Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Dysrhythmias
Ch. 36
| Question | Answer |
|---|---|
| What are the four properties of cardiac cells that enables the conduction system to start an electrical impulse, send it through the cardiac tissue, and stimulate muscle contraction? | Automaticity Excitability Conductivity Contractility |
| The ability to initiate an impulse spontaneously and continuously. | automaticity |
| The ability to be electrically stimulated. | excitability |
| The ability to transmit an impulse along a membrane in an orderly manner. | conductivity |
| The ability to respond mechanically to an impulse. | contractility |
| What is the normal pathway for cardiac impulses? | Begins in the sinoatrial (SA) node causing atrial contraction, to the atrioventricular (AV) node, through the Bundle of His, down the left and right bundle branches, and ends in the Purkinje fibers, which transmit the impulse to the ventricles. |
| These can result from disorders of impulse formation, conduction of impulses, or both? | dysrhythmias |
| What is the normal pacemaker of the heart? | SA node |
| What is the normal heart rate when the impulse begins at the SA node? | 60-100 beats/minute |
| What is the heart rate when the impulse starts at the AV node? | 40-60 beats/minute |
| What is the heart rate when the impulse begins in the Bundle of His or Purkinje fibers? | 20-40 beats/minute |
| What does the P wave represent on an ECG? | The time for the passage of the electrical impulse through the atrium causing atrial depolarization (contraction). |
| What represents the time taken for the impulse to spread through the atria, AV node, and bundle of His, the bundle branches, and Purkinje fibers to a point immediately preceding ventricular contraction. | PR interval (PRI) |
| On an ECG, the waves pointing up (P, R, T) represent a ______ deflection, while the waves pointing down (Q, S) represent a ______ deflection. | positive; negative |
| On an ECG, which wave represents the time taken for depolarization (contraction) of both ventricles (systole)? | QRS complex |
| How is the PR interval measured? | Measure from the beginning of the P wave to the beginning of the QRS complex. |
| What part of an ECG represents the time between ventricular depolarization and repolarization (diastole)? It should be isoelectric (flat). | ST segment |
| On an ECG, this wave represents the time for ventricular repolarization. It should be upright. | T wave |
| On an ECG, what represents the time taken for entire electrical depolarization and repolarization of the ventricles? How is this measured? | Q-T interval is measured from the beginning of the QRS complex to the end of the T wave. |
| A rhythm strip consists of large squares with each large square consisting of 25 smaller squares (5 horizontal, 5 vertical), what does each of the horizontal smaller (1 mm) squares represent? | 0.04 seconds |
| On a rhythm strip, what does a large square represent? | 0.20 seconds |
| On a rhythm strip, 300 large squares equals? | 1 minute |
| On a rhythm strip what do the vertical smaller squares represent? | 0.1 millivolt (mV) |
| How many millivolts (mV) does one large square represent? | 0.5 mV |
| What is the most accurate way of calculating the HR | Count the number of QRS complexes in 1 minute. |
| What is a simple way of calculating the HR that gives an estimated number of bpm? | A marker appears every 3 seconds on the ECG paper. Count the number of R-R intervals in 6 secs and multiply that number by 10. |
| Another way to calculate HR is to count the number of ____ squares between one R-R interval and divide this number into 1500 to get the HR. | small |
| To calculate HR you can count the number of large squares between one R-R interval and divide this number into ____ to get the HR. | 300 |
| How do you prep a patient that is about to have an ECG done? | Clip excessive hair on the chest wall w/scissors. Gently rub the skin with dry gauze til slightly pink. If skin is oily wipe w/alcohol first. If the pt is diaphoretic, apply a skin protectant before placing the electrode. |
| This is a distortion of the baseline and waveforms seen on the ECG. They are often seen when leads and electrodes are not secure, or if there is muscle activity (e.g. shivering), or electrical interference. | artifacts |
