Cardiovascular System Flashcards
functions of the CV system
transport mechanism for the body
immunity - WBC
tissue repair - blood clotting
body temp - constriction and dilation to regulate
what things do the cardiovascular system transport?
- macro and micronutrients
- gases: O2 and CO2
- end products of metabolism (such as lactate which can be used as fuel for the brain and heart), hormones
components of the CV system
1. heart: 2 pumps, L side and R side left pumps to body right pumps to lungs 2. blood vessels - network of tubes 3. blood - fluid contained w/in CV sys
pulmonary circulation
blood vessel leaves right side of heart and is pumped to lungs to become oxygenated
- the lungs have lots of capillaries
functions of the heart
- generating BP which dictates blood volume
- routing blood and keeping pulmonary, systemic and coronary circulations separate
- valves prevent backflow
- regulating blood supply through stroke volume and heart rate
heart location
mediastinum
- close to midline but 2/3 of it is located more to the left side of the body
apex
cone shaped, inferior portion of heart
- directed anteriorly, inf and to the left
pericardium
serous membrane around the heart
- 2 main layers:
fibrous pericardium
serous pericardium
mediastinum
area in thoracic cavity that contains everything but the lungs
base
flat part of heart at opposite end of apex
- where atria are found and great vessels enter and exit the heart
- directed posteriorly, superiorly and to the right
fibrous pericardium
dense irregular CT
- forms tough CT sac that attaches to great vessels and anchors the heart to the diaphragm
- dictates distention of the heart
endocardium
inner layer of the heart wall
myocardium
cardiac muscle
thicker in certain regions of the heart
serous pericardium
thin, transparent double layer of simple squamous epithelium (mesothelium)
- 2 layers:
parietal and visceral (epicardium)
parietal pericardium
lines the fibrous outer layer
trabeculae carnae
found in ventricles only
extensions of cardiac muscle that make bumpy grooves to prevent suction action of the heart
visceral pericardium
aka the epicardium
covers the surface of the heart
pericardial fluid
serous fluid found in pericardial cavity b/w visceral and parietal pericardium
- helps prevent friction
how are the chambers of the heart arranged?
4 chambers:
2 upper atria (w 2 auricles that are like flaps/side chambers that extend off atria)
2 lower ventricles
sulci
grooves on surface of the heart containing coronary blood vessels and fat
coronary sulcus
around the heart, encircles and marks boundary b/w atria and ventricles
valves
ensure one way flow of blood
posterior interventricular sulcus
marks boundary b/w the ventricles posteriorly
atrioventricular (AV) valves
- flat leaf like cusps attached to papillary muscles by chordae tendinae
- right (tricuspid) has 3 cusps, left (mitral/bicuspid) has 2
- when valve is open, the canal is the atrioventricular canal
semilunar valves
- each valve has 3 cup like cusps
right is pulmonary, left is atrial - when cusps are filled, valve is closed. when cusps are empty, valve is open
anterior interventricular sulcus
marks boundary b/w ventricles anteriorly
is the thickness of the muscle walls even around the heart
no. ventricle walls are thicker than atria walls
also left side is thicker than right side
people who have aerobically trained have thicker walls and larger ventricles
chordae tendinae
extensions of CT that make tendons
keep valves from inverting due to pressure in ventricles
attach to trabeculae carnae via extensions called papillary muscles
fibrous skeleton of the heart
plate of dense fibrous CT b/w atria and ventricles
- acts as anchor for muscles of heart- muscles contract towards plate
- fibrous rings around valves sere as support
electrical insulation: cardiac muscle in atria and ventricles don’t touch bc we want them to contract at diff times
path of blood flow through the heart
R atrium (deoxygenated) > tricuspid valve > right ventricle > pulmonary valve to pulm trunk and pulm arteries > pulm capillaries (loses CO2, gains O2) > pulm veins (oxygenated) > L atrium > bicuspid valve > L ventricle > aortic valve > aorta to systemic circulation (loses O2, gains CO2) > sup/inf vena cava and coronary sinus > R atrium
papillary muscles
contract when the ventricles contract
- are extensions of the trabeculae carnae
coronary circulation
blood supply to the heart
- when heart relaxes, high pressure of blood in aorta pushes blood into coronary vessels
anastomosis
