Cardiac Dysrhythmias exams Questions & Answers 2023/2024 with assured success, Exams of Nursing

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Cardiac Dysrhythmias exams

Questions & Answers 2023/2024 with

assured success

 Dysrhythmia - ✓✓✓Also called arrhythmia. Is a conduction disorder that results in an abnormally slow or rapid heart rate or one that does not proceed through the conduction system in the usual manner.  Sinus Bradycardia - ✓✓✓dysrhythmia that proceeds normally through the conduction SLOWERpathway but at a s than usual rate. less than or equal to 60 beats per minute.  Sinus Bradycardia pathology - ✓✓✓pathologic in clients with heart disorders, ICP, hypothyroidism, or digitalis toxicity. The danger in this is that the slow rate may be insufficient to maintain cardiac output.

 Sinus Bradycardia Drugs - ✓✓✓Atropine sulfate, a cholinergic blocking agent, is given IV to increase a dangerously slow heart rate.  Characteristics of Normal Sinus Rhythm - ✓✓✓-HR is b/t 60-100 beats.min.

• The SA node initiates the impulse (upright P wave before each QRS complex).
• Impulse travels to the AV node in 0.12-0. second (the PR interval).
• The ventricles depolarize in 0.12 seconds or less ( the QRS complex).  -Each impulse occurs regularly (evenly spaced).  Atropine Sulfate considerations - ✓✓✓A dose of 0.5 - 1 mg of this may be given every 1-2 hrs to increase the HR. A max of 2 mg is given IV. Closely monitor heart rate for drug response.  Isoproterenol (Isuprel) Considerations - ✓✓✓a beta- adrenergic blocker is also used to treat severe

bradycardia. Closely monitor pulse rate for drug response.  Sinus Tachycardia - ✓✓✓dysrhythmia that proceeds normally through the conduction pathway but at a FASTER than usual rate. 100-150 beats/min.  P wave - ✓✓✓Atrial depolarization  QRS - ✓✓✓Ventricular Depolarization  T - ✓✓✓Ventricular repolarization  Premature Atrial Contractions (PAC) - ✓✓✓Occasionally, neural tissue in the atrial conduction system initiates an early electrical impulse called this. It is identified by an irregularity in the underlying rhythm. P wave may differ slightly because it is initiated somewhere in the atria other than the SA node.

 Reasons for PACs - ✓✓✓consumption of caffeine, use of nicotine or other sympathetic nervous system stimulants, or in response to heart disease or metabolic disorders such as hyperthyroidism. Eliminating the cause usually controls PACs.  Ectopic Pacemaker site - ✓✓✓one that initiates an electrical impulse independently of the SA node, can lead to more serious dysrhythmias such as supraventricular tachycardia.  Supraventricular Tachycardia SVT - ✓✓✓a dysrhythmia in which the heart rate has a consistent rhythm but beats at a dangerously high rate. greater than or equal to 150 beats/min. Diastole is shortened and the heart does not have sufficient time to fill.  Signs and Symptoms of low cardiac output and impending heart failure for SVT - ✓✓✓Cardiac output drops dangerously low and heart failure can occur.

Angina, tachycardia, hypotension, syncope, reduced renal output.  CAD and SVT - ✓✓✓Pts. can develop chest pain because coronary blood flow cannot meet the increased need of the myocardium for oxygen imposed by the fast rate.  Drugs for SVT - ✓✓✓Digitalis, adrenergic blockers, and calcium channel blockers are used to slow the heart rate.  Atrial Flutter - ✓✓✓a single impulse outside the SA node causes the atria to contract at an exceedingly rapid rate (200-400 contractions/min.) AV node conducts only some impulsesto the ventricle, resulting in a ventricular rate that is slower than the atrial rate. Atrial waves in atrial flutter have a sawtooth pattern.

