Download Cardiovascular System Review

Cardiovascular System
Anatomy:
 Pulmonary artery- only artery to carry deoxygenated blood (carries blood to
lungs)
 Pulmonary vein- only vein to carry oxygenated blood (from the lungs)
 Left ventricle wall thicker because pumps blood to whole body
 Left valve is bicuspid- only two flaps
 Papillary muscles pull on the chordae tendineae, which pull on the cuspids, that
forces the valves shut
 Murmur: abnormal third heart sound- left ventricle blood goes back into the
atrium
 Not all blood cells will make it over the aortic arch, some falls back on the semilunar
valves, which catch it and force the valve shut
Problems:
 Angina pectoris: partial obstruction of coronary blood flow can cause chest paincan’t pick up enough oxygen during exercise causes your chest to hurt
 Myocardial infarction- true cell death, complete obstruction causes death of
cardiac cells in an affected area, too much of this for too long causes a heart attack
o Exercise induced cardioprotection- exercise prevents heart tissue death
following a heart attack
 Myocardial stunning- temporary blockage, does not result in cell death
 Tachycardia- abnormally fast heartbeat
 Bradycardia- abnormally slow heart rate
Defects of intrinsic conduction system:
 Arrythmias- irregular heart rhythms
 Uncoordinated atrial and ventricular contractions
 Fibrillation: rapid, irregular contractions that are useless for pumping blood
(dead person)
 Defective SA node: ectopic focus- something else setting the pace, causes
junctional rhythm (no P wave) if AV node takes over (40-60 bpm)
 Defective AV node: may result in partial or total heart block, few or no impulses
from SA node reach the ventricles, electrical signal stops
How Heart Contracts:
 1% of cardiac cells are self-excitable, so don’t need nerve stimulation to contract,
depolarize the rest (why heart can beat out of the body for transplants)
 Depolarization opens Na+ channels, -90 to 30, causes SR to release Ca2+
 ALSO opens slow Ca2+ channels in the sarcolemma that prolong the depolarization
phase (increases refractory period=decreases chance of having another AP mess up
the heart rhythm)
 Ca2+ influx triggers opening of Ca2+ sensitive channels in the SR, which liberates
bursts of Ca2+
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E-C coupling occurs as Ca2+ binds to troponin and filament sliding begins
Autorhythmic Cells
 Pacemaker potentials 0 unstable due to open of slow Na+ channels
 Explosive Ca2+ influx produces rising phase of Aps, repolarization= closing of Ca2+
and opening of voltage gated K channels
 HAPPENS IN FAST CELLS ONLY?
 Sodium starts to leak in again = pacemaker potential so line never goes flat
Excitation
 1. SA node- pacemaker that sets the rhythm, depolarizes the fastest than any other
part in the heart (easier for SA node when sympathetic tone increases)
 2. AV node- delays the impulse because of smaller diameter fibers and fewer gap
junctions (depolarizes A LOT in absence of SA node input)
 3. Atrioventricular bundle (bundle of his) only electrical connection between atria
and ventricles
 4. Right and left bundle branches- two pathways in the septum that carry impulses
to the apex of the heart
 5. Purkinje fibers- complete the pathway into the apex and ventricular walls
EKG
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Definition: a composite of all the action potentials generated by nodal and
contractile cells at a given time
o P wave: atrial depolarization (SA node depolarization)
o QRS complex: ventricular depolarization (atrial repolarization masked)
o T wave: ventricular repolarization
o Change in direction of blood flow makes the weird angles on the graph
o Height affected by the size of what’s depolarizing
Irregular graphs:
o No obvious waves of any kind=dying person=fibrillation
o Junctional rhythm- P waves are absent=living person= no functional SA node
(two obvious spikes)
o Second degree heart block: missing QRS every other time, some waves are
not conducted through the AV node, so more P waves than QRS
Cardiac Rhythm:
 Systole- ventricular contraction
 Diastole- ventricular relaxation/filling
 1. Rising pressure opens the semilunar valves and blood is rapidly ejected
o This amount ejected is the stroke volume: 70mL at rest
o SV/End diastolic volume= ejection fraction; at rest 54%, vigorous exercise as
high as 90%, diseased heart less than 50%
o End systolic volume: amount left in the heart after contraction
 Cardiac Output= heart rate x stroke volume
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o To maintain steady cardiac volume, if one factor increases, the other
decreases
o At rest: 75 bpm x 70 mL/beat = 5.25 mL/min
o Cardiac reserve: difference between resting
o Heart rate increases, so does milk yield in mammals
Stroke Volume:
o EDV (end diastolic volume)- ESV (end systolic volume/end of contraction)
o Three main factors:
Preload: adding a slight stretch to the ventricles optimizes myosin/actin overlap,
causing better contractions and more force to be enacted. This causes more blood to
leave the heart=larger stroke volume
Contractility: contractile strength at a given muscle length, independent of muscle
stretch and EDV
o Increased Ca2+ influx due to sympathetic stimulationmore cross bridges
formedmore forcemore blood leaveslarger SV/leads to preloading
o Decreased contractility: acidosis, increased extracellular K, calcium blockers
Afterload: pressure that must be overcome to eject blood
o Hypertension increases afterload, resulting in increased ESV and decreased
SV
Extrinsic Innervation of the heart: centers located in medulla oblongata
 Cardioacceleratory center innervates SA/AV nodes, heart muscle, coronary
arteries through sympathetic neurons
 Cardioinhibitory center- inhibits SA/AV nodes, through parasympathetic
fibers in the vagus nerves
 Atrial (Bainbridge) reflex: a sympathetic reflex initiated by increased venous
return (Stretch of atrial walls stimulates the SA node, also stimulates atrial
stretch receptors, activating sympathetic reflexes
 Proprioceptors: