CCRN Review part 1

““Never let what you cannot doNever 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


TOPICSTOPICS

Acute Coronary SyndromesAcute Coronary Syndromes

Acute Myocardial InfarctionAcute Myocardial Infarction

Heart BlocksHeart Blocks

Heart FailureHeart Failure

Cardiac AlterationsCardiac Alterations

Aortic AneurysmsAortic Aneurysms

CardiomyopathyCardiomyopathy

Shock StatesShock 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


OBJECTIVESOBJECTIVES
1.1. 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 ofIdentify 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.


OBJECTIVESOBJECTIVES
15.15. 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 respiratoryRecognize 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 hemodynamicRecognize 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 availableDescribe the signs & symptoms of acute pancreatitis and available
treatments.treatments.


Acute CoronaryAcute Coronary
SyndromesSyndromes

Acute MIAcute MI


Cardiac AlterationsCardiac Alterations
Cardiovascular ConditionsCardiovascular Conditions


Heart BlocksHeart Blocks


Shock StatesShock States


DEFINITIONSDEFINITIONS
– Term used to cover a group of symptomsTerm used to cover a group of symptoms
compatible with acute myocardial ischemiacompatible with acute myocardial ischemia
– Acute myocardial ischemia is insufficient bloodAcute myocardial ischemia is insufficient blood
supply to the heart muscle usually resulting fromsupply to the heart muscle usually resulting from
coronary artery diseasecoronary artery disease
Acute Coronary SyndromeAcute Coronary Syndrome


DEFINITIONDEFINITION
– Infarction occurs due to mechanical obstructionInfarction occurs due to mechanical obstruction
of a coronary artery (or branch) caused by aof a coronary artery (or branch) caused by a
thrombus, plaque rupture, coronary spasmthrombus, plaque rupture, coronary spasm
and/or dissection.and/or dissection.
– STEMI vs. NSTEMI (non-STEMI)STEMI vs. NSTEMI (non-STEMI)


SIGNS & SYMPTOMSSIGNS & SYMPTOMS
– Complains VaryComplains Vary

May include crushing chest pain (which may or mayMay include crushing chest pain (which may or may
not radiate), back, neck, jaw, teeth and/or epigastricnot 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


↑↑ 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 abnormalDiabetics and women often present abnormal
symptomssymptoms

Coronary CirculationCoronary Circulation

II AVRAVR V1V1
V4V4
IIII AVL V2 V5AVL V2 V5
IIIIII AVF V3 V6AVF V3 V6
IIII
VV
12 Lead ECG12 Lead ECG


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 aVFLeads 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

 ST ELEVATIONSST ELEVATIONS
– Lateral Wall MILateral Wall MI
 I, aVL, VI, aVL, V55 and Vand 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

Coronary ArteriesCoronary Arteries

Anterior Wall MIAnterior Wall MI

Inferior Wall MIInferior Wall MI

 COMPLICATIONSCOMPLICATIONS
– Dysrhythmias, heart failure, pericarditis,Dysrhythmias, heart failure, pericarditis,
ventricular aneurysms, ventricular thrombus,ventricular aneurysms, ventricular thrombus,
VSD, mitral regurgitation, papillary muscle (orVSD, mitral regurgitation, papillary muscle (or
chordae tendineae) rupture, pericardialchordae tendineae) rupture, pericardial
effusions, pericarditiseffusions, pericarditis


NURSING INTERVENTIONSNURSING INTERVENTIONS
– OO22
– BedrestBedrest
– Serial ECG’sSerial ECG’s
– Serial cardiac enzymesSerial cardiac enzymes
– Keep pain free (NTG. MSOKeep pain free (NTG. MSO44))
– MONAMONA (Morphine, O2, Nitroglycerin, Aspirin),(Morphine, O2, Nitroglycerin, Aspirin),
Heparin, beta-blockers, and ace inhibitors. May alsoHeparin, beta-blockers, and ace inhibitors. May also
include thrombolytics or Gp2b3a inhibitorsinclude thrombolytics or Gp2b3a inhibitors
– PCI, PTCA, IABP, CABGPCI, PTCA, IABP, CABG


TREATMENTTREATMENT
– Time Is Heart MuscleTime Is Heart Muscle
– Prompt ECGPrompt ECG
– Goals: Relieve pain, limit the size of theGoals: Relieve pain, limit the size of the
infarction and to prevent complicationsinfarction and to prevent complications
(primarily lethal dysrhythmias)(primarily lethal dysrhythmias)


