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28 Cards in this Set
- Front
- Back
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the heart
Location, location, location |
Thorax Cavity
Mediastinum |
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Mediastinum
surrounded by |
fibrous pericardium
serous pericardium epicardium, myocardium, endocardium |
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serous pericardium
made up of |
parietal layer
visceral layer |
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Microscopic anatomy of
heart |
striated
intercalcated discs - desmosomes and gap junctions mitochondria ~25% of cell volume typical sarcomeres |
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Mechanisms of contractions
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stimulations-auto-rhythmicity
impulses initiated contraction/or no contraction |
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Length of refractory period
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250 ms
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contraction sequence
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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 |
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Entery Requirments
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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 |
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Intrinsic conduction system
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gap junctions with cells tied at intercalcated discs
in-house conduction system |
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Auto-rhythmic cells
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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++ |
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Sequence of excitation
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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 |
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Sinoatrial node
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Inherent rate ~ 100x/min without hormonal factors
Fastest depolarization rate and sets pace for heart as a whole |
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AV node
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Located immediately above tricuspid valve
Activates ventricles - impulse delayed about 0.1 seconds |
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AV Bundle
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only electrical connection between artria and ventricles
also called bundle of HIS |
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Extrinsic enervation of the heart
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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 |
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ECG (EKG)
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 |
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ECG (EKG)
Intervals |
P-Q beginning of atrial excitation to ventricle excitation
Q-T intervals - whole heart depolarized |
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Cardiac Cycle
Terms |
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 SV=EDV-ESV |
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Cardiac cycle
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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 |
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Cardia Cycle
Ventricular systole |
pressure closes AV valves
Pressure forces open semi-lunar valves BP in aorta reaches about 120 mm Hg |
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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 |
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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 |
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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 |
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Cardiac Cycle
After load |
pressure ventricles must overcome to eject blood into arterial system - 1. Hypertension reduces SV
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Cardiac Cycle
ANS |
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 |
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Cardiac Cycle
Other Hormones |
epinephrine - stimulate
thyroxing - stimulate Ione balance heat |
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Cardiac Cycle
Development |
Arises from mesoderm
heart goes through multiple changes through second month without missing a beat |
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Heart & Health
Factors |
LDL - bad below 90
HDL - good above 45 VLDL & triglycerides homocistine history weight, BP, exercise cures |
