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pance study guide > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Stable Bradycardia Treatment

A

Monitor and observe

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2
Q

Unstable Bradycardia Treatment

A

Atropine (1st line)

Others: Epi, Dopamine, Transcutaneous Pacing

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3
Q

Shockable Rhythms

A

1) V-Fib

2) Pulseless V-Tach

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4
Q

Unstable Tachycardia Treatment

A

SYNCHRONIZED Cardioversion

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5
Q

Stable Tachycardia (Wide QRS) Treatment

A

Amiodarone (1st line)

Others: Lidocaine, Procainamide

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6
Q

Stable Tachycardia (Narrow QRS) Treatment

A

Adenosine (1st)

Then, Beta-blocker, CCB

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7
Q

Acute A-Fib Treatment

A

Beta-blocker or CCB

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8
Q

WPW Treatment

A

Procainamide preferred (avoid AV nodal blockers)

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9
Q

AV Nodal Blockers

A 
ABCD=
Adenosine
Beta Blockers
CCB
Digoxin
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10
Q

Normal PR interval

A

0.12 - 0.2

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11
Q

Normal QRS time

A

<0.12 sec (if normal, there is no bundle branch block*)

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12
Q

Anterior Leads

A

V1-V4

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13
Q

Lateral Leads

A

I, aVL, V5, V6

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14
Q

Anterolateral leads

A

I, aVL, V4-V6

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15
Q

Inferior Leads

A

II, III, aVF

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16
Q

Posterior Leads

A

ST DEPRESSIONS in V1-V2

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17
Q

Causes of Left Axis Deviation

A 
LBBB
LVH
Inferior MI
Elevated Diaphragm (pregnancy, obesity)
Left anterior hemiblock
WPW
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18
Q

Causes of Right Axis Deviation

A

RVH
Lateral MI
COPD
Left posterior hemiblock

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19
Q

Normal Sinus Rhythm Determination

A

Every P-wave followed by QRS
P waves are positive/upright in I, II, and aVF
P waves are negative in aVR
Rate is 60-100

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20
Q

Sick Sinus Syndrome (What is it?/Caused by?)

A

Combination of sinus arrest with alternativing paroxysms of atrial tachyarrhythmias & bradyarrhythmias
Caused by sinoatrial node disease and corrective cardiac surgery

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21
Q

Sick Sinus Syndrome Management

A

+/- permanent pacemaker if symptomatic

If brady alternating with v-tach –> permanent pacemaker with automatic implantable cardioverter-defibrillator

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22
Q

First Degree AV Block Definition

A

Constant, prolonged PR-Interval (>0.20 sec)

QRS follows every P wave

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23
Q

First Degree AV Block Treatment

A

None, observation

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24
Q

Second Degree AV Block Type I Definition

A 
Mobitz I (Wenckebach):
Progressive PRI lengthening --> Dropped QRS
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25
Q

Second Degree AV Block Type I Treatment

A

Symptomatic –> Atropine (treat like brady)

Asymptomatic –> Observation +/- cardiac consult

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26
Q

Second Degree AV Block Type II Definition

A

Mobitz II:

Constant/Prolonged PRI –> Dropped QRS

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27
Q

Second Degree AV Block Type II Treatment

A

Atropine or temporary pacing

Progression to 3rd degree block is common so permanent pacemaker is the definitive treatment!

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28
Q

Which heart block is most likely to progress to 3rd degree

A

Mobitz II

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29
Q

Third Degree AV Block Definition

A

AV dissociation: P waves NOT related to QRS

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30
Q

Third Degree AV Block Treatment

A

Acute: Temporary pacing –> PPM
Definitive: PPM

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31
Q

Atrial Flutter Management

A

Stable: Vagal, B-blocker, or CCB
Unstable: Synchronized cardioversion
Definitive: Radiofrequency ablation

*Anticoagulation similar to A-Fib

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32
Q

Most common chronic arrhythmia

A

A-Fib

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33
Q

Stable A-Fib Management

A

RATE CONTROL (preferred in symptomatic Afib)

