Heart Embryology
starts 3rd week
develops from splanchnic mesoderm
neural crest cells
formation of a single tube
cardiac looping
cardiac looping
by week 4
defect can lead to dextrocardia
primitive circulation begins by week 4
adult derivatives of embryonic structure
Septation of the chambers
Atria
septum primum grows toward endocardila cushion
Subtopic 1
secundum forms in septum primum
septum secundum develops as foramen secundum maintains right-to-left shunt
septum secundum expands and covers most of the foramen secundum. The residual is the foramen ovale
Remaining portion of the septum primum forms valve of the foramen valve
septum secundum and septum primum fuse to form the atrial septum
Foramen ovale usually closes soon after birth because of the increase LA pressure
Patent Foramen Ovale caused by failure of septum primum and septum secundum to fuse after birth
Can lead to paradoxical emboli
ASD( L TO R)
Ostium Primum
Down syndrome
Ostium Secundum
Most common
Ventricles
Muscular IV forms
Subtopic 1
aorticopulmonary septum forms and fuses with muscular IV to from membranous IV
growth of endocardial cushions separates atria from ventricles
VSD(L TO R)
Membranous
Muscular
Anatomy
Fetal circulation
Subtopic 1
Subtopic 2
Subtopic 3
adult derivatives of fetal structures
Characteristic of the valves
Layers of the heart
pericaridum
Fibrous pericardium(tough)
Visceral pericardium(surrounding heart)
Pericarditits
contains pericardial fluid
pericardial effusion
cardiac tamponade
Becks Triad
Hypotension
Distended neck veins
Muffled voices
endocardium
epicardium(visceral pericardium)
Coronary arteries
SA node supplied by RCA
AV node supplied by PDA
Right dominant circulation
PDA from RCA
Left dominant circulation
PDA from LCX
Codominant circulation
PDA from RCA and LCX
Cornonary artery occlusion common in LAD
Coronary blood flow peaks in early diastole
Floating Topic
Sites of auscultation with murmurs
Physiology
Cardiac muscle contraction
calcium induced calcium release via ryanodine receptor
Cardiac output
C0=SVxHR
determinants of cardiac output
stroke volume
preload
approximated by EDV
afterload
approximated by MAP
contractility
sympathetic stimulation via B1
increase intracellular calcium
digitalis
cardiac glycoside
digoxin
blocks NA+/K+ pump
increases intracellular CA2+
heart rate
Frank-starling's law
increase in volume(EDV)
increase in force of contraction(increase in stretch of myofibers )
increase in SV
Blood pressure
MAP=COxTPR
Systolic or diastolic
Pulse difference
Systolic-diastolic
atherosclerosis/aging
aortic regurgitation
PDA
Aortic stenosis
resistance
Diameter
mainly determined by arterioles
viscosity
length
blood vessels
arterioles(35mmHg)
regulars of MAP
capillaries
slowest velocity
largest cross sectional areas
Gas exchange
veins/venules(16mmHg)
capacitance vessels
reservoirs for blood volume
more compliant
Vena cava 0 mmHg
Aorta 120 mmHg
cardiac and vascular function curves
pressure volume loop
isovolumetric contraction
systolic ejection
isovolumetric relaxation
rapid filling
reduced filling
Cardiac cycle
heart sounds
Cardiac and Vascular function curves
Floating Topic
Electrophysiology and arrhythmias
Myocardial Action Potential
Phase 0
rapid upstroke and deoplarisation
fast voltage gated Na+ channels open
initial reoplarisation
fast Na+ close
fast voltage gated K+ open
Phase 2
Plateau
Ca2+ influx balances K+ efflux
Ca2+ triggers Ca2+ release from SR and myocyte contraction
Phase 3
Rapid repolarisation
K+ efflux through slow K+ channels and closure of Ca2+ channels
Phase 4
Resting Potential
High K+ permeability through K+ channels
Pacemaker Action Potential
Phase 0
upstroke
Opening of Ca2+...Fast Na+ permanently inactivated
Phase 3
reoplarisation
inactivation of C2+ channels
opening of K +
K+ efflux
Phase 4
slow spontaneous diastolic depolarization due to If channels(slow Na+ channels open
Accounts for automaticity of SA and AV nodes.