 Atrial Fibrillation - ✓✓✓several areas in the R atrium initiate impulses resulting in disorganized, rapid activity. Atria quiver rather than contract.  Cheif complaint of A fib - ✓✓✓Formation of blood clots within the atria that may become stroke-causing emboli if they enter the circulation.  Stroke gerontologic considerations - ✓✓✓Among 2. million people in the US with A fib, th eincidence and complication for stroke increases with age. Strokes occur b/t 2 and 7 times more often than in those without A fib. Therefore, the need to restore normal sinus rhythm is critial.  Pharmacologic considerations for A fib - ✓✓✓Heparin is generally prescribed initially if A fib persists longer than 48 hrs. Clients with persistent A fib may be prescribed an oral anticoagulant such as warfarin (Coumadin); rivaroxaban (Xarelto); Dabigatran

(Pradaxa); or a daily aspirin to prevent stroke or its reccurrence.  rivaroxaban ( Xarelto) - ✓✓✓a new anticoagulant that acts as an antagonist of Factor Xa in the clotting pathway, preventing the conversion of prothrombin to thrombin. For A fib.  Dabigatran (Pradaxa) - ✓✓✓a recently developed anticoagulant which is a direct thrombin inhibitor; for A fib.  Advantage of new oral anticoagulants - ✓✓✓They do not require leb monitoring of PT or INRs.  Ibutilide (Corvert) - ✓✓✓an antidysrhythmic drug used to convert new-onset A fib into sinus rhythm.  Flecainide (Tambocor) and Propafenone (Rythmol) - ✓✓✓used to prevent A fib.

 Chemical cardioversion - ✓✓✓Use of drugs to eliminate a dysrhythmia.  Maze Procedure - ✓✓✓The surgeon restores the normal conduction pathway in the atria by eliminating the rapid firing of ectopic pacemaker sites using scar- forming techniques.Clients with A fib who are not candidates for cardioversion and fail to respond to conventional measures may be candidates for this.  ways of the Maze procedure - ✓✓✓Traditionally requires open-chest incision. New method using closed-chest, using cath directed energy at the tissue creating abnormal electrical impulses. (mini-maze).  Heart block - ✓✓✓referes to disorders in the conduction pathway that interfere with the transmission of impulses from the SA node through the AV node to the ventricles.Can be 1st, 2nd, or 3rd degree.

 1st and 2nd degree heart block - ✓✓✓impulse is delayed.  3rd degree heart block (Complete heart block) - ✓✓✓atrial impulse never gets through and the ventricles develop their own rhythm independent of atrial rhythm. The ventricular rate is slow (30- beats/min).  Treatment for complete heart block - ✓✓✓Pacemaker insertion  Premature Ventricular Contration (PVC) - ✓✓✓a ventricular contraction that occurs early and independently in the cardiac cycle before the SA node initiates an electrical impulse. No P wave precedes the wide, bizarre-looking QRS complex. Many people experience them occasionally and are usually harmless. May be related to anxiety, stress, fatigue, alcohol withdrawl, or tabacco use.

 Signs and symptoms of PVC - ✓✓✓Flip-Flop sensation in chest, sometimes described as "fluttering", pallor, nervousness, sweating, and faintness.  Precursor of lethal dysrhythmias - ✓✓✓in presence of acute heart injury, such as after cardiac surgery or acute MI. PVCs of certain patterns suggest myocardial irritability.

• 6 or more PVCs/min.
• Runs of bigeminy (every other beat is a PVC).
• 2 PVCs in a row (couplets).  -Runs of PVCs (3 or more in a row).
• Mutifocal PVCs (originating from more than on location).
• A PVC whose R wave falls on the T wave of the preceding complex ( R-on-T phenomenon).  When dangerous PVCs occur - ✓✓✓Pt is given IV bolus of lidocaine followed by a continuous IV infusion of the drug.

