cardio vascular dysfunction - nursing lijan

Cardio Vascular Dysfunction

KEEP YOUR HEART HEALTHY

Objectives

At the end of this discussion, YOU will be able to:

• Review circulatory changes at birth

• Identify the classifications of Congenital Heart Diseases (CHD)

• Discuss the description and pathophysiology of each CHD

• Explain the therapeutic management and prognosis of each CHD

Introduction

11/3/2020 Suhaila Halasa RN, PhD, CIMI,CPT 4

Introduction


https://www.youtube.com/watch?v=rYVGjbzmAtg


https://www.youtube.com/watch?v=rYVGjbzmAtg

• During fetal life, blood carrying oxygen and nutritive material

from the placenta enters fetal system through the umbilical veins

• Oxygenated blood enters the heart by way of the inferior vena

cava

Circulatory changes at birth

• Because of the higher pressure of blood entering the right

atrium, it is directed posteriorly in a straight pathway across

the right atrium and through the foramen ovale to the left

atrium


• In this way the better –oxygenated blood enters the left atrium and

ventricle to be pumped through the aorta to head and upper extremities

• Blood from the head and upper extremities entering the right atrium

from superior vena cava is directed down ward through the tricuspid

valve into the right ventricle


• From here, it is pumped through the

pulmonary artery, where the major portion is

shunted to the descending aorta via the

ductus arteriosus

• Only small amount of blood flows to and

from non functioning fetal lung


• Before birth, the pulmonary vascular resistance created by the collapsed

fetal lung causes greater pressure in the right side of the heart and

pulmonary artery

• At the same time, the free flowing placental circulation and the ductus

arteriosus produce a low vascular resistance in the reminder of the fetal

vascular system


• With the cessation of placental blood flow from clamping of the umbilical cord and the expansion of lung at birth, the hemodynamics of fetal vascular system undergo pronounced and abrupt changes

• With the first breath, the lungs are expanded, the increased oxygen causes pulmonary vasodilation

• Pulmonary start to fall as systemic pressure, given the removal of the placenta start to rise


• Normally, the foramen oval closes as the pressure in the left atrium

exceeds the pressure in the right atrium

• Ductus arteriosus starts to close in the presence of increased oxygen

concentration in the blood and other factors


The Heart Valves

Suhaila Halasa RN, PhD, CIMI,CPT 16http://classroom.materials.ac.uk/caseHeart.php

• Normally the pressure on the right side of the heart is lower

than that on the left side, and the resistance in the pulmonary

circulation is less than that in the systemic circulation

Altered Hemodynamic

• Vessels entering in the champers have corresponding pressures

• Therefore, if an abnormal connection exist between the heart chambers

such as septal defect, blood will necessarily from an area of higher

pressure (left side) to one of lower pressure (right side)

Altered Hemodynamic

• Such a flow of blood is termed a left-to-right shunt

• Anomalies resulting in cyanosis may result from a change in pressure so

that the blood is shunted from the right to left side of the heart ( right-to

–left shunt) because of either increased pulmonary vascular resistance or

obstruction to blood flow through the pulmonic valve and artery

Altered Hemodynamic

• Cyanosis may also result from a defect that allows mixing of

oxygenated and deoxygenated blood within the heart

chambers or great arteries

Altered Hemodynamic

Please Wait ------

Please Wait ------YOU BROKE MY HEART-----

Circulatory Changes at Birth

https://www.google.jo/search?hl=en&tbm=isch&source=hp&biw=1366&bih=662&ei=eQwgWsOkMs3fwQLtlKDYCw&q=Circulatory+changes+at+birth+&oq=Circulatory+changes

Congenital Heart Defects

Causes:

• The exact etiology of CHD is unknown

• a complex interaction of genetic and environmental factors

Risk factors:

• Maternal factors (chronic illnesses such as diabetics)

• Alcohol consumption

Congenital Heart Defects

Risk factors:

• Exposure to environmental toxins

• Infections

• Family history

• Chromosomal abnormalities

• Syndromes

• Down syndrome (trisomy 21) and trisomy 13 and 18

More than 35 types of congenital heart defect (CHD) have been identified

• The Traditional classification is A cyanotic defects and cyanotic defects:

• Clinically, this system is challenging because children with A cyanotic defects may develop cyanosis

OR

• Children with cyanotic defects may appear pink

Classification of Congenital Heart Defects

• A more useful classification system is based on hemodynamic characteristic (blood flow patterns within the heart).

