Exam 1 Med Surg 3 Study Guide:QUESTIONS AND ANSWERS LATEST UPDATE 2023 GUARANTEED SUCCESS, Exams of Nursing

Download Exam 1 Med Surg 3 Study Guide:QUESTIONS AND ANSWERS LATEST UPDATE 2023 GUARANTEED SUCCESS and more Exams Nursing in PDF only on Docsity! Exam 1 Med Surg 3 Study Guide:QUESTIONS AND ANSWERS LATEST UPDATE 2023 GUARANTEED SUCCESS TOP RANKED SOLUTIONS PP 1/ 7 The Synergy Model • Basic Concepts o The needs or characteristics of clients and families influence and drive nurse’s competencies o Synergy results in the needs & characteristics of a client, clinical unit or system are matched with a nurse’s competencies o American Academy of Cardiology nursing o Critical patients- require different nurse competencies to care for patients o Linking critical nursing practice with patient outcomes o RN II start o Used for nursing staff ratio to complete nursing assignments • Client Characteristics are unique to each care situation  8 client characteristics o 1. Resiliency ▪ Capacity to return to a restorative level of functioning using compensatory/coping mechanisms; ▪ The ability to bounce back quickly after an insult ▪ Level one – minimally resilient – unable to mount a response ▪ Level five - highly resilient ▪ Restore to original level ▪ Family support/ involvement, o 2. Vulnerability ▪ Susceptibility to actual or potential stressors that may adversely affect outcomes ▪ Level one – highly vulnerable ▪ Level five- Minimally vulnerable o 3. Stability ▪ Ability to maintain a steady-state; equilibrium ▪ Level one – Minimally stable / unstable, not responding to therapies like we would want them to ▪ Level five – Highly stable, responsive to therapies, decreased risk of death o 4. Complexity ▪ Entanglement of 2 or > systems • Body, family, therapies ▪ Level one – highly complex ▪ Level five – minimally complex ▪ Pay attention to comorbidities o 5. Resource Availibility ▪ Extent of resources the client/family/community bring to situation • Technical • Fiscal [Type here] [Type here] [Type here] [Document title] • Personal • Psychological • Social ▪ Support groups, outside help available ▪ Best resource: case management ▪ Arrange for home health, meals on wheels, dialysis in outpatient setting, etc. ▪ Level one - few resources ▪ Level five – good knowledge of resources [Type here] [Type here] [Type here] [Document title] o 5. Systems Thinking ▪ Body of knowledge & tools that allow the nurse to manage environmental & system resources available o 6. Responsiveness to Diversity ▪ Sensitivity to recognize, appreciate, & incorporate differences into provision of care. ▪ Difference may include: • Culture • Spiritual • Gender • Race • Ethnicity • Lifestyle • Socioeconomic status • Age • Values o 7. Facilitation of Learning ▪ Ability to facilitate learning for: • Clients/families • Nursing staff • Members of health care team • Community ▪ May include both informal & formal learning o 8. Clinical Inquiry/Evaluator ▪ Ongoing process of questioning & evaluating practice ▪ Creating practice changes through research utilization & experiential learning • The goal of nursing is to restore a client to an optimal level of wellness as defined by the client. [Type here] [Type here] [Type here] [Document title] PP 2/7 Cardiac Dysrhythmia: Review • Dysrhythmias o Disorder of the formation or conduction of the electrical impulse within the heart o Irregularity causes disturbances in: ▪ Heart Rate ▪ Heart Rhythm ▪ Both o Hemodynamic effects o Regular rate and rhythm required to circulate oxygenated blood and life- sustaining nutrients to body organs o Diagnosed by analyzing the electrocardiogram o Named according to site of origin o Asssessment with dysrhythmia: ▪ Chest pain, SOB, irregular HR on monitor, c/o dizziness, fatigue, N/V o Electrical conduction starts in SA node (in atrium), SA node is also the natural pacemaker of the heart • Normal Electrical Conduction • Review of Cardiac Conduction System SA Node Internod al Pathway s AV Junction, AV node, Bundle of His Bundle Branch es Purkinje Network Firing rate Transfer impulse Slows impulse Two main Spreads impulse throughout th of 60-100 from the SA node Intrinsic firing branches (left ventricles bpm throughout the rate of 40-60 and right) Intrinsic firing rate of 20-40 atria to the AV bpm transmit [Type here] [Type here] [Type here] [Document title] junction impulses to the ventricles *** If the pace is originating from other areas other than the SA node, be cautious with beta blockers & calcium channel blockers. [Type here] [Type here] [Type here] [Document title] ▪ Measured from the beginning of the P wave to the beginning of the QRS complex • Represents time needed for sinus node stimulation, atrial depolarization and conduction through the AV node ▪ 0.12-0.20 seconds in length o QRS Complex ▪ Represents ventricular depolarization • 1st negative deflection: Q wave • 1st positive deflection: R wave • 1st negative deflection after the R wave: ▪ S wave ▪ <0.12 seconds in length o ST Segment ▪ Represents early ventricular repolarization ▪ Lasts from the end of the QRS complex to the beginning of the T wave ▪ Normally isoelectric • Analyzed above or below the baseline o T Wave ▪ Represents ventricular muscle repolarization ▪ Resting phase ▪ Follows the QRS complex; usually in the same direction as the QRS ▪ HR 140s because the monitor is counting the elevated Q and the T each as a beat ▪ Lead 2? o General Rules in Identifying Heart Rhythms ▪ Rapid assessment of your patient first ▪ Read every strip from left to right, starting at the beginning of the strip ▪ Apply a systematic approach ▪ Avoid shortcuts and assumptions ▪ Ask and answer each question in the five-step approach…this is important for consistency! ▪ Assess the pt if something is off on the monitor before acting on a code blue o Systematic Analysis of the ECG ▪ Identify P wave: is there a p-wave before every QRS? ▪ Identify the P wave shape: consistent? Upright? ▪ Determine each PR interval: Consistent? Irregular but with a pattern? Irregular? ▪ Identify the QRS: Duration consistent? Shape consistent? ▪ Evaluate the ST segment: Isoelectric? Depression vs. Elevation? Peaked? ▪ Identify the T wave: Upright? Inverted? ▪ Identify ventricular rate and rhythm • No p coming from somewhere other than the atrium (consider a- flutter or a- fib) ▪ 30 boxes in a 6 second strip ▪ 1500/R to R ▪ Consider the ^ second strip, ignore the extra ▪ Atrial rate – look at p to p waves ▪ Ventricular rate – look at r to r [Type here] [Type here] [Type