A & P: Test 3 (5) Cardiac Output/BV and Physiology of Circulation

Biology 2452 with P at Texas State University-San Marcos

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By: Brittany Snyder
Created: 2011-04-14
Size: 38 flashcards
Views: 9

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Cardiac Output (CO)

volume of blood pumped out by one ventricle in one minute
changes according to needs of the body

CO =

stroke volume (sv) x heart rate

SV (stroke volume)

the volume of blood pumped out by one ventricle during one systole, and the avg value is 70 ml

Cardiac Reserve

difference between the basic CO at rest and the max XO while exercising
an indication of how good your cardiovascular system is
well-trained athlete: high CR---35L/min, 7 times basic CO)
non-athlete: CR--20-25L/min (4 to 5 times the basic CO)

Regulation of SV

SV = EDV-ESV

EDV- end diastolic volume (120 ml of bld)
ESV- end systolic volume (50 ml of bld)

Factors that may change the EDV & ESV

pre-load
contractility
after load

1. Pre-load

refers to the pressure exerted by blood on the wall of ventricle at the end of vent diastole

----Frank-Starling's law of the heart

*SV is directly proportional to the degree of stretch of the myocardium

Increase in EDV will increase the degree of stretch, and thereby increase the force of contraction.
EDV will increase when venous return increases as during exercise

2. Contractility

increase in the force of contraction also increase SV.
Norepinephrine (NE)- inc force
Cal ions, glucagon, and thyroxine also increase

---Inotropic Agents

positive: all factors that increase the contractility
negative: slow down or inhibit heart's contractility (excess hydrogen ions in bld that inc acidity, inc levels of potassium ions)

3. After-load

refers to back-pressure by aortic blood (80 mm of HG), and blood in pulmonary blood (8 mm of HG) on SLVs.
When back pressure increases as during HB pressure (hypertension), ESV increases and SV decreases

***Regulation of Heart Rate

Sinus rhythm- at rest, initiated/coordinated by the SA node, but altered by

(1) ANS

(2) pressure receptors (baroreceptors)

(3) hormones

(4) ions

(5) physical factors

1. ANS (autonomic nervous system)

---cardiac center in medulla oblongata has 2 components

(a) CAC

(b)CIC

(a) CAC (cardiac acceleratory center)

when body is under stress, this is activated.
by means of sympathetic fibers and NE stimulate the heart and increases the HR

(b) CIC (cardiac inhibitory center)

at rest, this, by means of vagus nerve (parasympathetic) and ACh inhibits HR.

----Vagal tone

at rest, heart is under the influence of the vagus nerve and in this

3. Presso-receptors (baroreceptors)

detects blood pressure changes,and help regulate BP by changing HR
receptors in the wall of aorta and carotid sinus send impulses to CIC when the arterial blood pressure increases
CIC reduces HR, and tends to bring down the bp temporarily

---baroreceptors

located in wall of atria detect increase in venous bp when venous return to heart increases as during exercise.
these then send impulses to CAC to increase HR in order to clear off the increased venous and prevent heart congestion

---Bainbridge reflex

baroreceptors impulses to CAC to inc HR--prevent congestion

3. Hormones

epinephrine, norepinephrine and thyroxine increase HR

4. Ions

(a) Calcium

(B) Sodium

(a) Calcium Ions

decreased bld cal levels (hypocalcemia) reduces HR
increased bld cal levels (hypercalcemia) increases HR to such an extent, heart beast with very little rest, pump very little blood (spastic)

(b) Sodium Ions

low sodium does not affect HR, but High sodium in bld (Hypernatremia) adversely affect heart functions

----ANP (atrial natreuretic peptide)

when sodium content in bld increases, heart releases this hormone
which inhibits aldosterone and decreases sodium absorption and retention by the kidneys

low potassium level in blood (hypohalemia) weakens the heart and causes irregular heart beat (arrhythmia)
high potassium content (hyperkalemia) slows down the depolarization of cardiac fibers, leads to heart block and cardiac arrest, death.

5. Physical Factors

age affects HR
Infants- high (140-160/min)
HR declines w/ age
in females is higher (72-80/min)
males (64-72/min)
cold decreased HR
head increases HR

MAP in distribution arteries

around 90 mm Hg
becomes 20m Hg by the time blood reaches capillaries
BP in veins 15 mm Hg
in vena cava close to 0

Short-term changes in BP

brought about by vasoconstriction and vasodilation, controlled by the vasomotor center in medulla oblongata
vasoconstriction increases peripheral resistance and increases systemic bp

Long-term changes in BP

regulated by the kidneys which control the amount of fluid retained by the body

Arteries

take blood away from heart
thick smooth muscle layer, w/ plenty of elastic tissue
blood under systolic pressure
BP declines as the blood reaches bld capillaries
except pulm. trunk, arteries carry oxygenated blood

Distribution arteries

muscular arteries
smaller arteries with very little elastic tissue

Conduction Arteries

elastic arteries
act as "elastic tubes"
aorta and its branches close to heart

Arteioles

very small arteries w/ a relatively thin layer of smooth muscles
branch out to form blood capillaries

Veins

take blood towards the heart
thick outer conn tissue layer, thin smooth muscle layer
blood flow directed by pocket valves
except for pulm veins, veins carry deoxygenated

Venules

veins are formed by these
small veins
formed by blood capillaries

Blood Capillaries

exchange area in blood circulation
microscopic blood vessels with one-cel thick walls (made of one layer of endothelium)

Mean Arterial Pressure (MAP)

is equal to diastolic pressure + 1/3 of pulse pressure
keeps the blood flowing through the arteries

Coronary atherosclerosis

clogging of the coronary arteries reduces oxygen supple to myocardium and causes Hypoxia

About this deck

By: Brittany Snyder
Created: 2011-04-14
Size: 38 flashcards
Views: 9

About StudyBlue

“I have been getting MUCH better grades on all my tests for school. Flash cards, notes, and quizzes are great on here. Thanks!”
Kathy