Pediatric Enhancement: Fundamentals of Pediatric Cardiology Flashcards
Tools for Evaluation of the Pediatric Cardiovascular System
•History •Physical •Routine studies: –EKG –CXR •Studies for the cardiac patient: –cardiac cath –echocardiogram
Perinatal infections account for 2% to 3%
of all congenital anomalies
TORCH:
–are some of the most common infections associated with congenital anomalies (a lot of eye and skin findings in common) including cardiac defects
–Most of the TORCH infections cause mild maternal morbidity, but have serious fetal consequences
–Toxoplasmosis
–Other (syphilis, varicella-zoster, parvovirus B19, HIV)
–Rubella(think “bluebella”)
»congenital rubella syndrome includes cardiacmanifestations: PDA, PS
–Cytomegalovirus(CMV)
–HSV
–Again, they can have really serious fetal consequences, or fetal loss
Coxsackievirus B, CMV, HSV
»In early pregnancy are teratogenic; later in pregnancy may cause myocarditis
»Active HSV lesions at time of delivery is an indication for cesarean section
PRENATAL exposures (cont’d)
Meds
•Amphetamines >VSD, PDA, ASD, TGA
•Anticonvulsants
–hydantoin: PS, AS, coarc, PDA
–trimethadione: TGA, TOF, hypoplasticleft heart
•Alcohol >FAS: in which VSD, PDA, ASD, and TOF are common
prenatal exposures
maternal condition
–Of course, maternal congenital heart disease: increases risk of CHD from 1% to 15%.
–Infant of diabetic mothers (IDM):
•cardiomyopathy, TGA, VSD, PDA
•Also hypoglycemia, hypocalcemia, polycythemia, LGA (large for gestational age)or SGA (small for gestational age)
–Maternallupus/mixed connective tissue disease: congenital heart block
POSTNATAL history
(they may be presenting with these as chief complaints): –Poor growth (aka FTT = failure to thrive) –Poor feeding (secondary to fatigue and dyspnea) –Tachypnea –Cyanosis –Dyspnea, puffy eyelids –Frequent respinfections –Exercise intolerance –Murmur –Chest pain –Palpitations –Joint symptoms –Neuro symptoms
*Buzz words of presentation:
infant who presents with diaphoresis and tachypnea with feeding, cyanosis, FTT (feeding is all they do = exertional symptoms)
Family history
–Hereditary disease
–Congenital heart disease
–Rheumatic fever
*•Frequently occurs in more than one family member: higher incidence among relatives of rheumatic children, unknown genetic component
–Hypertension, atherosclerosis
Physical Exam
•General: well nourished, well developed “WN/WD”
–“Abnormal facies?” implies chromosomal syndrome
–Examples of syndromes with cardiac manifestations:
•Cornelia de Lange (thick eyebrows, distinct facial features): VSD, ASD
•CHARGE: Coloboma, Heart defects, choanal Atresia, growth/mental Retardation, GU anomalies and genital hypoplasia, Ear anomlies
–conotruncal anomalies (truncus, TOF)
–aortic arch anomalies
•Holt Oram(cardiac-limb): defects or absence of thumb or radius
–ASD
–VSD
- Color (keep in mind the newborn always has acrocyanosis!)
- Clubbing
- Pectus excavatum: rarely causes cardiac disease
CHARGE
Coloboma, Heart defects, choanal Atresia, growth/mental Retardation, GU anomalies and genital hypoplasia, Ear anomlies
–conotruncal anomalies (truncus, TOF)
–aortic arch anomalies
Coloboma
normal tissue in or around the eye is missing from birth
Choanal atresia
blue but pink when cry, try to pass catheter
Cornelia de Lange
Cornelia de Lange (thick eyebrows, distinct facial features): VSD, ASD
Holt Oram
Holt Oram(cardiac-limb): defects or absence of thumb or radius
–ASD
–VSD
*BP norms are based
on age, gender, and height percentile
*wide and fixed split S2 is
abnormal
Murmurs
•Remember to think about murmurs in terms of:
–Timing (systolic or diastolic)
–Intensity (grade I-VI)
–Quality (musical, harsh, high or low pitched)
- Not present in many severe forms of CHD, such as tricuspid atresia, coarctation of the aorta and transposition of the great vessels.
- When a murmur is associated with a cardiac defect, the intensity of the murmur is unrelated to the severity of the abnormality.
