A CASE STUDY IN CARDIO EMBOLIC STROKE,CAD,HCVD

SUBMITTED BY:
CHERRY ANN FLORES,RN MILLAN JOY FAMOSO, RN CHARMELLE KRITEAN ESTABILLO, RN SWET MAE FERNANDEZ, RN

INTRODUCTION
(BACKGROUND OF THE STUDY)

The heart

established as an important source for the development of

emboli. Cardio embolic stroke occurs when the heart pumps unwanted materials into the brain circulation, resulting in the occlusion of a brain blood vessel and damage to the brain tissue .Left Atrial Thrombi is the most common cause of a cardioembolic stroke. The reduced atrial contraction associated with atrial fibrillation leads to blood stasis, which facilitates thrombus formation in the left atrial appendage .Left Ventricular Thrombi thrombus formation is frequently associated with ischemic heart disease because of stasis caused by regional or global myocardial dysfunction. Dilated cardiomyopathy is a well-known risk factor for arrhythmias and mural thrombi, both of which are potential risk factors for stroke.

Cardioembolic stroke is one of the more devastating causes of stroke. In recent years, significant progress has been made in identifying patients at high risk for cardioembolic stroke. With the aging of the population, an increasing number of patients are at risk for cardioembolism.

Cardioembolic stroke accounts for 14-30% of all cerebral infarctions. Cardioembolic ischemic stroke accounts for one quarter of all cerebral infarcts .Cardioembolic ischemic stroke is the most severe ischemic stroke subtype, with a low frequency of absence of neurological dysfunction at hospital discharge and a non-negligible risk of early embolic recurrence (1-10%) Cardioembolic stroke is also the stroke subtype with the highest in-

hospital mortality (6-27%) .Cardioembolic stroke is a homogeneous subtype of ischaemic stroke characterized by sudden onset of neurological deficit . Patients with acute ischemic stroke of cardioembolic origin show maximal neurological at stroke onset or within a few minutes after the onset of symptoms, which is contrast with patients suffering from atherothrombotic stroke or lacunar infarction (LI) in which neurological dysfunction is progressively established in the course of several hours. Progression was most frequent in patients with LI (37%) and large-artery occlusive disease (33%) and least frequent in patients with embolism (7%)

Spontaneous early neurological deterioration (END) has been reported in 12 to 43% of patients with acute ischaemic stroke and is associated with an unfavourable outcome, with increased morbidity and mortality. However, there is little data on END when patients are individualized by the different subtypes of ischaemic stroke. Therefore, progressing or deteriorating stroke is uncommon in cardioembolic stroke and clinical factors and prognosis associated with early neurological deterioration in this stroke subtype have been scarcely assessed In the Philippines 27% of the population and in Davao regional according to Medical Records 79 patients admitted due to Cardioembolic stroke fro 2011 to present.

Objective of the Study: The Main objective of this case study is to find out the extent of Cardioembolic stroke that could affecthuman normal function. Specifically sought the following objective: 1.) To be able to discuss the origin of Cardioenbolic stroke. 2.) To determine the factors that causes the illness. 3.) To be able to better understand the behavior of Cardioembolic stroke patient. 4.) To be able to establish good relationship to the patient and to the family to have an comfortable communication for the case study 5.) To be able to Gather necessary information concerning the patient history and on the present condition of the patient that will attribute to the illness. 6.) To be able to present the latest medical development ofCardioembolic Stroke. 7.) To Illustrate the Anatomy and physiology of Cardioembolic stroke 8.) Discuss thoroughly the pathophysiology of cardioembolic stroke 9.) Elucidatemedication administered to our ptient 10.) 11.) Formulate applicable nursing care plan that will help to his condition To explain briefly the appropriate discharge plan that will apply to the

patient.

PATIENTS PROFILE

HEALTH HISTORY

GENOGRAM(narrative) The interview was conducted last February 15, 2012 at Medicine Ward. Our informant was Mr. Alfred the son of our patient. Our patient Mr.Daping is second child among the six children of Mr. Rodolfo and Ms. AngelitaBandaja. Mr. Daping was married to Ms.Julia and had two children.

PAST HEALTH HISTORY Our patient Mr.Daping, 63 years old. According to his Son he had hypertension and had maintenance medicine captopril or metoprolol. He also had onset of headache and just take over the counter drugs like paracetamol, he told us that they never had monitor the blood pressure of their father. His son told us also that his father started smoking and drinks occasionally in his adolescent years. Their family usually eats vegetables and and other poultry products.

Present health history

According to his son, two days prior to admission, patient had sudden onset of left sided weakness and vomiting. They decided to admit patient to local hospital as a case of CVA but referred to Davao Regional Hospital for CT-scan with regard to his condition, patient was admitted in the institution. Under the service of Dr.Pangarintao with admitting diagnosis of Cardioembolic stroke, HCVD, CAD.

PHYSICAL ASSESSMENT

Head and face Configuration- normocephalic;Hair- normal texture;Scalp- tenderness;The

skull is proportionate to the body size;notenderness;Face is symmetrical and symmetrical facial movement

Eyes: Symmetrical; sclera is white;Pupil equally round;reactive to light Ears: Auditory Canal- normal;same color as face,centralposition;no pain assessed;External Ear- nolesions, masses, tenderness Nose: Septum- midline;Inferior and Middle Turbinates normal Throat and Mouth: Teeth: Present and in good dentition;Pharynx and Tonsillar Fossa: normal Skin Brown; No bleeding; No lesions; Skin is dry; W a r m a n d e q u a l bilaterally Skin sprung back rapidly when pinched;noedema present Hair Hair appears black; even distributionof hair ;no infestation or lesions;hair is thick Nails Brown cast nails; good capillary refill; s u r f a c e i s s m o o t h a n d slightly rounded flat curved nails Mouth Lips is pale,semmetrical,palemucosa,tonue is in midline Neck The skin is uniform in color;neck muscles are equal in size and no tenderness Breast and Axilla No masses; tenderness upon palpation Abdomen Abdominal contour rounded; Symmetrical movement, uniform in color; No scars; Gurgling soundsin abdomen Upper extremities No deformities No edema or tenderness:there is left sided weakness Lower extremities No deformities No edema or tenderness;there is left sided weakness Neurologic

 GLASCO COMA SCALE

COURSE IN THE WARD

ANATOMY AND PHYSIOLOGY

CARDIOVASCULAR SYSTEM

The cardiovascular system can be thought of as the transport system of the body. This system has three main components: the heart, the blood vessel and the blood itself. The heart is the system's pump and the blood vessels are like the delivery routes. Blood can be thought of as a fluid which contains the oxygen and nutrients the body needs and carries the wastes which need to be removed. The following information describes the structure and function of the heart and the cardiovascular system as a whole.

