NCM118 LEC Acute Biological Crisis - 1st Semester 2022-2023 PDF

|NCM118 LEC 1st SEMESTER A.Y. 2022 – 2023...

|NCM118 LEC 1st SEMESTER A.Y. 2022 – 2023 [PRELIM] NCM118 LEC ACUTE BIOLOGICAL CRISIS 2. INITIAL ASSESSMENT Condition that may result to patient mortality if left Initial impression unattended in a brief period of time. Mental status Condition that warrants immediate attention for the ABCs reversal of disease process and prevention of further Assign priority morbidity and mortality. Stable CRITICAL CARE NURSING Unstable Nursing specialty that deals specifically with Treatment & transport decisions human responses to life-threatening problems. Sequence depends on patient’s condition A critical care nurse is a licensed professional Components: nurse who is responsible for ensuring that acutely A. History of present illness and critically ill patients and their families receive B. Assessment of complaints, signs, symptoms (OPQRST) optimal care. Critically ill patients are those Onset Provocation Quality Radiation Severity Time patients who are at high risk for actual or potential C. SAMPLE history  life-threatening health problems. The more D. Rapid assessment  critically ill the patient is, the more likely he/she is E. Baseline VS  to be highly vulnerable, unstable and complex, F. Emergency medical care thereby requiring intense and vigilant nursing A. HISTORY OF PRESENT ILLNESS care. Why was EMS called? THE FOCUS OF CRITICAL CARE NURSING Elaboration on chief complaint Goal of critical care nursing Chief Complaint to provide comfort and facilitate healing of What patient states in his/her own words is primary patients whose lives are under threat from illness or problem trauma, whether sudden or chronic, accidental or OPQRST EMS ACRONYMS surgical. Onset What was the patient doing when Critical illness influences all body systems and has the signs and symptoms first a profound impact on the people it affects occurred? Was the onset sudden or ASSESSMENT gradual? A. Focused History/PE Provocation or Is there anything that makes the B. Comprehensive History/ PE Palliation symptom better or worse? 1. FOCUSED HISTORY/PE Quality Description of what the patient is o Taken in 8-14 minutes that addresses the patient’s feeling. For example, the pain can presenting health issue. be described as dull, sharp, Goals of assessing medical patients crushing, aching, tearing, o Explore and characterize the patient’s main throbbing, etc. health concern. Region and Where is the pain located and does o No need to go into each item of critical radiation it move to another part of the body background history in great detail, but should Severity How severe is the symptom based briefly touch on each item or at least consider on a scale of 1 to 10? them Time When did the signs and symptoms o Differentiate between critical & noncritical first occur? conditions B. MEDICAL PATIENT ASSESSMENT o Gather focused history & choose appropriate OPQRST—important for qualifying patient conditions assessment 1. Pain FOCUSED HISTORY/PE 2. Respiratory difficulties 1. Scene size-up 3. Altered mental status 2. Initial assessment 4. Allergic reaction 3. Focused history & physical exam 5. Poisoning/overdose 4. Rapid assessment 6. Environmental emergencies 5. Vital signs (VS) 7. Obstetric conditions 6. Ongoing assessment 8. Behavioral emergencies/psychiatric emergencies 1. SCENE SIZE-UP C. SAMPLE HISTORY BSI (Body Substance Isolation) precautions Signs & symptoms Evaluating scene safety Allergies Determining the MOI/NOI Medications Determining the total number of patients Past medical history Determining the need for additional resources Last oral intake Events leading up to episode Loue Jean S. Gulfan | 1 Nc m118 LEC 1st SEMESTER VASODILATORS D. RAPID ASSESSMENT Lower the systemic vascular resistance (afterload) Conscious patients—history first Reduce workload on the left ventricle Increase tissue Critical/unstable patients—history & assessment perfusion of vital organs simultaneously Unresponsive patients—assessment first, then Reduce preload history o Head-to-toe order Reduce preload o Focused assessment for responsive patients Decrease pulmonary congestion o Unresponsive patients IV NITROGLYCERIN and NITROPRUSSIDE o Head used as vasodilators to reduce preload and o Neck afterload. o Chest For oral use, ACE INHIBITORS. o Abdomen CARVEDILOL - non-selective beta blocker and o Pelvis alpha 1 blocker = decreases the HR and lowers o Back the systemic vascular resistance (vasodilation) o Extremities MINOXIDIL, HYDRALAZINE Trauma Calcium Channel Blockers - reduce the afterload o DCAPBTLS - Deformities, Contusions, but with negative inotropic properties. Abrasions, Penetrations, Burns, INOTROPIC AGENTS Tenderness, Lacerations, Swelling Stimulate the heart to contract more forcefully Medical o Function Increase CO o Guarding o Masses Reduce pulmonary congestion Improve tissue perfusion o Pain IV dobutamine, amrinone, milrinone o Tenderness Oral = digoxin E. VITAL SIGNS Loop diuretics = furosemide ✓ Baseline DIGITALIS GLYCOSIDES ✓ Trending with multiple sets Digoxin (Lanoxin) o Changes in condition o Positive inotropic effect (increased force o Response to treatment of myocardial contraction) F. EMERGENCY