TREATMENTTREATMENT
– MONAMONA (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 Gp2b3aMay 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

Balloon AngioplastyBalloon Angioplasty

Vascular Stent DeploymentVascular Stent Deployment

 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


– A bulge or ballooning of the aortaA bulge or ballooning of the aorta

When the walls of the aneurysm include all threeWhen 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 theWhen 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


CAUSESCAUSES

AtherosclerosisAtherosclerosis

Marfan syndromeMarfan syndrome

HypertensionHypertension

Crack cocaine usageCrack cocaine usage

SmokingSmoking

TraumaTrauma

Aortic Aneurysms RuptureAortic Aneurysms Rupture
 An aortic aneurysm, depending on its size, mayAn 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 theThe risk of an aneurysm rupturing increases as the
aneurysm gets largeraneurysm gets larger
 The risk of rupture also depends on the location ofThe risk of rupture also depends on the location of
the aneurysmthe aneurysm
 Each year, approximately 15,000 Americans die of aEach year, approximately 15,000 Americans die of a
ruptured aortic aneurysm.ruptured aortic aneurysm.

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


– Often produces no symptomsOften produces no symptoms
– If an aortic aneurysm suddenly ruptures it presentsIf an aortic aneurysm suddenly ruptures it presents
with extreme abdominal or back pain, a pulsatingwith extreme abdominal or back pain, a pulsating
mass in the abdomen, and a drastic drop in bloodmass in the abdomen, and a drastic drop in blood
pressurepressure
– An increase in the size of an aneurysm means anAn increase in the size of an aneurysm means an
increased in the risk of ruptureincreased in the risk of rupture


THORACIC SIGNS & SYMPTOMSTHORACIC SIGNS & SYMPTOMS
– Back, shoulder or neck painBack, shoulder or neck pain
– Cough, due to pressure placed on the tracheaCough, due to pressure placed on the trachea
– HoarsenessHoarseness
– Strider, dyspneaStrider, dyspnea
– Difficulty swallowingDifficulty swallowing
– Swelling in the neck or armsSwelling in the neck or arms

Aortic DissectionsAortic Dissections

– Tearing of the inner layer of the aortic wall, whichTearing of the inner layer of the aortic wall, which
allows blood to leak into the wall itself and causesallows blood to leak into the wall itself and causes
the separation of the inner and outer layersthe separation of the inner and outer layers
– Usually associated with severe chest pain radiatingUsually associated with severe chest pain radiating
to the backto the back

A.A. DissectionDissection
beginning in thebeginning in the
ascending aortaascending aorta
B.B. Whenever theWhenever the
ascending aortaascending aorta
is not involvedis not involved


COMPLICATIONSCOMPLICATIONS

RuptureRupture

PeripheralPeripheral embolizationembolization

InfectionInfection

SpontaneousSpontaneous occlusionocclusion of aortaof aorta


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 surgicalMarfan patients will require surgical
correction or endovascular stent placementcorrection or endovascular stent placement

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


CLASSIFICATIONSCLASSIFICATIONS
– Primary / Idiopathic (intrinsicPrimary / Idiopathic (intrinsic))

Heart disease of unknown cause, although viralHeart 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, valvularsuch as autoimmune diseases, CAD, valvular
disease, severe hypertension, or alcohol abusedisease, severe hypertension, or alcohol abuse


Hypertropic CardiomyopathyHypertropic Cardiomyopathy

Restrictive CardiomyopathyRestrictive Cardiomyopathy

Dilated CardiomyopathyDilated Cardiomyopathy


Bizarre hypertrophy of the septumBizarre hypertrophy of the septum
– Previously called IHSSPreviously called IHSS

Idiopathic Hypertropic Subaortic StenosisIdiopathic Hypertropic Subaortic Stenosis
– Known as HOCMKnown as HOCM

Hypertropic Obstructive CardiomyopathyHypertropic Obstructive Cardiomyopathy

Positive inotropic drugs ShouldPositive inotropic drugs Should NotNot Be UsedBe Used
↑↑ Contractility willContractility will ↑↑ outflow tract obstructionoutflow tract obstruction

Nitroglycerin ShouldNitroglycerin Should NotNot Be UsedBe Used
– Dilation Will Worsen The ProblemDilation Will Worsen The Problem