- However, murmur type, along with other heart sounds, is useful in differentiating mild defects from severe abnormalities
Innocent Murmurs
- in children, physiologic murmurs are more common than in adults
- •Low pitched (non-turbulent, not high velocity)
- Still’s: low-pitched sounds heard at the lower left sternal area, “musical.” These most commonly occur between age 3 and adolescence. Low pitched -best heard with the bell of the stethoscope. Can change with position alteration and then can decrease or disappear with the Valsalva maneuver. No clicks are present.
- venous hum: low-pitched continuous murmurs made by blood returning from the great veins to the heart -bell
- pulmonary flow murmur:upper left sternal border. High pitched -best heard with the diaphragm. Also known as benign peripheral pulmonary stenosisof the newborn. Also seen in adolescents or in children with pectus excavatum. Prominent in high-flow situations, such as when a child has a fever or is anemic.
*suspicious murmurs
all of it was in red
- high-pitched
- harsh
- S1 coincident (holosystolic)
- diastolic murmurs
Still’s
low-pitched sounds heard at the lower left sternal area, “musical.” These most commonly occur between age 3 and adolescence. Low pitched -best heard with the bell of the stethoscope. Can change with position alteration and then can decrease or disappear with the Valsalva maneuver. No clicks are present.
Associated ejection clickalong with a high intensity murmur?
stenotic valve
Transient systolic murmur in first hours after birth
Closing pda
The Seven S’s: Key Features of Innocent Murmurs
- Sensitive (changes with child’s position or with respiration)
- Short duration (not holosystolic)
- Single (no associated clicks or gallops)
- Small (murmur limited to a small area and nonradiating)
- Soft (low amplitude)
- Sweet (not harsh sounding)
- Systolic (occurs during and is limited to systole)
Pulses
–Differences between upper and lower? coarctation of the aorta
–Differences between right upper and left upper? coarctation of the aorta proximal to or near the origin of left SC artery, or supravalvular AS
–Bounding? PDA, AR, AVF, rarely persistent truncus
EKG*
–Right ventricular dominancein newborns
–Manifested by right axis deviation
–Several interval lengths vary with age
CXR
–Large thymus! sail sign
–Film during expiration affects view of the heart shadow
Thymic Shadow
An important feature to recognize in the pediatric chest is the normal thymic tissue in the anterior mediastinum. Normal thymic tissue, as demonstrated on this image, should not be confused with a mediastinal or pulmonary mass. This is known as the “sail sign.”
Studies for the cardiac patient: echocardiogram
–Echocardiogram
•Basic principles:
–M mode technique uses one US beam passing through heart in a single axis to measure wall/chambers
–2D: transducer beam through a number of cross-sectional planes; four transducer locations
- Transesophageal echocardiogram (TEE): great to visualize valves
- Doppler flow:combines structure and blood flow
- fetal echo
Perinatal and Neonatal Circulation
•Four shunts in fetal circulation –Placenta –Ductus venosus –Foramen ovale –Ductus arteriosus •Changes at birth –Interruption of umbilical cord flow: •Increased SVR with removal of the low resistance placenta. •Closure of the ductus venosus because of lack of blood return from the placenta –Lung expansion •Decreased PVR, increased PBF, fall in PA pressure •Functional closure of foramen ovale •Closure of PDA
Cardiac defects in Genetic Disorders and Nonhereditary Syndromes
–Down:endocardial cushion defect, VSD –Turner:coarc, AS, ASD –Noonan:PS, ASD, AVSD (partial), coarc, HCM –Williams: SVAS –Marfansyndrome –FAS:VSD, PDA, ASD, TOF –Rubella –DiGeorge: interrupted aortic arch, truncus arteriosus, VSD, PDA, TOF
Down*
endocardial cushion defect, VSD
Turner*
coarc, AS, ASD
Noonan*
PS, ASD, AVSD (partial), coarc, HCM
FAS*
VSD, PDA, ASD, TOF
Congenital Heart Defects
•Present in nearly 1% of―or about 40,000―births per year
•VSD is the most common
•25% of babies with a CHD have a critical CHD. Infants with critical CHDs generally need surgery or other procedures in their first year of life.
•Infant deaths due to CHDs often occur when the baby is less than 28 days old(the neonatal period). In a study of neonatal deaths, 4.2% of all neonatal deaths were due to a CHD –one of leading causes of neonatal death secondary to birth defects.
