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CM I - Exam 1 (Cardio) > Arrhythmias > Flashcards

Arrhythmias Flashcards

1
Q

a fib

A

rapid, irregular, atrial activation (atria quiver instead of contracting properly, causes blood to pool & form a clot –> increased r/o stroke)
-very common
-increased risk w/ age

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2
Q

a fib sx

A

-may be asx
-palpitations (all arrhythmias), tachycardia (100-200 bpm), fatigue, weakness, mild dyspnea
-irregularly irregular pulse
others: stroke, thromboembolism

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3
Q

Dx studies for a fib

A

EKG: no p waves, ventricular rhythm lacks a repetitive pattern

ECHO: should be done on all pts w/ new onset a. fib to look for clots

Labs: CBC, electrolytes, renal fxn

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4
Q

a fib tx (address rhythm)

A

-cardiac ablation: better than drugs but higher r/o stroke (ex. atrioventricular junction ablation w/ cardiac resynchronization therapy - destroys link btwn LA and LV, f/b pacemaker implantation)
-drugs: AMIODARONE has least cardiotoxic AEs & is more effective than sotalol, donedarone, propafenone, flecainide; start in hosp to closely monitor!
-cardioversion: must be on AC for 3 wks and have TEE prior

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5
Q

A fib: tx of rate vs rhythm

A

-for decades, rate control was deemed most important d/t AEs of anti-arrhythmics and “noninferiority” of rate control agents
-recent studies, lean towards prioritizing rhythm control
-there are times when both are important

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6
Q

a fib tx (address rate)

A

-indications: asx, elderly, long-standing afib, markedly enlarged left atrium
-1st line: B-blockers and non-DHP (CCB) ***avoid CCB in pts w/ CHF
-less aggressive rate control (<110bpm) is preferred over more intense rate control (<80bpm)

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7
Q

a fib tx (address stroke risk)

A

Calc CHA2DS2-VASc score –>
-start oral AC if 2+ in men or 3+ in women
-may consider LAA closure (i.e. WATCHMAN device) depending on score

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8
Q

What does CHA2DS-VASc score stand for/consider

A

CHF
HTN
Age 75+ (doubled)
DM
Stroke (prior stroke, TIA, or thromboembolism) (doubled)
Vascular dz
Age 65-74
Sex category

*each is worth 1 pt unless it says “doubled”

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9
Q

Stroke risk AC: new oral AC (NOACs) that are now recommended over warfarin

A

-Dabigatran (Pradaxa)
-Apixaban (Eliquis)
-Rivaroxaban (Xarelto)
-Edoxaban

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10
Q

When is warfarin still recommended over other NOACs

A

if pt has moderate/severe mitral stenosis, advanced kidney dz, or if pt has an artificial heart valve

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11
Q

Supraventricular tachycardias

A

-caused by premature signaling in atria
-often paroxysmal (PSVT)

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12
Q

Supraventricular tachycardia S/S

A
  • > 100 bmp (often 150-200)
    -narrow QRS
    -palpitations, dyspnea, dizziness, chest discomfort, syncope
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13
Q

3 types of supraventricular tachycardia (most to least common) and their changes on EKG

A
  1. AVNRT (atrioventricular node reentry): retrograde p wave falls w/in or just after QRS
  2. AVRT: reentry involving an accessory pathway (i.e. WPW - short PR interval)
  3. Focal & Multifocal Atrial tachycardia: p waves immediately in from of QRS complex

*supraventricular –> think above ventricles, which lies the atria; on EKG the p wave represents the atria, therefore these will have p wave abnormalities

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14
Q

AVNRT (AV nodal reentrant tachycardia)

A

-MC type of PSVT
-reentry circuit involving the AV node & nearby atrial tissue –> leads to separate pathways w/in the AV node, resulting in tachycardia d/t premature beats
-usu presents after age 20

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15
Q

Dx of AVNRT (s/s, dx test results)

A

-HR of 150-250 bpm
-palpitations, lightheadedness, dizziness, dyspnea
-neck pounding secondary to CANNON WAVES is pathognomonic
-EKG (PAC w/ prolonged PR at beginning, p wave in or just after QRS - may be superimposed (“pseudo-r”))

*pathognomonic = specifically typical of that disease
*cannon waves are d/t atria & ventricles contracting simultaneously causing waves in the blood

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16
Q

what are cannon waves and what condition is this associated with?

