Anatomy, Physiology, Investigations Flashcards
four key adaptations in foetal circulation, and what they become after birth
- umbilical arteries = superior vesical arteries, and umbi veins = round ligament of liver
- ductus venosus = ligamentum venosum
- foramen ovale = fossa ovalis
- ductus arteriosus = ligamentum arteriosum
where does oxygenation occur in utero?
placenta
blood flow through the foetus
placenta > ox blood via umb vein > portal vein > liver»_space; deoxy blood > hepatic vein > IVC + SVC > RA
either A) RA > FO > LA > LV > aorta
or B) some RA > RV > pulmonary artery > PDA > aorta
aorta > common iliac > (ext) and int iliac arteries that lead into umbilical artery»_space; deoxy blood back to placenta
foetal cardiac pressure - higher in right vs left and why?
right - hypoxic VC of pulmonary vasculature»_space; high pulmonary artery pressure
what happens to the foetal vascular adaptations once birth occurs?
1) crying > reduced pulmonary vasculature pressure > right heart pressure falls > foramen ovale slams shut (functional closure)
2) lower pulmonary artery pressure > less flow through PDA. this plus higher O2 levels causing vasoconstriction, and less PGE»_space; PDA closure in a few hours
3) wharton’s jelly constricts in the cold > umbi arteries flatten
4) ductus venosus starts to clot up as does umbi veins
roles of the four key foetal circulation adaptations?
- umbilical arteries = deoxy to placenta, veins = oxy to foetus
- ductus venosus = bypass liver, umbi vein to IVC
- foramen ovale = avoids pulmonary circulation
- ductus arteriosus = avoids pulmonary circulation
cardiac embryology: development starts and ends when?
week 3 to week 9
heart develops from which embryo layer
mesoderm
what do the following foetal cardiac structures eventually form?
Sinus venosus and atrium
Primitive ventricle
Bulbus cordis
Truncus arteriosus
Sinus venosus and atrium becomes R+L atrium
Primitive ventricle becomes the L ventricle
Bulbus cordis becomes the R ventricle
Truncus arteriosus becomes aorta and pulmonary artery
what are the four processes of cardiac septation in embryology?
- endocardial cushions divide atria from ventricles, and AV valves
- atrial septation D30: septum primum grows down towards endocardial cushion completely separately atria, before ostium secundum and septum secundum appear to form flap valve and FO
- ventricular septation D25 from apex to endocardial cushion
- conotruncal septum divides truncus into aorta and pulmonary artery, and then the semilunar valves
left coronary artery
- origin
- branches
- supplies
from left coronary sinus
1) Left anterior descending down IV septum to apex
- Supplies: ventricles and anterior IV septum
2) Left circumflex
- travels in left sulcus, has left marginal branches for LV
left atrium, posterior LV
right coronary artery
- origin
- branches
- supplies
- right coronary sinus
1) R marginal branch for RA
AV nodal branch – branches off to AV node
2) R posterior descending (posterior interventricular artery) for posterior ventricles and posterior IV septum
Travels down posterior interventricular sulcus
newborn ECGs: RVH or LVH?
RVH - in foetus, RV is larger and more dominant than the LV - RV handles 55% of the combined ventricular output
ductus arteriosus and FO closure:
permanent vs functional closure
FO - by 3rd month
ductus arteriosus:
- functional closure: starts at 12h, 24 hours (20% closed), 48 hours (85% closed), 96 hours (100% closed)
- anatomical closure by 2-3 weeks
where does most of this blood come from:
A) foetal pulmonary blood flow
B) upper 1/3 of body
C) lower 1/3 of body
A) foetal pulmonary blood flow - from SVC, and preferentially flows through RV, not through FO
B) upper 1/3 of body - usually from foramen ovale then from LV
lower
B) lower 1/3 of body - usually from RV
why are beta haem diseases not see in a newborn?
foetus has alpha and gamma Hb only, which helps with left shift so it can grab as much O2 from mother
only at 6mo start to make beta Hb
stimuli for ductus arteriosus closure
- and therefore, what can we use to close significant PDAs vs
- what can we use to keep ductus open?
- oxygen is STRONGEST
- decreasing PGE2
- then bradykinin and ACh
so - to close use NSAID! to open, use IV PGE2 infusion!
why do premmie ductus arteriosus’ stay open for longer
responds less well to O2 stimulus - NOT due to lack of smooth muscle development!
what kind of stimuli causes pulmonary artery dilation vs constriction?
OPPOSITE to ductus arteriosus!
i.e. dilation = O2, vagal stimulation
constriction = hypoxia, acidosis, sympathetic
why do we even care about the rate of pulmonary vascular resistance decrease?
because it influences the timing of clinical appearance of many congenital heart lesions that are dependent on the relative levels of systemic and PVR
quickest in 1st week, then to two months…up to 2 years!
explain the paradoxical later development of CHF in large VSDs vs smaller VSDs
smaller - LVP doesn’t transmit to PA, so PVR falls quickly
larger - LVP directly transmits to PA, keeping PVR high»_space; CHF develops later
name four factors affecting neonatal PVR
- altitude - less O2, delayed PVR fall
- lung disease / acidaemia
- high PA pressure (from large VSD / PDA)
- increased left atrial / pulmonary vein pressure
describe process of action potential for a cardiac myocyte
4 = resting, -90mV.
