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Cardiology > Cardiology Part 2 > Flashcards

Cardiology Part 2 Flashcards

1
Q

Warfarin Interactions

A

x

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2
Q

increase warfarin effect (increase INR)

A

x

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3
Q

what are examples of drugs that increase warfarin effects?

A

metronidazole, quinolones, azoles, amiodarone, acetaminophen

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4
Q

mechanism

A

x

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5
Q

by what mechanism does metronidazole and quinolones increase warfarin effect?

A

alteration of intestinal flora

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6
Q

by what mechanism does azoles and amiodarone increase warfarin effect?

A

CYP2C9 inhibition

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7
Q

how do you adjust dose of warfarin for someone starting amiodarone?

A

reduce warfarin by 25-50%, monitor the INR closely for several weeks

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8
Q

by what mechanism does acetaminophen increase warfarin effect?

A

decrease vitamin K recycling

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9
Q

decrease warfarin effect (decrease INR)

A

x

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10
Q

what are examples of drugs that decrease warfarin effects?

A

rifampin , phenytoin, SJW (st john’s wort), oral contraceptives, green leafy vegetables

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11
Q

mechanism

A

x

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12
Q

by what mechanism does rifampin, phenytoin, SJW decrease warfarin effect?

A

CYP2C9 induction

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13
Q

by what mechanism does OCP decrease warfarin effect?

A

increase coagulation factors

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14
Q

by what mechanism does green leafy vegetables decrease warfarin effect?

A

increase vitamin K ingestion

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15
Q

INR independent interaction

A

x

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16
Q

what drugs have an INR independent interaction with warfarin?

A

NSAIDs, clopidogrel, ginkgo biloba

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17
Q

mechanism

A

x

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18
Q

by what mechanism do NSAIDs and clopidogrel interact with warfarin?

A

inhibition of platelet fxn

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19
Q

by what mechanism do Ginkgo biloba interact with warfarin?

A

increase bleeding (unknown mechanism)

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20
Q

Cardiogenic Syncope

A

x

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21
Q

syx

A

x

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22
Q

what is the syx of cardiogenic syncope?

A

loss of consciousness w/o prodromal symptoms. Palpitations prior to an episode of syncope or absence of preceding autonomic prodromal symptoms (likely due to Vtach)

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23
Q

what are clues of a benign vasovagal syncope event?

A

presence of autonomic prodromal syx (eg nausea, pallor, diaphoresis, feeling warmth)

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24
Q

causes

A

x

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25
Q

causes of cardiogenic syncope?

A

aortic stenosis or HCM, VTach, Sick Sinus Syndrome, Advanced AV block, Torsades de pointes

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26
Q

clues of type of cardiogenic syncope

A

x

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27
Q

exterional syncope, systolic murmur on exam?

A

aortic steonosis or HCM

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28
Q

preceding fatigue or dizzines, sinus pauses on EKG?

A

Sick sinus syndrome

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29
Q

bifascicular block on EKG, dropped QRS complexes on EKG?

A

Advanced AV Block

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30
Q

No preceding syx, medications that prolong QT interval , hypokalemia or hypomagnesemia?

A

Torsades de pointes

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31
Q

Ventricular Tachycardia

A

x

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32
Q

syx

A

x

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33
Q

what are the syx of VTach?

A

absence of prodromal syx leading to syncope

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34
Q

no preceding syx, hx of cardiomyopathy or previous MI?

A

VTach

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35
Q

risk

A

x

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36
Q

what other clues specifically suggest VTach?

A

presence of underlying structural heart disease (eg ischemic scarring, cardiomyopathy w low EF)

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37
Q

dx

A

x

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38
Q

what should be done after suspcion of VTach in a patient?

A

admitted to hospital to undergo telemetry (to detech arrhythmia) and echocardiography (to evaluate LVF and identify wall motion abnormalities)

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39
Q

trx

A

x

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40
Q

what is the trx of VTach?

A

combination of amiodarone , catheter ablation, or placement of ICD

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41
Q

complicaitons

A

x

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42
Q

what is a very serious complicaiton of VTach?

A

sudden cardiac death

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43
Q

Vasovagal Syncope (neurocardiogenic syncope)

A

x

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44
Q

syx

A

x

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45
Q

what are the syx of vasovagal syncope?

A

sudden neurocardiogenic LOC usually with prodrome

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46
Q

what are the other prodromal symptoms associated with vasovagal syncope?

