Acute Coronary syndrome part 2
What is Acute Coronary Syndrome?
Acute Coronary Syndrome develops when Ischemia is prolonged and not immediately reversible. Acute Coronary Syndrome compromises of 1.Unstable Angina (UA), 2.non-ST-segment-elevation Myocardial Infarction(NSTEMI), 3. ST-segment-elevation Myocardial Infarction (STEMI). Each is distinct but reflect nomenclature (ACS) reflects the relationship among the disorders.
Acute Myocardial Infarction
Acute myocardial infarction in the posterolateral wall of the left ventricle. This is demonstrated by the absence of staining in the areas of necrosis (white arrow). Note the scarring from a previous anterior wall myocardial infarction (black arrow).
Chronic Stable Angina and ACS Nursing Diagnoses
-Decreased cardiac output related to altered contractility and altered heart rate and rhythm as evidenced by decrease in BP, elevation in HR, dyspnea, dysrhythmias, diminished pulses, peripheral edema, and/or pulmonary edema -Acute pain related to an imbalance between myocardial oxygen supply and demand as evidenced by patient's report of severe chest pain and tightness with radiation of pain to the neck and arms, elevated cardiac markers, ECG changes -Anxiety related to perceived or actual threat of death, pain, and/or possible lifestyle changes as evidenced by restlessness, agitation, and verbalization of concern over lifestyle changes and prognosis as evidenced by patient's statement of "What if I die ... everyone relies on me." -Activity intolerance related to general weakness secondary to decreased cardiac output and poor lung and tissue perfusion as evidenced by patient's report of fatigue with minimal activity, inability to care for self without dyspnea, and increased heart rate Ineffective self-health management related to lack of knowledge of disease process, risk factor reduction, rehabilitation, home activities, and drugs as evidenced by frequent questioning about illness, management, and care after discharge
Unstable Angina and Myocardial Infarction Diagnostic Studies
-Detailed health history -12-lead ECG(change in QRS complex, ST segment, and T wave) 12-lead ECG -Distinguish b/w STEMI and NSTEMI Pathologic Q wave -coronary angiography: Coronary Angiography The patient with UA or NSTEMI may or may not undergo coronary angiography to evaluate the extent of the disease. Guidelines suggest that it is reasonable to do coronary angiography on stable but high-risk patients with UA/NSTEMI. If appropriate, a PCI is performed at this time. Some patients may be treated with conservative medical management. Coronary angiography is the only way to confirm the diagnosis of Prinzmetal's angina. Exercise or pharmacologic stress testing and echocardiogram are used when a patient has an abnormal but nondiagnostic baseline ECG. A dobutamine (Dobutrex), dipyridamole (Persantine), or adenosine (Adenocard) stress echocardiogram stimulates the effects of exercise and is used in patients unable to exercise -Exercise or pharmacologic stress testing -Echocardiogram
Collaborative care Acute Coronary Syndrome
-Ongoing monitoring pt=will receive ongoing care in a critical care unit or telemetry unit, where continuous ECG monitoring is available. TREATS =dysrhythmias according to established protocols Frequent vital sign monitoring Bed rest/limited activity for 12-24 hours -patient with UA or NSTEMI w/ negative markers and ongoing angina= A combination of Aspirin, heparin, and glycoprotein inhibitor is Recommended Coronary angiography with PCI once stable. -Monitor=vital signs, including pulse Oximetry, frequently during the first few hours after admission and closely thereafter. Maintain=bed-rest and limitations of activity for 12-24hrs, with gradual increase in activity unless contraindicated. Coronary angiography= w/ PCI is considered once the patient is stabilized and angina is controlled, or if angina returns or increases in severity.
Myocardial Infarction Healing Process
100 to 14 days after MI, scar tissue is still weak Myocardium vulnerable to stress **Monitor patient carefully as activity level increases By 6 weeks after MI=scar tissue has replaced necrotic tissue. Area=is healing, less compliant ventricular remodeling: normal myocardium will hypertrophy and dilate in an attempt to compensate for infarcted muscle.
