““Never let what you cannot doNever let what you cannot dointerfere with what you can do”interfere with what you can do”--...
TOPICSTOPICSAcute Coronary SyndromesAcute Coronary SyndromesAcute Myocardial InfarctionAcute Myocardial InfarctionHear...
OBJECTIVESOBJECTIVES1.1. Understand the different types of acute coronary syndromes.Understand the different types of acu...
OBJECTIVESOBJECTIVES15.15. Distinguish between arterial and venous peripheral vascular disease.Distinguish between arteri...
Acute CoronaryAcute CoronarySyndromesSyndromesAcute MIAcute MIAortic AneurysmsAortic AneurysmsCardiac AlterationsCardi...
DEFINITIONSDEFINITIONS– Term used to cover a group of symptomsTerm used to cover a group of symptomscompatible with acute...
DEFINITIONDEFINITION– Infarction occurs due to mechanical obstructionInfarction occurs due to mechanical obstructionof a ...
SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Complains VaryComplains VaryMay include crushing chest pain (which may or mayMay inclu...
SIGNS & SYMPTOMSSIGNS & SYMPTOMS↑↑ PAWP,PAWP, ↓↓ CO,CO, ↑↑SVR, dysrhythmias, SSVR, dysrhythmias, S44,,cardiac failure, ca...
Coronary CirculationCoronary Circulation
II AVRAVR V1V1V4V4IIII AVL V2 V5AVL V2 V5IIIIII AVF V3 V6AVF V3 V6IIIIVV12 Lead ECG12 Lead ECG
ST ELEVATIONSST ELEVATIONS– Anterior Wall MIAnterior Wall MI Leads VLeads V11-V-V44Reciprocal changes in leads II, III,...
 ST ELEVATIONSST ELEVATIONS– Lateral Wall MILateral Wall MI I, aVL, VI, aVL, V55 and Vand V66 Area supplied by the Circ...
Coronary ArteriesCoronary Arteries
Anterior Wall MIAnterior Wall MI
Inferior Wall MIInferior Wall MI
 COMPLICATIONSCOMPLICATIONS– Dysrhythmias, heart failure, pericarditis,Dysrhythmias, heart failure, pericarditis,ventricu...
NURSING INTERVENTIONSNURSING INTERVENTIONS– OO22– BedrestBedrest– Serial ECG’sSerial ECG’s– Serial cardiac enzymesSerial ...
TREATMENTTREATMENT– Time Is Heart MuscleTime Is Heart Muscle– Prompt ECGPrompt ECG– Goals: Relieve pain, limit the size o...
TREATMENTTREATMENT– MONAMONA (Morphine, O2, Nitroglycerin, Aspirin)(Morphine, O2, Nitroglycerin, Aspirin),,Heparin, beta-...
Balloon AngioplastyBalloon Angioplasty
Vascular Stent DeploymentVascular Stent Deployment
AtherectomyAtherectomy
 SPECIFIC TREATMENTSSPECIFIC TREATMENTS– Inferior Wall (IWMI)Inferior Wall (IWMI) FluidsFluids (with RV infarct)(with RV...
Aortic AneurysmsAortic AneurysmsDEFINITIONDEFINITION– A bulge or ballooning of the aortaA bulge or ballooning of the aort...
Aortic AneurysmsAortic AneurysmsCAUSESCAUSESAtherosclerosisAtherosclerosisMarfan syndromeMarfan syndromeHypertensionHy...
Aortic Aneurysms RuptureAortic Aneurysms Rupture An aortic aneurysm, depending on its size, mayAn aortic aneurysm, depend...
Aortic AneurysmsAortic AneurysmsCLASSIFICATIONSCLASSIFICATIONS– Classified by shape, location along the aorta,Classified ...
Aortic AneurysmsAortic Aneurysms
Aortic AneurysmsAortic AneurysmsSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Often produces no symptomsOften produces no symptoms– I...
Aortic AneurysmsAortic AneurysmsTHORACIC SIGNS & SYMPTOMSTHORACIC SIGNS & SYMPTOMS– Back, shoulder or neck painBack, shou...
Aortic DissectionsAortic DissectionsDEFINITIONDEFINITION– Tearing of the inner layer of the aortic wall, whichTearing of ...
Aortic DissectionsAortic DissectionsA.A. DissectionDissectionbeginning in thebeginning in theascending aortaascending aort...
Aortic DissectionsAortic DissectionsA.A. DissectionDissectionbeginning in thebeginning in theascending aortaascending aort...
Aortic DissectionsAortic Dissections
Aortic DissectionsAortic Dissections
Aortic AneurysmsAortic AneurysmsCOMPLICATIONSCOMPLICATIONSRuptureRupturePeripheralPeripheral embolizationembolizationI...
Aortic AneurysmsAortic AneurysmsTREATMENTTREATMENTMedical managementMedical management– Controlled BP (within specific r...
CardiomyopathyCardiomyopathyDEFINITIONDEFINITION– Diseases of the heart muscle thatDiseases of the heart muscle thatcause...
CardiomyopathyCardiomyopathyCLASSIFICATIONSCLASSIFICATIONS– Primary / Idiopathic (intrinsicPrimary / Idiopathic (intrinsi...
CardiomyopathyCardiomyopathyHypertropic CardiomyopathyHypertropic CardiomyopathyRestrictive CardiomyopathyRestrictive Ca...
Hypertropic CardiomyopathyHypertropic CardiomyopathyBizarre hypertrophy of the septumBizarre hypertrophy of the septum– P...
HarleyHarley
Hypertropic CardiomyopathyHypertropic CardiomyopathyTREATMENTTREATMENT– Relax the ventriclesRelax the ventricles Beta Bl...
Restrictive CardiomyopathyRestrictive CardiomyopathyRigid Ventricular WallRigid Ventricular Wall– Due to endomyocardial f...
Restrictive CardiomyopathyRestrictive CardiomyopathyTREATMENTTREATMENT– Positive InotropicsPositive Inotropics– Diuretics...
Dilated CardiomyopathyDilated CardiomyopathyGrossly dilated ventricles without hypertrophyGrossly dilated ventricles with...
Dilated CardiomyopathyDilated CardiomyopathyTREATMENTTREATMENT– Positive InotropesPositive Inotropes– Afterload ReducersA...
CardiomyopathiesCardiomyopathies
CardiomyopathyCardiomyopathyGENERALIZED TREATMENTGENERALIZED TREATMENT– Positive InotropesPositive InotropesExcept with ...
BREAK!BREAK!CCRN REVIEW PART 1CCRN REVIEW PART 1
Conduction DefectsConduction DefectsSTABLE VS UNSTABLESTABLE VS UNSTABLE– StableStableStart with medicationsStart with m...
Normal Sinus RhythmNormal Sinus RhythmHeart RateHeart Rate 60 - 100 bpm60 - 100 bpmRhythmRhythm RegularRegularP WaveP Wave...
Atrial FibrillationAtrial Fibrillation AFibAFib– Multifocal atrial impulses at rate 300-600/minMultifocal atrial impulses...
Atrial FlutterAtrial Flutter AFLAFL– Atrial impulses at rate of 250-350/minAtrial impulses at rate of 250-350/min– Regula...
Wandering Atrial PacemakerWandering Atrial PacemakerWAPWAP– Multiple ectopic foci in the atriaMultiple ectopic foci in th...
Supraventricular TachycardiaSupraventricular TachycardiaSVTSVT– Supraventricular rhythm at rate 150-250Supraventricular r...
Ventricular TachycardiaVentricular Tachycardia VTVT– Ventricular rate of 100-250/minVentricular rate of 100-250/min– Wide...
Torsades de PointesTorsades de Pointes Polymorphic VTPolymorphic VT– VT with alternating ventricular focusVT with alterna...
Heart Blocks (AV Blocks)Heart Blocks (AV Blocks)Sinus Rhythm with First Degree AV BlockSinus Rhythm with First Degree AV B...
 DEFINITIONDEFINITION– A condition in which the heart cannot pumpA condition in which the heart cannot pumpsufficient blo...
DEFINITIONDEFINITION– Pulmonary EdemaPulmonary EdemaFluid in the alveolus that impairs gas exchange byFluid in the alveo...
COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS– Sympaththetic nervous system stimulationSympaththetic nervous system stim...
FUNCTIONAL CLASSIFICATIONSFUNCTIONAL CLASSIFICATIONS– Class IClass I– Class IIClass II– Class IIIClass III– Class IVClass...
COMPLICATIONSCOMPLICATIONS– HypotensionHypotension– DysrhythmiasDysrhythmias– Respiratory FailureRespiratory Failure– Pro...
TREATMENTTREATMENT– Improve OxygenationImprove Oxygenation– Decrease Myocardial Oxygen DemandDecrease Myocardial Oxygen D...
Vascular DiseaseVascular DiseaseAorto/Iliac Disease: Pre & Post PTA/StentAorto/Iliac Disease: Pre & Post PTA/Stent
Peripheral Vascular DiseasePeripheral Vascular DiseaseSYMPTOMSSYMPTOMSPAINPAINPAIN RELIEFPAIN RELIEFEDEMAEDEMAPULSESPULSES...
