Cardiac Complications Flashcards
What are examples of acquired heart disease in ped pts?
- Pulmonary Artery Hypertension (discussed with CHD)
- Myocarditis/Endocarditis
- Cardiomyopathy
- Kawasaki Disease
- Rheumatic Fever/Rheumatic Heart Disease
Describe endocarditis and its risk factors.
- Infective process invading the endocardium - infection of inside of heart
- heart actually doesn’t have good blood supply - so IV abx need to be given for a LONG period of time
- Risk factors:
- CHD, artificial valves, central lines, piercings of nose/tongue, tattoos
How is endocarditis diagnosed and treated?
- Diagnosed by signs and symptoms of an infection or flu – usually already cardiac pts
- Long term antibiotics (cillins, mycins) will be required for bacterial endocarditis. (6 weeks, usually)
- May need valve replacement.
- Must maintain good dental health
- Prophylaxis before surgery and dental visits (No longer done in adults, still done in kids)
What is myocarditis?
- Infective process invading the myocardium after a systemic infection in a normal child
- Main symptom is failure to bounce back after a viral infection
- recover from myocarditis, but then cardiomyopathy is what we see (come in)
What is the ⅓ rule for myocarditis?
There is a 1/3 1/3 1/3 rule for these children
- 1/3 will have a mild case, recover and be fine
- 1/3 will get sick, require extensive support but recover
- 1/3 will get gravely ill with significant medical support up to and including a transplant
Describe cardiomyopathy.
CHAMBERS BECOME ENLARGED - difficult for heart to pump blood
- Many causes (including post myocarditis, congenital heart disease (CHD), HTN, many idiopathic (unknown cause)
- 3 types: Restrictive, Dilated, Hypertrophic
- We see DILATED myocarditis the most
- Monitor patient and treat depending upon severity of symptoms
- Treated similarly to adults
What is Congestive Heart Failure in kids?
“CHF and Shock are similar in they both are conditions of cardiac output that is inadequate to meet the metabolic demands of the body.”
- A condition in which the heart cannot pump enough oxygenated blood to meet the needs of the body’s other organs.
- A clinical syndrome in which the heart is unable to pump enough blood to dispose of venous return adequately
- A combination of the two
What are the causes of CHF?
- CHD (#1 in infant CHF)
- Myocardia Dysfunction
- Decreased contractility
- Infection of the myocardium or valves
- Arrhythmias
- Cardiomyopathy
- Anemia
- High cardiac output demands (i.e. septic shock)
- Chronic lung disease
- Hypertension
- Diabetes
- Overload
- Volume overload
- Pressure overload
- Volume overload
- Combination of the above factors
What are the symptoms of CHF? (same as adult CHF)
- Impaired myocardial function
- Tachycardia, gallop, diaphoresis, decreased perfusion, cardiomegaly on CXR, fatigue, poor feeding
- Pulmonary congestion
- Tachypnea, cyanosis, respiratory distress, pulmonary edema on CXR, orthopnea, wheezing, cough
- Systemic venous congestion
- Hepatomegaly, edema, weight gain, ascites, pleural effusion
What are the symptoms of LS HF?
- Pulmonary venous engorgement
- Tachypnea
- Grunting
- FTT (poor feeding for infants)
- Orthopnea in older child
- Wheezing/rales
What are the symptoms of RS HF?
- Systemic venous engorgement Hepatomegaly
- Splenomegaly
- Pitting edema
- Periorbital edema or distended neck veins (not visible in infants…their necks are not visible!)
What are the S/S in Infants with CHF?
- Poor feeding of recent onset
- Tachypnea that worsens during feeding
- Vomiting with feeds
- Poor weight gain
- Cold sweat on the forehead
What are S/S in Older Children with CHF?
- Shortness of breath, especially with activities
- Easy fatigability
- Puffy eyelids
- Swollen feet
What are the goals of CHF management and nursing considerations: Same as an Adult!
- Improve cardiac function
- Medications: digoxin, afterload reduction, IV inotropes
- Diuresis/ fluid restriction
- Lasix; strict I&O, monitor electrolytes closely
- Fluid and sodium restriction (usually in older children)
- Decrease metabolic O2 demands
- Conservation of energy (clustered care)
- N/G feeds (PO requires energy and may be difficult with tachypnea)
- Normothermia
- Improve tissue oxygenation
- Possibly administer O2
- Reduce work of breathing, proper positioning
What is Kawasaki Disease?
