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Flashcards in Cardiology_1 Deck (351):
1

Truncus arteriosus gives rise to what?

ascending aorta and pulmonary trunk

2

bulbus cordis gives rise to what?

smooth parts (outflow tract) of left and right ventricles

3

primitive ventricle gives rise to what?

trabeculated left and right ventricles

4

primitive atria give rise to what?

trabeculated left and right atria

5

left horn of sinus venosus gives rise to what?

coronary sinus

6

right horn of SV gives rise to what?

smooth part of right atrium

7

right common cardinal vein and right anterior cardinal vein give rise to what?

SVC

8

what happens in the normal development of the truncus arteriosus?

neural crest migration → truncal and bulbar ridges that spiral and fuse to form the aorticopulmonary (AP) septum→ ascending aorta and pulmonary trunk

9

what are the truncus arteriosus pathologies?

1. TGA • 2. ToF • 3. TA

10

what is the defect in transposition of the great vessels?

failure to spiral

11

what is the TA defect in tetralogy of Fallot?

skewed AP septum development

12

what is the defect in persistent TA?

partial AP septum development

13

3 steps in embryologic formation of interventricular septum?

1. muscular ventricular septum forms- opening= interventricular foramen • 2. AP septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing interventricular foramen • 3. Growth of endocardial cushions separates atria from ventricles and contributes to both atrial separation and membranous portion of the interventricular septum

14

improper neural crest migration into the TA can result in what?

transposition of the great arteries or a persistent TA

15

in interventricular septum development, membranous septal defect causes what?

an initial left to right shunt, which later reverses to a right to left shunt due to onset of pulmonary hypertension (Eissenmenger's syndrome)

16

8 steps in interatrial septum development?

1. foramen primum narrows as septum primum grows toward endocardial cushions • 2. perforations in septum primum form foramen secundum (foramen primum disappears • 3. foramen scundum maintains right to left shunt as septum secundum begins to grow • 4. septum secundum contains a permanent opening (foramen ovale) • 5. foramen secundum enlarges and upper part of septum primum degenerates • 6. remaining portion of septum primum forms the valve of the foramen ovale • 7. septum secundum and septum primum fuse to form the atrial septum • 8. foramen ovale usually closes soon after birth because of ↑ LA pressure

17

what happens in pathology of interatrial septal development?

patent foramen ovale, caused by failure of the septum primum and septum secundum to fuse after birth

18

when is there fetal erythropoiesis in the yolk sac?

3-10wk

19

when is there fetal erythropoiesis in the liver?

6wk-birth

20

when is there fetal erythropoiesis in the spleen?

15-30wk

21

when is there fetal erythropoiesis in the bone marrow?

22wk-adult

22

mnemonic for fetal erythropoiesis?

young liver synthesizes blood

23

structure of HbF?

α2γ2

24

structure of HbA?

α2β2

25

O2 content of fetal blood in the umbilical vein?

PO2~30 • 80% saturated with O2

26

O2 sat of umbilican arteries?

low

27

sites of 3 important shunts of fetal circulation?

1. ductus venosus • 2. foramen ovale • 3. ductus arteriosus

28

action of shunt at ductus venosus in fetal circulation?

blood entering the fetus through the umbilical vein is coducted via the ductus venosus into the IVC to bypass the hepatic circulation

29

action of the shunt at the foramen ovale in fetal circulation?

most oxygenated blood reaching the heart via the IVC is diverted through the foramen ovale and pumped out the aorta to the head and body

30

action of the shunt at the ductus arteriosus in fetal circulation?

deoxygenated blood entering the RA from the SVC enters the RV, is expelled into the pulmonary artery, then passes through the ductus arteriosus into the descending aorta

31

what happens to fetal circulation at birth when the infant takes a breath?

↓ resistance in pulmonary vasculature causes ↑ LA pressure vs RA pressure→ • foramen ovale closes (now called fossa ovalis) → • ↑ in O2 leads to ↓ in prostaglandins, causing closure of ductus arteriosus

32

what helps close PDA?

indomethacin

33

what keeps PDA open?

