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Exam #2
MedSurg
| Question | Answer |
|---|---|
| How are MI's related to Cardiac Output? | |
| Excessive Ventricular filling. | Results in excessive LVED voulme (left ventricle end diastolic volume)and pressure, however, and may result in decreased cardiac output. |
| Venules and Arterioles. What happens in supine position? | Hydrostatic pressure is decreased when client is lying down. There is less hindrance of venous return to the heart. Blood returns easier and faster. |
| Mean Arterial Pressure (MAP) | MAP maintains adequate blood flow through the coronary arteries. It is necessary to maintain perfussion of major body organs such as kidneys and brain. map should be at least 60-70mmHg. |
| NY Heart Association Class I. | Cardiac disease/ No physical limitations/ Activity doesnt cause fatigue,palpitation, or aginal pain. |
| NY Heart Association Class II. | Cardiac disease/ Slight physical limitations/ Comfortable at rest/ Activty causes fatigue, palpitation, dyspnea or anginal pain. |
| NY Heart Association Class III. | Cardiac disease/ Marked limitations/ Comfortable at rest/ Less than ordinary activity causes fatigue, palpitation, dyspnea or aginal pain. |
| NY Heart Association Class IV. | Cardiac disease/ Inability to have activity/ Symptoms of cardiac insuffiency evident at rest/ Discomfort increased with physical activity. |
| S1 (Normal heart sound). How to assess and location 1. | Produced by closure of heart valves (AV valves, mitral & tricuspid). 1st heart sound (LUB). Heard best at the lower left sternal border of the apex. Softer and longer than S2. Incresed sound during excercise, hyperthyroidism, and mitral stenosis. |
| S1 (Normal heart sound). How to assess and location 2. | Decreased sound during mitral regurgitationa and heart failure. Marks the beginning of ventricular systole and occurs right after the QRS complex on ECG. Longer phase. Soft pitch. |
| S2 (Normal heart sound). How to assess and location. | Produced by closure of heart valves Semilunar valves, pulmonic & aortic). 2nd heart sound (DUB). Heard best at the base of the heart at the end of ventricular systole.Shorter phase. High pitched. |
| Splitting of S1 & S2. (Normal heart sound) | S1-closure of mitral valve followed by closure of the tricuspid valve-left ventricle contraction occurs slightly before right ventricle contraction(often not heard). S2-normal splitting occurs because of the longer systolic phase of the right ventricle. |
| Paradoxical Splitting (Abnormal heart sound) | Abnormal splitting of S2. Characteristic of a wider split heard on exhpiration. Heard in clients with severe myocardial depression that causes early closure of the pulmonic valve or delay of the aortic valve closure. |
| Paradoxical Splitting Causes. | Myocardial infarction, left bundle branch block, aortic stenosis, aortic regurgitation, right ventricular pacing. |
| Gallops(Abnormal heart sound) | Produced when blood from the atrium enters a noncompliant ventricular chamber (decreased compliance) during rapid ventriclar filling in right, left or both ventricles. Sounds arise from vibrations of the valves and supporting structures. Commonly heard i |
| S3-Gallop (Abnormal heart sound) | Ventricular gallop.Left ventricular filling sounds heard best with person lying on left side with bell placed at the apex and left sternal border during during expiration. Usually normal in cildren and up to 30 years old. |
| S3-Gallop Continued | Abnormal in people >35-represents a decrease in ventricular comliance. Can be detected as an early sign of heart failure or as a ventricular septal defect(VSD). Heard during early diastole. |
| S4-Gallop (Abnormal heart sound) | Atrial gallop. Heard in those with hypertension, anemia, ventricular hypertrophy, myocardial infarction, aortic or pulmonic stenosis, and pulmonary emboli. may also be heard in advanced age(stiffened ventricla. Heard during late diastole. |
