Cardio Flashcards
truncus arteriosus gives rise to
ascending aorta and pulmonary trunk
bulbus cordis gives rise to
smooth parts of left and right ventricles
endocardial cushion gives rise to
atrial septum, membranous interventricular septum, AV and semilunar valves
primitive atrium/ventricle gives rise to
trabeculated part of left and right atria/ventricles
primitive pulmonary vein gives rise to
smooth part of left atrium
left horn of sinus venosus gives rise to
coronary sinus
right horn of sinus venosus gives rise to
smooth part of right atrium
right common cardinal vein and right anterior cardinal vein give rise to
superior vena cava
first function organ in neonates
heart, works at week 4 (also heart looping begins)
how Kartageners leads to dextrocardia
defect in left-right dynein
atrial septation morphogenesis
- septum primum towards endocardial cushions
- foramen secundum in septum primum
- septum secundum develops
- septum secundum grows, foramen secundum becomes foramen ovale
- septum primum forms valve
- primum and secundum fuse
cause of patent foramen ovale
failure of primum and secundum to fuse, paradoxical emboli
ventricular septation morphogenesis
- muscular interventricular septum forms
- aorticopulmonary septum rotates and fuses to form membranous septum
- endocardial cushion separates atria from ventricles
most common cardiac anomaly
VSD
cardiac abnormalities associated with neural crest migration
- transposition of great vessels
- Tetralogy of Fallot
- persistent truncus arteriosus
valve derivation
- aortic/pulmonary = endocardial cushions
- mitral/tricuspid = fused endocardial cushions of AV canal
3 shunts in fetal blood
- ductus venous bypasses portal circulation
- foramen ovale
- ductus arteriosus
allaNtois/urachus becomes
median umbilical ligament
ductus arteriosus becomes
ligamentum arteriosus
ductus venosus becomes
ligamentum venosum
notochord becomes
nucleus pulposus
umbiLical arteries becomes
lateral umbilical ligament
umbilical vein becomes
ligamentum teres hepatis (round ligament) - in falciform ligament
SA and AV nodes supplied by…
branches of RCA
most common sided dominant heart
right
coronary blood flow peaks in….
early diastole - valves are closed, pressure from aorta fills vessels
pericardium is innervated by…
phrenic nerve - pericarditis can go to shoulder
cardiac output equation
CO = SV * HR
MAP equation
MAP = TPR * CO (change in pressure = resistance * flow)
how to calculate MAP
2/3 diastolic + 1/3 systolic
cases of increased/decreased pulse pressure
increased - hyperthyroidism, aortic regurg, aortic stiffening, obstructive sleep apnea, exercise
decreased - aortic stenosis, cardiogenic shock, cardiac tamponade, HF
stroke volume is affected by what three things
afterload, preload and contractilitiy
contractility is increased with…
- catecholamine stimulation via B1 - increased calcium and phospholamban phosphorylation
- higher intracellular calcium
- decreased extracellular sodium
- digitalis - blocks Na/K pump
contractility is decreased with
- beta blockade
- HF with systolic dysfunction
- acidosis
- hypoxia/hypercapnia
- non-dihydropyridine Ca blockers
myoCARDial demand is increased by
Contractility
Afterload
heart Rate
Diameter of ventricle
venous dilators have what effect on preload
decrease
arterial vasodilators do what to afterload
decrease it (hydrAlAzine)
ejection fraction
stroke volume / EDV - or what ratio of blood is ejected each beat
blood viscosity changes based on…
hyperproteinemia states (myeloma, polycythemia)
a wave
AAtrial contraction - absent in afib
c wave
RV Contraction - bulging of tricuspid valve
v wave
right atrial pressure increase due to villing against valve
y descent
RA emptying in RV - prominent in constrictive pericarditis, absent in cardiac tamponade
splitting occurs in what sound
S2 - closure of aortic and pulmonic valves
normal splitting
inspiration causes drop in pressure, increase venous return, increase RV filling and stroke volume, increased RV ejection time = delayed closure of pulmonic valve
also increased capacity of pulmonary circulation
wide splitting
delay in RV emptying - pulmonic stenosis or RBBB
fixed splitting
meaning it doesnt change with breathing - due to ASD because of higher volume and no effect on breathing
paradoxical splitting
delay in aortic valve closure - aortic stenosis or LBBB
inspiration improves split so it is paradoxical
inspiration bedside maneuver
increase intensity of right heart sounds due to increased venous return
hand grip bedside maneuver
leads to increase in afterload
- higher intensity MR, AR and VSD
- less hyptertrophic cardiomyopathy and AS murmurs, MVP: later click
valsalva (phase 2) and standing bedside maneuver
decrease in preload
- lower intensity murmurs
- more hyptertrophic cardiomyopathy
- MVP: earlier click
rapid squatting bedside maneuver
increase venous return, preload and afterload
- less hypertrophic cardiomyopathy
- increase in AS, MS and VSD
- MVP: later click
