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n342 peds > midterm cardio > Flashcards

midterm cardio Flashcards

1
Q

Know about digoxin

normally pressure is greater on left than right

infants cannot increase stroke volume to increase CO

A
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2
Q

circulation

A

CO is dependent on HR until school age (don’t have stroke volume)

decreased BP and HR is a late ominous sign

higher metabolic rate

cannot concentrate urine = urine output higher (2ml/kg/hr)

heat and greater insensible water loss and higher fluid eq

relatively anemic

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3
Q

SA for CO - 2 defects

A
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4
Q

general physical signs of heart defect

A

tire easily

eating and getting diaphoretic

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5
Q

normal

A

heart dev 4-8 wks gestation

atrial septum dev at 4 wks

ventricular septum dev at 4-8 wks

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6
Q

normal blood flow

A

blood comes through umbilicus from vein, to liver. divides. Some enters hepatic portal and circulates liver. Rest goes to inferior vena cava, through the ductus venosus

Blood from head goes into right ventrical then to pulm artery

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7
Q

where is the pressure the greatest in a fetus

A

pressure greatest on right side because the pressure directed from the right atrium to the left across the foramen ovale

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8
Q

What is the pressure in the pulmonary arteries

A

pulm vascular resistance is high = hard to send blood into lungs = most blood gets shunted across ductus arteriosus, then to rest of body

Pulm vasc resistance decreases after first breath
large volume of blood shifts from placenta to the pulm system
alveolar oxygen tension shifts

At first breath, oxygen decreases vasoconstriction, vasodilates, and lowers pressure significantly

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9
Q

Fetus lungs

A

lungs are collapsed = this produces a high pressure dt resistance

high pulmonary vasc. resistance in utero dt collapsed lungs = greater pressure on right side of heart and pulm atery

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10
Q

Change of blood flow

A

at birth, change in blood flow causes changes in left side of heart
-forces foramen ovale to close (like a trap door) and pressure on left side gets higher

-arterial oxygenation stops since shunting across ductus arteriosus stops by 72 hrs of life

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11
Q

change in heart thickness

A

thickness during utero/at birth: equal

left side eventually grows in thickness and develops a larger muscle

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12
Q

conduction system

A

electrical pulses that initiate mechanical contraction and initiates circulation of blood

systole - contraction
diastole - relaxation

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13
Q

Cardiac output

A

the volume of blood ejected by the heart in 1 min

CO = HR x Stroke Volume

infants and young children can only increase HR as compensation to increase CO because they aren’t able to increase SV

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14
Q

Stroke volume

A

Stroke volume: blood volume ejected by ventricles per minute

3 things affect stroke volume:

1) preload: vol returning to heart (circulating vol)

2) afterload: resistance heart must pump against to eject blood (systemic vascular resistance or pulmonary vascular resistance)

3) Contractility: how efficient the heart muscle is (how efficient the myocardial fibers shorten and how easily the heart pumps)
measured by perfusion (pulses, temp, cap refill) and urine output

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15
Q

What is HR influenced by?

A

HR is influenced by autonomic nervous system

neonates cannot increase SV = depend on HR to increase CO

If HR is too fast:
-decreased filling time
-diastolic filling time not efficient = not enough blood to be pumped out

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16
Q

What does tissue perfusion depend on?

A

HR

Circulating blood volume

Heart pumping function

systemic and vascular resistances

capillary permeability

tissue utilization of O2

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17
Q

Heart Failure

A

Inability of heart to pump adequate amount of blood to systemic circulation at normal filling pressures to meet the body’s metabolic demands

Causes:
-any interference with normal mechanisms regulating CO
-volume overload of hypertrophied muscle
-pressure overload
-decreased contractility; cardiomyopathy (muscles not working or developed properly, cardiac ischemia, asphyxia) - body deprived of O2 causing death
-high CO demands = septic

in children, HF is common in kids w/ secondary congenital heart defects (structural anomalies where blood cant flow OR increases pressure in heart

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18
Q

What is the first thing the body does to compensate when it needs more O2?