| Assessment of Cardiac Rhythms: Step 1 | Look for the presence of the P wave. Is it upright or inverted? Is there one for every QRS complex or more than one? Are there atrial fibrillatory or flutter waves present? |
| Assessment of Cardiac Rhythms: Step 2 | Evaluate the atrial rhythm. Is it regular or irregular? |
| Assessment of Cardiac Rhythms: Step 3 | Calculate the atrial rate |
| Assessment of Cardiac Rhythms: Step 4 | Measure the duration of the P-R interval. Is it normal duration or prolonged? |
| Assessment of Cardiac Rhythms: Step 5 | Evaluate the ventricular rhythm. Is it regular or irregular? |
| Assessment of Cardiac Rhythms: Step 6 | Calculate the ventricular ratte. |
| Assessment of Cardiac Rhythms: Step 7 | Measure the duration of the QRS complex. Is it normal duration or prolonged? |
| Assessment of Cardiac Rhythms: Step 8 | Assess the ST segment. Is it isoelectric (flat), elevated, or depressed? |
| Assessment of Cardiac Rhythms: Step 9 | Measure the duration of the QT interval. Is it normal duration or prolonged? |
| Assessment of Cardiac Rhythms: Step 10 | Note the T wave. Is it upright or inverted? |
| This rhythm starts in the SA node at a rate of 60-100 bpm, follows the normal conduction pathway, and is regular. All of the waves are as they should be in shape and duration. | normal sinus rhythm |
| This rhythm fires at the SA node at a rate less than 60 bpm, is regular, P wave precedes each QRS complex, PRI is normal, and QRS complex is normal. | sinus bradycardia |
| Sinus bradycardia may be a normal sinus rhythm with what kind of people? | aerobically trained athletes and in some people during sleep |
| What are some other ways sinus bradycardia can occur? | carotid sinus massage, Valsalva maneuver, hypothermia, increased intraocular pressure, vagal stimulation, and administration of certain drugs (B-adrenergic blockers, CCBs) |
| What diseases can cause sinus bradycardia? | hypothyroidism, increased ICP, hypoglycemia, and inferior MI |
| What are the clinical manifestations of sinus bradycardia? | hypotension, pale, cool skin, weakness, angina, dizziness or syncope, confusion or disorientation, SOB |
| How would you treat a patient with sinus bradycardia? | Administration of atropine (an anticholinergic drug), pacemaker may be required, if brady is due to drugs then holding or discontinuing the drug, or reducing dosage. |
| This rhythm starts in the SA node at a rate of 101-200 bpm but all of the waves and QRS complexes, and PRIs are normal. | sinus tachycardia |
| How can sinus tachycardia occur? | By vagal inhibition or sympathetic stimulation. It's associated w/physiologic and psychologic stressores. Drugs can also increase HR. |
| What are some physiologic and psychologic stressors that can cause sinus tachycardia? | Exercise, fever, pain, hypotension, hypovolemia, anemia, hypoxia, hypoglycemia, myocardial ischemia, heart failure (HF), hyperthyroidism, anxiety, and fear |
| What drugs can cause sinus tachycardia? | epinephrine (Epipen), norepinephrine (Levophed), atropine (AtroPen), caffeine, theophylline (Theo-Dur), or hydralazine (Apresoline), OTC cold remedies have active ingrediieents (e.g. pseudoephedrine-Sudafed) |
| What are some clinical manifestations of sinus tachycardia? | dizziness, dyspnea, hypotension, angina in pts with CAD |
| How do you treat a pt with sinus tachycardia? | Find the underlying cause of the tachy (e.g. treat pain). In clinically stable pts vagal maneuvers can be attempted. Drugs such as B-adrenergic blockers (e.g. metoprolol-Lopressor) can be given to reduce HR and decrease myocardial oxygen consumption. |
| This rhythm the HR varies and is irregular. The P wave is a different shape than the original P wave from the SA node or may be hidden in the T wave. PRI may be shorter or longer than PRI from SA node but is w/i normal limits. QRS is usually normal. | premature atrial contraction (PAC) |
| What is a PAC? | A contraction starting from an ectopic focus in the atrium (i.e. a location other than the SA node) and coming sooner than the next expected sinus beat. |
| With a PAC the ectopic signal starts in the left or right atrium and travels across the atria by an abnormal pathway which can cause what? | a distorted P wave |
| With a PAC what occurs at the AV node? | It may be stopped (nonconducted PAC), delayed (lengthened PRI), or conducted normally. If the signal moves through the AV node, in most cases it is conducted normally through the ventricles. |
