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cardiology Flashcards

1
Q

Truncus arteriosus GIVES RISE TO

A

Ascending aorta and pulmonary trunk

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2
Q

Bulbus cordis GIVES RISE TO

A

Smooth parts (outflow tract) of left and right ventricles

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3
Q

Endocardial cushion GIVES RISE TO

A

Atrial septum, membranous interventricular septum; AV and semilunar valves

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4
Q

Primitive atrium GIVES RISE TO

A

Trabeculated part of left and right atria

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5
Q

Primitive ventricle GIVES RISE TO

A

Trabeculated part of left and right ventricles

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6
Q

Primitive pulmonary vein GIVES RISE TO

A

Smooth part of left atrium

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7
Q

Left horn of sinus venosus GIVES RISE TO

A

Coronary sinus

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8
Q

Right horn of sinus venosus GIVES RISE TO

A

Smooth part of right atrium (sinus venarum)

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9
Q

Right common cardinal vein and right anterior cardinal vein GIVES RISE TO

A

Superior vena cava (SVC)

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10
Q

First functional organ in vertebrate embryos

A

heart

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11
Q

Primary heart tube loops to establish _____

A

left-right polarity

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12
Q

Cardiac looping begins in week ____ of gestation.

A

week 4

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13
Q

Defect in left-right dynein (involved in L/R asymmetry) can lead to ____

A

dextrocardia

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14
Q

dextrocardia seen in____

A

Kartagener syndrome (primary ciliary dyskinesia)

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15
Q

Septum secundum and septum primum fuse to form the___

A

atrial septum

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16
Q

Patent foramen ovale is caused by ____

A

failure of septum primum and septum secundum

to fuse after birth

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17
Q

Patent foramen ovale can lead to

A

paradoxical emboli

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18
Q

abnormalities associated with failure of neural crest cells to migrate:

A

ƒ-Transposition of great vessels.
ƒ -Tetralogy of Fallot.
ƒ -Persistent truncus arteriosus.

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19
Q

Aortic/pulmonary valve derived from ___

A

endocardial cushions of outflow tract

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20
Q

Mitral/tricuspid valve derived from ___

A

fused endocardial cushions of the AV canal.

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21
Q

3 important fetal circulation shunts:

A

1 Ductus venosus
2 Foramen ovale
3 Ductus arteriosus

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22
Q

Blood entering fetus through the___

A

umbilical vein

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23
Q

Blood entering fetus through the umbilical vein is conducted via the _____

A

ductus venosus

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24
Q

Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the ____

A

IVC

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25
Q

Blood entering fetus through the umbilical vein is conducted via the ductus venosus into the IVC, bypassing ____

A

hepatic circulation

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26
Q

Most of the highly oxygenated blood reaching the heart via the ____

A

IVC

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27
Q

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the __

A

foramen ovale

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28
Q

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the ___

A

aorta

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29
Q

Most of the highly oxygenated blood reaching the heart via the IVC is directed through the foramen ovale and pumped into the aorta to supply the ____

A

head and body

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30
Q

Deoxygenated blood from the SVC passes through the RA -> 􏰀RV􏰀 ->____ -> ___ -> ___

A

main pulmonary artery

patent ductus arteriosus

descending aorta

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31
Q

At birth, infant takes a breath; ___ resistance

in pulmonary vasculature, causing ___ left atrial pressure vs right atrial pressure, causing ____ to close􏰀

A

↓

↑

foramen ovale

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32
Q

At birth, infant takes a breath… __ O2 (from respiration) and ___ prostaglandins (from placental separation)􏰀 leads to closure of ____

A

ductus arteriosus

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33
Q

Indomethacin helps ___

A

close PDA

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34
Q

remnant of ductus arteriosus)

A

ligamentum arteriosum

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35
Q

Prostaglandins E1 and E2

A

kEEp PDA open

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36
Q

SA and AV nodes are usually supplied by ___

A

Right coronary artery (RCA)

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37
Q

RCA supplies ___

A

SA and AV nodes

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38
Q

Right-dominant circulation %

A

85%

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39
Q

Right-dominant circulation (85%) = PDA arises from __

A

RCA.

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40
Q

Left-dominant circulation ___

A

(8%)

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41
Q

Left-dominant circulation (8%) = PDA arises from ___

A

Left circumflex coronary artery (LCX)

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42
Q

Codominant circulation (7%) = PDA arises from both ____ and ___

A

LCX and RCA

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43
Q

Coronary artery occlusion most commonly occurs in the ___

A

Left anterior descending

artery (LAD)

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44
Q

Coronary blood flow peaks in __

A

early diastole

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45
Q

most posterior part of the heart

A

left

atrium

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46
Q

left
atrium enlargement can cause ___ (due to compression of the ___) or ___ (due to compression of the____, a branch of the ___).

