Cardiology Flashcards
How is WPW treated?
Observation for asymptomatics
Acute therapy is procainamide or amiodarone
SVT gets worse after CCBs or digoxin (dangerous in WPW).
Radiofrequency catheter ablation is curative
Clinical features of hypertrophic cardiomyopathy?
Harsh systolic ejection crescendo-decrescendo murmur in the lower left sternal edge
↑ with ↓ preload (eg, Valsalva maneuver, standing)
↓ with ↑ preload (eg, passive leg raise)
Sustained apical impulse
S4 gallop
paradoxical S2
Abnormal bifid or bisferiens pulse (sudden quick rise followed by a slower longer rise due to LV outflow tract obstruction).
Firstline treatment for hypertrophic cardiomyopathy?
B Blocker
Inferior MI - ECG and coronary blood vessel involved
AvF, II, III
RCA
Anterior MI - ECG and coronary blood vessel involved
V1-V4
LAD
Lateral - ECG and coronary blood vessel involved
I, aVL, and V5–V6
LAD
What are the clinical features of AS?
Pulsus parvus et tardus (weak, delayed carotid upstroke)
Single or paradoxically split S2 sound;
Systolic crescendo- decrescendo murmur at the right second intercostal space radiating to the carotids
What murmur is heard in MR? What is the treatment?
Holosystolic radiating to the axilla
ACEIs or ARBs to vasodilate and ↓ rate of progression.
Antiarrhythmics if necessary (AF is common with LAE).
Digoxin and diuretics may be needed in CHF
Valve repair or replacement for severe cases
Murmur of AR
Treatment
Early blowing diastolic murmur at the left sternal border, mid-diastolic rumble (Austin Flint murmur), and midsystolic apical murmur
Widened pulse pressure causes de Musset sign (head bob with heartbeat), Corrigan sign (water-hammer pulse; wide and bounding), and Duroziez sign (femoral bruit)
Treat with venodilators e.g. ACEi CCB
What are the causes of cyanotic congenital heart disease?
Truncus arteriosus
Transposition
Tetraology of fallot
Tricuspid atresia
TAPVR
What happens with truncus arteriosus
The outflow tract of the heart remains fused. Associated with VSD (holosystolic, loudest at tricuspid area, harsh)
Transposition of the vessels
Aorta off RV
PA off LV
Not compatible with life unlesss there is some form of shunt, VSD, PDA, PFO)
Tetralogy of Fallot
- most common cause of childhood cyanosis
Pulmonary stenosis
RVH with boot shaped heart
Overriding aorta
VSD
“Tet spells’ Worsening of cyansosis during exercise, feeding, crying due to worsening of the R outflow obstruction.
Squatting increases systemic vascular resistance, decreases R-L shunt and improved cyanosis.
Ebstein anomaly
TCV downwards into RV
TCV regurg
Accessory conduction pathways
Right sided HF
Can be caused by lithium exposure in utero
VSD
Most common congenital defect
Harsh, pansystolic murmur heard best at the tricuspid area