TREATMENTTREATMENT
– Relax the ventriclesRelax the ventricles
 Beta BlockersBeta Blockers
 Calcium Channel BlockersCalcium 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


Rigid Ventricular WallRigid Ventricular Wall
– Due to endomyocardial fibrosisDue to endomyocardial fibrosis
– Obstructs ventricular fillingObstructs ventricular filling

Least common formLeast common form


TREATMENTTREATMENT
– Positive InotropicsPositive Inotropics
– DiureticsDiuretics
– Low Sodium DietLow Sodium Diet


Grossly dilated ventricles without hypertrophyGrossly dilated ventricles without hypertrophy
– Global left ventricular dysfunctionGlobal left ventricular dysfunction
– Leads to pooling of blood and embolic episodesLeads to pooling of blood and embolic episodes
– Leads to refractory heart failureLeads to refractory heart failure
– Leads to papillary muscle dysfunction secondary toLeads to papillary muscle dysfunction secondary to
LV dilationLV dilation


TREATMENTTREATMENT
– Positive InotropesPositive Inotropes
– Afterload ReducersAfterload Reducers
– Anticoagulants with Atrial FibAnticoagulants with Atrial Fib

CardiomyopathiesCardiomyopathies


GENERALIZED TREATMENTGENERALIZED TREATMENT
– Positive InotropesPositive Inotropes

Except with Hypertropic CardiomyopathyExcept with Hypertropic Cardiomyopathy
– VasodilatorsVasodilators

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

BREAK!BREAK!

Conduction DefectsConduction Defects

STABLE VS UNSTABLESTABLE VS UNSTABLE
– StableStable

Start with medicationsStart with medications
– UnstableUnstable

Shock (cardioversion or defibrillation)Shock (cardioversion or defibrillation)

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

Atrial FibrillationAtrial Fibrillation
 AFibAFib
– Multifocal atrial impulses at rate 300-600/minMultifocal atrial impulses at rate 300-600/min
– Irregular conduction to ventriclesIrregular conduction to ventricles

Atrial FlutterAtrial Flutter
 AFLAFL
– Atrial impulses at rate of 250-350/minAtrial 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

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

Supraventricular TachycardiaSupraventricular Tachycardia

SVTSVT
– Supraventricular rhythm at rate 150-250Supraventricular rhythm at rate 150-250
– P waves cannot be positively identifiedP waves cannot be positively identified
Atrial Tach = supraventricular rhythm with p wave morphologyAtrial Tach = supraventricular rhythm with p wave morphology
that is noticeably different from the sinus p wavethat is noticeably different from the sinus p wave

Ventricular TachycardiaVentricular Tachycardia
 VTVT
– Ventricular rate of 100-250/minVentricular rate of 100-250/min
– Wide QRSWide QRS

Torsades de PointesTorsades de Pointes
 Polymorphic VTPolymorphic VT
– VT with alternating ventricular focusVT with alternating ventricular focus
– Often associated with prolonged QT Rate < 100Often associated with prolonged QT Rate < 100

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

 DEFINITIONDEFINITION
– A condition in which the heart cannot pumpA condition in which the heart cannot pump
sufficient blood to meet the metabolic needs ofsufficient 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.


– 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 cardiogenicAcute left ventricular failure causes cardiogenic
pulmonary edemapulmonary edema

Non-cardiogenic pulmonary edema is a synonym forNon-cardiogenic pulmonary edema is a synonym for
Adult Respiratory Distress Syndrome (ARDS)Adult Respiratory Distress Syndrome (ARDS)


COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS
– Sympaththetic nervous system stimulationSympaththetic nervous system stimulation

TachycardiaTachycardia

Vasoconstriction and increased SVRVasoconstriction and increased SVR
– Renin-angiotensin-aldosterone systemRenin-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


FUNCTIONAL CLASSIFICATIONSFUNCTIONAL CLASSIFICATIONS
– Class IClass I
– Class IIClass II
– Class IIIClass III
– Class IVClass IV
(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)


– HypotensionHypotension
– DysrhythmiasDysrhythmias
– Respiratory FailureRespiratory Failure
– Progressive DeteriorationProgressive Deterioration
– Acute Renal FailureAcute Renal Failure
– Fluid & Electrolyte ImbalancesFluid & Electrolyte Imbalances


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!