A

dysphagia

esophagus

hoarseness

left recurrent laryngeal nerve

vagus

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47
Q

Pericardium consists of 3 layers (from outer to inner):

A 
1) Fibrous pericardium
ƒ 
2) Parietal layer of serous pericardium
ƒ 
3) Visceral layer of serous pericardium
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48
Q

Pericardial cavity lies between __ and

__ layers.

A

parietal

visceral

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49
Q

stroke volume (SV) × heart rate (HR)

A

CO

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50
Q

Fick principle:

A

CO = rate of O2 consumption/

arterial O2 content − venous O2 content

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51
Q

Mean arterial pressure (MAP) =

A

CO × total peripheral resistance (TPR)

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52
Q

2 ⁄3 diastolic pressure + 1⁄3 systolic pressure =

A

MAP

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53
Q

Pulse pressure =

A

systolic pressure – diastolic pressure

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54
Q

Pulse pressure is proportional to ___ and inversely proportional to ___

A

SV

arterial compliance

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55
Q

proportional to SV, inversely proportional to arterial compliance.

A

Pulse pressure

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56
Q

SV =

A

= (EDV) − (ESV)

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57
Q

During the early stages of exercise, CO is maintained by ___

A

↑ HR

and

↑ SV

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58
Q

During the late stages of exercise, CO is maintained by ___

A

↑ HR only (SV plateaus)

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59
Q

Diastole is preferentially shortened with ___ causing ___ filling time leading to ___ 􏰀􏰁(eg, ventricular tachycardia).

A

↑ 􏰂HR

less

↓CO

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60
Q

Inc. in pulse pressure is seen in ___

A

hyperthyroidism

aortic regurgitation

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61
Q

Dec. pulse pressure is seen in ___

A

aortic stenosis

cardiogenic shock

cardiac tamponade

HF

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62
Q

↑ SV with: “SV CAP”

A

↑ Contractility (eg, anxiety, exercise) ƒ 􏰂

↑ Preload (eg, early pregnancy)

↓ ƒ􏰁Afterload

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63
Q

Contractility (and SV)􏰂 ↑ with:

A

Catecholamines

increased 􏰂intracellular Ca2+

↓ extracellular Na+

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64
Q

Catecholamines (inhibition of

___ ) →__ Ca2+ entry into__→Ca2+ induced ___ release)

A

phospholamban

increase

sarcoplasmic reticulum􏰀

Ca2+

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65
Q

Contractility (and SV)􏰂 ↓ with:

A
  • β1-blockade (􏰁 dec. cAMP)
  • HF with systolic dysfunction
  • Acidosis
  • Hypoxia/hypercapnia
  • Non-dihydropyridine Ca2+ channel blockers
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66
Q

↑ MyoCARDial O2 demand is􏰂 ↑ by:
ƒ 􏰂 __ Contractility
ƒ 􏰂 __ Afterload (proportional to ___) ƒ􏰂heart Rate
__ ƒ􏰂Diameter of ventricle (􏰂__ wall tension)

A

↑ Contractility

↓ Afterload

arterial pressure

↑ ƒ􏰂Diameter of ventricle

↑ wall tension

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67
Q

Preload approximated by ___

A

ventricular EDV

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68
Q

VEnodilators (eg, ___) …. __ preload

A

nitroglycerin

↓ preload

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69
Q

Afterload approximated by ___

A

MAP

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70
Q

LV compensates for􏰂afterload by ___ in order to __ 􏰁wall tension

A

thickening (hypertrophy)

↓

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71
Q

VAsodilators (eg, ___) …. ___ 􏰁Afterload (Arterial).

A

hydrAlAzine

↓

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72
Q

ACE inhibitors and ARBs 􏰁both ____ preload and afterload.

A

↓

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73
Q

Chronic hypertension (􏰂__MAP) leads to ___.

A

increases

􏰀LV hypertrophy.

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74
Q

Left ventricular EF is an index of ____

A

ventricular contractility

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75
Q

normal EF is ___

A

≥ 55%

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76
Q

EF􏰁 ___ in systolic HF.

EF ___ in diastolic HF.

