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Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 1 LJ Myocardial Infarction Definition: necrosis of the heart muscle due to interruption of the oxygen supply. This interruption may be from: Plaque Thrombus Spasm—most common cause in young, healthy people Combination of all Three Terminology Transmural infarct: more common. Ischemic necrosis involves full thickness of ventricular wall. Serious and more common Can cause rupture or aneurysm The wall becomes necrotic and can pouch out and rupture. Rupture = immediate death. Nontransmural Infarct Necrosis limited to inner 1/3 to 1/2 of the ventricular wall. Sites of MI: Can occur in any area of the heart. Most common is left ventricle because it does the most work. Severity of MI depends on: Which vessel is affected Where in the vessel Number of vessels involved. Many = more severe MI Collateral circulation—new circulation that grows around occlusion. Younger patients do not have collateral circulation that is as well developed as older people. Collateral circulation takes “a while to develop.” Bull’s Eye Theory Picture a bull’s eye. The center is dead tissue (necrotic). No repair. Dead tissue. The next ring is an area of injury. (ischemic) Goal is to try to keep it from becoming necrotic. Irritated, red, etc.“Extended MI” means ischemic area became necrotic. The third ring is an area of swelling. Edema of heart muscle. Three Systems of the Heart: Electrical conduction system Blood supply Pumping Diagnosis of MI Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 2 LJ CPK: Creatinine Phosphokinase: Released from dead muscle. Starts going up 6-8 hours after damage, peaks in 12-18 hours. Returns to normal 3-4 days. Goes up with any muscle damage. Use as a broad idea of how large the infarct is. (Generally, the higher the CPK, the larger the infarct) = more muscle damage. Usually see an order: CPK Q8 times 3 (to check for rise in CPK) CPK Isoenzymes (CKI, CPKI, CKMB) Differentiates between heart and other muscle. May not be as high as you expect because there isn’t enough circulation to the area to pick up the enzymes. A patient receiving thrombolytics may have very high CPK. LDH (Lactic Dehydrogenase) Rises about 48-72 hours after CPKs. (2-3 days) Not beneficial in early MIs Troponin: Rises in 3-6 hours Peaks in 14-24 hours Returns to normal in 10-15 days Cardiac sensitive and specific in late MIs EKG ST elevation and Q wave indicate area of MI Treatment Goals Relieve distress (pain) Limit size of infarct—keep necrotic areas as small as possible Decrease cardiac work with meds to allow heart to rest Prevent complications—CHF, arrhythmias, etc. Thrombolytic Therapy ***Understand the difference between thrombolytic therapy and heparin Thrombolytics: Enzymes that dissolve clots. Heparin: keeps clots from getting larger and allows body’s own mechanisms to dissolve the clot. Contraindicated in patients with ulcers, surgery within past month, female on period, recent CVA, Systolic BP >180, history of bleeding for any reason. No “reverser”/antidote for Thrombolytics. Protamine sulfate is antidote for Heparin. Must be given as soon as possible after onset of chest pain (within 6 hours, preferably 4 hours). If given later, med will dissolve clot, but no use as tissue is dead. Purpose of Thrombolytic therapy is to prevent more muscle damage. Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 3 LJ If thrombolytics are given after 8 hours, the area that’s been without blood supply is most likely necrotic already. Most common thrombolytics: Streptokinase: Actually a strep bacteria, so pt may develop fever, sore throat, rash, aching—can actually give the patient a strep infection. Nice. Don’t use it much anymore for these reasons. TPA (Tissue Plasminogen Activator) $2,500/dose, but only one does is needed. No “flu” symptoms Controversial b/c of cost. Urokinase Rarely used for MIs, but still available. Retavase: most commonly used now! Given in continuous IV infusion bag over 12 hours Lyses clot Complications of thrombolytic therapy: Bleeding—most common MI Patient in CCU Equipment Cardiac Monitor IVs—at least two. Depending on severity: Ventilator Swan-Ganz Arterial Line Intra-aortic balloon pump Foley Nursing Care: 1. Continuous cardiac monitoring in CCU. Treat arrhythmias. a. Ventricular: Lidocaine or amnioterone: PVC and Vtach b. Bradycardia: Atropine c. Ventricular fibrillation—defibrillate. 