•About 75% of babies born with a critical CHD are expected to survive to one year of age. About 69% of babies born with critical CHDs are expected to survive to 18 years of age
•Basic categories:
–Acyanotic (left to right)
–Cyanotic (the T’s)
–Malpositions
–Obstructive and valvular disease
Most common congenital heart defect*
VSD
Basic Categories of congenital heart defects*
–Acyanotic (left to right)
–Cyanotic (the T’s)
–Malpositions
–Obstructive and valvular disease
Left to Right Congenital Heart Diseaseaka acyanotic
ASD
VSD
PDA
endocardial cushion defects
Partial TAPVR
ASD
–Often asymptomatic; 87% of secundumtypes close by age 4.
–Primary and sinus types require surgery.
–Late sequelae include mitral valve prolapse, atrial fibrillation or flutter, and pulmonary hypertension
VSD
–Size of defect dictates hemodynamic presentation.
Cardiomegaly in moderate to large VSDs
–In 30 to 40% of cases, spontaneous closure occurs within the first 6 months
–Surgical repair required if infant exhibits failure to thrive, pulmonary hypertension, or right-to-left shunt > 2:1
PDA
–In premature infants, spontaneous closure or indomethacin-induced closure may occur.
–In term infants, spontaneous closure is less likely, and indomethacin is not helpful.
•Surgical ligation usually required. No long-term sequelae if adequately treated
Endocardial cushion defects
–Combination of the primum type of atrial septal defect, ventricular septal defect and common atrioventricular valve.
–Presentation similar to that of ventricular septal defect.
–Palliative pulmonary artery banding in refractory congestive heart failure.
Cyanotic Congenital Heart Disease
*Presentation>is it always obvious cyanosis at birth?
whole slide*
–No; many will do fine and then develop s/sx of excessive pulmonary blood flow and heart failure after PVR decreases (after newborn period)
–Sometimes ductal patency may persist for weeks (even months) constriction and closure of ductus cause decreased systemic blood flow, oliguria, acidosis, pulmonary edema, and heart failure can lead to ischemia and ventricular dysfunction and death.
–Clinical presentation of left heart obstructive disease may mimic sepsis
•Tachypnea, mottled gray skin, poor perfusion, decreased pulses
•Clinical clues that are critical are gallop rhythm and hepatomegaly or cardiomegaly
Cyanotic Congenital Heart Disease
•5 T’s: –Tetralogy of Fallot: “Tet spells” in infancy –Transposition of the Great Arteries –TAPVR –Truncus arteriosus –Tricuspid Atresia
- Hypoplastic Left Heart
- Ebstein Anomaly (right sided heart abnormality)
- Pulmonary Atresia
- Single ventricle
- Double Outlet Right Ventricle
Transposition of Great Vessels*
**TGV is associated with severe cyanosis in the first hours after birth (in other words, TGV is the mostly likely diagnosis in a severely cyanotic neonate who is just a few hours old)
Transposition of Great Vessels
- Ductus-dependent lesion (no mixing!)
- Consider palliative balloon atrial septostomy, but definitive surgical switch of aorta and pulmonary artery required as soon as possible.
- Late complications include pulmonary stenosis, mitral regurgitation, aortic stenosis, coronary artery obstruction, ventricular dysfunction and arrhythmias.
Tetralogy of Fallot
1.VSD
2. Overriding aorta
3. RV outflow obstruction
4. RV hypertrophy
•Think of it as an Aortic Takeover!
•Most common cyanotic CHD beyond infancy.
•Intermittent episodes of hyperpnea, irritability, cyanosis with decreased intensity of murmur
•Palliative shunting may be necessary
•Surgical repair required before age 4
TOF xray
boot shaped heart (sometimes seen in tricuspid atresia –EKG will differentiate)
Egg shaped heart (”egg on a string” = narrow mediastinum)
TGA
snowman
tapvr
coarctation of aorta
rib notching
Malpositions
- Situs Inversus
- Vascular Rings and Slings
- Anomalous Origin of Left Coronary Artery
Pulmonic stenosis
–May be asymptomatic or may result in severe congestive heart failure. Prostaglandin E1 infusion at birth may be helpful. Valvular type may require balloon valvuloplasty.
