Cardiac

Fetal circulation structures

• Fetal circulation is pink/red due to the diversion of blood away from the lungs- no oxygenated blood returns.

• Umbilical vein; umbilical arteries

• Placenta carries blood and nutrients through fetal circulation through the umbilicus by way of the large umbilical vein.

• Blood returns to placenta via the umbilical artery

• Foramen ovale

• 1 way trap door that connects the right atrium to left atrium and allows the diversion of blood to the lungs

• Ductus arteriosus

  • Connects the left atrium directly to the aorta- diverts blood away from the lungs.

• Ductus venosus

  • Diverts blood from the umbilical vein and portal system directly to the inferior vena cava- directly to right atrium.

    • Closes when vein is no longer necessary- at 2 months becomes a ligament

• Lungs

  • In utero the lungs are collapsed

  • Utilizes Mom’s oxygen

  • **You want the blood with the highest oxygen concentration going to heart and brain.

Circulatory changes after birth

• Normal pressures higher in ventricles than atria (NORMAL LEFT> RIGHT PRESSURE)

  •   When the placenta is removed, the heart takes over and the systemic vascular resistance increases

  •   Leads to increase LV wall thickening

• Pressure flows from higher to lower; toward path of least resistance

  •   Left side pressures increases over the right side pressure

• Resistance in pulmonary circulation (R) less than in systemic (L)

  •   Increase pulmonary blood flow causes increase in oxygenation which, in turn, causes a vasodilating effect

•   This lowers pulmonary vascular resistance

•   Right side pressure drops- does not have to work against pvr

Transition from fetal to pulmonary circulation

• Occurs within a few hours after birth and completes at approximately days 10 to 21

• BEGINS- with removal of placenta

• ENDS- with permanent closure of ductus arteriosus (between day 10-21)

• Hemodynamics change with FIRST breath

• Increased pulmonary blood flow

• Decreased pulmonary vascular resistance

• Left Atrium

  • Increase blood flow from the lungs (pulmonary veins)

  • Increase pressure due to increase blood flow

  • Stimulates the closure of the Foramen Ovale

• Right atrium

  • Pressure decreases due to increased blood flow in pulmonary circulation– lungs expand– increased oxygen stimulates the vasodilation

  • Stimulates the closure of PDA

Neonatal Circulation

• GREATER RISK FOR HEART FAILURE DUE TO HEARTS ARE IMMATURE

• MORE SENSITIVE TO VOLUME OR PRESSURE OVERLOAD

• LOWER STRENGTH IN LV OF NEWBORN/INFANTS

  • Lower SBP

• Remember

  •   Infants are at a greater risk for heart failure than adults because their hearts are immature and are much more sensitive to volume or pressure overload.

  • Size of heart is of fist

  • Heart position- middle, slightly to left

• Cardiac Output- volume of blood ejected by heart in one minute

• Ways to assess without machines:  NO MONITORING NEEDED

• Cardiac   

• Pulse strong   

• Adequate HR 

• Cap Refill

• Color

• Kidney Perfusion

  • Urinary output

• Neuro Perfusion

  • Lethargy

  • Orientation status

Normal chamber pressure: RA - 72-80%; LA - 95%

CARDIAC DYSFUNCTIONS

Assessment: pediatric indicators of cardiac dysfunction

• physical

  • Poor feeding

    • Typical indicator

    • Difficulty coordinating suck, swallow, and breathe - WEARS THEM OUT

  • Tachypnea

    • Typical indicator

    • Working hard

  • Tachycardia

    • Typical indicator

    • Working hard

  • Failure to thrive

    • Poor feeders

    • Infant exemplify as poor feeding

    • Older children just cannot keep up with foods (Intolerance)

• Developmental

  • Developmental delays

  • Prenatal history

  • Family history of cardiac disease

• Prenatal history - Get a thorough prenatal

  • Maternal

    • Rubella

    • Alcohol

    • Dilantin

    • Diabetes

    • Lupus

    • SIDS

    • Frequent fetal death

    • Family history of cardiac disease

  • Fetal

    • We have congenital anomalies

    • High birthweight have higher incident of cardiac disease

Assessment: Murmurs

• Definition

  • Heart sounds that reflect the flow of blood within the heart

  • High flow rates through normal or abnormal valves

• Assessment

  • ausculation

    • High frequency sounds

    • Low frequency sounds

    • Loud and distinct

  • Palpitation

    • Thrill

  • Causes

    • Forward flow of blood

      • Constructed/Irregular valve

      • Dilated vessel/Chamber

    • Regurgitation flow - Backflow

      • Incompetent valve/defect

• Innocent Murmurs

  • Innocent/functional (VS. PATHOLOGICAL)

