Apex- Monitors and Equipment > Cardiac rhythms Flashcards

Question

All of the following are effective for treatment of afib EXCEPT: A. Verapamil B. Digoxin C. Metoprolol D. Adenosine

Answer 1

Adenosine -it slows conduction through the AV node - stimulates cardiac adenosine-1 receptor; adenosine activates K+ currents → hyperpolarizes cell membrane and reduces AP duration | not efficaious for afib, flutter, torsades, or VT ## Footnote works well for SVT and WPW with a narrow QRS

Answer 2

sinus arrhythmia → occurs wehn the SA node's pacing rate varies with respiration (usually benign) Bainbridge reflex can cause this! Inhalation → decreased intrathoracic pressure → increased venous return → increased HR Exhalation → increased intrathoracic pressure → decreased venous return → decreased HR

Answer 3

increased vagal tone

Answer 4

Atropine ## Footnote underdosing it (<0.5mg IV) can cause paradoxical bradycardia which is thought to be mediated by presynaptic muscarinic receptors THEN WHY TF DOES IT COME IN 0.4mg/ml VIALS?

Answer 5

immediate transcutaneous pacing

Answer 6

Glucagon initial dose = 50-70mcg/kg q 3-5min can be followed by infusion of 2-10mg/hr it stimulates glucagon receptors on the myocardium, which increases cAMP → increased HR, contractility, AV conduction

Answer 7

Cardioversion - start at 100j

Answer 8

if afib onset is >48hrs ago or if onset is unknown ## Footnote to r/o atrial thrombus

Answer 9

afib | POD 2-4 ## Footnote older patients after CT sugery

Answer 10

True *Atropine 0.5mg IV can be given if hemodynamics are affected ## Footnote can progress to junctional tachycardia (narrow complex tachycardia) > can produce hemodynamic instability

Answer 11

1. Frequency > 6/min 2. polymorphic 3. runs of 3 or more ## Footnote 1. Reverse underlying cause : hypoxia, hypercarbia, d/c QT prolonging drugs, tx lytes 2. If symptomatic - Lidocaine 1-1.5mg/kg followed by a gtt @ 1-4mg/min if continues

Answer 12

Brugada Syndrome | males from southeast asia ## Footnote Right BBB and persistent ST elevation in precordial leads V1-V3 -pt may require ICD or pad placement during surgery

Answer 13

1 & 2 > ST elevations >/= 2mm 1 → DOWNSLOPING ST segment & INVERTED T-wave 2 → "saddle back" (think 2 words = 2) ST-wave configuration & UPRIGHT or Biphasic (2) T wave

Answer 14

Second degree heart block- Mobitz 2 ## Footnote Some P's conduct to the ventricles, while others don't (usually there is a set ratio of 2:1 or 3:1). After the dropped QRS, the next P arrives right on time

Answer 15

Second degree heart block- Mobitz 2 ## Footnote Some P's conduct to the ventricles, while others don't (usually there is a set ratio of 2:1 or 3:1). After the dropped QRS, the next P arrives right on time

Answer 16

PR > 0.20 ## Footnote usually asymptomatic and no treatment required

Answer 17

1 → wenchebach- PR longer longer drop 2 → Some P's conduct to the ventricles while others dont (usually set ratio of (2:1 or 3:1) | often asympomatic ## Footnote 1 → atropine if symptomatic 2 → pacing

Answer 18

False - Mobitz 1 ## Footnote Mobitz 2 often does not respond to Atropine and pacing is required

Answer 19

1. age related degenerative changes 2. CAD 3. drugs: dig/amio

Answer 20

1st degree heart block ## Footnote monitor (usually asymptomatic)

Answer 21

Second degree- Mobitz 1 (Wenkebach) ## Footnote asymptomatic - nothing symptomatic - atropine

Answer 22

1. fibrotic degeneration of the atrial conduction system 2. Lenegres Disease

Answer 23

CHB ## Footnote mechanical pacemaker (transcutaenous, transvenous, implantable) chemical pacemaker (isoproterenol)

Answer 24

CHB - decreased CO → decreased cerebral perfusion → syncope

Answer 25

Mobitz 2 & CHB

Answer 26

Isoproterenol

Answer 27

1 → Lidocaine 2 → Propanolol 3 → Amiodarone 4 → Verapamil ## Footnote 1 → inhibit fast sodium channels 2 → decrease rate of depolarization 3 → inhibit potassium ion channels 4 → inhibit slow calcium channels

