A & P II Exam #3

R & L coronary arteries

first branches, minor arteries

L coronary artery branches into…

ant. interventricular & circumflex arteries

post. interventricular artery is the joining of…

R coronary & circumflex arteries

cardiac veins

receive blood from heart → coronary sinus → right atrium

blood flow thru heart (deoxygenated)

venae cavae → right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary trunk → pulmonary arteries → lungs

why are there 5 pulmonary arteries?

they go to each lobe of the lungs

blood flow thru heart (oxygenated)

pulmonary veins (4-5) → left atrium → aortic semilunar valve → ascending aorta → throughout body → back to venae cavae

self-excitability

create own action potential without neural stimulation

• “autorhythmicity”

MAP in conducting system

• moves cell-cell

• contraction is wave-like

sino-atrial node

group of cells in right atrium just inf. to opening of sup. vena cava → where impulse begins

atrioventricular node

• inside inf. interatrial septum

• made of Purkinje fibers

purkinje fibers

form AV bundle → bundle branches → apex

from SA node…

AP spreads down right atrium & across to left atrium thru conducting cells

depolarization causes…

atria to contract → AV node depolarizes → travels thru AV bundle → apex & out to ventricular tissues → ventricles depolarize from apex upward

• ventricles also contract

SA & AV nodal cells CANNOT maintain stable resting potential because…

after repolarization, ions leak IN & their MP gradually depolarizes toward threshold→prepotential→AP

since SA node reaches threshold first…

it establishes heart rate

electrical event followed by…

contraction event

atria contract first…

then ventricles contract

ventricular contraction must start where?

@ apex

• push blood UP to great vessels

caffeine increases…

rate of depolarization in SA node

• prepotential is shorter

heart rate is altered by…

autonomic nervous fibers

• impulse begins @ SA node

heart beat comes from…

heart

heart rate comes from…

hormones

sympathetic ______ HR

increases

• “fight or flight”

parasympathetic _______ HR

decreases

• “rest and digest”

stimuli that affect HR (2)

• change in blood pressure & blood chemicals

  • ex: low O2 = increase HR

• change in temp & emotions

  • tied to PS & S

electrocardiogram (EKG)

electrical events in heart detected on surface of body

• EKG records electrical changes

P wave

atrial depolarization

QRS complex

ventricular depolarization

• wave is larger because ventricles are larger

• atrial repolarization is masked

T wave

ventricular repolarization

• little taller than P wave

P-R interval

impulse starts & moves from atria to ventricles

• distance lengthens if conduction pathway is damaged (travels around blockage)

S-T interval

time between end of ventricular depolarization (QRS) to end of ventricular repolarization (T)

• indicates myocardial infarction

if cardiac muscle cells are damaged…

they no longer conduct APs→changes in EKG

any other change in EKG indicates…

heart disease/disorder

if injury is in ventricles…

depolarization takes less time (fewer cells)→QRS complex will be smaller→smaller waves→possible death of cardiac cells

what does excessively large QRS complex mean?

enlarged heart

tissue damage causes abnormalities in HR (2)

• tachycardia

• bradycardia

tachycardia

faster than normal

bradycardia

slower than normal

cardiac cycle

physical events from beginning of one heartbeat

systole

contraction phase of a chamber

• EXPELS blood

diastole

relaxation phase of a chamber

• filling occurs (dilate)

cardiac cycle phases (3)

1. atrial systole

2. atrial diastole/ventricular systole @ same time

3. ventricular diastole

atrial systole

atria “top off” filling of ventricles

atrial diastole & ventricular systole

• ventricles contract

  • pressure increases → pushes AV valves closed

• isovolumetric contraction

  • ventricles still contract & pressures increases more

  • all 4 valves closed!

• pressure build until semilunar valves open→blood ejected into great vessels

• atria are filling @ same time

ventricular diastole

• ventricles relax

  • pressure decreases→semilunar valves closed

• isovolumetric relaxation

  • all 4 valves closed!