Also Mucocutaneous lymph node syndrome
A type of disease that primarily affects young children and is believed to be caused by a non-contagious infection. Symptoms include:
- pink eye
- oral mucosal change
- enlarged lymph nodes
- patchy rash
- peeling skin
How is Kawasaki Disease diagnosed?
CDC CRITERIA FOR DIAGNOSIS OF KAWASAKI DISEASE
Fever >5 days and at least four of the five following physical findings with no other more reasonable explanation for the observed clinical findings:
1. Bilateral conjunctival injection
2. Oral mucosal changes (erythema of lips or oropharynx, strawberry tongue, or drying or fissuring of the lips)
3. Peripheral extremity changes (edema, erythema, or generalized or periungual desquamation) **usually painful
4. Rash
5. Cervical lymphadenopathy >1.5 cm in diameter
Describe the timeline for Kawasaki Disease.
Acute (1st 10 days with high fever)
Sub Acute (after 10 days)
–Symptoms appear
Convalescent (begins 6-8 weeks after onset)
–this time span may be more rapid with IVIG dosing–Symptoms start to disappear–Aneurysms developMay have persistent arthritis
What are the clinical manifestations of Kawasaki?
- Typical child - Children < 5 yr (77%)
- Most common in Asian heritage
- Sudden onset of high fever
- Non-infective Conjunctivitis
- Non-purulent
- Bilateral
- Changes in lips and oral cavity
- Reddening and fissuring of lips
- Erythema of the buccal mucosa
- Strawberry tongue
- Polymorphous exanthem
- Morbilliform, scarlatiniform or erythema multiforme
- Evanescent in some patients
- Begins in diaper area and spreads to torso and extremities
What are the clinical manifestations of Kawasaki in the acute phase of the disease progression? (1st 1-2 weeks)
- Erythema and edema of hands and feet
- Swelling of proximal interphalangeal joints of the hands
- Constant pain and discomfort
- Refusal to move hands or bear weight
What are the clinical manifestations of Kawasaki in the subacute phase?
- Desquamation
- Starts in the subungual regions
- Spreads to palms, soles & Diaper area
- Gangrene of fingers and toes
- Occurs rarely in very young infants of non-Asian background.
What are the manifestations of Kawasaki Disease in the convalescent phase (several months to years)?
resolution of symptoms
labs normalizing
possible (not always) resolution of aneurysms
What are the possible complications of Kawasaki disease?
Aneurysms usually first noted 12-28 days after onset of the disease. Rarely appear > 28 days after onset.
Aneurysms may thrombose leading to myocardial infarction and death
Aneurysms may rupture (rarely)
A pancarditis is often present in the first 10 days of the illness (Simultaneous inflammation of the heart muscle and of the endocardium and pericardium). Pericardial effusions may accompany this.
Describe the nursing care for Kawasaki disease?
- Bedrest for until afebrile for > 72 hours and pain diminished
- Become familiar with IVIG administration
- Restrict activity even when mobile
- Provide oral care
- Provide analgesia
- Educate family of importance of follow-up
How is Kawasaki managed?
- Anti-inflammatory agent
- (ASA 80-100mg/kg/day to wean after 2 weeks but keep taking
for up to 8 weeks)
- (ASA 80-100mg/kg/day to wean after 2 weeks but keep taking
- IVIG
- If given within acute phase reduces fever and prevents
aneurysms (80-90% of time) - 1-2 gms/kg in onetime dose over 12 hours
- infusion rate
- NO live virus vaccines for 11 months after IVIG
- Follow-up cardiac catheterizations/ echocardiograms to evaluate/rule out coronary artery aneurysms
- First ECHO usually done day after admit
- If given within acute phase reduces fever and prevents
What to watch for in complications of Kawasaki Disease?
Aspirin toxicity
Immunosuppression
Describe rheumatic fever.
- Cause: Auto-immune reaction to Group A beta-hemolytic streptococcal (pharyngitis)
- Prevention: throat cultures, prompt/total treatment for strep throat
- Strep migrates to myocardium (valves), joints, skin, CNS several weeks later
- As many as 39% of pts with RF will develop Rheumatic Heart Disease
What are the presenting symptoms of rheumatic fever?