| What can cause PACs? | stress, fatigue, caffeine, tobacco, alcohol, hypoxia, electrolyte imbalance, disease states |
| What diseases can cause PACs? | hyperthyroidism, COPD, heart disease including CAD and valvular disease |
| What are the clinical manifestations PACs? | palpitations, a sense that their hearts "skipped a beat" |
| How are PACs treated? | Depends on the pt's symptoms. Withdrawal of sources of stimulation such as caffeine or sympathomimetic drugs may be needed. B-adrenergic blockers may be used to decrease PACs. |
| This dysrhythmia starts in an ectopic focus anywhere above the bifurcation of the bundle of His. HR is 150-220 bpm, regular or slightly irregular. P wave is hidden in the T wave (may be abnormal shape). PRI shortened or normal, QRS normal. | paroxysmal supraventricular tachycardia (PSVT) |
| How do PSVTs occur? | B/c of a reentrant phenomenon (reexcitation of the atria when there is a one-way block). Usually a PAC triggers a run of repeated premature beats. |
| In the normal heart PSVT can be associated with what? | overexertion, emotional stress, deep inspiration, and stimulants such as caffeine and tobacco |
| What are some other ways PSVT can occur? | with rheumatic heart disease, digitalis toxicity, CAD, and cor pulmonale (right sided HF) |
| What are the clinical manifestations of PSVT? | HR is 150-220 bpm, HR > 180 leads to decreased CO and stroke volume, hypotension, dyspnea, angina |
| How is PSVT treated? | vagal stimulation (Valsalva, carotid massage, coughing), IV adenosine, IV B-adrenergic blockers (sotalol), CCBs (diltiazem), amiodarone, direct current (DC) cardioversion (if all else fails & pt is unstable) |
| This rhythm has recurring, regular, sawtooth shaped F waves. Atrial rate is 200-350 bpm, ventricular rate varies usually 150 bpm, PRI varies & not measurable. QRS is usually normal. | atrial flutter |
| What can cause atrial flutter? | Rarely occurs in a healthy heart. Associated with CAD, HTN, mitral valve disorders, PE, chronic lung disease, cor pulmonal, cardiomyopathy, hyperthyroidism, and drugs. |
| What drugs can cause atrial flutter? | digoxin, quinidine, epinephrine |
| Why are patients with atrial flutter at an increased risk of stroke? What would be given to these patients? | Due to the risk of thrombus formation in the atria from the stasis of blood. Patients are given warfarin (Coumadin) to prevent strokes. |
| What is the primary goal in treatment of atrial flutter? | To slow the ventricular response by increasing AV block. |
| How is atrial flutter treated? | pharmacologic agents, electrical cardioversion, radiofrequency ablation |
| What drugs are used to control ventricular rate? | CCBs (diltiazem) and BBs (metoprolol) |
| What drugs are used to convert atrial flutter to sinus rhythm or to maintain sinus rhythm? | Antidysrhythmia drugs such as ibutilide (Corvert); amiodarone, flecainide (Tambocor), dronedarone (Multaq) to maintain sinus rhythm |
| In emergency situations if drugs don't work for atrial flutter what can be done to convert it back to sinus rhythm? | electrical cardioversion |
| What is the treatment of choice for atrial flutter? | radiofrequency catheter ablation |
| This procedure is done in the EP lab and involves placing a catheter in the right atrium. Uses low-voltage, high-frequency form of electrical energy, the tissue is destroyed, dysrhythmia is ended, & NSR is restored. | radiofrequency catheter ablation |
| This rhythm is characterized by a total disorganization of atrial electrical activity due to multiple ectopic foci resulting in loss of effective atrial contraction. | atrial fibrillation |
| What does A fib look like on an ECG? | Atrial rate may be as high as 350-600 bpm. P waves replaced w/chaotic fibrillatory waves. Ventricular rate varies & rhythm is irregular. PRI isn't measurable, and QRS usually normal. |
| In A fib when the ventricular rate is b/t 60-100 bpm it is known as? | atrial fibrillation with a controlled ventricular response |
| In A fib when the ventricular rate is greater than 100 bpm it is known as? | atrial fibrillation with a rapid (uncontrolled) ventricular response |
| A fib is the most common dysrhythmia and may be ____ (begins and ends spontaneously) or _____ (lasting more than 7 days). | paroxysmal; persistent |
| A fib usually occurs in patients with what? | Underlying heart disease such as CAD, rheumatic heart disease, cardiomyopathy, hypertensive heart disease, HF, and pericarditis. |