A

pallor, nausea, diaphoresis, generalized warmth. Consciousness regained rapidly (eg <1 minute)

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47
Q

what is a common neurocardiogenic syncope symptom that can help distinguish from more serious etiologies of syncope (eg cardiogenic)

A

autonomic prodrome of (nausea, pallor, diaphoresis, generalized warmth, and fatigue) following the syncope that persist for a brief period

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48
Q

pathophys

A

x

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49
Q

what is the pathophys of vasovagal syncope?

A

sudden stress or pain causing a decreased sympathetic drive (leading to vasodilation) combined with an increased parasympathetic response (causing bradycardia)

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50
Q

cause

A

x

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51
Q

what is the cause of vasovagal syncope?

A

prolonged standing, emotional stress

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52
Q

dx

A

x

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53
Q

how is the diagnosis made?

A

mainly clinical diagnosis, upright til table testing in uncertain cases (helps distinguish neurocardiogenic from orthostatic)

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54
Q

trx

A

x

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55
Q

what is the treatment?

A
  • reassurance and discharge home with syncope education.
  • avoidnce of triggers
  • counterpressure techniques for recurrent episodes (assume supine position with raised legs, leg crossing with tensing of muscles, tensing of arm muscles with clenched fists)
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56
Q

Hemodynamic measurements in Shock

A

x

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57
Q

measurements

A

x

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58
Q

what are normal parameter measurements for hemodynamics?

A 
RA pressures (preload)= 4mmHg
PCWP (preload)= 9mmHg
Cardiac Index (pump fxn)= 2.8-4.2
SVR (afterload)= 1,150 dyne-sec/cm5
MvO2 (mixed venous oxygen saturation)= 60-80%
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59
Q

Hypovolemic Shock

A

x

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60
Q

how do the measurements change in hypovolemic shock?

A 
RA pressure decrease, 
PCWP decrease, 
Cardiac index decrease
SVR increase
MvO2 decrease
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61
Q

how do the measurements change in cardiogenic shock?

A 
RA pressure increase, 
PCWP increase, 
Cardiac index very much decrease
SVR increase
MvO2 decrease
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62
Q

how do the measurements change in septic shock or neurogenic shock (distributive shock)?

A 
RA pressure normal or decrease, 
PCWP normal or decrease, 
Cardiac index increase
SVR decrease
MvO2 increase
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63
Q

how do the measurements change in cardiac tamponade?

A

increase in right atrial and ventricular pressures, along with equalization of right atrial, right ventricular end diastolic, and PCWPs

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64
Q

how do the measurements change in pulmonary embolus?

A

elevated right atrial, right ventricular, and pulmonary artery pressures. Increased Cardiac index. PCWP and SVR unaffected

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65
Q

Cardiogenic Shock

A

x

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66
Q

syx

A

x

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67
Q

what are the symptoms of cardiogenic shock?

A

CP, tachycardia, hypotension

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68
Q

risk

A

x

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69
Q

what are the risks of cardiogenic shock?

A

recent complicated PCI

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70
Q

pathophys

A

x

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71
Q

what is the pathophys of cardiogenic shock?

A

abrupt coronary occlusion leading to impaired contractility of the involved myocardium

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72
Q

Perioperative Medication Management

A

x

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73
Q

management

A

x

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74
Q

what drug class when withdrawn can cause HTN, and should be continued during surgery?

A

beta blockers

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75
Q

what drug class when withdrawn can cause HTN, and should be continued during surgery?

A

alpha 2 agonist (eg clonidine)

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76
Q

what drug class when used can cause slightly increased risk of bleeding, and should be continued during surgery?

A

CCB

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77
Q

what drug class when used can cause hypotension, and should be continued during surgery for CHF patients and held the night before for all other patients?

A

ACEi

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78
Q

what drug class when used can cause hypovolemia and hypotension, and should be continued up to day of surgery and hold that morning?

A

diuretics

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79
Q

what drug class when used can cause slight riks of myopathy , and should be continued during surgery?

A

statins

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80
Q

what drug class when used can cause increased risk of dVT, and should be discontinued 4 weeks prior to any surgical procedure (eg knee replacement)?

A

SERM (both raloxifene and tamoxifen)

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81
Q

Aortic Injury

A

x

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82
Q

cause

A

x

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83
Q

what is the common cuase of death after MVA?

