MI.docx

**NCA 2 Midterm 2** **MYOCARDIAL INFARCTION** \* A life-threatening condition characterized by the formation of localized necrotic areas within the myocardium caused by interruption of the myocardium\'s blood supply. \* Irreversible- with dead tissues \- 70% obstruction of the lumen of the arter...

**NCA 2 Midterm 2** **MYOCARDIAL INFARCTION** \* A life-threatening condition characterized by the formation of localized necrotic areas within the myocardium caused by interruption of the myocardium\'s blood supply. \* Irreversible- with dead tissues \- 70% obstruction of the lumen of the artery the client will have symptoms \- 100% occlusion can cause death of tissues- can cause anaerobic metabolism- death of tissues, pain \- Vagovagal reflexes causes client to manifest epigastric pain \- Severe reduction of CO cause a decrease flow of blood to all organs \- Clients with MI should be assessed in all organs \- Left ventricle is a common and dangerous location for an MI, because it is the main pumping chamber of the heart. **Clinical Manifestations** \* Chest pain \- Severe, diffuse steady substernal pain of a crushing and squeezing nature \* Not relieved by rest or sublingual vasodilator therapy, but requires opioids (morphine) \* May radiate to the arms (usually the left), shoulders, neck, back, and/or jaw \* Continues for more than 15 minutes \* May produce anxiety and fear, resulting in an increase in heart rate, BP, and respiratory rate \* Diaphoresis, cool clammy skin, facial pallor, increased HR \* Hypertension or hypotension (hypertension initially, hypotension after) \* Bradycardia or tachycardia \* Premature ventricular and/or atrial beats, **ARRHYTHMIAS** (common complications with MI; prevalent cause of death) \* severe anxiety \* Disorientation, confusion, restlessness \* dyspnea \* Fainting, marked weakness \* Nausea, vomiting, hiccups \* **ATYPICAL symptoms:** epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, extreme fatigue (women and elderly) **Diagnostic Evaluation** 1\. ECG Changes \* Generally occur within 2 to 12 hours, but may take 72 to 96 hours. \* Necrotic, injured, and ischemic tissue alter ventricular depolarization and repolarization. \- ST ELEVATION (no O2) \- ST DEPRESSION (low O2) \- T WAVE INVERSION **Effects of Ischemia, Injury, and Infarction on ECG** \* **Zone of ischemia -** region of the heart muscle surrounding the area of injury, which is ISCHEMIC and VIABLE; not endangered unless extension of the infarction occurs; reversible (ST wave depression, T wave inversion) \- not endangered unless infarction occurs; if ischemic, still reversible \* **Zone of injury -** region of the heart muscle surrounding the area of necrosis; INFLAMED and INJURED, but still viable if adequate oxygenation can be restored
(ST wave elevation) \* **Zone of infarction** - DEATH to the heart muscle caused by extensive and complete oxygen DEPRIVATION; irreversible damage (pathologic Q wave- absence of electrical activity) \- irreversible damage; q wave is a permanent result in ecg tracing- sign of previous mi **SPECIFIC CARDIAC MARKERS** \* **Cardiac-specific TROPONIN T and Troponin** I: proteins released during myocardial infarction \- Troponin I: Most sensitive early marker, not detectable in people without cardiac injury \- Released 6-8 hrs. after injury, peak 12-24 hrs. - remain elevated for up to 7-10 days \*when cardiac cells are necrosed or damaged, they release troponin \*best indicator of acute MI \- Range: 0-0.4 mg/dl \- Peak: Can remain elevated for as long as 3 weeks \* **MYOGLOBIN** is a heme protein that helps to transport oxygen. \- starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms. \- rapid decline after 7 hours \- Myoglobin has high sensitivity but poor specificity. It may be useful for the early detection of myocardial infarction. \- increased during MI \*lacks specificity but a negative sign is good for ruling out MI \- Range: 5-70 mg/dl \- Peak: 12 hrs **\* CK-MB: subset of CK specific to cardiac muscle** \- CK-MB levels increase within 3-12 hours of onset of chest pain, reach peak values within 18 hours, and return to baseline after 48-72 hours. \*troponin is preferred than ckmb, bc troponin has longer duration \- Range: 0-5 mg/do \- Peak: 24 hrs \* **LDH