Peripheral Vascular DiseasePeripheral Vascular DiseaseTREATMENTSTREATMENTS– MedicalMedicalAre they taking ASA, Coumadin,...
Peripheral Vascular DiseasePeripheral Vascular DiseaseBypass GraftsBypass Grafts
 DEFINITIONDEFINITION– Inadequate perfusion to the body tissuesInadequate perfusion to the body tissues– Low blood pressu...
TYPES OF SHOCKTYPES OF SHOCK– Hypovolemic ShockHypovolemic Shock– Cardiogenic ShockCardiogenic Shock– Distributive ShockD...
ShockShockCOMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS–TachycardiaTachycardiaAttempts to deliver more blood to the tis...
Types of ShockTypes of ShockHypovolemic ShockHypovolemic Shock– Inadequate perfusion to the tissues due to insufficient i...
Hypovolemic ShockHypovolemic ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaOrthostatic Hypotens...
Hypovolemic ShockHypovolemic ShockTREATMENTTREATMENT–Volume (IVF, Blood)Volume (IVF, Blood)
Cardiogenic ShockCardiogenic ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP RestlessnessRestlessnessAgitation (or list...
TREATMENTTREATMENTBedrestBedrest O2O2↑↑ COCO Positive InotropesPositive Inotropes↓↓ Preload & AfterloadPreload & Afterloa...
Anaphylactic ShockAnaphylactic ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaRestlessnessRestle...
TREATMENTTREATMENT– EpinephrineEpinephrine– IVFIVF– VasoconstrictorsVasoconstrictors– Support/Maintain AirwaySupport/Main...
Obstructive ShockObstructive ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaRestlessnessRestless...
Obstructive ShockObstructive ShockCAUSESCAUSESPulmonary EmbolusPulmonary Embolus TamponadeTamponadeTension PneumothoraxTe...
Cardiogenic Shock is the only shock withCardiogenic Shock is the only shock with  PAWPPAWPEarly (Hyperdynamic) Shock i...
SIRS Sepsis Severe Septic MODS DeathSIRS Sepsis Severe Septic MODS DeathInfectionInfection Sepsis ShockSepsis ShockSepsis ...
 Sepsis– SIRS’ response with presumed/confirmed infectionSIRS’ response with presumed/confirmed infection Severe Sepsis–...
EARLY STAGE (Hyperdynamic)EARLY STAGE (Hyperdynamic)Normal BPNormal BP TachycardiaTachycardiaConfusionConfusion Agitation...
Homeostasis Gets LostHomeostasis Gets Lost
3.3. Improve PerfusionImprove Perfusion– Prevent organ dysfunctionPrevent organ dysfunction– Treat temp as neededTreat tem...
HEMODYNAMICSHEMODYNAMICS
Invasive PA CatheterInvasive PA CatheterCONTRAINDICATIONSCONTRAINDICATIONSMechanical Tricuspid or Pulmonary ValveMechanic...
BasicBasic ConceptsConceptsCO = HR X SVCO = HR X SVBP = CO x SVRBP = CO x SVRCO and SVR are inversely relatedCO and SVR...
StrokeStroke VolumeVolume Components Stroke VolumeComponents Stroke Volume– PreloadPreload:: the volume of blood in the v...
PAC Insertion SequencePAC Insertion Sequence
Phlebostatic AxisPhlebostatic Axis4th ICS Mid-chest, regardless of head elevation4th ICS Mid-chest, regardless of head ele...
 RAP (CVP)RAP (CVP) RVPRVP PAPPAP PAWPPAWP SVRSVR0-8 mmHg0-8 mmHg15-30/0-8 mmHg15-30/0-8 mmHg15-30/6-12 mmHg15-30/6-1...
Normal Hemodynamic ValuesNormal Hemodynamic ValuesValues normalized for body size (BSA)Values normalized for body size (B...
Mixed Venous Oxygen SaturationMixed Venous Oxygen SaturationSvO2SvO2 End result of O2 delivery andEnd result of O2 delive...
Stroke Volume Variation (SVV)Stroke Volume Variation (SVV) Minimally Invasive Flo TracMinimally Invasive Flo Trac Measur...
Measuring PA PressuresMeasuring PA PressuresMeasure All Hemodynamic ValuesMeasure All Hemodynamic Valuesat End-Expiration...
Spontaneous RespirationsSpontaneous Respirations
Measure all pressures atMeasure all pressures at end-expirationend-expirationAtAt top curvetop curve with Spontaneous Re...
Measure all pressures atMeasure all pressures at end-expirationend-expirationAtAt bottom curvebottom curve with mechanic...
 a-wavea-wave– Atrial contractionAtrial contraction– Correct location for measurement of PAWPCorrect location for measure...
c-wavec-wave– Rarely presentRarely present– Represents mitral valve closureRepresents mitral valve closurev-wavev-wave– ...
PAWP WaveformPAWP Waveform
BREAK!BREAK!CCRN REVIEW PART 1CCRN REVIEW PART 1
ARDSARDSDrowningDrowningPneumothoraxPneumothoraxRespiratoryRespiratoryFailureFailureRespiratory AlterationsRespiratory...
ARDSARDSDEFINITIONSDEFINITIONS– Severe respiratory failure associated with pulmonarySevere respiratory failure associated...
Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome
ARDSARDSPATHOPHYSIOLOGYPATHOPHYSIOLOGY– Inflammatory mediators are released causing extensiveInflammatory mediators are r...
ARDSARDSCXR CHARACTERISTICSCXR CHARACTERISTICS– Normal size heartNormal size heart– No pleural effusionNo pleural effusio...
ARDSARDS
ARDSARDSSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Symptoms develop 24 to 48 hours of injurySymptoms develop 24 to 48 hours of inj...
ARDSARDSCommon RiskCommon RiskFactorsFactorsOther Risk FactorsOther Risk FactorsSepsisSepsisMassiveMassiveTraumaTraumaShoc...
ARDSARDSTREATMENTTREATMENT– Respiratory SupportRespiratory Support– PEEP, CPAPPEEP, CPAP
Chronic Lung DiseaseChronic Lung DiseaseCOPDCOPD– Presents with hyper-inflated lung fieldsPresents with hyper-inflated lu...
Chronic Lung DiseaseChronic Lung DiseaseCOPD TREATMENTCOPD TREATMENT– Avoid overuse of oxygenAvoid overuse of oxygen (exc...
Near DrowningNear DrowningSalt WaterSalt Water– Causes body fluids to shift into lungsCauses body fluids to shift into lu...
PneumoniaPneumoniaLung infection (bacterial, viral, or fungal)Lung infection (bacterial, viral, or fungal)– Most commonly...
PneumothoraxPneumothoraxDEFINITIONSDEFINITIONS– Simple pneumothoraxSimple pneumothoraxResults from buildup of air or pre...
PneumothoraxPneumothorax
Tension PneumothoraxTension Pneumothorax
PneumothoraxPneumothoraxCAUSESCAUSES– BarotraumaBarotrauma– InjuryInjury– BlebsBlebs
PneumothoraxPneumothoraxSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Standard PneumothoraxStandard PneumothoraxSharp "pleuritic" ch...
PneumothoraxPneumothoraxTREATMENTTREATMENTSpontaneous pneumothoraxSpontaneous pneumothorax– Depends on symptoms & size o...
TREATMENTTREATMENT– PleurodesisPleurodesisPneumothoraxPneumothoraxChemical or surgical adhesion of the lungChemical or s...
Flail ChestFlail Chest
 DefinitionDefinition Signs & SymptomsSigns & SymptomsPulmonary EmbolismPulmonary Embolism– Arterial embolus that obstru...
Diagnostic TestsDiagnostic Tests– CXRCXR– VQ ScanVQ Scan– Spiral CTSpiral CT– Pulmonary arteriogram/angiogramPulmonary ar...
TreatmentTreatment– Requires immediate interventionRequires immediate intervention– Provide respiratory supportProvide re...
Respiratory FailureRespiratory FailureDEFINITIONSDEFINITIONS– Failure to maintain adequate gas exchangeFailure to maintai...
Respiratory FailureRespiratory FailureTYPE ITYPE I HypoxemiaHypoxemia withoutwithout hypercapniahypercapniaTYPE IITYPE II ...
Respiratory FailureRespiratory FailureCAUSESCAUSES– V/Q MismatchingV/Q Mismatching– Intrapulmonary ShuntingIntrapulmonary...
Respiratory FailureRespiratory FailureV/Q MISMATCHINGV/Q MISMATCHING– COPDCOPD– Interstitial Lung DiseaseInterstitial Lun...
Respiratory FailureRespiratory FailurePULMONARY SHUNTINGPULMONARY SHUNTING– AV fistulas/malformationsAV fistulas/malforma...
Respiratory FailureRespiratory FailureSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Restlessness / AgitationRestlessness / Agitation–...
Respiratory FailureRespiratory FailureARTERIAL BLOOD GASESARTERIAL BLOOD GASES– pH 7.30 / pO2 45 / pCO2 80pH 7.30 / pO2 4...
Respiratory FailureRespiratory FailureTREATMENTTREATMENT– Ensure Adequate VentilationEnsure Adequate Ventilation↑↑ FiO2Fi...
