bsc2094 m1 - the heart physiology

physiology of the heart *cries*

ekg and ecg

same thing, used in diff regions. both show action potentials and re/depolarization (which triggers contractions)

heart muscle

stimulated by nerves and is self excitable (automaticity) (brain doesn’t make heart stop beating, can speed up or down)

cardiac musc contraction

is like skeletal musc contraction w two main diff:

slower, contraction as one cell results in contraction of all other cells (all-or-nothing principle)

intrinsic conduction system - autorhythmic cells

act as a pacemaker - sets rhythm of electrical excitation that causes contraction of heart; make up 1% cardi tissue

spontaneous depo is a pacemaker potential: when the pacemaker potential reaches certain threshold, it triggers an action potential

where autorhythmic cells are found: PICTURE

sinoatrial node (SA), atrioventricular node (AV), atrioventricular bundle, R/L bundle branches, Purkinje fibers

sequence of excitation PICTURE 2

sinoatrial (SA) node → atrioventricular (AV) node → atrioventricular bundle (bundle of His) → bundle branches → Purkinje fibers

sinoatrial (SA) node

generates impulses abt 100x/min; responsib for initiation of heartbeat + sets pace (pacemaker)

happens when enough Na+ and Ca²+ leak into cells of SA node to reverse resting potentials

pacemaker potentials (PP) propagates thru both atria by gap junctions; both A contract and pumps blood A → V

atrioventricular (AV) node

located in lower RA

AV node delays impulse approx 0.1 sec; hesitation allows V to fill; AV fires

AV bundle (bundle of His)

impulse passes from atria to ventricles thru bundle; splits into two pathways in interventricular septum (bundle branches)

A and V not just connected by gap junctions - AV bundle is the only electrical connection between them

bundle branches

carry impulse toward apex of the heart

Purkinje fibers

carry impulse to heart apex and ventricular walls

keeps papillary muscs contracted in AV valves and V contract

bpm per sequence: SA, AV n and b, branch and purk

SA node - 75bpm (60~100)

AV node and bundle - 40~60

bundle branches and Purkinje - 20~40

action potentials

autorhythmic cells have special ability to depo spontaneously + thus pace heart; an action potential is prod, which stims cardi musc

sinoatrial node action potential PICTURE

threshold -40mV → rapid influx of Ca²+ to ~20mV → outflux of K+ for repo -60mV (resting mm potential) → slow influx Na+ for prepotential, returns to -40mV → cycle repeats

PICTURE of SA node process

contractile cells PICTURE

connected to nodal cells by gap junctions

contractile cells action potential

threshold -90mV → rapid depo, voltage gated ion channels open, influx of Na+ -85mV to 30mV → plateau phase: Na+ channels close 30mV, slow Ca2+ channels open ~0mV → repo: slow Ca2+ channels close (gain +) ~0mV → K+ channels close ~-90mV → cycle repeats

picture of graph

picture of diagram

electrocardiogram (EKG or ECG) PIC of labeled ecg

graphic record of heart activity, composite of all action potentials gen by nodal and contractile cells at a given time

can determine: if conduction pathway is abnormal, heart is enlarged, or certain parts of heart are damaged

P wave

atria depolarize; approx 0.1 sec afper P wave begins, atria contract

QRS complex

results from ventricular depo, precedes V contraction

has complicated shape bc paths of depo waves thru V walls change continuously, prod corresponding changes in current direction

T wave

V repo

repo slower than depo, so T wave more spread out + lower amp (height) than QRS wave

P-R(Q) interval

time it takes for elec impulse to travel from A to V

P-Q (R) segment

time when A contractile fibers are contracted

S-T segment

time when V contractile fibers are contracted

Q-T interval

time from ventricular depo to end of repo

T-P interval

ok we changing stuff up, go to study guide set