redundancy in blood vessels so that if one gets blocked, then blood still reaches most important areas
right coronary artery
exits aorta just superior to point where aorta exits heart
- lies in coronary sulcus
- extends to post aspects of heart
branches of right coronary artery
right marginal artery
posterior interventricular artery
left coronary artery
exits aorta just superior to the point where aorta exits heart
branches of left coronary artery
anterior interventricular artery
circumflex artery
right marginal artery
branches from right coronary artery
supplies lateral wall of right ventricle
posterior interventricular artery
branches from right coronary artery
lies in posterior interventricular sulcus
- supplies posterior and inferior aspects of the heart
anterior interventricular artery
branches from left coronary artery
aka left anterior descending artery or the widow maker
- main artery that supplies the left side of the heart
- sits in anterior interventricular sulcus
circumflex artery
branches from left coronary artery
- extends to posterior aspect of heart
- also runs in coronary sulcus
great cardiac vein
drains left side of heart
- sits in anterior interventricular sulcus
small cardiac vein
drains right margin of heart
similar in location to right coronary artery
coronary sinus
large venous cavity that empties into right atrium
- loc on posterior in coronary sulcus
smaller veins that drain other regions of the heart are?
middle cardiac vein: sits in posterior interventricular sulcus
anterior cardiac vein: sits somewhat where marginal branch of right cardiac artery is
cardiac muscle cells
- have very few nuclei (1-2), found centrally bc there are fewer myofibrils than in skeletal muscle
- elongated and branching cells, don’t run entire length of muscle
- contain actin and myosin myofilamnets
- myofibrils aren’t quite as organized as in skeletal muscle
what do gap junctions in cardiac muscle allow for?
for cardia muscle of atria and of the ventricles to behave as a single unit electrically
intercalated disks
specialized cell to cell contacts
- folds in sarcomere that hold cells together and allow them to fit together
desmosomes
- plasma membrane structures used to hold cells together
- act as staples to keep cells together when cardiac muscle cells contract
sarcoplasmic reticulum
- releases Ca2+
- not as highly organized as and has less contact w t-tubules
t-tubules
transverse tubules
- larger and less frequent
- located where z-disc is located
path of conduction through the heart
label them on a diagram
SA node AV node AV bundle/bundle of his R & L branches purkinje fibers
SA node
sinoatrial node
- depolarizes quickly
- generates spontaneous APs that pass to atrial muscle cells and to the AV node
- located near opening of sup. vena cava
- dictates pace of whole heart system
AV node
atrioventricular node
- APs conducted more slowly here than any other part of system
- this ensures that ventricles get the signal to contract after the atria have fully contracted to squeeze blood into ventricles before they contract
- found near coronary sinus and AV valve
AV bundle
bundle of his
- passes through hole in fibrous cardiac skeleton to reach interventricular septum
- this hole is the only place that a signal can go from atria to ventricles
right and left branches
- extend to beneath endocardium to apices of right and left ventricles and through interventricular septum
- number of gap junctions increase and also diameter of cardiac cells increase. this allows for FAST AP conduction through L & R branches
purkinje fibers
- large diameter cardiac muscle cells with few myofibrils (muscle cells) because job is to send fast signal, not contraction
- many gap junctions conduct AP to ventricular muscle cells quickly
node
lump or mass of specialized cardiac cells
tetanus
sustained contraction of the heart
regular cardiac cell resting membrane potential
~90mV
- extracellular fluid high in concentration in Na+ and Ca2+
- intracellular fluid is high in conc of K+
- these concentrations are v similar to in a neuron
regular cardiac cell depolarization
- occurs rapidly when voltage gated fast sodium channels open and Na+ flows into cell
- contraction happens slightly after depolarization
regular cardiac cell plateau
- maintained depolarization
- Na+ channels close, K+ channels open and K+ leaves cell; results in slight repolarization
- to compensate for this, voltage gated slow Ca2+ channels open and Ca2+ enters cell, balancing and resulting in little change in membrane potential