BREAK!BREAK!CCRN REVIEW PART 1CCRN REVIEW PART 1
GI BleedGI BleedPancreatitisPancreatitisGastrointestinal AlterationsGastrointestinal Alterations
CAUSESCAUSES– UGI BleedingUGI BleedingIncludes the esophagus, stomach, duodenumIncludes the esophagus, stomach, duodenum...
Gastrointestinal BleedingGastrointestinal Bleeding
Gastrointestinal BleedingGastrointestinal BleedingHematemesisHematemesis – vomiting of blood (or coffee ground– vomiting ...
Gastrointestinal BleedingGastrointestinal BleedingHematemesisHematemesis –– always UGI sourcealways UGI sourceMelanaMela...
TREATMENTTREATMENT– Find the underlying causeFind the underlying cause– Fluid volume replacementFluid volume replacement–...
The PancreasThe PancreasThe Pancreas secretes digestive enzymes,The Pancreas secretes digestive enzymes,bicarbonate, wate...
PancreatitisPancreatitisDEFINITIONDEFINITION– An autodigestive process resultingAn autodigestive process resultingfrom pr...
PancreatitisPancreatitisPATHOSHYSIOLOGYPATHOSHYSIOLOGY• Inactive pancreatic enzymes are activated outsideInactive pancrea...
PancreatitisPancreatitisMANY CAUSESMANY CAUSES– AlcoholismAlcoholism– Biliary DiseaseBiliary Disease– GallstonesGallstone...
PancreatitisPancreatitisSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Abdominal PainAbdominal Pain– Nausea & VomitingNausea & Vomitin...
PancreatitisPancreatitisCOMPLICATIONSCOMPLICATIONS– HypocalcemiaHypocalcemia– HypotensionHypotension– Acute Tubular Necro...
PancreatitisPancreatitisTREATMENTTREATMENT– StabilizationStabilizationCorrect Fluid AndCorrect Fluid AndElectrolyte Stat...
PancreatitisPancreatitisFULMINATING PANCREATITISFULMINATING PANCREATITIS• Overwhelming formOverwhelming form• Necrotizing...
PancreatitisPancreatitisFULMINATING PANCREATITISFULMINATING PANCREATITIS• Signs & SymptomsSigns & SymptomsTachycardia & ...
THE ENDTHE ENDPART 1PART 1CCRN REVIEWCCRN REVIEW
THANK YOUTHANK YOUCCRN REVIEW PART 1CCRN REVIEW PART 1
ReferencesReferences American Heart Association. (2005). Guidelines 2005 for CardiopulmonaryResuscitation and Emergency C...
References ContinuedReferences Continued Urden, L., Lough, M. E. & Stacy, K. L. (2009). Thelans Critical Care Nursing:Dia...
CCRN Review part 1
CCRN Review part 1
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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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  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 As plaque develops and the coronary arteries become increasingly narrower, collateral branches form to help supply those areas of heart muscle. MI’s with no collateral circulation tend to suffer more severe infarctions and more hemodynamic compromise. Edema and color changes (within the heart) are evident 6 hours after an MI. LV function is altered immediately in ischemic states as well as in infarctions. Wall thickness decreases 8 to 10 days later due to a natural physiological cleanup and/or necrotic tissue removal. Scar tissue and tissue remodeling occur later and may lead to cardiac failure. Transmural MI involves full thickness of the myocardium whereas subendocardial MI (non-Q wave) involves partial thickness.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Cardiac Enzymes: Troponin The troponin level rises within 4-6 hours after an AMI, peaks in 24 hours, and returns to baseline within 7-10 days. CK or CPK MB-CK is the cardiac specific isoenzyme MB-CK is normally less then 5% of the CK The CK level rises within 4-8 hours, peaks in 8-58 hours (with an average of 24 hours), and returns to baseline within 3-4 days. LDH LDH 1 is the cardiac specific isoenzyme When LDH 1 > LDH 2 , an AMI is probably occurring The LDH level rises within 24-48 hours, peaks within 3-6 days, and returns to baseline within 8-14 days. False positives enzyme levels may be seen in conditions that involve muscle injury (trauma, disease, vigorous exercise or rhabdomyolysis)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Coronary Circulation: RCA Supplies the SA node, AV node, bundle of his, posterior papillary muscles, inferior wall of the left ventricle, and the posterior third of the septum The RCA supplies most of the blood supply to the inferior wall of the left ventricle for most people A person is said to be right dominant when the RCA supplies most of the blood supply to the inferior wall (of the left ventricle) IWMI usually due to RCA occlusion Watch for problems associated with the SA node (tachycardia, bradycardia, sick sinus or sinus arrest), the AV node (AV blocks), the right ventricle (RV involvement), and the posterior papillary muscles (MR or papillary muscle rupture). LAD (branches off left main artery) Supplies the anterior wall of the left ventricle, some of the lateral wall, and most of the intra-ventricular septum (including it’s conduction system) AWMI usually due to LAD occlusion Watch for problems involving large areas of the anterior left ventricle (cardiogenic shock) and problems involving the septum (blocks and VSD). Circumflex (branches off left main artery) Supplies the lateral and posterior walls of the left ventricle A small percentage of people have a short RCA and the circumflex artery then wraps around and supplies most of the inferior wall A person is said to be left dominant when the circumflex artery supplies most of the blood supply to the inferior wall (of the left ventricle) Lateral and/or posterior wall MI usually due to circumflex occlusion
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Two or more leads of a group: IWMI Leads II, III and aVF view the inferior wall (of the left ventricle) Reciprocal changes are seen in leads I, and aVL AWMI Leads V 1 -V 4 view the anterior-septal wall (left ventricle) Reciprocal changes are seen in leads II, III, and AVF Lateral wall MI Leads I, aVL, V 5 and V 6 view the lateral wall (left ventricle) Reciprocal changes are seen in leads II, III, and aVF Posterior wall MI Posterior MI’s are difficult to detect on a 12 lead EKG because no leads are placed directly over the posterior Changes are reflected on the opposite walls (Instead of ST elevations, you will see ST depression. Instead of Q waves, you will see tall R waves. Instead of T wave inversions, you will see upright T waves) Reciprocal changes may be seen in leads V 1 and V 2 Right Ventricle Leads V 3 R – V 6 R view the RV
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Two or more leads of a group: IWMI Leads II, III and aVF view the inferior wall (of the left ventricle) Reciprocal changes are seen in leads I, and aVL AWMI Leads V 1 -V 4 view the anterior-septal wall (left ventricle) Reciprocal changes are seen in leads II, III, and AVF Lateral wall MI Leads I, aVL, V 5 and V 6 view the lateral wall (left ventricle) Reciprocal changes are seen in leads II, III, and aVF Posterior wall MI Posterior MI’s are difficult to detect on a 12 lead EKG because no leads are placed directly over the posterior Changes are reflected on the opposite walls (Instead of ST elevations, you will see ST depression. Instead of Q waves, you will see tall R waves. Instead of T wave inversions, you will see upright T waves) Reciprocal changes may be seen in leads V 1 and V 2 Right Ventricle Leads V 6 R - V 3 R view the RV
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 NTG Dilates coronary arteries Decreases preload (decreases, afterload some) MSO 4 Morphine is the analgesic of choice with AMI because it also reduces preload and decreases myocardial oxygen demand. Morphine decreases anxiety, restlessness, and autonomic nervous system activity. Aspirin Inhibits platelet aggregation Heparin Prevents further extension of existing thrombi and/or new clot formation (blocks conversion of prothrombin to thrombin and fibrinogen to fibrin) Beta Blockers Slow heart rate and lower BP Encourages electrical stability Improves mortality ACE Inhibitors Reduce afterload (vasodilatation) Reduces work of heart Decreases remolding effects GP IIb IIIa Inhibitors (anti-thrombolytics) Integrilin Reopro Thrombolytics Given up to 12 hours from the onset of an AMI Contraindicated in patients with active bleeding, BP>200/120, major surgery within 2 weeks, CPR >10 min, recent head trauma, suspected aortic dissection, pregnancy, CVA within 1 year, history of a hemorrhagic CVA, of major illnesses or cancers Anti-Lipidemics HDH is associated with  risk LDH is associated with  risk Look at the HDL : LDL ratio
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Increased incidence of sudden death or blood clots EDV) = the volume of blood in each ventricle at the end of diastole, usually about 120–130 mL but sometimes reaching 200–250 mL in the normal heart.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Increased incidence of sudden death or blood clots
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Generalized Treatment of Cardiomyopathy: Treat Symptoms Monitor For Signs of Worsening Heart Failure Daily Weights Prone To Digoxin Toxicity Due To  Renal Perfusion  Monitor Digoxin Levels Give Positive Inotropic Drugs (Except With Hypertropic Cardiomyopathy) Give Vasodilators (Except With Hypertropic Cardiomyopathy) Reduce Preload & Afterload Diuretics Calcium Channel Blockers As Indicated Beta Blockers As Indicated IABP Vasodilators As Indicated Fluid Restriction Give O2 With Exacerbations & As Needed Give Antidysrhythmic Agents As Needed Restrict Sodium Decrease Activity, Plan Activities & Rest Consider Heart Transplant Educate Patient & Family Give Emotional Support
