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
2
Q
What EKG leads will have a positive EKG deflection in a normal EKG
A
I and II
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
4
Q
What ECG leads will have an abnormal QRS deflection in R axis deviation?
A
Positive (+) deflction of QRS in lead III
5
Q
What is the normal length of QRS complex
A
- Normally < 120 msec (e.g. 3 boxes)
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
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
8
Q
Rank the parts of the conduction pathway from fastest to slowest
A
- Purkinje > atria > ventricles > AV node
9
Q
Causes of L axis deviation
A
- Inferior wall MI
- L anterior fascicular block
- LV hypertrophy
- LBBB
- High diaphragm
10
Q
Causes of R axis deviation
A
- RV hypertrophy
- Acute right heart strain (e.g. massive PE)
- L posterior fascicular block
- RBBB
- Dextrocardia
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
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)
13
Q
Defining ECG characteristics of atrial flutter
A
- Identical, back-to-back atrial depolarizations = consecutive P waves
- Sawtooth pattern
- Regular
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)
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
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
Describe the underlying defect and ECG findings in Wolff-Parkinson-White syndrome
* 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
Describe complication and treatment of Wolff-Parkinson-White
* May result in supraventricular tachycardia
* Treatment:
* Procainamide (Class IA)
* Amiodarone (Class III)
27
Describe the MOA of baroreceptors
* 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
What is a Cushing reaction, and what is it in response to?
* Triad of hypertension, bradycardia, and respiratory depression in response to increased intracranial pressure
29
Describe the pathogenesis behind a Cushing reaction
* 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
What are the different triggers of peripheral vs. central chemoreceptors
* 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
What is the trigger of aortic arch baroreceptor, and via what structure does it deliver its signal
Aortic arch responds to increase (only) in BP via vagus nerve to solitary nucleus of medulla
32
What is the trigger of carotid body baroreceptor, and via what structure does it deliver its signal
* Carotid sinus responds to increase or decrease in BP via glossopharyngeal nerve to solitary nucleus
33
What BP values define HTN and preHTN
* Prehypertension \> 120/80
* Hypertension \> 140/90
34
What is the difference betwen hypertensive urgency and hypertensive emergency
* 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
What will you see on CXR in an aortic dissection
Widening of the mediastinum
36
Differentiate Stanford A vs. Stanford B aortic dissection
* Stanford Type A
* Involves ascending aorta
* Stanford Type B
* Confined to descending aorta, distal to L subclavian
37
Treatment of Stanford type A and type B aortic dissection
Type A = surgery
Type B = medical: beta-blockers