A

↓

normal

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77
Q

Force of contraction is proportional to ___

A

preload

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78
Q

increase 􏰂contractility with ___

A
  • catecholamines

- positive inotropes (eg, digoxin)

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79
Q

decrease 􏰂contractility with ___

A
  • loss of myocardium (eg, MI)
  • β-blockers (acutely)
  • non-dihydropyridine Ca2+ channel blockers
  • dilated cardiomyopathy
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80
Q

ΔP =

A

Q × R

a change in pressure in a vessel is equal to flow times resistance

this is similar to Ohm’s law where a change in voltage is equal to current times resistance: ΔV = IR

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81
Q

Volumetric flow rate (Q) =

A

flow velocity (v) × cross-sectional area (A)

82
Q

Resistance

A

(driving pressure ΔP) / (flow Q) = 8η (viscosity) x length / (πr4)

83
Q

Total resistance of vessels in series:

A

RT = R1 + R2 + R3 . . .

84
Q

Total resistance of vessels in parallel:

A

1/RT = 1/R1 + 1/R2 + 1/R3

85
Q

Viscosity depends mostly on ____

A

hematocrit

86
Q

Viscosity􏰂 increases in ____ states (eg,

_____ ) and _____

A 
hyperproteinemic states (eg,
multiple myeloma)

polycythemia

87
Q

Viscosity decreases 􏰁in ____

A

anemia

88
Q

Removal of organs in parallel arrangement (eg, ____)􏰀􏰁 = ___TPR and􏰂 ___CO.

A

nephrectomy

↓ TPR

increase CO

89
Q

Pressure gradient drives flow from __ pressure to ___ pressure.

A

high

low

90
Q

____ account for most of TPR.

A

Arterioles

91
Q

___ provide most of blood storage capacity.

A

Veins

92
Q

Inotropy curve Effects

A

Changes in contractility􏰀 → altered CO for a given RA pressure (preload) or EDV.

93
Q

⊕ Intropy

A

Catecholamines

digoxin

94
Q

⊝ Intropy

A

Uncompensated HF

narcotic overdose

95
Q

Venous return curve Effects

A

Changes in circulating volume or venous tone → 􏰀altered RA pressure for a given CO.

Mean systemic pressure (x-intercept) changes with volume/venous tone.

96
Q

⊕ volume, venous tone

A

Fluid infusion, sympathetic activity

97
Q

⊝ volume, venous tone

A

Acute hemorrhage

spinal anesthesia

98
Q

Total peripheral resistance curve Effects

A

At a given mean systemic pressure (x-intercept) and RA pressure, changes in TPR􏰀 → altered CO.

99
Q

⊕ TPR

A

Vasopressors

100
Q

⊝ TPR

A

Exercise

AV shunt

101
Q

exercise: __ 􏰂inotropy and ___ 􏰁TPR to maximize ___

A

↑

↓

CO

102
Q

HF: ___ 􏰁inotropy → 􏰀fluid retention to __ preload to maintain ___

A

↓

↑

CO

103
Q

fetal erythropoiesis WK 3-10

A

yolk sac

104
Q

fetal erythropoiesis WK 6-birth

A

liver

105
Q

fetal erythropoiesis WK 15-30

A

spleen

106
Q

fetal erythropoiesis WK 22-adult

A

bone marrow

107
Q

fetal hemoglobin

A

A2Y2

108
Q

adult hemoglobin

A

A2B2

109
Q

truncal and bulbar ridges spiral and fuse to form

A

aorticopulmonary septum

110
Q

___ separates the ascending aorta and pulmonary trunk

A

aorticopulmonary septum

111
Q

aorticopulmonary septum formed from ___

A

cardiac neural crest

112
Q

notocord postanatal called ___

A

nucleus pulposus

113
Q

foramen ovale postnatal called ____

A

fossa ovalis

114
Q

period between mitral valve closing and aortic valve opening;

A

Isovolumetric contraction

115
Q

period between aortic valve opening and closing

A

Systolic ejection

116
Q

period between aortic valve closing and mitral valve opening

A

Isovolumetric relaxation

117
Q

period just after mitral valve opening

A

Rapid filling

118
Q

period just before mitral valve closing

A

Reduced filling

119
Q

period of highest O2 consumption

A

Isovolumetric contraction

120
Q

4 phases of cardiac cycle :

A
  1. Isovolumetric contraction
  2. Systolic ejection
  3. Isovolumetric relaxation
  4. Rapid filling
  5. Reduced filling
121
Q

mitral and tricuspid valve closure. heart sound?

A

S1

122
Q

S1 loudest at _____

A

mitral area

123
Q

S2 Loudest at ____

A

left upper sternal border.

124
Q

aortic and pulmonary valve closure. heart sound?

A

S2

125
Q

in early diastole during rapid ventricular

filling phase. heart sound?

A

S3

126
Q

heart sound associated with􏰂filling pressures (eg, mitral regurgitation, HF) and more common in dilated ventricles (but can be normal in children and young adults).

