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anatomy 1412 > cardiovascular physiology > Flashcards

cardiovascular physiology Flashcards

1
Q

what are the parts of the cardiac physiology

A
  1. heart - dual pump with valves
  2. conduction system
    - non-contractile cardiac muscle cells modified to initiate and distribute impulses throughout the heart
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2
Q

parts of conduction system

A
  1. sinoatrial (SA) node - in right atrium
  2. atrioventricular (AV) node - in right atrium
  3. bundle of His (AV bundle)
    - originates at AV node
    - only route for electrical activity to go from atria to ventricles
  4. purkinje fibres
    - terminal fibers - stimulate contraction of the ventricular myocardium
    - 30 APs/min
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3
Q

what are the phases of pacemaker activity

A
  1. pacemaker potential
    - low K+ permeability
    - slows inwards leak of Na
    - causes slow depolarization toward threshold (-40mV)
  2. AP depolarization
    - at threshold - AP
    - Ca++ voltage open - Ca moves in depol gates close at threshold
  3. AP repolarization
    - K voltages gates open at peak lets K out - repolarization
    - K gates close below threshold
  4. Na channels open at -50mV
    - starts pacemaker potential again once K+ gates close (continuous cycle)
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4
Q

APs in ventricular myocardium

A
  • cells=contractile
  • purkinje fibre AP = ventricular myocardial AP (spread cell to cell by gap junction)
  • resting MP= -90mV
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5
Q

absolute refractory period

A

-long - Na + channels inactivated until MP closes to -70mV

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6
Q

excitation-contraction coupling in myocardial cells

A
  1. open voltage-gated Ca channels of AP
  2. opens chemically-gated Ca channels on SR making the cytosolic Ca+ increase
  3. contraction
    - sliding filament mechanism
    - begins a few msec after AP begins
    - duration of AP
    - result: no summation
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7
Q

what are the 3 components of the cardiac cycle

A
  1. electrical activity (ECG)
    - small currents due to depol/repol of heart
    - seen as waves
  2. mechanical activity
    a. systole - contraction, emptying
    b. diastole - relaxation, filling
    - both initated by electrical activity
  3. blood flow through heart
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8
Q

ECG waves

A

a. P wave = atrial depol. - followed by contraction
b. QRS wave = ventricular depol - contraction. aslo atrial repol. (relaxation)
c. T wave = ventricular repol - followed by relaxation

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9
Q

ECG intervals

A

a. P-Q = atria contracted, signals passing through AV node
b. S-T = ventricles contracted, atria relaxed
c. T-P heart at rest

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10
Q

abnormalities of heart beat

A
  1. tachycardia - resting HR more than 100 bpm
  2. bradycardia - resting HR less than 60 bpm
  3. heart block - when conduction through the AV node slowed
    - ventricles may not contraction after each atrial contraction
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11
Q

what is the timing of mechanical events

A
  • average resting heart rate =75beats/min
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12
Q

blood flow through heart is due to

A

a. pressure changes
b. valves
c myocardial contraction (raises P)
- in diast. ventricles have lowest P blow flows into them
- in syst - ventricles have highest P blood flows out of them

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13
Q

during ventricular systole

A

a. high P in ventricles than atria forces AV valves shut causing turbulence of blood gives first heart sound
b. P rises - higher P in ventricle than aorta/pulm trunk pushes semilunar valves open - blood enters vessels

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14
Q

during ventricular diastole

A

a. P drops - higher P in aorta/pulm trunk than ventricles forces semilunar valves shut making 2nd heart sound
b. AV valves open when P in ventricles drop below P in atria

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15
Q

turbulent flow

A

noisy due to blood turbulence when valves shut

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16
Q

laminar flow

A

no sounds

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17
Q

what are the sounds of korokoff

A

turbulence heard in brachial artery during blood pressure measurements

  • begin=systolic pressure
  • stop = diastolic pressure
  • due to cardiac cycle events
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18
Q

cardiac output (CO)

A

volume of blood ejected by each ventricle in 1 min.

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19
Q

stroke volume

A

volume ejected by each ventricle per beat

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20
Q

end diastolic volume (EDV)

A

volume of blood in each ventricle at end of ventricular diastole
120ml

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21
Q

end systolic volume (ESV)

A

volume of blood in each ventricle at the end of ventricular systole
50ml

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22
Q

what are the controls of CO

A
  1. control of heart rate

2. stroke volume

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23
Q

control of heart rate

A
  • basic rate set by SA node (intrinsic control)

- modifiers of HR

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24
Q

types of entrinsic control

A
  1. neural
    - SNS: Na channels open wider
    - PSNS : keeps resting HR lower than pace set by SA node
  2. hormonal
    -epinephrine, NE
    - thyroid hormone - direct effect to increase HR
  3. other factors
    I. ions e.g. high K in ISF
    ii) fever
    -higher temp = higher HR
    iii)age
    - newborn =high
    iv) fitness
    - higher fitness lower HR
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25
Q

control of stroke volume: intrinsic control

A

a. intrinsic control: ( hearts build-in ability to vary SV - adjust to demands)
- increase venous return leads to increased EDV which leads to increase hear muscle stretch and increased force of contraction. increasing SV.
- more blood in = more blood out

