Cardiology embryo and physio Flashcards
gives rise to :
- smooth parts (outflow tract) or left and right ventricles
- atrial septum, membraneous interventricular septum, (AV and semilunar valves)
- coronary sinus
- inferior vena cava
- trabeculated part of the left and right atria
- smooth part of left atrium
- tracbeculated part of the left and right ventricles
- superior vena cava
- smooth part of the right atrium (sinus venarum)
- ascending aorta and pulmonary trunk
- bulbus cordis
- endocardial cushion
- left horn of sinus venosus
- posterior, subcardinal and supracardinal veins
- primitive atrium
- primitive pulmonary vein
- primitive ventricles
- right common cardinal vein, and right anterior cardinal vein
- right horn of sinus vensous
- truncus arteriosus
primary heart tube loops to establish L-R polarity beginning week 4 of gestation
Defect in L-R Dynein can lead to dextrocardia as seen in kartagener syndrome (primary ciliary dyskinesia)
cardiac looping
what is the process of sepatation of the chambers
atria
- septum primum grows toawrd endocardial cushions, a narrow foramen primum forms
- foramen secundum forms in septum primum (foramen primum disappears)
- septum secundum develops as the foramen secundum maintain R-L shunt
- septum secundum expands and covers most of the foramen and form the foramen ovale
- remaining portion of the septum primum forms valve of the foramen ovale
- septum secundum and septum primum fuse to form the atrial septum
- foramen ovale usually closes soon after birth because of increase LA and decrease RA pressure
what happens when the septum primum and septum secundum fails to fuse after birth?
patent foramen ovale- if left untreated can lead to paradoxical emboli (venous thromboemboli that enter systemic arterial circulation) similar to those resulting from the ASD.
ventricles
- muscular interventricular septum forms to form the opening of the interventricular foramen
- aorticopulmonary septum rotates and fuse with muscular ventricular septum to form the membranous interventricular septum, closing the interventricular foramen
- growth of endocardial cushion separates atria from ventricles
what is the most common congenital cardiac anomaly that occur int he membranous septum?
ventricular septal defect
- what forms the ascending aorta and pulmonary trunk?
- what fuses to form that?
- what structures migrate to form that?
- aorticopulmonary septum
- truncal and bulbar ridges
- neural crest and endocardial cushion
- aortic/ pulmonary valves derived from?
- mitral/tricuspid: derived from what?
- endocardial cushions of outflow tract
- fused endocardial cushions of AV canal
what is the process of fetal circulation?
remember umbilical vein carries oxygenated blood and umbilical arteries carried deoxygenated blood.
- blood enters fetus through umbilical vein conducted via ductus venosus into the IVC to bypass the hepatic circulation
- high oxygenated blood that reaches the heart via IVC is directed by the foramen ovale
- deoxygenated blood from SVC pass through the RA–> RV–> main pulmonary artery –> ductus arteriosus–> descending aorta due to high pulmonary artery resistance
what happens are birth that changes every?
infant takes breath leading to reduced resistance in pulmonary vasculature –> increase left atrial pressure compared to RA pressure–> foramen ovale closes (now called fossa ovalis).
the increase O2 and decrease prostaglandins (from the placental separation) –> closure of the ductus arteriosus
- indomethacin helps PDA –> ligamentum arteriosum
- prostaglandiss E1 and E2 keeps the PDA open
fetal structures
- allantois–> urachus
- ductus arteriosus
- ductus venosus
- foramen ovale
- notochord
- umbilical arteries
- umbilical vein
post-natal derivates
- median umbilical ligament
- note: urachus is part of the allantoic duct between bladder and umbilicus - ligamentum arteriosum
- note: near the left recurrent largyneal nerve - ligamentum venosum
- fossa ovalis
- nucleus pulposus
- medial umbilical ligaments
- ligamentum teres hepatis (round ligament)
- note: contained in falciform ligament
- what is the most most posterior part of the heart?
- enlargement can causes dysphagia (due to compression of the esophagus) or horseness (compression of the left recurrent (a branch of the vagus nerve))
- which chamber is the most anterior part of the heart making it prone to injury and trauma?
- LA
- RV
3 layers of the heart (from outer to inner)
- fibrous pericardium
- parietal layer of the serous pericardium
- visceral layer of the serous pericardium
pericardial cavity is between the parietal and viceral layer
1. which nerve innverate the pericardium?
2. where does pericarditis referred pain to?
- phrenic nerve
- pericarditis referred pain to the neck, arms, and one or both shoulders (often the left)
LAD-and its branches supply the anterior 2/3 of the interventricular septum, anteriolateral papillary, anterior surface of the LV and most commonly occluded
PDA- supplies AV nodes (dependent on dominance), 1/3 of interventricular septum and posterior 1/3 of the ventricle wall. supplies posteriomedial papillary muscles
-right marginal artery supplies RV
RCA- supplies SA node (independent of dominance). infarct may cause nodal dysfucntion (bradycardia or heart block)
describe the dominance
right dominance circulation (85%) = PDA arises from RCA
Left-dominant circulation (8%) = PDA arises from LCX
codominant circulation (7%)= PDA arises from LCX an RCA
coronary flow peaks during diastole
- which volume is affected by contractility, afterload and preload?