A

stimulates SNS - as CO falls, stretches and barrow receptors stimulate SNS to release catecholamine = causes sweating

increased HR and force of contraction (in children, just increase HR)

peripheral vasoconstriction = increase vasc. tone

decreased kidney perfusion triggers production of ADH, renin, and aldosterone = Na and water retention = increases blood volume for Preload = systemic and pulm venous engorgement

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19
Q

Cardiac reserve

A

how much reserve the heart muscle has
-poor cardiac reserve = the inability to increase cardiac output to meet the metabolic requirements during exercise

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20
Q

What happens when the heart hypertrophies?

A

less compliance because it doesn’t contract and produce stroke volume (only works to a point)

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21
Q

clinical manifestations of HF in impaired myocardial function

A

tachycardia, galloping rhythm
>160 bpm = earliest sign and is a direct result of SNS

at the slightest exertion, HR goes way up (stress, crying, feeding)

-infant tires easily, esp during feeding

-ventricular dilation and excess preload = extra heart sounds S3/4 gallop rhythm

-diaphoresis, irritability

-weight loss/poor weight gain, dev. delays (esp gross motor)

-frequent infections

-poor perfusion - cardiogenic shock
-cold extremities, weak pulses, slow cap refill, low BP, mottling, pallor/duskiness = OMINOUS SIGNS

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22
Q

clinical manifestations of HF in pulm congestion

A

tachypnea, nasal flaring, retractions, cough, crackles, wheezing, hoarseness
-cyanosis
-orthopnea - relieved by sitting up

-LATE sign: grunting/gasping resps

typically LEFT sided HF because BP and volume increase in the left atrium and backs up into lungs. capillary pressure is more = causes pulm edema

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23
Q

clinical manifestations of HF in systemic venous congestion

A

RIGHT sided HF

hepatomegaly
cardiomegaly
edema -
weight gain - periorbital, facial, sacrum, scrotal
ascites, pleural effusions

-distended neck and peripheral veins (usually noted in older children

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24
Q

When and what happens during the transition from fetal to pulm circulation?

A

occurs within a few hours after birth

completes 10-21 days post birth with permanent closure of ductus arteriosus

cord is cut which stimulates baby to breathe

foramen ovale - pressure decreases between 2 atria

Hemodynamic changes:
-increased pulm blood flow
-decreased pulm vasc resistance
-left atrium increases blood flow (from lungs thru pulm veins)

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25
Q

Hemodynamic changes in the heart chambers

A

-right atrial pressure falls

-increase pressure in left atrium

-higher O2 sat than in fetal circulation = stimulates closure of ductus arteriosus

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26
Q

What should you consider when taking the mother’s health, pregnancy, and birth hx?

A

-chronic health conditions (lupus, DM)
-medications (phenytoin)
-maternal alcohol or illicit drug use
-exposure to infections (rubella)
-infants with LBW dt IUGR
-high birth weight infants (infant of diabetic mother)

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27
Q

what shoulder you consider when taking the hx of an infant/young child?

A

-feeding difficulties dt fatigue, vomiting, rapid breathing, sweating w/ feeds, poor weight gain, developmental stage

-incidence of resp infections and breathing

-onset and frequency of colour changes (cyanosis that worsens with feeding/activity)

-parents feel baby’s heart race

-weak cry

-irritable

most comfortable person, HOB elevated, squatting

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28
Q

What should you consider when taking the hx of an older child?

A

exercise tolerance

presence of edema

resp problems, chest pain, palpitations

neurologic problems - fainting, headaches

recent infections or toxic exposures (ex. cardiomyopathy, rheumatic fever - they weaken heart valves)

*acquired heart disease usually comes from infections later in life

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29
Q

What should you consider when taking the health hx of ALL children?

A

review all other health problems

presence of other congenital anomalies

meds including OTC, herbal supplements

physical examination:
-general appearance - weak, irritable, in distress

Nutritional status:
-undernourished, underweight
-height below average

Size, shape, symmetry of chest
-retracts, heaves, or lifts
-enlargement over heart
-asymmetrical chest movement
-active precordium
-heart fluttering on chest dt possible patent ductus arteriosus
-point of maximum intensity (PMI)

Skin:
-pallor, cyanosis
-mucous membranes, sclera, palm, soles of feet
-clammy, sweating w/ feeding, activity
-scars from previous surgeries
-edema (RS HF) - sometimes periorbital in am, scrotal for males
-nail beds - cyanotic, clubbed

