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CCRN Review part 1

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The CCRN Review prepares critical care nurses for the CCRN and PCCN certification exams and is an excellent review for other nurses and other health care professionals.
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Never let what you cannot do Never let what you cannot do interfere with what you can do” interfere with what you can do” - - John Wooden John Wooden - - CCRN REVIEW PART 1 CCRN REVIEW PART 1 Sherry L. Knowles, RN, CCRN, CRNI Sherry L. Knowles, RN, CCRN, CRNI
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Page 1: CCRN Review part 1

““Never let what you cannot do Never let what you cannot do

interfere with what you can do”interfere with what you can do”- - John WoodenJohn Wooden - -

CCRN REVIEW PART 1CCRN REVIEW PART 1

Sherry L. Knowles, RN, CCRN, CRNISherry L. Knowles, RN, CCRN, CRNI

Page 2: CCRN Review part 1

TOPICSTOPICS Acute Coronary SyndromesAcute Coronary Syndromes Acute Myocardial InfarctionAcute Myocardial Infarction Heart BlocksHeart Blocks Heart FailureHeart Failure Cardiac AlterationsCardiac Alterations Aortic Aneurysms Aortic Aneurysms CardiomyopathyCardiomyopathy Shock States Shock States Peripheral Vascular DiseasePeripheral Vascular Disease HemodynamicsHemodynamics

ARDSARDS Chronic Lung DiseaseChronic Lung Disease DrowningDrowning PneumoniaPneumonia PneumothoraxPneumothorax Pulmonary EmbolismPulmonary Embolism Respiratory FailureRespiratory Failure Gastrointestinal AlterationsGastrointestinal Alterations GI BleedingGI Bleeding PancreatitisPancreatitis

CCRN REVIEW PART 1CCRN REVIEW PART 1

Page 3: CCRN Review part 1

OBJECTIVESOBJECTIVES1.1. Understand the different types of acute coronary syndromes.Understand the different types of acute coronary syndromes.

2.2. Identify basic coronary circulation and how it relates to different types of Identify basic coronary circulation and how it relates to different types of myocardial infarctions.myocardial infarctions.

3.3. Anticipate potential complications associated with an AMI.Anticipate potential complications associated with an AMI.

4.4. Identify the standard treatment of an AMI.Identify the standard treatment of an AMI.

5.5. Distinguish between various AV blocks.Distinguish between various AV blocks.

6.6. Recognize the signs & symptoms of heart failure.Recognize the signs & symptoms of heart failure.

7.7. Identify the treatment of heart failure.Identify the treatment of heart failure.

8.8. Recognize the general definition and classifications of aortic aneurysms.Recognize the general definition and classifications of aortic aneurysms.

9.9. Understand the different types of aortic dissections.Understand the different types of aortic dissections.

10.10. Recognize the signs & symptoms of cardiomyopathy.Recognize the signs & symptoms of cardiomyopathy.

11.11. Differentiate between the different types of cardiomyopathy.Differentiate between the different types of cardiomyopathy.

12.12. Identify the treatment for the different types of cardiomyopathy.Identify the treatment for the different types of cardiomyopathy.

13.13. Understand the different stages of shock.Understand the different stages of shock.

14.14. Differentiate between different types of shock.Differentiate between different types of shock.

CCRN REVIEW PART 1CCRN REVIEW PART 1

Page 4: CCRN Review part 1

OBJECTIVESOBJECTIVES15.15. Distinguish between arterial and venous peripheral vascular disease.Distinguish between arterial and venous peripheral vascular disease.

16.16. Identify the various treatments for peripheral vascular disease.Identify the various treatments for peripheral vascular disease.

17.17. Define respiratory failure.Define respiratory failure.

18.18. Identify the various treatments for acute respiratory failure.Identify the various treatments for acute respiratory failure.

19.19. Recognize the signs & symptoms and causes of various respiratory Recognize the signs & symptoms and causes of various respiratory alterations.alterations.

20.20. Identify the standard treatment for various respiratory alterations.Identify the standard treatment for various respiratory alterations.

21.21. Identify the components of cardiac output and stroke volume.Identify the components of cardiac output and stroke volume.

22.22. Recognize the pulmonary artery catheter waveforms.Recognize the pulmonary artery catheter waveforms.

23.23. Recognize the basic treatments used for commonly seen hemodynamic Recognize the basic treatments used for commonly seen hemodynamic profiles.profiles.

24.24. Explain the common causes of gastrointestinal bleeding. Explain the common causes of gastrointestinal bleeding.

25.25. Describe the most commonly seen treatments for GI bleeding.Describe the most commonly seen treatments for GI bleeding.

26.26. Describe the signs & symptoms of acute pancreatitis and available Describe the signs & symptoms of acute pancreatitis and available treatments.treatments.

CCRN REVIEW PART 1CCRN REVIEW PART 1

Page 5: CCRN Review part 1

Acute Coronary Acute Coronary SyndromesSyndromes

Acute MIAcute MI

Aortic AneurysmsAortic Aneurysms

Cardiac AlterationsCardiac Alterations

Cardiovascular ConditionsCardiovascular Conditions

CardiomyopathyCardiomyopathy

Heart BlocksHeart Blocks

Heart Failure Heart Failure

Shock StatesShock States

Page 6: CCRN Review part 1

DEFINITIONSDEFINITIONS

– Term used to cover a group of symptoms Term used to cover a group of symptoms compatible with acute myocardial ischemiacompatible with acute myocardial ischemia

– Acute myocardial ischemia is insufficient blood Acute myocardial ischemia is insufficient blood supply to the heart muscle usually resulting from supply to the heart muscle usually resulting from coronary artery disease coronary artery disease

Acute Coronary SyndromeAcute Coronary Syndrome

Page 7: CCRN Review part 1

DEFINITIONDEFINITION

– Infarction occurs due to mechanical obstruction Infarction occurs due to mechanical obstruction

of a coronary artery (or branch) caused by a of a coronary artery (or branch) caused by a

thrombus, plaque rupture, coronary spasm thrombus, plaque rupture, coronary spasm

and/or dissection.and/or dissection.

– STEMI vs. NSTEMI (non-STEMI)STEMI vs. NSTEMI (non-STEMI)

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 8: CCRN Review part 1

SIGNS & SYMPTOMSSIGNS & SYMPTOMS

– Complains Vary Complains Vary

May include crushing chest pain (which may or may May include crushing chest pain (which may or may not radiate), back, neck, jaw, teeth and/or epigastric not radiate), back, neck, jaw, teeth and/or epigastric pain, SOB, nausea/vomiting and dizzinesspain, SOB, nausea/vomiting and dizziness

– ST elevations on ECGST elevations on ECG

– Elevated cardiac enzymesElevated cardiac enzymes

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 9: CCRN Review part 1

SIGNS & SYMPTOMSSIGNS & SYMPTOMS

PAWP, PAWP, CO, CO, SVR, dysrhythmias, SSVR, dysrhythmias, S44, ,

cardiac failure, cardiogenic shockcardiac failure, cardiogenic shock

– Diaphoresis, pallor, referred painsDiaphoresis, pallor, referred pains

– Diabetics and women often present abnormal Diabetics and women often present abnormal

symptomssymptoms

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 10: CCRN Review part 1

Coronary CirculationCoronary Circulation

Page 11: CCRN Review part 1

I I AVRAVR V1 V1 V4V4

II II AVL V2 V5 AVL V2 V5

III III AVF V3 V6 AVF V3 V6

II II

VV

12 Lead ECG12 Lead ECG

Page 12: CCRN Review part 1

ST ELEVATIONSST ELEVATIONS– Anterior Wall MIAnterior Wall MI

Leads VLeads V11-V-V44

Reciprocal changes in leads II, III, and aVFReciprocal changes in leads II, III, and aVF Area supplied by the LADArea supplied by the LAD

– Inferior Wall MIInferior Wall MI Leads II, III and aVF Leads II, III and aVF Reciprocal changes in leads I, and aVLReciprocal changes in leads I, and aVL Area usually supplied by the RCAArea usually supplied by the RCA

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 13: CCRN Review part 1

ST ELEVATIONSST ELEVATIONS– Lateral Wall MILateral Wall MI

I, aVL, VI, aVL, V55 and V and V66

Area supplied by the Circumflex arteryArea supplied by the Circumflex artery

– Posterior Wall MIPosterior Wall MI Reflected on the opposite wallsReflected on the opposite walls Opposite deflectionsOpposite deflections

