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Cardiology Flashcards

1
Q

Describe development of the the embryonic heart.

A
  • initially there is a single heart tube which the sinus venous caudally and the aortic roots cranially
  • differential growth causes this tube to loop, establishing left-right polarity
  • endocardial cushions then develop to separate the atria from the ventricles and to divide the atrial-ventricular septum into a left and right
  • from there, the atrial and ventricular septa arise by various processes as does the aorticopulmonary septum
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2
Q

Describe the separation of the left and right atria.

A
  • initially, the septum primum grows toward the endocardial cushions, narrowing the foramen primum
  • as it reaches the endocardial cushions and the foramen primum is closed, the septum secundum develops through PCD of cells within the septum primum
  • this maintains the right-to-left shunt through the atria
  • the septum secundum then expands, covering most of the foramen secundum (like a one-leaf valve)
  • right atrial pressure drives blood through the foramen ovale of the septum secundum and the foramen secundum of the septum primum
  • after birth, pressure rises in the left atria and the septum secundum and septum primum fuse to form the atrial septum
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3
Q

Patent Foramen Ovale

A
  • failure of the septum primum and septum secundum to fuse after birth
  • typically asymptomatic and untreated because left atrial pressure keeps the the foramen closed
  • it can, however, lead to paradoxical emboli
  • associated with Down’s syndrome
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4
Q

What are paradoxical emboli?

A

venous thromboemboli that enter the systemic arterial circulation, most often due to an atrial septal defect or patent foramen ovale

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5
Q

When does the embryonic heart begin beating?

A

by week 4 of development

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6
Q

What is the truncus arteriosus?

A

the cranial most portion of the primitive heart tube, which gives rise to the ascending aorta and pulmonary trunk

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7
Q

What is the bulbus cordis?

A

a portion of the primitive heart tube just caudal to the truncus arteriosus, which gives rise to the smooth outflow tracks of the adult ventricles

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8
Q

The endocardial cushions contribute to what adult heart structures?

A
  • atrial septum
  • membranous inter ventricular septum
  • AV and semilunar valves
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9
Q

The primitive atria and ventricles give rise to what adult heart structures?

A

the trabeculated part of each

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10
Q

What is the sinus venosus? What adult heart structures does it give rise to?

A
  • it is the caudal most portion of the primary heart tube with two roots/horns
  • the left horn gives rise to the coronary sinus
  • the right horn gives rise to the smooth part of the right atrium known as the sinus venarum
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11
Q

What embryonic heart structures give rise to the smooth and trabeculated portions of each heart chamber?

A
  • right atrium: right horn of sinus venosus gives rise to the smooth part and the primitive atrium gives rise to the trabeculated
  • left atrium: primitive pulmonary vein gives rise to the smooth part and the primitive atrium gives rise to the trabeculated
  • right ventricle: bulbus cordis gives rise to the smooth outflow tract and the primitive ventricle gives rise to the trabeculated
  • left ventricle: bulbus cordis gives rise to the smooth outflow tract and the primitive ventricle gives rise to the trabeculated
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12
Q

Describe the separation of the left and right ventricles in the embryonic heart.

A
  • a muscular interventricular septum forms from the caudal surface toward the endocardial cushion, leaving a space cranially called the interventricular foramen
  • the interventricular foramen is covered by a membranous interventricular septum as the aorticopulmonary septum rotates and fuses with the muscular ventricular septum
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13
Q

What is the most common congenital cardiac anomaly?

A

ventricular septal defect

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14
Q

In which portion of the ventricular septum is a defect most likely?

A

the membranous septum

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15
Q

Describe the sedation of the truncus arteriosus to form the aortic and pulmonic outflow tracts.

A
  • truncal and bulbar ridges form from neural crest and endocardial cells
  • these ridges spiral and fuse to form the aorticopulmonary septum, dividing the ascending aorta and pulmonary trunk
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16
Q

Which portion of the heart is derived from neural crest cells?

A

the conotruncal ridges

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17
Q

Failure of neural crest cells to migrate to the embryonic, developing heart, is associated with which congenital anomalies?

A

conotruncal anomalies like:

  • transposition of the great vessels
  • tetralogy of Fallot
  • persistent truncus arteriosus
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18
Q

Describe development of the heart valves.

A
  • the aortic and pulmonary valves are derived from the endocardial cushions of the outflow tract
  • the mitral and tricuspid are derived form the fused endocardial cushions of the AV canal
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19
Q

Which side of the heart are the tricuspid and mitral valves located on?

A
  • tricuspid is on the right

- mitral is on the left

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20
Q

Which delivers newly oxygenated blood to the fetus, the umbilical artery or vein?

A

the umbilical vein

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21
Q

What is the PO2 and O2 saturation of blood within the umbilical vein?

A
  • PO2 = 30 mmHg

- Saturation = 80%

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22
Q

Describe the path of fetal blood flow.

A
  • oxygenated blood is delivered via the umbilical vein
  • it by passes the hepatic circulation as it enters the IVC via the ductus venosus
  • from there it is delivered into the right atrium and passes through the foramen ovale into the left atrium
  • it fills the left ventricle and is pumped into the ascending aorta to supply the head and body
  • deoxygenated blood from the superior vena cava returns to the right atrium and then fills the right ventricle
  • it is pumped out of the pulmonary artery but diverted through the ductus arteriosus into the aortic arch
  • blood in the aorta, then, is a mix of oxygenated and deoxygenated blood that passes through the body and exits the fetus via the umbilical arteries
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23
Q

What is the ductus venosus?

A
  • a shunt in the developing fetus that allows blood entering the fetus to initially bypass the hepatic circulation and enter the IVC directly
  • it becomes the ligament venosus
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24
Q

What is the ductus arteriosus?

A
  • a shunt that connects the pulmonic artery with the aortic arch and allows deoxygenated blood from the superior vena to pass from the right ventricle into the descending aorta and out the fetus via the umbilical arteries
  • it becomes the ligament arteriosus
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25
Q

The umbilical arteries become what adult structures? What about the umbilical vein?

A
  • arteries: the medial umbilical ligaments

- vein: ligamentum teres hepatis, contained in the falciform ligament

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26
Q

What embryonic structures give rise to the median and medial umbilical ligaments?

A
  • median: allantois/urachus

- medial: umbilical arteries

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27
Q

How does fetal circulation change at birth? What factors mediate these changes?

A
  • at birth, clamping of the umbilical cord, initiates the first breathe
  • this lowers resistance in the pulmonary vasculature and increases the left atrial pressure compared to the right
  • this pressure differential closes the foramen ovale, closing the right-left shunt
  • the rise in PO2 that comes with respiration rather than having partially oxygenated blood delivered from the mother, along with a decrease in prostaglandins as the placenta separates, cause closure of the ductus arteriosus
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28
Q

What drugs are given to close the ductus arteriosus or keep it open after birth?

A
  • prostaglandin E1 and E2 keep the PDA open

- indomethacin, an NSAID, can be used to close it

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29
Q

List the major coronary arteries and describe their arrangement.

A
  • the right coronary comes off the aorta and passes between the pulmonic artery and superior vena cava
  • as it wraps around to the posterior surface of the heart, the right coronary gives off the right marginal artery toward the apex
  • in the back, the RCA usually forms the posterior descending artery that runs on the interventicular septum
  • the left coronary artery comes off the aorta and immediately gives rise to the left anterior descending artery that runs caudally to the apex
  • the left circumflex continues posteriorly
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30
Q

The SA and AV nodes are supplied by which coronary artery?

A

SA: the right coronary artery
AV: PDA

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31
Q

Why is a RCA obstruction problematic?

A

because the RCA serves the SA and AV nodes, and ischemia/infarction of these tissues may lead to bradycardia or heart block

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32
Q

What is left-dominant circulation of the coronary vasculature?

A

it is an infrequent variation of the coronary vasculature in which the posterior descending artery arises from the left circumflex rather than the right coronary artery

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33
Q

Coronary artery occlusions are most common in which vessel?

A

the left anterior descending

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34
Q

When is coronary blood flow greatest?

A

in early diastole

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35
Q

What cardiac tissue is supplied by the right marginal artery?

A

the right ventricle

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36
Q

What cardiac tissue is supplied by the right coronary artery?

A
  • the SA and AV nodes

- the right atrium

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37
Q

What cardiac tissue is supplied by the posterior descending artery?

A
  • the posterior ⅓ of the interventricular septum
  • the posterior walls of the ventricles
  • the posteromedial papillary muscle of the mitral valve
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38
Q

What cardiac tissue is supplied by the left circumflex artery?

A
  • the lateral and posterior walls of the left ventricle

- the anterolateral papillary muscle of the mitral valve

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39
Q

What cardiac tissue is supplied by the left coronary artery?

A

the left atrium

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40
Q

What are the papillary muscles of the heart? Which coronary arteries supply their blood flow?

A
  • those that attach the the atrioventricular valves via the chordae tindineae and contract to prevent valve prolapse
  • the posteromedial papillary muscle is supplied by the PDA while the anterolateral papillary muscle is supplied by the LCX
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41
Q

What cardiac tissue is supplied by the left anterior descending artery?

A
  • anterior ⅔ of the interventricular septum
  • anterolateral papillary muscle
  • anterior surface of the left ventricle
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42
Q

What are the layers of the pericardium from outer to inner?

A
  • fibrous pericardium
  • parietal layer of the serous pericardium
  • visceral layer of the serous pericardium
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43
Q

Where is the pericardial cavity?

A

between the parietal and visceral layers of the serous pericardium

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44
Q

What is the most posterior part of the heart? What clinical implications does this have?

A
  • the left atrium is most posterior
  • enlargement can cause dysphagia or hoarseness due to compression of the esophagus or left recurrent laryngeal nerve, respectively
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45
Q

Give two equations for calculating cardiac output.

A
  • CO = SV x HR

- CO = (rate of O2 consumption)/(arterial O2 - venous O2)

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46
Q

What equation relates CO, MAP, and TPR?

A

MAP = CO x TPR

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47
Q

How is MAP calculated from systolic and diastolic pressure?

A

MAP = diastolic pressure + (⅓) systolic pressure

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48
Q

What is pulse pressure proportional to? How is it calculated?

A
  • pulse pressure = systolic pressure - diastolic pressure

- it is proportional to the SV

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49
Q

How is cardiac output maintained during exercise?

