Management of Arrhythmias and Conduction Problems Review Anatomy of the Heart - Hollow, muscular organ - Pumps blood to the tissues, supplying them with oxygen and other nutrients - Location: center of the thorax (where it occupies the space between the lungs and rests on the diaphragm) The heart is composed of 3 layers: 1. Endocardium: inner layer - consists of endothelial tissue and lines the inside of the heart and valves 2. Myocardium: middle layer - made up of muscle fibers and is responsible for the pumping action 3. Epicardium: exterior layer The heart is encased in a thin, fibrous sac called the pericardium that is composed of two layers: 1. Visceral pericardium - adheres to the epicardium (exterior layer) 2. Parietal pericardium - envelops the visceral pericardium and is a tough fibrous tissue that attaches to the great vessels, diaphragm, sternum, and vertebral column and supports the heart in the mediastinum The space between these two layers ^ is called the pericardial space and is normally filled with about 20mL of fluid, which lubricates the surface of the heart and reduces friction during systole (the phase of the heartbeat when the heart muscle contracts and pumps blood from the chambers into the arteries). Heart Chambers - The pumping action of the heart is accomplished by the rhythmic relaxation and contraction of the muscular walls of its two top (atria) and bottom chambers (ventricles) ● Diastole (ventricular filling): relaxation phase, all chambers relax simultaneously which allows the ventricles to fill in preparation for contraction ● Systole: contraction of the atria and ventricles - The atrial systole contracts first, followed by the ventricular systole. - This synchronization allows the ventricles to fill completely prior to the ejection of blood from these chambers. Right side of the heart: distributes deoxygenated blood (venous blood) to the lungs through the pulmonary artery. - Right atrium: receives venous blood returning to the heart from the superior vena cava (head neck, and upper extremities), inferior vena cava (lower extremities) and coronary sinus (coronary circulation) - Right ventricle - Pulmonary artery - the only artery in the body that carries deoxygenated blood Left side of the heart: distributes oxygenated blood to the remainder of the body through the aorta (systemic circulation) - Left atrium: receives oxygenated blood from pulmonary circulation through the four pulmonary veins - Left ventricle - Aorta The Heart’s Valves - There are four valves in the heart that permit blood to flow in only one direction - Valves are made up of thin leaflets of fibrous tissue that open and close in response to the movement of blood and pressure - There are (2) types of valves: 1. Atrioventricular (AV) 2. Semilunar (1) Atrioventricular valves: separates the atria from the ventricles - Tricuspid valve is also known as the right atrioventricular valve separates the right atrium from the right ventricle - The mitral or bicuspid valve also known as the left atrioventricular valve lies between the left atrium and left ventricle During diastole, the tricuspid and mitral valves are open and allow blood in the atria to flow freely into the ventricles. As the ventricular systole begins, the ventricles contract and blood flows upward into the cusps of the tricuspid and mitral valves causing them to close. As the pressure against these valves increases, two additional structures, the papillary muscles and the chordae tendineae, maintain valve closure. During ventricular systole, contraction of the papillary muscles causes the chordae tendinae to become taut, keeping the valve leaflets approximated and closed. This action prevents backflow of blood into the atria (regurgitation) as blood is ejected out into the pulmonary artery and aorta. (2) Semilunar valves: - Two semilunar valves are composed of three leaflets that are shaped like half moons - Pulmonic valve: the valve between the right ventricle and pulmonary artery - Aortic valve: valve between the left ventricle and the aorta The semilunar valves are closed during diastole. At this point, the pressure in the pulmonary artery and aorta decreases, causing blood to flow back toward the semilunar valves. This action fills the cusps with blood and closes the valves. The semilunar valves are forced open during ventricular systole as blood is ejected from the right and left ventricles into the pulmonary artery and aorta respectively. Coronary Arteries The left and the right coronary arteries and their branches supply arterial blood to the heart. These arteries are just above the aortic valve leaflets. 