b&b cardiovasc

*2010 Laurel R. Talabere, PhD, RN, AE-C*The Child a with Cardiovascular Alteration Laurel R. Talabere, PhD, RN, AE-C, Professor EmeritaCapital UniversityDepartment of NursingColumbus, OH 43209 USA

Ball & Bindler, Chapter 21(See p. 795: Explore Media Link for additional resources for this chapter)

Holloway, Moredich & Addudellpp. 114-115, 145-146

2010 Laurel R. Talabere, PhD, RN, AE-C

*2010 Laurel R. Talabere, PhD, RN, AE-C*The mystical heart of a child is a precious and beautiful thing. It is marred only by wounds of a thoughtless and not too intelligent world. In a physical sense, the heart is a tough organ a marvelous mechanism that mostly, without repairs, will give valiant service for up to 100 years. In an emotional sense, it is susceptible to wounds of indifference, thoughtlessness, and neglect. During episodes of illness, it is especially vulnerable.Author Unknown


*2010 Laurel R. Talabere, PhD, RN, AE-C*Learner Objectives

Describe measures to assess infants & children with cardiovascular alterations.

Compare & contrast anatomical & physiological differences between fetus, infant, child & adult.

Analyze assessment data for selected cardiovascular alterations.

Discuss epidemiology, etiology, pathophysiology, clinical presentation, diagnosis & management of selected congenital & acquired cardiovascular alterations.

Apply the nursing process in selected situations.


*2010 Laurel R. Talabere, PhD, RN, AE-C*How would you assess heart rate in an infant?

How might crying affect BP in an infant?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Pediatric Differences in A & P1. Blood volume:Absolute blood volume is smallerRelative blood volume is greater90ml/Kg infant70ml/Kg adult

2. Heart rateNormally fasterTachycardia with stressearly sign of decompensation

3. Hgb concentration > neonate

4. BP lower but labile w/ stress, cry

5. Heart & vessels grow unevenly


*2010 Laurel R. Talabere, PhD, RN, AE-C*AssessmentNeurologicalRestlessness early sign of hypoxiaChanges in LOCSkin colorPallorCyanosis -- late sign of hypoxiaHeartApical pulse, PMIHeart rate & rhythm; sinus arrhythmia may be nlAdditional heart sounds - murmursLungsHepatic & splenic bordersPosition of comfortNutritional statusExercise intoleranceExtremitiesPulses - bilateralCapillary refillEdemaDigital clubbing

In Chronic Hypoxemia look for polycythemia & clubbing


*2010 Laurel R. Talabere, PhD, RN, AE-C*Assessment Techniques:LocatingPulsesFigure 5-35


*2010 Laurel R. Talabere, PhD, RN, AE-C*Assessment Techniques:Heart SoundsKnow location of atria, ventricles, valves & rib interspaces

Auscultate in both sitting & in reclining positions

S1 is synchronous with carotid pulseAortic areaPulmonic areaTricuspid areaApex or mitral areaFigure 5-34


*2010 Laurel R. Talabere, PhD, RN, AE-C*Assessment Techniques:Heart MurmursInnocent murmurs50% of childrenNo pathology

Grading murmursGrade 1- barely audible, even in quiet roomGrade 2 - audible but faintGrade 3 - louder, easy to hearGrade 4 loud with palpable thrill on chest wallGrade 5 very loud, can hear with part of stethoscope lifted off chestGrade 6 loudest, can hear with entire stethoscope just above chest wall


*2010 Laurel R. Talabere, PhD, RN, AE-C*QuestionPolycythemia compensates for

______________________________

Why does this compensatory response occur?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Question

One of the earliest signs of impaired myocardial functioning is _____________________.

Why does this compensatory response occur?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Diagnostic TestsHeart rhythms1st waveP waveElectrical activity of atria2nd waveQRS waveElectrical activity of ventricles3rd waveT waveHearts return to resting state

Cardiac arrhythmias PACs / PVCs Very common in normal children & teensUsually no pathologyTachycardiaSVT (supraventricular tachycardia) most common abnormal tachycardia in children (see pp. 783-84)Involves both atria & ventriclesUsually not life threatening


*2010 Laurel R. Talabere, PhD, RN, AE-C*Diagnostic TestsPulse oximetry

Chest x-rayHeart sizePulmonary blood flow patterns

EKG (ECG)Measures electrical activity of heartBedside cardiac monitorHolter monitor 24-48 hrsEvent recorder

