Cardiology Flashcards
Bulbus cordis gives rise to…
Smooth/outflow parts of L and R ventricles
Endocardial cushion gives rise to…
Atrial septum
Membranous interventricular septum
AV and semilunar valves
Primitive pulmonary vein gives rise to…
Smooth part of L atrium
Right horn of sinus venosus gives rise to…
Smooth part of R atrium
Right cardinal veins give rise to…
SVC
Note - Target of central line
Embryologic mechanism of dextrocardia (e.g. Kartagener syndrome).
Defect in left-right dynein involved in L/R asymmetry during cardiac looping (4 weeks).
Age at which heart beats spontaneously
4 weeks
Steps of atrial separation (4)
Septum primum (top) grows towards endocardial cushion (bottom) narrowing foramen primum
Foramen secundum forms in septum primum as it continues to close foramen primum
Septum secundum (top) grows down to cover most of foramen secundum - residual is foramen ovale
Septum primum degenerates with remainder forming valve of foramen ovale - after birth fuse to form atrial septum due to increasing LA pressure
Note - Increasing RA pressure (straining) allows R to L shunt and may lead to cryptogenic stroke
Steps of ventricular separation (3)
Muscular interventricular septum (bottom) forms with opening called interventricular foramen
Aorticopulmonary septum (truncal/bulbar ridges) rotates and grows down to fuse with muscular septum - forms membranous interventricular septum and closes interventricular foramen
Endocardial cushions grow horizontally to separate atria from ventricles - also contributes to membranous interventricular septum
Mechanism of conotruncal abnormalities…
Persistent truncus arteriosus
Transposition of great vessels
Tetralogy of fallot
Failure of neural crest cells to migrate
Fetal circulation
Oxygenated blood from umbilical vein joins IVC via ductus venosus - mostly bypasses hepatic circulation
Enters RA and goes directly to LA via foramen ovale
Deoxygenated blood from SVC goes to RA, RV, and pulmonary artery, but is shunted to descending aorta (after left subclavian) via ductus arteriosus - due to high fetal pulmonary artery resistance (low O2 tension)
Deoxygenated blood returns via umbilical arteries off of internal iliacs
Mechanism of closure of fetal circulation
Decreased resistance in pulmonary vasculature leads to increased LA pressure - foramen ovale closes
Increased O2 and decreased prostaglandins (E1/E2) from placental separation lead to closure of ductus arteriosus - closed with Indomethacin
Postnatal derivative of... Allantois/urachus Ductus venosus Ductus arteriosus Notochord Umbilical arteries Umbilical vein
Median umbilical ligament Ligamentum venosum Ligamentum arteriosum Nucleus pulposus Medial umbilical ligaments Ligamentum teres
Right acute marginal artery supplies…
Right ventricle
Posterior interventricular/Posterior descending artery (PDA) supplies…
Note - 85% have PDA come off of RCA, while minority have PDA come off of LCX
Posterior ventricular walls
Posterior 1/3 of interventricular septum
Posteromedial papillary muscles
Left circumflex artery (LCX) supplies…
Lateral and posterior walls of LV
Anterolateral papillary muscles (via obtuse/marginal)
Anterior interventricular/Left anterior descending (LAD) supplies…
Anterior surface of LV
Anterior 2/3 of interventricular septum
Anterolateral papillary muscle
Blood supply to the SA and AV nodes…
Note - infarct may cause nodal dysfunction resulting in bradycardia and heart block
RCA
Fick’s principle
CO = rate O2 consumption/(arterial O2 - venous O2)
Maintenance of CO (SV x HR) during early and late exercise
Note - SV = EDV - ESV
Early both HR and SV
Late only HR - SV plateaus
Equation for MAP (afterload)
CO x TVR
OR
(2/3)Diastolic pressure + (1/3)Systolic pressure
Mechanism for decreased CO in VT
Diastole is preferentially shortened with increasing HR, decreasing filling time
Pulse pressure in... Hyperthyroidism Aortic regurgitation Aortic stiffening (isolated systolic HTN in elderly) OSA (sympathetic tone) Exercise
Increased
Pulse pressure in... Aortic stenosis Cardiogenic shock Cardiac tamponade Advanced HF
Decreased
Mechanism of catecholamine induced inotropy (and SV).