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CABG surgery consists of the placement of conduits to transport blood between the aorta, or other major arteries, and the myocardium distal to the blocked coronary artery (or arteries). CABG surgery requires a sternotomy (opening of the chest cavity) and cardiopulmonary bypass (CPB). The procedure may involve one or more grafts using the internal mammary artery, saphenous vein, radial artery, gastroepiploic artery, and/or inferior epigastric artery. Minimally invasive direct coronary artery bypass (MIDCAB) is a technique that offers patients with limited disease an approach to surgical treatment that does not involve a sternotomy and CPB. The technique requires several small incisions between the ribs. A thoracoscope is used to dissect the IMA. The heart is slowed using a β-adrenergic blocker (e.g., esmolol [Brevibloc]) or stopped temporarily with adenosine. A mechanical stabilizer immobilizes the operative site.
What are Clinical Manifestation of Acute Coronary Syndrome of Myocardial Infarction?
Clinical Manifestation of ACS Myocardial Infarction 1.Pain - Severe, immobilizing chest pain not relieved by rest, position change, or nitrate administration - persistent and unlike any other pain such as Heaviness, pressure, tightness, burning, constriction, crushing -Locations: Substernal, retrosternal, epigastric Occurs when pt is active or at rest, or asleep or awake. however, it most Commonly happen in the morning. Duration =20 mins or longer, more severe than usual anginal pain. *More common in AM Atypical= women Elderly=change in mental status, shortness of breath No Pain= if Cardiac neuropathy (diabetes) fyi patient with diabetes are asymptomatic.
What are the Complications of Myocardial Infarction?
Complications of Myocardial Infarction are: 1. Dysrhythmias -most common complication -present=80% of MI patients can be caused by Ischemia, electrolyte imbalances, or SNS stimulation Life-threatening dysrhythmias seen most often with anterior MI, heart failure, or shock 2. Heart failure occurs when the pumping power of the heart has diminished can be subtle or severe 3. Cardiogenic shock occurs because of severe LV failure **Requires Aggressive management 4.Papillary muscle dysfunction causes Mitral Valve regurgitation Aggravates an already compromised LV-rapid clinical deterioration 5.Ventricular aneurysm Myocardial wall=becomes thinned and bulges out during contraction. Leads=to HF, dysrhythmias, and angina 6. Acute Pericarditis An inflammation of visceral and/or parietal pericardium May result in cardiac tamponade, low= LV filling and emptying, emptying, heart failure, chest pain, Pericardial friction, ECG changes.Chest pain TREATED= with antiflammatory agents 7. Dressler syndrome Pericarditis with effusion and fever that develops 4 t0 6 weeks after MI Pericardial (Chest) pain pericardial friction rub pericardial effusion Arthralgia TREATED=with short-term corticosteroids
Cardiopulmonary Bypass
During CPB, blood is diverted from the patient's heart to a machine where it is oxygenated and returned (via a pump) to the patient. This allows the surgeon to operate on a quiet, nonbeating, bloodless heart while perfusion to vital organs is maintained.