    • Grade 3 or less

    • Low pitched

    • Normal S1 and two

    • Systolic in timing

    • Here, supine and disappears when sitting

    • Occurs in up to 50% of all children at sometime

• Test cardiac function

  • ECG

  • Chest x-ray

  • Echocardiography

  • Cardiac catheterization

Cardiovascular dysfunction/Disorders

• congenital heart disease

  • CHD – a child born with a heart disease

• Incidence

  • 5 to 8 per 1000 life births

  • About 2 to 3 of these are symptomatic and first year of life

  • Major causes of death and first year of life and prematurity

  • Most common anomaly in VSD

  • 28% of kids with CHD have another recognize anomaly

    • Trisomy 21, 13, 18, +++

  • The heart develops within the 4 to 7 week gestation

    • Most susceptible to teratogens

    • Do not even know they are pregnant

    • Most important for cardiac development

• Causes

  • •Chromosomal/genetic = 10%-12%

    •Maternal or environmental = 1%-2%

    •Maternal drug use

    •Fetal alcohol syndrome—50% have CHD

    •Maternal illness

    •Rubella in 1st 7 wks of pregnancy→50% risk of defects including PDA and pulmonary branch stenosis

    •CMV, toxoplasmosis, other viral illnesses>> cardiac defects

    •IDMs = 10% risk of  CHD (VSD, cardiomyopathy, TGA most common)

    •Multifactorial = 85%

• Classification

  • Older

    Acyanotic

    May become cyanotic

    Cyanotic

    May be pink

    May develop CHF

    Newer

    Hemodynamic characteristics

    Increased pulmonary blood flow

    Decreased pulmonary blood flow

    Obstruction of blood flow out of the heart

    Mixed blood flow

• Consequences

  • Severity of Cardiac Defect + Altered Hemodynamics= Clinical Consequence

  • uCongestive Heart Failure

    uDefects that lead to left to right shunting (increase pulmonary blood flow)

  • uHypoxemia

    uDefects that result in decrease pulmonary blood flow.

  • Older Classifications of CHD

    Acyanotic

    May become cyanotic

    Cyanotic

    May be pink

    May develop CHF

    Newer Classification of CHD

    Hemodynamic characteristics

    Increased pulmonary blood flow

    Decreased pulmonary blood flow

    Obstruction of blood flow out of the heart

    Mixed blood flow

    TGV- Transposition of Great Vessels

    TAPVR- Total Anomalous pulmonary venous return

    HLHS- Hypoplastic Left heart syndrome

Congestive heart failure

• 1.Inability of heart to pump adequate amount of blood to systemic circulation to meet metabolic demands of the body

  1.Heart failure is secondary to some structural abnormality that results in the increase in blood flow and pressure in heart

  2.This results in the increase of cardiac demands on the body- metabolic sepsis, anemia or hypothyroidism

  2.R Failure- RV cannot pump effectively in pulmonary artery

  3.L failure- Cannot pump into systemic circulation effectively

  4.High output failure- nothing wrong with the heart but something is going on to warrant an increase in the needs of the body- sepsis, anemia hypothyroidism

  1.Results in a change of pressure in LA and PV and lungs become congested with blood leading to pulmonary edema “Classic CHD”

  5.Children- hard to differentiate r vs l failure

  1.Need to correct due to the loss of cardiac damage

• •Inability of heart to pump adequate amount of blood to systemic circulation

  •Right-sided failure

  •Left-sided failure

  •In children is rare to observe clinical signs of solely right or left-sided failure

• CHF: CAUSES

  • •Volume Overload

    •RV Hypertrophy that can cause L to R shunt

    •Pressure Overload

    •Obstructive lesion; pressure proximal to where the obstruction is located

    •Decreased Contractility

    •Ischemia, anemia, electrolyte issues/problems

    •Cardiac Output Demands

    •Sepsis, anemia, hypothyroid

    •Cor Pulmonale

    •Heart disease caused from lung disease

• CHF: PRESENTATION IN CHILDREN

  • Impaired Myocardial Function

    • Tachycardia

    • Fatigue

    • Weakness

    • Restless

    • Pale

    • Cool Extremities

    • Decreased BP

    • Decreased UO

    • Diminished contractility

  • Pulmonary Congestion

    • Commonly seen in L heart failure

    • Tachypnea

    • Dyspnea

    • Respiratory Distress

    • Exercise Intolerance

    • Cyanosis

• Systemic Venous Congestion

  • Generalized body edema

  • Periorbital Edema

  • Weight gain

  • Ascites

  • Hepatomegaly

  • Neck Vein distention (JVD)

CHF:ASSESSMENT

• ALWAYS LISTEN TO CAREGIVER- THEY KNOW THE PATIENT BETTER! 

