Cardiovascular Physiology Flashcards
what is cardiac output
amount of blood pumped by each ventricle in one minute
-normal adult blood volume: 5 liters
how often does blood volume pass through the heart
once every minute
cardiac cycle
events that occur during one heart beat
ventricular systole
contraction/ejection
diastole
relaxation/filling
what is the normal heart rate
72 beats/min
heart general facts
250-250 grams
- pyramidal shaped
- lies in pericardium in mediastinum
what are the heart surfaces
3 surfaces
- anterior (sternocostal surface): formed by right atria and right ventricle
- inferior (diaphragmatic surface): formed by R & L ventricles separated by inter ventricular groove, also surface of right atrium where IVC opens
- base of heart (posterior surface): formed by left atrium
where does the heart rest
in the diaphragmatic surface
does NOT rest on its BASE
mediastinum
contains all heart and thoracic viscera except the lungs
anterior mediastinum
thymus, fat, lymphatics
posterior mediastinum
descending aorta, esophagus, azygous veins, autonomics, thoracic ducts
middle mediastinum
heart, pericardium, aorta, trachea, main bronchi, lymph nodes
superior mediastinum
above sternal angle, aortic arch
inferior mediastinum
contains anterior, middle and posterior mediastinum
what does the pulmonary circuit consist of
- right side of the heart
- pumps blood to the lungs
- CO2 unloaded, O2 picked up
what does the systemic circuit consist of
- left side of heart
- pumps blood to the tissues, delivering O2 and picking up CO2 and wastes
where is the base of the heart directed towards
toward the right shoulder
where is the apex of the heart directed toward
the left hip
what is the heart inclosed in
pericardium sac
deep to the pericardium is what
the serous pericardium
what lies the inside of the pericardium
the parietal pericardium
what covers the surface of the heart
the visceral pericardium
aka epicardium
functions of the fibers skeleton
- valve support structure
- prevent over-stretching of valves
- electrical isolation b/w atria and ventricles
- cardiac muscles anchored to fibrous ring
cardiac muscle details
- self contracting and auto regulated
- y shaped
- shorter and wider than skeletal muscle
- predominantely mononucleated
- posses many many mitochondria and myoglobin
- ATP mostly aerobic
some of the cardiac muscles are auto rhythmic. what does that mean?
that they contract even w/o neurological innervation such as from pacemaker cells
what are intercalated discs?
located b/w cardiac muscle cells
- allows cardia muscles to contract and work as pump
- contain gap junction and desmosomes
what do gap junctions help
forms channels b/w adjacent cardiac muscle fibers that allow depolarizing current to flow form one cardiac muscle to the next
-allows quick transmission of action potential
what do desmosomes help?
anchors the end of cardiac muscle fibers together
how fast does cardiac muscles repolarize and how does that help cardiac muscles?
- repolarization takes much longer to occur
- are not able to go into tetanus (sustained contraction)
sarcolemma
membrane around striated muscle cells
intercalated disc
connect cardiac myocytes together
gap junction
facilitate electrical activity to spread to adjacent cells
T-tubules
invaginate the sarcolemma
-allow impulses to penetrate the cell and activate the sarcoplasmic reticulum
sarcoplasmic reticulum
releases calcium ions during muscle contraction and absorb during relaxation
what supplies blood to the heart
ivc svc coronary sinus pulmonary veins thebesian veins bronchial veins
what do the bronchial veins drain into
- pulmonary veins or left atrium
- into azygous vein (right) or superior intercostal vein (left)
what do tricuspid and bicuspid valves prevent
prevent black flow into the atria
-electrically insulate the ventricles from the atria except AV node
what is the AV node
the only conducting path b/w atria and ventricles
when the heart is relaxed, the av valves are
open
when the heart contracts, the av valves are
closed
what do the aortic and pulmonary valves prevent
black flow into the ventricles
when the heart is relaxed, the aortic and pulmonary valves are
closed
when the heart contracts, the aortic and pulmonary valves are
open
durin isovolumeric contraction, how are the valves
all valves are closed
blood does not move in or out of ventricles
describe the path of blood flow