  • B-blocker (metoprolol*, esmolol)
  • CCB (diltiazem*, verapamil (nondihydropyridines))
  • Digoxin +/- in elderly (preferred rate control in patients with hypotension or CHF)

RHYTHM CONTROL (may be used in younger patients with lone AFib)

  • Direct current (synchronized) cardioversion (DCC) is preferred over pharmacologics; DCC can be done if AF present for <48 hours OR after 3-4 weeks of anticoagulation and TEE shows no atrial thrombi
  • Pharm control: Ilbutilide, Flecainide, Sotalol, Amiodarone
  • Radiofrequency ablation
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34
Q

Stable A-Fib Management in patient with hypotension or CHF

A

Digoxin

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35
Q

Unstable A-Fib Management

A

DCC

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36
Q

A-Fib Anticoagulation Risk Stratification

A

CHA2DS2-VASc Score:

  • CHF - 1 point
  • HTN - 1 point
  • Age(2) >75 - 2 points
  • DM - 1 point
  • Stroke, TIA, Thrombus - 2 points
  • Vascular disease (prior MI, aortic plaque, PAD) - 1 point
  • Age 65-74 - 1 point
  • Sex (female) - 1 point

Max Score: 9; 2 or more is high risk, 1 is low risk
High risk: chronic oral anticoagulation recommended
Low risk: clinical judgment

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37
Q

Anticoagulation options

A

NOACs (now preferred over warfarin)
Warfarin
Dual antiplatelet therapy (ex. Aspirin + Clopidogrel) –> reserved for patients who cannot be treated with anticoagulation

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38
Q

Types of NOACs

A

Dabigatran (direct thrombin inhibitor)

Rivaroxaban, Apixaban, Edoxaban (factor Xa inhibitors)

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39
Q

Anticoagulation preference in A-Fib

A

NOACs

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40
Q

Warfarin Indications for A-Fib

A

Preferred in patients with severe chronic kidney disease, contraindications to NOAC (HIV patients on protease inhibitor therapy, patients on CP450 inducing antiepileptic meds), patient preference, cost

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41
Q

INR goal for A-Fib

A

2-3

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42
Q

Long QT Syndrome Etiology

A

Congenital

Acquired (macrolides, TCAs, electrolyte abnormalities)

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43
Q

Long QT Clinical Manifestations

A

Recurrent syncope (Get EKG in ALL Syncope)
Ventricular arrhythmias
Sudden cardiac death

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44
Q

Management of Long QT Syndrome

A

Discontinue offending drugs and correct electrolyte abnormality
Implantable cardiodefibrillator is definitive for congenital or recurrent ventricular arrhythmias

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45
Q

Paroxysmal SVT (PSVT) EKG

A

HR > 100
Rhythm usually regular with narrow QRS
P waves hard to discern

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46
Q

PSVT Management

A

Stable (Narrow complex):
Vagal Maneuvers
Adenosine (1st line medical treatment)
AV nodal blockers (B-blockers, CCB)

Stable (Wide Complex):
Antiarrhythmics (amiodarone, procainamide if WPW)

Unstable:
DCC

Definitive:
Radiofrequency ablation

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47
Q

Wandering atrial pacemaker (WAP) vs Multifocal atrial tachycardia (MAT) EKG

A

WAP:
HR < 100
3 or more p wave morphologies

MAT:
HR > 100
3 or more p wave morphologies

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48
Q

What condition is MAT associated with?

A

Severe COPD

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49
Q

Tx for WAP and MAT

A

CCB or B-blocker if LV function preserved

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50
Q

Stable WPW management

A

Vagal, antiarrhythmics (procainamide preferred)

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51
Q

Unstable WPW Management

A

DCC

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52
Q

Definitive WPW management

A

Radioablation

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53
Q

Junctional Rhythm EKG

A

P waves inverted (if present) or not seen
Narrow QRS
Regular Rhythm
HR 40-60 bpm (reflecting intrinsic rate of AV junction)

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54
Q

Accelerated junctional rhythm EKG

A

HR 60-100 w/out pwaves (or inverted if present)

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55
Q

Junctional tachycardia

A

HR >100 w/out pwaves (or inverted if present)

