Heart Conduction System

Heart Conduction System Review

• The sinoatrial node (SA node) acts as the primary pacemaker of the heart
• The SA Node generates 60-100 impulses per minute under normal conditions
• The atrioventricular node (AV node) is situated in the right atrial wall near the tricuspid valve
• The AV node is responsible for coordinating incoming electrical impulses from the atria
• The AV node relays impulses to the ventricles after a slight delay
• The AV node generates 40-60 impulses per minute
• The Bundle of His consists of specialized conducting tissue
• The right bundle branch conducts impulses to the right ventricle
• The left bundle branch conducts impulses to the left ventricle
• The left bundle branch further divides into the left anterior and posterior bundle branches
• Purkinje fibers are the terminal point in the conduction system
• Purkinje fibers specialize in rapidly conducting impulses through the thick ventricular walls
• Purkinje fibers generate 30-40 impulses per minute

Congenital Heart Defects (CHD)

• Incidence of CHD is ~1% of births, this equates to around 40,000 births per year
• Ventricular Septal Defect (VSD) is the most common anomaly
• 25% of babies with CHD are in critical condition, and need surgery in year one
• 15% of CHD cases are linked with genetic conditions
• 28% of children with CHD have another recognised anomaly, like trisomy 21

Classification of CHD

• CHDs are classified as either Acyanotic or Cyanotic
• Acyanotic: involves increased pulmonary blood flow, or obstruction to blood flow from ventricles
• Acyanotic defects include atrial septal defect, ventricular septal defect, patent ductus arteriosus and any atrioventricular canal defect
• Aslo included in Acyanotic defects can be coarctation of the aorta, aortic stenosis and pulmonic stenosis
• Cyanotic: involves decreased or mixed blood flow
• Cyanotic defects include tetralogy of Fallot or tricuspid atresia
• Cyanotic defects include transposition of the great arteries, total anomalous pulmonary venous return, truncus arteriosus and hypoplastic left heart syndrome

Atrial Septal Defect (ASD)

• ASD involves an abnormal opening between atria, causing blood to flow from higher pressure in the left atrium (LA) to lower pressure in the right atrium (RA)
• ASD results in increased oxygenated blood entering the right side of the heart
• ASD leads to enlargement of the right atrium (RA) and right ventricle (RV)
• Cardiac failure is unusual in uncomplicated ASD
• ASD may be asymptomatic if the defect is small
• Symptomatic ASD can manifest as dyspnea, fatigue, and poor growth
• A soft systolic murmur in the pulmonic area (splitting S2) may be present
• An individual with ASD may develop Congestive Heart Failure (CHF)
• Diagnostic 2D echo reveals enlargement of the right side of the heart and increased pulmonary circulation
• Cardiac catheterization demonstrates separation of RA, identifying an increased O2 saturation in the RA
• ASD can be surgically repaired, using a Dacron patch closure
• Surgical repair of ASD involves open repair with cardio-pulmonary bypass during school age
• ASD may be closed non-surgically using devices during cardiac catheterization

Nursing Management for Atrial Septal Defect (ASD)

• Provide the parent with information and explain the purpose of diagnostic tests and necessary procedures
• Discuss nutrition guidelines, teach coping strategies, promote rest, and support child development pre-operatively
• Teach the parents signs of congestive heart failure and the signs of infection
• Prepare the parents and child for surgery by going to the intensive care unit with them
• Explain all equipment and sounds that they will find in the unit
• If the patient is an older child, prepare them for surgery, coughing and breath exercises, and movement restrictions
• Discuss the need for antibiotic prophylaxes, to protect from subacute bacterial endocarditis

Ventricular Septal Defect (ASD)

• VSD is a defect in the ventricular septum, typically resulting from an error in early fetal development
• VSD can occur in the muscle or membranous ventricular septum
• 20-25% of all CHDs are VSDs
• In VSD, pressure from the left ventricle (LV) flows to the right ventricle (RV)
• Pressure from systemic arterial circulations flows to pulmonary circulation
• Blood flows through the defect and into the pulmonary artery
• The RV becomes enlarged (hypertrophied), and the RA may distend over time
• VSD symptoms include tachypnea and dyspnea
• Additional VSD symptoms include poor growth and/or reduced fluid intake
• Palpable thrills may be present
• A systolic murmur is typically heard at the left lower sternal border
• An individual may develop CHF
• VSD is treated with furosemide, that removes excess fluid
• Digoxin for VSD, helps the heart pump more effectively
• Angiotensin-converting enzyme (ACE) inhibitors are used to relax blood vessels assisting the hearts pumping
• Surgical repair with bypass is a treatment option
• Pulmonary artery banding or patch repair can be done if the defect is not too large

