Cardiac Flashcards
Cardiac: In utero
Oxygenation is provided by the placenta, not the lungs
The heart develops in the first 3 weeks and fetal circulation by 8 weeks
Lungs are not expanded and air is not used during utero, therefore connections must close by birth
Cardiac: After birth
Fetal connections close and the lungs begin to take over oxygenation
Heart starts out..
As a simple tube and grows into a complex organ
One end of the tube is arterial and one end is venous
Middle part of the tube widens, folds, and bulges into 4 chambers by the 3rd week of fetal life (heart beat)
Heart starts to beat at the 4th and 5th week
Atrium and ventricles are developed
How to bypass the lungs
Openings that are closed by birth Foramen ovale (atria Right to left) Ductus venosus (shunts blood from belly button to vena cava) Ductus arteriosus (aortic arch)- the most common one that does not close These open so that oxygen is exchanged while the baby is in utero
Fetal circulation
The fetus does not rely on the lungs for oxygenation, it relies on the umbilicus
The blood goes from the placenta to the umbilical cord, which then goes up the fetal abdomen, to the liver where its divides into 2
The liver. and the one vena cava through the ductus venosus, then goes into the atrium through the foramen ovale, to the left atrium, then to the left ventricle, and the upper body getting oxygenated rich blood to the highest level of the body causing encephalocoele developmental head to rump
Fetal HR
110-160 bpm, greater cardiac output per minute thena the adult
Cardiac: Changes after birth
No longer has a placenta so the blood need the lungs for oxygenation
Pulmonary vascular resistance decreases causing vasodilation in the pulmonary vascular bed
Pulmonary blood flow increases
Systemic vascular resistance increases
Blood flow through the ductus arteriosus becomes primarily left to right
Foramen ovale closes
Baby’s firsts breath →lungs inflate→reducing PVR to blood flow→pulmonary artery pressure drops→pressure in the right atrium to decrease.
Blood flow to the left side of the heart increases the pressure in the left atrium closing the feremonal valle.
Baby crying causes temporary reversal with mild cyanosis
Pressure in the pulmonary artery promotes closure of the ductus arteriosus, Decrease in Prostaglandin E causes this to close (usually happens in the first few hours and permanently within the first 3 wks, unless the baby is premature it is needs to stay open due to other cardiac defects), open = murmur
Cardiac: Compensation
Infants have a limited ability to increase their stroke volume to compensate for increased demands
Leads to tachycardia
Heart rate is primary compensatory mechanism for children when metabolic demands increase
Tachycardia may decrease cardiac output by decreasing filling time
Bradycardia has a profound effect on cardiac output
Cardiac: Major groups of problems
Congenital
Acquired
Cardiac: Congenital problems
Anatomical disorders that are present at birth
Cardiac: Acquired problems
Issues that happen after birth, the components that develop in-utero during the 4th of gestation until about the 8th week, and then the heart begins to mature
DiGeorge Syndrome
Caused by a defect in chromosome 22, may be signs you can see at birth. Some may develop later. These include bluish skin, seizures, twithing, learning delays, developmental delays, and failure to gain weight.
There are heart defect issues and facial issues
Congenital defects: Etiology
Most are unknown
Genetic predisposition interacting with environmental triggers
Chromosomal abnormalities account for almost 10% (downs, turner, DiGeorge)
Environmental or adverse maternal conditions accounts for 2-4% (maternal DM, phenylketonuria, Rubella and other viruses, Maternal ingestion of alcohol, anticonvulsants, lithium…)
Congenital defects: Etiology: Family history
Heart disease are usually dx at birth or in the first 4-6wks of age. Incidences are 2x greater than per-term babies Genetic make up and chromosomal defects Sudden death Diabetes Heart disease HTN Hyperlipidemia Congenital heart defects Family members with cardiac risk factors
Cardiac: History of infant
How is the infant/child feeding? Getting diaphoretic or cyanotic around the mouth or extremities when they eat?
Wt loss or failure to gain wt?
How are they breathing? Persistent, peaceful tachypnea RR >60, Cyanosis, pale?
