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Cardiology Flashcards

1
Q

Embryology: Truncus arteriousus

A

ascending aorta and pulmonary trunk

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2
Q

Embryology: Bulbus cordi

A

smooth parts (outflow tract) of left and right ventricles

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3
Q

Embryology: endocardial cushion

A

atrial septum, membranous interventricular septum, AV and semilunar valves

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4
Q

Embryology: primitive atrium

A

trabeculated part of left and right atria

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5
Q

Embryology: primitive ventricle

A

trabeculated part of left and right ventricles

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6
Q

Embryology: primitive pulmonary vein

A

smooth part of left atrium

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7
Q

Embryology: left horn of sinus venosus

A

coronary sinus

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8
Q

Embryology: right horn of sinus venosus

A

smooth part of right atrium (sinus venarum)

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9
Q

Embryology: right common cardinal vein and right anterior cardinal vein

A

Superior vena cava

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10
Q

Heart beats by what week?

A

4 weeks

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11
Q

cardiac looping

A

primary heart tube loops to establish left-right polarity; begins in week 4 of gestation

problems with cardiac looping cause a defect in left-right dynein (involved in LR asymmetry) can lead to dextrocardia, as seen in kartagener syndrome (primary ciliary

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12
Q

______is a rare heart condition in which your heart points toward the right side of your chest instead of the left side.

A

Dextocardia

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13
Q

which two structures fuse to form the foramen ovale

A

septum secundum and septum primum fuse

soon after birth the foramen ovale closes due to increased left atrial pressure

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14
Q

Septation of the chambers

A

1) septum primum grows towards the endocardial cushions, narrowing foramen primum
2) foramen secundum forms in septum primum. Foramen primum disappears
3) septum secundum develops as foramen secundum maintains right to left shunt
4) septume secundum expands and covers most of the foramen secundum. The residual foramen is the foramen ovale
5) remainder of septum primum forms valve of foramen ovale

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15
Q

Ventricles morphogenesis

A

1) muscular interventricular septum forms. Opening is the interventricular foramen
2) aorticopulmonary septum rotates and fuses with muscular ventricular septum to form membranous interventricular septum, closing the interventricular foramen
3) growth of the endocardial cushions separates atria from ventricles and contributes to both atrial septation and membranous portions of the interventricular septum

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16
Q

Most common congenital cardiac anomaly?

A

Ventricular septal defect

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17
Q

Aortic/pulmonary valves are derived from

A

endocardial cushions of outflow tract

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18
Q

mitral/tricuspid valves are derived from

A

fused endocardial cushions of the AV canal

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19
Q

Fetal circulation

A

From placenta –> umbilical vein (PO2 of 30 mmHg and is 80% saturated with O2) –> liver OR ductus venosus –> ductus venosus bypasses hepatic circulation –> IVC –> foramen ovale –> aorta –> head and body

Deoxy blood from SVC goes from RA to RV –> main pulmonary artery –> ductus arteriosus (connecting the main pulmonary artery to the proximal descending aorta.) –> descenting aorta

shunt is due to high fetal pulmonary artery resistance due to low O2 tension.

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20
Q

Why does the ductus arteriosus close

A

Increase in O2 due to respiration and decrease in prostaglandins from placental separation causes closure of ductus arteriorsus

Indomethacin helps close PDA/patent ductus arteriosus –> ligamentum arteriosum

Prostaglandins E1 and E2 keep the PDA open

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21
Q

Why does the foramen ovale close

A

At birth –> take breathe –> decreases resistance in pulmonary vasculature –> increases left atrial pressure vs right atrial pressure–> foramen ovale closes (now fossa ovalis)

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22
Q

Fetal postnatal derivatives: Allantois–> urachus

A

Median umbilical ligament

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23
Q

Fetal postnatal derivatives: ductus arteriosus

A

ligamentum arteriosum

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24
Q

Fetal postnatal derivatives: ductus venosum

A

ligamentum venosum

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25
Q

Fetal postnatal derivatives: foramen ovale

A

fossa ovalis

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26
Q

Fetal postnatal derivatives: notochord

A

nucleus pulposus

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27
Q

Fetal postnatal derivatives: umbilical arteries

A

medial umbilical ligaments

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28
Q

Fetal postnatal derivatives: umbilical vein

A

ligamentum teres hepatis (round ligament). contains the falciform ligament

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29
Q

What artery supplies the lateral and posterior walls of the left ventrical and anterolateral papilalry mm

A

left circumflex coronary artery

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30
Q

What artery supplies anterior 2/3 of interventricular spetum, anterolateral papilalry muscle, and anterior surface of left ventricle

A

Left anterior descending artery

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31
Q

What artery supplies the right ventricle

A

Right(acute) marginal artery

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32
Q

What artery supplies the AV node, posterior 1/3 of interventricular septum, posterior 2/3 walls of ventricles and posteromedial papilalry mm

A

posterior descending/interventricular artery (PDA)

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33
Q

What supplies the SA node

A

RCA

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34
Q

what supplies the AV node

A

PDA

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35
Q

Right vs left dominant circulation

A

Right dominant circulation (85%) = PDA arises from RCA

Left dominant circulation (8%) = PDA arises from LCX

Codominant circulation = PDA from both LCX and RCA

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36
Q

Where does coronary artery occlusion most commonly occur?

A

Left anterior descending artery (LAD)

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37
Q

When does coronary blood flow peak?