• Respiratory- Respiratory status is early sign!!!

  •   Listen to breath sounds- not just the rate

  •   Congestion

  •   Cough

  •   Pulse- Weak/thready

• Pediatric Indicators of Cardiac Dysfunction- Tachycardia, tachypnea and poor feed

CHF: THERAPEUTIC MANAGEMENT GOALS

• Need to stabilize medically before surgical repair

    Improve cardiac function

    Increase cardiac output

    Decrease venous pressure

    Eliminate edema

    Increase myocontractility

    which will then decrease HR

• IMPROVE

  • CARDIAC FUNCTION

    • DIGOXIN

    • ACE INHIBITORS

  • OXYGENATION

    • DECREASE OXYGEN CONSUMPTION

• REMOVE

  • ACCUMULATED FLUID AND SODIUM

    • DIURETICS

• DECREASE

  • CARDIAC DEMANS

    • LIMIT ACTIVITY

CHF: nursing considerations

• improve cardiac function

  • Cardiac glycoside

    • Digoxin

      • Fine line between therapeutic and toxic doses

          Historically, a lot of med errors have occurred, now we have safety nets

          2 RN check dose, medication and sign off

          May require 2 MD to order

          Apical pulse for one full minute

          90-110 bpm- hold and call MD

          Range is 0.8mcg-2.0mcg- should be less than 1 ml.

          Green liquid- 1 ml syringe

          Toxicity S/S’s: Vomiting  Bradycardia    DO NOT REGIVE. CALL MD>

  • Ace inhibitors

    • Captopril

      • Interferes with angiotensin 2- causing vasodilation

          Decreases pulmonary resistance and SVR

          Vessels enlarge, results in decreased BP

          TAKE BP prior to administration

    • Enalapril

    • Vasotec

• Decrease cardiac demands

  • Treat fever/infection

  • Rest

  • Feeding adjustment

• Reduce respiratory distress

  • HOB elevated

• Maintain nutritional status

  • Elevated BMR

    • Need to supplement with feeds

        Orogastric due to babies are nasal breathers- NG may block the nare

        Higher kcal per ounce than normal due to high BMR

        Shorter more frequent feeds

  • Orogastric feeds

• Promote fluid loss

  • Diuretics

    • Furosemide

    • Chlorothiazide

    • Sprionolactone

  • Furosemide and chlorothiazide - do not spare potassium

    •   Monitor for hypokalemia

        Muscle weakness

        Teach parents foods rich in potassium- bananas, oranges, green leafy veg

        Sironolactone- spares potassium.

• Support child and family

  • Bundle care

Hypoxemia

• decreased oxygen levels in the blood

Hypoxemia: presentation in children

• uDecreased oxygen in circulating blood stream

• uCyanosis

  • Chronic hypoxemia

  • 02 sat between 80-85%

• uPolycythemia

  • Body interprets that body needs more oxygen so more RBCs are made (to increase Hgb molecule)

      Hematocrit then becomes elevated (Normal can vary, but typically 33-40%).

      Over 50% is a problem

      55-60 DANGEROUS

      Blood becomes very viscous

      Increase risk of thromboembolism--- leading to STROKE

• uClubbing

• uTet Spell

Hypoxemia: nursing consideration

• TET spells

  • STOP

  • SQUAT

  • Changes venous pressures and shunts blood back to major organs

      Breathes easier 

      Squat- older children

      Knee to chest- infants

• Polycythemia

  • Hydration

• Support and family

  • Bundle care

Hypoxia

• decreased oxygen levels in the tissue

Cardiovascular dysfunction - congenital heart disease - anomalies

• Newer Classification of CHD

  Hemodynamic characteristics

  Increased pulmonary blood flow

  Decreased pulmonary blood flow

  Obstruction of blood flow out of the heart

  Mixed blood flow

  TGV- Transposition of Great Vessels

  TAPVR- Total Anomalous pulmonary venous return

  HLHS- Hypoplastic Left heart syndrome

Increased pulmonary blood flow defects

• most common of defects

• uAbnormal connection between two sides of heart

  uSeptum

  uGreat Vessels

  uIncreased blood volume on the right side of heart

  uIncreased pulmonary blood flow

  uDecreased systemic blood flow

• L to R shunting of pulmonary blood flow

  Due to increase pulmonary blood flow, pulmonary resistance increases

  Overtime if the defect continues with the increase Pulm resistance, the body will compensate and these kids will eventually have pulmonary HTN