- what causes answer volume in terms of these variables?
- what happens during heart failure?
- stroke volume
- increased contractility, increased preload, decrease afterload
- decreased SV
catecholamines stimulate beta-recetors –> calcium channels get phosphorylated–> increase calcium entry–> Ca induce more Ca release from sarcoplasmic reticulum
phospholamban phosphorylation activate Ca ATPase to increase Ca storage in SR
-
phospholamban is an inhibitor of cardiac muscle sarcoplasmic reticulum Ca++-ATPase (SERCA2) which transports calcium from cytosol into the sarcoplasmic reticulum. When phosphorylated (by PKA) - disinhibition of Ca++-ATPase of SR leads to faster Ca++ uptake into the sarcoplasmic reticulum
- increase intracellular Ca
- decrease intracellular Na (decrease activity of Na/Ca exchanger)
what does digitalis do?
which factors can decrease contractility?
digitalis- block Na/K pump to increase Na intracellularly leading to decrease Na/Ca exchanger–> increase intracellular Ca
factors decreases contractility
B1-blackers
HF with systolic dusfunction
acidosis
hypoxia/hypercapnia
non-dihydropyridine Ca channel blockers
preload determined by ventricular EDV and depends on venous tone and circulating blood
what drugs can decrease preload?
venous vasodilator (nitroglycerin)
afterload approximated by MAP
increase afterload–> increase pressure–> increase wall tension per Laplace’s law
1. How does the LV compensate for the increased afterload?
2. which drugs decrease afterload?
- the LV hypertrophy to decrease the wall tension
2. arterial vasodilator (hydralazine) decreases afterload
ACE inhibitor and ARB decrease both preload and afterload
chronic HTN (MAP) –> LV hypertrophy
- isovolumetric contraction-period between mitral closing and aortic opening
- systolic ejection- between aortic opening and closing
isovolmetric relaxation-between aortic closing and mitral opening
reduced filling- period just before mitral closing
heart sounds
S1: mitral and tricuspid closure (loudest at mitral area)
S2: aortic and pulmonary valve closure (loudest at left upper sternal border)
S3: early diastolic during rapid ventricular filling phase associated with increaed filling pressure
-mitral regurg, HF) and dilated ventricles normal in children and yound adults
S4: late diastolic (atrial kick) best heard at apex in lateral recumbent
-high arterial pressure (hypertrophy)-LA pushing against stiff LV wall, consider abnormal regardless of age.
Jugular venous pulse (JVP)
a wave- atrial contraction- absent in atrial fibrillation
c wave- RV contraction- (closed tricuspid bulging into atrium)
x descent- downward displacement of tricuspid valve during ejection phase, reduced or absent in tricuspid regurgitation and right HF because pressure gradient reduced
v wave- increased atrial pressure due to filling against closed tricuspid valve
y descent- RA emptying into RV prominent in constrictive pericarditis, absent in cardiac tamponade
aortic stenosis: LV, ESV, EDV, SV
mitral regurg: ESV, EDV, SV
Aortic regurg: EDV, SV, pulse pressure
mitral stenosis: LA pressure, EDV, ESV, SV
aortic stenosis-increased LV pressure, and ESV,
no change to EDV
decrease SV
ventricular hypertrophy–> decrease ventricular compliance–> increase EDP for given EDV
mitral regurgitation-
no true isovolumetric phase,
decrease ESV due to decrease resistence increase regurg into LA uring systole,
increase EDV due to increase LA volume/pressure from regurg–> increase ventricular filing increase SV
aotic regurgitiation
- no true isovolumetric phase,
increase EDV, SV, pulse pressure
mitral stenosis-
increased LA pressure,
decreased EDV because of impaired ventricular filling,
decrease ESV and SV
normal splitting- inspiration–> drop intrathoracic pressure –> increase venous retrun –> increased RV stroke volume–> increased RV ejection time–> delayed closure of pulmonic valves –> decreased pulmonary impedance (increase capacity of the pulmonary circulation) also occurs during inspiration, contribute to delayed closure of the pulmonic valve
wide splitting- seen in delayed RV emptying )pulmonic stenosis, right bundle branch block)-caused delayed pulmonic sound on inspiration (an exageration of of normal splitting)
fixed splitting-heard in ASD–> L-R shunt–> increase RA and RV volumes–> increase flow through pulmonic valve regardless of breath. pulmonic closure is greatly delayed
paradoxical splitting- heard in condition that delay aortic valve closure (aortic stenosis, left bundle branch block. P2 sound occurs before delayed A2 sound
-therefore, inspiration P2 closes later and moves closer to A2, thereby “paradoxically” eliminating the split (usually heard in expiration)
inspiration (increase venous reutrn to right atrium)-increase intensity of right heart sounds
hand grip (increase afterload)
-increase intensity or MR, AR, VSD
decrease hypertrophy cardiomyopathy and AS murmurs
MVP: later onset of click/murmur
valsalva (phase 2), standing up (decrease preload)