A

in early diastole

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38
Q

What is the most posterior part of the heart? Its enlargement causes what problems?

A

Left atrium

causes dysphagia due to compression of the esophagus

Causes hoarseness due to compression of the left recurrent laryngeal nerve

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39
Q

The layers of the pericardium and its innervation

A

1) (outer) Fibrous pericardium
2) Parietal layer of serous pericardium
- —pericardial cavity—
3) Visceral layer of serous pericardium

Innervation is phrenic nerve. Referred pain to shoulder

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40
Q

Cardiac output

A

CO= SV x HR

during early exercise: CO maintained by increase HR and SV

during late exercise: CO maintained by only increase HR and SV plateaus

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41
Q

Ficks principle of Cardiac Output

A

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

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42
Q

Mean arterial pressure

A

MAP = CO x Total Peripheral resistance (TPR)

MAP at resting HR= 2/3 diastolic pressure + 1/3 systolic pressure

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43
Q

Pulse pressure

A

Pulse pressure = systolic pressure - diastolic pressure

proportional to SV
Inversely proportional to arterial compliance

increases in hyperthyroidism, aortic regurg, aortic stiffening(isolated systolic hypertension), obstructive sleep apnea (increased sympathetic tone), anemia, exercise

decreases in aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF

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44
Q

Stroke volume

A

SV= EDV-ESV

affected by contractility, afterload, and preload

SV increase with increase contractility, increased preload (i.e. early pregnancy), and decreased afterload

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45
Q

What happens to diastole as HR increases?

A

shortened because less filling time and drop in CO

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46
Q

What effect does Catecholamine stimulation have on stroke volume? contractility? How?

A

Increases stroke volume and contractility via stimulation of β1 receptor.

Ca channels are phosphorylated –> increases Ca entry –> increases Ca induced Ca release and Ca storage in sarcoplasmic reticulum

phospholamban (membrane protein that regulates the Ca2+ pump in cardiac muscle cells) phosphorylation –> active Ca ATPase –> increases Ca storage in sarcoplasmic reticulum

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47
Q

What effect does Digitalis have on stroke volume? contractility? How?

A

Increases stroke volume and contractility by blocking Na/K pump

This increases intracellular Na –> decrease Na/Ca exchanger activity –> increases intracellular Ca

note: decrease in extracellular Na causes increase in SV and Contractility by decreasing activity of Na and Ca exchanger

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48
Q

Preload

A

preload is the end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand.

depends on venous tone and circulating blood volume. If you use vasodilators it decreases your preload.

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49
Q

Afterload

A

Afterload is the pressure against which the heart must work to eject blood during systole (systolic pressure). The lower the afterload, the more blood the heart will eject with each contraction.

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50
Q

What determines afterload

A

It is approximated by MAP

Increase in afterload -> increase in pressure –> increase wall tension per Laplace law. The left ventrical will compensate for this by thickening the wall muscle and thus decreasing wall tension

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51
Q

What effect does ACE inhibitors and ARBs have on preload? afterload?

A

Decrease both

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52
Q

Wall tension

A

follows Laplace’s law

Wall tension = pressure x radius

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53
Q

Wall stress

A

Wall stress=(pressure x radius)/(2*wall thickness)

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54
Q

Ejection fraction

A

Index of ventricular contractility

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

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55
Q

Starlings curve

A

y axis: SV or CO
X axis: Ventricular EDV or preload

force of contraction is proportional to end diastolic length of cardiac mm fiber (preload)

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56
Q

How does the starling curve shift with exercise

A

Left (increased contractility/inotropy)

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57
Q

How does the starling curve shift with HF+digoxin? HF alone?

A

Both shift right (decreased contractility/inotropy)

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58
Q

How does the starling curve shift with catecholamines, positive inotropes like digoxin?

A

Left (increased contractility/inotropy)

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59
Q

How does the starling curve shift with loss of myocardium (MI), beta blockers, non-dihydropyridine Ca blockers, dilated cardiomyopathy, narcotic overdose, HF with reduced EF, sympathetic inhib?

A

shift right (decreased contractility/inotropy)

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60
Q

Resistance, pressure, and flow equations

A

ΔP=change in pressure= Q x R

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

R=ΔP/Q= 8ηL/πr^4
η=viscosity which depends on hematocrit

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61
Q

Total resistance of vessels in series

A

R1 +R2 etc

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62
Q

Total resistance of essels in parallel

A

1/R1 + 1/R2 etc

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63
Q

What has the lowest flow velocity?

A

Capillaries due to high cross sectional area

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64
Q

What accounts for most of total peripheral resistance (TPR)?

A

Arterioles

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65
Q

Compliance

A

= ΔV/ΔP

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66
Q

In the cardiac and vascular fx curves, what does the intersection of the two curves mean?

A

operating point of the heart

venous return=CO

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67
Q

S1 heart sound

A

mitral and tricuspid valve closure.