A
  • in the early stages, both HR and SV are increased

- in the later stages, SV plateaus and only HR is increased

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50
Q

What effect does heart rate have on cardiac output?

A
  • it tends to increase cardiac output but only to a certain limit
  • after this, it preferentially shortens diastole and allows for less filling time, reducing cardiac output
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51
Q

List five diseases that increase pulse pressure and four that decrease it.

A
  • increase: hyperthyroidism, aortic regurgitation, aortic stiffening (causes LV hypertrophy), obstructive sleep apnea (due to decreased Po2 and increased CO2), exercise
  • decrease: aortic stenosis, cardiogenic shock, cardiac tamponade, advanced heart failure
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52
Q

What three factors affect stroke volume?

A

preload, afterload, and inotropic state

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53
Q

How is ejection fraction calculated?

A

it is the stroke volume divided by the EDV

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54
Q

What is a normal ejection fraction?

A

> 55%

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55
Q

In what sort of heart failure is ejection fraction reduced?

A

systolic heart failure

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56
Q

Preload is dependent on what two circulatory factors?

A
  • venous tone

- circulating blood volume

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57
Q

What is Laplace’s Law?

A
  • an equation for wall tension within the heart

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

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58
Q

List four things/drugs that will increase the inotropic state of the heart.

A
  • catecholamines
  • high intracellular calcium
  • low extracellular sodium
  • digitalis
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59
Q

How does hyponatremia affect the inotropic state of the heart?

A
  • it increase inotropy
  • low extracellular sodium reduces the activity of the Na/Ca exchanger and keeps intracellular calcium high for a longer period
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60
Q

How does digitalis affect the inotropic state of the heart?

A
  • it increases inotropy
  • it competes with potassium for the Na/K exchanger and raises intracellular sodium, which inhibits the Na/Ca exchanger
  • the net effect is an increase in intracellular calcium
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61
Q

List five things that reduce the inotropic state of the heart.

A
  • beta blockers
  • systolic dysfunction
  • acidosis
  • hypoxia/hypercapnia
  • non-dihydropyridine calcium channel blockers
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62
Q

Describe the effects of each of the following on inotropy:

  • catecholamines
  • digitalis
  • beta-blockers
  • hyponatremia
  • acidosis
  • non-dihydropyridine calcium channel blockers
  • systolic HF
A
  • catecholamines increase
  • digitalis increases
  • beta blockers decrease
  • hyponatremia increases
  • acidosis decreases
  • CCBs decrease
  • systolic HF decreases
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63
Q

Describe how HR, inotropic state, afterload, and preload are reflected in a Starling curve.

A
  • as HR increases, filling time decreases and EDV is reduced, thus you move down the curve
  • as preload increases, EDV increases, thus you move up the curve
  • as inotropic state increases, greater SV is achieved at the same EDV, so the curve is shifted upward
  • as afterload increases, SV is lower at the same EDV, so the curve is shifted downward
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64
Q

Which vessels constitute the greatest proportion of the total cross-sectional area of the vasculature? What does this mean for flow?

A
  • the capillaries have the highest total cross-sectional area
  • thus flow velocity is the slowest in capillaries
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65
Q

How does cross-sectional area of vasculature related to flow rate?

A

volumetric flow rate = flow velocity x cross-sectional area

Q = vA such that greater cross-sectional area corresponds to a slower rate of flow

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66
Q

How is resistance to blood flow calculated?

A 
R = (driving pressure)/flow = (LVP - RA)/(v x A)
R = [8(viscosity) x length]/(pi x r^4)
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67
Q

What are the equations for resistance of organs in series and organs in parallel?

A
  • series: total R = R1 + R2 + R3 + … + Rn

- parallel: 1/total R = 1/R1 + 1/R2 + … + 1/Rn

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68
Q

The viscosity of blood is primarily dependent on what factor?

A

the hematocrit

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69
Q

Draw a normal pressure-volume loop. How does this change with increasing inotropy, afterload, and preload?

A

see page 270 of FA

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70
Q

What do the vertical lines on a pressure-volume loop reflect?

A

isovolumetric contraction and relaxation

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71
Q

What do S1 and S2 heart sounds reflect?

A
  • S1 reflects atrioventricular valve closure

- S2 reflects aortic and pulmonic valve closure

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72
Q

What is an S3 heart sounds? Describe it. What is it associated with? Under what circumstances is it considered normal?

A
  • it is a sound in early diastole after S2 during rapid passive filling of the ventricles
  • it is often described as a “ken-tuck-y” sound (1 2 2)
  • it is associated with increased filling pressures and occurs with sudden cessation of filling as the ventricle reaches its elastic limit
  • may be normal in individuals under 40 or during pregnancy
  • pathologic in systolic heart failure, mitral regurgitation, and high-output states
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73
Q

What is an S4 heart sounds? Describe it. What is it associated with? Under what circumstances is it considered normal?

A
  • it is a late diastolic sound best heart at the apex just before S1
  • it is often described as a “ten-nes-see” sound (1 1 2)
  • it occurs after atrial contraction as blood is forced into a stiff ventricle
  • may be normal in healthy older adults
  • pathologic in younger adults and in those with diastolic dysfunction
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74
Q

Describe the jugular venous pulse curve.

A
  • a wave: rise associated with atrial contraction
  • c wave: moderate peak associated with RV contraction and bulging of the tricuspid into the RA
  • x descent: fall in JV pressure during atrial relaxation with downward displacement of the closed tricuspid valve
  • v wave: rise associated with atrial filling
  • y descent: fall associated with emptying of the RA into the RV
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75
Q

What would make the x descent of jugular venous pulse absent?

A
  • absent: tricuspid regurgitation or right heart failure
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76
Q

What would make the y descent of jugular venous pulse absent or more prominent?

A
  • absent: cardiac tamponade

- prominent: constrictive pericarditis

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77
Q

Why does physiologic splitting of S2 arise?

A
  • a splitting of S2 that occurs during inspiration
  • inspiration causes a drop in intrathoracic pressure
  • this contributes to increased venous return and RV filling
  • as a result RV stroke volume is increased as is ejection time
  • this delays closure of the pulmonic valve
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78
Q

What is wide splitting of S2? Under what circumstances does it arise?

A
  • seen in conditions that delay RV emptying such as pulmonic stenosis or right bundle branch block
  • this causes an exaggerated delay in pulmonic valve closure compared to aortic and physiologic splitting is increased during inspiration but not as much during expiration (differentiates it from fixed splitting)
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79
Q

What is fixed splitting of S2? Under what circumstances and through what mechanism does it arise?

A
  • it is a splitting of S2 that doesn’t change regardless of breathing pattern
  • primarily heard in those with an atrial septal defect
  • the left-to-right shunt increases RA and RV volumes
  • flow through the pulmonic valve is therefore etxtended and pulmonic closure is greatly delayed
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80
Q

What is paradoxical splitting? Under what circumstances and through what mechanism does it arise?

A
  • seen in conditions that delay aortic valve closure like stenosis or left bundle block
  • it paradoxical splitting, the aortic valve closes after the pulmonic and inspiration shortens or “paradoxically” eliminates the split because it shifts the pulmonic closure later and toward the aortic closure
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81
Q

What sort of S2 splitting occurs in each of the following:

  • healthy individuals
  • right bundle branch block
  • left bundle branch block
  • aortic stenosis
  • pulmonic stenosis
  • atrial septal defect
A
  • healthy individuals: physiologic S2 splitting
  • right bundle branch block: wide splitting
  • left bundle branch block: paradoxical splitting
  • aortic stenosis: paradoxical splitting
  • pulmonic stenosis: wide splitting
  • atrial septal defect: fixed splitting
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82
Q

Describe the phases and currents of a myocardial action potential in the ventricular tissue.

A
  • phase 0: threshold is met, voltage-gated sodium channels open and there is a rapid upstroke and depolarization
  • phase 1: there is an initial repolarization as voltage-gated potassium channels begin to open and voltage-gated sodium channels begin to close
  • phase 2: there is a plateau as the potassium current through voltage-gated potassium channels is balanced by the L-type calcium channel current
  • phase 3: as L-type calcium channels close, the potassium current predominates and repolarization occurs
  • phase 4: resting potential at which fractional conductance and nernst potential of potassium predominates
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83
Q

Give three ways in which the action potentials of cardiac myocytes differ from those of skeletal muscle cells.

A
  • cardiac muscle APs have a plateau not seen in skeletal muscle APs
  • cardiac muscle contraction requires calcium influx to induce calcium release from the SR while skeletal muscle requires only depolarization
  • cardiac myocytes are electrically coupled to each other through gap junctions
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84
Q

Describe the phases and currents of an action potential in the SA and AV nodes.

A
  • phase 0: threshold is met and voltage-gated calcium channels open, generating an upstroke and depolarization
  • phase 1 and 2 are absent
  • phase 3: inactivation of calcium channels and opening of potassium channels causes repolarization
  • phase 4: a slow, spontaneous depolarization occurs due to a funny sodium current
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85
Q

Which cardiac tissue is least excitable and conducts action potentials the slowest? Why is this important?

A
  • the AV node has the slowest conduction velocity

- this helps delay ventricular contraction until filling has had time to occur

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86
Q

What molecular difference accounts for the slow conduction velocity through the AV node?

A
  • cells in the AV node have a less negative resting potential
  • as a result, fast voltage-gated sodium channels are permanently inactivated
  • this slows depolarization and conduction velocity
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87
Q

Which cardiac tissues rely on a calcium current for depolarization?

A

the SA and AV nodes

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88
Q

What is the effect of sympathetic, noradrenergic activity in the heart?

A
  • sympathetic nerves release NE on B1 receptors in the SA and AV nodes
  • this increases funny sodium current, current through L-type calcium channels, and potassium current
  • net result is an increase in heart rate and conduction velocity through the AV node as well as great inotropy
  • on an ECG, there is a shorter PR interval, spiked T wave, and shorter QT interval
  • does not affect the magnitude of sodium current in the atria or ventricles so there is no change in the QRS complex or P wave
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89
Q

Describe the pathway for conduction of action potentials through the heart.

A
  • SA node
  • atria
  • AV node
  • bundle of His
  • right and left bundle branches (left branch divides into anterior and posterior fascicles)
  • purkinje fibers
  • ventricles
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90
Q

Order the various segments of the cardiac conduction pathway from highest to lowest pacemaker rate.

