyed and replaced
with fibrotic tissue, results impaired hepatic function: ¾ of liver can be
destroyed before symptoms appear. Distortion, twisting, and constriction of
central sections cause impedance of portal blood flow and portal hypertension
occurs
o Portal Hypertension: esophageal varices, splenomegaly—
thrombocytopenia, vitamin K deficiency, inability to produce adequate amount
of bile, impaired carbohydrate (CHO), fat, protein metabolism, inability to store
vitamins and manufacture clotting factors
o Inability to detoxify toxins and drugs or to remove bacteria
o Ammonia production—break down of protein to ammonia
 Liver converts ammonia to urea and is eliminated by the kidney

High ammonia levels lead to hepatic encephalopathy

o Fulminant Live Failure: Jaundice, tachycardia, hypotension, fluid

retention, ascites, decreased urine output, spider nevi, palmer erythema,
bleeding, electrolyte imbalance, asterixis, hyperventilation—causing a
respiratory alkalosis and right pleural effusions, increased ICP (intracranial
pressure), sepsis portal hypertension
o Cirrhosis: Azotemia, bruising, bleeding, nutritional abnormalities,
fatigue, weight loss, impaired bilirubin metabolism

 Management:
o Identify and treat cause of liver failure, avoid hepato-toxic drugs,
avoid ETOH, monitor LFT’s, ABC’s, and monitor for aspiration
o Ascites and fluid overload, pleural effusion (on right), LeVeen or
Denver Shunts
o Renal insufficiency, fluid restrictions, diuresis, (aldosterone
antagonists—Aldactone)
o Immune-compromised
o Electrolyte imbalances: low K+ and low Ca++
o Empty the bowel—neomycin, lactulose

 Complications:
o Malnutrition
o Immunosuppression, poor wound healing, edema and ascites
o Hemorrhage: esophageal varices, coagulopathy, DIC
o Glucose abnormalities
o Electrolyte imbalance

House-Fancher 28
 o ARDS
o Peritonitis
o Sepsis
o Hepatorenal syndrome
o Acute Tubular Necrosis (renal failure)
o Cerebral edema

Pancreatitis:

 Definition: acute inflammation of the pancreas:

o Interstitial: edematous pancreas, hypovolemia
o Hemorrhagic: extensive necrosis of the pancreas and peri-pancreatic tissue
and fat, erosion into blood vessels, hemorrhage, SIRS often occurs
Acute pancreatitis (AP) and Severe Acute Pancreatitis (SAP)
 Etiology: alcoholism, obstruction of common bile duct—Cholelithiasis, Post ERCP,
hypertriglyceridemia, drug induced, trauma, radiation, pregnancy, infection,
ischemia, idiopathic (20%)
 Pathophysiology: etiological factor triggers activation of pancreatic enzymes and
pancreatic cell injury, which leads to auto-digestion of pancreas from proteolytic
enzymes--this causes damage to acinar cells with erosion into vessels causes
inflammatory process with necrosis of fat and exudates with high albumin content,
Hypoalbuminemia and ascites
o Hypocalcemia
o Release of necrotic toxins (inflammatory response) may cause
SIRS and Sepsis
 Clinical presentation: acutely ill, hyperthermic, pain, nausea & vomiting,
dyspepsia, flatulence, weight loss, weakness, look like STEMI with tachycardia, fever,
hypotension, jaundice, Grey Turner’s sign, abdominal distention, ascites, decreased
bowel sounds, steatorrhea, respiratory distress, shock
o Low Ca++, low K+, and hyperglycemia
 Serum amylase and lipase elevated
 Urine amylase increased
 LFT’s abnormally high
 CT scan, MRI, pancreatic swelling edema or necrosis

 Treatment: Always ABC’s

o Decrease release of and destruction by pancreatic enzymes
o Pain management
o Nutritional support
o Prevent infection, ETOH withdrawal
o Prevent complications: Hypoglycemia, hypocalcemia, pseudo-cysts, pancreatic
abscess, pancreatic fistula, hypovolemia, ARDS, DIC, perforation, bleeding,
ETOH withdrawal, immobilization, SIRS, and sepsis

Intestinal Infarction:

 Definition: necrosis of intestinal wall resulting from ischemia

 Etiology: arteriosclerosis, vasculitis, mural thrombus, emboli (atrial fibrillation),

House-Fancher 29
 hyper-coagulopathy, surgical procedures (aorta clamped), vasopressors, strangulated
intestinal obstruction, intra-abdominal infection or hypertension, cirrhosis
 Clinical presentation: anorexia pallor, abdominal pain, severe cramping or
Non-specific and diffuse: objective data: tachycardia, hypotension, tachypnea, fever,
dehydration, vomiting and persistent and/or bloody diarrhea, abdominal guarding
and rigidity
 Management: ABC’s
o Maintain adequate circulating volume,
o D/C vasopressors with bowel ischemia
o Prevent and treat pain
o Prevent perforation, bowel rest, NPO, elevate HOB, NG tube—decompress
stomach
o Prepare for procedures (CT scan and labs) and possible surgical intervention

INTRA-ABDOMINAL HYPERTENSION

Renal Dysfunction

Respiratory Compromise

Abdominal Pressure greater than 18mmHg

GI Infections
Diarrhea: viral infections, parasites, bacterial toxins, consequence of critical illness

C. Difficile: species of gram-positive bacteria

Pseudomembraneous colitis
Diagnosis: Greater than 3 days of watery foul smelling stool, with history of
antibiotic therapy, and colitis (abdominal pain)
Treatment: ASAP, Flagyl 500 mg 3X daily, or Oral Vancomycin 125 mg 4X daily
Both for 10-14 days
Proper antibiotic use and infection control measures

Remember the gut: nutritional support, electrolytes

GI PEARLS

 Arterial perfusion of the small intestine: superior mesenteric artery

 Complications of pancreatitis: bilateral riles, atelectasis of left base, pleural

 effusion and ARDS, HHNK, low Ca++

 Cullen’s Sign: ecchymosis around umbilicus

 **Ker’s Sign: Splenic rupture or air or fluid (blood) in free space of the abdominal
compartment

House-Fancher 30
The administration of vasopressin should be most carefully monitored in patients who
have:

A. Diabetes Insipidus
B. CAD
C. Hypotension secondary to GI bleed
D. DM

The inability of the liver to conjugate what substance is a primary contributor to hepatic
coma?

A. Ammonia
B. Urea
C. Fatty Acids
D. Bilirubin

Cimetidine or ranitidine acts to reduce stress ulcers by inhibiting the production of

which substance?

A. Histamine
B. Gastrin
C. Acetylcholine
D. Calcium

Which of the following laboratory findings is MOST specific for pancreatitis?

A. Leukocytosis
B. Elevated serum and urine amylase
C. Hyperglycemia and hypokalemia
D. Decreased serum albumin and total protein

House-Fancher 31
Neurology

 The brain requires a constant oxygen and glucose supply

 The brain is a closed vault with little additional space: blood, cerebral spinal fluid
(CSF), and brain matter: if any of these increase in volume, there is little area to
expand; pressure increases, herniation and death
o Monro-Kellie Doctrine

 Cerebral Blood Flow: amount of blood within the brain vault, auto-regulated to
maintain the needs of the brain tissue. Blood to the brain must be pumped with
pressure. The pressure required to maintain adequate perfusion to all cells
(deep brain, and cortex) is called cerebral perfusion pressure (CPP)

CPP = mean arterial pressure (MAP) – intracranial pressure (ICP)

 Changes in MAP or ICP affect CPP

Normal CPP 60-100 (remember 70)

Normal ICP 5-15
Normal MAP 70-105

 In the brain injured patient the MAP is an important assessment tool

 Look at CPP: things that increase cerebral blood flow (CBF) in the head injured
patient are NOT good, such as:

Increase CBF Decrease CBF

Hypercapnia Hypocapnia (32-35)

Hypoxemia Hyperoxemia
Blood viscosity Blood viscosity
Hyperthermia Hypothermia
Drugs Drugs

 Neurological Assessment:
o Mental status—behavior
o Motor function
o Sensory function
o Cranial nerves
o Deep tendon reflexes (DTR’s)