Loudest at mitral area

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68
Q

S2 heart sound

A

aortic and pulmonary valve closure

loudest and left upper sternal border

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69
Q

S3 heart sound

A

S2 S3 S1

early diastole
Rapid ventricullar filling phase

associated with increased filling pressures (mitral regurg or HF or dialted ventricles)

Can be normal in children, young adults, pregnant women

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70
Q

S4 heart sound

A

S4 S1 S2

late diastole

best heart at apex with patient in left lateral decubitus position

Due to high atrial pressure or ventricular noncomplaince because left atrium must push against stiff LV wall.

always abnormal

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71
Q

Jugular venous pulse (JVP) - a wave

A

atrial contraction

absent in a fib

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72
Q

Jugular venous pulse (JVP) - c wave

A

RV contraction

closed tricuspid valve bulging into atrium

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73
Q

Jugular venous pulse (JVP) - x descent

A

downward displacement of closed tricuspid valve during rapid ventricular ejection phase

reduced or absent in tricuspid regurg and right HF because pressure gradients are reduced

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74
Q

Jugular venous pulse (JVP) - v wave

A

increase in RA pressure due to filling against closed tricuspid valve

think “villing”

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75
Q

Jugular venous pulse (JVP) - y descent

A

RA emptying into RV

prominent in constrictive pericarditis
absenct in cardiac tamponade

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76
Q

Why does normal splitting occur

A

on Inspiration

drop in intrathoracic pressure which increases venous return and RV filling. This causes an increase in RV SV and RV ejection time. There is a delay in the closure of pulmonic valve

S2 (aortic and pulmonic valve) –> now A2 and delayed P2

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77
Q

Why does wide splitting occur

A

Conditions that delay RV emptying (pulmonic stenosis, RBBB)

exaggeration of normal splitting where S2 has a normal A2 but an exaggerated delay in P2.

there is normally a delay on inspiration but now its exaggerated

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78
Q

Why does fixed splitting occur

A

Atrial septal defect

ASD there is a left to right shunt which increases RA and RV volumes. This increase in volume also increases the flow through the pulmonic valve, such that regardless of inspiration or expiration…there is a greatly delayed pulmonic valve closure

Sa –> A2 ———> P2

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79
Q

Why does paradoxical splitting occur?

A

Conditions that delay aortic valve closure ( aortic stenosis, LBBB). A split that is heard on expiration but reduced on inspiration.

normal order is reversed and P2 sounds occur before delayed A2 sounds. Therefor when on inspiration –> there is a delay in P2 sounds which bring P2 closer to the A2. Thereby paradoxically eliminating the split.

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80
Q

Murmur heard at Aortic area? conditions that could cause it?

A

Systolic murmur

Aortic senosis
Flow murmur
Aortic valve sclerosis

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81
Q

Murmur heard at the Pulmonic area? conditions that cause it?

A

Systolic ejection murmur

pulmonic stenosis
flow murmur
atrial septal defect

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82
Q

Murmur heard at tricuspid area? conditions that cause it?

A

Holosystolic murmur due to tricuspid regurg and ventricular septal defect

Diastolic murmur due to tricuspid stenosis

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83
Q

Murmur heard at mitral area? conditions that cause it?

A

Holosystolic murmur due to mitral regurg

Systolic murmur due to mitral valve prolapse

Diastolic murmur due to mitral stenosis

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84
Q

What is a holosystolic murmur?

A

A holosystolic murmur begins at the first heart sound (S1) and continue to the second heart sound (S2)

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85
Q

Heart murmur related to aortic stenosis?

A
  • crescendo-decrescendo systolic ejection murmur
  • soft S2 (ejection click may be present)
  • LV pressure > aortic pressure during systole
  • Loudest at heart base and radiates to the carotids
  • “pulsus parvus et tardus” - pulses are weak with a delayed peak
  • SAD –> syncope, angina, dyspnea
  • mostly due to calcification of bicuspid aortic valve

S1 /\/\/\/\/\/~~~~~S2

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86
Q

what is a crescendo-decrescendo murmur?

A

crescendo—decrescendo murmurs (diamond or kite-shaped murmurs), a progressive increase in intensity is followed by a progressive decrease in intensity.

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87
Q

Heart murmur related to mitral/tricuspid regurg?

A
  • Holosystolic, high pitched “blowing murmur”
  • Both can be due to rheumatic fever and infective endocarditis
  • Mitral regurg is loudest at apex and goes to axilla. Usually due to ischemic heart dz post MI, mitral valve prolapse, LV dilation
  • Tricuspid regurg is loudest at tricuspid area. Usually due to RV dilation

S1/\/\/\/\/\/\/\/\/\/\/\S2

88
Q

Heart murmur associated with mitral valve prolapse?

A

Most frequent valvular lesion and best heard over apex. Usually benign

Late systolic crescendo (high intensity just before S2) murmur with midsystolic click due to sudden tensing of chordae tendineae

can be due to myxomatous degeneration ( due to marfan or ehlers danlos syndrome), rheumatic fever, chordae rupture

S1———CLICK-/\/\/\/\/\/\/\ S2

89
Q

Heart murmur associated with ventricular septal defect?

A

holosystolic, harsh sounding murmur

loudest at tricuspid

S1/\/\/\/\/\/\/\/\/\/S2

90
Q

Heart murmur associated with aortic regurg?

A

High pitched blowing

Early long diastolic decrescendo (low intensity) murmur

hyperdynamic pulse

Head bobbing when severe and chronic

wide pressure pulse

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

S1 S2 /\/\/\/\/~~~~~~~~~~~~~~~

91
Q

Heart murmur associated with mitral stenosis?

A

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

mid to late diastolic murmur.

Decreased delay between S2 and snap means greater severity

LA&raquo_space;» pressure than LV

Due to rheumatic fever. Can also get because chronic MS can result in LA dilation –> compress esophagus and L recurrent laryngeal nerve –> dysphagia and hoarseness

S1 S2 SNAP ~~~~~~~~

92
Q

Heart murmur associated with patent ductus arteriosus?