Birth weight related to UGR
Pregnancy history: what meds mother took before and during pregnancy
Be sure you’re not implying any blame on the mother!1
Cardiac: History of Older children
Do they tire easily? Syncope? Recurrent respiratory problems that dont get better including asthma Poor wt gain Palpitations Lower extremity swelling Clubbing of the fingers Chest pain - rare that this is a cardiac condition in children
Cardiac: Physical assessment
Nutrition - how long do they eat? Color Chest and deformities Unusual pulsations Respiratory excursion Clubbing of fingers Cyanosis Palpate pulses Abdomen Peripheral pulses, femoral pulses: coarctation of the aorta may indicate weaker pulses and blood pressures in the lower extremities Heart rate and rhythm Character of heart sounds
Cardiac: Physical assessment: Clubbing of fingers
Early as 3 months
Could be due to hypoxia and the presence of right and left intracardiac shunt and an increase Hgb and HCT
Cardiac: Physical assessment: Pulses
Apical pulses, heaves, thrills, rate, rhythm
Apical pulse in <4yr old: felt 4th intercostal space- mid clavicular line
4-7 y/o: midclavicular line
>7y/o: 5th intercostal space, right mid-clavicular line
Cardiac: Diagnostic tests
Chest x-ray ECG Holter monitor Echocardiography Cardiac catheterization Exercise stress test Cardiac MRI
Heart sounds: S1
Beginning systole, loudest at apex and best heard over the mitral and tricuspid areas
Closure of AV valves
Heart sounds: S2
Loudest at the base
Closure of the semilunar valves, best heard over the pulmonic and aortic areas
Heart sounds: S3
Norml in some children and young adults
Best heard over the mitral area
Heart sounds: S4
Nt usually good to hear
Murmur
Sound that is produced by vibrations within the heart chambers or the major arteries from the back and forth flow of blood
Maybe innocent (stills) or pathological
Kid could grow out of it
Most pathological murmurs are diastolic in nature, expect venous hum
Rated on a scale of 1-6 with grade 1 and 2 barely audible
Heart defects: Acyanotic: Increased pulmonary blood flow
Atrial septal defect- hole b/w the atrias
Ventricular septal defect- hole b/w ventricles
Patent ductus arteriosus- did not close at the right time
Atrioventricular canal
Heart defects: Cyanotic: Decreased pulmonary blood flow
Tetralogy of fallot (the right ventricle is connected to the left ventricle via VSD) Tricuspid atresia (underdeveloped right ventricle)
Heart defects: Acyanotic: Obstruction to blood flow from ventricles
Coarctation of the aorta
Aortic stenosis
Pulmonic stenosis
Heart defects: Cyanotic: Mixed blood flow
Transposition of great arteries (aorta connecting to the pulmonary artery)
Total anomalous pulmonary venous return (pulmonary veins connecting to the superior vena cava)
Truncus arteriosus (pulmonary veins connecting to the aorta)
Hypoplastic left heart syndrome
PDA (patent ductus arteriosus)
Defect of increased pulmonary blood flow
Connects the aorta with pulmonary artery
Usually is closed off upon birth within the first 48 hr.
Failure of the fetal ductus arteriosus to close within the first weeks of like makes a reversal in blood flow due to the increased aortic pressure
After birth the pulmonary vascular resistance decreases, the pulmonary artery pressure is low, the aortic pressure is high. Blood shunts from the aorta to the PA, the amount of shunt is depending on the size of the PDA, systemic resistance and pulmonary resistance – includes left to right shunting
At risk for endocarditis and pulmonary vascular obstructive disease
Failure to close leads to continued blood flow from left to right shunt (aorta to PA)
Oxygenated blood is getting re-oxygenated again.