1.Increased pulmonary blood flow ( A cyanotic):

• Defects that allow blood flow from the higher pressure left side

of the heart to the lower pressure right side (left-to-right shunt)

result in increased pulmonary blood flow and cause CHF

Congenital Heart Disease CHD

1. Increased pulmonary blood flow ( A cyanotic):

Types:

• Atrial Septal defect (ASD)

• Ventricular septal defect (VSD)

• Patent ductus arteriosus (PDA)


A more useful classification system is based on hemodynamic characteristic (blood flow patterns within the heart).

2. Obstruction of blood flow from ventricles( A cyanotic):

• Coarctation of aorta (CoA)

• Aortic stenosis (AS)

• Pulmonic stenosis (PS)


3. Decrease blood flow ( cyanotic):

• Tetralogy of Fallot (ToF)

• Tricuspid atresia (TA)

4. Mixed blood flow ( cyanotic):

• Transposition of great arteries (TGA)

• Truncus arteriosus (TA)


https://www.youtube.com/watch?v=UNWxKDvBFik

• Abnormal opening between the atria allowing blood from the higher

pressure left atrium to flow into the lower pressure right atrium


1. Increased pulmonary blood flow ( A cyanotic):

https://www.youtube.com/watch?v=UNWxKDvBFik

Types:❑ ASD1 (Ostium primum): opening at the lower end of the septum; may be

associated with mitral valve abnormalities

❑ ASD2: (Ostium secundom): opening near center of the septum

❑ Sinus venous defect: opening near junction of superior vena cava and

right atrium; may be associated with partial anomalous pulmonary venous connection

Atrial Septal Defect (ASD)


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https://www.google.jo/search?hl=en&biw=1366&bih=662&tbm=isch&sa=1&ei=uSIgWuW2IZDZwALS_qPABA&q=atrial+septal+defect&oq=atrial+septal+defect&gs_l=

Pathophysiology:

Because left atrial pressure highly exceeds right atrial pressure, blood flows from the left to the right atrium causing an increased flow of oxygenated blood into the right side of the heart


Clinical manifestations:

• May be a symptomatic

• May develop congestive heart failure in

their 30s or 40s

• Systolic or diastolic murmur

Atrial septal defect (ASD)


• At risk of atrial dysrhythmia, pulmonary

obstructive disease and emboli formation later

due to chronically increased pulmonary blood flow

Atrial septal defect (ASD)

Surgical treatment:

• Surgical patch closure (pericardial Dacron patch) for moderate and large

defect

• A Dacron graft can be used as a stent to repair an artery, blood vessel, or

other hollow structure in the body


Surgical treatment:

• Open repair of cardiopulmonary bypass before school age

• The sinus venosus defect requires patch placement

• For ADS1: it might require mitral valve repair or replacement of the mitral valve


Therapeutic Management

Non surgical treatment:

• Transcatheter closure: ADS2 closure device during cardiac cauterization

• Child receive low dose aspirin for 6 months

• Prognosis: operative mortality is very low less that 1%

https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/acyanotic-heart-diseases/v/rn-ventricular-septal-defect


https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/acyanotic-heart-diseases/v/rn-ventricular-septal-defect

Abnormal opening between the right and left ventricles

Ventricular Septal Defect (VSD)

https://www.google.jo/search?hl=en&biw=1366&bih=662&tbm=isch&sa=1&ei=uSIgWuW2IZDZwALS_qPABA&q=atrial+septal+defect&oq=atrial+septal+defect&gs_l=psy-ab.12...0.0.0.11461.0.0.0.0.0.0.0.0..0.0....0...1c..64.psy-

ab..0.0.0....0.jAW5XpLpLVQ

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• Abnormal opening between the ventricles