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56
Q

MC rhythm seen with digitalis toxicity

A

Junctional rhythms

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57
Q

PVC management

A

No treatment usually needed

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58
Q

MC cause of V-tach

A

Prolonged QT

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59
Q

MC cause of Torsades

A

Hypomagnesemia

Other: Hypokalemia, prolonged QT, V-tach

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60
Q

Stable Vtach treatment

A

Antiarrhythmics (Amiodarone*, lidocaine, procainamide)

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61
Q

Unstable Vtach w/ a pulse

A

Synchronized cardioversion

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62
Q

Vtach w/out pulse

A

Defibrillation (UNsynchronized cardioversion) + CPR (treat as VFib)

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63
Q

Torsades treatment

A

IV magnesium

Correct any electrolyte abnormalities

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64
Q

VFib treatment

A

Defibrillation + CPR

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65
Q

Pulseless electrical activity (PEA) definition

A

Organized rhythm on monitor, but patient does not have a palpable pulse (electrical activity is not coupled with mechanical contraction)

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66
Q

PEA treatment

A

CPR + Epinephrine + Check for shockable rhythm every 2 minutes

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67
Q

Asystole treatment

A

CPR + Epinephrine + Check for shockable rhythm every 2 minutes

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68
Q

Increased JVP + crackles/rales in lungs

A

CHF

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69
Q

Increased JVP + normal pulm exam

A

Pericardial tamponade

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70
Q

Increased JVP + decreased breath sounds

A

Tension pneumothorax

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71
Q

Causes of ST Depression

A

ST depression usually = ISCHEMIA

May be benign (upsloping)

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72
Q

Which ST depressions are pathologic

A

Horizontal and downsloping

73
Q

Which ST elevations are pathologic

A

Convex down (most likely ischemic)

74
Q

Which ST elevations may be benign

A

Concave up

75
Q

Etiologies of ST elevation

A
  1. Acute MI
  2. LVH
  3. LBBB
  4. Acute Pericarditis
  5. Early repolarization abnormalities
  6. Coronary artery vasopasm/prinzmetal angina/cocaine
  7. Brugada syndrome
76
Q

Early repolarization abnormalities EKG

A

DIFFUSE CONCAVE ST elevations
Large T waves
Tall QRS voltage
Fishook (slurring/notching) at the j point

77
Q

Acute pericarditis EKG

A
  • DIFFUSE CONCAVE ST elevations in the precordial leads (V1-V6)
  • PR depressions in the same leads with the ST elevations
  • Lead aVR: ST depression and PR elevation (opposite of precordial leads)
  • NO reciprocal changes
78
Q

Brugada Syndrome EKG

A
  • RBB pattern (often incomplete) in V1-V3
  • ST elevation in V1-V3 (often downsloping)
  • Twave inversions in V1 and V2 +/- S wave in lateral leads
79
Q

Demographic group associated with Brugada

A

Asian males

80
Q

Brugada syndrome cause and manifestations

A

Genetic disorder associated with syncope, sudden cardiac death

81
Q

Most common arrhythmia with brugada

A

Ventricular arrhythmias

82
Q

Brugada management

A

AICD to prevent death from V Fib

83
Q

When are left sided murmurs best heard in regards to breathing?

A

End expiration

84
Q

When are right sided murmurs best heard in regards to breathing?

A

End inspiration

85
Q

What does inspiration do to stroke volume

A

Decreases, but CO stays the same due to an increase in HR

86
Q

Gold standard test for diagnosing CAD, PAD, renal artery stenosis, and AAA

A

Angiography

87
Q

Most useful test to diagnose heart failure

A

Echocardiogram

88
Q

Biggest risk factor for CAD

A

Diabetes

89
Q

Most important modifiable risk factor for CAD

A

Smoking

90
Q

How much of the lumen is occluded to cause symptomatic CAD?

A

> 70%

91
Q

Class I Angina

A

Angina only with unusually strenuous activity. No limitations of activity.

92
Q

Class II Angina

A

Angina with more prolonged or rigorous activity. Slight limitation of physical activity.

