Dysrhythmias Flashcards
Main Concern of Dysrhythmias
- Ineffective Tissue Perfusion
Dysrhythmias
- Any disturbance or irregularity in the electrical system of the heart
Electrophysiologic Properties
-Automaticity
- Ability of the pacemaker cells to initiate an electrical impulse
Electrophysiologic Properties
-Excitability
- Ability to respond to electrical impulse
Electrophysiologic Properties
-Conductivity
- Ability to transmit impulse from cell to cell
Electrophysiologic Properties
-Contractility
- Ability of muscle fibers to shorten in response to impulse
P Wave
- Atrial depolarization
QRS Wave
- Ventricle Depolarization
2. Atrial re-polarization
T Wave
- Ventricle Re-polarization
Refractory Periods
-Absolute Refractory Period
- Cell is unresponsive to another stimulus
Refractory Periods
-Relative Refractory Period
- A stimulus could initiate an action potential and cause a dysrhythmia
- Located at the last half of the T wave
QT Interval
- Ventricular Cycle
Normal PR Interval
- .12 to .20
- Time the impulse travels to AV node and bundle branches
Normal QRS Complex
- .06 to .10 seconds ( above .13 is considered above)
- Ventricular depolarization
- Q wave - first negative deflection
- R Wave - first positive deflection
- S Wave - First negative after R wave
ST Segment
-What to look for?
- If ST is Elevated, it indicates myocardial ischemia
Normal QT Interval
- 0.32 to 0.44
- Beginning of QRS to end of T wave
U Wave
- Usually NOT SEEN
2. May be seen with HYPOKALEMIA
Sick Sinus Syndrome
- Problems with impulse formation, transmission, & Conduction
Sinus Bradycardia
-Occurs in response to?
- Carotid sinus massage
- Hypothermia
- Increased vagal tone
- Parasympathomimetic drugs
- Hypothyroidism
- Obstructive jaundice
Sinus Bradycardia
-Clinical Significance
- Dependent on Symptoms
- Hypotension
- Pale, cool skin
- Weakness
- Angina
- Dizziness or syncope
- Confusion or disorientation // SOB
Sinus Bradycardia
-Treatment
- Atropine
2. Pacemaker may be required
Sinus Tachycardia
-Clinical Associations
- Associated w/ physiologic stressors
- Exercise
- Pain
- Hypovolemia
- MI, HF, Fever
Sinus Tachycardia
-Clinical Significance
- Dizziness & hypotension
2. Increased Myocardial oxygen consumption may lead to angina
Sinus Tachycardia
-Treatment
- Beta-adrenergic blockers to reduce HR and myocardial oxygen consumption
- Antipyretics to treat fever
- Analgesics for pain
Premature Atrial Contraction (PAC)
- Contraction originating from ECTOPIC focus in atrium (not in SA node)
- Travels across atrial by abnormal pathway
- Creates distorted P wave - May be stopped, delayed, or conducted normally at the AV node
Premature Atrial Contraction (PAC)
-Clinical Associations (Can result from)
- Emotional stress
- Use of caffeine, tobacco, alcohol
- Hypoxia
- Electrolyte imbalances
- COPD
- Valvular disease
Premature Atrial Contraction (PAC)
-Clinical Significance
- Isolated PAC’s are NOT SIGNIFICANT in those with healthy hearts
- In persons w/ heart disease, may be warning of more serious dysrhythmia
Premature Atrial Contraction (PAC)
-Treatment
- Depends on symptoms
- Beta-Adrenergic blockers may be used to decrease PAC’s
- Reduce or eliminate caffeine
Paroxysmal Supraventricular Tachycardia (PSVT)
- Originates in ectopic focus anywhere above bifurcation of bundle of HIS
- Some degree of AV block may be present
- Can occur in presence of Wolff-Parkinson-White syndrome
Paroxysmal Supraventricular Tachycardia (PSVT)
-Clinical Association In a Normal Heart
- Overexertion
- Emotional stress
- Stimulants
Paroxysmal Supraventricular Tachycardia (PSVT)
-Clinical Associations
- Digitalis toxicity
- Rheumatic heart disease
- CAD
- Cor pulmonale
Paroxysmal Supraventricular Tachycardia (PSVT)
-Clinical Significance
- Prolonged episode of HR > 180 BPM may precipitate decreased cardiac output
- Palpitations
- hypotension
- Dyspnea
- Angina
Paroxysmal Supraventricular Tachycardia (PSVT)
-Treatment
- Vagal maneuvers: Valsalva, coughing
- IV adenosine
- Cardioversion (make sure machine is set to synchronize)
- Ablation
- Wolff-Parkinson-White (WPW)
Atrial Flutter
- Atrial Tachydysrhythmia identified by recurring, regular, SAWTOOTH-SHAPED flutter waves
- Originates from a single ectopic focus
- Loss of atrial kick
- Ration 4:1, 3:1, 2:1
Atrial Flutter
-Occurs with
- CAD, HTN
- Mitral valve disorders
- Pulmonary embolus
- Hyperthyroidism
- Digoxin, quinidine, epinephrine
Atrial Flutter
-Clinical Significance
- High Ventricular rates (>100) and loss of the atrial kick can decrease CO and precipitate HF, Angina
- Risk for Stroke due to risk of THROMBUS FORMATION in the atria
Atrial Flutter
-Treatment
- Drugs to slow HR: CCB, B-adrenergic blockers
- Electrical cardioversion
- Antidyshrythmia meds (amiodarone)
- Radiofrequency catheter ablation
Atrial Fibrillation
- Total disorganization of atrial electrical activity due to MULTIPLE ectopid foci
- Loss of effective atrial contraction and “kick”
- MOST COMMON dysrhythmia
- Prevalence increases w/ age
- “Irregularly Irregular”
Atrial Fibrillation
-How NCLEX describes it?