Phosphorylation of Phospholamban
Decreased inhibition of SERCA (Ca-ATPase)
Increased Ca entry into SR during relaxation
Upon next contraction…
Increased Ca-induced Ca release via RyR2 channels
Increased Ca-Troponin complex removal of Tropomyosin
Note - Na/Ca exchanger moves Ca out of cell instead of into SR during relaxation
Note - In smooth muscle Calmodulin instead of Troponin
Law explaining…
Increased O2 demand with increasing ventricular diameter
LV hypertrophy to compensate for increased afterload
LAPLACE’S LAW
Wall tension = (pressure x radius)/(2 x wall thickness)
Increased radius means increased wall tension/O2 demand
Increased wall thickness means decreased wall tension caused by increased afterload
Ejection fraction
Normal is > 55 - decreased in systolic HF but normal in diastolic HF
EF = SV/EDV = (EDV - ESV)/EDV
Action of the following on preload and afterload…
Venodilators (e.g. Nitrates)
Arteriolar vasodilators (e.g. Hydralazine)
Nitroprusside
Decreased preload (decreased O2 demand, reduced compression of coronary arteries during diastole)
Decreased afterload (activates RAAS)
Decreased preload and afterload (no effect on SV)
Note - ACEi/ARBs also affect both preload and afterload
Relationship between EDV and SV/CO (Frank-Starling curves)
Along a curve as EDV (preload) increases SV increases - force of contractility is proportional to end diastolic length of cardiac muscle fibers
As inherent contractility (inotropy) increases curve is shifted to the left - higher contractility at the same EDV
Volumetric flow rate equation
Q = flow velocity x cross sectional area (inverse of R)
Note - Capillaries have lowest velocity and highest cross sectional area
Relationship of RA pressure and venous return/CO (vascular function curves)
Increasing RA decreases venous return/CO via decreasing pressure gradient
When CO is at 0 (x-intercept) you get mean systemic pressure
When RA pressure is at 0 CO begins to plateau due to collapsing of vena cava
Location of pericardial cavity
Between fibrous pericardium/parietal pericardium and visceral pericardium.
Most posterior portion of the heart - responsible for dysphagia and hoarseness
Left atrium
Most anterior portion of the heart
Right ventricle
Note - Injury directly to LLSB will puncture lung pleura and right ventricle but not the lung
Relationship between Frank-Starling (cardiac) and vascular function curves.
Intercept of two curves is where the venous return and CO are equal = operating point of the heart
Note - cardiac function curves maintain an x/y intercept of 0
Cardiac/vascular function curve with increase in contractility
http://i.imgur.com/UFwPm59.png
Increased CO at lower RA pressure
Cardiac/vascular function curve with increase in volume/venous tone
http://i.imgur.com/Brgkvxj.png
Increased CO at higher RA pressure
Cardiac/vascular function curve with decrease in TPR (exercise, AV shunt)
http://i.imgur.com/QKvFuLN.jpg
Increased CO while maintaining same RA pressure
Note - alternatively, increase in TPR (vasopressors) will cause decreased CO while maintaining same RA pressure
Cardiac/vascular function curve in HF
http://i.imgur.com/VLyZQxu.png
Decrease in CO due to decreased inotropy (A to B) partially offset by increase in volume/venous tone (A to C)
Phases of left ventricular contraction (PV loop)…
Increased LVP at stable LVV (EDV)
Decreasing LVV (EDV to ESV) at increasing (rapid) then decreasing (reduced) LVP
Decreasing LVP at stable LVV (ESV)
Increasing LVV (ESV to EDV) at relatively stable LVP
Isovolumetric contraction - period between mitral valve closing and aortic valve opening (highest O2 consumption)
Systolic ejection - period between aortic valve opening and closing