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 AFib TREATMENT O2 and monitor. Slow rate when necessary. ECG Attempt to convert with medications if relatively new rhythm and hemodynamically stable. Prepare for synchronized cardioversion if hemodynamically unstable. Chronic atrial fibrillation usually treated with coumadin, ASA, etc.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 AFL TREATMENT O2 and monitor. ECG Attempt to convert with medications if relatively new rhythm and hemodynamically stable (beta-blockers, calcium channel blockers, digoxin). Prepare for synchronized cardioversion if hemodynamically unstable.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 WAP TREATMENT O2 and monitor ECG
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Atrial or Supraventricular tachycardia (SVT) is a fast heart rate that starts in the upper chambers of the heart. Some forms are called paroxysmal atrial tachycardia (PAT) or paroxysmal supraventricular tachycardia (PSVT). SVT TREATMENT O2 and monitor. ECG May attempt vagal maneuvers. May require beta-blockers, calcium channel blockers, etc. Prepare for synchronized cardioversion if hemodynamically unstable.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 VT TREATMENT Immediate defibrillation or cardioversion. CPR and ACLS
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Torsades TREATMENT MgSO4 Immediate defibrillation. CPR and ACLS.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Pulmonary (LVF) and/or systemic (RVF) congestion is present. The weakened LV doesn’t empty properly and backs up toward the pulmonary vasculature. The increased pressures allow fluid to leak back into the pulmonary interstitial spaces and into the alveolus. Back pressure form the RV to the systemic venous system leads to increased venous pressures with engorgement of the liver and spleen and third-spacing of fluid into interstitial spaces, causing peripheral edema and ascites.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Cardiogenic Pulmonary Edema = Elevated PAP, Elevated PAWP Non-cardiogenic Pulmonary Edema = Elevated PAP, Normal PAWP
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 When blood volume is low, juxtaglomerular cells in the kidneys secrete renin directly into circulation. Plasma renin then carries out the conversion of angiotensinogen released by the liver to angiotensin I. Angiotensin I is subsequently converted to angiotensin II by the enzyme angiotensin converting enzyme found in the lungs.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Class I: Patient with cardiac disease without resulting limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitations, dyspnea or angina.   Class II: Patient with cardiac disease resulting in slight limitation of physical activity. They are comfortable at rest but ordinary physical activity results in fatigue, palpitations, dyspnea or angina. Class III: Patient with cardiac disease resulting in marked limitations of physical activity. They are comfortable at rest but, less than ordinary activity causes fatigue, palpitations, dyspnea or angina. Class IV: Patient with cardiac disease resulting in inability to do any physical activity without discomfort. Symptoms of cardiac insufficiency or angina are increased when any activity is attempted.  
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 OPTIMIZE CARDIAC OUTPUT Improve Oxygenation O 2 Intubation PEEP Diuretics Decrease Myocardial Oxygen Consumption Bedrest (HOB elevated) Physical comfort (temperature control) Emotional control (keep informed, sedative prn) Gradually increase activity as tolerated, rest between activities Decrease Preload Diuretics (usually loop diuretics such as furosemide) High fowler’s position (legs dependent) Venous vasodilator (NTG, MSO 4 ) Sodium and fluid restriction Increase Contractility Cardiac glycosides (digoxin) Positive Inotropics (dopamine, dobutamine) Decrease Afterload Ace Inhibitors (captopril, enalapril) Nitroprusside (if hypertensive) Calcium channel blockers Dobutamine, Primacor Pulmonary vasodilators (aminophylline) IABP Prevent Valsalva Maneuvers Stool softeners Exhaling when turning Manage Dysrhythmias Atrial: Digoxin may be used to decrease ventricular rate by increasing refractoriness of the AV node. Ventricular: Lidocaine or amiodarone if necessary (procainamide and bretlium may significantly decrease contractility) Beta Blockers Used for mild CHF Protects heart form excessive catecholamines Cor Pulmonale (RVF) O 2 Therapy Pulmonary Vasodilators RVF Due to Pulmonary Embolus O 2 Therapy Anticoagulants Thrombolytics (if significant RVF or hypoxia)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002          
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Hypovolemic Shock Inadequate perfusion to the tissues due to insufficient intravascular volume.   Cardiogenic Shock Inadequate perfusion to the tissues due to heart failure.   Distributive Shock (Anaphylactic, Septic, and Spinal Shock) Inadequate perfusion to the tissues due to maldistribution of blood flow out of the intravascular space causing insufficient intravascular volume.   Obstructive Shock Inadequate perfusion to the tissues due to obstruction of blood flow. Causes: Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Orthostatic Hypotension
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Self destructive form of shock High mortality rate (75-100%) Occurs in 10% of AMI’s Usually means loss of at least 40% LV function Ventricular gallop = S3
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Optimize Cardiac Output
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Histamines cause massive vasodilatation
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Causes of Obstructive Shock: Pulmonary Embolus Tamponade Tension Pneumothorax Aortic Aneurysm
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Cardiac Tamponade & Beck’s Triad: 1. Low BP 2. Distended Neck Veins 3. Muffled Heart Sounds May have Narrowed Pulse
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 MODS = Multiple Organ Dysfunction Syndrome
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Definitions – ACCP/SCCM Consensus Conference Definition Bone et al.1992. Chest 101:1644-1655. Sepsis: a systemic inflammatory response to infection Severe Sepsis: systemic inflammation, coagulation and impaired fibinolysis. Septic Shock: severe sepsis defined as sepsis-induced hypotension (systolic blood pressure < 90mmHg or a reduction of=40mmHg from baseline in the absence of other causes for hypotension) despite adequate fluid resuscitation along with the presence of perfusion abnormalities. Patients receiving inotropic or vasopressor agents may no longer be hypotensive by the time that they manifest hypoperfusion abnormalities or organ dysfunction, yet they would be considered having septic shock.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Toxins and bradykinins cause massive vasodilatation, a positive inotropic effect and stimulate the respiratory rate. May cause release of myocardial depressant factor in late phase. May stimulate the clotting cascade. Often leads to ARDS or/and DIC.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Optimize intravascular volume Consider Xygris (Activated Protein C)
  • Definition: Measuring and monitoring the factors that influence the force and flow of blood. COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • The Fick Principle : Calculates consumption of O2 over time NIC0 : Partial CO2 rebreathing (NICO) Thermodilution : PA Catheter TEBCO : Electrical impedance of the thorax (TEB) NICCO : ECHO : Uses doppler ultrasound MUGA Scan : Nuclear heart scan SVV : CCO, SVV / SV, SVR COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • 1) Normal Values: CVP = 1-7 mmHg PAWP = 6-12 mmHg CO = 4.0-8.0 L/Min. CI = 2.5-4.0 L/Min. SVR = 700=1500 dynes/sec/cm 5 PVR = 100-250 dynes/sec/cm 5 RVSW = 10-15 gm 2 /beat LVSW = 60-80 gm 2 /beat COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • 1) Normal Values: CVP = 1-7 mmHg PAWP = 6-12 mmHg CO = 4.0-8.0 L/Min. CI = 2.5-4.0 L/Min. SVR = 700=1500 dynes/sec/cm 5 PVR = 100-250 dynes/sec/cm 5 RVSW = 10-15 gm 2 /beat LVSW = 60-80 gm 2 /beat COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • Normal SvO2 = 75% COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • SVV: Arterial pulse pressure falls during inspiration and rises during expiration due to changes in intra-thoracic pressure secondary to negative pressure ventilation. Variations over 10mmHg have been referred to as pulsus paradoxus. Pulsus Paradoxus is the origin of SVV value. Occurs with spontaneously breathing patients. Reverse Pulsus Paradoxus occurs during positive pressure ventilation. COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Looks like a CVP waveform, but the timing is different
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Looks like a CVP waveform – just occurs later
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 May do carotid ultrasound.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Type I often preceded Type II.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 In COPD, bronchospasm, mucus plugs, inflammation and airway obstruction in general worsen ventilation disrupting the balance between ventilation and perfusion.
