Cardiac Rhythm Disturbances (Atrial, Junctional, Ventricular) Flashcards
MAT (multifocal atrial tachycardia) is seen most commonly in people who have what condition?
-Chronic Lung Disease
Cor pulmonale is
-Right heart failure due to lung disease
People with Brugadda syndrome are prone to
- Sudden death from V-fib or V-tach
- Usually Middle eastern/Asian descent
- Collapses suddenly
WPW
- congenital
- HR 280-300
- from the presence of an accessory bypass tract
Principles
- Treat the patient–not the ECG
- Establish urgency of treatment–responsiveness, ABCD survey differential diagnosis, treat reversible causes (hypoxia, hypokalemia, hypovolemia)
- Access hemodynamic stability (LOC, BP, HR)
- Antiarrhythmic/electrical therapy
Arrhythmias symptoms
- Palpitations–skips, pounds, irregular
- Lightheadedness-faint like
- Syncope (near syncope)
- Chest pain
- Dyspnea
- Sudden death
Etiology
- Stress
- Ischemia (CAD), MI, HF
- Hypoxia, PE, COPD
- Metabolic acidosis
- Infection–Endocarditis, RF
- Inflammation–myocarditis, pericarditis
- Cardiomyopathy/alcohol; chemotherapy
- Electrolytic imbalance (low K, Mg, Ca)
- Drugs–caffeine, nicotine, thyroid, aminophylline, OTC
- Hypertension
Sinus Tachycardia causes
- Physiologic/pathologic process
- Need to look for cause!! :
- Emotion, anxiety, fear, drugs, hyperthyroid
- Fever, pregnancy, anemia, CHF
- Hypovolemia
- Treat underlying cause!
Sinus node
- Normally, the dominant cardiac pacemaker because of its intrinsic discharge rate is the highest of all potential cardiac pacemakers
- Bradycardia <60 beats/min
Medical conditions/situations associated with bradycardia
- Normal people
- Healthy athlete–well trained, good physical endurance
- Physiologic component to sleep, fright, carotid sinus massage, carotid hypersensitivity, avoid tight collars, shave neck lightly, massage or ocular pressure (glaucoma), mental control–yoga training
- Obstructive jaundice–effect of bile salts on SAN
- Sliding hiatal hernia
- Valsalva maneuver–lifting heavy objects, straining bowels
Other diseases associated with bradycardia
- Diseases of atrium or SAN–CAD:
- Inflammation
- Invasive neoplasm
- Cardiomyopathy
- Muscular dystrophy
- Amyloidosis
Drugs associated with bradycardia
- Digitalis, quinidine, hyperkalemia
- Drugs used for hypertension–mech to inhibit sympathetic tone (clonidine, methyldopa, reserpine)
- Beta blockers–propranolol, metoprolol
Acute inferior MI commonly present with
BRADYCARDIA!!
More conditions associated with bradycardia
- Acute inferior MI
- Ischemia
- decreased oxygen
- increased carbon dioxide
- decreased pH
- increased BP
- SSS (Sick sinus syndrome)–tach alternating with brady–older pt, vascular disease, advanced heart disease; Tx=pacemaker to control slow and meds to tx fast
- Convalescence from dig toxicity
Causes of bradycardia
- Sinus bradycardia
- Non conducted atrial bigeminy
- Sino atrial block
- AV block-incomplete/complete: sinus rhythm with 2:1 AV block, sinus tach with 3:1 AV block, sinus rhythm or tach with complete block; atrial flutter with complete block; A fib with complete block
Sinus arrhythmia
- SAN forms impulses irregularly
- waxes/wanes with phases of respiration
- HR increase with inspiration
- HR decreases with expiration
- sinus arrhythmia is a normal finding
EKG of sinus bradycardia
- P wave represents formation of sinus impulses
- Each atrial impulse is followed by a ventricular beat
- Rate less than 60/min
- P wave of sinus origin (normal axis)
- constant and normal PR interval (0.12-0.20)
- Constant P wave configuration in each lead
- regular or slightly irregular P-P cycle or R-R cycle
Most common cause of an unexplained pause in ECG is
-nonconducted premature atrial contraction (nonconducted PAC)
Sick sinus syndrome characteristics
tach alternating with brady–older pt, vascular disease, advanced heart disease
- S arrest
- SA block–>slow junctional rhythm
SSS seen in? Symptoms? Tx?
