LOUISIANA STATE UNIVERSITY HEALTH AND SCIENCE CENTER SCHOOL OF NURSING NURSING 4352 A.

Sinus - impulse originates from SA node 1. Normal Sinus Rhythm (NSR) a. Characteristics - In analysis, everything is normal in conduction (PQRST); 60-100 bpm with normal P-R interval (from intrinsic SA mode) Sinus Bradycardia (SB) a. Characteristics - like NSR, but slower. (< 60 bpm) b. Causes: Increase ICP REM Athletes After A.M.I - inferior Drugs digoxin, beta-blocker Vagal stimulation Carotid massage sleep hypoxia common in elderly trach suctioning gagging/vomiting

2.

c. Significance: Depends on hemodynamic consequence and cause with S&S -dizziness, syncope, pallor, HBP, chest pain. d. Treatment: If hemodynamically unstable Maintain patent airway; assist breathing PRN Give oxygen Monitor ECG (identify rhythm), B/P, Oximetry Establish IV access Prepare for transcutaneous pacing Consider Atropine 0.5 mg IV while awaiting pacer... May repeat to a total dose of 3 mg... If ineffective begin pacing Consider Epinephrine (2-10micrograms/min or Dopamine (2-10 microgram/kilogram / min.) infusion while awaiting pacer or if pacing ineffective Prepare for Tran venous pacing Treat causes

3.

Sinus Tachycardia (ST) a. Characteristics - like NSR, but faster (generally 100-150 bpm) b. Causes Exercise, fever Meds (i.e.-Atropine, Epinephrine, Isuprel, Dopamine, Aminophyllline) Heart failure, hypotension, hypovolemia, hypoxia, anemia, shock, stress, fear/anxiety, hyperthyroidism, stimulants (Caffeine), ETOH. MI (initially) d/t sympathetic response to increased coronary blood flow. c. Significance: There may be a significant underlying disorder -warning Sinus Tachycardia (ST) (cont) Significance (cont): Dysrrhythmia Increases the workload of the heart with decreased 02 supply to coronary arteries, & increase filling time. d. Treatment: (Seldom required unless hemodynamically significant) ST with pulses: Assess and support ABCs as needed Give oxygen Monitor EKG(identify rhythm), B/P, oximetry Identify and treat reversible causes Establish IV access Monitor QRS for width(wide or narrow) Determine if rhythm is regular or irregular Narrow QRS(rhythm: a. Attempt vagal maneuvers b. Give Adenosine 6 mg rapid IVP c. If no conversion, give 12 mg rapid IVP; may repeat 12 mg does once d. If rhythm converts observe for recurrence and treat with Adenosine or longer-acting AV nodal blocking agents such as Diltiazen Wide QRS (rhythm) Uncertain rhythm

a. Regular Amiodarone 150 mg IV over 10 min. Repeat PRN to a maximum dose of 2.2 grams/ 24 hours b. Prepare for elective synchronized cardioversion c. Irregular Control rate with Beta Blockers such as diltiazem Primarily treat the underlying cause!

4.

Sinus Arrhythmia: a. Characteristics - Slightly irregular rhythm; otherwise normal conduction in analysis. A normal variation of NSR. Rate decreases with expiration & increases with inspiration. (d/t vagal inhibition) b. Causes - Often seen in children, young adults & C.O.P.D. patients, but can occur in anyone. Also seen with increased Intracranial pressure, inferior wall MI & dig. toxicity. c. Significance: Look for cause. Benign rhythm. d. Treatment: (See Bradycardia) Treat cause, if d/t something else. Usually treatment of rhythm unnecessary unless hemodynamically unstable (with decreased rate).

B.

Atrial 1. Premature atrial contraction (PAC or APC) a. Atria contract early d/t impulses from irritable atrial foci reaching AV node before impulse from SA node; early, abnormally shaped P wave P-P interval is shorter for early cycle with a narrow QRS Underlying rhythm is usually normal (but be sure to assess!)--identified as NSR with PACs - nonconducted PAC b. Causes: (Seen in abnormal and normal conditions) ETOH, smoking, anxiety, pain, apprehension, caffeine, drugs (cocaine, amphetamines) c. Significance: Minor dysrrhythmia 3

