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Review / Wrong Answers > DIT review - Cardiology 5 > Flashcards

DIT review - Cardiology 5 Flashcards

1
Q

Describe the direction of each of the 6 major ECG leads (I, II, III, aVF, aVR, aVL)

A
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2
Q

What EKG leads will have a positive EKG deflection in a normal EKG

A

I and II

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3
Q

What ECG leads will have an abnormal QRS deflection in L axis deviation?

A

Negative (-) deflection of QRS in lead aVF and II

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4
Q

What ECG leads will have an abnormal QRS deflection in R axis deviation?

A

Positive (+) deflction of QRS in lead III

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5
Q

What is the normal length of QRS complex

A
  • Normally < 120 msec (e.g. 3 boxes)
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6
Q

What does it indicate if the QRS complex is widened?

A
  • Narrow QRS = Normal conduction pathway
    • Signal coming through AV node and down Purkinje system
  • Wide QRS = abnormal conduction pathway:
    • Premature ventricular contraction (PVC)
    • Ventricular tachycardia
    • Bundle branch block
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7
Q

Describe the effects of hyper- and hypokalemia on ECG

A
  • Hyperkalemia = high, peaked T wave
  • Hypokalemia = flat T wave with possible U wave
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8
Q

Rank the parts of the conduction pathway from fastest to slowest

A
  • Purkinje > atria > ventricles > AV node
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9
Q

Causes of L axis deviation

A
  • Inferior wall MI
  • L anterior fascicular block
  • LV hypertrophy
  • LBBB
  • High diaphragm
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10
Q

Causes of R axis deviation

A
  • RV hypertrophy
  • Acute right heart strain (e.g. massive PE)
  • L posterior fascicular block
  • RBBB
  • Dextrocardia
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11
Q

Defining ECG features of atrial fibrillation

A
  • Chaotic and erratic baseline with no discrete P waves in between irregularly spaced QRS complexes
  • Irregularly irregular (spacing between R waves are inconsistent)
  • Absent P waves
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12
Q

Treatment of atrial fibrillation

A
  • Anticoagulation (to remove clots) – Heparin, Enoxaparin, Coumadin (Warfarin)
  • Rate control – Digoxin, Beta-blockers (Class II), Calcium channel blockers (Class IV)
  • Rhythm control – Amiodarone or Sotalol (Class IV), Flecainide (Class IC)
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13
Q

Defining ECG characteristics of atrial flutter

A
  • Identical, back-to-back atrial depolarizations = consecutive P waves
  • Sawtooth pattern
  • Regular
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14
Q

Treatment of atrial flutter

A

Same as A-fib

  • Anticoagulation (to remove clots) – Heparin, Enoxaparin, Coumadin (Warfarin)
  • Rate control – Digoxin, Beta-blockers (Class II), Calcium channel blockers (Class IV)
  • Rhythm control – Amiodarone or Sotalol (Class IV), Flecainide (Class IC)
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15
Q

Defining feature of ventricular tachycardia

A
  • Defined as 3 or more successive ventricular (QRS) complexes
  • May be non-sustained (< 30 s) or sustained (> 30 s)
  • Rhythm is usually regular
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16
Q

Describe Torsades de Pointes, its predisposing condition, and its feared complication

A
  • Type of ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG
    • Amplitude going back and forth between tall and short
  • Can progress to ventricular fibrillation
  • Long QT intervals predispose to Torsades de Pointes
17
Q

What drugs prolong the QT interval, and therefore predispose to Torsades de pointes?

