Cardiovascular Nursing Part II

1. Cardiovascular NursingPart II Welcome Back to the Heart of Nursing!Welcome Back to the Heart of Nursing!

2. Code Teams – respond specifically to patients who have arrested. Rapid Response teams – Created to reduce inpatient mortality rates for preventable deaths from cardiac arrest. System failures typically contribute to these mortality rates: Failure in planning (assessments, tx., goals) Failure in communication (staff to staff or staff to MD) Failure to recognize the warning signs of patient instability Failure related to handoffs Similar to code teams but are different, nurse led versus physician led. SBAR Situation Background Assessment Recommendations Centers of Excellence - Organizations may seek certification for clinical programs for virtually any chronic disease or condition. Primary Stroke Centers – JCAHO can certify hospitals that make exceptional measures to improve patient outcomes and survival rates Magnet Status - Developed by the ANA to recognize healthcare organizations committed to nursing excellence. There are 14 qualities that hospitals are evaluated on and must maintain even after achieving this high honor Core Measures – we will look at these specifically when we discuss MI’s and CHF Clinical practice guidelines for management of specified disease processes. Guidelines are based on: Research Expert opinion Standards of Care National Patient Safety Goals Established by JCAHO (accrediting body for hospitals and other organizations) Reviewed/Revised annually by JCAHO Organizations accredited by JCAHO must adhere to these goals This years goals are listed in your course syllabusCode Teams – respond specifically to patients who have arrested. Rapid Response teams – Created to reduce inpatient mortality rates for preventable deaths from cardiac arrest. System failures typically contribute to these mortality rates: Failure in planning (assessments, tx., goals) Failure in communication (staff to staff or staff to MD) Failure to recognize the warning signs of patient instability Failure related to handoffs Similar to code teams but are different, nurse led versus physician led. SBAR Situation Background Assessment Recommendations Centers of Excellence - Organizations may seek certification for clinical programs for virtually any chronic disease or condition. Primary Stroke Centers – JCAHO can certify hospitals that make exceptional measures to improve patient outcomes and survival rates Magnet Status - Developed by the ANA to recognize healthcare organizations committed to nursing excellence. There are 14 qualities that hospitals are evaluated on and must maintain even after achieving this high honor Core Measures – we will look at these specifically when we discuss MI’s and CHF Clinical practice guidelines for management of specified disease processes. Guidelines are based on: Research Expert opinion Standards of Care National Patient Safety Goals Established by JCAHO (accrediting body for hospitals and other organizations) Reviewed/Revised annually by JCAHO Organizations accredited by JCAHO must adhere to these goals This years goals are listed in your course syllabus

3. V-O-M-I-T V= Vital Signs O = Oxygen M = Monitor I = IV Access T = Treatment I want you to think about this acronym when approaching patient assessment and treatment Vital Signs Touch the patient (Hands-on) Take vital signs Pay attention to pulse pressure Also includes looking at their med list, current labs and x-ray reports Oxygen Administer O2 at 2 liters NC Monitor Put them on a bedside monitor Evaluate heart rhythm IV access Get a patent site Draw labs and send them off for Stat analysis Call primary or the most appropriate M.D. with all of the information Treatment Based on standing protocols or M.D. ordersI want you to think about this acronym when approaching patient assessment and treatment Vital Signs Touch the patient (Hands-on) Take vital signs Pay attention to pulse pressure Also includes looking at their med list, current labs and x-ray reports Oxygen Administer O2 at 2 liters NC Monitor Put them on a bedside monitor Evaluate heart rhythm IV access Get a patent site Draw labs and send them off for Stat analysis Call primary or the most appropriate M.D. with all of the information Treatment Based on standing protocols or M.D. orders

5. CV Disease Risk Factors Smoking Metabolic Syndrome* Sedentary lifestyle, obesity Diabetes HTN Hyperlipidemia Diet, drugs Anger, stress, depression Genetics Gender depending on age Age Modifiable vs. Non-Modifiable Metabolic syndrome – term indicating group of risk factors that are connected: obesity, HTN, Diabetes, ? cholesterol, ? TriglyceridesModifiable vs. Non-Modifiable Metabolic syndrome – term indicating group of risk factors that are connected: obesity, HTN, Diabetes, ? cholesterol, ? Triglycerides

6. Coronary Artery Disease Inflammatory disorder: Atherosclerosis main cause R/T: Endothelial injury from Inflammatory response- (strongest theory) Low density lipoproteins (LDL) and growth factor from platelet aggregation prevent repair of endothelium Many things can cause injury to endothelial lining. These are what we refer to as Risk Factors: Modifiable Non ModifiableMany things can cause injury to endothelial lining. These are what we refer to as Risk Factors: Modifiable Non Modifiable

7. Big 4 Modifiable Risk Factors Elevated serum lipids (?LDL, ? HDL) Hypertension Cigarette smoking ( other) Physical Inactivity Diabetes - partially modifiable Cholesterol > 200 B/P > 140/90 Cigarettes – The more you smoke. The greater your risk Diabetes - leading cause of CAD todayCholesterol > 200 B/P > 140/90 Cigarettes – The more you smoke. The greater your risk Diabetes - leading cause of CAD today

8. CAD mortality drops to non-smoker level in 12 months! 12 months after smoking cessation, the risk level drops to that of a non-smoker! Nicotine in the smoke causes release of epinephrine/Norepinephrine ?HR ?B/P Peripheral vasoconstriction ?Platelet aggregation Others at risk: Exposure to second hand smoke Non-inhaling pipe & cigar smokers Pipe & Cigar smokers who do not inhale have an ? Risk for CAD like those who are exposed to second-hand smoke12 months after smoking cessation, the risk level drops to that of a non-smoker! Nicotine in the smoke causes release of epinephrine/Norepinephrine ?HR ?B/P Peripheral vasoconstriction ?Platelet aggregation Others at risk: Exposure to second hand smoke Non-inhaling pipe & cigar smokers Pipe & Cigar smokers who do not inhale have an ? Risk for CAD like those who are exposed to second-hand smoke

9. Benefits of physical exercise ? HDL Levels ? fibrinolytic activity ? oxygen perfusion to muscles Goal = 30 minutes 5X/Week Need to sweat ?HR 30-50 beats/minute Encourages development of collateral circulation

10. Cardiology and Gender Heart Disease use to be considered a “Man’s Disease” Heart disease kills 10 times more women than breast cancer Symptoms are more like angina, sometimes very vague Higher mortality rate one year after an MI than men More likely to have re-infarction in one year Diabetes most single powerful predictor of CAD in women Have a higher mortality rate post CABG (probably because they are older, smaller arteries Estrogen replacement does not reduce risk of CAD Smoking linked to increase in estrogen levels and early menopause Smoking most powerful contributor to heart disease for women <50. Women need close observation for complications post MI and CABGHeart Disease use to be considered a “Man’s Disease” Heart disease kills 10 times more women than breast cancer Symptoms are more like angina, sometimes very vague Higher mortality rate one year after an MI than men More likely to have re-infarction in one year Diabetes most single powerful predictor of CAD in women Have a higher mortality rate post CABG (probably because they are older, smaller arteries Estrogen replacement does not reduce risk of CAD Smoking linked to increase in estrogen levels and early menopause Smoking most powerful contributor to heart disease for women <50. Women need close observation for complications post MI and CABG

11. Un-Modifiable Risk Factors Diabetes (partially un-modifiable!) Age Gender Family hx Heredity- Familial hypercholesterolemia Diabetes is the leading cause of CAD todayDiabetes is the leading cause of CAD today

12. Lipid Control Lipid panel every 5 years Treat serum cholesterol > 200 mg/dl LDL >160 Treatment consist of: Dietary modifications & exercise Resins (Questran), Fibrins( Tricor, Lopid), Statins (Zocor, Lipitor, Crestor, pravachol), ( Zetia) Lipid Lowering agent as well Treatment for elevated cholesterol levels consist of: Decreased dietary fat and cholesterol ? caloric intake if overweight Re-check cholesterol levels in 6 weeks, if little change in cholesterol levels: Consider alternative therapies: Niacin, garlic, Omega-3 fatty acids, phytosterols found in nuts, seeds, soybeans, Red yeast rice, soy Consider drug therapy Review the categories of cholesterol meds as discussed in detail in Part I and your textbook Fibrins – inhibits triglyceride synthesis Statins: inhibit synthesis of cholesterol Side Note: Increased cholesterol could be due to Hypothyroidism Treatment for elevated cholesterol levels consist of: Decreased dietary fat and cholesterol ? caloric intake if overweight Re-check cholesterol levels in 6 weeks, if little change in cholesterol levels: Consider alternative therapies: Niacin, garlic, Omega-3 fatty acids, phytosterols found in nuts, seeds, soybeans, Red yeast rice, soy Consider drug therapy Review the categories of cholesterol meds as discussed in detail in Part I and your textbook Fibrins – inhibits triglyceride synthesis Statins: inhibit synthesis of cholesterol Side Note: Increased cholesterol could be due to Hypothyroidism