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 14: CCRN Review part 1

Coronary ArteriesCoronary Arteries

Page 15: CCRN Review part 1

Anterior Wall MIAnterior Wall MI

Page 16: CCRN Review part 1

Inferior Wall MIInferior Wall MI

Page 17: CCRN Review part 1

COMPLICATIONSCOMPLICATIONS

– Dysrhythmias, heart failure, pericarditis, Dysrhythmias, heart failure, pericarditis,

ventricular aneurysms, ventricular thrombus, ventricular aneurysms, ventricular thrombus,

VSD, mitral regurgitation, papillary muscle (or VSD, mitral regurgitation, papillary muscle (or

chordae tendineae) rupture, pericardial chordae tendineae) rupture, pericardial

effusions, pericarditiseffusions, pericarditis

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 18: CCRN Review part 1

NURSING INTERVENTIONSNURSING INTERVENTIONS– OO22

– BedrestBedrest

– Serial ECG’sSerial ECG’s

– Serial cardiac enzymesSerial cardiac enzymes

– Keep pain free (NTG. MSOKeep pain free (NTG. MSO44))

– MONA MONA (Morphine, O2, Nitroglycerin, Aspirin),(Morphine, O2, Nitroglycerin, Aspirin), Heparin, beta-blockers, and ace inhibitors. May also Heparin, beta-blockers, and ace inhibitors. May also include thrombolytics or Gp2b3a inhibitorsinclude thrombolytics or Gp2b3a inhibitors

– PCI, PTCA, IABP, CABG PCI, PTCA, IABP, CABG

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 19: CCRN Review part 1

TREATMENTTREATMENT

– Time Is Heart MuscleTime Is Heart Muscle

– Prompt ECGPrompt ECG

– Goals: Relieve pain, limit the size of the Goals: Relieve pain, limit the size of the infarction and to prevent complications infarction and to prevent complications (primarily lethal dysrhythmias) (primarily lethal dysrhythmias)

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 20: CCRN Review part 1

TREATMENTTREATMENT

– MONA MONA (Morphine, O2, Nitroglycerin, Aspirin)(Morphine, O2, Nitroglycerin, Aspirin), , Heparin, beta-blockers, and ace inhibitors. Heparin, beta-blockers, and ace inhibitors. May also include thrombolytics or Gp2b3a May also include thrombolytics or Gp2b3a inhibitorsinhibitors

– Cardiac Catheterization (with angioplasty, Cardiac Catheterization (with angioplasty, atherectomy and/or stent)atherectomy and/or stent)

– IABP, CABG, EducationIABP, CABG, Education

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 21: CCRN Review part 1

Balloon AngioplastyBalloon Angioplasty

Page 22: CCRN Review part 1

Vascular Stent DeploymentVascular Stent Deployment

Page 23: CCRN Review part 1

AtherectomyAtherectomy

Page 24: CCRN Review part 1

SPECIFIC TREATMENTSSPECIFIC TREATMENTS– Inferior Wall (IWMI)Inferior Wall (IWMI)

FluidsFluids (with RV infarct) (with RV infarct) InotropicsInotropics Afterload reducing medicationsAfterload reducing medications

– Anterior Wall (AWMI)Anterior Wall (AWMI) DiureticsDiuretics InotropicsInotropics Afterload reducing medicationsAfterload reducing medications

Acute Myocardial InfarctionAcute Myocardial Infarction

Page 25: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

DEFINITIONDEFINITION– A bulge or ballooning of the aorta A bulge or ballooning of the aorta

When the walls of the aneurysm include all three When the walls of the aneurysm include all three layers of the artery, they are called true aneurysmslayers of the artery, they are called true aneurysms

When the wall of the aneurysm include only the When the wall of the aneurysm include only the outer layer, it is called a pseudo-aneurysmouter layer, it is called a pseudo-aneurysm

– May be thoracic or abdominalMay be thoracic or abdominal

Page 26: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

CAUSESCAUSES Atherosclerosis Atherosclerosis

Marfan syndrome Marfan syndrome

Hypertension Hypertension

Crack cocaine usage Crack cocaine usage

Smoking Smoking

Trauma Trauma

Page 27: CCRN Review part 1

Aortic Aneurysms RuptureAortic Aneurysms Rupture

An aortic aneurysm, depending on its size, may An aortic aneurysm, depending on its size, may rupture, causing life-threatening internal bleedingrupture, causing life-threatening internal bleeding

The risk of an aneurysm rupturing increases as the The risk of an aneurysm rupturing increases as the aneurysm gets largeraneurysm gets larger

The risk of rupture also depends on the location of The risk of rupture also depends on the location of the aneurysmthe aneurysm

Each year, approximately 15,000 Americans die of a Each year, approximately 15,000 Americans die of a ruptured aortic aneurysm. ruptured aortic aneurysm.

Page 28: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

CLASSIFICATIONSCLASSIFICATIONS

– Classified by shape, location along the aorta, Classified by shape, location along the aorta, and how they are formedand how they are formed

– May be symmetrical in shape (fusiform) or a May be symmetrical in shape (fusiform) or a localized weakness of the arterial wall (saccular)localized weakness of the arterial wall (saccular)

Page 29: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

Page 30: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

SIGNS & SYMPTOMSSIGNS & SYMPTOMS

– Often produces no symptoms Often produces no symptoms

– If an aortic aneurysm suddenly ruptures it presents If an aortic aneurysm suddenly ruptures it presents with extreme abdominal or back pain, a pulsating with extreme abdominal or back pain, a pulsating mass in the abdomen, and a drastic drop in blood mass in the abdomen, and a drastic drop in blood pressure pressure

– An increase in the size of an aneurysm means an An increase in the size of an aneurysm means an increased in the risk of rupture increased in the risk of rupture

Page 31: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

THORACIC SIGNS & SYMPTOMSTHORACIC SIGNS & SYMPTOMS– Back, shoulder or neck pain Back, shoulder or neck pain

– Cough, due to pressure placed on the tracheaCough, due to pressure placed on the trachea

– Hoarseness Hoarseness

– Strider, dyspneaStrider, dyspnea

– Difficulty swallowing Difficulty swallowing

– Swelling in the neck or armsSwelling in the neck or arms

Page 32: CCRN Review part 1

Aortic DissectionsAortic Dissections

DEFINITIONDEFINITION

– Tearing of the inner layer of the aortic wall, which allows blood to leak into the wall itself and causes the separation of the inner and outer layersTearing of the inner layer of the aortic wall, which allows blood to leak into the wall itself and causes the separation of the inner and outer layers

– Usually associated with severe chest pain radiating to the backUsually associated with severe chest pain radiating to the back

Page 33: CCRN Review part 1

Aortic DissectionsAortic Dissections

A.A. Dissection Dissection beginning in the beginning in the ascending aorta ascending aorta

B.B. Whenever the Whenever the ascending aorta ascending aorta is not involved is not involved

Page 34: CCRN Review part 1

Aortic DissectionsAortic Dissections

A.A. Dissection Dissection beginning in the beginning in the ascending aorta ascending aorta

B.B. Whenever the Whenever the ascending aorta ascending aorta is not involved is not involved

Page 35: CCRN Review part 1

Aortic DissectionsAortic Dissections

Page 36: CCRN Review part 1

Aortic DissectionsAortic Dissections

Page 37: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

COMPLICATIONSCOMPLICATIONS

RuptureRupture

Peripheral Peripheral embolization embolization

InfectionInfection

Spontaneous Spontaneous occlusionocclusion of aorta of aorta

Page 38: CCRN Review part 1

Aortic AneurysmsAortic Aneurysms

TREATMENTTREATMENT

Medical managementMedical management

– Controlled BP (within specific range)Controlled BP (within specific range)

Surgical repairSurgical repair

> 4.5 cm in Marfan patients or > 5 cm in non-> 4.5 cm in Marfan patients or > 5 cm in non-Marfan patients will require surgical Marfan patients will require surgical correction or endovascular stent placementcorrection or endovascular stent placement

Page 39: CCRN Review part 1

CardiomyopathyCardiomyopathy

DEFINITIONDEFINITION

– Diseases of the heart muscle that Diseases of the heart muscle that cause deterioration of the function of cause deterioration of the function of the myocardiumthe myocardium

Page 40: CCRN Review part 1

CardiomyopathyCardiomyopathy

CLASSIFICATIONSCLASSIFICATIONS– Primary / Idiopathic (intrinsicPrimary / Idiopathic (intrinsic))

Heart disease of unknown cause, although viral Heart disease of unknown cause, although viral infection and autoimmunity are suspected causesinfection and autoimmunity are suspected causes