**- Increases within 24-48 hours, peaks within 2-4 days, and lasts 7-14 days
- LDH1 is more specific for MI - rises 8-24 hours
- Not used as sole indicator \* **Leukocytosis** (may be elevated up to 15,000 cells/mm3)
- Appears on the 2nd day after MI and disappears in 1 week
- Due to inflammatory process
- May indicate complications such as embolization, infection, pericarditis \* **AST (Aspartate Aminotransferase)** \- Rise within several hours after the onset of chest pain, peaks within 12 -18 hours and return to normal within 3-4 days **Other Findings:** \* Lipid profile \- Cholesterol \>200 mg/dl (\ 110 mmHg \- 0.4 mg nitroglycerin SL q 5 min. until pain is gone or max 3 doses \- Pain UNRELIEVED by nitro, 2-4 mg MORPHINE slow IV pump, max 20 mg \*SNS is stimulated with pain- increased cardiac workload; morphine counteracts with pain and decreases SNS stimulation; morphine dilate peripheral blood vessels and anxiety and fear \* Systolic BP \< 110 mmHg \- Shock position \- 250 ml NS bolus to achieve SBP 110, max 1L, monitor breath sounds \- Morphine \*when there is still pain when morphine is given, that is MI; when already diagnosed with mi and still not responding with morphine, more tissues are necrosed ***UPON ADMISSION*** \- Collect cardiac enzymes \- Strict bedrest **STEMI (elevation of cardiac markers) MANAGEMENT** \* **GOAL**: Acute Episode \- Door-to-balloon time of 60-90 minutes (PCTA) \- Door-to-drug time of 30 minutes from onset of signs and symptoms or chest pain (THROMBOLYTIC AGENTS) \* Goal is to open the artery as soon as possible, and preferably within 90 minutes of the patient presenting to the emergency room. \* **Primary angioplasty (Percutaneous Transluminal Coronary Angioplasty -PTCA)** \- insertion of balloon catheter to the artery with plaque and is inflated and deflated intermittently so as to flatten the plaque; oxygenated blood can be reperfused to targeted tissue \- Left descending coronary artery- most with plaques \* Intracoronary stent \- stent with balloon \- a balloon catheter bearing the stent is inserted into the coronary artery and positioned at the site of the occlusion; deployed by balloon inflation \- Reopens the blocked artery without reocclusion \- However, fibrins or clots are formed in stents; that's why clients are given anticoagulants and antiplatelets post stenting \- Meshed aluminum content **NSTEMI (no elevation of cardiac markers) MANAGEMENT** \* NO thrombolytics given \* Given anti-ischemic agents (vasodilators) \* May be candidates for PCI **PREPARATION**- cardiac catheterization: \* Check for allergy to iodine and metformin supplementation. \- installation of radiopaque dyes (check for iodine and seafoods allergies) \- If taking metformin, STOP 48 hours before and after procedure - TO PREVENT LACTIC ACIDOSIS \- metformin reacts with iodine causing lactic acidosis \* Withhold solid food (6-8 hrs, liquid (4 hrs) \* Baseline VS and peripheral pulses (esp of inserted limb) \* Inform client: fluttery feeling as the catheter passes through the heart; a flushed and warm feeling when the dye is injected \- monitor for presence of arrhythmia \- inserted at femoral artery and endpoint is at the ascending aorta and brought to the coronary artery; \- for diagnostic and pci purposes **POST PROCEDURE INTERVENTION** \* Supine position. (not semi-fowler\'s) \- sf position occludes the catheter that may cause embolism \* Monitor VS and cardiac rhythm at least every 30 minutes for 2 hours initially. \* Monitor for bleeding at catheter site. \- arterial pressure is influenced by cardiac output \* Monitor peripheral pulses and the color, warmth, and sensation