Cardiology part 4 Flashcards

1
Q

Antiplatelet therapy after Coronary Stenting

A

x

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2
Q

trx

A

x

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3
Q

what is the recommended duration of therapy antiplatelet therapy after coronary stenting?

A
  • DAPT (dual antiplatelet therapy=aspirin + P2Y12 receptor blocker) for minimum of 6-12 months after Bare Metal stent or Drug eluting stent placement
  • DAPT for minimum of 4 weeks in select patients after BMS
  • Continue DAPT for a total of 30 months if pos
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4
Q

what is perioperative management of antiplatelet therapy after coronary stenting if elective surgery?

A

defer surgery until after minimum DAPT duration

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5
Q

what is perioperative management of antiplatelet therapy after coronary stenting if urgent surgery?

A

continue P2Y12 receptor blocker or hold for shortest duration possible

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6
Q

what is perioperative management of antiplatelet therapy after coronary stenting if high risk of severe surgical bleeding?

A

continue aspirin unless high risk of severe surgical bleeding

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7
Q

Trastuzumab

A

x

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8
Q

side effects

A

x

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9
Q

what are the side effects of trastuzumab?

A

cardiotoxicity

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10
Q

what is the incidence of cardiotoxicity?

A

5% with trastuzumab monotherapy, but it is 25% with trastuzumab combined with anthracycline (eg doxorubicin) and cyclophosphamide.

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11
Q

MOA

A

x

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12
Q

how does trastuzumab work?

A

monoclonal Ab that targets HER2

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13
Q

managment

A

x

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14
Q

what is the management of trastuzumab only cardiotoxicity?

A

reversible

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15
Q

what is the management of chronic anthracycline + trastuzumab cardiotoxicity?

A

not reversible because dose related due to myocyte necrosis , destruction, and replacement of fibrous tissue

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16
Q

when should you hold trastuzumab?

A
  • if CHF develops

- if LVEF decreases by >=16% from baseline, or by 10-15% from baseline to below the lower limits of normal

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17
Q

Statin induced Myopathy

A

x

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18
Q

risk

A

x

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19
Q

what are the risks that lead to statin induced myopathy?

A

prolonged vigorous excercise

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20
Q

management

A

x

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21
Q

what are the indications for discontinuation of statin therapy?

A

Asyx patients with CK > 10 x Upper Limit of Normal

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22
Q

if the elevation of CK is temporally related to excercise, then what should you do?

A

recheck CK levels and restart atorvastatin if the levels have normalized

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23
Q

RBC transfusion

A

x

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24
Q

indications

A

x

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25
Q

what are the general indications for RBC transfusion?

A

Hgb <7g/dL

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26
Q

when would transfusion be appropriate for Hgb of 7-8?

A

cardiac surgery, oncology patients in trx, CHF

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27
Q

when would transfusion be appropriate for Hgb of 8-10?

A
  • syx anemia,
  • ongoing bleeding
  • ACS
  • noncardiac surgery
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28
Q

if Hgb >10, would you ever transfuse?

A

nope not generally

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29
Q

Heart Auscultation

A

x

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30
Q

where do you hear the aortic valve best?

A

2nd ICS to the right of sternal border

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31
Q

where do you hear the pulmonic valve best?

A

2nd ICS to the left of sternal border

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32
Q

where do you hear Erbs point ?

A

3rd ICS to the left of sternal border

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33
Q

where do you hear Tricuspic Valve best?

A

5th ICS to the lower left of sternal border

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34
Q

where do you hear Mtiral valve Best?

A

apex, PMI and 5th intercostal space at mid clavicular line

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35
Q

Antithrombotic Therapy in Patients with mechanical Heart Valves

A

x

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36
Q

risk

A

x

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37
Q

what are the risks of throomboembolism in patients per year with mechanical prosthetic valves with no anticoag vs with aspirin vs with warfarin?