House-Fancher 32
  Additional assessment includes:
o Blood pressure changes (PP)
o Respiratory rate and rhythm
o Bradypnea: central nervous system (CNS) depression
o Cheyne-Stokes: cerebral hemisphere
o Hyperventilation: lower midbrain or upper Pons
o Apneustic: mid to lower Pons
o Ataxic: medulla
o Temperature: central vs. peripheral fever

 Overall nursing care of the brain-injured patient should include:

1. ABC’s 7. Infection
2. Airway, ventilation 8. Complications of bed rest
3. Aspiration 9. DVT/PE
4. ICP/CPP/MAP 10. Rehabilitation potential
5. Volume status 11. Function
6. Bowel and bladder function 12. Psychosocial issues, family

 Clinical picture of increasing ICP

o First always, change in mental status: behavioral change, LOC change: early
and late
o Vital sign changes: pulse pressure widens: systolic pressure increases and
diastolic pressure decreases with a bradycardia
o Cranial Nerve changes: change in pupil size and reaction (smaller and less
reactive at first), vision, corneal reflex, swallow, contralateral motor changes,
vomiting, headache, seizure activity

 Early signs of ICP include

 Cushing’s Triad
1. Change in behavior
2. Change in vital signs (increasing pulse pressure, bradycardia)
3. Pupils constrict and become sluggishly reactive

 Complications of increased ICP:

o Further ischemia
o Seizure activity
o Diabetes insipidus (DI) or syndrome of inappropriate ADH (SIADH)
o Hydrocephalus
o DVT, stress ulcers
o Respiratory insufficiency, pneumonia

House-Fancher 33
Neurological Problems
 Hydrocephalus: excessive accumulation of CSF causing increased intracranial
pressure
o Congenital
o Acquired: communicating: CSF blocked after leaving the ventricle
o Non-communicating: obstructed
o Ex-vacuo: stroke or traumatic injury that causes brain damage
o Normal hydrocephalus: normal pressure, more commonly in the elderly,
subarachnoid hemorrhage, head trauma, infection, tumor or complications of
surgery, idiopathic
o Diagnosis: CT scan, ultrasound, MRI
o Treatment: shunt placement

 Neuromuscular Disorders: neurologic induced muscular weakness

o Think: respiratory compromise

 Muscular Dystrophy: genetic disorder, complications: cardiomyopathies with

resultant heart failure, decreased mobility, over all muscle weakness, mental
impairment, respiratory compromise, scoliosis, nutritional and swallowing
abnormalities, risk for falls
 Guillain-Barre: inflammatory peripheral neuropathy, syndrome, autoimmune
response, myelin sheath is lost, respiratory compromise
 Myasthenia Gravis: neuromuscular transmission disorder, autoimmune
response, anticholinesterases, steroids, Mestinon, thymectomy, respiratory
compromise, monitor calcium levels

 Muscle weakness: Nursing care of the debilitated patient

 Primary Types of Head Injury

o Trauma: concussion, contusion, sheer injury
o Ischemia: global, regional
o Inflammatory: meningitis – infection
o Compression tumor: edema, hematoma
o Metabolic encephalopathies

 Closed Head Injury: Etiology usually blunt trauma

 Contusion: partial or complete dysfunction for less than 24 hours, bruising,

petechial hemorrhages, laceration may occur, areas of infarction and necrosis may
occur
 Concussion: transient state of partial or complete paralysis of cerebral
functioning with complete recovery within 12 hours, headache
 Diffuse axonal injury: severe mechanical disruption of axons and neuronal
pathways in both cerebral hemispheres, diencephalon, and brainstem
 Hypoxic brain damage: occurs most frequently in the arterial distribution
between anterior cerebral artery and the middle cerebral artery (MCA)

House-Fancher 34
 Management:
 ABC’s
 Assess for additional injuries
 Prevent/detect intracranial hypertension and secondary brain injury (edema)
 Maintain CPP > 70
 Prepare for OR or IR
 Institute seizure precautions

 Brain Death
 Cardinal finding in brain death:
o Coma or complete unresponsiveness,
o Absence of cerebral motor responses to pain in all extremities,
o Absence of brain stem reflexes,
o Apnea
 Demonstrate that there is no flow or electrical activity
o Cerebral angiography,
o EEG,
o Transcranial doppler,
o Somatosensory and brain stem auditory evoked potentials,
o Technetium Tc 99m brain scan—no uptake

 Intracranial Hematoma
o Subdural hematoma: venous bleed spontaneously, older, ETOH
 Treatment: possibly a burr-hole evacuation
o Epidural hematoma: Linear skull fracture, usually arterial bleeding, history of
precipitating event
 Classic presentation: event causing unconsciousness, awake and
normal, rapid decline and unconsciousness again—requires intervention

 Stroke: Brain Attack: sudden, severe disruption of cerebral circulation VOMIT

o Ischemic Stroke:
 Etiology: atrial fibrillation, atherosclerosis, hypertension,
hypercoagulability
 Clinical: sudden onset
 Diagnosis: CT, MRI, and cerebral angiogram
 Risk Factors:
1. Family history 6. Substance abuse
2. Hypertension 7. Oral contraceptives
3. Smoking 8. Dysrhythmias
4. Hyperlipidemia 9. Hypercoagulability
5. Obesity 10. Sedentary life style

 Management: VOMIT
o ABC’s, vital signs, oxygenation, serum glucose
o Essential care: identification of type of stroke and timing of symptoms
o Oxygenation, ventilation, prevent aspiration

House-Fancher 35
 o Decrease metabolic requirements: head of bed elevated, temperature control,
labs
o Maintain cerebral perfusion: head of bed elevated
o Platelet aggregation inhibitors
o Anticoagulants
o Fibrinolytics—if prescribed
o Prevent complications

 Hemorrhagic Stroke: Etiology--Neurological deficit caused by interruption of blood

flow to the brain caused by vessel rupture
o Intracerebral Hemorrhage (ICH): trauma, hypertension, tumor, fibrinolytics,
anticoagulants, bleeding disorder

 Subarachnoid hemorrhage (SAH): Intracranial bleed into the CSF-filled space

between the arachnoid and pia mater membranes on the surface of the brain and
basal cisterns, bleeding into ventricular system
o Most frequent cause of SAH: aneurysm formation with leak, HTN
 Clinical Presentation:
 Change in LOC, seizures activity, HTN
 Severe Headache
 Change in LOC, neurological defect, and meningeal irritation signs
o Diagnosis: CT scan, lumbar puncture, MRI, cerebral angiogram
o Treatment:
o ABC’s
o Prevent/monitor clinical indications of increased ICP
o Prevent/monitor for delayed ischemia following SAH
o Identify vasospasm: 3-21 days
o Treatment of vasospasm
 Triple H Therapy: Calcium Channel Blockers
 Hypertension
 Hypervolemia
 Hemodilution
o This produces a fluid stent
o Procedures: surgical—clipping, wrapping, ligation: or endovascular
o Post-operative/procedure
o Monitor: vasospasm, re-bleeding, cerebral edema and increased ICP,
hydrocephalus, SIADH, seizures

 Overall Stroke Treatment Goals

o Minimize damage and maximize recovery
o Essential initial care: VOMIT
o Stabilize patient airway and breathing
o Optimization of cardiovascular function
o BP management—driving pressure to maintain perfusion
o Treatment of dysrhythmias
o Treatment of elevated ICP
o CV: dysrhythmias, AMI, 20% will have elevation of CK-MB Bands, and
diffuse ECG changes including ST-T segment depression
House-Fancher 36
 o Bronchial hygiene (pulmonary care)
o Monitor for seizures, hyperglycemia, nutrition, bowel function, DVT, pressure
sores, fever (33%), depression

 Spinal Cord Injury:

o Assessment:
 Clinical observation and presentation
 Overall assessment
 Respiratory function, sensory/motor function

 Spinal Shock: occurs within minutes and may last up to 3 months: T6 or higher
injury
o Classic finding: vasodilation with significant hypotension and bradycardia,
flaccidity, poikilothermy (loss of temperature regulation from hypothalamus)
o Diagnosis: CT scan, MRI
o Injury types: Brown-Sequard
 Hemisection cord injury
 Ipsilateral paralysis and loss of vibratory sense
Contralateral loss of pain and temperature sensation
o Management:
o ABC’s
o Prevent further damage to spinal cord
o Immediate immobilization
o Prevention of further edema
o Monitor and treat spinal shock: fluid and steroids
o Prevent/treat complications