• May be classified according to its location:

• Membranous (80%) or muscular

• May vary in size from a small pinhole to absence of septum which results in common ventricle


https://www.google.jo/search?hl=en&biw=1366&bih=662&tbm=isch&sa=1&ei=uSIgWuW2IZDZwALS_qPABA&q=atrial+septal+defect&oq=atrial+septal+defect&gs_

• VSD associated with other defects such as pulmonary stenosis

• 20-60% of VSD will close spontaneously in the

first year of life in children with moderate defect


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Pathophysiology:

Because the higher pressure within

the left ventricle and because the

systemic arterial circulation offer

more resistance than the pulmonary circulation,

blood flows through the defect into pulmonary artery


Pathophysiology

• The increased blood volume is pumped into the lung lead to

increase pulmonary vascular resistance

• Increase pressure in the right ventricle as a result of left –to-

right shunt and pulmonary resistance causes muscle

hypertrophy

Pathophysiology

• If the right ventricle is unable to accommodate the increased

workload, the right atrium may also enlarge as it attempts to

overcome the resistance offered by incomplete right

ventricular emptying


• CHF common

• Holosystolic Murmur heard best at the left sternal border

• Children at risk of bacterial endocarditis and pulmonary vascular diseases


Surgical repair:

• Palliative: pulmonary artery banding may be done in infant with multiple muscular defect

• Complete repair: (procedure of choice): small defect is repaired with suture


Surgical repair:

• Large defect require patch (knitted Dacron Patch sewn over opening) through cardiopulmonary bypass

• Postoperative complications include:

residual VSD

conduction disturbances


Transcatheter closure: device closure during cardiac catheterization for muscular defect

Prognosis: risk depends on the location of defect, the number of defects and presence of other defects

• Single muscular defect has low mortality Less than 2%

• Multiple muscular defect carry a higher risk


• https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/acyanotic-heart-diseases/v/patent-ductus-arteriosus

• https://www.youtube.com/watch?v=7DKaCqubuSg

Patent Ductus Arteriosus

https://www.khanacademy.org/science/health-and-medicine/circulatory-system-diseases/acyanotic-heart-diseases/v/patent-ductus-arteriosus

https://www.youtube.com/watch?v=7DKaCqubuSg

https://www.google.jo/search?hl=en&biw=1366&bih=662&tbm=isch&sa=1&ei=lyMgWrvlGMbdwAKMgKW4BQ&q=Patent+ductus+arteriosus&oq=Patent+ductus+arteriosus&gs_l=


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• Failure of fetal ductus arteriosus (artery connecting the aorta and

pulmonary artery) to close within the first week of life

• The continued patency of this vessels allows blood to flow from higher

pressure aorta to lower pressure pulmonary artery which cause left to

right shunt



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Pathophysiology

• At birth, the resistance in the pulmonary and systematic circulations is almost identical, so that resistance in pulmonary artery and aorta is equalized

• As systematic pressure comes to exceed the pulmonary pressure, blood begins to shunt from aorta across the duct of the pulmonary artery (left to right shunt)


Clinical Manifestations:

• May be asymptomatic or show signs of CHF

• There is a characteristics of machinery like murmur

• Widened pulse pressure and bounding pulse

• At risk of bacterial endocarditis and pulmonary vascular obstructive disease


Medical Management:

• Endomethacin ( prostaglandin inhibitor) to close PDA in preterm infants and some newborns

Surgical RX: ligation of the patent vessel via a left thoracotomy


Transcatheter treatment: coils to occlude the PDA during catheterization

Coil (loop) occlusion: is a procedure to close the opening between infant's aorta and pulmonary artery.

Prognosis: both surgical and non surgical procedures can done at low risk less than 1% mortality


• Obstructive defects are those in which blood existing the heart meets an

area of anatomic narrowing(stenosis)

• The pressure in the ventricle and great artery before the obstruction

increased and the pressure in the area beyond the obstruction is

decreased

Obstructive Defect

The location of narrowing usually near the valve as following:

• Valvular: at the site of valve itself

• Sub valvular: narrowing in the ventricle below the valve

• Supra valvular: narrowing in the great artery above the valve

Obstructive Defect

Coarctation of Aorta CoA


• Description:

- Localized narrowing near the insertion of the ductus arteriosus.

