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Cardio II Final > Arrythmias > Flashcards

Arrythmias Flashcards

1
Q

Symptoms of arrhythmias

A
  • Palpitations – skips, pounds, irregular
  • Lightheadedness – faint like, Syncope (near syncope)
  • CP, Dyspnea
  • Sudden Death
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2
Q

Etiology of arrhythmias

A
  • Stress, HTN
  • Ischemia (CAD), MI, HF
  • Hypoxia, PE, COPD
  • Metabolic acidosis
  • Infection – Endocarditis, RF
  • Inflammation – myocarditis, pericarditis
  • Cardiomyopathy/etOH, chemotherapy
  • Electrolytic imbalance – low K, Mg, Ca
  • Drugs – caffeine, nicotine, thyroid, aminophylline, OTC
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3
Q

Physiologic sinus arrhythmia

A

HR speeds up with inhalation, slows with exhalation

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4
Q

Automaticity

A

cardiac cell’s ability to depolarize spontaneously during phase 4 leading to generation of impulse
o Ischemia – have higher reactivity which can precipitate arrhythmias

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5
Q

Premature atrial contraction ECG

A 
can be conducted or non-conducted
•	Non-conducted – no QRS following
o	SA node resets to PAC timing
•	Change in P wave 
•	Atrial Bigeminy – Happens every other beat, looks like couplets, p wave biphasic
•	Atrial Trigeminy – every 3 beats
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6
Q

PACs

A
  • Associated with stress, etOH, tobacco, coffee, COPD, CAD
  • Most common cause of a pause!
  • T waves do not cause a pause
  • Treatment: if symptomatic
  • Reverse causes
  • Beta-adrenergic antagonist
  • Metoprolol 25-50 mg BID-TID
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7
Q

Atrial fibrillation

A

Atrial rate > 350-600/min
• Undulating baseline, no discernable P waves
• Irregular RR interval (QRS complex)
• Irregularly irregular ventricular rhythm
• Can form clots – stasis

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8
Q

Atrial flutter

A

Saw tooth appearance” 250-350/min
• Leads II, III, AVF, V, often best leads
• Can form clots – stasis; tolerate if ventricular rate under control, problems w/ stress

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9
Q

Premature junctional beat

A
  • P waves prior to, after (in ST segment), or in QRS complex
  • Each P’ is inverted in leads with upright QRS
  • Can have bigeminy or trigeminy
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10
Q

Causes of Bradycardia

A

o Normal or healthy athletes
o Physiologic component of sleep, fright, carotid sinus massage, carotid hypersensitivity (avoid tight collars, shave neck lightly), massage, or ocular pressure (glaucoma), mental control – yoga training
o Obstructive jaundice – bile salts effect on SA node
o Sliding hiatal hernia
o Valsalva maneuver – lifting, straining
o Inflammation or ischemia to SA node
o Drugs – beta blockers, central acting agents, digitalis

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11
Q

Medical conditions associated with bradycardia

A 
o	Acute inferior MI (RCA feeds the SA node) – Weckenbach, heightened vagal tone
o	Ischemia
o	Decreased pO2
o	Increased pCO2
o	Decreased pH
o	Increased BP
o	SSS – tachycardia alternating with bradycardia; older patients, tx pacemaker
o	Convalescence from dig toxicity
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12
Q

ECG findings for sinus bradycardia

A
  • P wave before each QRS complex
  • Rate less than 60/min
  • Normal axis
  • Constant and normal PR interval
  • Constant P wave configuration in each lead
  • Regular or slightly irregular P-P cycle or R-R cycle
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13
Q

Symptoms of hemodynamically compromised sinus bradycardia

A
  • Decreased BP
  • Decreased cardiac output, stroke volume, and renal perfusion (→ oliguria)
  • SOB, decreased cerebral profusion (→ confusion)
  • CP, cool, clammy, diaphoretic
  • Syncope, dizziness, fatigue
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14
Q

Sinus bradycardia

A

o Commonly seen in acute inferior MI especially in 1st few hours
• SN ischemia or vagal reflex initiated in ischemic area

o Tx: if HR less than 45-50 with hemodynamic compromise or unstable acute situations
• Depends on clinical setting/Dx the cause – may not need to be treated
• Depends on hemodynamics/impaired
• Depends on circulation
• No or few symptoms – no treatment