decrease intensity of most murmur
increase intensity of hypertrophic cardiomyopathy murmur
MVPL early onset of click/murmur
rapid squating (increased venous return, increase preload, increase afterload, increase peripheral resistance)
decrease intensity of hypertrophic cardiomyopathy murmur
increase intensity of of MR, AR, VSD
MVP: late onset
systolic murmurs- aortic/pulmonic stenosis, mitral/tricuspid regurgitation, VSD, MVP, hypertrophic cardiopathy
diastolic heart sound include murmur of aortic/pulmonic regurgitation, mitral/tricuspid stenosis
murmurs
SYSTOLIC MURMUR
aortic stenosis
-crescendo-decresendo systolic ejection murmur. loudest at heart base; radiates to carotids
pulsus parvus et tardus-weak delayed pulses
can lead to Syncope, Angina, Dyspnea on extertion (SAD)
commonly due to calcification older patients or in younger patients with early-onset in younger adults with calcification on bicuspid valve
mitral/tricuspid regurgitation
holosystolic, high pitched “blowing murmur”
mitral is loudlest at apex and radiate to axilla, MR are often due to ischemic heart disease (post-MI), MVP, LV dilation
tricuspid- loudest at tricuspid area, commonly due to RV dilation,
rhematic fever, infective endocarditis can cause both MR and TR
mitral valve prolapse
late systolic cresendo murmur with mid-systolic click due to suddent tensing of chordae tendineae
(chordae cause cresendo with click)
most frequent valvular lesion best heard over apex, loudest just befor S2
predisposed to IE, can be caused by myxomatous degeneration (marfan or Ehler’s Danlos syndrome) rheumatic fever, chordae rupture
ventricular septal defect
holosystolic-sounding murmur, loudest at tricuspid area
DIASTOLIC MURMUR
aortic regurgitation
high-pitched blowing murmur with early diastolic decresendo with low diastolic murmur, hyperdynamic pulse (bounding pulses), head bobbing when severe/chronic
wide pulse pressure- (high pulse pressure)
often due to aortic root dilation, biscuspid aortic valve, endocarditis, rheumatoid fever, progresses to left HF
mitral stenosis
opening snap (due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion at leaflet tips
delayed rumbling diastolic murmur
often a late sequela of rheumatic fever, chronic MS can result in LA dilation–> dysphagia/hoarseness viacompression of eosphagus/left recurrent
CONTINUOUS
patent ductus arteriosus-continous machine-like murmur best heard at left infraclavicular area, loudest at S2
often due to rubella or prematurity
Tosrades de pointes (twisting of points) -ventricular tachycardia characterised by shifting sinusoidal waveforms that progress to ventricular fibrillation
long QT interval predisposes condition
caused by drugs that decrease K, Mg, Ca, congenital anomalites
TX with magnesium sulfate
drugs classes that induce QT prolongation
- antiarrhythmics (class 1A, 3)
- Antibiotics (macrolides)
- anticythotic (haloperidol)
- antidepressants
- antimetics (ondansetron)
congenital long QT syndrome-defect of myocardial repolarization due to channel defect (increase risk of sudden cardiac death due to torsades de pointes
- autosomal dominant, pure cardiac phenotype (no deafness) what is this?
2. autosomal rrecessive, sensorineural deafness what is this?
-
AD most common in asian males, ECG pattern of pseudo-right bundle branch block and ST elevation in V1-3. what is this?
- increase risk of Vtach and SCD (prevented SCD with implantable cardioverter-defibrillator (ICD) - most common type of ventricular preexcitation syndrome. abnormal fast accessory conduction pathway bypassing the srate-slowing AV node via bundle of Kent. what is this?
the ventricule begin to depolarize earlier–>characteristic delta wave with wide QRS and shorten PR
can result in reentry circuit–> supraventricular tachycardia
1. Romano-Ward syndrom
2. Jervell and Lange- Nielsen sydrome
1. Brugada syndrome
1. Wolff-Parkinson-White (WPW) syndrome
- choatic, erratic baseline with no discrete P wave, most common risk factor include HTN, CAD, occasionally seen after binge drining. can lead to thromboembolic event (stroke)
Tx with anticoagulation, rate controlm rhythm control and cardioversion
- rapid succesion of identical back to back atrial depolarization thta looks like sawtooth
Tx- like A fib, definitive treatment with catheter ablation
- atrial fibrillation
- artial flutter
- completely erratic rhythm with no identifiable waves, fatal arrhythmia without immediate CPR and defibrillation
- PR interval prolonged >200msec). benign and asymptomatic (no tx)
- Ventricular tachycardia
- 1st degree AV block
progressive lengthening of PR interval until beat is “dropped” (a P wave not followed by QRS complex) asymptomatic
dropped beats that are not preceded by a change in length of PR, may progress to 3rd degree block
tx with pacemaker
atria and ventricles beat independently of each other. P waves and QRS complexes not rhythmically associated. Atrial rate > ventricular rate. usually treated with pacemaker, can be caused by lyme disease