A
  • Drugs that prolong QT interval – ABDCE
    • AntiArrhythmics (IA, III)
    • AntiBiotics (e.g. macrolides, chloroquine)
    • Anti”C”ychotics (e.g. Haloperidol)
    • AntiDepressants (e.g. TCAs)
    • AntiEmetics (e.g. ondansetron)
18
Q

Treatment of Torsades de pointe

A

Magnesium

19
Q

Describe ECG of ventricular fibrillation and resulting complications

A
  • Erratic rhythm with no identifiable waves
  • Fatal without immediate CPR and defibrillation
20
Q

Describe first degree AV block

A
  • Prolonged PR interval > 200 msec (5 blocks)
    • Recall that PR interval is time between atrial and ventricular depolarization (hence, AV block)
  • Asymptomatic
  • No treatment needed
21
Q

What are the different types of second degree AV block

A

Mobitz type I (aka Wenckebach)

Mobitz type II

22
Q

Describe Mobitz type I AV block

A
  • Progressive lengthening of PR interval until a beat is “dropped”
    • P wave not followed by a QRS complex
  • Usually asymptomatic
23
Q

Describe Mobtiz type II AV block

A
  • “Dropped” beats without a warning
    • Not preceded by change in length of PR interval
  • May progress to third degree block
  • Treated with pacemaker
24
Q

Describe 3rd degree AV block

A
  • Atria and ventricles beat independently of each other
    • No correlation between P waves and QRS complex
  • Atrial rate > ventricular rate
  • Usually treated with pacemaker
  • Associated with Lyme disease
25
Q

Describe the underlying defect and ECG findings in Wolff-Parkinson-White syndrome

A
  • Accessory conduction pathway from atrium to ventricle that bypasses the rate-slowing AV node
    • Bundle of Kent is a common accessory pathway
  • Causes ventricles to depolarize earlier
  • Delta-wave with widened QRS complex and shorted PR
26
Q

Describe complication and treatment of Wolff-Parkinson-White

A
  • May result in supraventricular tachycardia
  • Treatment:
    • Procainamide (Class IA)
    • Amiodarone (Class III)
27
Q

Describe the MOA of baroreceptors

A
  • Hypotension = decreased arterial pressure = decreased stretch = decreased afferent baroreceptor firing = increased efferent sympathetic firing and decreased efferent parasympathetic firing = vasoconstriction, increased HR, increased contractility, increased BP
28
Q

What is a Cushing reaction, and what is it in response to?

A
  • Triad of hypertension, bradycardia, and respiratory depression in response to increased intracranial pressure
29
Q

Describe the pathogenesis behind a Cushing reaction

A
  • Increased ICP = pressure constricts arterioles in brain = cerebral ischemia = sympathetic response increases peripheral vasoconstriction, thus increasing BP = aortic baroreceptors sense increased BP = respond with reflex bradycardia and respiratory depression
30
Q

What are the different triggers of peripheral vs. central chemoreceptors

A
  • Peripheral
    • Stimulated by decreased pO2, increased pCO2, and decreased pH
  • Central
    • Stimulated by increased pCO2 and decreased pH
    • Does not directly respond to pO2
31
Q

What is the trigger of aortic arch baroreceptor, and via what structure does it deliver its signal

A

Aortic arch responds to increase (only) in BP via vagus nerve to solitary nucleus of medulla

32
Q

What is the trigger of carotid body baroreceptor, and via what structure does it deliver its signal

A
  • Carotid sinus responds to increase or decrease in BP via glossopharyngeal nerve to solitary nucleus
33
Q

What BP values define HTN and preHTN

A
  • Prehypertension > 120/80
  • Hypertension > 140/90
34
Q

What is the difference betwen hypertensive urgency and hypertensive emergency

A
  • Hypertensive urgency:
    • BP > 180/20
    • With no evidence of end organ damage
  • Hypertensive emergency:
    • BP > 180/120
    • With evidence of end organ damage:
      • Encephalopathy, stroke, retinal hemorrhage, papilledema, MI, HF, aortic dissection, kidney injury, microangiopathic hemolytic anemia, eclampsia
35
Q

What will you see on CXR in an aortic dissection

A

Widening of the mediastinum

36
Q

Differentiate Stanford A vs. Stanford B aortic dissection

A
  • Stanford Type A
    • Involves ascending aorta
  • Stanford Type B
    • Confined to descending aorta, distal to L subclavian
37
Q

Treatment of Stanford type A and type B aortic dissection

A

Type A = surgery

Type B = medical: beta-blockers

Review / Wrong Answers (140 decks)

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