13. Hypertension > 140 SBP and/or > 90 DBP over extended period of time Stress from continual elevated B/P-?rate of atherosclerotic development Atherosclerosis causes narrowed arteries, requiring more force to pump blood = ?B/P Cardiac implications = CAD, LVH, Heart Failure, Atrial hypertrophy, PVD SVR = Systemic Vascular Resistance Resistance to the flow of blood in the vessel ? B/P causes endotheilial injury which leads to inflammation = atherosclerosisSVR = Systemic Vascular Resistance Resistance to the flow of blood in the vessel ? B/P causes endotheilial injury which leads to inflammation = atherosclerosis

14. Patient Teaching: Focus on Monitor & control blood glucose levels B/P control Reduction of cholesterol & Triglycerides Eliminate all tobacco products Physical exercise Manage stressful situations Maintain appropriate body weight Table 34-3

15. Clinical Manifestations of  CAD/ACS Angina Pectoris Stable/Unstable Angina Silent Ischemia Prinzmetals’ Angina Nocturnal Angina Myocardial Infarction WE are going to look at the S/S of Angina versus an MI Prinzmetals Angina Typically Occurs at rest Due to coronary artery spasm Seen in people with migraine headaches and Raynaud’s phenomenon Not associated with increased physical demand Can resolve on it’s own, quickly, short bursts Treated with calcium channel blockers like Nifedipine (Procardia) Silent Ischemia Absence of symptoms Seen more in diabetics due to neuropathy affecting nerves of the CV systemWE are going to look at the S/S of Angina versus an MI Prinzmetals Angina Typically Occurs at rest Due to coronary artery spasm Seen in people with migraine headaches and Raynaud’s phenomenon Not associated with increased physical demand Can resolve on it’s own, quickly, short bursts Treated with calcium channel blockers like Nifedipine (Procardia) Silent Ischemia Absence of symptoms Seen more in diabetics due to neuropathy affecting nerves of the CV system

16. Angina Supply vs. Demand Ischemia is limited and does not cause permanent damage ECG may or may not show changes CPK--MB will be negative Rest and Nitroglycerin should alleviate Pain is usually less than 5 minutes A temporary imbalance between the coronary arteries’ ability to supply oxygen and the cardiac muscle’s demand for oxygen Read slideA temporary imbalance between the coronary arteries’ ability to supply oxygen and the cardiac muscle’s demand for oxygen Read slide

17. Stable vs. Unstable Angina Stable: widespread, irregular disease in the coronary arteries Fixed Obstruction Usually occurs with activity Sufficient blood gets through when the heart slows down and rests Intermittent and sometimes predictable May have ST segment depression Unstable: caused by sudden interruption of blood flow Occurs at rest, asleep, or activity Stable angina results from a fixed obstruction of blood flow to the heart. Not enough blood for an ?HR , but sufficient blood can get through when the heart slows down and the individual is at rest. Stable angina = widespread, throughout the coronary arteries. The blockages that result may not seriously hinder the flow of blood, and they usually do not damage the heart unless a plaque (atheroma; fatty deposit within a blood vessel) suddenly ruptures. Unstable angina = sudden interruption of blood flow to the heart due to a partial or complete blockage of the artery. Occurs at rest, asleep, or during physical exertion Symptoms may become more frequent or increase in intensity. Stable angina results from a fixed obstruction of blood flow to the heart. Not enough blood for an ?HR , but sufficient blood can get through when the heart slows down and the individual is at rest. Stable angina = widespread, throughout the coronary arteries. The blockages that result may not seriously hinder the flow of blood, and they usually do not damage the heart unless a plaque (atheroma; fatty deposit within a blood vessel) suddenly ruptures. Unstable angina = sudden interruption of blood flow to the heart due to a partial or complete blockage of the artery. Occurs at rest, asleep, or during physical exertion Symptoms may become more frequent or increase in intensity.

18. Characteristics of Angina Vague pressure, ache, heaviness or tightness. Does not change with breathing or position May be anxious, a sense that someth9ing is wrong, sweating, nauseous, SOB or fatigued. Usually relieved with NTG. ST Segment Depression Read slide Women: more vague symptoms: Nausea Malice Indigestion PQRST= P= precipitating event Q = Quality of pain R = Radiation of pain S = Severity of Pain T = Timing, when and what were you doing when pain occurred Table – 33-10 Body compensates by building collateral circulation over timeRead slide Women: more vague symptoms: Nausea Malice Indigestion PQRST= P= precipitating event Q = Quality of pain R = Radiation of pain S = Severity of Pain T = Timing, when and what were you doing when pain occurred Table – 33-10 Body compensates by building collateral circulation over time

19. Collateral Circulation

20. Treatment Goal = ? O2 consumption Control the HR = ? Initial Therapeutic intervention Includes: Apply oxygen at 2 liters N/C ? Coronary Blood Flow Nitrates: Nitro SL, Nitro paste, Nitro Spray Controls pain, anxiety Additional Treatment includes: Anti-platelet therapy = ASA for stable Angina Plavix for Unstable Angina Can reduce progression to an MI Beta blockers, - preferred drug for chronic stable angina ACE Inhibitors - B/P control and ?Ventricular Remodeling PCI PTCA/stent CABG Decrease oxygen consumption = get the heart rate down or controlled Control pain with Nitrates Give ASA – Drug of choice to reduce progression of unstable angina to an MI Review of Beta-Adrenergic Blockers = ?HR, ?B/P, ?SVR, ?contractility = ?oxygen demand of the heart Controls arrhythmias, decrease severity and frequency of anginal attacks Reduces the workload of the heart Used for prevention of MI’s Percutaneous Transluminal Coronary Angioplasty Percutaneous Coronary Intervention Ventricular Remodeling - refers to decline in the functioning of the ventricle that is related to the size, shape and function. Future treatment - will consist of attacking platelet aggregation on 3 levels. Therefore expect treatment to include all three: ASA Persantine Coumadin Decrease oxygen consumption = get the heart rate down or controlled Control pain with Nitrates Give ASA – Drug of choice to reduce progression of unstable angina to an MI Review of Beta-Adrenergic Blockers = ?HR, ?B/P, ?SVR, ?contractility = ?oxygen demand of the heart Controls arrhythmias, decrease severity and frequency of anginal attacks Reduces the workload of the heart Used for prevention of MI’s Percutaneous Transluminal Coronary Angioplasty Percutaneous Coronary Intervention Ventricular Remodeling - refers to decline in the functioning of the ventricle that is related to the size, shape and function. Future treatment - will consist of attacking platelet aggregation on 3 levels. Therefore expect treatment to include all three: ASA Persantine Coumadin

21. Nitroglycerin SL (Nitrostat) Keep in brown bottle (sensitive to light) Keep away from heat Including body heat ( keep out of pants pocket) Destroys the medication Good for 6 months Instruct patient: Should have tingling sensation May have Headache – can take tylenol May feel increase in HR Should take effect within 3 minutes and last up to 30 minutes Caution to rise slowly – causes Orthostatic Hypotension Place one under tongue – allow to dissolve if no relief within 3-5 minutes call 911 May also be used prophalactally prior to sexual activity Contraindicated when sexual enhancement drugs like Viagra have been used within 24 hours. Tingling sensation should occur, this indicates the drug has not lost it’s potency Nitro paste or patches should be removed for an 8-hour period due to tolerance build-upContraindicated when sexual enhancement drugs like Viagra have been used within 24 hours. Tingling sensation should occur, this indicates the drug has not lost it’s potency Nitro paste or patches should be removed for an 8-hour period due to tolerance build-up

22. Myocardial Infarction

23. Myocardial Infarction Myocardial tissue is abruptly and severely deprived of oxygen Ischemia develops when blood flow is reduced by > 80--90 % Ischemia is not reversed Tissue necrosis occurs Described by the area of the heart affected: Anterior Inferior Lateral Posterior Anterolateral Anteroseptal Subendocardial MI Area of infarct is determined by 12-Lead EKG ECG placement and monitoring is extremely important and valuable when assessing/determining the cause of chest pain! Ischemia can last 20 minutes before cardiac necrosis develops The Subendocardium becomes ischemic first Takes 4-6 hours for the entire thickness of the heart muscle to become damaged (necrotic)Area of infarct is determined by 12-Lead EKG ECG placement and monitoring is extremely important and valuable when assessing/determining the cause of chest pain! Ischemia can last 20 minutes before cardiac necrosis develops The Subendocardium becomes ischemic first Takes 4-6 hours for the entire thickness of the heart muscle to become damaged (necrotic)