Obstructive and valvular disease
Pulmonic stenosis
Peripheral pulmonic branch stenosis
Aortic disease
Mitral valve stenosis, prolapse, and regurgitation
Mitral valve stenosis, prolapse, and regurgitation
Tricuspid Stenosis
Aortic disease
–Stenosis (may be asymptomatic. Valve replacement and anticoagulation may be required)
–Aortic regurgitation
–Supravalvular aortic stenosis
–*Coarctation of the aorta
•98% of cases occur at origin of left subclavian artery.
•Blood pressure higher in arms than legs, bounding pulses in arms,
•Surgical repair usually required between 2 and 4 years of age.
–Hypoplasia
Coarctation of the Aorta*
- While the presentation in the first year of life can be rather dramatic (heart failure, circulatory collapse, death), later in life the presentation can be more insidious and can go overlooked or underappreciated. Late presentation (with HTN or murmur) is because of less obstruction and good collateral blood flow.
- (1)Systolic murmur (often conducted to back)
- (2)Weak or absent femoral pulses (radio-femoral delay in older patients)
- (3)Upper limb hypertension
- (4)Exercise intolerance
- (5)Leg claudication
Acquired heart disease
- Disorders of Myocardium: cardiomyopathy, myocarditis
- Kawasaki
- Rheumatic Heart Disease
- Endocarditis
- Pericardial disease
Myocarditis*
–Inflammation of myocardial tissue
–*Etiology: viral
•Coxsackievirus, echovirus, poliomyelitis, mumps, rubella, CMV, HIV, arbovirus, adenovirus, influenza
–Sxs: nonspecific and inconsistent, depends on severity of disease
•Anorexia
•Lethargy
•Emesis
•Lightheadedness
•Cool extremities
•SOB
Myocarditis Diagnosis*
–EKG: low voltage throughout, *ST changes, prolonged QT, arrhythmias (premature contractions, AV block)
–CXR
•Variable cardiomegaly and pulmonary edema
–Echo findings
•Enlargement of heart chambers, impaired LV function
–Labwork:
* •PCR:used to find the viral genome in myocardial cells; it is rapid and sensitive, and it may become the test of choice for the diagnosis of viral myocarditis
–Treatment
•Bedrest, diuretics, inotropes. Digoxin, gamma globulin, ACEI, possible steroids, heart transplant.
*•IVIGhas been associated with improved left ventricular function and improved survival, though still controversial
Cardiomyopathy dilated*
Dilated:
•20-50% familial
•Acquired: often viral illness triggers myocarditis that leads to dilated cardiomyopathy
cardiomyopathy hypertrophic*
Hypertrophic (HCM)
•*Autosomal dominant genetic disorder that has a variable presentation and carries a high incidence of sudden death.
•myocardial hypertrophy that is inappropriate and often asymmetrical and that occurs in the absence of an obvious inciting hypertrophic stimulus
Kawasaki diagnostic criteria*
–High fever for FIVEdays
PLUS*
–At least FOUR of the following (head to toe):
- Bilateral bulbar *conjunctival injection, without exudate
- Erythematous mouth and pharynx, *strawberry tongue, and/or red, cracked lips
- *Cervical lymphadenopathy(> 1.5 cm in diameter), usually single and unilateral
- Polymorphous exanthem(morbilliform, maculopapular, or scarlatiniform)
- *Swelling of hands and feetwith erythema of palms and soles
–Infants can have atypical presentation
Kawasaki other findings
•Etiology unknown •Other clinical findings irritability, abdominal pain, V/D, anterior uveitis (80%), arthritis/arthralgias, aseptic meningitis, pericardial effusion or arrhythmias, gallbladder hydrops, carditis, perineal rash with desquamation •Lab findings –Leukocytosis with left shift –Elevated CRP or ESR –Thrombocytosis (after first week, peaking at 2 weeks) –Normocytic/normochromic anemia –Sterile pyuria (70%) –Increased LFTs (40%)
Kawasaki cont’d*
•Why are we talking about this in pediatric cardiology??
•CV complications!
–If untreated, *15-25% develop coronary artery aneurysmsand dilatation (peak prevalence 2-4 wks post onset of disease) and are at risk for coronary thrombosis acutely and coronary stenosis chronically
–Carditis, valvular regurgitation (AR, MR, and TR)
- Management: IVIG and ASA
- Follow up long term
rule out kawasakis it is most likely
adenovirus
Kawasaki is also known as
mucocutaneous lymph node syndrome
Rheumatic Heart Disease
- Up to 39% of patients with acute rheumatic fever may develop varying degrees of pancarditis with associated valve insufficiency, heart failure, pericarditis, and even death.