| S3 & S4 Summation(Abnormal heart sound) | Summation or a quadruple gallop. Indication of severe heart failure. If present with tachycardia (shortened diastole), the sounds may be close together and sound like a galloping horse. |
| Snaps & Clicks (Abnormal heart sound) | Related to stenoic valve. |
| Murmurs Abnormal heart sound) | Represnts turbulent blood flow through normal or abnormal heart valves. Classified according to their timing in cardiac cycle. Can occur during presystole, midsystole,or late systole or diastole,or can last thoughout both phases of cardiac cycle. |
| Murmur Classification | Systolic Murmur-aortic stenosis and mitral regurgitation occur between S1 & S2. Diastolic Murmur-mitral stenosis and aortic regurgitation occur between S1 & S2-related to turbulent blood flow as seen with hyperdynamic states. |
| Murmur Decsription | Murmurs are described by 1.location and area of rediation(if any) 2.Configuration-Cresendo(increased intensity)or Decresendo(decreased intensity) 3.Quality (harsh, blowing, whistlding, rumbling, squeaking) 4. Pitch (high, low). |
| Murmur Grading | Graded according to their intensity (level of loudness). Grades are I-VI |
| Grade I. | Very faint. |
| Grade II. | Faint, but recognizable. |
| Grade III. | Loud, but moderate in intensity. |
| Grade IV. | Loud and accompanied by a palpable thrill. |
| Grade V. | Very loud, accompanied by a palpable thrill and audble with the stetescope partially off the chest wall. |
| Grade VI. | Extremely loud, may be heard with the stetescope slightly above the chest wall and accompnied by palpible thrill. |
| Friction Rub (Abnormal heart sound) | Originates from pericardial sac & occurs with movement of the heart during the cardiac cycle. Usually a sign of inflammation, infection or infiltration. Can beheard in clients with pericarditis from MI and cardiac tamponade. |
| Friction Rub Continued | Best auscultated with person sitting up, leaning forward, and exhaling ( use diaphragm of stetescope). Harsh grating sound heard during systole and diastole caused by abrasion of pericardial surfaces. |
| Lab Tests (Serum Markers) | Increase in circulating enzymes due to cellular tissue injury. MI (acute coronary syndrome) can be confirmed by abnormally high levels of enzymes or isoenzymes. Detected by serum studies (cardiac markers). Tropinin, Myoglobin & Creatine Kinase, CKMB, LDH |
| Myoglobin | Heme low molecular weight protein rapidly released after myocardial damage. Elevations can occur with renalor skeletal muscle damage. Early marker of MI. Rises in 1-3 hours after MI/Peaks in 4-12 hours/Returns to normal in 24 hours. |
| Creatine Kinase (CK-MB) | Enzyme specific to myocardium. Isoenzyme indicate which organ is damaged. Predicatable rise and fall in 3 days. After acute MI, are the first enzymes to rise. Rise in 3-8 hours/Peak at 12-24 hours/Returns to normal in 2-3 days. |
| Tropinin I | Contractile protein only found in cardiac muscle. Specific marker of myocardial damage. Rises within 3-4 hours/Peaks in 4-24 hours/Remains elevated for several weeks. |
| Lactate Dehydrogenase (LDH) | Rise & Peak in 2-3 days. |
| Genetics and Atherosclerosis | People with a genetic predisposition to familial hyperlipidemia is suseptible to atherosclerosis because the liver makes excessive amounts of cholsterol and other fats (which cause hyperlipidemia). This contributes to the development of atherosclerosis. |
| Orthostatic (Postural Hypotension) | Occurs when the B/P is not adquately maintained while moving from a lying position to a siiting or standing position. Evidenced by a decrease of more than 20mmHg systolic or more than 10mmHg diastolic as well as a 10%-20% increase in heart rate. |
| ECG (Electrocardiogram) | Records electrical activity of the heart. Requires placement of electrodes to view myocardialelectrical conduction from different axes or positions. Client is placed in supine position. Wash skin to remove oils. |
