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Dysrhythmias
| Term | Definition |
|---|---|
| Automaticity | Ability to INITIATE an impulse spontaneously and continuously |
| Contractility | Ability to RESPOND mechanically to an impulse |
| Conductivity | Ability to TRANSMIT an impulse along a membrane in an orderly manner |
| Excitability | Ability to be electrically STIMULATED |
| Autonomic nervous system responsible for: | • RATE of impulse formation • SPEED of conduction • STRENGTH of cardiac contraction |
| Vagus nerve (Parasympathetic nervous system) stimulation results in: | • Decreases rate • Slowing of impulse conduction • Decreases force of contraction |
| Sympathetic nervous system stimulation causes: | • Increases rate • Increases force of contraction |
| P wave | Atrial depolarization. Represents the time it takes for the electrical impulse to pass through the atrium. Usually upright and round Duration is 0.06-0.12 seconds |
| PR Segment | The point immediately before ventricular contraction. Represents the time taken for impulse to spread through the atria, the AV node and bundle of His, the bundle branches, and Purkinje fibers Duration is 0.12-0.20 seconds |
| QRS Complex | Ventricular depolarization (CONTRACTION) Contraction of both ventricles represents systole Duration is 0.06-0.10 seconds |
| ST segment | Interval between ventricular depolarization and repolarization |
| T wave | Ventricular repolarization. Upright |
| QT interval | Time taken for entire electrical depolarization and repolarization of the ventricles. Longest duration: 0.34-0.43 |
| Isoelectric line | The baseline of an ECG tracing found by looking at the T-P segment. Denotes resting membrane potentials. |
| How to calculate Regularity | Measure R-R |
| How to calculate Rate | 1) Count the number of QRS complexes in 1 minute 2) Number of R-R intervals multiplied by 10 For regular rhythms: 3) 1500 divided by the number of small squares in R-R interval 4) 300 divided by the number of large squares in R-R interval |
| Sinus Rhythm | Rate: 60-100 bpm Rhythm: Regular P wave: Precedes every QRS wave, normal shape/duration PR Interval: 0.12-0.20 seconds (normal) QRS Complex: 0.06-0.10 seconds (normal) |
| Sinus Bradycardia conduction pattern | Rate: <60 bpm Rhythm: Regular P wave: Precedes every QRS wave, normal shape/duration PR Interval: 0.12-0.20 seconds (normal) QRS Complex: 0.06-0.10 seconds (normal) |
| Sinus Tachycardia | Rate: >100 bpm Rhythm: Regular P wave: Precedes every QRS wave, normal shape/duration PR Interval: 0.12-0.20 seconds (normal) QRS Complex: 0.06-0.10 seconds (normal) |
| Premature Atrial Contraction (PAC) | Contraction from an Ectopic focus before the next beat Distorted P Wave by impulse traveling across the atria through an abnormal pathway |
| Paroxysmal Supraventricular Tachycardia (PSVT) | Originates in ectopic focus above bifurcation of the bundle of His Premature beats (PAC) with abrupt onset and termination (Paroxysmal) Rate: 151-220 bpm Rhythm: regular or slightly irregular |
| Atrial Flutter | Recurring, regular, sawtooth-shaped flutter waves from a single ectopic focus Atrial rate (frequency of P waves): 250-350 bpm Rhythm: regular (atrial and ventricular) QRS Complex: usually normal |
| Atrial Fibrillation | Multiple ectopic foci and loss of effective atrial contraction Rate: 600 bpm (atrial) or 50-180 bpm (ventricular) Rhythm: usually irregular (ventrical) P wave: replaced by chaotic, fibrillatory waves PR Interval: not measurable QRS Complex: normal |
| Premature Ventricular Complex (PVC) | Contraction originating in ectopic focus of the ventricles P wave: absent Rhythm: irregular QRS Waves: Premature, wide, distorted, >0.12 sec |
| Ventricular Tachycardia | Ectopic focus fire repetitively and the ventricle takes control of the pacemaker; 3 or more PVCs Considered life-threatening because of decreased CO and the possibility of deterioration to ventricular fibrillation |
| Ventricular Fibrillation | Firing of multiple ectopic foci in the ventricle (severe derangement of rhythm) Ventricle is quivering - No effective contraction or CO occurs HR not measurable, rhythm is irregular and chaotic |