– Secondary (extrinsicSecondary (extrinsic)) Heart disease as a result of other systemic diseases, Heart disease as a result of other systemic diseases,

such as autoimmune diseases, CAD, valvular such as autoimmune diseases, CAD, valvular

disease, severe hypertension, or alcohol abusedisease, severe hypertension, or alcohol abuse

Page 41: CCRN Review part 1

CardiomyopathyCardiomyopathy

Hypertropic CardiomyopathyHypertropic Cardiomyopathy

Restrictive CardiomyopathyRestrictive Cardiomyopathy

Dilated CardiomyopathyDilated Cardiomyopathy

Page 42: CCRN Review part 1

Hypertropic CardiomyopathyHypertropic Cardiomyopathy

Bizarre hypertrophy of the septumBizarre hypertrophy of the septum– Previously called IHSS Previously called IHSS

Idiopathic Hypertropic Subaortic StenosisIdiopathic Hypertropic Subaortic Stenosis

– Known as HOCM Known as HOCM Hypertropic Obstructive CardiomyopathyHypertropic Obstructive Cardiomyopathy

Positive inotropic drugs Should Positive inotropic drugs Should NotNot Be Used Be Used Contractility will Contractility will outflow tract obstruction outflow tract obstruction

Nitroglycerin Should Nitroglycerin Should NotNot Be Used Be Used– Dilation Will Worsen The Problem Dilation Will Worsen The Problem

Page 43: CCRN Review part 1

HarleyHarley

Page 44: CCRN Review part 1

Hypertropic CardiomyopathyHypertropic Cardiomyopathy

TREATMENTTREATMENT– Relax the ventriclesRelax the ventricles

Beta BlockersBeta Blockers Calcium Channel Blockers Calcium Channel Blockers

– Slow the Heart RateSlow the Heart Rate Increase filling timeIncrease filling time

– Use Negative InotropesUse Negative Inotropes Optimize diastolic fillingOptimize diastolic filling

– Do Not use NTGDo Not use NTG Dilation will worsen the problemDilation will worsen the problem

Page 45: CCRN Review part 1

Restrictive CardiomyopathyRestrictive Cardiomyopathy

Rigid Ventricular WallRigid Ventricular Wall

– Due to endomyocardial fibrosis Due to endomyocardial fibrosis

– Obstructs ventricular fillingObstructs ventricular filling

Least common formLeast common form

Page 46: CCRN Review part 1

Restrictive CardiomyopathyRestrictive Cardiomyopathy

TREATMENTTREATMENT

– Positive InotropicsPositive Inotropics

– Diuretics Diuretics

– Low Sodium DietLow Sodium Diet

Page 47: CCRN Review part 1

Dilated CardiomyopathyDilated Cardiomyopathy

Grossly dilated ventricles without hypertrophyGrossly dilated ventricles without hypertrophy

– Global left ventricular dysfunction Global left ventricular dysfunction

– Leads to pooling of blood and embolic episodesLeads to pooling of blood and embolic episodes

– Leads to refractory heart failure Leads to refractory heart failure

– Leads to papillary muscle dysfunction secondary to Leads to papillary muscle dysfunction secondary to LV dilation LV dilation

Page 48: CCRN Review part 1

Dilated CardiomyopathyDilated Cardiomyopathy

TREATMENTTREATMENT

– Positive InotropesPositive Inotropes

– Afterload ReducersAfterload Reducers

– Anticoagulants with Atrial FibAnticoagulants with Atrial Fib

Page 49: CCRN Review part 1

CardiomyopathiesCardiomyopathies

Page 50: CCRN Review part 1

CardiomyopathyCardiomyopathy

GENERALIZED TREATMENTGENERALIZED TREATMENT– Positive InotropesPositive Inotropes

Except with Hypertropic CardiomyopathyExcept with Hypertropic Cardiomyopathy

– Vasodilators Vasodilators Except with Hypertropic CardiomyopathyExcept with Hypertropic Cardiomyopathy

– Reduce Preload & AfterloadReduce Preload & Afterload– DiureticsDiuretics– Beta BlockersBeta Blockers– Calcium Channel BlockersCalcium Channel Blockers– IABPIABP– Vasodilators (as indicated)Vasodilators (as indicated)– Fluid RestrictionFluid Restriction

– Daily weights, prn O2, planned activities, Daily weights, prn O2, planned activities, education, and emotional supporteducation, and emotional support

– Consider Heart TransplantConsider Heart Transplant

Page 51: CCRN Review part 1

BREAK!BREAK!

CCRN REVIEW PART 1CCRN REVIEW PART 1

Page 52: CCRN Review part 1

Conduction DefectsConduction Defects

STABLE VS UNSTABLESTABLE VS UNSTABLE

– StableStable

Start with medicationsStart with medications

– UnstableUnstable

Shock (cardioversion or defibrillation)Shock (cardioversion or defibrillation)

Page 53: CCRN Review part 1

Normal Sinus RhythmNormal Sinus Rhythm

Heart RateHeart Rate 60 - 100 bpm60 - 100 bpm

RhythmRhythm RegularRegular

P WaveP Wave Before each QRS & identicalBefore each QRS & identical

PR Interval (in seconds)PR Interval (in seconds) 0.12 to 0.200.12 to 0.20

QRS (in seconds)QRS (in seconds) < 0.12< 0.12

Page 54: CCRN Review part 1

Atrial FibrillationAtrial Fibrillation

AFibAFib– Multifocal atrial impulses at rate 300-600/min Multifocal atrial impulses at rate 300-600/min

– Irregular conduction to ventriclesIrregular conduction to ventricles

Page 55: CCRN Review part 1

Atrial FlutterAtrial Flutter

AFLAFL– Atrial impulses at rate of 250-350/min Atrial impulses at rate of 250-350/min

– Regularly blocked impulses at the AV nodeRegularly blocked impulses at the AV node

– Saw tooth flutter wavesSaw tooth flutter waves

Page 56: CCRN Review part 1

Wandering Atrial PacemakerWandering Atrial Pacemaker

WAPWAP– Multiple ectopic foci in the atriaMultiple ectopic foci in the atria

– Three or more p wave morphologiesThree or more p wave morphologies

– Rate < 100Rate < 100

Page 57: CCRN Review part 1

Supraventricular TachycardiaSupraventricular Tachycardia

SVTSVT– Supraventricular rhythm at rate 150-250 Supraventricular rhythm at rate 150-250

– P waves cannot be positively identifiedP waves cannot be positively identified

Atrial Tach = supraventricular rhythm with p wave morphology Atrial Tach = supraventricular rhythm with p wave morphology that is noticeably different from the that is noticeably different from the

sinus p wavesinus p wave

Page 58: CCRN Review part 1

Ventricular TachycardiaVentricular Tachycardia

VTVT– Ventricular rate of 100-250/minVentricular rate of 100-250/min

– Wide QRSWide QRS

Page 59: CCRN Review part 1

Torsades de PointesTorsades de Pointes

Polymorphic VTPolymorphic VT– VT with alternating ventricular focus VT with alternating ventricular focus

– Often associated with prolonged QT Rate < 100Often associated with prolonged QT Rate < 100

Page 60: CCRN Review part 1

Heart Blocks (AV Blocks)Heart Blocks (AV Blocks)

Sinus Rhythm with First Degree AV BlockSinus Rhythm with First Degree AV Block

Sinus Rhythm with Second Degree AV Block, Type 2Sinus Rhythm with Second Degree AV Block, Type 2

Sinus Rhythm with Second Degree AV Block, Type 1Sinus Rhythm with Second Degree AV Block, Type 1

Third Degree AV BlockThird Degree AV Block

Page 61: CCRN Review part 1

DEFINITIONDEFINITION

– A condition in which the heart cannot pump A condition in which the heart cannot pump sufficient blood to meet the metabolic needs of sufficient blood to meet the metabolic needs of the bodythe body

– Pulmonary (LVF) and/or systemic (RVF) Pulmonary (LVF) and/or systemic (RVF) congestion is present.congestion is present.