A

continuous machine like murmur

best heard at left infraclavicular area

loudest at S2

due to congenital rubella or prematurity

S1 ~~~~~/\/\/\/\S2\/\/\/\~~~~~~

93
Q

Mycocardial AP phases 0-4

A

0) voltage gated Na channels open (rapid upstroke and depolarization)
1) Inactivation of voltage gated Na channels and voltage gated K channels begin to open. (Initial repolarization)
2) Calcium influx through voltage gated Ca channels balances K+ efflux. Ca influx triggers Ca release from sarcoplasmic reticulum and myocyte contraction. (Plateau)
3) massive K+ efflux due to opening of voltage gated slow K+ channels and closure of voltage gated Ca channels (rapid repolarization)
4) High K+ permeability through K+ channels (resting potential (-85 mV)

94
Q

Hand grip

A

Increases afterload

Increases intensity of mitral regurg, aortic regurg, and ventricular septal defect murmurs

decreases hypertrophic cardiomyopathy and aortic stenosis murmurs

Later onset of click/murmur for mitral valve prolapse

95
Q

Valsalva (phase II)

Standing up

A

standing up decreases preload

decreases intensity of most murmurs
increases intensity of hypertrophic cardiomyopathy murmur

Mitral valve prolapse has an earlier onset of click

96
Q

Rapid squatting

A

Increases venous return
which increases preload
Which increases afterload

Decreases intensity of hypertrophic cardiomyopathy murmur
Increases intensity of AS, MR, and VSD murmur

Mitral valve prolapse has a later onset of click

97
Q

Cardiac vs skeletal mm AP differences

A

Cardiac mm AP has a plateau which is due to Ca influx and K efflux

Cardiac mm contraction requires Ca influx from ECF to induce Ca release from SR

Cardiac myocytes are electrically coupled to each other by gap junctions

98
Q

Pacemaker action potential

A

SA and AV nodes

phase 4: slow spontaneous diastolic depolarization due to If (funny current) from If channels. If channels are slow mixed Na/ K inward current, they are what causes the automaticity of SA and AV nodes. The slope is in the SA node and determines HR.

Phase 0: upstroke - opening of the voltage gated Ca channels. Fast voltage gated Na channels are premanently inactivated. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to the ventricles

Phase 1: absent

Phase 2: absent

Phase 3: re-polarization due to inactivation of the Ca channels and increase activation of K+ channels which increases K+ efflux

99
Q

Conduction pathway in the heart

A

SA node –> atria –> AV node –> bundle of his –> right and left bundle branches –> purkinje fibers –> ventricles

100
Q

What is the pacemaker of the heart?

A

SA node

101
Q

Where is the AV node and why is it important?

A

interatrial septum

blood supply usually the RCA

100msec delay that allows for the ventricular filling before contraction

102
Q

Speed of conduction in the heart (greatest to lowest?

A

purkinje>atria>ventricles>AV node

103
Q

P wave?
QRS interval?
T wave?
U wave?

A

P wave - atrial depolarization
QRS interval - venricular depolarization
T wave - ventricular repolarization (inversion may indicate ischmia or recent MI)
U wave? prominent in hypUkalemia. Smal wave after T wave

104
Q

Torsades de pointes

A

polymorphic ventricular tachycardia

From: long QT interval
Becomes: v fib

causes? drugs, low potassium, low Mg,

Tx? magnesium sulfate

105
Q

Drugs that induce long QT?

A 
A - antiArrhythmics (classIA and III)
B- antiBiotics
C - antiCychotics
D- antiDepressants
E-antiEmetics
106
Q

Congenital syndromes that can cause a long QT?

A

Romano-ward syndrome-autosomal dominant, pure cardiac phenotype with no deafness

Jervell and Lange-nielsen syndrome - autosomal recessive, sensorineural deafness

107
Q

The most common type of ventricular preexcitation syndrome? with characteristic delta wave?

A

Wolff-parkinson white syndrome

abnormal fast accessory conduction pathway from atria to ventricle (bundle of kent) bypasses the rate slowing AV node

ventricles begin to partially depolarize earlier causing the delta wave with widened QRS complex and shortened PR interval

may result in reentry circuit –> supraventricular tachycardia

108
Q

What ECG tracing causes irregularly irregular heartbeat?

A

Atrial fibrillation

Can lead to stroke

109
Q

What ECG tracing causes a sawtooth patttern?

A

Atrial flutter

back to back depolarization

definitive treatment is catheter ablation

110
Q

What ECG tracing has no discernible rhythm and need immediate CPR and defib?

A

V fib

111
Q

Which block pattern has a prolonged PR?

A

First degree AV block

prolonged but same PR interval for each

benign and no tx needed

112
Q

Which block pattern has a progressive lengthening of PR intervals until a beat is dropped?

A

Mobitz type I (wenckebach)

113
Q

Which block pattern has dropped beats without a change in the PR interval length?

A

Mobitz type II

Treat with pacemaker or it will progress to a type III

114
Q

Which block pattern shows atria and ventricles beating independently of eachother?

A

third degree (complete) AV block

arial rate> ventricular rate

needs pacemaker

can be caused by lyme disease

115
Q

What peptide is released in response to increased blood volume and atrial pressure?

A

atrial natriuretic peptide (ANP) is released from the atrial myocytes

acts via cGMP to cause vasodilation and decrease Na reabsorption at the renal collecting tubules

It also contributes to the aldosterone escape mechanism by dialating afferent renal arteriolsies and constricting efferent arterioles thus promoting diuresis

116
Q

What peptide is released in response to increased tension?

A

B type (brain) natriuretic peptide is released by the ventricular myocytes

similar to ANP except longer half life

117
Q

What peptide is a good blood test for diagnosing HF?

A

BNP has a very good negative predictive value

can also be used for treatment in HF via recombinant form (nesiritide)

118
Q

How do the receptors in the aortic arch transmit information? and to where?

A

via vagus nerve to the solitary nucleus of medulla

119
Q

How do teh receptors in the carotid sinus transmit information? and to where

A

via glossopharyngeal nerve to solitary nucleus of medulla

120
Q

What does the carotid massage do and how does it happen?

A

The carotid massage decreases HR

By pushing down on the carotid –> increase pressure –> increases the signals back to the solitary nucleus via glossopharyngeal –> ultimately causes an increase in the AV node refractory period –> decreases HR

121
Q

The cushings reflex

A

triad of HTN, bradycardia, and respiratory depression

The increase in the intracranial pressure constrict arterioles and causes cerebral ischemia. This causes an increase in the partial pressure of pCO2 and decrease pH

This results in the central reflex –> increase in sympathetics –> increase in perfusion pressure (HTN) –> increase stretch –> peripheral reflec baroreceptors induce bradycardia

122
Q

peripheral chemoreceptors

A

carotid and aortic bodies respond to high pCO2, low pO2, low pH

123
Q

central chemoreceptors

A

stimulated by changes in pH and pCO2 in brain which depends on arterial pCO2 levels

DO NOT directly respond to pO2

124
Q

Pulmonary capillary wedge pressure

A

Left atrial pressure

measured by a pulm artery catheter (swan-Ganz catheter)

125
Q

Autoregulation in the heart

A

Vasodilatory via adenosine, NO, CO2 (pH), decrease O2

126
Q

Auto regulation in the brain

A

vasodilatory via CO2 (pH)

127
Q

Autoregulation via in the lungs

A

the pulmonary vasculatory is unique because hypoxia causes vasoconstriction so that only well ventilated areas are perfused

128
Q

Net fluid flow equation for capillary fluid exchange

A

Jv=net fluid flow= Kf[(Pc-Pi)-σ(πc-πi)]

kf=capillary permeability
Pc=capillary pressure
Pi=interstitial pressure
σ= reflection coefficient that measures capillary permeability to protein
πc=plasma oncotic pressure pulls fluid into capillary
πi=interstitial fluid oncotic pressure pulls floid out of capillary

129
Q

Right to left shunts have ____ babies? What anomalies cause it? how to treat it?

A

Blue babies - think “eaRLy” cyanosis tx with maintenance of PDA via prostaglandin administration

5 Ts:

1) Truncus arteriosus ( 1 vessel)
2) Transposition ( 2 switched vessels)
3) Tricuspid atresia (3=tri)
4) Tetralogy of fallor (4=tetra)
5) TAPVR (5 letters)

130
Q

Persistent truncus arteriosus

A

fails to divide into pulm trunk and aorta

R–>L

blue baby

131
Q

D transposition of great vessels

A

Aorta leaves RV and pulmn trunk leaves LV

systemic and pulmonary circulation is seperated

fatal - needs surgery or VSD/PDA/patent foramen ovale

R–> L blue baby

132
Q

Tricuspid atresia

A

absent tricuspid and RV hypoplastic

needs both ASD and VSD

R–> L blue baby

133
Q

Tetralogy of fallot

A

MOST COMMON cause of cyanosis/ blue baby. R–> L

caused by the anterosuperior displacement of the infundibular septum

Think PROVe

1) Pulm infundibular stenosis - important for prognosis because it forces the R–>L flow across the VSD and causes RVH
2) RV hypertrophy –> boot shape
3) Overriding aorta
4) VSD

pt has “tet spells” - crying, fever, exercise due to exacerbation of RV outflow obstruction.

R–> L blue baby

134
Q

How does squatting help with tet spells in tetralogy of fallot?

A

Squatting increases SVR which then causes a decrease in the R–> L shunt and improves cyanosis

135
Q

Total anomalous pulmonary venous return

A

pulmonary veins drain into right heart circulation

normally pulmonary veins drain into the left atrium and bring oxygenated blood from the lungs

R–>L blue baby

136
Q

Ebstein anomaly

A

Displacement of tricuspid valve leaflets downward into RV causing tricuspid regurg, accessory conduction pathways, and right sided HF

lithium exposure in utero

R—> L blue baby

137
Q

Left to right shunt have ______ babies? what congenital conditions?

A

think L–> R as LateR cyanosis. Babies are acyanotic on presentation

1) VSD
2) ASD
3) PDA
4) Eisenmenger syndrome

138
Q

What is the most common congenital cardiac defect?

A

Ventricular septal defect - increase O2 saturdation in RV and Pulm artery

VSD>ASD>PDA

139
Q

Atrial septal defect

A

wide split fixed S2

ostium secundum defect is most common

O2 saturation increases in RA,RV, and pulmonary artery

may lead to paradoxical emboli- systemic venous emboli bypass lungs and become systemic arterial emboli

140
Q

Patent ductus arteriousus

A

machine like continuous mumur

Maintain patency with PGE and low O2 tension. This is important in conditions like transposition of the great vessels.

Indomethancin (think ENDomethacin) ends patency

141
Q

What syndrome do we worry about in an uncorrected L–> R shunt that can become a R–>L shunt pathologically?

A

Eisenmenger syndrome

uncorrected left to right shunt causes increase in pulmonary blood flow–> pathological remodeling of vasculature –> pulmonary arterial HTN –> RVH to compensate –> now a right to left shunt

signs: late cyanosis, clubbing, polycythemia

142
Q

Coarctation of the aorta

A

Aortic narrowing near insertion of ductus arteriosus

HTN in UE and weak delayed pulse in LE

Associated with turners syndrome and HF, increased risk of berry aneurysm, aortic rupture, endocarditis

143
Q

Primary (essential hypertension)

A

due to increased CO or increased TPR

most HTN cases

144
Q

Secondary HTN

A

renal/renovascular dz related such as fibromuscular dysplasia ( string of beads appearance of renal artery)

145
Q

HTN urgency? emergency?

A

urgency is >= 180/120 but no end organ damage

Emergency is HTN with end organ damage

146
Q

pt presents with hypercholesterolemia and are at risk of ____ affecting their eye?

A

Corneal arcus

elderly pt

147
Q

Two types of arteriolosclerosis (small vessels and arterioles)

A

1) hyaline - thickening of vessel walls in essential HTN or DM
2) hyperplastic - onion skinning in severe HTN with proliferation of smooth MM cells

148
Q

Arteriosclerosis that affects medium sized vessels. Internal elastic lamina and media of arteries are calcified

A

Monckeberg sclerosis (medial calcific sclerosis)

vascular stiffening without obstruction

pipestem appearance on xray

149
Q

Atherosclerosis is

A

a type of arteriosclerosis caused by buildup of cholesterol plaques

Abdominal aorta> coronary artery>poplitieal artery>carotid artery

150
Q

pathogenesis of atherosclerosis

A

inflammation important

endothelial cell dysfunction –> macrophage and LDL accumulation –> foam cell formation –> fatty streaks –> smooth mm cell migration, proliferation, and extracellular matrix deposition –> fibrous plaque –> complex atheromas

151
Q

Aortic aneurysm

A

abdominal infrarenal typically associated with atherosclerosis

thoracic ones are associated with cystic medial degeneration. CT diseases are a risk factor (i.e marfan which also has risk of aortic dissection) and tertiary syphilis

trauma related is mostly at aortic isthmus

152
Q

pt with back pain that has different BP in arms

A

aortic dissection!

Stanford type A: proximal. Ascending aorta. Can result in aortic regurg or cardiac tamponade. Needs surgery

Stanford type B: distal. descending aorta Below ligamentum arteriosum. give Beta blockers then vasodilators

153
Q

Chest angina

A

Chest pain due to ischemia secondary to coronary artery narrowing or spasm

stable: pain on exertion, ST depression
unstable: pain at rest, ST depression and or T wave inv
vasospastic: coronary artery spasm, transient ST elevation

154
Q

Pt has coronary stenosis and is resulting in maximally dilated vessels distal to the stenosis. Think pharmacologic stress test.

A

Coronary steal syndrome

give vasodilators –> dilation –> so blood is shunted toward well perfused areas but then ischemia in myocardium perfused by stenosed vessels

155
Q

NSTEMI

A

subendocardial infarct
subendocardium (inner 1/3) especially vulnerable to ischemia
ST depression on ECG

156
Q

STEMI

A

Transmural infarct
fullthickness of myocardial wall involved
ST elevation
Q waves

157
Q

Pt has a ruptured coronary artery atherosclerotic plaque that has caused acute thrombosis.

A

MI

elevated CK-MB and Troponins are diagnostic

158
Q

What is the order of arteries most common sclerosed in an MI

A

LAD>RCA>circumflex

159
Q

0-24 hrs after an MI

A

early coagulative necrosis , wavy fibers, neutrophils

reperfusion injury concern

160
Q

1-3 days after an MI

A

extensive coagulative necrosis

Hyperemia

tissue surrounding infarct has acute inflammation with neutrophils

postinfarction fibrinous pericarditis –> friction rub

161
Q

3-14 days after an MI

A

hypereremic border, central yellow brown softening.

macrophages then granulation tissue at margins

free wall rupture can result in cardiac tamponade

papillary muscle rupture can cause mitral regurg

interventricular septal rupture due to macrophage mediated structural degradation

LV pseudo aneurysm due to a contained free wall rupture

162
Q

2 wks to several months after an MI

A

Now gray white

contracted scar complete

True ventricular aneurysm

Dressler syndrome - autoimmune phenomenon resulting in fibrinous pericarditis “dress for your heart”

163
Q

DX of MI in first 6 hours

A

first 6 hours: ECG gold standard

164
Q

When is cardiac troponin begin to rise? peak? how long does it remain high?

A

cardiac troponin rises at 4 hours and peaks at 24 hours and is high for 7-10 days

165
Q

When is CK-MB begin to rise? peak? how long does it remain high?

A

rises after 6-12 hours
peaks at 16-24 hours
returns to normal at 48 hours

good for acute MI

166
Q

Anteroseptal leads and what is their blood supply

A

V1-V2

LAD

167
Q

Anteroapical leads and bloody supply

A

V3-V4

distal LAD

168
Q

Anterolateral leads and blood supply

A

V5-V6

LAD or LCX

169
Q

Lateral leads and blood supply

A

I, aVL

LCX

170
Q

Inferior leads and blood supply

A

II,III,aVF

RCA

171
Q

Posterior leads

A

V7-V9

PDA

172
Q

What is a pt with an MI likely to die from before reaching the hospital and within the first 24 hours post MI?

A

cardiac arrhythmia

173
Q

Unstable angina/NSTEMI treatment

A 
Anticoagulation (heparin)
Anti platelet therapy (aspirin)
ADP receptor inhibitors 
Beta blockers
ACEi
Statins
SX control with nitroglycerin and morphine
174
Q

STEMI tx

A 
Anticoagulation (heparin)
Anti platelet therapy (aspirin)
ADP receptor inhibitors 
Beta blockers
ACEi
Statins
SX control with nitroglycerin and morphine 
Reperfusion therapy is most important - percutaneous coronary intervention preferred over fibrinolysis
175
Q

Most common cardiomyopathy that present swith HF, S3, systolic regurg murmur

A

Dilated cardiomyopathy –> balloon appearance of heart on CXR. Leads to a systolic dysfunction and has eccentric hypertrophy. Sarcomeres are added in series.

Chronic alcohol abuse
Wet beriberi
Coxsackie B viral myocarditis
Chronic cocaine use
Chagas disease
Doxorubicin toxicity

tx: Na restriction, ACE inhib, beta blockers, diuretics, digoxin, ICD, heart transplant

176
Q

pt presents with ventricular apical balloon after a stressful situation

A

Takotsubo cardiomyopathy

broken heart syndrome

177
Q

Pt is a young athlete that was exercising and experienced a syncope. Physical exam findings included a S4 and systolic murmur. Mitral valve closure was also impaired. Pt was pronounced dead later.

A

Hypertrophic obstructive cardiomyopathy - a diastolic dysfunction. most commonly due to mutations in genes encoding sarcomeric proteins such as myosin binding protein C and beta myosin heavy chain. Sarcomeres are added in parallel.

death due to ventricular arrhythmia

cease high intesity exercise, beta blockers, or non dihydropyridine Ca channel blockers.

178
Q

Physiology behind hypertrophic obstructive cardiomyopathy

A

asymmetric septal hypertrophy and systolic anterior motion of mitral valve. This causes an outflow obstruction and ultimately dyspnea and syncope. An arrhythmia can cause death in these patients

179
Q

Type of restrictive/infiltrative cardiomyopathy with hypereosinophilic syndrome

A

Loffler endocarditis

histology shows eosinophilic infiltrates in myocardium

180
Q

What is the most likely cause of RHF

A

LHF

cor pulmonale though refers to an isolated cause due to pulmonary cause

181
Q

systolic vs diastolic dysfunction

A

systolic: reduced EF and increased EDV. Decreased contractility
diastolic: preserved EF, normal EDV, decreased compliance(increased end diastolic pressure)

182
Q

Signs of left heart failure

A

orthopnea (SOB when supine)
paroxysmal nocturnal dyspnea ( breathlessness waking you up)
Pulmonary edema (increase in pulm VP –> venous distention and transudation of fluid)

presence of hemosiderin laden macrophages in lungs

183
Q

Presence of hemosidern laden macropages in the lungs indicates

A

Left HF

184
Q

Signs of right heart failure

A

Hepatomegaly (nutmeg liver)
Jugular venous distention
Peripheral edema

185
Q

Obstructive shock

A

cardiac tamponade
pulmonary embolism
tension pneumothorax

186
Q

Distributive shock

A

sepsis
anaphylaxis
CNS injury

compared to other forms of shock (cold and clammy), distributive can be warm or dry. If its warm then there is deceased preload, increased CO, and decreased afterload/SVR. If it is dry then its decreased preload, decreased CO, decreased afterload/SVR.

187
Q

Symptoms of bacterial endocarditis

A

FROM JANE

Fever
Roth spots
Osler nodes
Murmur
Janeway lesions
Anemia
Nail bed hemorrhage
Emboli
188
Q

Acute vs subacute bacterial endocarditis

A

Acute is caused by S aureus with high virulence. It results in large vegetaions on previously normal valves. Rapid onset.

subacute- viridans strep with low virulence. smaller vegetation on congenitally abnormal or diseased valves.

189
Q

What are you at risk for due to dental procedures

A

subacute bacterial endocarditis

190
Q

What valve is most commonly involved in bacterial endocarditis

A

mitral valve

191
Q

What valve is most commonly involved in IV drug users

A

tricuspid valve

“dont tri drugs”

192
Q

A consequence of pharyngeal infection with group A beta hemolytic infection

A

Rheumatic fever –> rheumatic heart dz affecting mitral >aortic>tricuspid

early: mitral regurg
late: mitral stenosis

193
Q

This is associated with aschoff bodies (granuloma with giant cells), anitschkow cells (enarged macrophages with ovoid,wavy,rod like nucleus), increase in antistreptolysin O titers

A

Rheumatic fever

J<3NES criteria

J-joints (migratory polyarthritis)
<3 carditis
N-nodules (subq)
E-erythema marginatum (evanescent rash with ring margin)
S-sydenham chorea
194
Q

PT presents with a sharp chest pain that is worse on inspiration. He improves when sits up and leans forward

A

acute pericarditis

often complicated by pericardial effusion

presents with friction rub

195
Q

What causes widespread ST segment elevation and or PR depression

A

acute pericarditis

196
Q

What is a major cause of sudden cardiac death in adults < 40 yo

A

myocarditis- global enlargement of heart and dilation of chambers due to inflmmation of myocardium

