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
Obtuse marginals
supply blood to the LV
26
Left atrial branch
supplies blood to the LA
27
Diagonal branches
supply blood to the anterior LV free wall
28
Acute marginals
to the right ventricular free wall
29
Septal perforators
supply blood to the inter ventricular septum anteriorly
30
Starling's Law
an increase in ventricular filling pressure (preload) will be met with a proportional increase in contractile force
31
Baroreceptors response
to detection of low or high blood pressure
32
Medullary Ischemic response
decreased blood flow to medulla results in increased blood pressure
33
Chemoreceptors response to high carbon dioxide
vasoconstriction
34
SA nodal
to the sinoatrial node
35
Acute marginals
to the right ventricular free wall
36
AV nodal
to the atrioventricular node
37
Posterior descending artery
supplies blood to the posterior third of the IVS
38
posterolateral branches
perfuse the inferior or inferoposterior LV wall