 Autonomic Dysreflexia: After spinal shock is over

o Etiology: massive sympathetic discharge that cannot traverse the spinal cord
to communicate with the brain:
o Common noxious stimuli: full bladder, stool impaction, and skin pain
o Treat: eliminate cause—move patient, check bladder and bowel, anti-
hypertensives

 Status Epilepticus:
o Definition: sudden, paroxysmal episode of exaggerated activity
o Etiology: withdrawal symptoms, toxic levels of drugs
o Treatment: ABC’s, assess causes or contributing factors, protect patient from
injury, stop seizure activity, monitor and prevent complications, monitor and
document duration of seizure activity, fluid and electrolytes
 Prevent seizure activity, administer medications
 Obtain and monitor drug levels
 Fluid and electrolytes

House-Fancher 37
Behavioral

 Behavioral: abuse, antisocial behavior, delirium, dementia, developments delays,

failure to thrive, mood disorders, substance abuse

 Delirium: acute onset of mental status changes, and inattention and/or

disorganized thinking/altered level of consciousness
o Imbalance of neurotransmitters
o Risk: everyone
o 66-90%, onset ICU day 2—4 days, 10% remain delirious at time of discharge
o Associated with: increased length of stay, increased time on ventilator, higher
costs, increased mortality, 3-fold increase death at 6 months
o Treatment: identify etiology, modify risk factors, Haldol 2-10 mg IV every 20-
30 minutes, then 25% of loading dose every 6 Hours
o Monitor QT interval
o Develop a protocol, continued assessments, do not over-sedate, aspiration
precautions

 Dementia: loss of mental functions, not a disease, Alzheimer’s most common form

Delirium Dementia

Rapid Onset Slow Onset

Reversible Progressive
Irreversible
Worse Clinical Outcomes

 Depression: depressive disorder, negative thoughts, moods and behaviors

Treatment: SSRIs—Paxil, Zoloft, Celexa, Luvox and Lexapro
Second line: dual-action antidepressants: Effexor, Cymbalta
Atypical: Serzone, Desyrel, Wellbutrin, electroconvulsive therapy
Psychotherapies

Depression afflicts 1 in 6 Americans

Lifetime incidence
20% Woman
12% Men
More common in people with medical illness

 Substance Abuse: ETOH, drugs, withdrawal and stages of withdrawal:

benzodiazepines

House-Fancher 38
 Suicide: Are you planning of killing yourself? Steps to detect actual precautions

Points to remember
Suicide 4th leading cause of death in adults
Risk factors for suicide: dys-regulated impulse control,
propensity to intense psychological pain—
Hopelessness, mood disorders

NEUROLOGICAL PEARLS

 Multisystem effects of ICP

 Airway issues—pulmonary compromise

 ECG abnormalities—hemodynamics

 GI bleeding

 Effects of bed rest

 Temperature; regulated by hypothalamus

 Amicar: antifibrinolytic; used to prevent re-bleeding

QUESTIONS:

The patient suddenly becomes unresponsive as you are speaking to him, and develops
trembling of all extremities. Your priority is to:

A. Notify MD
B. Administer diazepam IV
C. Establish an airway
D. Perform a rapid neurologic check

The most common cause of subarachnoid hemorrhage is:

A. Aneurysms
B. Coagulopathy
C. Trauma from falls
D. Ischemia

House-Fancher 39
In a patient with increased intracranial pressure, cerebral perfusion pressure should be
maintained at:

A. 40 mmHg
B. 50 mmHg
C. 60 mmHg
D. 70 mmHg

The single most important index of neurologic state is the:

A. Level of consciousness
B. Pupillary reaction
C. Extremity movement
D. Vital signs

A patient is admitted to the ICU after sustaining a knife wound to the back. Assessment
findings include loss of pain and temperature on the right side and loss of motor
function on the left. Vital signs are stable and he is alert and oriented. No other
injuries are noted.
Based on the preceding information, which type of neurologic syndrome is likely to be
developing?

A. Central Cord
B. Brown-Sequard
C. Anterior Cord
D. Horner

Which of the following is a necessary immediate assessment for an injury of C3-C4?

A. Motor Ability
B. Heart Rate
C. Temperature
D. Ventilation

Which vital sign changes (due to loss of sympathetic nervous stimulation) would occur
after a spinal cord lesion about T5?

A. Bradycardia and hypotension

B. Bradycardia and hyperthermia
C. Tachycardia and hypotension
D. Hypertension and bradycardia

House-Fancher 40
Renal

 Regulation of homeostasis
 Production and release of hormones
o Aldosterone and Antidiuretic Hormone (ADH)
o Erythropoietin

 Renal Blood Flow

o Receives 20-25% of cardiac output
o Autoregulation maintains constant to protect glomerular filtration rate
(GFR)
o MAP 80-180 mmHg
o Filtration ceases with MAP less than 40 mmHg
 **Renal Function Assessment:
 Creatinine
 GFR
 Hourly urine output

 Renal Assessment
o Weight and fluid changes
o Serum osmolality: 275-295 mOsm/liter
o BUN/Creatinine Ratio 10:1
 BUN is elevated disproportionate to creatinine:
 Dehydration
 Catabolic state
 Blood in gut

 Pathophysiology
o Hypovolemia
 Tachycardia, orthostatic hypotension, low filling pressures, high systemic
vascular resistance, flat jugular veins, weakness, lethargy, anorexia, poor
skin turgor, thirst, low-grade fever, syncope, oliguria, increased BUN
with normal creatinine, high serum osmolality, increased H+H
 Hemo-concentration
o Management: return volume
o Hypervolemia
 Excessive fluid intake
 Retention of Na+ and water
 Stress response, steroid therapy, heart failure, liver failure,
nephrotic syndrome, acute or chronic renal failure
o Clinical presentation:
 Tachycardia, high blood pressure, high filling pressures, weight gain,
jugular vein distension, tachypnea, dyspnea, lethargy, apathy,
disorientation, indications of pulmonary or cerebral edema, low
hemoglobin, low serum osmolality, decreasing BUN with normal
creatinine

House-Fancher 41
 o Treatment
 Monitor intake + output
 Decrease excess volume
 Fluid restriction
 Diuretics
 Hemodialysis
 Prevent complications

 Acute Renal Failure:

o Definition: any sudden severe impairment or cessation of kidney function:

characterized by accumulation of nitrogenous wastes and fluid and electrolyte
imbalance

o Pre-renal Failure: disrupted blood flow to kidney

 Decreased intravascular volume
 Poor cardiac function with resultant decreased renal artery perfusion
 Renal artery stenosis
 Most common cause of renal failure in the progressive care unit patient

o Cortical: intra-renal damage to renal tissue: glomerulonephritis

o Medullary: acute tubular necrosis:

o Nephrotoxic drugs, prolonged ischemic injury, any causes of pre-renal
failure that is prolonged, diabetes
o Most common is the ICU patient

o Post-renal: disrupted urine flow

o Mechanical obstruction, functional obstruction: neurogenic bladder, diabetic
neuropathy
o Least common

House-Fancher 42
 Stages of Acute Renal Failure
o Onset: period of time from the precipitating event to beginning of oliguria/anuria
o Duration: hours to days
o BUN/Creatinine: normal or slightly increased
o Mortality: 5%

 Oliguric-Anuric Phase: when urine output is less than 400 mL/24 hours
o Duration 1-2 weeks
o BUN/Creatinine: elevated
o Mortality: 50-60%
o Metabolic Acidosis: water gain with dilutional hyponatremia, hyperkalemia,
hyperphosphatemia, hypocalcemia, hypermagnesemia, and azotemia

 Diuretic Phase: urine output is greater 400 mL/24 hours

o Duration: 1-2 weeks
o Urine Output: may increase to 3-4 liters/24 hours
o BUN/Creatinine stabilize
o Mortality: 25%
o Continues metabolic abnormalities with elevated potassium