| Asystole | Represents total absence of ventricular electrical activity No ventricular contraction (CO) occurs because depolarization does not occur Unresponsive, pulseless, and apneic state CPR with initiation of ACLS measures |
| Pulseless Electrical Activity | Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the client has no pulse CPR followed by intubation and IV epinephrine Epinephrine 1 mg every 3–5 minutes |
| SA Node rate | Pacemaker of the heart. 60-100 bpm (normal heart rate) |
| AV Node rate | 40-60 bpm |
| His-Purkinje system rate | 20-40 bpm |
| Sinus Bradycardia Clinical Significance and Treatment | •Hypotension • Pale, cool skin • Weakness • Angina (chest pain) • Dizziness or syncope • Confusion or disorientation • Shortness of breath •Reduce or stop medications that decrease HR • Atropine • Epinephrine • Dopamine • Pacemaker |
| Drugs that lower HR | Beta blockers (βBs) blocking epinephrine, non-dihydropyridine calcium channel blockers and ivabradine |
| Drugs that increase HR | Dopamine Epinephrine reuptake inhibitors Atropine: blocking the parasympathetic influences on the heart |
| Sinus Tachycardia Clinical Significance (5) | • Increased myocardial oxygen consumption • Angina (chest pain) • Dizziness • Dyspnea (shortness of breath) • Hypotension due to decreased CO |
| Sinus Tachycardia Treatment | • B-adrenergic blockers, calcium channel blockers to reduce HR and myocardial oxygen consumption • Antipyretics to treat fever • Analgesics to treat pain • Clinically unstable patients may need synchronized cardioversion |
| PSVT Clinical Significance | Prolonged episode and HR >180 bpm may precipitate decreased CO • Hypotension • Dyspnea (shortness of breath) • Angina (chest pain) |
| PSVT Treatment | •Vagal manoeuvres: Valsalva, coughing • IV adenosine • Short half life (1.5-10 sec) • Brief period of asystole can occur • Beta-adrenergic blockers, CCB, amiodarone • synchronized cardioversion in extreme cases |
| Atrial flutter Clinical Significance | • High ventricular rates (>100) and loss of the atrial “kick” can DECREASE CO and precipitate Heart failure (HF), angina (chest pain) • Risk for STROKE due to risk of thrombus formation in the atria from stasis of blood |
| Atrial Flutter Treatment | • Drugs to slow HR • Electrical cardioversion • Antidysrhythmic drugs (e.g., amiodarone, propafenone) • Radiofrequency catheter ablation: tissue with abnormal atrial automaticity is located and destroyed |
| Atrial Fibrillation Clinical Significance | • Decrease in CO due to ineffective atrial contractions (loss of atrial kick) and rapid ventricular response • Thrombi in the atria as a result of blood stasis • Embolus may develop and travel to the brain, causing a stroke |
| Atrial Fibrillation Treatment | • Meds to decrease HR • Long-term anticoagulation therapy • Conversion to sinus rhythm may be considered • Antidysrhythmic drugs • Cardioversion (anticoagulation pre/post) • Radiofrequency ablation (similar to atrial flutter) |
| PVC Clinical Significance | In heart disease PVCs may decrease CO and precipitate angina and HF if >10/minute Lack of sufficient ventricular contraction= no peripheral pulse (listen to apical pulse and palpate radial pulse to identify pulse deficit) |
| PVC Treatment | • Oxygen therapy for hypoxia • Electrolyte replacement • Assess for signs of decreased cardiac output and if patient is symptomatic • Dizziness, chest pain • Medications such as beta blockers, lidocaine, amiodarone |
| Ventricular Tachycardia Clinical Significance | •Stable (pulse) or Unstable (no pulse) •Decreased ventricular diastolic filling time and loss of atrial contraction Hypotension Pulmonary edema Decreased cerebral blood flow Cardiopulmonary arrest Ventricular fibrillation may develop |
| Ventricular Fibrillation Clinical Significance (4) | • Unresponsive • Pulseless • Apneic state (temporal cessation of breathing) • If not treated rapidly, death will result. |
| Ventricular Fibrillation Treatment (4) | Assessment of circulation, airway, and breathing (CAB) Immediate initiation of CPR and use of defibrillation and definitive drug therapy (ACLS) Epinephrine Amiodarone and/or lidocaine (antidysrhythmic) |
Created by:
selenay15
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