VS:
HR - tachy or brady
RR - increased even at rest? Laboured?
BP: HTN - difference in arms and legs?
BP normally higher in legs than arms
SBP 8-10 mmHg higher in RIGHT arm than in left may be significant dt coarctation of the aorta (narrowing after aortic arch)
Pulses: bounding

Heart auscultation:
-+- murmur. If present, not intensity, quality, timing, systolic/diastolic
-other: split sounds, gallops, rubs
-irregular rhythm

Lung auscultation:
-crackles, wheezing, grunting, decreased or absent breath sounds

Liver and splenic edges:
-palpation - RS HF

Tests for cardiac function:
-radiography -
CXR to check size
fluoroscopy
-ECG
-Echocardiogram - to see blood flow
-cardiac catheterization - go in thru femoral
-exercise stress test
-Cardiac MRI

30
Q

Congenital heart disease (CHD)

A

since birth
most common congenital anomaly

etiology (cause):
-90% unknown
-multifactorial- family hx, maternal factors, associated w/ chromosomal abnormalities, syndromes, or cong. defects in other body systems
-gene mapping research

-40% of children w/ down syndrome have a cardiac defect

31
Q

Hemodynamics

A

pressures generated by blood and pathways the blood takes through the heart and pulm system

blood flows from high to low pressure to the path of least resistance

32
Q

normally

A

pressure on right side is LOWER than left

resistance in pulm circulation is less than in systemic

33
Q

what happens when blood O2 saturations mix?

A

depending on defect, it can cause varying degrees of hypoxemia & cyanosis

34
Q

The 4 hemodynamic classifications

A

1) Decreased Pulm. Blood flow

2) Increased Pulm. Blood flow

3) Obstruction to Systemic Circulation

4) mixed blood flow

35
Q

which of the 4 classes are most vs least likely to cause cyanosis?

A

Most likely to cause cyanosis:
1)decreased pulm blood flow

Least likely to cause cyanosis:
2) increased pulm blood flow

36
Q

What happens in 1) decreased pulm blood flow

A

right to left shunt if septal defect is present dt right side pressure exceeds > left side pressure

little/no blood reaches the lungs to get oxygenated

cyanosis that does not respond to supp O2

37
Q

What happens in 2) increased pulm blood flow

A

left to right shunt

causes congestive HF

more blood flow to lungs -> vasoconstrict -> pulm HTN -> right vent. muscle hypertrophies to counteract the increased pulm vasc resistance

38
Q

What happens in 3) obstruction to systemic blood flow

A

increased pressure load on left ventricle -> decreased CO (shock)

obstruction to systemic blood flow = signs of poor CO, HF

39
Q

What happens in 4) mixed blood flow

A

saturated and desaturated blood mix within heart/great arteries = variable clinical picture

cyanosis

40
Q

causes of HF

A

volume overload

pressure overload

decreased contractility

high CO demands

41
Q

TX of HF

A

Goals of tx:
-improve cardiac function: increase contractility, decrease afterload

-remove accumulated fluid and sodium: decreased preload volume

-decreased CO demands

-improve tissue oxygenation and decrease O2 consumption

42
Q

nursing considerations for HF

A

Adx digitalis glycosides

Adx ACE inhibitors

Adx diuretics

nursing considerations for Digitalis glycosides (Digoxin):
-increases force of contraction
-decreases HR and slows conduction of impulses thru AV node
-indirectly enhances diuresis by improving renal perfusion

-loading does: are high, then go on maintenance doses, then check levels in blood

-check apical pulse before admin
-exact med calculations and measuring are critical = check decimal point because rare to give >1.0 ml
-observe for toxicity (bradycardia, anorexia, n&v)

discharge teaching:
-signs of toxicity - bradycardia, anorexia, n,v
-how to check pulse (not as important when on maintenance doses)
-signs of low HR
-know # for poison control
-know how to draw it up

43
Q

Nursing considerations for ACE inhibitors (-pril)

A

ACE inhibitors to improve cardiac function
by reducing afterload

-monitor BP before and after admin for hypotension

-monitor serum electrolytes (because drug blocks aldosterone and are potassium sparing)

