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Cardiovascular emergencies 2011

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    Cardiovascular emergencies 2011 Cardiovascular emergencies 2011 Presentation Transcript

    • Nelia B. Perez RN, MSN PCU – MJCN NCM 103
    •  Chest pain or pressure Shortness of breath Edema and weight gain Palpitations Fatigue Dizziness or loss of consciousness
    •  S1 and S2 S3 and S4 Gallop sounds Snaps and clicks Murmurs Friction Rub
    •  Cardiac Enzyme Analysis Blood Chemistry  Lipid profile  Cholesterol levels  Serum electrolyte  Blood urea nitrogen  Serum glucose Coagulation Studies Hematologic Studies
    •  Chest radiography and fluoroscopy Electrocardiography Cardiac stress testing Echocardiography Radionuclide Imaging Cardiac Catheterization Angiography Electrophysiologic testing
    •  Central Venous Pressure Pulmonary Artery Pressure Intra-arterial BP monitoring
    •  Ischaracterized by the accumulation of plaque within coronary arteries, which progressively enlarge, thicken and calcify. This causes critical narrowing of the coronary artery lumen (75% occlusion), resulting in a decrease in coronary blood flow and an inadequate supply of oxygen to the heart muscle.
    • Ischemia may be silent (asymptomatic but evidenced by ST depression of 1 mm or more on electrocardiogram (ECG) or may be manifested by angina pectoris (chest pain).
    • Risk factor for Coronary Artery Disease include dyslipidemia, smoking, hypertensio n, male gender (women are protected until menopause), aging, non-white race, family history, obesity, sedimentary lifestyle, diabetes mellitus, metabolic syndrome, elevated
    • Acute coronary syndrome is a complication of CAD due to lack of oxygen to the myocardium. Mnaifestations include unstable angina, non ST-segment elevation infarction, and ST- segment elevation infarction.
    • Other causes of angina include coronary artery spasm, aortic stenosis, cardiomyopathy, severe anemia, and thyrotoxicosis.
    •  Chest pain is provoked by exertion or stress and is relieved by nitroglycerin and rest. Character. Substernal chest pain, pressure, heaviness, or discomfort. Other sensations include a squeezing, aching, burning, choking, strangling, or cramping pain.
    •  Severity.Pain maybe mild or severe and typically present with a gradual buildup of discomfort and subsequent gradual fading away. Location.Behind middle or upper third of sternum; the patient will generally will make a fist over the site of pain (positive Levine sign; indicates diffuse deep visceral pain), rather than point to it with fingers.
    •  Radiation. Usually radiates to neck, jaw, shoulders, arms, hands, and posterior intrascapular area. Pain occurs more commonly on the left side than the right; may produce numbness or weakness in arms, wrist, or hands. Duration. Usually last 2 to 10 minutes after stopping activity; nitroglycerin relieves pain within 1 minute.
    •  Precipitating factors. Physical activity, exposure to hot or cold weather, eating a heavy meal, and sexual intercourse increase the workload of the heart and, therefore, increase oxygen demand. Associated manifestation. Diaphoresis, nausea, indigestion, dyspnea, tachycardia, and increase in blood pressure.
    •  Resting ECG may show left ventricular hypertrophy, ST-T changes, arrhythmias, and possible Q waves. Exercise stress testing with or without perfusion studies shows ischemia. Fasting blood levels of cholesterol, low density lipoprotein, high density lipoprotein, lipoprotein A, homocysteine, and triglycerides may be abnormal. Coagulation studies, hemoglobin level, fasting blood sugar as baseline studies.
    •  Cardiac catheterization shows blocked vessels. Position emission tomography may show small perfusion defects. Radionuclide ventriculography shows wall motion abnormalities and ejection fraction.
    •  Fasting blood levels of cholesterol, low density lipoprotein, high density lipoprotein, lipoprotein A, homocysteine, and triglycerides may be abnormal. Coagulation studies, hemoglobin level, fasting blood sugar as baseline studies.
    •  Antianginal medications (nitrates, beta- adrenergic blockers, calcium channel blockers, and angiotensin converting enzyme inhibitors) to promote a favorable balance of oxygen supply and demand. Antilipid medications to decrease blood cholesterol and tricglyceride levels in patients with elevated levels. Antiplatelet agents to inhibit thrombus formation. Folic acid and B complex vitamins to reduce homocysteine levels.
    •  Percutaneous transluminal coronary angioplasty or intracoronary atherectomy, or placement of intracoronarystent. Coronary artery bypass grafting. Transmyocardial revascularization.