A

SA > AV > bundle of His > Purkinje fibers

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91
Q

Order the various segments of the cardiac conduction pathway from highest to lowest speed of conduction.

A

Purkinje fibers > atria > ventricles > AV node

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92
Q

To what do the P wave, PR segment, QRS complex, ST segment, and T wave correspond?

A
  • P wave: atrial depolarization
  • PR segment: stalling at the AV node
  • QRS complex: ventricular depolarization
  • ST segment: phase 2 of ventricular AP
  • T wave: ventricular repolarization
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93
Q

Where are the Sa and AV nodes located?

A
  • SA: posterior wall of the right atrium where the superior vena cava enters
  • AV: posterioinferior part of the interatrial septum
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94
Q

Describe the units on a standard ECG.

A
  • each small box is 1 mm
  • 5 mm (big box) = 0.2 seconds along the x-axis
  • 5 mm (big box) = 0.5 mV along the y-axis
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95
Q

What is the normal length of the PR interval and QRS complex

A
  • PR interval < 200 msec

- QRS complex < 120 msec

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96
Q

Where does the PR interval begin on an ECG?

A
  • begins at the start of the P wave

- ends at the beginning of the QRS complex

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97
Q

Why isn’t atrial repolarization seen on an ECG?

A

it is masked by ventricular depolarization

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98
Q

During which phase of an ECG does mechanical contraction of the ventricles occur?

A

the QT interval

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99
Q

Where is the J point of an ECG?

A

it is the end of the QRS complex and beginning of the ST segment

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100
Q

What is a U wave on an ECG?

A
  • a wave after the T wave

- prominent in those with hypokalemia or bradycardia

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101
Q

T-wave inversion is indicative of what pathology?

A

recent MI

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102
Q

Torsades de Pointes

A
  • polymorphic ventricular tachycardia
  • characterized by shifting sinusoidal waveforms on ECG
  • patients with a long QT interval are predisposed; this includes those with hypokalemia, low magnesium, or congenital abnormalities
  • ABCDE drugs can induce long QT as well (IA/III anti-Arrhythmics, anti-Biotics, anti-Cychotics like haloperidol, anti-Depressants, and anti-Emetics)
  • risk is that this will progress to ventricular fibrillation and death
  • treat with magnesium sulfate
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103
Q

Congenital Long QT Syndrome

A
  • an inherited disorder of myocardial repolarization
  • most often due to ion channel defects
  • includes Romano-Ward syndrome as well as Jervell and Lange-Nielsen syndrome
  • Romano-Ward is an autosomal dominant condition without extracardial symptoms whereas Jervell and Lange-Nielsen syndrome is autosomal recessive and associated with sensorineural deafness
  • long QT increases the risk of sudden cardiac death due to tornadoes de pointes
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104
Q

Brugada syndrome

A
  • an autosomal dominant disorder
  • most common amongst Asian males
  • characterized by an ECG pattern of pseudo-right bundle branch block and ST elevations in nodes V1-V3
  • have an increased risk of ventricular tachyarrhythmias and sudden cardiac death
  • typically treated with implantation of a cardioverted-defibrillator
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105
Q

Wolff-Parkinson-White syndrome

A
  • the most common type of ventricular pre-excitation syndrome
  • results from an abnormal fast accessory conduction pathway from the atria to the ventricles, bypassing the AV node, called the Bundle of Kent
  • ECG demonstrates characteristic delta waves, widened QRS complex, and shortened PR interval/segment
  • increases risk for a supraventricular tachycardia
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106
Q

What is a delta wave on ECG?

A
  • a wave between the PR interval and QRS complex

- indicative of a Bundle of Kent (Wolff-Parkinson-White syndrome)

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107
Q

Which drugs increase the risk for torsades de pointes and sudden cardiac death?

A

ABCDEs

  • anti-Arrhythmics (class IA and III)
  • anti-Biotics
  • anti-“C”ychotics (e.g. haloperidol)
  • anti-Depressants
  • anti-Emetics
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108
Q

Atrial Fibrillation

A
  • chaotic and erratic baseline ECG with no discrete P waves and irregularly spaced QRS complexes
  • rhythm is irregularly irregular
  • risk factors include CAD and hypertension
  • can leads to thromboembolic events and should be treated with anti-coagulation, rate control, rhythm control, and/or cardioversion
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109
Q

Atrial Flutter

A
  • a rapid succession of identical, back-to-back atrial depolarizations with regular QRS complexes
  • has a “saw tooth” appearance of ECG and rhythm is regularly irregular
  • treat medically with anti-coagulation, rate control, rhythm control, and/or cardioversion
  • definitive treatment with catheter ablation
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110
Q

Ventricular Fibrillation

A
  • a completely erratic rhythm without identifiable waves

- a serious and fatal without CPR and defibrillation since cardiac output is essentially zero

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111
Q

What are first, second (type 1 and 2), and third degree AV heart blocks?

A
  • first degree: prolonged PR interval
  • second degree, Mobitz type I: progressive lengthening of PR interval until a QRS complex is dropped
  • second degree, Mobitz type II: consistent PR interval with randomly dropped QRS complexes
  • third degree: atria and ventricles beat independently of one another
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112
Q

How are first, second, and third degree AV blocks treated?

A
  • first degree and second degree type 1 are usually asymptomatic and not treated
  • second degree type 2 and third degree often require a pacemaker
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113
Q

In those with third degree heart block, is atrial or ventricular rate greater?

A

atrial rate is greater because the SA node has the highest pacemaker rate

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114
Q

Which heart block can be caused by an infectious disease?

A

a third degree heart block can be caused by Lyme disease

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115
Q

What are ANP and BNP? Where are they released from and in response to what?

A

ANP and BNP are release from atrial and ventricular myocytes, respectively, in response to increased blood volume and tension on the chamber wall

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116
Q

What is nesiritide?

A

recombinant BNP used in the treatment of heart failure

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117
Q

Where are the baroreceptors and chemoreceptors that sense changes within the vascular system located?

A
  • baroreceptors can be found in the aortic arch and carotid sinus just before the bifurcation
  • peripheral chemoreceptors are found in the same places
  • central chemoreceptors, however, are located within the brain
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118
Q

How does the aortic baroreceptor respond to an increase in blood pressure?

A
  • hypertension causes more stretch of the vessel wall, which increases the firing rate of the vagal afferent (CN X)
  • these afferents terminate in the solitary nucleus of the medulla and firing increases the parasympathetic-to-sympathetic ratio of efferent activity
  • the shift toward parasympathetic activity reduces arterial tone, heart rate, and inotropic state
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119
Q

How does the carotid baroreceptor respond to an increase in blood pressure?

A
  • hypertension causes more stretch of the vessel wall, which increases the firing rate of the glossopharyngeal afferent (CN IX)
  • this nerve terminates in the solitary nucleus of the medulla and increased firing of the afferent increases parasympathetic efferent and decreases sympathetic efferent activity
  • this serves to decrease arterial tone, heart rate, and inotropic state
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120
Q

Where do peripheral baroreceptors project to? What nerves carry these afferents?

A
  • both the carotid and aortic baroreceptors project to the solitary nucleus of the medulla
  • the aortic via the vagus and the carotid via the glossopharyngeal
121
Q

Why does a carotid massage slow heart rate?

A
  • massage increases pressure on the carotid sinus, which is sensed as a rise in blood pressure
  • the glossopharyngeal nerve afferent increases firing rate, which impairs sympathetic efferents and promotes parasympathetic efferents
  • the net result is a decrease in heart rate
122
Q

What is a Cushing reaction? Describe the mechanisms.

A
  • a triad of hypertension, bradycardia, and respiratory depression following a rise in intracranial pressure
  • increased intracranial pressure constricts arterioles and contributes to cerebral ischemia
  • pCO2 rises and pH drops, triggering the central chemoreceptor to initiate reflex sympathetic activity
  • this increases perfusion pressure (hypertension), which stretches the carotid wall and activates the carotid baroreceptor
  • the effect is bradycardia
123
Q

Describe central and peripheral chemoreceptors? What do they sense? What effect do they elicit?

A
  • peripheral chemoreceptors are located at the carotid and aortic bodies; they are stimulated by low PO2, high PCO2, and low pH
  • central chemoreceptors are located in the brain and respond only to changes in PCO2 and pH; they do not directly respond to PO2
124
Q

Pulmonary capillary wedge pressure is a good estimation of pressure where else in the cardiovascular system?

A

the left atrium

125
Q

What would cause pulmonary capillary wedge pressure to increase above LV end diastolic pressure?

A

mitral valve stenosis

126
Q

What are the normal pressures found in the atria, ventricles, aorta, pulmonary artery and pulmonary capillaries.

A
  • right atrium: < 5 mmHg
  • right ventricle: 25/5
  • pulmonary artery: 25/10
  • PCWP: 4-12
  • left atrium: 4-12
  • left ventricle: 130/10
  • aorta: 130/90
127
Q

What local metabolites promote vasodilation in skeletal muscle?

A

CHALK (during exercise)

  • CO2
  • H+
  • Adenosine
  • Lactate
  • K+
128
Q

How does pulmonary vasculature respond to hypoxia?

A

in contrast to all other tissues, it responds with vasoconstriction in an effort to move blood to ventilated alveoli

129
Q

What mechanisms are in place for auto-regulation of blood flow in the kidneys?

A
  • myogenic

- tubuloglomerular feedback

130
Q

What local metabolites promote vasodilation in the brain?

A

primarily a rise in CO2 or drop in pH

131
Q

What metabolites promote vasodilation in the heart?

A
  • adenosine
  • NO
  • CO2
  • low O2
132
Q

What factors affect the rate of capillary fluid exchange and can contribute to edema?

A
  • plasma and interstitial hydrostatic pressure
  • plasma and interstitial oncotic pressure
  • membrane permeability to fluid or protein
133
Q

What might cause edema by decreasing plasma oncotic pressure? Give three examples.

A

anything that results in low plasma proteins

  • nephrotic syndrome
  • liver failure
  • protein malnutrition
134
Q

How do burns contribute to edema?

A

they increase the permeability of the capillary to fluid

135
Q

How would you describe aortic regurgitation, aortic stenosis, mitral stenosis, and mitral regurgitation murmurs?