 Recovery Phase: period of time between onset and when the lab values stabilize
o Duration: 3-12 months
o BUN/Creatinine: back to 100% baseline
o Mortality: 10-15%
o Metabolic processes gradually resolve

 Treatment of Acute Renal Failure:

o Goal of treatment: Support renal perfusion and improve GFR
o Volume
House-Fancher 43
 Inotropes
o
Administer diuretic challenge
o
Maintain fluid and electrolytes
o
Diminish accumulation of nitrogenous wastes
o
Prevent further damage to kidney
o
 Nephrotoxic agents
 Nutrition
o Prevent infection
o Monitor and treat anemia (Epogen)
 Management of Complications
o Renal failure increases overall mortality
o Chronic renal failure occurs in 25% of all patients with acute renal failure
o Cardiovascular system: dysrhythmias, hypertension, pericarditis, pulmonary
edema, heart failure
o Neurologic system: change in level of consciousness, coma, seizures
o Metabolic: electrolyte imbalance
o GI System: peptic ulcer disease, hemorrhage, anorexia, nausea/vomiting,
abdominal distention, pancreatitis, ileus
o Hematological system: anemia, uremic coagulopathies, increased WBC’s,
platelet dysfunction, infection, immunocompromised
o Pulmonary system: pulmonary edema, hyperventilation, acid-base imbalance
o Therapies:
 Dialysis: semipermeable membrane, blood/dialysate
 Types: peritoneal, hemodialysis, continuous renal replacement therapy

Acute Renal Failure

Pre-renal Acute Tubular Necrosis

Urine Na+ < 20 Urine Na+ > 40-100

BUN/CR >20:1 BUN/CR 10:1
Fluid + Lasix Urine Fluid + Lasix NO Urine

Chronic Renal Failure: slowly progressive disease that causes gradual loss of kidney
function, progressive over years, asymptomatic.
 Incidence: 2 out of 1000 people in US. DM and HTN two most common causes and
account for most cases. Other causes: HF, hypotension, glomerulonephritis, kidney
stones, obstruction
 Course:
 Ability to concentrate urine declines early
1. Inability to excrete phosphate, acid and potassium
2. Ability to dilute urine is lost
3. Plasma concentrations of creatinine and urea rise
4. Progression continues: abnormal Ca++, phosphate, parathyroid hormone, vitamin D
metabolism, renal osteodystrophy occur, secondary hyperparathyroidism is
common
 Symptoms
 Fatigue: anemia, frequent hiccups, general ill feeling, generalized itching

House-Fancher 44
 (pruritus), headache, nausea/vomiting, unintentional weight loss
 Late symptoms: hyper-vomiting, confusion, decreased sensation in hands and
feet, easy bruising, increased or decreased urine output, muscle twitching,
cramps
 Diagnosis: UA, creatinine, creatinine clearance, potassium, metabolic acidosis,
CT scan, abdominal MRI, ultrasound, renal biopsy

End-Stage Renal Disease: 90% of nephrons damaged, patient now requires artificial
support to sustain life
 Treatment: Goal: control symptoms, reduce complications, and slow the progress of the
disease
 Fluid restriction, diet control, blood pressure control, diabetes control,
vitamin D supplements, drug monitoring, dialysis??
 Control blood sugar
 Control blood pressure
 Medications: dose and range
 Nutrition: moderate protein restriction

RENAL PEARLS

 Seizures are seen with hyperphosphatemia

 Signs and symptoms of hypophosphatemia: weakness, reciprocal

hypercalcemia, apathy and confusion

 Creatinine is best indicator of renal function

 Creatinine is inversely proportional to GFR

 Low serum sodium causes aldosterone release

 Know the electrolytes: remember additional material at end of book

 Know all the electrolytes for all the systems!

QUESTIONS

Mr. J., age 24, boxes on the weekends and has sustained blunt trauma to the left kidney
during a boxing match. Which of the following indicates renal trauma?

A. Severe flank pain and diaphoresis

B. Hematuria and flank tenderness
C. Urethral bleeding
D. Side pain and hemoptysis

House-Fancher 45
A patient with chronic renal failure asks the nurse why he is anemic. The nurse
explains that anemia accompanies chronic renal failure due to:

A. Blood loss via the urine

B. Renal insensitivity to Vitamin A
C. Inadequate production of Erythropoietin
D. Inadequate retention of serum iron

The primary etiology of hyperphosphatemia is:

A. Over-replacement
B. Hypercalcemia
C. Renal failure
D. Hypoalbuminemia

Bradycardia, tremors and twitching muscles are associated with which electrolyte
disorder?

A. Hypokalemia
B. Hyperkalemia
C. Hypophosphatemia
D. Hyperphosphatemia

Hyponatremia is usually associated with:

A. Fluid overload
B. Dehydration
C. Diuresis
D. Over-administration of normal saline

House-Fancher 46
 Pulmonary

 The purpose of the heart is to drive hemoglobin to the cell

 The purpose of the lungs is to oxygenate and ventilate that hemoglobin
 The heart and lungs work together: cannot separate the functions

 To oxygenate and ventilate the hemoglobin, 3 things must be working well:

o Brain: controls the rate and character of respiration

 Neural control by the medulla
 Chemical control: pH of cerebrospinal fluid
 Peripheral chemical control – chemoreceptors at the bifurcation of the
internal and external carotid bodies
o Bellows: the thoracic cage: neuromuscular pathways,
o Muscles of respiration,
 Diaphragm, intercostals, and accessory muscles
o Rib cage, sternum and spine—boney cage
o Alveolar-capillary Membrane (AC Membrane)—where respiration occurs

The The
Right Left
Ventricle Ventricle

House-Fancher 47
Alveolar Structure and Function

Ventilation and Perfusion: The Match

 Important concept in pulmonary medicine: matching ventilation (gas in the
alveolar sac) and perfusion (blood in the capillary associated with that alveoli)
 The goal is to have gas in the alveoli and blood in the capillary bed so that:

Ventilation (V) and Perfusion (Q) Match

A
Normal V/Q
in the upright
lung

B
In supine
position V/Q
is
mismatched

C
In exercise,
perfect V/Q
matching

House-Fancher 48
 Ventilation/Perfusion Matching/Mismatching

Normal V/Q Matching

The The
Right Left
Ventricle Ventricle

Abnormal Matching

The
Right The
Ventricle Left
Ventricle

What can cause this situation?

 Great ventilation, poor perfusion

 Perfusion problems: low right ventricle cardiac output, low volume status, and
pulmonary emboli

House-Fancher 49
 Abnormal Matching

The The
Right Left
Ventricle Ventricle

 What can cause this?

 Great blood flow, poor ventilation
Collapse of alveoli, mucous plug, and fluid, foreign body

Remember the goal is to have V/Q Matching: keep alveoli open and capillary open with
flow: so:
 Keep alveoli open: recruitment---incentive spirometer, or PEEP
 Keep the capillary open: recruitment--good right ventricle function, volume
status, pulmonary artery pressures

House-Fancher 50
 Oxy-Hemoglobin Curve: Demonstrates the Relationship of Oxygen to Hemoglobin

What’s Important?

