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One Time For the Patho Hoes > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

Normal Electrical Conduction Pathway

A

SA Node –> AV Node–> Bundle of His –> Bundle Branches –> Purkinje fibers

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2
Q

Bpm for:

  • SA Node
  • AV Node
  • His/ Purkinje fibers
A
  • SA Node: 60-100 bpm
  • AV Node: ~40-50 bpm
  • His/ Purkinje fibers: <40 bpm
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3
Q

What method is used to assess heart’s electrical activity?

A

Electrocardiogram (ECG)

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4
Q

Electrocardiogram waves:

  • Name of Waves?
  • What does each wave represent?
A
  1. P-wave: atrial depolarization
  2. QRS Complex: ventricular depolarization
  3. T-wave: ventricular repolarization
  4. PR Segment: impulse conduction pause in the AV node
  5. QT interval: time from ventricular depolarization to repolarization (important for drug dosing!)
  6. Isoelectric point: No deflection from electrical activity (baseline)
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5
Q

Which ECG wave is most important for drug monitoring?

A

QT interval: time from ventricular depolarization to repolarization

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6
Q

Ventricular Cardiac Action Potential:
-Phases
-Electrolyte movement at each phase
~Sorry I can’t put in pictures friends, I’m pooro pooro~

A

Phase 4: Spontaneous pacemaker current- Gradual spontaneous conduction, mainly sodium ions

Phase 0: Rapid depolarization- Rapid inward sodium channel → rapid ventricular depolarization

Phase 1: Rapid repolarization- Outward K, Cl, transient outward current

Phase 2: Plateau phase- Inward sodium and calcium, outward potassium ions (balanced)

Phase 3: Rapid repolarization - Outward potassium → ventricular repolarization

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7
Q

Abnormal impulse formation vs Abnormal impulse conduction

A

Abnormal impulse formation
– SA or AV node is not working
– Impulse formation is coming from somewhere else = ectopic beat

Abnormal impulse conduction
– Blockade somewhere in the conduction system
– Reentry loop

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8
Q

Arrhythmias occur due to?

A

Scarring or fibrotic tissue (Caused by):
• Ischemic heart disease
• Cardiomyopathy
• Fibrotic diseases

Changes to the cardiac action potential:
• Electrolyte abnormalities
• Drugs

Other: • Genetic diseases

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9
Q

Types of Tachyarrhythmias (HR>100)

A
  • Sinus Tachycardia
  • Atrial Fibrillation
  • Atrial flutter
  • AV Node Reentrant Tachycardia
  • AV Reentrant Tachycardia
  • Ventricular Tachycardia
  • Ventricular Fibrillation
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10
Q

Types of bradycardias (HR < 60bpm)

A
  • Sinus Bradycardia
  • First degree heart block
  • Second degree heart block
  • Third degree heart block
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11
Q

Sinus tachycardia:

a. Bpm
b. Causes

A

a. Bpm: > 100 bpm
b. Causes: increased firing of the SA node
• Non-pathologic: common during exercise or excitement
• Pathologic: – Often compensating for decreased stroke volume or blood pressure
– Due to autonomic disturbances
– If pathologic often leads to other tachycardic arrhythmias

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12
Q

Atrial Flutter

  • Bpm
  • ECG pattern
  • Patho
A

BPM:
Atria =300 bpm
Ventricles: Any factor of 300 depending on the AV node (1:2 A flutter = 150 bpm, 1:3 A flutter = 100 bpm, 1:4 A flutter = 75 bpm)

ECG pattern: Sawtooth/ flutter waves

Patho:
Due to a predictable and rhythmic reentry loop in the R atrium

-Cavotricuspid isthmus: tissue in the lower R
atria between the inferior vena cava and the tricuspid valve that can conduct

-If this isthmus gets stimulated, it can recreate a reentry loop within the right atria

Notes: Very similar to Afib, often patients switch back and forth between Afib and atrial flutter
– Many of the same complications and symptoms as atrial fibrillation

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13
Q

AV NODE REENTRANT TACHYCARDIA (AVNRT)

-Patho

A

Reentry loop in the AV node due to an
ectopic atrial beat

  • Normally, there is only one entry path into the AV node.
  • In AVNRT, the patient has two entry paths – one slow (quickly repolarizing) and one fast (slowly repolarizing) entrance!

• Clinical manifestations: similar to other
tachycardias

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14
Q

ATRIAL VENTRICULAR REENTRANT TACHYCARDIA (AVRT)

-Patho

A

Reentry loop between the atria and ventricles
• Pathogenesis: reentry + ectopy in a heart with
an accessory pathway between the atria and ventricles

• Clinical manifestations: similar to other
tachycardias

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15
Q

VENTRICULAR TACHYCARDIA (VT)

  • What is it
  • Non sustained vs sustained VT
  • Causes
  • Clinical Manifestations
A

• Series of 3 or more premature ventricular beats

– Non-sustained VT: < 30 seconds, terminates spontaneously
– Sustained VT: > 30 seconds
Sustained VT may degenerate into ventricular fibrillation which can lead to sudden cardiac death!!

