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)
Cardiac Catheterization: Fluoroscopy
Used to help guide the catheter
Cardiac Catheterization: Contrast media
Injected when catheter is in heart chambers (up and around heart chambers). Films are taken for an angiography. measurements are done for different pressure readings. Pressure readings can be obtained from different parts of heart
Cardiac Catheterization: Diagnostic
Catheter enters femoral vein or artery, up circulatory system then to heart (right atrium for right side of heart, through artery and aorta, then to left side of heart) and look for abnormal pulses or identify any structural problems
Cardiac Catheterization: Interventional/therapeutic
Might have balloon on end. Dacron patch. Ream out stenosis. Ability to alter the anatomy
Cardiac Catheterization: Electrophysiology studies
Record heart impulses or destroy parts of heart generating abnormal conduction
Cardiac Catheterization: Nursing considerations
Often an outpatient procedure unless child is already in NICU or PICU
Cardiac Catheterization: Risks
Hemorrhage from insertion site
N/V
Side effects from dye or anesthetic agent
Low-grade fever due to foreign object being inserted
Loss of pulse at cath insertion site could be from clot or hematoma or from a tear
Dysrhythmias-insertion of foreign objects into heart could interrupt normal condition
Cardiac Catheterization: Pre-op considerations
Assess for allergies to contrast, Ht and wt. so know length of catheter needed to get to the heart, mark pulses (pedal and tibial)- so that we know where to palpate post-op, baseline SpO2, monitor for infection, NPO 4-6hr prior to catheterization
-Prepare child and/or parents by description of the cath room. Explain what they need to have done: earphones might be used by older children to help distract them, oral or IV sedation might be used, let them know they might need an IV started if doesn’t already
Cardiac Catheterization: Post op considerations
General post-op care
Return directly to the room if inpatient or holding until if outpatient
Cardiac monitor and pulse ox initial hours
Lie flat after procedure (in mothers lap with straight legs, sitting in bed, sitting in chair with propped legs
Venous access: 4-6hr
Arterial access: 6-8hr
Remove pressure dressing day after surgery. Can shower but no baths for a few days
Observe site
No strenuous exercise allowed
Might be given ibuprofen or tylenol for pain
Important f/u appointments
Cardiac Catheterization: Post op Assessment
6Ps (pain, pulse, pallor, paresthesia, paralysis, pressure)
Pulses distal to insertion site (might be weak the first few hours due to edema and inflammation), fluids (prevent dehydration, they’ve lost blood, give dextrose IV, dye is a diuretic)
Temp, color of extremity (look for any type of bleeding)
VS (BP and pulses for 1 min for dysrhythmias, bradycardia, hypotension indicate hemorrhage)
BG (might be hypoglycemic)
Congestive Heart Failure
Often a consequence of congenital heart disease
Inability of the heart to pump an adequate amount of blood into systemic circulation to meet body’s demands
Occurs secondary to structure anomalies (septal defects causing increased blood volume in heart and pressure. Failure where contractility is impaired such as myopathy or dysrhythmias.
Can also occur due to excessive demands as in sepsis and severe anemia
Congestive Heart Failure: Patho left sided
Left ventricle unable to pump blood into circulation
Increased left atrial pressure
Lungs congested with blood- pulmonary edema
Congestive Heart Failure: Patho Right sided
Right ventricle unable to pump blood effectively into pulmonary artery
Increased right atrial pressure and systemic venous circulation- hepatosplenomegaly, with edema
Congestive Heart Failure: Symptoms: Impaired myocardial function
Tachycardia Sweating Pale Decreased urinary output Weakness Restlessness Anorexia Extremities that are pale and cool to the touch Cardiomegaly
Congestive Heart Failure: Symptoms: Pulmonary congestion
Crackles Tachypnea Dyspnea Restractions Nasal flaring Cyanosis Grunting Wheezing
Congestive Heart Failure: Symptoms: Systemic venous congestion
Wt gain from edema Hepatomegaly Periorbital edema Peripheral edema Ascites Neck vein distention
Congestive Heart Failure: Be alert to parental statements of
Baby drinks a small amount and then stops and then wants to eat again really soon.
Baby seems to perspire a lot during feeding.
Baby is more comfortable when sitting ip or on my shoulder than when flat.