 Ventricular tachycardia - ✓✓✓caused by a single, irritable focus in the ventricle that initiates and then continues the same repetitive pattern. Ventricles beat very fast (150-250 beats/min). and cardiac output is decreased. May progress to V fib.  Signs and Symptoms of V tach - ✓✓✓Depending on how long the dysrhythmia is present, the client may lose consciousness and become pulseless. Sometimes V tach ends abruptly without intervention but often requires defibrilation.  Ventricular Fibrillation - ✓✓✓rhythm of a dying heart. Ventricles do not contract effectively, and there is no cardiac output.Indication for CPR and immediate defibrillation.  Dysrhythmias for gerontologics - ✓✓✓Age increases the risk for dysrhythmias as a result of a decreased number of cells in the SA node and altered function of

the cells from accumulated fat and calcium. In older adults, stress, exercise, or illness may cause dysrhythmias and other cardiac disorders such as hear failure and myocardial ischemia.  Tachydysrhythmias - ✓✓✓Abnormally fast rhythms. pts with this describe palpitations or fluttereings in their chest. BP is usually low, pulse is irregular or difficult to palpatate; the rate is unusually fast or slow,Apical and radial pulse may differ, skin may be pale and cool, client may be disoriented and confused if brain is not getting enough oxygen or may be LOC and even clinical death.  Electrophysiology study - ✓✓✓can locate dysrhythmias. A procedure that enables the physician to examine the electrical activity of the heart; produce actual dysrhythmias by stimulating structures in the conduction pathway; determine the best method for preventing furthur dysrhythmic episodes; and in some

cases' eradicate tissue in the area of the heart that is producing the dysrhythmias.  Performing an Electrophysiology study - ✓✓✓Is performed by passing three flexible wire electrode caths into veins in the neck and groin. The caths are advanced into the heart in each of the following locations: R atrium, bundle of His, and R ventricle. Electrode caths monitor and record the hearts rhythm. Physician can use these same caths to reproduce the abnormal heart rhythm that client usually experiences by stimulating areas in the conduction system. When dysrhythmia is produced, the physician uses several drugs to evaluate each one's efficacy at restoring normal heart rhythm.  How to determine what drug works best for a pts dysrhythmia. - ✓✓✓Physician can use these same caths that were used for the electrophysiology study to reproduce the abnormal heart rhythm that client usually experiences by stimulating areas in the

conduction system. When dysrhythmia is produced, the physician uses several drugs to evaluate each one's efficacy at restoring normal heart rhythm.  Elective Electrical Cardioversion - ✓✓✓a nonemergency procedure by a physician to stop rapid, but not necessarily life-threatening, atrial dysrhythmias. Simialr to defibrillation. Different than defibrillation because it waits to detect the R wave so to prevent disrupting the heart during the critical persiod of ventricular repolarization.  Performing elective electrical cardioversion - ✓✓✓Client is sedated.Electrodes are lubricated with a special gel or moist saline pads are applied to chest wall. When discharge buttons on the paddles are depressed and the heart is in ventricular depolarization, the electrical energy is released. It completly depolarizes the entire myocardium and as the heart repolarizes ideally, the normal pacemaker

regains control and restores continued normal conduction through heart.  Defibrillation - ✓✓✓the only treament for life- threatening ventricular dysrhytmias. has the exact same effect as cardiversion except that it is used when there is no fuctional ventricular contractions. without this the client will die.  When is Defibrillation used? - ✓✓✓During pulseless ventricular tachycardia, ventricular fibrillation, and asystole (cardiac arrest) when no identifiable R wave is present.  Automatic External Defibrillation (AED) - ✓✓✓if performed within the first 3 minutes of ventricular fibrillation or sudden cardiac arrest, the potential for survival is 74%. Survival decreases 7% to 10% with every minute that defibrillation is delayed.

