A&p Ii - Lecture - Week Of 2/7

Front 1

Cardiac Output –

Back 1

Amount of blood pumped in one minute. CO= SV x HR (5250 mL/min=70beats/min x 75 beats/minute. About 4-6L of blood in the body)

Front 2

Heart rate increased by –

Back 2

norepinephrine, epinephrine, thyroxine

Front 3

Heart rate decreased by –

Back 3

Acetylecholine.

Front 4

Norepinephrine –

Back 4

increases heart rate and force of contraction. B1 adrenergic receptors. Norepinephrine effects is blocked by beta blockers

Front 5

Two ways to alter cardiac output –

Back 5

Heart rate or stroke volume

Front 6

Pre load –

Back 6

The amount the heart stretches just before it contracts. Stretchy-er heart raises EDV

Front 7

Slower ______ _______ allows more time for ventricular filling (affects EDV)

Back 7

heart rate

Front 8

Exercise strengthens mycocardium so ______ ______ increases. Heart rate goes down and cardiac output need is still met.

Back 8

stroke volume

Front 9

Muscular pump –

Back 9

when exercise causes squeezing in on veins to return blood to the heart. Veins have valves to prevent backwards leaking. (affects EDV)

Front 10

Veins are _____ pressure

Back 10

low

Front 11

At rest, average EDV:

Back 11

~120 mL

Front 12

At rest, average ESV:

Back 12

~150 mL

Front 13

At rest, stroke volume:

Back 13

~70 mL

Front 14

Affects EDV –

Back 14

preload, venous return, filling time

Front 15

Affects ESV –

Back 15

Strength of contraction and pressure in aorta

Front 16

Contractility –

Back 16

Strength of contraction

Front 17

Afterload –

Back 17

Blood pressure in aorta. Increased afterload means decreased cardiac output.

Front 18

Contractility –

Back 18

Efficiency of actin/myosin units. Affected by amount of calcium available. Thyroxine and epinephrine directly increase contractility

Front 19

Venous Return –

Back 19

amount of blood returning to the heart. A healthy heart has more time between each beat, therefore a bigger venous return, which means an increases preload (sort of) which increases EDV.

Front 20

If someone has a high blood pressure, the heart has to work ______ . Can leaded to an enlarged but weakened heart.

Back 20

Harder

Front 21

HR regulation: sympathetic –

Back 21

Norepinephrine binds to B1-adrenergic receptors and decreases threshold for action potentials, also increases calcium available.

Front 22

HR regulations: parasympathetic –

Back 22

Acetylcholine increases threshold for action potentials

Front 23

Vagal tone –

Back 23

dominant influence on heart rate at rest is parasympathetic.

Front 24

HR regulation: Hormones –

Back 24

Epinephrine and thyroxin increase heart rate.

Front 25

_______ binds to b1-adrenergic receptors and decreases threshold.

Back 25

Norepinephrine.

Front 26

Hypocalcemia –

Back 26

depresses heart rate (lack of calcium)

Front 27

Hypercalcemia –

Back 27

increases heart rate and can lead to dysrhythmias.

Front 28

Dysrhythmias –

Back 28

Hyper-excitability of SA node

Front 29

Many medicines work by decreasing or increasing __________ entry into muscle fibers

Back 29

calcium

Front 30

Hyperkalemia –

Back 30

lowers resting potential and can block action potentials all together. Leads to cardiac arrest or dysrhythmias

Front 31

Heart attack –

Back 31

myocardial infarction

Front 32

Multiple myocardial infarctions

Back 32

– can lead to congestive heart failure. dead cells are replaced with scar tissue

Front 33

Chronic hypertension –

Back 33

High blood pressure. Weakens heart because afterload is great. Called “the silent killer” because symptoms are not obvious, heart is being weakened, and blood vessel damaged without person knowing about it.

Front 34

Congestive heart failure –

Back 34

when cardiac output cannot meet the demands of the tissues. Degenerative. Prognosis is poor. Four causes/types: Coronary atherosclerosis, persistent high blood pressure, multiple myocardial infarcts, and dilated cardiomyopathy

Front 35

Persistent high blood pressure –

Back 35

Enhanced afterload begins and can lead to an elevated ESV. The heart then works too hard to try to keep up with demand and begins to weaken

Front 36

Dilated cardiomyopathy –

Back 36

ventricles stretch, myocardium becomes fat-filled

Front 37

Left ventricular failing –

Back 37

pulmonary congestion. As blood waits to enter the left atrium, it pools in the lungs. Pressure leads to pulmonary edema

Front 38

Right ventricle failings –

Back 38

peripheral congestion as blood waits in capillaries. Peripheral/systemic edema

Front 39

Cardiac Output disorders –

Back 39

Coronary atherosclerosis

Front 40

Coronary atherosclerosis –

Back 40

fatty build up that blocks coronary arteries (especially the anterior interventricular). Ischemia of myocardium results.

Front 41

Pulmonary edema –

Back 41

fluid seeping into lungs

Front 42

Lumen –

Back 42

Blood containing space.

Front 43

The layers of blood vessels –

Back 43

Tunica intima, tunica media, and tunica externa.

Front 44

Tunica intima –

Back 44

closest layer of the blood vessel. Made of endothelial, simple squamous cells. Capillaries are made of tunica intima only

Front 45

Tunica media –

Back 45

middle layer of blood vessels. Contains smooth muscles that are important to blood pressure regulation. Arteries have thicker tunica media than veins do.