  HIGH BMR

  SUSCEPTIBLE TO RESPIRATORY INFECTIONS

Clinical presentation

• ØElevated BMR

  ØCongestive Heart Failure

  uTachycardia

  uTachypnea

  uHypotension

  uIncrease cap refill

  uEdema

  uSusceptible to Respiratory Infections

• Atrial septal defect

• Ventricular septal defect

• Patent ductus arteriosus

Atrial septal defect

• low mortality

• Few complications

• Treatments

  • Cardiac cath and coil

  • Open heart with patch

• Left to Right shunt- PRESSURES

    Increase in oxygenated blood to right atrium

  Kids with small ASD may be asymptomatic

  Symptoms can progress over time

  IF found and NOT corrected these kids can have:

    Atrial dysrhythmias- due to atrial enlargement and stretching of conduction fibers

    PULM HTN- due to prolonged increase in pulmonary resistance

    Emboli- from chronic increased, stagnate blood flow

  Treatment

  Small- Cardiac Cath & coil

  Large- Open Heart with patch

Ventricular septal defect

• most common

• MOST COMMON ANOMALY

  Frequently associated with other defects- Down’s Syndrome

  May close on its own

  Characteristic murmur

  Treatment

  Small- Cardiac Cath with purse string sutures

  Large- Open Heart with patch

Patent ductus arteriosus

• Most common in preemies

  With 1st breath, there is a drop in PROSTAGLANDIN along with the introduction of oxygen

  IF other anomalies exist- this will NOT close

  Having ductus- enables increased oxygenated blood to lungs

    Thus increase in pulmonary blood flow----- Sx’s of CHF

  Treatment

  Small- close on own

  Large- Indocin or Ibuprofen

    cath clip and coil

Obstructive defects

• blood exiting the heart meets a narrowing or stenosis

• Increase the pressure load on ventricle

• Decreased output

• Low mortality

• Clinical presentation

  • ØDepends on the location of the obstruction

    uLeft side obstruction:

    uCHF symptoms

    uRight side obstruction:

    uCyanotic symptoms

  • Coarctation of the aorta

  • Aortic stenosis

  • Pulmonic stenosis

Coactation of the aorta (COA)

• Left side obstruction

  Localized narrowing near the insertion of the ductus arteriosus

    Results in increase pressure proximal to the defect (head and UE’s)

    Also results in decrease pressure distal to the defects (LE’s) 

  Clinical Presentation

    In addition to CHF presentation due to a back up of blood from the lungs:

    Increase BP and bounding pulses in UE

    Weak/absent femoral pulses and a Low BP in LE’s

  Treatments:

    Balloon Angioplasty for older infants and children

    Adolescents may only need Aortic Stent

    6 months and younger- surgery

    Resection and Anastomosis of aorta

    Outside of heart- OPEN HEART IS NOT NEEDED

Aortic stenosis

• Left sided obstruction

  Aortic Valve- highest pressure and narrowing stricture that causes resistance to left ventricle  - hard for left ventricle to pump out through aorta 

  Clinical Presentation

    Decrease in Cardiac Output

    Left Ventricular hypertrophy

    In addition to CHF presentation due to a back up of blood from the lungs

    Interferes with the perfusion to the heart- Coronary artery perfusion

    Increase risk for MI

  Infants:

    Weak pulses

    Hypotension

    Poor Feeder

    Tachycardia

  Older children:

    Dizzy

    Exercise intolerance

    Chest pain

  Treatments:

    Cardiac cath for Balloon Angioplasty to dilate valve. MAY NEED REPEATf

    Ross Procedure

    Valve replacement

    Konno Procedure

    Patch to enlarge left ventricular outflow and (enlarging the aortic root by an anterior approach)

    Modified Ross- Konno Procedure

    Amends to ventricular septal incision. The left ventricular outflow tract is widened so that it spares any possible of conduction issues (near the left main coronary)

Pulmonary stenosis

• Right side obstruction:

  Narrowing at the entrance of the Pulmonary Artery

  Resistance of blood to flow out results in:

    R ventricular hypertrophy

    Decreased pulmonary blood flow. --- this can cause cyanosis!