crescendo-decrescendo systolic ejection murmur
aortic stenosis - ejection click
holosystolic, pitched blowing murmur
mitral regurg
late systolic crescendo murmur with midsystolic click
mitral valve prolapse
holosystolic harsh murmur
VSD - loudest at tricuspid area
early diastolic decrescendo blowing murmur
aortic regurg
delayed rumbling mid-late diastolic murmur
mitral stenosis - follows opening snap
continuous machine like murmur
PDA - loudest at S2
facts about aortic stenosis
- pressure difference (higher in LV)
- loudest at base, radiates to carotid
- pulses are weak with delayed peak
- age related calcifications or younger bicuspid valve
facts about mitral regurg
- loudest at apex, radiates toward axila
- due to ischemic heart disease or rheumatic fever and infective endocarditis
facts about mitral prolapse
- most common
- heard at apex
- predispose to infective endocarditis
- myxomatous degeneration
- rheumatic fever, chordae rupture
facts about aortic regurg
- hyperdynamic pulse with head bobbing
- wide pulse pressure (due to back flow of blood, lowering diastolic pressure)
- due to aortic root dilations, bicuspid valve, endocarditis, rheumatic fever
facts about mitral stenosis
- pressure difference (higher in LA)
- late complication of rheumatic fever
- can be in chronic MS
myocardial action potential
- Na channels open - rapid upstroke
- Na channel inactivated, K open - initial repolarization
- Ca influx balances K efflux - plateau
- K efflux, closure of Ca - rapid repolarization
- high K permeability - resting
differences in mycardial physiology
- action potential plateau due to Ca influx
- contraction requires Ca influx to induce Ca release from SR
- electrical coupling by gap junctions
pacemaker action potential
- opening of Ca channels, fast Na channels are inactivated resulting in slower polarization
- absent
- absent
- inactivation of Ca, activation of K (K efflux)
- slow depolarization due to funny current (slope determines HR)
effect of sympathetics on funny current
increase likelihood that they are open, leading to increase in HR
conduction pathway of heart
SA - atria - AV - bundle of His - right and left bundle branches - Purkinje - ventricles
speed of conduction
purkinje > atria > ventricles > AV node
u wave prominent in….
hypokalemia and bradycardia
causes of torsades de pointes
long QT intervals, drugs, low K, low Mg, congenital abnormalities
drugs inducing long QT
antiArrhythmics (class 1A,3) antiBiotics (macrolides) antiCychotics (haloperidol) antiDepressants (TCA) antiEmetics (ondansetron)
Romano-Ward syndrome
autosomal dominant disorder leading to congenital QT prolongation, no deafness
Jervell and Lange-Nielsen syndrome
autosomal recessive disorder leading to congenital QT prolongation, sensorineural deafness
brugada syndrome
pseudo- RBBB and ST elevations in V1-V3
- increase chance of tachyarrhythmias and sudden death, prevent with defibrillator
wolf-Parkinson White syndrome
- abnormal accessory conduction pathway bypasses AV node
- delta wave with widened QRS and short PR
- may cause supraventricular tachycardia
atrial fibrillation
- no discreet P waves**
- irregularly irregular heartbeat**
- caused by CAD, can lead to thromboembolus
- treatment is anticoag, rate/rhythm control, carvioversion
atrial flutter
- sawtooth on EKG**
- consistent interval
- treat like afib, requires ablation
first degree AV block
prolonged PR > 200ms
second degree type 1 block
Wenckebach - progressive lengthening followed by drop - asymptomatic
second degree type 2 block
drop with no PR lengthening - treated with pacemaker
third degree heart block
atria and ventricles beating independently - can be caused by Lyme
ANP
released from atria in response to increased blood volume and pressure
- acts via cGMP
- causes vasodilation, less Na reabsorption ar renal tubule
- dilates afferent, constricts efferent, promoting diuresis
BNP
release from ventricular myocytes in response to tension, same effect as ANP
diagnosis of HF
use BNP - good negative predictive value
carotid sinus
baroreceptor
carotid body
chemoreceptor
aortic arch transmits via…
vagus nerve
carotid sinus transmits via…
glossopharyngeal nerve
peripheral chemoreceptors
carotid and aortic bodies are stimulated by low PO2, high PCO2 and low pH
central chemoreceptors
stimulated by change in pH and PCO2 of brain fluid - ** does not respond to O2
autoregulation
how blood flow remains constant over range of perfusion pressures
autoregulation factors of heart
local metabolites (vasodilators): adenosine, NO, CO2, low O2
autoregulation factors of brain
local metabolites (vasodilators): CO2 (pH) - not O2
autoregulation factors of kidneys
myogenic and tubuloglomerular feeback
autoregulation factors of lungs
hypoxia causes vasoconstriction to ensure perfusion of well ventilated areas
autoregulation factors of skeletal muscle
local metabolites during exercise (CHALK): CO2, H, Adenosine, Lactae, K
autoregulation factors of skin
sympathetic stimulation for temp control