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

SYMPTOMSSYMPTOMS
PAINPAIN
PAIN RELIEFPAIN RELIEF
EDEMAEDEMA
PULSESPULSES
INTEGUMENTINTEGUMENT
CHANGESCHANGES
ULCERSULCERS
SKIN TEMPERATURESKIN TEMPERATURE
SEXUAL ISSUESSEXUAL ISSUES
ARTERIALARTERIAL
Upon walkingUpon walking
On resting, standing orOn resting, standing or
dependent position of lower limbsdependent position of lower limbs
NoneNone
Decreased or absentDecreased or absent
Hair lossHair loss
Skin shinySkin shiny
Nail thickeningNail thickening
Pallor when elevatedPallor when elevated
Red when dependentRed when dependent
Ulcers located on toes, lateralUlcers located on toes, lateral
areas or site of traumaareas or site of trauma
Gangrene possibleGangrene possible
CoolCool
ImpotencyImpotency
Sexual 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 pigmentation
May be cyanotic whenMay 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


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

Bypass GraftsBypass Grafts

 DEFINITIONDEFINITION
– Inadequate perfusion to the body tissuesInadequate perfusion to the body tissues
– Low blood pressure with impaired perfusionLow blood pressure with impaired perfusion
to the end organsto the end organs
– May result in multiple organ dysfunctionMay result in multiple organ dysfunction
ShockShock


TYPES OF SHOCKTYPES OF SHOCK
– Hypovolemic ShockHypovolemic Shock
– Cardiogenic ShockCardiogenic Shock
– Distributive ShockDistributive Shock
– Obstructive ShockObstructive Shock
ShockShock

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 toAttempts 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 toADH makes the body hold onto water in an effort to
maintain volume and thus enough blood pressure tomaintain volume and thus enough blood pressure to
perfuse the body tissuesperfuse the body tissues

Types of ShockTypes of Shock

Hypovolemic ShockHypovolemic Shock
– Inadequate perfusion to the tissues due to insufficient intravascularInadequate 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 theInadequate 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


Low BPLow BP TachycardiaTachycardia
Orthostatic HypotensionOrthostatic Hypotension RestlessnessRestlessness
ConfusionConfusion Agitation (or listless)Agitation (or listless)
ThirstThirst PallorPallor
Cool, Clammy SkinCool, Clammy Skin ↑↑ Resp. RateResp. Rate
↓↓ UOPUOP ↓↓ COCO
↓↓ PAWPPAWP ↓↓ CVPCVP
↑↑ SVRSVR ↑↑ Lactate LevelsLactate Levels


TREATMENTTREATMENT
–Volume (IVF, Blood)Volume (IVF, Blood)


Low BPLow BP RestlessnessRestlessness
Agitation (or listless)Agitation (or listless) ConfusionConfusion
TachycardiaTachycardia PallorPallor
↑↑ PAWP (low with RVF)PAWP (low with RVF) ↑↑CVPCVP
↑↑ SVRSVR ↑↑ Lactate LevelsLactate Levels
JVDJVD Peripheral EdemaPeripheral Edema
Ventricular Gallop (S3)Ventricular Gallop (S3) DyspneaDyspnea
Pulmonary CracklesPulmonary Crackles


TREATMENTTREATMENT
BedrestBedrest O2O2
↑↑ COCO Positive InotropesPositive Inotropes
↓↓ Preload & AfterloadPreload & Afterload DiureticsDiuretics
↓↓ VasodilatorsVasodilators PositioningPositioning
↓↓ Myocardial DemandMyocardial Demand IABPIABP

Anaphylactic ShockAnaphylactic Shock

RestlessnessRestlessness ConfusionConfusion
Agitation (or listless)Agitation (or listless) ThirstThirst
PallorPallor Warm FeelingWarm Feeling
PruritusPruritus HivesHives
AngioedemaAngioedema BronchoconstrictionBronchoconstriction
WheezingWheezing Laryngeal EdemaLaryngeal Edema
DyspneaDyspnea Cool, Clammy SkinCool, Clammy Skin
↓↓ PAWPPAWP ↓↓ CVPCVP
↓↓ SVRSVR ↑↑ Lactate LevelsLactate Levels


TREATMENTTREATMENT
– EpinephrineEpinephrine
– IVFIVF
– VasoconstrictorsVasoconstrictors
– Support/Maintain AirwaySupport/Maintain Airway
Anaphylactic ShockAnaphylactic Shock