93
Q

Class III Angina

A

Angina with usual daily activity. Marked limitation of physical activity.

94
Q

Class IV Angina

A

Angina at rest. Often unable to carry out any physical activity.

95
Q

Levine’s Sign

A

Clenched fist over chest

96
Q

Classic angina description

A

Substernal chest pain brought on by exertion/anxiety (sometimes radiating to arm/jaw) and relieved with rest/nitroglycerin (predictable pattern)

97
Q

Classic EKG finding for angina

A 
ST depression (horizontal or downward)
if LVH present = increase in adverse outcomes
98
Q

Most useful noninvasive screening tool for angina

A

Stress Testing

99
Q

Angina definitive management

A
  1. Percutaneous Transluminal Coronary Angioplasty

2. CABG

100
Q

Indication for percutaneous transluminal coronary angioplasty

A

1 or 2 vessel disease NOT involving the left main coronary artery and in whome ventricular function is normal/near normal.

101
Q

CABG indications

A

Left main coronary artery disease
Symptomatic or critical (>70%) stenotic 3-vessel disease
Decreased left ventricular ejection fraction (<40%)

102
Q

Medical management of angina

A
  1. Nitrates
  2. B-Blockers
  3. CCB
  4. Aspirin
103
Q

1st line drug for chronic management of angina

A

B-Blockers

104
Q

Contraindication to nitrates

A

SBP <90
RV infarct
Use of sildenafil & other PDE-5 inhibitors

105
Q

UA/NSTEMI EKG

A

ST depressions &/or T-wave inversions = Subtotal occlusion (EKG may be normal)

106
Q

STEMI EKG

A

ST elevations in two or more consecutive leads = Total occlusion

107
Q

UA vs NSTEMI

A

Cardiac enzymes elevated in NSTEMI (EKG may be the same)

108
Q

Patients with “silent MI”

A

Women, elderly, diabetics, & obese

109
Q

Symptoms of atypical MI

A

abdominal pain, jaw pain, or dyspnea WITHOUT chest pain

110
Q

Inferior MI physical exam findings

A

Chest pain + bradycardia +/- S4

111
Q

Progression of EKG changes in STEMI

A

Hyperacute (peaked) T-waves –>
ST elevations –>
Q waves –>
T wave inversions

112
Q

Pathologic Q-wave definition

A

Q wave > 0.03 sec & 0.1 mv deep

Q wave depth at least 25% of associated R wave

113
Q

Most sensitive and specific cardiac marker

A

Troponin

114
Q

Other causes of increased troponin

A

Renal failure
Advanced heart failure
Acute PE
CVA

115
Q

Management of STEMI

A
  1. Reperfusion therapy (most important) - PCI or thrombolytics
  2. Antithrombotics - Asprin, Heparin
  3. Adjuntive therapy - B-Blockers, ACE, Nitrates, Morphine
116
Q

PCI indication in STEMI

A

Best w/in 3 hours of sx onset (esp w/in 90 min)

PCI is superior to thrombolytics

117
Q

Thrombolytic indication in STEMI

A

PCI is not an option/unable to get PCI early

118
Q

CI of Betablockers in STEMI

A 
HR <50
SBP <100
Decompensated CHF
2nd/3rd degree heart block
Severe asthma/COPD
Shock
Cocaine induced MI
119
Q

CI of ACE Inhibitors in STEMI

A

Renal failure

SBP <100

120
Q

AMI protocol for ACS

A

EKG w/in 10 min
Door to thrombolytics w/in 30 min
Door to PCI w/in 90 min

121
Q

STEMI AMI protocol

A 
B-Blockers
Nitro
Asprin
Heparin
ACEI
Reperfusion!!!
122
Q

UA or NSTEMI AMI Protocol

A 
B-Blockers
Nitro
Asprin
Heparin
NO emergent reperfusion or ACEI (unlike STEMI)
123
Q

Cocaine Induced MI AMI protocol

A 
Aspirin
Nitro
Heparin
Anxiolytics
(*AVOID B-Blockers b/c of vasospasm)
124
Q

Dressler syndrome

A

Post-MI pericarditis +
Fever +
Pulmonary infiltrates

125
Q

Prinzmetal Angina Tx

A

CCBs (drug of choice)