start at right heart with O2 poor blood -right atrium -tricuspid valve -right ventricle -pulmonary valve -pulmonary circulation -pulmonary artery -pulmonary capillaries (gas exchange) -pulmonary veins return to the left heart with O2 rich blood -right atrium -mitral valve -right ventricle -aortic valve -aorta -branching arteries -systemic capillaries (gas exchange) -systemic veins -SVC and IVC -return to right of heart
what is the electrical activity of heart
the heart beats rhythmically as a result of action potentials
what are the two types of muscle cells
- contractile cells
- autorhythmic cells
what do contractile cells do
- mechanical work of pumping
- do not initiate their own AP
- ex: neurons, skeletal muscles, heart muscles
what do autorhythmic cells do
- specialized cells that initiate and conduct AP
- display pacemaker activity
- ex: pacemaker tissues, SA node, AV node, atrial foci, ventricular foci
what are the components of the conducting system of the heart
specialized cardiac muscle in SA node, AV node, and atrioventricular bundle w/ right and left terminal branches
-perkinje fibers
what are perkinje fibers
specialized cardiac muscle fibers that form the conducting system of the heart
what is the function of the conducting system of the heart and what influences it
- responsible for generating rhythmic cardiac impulses and conducting them rapidly throughout myocardium
- influenced by autonomic nerve supply of heart
how does the parasympathetic and sympathetic system influence the heart
- parasympathetic: slows the rhythm and diminish speed of conduction
- sympathetic: does opposite of parasympathetic
what do the internal pathways do and how many are there
- 3 intermodal pathways
- in atrial wall
- help impulses travel from SA node to AVB node more rapidly than they can pass through the muscle of heart
anterior internodal pathway
leaves anterior end of SA node and passes anterior to the SVC to end in AV node
Bachmann’s bundle
- aka interartrial tract
- branch of anterior internal tract that resides on inner of left atrium
middle internodal pathway
leaves posterior of SA node and passes posterior to SVC and ends in AV node
posterior internodal pathway
leaves posterior of SA node and down through cresta terminalis to end in AV node
sinuatrial node
- wall of right atrium, to the right of opening of SVC
- origin spontaneously to rhythmical impulses that spread in all direction through the cardiac muscle of the atria
- result in atria muscle contracts
atrioventricular node
- lower part of right atrium just above attachment of spatial cusps of the tricuspid valve
- impulse conducted from atria to ventricles
- speed is slow to allow sufficient time for atria to empty blood into ventricles completely
atrioventricular bundle
- aka Bundle of His
- only pathway that connects myocardium of atria to myocardium of ventricles electrically
- only route of impulse from atria to ventricles
what is the only route of impulse from atria to ventricles
atrioventricular bundle
or bundle of HIS
where is the atrioventricular bundle
bundle descended through fibrous skeleton to membranous part of ventricular septum, then divides into two branches (R & L)
-become continuous with the fibers of Purkinje plexus
what does electrical communication start with
starts with AP in autorhythmic cells
what is the pathway of electrical conduction that coordinates contractions
- electrical communication starts with AP in autorhythmic cells
- depolarization spreads quickly to adjacent cells through gap junctions in intercalated disks, followed by wave of contraction that goes to atria then ventricles
- heart contracts as a functional syncytium
what does contract as a function syncytium mean
atria as well as ventricles contract as a single unit
what is normal sinus rhythm driven by
SA node
what is junctional rhythm driven by
AV node
what is 1st degree heart block
-prologation of the p-q interval due to refractoriness of conductive cells in the AV node
what is 2nd degree of heart block
a fraction of atrial depolarizations are conducted through the AV node
- results in more P waves than QRS complexes
- block may be before or below bundle
- below bundle = more severe
what is 3rd degree of heart block
complete heart block, no atrial depolarization s are conducted through the AV node
- intrinsic depolarization of ventricles (about 32 bpm) often result in syncope