here] [Document title] ▪ [Type here] [Type here] [Type here] [Document title] o Heart Rate Determination ▪ Regular • 1- minute strip contains 300 large boxes (1500 small boxes) • Count number of small boxes within an RR interval and divide 1,500 by that number ▪ Irregular • Less accurate method: • Top of ECG paper is marked at 3-second intervals (15 large boxes horizontally) • Count the number of RR intervals (not QRS complexes) in 6- seconds and multiply that number by 10 ▪ RR interval used to determine ventricular rhythm ▪ PP interval used to determine atrial rhythm ▪ If intervals are the same: regular rhythm ▪ If intervals are different: irregular rhythm [Type here] [Type here] [Type here] [Document title] AA opne OS m8 Le * MXit pcr ‘Pees XS cbse] Z-5 evinded [Type here] [Type here] [Type here] o Atrial Flutter ▪ Conduction defect in the atrium ▪ Creates atrial rate between 250-400 times/minute (Ventricular rate 75-150) ▪ Not all impulses conducted to ventricle: therapeutic block at AV node ▪ 2:1, 3:1, 4:1 ▪ Flutters are coming at high rate ▪ Ratios: 1 are representing the QRS…. The number of flutters between determine what the first number in the ratio is ▪ Aflutter afib switching back and forth is possible ▪ ▪ Regular atrial activity ▪ P wave= “saw tooth” appearance ▪ HR > 100 bpm ▪ “uncontrolled” ▪ HR > 150 bpm ▪ “rapid ventricular rate” ▪ CAUSES: • COPD • Pulmonary HTN • Valvular disease • Thyrotoxicosis • Open heart surgery ▪ CLINICAL MANIFESTATIONS: • Clinical Manifestations: • Chest pain • Dyspnea • Hypotension ▪ Management: • Electrical Cardioversion for unstable patient • See treatment for atrial fibrillation • Medications to slow the ventricular response: o Beta blockers o Calcium channel blockers o Digitalis ▪ In the atrium, the blood is pooling causing SOB and increased risk for clotting ▪ Cardioversion- syncronize it with the heart (syncronized with the R) ▪ Try medication first before cardioversion (if pt is on long term anticoagulation therapy this increases the risk of complication of a cardioversion) ▪ Try amiodarone first, or CCC, or dig [Type here] [Type here] [Type here] [Document title] • Atrial Fibrillation o Rapid, disorganized and uncoordinated twitching of atrial muscle o Paroxysmal or chronic o Rapid ventricular response; loss of atrial kick (25-30% of cardiac output) [Type here] [Type here] [Type here] [Document title] Exam 1 Med Surg 3 Study Guide:QUESTIONS AND ANSWERS LATEST UPDATE 2023 GUARANTEED SUCCESS TOP RANKED SOLUTIONS PP 1/ 7 The Synergy Model • Basic Concepts o The needs or characteristics of clients and families influence and drive nurse’s competencies o Synergy results in the needs & characteristics of a client, clinical unit or system are matched with a nurse’s competencies o American Academy of Cardiology nursing o Critical patients- require different nurse competencies to care for patients o Linking critical nursing practice with patient outcomes o RN II start o Used for nursing staff ratio to complete nursing assignments • Client Characteristics are unique to each care situation  8 client characteristics o 1. Resiliency ▪ Capacity to return to a restorative level of functioning using compensatory/coping mechanisms; ▪ The ability to bounce back quickly after an insult ▪ Level one – minimally resilient – unable to mount a response ▪ Level five - highly resilient ▪ Restore to original level ▪ Family support/ involvement, o 2. Vulnerability ▪ Susceptibility to actual or potential stressors that may adversely affect outcomes ▪ Level one – highly vulnerable ▪ Level five- Minimally vulnerable o 3. Stability ▪ Ability to maintain a steady-state; equilibrium ▪ Level one – Minimally stable / unstable, not responding to therapies like we would want them to ▪ Level five – Highly stable, responsive to therapies, decreased risk of death o 4. Complexity ▪ Entanglement of 2 or > systems • Body, family, therapies ▪ Level one – highly complex ▪ Level five – minimally complex ▪ Pay attention to comorbidities o 5. Resource Availibility ▪ Extent of resources the client/family/community bring to situation • Technical • Fiscal [Type here] [Type here] [Type here] [Document title] • Personal • Psychological • Social ▪ Support groups, outside help available ▪ Best resource: case management ▪ Arrange for home health, meals on wheels, dialysis in outpatient setting, etc. ▪ Level one - few resources ▪ Level five – good knowledge of resources [Type here] [Type here] [Type here] [Document title] o 5. Systems Thinking ▪ Body of knowledge & tools that allow the nurse to manage environmental & system resources available o 6. Responsiveness to Diversity ▪ Sensitivity to recognize, appreciate, & incorporate differences into provision of care. ▪ Difference may include: • Culture • Spiritual • Gender • Race • Ethnicity • Lifestyle • Socioeconomic status • Age • Values o 7. Facilitation of Learning ▪ Ability to facilitate learning for: • Clients/families • Nursing staff • Members of health care team • Community ▪ May include both informal & formal learning o 8. Clinical Inquiry/Evaluator ▪ Ongoing process of questioning & evaluating practice ▪ Creating practice changes through research utilization & experiential learning • The goal of nursing is to restore a client to an optimal level of wellness as defined by the client. [Type here] [Type here] [Type here] [Document title] PP 2/7 Cardiac Dysrhythmia: Review • Dysrhythmias o Disorder of the formation or conduction of the electrical impulse within the heart o Irregularity causes disturbances in: ▪ Heart Rate ▪ Heart Rhythm ▪ Both o Hemodynamic effects o Regular rate and rhythm required to circulate oxygenated blood and life- sustaining nutrients to body organs o Diagnosed by analyzing the electrocardiogram o Named according to site of origin o Asssessment with dysrhythmia: ▪ Chest pain, SOB, irregular HR on monitor, c/o dizziness, fatigue, N/V o Electrical conduction starts in SA node (in atrium), SA node is also the natural pacemaker of the heart • Normal Electrical Conduction • Review of Cardiac Conduction System SA Node Internod al Pathway s AV Junction, AV node, Bundle of His Bundle Branch es Purkinje Network Firing rate Transfer impulse Slows impulse Two main Spreads impulse throughout th of 60-100 from the SA node Intrinsic firing branches (left ventricles bpm throughout the rate of 40-60 and right) Intrinsic firing rate of 20-40 atria to the AV bpm transmit [Type here] [Type here] [Type here] [Document title] junction impulses to the ventricles *** If the pace