Structure and Function of the Heart

Function and Location of the Heart The heart's job is to pump blood around the body. The heart is located in between the two lungs. It lies left of the middle of the chest. Structure of the Heart The heart is a muscle about the size of a fist, and is roughly cone-shaped. It is about 12cm long, 9cm across the broadest point and about 6cm thick. The pericardium is a fibrous covering which wraps around the whole heart. It holds the heart in place but allows it to move as it beats. The wall of the heart itself is made up of a special type of muscle called cardiac muscle. Chambers of the Heart The heart has two sides, the right side and the left side. The heart has four chambers. The left and right side each have two chambers, a top chamber and a bottom chamber. The two top chambers are known as the left and right atria (singular: atrium). The atria receive blood from different sources. The left atrium receives blood from the lungs and the right atrium receives blood from the rest of the body. The bottom two chambers are known as the left and right ventricles. The ventricles pump blood out to different parts of the body. The right ventricle pumps blood to the lungs while the left ventricle pumps out blood to the rest of the body. The ventricles have much thicker walls than the atria which allows them to perform more work by pumping out blood to the whole body. There are also microscopic blood vessels which connect arteries and veins together called capillaries. There are a few main blood vessels which connect to different chambers of the heart. The aorta is the largest artery in our body. The left ventricle pumps blood into the aorta which then carries it to the rest of the body through smaller arteries. The pulmonary trunk is the large artery which the right ventricle pumps into. It splits into pulmonary arteries which take the blood to the lungs. The pulmonary veins take blood from the lungs to the left atrium. All the other veins in our body drain into the inferior vena cava (IVC) or the superior vena cava (SVC). These two large veins then take the blood from the rest of the body into the right atrium. Valves Valves are fibrous flaps of tissue found between the heart chambers and in the blood vessels. They are rather like gates which prevent blood from flowing in the wrong direction. They are found in a number of places. Valves between the atria and ventricles are known as the right and left atrioventricular valves, otherwise known as the tricuspid and mitral valves respectively. Valves between the ventricles and the great arteries are known as thesemilunar valves. The aortic valve is found at the base of the aorta, while the pulmonary valve is found the base of the pulmonary trunk. There are also many valves found in veins throughout the body. However, there are no valves found in any of the other arteries besides the aorta and pulmonary trunk. What is the Cardiovascular System The cardiovascular system refers to the heart, blood vessels and the blood. Blood contains oxygen and other nutrients which your body needs to survive. The body takes these essential nutrients from the blood. At the same time, the body dumps waste products like carbon dioxide,

back into the blood, so they can be removed. The main function of the cardiovascular system is therefore to maintain blood flow to all parts of the body, to allow it to survive. Veins deliver used blood from the body back to the heart. Blood in the veins is low in oxygen (as it has been taken out by the body) and high in carbon dioxide (as the body has unloaded it back into the blood). All the veins drain into the superior and inferior vena cava which then drain into the right atrium. The right atrium pumps blood into the right ventricle. Then the right ventricle pumps blood to the pulmonary trunk, through the pulmonary arteries and into the lungs. In the lungs the blood picks up oxygen that we breathe in and gets rid of carbon dioxide, which we breathe out. The blood is becomes rich in oxygen which the body can use. From the lungs, blood drains into the left atrium and is then pumped into the left ventricle. The left ventricle then pumps this oxygenrich blood out into the aorta which then distributes it to the rest of the body through other arteries. The main arteries which branch off the aorta and take blood to specific parts of the body are:

Carotid arteries, which take blood to the neck and head Coronary arteries, which provide blood supply to the heart itself Hepatic artery, which takes blood to the liver with branches going to the stomach Mesenteric artery, which takes blood to the intestines Renal arteries, which takes blood to the kidneys Femoral arteries, which take blood to the legs The body is then able to use the oxygen in the blood to carry out its normal functions. This blood will again return back to the heart through the veins and the cycle continues.

What is the Cardiac Cycle The cardiac cycle is the sequence of events that occurs in one complete beat of the heart. The pumping phase of the cycle, also known as systole, occurs when heart muscle contracts. The filling phase, which is known asdiastole, occurs when heart muscle relaxes. At the beginning of the cardiac cycle, both atria and ventricles are in diastole. During this time, all the chambers of the heart are relaxed and receive blood. The atrioventricular valves are open. Atrial systole follows this phase. During atrial systole, the left and right atria contract at the same time and push blood into the left and right ventricles, respectively. The next phase is ventricular systole. During ventricular systole, the left and right ventricles contract at the same time and

pump blood into the aorta and pulmonary trunk, respectively. In ventricular systole, the atria are relaxed and receive blood. The next phase is ventricular systole. During ventricular systole, the left and right ventricles contract at the same time and pump blood into the aorta and pulmonary trunk, respectively. In ventricular systole, the atria are relaxed and receive blood. Following this phase, the ventricles relax that is ventricular diastole occurs. The semilunar valves close to stop the blood from flowing back into the ventricles from the aorta and pulmonary trunk. The atria and ventricles once again are in diastole together and the cycle begins again.

