Week 6 Flashcards
Primitive heart tube structure and changes during development
Formed from cardiogenic plate of mesodermal tissue at cranial end of embryonic disc
Tube grows quicker than rest of embryo and is fixed at both ends so fold to the right/D-looping or uncommonly to the left/L-looping
Right horn of sinus venosus forms walls of right ventricle, left horn form coronary sinus
Role of endocardial cushions in heart development
AV/endocardial cushions within AV canal -> chordae tendinae + AV valves
How do aorta and pulmonary artery form
Bulbar cushions in bulbus cordis and truncal cushions in truncus arteriosus fuse forming aorticopulmonary septum up the truncus arteriosus
Explain the partitioning of the AV canal, artium and ventricles
Interatrial septum formed by septum primum growing towards AV cushions forming foramen primum
Septum secundum develops to maintain R to L blood flow
Interventricular septum from caudal expansion and hypertrophy of bulbis cordis and primitive ventricles - grow in caudoventral direction
Growth of AV cushions -> closes interventricular septum
Ventricles dilate, walls hypertrophy, trabeculation occurs, endodermal cell death
Strands of cell wall mesenchyme from AV cushions to ventricle walls remain forming cusps of AV valves and chordae tendinae
Formation and fusion of truncal ridges -> 3 swellings in walls of aorta and PA trunks -> expand into lumen of each vessel -> become thin with cellular degradation -> aortic and pulmonic valve formed
Foetal circulation
O2 and nutrients from mothers blood transferred across placenta -> umbilical vein -> liver
DUCTUS VENOSUS - some blood to liver, rest -> caudal vena cava -> RA
FORAMEN OVALE - RA -> LA
LA -> LV -> aorta -> body
Deoxy blood -> RA -> RV -> PA
DUCTUS ARTERIOSUS - PA -> descending aorta -> umbilical arteries -> placenta
Abnormalities due to failure of normal heart development
Mitral/tricuspid dysplasia - present a murmur
Persistent truncus arteriosus - PA and aorta don’t divide
Tetralogy of fallot - VSD + pulmonary stenosis + RV hypertrophy + overriding aorta (aortic valve over VSD rather than LV)
Patent foramen ovale - atria have similar pressures so usually benign
Ventricular septal defect (VSD) - insignificant if small - LV has high pressure -> RV
Aortic/pulmonary stenosis - narrowing of valves
Patent ductus arteriosus - shunt of blood from aorta -> PA = serious problem
Lead I,II and III ECG
Lead I - RF - LF
Lead II - RF - LH
Lead III - LF - LH
PQRST, PR, ST
P = atrial depolarisation
QRS = ventricle depolarisation
T = ventricular repolarisation
PR = time impulse travels from SA to Av
ST = ventricles are depolarised but haven’t started repolarising
Tall P wave
Wide P wave
Tall R wave
Deep S wave
R atrial enlargement
L atrial enlargement
L ventricular enlargament
R ventricular enlargement
Wide and bizarre complexes
Ventricular premature complexes
Can happen if conducting system is damaged
P wave initiated but impulse not conducted normally
Sinus arrest:
Bradydysrythmia
Failure of pacemaker to discharge - next fastest pacemaker takes over after pause
Persistant atrial standstill:
Bradydysrythmia
no P waves
next fastest pacemaker takes over - slow but regular HR
AV blocks ECG
Bradydysrythmias
1st degree = prolonged R-R interval
2nd degree = P wave not conducted through AV node - P but no QRS
3rd degree/complete = persistent failure of conduction through AV node - ventricle depolarisation from ventricular focus - wide and bizarre escape complexes
Supraventricular premature complex
Premature P wave interrupts normal P wave
QRST is normal
runs of 3 or more = supraventricular tachycardia
Ventricular premature complex
Site of origin with ventricles
wide and bizarre QRST complexes interrupt rhythm
Runs of 3 or more = ventricular tachycardia
Formation and control of cardiac action potential
Mediated mostly by Ca channels as they open and close slower so APs develop over long time
Nor-adrenaline -> increased cAMP ->more Ca earlier -> increased force and HR