A

steering wheel injuries leading to aortic injury

84
Q

pathophys

A

x

85
Q

what is the pathophys of aortic injury?

A

rapid deceleration produces a shearing force along the aortic arch where the aorta is firmly attached (usually observed in the area of the ligamentum aretriosum, aortic root, and diaphragmatic hiatus).

86
Q

Peripheral Edema

A

x

87
Q

cause

A

x

88
Q

what is a common cause of LE edema?

A

CCB (amlodipine and nifedipine&raquo_space;> dilitizama and verapamil)

89
Q

pathophys

A

x

90
Q

what is the pahthophys of CCB causing LE edema?

A

related to preferential dilation of precapillary vessels (arteriolar dilation) which leads to increased capillary hydrostatic pressure and fluid extravasation into the interstitium.

91
Q

side effects

A

x

92
Q

what are other side effects of CCB?

A

headache, flushing, dizziness

93
Q

Glyburide

A

x

94
Q

side effects

A

x

95
Q

what are side effects of glyburide?

A

photosensitivity reactions, maculopapular eruptions, purpura, or urticaria

96
Q

HCTHz (hydrochlorothiazide)

A

x

97
Q

side effects

A

x

98
Q

what are side effects of HCTHz?

A

hyponatremia, hypokalemia, renal failure, hyperuricemia (may percipitate gout), and elevated glucose and lipids

99
Q

ACEi (eg enalapril) Ace Inhibitors

A

x

100
Q

side effects

A

x

101
Q

what are side effects of ACEi?

A

nonpitting swelling of the subQ or submucosal tissue and affect lips, tongue, face, and upper airway

102
Q

Cardiac Tamponade

A

x

103
Q

cause

A

x

104
Q

what are the causes of cardiac tamponade?

A
  • aortic aneurysm or postmyocardial infarction
  • malignancy or radiation therapy
  • infxn (viral, TB)
  • CTD (SLE)
  • Cardiovascular surgery
105
Q

signs

A

x

106
Q

what are the clinical signs of cardiac tamponade?

A
  • beck triad: hypotension, JVD, decreased heart sounds

- pulsus paradoxus (SBP decreased >10 mm Hg with inspiration)

107
Q

PE

A

x

108
Q

what is the classic physical exam findings of constrictive pericarditis, restrictive cardiomyopathy but rarely seen in cardiac tamponade?

A

Kussmaul sign (abnormal increase or lack of a decrease) in JVP during inspiration

109
Q

what is a classic physical exam finding in cardiac tamponade?

A

pulsus paradoxus : an exaggerated drop in SBP >10 mmHg due to bowing of the right ventricle into the left ventricle during inspiration

110
Q

dx

A

x

111
Q

what does the EKG show for cardiac tamponade?

A

low voltage QRS, electrical alternans

112
Q

what does the CXR show for cardiac tamponade?

A

enlarged cardiac silhouette, clear lungs

113
Q

what does the echo show for cardiac tamponade?

A

right atrial and ventricular collapse, plethora of the IVC

114
Q

what is the most specific findings of echo tamponade physiology?

A

early diastolic collapse of the right ventricle and right atrium

115
Q

what are other findings on echo of cardiac tamponade?

A

exaggerated respiratory variation of cardiac and venous flow and plethora of the IVC with lack of inspiratory collapse

116
Q

pathophys

A

x

117
Q

what is the pathophys of cardiac tamponade?

A

impaired diastolic filling of the right side of the heart, as the pericardial effusion increases hypotension and distant heart sounds can eventually develop

118
Q

syx

A

x

119
Q

what are the syx of cardiac tamponade?

A

progressive dyspnea, fatigue, LE edema

120
Q

trx

A

x

121
Q

what is the trx of cardiac tamponade?

A

removal of pericardial fluid, which can be performed with catheter pericardiocentesis or surgical pericaridal window

122
Q

Jugular Venous Pulsation

A

x

123
Q

define

A

x

124
Q

what is the Jugular venous pulsation tracing?

A

you have a tracing of jugular veins blood flow as the right atrium fills and contracts

125
Q

signs

A

x

126
Q

what does the tracing look like on paper?

A

peak a wave then a drop x descent, with a bump c wave on the way down to x. So rise with a then c bump as you drop with x, then v bump up then y descent

127
Q

what does a represent?