The relationship of
shifting the curve to
the left: oxygen is
not disassociated
from the hemoglobin

Pulmonary Assessment: VOMIT

 Respiratory rate and rhythm, oxygen saturations, tracheal deviation, breath sounds
 Tracheal Deviation: the trachea moves away from increasing air, and toward
increasing fluid
 Tension Pneumothorax: trachea moves away from pneumothorax
 Pleural Effusion: the trachea moves toward the effusion, or pneumonia
 Breath Sounds

Pulmonary Exam
ABG
Chest X-Ray

ABG Interpretation
 Steps to review ABG:
o Is pH acidotic, normal, or alkalotic?
o Which parameter is abnormal?
 Respiratory or Metabolic
o Is pH normal or not? -If normal with abnormal CO2 or metabolic abnormality
compensated
o Assess oxygenation
o Assess metabolic pathway

pH 7.55 7.21
CO2 28 28
O2 88 97
House-Fancher 51 Bicarb 24 14
ETCO2 Monitoring

Pulmonary Hypertension (PAH):

 Primary PAH: primary lung disorder, rare—usually in young women, pressure in

the lung circulation is high with a Mean PAP of greater than 25 mmHg at rest and
greater than 30 mmHg during exercise
o Causes: Raynaud’s Disease, appetite suppressants, cocaine, HIV infection
o Symptoms: fatigue, dizziness, Right heart failure symptoms (leg edema,
shortness of breath), pulmonary failure
o Treatment: underlying disease and to lower the pulmonary pressures
 To the catheterization lab to measure pressures and oxygenation in
each chamber
o Measure response to oxygen supplementation
 If responder: place on home O2 at night
 If does not respond to oxygen therapy: Calcium Channel Blockers
IV prostacyclin, endothelin receptor antagonists, and/or
transplantation

--
 Secondary PAH: other reasons for pulmonary pressure increases, much more
common, what we see every day in critical care
o Pulmonary emboli
o Heart Failure,
o Obstructive Sleep Apnea (OSA)
o Hypoxia
o HIV Disease
o Valvular Disease
Treatment: Underlying disease

Anything that affects the lung tissue and increases pulmonary pressures, causes
increased right ventricular work load—afterload—cor pulmonale

Lung Abnormalities

 Obstructive: inability to exhale lung volume, air trapping, prolonged exhalation time,
barrel chest
o Asthma
o Chronic Bronchitis
o Emphysema

House-Fancher 52
  Restrictive: inability to inhale volumes, chest wall abnormality and/or lung tissue
abnormality
o Structural abnormality: chest wall restriction, muscle
o Atelectasis
o Pneumonia
o Pneumothorax
o Pulmonary edema
o Pulmonary fibrosis
o ARDS
o Obesity

Acute Respiratory Failure: Pulmonary system is no longer able to meet the metabolic
Hypoxemia: PaO2 less than 50
Hypercapnia: PaCO2 greater than 50

Hypoxia: V/Q mismatch is primary cause of hypoxia in critical care patient

Shunt Effect: De-recruiting
Treatment: Recruit the alveoli open: Incentive Spirometer: for the patient on
mechanical ventilation the recruitment tool is PEEP
Assessment of Hypoxia:
Tachycardia and dysrhythmias
Dyspnea
Restlessness-confusion-lethargy-coma
Accessory muscle use
Cyanosis

Hypercapnia: Abnormality of alveolar minute ventilation

Tidal Volume (Vt), dead space and frequency (f) of ventilation

Alveolar Minute Ventilation = Vt – Dead Space X Frequency

In reality, at the bedside, the equation is

Alveolar Minute Ventilation = Vt X f

Hypercapnic Failure:

Causes:
Central Nervous System Depression (brain injury or drugs)
Neuromuscular Problem
Abnormalities of chest wall (restriction)
Abnormalities of gas flow in airways (obstruction)
Increased Dead Space (air that sees no blood—pulmonary emboli)
Increased CO2 production (seizure activity, increased work of breathing)

Assessment: tachycardia and dysrhythmias, Bradypnea, irritability, inability to

concentrate, somnolence, headache
Treatment: improve Vt and/or the rate

House-Fancher 53
Assessment of Acute Respiratory Failure: altered mental status, increased work of
breathing, and signs of stress-catecholamine release

Airways Management of Acute Respiratory Failure

Cannula 40% Oxygen supplementation
Simple Mask 40-60% Tracheal Intubation and Mechanical Ventilation (MV)
Partial Rebreather 60-80% Pharmacologic Adjuncts:
Nonrebreather 100%
NPPV 40-100% Beta2 agonist
Anticholinergic agents
Corticosteroids
Antibiotics

Mechanical Ventilation (MV) Indications:

Strategies of Ventilation
Indications for MV
AC and SIMV
Clinical or laboratory signs that the patient cannot
BASIC VENTILATOR
FIO2 maintain an airway
FREQUENCY Adequate oxygenation or ventilation with
VT A RR greater than 30breaths/min
FLOW: PRESSURE Maintain arterial O2 saturations > 90% with
PIP
FiO2 > 60%
MAP
Increased CO2 >50 mmHg with pH<7.25
Ventilatory Failure
Reduced respiratory drive
Chest wall abnormalities
Respiratory muscle weakness
Inefficient Gas Exchange
Intrapulmonary Shunt
Ventilation-perfusion mismatch
Deceased FRC
AACN’s Indications for MV
Acute ventilatory failure with acidosis
Hypoxemia despite adequate oxygen therapy (ARDS)
CO2 retention
Apnea

Prove Beneficial
Decrease systemic and/or MVO2
Permit sedation
Reduce intracranial pressure
Prevent atelectasis
Secure airway

House-Fancher 54
 Types of Ventilators: Positive Pressure
 Inspiration: created with positive pressure
 Expiration: passive
 Classification: pressure-cycled, volume-cycled
 Ventilator strategies per patient disease process
 Goals of mechanical ventilation:
 Reduction in work of breathing
 Assurance of patient comfort
 Synchrony with ventilator
 Adequacy of ventilation and oxygenation
 Airway protection

Three main strategies today: lung protective ventilation

Protect the lung: low tidal volume
Recruit the alveoli: PEEP
Perfuse the lung: right ventricle is filled and contracting

Strategies of Ventilation
 Improve oxygenation: PEEP
 Physiologic: 3-5 cm H2O
 Actions: improves the PaO2 without increasing FiO2, decreases surface
tension, decreases intrapulmonary shunt
 Uses: severe hypoxemia, ARDS, drowning, sepsis, Acute Respiratory Failure
 Adverse effects: hemodynamic changes, baro-biotrauma
 Contraindications: ???

 Improve removal of CO2: Improve Ventilation

 Frequency
 Tidal volume
 Flow Rate: compliance and alveolar recoil

 Basic guideline:
o Initial intubation—use ACLS protocols
o FiO2 100%, then wean to keep O2 saturation at predetermined
percentage
o Initial Vt 5-10mL/kg of IBW (ideal body weight): ARDS 4-
6mL/kg IBW
o Respiratory rate: determined by pH and PaCO2
o Add PEEP: diffuse lung injury and reduce FiO2

 Assessment of patient with mechanical ventilation

 Physical assessment: chest excursion, breath sounds, type of airway,
ventilatory mechanics
 Pulse oximetry: ABG’s, chest X-ray
 System review:
o Cardiovascular: hear rate, rhythm response to positive pressure ventilation
o Hemodynamic response
o Neurologic

House-Fancher 55
 o Renal and metabolic
o Gastrointestinal: bowel sounds, feeding, distention, and prevention of
aspiration
o Immunologic
o Psychological

 Complications of mechanical ventilation

o Decreased cardiac output
o Fluid retention
o Baro-biotrauma
o Atelectasis, hyper-hypocapnia, oxygen toxicity, aspiration, GI effects,
infections, asynchrony, anxiety, inability to wean from ventilator

 Post Extubation:
o Complications: remember the ABC’s
o Hoarseness
o Difficulty swallowing, risk of aspiration
o Severe glottic edema leading to post-extubation stridor and obstruction

Acute Respiratory Distress Syndrome (ARDS)

 Definition: syndrome of acute respiratory failure characterized by noncardiac
pulmonary edema and manifested by refractory hypoxemia caused by
intrapulmonary shunting
 Risk factors: direct and indirect lung injury
 Pathophysiology:
 Injury to alveolar-capillary membrane
 Inflammatory release of mediators that cause complex reaction of tissue
edema, movement of fluid to the alveolar spaces, production of clot formation
in the pulmonary vessels
 Results in fluid in the alveolar space and obstructed blood flow

NO gas, NO blood

House-Fancher 56
 Clinical Presentation: severe oxygen defect
o Signs and symptoms of hypoxia
o Chest X-ray: diffuse bilateral infiltrates
o Static compliance: stiff lung disease
o Hemodynamics: remember this is a lung problem not a left heart problem
 Acute elevation of PAP—with normal wedge (this depends on age of patient
and other problems that may be present—such as, COPD and left heart failure),
acute right ventricular failure
o ABG’s: acute hypoxemia unrelieved with oxygen therapy
o Low lung volumes: Vt and FVC are low
 Treatment: Goal is to restore oxygenation: Improve delivery and reduce demand
o Maintain airway and ventilation
o Mechanical ventilation: low Vt and high PEEP
o Decrease intra-alveolar fluid: diuresis if possible (remember the right
ventricle)
o Hemodynamic monitoring
o Inotropes as indicated by cardiac output
o Decrease pulmonary hypertension
o General support

House-Fancher 57
 Pneumonia: Definition: acute infection of the lung parenchyma, including alveolar
spaces and interstitial tissue
o Etiology
o Predisposing factors: general condition, mouth health, and immunologic
system
o Diagnosis
 Fever
 WBC
 Sputum
 Chest X-ray
 Increased Respiratory Rate
o Treatment: PREVENTION
 Maintain airway, oxygenation and ventilation
 Positioning—turning
 Organism-specific antibiotics
 Hydration
 Bronchial hygiene
 Bronchoscopy
 Mechanical ventilation
o Complications: Death
 Acute respiratory failure
 Pleural effusion
 Empyema
 Septic shock

 Aspiration Pneumonia: Definition: lung injury related to the inhalation of stomach

contents, saliva, food, or other foreign material into the tracheobronchial tree
o Pathophysiology: oropharyngeal secretions are most common
o Risk Factors: altered consciousness and/or gag reflex
 Anesthesia, CNS disorder, altered anatomy, GI conditions
(hiatal hernia and vomiting), prolonged intubation, Enteral nutritional
support
 NG tube
 Position
 Residual contents

 Status Asthmaticus: Definition: recurrent, reversible airway disease characterized

by increased airway responsiveness to a variety of stimuli that produce airway
narrowing.
o Status: exacerbation of acute asthma not relieved after 24 hours of maximal
therapy
o Management:
 ABC’s
 Oxygen
 Bronchodilators—short acting—Albuterol
 Anticholinergics
 STEROIDS

House-Fancher 58
Pulmonary Embolism: Definition: obstruction of blood flow to one or more arteries of
the lung by a thrombus lodged in a pulmonary vessel: fat, air, amniotic fluid, tumor,
foreign body
o Etiology: hypercoagulability, alteration in vessel wall, venous stasis
o Pathophysiology: 90% of pulmonary emboli develop in deep veins of lower
extremities—DVT
o Clinical presentation: the great pretender
 Anxiety, dyspnea, tachypnea, tachycardia, chest pain, cough, feeling
of impending doom, fever, hemoptysis, mental status clouding,
cyanosis, hypotension, pulseless electrical activity

o MOST COMMON
o Symptoms: Dyspnea, pleuritic pain, cough
o Signs: Tachycardia, rales

o Hemodynamics:
o High PAP
o High CVP
o Low to normal PCWP (PAOP)
o Low to normal cardiac output
o ECG dysrhythmias: tachycardia, atrial fibrillation
o Heart blocks
o Tall, peaked P-waves, (P-pulmonale)
o New development of bundle branch blocks
o R axis deviation, and right ventricle strain pattern (Right BBB)
o Diagnostics:
o ABG, chest X-ray, ECG, Echo
o V/Q scan
o CT Scan with PE protocol (spiral CT scan)
o Pulmonary angiography

o Treatment: Prevention (DVT prophylaxis)

o Acute:
 ABC’s
 Diagnostics
 Restore circulation and oxygenation
 Arrest thrombus: baseline clotting profile, fibrinolytic therapy if
candidate
 Heparin therapy
 Oral anticoagulants: Coumadin 3-6 months
 Pulmonary embolectomy
 Surgical interruption of IVC: filter

o Complications; pulmonary infarction, cerebral infarction, myocardial

infarction, right ventricle failure, hepatic congestion, pneumonia, empyema,
pulmonary abscess, acute respiratory failure, DIC, hemodynamic compromise,
bleeding secondary to treatment, death

House-Fancher 59
Chest Trauma: Flail Chest

TENSION PNEUMOTHORAX

House-Fancher 60
Pulmonary Pearls

 Asthma: ominous sign is absence of wheezing, increased CO2

 Low CO2 and O2 with ARDS does not improve with oxygen therapy due to

shunting, treatment low Vt and high PEEP

 Ventilatory Adjuncts:
 Aerosol treatment: bronchodilators and mucolytics
 iNO, helium, prone position, rotational beds
 IV Magnesium: acts as bronchodilator, decreases inflammation, 2 gm IV,
effective with respiratory failure

QUESTIONS

The hallmark of acute respiratory distress syndrome is:

A. Refractory hypercapnia
B. Refractory hypoxemia
C. Low functional residual capacity
D. Increased compliance

The most common ECG changes that occur during pulmonary embolus are:

A. Q-waves in AVR and Lead I

B. Tachycardia and atrial fibrillation
C. Bradycardia and ST-segment depression
D. High-degree AV Block

House-Fancher 61
The principle contributing factors to venous thrombosis include all of the following
EXCEPT:

A. Atrial fibrillation
B. Stasis of blood flow
C. Endothelial injury or vessel wall abnormality
D. Hypercoagulability

Which of the following features of pleural drainage systems indicates an active pleural
leak?

A. Bubbling in the water-seal chamber

B. Bubbling in the suction control chamber
C. Fluctuation of water level in the water-seal chamber with respiration
D. No fluctuation of water level in the water-seal chamber with respiration

Which type of condition can lead to a tension pneumothorax?

A. Closed pneumothorax
B. Open pneumothorax
C. Subcutaneous emphysema
D. Pneumomediastinum

You are helping another nurse to move a patient up in bed when the low-pressure alarm
on the ventilator goes off. It also indicates a low tidal volume. The patient is becoming
short of breath and his SpO2 has dropped from 0.95 to 0.84. The PETCO2 waveform is
absent. The endotracheal tube appears to be in place and there is no obvious
disconnection from the ventilator. The other nurse goes to call respiratory therapy.
What should you do?

A. Increase the Vt on the ventilator while instructing the patient to remain calm
B. Increase the FiO2 on the ventilator while instructing the patient to remain calm
C. Remove the ventilator and begin manual respiration (Ambu bag)
D. Increase the ventilator respiratory rate and peak flow

The major signs and symptoms of acute respiratory failure include:

A. Increased respiratory rate, tachycardia, change in mental status

B. No change in respiratory rate, tachycardia
C. The major sign is the compliant of shortness of breath
D. There are no early signs of respiratory failure.

House-Fancher 62
Additional Summary Slide of Failure to Oxygenate

House-Fancher 63
Multisystem Failure

MSOF: Multisystem Organ Failure—MODS: Multisystem Organ Dysfunction Syndrome

Shock: Malperfusion

 Shock: Definition: Condition of insufficient perfusion of cells and vital organs,

causing tissue hypoxia, perfusion is inadequate to sustain life—results in cellular,
metabolic and hemodynamic derangements
o Malperfusion
o MSOF/MODS

 Systemic Inflammatory Response Syndrome: the systemic response to a variety of

insults that begin as local inflammation
o Collection of immune-mediated responses to infections, foreign materials,
tissue ischemia and reperfusion injuries

 The Inflammatory Cascade

o Clinical Presentation:
o Criteria: 2 or more of the following
o Tachycardia (>90)
o Hyperpnea (RR>20/minute or PaCO2 <32mmHg)
o Hypothermia (<36⁰C) or hyperthermia (>38⁰C)
o WBC >12,000 or <4,000

 Definitions:
Fever + Leukocytosis = SIRS
SIRS + Infection = Sepsis
Sepsis + MODS = Severe Sepsis
Severe Sepsis + Refractory Hypotension = Septic Shock

Classifications of Shock

 Hypovolemia: caused by inadequate intravascular volume: external or

internal losses
 Cardiogenic: caused by impaired ability of heart to pump blood: contractility,
filling and/or emptying
 Distributive or vasogenic: caused by massive vasodilatation caused by release
of mediators of inflammatory process in response to overwhelming infection,
allergy, or neurogenic cause: septic, anaphylactic, and neurogenic shock

 Important to remember:
o Preload
o Afterload
o Contractility
o Heart rate
o Perfusion

House-Fancher 64
House-Fancher 65
Treatment:

Cardiac: fix the pump

 Oxygen
 Drugs: preload, afterload, and contractility
 IABP

 What does this patient look like: VOMIT

o Treatment of cardiogenic shock
 Decrease preload
 Decrease afterload
 Increase contractility

Hypovolemic: Volume Loss

o Etiology of loss: Stop the loss

 Classes of Hypovolemia
I. 750-1500 mL loss ↑HR, narrow pulse pressure, ↓ urine output
II. 1500-2000 mL loss ↑HR, ↑RR, ↓BP, LOC change, ↓urine output
III. 2000 mL loss or greater ↑HR, shallow respirations, obtunded, anuria
IV. Exsanguination

 Specific to Hypovolemia: ABC’s

o Volume resuscitation
o Treat the cause: stop fluid loss, restore intravascular volume
o Inotropes: after volume is restored
o Utilize mechanical support

Anaphylactic
 Remove the offending agent, antigen
 Maintain a patent airway (ABC’s)
 Volume resuscitation
 Modify or block the effects of biochemical mediators
 Administer sympathomimetic:
o Epinephrine
o Antihistamines
o Bronchodilators
o IV Steroids

Neurogenic
 Spinal Cord immobilization
 Warming measures
 Maintain MAP: Fluid resuscitation
 Prevent venous stasis
 Volume replacement
 Monitor for complications of shock, or other reasons for shock
 Steroids

House-Fancher 66
Septic
 Prevent infection
 Avoid NPO Status
 Antibiotic Therapy
 Control Hyperthermia
 Volume Status

Management of Septic Shock

ID Infection

Maximize O2 Delivery Minimize O2 Consumption

Fluids Mechanical ventilation
Vasopressors Monitor SvO2
Maintain Hct >30% Control temperature & electrolytes
Inotropes Nutritional status
Control pain and anxiety
Prevent complications

QUESTIONS:

One of the most effective therapies in the treatment of sepsis is:

a. Early antibiotic therapy

b. Early treatment with multiple cardiac inotropes.
c. Early treatment with mechanical ventricular assistance
d. No treatment has been shown to be successful

In the treatment of shock, the team should:

a. Promote oxygenation and ventilation

b. Enhance oxygen delivery
c. Decrease oxygen consumption
d. All the above

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Helpful Web Sites

 www.aacn.org

 www.theheart.org

 www.sccm.org

 www.guideline.gov

 www.lungusa.org

 www.medscape.com

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Reference: Material

Electrolyte Abnormalities:

Potassium (3.5-5 mEq/L)

1. Acquired in diet, excreted in urine, must be replaced daily

2. Major intracellular cation
3. Functions:
a. Maintains osmotic pressure inside cells
b. Maintains electrical potential
c. Maintains acid/base balance
d. Participates in metabolism

4. Hyperkalemia
a. Common causes:
i. Renal failure
ii. Over-replacement
iii. Cell damage / shift out of cells
1. Acidosis
2. Hemolysis
3. Sepsis
4. Chemotherapy
iv. Spironolactone administration
b. Manifestations
i. Bradycardia
ii. Tremors, twitching
iii. Nausea / vomiting
iv. EKG changes: ( K+ suppresses the SA node)
1. Peaked T-waves
2. Shortened S-T segment
3. Flattened P-wave
4. Long P-R interval
5. Blocks
6. PVC’s, ventricular arrhythmias
c. Treatment
i. Kayexelate
ii. Insulin / glucose
iii. Dialysis
iv. HCO3, Ca++
v. Albuterol aerosol

If a patient is NPO, he will require 40 mEq of potassium per day to

maintain his potassium level. 200 mEq or more may be required to
replace lost stores.

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 5. Hypokalemia (aLKylosis is associated with a Low K+)
a. Common causes:
i. Poor intake
ii. Renal loss
1. Diuretics
2. Renal tubular acidosis
3. Gentamycin, Amphotericin
iii. GI loss
1. Diarrhea
2. Vomiting
iv. Shift into cells
1. Excessive insulin administration in DKA
2. Alkalosis
b. Manifestations
i. Tachycardia
ii. Hypotension
iii. Flaccid muscles
iv. EKG changes:
1. Flattened T-waves
2. Long S-T segment
3. U-waves
4. Peaked P-wave
5. Long P-R interval
6. PVC’s, ventricular arrhythmias
c. Treatment
i. Oral replacement is preferable (allows slower equilibration with
intracellular compartment)
ii. IV: no faster than 20 mEq/hour
6. Testing Implications:
a. Potassium levels change inversely to serum pH
b. Opening and closing the fist with a tourniquet in place  K+ level
c.  K+ can lead to digoxin toxicity

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Calcium (8.4-10.2 mg/dl)

1. Ionized (active fraction)

2. Inactive fraction (bound to albumin)
3. Adjusted calcium level
a. [(4-Alb) X 0.8] + Calcium = Adjusted calcium

4. Essential for the functioning of:

a. Neuromuscular activity
b. Integrity of cell membrane Chvostek’s sign:
c. Cardiac activity  Tap the facial nerve just
d. Blood coagulation below the temple
5. Increases in PTH,  Ca++ level  Twitch of the lip or nose is a
6. Hypercalcemia positive sign
a. Etiology:
i. Hyperparathyroidism Trousseau’s sign:
ii. Paget’s disease  Contraction of the hand or
iii. Excessive Vitamin D intake fingers when arterial flow is
b. Manifestations occluded for 5 minutes.
i. Anorexia, nausea, vomiting
ii. Coma
iii. Acute renal failure
iv. Flaccid muscles
v. EKG changes
(1) Short S-T
(2) Short Q-T
(3) Steep drop off of T-wave
c. Treatment
i. Fluids / Lasix
ii. Oral or IV Phosphate

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 7. Hypocalcemia
a. Etiology:
i. Surgical Hypoparathyroidism
ii. Malabsorption
iii. Acute pancreatitis
iv. Renal failure
v. Vitamin D deficiency
vi. Hypoalbuminemia
vii. Excessive administration of citrated (banked) blood
b. Manifestations
i. Laryngeal spasm
ii. Seizures & muscle cramps
iii. Hypotension
iv. Hyperactive reflexes
v. Trousseau’s sign
vi. Chvostek’s sign
vii. EKG changes:
(1) Prolonged Q-T interval
(2) Flat S-T
(3) Small T-wave
c. Treatment
i. Oral route is safer
ii. IV: 10-20 mL of 10% calcium gluconate over 5-10 minutes
iii. Monitor EKG during treatment
8. Implications:
a. Ionized calcium level is inversely proportional to serum pH
b. Serum Ca++ levels should be assessed in conjunction with serum albumin
levels

Magnesium (1.5-1.95 mEq/L)

1. Intracellular enzymatic reactions and utilization of ATP

2. CNS transmission
3. Cardiovascular tone Magnesium is cardio-
4. Hypermagnesemia (rare) protective, and may be given
a. Etiology to a patient with myocardial
i. Renal disease infarction even if the Mg++
ii. Adrenal insufficiency level is normal.
b. Manifestations
i. Flushing and hypotension
ii. Hypotension & bradycardia
iii. Respiratory depression
iv. Hypoactive reflexes
v. CNS depression

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 c. Treatment
i. IV calcium: 10-20 mL of a 10% calcium gluconate
ii. Mechanical ventilation
iii. Temporary pacemaker
iv. Dialysis
5. Hypomagnesemia (common electrolyte disorder)
a. Etiology
i. Chronic renal failure
ii. Pancreatitis
iii. Hepatic cirrhosis
iv. GI losses
v. Alcoholism
vi. Treatment of DKA
b. Manifestations
i. Increased reflexes
ii. + Trousseau’s sign
iii. + Chvostek’s sign
iv. Tachycardia
v. EKG changes:
1. P-R & Q-T prolongation
2. Widened QRS
3. S-T depression
4. T wave inversion
vi.  K+,  Ca++,  PO4 -
c. Treatment:
i. Dietary replacement
ii. IV magnesium acts as a vasodilator (expect flushing and hypotension)
1. Acute hypomagnesemia
a. 1-2 grams IV over 60 minutes
2. During a code for VT/VF
a. 1-2 grams IV push (over 1-2 minutes)
6. A 24-hour urine magnesium level may be helpful in assessing deficiency