24. Clinical manifestations Pain/Pressure, not relieved by rest or nitro SL Nausea, vomiting Diaphoresis Vasoconstriction of peripheral nerves, BP/HR changes Fever due to necrosis of tissue Can start within 24 hours and last 7 days ST elevation of > 1mm in two or more leads Elevated cardiac markers ( CKMB, Troponin, BNP, Myoglobin ) Pain/Pressure = mid sternal, radiating pain to the jaw or L. arm, L. Shoulder, both arms, Epigastric, neck and jaw pain, Intrascapular BP/HR increase initially then decrease due to decrease in CO Urine Output may decrease later Crackles in lungs for several days Additional heart sounds (S3,S4) Myoglobin More sensitive than CK isoenzymes but not as specific Increased levels occurring within 3 hours indicate cardiac injuryPain/Pressure = mid sternal, radiating pain to the jaw or L. arm, L. Shoulder, both arms, Epigastric, neck and jaw pain, Intrascapular BP/HR increase initially then decrease due to decrease in CO Urine Output may decrease later Crackles in lungs for several days Additional heart sounds (S3,S4) Myoglobin More sensitive than CK isoenzymes but not as specific Increased levels occurring within 3 hours indicate cardiac injury

25. Premature Ventricular Contraction Arrhythmias are most common complications of an MI The more heart tissue damaged, the greater the irritability of the conduction system (due to lack of O2). leading to > of PVC’s which can trigger…. VTArrhythmias are most common complications of an MI The more heart tissue damaged, the greater the irritability of the conduction system (due to lack of O2). leading to > of PVC’s which can trigger…. VT

26. Ventricular Tachycardia Life-Threatening, Heart not perfusing Stable versus unstable Stable requires antiarrhythmics, sedation and synchronized cardioversion Pulsesless VT: CPR for 2 minutes Defibrillate, CPR x 2 min. Epinephrine or (Vasopressin only once) Defibrillate, CPR x 2 min Amiodarone or Lidocaine Defibrillate, CPR x 2 min. Continue sequenceLife-Threatening, Heart not perfusing Stable versus unstable Stable requires antiarrhythmics, sedation and synchronized cardioversion Pulsesless VT: CPR for 2 minutes Defibrillate, CPR x 2 min. Epinephrine or (Vasopressin only once) Defibrillate, CPR x 2 min Amiodarone or Lidocaine Defibrillate, CPR x 2 min. Continue sequence

27. Multi focal PVC’s Multiple areas of the heart are irritated and firing Medication treatment – Lidocaine or Amiodarone –IV Bolus followed by dripMultiple areas of the heart are irritated and firing Medication treatment – Lidocaine or Amiodarone –IV Bolus followed by drip

28. Very Bad! Ventricular Tachycardia and Fibrillation Heart not perfusing V-Fib same as pulseless v-tach V-Fib unwitnessed, 2 minutes of CPR then defibrillate, want to establish circulation to perfuse heartVery Bad! Ventricular Tachycardia and Fibrillation Heart not perfusing V-Fib same as pulseless v-tach V-Fib unwitnessed, 2 minutes of CPR then defibrillate, want to establish circulation to perfuse heart

29. Initial Treatment for AMI Goal = Reduce the size of the infarct Remember = VOMIT Monitor for arrhythmias--number one complication of MI Oxygen, Aspirin, Nitroglycerin, Morphine, Beta blockers, MONA plus Beta Blocker (ACLS) Lab tests = Enzymes - CPK, Triponins EKG--12 lead/15 lead Reperfusion: Fibrinolytic Therapy if no access to cath lab Cardiac Cath w/ PTCA/Stent - 90 minutes *NEW EBP* = Hypothermia as endorsed by the AHA (ANA, 2007) “Time is muscle and Muscle is life” ACLS treatment: Mona + Beta Blocker Pt may need other meds like: anti-anxiety (Xanax), anti-arrhythmic, ACE inhibitors What does morphine do? Decreases pre-load and after load = increased CO Decrease anxiety Watch giving morphine when diastolic is low = ? mortality 15 Lead EKG’s – add a V4R, V8, V9 – increases the likely hood of detecting a posterior wall MI, and a R. Ventricular wall MI Fibrinolytics: Streptokinase Urokinase Reteplase Goal is to transport patient to the cardiac cath lab within 90 minutes of ED arrival Hypothermia: Cardiac Arrest with return of spontaneous circulation within 1-4 hours VT or VF Persistent coma Use cooling blankets tah can be easily monitored and controlled Cool between 32° and 34° C (89.6° to 93.2° Keep cool between 12-24 hours Rewarm the patient slowly 0.5° to 1.0° per hour “Time is muscle and Muscle is life” ACLS treatment: Mona + Beta Blocker Pt may need other meds like: anti-anxiety (Xanax), anti-arrhythmic, ACE inhibitors What does morphine do? Decreases pre-load and after load = increased CO Decrease anxiety Watch giving morphine when diastolic is low = ? mortality 15 Lead EKG’s – add a V4R, V8, V9 – increases the likely hood of detecting a posterior wall MI, and a R. Ventricular wall MI Fibrinolytics: Streptokinase Urokinase Reteplase Goal is to transport patient to the cardiac cath lab within 90 minutes of ED arrival Hypothermia: Cardiac Arrest with return of spontaneous circulation within 1-4 hours VT or VF Persistent coma Use cooling blankets tah can be easily monitored and controlled Cool between 32° and 34° C (89.6° to 93.2° Keep cool between 12-24 hours Rewarm the patient slowly 0.5° to 1.0° per hour

30. Treatment (cont’d) Bed rest up to 48 hours – depends on severity ( usually allow BSC) Up to chair within 12-24 hours – depends on severity Supervised OOB and ambulation activity Hospital stay (uncomplicated) 3-5 days Discharge teaching: activity based on how pt. feels, S/S of angina & MI, medication therapy, sexual activity (7-10 days – 2 flights of stairs), return to work depends on occupation, quit smoking Cardiac Rehab (AMI) & Mended Hearts (CABG) Takes 6 weeks for heart to heal (scar tissue replaces necrosis) Table 34-21

31. Patient Tracking Scenario Emergency Department RN Assigned 3 patient rooms and one empty room One hour into your shift you receive a patient from the waiting room who is complaining of chest pain. Let’s discuss how you will respond when the patient lays down on your stretcher. This discussion will include your responsibilities as a critical thinking RN and the reasons behind your actions! If you are listening to this lecture only as a podcast or you are only viewing these PowerPoint's, stop and take a few minutes to write down what you would do. Feel free to discuss with me your response to this activity in order to validate the correct steps involved. If you are listening to this lecture only as a podcast or you are only viewing these PowerPoint's, stop and take a few minutes to write down what you would do. Feel free to discuss with me your response to this activity in order to validate the correct steps involved.

32. Complications of MI Arrhythmias Congestive Heart Failure Cardiogenic Shock Papillary Muscle dysfunction Ventricular aneurysm Pericarditis Dressler Syndrome Pulmonary Embolism Cardiogenic Shock: Cardiogenic Shock = heart unable to pump enough blood to organs and tissues Only 20% of patients survive 5% to 10% of MI patients will experience cardiogenic shock within 48 hours S&S: tachycardic, hypotension, narrowed pulse pressure, tachypneic, crackles from pulmonary congestion, arrhythmias Life-threatening, needs immediate intervention to increase oxygen to the body Drugs to increase contractility, reduce fluid overload to lungs, decrease oxygen consumption Papillary Muscle dysfunction Cause mitral valve regurgitation, valve can rupture requiring immediate management and surgery Ventricular Anerysm Rupture Thrombi Arrythmias LV dysfunction Pericarditis Inflammation of pericardium Can be heard as friction rub Can occur 2-3 days after an MI Chest pain aggravated by inspiration May be relieved by sitting forward Pain is different than an MI Fever Friction rub ST Segment elevation in all 12 Leads Tx. ASA, corticosteroids or nonsteroidal anti-inflammatory drugs Dressler Syndrome Pericarditis with effusion and fever 1-4 weeks post MI/CABG Pulmonary Embolus Thrombous to the lung Prolonged bed rest Arrhythmias Pt C/O Dyspnea, anxiousness, and chest painCardiogenic Shock: Cardiogenic Shock = heart unable to pump enough blood to organs and tissues Only 20% of patients survive 5% to 10% of MI patients will experience cardiogenic shock within 48 hours S&S: tachycardic, hypotension, narrowed pulse pressure, tachypneic, crackles from pulmonary congestion, arrhythmias Life-threatening, needs immediate intervention to increase oxygen to the body Drugs to increase contractility, reduce fluid overload to lungs, decrease oxygen consumption Papillary Muscle dysfunction Cause mitral valve regurgitation, valve can rupture requiring immediate management and surgery Ventricular Anerysm Rupture Thrombi Arrythmias LV dysfunction Pericarditis Inflammation of pericardium Can be heard as friction rub Can occur 2-3 days after an MI Chest pain aggravated by inspiration May be relieved by sitting forward Pain is different than an MI Fever Friction rub ST Segment elevation in all 12 Leads Tx. ASA, corticosteroids or nonsteroidal anti-inflammatory drugs Dressler Syndrome Pericarditis with effusion and fever 1-4 weeks post MI/CABG Pulmonary Embolus Thrombous to the lung Prolonged bed rest Arrhythmias Pt C/O Dyspnea, anxiousness, and chest pain

