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XIO > Traffic - week 9 > Flashcards

Traffic - week 9 Flashcards

1
Q

Basics of cardiovascular system and heart (heart bike)

A
  • function of CV system is transport
    1. heart is the pump
    a. establishes a pressure gradient (flow occurs from greater ➝ lesser pressure)
    2. blood vessels are passageways
    3. blood is the transport medium
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2
Q
  • heart is a double pump
A

. pulmonary circuit

a. heart ➝ lungs and back (at lungs, picks up O2, releases CO2)
b. right side is pump
2. systemic circuit
a. heart ➝ body tissues and back (at tissues, picks up CO2, releases O2)
b. left side is pump

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3
Q

valves prevent backflow of blood (chord)

A
  1. AV valves attached by chordae tendinae to papillary muscles so that they open in one direction only
  2. semilunar valves are shaped like cups, this structure prevents them from opening backward
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4
Q

When pressure is greater behind the valve

A

it opens

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5
Q

When pressure is greater in

front of the valve

A

it closes. Note that when pressure is greater in front of the valve, it does not open in the opposite direction; that is, it is a one-way valve

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6
Q

fibrous skeleton (skeleton)

A
  1. provides attachment for valves and muscle

2. separates atria from ventricles (important so they contract at different times)

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7
Q

pericardial sac (cardigan)

A

fibrous covering continuous with epicardium

a. anchors heart
b. filled with fluid to prevent friction

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8
Q

Electrical activity of heart (rhythm) - cells

A

auto rhythmic cells

1. specialized cells that initiate and conduct APs

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9
Q

display pacemaker activity - electrical activity of heart

A

K out, Na in - funny channels, slow depolarization. near threshold voltage-gated transient Ca2+ channels open, threshold, voltage-gated long-lasting Ca2+ channels open (more Ca and then AP), peak voltage-gated K+ channels open, repolar.

(no resting potential changes in potential due to voltage-gated Na+, K+ and Ca2+ channels) decreased flow of K+ out and increased inward flow of Na+ through “funny” channels results in slow depolarization

b. near threshold, voltage-gated transient Ca2+ channels open and bring membrane to threshold (Ca2+ flows in)
c. at threshold voltage-gated long-lasting Ca2+ channels open, more Ca2+ flows in (this is the AP)
d. at peak of depolarization, voltage-gated K+ channels open and repolarization occurs

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10
Q

SA node (sinoatrial) (sinus)

A

(1) right atrium
(2) fastest rate of autorhythmicity, it’s the pacemaker of the heart (under usual conditions initiates APs)
(3) interatrial pathway extends to left atrium (spreads AP, atria contract)
(4) internodal pathway extends to next node

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11
Q

AV node (atrioventricular)

A

(1) electrical connection between atria and
ventricles
(2) signal slightly delayed (.1 sec) to allow atria to finish contracting - more efficient blood pumping

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12
Q

AV bundle branches into…(bundle of His)

A

ventricles

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13
Q

Purkinje fibers branch..

A

throughout ventricular myocardium (ventricles contract)

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14
Q

contractile cells (contractor)

A

APs spread from cell to cell
a. adjacent cells joined by intercalated discs
(1) desmosomes resist mechanical stress
(2) gap junctions allow spread of electrical
signals

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15
Q

cardiac muscle APs -

A

a. cell depolarized by autorhythmic activity
b. voltage-gated Na+ channels open, Na+ ➝ in, cell depolarized to +30 mV
c. at the peak of depolarization, Na+ channels close, voltage-gated slow Ca2+ channels open (Ca2+ flows in
- results in plateau, the channels are a “slow” version of the long-lasting Ca2+ channels in autorhythmic cells)
d. at the end of the plateau, Ca2+ channels close, voltage- gated K+ channels open
(K+ ➝ out, repolarization)

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16
Q

excitation-contraction coupling (sliding filament) (ap in cardiac contractile cell)