My baby has episodes of rapid breathing and grunting
Difficulty feeding and easily tired
Congestive Heart Failure: Treatment Goals
Treat underlying cause
Increase cardiac function by increasing contractility and decreasing afterload
Remove accumulated fluids and Na to decrease cardiac demands
Improve tissue oxygenation to decrease O2 consumption
Congestive Heart Failure: Treatment: Goal #1: Improve cardiac function
Digoxin
Improves contractility
Helps bundle fibers work in sync together
Increases cardiac output, decreased heart size, decreases venous pressure, relieves edema (result of backflow of blood from the heart)
Used due to rapid onset (PO, IV)
Calculated in mcg
High potential for error and overdose
Require 2 RN check
🚩Anything bigger than 1mL
Monitor serum K level- leads to dig toxicity
Congestive Heart Failure: Treatment: Goal #1: Digitalization
Can be done initially- where ECG monitoring is done while IV or PO digoxin given over 24 hr period, several doses given over 24 hr and maintenance given usually BID. This is to reach the body’s threshold or need for Dig
Congestive Heart Failure: Treatment: Goal #1: Digoxin S/E
GI (N/V anorexia)
Cardiac (bradycardia, dysrhythmias)
Congestive Heart Failure: Treatment: Goal #1: Nursing care
Watch for toxicity
GI (N/V, anorexia)
Cardiac (bradycardia, dysrhythmias)
Correct dosing
Congestive Heart Failure: Treatment: Goal #1: Parent education
Check apical pulse prior to admin for full min
Young child: hold if pulse less than 90-110
Older children hold is pulse less than 70
Observe the parents as they administer the med (BID)
Give before or 2 hours after eating, best on an empty stomach
Do not mix with food or liquid
Do not repeat dose if child vomits
If overdose occurs: call poison control right away
Congestive Heart Failure: Treatment: Goal #1: Digoxin antidote
Digibind
Digiband
Look at EKG strip to see if theres an increase in PR interval: indicates Dig tox
Congestive Heart Failure: Treatment: Goal #2: Afterload reduction: ACE inhibitors
Captopril & Enalapril
Assess for hypotension, cough, renal functionality
Blocks angiotensin 1 conversion to angiotensin 2: vasodilation occurs, blocks aldosterone secretion (causing hyperkalemia)
reduces preload of heart by preventing volume expansion from fluid retention and decreases hypokalemia
Sparing K and excreting Na
Congestive Heart Failure: Treatment: Goal #2: Afterload reduction: Beta blockers
Blocks alpha and beta adrenergic receptors, causing decreased HR and BP and vasodilation
Good response shown in adults, used selectively in children
S/E: dizziness, HA, hypotension
Congestive Heart Failure: Treatment: Goal #2: Afterload reduction: CRT
Cardiac Resynchronization therapy
Is relatively new; used for severe ventricular dysfunction
Congestive Heart Failure: Treatment: Goal #2: Afterload reduction: Nursing care
Monitor for hypotension, dizziness
Monitor electrolytes and renal function: Pay attention to K!!!!
Congestive Heart Failure: Treatment: Goal #3: Remove accumulated fluid/sodium: Diuretics
Lasix (get rid of K, need K supplement)
Thiazides (gets rid of K, need K supplement)
Aldactone (K sparing)
Congestive Heart Failure: Treatment: Goal #3: Remove accumulated fluid/sodium: Fluid restriction
This is rarely needed as these children self regulate. Its hard to get them to drink with CHF
Congestive Heart Failure: Treatment: Goal #3: Remove accumulated fluid/sodium: Na restriction
Not used in kids because of negative effects on appetite
If must be used, be sure to check their trays: no added salt diet (is more realistic) and potato chips
Congestive Heart Failure: Treatment: Goal #3: Remove accumulated fluid/sodium: Nursing care
Wt. same time, same amount of clothes, same scale each day
Monitor electrolytes, dehydration status
Give med same time each day
Congestive Heart Failure: Treatment: Goal #3: Remove accumulated fluid/sodium: K rich foods and supplements
Due to K losing diuretics
Bananas, oranges, green leafy veggies, whole grain
Might need K supplements elixir. K supplements: super salty, administer with orange or grape juice to hide taste
Be careful of dehydration. Children who are cyanotic and have polycythemia can have blood clots, keep them hydrated
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Cardiac workload
Reduced through decreasing metabolic needs
Limiting physical activity
Treat existing infection
Body temp preservation-not having the stress of becoming cold
Decrease work of breathing - by placing them in a semi fowler position
Medication to sedate an an irritable child as needed
Provide rest
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nursing care: Rest
Cluster care to minimize interruption and provide uninterrupted sleep, parents can stay for holding and rocking; change linen only when necessary; bath only when necessary; feed only when they’re hungry, not when they’re crying
