Cardiovascular anatomy Flashcards

1
Q

What is the blood supply of the SA Node?

A

Commonly supplied by RCA (blood supply independent of dominance)

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2
Q

What is the blood supply of the AV Node?

A

Supplied by the PDA

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3
Q

Describe effects of PDA infarct

A

Infarct may cause AV nodal dysfunction (bradycardia or heart block)

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4
Q

Describe the prevalence and features of a right-dominant circulation

A

85% of people PDA arises from RCA

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5
Q

Describe the prevalence and features of a left-dominant circulation

A

8% of people, PDA arises from LCX

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6
Q

Describe the prevalence and features of a Codominant circulation

A

7% of people, PDA arises from both LCX and RCA

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7
Q

What is the most common site of coronary artery occlusion?

A

Coronary artery occlusion most commonly occurs in the LAD

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8
Q

When does coronary blood flow peak?

A

Coronary blood flow peaks in early diastole

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9
Q

The left circumflex coronary artery supplies?

A

Supplies lateral and posterior walls of left ventricle, anterolateral papillary muscle

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10
Q

LCX AKA

A

Left circumflex coronary artery

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11
Q

LAD AKA

A

Left anterior descending coronary artery

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12
Q

LAD supplies

A

Anterior 2/3 of interventricular septum, anterolateral papillary muscle, anterior surface of the left ventricle

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13
Q

PDA AKA

A

Posterior descending/interventricular artery

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14
Q

PDA supplies

A

AV node, posterior 1/3 of interventricular septum, posterior 2/3 walls of ventricles and posteromedial papillary muscle

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15
Q

Right acute marginal artery supplies

A

Right ventricle

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16
Q

What is the most posterior part of the heart?

A

Left atrium

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17
Q

Left atrial enlargement can cause?

A

Dysphagia, (due to compression of the esophagus), or hoarseness (due to compression of the left recurrent laryngeal nerve, a branch of the vagus nerve)

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18
Q

What are the layers of the pericardium?

A

From outer to inner Fibrous pericardium Parietal layer of serous pericardium Visceral layer of serous pericardium

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19
Q

Where is the pericardial cavity?

A

Lies between parietal and visceral layers of the pericardium

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20
Q

Innervation of the pericardium

A

Phrenic nerve

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21
Q

Pericarditis pain location

A

Can cause referred pain to the shoulder

22
Q

CO equation

A

SV x HR = CO

23
Q

Fick Principle

A

Rate of O2 consumption / (arterial O2 content - venous O2 content)

24
Q

MAP equation

A

MAP = CO x TPR

25
Q

MAP at resting HR

A

(2/3 diastolic + 1/3 systolic)

26
Q

Pulse pressure equation

A

Systolic pressure - diastolic pressure

27
Q

Pulse pressure is proportional to?

A

SV

28
Q

Pulse pressure is inversely proportional to?

A

Arterial compliance

29
Q

SV equation

A

EDV - ESV

30
Q

Describe CO control in exercise

A

During the early stages of exercise CO is maintained by Increased HR and increased SV During the late stages of exercise CO is maintained only by increased HR as SV plateaus

31
Q

Increased HR effect on SV

A

Diastole is shortened with increased HR because there is less filling time so CO is decreased such as in ventricular tachycardia)

32
Q

Causes of increased pulse pressure

A
  • Hyperthyroidism
  • Aortic regurgitation
  • Aortic stiffening (isolated systolic hypertension in the elderly)
  • Obstructive sleep apnea (increased sympathetic tone)
  • Anemia
  • Exercise (transient)
33
Q

Causes of decreased pulse pressure

A
  • Aortic stenosis
  • Cardiogenic shock
  • Cardiac tamponade
  • Advanced heart failure
34
Q

SV is increased by

A
  • Increased contractility
  • Increased preload
  • Decreased afterload
35
Q

SVCAP

A

Stroke volume is affected by contractility, afterload and preload

36
Q

Contractility (and SV) are increased with

A
  • Catecholamine stimulation via B1 receptor
  • Increased intracellular Ca2+
  • Decreased extracellular Na+ (reduced activity of Na/Ca exchanger)
  • Digitalis (bocks Na/K pump -> increased intracellular Na -> decreased Na/Ca exchanger activity -> increased intracellular Ca
37
Q

Describe the pathway of B1 stimulation

A
  • Ca channels phosphorylated -> increased Ca entry -> increased Ca-induced Ca-release and increased Ca storage in the sarcoplasmic reticulum
  • Phospholamban phosphorylation results in active CaATPase -> increased Ca storage in the sarcoplasmic reticulum
38
Q

Describe Phospholamban phosphorylation

A

results in active CaATPase -> increased Ca storage in the sarcoplasmic reticulum

39
Q

Describe the function of digitalis

A

Digitalis blocks the Na/K pump -> increased intracellular Na -> decreased Na/Ca exchanger activity -> increased intracellular Ca and thereby increasing contractility

40
Q

Contractility is decreased by

A
  • B1 blockade (decreased cAMP)
  • HF with systolic dysfunction
  • Acidosis Hypoxia/hypercapnia (decreased PO2/ increased PCO2)
  • Non-dihydropyridine Ca2 channel blockers
41
Q

How is preload determined?

A

It is approximated by ventricular EDV and depends on venous tone and circulating blood volume

42
Q

Venous vasodilators effect on preload

A

Decrease preload

43
Q

Nitroglycerin effect on venous circulation

A

Venous vasodilation and decreased preload through reduced venous return

44
Q

How is afterload determined?

A

Afterload is approximated by MAP Increased afterload -> increased pressure -> increased wall tension per Laplace’s Law

45
Q

What is the adaptive response to increased afterload?

A

The left ventricle compensates for increased afterload by thickening (hypertrophy) in order to reduce wall tension

46
Q

Arterial vasodilators affect on afterload

A

Decrease afterload

47
Q

ACE inhibitors affect on afterload and preload

A

Decrease afterload and preload

48
Q

Chronic hypertension (MAP) leads to what heart changes?

A

LV hypertrophy

49
Q

Myocardial O2 demand is increased by?

A
  • Increased contractility
  • Increased afterload
  • Increased heart rate
  • Increased diameter of the ventricle (increased wall tension)
50
Q

Wall tension principle

A

LaPlace’s Law