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Somatostatin is classified as an inhibitory hormone, whose main actions are to: Inhibit the release of growth hormone (GH) Inhibit the release of thyroid-stimulating hormone (TSH) Suppress the release of gastrointestinal hormones Gastrin Cholecystokinin (CCK) Secretin Motilin Vasoactive intestinal peptide (VIP) Gastric inhibitory polypeptide (GIP) Enteroglucagon (GIP) Lowers the rate of gastric emptying, and reduces smooth muscle contractions and blood flow within the intestine. Suppress the release of pancreatic hormones Inhibit the release of insulin Inhibit the release of glucagon Suppress the exocrine secretory action of pancreas. Somatostatin opposes the effects of Growth Hormone-Releasing Hormone (GHRH)
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002 Sphincter or Oddi
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
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  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
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  • COMMON CRITICAL CONDITIONS Part One July 2004November 2002
  • CCRN Review part 1

    1. 1. ““Never let what you cannot doNever let what you cannot dointerfere with what you can do”interfere with what you can do”-- John WoodenJohn Wooden --CCRN REVIEW PART 1CCRN REVIEW PART 1Sherry L. Knowles, RN, CCRN, CRNISherry L. Knowles, RN, CCRN, CRNI
    2. 2. 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PancreatitisPancreatitisCCRN REVIEW PART 1CCRN REVIEW PART 1
    3. 3. 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 ofIdentify basic coronary circulation and how it relates to different types ofmyocardial 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
    4. 4. 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 respiratoryRecognize the signs & symptoms and causes of various respiratoryalterations.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 hemodynamicprofiles.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 availabletreatments.treatments.CCRN REVIEW PART 1CCRN REVIEW PART 1
    5. 5. Acute CoronaryAcute CoronarySyndromesSyndromesAcute MIAcute MIAortic AneurysmsAortic AneurysmsCardiac AlterationsCardiac AlterationsCardiovascular ConditionsCardiovascular ConditionsCardiomyopathyCardiomyopathyHeart BlocksHeart BlocksHeart FailureHeart FailureShock StatesShock States
    6. 6. DEFINITIONSDEFINITIONS– Term used to cover a group of symptomsTerm used to cover a group of symptomscompatible with acute myocardial ischemiacompatible with acute myocardial ischemia– Acute myocardial ischemia is insufficient bloodAcute myocardial ischemia is insufficient bloodsupply to the heart muscle usually resulting fromsupply to the heart muscle usually resulting fromcoronary artery diseasecoronary artery diseaseAcute Coronary SyndromeAcute Coronary Syndrome
    7. 7. DEFINITIONDEFINITION– Infarction occurs due to mechanical obstructionInfarction occurs due to mechanical obstructionof a coronary artery (or branch) caused by aof a coronary artery (or branch) caused by athrombus, plaque rupture, coronary spasmthrombus, plaque rupture, coronary spasmand/or dissection.and/or dissection.– STEMI vs. NSTEMI (non-STEMI)STEMI vs. NSTEMI (non-STEMI)Acute Myocardial InfarctionAcute Myocardial Infarction
    8. 8. SIGNS & SYMPTOMSSIGNS & SYMPTOMS– Complains VaryComplains VaryMay include crushing chest pain (which may or mayMay include crushing chest pain (which may or maynot radiate), back, neck, jaw, teeth and/or epigastricnot radiate), back, neck, jaw, teeth and/or epigastricpain, SOB, nausea/vomiting and dizzinesspain, SOB, nausea/vomiting and dizziness– ST elevations on ECGST elevations on ECG– Elevated cardiac enzymesElevated cardiac enzymesAcute Myocardial InfarctionAcute Myocardial Infarction
    9. 9. 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 abnormalDiabetics and women often present abnormalsymptomssymptomsAcute Myocardial InfarctionAcute Myocardial Infarction
    10. 10. Coronary CirculationCoronary Circulation
    11. 11. II AVRAVR V1V1V4V4IIII AVL V2 V5AVL V2 V5IIIIII AVF V3 V6AVF V3 V6IIIIVV12 Lead ECG12 Lead ECG
    12. 12. 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 RCAAcute Myocardial InfarctionAcute Myocardial Infarction
    13. 13.  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 deflectionsAcute Myocardial InfarctionAcute Myocardial Infarction
    14. 14. Coronary ArteriesCoronary Arteries
    15. 15. Anterior Wall MIAnterior Wall MI
    16. 16. Inferior Wall MIInferior Wall MI
    17. 17.  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 (orchordae tendineae) rupture, pericardialchordae tendineae) rupture, pericardialeffusions, pericarditiseffusions, pericarditisAcute Myocardial InfarctionAcute Myocardial Infarction
    18. 18. 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 alsoinclude thrombolytics or Gp2b3a inhibitorsinclude thrombolytics or Gp2b3a inhibitors– PCI, PTCA, IABP, CABGPCI, PTCA, IABP, CABGAcute Myocardial InfarctionAcute Myocardial Infarction
    19. 19. 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 theinfarction and to prevent complicationsinfarction and to prevent complications(primarily lethal dysrhythmias)(primarily lethal dysrhythmias)Acute Myocardial InfarctionAcute Myocardial Infarction
    20. 20. 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 Gp2b3ainhibitorsinhibitors– Cardiac Catheterization (with angioplasty,Cardiac Catheterization (with angioplasty,atherectomy and/or stent)atherectomy and/or stent)– IABP, CABG, EducationIABP, CABG, EducationAcute Myocardial InfarctionAcute Myocardial Infarction
    21. 21. Balloon AngioplastyBalloon Angioplasty
    22. 22. Vascular Stent DeploymentVascular Stent Deployment
    23. 23. AtherectomyAtherectomy
    24. 24.  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 medicationsAcute Myocardial InfarctionAcute Myocardial Infarction
    25. 25. Aortic AneurysmsAortic AneurysmsDEFINITIONDEFINITION– 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 threelayers 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 theouter layer, it is called a pseudo-aneurysmouter layer, it is called a pseudo-aneurysm– May be thoracic or abdominalMay be thoracic or abdominal
    26. 26. Aortic AneurysmsAortic AneurysmsCAUSESCAUSESAtherosclerosisAtherosclerosisMarfan syndromeMarfan syndromeHypertensionHypertensionCrack cocaine usageCrack cocaine usageSmokingSmokingTraumaTrauma
    27. 27. Aortic Aneurysms RuptureAortic Aneurysms Rupture An aortic aneurysm, depending on its size, mayAn aortic aneurysm, depending on its size, mayrupture, 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 theaneurysm gets largeraneurysm gets larger The risk of rupture also depends on the location ofThe risk of rupture also depends on the location ofthe aneurysmthe aneurysm Each year, approximately 15,000 Americans die of aEach year, approximately 15,000 Americans die of aruptured aortic aneurysm.ruptured aortic aneurysm.
    28. 28. 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 aMay be symmetrical in shape (fusiform) or alocalized weakness of the arterial wall (saccular)localized weakness of the arterial wall (saccular)
    29. 29. Aortic AneurysmsAortic Aneurysms
    30. 30. Aortic AneurysmsAortic AneurysmsSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Often produces no symptomsOften produces no symptoms– If an aortic aneurysm suddenly ruptures it presentsIf an aortic aneurysm suddenly ruptures it presentswith extreme abdominal or back pain, a pulsatingwith extreme abdominal or back pain, a pulsatingmass in the abdomen, and a drastic drop in bloodmass in the abdomen, and a drastic drop in bloodpressurepressure– An increase in the size of an aneurysm means anAn increase in the size of an aneurysm means anincreased in the risk of ruptureincreased in the risk of rupture
    31. 31. Aortic AneurysmsAortic Aneurysms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
    32. 32. Aortic DissectionsAortic DissectionsDEFINITIONDEFINITION– Tearing of the inner layer of the aortic wall, whichTearing of the inner layer of the aortic wall, whichallows blood to leak into the wall itself and causesallows blood to leak into the wall itself and causesthe 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 radiatingto the backto the back
    33. 33. Aortic DissectionsAortic DissectionsA.A. DissectionDissectionbeginning in thebeginning in theascending aortaascending aortaB.B. Whenever theWhenever theascending aortaascending aortais not involvedis not involved
    34. 34. Aortic DissectionsAortic DissectionsA.A. DissectionDissectionbeginning in thebeginning in theascending aortaascending aortaB.B. Whenever theWhenever theascending aortaascending aortais not involvedis not involved
    35. 35. Aortic DissectionsAortic Dissections
    36. 36. Aortic DissectionsAortic Dissections
    37. 37. Aortic AneurysmsAortic AneurysmsCOMPLICATIONSCOMPLICATIONSRuptureRupturePeripheralPeripheral embolizationembolizationInfectionInfectionSpontaneousSpontaneous occlusionocclusion of aortaof aorta