Blood doesn’t get out systemically and this increases the workload of the left heart. Pulmonary vascular congestion can occur and right ventricular hypertrophy can occur
PDA (patent ductus arteriosus): Clinical signs
Asymptomatic or show signs of CHF, presence of a murmur, bounding pulses and widening pulse pressure
Frequent URI
Children may become diaphoretic while eating and they may tire while eating
PDA (patent ductus arteriosus): Treatment
Indomethacin soon after birth
Surgical division or ligation (if medication doesn’t work, place a clip on the ductus is being done as well)
Use of coils in the cath lab
Antibiotics post op for any of these procedures
Ibuprofen (not as effective as indomethacin in low birth wt babies or less than 27wk gestation)
Low risk of mortality in these babies
PDA (patent ductus arteriosus): Treatment: Indomethacin
Prostaglandin inhibitor (prostaglandins keep it open) Only can give 3 doses and watch for necrotizing enterocolitis, GI bleed, and renal flow
ASD (atrial septal defect):
Defect of increased pulmonary blood flow
Abnormal opening between the atria, allowing blood from the higher pressure left atrium to low into the lower pressure right atrium
More common in females
ASD (atrial septal defect): Clinical signs
Asymptomatic
Fatigue
SOB on exertion
Development of CHF and respiratory infections
Presence of murmur (2nd intercostal space in systole and may be accompanied by a thrill)
Dysrhythmias, pulmonary vascular disease and emboli, can lead to stroke an this is from chronically increased pulmonary blood flow
ASD (atrial septal defect): Treatment
Use a Dacron patch for closure of moderate to large, open bypass before school and possible mitral valve replacement. Surgical interventions need to be careful of where the SA and AV node is for conduction purposes
Small defects can be closed in the cath lab (pt will receive low doses of aspirin for 6 months after closure)
It may close on its own before 4yr of life
VSD (ventricular septal defect)
Increased pulmonary blood flow
Abnormal opening between the right and left ventricles
This shunts the left to right
Some spontaneously close during the first year of life
Most common CHD
VSD (ventricular septal defect): Clinical signs
Small VSD: asymptomatic and may close with normal growth
CHF is common, presence of murmur, at risk for endocarditis, and pulmonary vascular disease
Children may also have increased respiratory infections and poor wt gain and fatigue
VSD (ventricular septal defect): Treatment
May close on its own during 1st yr of life
VSD (ventricular septal defect): Treatment: Asymptomatic
Wait for closure which could take up to school age. Manage the child with digoxin and lasix as needed and observe for signs of pulmonary HTN, prophylactically treat with abx and may use captopril id needed for afterload reduction
VSD (ventricular septal defect): Treatment: Symptomatic
Surgical closure- open or cath can be don at anytime. A medium sternotomy with bypass and aortic clamping might be done. The hole can be close with the patch or stitches. The child is put on abx to help prevent bacterial endocarditis
TET (Tetralogy of Fallot): defects
Decrease pulmonary blood flow
4 defects: Ventricular septal defect, Pulmonic stenosis, Overriding aorta, Right ventricular hypertrophy
TET (Tetralogy of Fallot): defects: Ventricular septal defect
Opening in the ventricles- The VSD is usually large and unrestricted, which allows for equal systolic pressure in both ventricles
TET (Tetralogy of Fallot): defects: Pulmonic stenosis
May be infundibular, valvular, supraventricular or any combination thereof, the degree of the stenosis determines the degree of cyanosis, pulmonary valve may be normal or hypoplastic
TET (Tetralogy of Fallot): defects: Overriding aorta
Aorta mixes with right and left ventricle, blood mixes together, usually straddles the VSD and the degree of overriding aorta does vary
TET (Tetralogy of Fallot): defects: Right ventricular hypertrophy
Right ventricle muscle is enlarged, resulting from high ventricular pressure
TET (Tetralogy of Fallot): Manifestations
Decrease pulmonary blood flow depending on the degree of PS
High pressure in the RV due to outflow tract obstruction causing shunting of blood through VSD to LV
Some blood flow maybe from RV to aorta depends on the degree of overriding
Some infants maybe cyanotic at birth, others may have mild cyanosis that progresses over the first year of life
Most common cyanotic HD
If cyanosis present at birth, will administer prostaglandin to increase pulmonary blood flow and surgery to keep the PDA open to allow more mixture of blood
Presence of murmur
Presence of tet spells (episodes of cyanosis or hypoxia because the infants O2 requirements exceed the blood supply usually during crying or after feeding - use calm approach, give O2, morphine, place knees to chest (morphine: decrease defibrillation, spasming on ventricles of the heart)
Possible neurological complications and dehydration may occur as well
Poor wt gain, short stature
Children playing on a playground might squat down to prevent an episode
TET (Tetralogy of Fallot): Treatment
Palliative shunt (provides blood flow to the pulmonary arteries from the left or right subclavian artery via a tube graft until correction of TET can be done) Complete surgical repair by putting child on bypass with aortic clamping Risk of dysrhythmias, sudden death, CHF
