CVRN BC REVIEW ANSWERS AND QUESTIONS SET
A+
✔✔Grade 5 murmur - ✔✔Very loud, with thrill. May be heard when the stethoscope is
partly off the chest
✔✔Grade 6 murmur - ✔✔Audible without stethoscope
✔✔Lead 1 is good to see what kind of rhythms? - ✔✔ventricular
✔✔Lead 2 is good to see what kind of rhythms? - ✔✔atrial
✔✔What leads to you check to see where VT is coming from? - ✔✔V1 and V6
✔✔If QRS is positive and wide in V1, consider what 3 issues? - ✔✔RBBB, left
ventricular ectopic beats, WPW syndrome
✔✔If QRS is wide in V1, what lead do you also check? - ✔✔V6
✔✔What med do you avoid in SVT? - ✔✔cardizem, can cause pt to code
✔✔tx for symptomatic SVT - ✔✔adenosine
✔✔tx for persistent symptomatic SVT - ✔✔cardiovert
✔✔Left ventricular rhythms mimic what in V1 - ✔✔RBBB
✔✔Right ventricular rhythms mimic what in V1? - ✔✔LBBB
✔✔Ventricular Escape rhythm - ✔✔20-40 bpm
✔✔Accelerated Ventricular Rhythm - ✔✔50-100 bpm
,✔✔HR for ventricular tachycardia - ✔✔100+ bpm
✔✔If QRS in V6 is negative and wide - ✔✔VT indicator
✔✔WPW syndrome - ✔✔short PR interval, delta waves (slur on the upstroke of the
QRS) and wide QRS
✔✔Nadir <0.06 - ✔✔LBBB
✔✔nadir - ✔✔lowest point of QRS complex
✔✔nadir >0.07 - ✔✔right ventricular ectopy
✔✔Junctional Escape Rhythm - ✔✔40-60 bpm
✔✔Accelerated Junctional Rhythm - ✔✔60-100 bpm
✔✔Junctional Tachycardia - ✔✔100+ bpm
✔✔Junctional Rhythm - ✔✔heart is paced by the AV node
✔✔"Scooped out" ST segment indicative of - ✔✔dig toxicity
✔✔What med is notorious for causing junctional arrhythmias - ✔✔Digoxin
✔✔PR interval >0.20 seconds - ✔✔1st degree AV block
✔✔2nd degree AV block type I (Wenckebach) - ✔✔Progressively prolonged PR interval
until eventually dropped (P wave followed by missing QRS)
✔✔Second degree AV block type II - ✔✔P-R interval fixed and normal, random
dropping of one QRS complex, QRS wide DT BBB.
✔✔Complete AV block (3rd degree) - ✔✔no relationship between P and QRS.
✔✔Tall peaked T waves, flattened P waves, ST segment depression, wide QRS interval
- ✔✔hyperkalemia
✔✔U waves on EKG - ✔✔hypokalemia
✔✔Camel Hump and McDonalds on EKG - ✔✔hypokalemia
, ✔✔What leads are best to see electrolyte disturbances - ✔✔V2-V4
✔✔ST segment leaning towards QRS, prolonged Q-T interval, lengthened ST segment
- ✔✔hypercalcemia
✔✔What are the stages of Acute Coronary Syndrome (ACS) - ✔✔First stage,
Intermediate stage, Advanced stage
✔✔First stage of ACS - ✔✔Begins with fatty streaks
Infiltration, leukocytes, lipids and macrophages accumulate
Foam cells created
✔✔Atheroma
Endothelial cell injury via platelet aggregation and PDGF = proliferation of smooth
muscle cells that becomes foam cells
Edothelial dysfunction that permits various blood components into intimal layer
Inflammation with eventual bulging onto the arterial lumen - ✔✔Intermediate stage of
ACS
✔✔Athermoa - ✔✔consists of foam cells, smooth muscle cells, connective tissue
✔✔Fibrous cap over fatty lesion = complex (crescent moon) lesion
Complicated lesion of fibrous plaques
Plaque rupture - ✔✔Advanced stage ACS
✔✔Responsible for 75% of the thrombi associated with ACS - ✔✔Disrupted plaques
✔✔What med decreases inflammation and creates fibrous caps to make sure plaque
doesn't rupture - ✔✔Statins
✔✔Acute Coronary Syndrome (ACS) - ✔✔The clinical manifestation of plaque rupture
with subtotal or total occlusion of the affected artery
✔✔How to diagnose ACS according to the WHO - ✔✔Must have two of the three
criteria:
-Clinical hx of ischemic type CP
-Changes on serial ECG tracings
-A rise and fall in serum cardiac markers
✔✔CAD generally develops silently until a crisis occurs. List three. - ✔✔Stenosis
Thrombosis