Components of the Heartbeat

The adult heart beats around 70 to 80 times a minute at rest. When you listen to your heart with a stethoscope you can hear your heart beat. The sound is usually described as "lubb-dupp". The "lubb" also known as the first heart sound, is caused by the closure of the atrioventricular valves. The "dupp" sound is due to the closure of the semilunar valves when the ventricles relax (at the beginning of ventricular diastole). Abnormal heart sounds are known as murmurs. Murmurs may indicate a problem with the heart valves, but many types of murmur are no cause for concern. (For more information see: (see Valvular Heart Disease)

The Electrocardiogram
The heart has an inbuilt rhythm of contraction and relaxation. A small group of heart muscle cells called the pacemaker help achieve this. The pacemaker generates an electrical impulse which spreads over the atria, making them contract. This impulse then spreads to the ventricles, causing them to contract. The electrical changes that spread through the heart can be detected at the surface of the body by an instrument called the electrocardiograph. Electrodes are placed in a number of positions over the chest and the electrical changes are recorded on moving graph paper as an electrocardiogram (ECG).

PATHOPHYSIOLOGY

NARRATIVE DISCUSSION

Embolus arises from elsewhere,it is due to fatty deposit, imbalance in the blodd coagulation system that can cause clot formation. Thus, the source of the embolus must be identified. Because the embolic blockage is sudden in onset, symptoms usually are maximal at start. Also, symptoms may be transient as the embolusis partially resorbed and moves to a different location or dissipates altogether. It occurs in different factors, it can be predisposing and precipitating.In predisposing factors it includes the age,race and hereditary while in precipitating factor it include the patient diet, lifestyle, obesity and systemic embolism. Fatty plaques develop on the inner wall(atheroma). Atherosclerosis may disrupt the blood supply by narrowing the lumen of blood vessel leading to reduction of blood flow, by causing the formation of blood clots within the vessel, or by releasing showers of smallembolithrough the disintegration of atherosclerotic plaques.This time our compensatory mechanism activated by increasing blood pressure and work load of the heart to sustain exact distribution of blood.By the great pressure the thrombus detached from the vessel wall that most of the time lodges in the mid coronary artery that can causes blockage of the blood flow. Coronary artery supply blood flow to the heart, they ensure adequate oxygenation of the myocardium at all level of the cardiac activity. Due from the blockage of the blood flow it decrease tissue perfusion that insufficient gas exchange takes place. Ischemia occur cause by constriction or blockage of the blood vessels supplying it.Ischemia of the heart muscle produces angina pectoris that is chest pain that can be relieve by rest or taking nitroglycerin.Ischemia can lead to necrosis if not treated. Since blood vessels are now occluded, it becomes low in energy, and thus it resorts into usinganaerobic respiration within the region of tissue affected by ischemia which stimulate the sympathetic nervous response to increase blood pressure and cardiac rate. Unfortunately, this kind of respiration produces less adenosine triphosphate (ATP)( a compound that contains adenine, ribose and three phosphate groups and occurs in the cell and the chemical bond of the phosphate groups store energy needed by the cell for muscle contraction) but releases a byproduct calledlactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-base balance, increase lactic acid can also cause chest pain.Unfortunately, this kind of respiration produces less adenosine triphosphate (ATP)( a compound that contains adenine, ribose and three phosphate groups and occurs in the cell and the chemical bond of the phosphate groups store energy needed by the cell for muscle contraction) but releases a by-product called lactic acid. Lactic acid is an irritant which could potentially destroy cells since it is an acid and disrupts the normal acid-base balance, increase lactic acid can also cause chest. Decrease oxygenation of the tissue can cause impaired left ventricular function

of the heart.The Ventricle cannot overcome the resistant to eject blood or decrease afterload of the heart and that can lead in to decrease cardiac output. Left sided congestive heart failure occur because of blood accumulation in the left ventricle and can lead to pulmonary congestion in manifestation of dypnea, cough,pink fruity sputum.Due to the said congestion,regurgitation occur. If treated the medical management of the said disease are nitrates,calcium channel blocker,reduce the blood pressure and blood glucose, Lifestyle modification. The surgical manifestation are atherectomy to remove plaque in the blood vessels,andioplasty to remo0ve significant atherosclerosis narrowing the carotid artery, endartectomy a surgical re-bore of the artery that has become obstructed by the atheroma ,the inner part of the wall remove together with any clot that is present.If not treated it can cause hemorrageconvertion that lead to brain edema that manifest increase Intra cranial Pressure that can develop to brain hernation and result to death of the patient.

DIAGRAM PRESENTATION

IDEAL and MEDICAL(including drugs and meds)and SURGICAL MANAGEMENT IDEAL MEDICATION

Warfarin: Reduces blood clot formation by blocking clotting factors from forming in the blood. This drug is used to prevent strokes, heart attacks and blood clot formation in the lungs, arteries and veins. Heparin Reduces the blood's ability to clot so that clots cannot form in the veins, arteries or lungs. This drug can be used during surgical procedures that create a high risk of blood clot formation. It can also be used to treat heart, lung and blood vessels conditions that increase the likelihood of dangerous clots. Patients taking heparin should not take drugs that contain aspirin or ibuprofen, as these drugs can change the way heparin works and cause serious side effects. Easy bruising and bleeding are the most common side effects of this drug. Clopidogrel Used in the prevention or management of strokes and heart attacks. This drug is an anti-platelet drug, which means that it prevents platelets from sticking together and forming blood clots that can lead to strokes and heart attacks. People with bleeding ulcers, brain bleeds or other bleeding conditions may not be able to take this drug. Ticlopidine A medication used to prevent strokes by preventing excessive blood clotting. This drug should be used with caution in people who have liver disease, low blood cell counts, high cholesterol, kidney disease, high triglycerides and bleeding disorders. Patients should inform their doctors about all prescription and over-the-counter medications they are taking, as well as any vitamins or supplements. Enoxaparin Anticoagulant used to prevent blood clots in people who are immobile because of major surgery or the need for bed rest. It can also be used with aspirin to prevent heart attacks or with warfarin to treat the formation of blood clots in the legs. This drug should be used with caution in people who have or

have had heart infections, bleeding disorders, kidney disease, strokes, low platelet counts or ulcers.