- small, painless nodules under the skin
- rash - erythema marginatum
- chest pain
- rapid fluttering or pounding chest palpitations
- tic
- lethargy or fatigue
- nosebleeds
- stomach pain
- painful or sore joints in the wrists, elbows, knees, and ankles
- pain in one joint that moves to another joint
What is rheumatic heart disease?
Mitral Valve affected most often (followed by Aortic Valve)
Poor valve function may produce CHF
Usually resolves but in 10-40% of patients, permanent valve damage develops
What diagnostic testing is available for rheumatic fever/rheumatic heart disease?
EKG (16 Lead, Left side AND Right side)
ECHO
Cardiac Catheterization
Labs to know
CBC – H/H, differential
C-Reactive Protein (CRP)
Erythrocyte Sedimentation Rate (ESR)
Anti-streptolysin-O antibody titer (ASO/ASLO)
Describe embryonic heart development.
Describe ductus arteriosus, ductus venosus, foramen ovale and why they’re important.
Compare prenatal and postnatal blood flow.
Describe Congenital Heart Disease: defn and etiology/
Definition: a group of cardiovascular malformations that results from abnormal structural development of the heart and/or a persistence of fetal vessels
Etiology: >80% of the etiology is unknown
multifactorial etiology
Incidence: 8-10 per 1000 live births
Now have >1,400,000 adults in US with CHD
kids w/ down - 30% have CHD
Risk factors for CHD - gestational and natal hx
- Infection (maternal rubella, CMV, herpes virus, coxsackievirus B)
- Medications (amphetamines, phenytoin, trimethadione, lithium, thalidomide)
- Maternal conditions (diabetes, maternal lupus erythematous, mother has CHD, maternal age >40 years
- Birth Weight
- Excessive smoking
- Alcohol consumption
Family Hx risk factors for CHD
Hereditary disease
CHD
Rheumatic fever
Sudden unexpected death
Diabetes mellitus, arteriosclerotic heart disease, hypertension
Long QT syndrome
Marfan’s syndrome
Infant s/s of CHD
Feeding problems (Failure to Thrive)
Dysphagia
Dyspnea
Cyanosis
Exercise intolerance
What would you assess for on physical exam for CHD?
Growth failure
Color (ie. Pale, dusky, or cyanosis)
Diaphoretic
Tachypnea
Tachycardia
Hepatomegaly
What is the genetic pattern in CHD?
- About 15% of CHD’s related to genetics
- Increase chance of CHD if the following
- sibling(s) with a heart defect
- parent(s) with CHD
- a chromosomal aberration, eg, Down’s syndrome
- Another non-cardiac congenital anomaly
What are associated defects and chromosomal abnormalities with CHD?
- Associated Defects
- tracheoesophageal fistulas
- renal agenesis
- diaphragmatic hernias
- Chromosomal Abnormalities
- Down Syndrome
- Turner Syndrome
What is the Management for Patients with CHD?
- Refer to pediatric cardiologist
- RN role
- Was the CHD diagnosed prenatally?
- Reducing parental anxiety: the blame game
- Recognize that children with chronic illness have an increase in sibling rivalry, hostility, and anger between the ill child and healthy child
- Children with CHD are more socially isolated than other children with chronic illness
How can you help families/pts deal with CHD?
- Know your community resources
parental support groups
insurance resources
internet sites - Help families deal with common threads
fear
isolation
shock
disbelief
Anger (the stages of death)
feelings of being overwhelmed
attempts to place guilt & blame
Why are pressure gradients important to understand in CHD?
- Pressure Gradients
-generally lower on the right side v. left side of the heart - resistance
-lower in the pulmonary circuit v. systemic circulation - presence of an abnormal communication
-leads to shunting from higher pressure circuits to lower pressure circuits (left-to-right)
*Trinka observation: blood is lazy!
Describe palliation vs. correction in CHD?
- Correction:
- Heart defect is completely gone and heart looks/functions normally
- Palliation:
- Surgical procedure so child will live CANNOT fix the heart to look/function normally
What are the classifications of CHD?
- Increased pulmonary blood flow
Left to Right Shunts (acyanotic) - Decreased pulmonary blood flow
Right to Left Shunts (cyanotic) - Obstructive lesions
- Complex
(..or any combination of the above)
Describe incr pulmonary blood flow (acyanotic defects).
- Atrial Septal Defect
Opening between the atria - Ventricular Septal Defect
Opening between the ventricles - Patent Ductus Arteriosus
Failure of ductus arteriosus to close - Atrioventricular Canal Defect
Opening between the atria, ventricles and one common A-V valve
What symptoms would we treat w/incr pulmonary blood flow?