| ECG Continued | Can be used to diagnose dysrhythmias, conduction abnormalities, enlarged heart chambers, myocardial ischemia or infarct, high or low calcium and potassium levels, and effects of some medications. |
| EPS (Electrophysiologic Testing) | Test performed on clients with Hx of MI, recurrent tachydysrythmias or syncopal episodes. Distinguish atrial fron ventrical dysrhythmias. Done in cath lab because risks are similiar to cardiac catherization. Evaluates node function. |
| EPS Continued | Catether is placed in (RA) & (RV). The test lastes 2-6 hours. Client may complain of back pain due from lying supine for extensive time. Client may experience memory loss of procedure. chest discomfort in area where electrical current was applied. |
| Stress Test (Electrocardiography) | Exercise tolerance. Noninvasive, evaluate respose of cardiovascular system to workload or stress. Screens for asymptomatic coronary artery disease. Obtain written consent. Instruct client to get planty rest the night before the procedure. |
| Stress Test Continued | May have lite meal 2 hours before test. No smoking alcohol or caffeine day of test. May be done on bike or treadmill. Monitor ECG and BP until client recover. Avoid hot showers for 2 hours after test, may cause hypotension/vasoconstriction-May pass out. |
| Cardiac Catherization & Coronary Arteriography(Angiography) | Invasive diagnostic procedure. Radiopague arteial and venous catheters put into blood vessels of the right & left sides of heart. Catheter advanced via fluoroscopy. Pressure and O2 satuation is measured. |
| Cardiac Catherization Continued | Used to diagnose CAD, assess patency of coronary artery, determine extent of aterosclerosis by degree of coronary ccclusion. Contrast injected to visualize coronary arteries. Check for allergy to shellfish/iodine.Signed consent. Results determine bypass. |
| Right Heart Catherization | Preceds left heart catherization. cath advanced from antecubital or femoral vein into RA-RV-Pulmonary artery-and Pulmonic arterioles. Pressures and O2 satuartion of areas are obtained and recorded. |
| Complications of Right Heart Catherization | Thrombophlebitis/ Pulmonary embolism/ Vagal responses/ Cardiac dysrhythmias/ Venous spasm |
| Left Heart Catherization | Evaluates patency of coronary arteries and function of left ventricle and mitral and aortic valve. retrograde placement from right brachial or femoral artery and advanced into aorta and left ventricle. |
| Complications of Left Heart Catherization | Myocardial infarct/ stroke/ Arterial bleeding or thromboembolism/ Dysrhythmias/ Perforation of heart or great vessels. |
| General Complications of Cardiac Catherization | Cardiac tamponade/ Hypovolemia/ Pulmonary edema/ Hematoma or blood loss at insertion site/ Infection at insertion site/ Reaction to contrast medium. |
| Nurse Assessment/Interventions Post-Ateriograph | Monitor V/S every 15 minutes for 1 hour, then every 30 minutes for 2 hours or until vitals are stable, then every 4 hours. Assess for hematoma or bloody drainage at insertion site. Check peripheral pulses, skin temp and color in affected extremity. |
| Nurse Assessment/Intervention Continued | Restrict client to bedrest, should remain in bed 4-6 hours unless a special closure was used. HOB may be elevate 30-45 degrees. Keep extremity of insertion site straight. Contrast medium acts as osmotic diuretic, so monitor urine output. |
| Nurse Assessment/Intervention Continued | Ensure client receives oral and IV fluids to assist with excretion of contrast medium. Pain meds may be given for back discomfort or insertion site. Report neurological changes. Report pulse changes in periperal extremities. Soft brace for extremity. |
| Normal B/P | Less than 120 systolic. Less than 80 diastolic. |
| Prehypertension | 120-139mmHg systolic or 80-89mmHg diastolic. |
| Hypertension | Stage 1:140-159 Systolic or 90-99 Diastolic. Stage 2:Above or equal to 160mmHg Systolic or above or equal to 100mmHg Diastolic. |