1. Left coronary artery: has 3 branches - Left main coronary artery: the artery from the point of origin to the first major branch - - Left anterior descending artery: courses down the anterior wall of the heart Circumflex artery: which circles around to the lateral left wall of the heart 2. Right coronary artery: travels to the inferior wall of the heart. The posterior wall of the heart receives its blood supply by an additional branch from the right coronary artery called the posterior descending artery. Superficial to the coronary arteries are the coronary veins. Venous blood from these veins return to the heart primarily through the coronary sinus which is located posteriorly in the right atrium. Myocardium - The middle layer of the atrial and ventricular walls - Composed of myocytes - which form an interconnected network of muscle fibers - Myocytes encircle the heart in a figure of eight pattern forming a spiral from the base of the heart to the bottom - During contraction, this muscular configuration facilitates a twisting and compressive movement of the heart that begins in the atria and moves to the ventricles Subido’s Notes Electrocardiogram - The electrical impulse that travels through the heart can be measured through an electrocardiogram - May be used to monitor heart rate - Measures the conduction system of the heart. Explanation: The impulse is going to enter the pacemaker of the heart which is the SA node and is seen in the upper part of the right atrium as the impulse is received by the SA node the RA is starting to contract, and will be followed by the left atrium so when it is received by the SA node, the atrium is already contract so that the atrioventricular bulb opens. So that it is giving blood to the ventricles. Once the impulse is received, the bi and tricuspid valve closes and the ventricles start contracting, pushing blood towards the pulmonary trunk allowing for oxygenating. Coronary arteries give oxygenated blood to the heart so it is able to function properly. The right RCA is much bigger than the LCA. The heart has valves. We have valves to prevent the backflow of blood so that the blood will only flow in one direction. Once the impulse is received by the SA node, the RA immediately contracts (much earlier than the LA) as the atriums are contracting, the bi and tricuspid valves begin to open so that more blood goes into the ventricles. The impulse is received by the AV node and tries to hold the valves open so that more blood is received by the ventricles. When blood is received in the bundle of his The RV will push unoxygenated blood to the pulmonary blood The LV will also contract when the RV also contracts, the LV will push oxygenated blood towards the AV to the Ascending aorta so that oxygenated blood will be distributed to multiple organs of the body. If the valve is incompetent, less blood is ejected. When the tri and bi cuspid valve are closed, that means the impulse is already received by the right bundle of HIS plus the fibers, the RV is pushing unoxygenated valve in to the pulmonary artery going into lungs for oxygenated The Sinoatrial Node is the pacemaker of the heart seen at the upper part of the RA It is the only pacemaker that can give us the normal cardiac rate which is 60-100 bpm - A normal heartbeat is initiated in the SA node It causes the atria to contract first right atrium and left atrium the valves will OPEN then it will give blood to your ventricles AV NODE - Back up pacemaker with an intrinsic rate of 40-60 bpm - If you destroy your pacemaker the AV node, bundle of His, or BF take over - Receives the atrial impulse - - Cardiac output is the amount of blood ejected by the heart per minute Normal cardiac output is 5-6L per minute Blood is important because it contains oxygen, nutrients, and glucose which is needed for the survival of our cells PURKINJE FIBERS - Backup pacemaker with an intrinsic rate of 20-40 bpm - A complex network that mingles with ventricular myocardial cells - It will rapidly stimulate ventricular muscle fibers (ventricular depolarization - contraction) - If its destroyed, you will get a artificial pacemaker implanted in your chest Pacemakers of the Heart SA NODE (60-100) AV NODE (40-60) PURKINJE FIBERS (20-40) ECG P: Atrial depolarization - contraction - It stops in the middle (the RA is contracting) - When the whole P curves, BOTH atriums are contracting, the valves are open, and blood is given to the ventricles which is P WAVE - tricuspid and bi cuspid valve should be open - The right atrium beats faster than the left - 2.5mm in height - Last 0.06-0.12 seconds - Measures horizontally - Occupies three small boxes - to be normal PR Segment - Horizontal line between the end of the P wave and beginning of the QRS - Represents the activation of the AV node, the Bundle of His, the bundle branches and the Purkinje fibers - Atrial repolarization occurs during this period Depressed PR segment : can mean ventricular hypertrophy or chronic pulmonary disease QRS: Ventricular depolarization contraction Q represents depolarization of the interventricular septum - q is the SEPTUM part of the heart that is contracting - downward deflection - Always a negative waveform - - - The right and left ventricle are contracting The right ventricle will contract and will push oxygenated blood to the pulmonary valve so that it can go to the lungs for oxygenated, at the same time the L ventricle will push oxygenated blood to the aorta to push blood to the whole body The atrium is already closed When the R and L ventricle are contracting, blood leaves the heart through the aortic valve, into the aorta and to the body 0.04 second duration (only one block) and less than ⅓ of the height of the R wave in that lead R and S WAVES - Represent simultaneous depolarization of the right and left ventricles Layman's term: there is simultaneous contraction of the right and left ventricles - R wave is the first positive upright waveform following the P wave R wave is always positive Duration: 0.06-0.10 or one half of the PR interval S-T: Early ventricular relaxation repolarization T wave: Ventricular repolarization - complete ventricular relaxation - Slightly asymmetric - Direction of the T wave is the same as the QRS that precedes it - Less