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Description : Check out this medical presentation on Arrhythmia, which is titled "ECGs", to know about Arrhythmias, abnormal cardiac rhythms and prompt assessment of abnormal cardiac rhythm and patient’s response is critical.

Tags : Arrhythmia, ECGs, abnormal cardiac rhythms, assessment

Published on : Jun 02, 2021 | Views : 1534 | Downloads : 13

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Slide 1-

ECGs
Slide 2-

Arrhythmias Abnormal cardiac rhythms Prompt assessment of abnormal cardiac rhythm and patient’s response is critical
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Phases of Cardiac Action Potential Fig. 35-1
Slide 4-

12-Lead ECG Fig. 35-3
Slide 5-

Assessment of Cardiac Rhythm Fig. 35-5
Slide 6-

Assessment of Cardiac Rhythm Fig. 35-6
Slide 7-

Assessment of Cardiac Rhythm Fig. 35-9
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Sinus Bradycardia Sinus node discharges at a rate < 60 bpm Normal rhythm in aerobically trained athletes and during sleep
Slide 9-

Sinus Bradycardia Fig. 35-11, A
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Sinus Bradycardia Clinical Association Occurs in response to Carotid sinus massage Hypothermia Increased vagal tone Administration of parasympathomimetic drugs
Slide 11-

Sinus Bradycardia Clinical Association Occurs in disease states Hypothyroidism Increased intracranial pressure Obstructive jaundice Inferior wall MI
Slide 12-

Sinus Bradycardia Significance Hypotension with decreased CO may occur An acute MI may predispose the heart to escape arrhythmias and premature beats
Slide 13-

Sinus Bradycardia Treatment Consists of atropine Pacemaker may be required
Slide 14-

Sinus Tachycardia Discharge rate from the sinus node is increased as a result of vagal inhibition and is > 100 bpm
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Sinus Tachycardia Fig. 35-11, B
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Sinus Tachycardia Clinical Associations Associated with physiologic stressors Exercise Hypotension Hypovolemia Myocardial ischemia CHF
Slide 17-

Sinus Tachycardia Significance Patients may have symptoms of dizziness and hypotension may occur Increased myocardial oxygen consumption is associated with increased HR
Slide 18-

Sinus Tachycardia Significance Angina or increase in infarct size may accompany persistent tachycardia in patient with acute MI
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Sinus Tachycardia Treatment Determined by underlying causes -adrenergic blockers to reduce HR and myocardial oxygen consumption
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Atrial Flutter Atrial tachyarrhythmia identified by recurring, regular, sawtooth-shaped flutter waves Associated with slower ventricular response
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Atrial Flutter Fig. 35-14, A
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Atrial Flutter Clinical Associations Usually occurs with: CAD Mitral valve disorders Pulmonary embolus Chronic lung disease Cardiomyopathy
Slide 23-

Atrial Flutter Significance High ventricular rates with atrial flutter can decrease CO and cause serious consequences such as heart failure Risk for stroke because of risk of thrombus formation in the atria Coumadin used for atrial flutter > 48h
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Atrial Flutter Treatment Primary goal is to slow ventricular response by increasing AV block Electrical cardioversion may be used to convert atrial flutter to sinus rhythm in emergency situation
Slide 25-

Atrial Flutter Treatment Diltiazem, digoxin, and -adrenergic blockers used to control ventricular rate Antiarrhythmic drugs used to convert atrial flutter to sinus rhythm or maintain sinus rhythm Radiofrequency catheter ablation used as curative therapy
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Atrial Fibrillation Total disorganization of atrial activity without effective atrial contraction Chronic or intermittent
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Atrial Fibrillation Fig. 35-14, B
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Atrial Fibrillation Clinical Associations Usually occurs with Underlying heart disease, such as rheumatic heart disease Cardiomyopathy CHF Pericarditis
Slide 29-

Atrial Fibrillation Clinical Associations Often acutely caused by Thyrotoxicosis Alcohol intoxication Caffeine use Electrolyte disturbance Cardiac surgery
Slide 30-

Atrial Fibrillation Significance Can often result in decrease in CO because of ineffective atrial contractions and rapid ventricular response
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Atrial Fibrillation Significance Thrombi may form in atria and may pass to brain, causing stroke Risk for stroke increases five-fold in atrial fibrillation Risk even higher in structural heart disease, HTN, and an age over 65
Slide 32-

Atrial Fibrillation Significance Anticoagulation with Coumadin used to prevent stroke
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Atrial Fibrillation Treatment Goals are decreased in ventricular response and conversion to sinus rhythm Drugs for rate control include digoxin, - adrenergic blockers, and calcium channel blockers
Slide 34-