A

no anticoag: 4%
w aspirin: 2%
w warfarin: <1%

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38
Q

who has higher risk of stroke mitral mechanical valves or aortic valve prosthesis?

A

mitral valve have twic the risk of stroke

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39
Q

risk

A

x

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40
Q

what are considered risk factors/comorbidities in those with artificial valves?

A

Atrial fibrillation, severe left ventricular dysfunction EF <=30%, prior thromboembolism, presence of hypercoagulable state

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41
Q

management

A

x

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42
Q

what are current guidelines for INR for patients with aortic valve replacements and no risk factors (i.e. no a fib, severe left ventricular dysfunction EF <=30%, prior thromboembolism, presence of hypercoagulable state)?

A

INR of 2-3 using aspirin and warfarin

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43
Q

what is the goal warfarin INR if patients have mitral valve replacement, aortic valve replacement with presence of risk factors, in the first 3 months after aortic valve replacement?

A

INR of 2.5 to 3.5 using aspirin and warfarin

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44
Q

in patient who can’t take warfarin, how much aspirin do you give?

A

75-325mg/day

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45
Q

in all patients who have aortic or mitral valve replacements, how much aspirin do you give in addition to warfarin?

A

75-100mg/day

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46
Q

Approach to Adult Cardiac Arrest

A

x

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47
Q

Approach to Adult Cardiac Arrest

A

x

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48
Q

Step 1 of cardiac arrest is?

A

start CPR, give oxygen and attach monitor/defibrillator

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49
Q

Step 2 are assess rhythm and decide if it is either ____ or ____

A

VF/pulseless VT or PEA/Asystole

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50
Q

if VF/Pulseless VT, then what do you do?

A

defibrillator shock

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51
Q

if VF/Pulseless VT, then what do you do after you defibrillator shock?

A

CPR x 2min, airway, IV/IO access, epinephrine every 3-5 minutes.

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52
Q

if PEA/Asystole, then what do you do ?

A

CPR x 2min, airway, IV/IO access, epinephrine every 3-5 minutes, so no shock needed.

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53
Q

After CPR x 2min, airway, IV/IO access, epinephrine every 3-5 minutes, what do you do?

A

pulse and rhythm check every 2 min, treat reversible causes

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54
Q

what do you after checking pulse and rhythm check?

A

identify if shockable rhythm (VF/pulseless VT) or unshockable rhythm (PEA/Asystole)

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55
Q

what should you always remember to do instead of giving epi on the third shockable rhythm?

A

give amiodarone

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56
Q

Adult Tachycardia Algorithm (with pulse)- ACLS

57
Q

what is the first steps of ACLS with pulse?

A

identify and treat underlying cause:

  • maintain patent airway; assist breathing if needed
  • oxygen
  • cardiac monitor to identify rhythm; monitor blood pressure and oximetry
58
Q

if you ask yourself is there persistent tachyarrythmia causing hypotension, AMS, signs of shock, ischemic chest discomfort, acute heart failure, and the answer is yes, what is the next step?

A
  • synchronized cardioversion,

- if regular narrow complex, consider adenosine

59
Q

if you ask yourself is there persistent tachyarrythmia causing hypotension, AMS, signs of shock, ischemic chest discomfort, acute heart failure, and the answer is no, what is the next step?

A

ask if the QRS is >0.12 seconds

60
Q

if you ask yourself is there persistent tachyarrythmia causing hypotension, AMS, signs of shock, ischemic chest discomfort, acute heart failure, and there is prolonged QRS, what is the next step?

A

IV access, 12 lead EKG, give adenosine if regular and monomorphic, consider antiarrhythmic infusion, consider exper consultation

61
Q

if you ask yourself is there persistent tachyarrythmia causing hypotension, AMS, signs of shock, ischemic chest discomfort, acute heart failure, and the QRS is not prolonged, what is the next step?

