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Atrial Flutter


saw tooth appearing p waves (look in V1) with rate 200-350 / usually with 2:1 or 3:1 AV block / similar (but not identical) treatment as atrial fibrillation / atrial flutter is often curable with ablation / 40% with some tachyarrhythmia / also causes thrombus (needs to be anticoagulated like atrial fibrillation)
Wandering Pacemaker – benign

usually benign, mostly in young persons (athletes) / will have more than one p wave morphology


Multifocal atrial tachycardia (MAT)

Associated with COPD, digitalis, theophylline, severe hypokalemia, hypomagnesemia

Must have at least 3 different P wave morphologies on ECG / rate 100-130

can use adenosine to attempt to distinguish from coarse atrial fibrillation


Premature junctional beat (PJB)

May produce aberrant conduction

May produce retrograde (inverted) P1 (SA pacing will be reset to P1)

Can get junctional bigeminy/trigeminy


Paroxysmal junctional tachycardia (PJT)

may have aberrant conduction (150-250)


Nonparoxysmal junctional tachycardia (NPJT)

may be treated with AV nodal agents, possibly including adenosine


AV nodal re-entrant tachycardia (AVNRT)

circus re-entry (normal impulse goes through AV node, but instead of terminating in ventricle, it goes back up into AV node and loops back around to stimulate ventricle again; hard to distinguish from JT)



Treatment: catheter ablation in young patients (90% success) / drug therapy: ß-blockers, Ca channel blockers, digoxin (be careful in WPW)
Wolf Parkinson White

AV muscle bridge (accessory pathway or Bundle of Kent)

Findings: short PR interval ( < .12 sec) and delta waves


  • atrial arrhythmias may carry over to ventricles (loss of AV protection mechanism)

  • ventricular tachyarrhythmias from re-entry

Treatment: for sustained VT or VT with hypotension, use DC cardioversion 1st / avoid AV blocking agents like adenosine, ß-blockers, Ca channel blockers, digoxin which may only worsen arrhythmias by increasing conduction through accessory pathway / can use procainamide, lidocaine, some say ibutilide

Ventricular Arrhythmias
Causes of ventricular irritability

Low O2

Low K

Adrenergic stimulation (to a lesser extent)


PVC or Premature Ventricular Contraction

    • 6/min is pathological / > 3 PVC’s in a row is VT / > 30 seconds is sustained VT

    • usually opposite polarity of QRS / enormous complex with QRS much longer than > .14 ms / long pause (does not disrupt sinus pacing, thus there is a punctual, but ineffective P wave)

    • may occur in normal, healthy individuals (women > men) (usually disappear after exercise) in which case reassurance is treatment of choice and if needed, can try B-blockers / studies have shown reduction of PVCs (even in post-MI) patients cannot be used as an endpoint on its own (does not improve mortality)


R on T


During vulnerable period (after peak or during downslope of T) / vulnerable period extended by hypoxia / PVCs with R on T are more worrisome for triggering VT
Criteria for wide complex tachycardia
1. AV dissociation (may see fusion or capture beats)

2. QRS width > 0.14 s w/ RBBB, > 0.16 s w/ LBB

3. QRS axis: LAD w/ RBB morphology

4. concordance of QRS in precordial leads


SVT vs. VT











fusion/capture

extreme RAD

Q in V6

VT

CAD

QRS > 0.14

yes

yes

yes

SVT

uncommon

QRS < 0.14

rare

rare

rare

Note: canon a waves in jugular venous pulsations occur from atria contracting against closed tricuspid valve (only seen with VT/AV dissociation)


Non-sustained ventricular tachycardia (NSVT)

Duration < 30 seconds / yes, it is a signal that something is not right

Treatment: B-blockers and type III drugs (lidocaine)

Ventricular tachycardia (VT)


150-250 bpm

Causes: ischemia, HOCM, AS, long QT

Treatment: ACLS measures (shock, medication), refractory cases (consider LVAD)
Polymorphic VT

Treatment: magnesium + other ACLS measures


Torsades de Pointes (twisting of the points)

ventricular arrhythmia associated with prolonged QT and characteristic EKG pattern / described by Dessertenne in 1966, related to 2 competing ventricular foci and abnormal electrolytes / whites > blacks / females > males



Causes: hypomagnesemia, hypocalcemia, intracranial events, bradyarrhythmias, many drugs (see below)

Course: TdP may either revert to normal or evolve into ventricular fibrillation

Treatment: give magnesium; cardioversion insufficient (must do external ventricular pacing; overdrive pacing will shorten QT interval)
Drugs associated with Torsades de Pointes:

Anti/Pro arrhythmics: amiodarone, sotalol, bretylium, procainamide, propafenone, flecainide, encainide, disopyramide

Antibiotics: fluoroquinolones, ganciclovir, pentamidine, macrolides (e.g. erythromycin, clarithromycin), amphotericin B, itraconazole, ketoconazole, ? fluconazole, co-trimoxazole, indapamide

Protease Inhibitors: amprenavir, indinavir, nelfinavir, ritonavir, saquinavir

Antipsychotics: droperidol, phenothiazines, chlorpromazine, thioridazine, moricizine, haldol

Antidepressants: doxepin, amitriptyline, imipramine

Other: tacrolimus, quinidine, quinine

drugs that I can’t remember what they are: terfenadine, terodiline, astemizole, bepridil, , maprotiline, ibutilide, ketanserin, perhexiline, prenylamine, probucol, sultopride

drugs not commonly prescribed: cocaine, arsenic
Prolonged QT syndromes
Jervell-Lange-Nielsen (JLN)

hereditary deafness and prolonged QT interval / syncope, sudden death

Treatment: B-blockers
Romano-Ward

prolonged QT interval / syncope, sudden death


Leopard syndrome [dermis]