RestlessnessRestlessness ConfusionConfusion
Agitation (or listless)Agitation (or listless) PallorPallor
Cool, Clammy SkinCool, Clammy Skin ↓↓ CO ,CO , ↓↓ UOPUOP
Symptoms related to causeSymptoms related to cause


CAUSESCAUSES
Pulmonary EmbolusPulmonary Embolus TamponadeTamponade
Tension PneumothoraxTension Pneumothorax Aortic AneurysmAortic Aneurysm

TREATMENTTREATMENT
Treat the CauseTreat the Cause


Cardiogenic Shock is the only shock withCardiogenic Shock is the only shock with  PAWPPAWP

Early (Hyperdynamic) Shock is the only shock withEarly (Hyperdynamic) Shock is the only shock with  CO andCO and 
SVRSVR

Neurogenic Shock is the only shock withNeurogenic Shock is the only shock with  BradycardiaBradycardia

Anaphylactic Shock has the definitive characteristic of wheezing dueAnaphylactic 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

SIRS Sepsis Severe Septic MODS DeathSIRS Sepsis Severe Septic MODS Death
InfectionInfection Sepsis ShockSepsis Shock
Sepsis SyndromeSepsis Syndrome

 Sepsis
– SIRS’ response with presumed/confirmed infectionSIRS’ response with presumed/confirmed infection
 Severe Sepsis
– Sepsis associated with organ dysfunction, hypoperfusionSepsis 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 hypotensionSepsis with perfusion abnormalities and hypotension
despite adequate fluid resuscitationdespite adequate fluid resuscitation
Sepsis SyndromeSepsis Syndrome


EARLY STAGE (Hyperdynamic)EARLY STAGE (Hyperdynamic)
Normal BPNormal BP TachycardiaTachycardia
↑↑ Respiratory RateRespiratory Rate TemperatureTemperature
Normal ColorNormal Color Normal orNormal or ↑↑ UOPUOP
Normal PAWPNormal PAWP ↑↑ COCO ↓↓ SVRSVR

LATE STAGE (Hypodynamic)LATE STAGE (Hypodynamic)
Orthostatic HypotensionOrthostatic Hypotension RestlessnessRestlessness
ThirstThirst PallorPallor
Cool, Clammy SkinCool, Clammy Skin ↓↓ UOPUOP
↓↓ COCO ↓↓ PAWPPAWP
↓↓ CVPCVP ↑↑ SVRSVR
↑↑ Lactate LevelsLactate Levels
Septic ShockSeptic Shock

Homeostasis Gets LostHomeostasis Gets Lost

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, antibioticsPan 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

Invasive PA CatheterInvasive PA Catheter
CONTRAINDICATIONSCONTRAINDICATIONS

Mechanical Tricuspid or Pulmonary ValveMechanical 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

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

StrokeStroke VolumeVolume
 Components Stroke VolumeComponents Stroke Volume
– PreloadPreload:: the volume of blood in the ventriclesthe volume of blood in the ventricles
at end diastole and the stretch placed on theat end diastole and the stretch placed on the
muscle fibersmuscle fibers
– AfterloadAfterload:: the resistance the ventricles mustthe resistance the ventricles must
overcome to eject it’s volume of bloodovercome to eject it’s volume of blood
– Contractility:Contractility: the force with which the heartthe force with which the heart
muscle contracts (myocardial compliance)muscle contracts (myocardial compliance)

PAC Insertion SequencePAC Insertion Sequence

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

 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
700-1500700-1500 dynes/sec/cmdynes/sec/cm22
Normal Hemodynamic ValuesNormal Hemodynamic Values

Normal Hemodynamic ValuesNormal Hemodynamic Values

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-5/m21970 – 2390 dynes/sec/cm-5/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

Mixed Venous Oxygen SaturationMixed Venous Oxygen Saturation
SvO2SvO2
 End result of O2 delivery andEnd result of O2 delivery and
consumptionconsumption
 Measured in the pulmonary arteryMeasured in the pulmonary artery
 An average estimate of venous saturation forAn average estimate of venous saturation for
the whole body.the whole body.
 Does not reflect separate tissue perfusion orDoes not reflect separate tissue perfusion or
oxygenationoxygenation