A

S3

127
Q

late diastole (“atrial kick”). heart sound?

A

S4

128
Q

heart sound best heard at apex with patient in left lateral decubitus position.

A

S4

129
Q

heart sound associated with ventricular noncompliance (eg, hypertrophy). Left atrium must push against stiff LV wall. Consider abnormal, regardless of patient age.

A

S4

130
Q

[JVP] a wave—

A

atrial contraction

131
Q

Absent in atrial fibrillation (AF). [JVP]

A

a wave

132
Q

c wave— [JVP]

A 
RV contraction (closed tricuspid valve
bulging into atrium).
133
Q

x descent— [JVP]

A

atrial relaxation and downward

displacement of closed tricuspid valve during ventricular contraction.

134
Q

Absent in tricuspid regurgitation. [JVP]

A

x descent

135
Q

Prominent in tricuspid insufficiency and right HF. [JVP]

A

x descent

136
Q

v wave— [JVP]

A

􏰂right atrial pressure due to filling (“villing”) against closed tricuspid valve.

137
Q

y descent— [JVP]

A

RA emptying into RV

138
Q

Prominent in constrictive pericarditis [JVP]

A

y descent

139
Q

absent in cardiac tamponade. [JVP]

A

y descent

140
Q

Continuous machine-like murmur. Loudest at S2. Often due to congenital rubella or prematurity.

A

Patent ductus arteriosus

141
Q

Best heard at left infraclavicular area.

A

Patent ductus arteriosus

142
Q

Holosystolic, harsh-sounding murmur. Loudest at tricuspid area.

A

Ventricular septal defect

143
Q

continuous heart murmur

A

Patent ductus arteriosus

144
Q

Diastolic heart murmurs:

A

Aortic regurgitation

Mitral stenosis

145
Q

Systolic Heart murmurs:

A

Aortic stenosis
Mitral/tricuspid regurgitation
Mitral valve prolapse
Ventricular septal defect

146
Q

Crescendo-decrescendo systolic ejection murmur

A

Aortic stenosis

147
Q

murmur Loudest at heart base; radiates to carotids.

A

Aortic stenosis

148
Q

murmur with “Pulsus parvus et tardus”—pulses are weak with a delayed peak.

A

Aortic stenosis

149
Q

murmur Can lead to Syncope, Angina, and Dyspnea on exertion (SAD).

A

Aortic stenosis

150
Q

Murmur most commonly due to age- related calcification in older patients (> 60 years old) or in younger patients with early-onset calcification of bicuspid aortic valve.

A

Aortic stenosis

151
Q

Holosystolic, high-pitched “blowing murmur.”

A

Mitral/tricuspid regurgitation

152
Q

murmur loudest at apex and radiates toward axilla.

A

Mitral regurgitation

153
Q

murmur is often due to ischemic heart disease (post-MI), MVP, LV dilatation.

A

Mitral regurgitation

154
Q

murmur loudest at tricuspid area and radiates to right sternal border

A

tricuspid regurgitation

155
Q

murmur commonly caused by RV dilatation.

A

tricuspid regurgitation

156
Q

Rheumatic fever and infective endocarditis can cause what murmurs?

A

Mitral regurgitation

tricuspid regurgitation

157
Q

Late systolic crescendo murmur with midsystolic click (MC; due to sudden tensing of chordae tendineae).

A

Mitral valve prolapse

158
Q

Murmur most frequent valvular lesion.

A

Mitral valve prolapse

159
Q

Murmur loudest just before S2. Usually benign.

A

Mitral valve prolapse

160
Q

Murmur best heard over apex.

A

Mitral valve prolapse

161
Q

murmur can predispose to infective endocarditis.

A

Mitral valve prolapse

162
Q

murmur can be caused by myxomatous degeneration (1° or 2° to connective tissue disease such as Marfan or Ehlers-Danlos syndrome), rheumatic fever, chordae rupture.

A

Mitral valve prolapse

163
Q

High-pitched “blowing” early diastolic decrescendo murmur. Long diastolic murmur, hyperdynamic pulse, and head bobbing when severe and chronic. Wide pulse pressure.

A

Aortic regurgitation

164
Q

murmur often due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever. Progresses to left HF.

A

Aortic regurgitation

165
Q

murmur follows opening snap (OS; due to abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips).

A

Mitral stenosis

166
Q

murmur with delayed rumbling late diastolic murmur (􏰁interval between S2 and OS correlates with􏰂severity). LA&raquo_space; LV pressure during diastole.

A

Mitral stenosis

167
Q

murmur often occurs 2° to rheumatic fever. Chronic MS can result in LA dilatation.