Patent Ductus Arteriosus (PDA)

• The ductus arteriosus SHOULD close ~15 hours post-birth
• Some blood shunting may occur for up to 24 hours
• The ductus closes as arterial O2 concentration increases, after pulmonary function begins
• Prostaglandin E assists closure of the PDA
• PDA facilitates blood flow from left to right, increasing flow to the lungs
• Small PDA presents as asymptomatic
• Bounding peripheral pulses are a notable sign
• Widened pulse pressure (>25) occurs
• Loud, machine-like murmur at upper left sternal border (Left infraclavicular area) is usual
• A complication is CHF with tachypnea, dyspnea, and hoarse cry when PDA is large
• Definitive diagnosis is ECHO
• Indomethacin closes PDA's in premature babies
• Surgical ligation is done if meds fail
• Prophylactic antibiotics reduce risk of bacterial endocarditis
• Surgical repair is done between 1-2 years of age

Obstructive Defects

• Blood flow meets an area of narrowing (stenosis), resulting in obstruction of blood flow
• Ventricle and great artery pressure increases, before the obstruction; beyond the obstruction, the pressure decreases
• Location of narrowing occurs near the valve:
  • At the valve itself, that involves the location (Valvular)
  • Ventricular outflow tract (subvalvular)
  • In the aorta above the valve, supravalvular narrowing
• (+) pressure load on the ventricle decreases cardiac output
• Individual presents s/s of CHF
• Mild obstruction: asymptomatic, may be unnoticed
• Severe stenosis: hypoxemia (rare)

Coarctation of Aorta

• The aorta narrows near the ductus arteriosus
• Increased pressure develops proximal to the defect
• High blood pressure and bounding pulses in arms occurs with coarctation
• Weak or absent femoral pulses, cool lower extremities with low blood pressure also appear
• Signs of CHF can appear in infants
  • There may be rapid condition deterioration
• Dizziness, headache, fainting, and nosebleeds can appear with coarctation
• Risk of ruptured aorta, aortic aneurysm, or stroke is a possibility
• Treatment involves non-surgical balloon angioplasty, that is usually effective
• Surgical repair is done, requiring no bypass since the defect is outside the pericardium
• Post-surgical complication is hypertension
• Repair is usually done before age 2
• Risk of a recurring coarctation is possible

Aortic Stenosis

• Aortic valve narrowing is usually malformed in BI- rather than TRI-cuspid valve
• Resistance in the left ventricle increases, cardiac output decreases, and the left ventricle hypertrophies
• Pulmonary vascular congestion occurs
• Increased pulmonary vascular resistance and pulmonary hypertension also occur
• Significant hypertrophy causes decreased coronary artery perfusion and increased risk of MI
• Clinical manifestations involve decreased cardiac output.
• Faint pulses, hypotension, poor feeding and tachycardia may occur
• Heart murmur and exercise intolerance are also common along with chest pain and dizziness
• Treatment includes balloon angioplasty to dilate the aortic valve
• Some require a Konne procedure (valve replacement)
• Repeat procedures may be needed

Pulmonary Stenosis

• Pulmonary valve is stenosed
• Narrowing takes place at entrance to pulmonary artery
• Right ventricular hypertrophy and decreased pulmonary blood flow can occur
• Pulmonary atresia, an extreme form of PS, involves total fusion of the commisures with complete obstruction
• PS causes right ventricular hypertrophy, right ventricular failure, and increased right atrial pressure
• Foramen ovale may reopen
• Unoxygenated blood shunts to the left atrium, creating systemic cyanosis
• CHF may develop
• Individuals often have PDA
• Cardiomegaly can appear on CXR
• Treatment includes balloon angioplasty to dilate the stenotic valve
• Some may have surgical Breck procedure, including bypass to do valvotomy
• Catheterization may be possible

Defects of Decreased Pulmonary Blood Flow

• Obstruction of pulmonary blood flow appears, along with an anatomic defect (ASD/VSD) between the right and left sides of the heart
• Difficulty of blood exiting the right heart can occur via the pulmonary artery
• Desaturated blood that shunts from right to left enters systemic circulation
• Hypoxemia & cyanosis are expected