-carefully assessing renal function

44
Q

Other drugs for HF

A

Beta-blockers: metoprolol, carvedilol

45
Q

Nursing considerations for decreasing cardiac demands

A

organize care to allow periods of rest

minimal handling

minimize unnecessary stress

maintain neutral thermal environment (NTE): modern incubators (problem is that there’s a possibility to miss fever to low temp when septic)

monitor temp

prevent skin breakdown from edema

prevent/tx infections promptly

46
Q

nursing considerations: managing resp distress

A

count RR full minute

position HOB elevated, sitting up

provide for unrestricted chest expansion
*infants are diaphragmatic breathers

supp O2

47
Q

maintaining nutritional status: nursing considerations

A

greater caloric needs but impaired ability to take in adequate calories

well rested before feeds, feed soon after awakening - to minimize crying which is energy expenditure

Q3h feeding schedule

allow no more than 30 min to complete feed with NG prn

increase caloric density of formulas by adding corn oil or MCT (medium chain triglycerides) oil to formula or HMF (human milk fortifier) to breast milk

if fully BF, then feeds can be on demand

no fluid restriction for babies = must increase caloric density

48
Q

Manage accumulation of fluid and Na: nursing considerations

A

Adx diuretics (give early in day, not at night or child will pee during night)

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 awake hours

possible sodium restriction

49
Q

Hypoxemia

A

PaO2 < normal

desaturated venous blood enters systemic circ w/o passing thru lungs

amount of o2 in the blood

normal PaO2 range: 80-100mmHg

3 types of defects that cause cyanosis:
1) category 1) decreased pulm blood flow aka Right to left shunting
ex tetralogy of fallot

2) category 4) mixing of arterial and venous blood within heart chambers
ex single ventricle

3) transposition of great arteries

50
Q

Know

-which of the 4 categories

-anatomy

-hemodynamics

-expected manifestations

A

x2, from different categories

51
Q

Category 1: decreased pulm blood flow

A

Tetralogy of Fallot

ANATOMY:

x4 abnormalities:
1. Pulmonic stenosis: valve doesn’t open all the way/narrow = less blood reaches lungs = increases backup pressure

  1. Right vent hypertrophy: because blood has to be pumped against resistance of stenotic valve
  2. Overriding aorta: moved forward, right in front of VSD. It also compresses pulm artery which is why there is pulm stenosis. O2 and deO2 blood enters aorta
  3. Ventricular septal defect VSD: hole between vents. blood shunts LEft to Right

L to R shunt

HEMODYNAMICS

overriding aorta and VSD allow deO2 to pass lungs and enter systemic circ

Less deO2 blood enters lungs dt pulm stenosis

“pink” tetralogy of fallot:
-no/minimal right vent outflow obstruction (RVOTO) w/ little aortic override. behaves like VSD and left-right shunt
SaO2100%

“blue” tetralogy of fallot:
-classic ToF has a degree of RVOTO and aortic override
-hypoxia

“profound cyanosis”
-severe or complete RVOTO
-increasing left to right shunting
-hypercyanotic spells!

Clinical manifestations of hypercyanotic spells:
-cyanosis
-pallor, poor perfusion
-increase rate and depth of resps
-increased HR
-agitation, irritability -> may lead to limpness or seizures

Tx: knee-chest position : instinctive. To decrease return of systemic venous blood to heart
-admin 100% O2
-give SC or IV morphine
-gegin IV fluid replacement and volume expansion prn
-repeat morphine

ToF Assessment:

-Tet spells
-cyanosis
-O2 admin
-systolic murmur in pulmonic area
-thrill may be palpated in pulmonic area

Interventions:

-prevent hypercyanotic spells
-prevent dehydration
-monitor CBC
-monitor for bleeding
-surgery

52
Q

Category 1) decreased pulm blood flow

A

Pulmonic Stenosis

ANATOMY

-narrowing of pulmonic valve or great artery above valve

-increases preload (vol in ventricle at end of diastole) = results in right vent hypertrophy dt heart working harder to pump blood thru obstruction

Neonates: with mod-severe stenosis, may dev a right-left shunt thru foramen ovale between atria => cyanosis

HEMODYNAMICS

-decrease blood flow to lungs = deO2 blood entering syst circ

MANIFESTATIONS

asymptomatic, dev normally

-moderate stenosis = dyspnea, fatigue on exertion

-signs of CHF

-loud systolic murmur and widely split S2 and thrill heard in pulmonic area
-murmur louder indicates increased severity

53
Q

Category 2) increased pulm blood flow

A

3 examples:

PDA Patent ductus arteriosus <3.1
ASD Atrial septal defect
VSD Ventricular septal defect

Left to right shunt

general characteristics:
-increased blood volume on right side increased pulm blood flow at expense of systemic circulation

54
Q

PDA - Patent Ductus Arteriosus <3.1

Cat 2) increased pulm blood flow

left-right

A

ANATOMY

Because of the physiologic effects of prematurity like resp distress syndrome and hypoxia, the ductus arteriosus is prevented from closing naturally

When pulm circulation is established and systemic resistance increases at birth, pressures in the aorta become greater than in the pulm arteries. Aorta pressure> pulm arteries
blood is then shunted from aorta to pulm arteries thru the PDA= increasing blood flow to pulm system

compensation: pulm vasoconstriction = try to control blood flow increase BUT this makes it harder for right ventricle to pump against resistance

HEMODYNAMICS

Oxygenated blood from aorta shunts thru PDA into pulm arteries, creating a mix of saturated and unsaturated blood going into lungs

CLINICAL MANIFESTATIONS

-dyspnea, tachypnea, tachycardia
-symps associated w/ edema and CHF
bounding pulses
hepatomegaly, poor growth if PDA is large
-“machinery” murmur during sys&diastole
-active prercordium
-risk for frequent resp infections and pneumonia dt moist environment
-no cyanosis
-hypotension with low CO
-intercostal retractions

55
Q

ASD - Atrial septal defect

category 2) increased pulm blood flow

left to right

A

ANATOMY

-opening in atrial septum allows left to right shunt

-can be small (foramen ovale fails to close) or large opening (septum completely absent)

HEMODYNAMICS

-oxygenated blood goes back into right atrium

-causes pulm constriction and build up of pressure on right side -> RS HF

-less O2 blood in systemic circ

CLINICAL MANIFESTATIONS

happens in 40s. Asymptomatic til adulthood
small enough hole = no major surgery

-large ASD = CHF
-easy tiring
-poor growth
-soft ejection murmur in pulmonic area with fixed wide splitting of S2 through all phases of respiration

56
Q

VSD - ventricular septal defect

Cat 2) increased pulm blood flow

left to right shunt

A

ANATOMY

-opening in vent septum results in increased pulm blood flow

-can occur in any area of septum

HEMODYNAMICS

oxygenated blood enters from left vent to right vent dt greater pressure in left side

-mixed blood from right vent enters pulm arteries = this extra blood being pumped into the lungs forces the heart and lungs to work harder.

CLINICAL MANIFESTATIONS

-infants and children may have no symptoms

-murmur - systolic murmur at 3rd or 4th LICS at sternal border

-thrill

-no cyanosis

-moderate and large VSD’s = CHF
tachypnea, dyspnea, poor growth

-increased pulm infections and pulm HTN

57
Q

Category 3) defects that obstruct systemic blood flow

A

examples:

Coarctation of the aorta

Aortic stenosis

Hypoplastic left heart syndrome

general patho:

-blood existing heart meets area of anatomic stenosis causing obstruction to blood flow

PRESSURES:

-increased pressure in ventricle and greater artery BEFORE obstruction

&
-decreased pressure in area AFTER obstruction

58
Q

Coarctation of the aorta

Cat 3) Defects that obstruct systemic blood flow

A

ANATOMY

-narrowing or constriction of descending aorta, often dear ductus arteriosus OR left subclavian artery = obstructs systemic blood outflow

1st brachiocephalic/right subclavian/right common carotid artery
2nd left common carotid artery
3rd left subclavian artery

HEMODYNAMICS

-Increase pressure load on left ventricle because blood is backing up at the top of the aorta and not making it all the way thru

-increased pressure going into head and upper extremities

CLINICAL MANIFESTATIONS

-bounding pulses on upper extremities and weak/absent pulses on lower extremities

-differences in BP: Increase BP in upper , decreased BP in lower

-nose bleeds

-worse case: aorta ruptures

-older children may complain of weakness, pain in legs after exercise

-children usually asymptomatic and grow normally

*nursing considerations when taking BP for pt w/ coarctation of the aorta:
-take BP in all 4 limbs