MEDICAL MEDICATION: 1. 2. 3. 4. 5. 6. 7. 8. CEFUROXIME 1.5 mg every 6 hours ATORVASTATINE HYDRATE 80 mg 1 tab ance a day METOPROLOL 5 mg 1 tab two times a day RANITIDINE 50 mg 1 amp every 6 hours CAPTOPROL 50 mg1 tab SL every 6 hours for BP more than 160/100 KETOSTERIL 60 mg 1 tab three times a day CITICOLINE 1 gm 1 amp two times a day AMLODIPINE 10 mg 1 tab once a day

SURGICAL MANAGEMENT: 1. angioplasty- can be used to remove significant atherosclerotic narrowing (stenosis) of the carotid artery, which supplies blood to the brain. There is a large body of evidence supporting this procedure in selected cases. 2. endarterectomy-surgical re-bore of an artery that has become obstructed by atheroma.the inner part of the wallis removed together with any clot that is present. This restores patency and arterial blood flow to the tissue beyond the obstruction. 3. ATHERECTOMY- removal of plaques from the blood vessels.

SOURCE/BIBLIOGRAPHY
1. ^ Sims NR, Muyderman H (September 2009). "Mitochondria, oxidative metabolism and cell death in stroke". BiochimicaetBiophysicaActa1802 (1): 8091. doi:10.1016/j.bbadis.2009.09.003. PMID 19751827. 2. ^ abcdefghijklmDonnan GA, Fisher M, Macleod M, Davis SM (May 2008). "Stroke". Lancet371 (9624): 161223. doi:10.1016/S0140-6736(08)60694-7. PMID 18468545. 3. ^Feigin VL (2005). "Stroke epidemiology in the developing world". Lancet365 (9478): 21601. doi:10.1016/S0140-6736(05)66755-4. PMID 15978910. 4. ^ Miwa K, Hoshi T, Hougaku H, et al. (2010). "Silent cerebral infarction is associated with incident stroke and TIA independent of carotid intima-media thickness". Intern. Med.49 (9): 81722. doi:10.2169/internalmedicine.49.3211. PMID 20453400. http://joi.jlc.jst.go.jp/JST.JSTAGE/internalmedicine/49.3211?from=PubMed. 5. ^ abHerdersche D, Hijdra A, Algra A, Koudstaal PJ, Kappelle LJ, van Gijn J (September 1992). "Silent stroke in patients with transient ischemic attack or minor ischemic stroke. The Dutch TIA Trial Study Group". Stroke23 (9): 12204. doi:10.1161/01.STR.23.9.1220. PMID 1519274. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=1519274. 6. ^ Leary MC, Saver JL (2003). "Annual incidence of first silent stroke in the United States: a preliminary estimate". Cerebrovasc. Dis.16 (3): 2805. doi:10.1159/000071128. PMID 12865617. http://content.karger.com/produktedb/produkte.asp?DOI=71128&typ=pdf. 7. ^ Vermeer SE, Koudstaal PJ, Oudkerk M, Hofman A, Breteler MM (January 2002). "Prevalence and risk factors of silent brain infarcts in the population-based Rotterdam Scan Study". Stroke33 (1): 215. doi:10.1161/hs0102.101629. PMID 11779883. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=11779883. 8. ^"Brain Basics: Preventing Stroke". National Institute of Neurological Disorders and Stroke. http://www.ninds.nih.gov/disorders/stroke/preventing_stroke.htm. Retrieved 2009-10-24. 9. ^Shuaib A, Hachinski VC (September 1991). "Mechanisms and management of stroke in the elderly". CMAJ145 (5): 43343. PMC 1335826. PMID 1878825. http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pmcentrez&artid=1335826. 10. ^ abStam J (April 2005). "Thrombosis of the cerebral veins and sinuses". The New England Journal of Medicine352 (17): 17918. doi:10.1056/NEJMra042354. PMID 15858188. 11. ^Guercini F, Acciarresi M, Agnelli G, Paciaroni M (April 2008). "Cryptogenic stroke: time to determine aetiology". Journal of Thrombosis and Haemostasis6 (4): 54954. doi:10.1111/j.1538-7836.2008.02903.x. PMID 18208534. 12. ^Bamford J, Sandercock P, Dennis M, Burn J, Warlow C (June 1991). "Classification and natural history of clinically identifiable subtypes of cerebral infarction". Lancet337 (8756): 15216. doi:10.1016/0140-6736(91)93206-O. PMID 1675378. Later publications distinguish between "syndrome" and "infarct", based on evidence from imaging. "Syndrome" may be replaced by "hemorrhage" if imaging demonstrates a bleed. See Internet Stroke Center. "Oxford Stroke Scale". http://www.strokecenter.org/trials/scales/oxford.html. Retrieved 2008-11-14.