than 5 mm in height - Horizontal line is much more significant - There are no definite rules for height - T wave generally shouldn’t be taller than half the size of the preceding QRS - If you see the T increase multiple causes can be hyperkalaemia, acute myocardial infarction Abnormal t waves - T wave in the opposite direction as the QRS that precedes it ventricular rhythms bundle branch blocks - Negative t waves- myocardial ischemia (coronary arteries are blocked with clotted bloods or fats) what is the artery that supplies the blood with oxygenated blood? - right and left coronary arteries, if that coronary artery is blocked with fats or clotted blood, there is less blood going into the heart, then the ECG will show a negative T wave. - The coronary arteries are the arteries that will deliver oxygenated blood - - - Myocardial ischemia - the lumen becomes smaller, and the circulation becomes sluggish When you lessen the blood supply, the myocardial becomes inflammed, painful, and swollen. Tall, peaked t waves - hyperkalemia Low t waves- hypokalemia : ● ST segment is depressed ● Flattening of the t wave ● Appearance of U wave Hypo and hyperkalemia can cause cardiac arrest Causes of abnormal U wave - Electrolyte imbalance - Medications (quinidine, procainamide, digitalis - Hyperthyroidism - CNS disease - QST syndrome 3. V3 halfway between V2 and V4 4. V4 5th ICS L midclavicular line 5. V5 5th ICS L ant. Axillary Line 6. V6 - 5th ICS L Mid axillary Line 7. V3R halfway between V1 and V4R 8. V4R-5th R midclavicular line 6 ANTERIOR LEADS V1 and V2 - reflect the right side of the heart V3 and v4 - reflect the interventricular septum (location of His Bundle and right and Left bundle branches) V5 and V6 - Reflect the left side of the heart ECG Grid Shows the horizontal axis and vertical axis and their respective measurement values If you are measuring going up: you are measuring voltage U wave - Small waveform that follows the T wave - One theory: represented repolarization of Purkinje fibers - Normally it should not be present HORIZONTAL AXIS BLOCKS If you are measuring horizontally: you are measuring the time Each small block equals 0.04 seconds Depolarization- contracting repolarization - resting Basics of ECG - Position of Chest Leads (Precordial leads) 1. V1 - 4th R Sternal Border 2. V2 4th ICS L sternal border 5 small blocks form a large block which equals 0.20 seconds 5 large blocks is equal to 1 second VERTICAL AXIS BLOCKS - The ECG strips vertical axis measures AMPLITUDE in millimeters or electrical voltage in millivolts - Each small block represented 1 millimeter or 01 millivolt - Each large block represents 5 millimeters or 0.5 millivolts IF there is pulmonary stenosis - can be seen in QRS, you are accumulating blood in the right ventricle and P wave will be abnormal If the valves don’t close completely then tricuspid stenosis may occur. Abnormalities in QRS Ventricular fibrillation - Sometimes you can see P and sometimes you can’t - Heart may be beating 200 bpm Ventricular tachycardia - You cannot see the P - Heart may be beating 400 bpm - If impulse originating from ectopic pacemaker, duration usually prolonged more that 0.12 - more than 3 small boxes Arrhythmia disorder of the formation or conduction of the electrical impulse within the heart, altering the heart rate, heart rhythm, or both and potentially causing altered blood flow (also referred to as dysrhythmia) - - Treatment is based on the frequency and severity of the symptoms produced They are named according to the site of origin of the electrical impulse and the mechanism of formation or conduction involved Atrial Fibrillation - - A type of arrhythmia Very common arrhythmia Results from abnormal impulse formation that occurs when structural or electrophysiological abnormalities alter the atrial tissue causing a rapid, disorganized, and uncoordinated twitching of the atrial musculature Causes a loss in AV synchronicity (the atria and ventricles contract at different times), the atrial kick (the - last part of diastole and ventricular filling, which accounts for 25-30% of the cardiac output) is also lost. Some patients with atrial fibrillation are asymptomatic, others experience palpitations and clinical manifestations What is the cause? - The extrinsic and intrinsic cardiac autonomic nervous system are thought to play a role in the initiation and continuance of atrial fibrillation - The cardiac autonomic system consists of a highly interconnected network of autonomic ganglia and nerve cell bodies embedded within the epicardium, largely within the atrial myocardium and pulmonary veins. Hyperactive autonomic ganglia in the CANS are thought to play a critical role in atrial fibrillation resulting in impulses that are initiated from the pulmonary veins and conducted through to the AV node. - The ventricular rate of response depends on the conduction of atrial impulses through the AV node, presence of accessory electrical conduction pathways and therapeutic effect of medications. Classification of Atrial Fibrillation Type Description Paroxysmal Sudden onset with termination that occurs spontaneously or after an intervention - Lasts < days, but may recur Persistent Continuous, lasting than > 7 days Long-standing persistent Continuous, lasting >12 months Permanent Persistent, but decision has been made not to restore or maintain sinus rhythm Nonvalvular Absence of moderate-to-severe mitral stenosis or mechanical