slope of phase 4 determines HR
Floating Topic
Subtopic 1
Subtopic 1
Electrocardiogram
P wave
atrial depolarisation
PR interval
AV nodal delay
0.12-0.2 s
QRS complex
-
Q wave
Septal deoplarisation
R Wave
Ventricles deoplarisation
S wave
Basal deoplarisation
<0.12 s
QT interval
Ventricular depolarization and Ventricular repolarization
<0.43
T wave
Ventricular repolarisation
J point
junction between end of QRS complex and start of ST segment
ST segment
Isoelectric,ventricles deoplarised
U wave
prominent in hypokalemia , bradycardia
Cardiac arrhythmias
Mechanism
Increased automaticity
triggered activity
Reentry
Cardiac Axis
Tachycardia > 100 bpm
supraventricular (narrow QRS complex)
SA node:Sinus tachycardia
AV node/atria
Paroxysmal supraventricular tachycardia (PSVT)
Atrial flutter
Saw toothed shape
Subtopic 1
Atrial fibrillation (Afib)
irregularly irregular heart beat
Subtopic 1
ventricular (wide QRS complex)
premature ventricular contraction
ventricular tachycardia (VT)
monomorphic VT
polymorphic VT
Torsades de pointes :type of polymorphic VT
treatement
magnesium sulfate
caused by
drugs:
antibiotics: macrolides- ezythromyocin
hypokalemia and hypomagnesia
Subtopic 1
Long QT interval
Ventricular fibrillation (VF)
completely irregular rhythm with no identifiable waves
fatal
needs CPR and defibrillation
Bradycardia <60 bpm
SA node:Sinus bradycardia
Sick sinus Syndrome
syncope
dizziness
AV node: AV blocks
first degree
Subtopic 1
second degree
Mobitz type 1 (Wenckeback)
asymptomatic
Mobitz type 2
symptomatic
third degree
Bundle branch blocks
RBBB
LBBB
Can be classified into
Floating Topic
Starlings curve
Floating Topic
Floating Topic
Floating Topic
Floating Topic
Congenital Long QT syndrome
inherited disorder of myocardial repolarisation
due to ion channel defects
increased risk of sudden cardiac death
Pathology
Congenital Heart disease
Floating Topic
Floating Topic
Floating Topic
Floating Topic
RVH to compensate
shunt becomes right to left
causes late cyanosis
clubbing
polycythemia
Other anomalies
coarctation of the aorta
Acyanotic
Ventricular septal defect
most common
most resolve
larger lesions may lead to LV overload and HF
TYPES
muscular
membranous
Atrial septal defect
defect in the interatrial septum
wide fixed split S2
ostium secundum more common
may lead to paradoxical emboli
Patent ductus arteriosus
continuous machinery murmur
patency maintained by PGE synthesis and low oxygen tension
treatment
Endomethicin
decreases PGE
uncorrected left to right shunt leads to
Eisenmenger syndrome
increased pulmonary blood flow
pathologic remodeling of vasculature
pulmonary hypertension
Early cyanosis (5Ts)
Persistent Truncus arteriosus
truncus arteriosus fails to divide
lack of aorticopulmonary septum
most Patients have VSD
Transposition of great vessels
aorticopulmomary septum fails to divide
Aorta leaves RV
Pulmonary trunk leaves LV
Not compatible with life
patients present with
VSD
PDA
Patent foramen ovale
Tricuspid atresia
absence of tricuspid valve and hypoplastic RV
requires both ASD and VSD for survival
Tetralogy of Fallot
Pulmonary infundibular stenosis
pulmonary stenosis
forces RIGHT TO LEFT across VSD and causes RVH
Right ventricular hypertrophy
boot-shaped heart
Overriding aorta
VSD
children often squatt
Total anomalous of Pulmonary return
Pulmonary veins drains into right heart circulation ( SVC, coronary sinus)
associated with ASD, PDA
Ebstein anomaly
displacement of tricuspid valve leaflets into RV
associated with tricuspid regurgitation