33. Myocardial Injury/Infarction ST abnormalities signify acute process ST segment returns to baseline over time Q wave associated with ST elevation indicates acute or recent injury Non-q wave or ST depression may indicate sub-endocardial injury

34. Myocardial Necrosis 1mm wide or 1/3 amplitude of QRS complex Q waves may be permanent; check other criteria to determine if infarction is old or acute Q wave can indicate an MI past or present New MI must be evaluated by current S&S, diagnostics and labQ wave can indicate an MI past or present New MI must be evaluated by current S&S, diagnostics and lab

35. Anterior Infarction -picture FYI – Not tested on this Occlusions related to LAD Clinical Sign = TachycardiaFYI – Not tested on this Occlusions related to LAD Clinical Sign = Tachycardia

36. Inferior Infarction - picture FYI – Not tested on this Occlusions related to RCA Typical symptoms = Bradycardia and N/VFYI – Not tested on this Occlusions related to RCA Typical symptoms = Bradycardia and N/V

37. Lateral Wall Infarction - picture FYI – Not tested on this Occlusions related to Left Circumflex artery I, AVL - High Lateral V5, V6 - Low LateralFYI – Not tested on this Occlusions related to Left Circumflex artery I, AVL - High Lateral V5, V6 - Low Lateral

38. Nursing Considerations Nursing Considerations for Your patients: Pain Tissue perfusion Cardiac Output Anxiety/depression Activity intolerance related to tissue perfusion Lack of knowledge Refer to Cardiac Rehab Phase I – inpatient educational program Phase II Outpatient – Closely monitored exercise program (usually 12 weeks) Phase III Outpatient Exercise program (Supervision provided, but typically not cardiac monitored with telemetry) Nursing Considerations for Your patients: Pain Tissue perfusion Cardiac Output Anxiety/depression Activity intolerance related to tissue perfusion Lack of knowledge Refer to Cardiac Rehab Phase I – inpatient educational program Phase II Outpatient – Closely monitored exercise program (usually 12 weeks) Phase III Outpatient Exercise program (Supervision provided, but typically not cardiac monitored with telemetry)

39. Acute Coronary Syndrome (ACS) Umbrella term that encompasses: Unstable angina Myocardial Infarction which may or may not have elevated ST segment (NSTEMI vs. STEMI) Goes from a stable to unstable atherosclerotic plaque rupture cover any group of clinical symptoms compatible with acute myocardial ischemia.  Acute myocardial ischemia is chest pain due to insufficient blood supply to the heart muscle that resulting from coronary artery disease (also called coronary heart disease) symptoms of acute myocardial ischemia may or may not have an elevated ST elevation Acute coronary syndrome covers clinical conditions from unstable angina to non-Q-wave myocardial infarction and Q-wave myocardial infarction cover any group of clinical symptoms compatible with acute myocardial ischemia.  Acute myocardial ischemia is chest pain due to insufficient blood supply to the heart muscle that resulting from coronary artery disease (also called coronary heart disease) symptoms of acute myocardial ischemia may or may not have an elevated ST elevation Acute coronary syndrome covers clinical conditions from unstable angina to non-Q-wave myocardial infarction and Q-wave myocardial infarction

40. Care Plan Practice Generate 3 Nursing diagnosis and at least 3 interventions for each diagnosis. Be Specific with your goals and interventions Do this for the patient with: Angina MI/ACS Pain R/T MI & decreased myocardial O2 supply AEB… Chest pain, pressure or tightness, radiation of pain Ineffective Tissue Perfusion R/T MI AEB… ? B/P, HR, peripheral edema, SOB, oliguria, arrhythmias Anxiety Risk for decreased Cardiac output R/T Myocardial tissue damage AEB… List Goals & Interventions for each Chapter 34 Case Study = MI/ACS – Handout on projector #1 AnimationPain R/T MI & decreased myocardial O2 supply AEB… Chest pain, pressure or tightness, radiation of pain Ineffective Tissue Perfusion R/T MI AEB… ? B/P, HR, peripheral edema, SOB, oliguria, arrhythmias Anxiety Risk for decreased Cardiac output R/T Myocardial tissue damage AEB… List Goals & Interventions for each Chapter 34 Case Study = MI/ACS – Handout on projector #1 Animation

41. AMI Core Measures Reperfusion Therapy (PTCA/Stent, Fibrinolytics) ASA within 24 hours of arrival to hospital ASA at discharge Beta-Blockers at discharge unless contraindicated ACE Inhibitor at discharge for LVF or EF < 40% unless contraindicated Lipid Control = Statin Smoking cessation education Not tested on this material Need to be aware of this info., because you will want to make sure your patient is receiving care based on EBP.Not tested on this material Need to be aware of this info., because you will want to make sure your patient is receiving care based on EBP.

42. Heart Failure Definition of HF is evolving as to what actually causes it. Most common causes: CAD, LV Infarct, Ischemic cardiomyopathy Has many etiologies but nursing care is similar for all patients recognizing early symptoms is essential in preventing mortality and permanent disability This is becoming a specialization in medicine - HF CardiologistDefinition of HF is evolving as to what actually causes it. Most common causes: CAD, LV Infarct, Ischemic cardiomyopathy Has many etiologies but nursing care is similar for all patients recognizing early symptoms is essential in preventing mortality and permanent disability This is becoming a specialization in medicine - HF Cardiologist

44. Heart Failure Inability of the heart to pump sufficient blood to meet the demands of the body Systolic or Diastolic failure or mixed Can occur rapidly or over time without notice Can be divided into left or right ventricular failure Most common cause is CAD and Myocardial Infarction Not a disease Characterized by a variety of symptoms associated with CV diseases CAD & ? age are the primary risk factors Major causes can be grouped into primary & precipitating causes Table 35-1 & 35-2Not a disease Characterized by a variety of symptoms associated with CV diseases CAD & ? age are the primary risk factors Major causes can be grouped into primary & precipitating causes Table 35-1 & 35-2

45. Heart Failure Society

46. Grading Heart Failure NYHA Class I No limitation Class II slight limitation Class III Marked limitation Class IV Inability to carry on any physical activity without discomfort AHA Stage A Stage B Stage C Stage D Class 2:No symptoms at rest, fatigue/dyspnea with activity Class 3: Mainly comfortable at rest, increased limitation of activity Class 4: All physical activity causes discomfort, even at restClass 2:No symptoms at rest, fatigue/dyspnea with activity Class 3: Mainly comfortable at rest, increased limitation of activity Class 4: All physical activity causes discomfort, even at rest

47. Left Ventricular Failure(most common) Signs and Symptoms: Tachycardia (early sign) Exertional and nocturnal dyspnea Orthopnea Dry Cough Nocturia Crackles in the lungs? Pulmonary Edema S3 and S4 heart sounds ? HR (early sign) PMI displaced Fatigue Mental Confusion Table 35-3 Blood backs up through the left atrium and into the pulmonary veins Signs are pulmonary congestion and edema Orthopnea = SOB while lying down (defined by the number of pillows one has to prop up on) Exertional – SOB with activity Nocturnal – SOB while sleeping ( wakes up panic stricken, feelings of suffocation) S3 sound - occurs because new blood dumping into venticle with blood still left in it - so it splashes, making the S3 sound S4 sound - occurs from stiff ventricle Blood backs up through the left atrium and into the pulmonary veins Signs are pulmonary congestion and edema Orthopnea = SOB while lying down (defined by the number of pillows one has to prop up on) Exertional – SOB with activity Nocturnal – SOB while sleeping ( wakes up panic stricken, feelings of suffocation) S3 sound - occurs because new blood dumping into venticle with blood still left in it - so it splashes, making the S3 sound S4 sound - occurs from stiff ventricle