Isovolumetric relaxation - period between aortic valve closing and mitral valve opening
Rapid/reduced filling - period between mitral valve opening and closing
Effect of increased afterload on PV loop
Increased ESV and maximum LVP - decreased SV (area in loop)
Effect of increased preload on PV loop
Increased EDV with stable ESV - increased SV (area in loop) without increase in EF
Effect of increased contractility on PV loop
Decreased ESV with stable EDV - increased SV (area in loop) and EF
Note - Line from origin of graph to top left point of loop is the Frank-Starling line
Valves/stage of cardiac cycle associated with S1 (loudest at mitral area/apex)
Closure of mitral and tricuspid valves at the beginning of isovolumetric contraction/systole
Valves/stage of cardiac cycle associated with S2 (loudest at LUSB)
Closure of aortic and pulmonary valves at the beginning of isovolumetric relaxation/diastole
Mechanism/stage of cardiac cycle associated with S3 (loudest at apex in LLD position at end expiration)
(“Kentuk-ey”)
Increased filling pressures (MR, HF) or dilated ventricle - occurs with rapid ventricular filling/early diastole
Note - may be normal in children and young adults
Mechanism/stage of cardiac cycle associated with S4 (loudest at apex in LLD position)
(“Ten-nessee”)
Increased atrial pressure and ventricular noncompliance (atrial kick against stiff LV) - occurs with atrial systole/late diastole
Stages of JVP…
a wave (absent in afib, prominent in tricuspid stenosis)
c wave
x descent (absent in tricuspid regurg)
v wave
y descent (absent in tricuspid stenosis and tamponade, prominent in constrictive pericarditis)
RA contraction
RV contraction resulting in tricuspid valve bulging into atrium
RA relaxation resulting in downward displacement of tricuspid valve during ventricular contraction
Increased RA pressure due to filling against closed tricuspid valve
RA emptying into RV prior to RA contraction
Mechanism of wide splitting as seen in pulmonary stenosis and RBBB
Delayed RV emptying delay pulmonic sound especially on inspiration
Exaggeration of normal splitting on inspiration due to increased venous return and decreased pulmonary impedance
Mechanism of fixed splitting as seen in ASD
Note - Also loud S1
L to R shunt increases RA/RV volumes so that there is increased flow through pulmonary valve regardless of inspiration
Mechanism of paradoxical splitting as seen in aortic stenosis and LBBB
Delayed aortic valve closure causes a “fixed split” during expiration - disappears during inspiration as pulmonary valve closure occurs later and “catches up” to aortic valve closure
Harsh crescendo-decrescendo systolic murmur
Loudest at mid systole - may eliminate S2
Loudest at RUSB (base)
Pulsus parvus et tardus
Radiates to carotids
Note - Concentric hypertrophy (pressure overload)
AORTIC STENOSIS
Calcification in older patients
Bicuspid aortic valve in younger patients
Holosystolic, high-pitched blowing murmur
Loudest at apex
Radiates to axilla
Note - Eccentric hypertrophy (volume overload)
MITRAL REGURGITATION
Treat with afterload reduction
Post-MI Infective endocarditis MVP LV dilation (functional/reversible) Acute rheumatic fever (initially)
Note - Acutely regurgitant syndromes present with increased pressure and decreased CO as heart has not had time to adapt
Holosystolic, high-pitched blowing murmur
Loudest at LLSB
Radiates to RSB
Note - Increases with inspiration (unlike MR)
TRICUSPID REGURGITATION
RV dilation
Infective endocarditis
Ebstein anomaly
Midsystolic click (chordae tendinae tensing) occurring earlier with inspiration
Late systolic crescendo murmur
Loudest right before S2
Loudest at apex
MITRAL VALVE PROLAPSE
Myxomatous degeneration
Chordae rupture
Predisposes to infective endocarditis