    38. 38. 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 surgicalMarfan patients will require surgicalcorrection or endovascular stent placementcorrection or endovascular stent placement
    39. 39. CardiomyopathyCardiomyopathyDEFINITIONDEFINITION– Diseases of the heart muscle thatDiseases of the heart muscle thatcause deterioration of the function ofcause deterioration of the function ofthe myocardiumthe myocardium
    40. 40. CardiomyopathyCardiomyopathyCLASSIFICATIONSCLASSIFICATIONS– Primary / Idiopathic (intrinsicPrimary / Idiopathic (intrinsic))Heart disease of unknown cause, although viralHeart disease of unknown cause, although viralinfection 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, valvulardisease, severe hypertension, or alcohol abusedisease, severe hypertension, or alcohol abuse
    41. 41. CardiomyopathyCardiomyopathyHypertropic CardiomyopathyHypertropic CardiomyopathyRestrictive CardiomyopathyRestrictive CardiomyopathyDilated CardiomyopathyDilated Cardiomyopathy
    42. 42. Hypertropic CardiomyopathyHypertropic 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
    43. 43. HarleyHarley
    44. 44. Hypertropic CardiomyopathyHypertropic Cardiomyopathy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
    45. 45. Restrictive CardiomyopathyRestrictive CardiomyopathyRigid Ventricular WallRigid Ventricular Wall– Due to endomyocardial fibrosisDue to endomyocardial fibrosis– Obstructs ventricular fillingObstructs ventricular fillingLeast common formLeast common form
    46. 46. Restrictive CardiomyopathyRestrictive CardiomyopathyTREATMENTTREATMENT– Positive InotropicsPositive Inotropics– DiureticsDiuretics– Low Sodium DietLow Sodium Diet
    47. 47. Dilated CardiomyopathyDilated Cardiomyopathy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 toLV dilationLV dilation
    48. 48. Dilated CardiomyopathyDilated CardiomyopathyTREATMENTTREATMENT– Positive InotropesPositive Inotropes– Afterload ReducersAfterload Reducers– Anticoagulants with Atrial FibAnticoagulants with Atrial Fib
    49. 49. CardiomyopathiesCardiomyopathies
    50. 50. CardiomyopathyCardiomyopathy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
    51. 51. BREAK!BREAK!CCRN REVIEW PART 1CCRN REVIEW PART 1
    52. 52. Conduction DefectsConduction DefectsSTABLE VS UNSTABLESTABLE VS UNSTABLE– StableStableStart with medicationsStart with medications– UnstableUnstableShock (cardioversion or defibrillation)Shock (cardioversion or defibrillation)
    53. 53. Normal Sinus RhythmNormal Sinus RhythmHeart RateHeart Rate 60 - 100 bpm60 - 100 bpmRhythmRhythm RegularRegularP WaveP Wave Before each QRS & identicalBefore each QRS & identicalPR Interval (in seconds)PR Interval (in seconds) 0.12 to 0.200.12 to 0.20QRS (in seconds)QRS (in seconds) < 0.12< 0.12
    54. 54. 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
    55. 55. 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
    56. 56. 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
    57. 57. 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 identifiedAtrial Tach = supraventricular rhythm with p wave morphologyAtrial Tach = supraventricular rhythm with p wave morphologythat is noticeably different from the sinus p wavethat is noticeably different from the sinus p wave
    58. 58. Ventricular TachycardiaVentricular Tachycardia VTVT– Ventricular rate of 100-250/minVentricular rate of 100-250/min– Wide QRSWide QRS
    59. 59. 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
    60. 60. Heart Blocks (AV Blocks)Heart Blocks (AV Blocks)Sinus Rhythm with First Degree AV BlockSinus Rhythm with First Degree AV BlockSinus Rhythm with Second Degree AV Block, Type 2Sinus Rhythm with Second Degree AV Block, Type 2Sinus Rhythm with Second Degree AV Block, Type 1Sinus Rhythm with Second Degree AV Block, Type 1Third Degree AV BlockThird Degree AV Block
    61. 61.  DEFINITIONDEFINITION– A condition in which the heart cannot pumpA condition in which the heart cannot pumpsufficient blood to meet the metabolic needs ofsufficient blood to meet the metabolic needs ofthe bodythe body– Pulmonary (LVF) and/or systemic (RVF)Pulmonary (LVF) and/or systemic (RVF)congestion is present.congestion is present.Heart FailureHeart Failure
    62. 62. DEFINITIONDEFINITION– Pulmonary EdemaPulmonary EdemaFluid in the alveolus that impairs gas exchange byFluid in the alveolus that impairs gas exchange byaltering the diffusion between alveolus andaltering the diffusion between alveolus and capillarycapillaryAcute left ventricular failure causes cardiogenicAcute left ventricular failure causes cardiogenicpulmonary edemapulmonary edemaNon-cardiogenic pulmonary edema is a synonym forNon-cardiogenic pulmonary edema is a synonym forAdult Respiratory Distress Syndrome (ARDS)Adult Respiratory Distress Syndrome (ARDS)Heart FailureHeart Failure
    63. 63. COMPENSATORY MECHANISMSCOMPENSATORY MECHANISMS– Sympaththetic nervous system stimulationSympaththetic nervous system stimulationTachycardiaTachycardiaVasoconstriction and increased SVRVasoconstriction and increased SVR– Renin-angiotensin-aldosterone systemRenin-angiotensin-aldosterone systemactivation (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 dilationHeart FailureHeart Failure
    64. 64. FUNCTIONAL CLASSIFICATIONSFUNCTIONAL CLASSIFICATIONS– Class IClass I– Class IIClass II– Class IIIClass III– Class IVClass IVHeart 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)
    65. 65. COMPLICATIONSCOMPLICATIONS– HypotensionHypotension– DysrhythmiasDysrhythmias– Respiratory FailureRespiratory Failure– Progressive DeteriorationProgressive Deterioration– Acute Renal FailureAcute Renal Failure– Fluid & Electrolyte ImbalancesFluid & Electrolyte ImbalancesHeart FailureHeart Failure
    66. 66. 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
    67. 67. Vascular DiseaseVascular DiseaseAorto/Iliac Disease: Pre & Post PTA/StentAorto/Iliac Disease: Pre & Post PTA/Stent
    68. 68. Peripheral Vascular DiseasePeripheral Vascular DiseaseSYMPTOMSSYMPTOMSPAINPAINPAIN RELIEFPAIN RELIEFEDEMAEDEMAPULSESPULSESINTEGUMENTINTEGUMENTCHANGESCHANGESULCERSULCERSSKIN TEMPERATURESKIN TEMPERATURESEXUAL ISSUESSEXUAL ISSUESARTERIALARTERIALUpon walkingUpon walkingOn resting, standing orOn resting, standing ordependent position of lower limbsdependent position of lower limbsNoneNoneDecreased or absentDecreased or absentHair lossHair lossSkin shinySkin shinyNail thickeningNail thickeningPallor when elevatedPallor when elevatedRed when dependentRed when dependentUlcers located on toes, lateralUlcers located on toes, lateralareas or site of traumaareas or site of traumaGangrene possibleGangrene possibleCoolCoolImpotencyImpotencySexual dysfunctionSexual dysfunctionVENOUSVENOUSWhile standingWhile standingElevation of extremitiesElevation of extremitiesPresent, edematousPresent, edematousMay be difficult to palpateMay be difficult to palpateBrownish pigmentationBrownish pigmentationMay be cyanotic whenMay be cyanotic whenextremities are dependentextremities are dependentUlcers located on ankles,Ulcers located on ankles,medial or pre-tibial areasmedial or pre-tibial areasNormal or warmNormal or warmNot presentNot present
    69. 69. 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
    70. 70. Peripheral Vascular DiseasePeripheral Vascular DiseaseBypass GraftsBypass Grafts
    71. 71.  DEFINITIONDEFINITION– Inadequate perfusion to the body tissuesInadequate perfusion to the body tissues– Low blood pressure with impaired perfusionLow blood pressure with impaired perfusionto the end organsto the end organs– May result in multiple organ dysfunctionMay result in multiple organ dysfunctionShockShock
    72. 72. TYPES OF SHOCKTYPES OF SHOCK– Hypovolemic ShockHypovolemic Shock– Cardiogenic ShockCardiogenic Shock– Distributive ShockDistributive Shock– Obstructive ShockObstructive ShockShockShock
    73. 73. 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 toadequately 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 tomaintain volume and thus enough blood pressure tomaintain volume and thus enough blood pressure toperfuse the body tissuesperfuse the body tissues
    74. 74. Types of ShockTypes of ShockHypovolemic ShockHypovolemic Shock– Inadequate perfusion to the tissues due to insufficient intravascularInadequate perfusion to the tissues due to insufficient intravascularvolumevolume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 theintravascular 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
    75. 75. Hypovolemic ShockHypovolemic ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaOrthostatic HypotensionOrthostatic Hypotension RestlessnessRestlessnessConfusionConfusion Agitation (or listless)Agitation (or listless)ThirstThirst PallorPallorCool, Clammy SkinCool, Clammy Skin ↑↑ Resp. RateResp. Rate↓↓ UOPUOP ↓↓ COCO↓↓ PAWPPAWP ↓↓ CVPCVP↑↑ SVRSVR ↑↑ Lactate LevelsLactate Levels
    76. 76. Hypovolemic ShockHypovolemic ShockTREATMENTTREATMENT–Volume (IVF, Blood)Volume (IVF, Blood)