Again, importance depends on precipitating factors and hemodynamic consequences. May precipitate a more serious atrial dysrrhythmia, especially when heart disease present. Premature atrial contraction (cont) a. Treatment (if at all): Treat cause and monitor for further problems. (SOB, CP, worse arrhythmia erratic, faster PSVT or A. fib) b. Goal: Prevent worsening arrhythmia 2. Atrial Tachycardia (aka Paroxysmal Atrial Tachycardia - PAT or Paroxysmal Supraventricular Tachycardia - PSVT) a. Characteristics: Paroxysmal-def: starts and stops abruptly; like ST but faster (>150 bpm). Rhythm regular; P waves often blend in with previous T waves because of the rapid rate. b. Cause: same as sinus tach, mitral valve problems, thyroitoxicosis, CHF (especially if with cardiac disease). May be preceded by PACs c. Significance: decreased filling time & increased workload more serious than PACS d. Treatment: (See Tachycardia). May attempt to cardiovert to NSR. e. Goal: decrease rapid ventricular rate *Wolff-Parkinson white syndrome presence of delta waves 3. Atrial Fibrillation a. Characteristics: R-R interval is NOT Regular, irregularly irregular Uneven baseline; No definite P-wave. Electrical stimulus is from multiple areas of the atria Atrial rate is indeterminate. Vent. rate is slow, normal, or fast, but always irregular; ventricular rate > 100 = uncontrolled a. fib; < 100 = controlled a fib. Usually normal QRS interval (<0.12 sec) b. Causes:

valve problems, rheumatic heart disease, COPD, CHF, Cardiomyopathy, increased BP, Dig. toxicity, CAD. c. Significance: May precipitate or aggravate CHF. Peripheral & pulmonary emboli-developed in quivering atrium R/T incomplete ejection (decreases C.O. by at least 20% with atrial kick = decreased vent filling and S&S = anxiety, SOB, CP, palpitations. Decreased C.O. d. Treatment: (See Tachycardia); Maze procedure e. Goal = control ventricular rate; prevent embolus (coumadin, if chronic) 4. Atrial Flutter - Serious a. Characteristics: Sawtooth appearance. - Regular or irregular ventricular response; always regular atrial rhythm - T-wave not seen (Q-T immeasurable) - Instead of P-waves, see F-waves (flutter)-(PR immeasurable) - Less common than A.fib. and harder to treat successfully. - Atrial rate = 250 - 350 bpm Atrial conduction ratio (A: V): 2 P-waves for every QRS = 2:1 (common) 3 P........................... = 3:1, etc. or variable ratio b. Causes - Fluid overload, Hypoxia, CHF, seen in elderly, rarely occurs without heart disease. c. Significance: depends on ventricular response rate; serious dysrrhythmia d\t poor A. filling and decreased C.O. with rapid ventricular response with 1:1 & 2:1 d. Treatment: (See Tachycardia)
e.

Goal: convert to NSR

C.

Nodal or junctional rhythm - Junctional escape rhythm (40-60 bpm) accelerated junctional (60-100 bpm) and Junctional tachycardia (>100) a. Characteristics: Supraventricular rhythm originating from AV junction; AV node firing before the SA node indicated by no P Wave or inverted P Wave An escape rhythm or safety mechanism with failure of SA mode b. Causes: Can result from anything that depresses conduction through SA node or 8 automaticity of AV node. c. Significance: Failure of higher intrinsic pacemaker (SA node) Unreliable SA node. Allows time for irritable foci. Serious, but not life threatening unless hemodynamically significant. Treatment: (See Bradycardia) Treat cause.

d. D.

Ventricular-In general, more serious than atrial or junctional; if it occurs rapidly, often fatal; width of the QRS, not the height, that is important in diagnosis 1. Premature ventricular contraction (PVC or VPC) a. Characteristics: Wide, bizarre QRS; no P-wave; T wave deflection opposite QRS; ectopic-outside usual pathway; originates in ventricle with retrograde conduction. Important to observe frequency and pattern of occurrence. - Compensatory pause b. Types: i. Isolated ii.Bigeminy - ventricular Bigeminy iii. Trigeminy iv. Sequentials or Salvos Couplets Triplets Runs v. Unifocal vs. Multifocal - Underlying rhythm must be described c. Causes: 6