MEDICAL CARE o Negative chronotropic effect (decreased HR) When assessment is complete, plan or initiate care Indications: Care should be focused on signs & symptoms o Moderate to severe systolic HF not Unresponsive medical patient responsive to diuretics and ACE inhibitors Rely on patient’s presentation & information from o Atrial fibrillation, atrial flutter, paroxysmal bystanders/family tachycardia Pay attention to environment for clues o Loading dose = digitalization Consider ACLS intercept (clinical interventions for o Check apical pulse before urgent emergencies) administration. DRUGS FOR HEART FAILURE o Check quality of pulse and rhythm. o Administer IV doses very slowly at least 5 Compensatory Mechanisms of Heart Failure minutes. SNS – epi, norepi o Avoid giving via IM injections. Renin-angiotensin-aldosterone system o Weigh patient daily. Increase production of ADH o Avoid administering with food and Increase sodium reabsorption antacids. Signs and Symptoms o Therapeutic level = 0.5 – 2 ng/ml Dyspnea Digitalis Toxicity Chest pain Usually occurs in the elderly because digitalis has Fatigue a long half-life Edema Anorexia, mild nausea Syncope Digitalis intoxication: any change in pulse rhythm palpitations and rate, changes in mental status, changes in color vision, hallucinations Children = development of atrial arrhythmias Loue jean s. Gulfan | 2 Nc m118 LEC 1st SEMESTER Stop digitalis and any potassium-depleting diuretics, check serum K levels, and administer potassium as indicated. Administer anti-arrhythmic drugs (phenytoin and lidocaine). Prescribe atropine for sinus bradycardia. ANTIDOTE: DIGOXIN IMMUNE FAB (Digibind) PHOSPHODIESTERASE INHIBITORS Inotropic Amrinone (Inocor) o Incompatible with dextrose solutions o Bolus given slowly o Furosemide is incompatible with amrinone Milrinone (Primacor) o Possible diluents = 0.45% or 0.9% NaCl and D5W o Incompatible with furosemide Cardiac/Heart Failure (HF) -is a clinical syndrome resulting from structural or functional cardiac disorders that impair the ability of the ventricles to fill or eject 2 major types of HF: Identified by assessment of left ventricular function, usually by echocardiogram 1. Systolic heart failure - most common type; alteration in ventricular contraction characterized by a weakened heart muscle. - 1/3 of patients w/ HF have systolic dysfunction 2. Diastolic heart failure - characterized by a stiff & noncompliant heart muscle, making it difficult for the ventricle to fill. - 1/3 of HF patients have diastolic dysfunction. Assessment of ejection fraction (EF) is performed by echocardiogram to assist in determining the type of HF. EF=amount of blood present at the end of diastole – amount of blood pres in the left ventricle at the end of systole. Calculate the % of blood ejected. Normal EF= 55% to 65% of the ventricular volume If EF is normal in diastolic HF--- heart failure w/ preserved EF Diastolic heart failure - characterized by a stiff & noncompliant heart muscle, making it difficult for the ventricle to fill. 1/3 of HF patients have diastolic dysfunction. Etiology of HF: 1. Coronary Artery Disease 2. Hypertension 3. Cardiomyopathy 4. Valvular disorders 5. Renal dysfunction w/ volume overload 6. Diabetes Clinical Manifestations of HF 7. Atherosclerosis of the coronary arteries- primary CONGESTION cause of HF Dyspnea Orthopnea Paroxysmal nocturnal dyspnea Cough (recumbent or exertional) Loue jean s. Gulfan | 3 Nc m118 LEC 1st SEMESTER Pulmonary crackles that do not clear w/ cough weights gain dependent edema abdominal bloating or discomfort ascites - Jugular venous distention Sleep disturbance (anxiety or air hunger) Fatigue Poor perfusion/ Low CO Decreased exercise tolerance Muscle wasting or weakness Anorexia or nausea Unexplained weight loss Lightheadedness or dizziness Unexplained confusion or altered mental status - Resting tachycardia Daytime oliguria w/ recumbent nocturia Cool or vasoconstricted extremities Pallor or cyanosis Left-sided heart failure Pulmonary congestion occurs when the left ventricle cannot effectively pump blood out of the ventricle into the aorta & the systemic circulation Clinical manifestations: Dyspnea; Orthopnea Cough- initially dry & nonproductive Pulmonary Crackles Low oxygen saturation levels Right-sided heart failure When the right ventricle fails, congestion in the peripheral tissues & the viscera predominates Right side of the heart cannot eject blood effectively & cannot accommodate all the blood that normally returns from the venous circulation. When the right ventricle fails, congestion in the peripheral tissues & the viscera predominates Right side of the heart cannot eject blood effectively & cannot accommodate all the blood that normally returns from the venous circulation. SYSTEMIC Clinical manifestations: Edema of the lower extremities (dependent edema) Hepatomegaly- enlargement of the liver ascites- accumulation of fluid in the peritoneal cavity Weight gain due to fluid retention Loue jean s. Gulfan | 4 Nc m118 LEC 1st SEMESTER Noninvasive radionuclide ventriculography or invasive ventriculography as part of a cardiac catheterization procedure A type of angiography in which x-rays are taken; a radiopaque contrast agent is injected into the left or right ventricle of the heart through a catheter done during cardiac catheterization Chest x-ray & 12-lead electrocardiogram (ECG) assist in the diagnosis ECG is a medical test that detects heart problems by measuring the electrical activity generated by the heart as it contracts. Chest X-ray- shows the size of your heart & if there is fluid build-up around the heart & lungs. Laboratory studies includes serum electrolytes, Blood urea nitrogen, creatinine, liver function test, thyroid stimulating hormone, complete blood count, BNP, routine urinalysis B-type natriuretic peptide (BNP) - BNP level is a key diagnostic indicator of HF 1. BNP is released in response to atrial and ventricular stretch; it serves as a marker for heart failure. 