A & P Flashcards

1
Q

V1 and V2

A
  • septal leads

- septal perforators off of LAD

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2
Q

V3 and V4

A
  • anterior lead

- LAD

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3
Q

L1 and V5 and V6 and aVL

A
  • lateral wall leads

- left circumflex artery

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4
Q

L2 and L3 and aVF

A
  • inferior leads

- right coronary artery

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5
Q

First branch off off right coronary artery

A

conus

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6
Q

Afterload

A

resistance to ejection of blood from ventricles

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7
Q

Afterload - Increased in

A
  • vasoconstriction as from sympathetic nervous system stimulation or vasopressors
  • hypertension
  • aortic valve disease
  • hypercoagulability
  • pulmonary hypertension
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8
Q

Afterload - Deceased in

A
  • hypotension
  • vasodilation
  • vasodilators
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9
Q

Preload

A

end-diastolic; “filling pressure”

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10
Q

Preload - Increased in

A
  • heart failure
  • hypervolemia
  • bradydysrhythmias
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11
Q

Preload - Decreased in

A
  • hypovolemia
  • excessive vasodilation
  • increased intrathoracic pressure
  • cardiac tamponade
  • right ventricular failure or infarction
  • tachydysrhythmias
  • loss of atrial contraction
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12
Q

Cardiac Output

A
  • the amount of blood pumped by the heart in liters per minute
  • calculated as heart rate x stroke volume
  • normal range is 4.0 to 6.0 liters per minute
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13
Q

Rapid diastolic filling

A

passive filling

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14
Q

Reduced diastolic filling

A

“diastasic”

-coronary blood flow is optimal

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15
Q

Atrial contraction

A
  • this subphase is also referred to as “atrial kick” or “atrial systole”
  • contributes to 15 to 30% of diastolic filling volume
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16
Q

Isovolumetric contraction

A
  • contraction increases pressure in the ventricles, but there is no change in volume due to the AV valves are closed and the semilunar valves have not yet opened
  • this subpage accounts for 2/3 of oxygen consumption of the ventricles
17
Q

Rapid ventricular ejection

A

aortic and pulmonary arterial pressures increase rapidly and ventricular volume decreases rapidly

18
Q

Reduced Ejection

A

“protodiastole”

19
Q

Isovolumetric Relaxation

A
  • relaxation occurs and ventricular pressure decreases

- volume does not change because the semilunar valves are closed and the atrioventricular valves have not yet opened

20
Q

Chemoreceptors

A

input from carbon dioxide-sensing cells in the carotid bodies and the aorta

21
Q

Baroreceptors

A

pressure - sensing cells in the carotid bodies (located at the carotid bifurcation) and the aortic arch

22
Q

Medullary Ischemic Response

A

cerebral perfusion in the difference between mean arterial pressure and intracranial pressure

23
Q

Increased Inotropy

A
  • stroke volume and cardiac output
  • increases workload of the heart and myocardial oxygen requirements
  • sympathetic stimulation
24
Q

Decreased Inotropy

A
  • myocardial ischemia or infarction
  • cardiomyopathy
  • hypoxemia
  • acidosis
25
Q

Obtuse marginals

A

supply blood to the LV

26
Q

Left atrial branch

A

supplies blood to the LA

27
Q

Diagonal branches

A

supply blood to the anterior LV free wall

28
Q

Acute marginals

A

to the right ventricular free wall

29
Q

Septal perforators

A

supply blood to the inter ventricular septum anteriorly

30
Q

Starling’s Law

A

an increase in ventricular filling pressure (preload) will be met with a proportional increase in contractile force

31
Q

Baroreceptors response

A

to detection of low or high blood pressure

32
Q

Medullary Ischemic response

A

decreased blood flow to medulla results in increased blood pressure

33
Q

Chemoreceptors response to high carbon dioxide

A

vasoconstriction

34
Q

SA nodal

A

to the sinoatrial node

35
Q

Acute marginals

A

to the right ventricular free wall

36
Q

AV nodal

A

to the atrioventricular node

37
Q

Posterior descending artery

A

supplies blood to the posterior third of the IVS

38
Q

posterolateral branches

A

perfuse the inferior or inferoposterior LV wall