| Patient Teaching of Hypertension | Avoid salt intake/ Read labels/ Avoid high sodium foods(bacon, ham, processed snacks)/ Loss weight/ Excercise/ Stop smoking/ Avoid alcohol/ Monitor BP. |
| Venous Ulcers | Chronic nonhealing ulcer/ No claudination or rest pain/ Moderate ulcer discomfort/ Complaints of ankle or leg swelling/ Ulcers located in ankle area/ Brown pigmentation/ Ulcer bed pink/ Usually superficial with uneven edges/ Granulation tissue present/ |
| Venous Ulcers | Ankle discoloration and edema/ Full veins when leg slightly dependent/ No neurologic deficit/ Pulses present/ May have scarring from previous ulcers/ Long term care-Unna boot, wet to dry dressing/ Elevate etremity/ Prevent infection/ Client education. |
| Arterial Ulcers | Client complains of claudination after walking appr. 1-2 blocks/ Rest pain usually present/ Pain at ulcer site/ Two or three risk factors present/ Located at end of toes/ Between toes/ Deep/ Ulcer bed pale with eevn edges/ Little granulation tissue/ |
| Arterial Ulcers | Cool or cold foot/ Decreades or absent pulses/ Atrophy of skin/ Hair loss/ Pallor with elevation/ Dependent rubor/ Possible gangrene/ When acute, neurologic deficits noted/ Treat underling cause (surgical, revascularization)/Prevent trauma and infection. |
| Signs/Symptoms of Arterial Insufficiency/ Disease. Who it affects most. | Atherosclerosis is a common cause of of chronic altered blood flow. At risk is clients with hypertension/ hyperlipidemia/ diabetes/ smoking/ obesity familial predisposition/ Black people/ Postmenopausal women/ Men older than 45 |
| S/S of Arteial Insufficiency | Hair loss on the lower calf, ankle and foot/ Dry, scaly, dusky, pale or mottled skin/ Thickened toenails/ Cold and cyanotic extremity/ Pallor in extre. when elevated/ Rubor when the extre. is lowered/ Muscle atrophy/ Ulcers/ Bruits or aneurysm/ Gangrene |
| CAL (Chronic Airflow Limitations) | Group of chronic lung diseases that include asthma, chronic bronchitis and pulmonary emphysema. |
| COPD (Chronic Obstructive Pulmonary Disease) | Emphysema and chronic bronchitis, characterized by bronchospasm and dyspnea. The tissue damage is irreversible and increases with severity, eventually leading to respiratory failure. |
| Asthma | Unlike COPD, it is an intermittent disease with reversible airflow obstruction and wheezing. Airflow obstruction affects the airway only, not the alveoli. Two causes 1. Inflammation(lumen obstruction 2.Airway hyperresponsiveness(airway twitching) |
| Asthma | Hyperresponsiveness cause bronchspams, narrowing of the bronchial tubules through constriction of the smooth muscle. Asthma is best treated with Bronchodilators(Beta-agonist. Also corticoidsteriods if inflammation is present. |
| Corticosteroids | Decrease the inflammation in the airways. Suppresses immune system. Client at risk for developing infections. |
| Medications that Cause Anaphylaxis | Asprin and NSAIDs. |
| Post Operative Pulmonary Care | Treat with bronchodilators and mucolytics/ Pulmonary hygiene-incentive spirometer 10 times per hour while awake/ Chest PT 1st day after surgery and hourly assessment/ Pain management with opiods (epidural). |
| Breathing Excercises | Helps manage dyspnea. Diaphragmatic/Abdominal Breathing-client consciously increase movement of the diaphragm. Lying on back allows the abdomen to relax. |
| Breathing Excercises | Pursed Lip Breathing- breathing through pursed lips uses the mild resistance of partially closed lips to prolong exhalation and to increase airway pressure. This technique dealys airway compression and reduces airway trapping. Used with D/A breathing. |
| Effects of Chemotherapy | Alopecia (temporary hair loss)/ NV/ Mucositis(open sores on mucus membranes)/ Immunosupression/ Anemia/ Thrombocytopenia(decresed platelets)/ Clients administered emetogenic agaents to treat nausea/vomiting. |