    77. 77. Cardiogenic ShockCardiogenic ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP RestlessnessRestlessnessAgitation (or listless)Agitation (or listless) ConfusionConfusionTachycardiaTachycardia PallorPallor↓↓ UOPUOP ↓↓ COCO↑↑ PAWP (low with RVF)PAWP (low with RVF) ↑↑CVPCVP↑↑ SVRSVR ↑↑ Lactate LevelsLactate LevelsJVDJVD Peripheral EdemaPeripheral EdemaVentricular Gallop (S3)Ventricular Gallop (S3) DyspneaDyspneaPulmonary CracklesPulmonary Crackles
    78. 78. TREATMENTTREATMENTBedrestBedrest O2O2↑↑ COCO Positive InotropesPositive Inotropes↓↓ Preload & AfterloadPreload & Afterload DiureticsDiuretics↓↓ VasodilatorsVasodilators PositioningPositioning↓↓ Myocardial DemandMyocardial Demand IABPIABPCardiogenic ShockCardiogenic Shock
    79. 79. Anaphylactic ShockAnaphylactic ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaRestlessnessRestlessness ConfusionConfusionAgitation (or listless)Agitation (or listless) ThirstThirstPallorPallor Warm FeelingWarm FeelingPruritusPruritus HivesHivesAngioedemaAngioedema BronchoconstrictionBronchoconstrictionWheezingWheezing Laryngeal EdemaLaryngeal EdemaDyspneaDyspnea Cool, Clammy SkinCool, Clammy Skin↓↓ UOPUOP ↓↓ COCO↓↓ PAWPPAWP ↓↓ CVPCVP↓↓ SVRSVR ↑↑ Lactate LevelsLactate Levels
    80. 80. TREATMENTTREATMENT– EpinephrineEpinephrine– IVFIVF– VasoconstrictorsVasoconstrictors– Support/Maintain AirwaySupport/Maintain AirwayAnaphylactic ShockAnaphylactic Shock
    81. 81. Obstructive ShockObstructive ShockSIGNS & SYMPTOMSSIGNS & SYMPTOMSLow BPLow BP TachycardiaTachycardiaRestlessnessRestlessness ConfusionConfusionAgitation (or listless)Agitation (or listless) PallorPallorCool, Clammy SkinCool, Clammy Skin ↓↓ CO ,CO , ↓↓ UOPUOPSymptoms related to causeSymptoms related to cause
    82. 82. Obstructive ShockObstructive ShockCAUSESCAUSESPulmonary EmbolusPulmonary Embolus TamponadeTamponadeTension PneumothoraxTension Pneumothorax Aortic AneurysmAortic AneurysmTREATMENTTREATMENTTreat the CauseTreat the Cause
    83. 83. 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 dueto bronchospasmto bronchospasmParameter Hypovolemic Cardiogenic Neurogenic Anaphylactic Early Septic Late SepticCVP/RAP      PAWP      or Norm CO      BP      SVR      HR     Normal Shock ProfilesShock Profiles
    84. 84. SIRS Sepsis Severe Septic MODS DeathSIRS Sepsis Severe Septic MODS DeathInfectionInfection Sepsis ShockSepsis ShockSepsis SyndromeSepsis Syndrome
    85. 85.  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.), orhypotension (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 hypotensiondespite adequate fluid resuscitationdespite adequate fluid resuscitationSepsis SyndromeSepsis Syndrome
    86. 86. EARLY STAGE (Hyperdynamic)EARLY STAGE (Hyperdynamic)Normal BPNormal BP TachycardiaTachycardiaConfusionConfusion Agitation (or listless)Agitation (or listless)↑↑ Respiratory RateRespiratory Rate TemperatureTemperatureNormal ColorNormal Color Normal orNormal or ↑↑ UOPUOPNormal PAWPNormal PAWP ↑↑ COCO ↓↓ SVRSVRLATE STAGE (Hypodynamic)LATE STAGE (Hypodynamic)Low BPLow BP TachycardiaTachycardiaOrthostatic HypotensionOrthostatic Hypotension RestlessnessRestlessnessConfusionConfusion Agitation (or listless)Agitation (or listless)ThirstThirst PallorPallorCool, Clammy SkinCool, Clammy Skin ↓↓ UOPUOP↓↓ COCO ↓↓ PAWPPAWP↓↓ CVPCVP ↑↑ SVRSVR↑↑ Lactate LevelsLactate LevelsSeptic ShockSeptic Shock
    87. 87. Homeostasis Gets LostHomeostasis Gets Lost
    88. 88. 3.3. Improve PerfusionImprove Perfusion– Prevent organ dysfunctionPrevent organ dysfunction– Treat temp as neededTreat temp as needed2.2. 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 cause1.1. Stabilize The PatientStabilize The Patient– Fluids (lots of fluids) 150ml/hr or moreFluids (lots of fluids) 150ml/hr or more– VasoconstrictorsVasoconstrictorsTreatment for SepsisTreatment for Sepsis
    89. 89. HEMODYNAMICSHEMODYNAMICS
    90. 90. Invasive PA CatheterInvasive PA CatheterCONTRAINDICATIONSCONTRAINDICATIONS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
    91. 91. 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 relatedCO and SVR will change before BP changesCO and SVR will change before BP changes
    92. 92. StrokeStroke VolumeVolume Components Stroke VolumeComponents Stroke Volume– PreloadPreload:: the volume of blood in the ventriclesthe volume of blood in the ventriclesat end diastole and the stretch placed on theat end diastole and the stretch placed on themuscle fibersmuscle fibers– AfterloadAfterload:: the resistance the ventricles mustthe resistance the ventricles mustovercome 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 heartmuscle contracts (myocardial compliance)muscle contracts (myocardial compliance)
    93. 93. PAC Insertion SequencePAC Insertion Sequence
    94. 94. Phlebostatic AxisPhlebostatic Axis4th ICS Mid-chest, regardless of head elevation4th ICS Mid-chest, regardless of head elevation
    95. 95.  RAP (CVP)RAP (CVP) RVPRVP PAPPAP PAWPPAWP SVRSVR0-8 mmHg0-8 mmHg15-30/0-8 mmHg15-30/0-8 mmHg15-30/6-12 mmHg15-30/6-12 mmHg8 - 12 mmHg8 - 12 mmHg700-1500700-1500 dynes/sec/cmdynes/sec/cm22Normal Hemodynamic ValuesNormal Hemodynamic Values
    96. 96. 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
    97. 97. Mixed Venous Oxygen SaturationMixed Venous Oxygen SaturationSvO2SvO2 End result of O2 delivery andEnd result of O2 delivery andconsumptionconsumption Measured in the pulmonary arteryMeasured in the pulmonary artery An average estimate of venous saturation forAn average estimate of venous saturation forthe whole body.the whole body. Does not reflect separate tissue perfusion orDoes not reflect separate tissue perfusion oroxygenationoxygenation
    98. 98. 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
    99. 99. Measuring PA PressuresMeasuring PA PressuresMeasure All Hemodynamic ValuesMeasure All Hemodynamic Valuesat End-Expirationat End-Expiration– ““Patient PeakPatient Peak””– ““Vent ValleyVent Valley””
    100. 100. Spontaneous RespirationsSpontaneous Respirations
    101. 101. 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 duringduringspontaneous inspirationspontaneous inspiration– Negative deflection on waveformsNegative deflection on waveformsIntrathoracic pressureIntrathoracic pressure increasesincreases duringduringspontaneous expirationspontaneous expiration– Positive deflection on waveformsPositive deflection on waveformsMeasuring PA PressuresMeasuring PA Pressures
    102. 102. 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 duringduringpositive pressure ventilations (inspiration)positive pressure ventilations (inspiration)– Positive deflection on waveformsPositive deflection on waveformsIntrathoracic pressureIntrathoracic pressure decreasesdecreases duringduringpositive pressure expirationpositive pressure expiration– Negative deflection on waveformsNegative deflection on waveformsMeasuring PA PressuresMeasuring PA Pressures
    103. 103.  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 QTsegmentsegment Delayed ECG correlation from CVP sinceDelayed ECG correlation from CVP sincePA catheter is further away from left atriumPA catheter is further away from left atriumPAWP WaveformPAWP Waveform
    104. 104. 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 wavePAWP WaveformPAWP Waveform
    105. 105. PAWP WaveformPAWP Waveform
    106. 106. BREAK!BREAK!CCRN REVIEW PART 1CCRN REVIEW PART 1
    107. 107. ARDSARDSDrowningDrowningPneumothoraxPneumothoraxRespiratoryRespiratoryFailureFailureRespiratory AlterationsRespiratory AlterationsChronicChronic LungLungDiseaseDiseasePneumoniaPneumoniaPulmonaryPulmonaryEmbolismEmbolism
    108. 108. ARDSARDSDEFINITIONSDEFINITIONS– Severe respiratory failure associated with pulmonarySevere respiratory failure associated with pulmonaryinfiltrates (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 ordepressed 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 thealveolar-capillary membranealveolar-capillary membrane
    109. 109. Acute Respiratory Distress SyndromeAcute Respiratory Distress Syndrome
    110. 110. ARDSARDSPATHOPHYSIOLOGYPATHOPHYSIOLOGY– Inflammatory mediators are released causing extensiveInflammatory mediators are released causing extensivestructural damagestructural damage– Increased permeability of pulmonary microvasculatureIncreased permeability of pulmonary microvasculaturecauses 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
    111. 111. 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 rapidlyprogress to complete whiteoutprogress to complete whiteout
    112. 112. ARDSARDS
    113. 113. 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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
    114. 114. ARDSARDSCommon RiskCommon RiskFactorsFactorsOther Risk FactorsOther Risk FactorsSepsisSepsisMassiveMassiveTraumaTraumaShockShockMultipleMultipleTransfusionsTransfusionsPneumoniaPneumoniaAspirationAspirationInfectionInfectionSmoke inhalationSmoke inhalationInhaled toxinsInhaled toxinsBurnsBurnsNear DrowningNear DrowningDKADKAPregnancyPregnancyEclampsiaEclampsiaAmniotic Fluid EmbolusAmniotic Fluid EmbolusDrugsDrugsAcute PancreatitisAcute PancreatitisDICDICHead InjuryHead Injury↑ ICPICPFat EmboliFat EmboliBlood ProductsBlood ProductsHeart/Lung BypassHeart/Lung BypassTumor LysisTumor LysisPulmonary ContusionPulmonary ContusionNarcoticsNarcoticsRISK FACTORSRISK FACTORS