- “Irregularly Irregular”
Atrial Fibrillation
-Usually occurs with?
- Underlying heart disease, such as rheumatic heart disease, CAD
- Cardiomyopathy
- HF
- Pericarditis
Atrial Fibrillation
-Often acutely caused by?
- Thyrotoxicosis
- Alcohol intoxication
- Caffeine use
- Electrolyte disturbance
- Cardiac surgery
Atrial Fibrillation
-Clinical Significance
- Can result in decrease in CO
- Thrombi may form in the atria as a result of blood stasis
- Embolus may develop and travel to the brain, causing a stroke
Atrial Fibrillation
-Treatment for rate control?
- Digoxin
- B-adrenergic blockers
- CCB
Atrial Fibrillation
-Treatment (Long-term anticoagulation)
- Coumadin
Atrial Fibrillation
-Treatment used for Conversion
- Amiodarone
Atrial Fibrillation
-DC Cardioversion
- DC cardioversion may be used to convert atrial fibrillation to normal sinus rhythm
Atrial Fibrillation
-Rapid Ventricular Response
- This is very dangerous and needs to be put under control
2. Give pt Antidyshrythmia med
Atrial Kick
- When the atria contract, it is responsible for pushing an extra 30% of blood into the ventricles
- The rest of the blood flows passively into the ventricles
Electrophysiologic Properties
-All Properties
- Automaticity
- Excitability
- Conductivity
- Contractility
Junctional Dysrhythmias
- Dysrhythmia that originates in area of AV node
- SA node has failed to fire or impulse has been blocked at the AV node
- Occasional retrograde conduction - inverted P wave
Junctional Dysrhythmias
-Retrograde conduction
- Inverted P wave
Junctional Dysrhythmias
-Clinical Associations
- CAD, HF
- Electrolyte imbalances
- Digoxin, amphetamines, caffeine, nicotine
Junctional Dysrhythmias
-Clinical Significance
- Serves as safety mechanism when SA node has not been effective
- Escape rhythms should NOT be suppressed
- If rhythms are rapid, may result in reduction of CO and HF
Junctional Dysrhythmias
-Treatment if symptomatic?
- Atropine if the Junctional dysrhythmia is slower than normal
- If it is faster (caused by digoxin) stop the underlying cause
Junctional Dysrhythmias
-Treatment for Accelerated Junctional Rhythm
- If accelerated junctional rhythm and junctional tachycardia caused by digoxin toxicity…
- Digoxin is HELD
Junctional Dysrhythmias
-Contraindicated treatment?
- Cardioversion is contraindicated
Junctional Dysrhythmias
-Treatment if not caused by Digoxin Toxicity
- B-Adrenergic blockers
- CCB
- Amiodarone
- Used for rate control for Junctional tachycardia
Ventricular Dysrhythmias
- Affect CO and tissue perfusion
- Wide, bizarre QRS
- P wave w/ no relation to QRS, abnormal ST segment
- T wave w/ opposite deflection of QRS
Premature Ventricular Contractions
- Contraction originating in ectopic focus of the ventricles
- Premature occurrence of wide and distorted QRS
- If it happens less than 3 times it is a PVC
- Always Say the Underlying rhythm **
Premature Ventricular Contractions
-Clinical Associations
- Stimulants
- DIgoxin
- Electrolyte imbalance
- Hypoxia
- Fever
Premature Ventricular Contractions
-Disease states that cause PVC’s?