Tetralogy of Fallot

• This involves four heart defects
  • Ventricular Septal Defect
  • Pulmonary stenosis
  • Right ventricular hypertrophy
  • Overriding aorta
• Hemodynamics vary depending on the extent of pulmonic valve stenosis and size of VSD
• With a large VSD, pressures in right and left ventricles equalize
• Blood shifts in direction of least resistance, either pulmonary or systemic vessels
• Pulmonary Vascular Resistance (PVR) greater than systemic vascular resistance causes right-to-left shunting

Clinical Manifestations of Tetralogy of Fallot

• "TET SPELLS" or "blue spells" occur with acute episodes of cyanosis and hypoxia
• Anoxic spells often occur after feeding or crying, increasing the risk of emboli, LOC, sudden death, and seizures
• Repairs is indicated when Tet spells and hypercyanotic spells increase
• Stage 1 involves a Blalock or modified Blalock shunt moves blood to pulmonary arteries from the left or right subclavian artery
• Complete repair, usually in first year, involves repair of VSD, stenosed area resection, and R ventricular outflow patch

Tricuspid Atresia

• Tricuspid valve fails to develop
• No communication exists between the right atrium and the right ventricle
• Blood flows through an ASD or patent foramen ovale (FO) to the left side of the heart, travels via the VSD to the right ventricle, reaching the lungs
• Often associated with pulmonary stenosis (PS) and transposition of great arteries (TGA)
• Complete mixing of unoxygenated and oxygenated blood takes place in the left side of the heart
• Systemic desaturation and pulmonary obstruction leads to decreased pulmonary blood flow
• Patent FO (or ASD) is needed at birth to permit blood flow across septum into the left atrium
  • PDA allows blood flow to pulmonary artery for oxygenation
• Manifestations: cyanosis, tachycardia, dyspnea, hypoxemia, and clubbing
• Risk for bacterial endocarditis and brain abscess, stroke increases with tricuspid atresia
• Initial management depends on pulmonary blood flow being dependent on PDA
  • Continuous infusion of Prostaglandin E1 (PGE1) until surgery is indicated
  • Palliative: shunt (pulmonary-to-systemic artery anastomosis)
  • Pulmonary artery banding
  • Modified Fontan procedure

Mixed Defects

• Postnatal survival depends on mixing blood from pulmonary systemic circulation within cardiac chambers
• Blood is mixed from pulmonary and systemic circulations within the heart chambers, causing relative desaturation of blood in systemic blood flow
• Cardiac output decreases because of volume load on ventricle
• Signs of desaturation, cyanosis, and CHF vary depending on anatomy
• Degree of cyanosis might not be visible & signs of CHF can be present
  • Severe cyanosis in first day indicates transportation of great arteries, which will appear as Congestive Heart Failure later
  • Truncus arteriosus indicates sever Congestive Heart Failure and mild desaturation

Hypoplastic Left Heart Syndrome (HLHS)

• The left side of the heart is underdeveloped
• The left ventricle is small, the aorta is atretic
• Most blood flow is directed across patent foramen ovale (PFO) to the R atrium, R ventricle, then pulmonary
• Descending aorta receives blood from patent ductus arteriosus (PDA) to supply the systemic circulation
• PDA closure results in rapid deterioration and CHF
• HLHS treatment involves keeping the ductus open with Prostaglandin E infusion

Surgical Treatment for Hypoplastic Left Heart Syndrome

• Norwood procedure creates a new aorta using the main pulmonary artery
• Creation of a large ASD facilitates blood flow
• Bidirectional Glenn Shunt, 6-9 months of age, reduces volume load on the R ventricle
• The Modified Fontan procedure, similar to Tricuspid atresia repair, redirects blood flow
• Transplantation can be an option
• There is a high mortality rate (30%-50%)

Transposition of the Great Vessels

• Pulmonary artery leaves the L ventricle, and the aorta exits from the R ventricle
• No communication between the systemic and pulmonary circulations
• Must have PDA or septal defect for blood flow

Surgical Treatment for Transposition of the Great Vessels

• An arterial switch procedure involves resecting and reanastomosing great vessels
• Coronary arteries must be reimplanted
• Other procedures are possible depending on the defect

Total Anomalous Pulmonary Venous Connection (TAPVC)