heart valve Risk Factors - Atrial Fibrillation Increasing age Hypertension Diabetes Obesity Valvular heart disease Heart failure Obstructive sleep apnea Alcohol abuse Hyperthyroidism Myocardial infarction Smoking Exercise Cardiothoracic surgery Increased pulse pressure European ancestry Family history Characteristics ~ Atrial Fibrillation Ventricular and atrial rate - Atrial rate: 300-600 bpm Ventricular rate: 120-200 bpm in untreated atrial fibrillation Ventricular and atrial rhythm Highly irregular QRS shape and duration Usually normal, but may be abnormal P wave No discernable P waves; irregular undulating waves that vary in amplitude and shape pare seen and referred to as fibrillatory or f waves PR interval Cannot be measured P: QRS ration Many: 1 Medical Management Treatment of atrial fibrillation depends on the cause, pattern, and duration of the arrhythmia, the ventricular response rate, as well as the presence of structural or valvular heart disease and other cardiac conditions such as coronary artery disease or heart failure. Management of atrial fibrillation may not only be different in different patients, but it also may change over time for one patient Medical management revolves around preventing embolic events such as a stroke with anticoagulant medications, controlling the ventricular rate of response with antiarrhythmic agents, and treating the arrhythmia as indicated so that it is converted to a sinus rhythm Pharmacologic Therapy Antithrombotic Medications Medications that control heart rate Medications that convert the heart rhythm or prevent atrial fibrillation Includes anticoagulants and antiplatelet drugs This is a strategy to control the ventricular rate of response so that the resting heart rate is less than 80 bpm Patients with atrial fibrillation lasting 48 hours or longer: - Coagulation (to restore sinus rhythm) To decrease the ventricular rate in patients with paroxysmal, persistent, or permanent atrial fibrillation: - Beta Blocker Medications that may be given to achieve pharmacologic cardioversion to sinus rhythm include: - Flecainide - Dofetilide Oral antithrombotic therapy is indicated for most patients with nonvalvular atrial fibrillation because it reduces the risk of stroke. Patients with atrial fibrillation with valvular heart disease or bioprosthetic heart valves may be prescribed: - Warfarin - Direct acting oral anticoagulant - Factor Xa inhibitor - non -dihydropyridine calcium channel blocker is generally recommended For patients with mechanical heart valves: - Wafarin If Immediate or short term anticoagulant is necessary the patient may be placed on: - IV - Low molecular weight heparin until warfarin therapy can be started and the international normalized ratio (INR) reaches a therapeutic range consistent with antithrombosis. Home monitoring is an option for some patients - Propafenone - Amiodarone - IV ibutilide These medications are most effective if given 7 days of the onset of atrial fibrillation. Patients who were prescribed dofetilide should be hospitalized so that the QT interval and renal function are monitored. Dofetilide is also a preferred medication because it is highly effective at converting atrial fibrillation to sinus rhythm and has fewer drug to drug interactions and is better tolerated by patients than other medications. Clients with recurrent atrial fibrillation may be prescribed: - Flecainide To administer at home Preoperative administration of beta blockers has resulted in a significant reduction in atrial fibrillation after cardiac surgery Cholesterol lowering drugs such as the HMG-CoA reductase inhibitors may also be prescribed to prevent new onset atrial fibrillation following cardiac surgery IF symptomatic paroxysmal atrial fibrillation is refractory to at least one Class 1 or Class 3 antiarrhythmic medication, rhythm control is desired and catheter ablation may be indicated. Antithrombotic Medication Guidelines Antithrombotic therapy is selected based on risk factors outlined in the mnemonic CHA2DS2 VASc with each risk factor assigned points tallied for a total score that indicates an overall risk of stroke 1. Patients with nonvalvular atrial fibrillation with a CHA2 DS VASc score of zero may choose the option of no antithrombotic therapy 2. Patients with nonvalvular atrial fibrillation with CHA2 DS VASc score of one may choose no thrombotic therapy, treatment with an oral anticoagulant or aspirin 3. Patients with nonvalvular atrial fibrillation with a CHA 2 DS2 VASc score of 2 or higher for men and 3 or higher for women may choose warfarin or a direct thrombin inhibitor (e.g( dabigatran or an Factor Xa inhibitor (E.g rivaroxaban, apixaban, edoxaban) Procedures done for Atrial Fibrillation 1. Electrical Cardioversion - Indicated for patients with atrial fibrillation who are hemodynamically unstable (e.g. acute alteration in mental status, chest discomfort, hypotension) and do not respond to medications - Flecainide, propafenone, amiodarone, dofetilide, or sotalol may be given prior to cardioversion to enhance the success of cardioversion and maintain sinus rhythm - Warfarin is indicated for at least 4 weeks after the procedure Cardiac Rhythm Therapies: 1. Catheter Ablation Therapy: destroys specific cells that are the cause of a tachyarrhythmia - Involves a procedure similar to a cardiac catheterization; however in this instance a special catheter is advanced at or near the origin of the arrhythmia, where