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Terms in this set (114)

Regularity: Regular
Rate: Atrial: >100-160 bpm, Ventricular:>100-160 bpm
P Waves: One P wave precedes every QRS; P waves are consistent in shape.
PR Interval: 0.12-0.20 sec. and consistent.
QRS: 0.04-0.10 sec. QRS is normal configuration. A QRS follows each P wave.
Interpretation: In ST, the impulse is being generated in the SA node at a rate that is faster than normal. The route through the conduction system is normal.
Effect
-Decreased filling times
-Decreased mean arterial pressure
-Increased myocardial demand
Patho
-Catecholamines: rise in resting potential and calcium influx
-Fever: unknown
-Early heart failure: Compensatory response to decreased stroke volume
-Lung disease: hypoxic cell metabolism
-Hypercalcemia
Treatment
-Oxygen
-Bed Rest
-Calcium Blockers
(Causes: can be normal response to exercise, pain, stress, fever, or strong emotions, such as fear and anxiety. Can also occur in certain cardiac conditions, such as heart failure, cardiogenic shock and pericarditis; as a compensatory mechanism in shock, anemia, respiratory distress, pulmonary embolism, sepsis, and hyperthyroidism; and when taking such drugs as atropine, isoproterenol (Isuprel), aminophylline, dopamine, dobutamine, epinephrine, alcohol, caffeine, nicotine, and amphetamines.)
Tachycardia can lower cardiac output by reducing ventricular filling time and the amount of blood pumped by the ventricles during each contraction. Normally, ventricular volume reaches 120-130ml during diastole. In tachycardia, decreased ventricular volume leads to hypotension and decreased peripheral perfusion.
As cardiac output plummets, arterial pressure and peripheral perfusion decrease. Tachycardia worsens myocardial ischemia by increasing the heart's demand for oxygen and reducing the duration of diastole- the period of greatest coronary flow.
Regularity: Regular
Rate: Atrial:<60 bpm ,Ventricular: <60 bpm
P Waves: One P wave precedes every QRS; P waves are consistent in shape.
PR Interval: 0.12-0.20 sec. and consistent.
QRS: 0.04-0.10 sec. QRS is normal configuration. A QRS follows each P wave.
Interpretation: In SB, the impulse is being generated in the SA node at a rate that is slower than normal. The route through the conduction system is normal. Therefore, SB meets all criteria for Sinus Rhythm except the rate.
Effect
-Increased pre-load
-Decreased mean arterial pressure
Patho
-Hyperkalemia: slows depolarization
-Vagal Hyperactivity: unknown
-Digoxin Toxicity common
-Late Hypoxia: lack of adenosine triphosphate (ATP)
Treatment
-Only treat if symptomatic
-If hypotensive: treat cause
-Sympathomimetics, anticholinergics
-Atropine
-Pacemaker implantation
Causes: May be a normal physiological variant, especially in athletes or during sleep.
Pathologies associated with SB include myxedema coma, increased intracranial pressure, and glaucoma.
Increased vagal tone or stimulation can also slow the rate.
Drugs that slow the heart rate include beta-blockers, calcium-channel blockers, or digoxin.
Digitalis toxicity is a common cause of SB.
Inferior myocardial infarction.
Significance: Decreases cardiac output with clinical signs of hypotension and decreased organ perfusion.
Treatment: Only treat when symptomatic (i.e. hypotension, chest pain, shortness of breath, dizziness or lethargy, or signs of congestive heart failure) (see table above)
Any wide complex Tachycardia is V-Tach until proven otherwise
Regularity: Regular during tachycardia; may be slightly irregular at onset and cessation of tachycardia.
Rate: Atrial: Depends on the underlying atrial rhythm. It may be impossible to calculate the atrial rate, Ventricular: >100 bpm.
P-waves: If seen, P-waves are generally dissociated from the QRSs.
PR interval: If P-waves are noted, the P-R interval will vary.
QRS: Wide and bizarre, >0.10 sec.