Echocardiography (ECHO)High frequency sound waves produce image of heart structuresMay replace need for cardiac cath

Exercise stress test

MRI - images extracardiac vascular structures See Diagnostic Procedures & Laboratory Tests to Evaluate Cardiac Conditions, pp. 743-745.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Diagnostic TestsCardiac cathMost invasiveOne or both sides Usual entry through femoral veinMeasures pressures & O2 sats in heart chambersUsually combined with angiography (use of contrast material)May do biopsyUsually diagnostic, may be interventionalNursing care:Pre-procedure: assess for illness & allergies, get baseline pedal pulses, NPO, age-appropriate preparation (see HH), topical EMLA

Post-procedure: watch for hemorrhage or hematoma, fever, loss of pulse below site, vessel obstruction, transient dysrhythmia, N&VColumbus Children's Hospitals Hybrid Cardiac Cath Lab. Interventional & surgical techniques can be combined to correct congenital defects in one procedure. Also used to treat adult congenital heart clients, often with no surgery required.http://www.columbuschildrens.com/gd/templates/pages/pfv/PFV.aspx?page=193


*2010 Laurel R. Talabere, PhD, RN, AE-C*Cardiac catheterizationSee the top part of Table 21-2: Clinical Interventions for Congenital Heart Defects: Cardiac Catheterization, p. 749.



What is the purpose of a cardiac catheterization?

What is the difference between diagnostic & interventional cardiac catheterization?

Think about the words "diagnosis" & "intervention." How could a cardiac cath be used for both of these purposes?


*2010 Laurel R. Talabere, PhD, RN, AE-C*QuestionIdentify 2 priority risks for a child following a cardiac catheterization.

Why?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Normal Cardiopulmonary Circulation


*2010 Laurel R. Talabere, PhD, RN, AE-C*Normal pressures (mm Hg) & O2 sats (SaO2) in cardiac chambers & great arteries. Figure 21-1.


*2010 Laurel R. Talabere, PhD, RN, AE-C*What are some differences between fetal & postnatal circulation?


*2010 Laurel R. Talabere, PhD, RN, AE-C*http://heart.healthcentersonline.com/animations/show_all_animations.cfm

Click on the above link. When the webpage opens, scroll down to Prenatal Heart Circulation and click on the picture that matches the one above. This video segment, which is 2:11 minutes long, may take a minute or so to load.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Pre- and Postnatal CirculationSee As Children Grow: Transition of Fetal Circulation to Pulmonary Circulation, p. 742.



Is the ductus arteriosis a pre- or post-natal structure?

What is the function of the ductus arteriosis?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Pre- and Postnatal CirculationLV


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congential Heart DefectsFrequency - 8:1000 live birthsMost common type of birth defect in live birthsAt least 35 different defectsCombination defects occurWide range of severityEtiologyUnknown in most casesAssociated factors: maternal exposure to environmental factors, medications; maternal diabetes; geneticsSurgical repairRequired for most defectsMay require stagingCPB may be necessaryECMO = Extracorporeal Membrane Oxygenation(See NCH Helping Hand)


*2010 Laurel R. Talabere, PhD, RN, AE-C*Classification of Congential Heart Disease:Comparison of Selected ConditionsCoarctation of aortaAortic stenosis_____ Hypoplastic left heart syndromeAtrial septal defectVentricular septal defectPatent ductus arteriosusAtrioventricular canalPulmonic stenosis Tetralogy of FallotPulmonary or tricuspid atresiaDecreased pulmonary blood flowIncreased pulmonary blood flowObstruction of systemic blood flowTransposition of great vesselsTruncus arteriosusTotal anomalous pulmonary venous returnMixed defectsAcyanoticCyanotic


*2010 Laurel R. Talabere, PhD, RN, AE-C*What are some of the clinical differences between acyanotic & cyanotic congenital heart defects?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congential Heart Disease: PathophysiologySee Clinical Manifestations: Heart Defects by Pathophysiology (p. 746) for a comparison of the clinical signs & symptoms in the 4 major congenital heart defect categories.