Front 46

Tunica Externa –

Back 46

outer coat of blood vessel. Made of collagen fibers. “Aventicia”

Front 47

Vasoconstriction –

Back 47

Reduces blood vessel size

Front 48

Vasodilation –

Back 48

increased blood vessel size.

Front 49

Arterioles –

Back 49

Smallest arteries. Very important to blood pressure regulation.

Front 50

Venules –

Back 50

tiny veins

Front 51

Capillaries have only one layer:

Back 51

tunica intima

Front 52

Angiogenesis –

Back 52

Growth of new blood vessels from existing ones

Front 53

TPR –

Back 53

Total peripheral resistance. The amount of resistance in the blood vessels. Affected by three main factors: viscosity (short term), length (long term), and diameter (short term).

Front 54

Systolic pressure –

Back 54

120 mmHg is enough pressure to get the blood all the way around

Front 55

Diastolic pressure –

Back 55

80mmHg

Front 56

BP of arteries –

Back 56

Around 80-90mmHg

Front 57

BP of arterioles –

Back 57

Pulse pressure disappears, drops down to about 35 mmHg

Front 58

BP of capillaries –

Back 58

drops down to about 15mmHg

Front 59

BP of Venules –

Back 59

almost 0mmHg

Front 60

Three main areas of BP control –

Back 60

Neural, hormonal, and renal.

Front 61

4 types of Neural BP Control:

Back 61

vasomotor center, baroreceptor reflexes, chemoreceptor reflexes, and hypothalamic controls

Front 62

Neural BP Control: Vasomotor Center –

Back 62

Located in medulla, controls constriction of arterioles via sympathetic fibers. Vasomotor fibers of the skeletal system control dilation by releasing acetylcholine

Front 63

Neural BP Control: Baroreceptor reflexes –

Back 63

High BP stimulates stretch receptors found in aortic arch and carotid bodies send more frequent signals to the medulla (via vagus and glossopharyngeal) which inhibits vasomotor and cardioacceleratory centers. Stimulates cardioinhibitory center and vasodilation

Front 64

Baroreceptors: increased stimulation in the cardioregulatory stimulates _________ stimulation to the heart, which decreases HR

Back 64

parasympathetic

Front 65

Neural BP Control: Chemoreceptors –

Back 65

Low oxygen, low pH, or high CO2 stimulate these receptors (also on aortic arch and carotid arch) and sends signals to the medulla (via vagus and glossopharyngeal) to stimulate cardioaccelatory center and vasomotor center. Decreaes parasympathetic stimulation so hr goes up

Front 66

Neural BP Control: Hypothalmic

Back 66

controls as influenced by emotion, temperature, etc.

Front 67

Hormonal BP Controls: Adrenal –

Back 67

Adrenal Medulla hormones: Epinephrine and norepinephrine

Front 68

Hormonal BP Controls: Atrial Natiuretic Peptide –

Back 68

Released from the heart when blood pressure is high, blocks aldosterone to allow salt/water loss.

Front 69

Hormonal BP Controls: ADH –

Back 69

Stimulates water retention by kidneys, released by pituitary

Front 70

Hormonal BP Controls: Angiotensin –

Back 70

Renin from kidneys eventually activates AII. AII stimulates aldo, vasoconstriction, and ADH.

Front 71

Renal BP Control Types –

Back 71

Direct and indirect.

Front 72

Renal BP Control: Direct –

Back 72

Amount of water the kidneys retains

Front 73

Renal BP Control: Indirect –

Back 73

renin-angiotensin

Front 74

Pulse =

Back 74

systolic pressure – diastolic pressure

Front 75

Hypotension –

Back 75

Systolic below 100

Front 76

Hypertension –

Back 76

Systolic over 140/90. Called “Silent Killer”. Strains heart and arteries. Builds up atherosclerosis and increases afterload.

Front 77

Net filtration =

Back 77

net hydrostatic pressure –oncotic pressure

Front 78

The vasomotor center controls constriction of arterioles via ____________ fibers

Back 78

sympathetic

Front 79

Key points to how blood pressure changes through out circulation:

Back 79

1) blood vessels are regulated by vasoconstriction of arteries, NE from sympathetic motor neuron binds to L receptors or B receptors on the tunica medials
2) Pulse is gone before it reaching capillaries
3) Mean arterial pressure (MAP). Diastolic +pp/3 =

Front 80

Blood pressure =

Back 80

cardiac output x total peripheral resistance

Front 81

Hormonal controls –

Back 81

1) Atrial naturetic peptide released from right atrium when blood pressure is high. Targets kidneys to cause more salt loss (water follows)
2) Epinephrine – released from adrenal medulla. Targets many organs. Increases heart rate and force of contraction. Targets smoot muscle of the blood vessels. Alpha adrenergic receptor cause constriction in skin, reproductive organs, kidneys, and intestinal arteries. But causes dilation in heart muscle, lung and skeletal muscle arteries
3) Agiotensin. Kidney releases renin into the blood when it senses low blood volume or low oxygen. Renin converts angiotensinogen into angiotensin I. Agitenisin Converting Enzyme (ACE)converts angiotensin I into angiotensis ii

Front 82

Angiotensis II – Three key effects:

Back 82

1) Potent vasoconstricter (immediate)
2) Stimulates release of antideurtic hormone (released from post. Pituitary and causes H2O re-absorption in the kidneys). Therefor increase blood volume, which increases blood pressure.
3) Stimulates aldosterone (released from adrenal cortex and targets kidneys and causes salt retention

Front 83

120/80 –

Back 83

typical blood pressure sys