- condition is one most common requiring artificial pacemaker
what does ectopic foci cause
may cause premature atrial or ventricular contractions which prevent proper ventricular filling
atrial contraction
- starts in SA node and spreads throughout both atria via gap junctions
- two conduction pathways to speed up conduction
what are the two conduction pathways that speed up conduction in atrial contraction
- interarterial pathway: SA node branch off of the anterior internodal pathway to left atrium: Bachmann’s Bundle, ensures that both atrias depolarize to contract simultaneously
- internodal pathway: SA node to AV node (3 nodes: anterior, middle, posterior), ensures sequential contracting of the ventricles following atrial contraction
ventricular contraction
- ATP is conducted slowly at AV node b/c fewer gap junctions
- one way conduction through the AV bundle prevents re-entry of action potentials from ventricle to atria
what is the effect of ATP being conducted slowly at AV node
-causes AV nodal delay to enable atria to completely depolarize and contract before ventricles do
pacemaker potential
slow depolarization due to opening of Na+ channels and closing of K+ channels
depolarization happens when
AP begins when pacemaker potential reaches threshold
-is caused by Ca2+ influx through Ca 2+ channels
depolarization happens when
Ca2+ channels inactivating
-K+ channels opening causing K+ influx, which results in membrane potential back to most negative voltage
what is the voltage of unstable membrane potential
-60 mV
what is the threshold membrane potential
-40 mV
what happens whenever pacemaker potential depolarizes to threshold
autorhythmic cell fires an AP
how long does AP usually last
200 msec or more
what is the refractory period
time following AP which a normal stimulus cannot trigger a 2nd AP until an excitable membrane has recovered
what is the purpose of a refractory period
to protect the heart to ensure alternating periods of contraction and relaxation
what are the three types of ions that determines all aspects of conduction, contraction, and repolarization?
- calcium (Ca++) ions: cause myosite contraction
- potasium (K+) ions: outflow causes repolarization
- sodium (Na+) ions: produces cell to cell conduction (of depolarization) I the heart, except in AV node b/c of slow movement of Ca2+ ions
bradychardia
heart rate less than 60 bpm
tachychardia
heart rate greater than 100 bpm
normal heart rate
60-100 bpm
describe the systole/diastole ion pathway
- Ca2+ influx stops at the end of systole
- movement reversed = now Ca2+ is pumped into sarcoplasmic reticulum by Ca2+ pump
- phosphorylation of troponin 1
- binding of Ca2+ to troponin C
- binding sites b/w actin and myosin are blocked
- diastole: Ca2+ surplus removed by a 3 Na+ - 1 Ca2+ exchanger and by an electrogenic Ca2+ pump
describe the Ap of cardiac contractile cells
- phase 4: resting membrane potential: -90 mV
- phrase 0: depolarization: voltage gated Na+ channels open, Na+ enter cell and rapidly depolarize
- phase 1: initial repolarization: Na+ channels close, cell begins to repolarize as K+ leaves through open K+ channels
- phase 2: plateau: combo of Ca2+ influx and decrease K+ efflux
- phrase 3: rapid repolarization: slow K+ channels open, K+ exits rapidly, returning cell to resting potential
mechanical events of cardiac cycle
heart contracts to empty and relaxes to fill
both the atria and ventricle have their own cycles of systole and diastole
systole:
contraction and emptying
spread of excitation
diastole
relaxation and filling
subsequent repolarization
early diastole
atria and ventricles relaxed
ventricular pressure is close to zero
AV valve are open
80% of ventricular filling occurs
late diastole (atrial contraction)
atrial pressure is increased causing increase blood in ventricle
ventricular pressure increases slightly
end diastole volume (EDV)
volume of blood in ventricle at the end of diastole
isovolumetric ventricular contraction (early systole)
- beginning of ventricular systole
- impulse travels to AV node to excel ventricule
- sharp rise in ventricular pressure
- AV valve closed and SL valves closed
- ventricular volume does not change
ventricular ejection (systole)
- ventricular pressure greater than aortic pressure
- aortic valve opens, ventricular volume decreases
- rise in aortic pressure from blood volume entering faster than leaving aorta