Atrial Fibrillation Treatment Antiarrhythmic drugs used for conversion DC cardioversion may be used to convert atrial fibrillation to normal sinus rhythm
Slide 35-

Atrial Fibrillation Treatment Anticoagulant therapy recommended for 3 to 4 weeks in atrial fibrillation > 48 h before attempt at conversion to sinus rhythm
Slide 36-

First-Degree AV Block Every impulse is conducted to the ventricles, but duration of AV conduction is prolonged
Slide 37-

First-Degree AV Block Fig. 35-16, A
Slide 38-

First-Degree AV Block Clinical Associations Usually occurs with: Chronic ischemic heart disease MI Rheumatic fever Vagal stimulation Drugs such as digitalis, -adrenergic blockers, flecainide, and IV verapamil
Slide 39-

First-Degree AV Block Significance May be a precursor to higher degrees of AV block No treatment
Slide 40-

Second-Degree AV Block, Type 1 Includes gradual lengthening of the PR interval, which occurs because of prolonged AV conduction time Most commonly occurs at AV node, but can occur in His-Purkinje system
Slide 41-

Second-Degree AV Block, Type 1 Fig. 35-16, B
Slide 42-

Second-Degree AV Block, Type 1 Clinical Associations May result from drugs such as digoxin or -adrenergic blockers Associated with ischemic cardiac disease and other diseases slowing AV conduction
Slide 43-

Second-Degree AV Block, Type 1 Significance Usually a result of myocardial ischemia on an inferior MI May be warning signal of impending significant AV conduction disturbance
Slide 44-

Second-Degree AV Block, Type 1 Treatment If symptomatic, atopine is used to increase HR or pacemaker may be needed If asymptomatic, rhythm closely observed with transcutaneous pacemaker on standby
Slide 45-

Second-Degree AV Block, Type 2 P wave not conducted without progressive antecedent PR lengthening Almost always occurs when bundle branch block is present Certain number of impulses from the sinus node are not conducted to the ventricles
Slide 46-

Second-Degree AV Block, Type 2 Fig. 35-16, C
Slide 47-

Second-Degree AV Block, Type 2 Clinical Associations Associated with rheumatic heart disease, CAD, acute anterior MI, and digitalis toxicity
Slide 48-

Second-Degree AV Block, Type 2 Significance Often progresses to third-degree and is associated with poor prognosis May result in decreased CO with subsequent hypotension and myocardial ischemia
Slide 49-

Second-Degree AV Block, Type 2 Treatment Before the insertion of a permanent pacemaker may involve use of temporary transvenous or transcutaneous pacemaker Temporary drug measures to increase HR until pacemaker is available
Slide 50-

Third-Degree AV Heart Block Complete heart block Constitutes one-fourth of AV dissociation in which no impulses from atria are conducted to ventricles
Slide 51-

Third-Degree AV Heart Block Ventricular rhythm is escape rhythm, and ectopic pacemaker may be above or below bifurcation of His bundle
Slide 52-

Third-Degree AV Heart Block Fig. 35-16, D
Slide 53-

Third-Degree AV Heart Block Clinical Associations Calcification or fibrosis of conduction system CAD MI Cardiomyopathy
Slide 54-

Third-Degree AV Heart Block Significance Almost always results in reduced CO with subsequent ischemia and heart failure Syncope may result from severe bradycardia or periods of asystole
Slide 55-

Third-Degree AV Heart Block Treatment Temporary transvenous or transcutaneous pacemaker may be used on an emergency basis in a patient with acute MI Drugs used to temporarily increase HR and support blood pressure before pacemaker insertion
Slide 56-

Premature Ventricular Contractions Contraction originating in ectopic focus of the ventricles Premature occurrence of QRS complex Multifocal, unifocal, ventricular bigeminy, ventricular trigeminy, couples, and triplets
Slide 57-

Premature Ventricular Contractions Fig. 35-17
Slide 58-

Premature Ventricular Contractions Clinical Associations Stimulants Hypokalemia Exercise MI Mitral valve prolapse
Slide 59-

Premature Ventricular Contractions Significance Usually a benign finding in patient with a normal heart In heart disease, PVCs may reduce CO and precipitate angina and heart failure In ischemic heart disease or acute MI, represents ventricular irritability
Slide 60-

Premature Ventricular Contractions Significance May also occur in reperfusion arrhythmias after lysis of a coronary artery clot with thrombolytic therapy in acute MI, or following plaque reduction after percutaneous coronary intervention
Slide 61-

Premature Ventricular Contractions Treatment Assessment of hemodynamic status is important to determine if drug therapy is indicated -adrenergic blockers, procainamide, amiodarone, or lidocaine
Slide 62-

Ventricular Tachycardia Run of three or more PVCs occurs Monomorphic, polymorphic, sustained, and nonsustained Considered life-threatening because of decreased CO and the possibility of deterioration of ventricular tachycardia to ventricular fibrillation
Slide 63-