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26
Q

Frank-starling’s law of the heart

A

force of ejection is directly proportional to length of ventricular contractile fibres

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27
Q

getting an increase of venous return is due to

A
  • exercise: venous return speeded up

- lower HR: has longer to fill, less of an effect than exercise

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28
Q

extrinsic controls: ANS-SNS`

A
  • increase force of contraction.
  • increase SV but SNS also increases HR which is less time to fill. this leads to a decrease in EDV at higher HR. however, increase force increases ESV
  • PSNS no significant eggect
  • overall SNS increases, PSNS decreases
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29
Q

extrinsic controls: hormones

A
  • epi, NE: same mechanism as SNS which increases force

- thyroid hormone increases force

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30
Q

extrinsic controls: other factors

A 
force is increased by:
- increased external Ca++
-digitalis (drug) - increases Ca++ inside 
force is decreased by;
-acidosis 
- increased external K+
- Ca++ channel blockers (drugs)
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31
Q

blood circulation

A
  • blood flow: volume of blood flowing through any tissue and in a vessel is determined by pressure and resistance
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32
Q

what is the relationship of blood circulation

A

F= (triangle)(P)/ R

f= flow
(triangle)(P) = blood pressure gradient 
R= resistance
- opposes flow 
- depends on:
1. vessel length
2. viscosity of blood 
3. radius of arterioles *most important*
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33
Q

blood flow to organs is controlled by

A
  1. vasoconstriction
    - radius decreases raising R and decreasing Flow
    - P in artery increases
    - P in organ decreases
  2. vasodilation
    - radius increases making the R decrease and flow increase
    - P in artery decreases
    - P in organ increases
34
Q

if vasoconstriction is local what happens

A

no observable change in systemic (Arterial) BP

35
Q

if vasoconstriction is systemic what happens

A

systemic BP will change

36
Q

what is the vasoconstriction/dilation controlled by

A
  1. intrinsic regulation
    - allows organs to control it own blood flow
  2. extrinsic regulation
    - external control by NS and endocrine system
37
Q

myogenic regulation

A

when smooth muscle is stretched it contracts. if systemic blood increases P arterioles constrict.

38
Q

metabolic regulation

A

if blood levels of e.g. O2 decrease, CO2 increase, pH decreased - endothelial cells + hemoglobin release nitric oxide which increases blood flow to organs

39
Q

neural regulation

A
  • arteriolar vasocon
  • vasodilation due to decrease in SNS signals
  • also venoconstriction
40
Q

hormonal regulation

A

I) epinephrine

  • vasocon: skin, viscera
  • vasodil: heart, skel muscle, liver opposes SNS
41
Q

SNS causes release of epinephrine, what is the arteriolar response

A
  • in skin, viscera: both vascon (blood shifts to where its needed)
  • in heart skeletal muscles and liver has opposite effects, response mainly determined by metabolic regulation
42
Q

systolic pressure

A

arterial bp produced by ventricular contraction

43
Q

diastolic pressure

A

arterial bp due to recoil of elastic arteries (when ventricles are relaxed)

44
Q

how do we measure blood pressure

A
  • syst/diast.

- normal bp is 120/80

45
Q

how do we measure pulse pressure

A

systolic -diastolic

46
Q

mean arterial pressure (MAP)

A

regulated by the body i.e. what the body measures

47
Q

how does MAP regulate

A
  1. cardiac output
  2. TPR(Arteriolar radius)
  3. blood volume
48
Q

extrinsic regulation of MAP

A
  1. neural control
    a. baroreceptor reflexes: short term changes e.g. standing
    b. chemoreceptor reflexes
    - peripheral chemoreceptors responds to pH, CO2. found in the aortic arch
  2. hormonal control
    a. epinephrine
    b. renin-angiotensin system
    c. atrial natriuretic peptide (ANP)
    - causes decrease in renin, aldosterone, ADH whiche increase urine production
49
Q

how do stretch receptors monitor MAP

A
  1. ceratoid sinus (brain bp)

2. aortic arch (systemic bp)

50
Q

angiotensin II causes

A
  • increase vasocon, increase venocon which increases MAP

- increase aldosterone, ADH results in increase renal Na, h20 abs, increase thirst and blood volume