high frequency, low energy sound waves are passed through the catheter, causing thermal injury, localized cell destruction, and scarring. - Ablation may also be accomplished using a special catheter to apply extremely cold temperature to destroy selected cardiac cells, called cryoablation - The goal or each ablation procedure is to eliminate the arrhythmia by preventing the ectopic activity arising from the pulmonary veins from reaching the atria, thereby stopping the fibrillation Nursing Management: - Frequent monitoring for arrhythmias and for signs and symptoms of a stroke and vascular access site complications - Administering any pain medications the nurse may help to alleviate this pain by placing rolled towels under the patient’s knees and waist 2. Maze and Mini-Maze Procedures Maze Procedure - An open heart surgical procedure for refractory atrial fibrillation - Small transmural incisions are made throughout the atria. The resulting formation of scar tissue prevents reentry conduction of the aberrant electrical impulse - Reserved only for those patients undergoing cardiac surgery for another reason - Some patients may need a permanent pacemaker after this surgery because of subsequent injury to the SA node Mini Maze Procedure - Modification of the maze procedure - Minimally invasive maze surgery - Performed by making small incisions between the ribs, through which video guided instruments are inserted. - The pulmonary veins are encircled with surgical incisions within the left atrium - This surgery eliminates the need for opening the sternum, heart lung bypass, and the use of cardioplegia - This results in a shorter recovery time and a lower risk of infection 3. Convergent Procedure - Utilizes a hybrid approach to ablation requiring the skills of both a cardiothoracic surgeon and an electrophysiologist, a cardiologist with special training - This procedure has lower rates of arrhythmias but more complications within 30 days of the procedure - The surgeon creates a few small incisions in the abdomen so that a special catheter that allows visualization can be inserted through the diaphragm and toward the posterior wall of the heart - The surgeon performs ablation of the epicardial wall in the area around the pulmonary veins and the electrophysiologist performs ablation around the endocardial area of the pulmonary veins - The patient usually has a 3 day hospital length of stay - The patient may experience mild dull chest pain caused by resulting inflammation from the ablation that usually resolves within a few days - - The pain is usually alleviated by treatment with acetaminophen as needed If the phrenic nerve was affected the patient may experience shortness of breath that may take days to weeks to resolve 4. Left Atrial Appendage Occlusion (LAAO) - An alternative to antithrombotic medications for stroke prevention in patients with nonvalvular atrial fibrillation - The LAA is the area where the majority of stroke causing blood clots form in patients with nonvalvular atrial fibrillation - Candidates for LAAO include those patients with increased risk of stroke based on CHA 2DS2-VASC scores of one or higher and those patients seeking a nonpharmacologic alternative to treatment - Commonly used is the WATCHMAN a device typically inserted while the patient is under general anesthesia - Similar to a percutaneous coronary intervention procedure, a small incision is made in the femoral area and a catheter is then inserted that guides the device into position. The parachute-shaped device is threaded through to the opening of the LA sealing it off and preventing it from releasing clots - Patients are prescribed aspirin and warfarin post procedure approximately 6 weeks post procedure and should return to the clinic for a TEE to confirm that the device has effectively occluded the LAA. If LAAO has occurred, then the patient may stop taking warfarin and - is prescribed clopidogrel, an antiplatelet medication. After 6 months the patient may stop taking clopidogrel but must continue taking daily aspirin indefinitely - - Wolff Parkinson- White Syndrome - - - - If the QRS is wide and the ventricular rhythm is very fast, an accessory pathway should be suspected An accessory pathway is typically congenital tissue between the atria, bundle of His, AV node, Purkinje fibers, or ventricular myocardium This anomaly is known as Wolf-Parkinson-White Syndrome Electrical cardioversion is the treatment of choice or atrial fibrillation in the presence of WPW syndrome that causes hemodynamic instability Medications that block AV conduction (e.g digoxin, diltiazem, verapamil) should be avoided in WPW because they can increase the ventricular rate If the patient is hemodynamically stable, procainamide, propafenone, flecainide or amiodarone are recommended to restore sinus rhythm Catheter ablation is performed for long term management Atrial Flutter Occurs because of a conduction defect in the atrium and causes a rapid, regular atrial impulse at a rate between 250-400 bpm - Because the atrial rate is faster than the AV node can conduct, not all atrial impulses are conducted into the ventricle, causing a therapeutic block at the AV node. - This is an important feature of the arrhythmia. If all atrial impulses were conducted to the ventricle, the ventricular rate would also be 250 400 bpm, which would result to ventricular fibrillation which is life threatening Serious signs and symptoms: - Chest