• AV valves open→blood moves passively into ventricles

end-diastolic volume (EDV)

ventricular volume when filled

• about 130mL

end-systolic volume (ESL)

blood remaining in ventricles after emptying

• about 50mL

stroke volume (SV)

volume of blood ejected by ventricles out to organs

• about 70-80mL

• SV=EDV-ESV

ejection fraction

% of EDV ejected during ventricular systole

• about 55-70%

heart sounds

generated by closing of valves & turbulence of blood when valves close

• lubb & dupp

lubb

closure of AV valves due to ventricular systole

• louder of the two

dupp

closure of semilunar valves due to ventricular diastole

• ventricles begin diastole→blood in great vessels tries to re-enter ventricles

cardiac output

amount of blood pumped/min & delivered to tissues

• cardiac output=SVxHR

the lower/higher the SV or HR is…

the lower/higher the cardiac output is

• direct relationship

factors that affect heart rate (4)

1. S & PS fibers innervate SA /AV nodes & cardiac muscle cells

2. cardiac center

   1. S releases NE→increase HR

   2. PS releases ACh→decrease HR

3. baroreceptors

4. chemoreceptors

baroreceptors

monitor BP

chemoreceptors

monitor chemicals like O2, H, & CO2

factors that affect stroke volume (4)

1. preload

2. contractility

3. afterload

4. autonomic activity

preload

degree of stretch on ventricular cells due to filling (diastole)

• sarcomere need to be somewhat stretched to contract efficiently

Frank-Starling Principle

more filling causes greater stretch followed by stronger contraction

• more in = more out

contractility

force of contraction

positive inotropic effect

anything that increases force

• sympathetic NS

• stronger contraction = increased SV

negative inotropic effect

anything that decreases force

• parasympathetic NS

• less strong contraction = decreased SV

afterload

amount of tension needed during contraction to force semilunar valves open→blood is ejected

• increases due to any factor that restricts blood flow thru arteries→blockage or constriction of peripheral arteries

autonomic activity (affects SV)

related to S & PS NS

coronary artery disease (CAD)

areas of partial/complete blockage of coronary circulation causing ischemia (insufficient blood supply)

CAD causes

• fatty deposits (plaque)

• thrombus (blood clot)

CAD symptoms

angina pectoris (chest pain)

• sensation of pressure/pain in chest

• radiates into left shoulder & arm

in women:

• dizziness

• anxiety

• nausea

• can’t catch breath

• clamminess/sweating

CAD treatments

• catheter: tube to remove plaque

• balloon angioplasty: inflatable balloon→expanded→compresses plaque

• stent: “cage” inserted in vessel to keep it open

• coronary artery bypass grate (CABG): section of vessel is used to make detour around obstruction

  • usually uses great saphenous vein or internal thoracic artery

blood vessel & circulation histology→layers

1. tunica intima/interna

2. tunica media

3. tunica externa

tunica intima/interna

inner layer; simple squamous epithelium; closest to blood

tunica media

medial layer; thickest layer; elastic fibers & smooth muscle for elasticity & contraction

tunica externa

external layer; elastic & collagen fibers

order from arteries to veins

arteries→arterioles→capillaries→venules→veins

arteries & arterioles function

*vasomotor center*

• control diameter of blood vessel

• has 2 cell groups

  • one causes widespread vasoconstriction

  • one causes vasodilation

• uses sympathetic NS

capillaries structure & function

thin-walled so exchange can occur quickly (t. interna)

• smaller in diameter than RBCs

• have pores (fenestrations) that allow faster exchange

• capillary beds connect arteriole to venule

veins & venules structure & function

in extremities, valves prevent backflow

• blood moves due to “milking” action of skeletal m.

• have high capacitance & allow large volume changes

if vein walls become weak or stretched…

valves don’t work properly→become incompetent & blood can pool→varicose veins form

blood vessel function

maintain adequate blood flow to tissues & organs (perfusion)

• changes in cardiac output will change perfusion, which is adjusted to maintain homeostasis

• hydrostatic pressure: force exerted against fluid→moves to area of lower pressure

blood pressure

pressure exerted on walls of blood vessels by blood

blood pressure is established by