59
Q

Aortic Stenosis

Cat 3) Defects that obstruct systemic blood flow

A

ANATOMY

-narrowing of aortic valve = obstructs blood flow to systemic circulation

-narrowing may be sub valvular, @ the valve, or supra valvular

-defect associated often w/ bicuspid (2 valve leaflets) rather than normal tricuspid valve

-pressure gradient across valve usually increases during periods of rapid growth w/ associated increase CO dt valve does not grow at comparable rate

-left vent hypertrophies to force blood pasta narrowed valve opening -> may progress to left vent failure

HEMODYNAMICS

-decreased oxygenation blood flow to peripheries

CLINICAL MANIFESTATIONS

-most infants/young children asymptomatic and develop normally

-CHF

-BP normal but narrow pulse

-weak peripheral pulses

-fainting, dizziness

-chest pain & dyspnea after exercise

-systolic murmur and thrill

-ejection click

-splitting of S2 with severe stenosis

-high pitched diastolic decrescendo murmur along left sternal border near mitral valve

60
Q

Cat 4) Mixed blood

A

examples:

TGA - transposition of the great arteries <3.2

Truncus arteriosus

61
Q

TGA - transposition of the great arteries <3.2

Category 4) mixed blood

Blue color of the skin (cyanosis)
Shortness of breath
Weak pulse
Lack of appetite
Poor weight gain

A

ANATOMY

-Aorta and the pulm artery are switched

-Aorta connected to right ventricle and sends deO2 blood to head and extremities w/o going to the pulm circ

-Pulm artery is connected to left ventricle

HEMODYNAMICS

-aorta connected to right ventricle: blue blood from body enters right atrium/ventricle and goes into aorta and to systemic circ

Pulm artery connected to left ventricle: red blood goes from pulm artery into ductus arteriosus to systemic circ

-MIXED blood as red O2 blood enters patent ductus arteriosus to systemic circ

-patent foramen ovale or atrial septal defect) between the two collecting chambers (atria) of the heart -this allows some mixing to occur. After birth, the hole and the duct tend to shut off. Keeping them open is the first step in the treatment of this condition.

CLINICAL MANIFESTATIONS

-Polycythemia )increased RBC
risk for thromboembolism (blood becomes thick and RBC’s clump)

-Clubbing - dt chronic tissue hypoxemia and polycythemia

-CNS injury
increased risk for stroke, meningitis, brain abscess

-Dehydration - hemoconcentration

-Hematologic abnormalities like thrombocytopenia (lack platelets) = prolonged clotting time

-Bacterial endocarditis

-fatigue w/ feeding poor weight gain, tachypnea, dyspnea on exertion, poor exercise tolerance

-Squatting: hypercyanotic spells -blue spells or “tet” spells

Blue color of the skin (cyanosis)
Shortness of breath
Weak pulse
Lack of appetite
Poor weight gain

62
Q

Truncus arteriosus

Cat 4) mixed blood

A

ANATOMY

-a single trunk empties both ventricles and provides blood flow to pulm, systemic, and coronary circs

  • fails to separate completely during development, leaving a connection between the aorta and pulmonary artery

-VSD usually present

HEMODYNAMICS

-blue blood from right side and red blood from left side mix then divide into lungs and systemic circ

CLINICAL MANIFESTATIONS

-cyanosis soon after birth
*cyanosis also a manifestation of decreased pulm blood flow cat 1)

-CHF develops within 2 weeks after birth w/ signs of:
-tachypnea, dyspnea, retractions
-fatigue, poor feeding, poor growth
-polycythemia
-clubbing
-increasaed pulse pressure
-widened pulse pressure (diff. between sys
and diastolic BP)
-frequent resp infections

-VSD produces harsh systolic murmur in lower sternal border

-systolic click may be auscultated in apex and pulmonic area

63
Q

Acquired Heart Disease

A

x4

  1. Rheumatic Fever
  2. Bacterial infective Endocarditis
  3. Kawasaki Disease
  4. MIS-C
64
Q
  1. Rheumatic Fever
A

follows strept throat (pharyngitis) group beta-hemolytic streptococci
may lead to permanent heart valve damage

65
Q
  1. Bacterial (infective) Endocarditis
A

inflammation of lining, valves and arterial vessels

streptococcus or staphylococcus

-prevention w/ prophylactic antibiotics before dental procedures

66
Q
  1. Kawasaki Disease
A

-unique disease to children

-acute systemic inflammatory disease of small& medium-sized blood vessels
-coronary arteries are most susceptible. May lead to dilation of coronary arteries and aneurysm formation

