Chapter 5 Flashcards
Tributaries of SVC
External jugular veins Internal jugular veins Subclavian veins Brachiocephalic veins Posterior intercostal veins Azygos vein
Fetus and placenta
Thymus Placenta Umbilical cord Umbilical arteries Umbilical vein
Branches of aortic arch
Brachiocephalic artery
Common carotid arteries
Subclavian arteries
Branches of thoracic aorta:
Posterior intercostal arteries
Respiratory and Digestive Structures:
Trachea Main bronchi Lungs Secondary bronchi Pleurae Esophagus
lungs
- Apex
- Base
- Root
Pleurae
Parietal pleurae
Visercal pleurae
Pleural cavities
Nerves
Vagus nerves
Phrenic nerves
Sympathetic trunk ganglion
left recurrent laryngeal nerve
branches off the vagus nerve
major vasculature in the thoracic cavity
superior vena cava (SVC), inferior vena cava (IVC), aortic arch, brachiocephalic trunk, common carotids, subclavian arteries, subclavian veins, and azygos vein.
venous blood
deoxygenated blood is brought TO the heart
arterial blood
oxygenated blood flow AWAY from heart
heart and lungs
2 important organs that help sustain life and propel “life fluid”, or oxygenated blood throughout the body
intrinsic conduction system
how blood flows through the heart, cardia output and stroke volume, and neural and hormonal inputs
function of heart
pump deoxygenated blood to the lungs, and oxygenated blood to the rest of the body
right and left coronary artieries
bring oxygenated blood from the aorta and bran into the right & left sides of the cardiac muscle
blood transfuses through
the myocardium, and then the venous blood drains into the the coronary sinus and dumps into the right atrium to join the rest of the deoxygenated blood
neural input, hormonal signals, and intrinsic conduction system
control the rhythm of the heart contractions
with no neural input or hormones to affect sinus rhythm
the heart would beat an average of 100 beats per minute
how is it that the heart can generate its own sinus rhythm without neural stimulation?
it contains cells with an “unstable resting potential”, called cardiac pacemaker cells
cardiac pacemaker cells
aka autorhythmic cells
3 phases of action potential to initiate heart contractions
1) pacemaker potential
2) depolarization
3) repolarization
pacemaker potential
there is a slow opening of Na+ channels, while the K+ channels are closing, thus becoming more positive, initating action potential and entering the depolarization phase
membrane potential
~40mV, depolarization has began
Depolarization
Ca2+ channels open, causing increase in positivity, thus a peak, that is short lived (bc excitable cells)
Repolarization
membrane potential becomes more negative, the K+ channels open, allowing K+ to exit out of the cell.
Cycle begins again
when K+ channels begin to close, and Na+ channels begin to open again
Major concentration site of pacemaker cells
SA (sinoatrial) node, located in the right atrium
SA Node
is where sinus rhythm is established, it is the determinant of heart rate
Internodal path
within right atrium, that connects the SA node to the AV (atrioventricular) node
Impulse of the AP is carried along the internodal path
and pauses for 0.1 seconds at the AV nose, this allows the atria to contract, forcing blood into the ventricles
Impulse is then continued towards the AV node to the
bundle of HIS, located in the superior portion of the interventricular septum
From the bundle of HIS
the path is split into 2 bundle branches and continues along the interventricular septum towards the apex
At the apex
each branch travels up their respective side and forms of network fibers, Purkinje fibers
Purkinje fibers
located within the ventricular walls, the contractile cells of the ventricle become depolarized
Total time from SA node initiation to the depolarization of the last contractile cells of the ventricle
0.22s
What happens when our biological pacemaker cells no longer generate a normal sinus rhythm for the heart?