A

right atrial contraction

128
Q

what does c represent?

A

bulgin of tricuspid valve during right ventricular contraction

129
Q

what does x represent?

A

right atrial relaxation

130
Q

what does v represent?

A

continued inflow of venous blood

131
Q

what does y represent?

A

passive emptying of the right atrium after tricuspid valve opening

132
Q

Klinefelter Syndrome

A

x

133
Q

genetics

A

x

134
Q

what is the genetics of Klinefelters Syndrome?

A

47, XXY

135
Q

PE

A

x

136
Q

what are the physical exam findings of Klinefelter Syndrome?

A

gynecomastia , small or cryptoorchid testes

137
Q

Multifocal Atrial Tachycardia (MAT)

A

x

138
Q

cause

A

x

139
Q

what are the causes of MAT?

A
  • Exacerbation of pulmonary disease (eg COPD)
  • Electrolyte disturbance (eg hypokalemia, hypomagnesemia)
  • Catecholamine surge (eg sepsis)
140
Q

syx

A

x

141
Q

what are the syx of MAT?

A

typically asyx, may have palpitations, but may have progressive SOB and cough productive of yellowish sputum that is underlying lung disease

142
Q

PE

A

x

143
Q

what are phsyical exam findings of MAT?

A

rapid, irregular pulse

144
Q

dx

A

x

145
Q

what is the dx finding on EKG?

A

> = 3 P wave forms and atrial rate >100 bpm, irregular R-R waves

146
Q

trx

A

x

147
Q

what is the treatment of MAT?

A
  • correct underlying disturbance (administer bronchodilators, systemic corticosteroids, and noninvasive ventilation)
  • AV nodal blockade (eg verapamil) if persistent
148
Q

epid

A

x

149
Q

most commonly MAT is seen in which population?

A

elderly (> 70 yo)

150
Q

Mobitz Type II 2nd Degree AV block

A

x

151
Q

dx

A

x

152
Q

what is the classic finding of EKG for mobitz type II 2nd degree AV block?

A

intermittent nonconducted P waves and a regular PR interval

153
Q

causes

A

x

154
Q

what are the casues of mobitz type II 2nd degree AV block?

A

ischemia, electrolyte abnormalitites, medications (eg beta blockers, verapamil and diltiazam, infiltrative disease (eg sarcoidosis), or age related fibrosis can lead to impaired electrical conduction across the AV node

155
Q

syx

A

x

156
Q

what are the symptoms of Mobitz Type II 2nd Degree AV block?

A

dyspnea, lightheadedness, syncope

157
Q

complication

A

x

158
Q

what is a major concern of mobitz type II 2nd degree AV Block?

A

third degree AV block

159
Q

trx

A

x

160
Q

what is the treatment of mobitz type II 2nd degree AV block?

A

permanent pacemaker, in the absence of reversible causes like hyperkalemia, MI, pharmacological AV nodal blockade)

161
Q

what should always be done in the setting of AV block where there is suspicion for ischemia as a reversible cause prior to cath?

A

temporary pacemaker

162
Q

Predictors of Major Cardiac Complications with noncardiac surgery (Revised Cardiac Risk Index)

A

x

163
Q

clinic risk factors

A

x

164
Q

what are clinical risk factors for Revised Cardiac Risk Index?

A
  • high risk surgery (eg vascular)
  • hx of ischemic heart disease
  • heart failure
  • hx of stroke
  • DM treated with insulin
  • preop Creatinine >2 mg/dL
165
Q

what is the rate of cardiac death, nonfatal cardiac arrest, or nonfatal MI in RCR-I?

A

no risk factors: 0.4%
1 risk factor: 1.0%
2 risk factor: 2.4%
>=3 risk factors: 5.4%

166
Q

cardiac risk stratification for noncardiac surgical procedures

A

x

167
Q

risk of cardiac death or non fatal MI categories

A

x

168
Q

high risk (>5%) type of surgery

A
  • aortic or other major vascular surgery

- peripheral vascular

169
Q

intermediate risk (1-5%) type of surgery

A
  • CEA
  • head and neck
  • intraperitoneal and intrathoracic
  • orthopedic
  • prostate
170
Q

low risk (<1%) type of surgery

A
  • ambulator or superficial procedure
  • endoscopic procedure
  • cataract
  • breast
171
Q

Active Cardiac Conditions that increase perioperative cardiovascular risk

A

x

172
Q

requires further evaluation and treatment before noncardiac surgery

A
  • unstable angina or recent MI
  • decompensated heart failure
  • significant arrhythmia (symptomatic bradycardia, high grade AV block, SVT, symptomatic or new onset VT)
  • Severe valvular disease (severe aortic stenosis, syx mitral stenosis)
173
Q

how to assess if patient has reduced functional capacity if they are undergoing potential low, medium, or high risk surgery ?

