• Disorganized atrial conduction with irregular conduction to
• No discernable p- wave with irregular QRS
• QRS narrow unless BBB
• Unstable: Synchr Cardioversion (less success if chronic AF or
• Stable: Rate control- BB, CCB, Digoxin, Amiodarone,
Anticoagulation-ASA, Heparin, Warfarin based on CHADS2
Multifocal Atrial Tachycardia
• Often mistaken for A-fib, but 3 or more discernable p- waves,
Irregular rate, 100-180 BPM.
• Narrow QRS, but can be wide QRS with BBB
• 2/2 lung dz
• Treat underlying lung dz, Rate control with CCB
• Reentry Tachycardia
• Abrupt onset and termination differentiates from Sinus Tach
• Precipitated by PAC or PVC (if AVRT)
• Requires 2 different conduction pathways with different refractory
• Regular rate, p- waves absent, QRS narrow unless BBB
• AVNRT- Conduction pathways within AV node
• AVRT- Conduction pathways between Atria and Ventricle
• Atrial Reentry Tachycardia- Conduction pathways within atria
• Unstable-Synchr. Cardioversion
• Stable- Vagal maneuver, Adenosine, BB, CCB, Procainamide
• Preexitation Syndromes- WPW
• Men> Women, 10% of Ebstein Anomaly (Tricuspid anomaly- atrialization of RV/ CHD)
• Accessory pathway/ Bundle of Kent circumvents AV node, connect. atrium to bundle of His.
• Orthodromic SVT/ Narrow QRS (95%):
• Antegrade conduction vie AV node/Retrograde via accessory pathway.
• Unstable- Synchr. Cardioversion
• Stable- CCB, BB, Adenosine, Procainamide
• Antidromic SVT/ Wide QRS and short PR (5%):
• Antegrade conduction via accessory pathway, retrograde via AV node.
• Wide QRS/ Delta wave. Can be indistinguishable from V-Tach.
• Unstable: Synchr. Cardioversion
• Stable: Procainamide, Amiodarone
• NO CCB/BB/Dig, Adenosine (blocks AVN, allowing conduction via accessory
Monomorphic Ventricular Tachycardia
• Single ventricular ectopic focus with wide QRS 2/2 depolarization via myocardium (not
as rapid as His- Purkinje fibers).
• Absent P- waves, rate >140, QRS> 160 mS
In favor of VT vs SVT w/ aberrancy:
• Fusion beats- fusion of wide ectopic beats and normal QRS
• Capture beats- Narrow QRS captured between wide QRS
• AV dissociation
• >50 yrs, cardiac dz
• Unstable: Pulse- Synchronized cardioversion, Pulseless- unsynchronized defibrillation
• Stable: Amiodarone, Procainamide, correct underlying etiology
Polymorphic Ventricular Tachycardia (Torsade de Pointes)
• Wide complex QRS, 180-240, wave like appearance.
• Baseline EKG may show long QT
• Congenital: Jervell-Lange- Nielson, Romano-Ward
• Meds: Antiarrhythmics 1A, IIIA, TCA, Phenothiazine, antipsychotics
• Electrolyte: Hypo K, Hypo Mg
Unstable: Pulse- Synchr cardioversion, Pulseless- Defibrillation
Stable: Mg, Overdrive pacing or Isoproterenol (incr HR-> Shorter QT)
• Hyperirritable ventricular myocardium 2/2 Ischemia, scarring,
antiarrhythmics, a-fib, cardioversion.
• Disorganized, irregular rapid waveform with no discernable P or QRS.
• ACLS, Defibrillation, or will degenerate in to Asystole.
• Epinephrine, Amiodarone, Mg
Ventricular Pacing- Temporary
• Bradycardia with hemodynamic Instability
• Bradycardia with significant escape rhythms
• Overdrive pacing
• Standby for:
• Stable bradycardia
• Acute MI with Sinus node dysfunction
• Mobitz II or third degree block
• Cardiac Ischemia with new LBBB or RBBB
• Transcutaneous pacer- pads to ant-post chest. Limited by body habitus.
• Transvenous pacer- via Cordis catheter to IJ or SC.