A

cannon waves are d/t atria & ventricles contracting simultaneously causing waves in the blood

associated with AVNRT

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17
Q

AVNRT: acute management tx

A

-if hemodynamically stable, try vagal maneuvers (Valsalva)
-if Valsalva doesn’t work, give IV adenosine
-If adenosine is ineffective, give IV verapamil or IV metoprolol
-If all fails, OR if pt is hypotensive, has angina pectoris, or has CHF, then cardioversion is performed
*if refractory (resistant to tx) then perform advanced CV life support (ACLS)

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18
Q

how does the Valsalva maneuver work

A

holding your breath and bearing down decreases blood return to the heart –> stim symNS –> increased HR and contractility –> stim parasymNS to compensate for overstim of symNS –> decreased HR and contractility

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19
Q

AVNRT: preventative therapy

A

depends on frequency of arrhythmia, severity, pt preference, etc.

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20
Q

Tx for recurrent AVNRT (Cure rate)

A

catheter ablation
-95% cure rate

*if pt can’t undergo ablation, then use B-blockers, non-DHP (CCB), anti-arrhythmics

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21
Q

WPW

A

<1% of population
-accessory pathways connect the atria and ventricles; AV node is bypassed
-dx in teenager/early adulthood

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22
Q

Sx of WPW

A

dizziness
syncope
SOB
weakness
chest pain

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23
Q

EKG findings w/ WPW

A

short PR interval
delta wave

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24
Q

WPW: Tx

A

-Goals: reduce sx and prevent life-threatening arrhythmia
-urgent cardioversion if hemodynamically unstable (low BP, elevated HR)
-Vagal maneuvers
-Adenosine 1st choice if vagal maneuvers fail; Verapamil 2nd line
-Long-term management: catheter ablation

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25
Q

Focal Atrial Tachycardia (what is it, what causes it, EKG findings, long-term therapy)

A

-small area in atria generates impulses that override SA node
-can be d/t meds, caffeine, alcohol, or idiopathic
-EKG: abnormal p wave morphology, QRS is normal
-Long-term therapy: uncertain, drugs (???), catheter ablation may be effective in 70-90%

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26
Q

Multifocal Atrial Tachycardia (MAT)

A

100-130bpm
-3+ morphologically distinct p waves
-irregular
-multiple areas of the atria are sending electrical impulse randomly
(same sx as other arrhythmias)

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27
Q

what diseases are MAT associated with

A

respiratory dz (MAT is secondary to COPD, hypoxia, pulm HTN)
CHF

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28
Q

MAT: Tx

A

tx underlying problems (oxygen)
rate control w/ Metoprolol or Verapamil

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29
Q

atrial flutter

A

rapid, circular (more organized than a fib), reentrant atrial arrhythmia

30
Q

clinical presentation of atrial flutter (s/s)

A

-unusual in pts w/o cardiac dz (a fib, valvular dz, cardiomyopathy) or pulm dz
-palpitations, fatigue, dizziness, dyspnea
-tachycardia, hypotension, diaphoresis

31
Q

Atrial flutter: Dx tests

A

EKG: ventricular rate ~150bpm, p waves absent, “sawtooth” pattern in II, III, aVF

Echo: perform in all new diagnoses

32
Q

Atrial flutter: Tx/Management

A

-rate control
-AC

33
Q

comparing presentation and tx of a fib and a flutter

A

presentation is the same

tx for both is rate control and AC but for a fib you can consider cardioversion & anti-arrhythmics

34
Q

Ventricular tachyarrhythmias (organized re-entry vs disorganized re-entry)

A

Organized re-entry (>120bpm): non-sustained VT (<30 secs, may be asx) and sustained VT (lasts 30+ secs)

Disorganized re-entry: V fib (350-450 bpm), Torsades de Pointes(250-350 bpm)

*all except non-sustained VT can lead to cardiac arrest

35
Q

Ventricular tachycardia: monomorphic vs polymorphic

A

Monomorphic: single focus or reentrant pathway; regular identical QRS complexes

Polymorphic: several foci or pathways; irregular, varying QRS complexes

36
Q

Ventricular tachycardia

A

3+ consecutive ventricular beats at 120+ bpm
-occurs MC in pts w/ past MI or cardiomyopathy
-frequently deteriorates to ventricular fibrillation (scary!)

37
Q

Sx of VT

A

variable
-if sustained, pt may have palpitations, hemodynamic compromise (decreased BF to body/shock), or sudden cardiac death

38
Q

Dx of VT

A

any wide QRS complex tachycardia should be considered VT until proven otherwise

39
Q

VT: Tx depending on type of VT

A

Non-sustained VT: no immediate tx unless sx occur; if sx occur drugs are usually used

Hemodynamically stable sustained VT: cardioversion or antiarrhythmics (lidocaine, procainamide, amiodarone)

Pulseless VT (hemodynamically unstable): defibrillation

ICD is often used for long-term prevention of sudden death

40
Q

What may occur if CCB are used in a pt w/ VT

A

hemodynamic collapse, so AVOID CCB!!!