48. Right Ventricular Failure Tachycardia (early sign) By itself usually from pulmonary disease Most often occur 2nd-ary to Left Heart Failure Ascites, GI Disorders (nausea), abd. pain Liver and Spleen engorgement JVD Dependent bilateral edema Weight Gain Murmurs Anxiety Anorexia Nocturia Fatigue Blood backs up through the right atrium, causing venous congestion Usually cause of right sided failure is left sided failure Cor pulmonale - RV dilation and hypertrophy Almost any disorder that affects the respiratory system can cause this. Anasarca – extreme generalized body edema Both types can cause chest pain due to ? CO = ? perfusionBlood backs up through the right atrium, causing venous congestion Usually cause of right sided failure is left sided failure Cor pulmonale - RV dilation and hypertrophy Almost any disorder that affects the respiratory system can cause this. Anasarca – extreme generalized body edema Both types can cause chest pain due to ? CO = ? perfusion

49. Jugular Vein Distention (JVD)

50. Diagnostics of Acute Heart Failure CXR EKG MUGA Scan ECHO Pressure monitoring catheters PA Catheter Swan-Ganz Arterial line; SBP, DBP, MAP Muga Scan – A nuclear scan that evaluates the pumping action of the Ventricles ECHO These tests can determine the EF = amount of blood ejected by the ventricle (normal > 50%) Pulmonary artery catheter ( Swan-Ganz), determines fluid volume status and end-diastolic pressure Muga Scan – A nuclear scan that evaluates the pumping action of the Ventricles ECHO These tests can determine the EF = amount of blood ejected by the ventricle (normal > 50%) Pulmonary artery catheter ( Swan-Ganz), determines fluid volume status and end-diastolic pressure

51. MUGA SCAN Nuclear Study Evaluates the structure and the function of the heart Can specifically evaluate the function of the left ventricle ( useful in CHF)Nuclear Study Evaluates the structure and the function of the heart Can specifically evaluate the function of the left ventricle ( useful in CHF)

52. MUGA SCAN Images

53. Goals & Treatment of HF ? Gas exchange/oxygenation ? Cardiac Function ? Preload ? Afterload ? Anxiety

54. Treatment of Heart Failure Preload = Low Sodium Diet (Refer to Table 35-11 & 13) 500 - 2500 mg/day Preload = Daily Weights > 3 lbs. within 2 days should be reported to MD/ARNP Preload = Fluid Restrictions typically reserved for Class III & IV patients Strict I & O records Assess for depression Assess for family or social support Cardiac Rehab for some Stop Smoking Medication & diet adherence teaching ?Gas Exchange = Oxygen Reference: Cunningham, C. (2006). Managing hospitalized patients with heart failure. American Nurse Today, 1, 44-50. Expect a test question regarding low sodium food choices (hint, hint) Goals ? patient symptoms ? quality of life ? mortality & morbityReference: Cunningham, C. (2006). Managing hospitalized patients with heart failure. American Nurse Today, 1, 44-50. Expect a test question regarding low sodium food choices (hint, hint) Goals ? patient symptoms ? quality of life ? mortality & morbity

55. CHF Treatment (cont’d.) CF = ACE inhibitors * ? CO Preload = Diuretics *, NTG, Vasodilators Potassium-sparing Diuretics and ACE Inhibitors both spare potassium. Pts. Taking both types of meds are at risk for Hyperkalemia Afterload = Vasodilators, ACE Inhibitors CF = Cardiac Glycosides--Digoxin = Inotropics/Adrenergics--Dopamine, Dobutamine Beta Blockers (Coreg is best) and ARB Afterload, Preload, anxiety = Morphine Preload = Position patient to ? Venous return Horizontal in bed or dangling at bedside Gas = Rest-activity Circulatory assist devices – VAD Cardiac Transplantation Diuretics – reduce venous return, which decreases blood going to the LV, therefore the LV contracts more efficiently without the over volume of blood Vasodilators - Reduce preload (Natrecor) - used cautiously especially in renal pts. Can cause decrease in b/p and mental confusion Dosage = 2mcg/kg/min Nipride Reduces pre-load (Volume – venous return) and afterload (Arterial resistance) of the heart ACE Inhibitors - Reduce Afterload (amount of wall tension the LV has to develop [amount of work] to eject blood into the aorta Now considered the main drug of choice for chronic HF. & newly diagnosied CHF post MI Cardiac Glycosides - increase contractility of the heart. Cause increased O2 consumption, not good for HF patients Only used for chronic CHF if other meds are insuffcient Morphine – reduces preload and afterload, by dilating pulmonary and systemic blood vessels Improves exchange of gases Reduces anxiety How will you know if the drug therapy has been effective??? Increase in actiivty tolerance (ADL’s) Decrease in patient symptoms Diuretics – reduce venous return, which decreases blood going to the LV, therefore the LV contracts more efficiently without the over volume of blood Vasodilators - Reduce preload (Natrecor) - used cautiously especially in renal pts. Can cause decrease in b/p and mental confusion Dosage = 2mcg/kg/min Nipride Reduces pre-load (Volume – venous return) and afterload (Arterial resistance) of the heart ACE Inhibitors - Reduce Afterload (amount of wall tension the LV has to develop [amount of work] to eject blood into the aorta Now considered the main drug of choice for chronic HF. & newly diagnosied CHF post MI Cardiac Glycosides - increase contractility of the heart. Cause increased O2 consumption, not good for HF patients Only used for chronic CHF if other meds are insuffcient Morphine – reduces preload and afterload, by dilating pulmonary and systemic blood vessels Improves exchange of gases Reduces anxiety How will you know if the drug therapy has been effective??? Increase in actiivty tolerance (ADL’s) Decrease in patient symptoms

56. CHF Core Measures Documentation of Heart Failure education by nursing or case management ACE Inhibitor for patients with LVF or EF < 40% unless contraindicated Prior to discharge - LV Assessment by Nuclear Medicine, Echo or Cardiac Cath unless a valid documented reason why the assessment was not obtained. Smoking cessation education Table 35-8

57. Heart Failure Complications Pleural Effusion Arrhythmias Thrombus Pulmonary Edema Hepatomegaly Renal Failure Effusion – fluid shifts from the capillaries into the pleural space between the pleura Arrhythmias may occur when tissue has been stretched, which can cause a change in the electrical conduction system Thrombus – increase in fluid in the chambers, and chambers not emptying correctly because they are enlarged and engorged, blood clot can occur Anticoagulation is recommended with EF less than 20% and if patient is in A-Fib Liver becomes engorged with blood that has backed up, leading to impaired function – can develop to cirrhosis Renal Failure due to ? CO causes ? Kidney perfusionEffusion – fluid shifts from the capillaries into the pleural space between the pleura Arrhythmias may occur when tissue has been stretched, which can cause a change in the electrical conduction system Thrombus – increase in fluid in the chambers, and chambers not emptying correctly because they are enlarged and engorged, blood clot can occur Anticoagulation is recommended with EF less than 20% and if patient is in A-Fib Liver becomes engorged with blood that has backed up, leading to impaired function – can develop to cirrhosis Renal Failure due to ? CO causes ? Kidney perfusion

58. Pleural Effusion

59. CXR – Pleural Effusion

60. Arrhythmias - Atrial Fibrillation A-fib decreases CO by 10%-20% If patient does not convert back to NSR within 24-48 hours medication administration will be required. Drugs – Initially Heparin bolus, followed by heparin drip, D/C after APTT is in therapeutic range of 46-71 (LRMC guidelines) Coumadin – requires therapeutic INR range of 2.0-3.0 prior to discharge IF rapid rate: Cardizem/Diltiazem, or Amiodarone/Cordarone (Antiarrhythmics – Calcium Channel Blocker/inhibits adrenergic stimulation CardioversionA-fib decreases CO by 10%-20% If patient does not convert back to NSR within 24-48 hours medication administration will be required. Drugs – Initially Heparin bolus, followed by heparin drip, D/C after APTT is in therapeutic range of 46-71 (LRMC guidelines) Coumadin – requires therapeutic INR range of 2.0-3.0 prior to discharge IF rapid rate: Cardizem/Diltiazem, or Amiodarone/Cordarone (Antiarrhythmics – Calcium Channel Blocker/inhibits adrenergic stimulation Cardioversion