Heart FailureHeart Failure

Page 62: CCRN Review part 1

DEFINITIONDEFINITION– Pulmonary EdemaPulmonary Edema

Fluid in the alveolus that impairs gas exchange byFluid in the alveolus that impairs gas exchange by altering the diffusion between alveolus andaltering the diffusion between alveolus and capillarycapillary

Acute left ventricular failure causes cardiogenic Acute left ventricular failure causes cardiogenic pulmonary edemapulmonary edema

Non-cardiogenic pulmonary edema is a synonym for Non-cardiogenic pulmonary edema is a synonym for Adult Respiratory Distress Syndrome (ARDS)Adult Respiratory Distress Syndrome (ARDS)

Heart FailureHeart Failure

Page 63: CCRN Review part 1

COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS– Sympaththetic nervous system stimulationSympaththetic nervous system stimulation

TachycardiaTachycardia Vasoconstriction and increased SVRVasoconstriction and increased SVR

– Renin-angiotensin-aldosterone system Renin-angiotensin-aldosterone system activation (RAAS)activation (RAAS)

Hypo perfusion to the kidneys (renin)Hypo perfusion to the kidneys (renin) Vasoconstriction (angiotensin)Vasoconstriction (angiotensin) Sodium and water retention (kidneys)Sodium and water retention (kidneys) Ventricular dilationVentricular dilation

Heart FailureHeart Failure

Page 64: CCRN Review part 1

FUNCTIONAL CLASSIFICATIONSFUNCTIONAL CLASSIFICATIONS

– Class I Class I

– Class IIClass II

– Class IIIClass III

– Class IVClass IV

Heart FailureHeart Failure

(without noticeable limitations)(without noticeable limitations)

(symptoms upon activity)(symptoms upon activity)

(severe symptoms upon activity)(severe symptoms upon activity)

(symptoms at rest)(symptoms at rest)

Page 65: CCRN Review part 1

COMPLICATIONSCOMPLICATIONS– HypotensionHypotension

– DysrhythmiasDysrhythmias

– Respiratory FailureRespiratory Failure

– Progressive DeteriorationProgressive Deterioration

– Acute Renal FailureAcute Renal Failure

– Fluid & Electrolyte ImbalancesFluid & Electrolyte Imbalances

Heart FailureHeart Failure

Page 66: CCRN Review part 1

TREATMENTTREATMENT– Improve OxygenationImprove Oxygenation

– Decrease Myocardial Oxygen DemandDecrease Myocardial Oxygen Demand

– Decrease PreloadDecrease Preload

– Decrease AfterloadDecrease Afterload

– Increase ContractilityIncrease Contractility

– Manage DysrhythmiasManage Dysrhythmias

– Educate!Educate!

Heart FailureHeart Failure

Page 67: CCRN Review part 1

Vascular DiseaseVascular Disease

Aorto/Iliac Disease: Pre & Post PTA/StentAorto/Iliac Disease: Pre & Post PTA/Stent

Page 68: CCRN Review part 1

Peripheral Vascular DiseasePeripheral Vascular DiseaseSYMPTOMSSYMPTOMS

PAINPAIN

PAIN RELIEFPAIN RELIEF

EDEMAEDEMA

PULSESPULSES

INTEGUMENT INTEGUMENT CHANGESCHANGES

ULCERSULCERS

SKIN TEMPERATURESKIN TEMPERATURE

SEXUAL ISSUESSEXUAL ISSUES

ARTERIALARTERIAL

Upon walkingUpon walking

On resting, standing or On resting, standing or dependent position of lower limbs dependent position of lower limbs

NoneNone

Decreased or absentDecreased or absent

Hair lossHair lossSkin shinySkin shinyNail thickeningNail thickeningPallor when elevatedPallor when elevatedRed when dependentRed when dependent

Ulcers located on toes, lateral Ulcers located on toes, lateral areas or site of traumaareas or site of traumaGangrene possibleGangrene possible

CoolCool

ImpotencyImpotencySexual dysfunctionSexual dysfunction

VENOUSVENOUS

While standingWhile standing

Elevation of extremitiesElevation of extremities

Present, edematousPresent, edematous

May be difficult to palpateMay be difficult to palpate

Brownish pigmentationBrownish pigmentationMay be cyanotic when May be cyanotic when extremities are dependentextremities are dependent

Ulcers located on ankles, Ulcers located on ankles, medial or pre-tibial areasmedial or pre-tibial areas

Normal or warmNormal or warm

Not presentNot present

Page 69: CCRN Review part 1

Peripheral Vascular DiseasePeripheral Vascular Disease

TREATMENTSTREATMENTS– MedicalMedical

Are they taking ASA, Coumadin, Ticlid, Plavix, Are they taking ASA, Coumadin, Ticlid, Plavix, Oral Contraceptives, Hormones?Oral Contraceptives, Hormones?

– InvasiveInvasive PTA, atherectomy, stentsPTA, atherectomy, stents

– SurgicalSurgical GraftsGrafts

Page 70: CCRN Review part 1

Peripheral Vascular DiseasePeripheral Vascular Disease

Bypass GraftsBypass Grafts

Page 71: CCRN Review part 1

DEFINITIONDEFINITION

– Inadequate perfusion to the body tissuesInadequate perfusion to the body tissues

– Low blood pressure with impaired perfusion Low blood pressure with impaired perfusion to the end organsto the end organs

– May result in multiple organ dysfunctionMay result in multiple organ dysfunction

ShockShock

Page 72: CCRN Review part 1

TYPES OF SHOCKTYPES OF SHOCK

– Hypovolemic ShockHypovolemic Shock

– Cardiogenic ShockCardiogenic Shock

– Distributive Shock Distributive Shock

– Obstructive ShockObstructive Shock

ShockShock

Page 73: CCRN Review part 1

ShockShock

COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS –TachycardiaTachycardia

Attempts to deliver more blood to the tissuesAttempts to deliver more blood to the tissues

–VasoconstrictionVasoconstriction Attempts to maintain adequate BP in order to Attempts to maintain adequate BP in order to

adequately perfuse the body tissuesadequately perfuse the body tissues

–Increased ADH SecretionIncreased ADH Secretion ADH makes the body hold onto water in an effort to ADH makes the body hold onto water in an effort to

maintain volume and thus enough blood pressure to maintain volume and thus enough blood pressure to perfuse the body tissuesperfuse the body tissues

Page 74: CCRN Review part 1

Types of ShockTypes of Shock

Hypovolemic ShockHypovolemic Shock– Inadequate perfusion to the tissues due to insufficient intravascular Inadequate perfusion to the tissues due to insufficient intravascular

volumevolume

Cardiogenic ShockCardiogenic Shock– Inadequate perfusion to the tissues due to heart failureInadequate perfusion to the tissues due to heart failure

Distributive ShockDistributive Shock– Inadequate perfusion to the tissues due to blood flow out of the Inadequate perfusion to the tissues due to blood flow out of the

intravascular space causing insufficient intravascular volumeintravascular space causing insufficient intravascular volume

– Anaphylactic, Septic, and Spinal ShockAnaphylactic, Septic, and Spinal Shock Obstructive ShockObstructive Shock

– Inadequate perfusion to the tissues due to obstruction of blood flowInadequate perfusion to the tissues due to obstruction of blood flow

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Hypovolemic ShockHypovolemic Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardia

Orthostatic Hypotension Orthostatic Hypotension RestlessnessRestlessness

Confusion Confusion Agitation (or Agitation (or listless)listless)

Thirst Thirst PallorPallor

Cool, Clammy SkinCool, Clammy Skin Resp. Rate Resp. Rate

UOPUOP CO CO

PAWPPAWP CVP CVP

SVR SVR Lactate Levels Lactate Levels

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Hypovolemic ShockHypovolemic Shock

TREATMENTTREATMENT

–Volume (IVF, Blood)Volume (IVF, Blood)

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Cardiogenic ShockCardiogenic Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP RestlessnessRestlessness

Agitation (or listless)Agitation (or listless) ConfusionConfusion

TachycardiaTachycardia PallorPallor

UOPUOP CO CO

PAWP (low with RVF) PAWP (low with RVF) CVPCVP

SVR SVR Lactate Levels Lactate Levels

JVDJVD Peripheral EdemaPeripheral Edema

Ventricular Gallop (S3)Ventricular Gallop (S3) DyspneaDyspnea

Pulmonary CracklesPulmonary Crackles

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TREATMENTTREATMENTBedrestBedrest O2O2

COCO Positive InotropesPositive Inotropes

Preload & AfterloadPreload & Afterload DiureticsDiuretics

VasodilatorsVasodilators PositioningPositioning

Myocardial DemandMyocardial Demand IABPIABP

Cardiogenic ShockCardiogenic Shock

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Anaphylactic ShockAnaphylactic Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaRestlessnessRestlessness Confusion Confusion Agitation (or listless)Agitation (or listless) Thirst Thirst PallorPallor Warm FeelingWarm FeelingPruritusPruritus HivesHivesAngioedemaAngioedema BronchoconstrictionBronchoconstrictionWheezingWheezing Laryngeal EdemaLaryngeal EdemaDyspneaDyspnea Cool, Clammy SkinCool, Clammy Skin UOPUOP CO CO PAWPPAWP CVP CVP

