Arrythmias Flashcards
Symptoms of arrhythmias
- Palpitations – skips, pounds, irregular
- Lightheadedness – faint like, Syncope (near syncope)
- CP, Dyspnea
- Sudden Death
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
Physiologic sinus arrhythmia
HR speeds up with inhalation, slows with exhalation
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
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
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
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
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
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
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
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
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
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
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
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
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
Sinus tachycardia
o Look for cause, tx underlying cause • Physiologic/pathologic process • Emotion, anxiety, fear, drugs, hyperthyroid • Fever, pregnancy, anemia, CHF • Hypovolemia
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
PAT with AV block
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
o 3 or more different P waves
o PR interval varies
o Irregular ventricular rhythm
o Atrial rate >100
MAT associated conditions
- Lung disease – COPD, pneumonia, ventricular theophylline
- Beta agonists
- Electrolyte abnormalities (low K+, Low Mg)
- Digitalis toxicity
- Sepsis
Treatment of MAT
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
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
- 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