0 = depolarisation
A) -90 to -70 from some Ca influx
B) threshold potential reached > Na open +++ > +20
1 = early repol = Na close, K open
2 = plateau repol = K out but now Ca opens to let Ca in»_space; myocytes contract bc Ca binds with tropomyosin
3 = Ca close, K stay open > back down to -90
effect of PNS and SNS on the myocyte AP
PNS ACh = opens K channels, so harder to depolarise, so decr HR
SNS NA = opens Na so inc HR, and increases Ca so more contractile
what are the classes of anti-arrhythmics?
NAB-KC: I = Na channel blockers II = Beta blockers III = K Channel blockers IV = Ca channel blockers V = unclassified e.g. digoxin
briefly differentiate: class Ia, Ib and Ic drugs
Ia = quinidine = blocks Na (also K) i.e. less depol, and longer refractory period/QT. use dependent Na blockade, and reverse use dependent K blockade
Ib = lignocaine = blocks Na, more likely in ischaemic cells and NOT in atria. quickly dissociates.
Ic = flecainide = blocks OPEN Na, and slow to dissociate = use dependence and MOST LIKELY to cause arrythmia; they super potent
beta blockers
- actions and overall effects
All will act at SA (and AV) to slow HR down
non-selective beta-blockers (second half of alphabet e.g. propranolol/timolol) will also reduce contractility
main side effects of beta blockers
heart block
hypoglycaemic unawareness
bronchospasm + dyspnoea
and can’t use in phaeochromocytoma if not the alpha receptor activity will be unopposed
amiodarone
- actions
- half life
- main side effects
- technically class III, but also act as I, II and IV!
- very toxic, bloody long half life (20-100 days)
- thyroid dysfunction, pulmonary fibrosis, skin discolouration, constipatino, corneal deposits, tremor
sotalol
- actions
- class III, but as a ‘lol’ can also act as non-selective beta-blocker, causing reduced HR and contracility
- reverse use dependence!
class III anti-arrhythmics - important side effect
prolonged repolarisation, so can prolong QT and cause torsades des pointes!
CCB and beta blockers - why contraindicated to use together?
both can slow down SA and AV node - so you’d be really at risk of AV block
types of CCBs
DHPs eg nifedipine, amlodipine - selective for Ca channel in peripheral vessel smooth muscle i.e. used for HTN
non-DHPs e.g. verapamil (is VERY cardiac selective) or diltiazem (less so), are more cardiac selective.
adenosine
- action
- uses
- side effects
- adenosine receptors on pacemaker cells, which act to open K channels and inhibit Ca channels
- quick onset: WPW, SVT
- sense of doom, bronchospasm, AF, hypotension, chest pain
what kind of arrhythmia is very specific to digoxin toxicity?
atrial tachycardia with AV block - CAN’T be given in WPW!
what is the concept of cardiac afterload? preload?
preload = amount of tension in the ventricular myocardium prior to contraction
afterload = the force the ventricles need to push against to eject blood
normal:
- RV vs LV pressure
- mean pulmonary artery pressure
- PVR vs SVR
a. RV pressure should be 1/3 of LV pressure
b. Mean pulmonary artery pressure should be < 20
c. PVR 1/6th of SVR
features that suggest a pathological, not innocent, murmur
diastolic holosystolic harsh >grade 3 abnormal S2 systolic click louder standing extra sounds eg click
how to grade murmurs
I = very bloody soft II = faint, but it's there mate III = hear, don't feel IV = hear and feel V = my steth is half off your chest and i can hear it VI = farked
what kind of pathological murmurs are asymptomatic, and so should therefore carefully consider innocent vs pathological murmur?
ASD
VSD
PS and AS
coarctation, PDA
innocent murmurs
- be still in the middle, that music hits you low - Stills, mid systolic, musical, loudest LLSE
- adolescents - early ejection blows you up and out - pulmonary ejection systolic, early-mid systolic, blowing, LUSE
- newborns make you get up and sing ABC - pulmonary flow murmur of newborn (disappears 6mo), transmits to axillae back and carotid, loudest LUSE
- continuously hum while you clap(v) not on your back - venous hum is continuous, loudest at clavicle, soft when supine
pulsatile liver =
aortic regurg
sacral vs peripheral oedema sign of?
sacral oedema = left heart failure
peripheral oedema = right heart failure
what is pulsus paradoxus and what can cause it? (mnemonic)
excessive >10mmHg drop in BP during inspiration, occurs bc there’s competition between right and left heart to fill
TAPE tamponade asthma pericarditis (pericardial) effusion
what does a heave vs tap indicate on cardiac palpation?
- Heave = slow rising, diffuse impulse (volume overload)
* Tap = well localised, sharp risking tap (pressure overload)
these thrills suggest what defects? • LUSE: • RUSE: • LLSE: • Suprasternal notch: • Intercostal spaces –
- LUSE: PS, PA stenosis, PDA
- RUSE: aortic stenosis
- LLSE: VSD
- Suprasternal notch: AS, PS, PDA, COA
- Intercostal spaces – severe COA with collaterals
how can physiological splitting occur during inspiration?
increased venous return to RH ‘slows’ systole, so P2 is slightly after A2
S3 vs S4 heart sounds
S3 = ventricular gallop
- just after S2, in early diastole
- MV opens and blood strikes the LV
S4 = atrial gallop
- just before S1, pre-systole
- from atria trying to force blood into ventricle