pain - Shortness of breath - Low blood pressure Characteristics of Atrial Flutter: Ventricular and atrial rate Ventricular and atrial rhythm QRS shape and duration P wave PR interval P:QRS ratio Atrial rate ranges between 250-400 bpm Atrial rhythm is regular Usually normal, but may be abnormal or absent Saw-toothed shape; these waves are referred to as F waves Multiple F waves may make it difficult to determine the PR interval 2:1 3:1 4:1 Ventricular rate Ventricular rhythm is usually regular but usually ranges between 75-150 bpm may be irregular because of a change in the AV conduction Medical Management for Atrial Flutter - Use of vagal maneuvers Trial administration of adenosine (which causes sympathetic block and slowing of conduction through the AV node); it may terminate tachycardia, optimally facilitating visualization of flutter waves for diagnostic purposes Adenosine is given via IV by rapid administration and immediately followed by a 20-mL saline flush and elevation of the arm with the IV line to promote rapid circulation of the medication Antithrombotic therapy Rate control Rhythm control Electrical cardioversion Ventricular Tachycardia Defined as three or more PVCs in a row, occurring at a rate exceeding 100 bpm. - The causes are similar to those of PV - VT is an emergency because the patient is nearly always unresponsive and pulseless Characteristics: Ventricular and atrial rate Ventricular and atrial rhythm QRS shape and duration P wave PR interval P:QRS ratio Ventricular rate: 100-200 bpm Ventricular rhythm: usually regular 0.12 seconds or more; bizarre, abnormal shape Very difficult to detect, so the atrial rate and rhythm may be indeterminable Very irregular, if P waves are seen Difficult to determine, but if P waves are apparent, there are usually more QRS complexes than P waves Atrial rate: depends on the underlying rhythm (e.g; sinus rhythm) Atrial rhythm: may also be regular Medical Management for Ventricular Tachycardia Several factors determine the initial treatment: - Identifying the rhythm as monomorphic (having a consistent QRS shape and rate) or polymorphic (having varying QRS shapes and rhythms) - Determining the existence of a prolonged QT interval before the initiation of VT, any comorbidities and ascertaining the patient’s heart function (normal or deceased) IF the patient is stable, continuing the assessment, especially obtaining a 12 lead ECG, may be the only action necessary Antiarrhythmic medications ( Procainamide, amiodarone, sotalol, and lidocaine) Antitachycardia pacing Direct cardioversion or defibrillation: - Cardioversion is the treatment of choice for monophasic VT in a patient who is symptomatic - Defibrillation, which uses an electrical current given to stop the arrhythmia that is not set to synchronize with the patient’s QRS, is the treatment of choice for pulseless VT. (Any type of VT in a patient who is unconscious and without a pulse is treated in the same manner as ventricular fibrillation: immediate defibrillation is the action of choice For long term management, patients with an ejection fraction less than 35% should be considered for an implantable cardioverter defibrillator With an ejection fraction greater than 35%, may be managed with antiarrhythmic medications. Torsades de pointes is a polymorphic VT - Proceeded by a prolonged QT interval, which could be congenital or acquired Common causes: ● Central nervous system disease ● Certain medications (ciprofloxacin, erythromycin, haloperidol, lithium, methadone) ● Low levels of sodium, potassium, or magnesium ● Congenital QT (because the rhythm is likely to cause the patient to deteriorate and become pulseless) Ventricular Fibrillation The most common arrhythmia in patients with cardiac arrest - Rapid, disorganized ventricular rhythm that causes ineffective quivering of the ventricles - Always characterized by the absence of an audible heartbeat, a palpable pulse, and respirations - No atrial activity is seen on the ECG Causes: - The most common cause is coronary artery disease and the resulting acute MI - Untreated or unsuccessfully treated VT - Cardiomyopathy - Valvular heart disease - Several proarrhythmic medications - Acid base and electrolyte abnormalities - Electrical shock - Brugada syndrome: the patient (mostly Asian descent) has a structurally normal heart, few or no risk factors for coronary artery disease and a family history of sudden cardiac death Characteristics Ventricular Rate Ventricular rhythm QRS shape and duration Greater than 300 bpm Extremely irregular, without a specific pattern Irregular, undulating waves with changing amplitudes. There are no recognizable QRS complexes Medical Management - Early defibrillation is critical to survival, with administration of immediate bystander cardiopulmonary resuscitation (CPR) until defibrillation is available For refractory ventricular fibrillation, administration of: ● Amiodarone ● Epinephrine may facilitate the return of a spontaneous pulse after defibrillation Cardioversion and Defibrillation Used to treat tachyarrhythmias by delivering an electrical current that depolarizes a critical mass of myocardial cells - When the cells depolarize, he SA nodes is usually able to recapture its role as the heart’s pacemaker - Defibrillators are used for BOTH cardioversion and defibrillation — the electrical voltage required to defibrillate the heart is usually greater than that required for cardioversion and may