Stroke Volume Variation (SVV)Stroke Volume Variation (SVV)
 Minimally Invasive Flo TracMinimally Invasive Flo Trac
 Measured through Arterial LineMeasured through Arterial Line
 Measures preload responsivenessMeasures preload responsiveness
 SVV > 10-15 % = preload responsiveSVV > 10-15 % = preload responsive
(responsive to fluids)(responsive to fluids)
 SVV > 10-15% = pulsus paradoxusSVV > 10-15% = pulsus paradoxus
 SVV < 10–15% = not preload responsiveSVV < 10–15% = not preload responsive

Measuring PA PressuresMeasuring PA Pressures

Measure All Hemodynamic ValuesMeasure All Hemodynamic Values
at End-Expirationat End-Expiration
– ““Patient PeakPatient Peak””
– ““Vent ValleyVent Valley””

Spontaneous RespirationsSpontaneous Respirations


Measure all pressures atMeasure all pressures at end-expirationend-expiration

AtAt top curvetop curve with Spontaneous Respirationwith Spontaneous Respiration
““patient-peak”patient-peak”

Intrathoracic pressureIntrathoracic pressure decreasesdecreases duringduring
spontaneous inspirationspontaneous inspiration
– Negative deflection on waveformsNegative deflection on waveforms

Intrathoracic pressureIntrathoracic pressure increasesincreases duringduring
spontaneous expirationspontaneous expiration
– Positive deflection on waveformsPositive deflection on waveforms


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 duringduring
positive pressure ventilations (inspiration)positive pressure ventilations (inspiration)
– Positive deflection on waveformsPositive deflection on waveforms

Intrathoracic pressureIntrathoracic pressure decreasesdecreases duringduring
positive pressure expirationpositive pressure expiration
– Negative deflection on waveformsNegative deflection on waveforms

 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 QTBegins near the end of QRS or at the QT
segmentsegment
 Delayed ECG correlation from CVP sinceDelayed ECG correlation from CVP since
PA catheter is further away from left atriumPA catheter is further away from left atrium
PAWP WaveformPAWP Waveform


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


ARDSARDS

DrowningDrowning


RespiratoryRespiratory
FailureFailure
Respiratory AlterationsRespiratory Alterations

ChronicChronic LungLung
DiseaseDisease

PneumoniaPneumonia

PulmonaryPulmonary
EmbolismEmbolism

ARDSARDS

– Severe respiratory failure associated with pulmonarySevere 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 orPulmonary 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 theOriginates from a number of insults involving damage to the
alveolar-capillary membranealveolar-capillary membrane

Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome

ARDSARDS

PATHOPHYSIOLOGYPATHOPHYSIOLOGY
– Inflammatory mediators are released causing extensiveInflammatory mediators are released causing extensive
structural damagestructural damage
– Increased permeability of pulmonary microvasculatureIncreased permeability of pulmonary microvasculature
causes leakage of proteinaceous fluid across the alveolar–causes leakage of proteinaceous fluid across the alveolar–
capillary membranecapillary membrane
– Also causes damage to the surfactant-producing type II cellsAlso causes damage to the surfactant-producing type II cells

ARDSARDS

CXR CHARACTERISTICSCXR CHARACTERISTICS
– Normal size heartNormal size heart
– No pleural effusionNo pleural effusion
– Ground GlassGround Glass appearanceappearance
– Often normal early in the disease but may rapidlyOften normal early in the disease but may rapidly
progress to complete whiteoutprogress to complete whiteout

ARDSARDS

– 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

HypoxemiaHypoxemia REFRACTORYREFRACTORY to O2to O2

Decreased lung complianceDecreased 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

ARDSARDS
Common RiskCommon Risk
FactorsFactors
Other Risk FactorsOther Risk Factors
SepsisSepsis
MassiveMassive
TraumaTrauma
ShockShock
MultipleMultiple
TransfusionsTransfusions
PneumoniaPneumonia
AspirationAspiration
InfectionInfection
Smoke inhalationSmoke inhalation
Inhaled toxinsInhaled toxins
BurnsBurns
Near DrowningNear Drowning
DKADKA
PregnancyPregnancy
EclampsiaEclampsia
Amniotic Fluid EmbolusAmniotic Fluid Embolus
DrugsDrugs
Acute PancreatitisAcute Pancreatitis
DICDIC
Head InjuryHead Injury
↑ ICPICP
Fat EmboliFat Emboli
Blood ProductsBlood Products
Heart/Lung BypassHeart/Lung Bypass
Tumor LysisTumor Lysis
Pulmonary ContusionPulmonary Contusion
NarcoticsNarcotics