- Results in increased pressure proximal to the defect (head and upper

extremities) and decreased pressure distal to the obstruction( body and

lower extremities).


Pathophysiology:

• The effect of a narrowing within the aorta is increased pressure

proximal to the defect (upper extremities) and decreased pressure

distal to it (lower extremities).



- May have high blood pressure and bounding pulse in the arms

- Weak or absent femoral pulse and cool lower extremities with lower blood pressure.

- There are signs of CHF in infants.

- In infants with critical Coarctation the hemodynamics condition may deteriorate rapidly with sever acidosis and hypotension.



- Mechanical ventilation and is often necessary before surgery.

- Older children may experience dizziness, headaches, fainting, and epistaxis resulting from hypertension.

- At risk for hypertension, ruptured aorta, aortic aneurysm (enlargement or dilation of the aorta to greater than 1.5 times normal size), and stroke.


Surgical treatment:

The treatment of choice for:

- Infants less than 6 months of age

- Children with long-segment stenosis or complex anatomy


• Surgical treatment: Repair by:

- Either resection of the coarcted portion with an end-to end

anastomosis of the aorta

OR

- Enlargement of the constricted section using a graft of prosthetic

material or a portion of the left subclavian artery.


• Surgical treatment:

- Elective surgery for CoA is advised within the first 2 years of life (to

prevent hypertension at rest and exercise-provoked systemic hypertension

after repair

- There is a 5%-10% risk of recurrent narrowing in children who underwent

surgical repair as infants


• Transcatheter treatment:

- Angioplasty: (any procedure to widen vessels narrowed by stenosis or

occlusions)

- A primary intervention for CoA is being performed in some centers.


Prognosis:

- Low rates of morbidity and mortality

- Major long-term complications:

- Recoarctation

- Aortic aneurysm (weakening of the wall)

- Systemic hypertension


Types of Heart Valves

11/3/2020 Suhaila Halasa RN, PhD, CIMI,CPT 76https://www.heartandstroke.ca/heart/conditions/valvular-heart-disease

Aortic Stenosis


Description:

- Narrowing or stricture of the aortic valve,

- Causing resistance to blood flow in the left ventricle, decreased cardiac

output, left ventricular hypertrophy, and pulmonary vascular congestion.

Aortic Stenosis (AS)

Description:

- The prominent anatomic consequence of AS is the hypertrophy of the left

ventricular wall, which eventually will lead to increased end-diastolic

pressure, resulting in pulmonary venous and pulmonary arterial

hypertension.


Types of AS

http://www.pted.org/?id=aorticstenosis611/3/2020 Suhaila Halasa RN, PhD, CIMI,CPT 80

Types of AS:

➢Valvular Aortic stenosis: anomaly of the valves result in a bicuspid

rather than tricuspid valve (the most common type)

➢Subvalvular stenosis: is a structure caused by fibrous ring below a

normal valve (obstruction in the ascending aorta)


Types of AS:➢Supravalvular stenosis: occurs infrequently an obstruction in the left

ventricular outflow

Valvular AS is a serious defect:• Obstruction tends to be progressive

• Sudden episodes of myocardial ischemia or low cardiac output (leads to death)

• Surgical repair rarely results in a normal valve



• Newborn with critical AS demonstrate signs of decreased cardiac output with faint pulses, hypotension, tachycardia, and poor feeding.

• Children show signs of exercise intolerance, chest pain, and dizziness when standing for a long period.

• A systolic ejection murmur may or may not be present.

• Children are at risk for bacterial endocarditis coronary insufficiency, and ventricular dysfunction.


• Valvular Aortic Stenosis:


- Balloon dilation in the catheterization laboratory is the first-line procedure.

- Aortic valvotomy is performed under inflow occlusion.