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nursing care: Small feedings
Q3H
Planned with sleeping periods
Gavage when necessary to allow rest; putting feeding tube in
Lavage = take out
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nursing care: Decrease anxiety
Plan with older children: school at home
Sedate infant to facilitate sleep as necessary
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nursing care: Temperature regulation
Hyper/hypothermia- need more O2
Be aware of children getting cool humidified O2 so they don’t get too cold
Treat infections promptly
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nursing care: Skin care
If edematous- change positions frequently and watch for skin tears
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nutrition status and maintenance
Metabolic need greater due to poor cardiac function, increased heart and respiratory rates so they’re often fatigued
Congestive Heart Failure: Treatment: Goal #4: Decrease Cardiac Demands: Nutrition nursing care
Rested to eat: feed when first wake up and about Q3H
Easy to suck nipple (enlarged slit or has hole and aoft)
Stimulate on jaw or cheek to get suck
Timing (don’t do >30 min as can be more tiring and use up more calories than taking in)
Gavage ( what they would not take in 30 min of if tachypnic)
Caloric density might need to be increased (ass corn oil or MCT, oil or polycose to formula, increase from 20-30 calories/oz, adding slowly at rate of 2 calories/oz/day to avoid irritation of GI tract)
Supplement breast milk with high-calorie formula or add calories to breast milk
Normal healthy baby feeding goal
108kcal/kg/day
Cardiac Disease baby feeding goal
up to 120kcal/kg/day
Congestive Heart Failure: Treatment: Goal #5: Reduce Resp. distress and improvement in tissue O2
Improve myocardial function
Lessening tissue O2 demands
Use cool humidified O2 to increase the amount of available O2 during inspiration. O2 is a vasodilator, decreases pulmonary vascular resistance, O2 is a drug and requires an MD order. Can be given via hood, tent, NC, or mask
Congestive Heart Failure: Treatment: Goal #5: Reduce Resp. distress and improvement in tissue O2: Nursing care
Assessment (1 min after administering for any respiratory distress signs, which can worsen CHF. Assess rate and ease of breathing, saturation, and color)
Positioning to maximize chest expansion (infant seat, hold at 45 degree angle, several pillows for the older kids to sleep with, loose clothing and diaper, safety restraint low on abdomen)
infection control (infection is worse on child with CHF, encourage good hand washing to everyone entering room and to family. Start on abx as soon as they show signs of infection
O2 administration
Hypoxemia
Altered O2 tension (pressure) less than normal and identification by decreased arterial saturation levels
Decreased PaO2
Hypoxia
Reduction in tissue oxygenation from low O2 saturation
Chronic hypoxemia: Polycythemia
Increased RBCs, blood viscosity, crowds clotting factors; can develop a CVA, developmental delays
Chronic hypoxemia: Clubbing
Thickening and flattening of tips of fingers and toes
All the shunting of blood from the R and L allows air in venous system to go directly to brain
IV lines need filters, need to be primed and check for no air bubbles
Chronic hypoxemia: Squatting
Child will do this to get oxygenated blood back to the heart when going through hypercyanotic spells
Chronic hypoxemia: Hypercyanotic spells (TET)
Infundibular venous spasm decreasing pulmonary blood flow, increases right to left blood flow or shunting; occurs when communication between the ventricle and/or obstruction of pulmonary blood flow is decreased. Child becomes acutely cyanotic and hyper apneic because of this. Happens when baby is primarily >2 months of age and in first year of life often when blood draw is done or IV started
Chronic hypoxemia: Risk for neuro involvement
CVA, Abscess, developmental delays
Will need fluid to decrease risk of CVA
Chronic hypoxemia: TET Treatment
Morphine subQ or IV to decrease infundibular venous spasm, oxygen via face mask, knee to chest position helps as it reduces system venous return, and calm them down
Cardiac: Nursing care - Family foucs
Diagnosis of heart disease affect the whole family
Goal: help family adjust to the disorder (initally shock, then anxiety and fear)
Educate family about disorder
Help family cope with effects, the more they know, the more prepared they are, the better they can take car of their child
Prepare child and family for upcoming surgery
Often times need to help the family treat the child as normal as possible, with limit setting and discipline and allow normal socialization and play
Parent might need help to learn how to manage