- ischemic, sclerotic, inflammatory changes in SAN
- may cause syncope, dizziness, fatigue, heart failure
- Tx with pacemaker for bradycardia and meds for tachycardia
Treatment for sinus bradycardia
- Depends on clinical setting/Dx the cause–may not need to be treated
- Depends on hemodynamics/impaired
- Depends on circulation
- Maybe no or few symptoms–No Rx
In sinus bradycardia, if hemodynamically compromised, may get combination of:
- low BP
- Low CO, los SV, low renal perfusion–oliguria
- SOB, low cerebral perfusion–confusion
- CP, cool, clammy, diaphoretic
- syncope, dizziness
- Fatigue
Commonly see Sinus bradycardia in
- Acute inferior MI, especially in 1st few hours (secondary to heightened vagal tone)
- This is related to SN ischemia or to a vagal reflex initiated in the ischemic area
- RX–if HR<45-50 with hemodynamic compromise/unstable acute situations
Drug used to treat sinus bradycardia
- Atropine–0.3–>0.5–>2mg IV
- Repeat 10 min
- Can also use epinephrine 2-10 ug/min, isoproterenol 1mg in 500 cc D5W 1-4 ug/min IV, pacemaker
Use caution in using atropine in patients with
-glaucoma–can increase Intraocular pressure
SE of atropine:
- Urinary retention
- Abdominal distension
- Transient
What is automaticity?
-Property of a cardiac cell to depolarize spontaneously during phase 4 of action potential/ leads to generation of an impulse
Atrial arrhythmias are caused by and seen in
- Premature atrial contraction (PAC) also APC
- seen in absence of significant heart disease; associated with stress, alcohol, tobacco, coffee, COPD and CAD
Premature beats
- an irritable focus spontaneously fires a single stimulus
- Premature atrial beat
- Premature junctional beat
- Premature ventricular beat
PAB does what to SA node
- resets SA node pacing
- SA node resets in step with premature atrial beat
Treatment of PACs
- If symptomatic:
- reverse causes
- Beta adrenergic antagonist (BB)
- Metoprolol 25-50mg BID-TID
Paroxysmal Atrial Tachycardia (PAT)
- Sudden heart rate greater than 100
- Rate 150-250/min
- Identify “irritable focus”; P’ wave
Types of Paroxysmal (sudden) tachycardia–very irritable automaticity focus suddenly paces rapidly
- Paroxysmal Atrial Tachycardia
- Parodysmal Junctional Tachycardia
- Paroxysmal ventricular tachycardia
PAT with AV block seen as?
-suspect what in this case?
- Greater than one P’ wave/QRS complex; 2P’ waves for each QRS
- Suspect digitalis toxicity
- Rapid rate, spiked P’ waves; 2:1 ratio of P’:QRS
Criteria for Multifocal Atrial Tachycardia
- 3 or more different P waves
- PR interval varies
- Irregular ventricular rhythm
- Atrial rate >100
Multifocal atrial tachycardia associated with
- Associated with LUNG DISEASE!!! (COPD, pneumonia, ventilator theophylline),
- Other causes: beta agonists, electrolyte abnormalities (low potassium, low magnesium), digitalis toxicity, sepsis
Tx for Multifocal Atrial Tachycardia
- DC theophylline
- IV MG S04 (Mg sulfate)
- Non-DHP CCB to control ventilatory rate and decrease ectopic atrial impulses
- Diltiazem IV
- IV verapamil (caution with pts with impaired EF)
- DONT GIVE B-BLOCKERS bc it exacerbates lung disease!