is originating from other areas other than the SA node, be cautious with beta blockers & calcium channel blockers. [Type here] [Type here] [Type here] [Document title] ▪ Measured from the beginning of the P wave to the beginning of the QRS complex • Represents time needed for sinus node stimulation, atrial depolarization and conduction through the AV node ▪ 0.12-0.20 seconds in length o QRS Complex ▪ Represents ventricular depolarization • 1st negative deflection: Q wave • 1st positive deflection: R wave • 1st negative deflection after the R wave: ▪ S wave ▪ <0.12 seconds in length o ST Segment ▪ Represents early ventricular repolarization ▪ Lasts from the end of the QRS complex to the beginning of the T wave ▪ Normally isoelectric • Analyzed above or below the baseline o T Wave ▪ Represents ventricular muscle repolarization ▪ Resting phase ▪ Follows the QRS complex; usually in the same direction as the QRS ▪ HR 140s because the monitor is counting the elevated Q and the T each as a beat ▪ Lead 2? o General Rules in Identifying Heart Rhythms ▪ Rapid assessment of your patient first ▪ Read every strip from left to right, starting at the beginning of the strip ▪ Apply a systematic approach ▪ Avoid shortcuts and assumptions ▪ Ask and answer each question in the five-step approach…this is important for consistency! ▪ Assess the pt if something is off on the monitor before acting on a code blue o Systematic Analysis of the ECG ▪ Identify P wave: is there a p-wave before every QRS? ▪ Identify the P wave shape: consistent? Upright? ▪ Determine each PR interval: Consistent? Irregular but with a pattern? Irregular? ▪ Identify the QRS: Duration consistent? Shape consistent? ▪ Evaluate the ST segment: Isoelectric? Depression vs. Elevation? Peaked? ▪ Identify the T wave: Upright? Inverted? ▪ Identify ventricular rate and rhythm • No p coming from somewhere other than the atrium (consider a- flutter or a- fib) ▪ 30 boxes in a 6 second strip ▪ 1500/R to R ▪ Consider the ^ second strip, ignore the extra ▪ Atrial rate – look at p to p waves ▪ Ventricular rate – look at r to r [Type here] [Type here] [Type here] [Document title] ▪ [Type here] [Type here] [Type here] [Document title] o Heart Rate Determination ▪ Regular • 1- minute strip contains 300 large boxes (1500 small boxes) • Count number of small boxes within an RR interval and divide 1,500 by that number ▪ Irregular • Less accurate method: • Top of ECG paper is marked at 3-second intervals (15 large boxes horizontally) • Count the number of RR intervals (not QRS complexes) in 6- seconds and multiply that number by 10 ▪ RR interval used to determine ventricular rhythm ▪ PP interval used to determine atrial rhythm ▪ If intervals are the same: regular rhythm ▪ If intervals are different: irregular rhythm [Type here] [Type here] [Type here] [Document title] AA opne OS m8 Le * MXit pcr ‘Pees XS cbse] Z-5 evinded [Type here] [Type here] [Type here] o Atrial Flutter ▪ Conduction defect in the atrium ▪ Creates atrial rate between 250-400 times/minute (Ventricular rate 75-150) ▪ Not all impulses conducted to ventricle: therapeutic block at AV node ▪ 2:1, 3:1, 4:1 ▪ Flutters are coming at high rate ▪ Ratios: 1 are representing the QRS…. The number of flutters between determine what the first number in the ratio is ▪ Aflutter afib switching back and forth is possible ▪ ▪ Regular atrial activity ▪ P wave= “saw tooth” appearance ▪ HR > 100 bpm ▪ “uncontrolled” ▪ HR > 150 bpm ▪ “rapid ventricular rate” ▪ CAUSES: • COPD • Pulmonary HTN • Valvular disease • Thyrotoxicosis • Open heart surgery ▪ CLINICAL MANIFESTATIONS: • Clinical Manifestations: • Chest pain • Dyspnea • Hypotension ▪ Management: • Electrical Cardioversion for unstable patient • See treatment for atrial fibrillation • Medications to slow the ventricular response: o Beta blockers o Calcium channel blockers o Digitalis ▪ In the atrium, the blood is pooling causing SOB and increased risk for clotting ▪ Cardioversion- syncronize it with the heart (syncronized with the R) ▪ Try medication first before cardioversion (if pt is on long term anticoagulation therapy this increases the risk of complication of a cardioversion) ▪ Try amiodarone first, or CCC, or dig [Type here] [Type here] [Type here] [Document title] • Atrial Fibrillation o Rapid, disorganized and uncoordinated twitching of atrial muscle o Paroxysmal or chronic o Rapid ventricular response; loss of atrial kick (25-30% of cardiac output) [Type here] [Type here] [Type here] [Document title] ▪ CXR ▪ Exercise test ▪ Holter monitoring o As we age, the risk for delevopment of dysrhythmias increases o CXR could show enlarged heart or calcifications that could cause afib o Management of AFib ▪ Rhythm control vs. rate control ▪ Hemodynamically unstable? • Electrical cardioversion if < 48 hours • >48 hours: TEE to confirm mural wall thrombus. o If absent: Heparin prior to cardioversion o High risk of embolization of atrial thrombi if cardioverted if AF duration > 48 hours o Coumadin x 4 weeks after cardioversion o Amiodarone, Betapace, Rhythmol prior to cardioversion • Pharmacologic cardioversion o Tikosyn, Ibutelide= required patient hospitalization ▪ HR control ▪ Beta blocker • Contraindicated with bronchospasm ▪ Calcium channel blocker • Contraindicated with impaired ventricular function AV block ▪ IV amiodarone or digoxin ▪ Antithrombotic therapy indicated for all patients with A Fib ▪ Heparin therapy until INR therapeutic with Coumadin • Xarelto, Pradaxa o Premature Atrial Complex (PAC) ▪ Single, ECG complex occurs when an electrical impulse starts in the atrium before the next normal impulse of the sinus node ▪ Atrial bigeminy, trigeminy ▪ Interrupts the sinus rhythm ▪ Etiology: PACs • Caffeine • Alcohol [Type here] [Type here] [Type here] [Document title] • Nicotine • Anxiety • Hypokalemia • Stretched atrial myocardium (Hypovolemia) [Type here] [Type here] [Type here] [Document title] • Hypermetabolic states • Atrial ischemia, injury or infarction ▪ Clinical Manifestations: • “Skipped beat” • Etiology • Caffeine intake • Hypokalemia ▪ Management: • Treat the underlying cause • If infrequent: no treatment necessary • If > 6 per minute: treat underlying cause ▪ Cut down on caffeine intake o AV Nodal Re-entry Tachycardia (AVNRT) ▪ Impulse conducted in the AV node that causes the impulse to be rerouted back into the same area over and over again at a very fast rate ▪ Causes fast ventricular rate ▪ Abrupt onset and abrupt cessation ▪ QRS normal duration ▪ Atrial rate150-250 (P