RISK FACTORSRISK FACTORS

ARDSARDS

TREATMENTTREATMENT
– Respiratory SupportRespiratory Support
– PEEP, CPAPPEEP, CPAP


COPDCOPD
– Presents with hyper-inflated lung fieldsPresents 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 pulmonaleMay 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


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

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

PneumoniaPneumonia

Lung infection (bacterial, viral, or fungal)Lung infection (bacterial, viral, or fungal)
– Most commonly caused by SMost commonly caused by Streptococcustreptococcus
pneumoniaepneumoniae

Symptoms include fever, pleuretic chestSymptoms include fever, pleuretic chest
pain, productive cough, and tachypneapain, productive cough, and tachypnea
– Often presents bronchial breath sounds over theOften presents bronchial breath sounds over the
lung arealung area

Treatment involves giving the right antibioticTreatment involves giving the right antibiotic


– 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 andThe 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 toInvolves 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

Tension PneumothoraxTension Pneumothorax


CAUSESCAUSES
– BarotraumaBarotrauma
– InjuryInjury
– BlebsBlebs


– 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 irritationDry, hacking cough (may occur due to irritation
of the diaphragm)of the diaphragm)

May cause mediastinal shiftMay cause mediastinal shift
– Tension pneumothoraxTension pneumothorax

Signs of standard pneumothorax with signs ofSigns of standard pneumothorax with signs of
cardiovascular collapsecardiovascular collapse

Immediately life threateningImmediately life threatening

May cause mediastinal shiftMay cause mediastinal shift


TREATMENTTREATMENT

Spontaneous pneumothoraxSpontaneous pneumothorax
– Depends on symptoms & size of pneumothoraxDepends on symptoms & size of pneumothorax
– Provide respiratory supportProvide respiratory support
– May need chest tube or needle decompressionMay need chest tube or needle decompression

Some resolve without interventionSome resolve without intervention

Tension pneumothoraxTension pneumothorax
– RequiresRequires immediateimmediate interventionintervention
– May cause cardiovascular collapseMay cause cardiovascular collapse
– May need chest tube or needle decompressionMay need chest tube or needle decompression

22ndnd
intercostal spaceintercostal space


TREATMENTTREATMENT
– PleurodesisPleurodesis

Chemical or surgical adhesion of the lungChemical or surgical adhesion of the lung
to the chest wallto the chest wall

Used for multiple collapsed lungs orUsed for multiple collapsed lungs or
persistent collapsepersistent collapse

 DefinitionDefinition
 Signs & SymptomsSigns & Symptoms
– Arterial embolus that obstructs blood flow to the lungArterial embolus that obstructs blood flow to the lung
– Symptoms include sudden dyspnea, cough, chestSymptoms 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


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-DimerD-Dimer


TreatmentTreatment
– Requires immediate interventionRequires immediate intervention
– Provide respiratory supportProvide respiratory support
– Treat pain & comfortTreat pain & comfort
– Usually includes intravenous heparinUsually includes intravenous heparin

Heparin reduces risk of secondaryHeparin 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 filterMay need umbrella filter
– May need long term anticoagulantsMay need long term anticoagulants


– Failure to maintain adequate gas exchangeFailure to maintain adequate gas exchange
– Inadequate blood oxygenation or CO2 removalInadequate blood oxygenation or CO2 removal
– PaO2 < 50 mmHg and/or PaCO2 > 50 mmHgPaO2 < 50 mmHg and/or PaCO2 > 50 mmHg
and/or pH < 7.35and/or pH < 7.35 on Room Airon Room Air

TYPE ITYPE I HypoxemiaHypoxemia withoutwithout hypercapniahypercapnia
TYPE IITYPE II HypoxemiaHypoxemia withwith hypercapniahypercapnia


CAUSESCAUSES
– V/Q MismatchingV/Q Mismatching
– Intrapulmonary ShuntingIntrapulmonary Shunting
– Alveolar HypoventilationAlveolar Hypoventilation


V/Q MISMATCHINGV/Q MISMATCHING
– COPDCOPD
– Interstitial Lung DiseaseInterstitial Lung Disease
– Pulmonary EmbolismPulmonary Embolism