Phosphorus (2.5-4.7 mg/dl)

1. Phosphorus is an important part of all body tissue

2. Phosphate has a marked diurnal variation; therefore single measurements are of
little use.
3. Mostly stored intracellular
4. Phosphate is cleared by the kidney; therefore renal function must be monitored as
well.
5. Hyperphosphatemia
a. Etiology
i. Renal failure
ii. High PO4 intake
iii. Chemotherapy
iv. Lactic acidosis

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 b. Manifestations
i. Most often is asymptomatic
ii. Numbness, tingling of hands and mouth
iii. Muscle spasms
iv. Precipitation of Ca++ salts can lead to hypocalcemia
c. Treatment
i. Treat underlying disorder
ii. Phosphate-binding agents (Amphogel)
iii. IV fluids
iv. D50 & insulin
v. Dialysis
6. Hypophosphatemia
a. Etiology
i. Re-feeding syndrome (re-feeding after severe malnutrition)
ii. Calcium and magnesium deficiency
iii. Acute respiratory disorders
iv. Alcoholism
v. DKA, insulin administration

Acute
Respiratory
Disorder
Hypophosphatemia

Acute
Respiratory
Distress

b. Manifestations
i. Hemolysis & anemia
ii. Muscle pain & weakness
iii. Respiratory muscle weakness
iv.  LOC, paresthesias
c. Treatment
i. Treat the primary disorder
ii. Nutrition
iii. Oral or IV replacement
7. Sudden  in serum PO4 level during treatment can cause hypocalcemia
8. Introduce nutrition gradually to the malnourished patient
9. Phosphorus levels are inversely related to Ca++ levels
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Imbalances in Sodium and Water

Sodium (135-145 mEq/L)

a. Most important ion in maintaining extracellular fluid balance

b. Balance is controlled by CNS & endocrine systems
c. Imbalance will result in fluid shifts and edema or dehydration

d. Osmolality = 2 X Na+ + Glucose / 18 + BUN / 2.8

e. Blood osmolality is normally 280-300 mOsm/kg H2O
f. Maximum daily sodium load is 400 mEq/day (0.9% NaCl @125ml/hour
provides 465 mEq/day)
g. Hyponatremia is more common
h. Hypernatremia has 40-60% mortality

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 2. Normal volemic states
a. Hypernatremia ( TBW, near normal TBNa)
i. Etiology:
1. Diabetes Insipidus (lack of response to ADH)
2.  insensible losses without replacement of water
ii. Signs and symptoms:
1. Thirst
2. CNS depression
iii. Treatment:
1. Water replacement
2. ADH for diabetes insipidus

b. Hyponatremia
i. Etiology:
1. Water ingestion > 25 L/day
2. Defect in renal diluting ability
3. Post-operative fluid administration / non-osmotic ADH release
4. Drugs:
a. NSAIDS
b. Oxytocin
ii. Signs and symptoms:
1. Edema
iii. Treatment:
1. Water restriction
2. Sodium replacement
3. General Management Principles:
a. Hyponatremia:
i. Mild (Na+ <120)
1. Usually asymptomatic
2. Treat underlying cause
ii. Moderate (Na+ <115)
1. CNS depression
2. Replace with 0.9% NaCl
3. Fluid restriction (<1000cc/day)
iii. Severe (Na+ <110)
1. Coma, seizures, and death
2. Replace with 0.9% NaCl or hypertonic saline (3%)
3. Do not  serum Na+ by more than 1 mEq/L/hour or
10 mEq/L/day.

Free Water Deficit = (kg weight. X 0.6) X [(Na/140) – 1]

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 The Test and Test Taking Strategies

 After you sign in at the testing center with your authorization number, you will go
to the testing area.

 When you sit at the computer and enter your authorization number, the computer
will take your picture. Smile :)

 There will be several pre-test questions, only to orient you to the computer system.

 When completed, you will be asked if you are ready to begin—answer YES.

 The test will then begin as well as the timer.

 The entire test is randomized—all systems are randomized throughout the entire
exam

 You must complete the entire exam: this is NOT like the boards, you must answer
each question (you cannot complete the test in fewer questions if you are doing
well)

 As you are taking the exam, please answer each question.

 You will receive a piece of paper and pencil as you enter the test, you may write
anything you wish on the paper. It is your paper for the test; it will be turned
back in to the proctor at the end of the exam.

 If you cannot answer a question, do not spend too much time, skip it and move on
to the next question. You are able to go back and answer the question at any time.

 Answer each question, even if you must eliminate and guess.

 Do not leave any question blank, answer each one.

 After you finish, there is a short post-test questionnaire. When completed you will
leave the test area. There will be a fax for you from AACN with your total score, %
in each category and if you passed or not. Your picture will be in the top right
corner.

 As you answer the questions remember:

o You must answer each question
o The test will NOT click you out if you are doing well or poorly—you must
take each and every question
o The test is timed, do not spend too much time on any single question

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Types of Questions: Three major types

 KNOWLEDGE: a simple question with only one answer

Drugs that have a positive inotropic action are effective because they increase:
A. Myocardial contractility
B. Systemic vascular resistance
C. Apical pulse rate
D. Pulmonary compliance

• (Answer A): The test is just looking for the definition of inotropic. These are the
easy questions you will fly through them. Careful though, read each word……

 APPLICATION/ANALYSIS: more in-depth question that may require analysis of data

 (Answer: B) Here, the test is looking for you to analysis the lab data.

SYNTHESIS AND EVALUATION: This type of question is more complex and may ask
about signs and symptoms and treatment plans.

Patient is admitted to ICU after an accident in which he inhaled methane gas. He is

producing large amounts thin, pink, frothy sputum and is intubated with 10cm PEEP.
PIP (peak inspiratory pressure) suddenly increases; blood pressure decreases, heart rate
increases and breath sounds are unequal. Pulse oximetry decreases.

Which of the following conditions would most likely explain the patient’s signs and
symptoms?
A. Pulmonary embolus
B. Cardiac tamponade
C. Pneumothorax
D. Hemothorax

• (Answer: C): The test question has nothing to do with inhaled methane gas—this
is the distractor. The question is what is one of the complications of mechanical
ventilation with a PEEP of 10 cmH2O.

 Do not study the day of the exam.

 Answer each question: if you do not know, eliminate and pick the best answer—

even if you have to guess.

 Study the electrolyte lecture the night before the exam only.

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  Be prepared to be at the examination site early.

 Allow one minute per question.

 Look for key words, such as, never, always, cardinal, or first.

 More than one answer is usually correct; pick the best for the priority of the

patient. Remember the ABCDs (Airway, Breathing, Circulation, Drugs).

 Read and eliminate all distractors--words/terms that you have never heard/seen

before and do not fit. They are not correct.

 Do not take the exam after work.

 Do not “read” into the question, if it does not mention renal function—it does not

matter to the answer.

 Have confidence in yourself.

 DO NOT change your answers.

 Trust your clinical knowledge.

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References for CCRN Review

Ahrens TS, Prentice D, Kleinpell RM. Critical Care Nursing Certification. 2010. 6th
Edition, McGraw-Hill.

Diepenbrock NH. Quick Reference to Critical Care. 2011. 4th Edition, Lippincott
Williams and Wilkins.

Donohoe-Dennison R. Pass CCRN. 2013. 4th Edition, Mosby.

Donohoe-Dennison, R. Studyguide for Pass CCRN. 2011. Content Technologies, Inc.

Darovic FO. Hemodynamic Monitoring: Invasive and Noninvasive Clinical Application.

2002. 3rd ed. Philadelphia: WB Saunders/Elsevier.

Kaplan, et al. CCRN: Certification for Adult Critical Care Nurses. 2013. 4th Edition.
Kaplan Publishing.

Urden LD, Stacy KM, et al. Critical Care Nursing: Diagnosis and Management. 7th
edition. 2013. Elsevier Health Sciences.

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 THANK YOU

Take your time, read each question

carefully and fully!!! Answer each
question. Best of luck. Please let me
know how you did on the test, and if
there is anything I can do to help you in
the future.
Cammy House-Fancher, ACNP, MSN, CCRN-
CSC/CMC, PCCN

cam4230@gmail.com

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