 Automatic implnted cardioverter Defibrillator (AICD) - ✓✓✓An internal electrical device used for selected clients with recurrent life-threatening tachydysrhythmias. Consists of a generator with a battery and one (sometimes 2) electrical leads that resembles a wire. The lead sense the cardiac rhythm which transmits to the generator. The generator, which is programmed for various responses depending on the sensed rhythm, delivers and electrical shock through the lead to restore a life- sustaning cardiac rhythm, reocords the data and then resets itself. Can also pace the heart to obliterate a tachydysrhythmias and perform low-energy cardioversion.  Candidates for an AICD include - ✓✓✓1. patient has survived at least one episode of cardiac arrest ventricular dysrythmia 2. they have experienced recurrent episodes of ventricular tachycardia or 3. they are at risk for sudden cardiac death because of

structural heart disease such as cardiomyopathy with poor ventricular function.  pts with an AICD - ✓✓✓it is checked every 3 to 4 months. Info retrieved by passing an electromagnectic wand over the implanted generator. Can be reprogrammed the same way. Can last for 3 to 6 years before replacing battery. Can deliever 200 to 250 discharges. Driving usually restricted for 6 months.Need to wear medical braclet or necklace with medical info on it about the AICD. Inform physician immediatley if you think the generator has gone off.  Things to avoid with an AICD - ✓✓✓MRI devices, extracorporeal shock wave lithotripsy machines, electrocauteryand diathermy devices, peripheral nerve stimulators, large industrial electrical motors, and arc welding equipment. Also elctrical signal from digital cellular telephones can minic abnormal heart rhythm activating AICD. Hand serch id preferred to scan with metal detector at airports.

 Pacemaker - ✓✓✓Provides an electrical stimulus to the heart muscle to treat an ineffective bradydysrhythmia(slow abnormal dysrhythmia).  Demand (synchronous) mode pacemaker - ✓✓✓self- activate when the clients pulse falls below a certian level. if set at 72 bets/min, it will not go off unless the rate falls below that.  Fixed-rate (asynchronous) mode pacemakers - ✓✓✓produce an electrical stimulus at a present rate usually 72 to 80 beats/min) despite the clients natural rhythm. Used less frequently than the deamand mode pacemaker.  transcutaneous paemaker (temporary) - ✓✓✓an emergency measure for maintaining adequate heart rate. Uses disposable self-adhearing leads to the chest.

 Transvenous pacemaker (temporary) - ✓✓✓temporary pulse generating device that sometimes is necessary to manage transient bradydysrhythmias such as those that occur during acute MIs or after coronary artyery bypass graft surgery or to overide tachydysrhythmias.  Placement of transvenous pacemaker - ✓✓✓Electrical lead is introduced through the subclavian, external of internal jugular, or cephalic vein and threaded first into the R atrium, then into the R ventricle. May be inserted at the bedside. Fluoroscopy and cardiac monitor are used to determine the correct placement of the tip of the pacemaker lead.  transthorasic pacemaker - ✓✓✓inserted during open heart surgery. extened from the chest incision. if client requires cardiac pacing during postop recovery, the leads are connected to a temporary pacing unit.

 Permanent (implacted) pacemaker - ✓✓✓totally implanted electrical device used to manage a chronic bradydysrhythmia. Needed for a complete or 2nd degree block accompanined by a slow ventricular rate.  radiofrequency cath ablation - ✓✓✓Procedure in which a heated cath tip destroys dysrhythmia- producing tissue. its threaded transvenously into the heart. Once the location of the dysrhythmia- generating tissue is identified, ekectrical energy is sent to the cath tip. the heat destroys the errant tissue, allowing impulse conduction to travel over appropriate pathways.  Risks associated with Radiofrequency cath ablation - ✓✓✓bleeding from insertion site,perforating of the cathed vein, and vascular complications such as thrombus formation. When cath is in the heart itself, it may pierce the myocardium leading to pericardial tamponade. Also possible for the heated tip to

