Physiology Chapter 14: Cardiac Function Terms & Definitions

as organisms evolved with more cells, couldn't use solely diffusion from the extracellular environment

needed a circulatory system to bring nutrients and remove wastes from the innermost cells of the body

why do you need a circulatory system

fluid (blood) - help nutrients move

pump (heart) - push fluid around

channels (vessels) - ensures fluid goes to the right places

list and explain the 3 basics of a circulatory system

transport of oxygen and carbon dioxide

distribution of nutrients

transport of waste

distribution of hormones

regulation of body temperature

protection of the body against blood loss and disease

list the six functions of the circulatory system

when hot, blood rushes to the surface of the body to try to cool it down

when cold, blood goes to the interior to try and keep it warm

how does blood maintain body temperature

transport of nutrients, gases, hormones, wastes

immune response

what are the functions of blood

plasma: 55-60% of blood volume

cellular fraction: 40-45% of blood volume

list and explain the two components of blood

90% water

10% molecules of dissolved proteins, nutrients, hormones, gases, ions, and wastes

what is plasma composed of

red blood cells: 99% of total cellular component of blood , carry oxygen bound to hemoglobin from lungs to tissue and buffer carbon dioxide carried from tissues

white blood cells: less than 1% of total cellular component, five types that all fight off infection and are part of the immune response

platelets: way less than 1% of total cellular component, cellular fragments from megakaryocyte in bone marrow that function in blood clotting

list and explain the components of the cellular fraction in blood

biconcave discs

what shape are normal red blood cells

percentage of cellular components relative to the total blood volume

define hematocrit

males usually have higher hematocrit because they do not have menstrual cycles

which gender usually has a higher hematocrit and why

fewer RBCs so the hematocrit levels are lower than normal

plasma levels are elevated

leads to inadequate delivery of oxygen but it flows well

what does the hematocrit look like for someone who is anemic

too many RBCs so the hematocrit levels are higher than normal

plasma levels are low (blood is too viscous)

really good at delivering oxygen but need more pressure to push the blood which is bad for the heart and vessels

what does the hematocrit look like for someone who has polycythemia

normal number of red blood cells so normal hematocrit

plasma levels are low (blood is too viscous)

need more pressure to push the blood around which is bad for heart and lungs

easy to fix, just need an IV

what does the hematocrit look like for someone who is dehydrated

sickle cell anemia is a genetic disorder where in one amino acid change, resulting in red blood cells having a sickle shape instead of a biconcave disc shape

iron deficiency anemia is a nutritional disorder where there is a deficiency of iron in the diet that results in defective hemoglobin that can't carry oxygen

what is the difference between sickle cell anemia and iron deficiency anemia

kidney can tell how much oxygen they are getting through the blood

if there is not adequate amounts over long periods of time, they release EPO that will travel to the bone marrow to stimulate the production of more mature RBCs from the stem cells

the mature red blood cells are released and increase the capacity to carry oxygen through the blood

if the kidney senses an increase of oxygen, it will stop the secretion of EPO

explain how RBCs are regulated in the body

composed mostly of myocardium

size of the human fist

enclosed in pericardium in chest midline

explain the heart in general

like skeletal fibers in design and regulation but shorter

have striations so have sarcomeres

jointed at the ends with intercalated discs

what is the cell structure of a cardiac muscle fiber

gap junctions for communication

desmosomes (adhering junctions) to keep cells together

what is included in the intercalated disc of cardiac muscle fibers

intercalated discs

what connects cardiac muscle cells

double-membrane that surrounds the heart and secretes viscous fluid (pericardial fluid) into the pericardial sac to lubricate the heart

describe the pericardium

protect the heart from irritation when rubbing back and forth

what is the function of fluid in the pericardial sac

chest in the midline, under the sternum

so it can pump blood to the head as well as the rest of the body

little more to the left side because the myocardium in the left ventricle is bigger than the right ventricle

between two bones so that when giving CPR, it can squeeze the heart to pump blood

describe how the position of the heart in important relative to how the body works

no, they are mono-nucleated

do cardiac muscle cells have many nuclei

contractile tissue (myocardium) - 99% of the heart, no pacemaker potential

autorhythmic cells - 1% of the heart, does have pacemaker potential

list and explain the two types of cardiac muscle tissue

SA node

Av node

Bundle of His

Purkinje fibers

what are the autorhythmic cells

around -60mV, voltage-gated K+ channels close but there is steady influx of Na+ from Na+ leak channels