13. ^Bamford JM (2000). "The role of the clinical examination in the subclassification of stroke". Cerebrovascular Diseases10 Suppl 4: 24. doi:10.1159/000047582. PMID 11070389. 14. ^ Adams HP, Bendixen BH, Kappelle LJ, et al. (January 1993). "Classification of subtype of acute ischemic stroke. Definitions for use in a multicenter clinical trial. TOAST. Trial of Org 10172 in Acute Stroke Treatment". Stroke24 (1): 3541. doi:10.1161/01.STR.24.1.35. PMID 7678184. http://stroke.ahajournals.org/cgi/pmidlookup?view=long&pmid=7678184. 15. ^ Goldstein LB, Simel DL (May 2005). "Is this patient having a stroke?".JAMA293 (19): 2391402. doi:10.1001/jama.293.19.2391. PMID 15900010. 16. ^Harbison J, Massey A, Barnett L, Hodge D, Ford GA (June 1999). "Rapid ambulance protocol for acute stroke". Lancet353 (9168): 1935. doi:10.1016/S0140-6736(99)009666. PMID 10371574. 17. ^ Kidwell CS, Saver JL, Schubert GB, Eckstein M, Starkman S (1998). "Design and retrospective analysis of the Los Angeles Prehospital Stroke Screen (LAPSS)". Prehospital Emergency Care2 (4): 26773. doi:10.1080/10903129808958878. PMID 9799012. 18. ^ Kothari RU, Pancioli A, Liu T, Brott T, Broderick J (April 1999). "Cincinnati Prehospital Stroke Scale: reproducibility and validity". Annals of Emergency Medicine33 (4): 3738. doi:10.1016/S0196-0644(99)70299-4. PMID 10092713. 19. ^ abNational Institute for Health and Clinical Excellence. Clinical guideline 68: Stroke. London, 2008. 20. ^ Nor AM, Davis J, Sen B, et al. (November 2005). "The Recognition of Stroke in the Emergency Room (ROSIER) scale: development and validation of a stroke recognition instrument". Lancet Neurology4 (11): 72734. doi:10.1016/S1474-4422(05)70201-5. PMID 16239179.

DIAGNOSTIC and OTHERV LABS PROCEDURE CT SCAN SECTION

Case No: 3855765 CT Film No: 120254 MED Name: mr. X Address: Caraga Part of Examned: Cranium Plain Referedby:Dr. Quilisadio FINDINGS Multiple plain axial CT Image of the head were obtained.

Date of examined: 2-8-13 Age: 63 Sex: M Dept:

Curvilinear hypodense collection are seen in both frontal convexeties with the large focus seen in the right and has a maximal thickness of 0.5 cm. Hyperdense collection is noted in the right thalamus and posterior limb of the right internal capsule having the approximate volume of 3cc. Patchy hypodence changes and noted in the preventicular white matter. A subcentemeter calcification is noted in the left posterior parietal lobe. Gyn, suici, tissue and cistem are intact. The right lateral ventricle is compressed. Medicine structure are not displaced. Sella, orbits, paranasal sinuses and petramostoid are unremarkable. Calvarium and visualized facial bones are intact with no deficit evidence of fration. Extracalverial soft tissue are unremarkable. No other signaficant findings. IIMPRESSION: -ACCUTE BLEED IN THE RIGHT HYPOTHALAMUS AND INTERNAL CAPSULE -PATCHY HYPODENSE CHANGED IN THE PERIVENTRICULAR WHITE MATTER SUGGESTIVE SMALL VESSEL ISCHEMIC DISEASE. BIFRONTAL SUBDURAL HYGROMA. NONSPECIFIC CALCIFICATION OF THE LEFT PARIETAL LOBE

Laboratory Result/ Report DAVAO REGIONAL HOSPITAL LABORATORY DEPARTMENT APOKON, TAGUM CITY CLINICAL CHEMESTRY Name: Mr. X Age: 63 y.o Date: 2-10-122 Ward: MED

Sex: Male

Case No.

CREATENINE

114.7

Normal Value: SI Unit M: 53.0 115.0: F: 44.0 96.0 mmol/ L

Significance of a change: Increase createnine- in some kidney disorder

Davao Regional Hospital Apokon, Tagum City ECHOCARDIOGRAPHY AND COLOR FLOW DOPPLER

Name: Mr. X

Medicine No:_________

Category: DOPPLER Department: Medicine Study Date: 2-13-2012

Age: 63 years old

Sex: M QUANTITATIVE NORMAL DIMENTION MEASUREMENT (4.5-5.0) LVEDV 125.0 LVESV 53.6 (0.8-11) SV 71.4 CO EF 57.12% FS 24.59% VCF LV MASS
DIASTOLIC FUNCTION

DIMENTION MEASUREMENT LV(ed) 5.0 LV(es) 3.7 IVS(ed) 1.4 LVPW(ed) 1.5 LVPW(es) 1.3 Aorta 1.9 LA (Apdiam) 3.9 MPA 3.4 Aortic Valve EPSS LVOIT RV RA AV Annulus TV Annulus

NORMAL

SIMSONS

(55.0-77. (29-42) (0.5-1.5)

(< 1.0) 3.4 4.5 (3.0 4.0) (3.5 4.5)

PARAMETER Decel Time IVRT HR

PATIENT 216

NORMAL

1. Concentric LVH with segmental wall motion abnormality consistent with CAD with borderline systolic function. The anterioi IVS and anterior IV free wall are hypokinetic from basev to apex. The inferior and lateral wall contract adequately. The visual EF is 40-45%. 2. Atheriosclerosis aortic root. 3. Dilated left atrium without thrombus. 4. Normal left atrium, right atrim, right ventricle, main pulmonary artery dimention. 5. Structualy normal mitral, tricuspid and pulmonic valve. 6. Aortic sclerosis with no restriction of motion. 7. No intra cardiac thrombus or pericardial effusion. 8. Mild Pulmonary artery Hypertention.

Laboratory Result/ Report DAVAO REGIONAL HOSPITAL LABORATORY DEPARTMENT APOKON, TAGUM CITY CLINICAL CHEMESTRY Name: Mr. X Age: 63 y.o Date: 2-1-12 Ward: MED

Sex: Male

Case No.