A
  • aortic regurgitation: HARD FALL: diastolic decrescendo
  • aortic stenosis: ASS BUMP: systolic crescendo-decrescendo
  • mitral stenosis: MSD YOU: diastolic decrescendo-presystolic crescendo
  • mitral regurgitation: MRS THROUGH: pansystolic
136
Q

What are you hearing when you hear a heart murmur? What does volume relate to?

A
  • you are hearing blood moving past the defect

- the volume corresponds to the pressure difference between the two spaces it is passing between

137
Q

What is the leading cause of death in the US?

A

ischemic heart disease

138
Q

Ischemic heart disease is most often due to what?

A

atherosclerosis

139
Q

Compare and contrast stable and unstable angina.

A
  • stable arises with exertion or emotional stress while unstable occurs at rest
  • stable arises due to incomplete occlusion of a vessel by atherosclerosis whereas unstable arises from rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion
  • both represent reversible injury to myocytes and ST depression due to subendocardial ischemia
  • both are relived by NO
140
Q

Stable Angina

A
  • chest pain that arises with exertion or emotional stress
  • due to partial occlusion of a coronary artery by atherosclerosis inducing a subendocardial ischemia
  • this represents reversible injury
  • presents with pain lasting less than 20 minutes but which radiates to the left arm or jaw and is accompanied by diaphoresis and shortness of breath
  • ECG would reveal ST depression due to subendocardial ischemia
  • treat with rest and nitroglycerine
141
Q

Unstable Angina

A
  • chest pain that arises at rest as the result of atherosclerotic plaque rupture and thrombosis causing partial occlusion of a coronary artery and subendocardial ischemia
  • this represents reversible injury
  • presents with pain lasting less than 20 minutes but which radiates to the left arm or jaw and is accompanied by diaphoresis and shortness of breath
  • ECG would demonstrate ST depression due to subendocardial ischemia
  • treatment is with nitroglycerine
142
Q

Angina is indicative of ischemic damage to what part of the heart?

A

the endothelium

143
Q

What causes ST depression on ECG?

A

subendocardial ischemia as might be seen in those suffering from stable and unstable angina

144
Q

Prinzmetal Angina

A
  • angina that arises unrelated to exertion due to coronary artery vasospasm
  • it incurs reversible injury to myocytes
  • ECG will show ST elevation due to transmural ischemia
  • relieved by nitroglycerine and calcium channel blockers
  • related to smoking; tx: cessation
  • triggers: cocaine, alcohol, triptans
145
Q

Calcium channel blockers play a role in treating what kind of angina?

A

prinzmetal (vasospastic) ischemia because CCBs relieve the vasospasm

146
Q

How do the ECGs of stable, unstable, and prinzmetal angina differ? Why is this?

A
  • stable and unstable angina are characterized by ST depression because there is only sub endothelial ischemia
  • prinzmetal angina involves transmural ischemia and presents with ST elevation
147
Q

What are the layers of the heart?

A
  • pericardium
  • myocardium
  • endocardium
148
Q

Atherosclerosis is typically asymptomatic (without angina) until what point?

A

until there is greater than 70% coronary artery occlusion

149
Q

What is the primary difference between angina and MI?

A
  • although both involve ischemic injury, angina is a term applied to ischemic injury that lasts fewer than twenty minutes and is therefore considered reversible
  • MIs result from ischemia that lasts longer than twenty minutes because at that point, the injury becomes irreversible and myocyte necrosis ensues
150
Q

Myocardial Infarction

A
  • necrosis of cardiac myocytes
  • most often due to rupture of an atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery; but occasionally due to vasospasm, emboli, or vasculitis
  • presents with severe, crushing chest pain lasting more than twenty minutes which radiates to the left arm or jaw most frequently
  • often accompanied by diaphoresis and dyspnea
  • initially, there is subendocardial necrosis with ST depression followed by transmural necrosis and ST elevation
  • ECG is the gold standard for diagnosis in the first six hours
  • troponin I is the most sensitive and specific marker for MI
  • not relieved by nitroglycerin
  • treatment involves aspirin/heparin, supplemental O2, nitrates, a beta blocker, an ACE inhibitor, and fibrinolysis or angioplasty
  • reperfusion injury may occur, mediated by ROS, or a calcium influx may induce contraction band necrosis
  • post-MI complications are directly tied to the microscopic and macroscopic changes that can be sen in the hours, days, and weeks following
151
Q

MI most often involves what part of the heart? Why?

A

the left ventricle is most often involved because of the coronary arteries that are most often occluded

1) left anterior descending
2) posterior descending
3) left circumflex

152
Q

How does the ECG typically change during an MI?

A
  • in the early phase, infarction leads to subendocardial necrosis (because it becomes ischemic first) and ST depression
  • later, the area of infarction expands to become transmural, leading to ST elevation
153
Q

What role does ECG play in diagnosing ischemic heart disease?

A
  • ECG is the gold standard in the first 6 hours
  • subendocardial ischemia and necrosis will appear as ST depression
  • transmural ischemia and necrosis will appear as ST elevation
154
Q

What roles do troponin I and CK-MB play in the diagnosis of ischemic heart disease? What characteristics of these make them appropriate for their respective roles?

A
  • troponin I is a highly sensitive and specific marker for MI; levels rise 2-4 hours after infarction, peak at 24 hours, and return to normal within 7-10 days
  • CK-MB is useful in that it’s levels rise in 4-6 hours, peak at 24 hours, and return to normal by 72 hours; this makes it a better marker for detecting re-infarction in the days following initial MI
155
Q

When do troponin I and CK-MB levels rise, peak, and return to normal?

A
  • troponin I: rise in 2-4 hours, peak at 24 hours, and return to normal within 7-10 days
  • CK-MB: rise in 4-6 hours, peak at 24 hours, and return to normal within 72 hours
156
Q

How is MI treated? (6) things

A
  • aspirin or heparin to limit thrombosis
  • supplemental O2 to minimize ischemia
  • nitrates to vasodilator veins and coronary arteries
  • beta blockers to decrease oxygen demand and the risk for arrhythmias
  • ACE inhibitors to limit LV dilation
  • fibrinolysis or angioplasty to re-open the blocked vessel
157
Q

What is contraction band necrosis?

A
  • a form of necrosis that follows reperfusion after an MI
  • reperfusion of irreversibly-damaged cells results in a calcium influx, which hypercontracts myofibrils
  • the result is contraction band necrosis
  • histology reveals myocytes without nuclei (necrosis) and pink bands running perpendicular to myocyte orientation
158
Q

Describe the gross and microscopic changes in the hours, days, and weeks following MI.

A
  • there are no changes at the four hour mark
  • 4-24 hours after MI, there is coagulative necrosis microscopically and a corresponding dark discoloration macroscopically
  • 1-3 days after MI, there is a neutrophil infiltrate and the tissue takes on a yellow pallor on gross exam
  • 4-7 days after MI, there is a macrophage infiltrate and the yellow pallor persists
  • 1-3 weeks post-MI, granulation tissue forms an a red border emerges from the edge of the infarct
  • in the month following, there is fibrosis (replacement of type III collagen in the granulation tissue with type I) and a white scar forms
159
Q

What complications arise from the microscopic and macroscopic changes following MI?

A
  • from 0-4 hours there is risk for arrhythmia, cariogenic shock, and heart failure
  • with coagulative necrosis in the first 4-24 hours, there is an increased risk of arrhythmia
  • in the 1-3 days post-MI there is a risk for fibrinous pericarditis if the damage was transmural as neutrophils invade the myocardium and may invade the pericardium; this would present with chest pain and a friction rub
  • 4-7 days post-injury, macrophage activity makes the wall weak and there is a risk of rupturing the wall, papillary muscle or interventricular septum
  • in the months following, as granulation tissue turns to scar tissue, there is a risk of aneurysm, mural thrombus, and Dressler syndrome
160
Q

What is Dressler syndrome?

A
  • a complication of MI that arises 6-8 weeks post-injury
  • results from auto-antibodies that form after immune cells are exposure to pericardial antigens
  • the end result is fibrinous pericarditis
161
Q

Sudden Cardiac Death

A
  • unexpected death due to cardiac disease, either without symptoms or less than one hour after symptoms arise
  • usually due to a fatal ventricular arrhythmia
  • most common etiology is acute ischemia as most patients have pre-existing severe atherosclerosis (CAD)
  • may also arise as the result of mitral valve prolapse, cardiomyopathy, or cocaine abuse
162
Q

Chronic Ischemic Heart Disease

A
  • poor myocardial function due to chronic ischemic damage, with or without infarction
  • progresses to CHF
163
Q

Left-Sided Heart Failure

A
  • failure of the heart to adequately supply blood to the systemic circulation and peripheral tissues
  • caused by ischemic heart disease, hypertension, dilated cardiomyopathy, or restrictive cardiomyopathy
  • presentation relates to decreased forward perfusion and pulmonary congestion
  • pulmonary edema presents with dyspnea, paroxysmal nocturnal dyspnea (breathless awakening from sleep), orthopnea (when supine), and crackles; decreased flow to the kidneys leads to activation of the renin-angiotensin system and fluid retention which exacerbates CHF
  • mainstay for treatment is ACE inhibitors
  • histology of the lungs will reveal “heart failure cells,” which are hemosiderin-laden macrophages that have cleaned up intra-alveolar hemorrhages as pulmonary congestion leads capillaries to burst
164
Q

Describe heart failure cells including how they arise and what they are indicative of.

A
  • a histologic sign of left-sided heart failure
  • left-sided heart failure leads to pulmonary congestion and rupture of capillaries in the lungs
  • alveolar macrophages clean up this debris and become hemosiderin-laden
165
Q

Why do those with left-sided heart failure experience paroxysmal nocturnal dyspnea?

A
  • because when they lay down, there is increased venous return
  • the heart isn’t able to pump this extra volume forward, so it adds to the already present pulmonary congestion, worsening pulmonary symptoms
166
Q

What kind of edema are characteristic of left- and right-sided heart failure?

A
  • left: pulmonary edema

- right: pitting edema

167
Q

Right-Sided Heart Failure

A
  • arises most commonly as a result of the increased afterload from left-sided heart failure
  • also caused by left-to-right shunts and chronic lung disease
  • presents with JVD, painful hepatosplenomegaly with a characteristic “nutmeg” liver and potentially cardiac cirrhosis, and dependent pitting edema
168
Q

What is the most common cause of right-sided heart failure?