  Pulmonary atresia is the most severe/extreme form

    Total fusion of the valve- thus NO BLOOD FLOW at all!! – definite cyanosis

    The resistance to blood flow causes:

    Right ventricular hypertrophy

    Right atrial pressures increase

    This can cause the foramen ovale to re-open

    This shunts blood from the left atrium (right to Left shunt)- keeping some volume in left side of heart to go to aorta and re-circulate into pulmonary artery- lungs – pulmonary viens- left atrium a- left ventricle- body

    Systemic cyanosis

  Clinical Presentation

  Depending on severity of the stenosis

    Mild- may be asymptomatic or mild cyanosis 

    Moderate- Heart failure

    Severe- Cyanosis

   

  Treatments: 

    May want to keep PDA open so that oxygenated blood gets to system

    Hopefully seen in utero

    Give prostaglandin----INDOCIN

    This provides good avenue of blood flow from the aorta to the pulmonary artery and lungs

    Balloon Angioplasty

    Brock Procedure

    Valve replacement

Decreased pulmonary blood flow defects

• uObstruction of pulmonary blood flow and defect between the right and left sides of heart.

  uLack of blood flow in the lungs

• Clincial manifestation

  • Cyanosis

      Not enough blood to the lungs- no oxygen to the system

    Hypercyanotic spells

      Babies get agitated and pass out due to lack of circulatorry oxygen

    Poor weight gain

      Suck, Swallow and breath

    Polycythemia

      Bone marrow responds to the lack of oxygen – Chronic Hypoxia

      presents as the need to make more RBCs for more Hgb to carry oxygen

      erythrocytosis is the production of more RBC

      This increases the hematocrit

      Normal level- 32-42%

      > 50% is serious

      55-60% or greater- VERY VISCOUS and thick---HIGH RISK for Thromboembolism and Stroke

• Tetralogy of fallout

• Tricuspid atresia

Tetralogy of fallot

• Hemodynamics of the defect can vary, depending on the severity of the Pulmonic Stenosis and size of VSD.

  Because the VSD is usually large:

    Heart pressures can equal in both ventricles

    Shunt direction depends on pulmonary and systemic vascular resistance

    High pulmonary resistance- R to L shunt

    High systemic resistance- L to R shunt

  Pulmonary Stenosis

    Decrease blood flow to lungs and O2 blood that returns to L side of heart

  Overriding Aorta

    Aorta is directly over the VSD rather than the Left Ventricle

    Blood from both ventricles go back into the system

  Clinical Presentation:

    Hypoxemia  Lethargy

    Cyanosis  Decreased activity level

   ****Avoid crying***- Tet Spell   STOP

  Treatments: 

    Surgery to correct all defects within the first year of life- Repair of VSD, Stenosis and Aorta

Tricuspid atresia

• Failure of the valve to develop

  NO COMMUNICATION between the right atrium and right ventricle

  MUST have 

    ASD ---- shunts from right to left into left atrium (Unoxygenated blood to left side of heart- results in decreased oxygen to body

    –or-

    Formane Ovale – same as ASD 

    –or-

    VSD----- Shunts from left to right (increase pressures) out to the lungs for some oxygenated bood

  A complete mixing of unoxygenated and oxygenated blood on the left side of the heart

  Often associated with pulmonic stenosis or other anomalies

  Clinical Presentation

  As with decreased pulmonary blood flow slide

    Increased HR  Cyanosis  Poor weight gain

    Dyspnea  Tet spells  Polycythemia

   

  Treatments: 

    May want to keep PDA open so that oxygenated blood gets to system

    Hopefully seen in utero

    Give prostaglandin----INDOCIN

    This provides good avenue of blood flow from the aorta to the pulmonary artery and lungs

    Palliative Shunt- increases blood flow to lungs

    Fontan Procedure   It involves diverting the venous blood from the inferior vena cava and superior vena cava to the pulmonary arteries. 

Mixed blood flow defect

• uOverlapping with decreased pulmonary blood flow defects

  uVery complex

  uSurvival postnatally depends on the mixing of blood from pulmonic and systemic circulations of the heart

• Clinical manifestation

  • ØPulmonary congestion

    ØDecreased cardiac output

    ØCHF symptoms

    ØVolume overload

    ØRelative desaturation of systemic circulation is typical

    ØMay or may not be hypoxemia

  • Transposition or the great vessels

  • Total anomalous pulmonary venous connection (TAPVC)

  • Hypoplasstic left heart syndrome

Transposition of the Great Vessels

• Pulmonary artery leaves the left ventricle

  Aorta exits off the right ventricle

  NO COMMUNICATION BETWEEK PULMONIC CIRCULATION AND SYSTEMIC CIRCULATION

    Parallel circulations

  Prenatal care is CRITICAL

  ASD/VSD (Septal Defect) or PDA MUST be present to permit some mix of oxygenated/unoxygenated blood