ACLS Guidelines (will supply pic of algorithm here)


  • For VF or hypotensive VT shock at 200 then 300 then 360 then 360 then amiodarone 150 mg IV x 1 or lidocaine 1-1.5 mg/kg/IV x 1 / may also be indications for magnesium sulfate or procainamide


Hypothermia


  • EKG: J-point elevation or Osborn waves [pic] and QT prolongation

  • occurs at temperatures below 30C



Pericardial Disease

[restrictive pericarditis] [cardiac tamponade]


Pericardial effusions

Acute pericarditis

Infectious pericarditis (viral, TB)

Dressler’s syndrome

Uremic pericarditis
Pericardial effusion
serous non-bacterial / some WBCs

fibrinous uremia, rheumatic heart disease

serofibrinous

purulent/suppurative infection

hemorrhagic blood, fibrin, pus, neoplasm

cholesterol rare

chronic adhesive result of fibrinous

constrictive result of purulent or hemorrhagic


Acute Pericarditis

Causes:

Infectious: (see below)

Cardiac: acute MI, post-radiation, postcardiac injury (postpericardiotomy, trauma, Dressler’s, chylopericardium), aortic dissection

Immune: sarcoidosis, SLE, RA, scleroderma (less), rheumatic fever, IBD

Other: uremia, myxedema

Drug induced: procainamide, hydralazine, INH, etc

Malignancy: primary (mesothelioma), metastatic malignancy (lung, breast, melanoma, lymphoma)

Presentation: fever (implies infection) occurs before pain (unlike MI where fever is after pain), 1-2 wks after viral illness / pain may resemble MI, radiate to back, shoulders, arms (less), pain may be pleuritic, altered by postural changes

Physical Exam:

  • Pericardial friction rub (50%): monophasic, triphasic (early, late, diastolic) < biphasic / may decrease with onset and increased size of pericardial effusion (but can co-exist with effusion) / distinguish from pleural friction rub by having patient hold breath / rub changes w/ position

  • Pericardial Effusion: elevated JVD, pulsus paradoxus, prominent x descent, reduced y descent, peripheral edema, and disproportionate ascites, Kussmaul’s sign (constrictive pericarditis)

Diagnosis:

  • ECG: PR ↓, J-point ↑, characteristic ST ↑  restated: diffuse ST elevation (concave) with T wave inversion occurring temporally after ST resolution (unlike MI), PR depression / also ST-elevation to T-wave amplitude in V6 > 0.24 is very suggestive [pic]

  • Radiographic: pleural effusion [pic] in constrictive pericarditis, calcified pericardium (50%), enlargement of cardiac silhouette (with pericardial effusion > 250 ml) [pic] / CT or MRI may reveal thickened pericardium / other studies include left/right heart catheterization and fluid challenge

Labs: mild elevated WBC, ESR

Complications: cardiac tamponade, arrhythmias (resting tachycardia, atrial fibrillation)

Treatment: avoid anticoagulation!!! (may bleed causing hemopericardium/tamponade) / NSAIDs 1st line (e.g. indocin 25-50 tid until 1 week after Sx resolve) / steroids 2nd line (20-60 mg P qd) / prolonged/relapse may require colchicine 1 mg/d and/or pericardiectomy to prevent constrictive pericarditis / some argue for colchicine as first line (2009)

Prognosis: most cases improve in 2-3 weeks
Infectious Pericarditis:

Viral: coxsackie A/B, echovirus, adenovirus, mumps, influenza, EBV, VZV, CMV, HSV,

HBV(really?)

Bacterial: 30% mortality / antibiotics and drainage, not steroids

Organisms: S. pneumo and other strep, S. aureus, N. meningitidis and gonorrhea, H.

influenzae, Enterobacteriaceae, Campylobacter, Brucella, Actinomyces, Nocardia, Listeria, M. pneumoniae, Legionella, Chlamydia, Borrelia, M. tuberculosis, MAI



  1. contiguous spread from chest infection (outside heart or endocarditis) or (peri or post) trauma/surgery

  2. bacterial pericarditis from contiguous pneumonia usually occurs only after prolonged, untreated infection

Fungus (most of them)

Parasites: Toxoplasma, E. histolytica, Schistosomes
Viral pericarditis

friction rub – LLS border / more w/ leaning forward / pain come and goes / diffuse ST elevation / normalized by 1-2 days, then T inversion


TB pericarditis

5 to 10% of acute pericarditis / 1% of pulmonary Tb / serous (20%) or serosanguinous (80%)

hematogenous or contiguous / granulomatous (Langerhans cells)

Effusate: high protein, high PMNs early, high lymphocytes later



Complications: constrictive pericarditis (may be predicted by elevated adenosine deaminase), pericardial calcification, myocarditis, dissemination

Treatment: HRZE for 8 weeks then INH/rifampin / some evidence favors steroids / pericardiectomy recommended for pericardial thickening (over ½ will have some procedure)

Note: 2.6:1 odds that patient will have AIDS, 6:1 if disseminated Tb
Dressler’s syndrome

Presentation: pleuritis, malaise, CP occurring 1-4 weeks to months after MI

Findings: pleural/pericardial effusions, fever (up to 40c), leukocytosis, elevated ESR

Note: may consider biopsy of heart muscle to rule out ongoing inflammation

Treatment: NSAIDs (1st) / steroids (2nd)

Course: autoimmune process which may relapse up to 2 yrs later
Uremic pericarditis

often hemorrhagic / avoid anticoagulation




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