2. BNP levels should be < 100 pg/mL (< 100 ng/L); the higher the level, the more severe the heart failure. Other findings Serum Electrolytes- abnormal result due to causes such as fluid retention or renal dysfunction Urinalysis- may reveal proteinuria associated with cardiovascular disease, BUN & creatinine level (blood urea nitrogen- N=10- 20 mg/dl; children= 5-18 mg/dl) indicate decreased renal blood flow Liver function tests- show elevated liver enzyme levels and indicate liver dysfunction due to heart failure Cardiac stress testing or cardiac catheterization to determine whether coronary artery disease & cardiac ischemia are causing the HF Loue jean s. Gulfan | 5 Nc m118 LEC 1st SEMESTER DRUGS FOR ANGINA PECTORIS Ultrafiltration is the movement of fluid across a Classification of ANGINA PECTORIS semipermeable membrane as a result of an artificially CHRONIC STABLE angina - precipitated by created pressure gradient. Ultrafiltration improves physical exertion and stress. congestion, lowers right atrial and pulmonary arterial UNSTABLE angina - has unpredictable onset, wedge pressures, improves cardiac output, decreases frequency, duration, and intensity. neurohormone levels, corrects hyponatremia, restores VARIANT angina - occurs when the patient is at diuresis, and reduces diuretic requirements. rest. DRUG THERAPY for ANGINA PECTORIS Nitrates 0Beta Blockers Calcium Channel Blockers Platelet-active agents (aspirin, clopidogrel, ticlopedine) NITRATES Induce relaxation of the peripheral vascular smooth muscles. Increase myocardial oxygen supply by dilating large coronary arteries and redistributing blood flow, thus enhancing oxygen supply to the ischemic areas. Oldest effective therapy for angina pectoris. Nitroglycerin is currently the DOC. Amyl nitrite = available in small glass ampules for inhalation. SIDE EFFECTS Excessive hypotension Dizziness Nausea, flushing, rarely syncope Prolonged headache Tolerance DRUG INTERACTION Alcohol accentuates vasodilation and postural hypotension of the nitrates. Calcium channel blockers and beta blockers may lower BP. Tablet fizzles or burns which indicates potency. Protect from heat and light. SR forms with water; not to chew or crush = these preparations need to reach the GI intact. Rotate sites of topical forms to decrease the risk of skin breakdown and abrasion. Loue jean s. Gulfan | 6 Nc m118 LEC 1st SEMESTER Avoid alcohol. Reduce arterial clot formation (white thrombus) BETA BLOCKERS by preventing platelet aggregation. Block beta receptors of the heart ANTICOAGULANTS Used in the prevention of arterial and venous Reduce myocardial oxygen demand thrombi in predisposed patients. BETA BLOCKERS Prevent new clots from forming Goal of beta blocker therapy: Warfarin, heparin o Reduce the number of anginal attacks Heparin derivatives or low molecular weight o Minimize nitroglycerin use heparins (LMWH) = ardeparin, dalteparin, o Improve exercise tolerance enoxoparin Acebutolol THROMBOLYTIC Atenolol Used to dissolve thromboemboli that are already Betaxolol formed metoprolol Streptokinase, alteplase CALCIUM CHANNEL BLOCKERS PLATELET INHIBITORS Decrease myocardial oxygen demand Aspirin (decreased workload). 2 – 4 times daily 0 Administer with food or milk. 0 Increase myocardial blood supply by dilating the Clopidogrel (Plavix) coronary arteries. OD with food or on empty stomach Inhibit smooth muscle contraction. Dipyridamole (Persantine) Amlodipine Used in combination with warfarin to prevent Nifedipine formation of thromboembolism after valve Verapamil replacement. Diltiazem Ticlopidine (Ticlid) nicardipine 50mg BID with meals DRUGS FOR THROMBOEMBOLIC DISORDERS ANTICOAGULANTS PATHOPHYSIOLOGY Warfarin (Coumadin) Thrombosis = process of forming a fibrin blood clot Oral; interferes with the formation of vitamin K (thrombus) dependent clotting factors in the liver. Embolus = small fragment of thrombus that breaks Used for prolonged effects. off and travels through the bloodstream until it Antidote: Vitamin K becomes trapped in a capillary. Monitor PT (prothrombin time) Coronary artery = myocardial infarction (MI) Heparin Brain = cerebrovascular accident (CVA) or stroke Blocks the conversion of fibrinogen to fibrin. Lungs = pulmonary embolism IV, SQ Legs = deep vein thrombosis (DVT) Does not cross the placenta. 