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STEP > Cardio > Flashcards

Cardio Flashcards

1
Q

Truncus arteriosus–>

A

Ascending aorta and pulmonary trunk

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2
Q

Bulbus cordis–>

A

smooth parts (outflow tract) of left/right ventricles

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3
Q

Endocardial cushion–>

A

Atrial septum, membranous IV septum, AV and semilunar valves

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4
Q

Primitive atrium–>

A

Trabeculated part of rt/lt atria

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5
Q

Primitive ventricle–>

A

Trabeculated part of rt/lt ventricle

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6
Q

Primitive pulmonary vein–>

A

Smooth part of lt atrium

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7
Q

Left horn of sinus venosus–>

A

coronary sinus

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8
Q

Right horn of sinus venosus–>

A

Smooth part of rt atrium (sinus venarum)

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9
Q

Right common cardinal vein and rt anterior cardinal vein

A

SVC

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10
Q

What part of IV septum most often malformed in VSD?

A

Membranous

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11
Q

Ductus venosus

A

Allows bypass of hepatic circulation

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12
Q

Foramen ovale

A

Allows bypass of pulmonary circulation

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13
Q

Ductus arteriosus

A

Allows blood to leave pulmonary circulation

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14
Q

Closed foramen ovale

A

Fossa ovalis

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15
Q

What causes ductus arteriosus closure?

A

Low prostaglandins – can use indomethacin

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16
Q

Allantois–>

A

Urachus–>mediaN umbilical ligament

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17
Q

Ductus arteriosus–>

A

Ligamentum arteriosum

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18
Q

Ductus venosus–>

A

Ligamentum venosum

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19
Q

Notochord–>

A

nucleus pulposus

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20
Q

Umbilical aa’s–>

A

MediaL umbilical ligaments

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21
Q

Umbilical vvs–>

A

Ligamentum teres hepatis (round ligament) in the falciform ligament

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22
Q

SA and AV nodal blood supply

A

RCA

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23
Q

LCX goes to

A

Lateral/post walls of left ventricle, antlat papillary muscle

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24
Q

LAD goes to

A

Anterior 2/3 of IV septum, anterlat papillary muscle, anterior surface of lft ventricle

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25
Q

PDA goes to

A

AV node, posterior 1/3 IV septum, post 2/3 walls of ventricles, posteromed papilary muslce

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26
Q

Right marginal a goes to

A

Right ventricle

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27
Q

Innervation of pericardium

A

Phrenic n (referred shoulder pain)

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28
Q

CO=

A

SV*HR

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29
Q

Fick principle

A

CO=rate O2 consumed/(art O2-venousO2)

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30
Q

MAP=

A

CO*TPR
or
2/3 diastolic P+1/3systolic P

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31
Q

Pulse pressure

A

Systolic-diastolic

Proportional to SV, inverse proportional to arterial compliance

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32
Q

SV

A

EDV-ESV

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33
Q

Increase pulse pressure states

A

Hyperthyroidism, aortic regurg, aortic stiffening, OSA, exercise

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34
Q

Lower pulse pressure states

A

Aortis stenosis, cardiogenic show, cardiac tamponade, advanced HF

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35
Q

SV increases with…

A

Higher contractility
Higher preload
Lower afterload

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36
Q

Contractility increases with…

A 
B1 activation (calcium channels opened, phospholamban phosphorylation)
Catecholamines
More IC Ca
Lower EC Na
Dig (blocks Na/K pump)
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37
Q

Contractility decreases with…

A 
B1 block (less cAMP)
Loss of myocardium
Dilated cardiomyopathy
HF w/ systolic dysfxn
Acidosis
Hypoxia/hypercapnia
Non DHP Ca channel blockers
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38
Q

Oxygen demand for heart increased with…

A

Increased Contractility
Increased Afterload (proportional to art. P)
Increased hR
Increased Diameter of ventricle

CARD

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39
Q

Wall tension =

Walls stress =

A

Tension= P*r

Stress=(Pr)/(2wall thickness)

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40
Q

Approximation, contributors, pharm affecting preload

A

Ventricular EDV
Depends on venous tone and circulating blood volume
Lowered w/ nitroglycerin (venous vasodil.)

