Internal Medicine: Cardio - Arrhythmias

Front 1

Premature Atrial Complexes (PACs)

Back 1

Early heartbeat arising when atria fire on their own --> not from SA node

*Causes: adrenergic excess, drugs, EtOH, tobacco, electrolyte imbalance, ischemia, infection

Front 2

Premature Ventricular Complexes (PVCs)

Back 2

Early ventricular beat fires on its own from a focus in the ventricle and then spreads to the other ventricle
Wide, bizarre QRS complexes followed by compensatory pause

*Causes: caffeine & other stimulants, hypoxia, electrolyte abnormalities, medications

Front 3

General characteristics of Atrial Fibrillation (AFib)

Back 3

1) Multiple foci in the atria fire continuously in chaotic pattern (atrial quiver) --> totally irregular, rapid ventricular rate (IRREGULARLY IRREGULAR)
2) Atrial rate is over 400 bpm; ventricular rate between 75-175 bpm

*Pts with AFib and underlying heart disease at increased risk of thromboembolism and hemodynamic instability
*Dx: EKG

Front 4

Causes of AFib

Back 4

1) Heart disease
2) Pericarditis & pericardial trauma
3) Pulmonary disease
4) Hyper or Hypothyroidism
5) Systemic illness (sepsis, DM)
6) Stress
7) Excessive EtOH intake ("Holiday heart syndrome")
8) Sick sinus syndrome
9) Pheochromocytoma

Front 5

Clinical features of AFib

Back 5

1) Fatigue and exertional dyspnea
2) Palpitations, dizziness, angina, syncope
3) Irregularly irregular pulse
4) Blood stasis, leading to intramural thrombi

Front 6

Cardioversion

Back 6

Delivery of a shock in synchrony with QRS complex
Terminates certain dysrhythmias

*Timed not to hit the T wave
*Indications: AFib, atrial flutter, VT w/ a pulse, SVT

Front 7

Defibrillation

Back 7

Delivery of shock NOT in synchrony with QRS complex
Converts dysrhythmia into normal sinus rhythm

*Indications: VFib, VT w/o a pulse

Front 8

Automatic Implantable Defibrillator

Back 8

Surgically implanted device that delivers electric shock upon detection of lethal dysrhythmia

*Indications: VFib, VT not controlled medically

Front 9

Treatment of acute AFib in hemodynamically unstable patient

Back 9

Immediate electrical cardioversion to sinus rhythm

Front 10

Treatment of acute AFib in hemodynamically stable patient

Back 10

1) Rate control w/ calcium channel or beta-blockers
2) Cardioversion to sinus rhythm
3) Anticoagulation to prevent CVA

*If AFib present for >48 hours, anti-coagulate for 3 weeks before and 4 weeks after cardioversion; can also do TEE to check for emboli

Front 11

Treatment of chronic AFib

Back 11

1) Rate control
2) Anticoagulation

*Aspirin w/ lone AFib and <60 yrs old; warfarin otherwise

Front 12

Atrial rate in Atrial Flutter

Back 12

250 - 350 bpm

*Ventricular rate is one-half to one-third atrial rate

Front 13

Causes of Atrial Flutter

Back 13

1) COPD - MC association
2) Rheumatic heart disease, CAD, CHF
3) ASD

Front 14

ECG findings in Atrial Flutter

Back 14

1) Saw-tooth pattern
2) QRS after every 2nd or 3rd "tooth"
(P-wave)

*Saw-tooth flutter best seen in inferior leads (II, III, avF)

Front 15

Agents used for pharmacological cardioversion

Back 15

1) Ibutilide
2) Procainamide
3) Flecainide
4) Sotalol
5) Amiodarone

Front 16

Multifocal Atrial Tachycardia

Back 16

Variable P=wave morphology with variable PR and RR intervals
*3 different P wave morphologies necessary for diagnosis
*Seen with SEVERE pulmonary disease (COPD)
*Treat by improving oxygenation and ventilation

Front 17

True or False: Electrical cardioversion is the treatment of choice for Multifocal Atrial Tachycardia

Back 17

False; it is ineffective and should not be used

Front 18

How is AV nodal reentrant tachycardia distinguished from Orthodromic AV reentrant tachycardia on ECG?

Back 18

Orthodromic AV reentrant tachycardia may have discernible P waves, depending on rate because reentrant rate is longer and atria and ventricles are activated at different times;
With AV nodal reentrant tachycardia, P waves are buried within narrow QRS because reentrant circuit is short and atria and ventricles are activated simultaneously

Front 19

Causes of Paroxysmal Supraventricular Tachycardia (PSVT)

Back 19

1) Ischemic heart disease
2) Digoxin toxicity (2:1 block)
3) AV node reentry
4) Atrial flutter with rapid ventricular response
5) AV reciprocating tachycardia (accessory pathway)
6) Excessive caffeine or EtOH

Front 20

Maneuvers that stimulate the vagus nerve

Back 20

1) Valsalva
2) Carotid sinus massage
3) Breath holding
4) Head immersion in cold water (or ice to the face)