CREATENINE SODIUM POTASSIUM CALCIUM

124.2 149.3 3.51 1.19

Normal Value: SI Unit M: 53.0 115.0: F: 44.0 96.0 mmol/ L 135 145 mmol/ L 3.5 5.0 mmol/L 1.13 1.32 mmol/L

Significance of a change: Createnineincrease- some kidney disorder

Potassium-

increase- in hypoaldosteronism increase- in acute kidney failure decrease- in vomiting or diarrhea decrease- in starvation

Sodium increase- in starvation Increase- in dehydration Decrease- acute kidney failure Decrease-in cushing syndrome Calcium increase- hyperparathyroidism Decrease- hypoparathyroid

PHARMACOLOGY

Ranitidine Date Ordered: February 7,2012 Ordered Dode: 50mg IVTT q8 MECHANISM OF ACTION Inhibits the action of histamine at the H2 receptor site located primarily in gastric parietal cells, resulting in inhibition of gastric acid secretion. In addition, ranitidine bismuth citrate has some antibacterial action against H. pylori. INDICATION: Treatment and prevention of heartburn, acid indigestion, and sour stomach. CONTRA INDICATIONS Hypersensitivity, Cross-sensitivity may occur; some oral liquids contain alcohol and should be avoided in patients with known intolerance.Use Cautiously in: Renal impairment SIDE EFFECTS/ ADVERSE EFFECTS CNS: Confusion, dizziness, drowsiness, hallucinations, headache CV: Arrhythmias GI: Altered taste, black tongue, constipation, dark stools, diarrhea, drug-induced hepatitis, nausea GU: Decreased sperm count, impotence ENDO: Gynecomastia HEMAT: Agranulocytosis, Aplastic Anemia, neutropenia, thrombocytopenia NURSING IMPLICATIONS/RESPONSIBILITIES Assess patient for epigastric or abdominal pain and frank or occult blood in the stool, emesis, or gastric aspirate.

 Inform patient that it may cause drowsiness or dizziness. Inform patient that increased fluid and fiber intake may minimize constipation. Advise patient to report onset of black, tarry stools; fever, sore throat; diarrhea; dizziness; rash; confusion; or hallucinations to health car professional promptly Inform patient that medication may temporarily cause stools and tongue to appear gray black.

Citicoline Date Ordered: February 7,2012-02-23 Ordered Dode: 1gm IVTT q12 Mechanism of Action Citicoline seems to increase a brain chemical called phosphatidylcholine. This brain chemical is important for brain function. Citicoline might also decrease brain tissue damage when the brain is injured.It is usually known that phospholipid, especially lecithin, decreases following decline in brain activity with cerebral trauma. Citicoline, which is a co-enzyme, accelerates the biosynthesis of lecithin in the body. Indication Parkinsons disease,Headinjury,Cerebral vascular disease,Alzheimersdisease,Cerebral surgery or acute cerebral disturbance,Disturbance of consciousness following brain surgery Side Effects Body temperature elevation;Restlessness;Headaches;Nausea and vomitingDiarrhea;Low or high blood pressure;Tachycardia;Sleeping troubles or insomniaBlurredvision;Chest pain. Nursing Responsibility Monitor Vital signs,BP and cardiac output Monitor the intake and output

Mannitol Date Ordered: February 7, 2012 Ordered ordered: 150 cc q6 x 4 doses then 75cc q6 x 8 doses then D/C
Mechanism of Action: Elevates plasma osmolality, causing water to flow from tissues, such as brain and eyes, and from CSF, into extracellular fluid, thereby decreasing intracranial and intraocular pressure.As an osmotic diuretic, mannitol increases the osmolarity of glomerular filtrate, which decreases water reabsorption. This leads to increased excretion of water, sodium, chloride, and toxic substances. Indications: To reduce intracranial or intraocular pressure,To diagnose oliguria or inadequate renal function, To prevent oliguria or acute renal failure, To treat oliguria,To promote diuresis in drug toxicity, To promote diuresis in hemolytic transfusion reaction,To provide irrigation during transurethral resection of prostate gland Adverse Reactions: : CNS: Chills, dizziness, fever, headache, seizuresCV: Angina-like Chest pain, heart failure, hypertension, tachycardia, thrombophlebitis, hypotension, vascular overloadEENT: Blurred vision, dry mouth, rhinitisGI: Diarrhea, nausea, thirst, vomiting, dry mouth

Contraindications Contraindicated in patients hypersensitive to drug.Active intracranial bleeding (except during craniotomy), anuria, hepatic failure, hypersensitivity to mannitol or its components, frank pulmonary edema, severe dehydration, severe heart failure, severe pulmonary congestion, severe renal insufficiency, severe dehydration, metabolic edema, progressive renal disease or dysfunction Nursing Responsibilities: If crystals form in mannitol solution exposed to low temperature, place solution in hot-water bath to redissolve crystals.. During I.V. infusion of mannitol, monitor vital signs, central venous pressure, and fluid intake and output every hour. Measure urine output with indwelling urinary catheter, as appropriate.

 Provide frequent mouth care to relieve thirst and dry mouth. Inform patient that he may experience dry mouth and thirst during mannitol therapy. Instruct patient to report chest pain, difficulty breathing, or pain at I.V. site..

Metoprolol Date Ordered: February 7, 2012 Ordered ordered: 50mg 1tab BID Therapeutic actions Competitively blocks beta-adrenergic receptors in the heart and juxtaglomerular apparatus, decreasing the influence of the sympathetic nervous system on these tissues and the excitability of the heart, decreasing cardiac output and the release of renin, and lowering BP; acts in the CNS to reduce sympathetic outflow and vasoconstrictor tone Indications Hypertension, alone or with other drugs, especially diuretics Prevention of reinfarction in MI patients who are hemodynamically stable or within 3 10 days of the acute MI (immediate-release tablets and injection) Treatment of angina pectoris Contraindications Contraindicated with sinus bradycardia (HR <> 0.24 sec), cardiogenic shock, CHF, systolic BP <> Adverse effects Pharyngitis, erythematous rash, fever, sore throat, laryngospasm Dizziness, vertigo, tinnitus, fatigue, emotional depression, paresthesias, sleep disturbances, hallucinations, disorientation, memory loss, slurred speech CHF, cardiac arrhythmias, peripheral vascular insufficiency, claudication, CVA, pulmonary edema, hypotension Rash, pruritus, sweating, dry skin Eye irritation, dry eyes, conjunctivitis, blurred vision

 Gastric pain, flatulence, constipation, diarrhea, nausea, vomiting, anorexia, ischemic colitis, renal and mesenteric arterial thrombosis, retroperitoneal fibrosis, hepatomegaly, acute pancreatitis Nursing considerations Do not discontinue drug abruptly after long-term therapy (hypersensitivity to catecholamines may have developed, causing exacerbation of angina, MI, and ventricular arrhythmias). Taper drug gradually over 2 wk with monitoring. Give oral drug with food to facilitate absorption. Provide continual cardiac monitoring for patients receiving IV metoprolol.