- Digitalis not helpful and DC cardioversion isn’t effective
Atrial Fibrillation ECG
- Atrial Rate >350-600/min
- undulating baseline, no discernible p waves, irregular RR intervals (QRS complex) “irregularly irregular” ventricular rhythm
- multiple foci discharging rapidly
- continuous chaotic atrial spikes
Atrial Flutter
- Saw tooth appearance
- Leads II, III, AVF, V often best leads
- 250-350/min
- may see better in inverted tracing or during valsalva maneuver
Pericarditis
- causes diffuse ST elevations in multiple leads
- Can also have atrial flutter associated with it
A junctional automaticity focus may cause
- Retrograde atrial depolarization
- Each P’ is inverted in leads with an upright QRS
Junctional (nodal) rhythms
- Paroxysmal junctional tachycardia (150-250/min)
- P wave may be lost (buried), inverted before or after each QRS
- Junctional foci (inherent rate 40-60/min)
Mechanism of AV nodal reentrant tachycardia
1) premature atrial impulse enters the slow pathway but is blocked at the fast pathway
2) The impulse is conducted anterogradely through the slow pathway
3) The ventricles are activated synchronously
4) Impulse is conducted retrogradely through the fast pathway
5) Impulse activates the atria retrogradely and reenters the slow pathway
-NO P WAVES IN THAT NODAL RUN
SVT morphology
- fast ventricular rate
- NO p waves
- Tx using ADENOSINE!!
Premature Ventricular Contractions Etiology
- Normal heart
- CAD, MI, myocardial ischemia, hypoxia
- Valvular heart disease, congenital heart disease
- Cardiomyopathy, electrolyte abnormalities
- Acid base imbalance
- Hyperthyroid
- Drugs
ECG characteristics of PVC
- PRemature bizarre wide QRS
- No preceding p wave; may produce a retrograde P wave in ST segment
- ST-T wave moves in opposite direction of QRS
- Usually full compensatory pause
- Comes from one irritable foci (unifocal)
- IF there are multiple irritable foci you get multifocal ventricular ectopics and all the PVCS look different
Ventricular rhythm disturbances Principals of treatment
- Consider setting: normal, stress, hypoxia
- Drugs: nicotine, caffeine, thyroid, aminophylline, digitalis, intoxication
- Heart failure
- Acute myocardial infarction (AMI)
- Ischemic heart disease
- Cardiomyopathy
- Electrolyte disorder: hypokalemia, hyperkalemia, hypomagnesemia
Accelerated idioventricular rhythm commonly seen in
- patients that have been given thrombolytic agent following MI
- fast rate, QRS wide, ST segments are in opposite direction of QRS complex
Treatment of PVCs
- If stable no Tx
- If symptomatic or in setting of ACS–metoprolol 2.5-10mg IV
- If unstable–Amiodorone, Lidocaine (1-1.5 mg/kg), Procainamide
Stimulants associated with
PVCs
Ventricular Tachycardia (VT) criteria
- 3 or more consecutive bizarre QRS complex
- Ventricuar rate 120-200 (100-250)
- Usually regular wide QRS (>0.12 sec)
- P wave often lost; if seen no relationship to QRS (AV dissociation)
- Lasts longer than 30 sec (sustained)
- Fusion beats (Dressler)
- Capture beats
- Suddenly a very irritable ventricular focus paces rapidly
Ventricular fibrillation (VF)
- Disorganized depolarization
- Not effective pump
- Clinical setting–AMI, HF, IHD, K+ disturbance (low or high)
- Tx: ABCs and defribillator
Torsades de Pointes
- Twisting of the points
- QRS swings from positive to negative direction
- May be inherited (prolonged QT) or acquired (class I, II, antiarrhythmias, alcohol, TCA, electrolyte imbalance–K, Ca, Mg)