❑Prognosis:

- Aortic valve (palliative procedure) replacement offers a good treatment option

and may lead to normalization of left ventricular size and function.

- Results of aortic valvotomy (cutting through a stenosed cardiac valve to relieve

the obstruction)


❑Prognosis:

- Aortic valvotomy remains a palliative procedure, and

approximately 25% of children require additional surgery within

10 years for recurrent stenosis.


• Nonsurgical treatment:

- The narrowed valve is dilated using balloon angioplasty in the catheterization laboratory. this procedure is usually the first intervention

- Complication include aortic insufficiency or Valvular regurgitation, tearing of the valve leaflets, and loss of pulse in the catheterized limb.


• Subvalvular aortic stenosis:

(obstruction in the left ventricular outflow)

- Surgical treatment:

- if the obstruction results from narrowing of the left ventricular outflow tract and a small aortic valve annulus, a patch may be required to enlarge the entire left ventricular outflow tract and annulus and replace the aortic valve; this is known as the Konno procedure.




- Prognosis:

- mortality is less than 5%, about 20% patients develop recurrent subaortic stenosis and require additional surgery.




- Konno procedure:

- It involves the replacement of the aortic valve and the widening of the ventricular septum in the region of the valve with a patch

- Prognosis: mortality is less than 5%, about 20% patients develop recurrent subaortic stenosis and require additional surgery.


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Pulmonic Stenosis (PS)

• Description:

- Narrowing at the entrance to the pulmonary artery.

- Resistance to blood flow causes right ventricular hypertrophy and decreased

pulmonary blood flow.


• Description:

• Pulmonary atresia is the extreme form of Pulmonic stenosis (PS) in that

there is total fusion of the commissures and no blood flow to the lungs

• The right ventricle may be hypoplastic.


• Pathophysiology:- Resistance to blood flow causes right ventricular hypertrophy

- If right ventricular failure develops, then ----

- Right atrial pressure increases --- may result in reopening of the foramen

oval

- Shunting of deoxygenated blood into the left atrium – systemic cyanosis


• Pathophysiology:

• If PS is sever:

- HF occurs

- associated defect (patent ductus arteriosus) to

compensates for obstruction by shunting blood from aorta

to the pulmonary artery and into the lung


• Clinical manifestations:

- May be asymptomatic

- Some have mild cyanosis HF

- Progressive narrowing causes increased symptoms

- Newborns with sever narrowing will be cyanotic

- Aloud systolic ejection murmur at the upper left sternal border may be present.



- In sever ill Children, the murmur may be much softer due to decreased cardiac output and shunting of blood.

- Cardiomegaly is evident on chest radiographic films

- Children at risk for infective endocarditis



• Need for surgical treatment is rare with widespread use of balloon angioplasty techniques.

- Pulmonary valvotomy with cardiopulmonary bypass is necessary


• Transcatheter treatment:

- Balloon angioplasty in the cardiac catheterization laboratory to dilate the valve

- It is treatment of choice for discrete PS in most centers and can be done safely in neonates


• Prognosis:

- Risk is low for both surgical and nonsurgical procedures.

- Mortality rate is low, slightly higher in neonates

- Both balloon dilation and surgical valvotomy leave the pulmonic valve

incompetent because they involve opening the fused valve leaflets.

- Long term problem with restenosis or valve incompetence may occur.

Tetralogy of Fallot TOF

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11/3/2020 Suhaila Halasa RN, PhD, CIMI,CPT 102https://www.google.jo/search?hl=en&biw=1366&bih=662&tbm=isch&sa=1&ei=lyMgWrvlGMbdwAKMgKW4BQ&q=Patent+ductus+arteriosus&oq=Patent+ductus+arteriosus&gs_l=psy-ab.12..0l2j0i67k1j0l7.406300.411234.0.412512.33.11.0.0.0.0.193.758.0j5.7.0....0...1c.1j2.64.psy-ab..29.2.322.0..0i24k1.120.3a1yZeczj94

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Tetralogy of Fallot TOF• Description:

The classic form includes four defects:

1. Ventricular septal defect VSD

2. Pulmonic Stenosis PS

3. Overriding aorta

4. Right ventricular hypertrophy



- Some infants may be acutely cyanotic at birth.