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41
Q

Afterload approximation, pharm affecting

A

MAP

Lowered with arterial vasodilators like hydralazine, ACE inhibs/ARBs (lower preload and afterload)

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42
Q

Response to high afterload

A

LV hypertrophy (increase wall thickness) to decrease wall tension

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43
Q

EF=

A

SV/EDV
or
(EDV-ESV)/EDV
Index of ventricular contractility (lower in systolic HF)

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44
Q

Starling princiciple

A

Force of contraction is proportional to end diastolic length of cardiac muscle fiber (preload) up to a point where the increased tension impedes hearts ability to pump

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45
Q

ChangeP=

A

Q*R

Where Q=volumetric flow rate

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46
Q

Q=

A

Flow velocity(v)*Cross sectional area(A)

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47
Q

R=

A

changeP/Q
or
8n(viscosity)length/(pir^4)
SO RADIUS IS THE BIG VARIABLE

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48
Q

Total resistance in series

A

R=R1+R2+R3…

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49
Q

Total resistance in parallel

A

1/R=1/R1+1/R2+1/R3…

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50
Q

What accounts for most of TPR?

A

Arterioles

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51
Q

What provides storage capacity?

A

Venous circ

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52
Q

a wave

A

Atrial contraction (absent in A fib)

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53
Q

c wave

A

RV contraction (closed tricuspid bulges into atrium)

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54
Q

x descent

A

Downward displacement of close tricuspid valve during rapid vent. ejection phase
Reduced/absent in tricuspid regurg, right HF because lower pressure gradient

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55
Q

v wave

A

Increased RAP due to filling against closed tricuspid valve

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56
Q

Y descent

A

RA emptying into RV
Prominent in constrictive pericarditis
Absent in cardiac tamponade

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57
Q

Wide splitting

A

In conditions that delay RV emptying (e.g. pulmonic stenosis, right branch bundle block)–exaggeration of normal splitting

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58
Q

Fixed splitting

A

Heard in ASD, i.e. lft–>rt shunt–>delayed closure of pulmonic valve

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59
Q

Paradoxical splitting

A

Delay aortic valve closure (aortic stenosis, lft bundle branch block), A2 after P2; On inspiration P2 moves closer to A2 (I.e. split best heard in exhalation)

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60
Q

Inspiration’s effect on heart sounds

A

Increases venous return to rt atrium –> increased intensity of rt heart sounds

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61
Q

Hand grip’s effect on heart sound

A

Increases afterload –> increased intensity of MR, AR, VSD murmurs

  • -> lowered intensity of hypertrophic cardiomyopathy, AS murmurs
  • -> later click in MVP
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62
Q

Valsalva/standing effect on heart sound

A

Decreases preload –> decreased intensity of most murmurs
Increased intensity of hypertrophic cardiomyopathy
Earlier click in MVP

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63
Q

Rapid squatting effect on heart sound

A

Increases venous return, increases preload, increases afterload
Decreased intensity of hypertrophic cardiomyopathy murmur
Increased intensity of AS, MR, VSD
Later click in MVP

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64
Q

Aortic stenosis

A

Crescendo-decrescendo systolic (w/ or w/o ejection click)
Heard loudest at heart base, radiates to carotids
Can lead to syncope, angina, dyspnea on exertion
Usually due to age related calcification or in younger patients with congenital bicuspid aortic valve (e.g. Turners)

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65
Q

Mitral/tricuspid regurg

A

Holosystolic, high pitched, blowing
Mitral – loudest at apex and radiates towards axilla; often due to iscehmic heart disease after MI, MVP, LV dilatation
Tricuspid – loudest at tricuspid area; usually caused by RV dilatation
Can be caused by rheumatic fever/infective endocarditis

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66
Q

MVP

A

Late systolic crescendo w/ mid systolic click (sudden tensing of chordae tendinae) – loudest just before S2
Most frequent lesion, usually benign
Best heard over apex
Causes: myxomatous degeneration (e.g.in Margans), rheumatic HD, chordae rupture

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67
Q

VSD

A

Holosystolic harsh sounding murmur heard best at tricuspid area

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68
Q

aortic regurg

A

High pitched “blowing” early diastolic decrescendo murmur
Long diastolic murmur, hyperdynamic pulse, head bobbing when severe/chronic, wide pulse pressure
Usually due to aortic root dilatation, bicuspid aortic valve, endocarditis, rheumatic fever
Progresses to lft HF

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69
Q

Mitral Stenosis

A

Follows opening snap (abrupt half in leaflet motion in diastole – after rapid opening due to fusion at leaflet tips)
Delayed rumbling mid/late diastolic murmur
(Prognosis worse if closer to S2)
Highly specific for late rheumatic fever and can lead to LA dilatation

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70
Q

PDA

A

Continuous machine-like murmur loudest at S2 – congenital rubella or prematurity; best heard at left infraclavicular area

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71
Q

Phase 0 (myocardium)

A

Rapid upstroke/depol due to opening of voltage gated Na channels

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72
Q

Phase 1 (myocardium)

A

Initital repol due to inactivation of Na channels – voltage gated K channels begin to open

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73
Q

Phase 2 (myocardium)

A

Plateau due to Ca influx through voltage gate Ca channels (balances K efflux) –> triggers Ca release from SR and myocyte contraction

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74
Q

Phase 3 (myocardium)

A

Rapid repolarization due to K efflux – opening of slow K channels and Ca channels close

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75
Q

Phase 4 (myocardium)

A

Resting potential characterized by high K permeability

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76
Q

Phase 0 (nodal)

A

Upstroke due to opening of voltage gated Ca channels, fast voltage gated Na chennels permanently inactivated because resting potential is less negative –> slow conduction velocity to prolong transmission from atria to ventricles

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77
Q

Phase 3 (nodal)

A

Inactivation of Ca channels and increased activation of K channels –> K efflux

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78
Q

Phase 4 (nodal)

A

Slow spontaneous diastolic depol due to If funny current –> slow Na/K inward current; gives automaticity and slope determines HR
Ach/Adenosine decrease rate of diastolic depol/HR
Catecholamines increase rate of diastolic depol/HR (sympathetic stim opens If)

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79
Q

SA node location

A

Near entry of SVC

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80
Q

AV node location

A

Posterinferior part of interatrial septum near opening of coronary sinus

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81
Q

Pacemaker rates

A

SA>AV>bundle of His/Purkinje/Ventricles

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82
Q

Speed of conduction

A

Purkinje>atria>vent>AV node

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83
Q

P wave

A

Atrial depol

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84
Q

QRS

A

Ventricular depol (<120s)

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85
Q

QT interval

A

Vent depol, contraction, repol

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86
Q

T wave

A

Vent repol

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87
Q

J point

A

Jxn between end of QRS and start of ST

88
Q

ST segment

A

Isoelectric – vents are depol

89
Q

U wave

A

Prominent in hypokalemia and bradycardia

90
Q

Causes of Torsades

A 
Low K
Low Mg
Congenital abnormalities (long QT syndrome -- ion channel defects --> risk of SCD and torsades)
Drugs
AntiArrhythmics (IA, III)
AntiBiotics (macrolides)
AntiCychotics (Haloperidol)
AntiDepressants (TCAs)
AntiEmetics (Odansetron)
ABCDE
91
Q

Romano Ward

A

AD pure cardiac congenital long QT syndrome; K channel

92
Q

Jervell Lange Nielsen

A

AR, congenital long QT syndrome w/ sensorineural deafness; K channels

93
Q

Brugada syndrome

A

AD in Asian males; pseudo right branch bundle block w/ ST elevations in V1-V3; increased risk of vent tachyarrhymthias and SCD – give implantable cardioverter-defibrilator

94
Q

Wolff Parkinson White

A

Most common ventricular preexcitation syndrome
Abnormal fast accessory pathway from atria to ventricle (bundle of Kent) that bypasses rate slowing AV node resulting in partial ventricular depol earlier –> delta wave with widened QRS and shorter PR
Can cause reentry circuit –> SVT

95
Q

Risk factors for A fib

A

HTN, CAD

96
Q

1st degree heart block

A

PR >200ms

97
Q

2nd degree type I/Wenckebach HB

A

Progressive lengthening of PR interval until beat dropped

98
Q

2nd degree type II HB

A

Dropped beats not preceeded by change in length of PR interval

99
Q

3rd degree HB

A

Atria and ventricles independent (Arate>Vrate)

Can be caused by lyme disease

100
Q

ANP release from

A

Atrial myocytes in response to increased blood volume/atrial P

101
Q

ANP actions

A

via cGMP –> vasodilation and less Na reabsorption at renal collecting tubule, dilates afferent renal arterioles and contricts efferent –> diuresis and contributes to aldosterone escape

102
Q

BMP release from

A

Ventricular myocytes in response to increased tension

103
Q

Aortic arch receptor

A

Transmits via vagus to solitary nuc of medulla in response to BP change

104
Q

Carotid sinus receptor

A

Transmits via glossopharyngeal (9) to solitary nucleus of medulla in response to BP change

105
Q

Peripheral vs central chemoreceptors

A

Peripheral respond to O2, CO2 and pH while central only CO2 and pH

106
Q

How do you measure LAP?

A

PCWP

107
Q

Heart autoregulation of blood flow

A

Local vasodilatory metabolites: adenosine, NO, CO2, low O2

108
Q

Brain autoregulation of blood flow

A

Local vasodilatory metabolites: Co2 (pH)

109
Q

Kidneys autoregulation of blood flow

A

Mygenic and tubuloglomerular feedback

110
Q

Lungs autoregulation of blood flow

A

Hypoxia –> vasoconstriction (this is weird but maintains ventilation/perfusion match)

111
Q

Skeletal muscle autoregulation of blood flow

A

Local metabolites during exercise: lactate, adenosine, K, H, CO2

112
Q

Skin autoregulation of blood flow

A

Symp stim helps in temp control

113
Q

Net fluid flow equation

A

Jv=Kf[(Pc-Pi)-C(pic-pii))]

Kf = capillary permeatbility to fluid

114
Q

Right to left shunts

A 
Truncus arteriosus (1 vessel)
Transposition (2 switched vessels)
Tricuspid atresia
Tetralogy of fallot
TAPVR
(5Ts)
115
Q

Persistent truncus arteriosus

A

Doesn’t divide into aorta/pulmonary trunk due to lack of aorticopulmonary septum formation (usually accompanied by VSD)

116
Q

D-transposition of great vessels

A

Septation did not spiral – must have shunt present for mixing w/ blood

117
Q

Tricuspid atresia

A

Absence of tricuspid valve and hypoplastic RV (requires ASD and VSD)

118
Q

Tetralogy of fallot

A

Anterior superior displacement of infundibular septum – most common cause of early childhood cyanosis
-Pulmonary infundibular stenosis/RVOTO (PROGNOSIS!)
-Right ventricular hypertrophy (boot shaped heart)
-Overriding aorta
-VSD
Squatting –> increases SVR –> less right/left shunt (higher left sided pressure) –> improves cyanosis

119
Q

TAPVR

A

Total anomalous pulmonary venous return

Pulonary veins drain into right heart – assoc w/ ASD/PDA to allow right–>left shunting to maintain CO

120
Q

Ebstein anomaly

A

Displacement of tricuspid vavle leaflets down into RV, “atrializing” the ventricle –> tricuspid regurg and right HF
Assoc w/ utero Li exposure

121
Q

Left to right shunts

A

VSD>ASD>PDA

122
Q

ASD

A

Loud S1, wide fixed split S2

Ostium secundum defects are common

123
Q

Eisenmenger syndrome

A

Uncorrected left–>rt shunt –> increased pulmonary blood flow –> pathologic remodeling of vascularture –> pulmonary arterial HTN–>RVH to compensate–>rt to lft shunt (reversed) –> late cyanosis, clubbing, polycythemia

124
Q

Coarc of aorta

A

Aortic narrowing near insertion of ductus arteriosus
Assoc w/ bicuspid aortic valve, Turner syndrome
HTN in upper extremities and weak lower extremity pulses
W/ time intercostal aas enlarge to create collateral circ –> erode into ribs –> notched appearance on CXR
Complications: HF, increased risk of cerebral hemorrhage (berry aneurysm), aortic rupture, endocarditis

125
Q

Alcohol exposure in utero–>

A

VSD, PDA, ASD, tet oF

126
Q

Congenital rubella–>

A

PDA, pulm a. stenosis, septal defects

127
Q

Diabetes in mother –>

A

Transposition of great vessels

128
Q

DS–>

A

AVSD (endocard cushion defect), VSD, ASD

129
Q

Marfan –>

A

MVP, thoracic aortic aneurysm and dissection, aortic regurg

130
Q

Li exposure in utero–>

A

Ebstein anomaly

131
Q

Turner syndrome–>

A

Bicuspid aortic vavle, coarc

132
Q

Williams syndrome

A

Supravalvular aortic stenosis

133
Q

22q11 syndromes–>

A

Truncus arteriosus, Tet oF

134
Q

Hypertensive urgency

A

> 180/>120 w/ no end organ damage

135
Q

Hypertensive emergency

A

evidence of acute end organ damage – encephalopathy, stroke, retinal hemorrhages/exudates, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia

136
Q

HTN predisposes to

A

CAD, LVH, HF, a fib, aortic dissection, aortic aneurysm, stroke, CKD (hypertensive nephropathy), retinopathy

137
Q

Hyaline arteriolosclerosis

A

Thickening of vessel walls as in essential HTN or diabetes

138
Q

Hyperplastic arteriolosclerosis

A

Onionskinning in in severe HTN w/ proliferation of smooth muscle cells

139
Q

Monckeberg sclerosis

A

Aka medial calcific sclerosis – medium sized arteries
Calcifications of internal elastic lamina and media –> vascular stiffening without obstruction
Pipstem appearance on x ray, does not obstruct blood flow and intima NOT involved

140
Q

Atherosclerosis

A

Large/medium sized muscular arteries – arteriolosclerosis caused by cholesterol plaques

141
Q

Location of atherosclerosis

A

Abdominal aorta>coronary artery>popliteal artery>carotid artery

142
Q

GF involved in smooth muscle cell migration in atherosclerosis

A

FGF, PDGF

143
Q

Abdominal aortic aneurysm risk factors and sxs

A

Atherosclerosis, tobacco use, age, male, family hx

Present: palpable pulsatile abdominal mass

144
Q

Thoracic aortic aneurysm risk factors

A

Assc w/ cystic medial degeneration, risk factors: HTN, bicuspid aortic valve, Marfans, 3o syphillis (obliterative endarteritis of the vasa vasorum) –> aortic root dilatation –> aortic regurg

145
Q

Traumatic aortic rupture

A

Trauma/deceleration injury –> at aortic isthmus most often (just distal to origin of lft subclav a.)

146
Q

Associations w/ aortic dissection

A

HTN, bicuspid aortic vavle, connective tissue disorders

147
Q

Aortic dissection presents

A

Tearing sudden pain radiating to back, can have unequal BP in arms, CXR shows mediastinal widening

148
Q

Types of aortic dissection

A

Stanford A: proximal –> ascending aorta, may extend to aortic arch or descending, may cause acute aortic regurge or tamponade (REQ SURG)
Stanford B: distal –> only descending aorta (Tx w/ B blockers and then vasodilators)

149
Q

Risk factors for prinzmetal angina

A

Smoking (not HTN or hypercholestrol)

150
Q

Coronary steal

A

Give a vasodilator and causes dilation in normal coronary vessels rather than stenosed; pharm stress tests

151
Q

STEMI

A

Transmural w/ ST elevation

152
Q

NSTEMI

A

Subendocardial infarct w/ ST depression

153
Q

First 24 hours post MI

A

Wavy fibers –> neutrophils appear; complications: Vent arrhythmia, HF, cardiogenic shock

154
Q

1-3 days post MI

A

Extensive coag necrossis w/ neutrophils; complication postinfarction fibrinous pericarditis

155
Q

3-14 days post MI

A

Macrophages and then granulation tissue; complications: free wall rupture –> tamponade, papillary m rupture –> mitral regurge, IV septal rupture (macrophage mediated structural degradation), LV pseudoaneurysm

156
Q

2 weeks-months post MI

A

Contracted scar; complications: Dressler syndrome, HF, arrhthmias, true vent aneurysm (mural thrombus)

157
Q

Troponin rises in x hours and peaks at x hours then remains elevated for x days

A

4, 24, 7-10

158
Q

CK-MB rises in X hours, peaks at X hours, returns to normal in X hours

A

6-12, 16-24, 48 – making it good to follow

159
Q

Anteroseptal MI

A

LAD – V1-V2

160
Q

Anteroapical MI

A

distal LAD – V3-V4

161
Q

Anterolateral MI

A

LAD or LCX – V5-V6

162
Q

Lateral MI

A

LCX – I, aVL

163
Q

Inferior MI

A

RCA–II, III, aVF

164
Q

Posterior MI

A

PDA V7-V9; depression in V1-3 w/ tall R waves

165
Q

Tx for NSTEMI/unstable angina

A

Anticoag, antiplt, ADP receptor inhib (clopedogrel), B blocker, ACE inhib, statins, symptoms controlled w/ nitroglyerin and morphin

166
Q

Tx for STEMI

A

NSTEMI + Reperfusion therapy

167
Q

Dilated cardiomyopathy causes

A

Alcohol, wet Beriberi, Coxsacki B viral myocarditis, chornic Cocaine use, Chagas, Doxorubicin, hemochromatosis, sarcoidosis, peripartum cariomyopathy

ABCCCD

168
Q

Findings in dilated cardiomyopathy

A

HF, S3, regurg murmur, dilated heart on echo, balloon appearance on CXR; leads to systolic dysfuction, eccentric hypertrophy

169
Q

Tx for dilated cardiomyopathy

A

Na restriction, ACE inhib, B blockers, diuretics, dig, ICD, heart transplant

170
Q

Takotsubo cardiomyopathy

A

Ventricular apical balooning due to increased sypathetic stim (stress)

171
Q

Hypertrophic cardiomyopathy causes

A

Mostly familial – mutations in sarcomeric proteins like myosin binding prot C and beta myosin heavy chain, assc w/ Freidrich ataxia

172
Q

Hypertrophic cardiomyopathy sx

A

Syncope during exercise, can lead to sudden death, S4, systolic murmur, mitral regurge due to impaired mitral valve closure; leads to diastolic dysfxn; has marked concentric hypertrophy and myofibrillar disarray/fibrosis

173
Q

Hypertrophic obstructive cardiomyopathy

A

Hypertrophic CM w/ asymmetric septal hypertrophy/systolic anterior motion of mitral valve–>outflow obstruction–>dyspnea, syncope

174
Q

Tx of hypertrophic CM

A

Cessation of high-intensity athletics, Bblockers or nonDHP CCBs, ICD if high risk

175
Q

Restrictive/infiltrative CM causes

A

Postradiation fibrosis, Loffler syndrome, Endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), amyloidosis, sarcoidosis, hemochromatosis (though more often dilated)
Puppy LEASH

176
Q

Restrictive/infiltrative CM results in

A

Diastolic dysfxn – low voltage ECG despite thick myocardium (esp w amyloid)

177
Q

Loffler endocarditis

A

Assc. w/ hypereosinophilic syndrome; histology shows eosinophilic infiltrate in myocardium

178
Q

HF syndrome

A

Cardiac pump dysfxn –> congestion, low perfusion; sx: dyspnea, orthopnea, fatigue, S3, rale, JVD, pitting edema

179
Q

Systolic dysfxn

A

Reduced EF, higher EDV, lower contractility (2o to ischemia/MI or dilated CM)

180
Q

Diastolic dysfxn

A

Preserved EF, normal EDV, lower compliance (2o to myocardial hypertrophy)

181
Q

Drugs that decrease mortality in HF

A

ACE Inhibs or ARBs, B blockers (EXCEPT acute decomp), spirinolactone

182
Q

Hypovolemic shock causes

A

Hemorrhage, dehydration, burns

183
Q

Hypovolemic shock skin, PCWP, CO, SVR

A

Cold clammy skin
Much lower PCWP (preload)
Lower CO
Increased SVR

184
Q

Tx of hypovolemic shock

A

IV fluids

185
Q

Cardiogenic shock causes

A

Acute MI, HF, valvular dysfxn, arrhythmia

186
Q

Obstructive shock causes

A

Cardiac tamponade, PE, tension pneumothorax

187
Q

Cardiogenic/obstructive skin, PCWP, CO, SVR

A

Cold, clammy skin
PCWP can go either way
CO much lower
SVR goes up

188
Q

Tx of cardiogenic shock

A

Inotropes, diuresis

189
Q

Tx of obstructive shock

A

Relieve obstruction

190
Q

Distributive shock cause

A

Sepsis, anaphylaxis, CNS injury

191
Q

Sepsis/anaphylaxis shock skin, PCWP, CO, SVR

A

Skin warm
Lower PCWP
Higher CO
Much lower SVR

192
Q

CNS injury shock skin, PCWP, CO, SVR

A

Skin dry
Lower PCWP
Lower CO
Much lower SVR

193
Q

Tx of distributive shock

A

IV fluids, presors

194
Q

Roth spot

A

White spot on retina surrounded by hemorrhage, found in bacterial endocarditis

195
Q

Osler nodes

A

Painful notes on fingers. toe pads due to immune complex deposition, found in bact ECitis

196
Q

Janeway lesions

A

Small, painless erythematous lesions in palm or sole, found in bact ECitis

197
Q

Most common bact. endocarditis buts

A

Acute: s.auerus (large veg on perviously normal valve, rapid onset)
Subacute: viridians strep – smaller veg on damaged/abnormal valve after dental procedure, gradual onset
S bovis in colon cancer
S. epi on prosthetic valves

198
Q

Causes of NBTE

A

Malignancy, hypercoagulable state, lupus

199
Q

Most frequently involved valve in Bact EC itis

A

Mitral

200
Q

Tricuspid valve ECitis associations

A

IVDU, S. aureus, Pseudomonas, candida

201
Q

Culture negative ECItis bugs

A

Coxiella burnietti, Bartonella, HACEK (Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella)

202
Q

Early and late lesion in rheumatic fever

A

Early – mitral regurg

Late – mitral stenosis

203
Q

Histology of rheumatic fever

A

Aschoff bodies (granduloma) and Anitschkow cells (large macs w/ ovoid/wavy rod-like nucleus)

204
Q

Type of hypersensitivity of RF

A

Type II (abs to M protein cross react – molecular mimicry)

205
Q

Tx/prophylaxis of RF

A

Penicillin

206
Q

JONES criteria

A 
Joint (migratory polyarthritis)
Oheart (carditis)
Nodules in skin (subcutaneous)
Erythema marginatum
Sydenham chorea
207
Q

Presentation of acute pericarditis

A

Sharp pain aggravated by inspiration and relieved by sitting up/leaning forward, friction rub, widespread ST segment elevation or PR depression; can have effusion

208
Q

Acute pericarditis causes

A

Idiopathic (most, probably viral), confirmed infxn (e.g. coxsackie), neoplasia, autoimmune (e.g. SLE, RA), uremia, cardiovascular (acute STEMI, Dressler), radiation

209
Q

Cardiac tamponade findings

A

Beck triad (hypotension, distended neck veins, distant heart sounds), increased HR, pulsus paradoxus (large lowered BP on inspiration), low voltage QRS and electrical alternans

210
Q

Where is pulsus paradoxus seen?

A

Cardiac tamponade, asthma, OSA, pericarditis, croup

211
Q

3o syphillis effect on heart

A

Disrupts vasa vasorum–>dilatation of aorta and valve ring–>atrophy of vessel wall (looks like tree bark)
May see calcification of aortic roots, ascentidng archm thoracic aorta, aneurysm of ascending aorta, arch or aortic insufficiency

212
Q

Most common heart tumor

A

Metastatis

213
Q

Most common primary cardiac tumor in adults

A

Myxoma – ball vavle ovstruction in lft atrium assc w/ syncopal episodes, may auscultate plop

214
Q

Myxoma histology

A

Myxioid gelatinous material, myxoma cells in GAGs

215
Q

Most frequent cardiac tumor in kiddos

A

Rhabdomyoma (assc w/ tuberous sclerosis) – basically a hamartoma

216
Q

Kussmaul sign

A

Increased JVP on inspiration (normal is decreased)

Seen w/ constrictive pericarditis, restrictive cardiomyopathies, right atrial/ventricular tumors

STEP (15 decks)

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