0 Anticoagulant of CAUSES choice for lactating mothers. Immobilization with venous stasis Antidote: Protamine sulfate Surgery and post-operative period LOW MOLECULAR WEIGHT HEPARINS Trauma to the lower limbs Ardeparin Certain illnesses eg. HF, vasospasm, ulcerative Dalteparin (Fragmin) colitis Enoxaparin (Lovenox) Cancers of the lung, prostate, stomach, pancreas Used to prevent DVT after knee replacement Pregnancy and oral contraceptives therapy. Heredity Administer DEEP SC. THROMBI Do not administer IM. RED THROMBUS Inject the drug slowly, leaving the needle in place Venous thrombus for 10 seconds after injection. 0Do not rub site of Composed almost entirely of fibrin and RBC injection. Formed in response to venous stasis FIBRINOLYTIC Most common cause: DVT of the lower extremitie Streptokinase WHITE THROMBUS Urokinase Develop in the arteries Anistreplase Composed of fibrin and platelets Alteplase or Tissue Plasminogen Activator (t-PA) Form in areas of high blood flow in response to Reteplase (t-PA) injured vessel walls. HEMOSTATIC AGENTS Example: coronary artery occlusion = MI Used to stop bleeding. DRUG THERAPY Aprotinin PLATELET INHIBITORS or ANTIPLATELET 02.) aminocaproic acid Loue jean s. Gulfan | 7 Nc m118 LEC 1st SEMESTER CARDIOVASCULAR PHYSIOLOGY Conductivity Cardiac Cycle ability of cardiac cells to transfer the action Actual time sequence between ventricular potential generated at the sino-atrial node from contraction and relaxation cell to cell. An action potential moves through the Cardiac Output heart at a rate of 1 meter per second Amount of blood pumped by the left ventricle in 1 Contractility minute (SV Stroke volume x HR) cardiac muscle cell’s ability to transform an Average resting adult= 5 L/minute; can increase electrical signal originating at sino-atrial node into 5- fold during exercise mechanical action Stroke Volume- volume of blood pumped out of left Rhythmicity ventricle in a single beat or contraction (70 ml) a property of cardiac muscle cells which Systole- cardiac muscle is contracting to push describes their ability to contract regularly without blood out of the chamber the involvement of any nerves. Diastole- cardiac muscle cells relax to allow the MOVEMENT OF IONS chamber to fill with blood Intracellular (K, Mg, Ca) Blood pressure increases in the major arteries Extracellular (Na) during ventricular systole and decreases during Polarization- resting potential ventricular diastole. Depolarization- action potential Repolarization- recovery state NORMAL IMPULSE CONDUCTION Sinoatrial node AV node Bundle of His Bundle Branches Purkinje fibers ELECTRICAL CONDUCTION SYSTEM P wave: During normal atrial contraction, the SA SA Node Firing rate 60-100 BPM node sends an electrical signal to the AV node (Dominant Pacemaker) which spreads from the right atrium to the left Internodal Pathways Transfer impulse from the atrium. SA node throughout the QRS complex: Represents contraction of both atria to the AV junction ventricles. AV Junction (AV Node Slow impulse; intrinsic firing T wave: Relaxation and recovery (repolarization). and Bundle) rate of 40-60 BPM (Back- The interval from the beginning of the QRS up Pacemaker) complex to the apex (highest point) of the T wave Bundle Branches Two main branches (left is referred to as the absolute refractory period; and right) transmit impulse during this phase no action potential can be to ventricles generated. The last half of the T wave is referred Purkinje’s Network Spreads impulse to as the relative refractory period. throughout the ventricles; BASIC ELECTROPHYSIOLOGY intrinsic firing rate of 20-40 Primary Cardiac Cell Characteristics BPM (Back-up Characteristic Location Function Pacemaker) Automaticity/ SA node, AV Electrical rhythmicity junction, Purkinje PHARMACOLOGIC THERAPY fibers ACE inhibitors (Angiotensin-converting enzyme Excitability All cardiac cells Electrical Promotes vasodilation & diuresis. Vasodilation Conductivity All cardiac cells Electrical reduces resistance to left ventricular ejection of Contractility Myocardial Mechanical blood, diminishing the heart’s workload & muscle cells improving ventricular filling. ex.: Lisinopril (Prinivit); CARDIAC CELL CHARACTERISTICS Enalapril (Vasotec) Excitability Angiotensin Receptor Blockers cardiac cells respond to a suitable amount of blocks the vasoconstricting effects of angiotensin stimuli and produce an electric II at the angiotensin II receptors. Use as an potential/electrical impulse. This electrical impulse alternative to ACE inhibitors. - E.g. Valsartan ( spreads across the heart, causing it to beat diovan); Losartan ( Cozaar) Loue jean s. Gulfan | 8 Nc m118 LEC 1st SEMESTER 2. Excess fluid volume 3. Anxiety Hydralazine & Isosorbide Dinitrate ( Dilatrate) 4. Powerlessness another alternative for patients who cannot take 5. Ineffective family health management ACE inhibitors. COLLABORATIVE/ POTENTIAL COMPLICATIONS: Nitrates (e.g. Isosorbide dinitrate) cause venous NURSING DIAGNOSES dilation, w/c reduces the amount of blood return hypotension, poor perfusion, & cardiogenic shock to the heart & lowers preload. dysrhythmias Hydralazine- lowers systemic vascular resistance & thromboembolism ventricular afterload. pericardial effusion & cardiac tamponade Beta- Blockers/ Beta-Adrenergic Blocking Agents They relax blood vessels, lower blood pressure, NURSING INTERVENTIONS decrease afterload, & decrease