| What other disease states can cause A fib? | Develops acutely with thyrotoxicosis, alcohol intoxication, caffeine use, electrolyte disturbances, stress, and cardiac surgery. |
| These rhythms cause a decrease in CO and an increased risk of stroke. | atrial flutter and atrial fibrillation |
| What are the goals of treatment for A fib? | Decrease in ventricular response (to less than 100 bpm), prevention of stroke, and conversion to sinus rhythm, if possible. |
| What are some treatments for A fib? | drugs, electrical cardioversion, anticoagulation, radiofrequency ablation, maze procedure with cryoablation |
| What drugs are used to control ventricular rate in A fib? | CCBs (diltiazem), BBs (metoprolol), digoxin (Lanoxin), dronedarone |
| The most common antidysrhythmia drugs used for conversion to and maintenance of sinus rhythm are what? | amiodarone and ibutilide |
| If a patient is in A fib for longer than 48 hours, what is needed 3-4 wks before the cardioversion and for several wks after successful cardioversion? | anticoagulation therapy with warfarin |
| Why is anticoagulation therapy necessary before cardioversion? | Clots may have formed and if cardioversion is performed with clots present than the procedure could dislodge the clot causing a stroke or PE. |
| What can be used to rule out the presence of clots in the atria? | A transesophageal echocardiogram, if no clots are present then anticoagulation therapy may not be required before cardioversion. |
| What happens if drugs or cardioversion do not convert A fib to NSR? | long term anticoagulation therapy is required |
| Warfarin is the drug of choice for long term anticoagulation therapy. What is monitored with these patients? | PT and INR |
| This is a surgical intervention that stops A fib by interrupting the ectopic electrical signals that are responsible for the dysrhythmias. Incisions are made in both atria & cold therapy stops the formation & conduction of these signals & resores NSR. | Maze procedure |
| Every impulse is conducted to the ventricles but the time of the AV conduction is prolonged. After the impulse moves through the AV node, the ventricles usually respond normally. HR normal, regular, PRI >0.20 sec, P wave & QRS normal. | First-degree AV block |
| What can cause 1st degree AV blocks? | Associated with MI, CAD, rheumatic fever, hyperthyroidism, electrolyte imbalances (hypokalemia), vagal stimulation, and drugs. |
| What are some drugs that can cause 1st degree AV blocks? | digoxin, B-adrenergic blockers, CCBs, and flecainide |
| What is the treatment for 1st degree AV blocks? | Usually not serious so there is no treatment for these blocks. Monitor patients for any new changes in heart rhythms (e.g. more serious block). |
| This block includes a gradual lengthening of the PRI. Atrial rate is normal, vent. rate slower b/c of nonconducted or blocked QRS resulting in brady. Once a vent. beat is blocked, the cycle repeats itself. Vent. rhythm irreg. P wave normal. QRS normal. | Type 1 second-degree AV block (Mobitz 1 or Wenckebach) |
| What could cause a 2nd degree type 1 AV block? | Drugs such as digoxin or BBs. Associated w/CAD & other diseases that can slow AV conduction. Usually a result of myocardial ischemia or inferior MI. |
| The 2nd degree type 1 AV block is usually transient and well tolerated except in these patients? | Patients with acute MIs b/c it may be a warning sign of a more serious AV conduction disturbance (e.g. complete heart block). |
| How is the 2nd degree type 1 AV block treated? | If pt is symptomatic atropine is used to increase HR, or a temporary pacemaker may be need, esp if the pt has had an MI. If pt is asymptomatic monitor closely w/transcutaneous pacemaker on standby. |
| P wave is nonconducted, no progressive PR lengthening, occurs when block in bundle branches, PRI is constant, may be normal or prolonged. Atrial rate normal and regular, vent. rate varies and irregular. QRS >0.12 sec b/c of bundle branch block (BBB). | Second degree AV block, Type 2 (Mobitz II) |
| Second degree type II blocks are associated with what? | rheumatic heart disease, CAD, anterior MI, and drug toxicity |
| How is a second degree type 2 block treated? | pacemaker; temporary pacemaker may be needed if pt becomes symptomatic (e.g. hypotension, angina) |
| This is a complete heart block, in which no impulses from the atria are conducted to the ventricles. The atria contract independently of the ventricles. The vent. rhythm is an escape rhythm. | Third degree AV block |