*2010 Laurel R. Talabere, PhD, RN, AE-C*http://heart.healthcentersonline.com/animations/show_all_animations.cfmClick on the above link. When the webpage opens, scroll down to Congenital Heart Disease and click on the picture that matches the one above. This video segment, which is 2:37 minutes long, may take a minute or so to load.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Defects with Increased Pulmonary Blood Flow (acyanotic)What do these defects have in common?See Table 21-3


*2010 Laurel R. Talabere, PhD, RN, AE-C*Atrial Septal Defect (ASD): Defect with Increased Pulmonary Blood FlowAn ASD is an abnormal opening in the wall between the two atria.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Ventricular Septal Defect (VSD): Defect with Increased Pulmonary Blood FlowMost common congenital heart defect.A VSD is an abnormal opening in the wall between the two ventricles.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Patent Ductus Arteriosus (PDA): Defect with Increased Pulmonary Blood FlowA PDA occurs when this prenatal structure fails to close.

The incidence is increased in premature infants . WHY??May be treated with IV indomethacin, an NSAID which inhibits prostaglandin synthesis. This med stimulates closure of the PDA.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Atrioventricular Canal Defect (AVC): Defect with Increased Pulmonary Blood FlowMost common heart defect in infants with Down Syndrome (Trisomy 21).An AVC is an abnormal opening in the wall between the two atria and the two ventricles.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Defects with Obstruction of Systemic Blood FlowWhat do these defects have in common?See Table 21-6


*2010 Laurel R. Talabere, PhD, RN, AE-C*Coarctation of the Aorta (COA): Obstructive Defect (acyanotic)Coarctation means the narrowing of a structure.

In this defect, the BP is elevated before the COA & decreased beyond the COA.

Where would you expect to find elevated BP? Decreased BP?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Aortic Stenosis (AS): Obstructive Defect (acyanotic)Stenosis means a narrowing of a normal body opening. In this defect, the opeing of the aorta where it leaves the left ventricle is narrowed.

What is the effect on blood flow through the heart??


*2010 Laurel R. Talabere, PhD, RN, AE-C*Hypoplastic Left Heart Syndrome (HLHS): Obstructive Defect (cyanotic)Atresia of the Mitral Valve


*2010 Laurel R. Talabere, PhD, RN, AE-C*Defects with Decreased Pulmonary Blood Flow (Cyanotic)Tetralogy of FallotPulmonary or Tricuspid AtresiaWhat do these defects have in common?See Table 21-4Pulmonic Stenosis


*2010 Laurel R. Talabere, PhD, RN, AE-C*Pulmonic Stenosis (PS): Defect with Decreased Pulmonary Blood FlowPS is narrowing of pulmonary artery where it leaves the right atrium.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Tetralogy of Fallot (TOF): Defect with Decreased Pulmonary Blood FlowTOF is a combination of 4 abnormalities.

Can you find all 4 of them in the illustration?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Position of Comfort for TOFHolding infant in knee-chest position


*2010 Laurel R. Talabere, PhD, RN, AE-C*Position of Comfort for TOFSquatting position for child with cyanotic heart defect to relieve chronic hypoxia & blue (tet) spellsFigure 21-6


*2010 Laurel R. Talabere, PhD, RN, AE-C*Tricuspid or Pulmonary Atresia: Defect with Decreased Pulmonary Blood FlowBoth tricuspid pulmonary atresia alone are incompatible with life. WHY??

What compensatory defects must also be present?Atresia means congenital closure or absence of a normal body opening. In this defect, either the tricuspid valve or the pulmonary artery is closed.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Mixed Defects (Cyanotic)What do these defects have in common?See Table 21-3http://www.med.umich.edu/mott/chc/images/truncus-defect.gifhttp://www.med.umich.edu/mott/chc/images/avpr1.jpgTotal Anomalous Pulmonary Venous ReturnTruncus Arteriosus


*2010 Laurel R. Talabere, PhD, RN, AE-C*Transposition of the Great Vessels or Arteries(TGV or TGA): Defect with Decreased Pulmonary Blood FlowTGV alone is incompatible with life. What defects must also be present?

If PDA present, prostaglandin E1 is given. WHY??TGV is a complete switch or transposition of the aorta and the pulmonary artery.

What impact does this altered placement of these great vessels have on circulation?


*2010 Laurel R. Talabere, PhD, RN, AE-C*QuestionWhat action would you take for an infant or child experiencing a hypercyanotic episode?