PULMONARY SHUNTINGPULMONARY SHUNTING
– AV fistulas/malformationsAV fistulas/malformations
– Alveolar collapse (atelectasis)Alveolar collapse (atelectasis)
– Alveolar consolidation (pneumonia)Alveolar consolidation (pneumonia)
– Excessive mucus accumulationExcessive mucus accumulation


– Restlessness / AgitationRestlessness / Agitation
– Confusion /Confusion / ↓↓ LOCLOC
– Tachycardia / DysrhythmiasTachycardia / Dysrhythmias
– Tachypnea / DyspneaTachypnea / Dyspnea
– Cool, clammy, pale skinCool, clammy, pale skin


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 22pH 7.55 / pO2 65 / pCO2 22


TREATMENTTREATMENT
– 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 retainersChronic hypercapnia causes CO2 retainers
to use hypoxic driveto use hypoxic drive
– Too much O2 can depress respirationsToo much O2 can depress respirations


GI BleedGI Bleed

Gastrointestinal AlterationsGastrointestinal Alterations


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, rectumIncludes the jejunum, ileum, colon, rectum
– Colorectal cancer, Polyps, Hemorrhoids, IBDColorectal cancer, Polyps, Hemorrhoids, IBD
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


HematemesisHematemesis –– always UGI sourcealways UGI source

MelanaMelana –– indicates blood has been in GI tractindicates blood has been in GI tract
for extended periodsfor 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)


TREATMENTTREATMENT
– Find the underlying causeFind the underlying cause
– Fluid volume replacementFluid volume replacement
– Endoscopy or colonoscopyEndoscopy or colonoscopy
– Medical and /or surgical therapyMedical 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)

The PancreasThe Pancreas

The Pancreas secretes digestive enzymes,The Pancreas secretes digestive enzymes,
bicarbonate, water, and some electrolytes intobicarbonate, water, and some electrolytes into
the duodenum via the pancreatic ductthe duodenum via the pancreatic duct
– Lipase, Amylase, TrypsinLipase, Amylase, Trypsin

The Pancreas also producesThe Pancreas also produces
and secretes insulinand secretes insulin


– An autodigestive process resultingAn autodigestive process resulting
from premature activation offrom premature activation of
pancreatic enzymespancreatic enzymes


PATHOSHYSIOLOGYPATHOSHYSIOLOGY
• Inactive pancreatic enzymes are activated outsideInactive pancreatic enzymes are activated outside
of the duodenumof the duodenum
• The swelling pancreas causes fluids to shift intoThe swelling pancreas causes fluids to shift into
the retro peritoneum and bowelthe retro peritoneum and bowel
• Fluid shifts can cause severe hypovolemia andFluid shifts can cause severe hypovolemia and
hypotensionhypotension
• Inflammation cause commotion around pancreasInflammation cause commotion around pancreas


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


– 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’sLipase, LDH, AST, WBC’s
BUN, and GlucoseBUN, and Glucose


– 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
– HypoxemiaHypoxemia
– AtelectasisAtelectasis
– ARDSARDS
– Pericardial EffusionPericardial Effusion
– Mediastinal AbscessMediastinal Abscess
– HyperglycemiaHyperglycemia
– HypertriglyceridemiaHypertriglyceridemia
– EncephalopathyEncephalopathy


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 OfWatch For Signs Of
InfectionInfection
– PrayPray


FULMINATING PANCREATITISFULMINATING PANCREATITIS
• Overwhelming formOverwhelming form
• Necrotizing formNecrotizing form
• Extreme symptomsExtreme symptoms
• Seen with ESRF patientsSeen with ESRF patients
• May lead to ARDS & DICMay lead to ARDS & DIC


FULMINATING PANCREATITISFULMINATING PANCREATITIS
• Signs & SymptomsSigns & Symptoms

Tachycardia & low BP (may be the only sign)Tachycardia & low BP (may be the only sign)

Pulmonary & cerebral insufficiencyPulmonary & cerebral insufficiency

Acute diabetic ketosis or oliguriaAcute diabetic ketosis or oliguria

Hemorrhagic pancreatitis may appearHemorrhagic pancreatitis may appear

THE ENDTHE END
PART 1PART 1
CCRN REVIEWCCRN REVIEW

THANK YOUTHANK YOU

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.

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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