- about 2/3 (65 %) of blood in ventricles is ejected into arteries
stroke volume
volume of blood ejected from each ventricle in a single contraction/beat
SV = EDV - ESV
_____ of blood is ejected during systole
-not all of blood is ejected during systole
end systolic volume (ESV)
volume of blood in ventricle at the end of systole
ejection fraction
SV/EDV
isovolumetric ventricular relaxation ( early diastole)
both AV and pulmonary valve closed
no blood enters or leaves
cardiac output
amount of blood pumped out of a ventricle per minute
- calculated as the product of heart rate and stroke volume
- CO = SV x HR
heart rate
determine by autonomic influence on the AV node
how does the parasympathetic innervation effect heart rate
decrease heart beat
decrease cardiac output
decrease AV node conduction (via Vagus nerve)
-primarily supplies atrium (esp SA and AV nodes) and the ventricles
how does the sympathetic innervation effect heart rate
increase heart rate increase cardiac output increase contractility increase AV node conduction (shorten P-R interval) -supplies the atria and ventricles
conduction velocity is altered by
- increase sympathetic stimulation and adrenergic drugs (norepinephrine, epic, phenylephrine)
- decrease parasympathetic stimulation (vagus), ischemia, hypoxia and beta blockers
nenoates can only change their ___ and not their ___
heart rate and not their SV
stroke volume is regulated by three things…
preload
contractility
afterload
preload
frank starling law states that critical factor controlling stroke volume is the degree of stretch of cardiac muscles cells immediately before they contract
-preload affected by venous return to heart and volume status
EDP
- aka end diastole pressure
- estimated by LAP, RAP, CVP
contractility
stretch allows the sarcoma to contract farther, generating more force
afterload
ventricular pressure must be overcome before blood can be ejected from the heart
- indicated by the diastolic blood pressure
- PVR effects the right ventricle
- SVR effects the left ventricle
- affected by vasoconstriction, vasodilation, obstructure lesions
othostatic hypertenstion
“postural hypertension”
- common form of low blood pressure
- occurs after a change in body positioning: when stands up from a seated or lying position
- occurs from a decrease in cardiac output
- causes: hypovalemia, bp meds, psychiatric medications
coronary circulation
- heart receives about 5% of cardiac output
- coronary blood flow is about 250 ml/min
- increases in myocardial oxygen demand must be met by an increase in coronary blood flow
coronary blood flow occurs predominantly during
diastole
blood pressure
- force exerted by the blood against a vessel wall
- highest in arteries
- lowest in veins
pulse pressure
pressure different b/w systolic and diastolic pressure
mean arterial pressure (MAP)
average pressure driving blood forward, monitored and regulate by the body
- MAP = diastolic pressure + (1/3) x pulse pressure
- 2/3 cardiac cycle in diastole
- 1/3 in systole
velocity of blood flow: where does it change and where is it fastest
- changes as it passes through systemic circulation
- fastest in aorta
- declines as vessel diameter decreases and then increases on the venous side as vessel diameter increases again
what causes an increase in blood volume
increase bp, cardiovascular system, and kidneys to maintain homeostatic balance
what is blood distribution determine by
diameter of the veins
what does venous constriction forces
more blood into arterial circulation = increase cardiac output
neural control of the heart is done by
sympathetic and parasympathetic stimulation
sympathetic stimulation
speeds up the SA node and vagal activity slows the node
- norepinephrine (NE) from sympathetic transmitter
- adrenaline (EPI) from adrenal glands: cause increase contractility, frequency, conduction, velocity, and irritability
parasympathetic stimulation
by ACH, activating muscarinic receptors and vagal simulation
-reduces contractility, frequency, conduction velocity, and irritability
sympathetic (thoracolumbar) fibers
- arise from cervical and upper thoracic portions of the sympathetic trunk
- end of SA node, AV node, cardiac muscle fibers, and coronary arteries
parasympathetic (craniosacral) fibers
- comes from vagus nerve
- terminate on SA node, AV node, and coronary arteries
- NOT ON CARDIAC MUSCLE FIBERS
