EEOB 2520 exam 11

inter ventricular septum

wall between two ventricles

what chamber is bigger?

Left is bigger due to pumping oxygenated blood to entire body; ventricles are bigger than atria thicker muscle wall more APs happening here

properties of myocardium

striated (parallel myosin and actin), short and branched myofibers; intercalated discs

what are intercalated discs

two junction connections of how myofibers are attached; strongest (desmosomes) and gap junction

strongest junction of the intercalated discs

desmosomes; hold cells together

what do the two junctions of the intercalated discs do

desmosomes- hold cells together

gap junctions- electrical synapses; quickest movement for synchronous contraction)

another name for contraction of myocardium

Calcium induced calcium release; calcium helps to get other calcium to be released

how does the myocardium relax

remove calcium by putting it back to its two locations

where is the calcium put back during relaxation of myocardium

both to the sarcoplasmic reticulum and the plasma membrane by ATPase pumps

what happens if you do not put the calcium back to where it came from for relaxation

parts of the process will end up failing; need to put it outside the cell so we can have calcium there to start the whole process; need to put it back to SR so we can get bigger amount of calcium for bigger tension later in the process

which was does atria contract

top to bottom

what kind of synapse is used for contracting of heart and why

electrical because it is quicker than chemical

is there an indirect or direct relationship between the atria and ventricles communication

indirect by AV node

where is the bundle of His located

interventricular septum

how does the ventricular cells contract

bottom to top

what is the line made up of that separates atria from ventricles

lipids/fats; preventing APs from moving directly from our atrial cells to ventricular cells

what helps us communicate between atria and ventricles

atrioventricular node

what kind of measurement is an EKG/ECG

gross measurement

P wave

atrial depolarization; small upward blip not a lot of variation; all the APs are moving and getting all of the atrial cells to contract

QRS complex

ventricular depolarization (atrial repolarization); more complex; down, big up, down again; more APs happening in ventricles so more deflection seen; ventricles are contracting; atrial cells relax/repolarize

T wave

ventricular repolarization; ventricles relax and expand out to their original position

what two sounds does the heart make

lub dub

lub

just post QRS= cuspids closing (AVs)

dub

just post T wave= semilunar closing

What comes first sound or visual for the heart

first you see it on the EKG then hear it

is there a P wave sound

nope

do our muscles make noise

nope

what makes the Lub dub sound

valves slamming close

ventricles squeeze blood out of chamber and ventricles fill with blood

heart murmur

extra noise; Lub shh dub or Lub dub shh; back flow of blood occurring due to failed closure

what is blood pressure

change in size of atria or ventricles; due to space contraction

PV=nRT blood pressure

T= 98.6 typically;R= constant; n= same amount of blood so constant

P=c/V

what kind of relationship exists between volume and pressure for BP

inverse relationship; as we change V we change P; increase of V decreases P; decrease of V increases P

how many phases in one stroke (cycle)

two; systole and diastole

systole

contraction to empty (squeeze out of chamber)

decrease V increase P

~1/3 time squeezing

diastole

relax to fill

increase V decrease P

~2/3 time relaxing

stroke volume

measures the difference between what's there before we do our contraction and whats there after contraction

EDV - ESV

End diastolic volume (EDV)

pre-contraction; maximum V; ~135 mL

End systolic volume (ESV)

post-contraction; minimum V; ~65 mL

what is heart rate

number of strokes (cycles) per min;

typical adult is 70 bpm

stroke V ~70 mL

Cardiac output

heart rate x stroke volume ; 4.9 L/min ; good movement happening not for the individual stroke but for the fact we keep repeating it so well; bigger movement happening

what is cardiac output dependent on

heart rate and stroke volume

EDV and ESV because those are what our SV is dependent on

is HR independent or dependent on SV

relatively independent; can alter one without impacting the other

what impacts HR regulation

autonomic nervous system

what impact does sympathetic and parasympathetic have on HR

increase HR with sympathetic (fight or flight)

decrease HR with parasympathetic

what autonomic NS impacts on HR

input to SA node (sympathetic vs parasympathetic)

conduction velocity (amount of gap junctions present)

other impacts on HR

epinephrine ; body temperature ; electrolytes (ions) ; endocrines

what impact does epinephrine have on HR

acts as an endocrine helps get our heart to do its job faster

what impact does body temp have on HR

too hot or too cold will increase your HR so you want to get to normal temp 98.6

what impact does electrolytes have on HR

Calcium: critical for our electrical activity for contraction to happen so issues with contraction and electrical movements

Sodium, Potassium, Magnesium: issues with electrical movement

what impact do endocrines have on HR

cortisol, testosterone, estrogen

heart problems in people of older age taking sex endocrine therapy when theirs drops

want your sex endocrines to drop as you age so the heart isn't overworking

what happens when EDV is increased for SV regulation

heart stretches (not fixed volume)

increases contraction force when stretched a little

increases potential for cross bridge cycling to occur

what happens when you overstretch the sarcomere

plummets force when too much stretch (congestive heart failure)

actin and myosin is pulled too much there is no overlap so no CBC can occur and it will tear/rip

congestive heart failure

heart overfills and stretched too much and ability to cross bridge cycle plummets

what happens to ESV when EDV is increased

ESV decreases

better squeeze from EDV results in ESV gets smaller

what happens when arterial pressure is changed

ventricles eject into arteries

what happens as result of pressure gradient increasing in arteries

resistance:

less blood therefore smaller SV is going to happen because you can't just push it out due to resistance

regardless of EDV what will increase contraction force

norepinephrine / epinephrine due to sympathetic NS response

better squeeze lowers ESV regardless of starting EDV

position for cross bridge cycling at rest

deflexed/cocked position (same as skeletal)

composition of adrenal gland

sits atop of kidney, cortex = gland, medulla = sympathetic ganglio

endocrines for adrenal gland

corticosteroids (cortisol)

impacts of corticosteroids on the adrenal gland

metabolic saving (limits starvation), alters liver activity (increase glucose catabolism and increases fats, proteins, then bones), increase epi/norepi to impact BP, decreases immune, decrease growth and reproduction

what happens if there is no cortisol in the system?

dead within days

adrenal insufficiency

Addison’s syndrome, no energy sources getting put into the system (weak), low glucose, low BP

hypercotisolism

Cushing’s syndrome, making to much cortisol that isn’t matching whats going on around them, increase glucose, increase BP, decrease immune, fragile bones, distint obesity pattern

somatic growth process

adding non-reproductive cells via mitosis

somatic growth needs

increase protein synthesis, (increase glucose and adipose catabolism), increase bone growth at epiphyseal plates