A

left-sided heart failure

169
Q

JVD is a sign of what?

A

right-sided heart failure

170
Q

What is “nutmeg liver”?

A

nutmeg is used to describe the splotches of red in the liver that arise due to congestion of the capillaries within the liver, secondary to right-sided heart failure

171
Q

What is cardiac cirrhosis?

A

cirrhosis of the liver that arises secondary to right-sided heart failure and congestion of the hepatic vasculature

172
Q

Are most congenital cardiac defects sporadic or familial?

A

sporadic

173
Q

Describe the mechanism by which a left-to-right shunt becomes symptomatic?

A
  • this shunt tends to increase flow through the pulmonary circulation
  • the result is pulmonary hypertension, increasing the pressure in the right heart
  • eventually the pressure in the right heart is high enough that the shunt is reversed and becomes right-to-left
  • at this point it often becomes symptomatic
  • this process is known as Eisenmenger syndrome
174
Q

Which kind of shunt is typically symptomatic at birth, a left-to-right or right-to-left cardiac shunt?

A

right-to-left

175
Q

Why don’t left-to-right cardiac shunts present until adulthood?

A

because they typically have to reverse to right-to-left shunts before they become symptomatic and this takes time as pressure builds in the right hearts

176
Q

What is Eisenmenger syndrome?

A

the process by which a left-to-right shunt reverses to a right-to-left shunt and becomes symptomatic

  • this shunt tends to increase flow through the pulmonary circulation
  • the result is pulmonary hypertension, increasing the pressure in the right heart
  • eventually the pressure in the right heart is high enough that the shunt is reversed and becomes right-to-left
177
Q

What are the presenting syndromes in someone with Eisenmenger syndrome (right-to-left shunt?

A
  • right ventricular hypertrophy (from when the shunt was left-to-right)
  • late/adult onset cyanosis with reactive polycythemia (due to decreased O2 content = try to increase RBC)
  • clubbing
178
Q

Ventricular Septal Defect

A
  • the most common congenital heart defect
  • strongly associated with fetal alcohol syndrome
  • results in a left-to-right shunt and a large defect can lead to Eisenmenger syndrome (late cyanosis, polycythemia, clubbing, and right ventricular hypertrophy)
  • usually presents with a holosystolic, harsh-sounding murmur loudest at the tricuspid area and increased with the hand grip maneuver, which increases afterload
  • additionally, could hear a fixed split S2
  • may spontaneously resolve or be asymptomatic if small, but larger defects require surgical closure
  • O2 saturation will be elevated in the RV and pulmonary artery
179
Q

Atrial Septal Defect

A
  • the most common type is ostium secundum but ostium primum has an association with Down syndrome
  • results in a left-to-right shunt and fixed split S2
  • most likely murmur is a diastolic murmur heard best at the tricuspid area due to the increased volume flowing across this valve
  • paradoxical emboli are an important complication
  • O2 saturation will be elevated through the right side of the heart
180
Q

What kind of congenital heart defect is associated with Down syndrome?

A

ostium primum type atrial septal defect

181
Q

Patent Ductus Arteriosus

A
  • a failure of the ductus arteriosus to close after birth, leaving a left-to-right shunt between the aorta and pulmonary arteries
  • strongly associated with congenital rubella
  • asymptomatic at birth with a continuous, machine-like murmur loudest at the left infraclavicular area
  • may progress to Eisenmenger syndrome with lower extremity cyanosis (upper extremity perfusion largely preserved based on location of the shunt)
  • treatment involves indomethacin, which inhibits PGE, and closes the duct
182
Q

Tetralogy of Fallot

A
  • a set of cardiac anomalies caused by anterosuperior displacement of the infundibular septum
  • includes stenosis of the right ventricular outflow tract, right ventricular hypertrophy, VSD, and an aorta that overrides the VSD
  • the overriding aorta forms a right-to-left shunt that presents with early cyanosis
  • the degree of right ventricular outflow tract stenosis determines the extent of shunting and cyanosis
  • CXR reveals a boot-shaped heart
  • patients will learn to squat in response to a cyanotic spell, because this increases arterial resistance and decreases shunting
183
Q

Transposition of the Great Vessels

A
  • a congenital anomaly in which the pulmonary artery arises from the left ventricle and the aorta arises form the right ventricle, forming two separate circuits
  • associated with maternal diabetes
  • presents with early cyanosis and results in hypertrophy of the right ventricle and atrophy of the left
  • PGE can be administered at birth to maintain a patent ductus arteriosus and a link between the two circuits until surgical repair can occur
184
Q

Maternal diabetes is associated with what congenital cardiac anomaly?

A

transposition of the great vessels

185
Q

Truncus Arteriosus

A
  • a congenital cardiac anomaly in which a single large vessel arises from both ventricles after which the pulmonary and aortic circulations separation
  • most patients have an accompanying VSD
  • presents with early cyanosis
186
Q

Tricuspid Atresia

A
  • failure of the tricuspid valve orifice to develop; often associated with an atrial septal defect
  • the right ventricle becomes hypoplastic as no blood passes through it; instead passing to the left heart via the ASD
  • presents with early cyanosis
187
Q

Infantile Coarctation of the Aorta

A
  • a congenital cardiac anomaly with narrowing of the aorta
  • the coarctation lies distal to the aortic arch but proximal to a patent ductus arteriosus
  • this infantile form presents with lower extremity cyanosis at birth since there is a right-to-left shunt
  • associated with Turner syndrome
188
Q

Adult Coarctation of the Aorta

A
  • a congenital cardiac anomaly with narrowing of the aorta
  • the coarctation is not associated with a PDA and arises after the aortic arch
  • it is associated with a bicuspid aortic valve
  • presents with hypertension in the upper extremities and hypotension with weak pulses in the lower extremities
  • notching of the ribs is present on x-ray as collateral circulation develops and expands the intercostal arteries
189
Q

Acute Rheumatic Fever

A
  • a systemic complication of pharyngitis due to a group A B-hemolytic strep (increase in anti-Streptolysin O titers)
  • due to molecular mimicry of the bacterial M protein (type II hypersensitivity)
  • arises 2-3 weeks after an episode of strep throat
  • presents with migratory polyarthritis (migratory swelling and pain in large joints), pancarditis, subcutaneous nodules, erythema marginatum (annular, nonpuritis rash with erythematous borders), and sydenham chorea (rapid, involuntary muscle movements) - the so-called “JONES criteria” (joints, heart, nodules, erythema marginatum, and sydenham chorea)
  • endocarditis affects the mitral valve more than the aortic with small vegetations along the lines of closure leading to regurgitation
  • myocarditis with Aschoff bodies (foci of chronic inflammation, reactive histiocytes with slender, wavy nuclei called Anitschkow cells, giant cells, and fibrinoid material)
  • pericarditis presents with friction rub and chest pain
  • myocarditis is the most common cause of death in the acute phase
  • treat with penicillin
  • usually resolves, but repeat exposure to group A B-hemolytic strep results in relapse of the acute phase and increase the risk of progression to chronic rheumatic heart disease
190
Q

Acute rheumatic fever and chronic rheumatic heart disease preferentially affect which heart valve?

A

the mitral valve

191
Q

Describe the cardiac features of acute rheumatic fever

A

there is a pancarditis, but myocarditis is the most common cause of death in the acute phase

  • endocarditis preferentially affects the mitral valve over the aortic valve and small vegetations along the closure lines lead to regurgitation
  • there is a distinct myocarditis with Aschoff bodies characterized by foci of chronic inflammation, Anitschokow cells (reactive histiocytes with slender, wavy nuclei), giant cells, and fibrinoid material
  • pericarditis presents with a friction rub and chest pain
192
Q

What are Anitschkow cells?

A
  • reactive histiocytes with slender, wavy nuclei called “caterpillar nuclei”
  • present in Aschoff bodies, a unique histologic finding seen in those with acute rheumatic fever myocarditis
193
Q

What is the etiologic agent responsible for acute rheumatic fever?

A

a group A beta-hemolytic streptococci

194
Q

What mechanism serves to bring about acute rheumatic fever?

A

molecular mimicry between the bacterial M protein of group A beta-hemolytic strep and human tissue

195
Q

Chronic Rheumatic Heart Disease

A
  • a complication of acute rheumatic fever (secondary to group A beta-hemolytic strep and mediated by molecular mimicry)
  • defining feature is valve scarring as a consequence of the rheumatic fever, resulting in stenosis
  • mitral valve is preferentially affected and takes on a “fish-mouth” appearance with stenosis along with thickening of the chordae tendineae and cusps
  • if the aortic valve is affected, there is fusion of the commissures
  • the primary complication is infectious endocarditis
196
Q

What are the cardiac features of chronic rheumatic heart diseases?

A
  • stenosis of the mitral valve with thickening of the chordae tendineae and cusps
  • stenosis has a “fish-mouth” appearance
  • if the aortic valve is affected, there is fusion of the commissures, which distinguishes this aortic stenosis from that of normal aging and wear and teat
197
Q

Aortic Stenosis

A
  • a narrowing of the aorta
  • usually due to fibrosis and calcification from “wear and tear” with presentation in late adulthood
  • risk is increased by a bicuspid aortic valve which also hastens disease onset or it can arise as a consequence of chronic rheumatic heart disease (with fusion of commissures)
  • there is a long asymptomatic stage during which the heart compensates; during this period there is a systolic ejection click followed by a crescendo-decrescendo murmur; this murmur will increase with squatting and decrease upon standing because of the change in preload
  • pulse is weak with a delayed peak
  • complications include left ventricular hypertrophy, angina, syncope with exercise, and microangiopathic hemolytic anemia
  • treatment is a valve replacement after the onset of complications
198
Q

How can you distinguish aortic stenosis due to aging/wear and tear from that associated with chronic rheumatic heart disease?