Acute ischemic with Myocardial Damage or hypoxemia; interruption in conduction pathway with ventricular aneurysm or cardiomyopathy Acid-base Imbalance (usually acidosis) Electrolyte Imbalance (hypokalemia & hypomagnesemia); Dig. Toxicity (refractory PVCs seen); stress of pregnancy, increased irritability with cardiac cath or SG insertion d. Significance: SERIOUS! especially with ischemic heart i. increasing ventricular irritability ii. progression to lethal arrhythmias S&S- May feel skipped beats; pulse feels irregular e. Treatment: (if frequent, close together, multifocal, symptomatic; or close to T- wave - R-on-T Phenomenon Drugs Amiodarone Lidocaine Procainamide (Pronestyl) Bretylium - ICD Treat cause - Case study in 1987 2. Ventricular Tachycardia more than 3 PVCs in a row; very dangerous if sustained a. Characteristics: >100/min, regular, no P wave; wide QRS - Ghosts, Tombstones >Torsades de pointes b. Causes: same as PVCs; Dig Toxicity, Cocaine; MV problems, Rheumatic HD, chronic severe heart disease c. Significance: LETHAL! Poor cardiac output Inadequate circulation & perfusion Decreased blood pressure, chest pain, shock Loss of consciousness May deteriorate to V. fib

d. Treatment: (See Tachycardia Algorithm or Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm) Treatment determined by pulse or pulseless and if pulse, stable or unstable. * Significance of VT versus SVT 3. Ventricular Fibrillation a. Characteristics: Irregular, quivering wave; no PQRST, fibrillatory waves; no pulse b. Causes: Mainly Acute MI; deteriorating ventricular dysrrhythmia c. Significance: LETHAL!!! Rapid discharge of ventricular foci, Ventricles unable to respond, & quiver Circulation STOPS d. E. Treatment: (See Ventricular Fibrillation/Pulseless Ventricular Tachycardia Algorithm)

Atrioventricular Blocks (A-V Blocks) or Impulse Conduction Disorders-delay through AV node 1. First Degree A-V Block a. Characteristics: Prolonged PR interval b. Causes: Dig. Toxicity Infarct of Right Coronary Artery (Inferior M.I.) - impaired blood flow to SA node Anesthesia (resolves spontaneously) Post-op heart surgery c. Significance: Usually not clinically significant. If MI, may deteriorate to higher degree block d. Treatment: (See Bradycardia) if symptomatic treat cause; monitor for progression to 2o or 3o 2. Second Degree A-V Block Mobitz Type I (Wenckebach) a. Characteristics: P-R Interval gets longer with each complex until QRS is dropped. b. Cause: Dig toxicity, inf. MI c. Significance: usually benign and d/t ischemia; resolves with resolved ischemia. May progress to complete block. 8

d. Treatment: (See Bradycardia) especially if decreased HR. Temporary Pacemaker until resolved (if unstabletreat cause) 3. Second Degree AV Block - Mobitz Type II a. Characteristics: P-R Interval is consistent with each complex; with dropped QRS; all or nothing situation b. Cause: Same as Mobitz I c. Significance: More serious; often precursor of 3o almost never occurs with healthy heart. d. Treatment: (See Bradycardia Algorithm) Atropine is palliative-needs pacemaker. Third Degree A-V Block (Complete Heart Block) a. Characteristics: The atrial & ventricular rates are different and from own intrinsic pacemakers. All atrial impulses blocked at AV junction - none get through. P-R intervals vary widely b. Cause: Same as above c. Significance: Slow ventricular rate with decreased C.O. resulting. d. Treatment: (See Bradycardia) - Pacemaker, Ventricular standstill can occur!! e. Goal: increased ventricular rate, correct cause

4.

F.

Pulseless Electrical Activity (PEA) - aka Electromechanical Dissociation (EMD) a. Characteristics: Electrical activity with no mechanical response; no pulse/any cardiac rhythm pattern may be seen on monitor and eventually deteriorates to ultimately flatline within minutes. NON SCHOCKABLE Resume CPR immediately for 5 cycles When IV/ IO available, give vasopressor Epinephrine 1 mg IV/IO Repeat every 3-5 min or give 1 dose of vasopressin 40 units IV/IO to replace first or second dose of epinephrine Consider atropine 1 mg IV/IO for Asystole or slow PEA rate. Repeat every 3-5 min. (up to 3 doses) b. Causes: Hypovolemia Acidosis Hyperkalemia Hypoxia Drug Overdose Pulmonary Embolism Hypothermia AMI-with excessive Pericardial Myocardial damage Tamponade Tension Pneumothorax 9

c.