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15
Q

Drug therapy for sinus bradycardia

A
  • Atropine .3 → .5 → 2 mg IV
  • Repeat in 10 min
  • Caution in glaucoma, can increase intraocular pressure (narrow angle)
  • Side effects: urinary retention, abdominal distention, transient
  • If Atropine fails, treat with (in order to try):
  • Epinephrine 2-10 ug/min
  • Isoproterenol 1 mg in 500 cc D5W 1-4 ug/min IV
  • Pacemaker
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16
Q

Sick Sinus Syndrome

A

tachy-brady
o EKG:
• Sinus bradycardia
• Sinus arrest
• SA block – slow junctional rhythm
o Causes: ischemic, sclerotic, inflammatory changes in SA node
o Symptoms: syncope, dizziness, fatigue, heart failure
o Tx: pacemaker for brady; medications to suppress tachycardia

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17
Q

Sinus tachycardia

A 
o	Look for cause, tx underlying cause
•	Physiologic/pathologic process
•	Emotion, anxiety, fear, drugs, hyperthyroid
•	Fever, pregnancy, anemia, CHF
•	Hypovolemia
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18
Q

Paroxysmal tachycardia

A 
Supraventricular Tachycardia (SVT)
o	Sudden HR >100 (rate 150-250/min)
o	Identify “irritable focus”, P’ wave
o	Change in T wave signals the change, P wave changes after tachycardia sets in
o	More vulnerable in elderly
o	Can occur as:
•	Paroxysmal Atrial Tachycardia (PAT)
•	Paroxysmal Junctional Tachycardia
•	Paroxysmal Ventricular Tachycardia
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19
Q

PAT with AV block

A

o Greater than 1 P’ wave to 1 QRS – typically 2 P’ waves for each QRS
• Can have the P’ wave superimposed on the T wave
o Typically seen in digitalis toxicity 2:1 pattern

20
Q

Multifocal atrial tachycardia - ECG

A

o 3 or more different P waves
o PR interval varies
o Irregular ventricular rhythm
o Atrial rate >100

21
Q

MAT associated conditions

A
  • Lung disease – COPD, pneumonia, ventricular theophylline
  • Beta agonists
  • Electrolyte abnormalities (low K+, Low Mg)
  • Digitalis toxicity
  • Sepsis
22
Q

Treatment of MAT

A

o Treat the cause
• Discontinue theophylline
• IV Mg SO4 2 gm in 50 cc saline over 1 min, then 6 g in 500 cc saline 6 hrs (1-2 g/hr), Amiodarone/Adenosine
• Helps stabilize rhythm
• Caution with beta blocker – pulmonary problems
• Calcium channel blocker – control vent rate and decrease ectopic atrial impulses
• IV verapamil 5-10 mg
o Avoid if EF less than 40% - can exacerbate heart failure
• Diltiazem 20 mg IV, then 5-15 mg/hr drip
• Digitalis isn’t helpful and DC cardioversion isn’t effective

23
Q

Paroxysmal junctional tachycardia

A

o 150-250/min
o P wave may be lost (buried), inverted before or after each QRS
o QRS complex is NOT wide (if it were wide it would be ventricular tachycardia)
o Looks identical to “AV Nodal Re-entry” – no P waves

24
Q

PVC ECG findings

A
  • Premature, bizarre, wide QRS
  • No preceding P wave; may produce a retrograde P wave in ST segment
  • P wave not conducting to ventricle
  • ST-T wave moves in opposite direction of QRS
  • Usually full compensatory pause
  • Can have ventricular bigeminy, trigeminy, quadrigeminy
  • Can be multifocal – each foci will have it’s own pattern
  • Can be up or down
25
Q

Etiology of PVCs

A
  • Normal heart
  • CAD, MI, HF, myocardial ischemia, hypoxia
  • Valvular heart disease, congenital heart disease
  • Cardiomyopathy, electrolyte abnormalities
  • Acid base imbalance
  • Hyperthyroid
  • Drugs
26
Q

Treatment of PVCs

A
  • Consider setting: normal, stress, hypoxia
  • Drugs: nicotine, caffeine, thyroid, aminophylline, digitalis intoxication
  • Heart Failure, AMI, Ischemic HD, cardiomyopathy
  • Electrolyte disorder – hypokalemia, hyperkalemia, hypomagnesemia
  • If stable – no Rx; if symptomatic or in setting of ACS – Metoprolol 2.5-10 mg IV
  • If unstable – Amiodarone, Lidocaine (1-1.5 mg/kg up to 3 mg/kg), Procainamide
27
Q