Holosystolic harsh murmur
Loudest at LLSB
VENTRICULAR SEPTAL DEFECT
Associated with fetal alcohol syndrome
High-pitched “blowing” diastolic decrescendo murmur
Loudest at early diastole - may eliminate S1
Loudest at LUSB and leaning forward
No inspiratory increase (unlike pulm regurg)
Hyperdynamic/bounding pulse (increased systolic, decreased diastolic) - may see head bobbing
Palpitations at night
Note - Eccentric hypertrophy (volume overload)
AORTIC REGURGITATION
Aortic root dilatation
Bicuspid aortic valve
Endocarditis
Note - Occasionally occurs from rheumatic fever (fusion of commissures) but will always occur with mitral valve stenosis
Early diastolic opening snap Rumbling mid diastolic murmur Decrescendo with presystolic accentuation Loudest at apex PCWP > LVEDP
Note - Patients also tend to have afib if severe, which might make accentuation disappear
MITRAL STENOSIS
Chronic rheumatic fever (late lesion) - commissural fusion
Note - More severe stenosis results in shorter A2-OS interval (earlier maximum diameter)
Continuous machine-like murmur
Loudest at left infraclavicular area
Lower extremity cyanosis
PATENT DUCTUS ARTERIOSUS
Congenital rubella
Prematurity
Note - Lower extremity cyanosis requires Eisenmenger’s syndrome
Diastolic and systolic murmurs loudest at LUSB
Systolic:
HOCM
Pulmonary stenosis
Flow murmur
Diastolic:
Aortic regurgitation
Pulmonary regurgitation
Diastolic and systolic murmurs loudest at LLSB
Systolic:
Tricuspid regurgitation
VSD
Diastolic:
Tricuspid stenosis
ASD
Effect of hand grip (increased afterload) on murmurs
Increased:
Mitral regurgitation
Aortic regurgitation
VSD
Decreased:
HOCM
Effect of valsalva/standing up (decreased preload) on murmurs…
Increased:
HOCM
MVP
Decreased: Most murmurs (including aortic stenosis)
Effect of rapid squatting/leg raise (increased preload, increased afterload) on murmurs
Increased: Most murmurs (including aortic stenosis)
Decreased:
HOCM
MVP
Phases (0-5) of cardiac action potential
Rapid depolarization due to voltage-gated Na channels
Initial repolarization due to inactivation of voltage-gated Na channels and opening of voltage-gated K channels
Plateau due to balance between voltage-gated K channels and voltage-gated Ca channels (Ca-induced Ca release)
Rapid repolarization due to massive efflux from voltage-gated slow K channels - Ca channels now closed
Resting potential maintained by high K permeability through K channels
Phases (0, 3, 4) of pacemaker action potential
Slow upstroke due to opening of voltage-gated L-Ca channels (allows for AV delay) - fast voltage-gated Na channels permanently inactivated due to high resting potential
Repolarization due to inactivation of L-Ca channels and increased activation of K channels
Slow spontaneous diastolic depolarization due to If/funny (Na) current - certain threshold opents T-type Ca channels
Mechanism of effect of Ach/adenosine, catecholamines, and sympathetic activation on HR
Ach/Adenosine decrease rate of diastolic depolarization decreasing SA activity, slow AV conduction, and prolong AV refractory period
Catecholamines increase rate of diastolic depolarization increasing SA activity, increasing AV conduction, and shortening AV refractory period
Note - SA node located near SVC opening
Relative speed of conduction of atria, AV node, Purkinje fibers, and ventricles
Purkinje (contraction) > atria > ventricles > AV node (delay)
Responsible for conduction to LA from SA node
Bachmann bundle
U-wave (after T wave) indicates…
Hypokalemia
Bradycardia
Mechanical action of heart during…
QRS (ventricular depolarization)
ST
T-wave (ventricular repolarization)
Mechanical function lags behind electrical activity
Isovolumetric contraction
Rapid ejection
Reduced ejection