2. Respiratory a. Oxygen b. Ventilator c. Lung sounds—crackles, edema b/c of fluid secondary to CHF 3. Heart Sounds a. Murmur? Is there a murmur developing? If the vessel affected is feeding a valve, then the valve can be damaged. Murmur is the 1st sign of damaged valve. Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 4 LJ b. S3 or S4? 4. Urine Output: a. Low—decreased CO = decreased kidney output. 5. Abdomen: a. Decreased bowel tones b/c of decreased CO and intestinal perfusion. 6. Pulses: a. Weak? Thready? 7. Neuro a. Alert? Oriented? Cooperative? b. Able to follow commands? 8. Edema: a. Especially pedal edema = CHF sign 9. Chest pain: New pain could be: a. New occlusion of vessel (e.g. secondary to stint placement) b. Pericarditis—inflammation of pericardial sac c. Treatment: Morphine 2-4 mg IV; Nitroglycerine IV or Sublingual—dilates blood vessels so more oxygen and blood can get to painful area. 10. Monitor Lab values: a. K+ Increased or decreased can cause arrhythmias b. Magnesium = arrhythmias c. CPK (CKI) cardiac enzymes d. PT/PTT especially if pt is on heparin or thrombolytics 11. Bedrest or bathroom privileges 12. frequent VS. Low BP may indicate decreased CO 13. Be prepared for Code Blue 14. Diet—may be on clear liquids 1st day. 2 gm sodium (low sodium and low fat diet) 15. Maintain a therapeutic environment 16. Restrict visitors first few days 17. Denial of MI is common. Anxiety and mood changes reflect coping mechanisms 18. Explain all procedures and tests. Common Medications Used in the Treatment of MIs 1. ASA (aspirin therapy) decreases platelet aggregation. Does not affect clotting mechanism, but makes the platelets “slippery so that they slide through.” 2. Nitroglycerine (Tridil)continuous IV drip 3. Heparincontinuous IV drip—Does not dissolve clots. Dose individual to maintain PTT at twice the normal. 4. Dopamine—continuous IV drip 5. Anti-arrhythmic IV (To tx arrhythmias) 6. Oral vasodilator 7. Stool softenerto decrease straining with stools and decrease Valsava maneuver. (Valsava stimulation can cause client to “pass out.”) 8. Diuretic Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 5 LJ 9. Lovenox: Not used in acute phase b/c it’s SubQ. Use when on the floor and stable. New National guidelines for patients with MIs: 1. 2. 3. 4. Aspirin Beta blocker ACE inhibitor If client is a smoker, must address that issue with client and document in the chart. **Significant research suggests that survival rate post-MI and reinfarcts are reduced with this treatment. These guidelines should hopefully be in effect within 18 months in all US hospitals. Complications of MIs 1. Heart failureoccurs in 2/3 of all patients 2. Hypoxemiamontior O2 sats and administer O2. 3. HypotensionDetermine cause and treat. (Hypovolemia, Nitroglycerin, large MI) 4. Cardiogenic ShockHeart cannot pump enough blood to adequately provide O2 to organs and tissues. Pt. goes into shock state where the organs in body do nto get enough O2/blood supply. Congestive Heart Failure Definition: Failure of the heart to function as a pump so that it cannot deliver an adequate supply of oxygenated blood to the tissues. Causes: MI Valve disease (valve stuck open or closed) Cardiomyopathy Fluid volume overload Hypertension—Higher bp = harder work for the Left ventricle to adequately perfuse the body. Terminology Preload: The force distending the relaxed myocardial fibers. Filling pressure. Blood coming to the right heart—pressure before contraction. After-load: The force necessary to initiate output to overcome the resistance in the vascular system. Amount of resistance after contraction. Stroke volume: The amount of blood ejected by the left ventricle during systole. Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 6 LJ Compensatory Mecanisms: When the tissues stop receiving adequate perfusion, the body makes some adjustments to try to increase perfusion. These are called compensatory mechanisms: Increase heart rate Starling’s law: Stretching and extension of myocardial muscle fibers. At first this increases force of contractions but only works up to a point. Rubber band analogy: Professor’s brother’s used to snap her with rubber bands. After repeated stretching of rubber band, the rubber band would lose it’s stretch. Same with this compensatory mechanism of the heart. Will end up with heart muscle overextension and decreased ability of the muscle to contract back down to original size. Increase stroke volume Increase oxygen extraction: Tissues can increase oxygen extraction. Take out more O2 when blood supply gets there. Left Heart Failure: Decreased cardiac output to the system Blood backs up into the lungs S&S: Dyspnea, Rales Tachycardia Paroxysmal nocturnal dyspnea—PND=cannot breathe laying down. Fluid redistributes when supine. S3 gallop SOB Acute Pulmonary Edema: Severe Stage of L ventricle failure. Life threatening manifestation of acute left vent failure. There is rapid movement of plasma fluid into interstitial spaces and alveoli. S&S: Extreme dyspnea: SOB Cyanosis Tachypnea—heavy, fast breathing Restlessness Anxiety Sense of suffocation Pale skin Thready pulse: “Thin” pulse. Can feel the pulse, but it feels thin. Sweating Labored respirations Pink frothy sputum—looks like pink, foamy bubble suds May hear rales up to apices of lungs. MEDICAL EMERGENCY! Right Heart Failure: Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 7 LJ Right heart unable to pump blood sufficiently to the lungs Blood backs up into the system S&S Enlarged tender liver Edema of lower extremities Jugular vein distension Ascites: fluid collection into abdomen Cyanosis—not usually seen unless very severe R sided failure. Treatment of Heart Failure: depends on what stage of failure the patient is in. Rest: Sedate if necessary Decreases heart rate and work load Elevate HOB Rhythm Evaluate and treat arrhythmias: PVCs, PACs (premature atrial contractions), etc. PVC’s and PAC’s usually improve as congestion subsides. Diuretics: Lasix: 20-40 mg IV. Can be up to 80 mg Q2 hours! The BIG treatment! Acts as a potent venodilator before the onset of diuresis and thus decreases venous return in early treatment. Pulls off potassium. Monitor K+ and supplement prn. Digitalis/Digoxin: Increases myocardial contractile force: helps heart pump stronger Increases renal blood flow Slows heart rate—if tachy, will slow down heart rate. Note: Dig toxicity: Must watch for and assess for S&S of digoxin toxicity! **Extra Notes on Digoxin: Administration: Ascultate apical pulse checked for one full minute immediately before giving dose. Hold if apical pulse is <60 in adults or <90-100 in children Monitor serum digoxin level and hold if level is > 2.0 ng/dL Draw serum digoxin levels 6-8 hours after dose or just before administering next dose. Digoxin Toxicity S&S: N/V Visual disturbances: especially “yellow or blue tints to lights” Bradycardia Assess for hypokalemia. If K+ < 3.5 cannot give Digoxin. If you give digoxin in a hypokalemic state, you will induce dig toxicity. If on Lasix, you will most likely give K+ supplements as lasix is a potassium depleting diuretic. Myocardial Infarction; Congestive Heart Failure Lecture Date 03-03-03 8 LJ Treatment of digtoxicity: Digibind: Increases renal excretion of Digoxin—usually given with 10-15 ng/ml (severe toxicity). Life threatening arrhythmias, hypotension or LOC. Vasodilators: Act on arteries or veins but most have mixed effect Nitroprusside (Nipride)—relaxes veins and arteries’ resistance Apresoline—dilates arteries and decreases peripheral vascular resistance Nitrates—primarily vein dilators with lesser effects on arteries. Watch for headache and hypotension. ACE Inhibitors: Effective in patients with advanced failure Decreases afterload, increases cardiac output Dobutaminemcg/kg/min continuous infusion. Causes heart muscle to pump with more force. Stronger than digoxin. Cardiac Monitoring Arrhythmias Nursing Care Respiratory Rales/crackles Cyanosis SOB Ventilator Heart Sounds S3 Gallop—indication of fluid overload Urine Output Decrease = not enough cardiac perfusion or decreased CO Abdomen Ascites Decreased bowel tones Pulses Weak/thready—heart failure Bounding—fluid overload/CHF Neuro—confusion secondary to inadequate perfusion Edema Lab Values CPK initially to rule out MI K+ always monitor—especially if on Lasix, Digoxin Bedrest Elevate HOB