regular cardiac cell repolarization
- Ca2+ channels close
- voltage gated K+ channels open and K+ leaves cell
Na+/K+ pump works to re-establish resting membrane potential
regular cardiac cell refractory period
is longer than contraction period
- this allows the heart to fully contract and relax and allow the chambers of the heart to fully fill before contracting again
calcium-induced calcium release (CICR)
movement of Ca2+ though plasma membrane and T-tubules into sarcoplasm and stimulates the release of more Ca2+ from the SR
- allows contraction to occur for sustained amount of time
some diff b/w cardiac and skeletal muscle physiology
- cardiac APs conducted from cell to cell;
skeletal AP conducted along length of entire fiber - cardiac rate of propagation is slow bc of gap junctions and small diameter fibers;
skeletal AP propagation is faster bc of large diameter fibers and it is conducted along a single cell fiber
autorhythmicity
- SA node action potentials
- self generating APs at regular time intervals
autorhythmic resting membrane potential
-60mV – threshold is about -50mV
isn’t really stable, but is very close to threshold therefore makes it easier to generate APs
autorhythmic pacemaker potential
Na+ leakage into cells causes resting membrane potential to move towards threshold, results in
- inside of cell becoming more electrically positive
- K+ channels closing
autorhythmic depolarization phase
Ca2+ channels open
K+ channels close
autorhythmic repolarization phase
Ca2+ channels close
K+ channels open
APs in pacemaker cells
take longer to reach threshold as they go down this list
SA node: 100bpm
AV node: 60-70bpm
Purkinje fibers: 25-30bpm
artificial pacemaker
stimulates depolarization at a regular interval if something was wrong w SA node
which area of the heart would be least detrimental to function if it were injured
left atrium bc no important autorhythmic cells in there
electrocardiogram
ECG/EKG
a record of electrical events in the myocardium that can be correlated with mechanical events
– basically measures the movement of APs through the heart
P wave
depolarization of atrial myocardium
- signals onset of atrial contraction
QRS complex
ventricular depolarization
- signals onset of ventricular contraction
- repolarization of atria simultaneously
T wave
repolarization of ventricles
- ventricular relaxation
PQ interval
aka PR interval
- 16 seconds
- start of atrial excitation to start of ventricular excitation
ST segment
represents time b/w beginning of depolarization and repolarization (plateau phase)
QT interval
- 36 seconds
- start of ventricular depolarization to end of ventricular repolarization
the cardiac cycle
all events that happen within 1 beat of the heart
- repetitive systole (contraction) and diastole (relaxation) of heart chambers
- blood moves from areas of high to low pressure; contraction of the heart produces the pressure and these pressure changes open and close valves
systole
chamber contracts and ejects blood from the one chamber to whatever’s next
diastole
relaxation of cardiac muscle
- chamber fills w blood in this time
- atria and ventricles differ slightly in their timing of each state
phases of the cardiac cycle
atrial contraction/systole isovolumetric contraction ventricular ejection isovolumetric relaxation passive ventricular filling
atrial contraction/systole
1st
active ventricular filling when atria contract so that all blood gets into ventricles
isovolumetric contraction
2nd
systolic, no volume changes, all valves closed, causing pressure to increase
ventricular ejection
3rd
when enough pressure builds up in ventricles, it pushes semilunar valves open
isovolumetric relaxation
4th
diastole
- vent begin to relax, no volume changes, valves closed causing pressure to drop
ventricular filling
5th aka passive filling
- atria had been continuing to fill w blood and pressure increases causing valves to open and blood moves to area where pressure is lower
when do mechanical events in the heart happen relative to electrical events?
electrical events happen just before mechanical events
pressure changes in the heart
- atrial pressure stays pretty low
- if the pressure after a valve is greater than the pressure before a valve, the valve will not open
why is having high BP a bad thing?
the higher the pressure is in your heart, the harder your heart has to work to build pressure in order to open/close valves to get blood to move
when do AV valves open?
when the atrial pressure exceeds ventricular pressure
when do semilunar valves open?