• There is an anomalous (incorrect) connection existing with the location in which the veins drain
• Very rare, requires a venous connection to be connected to RA, or a tributary of the RA to survive
• Treatment:
  • Administer furosemides and thiazides, and Spironolactone
  • Administer fluid and sodium restriction
  • Decrease cardiac demands
• Decrease cardiac demands is done by:
  • Providing bed rest
  • Treat any infection
    • Keep body temperature stable
• Lower the effort of breathing by placing patient in semi-fowlers position
• Sedate irritable child
• Improve tissue and oxygen, and decrease oxygen consumption by providing:
  • Oxygen (O2) Vasodilators
  • Humidified Cool Oxygen Supply

Acquired Cardiovascular Disorders

• Congestive Heart Failure

Congestive Heart Failure

• The Inability of heart to pump blood adequately into systemic circulation at normal pressures to meet the body's metabolic needs
• Structural issues are a structural deformity in children (septal defects), this increases blood volume and leads to myocardial failure
• This can cause:
  • Cardiomyopathy
  • Dysrhythmia
  • Severe imbalance in electrolytes
• The causes of this can be from the demands on regular cardiac muscle (like with anemia or a case of sepsis)

Types of Congestive Heart Failure

• Right Sided Heart Failure
  • Right Ventricle can't pump blood into pulmonary artery, increasing systemic venous pressure, eventually leading to hepatosplenomegaly
• Left Sided Heart Failure
  • Left Ventricle can't pump blood into systemic circulation increases pressure in the left atrium
  • This goes into congestion, eventually edema, resulting in pulmonary hypertension

Signs and Symptoms of CHF

• Each side of the heart depends on the others adequate function
  • Failure of one chamber affects the opposite chamber which lead to cardiac damage, and thus, inadequate supply to the body
• Decreased CO leads to inadequate blood supply to the kidneys, causing sodium/ water retention and increased workload of the cardiovascular system

Congestive Heart Failure in Children

• Impaired myocardial function includes:
  • Fatigue
  • Tachycardia
  • Cool & pale Extermities
  • Restlessness
  • Declined urine output
• Pulmonary congestion means:
  • Exercise intolerance
  • Dyspnea & Orthopnea
  • Weezing
• Also systemic venous congestion and edema/distention
• Peripheral and periorbital edema
• Increased body weight

Congestive Heart Failure (CHF) Treatment

• Improve cardiac function with Digoxin to - Increase CO and reduce edema

• Reduce strain on the kidneys with drugs like ACE Inhibitors, to allow vasodilation

• Remove fluid build-up using diuretics or Bidirectional Glenn

• In extreme situations:

  • Hydrate to keep hemocrit/fluid levels normal
  • Respiratory therapy using antibiotics

Endocarditis (Bacterial Infective Endocarditis)

• Occurs either as BE/IE/SBE
• Resulting infection stems from valves in the endocardium, or in blood from sepsis in a child
• It happens in abnormal valves, surgeries, in-dwelling lines, valve and drug abuse

Types & causes of Endocarditis

• Gram negative strands that come from dental issues, UTI's, cardiac caths and surgeries
• This will lead to organisms leading to the endocardium to vegetate - causing fibrin, platelet and ultimately breaks and embolizes
• Leads to death depending on tissue reached

Diagnosing Endocarditis

• Blood cultures in the definitive tests, which are further elaborated by ECG and increased tests of blood, like ESR tests, anemia tests
• The 2D-echo then further evaluates the severity, focusing then on the valve functionality

Symptoms of Endocarditis

• Initial indications can be very broad, low grade fevers, achiness, weight loss and fatigue.
• Further signs of it:
  • Extracardiac emboli
  • Thinn black line under nails
  • Osler's Nodes are inflamed, usually on phalanges
  • Red lesions, or Panes around skin can indicate this
• Some indicate CHF from the new murmur/arrhythmia

How to Treat Endocarditis

• IV antibiotics as prescribed over a period of 4 weeks
• Give Amphoterican if found as fungal
• Ultimately: 2-8 weeks, if no change can indicate eventual damage and will require a prosthetic

Preventative Care for Endocarditis

• Prophylaxes/evaluate current needs and history from a medical professional about heart as a precaution in different events
• Medical assessment from a dentist would be best, to see if any issues could be from here

Rheumatic Fever (RF)