A

a. AP travels down T tubules, voltage-gated Ca2+ channels open, Ca2+ ➝ in from ECF
b. Ca2+ influx triggers further release of Ca2+ from sarcoplasmic reticulum
c. Ca2+ binds with troponin-tropomyosin complex, cross bridge cycling occurs
d. Ca2+ actively pumped back to ECF and SR
e. extent of cross bridge cycling depends on amount of Ca2+ that enters cytosol (unlike in skeletal muscle, where enough Ca2+ for maximum contraction is always released)

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17
Q

long contractions due to

A

lots of Ca2+ from ECF and SR

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18
Q

long refractory period

A

a. due to inactivation of Na+ channels during plateau
b. tetanus does not occur (no summation)
c. keeps cardiac functioning efficient

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19
Q

Cardiac cycle (sis and di)

A

systole (contraction) and diastole (relaxation) occur in atria and ventricles - most often refers to ventricles

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20
Q

diastole (ava di)

A

AV valves open

b. blood fills ventricles (amount at end of diastole is called end-diastolic volume, EDV is about 135 ml)
c. atria contract

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21
Q

systole (stove-sis)

A

a. ventricles contract, closing AV valves
b. semilunar valves open
c. blood ejected (amount of blood still in ventricles is end- systolic volume, ESV is about 65 ml)

22
Q

Cardiac output (CO - 1 min)

A

CO is the volume of blood pumped by each ventricle in one minute (left and right normally equal)

23
Q

CO =

A 
heart rate (beats/min) x stroke volume
(ml/beat). typically about 5 liters/min at rest (entire blood volume).
24
Q

CO can (elite athlete - reserved)

A

increase to 20-25 l/min

a. difference between CO at rest and maximum CO is cardiac reserve

25
Q

factors influencing heart rate (HR) - parasympathetic

A

parasympathetic effects (ACh, decrease HR)

a. primarily supplies atria (SA and AV nodes)
b. acts on SA node
(1) increases PK+ by slowing K+ channel closure, resulting in hyperpolarization, takes longer to reach threshold
c. also increases PK+ at AV node, lengthening delay
d. acts on atrial contractile cells, weakening contraction
(1) shortens the plateau phase, by decreasing Ca2+ influx
e. little effect on strength of ventricular contraction

26
Q

. sympathetic effects (NE and E, increase HR) on HR

A

acts on SA node
(1) decreases PK+ by speeding up inactivation of K+ channels, resulting in “hypopolarization”, threshold reached more quickly
b. reduces delay at AV node, probably by
enhancing influx of Ca2+
c. speeds spread of AP throughout nodal system by enhancing Ca2+ influx

27
Q
  • factors influencing stroke volume (SV) - intrinsic control -
A

intrinsic control

a. resting cardiac muscle is at less than optimal length - stretching fibers by increasing EDV (increasing venous return) results in a more forceful contraction (increases SV)
b. important to match stroke volume to venous return
(1) automatically equalizes flow through pulmonary and systemic circuits (blood does not “back up”)

28
Q

increasing contractility (increasing SV)

A

a. sympathetic stimulation increases Ca2+ influx (atria and ventricles) resulting in greater cross bridge cycling and more forceful contraction
(1) also enhances venous return by constricting veins, squeezing more blood toward heart

29
Q

Coronary circulation (corona - lamp)

A

heart receives O2 and nutrients from coronary arteries branching off the aorta (coronary veins empty into right atrium)

30
Q

(coronary circulation - blood for heart only) most blood flow occurs during..

