Cardiology Flashcards
List 4 infectious causes of myocarditis
Enterovirus Coxsackie virus Adenovirus Parvovirus EBV/CMV Rickettsia Diptheria Hep C
List 3 cardiac defects associated with DiGeorge
Conotruncal defects
- TOF-usually PA, MAPCAs***
- TA**
- DORV
- Subarterial VSD
Branchial arch defects
- CoA
- Interrupted aortic arch (type 2B!)***
- Right aortic arch
List steps in transitional circulation
- UA closes, UV remains more patent
- Cord clamped–>removal of placenta–>ductus venosus closes–>↑SVR
- ↓PVR from (1) mechanical expansion of lungs and (2) ↑ in arterial PAO2 (causing ↑ in vasodilation)
- PVRoutput from right heart flows through lungs
- PDA closure (due to o ↑ arterial PAO2 )
- PFO closure (due to ↑ volume of flow returning to left atrium)
In what % of adults does PFO persist?
1/3
What is the incidence of CHD i?
0.8% of live births
What is the common CHD ?
VSD (1/3)
What cardiac lesions cause in utero heart failure (hydrops)?
Severe RVOTO
Severe AVVR
Ebstein
List 3 genetic counselling points for CHD
- 1 affected sib risk increased to 2-6%, 2 sibs 10% (vs. 0.8% in general population)
- If 2 1st degree relatives, risk 20-30% in subsequent
- Tend to be similar class (conotruncal, atrioventricular septal, Rt obstruction, Lt obstruction)
How do you perform a hyperoxia and what do the results mean?
Apply 100% O2 x 15 min, then ABG taken from right radial artery
If Pao2 rises > 150 mm Hg: intracardiac right–left shunt essentially excluded
If PaO2 remains < 50 mmHg, cyanotic CHD vs severe PPHN/lung disease
CXR findings in TGA
Egg on a string
Thin mediastinum
CXR findings in TA
Wide mediastinum
CXR findings in Ebstein
Wall to wall heart
What is the primary defect in TOF?
Abnormal infundibular septum, that separates aortic/pulmonary outflow tracts
4 components of TOF
(1) RVOTO (pulmonary stenosis + subpulmonic area)
(2) VSD
(3) aorta that overrides ventricular septum
(4) RVH
Which component of TOF determines degree of cyanosis?
RVOTO
List 4 treatments for TOF spell and how they work
(1) Prone in knee-chest position (increases afterload thus decreasing R to L shunting)
(2) Supplemental O2
(3) Calming and holding
(4) Morphine (treat hyperpnea and decrease systemic catecholamines)
(5) Phenylephrine (increases afterload)
(6) β blockers (to block beta receptors in infundibulum therefore lessening RVOTO)
Describe the murmur in TOF
Loud harsh SEM at LUSB, sounding more holosytolic at LLSB
S2 single or soft P2 component
List CXR findings in TOF
Normal heart size
“Boot shaped heart” (elevation of apex, concavity of main PA area)
Right-sided AoA
↓ pulmonary vascularity
Repair and treatment of TOF
Repair in infancy
Severe RVOTO requires PGE infusion
List 2 long term complications patients with repaired TOF
Pulmonary insufficiency
RV dilatation (QRS duration increases)
Ventricular arrhythmias
Increased risk of SCD
Describe the physiology of tricuspid atresia
Single ventricle physiology!
All systemic venous return moves from RA to Lt side of heart by ASD
Blood then enters LV and is ejected to systemic circulation (through aorta) and to pulmonary circulation (by Lt–Rt shunt either by a PDA or a VSD)
What is the classic ECG finding in tricuspid atresia
Leftward superior axis on ECG, LVH (similar to AVSD)
Murmur in tricuspid atresia
Holosystoic murmur LSB
Prominent LV impulse (in most cyanotic CHD there is ↑d RV impulse)
Describe the pathophysiology of Ebstein’s
Downward displacement of an abnormal tricuspid valve into the RV
Leaflets adherent to wall
TV is insufficient resulting in TR
Extra volume of desaturated right atrial blood shunted right–left across an ASD or PFO
Due to combo of TR, poorly functioning small RV, and RVOTO from large sail-like TV leaflet, the effective output from Rt heart ↓s; if patent, PDA provides additional pulmonary flow
Due to TR, RA becomes enlarged