obliterate normal conductive tissue requiring permenant pacemaker to ensure heart contraction.  Nursing management for dyarhythmias - ✓✓✓constant monitoring and documentation of symptoms. Frequent rhythm analyses important.Administering and monitoring effects of antidysrhythmics drugs. Provides health teaching that promotes the client's ability to maintain self- management after discharge.  Digitalis toxicity - ✓✓✓usually treated by discontinuing the prepartation, which allows digitalis levels to return to normal within a short time. If digoxin levels are severly elevated to a life-threatening level, 800 mg of the digitalis antidote, digoxin immune fab (Digibind), is given IV over 30 mins.  Signs of toxocity of cardiac glycosides and disitalis - ✓✓✓Anorexia, N/V/D,visual disturbances, abd discomfort, and dysrythmias such as bradycardia and

tachycardia. With hold the drug and notify primary healthcare provider if the heart rate is less than 60 beats/min.  transcutaneous pacemaker nursing instructions - ✓✓✓- attaches the anterior electrode patch to the L sode of the chest, halfway b/t the xiphoid process to below the L nipple.

• Adheres the posterior electrode patch to the L posterior chest beneath the scapula and lateral to the spine.  -Adjusts the rate knob beginning at 40 beats/min in increments of 10 until reaching the rate prescribed by the physician or established by agency.  -Regulates the current knob, which has a capacity starting at zero and advancing to 120 milliamps, until capturing is observed- that is, a QRS complex follows each spike of the pacemaker; capturing usually occurs b/t 50 to 100 milliamps.  -selects the demand mode, which programs the pacemaker to produce an electrical stimulus

wheneverthe heart rate falls below a preset rate but remains inactive when the clients hear beats naturally at an adequate rate.  -Palpates the pulse and observes the client's response.  postimplantaion instructions for Permanent pacemaker - ✓✓✓- Avoid strenuous movement, especially of the arm on the side where the pacemaker is inserted.

• Keep the arm on the side of the pacemaker lower than the head except for breif moments when dressing or performing hygiene.  -Delay for at least 8 weeks such activities as swimming, bowling, playing tennis, vacumm cleaning, carrying heavy objects, chopping wood, mowing or raking, and shoveling snow.  -Avoid sources o electrial interference similar to those problematic for people with AICDs.

 Sinus Brady chardia characteristics - ✓✓✓Rhythm: regular, Atrial rate: less than 60 beats/min., Ventricular rate: less than 60 beats/min., Treatment: None unless symptomatic; atropine  Sinus Tachycardia characteristics - ✓✓✓Rhythm: Regular, Atrial rate: 100-150 beats/min, Ventricular rate: 100-150 beats/min, Treatment: None unless symptomatic; treat underlying disease.  Premature artrial contraction characteristics - ✓✓✓Rhythm: Irregular, Atrial rate: 60-100 beats/min., Ventricular rate: 60-100 beats/min., Treatment: None or treat underlying cause, if known  Supraventricular tachycardia charachteristics - ✓✓✓Rhythm: Regular, Atrial rate: 150-250 beats/min., Ventricular rate: 150-250 beats/min., Treatment: Valsalva maneuver, unilateral carotid massage, immersion of face in ice water,

administration of IV adenosine, cardioversion, radiofrequency ablation.  Atrial flutter characteristics - ✓✓✓Rhythm: Usually regular, Atrial rate: 250-350 beats/min., Ventricular rate: 75-175, Treatment: Cardioversion, digitalis, quinidine, propranolol, verapamil.  Atrial fibrillation characteristics - ✓✓✓Rhythm: Grossly irregular, Atrail rate: 400-600 beats/min, Ventricular rate: 100-160 beats/min., treatment: Digitalis, quinidine, cardioversion, verapamil, ibutilide, flecainiide, amiodarone, anticoagulant.  First degree AV block characteristics - ✓✓✓Rhythm: Regular, Atrial rate: 60-100 beats/min., ventricular rate: 60-100 beats/min., Treatment: None unless symptomatic.  Second degree AV block characteristics - ✓✓✓Rhythm: Regular, Atrial rate: 60-100 beats/min.,