- With chronic rheumatic heart disease, patients develop valve stenosis with varying degrees of regurgitation, atrial dilation, arrhythmias, and ventricular dysfunction.
- Chronic rheumatic heart disease remains the leading cause of mitral valve stenosis and valve replacement in adults in the United States.
Endocarditis
- Sticky valves, wimpy bugs
* Smooth valves, sticky bugs
Pericardial disease
- Pericarditis
- Pericardial effusion
- Tamponade
- Constrictive pericarditis
- Postpericardiotomy
Other cardiac issues in pediatrics
- HTN
- Arrhythmias (prolonged QT, SVT)
- Pulmonary Hypertension
- Syncope
- Chest pain in children (cardiac vs noncardiac)
- Sports PE screening
Hypertension in pediatric patients*
•Obesity is a strong risk factor for developing childhood hypertension
•Before puberty –secondary cause of HTN
–**The younger the child and the higher the BP, the more likely it is a secondary to an identifiable cause (such as renal disease)
•After puberty –likely essential HTN (primary cause)
Arrhythmias*
•*Less common in children than in adults
•Conduction abnormalities
–*prolonged QT: disorder of myocardial repolarization characterized by prolongation of QT interval on the electrocardiogram and an increased risk of sudden death (due to the potential to degenerate into polymorphic ventricular tachycardia)
Sinus tachycardia
–Compatible history consistent with known cause
–P waves present and normal
–Variable R-R with constant PR
–Infants HR
SVT
–Compatible history –(vague, nonspecific, h/o abrupt rate change) –P waves absent or abnormal –HR not variable with activity –Infants HR >220 –Children HR >180
Syncope
•DDx –Noncardiac •Vasovagal (fear, anxiety, prolonged standing) •Hypovolemia –Cardiac •Arrhythmia •HCM •Evaluation? –History –Orthostatic BP/P (“Tilt” test) –EKG
Chest pain in children
noncardiac problems*
*(much more common than cardiac etiology)!
–Musculoskeletal etiology very common
•Costochondritis
•Tietze syndrome (recent URI) –similar to costochondritis but often a single joint with associated warmth, swelling, tenderness
•Nonspecific
•Slipping rib syndrome
•Trauma, strain
•Precordial catch (Texidor twinge): posture or pinched nerve related
•Xiphodynia (reproducible)
–GI (GERD)
–Psychogenic (anxiety)
–Zoster (superficial pain
–before lesions appear)
–Spinal cord/nerve root compression in conjunction with scoliosis
pain out of porpotion is
zoster or necrotizing fasciitis
Costochondritis
number 1 diff for kids with chest pain found on palpation
Chest pain in children
Cardiac causes
Inflammatory
Increased myocardial demand or decreased supply
cardiomyopathy
LVOT
Arrhythmias
Coronary artery abnormalities
Miscellaneous Aortic dissection Rupture of aortic aneurysm Pulmonary HTN MVP Atrial myxomas Cardiac device/stent complications
Drugs
Cocaine
Overdose of sympathomimetics
Chest Pain
•When to refer?*
–Abnormal cardiac findings –*Exertional chest pain –*Exertional syncope –Chest pain with palpitations –EKG abnormalities –*Significant family historyof arrhythmias, sudden death, or genetic disorders –Heart transplant –h/o Kawasaki –First degree relative with familial hypercholesterolemia
Sports PE screening
Refer for*:
•*Family h/o early sudden death
–Cardiac, seizure, one car accident, unknown (could be arythymia
- *Murmurs (HCM)
- *Marfan’s stigmata
- Simultaneous palpation of radial and femoral pulses (undiagnosed coarc) reveals unequal pulses
- *Other PE findings consistent with cardiac disease
Palliative systemic to pulmonary artery shunts*
use of systemic arterial flow to increase pulmonary blood flow in cardiac lesions with impaired pulmonary perfusion (TOF, hypoplastic right heart, TA, PS)
Blalock-Taussig shunt*
Palliative cava to pulmonary artery shunts: use of systemic venous flow to increase pulmonary blood flow, usually in older children with lower PVR, as an intermediate step to Fontan: Glen
Fontan*
anastomosis of SVC to RPA (Glenn shunt), and anastomosis of RA and/or IVC to pulmonary arteries, separates systemic and pulmonary circulations when there is a functionally single ventricle
norwood*
repair of hypoplastic left heart, also 2 stages
Special Considerations: recent cath or cardiac surgery
- Embolization or compression of adjacent structures
- Can have MI
- Fever and chest pain worse when supine: postpericardiotomy syndrome
You are seeing a 3 day old infant in the emergency department.