*2010 Laurel R. Talabere, PhD, RN, AE-C*QuestionWhat abnormal signs would you expect to find when assessing an infant with coarctation of the aorta?


*2010 Laurel R. Talabere, PhD, RN, AE-C* Question

A cyanotic heart defect is one in which there is a _____________ to _______________ shunting of blood.

Why?


*2010 Laurel R. Talabere, PhD, RN, AE-C*What is the most common cause of congestive heart failure in infants and children?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congestive Heart Failure: PathophysiologySpecific causes:Volume overload (preload)L ---> R shunt ---> cor pulmonalePressure overload (afterload)Obstructive lesions ---> increased left ventricular pressureDecreased contractilityDecreased K+, glucose, Ca++, Mg++Severe anemiaOxygen demands exceed cardiac output (CO)HyperthyroidismSepsisSevere anemiaBall, J.W. & Bindler, R.C. (2006).


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congestive Heart Failure: PathophysiologyFigure 21-9.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congestive Heart Disease: Nursing Management1. Improve cardiac functionDigoxinMaintain K+

2. Remove accumulated fluid & Na+DiureticsMay need K+ supplements When K+ decreased, increased risk of digitalis toxicity (KNOW THE SIGNS Possible fluid & Na+ restriction


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congestive Heart Disease: Nursing Management3. Decrease cardiac & respiratory demandsAvoid cold stress in infantsIncreases BMR & O2 demand pulmonary & peripheral vasoconstriction decreased O2 uptake in Iungs & O2 delivery to tissuesTreat infectionsReduce WOBSedate irritable / restless child as neededProvide restMinimize environmental stimuliPosition appropriatelyFit diapers & clothing looselyProtect from respiratory infectionsBall, J.W. & Bindler, R.C. (2006).


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congestive Heart Disease: Nursing Management4. Maintain nutritional statusClinical signs:Wt & ht low on growth chartIncreased BMR due to poor cardiac function

InterventionsIncrease calorie density of formulaImpaired ability for intake due to fatigueFeed by N/G or G-tube in addition to or in place of oral feedings as neededFigure 21-10.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congestive Heart Disease: Nursing Management5. Provide child & family support to facilitate adjustment & copingRecognize impact of stress on child & familySerious complicationStress increases cardiac & respiratory demandUse anxiety reduction techniquesTeaching with written instructionsCommunicationAppropriate reassuranceMake referralsOutpatient servicesCommunity resourcesHome carehttp://www.columbuschildrens.com/Media_Center/pr/release.cfm?type=search&id=44



Name three signs of digoxin toxicity: __________________, __________________, and __________________.

What nursing action would you take?



You are caring for a child with congestive heart disease secondary to a congenital heart defect. Identify two nursing interventions that would help this child achieve improved cardiac output.

Think about an important medication that you might give. Think about the effects on the heart of fluid retention& what can be done to correct it. Consider how you might reduce demands on the heart & lungs.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congential Heart Disease: ManagementNon-surgicalBalloon angioplasty COAValvuloplasty - PSCoils to occlude during cardiac cath - PDAClose septal defect during cardiac cath - ASD, VSD

ValvuloplastySeptal occluder used to close an atrial septal defect (ASD) and less commonly to close a ventricular septal defect (VSD).Coil used to close a patent ductus arteriosus (PDA). The coil of wire covered with tiny fibers occludes the ductus arteriosis when a thrombus forms in the mass of fabric and wire.See the bottom part of Table 21-2: Clinical Interventions for Congenital Heart Defects: Surgical Procedure, p. 749.


*2010 Laurel R. Talabere, PhD, RN, AE-C*Congential Heart Disease: ManagementSurgical - varies with defect(s)Patch - septal defectsGraft - valve defectsArterial switch TOGVShunts HLHS, TA, TOFChild with ASD repairFigure 21-7.See the bottom part of Table 21-2: Clinical Interventions for Congenital Heart Defects: Surgical Procedure, p. 749.Figure 21-4.



What congenital heart defect is the most common indication for a heart transplant?

Why is a heart transplant the only real solution?



Identify 4 congenital heart defects that cause increased pulmonary blood flow.