waves??) ▪ Ventricular rate 120-200 ▪ No P waves ▪ Once it says AV node– there will not be ▪ ▪ Etiology: AVNRT • Caffeine • Nicotine • Hypoxemia • Stress • Coronary artery disease • Cardiomyopathy ▪ Clinical Manifestations: • Reduced cardiac output • Restlessness • Chest pain • SOB • Pallor • Hypotension • Loss of consciousness ▪ Management: • Treatment aimed at breaking reentry of impulse [Type here] [Type here] [Type here] [Document title] o Vtach  deadly rhythm o o [Type here] [Type here] [Type here] [Document title] o PVCs ▪ More recent research shows that the following are NOT precursors to VT: ▪ More frequent than 6/minute ▪ Multifocal ▪ Occur two in a row ▪ Occur on the T wave ▪ p. 708 ▪ We become worried when we have more than 6 beats occuring… look closer at the patient ▪ PVC here and there  check the patient’s electrolytes (K+ low or high, Magnesium) ▪ Etiology of PVCs • Cardiac ischemia/infarction • Increased workload on the heart (heart failure/tachycardia) • Digitalis toxicity • Hypoxia • Acidosis • Electrolyte imbalance • Healthy people: caffeine, nicotine, alcohol • Reperfusion beats • When PVCs are grouped together (6 PVCs in one 6 second strip) runs of vtach • Heart is irritated (cardiac cath or CABG could result in PVCs) ▪ PVC Patterns • Ventricular Bigeminy o Occurs when every other beat is a PVC • Ventricular Trigeminy o Occurs when every third beat is a PVC • Ventricular Quadrigeminy o Occurs when every fourth beat is a PVC • Ventricular Couplets o Two PVC’s occurring together without a normal complex in between • Bigeminy: QRS.PVC.QRS.PVC.QRS.PVC • Trigeminy: QRS.PVC.QRS.QRS.PVC.QRS.QRS.PVC.QRS.QRS. • Quadreminy: QRS.QRS.QRS.PVC.QRS.QRS.QRS.PVC. ▪ Ventricular Bigeminy ▪ Ventricular Trigeminy [Type here] [Type here] [Type here] [Document title] ▪ Ventricular Quadrigeminy ▪ PVC Management • PVC’s are usually not serious • Frequent and persistent PVC’s may be treated with amiodarone or sotalol • Long-term therapy not usually indicated o Ventricular Tachycardia (VT) ▪ Three or more PVC’s in a row ▪ Rate exceeds >100 BPM ▪ Etiology • Same as PVC • At risk for Lethal VT • Larger AMI • Lower ejection fraction ▪ Characteristics • Ventricular rate: 100-200 BPM • QRS: Duration > 0.12, abnormal • P wave: difficult to detect [Type here] [Type here] [Type here] [Document title] ▪ IACD shock can occur anywhere ▪ Tx: magnesium for Torsades de point (top strip) o Ventricular Fibrillation ▪ Rapid, disorganized ventricular rhythm (>300 bpm) ▪ Causes ineffective quivering of ventricles ▪ No atrial activity [Type here] [Type here] [Type here] [Document title] ▪ Irregular and undulating waves without recognizable QRS complex ▪ Electrical impulses initiated by multiple sites ▪ Vfib will run until the heart gives up and you flatline ▪ ***** If vfib you dfib ▪ Print strips from vtach to flatline ▪ Etiology • Most common: CAD and resulting AMI • Untreated or unsuccessfully treated VT • Cardiomyopathy • Valvular heart disease • Pro-arrhythmic medications • Acid-base and electrolyte disorders • Electrical shock ▪ Clinical Manifestations: • Fatal dysrhythmia • Pulseless • Apneic • No coordinated cardiac activity • Cardiac arrest and death imminent if VF not corrected ▪ Management: • CPR until defibrillator arrives • Immediate Defibrillation • 5 cycles of CPR alternating with defibrillation • Epinephrine every 3-5 minutes • One dose of vasopressin instead of epinephrine • Anti-arrhythmic o Amiodarone o Lidocaine o Magnesium • Intubation/airway management ▪ You can not shock asystole  do CPR ▪ If you are going to give vasopressin (one time dose), don’t give epi ▪ Push epi first for a few doses, then try vasopressin in place of the next dose of epi. If pressin doesn’t work then continue with pushing epi ▪ Airway  need intubation (nurse for CPR, nurse for document, nurse for meds, doctor and respiratory at bedside) ▪ VF Management • Hypothermia protocol o Mild hypothermia in comatose adults (32-34 °C) [Type here] [Type here] [Type here] [Document title] o Induction started as soon as circulation is restored o Maintained 12-24 hours • Nursing Management [Type here] [Type here] [Type here] [Document title] o General information ▪ Identify underlying rhythm ▪ Assess PR interval • AV blocks occur when the conduction through the AV nodal or His bundle is decreased or stopped) o Medications (CCB, BB) o Myocardial ischemia/infarction o Cardiomyopathy o Increased vagal tone • Block in conduction system, tend to be problematic as we age • If the blockers are causing the heart block, stop the blockers and inform the doctor o Clinical Manifestations ▪ Vary with resulting ventricular rate and severity of underlying disease process • Asymptomatic • Hemodynamic instability o Decreased perfusion to vital organs (brain, heart, kidneys, lungs, skin) o Treat the patient not the monitor o Treatment base don hemodynamic effect of the rhythm • Usually pts are asymptomatic with first degree, and second degree type one o Classification of AV Blocks ▪ First-degree AV block ▪ Second-degree AV block Type I (Wenckebach) ▪ Second-degree AV block Type II ▪ Third-degree AV block • Symptomatic for second degree type II and third degree o First Degree AV Block ▪ Occurs when all atrial impulses are conducted thorough the AV node into the ventricles ▪ Rate is slower than normal ▪ P wave is in front of the QRS ▪ PR interval • > 0.20 seconds • PR interval is constant ▪ PR interval is prolonged ▪ Do not get fooled thinking it is sinus rhythm. You need to measure PR interval!!! ▪ If the PR interval is 0.24 it will be uniform throughout the strip ▪ P to P is regular and so is R to R [Type here] [Type here] [Type here] [Document title] o Second Degree AV Block Type I (Wenckebach) ▪ Repeating pattern in which all but one of a series of atrial impulses are conducted through the AV node into the ventricles ▪ Each atrial impulse takes a longer time for conduction than the one before [Type here] [Type here] [Type here] [Document title] ▪ Finally, one impulse is blocked ▪ P wave • In front of the QRS ▪ PR interval • PR interval becomes longer with each succeeding ECG complex until there is a P wave not followed by QRS ▪ QRS: normal or abnormal • Winkybach • PR interval is becomes progressively longer as the strip then it DROPS then it starts over and gets longer progressively again • *Longer, longer, longer, drop, then you have a winkybach* • WHEN YOU HAVE A DROP  it causes an irregular R to R o Second Degree VA Block Type II ▪ Only some of the atrial impulses are conducted