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Cardiovascular basic science, Physiology, Embryology, Anatomy - Coggle…
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Physiology
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cardiac output
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↑pulse pressure: hyperthyroidism, aortic regurgitation, aortic stiffening, obstructive sleep spnea, anemia, exercise
pulse pressure=systolic-diastolic, (proportional to SV, inversely proportional to arterial compliance)
↓pulse pressure: aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure
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variables
stroke volume: ↑contractility, ↑preload, ↓afterload→↑SV
contractility: catecholamine stimulation via β₁ receptor (Ca²⁺ channel, phospholamban phosphorylation), ↑intracellular Ca²⁺, ↓extracellular Na⁺, digitalis →↑contractility
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myocardial oxygen demand: ↑contractility, ↑afterload, ↑heart rate, ↑diameter of ventricle→↑↑↑
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resistance, pressure, flow
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electrocardiogram
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wave
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PR interval: time from start of atrial depolarization to start of ventricular depolarization (normally <200msec)
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QT interval: ventricular depolarization, contraction, repolarization
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U wave: prominent in hypokalemia, bradycardia
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AV node: located in posteroinferior part of interartrial septum, blood suply from RCA, 100 msec delay
pathway
SA node→atria→AV node→bundle of His→right and left bundle branches→Purkinje fiber→ventricles (left branch have anterior and posterior fascicle)
pre-excitation disorder
Torsades de pointes
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caused by drugs, ↓K⁺, ↓Mg²⁺, congenital abnormalities
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ECG tracing
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AV block
second degree
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mobitz type 2
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often treat with pacemaker, may progress to 3rd
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atrial flutter(心房粗動)
treat like atrial fibrillation, catheter ablation
identical, back to back atrial depolarization wave, "sawtooth"
atrial fibrillation(AF)
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risk factor: hypertension, coronary artery disease
treatment: anticoagulation, rate control, rhythm control, cardioversion
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starling curve
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↑contractility with catecholamines, positive inotropes(eg. digoxin)
↓contractility with loss of myocardium, β-blocker, non-dihydropyridine Ca²⁺ channel blocker, dilated cardiomyopathy
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splitting
wide splitting
delay RV emptying (eg. pulmonic stenosis, RBBB)
caused delayed pulmonic sound, exaggeration of normal splitting
fixed splitting
ASD→left-to-right shunt→↑RA and RV volume→↑flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed
normal splitting
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inspiration→↓intrathoracic pressure→↑venous return→↑RV filling→↑RV stroke volume→↑RV stroke time→delayed closure of pulmonary valve
paradoxical splitting
delay aortic valve closure (eg. aortic stenosis, LBBB)
on inspiration, P2 closes later and moves closer to A2
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hear murmur
diastolic
AR
due to aortic dilation, bicuspid aortic valve, endocarditis, rheumatic fever
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MS
chronic MS lead to LA dilatation→dysphagis, hoarseness
opening snap, delayed rumbling
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systolic
MR, TR
MR: loudest at apex and radiates toward axilla, MR is due to ischemic heart disease, MVP(僧帽弁逸脱症), LV dilatation
TR: loudest at tricupsid area, caused by RV dilatation
holosystolic, high pitched blowing murmur
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aortic stenosis
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lead to syncope(失神), angina, dyspnea
VSD
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holosystolic, harsh-sounding murmur
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normal cardiac pressure
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autoregulation
heart: adenosine, NO, CO₂, ↓O₂
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skeletal muscle: CO₂,H⁺,adenosine, lactate, K⁺
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RA<5,RV=25/2, PA=25/10, LA<12, LV=130/10, Ao=130/90
capillary fluid exchange
determination factor: capillary pressure(Pc), interstitial fluid pressure(Pi), plasma colloid osmotic pressure(πc), interstitial fluid colloid osmotic pressure(πi)
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edema
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caused by: ↑capillary pressure, ↓plasma protein, ↑capillary permeability, ↑interstitial fluid colloid osmotic pressure
natriuretic peptide
ANP(心房性ナトリウム利尿ペプチド)
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dilate afferent renal arterioles and constrict efferent arterioles, promoting diuresis and aldosterone escape
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BNP(脳性ナトリウム利尿ペプチド)
similar to ANP, with longer half time
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Embryology
heart embryology
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endocardial cushion: artial septum, membranous interventricular septum, AV and semilunar valve
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Fetal circulation
at birth,,, ↑O2 and ↓prostagrandin→closure of ductus arteriosus
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at birth,,, breath→↓resistance of pulmonary vasculature→↑left artrial pressure→foramen ovale closed
PO₂=30mmHg, 80% saturated
morphogenesis
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septation
outflow tract
neural crest and endocardial cell migration→truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum→ascending aorta and pulmonary trunk
failure of neural crest cell to migrate: transposition of great vessel, tetralogy of fallot, persistent truncus arteriosus
ventricle
- muscular interventricular septum forms
- aorticopulmonary septum rotate and fuse with muscular ventriculr septum to membranous intraventricular septum
- growth of endocardial cushion separete atria from ventricles and contribute to both atrial septation and membranous portion of the interventricular septum
ventricular septal defect: most common congenital cardiac anomaly, usually in membranous septum
atria
- septum primum (一次中隔) grows toward endocardial cushion, narrowing foramen primum(一次口)
- foramen secundum forms in septum primum
- septum secundum develops as foramen secondum maintain right-to-left shunt
- septum secundum expands and covers most of foramen secundum, the residual foramen is foramen ovale(卵円孔)
- remaining portion of septum primum forms valve of foramen ovale
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patent foramen ovale: failure of two septums to fuse, can lead to paradoxical wmboli(奇異性塞栓)
cardiac looping
establish left-right polarity, begins at 4 week of gestation
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valve development
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stenosis(狭窄), regurgitant(逆流), atretic(閉鎖), displaced(Ebstein anomaly)
Anatomy
Anatomy of heart
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LCA; left main coronary artery; LCX; left circumflex coronary artery; LAD: left anterior descending artery; RCA: right coronary artery; PDA: posterior descending artery
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most posterior part is LA; enlargement→dysohagia, hoarness
right-dominant circulation (85%)=PDA arises from RCA, left-dominant (8%)=PDA arises from LCX, codominant(7%)
pericardium consists of 3 layers: fibrous pericardium(線維性心膜), parietal layer of serous pericardium(壁側漿膜), visceral layer of serous pericardium(臓側漿膜)
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