*2010 Laurel R. Talabere, PhD, RN, AE-C*What is the difference between congenital & acquired heart disease?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Bacterial (Infective) Endocarditis Also known as:Subacute Bacterial Endocarditis (SBE)

Infection of valves & endocardium

Usually occurs w/ great vessel anomalies

EtiologyUsually Strep viridans or StaphEntry - bacteremia following dental work, UTIs, long-term catheters, cardiac surgery


*2010 Laurel R. Talabere, PhD, RN, AE-C*Bacterial (Infective) Endocarditis

Clinical presentationSubacute sx - slow onset, low-grade fever, anorexia, malaiseAcute (& more serious) sx - rapid onset, high fever, stiffness

DiagnosisECG changesBlood culturesECHO

ManagementHigh dose IV antibiotics for 4-6 weeks

PreventionProphylactic antibiotics for high risk children. WHY??


*2010 Laurel R. Talabere, PhD, RN, AE-C*Rheumatic Fever (RF)Leading cause of acquired heart disease in developing countries

Can cause cardiac valve damage

EtiologyProbably autoimmune response to proteins in Group A -hemolytic Streptococcus

PathophysiologyAutoimmune response to untreated or partially treated strep throat

Risk of recurrence


*2010 Laurel R. Talabere, PhD, RN, AE-C*Rheumatic Fever (RF)Clinical presentation multiple systems involvedCarditis - characteristic murmur, CHF may develop

Sydenham Chorea (St. Vitus dance) - involuntary, purposeless movements; exacerbated with fatigue; transitory but may persist

Erythema marginatum - transitory, nonpruritic rash

Polyarthritis - reversible

Ashoff bodies (lesions in subcutaneous tissue near joints & in connective tissue in heart)

See Guidelines for Diagnosis of Initial RF (Jones Criteria), Table 21-7


*2010 Laurel R. Talabere, PhD, RN, AE-C*Rheumatic Heart Disease (RHD)

What are the consequences of these valvular changes?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Rheumatic Fever (RF)DiagnosisClinical presentationAntibody titersElevated ESREKGECHOManagementAcute phaseBedrestMonitor carefully for carditisAntibioticsASA for 3-4 wksSteroids if severe carditis developsSecondary prophylaxisLong term antibiotics (into adulthood)Reduce risk of recurrenceReduce risk of infectious endocarditisPrevention is KEY for nursing care:

F/U of sore throats in child & family members

Emphasize importance of long term F/U care

Emphasize importance of prophylaxis


*2010 Laurel R. Talabere, PhD, RN, AE-C*QuestionAdequate treatment of ___________________ significantly reduces the risk of rheumatic fever.

Why?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Kawasaki SyndromeHighest incidence:

*2010 Laurel R. Talabere, PhD, RN, AE-C*Kawasaki SyndromeClinical presentationHigh fever unresponsive to antibiotics or antipyreticsLymphadenopathy & conjunctivitisLips cracked, mouth & pharynx inflammed (see Figure 21-11)Strawberry tongueSwollen hands & feetDiagnosis - no specific testsHistoryLab tests: anemia, leukocytosis, elevated ESREchocardiogramsManagementHigh dose IV immune globulin (IVIG)ASA, other anticoagulants if neededMaintain BP & cholesterol WNL to reduce risk of later HDBall, J.W. & Bindler, R.C. (2006). See Box 21-1 for Diagnostic Criteria


*2010 Laurel R. Talabere, PhD, RN, AE-C*DyslipidemiaDiagnosisFull lipid profile (12-hr fasting)Abnormal valuesTotal cholesterol >200 mg/dLLDL > 130 mg/dLTriglycerides > 200 mg/dLHDL < 40 mg/dLManagementDietary reduction of saturated fatsMedicationsSee Table 21-8 (Lab Values) & Table 21-9 (Recommended Nutrient Intake for Dyslipidemia)


*2010 Laurel R. Talabere, PhD, RN, AE-C*DyslipidemiaRecommendations Education for preventionLower cholesterol levels in all children by changing eating patternsEffect of aerobic exercise on cholesterol levels

Early detectionScreen children & adolescents with family hx of cardiac disease or one parent with cholesterol >240


*2010 Laurel R. Talabere, PhD, RN, AE-C*Systemic Hypertension (HTN)CategoriesEssential HTN - idiopathicGenetic factors: African-Americans - higher incidence, develops earlier, more severeEnvironmental factors: obesity, salt, smoking, stress

Secondary HTN - identified causeIn children, usually structural anomaly or other disease (cardiovascular, endocrine, renal)


*2010 Laurel R. Talabere, PhD, RN, AE-C*Systemic Hypertension (HTN)Diagnosis Significant HTN - persistent BP in 95th-99th percentiles for age & genderSevere HTN - persistent BP at or above 99th percentile for age & genderBright Futures: Appendix I: Hypertension Screening http://www.bright futures.org/bf2/pdf/pdf/Appendices.pdf

ManagementLifestyle changes / reduction of risk factorsMedicationTreatment of underlying disease



What is the underlying pathology that occurs with shock?

