Study your flashcards anywhere!

Download the official Cram app for free >

  • Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off

How to study your flashcards.

Right/Left arrow keys: Navigate between flashcards.right arrow keyleft arrow key

Up/Down arrow keys: Flip the card between the front and back.down keyup key

H key: Show hint (3rd side).h key

A key: Read text to speech.a key


Play button


Play button




Click to flip

23 Cards in this Set

  • Front
  • Back
3 phases of cardiac cycle (systole/diastole)
1) ventricular filling (diastole)/ atrial systole
2) ventricular systole/ atrial diastole/ ejection of blood from ventricles (pressure in ventricles increases: AV valve closes, blood begins to flow into aorta or pulmonary trunk)
3) relaxation of atria and ventricles
end diastolic volume
max. vol. of blood in ventricles at end of ventricular diastole.
end systolic volume
amt of blood left in ventricles after ventricular systole
stroke volume
amount of blood moved in each beat of the heart
cardiac output
CO = SV x bpm
volume pumped by heart per minute
3 things that affect stroke volume
1) preload: amt. of blood entering the heart; stretching of heart increases contraction strength (high EDV = high SV)
2) contractility: – epinephrine or norepinephrine (from sympathetic neurons or as hormones) increases Ca++ influx, which increases the force of contraction (increases SV)
3) afterload: arterial blood pressure determines how much blood can be ejected from ventricles (low pressure in aorta = high SV)
heart rate can be modified by:
autonomic innervation:
1) vagus nerve: parasympathetic - decelerates heart rate
2) cardiac nervE: sympathetic - increases heart rate
-cardiac centers are in the medulla
Cardiac muscle contraction (3 steps)
1) Depolarization caused by opening of voltage-gated Na+ channels --leads to action potential
2) Action potential opens Ca++ channels and triggers Ca++ release from extracellular space and SR
3) Excitation-contraction coupling occurs
Cardiac conduction through autorhythmic cell contraction
1) Slow influx of Na+ causes potential to slowly rise -leads to depolarization of pacemaker potential
2) Depolarization reaches a threshold for action potential that opens Ca++ channels which causes rapid depolarization
3) Repolarization occurs, K+ efflux restores negative potential
the P wave in EKG
corresponds to atrial depolarization
the QRS complex in EKG
Q wave corresponds to atrial repolarization; R wave corresponds to ventricular depolarization
the T wave in EKG
corresponds to ventricular repolarization
3 layers of arteries and veins
the three tunica layers: tunica intima, tunica media, tunica externa
tunica intima (interna)
inside endothelial layer that lines the lumen of all vessels
tunica media
smooth muscle and elastic fiber layer, regulated by sympathetic nervous system; controls diameter of vessel thru vasoconstriction/vasodilation of vessels
tunica externa (adventitia)
outer layer tha tprevents vessel from getting too big; has collagen fibers that protect and reinforce; restrict amt of stretching; larger vesselgs have vasa vasorum (small vessels of their own)
3 types of arteries
1) elastic arteries/conducting vessels; most elastic- including aorta and its major branches
2) muscular arteries/distributing vessels
3) arterioles- lead into capillary bed
3 types of capillaries
1) continuous capillaries- most common; diffusions occurs thru intercellular cleft; held together by tight jxns
2) fenestrated capillaries- has many pores- found in small intestine, endocrine glands, kidneys)
3) sinusoid capillaries- leaky, with large holes; allow passage of proteins and large molecules from surrounding tissues; found in liver, bone marrow, lymphoid tissue, and in some endocrine organs
3 factors contributing to movement of blood through veins
1) respiratory pump- when diaphragm contracts, abdomen increases in pressure (when inhale); blood draw towards heart
2) muscular pump- contraction of skeletal muscle causes increase in pressure which "milks" blood towards heart
3) valves prevent backflow during venous return/ blood flows down to heart b/c of gravity
neural control (short-term mechanism) that controls blood pressure
neural controls from symp and parasymp NS; maintain MAP by vasodconstriction (SNS) and vasodilation (lack of SNS control); regulated by vasomotor centers of medulla
chemical control (short-term mechanism) that controls blood pressure
BP regulated by chemoreceptor reflexes sensitive to O2 and CO2; chemorecep in carotid and aortic bodies; reflexes that regulate blood pressure are integrated in medulla; if body has high CO2 and low O2 -blood vessels dilate (pressure decreases)
chemicals that increase blood pressure
adrenal medulla hormones: norepinephrine and epinephrine
antidiuretic hormone (ADH): causes intense vasoconstriction in cases of extremely low BP
angiostensin II - kidney release of renin generates angiotensin II, which causes intense vasoconstriction
endothelium-derived factors
chemicals that decrease blood pressure
atrial natriuretic peptide (ANP): causes blood volume and pressure to decline
nitric oxide (NO)- has brief but potent vasodilator effects
inflammatory chemicals- histamine, prostacyclin, kinins are potent vasodilators
alcohol- cause BP to drop by inhibiting ADH