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Fall 2014 - CM Cardio > Conduction Disorders (Cardio 1) > Flashcards

Conduction Disorders (Cardio 1) Flashcards

1
Q

What characteristics must a rhythm have to be considered a SINUS rhythm?

A
  1. regular, upright P waves
  2. normal PR interval (.12-.20)
  3. regular QRS with normal width (.08-.12)
  4. P:QRS relationship is 1:1
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2
Q

Normal Sinus Rhythm Characteristics

A
  • rate is 60-100
  • regular, upright P waves
  • normal PR interval
  • regular QRS with normal width
  • P:QRS is 1:1
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3
Q

Sinus Bradycardia Characteristics

A
  • rate < 60
  • normal sinus P’s
  • normal PR interval
  • 1:1 AV conduction
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4
Q

Causes of Sinus Bradycardia

A
  1. physiologic: well-conditioned athlete, sleep, vagal stimulation
  2. pharmacologic: digoxin, beta blockers, calcium channel blockers
  3. pathologic: inferior MI, increased intracranial pressure, hypothyroidism
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5
Q

Clinical Significance of Sinus Bradycardia

A

-depends on cause

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6
Q

Sinus Tachycardia Characteristics

A
  • acceleration of sinus rate (100-160)
  • normal sinus P’s
  • normal PR interval
  • 1:1 AV conduction
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7
Q

Causes of Sinus Tachycardia

A
  1. physiologic: infants/kids, exertion, anxiety
  2. pharm: atropine, epinephrine, nicotine, caffeine, cocaine
  3. pathologic: fever, hypoxia, anemia, pulmonary embolus
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8
Q

Tx of Sinus Tachycardia

A
  • usually none, but need to investigate underlying cause

- in setting of acute MI, consider beta blockers

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9
Q

Sinus Arrhythmia Characteristics

A
  • variation in sinus node discharge rate (irregular)
  • normal P waves
  • normal PR interval
  • 1:1 AV conduction
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10
Q

Sinus Arrhythmia Causes

A
  • most common in kids, young adults
  • usually results from change in vagal tone during respiration (rate does not speed up w/ inspiration, it SLOWS with expiration)
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11
Q

Clinical Significance of Sinus Arrhythmias

A
  • benign

- usually asymptomatic

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12
Q

Tx of Sinus Arrhythmias

A

none

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13
Q

For irregular rates, how are these estimated and reported?

A
  • take an average of the rate for the shortest QRS interval and longest interval
  • for irregular rates, must put about 80 or 80I
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14
Q

How do you determine regular vs. irregular on a rhythm strip?

A

-look at the QRS spacing

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15
Q

Atrial Flutter Characteristics

A
  • regular atrial rate 250-350 bpm (300 most common; get this by looking @ the P waves)
  • sawtooth flutter waves
  • AV block, usually P: QRS of 2:1 (ventricular rate 150)
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16
Q

Where in the heart is the problem spot in atrial flutter?

A

above the AV node b/c things are normal on the rhythm strip once it hits AV (QRS is normal)

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17
Q

Causes of Atrial Flutter

A
  • 60% due to underlying heart dz (ischemic heart dz, acute MI, HTN)
  • 30% no cause
  • also seen with pulmonary embolus, digoxin toxicity
  • may be transitional arrhythmia between sinus rhythm and atrial fibrillation
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18
Q

Symptoms of Atrial Flutter

A
  • palpitations (heart jumping or feeling funny)
  • fatigue
  • dyspnea
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19
Q

Tx of Atrial Flutter

A
  • carotid sinus massage may transiently slow conduction rate to make atrial flutter and make sawtooth more evident
  • low energy electrical cardioversion >90% success
  • may control ventricular rate with digoxin, calcium channel blockers, beta blockers
  • chemical conversion using type Ia, Ic, III
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20
Q

What is actually happening in the heart during atrial flutter?

A
  • atria depolarize/contract and dump blood to ventricles, depolarize and dump, depolarize and dump
  • ventricles now have more blood in them than they should
  • blood not getting to lungs = SOB
  • then ventricles contract
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21
Q

Atrial Fibrillation Characteristics

A
  • no organized P waves, only shimmering baseline
  • irregular ventricular rhythm (usually rapid 160-180)
  • normal QRS width
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22
Q

Causes of Atrial Fibrillation

A
  • most common: rheumatic heart dz, HTN, ischemic heart dz, thyrotoxicosis
  • other: COPD, pulmonary embolus, pericarditis, ETOH
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23
Q

Clinical Significance of Atrial Fibrillation

A
  • multiple areas of atria continuously depolarizing
  • no uniform atrial depolarization (bag of worms, quivering)
  • atrial depolarization rate >400, but refractory period of AV node means a slower ventricular response
  • loss of atrial contraction can lead to heart failure in patients with underlying left ventricular dysfunction
  • rapid ventricular response may lead to myocardial ischemia, hypotension, shock
  • increased risk of stroke
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24
Q

Tx of Unstable A Fib Patient

A

-immediate electrical cardioversion (if hypotension, shock, pulmonary edema)