Tricuspid Atresia
Failure of the tricuspid valve to develop. There is no communications between R atrium and R ventricle
Blood flows through the ASD or patent ovale to the left side of the heart and allows blood to get to the lungs
Allows the mixing of blood in the left side of the heart
Tricuspid Atresia: Manifestations
Cyanosis in newborn period, tachycardia, dysrhythmias
Other children: signs of chronic hypoxemia and bleeding
Tricuspid Atresia: Treatment
Risk for endocarditis, brain abscess and stroke
Newborns: given continuous infusion of prostaglandin E until surgical intervention arranged so the foraminal valley and ductus arteriosus can stay open
Pulmonary to systemic artery shunt is placed to increase the blood flow
Glenn shunt (placed in the 2nd stage when the child is 4-9mo)
Modified Fontaine procedure is the final correction
Tricuspid Atresia: Complications of surgerys
Dysrhythmias, systemic venous hypertension, pleural and pericardial effusion, ventricular dysfunction
Obstruction disorder: Coarctation of the Aorta
Narrowing of the aorta usually is distal to the origin of the left subclavian artery, thereby the head and upper body is affected
There is a decreased pressure to the lowe body
Most common site is the ductus
Increases resistance to aortic flow
Increase left ventricular pressure and workload (afterload)
Blood flow to lower part of the body is decreased
Associated with other defects (VSD most common)
More common in white males
1/3 of girls born with Turners
Different degrees of abnormalities
Obstruction disorder: Coarctation of the Aorta: Clinical manifestations
Closed PDA will have increased afterload of the LV
Open PDA will have increased pulmonary blood flow and volume overload to the left side of the heart
Older children: increased blood flow to the upper body and decreased blood flow to the lower body, increase afterload to the LV
Renal arteries receiving decreased flow
Renin released, causing HTN in the ascending aorta
Development of collateral circulation to the lower body
Difference in extremity BP and pulse. The upper body will be hypertensive and bounding pulse, while the lower extremities will be hypotensive and faint pulses
Most deteriorate rapidly with HTN
Decrease systemic perfusion
Obstruction disorder: Coarctation of the Aorta: Treatment
Need supportive care before correction
Surgical repair (may be emergent or electively done at 2-4yr. Surgery is tx of choice for babies less than 6mo. Usually done via left thoracotomy with aortic cross clamping)
End-to-end anastomosis (done with stenosed area being exercised)
Balloon angioplasty
Abx prophylaxis
Obstruction disorder: Coarctation of the Aorta: Complications
CVA/Stoke
Bleeding
Lower extremity paralysis
HTN that may last for a few weeks or months after surgery (tx with nipride)
Chylothorax (type of flymph fluid called chyle that leaks into the thoracic apsce through the chest tube, accumulates in the chest cavity or the thoracic space, tx with draining, ways to stop production of chyle: give fat restricted diet and supplement with medium chain)
Recoarctation
Transposition of the great vessels
Mixed defect
Pulmonary artery leaves the left ventricle
Aorta exits from the right ventricle
Results in co communication between the systemic and pulmonary circulation
Children may need a septal defect or a PDA to make the blood communicate, also may have a patent foramen ovale or VSD
Transposition of the great vessels: Treatment
Intracardiac mixing with prostaglandin E
May have a cardiac cath to increase mixing
Surgery performed with in 1st weeks of life
Later surgery, you may risk of dysrhythmia and ventricular dysfunction later in life
Surgery may require multiple surgeries before it can be corrected
Transposition of the great vessels: Manifestations
Severely cyanotic and depressed at birth
Symptoms of CHF, murmur, cardiomegaly
Heat defects: Impacts on family
Adjustment to a child with special needs
Shock, denial, angry
How does this affect the parent-infant interaction?
Protective?
Discipline? (children to be as normal as possible regarding their social interactions and not part of a bubble, Parents need boundaries and discipline)
Most require initial surgical intervention and then later on, ongoing sx interventions
Heart defects: Helping families cope
Listen-be present
Educate
Remember the stage of development
Support groups
Hypoplastic left heart syndrome
Underdevelopment of the left side of the heart, resulting in a hypoplastic left ventricle and aortic atresia
Most blood from the left atrium flows across the patent foramen ovale to the right atrium, to the right ventricle, and out the pulmonary artery.
The descending aorta receives blood from the PDA supplying systemic blood flow
Hypoplastic left heart syndrome: Treatment
Mechanical ventilation Inotropic support preoperatively Infusion of prostaglandin E Surgical approach: First step: anastomosis of the main pulmonary artery to the aorta to create the new aorta, then repair the right ventricle to pulmonary artery. Second step: Glenn shunt to bypass the right atrium Transplant
Cardiac electrode placement
Right side of the chest above the heart (white)
Abdomen- grounding lead(green/red)
Left side of chest (black)
Cardiac Catheterization: Catheter
Inserted through a peripheral blood vessel into the heart
Through a large needle inserted either in a vein or an artery (usually femoral artery)