| In a 3rd degree block the atrial rate is usually 60-100 bpm, but the vent. rate depends on the site of the block. What is the vent. rate if the block is in the AV node? In the His-Purkinje system? | AV node: 40-60 bpm; His-Purkinje system: 20-40 bpm |
| What would a 3rd degree block look like on an ECG? | Atrial & vent. rhythms are regular but unrelated to each other. P wave normal. PRI variable w/no relationship b/t the P wave & QRS. QRS complex normal if escape rhythm occurs at the His or above; widened if it occurs below His. |
| What disease states are associated with 3rd degree blocks? | severe heart disease (CAD, MI, myocarditis, cardiomyopathy), some systemic diseases (amyloidosis, scleroderma) |
| What drugs can cause 3rd degree blocks? | digoxin, BB's, CCB's |
| What usually results from 3rd degree blocks? | Reduced CO w/subsequent ischemia, HF, and shock |
| If a pt with 3rd degree block has severe bradycardia, what can occur? | syncope or even periods of asystole |
| If a pt has a 3rd degree block and is symptomatic, how is it treated? | A transcutaneous pacemaker is used until a temporary transvenous pacemaker can be inserted. A permanent pacemaker is needed asap. |
| What are some temporary measures that can be done to treat 3rd degree blocks until temporary pacing is started? | Drugs such as atropine, dopamine (Intropin), and epinephrine is used to increase HR and support blood pressure. |
| This is a contraction coming from an ectopic focus in the ventricles. It is the early occurrence of a QRS complex. | premature ventricular contraction (PVC) |
| What would a PVC look like on a rhythm strip? | Is wide & distorted compared to a normal QRS complex. HR varies and irregular, P wave rarely visible & usually lost in QRS. PRI not measurable. QRS wide, distorted, lasts >0.12 sec. T wave large & opposite in direction of the QRS. |
| PVCs that arise from different foci appear different in shape from each other are called? | multifocal PVCs |
| PVCs that have the same shape are called? | unifocal PVCs |
| When every other beat is a PVC, the rhythm is called? | ventricular bigeminy |
| When every third beat is a PVC, it is called? | ventricular trigeminy |
| Two consecutive PVCs are called? | couplet |
| When there are three or more consecutive PVCs this is known as? | ventricular tachycardia |
| R on T phenomenon occurs when a PVC falls on the T wave of a preceding beat. Why is this especially dangerous? | The PVC is firing during the relative refractory phase of ventricular repolarization. Excitability of the cardiac cells increases during this time, & risk for PVC to start V tach or V fib is great. |
| What can cause PVCs? | stimulants (e.g. caffeine, alcohol, nicotine, aminophylline, epinephrine, isoproterenol, digoxin), electrolyte imbalances, hypoxia, fever, exercise, emotional stress, MIs, mitral valve proplapse, HF, & CAD |
| PVCs are usually not harmful in the pt with a normal heart, but what can occur with pts with heart disease? | May reduce the CO andd lead to angina and HF depending on the frequency. PVCs in CAD or acute MIs indicate ventricular irritability. |
| Why should the nurse obtain the pts apical-radial pulse rate with PVC pts? | PVCs often don't generate a sufficient ventricular contraction to result in a peripheral pulse. This can lead to a pulse deficit. |
| How are PVCs treated? | Treatment r/t the cause of the PVCs (e.g. O2 therapy for hypoxia, electrolyte replacement). Assess pts hemodynamic status to determine whether drug therapy is needed. |
| What are some drugs used to treat PVCs? | BB's, procainamide (Pronestyl), or amiodarone |
| Run of 3 or more PVCs, vent. rate 150-250 bpm, rhythm reg/irreg, P wave buried in the QRS complex, PRI not measurable, QRS is distorted and wide (>0.12 sec), T wave is in opposite direction of the QRS complex. | ventricular tachycardia (V tach) |
| What occurs with V tach? | An ectopic focus or foci fire repeatedly and the ventricle takes control as the pacemaker. |
| There are different forms of V tach depending on the QRS configuration. What are they? | Monomorphic V Tach, Polymorphic V Tach |
| This type of V Tach occurs when the QRS complexes gradually change back and forth from one shape, size, and direction to another over a series of beats. | polymorphic V Tach |