Answer 28

1 → Sodium channel blockers 2 → Beta blockers 3 → K+ channel blockers 4 → Calcium channel blockers ## Footnote 1 → quinidine, procainamide, disopyramide; lidocaine & phenytoin; flecainide, propafenone 2 → obvious ones 3 → amiodarone & bretyium 4 → verapamil & diltazem

Answer 29

1 → depression of phase 0 & phase 3 repolarization 2 → slows phase 4 depolarization in the SA node 3 → prolongs phase 3 repolarization 4 → decreases conduction velocity through the AV node ## Footnote 1→ sodium channel blockers (lido) 2 → betablockers 3 → k+ channel blockers (amio) 4 → calcium channel blockers (verapamil and cardizem)

Answer 30

It prolongs phase 3 repolarization (increases Qt), increases effective refractory period | K* channel blocker ## Footnote bretium also in this class (class 3)

Answer 31

class 1 = sodium channel blockers (phases 0 and 3) 1A: *mod* ↓phase 0; *prolonged* phase 3 (increased Qt) 1B: **weak** ↓phase 0;** shortened **phase 3 1C: STRONG ↓phase 0, little effect on phase 3 ## Footnote 1A → quinidine, procainamide, disopyramide 1B → lidocaine, phenytoin 1C → flecainide, propafenone

Answer 32

* Slowing of phase 4 depolarization → Class 2→ betablockers * Strong depression of phase 0, little effect on phase 3 repolarization → class 1c → Na channel blockers - flecanide & propafenone * Prolonged phase 3 repolarization → K+ channel blocker (increased QT) → amio & bretyium * Moderate depression of phase 0 depolarization + prolonged phase of phase 3 repolarization (increased QT) → Class 1A → quinidine, procainamide, disopyramide * Decreased conduction velocity trhough AV node → Class 4 → Ca++ channel blockers → verapamil and diltazem * Weak depression of phase 0, shortened phase 3 repolarization → class 1B (NA++ blockers) → lidocaine and phenytoin ## Footnote *When thinking about how antidysrhythmics work, ask yourself: 1. Are they depressing phase 0 (class 1) 2. Are they effecting phase 3 repolarization (class 1, 3) 3. Or are they slowing phase 4 depolarization (class 2)

Answer 33

Yep, it slows conduction through the AV node ## Footnote it stimulates the cardaic adenosine-1 receptors and promotes potassium efflux, hyperpolarizing hte cell membrane, and slowing conduction

Answer 34

rapidly in the plasma ## Footnote 5 seconds

Answer 35

FALSE ## Footnote not useful for afib/flutte -- only SVT and WPW with narrow complex

Answer 36

Peripheral 6mg → 12mg Central 3mg → 6mg ## Footnote *AC preferrerd for peripheral - closest to heart

Answer 37

C. A-V reentry ## Footnote * WPW occurs when an accessory pathway joins the atrium to the ventricles (kent's bundle)

Answer 38

Re-entry pathways

Answer 39

Cardioversion and Procainamide

Answer 40

refractory period ## Footnote in the accessory pathway, there is no delay, so the impulse quickly moves from the atrium to the ventricle → there is no gate keeper (slowed movement thru the AV node)

Answer 41

* Delta wave | Short PR (<0.12), Wide QRS, Possible T-wave inversion ## Footnote After the SA node depolarizes, the electricle impulse travels through the accessory pathway and the same time as the AV node; the accessory pathway route is not delayed like the AV route and arrives at the ventricle earlier, causing the delta wave.

Answer 42

## Footnote antidromic is more dangerous bc the gatekeeper function of the AV node is bypassed and the heart rate can increase well beyond the heart's pumping ability (dramatically reducing filling time)

Answer 43

Lidocaine Adenosine Beta-blockers Calcium channel blockers Digoxin (L-ABCD) (Love ABCD) ## Footnote Bc if you give a drug that preferentially blocks the AV node to an antidromic AVNRT, then you'll force conduction along the acessory pathway which can induce vfib!

Answer 44

bc during afib the atria can depolarize up to 300 times a mintue, and combining this with WPW can preciptate CHF, vfib, and death. ## Footnote *Procainamide is the treatment of choice bc it increases the refractory period in the accessory pathway. If the patient is hemodynamically unstable, then cardioversion is the best option *avoid drugs that increase the refractory period of the AV node

Answer 45

radiofrequency ablation of the accessory pathway

Answer 46

it can cause hypokalemia and hypomagnesia which both can prolong the QT ## Footnote when asked about how something affects the QT interval - think does it affect the lytes? low lytes = long qt

Answer 47

hyperventilation shifts K+ into the cells → decreased serum K can prolong the QT interval