A

IV access, 12 lead EKG, vagal maneuvers, adenosine (if regular rhythm), beta blocker or CCB, consider exper consultation

62
Q

PEA/Asystole

63
Q

define

64
Q

what does PEA mean?

A

refers to an organized cardiac rhythm (eg sinus bradycardia, atrial fibrillation) that is unable to generate sufficient cardiac output to create a measurable blood pressure or palpable pulse

65
Q

cause

66
Q

what is the underlying cause typically?

A

severe hypovolemia, massive PE, markedly impaired left ventricular contractility

67
Q

risk

68
Q

what is a risk for PEA and asystole?

A

lightning injury, rhabdomyloyslsis w renal failure,

69
Q

managment

70
Q

what is the management of Asystole ?

A

chest compressions while giving vasopressors (epi or vasopressin) and identifying and treating reversible causes

71
Q

complications

72
Q

what is a complication of PEA?

A

asystole (complete absence of organized cardiac electrical activity

73
Q

reversible causes

74
Q

what are reversible causes of Asystole/PEA?

A

5 H’s: Hypovolemia, Hypoxia, Hydrogen ions (acidosis), hypokalemia or hyperkalemia, hypothermia

5T’s: Tension Pneumo, Tamponade cardia, Toxins (narcotics, BDZs), Thrombosis (Pulmonary or Coronary), Trauma

75
Q

Narrow Complex Tachycardias

76
Q

Trx

77
Q

what is treatment for Narrow Complex Tachycardias that is HD stable?

78
Q

what is treatment for Narrow Complex Tachycardias that is HD unstable?

A

synchronize cardioversion

79
Q

Types

80
Q

what are types of Narrow Complex Tachycardias ?

A

SVT’s (i.e. Afib with RVR)

81
Q

what are various types of SVT?

A

AVNRT (atrioventricular nodal reentrant tachycardia), Sinus tachy, AV reentrant tachycardia (AVRT), Afib, and A flutter

82
Q

define

83
Q

what are the components of SVT arrhythmias?

A
  • mostly narrow QRS complex tachcyardia.
  • usually there are no regular P waves as they are buried in the QRS complexes, but retrograde P wave can occur.
  • retrograde P waves : seen in the beginning or end of a QRS complex when the atria and ventricles a
84
Q

Abdominal Aortic Aneurysm (AAA)

85
Q

Anatomy

86
Q

what is the anatomy of AAA?

A

most commonly affects infrarenal aorta (>=3cm)

87
Q

Risks

88
Q

what are the risks of AAA?

A

smoking (highest risk), male sex, older, white ethnicity, family hx of AAA, atherosclerotic disease

89
Q

Screening

90
Q

what is the screening of AAA?

A

abd ultrasound in men age 65-75 y.o. who have ever smoked

91
Q

symptoms

92
Q

what are the syx of AAA?

A
  • mostly asyx,
  • may have abd, back or flank pain
  • lower limb ischemia and/or thromboembolism
  • rupture often presents with Abd distention and shock
93
Q

management

94
Q

what is the management of AAA?

A
  • smoking cessation is key!

- aspirin and statin therapy

95
Q

when is elective repair recommnded for?

A
  • Large (>=5.5 cm) aneurysms
  • rapidly enlarging aneurysms (>= 0.5cm in 6 months)
  • AAA associated with PAD or aneurysm
96
Q

follow up imaging

97
Q

what is follow up imaging for AAA?

A
medium artery (4-5.4cm): U/S q 6-12 months
smaller: U/S q 2-3 years
98
Q

risks of rupture

99
Q

what are the three biggest risk factors for aneurysmal ruptures?

A

large diameter (20% risk in aneurysms >6cm), rate of expansion (>0.5 cm in 6 months), and current cigarette smoking

100
Q

Cardiovascular Effects of Cocaine Intoxication

101
Q

pathophys

102
Q

what are the pathophysiology of cardiovascular effects of cocaine intoxication?