SVR SVR Lactate Levels Lactate Levels

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TREATMENTTREATMENT– Epinephrine Epinephrine

– IVFIVF

– VasoconstrictorsVasoconstrictors

– Support/Maintain AirwaySupport/Maintain Airway

Anaphylactic ShockAnaphylactic Shock

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Obstructive ShockObstructive Shock

SIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP

TachycardiaTachycardiaRestlessnessRestlessness Confusion Confusion

Agitation (or listless)Agitation (or listless) Pallor Pallor Cool, Clammy SkinCool, Clammy Skin CO , CO ,

UOPUOP

Symptoms related to causeSymptoms related to cause

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Obstructive ShockObstructive Shock

CAUSESCAUSESPulmonary EmbolusPulmonary Embolus TamponadeTamponade

Tension PneumothoraxTension Pneumothorax Aortic AneurysmAortic Aneurysm

TREATMENTTREATMENTTreat the CauseTreat the Cause

Page 83: CCRN Review part 1

Cardiogenic Shock is the only shock with Cardiogenic Shock is the only shock with PAWP PAWP

Early (Hyperdynamic) Shock is the only shock with Early (Hyperdynamic) Shock is the only shock with CO and CO and SVRSVR

Neurogenic Shock is the only shock with Neurogenic Shock is the only shock with BradycardiaBradycardia

Anaphylactic Shock has the definitive characteristic of wheezing due Anaphylactic Shock has the definitive characteristic of wheezing due to bronchospasmto bronchospasm

Parameter Hypovolemic Cardiogenic Neurogenic Anaphylactic Early Septic Late Septic

CVP/RAP

PAWP or Norm

CO

BP

SVR

HR Normal

Shock ProfilesShock Profiles

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SIRS Sepsis Severe Septic MODS DeathSIRS Sepsis Severe Septic MODS DeathInfection Infection Sepsis Shock Sepsis Shock

Sepsis SyndromeSepsis Syndrome

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Sepsis– SIRS’ response with presumed/confirmed infectionSIRS’ response with presumed/confirmed infection

Severe Sepsis– Sepsis associated with organ dysfunction, hypoperfusion Sepsis associated with organ dysfunction, hypoperfusion

(lactic acidosis, oliguria, altered mental status etc.), or (lactic acidosis, oliguria, altered mental status etc.), or hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)

Septic Shock– Sepsis with perfusion abnormalities and hypotension Sepsis with perfusion abnormalities and hypotension

despite adequate fluid resuscitationdespite adequate fluid resuscitation

Sepsis SyndromeSepsis Syndrome

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EARLY STAGE (Hyperdynamic)EARLY STAGE (Hyperdynamic)Normal BPNormal BP TachycardiaTachycardiaConfusion Confusion Agitation (or listless)Agitation (or listless) Respiratory RateRespiratory Rate TemperatureTemperatureNormal ColorNormal Color Normal or Normal or UOP UOPNormal PAWPNormal PAWP CO CO SVR SVR

LATE STAGE (Hypodynamic)LATE STAGE (Hypodynamic)Low BPLow BP TachycardiaTachycardiaOrthostatic Hypotension Orthostatic Hypotension RestlessnessRestlessnessConfusion Confusion Agitation (or listless)Agitation (or listless)Thirst Thirst PallorPallorCool, Clammy SkinCool, Clammy Skin UOP UOP COCO PAWP PAWP CVPCVP SVR SVR Lactate LevelsLactate Levels

Septic ShockSeptic Shock

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Homeostasis Gets LostHomeostasis Gets Lost

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3.3. Improve PerfusionImprove Perfusion– Prevent organ dysfunctionPrevent organ dysfunction– Treat temp as neededTreat temp as needed

2.2. Treat The CauseTreat The Cause – Pan culture, antibiotics Pan culture, antibiotics

– Seek primary site of infectionSeek primary site of infection

– Direct therapy to primary causeDirect therapy to primary cause

1.1. Stabilize The PatientStabilize The Patient– Fluids (lots of fluids) 150ml/hr or moreFluids (lots of fluids) 150ml/hr or more

– VasoconstrictorsVasoconstrictors

Treatment for SepsisTreatment for Sepsis

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HEMODYNAMICSHEMODYNAMICS

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Invasive PA Catheter Invasive PA Catheter CONTRAINDICATIONSCONTRAINDICATIONS

Mechanical Tricuspid or Pulmonary Valve Mechanical Tricuspid or Pulmonary Valve

Right Heart Mass (thrombus and/or tumor)Right Heart Mass (thrombus and/or tumor)

Tricuspid or Pulmonary Valve EndocarditisTricuspid or Pulmonary Valve Endocarditis

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BasicBasic ConceptsConcepts

CO = HR X SVCO = HR X SV

BP = CO x SVRBP = CO x SVR

CO and SVR are inversely relatedCO and SVR are inversely related

CO and SVR will change before BP changesCO and SVR will change before BP changes

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StrokeStroke VolumeVolume

Components Stroke VolumeComponents Stroke Volume

– PreloadPreload:: the volume of blood in the the volume of blood in the ventricles at end diastole and the stretch ventricles at end diastole and the stretch placed on the muscle fibersplaced on the muscle fibers

– AfterloadAfterload:: the resistance the ventricles the resistance the ventricles must overcome to eject it’s volume of must overcome to eject it’s volume of bloodblood

– Contractility:Contractility: the force with which the the force with which the heart muscle contracts (myocardial heart muscle contracts (myocardial compliance)compliance)

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PAC Insertion SequencePAC Insertion Sequence

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Phlebostatic AxisPhlebostatic Axis

4th ICS Mid-chest, regardless of head elevation4th ICS Mid-chest, regardless of head elevation

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RAP (CVP)RAP (CVP)

RVPRVP

PAPPAP

PAWPPAWP

SVRSVR

0-8 mmHg0-8 mmHg

15-30/0-8 mmHg15-30/0-8 mmHg

15-30/6-12 mmHg15-30/6-12 mmHg

8 - 12 mmHg8 - 12 mmHg

700-1500 700-1500 dynes/sec/cmdynes/sec/cm22

Normal Hemodynamic ValuesNormal Hemodynamic Values

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Normal Hemodynamic Normal Hemodynamic ValuesValues Values normalized for body size (BSA)Values normalized for body size (BSA)

CI:CI: 2.5 – 4.5 L/min/m2.5 – 4.5 L/min/m22

SVRI:SVRI: 1970 – 2390 dynes/sec/cm-1970 – 2390 dynes/sec/cm-

5/m25/m2

SVI or SI:SVI or SI: 35 – 60 mL/beat/m235 – 60 mL/beat/m2

EDVI:EDVI: 60 – 100 mL/m260 – 100 mL/m2

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Mixed Venous Oxygen Mixed Venous Oxygen SaturationSaturationSvO2SvO2

End result of O2 delivery and End result of O2 delivery and consumptionconsumption

Measured in the pulmonary arteryMeasured in the pulmonary artery An average estimate of venous saturation for An average estimate of venous saturation for

the whole body.the whole body.

Does not reflect separate tissue perfusion or Does not reflect separate tissue perfusion or oxygenationoxygenation

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Stroke Volume Variation (SVV)Stroke Volume Variation (SVV)

Minimally Invasive Flo Trac Minimally Invasive Flo Trac

Measured through Arterial LineMeasured through Arterial Line Measures preload responsivenessMeasures preload responsiveness

SVV > 10-15 % = preload responsive SVV > 10-15 % = preload responsive (responsive to fluids)(responsive to fluids)

SVV > 10-15% = pulsus paradoxusSVV > 10-15% = pulsus paradoxus

SVV < 10–15% = not preload responsive SVV < 10–15% = not preload responsive   

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Measuring PA PressuresMeasuring PA Pressures

Measure All Hemodynamic Values Measure All Hemodynamic Values at End-Expirationat End-Expiration

– ““Patient PeakPatient Peak””

– ““Vent ValleyVent Valley””

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Spontaneous RespirationsSpontaneous Respirations

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Measure all pressures atMeasure all pressures at end-expirationend-expiration

AtAt top curve top curve with Spontaneous Respirationwith Spontaneous Respiration

““patient-peak”patient-peak”

Intrathoracic pressure Intrathoracic pressure decreasesdecreases during during spontaneous inspirationspontaneous inspiration

