Path 12: Heart go brrrrrrrrr Flashcards
Layers of tri-layer architecture of cardiac valves
Endothelium
Fibrosa
Ventricularis/Atrialis Layer
Cardiac myocytes rely on ________ for energy
oxidative phosphorylation
Diastole comprises ____ [fraction] of the cardiac cycle
2/3
With tachycardia, the relative duration of ____ decreases
diastole
Frank-Starling mechanism
1) Increased filling volumes dilate the heart
2) Actin-myosin crossbridge formation increases
3) Contractility increases
Normal EF
45-65%
Causes of hypertrophy
Pressure overload
Volume overload
Trophic signals (aka ß activation)
Hypertrophic myocyte cellular characteristics
1) increased protein synthesis
2) Increased mitochindira
3) Multiple/enlarge nuclei
4) DNA ploidy
Patterns of hypertrophy
Pressure overload: sarcomeres are PARALLEL to long axes of cells. Wall thickness increases
Volume overload: sarcomeres assembled in series with existing ones. Heart weight increases, but wall thickness does not. Dilation of ventricle
Why does hypertrophy make heart vulnerable to ischemia
1) Increased oxygen demand
2) Hypetrophic growth not accompanied by capillary growth
3) Fibrous tissue resists diastolic filling
Genes expressed in hypertrophic myocytes
FOS
JUN
MYC
EGR1
Most common left HF causes
1) Ischemia
2) HTN
3) Aortic/mitral dx
4) Primary myocardial dx
Pulmonary changes from pulmonary edema
1) Perivascular and interstitial edema
2) Progressive widening of alveolar septa
3) Accumulation of fluid in alveolar spaces
Histologic changes pointing to previous episodes of pulmonary edema
Hemosiderin laden macrophages
AKA Heart Failure Cells
Mechanism of hemosiderin laden macrophages
Extravasated red cells phagocytosed and accumulated iron is hemosiderin
CHF auscultation findings
1) Fine rales in bases (inspiratory)
2) S3 (volume overload)
3) S4 (increased myocardial stiffness
Mitral regurgitation in HF caused by
Dilation of heart outwardly displaces papillary muscle
Most common cause of right HF
Left HF
Isolated right HF caused by
Usually pulmonary pathologies
Marker used to quantitatively assess CHF progression
BNP
Cardiac cell embryologic origin
Mesoderm
First wave of cardiac folding in embryo produces
Left ventricle
Second wave of cardiac folding in embryo produces
Right ventricle, outflow tract, atria
Most common genetic cause of congenital heart dx
Down syndrome
Left-to-right shunts types
ASD
VSD
PDA
Atrial Septal Defect presentation
Usually silent till adulthood
Pulmonary valve murmur
Patent foramen ovale
Persistent foramen can open when right sided pressures are elavated, sometimes creating a right-left shunt or paradoxial embolism
90% of VSDs happen in
Membranous interventricular septum
VSD below pulmonary valve
Infundibular VSD
VSD presentation age
Manifest in children
VSD clinical features (morphology changes)
Irreversible pulmonary vascular disease
Right hypertrophy
Pulmonary hypertension
VSD treatment
Most close spontaneously so surgery is delayed
Surgery if no closure
PDA structure
PA joins aorta just distal to left subclavian
PDA auscultation
Persistent machinery like murmur
Mechanisms that close Ductus arteriosus
Increased atrial oxygenation
Decreased pulmonary vascular resistance
Declining prostaglandin E2 levels
Causes of PDA
Hypoxia in infant
Other defects increase pulmonary vascular resistance
Treatments to close PDA
Prostaglandin inhibitors
Percutaneous/surgical
When should a PDA be preserved
Co-occurring defects that obstruct pulmonary outflow tracts
Done by admin of Prostaglandin E1
Four features of Tetralogy of Fallot
1) VSD
2) Obstruction of the right ventricular outflow tract
3) Overriding aorta
4) Right ventricular hypertrophy (secondary to to pressure overload)
Tetralogy of Fallot classic presentation
Cyanotic at birth
Loud murmur
Transposition of great vessels types
L- uncommon, often well tolerated (corrected)
D- most common, leads to death without shunting
Cause of tricuspid atresia
unequal canal division makes tricuspid smaller and mitral larger
Tricuspid atresia symptom
Cyanosis
How is circulation maintained in tricuspid atresia?
VSD/ASD providing shunting
Coarctation of aorta patient population
Males and Turner syndrome