Effect
-Decreased cardiac output from loss of atrial contribution to ventricular preload
-Increased myocardial demand because of tachycardia
Pathophysiology
-Hyperkalemia (5.4-6)
-Hypercalcemia, hypoxia, and elevated preload: cell membrane disturbances
Treatment
-Treat underlying cause
-Treatment for the stable patient will include IV antiarrhythmic medications, such as Amiodarone and Lidocaine.
-Treatment for the unstable but conscious patient will include synchronized electrical cardioversion.
-Treatment for the pulseless patient will include CPR, defibrillation, and IV medications such as epinephrine, Amiodarone, or Lidocaine
-Management of the patient who is at risk for recurrence of V-tach may include
radio-frequency ablation
antiarrhythmic medications
-placement of an implanted cardioverter defibrillator (ICD)
(Causes: Myocardial ischemia; MI; coronary artery disease; vavular heart disease; heart failure; cardiomyopathy; electrolyte imbalances such as hypokalemia, drug intoxication from digoxin (Lanoxin), procainamide, quinidine or cocaine; proarrhythmic effects of some antiarrhythmics)
Ventricular tachycardia is significant because of its unpredictability and potential to cause death. A patient may be stable with a normal pulse and adequate hemodynamics or unstable with hypotension and no detectable pulse. Because of reduced ventricular filling time and the drop in cardiac output, the patient's condition can quickly deteriorate to ventricular fibrillation and complete cardiac collapse.(Lippencott 137)
Vfib is a PULSELESS Rhythm. Verify and Defibrillate immediately.
Regularity: Irregular
Rate: Atrial: None, Ventricular: None
P-waves: None.
PR interval: None.
QRS :None.
Interpretation: Irregular, chaotic fibrillatory waves are seen. They may be coarse or fine.
Effect
-No cardiac output
-Not compatible with life Hyperkalemia (5.4-6)
Patho
-Hypercalcemia, hypoxia, and elevated preload: cell membrane disturbances
-Aging
-Induction of anesthesia
-Impulse originates in cell outside normal conduction system and spreads through intercalated disks
-Rapid infusion of potassium
Treatment
-Pharmacological interventions to change thresholds, refractory period; reduce myocardial demand, increase supply
-Electrical Cardioversion
(Causes: Severe hypoxemia, ischemia, MI, acidosis, profound electrolyte imbalance, severe hypothermia, electric shock, or drug toxicity (digoxin, Quinidine, and Procainamide). V-tach may deteriorate to V-fib.)
• With ventricular fibrillation the ventricles quiver instead of contract, so cardiac output falls to zero. If fibrillation continues, it leads to ventricular standstill and death. (Lippencott 142)
• The patient in V-Fib is in full cardiac arrest, unresponsive, and without detectable blood pressure or carotid or femoral pulse. Whenever you see a pattern resembling ventricular fibrillation, check the patient immediately, check the rhythm in another lead, and start treatment. (Lippencott 142)
• Be aware that other factors can mimic V-Fib on an ECG strip. Interference from an electric razor is one such mimic, as is muscle movement form shivering. (Lippencott 142)
Regularity: Grossly irregular.
Rate: Atrial: Indeterminate, >400 bpm. Ventricular: Varied depending on the AV node's ability to conduct to the ventricles; if uncontrolled generally160-180 bpm, controlled generally at 60-70 bpm.
P waves: No discernable P waves, as the atria never depolarize as a whole. Atria are quivering and not contracting. The baseline is chaotic and may appear fine or coarse. T waves may also be difficult to distinguish within the chaotic baseline.
PR Interval: None, due to a lack of P wave
QRS: Typically normal, unless aberrant conduction occurs causing widening of the QRS complex which is common at faster rates.
Effect
-Decreased filling time
-Decreased mean arterial pressure
Patho
-Electrolyte disturbances(especially hypercalcemia): alter action potentials
-Hypoxia and elevated preload: cell membrane disturbances
-Leads to increased atrial automaticity, atrial reentry
-Digoxin toxicity: common
-Aging
Treatment
-control ventricular rate
-digoxin, calcium channel blockers, vagus stimulation
-pacemaker to override atrial conduction
(Cause: CAD, MI, ischemia, rheumatic heart disease, vavlular heart disease, pericarditis, cardiomyopathy, CHF, hypermetabolic states, pulmonary disease, stimulants/intoxicants, hypokalemia, cardiac surgery, chronic HTN, and hypoxia.)