Etiology and Pathosiology of Acute Coronary Syndrome
E & Patho: Plague deteriorates-Rupture-platelets aggregation-Thrombus. Acute Coronary Syndrome=deterioration of a once stable atherosclerotic plague. once the stable plague ruptures, it expose the intima to blood and stimulates platelet aggregation and local vasoconstriction with thrombus formation. "Unstable Lesion: * Partially Occluded by a thrombus will manifest as UA or NSTEMI. *Totally Occluded by a thrombus manifest as STEMI. what causes Coronary plague to suddenly become unstable isn't well understood, BUT Systemic Inflammation is thought to play a role. Patient suspected of Acute Coronary Syndrome require immediate Hospitalization. *Results Partial occlusion of coronary artery: UA or NSTEMI Total occlusion of coronary artery: STEMI
Thrombolytic Therapy
Each Hospital has a protocol =giving Thromolytic Therapy However, there are several common factors. -Draw blood to obtain baseline laboratory values and start 2 or 3 Lines for IV Therapy. All other invasive are done before the thrombolytic agent is given to reduce the possibility of bleeding. varies on Drug selected, therapy administered in One IV Bolus or over a period of time (30 to 90) minutes. - Monitor heart rhythm, vital signs, and pulse Oximetry and assess the heart and lungs frequently to evaluate the patients response to therapy. Assess regularly for changes in Neuro= indicate Cerebral Bleed. Assess for perfusion= return of ST wave to baseline best marker. Present of reperfusion dysthymias=unreliable marker A major concern with thrombolytic therapy is reocclusion of the artery. The site of the thrombus is unstable, and another clot may form or spasm of the artery may occur. Because of this possibility, IV heparin therapy is initiated.
Drug Therapy
IV NTG (Tridil) is used in the initial treatment of the patient with ACS. The goal of therapy is to reduce anginal pain and improve coronary blood flow. IV NTG decreases preload and afterload while increasing the myocardial oxygen supply. The onset of action is immediate. Titrate NTG to control and stop chest pain. Because hypotension is a common side effect, BP is closely monitored during this time. Patients who do become hypotensive are often volume depleted and can benefit from an IV fluid bolus. Morphine sulfate is the drug of choice for chest pain that is unrelieved by NTG. As a vasodilator, it decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility, and decreasing BP and HR. In addition, morphine can help reduce anxiety and fear. In rare situations, morphine can depress respirations. Monitor patients for signs of bradypnea or hypotension, conditions to avoid in myocardial ischemia and infarction. β-adrenergic blockers decrease myocardial oxygen demand by reducing HR, BP, and contractility. The use of these drugs in patients who are not at risk for complications of MI (e.g., cardiogenic shock) reduces the risk of reinfarction and the occurrence of HF. The continuation of β-adrenergic blockers indefinitely is recommended. ACE inhibitors should be started and continued indefinitely in patients recovering from STEMI with an EF of 40% or less. The use of ACE inhibitors can help prevent ventricular remodeling and prevent or slow the progression of HF. For patients who cannot tolerate ACE inhibitors, angiotensin II receptor blockers should be considered. Dysrhythmias are the most common complications after an MI. In general, they are self-limiting and are not treated aggressively unless they are life threatening (e.g., sustained ventricular tachycardia). A lipid panel is obtained on all patients admitted with ACS. All patients with elevated triglycerides and LDL cholesterol should receive lipid-lowering drugs. After an MI, the patient may be predisposed to constipation because of bed rest and opioid administration. Stool softeners (e.g., docusate sodium [Colace]) are given to facilitate bowel movements. This prevents straining and the resultant vagal stimulation from the Valsalva maneuver. Vagal stimulation produces bradycardia and can provoke dysrhythmias.
Nutritional Therapy
Initially, patients may be NPO (nothing by mouth), except for sips of water, until stable (e.g., pain free, nausea resolved). You advance the diet as tolerated to a low-salt, low-saturated fat, and low-cholesterol diet
Myocardial Infarction from Occlusion
Myocardial Infarction are described based on Locations of the damage (for ex: anterior, inferior, lateral, septal, or posterior wall infarction). Most involve some portion of the left ventricle. The location of the infarction correlates with the involved coronary circulation. For example, the right coronary artery provides blood supply to the inferior wall. Blockage of the right coronary artery will result in an inferior wall MI. Anterior wall infarctions result from blockages in the left anterior descending artery, as shown in this figure. Blockages in the left circumflex artery usually cause lateral and/or posterior wall MIs. Damage can occur in more than one location, especially if more than one coronary artery is involved (e.g., anterolateral MI, anteroseptal MI). The degree of preexisting collateral circulation also influences the severity of infarction. An individual with a long history of CAD will develop collateral circulation to provide the area surrounding the infarction site with a blood supply. This is one reason why a younger person may have a more serious first MI than an older person with the same degree of blockage.