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25
Q

Tx of Stable A Fib Patient

A
  • control ventricular rate with IV or oral calcium channel blockers or beta blocker
  • chemical cardioversion Ia, Ic, III
  • can consider electric cardioversion of stable pt prior to 7 days but do not cardiovert if a fib. present >48 hours (higher risk of systemic emboli; must anticoagulate coumadin at least 3 weeks prior to cardioversion)
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26
Q

Chemical Cardioversion Agents

A
  • Ia: procainamide, qunidine
  • Ic: flecanide, propafenone
  • III: ibutilide, amiodarone
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27
Q

Supraventricular (Atrial) Tachycardia Characteristics

A
  • regular, rapid atrial rhythm (160-200)
  • P waves often difficult to see (might be buried in T waves)
  • QRS complexes usually normal width
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28
Q

Causes of Supraventricular Tachycardia

A
  • fairly common (2/1000)
  • can occur in otherwise normal heart
  • no age or sex predisposition
  • sometimes seen in association with MI, rheumatic heart dz, pericarditis, mitral valve prolapse
  • due to “reentry” of depolarization
29
Q

Clinical Significance Supraventricular Tachycardia

A
  • abrupt onset of tachycardia caused by reentry of electrical impulse in atria via closed loop of conducting tissue
  • usually well-tolerated in young healthy patients; may cause palpitations, lightheadedness, dizziness, SOB
  • in elderly patients or those with heart dz: syncope, pulmonary edema, myocardial ischemia
30
Q

Tx of Supraventricular Tachycardia

very general categories… will ask for detail on other cards

A
  • vagal maneuvers in stable, young patient
  • adenosine
  • verapamil
  • electrical cardioversion if unstable and refractory to above methods
  • can usually cure with radiofrequency ablation
31
Q

Vagal Maneuvers for Supraventricular Tachycardia

A
  • increase vagal tone
  • slow conduction and prolong the refractory period in the AV node
  • examples: carotid sinus massage, diving reflex, Valsalva maneuver (bearing down like pooping)
32
Q

Adenosine for Supraventricular Tachycardia

A
  • ultra-short acting AV nodal blocker
  • most commonly used SVT med
  • will stop the heart at first (5-7 secs)
33
Q

Verapamil for Supraventricular Tachycardia

A
  • a calcium channel blocker
  • longer acting than adenosine
  • blocks AVnode
34
Q

Ventricular Tachycardia Characteristics

A
  • three of more ectopic (aberrant) beats in a row
  • wide QRS
  • rate > 100 (usually 150-200)
  • usually a regular rhythm
  • may occur in short episodes or sustained
  • in v tach, you usually cannot identify P waves
35
Q

Causes of Ventricular Tachycardia

A
  • rarely seen in pts w/o underlying heart dz
  • usually seen w/ ischemic heart dz or acute MI
  • other causes: drugs, metabolic abnormalities, cardiomyopathies
36
Q

Clinical Significance of Ventricular Tachycardia

A

PATIENT MAY BE:

  • relatively stable (alert, good BP, asymptomatic) but few are like this
  • symptomatic (hypotension, chest pain, SOB, syncope)
  • pulseless in cardiac arrest
37
Q

Tx of Ventricular Tachycardia

A
  • if unstable/pulseless: immediate electric biphasic shock (100-200 J)
  • if stable, use IV antiarrhythmics: amiodarone, lidocaine, bretylium, procainamide; can try synchronized cardioversion (50-200 J) if needed
38
Q

What is synchronized cardioversion?

A

-delivers shock at the peak of the QRS complex

39
Q

What is really happening in the heart during Ventricular Tachycardia?

A
  • ventricles in charge of rhythm

- atria sort of just depolarizing w/o inducing ventricular depolarization

40
Q

Ventricular Fibrillation Characteristics

A
  • irregular zigzag pattern with no P waves or QRS
  • may be coarse (early) or fine (late) pattern
  • looks like squiggles
41
Q

Ventricular Fibrillation Causes

A
  • usual etiology: severe ischemic heart dz with or w/o acute MI
  • other: digoxin toxicity, hypothermia, blunt chest trauma, severe electrolyte imbalance (eg hyperkalemia)
42
Q

Ventricular Fibrillation Clinical Significance

A
  • totally disorganized, chaotic depolarization of small areas of the ventricle
  • no effective ventricular pumping
  • pt is pulseless and in cardiac arrest
43
Q

Ventricular Fibrillation Tx

A
  • immediate electrical defibrillation
  • CPR!
  • IV amiodarone, lidocaine and/or bretylium with repeated shocks after each dose
44
Q

AV Block First Degree Characteristics

A
  • delay in AV conduction
  • each atrial impulse is conducted to ventricles, but slower than normal
  • PR interval > .20 seconds
45
Q

AV Block First Degree Cause

A
  • sometimes found in normal hearts
  • increased vagal tone
  • digoxin toxicity
  • inferior MI
  • myocarditis
46
Q