61. Arrhythmias - Atrial Flutter Another complicationAnother complication

62. Pulmonary Edema Results from Left Heart Failure Signs and Symptoms: Severe dyspnea Pink, blood tinged, frothy sputum Crackles, wheezes, rhonchi Anxiety Pale/clammy/cold skin Tachypnea > 30 Increased Heart rate Acute life-threatening state Alveoli become filled with serosanguineous fluid Read slideAcute life-threatening state Alveoli become filled with serosanguineous fluid Read slide

63. CXR picture

64. Picture- fluid shift Fluid shift from the capillaries into the interstitial space and into the alveoliFluid shift from the capillaries into the interstitial space and into the alveoli

65. Treatment of Pulmonary Edema Oxygen Morphine in small doses Diuretics with Potassium supplementation Nitrates High Fowler’s position C-PaP Possible endotracheal intubation with ventilator assistance

66. Nursing Care Plan Considerations Gas Exchange Fluid Balance Anxiety Activity Knowledge Deficit Impaired Gas Exchange R/T increase in preload Fluid Volume Excess R/T CHF or pulmonary edema Anxiety R/T SOB Activity Intolerance R/T fluid volume overload Knowledge Deficit R/T new diagnosis or repeated admissionsImpaired Gas Exchange R/T increase in preload Fluid Volume Excess R/T CHF or pulmonary edema Anxiety R/T SOB Activity Intolerance R/T fluid volume overload Knowledge Deficit R/T new diagnosis or repeated admissions

67. Discharge Teaching Focus re: CHF Understand the cause Progressive disease Patient controls symptom management Daily weights, Medications, Exercise, ? Na diet Stop smoking Conserve Energy Support Systems important to combat depression Goal ? To manage the disease process outside of the hospital Evidenced Based Practice (EBP) – supports 1 hour of patient education session at time of discharge Goal is to increase clinical outcomes, increase patient compliance, decrease costsEvidenced Based Practice (EBP) – supports 1 hour of patient education session at time of discharge Goal is to increase clinical outcomes, increase patient compliance, decrease costs

68. Cardiomyopathy Used to describe a group of Diseases affecting the structure or function of the heart Not common Can lead to Cardiomegaly – Enlarged heartUsed to describe a group of Diseases affecting the structure or function of the heart Not common Can lead to Cardiomegaly – Enlarged heart

69. Types Primary Secondary Dilated Hypertrophic Restrictive Primary – disease is unknown Secondary: Dilated – most common, structural damage to the heart tissue (alcohol abuse) Can result in Cardiomegaly (enlarged heart due to ventricular dilation) * not the same as CHF where the walls of the ventricles become hypertrophied Hypertrophic – Stiff left ventricle resulting in ? diastolic filling, More common in men between ages of 30-40 Restrictive – rarest, results in restriction of filling of ventricles Symptoms similar to CHF Diagnosis based on pt’s history, ruling out other conditions Treatment very similar to CHF Try to maintain cardiac output/ manage congestive heart failure, fix the cause, transplant in end stage if a candidate Primary – disease is unknown Secondary: Dilated – most common, structural damage to the heart tissue (alcohol abuse) Can result in Cardiomegaly (enlarged heart due to ventricular dilation) * not the same as CHF where the walls of the ventricles become hypertrophied Hypertrophic – Stiff left ventricle resulting in ? diastolic filling, More common in men between ages of 30-40 Restrictive – rarest, results in restriction of filling of ventricles Symptoms similar to CHF Diagnosis based on pt’s history, ruling out other conditions Treatment very similar to CHF Try to maintain cardiac output/ manage congestive heart failure, fix the cause, transplant in end stage if a candidate

70. Widened QRS seen with ventricular hypertrophy

71. Cardiac Transplantation Treatment of choice for end-stage heart disease >50% of patients have cardiomyopathy 40% In-operable CAD Extensive evaluation process to determine acceptability Long Wait time An artificial heart now exists to decrease wait time for transplantation Chapter 35 HF case study - projectorChapter 35 HF case study - projector

72. Inflammatory Heart Diseases  Infective Endocarditis Myocarditis Rheumatic Fever Rheumatic Heart Disease Pericarditis Each one will be discussed in the following slidesEach one will be discussed in the following slides

73. Infective Endocarditis Infection of the endocardium of the heart Etiology : Aging process IV drug & cocaine abusers Clients who have had valve replacements Recent dental or surgical procedures Signs and Symptoms: Flu like Symptoms 80% develop either aortic or mitral valve murmurs Diagnostics: + Blood Cultures Cultures should be done prior to antibiotic administration New or changed murmur Treatment: Prophlatic antibiotics prior to dental or surgical procedures Infection of the endocardium of the heart Most commonly caused by bacterial streptococcus and Staphylococcus Usually affect the valves Symptoms: (Flu-like) fever, chills, weakness, malaise, fatigue, anorexia, back pain, headache, weight loss, petechiae (ankles, folds of the skin)Infection of the endocardium of the heart Most commonly caused by bacterial streptococcus and Staphylococcus Usually affect the valves Symptoms: (Flu-like) fever, chills, weakness, malaise, fatigue, anorexia, back pain, headache, weight loss, petechiae (ankles, folds of the skin)

74. Myocarditis Inflammation of the myocardium Due to: infection, radiation, meds Most common: viruses (flu) Associated with acute Pericarditis S&S are benign to severe heart involvement, even sudden death Cardiac involvement can be seen 7-10 days after viral infection

75. Myocarditis (cont’d) S&S: Pleuritic Chest pain, friction rub, S3, crackles, JVD Diagnosis: ECG & Lab findings are vague Biopsy most diagnostic Goal: Manage the symptoms of poor cardiac function Tx: Oxygen, Rest, restricted activity, Digoxin Nursing Mgt: monitor & tx for CHF

76. Rheumatic Fever Inflammation that can affect up to all three layers of the heart May or may not cause permanent structural damage to the heart Occurs 2-3 weeks after Strept infection Other contributing Factors: Lower socioeconomic groups (overcrowding) Familial tendencies Altered Immune response The exact mechanism of how the b-Hemolytic Steptococcal organism causes inflammation of the heart and other body tissues is not well known at this time. In addition to the heart it can affect joints and the CNS.The exact mechanism of how the b-Hemolytic Steptococcal organism causes inflammation of the heart and other body tissues is not well known at this time. In addition to the heart it can affect joints and the CNS.

77. Diagnosing Rheumatic Fever No single test Throat cultures are usually negative by the time the individual seeks medical care CRP and ESR are + indicating systemic inflammation ? WBC, Fever Echo – valve insufficiency and pericardial fluid CXR – enlarged heart if CHF is present Tx – Antibiotics, NSAIDS, cortcosteroids

78. Rheumatic Heart Disease Chronic Condition Results from scarring and deformity of the heart valves Term used to signify when damage has occurred to the heart from Rheumatic Fever

79. Pericarditis An inflammation or alteration of the pericardium Signs and Symptoms: Pain usually sharp & stabbing, but can be dull ache is minority of cases Pain that radiates to shoulder or back Pain aggravated by breathing Pain aggravated by lying down Slow shallow breaths Pericardial friction rub on auscultation ST segment elevation in all 12 Leads Pericardium is comprised of two layers Function is to provides lubrication to decrease friction during a heart beat Multiple causes: infectious (viral, bacterial, fungal), noninfectious (acute MI), autoimmune response related to rheumatoid arthritis, systemic lupus See this occasionally post CABG Pericardium is comprised of two layers Function is to provides lubrication to decrease friction during a heart beat Multiple causes: infectious (viral, bacterial, fungal), noninfectious (acute MI), autoimmune response related to rheumatoid arthritis, systemic lupus See this occasionally post CABG

80. Treatment of Pericarditis Identify and treat the underlying problem NSAIDS ASA Rest Overbed table for leaning forward Corticosteroids Antibiotics if bacterial Pericardiocentesis if there is an ? in fluid between the layers of the pericardial sac Watch for arrhythmias, pneumothorax Pericardiocentesis – needle inserted into the pericardial space to remove fluidPericardiocentesis – needle inserted into the pericardial space to remove fluid

81. Complications Pericardial Effusion Distant heart sounds Cough, dyspnea, tachypnea Cardiac Tamponade Agitation, confusion, restlessness Tachycardia, tachypnea Distended neck veins Effusion – accumulation of excess fluid in the pericardium Tamponade – occurs as the effusion grows Increase in intrapericardial pressure Results in compression of the heart Effusion – accumulation of excess fluid in the pericardium Tamponade – occurs as the effusion grows Increase in intrapericardial pressure Results in compression of the heart