PVC with R on T phenomenon

A
  • Ectopic lands early in relative recovery phase of repolarization
  • Can lead to ventricular tachycardia and ventricular fibrillation
28
Q

Accelerated idioventricular rhythm (AIVR)

A
  • Common rhythm in thrombolytic therapy – post MI

* Can have a fusion beat

29
Q

Ventricular tachycardia

A

o 3 or more consecutive bizarre wide QRS complexes
o ST segments going in opposite directions
o Ventricular rate 120-200/min (100-250)
o Usually regular, wide QRS (>.12 sec)
o P wave often lost, no relationship to QRS (AV dissociation)
o Lasts longer than 30 seconds (sustained)
o Fusion beats (Dressler)
o Capture beats
o Tx: cardioversion if sudden changes in clinical picture

30
Q

Ventricular fibrillation

A

o Disorganized depolarization
o No effective pump
o Clinical setting: AMI, HF, IHD, K+ disturbance (high or low)
o Defibrilate

31
Q

Ventricular flutter

A

o 250-350/min

o Sine waves – leads to ventricular fibrillation

32
Q

Torsades de Pointes

A

o QRS swings from positive to negative direction
o May be inherited (prolonged QT) or acquired (class I, II antiarrhythmics, etOH, TCA, electrolyte imbalance (K, Ca, Mg))
o Can degenerate to ventricular fibrillation
o Tx:
• MgSO4, 1-2 g IV bolus
• Overdrive pacing
• Isoproternol

33
Q

Hypokalemia

A

lowers resting membrane potential, enhances automaticity
• Causes:
• Diretics, metabolic alkalosis (transcellular shift of K+ into cell), high aldosterone (Conn’s, Cushings), beta-agonist overdose, diarrhea, renal loss
• ECG: II, III, AVF
• U waves
• Increased QT interval
• Flat or inverted T wave

34
Q

Hyperkalemia

A

raises RMP, slows conduction, widens QRS

Causes:
• Renal failure (insufficiency), metabolic acidosis, DKA, cell breakdown (hemolysis, Rhabdomyolysis)

ECG:  
•	Peaked T wave (tombstone T waves)
•	Wide QRS (not tachy, looks like slow VT)
•	Increased PR interval
•	Loss of P wave
Tx:
•	Dialysis
•	Insulin & glucose
•	NaHCO3
•	Albuterol
•	Rezin binding agents
35
Q

Hypocalcemia

A

prolongs QT interval – triggers arrhythmias (Torsades de pointes)
• Chronic renal failure, Vit D deficiency, hypoparathyroidism, acute pancreatitis, hypomagnesium

36
Q

Hypercalcemia

A

shortens QT interval, short ST segment
• Hyperparathyroidism, malignancy, granulomatous disorders (TB, sarcoid), endocrine disorders (adrenal insufficiency, hyperthyroid)

37
Q

Hypomagnesemia

A

prolongs QT Interval (Torsades), prolonged PR, wide QRS, decreased T wave
• Poor nutrition, alcoholism, decreased absorption, renal magnesium loss, diuretics
• Renal failure, magnesemia containing drugs

38
Q

Hypermagnesemia

A

Shortens QT interval

39
Q

Hypothermia

A

Less than 35C (95F)
o Bradycardia
o J wave (Osborne wave)

40
Q

Pulmonary embolus

A 
o	Sudden dyspnea, clear lung, and normal CXR = PE
o	Tachycardia
o	Non-specific ST-T changes
o	ECG:  
•	S1 Q3 T3
•	T wave inversion V1-V4
•	Transient RBBB
41
Q

Cor Pulmonale

A

o Strain in II, III, AVF
o Right atrial enlargement
o Low voltage

42
Q

Cerebral Hemorrhage

A

impressive ST-T changes

43
Q

Hypothyroidism

A

o Widespread flattening or mild inversion of T waves without ST segment displacement
o Low voltage QRS complex
o Sinus bradycardia
o Check TSH

44
Q

Brugada syndrome

A 
o	Asian, Middle East decent
o	Prone to sudden death
o	RBBB with ST elevation in V1, V2, V3
•	“Ski slope” to QRS complex
o	Defibrilator
45
Q

Wolff-Parkinson-White Syndrome (WPW)

A

o Short PR Interval
o Slurred upstroke (delta wave) of QRS complex
o Accessory AV conduction pathway (Bundle of Kent)
o Prone to palpitations, near fainting spells for several months
o Procainamide to stabilize rhythm

Cardio II Final (15 decks)

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