-Mucocutaneous Lymph Node syndrome

-etiology unknown

-primary cause thought to be infection with organism or toxin but not spread person to person

-hospital admissions late winter, early spring

Dx:

Fever for at least 5 days and unresponsive to antipyretics and antibiotics

must have 4 of the following:
-erythema and edema of hands and soles of feet

-peeling of hands and feet in 2-3rd wk

-both eyes inflamed w/o drainage (difference: pink eye has exudate)

-polymorphous rash

-strawberry tongue, dry cracked lips

-swollen lymph nodes

tests: CPR for inflammation markers
ESR, Echo

Sed rate, or erythrocyte sedimentation rate (ESR), is a blood test that can reveal inflammatory activity in your body. A sed rate test isn’t a stand-alone diagnostic tool, but it can help your doctor diagnose or monitor the progress of an inflammatory disease.

When your blood is placed in a tall, thin tube, red blood cells (erythrocytes) gradually settle to the bottom. Inflammation can cause the cells to clump. Because these clumps are denser than individual cells, they settle to the bottom more quickly.

67
Q

Stages of Kawasaki Disease

A

Acute stage:
-5+ days
-fever
-strawberry tongue
-edema hands/feet
-enlarged cervical lymph nodes
-irritable
-conjuctival hyperemia

Subacute stage:
-cracking lips
-desquamation of skin on fingertips, toes
-joint pain
-irritability continues

Convalescent stage:
-appears normal but lingering signs of inflammation
-ESR remains increased even after symptoms are gone
-6-8wks after onset, all blood values return to normal

severe: cardiac involvement like MI

68
Q

Kawasaki Tx

A

Tx:

IVIG - immunoglobulin to reduce fever, inflamm

Aspirin. Usually, aspirin is not recommended for kids dt risk of Ryes syndrome but this is the only time Aspirin is given to kids because in Kawasaki disease, it actually responds to Aspirin
(salicylates- reduce fever )

Nursing care:
-asses for edema, eye pain, redness in mouth, rashes, desquamation, fluid balance, heart sounds, temperature, Side effect of Aspirin - GI upset and bleeding

-ROM

-discharge teaching for aspirin, cardiac follow-up

69
Q
  1. MIS-C. Multi-System Inflammatory Syndrome in Children
A

reportable condition

associated with covid 19

-presents with fever, lab evidence of inflammation, evidence of severe illnesses requiring hospitalization with multisystem >2 organ involvement (cardiac, renal, resp, hematologic, GI, dermatologic, or neurological) AND
no alternative plausible dx
AND
positive antigen or serology for recent SARS - CoV 2 infection OR covid-19 exposure within 3 wks prior to onset of symptoms

pt presentation:

systemic inflammation:
-tachycardia, hypotension, hypo or hypoperfusion, lymphadenitis

Mucocutaneous:
-rash, lip cracking, strawberry tongue, extremity swelling, conjunctivitis, blisters

GI:
-n,v, d, abd pain

Cardiopulmonary:
-resp distress, chest pain

Neurologic:
-headache, altered mental status, meningismus, focal deficits, seizure

Management:

-isolation

-close VS monitoring for stability

-dx testing- blood, EKG, CXR, Echo, septic work up

Meds - IVIG, steroids, Aspirrin

Antibiotics- until infection ruled out

Anticoagulation therapy

Discharge and follow-up:

Discharge criteria:
-no fever for 48 hrs without antipyretics
-improvement of presenting symptoms
-improvement in lab markers
-influenza vaccine

follow up:
-with pediatrician or family doc within 1 week of discharge
-cardiology - repeat Echo in 2 weeks
-follow up with rheumatology, immunology, neuro, GI services as needed

Return to ED if:
-fever >38
-recurrence of presenting symptoms or unwell with other symptoms
-resp distress or SOB

70
Q

jeoprody:

heart defect episode with limpness, resp distress, ___.

A

TET spell or hypercyanotic spell

put them in knee to chest position

71
Q

DIGOXIN TOXICITY

A

signs of digoxin toxicity:
-bradycardia
-GI upset
-visual disturbances

bradycardia, anorexia, n,v

n342 peds (13 decks)

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