A

diastole

31
Q

coronary circulation (blood just for the heart) uses (oxy)

A

oxidative phosphorylation

a. uses mostly free fatty acids, but can use glucose

32
Q

(coronary circulation - blood for the heart only) during exercise, increased demands for O2 are met by

A

by vasodilation (dilation of blood vessels)

a. adenosine (formed from breaking down ATP) released from muscle cells
(1) during O2 deficit
(2) during increased activity (using more ATP)
(3) induces dilation of vessels (smooth muscle relaxes)

33
Q

heart failure (heart can’t keep up with demands of body) (lunar stint)

A

a. damage from heart attack or impaired circulation to cardiac muscle
b. prolonged pumping against increased afterload (stenotic (too stiff) semilunar valve or chronically elevated blood pressure)

34
Q

heart failure - contractility of heart is decreased (umbrella desk)

A

stroke volume decreased for a given EDV (Frank-Starling curve shifts down to right)
b. body compensates with increased sympathetic activity and retaining salt and water to expand blood volume and increase EDV
c. eventually body can’t compensate
(1) backward failure - blood pools in venous system (congestive heart failure)
(2) forward failure - inadequate supplies to tissues
(3) left-sided failure worse
backward - fluid accumulates in lungs
(pulmonary edema), forward – kidney function depressed and they retain even more water and salt

35
Q

atherosclerosis and its effects on the heart (called coronary artery disease when it occurs in coronary vessels) (athlete olympics)

A

complications of disease are leading cause of death in US

can lead to myocardial ischemia (insufficient O2 to heart)

36
Q

thromboembolism (throm)

A

plaque breaks through lining of blood vessels and platelets form abnormal clots
(thrombus) if clot breaks free (embolus) it can block small vessels (complete blockage causes myocardial infarction - heart attack)

37
Q

transient ischemia causes angina pectoris (chest pain) (milk)

A

usually during physical or emotional stress

b. may be due to accumulation of lactic acid as heart makes ATP anaerobically

38
Q

risk factors - coronary artery disease GOOSHHD NE

A

GOOSHHD NE

genetics, obesity, old age, smoking,
high blood pressure, diabetes, lack of exercise, nervous tension, high blood cholesterol levels

39
Q

specific indicators of risk -coronary artery disease

A

a. high blood levels of homocysteine (promotes smooth muscle growth and causes oxidation)
b. high blood levels of C-reactive protein (an indicator of inflammation)

40
Q

cholesterol (window - lip)

A

a. carried in blood as lipoprotein complexes
b. low density lipoproteins (LDL) transport to cells (“bad cholesterol”)
c. high density lipoproteins (HDL) transport to liver and some excreted from body (“good cholesterol”)

41
Q

factors causing ischemia - vascular spasm (kitchen table)

A

decreased O2 triggers platelet activating factor (PAF) release from vessels, causing spastic constriction, further decreasing O2 to heart

42
Q

cholesterol needed for (cell)

A

cell membranes, hormones, bile salts - but high levels of LDL associated with atherosclerosis

43
Q

factors causing ischemia - atherosclerotic plaques (kitchen table)

A

accumulation of lipid and overgrown smooth muscle reduce blood flow, in later stages Ca2+ accumulates (“hardening of the arteries”)

44
Q

systemic (arteries and veins) - direction of movement

A

arteries - oxygen rich, away from heart. veins, oxygen poor, towards heart

45
Q

pulmonary (arteries and veins)

A

arteries - oxygen poor, veins - oxygen rich

46
Q

electrical activity in autorythmic cells causes(what channels open)….

A

(funny channels) then the muscle fibers have ap (transient)

47
Q

increased EDV =

A

increased stroke volume

48
Q

pulmonary edema much worse than..

A

systemic edema

49
Q

heart is lined with

A

endothelial cells

50
Q

heart wall is 3-layered

A

heart wall is 3-layered

  1. endocardium (epithelial lining)
  2. myocardium (muscle)
  3. epicardium (thin fibrous connective tissue layer)
51
Q

contractions are not, an all or

A

nothing effect

52
Q

sympathetic effects do not include..

A

increasing the permeability to potassium in the autorhythmic cells, which increases the heart rate

XIO (393 decks)

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