Myocardial Infarctioneeee Healing Process
Myocardial healing Process The body's response to cell death is the inflammatory process. w/in 24 hours, leukocytes infiltrate the area of cell death. on the Fourth Day: proteclytic enzymes of the neutrophils and macrophages begin to remove necrotic tissue. During this time, the necrotic muscle wall is thin. The necrotic zone is identifiable by ECG changes and by nuclear scanning after the onset of symptoms. At this point, the neutrophils and monocyte's have cleared the necrotic debris from the injured area and the collagen matrix that will eventually form At this point, the neutrophils and monocytes have cleared the necrotic debris from the injured area, and the collagen matrix that will eventually form scar tissue is laid down.
Nursing Management Chronic Stable Angina and ACS
Nursing Assessment subjective data Obtain the following health information from the client: Past health history: Previous history of CAD, chest pain/angina, MI, valve disease (e.g., aortic stenosis), heart failure, or cardiomyopathy; hypertension, diabetes, anemia, lung disease; hyperlipidemia Drugs: Use of antiplatelets/anticoagulants, nitrates, angiotensin-converting enzyme inhibitors, β-adrenergic blockers, calcium channel blockers; antihypertensive drugs; lipid-lowering drugs; over-the-counter drugs (e.g., vitamin and herbal supplements) History of present illness: Description of events related to current illness, including any self-treatments and response
Radial Artery Grafts
Other conduits include the gastroepiploic or inferior epigastric artery. However, they are rarely used as the dissection of these arteries is extensive. This increases the length of surgery and the risk for wound complications at the harvest site, especially in an obese or diabetic patient.
Acute Coronary syndrome
Part Two
Acute Coronary Syndrome "ACUTE INTERVENTION"
Priority interventions are aimed at decreasing the oxygen needs of a compromised myocardium and reducing the risk of complications. Provide NTG, morphine sulfate, and supplemental oxygen as needed to eliminate or reduce chest pain. Ongoing evaluation and documentation of the effectiveness of the interventions is important. Maintain continuous ECG monitoring while in the ED and intensive care unit and after transfer to a step-down or general unit. Dysrhythmias need to be identified quickly and treated. During the initial period after MI, ventricular fibrillation is the most common lethal dysrhythmia. In many patients, premature ventricular contractions or ventricular tachycardia precedes this dysrhythmia. Monitor the patient for the presence of reinfarction or ischemia by monitoring the ST segment for shifts above or below the baseline of the ECG. Silent ischemia can occur without clinical symptoms such as chest pain. Its presence places a patient at higher risk for adverse outcomes and even death. If you note ST segment changes, notify the physician. Perform a physical assessment to detect deviations from the patient's baseline findings. Assess heart and breath sounds and any evidence of early HF (e.g., dyspnea, tachycardia, pulmonary congestion, distended neck veins). In addition to routine vital signs and pulse oximetry, monitor intake and output at least once a shift. It is important to promote rest and comfort with any degree of myocardial injury. Bed rest may be ordered for the first few days after an MI involving a large portion of the ventricle. A patient with an uncomplicated MI (e.g., angina resolved, no signs of complications) may rest in a chair within 8 to 12 hours after the event. The use of a commode or bedpan is based on patient preference. When sleeping or resting, the body requires less work from the heart than it does when active. It is important to plan nursing and therapeutic interventions to ensure adequate rest periods free from interruption. Comfort measures that can promote rest include a quiet environment, use of relaxation therapy (e.g., guided imagery), and assurance that staff are nearby and responsive to the patient's needs. Phase 1 of cardiac rehab occurs in the hospital. It is important that the patient understands the reasons why activity is limited but not completely restricted. Gradually increase the patient's cardiac workload through more demanding physical tasks so that the patient can achieve a discharge activity level adequate for home care. Phase 2 of rehab begins when the patient is discharged home and continues for 2 to 12 weeks. Phase 3 is long-term maintenance for optimal cardiac health.
