Cardiovascular Flashcards
Increased pulmonary blood flow heart defects
Atrial Septal Defect
Ventricular Septal Defect
Patent Ductus Arteriosus
Obstruction of systemic blood flow heart defects
Coarctation of the aorta
Aortic Stenosis
Hypoplastic Left Heart Syndrome
Decreased pulmonary blood flow heart defects
Tetralogy of Fallot
Pulmonic Stenosis
Mix blood flow heart defects
Transposition of the great arteries
Truncus Arteriosus
Septal development of the heart
Artrial, ventricular septum and heart all are developed between week 4-8 of gestation
What is fetal circulation?
umbilicus - liver (divides in two 1) hepatic system
2) inferior vena cava - heart - body
pressure of heart is higher on the R side
high pulmonary vascular resistance
What shunt spreads blood to the ret of the body in fetal circulation?
Ductus arteriosus
What does infant circulation look like?
Umbilical cord is cut (no more need of the ductus venosus)
Ductus arteriosus closes because of the use of the lungs and the oxygenated blood that enters the heart (10-21 days)
What are the hemodynamic changes with infant circulation?
Increased pulmonary blood flow
Decreased pulmonary vascular resistance (PVR)
Left atrium increased blood flow
Right atrial pressure falls, Increased pressure in left atrium (Stimulates closure of foramen ovale)
Higher oxygen saturation than fetal circulation (Stimulates closure of ductus arteriosus)
vasodilation
Difference between pulmonary blood vessels (fetal and neonatal)
F: Constricted with little blood flow; lungs not expanded
N: Vasodilation and increased blood flow; lungs expanded; increased oxygen stimulates vasodilation
Differences in systemic blood vessels (Fetal and neonatal)
F:Dialated, with low resistance, blood mostly in placenta
N: Arterial pressure rises due to loss of placenta; increased systemic blood volume and resistance
Differences in Ductus arteriosus (fetal and neonatal)
F: Large, with no tone, blood flow from pulmonary artery to aorta
N: Reversal of blood flow; now from aorta to pulmonary artery because of increased left atrial pressure. Ductus arteriosus is sensitive to increased oxygen and body chemicals and begins to constrict
Differences in foramen ovale (fetal and neonatal)
F: Patent, with increased blood flow from R atrium to L atrium
N: Increased pressure in left atrium attempts to reverse blood flow, closing flaps on the one-way valve
Differences in ductus venosus (fetal and neonatal)
F: Patent, blood flow from placenta to liver and inferior vena cava
N: Blood flow stops when umbilical cord is cut; ductus venosus begins to constrict
What does the SA node do for the heart?
pacemaker of the heart
leads to contraction
What does systole mean?
contraction of the heart
What does diastole means?
relaxation of the heart
What is cardiac output?
= volume of blood ejected by heart in 1 min
= heart rate x stroke volume
What is stroke volume?
= volume of blood ejected by ventricles per beat (in mLs)
What is stroke volume affected by?
Preload
Afterload – clinically measured by BP
Contractility – clinically measured by perfusion & urinary output
What is heart rate influenced by?
ANS
Can neonates change their stroke volume?
No, they can not increase their stroke volume
They depend of HR to increase CO
If the heart rate is too fast, it does not give the heart enough time to fill
What does tissue perfusion depend on?
HR, circulating blood volume, pump function, systemic and vascular resistances, capillary permeability and tissue utilization of oxygen
What do you want to include in a cardiac history?
Mothers health history, pregnancy and birth history
Detailed family history
What is included in the mothers health history?
Chronic health conditions (e.g. lupus, diabetes)
Medications (e.g. phenytoin)
Maternal alcohol use or illicit drug use
Exposure to infections (e.g. rubella)
Infants with LBW due to IUGR (intra uterine growth retardation)
High-birth-weight infants (e.g. IDM)
Cardiac history of infant/young child
Feeding difficulties with fatigue, frequent vomiting, rapid breathing, sweating with feeds, poor weight gain, developmental level
Incidence of respiratory infections & breathing problems
Onset & frequency of colour changes – cyanosis that worsens with feeding or activity
Parents feel baby’s heart race
Irritable; weak cry
Most comfortable position – HOB elevated, squatting
Cardiac history with Older child
Exercise tolerance & activities
Presence of edema & respiratory problems, chest pain, palpitations
Neurologic problems – fainting or headaches
Recent infections or toxic exposures; e.g. cardiomyopathy or rheumatic fever
Cardiac history with all children
review all other health problems
presence of other congenital anomalies
medications (OTC, herbal supplements)
Abnormal findings through physical examination
Weak, irritable, in distress
Undernourished, underweight
Chest retracts, heaves or lifts, enlargement over heart, asymmetrical chest movement
pallor, cyanosis, mucous membranes dry? clammy with activity/feeding, peripheral/periorbital edema, scars from surgery?