A

if it is due to aging there is no fusion of the commissures as there is in those with chronic rheumatic heart disease

199
Q

Aortic Regurgitation

A
  • arises due to aortic root dilation (as in the case of a syphilitic aneurysm and aortic dissection) or valve damage (as in the case of infectious endocarditis)
  • presents with a diastolic decrescendo murmur heard best at the left sternal border, increased pulse pressure, LV dilation, and eccentric hypertrophy
  • the increased pulse pressure (hyperdynamic pulse) may present as a bounding pulse, pulsating nail bed, or head bobbing
  • treatment is valve replacement once LV dysfunction develops
200
Q

Mitral Valve Prolapse

A
  • a ballooning of teh mitral valve into the left atrium during systole
  • due to myxoid degeneration of the valve making it floppy; the etiology for this is unknown but may be seen in Marfan syndrome or Ehlers-Danlos syndrome
  • auscultation finds a mid-systolic click with a late systolic crescendo murmur best heart at the apex
  • complications are rare but include infectious endocarditis, arrhythmia, and severe mitral regurgitation
  • treatment is valve replacement
201
Q

Mitral Regurgitation

A
  • a reflux of blood during systole
  • usually arises as a complication of mitral valve prolapse, but also in association with LV dilatation, infective endocarditis, acute rheumatic heart disease, or papillary muscle rupture after MI
  • presents with a holosystolic blowing murmur best hearts at the apex and radiating to the axilla, which is louder when squatting and during expiration
  • will ultimately result in volume overload and left-sided heart failure
202
Q

Mitral Valve Stenosis

A
  • narrowing of the mitral valve orifice, usually due to chronic rheumatic valve disease
  • auscultation finds an opening snap followed by a diastolic decrescendo-presystolic crescendo murmur
  • results in volume overload: dilatation of the left atrium, pulmonary congestion with edema and alveolar hemorrhage, pulmonary hypertension and eventual right-sided heart failure, atrial fibrillation with associated risk for mural thrombi
203
Q

What is the most common cause of each of the following:

  • aortic stenosis
  • aortic regurgitation
  • mitral valve prolapse
  • mitral valve regurgitation
  • mitral valve stenosis
A
  • aortic stenosis: normal wear and tear or bicuspid aorta
  • aortic regurgitation: aortic root dilation (syphilitic aneurysm) or valve damage (infective endocarditis)
  • mitral prolapse: myxoid degeneration (Marfan syndrome)
  • mitral regurgitation: mitral prolapse, LV dilatation, acute rheumatic fever, or post-MI papillary muscle rupture
  • mitral stenosis: chronic rheumatic valve disease
204
Q

Myxoma

A
  • a benign mesenchymal tumor
  • the most common primary cardiac tumor in adults
  • has a gelatinous appearance and abundant group substance on histology
  • usually forms a pedunculate mass in the left atrium that causes syncope due to obstruction of the mitral valve
205
Q

Rhabdomyoma

A
  • a benign hamartoma of cardiac muscle
  • the most common primary cardiac tumor in children
  • strongly associated with tuberous sclerosis
  • usually arises in the ventricle
206
Q

What are the most common primary cardiac tumors in children and in adults?

A
  • children: rhabdomyoma

- adults: myxoma

207
Q

What is the most common tumor of the heart?

A

metastatic tumors

208
Q

What cancers are most likely to metastasize to the heart?

A
  • breast carcinoma
  • lung carcinoma
  • melanoma
  • lymphoma
209
Q

Metastases to the heart, most commonly involve what tissue?

A

the pericardium, resulting in a pericardial effusion

210
Q

Metastatic Cancer of the Heart

A
  • the most common tumors of the heart
  • typically from breast or lung carcinoma, lymphoma, or melanoma
  • most often involving the pericardium, resulting in a pericardial effusion
211
Q

What is endocarditis?

A

inflammation of the endocardium that lines the surface of cardiac valves

212
Q

What is the most common etiology for endocarditis?

A

Sterptococcus viridans

213
Q

What is a subacute endocarditis versus an acute endocarditis? How do the etiologies differ?

A
  • a subacute endocarditis has a gradual onset and involves small vegetations that do not destroy the valve; this is most often due to a Streptococcus viridans infection (low virulence)
  • acute has a more rapid onset and involves larger vegetations that destroy the valve; this is most often due to Staphylococcus auerus
214
Q

What are the most common etiologic agents for endocarditis of the following kinds:

  • most common overall
  • most common cause of subacute endocarditis
  • most common in IV drug users
  • most common in those with a prosthetic valve
  • most common in those with underlying colorectal carcinoma
  • most common in those with negative blood cultures
A
  • overall: Strep viridans
  • subacute: Strep viridans
  • IV drug users: Staph aureus
  • prosthetic valve: Staph epidermidis
  • colorectal carcinoma: Strep bovis
  • negative blood cultures: Coxiella burnetii, Bartonella spp., and HACEK organism (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, Kingella)
215
Q

What are HACEK organisms?

A

the organisms most likely to cause a culture negative endocarditis

  • Haemophilus
  • Actinobacillus
  • Cardiobacterium
  • Eikenella
  • Kingella
216
Q

Endocarditis

A
  • an inflammation of the endocardium that lines the surface of cardiac valves
  • Strep viridans is the most common overall cause
  • may be subacute (small vegetations and no valvular destruction) or acute (larger vegetations with valvular destruction)
  • presents with fever, murmur (depending on valve affected by vegetations), Janeway lesions (erythematous, nontender on the plams and soles), Osler nodes (tender lesions on fingers or toes), splinter hemorrhages in the nail beds, Roth spots on the retina (due to septic emboli), and anemia of chronic disease
  • blood cultures are positive (unless it is a HACEK organism)
  • other findings include those associated with anemia of chronic disease (low Hg, low MCV, high ferritin, low TIBC, low serum iron, and low saturation)
  • trans esophageal echocardiogram can detect lesions on valves
217
Q

What is unique about Strep Viridans endocarditis?

A
  • it is the most common overall cause of endocarditis
  • it has low-virulence so it only infects previously damaged valves
  • the previously damaged endocardial surface develops thrombotic vegetations, which trap bacteria during periods of transient bacteremia (often as a sequelae of dental procedures)
  • results in a subacute endocarditis with small vegetations and no destruction of valves
218
Q

What is unique about Staph aureus endocarditis?

A
  • it is the most common cause of endocarditis in IV drug users
  • high virulence allows it to infect normal valves
  • most commonly affects the tricuspid because it enters via needles entering veins and travel first to the right atrium
  • presents with an acute endocarditis (large vegetations and valvular destruction)
219
Q

What is unique about Staph epidermidis endocarditis?

A

it is associated with endocarditis of prosthetic valves

220
Q

What is unique about Strep bovis endocarditis?

A

it is associated with endocarditis in patients with underlying colorectal carcinoma

221
Q

What is unique about HACEK endocarditis?

A

it is associated with culture-negative endocarditis

222
Q

Nonbacterial Thrombotic Endocarditis

A
  • an inflammation of the endocardium without infection
  • sterile vegetations arise in association with a hypercoagulable state, underlying adenocarcinoma, or SLE
  • most often arise in the mitral valve along lines of closure and result in mitral regurgitation
223
Q

Libman-Sacks Endocarditis

A
  • a form of endocarditis due to sterile vegetations that arise in association with SLE
  • uniquely, vegetations are present on both sides of the mitral valve
  • contributes to mitral valve regurgitation
224
Q

What are cardiomyopathies?

A

a group of myocardial disease that result in cardiac dysfunction

225
Q

Dilated Cardiomyopathy

A
  • a dilation of all four chambers of the heart
  • most commonly idiopathic; can be due to alcohol abuse, wet beriberi, coxsackie B viral myocarditis, cocaine, chagas disease, doxorubicin, thyrotoxicosis, carnitine deficiency, or pregnancy
  • takotsubo cardiomyopathy is “broken heart” due to ventricular apical ballooning in response to sympathetics
  • causes systolic dysfunction with heart failure, arrhythmia, systolic regurgitation and an S3 heart sound
  • manage by evaluating viral serologies, serum carnitine level, ECG, and echo
  • treat with sodium restriction, ACE inhibitors, B-blockers, diuretics, digoxin, transplant
226
Q

Myocarditis

A
  • an infection of the myocardium
  • most often due to a coxsackie A or B infection
  • characterized by a lymphocytic infiltrate in the myocardium
  • results in chest pain, arrhythmia with sudden death, and heart failure
  • dilated cardiomyopathy is a late complication
227
Q

Hypertrophic Cardiomyopathy

A
  • massive concentric hypertrophy of the left ventricle
  • most often due to an autosomal dominant mutation in sarcomere protein like B-myosin heavy chain or myosin binding protein C
  • can also be caused by chronic hypertension and Frederich ataxia
  • hypertrophy disproportionately affects the interventricular septum and the mitral valve is anteriorly displaced during systole, which cause an outflow tract obstruction, leading to syncope
  • major complication is ventricular tachycardia and SCD
  • can hear an S4 heart sound, systolic murmur at the left sternal border, and a mitral regurgitation murmur
  • biopsy reveals myofiber hypertrophy with disarray
  • treat with cessation of high-intensity athletics, beta-blockers, and non-dihydropyridine CCBs
228
Q

When young athletes drop dead, what is the most common cardiac finding?

A

sudden death due to ventricular arrhythmias secondary to hypertrophic cardiomyopathy

229
Q

Restrictive Cardiomyopathy

A
  • decreased compliance of the ventricular endomyocardium that restricts filling during diastole
  • caused by amyloidosis, sarcoidosis, endocardial fibroelastosis (thick firboelastic tissue in the endocardium of young children), hemochromatosis, Loeffler syndrome (endomyocardial fibrosis with a prominent eosinophilic infiltrate), and post radiation fibrosis
  • presents as diastolic heart failure with a low-voltage ECG
  • exercise intolerance, weakness, dyspnea, edema, hepatomegaly, ascites
  • treat with diuretics, beta-blockers, and CCBs
230
Q

What are the three layers of an artery?

A
  • endothelial intima
  • smooth muscle media
  • connective tissue adventitia
231
Q

Which forms of vasculitis affect large-vessels?

A
  • temporal (giant cell) arteritis

- takayasu arteritis

232
Q

What do large-vessel, medium-vessel, and small-vessel vasculitis conditions affect?