- Others have mild cyanosis that progresses over the first year of life as the PS worsens.

- There is a characteristic systolic murmur that is often moderate in intensity.



- Blue spells: acute episodes of cyanosis, dyspnea,

restlessness, decreased arterial PO2, decrease of

already compromised pulmonary blood flow, and

hypoxia

https://www.google.jo/search?hl=en&biw=1366&bih=662&tbm=isch&sa=

Tetralogy of Fallot (TOF)


- Infants may be acutely cyanotic at birth.

- Others have mild cyanosis that progresses over the first year of life

- Moderate systolic murmur

- Anoxic spells occur when the infant’s oxygen requirements exceed the blood supply,

usually during crying or after feeding.

Tetralogy of Fallot (TOF)

Children are at risk for:

- emboli

- seizure

- loss of consciousness

- sudden death following an anoxic spell.



- Complete repair: elective repair is usually performed in the first year of life. when increasing cyanosis and the development of hypercyanotic spells.

- Complete repair involves closure of the VSD and resection of the stenosis, with placement of a pericardial patch to enlarge the right ventricular outflow tract.


• Prognosis:

- Mortality rate for total correction is less than 3%

- Complications:

- Chronic regurgitation with right ventricular enlargement

- Aortic root dilation and oartic valve insufficiency

- Arrhymias

- Sudden cardiac death

• Many complex cardiac anomalies are classified together in the mixed

categories because survival in the post natal depend on mixing of blood

from the pulmonary and systemic circulations within the heart champers

• Fully saturated systemic blood flow mixes with desaturated pulmonary

blood flow

Mixed Defects

• Pulmonary congestion occurs because the differences pulmonary artery pressure and aortic pressure favor pulmonary blood flow

• Cardiac output decreases because of a volume load in the ventricle

• Children have variable picture that combines some degree of desaturation and signs of CHF

Mixed Defects

• Transposition of great vessels cause sever cyanosis in the first days of life and later cause CHF

• Truncus arteriosus causes sever CHF in the first weeks of life and mild desaturation

Mixed Defects

• Description:

• Great vessels are switched that the aorta arises from the right ventricle and the main pulmonary artery arises from the left ventricle.

• It causes complete separation from the two circulation.

• Transposition of great vessels cause sever cyanosis in the first days of life and later cause CHF

Mixed Defects

Transposition of Great Arteries (TGA)

•Description:

- Great vessels are switched that the aorta arises from the right ventricle

and the main pulmonary artery arises from the left ventricle causing

complete separation from the two circulation.

• Associated defects such as septal defect or PDA permit blood to enter the

systemic circulation and/or the pulmonary circulation for mixing of

saturation and desaturation blood.


• The most common defect associated with TGA is a patent foramen ovale

• VSD (increase the incidence of HF, because it permits blood to flow from

the right to the left ventricle, into the pulmonary artery then to the lung)



Clinical manifestation:

- Depends on the type and size of the defect.

- Newborns with minimal defect are severely cyanotic and depressed at

birth.

- Children with large septal defect or a PDA may be less cyanotic but have

symptoms of HF

- Cardiomegaly is usually evident a few weeks after birth .


• Therapeutic management:

- Prostaglandin (PGE1) IV may be given preoperatively to maintain potency

and ensure adequate systemic blood flow

- Anti-congestive measures –digoxin, diuretics, increased caloric density of formula and after loud reduction.


• Pharmacologic treatment:

- Prostaglandin (PGE1) should be initiated to maintain potency of the PDA.

- Anti-congestive measures –digoxin, diuretics, increased caloric density of formula


- Cardiac catheterization and balloon atrial septostom

- Repair by 3 months of life.

- A definitive repair consists of switching the right/left structures.

- Arterial switch procedure


• Pharmacologic treatment:

- Prostaglandin (PGE1) should be initiated to maintain potency of the PDA.