cardiac 1. Promoting activity tolerance workload. e.g. Carvedilol (Coreg); Bisoprolol 2. Managing fluid volume (Zebeta); Metoprolol (Lopressor, Toprol XL) 3. Controlling anxiety PHARMACOLOGIC THERAPY:.HF 4. Minimizing powerlessness Diuretics 5. Assisting patients and family to effectively manage remove excess extracellular fluid by increasing the health rate of urine produced in patients w/ signs & ACUTE MYOCARDIAL INFARCTION symptoms of fluid overload. Necrosis (death) of myocardial cells Loop diuretics- inhibit sodium & chloride A deficit of two oxygenation factors: supply and reabsorption mainly in the ascending loop of demand, which results in myocardial damage henle May lead to cardiogenic shock and death Thiazide diuretics e.g. metolasone(Zaroxolyn)- CATEGORY OF AMI early distal tubules Transmural Aldosterone antagonist such as spironolactone Entire thickness of all layers of the myocardium in (Aldactone)- block the effects of aldosterone in a specific region is affected (from endocardium the distal tubule & collecting duct. to epicardium) Digitalis AKA Q-wave MI (>1 mm wide, > 2 mm deep, > 25% increases the force of myocardial contraction & of depth of QRS complex. Seen in leads V1-3 slows conduction through the atrioventricular Non-transmural node. It improves contractility, increasing left Necrosis commonly affects inner layers of the ventricular output. e.g. Digitalis (Lanoxin) endocardium (subendocardial infarcts) IV infusions AKA non-Q-wave MI IV inotropes such as milrinone (Primacor), ST depression dobutamine (Dobutrex) T wave inversion may be seen they increase the force of myocardial contraction RISK FACTORS: used for pts who are unresponsive to routine pharmacologic therapy & w/ severe ventricular Non-modifiable dysfunction Age DOBUTAMINE Gender cathecolamine IV medication given to pts w/ Genetic significant ventricular dysfunction & hypoperfusion Race stimulates the beta-1 adrenergic receptors Pathologic Conditions action: increase cardiac contractility & renal Hypertension perfusion to enhance urine output. DM Other medications for HF Hyperlipidemia Anticoagulants - if client has history of atrial Lifestyle fibrillation or a thromboembolic event. Smoking Antiarrhythmic drugs such as amiodarone Obesity (Cordarone) for pts. w/ dysrhythmias Physical inactivity Medications that manage hyperlipidemia (e.g., Diet statins) PATHOPHYSIOLOGY NUTRITIONAL THERAPY Low Na diet (no more than 2 g/day)- reduce fluid Atherosclerosis triggers coronary artery spasm retention & symptoms of peripheral & pumonary congestion Decrease or complete blockage of blood flow Avoid excessive fluid intake NURSING DIAGNOSES Tissue damage triggers platelet aggregation causing a 1. Activity intolerance complete arterial obstruction Loue jean s. Gulfan | 9 Nc m118 LEC 1st SEMESTER ✓ Maintain cardiovascular stability Ischemia beyond 20 minutes to several hours can cause ✓ Decrease cardiac workload irreversible cellular death (necrosis) ✓Prevent complications ASSESSMENT FINDINGS: AHA GUIDELINES FOR THE MANAGEMENT OF PATIENTS WITH 1. Chest pain: substernal or precordial, may AMI INITIAL RECOGNITION AND MANAGEMENT IN THE radiate to neck jaw, shoulder(s), or left arm lasts EMERGENCY DEPARTMENT more than 15 to 20 minutes The initial evaluation of the patient ideally should be 2. Indigestion, heartburn, N/V accomplished within 10 minutes of his or her arrival in the 3. Tachycardia ED; certainly, no more than 20 minutes should elapse 4. Tachypnea before an assessment is made. 5. Hypotension or hypertension 1. Oxygen therapy 6. Delayed fever (48 hours after infarct) 2. Sublingual nitroglycerin therapy 7. Dyspnea, shortness of breath 3. Adequate analgesia (with morphine sulfate or 8. Cool-mottled skin Meperidine) 9. Diminished peripheral pulses 4. Aspirin, 160 to 325 mg orally 10. Abnormal heart sounds 5. 12-lead electrocardiogram (ECG) should be 11. Palpitations, dysrhythmias performed 12. Decreased level of consciousness 6. Immediate reperfusion therapy, either by thrombolytic or primary percutaneous LABORATORY FINDINGS: transluminal coronary angioplasty 1. CK (Creatine Kinase) THE FIRST 24 HOURS 2. CK-MB (Creatine Kinase Myocardial Band) 1. Continuous ECG and serum cardiac markers. Factor) 2. The patient's physical activities should be limited 3. Cardiac Muscles Troponin for at least 12 hours, and pain and/or anxiety 4. Myoglobin-N=0 to 85 ng/ml should be minimized with appropriate analgesics. 5. Cholesterol, LDL, HDL 3. Although the use of prophylactic antiarrhythmic agents in the first 24 hours of hospitalization is not recommended, Atropine, Lidocaine, transcutaneous pacing patches or a transvenous pacemaker, a defibrillator, and epinephrine should be immediately available. 4. When primary PTCA is performed, high-dose of intravenous heparin is recommended. 5. Aspirin, 160 to 325 mg daily, initially given in the ED, should be continued indefinitely. 6. The patient with evolving acute MI should receive early intravenous β-adrenergic blocker therapy, followed by oral therapy, provided that there is no contraindication. 