- MI
- Mitral Valve prolapse
- HF
- CAD
Premature Ventricular Contractions
-Clinical Significance w/ Normal Heart?
- Usually benign when heart is normal
Premature Ventricular Contractions
-Clinical Significance with Diseased Heart?
- May decrease CO and precipitate angina and HF
- Pt response to PVC’s must be monitored
- PVC’s often do not generate sufficient ventricular contraction to result in peripheral pulse
- Apical-radial pulse rate should be assessed to determine pulse deficit
Premature Ventricular Contractions
-Clinical Significance
- Shows that there is some ventricular irritability
- May occur after:
- Lysis of Coronary artery clot w/ Thrombolytic therapy in acute MI
- Following plaque reduction after percutaneous coronary intervention
Premature Ventricular Contractions
-Treatment
- Based on Cause of PVC’s
- O2 therapy for hypoxia
- Electrolyte replacement
- Drugs:
- –Beta-Adrenergic Blockers, Procainamide, Amiodarone, lidocaine
Ventricular Tachycardia
- Run of Three or more PVC’s
2. Considered life-threatening because of decreased CO and the possibility of deterioration ventricular fibrillation
Ventricular Tachycardia
-Classifications of V-Tach
- Monomorphic
- Polymorphic
- Sustained
- Non-sustained
Ventricular Tachycardia
-Clinical Associations
- Electrolyte imbalances
- Long QT syndrome
- Digitalis toxicity
- MI & CAD
- CNS disorders
Sustained Ventricular Tachycardia
-Clinical Significance
- Severe decrease in CO
- Hypotension
- Pulmonary edema
- Decreased cerebral blood flow
- Cardiopulmonary arrest
Ventricular Tachycardia
-Clinical Significance
- VT can be stable (PT has pulse) or unstable (No pulse)
- Treatment for VT must be rapid
- May recur if prophylactic treatment is not initiated
- V-Fib may develop
Ventricular Tachycardia
-Treatment
- Precipitating causes must be identified and treated (e.g hypoxia)
Ventricular Tachycardia
-Treatment if Pt is hemodynamically stable (pulse + LV function)
Nursing Priority is to look for cause
- IV procainamide
- Sotalol
- Amiodarone or lidocaine
Ventricular Tachycardia
-Treatment if Hemodynamically unstable
- Amiodarone or Lidocaine followed by CARDIOVERSION
Ventricular Tachycardia
-Treatment if Patient Has NO PULSE? Unstable
- Initiate ACLS
- CPR and rapid defibrillation (Nursing Priority is to shock PT)**
- Epinephrine (or Vasopressin) if defibrillation is unsuccessful
Ventricular Fibrillation
-Top Causes
- Acute MI causes 50% of V-fib
In V-Fib you Defib for treatment
Ventricular Fibrillation
- Severe derangement of the heart rhythm characterized on ECG by:
- Irregular undulations of varying contour and amplitude - No effective contraction of CO occurs
- Cardiac arrest
Ventricular Fibrillation
-Clinical Associations
- VF may occur during cardiac pacing or cardiac cath
- VF may occur with coronary reperfusion after fibrinolytic therapy
- Electrical shock
- Hyperkalemia
- hypoxia / Acidosis / Drug toxicity
* **Acute MI accounts for 50% of V Fib **TEST
Ventricular Fibrillation
-Clinical Significance
- Unresponsive, pulseless, and apneic state
- If not treated rapidly, death will result
- MUST BE DEFIBRILLATED
Ventricular Fibrillation
-Treatment
- Immediate initiation of CPR and ACLS
- Use of defibrillation and definitive drug therapy
Nursing Priority is to Defibrillate
Asystole
- Represents total absence of ventricular electrical activity
Asystole
-Clinical Associations
- Advanced cardiac disease
- Severe cardiac conduction system disturbance
- End-stage HF
Asystole
-Clinical Significance
- Unresponsive, pulseless, and apneic state
2. Prognosis for asystole is extremely poor
Asystole
-Treatment
- CPR w/ initiation of ACLS measures
-Intubation
-transcutaneous pacing
-IV therapy w/ epinephrine and atropine
NOT A SHOCKABLE RHYTHM (DO NOT DEFIBRILLATE)
Pulseless Electrical Activity
- Electrical activity can be observed on the ECG, but there is no mechanical activity of the ventricles and the patient has no pulse
Pulseless Electrical Activity
-Treatment
- CPR followed by intubation and IV epinephrine
- Atropine is used if the ventricular rate is slow
- Treatment is directed to correct underlying cause
Sudden Cardiac Death
- Death occurring w/in 1 hour of onset of cardiovascular symptoms
- 1/2 die before reaching the hospital
- 25% to 30% survive
- 50% of cases are R/T CHD
Sudden Cardiac Death
-Most Common Cause?