    MOST common is patent foramen ovale (ASD)

  Clinical Manifestations

    CHF

    Cyanosis @ birth and decrease function at birth

    Depending on size of FO or VSD- may be less cyanotic--- Sxs of CHF

    Decreased apgars- depressed- dependent on septal defect

  Treatments: 

    May want to keep PDA open so that oxygenated blood gets to system UNTIL SURGERY

    Hopefully seen in utero

    Give prostaglandin----INDOCIN

    This provides good avenue of blood flow from the aorta to the pulmonary artery and lungs

    Arterial Switch of the great arteries 

   

Total Anomalous Pulmonary Venous Connection

• “Easter Basket”

  Abnormal connection of the pulmonary vein connecting directly to the right atrium.

    Oxygenated blood from the pulmonary vein goes directly back into the right atrium (into the superior vena cava)

  Then Right to left shunt (pressure is higher on right side of heart due to lack of volume into the left atrium)

    Right side of heart hypertrophy occurs from overflow

    Left atrium remains small due to decreased blood volume

  Patent foramen ovale or ASD (septal defect)– allows systemic blood to shunt from high pressure (r atrium) to lower pressure (L atrium/ventricle)

  SURGICAL EMERGENCY

  Clinical Presentation

  As with decreased pulmonary blood flow slide

   

  Treatments: 

    May want to keep PDA open so that oxygenated blood gets to system

    Hopefully seen in utero

    Give prostaglandin----INDOCIN

    This provides good avenue of blood flow from the aorta to the pulmonary artery and lungs

    Palliative Shunt- increases blood flow to lungs

    Fontan Procedure   It involves diverting the venous blood from the inferior vena cava and superior vena cava to the pulmonary arteries. 

   

Hypoplastic Left Heart Syndrome (HLHS)

• Left side of the heart (ventricle) is underdeveloped

    Ventricle is small with enlarged wall

    Aortic atresia- valve closed due to decreased blood flow

  Blood mostly flows from the Left atrium across ASD/Foramen ovale in the right atrium----right ventricle----ultimately pulmonary artery

  Descending aorta receives oxygenated blood from the pulmonary artery (pressure is higher in PA)– then out the remaining portion of aorta to system.

    IF PDA CLOSES- Rapid deterioration- even death if not treated

  These patients have also a relative desaturation depending on the severity

  Clinical Presentation

    Mild Cyanosis 

    Potential Heart Failure

    Decreased cardiac output

    Cardiovascular Collapse 

  WITHOUT Intervention: Children will not survive

    Lactic acidosis  Gut ischemia  Cyanosis

    No urinary output  No CNS perfusion (Unconscious)

   

   

  Treatments: 

    May want to keep PDA open so that oxygenated blood gets to system

    Hopefully seen in utero

    Give prostaglandin---

    This provides good avenue of blood flow from the aorta to the pulmonary artery and lungs

    Palliative Shunt- increases blood flow to lungs

    Fontan Procedure   It involves diverting the venous blood from the inferior vena cava and superior vena cava to the pulmonary arteries. 

   

CARDIOVASCULAR DYSFUNCTION - POST-PROCEDURAL TREATMENT & CARE

• Interventional cardiac catherization

  • Balloon atrioseptostomy

      make a hole or enlarge a hole

    Balloon dilation

      dilates an area

    Coil occlusion

      occludes pda or maybe a vsd

  • Transcatheter device closure

      closes septal defect and/or septal occluded

    Stent placement

      to connect and open stenosis

    Radio-frequency ablation

      zap affected areas- dysrrhythmias

• Cardiac cathetierization nursing care

  • Pre-procedural

    • Preparation/explaation

    • Sedation

    • NPO

  • Post procedure

    • uCardiac & Pulse Ox monitoring

      uVital Signs

      uNeurovascular checks

      uDressing

      uI & O

      uBGL

• Surgical interventions

  • Cardiac Shunts

      One way to temporarily provide blood flow with defects until surgery

    Prepare Child & Family----- take to PICU

    Give accurate portrayal of procedure

    Prepare regarding ECMO

    Prepare family and patient regarding complications

      CHF- cardiac changes can occur

      Cyanosis can occur

      AIRWAY ALWAYS #1!!!