A

Mitral stenosis

168
Q

rapid upstroke and depolarization—voltage-gated Na+ channels open.

A

Myocardial action potential Phase 0

169
Q

initial repolarization—inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open.

A

Myocardial action potential Phase 1

170
Q

plateau—Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux. Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.

A

Myocardial action potential Phase 2

171
Q

rapid repolarization—massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels.

A

Myocardial action potential Phase 3

172
Q

resting potential—high K+ permeability through K+ channels.

A

Myocardial action potential Phase 4

173
Q

In contrast to skeletal muscle …Cardiac muscle: (3 differences)

A
  1. Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux. ƒ
  2. Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from
    sarcoplasmic reticulum (Ca2+-induced Ca2+ release).
    ƒ
  3. Cardiac myocytes are electrically coupled to each other by gap junctions.
174
Q

Occurs in the SA and AV nodes only

A

Pacemaker action potential

175
Q

upstroke—opening of voltage-gated Ca2+ channels. Fast voltage-gated Na+ channels are permanently inactivated because of the less negative resting potential of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles.

A

Phase 0

176
Q

what 2 phases are absent in Pacemaker action potential

A

Phases 1 and 2

177
Q

inactivation of the Ca2+ channels and􏰂activation of K+ channels􏰀􏰂K+ efflux.

A

Phase 3

178
Q

slow spontaneous diastolic depolarization due to If (“funny current”). If channels responsible for a slow, mixed Na+/K+ inward current; different from Ina in phase 0 of ventricular action potential. Accounts for automaticity of SA and AV nodes.

A

Phase 4

179
Q

The slope of phase 4 in the SA node determines

A

HR

180
Q

ACh/adenosine ___ 􏰁the rate of diastolic depolarization and􏰁 ___HR

A

↓

↓

181
Q

catecholamines􏰂 ___ depolarization and ___ 􏰂HR

A

↑

↑

182
Q

Conduction pathway

A

SA node → 􏰀atria→ 􏰀AV node→􏰀bundle of His→􏰀right and left bundle branches→􏰀Purkinje fibers→􏰀ventricles

183
Q

SA > AV > bundle of His/ Purkinje/ventricles.

A

Pacemaker rates

184
Q

Purkinje > atria > ventricles > AV node.

A

Speed of conduction

185
Q

Long QT interval predisposes to ____

A

torsades de pointes.

186
Q

Polymorphic ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG; can progress to ventricular fibrillation (VF)

A

torsades de pointes.

187
Q

Torsades de pointes caused by

A

drugs,􏰁

↓ K+

↓ 􏰁Mg2+

congenital abnormalities

188
Q

Torsades de pointes tx

A

magnesium sulfate

189
Q

Drug-induced long QT (ABCDE):

A

AntiArrhythmics (class IA, III)

AntiBiotics (eg, macrolides)

Anti“C”ychotics (eg, haloperidol)

AntiDepressants (eg, TCAs)

AntiEmetics (eg,ondansetron)

190
Q

Inherited disorder of myocardial repolarization, typically due to ion channel defects

A

Congenital long QT syndrome

191
Q

􏰂in Congenital long QT syndrome there is ↑ risk of ____ due to torsades de pointes.

A

sudden cardiac death (SCD)

192
Q

Congenital long QT syndrome 2 types:

A

Romano-Ward syndrome

Jervell and Lange-Nielsen syndrome

193
Q

Congenital long QT syndrome type that is “autosomal dominant, pure cardiac phenotype (no deafness).”

A

Romano-Ward syndrome

194
Q

Congenital long QT syndrome type that is “autosomal recessive, sensorineural deafness.”

A

Jervell and Lange-Nielsen syndrome

195
Q

Brugada syndrome genetically ___

A

Autosomal dominant disorder

196
Q

Brugada syndrome most common in ___

A

Asian males

197
Q

ECG pattern of pseudo-right bundle branch block and ST elevations in V1-V3.􏰂risk of ventricular tachyarrhythmias and SCD

A

Brugada syndrome

198
Q

Prevent SCD with ____

A

implantable cardioverter-defibrillator (ICD).

199
Q

Most common type of ventricular pre- excitation syndrome.

A

Wolff-Parkinson-White syndrome

200
Q

Wolff-Parkinson-White syndrome ECG findings:

A
  • characteristic delta wave
  • widened QRS complex
  • shortened PR interval
201
Q

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses the rate-slowing
AV node􏰀ventricles begin to partially depolarize earlier

A

Wolff-Parkinson-White syndrome

202
Q

Wolff-Parkinson-White syndrome- May result in reentry circuit… leading to ___

A

supraventricular tachycardia.

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