PGE1, PGE2

34

post natal derivative of the umbilical vein?

ligamentum teres hepatis, contained in falciform ligament

35

postnatal derivatives of umbilical arteries?

medial umbilical ligaments

36

postnatal derivatives of ductus arteriosus?

ligamentum arteriosum

37

postnatal derivative of ductus venosus?

ligamentum venosum

38

postnatal derivative of foramen ovale?

fossa ovalis

39

postnatal derivative of allantois?

urachus-median umbilical ligament

40

what is the urachus part of?

the allantoic duct between the bladder and the umbilicus

41

what finding is a remnant of the urachus?

urachal cyst, or sinus

42

postnatal derivative of the notochord?

nucleus pulplosus of intervertebral disc

43

LCX supplies what?

lateral and posterior walls of left ventricle

44

LAD supplies what?

anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of left ventricle

45

PD supplies what?

posterior 1/3 of interventricular septum and posterior walls of ventricles

46

acute marignal artery supplies what?

right ventricle

47

SA and AV nodes are usually supplied by what?

RCA

48

frequency and features of right dominant coronary circulation?

85% • PD arises from RCA

49

frequency and features of left-dominant coronary circulation?

8% • PD arises from LCX

50

frequency and features of codominant circulation?

7% • PD arises from both LCX and RCA

51

coronary artery occlusion most commonly occurs where?

in LAD

52

when do coronary arteries fill?

during diastole

53

most posterior part of the heart is what?

LA

54

enlargement of LA can cause what?

dysphagia (due to compression of the esophagus) or hoarseness (due to compression of the left recurrent laryngeal nerve)

55

transesophageal echocardiography is useful for diagnosing what?

LA enlargement • aortic dissection • thoracic aortic aneurysm

56

equations for cardiac output?

CO= SV x HR • • Fick's: • CO= (rate of O2 consumption)/((arterial O2 content)- (venous O2 content))

57

equation for MAP?

MAP= CO x TPR • • MAP= 2/3 diastolic pressure + 1/3 systolic

58

pulse pressure=?

systolic pressure - diastolic pressure

59

pulse pressure is proportional to what?

stroke volume

60

equations for stroke volume?

SV = CO/HR = EDV - ESV

61

during the early stages of exercise CO is maintained by what?

↑ HR and ↑ SV

62

during the late stages of exercise, CO is maintained by what?

↑ HR only (SV plateaus)

63

what happens during exercise if HR is too high?

diastolic filling is incomplete and CO ↓

64

cardiac variables that affect stroke volume?

SV CAP • Stroke Volume affected by Contractility, Afterload, and Preload

65

↑ SV when what?

↑ preload, ↓ afterload, ↑ contractility

66

contractility (and SV) ↑ with what?

1. catecholamines • 2. ↑ intracellular Ca++ • 3. ↓ extracellular Na+ • 4. Digitalis

67

how do catecholamines ↑ contractility?

↑ activity of Ca++ pump in sarcoplasmic reticulum

68

how does a ↓ in extracellular Na+ ↑ contractility?

↓ activity of Na+/Ca++ exchanger

69

how does digitalis ↑ contractility?

blocks Na+/K+ pump → ↑ intracellular Na+ →↓ Na+/Ca++ exchanger activity → ↑ intracellular Ca++

70

contractility and SV ↓ with what?

1. β blockade • 2. heart failure (systolic dysfunction) • 3. acidosis • 4. hypoxia/hypercapnia (↓PO2/↑PCO2) • 5. Non-dihydropyridine Ca++ channel blockers

71

effect of anxiety, exercise, and pregnancy on SV?

72

myocardial O2 demand is ↑ by what?

↑ afterload (proportional to arterial pressure) • ↑ contractility • ↑ heart rate • ↑ heart size (↑wall tension)

73

preload = ?

ventricular EDV

74

afterload=?

MAP (proportional to peripheral resistance)

75

agents that ↓ preload?

vEnodilators (nitroglycerin)

76

agents that ↓ afterload?

vAsodilators (hydrAlazine)

77

preload ↑ with what?

1. exercise (slightly) • 2. ↑ blood volume (overtransfusion) • 3. excitement (↑ sympathetic activity)

78

on Starling curve, force of contraction is proportional to what?

end-diastolic length of cardiac muscle fiber (preload)

79

on Starling curve, what are the factors that increase contractility?

sympathetic stimulation • catecholamines • digoxin

80

on starling curve, which factors ↓ contractility?

loss of myocardium (MI) • β blockers • Ca++ channel blockers

81

equation for EF?

EF= SV/EDV = (EDV-ESV)/EDV

82

EF is an index of what?

ventricular contractility

83

normal EF?

>=55%

84

EF ↓ in what?

systolic heart failure

85

ΔP =?

Q x R

86

equation for resistance?

resistance = (driving pressure ΔP)/(Flow Q)= (8ηl)/πr^4

87

equation for total resistance of vessels in series?

0

88

1/Toral Resistance of vessels in parallel?

= 1/R1 + 1/R2 + 1/R3...

89

viscosity ↑ in what?

1. polycythemia • 2. hyperproteinemic states (multiple myeloma) • 3. hereditary spherocytosis

90

viscosity ↓ in what?

anemia

91

pressure gradient drives blood flow where?

from high pressure to low pressure

92

resistance is proportional to what?

viscosity and vessel length

93

viscosity is inversely proportional to what?

the radius to the 4th power

94

what accounts for most of total peripheral resistance?

arterioles

95

what vessels regulate capillary flow?

arterioles

96

where is the operating point of the heart on the cardiac and vascular function curve?

intersection where cardiac output and venous return are equal

97

what causes the operating point of the heart on the cardiac and vascular function curve to shift straight down?

↑ TPR, hemorrhage before compensation can occur

98

what causes the operating point of the heart on the cardiac an vascular function curve to shift straight up?

↓ TPR, exercise, AV shunt

99

what causes the operating point of the heart to shift downward and rightward along the venous return curve on the cardiac and vascular function curve?

heart failure • narcotic overdose

100

what causes an upward shift in the CO curve?

#NAME?

101

what causes a downward shift in the CO curve?

#NAME?

102

what causes a rightward shift in the venous return curve?

↑ blood volume

103

what causes a leftward shift in the venous return curve?

↓ blood volume

104

what is the X intercept of the venous return curve?

mean systemic filling pressure

105

what are the 5 phases of the left ventricle in the cardiac cycle?

1. isovolumetric contraction • 2. systolic ejection • 3. isovolumetric relaxation • 4. rapid filling • 5. reduced filling

106

what is isovolumetric contraction?

period between mitral valve closure and aortic valve opening

107

what is the period of highest O2 consumption during the cardiac cycle?

isovolumetric contraction

108

what is systolic ejection?

period between aortic valve opening and closing

109

what is isovolumetric relaxation?

period between aortic valve closing and mitral valve opening

110

what is rapid filling?

period just after mitral valve opening

111

what is reduced filling?

period just before mitral valve closure

112

what causes a rightward EDV expansion without an upward pressure expansion in the LV cardiac cycle P/V curve?

↑preload → ↑SV

113

what causes a leftward ESV expansion with an upward pressure expansion on a LV cardiac cycle P/V curve?

↑ contractility • ↑ SV • ↑ EF • ↓ ESV

114

what causes a leftward ESV contraction with an upward pressure expansion on a LV cardiac cycle P/V curve?

↑ afterload • ↑ aortic pressure • ↓ SV • ↑ ESV

115

what causes S1 sound?

mitral and tricuspid valve closure

116

S1 is loudest where?

at mitral area

117

what causes S2 sound?

aortic and pulmonary valve closure

118

where is S2 loudest?

at left sternal border

119

when is S3 heard?

in early diastole during rapid ventricular filling phase

120

S3 is associated with what?

↑ filling pressures (MR, CHF)

121

S3 is more common in which types of ventricles?

dilated ventricles, but normal in children and pregnant women

122

when do you hear S4?

atrial kick in late diastole

123

what causes S4?

high atrial pressure • LA must push against stiff LV wall

124

S4 associated with what?

ventricular hypertrophy

125

what does JVP a wave correspond to?

atrial contraction

126

what does the JVP c wave correspond to?

RV contraction (closed tricuspid valve bulging into atrium)

127

what does the JVP x descent correspond to?

atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

128

what does the JVP v wave correspond to?

↑ right atrial pressure due to filling against closed tricuspid valve

129

what does the JVP y descent correspond to?

blood flow from RA to RV

130

what happens in normal splitting?

inspiration → • drop in intrathoracic pressure → • ↑ venous return to the RV → • ↑ RV stroke volume → • ↑ RV ejection time → • delayed closure of the pulmonic valve

131

what else contributes to the delayed closure of the pulmonic valve in normal splitting?

↓ pulmonary impedance ( ↑ capacity of the pulmonary circulation)

132

what does normal splitting sound like?

A2 and P2 are close during expiration, • A2 and P2 are only slightly more separated during inspiration

133

wide splitting is seen in which conditions?

those that delay RV emptying (pulmonic stenosis, RBB block)

134

what happens in wide splitting?

delay in RV emptying causes delayed pulmonic sound (regardless of breath)

135

what does wide splitting sound like?

an exaggeration of normal splitting • Ex: A2 and P2 are split as wide as normal inspiration • Ins: A2 and P2 are split much wider than normal

136

fixed splitting is seen in what?

ASD

137

what happens in fixed splitting?

ASD → left to right shunt → ↑ RA and RV volumes → ↑ flow through pulmonic valve such that, regardless of breath, pulmonic closure is greatly delayed

138

paradoxical splitting is seen in what?

conditions that delay LV emptying (aortic stenosis, LBB block)

139

what happens in paradoxical splitting?

normal order of valve closure is reversed so that P2 sound occurs before A2.

140

what does paradoxical splitting sound like?

on inspiration, P2 closes later and moves closer to A2, thereby 'paradoxically' eliminating the split

141

what can cause a systolic murmur in the aortic area?

aortic stenosis • flow murmur • aortic valve sclerosis

142

where is the aortic auscultation area?

2nd intercostal space RSB

143

what causes a systolic ejection murmur in the pulmonic area?

pulmonic stenosis • flow murmur (ASD, PDA)

144

where is the pulmonic area for ausculation?

2nd interspace LSB

145

what causes a pansystolic murmur at the tricuspid area?

tricuspid regurgitation • ventricular septal defect

146

what causes diastolic murmur at the tricuspid area?

tricuspid stenosis • ASD

147

where is the tricuspid area for auscultation?

5th interspace LSB

148

what causes a systolic murmur in the mitral area?

mitral regurgitation

149

what causes a diastolic murmur in the mitral area?

mitral stenosis

150

where is the mitral area for auscultation?

5th interspace mid clavicular line

151

what causes diastolic murmur at the left sternal border?

aortic regurgitation • pulmonic regurgitation

152

what causes systolic murmur at left sternal border?

hypertrophic cardiomyopathy

153

what are the auscultation findings in ASD?

pulmonary flow murmur • diastolic rumble (tricuspid) • blood flow across the ASD doesn't cause a murmur because there is no pressure gradient • murmur → louder diastolic murmur of pulmonic regurgitation from dilation of pulmonary artery

154

the continuous, machine-like murmur of PDA is best appreciated where?

left infraclavicular region

155

what is the effect of inspiration on ausculation?

↑ intensity of right heart sounds

156

what is the effect of expiration on auscultation?

↑ intensity of left heart sounds

157

what is the effect of hand grip maneuver on auscultation (↑ systemic vascular resistance)?

↑ intensity of MR, AR, VSD, MVP murmurs • ↓ intensity of AS, hypertrophic cardiomyopathy murmurs

158

what is the effect of the vasalva maneuver (↓ venous return) on auscultation?

↓ intensity of most murmurs • ↑ intensity of MVP, hypertrophic cardiomyopathy murmurs

159

what is the effect of rapid squatting (↑ venous return, ↑ preload, ↑afterload with prolonged squatting)?

↓ intensity of MVP, hypertrophic cardiomyopathy murmurs

160

conditions associated with systolic heart sounds include what?

aortic/pulmonic stenosis • mitral/tricuspid regurgitation • VSD

161

conditons associated with diastolic heart sounds include what?

aortic/pulmonic regurgitation • mitral/tricuspid stenosis

162

what does mitral/tricuspid regurgitation sound like?

holosystolic, high-pitched "blowing murmur"

163

mitral regurgitation is loudest where?

at apex and radiates to toward axilla

164

mitral regurgitation sound is enhanced by what?

maneuvers that ↑ TPR (squatting, hand grip) or LA return (expiration)

165

MR is often due to what?

ischemic heart disease, mitral valve prolapse, LV dilation

166

where is tricuspid regurgitation loudest?

loudest at tricuspid area and radiates to right sternal border

167

tricuspid regurgitation sound enhanced by what?

maneuvers that ↑ RA return (inspiration)

168

TR can be caused by what?

RV dilation

169

rheumatic fever and infective endocarditis can cause which heart sounds?

MR or TR

170

what does Aortic stenosis sound like?

crescendo-decrescendo systolic ejection murmur following ejection click • radiates to carotids/heart base

171

what causes ejection click in aortic stenosis?

EC due to abrupt halting of valve leaflets

172

pressure gradient in aortic stenosis?

LV>> aortic pressure during systole

173

pulse findings in aortic stenosis?

pulsus parvus et tardus' • pulses are weak with a delayed peak

174

aortic stenosis can lead to what?

Syncope, Angina, Dyspnea on exertion (SAD)

175

aortic stenosis is due to what?

age related calcific aortic stenosis or bicuspid aortic valve

176

what does VSD sound like?

holosystolic, harsh sounding murmur

177

where is VSD loudest?

tricuspid area

178

VSD sound can be accentuated how?

hand grip maneuver due to increased afterload

179

what does MVP sound like?

late systolic crescendo murmur with midsystolic click

180

what causes MC?

sudden tensing of the chordae tendineae

181

what is the most frequent valvular lesion?

MVP

182

MVP is best heard where?

over apex

183

when is MVP loudest?

S2

184

severity of MVP?

usually benign

185

MVP can predispose to what?

infective endocarditis

186

MVP can be caused by what?

myxomatous degeneration • rheumatic fever • chordae rupture

187

MVP enhanced by what?

maneuvers that ↓ Venous return (standing or vasalva)

188

what does aortic regurgitation sound like?

immediate high pitched "blowing" diastolic decrescendo murmur

189

pulses in AR?

wide pulse pressure when chronic; can present with bounding pulses and head bobbing

190

AR is often due to what?

aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever

191

what ↑ murmur in AR?

hand grip

192

effect of vasodilators on AR?

↓ intensity of murmur

193

what does MS sound like?

follows opening snap • delayed rumbling late diastolic murmur

194

what causes OS in MS?

abrupt halt in leaflet motion in diastole, after rapid opening due to fusion at leaflet tips

195

pressure gradient in MS?

LA>>LV during diastole

196

MS often occurs secondary to what?

rheumatic fever

197

chronic MS can result in what?

LA dilation

198

MS sound is enhanced by what?

maneuvers that ↑ LA return (expiration)

199

what does PDA sound like?

continuous machine like murmur

200

when is PDA loudest?

S2

201

PDA is often due to what?

congenital rubella or prematurity

202

where is PDA best heard?

left infraclavicular area

203

ventricular action potential also occurs where?

in bundle of His and Purkinje fibers

204

what happens in Phase 0 of ventricular action potential?

rapid upstroke- voltage gated Na+ channels open

205

what happens in Phase 1 of ventricular action potential?

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

206

what happens in Phase 2 of ventricular action potential?

plateau-Ca++ influx through voltage gated Ca++ channels balances K+ efflux • Ca++ influx triggers Ca++ release from sarcoplasmic reticulum and myocyte contraction

207

what happens in phase 3 of ventricular action potential?

rapid repolarization= massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage gated Ca++ channels

208

what happens in phase 4 of the ventricular action potential?

resting potential- high K+ permeability through K+ channels

209

difference between cardiac muscle AP and skeletal muscle?

1. cardiac muscle AP has a plateau, which is due to Ca++ influx and K+ efflux, myocyte contraction occurs due to Ca++ induced Ca++ release from the sarcoplasmic reticulum • 2. cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to If channels • 3. Cardiac myocytes are electrically coupled to eachother by gap junctions

210

what do If chanels do?

funny current channels responsible for a slow, mixed Na+/K+ inward current

211

what is the direction of the leak currents in cardiac ventricular myocytes?

K+ out • Na+, Ca++ in

212

pacemaker action potential occurs where?

in the SA and AV nodes

213

what happens in phase 0 of the pacemaker action potential?

upstroke- opening of VG Ca++ channels • fast VG Na channels are permanently inactivated because of the less negative resting voltage of these cells

214

permanent fast VG Na channel inactivation in the pacemaker cells results in what?

slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles

215

what happens in Phase 2 or pacemaker potential?

plateau is absent

216

what happens in phase 3 of the pacemaker potential?

inactivation of the Ca++ channels and ↑ activation of K+ channels→ ↑ K+ efflux

217

what happens in phase 4 of the pacemaker potential?

slow diastolic depolarization- membrane potential spontaneously depolarizes as Na+ conductance ↑ (If different from Ina in phase 0 of ventricular action potential)

218

phase 4 of the pacemaker potential accounts for what?

automaticity of SA and AV nodes

219

slope of phase 4 in the SA node determines what?

HR

220

effect of ACh/adenosine on SA node?

↓ the rate of diastolic depolarization and ↓ HR

221

effect of catecholamines on SA node?

↑ depolarization and ↑ heart rate

222

effect of sympathetic stimulation on SA/AV node?

↑ the chance that If channels are open and thus ↑ HR

223

P wave corresponds to what?

atrial depolarization

224

atrial repolarization in ECG?

masked by QRS complex

225

PR interval corresponds to what?

conduction delay through AV node

226

normal PR interval?

<200 ms

227

QRS complex correspondes to what?

ventricular depolarization

228

normal duration of QRS complex?

<120s

229

QT interval corresponds to what?

mechanical contraction of the ventricles

230

T wave corresponds to what?

ventricular repolarization

231

T wave inversion may indicate what?

recent MI

232

ST segment corresponds to what?

isoelectric, ventricles depolarized

233

U wave is caused by what?

hypokalemia • bradycardia

234

relative speed of conduction in the heart?

purkinje > atria > ventricles > AV nodes

235

relative speed of conduction in the pacemaker cells?

SA node> AV> Bundle of his/purkinje/ventricles

236

what is the conduction pathway in the heart?

SA node → atria → AV node → common bundle→ bundle branches→ purkinje fibers→ ventricles

237

dominant pacemaker in heart?

SA node pacemaker inherent dominance with slow phase of the upstroke

238

what is the delay in the AV node?

100ms delay- atrioventricular delay; allows time for ventricular filling

239

what happens in torsades de pointes?

ventricular tachycardia, characterized by shifting sinusoidal waveforms on ECG, can progress to ventricular fibrillation

240

what predisposes to torsades de pointes?

anything that prolongs the QT interval

241

treatment for torsades de pointes?

magnesium sulfate

242

congenital long QT syndromes are most often due to what?

defects in cardiac sodium or potassium channels

243

what condition has long QT syndrome that presents with severe sensorineural deafness?

Jervell and Lange-Nielsen syndrome

244

how does atrial fibrillation look?

chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes

245

atrial fibrillation can result in what?

atrial stasis and lead to stroke

246

tx for atrial fibrillation?

rate control • anticoagulation • possible cardioversion

247

what does atrial flutter look like?

a rapid succession of identical, back-to-back atrial depolarization waves • 'saw tooth' appearance

248

pharmacologic conversion to sinus rhythm in atrial flutter?

Class IA, IC, or III antiarrhythmics

249

rate control in atrial flutter?

β-blocker or calcium channel blocker

250

what does ventricular fibrillation look like?

a completely erratic rhythm with no identifiable waves

251

severity of ventricular fibrillation?

fatal arrhythmia without immediate CPR and defibrillation

252

features of 1st degree AV block?

prolonged PR interval >200ms • asymptomatic

253

features of 2nd degree AV block Mobitz type I (Wenckebach)?

progressive lenghtening of the PR interval until a beat is dropped • usually asymptomatic

254

features of Mobitz type II?

dropped beats that are not preceded by a change in the length of the PR interval

255

severity of Mobitz type II?

these abrupt, nonconducted p waves result in a pathologic condition

256

mobitz type II is often found as what?

2:1 block, where there are >=2 p waves to 1 QRS

257

mobitz type II often treated with what?

pacemaker

258

mobitz type II may progress to what?

3rd degree block

259

what happens in 3rd degree (complete) heart block?

the atria and ventricles beat independently of each other • both p waves and QRS complexes are present, though P waves bear no relation to the QRS complexes

260

which rate is faster in 3rd degree heart block?

atrial rate is faster than ventricular rate

261

3rd degree heart block is usually treated with what?

a pacemaker

262

which disease can result in 3rd degree heart block?

Lyme disease

263

ANP is released from where?

atrial myocytes

264

ANP is released in response to what?

↑ blood volume and pressure

265

ANP causes what?

generalized vascular relaxation and ↓ Na+ reabsorption at the medullary collecting tubule

266

effect of ANP on renal blood flow?

constricts efferent renal arterioles and dilates afferent arterioles (cGMP mediated), promoting diuresis and contributing to the escape from aldosterone mechanism

267

aortic arch baroreceptors transmit info where?

via vagus nerve to solitary nucleus of medulla (responds only to ↑ BP)

268

carotid sinus baroreceptor transmits info where?

via glossopharyngeal nerve to solitary nucleus of medulla (responds to ↑ and ↓ in BP)

269

what happens at baroreceptors in response to hypotension?

↓ arterial pressure → • ↓ stretch → • ↓ afferent baroreceptor firing→ • ↑ efferent sympathetic firing and ↓ efferent parasympathetic stimulation → • vasoconstriction, ↑ HR, ↑ contractility, ↑ BP

270

baroreceptors are important in the response to what?

severe hemorrhage

271

effect of carotid massage on baroreceptors?

↑ pressure on carotid artery → ↑ stretch → ↑ afferent baroreceptor firing → ↓ HR

272

baroreceptors contribute to which reaction?

Cushing reaction

273

what happens in Cushing reaction?

triad of hypertension, bradycardia, and respiratory depression

274

mechanism of Cushing reaction?

↑ ICP constricts arterioles→ cerebral ischemia and reflex sympathetic increase in perfusion pressure (hypertension)→ ↑ stretch → reflex baroreceptor induced-bradycardia

275

what happens in stimulation of peripheral chemoreceptors?

carotid and aortic bodies are stimulated by ↓ PO2 (<60mmHg), ↑ PCO2, and ↓ pH of blood

276

what happens in stimulation of central chemoreceptors?

are stimulated by changes in pH and PCO2 of brain interstitial fluid, which in turn are influenced by arterial CO2

277

central chemoreceptors do not directly respond to what?

PO2

278

what is the organ with the largest blood flow?

Lung (100% of CO)

279

what is the organ with the largest share of systemic cardiac output?

liver

280

which organ has the highest blood flow per gram of tissue?

kidney

281

which organ has the largest arteriovenous O2 difference?

heart

282

why does heart have the largest arteriovenous O2 difference?

becuase O2 extraction is 80%

283

how is O2 demand met in heart?

↑ O2 demand is met by ↑ coronary blood flow, not by ↑ extraction of O2

284

what is the normal pressure in the RA?

<5

285

what is the normal pressure in the RV?

25-May

286

what is the normal pressure in the PA?

25-Oct

287

what is the normal pressure in the LA?

<12

288

what is the normal pressure in the LV?

130/10

289

what is the normal pressure in the aorta?

130/90

290

PCWP is a good approximation of what?

left atrial pressure

291

when is PCWP> LV diastolic pressure?

mitral stenosis

292

how is PCWP measured?

Swan Ganz catheter

293

what is autoregulation?

how blood flow to an organ remains constant over a wide range of perfusion pressures

294

what are the factors determining autoregulation in the heart?

Local metabolites (vasodilatory)-CO2, adenosine, NO

295

what are the factors determining autoregulation in the brain?

Local metabolites (vasodilatory)-CO2 (pH)

296

what are the factors determining autoregulation in the kidneys?

myogenic and tubuloglomerular feedback

297

what are the factors determining autoregulation in the lungs?

hypoxia causes vasoconstriction

298

what are the factors determining autoregulation in skeletal muscle?

local metabolites- lactate, adenosine, K+

299

what are the factors determining autoregulation in the skin?

sympathetic stimulation most important mechanism-temperature control

300

what determines fluid movement through capillary membranes?

starling forces

301

what are the 4 starling forces?

Pc • Pi • πc • πi

302

what is Pc?

capillary pressure- pushes fluid out of capillary

303

what is Pi?

interstitial fluid capillary- pushes fluid into capillary

304

what is πc?

plasma colloid osmotic pressure- pulls fluid into capillary

305

what is πi?

interstitial fluid colloid osmotic pressure-pulls fluid out of capillary

306

equation for net filtration pressure?

Pnet= [(Pc - Pi) - (πc - πi)]

307

what is Kf?

filtration constant (capillary permeability)

308

what is Jv?

net fluid flow= Kf x Pnet

309

what is edema?

excess fluid outflow into interstitium

310

edema is commonly caused by what?

↑ capillary pressure (heart failure) • ↓ plasma proteins (nephrotic syndrome, liver failure) • ↑ capillary permeability (toxins, infections, burns) • ↑ interstitial colloid osmotic pressure (lymphatic blockage)

311

what is the most common cause of early cyanosis?

Tetralogy of Fallot

312

which congenital heart diseases make up the right to left shunts (early cyanosis)-blue babies?

5T's • Tetralogy of Fallot • Transposition of the great vessels • persistent Truncus arteriosus • Tricuspid atresia • Total anomalous pulmonary venous return

313

features of Persistent Truncus Arteriosus?

failure of truncus arteriosus to divide into pulmonary trunk and aorta

314

most patients with persistent truncus arteriosus have what?

accompanying VSD

315

tricuspid atresia is characterized by what?

absence of tricuspid valve and hypoplastic RV

316

tricuspid atresia requires what for viability?

both ASD and VSD

317

what happens in TAPVR?

pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc)

318

TAPVR is associated with what?

ASD and sometimes PDA to allow for right to left shunting to maintain CO

319

which congenital heart abnormalities make up the left to right shunts (late cyanosis)-blue kids?

VSD • ASD • PDA

320

what is the most common congenital cardiac anomaly?

VSD

321

findings in ASD?

loud S1, wide, fixed split S2

322

what do you use to close PDA?

indomethacin

323

what is the frequency of the congenital left to right shunts?

VSD > ASD > PDA

324

what happens in Eisenmenger's syndrome?

uncorrected VSD, ASD, or PDA causes compensatory pulmonary vascular hypertrophy, which results in progressive pulmonary hypertension

325

what happens in Eisenmenger's syndrome as pulmonary resistance increases?

the shunt reverses from left to right to right to left, which causes late cyanosis, clubbing, and polycythemia

326

tetralogy of fallot is caused by what?

anterosuperior displacement of the infundibular septum

327

what is the mnemonic for the components of ToF?

PROVe • 1. Pulmonary infundibular stenosis • 2. RVH • 3. Overriding aorta (overrides the VSD) • 4. VSD

328

what is the most important determinant for prognosis in ToF?

pulmonary infundibular stenosis

329

in ToF early cyanosis (tet spells) caused by what?

a right to left shunt across the VSD

330

difference between isolated VSD and VSD in ToF?

isolated VSDs usually flow left to right (acyanotic) • in tetralogy, pulmonary stenosis forces right to left (cyanotic) flow and causes RVH

331

how does RVH in ToF look?

boot shaped heart on CXR

332

patients with ToF learn what compensatory mechanism?

squat to relieve cyanotic symptoms

333

why do patients with ToF squat?

reduces blood flow to the legs, ↑ PVR, and thus ↓ the cyanotic right to left shunt across the VSD

334

what is the preferred treatment for ToF?

early, primary surgical correction

335

what happens in transposition of great vessels?

aorta leaves RV (anterior) and pulmonary trunk leaves LV (posterior)→ separation of systemic and pulmonary circulations

336

transposition of the great vessels not compatible with life unless what?

a shunt is present to allow adequate mixing of blood (VSD, PDA, or patent foramen ovale)

337

transposition of great vessels is due to what?

failure of aorticopulmonary septum to spiral

338

prognosis of transposition of great vessels?

without surgical correction, most infants die within the first few months of life

339

coarctation of the aorta can result in what?

AR

340

what is infantile type of coarctation of the aorta?

aortic stenosis proximal to insertion of ductus arteriosus (preductal)

341

preductal coarctation of the aorta is associated with what?

Turner syndrome

342

what needs to be checked in infantile coarctation of the aorta?

check femoral pulses on physical exam

343

what is adult type coarctation of the aorta?

stenosis is distal to ligamentum arteriosum (postductal)

344

postductal coarctation of the aorta is associated with what?

notching of the ribs (due to collateral circulation), hypertension in upper extremities, weak pulses in lower extremities

345

postductal coarctation of the aorta is most commonly associated with what?

bicuspid aortic valve

346

what is going on in patent ductus arteriosus in the fetal period?

shunt is right to left (normal)

347

what happens to patent ductus arteriosus in the neonatal period?

lung resistance ↓ and shunt becomes left to right with subsequent RVH and/or LVH and failure (abnormal)

348

patent ductus arteriosus is associated with what finding?

continuous machine like murmur

349

in PDA, patency is maintained with what?

PGE synthesis and low O2 tension

350

uncorrected PDA can eventually result in what?

late cyanosis in the lower extremities (differential cyanosis)

351

when is PDA normal?

PDA is normal in utero and only closes after birth