      May be on ionotropic drugs (increase contractility of the heart)

      Always monitor I & O & electrolytes

  • Open/closed heart

  • Staged procedures

  • Cardiac shunt

Care of the family and child with CHD

• üHelp family adjust to the disorder

  üEducate family

  üHelp family cope with effects of the disorder

  üPrepare child and family for surgery

  üAdapt the child to the best of their ability. Normalcy to life

Postoperative care

• Hemodynamic Monitoring

  • uIntracardiac monitoring

    uVital Signs (intraarterial BP)

    uArterial/Venous Pressures

    uRespiratory needs

    uComfort and pain management

    uRest

    uProgression of activity

• Fluid Status

  • uIntake

    uAll IV fluids

    uAll flushes, other intake

    uOutput

    uFrom all tubes/drains/Lab work

    uUrine output <1 ml/kg/hr = possible renal failure

    uConcern r/t decreased cardiac output

• From all sources

  • Chest tube, urine, NG, surgical drains; also include blood drawn for lab work

• Monitor chest tube drainage q hour for COLOR

  Immediate postop may be bright red, but changing to serous

  Monitor chest tube drainage for quantity

  Notify surgeon if chest tube drainage >3 ml/kg/hr ×3 consecutive hours OR 5-10 ml/kg in any 1 hour (possible hemorrhage)

  Be alert for cardiac tamponade (rapid onset; life threatening)

    fluid in pericardium—puts pressure on heart

    If fluid builds up- can rupture heart

    Symptoms

    Narrow pulse pressure

    Increased HR

    Dyspnea

• Complications

  • uCHF

    uDysrhythmias

    uDecreased Cardiac Output Syndrome

    uDecreased peripheral perfusion

    uPulmonary changes

    uNeurologic changes

• Post Operative Care Postpericardiotomy Syndrome

  • uOccurs in immediate postoperative period

    uAlso can occur later (postoperative day 7-21)

    uEtiology - Unknown

    uTheories of etiology

    uViral infection; auto immune response; reaction to blood in pericardium

  • uSymptoms

    uFever – High- 38.0C-40.0C

    uPericardial friction rub

    uPericardial and pleural effusion

    uMay require pericardiocentesis or pleurocentesis

CARDIOVASCULAR DYSFUNCTION - ACQUIRED HEART DISEASE (INFECTIOUS AND INFLAMMATORY CARDIAC DISORDERS)

• Happens at birth

  Can occur in normal heart or in addition to congenital defects

  Can include:

    Autoimmune response infections

    Environmental factors

    Familial tendencies

Endocarditis

• ØTypes

  ØBE-bacterial endocarditis

  ØIE-infective endocarditis

  ØSBE-subacute bacterial endocarditis

• ØInfection of valves and inner lining of heart

• ØStrep most common

• IE - PATHOPHYSIOLOGY

  • uAltered blood flow and turbulence inside the heart

    uDamage to valvular endothelium

    uRough endothelium increases fibrin and deposition of platelets

  • uMicroorganisms grow and form vegetation on the endocardium

    uLesion may invade adjacent tissues (valves and myocardium)

    uMay break off and embolize

• IE- CLINICA MANIFESTATION

  • uInsidious, low- grade fever

    uMalaise

    uAnorexia

    uHF Symptoms

    uFeeling intolerance

    uRespiratory Distress

    uTachycardia

  • uMurmur

    uNew

    uChange in previous murmur

    uSplenomegaly

    uOsler nodes

    uRed, painful nodes on pads of fingers

    uJaneway spots

    uPainless hemorrhagic spots on palms and soles

  • OLSER NODES (EXPLAIN)

  • JANEWAY SPOTS (EXPLAIN)

• IE- THERAPEUTIC MANAGEMENT

  • uHigh dose IV antibiotics 2-8 weeks

    uEvaluate effectiveness of antibiotics with repeat blood culturesA

  • uIf no response or minimal response to antibiotics

    uSurgical Approach

    uRemove vegetation

    uValve replacement with prosthetic waves

  • Typically PCN

    Fungal- Amphotericin

    Leads to valve damage

    Parent teaching on dental hygiene is imperative

• IE- THERAPEUTIC PREVENTION

  • uProphylactic antibiotics ONLY for high risk CHD patients

    uDental work

    uInvasive respiratory

    uProcedures on soft tissue infections

  • uNo prophylaxis needed for GI/GU procedures

    uAdminister 1 hour prior to procedure

Rheumatic Fever Rheumatic Heart Disease

• Rheumatic Fever

  ØInflammatory disease occurs after Group A B-hemolytic streptococcal pharyngitis

  ØInfrequently seen in U.S.; big problem in Third World

  ØSelf-limiting

  ØAffects joints, skin, brain, serous surfaces, and heart

• Rheumatic heart disease

  ØMost common complication of RF

  ØDamage to valves as result of RF

• RF - CLINCIAL MANIFESTATION

  • MAJOR

    • uCarditis

      uPolyarthritis

      uErythema marginatum

      uChorea

      uSubcutaneous nodes

      Aschoff bodies

  • Carditis

      Involved endocardium, pericardium and myocardium– most common is mitral valve

    Arthritis

      Reversible and migrates, especially in large joints (knewws, elbows, hips, shoulders, wrists)