197
Q

Pt presents with hypotension, distended neck veins, and distant heart sounds. ECG shows electrical alternans

A

Cardiac tamponade - becks triad

electrical alternans due to swinging movement of heart in large effusion

Also has pulsus paradoxus which is a decrease in amplitude of systolic BP by >10 mm Hg during inspiration

Pulses paradoxus. High yield caused by croup. Tamponade. Copd. Asthma. Restrictive lung disease. Sleep Apnea

198
Q

What conditions can you see pulsus paradoxus

A

cardiac tamponade, asthma, obsructive sleep apnea, pericarditis, croup

a decrease in amplitude of systolic BP by >10 mm Hg during inspiration

199
Q

syphilitic heart dz

A

disrupts vasa vasorum of the aorta –> atrophy of BV–> dilation of aorta and valve ring

calcification of aortic root, ascending arch, and thoracic aorta

leads to tree bark appreance of aorta

200
Q

Pt is a 70 yo woman complaining about a unilateral headache and pain in her jaw (jaw claudication). What are you most worried about?

A

Giant cell (Temporal)

involves the temporal artery. may lead to irreversible blindness due to ophthalmic artery occlusion

Most commonly affects branches of the carotid artery

associated with polymyalgia rheumatica

focal granulomatous inflammation

201
Q

Pt is an asian female presenting with fever, night sweats, arthritis, myalgia, and weak UE pulses

A

Takayasu arteritis

also see skin nodules and ocular disturbances

granulomatous thickening and narrowing of aortic arch and proximal great vessels

202
Q

Pt is a 45 yo man that recently tested positive for Hep B, he complains of a fever, weight loss, malaise and headache. What are you most worried about?

A

Polyarteritis nedosa

can also see abd pain and melena. HTN, neurological dysfx, cutaneous eruptions, renal damage

on labs you see transmural inflammation of the arterial wall with fibrinoid necorsis (usually renal and visceral). Also innumerable renal microaneurysms and spasms on angiogram

203
Q

A 3 yo asian child with high fever and a strawberry tongue. what are you most worried about?

A

kawasaki disease (mucocutaneous lymph node syndrome)

asian kids <4 yo

think CRASH and burn your motorcycle

C-conjunctival inhection
R-rash (polymorphous --> desquamating)
A-adenopathy (cervical)
S- strawberry tongue 
H-hand foot changes (edema and erythema)

burn=fever

204
Q

pt is a 35 yo male with a strong history of smoking. what are you most worried about?

A

Buerger disease or thromboangiitis obliterans

intermittent claudication –> gangrene
Raynaud phenomenon
segmental thrombosing vasculitis with vein and nerve inolvement

205
Q

Pt presents with a saddle nose and red urine and couging up blood

A

Wegeners (granulomatosis with polyangiitis)

triad: focal nectrotizing vasculitis, necrotizing granulomas in lung and upper airway, necrotizing glomerulonephritis

UR tract - perforation of nasal septum , chronic sinusitis, otitis media, mastoiditis

Renal - hematuria and red cell casts

c-ANCA/PR3-ANCA

206
Q

Microscopic polyangiitis

A

Necrotizing vasculitis commonly involving the lungs, kidneys, skin with pauci immune glomerulonephritis and palpable purpura

similar to wegners except no nasopharyngeal involvement

No granulomas

p-ANCA/MPO-ANCA

207
Q

p-ANCA?

A

anti myeloperoxidase

208
Q

c-ANCA?

A

anti proteinase 3

209
Q

Behcet syndrome

A

Turkish and eastern mediterranean descent

immune complex vasculitis

recurrent aphtous ulcers, genital ulcerations, uveitis, erythema nodosum

related to HSV or parvo virus

HLA-B51

210
Q

Churg strauss

A

Eosinophilic granulomatosis with polyangitis

granulomatous necrotizing vasculitis with eosinophilia

pANCA and increase IgE levels

asthma, sinusitis, skin nodules or purpura, peripheral neuropathy resulting in wrist and foot drop

211
Q

Henoch-Schonlein purpura

A

Immunoglobulin A vasculitis

Following an URI in children

classic triad: palpable purpura on buttocks and legs, arthralgia, abdominal pain associated with intssusception

212
Q

Most common cardiac tumor

A

metastasis

213
Q

most common primary cardiac tumor in adults

A

myxoma commonly in the left atrium

“ball valve” obstruction in left atrium . early diastolic tumor plop sound

multiple syncopal episodes

on histology there are gelatinous material, myxoma cells immersed in glycosaminoglycans

214
Q

most common primary cardiac tumor in children

A

rhabdomyomas

associated with tuberous sclerosis

on histology there are hamartomatous growth

215
Q

Kussmaul sign

A

increase JVP on inspiration instead of decrease

inspiration: negative intrathroacic pressure not transmitted to heart –> impiared filling of RV –> blood backs up into vena cava –> JVD

constrictive pericarditis, restricive cardiomyopathies, right atrial and ventricular tumors

216
Q

Osler Weber Rendu syndrome

A

Hereditary hemorrhagic telangiectasia is an inhereted disorder of BVs

blanching lesions or telangiectasia on skin and mucous membranes

recurrent epistaxis
skin discoloration
AV malformation
GI bleeding
Hematuria
217
Q

Hypertrophic cardiomyopathy mutation

A

missense mutation in beta mysoin heavy chain
and
myosin binding protein C

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