implant an artificial pacemaker to take over and continue the arduous task of sinus rhythm
pacemakers are implanted
superficial to the left pectoralis major muscle and leads are inserted into the left subclavian vein, into the superior vena cava, then to the heart of the right atrium
Pacemaker types
- dual chamber pacemakers
- biventricular pacemakeres
- implantable cardioverter defibrillator (ICD)
Arrhythmias uncontrollable via drugs
may require the use of a pacemaker
bradycardia symptoms
exercise intolerance, fatigue, dizzy spells, & even circulatory collapse
con of pacemakers
lead wears out, battery need changed
pocket infections
chest-wall generator due to surgery to replace pacemaker
Biological pacemaker
introducing specific ion channels into cardiomyocytes by gene transfer as well as the use of stem cells that were differentiated into cardiomyocytes
normal cardiac output
5 L/min
cardiac output equation
Q = HR X SV
stroke volume
volume of blood pumped out by one ventricle with each beat, the force determines how much blood is pumped out
stroke volume equation
SV = EDV – ESV
EDV & ESV
end diastolic and systolic volume
EDV
the amount of blood that has been collected in the ventricle prior to contraction (thus relaxation would be occurring).
preload (degree of stretch)
EDV, myocardial walls stretching
ESV
the amount of blood remaining in the ventricle after contraction has occurred (thus contraction would be occurring)
to increase SV
need to increase EDV and decrease ESV
Frank-Starling Law
relationship between the degree of stretch and how it impacts SV
average heart rate
70 bpm
sympathetic stimulation
180-200bpm
sympathetic trunk ganglion
send sympathetic stimulation to the heart
vagus nerve
stimulate rest and digest
2 major hormones produced by the heart?
atrial-natriuretic peptide (ANP) & brainnatriuretic peptide (BNP)
ANP
produced and released from atrial cardiomyocytes, reduces blood pressure
factors stimulating ANP
enlargement of the atria, increased levels of endothelin (a strong vasoconstrictor), and beta-adrenergic stimulation
ANP blocks
catecholamine action, which would otherwise vasoconstrict the vessels and increase blood pressure
ANP inhibits
hypertrophy by inhibiting norepinephrine-stimulated protein synthesis
BNP
released by the ventricular cardiomyocytes when there is excessive stretching of the
ventricles
patients with left ventricular dysfunction are usually indicative of heart failure
Elevated BNP levels
thyroxine (T4)
action is to increase beta1 receptors, which respond to norepinephrine (a “fight or flight” hormone)
beta1 receptors
will help increase heart contractility as well as heart rate, thereby increasing cardiac output
atrial fibrillation, a type of cardiac arrhythmia
elevated levels of T4
if volume increases
pressure decreases and vice versa
we inspire, or breathe in
our inspiratory muscles (diaphragm and external intercostal muscles) will contract
breathing in results in
diaphragm moving inferiorly and the rib cage elevating
thoracic cavity needs to obtain a pressure lower than the atmosphere
thoracic cavity needs to obtain a
pressure lower than the atmosphere
breath out
inspiratory muscles relax, which allows the diaphragm to move superiorly and the rib cage to move inferiorly, increased pressure!
How is respiration controlled?
respiratory centers in brain: ventral respiratory group (VRG), dorsal respiratory group (DRG), and pontine respiratory group (PRG)
VRG
located near the pons-medulla border and fires impulses during both inspiration and expiration
* inspiratory neurons fire, the signal is transmitted via the phrenic nerves and intercostal nerves to excite both the diaphragm & external intercostal muscles to contract, thereby increasing the volume wn the thoracic cavity
DRG
located in the brain stem as well as the aortic arch and carotid arteries. Carbon dioxide and oxygen are some examples of chemicals that these receptors monitor
*behind the assimilation of input from chemoreceptors and stretch receptors,
and then furthers this communication with the VRG
PRG
responsible for smoothing the transitions between inspiration
and expiration
*sleeping or exercise, and it too receives its information from sensory receptors, similar to the DRG
if you go to the gym and are running on the treadmill
your chemoreceptors should be picking up lower oxygen. They should then send signals that get assimilated by the DRG, which then sends the information to the VRG and the VRG will send more excitatory impulses via the phrenic and intercostal nerves to contract the inspiratory muscles
Hypocalcemia
depresses heart
Hypercalcemia
increase HR and contractility; excessive can lead to life threatening heart dysfunctions