    Erythema marginatum

      Rash, usually on trunk and proximal portion of extremities. Red macule with clear center and wavy, well-demarcated border 

      Upper arms

      Upper legs

    Chorea

      Involuntary movements

    Subcutaneous nodules

      Small nontender nodules appear over bony prominences: hands, feet, elbows, scalp, scapulae vertebrae

      Persists indefinitely after onset of the disease and resolve with no resulting damage

    Aschoff bodies

      Inflammed bullous lesions seen in microscope

  • MINOR

    • uArthralgia

      Fever

  • Inflammatory marker increases:

    •Sedimentation rate

    •C-reactive protein

• RF- PREVENTION

  • uTreatment of causative factor (Tonsillitis/Pharyngitis)

    uPenicillin G- IM x 1

    uPenicillin V- Oral x 10 days

    uSulfa – Oral x 10 days

    uErythromycin (if allergic to PCN)- Oral x 10 days

    uTreatment of recurrence is the same

  • Complete ALL po therapy---if non compliant--IM

    Educate for strep throat

    Need to prevent glomerular nephritis

    Labs to monitor:

      CRP

      ESR

Kawasaki Disease

• 6-8 weeks

  • uAcute systemic vasculitis

    uUnknown cause

    uSelf-limited, but without treatment 20% develop cardiac sequelae

    u3 stages:

    uAcute

    uSubacute

    uConvalescent

  • Acute systemic vasculitis -  inflammation small vessels

      Most distinctive

      Younger children prove to be at a greater risk for cardiac involvment

    Unknown cause

      Lead cause of acquired heart disease in North America

    Self-limited, but without treatment 20% develop cardiac sequelae

    3 stages:

    Acute

      High fever

      Not responsive to meds (antibiotics and antipyretics)

      1st week symptoms are evident

      Red conjuctivae

      Red pharynx and oral mucosa

    Subacute

      Fever is over

      Other symptoms prevail– hopefully in hospital

    Convalescent

      Disease is gone, but inflammatory markers remain abnormal

• Kawasaki- Clinical Manifestations

  • 1st weeks, the signs are evident

    Most at risk in subacute phase

      Fever has gone but other symptoms- in hospital

    Can progress to coronary artery aneurysm

      Damaged vessels can continue to enlarge after fever is gone (typically 2nd week)

      Vessels can enlarge up to 4-6 weeks of onset of illness

      Thrombocytosis and Hypercoagulability can lead to aneurysm and disrupted blood flow

      This leads to coronary aneurysm and Mis.

    Monitor with serial echos

  • uProlonged fever

    uConjunctival inflammation

    uChanges in oral mucosa

    u“Strawberry tongue”

    uEdema

    uPalms & soles

  • uErythema

    uPerineum most common

    uPeeling of hands and feet

    uCervical lymphadenopathy

• Kawasaki - presentation

  • This child has returned for one of her frequent follow-up visits to assess her cardiac status after treatment for Kawasaki syndrome. Notice the lips that show the inflammation and cracking.

• Kawasaki - Treatment

  • IVIG

      Reduces duration of fever and decreases the incidence of coronary artery abnormalities

      Give within 1st 10 days of illness (better in 1st 7)

    ASA

      Helps with fever

      Anti coag properties

      Anti inflammatory

      Decrease incidence of aneurysms- if it does develop switch to coumadin

    CAUTION Reye Syndrome

Systemic hypertension

• BP SCREENING

• •Primary = no known cause

  •Secondary = identifiable cause

  •Pediatrics—HTN generally secondary to structural abnormality or underlying pathology

  •Renal disease

  •CV disease

  •Endocrine or neurologic disorders

HYPERLIPIDEMIA

• •Presymptomatic phase of atherosclerosis begins in childhood

  •Identify high risk children by lipid screening

  •Treatment=Dietary control:↓ cholesterol and fats

  •If not response to diet→RX

  •Colestipol (Colestid)

  •Cholestyramine (Questran)

• No real symptoms until 60% occluded