when the ventricular pressure is greater than aortic/pulmonary trunk pressure
end diastolic volume
volume in the ventricle at end of diastole (relaxation), when the heart is full
end systolic volume
volume of blood leftover in the ventricle at the end of contraction
stroke volume (SV)
the amount of blood ejected from the left ventricle per heartbeat
- ml/beat
- norm is 80-100ml/beat
calculated by taking: EDV - ESV
heart sounds
made by turbulent flow of blood
lubb is 1st
dupp is 2nd
woosh is occasional 3rd and 4th
“lubb”
first sound
fluid vibrations made as AV valves close at beginning of ventricular systole
“dupp”
second sound
results from closure of aortic and pulmonary semilunar valves at beginning of ventricular diastole
“woosh”
occasional 3rd and 4th sounds
caused by turbulent flow of blood into ventricles detected near the end of first third of diastole or during atrial systole
cardiac output (CO)
the volume of blood pumped to the body per minute by the heart
- typically refers to the left ventricle
CO = HR x SV
heart rate (HR)
number of times the heart beats per minute
- measured in beats/min lol
cardiac reserve
diff between CO at test and max CO during exercise
regulation of stroke volume
3 factors regulate SV:
preload
afterload
contractility
preload
- amt of stretch of ventricle walls before contraction when heart is full
- frank-sterling law of the heart: the greater the stretch, the greater the force of contraction bc of recoil ability therefore the blood flows out faster
frank-sterling law of the heart
the greater the stretch (preload), the greater the force of contraction bc of recoil ability therefore the blood flows out faster
afterload
the pressure the contracting ventricles must produce to overcome the pressure in the aorta and move blood into the aorta (open semilunar valves)
contractility
the forcefulness of contraction of the ventricle muscle fibers
– basically the strength of contraction
controlled by inotropic agents
inotropic agents
substances that come in contact w cardiac uscle fibers and increase of decrease contractility of the heart
positive inotropic agents
open Ca2+ channels, increase contractility
sympathetic NS: cardiac accelerator nerves release norepinephrine OR hormones from adrenal medulla (epinephrine or NE)
negative inotropic agents
decrease contractility
drugs: calcium channel blockers, beta blockers (beta adrenergic receptors are triggered when epinephrine and norepinephrine bind
factors that regulate HR
age ANS hormones gender physical fitness temperature
neural and hormonal control of HR
parasympathetic nerve stimulation
sympathetic nerve stimulation
hormonal control by somatic NS
parasympathetic nerve stimulation w regards to HR
vagus nerve decreases HR bc NT Ach hyperpolarizes heart by opening more K+ channels therefore taking longer to reach threshold
sympathetic nerve stimulation w regards to HR
cardiac accelerator nerves increase HR and contractility
- NE released at SA and AV nodes and opens Ca2+ channels
hormonal control by somatic NS w regards to HR
epinephrine and NE from adrenal medulla released in response to many factors
- slower acting but lasts longer
where is the cardiovascular centre located?
in the brainstem
what do higher brain centres have the ability to do?
they can override input from sensory receptors
sensory receptors that input info to CV centre
proprioceptors: monitor movements
chemoreceptors: monitor blood chemical levels (O2 and CO2 levels)
baroreceptors: monitor BP
rheumatic fever and its effect on the mitral valve
it causes inflammation of muscles, joints and CT in body bc the “fever” it produces a protein similar to these structures that the immune system tried to attack.
- the result is a scarred and more fibrous mitral valve
stenosis
a narrowing of a passageway, where it doesn’t open as it should
what is an echocardiogram?
an ultrasound of the heart
it sents ultrasonic sound waves towards tissues and when the waves bounce off of them, they are collected and read
treatment for mitral valve stenosis (medications)
duretics, blood thinners, beta/calcium blockers, anti-arrythmics, antibiotics
treatment for mitral valve stenosis (procedures)
percutanious balloon mitral valvuloplasty where you put balloon in and inflate it where mitral valve is in hopes of making it work
mitral valve replacement: tissue valve from animal or human specimen or mechanical sewn in place
- ball and cage kind prone to clotting so they now do a different kind of artifical valve