AV Block First Degree Clinical Significance

A
  • delay usually at level of AV node

- generally benign

47
Q

AV Block First Degree Tx

A

none

48
Q

Second Degree Block Type 1 Characteristics

A
  • progressively longer PR interval until a dropped beat (blocked, non-conducted P wave)
  • cycle usually repeats itself
  • conduction ratio describes atrio-ventricular depolarizations
49
Q

Second Degree Block Type 1 Causes

A
  • acute inferior MI
  • digoxin toxicity
  • myocarditis
  • cardiac surgery
  • rheumatic heart dz
  • seen in high level athletes (increased parasympathetic tone)
50
Q

Second Degree Block Type 1 Clinical Significance

A
  • occurs at level of AV node
  • thought to be due to progressive prolongation of refractory period of AV node w/ each depolarization until AV node completely blocked; then AV node resets itself
  • generally does not progress to complete heart block
51
Q

Second Degree Block Type 1 Tx

A
  • if pt stable, no tx necessary

- if slow ventricular rate causes hypoperfusion, consider atropine and/or cardiac pacing

52
Q

Second Degree Block Type 2 Characteristics

A
  • constant PR interval (either normal or long), then a non-conducted P wave (missing QRS)
  • QRS may be narrow or wide, depending on whether or not bundle branch block also present
53
Q

Second Degree Block Type 2 Causes

A
  • acute anteroseptal MI

- cardiomyopathy

54
Q

Second Degree Block Type 2 Clinical Significance

A
  • block usually occurs in infranodal conducting system
  • prognosis worse than 2nd degree type 1
  • usually permanent
  • in setting of acute MI, may progress to complete heart block
55
Q

Second Degree Block Type 2 Tx

A
  • if slow perfusion rate produces hypoperfusion, atropine or pacing
  • most pts ultimately require pacemaker
56
Q

Third Degree Block Characteristics

A
  • atrial and ventricular depolarizations are independent of each other
  • P waves and QRS complexes have no consistent relationship
  • PR interval varies
  • QRS may be either narrow or wide
57
Q

Third Degree Block Causes

A
  • usually acute MI
  • drug effect (digoxin, beta blocker)
  • may be transient or permanent
58
Q

Third Degree Block Clinical Signficance

A

–no atrioventricular conduction

–escape pacemaker kicks in
+if nodal block: pacemaker above His bundle, produces narrow QRS escape rhythm (40-60)
+if infranodal block: pacemaker at or below His bundle, produces wide QRS escape rhythm (<40 bpm, unstable)

59
Q

Third Degree Block Tx

A
  • atropine and/or pacing
  • nodal blocks (narrow complex) more likely to respond to atropine
  • infranodal probably won’t respond to atropine and will require pacing
60
Q

Premature Atrial Contractions (PAC) Characteristics

A
  • ectopic P wave occurs sooner than expected
  • ectopic P wave has different shape than other Ps (originates from site other than sinus node)
  • ectopic P may or may not be conducted through AV node
61
Q

Premature Atrial Contractions (PAC) Causes

A
  • common in all ages, often in absence of heart dz
  • possible precipitants: stress, alcohol, caffeine, fatigue, tobacco
  • frequent PACs may be seen in chronic lung dz, heart dz, digoxin toxicity
62
Q

Premature Atrial Contractions (PAC) Clinical Significance

A
  • usually benign

- occasionally PACs may trigger other atrial arrhythmias (like atrial flutter/fib)

63
Q

Premature Atrial Contractions (PAC) Tx

A
  • stop any precipitating drugs
  • tx underlying disorder
  • PACs that trigger flutter/fib can be suppressed with quinidine, beta blockers
64
Q

Premature Ventricular Contractions (PVC) Characteristics

A
  • impulses arising prematurely from single or multiple areas in the ventricles
  • occurs before next expected sinus beat
  • no preceding P wave
  • wide and bizarre appearing QRS ( >.12 sec)
  • PVCs may be unifocal (same morphology) or multifocal (different morphs)
65
Q

Premature Ventricular Contractions (PVC) Causes

A
  • very common even in absence of heart dz
  • stress, alcohol, caffeine contribute
  • frequently occur in ischemic heart dz, acute MI, CHF
  • hypokalemia
  • hypoxia most common cause
  • sympathomimetic drugs
66
Q

Premature Ventricular Contractions (PVC) Clinical Sig.

A
  • common in AMI due to myocardium being electrically unstable
  • may lead to v fib
  • in absence of heart dz, PVCs have no prognostic significance
  • in pts w/ heart dz and decreased ejection fraction, frequent PVCs are risk for v fib and sudden death (need implantable defibrillator)
67
Q

Premature Ventricular Contractions (PVC) Tx

A
  • if otherwise healthy: give O2, avoid caffeine/alcohol/etc
  • for PVCs with acute MI: treat underlying cause rather than the PVCs
  • chronic PVCs: no evidence that anti-arrhythmics enhance survival; consider implantable defibrillator
68
Q

Asystole Characteristics

A
  • no atrial or ventricular activity
  • check lead placement
  • check circ, airway, breathing
  • CPR!!!

Fall 2014 - CM Cardio (5 decks)

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