- Symptomatic treatment of:
- CHF
- Failure to thrive
- Oxygenation
Describe cath lab or surgical repair for CHD.
Correction:
Close the holes
Fix the valves (if there’s an issue)
Expect normal heart/vital signs postoperatively
What are Increased Pulmonary Blood Flow specific post op/procedure problems?
- Post repair complications:
- Holes might remain leaky
- Valves could remain leaky
- If the electrical conduction was cut, heart blocks or arrhythmias in that area
- Expect normal heart/vital signs postoperatively
What is Pulmonary Artery Hypertension? (PAH)
2 types: short term and permanent.
Short term:
Congenital Heart Disease with increased pulmonary blood flow (AVC, VSD, TRU)
Surgical correction occurs, dropping the blood flow to normal
Pulmonary Arteries vasoconstrict to maintain higher pressures
Permanent:
Vascular changes occur from unrepaired CHD or PPHN of unknown etiology
Describe how PAH can lead to PVD.
- Since the vascular bed’s smooth muscles are very sensitive and easy to hypertrophy, Pulmonary Hypertension can become a permanent change as pulmonary vascular disease develops.
- Pulmonary Vascular Disease is irreversible and is treated by heart/lung transplantation when severe enough.
- PVD can also develop due to long-standing unrepaired defects (i.e. AVC, VSD, TA)
What are causes of PAH crisis?
- Alveolar Hypoxia (due to suctioning, increased 02 requirements–untreated)
- Hydrogen Ion (acidosis) Possibly due to sepsis, hyperthermia, or hypoventilation.
- Alveolar Hyperinflation
- Hypothermia (environmental)
- Stress/Overstimulation
How does a PAH crisis present?
- As pt starts the downward spiral, the trigger stimulates the smooth muscles of the vascular bed to vasoconstrict.
- Vasoconstriction (“Clamping down”) leads to hypoxia which increases vasoconstriction.
- At the same time, vasoconstriction leads to a backup of blood flow into the pulmonary bed that increases pressure.
- Vasoconstriction and hypoxia spiral which leads to acidosis which increases the spiral.
How is a PAH crisis treated?
- Alveolar ventilation
- Alkalosis
- Analgesia and sedation (up to and including anesthesia)
- Avoidance of stimulation
What are some PAH precautions?
Minimal stimulation ie. signs on the door
Hyper-oxygenate with 100% 02 for 1 full minute before suctioning and between each pass of the suction catheter
Avoid hypothermia
Keep pt alkalotic (pH >7.5)
What are defects that decr pulmonary blood flow (cyanotic defects)?
Tetralogy of Fallot
Tricuspid Atresia
What are TOF s/s?
- Hypercyanotic spells may occur (“Tet spells”)
- Cyanosis
- Dyspnea on exertion
- Clubbing
- Squatting
- Harsh systolic murmur
- CHF uncommon
What symptoms would you treat w/decr pulmonary blood flow?
- Symptomatic treatment of:
- Tet spells
- Failure to thrive
- Oxygenation
What are obstructive lesions?
- Pulmonary valve stenosis
- all other Atresia-s
- all other Stenosis-es
- Coarctation of the Aorta
What is diff b/n stenosis and atresia?
stenosis: narrowing
atresia: door is shut
How do you diagnosis coarctation of the aorta?
- 4 extremity bp b/c absent leg pressures, or 20 pt diff
- echocardiogram to diagnose finding
- pre and post pulse ox - if coarc is getting worse, the diff will be wider
What symptoms would you treat in obstructive lesions?
- Symptomatic treatment of:
- Hypoxia
- Failure to thrive no flow no grow
- Decreased perfusion - anything beyond obstruction is going to decr perfusion
What are some complex lesions?
“a little of everything” - when they divided out, divided incorreclty
- Transposition of the Great Arteries/Vessels - both arteries fused to wrong ventricle
- Truncus Arteriosus (TRU) - pulmonary artery and aorta never unfused
- Total/Partial Anomalous Pulmonary Venous Return (TAPVS, PAPVR) - pulmonary veins didn’t go to left atrium, (incl ductus venosis – > so all blood goes to liver)
- Hypoplastic Left Heart Syndrome (HLHS) - usually seen after they have atresia or severe stenosis of mitral valve or aorta
What symptoms would you treat in complex lesions?