CC: “She has not been feeding well since we took her home from the hospital, and I think she is breathing faster.”
Preliminary DDx?
Tip:
You can ask mom to feed the baby during encounter.
OB history –33 year old G1P1001 –good PNC throughout pregnancy –All prenatal labs unremarkable; GBS negative, no infections in pregnancy –Induced vaginal delivery at 41 weeks –APGARS 8/9 –Hep B received in NBN
Family hx: no congenital heart disease or early childhood deaths, no seizure disorders, no genetic syndromes •Social hx: –Diet as in HPI –Sleep –Who lives at home? –Any pets or smokers? –Any daycare? •ROS
Family hx: no congenital heart disease or early childhood deaths, no seizure disorders, no genetic syndromes •Social hx: –Diet as in HPI –Sleep –Who lives at home? –Any pets or smokers? –Any daycare? •ROS
•Coarctation of the aorta (corrected –previously an error here)
–Admit
–Consult pediatric cardiology, pediatric surgery
–Treatment of early presentation: surgery or balloon angioplasty
mona
morhine oxygen nitroglycerin and aspirin for mi
Causes of altered mental status in a neonate
- T–Trauma (nonaccidental and accidental)
- H–Heart disease andhypovolemia
- E–Endocrine (eg, congenital adrenal hyperplasia and thyrotoxicosis)
- M–Metabolic (electrolyte imbalance)
- I–Inborn errors of metabolism
- S–Sepsis (eg, meningitis, pneumonia, and urinary tract infection)
- F–Formula mishaps (eg, under-or overdilution)
- I–Intestinal catastrophes (eg, volvulus, intussusception, and
- necrotizing enterocolitis)
- T–Toxins and poisons
- S–Seizures
15 year old female athlete presents to you with syncope.
•Preliminary DDx?
- She was out on the soccer field and fainted while playing. Team members helped her to the ground.
- No known head injuries.
- Quickly returned to consciousness.
- She recalls sudden chest pain and dizziness before fainting.
- PMH is unremarkable
- General -WN/WD, healthy appearing teen in NAD
- Skin -pink
- HEENT -clear
- Lungs -CTAB
- Heart -ejection click with grade III/VI SEM at base of heart and RUSB, radiation to both carotid arteries.
- Abdomen soft, no organomegaly
- Extremities no c/c/e
- Neuro –alert, CNs 2-12 intact, strength 5/5 in all major muscle groups, DTRs 2/4 in all extremities, sensation intact in all extremities, cerebellar function intact to RAM, Romberg neg (aka: normal)
•EKG:
–Left ventricular hypertrophy and ST segment depression in left precordial leads suggestive of strain pattern caused by transient left ventricular subendocardial ischemia
•Echocardiogram
–Bicuspid aortic valve with moderate to severe aortic stenosis and LVH
- Adrenal Insufficiency and Adrenal Crisis
- Aneurysm, Abdominal
- Aortic Stenosis
- Asystole
- Atrial Fibrillation
- Brugada Syndrome
- Cardiomyopathy, Restrictive
- Dissection, Aortic
- Heart Block, Second Degree
- Heart Block, Third Degree
- Hypoglycemia
- Hyponatremia
- Long QT Syndrome
- Mitral Stenosis
- Multifocal Atrial Tachycardia
- Myocardial Infarction
- Pulmonary Embolism
- Pulmonic Valvular Stenosis
- Sinus Bradycardia
- Subarachnoid HemorrhageTetralogy of Fallot
- Torsade de Pointes
- Toxicity, Amphetamine
- Toxicity, Antidepressant
- Toxicity, Antidysrhythmic
- Toxicity, Beta-blocker
- Toxicity, Calcium Channel Blocker
- Toxicity, Cocaine
- Toxicity, Cyclic Antidepressants
- Wolff-Parkinson-White Syndrome
•EKG:
–Left ventricular hypertrophy and ST segment depression in left precordial leads suggestive of strain pattern caused by transient left ventricular subendocardial ischemia
•Echocardiogram
–Bicuspid aortic valve with moderate to severe aortic stenosis and LVH
12 year old male child presents with intermittent chest pain.