of the extremity distal to the insertion site at least every 30 minutes for 2 hours initially. \- neurovascular checking; pain, pallor, pulse, paresthesia, and paralysis \* Monitor for manifestations of clot formation: numbness and tingling, cool and pale extremity, cyanosis, absence of peripheral pulses - ***EMERGENCY - NOTIFY PHYSICIAN ASAP*** \* Keep extremity extended for 4-6 hours, as prescribed, keeping the leg straight to prevent arterial occlusion. \* Strict bedrest for 6-12 hours \* Patients who have undergone angioplasty continue treatment with aspirin or another antiplatelet medication indefinitely after the procedure BUT NOT given 6 hours from the procedure. (client is still prone to bleeding) \- If a stent has been implanted, clopidogrel (Plavix) is usually prescribed to be taken once a day for 2 to 4 weeks; to prevent GI irritation or bleeding; drink after meals \* IV nitroglycerin may be prescribed to prevent coronary artery vasospasm. \* Encourage fluids, if not contraindicated, to enhance renal excretion of dye. \* Monitor crea level (0.9-1.2) **Angioplasty Complications** \* Allergic reaction to iodine-based dye - dyes can damage kidneys \* Arrhythmias \* Bleeding at the insertion site \* Heart attack, stroke \* Infection at the insertion site \* Kidney failure \* Ruptured artery (dissection) **Administer Thrombolytic Agents/ Fibrinolytics** \- tissue plasminogen activator - TPA (Altiplase) - will not have allergic effects on patients bc it is innate on body; increases plasminogen present causing the clot to dissolve \- streptokinase - synthetic; horse (Streptase) (allergy risk) \- reteplase (Retavase)- synthetic; not derived from animals \- urokinase- synthetic; derived from animals \* To DISSOLVE the thrombus in a coronary artery, allowing blood to flow through again, minimizing the size of the infarction and preserving ventricular function; \* Monitor for bleeding (8 hour window) \- \"door-to-needle\" time in less than 30 minutes \- Effectiveness is highest within the first 2 hours \- if given \>12 hours after symptoms commenced, the risk of INTRACRANIAL BLEEDING is high \* Anticoagulants and antiplatelets are administered after thrombolytic therapy to maintain arterial patency **Contraindications of Thrombolytic agents:** **\* MNEMONIC: SHIP BLAST** **S - Stroke in the last 3 months** **H - Head injury in the last 3 months** **I- Intracranial hemorrhage** **P - PT \> 15 seconds** **B - BP above 185/110; severe uncontrolled HPN** **L - Lumbar puncture in the last 7 days** **A - Anticoagulant use/ Arterial puncture in the last 7 days/Active bleeding** **S - Surgery within the last 14 days** **T - Thrombocytopenia \ 6PVCs - leads to vfib \- Administer LIDOCAINE or amiodarone as ordered \- for pulseless V-tach: SYNCHRONIZED CARDIOVERSION - electric current is delivered at QRS complex; when the heart is in contraction \- V-fib: DEFIB (unsynchronized) with CPR and EPI \- Assess respiratory rate and breath sounds for signs of heart failure as evidenced by presence of crackles and wheezes or dependent edema. \- Place the client in a semi-fowler\'s position to enhance comfort and tissue oxygenation; stay with the client. \* Monitor for presence of Heart Failure and Pulmonary edema \* Monitor for Cardiogenic Shock caused by decreased myocardial contraction with diminished cardiac output \- Administer vasopressors:
dopamine and dobutamine to raise blood pressure Dopamine in low dose- renal arterial dilation Dopamine in high dose- peripheral dilation and increased blood flow to major organs and increasing blood pressure \- Vasodilators: nitroglycerin, nitroprusside: to reduce afterload and promote blood flow to microcirculation \- Inotropic agents: epinephrine \* Assess distal peripheral pulses and skin temperature (poor cardiac output may be identified by cool diaphoretic skin and diminished or absent pulses) \* Monitor BP closely after the administration of medications (if SP of \- BP is \