    •  Monitor blood pressure, apical heart rate, and respirations every 5 minutes during an anginal attack. Maintain continuous ECG monitoring or obtain a 12-lead ECG, as directed, monitor for arrhythmias and ST elevation. Place patient in comfortable position and administer oxygen, if prescribed, to enhance myocardial oxygen supply.
    •  Identify specific activities patient may engage in that are below the level at which anginal pain occurs. Reinforce the importance of notifying nursing staff whenever angina pain is experienced. Encourage supine position for dizziness caused by antianginals.
    •  Be alert to adverse reaction related to abrupt discontinuation of beta-adrenergic blocker and calcium channel blocker therapy. These drug must be tapered to prevent a “rebound phenomenon”; tachycardia, increase in chest pain, and hypertension.
    •  Explain to the patient the importance of anxiety reduction to assist to control angina. Teach the patient relaxation techniques. Review specific factors that affect CAD development and progression; highlight those risk factors that can be modified and controlled to reduce the risk.
    • a temporary chest pain that results from inadequate oxygen flow to the myocardium. It’s usually described as burning, squeezing, or a tight feeling in the substernal or precordial chest. This pain may radiate to the left arm, neck, jaw, or shoulder blade. Typically, the patient clenches his fist over his chest or rubs his left arm when describing the pain, which may also be accompanied by nausea, vomiting, fainting, sweating, and cool extremities.
    •  Angina commonly occurs after physical exertion, but may also follow emotional excitement, exposure to cold, or a large meal. It may also develop during sleep, and symptoms may awaken the patient.
    •  When assessing for anginal pain, older adults commonly have an increased tolerance for pain, and may be less likely to complain. Instead, they may compensate by slowing their activity levels. Older adults may not experience chest pain at all, but may report dyspnea, faintness, or extreme fatigue.
    •  The person’s health history may suggest a pattern to the type and onset of pain. If the pain is predictable and relieved by rest or nitrates, it’s called stable angina. If it increases in frequency and duration and is more easily induced, it’s referred to as unstable angina or unpredictable angina. Unstable angina may occur at rest and generally indicates extensive or worsening disease that may progress to an MI. Variant or Prinzmetal’s angina is caused by coronary artery spasm, and commonly occurs at rest without initial increased oxygen demand.
    •  Administer oxygen to relieve ischemia at a flow rate based on institutional policy and the patient’s condition. Assess and document continuous ECG rhythm, vital signs, mental status, heart and lung sounds. Assess and document pain characteristics: location, duration, intensity (have patient grade pain on a scale from 1 to 10), precipitating factors, relief measures and any symptoms that indicate changes in these parameters.
    •  Assess vital signs with complaints of chest pain, and compare to baseline. Begin IV nitroglycerin titrated until acute pain is relieved; check blood pressure every 15 minutes or according to institutional policy; maintain systolic blood pressure greater than 90 mm Hg or according to institutional protocol; document the patient’s response to therapy. Administer IV morphine in small doses to relieve pain and decrease preload.
    •  Give sublingual, oral, or topical nitroglycerin prophylactically for chronic pain. Consider calcium channel blockers with Prinzmetal’s angina to block the influx of calcium into the cell; calcium channel blockers produce vasodilation of coronary and peripheral arteries. Use beta-adrenergic blockers to decrease myocardial oxygen demand by decreasing contractility, heart rate, and blood pressure. Notify the doctor and obtain a 12-lead ECG at the onset of recurring chest pain.
    •  Maintain activity restrictions based on the patient’s activity tolerance to reduce myocardial oxygen demands. Begin the patient on a low- cholesterol, low-sodium diet to alleviate the modifiable risk factors. Consider percutaneous transluminal coronary angioplasty (PTCA) to improve blood flow through the stenotic coronary arteries.
    •  Remember that a coronary artery bypass graft (CABG) may be indicated when medical treatment has been unsuccessful, based on the patient’s symptoms and the cardiac catheterization report. Provide patient education, and ensure that the patient can recognize signs and symptoms necessitating medical attention (unrelieved chest pain after taking three nitroglycerin tablets sublingually 5 minutes apart).
    •  Work with the patient and family to identify the patient’s risk factors and necessary life style modifications. Refer the family to appropriate sources for cardiopulmonary resuscitation (CPR) training. Ensure that the family can activate the emergency medical system if any problems occur at home.