cause more myocardial damage - The electrical current may be delivered externally through the skin with the use of paddles or with conductor pads, or one pad may be - placed on the front of the chest and the other pad placed under the patient’s back just left of the spine (anteroposterior placement) Defibrillator malfunction conductor pads contain a conductive medium and are connected to the defibrillator to allow for hands off defibrillation — this method reduce the risk of touching the patient during the procedure and increases electrical safety (automated external defibrillators are found in many public areas and use this type of delivery for the electrical current Management: When using pads or paddles the nurse must OBSERVE two safety measures: 1. Good contact must be maintained between the pads or paddles and the patient’s skin with a conductive medium between them to prevent electrical current from leaking through the air when the defibrillator is discharge 2. No one is to be in contact with the patient or with anything that is touching the patient when the defibrillator is discharged, to minimize the chance that electrical current is conducted to anyone other than the patient Electrical Cardioversion Involves the delivery of a “timed” electrical current to terminate a tachyarrhythmia - The defibrillator is set to synchronize with the ECG on a cardiac monitor so that the electrical impulse discharges during the QRS complex. - The synchronization prevents the discharge from occurring during the vulnerable period of repolarization (T Wave) which could result in VT or ventricular fibrillation - The ECG monitor connected to the external defibrillator usually displays a mark or line that indicates sensing of a QRS complex - It’s important to ensure that the patient is connected to the monitor and to select a lead (not paddles) that has the most appropriate sensing of the QRS - Because there may be a short delay until the recognition of the QRS, the discharge buttons of an external manual defibrillator must be held - down until the shock has been delivered The amount of voltage used varies from 50-360 joules, depending on the defibrillator’s technology, the type and duration of the arrhythmia, and the size and hemodynamic status of the patient Management: - If cardioversion is elective and the arrhythmia has lasted longer than 48 hours: Anticoagulation for a weeks before cardioversion may indicated - Digoxin is usually withheld for 48 hours before cardioversion to ensure the resumption of sinus rhythm with normal conducted - The patient is instructed not to eat or drink for at least 4 hours before the procedure - Gel-covered paddles or conductor pads are positioned anteroposteriorly for cardioversion - Before cardioversion, the patient receives moderate sedation IV as well as an analgesic medication or anesthesia - Respiration is then supported with supplemental oxygen delivered by a bag valve mask device with suction equipment readily available - Airway patency must be maintained and the patient’s state of consciousness assessed - Vital signs and oxygen saturation are monitored are recorded until the patient is stable and recovered from sedation analgesic medications or anesthesia - ECG monitoring is required during and after cardioversion Indications of a successful response: - Conversion to sinus rhythm - Adequate peripheral pulses - Adequate blood pressure Defibrillation Is used in emergency situations as the treatment of choice for ventricular fibrillation and pulseless VT - Not used for patients who are conscious or have a pulse - The energy setting for the initial and subsequent shocks using a monophasic defibrillator should be set at 360 joules - The energy setting for the initial shock using a biphasic defibrillator may be set at 150-200 joules, with the same or an increasing dose with subsequent shocks - The sooner defibrillation is used, the better the survival rate - If immediate CPR is provided and defibrillation is performed within 5 minutes, more adults in ventricular fibrillation may survive with intact neurologic function - Epinephrine is given after initial unsuccessful defibrillation to make it easier to convert the arrhythmia to a normal rhythm with the next defibrillation ● This medication may also increase cerebral and coronary blood flow - Antiarrhythmic medications such as amiodarone, lidocaine, or magnesium may be given if ventricular arrhythmia persists — this treatment with continuous CPR, medication administration, and defibrillation continues until stable rhythm resumes or until it is determined that the patient cannot be revived Pacemaker Therapy A pacemaker is an electronic device that provides electrical stimuli to the heart muscle - Pacemakers are used when a patient has a permanent or temporary slower than normal impulse formation, or a symptomatic AV, or ventricular conduction disturbance - May be used to control some tachyarrhythmias that do not respond to medication - Biventricular pacing, also called cardiac resynchronization therapy (CRT) may be used to treat advanced heart failure. Pacemaker technology also may be used in conjunction with ICD - Can be permanent or temporary Pacemakers consist of two components: 1. Electronic pulse generator 2. Pacemaker electrodes (which are located on leads or wires) Generator: - Contains the circuitry and batteries that determine the rate (measured in bpm) and the strength or output (measured