Na+ influx is greater than K+ efflux

depolarization gets the membrane to threshold, opening Ca++ voltage-gated channels (causing Ca++ influx and depolarization) and triggering K+ voltage-gated channels to open

Ca++ influx continues to depolarize the membrane creating a self-induced AP

at about 10mV, Ca++ voltage-gated channels close and the K+ voltage-gated channels open, causing K+ efflux and repolarization

once membrane returns to about -60mV, K+ voltage-gated channels close again and Na+ leak channels continue to allow Na+ influx

explain pacemaker potential in autorhythmic cells

Na+ influx from Na+ leak channels

the pacemaker potential in cardiac cells is due to...

Ca++ influx

the rising phase of the AP in cardiac cells is due to...

K+ efflux

the falling phase of the AP in cardiac cells is due to...

no

they are either repolarizing or depolarizing due to Na+ leak channels

do autorhythmic cells have a RMP or proportionate ion flux

Na+ seap from Na+ leak channels

what gets autorhythmic cells to threshold

one heartbeat

one AP in cardiac muscle is equivalent to what

more Na+ influx = steeper slope for pacemaker potential = get to threshold quicker = more APs = increase heart rate

what is the effect of more Na+ seapage in pacemaker potential

less Na+ influx = less steep slope for pacemaker potential = takes longer to get to threshold = less APs = slower heart rate

what is the effect of less Na+ seapge in pacemaker potential

sympathetic stimulation increases the flow through Na+ leak channels and Ca++ voltage-gated channels (faster depolarization)

parasympathetic stimulation keeps the K+ voltage-gated channels open longer and closes Ca++ voltage-gated channels which hyperpolarizes the membrane (slower depolarization)

what two things would cause the rate of depolarization to change in the heart and how would it change

NorEpi on beta-1 adrenergic receptor

sympathetic NS uses which neurotransmitter and receptor in the heart

Ach on muscarinic

parasympathetic NS uses which neurotransmitter and receptor in the heart

skeletal - requires nervous system input for an AP

cardiac - doesn't need nervous system input for an AP but NS input does influence the rate of the AP

what is different about the action potentials in the heart versus skeletal muscle

SA node is the lead because it has the fastest intrinsic pacemaker potential, so once it depolarizes, gap junctions in the intercalated discs cause all cells in the heart to depolarize

what is the lead pacemaker in the heart? why?

non-contractile septum

this ensures that the AP stays in a coordinated fashion so that the ventricles contract from the bottom to top

prevents the top of the ventricles from prematurely contracting

what is found between the atria and ventricles? why is this important for the heart physiologically?

about 0.1 sec as the AP passes through the AV node and the non-contractile septum

explain what the AV nodal delay is

starts from pacemaker potential in the SA node - rapidly spreads to the atria - slows as it goes through the AV node (AV nodal delay) - rapidly spreads down the Bundle of His to the apex of the heart and up the Purkinje fibers to the rest of the ventricles

what is the pathway of an AP in the heart

-90mV (same as skeletal muscle)

what is the RMP for the contractile myocardium

pacemaker potential depolarizes surrounding myocardium through gap junctions which opens Na+ voltage-gated channels (allowing for Na+ influx) and triggers open K+ and Ca++ voltage-gated channels

at about +30mV, Na+ voltage-gated channels close and lock, K+ and Ca++ voltage-gated channels open, resulting in K+ efflux (repolarization) and Ca++ influx (depolarization) which creates a plateau (proportionate ion flux)

Ca++ voltage-gated channels close while K+ voltage-gated channels remain open, allowing only for K+ efflux and repolarization

at RMP (-90mV), K+ voltage-gated channels close and the Na+ voltage-gated channels go back to being closed but capable of being opened

explain the action potential in the contractile myocardium

autorhythmic cells: triggered by Na+ seapage

contractile myocardium: triggered by ion flux through gap junctions

what is the difference with how autorhythmic cells get to threshold versus the contractile myocardium

AP travels down the sarcolemma and T-tubules by local current flow

when AP reaches DHP receptor in the T-tubule, it flexes, opens, and acts directly as a voltage-gated Ca++ channel resulting in Ca++ spark