What are the Clinical Manifestations of Acute Coronary Syndrome?
The Clinical Manifestation of Acute Coronary Syndrome are: 1. UNSTABLE ANGINA Unstable Angina(UA) is a chest that is new in onset, occurs at rest, or has a worsening pattern. Patients with Chronic Stable Angina may develop UA, or UA may be the first clinical sign of CAD. Patient previously diagnosed Chronic Stable Angina will describe a significant change in the pattern of angina. occurs with increasing frequency and easily provoked by minimal or no exertion, during sleep, or even at rest. Unlike Chronic Stable Angina. Unstable Angina(UA) is UNPREDICTABLE and is an EMERGENCY. Despite national efforts to increase awareness, Women's symptoms continue to go unrecognized as heart related. These include Fatigue, Shortness of breath, indigestion & Anxiety. ** FATIGUE= is the most prominent symptom. Symptoms=can relate to different diseases and syndromes. it is b/c of these reasons that Women often present with Unstable Angina before Coronary Artery is diagnosed.
what is the Collaborative Care for Acute Coronary Syndrome?
The Collaborative Care of ACS are: -Initial Interventions 12-lead ECG Semi-fowler's position Oxygen IV access Nitroglycerine (SL) and ASA(chewable) Morphine **IMPORTANT: Its extremely important to rapidly diagnose and treat a patient with ACS to preserve cardiac muscle. Obtain= 12 lead ECG and start continuous ECG monitoring Position= patient in an upright position (fowler position) unless contraindicated and initiate oxygen by nasal cannula to keep oxygen saturation above 93%. Establish an IV route to provide an access for emergency drug therapy. Give sublingual NTG and aspirin(chewable) if not given before arrival at the ED. Morphine Sulfate is given for pain unrelieved by NTG.
Internal mammary artery
The internal mammary artery (IMA) is the most common artery used for bypass graft. It is left attached to its origin (the subclavian artery) but then dissected from the chest wall. Next, it is anastomosed (connected with sutures) to the coronary artery distal to the blockage. The long-term patency rate for IMA grafts is greater than 90% after 10 years. Saphenous veins are also used for bypass grafts. The surgeon removes the saphenous vein from one or both legs endoscopically. Sections are attached to the ascending aorta and then to a coronary artery distal to the blockage. The use of antiplatelet therapy and statins after surgery improves vein graft patency. Patency rates of these grafts are 50% to 60% at 10 years.
Nursing Mangament Chronic Stable Angina and ACS "PLANNING"
The overall goals for a patient with ACS include (1) relief of pain, (2) preservation of myocardium, (3) immediate and appropriate treatment, (4) effective coping with illness-associated anxiety, (5) participation in a rehabilitation plan, and (6) reduction of risk factors.
Collaborative Care of Acute Coronary Syndrome Coronary Surgical revaltiization.
he off-pump coronary artery bypass (OPCAB) procedure uses full or partial sternotomy to access all coronary vessels. OPCAB is performed on a beating heart using mechanical stabilizers and without CPB. It is usually reserved for patients with limited disease but who are at high risk for traditional surgery secondary to multiple co-morbidities. Robot-assisted cardiothoracic surgery incorporates the use of a robot in performing CABG or mitral valve replacement. The benefits of robotic surgery include increased precision, smaller incisions, decreased blood loss, less pain, and shorter recovery time. Transmyocardial laser revascularization (TMR) is an indirect revascularization procedure. It is used for patients with advanced CAD who are not candidates for traditional CABG surgery and who have persistent angina after maximum medical therapy. The procedure involves the use of a high-energy laser to create channels in the heart to allow blood flow to ischemic areas. The procedure is performed during cardiac catheterization as a percutaneous TMR or during surgery using a left anterior thoracotomy incision as an adjunct to CABG.