G.

Significance: Dead. Sudden loss of consciousness, no BP, no R, no P. d. Treatment: (Same as for BLS) Asystole and Pulseless Electrical Activity CPR following BLS Algorithm: Call for help, give CPR Give oxygen when available Attach monitor/ defibrillator when available Shockable- VF/VT give 1 shock Manual biphasic: device specific (typically 120 to 200 j) if unknown, use 200 j Monophasic: 360 j Resume CPR immediately Defibrillator Arrives Defibrillate Cardiac Arrest CPR Give Vasopressor, identify Contributing Factor, continue CPR and administer medications during CPR. Consider Atropine Treat cause Usually fatal Asystole a. Characteristics: flat line or P-waves only (no QRST) b. Causes: Severe metabolic deficiency; acute respiratory failure, excessive myocardial damage c. Significance: Dead!! Ventricular standstill d. Treatment: (See Asystole/ PEA)

IV.

OTHER TREATMENT MODALITIES A. Defibrillation 1. Definition: The process of applying electrical stimulation to the chest wall to produce a simultaneous electrical depolarization of all the myocardial muscle fibers. 2. Purpose: Successful defibrillation results in a unified contraction of the myocardium and allows the hearts normal rhythm to reestablish itself. Defibrillation is an emergency procedure for pulseless ventricular tachycardia and ventricular fibrillation only. Equipment a. energy source - direct current (dc) defibrillator b. paddles (2) - direct the energy flow 10

3.

c. conducting media - saline soaked pads, conduction gel or gel pads (preferable) d. placement of paddles - 1 below the right clavicle and 2nd left of the sternum at the apex (approximate placement) e. voltage - theoretically only as much as needed to depolarize the myocardium - approx 200 watt - seconds (or joules) 4. Procedure a. Assess the patient status - establish unresponsiveness and pulselessness. b. Initiate CPR until equipment is ready c. Verify ventricular fibrillation or pulseless ventricular tach. via EKG d. Turn on the machine to defib e. Select energy level at 360 J for monophasic manual defibrillator. Select device-specific energy level for biphasic manual defibrillator, typically 120-200 joules; if unknown select 200j. f. Apply gel or defibrillation pads g. Position paddles h. Clear the area - Call out One, Im clear; two, youre clear; three everybodys clear No one should be touching the patient or the bed! i. Activate the firing button while applying firm pressure with the paddles j. Assess the patients response - i.e., EKG rhythm, pulse BP, LOC k. If unsuccessful, defibrillate again. (continue CPR in between defibrillation)

B.

Cardioversion 1. Definition: The process of applying an electrical stimulus to the myocardium that is synchronized to the patients existing rhythm. 2. Procedure a. Prepare the patient; unless the cardioversion is part of an emergency situation, i.e., rapidly deteriorating ventricular tachycardia with pulse or atrial fibrillation with decreasing cardiac output, the physician should explain the procedure to the patient in non-technical terms and obtain an informed consent. The patient

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b. c.

d. e. f.

g. h. 4.

should have an IV line in place for administration of medication. Anesthesia should be on standby. Consider IV sedation, analgesia, or anesthesia. Prepare the equipment - turn on the equipment - set on synchronized - dial in the appropriate setting (100, 200, 300, 360 joules) - adjust the R-wave amplitude to allow the machine to sense the patients rate and rhythm - adjust the lead placement if necessary Establish an airway Apply gel pads and paddles to the patients chest Activate the firing button and hold until machine discharges impulse. This may not happen immediately as in defibrillation. The impulse MUST BE SYNCHRONIZED with the patients R-wave to prevent R-on-T phenomenon: & more lethal dysrrhythmia. Assess the patients status Observe for reoccurrence

Contraindications a. Cardioversion may provoke refractory ventricular tachycardia in the digitalized patient.

Complications a. local tissue damage b. myocardial damage c. ventricular fibrillation d. reoccurrence of the original dysrrhythmia *Please review antidysrrhythmic drugs in textbook. The following algorithms are based on the American Heart Associations Recommendations for Advanced Cardiac Life Support (2006).

5.

