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NSCC 7150 > Cardiac A&P Foundational Concepts > Flashcards

Cardiac A&P Foundational Concepts Flashcards

1
Q

Arteries

A
  • carry blood away from heart
  • arterial vessels are known as resistance vessels b/c they have the ability to change amount of resistance encountered by blood flowing through them and can redistribute blood flow through body by constricting/dilating
  • ax findings can provide info about cardiac output and perfusion of oxygenation blood to tissues
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2
Q

Veins

A
  • carry blood towards heart
  • capacitance vessels b/c they hold ~75% of body’s total blood volume
  • ax findings give info about total circulating blood volume and volume of blood returning to the heart
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3
Q

what is common in all blood vessels

A

have three layers:
1) outer CT layer
2) middle layer of smooth muscle and elastic tissue. accommodates large amount of blood in venous system
3) inner layer of endothelium and small amount of elastic tissue

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4
Q

which organs contain the largest reservoirs of blood?

A

spleen, liver, intestines
(Sp-L-In)

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5
Q

describe blood flow through the heart

A

inferior/superior vena cava -> R atrium -> tricuspid valve -> R ventricle -> pulm valve -> pulm arteries -> lungs -> pulm veins -> L atrium -> mitral valve -> L ventricle -> aortic valve -> aorta -> arterial and venous systems

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6
Q

_______ send _______ blood to the lungs

A

pulmonary arteries, deoxygenated

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7
Q

_____ send ______ blood to the heart

A

pulmonary veins, oxygenated

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8
Q

which structures of the heart are not separated by valves?

A

-inferior/superior vena cava and R atrium
-pulmonary veins and L atrium

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9
Q

what represents the time of greatest cardiac output?

A

ventricular systole (contraction)

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10
Q

describe the parasympathetic nervous system

A
  • rest and digest
  • outflow from brain to heart originates in medulla and enters heart as vagus nerve
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11
Q

what does stimulation of the PNS cause?

A

1) rate of impulse generation at SA node slows down
2) transmission of impulses through AV node
3) slows heart rate

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12
Q

atropine

A

given for bradycardia, blocks vagal influence on heart. does not speed up heart directly

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13
Q

describe the sympathetic nervous system

A
  • fight or flight
  • triggered by stress and increases HR and contractility; stimulates secretion of adrenaline/noradrenaline
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14
Q

what facilitates SNS effects?

A

alpha and beta receptors (adrenergic receptors)

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15
Q

alpha receptors

A
  • located in GI tract, skin, and peripheral blood vessels
  • cause vasoconstriction of arterioles
  • increase afterload, MAP and perfusion to major organs
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16
Q

beta-1 receptors

A
  • located in heart
  • increase speed of impulse transmission and conductivity, automaticity and force of contraction
    -increase contractility
  • increase CO, SV and HR
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17
Q

beta-2 receptors

A
  • found in lungs and skeletal muscle
  • cause bronchodilation
  • decrease airway resistance
  • increase ventilation and arterial O2 content
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18
Q

sympathomimetic drugs

A

mimic action of SNS stimulus on beta receptors, produce effects that match stimulus of beta receptors
ex) dobutamine, dopamine

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19
Q

what are the main neurotransmitters?

A

acetylcholine (secreted by PNS nerves and few SNS nerves), epinephrine, norepinephrine (secreted by SNS nerves at synaptic cleft)

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20
Q

cholinergic

A

nerves and receptors interact by means of acetylcholine (PNS)

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21
Q

adrenergic

A
  • nerves and receptors interact by means of norepinephrine/epinephrine (SNS)
  • also respond to catecholamines in general systemic circuit
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22
Q

what happens when stress is prolonged?

A

SNS response is sustained d/t effects of circulating catecholamines

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23
Q

cardiac output

A

amount of blood pumped by heart in a given time period; L/min

24
Q

formula for cardiac output

A

stroke volume x HR

25
Q

effects of increased HR are?

A
  • decreased ventricular filling time = decr preload and contractility
  • increased cardiac demand
  • decreased coronary artery filling time
26
Q

stroke volume

A

amount of blood ejected from the heart with each contraction; mL/beat

27
Q

formula for stroke volume

A

EDV (preload) - ESV (afterload)

determined by volume in blood at end of diastole - volume of blood expelled during systole

28
Q

what can affect stroke volume?

A

dysrhythmias

29
Q

what factors influence stroke volume?

A

1) preload
2) afterload
3) contractility

30
Q

preload

A

volume of blood in ventricles at end of diastole (EDV); amount of stretching of heart’s ventricles

31
Q

what factors could influence preload?

A

4VEN ACirc
1) venous return
2) circulating blood volume
3) ventricular filling time
4) atrial kick
5) ventricular contractility
5) ventricular compliance

32
Q

venous return

A

blood returning to the heart from the body

33
Q

what is venous return influenced by?