82. Pericardial Effusion When the pericardium becomes inflamed, sometimes the fluid between the two layers will increase causing a Pericardial Effusion MayoClinic (2005)

83. Cardiac Tamponade When fluid accumulates in the pericardial space it compromises cardiac filling and cardiac outputWhen fluid accumulates in the pericardial space it compromises cardiac filling and cardiac output

84. Clinical Signs of Tamponade

85. Treatment of Pericardial Effusion or Cardiac Tamponade Pericardiocentesis Additional Treatment: “A procedure in which an opening is made in the pericardium to drain fluid that has accumulated around the heart. A pericardial window can be made via a small incision below the end of the breastbone (sternum) or via a small incision between the ribs on the left side of the chest” (USC School of Medicine, n.d.). Window = drainage port through the pericardium into the peritoneum Left chest tube will be inserted to collect the fluid Additional Treatment: “A procedure in which an opening is made in the pericardium to drain fluid that has accumulated around the heart. A pericardial window can be made via a small incision below the end of the breastbone (sternum) or via a small incision between the ribs on the left side of the chest” (USC School of Medicine, n.d.). Window = drainage port through the pericardium into the peritoneum Left chest tube will be inserted to collect the fluid

86. Valvular Heart Disease Eventually valve disease can cause Hemodynamic problems Eventually valve disease can cause Hemodynamic problems

87. Understanding Terms Stenosis = Constriction or narrowing of orifice Regurgitation = Retrograde of the flow of blood from one chamber back into another Prolapse = valve leaflets billow back or buckle back into the atrium

88. Mitral Stenosis Mitral valve becomes narrow and constricted Causes ? L. Atrial pressure and volume Most are due to Rheumatic Heart disease Symptoms: murmur at 5th ICS Extended dyspnea and fatigue Other causes: congenital, systemic lupus, rheumatoid arthritis Valve becomes constricted and narrowed, creating pressure in the chamber to overcome the resistance Other causes: congenital, systemic lupus, rheumatoid arthritis Valve becomes constricted and narrowed, creating pressure in the chamber to overcome the resistance

89. Mitral Valve Prolapse Valve billows back into L. Atrium Cause is unknown Heard as a murmur Can be familial due to connective tissue disorder Most people asymptomatic, benign Most common valve disorder May lead to Mitral Valve Regurgitation Diagnosed by ECHO Prolapse – structural: cusps billow upward (Prolapse) into atrium Most common valve disorder in the U.S. Cause: may be genetic or environmental May hear regurge Could have atypical chest pain related to fatigue not exertion Increased risk for bacterial endocarditisProlapse – structural: cusps billow upward (Prolapse) into atrium Most common valve disorder in the U.S. Cause: may be genetic or environmental May hear regurge Could have atypical chest pain related to fatigue not exertion Increased risk for bacterial endocarditis

90. Mitral Regurgitation Retrograde blood flow from L. Ventricle to L. Atrium Etiology R/T: MI, Rheumatic heart disease, MVP Symptoms R/T acute or chronic murmur Heard best at 5th ICS May feel a thrill More common in women than men Valve leaflets become compromised, allowing blood to flow back into the chamber after the valve is closed Chamber dilation Clinically: acute: pulmonary edema, cool/clammy, weak thready peripheral pulses chronic: asymptomatic, weakness, fatigue Progressive worsening of regurgitation can lead to HF (left or right) leading to cardiomegaly Valve leaflets become compromised, allowing blood to flow back into the chamber after the valve is closed Chamber dilation Clinically: acute: pulmonary edema, cool/clammy, weak thready peripheral pulses chronic: asymptomatic, weakness, fatigue Progressive worsening of regurgitation can lead to HF (left or right) leading to cardiomegaly

91. Valvular Regurg - picture

92. Aortic Stenosis Blood flow restricted from L. Ventricle to Aorta Results in LVH, & ?myocardial oxygen consumption Causes: congenital, Rheumatic Fever, atherosclerosis Symptoms - ? S1 or S2 sound Murmur S4 aortic valve narrows causing diminished blood flow from LV to Aorta Symptoms develop gradually Symptoms :low systolic pressure, narrowed pulse pressure, slow HR, faint pulsesaortic valve narrows causing diminished blood flow from LV to Aorta Symptoms develop gradually Symptoms :low systolic pressure, narrowed pulse pressure, slow HR, faint pulses

93. Aortic Regurgitation Retrograde blood flow from the Ascending Aorta into L. Ventricle Results in: L. Ventricle dilation & LVH, leading to ?contractility of the heart murmur Soft S1, S3 or S4 Causes: Congenital, Rheumatic Heart Disease May have Orthopnea, Exertional dyspnea, paroxysmal nocturnal dyspnea Retrograde blood flow from the aorta into the LV Sudden clinical manifestations, resulting in a medical emergency Absent S1, may have an S3 or S4 Retrograde blood flow from the aorta into the LV Sudden clinical manifestations, resulting in a medical emergency Absent S1, may have an S3 or S4

94. Tricuspid Valve Disease Stenosis & Regurgitation Tricuspid Stenosis is uncommon R. Atrium enlargement & ?systemic venous pressure Tricuspid Regurgitation Volume overload in R. Atrium and Ventricle occurs Causes: R. Ventricular dysfunction, or pulmonary HTN

95. Diagnosing Valve Disease History and Physical Exam Echocardiography Cardiac Catheterization ECG

96. Collaborative Care for Valvular Disease Ask about history of Rheumatic Heart Disease Use of antibiotic prophylaxis Digitalis Diuretics Anticoagulation (ASA, Coumadin) Surgical repair or replacement

97. Nursing Management/Goals Maintaining normal cardiac function Monitoring Cardiac output, fluid volume excess Improving activity tolerance Educating patients on the disease process and preventative measures

98. Mitral Valve repair May be able to be repaired, first choice Suture of leaflets or cordae tendonae if not…..May be able to be repaired, first choice Suture of leaflets or cordae tendonae if not…..

99. Valve Replacement Mechanical/Biologic Antibiotics Lifelong anticoagulation therapy mechanical Good oral hygiene Prevent infections Mechanical: Last longer, requires anticoagulation Biological: Cow/pig or human tissue No coagulation Does not last as long Chapter 37 Case study Heart disease Rheumatic FeverMechanical: Last longer, requires anticoagulation Biological: Cow/pig or human tissue No coagulation Does not last as long Chapter 37 Case study Heart disease Rheumatic Fever

101. Synchronized Cardioversion The defibrillator is used to deliver a shock during the QRS complex (synchronized) Done for Stable and A-Fibrillation or SVT’s with a pulse greater than 150The defibrillator is used to deliver a shock during the QRS complex (synchronized) Done for Stable and A-Fibrillation or SVT’s with a pulse greater than 150

102. Procedure Requirements Consent Conscious sedation , Propofol/Diprivan 50 -100 joules initially Usually performed in procedure room/cath lab Can be performed in ER/ICU/Step-down unit/PCU Typically sedate the patient for this procedure using conscious sedation meds (ex. = Diprivan) and following institution’s policy. There are specific guidelines that have to be followed when conscious sedation is administered, and the patient recovers. It is a special procedure. Make sure charge Nurse is always aware. Docs don’t always know what hospital policies are, but as the nurse you are responsible for knowing! Typically sedate the patient for this procedure using conscious sedation meds (ex. = Diprivan) and following institution’s policy. There are specific guidelines that have to be followed when conscious sedation is administered, and the patient recovers. It is a special procedure. Make sure charge Nurse is always aware. Docs don’t always know what hospital policies are, but as the nurse you are responsible for knowing!

103. Defibrillation Treatment for Pulseless Ventricular Tachycardia & Ventricular Fibrillation Defibrillator – 2 Types Monophasic – delivers energy in one direction 360 joules Biphasic – delivers energy in two directions 150 or 200 joules Learn which type of defibrillator is located on the unit or department you work in.Learn which type of defibrillator is located on the unit or department you work in.