| Effects of Radiation | Immediate effects are skin irritation/ fatigue/ Nausea & taste changes/ Esophigitis may occur/ Advise clients to avoid sun exposure for 1 yaer after completion of treatment/ Do not use lotions/ointments unless prescribed by physisian or radiologist. |
| Creatine Kinase (CK) Normal Range | Females: 30-135units/L, Males:55-170units/L. CK-MB:0% of total CK(elevations occur with myocardial injury. |
| Serum Lipids Normal Range | Total Lipids: 400-1000mg/dL(elevation indicates increased risk for coronary artery disease CAD) |
| Cholesterol Normal Range | 122-200mg/dL, Older Adults>70: 144-280 (elevation increases risk of CAD). |
| Triglcerides Normal Range | Females: 35-135mg/dL, Males:40-160mg/dL, Older Adults>65: 55-260mg/dL (elevation increases risk of CAD). |
| HDL's High Density Lipoproteins (Good) | Females: mean 55-60mg/dL, Males: mean 45-50mg/dL, Older adult ranges increase with age. (elevations protect against CAD). |
| LDL's Low Density Lipoproteins (Bad) | 60-180mg/dL, Older Adults>65: 92-221mg/dL(elevations increases risk of CAD). |
| Type 1 Diabetes (Risk Factors, Genetic Predisposition) | Autoimmune disorder. Clients with tissue types HLA-DR3+/or HLA-DR4. Clients with certain viral infections(mumps, congeital rubella, coxsackie virus)-may trigger autoimmune response. Immune system attacks and destroys insulin secreting beta cells. |
| Type 2 Diabetes (Risk Factors, genetic Prediposition) | Progressive disorder in which pancreas makes less insulin over time. specific cause not known. Risks are obesity/ hypertension/ Heredity-offspring has 15% chance of development/ Physically inactive/ High choleterol/ Polycystic ovary syndrome/ |
| Type 2 diabets Continued | History of vascular disease/ Have IGT or IFG on previous screening/ Women having baby >9 lbs/ Gestational diabetes/ African, hispanic, Native Amer, Asian, Pacific Islander. |
| DKA-Diabetic Ketoacidosis (Risk Factors) | Total or partial insulin lack/ Occurs in Type /Caused by hyperglycemia/ Sudden onset/ Infection, other stressor, inadequate insulid dose/ Ketosis, Kussmaul respirations,fruity breath, nausea, abdominal pain, dehydration, electrolyte loss, weight loss, |
| DKA Continued | sunken eyes, soft eyeballs, coma, lethargy/Glcose>300mgdL/ Positive ketones/ pH<7.35/HCO3<15mEqL/ Na+ low, normal or high/ K, normal, elevated after acidosis/ BUN,>20/ Creatine,>1.5/ BUN,Creatine elevated due to dehydration/ 3 P's. |
| HHNS-Hyperglycemic Hyperosmolar Nonkinetic Syndrome | Caused by hyperglycemia/ Gradual onset/ Infection, other stressors, poor fluid intake/ Altered CNS function with neuroloic symptoms/ Dehydration and electolyte loss/ Glucose>600mgdL/ Osmolarity>350mOamL/ Negative ketones/ pH>7.4/ HCO3>20mEqL/ |
| HHNS Continued | Na+, normal or low/ K, normal or low/ BUN elevated/ Creatine elevated/ Hydration is key to treating HHNS. |
| Physiological of 3 P's (Causes Hyperglycemia) | Polyuria-frequent & excessive urination results by excessiveglucose in the urine from osmotic diuresis. Diuresis results in sodium, chloride and potassium extretion (electrolyte loss) in addition to dehydration. Polydypsia-excessive thirst resulting from |
| 3 P's continued | dehydration which stimulates thirst. Polyphagia-excessive eating or hunger results from cell starvation and despite eating large amounts of food, person remains in state of hunger until insulin is ready to move glucose into cells. |
| Metabolic Syndrome (Syndrome X) & Type 2 DM | Group of disorders with insulin resistance as a main feature. genetic predispostion to type 2 diabetes increases the risk for other metabolic syndrome health problems when compounded by obesity and sedentary lifestyle. Increases risk for atherosclerosis, |
| Metabolic Syndrome Continued | stroke, coronary heart disease, and early death. metabolic syndrome dont respond readily to drug therapy. Lifestyle changes can reduce the insulin resistence and diabetic manifestations. |
Created by:
Honeynut718
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