| This type of V Tach has QRS complexes that are the same in shape, size, and direction. | monomorphic V Tach |
| Why is the development of V Tach an ominous sign? | It is a life threatening dysrhythmia b/c of decreased CO and the possibility of development of ventricular fibrillation, which is a lethal dysrhythmia. |
| This is a polymorphic V Tach associated with a prolonged QT interval of the underlying rhythm usually caused by an electrolyte deficiency. | Torsades de Pointes |
| How would you treat a patient with Torsades? | give Magnesium |
| V Tach is caused by what? | heart disease, electrolyte imbalances, drugs, CNS disorder |
| What occurs with sustained V Tach? | A severe decrease in CO b/c of decreased ventricular diastolic filling times and loss of atrial contraction. |
| What can result from sustained V TAch? | hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest, V Fib may also develop |
| What is stable V Tach? | patient has a pulse |
| What is unstable V Tach? | patient is pulseless |
| How is V Tach treated? | Identify and treat underlying cause (e.g. electrolyte imbalance, ischemia), VTach w/pulse treat w/antidysrhythmics or cardioversion; pulseless VTach treat w/CPR and rapid defibrillation |
| What are some drugs to treat stable VTach? | antidysrhythmics |
| If the VTach is monomorphic and stable and has preserved left ventricular function, what drugs are given? | IV procainamide, sotalol, or amiodarone |
| If the VTach is polymorphic w/a normal baseline QT interval, what drugs can be used? | BBs, amiodarone, procainamide, or sotalol |
| What drugs can be used for a polymorphic VTach with a prolonged baseline QT interval? | IV magnesium, isoproterenol, phenytoin (Dilantin), or antitachycardia pacing |
| What drugs prolong the QT interval? | dofetilide (Tikosyn) |
| Unstable VTach is life threatening, how should it be treated? | CPR and rapid defib are first lines of treatment, followed by administration of vasopressors (e.g. epinephrine) and antidysrhythmics (e.g. amiodarone) if defib is unsuccessful. |
| Characterized on ECG by irregular waveforms of varying shapes and amplitude which represents the firing of multiple ectopic foci in the ventricle. The ventricle is simply "quivering" with no effective contraction & consequently no CO. Lethal dysrhythmia. | Ventricular fibrillation (Vfib) |
| What are the characteristics of Vfib on an ECG? | HR is not measurable. Rhythm is irregular and chaotic. P wave is not visible, and PRI and QRS interval are not measurable. |
| What diseases is Vfib associated with? | MI, ischemia, HF, and cardiomyopathy |
| Causes of Vfib. | Can occur during cardiac pacing or catherization, may occur w/coronary reperfusion after thrombolytic therapy, electric shock, hyperkalemia, hypoxemia, acidosis, and drug toxicity |
| What is the treatment for Vfib? | Immediate initiation of CPR and advanced cardiac life support (ACLS) w/use of defibrillation and drug therapy (epinephrine, vasopressin - Pitressin) |
| Represents total absence of ventricular electrical activity. Pts are unresponsive, pulseless, and apneic. A lethal dysrhythmia. | asystole |
| Causes of asystole. | Result of advanced cardiac disease, severe conduction disturbance, or end-stage HF. |
| How is asystole treated? | Immediate CPR and ACLS measures, epinephrine and/or vasopressin, intubation |
| Electrical activity can be observed on the ECG, but no mechanical activity of the ventricles is evident, and the patient has no pulse. | pulseless electrical activity (PEA) |
| Most common causes of PEA. Think H's and T's. | Hypovolemia, Hypoxia, Hydrogen ion (m. acidosis), Hyper/hypokalemia, hypoglycemia, hypothermia, toxins, tamponade (cardiac), thrombosis (MI & pulmonary), tension pneumo, trauma |
| How is PEA treated? | CPR followed by intubation and IV epinephrine. Tx directed toward correction of the underlying cause. |
| What is the tx of choice for Vfib and pulseless Vtach? | defibrillation (rapid defib w/i 2 mins is critical) |
| What are the differences b/t defibrillation and cardioversion? | Cardioversion is used on stable pts and uses a lower joule setting than defib and is synced to shock w/pts own rhythm (R wave). Defib is for unstable pulseless pts, at a higher joule, and shocked at any time. |
| An electronic device used when the normal conduction pathway is damaged. Consists of a power source (battery powered pulse generator w/one or more conducting lead to the myocardium. | pacemaker |
