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Flashcards in Cardiology Deck (620):
1

Romano-Ward syndrome

Q from the bond is a giant standing in the back/form of congenital long QT syndrome. Femdom chick whipping him/autosomal dominant. /pure cardiac phenotype (no deafness). Arthur spinning/can predispose to torsades de pointes, causing syncopal episodes + sudden cardiac death. /thought to result from mutations in a K= channel protein that contributes to the delayed rectifier current (Ik) of the cardiac action potential.

2

Jervell and Lange-Nielsen syndrome

Q from the bond is a giant /form of congenital long QT syndrome. Tyrion running down the hall/autosomal recessive. Nelson has big headphones on/sensorineural deafness. /common presentation = syncope in an otherwise healthy person. Arthur spinning/can predispose to torsades de pointes + sudden cardiac death. /thought to result from mutations in a K+ channel protein that contributes to the delayed rectifier current (Ik) of the cardiac action potential.

3

Brugada syndrome

Tuong: he’s being whipped by a FEMDOM/autosomal dominant disorder most common in Asian males. Huge bundle of sticks in the right corner + mountains on backwall with hat bone on left and hambone on right/ECG pattern of pseudo-right bundle branch block + ST elevations in V1-V3. Jonny kenser dead on the floor + /increased risk of ventricular tachyarrhythmias + SCD (sudden cardiac death). He has an implanted cardioverter-defibrillator/prevent SCD with implantable cardioverter-defibrillator (ICD).

4

Wolff-Parkinson-White syndrome

o Parker from woodlands. Electric shock to the chest and lightning bolt that has down wall and across floor and up to Parker/very common ventricular pre-excitation syndrome. Abnormally fast accessory conduction pathway from atria to ventricle bypasses the rate-slowing AV node ventricles begin to partially depolarize earlier. May result in reentry circuit SVT. Camouflaged delta commanders coming out of the ground that have suffered strokes and are slurring their words + a morbidly obese Q from James bond (QRS complex code) + a midget media crew shooting photos on left/ECG = characteristic delta wave, described as “slurred upstroke of the QRS complex” + widened QRS complex + shortened PR interval on ECF. Amy young riding her hippo is there + vera wing in the back + Aidan Melville juggling in front of door/treatment = amiodarone + adenosine + verapamil. Tigger firing rocket launcher at parker/digoxin is contraindicated (can enhance transmission of impulses through accessory pathways by reentry or possible triggered membrane activity) extremely fast ventricular rate OR Vfib.

5

Potassium channel problem in romano-ward

DELAYED rectifier potassium channel.

6

truncus arteriosus gives rise to...

ascending aorta + pulmonary trunk

7

bulbus cordis gives rise to

smooth parts (outflow tract) of left and right ventricles

8

endocardial cushions give rise to

1) atrial septum
2) membranous inter ventricular septum
3) AV and semilunar valves

9

AV valves

mitral and tricuspid

10

semilunar valves

aortic + pulmonary valves

11

Primitive atrium gives rise to...

Trabeculated part of left and right atria

12

Primitive ventricle gives rise to

trabeculated part of left and right ventricles

13

Primitive pulmonary vein gives rise to...

smooth part of left atrium

14

Left horn of sinus venosus gives rise to...

coronary sinus

15

Right horn of sinus venosus gives rise to...

Smooth part of right atrium (sinus venarum)

16

What is SVC derived from

right common cardinal vein + right anterior cardinal vein

17

When does cardiac looping begin?

Week 4

18

Dextrocardia etiology

Defect in left-right dynein (dynes are involved in L/R asymmetry)

19

PFO etiology

Failure of septum premum and septum secundum to fuse.

20

underlying etiology of paradoxical emboli

1) ASD
2) VSD
3) PFO

21

Separation of cardiac chambers

1) septum primum grows toward endocardial cushions, narrowing foramen primum.
2) Foramen secundum forms in septum premum (foramen premium disappears)
3) Septum secundum develops as foramen secundum maintains right-to-left shunt.
4) septum secundum expands and covers most of the foramen secundum. Residual foramen is foramen ovale.
5) Remaining portion of septum premum forms valve of foramen ovale.

22

Most common location of VSD

membranous septum

23

Ventricle formation/morphogenesis

1) Muscular inter ventricular septum forms. Opening is inter ventricular foramen
2) Aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous inter ventricular septum, closing inter ventricular foramen.
3) Growth of endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portion of interventricular septum.

24

Outflow tract formation

Neural crest and endocardial cell migrations lead to truncal and bulbar ridges that spiral and fuse to form aorticopulmonary septum. Lead to ascending aorta and pulmonary trunk.

25

Persistent truncus arteriosus etiology

Failed neural crest migration

26

Tetralogy of fallot etiology

failed neural crest migration

27

transposition of great vessels etiology

failed neural crest migration

28

aortic/pulmonary valve origin

derived from endocardial cushions of outflow tract.

29

Mitral/tricuspid origin

Derived from fused endocardial cushions of the AV canal.

30

PO2 of umbilical vein blood

30 mm HG

31

umbilical vein blood saturation

80%

32

Path of most highly oxygenated blood reaching heart...

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 body.

33

path of deoxygenated blood from the SVC

SVC --> RA --> RV --> main pulmonary artery --> PDA --> descending aorta.

34

closing of foramen ovale mechanism

Decreased resistance in pulmonary vasculature leads to increased left atrial pressure vs. right atrial pressure --> closes.

35

Closure of ductus mechanism

Increase in O2 + decrees in prostaglandins (from placental separation)

36

Remnant of ductus arteriosus

Ligamentum arteriosum

37

What can you use to maintain the PDA?

PGE1 + PGE2

38

Median umbilical ligament derived from...

urachus

39

Remnant of ductus venosus...

ligamentum venosum

40

Remnant of foramen ovale

Fossa ovalis

41

Remnant of notochord

nucleus pulposus

42

Medial umbilical ligaments derived from

umbilical arteries

43

remnant of umbilical vein

ligamentum teres hepatis (contained in falciform ligament)

44

What supplies the SA and AV nodes usually?

RCA

45

Which circulation type is more common

Right-dominant

46

When does coronary blood flow peak?

Early diastole

47

Most posterior part of the heart

Left atrium

48

Layers of pericardium (from outer to inner)

1) Fibrous pericardium
2) Parietal layer of serous pericardium
3) Visceral layer of serous pericardium

49

Where is the pericardial cavity?

Lies between parietal and visceral layers

50

How is CO maintained in early and late stages of exercise?

Early --> increased HR + SV
Late --> increased HR only (SV plateaus)

51

Examples of increased pulse pressure

1) hyperthyroidism
2) aortic regurgitation
3) aortic stiffening (isolated systolic hypertension in elderly)
4) OSA (due to increased sympathetic tone)
5) Exercise (transient)

52

Examples of decreased pulse pressure

1) aortic stenosis
2) cardiogenic shock
3) cardiac tamponade
4) advanced heart failure (HF)

53

Catecholamines and increased contractility mechanism

Inhibition of phospholamban leads to increased calcium entry into sarcoplasmic reticulum --> increased calcium induced calcium release.

54

What increases contractility?

1) catecholamines
2) increased intracellular calcium
3) decreased extracellular sodium (decreased activity of Na/Ca exchanger)
4) digitalis

55

digitalis mechanism

Blocks Na/K+ pump, leading to increased intracellular sodium, decreased Na/Ca exchanger activity, and increased intracellular calcium.

56

Causes of decreased contractility

1) Beta-blockade
2) HF with systolic dysfunction
3) acidosis
4) hypoxia/hypercapnia
5) non-dihydropyridine Ca2+ channel blockers

57

Wall tension (Laplace's law)

Wall tension = (pressure x radius)/(2 x wall thickness)

58

What approximates afterload?

MAP

59

Drugs that decrease both preload and after load...

ACE inhibitors and ARBs

60

Normal EF

greater than 55%

61

EF in systolic vs diastolic HF

Decreased in systolic HF, normal in diastolic HF

62

Other things that decrease contractility

1) Beta-blockers (acutely)
2) non-dihydropyridine Calcium channel blockers
3) narcotic overdose
4) uncompensated HF

63

Volumetric flow rate (Q)

Q = flow velocity (v) x cross-sectional area (A)

64

Total resistance of vessels in series

Rt = R1 + R2 + R3

65

What does viscosity depend on?

Primarily hematocrit

66

When is viscosity increased?

1) polycythemia
2) hyperproteinemic states (eg multiple myeloma)

67

Where is flow velocity lowest?

Capillaries

68

What is the effect of removing organs in parallel (eg nephrectomy)?

1) decreased TPR
2) increased CO

69

Factors that would cause a left shift in venous return graph

1) acute hemorrhage
2) spinal anesthesia

70

Exercise on cardiac function curve

1) increased inotropy
2) decreased TPR
*think about how this would affect graph

71

Compensated heart failure

Isotropy drops in order to maintain fluid retention and increase preload to maintain CO.

72

What will decrease TPR

1) exercise
2) AV shunt

73

vasopressor?

Antihypotensive meds. Anything that raises reduced blood pressure.

74

JVP: a wave

atrial contraction

75

JVP: c wave

RV contraction

76

JVP: x descent

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

77

Absent x was on JVP?

tricuspid regurgitation

78

Prominent x wave on JVP indicates...

1) Tricuspid insufficiency
2) right HF

79

V wave on JVP

Increased right atrial pressure due to filling against closed tricuspid valve.

80

Y descent on JVP?

RA emptying into RV

81

When is y descent prominent?

Constrictive pericarditis

82

When is y descent absent?

Cardiac tamponade

83

What is S1?

Mitral and tricuspid valve closure.

84

What is S2?

Aortic and pulmonary valve closure.

85

atrial kick?

S4

86

Isovolumetric contraction?

Period between mitral valve closing and aortic valve opening.

87

When is O2 consumption highest in cardiac cycle?

Isovolumetric contraction.

88

Systolic ejection on PV loop?

Period between aortic valve opening and closing.

89

Isovolumetric relaxation on PV loop?

Period between aortic valve closing and mitral opening.

90

Rapid filling on PV loop?

Period just after mitral valve opening.

91

Reduced filling on PV loop?

Period just before mitral valve closing

92

How will increased contractility affect PV loop?

FA 270

93

How will increased afterload affect PV loop?

FA 270

94

How will increased preload affect PV loop?

FA 270

95

What causes normal splitting?

Inspiration --> drop in intrathoracic pressure --> increased venous return --> increased RV filling --> increased RV stroke volume --> increased RV ejection time --> delayed closure of pulmonic valve.

96

pulmonary impedance?

capacity of the pulmonary circulation

97

When is wide splitting seen?

Conditions that delay RV emptying.

98

What does wide splitting indicate?

Delayed pulmonic, as seen in...
1) pulmonic stenosis
2) right bundle branch block

99

Why does fixed splitting occur in ASDs?

Delay in pulmonic closure due to increased flow through pulmonic valve due to left-to-right shunt.

100

When does paradoxical splitting occur?

Conditions that delay aortic valve closure.

101

Conditions in which paradoxical splitting is seen...

1) aortic stenosis
2) left bundle branch block

102

What is paradoxical splitting?

Normal order of valve closure is reversed so that P2 sound occurs before delayed A2 sound. Therefore in inspiration, P2 closes later and moves closer to A2, thereby "paradoxically" eliminating the split.

103

VSD -- systolic or diastolic?

systolic (holosystolic)

104

ASD -- systolic or diastolic?

diastolic

105

Where are ASD's best auscultated?

tricuspid area

106

Where are VSD's best auscultated?

tricuspid area

107

holosystolic murmurs...

1) Tricuspid regurgitation
2) VSDs
3) mitral regurgitation

108

Affect of hand grip?

Increase afterload

109

What will hand grip increase intensity of?

1) MR + AR + VSD murmurs

110

diastolic heart sounds

1) aortic/pulmonic regurgitation
2) mitral/tricuspid stenosis

111

Affect of increased after load on MVP?

Later onset of click/murmur

112

What will hand grip decrease intensity of?

hypertrophic cardiomyopathy

113

Affect of Phase II valsalva?

Decreased preload

114

What will valsava decrease intensity of?

Most murmurs (including AS)

115

Affect of valsalva on MVP?

Earlier onset of click/murmur.

116

What will valsava increase intensity of?

hypertrophic cardiomyopathy

117

Affect of rapid squatting?

1) increased venous return
2) increased preload
3) increased afterload

118

Affect of squatting on HOCM?

decrease intensity

119

Affect of squatting on AS?

increase intensity

120

Affect of squatting on MVP?

Later onset of click/murmur

121

AS radiation

Loudest at base; radiates to carotids.

122

"Pulses parvus et tardus"

Pulses are weak with a delayed peak.

123

AS presentation

syncope + angina + dyspnea on exertion

124

Murmur radiating to right sternal border

tricuspid regurg

125

Rheumatic fever caveat

Can cause either MR or TR

126

MVP murmur

Late systolic crescendo murmur with mid systolic click

127

What is mid systolic click due to

Sudden tensing of chordae tendinae.

128

Most frequent valvular lesion?

MVP

129

MVP best location for auscultation?

Apex

130

When is MVP loudest?

Just before S2.

131

Some causes of MVP

1) Marfan's
2) Ehlers-Dalos
3) rheumatic fever
4) chordae rupture

132

When are PDAs loudest?

S2

133

Most common causes of PDAs

1) congenital rubella
2) prematurity

134

Where are PDAs best heard?

Left infraclavicular area

135

aortic regurg murmur description

High-pitched blowing early diastolic decrescendo murmur.

136

aortic regurg characteristics

1) long diastolic murmur
2) hyperdynamic pulse
3) head bobbing when severe or chronic
4) wide pulse pressure

137

Aortic regurg causes

1) aortic root dilation
2) bicuspid aortic valve
3) endocarditis
4) RF

138

What causes opening snap in mitral stenosis?

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

139

What correlates with severity in mitral stenosis?

Decreased interval between S2 and OS.

140

Sequela of chronic mitral stenosis

LA dilatation

141

What underlies phase 1 in myocardial action potential?

1) inactivation of voltage-gated Na channels
2) voltage-gated K+ channels begin to open.

142

What underlies phase 2 in myocardial action potential?

Plateau..
1) Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflux.
2) Ca2+ influx triggers Ca2+ release from sarcoplasmic reticulum and myocyte contraction.

143

What underlies phase 3 in myocardial action potential?

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

144

What underlies phase 4 in myocardial action potential?

Resting potential--high K+ permeability through K+ channels.

145

What are the differences between myocardial action potential and skeletal muscle action potential?

1) Cardiac muscle action potential has a plateau, which is due to Ca2+ influx and K+ efflux.
2) Cardiac muscle contraction requires Ca2+ influx from ECF to induce Ca2+ release from sarcoplasmic reticulum (Ca2+ induced Ca2+ release).
3) electrical coupling with gap junctions.

146

Phases of pacemaker action potential...

Phase 0, phase 3, phase 4.
*NO phase 1 or 2.

147

What underlies phase 0 in pacemaker action potential?

Upstroke--opening of voltage-gated Ca2+ channels. Results in a slow conduction velocity that is used by the AV node to prolong transmission.

148

What underlies phase 3 in pacemaker action potential?

Inactivation of Ca2+ channels + increased activation of K+ channels leading to potassium efflux.

149

What underlies phase 4 in pacemaker action potential?

Slow spontaneous diastolic depolarization due to If (funny current).

150

If channels (funny current)

Slow, mixed Na/K inward current

151

What accounts for automacity of SA and AV nodes?

If channels (funny current)

152

What determines heart rate?

Slope of phase 4 in SA node.

153

Affect of adenosine on pacemaker action potential?

Decreases the rate of diastolic depolarization and decreases HR.

154

How does sympathetic stimulation increase HR?

Increases the chance that If channels are open and thus increases HR.

155

Conduction pathway in heart

SA node --> atria --> AV node --> bundle of His --> right and left bundle branches --> Purkinje fibers --> ventricles.

156

Why is the SA node the dominant pacemaker?

slow phase of upstroke

157

AV node location

Posteroinferior part of intertribal septum.

158

Pacemaker rates

SA, AV, bundle of His/Purkinje/ventricles

159

Speed of conduction

Purkinje, atria, ventricles, AV node

160

PR interval

Time from start of atrial depolarization to start of ventricular depolarization

161

Normal PR interval

Less than 200 msec

162

Normal QRS

less than 120 msec

163

What does QT interval represent?

ventricular depolarization + mechanical contraction of the ventricles + ventricular depolarization.

164

What does T wave represent?

Ventricular repolarization

165

What does a T-wave inversion indicate?

Recent MI.

166

What is the J point?

Junction between end of QRS complex and start of ST segment.

167

What does the ST segment represent?

Isoelectric period in which ventricles are depolarized.

168

When is a U wave prominent?

1) hypokalemia
2) bradycardia

169

treatment for torsades de pointes?

magnesium sulfate

170

What causes torsades de pointes?

1) long QT syndromes
2) drugs
3) hypokalemia
4) hypomagnesemia

171

Drugs causing torsades de pointes?

1) antiarrhythmics (class IA, III)
2) macrolides
3) haloperidol
4) TCAs
5) ondansetron

172

Wolff-Parkinson-White syndrome etiology

Abnormal fast accessory conduction pathway from atria to ventricle (bundle of Kent) bypasses rate-slowing AV node. This causes ventricles to depolarize early.

173

What is a delta wave?

shortened PR interval (due to early depolarization)

174

Wolff-Parkinson-White sequela

Reentry circuit leading to SVT.

175

Most common RF's for afib

1) HTN
2) CAD

176

definitive treatment for atrial flutter

catheter ablation

177

1st degree AV block

Prolonged PR interval. Benign and asymptomatic condition that doesn't require treatment.

178

Mobitz type I (wenckebach)

Type of 2nd degree heart block. Progressive lengthening of PR interval until a beat is "dropped" (a P wave not followed by a QRS complex). Variable RR interval with a pattern (regularly irregular)

179

Mobitz type I prognosis

usually asymptomatic

180

Mobitz type II

Form of second degree that block. Dropped beats that aren't preceded by a change in length of PR interval.

181

Mobitz type II sequela

Can progress to 3rd degree block.

182

Mobitz type II management

Often treated with a pacemaker.

183

3rd degree heart block pathophys

atria and ventricles beat independently of each other.

184

3rd degree heart block on ECG

P waves and QRS complexes not rhythmically associated.

185

3rd degree heart block management

pacemaker

186

ANP effects

1) vasodilation
2) decreased Na+ reabsorption at *collecting tubule
3) dilates afferent arterioles + constricts efferent arterioles, promoting diuresis and contributing to aldosterone escape.

187

Difference between ANP and BNP?

BNP has a longer half-life.

188

nesiritide

recombinant BNP

189

Diagnostic relevance of BNP?

Blood test used for diagnosing HF (very good negative predictive value)

190

aortic chemoreceptor pathway

Transmits via vagus nerve to solitary nucleus of medulla.

191

Carotid sinus pathway

Transmits via glossopharyngeal nerve to solitary nucleus of medulla.

192

Carotid massage mechanism

Increased pressure on carotid sinus leads to increased stretch --> increased afferent baroreceptor firing --> increased AV node refractory period --> decreased HR.

193

Cushing reaction setting

Triad of HTN + bradycardia + respiratory depression

194

Cushing reaction pathophys

Increased ICP constricts arterioles leading to cerebral ischemia leading to increased PCO2 and decreased pH --> central reflex sympathetic increase in perfusion pressure (HTN) --> increased stretch --> increased peripheral reflex baroreceptor-induced bradycardia.

Better explanation:
With increased ICP, cushing reflex increases MAP in an attempt to restore cerebral perfusion pressure. Bradycardia occurs because baroreceptors in the carotid and aortic arch don't know what's going on in brain and just ease hypertension.

195

What triggers peripheral chemoreceptors?

1) decreased Po2
2) increased PCO2
3) decreased pH

196

What triggers central chemoreceptors?

Changes in pH and pCO2 of brain interstitial fluid (which are influenced by arterial CO2).

197

How do you determine mitral stenosis from cardiac pressures?

PCWP greater than LV EDV.

198

Normal cardiac pressures

FA 280

199

cardiac pressures from codebook

o Code: covered in ivy/right atrium = 0,8. Covered in hair + nails pounded in everywhere/right ventricle = 4,25. Nails + big hoops/pulmonary artery = 9,25. Hens + walls made out of tin cans/left atrium = 2,12. Hoops on walls + mice drinking mimosas/left ventricle = 9,130. Mice drinking mimosas + carrying briefcases/aorta = 70,130. Wedge of tissue sitting in middle of road covered in tin cans/wedge pressure = 12 (remember that wedge pressure is an indication of left atrial pressure).
o Location: Intersection of montview and colorado

200

what determines auto regulation in the heart?

Local vasodilatory metabolites: adenosine, NO, CO2, decreased O2.

201

What determines auto regulation in the brain?

CO2 (pH)

202

What determines auto regulation in the kidney?

Myogenic + tubuloglomerular feedback

203

Tubuloglomerular feedback

just macula dense and RAAS mechanism

204

myogenic mechanism

reflex vasoconstriction that occurs when perfusion pressure increases

205

what determines skeletal muscle regulation with exercise?

local metabolites: lactate, adenosine, K+, H+, CO2

206

what determines skeletal muscle regulation at rest?

sympathetic tone

207

what determines auto regulation in the skin?

sympathetic stimulation most impt

208

Thing to remember about about capillary oncotic pressure

Pushes fluid into capillary.

209

Why does lymphatic blockage cause edema?

Increased interstitial fluid colloid osmotic pressure because proteins aren't drained into lymphatics

210

Managing early cyanosis

urgent surgery + maintain PDA

211

congenital heart diseases presenting with early cyanosis

5 Ts:
Truncus arteriosus
Transposition
Tricuspid atresia
Tetralogy of ballot
TAPVR

212

Persistent truncus arteriosus etiology

Truncus fails to divide into pulmonary trunk and aorta due to lack of aorticopulmonary septum formation; most patients have accompanying VSD.

213

Etiology of transposition of great vessels

Failure of aorticopulmonary septum to spiral.

214

hypoplastic RV in cyanotic newborn suggests...

tricuspid atresia

215

TOF etiology

anterosuperior displacement of the infundibular septum.

216

shunt in TOF

Pulmonary stenosis forces right-to-left flow across VSD leading to RVH

217

What are "tet spells"

characteristic of TOF. exacerbation of RV outflow obstruction.

218

Why does squatting help TOF patients?

Increased SVR, decreased right to left shunt, improves cyanosis.

219

TAPVR mechanism

Pulmonary veins drain into right heart circulation.

220

Epstein anomaly associations

Tricuspid regurgitation + right HF.

221

Relative frequency of ASD, PDA, VSD

VSD, ASD, PDA

222

difference in presentation between right-to-left and left-to-right shunts?

Right-to-Left shunts: eaRLy cyanosis.
Left-to-Right shunts: "LateR" cyanosis.

223

Most common congenital cardiac defect

VSD

224

How does VSD present in terms of O2 saturation?

Increased in RV and pulmonary artery.

225

More common defect in ASD

Ostium secundum defects most common.

226

Difference between ASD and PFO

In ASDs, septa are missing tissue rather than unfused.

227

Increased O2 sat in RA, RV, and pulmonary artery?

ASD

228

What happens to PDA in neonatal period?

With decreased pulmonary vascular resistance, shunt becomes left to right, leading to progressive RVH and/or LVH and HF.

229

Eisenmenger mechanism

Uncorrected left-to-right shunt (VSD, ASD, PDA) leads to increased pulmonary blood flow --> pathologic remodeling of vasculature --> increased pulmonary arterial HTN and compensatory RVH --> shunt switches to become right to left.

230

Eisenmenger presentation

Late cyanosis + clubbing + polycythemia.

231

aortic coarctation associations

1) bicuspid aortic valve
2) congenital heart defects
3) Turner syndrome

232

Complications of aortic coarctation...

1) HF
2) Increased risk of cerebral hemorrhage (berry aneurysm)
3) aortic rupture
4) endocarditis.

233

fetal alcohol syndrome congenital cardiac defect associations

ASDs, VSDs, PDA, TOF

234

congenital rubella congenital cardiac defect associations

1) PDA
2) pulmonary artery stenosis
3) septal defects

235

Infant of diabetic mother: congenital cardiac defect associations

transposition of great vessels

236

Marfan syndrome: congenital cardiac defect associations

1) MVP
2) aortic regurgitation
3) thoracic aortic aneurysm and dissection

237

Williams syndrome: congenital cardiac defect associations

supravalvular aortic stenosis

238

22q11 syndromes: congenital cardiac defect associations

1) truncus arteriosus
2) TOF

239

HTN ethnic incidence

AA, caucasian, asian

240

HTN definition

persistent systolic greater than 140 and/or diastolic greater than 90

241

most hypertension is primary (essential) and due to..

Increased CO or increased TPR

242

Classic radiologic finding in FMD

"string of beads" appearance of arteries

243

hypertensive urgency

severe (greater than 180 or greater than 120) HTN without acute end-organ damage.

244

Hypertensive emergency

Severe HTN with evidence of acute end-organ damage (eg encephalopathy, stroke, retinal hemorrhages and exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia).

245

Post-MI murmur?

Probably mitral regurg due to papillary muscle rupture.

246

Note -- don't assume VSD with holosystolic murmur.

OK

247

Flow rate expressed in...

L/min

248

calculation note: DO NOT forgot to convert units

OK.

249

Cubic centimeter in liter

1000 cubic cm = 1 liter

250

Pericarditis presentation

Sharp pain aggravated by inspiration + relieved by sitting up and leaning forward.

251

Characteristic physical exam finding in pericarditis

Friction rub (described as harsh as scratchy sound present in both systole and diastole)

252

Pericarditis associations

1) Idiopathic (presumed viral)
2) coxsackievirus
3) neoplasia
4) SLE
5) arthritis
6) uremia
7) cardiovascular (acute STEMI or Dressler syndrome)
8) radiation therapy

253

Hagemann factor Function

part of intrinsic pathway, activates kallikrein.

254

Important complication of horseshoe kidney

Variant arterial supply. Anomalous origins of multiple renal arteries to each kidney.

255

What do xanthomas consist of ?

lipid-laden histiocytes

256

xanthelaasma?

xanthomas in the eyelids

257

corneal arcus

Lipid deposits in cornea. Looks like ring around eye. Don't confuse with Kaiser-Fleischer rings.

258

Arteriosclerosis finding in essential HTN

Hyaline arteriolosclerosis

259

Diabetes mellitus arteriosclerosis finding

hyaline arteriolosclerosis

260

Severe HTN arteriosclerosis finding and etiology

Hyperplastic arteriosclerosis (onion skinning with proliferation of smooth muscle cells).

261

Monckeberg description

medial calcific sclerosis

262

Classic radiologic finding of Monckeberg's

pipestem appearance.

263

Monckeberg etiology

Calcification of internal elastic lamina and media. ***no intimal involvement.

264

atherosclerosis epidemiology location

abdominal aorta, coronary artery, popliteal, carotid

265

nonmodifiable RF's for atherosclerosis

1) Age
2) Sex
3) Family history

266

Sex at increased risk for atherosclerosis?

Increased in men + postmenopausal women

267

claudication is a sign of...

atherosclerosis.

268

atherosclerosis pathogenesis.

Inflammation impt. endothelial cell dysfunction --> macrophage and LDL accumulation --> foam cell formation --> fatty streaks --> smooth muscle cell migration, proliferation, and ECM deposition --> fibrous plaque --> complex atheroma.

269

What causes smooth muscle cell migration in atheroma formation?

PDGF and FGF

270

If someone has abdominal and/or back pain and a bulge/aneurysm what does this indicate?

Aneurysm is leaking, dissected, or rupture is imminent.

271

AAA RF's

1) tobacco use
2) increased age
3) male sex
4) family history

272

RF's for thoracic aortic aneurysms

1) HTN
2) bicuspid aortic valve
3) connective tissue disease (Marfan's)

273

abdominal vs thoracic aneurysms?

Abdominal associated with atherosclerosis, thoracic associated with HTN and cystic medial degeneration.

274

Aneurysm type in tertiary syphilis?

thoracic aortic aneurysm

275

cystic medial degeneration?

Degenerative breakdown of collagen, elastin, and smooth muscle.

276

Where does traumatic aortic rupture most commonly occur?

Aortic isthmus

277

What is the aortic isthmus?

Proximal descending aorta just distal to origin of left subclavian

278

Aortic dissection associations

1) HTN
2) **bicuspid aortic valve
3) inherited connective tissue disorders

279

Markedly unequal BP in arms suggests....

Aortic dissection

280

CXR finding of aortic dissection

Mediastinal widening.

281

Aortic dissection:
Stanford type A

Proximal aortic dissection; involves Ascending aorta. May extend to aortic arch or descending aorta.

282

Stanford type A treatment

surgery

283

Stanford type A complications

Acute aortic regurgitation or cardiac tamponade

284

Stanford type B aortic dissection

Distal. Involves descending aorta and/or aortic arch.

285

Stanford type B aortic dissection management.

B-blockers then vasodilators.

286

Angina caveat

No myocyte necrosis.

287

Stable angina on ECG

ST depression

288

Variant (prinzmetal) angina triggers

1) tobacco
2) cocaine
3) triptans

289

variant angina treatment

1) Ca2+ channel blockers
2) nitrates
3) smoking cessation

290

unstable angina pathophys

Thrombosis with incomplete coronary artery occlusion.

291

Unstable angina on ECG + markers

+/- ST depression and/or T wave inversion buT NO cardiac biomarker elevation.

292

How do you distinguish NSTEMI from unstable angina?

biomarker elevation with NSTEMI, none with unstable.

293

difference in presentation from stable and unstable angina

Stable usually exertion chest pain; unstable is either increase in frequency or intensity of pain or pain at rest.

294

coronary steal syndrome pathophy

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators dilates normal vessels and shunts blood toward well-perfused areas leading to decreased flow and ischemia in poststenotic region.

295

regadenoson

vasodilator

296

dipyridamole use and MOA

1) vasodilator, inhibits clot formation
2) phosphodiesterase inhibitor

297

SCD definition

death from cardiac causes within 1 hour of onset

298

large majority of cases of SCD are caused by...

CAD

299

What is chronic ischemic heart disease?

Progressive onset of HF over many years due to chronic ischemic myocardial damage.

300

STEMI pathophys

Transmural infarct. Full thickness of myocardial wall involved.

301

STEMI on ECG

ST elevation + Q waves

302

NSTEMI pathophys

subendocardial infarcts

303

commonly occluded coronary arteries

LAD, RCA, circumflex

304

finding I don't often think of with MI's

Pain in left arm and/or jaw

305

0-24 MI timeframe light microscopy

1) Early coagulative necrosis
2) release of necrotic cell contents into blood
3) edema, hemorrhage, wavy fibers.
4) neutrophils appear

306

0-24 MI etiology

Repercussion injury, associated with generation of free radicals, leads to hyper contraction of myofibrils through increased free calcium influx.

307

0-24 hr timeframe complications

1) ventricular arrhythmias
2) HF
3) cardiogenic shock

308

1-3 day timeframe complication

Postinfarction fibrinous pericarditis.

309

macroscopic appearance of heart in 1-3 day timeframe

hyperemia

310

hyperemia

increased blood flow to different tissues in body

311

1-3 day microscope chagnes

1) coagulative necrosis
2) *tissue surrounding infarct shows acute inflammation + neutrophils.

312

3-14 day macroscopic appearance

- hyperemic border; central yellow-born softening.
- maximally yellow and soft by 10 days.

313

Papillary muscle rupture leads to...

mitral regurgitation

314

morphologic appearance 2 weeks to several months

- Reanalyzed artery.
- Gray-white appearance

315

True vs false ventricular aneurysms

True occur later (after 2 weeks), false in 3-14 day timeframe.

316

complication of true ventricular aneurysm

Mural thrombus.

317

MI diagnosis and timeframe

- In the first 6 hours, ECG is the gold standard.
- Biomarkers afterward.

318

Troponin timeframe

1) Rises after 4 hours
2) Peaks at 24 hours
3) elevated for 7--10 days

319

CK-MB timeframe

1) Rises after 6-12 hours
2) Peaks at 16-24 hours
3) Returns to baseline at 48 hours

320

CK-MB downfall and use

It's also found in skeletal muscle so not as specific, but good at diagnosing reinfarction since levels fall earlier.

321

hyperacute T waves

peak T-waves

322

Other ECG findings related to MI's

1) hyper acute T waves
2) T-wave inversion
3) new left bundle branch block
4) pathologic Q waves
5) poor R wave progression

323

What does poor R wave progression on ECG indicate?

evolving or old transmural infarct. R wave should become progressively taller, but remains low.

324

Anteroseptal leads

V1-V2

325

Anteroapical leads

V3-V4

326

Anterolateral leads

V5-V6

327

Lateral leads

I, aVL

328

What leads will be elated with an anteroseptal (LAD) infarct?

V1-V2

329

What leads will be elated with an anteroseptal (distal LAD) infarct?

V3-V4

330

What leads will be elated with an anterolateral (LAD or LCX) infarct?

V5-V6

331

What leads will be elevated with a lateral (LCX) infarct?

I, aVL

332

What leads will be elated with an inferior (RCA) infarct?

II, III, aVF

333

What leads will be elated with a posterior (PDA) infarct?

V7-V9, ST depression in V1-V3 with tall R waves

334

tall R waves suggests..

posterior infarct

335

most impt complication within first 24 hours post-MI?

arrhythmia

336

What does a friction rub post MI indicate?

post infarction fibrinous pericarditis

337

Where is papillary muscle rupture most likely to occur and why?

Posteromedially, due to single blood supply from PDA.

338

When do inter ventricular septal ruptures occur?

3-5 days post MI

339

What mediates interventricualr septal ruptures?

Macrophages

340

Complications of ventricular pseudoaneurysms...

1) decreased CO
2) increased risk of arrhythmia
3) embolus from mural thrombus

341

sequela of free wall rupture

cardiac tamponade

342

How do true ventricular aneurysms present?

Outward bulge with contraction ("dyskinesia") associated with fibrosis.

343

Sign of LV infarction?

pulmonary edema

344

Sign of papillary muscle rupture?

mitral regurg leading to pulmonary edema

345

Unstable angina/NSTEMI management

1) heparin for anticoagulation
2) anti platelet therapy (aspirin + clopidogrel)
3) beta-blocker
4) ACE inhibitor
5) statins

346

clopidogrel mechanism

ADP receptor inhibitor

347

How do you control symptoms with unstable angina/NSTEMI?

Nitroglycerin + morphine.

348

STEMI management?

Same as NSTEMI but you need repercussion therapy with PCI (preferred over fibrinolysis).

349

Most common cardiomyopathy?

Dilated cardiomyopathy

350

Common dilated cardiomyopathy etiologies

1) chronic alcohol abuse
2) wet beriberi
3) coxsackie B
4) chronic cocaine use
5) Chagas disease
6) doxorubicin
7) hemochromatosis
8) sarcoidosis
9) peripartum cardiomyopathy

351

Murmur with dilated cardiomyopathy?

Systolic regurgitant murmur.

352

hypertrophy associated with dilated cardiomyopathy?

Eccentric hypertrophy.

353

Dilated cardiomyopathy treatment?

1) Na restriction
2) ACE inhibitors
3) beta-blockers
4) diuretics
5) digoxin
6) ICD
7) heart transplant

354

Eccentric hypertrophy etiology

sarcomeres added in series.

355

Concentric hypertrophy?

There's no overall enlargement of ventricle. The walls are thickened.

356

concentric hypertrophy associations

Volume overload, such as which HTN or aortic stenosis.

357

Auscultation findings in HOCM

1) S4
2) systolic murmur
3) Mitral regurg possible due to impaired mitral valve closure.

358

HOCM management

1) no high intensity sports
2) b-blocker or non-dihydropyridine Ca-blocker (verapamil)
3) ICD if high risk

359

HOCM macroscopic findings

myofibrillar disarray + fibrosis

360

Obstructive HOCM

subtype of HOCM characterized by asymmetric septal hypertrophy + systolic anterior motion of mitral valve, leading to outflow obstruction, dyspnea and possible syncope

361

infiltrative cardiomyopathy?

restrictive cardiomyopathy

362

What are some major causes of restrictive cardiomyopathy?

1) sarcoidosis
2) amyloidosis
3) postradiation fibrosis
4) endocardial fibroelastosis
5) Loffler syndrome
6) hemochromatosis

363

endocardial fibroelastosis?

thick fibroelastic tissue in endocardium of young children.

364

Loftier syndrome

Endomyocardial fibrosis with a prominent eosinophilic infiltrate.

365

ECG and restrictive cardiomyopathy

Low-voltage ECG

366

rales?

another name for crackles

367

systolic dysfunction characteristics

Reduced EF + increased EDV + decreased contractility

368

Diastolic dysfunction characteristics

Preserved EF + *normal EDV + decreased compliance (secondary to myocardial hypertrophy)

369

Most common cause of right HF

Left HF

370

cor pumonale

Isolated right HF due to pulmonary cause

371

Drug contraindicated in acute decompensated HF?

beta-blockers

372

What decreases mortality with heart failure?

1) ACEIs
2) ARBs
3) beta-blockers (except in acute decompensated)

373

What drugs improve both symptoms in mortality in HF patients?

Hydralazine with nitrate therapy.

374

Orthopnea etiology?

Increased venous return from redistribution of blood (gravity effect)

375

paroxysmal nocturnal dyspnea etiology

same as orthopnea, increased venous return from redistribution of blood

376

Rare complication of hepatomegaly?

cardiac cirrhosis

377

Causes of hypovolemic shock?

1) hemorrhage
2) dehydration
3) *burns

378

Obstructive shock

reduced CO due to cardiac tamponade or PE

379

Distributive shock and causes

Inadequate organ perfusion due to...
1) sepsis
2) anaphylaxis
3) CNS injury

380

Skin findings that distinguish distributive vs. other types of shock

Distributive shock presents with warm or dry skin. Other forms of shock present with cold, clammy skin.

381

Hypovolemic shock treatment

IV fluids

382

Cariogenic shock treatment

Inotropes + diuresis

383

Obstructive shock treatment?

Relieve obstruction

384

Sepsis, anaphylaxis, CNS injury shock treatment?

IV fluids + pressors

385

hypovolemic shock
1) PCWP
2) CO
3) SVR

1) very reduced. Remember - this is preload
2) reduced.
3) Increased. this is afterload

386

PCWP importance

= preload

387

obstructive shock
1) PCWP
2) CO
3) SVR

1) increased
2) decreased a lot
3) increased

388

SVR significance

afterload

389

cardiogenic shock
1) PCWP
2) CO
3) SVR

1) increased
2) decreased a lot
3) increased

390

Sepsis, anaphylaxis..
1) PCWP
2) CO
3) SVR

1) decreased
2) increased
3) severely decreased

391

Shock related to CNS injury..
1) PCWP
2) CO
3) SVR

1) decreased
2)**decreased
3) severely decreased

392

Skin findings with shock related to CNS injury

dry

393

Skin findings with shock related to sepsis, anaphylaxis...

warm

394

Roth spots description

Round white spots on retina surrounded by hemorrhage

395

osler nodes description

tender raised lesson on finger or toe pads

396

Janeway lesions description

Small, painless, erythematous lesions on palm or sole

397

caveat about bacterial endocarditis

You need multiple blood cultures for diagnosis.

398

vegetations in acute vs subacute endocarditis

With acute you get large vegetation on previously normal valves, with subacute you get smaller vegetations on congenitally abnormal or diseased valves.

399

Causes of nonbacterial endocarditis?

1) malignancy
2) hyper coagulable state
3) lupus

400

bugs causing tricuspid valve endocarditis

1) S aureus
2) pseudomonas
3) candida

401

bugs causing culture negative endocarditis

1) Coxiella brunette
2) bartonella
3) HACEK bugs

402

HACEK bugs

Haemophilus
Aggregatibacter (formerly actinobacillus)
Cardiobacterium
Eikenella
Kingella

403

Valves affected in RF in order

mitral then aortic then tricuspid (high-pressure valves affected most)

404

Anitschkow cells

Rheumatic fever

405

Anitschkow cell description

enlarged macrophages with ovoid, wavy, rod-like nucleus

406

rheumatic fever pathophys

Type II hypersensitivity. Antibodies to M protein cross-react with self antigens (molecular mimicry)

407

Rheumatic fever treatment

penicillin

408

joint presentation of rheumatic fever

migratory polyarthritis

409

common complication of acute pericarditis

Pericardial effusion

410

physical exam finding for pericarditis

friction rub

411

ECG for pericarditis

Widespread ST-segment elevation and/or PR depression

412

Causes of acute pericarditis

1) idiopathic (presumed viral)
2) coxsackie
3) neoplasia
4) SLE
5) RA
6) uremia
7) acute STEMI
8) dressler
9) radiation therapy

413

what happens to pressure in cardiac chambers with tamponade?

Equilibration of pressure in all 4 chambers.

414

ECG in tamponade

low-voltage QRS + electrical alternans

415

what is pulsus paradoxus?

Decrease in amplitude of systolic BP by greater than 10 mm Hg during inspiration.

416

Pulsus paradoxes seen in..

1) cardiac tamponade
2) asthma
3) OSA
4) pericarditis
5) croup

417

Most common heart tumor...

metastasis

418

What is kussmaul sign?

Increase in JVP on inspiration instead of a normal decrease.

419

JVD pathophys

inspiration --> negative intrathoracic pressure not transmitted to heart --> impaired filling of right ventricle --> blood backs up into venae cavae

420

Kussmaul sign + elevated JVP associations

1) constrictive pericarditis
2) restrictive cardiomyopathies
3) right atrial or ventricular tumors

421

Pathophys of eye injury with GCA

Ophthalmic artery can become occluded

422

What arteries are most commonly affected by GCA?

Branches of carotid

423

Takayasu affects..

Large-vessels: aortic arch and proximal great vessels

424

Takayasu presentatoin

1) "pulseless disease" (weak upper extremity pulses)
2) fever + night sweats + arthritis + myalgias + skin nodules + ocular disturbances

425

Takayasu treatment

corticosteroids

426

polyarteritis nodosa classic demographic

young adults

427

PAN presentation

Fever + weight loss + malaise + headache + abdominal pain + melon.
HTN + neurologic dysfunction + cutaneous eruptions + renal damage.

428

what arteries are usually involved in PAN?

Renal and visceral vessels, NOT pulmonary arteries.

429

Hypersensitivity type in PAN?

immune complex mediated

430

PAN treatment

1) corticosteroids
2) cyclophosphamide

431

Impt findings in PAN

1) transmural inflammation with fibrinoid necrosis
2) different stages of inflammation coexisting in different vessels
3) innumerable renal micro aneurysms and spasms on arteriogram.

432

Other name for Kawasaki

mucocutaneous lymph node syndrome

433

kawasaki presentation

conjunctival injection + rash (desquamating) + cervical adenopathy + strawberry tongue + hand foot changes + fever

434

strawberry tongue medical term

oral mucositis

435

Kawasaki treatment

IVIG + aspirin

436

Other name for Buerger's...

Thromboangiitis obliterans

437

other impt finding in Buerger's...

superficial nodular phlebitis

438

Wegener's upper respiratory presentation

1) perforated nasal septum
2) chronic sinusitis
3) otitis media
4) mastoiditis

439

mastoiditis

mastoid sits behind the ear (battle sign)

440

renal presentation of Wegener's

hematuria + red cell casts

441

wegener's triad

focal necrotizing vasculitis + necrotizing granulomas in lung and upper airway + necrotizing glomerulonephritis.

442

other term for c-ANCA

anti-proteinase 3

443

CXR in wegener's

large nodular densities

444

Wegener's treatment

Cyclophosphamide + corticosteroids

445

microscopic polyangiitis presentation

Necrotizing vasculitis commonly involved lung + kidneys + skin with pauci-immune glomerulonephritis and palpable purpura.

446

How do you differentiate microscopic polyangiitis from wagerer's?

in microscopic polyangiitsis, there's no nasopharyngeal involvement + no granulomas.

447

other name for p-ANCA

anti-myeloperoxidase

448

microscopic polyangiits treatment

cyclophosphamide + corticosteroids

449

Churn-Strauss presentation

asthma + sinusitis + skin nodules or purpura + peripheral neuropathy. Can involve heart, GI, kidneys.

450

churg-strauss path

Granulomatous, necrotizing vasculitis with eosinophilia.

451

Labs in churg-strauss

1) *increased IgE
2) MPO-ANCA/p-ANCA

452

HSP pathophys

IgA immune complex deposition

453

Essential HTN management

1) thiazides
2) ACEIs/ARBs
3) *dihydropyridine Ca2+ channel blockers

454

HTN with heart failure management

1) diuretics
2) ACEI's/ARBs
3) b-blockers (compensated) (to prevent cardiac remodeling)
4) aldosterone antagonists (to prevent from being fluid overloaded)

455

HTN with DM management

1) ACE/ARBs (both are protective against diabetic nephropathy)
2) Ca2+ channel blockers
3) thiazides
4) beta-blockers

456

Drugs for HTN in pregnancy?

1) hydrazine
2) labetalol
3) methyldopa
4) nifedipine

457

dihydropyridines vs nondihydropyridines

dihyropyridines act on vascular smooth muscle, non-dihydropyridines act on heart

458

dihydropyridines

all the -pines

459

non-dihydropyridines

dilimiazem + verapamil

460

Ca-channel blocker mechanism

Block voltage-dependent *L-type calcium channels of cardiac and smooth muscle leading to decreased contractility.

461

order of action of calcium channel blockers on vascular smooth muscle

Amlodipine + nifedipine, then diltiazem, then verapamil

462

order of efficacy of calcium channel blockers on heart

verapamil, diltiazem, amlodipine = nifedipine (verapamil for ventricle)

463

dihydropyridine you can't use for HTN, angina, or Raynaud's

nimodipine

464

clevidipine clinal use?

hypertensive urgency or emergency.

465

other use for non-dihydropyridines

afib/ a flutter

466

AE's of non-dihydropyridines

cardiac depression + AV block + hyperprolactinemia + constipation

467

AE's of dihydropyridines

peripheral edema + flushing + dizziness + gingival hyperplasia

468

hydrazine mechanism

increases cGMP leading to smooth muscle relaxation. Vasodilates arterioles more so than veins, leading to after load reduction.

469

when is hydralazine contraindicated?

angina/CAD (due to compensatory tachycardia)

470

hydralazine AE's

fluid retention + headache + angina + lupus-like syndrome

471

hypertensive emergency drugs

1) clevidipine
2) fenoldopam
3) labetalol
4) nicardipine
5) nitroprusside

472

Nitroprusside MOA

short acting, increases cGMP via direct release of NO.

473

Nitroprusside AE

can cause cyanide toxicity (releases cyanide)

474

Fenoldopam MOA

Dopamine D1 receptor agonist-- coronary, peripheral, renal, and splanchnic vasodilation. Decreases BP, increases natriuresis

475

What drug is commonly used postop for anti hypertension?

fenoldopam

476

Fenoldopam SE's

hypotension + tachycardia

477

nitrates effect on veins or arteries?

Dilate veins more than arteries, thus DECREASING preload

478

other use for nitrates

pulmonary edema

479

nitrates AE's

reflex tachycardia + hypotension + flushing + headache.

480

Describe Monday disease

exposure to nitrates leads to development of tolerance for the vasodilating action during the work week and loss of tolerance over the weekend. So they show up to work and become tachy, dizzy, and have a headache upon exposure.

481

MVO2

myocardial oxygen consumption

482

What beta-agonists are contraindicated in angina?

pindolol and acebutolol

483

pindolol MOA

partial B-antagonist (Only partial among nonselective)

484

B-blocker effect on EDV?

no effect or increased

485

Nitrate effect on ejection time?

decrease

486

Beta-blocker effect on ejection time?

Increase

487

Combined effect of nitrates + beta-blockers on
1) EDV
2) BP
3) contractility
4) HR
5) ejection time
6) MVO2

1) no effect or decreased
2) decreased
3) little/no effect
4) no effect or decreased
5) little/no effect
6) decreased significantly

488

**Ranolazine MOA

Inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption. *No affect on HR or contractility.

489

What is ranolazine used for?

angina refractory to other medical therapies

490

Ranolazine AE's

constipation + dizziness + headache + nausea + QT prolongation

491

Statin mechanism

HMG-CoA reductase inhibitors: inhibit conversion of HMG-CoA to mevalonate

492

Mevalonate

precursor to cholesterol

493

when is myopathy a concern with statins?

When used with fibrates or niacin.

494

Name bile acid resin drugs

1) cholestyramine
2) colestipol
3) colesevelam

495

Bile acid resins affect on...
1) LDL
2) HDL
3) triglycerides

1) decrease (2 arrows)
2) slight increase
3) slight increase

496

Bile acid AE's

1) GI upset
2) decrease absorption of other drugs and fat-soluble vitamins

497

Ezetimibe MOA

Prevents cholesterol absorption at small intestine brush border.

498

1) LDL
2) HDL
3) triglycerides

1) decrease (2 arrows)
2) null
3) null

499

Ezetimibe AE's

rare hepatoxicity + diarrhea

500

Fibrate affect on...
1) LDL
2) HDL
3) triglycerides

1) decrease
2) increase
3) major decrease

501

fibrate mechanism

1) up regulate LPL leading to increased TG clearance
2) activates PPAR-alpha to induce HDL synthesis

502

Vibrate AE

myopathy + cholesterol gallstones

503

Niacin affects on...
1) LDL
2) HDL
3) triglycerides

1) significant decrease (2 arrows)
2) significant increase
3) decrease

504

Niacin mechanism as a lipid lowering agent

1) Inhibits lipolysis (HSL) in adipose tissue. Thus this prevents FFA from getting into the bloodstream and uptake into liver where cholesterol synthesis occurs.
2) reduces hepatic VLDL synthesis

505

Other niacin AE's

hyperglycemia + hyperuricemia

506

Cholesterol synthesis pathway

Acetyl CoA --> HMG-CoA --> mevalonate --> cholesterol

507

digoxin affect on vagus nerve

Stimulates vagus nerve leading to decreased HR.

508

Factors predisposing to digoxin toxicity

1) renal failure
2) hypokalemia (this leads to increase binding at K+ binding site on ATPase because there's less potassium).
3) decreased clearance with verapamil, amiodarone, and quinidine

509

Management of digoxin toxicity

1) Slowly normalize K+
2) cardiac pacer
3) anti-dig FAB
4) Mg2+

510

Class IA antiarrhytmics

Quinine + procainamide + disopyramide

511

Class IA affects

1) Increased AP duration
2) increase effective refractory period
3) increase QT interval

512

When are class IA's used?

atrial and ventricular arrhythmias

513

Treatment for re-entrant and ectopic SVT and VT?

Class IA's

514

cinchonism

headache + tinnitus with quinidine

515

disopyramide AE

HF

516

Other 1A SE's

thrombocytopenia + torsades de pointes

517

1B drugs

Lidocaine + mexiletine + (phenytoin)

518

1B affects on action potential

Decrease AP duration.

519

1B MOA

Preferentially affect ischemic or depolarized Purkinje and ventricular tissue.

520

Best anti-arrhythmic post-MI?

IB's (IB is Best post MI)

521

Arrhythmias for digitalis induced?

1B's (lidocaine or mexiletine)

522

1B AE's

CNS stimulation/depression + cardiovascular depression

523

IC drugs

fleicanide + propafenone

524

IC mechanism

Significantly prolong ERP in AV node and accessory bypass tracts. No effect on ERP in purkinje and ventricular tissue.
- No affect on AP duration.

525

antiarrhythmics contraindicated post-MI?

IC (IC Contraindicated post MI)

526

antiarrhythmics contraindicated in structural and ischemic heart disease?

IC (IC contraindicated)

527

beta-blocker mechanism

Decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents.

528

How do beta-blockers suppress abnormal pacemakers?

Decreasing slope of phase 4.

529

esmolol caveat

very short acting

530

Why is PR interval increased with beta-blockers?

AV node particularly sensitive

531

metoprolol other AE

dyslipidemia

532

propranolol other AE

Can exacerbate vasospasm in prinzmetal angina

533

carvedilol and labetalol MOA

nonselective alpha and b-antagonists

534

Problem with giving b-blockers for cocaine toxicity or pheochromocytoma?

Cause unopposed alpha1 agonism if given alone.

535

Beta-Blocker overdose management

saline + atropine + glucagon

536

Class III antiarrhytmics mechanism

Increase AP duration + increase ERP + increase QT interval

537

Class IIIs used for V tach

amiodarone + sotalol

538

antiarrhythmics for afib

Anything except 1B or 1C

539

Sotalol AE's

torsades de pointes + excessive betablockade

540

Ibutilide AE's

torsades de pointes

541

amiodarone AE's

1) PF
2) hepatotoxic
3) hypothyroidism
4) *hyperthyroidism (amiodarone is 40% iodine by weight)
5) corneal deposits + blue/gray skin deposits resulting in photo dermatitis
6) neurologic effects
7) constipation
8) bradycardia + heart block + HF

542

What will class III look like on action potential graph?

markedly prolonged repolraization

543

Why does amiodarone cause corneal deposits and skin deposits?

Acts as a happen.

544

Caveat about amiodarone

Lipophilic and has class I, II, III, and IV effects.

545

Class IV mechanism

Decreased conduction velocity + increased ERP + increased PR interval

546

What do you use for rate control in fib?

Class IV channel blockers

547

Which anti arrhythmic can depress the sinus node?

class IV - verapamil, diltiazem.

548

adenosine

Moves K+ out of cells leading to hyper polarization of cell and decreased caclium

549

Drug of choice in diagnosing/terminating certain forms of SVT?

adenosine (very short acting)

550

Adenosine contraindications

theophylline + caffeine will blunt effects because both are adenosine receptor antagonists

551

Adenosine AE's

flushing + hypotension + chest pain + sense of impending doom + bronchospasm

552

What do you use to treat torsades de points?

Mg2+

553

Displaced PMI indicates...

cardiomegaly

554

Mixed osteolytic and blastic lesions

1) gastric
2) breast

555

acute decompensated heart failure

Decompensation of chronic stable heart failure. Eg from illness, MI, abnormal rhythm, uncontrolled HTN, or increased fluids.

556

Where do internal thoracics come off of?

subclavian

557

Pathophys of rib notching

with increased flow through the internal thoracic-anterior intercostal arterial system, retrograde flow through the posterior intercostal arteries develops, providing oxygenated blood to the descending aorta distal to the coarctation. /this is what causes rib notching (increased flow through the intercostals enlarges the arteries resulting in resorption of bone along the lower borders of the ribs.

558

murmur in aortic coarctation

harsh systolic ejection murmur.

559

carotid occlusion

procedure in which occlusion of the carotid results in less stretch of the carotid baroreceptors and less afferent nerve activity. Basically tricks body into thinking it has a lower blood pressure than it actually has. /thus, a baroreceptor reflex is elicited, leading to an increase in sympathetic tone increasing mean blood pressure + HR.

560

What happens to preload when CO decreases?

Increases because blood is redistributed to the veins. Blood flow ceases, and then flows from high pressure arterial system to low pressure venous system.

561

MCFP

mean circulatory filling pressure. Equilibrated pressure when pressure is equal throughout CV system.

562

Mean systemic filling pressure (MSFP)

Measure of volume of blood and compliance of vessels.

563

Relation of venous compliance to preload

Decreased compliance = increased preload.

564

Bainbridge reflex

Increase in HR due to increase in CVP.
Increased blood volume --> increased volume sensed by baroreceptors --> B-fibers reflex with heart affecting sympathetic and parasympathetic pathways --> increased HR.

565

Auto regulation of blood flow in heart?

ATP consumption increases with increased work --> increased adenosine --> vasodilation --> increased oxygen delivery.

566

What happens to arterial PO2 and arterial O2 sat at high elevation?

Low. Even with acclimatization since these are independent of hematocrit. Just depend on O2 availability.

567

Changes with acclimatization...

1) arterial PO2 and O2 sat stay low
2) systemic arterial O2 content increases to normal
3) pH normal (increased ventilation)

568

acute changes to altitude

decreased PAO2 and PaO2 + decreased PACO2 and PaCO2 + increased systemic arterial pH + decreased Hb% sat + decreased systemic arterial O2.

569

What happens to compliance and CVP with exercise?

Increased sympathetic activity causes venous smooth muscle constriction --> decreased compliance --> increased CVP --> increases CO

570

adenosine half-life

minutes

571

TPR and CO changes with dynamic, endurance exercise?

Increased CO + decreased TPR due to metabolic vasodilation.

572

static exercise changes in...
1) blood flow
2) MAP
3) ATP/ADP ratio

Contraction of skeletal muscles compress blood vessels and decreases blood flow. This increases vascular resistance + profound increase of MAP.
3) decreased.

573

What happens to blood flow with dynamic exercise?

Increased blood flow due to metabolic vasodilation of arterioles due to local vasodilator actions.

574

PV loop changes with LV dilation

Only slightly increased EDP (compliance increases but not a significant change in pressure).

575

Hypertonic contraction

Loss of hypotonic fluid

576

Hypertonic expansion

Excessive intake of sodium chloride.

577

Approach to Darrow Yannett diagrams

Just draw cell and think about osmolar effect.

578

Causes of isotonic fluid loss

1) hemorrhaging
2) diarrhea
3) vomiting

579

Affect of isotonic fluid loss on:
1) osmolarity
2) ICF volume
3) ECF volume

1) no change
2) no change (no force pushing fluid out of cell)
3) decreased

580

Causes of hypotonic fluid loss:

1) dehydration
2) DI
3) alcoholism

581

Affect of hypotonic fluid loss on:
1) osmolarity
2) ICF volume
3) ECF volume

1) Increased
2) decreased
3) decreased

582

Affect of isotonic fluid gain on:
1) osmolarity
2) ICF volume
3) ECF volume

1) no change
2) no change
3) increased

583

Causes of hypotonic fluid gain

1) hypotonic saline
2) water intoxication

584

Affect of hypotonic fluid gain on:
1) osmolarity
2) ICF volume
3) ECF volume

1) decreased
2) increased
3) increased

585

Premature contraction of the ventricle (PVC) on ECG

no P wave

586

Premature contraction of the ventricle (PVC)

presentation = either asymptomatic or palpitations or syncopale episodes. /can present after MIs in which tissue damage in ventricular tissue produces ectopic (non-SA node) sites of electrical activation. When these sites depolarize the ventricles contract independently and generate premature and abnormal QRS patterns seen on ECG.

587

afib on ECG

absent P waves + irregularly irregular QRS

588

premortem thrombi (lines of zahn) suggests...

afib prior to death

589

treatment of choice for V tach?

amiodarone

590

AV fistula
1) presentation
2) scenario
3) findings

1) coldness of extremity (due to lack of arterial flow)
2) post surgery
3) palpable thrill over area of wound. Continuous murmur. Diminished pulse. Doppler showing turbulence.

591

Nutmeg appearance of heart may also indicate...

right heart failure

592

Adult pressures in the cardiac chambers (minimum, maximum)

Code: covered in ivy/right atrium = 0,8. Covered in hair + nails pounded in everywhere/right ventricle = 4,25. Nails + big hoops/pulmonary artery = 9,25. Hens + walls made out of tin cans/left atrium = 2,12. Hoops on walls + mice drinking mimosas/left ventricle = 9,130. Mice drinking mimosas + carrying briefcases/aorta = 70,130. Wedge of tissue sitting in middle of road covered in tin cans/wedge pressure = 12

593

Common treatment for bradycardia?

atropine (decreases vagal influence on the SA and AV nodes).

594

valsalva maneuver pathophys

pathophys: pressure increase in chest forces blood out of pulmonary circulation into left atrium. ALSO return of systemic blood to the heart is impeded by increased pressure in chest. /effect = decreases preload + decreases afterload

595

What signifies the development of a complicated atheromatous plaque?

Calcification

596

"foci of calcification"

atherosclerotic plaque

597

ruptured free wall presentation

profound hypotension + dyspnea + muffled hear sounds and elevated JVP.

598

What does coronary sinus dilation often suggest

pulmonary hypertension.

599

bronchiolitis obliterans

lymphocytic inflammation and necrosis of bronchiolar walls, leading to scarring and progressive obliteration of small airway lumens.

600

SERCA proteins

Sarcoplasmic reticulum Ca ATPase. Pump Ca, and thus a net positive charge out of the cytosol into the sarcoplasmic reticulum (thus sequester Calcium)

601

sarcoplasmic reticulum

stores calcium

602

Ryanodine receptor functions

Mediates calcium-induced calcium release

603

When does ischemic injury become irreversible?

half hour

604

When does loss of cardiomyocyte contractility occur with ischemia?

after 60 seconds.

605

If radius of an artery decreases by 50%, what is change in blood flow?

Decreases by 1/16 (flow is proportional to radius ^ 4th power) so (1/2)^4 = 1/16

606

Systolic pressure in downstream arteries is actually slightly higher than in aorta.

So renal artery pressure is actually higher than aorta.

607

What happens with extra systolic beats?

There's more calcium in the myocyte so contractility increases. Thus, pulse pressure increases.

608

What does 2 P waves breeding each QRS complex indicate?

Only every other P wave is conducted through AV node to ventricle. Thus, conduction velocity through AV node must be decreased.

609

What determines pulse pressure?

Stroke volume

610

When is the aortic pressure highest in the cardiac cycle?

- Reduced ventricular filling (diastasis).
- Aortic pressure reaches its highest level immediately after rapid ejection of blood during systole.

611

Affect of histamine on vasculature

1) vasodilation of arterioles, thus increasing filtration.
2) constriction of veins

612

Hodgkin's lytic or blastic mets?

blastic

613

What happens to TPR during exercise?

Decreases. Although there is increased sympathetic flow to blood vessels, there is an overriding vasodilation of skeletal muscle arterioles.

614

During which phase of the cardiac cycle is ventricular volume lowest?

Isovolumetric ventricular relaxation (ventricle is relaxed just before filling occurs).

615

Why does standing cause an increase in HR?

Blood pools and due to decreased venous return, baroreceptors sense this and stimulate increased HR.

616

During which phase of ventricular action potential is membrane potential closest o K+?

Phase 4

617

What receptors mediate slowing of the heart?

Muscarinic (via ACh in the SA node)

618

Other cause of decreased inotropy...

- Acetylcholine (on atria)

619

How do sympathetic stimulation and NE increase contractility?

Increasing calcium entry during the plateau phase and increasing storage of Ca by the sarcoplasmic reticulum.96

620

pulses finding in AS

"pulses parvus et tardus"-- pulses are weak with a delayed peak.