A
  • large: the aorta and it’s major branches
  • medium: muscular arteries that supply organs
  • small: arterioles, capillaries, and venules
233
Q

Temporal Giant Cell Arteritis

A
  • a granulomatous vasculitis
  • classically involves the branches of the carotid artery
  • it is the most common form of vasculitis in older adults and affects more females than males
  • presents with headache, visual disturbances, and jaw claudication in addition to flu-like symptoms and an elevated ESR (>100)
  • biopsy reveals inflamed vessel wall with giant cells and intimal fibrosis
  • lesions are segmental so biopsy requires a long segment and a negative biopsy does not rule out disease
  • treat with corticosteroids as soon as suspected to prevent blindness
234
Q

Takayasu Arteritis

A
  • a granulomatous vasculitis
  • classically affects the aortic arch at branch points
  • classically presents in young (<50) Asian females with visual and neurologic symptoms with a weak or absent pulse in the upper extremity (aka pulseless disease)
  • treatment is corticosteroids
235
Q

Which forms of vasculitis are said to be medium-vessel vasculitis conditions?

A
  • polyarteritis nodosa
  • Kawasaki disease
  • Buerger disease
236
Q

Polyarteritis Nodosa

A
  • a necrotizing vasculitis affecting multiple organs EXCEPT the lungs, which is mediated by immune complexes
  • classically presents in young adults as hypertension (renal artery), abdominal pain with melena (mesenteric artery), neurologic disturbances, and skin lesions
  • associated with serum HBsAg
  • lesions are in varying stages of development: early ones consist of transmural inflammation with fibrinoid necrosis while later lesions have healed with fibrosis
  • this alternation of early and late lesions produces a “string-of-pearls” appearance on imaging as inflammation weakens segments that turn to aneurysms and fibrosis constricts others
  • treatment is corticosteroids and cyclophosphamide
237
Q

Kawasaki Disease

A
  • a medium-vessel arteritis
  • coronary artery involvement is common contributing to a risk for thrombosis with MI or aneurysm
  • classically affecting Asian children less than four y.o.
  • presents with nonspecific signs including erythematous rash on palms and soles (appears viral-like) and a cardiac event in a young child
  • treatment involves aspirin and IVIG but the disease is self-limiting
238
Q

Buerger Disease

A
  • a necrotizing vasculitis involving the digits
  • presents with ulceration, gangrene, and autoamputation of fingers and toes, often with Raynaud phenomenon
  • a disease of smoking
  • treatment is smoking cessation which halts disease progression
239
Q

Wegener Granulomatosis

A
  • a necrotizing granulomatous vasculitis involving the nasopharynx, lungs, and kidneys (We”c”ener Granulomatosis)
  • presents as a middle-aged male with sinusitis or nasopharyngeal ulceration, hemoptysis, and hematuria due to RPGN
  • serum c-ANCA correlates with disease activity
  • large necrotizing granulomas are seen on biopsy with adjacent necrotizing vasculitis
  • treat with cyclophosphamide and steroids
240
Q

Microscopic Polyangiitis

A
  • necrotizing vasculitis involving the lung and kidneys in particular
  • similar to Wegener without the nasopharyngeal involvement or granulomas
  • serum p-ANCA correlates with disease activity
  • treat with cyclophosphamide and steroids
241
Q

Churg-Strauss Syndrome

A
  • a small vessel necrotizing, granulomatous vasculitis with eosinophilia
  • affects the heart and lungs in particular
  • presents with asthma, skin nodules or purpura, and peripheral neuropathy
  • serum p-ANCA levels correlate with disease activity; IgE is elevated
242
Q

How is microscopic polyangiitis differentiated from Churg-Strauss Syndrome given that both are associated with serum p-ANCA?

A
  • microscopic polyangiitis lacks granulomatous inflammation

- Churg-Strauss is more likely to have asthma-like symptoms and a peripheral eosinophilia

243
Q

Henoch-Schonlein Purpura

A
  • a small-vessel vasculitis resulting from IgA immune complex deposition
  • the most common childhood systemic vasculitis
  • presents with palpable purpura on buttocks and legs, GI pain and bleeding, hematuria (IgA nephropathy)
  • often follows an upper respiratory tract infection
  • disease is self-limiting but steroids can be used if severe
244
Q

How do we define systemic hypertension?

A
  • normal: 120/80
  • elevated: 120-129/80
  • HTN 1: 130-139/80-89
  • HTN 2: 140/90
245
Q

What is the most common cause of secondary hypertension?

A

renal artery stenosis

246
Q

How does renal artery stenosis contribute to secondary hypertension?

A

it limits blood flow, reducing sodium delivery to the JGA, resulting in excess renin release

247
Q

What are the most common causes of renal artery stenosis?

A
  • men: atherosclerosis

- women: fibromuscular dysplasia

248
Q

What is fibromuscular dysplasia?

A
  • a developmental defect of the blood vessel wall, which results in irregular thickening of large- and medium-sized arteries, especially the renal artery
  • commonly causes renal artery stenosis and secondary hypertension in women
249
Q

What are hypertensive urgency and hypertensive emergency?

A
  • urgency: BP > 180/120 arising de novo or from pre-existing benign HTN without end-organ damage
  • emergency: severe hypertension with evidence of acute end-organ damage
250
Q

Atherosclerosis

A
  • an intimal plaque that obstructs flow through a large- or medium-sized vessel
  • most often in the abdominal aorta then coronary artery, popliteal artery, and finally carotid artery
  • consists of a necrotic lipid core with a fibromuscular cap, often undergoing dystrophic calcification
  • there are modifiable and non-modifiable risk factors
  • begins as a fatty streak of macrophage foam cells early in life and then progresses to a plaque
  • complications include stenosis and ischemia, plaque rupture with thrombosis and stroke, plaque rupture with embolization, or weakening of the vessel and aneurysm
251
Q

What are the modifiable and non-modifiable risk factors of atherosclerosis?

A
  • modifiable: HTN, hypercholesterolemia, smoking, diabetes

- non-modifiable: older age, male gender, low estrogen (post-menopausal), and genetics

252
Q

Describe the pathogenesis of atherosclerosis.

A
  • damage to endothelium allows lipids (mostly LDL) to leak into the intima
  • these lipids are oxidized and consumed by macrophages via scavenger receptors, resulting in foam cells
  • this lesion is known as the fatty streak
  • later inflammation and healing leads to deposition of ECM and the proliferation of smooth muscle, forming the fibromuscular cap
253
Q

Why does atherosclerosis increase the risk for aneurysm?

A

because intimal thickening reduces oxygen diffusion and delivery to the deeper layers of the artery, weakening the vessel wall

254
Q

What is arteriolosclerosis?

A

a narrowing of small arterioles either due to hyperplasia of smooth muscle or hyaline (proteins leaking into vessel wall)

255
Q

Hyaline Arteriolosclerosis

A
  • a narrowing of small arterioles due to proteins leaking into the vessel wall
  • a consequence of long-standing, benign HTN or diabetes
  • results in reduced caliber arterioles with end-organ ischemia
  • classically results in arteriolonephrosclerosis, glomerular scarring, and chronic renal failure
256
Q

Hyperplastic Arteriolosclerosis

A
  • a narrowing of small arterioles due to hyperplasia of smooth muscle
  • a consequence of malignant hypertension
  • biopsy reveals a characteristic “onion skin” appearance of concentric smooth muscle cells
  • contributes to end-organ ischemia
  • may lead to fibrinoid necrosis of the vessel wall with hemorrhage, which classically causes acute renal failure with a characteristic “flea-bitten” appearance of pin point hemorrhages
257
Q

Monckeberg Medial Calcific Sclerosis

A
  • a form of arteriosclerosis defined by calficiation of the media of medium-sized arteries
  • non-obstructive and not clinically significant
  • important to be aware of, however, because it can be an incidental finding on x-ray or mammography where it appears more linear than malignant calcification
258
Q

Aortic Dissection

A
  • an intimal tear with dissection of blood through the media of the aortic wall forming a false lumen
  • two forms: Stanford type A and type B
  • A is proximal and involves the ascending aorta, possibly resulting in acute aortic regurgitation or cardiac tamponade and requires surgery
  • B is distal, involving the descending aorta or aortic arch, and can be treated medically with beta blockers and vasodilators
  • most often occurs in the proximal 10cm of the aorta, which is under high stress, and only in the setting of pre-existig weakness
  • most common cause in adults is hypertension, which causes hyaline arteriolosclerosis of the vasa vasorum supplying O2 to the aortic media, resulting in atrophy
  • most common cause in children is an inherited CT defect like Marfan syndrome or Ehlers-Danlos syndrome
  • presents as a sharp, tearing chest pain radiating to the back
  • complications include pericardial tamponade, rupture, or obstruction of branching arteries (particularly renal or coronary)
259
Q

Thoracic Aortic Aneurysm

A
  • a dilation of the thoracic aorta
  • due to weakness in the aortic wall
  • classically resulting from tertiary syphilis, which causes endarteritis of the vasa vasorum and gives the aorta a “tree-bark” appearance
  • primary complication is dilation of the aortic valve root with subsequent aortic valve insufficiency
  • may also compress mediastinal structures or generate thrombi/emboli
260
Q

Abdominal Aortic Aneurysm

A
  • a dilation of the abdominal aorta, usually below the renal arteries but above the bifurcation
  • most often due to atherosclerosis and classically seen in male smokers over 60 with hypertension
  • presents as a pulsatile abdominal mass that grows with time
  • rupture is especially possible when more than 5 cm in diameter and will present with hypotension, pulsatile abdominal mass, and flank pain
  • may also compress local structures or generate thrombi/emboli as it grows and disrupts blood flow
261
Q

Hemangioma

A
  • a benign tumor comprised of blood vessels
  • commonly presents at birth and then regresses during childhood (so don’t remove surgically)
  • most often involves the skin or liver
  • importantly, it will blanch if you press on it, unlike a purpura because it is blood within formed vessels, not just blood in the skin
262
Q

Angiosarcoma

A
  • a high-grade malignant proliferation of endothelial cells
  • commonly found in the skin, breast, and liver
  • liver angiosarcoma is particularly associated with exposure to PVC, arsenic, and Thorotrast
263
Q

Angiosarcoma of the liver is strongly associated with what exposure?