Amplodipine Date Ordered: February 7, 2012 Ordered ordered: 50mg 1tab BID Therapeutic actions Inhibits the movement of calcium ions across the membranes of cardiac and arterial muscle cells; inhibits transmembrane calcium flow, which results in the depression of impulse formation in specialized cardiac pacemaker cells, slowing of the velocity of conduction of the cardiac impulse, depression of myocardial contractility, and dilation of coronary arteries and arterioles and peripheral arterioles; these effects lead to decreased cardiac work, decreased cardiac oxygen consumption, and in patients with vasospastic (Prinzmetal's) angina, increased delivery of oxygen to cardiac cells. Indications Angina pectoris due to coronary artery spasm (Prinzmetal's variant angina) Chronic stable angina, alone or in combination with other agents Essential hypertension, alone or in combination with other antihypertensives Contraindications

 Contraindicated with allergy to amlodipine, impaired hepatic or renal function, sick sinus syndrome, heart block (second or third degree), lactation. Adverse effects Dizziness, light-headedness, headache, asthenia, fatigue, lethargy, Peripheral edema, arrhythmias, Flushing, rash, Nausea, abdominal discomfort

Nursing considerations Monitor patient carefully (BP, cardiac rhythm, and output) while adjusting drug to therapeutic dose; use special caution if patient has CHF. Monitor BP very carefully if patient is also on nitrates. Monitor cardiac rhythm regularly during stabilization of dosage and periodically during long-term therapy. Administer drug without regard to meals.

Atorvastatin Date Ordered: February 7, 2012 Ordered ordered: 50mg 1tab OD at HS Indications Adjunct to diet in the treatment of elevated total cholestrol and LDL cholesterol with primary hypercholesterolemia (types IIa and IIb) in those unresponsive to dietary restriction of saturated fat and cholesterol and other nonpharmacologic measures To reduce the risk of stroke, TIA, MI in patients with coronary heart disease and hypercholesterolemia Treatment of patients with isolated hypertriglyceridemia Treatment of type III hyperlipoproteinemia Contraindications Contraindicated withallergy to simvastatin, fungal byproducts, pregnancy, lactation. Use cautiously with impaired hepatic and renal function, cataracts. Adverse effects Headache, asthenia, sleep disturbances, Flatulence, diarrhea, abdominal pain, cramps, constipation, nausea, dyspepsia, heartburn, liver failure, Sinusitis, pharyngitis, Rhabdomyolysis, acute renal failure, arthralgia, myalgia

Nursing considerations Ensure that patient has tried a cholesterol-lowering diet regimen for 36 mo before beginning therapy. Give in the evening; highest rates of cholesterol synthesis are between midnight and 5 AM. Advise patient that this drug cannot be taken during pregnancy; advise the use of barrier contraceptives. Arrange for regular follow-up during long-term therapy. Consider reducing dose if cholesterol falls below target.

Paracetamol Date Ordered: February 7, 2012 Ordered ordered: 600mg IVTT q4 RTC Therapeutic actions . Antipyretic effects are not fully understood, but aspirin probably acts in the thermoregulatory center of the hypothalamus to block effects of endogenous pyrogen by inhibiting synthesis of the prostaglandin intermediary. Indications Mild to moderate pain; Fever Contraindications Allergy to salicylates or NSAIDs (more common with nasal polyps, asthma, chronic urticaria); allergy to tartrazine (cross-sensitivity to aspirin is common); hemophilia, bleeding ulcers, hemorrhagic states, blood coagulation defects, hypoprothrombinemia, vitamin K deficiency (increased risk of bleeding); impaired renal function; chickenpox, influenza (risk of Reye's syndrome in children and teenagers); children with fever accompanied by dehydration; surgery scheduled within 1 wk; pregnancy (maternal anemia, antepartal and postpartal hemorrhage, prolonged gestation, and prolonged labor have been reported; readily crosses the placenta; possibly teratogenic; maternal ingestion of aspirin during late pregnancy has been associated with the following adverse fetal

effects: low birth weight, increased intracranial hemorrhage, stillbirths, neonatal death); lactation. Adverse effects Respiratory alkalosis, hyperpnea, tachypnea, hemorrhage, excitement, confusion, asterixis, pulmonary edema, convulsions, tetany, metabolic acidosis, fever, coma, cardiovascular collapse, Exacerbation of bronchospasm, rhinitis (with nasal polyps, asthma, rhinitis),Nausea, dyspepsia, heartburn, epigastric discomfort, anorexia, hepatotoxicity, Occult blood loss, hemostatic defect,Anaphylactoid reactions to anaphylactic shock, Dizziness, tinnitus, difficulty hearing, nausea, vomiting, diarrhea, mental confusion, lassitude (dose related) Nursing considerations Give drug with food or after meals if GI upset occurs. Give drug with full glass of water to reduce risk of tablet or capsule lodging in the esophagus. Do not crush, and ensure that patient does not chew sustained-release preparations. Do not use aspirin that has a strong vinegar-like odor. Institute emergency procedures if overdose occurs: gastric lavage, induction of emesis, activated charcoal, supportive therapy.