    •  Refersto a dynamic process by which one or more regions of the heart muscle experience a severe and prolonged decrease in oxygen supply because of insufficient coronary blood flow. The affected muscle tissue subsequently becomes necrotic.
    • Onset of Myocardial Infarction may be sudden or gradual, and the process takes 3 to 6 hours to run its course.
    •  Itis the most serious manifestation of acute coronary syndrome, a complication of coronary artery disease (CAD). Approximately 90% of Myocardial Infarction are precipitated by acute coronary thrombosis (partial or total) secondary to severe CAD (greater than 70% narrowing of the artery).
    •  Other causative factors include coronary artery spasm, coronary artery embolism, infectious diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or stress on the heart in the presence of significant coronary artery disease.
    •  Chest pain  Character: variable, but often diffuse, steady substernal chest pain. Other sensations include a crushing and squeezing feeling in the chest. Other sensations include a crushing and squeezing feeling in the chest.  Severity: pain may be severe; not relieved by rest or sublingual vasodilator therapy, requires opioids.
    •  Location: variable, but often pain resides behind upper or middle third of sternum. Radiation: pain may radiate to the arms (commonly the left), and to the shoulders, neck, back, or jaw. Duration: pain continues for more than 15 minutes.
    •  Associated manifestations include anxiety, diaphoresis, cool clammy skin, facial pallor,hypertension or hypotension, bradycardia or tachycardia, premature ventricular or atrial beats, palpitations, dyspnea, disorie ntation, confusion, restlessness, fain ting, marked weakness, nausea, vomiting, and hiccups.
    •  Atypicalsymptoms of MI include epigastric or abdominal distress, dull aching or tingling sensations, shortness of breath, and extreme fatigue (more frequent in women).
    •  Riskfactors for MI include male gender, age over 45 for men, age over 55 for men, smoking; high blood cholesterol levels, hypertension, family history of premature CAD, diabetes and obesity.
    •  Serial 12-lead electrocardiograms (ECGs) detect changes that usually occur within 2 to 12 hours, but may take 72 to 96 hours  ST-segment depression and T-wave inversion indicate a pattern of ischemia; ST elevation indicates an injury pattern.  Q waves indicate tissue necrosis and are permanent Nonspecific enzymes including aspartate transaminase, lactate dehydrogenase, and myoglobulin may be elevated More specific creatinine phosphokinase isoenzyme CK-MB will be elevated.
    •  Triponin T and I are myocardial proteins that increase in the serum about 3 to 4 hours after an MI, peak in 4 to 24 hours, and are detectable for upto 2 weeks; the test is easy to run, can help diagnose an MI up to 2 weeks earlier, and only unstable angina causes a false positive. White blood cell count and sedimentation rate may be elevated. Radionuclide imaging, positron emission tomography, and echocardiography may be done to evaluate heart muscle.
    •  Pain control drugs to reduce catecholamine- induced oxygen demand to injured heart muscle.  Opiate analgesics: Morphine  Vasodilators: Nitroglycerin  Anxiolytics: Benzodiazepines Thrombolytic therapy by I.V. or intracoronary route, to dissolve thrombus formation and reduce the size of the infarction. Anticoagulants or other anti-platelet medications such as adjunct to thrombolytic therapy.
    •  Reperfusion arrhythmias may follow successful therapy. Beta-adrenergic blockers, to improve oxygen supply and demand, decrease sympathetic stimulation to the heart, promote blood flow in the small vessels of the heart, and provide antiarrhythmic effects. Calcium channel blockers, to improve oxygen supply and demand.
    •  Monitor continuous ECG to watch for life threatening arrhythmias (common within 24 hours after infarctions) and evolution of the MI (changes in ST segments and T waves). Be alert for any type of premature ventricular beats- these may herald ventricular fibrillation or ventricular tachycardia. Monitor baseline vital signs before and 10 to 15 minutes after administering drugs. Also monitor blood pressure continuously when giving nitroglycerin I.V.
    •  Handle the patient carefully while providing care, starting I.V. infusion, obtaining baseline vital signs, and attaching electrodes for continuous ECG monitoring. Reassure the patient that pain relief is a priority, and administer analgesics promptly. Place the patient in supine position during administration to minimize hypotension.
    •  Emphasize the importance of reporting any chest pain, discomfort, or epigastric distress without delay. Explain equipment, procedures, and need for frequent assessment to the patient and significant others to reduce anxiety associated with facility environment.
    •  Promote rest with early gradual increase in mobilization to prevent deconditioning, which occurs during bed rest. Tell the patient that sexual relations may be resumed on advise of health care provider, usually after exercise tolerance is assessed.