A

HTN and Tachy, coronary vasoconstriction, increased platelet activity and thrombus formation

103
Q

syx

104
Q

what are syx of cocaine intox?

A

CP in the middle of chest and upper sternal area,nausea, mild occipital headache

105
Q

complications

106
Q

what are the complications of cocaine intoxication?

A

MI or infrarct, aortic dissection, neurologic ischemia or stroke

107
Q

trx

108
Q

what is the initial mangement treatement goals of MI due to cocaine intox?

A

reduction of myocardial oxygen demand and improvment in myocardial oxygen supply

109
Q

what is the initial treatment for cocaine intoxication in persistent CP with minimal EKG changes ?

A

-BDZ (reduce sympathetic outflow) and nitroglycerin (alleviates HTN and MI)

110
Q

what is the second line treatment for persistent chest pain with minimal EKG changes in the setting of cocaine intoxication?

111
Q

what is the treatment for persistent HTN in the setting of cocaine intoxication?

A

phentolamine (alpha receptor antagonist)

112
Q

if ST elevation persists in setting of cocaine intox, what is appropriate next step?

A

aspirin then PCI (cocain that encourage thrombus formation and cause thrombotic occlusion of coronary arteries) even in young patients.

113
Q

if there is an MI due to cocaine intox, what do you do?

114
Q

when are fibrinolytics (eg alteplase) recommended?

A

only in patients with STEMI for whom PCI cannot be performed within 2 hours of first medical contact

115
Q

complications

116
Q

what are the complications of cardiovascular effects of cocain intox?

A

acute aortic dissection of the ascending aorta

117
Q

acute aortic dissection of the ascending aorta

118
Q

syx

119
Q

what are syx of aortic dissection of the ascending aorta?

A

new neuro findings of right sided weakness, severe, sharp, tearing CP or Back Pain

120
Q

risk

121
Q

what are the risks associated iwth aortic dissections?

A

HTN (Most common), marfan sydnrome, cocaine use

122
Q

PE

123
Q

what are the physical exam findings of aortic dissection?

A

> 20mmHg variation in SBP between arms

124
Q

complications

125
Q

what are the complications of aortic dissection?

A

stroke (carotid arteries), acute aortic regurg (aortic valves), horner syndrome (superior cervical sympathetic ganglion), acute MI (coronary artery), pericardial effusion/cardiac tamponade (pericardial cavity), hemothorax (pleural cavity), LE weakness or ischemia (spinal or common iliac arteries), abd pain (mesenteric artery)

126
Q

dx

127
Q

what is the dx imaging needed for acute dissection of the ascending aorta?

A

CT angiography

128
Q

pathophys

129
Q

how do focal neuro deficits deficits occur?

A

carotid artery involvement (eg obstruction by intimal flap, extension of dissection into carotids) leading to cerebral ischemia

130
Q

Detection of Left to Right Shunt by Oximetry

131
Q

dx

132
Q

what is the best measure of oxygenation saturation changes between atria and ventricles?

A

right and left heart cath

133
Q

location of shunt

134
Q

what are the three most common locations of potential shunts?

A

atrial, ventricular , and great vessels

135
Q

causes of specific shunts

136
Q

if you’re in the level of the atria and you have step up in O2 % saturation from superior/inferior vena cava to right atrium, what are the possible causes?

A
  • ASD
  • Partial anomalous pulm venous drainage
  • Ruptured sinus of valsalva
  • VSD with tricuspid regurg
  • coronary fistula to right atrium
137
Q

if you’re in the level of the ventricle and you have step up in O2 % saturation from right atrium to right ventricle, what are the possible causes?

A
  • VSD
  • PDA with pulm regurg
  • coronary fistual to right ventricle
138
Q

if you’re in the level of the great vessels and you have step up in O2 % saturation from right ventricle to pulm artery, what are the possible causes?

A
  • PDA

- Aorto-pulmonary window