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28 Cards in this Set

  • Front
  • Back
the heart
Location, location, location
Thorax Cavity
surrounded by
fibrous pericardium
serous pericardium
epicardium, myocardium, endocardium
serous pericardium
made up of
parietal layer
visceral layer
Microscopic anatomy of
intercalcated discs - desmosomes and gap junctions
mitochondria ~25% of cell volume
typical sarcomeres
Mechanisms of contractions
impulses initiated contraction/or no contraction
Length of refractory period
250 ms
contraction sequence
Na+ influx
transmission of depolarization wave down t-tubules
Ca2+ provides signal of troponin binding and contraction
differences in stimulatoin to release Ca2+
-20% enters from intercellular space
- rest from SR
- typically, Ca2+ barred from cardiac muscle cells until Na+ is open, causing the cells to contract longer
- thus heart contraction tension last 200 ms rather than 15-100 ms as in skeletal muscle
Entery Requirments
needs loads of O2 due to high mitochondria
uses multiple fuel molecules-glucoses and fatty acids mostly
readily switches metabolic pathways, will even use lactic acid
real danger is lack of O2
Intrinsic conduction system
gap junctions with cells tied at intercalcated discs
in-house conduction system
Auto-rhythmic cells
do not have stable resting membrane potential
unstable, continuously depolarizing slowly toward threshold-pacemakers
membrane gradually reduces permeability to K+, interior becomes more positive, at threshold, Ca2+ has explosive entry, no the Na++
Sequence of excitation
sinoatrial node (pacemaker) activated atria
AV node
AV bundle
R & L budles branches - move along two branches to apex of heart
Purkinje fibers - penetrate through the heart apex and then turn upward to ventricles
Sinoatrial node
Inherent rate ~ 100x/min without hormonal factors
Fastest depolarization rate and sets pace for heart as a whole
AV node
Located immediately above tricuspid valve
Activates ventricles - impulse delayed about 0.1 seconds
AV Bundle
only electrical connection between artria and ventricles
also called bundle of HIS
Extrinsic enervation of the heart
ANS modifies
Sympathetic (stimulate via T-1, T-5, via chain ganglia to cardiac plexus to heart and SA % AV nodes
Parasympathetic-inhibits-via medulla via vagus nerve, to ganglia in heart wall
Three waves
P wave (~0.08 s) - SA node depolarizes and then atria contract
QRS complex (~0.08 s) - depolarization of the ventricles and AV node
T wave (~0.16 s) - ventricular repolarization
P-Q beginning of atrial excitation to ventricle excitation
Q-T intervals - whole heart depolarized
Cardiac Cycle
Systole - contraction
diastole - relaxation
Cardiac output - CO =HR x SV (stroke volume)
SV = difference between EDV (end diastolic volume) and end SYV (systolic); affected by length of diastole and pressure
Cardiac cycle
ventricular filling - mid to late diastole
Ventricular systole
Relaxation (early diastole)
Blood flow through the heart is controlled by pressure changes
blood flows down a pressure gradient
Pulmonary pressures about 8-24 mm Hg
Cardia Cycle
Ventricular systole
pressure closes AV valves
Pressure forces open semi-lunar valves
BP in aorta reaches about 120 mm Hg
Cardiac Cycle
Relaxation ( early diastole)
Blood in aorta and pulmonary trunk back flow
closure causes brief rise in aortic pressure, called dicrotic notch
atria fill during systole, as pressure builds up on artrial side valves open up and blood flows to ventricles
Cardiac Cycle
Preload-Frank-Sterling Law
Heart muscles normally shorter than optimum length
filling of ventricles (volume) affect contractile force
exercise and rest and heart health
Cardiac Cycle
Contractility-increase in contractile strength, independent of muscle stretch
more vigorous contractions a direct consequence of increased Ca2+
They lead to a greater SV
Driven by the sympathetic
Remember the rule of "set point"
Positive inotropic agents: digitalis, epinephrine, glucagon, thyroxin-affect forces of muscle contraction
negative inotropic agents: acidosis, High K+ levels, calcium channel blockers
Cardiac Cycle
After load
pressure ventricles must overcome to eject blood into arterial system - 1. Hypertension reduces SV
Cardiac Cycle
Sympathetic releases norepinephrine, binds to B1 andrenergic recepto-threshold &relaxation occure more quickly
para releases Ach which hyperpolarized by opening K+ cells - during rest this is dominant
Cardiac Cycle
Other Hormones
epinephrine - stimulate
thyroxing - stimulate
Ione balance
Cardiac Cycle
Arises from mesoderm
heart goes through multiple changes through second month without missing a beat
Heart & Health
LDL - bad below 90
HDL - good above 45
VLDL & triglycerides
weight, BP, exercise