Aneurysm or embolism
A+
✔✔Grade 5 murmur - ✔✔Very loud, with thrill. May be heard when the stethoscope is
partly off the chest
✔✔Grade 6 murmur - ✔✔Audible without stethoscope
✔✔Lead 1 is good to see what kind of rhythms? - ✔✔ventricular
✔✔Lead 2 is good to see what kind of rhythms? - ✔✔atrial
✔✔What leads to you check to see where VT is coming from? - ✔✔V1 and V6
✔✔If QRS is positive and wide in V1, consider what 3 issues? - ✔✔RBBB, left
ventricular ectopic beats, WPW syndrome
✔✔If QRS is wide in V1, what lead do you also check? - ✔✔V6
✔✔What med do you avoid in SVT? - ✔✔cardizem, can cause pt to code
✔✔tx for symptomatic SVT - ✔✔adenosine
✔✔tx for persistent symptomatic SVT - ✔✔cardiovert
✔✔Left ventricular rhythms mimic what in V1 - ✔✔RBBB
✔✔Right ventricular rhythms mimic what in V1? - ✔✔LBBB
✔✔Ventricular Escape rhythm - ✔✔20-40 bpm
✔✔Accelerated Ventricular Rhythm - ✔✔50-100 bpm
,✔✔HR for ventricular tachycardia - ✔✔100+ bpm
✔✔If QRS in V6 is negative and wide - ✔✔VT indicator
✔✔WPW syndrome - ✔✔short PR interval, delta waves (slur on the upstroke of the
QRS) and wide QRS
✔✔Nadir <0.06 - ✔✔LBBB
✔✔nadir - ✔✔lowest point of QRS complex
✔✔nadir >0.07 - ✔✔right ventricular ectopy
✔✔Junctional Escape Rhythm - ✔✔40-60 bpm
✔✔Accelerated Junctional Rhythm - ✔✔60-100 bpm
✔✔Junctional Tachycardia - ✔✔100+ bpm
✔✔Junctional Rhythm - ✔✔heart is paced by the AV node
✔✔"Scooped out" ST segment indicative of - ✔✔dig toxicity
✔✔What med is notorious for causing junctional arrhythmias - ✔✔Digoxin
✔✔PR interval >0.20 seconds - ✔✔1st degree AV block
✔✔2nd degree AV block type I (Wenckebach) - ✔✔Progressively prolonged PR interval
until eventually dropped (P wave followed by missing QRS)
✔✔Second degree AV block type II - ✔✔P-R interval fixed and normal, random
dropping of one QRS complex, QRS wide DT BBB.
✔✔Complete AV block (3rd degree) - ✔✔no relationship between P and QRS.
✔✔Tall peaked T waves, flattened P waves, ST segment depression, wide QRS interval
- ✔✔hyperkalemia
✔✔U waves on EKG - ✔✔hypokalemia
✔✔Camel Hump and McDonalds on EKG - ✔✔hypokalemia
, ✔✔What leads are best to see electrolyte disturbances - ✔✔V2-V4
✔✔ST segment leaning towards QRS, prolonged Q-T interval, lengthened ST segment
- ✔✔hypercalcemia
✔✔What are the stages of Acute Coronary Syndrome (ACS) - ✔✔First stage,
Intermediate stage, Advanced stage
✔✔First stage of ACS - ✔✔Begins with fatty streaks
Infiltration, leukocytes, lipids and macrophages accumulate
Foam cells created
✔✔Atheroma
Endothelial cell injury via platelet aggregation and PDGF = proliferation of smooth
muscle cells that becomes foam cells
Edothelial dysfunction that permits various blood components into intimal layer
Inflammation with eventual bulging onto the arterial lumen - ✔✔Intermediate stage of
ACS
✔✔Athermoa - ✔✔consists of foam cells, smooth muscle cells, connective tissue
✔✔Fibrous cap over fatty lesion = complex (crescent moon) lesion
Complicated lesion of fibrous plaques
Plaque rupture - ✔✔Advanced stage ACS
✔✔Responsible for 75% of the thrombi associated with ACS - ✔✔Disrupted plaques
✔✔What med decreases inflammation and creates fibrous caps to make sure plaque
doesn't rupture - ✔✔Statins
✔✔Acute Coronary Syndrome (ACS) - ✔✔The clinical manifestation of plaque rupture
with subtotal or total occlusion of the affected artery
✔✔How to diagnose ACS according to the WHO - ✔✔Must have two of the three
criteria:
-Clinical hx of ischemic type CP
-Changes on serial ECG tracings
-A rise and fall in serum cardiac markers
✔✔CAD generally develops silently until a crisis occurs. List three. - ✔✔Stenosis
Thrombosis
Aneurysm or embolism