Cardiac: Preparing for surgery
Introduce child to environment
Familiarize with equipment and procedures: show machines they’ll be hooked up to and how they can write and communicate, familiarize family to equipment so they wont be so scared walking into so many tubes and IV connections
Cardiac: Post op care
Delivered in ICU
Observe vitals very frequently
Maintain respiratory status
Monitor fluids (elevated BUN and Cr: signs of renal failure <1mL/kg/hr)
Cardiac: Surgical interventions
Open heart surgery
Closed heart surgery
Staged procedures- oftentimes, need more than 1 surgery to fix heart conditions
Prepare child and family for procedures
Cardiac: Shunt procedures
Temporary measures until corrective interventions can be done
Modified blalick-Taussig: subclavian artery to pulmonary artery shunt
Central shunt: ascending aorta to main pulmonary aorta
Bidirectional glenn procedure: Superior vena cava to the side of right pulmonary artery and both go to lungs
Aspirin often given prophylactically to prevent clots and thrombus
Cardiac: Post op child care
Monitor vitals and arterial/venous pressures
Intra Arterial monitoring of BP
Intracardiac monitoring
Respiratory needs such as intubation, off ET tube as quickly as possible, suction might be needed
Chest tube
Rest, comfort and pain management
Thoracic insertions usually more painful than sternal, continuous IV opioids and PCA if old enough
Fluid management: I&O, including ice chips, and IV flushes, watch for renal failure, notify MD if <1mL/kg/hr, check BUN and Cr and daily weights
Progression of activity: up and walking post-op day 2 usually after tubes are removed
Emotional support
Discharge planning
Cardiac: Post op: chest tube
Increased output first 12-24hr post op then begin to taper down and color begins to clear ip, usually removed day1-3, does hurt when removed, premedicate, cover hole with petroleum gauze right away and tape as if sealing it
Cardiac: Post op complications
Can be due to excessive pulmonary blood flow or fluid overload causing possible cardiac changes and CHF
Dysrhythmias due to electrolyte imbalance interfered SA or AV node from surgical intervention
Cardiac tamponade, cardiac infusion and restricted function of heart
Hypoxia due to respiratory difficulty or inadequate pulmonary blood flow
Decreased cardiac output syndrome and peripheral perfusion: due to hyperthermia or left ventricle unable to maintain circulation, treat with Dopamine. Use assistive device such as ECHMO if the medications fail. If ECHMO fails then they’ll need a transplant
Cardiac: Post op complications: Pulmonary changes
Pneumothorax
Pulm edema
Pleural effusion
Cardiac: Post op complications: Neurological changes
Cerebral edema, brain damage due to hypoxia, seizures and infection
Cardiac: Post op complications: Hema changes
Look at Hgb, Hct. might have RBC hemolysis, might have renal tubular necrosis, clotting issues after prolonged heparin, anemia
Bacterial endocarditis
Infection in the valve in the endocardium, grows an might break off, might go to adjunct tissues or valves or kidneys or spleen or cerebral nervous system. Usually sequelae form sepsis in children with cardiac disease or congenital anomalies
aka: BE, IE (infective endocarditis), SBE (subacute bacterial endocarditis)
Bacterial endocarditis: Caused by
Streptococci, staphylococci, candida, gram negative bacteria
May enter at any site, but most common is inheart (develop from dental procedures, UTI, catheters, venous lines, surgeries)
Bacterial endocarditis: Treatment
High-dose abx, will need blood cultures to evaluate effectiveness
2-8wk of abx, if not successful, can develop CHF and damage to valves. If they do have valvular damage then continue IV therapy and give IV abx at home
Bacterial endocarditis: Fungal infection treatment
Amphotericin (amphoTerrible)
Bacterial endocarditis: Prophylaxis
For dental work and other high risk procedures (bronchoscopy, cystoscopy, tonsillectomy)
Bacterial endocarditis: Education
Parents to report: malaise, fever, and anorexia and to take all medications
Rheumatic fever
Inflammatory disease occurs after group A strep such as upper respiratory involvement
Rheumatic fever: Caused by
beta-hemolytic streptococcal pharyngitis (2-3 wks after strep throat)
Big problem in 3rd world countries
Often in children not taking abx post strep throat or all abx course
Self limiting
Rheumatic heart disease
Most common complication of RF
Damage to valves as result of RF
Rheumatic fever: Major Manifestations: Carditis
Involving endocardium, pericardium, or myocardium
Most common involving mitral valve
Rheumatic fever: Major Manifestations: Polyarthritis
Reversible
Does migrate, especially in large joints such as knees, elbows, hips, shoulders, and wrists
They appear red and swollen
Rheumatic fever: Major Manifestations: Erythema marginatum