A

excercise capacity <4 METS (inaibility to climb 2 flights of stairs),

174
Q

Clinical Risk Assessment of Preop Cardiac Eval for Noncardiac Surgery

A

x

175
Q

if there is an active high risk cardiac condition (eg Unstable Angina, decompensated HF), then what is the next step?

A

stabilize prior to surgery

176
Q

if there is a low risk surgery and no active high risk cardiac surgery, then what?

A

proceed to surgery

177
Q

if there is a low risk surgery and patient RCRI <= 1%, then what?

A

proceed to surgery

178
Q

if there is a low risk surgery and patient RCRI <= 1%, and able to perform >=4 METS then what?

A

proceed to surgery

179
Q

if not a low risk surgery, RCRI >=1%, unable to perform >=4 METS, then what?

A

no further cardiac evaluation prior to surgery (eg TTE, stress testing)

180
Q

Acquired Long QT Syndrome (LQTS)

A

x

181
Q

causes

A

x

182
Q

what are the medications causing acquired long QT syndrome?

A

-diuretics (due to electrolyte imbalances)
-antiemetics (eg ondansetron)
-antipsychotics (eg haloperidol, quetiapine, risperidone)
-TCA
-SSRI (eg citalopram)
-Antiarrhythmics (eg amiodarone, sotalol, flecainide)
-antianginal drugs (eg ranolazine)
-

183
Q

what are the metabolic disorders causing long QT syndrome?

A
  • electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia)
  • starvation
  • hypothyroidism
184
Q

what are the bradyarrhythmias that cause long QT syndrome?

A
  • sinus node dysfunction

- AV block (2nd or 3rd degree)

185
Q

what are the other causes of long QT syndrome?

A
  • hypothermia
  • myocardial ischemia/infarction
  • intracranial disease
  • HIV infection
186
Q

Torsade de Pointes (TdP)

A

x

187
Q

dx

A

x

188
Q

what does the EKG show for TdP?

A

most commonly precipitated by PVC beats followed by a compensatory pause (short long RR intervals) that initiates the cycle of VT

189
Q

cause

A

x

190
Q

what is an unusual cause of LQTS (long QT syndrome leading to torsades)?

A

adrenergic surge (excercise or sudden arousal) in some patients with certain congenital forms of LQTS

191
Q

syx

A

x

192
Q

what are the symptoms of torsades de Pointes?

A

2 episodes of LOC associated with seizure like activity

193
Q

trx

A

x

194
Q

what is the treatment for torsade de Pointes? what if they have normal mag levels?

A

IV magnesium sulfate, still give IV MgSO4

195
Q

if they don’t respond to IV MgSO4, what would you give?

A

temporary transvenous pacing

196
Q

complication

A

x

197
Q

if patients have recurrent episodes of TdP in rapid succession, what happens?

A

risk of degenerating into Vfib and death

198
Q

Varicose Veins

A

x

199
Q

define

A

x

200
Q

what are varicose veins?

A

visible, palpable, and tortuous superficial veins of the legs usually on the calf or medial thihg

201
Q

syx

A

x

202
Q

what are the symptoms of varcose veins?

A

asyx but can include leg cramping, heaviness, fatigue, and swelling. Symptoms get worse in the evening w prolonged standing and improve with leg elevation

203
Q

trx

A

x

204
Q

what is the treatment for varicose veins?

A

aimed at alleviating syx:
first line= leg elevation, compression stockings,
second line= sclerotherapy, and surgical ligation

205
Q

when do you use second line trx for varicose veins?

A

in patients with large syx varicose veins with ulcers, bleeding, or recurrent thrombophlebitis of the veins

206
Q

when is injection sclerotherapy w or without anesthetics used?

A

symptomatic , small, varicose veins in patients who have failed >=3 - 6 months of conservative treatment

207
Q

when are compression stockings contraindicated?

A

in patients with arterial insufficiency

Cardiology (7 decks)

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