*Block reentry mechanism of PSVT

Front 21

Pharmacologic tx of PSVT

Back 21

1) IV Adenosine (DOC)
2) IV Verapamil, Esmolol, or Digoxin

Front 22

Side effects of Adenosine

Back 22

1) HA
2) Flushing
3) SOB
4) Chest pressure
5) Nausea

Front 23

Delta Wave

Back 23

Characteristic wave seen with Wolff-Parkinson-White Syndrome
Slurred upstroke in the QRS complex associated with a short PR interval

Front 24

Mechanism of Action of Digoxin

Back 24

1) Inhibits cardiac Na+/K+ pump -->
2) Increases intracellular Na+ -->
3) Decreases Na+/Ca2+ exchanger -->
4) Increases intracellular Ca2+ -->
5) Increases Ca2+ release from SR -->
6) Increases actin-myosin interaction, which increases contractile force

Front 25

Ventricular Tachycardia (VT)

Back 25

Rapid and repetitive firing of 3 or more PVC in a row at at rate between 100 - 250 bpm
AV dissociation; sinus P waves unaffected by tachycardia
Originates below bundle of His

Front 26

Causes of Ventricular Tachycardia

Back 26

1) CAD with prior MI (MCC)
2) Active ischemia, hypotension
3) Cardiomyopathies
4) Congenital defects
5) PROLONGED QT Syndrome
6) Drug toxicity

Front 27

Sustained VT

Back 27

Lasts longer than 30 seconds
Almost always symptomatic
Associated with marked hemodynamic compromise
Can progress to V-Fib --> Life-threatening

Front 28

Torsades de Pointes

Back 28

Rapid polymorphic VT - can lead to V-Fib
Caused by factors that prolong QT interval
*IV Mg2+ stabilizes the myocardium

Front 29

Factors that prolong the QT interval

Back 29

1) Congenital QT Syndromes
2) TCAs
3) Anti-cholinergics
4) Electrolyte abnormalities
5) Ischemia

Front 30

Non-sustained VT

Back 30

Brief, self-limited, often asymptomatic runs of VT

*Independent risk factor for sudden death when CAD and LV dysfunction

Front 31

Clinical features of V-tach

Back 31

1) Palpitations, SOB, lightheadedness, angina, impaired consciousness
2) Sudden cardiac death
3) Signs of cardiogenic shock
4) Cannon a waves (due to atrial contraction during ventricular contraction)

Front 32

Normal time of QRS interval

Back 32

120 ms

Front 33

True or False: VTach does not respond to vagal maneuvers or adenosine

Back 33

True

Front 34

Treatment of sustained VTach

Back 34

Hemodynamically stable: IV amiodarone, procainamide, or sotalol
Hemodynamically unstable: Immediate cardioversion followed by IV amiodarone

Front 35

Treatment of non-sustained VTach

Back 35

No underlying heart disease: No treatment (pts not at increased risk of sudden death)
Underlying heart disease: Order EP study --> ICD placement if positive

Front 36

Ventricular Fibrillation

Back 36

Multiple foci in ventricles fire rapidly --> chaotic quivering of ventricles with NO CARDIAC OUTPUT
If associated with MI (within 48 hrs): good prognosis
If unrelated to MI, recurrence is high and pts need chronic amiodarone or defibrillator
Fatal if untreated

Front 37

Causes of VFib

Back 37

1) Ischemic heart disease (MCC)
2) Anti-arrhythmics (prolonged QT)
3) AFib with very rapid ventricular response (Wolff-Parkinson-White)

Front 38

Clinical features of VFib

Back 38

1) Absent heart sounds and pulse
2) Patient unconscious
3) Leads to eventual sudden death

Front 39

Treatment of VFib

Back 39

1) Immediate defibrillation and CPR
2) Epinephrine (increases myocardial and cerebral blood flow and lowers threshold for defibrillation)
3) IV amiodarone followed by shock

Front 40

Sinus Bradycardia

Back 40

Sinus rate <60 bpm
Caused by ischemia, increased vagal tone, anti-arrhythmic drugs

*Atropine can elevate sinus rate by blocking vagal stimulation to SA node

Front 41

Sick Sinus Syndrome

Back 41

Persistent, spontaneous sinus bradycardia --> dizziness, confusion, syncope, fatigue, CHF
*Pacemaker implantation may be needed

Front 42

First-degree AV Block

Back 42

1) Prolonged PR interval (>200ms)
2) QRS followed by every P wave
3) Delay in AV node
4) Benign; no tx necessary

Front 43

Second-degree AV Block - Mobitz I (Wenckebach)

Back 43

1) Progressive prolongation of PR interval until there is a dropped PQRS
2) Block in AV node
3) Benign; no tx necessary

Front 44

Second-degree AV Block - Mobitz II

Back 44

1) Sudden drop in PQRS despite normal PR intervals
2) Progresses to complete heart block
3) Block in His-Purkinje fibers
4) Pacemaker necessaryt!

Front 45

Third-degree AV Block (Complete Block)

Back 45

1) Atrial impulses not conducted to ventricles
2) No correspondence between P waves and QRS complex
3) VENTRICULAR PACEMAKER MAINTAINS RATE AT 25-40 BPM
4) Pacemaker necessary!