in milliamperes) of the electrical stimulus delivered to the heart - Circuitry that can detect the intracardiac electrical activity to cause an appropriate response; this component of pacing is called - - - - - - - - - sensitivity and is measured in millivolts Sensitivity is set at the level that the intracardiac electrical activity must exceed to be sensed by the device Leads which carry the impulse created by the generator to the heart, can be threaded by fluoroscopy through a major vein into heart, usually the right atrium and ventricle (endocardial leads) or they can be lightly sutured onto the outside of the heart and brought through the chest wall during open heart surgery (epicardial wires). The endocardial leads may be temporarily placed with catheters through a vein (usually the femoral, subclavian, or internal jugular vein, usually guided by fluoroscopy) The leads may also be part of specialized pulmonary artery catheter The endocardial and epicardial wires are connected to a temporary generator which is about the size of a cell phone The energy source for a temporary generator is a common household battery Monitoring for pacemaker malfunctioning and battery failure is a nursing responsibility The endocardial leads may also be placed permanently, passed into the heart through the subclavian, axillary, or cephalic vein, and connected to a permanent generator these pace makers are also called transvenous pacemakers Most current leads have a fixation mechanism at the end of the lead that allows precise positioning and avoidance dislodgement The permanent generator, which often weighs less than 1 ounce, is usually implanted in a subcutaneous pocket created in the pectoral region . Below the clavicle in men, or behind the breast in women. - This procedure usually takes about an hour and is performed in a cardiac catheterization laboratory using a local anesthetic and moderate sedation - Close monitoring of the respiratory status is need until the patient is fully awake Leadless pacemakers are a newer type of permanent pacemakers and are 90% smaller than transvenous pacemakers - They feature a self contained, single unit pulse generator and electrode that is inserted transvenously directed into the right ventricle Permanent pacemaker generators are insulated to protect against body moisture and warmth and have filters that protect them from electrical interference rom most household devices, motors, and appliances IF a patient suddenly develops bradycardia, is symptomatic but has a pulse, and is unresponsive to atropine, emergency pacing may be started with transcutaneous pacing Large pacing ECG electrodes (sometimes the same conductive pads used for cardioversion and defibrillation) are placed on the patient’s chest and back - The electrodes are connected to the defibrillator which is the temporary pacemaker generator - Because the impulse must travel through the patient's skin and tissue before reaching the heart, transcutaneous pacing can cause significant discomfort (burning sensation and involuntary muscle contraction) and is intended to be used only in emergences for short periods of time - - This type of pacing necessitates hospitalization If the patient is alert, sedation and analgesia may be given After transcutaneous pacing, the skin under the electrode should be inspected for erythema and burns Transcutaneous pacing is not indicated for pulseless bradycardia - Complications of Pacemaker Use Most common: dislodgement of the pacing electrode - Minimizing patient activity can help prevent this complication Leadless pacemakers have fewer complications than transvenous pacemakers: - Fewer infections - Hematomas - Lead dislodgement - Lead fracture Potential Complications from Insertion of a Pacemaker Local infection at the entry site of the leads for temporary pacing - Prophylactic antibiotic and antibiotic irrigation of the subcutaneous pocket prior to generator placement has decreased the rate of infection Pneumothorax or hemothorax - Risk is reduced if cephalic vein is cut down, contrast venography, or ultrasound is utilized Bleeding and hematoma - Can be managed with cold compresses and discontinuation of antiplatelet and antithrombotic medication Ventricular ectopy and tachycardia from irritation of the ventricular wall by the endocardial electrode Movement or discoloration of the lead placed transvenously (perforation of the myocardium) Phrenic nerve, diaphragmatic (hiccupping may be a sign of skeletal muscle stimulation if the lead is dislocated or if the delivered energy is set high) Cardiac perforation resulting in pericardial effusion and rarely cardiac tamponade - May occur during implant Twiddler syndrome may occur when the patient manipulates the generator - Causing dislodgement or fracture of the lead Pacemaker syndrome - Hemodynamic instability caused by ventricular pacing and the loss of AV synchrony Nursing Management - Monitor patient’s heart rate and rhythm Monitor ECG Assess for anxiety, depression, or anger, which may be symptoms of ineffective coping with the implantation Preventing infection ● Change the dressing as needed and inspect the insertion site for redness, soreness, or any unusual drainage Promote Effective Coping ● Recognize both the patient’s and family perceptions of the situation and their resulting emotional state and assist them to explore their reactions and feelings Promoting Home, community based, and transitional care