– Negative deflection on waveformsNegative deflection on waveforms Intrathoracic pressure Intrathoracic pressure increasesincreases duringduring

spontaneous expirationspontaneous expiration

– Positive deflection on waveformsPositive deflection on waveforms

Measuring PA PressuresMeasuring PA Pressures

Page 102: CCRN Review part 1

Measure all pressures atMeasure all pressures at end-expirationend-expiration AtAt bottom curvebottom curve with mechanical ventilatorwith mechanical ventilator

““Vent-Valley”Vent-Valley”

Intrathoracic pressureIntrathoracic pressure increasesincreases during during positive pressure ventilations (inspiration)positive pressure ventilations (inspiration)

– Positive deflection on waveformsPositive deflection on waveforms Intrathoracic pressureIntrathoracic pressure decreases decreases during during

positive pressure expirationpositive pressure expiration

– Negative deflection on waveformsNegative deflection on waveforms

Measuring PA PressuresMeasuring PA Pressures

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a-wavea-wave– Atrial contractionAtrial contraction

– Correct location for measurement of PAWPCorrect location for measurement of PAWP Average the peak & trough of the a-waveAverage the peak & trough of the a-wave

– Begins near the end of QRS or at the QT Begins near the end of QRS or at the QT segmentsegment

Delayed ECG correlation from CVP since Delayed ECG correlation from CVP since PA catheter is further away from left atriumPA catheter is further away from left atrium

PAWP WaveformPAWP Waveform

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c-wavec-wave– Rarely presentRarely present

– Represents mitral valve closureRepresents mitral valve closure

v-wavev-wave– Represents left atrial fillingRepresents left atrial filling

– Begins at about the end of the T waveBegins at about the end of the T wave

PAWP WaveformPAWP Waveform

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PAWP WaveformPAWP Waveform

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BREAK!BREAK!

CCRN REVIEW PART 1CCRN REVIEW PART 1

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ARDSARDS

Drowning Drowning

PneumothoraxPneumothorax

Respiratory Respiratory

FailureFailure

Respiratory AlterationsRespiratory Alterations

ChronicChronic LungLung DiseaseDisease

PneumoniaPneumonia

PulmonaryPulmonary

EmbolismEmbolism

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ARDSARDS

DEFINITIONSDEFINITIONS

– Severe respiratory failure associated with pulmonary Severe respiratory failure associated with pulmonary infiltrates (similar to infant hyaline membrane disease)infiltrates (similar to infant hyaline membrane disease)

– Pulmonary edema in the absence of fluid overload or Pulmonary edema in the absence of fluid overload or depressed LV function (Non-cardiogenic pulmonary edema)depressed LV function (Non-cardiogenic pulmonary edema)

– Originates from a number of insults involving damage to the Originates from a number of insults involving damage to the alveolar-capillary membranealveolar-capillary membrane

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Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome

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ARDSARDS

PATHOPHYSIOLOGYPATHOPHYSIOLOGY

– Inflammatory mediators are released causing extensive Inflammatory mediators are released causing extensive

structural damagestructural damage

– Increased permeability of pulmonary microvasculature Increased permeability of pulmonary microvasculature

causes leakage of proteinaceous fluid across the alveolar–causes leakage of proteinaceous fluid across the alveolar–

capillary membrane capillary membrane

– Also causes damage to the surfactant-producing type II cellsAlso causes damage to the surfactant-producing type II cells

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ARDSARDS

CXR CHARACTERISTICSCXR CHARACTERISTICS– Normal size heart Normal size heart

– No pleural effusion No pleural effusion

– Ground GlassGround Glass appearance appearance

– Often normal early in the disease but may rapidly Often normal early in the disease but may rapidly

progress to complete whiteoutprogress to complete whiteout

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ARDSARDS

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ARDSARDS

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Symptoms develop 24 to 48 hours of injurySymptoms develop 24 to 48 hours of injury

Sudden progressive disorderSudden progressive disorder Pulmonary edemaPulmonary edema Severe dyspneaSevere dyspnea Hypoxemia Hypoxemia REFRACTORYREFRACTORY to O2 to O2 Decreased lung compliance Decreased lung compliance Diffuse pulmonary infiltratesDiffuse pulmonary infiltrates

– Symptoms may be minimal compared to CXRSymptoms may be minimal compared to CXR – Rales may be heardRales may be heard

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ARDSARDS

Common Risk Common Risk FactorsFactors Other Risk FactorsOther Risk Factors

Sepsis Sepsis Massive Massive Trauma Trauma Shock Shock MultipleMultiple

Transfusions Transfusions Pneumonia Pneumonia

Aspiration     Aspiration     InfectionInfection

Smoke inhalation Smoke inhalation Inhaled toxinsInhaled toxins

Burns Burns Near Drowning Near Drowning

DKA DKA Pregnancy Pregnancy Eclampsia Eclampsia

Amniotic Fluid EmbolusAmniotic Fluid EmbolusDrugsDrugs

Acute Pancreatitis Acute Pancreatitis DIC DIC

Head Injury Head Injury ICP ICP

Fat Emboli Fat Emboli Blood Products Blood Products

Heart/Lung BypassHeart/Lung Bypass Tumor Lysis Tumor Lysis

Pulmonary ContusionPulmonary ContusionNarcoticsNarcotics

RISK FACTORSRISK FACTORS

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ARDSARDS

TREATMENTTREATMENT

– Respiratory SupportRespiratory Support

– PEEP, CPAPPEEP, CPAP

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Chronic Lung DiseaseChronic Lung Disease

COPDCOPD– Presents with hyper-inflated lung fields Presents with hyper-inflated lung fields

Due to chronic air trappingDue to chronic air trapping

May be barrel chestedMay be barrel chested

– May lead to cor pulmonale May lead to cor pulmonale (right-sided heart failure)(right-sided heart failure)

Due to chronic high pulmonary pressuresDue to chronic high pulmonary pressures

– Often hypercarbic (high pCO2)Often hypercarbic (high pCO2) Often dependent upon hypoxic driveOften dependent upon hypoxic drive

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Chronic Lung DiseaseChronic Lung Disease

COPD TREATMENTCOPD TREATMENT– Avoid overuse of oxygenAvoid overuse of oxygen (except in emergencies) (except in emergencies)

– BronchodilatorsBronchodilators

– SteroidsSteroids

– HydrationHydration

– EducationEducation

Pursed Lip BreathingPursed Lip Breathing

Leaning UprightLeaning Upright

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Near DrowningNear Drowning Salt WaterSalt Water

– Causes body fluids to shift into lungsCauses body fluids to shift into lungs Osmosis: From low to high concentrationOsmosis: From low to high concentration Results in hemoconcentration & hypovolemiaResults in hemoconcentration & hypovolemia

– Results in acute pulmonary edemaResults in acute pulmonary edema Fresh WaterFresh Water

– Fluids shift into body tissuesFluids shift into body tissues Results in hemodilution & hypervolemiaResults in hemodilution & hypervolemia Can result in gross edemaCan result in gross edema

– Damaged alveoli fill with proteinaceous fluidDamaged alveoli fill with proteinaceous fluid May lead to pulmonary edemaMay lead to pulmonary edema

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PneumoniaPneumonia

Lung infection (bacterial, viral, or fungal)Lung infection (bacterial, viral, or fungal)

– Most commonly caused by SMost commonly caused by Streptococcus treptococcus pneumoniaepneumoniae

Symptoms include fever, pleuretic chest Symptoms include fever, pleuretic chest pain, productive cough, and tachypneapain, productive cough, and tachypnea

– Often presents bronchial breath sounds over the Often presents bronchial breath sounds over the lung area lung area

Treatment involves giving the right antibioticTreatment involves giving the right antibiotic

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PneumothoraxPneumothorax DEFINITIONSDEFINITIONS

– Simple pneumothoraxSimple pneumothorax Results from buildup of air or pressure in the pleural spaceResults from buildup of air or pressure in the pleural space

– Spontaneous pneumothoraxSpontaneous pneumothorax May be due to blebs that ruptureMay be due to blebs that rupture The 2 key risk factors are increased chest length and The 2 key risk factors are increased chest length and

cigarette smokingcigarette smoking

– Tension pneumothoraxTension pneumothorax Involves a buildup of air in the pleural space due to Involves a buildup of air in the pleural space due to

one-way movement of airone-way movement of air Progressively worsensProgressively worsens Requires immediate interventionRequires immediate intervention

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PneumothoraxPneumothorax

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Tension PneumothoraxTension Pneumothorax