104. Percutaneous Transluminal Coronary Angioplasty (PTCA)/Stent Previously discussed under diagnostic cardiac cath An invasive but technically nonsurgical technique Used to reduce frequency and severity of chest discomfort for clients with angina Also used with client with an evolving acute MI to reperfuse myocardium

105. PTCA(cont) Catheter is introduced through a guide wire Balloon is inflated to compress plaque Success rate can be as high as 90% upon initial reopening Re-occlusion rate is high without stentingRe-occlusion rate is high without stenting

106. Balloon Angioplasty - picture

107. % Blockages - picture

108. Stents Also now available are drug coated stentsAlso now available are drug coated stents

110. Coronary Artery Bypass Graft Surgery (CABG) Most common type of Cardiac Surgery Occluded coronary arteries are bypassed with client’s own blood vessels or synthetic grafts Saphenous Vein–66% patency rate @ 10 yrs Internal Mammary Artery Patency rate-90% @ 10 yrs Read Slide Book also describes the following procedure: MIDCABG Minimally Invasive Direct Coronary Artery Bypass Graft New technique For 1 vessel or LAD disease Small incisions between the ribs Scope used Heart is not stopped, only slowed Pain is greater with this procedure (thoracotomy incision causes more pain than sternotomy)Read Slide Book also describes the following procedure: MIDCABG Minimally Invasive Direct Coronary Artery Bypass Graft New technique For 1 vessel or LAD disease Small incisions between the ribs Scope used Heart is not stopped, only slowed Pain is greater with this procedure (thoracotomy incision causes more pain than sternotomy)

111. CABG (cont) Pre-Op care: May be elective or emergency Pre-Op teaching Check administration of cardiac meds, anticoagulants NPO after midnight Explain Post-Op procedure Teach Sternal Precautions

112. Cardiac Bypass- picture Minimally invasive techniqueMinimally invasive technique

113. Cardiac bypass - picture

114. CABG (cont) Post-Op: ICU for at least 24 hours Monitor for arrhythmias Monitor Vital Signs and Electrolytes Emotional status Discharge Planning and teaching Epicardial pacing wires Atrial attached to right atrial surface and exit the chest to the right of the sternum Ventricular wire attached to the surface of the right ventricle and exit the chest to the left of the sternum Allows for treatment of arrhythmias Chest tubes, drips to regulate heart rate, rhythm, preload and afterload Chapter 34 Case Study View animation #2Epicardial pacing wires Atrial attached to right atrial surface and exit the chest to the right of the sternum Ventricular wire attached to the surface of the right ventricle and exit the chest to the left of the sternum Allows for treatment of arrhythmias Chest tubes, drips to regulate heart rate, rhythm, preload and afterload Chapter 34 Case Study View animation #2

115. Intra-Aortic Balloon Pump Purpose: Provides temporary circulatory assistance to a compromised heart Indications: Cardiac Bypass surgery Acute Myocardial infarction with complications Awaiting cardiac transplantation Effects: Increased coronary perfusion Improved oxygen delivery Decreases anginal pain Decreases Afterload Decreases Preload Increases Stroke Volume Facilitates left ventricular emptying Used in a CVICU settingUsed in a CVICU setting

116. Intra-Aortic Balloon Pump Procedure: Catheter is inserted into femoral artery Advanced into descending Aorta Balloon inflates during Diastole Balloon deflates during Systole

117. Intraaoritc pump Inflates and deflates with each heart beatInflates and deflates with each heart beat

118. Ventricular Assist Devices(VAD) Purpose: Provides longer term support for a decompensated heart Assist or replace the action of the ventricle May be implanted or external Indications: Ventricular failure associated with an MI Waiting for a donor or artificial heart

119. Pacemakers Triggers electrical activity. Used in place of SA node Permanent or Temporary Single and Dual Chamber Permanent Pacemakers Atrial or Ventricular single chamber Atrial and Ventricular dual chambers (AV) CRT pacing technique that paces both ventricles Malfunctions can occur -R/T sensing or capture Pulse generator contains circuitry and insulated lead wire is usually placed into RV. Sensing – fails to recognize atrial or ventricular activity, Check battery, lead relocation Capture – fails when the electrical charge generated by the pacemaker is unable to produce a myocardial contraction Same reasons as abovePulse generator contains circuitry and insulated lead wire is usually placed into RV. Sensing – fails to recognize atrial or ventricular activity, Check battery, lead relocation Capture – fails when the electrical charge generated by the pacemaker is unable to produce a myocardial contraction Same reasons as above

120. Pacemaker Malfunction

121. Pacemaker Malfunction

122. Indications for Permanent pacing Symptomatic Brady arrhythmias Sick Sinus Syndrome Third Degree Heart Block Tachy arrhythmias Chronic A-Fib with a slow Ventricular rate See Table 35-10 Generates an electrical impulse from the pacemaker through the leads to the wall of the myocardium, causing the chamber to contract.Generates an electrical impulse from the pacemaker through the leads to the wall of the myocardium, causing the chamber to contract.

123. Care and Considerations Keep incision w/ staples dry No pushing, pulling, lifting or raising arm for 2 weeks Encourage use of sling Watch for s/s of infection Keep wallet card Avoid large electrical generators, and large magnets like MRI Teach pulse taking daily with log daily till MD visit

124. Pacemaker Insertion Leads are threaded through the subclavian vein to the heart. In AV pacemakers, one lead lies in the Right atrium, second tip lies in the right ventricle Placed under moderate sedation Immobilzation of the affected arm/shoulder for 24-48 hours (sling) Prevents dislodgement of tip of electrode Assess patient for chest pain, palpitations, dizziness, SOBLeads are threaded through the subclavian vein to the heart. In AV pacemakers, one lead lies in the Right atrium, second tip lies in the right ventricle Placed under moderate sedation Immobilzation of the affected arm/shoulder for 24-48 hours (sling) Prevents dislodgement of tip of electrode Assess patient for chest pain, palpitations, dizziness, SOB

125. Types of Pacemakers Indicated for: Symptomatic bradycardia Different types: Internal Single Chamber (Atrial or Ventricular) Dual Chamber (AV, Atrial & Ventricular) Rate Responsive Set at a specific rate, fires if HR drops below AICD 2. External Indicated for: Symptomatic bradycardia Different types: Internal Single Chamber (Atrial or Ventricular) Dual Chamber (AV, Atrial & Ventricular) Rate Responsive Set at a specific rate, fires if HR drops below AICD 2. External

126. External Pacemaker Indications: Used for Temporary pacing Pt waiting for permanent pacemaker surgery Post CABG surgery using Epicardial pacing wires Post MI See Table 35-11

127. Internal Automated Defibrillators

128. AICD

129. AICD’s Treats life threatening arrhythmias Detects abnormally fast rhythm and deliver small electrical charge to convert the heart into a normal rhythm. Leads placed via sub-clavian catheter into endocarium Treats life threatening arrythmias Rapid pacing is not felt by the patient, however strong shocks to initiate heart beat are felt. . Pt teaching; watch for s/s of infection insertion site, keep incision dry X 1 week, pulse taking, avoid MRI, avoid direct blows to generator, carry card at all times. Treats life threatening arrythmias Rapid pacing is not felt by the patient, however strong shocks to initiate heart beat are felt. . Pt teaching; watch for s/s of infection insertion site, keep incision dry X 1 week, pulse taking, avoid MRI, avoid direct blows to generator, carry card at all times.

130. Patient Teaching Lie down when it fires If pt. loses consciousness, call 911 Airport security should be alerted Do not allow for “wanding” to go over the site

131. Artificial Airways Oral or nasal ET (endotracheal tube) intubation Indications: Airway obstruction Respiratory distress Ineffective clearance of secretions High risk for aspiration Insertions: Physician (ED or Pulmonologist) Credentialed Respiratory Therapist

132. ET Tubes Oral Nasal

134. Goal of Mechanical Ventilation

135. Nursing Responsibilitiesfor Mechanical Ventilation Maintain correct tube placement Checked every 2-4 hours Ascultates for bilateral breath sounds Maintain proper cuff inflation Maintains at 20-25mm Hg Monitor oxygenation and ventilation Assess clinical data for ABG’s, SpO2 Assess for S/S of hypoxemia Confusion, anxiety, arrhythmias and dusky skin color) Assess for complications Maintain tube patency Open or Closed suctioning Provide oral care Maintain skin integrity Watch for skin breakdown on the face and lips Provide skin care daily and re-tape and secure ET tube

136. The Ventilated Patient

137. Ventilators Not a cure but a means to support patient breathing Negative pressure Positive Pressure – most common for acutely ill patients Several manufacturers Several types/modes Controlled Assist-controlled Intermittent Positive End-Expiratory (PEEP) CPAP High frequency/flow Process for weaning and extubation Do not need to study the types of ventilatorsDo not need to study the types of ventilators

138. Considerations for Mechanical Ventilation Consider the implications for short term-versus long-term need What is the long term goal for the patient/family Is the patient needing ventilation for acute reasons or for a chronic illness/disease Patients and families should discuss the implications for removal of ventilation support In Class exercise Chapter 34 – Case Study - MIIn Class exercise Chapter 34 – Case Study - MI

139. Remote Intensive Care Units

140. Resources www.theheart.org www.societyofcriticalcaremedicine.org www.guoideline.gov