through eh AV node into the ventricle ▪ P wave: in front of the QRS ▪ PR interval • PR interval is constant for those p waves just before the QRS ▪ QRS: normal or abnormal ▪ PR intervals are still prolonged, but they are equal throughout the strip until you drop one ▪ Same, same, same, drop, same same drop ▪ You don’t know when the drop is coming, making it more dangerous than Second Degree Type I ▪ P to P is regular [Type here] [Type here] [Type here] [Document title] o Deficient knowledge o Nursing Interventions: ▪ Evaluate BP, pulse, rhythm ▪ Evaluate rate and depth of respirations ▪ Auscultate breath sounds ▪ Assess for syncope, dizziness [Type here] [Type here] [Type here] [Document title] ▪ Obtain 12-lead ECG ▪ Medication administration ▪ Assess for factors which contribute to dysrhythmia ▪ Minimize anxiety, provide assurance ▪ Maximizes self-management ▪ Empathy o Collaborative Problems/potention complications ▪ Cardiac arrest ▪ Heart failure ▪ Thromboembolic event, especially with atrial fibrillation • Electricity: Pacemaker, Cardioversion, and Defibrillation o ****** o SA node o Then AV node (in the 50s without medications) o Cardioversion and Defibrillation ▪ Used to treat tachydysrhythmia ▪ Delivers an electrical current that depolarizes a critical mass of myocardial cells ▪ When cells repolarize; the SA node is usually able to recapture its role as heart’s pacemaker ▪ Cardioversion – synchronized, pt is already in some type of rhythm that is causing decreased cardiac output (SOB, dizziness, decreased perfusion, syncope, hypoTN). Try to fix with medications first but if the patient is symptomatic and the meds aren’t working, cardioversion may occur. Cardioversion acts like a pacemaker and syncs with the pt’s rhythm. Shocks patient right at the R. The electricity is a lot less than that of defibrillation. ▪ Defibrillation  in v-fib then SHOCK, if in v-tach see if they have a pulse first! o Defibrillator Technology ▪ Used for cardioversion and defibrillation ▪ Electrical current delivered through the skin ▪ AED ▪ Safety measures • Good contact must be maintained between pads and patient skin • No one is to be in contact with the patient or with anything touching the patient when the defibrillator is discharged • See chart 26-5, p. 716 • With pacer pads you do not need gel • If you are going to shock the pt and it is not an emergency  medicate them with versed o Electricity ▪ Cardioversion • Delivery of “timed” electrical current • Synchronized with the ECG to impulse is discharged during ventricular depolarization (QRS complex) • Sedation required if elective [Type here] [Type here] [Type here] [Document title] • ABC monitoring ▪ Defibrillation • Treatment of choice for V-fib and pulseless V-tach • Not used for patients who are conscious or with a pulse • Medications utilized to make it easier to convert: o Epinephrine/Vasopressin [Type here] [Type here] [Type here] [Document title] o Dilated cardiomyopathy o Symptomatic, refractory A Fib [Type here] [Type here] [Type here] [Document title] ▪ Nursing interventions and complications similar to pacemaker insertion • Depends on the rhythm the patient has and what rhythms they will go into • Settings: after 4 runs of vtach shock! Or 6 beats o Assessment ▪ Device function; ECG ▪ Cardiac output and hemodynamic stability ▪ Incision site ▪ Coping ▪ Patient and family knowledge o Diagnosis ▪ Risk for infection ▪ Risk for ineffective coping ▪ Knowledge deficit o Goals ▪ Goals include absence of infection, adherence to self-care program, effective coping, and maintenance of device function. [Type here] [Type here] [Type here] [Document title] PP 4/ 7 Hemodynamic Monitoring • Hemodynamic Monitoring o Critically ill patient require continuous assessment of the cardiovascular system to diagnose and manage medical conditions o Achieved via direct pressure monitoring systems ▪ Central venous pressure (CVP ▪ Pulmonary artery pressure (PAP) ▪ Intra-arterial blood pressure (Arterial line) o Nursing care ▪ Ensure system is set up and maintained properly ▪ Ensure stopcock is at level of atrium before measurements obtained ▪ Establish zero reference point o Measures BP inside the vein, heart, arteries, measure blood flow and oxygen concentration in the blood, MOST accurate way of monitoring your patient o Watch the tubing, monitor for infection • Complications o Uncommon o Pneumothorax o Infection ▪ See care bundle, page 687 o Air embolism o Do not give meds through arterial line! • What does HM measure: o Hemodynamic monitoring measures: ▪ Heart chamber pressures ▪ Cardiac output ▪ Preload ▪ Afterload ▪ Contractility o PRELOAD: o AFTERLOAD: • Cardiac Output o = Stroke Volume * HR o CO ▪ Total amount of blood ejected by the ventricle in liters per minute ▪ Resting adult: 4-6L/min ▪ Varies based on metabolic need o Stroke Volume ▪ Total amount of blood ejected by the ventricle per heartbeat ▪ Resting adult: 60-130 mL o Varies based on patients metabolic need • Effects of HR on CO o CO responds to changes in metabolic demands of tissues associated with stress, physical exercise, illness [Type here] [Type here] [Type here] [Document title] o Afterload ▪ Resistance to ejection of blood from the ventricle ▪ Resistance to left ventricular ejection: Systemic vascular resistance (SVR) ▪ Resistance to right ventricular ejection: pulmonary vascular resistance (PVR) Increased Afterload Decreased Afterload Afterload is increased due to arterial vasoconstriction Afterload is decreased due to arterial vasodilation Leads to decreased stroke volume Leads to increased stroke volume • Increased resistance to ejection • Decreased resistance to ejection • Contractility: the force generated by the contracting myocardium o Enhanced Contractility o Reduced Contractility o Circulating catecholamine's o Hypoxia o Increased sympathetic activity o Acidosis o Medications o Digoxin o Dopamine o Dobutamine o o Medication s Beta blockers • • Types of Monitoring Devices o CENTRAL VENOUS PRESSURE (CVP) MONITORING ▪ Measurement of the pressure in the vena cava or right atrium ▪ Vena cava, right atrium and right ventricle pressures are all equal at the end of diastole; thus, CVP also reflects right ventricle pressure= Measures right ventricular PRELOAD ▪ Normal CVP= 2-6 mm Hg ▪ Catheter is positioned in the right atrium ▪ Most valuable when monitored over time o CVP >6 mm Hg o CVP < 2 mm Hg o Hypervolemia o Right heart failure o Hypovolemia ▪ Evaluating venous return to the heart or right sided filling pressure ▪ Measures