- comes from different foci
Torsades de Pointes Treatment
- MgSO4, 1-2 grams IV bolus–FRONTLINE THERAPY
- Overdrive pacing
- Isoproternol
Asystole
- No rhythm
- Need CPR immediately
Potassium disturbances
- Low: lowers resting membrane potential (RMP)
- Enchances automaticity
- High: raises RMP, slows conduction, widens QRS
Calcium disturbances
- Low: prolongs QT interval; triggers arrhythmias (Torsades de pointes)
- High: shortens QT interval
Magnesium disturbances
- Low: prolongs QT (Torsades)
- High: shortens QT
Acidosis
- reduces threshold for VF
- sensitizes myocardium to re-entrainemnet arrhythmias
Hypokalemia etiology
- Diuretics!!! , metabolic alkalosis (transcellular shift of K+ into cell), high aldosterone (Conn’s, Cushings), beta-agonist overdose, diarrhea, renal loss
- common in hospital or office
ECG in hypokalemia
-U waves, increased QT interval, flat or inverted T wave
Hyperkalemia etiology
- Renal failure (insufficiency)
- Metabolic acidosis
- DKA
- Cell breakdown (hemolysis)
- Rhabdomyolysis
- ECG
- Peaked T wave
- Wide QRS
- Increased PR interval
- loss of P wave
Tx for hyperkalemia
- Dialysis
- Insulin and glucose
- Na HCO3
- Albuterol
- Rezin binding agents
Hypocalcemia etiology
- Chronic renal failure
- Vitamin D deficiency
- Hypoparathyroidism
- Acute pancreatitis
- hypomagnesium
Hypocalcemia ECG
-Prolongation of QT interval (QTc corrected for rate)
Hypercalcemia etiology
-Hyperparathyroidism, MALIGNANCY of bones, granulomatous disorders (TB, sarcoid), endocrine disorders (adrenal insufficiency, hyperthyroid)
Hypercalcemia ECG
- short QT interval
- short ST segment
Hypomagnesemia etiology
- Poor nutrition
- Alcoholism
- Decreased absorption
- Renal magnesium loss
- Diuretics
- Renal failure? Magnesemia containing drugs?
ECG for hypomagnesemia
- Prolonged PR
- Wide QRS
- Prolonged QT
- Dec T wave (flat)
Hypothermia
Temp <35 C (95 F)
- Slow heart rate (bradycardia)
- J wave (Osborne wave)
Pulmonary Embolus symptoms
- Sudden dyspnea + clear lung + normal X-ray=PE
- Tachycardia
ECG changes with Pulmonary embolus
- Non-specific ST-T changes
- S1Q3T3
- T wave inversion V1-V4
- Transient RBBB
Pulmonary Embolus ECG
- Large S wave in Lead I
- ST depression in II
- Large Q wave in III (with T wave inversion)
- T wave inversion V1-V4
- Transient RBBB
Cor Pulmonale
- Respiratory distress
- Sinus tachycardia
- Right Atrial Enlargement
- see best in leads II, III and AVF
- LOW VOLTAGE QRS SEEN IN LUNG DiSEASE!!
Cerebral hemorrhage
-Significant ST-T changes
Whenever you see widespread flattening or mild inversion of T waves without associated ST displacement, think ____
- Hypothyroidism
- 50% of the time will be hypothyroidism
Another consistent ECG finding in myxedema (hypothyroidism) is
- Low voltage QRS complex
- Sinus bradycardia often mentioned but less often seen
Brugada syndrome–more often seen in? ECG changes?
- Asian or middle eastern descent
- RBB with ST elevation in V1, V2 and V3
- susceptible to deadly arrhythmias!!
Wolff-Parkinson–White syndrome (WPW)
- Short PR interval
- Slurred upstroke (delta wave) of QRS complex
- Accessory AV conduction pathway (Bundle of Kent)
- have bypass tract
- prone to palpitations and syncope, tachyarrhythmias
preferred dug of choice for WBW
-Procaineamide
ON EXAM:
- A FIB
- A FLUTTER
- VTACH
- TORSADES
- HYPERKALEMIA
- HYPOKALEMIA
- WPW
- maybe HYPOKALEMIA