Rash usually on trunk in proximal portion of extremities; red macula with clear center and wavy well demarcated border
Rheumatic fever: Major Manifestations: Subcutaneous nodules
Small, non-tender nodules which appear over bony prominences such as hands, feet, elbows, scalp, scapulae, vertebrae
Persist indefinitely after onset of the disease and resolve with no swelling and resulting damage
Rheumatic fever: Major Manifestations: Chorea
Irregular movements or jerky movements
Rheumatic fever: Prevention of RHD
Full treatment of strep tonsillitis/pharyngitis
Treatment of recurrent RF: take abx or prevent getting strep
Ongoing and continued abx and prophylaxis, and salicylate for inflammation and pain. Monthly IM injections or PO doses, could be daily doses or given 5 years after last episode or 18 yr or up to adulthood every day if no valve involvement or to age 40 if there is valve involvement
Bed rest for the acute phase and prevent and treat
Get respiratory and throat cultures for sore throat
Rheumatic fever: Goal of therapy
Get rid of strep, prevent cardiac damage, manage symptoms, and prevent recurrences
Kawasaki disease:
Acute systemic vasculitis Usually children <5yr Not contagious, unknown etiology Greatest risk of heart problems Risk of cardiac sequelae Heart muscle inflamed around the heart there is potential for coronary artery aneurysm to be formed. Inflammation of arterioles, venules and capillaries Risk for coronary artery aneurysms
Kawasaki disease: Manifestations
Prolonged temp up to 4-5 days that is unresponsive to abx
Sore, red eyes which are not weepy
Red lips, might be cracked
Red tongue or red mouth (strawberry tongue)
Redness and peeling on hands and feet
Swollen hands and fingers
Rash all over body
Swollen glands in neck
Cough, diarrhea, sore joints, and sore neck
Not happy babies, Hard to console
Kawasaki disease: Acute phase
High fever
Abrupt onset
Unresponsive to abx and antipyretics
Very irritable
Kawasaki disease: Subacute phase
Resolution of fever, still very irritable
Risk for aneurysm (child will need ECHO to watch for development of aneurysm because one of the sequelae of Kawasaki’s is potential for the development of aneurysm)
Kawasaki disease: Convalescent phase
All but lab results are normal
6-8 wks to normalize
Kawasaki disease: Treatment: IV IgG
High dose, to reduce duration of fever and reduce risk of coronary artery abnormality
Needs to be given first 10 days of disease
Single large dose of 2g/kg infused over 10-12hr
Monitor infusion same way as you would when given blood transfusion: for anaphylaxis, AE…
Kawasaki disease: Treatment: Aspirin
High dose initially: 80-100mg/kg/day in divided doses/6 hr for fever and inflammation, until fever is gone
Then 3-5mg/kg/day- after fever is gone, you continue to give aspirin as an antiplatelet agent, given until platelet count is back to normal
Prophylactic aspirin for life if develop coronary artery abnormality or plavix or lovenox
Coumadin for children with giant aneurysm >8mm in size
Kawasaki disease: Nursing care
Might see arthritis for a few weeks, stiff in the morning
Might need to know how to do CPR at home depending on cardiac involvement
Live vaccines deferred for 11 months because of gamma globulin and antibody formation
Kawasaki disease: Nursing care: Monitoring
Cardiac status
I&O
Weight
Fluid with care due to myocarditis, watch for signs of CHF
Kawasaki disease: Nursing care: Gamma globulin administration
Monitor just like blood products with the frequent VS checks
Kawasaki disease: Nursing care:: Symptoms relief
Cool clothes, loose clothes, mouth and lip care, popsicle will help with lips and tongue
Kawasaki disease: Nursing care: Irritability management
Quiet environment, parents can comfort, could last up to 2 months- normal
Kawasaki disease: Nursing care: Parent teaching and expectations
Expected peeling of hands and feet 2-3 weeks -if painless
Hyperlipidemia: At risk
Obesity is becoming common in our society
Get fasting blood draw and look for an increased LDL in blood (because it carries cholesterol to the cells, want it to be <110 LDL)
Hyperlipidemia: Testing
LDL
HDL (carries the cholesterol to the liver then bile then excreted)
Look at excessive lipids and fats (high lipids and cholesterol leads to atherosclerosis or fatty plaques)
Hyperlipidemia: Treatment
Eat more whole grains, fruit, veggies
Restrict intake of cholesterol and fats
Increase exercise up to 60 min/day minimally
If not responsive to diet then start Rx
Congestive Heart Failure: Treatment: Goal #1: Digoxin therapeutic level
0.8-2mcg/L
Acquired Cardiovascular Disorders
Bacterial endocarditis Rheumatic fever Hyperlipidemia Cardiac dysrhythmias Cardiomyopathy Hypertension Kawasaki disease
Rheumatic fever: Manifestations: Minor criteria
Arthralgia
Fever
Increased ESR
Prolonged PR interval