Ca++ influx interacts with the Ryr channel on the lateral sac of the SR, causing even more Ca++ to enter the sarcoplasm

summation of Ca++ influx into the sarcoplasm from the DHP receptor and Ryr channel bind to troponin and cause the cross-bridge cycle

explain muscle contraction in cardiac muscle

Na+ influx

what causes the rising phase of contractile myocardium APs

proportionate ion flux from Ca++ influx and K+ efflux

what causes the cardiac plateau of contractile myocardium APs

K+ efflux

what causes the falling phase of contractile myocardium APs

both:

AP travels down the T-tubules by local current flow and activate the voltage-gated DHP receptors

cardiac:

DHP receptor acts directly as a Ca++ channel for entry from ECF

Ca++ entry acts as trigger Ca++ and opens the Ryr channel to further release more Ca++ into the sarcoplasm

Ca++ from both sources bind to troponin and cause cardiac plateau

smaller fibers and have single nucleus per fiber

have intercalated discs that contain gap junctions

T-tubules are larger and branch

SR is smaller

after AP, Ca++ has to go back to the SR and the ECF

compare the skeletal and cardiac muscle excitation-contraction processes

cardiac: amount of Ca++ released from an AP is variable and does not always open all binding sites on actin, leading to various strengths of contraction

skeletal: so much Ca++ is released that all binding sites are open, leading to an all-or-nothing response

what is different about strength of contractions in skeletal versus cardiac

skeletal: control the number of motor units that are stimulated

cardiac: control the amount of Ca++ in the sarcoplasm

how are the strengths of contractions controlled in skeletal muscle versus cardiac muscle

reduce the strength of the contraction of the heart because not as much Ca++ can bind to troponin

give to someone with high BP

what is the effect of Ca++ blocking agents? who would you give them to?

increases the strength of the contraction because there will be more Ca++ to bind to troponin

give to someone with congestive heart failure

what is the effect of Ca++ enhancers? who would you give them to?

no

is there a refractory period in autorhythmic myocardium

longer refractory period causes the AP to be lengthened which prevents tetanus

why is the cardiac plateau significant in contractile myocardium

there would be no pumping of blood or filling the heart with blood

why don't we want our heart to go into tetanus

summation of AP and tetanus

skeletal muscle lives in tetanus

short refractory periods allow for what

the refractory period lasts just about as long as the entire muscle twitch

in cardiac muscle fibers, how long is the refractory period compared to the actual twitch

recording at the skin surface of the electrical activity generated by cardiac action potentials

define an electrocardiogram

a different point of view

a lead in a ECG is just what

P wave - atrial depolarization, SA node first then the rest of the atria

PQ segment - atrial contraction, AV nodal delay

QRS complex - atrial repolarization, ventricular depolarization

ST segment - ventricular contraction

T wave - ventricular repolarization

explain the waves and segments in one cycle on an ECG

find abnormalities in heart rate (tachycardia and bradycardia)

find abnormalities in rhythm (arrhythmia, PVC)

cardiac myopathy

what are the clinical uses for an EKG

fast heart rate (greater than 100 bpm)

define tachycardia

slow heart rate (less than 60 bpm)

define bradycardia

any variation in rhythm

define arrhythmia

no

some are necessary. for example, heart undergoes an arrhythmia when you go from resting to a quick increase in physical activity

are all arrhythmias bad

abnormality in rhythm due to contraction from an ectopic pacemaker (Bundle of His, AV node, or Purkinje fibers)

what is preventricular contraction (PVC)

tissue necrosis from heart damage like a heart attack

what is cardiac myopathy

noninvasive

quick and easy

relatively cheap for hospitals

get good information from them

what are the pros of during an ECG

fibrillation is heart quivering

issue because depolarization is not spreading properly = no coordinated contraction = no blood pumping = death

what is fibrillation? why is this an issue?

the machine generates more energy than the heart

all cells are forced into depolarization (even those repolarizing)

goal is to get them all on the same page again so that the coordinated cycle of depolarization and repolarization can occur again

why do defibrillators work if someone is in fibrillation

the ventricles are still contracting and working properly so 2/3 of the blood is still getting into the ventricles by passive filling and leaving to go to the body

why is atrial fibrillation not a death sentence

there is no connection between the atria and ventricles (probably a problem with the AV node) so treatment is an artificial pacemaker that zaps both the atria and ventricles to cause contraction

what is the treatment for someone with a third degree block

right side (pulmonary) - to the lungs

left side (systemic) - to the body

how does the heart serve as a dual pump

blood from the right side goes to the lungs then goes back in on the left side to be sent to the body where it goes back to the right side

cycle continues

the two circulatory systems work in parallel. what does this mean?