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PneumothoraxPneumothorax

CAUSESCAUSES

– BarotraumaBarotrauma

– InjuryInjury

– BlebsBlebs

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PneumothoraxPneumothorax

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Standard PneumothoraxStandard Pneumothorax

Sharp "pleuritic" chest pain, worse on breathingSharp "pleuritic" chest pain, worse on breathing Sudden shortness of breathSudden shortness of breath Dry, hacking cough (may occur due to irritation Dry, hacking cough (may occur due to irritation

of the diaphragm)of the diaphragm) May cause mediastinal shift May cause mediastinal shift

– Tension pneumothoraxTension pneumothorax Signs of standard pneumothorax with signs of Signs of standard pneumothorax with signs of

cardiovascular collapse cardiovascular collapse Immediately life threateningImmediately life threatening May cause mediastinal shiftMay cause mediastinal shift

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PneumothoraxPneumothorax TREATMENTTREATMENT Spontaneous pneumothoraxSpontaneous pneumothorax

– Depends on symptoms & size of pneumothorax Depends on symptoms & size of pneumothorax

– Provide respiratory supportProvide respiratory support

– May need chest tube or needle decompression May need chest tube or needle decompression Some resolve without interventionSome resolve without intervention

Tension pneumothoraxTension pneumothorax– Requires Requires immediateimmediate intervention intervention

– May cause cardiovascular collapseMay cause cardiovascular collapse

– May need chest tube or needle decompression May need chest tube or needle decompression 22ndnd intercostal space intercostal space

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TREATMENTTREATMENT

– PleurodesisPleurodesis

PneumothoraxPneumothorax

Chemical or surgical adhesion of the lung Chemical or surgical adhesion of the lung to the chest wallto the chest wall

Used for multiple collapsed lungs or Used for multiple collapsed lungs or persistent collapsepersistent collapse

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Flail ChestFlail Chest

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DefinitionDefinition

Signs & SymptomsSigns & Symptoms

Pulmonary EmbolismPulmonary Embolism

– Arterial embolus that obstructs blood flow to the lung Arterial embolus that obstructs blood flow to the lung

– Symptoms include sudden dyspnea, cough, chest Symptoms include sudden dyspnea, cough, chest pain, hemoptysis and sinus tachycardiapain, hemoptysis and sinus tachycardia

– Blood gas shows low pO2 & low pCO2Blood gas shows low pO2 & low pCO2

– May present positive Homan’s SignMay present positive Homan’s Sign

– May present loud S2May present loud S2

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Diagnostic TestsDiagnostic Tests

– CXRCXR

– VQ ScanVQ Scan

– Spiral CTSpiral CT

– Pulmonary arteriogram/angiogramPulmonary arteriogram/angiogram

– Venous ultrasound of the lower extremitiesVenous ultrasound of the lower extremities

– ABG with low pO2 & low pCO2ABG with low pO2 & low pCO2

– D-Dimer D-Dimer

Pulmonary EmbolismPulmonary Embolism

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TreatmentTreatment– Requires immediate intervention Requires immediate intervention

– Provide respiratory supportProvide respiratory support

– Treat pain & comfortTreat pain & comfort

– Usually includes intravenous heparinUsually includes intravenous heparin Heparin reduces risk of secondary Heparin reduces risk of secondary

thrombus formation while clot is reabsorbedthrombus formation while clot is reabsorbed

– May require embolectomyMay require embolectomy

– May require thrombolysisMay require thrombolysis

– May need umbrella filter May need umbrella filter

– May need long term anticoagulantsMay need long term anticoagulants

Pulmonary EmbolismPulmonary Embolism

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Respiratory FailureRespiratory Failure

DEFINITIONSDEFINITIONS

– Failure to maintain adequate gas exchange Failure to maintain adequate gas exchange

– Inadequate blood oxygenation or CO2 removalInadequate blood oxygenation or CO2 removal

– PaO2 < 50 mmHg and/or PaCO2 > 50 mmHg PaO2 < 50 mmHg and/or PaCO2 > 50 mmHg

and/or pH < 7.35 and/or pH < 7.35 on Room Air on Room Air

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Respiratory FailureRespiratory Failure

TYPE ITYPE I Hypoxemia Hypoxemia withoutwithout hypercapnia hypercapnia

TYPE II TYPE II Hypoxemia Hypoxemia withwith hypercapnia hypercapnia

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Respiratory FailureRespiratory Failure

CAUSESCAUSES

– V/Q MismatchingV/Q Mismatching

– Intrapulmonary ShuntingIntrapulmonary Shunting

– Alveolar HypoventilationAlveolar Hypoventilation

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Respiratory FailureRespiratory Failure

V/Q MISMATCHING V/Q MISMATCHING

– COPDCOPD

– Interstitial Lung DiseaseInterstitial Lung Disease

– Pulmonary EmbolismPulmonary Embolism

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Respiratory FailureRespiratory Failure

PULMONARY SHUNTINGPULMONARY SHUNTING

– AV fistulas/malformationsAV fistulas/malformations

– Alveolar collapse (atelectasis)Alveolar collapse (atelectasis)

– Alveolar consolidation (pneumonia)Alveolar consolidation (pneumonia)

– Excessive mucus accumulation Excessive mucus accumulation

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Respiratory FailureRespiratory Failure

SIGNS & SYMPTOMSSIGNS & SYMPTOMS

– Restlessness / AgitationRestlessness / Agitation

– Confusion / Confusion / LOC LOC

– Tachycardia / DysrhythmiasTachycardia / Dysrhythmias

– Tachypnea / Dyspnea Tachypnea / Dyspnea

– Cool, clammy, pale skin Cool, clammy, pale skin

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Respiratory FailureRespiratory Failure

ARTERIAL BLOOD GASESARTERIAL BLOOD GASES

– pH 7.30 / pO2 45 / pCO2 80pH 7.30 / pO2 45 / pCO2 80

– pH 7.30 / pO2 55 / pCO2 65pH 7.30 / pO2 55 / pCO2 65

– pH 7.32 / pO2 50 / pCO2 50pH 7.32 / pO2 50 / pCO2 50

– pH 7.55 / pO2 65 / pCO2 22 pH 7.55 / pO2 65 / pCO2 22

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Respiratory FailureRespiratory Failure

TREATMENT TREATMENT – Ensure Adequate VentilationEnsure Adequate Ventilation FiO2FiO2

Ineffective with shuntingIneffective with shunting Prolonged O2 > 40% causes O2 toxicityProlonged O2 > 40% causes O2 toxicity Must use caution with CO2 retainersMust use caution with CO2 retainers

– Chronic hypercapnia causes CO2 retainers Chronic hypercapnia causes CO2 retainers to use hypoxic driveto use hypoxic drive

– Too much O2 can depress respirationsToo much O2 can depress respirations

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BREAK!BREAK!

CCRN REVIEW PART 1CCRN REVIEW PART 1

Page 142: CCRN Review part 1

GI BleedGI Bleed

PancreatitisPancreatitis

Gastrointestinal AlterationsGastrointestinal Alterations

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CAUSESCAUSES– UGI BleedingUGI Bleeding

Includes the esophagus, stomach, duodenumIncludes the esophagus, stomach, duodenum

– Peptic Ulcer Disease (PUD), or Esophageal VaricesPeptic Ulcer Disease (PUD), or Esophageal Varices

– ASA, NSAID’s, Anticoagulants, AlcoholASA, NSAID’s, Anticoagulants, Alcohol

– H. PyloriH. Pylori

– LGI BleedingLGI Bleeding Includes the jejunum, ileum, colon, rectum Includes the jejunum, ileum, colon, rectum

– Colorectal cancer, Polyps, Hemorrhoids, IBD Colorectal cancer, Polyps, Hemorrhoids, IBD

Gastrointestinal BleedingGastrointestinal Bleeding

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Gastrointestinal BleedingGastrointestinal Bleeding

Page 145: CCRN Review part 1

Gastrointestinal BleedingGastrointestinal Bleeding HematemesisHematemesis – vomiting of blood (or coffee ground – vomiting of blood (or coffee ground

material) (indicates bleeding above the duodenum )material) (indicates bleeding above the duodenum )

MelenaMelena – passage of black tarry stools > 50ml (indicates – passage of black tarry stools > 50ml (indicates degradation of blood in the bowel)degradation of blood in the bowel)

HematocheziaHematochezia – passage of red blood (rectal bleeding)– passage of red blood (rectal bleeding)

Occult BleedingOccult Bleeding – bleeding that is not apparent to the – bleeding that is not apparent to the patient and results from small amounts of bloodpatient and results from small amounts of blood

