Relias Dysrhythmia Basic Adult Care 3 Cardiac Blueprint

PR interval (P wave) 0.12-0.20 seconds P wave less than 0.12 seconds QRS complex 0.10 seconds QT interval 0.44 seconds sinus rhythm impulse initiated by the sinus node regular rhythm rate 60 to 100 beats/min P wave before each QRS Normal PR, QRS, and QT interval PR interval "0.12 to 0.20 seconds and constant QRS duration: 0.04 to 0.10 seconds sinus tachycardia sinus rhythm with a rate of 100 to 150 beats/min normal P wave P wave before every QRS assess for symptoms of low cardiac output assessment findings of sinus tachycardia fever diaphoresis decreased urine output decreased or increased BP causes of sinus tachycardia Hyperthyroidism, hypovolemia, heart failure, anemia, exercise, use of stimulants, fever, and sympathetic response to fear or pain and anxiety treatment for tachycardic If fever- give antipyretic. If dehydration- give fluids. If hypoxemia- give oxygen. If pain- give meds. Meds: 1. Beta-blockers 2. Calcium channel blockers. Other tx: vagal maneuvers sinus bradycardia impulse initiated in the sinus node sinus rhythm with rate less than 60 beats/min normal p wave each QRS produces various hemodynamic responses findings for sinus bradycardia Syncope Dizziness and weakness Confusion Hypotension Diaphoresis SOB Chest pain causes of sinus bradycardia vagal, drugs, ischemia, disease of the nodes, ICP, hypoxemia, and athletes (normal) treatments for sinus bradycardia Assess underlying cause If vomiting - give antiemetic If hypoxic - oxygen Hypothyroidism - give medications Medications to treat: Atropine Dopamine Epinephrine Other treatment: Pacemaker premature atrial contractions Early beats initiated by the atrium P waves and PR intervals may vary P wave may be in T wave Occurs when atrial tissue becomes irritable. This ectopic focus fires an impulse before the next sinus impulse is due. The premature P wave may not always be clearly visible because it can be hidden in the preceding T wave. PACs assessment findings asymptomatic palpitations causes of premature atrial contractions stress fatigue anxiety inflammation infection caffeine nicotine alcohol drugs such as epinephrine, sympathomimetics, amphetamines, digitalis or anesthetic agents atrial fibrillation irregularly irregular erratic impulse in atria no discernible p wave irregular ventricular rate aberrant ventricular conduction can occur results in loss of atrial kick high risk for pulmonary or systemic emboli AFIB assessment findings Asymptomatic or anxiety Fatigue Weakness SOB Dizziness Syncope Palpitations Chest discomfort Pain Hypotension treatment for AFIB Correct rhythm & rate Antidysrhythmic meds: Digoxin (if HF) Revised 1/2024 Diltiazem Amiodarone Dronedarone Flecainide Other meds: 1. Beta-blockers 2. Sotalol Anticoagulation: Warfarin Dabigatran Rivaroxaban Apixaban Other tx: Synchronized cardioversion EP study and ablation atrial flutter ectopic foci in atria, heart disease classic "sawtooth" pattern in leads II, III, and aVF atrial rate fast and regular (250 to 350 beats/min) with AV block description of atrial flutter be constant at 2:1, 3:1, 4:1, 5:1., and so forth or it may be variable atrial flutter causes lung disease ischemic heart disease hyperthyroidism hypoxemia heart failure alcoholism premature ventricular contractions Wide and bizarre beats Compensatory pause Patterns Bigeminy and trigeminy Couplets and triplets Unifocal vs multifocal QRS complex greater than 0.10 seconds Irregular rhythm Compensatory pause Absent P wave why are PVCs dangerous? Frequent Multifocal Two or more in a row R on T PVC falls into the vulnerable period of the T wave Ventricular tachycardia or fibrillation can result ventricular tachycardia rapid, life-threatening dysrhythmia three or more PVCs in a row fast rate 100 beats/min initiated by ventricles wide QRS complex; greater than 0.10 seconds usually regular may or may not have pulse - treat pulseless same as ventricular fibrillation significant loss of cardiac output hypotension ventricular fibrillation Chaotic pattern No discernible P, Q, R, S, or T waves Coarse Verus fine No cardiac output; life-threatening Emergent defibrillation There is no cardiac output or pulse and therefore no cerebral, myocardial, or systemic perfusion. This rhythm is rapidly fatal if not successfully ended within 3 to 5 minutes. asystole No P, Q, R, S, or T waveforms Assess in two leads No cardiac output Death 1st degree block Delayed conduction from SA node to AV node Prolonged PR interval Greater than 0.20 seconds Same PR interval for each beat If the R is far from the P, then you have a first degree typically asymptomatic potential causes for 1st degree aging ischemic heart disease valvular heart disease 2nd heart degree block type 1 Steadily lengthening PR interval Nonconducted P waves PP interval regular RR interval irregular QRS normal Self-limiting; rarely progresses May decrease cardiac output Longer, longer, drop must be the one and only Wenckebach asymptomatic unless frequent dropped QRS symptoms of decreased