Flashcards in 146 - Aortic Stenosis Deck (34):
what occurs during the filling stage of the cardiac cycle, what can be heard on auscultation and what can be seen on an ECG?
*opening of AV valve, atrial diastole ( ventricle fills passively), atrial systole (ventricle filled actively), AV valve closes when ventricular P>atrial P
*3rd HS (passive ventricular filling) & 4th HS (active ventricular filling)
*P-wave (elec stim of atria prior to atrial systole) &QRS (elec stim of ventricles prior to ventricular systole)
what occurs during the isovolumetric contraction stage of the cardiac cycle, what can be heard on auscultation and what can be seen on an ECG?
*closure of AV valve, ventricle contracts, ↑ventricular P, aortic valve opens
*1st HS (AV valve closing)
*end of QRS
what occurs during the ejection stage of the cardiac cycle, what can be heard on auscultation and what can be seen on an ECG?
*opening of aortic valve, 2/3 of blood ejected (80/120ml), early ejection ↑aortic P & elastic walls dilate as too quick to fill small arteries, late ejection ↓velocity of blood ↓aortic P but windkessel effect maintains high P,aortic valve closed
*T-wave (ventricular repolarisation)
what occurs during the Isovolumetric relaxation stage of the cardiac cycle, what can be heard on auscultation and what can be seen on an ECG?
*closing of aortic valve, small ↑aortic P as backflow against closed aortic valve, ventricular relaxation (volume constant ↓P), opening of AV valve
*2nd HS (closing of aortic & pulmonary valves)
*no ecg wave
describe the atrial cycle and abnormalities
*a wave - atrial contraction, ↑atrial P (lost in AF, large in tricuspid stenosis caused by atrail hypertrophy, canon when contraction with closed tricuspid valve)
*c-wave - closure of AV valve & AV valves bulge as ventricles contract, ↑atrial P
*x-descent - atria relax and start to fill & AV valves pulled back into ventricles, ↓atrial P
*V-wave - blood fills atria, ↑atrial P (giant in tricupid regurge)
*Y-descent - AV valves open & blood passively fill ventricles, ↓atrial P (steep in constrictive pericarditis)
what is the equation for cardiac output & how can you measure it?
CO= Heart rate x stoke volume (vol of blood ejected from one ventricle per minute)
*Ficks principle - rate of o2 uptake in blood (spirometer) =pulm blood flow x change in [o2]blood (blood conc in arteries (ABG) - that in rt atrium catheter)
*Hamilton's dye dilution, thermodilution, pulsed doppler
how is heart rate controlled?
by autonomic system acting on SA node & AV node. Baroreceptors sense BP & send signals to medulla via vagus/glossopharnygeal nerves. Parasympthetic stimulation causes ↓HR & sympathetic stimulation causes ↑HR & contractility
how is stroke volume controlled?
*arterial blood pressure - sympathetic, hormonal & vol controlling mechanisms
*contactile energy controlled by:
- frank starling law - ↑filling vol stretches muscle & they become more responsive to Ca2+ influx & ↓actin/myosin overlap causing ↑contraction
- sympathetic stim - noradrenaline binds to B1 receptor ↑ Ca2+ release
- catecholamines - circulating adrenaline/noradrenaline acts the same
how does ↑CVP affect cardiac output and venous return?
↑cardiac output causes ↓CVP as blood removed from R atrium. ↓CVP cause ↑venous return as P diff ↑ between arterial & venous systems ↑ flow
what happens to cardiac output and venous return in heart failure?
*↓Cardiac output causes ↓venous return and ↑CVP and P diff ↓ between arterial & venous systems. blood backs up in capilliary system and ↑P causes oedema. Body compensates and ↑Parterial and ↑ venous return by salt and water retention by kidneys - but this causes ↑CVP
what is aortic stenosis?
narrowing of aortic valve caused by calcific degeneration, bicuspid valve or rheumatic fever. As a result pressure builds up in L ventricle causing LV hypertrophy, LV dilatation & LV failure
what can be seen on examination of a px with aortic stenosis?
slow rising pulse, apex thrust, ejection systollic murmur radiating to carotids
how might you assess the severity of aortic stenosis on echo?
mean gradient (4(velocity^2), jet velocity and valve area
which valves does rheumatic fever affect?
autoimmune inflammation of tissues following Grp A streptococcal infection (scarlet fever). Predominantly affects mitral valve but also aortic valve. Leads to calcification & stenosis
how does calcification in aortic stenosis develop?
There is a chronic inflammatory response to epithelial damage due to turbulent blood flow. This causes lipid plaques & leukocyte infiltration (secrete chem stimulating interstitial cells to differentiate into osteoblasts which simulate bone nodules (calcification))
Due to the stenosis caused higher ventricular P req to push stoke vol through smaller hole leading to hypertrophy
what are the risk factors for aortic stenosis?
rheumatic fever, bicuspid aortic valve, hyperlipidaemia, hypertension, DM, smoking
how is angina caused in aortic stenosis?
myocardial o2 demand outstrips supply as:
*↑o2 demand via ↑work for myocytes to ↑P & ↑myocyte no (hypertrophy) req o2
*reduce o2 supply by ↓diastole as ↑systole due to ↑P req & blood in coronary vessels flow during diastole
* ↓aortic pressure in severe as LV unable to compensate causing ↓aortic P and ↓coronary perfusion
*↓ capillary density in hypertrophied muscle so ↓perfusion
how is dyspnoea caused in aortic stenosis?
hypertrophied LV less compliant so ↑atrial P req to fill it and this ↑back P in pulm veins causing pulmonary oedema & dyspnoea
how is syncope caused in aortic stenosis?