Obscure BleedingObscure Bleeding – occult or obvious but source not – occult or obvious but source not identifiedidentified

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Gastrointestinal BleedingGastrointestinal Bleeding

HematemesisHematemesis – – always UGI sourcealways UGI source

MelanaMelana – – indicates blood has been in GI tract indicates blood has been in GI tract for extended periods for extended periods – Mostly UGIMostly UGI– Small bowelSmall bowel– Rt colon (if bleeding relatively slow)Rt colon (if bleeding relatively slow)

HematocheziaHematochezia – Mostly colonMostly colon– Massive UGI bleeding (not enough time for degradation)Massive UGI bleeding (not enough time for degradation)

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TREATMENTTREATMENT– Find the underlying causeFind the underlying cause

– Fluid volume replacementFluid volume replacement

– Endoscopy or colonoscopyEndoscopy or colonoscopy

– Medical and /or surgical therapy Medical and /or surgical therapy SomatostatinSomatostatin IV or intra-arterial vasopressinIV or intra-arterial vasopressin SclerotherpaySclerotherpay Angiography with embolizationAngiography with embolization ElectrocoagulationElectrocoagulation Band ligationBand ligation Balloon tamponade (Sengstaken-Blackmore tube)Balloon tamponade (Sengstaken-Blackmore tube)

Gastrointestinal BleedingGastrointestinal Bleeding

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The PancreasThe Pancreas

The Pancreas secretes digestive enzymes, The Pancreas secretes digestive enzymes, bicarbonate, water, and some electrolytes into bicarbonate, water, and some electrolytes into the duodenum via the pancreatic ductthe duodenum via the pancreatic duct

– Lipase, Amylase, TrypsinLipase, Amylase, Trypsin

The Pancreas also produces The Pancreas also produces and secretes insulin and secretes insulin

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PancreatitisPancreatitis

DEFINITIONDEFINITION– An autodigestive process resulting An autodigestive process resulting

from premature activation of from premature activation of pancreatic enzymespancreatic enzymes

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PancreatitisPancreatitis

PATHOSHYSIOLOGYPATHOSHYSIOLOGY

• Inactive pancreatic enzymes are activated outside Inactive pancreatic enzymes are activated outside of the duodenumof the duodenum

• The swelling pancreas causes fluids to shift into The swelling pancreas causes fluids to shift into the retro peritoneum and bowel the retro peritoneum and bowel

• Fluid shifts can cause severe hypovolemia and Fluid shifts can cause severe hypovolemia and hypotensionhypotension

• Inflammation cause commotion around pancreasInflammation cause commotion around pancreas

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PancreatitisPancreatitis

MANY CAUSESMANY CAUSES– AlcoholismAlcoholism

– Biliary DiseaseBiliary Disease

– GallstonesGallstones

– InfectionsInfections

– HyperparathyroidismHyperparathyroidism

– HypertriglyceridemiaHypertriglyceridemia

– HypercalcemiaHypercalcemia

– Peptic Ulcer DiseasePeptic Ulcer Disease

– Cystic FibrosisCystic Fibrosis

– Vascular DiseaseVascular Disease

– Multiple DrugsMultiple Drugs

– Much Much MoreMuch Much More

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PancreatitisPancreatitis

SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Abdominal PainAbdominal Pain

– Nausea & VomitingNausea & Vomiting

– Abdominal DistentionAbdominal Distention

– JaundiceJaundice

– MalnutritionMalnutrition

– HematemesisHematemesis

– Grey Turner’s SignGrey Turner’s Sign

– Cullen’s SignCullen’s Sign

– Elevated Amylase, Elevated Amylase,

Lipase, LDH, AST, WBC’s Lipase, LDH, AST, WBC’s

BUN, and GlucoseBUN, and Glucose

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PancreatitisPancreatitis

COMPLICATIONSCOMPLICATIONS– HypocalcemiaHypocalcemia– HypotensionHypotension– Acute Tubular NecrosisAcute Tubular Necrosis– DICDIC– Obstructive JaundiceObstructive Jaundice– Erosive GastritisErosive Gastritis– Paralytic IleusParalytic Ileus– Pseudocyst or AbscessPseudocyst or Abscess– Bowel InfarctionBowel Infarction– Internal BleedingInternal Bleeding– Fat NecrosisFat Necrosis

– Pleural Effusion (left)Pleural Effusion (left)– Pulmonary InfiltratesPulmonary Infiltrates– Hypoxemia Hypoxemia – AtelectasisAtelectasis– ARDSARDS– Pericardial EffusionPericardial Effusion– Mediastinal AbscessMediastinal Abscess– HyperglycemiaHyperglycemia– HypertriglyceridemiaHypertriglyceridemia– EncephalopathyEncephalopathy

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PancreatitisPancreatitis

TREATMENTTREATMENT– StabilizationStabilization

Correct Fluid AndCorrect Fluid And Electrolyte StatusElectrolyte Status

– Respiratory SupportRespiratory Support – Control PainControl Pain

DemerolDemerol

– NG TubeNG Tube NPONPO

– TPNTPN Restricted DietRestricted Diet

– Monitor For ComplicationsMonitor For Complications

– Monitor Blood SugarMonitor Blood Sugar

– Drug TherapiesDrug Therapies Somatostatin, Somatostatin,

AnticholinergicsAnticholinergics

– Watch For Signs Of Watch For Signs Of InfectionInfection

– PrayPray

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PancreatitisPancreatitis

FULMINATING PANCREATITISFULMINATING PANCREATITIS• Overwhelming form Overwhelming form

• Necrotizing formNecrotizing form

• Extreme symptomsExtreme symptoms

• Seen with ESRF patientsSeen with ESRF patients

• May lead to ARDS & DICMay lead to ARDS & DIC

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PancreatitisPancreatitis

FULMINATING PANCREATITISFULMINATING PANCREATITIS• Signs & SymptomsSigns & Symptoms

Tachycardia & low BP (may be the only sign) Tachycardia & low BP (may be the only sign)

Pulmonary & cerebral insufficiency Pulmonary & cerebral insufficiency

Acute diabetic ketosis or oliguriaAcute diabetic ketosis or oliguria

Hemorrhagic pancreatitis may appear Hemorrhagic pancreatitis may appear

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THE ENDTHE ENDPART 1PART 1

CCRN REVIEWCCRN REVIEW

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THANK YOUTHANK YOU

CCRN REVIEW PART 1CCRN REVIEW PART 1

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ReferencesReferences American Heart Association. (2005). Guidelines 2005 for Cardiopulmonary

Resuscitation and Emergency Cardiovascular Care. Available at: www.americanheart.org.

Bridges EJ.(2006) Pulmonary artery pressure monitoring: when, how, and what else to use. AACN Adv Crit Care. 2006;17(3):286–303.

Chulay, M., Burns S. M. (2006). AACN Essentials of Critical Care Nursing. McGraw-Hill Companies, Inc., Chapter 23.

Finkelmeier, B., Marolda, D. (2004) Aortic Dissection, Journal of Cardiovascular Nursing: 15(4):15–24.

Hughes E. (2004). Understanding the care of patients with acute pancreatitis. Nurs Standard: (18) pgs 45-54.

Sole, M. L., Klein, D. G. & Moseley, M. (2008). Introduction to Critical Care Nursing. 5th ed. Philadelphia, Pa: Saunders.

Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis and Treatment for repair of abdominal aortic aneurysm. St. Louis, Mo.: Mosby/Elsevier. pg 145-188.

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References ContinuedReferences Continued Urden, L., Lough, M. E. & Stacy, K. L. (2009). Thelan's Critical Care Nursing:

Diagnosis and Management (6th ed). St. Louis, Mo.: Mosby/Elsevier.

Woods, S., Sivarajan Froelicher, E. S., & Motzer, S. U. (2004). Cardiac Nursing. 5th ed. Philadelphia, Pa: Lippincott Williams & Wilkins.

Wynne J, Braunwald E. (2004). The Cardiomyopathies in Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine (7th Edition). Philadelphia: W.B. Saunders, vol. 2, pps. 1659–1696, 1751–1803.

Zimmerman & Sole. (2001). Critical Care Nursing (3rd Edition). WB Saunders., pgs. 41-80, 176-180, 242-266.

Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular Nursing:15(4):1–14, July 2001.

Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. Lippincott Williams & Wilkins, Philadelphia: pgs. 35-548. 

Wung, S., Aouizerat, B. E. (Nov/Dec 2004). Aortic Aneurysms. Journal of Cardiovascular Nursing. Lippincott Williams & Wilkins, Inc.:19(6):409-416, 34(2).


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