    115. 115. ARDSARDSTREATMENTTREATMENT– Respiratory SupportRespiratory Support– PEEP, CPAPPEEP, CPAP
    116. 116. Chronic Lung DiseaseChronic Lung Disease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
    117. 117. 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
    118. 118. 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
    119. 119. PneumoniaPneumoniaLung infection (bacterial, viral, or fungal)Lung infection (bacterial, viral, or fungal)– Most commonly caused by SMost commonly caused by StreptococcustreptococcuspneumoniaepneumoniaeSymptoms include fever, pleuretic chestSymptoms include fever, pleuretic chestpain, productive cough, and tachypneapain, productive cough, and tachypnea– Often presents bronchial breath sounds over theOften presents bronchial breath sounds over thelung arealung areaTreatment involves giving the right antibioticTreatment involves giving the right antibiotic
    120. 120. 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 andThe 2 key risk factors are increased chest length andcigarette 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 toone-way movement of airone-way movement of airProgressively worsensProgressively worsensRequires immediate interventionRequires immediate intervention
    121. 121. PneumothoraxPneumothorax
    122. 122. Tension PneumothoraxTension Pneumothorax
    123. 123. PneumothoraxPneumothoraxCAUSESCAUSES– BarotraumaBarotrauma– InjuryInjury– BlebsBlebs
    124. 124. 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 irritationDry, hacking cough (may occur due to irritationof 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 ofcardiovascular collapsecardiovascular collapseImmediately life threateningImmediately life threateningMay cause mediastinal shiftMay cause mediastinal shift
    125. 125. PneumothoraxPneumothorax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22ndndintercostal spaceintercostal space
    126. 126. TREATMENTTREATMENT– PleurodesisPleurodesisPneumothoraxPneumothoraxChemical or surgical adhesion of the lungChemical or surgical adhesion of the lungto the chest wallto the chest wallUsed for multiple collapsed lungs orUsed for multiple collapsed lungs orpersistent collapsepersistent collapse
    127. 127. Flail ChestFlail Chest
    128. 128.  DefinitionDefinition Signs & SymptomsSigns & SymptomsPulmonary EmbolismPulmonary Embolism– 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, chestpain, 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
    129. 129. 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-DimerPulmonary EmbolismPulmonary Embolism
    130. 130. 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 secondarythrombus 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 anticoagulantsPulmonary EmbolismPulmonary Embolism
    131. 131. Respiratory FailureRespiratory FailureDEFINITIONSDEFINITIONS– 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 mmHgand/or pH < 7.35and/or pH < 7.35 on Room Airon Room Air
    132. 132. Respiratory FailureRespiratory FailureTYPE ITYPE I HypoxemiaHypoxemia withoutwithout hypercapniahypercapniaTYPE IITYPE II HypoxemiaHypoxemia withwith hypercapniahypercapnia
    133. 133. Respiratory FailureRespiratory FailureCAUSESCAUSES– V/Q MismatchingV/Q Mismatching– Intrapulmonary ShuntingIntrapulmonary Shunting– Alveolar HypoventilationAlveolar Hypoventilation
    134. 134. Respiratory FailureRespiratory FailureV/Q MISMATCHINGV/Q MISMATCHING– COPDCOPD– Interstitial Lung DiseaseInterstitial Lung Disease– Pulmonary EmbolismPulmonary Embolism
    135. 135. 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 accumulationExcessive mucus accumulation
    136. 136. Respiratory FailureRespiratory FailureSIGNS & SYMPTOMSSIGNS & SYMPTOMS– Restlessness / AgitationRestlessness / Agitation– Confusion /Confusion / ↓↓ LOCLOC– Tachycardia / DysrhythmiasTachycardia / Dysrhythmias– Tachypnea / DyspneaTachypnea / Dyspnea– Cool, clammy, pale skinCool, clammy, pale skin
    137. 137. 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 22pH 7.55 / pO2 65 / pCO2 22
    138. 138. Respiratory FailureRespiratory Failure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 retainersto use hypoxic driveto use hypoxic drive– Too much O2 can depress respirationsToo much O2 can depress respirations
    139. 139. BREAK!BREAK!CCRN REVIEW PART 1CCRN REVIEW PART 1
    140. 140. GI BleedGI BleedPancreatitisPancreatitisGastrointestinal AlterationsGastrointestinal Alterations
    141. 141. 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, IBDGastrointestinal BleedingGastrointestinal Bleeding
    142. 142. Gastrointestinal BleedingGastrointestinal Bleeding
    143. 143. Gastrointestinal BleedingGastrointestinal BleedingHematemesisHematemesis – vomiting of blood (or coffee ground– vomiting of blood (or coffee groundmaterial) (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 (indicatesdegradation 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 thepatient 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 notidentifiedidentified
    144. 144. Gastrointestinal BleedingGastrointestinal BleedingHematemesisHematemesis –– always UGI sourcealways UGI sourceMelanaMelana –– indicates blood has been in GI tractindicates blood has been in GI tractfor 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)
    145. 145. 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)Gastrointestinal BleedingGastrointestinal Bleeding
    146. 146. The PancreasThe PancreasThe Pancreas secretes digestive enzymes,The Pancreas secretes digestive enzymes,bicarbonate, water, and some electrolytes intobicarbonate, water, and some electrolytes intothe duodenum via the pancreatic ductthe duodenum via the pancreatic duct– Lipase, Amylase, TrypsinLipase, Amylase, TrypsinThe Pancreas also producesThe Pancreas also producesand secretes insulinand secretes insulin
    147. 147. PancreatitisPancreatitisDEFINITIONDEFINITION– An autodigestive process resultingAn autodigestive process resultingfrom premature activation offrom premature activation ofpancreatic enzymespancreatic enzymes
    148. 148. PancreatitisPancreatitisPATHOSHYSIOLOGYPATHOSHYSIOLOGY• Inactive pancreatic enzymes are activated outsideInactive pancreatic enzymes are activated outsideof the duodenumof the duodenum• The swelling pancreas causes fluids to shift intoThe swelling pancreas causes fluids to shift intothe retro peritoneum and bowelthe retro peritoneum and bowel• Fluid shifts can cause severe hypovolemia andFluid shifts can cause severe hypovolemia andhypotensionhypotension• Inflammation cause commotion around pancreasInflammation cause commotion around pancreas
    149. 149. 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
    150. 150. 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’sLipase, LDH, AST, WBC’sBUN, and GlucoseBUN, and Glucose
    151. 151. 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– HypoxemiaHypoxemia– AtelectasisAtelectasis– ARDSARDS– Pericardial EffusionPericardial Effusion– Mediastinal AbscessMediastinal Abscess– HyperglycemiaHyperglycemia– HypertriglyceridemiaHypertriglyceridemia– EncephalopathyEncephalopathy
    152. 152. PancreatitisPancreatitisTREATMENTTREATMENT– StabilizationStabilizationCorrect Fluid AndCorrect Fluid AndElectrolyte 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 OfInfectionInfection– PrayPray
    153. 153. PancreatitisPancreatitis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
    154. 154. 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 insufficiencyPulmonary & cerebral insufficiencyAcute diabetic ketosis or oliguriaAcute diabetic ketosis or oliguriaHemorrhagic pancreatitis may appearHemorrhagic pancreatitis may appear
    155. 155. THE ENDTHE ENDPART 1PART 1CCRN REVIEWCCRN REVIEW
    156. 156. THANK YOUTHANK YOUCCRN REVIEW PART 1CCRN REVIEW PART 1
    157. 157. ReferencesReferences American Heart Association. (2005). Guidelines 2005 for CardiopulmonaryResuscitation and Emergency Cardiovascular Care. Available at:www.americanheart.org. Bridges EJ.(2006) Pulmonary artery pressure monitoring: when, how, and whatelse 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 CardiovascularNursing: 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 CareNursing. 5th ed. Philadelphia, Pa: Saunders. Thelan, L. A., Urden, L. D., Lough, M. E. (2006). Critical care: Diagnosis andTreatment for repair of abdominal aortic aneurysm. St. Louis, Mo.:Mosby/Elsevier. pg 145-188.
    158. 158. References ContinuedReferences Continued Urden, L., Lough, M. E. & Stacy, K. L. (2009). Thelans 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 Braunwalds HeartDisease: 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 ofCardiovascular Nursing:15(4):1–14, July 2001. Irwin, R. S.; Rippe, J. M. (January 2003). Intensive Care Medicine. LippincottWilliams & Wilkins, Philadelphia: pgs. 35-548. Wung, S., Aouizerat, B. E. (Nov/Dec 2004). Aortic Aneurysms. Journal ofCardiovascular Nursing. Lippincott Williams & Wilkins, Inc.:19(6):409-416, 34(2).

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