AV valves (atrioventricular) - separate atria from the ventricles

right AV (tricuspid) - separates the right atrium and ventricle

left AV (bicuspid) - separates the left atrium and ventricle

semilunar valves - separate ventricle and corresponding artery

right semilunar valve (pulmonary) - separates the right ventricle and the pulmonary artery

left semilunar valve (aortic) - separates the left ventricle from the aorta

list and explain the valves in the heart

only by changes in pressure

how do the valves of the heart open and close

the valve opens

when pressure is greater behind the valve, what happens to it

the valve closes

this prevents backflow of blood

when pressure is greater in front of the valve, what happens to it

papillary muscles contract when the ventricle contracts which causes the chordiae tendineae to tense

this prevents the valves from collapsing during contraction (open backwards)

what is the job of the chordae tendineae and papillary muscles in the heart

late cardiac diastole (TP segment)

P wave

atrial systole (PQ segment)

QRS complex

ventricular systole (ST segment)

T wave

early cardiac systole (TP segment)

list the phases of the cardiac cycle and their associated wave/segment from an ECG in order

Ca++ is being released into the sarcoplasm leading to the cross bridge cycle

when a portion of the heart is depolarizing, what is going on at the cellular level

Ca++ is put back into the SR and ECF

when a portion of the heart repolarizes, what is going on at the cellular level

both the atria and ventricles are at rest

atria are receiving blood from body and lungs, increasing the atrial volume

once atrial pressure exceeds ventricular pressure, the AV valves open (semilunar valves closed) allowing for blood to flow into the ventricles (PASSIVE FILLING)

explain what happens during late cardiac diastole (TP segment)

P wave

SA node depolarizes and spreads to the rest of the atria

what triggers the heart into atrial systole

atria contract

atrial pressure continues to increase, pushing more blood into the ventricles (ACTIVE FILLING)

atrial volume decreases

AV nodal delay occurs here to let the atria fully contract and get blood into ventricles actively

explains what happens during atrial systole (PQ segment)

QRS complex

atria repolarize and relax

ventricles depolarize

what triggers the heart into ventricular systole

ventricles contract

ventricular volume decreases, pressure increases

once ventricular pressure is greater than atrial pressure, the AV valves close (semilunar still closed) resulting in isovolumetric ventricular contraction

ventricles continue to contract

since volume does not change, there is a rapid increase in ventricular pressure

once the ventricular pressure is greater than the arterial pressure, the semilunar valves open (AV still closed) resulting in the ejection phase

ventricular volume decreases as it is getting pushed into the artery

explain what happens during ventricular systole (ST segment)

T wave

ventricular repolarization

what triggers the heart into early cardiac diastole

as ventricle repolarizes and relaxes, ventricular volume increases which causes pressure to decrease

when ventricular pressure falls below arterial pressure, the semilunar valves close (AV valves still closed) resulting in isovolumetric ventricular relaxation

ventricles continue to relax

ventricular pressure rapidly decreases as volume stays the same

when the ventricular pressure falls below atrial pressure, the AV valves open (semilunar still closed) resulting in passive filling again

explain what happens during early cardiac diastole (TP segement)

atrial is always greater because AV valves have to be open for passive filling to occur

during cardiac diastole, which pressure is always greater: ventricular or atrial?

atrial is always greater because AV valves have to be open for active filling to occur

during atrial systole, which pressure is always greater: ventricular or atrial?

ventricular is always greater because AV valves are closed

in early ventricular systole, which pressure is always greater: ventricular or atrial?

both sets of valves are closed and the heart is undergoing isovolumetric ventricular contraction

as ventricles are contracting and the volume is staying the same, pressure rapidly increases

why does the ventricular pressure increase so rapidly during ventricular systole?

ventricular is higher than atrial

arterial is higher than ventricular

during isovolumetric ventricular contraction, which pressure is higher: ventricular or atrial and ventricular or arterial

ventricular because the semilunar valves have to be open in order for the ejection phase to occur

during the ejection phase, which pressure is higher: ventricular or arterial?

arterial has to be higher than ventricular

ventricular has to be higher than atrial

during isovolumetric ventricular relaxation, which pressure is higher: arterial or ventricular and atrial or ventricular?

atrial is higher because the AV valves have to be open for passive filling again

at the end of early cardiac diastole, which pressure is higher: ventricular or atrial?