| This pacemaker senses the heart's electrical activity and fire only when the HR drops below a preset rate. | demand pacemakers |
| What are the 2 distinct features of a demand pacemaker? | A sensing device that inhibits the pacemaker when the HR is adequate and a pacing device that triggers the pacemaker when no QRS complexes occur w/i a preset time period. |
| This type of pacing involves the delivery of a stimulus to the ventricle to end tachydysrhythmias (e.g. VT). | antitachycardia pacing |
| This type of pacing involves pacing the atrium at rates of 200 to 500 impulses/min in an attempt to terminate atrial tachycardias (e.g. Aflutter w/rapid ventricular response). | overdrive pacing |
| Totally implantable w/i the body. Power source is placed subcutaneously, usually over pectoral muscle on pts nondominant side. Leads are placed transvenously to rt. atrium & 1 or both ventricles & attached to power source. | permanent pacemaker |
| Why are permanent pacemakers used? | Inserted to treat pts w/chronic heart problems in which the heart beats too slowly to adequately support the body's circulation (ie AV blocks, Afib w/slow ventricular response, severe HF, cardiomyopathy, bundle branch block). |
| Resychronizes the cardiac cycle by pacing both ventricles (biventricular pacing). Promotes improvement in ventricular function. | cardiac resynchronization therapy (CRT) |
| Why is CRT used in most HF patients? | HF pts have intraventricular conduction delays causing abnormal ventricular contraction causing dyssynchrony b/t the rt and lt ventricles resulting in reduced systolic function, pump inefficiency, and worsened HF. |
| For pts w/severe left ventricular dysfunction, CRT is combined with what? | an implantable cardiovert defibrillator (ICD) for maximum therapy |
| A temporary pacemaker has the power source outside the body. What are the 3 types? | transvenous, epicardial, transcutaneous |
| This type of temporary pacemaker consists of a lead or leads that are threaded transvenously to the rt atrium and/or rt ventricle and attached to the external power source. | transvenous pacemaker |
| When are temporary transvenous pacemakers most often used? | Inserted in emergency depts and critical care units in emergent situations. They provide a bridge to insertion of a permanent pacemaker or until the underlying cause of the dysrhythmia is resolved. |
| Involves attaching an atrial and ventricular pacing lead to the epicardium during heart surgery. The leads are passed through the chest wall & attached to the external power source. | epicardial pacing |
| Why are epicardial pacing leads placed prophylactically? | In case any bradydysrhythmias or tachydysrhythmias occur in the early postoperative period. |
| Used to provide adequate HR and rhthn to the pt in an emergency situation. It is noninvasive, temporary procedure used until a transvenous pacemaker is inserted or until more definitive therapy is available. | transcutaneous pacemaker (TCP) |
| Where do you place the 2 large electrode pads when using a TCP? | One pad on the anterior part of the chest, ususally on the V4 lead position, and the other pad on the back b/t the spine and the left scapula at the level of the heart. |
| When using a TCP what current should always be used on the pt? | The lowest current that results in a ventricular contraction (capture) to minimize pt discomfort. |
| What should be provided to the pt whenever possible when using TCP? | analgesia or sedation while TCP is in use |
| Pacemaker malfunction primarily involves what? | a failure to sense or a failure to capture |
| This occurs when the pacemaker fails to recognize spontaneous atrial or ventricular activity, and it fires inappropriately. | failure to sense |
| What results when a pacemaker fails to sense? | Results in pacemaker firing during the excitable period of the cardiac cycle resulting in Vtach. |
| What causes a failure to sense in pacemakers? | Pacer lead damage, battery failure, sensing set too high, or dislodgement of the electrode. |
| This occurs when the electrical charge to the myocardium is insufficient to produce atrial or ventricular contraction. | failure to capture |
| What can result when a pacemaker fails to capture? | Can result in serious bradycardia or asystole. |
| What can cause a failure to capture in pacemakers? | pacer lead damage, battery failure, dislodgement of the electrode, electrical charge set too low, fibrosis at the electrode tip |