Intrinsic Causes                   
• Structural disease
– Ischemic heart disease
– Cardiomyopathy
– Surgical trauma
Extrinsic Causes
• Electrolyte abnormalities
– Hypokalemia
– Hypomagnesemia
• Medications
– Antiarrhythmic medications
Clinical Manifestations
• Patients can present with or without a pulse
– With pulse patients may experience:
o Palpitations
o Dizziness, light-headedness
o Hypotension, syncope

-Without a pulse bpm> with a pulse bpm

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16
Q

Ventricular Fibrillation

  • What is it?
  • Clinical Manifestation
A
  • Disordered, rapid stimulation of the ventricles with no coordinated contractions
  • Ventricular tachycardia degenerates into multiple smaller wavelets of reentry

– Clinical manifestation = NO CARDIAC OUTPUT → DEATH (Immediately life-threatening arrhythmia!!)

17
Q

Sinus bradycardia

a. bpm
b. causes
c. clinical manifestations

A

a. Bpm: < 60 bpm
b. Due to: decreased firing of the SA node

  • Non-pathologic: common during rest or sleep
  • Pathologic:
 Intrinsic Causes
 • Conduction disease :Decreased automaticity (aging)
 • Structural disease:
 – Ischemic heart disease
 – Cardiomyopathy
 – Surgical trauma

Extrinsic Causes
• Medications: Beta-blockers, calcium channel blockers
• Metabolic disease: Hypothyroidism
• Autonomic syndromes
• Electrolyte abnormalities: Hyper/hypokalemia, Hypermagnesemia

c. Clinical Manifestations:
• Often asymptomatic
• Fatigue, weakness
• Dizziness, light-headedness, syncope
• Exercise intolerance
18
Q

Heart Block

  • Degrees
  • What does each degree represent?
  • Causes
  • Clinical Manifestation of each degree
A

Three degrees of Heart Block
(higher degree = more severe)

First-degree: conduction delay in the AV node

Second-degree: conduction delay in AV node or bundle of His
– Type 1: less severe
– Type II: more severe

Third-degree (“complete heart block”): complete dissociation between the atria and ventricles

Second-degree type II and third degree heart block
are medical emergencies and require immediate
intervention!!

-Causes: same as sinus bradycardia
Pathologic:

Intrinsic Causes
• Conduction disease :Decreased automaticity (aging)
• Structural disease:
          – Ischemic heart disease
          – Cardiomyopathy
          – Surgical trauma

Extrinsic Causes
• Medications: Beta-blockers, calcium channel blockers
• Metabolic disease: Hypothyroidism
• Autonomic syndromes
• Electrolyte abnormalities: Hyper/hypokalemia, Hypermagnesemia

Clinical Manifestations:
1. First-degree: usually asymptomatic
2. Second-degree: usually symptomatic only at low heart rates
3. Third-degree (“complete heart block”):
– Fatigue, weakness
– Dizziness, light-headedness, syncope
– Exercise intolerance

19
Q

Which arrhythmia is the most common?

A

Atrial Fibrilation

20
Q

Atrial Fibrillation:

Types

A

Paroxysmal: Terminates within 7 days of onset

Persistent: Lasts > 7 days

Longstanding, persistent: Lasts > 12 months

Permanent: patient and clinician have decided that
there will be no more effort to restore
or maintain sinus rhythm

AFIB w/ rapid ventricular rate: 
Generally acute presentation
– Higher HRs (more conduction through AV node)
• Often needs immediate intervention
– May lead to syncope
21
Q 
ATRIAL FIBRILLATION (AFIB):
CLINICAL MANIFESTATIONS
A 
Fatigue
Palpitations
Shortness of breath
Hypotension
Dizziness, light-headedness
Syncope

Many patients are asymptomatic and may not know
they have Afib!

  1. Stroke or systemic embolism: 5-fold increase in risk
  2. Heart failure: 3-fold increase in risk
  3. Dementia: 2-fold increase in risk
  4. Hospitalization: 2-fold increase in risk
  5. Mortality: 2-fold increase in risk
22
Q

Atrial Fibrillation:

  • Electrical activity
  • Patho
  • BPM: Atria & Ventricles
A

Disorganized and irregular atrial electrical activity
– “Quivering”
– No distinguishable atrial depolarization/contraction (p-waves)

• Occurs when atrial tissue is modified due to abnormalities in structure or function

• Rate:
– Atrial: 600-800 bpm
– Ventricular: usually 100-180 bpm

23
Q

Atrial Fibrillation:

  • Patho
  • Risk Factors
A

• Triggered by rapidly firing ectopic beats in the atria
– Most common: where pulmonary veins connect to the atria
• Ectopic beats can occur due to previously discussed etiologies of arrhythmias

• Risk factors:
– Concomitant cardiac disease
– Diabetes mellitus
– Obesity
– Obstructive sleep apnea
– Hyperthyroidism
– Smoking

One Time For the Patho Hoes (7 decks)

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