7. ACE inhibitor should be initiated within hours of hospitalization, provided that the patient does not have hypotension or a contraindication. DIAGNOSTIC TESTS: AFTER FIRST 24 HOURS 1. ECG 1. Indefinitely with a β-adrenergic blocker 2. Radionuclide Imaging- A small amount of 2. ACE inhibitor for at least 6 weeks. radioactive material such as thallium or 3. Nitroglycerin should be infused intravenously for technetium is injected into a patient’s vein. The 24 to 48 hours, and magnesium sulfate should be radioactive material travels to the patient’s heart given as needed to replete magnesium deficits for muscle and pictures are taken with a special 24 hours. camera to obtain a three-dimensional image 4. Angiography and PTCA >procedure that uses a 3. Hemodynamic Monitoring- measures the blood special dye & x ray to see how blood flows through pressure inside the veins, heart, and arteries. It also the arteries in your heart 5. Continue Aspirin 160 to measures blood flow and how much oxygen is in 325 mg/day the blood. It is a way to see how well the heart is OTHER TREATMENTS: working. 1. Intra-aortic Balloon Pump (IABP) MEDICAL MANAGEMENT: 2. Percutaneous Transluminal Coronary Angioplasty Primary focus/ Goal: (PTCA) ✓ Relieve chest pain 3. Coronary Artery Bypass Graft (CABG) ✓ Reduce the extent of myocardial damage Loue jean s. Gulfan | 10 Nc m118 LEC 1st SEMESTER 4. Ventricular Assist Device ✓ LVAD- most common ✓ 2. Encourage verbalization of fears and concerns. RVAD- short term ✓ BIVAD ✓ Transcutaneous- short 3. Explain the need for frequent monitoring of vital signs term ✓ Implantable- long term and potential bleeding. 4. If needed, prepare for intubation and mechanical ventilation INTRA-AORTIC BALLOON PUMP (IABP) 5. Discuss continuing cardiac care and rehabilitation. ✓ Place patient on cardiac monitor ✓ Report any changes in mental status ✓ Monitor hemodynamic status ✓ Administer oxygen, continuous oximetry ✓ Monitor ABG, cardiac enzymes, electrolytes and CBC ✓ Maintain IV flow rate and assess insertion site ✓ Assume position as tolerated: semi to high fowler’s ✓ Schedule adequate rest periods and limit visiting PERCUTANEOUS TRANSLUMINAL CORONARY time ANGIOPLASTY (PTCA) ✓ Administer stool softener as ordered; avoid valsalva response STROKE/ CEREBRO VASCULAR DISORDERS Cerebrovascular disorders/strokes Refers to a functional abnormality of the CNS that occurs when blood supply to the brain is disrupted Cerebrovascular disorders/ stroke 2 major categories: 1. Ischemic (87%) - vascular occlusion & significant hypoperfusion occur 2. Hemorrhagic (13%) - extravasation of blood into the brain or subarachnoid space ISCHEMIC stroke Coronary artery bypass graft (CABG) “Brain attack” A healthy artery or vein from the body is Sudden loss of function resulting from disruption of connected, or grafted, to the blocked coronary the blood supply to a part of the brain. artery. The grafted artery or vein bypasses (that is, Cerebrovascular disorder/stroke: goes around) the blocked portion of the coronary 5 diff. types of ischemic stroke based on the cause: artery. This creates a new path for oxygen-rich 1. Large artery thrombotic strokes (20%) blood to flow to the heart muscle caused by atherosclerotic plaques in the Ventricular assist device large blood vessels of the brain. - is a mechanical pump that's used to support heart thrombus formation & occlusion results in function and blood flow in people who have ischemia & infarction Cerebrovascular weakened hearts. The device takes blood from a disorder/stroke: 2. lower chamber of the heart and helps pump it to 2. Small penetrating artery thrombotic the body and vital organs, just as a healthy heart strokes/lacunar strokes (25%) would affect one or more vessels NURSING DIAGNOSES Cerebrovascular disorder/stroke: 3. 1. Acute Pain 3. Cardiogenic embolic strokes (20%) 2. Anxiety and Fear associated w/ cardiac dysrhythmias, 3. Decreased cardiac output usually atrial fibrillation; can also be 4. Ineffective family coping associated w/ valvular heart disease & 5. Ineffective tissue perfusion thrombi in the left ventricle EXPECTED OUTCOMES: Cerebrovascular disorder/stroke: 1. Decrease pain scale 4. Cryptogenic strokes (30%) - no known cause 2. Verbalize reduced anxiety and fear 5. Other causes (5%) - illicit drug use (cocaine); 3. Demonstrate no signs of bleeding coagulopathies; migraine/vasospasm; 4. Maintain adequate cardiac output spontaneous dissection of the carotid or vertebral arteries NURSING MANAGEMENT: RISK FACTORS: 1. Instruct to report all chest pain; Administer pain medication as ordered. 1. Asymptomatic carotid stenosis 2. Atrial fibrillation Loue jean s. Gulfan | 11 Nc m118 LEC 1st SEMESTER 3. Diabetes 5. Antihypertensive medications - ACE inhibitors & 4. Dyslipidemia diuretics or a combination - used after the acute 5. Excessive alcohol consumption stroke period 6. Hypercoagulable states 6. Thrombolytic agents - dissolves blood clot by 7. Hypertension binding to fibrin & converting plasminogen to 8. Migraine plasmin, w/c stimulates fibrinolysis of the clot 9. Obesity Medical management 10. Sedentary lifestyle Endovascular treatment - devices that open the 11. Sleep Apnea blocked artery (stent) & restore blood flow to the 12. Smoking brain Pathophysiology Nursing diagnosis Thrombosis (blood clot within a blood vessel of the brain Impaired physical mobility or neck) Acute