| What are some complications a nurse should monitor for with pacemakers? | infections, hematoma formation at the insertion site, pneumothorax, failure to sense or capture, perforation of the atrial or ventricular septum by the pacing lead, and appearance of "end of life" battery power on testing the pacemaker |
| What measures can be used to prevent or assess for complications with pacemakers? | prophylactic IV antibiotic therapy before and after insertion, postinsertion chest x-ray to check lead placement and to rule out the presence of a pneumothorax, careful observation of insertion site, & continuous ECG monitoring of the pts rhythm |
| What kind of postprocedure care should be done after the pacemaker has been inserted? | The pt can be out of bed once stable. Have the pt limit arm & shoulder activity on the operative side to prevent dislodging the newly implanted pacing leads. Observe ins. site for bleeding & incision is intact. Note temp elevation or pain at site & treat |
| What should you teach the pt for management of the pacemaker? | Maintain follow up care to begin reg pcmkr function checks, report s/s of infection at inc. site, keep inc. dry for 4 days after, avoid lifting arm on pcmkr side above shoulder, avoid direct blows to site, monitor pulse, carry pcmkr ID, wear medicalert ID |
| What are some things you should avoid with a pacemaker? | Avoid close proximity to high output electric generators, MRI's, avoid standing near antitheft devices in doorways of dept stores and public libraries (walk through them at a normal pace), inform arprt sec of pcmkr, wand shouldnt be directly over pcmkr. |
| Uses electrical energy to "burn" areas of the conduction system as definitive treatment of tachydysrhythmias. | radiofrequency catheter ablation therapy |
| When is ablation therapy done? | After EPS has identified the source of the dysrhthmia. |
| An electrode tipped ablation catheter ablates (destroys) what? | accessory pathways or ectopic sites in the atria, AV node, and ventricles |
| Catheter ablation is considered the nonpharmacologic tx of choice for what? | atrial dysrhthmias |
| What is the result of catheter ablation in atrial dysrhythmias? | Rapid ventricular rates and AV nodal reentrant tachycardia refractory to drug therapy. |
| What are some ECG changes associated with Acute Coronary Syndrome (ACS)? | In myocardial ischemia: ST seg depression & T wave inversion; ST seg depression significant if at least 1 mm below isoelectric line. |
| In myocardial ischemia the depression in the ST seg &/or T wave inversion occurs in response to what? | Inadequate supply of blood & O2 which causes an electrical disturbance in the myocardial cells. |
| Myocardial injury represents a worsening stage of ischemia that is potentially reversible by may evolve to what? | MI |
| What ECG changes are seen with myocardial injury? | ST seg elevation; ST seg elevation is significant if it is greater than or equal to 1 mm above the isoelectric line. |
| With myocardial injury, if tx is prompt & effective, it's possible to restore O2 to the myocardium & avoid or limit infarction. The absence of what confirms there is nor infarct? | serum cardiac markers |
| What ECG changes can be seen with infarction? | ST seg elevation, a pathologic Q wave is the first negative deflection following the P wave (small & narrow <0.04 sec in duration) |
| A Q wave that is wide (>0.03 sec in duration) and deep (> than or = to 25% of height of the R wave) is known as what? | a Q wave MI |
| The ECG changes seen in injury and MI reflect electrical disturbances in the myocardial cells caused by what? | a prolonged lack of blood and oxygen leading to necrosis |
| A brief lapse in consciousness accompanied by a loss in postural tone (fainting), is a common dx of pts coming into the emergency dept. | syncope |
| What are some noncardiovascular causes of syncope? | stress, hypoglycemia, dehydration, stroke, and seizure |
| What is the most common cause of syncope? | cardioneurogenic syncope or "vasovagal" syncope (e.g. carotid sinus sensitivity) |
| What are some cardiovascular causes for syncope? | relate to dysrhythmias (e.g. tachycardias, bradycardias, prosthetic valve malfunction, PE, and HF) |
| What diagnostic studies are done for syncope? | ECG, stress test, EPS, head-up tilt test |
Created by:
eblanc1
Popular Nursing sets