• RF is an inflammatory disease occurring post Group A Beta-hemolytic streptococcal infection
• RF is self-limiting, affecting the joints, skin, brain, serious surfaces, and heart
• Risk factors for RF -Age (5-15 year old) -Being female -Housing and socioeconomic status -Rainy season -Genetic predisposition
• Clinical manifestations -Acute febrile-like illness (2-3 weeks after streptococcal throat infection) and non-specific symptoms
• Non-specific symptoms are fever, joint point, loss of appetite & muscle ache

Specific Clinical Manifestations of Rheumatic Fever

• Joints presenting swelling, pain of joints like knee, ankle, joints being rapid
• Heart, presenting (PANCARDITIS) Palpitation, chest pain, shortness of breathe/swelling
• Skin and tissues with rashes, painless and easy to move
• Late CNS issues including issues with limb movements, and weakness

Jones Criteria (Modified)

• Having 2 major or having 1 major + 2 minor factors, with possible strep

• Major indicators:

  • Rapid and disportional Carditis - heart infection
  • Involving various layers (Myo, pericardia)
  • Polyarthritis with pain that can migrate in large sections (knees/elbows)

• Additional Factors:

  • Major indicators will include rash-like effects and small nods

Another set of criteria

-Major St. Virus dance

• St. Virus in relation to CNS factors
• Minor involves pain and fever

Rheumatic Fever treatments (Medical)

• Increase in test values, will require tests on strep
• High ASO amount for a higher possibility
• Test to ensure proper heart support by checking through ECG/CRP

Goals in Treatment

• Eradicating with use of antibiotics and prevent with vaccines
• Prevent heart damage
• Reduce current systems and prevent further issues

Preventative Action for Rheumatic Fever

Treatment of recurrent tonsillitis with Penicillin or Salfa

General Care, During

• Salicylates to help with inflammation in areas
• Stay in bed if pain and fever occurs, but not being restrictive
• Medical visits after should be done for 5 years on how progress goes

Nursing and Caring Considerations

• Maintain compliance, but make it a positive adherence
• Provide monthly injections to keep good support system to continue treatments
• Provide support and facilitate support system while in illness
• Help patient cope at home after, providing support for parents

Complication of Rheumatic Fever (Rheumatic Heart Disease (RHD)

• Is its most common complication
• With RHD the valves may get damaged over time leading to stenosis, which causes the disruption and issues

Kawasaki Disease

• Mucocutaneous LN syndrome -Acute systemic vasculitis that is self limiting
• Under the age of 5, peak in toddlers
• 20% will develop long life cardio related systems
• Etiology unknown

Identifying S/S

• Conjunctivitis
• Rash
• Arthritis
• Strawberry like tongue
• Peeling of extremities

Area Involvement, Complications

• Infection in the CVS, mainly arterioles, veinles and capillaries
• Death as a complication for cardiac thrombus
• Tests aren't that specific
• Key check for Irritability for around 2 weeks is a key

Kawasaki treatment approach

• Help children cope and family adjust/Educate
• Prepare them in order to go through surgeries

Postoperative Treatment/Care:

• Track signals and vital signs
• Monitor blood pressure
• Address any respiration issues
• Keep patients comfortable

Surgical Post Complications:

• CHF caused by fluid build up in the lungs either from fluid input or from the procedure
• Hypoxia from lung complications
• ECG pattern problems along with odd apical pulse

More Extreme Care and Complications

• Cardiac Tamponade caused from sac build around vessels; use fluid relief in the cavity
• Low Co due to the shock as well, use a high-low volume to balance to create a regulated amount of blood volume around body parts
• Areas of Collapse from pressure, will cause area to have no oxygen

Testing and Analyzing

Echocardiography - Use vibrations to analyze turbulence of the liquids

Angiography, look at vessels in the blood stream

X-RAY to evaluate:

• Size and blood distribution problems around the heart.

• Other Test: EKG AND ABG*
• EKG is used to determine proper distribution of electric activity, not so great for exact diagnosis, just high level
• ABG, for if the patient is crashing to understand if some parts are lacking oxygen or are in acidosis

Cardiac Catheterization

Use and diagnosis heart function or values, a high level invasive test with risk related to inflammation

• A thin tube with a tracker that is inserted to track the area and can track its location from an X-Ray view.

Complications

• Infections (Infectious Endocarditis)
• Bruising and Bleeding from insertion
• Circulation changes

Care: What to do

• History exam before procedure is most effective
• After Procedure
  • Keep monitoring vitals
  • Ensure extremtities are normal and alert
  • Immobilize extremity used