51
Q

capillary exchange

A
  • between blood and ISF
52
Q

how do solutes enter and leave capillaries

A
  1. diffusion - major route (except brain)
    - CO2, O2, ions, glucose, hormones
  2. vesicular transport
    - large proteins
    - occurs via transcytosis
  3. mediated transport
    - requires a membrane carrier protein. mainly in brain
53
Q

fluid (water) enters or leave capillaries by

A
  1. osmosis

2. bulk flow - due to P difference

54
Q

what are the 4 pressures involved in bulk flow

A

a. blood hydrostatic P
b. . blood osmotic P
c. ISF hydrostatic P
d. ISF osmotic

55
Q

Net filtration pressure

A
  • sum of hydrostatic and osmotic pressures acting on the capillary
56
Q

circulatory shock

A

inadequate blood flow (decrease oxygen, nutrients to cells)

57
Q

hypovolemic shock

A
  • decrease blood volume

- due to: blood loss severe burns, diarrhea, vomiting

58
Q

vascular shock

A
  • blood volume normal, but vessels expanded

- due to: systemic vasodilation of blood vessels

59
Q

cardiogenic shock

A
  • pump failure result in decrease CO

- heart cannot sustain blood flow

60
Q

stages of shock

A
  1. compensatory
    - mechanisms can restore homeostasis by themselves
    - involves
    a. baroreceptors
    b. chemoreceptors
    c. ischemia of medulla
  2. progressive
    - mechanisms inadequate to restore homeostasis
    - decrease CO, BP, blood to brain
  3. irreversible
    - decrease CO - too little blood to heart
    - self-perpetuating cycle - leads to death
61
Q

what does the compensatory trigger

A
  • increase HR, generalized vasocon

- decrease blood flow to kidneys triggers renin release

62
Q

what does blood contain

A
  1. plasma (90.5% water

2. formed elements

63
Q

what does plasma contain

A

a. H20
b. proteins
- albumins
- globulins
- fibrinogen
c. electrolytes (ions)
d. other solutes

64
Q

what is the function of proteins in plasma

A
  1. produce osmotic pressure
  2. buffer pH
  3. globulins: transport lipids, metal ions, hormones
  4. y globulins = antibodies
  5. clot formation
65
Q

what is the function of electrolytes in plasma

A
  1. membrane excitability

2. buffers (HCO3)

66
Q

what other solutes does the plasma contain

A

nutrients, wastes, gases, hormones

67
Q

what formed elements does blood contain

A

a. red blood cells (RBCs)

b. White blood cells (WBCs)

68
Q

what are the functions of RBCs

A

1, transport

  1. buffer - globin binds to H reversibly
  2. carbonic anhydrase
69
Q

hemoglobin in RBCs

A
  • Hb = 4 hemes + 4 globins (proteins)
70
Q

how is hemoglobin broken down

A

by macrophages into:

  1. heme
    - iron is removed and stored
    - bone marrow make heme
    - non iron protein excreted by bile in liver
  2. globin
    - converted to amino acids : recycled
71
Q

granulocytes WBCs

A
  1. neutrophils
    - phagocytic
  2. eosinophils
    - attack parasites
    - break down chemical released in allergic reactions
  3. basophils
    - secret histamine
    - secrete heparin `
72
Q

agranulocytes WBCs

A
  1. monocytes
    - enter tissues, enlarge to become phagocytic marcophages
  2. lymphocytes
73
Q

T lymphocytes

A
  • helper T + cytotociv lymphocytes
74
Q

B lymphocytes

A

when activated give rise to plasma cells , secrete antibodies
- natural killer cells , attack foreign cells, abnormal cells

75
Q

platelets

A

cell fragments from megakaryocytes in red marrow

76
Q

functions of platelets

A

forms platelet plug which prevents excess blood loss

77
Q

hemostasis

A
  • process of stopping bleeding.
78
Q

what does hemostasis involve

A
  1. vascular spasm
    - vasoconstriction of damaged arteries, arterioles, decreases blood flow
  2. platelet plug formation
    - platelets stick to damaged blood vessel, releasing chemicals
    - healthy endothelial cells release chemicals to prevent spread of plug
  3. clot formation
  4. clot retraction + repair
    - retraction - blood vessel edges pulled together
    - repair - fibroblasts form new CT, new endothelial cells repair lining
  5. fibrinolysis
    - clot dissolution
    - digesting enzymes = plasmin
79
Q

what does the release of chemicals in platelet plug formation cause

A

a. cause more platelets to stick
b. promote clotting
c. begin healing

80
Q

what are the three stages of clot formation

A
  1. production of prothrombin
  2. prothrombin converted to thrombin
  3. fibrinogen converted to fibrin
    - positive feedback to increase its formation, thrombin trapped in clot, inactivated, washed away
81
Q

how is production of prothrombin activated

A
  1. extrinsic pathway
    - uses factors released by damaged tissues
  2. intrinsic pathway
    - uses factors contained in blood
    - require Ca++, tissue, platelet and or plasma factors
82
Q

hemophilia

A

clotting abnormal/absent

- about 83% = type A lack clotting factor

anatomy 1412 (13 decks)

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