41
Q

Cardioversion

A

different from defibrillation in that the shock is synchronized (given at certain time) and has less energy

42
Q

Long Q-T syndrome causes

A

can be congenital or acquired (d/t drugs, hypokalemia, or hypomagnesemia)

43
Q

Long-QT syndrome: Sx

A

most acquired cases are asymptomatic

sometimes pts have palpitations, syncope, cardiac arrest
**pay attention to hx of syncope

44
Q

Long-QT syndrome: Prognosis

A

-increased r/o sudden death if have congenital deafness, h/o syncope, female, and VT during monitoring

45
Q

What is your biggest fear with long QT syndrome

A

Torsades de Pointes (bc long QT synd messes w/ how your heart relaxes and recharges)

46
Q

What may be the result of untreated long QT syndrome

A

if untreated, 50% have experienced LOC or cardiac arrest by age 12

47
Q

Long QT syndrome: Tx

A

-B-blockers
-Surgical sympathectomy if unresponsive to drugs (removal of ganglion)

48
Q

Torsades de Pointes (“twisting of the points”)

A

a polymorphic VT w/ a long QT
-may degenerate into v fib (scary!)
-points & curves alternate up and down on EKG

49
Q

Torsades de Pointes: Tx

A

-MAGNESIUM in the short-term
-B-blockers (propranolol) in the long-term

50
Q

V fib

A

-uncoordinated quivering of ventricles
-results in no useful contractions (lethal bc no CO)
-on EKG rate and rhythm are fast and irregular, p waves and QRS are absent

51
Q

What % of cardiac arrest pts present with V fib

A

70%

52
Q

V fib Tx

A

-requires CPR and defibrillation, Epi q3-5minutes

53
Q

commonality of PVCs (premature ventricular contractions)

A

1/2 of all people have them

more likely in older pts

54
Q

If PVCs are found post-MI what does this mean

A

higher risk of death

55
Q

Increased risk of ____ if EF is <50% in conjunction w/ PVCs

A

cardiac arrest

56
Q

PVC Sx

A

mostly asymptomatic
-may have palpitations (MC), dizziness (uncommon)

57
Q

PVC signs

A

exam is usually normal, may be an irregular pulse during PVCs

58
Q

Dx tests for PVCs

A

EKG
ECHO if significant sx or suspicious of structural dz

59
Q

Tx of PVCs

A

-eliminate triggers if possible (alcohol, caffeine, thyroid dz, anemia, stress/anxiety)
-B-blockers, CCBs, ablation if medical therapy doesn’t work

60
Q

EKG findings for PVCs

A

P wave: usu doesn’t precede QRS; may be seen after QRS causing distortion of ST segment

QRS: wide, abnormal

ST segment & T wave: inverted

R-R interval: usu f/b a full compensatory pause

60
Q

bigeminy, trigeminy, couplet

A

Bigeminy: PVC after every normal beat

Trigeminy: PVC after every 2 normal beats

Couplet: Two PVCs in a row

61
Q

What % of pts >50yo have at least one PAC/hr

A

99% of pts over 50 have at least 1 PAC/hr

62
Q

PAC EKG findings

A

abnormal (shape) p waves
atria contract early so may have p wave early

63
Q

sinus bradycardia

A

sinus rhythm w/ <60 bpm

64
Q

Cause of sinus bradycardia

A

-may be normal in many healthy adults and children, particularly during sleep and in endurance athletes

-Pathological causes: dysfunctional SA node, meds (B-blockers), AMI, OSA, infectious diseases

65
Q

Sinus bradycardia: Sx

A

if sx occur, they include lightheadedness, fatigue, syncope

66
Q

Sinus bradycardia: Tx

A

-if no sx, then no tx required
-if tx is necessary, IV atropine is often used
*If atropine doesn’t help, then pacing is performed

67
Q

1st, 2nd, and 3rd degree Heart Block (poem)

A

If the R is far from P (slow transmission, long PR interval), then you have a 1st degree

Long, longer, longest, drop! Then you have a Wenkebach (Mobitz I)

If some Ps don’t get through (missing QRS-T), then you have Mobitz II (more likely to have sx and need tx)

If Ps (atria) and Qs (ventricles) don’t agree, then you have a 3rd degree

68
Q

Heart Block Sx (based on degree)

A

1st degree & Wenkebach: typically asx

Mobitz II (sometimes Wenkebach: palpitations

3rd degree: palpitations & syncope

69
Q

Heart block tx

A

Pacemaker for Mobitz II and 3rd degree blocks

CM I - Exam 1 (Cardio) (11 decks)

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