Captopril Date Ordered: February 7, 2012 Ordered ordered: 50mg 1tab SL PRN q6 BP > 160/90mmHg Indications Hypertension;Management of congestive heart failure (CHF) Reduces the risk of death or development of CHF after myocardial infarction (MI) Slows the progression of left ventricular dysfunction into overt heart failure Used to decreased the progression of diabetic neuropathy

Mechanism of Action ACE inhibitors block the conversion of angiotensin I to the vasoconstrictor angiotensin II. It also inactivates the vasodilator bradykinin and other vasodilatory prostaglandins. Contraindications Hypersensitivity;Cross sensitivity among Ace inhibitors;Pregnancy;Angioedema (hereditary or idiopathic)

Side Effects Dizziness or lightheadedness;Fatigue Headache;Insomnia;Weakness or excessive tiredness Cough;Hypotension Nursing reponsibility Monitor blood pressure and pulse frequently during initial dose adjustment and periodically during therapy. Oral care The nurse should keep in mind that Captopril may cause false-positive result for urine acetone. The drug should be administered 1 hour before or 2 hours after meals. It may be crushed if the patient has difficulty swallowing. Keep this medication in the container it came in, tightly closed, and out of reach of children. Store it at room temperature and away from excess heat and moisture (not in the bathroom). Inform the patient that Captopril tablets may have a slight sulfur odor (like rotten eggs).

Lactulose Date Ordered: February 7, 2012 Ordered ordered: 30cc OD at HS Indication constipation Mechanism of Action Lactulose promotes peristalsis by producing an osmotic effect in the colon with resultant
distention. In hepatic encephalopathy, it reduces absorption of ammonium ions and toxic nitrogenous compounds, resulting in reduced blood ammonia concentrations.

Side Effect Diarrhoea (dose-related), nausea, vomiting, hypokalaemia, bloating and abdominal cramps.
Potentially Fatal: Dehydration and hypernatraemia on aggressive treatment.

Contraindication Galactosaemia, intestinal obstruction. Patients on low galactose diet. Nursing Responsibility - May take up to 48 hours to act. - Diarrhoea may indicate the dose is too high. - Evaluate therapeutic response: decreased constipation or blood ammonia level. - Assess amount, colour and consistency of stool.

MANNITOL

STANDARD OF NURSING CARE IDEAL FOR THE PATIENT CONDITION

NURSING CARE PLAN

PROGNOSIS

PROGNOSIS Criteria 1. Onset of illness Poor 1 / Fair 2 Good 3 Justification The patient is experiencing this condition for the longiesttime,but last November,the condition of the client aggravated that prompted her admission.Thus, we rated him fair because this cause his many admission. The patient willing to be admitted during the onset of the illness. With that we rated him good in this category With regards to patients willingness , it can be considered to be good for: - He is subjected his self to take medications as prescribed by the doctor. -He takes it religiously. He is eager to listen to the health teaching being provided to him and is encouraged in putting them into practice. The factor that trigger his condition is in his adolescent years he engaged in many vices He has hypertension. In the entire duration of the patients healing/recovery, his family was always at his side to provide everything for the wellness of his condition.

2. Duration of illness Check lab tests 3. Willingness to take medication/ compliance to treatment regimen

4. Precipitating factor (e.g. obesity, sedentary lifestyle) 5. Predisposing factor 6.Family support

/ /

DISCHARGE PLAN

MEDICATION Advice patient to continue taking her prescribed medicines. Treatment regimen is important to have an immediate recovery. Instruct the patient to take the medications with exact dosage as ordered as prescribed. Exact amount and proper timing ensures the effectiveness of the medication and to avoid toxicity. Explain the medications how they work, there side effects, and precautions.
To decrease the anxiety when adverse effect occurs and for them to know that it is normal because he is under medication.

Instruct family or significant others to take patients medications with food if not contraindicated or to take the medicine one hour before the meal or one hour after meal. This helps in the prevention of gastric irritation of the G.I. tract that could lead to G.I. ulcerations. Instruct the client and family to the physician immediately if problem due to side effects of drugs occurs. The physician can re-evaluate the drugs immediately and prescribe new medicines. Instruct the patient to avoid taking medications that are not prescribed by
the physician.

OTC drugs may interfere with the effectiveness of the drugs prescribed. Synergetic or additive effect might happen that might cause further injury to patient

EXERCISE Be sure to get enough rest and sleep on a daily basis. Instructed patient and family member to performed passive range of motion to his affected side Avoid strenuous activities

TREATMENT Avoid stress, fatigue, sudden changes in temperature and excessive alcohol intake,. Encouraged to comply treatment regimen

HYGIENE Take bath daily. Wear masks especially when traveling for the first week after being discharged Promote frequent oral hygiene.

OUTPATIENT ORDERS/FOLLOW UPS Follow up check up

DIET Encouraged to limit intake of salty and fatty foods Eat a healthy, balanced diet and take in a sufficient amount of non-alcoholic fluids each day.

BIBLIOGRAPHY

Mosbys Pocket Dictionary of Medicine, Nursing & Allied Health Fourth Edition, p. 189 S. Smeltzer, B. Bare, J. Hinkle, K. CHeever; Brunner &Suddarths Textbook of MedicalSurgical Nursing Eleventh Edition; Copyright 2008 by Lippincott Williams & Wilkins, a Wolters Kluwer Business, P. 634 Websters Third New International Dictionary; Merriam Webster Inc.; p. 282 Miller-Keane, Encyclopedia& Dictionary of Medicine, Nursing, & Allied Health, W.B. Saunders Company, p. 240 Nursing 2008 drug handbook by Wolterkluwer; Lippincott Williams & Wilkins. Page 672-673 Lippincott Wiliams& Wilkins, Nursing 2006 drug Handbook, page 351 - 353 http://emedicine.medscape.com/article/803364-overview http://pneumonia-disease.blogspot.com/2009/09/risk-factors.html http://www.nhlbi.nih.gov/health/dci/Diseases/pnu/pnu_all.html www.sciencedaily.com http://www.healthline.com/galecontent/hemoptysis www.nursingscrib.com Medical Surgical nursing, brunner&sudarths , 10th edition http:/www.articleswave.com/article/hypertensive cardiovascular disease

Medical Surgical Nursing,m Tim conception