*aortic hypotension during exercise as vasculature dilates, CO cant ↑ to ensure BP maintained so ↓perfusion to brain
*↑Ventricular P stim bradycardiac reflex
how is bleeding caused in aortic stenosis?
caused by angiodysplasia especially in GIT, high shear forces damage vWF.
what causes a heaving apex beat in aortic stenosis?
LV hypertrophy and an ↑contractile force due to ↑P
what causes a slow rising pulse in aortic stenosis?
slow passage of blood through stenosed aortic valve
what causes a ejection systolic murmur in aortic stenosis?
turbulent flow through aortic valve inbetween 1st and 2nd HS. Ejection click (rarely heard) is sound of aortic valave opening and crescendo-decrescendo murmur is sounfs of turbulent flow & friction through aortic valve (gets louder then quieter)
how can aortic stenosis appear on a CXR?
dilated ascending aorta
describe the foetal circulation system
*oxygenated blood from placenta passes down umbilical vein and shunted through ductus venosus into IVC (some to liver)
*blood enters R atrium and majority passes through foramen ovale into L atrium & ventricle then into aorta - eustachian valve ensures oxygenated blood goes to head
*some blood enter R ventricle & into pulm artery. majority then passes through ductus arteriosus & into aorta. very little passes to lungs as vascular resistance is high
*blood passes down aorta into common iliac arteries & some returns to heart & some passes into interal iliac arteries then into umbilical arteries back to the placenta
what happens when a baby takes its first breaths?
*lungs oxygenate so pulm vasculature smooth muscle vasoldilates due to o2. Oxygenated lungs produce bradykinin which constricts smooth muscle of ductus arteriosus.
*↓pulm resistance> ↓pulm artery P below aortic P(↓ due to placenta disengagement) so blood reverses & flows from aorta to pulm artery through ductus arteriosus
*blood is more oxygenated in aorta & DA consticts & closes due to ↑o2, ↑bradykinin &↓prostaglandin levels from mother
*DA closes after 4-10 days and becomes ligamentum arteriosum
how does the foramen ovale close?
*lung expansion & vasodilation causes ↑blood into L atrium & ↓venous return from placenta causes ↓blood flow into R atrium
*L atrial P > R atrial P so septum primum pushed against septum secundum & foramen ovale closes to become fossa ovalis
how is persistent pulmonary hypertension of the newborn caused?
*failure of pulm vasodilation at birth due to prenatal foetal hypoxia (lung vasculature overly muscular) causing ductus arteriosus & formamen ovale to stay open. Seen by cyanosis, acidosis& ↓lower limb sats. MAnage with 02 & ventilation, NO & extracorpeal membrane oxygenation
what occurs with a patent ductus arteriosus?
shunt from aorta to pulm artery causing ↑pulm P which causes pulm oedema& R sided heart failure. Seen by dyspnoea & tachypnoea, tachycardia, systolic thrill & murmur, bounding pulse & cardiomegaly. treated with NSAIDS to block prostaglandin & surgical closure
what occurs with an atrial septal defect?
failure of atrial septum to develop so left to right shunt occurs. Seen by ejection systolic murmur & fixed spliting of 2nd HS, R atrial enlargement, ↓exercise tolerance. treat with surgical or percutaneous closure
how does vasculogenesis occur in foetus?
formation of new blood cells from scratch - blood islands form in mesoderm by differentiation of mesodermal cells into haemangioblasts. these then differentiate:
*in centre of islands become haematopoietic stem cells (blood cell precursor) and migrate to colonise liver then later the bone marrow
*peripheral cells become angioblasts which proliferate & differentiate into vascular endothelium (1ry vascular bed which is added to by angiogenesis (formation of new cells from existing vascular)
how does the early formation of the heart occur?
*blood islands form at cephalic end of embryo at wk3 into horse shoe shaped tube (heart tube). head grows over it to position it in ventral thorax.
*embryonic folding occurs leaving from top to bottom: truncus arteriosus, cono truncal segment, ventricle, atrium and sinus venosus.
*the sinus venosus then folds behind the ventricular/conotruncal segments to produce start of atria
how do the AV valves form and the partitioning of the atrium?
*the common atrioventricular valve formed at narrowing of neck between A&V. Endocardial cushions grow from sup & inf walls & meet to split valve into left & right AV canals
*septum primum develops from roof of atrium towards endocardial cushions & gap below is ostium primum. ostium secundum (foramen ovale) develops
*Septum secundum grow from roof in RA part & forms flap over foramen ovale preventing LA to RA flow