How does it relate to circulatory failure?

What is the triad of shock?


*2010 Laurel R. Talabere, PhD, RN, AE-C*Shockaka circulatory failure

Inadequate tissue perfusionmetabolic demands not metcellular dysfunctionorgan failure

Major physiological results ------------------------- >

What clinical signs would you expect to see?

HypotensionMetabolic acidosisTissue hypoxia


*2010 Laurel R. Talabere, PhD, RN, AE-C*How Shock Causes Circulatory Failure in Children


*2010 Laurel R. Talabere, PhD, RN, AE-C*ShockHypovolemicmost common form of serious shock

caused by loss of blood, plasma or ECF ---------> reduced circulating blood volume

dehydration from diarrhea or emesis

See Pathophysiology Illustrated: Hypovolemic Shock, p. 788.

See Clinical Manifestations: Hypovolemic Shock, p. 789.


*2010 Laurel R. Talabere, PhD, RN, AE-C*ShockMaldistributive (vasogenic)vascular abnormality leading to maldistribution of blood in bodyanaphylaxisneurogenic shocksepsis


*2010 Laurel R. Talabere, PhD, RN, AE-C*ShockCardiogenic (obstructive)decreased cardiac output from pneumothorax

What clinical signs would you expect to find?See Pathophysiology Illustrated: Mediastinal Shift in Obstructive Shock Figure 21-14.Also See Pathophysiology Illustrated: Cardiogenic Shock Figure 21-15.


*2010 Laurel R. Talabere, PhD, RN, AE-C*ShockSepticdefinition: sepsis with organ dysfunction & hypotensionsystemic inflammatory response syndrome (SIRS) -very exaggerated immune response

Incidence increasingmore immunosuppressed individualsmore invasive devices

Stages:1st - hyperdynamic, warm 2nd - normodynamic, cool 3rd - hypodynamic, cold See Pathophysiology Illustrated: Septic Shock Figure 21-13.


*2010 Laurel R. Talabere, PhD, RN, AE-C*ShockBodys ResponseCompensatednormal BPmild tachycardiadecreased perfusion in extremitiesirritabilityDecompensatednormal BP but narrowing pulse pressuretachypnea & increased tachycardiacool, pale extremities with poor cap refillconfusion, sleepiness, less responsivenessIrreversiblehypotensionthready, weak pulsepronounced peripheral vasoconstrictionlethargy, stupor, coma


*2010 Laurel R. Talabere, PhD, RN, AE-C*ShockManagementEarly detectionVentilationEstablish airwayOxygen therapyIntubation & ventilator supportFluid administrationRestore blood & fluid volumeColloids to retain fluid in the vascular compartmentVasopressor supportImprove cardiac outputDopamine improves cardiac output & renal perfusionAlsoNa+ bicarb & Ca++ chlorideDiureticsBroad spectrum antibiotics in septic shock

HypotensionMetabolic acidosisTissue hypoxia


*2010 Laurel R. Talabere, PhD, RN, AE-C*Selected Nursing Diagnoses, Outcomes & Interventions

Nsg DxOutcomesMajor InterventionsCardiac Output, DecreasedCardiac Pump, Effectiveness

Circulation Status

Vital SignsCardiac Care: Acute Hemodynamic RegulationShock Management: Cardiac

Circulatory Care: Arterial InsufficiencyCirculatory Care: Venous Insufficiency

Vital Signs MonitoringActivity IntoleranceEnergy Conservation

Physical FitnessEnergy ManagementEnvironmental Management

Activity TherapyExercise Promotion: Strength Training


ReferencesBall, J.W. & Bindler, R.C. (2006). Child health nursing: Partnering with children & families. Upper Saddle River, NJ: Pearson Prentice Hall.

*2010 Laurel R. Talabere, PhD, RN, AE-C*


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