pressure (in VC or RA or RV) and volume ▪ CVP > 6 = patient has too much volume or is in RSHF ▪ CVP < 2 = patient has very low volume [Type here] [Type here] [Type here] [Document title] ▪ RSHF symptoms ▪ LSHF symptoms ▪ CVP of 8 ➔ diuretic ▪ CVP 1 ➔ fluid replacement or blood transfusion, medications ▪ Pts with cardiac tamponade  you will see an increase in CVP, drain the fluid [Type here] [Type here] [Type here] [Document title] ▪ Restrictive pericarditis – get inflam down with antibiotics or nsaids ▪ Pulmonary HTN ▪ Give albumin with low CVPs o Phlebostatic Axis: Left Atrium ▪ ▪ Where the RA is located typically ???? o PULMONARY ARTERY PRESSURE (PAP) MONITORING ▪ Used in critical care to assess • Left ventricular function • Diagnose the etiology of shock • Evaluate response to interventions ▪ Balloon tipped, flow-directed catheters with multiple lumens ▪ May include specialty functions: cardiac pacing, oximetry, cardiac output measurements ▪ Used temporarily for cardiac pacing, measures cardiac output directly ▪ Proximal lumen opens to RA, could give meds and monitor CVP ▪ Distal lumen monitors pressure of the Pulmonary arteries ▪ Enables measurement of: • Right atrial pressure= 0-8 mm Hg • Pulmonary artery systolic pressure= 15-25 mm Hg • Pulmonary artery diastolic pressure= 8-15 mm Hg • Pulmonary artery wedge pressure ( Measures left ventricular PRELOAD)= 4- 12 mm Hg ▪ See page 656, figure 25-2 [Type here] [Type here] [Type here] [Document title] ▪ A- line o Dis section o Air embolism o Pain o Arteriospasm o Infection ▪ Pull ABGs from here ▪ NEED TO KNOW: what to monitor for ▪ You will bleed out faster than a venous line ▪ You do not give medications in an a line, however, there is a heparin solution in that line to keep it open! [Type here] [Type here] [Type here] [Document title] PP 5/ 7 Acute Coronary Syndrome and Myocardial Infarction o Emergent situation: acute onset of myocardia ischemia resulting in myocardia death if no intervention o Unstable angina and acute myocardial infarction (AMI) are considered to be the same process but different points along a continuum o Take second nitro and call 911 • Spectrum of ACS o Unstable Angina ▪ (USA) o Non-ST elevation myocardial infarction ▪ (NSTEMI) o ST elevation myocardial infarction ▪ (STEMI) o From the door you have 5 min to do EKG o Biomarkers don’t change (troponin, CK-MB) for unstable angina o Non ST elevation  no ST change but noticeable biomarker changes o St Elevation  ST change and biomarker change!!! o Troponin  cardiac specific o Myoglobin  cardiac specific o CK-MB is Cardiac SPECIFIC o CK is not CS o CRP (C Reactive Protein), very non specific but it will show if an inflammatory response is occurring in response to damage to the heart o No EKG changes -- .troponin can be non specific in renal patients (can be increased in renal patients) • Pathophysiology of ACS/MI o USA ▪ Reduced blood flow in a coronary artery ▪ Partial occlusion of an artery ▪ Atherosclerosis/plaque rupture o M I ▪ area of the myocardium is permanently destroyed ▪ Plaque rupture, thrombus formation ▪ Complete occlusion ▪ Ischemia and necrosis of myocardium supplied by artery o Vasospasm ▪ Sudden constriction or narrowing of a coronary artery ▪ Decreased oxygen supply ▪ Increased demand for oxygen o Decreased oxygen supply ▪ Etiology • Acute blood loss • Anemia [Type here] [Type here] [Type here] [Document title] • Low blood pressure o Increased oxygen demand ▪ Etiology [Type here] [Type here] [Type here] [Document title] ▪ Skin o U pper abdominal  get EKG (especially with diabetes/neuropathy) o EKG vomiting  ST elevation o ABC • Cool • Clammy • Diaphoretic • Pale or dusky ▪ Neurologic • Anxiety • Restlessness • Syncope • Headache • Changes in levels of consciousness • Dizziness • Lightheaded ▪ ***Do not confuse anxiety with chest pain ▪ If you can’t breath  you will be anxious ▪ If you have chest pain  you will be anxious ▪ All of these symptoms are from decreased CO ▪ Psychological • Fear • Impending doom • Denial ▪ They feel like they’re going to die with impending doom ▪ Bowel movement of death  from pressure build up ▪ Fear talk to patients and calm them down o Diagnostic Findings ▪ Presenting symptoms and assessment/HPI ▪ 12-lead ECG findings ▪ Laboratory results o Electrocardiogram ▪ Should be obtained within 10 minutes from time patient reports pain or arrives in ED ▪ “Time is Muscle”; changes evolve (evolution of MI) ▪ Serial ECG: evolution of MI ▪ Classic ECG changes • T-wave inversion • ST-segment elevation • Development of abnormal Q waves o Can be a non-q wave MI ▪ T wave inversion • Ischemia causes delay in myocardial repolarization, causing T wave to invert [Type here] [Type here] [Type here] [Document title] [Type here] [Type here] [Type here] [Document title] o ▪ ST Segment Elevation • Injured myocardial cells repolarize more rapidly than normal cells, causing ST segment to elevate at least 1 mm above the isoelectric line ▪ ^^^^Tomb stoning  pt needs IMMEDIATE intervention o Evolution of EKG Changes ▪ o Abnormal Q Waves ▪ Develops in 1-3 days ▪ Does not exist before the event ▪ c/p “Pain started about a week ago “ • Laboratory Assessment [Type here] [Type here] [Type here] [Document title] ▪ Point in time within process • Acute • Evolving [Type here] [Type here] [Type here] [Document title] • Old ▪ T wave inversion can be old or it can indicate ischemia ▪ **** KNOW^^tells us what part of the heart is being affected based on conduction ▪ Drug users often have enlarged, hypertrophic left ventricles o Medical Management ▪ Goal • Minimize myocardial damage • Preserve myocardial function • Prevent complications ▪ Goal Achieved via: • Emergency use of Thrombolytic Medications • PTCA for reperfusion • Reduction of myocardial oxygen demand • Increasing myocardial oxygen supply ▪ TPA ▪ Give thrombolytic ▪ PTCA  percutaneous transluminal coronary angioplasty or arteriogram ▪ The wall surrounding the area is weakened, requires a stent to be placed to [Type here] [Type here] [Type here] [Document title] reinforced o Goal Achieved [Type here] [Type here] [Type here] [Document title] • Lopressor, Toprol, Atenolol o ACE Inhibitors ▪ Prevent conversion of angiotensin from I to II ▪ In absence of angiotensin II; • BP decreases • Kidneys excrete sodium and fluid • Decreases oxygen demand of the heart ▪ Post-MI • Decreases mortality rate • Prevents the onset of heart failure ▪ Monitor potassium, creatinine, sodium, BP, U/O o Calcium Channel Blockers ▪ Negative inotropic effect ▪ Indicated in patients not responsive to beta-blocker ▪ Used as primary treatment for vasospasm • Norvasc • Cardizem • Plendil o Treatment Guidelines ▪ Evaluate for indications for reperfusion therapy • PTCI • Thrombolytics Continue therapy • IV heparin/LMWH • Plavix • GP IIb/IIIa inhibitor • Bed rest (12-24 hours) o Antiplatelet Medication ▪ Aspirin ▪ Plavix ▪ Glycoprotein IIb/IIIa • Reo-pro • Aggrastat • Integrilin ▪ Prevention of platelet aggregation o Anticoagulation ▪ Unfractionated heparin ▪ LMWH ▪ Platelet-inhibiting agents • Prevents further clot formation ▪ Lovenox ▪ Heparin • Surgical Interventions (will be discussed later in SG) [Type here] [Type here] [Type here] [Document title] o Thrombolytic Therapy ▪ Thrombolytic agents open the artery by lysis of the thrombus in the coronary artery (Activase, r-PA, TNKase) • Thrombolysis • Reperfusion • Minimize the size of the infarction • Preserve ventricular function • Doesn’t effect the underlying atherosclerotic lesion • Dissolves ALL clots in the body • **First-line therapy in facilities that lack resources to perform PCI ▪ Thrombolytic  clot buster, at risk for bleeding or emboli 9risk for stroke, worsening MI in another location) ▪ Works throughout the body, non specific due to circulation o Contraindications to Thrombolytic Therapy ▪ Active, internal bleeding ▪ Surgery, trauma or bleeding within 2 months ▪ Bleeding disorder ▪ Previous hemorrhagic stroke/AVM ▪ Severe, uncontrolled HTN ▪ Pregnancy o Thrombolytic Inclusion Criteria ▪ Chest pain for > 20 minutes, unrelieved by NTG ▪ ST segment elevation in at least two leads ▪ < 6 hours from onset of pain ▪ “Door-to-Needle Time” • 30 minutes o Nursing Considerations ▪ Minimize punctures ▪ Avoid IM ▪ Start IV lines prior to therapy ▪ Avoid NIBP ▪ Monitor for dysrhythmias/ hypo-tension ▪ Monitor for reperfusion ▪ Monitor s/s of bleeding • H/H • Oozing, back pain • Changes in LOC [Type here] [Type here] [Type here] [Document title] • Headache ▪ Avoid taking BP in the arm that the thrombolytic was administered in ▪ You may see reperfusion dysrhythmias [Type here] [Type here] [Type here] [Document title] PP 6/ 7 Acute Pulmonary Edema Congestive Heart Failure • Pulmonary Edema: definition o Abnormal accumulation of fluid in the interstitial spaces and alveoli of the lung ▪ Life-threatening condition ▪ Associated with acute decompensated HF o Cardinal sign  pink, frothy sputum o Pulmonary edema o 1. Complications of heart and lungs (pulmonary pressure building up secondary to cardiac dysfunction) • Pathophysiology of Acute Pulmonary Edema o Results from left ventricular failure ▪ AMI or acute exacerbation of CHF ▪ Non- cardiac disorders (renal failure) o Left ventricle fails => blood backs up into left atrium=> Rapid increase in atrial pressure=> increased pulmonary venous pressure=> interstitial edema o “flash pulmonary edema” o Fluids are backing up into the lungs, then backs up into right sided, then you would see JVD, ascites in abdomen, and lower extremity edema • Fluid within the alveoli creates a diffusion block: severely limits gas exchange [Type here] [Type here] [Type here] [Document title] • Clinical Manifestations o Decreased cerebral oxygenation ▪ Confusion, anxious, restless→stuporous o Sudden dyspnea o Sense of suffocation o Cold, moist, pale o Weak, rapid pulse o Cyanosis/ashen (Skin/nail beds) o Neck vein distention o Cough o Things that could cause pulm edema (non-cardiac) Opiate users/overdose (heart pumps very fast, could be vtach, CO decreased), Inhalation of irritated gas, rapid administration of IV fluids (especially elderly), o CHF typically elderly (heart starts slowing down at 65 and older), but could be younger o Lasix in between blood transfusions o Head injury can end up with neurologic pulm edema o Older people are at risk for decreased CO and heart failure o Pt complains that they are sufficating, the pt is actually drowning in their fluid o If restless  check o2 right away o Risk Factors: [Type here] [Type here] [Type here] [Document title] o Acute MI  blockage of the heart, pressures, are building, pulm emboli could form o Fluid volume overload o HTN o Valvular Heart Disease (mitral valve o Left sided HF [Type here] [Type here] [Type here] [Document title] o Airway  may require suction o Position in high fowlers o Dangle feet o Monitor oxygenation o May want non rebreather or even bipap or intubation o Monitor urine output o Oxygen Therapy ▪ Relieve hypoxemia and dyspnea ▪ NRB ▪ NIPPV ▪ Endotracheal intubation ▪ Mechanical ventilation o Diuretics ▪ Loop diuretic (IV) ▪ BP monitoring ▪ U/O monitoring ▪ I/O ▪ Daily weights ▪ Electrolytes ▪ Minimum 30 ccs per hour is ideal, but if they only put out 30 mls of urine in 2 hours call the doc ▪ Pt puts out 300 mls  • Medical and Nursing management o Vasodilators ▪ IV nitroglycerin ▪ IV nitroprusside ▪ Monitor BP ▪ Morphine; no longer recommended (increased need for mechanical ventilation, Increase LOS, increased mortality) o Nursing Management ▪ Upright ▪ Legs dangling ▪ Psychological support ▪ Monitoring medications o Vasodilators decrease preload and afterload, and will decrease BP o Nitro  tell someone your patient is on nitro (POTENT) • Nursing management o Assisting with intubation o Administer oxygen/monitor hypoxia o Administer and monitor response to medication ▪ I/O ▪ VS ▪ N/V ▪ EKG monitoring ▪ Electrolytes o Position to promote optimal circulation [Type here] [Type here] [Type here] [Document title] o Provide psychological support [Type here] [Type here] [Type here] [Document title] [Type here] [Type here] [Type here] [Document title] o One year post drug-eluting ▪ Stent is used as a first tx before open heart ▪ Those who go to open heart typically have a failed stent first ▪ They will clot again if noncompliant with antiplatelet clopidogrel (PLAVIX) 600mg loading dose of plavix immediately after stent placement ▪ Complications • Coronary artery dissection, perforation • Abrupt closure • Vasospasm • Acute MI • Acute dysrhythmias, cardiac arrest • Bleeding at insertion site • Hematoma • Acute kidney injury o PTCA Post Procedure Care ▪ Emergent (ACS): admit to ICU ▪ IV Heparin or thrombin inhibitor • GP IIb/IIIa ▪ Hemostasis achieved with • Angio-seal • Femostop • C-shaped clamps ▪ aPtt testing ▪ Flat in bed ▪ Affected leg straight until sheaths removed and then post-removal ▪ Vasovagal ▪ Analgesics/sedation ▪ Restart Heparin if high risk for re-occlusion ▪ Monitor site for hematoma ▪ Ambulatory after procedure • Pull out sheath when ACT (measures clotting time) is under 150  use a strip to test the blood, takes about 3 min • Shealth is in groin, shealth may be removed in the cath lab & then angio-seal is placed (square white gauze to assist with clotting) • Femostop  You can tighten it over pt groin, progressive loosen it (start at 20, then decrease in increments of 2 or 3) [Type here] [Type here] [Type here] [Document title] • Have to chart the time that hemostatis was achieved (aka bleeding stopped, note absence of hemotoma, & presence of pulses) • Use leg immoblizer [Type here] [Type here] [Type here] [Document title] • Once shealth is removed, BP can drop and they can brady down, make sur e you have at least 500 ml of NS and atropine at bed side. Ensure they have a working IV. • Ambu bag, suction, albumin, atropine (in CVICU) • HEPARIN  PTT • Post Cath Ambulation: First pt goes up to chair then they can walk after • Coronary Artery Revascularization o Indications for Surgical Intervention: CABG ▪ Alleviation of angina not controlled with meds or PCI ▪ Treatment of left main coronary artery stenosis or multi-vessel CAD ▪ Prevention/treatment of MI, heart failure, dysrhythmias ▪ Complications from unsuccessful PCI ▪ >70% occlusion ▪ Other • LV dysfunction • Number of disease coronary vessels • Signs/symptoms • Previous treatment ▪ Multiple vessel block ▪ If vessel (LAD for example) is 90% blocked, they may bypass a cath and skip to open heart o CABG ▪ Most common type of cardiac surgery ▪ Most common type of surgery for older adults [Type here] [Type here] [Type here] [Document title] ▪ Pain medication will be readily available o Prophylactic antibiotic 20-30 minutes pre-op o Teach them incentive spirometer o Inform they will be on ventilator • CABG: Intraoperative Management o Perioperative nursing responsibilities [Type here] [Type here] [Type here] [Document title] o Monitor for intraoperative complications o Bleeding- biggest complication in CABG. Units of blood usually given o Blood bank has 4 units packed on hold • CABG: Post-operative Nursing Process (Chart 27-13 Plan of Care) o Neurologic status o Cardiac status o Respiratory status o Peripheral vascular status o Renal function o Fluid and electrolyte status o Pain o Equipment o Stroke is major concern directly to CVICU from OR Weaned off ventilator o ABGs are performed to ensure they can be weaned of o On cardiac monitor, look at strips, rhythm, watch if pt goes into afib (at increased risk for afib) o Standing order for amiodarone in ICU typically o Monitor urine output, Cr, and BUN o F&E= K+, Mag, Na, Calcium o PAIN is major concern as well o Fentanyl, morphine, versed given IV until extubated, PO percocet after o Oxygen, suctioning for chest tubes, ambu bag, ventilator, check blood sugar (sx disturbs metabolic function) o BS q hour 150 and below is typically goal, Insulin drip may be administered • Potential Complications of Cardiac Surgery (Table 27-5) o Preload alterations o Persistent bleeding o Cardiac tamponade o Hypovolemia ▪ Hypotension ▪ Low CO o Increased afterload o F & E disturbances o Impaired gas exchange o Impaired cerebral circulation o Fluid overload o Hypertension o Cardiac failure o AMI [Type here] [Type here] [Type here] [Document title] o AKI o Stroke o Hepatic failure ▪ Persistent bleeding  watch chest tubes (>100/hr is concerning because we may need to transfuse) **** ▪ Cardiac tamponade can happen is BP maintains at a very high level (listen to doctor’s threshold for BP, otherwise tamponade may occur) ▪ Hypovolemia  give fluid or pressor (dopamine) [Type here] [Type here] [Type here] [Document title] therapy o * one of the most effective medications for controlling supraventricular and ventricular dysrhythmias o AE: pulmonary toxicity, photosensitivity, interaction with digoxin and warfarin [Type here] [Type here] [Type here] [Document title] ▪ Dig level will increase by 50% ▪ INR will increase by 50% ▪ Therefore reduce dig or warfarin dose by 50% when on amiodarone o Interactions: grapefruit juice o ASSESS: respiratory, thyroid (due to lipophilic properties), hepatic, dermatologic, and or HTN conditions o Encourage high fiber/fluid diet to prevent constipation and GI upset o Immediately report blue/grey discoloration of the skin (often after a year) and jaundice • B blockers o Adrenergic blocking (compete with epi and norepi) o Cardioselective BB are on the surface of the heart therefor they reduce myocardial stimulation ( decrease HR and slows conduction through AV node) o Nonselective BB block glycogenesis therefore can delay recovery from hypoglycemia OR can impede the secretion of insulin leading to increase blood glucose levels o *Esmolol is a short acting BB indicated for acute situations of rapid but temporary control of ventricular rate in patients with SVT o *Antidysrhythmic specific information: ▪ reduce SA node activity ▪ reduce ventricular contraction rate ▪ reduce CO and BP ▪ decrease automaticity o INDICATIONS: SV dysrhythmias and ventricular dysrhythmias o AE: could cause bradycardia, AV block, heart failure and changes in blood glucose levels • Ca Channel Blockers o Antihypertensive agents o Also Class IV Antidysrhythmics o MoA: cause smooth muscle relaxation by blocking the binding of calcium to its receptors (preventing muscle contraction) o Results: decreased peripheral SM tone, decreases systemic vascular resistance, decreased BP o IND: angina, HTN, dysrhythmias, migraine headaches, and Raynauds disease o SPECIFIC INDICTATIONS: Paroxysmal SVT and rate control for afib and aflutter o *diltiazem (Cardizem)  prevents afib o AE: hypotension, palpitations, tachycardia, constipation, peripheral edema, could cause heart block • Digoxin o Cardiac glycosides  have beneficial effects on the heart and control ventricular response to afib o MOA: positive inotropic effect, * negative chronotropic and dromotropic effects [Type here] [Type here] [Type here] [Document title] o Therapeutic level 0.5-2.0 o Low potassium (<3.5) increased digoxin’s toxicity levels (low magnesium does as well) o *Tell pt to report if they feel like their heart is racing o Effects: increase stroke volume, decrease venous BP, increase coronary circulation o Contraindications: allergy, second or third degree heart blocks, vfib, and heart failure resulting from diastolic dysfunction o ** Digoxin augments cholinergic stimulation via vagus nerve resulting in increased diastolic filling between heart beats secondary to reduced HR • Adenosine [Type here] [Type here] [Type here] [Document title]