cardiac output potential causes for second degree aging AV nodal blockers MI ischemia heart disease digoxin toxicity 2nd degree heart block type II More severe AV block Often associated with bundle branch block PR interval is fixed PP interval is regular Occasional P wave not followed by QRS What is the danger of this block? If some Ps don't get through (to ventricles), then you have Mobitz II Asymptomatic unless frequent dropped QRS symptoms of decreased cardiac output potential causes for second degree type II Aging Av nondual blockers MI Ischemia heart disease treatment for second degree block II possibly pacemaker 3rd degree heart block complete Atria and ventricles beat independently of each other. P waves not associated with QR complex - PP intervals regular - RR intervals regular Complete heart block May need pacemaker Hemodynamic status based on ventricular rate If Ps and Qs DON'T agree, then you have a third-degree 3rd degree complete heart block findings bradycardia decreased cardiac output 3rd degree complete heart block treatment pacemaker Remember while there is standard treatment for dysrhythmias, your interventions are dependent on the hemodynamic status of the patient! Evaluate the patient with dysrhythmias immediately for the presence of a life-threatening dysrhythmia or hemodynamic deterioration Assess the patient with a dysrhythmia for angina, hypotension, heart failure, and decreased cerebral and renal perfusion Consider these causes of dysrhythmias when taking the patient's history: hypoxia, drug toxicity, electrolyte imbalances, heart failure, and myocardial ischemia or infarction Assess the patient's level of education, hearing learning style, and ability to understand and recall instruction to determine the best approaches for teaching Assess the patient's ability to read written instructions Teach the patient the generic and trade names of prescribed antidysrhythmic drugs, as well as their purpose, dosage, side effects, and special instructions for their use Provide clear written instructions in basic language and easy to read print Provide a written drug dosage schedule for the patient, considering all the drugs the patient is taking and possible drug interactions Assess the patient for possible side effects or adverse reactions to drugs considering age and health status Teach the patient to take his or her pulse and to report significant changes in heart rate rhythm to the health care provider Inform the patient of available resources for blood pressure and pulse checks, such as BP clinics, home health agencies, and cardiac rehab programs Instruct the patient on the importance of keeping follow-up appointments with the health care provider and reporting symptoms promptly Include the patient's family members or significant other in all teaching whenever possible Teach the patient to avoid drinking caffeinated beverages, to stop smoking, to drink alcohol only in moderation, and to follow his or her prescribed diet nonmodifiable risk factors for CAD Age Men 45 years Women 55 years Gender: Men women Family history - first degree relative Modifiable risk factors for CAD smoking inactivity overweight cholesterol - high LDL - low levels of HDL diabetes hypertension stable angina Chest discomfort that occurs with moderate to prolonged exertion in familiar pattern Rarely requires aggressive treatment. Relieved by rest stable angina management Lifestyle modifications Cholesterol meds Cardio protective meds (betablockers, ace inhibitors) Antiplatelets for prevention unstable angina Chest pain at rest or with exertion T wave inversions or ST depression Usually has anxiety, diaphoresis, and hypertension going along with it Troponin likely normal MI A myocardial infarction occurs because of atherosclerosis and coronary artery disease. STEMI worse ST elevation Elevated troponin NSTEMI no ST elevation Elevated troponin may have T wave inversions or ST depressions or no EKG changes MI assessment findings Chest pain Shortness of breath Fatigue Palpitation Anxiety Diaphoresis Women Diabetes Troponin lab diagnostics for CAD and Acute Coronary syndrome EKG Exercise stress test Pharmacologic stress test Nuclear stress test Echocardiogram Cardiac catheterization and angiography ischemia lack of oxygen to the cardiac tissue, represented by ST segment depression, T wave inversion, or both infarction death of tissue, represented by a pathological Q wave medications used to treat acute coronary syndrome blood thinners clots blusters beta blockers Emergency care of ACS MONA Phosphodiesterase inhibitors - Glycoprotein IIb/IIa inhibitors - Fibrinolytic therapy - tissue plasminogen activator (tPA alteplase), reteplase, Tenecteplase Phosphodiesterase inhibitors sildenafil, tadalafil, avanafil, or vardenafil Glycoprotein IIb/IIa inhibitors abciximab, eptifibatide, or tirofiban post cardiac catherization care ??? Complication of Caths ?? nonmodifiable risks for vascular problems Age Men 45 years Women 55 years Gender Men women Family history - first degree relative