Answer 48

mag sulfate and cardiac pacing

Answer 49

Romano Ward & Timothy Timothy Romano Ward

Answer 50

men > 0.45 women > 0.47

Answer 51

bc the QT interval varies **inversely** with HR

Answer 52

Postion 1 → chamber Paced Position 2 → chamber Sensed Position 3 → Response to sensed event Postion 4 → Programability ## Footnote **PaSeR** Chamber **Pa**ced Chamber **Se**nsed **R**esponse of pacmaker if native activity is sensed

Answer 53

Single-chamber demand pacing | BACKUP MODE ## Footnote only fires wehn the native HR falls below a pre-determinded level AAI - atria paced, atria sensed, inhibition VVI - ventricle paced, ventricle sensed, inhibition *inhibition = if natative activity is sensed, the pacemaker is inhibited (won't fire -- unless under a certain rate)

Answer 54

DDD | dual paced, dual sensed, dual response ## Footnote ensures the atrium contracts first, followed by the ventricle and improves AV-synchrony

Answer 55

Asynchrounous pacing -Atrium is paced, no chamber is sensed, and no response to native cardaic electricle activity ## Footnote R-on-T

Answer 56

Single-chamber demand pacing Ventricle is paced and sensed & the pacer is inhibited if native electric activity is sensed

Answer 57

A. EtCO2 was 20mmHg ## Footnote The pacer failed to capture because hypocarbia (which caused hypokalemia) made the myocardium more resistant to depolarization. The same electrical stimulus from the pacer was no longer sufficent to depolarize the heart. You'll see the pacer spikes, but you wont see capture -when compared to ESU, the use of a ultrasonic harmonic scalpel decreases the risk of electromagnetic interference -changes from "coag to cutting" also reduces the risk of EMI -hypothermia makes the myocardium more resistant to to depolarization (also explains why hypothermia causes bradycardia)

Answer 58

Pacer → converts it to asynchronous mode (usually but not always) > asynchonous = delivers a constant rate despite underlying native activity ICD → suspends ICD and prevents shock delivery PACER+ICD: suspends ICD and prevents shock delivery; no effect on pacemaker function (interesting?)

Answer 59

what's their underlying rhythm - so you know how to prepare for device failure ## Footnote -can be treated with isoproterenol, epi, or atropine (depends on the underlying rhythm)

Answer 60

failure to sense -pacer is sending sporatic impulses -concern for R on T ## Footnote not sure wtf i would do other than consult cardiology to interrogate it?

Answer 61

failure to capture conditions that can hyperpolarizing the myocardium, making it more resistant to depolarization (electrical stimulus) - hyperkalemia, hypokalemia - hypocapnia (intracellular K shift) - hypothermia - MI - Fibrotic tissue builiding up on leads - Antiarrythmic meds ## Footnote can also be from electrode displacement or wire fracture

Answer 62

15cm ## Footnote (i read somewhere that concern should be have when operating above umbilicus)

Answer 63

far away from the generator, in a location that prevents a direct line of current thru it

Answer 64

False - the beam should be directed away from the generator

Answer 65

false ## Footnote MRI is the only contraindication (even though some newer ones are MRI safe)

Answer 66

A. Bundle of His ## Footnote It's Mobitz 2 - affected regions of this are the His bundle or bundle branches

Answer 67

A. Bundle of His ## Footnote It's Mobitz 2 - affected regions of this are the His bundle or bundle branches

Answer 68

B. Peaked T's ## Footnote - PR depression > pericarditis - Deep Q waves > MI - U waves > hypokalemia

Answer 69

Left axis devation Lead 1 is postive and AVF is negative

Answer 70

Bottom left

Answer 71

Bottom left

Answer 72

-90 to -30 degrees ## Footnote Normal = -30 to +90 Left axis = < -30 (L , to the Left) Right = > +90 (R, to the right)

Answer 73

A. PR segment ## Footnote The J point is where the QRS complex ends and the ST segment begins. By measuring this point relative to the PR segment, we can quantify the amount of elevation and depression

Answer 74

A. PR segment ## Footnote The J point is where the QRS complex ends and the ST segment begins. By measuring this point relative to the PR segment, we can quantify the amount of elevation and depression

Answer 75

FALSE - no one in the OR should be grounded, not even the patient ## Footnote it is a return electrode where electricty flows after it flows through the tip of the electrocautery > pt > exits patient through the return electrode

Answer 76

Torrsaddes (+Timothy disease)

Answer 77

CLASS 1A antidysrhythmic w procainamide and quinidine Mod phase 0, prolonged phase 3(qt)