Preliminary DDx?
•HPI –LUSB –sharp, stabbing –No radiation –5/10 severity –Intermittent for 5 days –Not worsening –No clear alleviating factors –Worse with deep inspiration
VSS
Pertinent PE
•Chest wall: pain upon palpation at LUSB, costochondral junction
•Heart* unremarkable exam
•Diagnosis based on physical exam finding: reproducible pain
Cardiac –Inflammatory –Increased myocardial demand or decreased supply cardiomyopathy LVOT Arrhythmias Coronary artery abnormalities Miscellaneous Aortic dissection Rupture of aortic aneurysm Pulmonary HTN MVP Atrial myxomas Cardiac device/stent complications Drugs Cocaine Overdose of sympathomimetics Noncardiac –Musculoskeletal etiology very common •Costochondritis •Tietze syndrome •Nonspecific •Slipping rib syndrome •Trauma, strain •Precordial catch •Xiphodynia –GI –Psychogenic –Zoster –Spinal cord/nerve root compression in conjunction with scoliosis
•Costochondritis –Normal findings –Well appearing child –Reproducible tenderness Treatment: NSAIDs, warm compresses if needed
Parents bring a 3 year old child to the clinic because of “lethargy” and fast breathing.
Preliminary DDx?
•Over the past week they’ve noticed that she has been fussy and less playful. She had a cold about a week and a half ago which seemed to have resolved.
•She has been lying around “lethargic” all day.
–Let’s take a moment to clarify lethargy!
•Decreased intake but normal urine output.
•No fevers
- VS –HR 180, RR 44, T 99.0F, BP 110/76, O2 sat: 88% RA
- General –tired appearing, tachypneic, WN/WD female
- Skin –no apparent cyanosis
- HEENT -clear
- Lungs –faint crackles bilateral bases, tachypnea, no retractions
- Heart -tachycardic, S1 and S2 present, S3 gallop noted, PMI displaced to anterior axillary line
- Abdomen –hepatomegaly
- GU –Tanner I
- Extremities –no c/c/e
- Neuro –alert and interactive
•See Dyspnea •Physiologic and mechanical •Fever –Feverincreases Respiratory Rateup to 10 breaths/min per degree Celsius •Exertion •Pain •Abdominal distention •Respiratory muscle paralysis •Obesity •Anxiety or Panic Disorder •Hypoglycemia •Cardiovascular (decreased perfusion or oxygen carrying capacity) •Congestive Heart Failure •Anemia •Hyperthyroidism •Pulmonary Embolism •Respiratory •Pneumonia(or Pediatric Pneumonia) •Chronic Obstructive Pulmonary Disease •Asthma •Pneumothorax •Hypoxemiaor Hypercapnia •Interstitial Lung Disease •Pulmonary edema •Compensatory acid-base •Metabolic Acidosis •Sepsis(Lactic Acidosisas well as fever) •Neurologic •Brain mass •Hepatic Encephalopathy •Medications •Salicylates •Sympathomimetics (Amphetamines, Cocaine) •Anticholinergics •Cholinergics (variable effect) •Hallucinogens (Ketamine, PCP) •Cannabinoids (Marijuana,
Acquired dilated cardiomyopathy of viral etiology
Treatment
-O2, IV, monitor
-Same as for CHF: preload reduction, afterload reduction, diuresis, and airway support.
Heart* -grade II/VI systolic ejection murmur best heard over interscapularregion; normal S1 and S2; femoral pulses weaker than brachial bilaterally
•Abdomen –slight hepatomegaly
Coarctation of the aorta (corrected –previously an error here)
Heart* -ejection click with grade III/VI SEM at base of heart and RUSB, radiation to both carotid arteries.
Aortic stenosis with LVH
Reproducible tenderness
costochondritis
tachycardic, S1 and S2 present, S3 gallop noted, PMI displaced to anterior axillary line
•Abdomen –hepatomegaly
Acquired dilated cardiomyopathy of viral etiology
