Transcript Heart
THE CARDIOVASCULAR
SYSTEM: HEART
Lab and Lecture Notes
LAB MATERIAL
Location
Thoracic cavity between two lungs
~2/3 to left of midline
surrounded by pericardium:
Fibrous pericardium Inelastic and anchors heart in place
Inside is serous pericardium- double layer
around heart
Parietal layer fused to fibrous pericardium
Inner visceral layer adheres tightly to heart
Filled with pericardial fluid- reduces friction during
beat.
Figure 15.1
Heart Wall
Epicardium- outer layer
Myocardium- cardiac muscle
Two separate networks via gap junctions in
intercalated discs- atrial & ventricular
Networks- contract as a unit
Endocardium- Squamous epithelium
lines inside of myocardium
Figure 15.2a
Figure 15.2b
Figure 15.2c
Chambers
4 chambers
2 upper chambers= Atria
Between is interatrial septum
Contains fossa ovalis- remnant of foramen ovalis
2 lower chambers = ventricles
Between is interventricular septum
Wall thickness depends on work load
Atria thinnest
Right ventricle pumps to lungs & thinner than left
Great Vessels Of Heart- Right
Superior & inferior Vena Cavae
Delivers deoxygenated blood to R. atrium
from body
Coronary sinus drains heart muscle veins
R. Atrium Tricuspid Valve R. Ventricle
pumps through Pulmonary Trunk
R & L pulmonary arteries
lungs
Great Vessels Of Heart-Left
Pulmonary Veins from lungs
oxygenated blood
L. atriumBicusid (Mitral) Valve Left
ventricle
ascending aorta body
Between pulmonary trunk & aortic arch is
ligamentum arteriosum
fetal ductus arteriosum remnant
Figure 15.3a
Figure 15.3b
Figure 15.3c
Valves
Designed to prevent back flow in response
to pressure changes
Atrioventricular (AV) valves
Between atria and ventricles
Right = tricuspid valve (3 cusps)
Left = bicuspid or mitral valve
Semilunar valves near origin of aorta &
pulmonary trunk
Aortic & pulmonary valves respectively
Figure 15.4ab
Figure 15.4c
Figure 15.4d
Figure 15.5a
Figure 15.5b
Blood Supply Of Heart
Blood flow through vessels in myocardium =
coronary circulation
L. & Right coronary arteries
branch from aorta
branch to carry blood throughout muscle
Deoxygenated blood collected by Coronary
Sinus (posterior)
Empties into R. Atrium
LECTURE MATERIAL
Conduction System
1% of cardiac muscle generate action
potentials= Pacemaker & Conduction system
Normally begins at sinoatrial (SA) node
Atria & atria contract
AV node -slows
AV bundle (Bundle of His)
bundle branches Purkinje fibers
apex and up- then ventricles contract
Pacemaker
Depolarize spontaneously
sinoatrial node ~100times /min
also AV node ~40-60 times/min
in ventricle ~20-35 /min
Fastest one run runs the heart = pacemaker
Normally the sinoatrial node
Figure 15.6
Electrocardiogram
Recording of currents from cardiac
conduction on skin = electrocardiogram
(EKG or ECG)
P wave= atrial depolarization
Contraction begins right after peak
Repolarization is masked in QRS
QRS complex= Ventricular depolarization
Contraction of ventricle
T-wave = ventricular repolarization
Just after ventricles relax
Figure 15.7
Cardiac Cycle
after T-wave ventricular diastole
Ventricular pressure drops below atrial & AV valves
open ventricular filling occurs
After P-wave atrial systole
Finishes filling ventricle (`25%)
After QRS ventricular systole
Pressure pushes AV valves closed
Pushes semilunar valves open and ejection occurs
Ejection until ventricle relaxes enough for arterial
pressure to close semilunar valves
Action Potential
Review muscle
Heart has addition of External Ca2+
creates a plateau
prolonged depolarized period.
Can not go into tetanus.
Figure 15.8
Flow Terms
Cardiac Output (CO) = liters/min pumped
Heart Rate (HR) = beats/minute (bpm)
Stroke volume (SV) = volume/beat
CO = HR x SV
Controls- Stroke Volume
(S.V.)
Degree of stretch = Frank-Starling law
Increase diastolic Volume increases strength of
contraction increased S.V.
Increased venous return increased S.V.
increased sympathetic activity
High back pressure in artery decreased S.V.
Slows semilunar valve opening
Controls- Heart Rate
Pacemaker adjusted by nerves
Cardiovascular center in Medulla
parasympathetic- ACh slows
Via vagus nerve
Sympathetic - norepinephrine speeds
Sensory input for control:
baroreceptors (aortic arch & carotid sinus)- B.P.
Chemoreceptors- O2, CO2, pH
Other Controls
Hormones:
Epinephrine & norepinephrine increase H.R.
Thyroid hormones stimulate H.R.
Called tachycardia
Ions
Increased Na+ or K+ decrease H.R. &
contraction force
Increased Ca2+ increases H.R. & contraction
force
Figure 15.9
Exercise
Aerobic exercise (longer than 20 min)
strengthens cardiovascular system
Well trained athlete doubles maximum
C.O.
Resting C.O. about the same but resting H.R.
decreased
Figure 15.10