A

PVC, arsenic, and Thorotrast

264
Q

Kaposi Sarcoma

A
  • a low-grade malignant proliferation of endothelial cells, associated with HHV-8
  • presents as purple patches, plaques, and nodules on the skin, but may also involve visceral organs
  • these lesions will not blanch because it is an endothelial cell tumor, not complete vessels
  • seen in older, Eastern European males (won’t spread), those with AIDS (spreads early, treat with antiretrovirals), and transplant recipients (decrease immunosuppression)
265
Q

How is hypertension treated in the setting of:

  • primary hypertension
  • hypertension with heart failure
  • hypertension with diabetes
  • hypertension in pregnancy
A
  • use ACE inhibitors, ARBs, dihydropyridine CCBs, and thiazide diuretics
  • use diuretics, ACE inhibitors/ARBs, and aldosterone antagonists; beta-blockers must be used cautiously in decompensated HF and not at all in cardiogenic shock
  • use ACE inhibitors/ARBs because these are protective against diabetic nephropathy
  • use hydrazine, methyldopa, nifedipine, and labetalol
266
Q

What are the two major groups of calcium channel blockers? How do they differ?

A
  • dihydropyridines end in -dipine” and act on vascular smooth muscle
  • verapamil and diltiazem act on the heart
267
Q

Which has a greater central effect, verapamil, diltiazem, or amlodipine?

A

verapamil > diltiazem > amlodipine

268
Q

What is the primary clinical use for dihydropyridines, nimodipine, clevidipine, and non-dihydropyridine CCBs?

A
  • dihydropyridines are used for hypertension, angina, and Raynaud phenomenon
  • nimodipine is used to prevent cerebral vasospasm in those with subarachnoid hemorrhage
  • clevidipine is used for hypertensive emergency
  • non-dihydropyridines are used for hypertension, angina, and atrial fibrillation/flutter
269
Q

What are the side effects associated with non-dihydropyridine and dihydropyridine CCBs?

A
  • non-dihydropyridine: cardiac depression, AV block, hyperprolactinemia, and constipation
  • dihydropyridine: peripheral edema, flushing, dizziness, and gingival hyperplasia
270
Q

Describe the mechanism, uses, and adverse effects of hydralazine.

A
  • increases cGMP to cause smooth muscle relaxation and preferentially dilate the arterioles, reducing afterload
  • used for severe hypertension and HF, especially in those who are pregnancy
  • usually coadministered with a beta-blocker to prevent reflex tachycardia; may also cause fluid retention, headache, angio, or a lupus-like syndrome
271
Q

List five drugs appropriate for treating hypertensive emergencies.

A
  • clevidipine
  • fenoldopam
  • labetalol
  • nicardipine
  • nitroprusside
272
Q

What is nitroprusside?

A

a short acting drug that directly releases NO and increases cAMP to cause vasodilation for the treatment of hypertensive emergency

273
Q

What is fenoldopam?

A
  • a D1 receptor agonist
  • decreases BP and increase natriuresis because it is a vasodilator of coronary, peripheral, renal, and splanchnic vessels
  • used for hypertensive emergency and as a post-op anti-hypertensive
  • may cause hypotension and reflex tachycardia
274
Q

Describe the mechanism, uses, and adverse effects of nitrates.

A
  • increase NO in vascular smooth muscle, causing a rise in cGMP and vasodilation
  • preferentially dilate veins and reduce preload
  • useful for treating angina, acute coronary syndrome, and pulmonary edema
  • may cause reflex tachycardia, hypotension, flushing, and headache (i.e. “monday disease”)
275
Q

Nitrates are often combined with what other drug?

A

beta blockers (except the partial B-agonists like pindolol and acebutolol)

276
Q

Ranolazine

A
  • inhibits the late phase of sodium current to reduce diastolic wall tension and oxygen consumption without impacting heart rate or contractility
  • used for angina refractory to other therapies
  • may cause QT prolongation, constipation, dizziness, headache
277
Q

Digoxin

A
  • a direct inhibitor of Na/K-ATPase and indirect inhibitor of the Na/Ca exchanger to increase inotropy; also stimulates the vagus nerve to reduce heart rate
  • used to treat heart failure and atrial fibrillation (depresses AV/SA nodes)
  • causes cholinergic side effects, a blurry yellow vision change, arrhythmias, AV block, and hyperkalemia
  • toxicity predicted by renal failure or drugs that reduce clearance and by hypokalemia
  • toxicity should be treated by slowly normalizing potassium, adding a cardiac pacer, giving magnesium, and using the anti-digoxin antibodies as needed
278
Q

What are statins?

A
  • HMG-CoA reductase inhibitors that inhibitor the rate-limiting step of cholesterol synthesis (HMG-CoA to mevalonate)
  • best drug for reducing LDL; also increase HDL and decrease triglycerides
  • may cause hepatotoxicity or cause myopathy when used with fibrates or niacin
279
Q

What are bile acid resins?

A
  • they include cholestyramine, colestipol, and colesnvelam
  • they prevent intestinal reabsorption of bile acids, so the liver must use cholesterol to make more
  • reduces LDL while slightly increasing triglycerides and HDL
  • may cause GI upset and reduce absorption of other drugs and fat-soluble vitamins
280
Q

What is ezetimibe?

A
  • a drug that prevents cholesterol absorption at the small intestine brush border
  • effective at reducing LDL but has no other effects on lipid profile
  • may cause diarrhea and rare hepatotoxicity
281
Q

What are fibrates?

A
  • drugs ending in “-fibrate” or “-fibrozil”
  • function to upregulate LPL and thus triglyceride clearance; also activate PPAR-a to induce HDL synthesis
  • most effective drug for reducing triglycerides and also have some benefit for lowering LDL and raising HDL
  • may cause myopathy when used with statins or cholesterol gallstones
282
Q

What is the mechanism, effect, and adverse effects associated with niacin as a lipid lowering agent?

A
  • it inhibits lipolysis in adipose tissue (hormone-sensitive lipase) and reduces hepatic VLDL synthesis
  • the best drug for increasing HDL, but also effectively reduces LDL and triglycerides
  • may cause flushing (reduce with time or NSAIDs), hyperglycemia, and hyperuricemia
283
Q

Total Anomalous Pulmonary Venous Return

A
  • a congenital defect in which the pulmonary veins drain into the right heart
  • associated with ASD and sometimes PDA to allow for right-to-left shunting and maintenance of CO
284
Q

Ebstein Anomaly

A
  • a displacement of the tricuspid valve leaflets downward into the right ventricle, artificially “atrializing” the ventricle
  • associated with in utero exposure to lithium
  • associated with tricuspid regurgitation and right HF
285
Q

Which congenital cardiac defects are associated with the following:

  • alcohol exposure in utero
  • congenital rubella
  • Down syndrome
  • Marfan syndrome
  • Turner syndrome
  • Williams syndrome
  • DiGeorge Anomaly
A
  • alcohol: VSD, PDA, ASD, tetralogy of Fallot
  • rubella: PDA, pulmonary artery stenosis, septal defects
  • Down syndrome: AV septal defect
  • Marfan: mitral prolapse, thoracic aortic aneurysm and dissection, aortic regurgitation
  • Turner: coarctation of the aorta and bicuspid aortic valve
  • Williams: supravalvular aortic stenosis
  • DiGeorge: truncus arteriosus and tetralogy of Fallot
286
Q

What are xanthomas?

A

lipid-laden histiocytes in the skin, especially the eyelids, indicative of xanthomas

287
Q

What is corneal arcus?

A

lipid deposits in the cornea, common in the elderly but appearing earlier in life in those with hypercholesterolemia

288
Q

Coronary Steal Syndrome

A
  • the principle behind pharmacologic stress test
  • distal to coronary stenosis, vessels are maximally dilated at baseline, so administration of vasodilators dilates normal vessels and actually reduces blood flow to ischemic areas
  • as a results, there is ischemia and angina in the post-stenotic region
289
Q

Why is CK-MB non-specific for MI?

A

because it can also be release by damaged skeletal muscle

290
Q

Where will a STEMI appear on ECG if the infarction is in the following areas:

  • anteroseptal (LAD)
  • anteroapical (distal LAD)
  • anterolateral (LAD or LCX)
  • lateral (LCX)
  • inferior (RCA)
  • posterior (PDA)
A
  • anteroseptal (LAD): V1-V2
  • anteroapical (distal LAD): V3-V4
  • anterolateral (LAD or LCX): V5-V6
  • lateral (LCX): I, aVF
  • inferior (RCA): II, III, aVF
  • posterior (PDA): V7-V9 with ST depression in V1-V3 with tall R waves
291
Q

Which is more likely to rupture following MI, the anterolateral and posteromedial papillary muscle of the mitral valve?

A

the posteromedial because it only has a single blood supply

292
Q

What is a ventricular pseudoaneurysm?

A

a contained free wall rupture seen in the 4-7 days after MI

293
Q

What is eccentric hypertrophy?

A

a characteristic feature of dilated cardiomyopathy in which sarcomeres are added in series

294
Q

What is cor pulmonale?

A

isolated right HF due to a pulmonary cause (rather than secondary to left HF)

295
Q

What is the difference between cardiogenic and obstructive shock?

A
  • both have an increase in preload, low CO, and increased afterload
  • but cariogenic is that caused by acute MI, HF, vulvular dysfunction, or arrhythmia and treated with inotropes and diuresis
  • obstructive is caused by cardiac tamponade or pulmonary embolism and is treated by relieving that obstruction
296
Q

What is the Kussmaul sign?

A
  • an increase in JVP with inspiration instead of the normal decrease
  • due to something that prevents the negative intrathoracic pressure from being transmitted to the heart
  • may be seen with constrictive pericarditis, restrictive cardiomyopathies, and right atrial or ventricular tumors
297
Q

Acute Pericarditis

A
  • an inflammation of the pericardium
  • most often idiopathic and presumed viral; other causes include confirmed infection, neoplasm, autoimmune, uremia, and radiation therapy
  • presents with friction rub and a sharp pain, aggravated by inspiration and relieved by sitting up and leaning forward
  • often complicated by pericardial effusion
  • ECG shows widespread ST elevation and/or PR depression
298
Q

Cardiac Tamponade

A
  • a compression of the heart by fluid in the pericardial space
  • presents with a classic triad of hypotension, distended neck veins, and distant heart sounds
  • also may see increase in HR, pulses paradoxes (a decrease in systolic BP > 10 mmHg during inspiration), low voltage QRS complexes and electrical alternans
  • all four heart chambers will equilibrate diastolic pressures
299
Q

Syphilitic Heart Disease

A
  • tertiary syphilis disruptes the vasa vasorum of the aorta, causing atrophy of the wall with dilation of the vessel and valve ring
  • may see calcification of the root and ascending arch with a “tree bark” appearance
  • can result in aneurysm or aortic insufficiency

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