- Symptomatic treatment of:
- Failure to thrive
- Hypoxia
- Decreased perfusion
What are some important things to know in general about CHD?
- Fluids are lazy and will always go the path of least resistance
- No FLOW, No GROW!
If poor perfusion to an area in utero, area will be small or absent at birth - Feed & Grow
All cardiac babies have growth issues and getting them big enough for their surgeries is a priority! - Ductal Dependent Lesions require a PDA or they die! (until repaired/paliated) (ie HLHS)
Which are ductal dependent lesions??
require a PDA or they die! (until repaired/paliated) (ie HLHS)
Describe Family Education in Care of CHD children.
- Identify Primary Caregivers (may or may not be the parent!)
- CPR
- When to call Pediatrician vs Cardiologist vs. 911
- Incision care/Sternal care (sternal precautions)
- HLHS parents have more education than others
- Safe-at-Home Program
- Feeding tube insertion and care
- Formula/Breast Milk supplements to increase calories/oz
- Medication administration
- Drawing up accurately
- Knowing actions and side effects
- Knowing if ok to re-administer in times of emesis
- When to hold meds (diuretics with N/V)
What is shock?
Definition - inadequate delivery of oxygen to tissues to meet metabolic demands of body despite cardiac output
If shock is not addressed and resolved it will lead to death 100% of the time
What are the types of shock?
- Hypovolemic - most common form
- Septic/neurogenic - inappropriate distribution of blood flow
- Obstructive – physical causes of inadequate tissue perfusion
- Cardiogenic
- CHD
- Myocarditis/Endocarditis
- SVT
Explain the 4 types of shock.
Hypovolemic - Pipes empty
Septic/neurogenic - Pipes leaking
Obstructive - Pipes are clogged
Cardiogenic - Pipes are fine BUT… Pump is bad
Give an overview of types of shock, causes and tx.
Describe compensated vs. hypotensive shock.
Compensated (early) shock - blood pressure is maintained.
Hypotensive (late) shock - blood pressure is NOT maintained, organs not perfused
Describe the stages of shock.
early shock → symptomatic shock → organ dysfunction
- Early: tissues start to get altered, decr perfussion. Heart will increase cardiac outpout. Immature hearts CANNOT incr stroke volume, so they do with incr HR. Periphery will get better and perfussion will improve. BUT if we don’t intervene, they will get worse.
- Symptomatic shock - heart can’t keep up anymore, so CPETC starts to drop b/c body goes into Triage Mode. BP is still maintained
- Organ dysfunction - no blood to perfuse main organs, LOC, BP, Urine Output goes. altered perfussion to liver, coags can go, perfussion to kidney - no perfussion - AKI
We need to catch early or at least symptomatic
With shock in peds, you always assess _____ first?
Always assess Perfusion First!!C PET C
C = color
P = pulses
E = edema
T = temperature
C = cap refill (>3 is BAD)
How would you conduct a rapid cardiopulmonary assessment?
CPETC – sometimes more important than ABCs. Unless ABCs are life altering, CPETC would be what you look at first.
- Evaluation of general appearance:
- Mental status
- Tone
- Responsiveness
- Physical examination of:
- Airway
- Breathing
- Circulation (ABCs)
- Classification of physiologic status (severity of the patient’s respiratory or cardiovascular dysfunction).
What vitals might you see with shock?
- Temperature:
hypothermia can be a symptom of shock - Pulse:
increased pulse rate, bounding pulse, weak pulse can all be signs of a shock state. WHICH ONE - Respirations:
increased Work of Breathing can be a sign of shock - Blood Pressure:
In early shock, the BP will be normal. A drop in blood pressure indicates late shock and is an ominous sign!
What is the treatment of shock?
- Assess and support ABCs.
- Activate Rapid Response or CodeTeam.
- (at what time would you call which team?)
- Provide oxygen and ventilation as needed.
- Attach monitor/defibrillator.
- Attach pulse oximeter.
- Establish vascular access.
- Prepare to provide volume expansion.
- Consider vasoactive infusions
- Prepare to provide volume expansion
- 20mL/kg of isotonic crystalloids
- 0.9% Sodium Chloride (Normal Saline)
- Lactated Ringers
- Normosol (rarely seen/used)
- Isolyte (rarely seen/used)
- Consider vasoactive infusions
- Inotropes
- Epinephrine
- Phenylephrine
- Inotropes
What is intraosseous access?