Revised: RM/2007

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BLS Adult HCP Algorithm No movement or Response Phone 911 of emergency number Get AED Or send second rescuer (if available to do this Open Airway, check Breathing If no breathing, give 2 breaths that make chest rise If no response, check pulse within 10 seconds? Definite Pulse- Give 1 breath every 5 to 6 seconds Recheck pulse every 2 mins. Give cycles of 30 compressions and 2 breaths Until AED defibrillator arrives, ALS providers take over, or victim starts to move AED/Defibrillator Arrives Check rhythm Shockable rhythm Shockable Give 1 shock Resume CPR immediately for 5 cycles Not Shockable Resume CPR immediately for 5 cycles check rhythm every 5 cycles Continue until ALS providers take over or victim starts to move

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BRADYCARDIA ALGORITHM (<60 bpm & symptomatic) ASSESS, 02, IV *ATROPINE IVP EVERY 3-5 MINUTES OR TRANSCUTANEOUS or TRANSVENOUS PACEMAKER IF AVAILABLE (ALSO For 2o II & 3o HB) EPINEPHRINE INFUSION-2-10 mcg/min DOPAMINE INFUSION 5-20 mcg/kg/min

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TACHYCARDIA ALGORITHM* ASSESS, 02, IV UNSTABLE

(with symptoms or vent. rate >150)

STABLE
_______________________________________________________________________________________________________________________________________

consider sedation

A fib or A flutter 1 normal cardiac function Control rate2 Covert rhythm Use only one: Ca-channel <48 hrs. >48 hrs. blockers cardioversion anticoag B-blockers Use only one: x3 wks. Amiodarone delay carIbutilide cardioversion Flecainide Propafenone Procainamide

PSVT vagal maneuvers adenosine normal cardiac EF<40% function No cardioCa+ channel version B-blocker Digoxin Digoxin Amiodarone Cardioversion Diltiazem consider: procainamide amiodarone sotalol

VTACH3

immediate cardioversion

normal cardiac function Any one: Procainamide Sotalol others acceptable: Amiodarone Lidocaine

EF<40% Amiodarone Lidocaine Cardioversion

NOTE:

1. 2. 3.

Treatment differs for Wolff-Parkinson-White Syndrome If >48 hours, use agents with caution in patient not receiving adequate anticoagulation. Treatment differs for polymorphic ventricular tachycardia

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PULSELESS ARREST BLS Algorithm: Call for help, give CPR Give Oxygen when available Attach monitor/defibrillator when available Check rhythm Shockable rhythm SHOCKABLE VF/VT No Pulse Precordial Thump Resume CPR immediately for 5 cycles (if defibrillation NOT available STAT) When IV/IO give same vasopres sors as for Shockable Consider atropine 1 mg IV/IO No Pulse CPR (until defibrillation available) for Asystole or slow PEA NOT SHOCKABLE Asystole/PEA No Pulse

5 min up to3 Quick Look Rhythm Defibrillate with biphasicdevice (120-200 J) if not available use 200J AED Specific: Monophasic Defibrillate 200-300J Monophasic Defibrillate 360J Resume CPR immediately, Intubate, IV/IO Give medication during CPR Epinephrine 1mg IVP or IO q3-5 min or vasopressin 40u IV, single dose, 1 time only to replace first or second dose of Epinephrine CPR Defibrillate 360J (always within 30-60 seconds after med) CPR

Repeat every 3doses

Amiodarone (300 mg IV/IO once) or Lidocaine (1 to 1.5 mg/kg IV/IO first dose then 0.5 to 0.75mg/kg IV/IO Maximum dose 3mg/kg or 3 doses Consider antiarrhythmics: magnesium loading dose 1-2 grams IV/IO for Torsades de pointes

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CPR Defibrillate CPR

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 CPR, INTUBATE, IV CONFIRM RHYTHM IN ANOTHER LEAD CONSIDER POSSIBLE CAUSES: (H (x4) AD) HYPOXIA HYPOKALEMIA HYPERKALEMIA HYPOTHERMIA ACIDOSIS (PREEXISTING) DRUG OVERDOSE CONSIDER IMMEDIATE TRANSCUTANEOUS PACING EPINEPHRINE IV OR IO ATROPINE IV /OR CONSIDER TERMINATION OF EFFORTS

ASYSTOLE

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