Cyanotic, clubbed finger nails
Pulses bounding
Liver through palpation
Physical examination = vital signs
HR - increased or decreased
RR - increased even at rest (raise HOB)
BP - differences in arms and legs (8-10 mmHg is concerning)
Tests of cardiac function
Radiography - chest x ray, fluoroscopy
Electrocardiography (ECG)
Echocardiography (where the blood is flowing)
Cardiac catheterization (femoral artery, invasive)
Exercise stress test
Cardiac MRI
What is the most common congenital heart disease with autistic children?
septal defect
What are the hemodynamics of the heart?
= pressures generated by blood & pathways blood takes through the heart & pulmonary system
Blood flows from high to low pressure path of least resistance
Normally, pressure on right side of heart is lower than left & resistance in pulmonary circulation is less than in systemic
What is HF?
Inability of the heart to pump adequate amount of blood to systemic circulation at normal filling pressures to meet body’s metabolic demands
What are the causes of HF?
Volume overload (too much in the ventricles)
Pressure overload (difficulty with blood leaving heart, narrowing of aorta)
Decreased contractility (cardinal myopathy, myocardial ischemia)
High cardiac output demands (needs more O2 than heart can deliver)
what are the compensatory mechanisms of HF?
Hypertrophy and dilation of cardiac muscle
Sympathetic nervous system
- Release of catecholamines which increases force and rate of contraction; peripheral vasoconstriction
- Sympathetic cholinergic fibers (sweating)
Renal system (Renin-angiotensin-aldosterone mechanism)
What is the first sign of impaired myocardial function?
tachycardia
Other signs of impaired myocardial function
Infant tires easily, especially during feeding (first sign)
Diaphoresis, irritability
Weight loss or poor weight gain (Developmental delays (gross motor))
Frequent infections
Poor perfusion (cardiogenic shock)
- Cold extremities, weak pulses, slow cap refil, low BP, mottled skin, extreme pallor, duskiness, cyanosis
Signs of pulmonary congestion
Tachypnea, nasal flaring, grunting, retractions, cough, crackles, wheezing, hoarseness
Cyanosis
Orthopnea – relieved by sitting up
Gasping & grunting respirations – late sign
Signs of systemic venous congestion (R sided)
Hepatomegaly
Cardiomegaly
Edema
- Weight gain; periorbital, facial, sacrum, scrotal
- Ascites, pleural effusions
Distended neck & peripheral veins (usually only noted in older children)
What does digitalis glycosides do? (digoxin)
Increases force of contraction
Decreases heart rate & slows conduction of impulses through AV node
Indirectly enhances diuresis by improving renal perfusion
Hold if HR is lower than 60BPM (adults), 100BPM (children) -apical pulse
First dose is loading dose (BLOOD LEVELS need to be done)
What are the signs of digitalis (digoxin) toxicity?
bradycardia, anorexia, N and V
What do ACE inhibitors do?
reduce afterload
What to do before giving ACE inhibitors?
Monitor BP before & after administration (hypotension)
Monitor serum electrolytes – block action of aldosterone & are potassium-sparing
Carefully assess renal function
How can we decrease cardiac demands?
Allow for uninterrupted rest
Minimal handling
Reduce stress
Maintain stable environment temp
Prevent skin breakdown
How can we care for respiratory distress?
Count RR for full minute
Position with HOB elevated or sitting up
Provide for unrestricted chest expansion
Remember: babies are diaphragmatic breathers!!
Oxygen administration
How can we maintain nutritional status?
Greater caloric needs but impaired ability to take in adequate calories
Well rested before feeds; feed soon after awakening (minimize energy expenditure on crying)
q3h feeding schedule – individualize to infant’s needs
Allow no more than ½ hour to complete feed (NG prn)
Increase caloric density of formulas - Add corn oil or MCT oil to formula or HMF to breastmilk
Metabolic needs are high with HF
How do we removed accumulated fluid and sodium?