Ventricular Tachycardia Fig. 35-18
Slide 64-

Ventricular Tachycardia Clinical Associations Associated with Acute MI Significant electrolyte imbalances Mitral valve prolapse Coronary reperfusion after thrombolytic therapy CNS disorders
Slide 65-

Ventricular Tachycardia Significance Have been observed in patients with no evidence of heart disease May cause severe decrease in CO Result may be pulmonary edema, shock, and decreased blood flow to the brain
Slide 66-

Ventricular Tachycardia Treatment If VT is monomorphic and patient is hemodynamically stable and has preserved left ventricular function IV procainamide, amiodarone or lidocaine is used Synchronized cardioversion is used when drug therapy is ineffective
Slide 67-

Ventricular Tachycardia Treatment If polymorphic with normal baseline QT interval, therapies include magnesium infusion, overdrive pacing, and IV -adrenergic blocker
Slide 68-

Ventricular Tachycardia Treatment Drugs prolonging QT should be discontinued Unsynchronized cardioversion may be needed
Slide 69-

Ventricular Tachycardia Treatment Ventricular tachycardia without a pulse is treated as ventricular fibrillation, rapid defibrillation is attempted
Slide 70-

Ventricular Tachycardia Accelerated idioventricular rhythm is a slow VT originating from ectopic pacemaker in ventricles Rate between 40 to 100 bpm
Slide 71-

Ventricular Tachycardia Clinical Associations Associated with acute MI and reperfusion of myocardium after thrombolytic therapy or angioplasty
Slide 72-

Ventricular Tachycardia Significance Can be escape mechanism Can be seen with digitalis toxicity Treatment Treat as VT if patient becomes symptomatic
Slide 73-

Ventricular Fibrillation Severe derangement of the heart rhythm characterized on ECG by irregular undulations of varying contour and amplitude No effective contraction or CO occurs
Slide 74-

Ventricular Fibrillation Fig. 35-19
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Ventricular Fibrillation Clinical Associations Occurs in Acute MI Myocardial ischemia Chronic diseases such as CAD Electrical shock Hyperkalemia Drug toxicity
Slide 76-

Ventricular Fibrillation Clinical Associations May occur during catheterization procedures or with coronary reperfusion after thrombolytic therapy
Slide 77-

Ventricular Fibrillation Significance Results in unconsciousness, absence of pulse, apnea, and seizures If untreated, patient will die
Slide 78-

Ventricular Fibrillation Treatment Immediate initiation of CPR and ACLS with use of drug therapy and defibrillation
Slide 79-

Pulseless Electrical Activity Electrical activity can be observed on ECG, but there is no mechanical activity of ventricles and patient has no pulse
Slide 80-

Pulseless Electrical Activity Clinical Associations Common causes Hypovolemia Drug overdose MI Hyper- or hypokalemia Pulmonary embolus
Slide 81-

Pulseless Electrical Activity Treatment CPR followed by intubation and IV therapy with epinephrine Directed toward correcting underlying cause
Slide 82-

Sudden Cardiac Death Death by an arrhythmia
Slide 83-

Proarrhythmia Antiarrhythmic drugs may cause life- threatening arrhythmias Significance Patient with left ventricular dysfunction is most susceptible
Slide 84-

Proarrhythmia Treatment Monitor first days of antiarrhythmic drugs in hospital setting
Slide 85-

Defibrillation Most effective method of terminating ventricular fibrillation Ideally performed within 15 to 20 seconds of onset of arrhythmia Passage of direct current electrical shock through heart to depolarize cells
Slide 86-

Defibrillation Intent is to allow SA node to resume role
Slide 87-

Defibrillation Fig. 35-21
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Cardioversion Choice therapy for hemodynamically unstable ventricular or supraventricular tachyarrhythmias Delivers countershock during QRS complex Done on non-emergency basis
Slide 89-

Implantable Cardioverter-Defibrillator Treatment for life-threatening ventricular arrhythmias Lead system placed via subclavian vein to endocardium Pulse generator is implanted over pectoral muscle
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Implantable Cardioverter- Defibrillator After sensing system defects in lethal arrhythmia, delivers shock to the patient’s heart muscle Initiate overdrive pacing of supraventricular and ventricular tachycardias
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Implantable Cardioverter-Defibrillator Provide backup pacing for bradyarrhythmias after defibrillation
Slide 92-

Implantable Cardioverter-Defibrillator Fig. 35-22
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Implantable Cardioverter-Defibrillator Electronic device used in place of SA node Paces both the atrium as well as the ventricle Increases HR when appropriate Used in management of heart failure, symptomatic bradyarrhythmias, and neurocardiogenic syncope