- Ventricular Fibrillation (80%)
Sudden Cardiac Death
-Threat of Recurrence
- Threat of recurrence is greatest in the first 6-18 months following a major cardiac event
Educate the patient during this period to help them change habits
Prodysrhythmia
-Clinical Significance
- Anti-dysrhythmic drugs may cause life-threatening dysrhythmias
Prodysrhythmia’s
-Risk increases w/:
- Severe LV dysfunction
2. Digoxin and class IA, IC, and III antidysrhythmia drugs
Prodysrhythmia’s
-Treatment
- First several days of drub therapy are the vulnerable period for developing Prodysrhythmias
- May oral antidysrhythmia drug regimens are initiated in a monitored hospital setting
Electrophysiology Studies
- Analyze components of the heart’s electrical conduction system
- Identifies sites of ectopic stimulation - Ablative therapy
- Destroys ectopic sites
Fast Sodium Channel Blockers (Class I)
- Decrease flow of Na into cell
- Treat
- PVC, VT, VF
Beta-Blockers (Class II)
- Decrease automaticity, conduction, and contraction
- Treat:
- SVT & prevent VF
Potassium Channel Blockers (Class III)
- Decrease flow of K out of the cell
- Treat
- VT, VF, SVT
Calcium Channel Blockers (Class IV)
- Block flow of calcium into cell
Defibrillation **
- Passage of electrical shock through the heart to depolarize the cells of the myocardium to allow the SA node to resume the role of pacemaker
Defibrillation
-Used for what??
- Most effective method of terminating VF and pulseless VT
Defibrillation
-How to use
- Use at any point in cardiac cycle
- VF and pulseless VT should be defibrillated immediately
- Remember “all clear” before shocking
Synchronized Cardioversion
- Direct electrical current synchronized w/ the client’s rhythm
- Get consent
- Synchronize to the R wave
Synchronized Cardioversion
-Uses
- SVT
- A Fib/Flutter
- Stable VT
Synchronized Cardioversion
-Preparation
- Consent
- Emergency equipment
- IV, labs, VS, NPO
- Sedation as directed
Synchronized Cardioversion
-Aftercare
- Reassessment of rhythm
- VS
- LOC
- Skin burns
Implantable Cardioverter-Defibrillator (ICD)
-Appropriate for Patients who?
- Have spontaneous sustained VT
- Have syncope w/ inducible V-Tach/Fib during EPS
- Are at high risk for future life-threatening dysrhythmias
Pacemaker Therapy
- Provides electrical stimulus to the heart when the heart fails to generate its own or the rate is too low
Pacemaker Therapy
-Transcutaneous
- Pace through the chest wall
- SEDATE THE PATIENT TEST
- Machine is set to pacing
One pad in the front of chest and one in the back
Pacemaker Therapy
-Transvenous
- Electrode threaded into Right Ventricle or implanted during cardiac surgery
Pacemaker Therapy
-Permanent
- Epicardial - sewn directly on the heart
- Endocardial -passed transvenously into the heart
- Subcutaneous pocket formed to hold generator
Pacemakers
-Sensing
- Ability of the pacemaker to detect the heart’s own activity
Pacemakers
-Pacing
- Atrial, Ventricular, Dual
- Rate
- Output
Pacemakers
-Capture
- Successful stimulation
2. Seen on the EKG
Catheter Ablation Therapy
- Electrode-tipped ablation catheter “burns” accessory pathways or ectopic sites in the atria, AV node, and ventricles
Catheter Ablation Therapy
-Non-pharmacologic treatment for:
- AV nodal re-entrant tachycardia
- Re-entrant tachycardia r/t accessory bypass tracts
- Control of ventricular response of certain tachydysrhythmias
Atrial fibrilation & Flutter
-At risk for?
- Thrombus **
Pt Returning from Cath Lab
-What to look for?
- Hiccups show that there has been perforation of Right ventricle
Torsades de Pointes
- Assess for long QT interval which can lead to torsades de pointes