    •  Be alert to signs and symptoms of sleep deprivation such as irritability, disorientation, hallucinat ions, diminished pain tolerance, and aggressiveness. Take measures to prevent bleeding if patient is thrombolitic therapy
    •  Interventional cardiology is a branch of cardiology that deals specifically with the catheter based treatment of structural heart diseases.
    •  AngioplastyAlso called percutaneous transluminal coronary angioplasty (PTCA), angioplasty is an intervention for the treatment ofcoronary artery disease.
    • Valvuloplasty It is the dilation of narrowed cardiac valves (usually mitral, aortic, or pulmona ry).
    •  Congenital heart defect correction Percutaneous approaches can be employed to correct atrial septal and ventricular septal defects, closure of a patent ductus arteriosus, and angioplasty of the great vessels. Percutaneous valve replacement: An alternative to open heart surgery, percutaneous valve replacement is the replacement of a heart valve using percutaneous methods.
    • Coronary thrombectomy Coronary thrombectomy involves the removal of a thrombus (blood clot) from the coronary arteries.[
    •  3]Cardiac ablation A technique performed by clinical electrophysiologists, cardiac ablation is used in the treatment of arrhythmias.
    • Disorders of the formation and/or conduction of electrical impulses in the heartCause disturbances of heart rate and/or heart rhythmMay be evidenced by changes in hemodynamicsDiagnosed by analyzing electrocardiogram
    •  Sinus Bradycardia Sinus Tachycardia Sinus Arrhythmia
    •  Premature Atrial Complex Atrial Flutter Atrial Fibrillation
    •  Premature Junctional Complex Junctional Rhythm Atroventricular Nodal Reentry Tachycardia  Supraventricular tachycardia
    •  Premature Ventricular Complex Ventricular Tachycardia Ventricular Fibrillation Idioventricular Rhythm Ventricular Asystole
    •  First-Degree Atrioventricular Block Second-Degree Atrioventricular Block, Type I Second-Degree Atrioventricular Block, Type II Third-Degree Atrioventricular Block
    •  Monitoring and managing the dysrhythmia Minimizing anxiety Teaching self-care
    •  Provides electrical stimuli to heart muscle Used for slower-than-normal impulse formation, to control some tachycardias, or for advanced heart failure May be permanent or temporary
    •  NASPE-BPEG code  First letter identifies chambers being paced  Second letter describes the chambers being sensed  Third letter describes type of response by pacemaker to what is sensed
    •  Delivery of electrical current to depolarize a critical mass of myocardial cells When cells repolarize the SA node, is usually able to recapture its role as pacemaker of heart Cardioversion involves use of “timed” electrical current to terminate a tachydysrhythmia
    • Defibrillation is used in emergency situations as treatment for ventricular fibrillation and pulseless VT
    •  Chronic heart failure managed based upon type, severity, and cause Diastolic heart failure Systolic heart failure Ejection performed to assist in diagnosis
    •  Pulmonary congestion occurs when left ventricle cannot pump well Dyspnea upon exertion, orthopnea, and paroxysmal nocturnal dyspnea Oliguria
    •  Congestion of viscera and peripheral tissues when right ventricle fails Jugular vein distention Dependent edema Hepatomegaly Ascites Weakness, anorexia, and nausea Weight gain
    •  Eliminate or reduce contributing factors Reduce workload of heart by reducing afterload and preload Pharmacologic Therapy  ACE inhibitors and ARBs  Hydralazine and isosorbide dinitrate  Beta-blockers  Diuretics  Digitalis  Calcium channel blockers  Other: anticoagulants and antianginal medications Low Sodium Diet
    •  I&O Weigh daily Auscultate lung sounds Determine degree of JVD Assess dependent edema Monitor VS
    • Exam skin turgor and mucous membranesAssess for symptoms of fluid overload
    •  Pulmonary Edema is abnormal accumulation of fluid in the lungs, interstitial spaces and/or alveoli Increasing restlessness and anxiety Cyanosis Weak, rapid pulse Incessant coughing with mucoid sputum
    • Pharmacologic Therapy  Oxygen  Morphine  Diuretics  Dobutamine  Milrinone  Nesiritide
    •  Myocardial rupture is rare. Can occur as result of MI, infectious process, cardiac trauma, pericardial disease, or other myocardial dysfunction Result is immediate death Cardiac arrest occurs when heart ceases to produce effective pulse and blood circulation Pulseless electrical activity Emergency Management is CPR