Administer diuretics (give early in day)
Accurate I&O
Daily weights (same time, same scale)
Observe for signs of dehydration or edema
Observe for signs of electrolyte imbalance
Fluid restriction rarely needed - If required, plan to give most fluids during waking hours
Possible sodium restriction
Whats normal PaO2 range?
80-100 mmHg
What does low PaO2 indicate?
hypoxemia
What causes hypoxemia
Desaturated venous blood enters systemic circulation without passing through lungs
Synonyms for hypercyanotic spells?
blue spells, tet spells
What are clinical manifestations for hypercyanotic spells?
Increased rate & depth of respiration
Increased cyanosis
Increased heart rate
Pallor & poor tissue perfusion
Agitation or irritability - may lead to limpness or seizures
Tx of tet spells
Knee-chest position
Calm, comforting approach
Administer 100% oxygen
Give SC or IV morphine
Begin IV fluid replacement & volume expansion, prn
Repeat morphine administration
What is rheumatic fever?
Follows infection by some strains of group A beta-hemolytic streptococci
May lead to permanent heart valve damage
If croup antibiotics aren’t used up, it can lead to this
What is bacterial infective endocarditis?
Inflammation of lining, valves, & arterial vessels
Streptococcus or Staphylococcus
Prevention important; e.g. prophylactic antibiotics before dental procedures
Pneumonia can lead to this
What is Kawasaki Disease?
Mucocutaneous Lymph Node Syndrome
Young children
Acute systemic inflammatory illness
Widespread inflammation of small & medium-sized blood vessels (coronary arteries most susceptible).
May lead to dilation of coronary arteries & aneurysm formation.
Primary cause theorized to be infection with organism or toxin but not spread person-to-person
Most often late winter & early spring
Kawasaki disease diagnostic critera
Fever for at least 5 days, unresponsive to antipyretics & antibiotics
Must have 4 of the following:
1. Changes in extremities
- Acute - erythema of palms & soles, edema of hands & feet
- Subacute - peeling of hands & feet in 2nd & 3rd week
2. Polymorphous rash (flat)
3. Bilateral conjunctival (pink eye without discharge) inflammation without exudate
4. Changes in lips & oral cavity
- Erythema, dryness & cracking of lips, oropharyngeal reddening, or “strawberry tongue”
5. Cervical lymphadenopathy (enlarged lymph nodes), usually unilateral
Acute stage of Kawasaki disease
Fever, conjunctival hyperemia, red throat, strawberry tongue, swollen hands & feet, rash, enlargement of cervical lymph nodes, +++ irritable
1-2 weeks
Subacute stage of Kawasaki disease
Cracking lips & fissures, desquamation of skin on tips of fingers & toes, joint pain, arthritis, cardiac disease, & thrombocytosis; irritability continues
2-4 weeks
Convalescent stage of Kawasaki disease
Appears normal but lingering signs of inflammation
Increased ESR
6-8 weeks after onset, all blood values returned to normal
Medication for Kawasaki disease
IVIG (intravenous immunoglobulins)
Aspirin (salicylates)
Why do we not normally give aspirin to children?
They can get Reye’s syndrome. They are given because of the risk of clotting with KD
Nursing care for Kawasaki disease
Assessment of signs & symptoms; Tolerance of medication
Promote comfort (soft solids for food)
Passive ROM
Discharge teaching re: aspirin, cardiac follow-up
What is the criteria for MIS-C?
< 21 years, presenting with fever, laboratory evidence of inflammation, & evidence of clinical severe illness requiring hospitalization , with multisystem (≥2) organ involvement (cardiac, renal, respiratory, hematologic, GI, dermatologic, or neurological); AND
No alternative plausible diagnoses; AND
Positive for current or recent SARS-CoV-2 infection, serology, or antigen test; or COVID-19 exposure within 3 weeks prior to onset of symptoms
What are the manifestations of MIS-C?
Myalgia, tachycardia, hypotension, hypo- or hyperperfusion, lymphadenopathy/lymphadenitis
Rash, lip swelling/cracking, strawberry tongue, extremity swelling/peeling, conjunctivitis, blisters or erosions
Nausea/vomiting, diarrhea, abdominal pain
Respiratory distress, chest pain
Headache, altered mental status, meningismus, focal deficits, seizure
What is the discharge criteria for MIS-C?
No fever for 48 hours without antipyretics
Improvement in presenting symptoms
Improvement in lab markers
Influenza vaccine
When do you want to return to the ED with MIS-C?
Fever > 38
Recurrence of presenting symptoms or unwell with other symptoms
Respiratory distress or SOB
