CARDIO Flashcards
MC cause of pediatric heart failure in children
Congenital heart disease
Volume overload lesions (VSD, ASD, PDA) MC in the first 6mos of life
Heart failure management (6)
IDAPAS
1. Inotropes: to improve cardiac contractility
2. Diuretics: reduce pulmo congestion
3.ACE/ARBs: reduce afterload
4. Penicillin/Prednisone
5. Aspirin/Antibx
5. Support
> high back rest
> Appropriate fluid therapy
> O2, ventilatory support
> Nutrition
MC pediatric cardiac tumor
Rhabdomyomas
> asstd w tuberous sclerosis
Matching type:
A. pressure work
B. volume load
C. intrinsic myocardial function
Afterload, Preload, Contractility
A. pressure work: Afterload
B. volume load: Preload
C. intrinsic myocardial function: Contractility
Saccular aneurysms seen in what phase of Kawasaki Disease?
1st phase: neutrophilic necrotizing arteritis
2nd phase: subacute/chronic vasculitis - Fusiform aneurysm
Principle criteria of Kawasaki Disease
CRASH+ Burn
1. Fever 38deg, at least 5 days
2. Conjunctivitis, bilateral non exudative w limbal sparing
3. Rash - polymorphic
4. Adenopathy - unilateral cervical at least >1.5cm
5. Strawberry tongue - erythema of oral and pharyngeal mucosa, dry cracked cherry lips
6. Hands and feet - edema and erythema
Highest risk of sudden death is seen in which phase of Kawaski disease?
- Subacute phase
* periungual desquamation of fingers and toes: 2-3 wks
* thrombocytosis
* development of CAA
* highest risk of sudden death
* lasts 3 weeks - acute febrile phase
* fever lasting 1-2wks
* acute phase: perineal desquamation - Convalescent phase
* all clinical signs of illness disappeared
* continues until ESR returns to normal
* 6-8wks after onset of illness
Diagnostic criteria for RHD
MAJOR (JONES)
1. Polyarthritis
2. Carditis
3. Subcutaneous nodules
4. Erythema maginatum
5. Syndenham chorea
MINOR (CAFE PAL)
1. elev CRP
2. Arthralgia- must not included if arthritis is included
> monoarthralgia in mid/high risk pop
3. Fever
Mod/High risk: >38degC
Low risk: >38.5degC
4. elev ESR
- >30mm/hr in mod/high risk
- >60mm/hr in low risk
5. Prolonged PR interval
6. Grp A Strep
> culture
> rapid ag tests
> ab titers
Circumstances where ARF diagnosis can be made WITHOUT strict criteria adherence
CIR
1. Chorea is the only major manifestation
2. Indolent carditis is the only manifestation in patients who first come to medic attention ony months after the apparent onset of ARF
3. Recurrences of ARF in high risk populations
Minimum # criteria to fulfil RHD diagnosis?
Initial attack:
Recurrent attacks:
Initial attack:
Evidence of GAS inx PLUS
> 2 major
> 1 major 2 minor
Recurrent attacks:
Evidence of GAS inx PLUS
> 2 major
> 1 major 2 minor
> or 3 minor in mod/high risk population
TRUE or FALSE. Myocarditis and/or pericarditis without evidence of endocarditis is almost never RHD.
TRUE
A substernal thrust indicates __.
A. LVH
B. RVH
C. RAE
D. LAE
B. RVH
An apical heave indicates __.
A. LVH
B. RVH
C. RAE
D. LAE
A. LVH
Murmur grading: I-VI
I: barely audible
II: medium intensity
III: loud, NO thrill
IV, loud with THRILL
V. very loud
VI: loud enough w stethoscope above the chest
Characteristics of innocent mumurs
INNOCENT MURMURS- 7S
1. soft
2. short
3. single
4. sweet (musical)
5. sensitive
6. small
7. systolic
- medium pitched
- vibratory
- musical
- short systolic ejection murmur
- at the LL or MSB
- bet 3-7yo
MC CHD in infancy
VSD
MC CHD beyond infancy
TOF
Components of TOF
DROP
1. VSD: shunting L –> R
2. RVH
3. Overriding of the VSD by the aorta
4. PS
Murmur of TOF is caused by:
A. VSD
B. PS
C. MR
D. PR
Pulmonary stenosis
> caused by the turbulence in the RVOT
> less audible during tet spell because blood is shunted away from RVOT via AV
Rib notching is appreciated in what CHD
A. VSD
B. TGA
C. TAPVR
D. COA
COA
Complications of uncorrected TOF (3)
Cerebral thromboses
Brain abscess
Bacterial endocarditis
Pathophy of tet spells
Pag agitated, crying, dehydrated, fever, exercise or play, there is an increase in pulmo vascular resistance. Therefore, walang BF sa already stenotic na Pulmo valve – kaya nawawala yung murmur ng PS
Squatting:
kinks the BV of the LE to increase systemic vascular resistance to decrease shunting of blood from right to left, therefore increasing BF to the pulmonary artery.
The primary developmental defect in tetralogy of Fallot that is responsible for the characteristic 4 cardiac defects is what?
A. Anomaly in arch development
B. Anterior displacement of the infundibular septum
C. Downward displacement of the tricuspid valve
D. Downward displacement of the tricuspid valve
B. Anterior displacement of the infundibular septum
> Tetralogy of Fallot is one of the conotruncal family of heart lesions in which the primary defect is an anterior deviation of the infundibular septum (the muscular septum that separates the aortic and pulmonary outflows)
Which cardiac defect has the worst prognosis, without immediate surgical correction?
A. d-TGA with no associated defects
B. l-TGA with no associated defects
C. d-TGA with large ASD
D. d-TGA with restrictive VSD
E. l-TGA with restrictive VSD
A. d-TGA with no associated defects
d-Transposition of the great arteries is a medical emergency. Cyanosis and tachypnea are most often recognized within the 1st hours or days of life. If it is not treated, the vast majority of these infants would not survive the neonatal period. Hypoxemia is usually moderate to severe, depending on the degree of atrial level shunting and whether the ductus is partially open or totally closed. Infants who remain severely hypoxic or acidotic despite prostaglandin infusion should undergo Rashkind balloon atrial septostomy. A successful Rashkind atrial septostomy should result in a rise in PaO2 to 35-50 mm Hg and elimination of any pressure gradient across the atrial septum. Some patients with TGA and VSD may require balloon atrial septostomy because of poor mixing, even though the VSD is large. If the VSD associated with d-TGA is small, the clinical manifestations, laboratory findings, and treatment are similar to those described previously for transposition with an intact ventricular septum. When the VSD is large and not restrictive to ventricular ejection, significant mixing of oxygenated and deoxygenated blood usually occurs and clinical manifestations of cardiac failure are seen. The degree of cyanosis may be subtle and sometimes may not be recognized until an oxygen saturation measurement is performed. The physiology of l-TGA is quite different from that of d-TGA. The double inversion of the atrioventricular and ventriculoarterial relationships result in desaturated right atrial blood appropriately flowing to the lungs and oxygenated pulmonary venous blood appropriately flowing to the aorta. The circulation is thus physiologically “corrected.” Without other defects, the hemodynamics would be nearly normal.