pain Self-care deficit Cerebral embolism (blood clot carried to the brain from Impaired comfort another part) Impaired swallowing Impaired urinary elimination Ischemia (decrease blood flow to an area of the brain) Constipation Clinical manifestations Acute confusion Numbness or weakness of the face, arm, or leg, Impaired verbal communication esp. on one side of the body Risk for impaired skin integrity Confusion or change in mental status Interrupted family processes trouble speaking or understanding speech Sexual dysfunction visual disturbances Nursing interventions difficulty walking, dizziness, or loss of balance or 1. Improving mobility & preventing joint deformities coordination - prevent shoulder adduction sudden severe headache - position the hand & fingers Assessment: - changing positions 1. Initial assessment focuses on airway patency - establishing an exercise program - compromised by loss of gag or cough reflexes & altered respiratory pattern; cardiovascular status (BP, -prepare for ambulation 2. Prevent shoulder pain cardiac rhythm & rate, carotid bruit); & gross neurologic - post stroke pain medications- amitriptyline deficits (Elavil); gabapentin (Neurontin); lamitrigine (Lamictal); Diagnostic findings pregabalin (Lyrica) 1. Non- contrast computed tomography scan - to 3. Enhancing self- care determine if the event is ischemic or hemorrhagic 4. Adjusting to physical changes 2 - approach pt on the side where visual perception is 2. 12 lead ECG intact. 3. Carotid ultrasound 5. Assisting w/ nutrition 4. Other studies - educate pt in alternative swallowing technique; - CT angiography or CT perfusion; magnetic advise to take smaller boluses of food & types of food resonance imaging (MRI); magnetic resonance that are easier to swallow. angiography; transcranial doppler flow studies; 6. Attaining bladder & bowel control transthoracic or transesophageal - intermittent catheterization w/ sterile technique echocardiography; xenon-enhanced CT scan; 7. Improving thought processes single-photon emission CT scan - collaborate w/ primary provider, psychiatrist, & other Pharmacologic Management professionals 8. Improving communication 1. Warfarin (Coumadin) - for pts. w/ atrial fibrillation - speech therapist or cardioembolic strokes 9. Maintaining skin integrity 2. New or novel oral anticoagulants (NOACs) - - frequent assessment of the skin esp. on bony & dabigatran (Pradaxa); apixaban (Eliquis); dependent parts of the body; turning sched edoxaban (Savaysa); rivaroxaban (Xarelto) 10. Improving family coping 3. Platelet-inhibiting medications - includes aspirin, - encourage to participate in counseling & use extended-release dipyridamole plus aspirin support system (Aggrenox); clopidogrel 11. Helping the pt cope w/ sexual dysfunction 4. Statin medications - simvastatin (Zocor) - 12. Monitoring & managing complications prevent secondary stroke Loue jean s. Gulfan | 12 Nc m118 LEC 1st SEMESTER - Decreased cerebral blood flow due to increased provide info about the affected arteries, veins, ICP, leading to inadequate oxygen delivery to the adjoining vessels & vascular branches. Diagnostic brain, & pneumonia findings…hemorrhagic stroke: - neurologic flow sheet is used to monitor & 3. Lumbar puncture document assessment parameters - performed if there is no evidence of IICP, CT scan Hemorrhagic stroke is negative, & subarachnoid hemorrhage is confirmed - Lumbar Puncture in the presence of Caused by bleeding into the brain tissue, the IICP can result to brain herniation or rebleeding ventricles, or the subarachnoid space GCS Result: 13-15- mild BI 9-12- moderate BI 8 or less- severe Hemorrhagic stroke BI Primary intracerebral hemorrhage - spontaneous rupture of small vessels accounts for 80% of hemorrhagic strokes - cause: uncontrolled hypertension; - cause in older adults: cerebral amyloid angiopathy Hemorrhagic stroke Subarachnoid hemorrhage - occur spontaneously from a ruptured intracranial aneurysm Hemorrhagic stroke Secondary intracerebral hemorrhage - associated w/ arteriovenous malformations (AVMs), intracranial aneurysms, intracranial Laboratory/Diagnostic Findings: neoplasms, or certain medications 1. Lumbar Puncture (anticoagulants, amphetamines) 2. Angiography Pathophysiology Radiopaque contrast Blood vessels rupture 3. EEG 4. Transcranial Ultrasound Doppler Blood enters the brain tissue, cerebral ventricles or 5. CT scan/MRI subarachnoid space Medical Management: 1. Antiplatelet- Aspirin, clopidogrel (Plavix), T Compressing adjacent tissues causing blood vessel spasm iclopidine (Ticlid) and cerebral edema 2. Anti-coagulant- Heparin, Warfarin 3. Corticosteroids – prednisone, dexamethasone Blood in the ventricles irritates the meninges and brain 4. Diuretics –lasix/ osmotic diuretic- mannitol tissue 5. Anticonvulsant- Phenytoin (Dilantin) Inflammatory reaction and impairing absorption and Surgical Management: circulation of CSF 1. Ventriculostomy - is a neurosurgical procedure that involves creating a Increase ICP may cause coma and death hole ("ostomy") within a cerebral ventricle for Clinical manifestations drainage Surgical Management: 2. Decompressed craniotomy Severe headache 3. Carotid Endarterectomy Nausea & vomiting Sudden change in level of