Physiology Flashcards
(52 cards)
Depolarization of free walls of ventricles
Endocardium to epicardium
Purkinjie fibers are located in the endocardial layer (Subendocardium)
Depolarization direction of IV septum
Left to right due to the shortness of Anterior LBB vs RBB
Depolarization of ventricles direction
Right ventricle completely depolarizes before the left because the outer wall is much thinner (fewer myocytes to take over cell to cell conduction after Purkinjie fibers)
Repolarization of ventricles
Epicardial cells
Duration of Epicardial cells is shorter than duration of action potentials for endocardial cells
Epicardium to endocardium.
Endocardial contracts sooner and lasts longer, epicardial contracts later and relaxes sooner
Split second heart sound during inspiration and expiration
Delayed right ventricular contraction,
RBBB
Prolonged right ventricular ejection
Paradoxical split
Split second heart sound heard during expiration but not inspiration
Delayed left ventricular contraction
LBBB
Or prolonged left ventricular ejection
Systolic murmurs
Stenosis of semilunar valves
Insufficiency of atrioventricular valve–holosystolic
Severe mitral–early systolic
Three general regions so AV node and cells they contain
AN-atrial muscle cells and nodal type cells
N-only nodal cells with slow changing pre potential (phase 4), slow rate of Phase 0, and low amplitude AP
NH zone–nodal cells and fibers of the bundle of His
—faster than N only zone because His fibers have a rapid rate of depolarization and large amplitude depolarization during phase 0
Systolic murmurs vs holosystolic murmurs
Systolic–mitral/tricuspid insufficiency and aortic/pulmonary stenosis
Holosystolic–mitral/tricuspid insufficiency
Reduced ejection (left vent pressure vs aorta)
Left vent.aortic
PR interval
Conduction time between atrial and ventricles
Completely depolarized ventricles, which segment
ST segment
RAD, LAD, Circumflex leads
RAD–II, III, aVF
LAD– V1, V2 (septal)(lad for the V’s)
Circumflex–I, aVL (I-alphabetically first, and L-fLEX)
P wave
Atrial depolarization and contraction
PR interval
Beginning of P wave to beginning of Q wave–initial depolarization of the ventricle
Varies with conduction velocity through the AV node–heart block (AV conduction decreases, PR increases)
Decreased by stimulation of SNS
Increased by PNS
Pathway of baroreceptor inhibition of SNS in brain
Caudal ventral lateral medulla in SNS vasodepressor center to rostral ventral lateral medulla in vasopressorlcenter… Inhibition using GABA.
CVLM (depressor—CD)
RVLM(pressor–PR)
First degree AV block
More than 1 large square for PR interval (greater than .2)
Consistent in every cycle
P-QRS-T order normal for every cycle
Conduction delay in AV node
Wenekebach/Type 1
One less QRS than P waves, (3:2, 4:3)
PR gradually increases
Final P fails to conduct QRS
Parasympathetic excess, so vagal makes it go from 3:2-4:3
QRS is normal (less than .2) because the block is the AV node
Mobitz/Type II
Located in purkenji/bundle of His 1 normal P-QRS-T, followed by just a P 2:1 or 3:1 QRS widened P-P normal. Vagal maneuver eliminates
Third degreee junctional
Atrial depolarization not conducted to ventricles
Upper AV blocked, junctional complex takes over
Normal/narrow QRS with a rate (RR) of 40-60 bpm (slower rate than PP)
Third degree AV block, ventricular focus
Slower than junctional (RR is approximately 20-40 bpm)
Cerebral blood flow compromised, syncope
Large, wide PVC-like complexes
Completely obliterated AV node or right below the AV node)
RBBB
Right axis deviation (+120-+180)
Widened QRS >0.12 (or 3 small squares)
Chester leads–V1, V2
R is left ventricle, r’ is right ventricle
LBBB
Left axis deviation (-30 to -90) QRS > .12 (3 small squares) Chest leads V5 and V6 R would be right ventricle R' is left ventricle
Depolarization of the heart proceeds in what direction
Endocardium to epicardium