Third degree block, Sick sinus, Severe CHF
Generator: generates impulse
Lead: deliver impulse
• Pacer spikes before P and QRS if paced.
• Wide QRS/ LBBB pattern.
• Demand pacemaker may not have spikes if rhythm is nml
• Generator- device or battery
• Lead- fracture, dislodging, migration of lead
• Myocardium- fibrosis, electrolyte imbalance
Pacer Failure on EKG
Rate less than preset= Generator failure
Bradycardia but absent spikes= Failure to pace
Impulses fires inappropriately despite nml rhythm= failure to sense
Impulse/ spike without causing P or QRS= failure to capture
Pacer falsely senses activity of heart therefore and inhibits pacing= Oversensing
Pacer incorrectly misses activity of heart and therefore sends impulses= Undersensing
• Pacer with thin coil to atrium, single ventricle or both ventricles
• Defibrillator with thicker shocking coil in atrium and ventricle
Interrogation/ Trouble shooting
• Use manufacturer specific magnet held close to Pacemaker.
• Most pacers will switch from demand to fixed mode (preset rate for each pacer) with
use of any magnet.
• IECD will turn off with magnet.
AICD (Automatic Inplantable Cardioverter Defibrillator)
• Delivers defibrillatory shock to apex of right ventricle if VF or VT
• Almost always combined with pacemaker
• High risk for dysrhythmia
• Sever CHF
• Brugada Syndrome
• Hypertrophic Cardiomyopathy
• Inappropriate discharge: Can turn off AICD with magnet
• Elevation of BP without acute end- organ injury.
• Potentially harmful if sustained, usually DBP >130 mmHg.
• Gradual reduction in BP over 24 hrs with Outpatient PO meds:
HCTZ, or BB (CAD), Lisinopril (CHF, RF, DM).
• Outpatient evaluation of labs for end- organ damage.
Hypertension with acute end- organ damage, usually >130 mmHg
• Hypertensive encephalopathy, ICH, Ischemic stroke
• Renal Failure
• ACS, CHF, Pulm edema
• Aortic Dissection
• Retinal hemorrhage/papilledema
• Reduce MAP by 20% over next hour with IV meds:
• Nicardipine (incr HR), Nitroglycerine (incr HR), Esmolol (short acting,
easily titrated), Labetalol (for PIH, worsen bronchospasm), Sodium
Nitroprusside (poss, cyanide tox, give w/ BB for elev of HR), Enalapril
(avoid in Renal Artery stenosis)
• Avoid Beta Blockers- allows unopposed alpha stimulation on blood
vessels-> further elevation of BP.
• Caution with cardioversion of dysrhythmia if hyperadrenergic state
since irritable myocardium.
• Phentolamine (alpha blocker) for Pheochromocytoma and Cocaine
Tear of aortic intima with blood leaking in to media
• Abrupt, excruciating pain epigastrum/ chest radiating through to back
• If aortic branch vessel occlusion:
• Neuro deficits, paraplegia, CHF, ACS, Abdominal pain, flank pain/RF, syncope
• Tamponade, HTN, unequal pulses, aortic insufficiency
• CXR: wide mediastinum, pleural effusion, apical cap, media separated from calcified
intima, blurred aortic knob.
• TEE, CT, CT Aortogram, MRI
• Debakey I: ascending/descending, II: ascending, III: descending
• Stanford A: Ascending , B: Descending
• Start IV BB for HR control (Esmolol, Labetalol). Add Vasodilator (Nitroprusside) if needed
to bring BP down to SBP ~100. Analgesia (morphine to reduce sympathetic output.
• Surgery for ascending dissection, Medical mgmt. for descending dissection.
• True aneurysm, >3cm or incr diameter by 50%. Rupture risk incr @ 5cm.
• MC abdominal and infra- renal. Grows 4 mm/yr once over 3cm. Most
commonly asymptomatic until rupture.
• White, smoker, hypertensive male with CAD.
• If pain, sudden onset in flank, abdomen, chest, back, often pulsatile
mass, hypotensive, unequal pulses.
Imaging: Abd XR, US, CT contrast, angiogram, MRI
• Immediate Surgery consultation/OR
• Optimize BP (not to low/ not to high: BP meds/ pressors)
• Crossmatch PRBC’s