Significance:
• Loss of atrial kick which attributes to 10-20% of ventricular filling therefore cardiac output decreases.
• High ventricular response rates exacerbate the decreased cardiac output
• Commonly blood clots form in the atria that may manifest as emboli.
When the ventricular rate is greater than 100 in the presence of atrial fibrillation, the person is said to have atrial fibrillation with a "rapid ventricular response" or "RVR". Atrial fibrillation is sometimes abbreviated as "Afib". Thus a "rapid afib" or atrial fibrillation with RVR is sometimes abbreviated as "afib with RVR".
Very similar to SVT but is irregular rate, where SVT is regular rate
Regularity: Atrial rhythm is regular. Ventricular rhythm is irregular. The R-R interval is irregular in a pattern of group beating. The R-R interval gets progressively shorter as the PR interval gets progressively longer
Rate : Atrial: Exceeds the ventricular rate because of blocked P's,Ventricular: Less than atrial rate
P Waves: The P waves will be normal size and configuration; some P waves not followed by QRS complexes
PR Interval:The PR interval gets progressively longer until one P wave is not followed by a QRS complex. After the blocked beat (dropped QRS), the cycle starts again (group beating)
QRS: Since depolarization will usually occur normally through the ventricles, the QRS has a normal configuration and duration of 0.04 - 0.10 sec.
Effect
-Occasional decrease in cardiac output
-Increase in preload for following beat
Patho
-Hypokalemia (<3.5)
-Faulty cell metabolism in AV node
-Severity increases as heart rate increases
-Supports theory that AV node is fatiguing
-Digoxin toxicity, beta blockade
-CAD, MI, hypoxia, increased prload, vavular surgery and disease, diabetes
Treatment
-conservative
-usually do not progress in severity
-pharmacologic treatment includes vagolytics, sympathomimetics, pacing
-Treatment is seldom necessary.
-Underlying cause
-Continue observation and monitoring.
-If symptomatic bradycardia occurs, Atropine and/or a temporary pacemaker may be used.

(Causes: Include inferior wall MI, digoxin toxicity, ischemic heart disease, acute rheumatic fever, post-cardiac surgery, electrolyte imbalance; Drugs such as beta blockers, Quinidine and Procainamide.)
Interpretation: Occurs when each successive impulse from SA node is delayed slightly longer than the previous impulse.
(Wide QRS complexes indicate origin of block is below the Bundle of His, leading to a higher incidence of lethal complications, If QRS narrow, block is above the Bundle of His, and is not associated with high mortality)
Regularity: Atrial rhythm is regular, Ventricular rhythm can be regular or irregular.
• Pauses correspond to dropped beats. When the block is intermittent or when the conduction ratio is variable, the ventricular rhythm is irregular. When there is a constant conduction ratio, the ventricular rhythm is regular.
Rate: Atrial: Exceeds the ventricular rate because of blocked P's, Ventricular:Less than atrial rate.
P Waves: The P waves will be normal size and configuration; some P waves not followed by QRS complexes.
PR Interval: PR interval is within normal limits or prolonged, but constant
QRS: If the block occurs at the bundle of His, the QRS will have a normal configuration and duration of 0.04 - 0.10 sec, If the block occurs at the bundle branches, the QRS will be wide >0.10 sec.
Interpretation: Hallmarks of this type of block, is PR interval does NOT lengthen before a dropped beat. More than one nonconducted beat can occur in succession.
Effect
-Occassional decrease in cardiac output
-Increase in preload for following beat
Pathophysiology
-Hypokalemia (<3.5)
-Faulty cell metabolism in AV node
-Antidysrhythmics, tricyclic antidepressants
-CAD, MI, hypoxia, increased preload, valvular surgery and disease, diabetes
Treatment
-More aggressively than Mobitz I, because can progress to type III
-Pacemaker after pharmacologic treatment
-In asymptomatic patients, monitor closely and be prepared to pace
-Atropine for patients experiencing symptomatic bradycardia
-Transcutaneous pacing should be immediately available
-IV Dopamine or epinephrine drips may also be used to increase CO.