Nitrates as needed

126
Q

Prinzmetal Angina EKG

A

Transient ST elevations that resolve with CCBs or nitro

127
Q

Prinzmetal Angina clinical manifestations

A

CP, usually NONexertional and occurring at rest

128
Q

Absolute contraindications to thrombolytics in ACS

A 
Previous intracranial hemorrhage
Non-hemorrhagic stroke w/in 6 months 
Closed head/facial trauma w/in 3 months
Intracranial neoplasm, aneurysm, AVM
Active internal bleeding
Suspected aortic dissection
129
Q

MC cause of heart failure

A

CAD

130
Q

MC cause of R-sided HF

A

L-sided HF

Also, pulmonary disease, mitral stenosis

131
Q

Systolic vs Diastolic HF

A

Systolic:

  • Decreased EF
  • +/- S3 gallop
  • Most common form of HF
  • Etiologies: Post-MI, DILATED cardiomyopathy, myocarditis

Diastolic:

  • Normal/Increased EF
  • +/- S4 gallop
  • Normal cardiac size (stiff/noncompliant ventricle)
  • Etiologies: HTN, LVH, elderly, valvular heart disease, cardiomyopathies, constrictive pericarditis
132
Q

Classifying of HF

A

Class I - No symptoms, no limitation during ordinary physical activity
Class II - Mild symptoms, slight limitation of activity
Class III - Sxs cause marked limitation in activity
Class IV - Symptoms present at rest

133
Q

MC sx of L-sided HF

A

Dyspnea

134
Q

Cheyne-Stokes breathing

A

Associated with L-side HF

Deeper, faster breathing w/ gradual decrease & periods of apnea

135
Q

R-sided HF physical exam

A

Peripheral edema
JVD
GI/hepatic congestion: anorexia, n/v, HSM, RUQ tenderness, hepatojugular reflex

136
Q

Diagnosis of HF

A

Echo (most useful)
CXR (esp useful in congestive HF)
BNP

137
Q

CXR findings with HF

A

Cephalization of flow –> Kerley B lines –> Butterfly pattern –> cardiomegaly
Pleural effusions –> pulmonary edema

138
Q

Initial management of HF

A

ACE + Diuretic (for sxs) –> Add beta blockers as needed

139
Q

Best 2 meds for decreasing mortality of HF

A

ACE > Beta-blockers

140
Q

Management of acute pulmonary edema/CHF

A

LMNOP:

Lasix, Morphine, Nitro, Oxygen, Position (place upright)

141
Q

2 MC causes of pericarditis

A

Idiopathic

Viral

142
Q

MC Viral causes of pericarditis

A

Enteroviruses-Coxsackie; Echovirus

143
Q

Drugs that cause pericarditis

A

Procainamide
INH
Hydralazine

144
Q

Clinical manifestations of pericarditis

A

3 P’s:

  • Pleuritic CP
  • Persistent CP
  • Postural CP (worse supine, relieved sitting forward)

Physical:
Pericardial friction rub (best heard at end expiration while upright and leaning forward

145
Q

Pericarditis diagnostics

A

EKG: DIFFUSE ST elevations in precordial leads (concave up in V1-V6)
Echo: Assesses complications (effusion/tamponade)

146
Q

Pericarditis management

A

Aspirin/NSAIDs x 7-14 days
Colchicine (2nd line)
+/- steroids if sxs >48 hours refractory to 1st line meds

147
Q

Pericardial effusion EKG

A

Low voltage QRS

Electrical alternans

148
Q

Management of pericardial effusion

A

Observation if small & no tamponade

+/- Pericardiocentesis if tamponade or large

149
Q

Knuckle sign

A

Lead aVR: PR elevation with ST depression reflects atrial injury in acute pericarditis

150
Q

Beck’s Triad

A

Associated with tamponade:

  1. Muffled heart sounds
  2. JVD
  3. Hypotension
151
Q

MC symptom of constrictive pericarditis

A

Dyspnea

152
Q

Kussmaul’s sign

A

Increased JVD during inspiration associated with constrictive pericarditis and restrictive cardiomyopathy

153
Q

Heart sound associated with constrictive pericarditis

A

Pericardial knock: high pitched 3rd heart sound due to sudden cessation of ventricular filling

154
Q

Treatment of constrictive pericarditis

A

Pericardiectomy (definitive treatment)

Diuretics for symptomatic control

155
Q

MC cause of myocarditis

A

Viral infection (enterovirus (esp. coxsackie))

Others: 
Bacteria (rickettsial, chagas, diptheria); 
Fungal;
Parasitic;
Scorpion envenomation;
SLE, rheumatic fever, rheumatoid arthritis, Kawasaki
Meds
Uremia
156
Q

Meds associated with myocarditis

A

Clozapine***

Methyldopa, tetracycline, penicllin, isoniazid, etc.

157
Q

Classic CXR with myocarditis

A

Cardiomegaly (may be normal)

158
Q

Gold standard of diagnosing myocarditis

A

Endomyocardial biopsy

159
Q

Management of myocarditis

A
  1. Supportive (mainstay) - diuretics, ACE I, inotropic drugs (dopamine, dobutamine, milrinone)
  2. Beta blockers not used in management of peds patients
  3. IVIG may be helpful in some patients
160
Q

MC cause of dilated cardiomyopathy

A

Idiopathic (50%)

161
Q

Apical left ventricular ballooning following stress

A

Takotsubo Cardiomyopathy

162
Q

MC cause of restrictive cardiomyopathy

A

Amyloidosis

Others: Sarcoidosis, idiopathic myocardial fibrosis

163
Q

Treatment of restrictive cardiomyopathy

A

No specific treatment, treat underlying cause

164
Q

MC initial complaint of hypertrophic cardiomyopathy

A

Dyspnea

165
Q

Hypertrophic cardiomyopathy murmur

A

Harsh systolic crescendo-decresendo murmur: best heart @ LLSB (similar to AS)
Decreased murmur intensity with INCREASED venous return (squatting, lying suping)
Increased intensity with DECREASED venous return

166
Q

Rheumatic Fever diagnostic criteria

A

JONES criteria

167
Q

JONES criteria for Rheumatic Fever

A

Major criteria (2 pts):

  • Joint (migratory polyarthritis)
  • Oh my heart (active carditis)
  • Nodules (subcutaneous)
  • Erythema marginatum
  • Sydenham’s chorea

Minor criteria (1 pt):

  • Fever >101.3
  • Arthralgia
  • Increased ESR/CRP/leukocytosis
  • Prolonged PR on EKG

PLUS supporting evidence of recent GAS infection

168
Q

MC valve affected by Rheumatic fever

A

Mitral (75%-80%)

Aortic (30%)

169
Q

Rheumatic fever management

A
  1. Aspirin x 2-6 weeks with taper +/- steroids

2. Pen G (erythromycin if PCN-allergic)

170
Q

Fixed split of S2

A

Left to Right shunts (ASD, VSD) or

Delayed pulmonary closure (pulmonary HTN, mitral regurgitation)

171
Q

Physiologic split of S2

A

Inspiration splits S2 into A2 followed by P2

172
Q

Systolic ejection click

A

Mitral valve prolapse

173
Q

Diastolic opening snap

A

Mitral valve stenosis

174
Q

MC valve affected by Rheumatic fever

A

Mitral (75%-80%)

Aortic (30%)

175
Q

Rheumatic fever management

A
  1. Aspirin x 2-6 weeks with taper +/- steroids

2. Pen G (erythromycin if PCN-allergic)

176
Q

Fixed split of S2

A

Left to Right shunts (ASD, VSD) or

Delayed pulmonary closure (pulmonary HTN, mitral regurgitation)

177
Q

Physiologic split of S2

A

Inspiration splits S2 into A2 followed by P2

178
Q

Systolic ejection click

A

Mitral valve prolapse

179
Q

Diastolic opening snap

A

Mitral valve stenosis

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