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

Arrythmias Flashcards by Autumn Brubaker

Symptoms of arrhythmias

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

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Etiology of arrhythmias

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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Physiologic sinus arrhythmia

HR speeds up with inhalation, slows with exhalation

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Automaticity

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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Premature atrial contraction ECG

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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PACs

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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Atrial fibrillation

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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Atrial flutter

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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Premature junctional beat

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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Causes of Bradycardia

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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Medical conditions associated with bradycardia

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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ECG findings for sinus bradycardia

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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Symptoms of hemodynamically compromised sinus bradycardia

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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Sinus bradycardia

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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Drug therapy for sinus bradycardia

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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Sick Sinus Syndrome

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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Sinus tachycardia

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

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Paroxysmal tachycardia

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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PAT with AV block

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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

Multifocal atrial tachycardia - ECG

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

MAT associated conditions

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

Treatment of MAT

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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

Paroxysmal junctional tachycardia

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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

PVC ECG findings

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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

Etiology of PVCs

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

Treatment of PVCs

* 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

PVC with R on T phenomenon

* Ectopic lands early in relative recovery phase of repolarization * Can lead to ventricular tachycardia and ventricular fibrillation

Accelerated idioventricular rhythm (AIVR)

* Common rhythm in thrombolytic therapy – post MI | * Can have a fusion beat

Ventricular tachycardia

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

Ventricular fibrillation

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

Ventricular flutter

o 250-350/min | o Sine waves – leads to ventricular fibrillation

Torsades de Pointes

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

Hypokalemia

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

Hyperkalemia

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 ```

Hypocalcemia

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

Hypercalcemia

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

Hypomagnesemia

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

Hypermagnesemia

Shortens QT interval

Hypothermia

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

Pulmonary embolus

``` 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 ```

Cor Pulmonale

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

Cerebral Hemorrhage

impressive ST-T changes

Hypothyroidism

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

Brugada syndrome

``` 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 ```

Wolff-Parkinson-White Syndrome (WPW)

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

Arrythmias Flashcards

(45 cards)