-A temporary pacemaker may be used until a permanent pacemaker can be inserted.

(Causes: Acute anterior or anteroseptal MI; Other causes include degenerative changes in the conduction system; severe coronary artery disease)
Above the Bundle of HIS
(Narrow QRS complexes indicate high block (above the Bundle of His) Usually benign. Usually associated with ischemia or toxic drug effects.)

Below the Bundle of HIS
• Regular Rhythm
• Rate: Atrial: Generally under the control of the SA node, 60 - 100 bpm, Ventricular: With a junctional escape rhythm the ventricular rate usually 40 - 60 bpm. With a ventricular escape rhythm the ventricular rate is usually below 40 bpm
• There is no PR interval!
• QRS interval: Configuration depends on location of escape mechanism pacing the ventricles:
o If junctional escape rhythm, the QRS will appear normal (0.04 - 0.10 sec.).
o If ventricular escape rhythm the QRS will be widened (>0.10 sec)

Interpretation: The atria and ventricles are depolarized from different pacemakers and beat independently of each other (AV dissociation). Complete absence of impulse conduction between the atria and ventricles; two independent rhythms. Atrial rate > ventricular rate.
Effect
Decreased cardiac output from loss of atrial contribution to ventricular preload
Pathophysiology
-Hypokalemia (<3.5)
-Faulty cell metabolism low in bundle of HIS MI, especially inferior wall, as nodal artery interrupted, results in ischemia of AV node
Treatment
-Pacemaker after pharmacologic treatment
-Temporary pacing if caused by inferior MI, because ischemia usually resolves
-goal is to increase cardiac output: transcutaneous pacing should be available
-If the QRS is wide IV Dopamine or epinephrine drips may also be used to increase cardiac output (CO)
(Causes: MI, AV node damage or ischemia, acute myocarditis, electrolyte imbalance; Toxic effect of drugs such as digoxin or beta blockers; Chronic degenerative changes in the bundle branches present in the elderly.)
•Rhythm irregular
•Rate dependent on the underlying rhythm
•P wave absent with PVC
•PR interval not measured for the PVC
•QRS in PVC is early with bizarre configuration that is wide
Effect
-Decreased cardiac output from loss of atrial contribution to ventricular preload for that beat
Pathophysiology
-Hyperkalemia (5.4-6)
-Hypercalcemia, hypoxia, and elevated preload
-Aging and induction of anesthesia
-Impulse originates in cell outside normal conduction system and spreads through intercalated disks
Treatment
-Pharmacological interventions to change thresholds, refractory periods; reduce myocardial demand, increase supply
-Correcting the underlying cause
-Antiarrhythmic medications may suppress the PVC's, Amiodarone, Betapace, Lidocaine, Mexilitine, Pronestyl, beta-blockers, and numerous others.

(Cause: Infrequent PVC's resulting from enhanced normal automaticity may be a normal; Frequent PVC's (> 6/minute) and couplets may be caused by electrolyte abnormalities, ischemia, infarction, hypoxemia, acidosis and with cardiomyopathies; Other causes include increase sympathetic stimulation, sympathomimetic drugs (like epinephrine and Isoproterenol), caffeine, alcohol, tobacco, drug intoxication (particularly cocaine, amphetamines and tricyclic antidepressants); Mechanical irritation by a pacemaker wire or pulmonary artery catheter may cause PVC's; Antiarrhythmic medications may have proarrhythmic effects, as do any medications that prolong the QT interval. )
Significance:
• May be a normal occurrence.
• Frequent PVC's may indicate a patient at risk for V-tach or ventricular fibrillation
• Patients with frequent PVC's may be mildly symptomatic
• Prematurity of ventricular systole and loss of atrial kick with the PVC limits ventricular filling time, resulting in a decreased stroke volume with each PVC