consciousness ✓ Removal of atherosclerotic plaque Possible seizure Pain & rigidity of the back of the neck (nuchal rigidity) & spine due to meningeal irritation Visual disturbances (visual loss, diplopia, ptosis)- if aneurysm is adjacent to the oculomotor nerve Tinnitus, dizziness & hemiparesis Diagnostic findings 1. CT scan or MRI - determines the type of stroke, size & location, presence or absence of ventricular blood & hydocephalus Diagnostic findings…hemorrhagic stroke: 2. Cerebral angiography - confirms the diagnosis of an intracranial aneurysm or AVM - shows the location & size; Loue jean s. Gulfan | 13 Nc m118 LEC 1st SEMESTER 4.Extracranial-intracranial Bypass 3. Brain tumor ✓ Bypass of the internal carotid, middle cerebral 4. Brain herniation or vertebral artery 5. Head injury Other therapy 6. Stroke 1. Physical Therapy helps prevent contractures Pathophysiology of IICP: and improve muscle strength and coordination Increased ICP from any cause > decreases 2. Occupational Therapy provides assistive Cerebral perfusion > swelling/edema > shift brain devices and a plan for regaining lost motor skills. tissue resulting in herniation 3. Speech Therapy Increased ICP> reduce cerebral blood flow> Nursing Diagnoses: ischemia and cell death 1. Ineffective tissue perfusion 2. Impaired verbal communication Assessment Findings of IICP: 3. Impaired physical mobility 1. Earliest sign 4. Impaired swallowing Change in LOC, agitation, slowing of 5. Incontinence bladder/bowel speech, delay in response to verbal 6. Self-care deficit suggestions 7. Altered thought process Restlessness (w/o apparent reason), 8. Sensory/perceptual alterations confusion, increasing drowsiness= results 9. Risk for impaired skin integrity from compression 2. 10. Social isolation 2. Late signs: 11. Sexual dysfunction stuporous, comatose, abnormal motor Nursing Management: response in the form of decortication, decerebration or flaccidity 1. Assess for communication ability and offer alternative methods of communication. 2. Assess neurologic status. 3. Monitor respiratory status and airway patency. Auscultate pulmonary sounds, and result of ABG’s. 4. Suction as necessary. 5. Administer oxygen as ordered. 6. Assess for skin breakdown. 7. Encourage ROM and turning. 8. Provide for rest. 9. Maintain fluid and electrolyte balance. 10.Apply anti-embolic stockings. INCREASED INTRACRANIAL PRESSURE Increased Intracranial Pressure An ICP exceeding 15 mmHg is a medical ICP Monitoring emergency 1. Components of monitoring: Rigid cranial vault contains: ✓ Sensor o Brain tissue- 1,400 g ✓ Transducer o Blood- 75 mL ✓ Recording device o CSF- 75 mL 2. ICP’s effect on the sensor which transmits Monro-Kellie Hypothesis information to transducer ICP values 3. An electrical signal is displayed via oscilloscope o Normal ICP 0-10 mmHg 4. Monitoring devices: o Upper limit of normal 15 mm Hg ✓ Intraventricular catheter- The catheter is Monro- kellie hypothesis/Monro-Kellie doctrine inserted through the brain into the lateral States that because of the limited space for ventricle expansion w/in the skull, an increase in any one of the components causes a change in the volume ✓ Epidural sensor- The epidural sensor is placed of the others. Compensation is accomplished by through a hole drilled in the skull. displacing or shifting CSF. ✓ Subarachnoid screw- it is place through the membrane that protects the brain and spinal Causes of IICP: cord (dura mater) ✓Occur in normal activities such as coughing, Nursing care of pts with ICP monitoring: sneezing, straining, or bending forward- minor changes in blood volume & CSF 1. Ensure continuous neurologic assessment. 1. Cerebral edema 2. ICP device: 2. Hydrocephalus ✓ Maintain closed system sterility Loue jean s. Gulfan | 14 Nc m118 LEC 1st SEMESTER ✓ Maintain transducer at the same level of the ear ✓ Do not permit air bubbles to enter transducer or tubing 3. Monitor pressures and waveforms. 4. Report and document pressure changes. 5. Remember that coughing, sneezing, or valsalva may cause a temporary change in pressure 6. Limit suctioning. Medical Management: Nursing Diagnoses: 1. Ineffective airway clearance 2. Altered tissue perfusion: cerebral 3. Altered thought process 4. Risk for infection 5. Risk for impaired skin integrity Nursing Management: 1. Assess neurologic status, including LOC, pupillary reactivity, ocular movement and general motor/sensory function. 2. Monitor VS. 3. Ensure that body temperature is maintain to prevent acceleration of oxygen consumption. 4. Maintain patent airway and adequate ventilation. 5. Assess respiratory rate and pattern. 6. Assess for cyanosis. 7. Suction as needed. Hyperoxygenate prior to suctioning. 8. Assist with mechanical ventilation to decrease CO2. 9. Monitor ABG to ensure adequate oxygenation 10. Maintain optimal patient positioning. ✓ Elevate head of bed 30-40 degrees in neutral position ✓ Turn patient every 2 hours ✓ When the client is alert, have him exhale during turning to block activation of valsalva maneuver 11. Monitor fluid balance. 12. Prevent precipitous increases in ICP. ✓ Provide quite environment ✓ Prevent coughing ✓ Avoid vomiting by administering antiemetic ✓ Prevent straining of stool Loue jean s. Gulfan | 15