A

a) conditions that cause venodilation and incr venous capacitance: allows blood to pool in peripheral circulation and decreases venous return . ex: incr temp, allergic responses, some meds like nitro

b) conditions that cause vasoconstriction and decr venous capacitance: increases venous return
ex: decr temp, some meds like epi

c) inc or decr in intrathoracic pressure can occur with invasive/non-invasive positive pressure ventilation

34
Q

how does intrathoracic pressure affect venous return?

A
  • increase in intrathoracic pressure decreases venous return (when + vent pressure is applied)
  • decrease in intrathoracic pressure increases venous return (when support is removed)
35
Q

What can increase/decrease circulating blood volume?

A

can be decreased by:
- blood loss
- vomiting/diarrhea
- over diuresis
- poor intake
- sepsis

can be increased by:
- over resuscitation with fluids/blood
- excessive oral fluid intake
- renal failure resulting in decreased urine output

36
Q

what affects ventricular filling time?

A
  • increased heart rate decreases amount of time the ventricles have to fill and vice versa
  • impacts volume of blood within ventricles and preload
37
Q

atrial kick

A

R and L ventricles relax, begin filling with blood. tricuspid and mitral valves open, blood flows passively into ventricles. 70-80% ventricular filling, end of diastole, atrium contract. atrial kick = last 20-30% of blood volume ejects into ventricles

38
Q

when does preload occur?

A

after atrial kick while AV valves are still open and ventricular filling is at its max

39
Q

what happens if there is a loss of atrial kick?

A

dysrhythmias!
ex) afib leading to decreased preload

40
Q

what happens when ventricular contractility is impaired?

A

ventricle doesn’t empty effectively during systole - blood is not being pumped forward - heart fills with more blood during next diastolic cycle = greater than normal amount of blood in ventricle = increased preload

41
Q

what happens when there’s fluid backup in the left ventricle and in the right ventricle?

A

left ventricle = increase pressure in pulmonary vasculature = pulm edema

right ventricle = increase pressure in systemic circulation = peripheral edema

42
Q

ventricular compliance

A

measure of distensibility or ability to stretch

43
Q

what happens if there is a decrease in ventricular compliance?

A

could occur as result of scarring associated with MI

decreased compliance = increased preload

44
Q

afterload

A

force or resistance against which the ventricles must pump in order to eject blood

45
Q

what happens if afterload is increased?

A

this means increased resistance. so ventricles must contract forcefully to maintain normal stroke volume which will cause increased myocardial workload and O2 demand

46
Q

what happens if afterload is decreased?

A

this means ventricles can’t generate enough force - decreased stroke volume and amount of blood leaving heart

47
Q

what factors is afterload influenced by?

A

BAV is DJ AFTERLOAD
1) vessel diameter
2) blood viscosity
3) aortic impedence

48
Q

vessel diameter

A

diameter of arteries/arterioles; is primary determinant of afterload

49
Q

what happens if vessel diameter is decreased? what is it caused by?

A

vasoconstriction is occurring, afterload is increased.

-circulating catecholamines
-compensatory mechanisms like RAAS
-hypothermia
-vasoconstrictive drugs (epi, norepi, vasopressin)

50
Q

what happens if vessel diameter is increased? what is it caused by?

A

vasodilation. afterload is decreased.

-hyperthermia
-inflammatory responses
-vasodilating drugs (nitro)

51
Q

what is good indicator of arterial tone and why?

A

dBP; its a measurement of pressure within the body’s vasculature between heart beats. is the resting pressure of system between influxes of blood flow and pressure caused by systole.

  • in a vasoconstricted system dBP is increased; in vasodilated system dBP is decreased
52
Q

contractility

A

ability of heart’s myofibrils to change their strength of contraction during systole

53
Q

what is contractility influenced by?

A

hormones, NTs, cardiac hx, chemical substances, availability of O2 and nutrients to cardiac muscle

54
Q

what can decrease contractility?

A
  • decreased preload (not stretching myofibrils enough)
  • increased preload (overstretching myofibrils)
  • increased afterload (increased pressure heart must pump against)
  • inadequate O2 supply to heart’s muscle
  • negative inotropic drugs
  • some electrolyte imbalances, especially hypocalcemia
  • tachycardia
  • pre-existing medical conditions
55
Q

what can increase contractility?

A

-stimulatory effect of SNS
-circulating catecholamines
- positive inotropic drugs
-balanced electrolytes, esp Ca+
-obtaining adequate preload
-decreased afterload

56
Q

starling’s law

A

describes relationship between amount of stretch experienced by myocardial fibers caused by preload during diastole, and the resulting force they can contract with during systole

as preload increases, contractility increases, but if myofibrils are overstretched, contractility becomes impaired

NSCC 7150 (10 decks)

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