- Anti-congestive measures –digoxin, diuretics, increased caloric density of formula


- Cardiac catheterization and balloon atrial septostomy

- Repair by 3 months of life.


•Surgical treatment:

- A definitive repair consists of switching the right/left structures.

- Arterial switch procedure

- Potential complications of the arterial switch include narrowing at the great artery anastomoses or coronary artery insufficiency.

Truncus Arteriosus (TA)


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Truncus Arteriosus (TA)Descriptions:

• Failure of normal separation and division of the embryonic bulbar trunk

into the pulmonary artery and aorta results in -----

- Development of a single vessel that overrides both ventricles

- Blood from both ventricles mixes in the common great artery, causing

desaturation and hypoxemia.


11/3/2020 Suhaila Halasa RN, PhD, CIMI,CPT 129https://www.slideshare.net/MissReith/ap2-chap18heartclass?next_slideshow=1


• Descriptions:

- Blood ejected from the heart flows preferentially to

the lower pressure pulmonary arteries, causing

increased pulmonary blood flow and reduced

systemic blood flow.


• Descriptions:

- There are three types:

➢Type I: a single pulmonary trunk arises near the base of the truncus and divides into the left and right pulmonary arteries

➢Type II: the left and right pulmonary arteries arise separately but in close proximity and at the same level from the back of the truncus

➢Type III: the pulmonary arteries arise independently from the sides of the truncus.

Types of (TA)

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A single pulmonary trunk arises near the base of the truncus and divides into the left and right pulmonary arteries

Types of TA/ Type 1

The left and right pulmonary arteries arise separately but in close

proximity and at the same level from the back of the truncus

Types of TA/ Type II

The pulmonary arteries arise independently from the sides of the truncus.

Types of TA/ Type III

Pathophysiology

• Blood ejected from the left and right ventricles enters the

common trunk, mixing pulmonary and systemic circulations.

• Blood flow is distributed to the pulmonary and systemic

circulations according to the relative resistances of each system.

Pathophysiology

• The amount of pulmonary blood flow depends on the size of the pulmonary

arteries and the pulmonary vascular resistance.

• The resistance to pulmonary blood flow is less than systemic vascular

resistance, resulting in better blood flow to the lungs.

• Pulmonary vascular disease develops at an early age in children with TA

Clinical Manifestations of TA

• Most infants are symptomatic with moderate to severe HF

• cyanosis

• poor growth

• activity intolerance.

• There is a characteristic murmur.


• Early repair in the first few month of life.

• It involves closing the VSD so that the TA receives the outflow from the

left ventricle, excising the pulmonary arteries from the aorta, and

attaching them to the right ventricle by means of a homograft

Therapeutic Management of TA


• Postoperative complications:

• persistent heart failure, bleeding, pulmonary artery hypertension, dysrhythmias, and residual VSD.

• Prognosis:

- Mortality is greater than 10%

Assist in measures to improve cardiac function:

• Administering correct dose of digoxin, observing for signs of toxicity and

instituting parental teaching regarding drug administration at home

• Drug is not given if pulse rate below 90-110 beats /min in infant and

young children or below 70 in older children

Nursing Care Management

Decrease cardiac demand:

• Infants require rest and conservation of energy for feeding

• Organize nursing activities to allow for interrupting periods of sleep

• Minimize infant crying

• Small frequent meals every 3 hours

• Reduce unnecessary stress for older children by explanation of what

happening to reduce anxiety


Reduce respiratory distress:

• Carful assessment, positioning and oxygen administration

• Respirations are counted for full one minute during a resting state

• Elevate the head of the bed


• Sleep on several pillows or semi-Fowler or high Fowler position

• Provide humidified O2 by nasal cannula, hood or mask

• Protect the child from persons with respiratory infections


• Maintain nutritional status

• Children metabolic rate is greater because of poor cardiac function and increased heart and

Respiratory rates

• They need more calories because they cant take adequate food due to fatigue


•Assist in measure to promote fluid loss

•When diuretics are given

•Record intake and output

•Monitor weight


• Support child and family


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