- IO is indicated when other vascular access is not already established.
- Blood from bone marrow of the tibia passes from emissary (intramedullary) veins into general circulation via popliteal vein.
- anything that can be given through venous access, can be given IO. If they are getting IO, they’re probably so sick they aren’t awake
- usually max 12 hours bc after 12 hours, you probably have enough fluid and we can go to IV access (PIVs or Central access)
What is the cause of each type of shock?
- hypovolemic - dehydration/hemorrhage
- septic/distributive shock - infective process, spinal cord injury
- cardiogenic shock - myocarditis, CHD, cardiomyopathy
- obstructive shock - physical cause, tension pneumo, tamponade, trauma/injuries
What are the symptoms of ALL types of shock?
Early: decr perfusion, tachycardia
Late: decr. LOC, drop in U/O, low B/P
What is the general tx for ALL types of shock?
Fluid, 20mL/kg, reassess. repeat (up to 3x… after 3, probably need to start a drip)
What will be the response to dehydration/hemorrhage with fluid tx.
May take several boluses but pt will improve with fluid alone.
What will be the response with septic/distributive shock with fluid tx.
If perfusion still poor after 3 boluses, consider going to inotropes.
What will be the response with cardiogenic shock with fluid tx?
Pt will get worse. Decr perfusion, CHF, gallop, fine crackles (rales) in lungs develop, tachycardia worsens, BP drops, tachypnea
What will be the response with obstructive shock with fluid tx?
Pt will get worse until causes is reversed.
Why do we give fluids with almost all cases of shock?
Many times, unable to determine cause of shock at onset so all kids get fluids. If they improve, they are either hypovolemic or septic (get pt hx/background from parents to determine which). If they get worse, need to determine if pt has cardiac issues or one of the obstructive causes.
Describe the progression from SIRS to Sepsis to Severe sepsis/septic shock.
SIRS: systemic inflammatory response syndrome - pt has altered vital signs or elevated WBC but cause is unknown. Some call this “warm shock” or “hyperdynamic shock”
- we will do a WBC differential, seg/neutrophils vs. lymphocytes
- Bands importance
Sepsis: cause identified and we will do a 24 hour culture or 24 hour culture
Severe shock /sepsis - sepsis with 2+ organ dysfunction involvement.
- follow fluid bolus rules, fluids vs. pressors.
What might you see with “leaky pipes” sepsis
purpura, mottling, petechiae
Always listen to parents *
What would you associate a “pink child” with?
CHF
Why is feed & grow so important with CHD?
Can’t operate until they’re big enough. Have to be as big and healthy as possible.
For what issues would you get 4 extremity blood pressures?
coarctation of the aorta
Give an example of an obstructive defect.
coarctation of the aorta
How do you do fluid resuscitation?
push pull method with 60 cc syringe
If you need to give more than 500ccs of fluid in 15 mins, what would you do?
use two pumps
What are the 4 defects of Tetralogy of Fallot?
(1) VSD (hole b/n ventricles big enough that aorta sits on fence b/n L&R ventricles (2) “overriding aorta” (3) narrowed pulmonary outflow tract (that’s why blood prefers to go from blue to red) , in utero, less blood went through to lungs, if no blood flow in utero, not big enough (small pulm arteries) (4) hypertrophy of right ventricle
What are treatments (non surgical) for Tet spells?
- knees to chest
- older: stop and squat
- positioning FIRST*
- second - give oxygen
- third - give morphine (calm AND vasodilate)
- propranolol - prevent TET spells, not treat
Treatment of tetralogy of fallot and coarctation
- tetralogy of Fallot - feed and grow first and then surgical repair
- coarctation of aorta - surgical repair
mitral valve atresia
no good left ventricle - hypoplastic left ventricle (HLHS)
HLHS treatment?
“Sacred cows”
Haven’t mastered as well
life expectancy is the same for a lot of correctable defects
HLHS - lower life expectancy
Three choices:
- go to a place for heart transplant
- 3 palliative surgeries
- take child home and 14 days PDA closes and child dies (only defect they allow child to go home on palliative care)
How would you distinguish petechiae vs. rash?
petechiae won’t blanch.
purpura - collection of petechiae. Really bad. starts to clot off - gangrene
mottling - could be altered CPETC (usually sign of altered perfusion. or child is really cold).
