Micu Case Study D1

PHILIPPINES COLLEGES of HEALTH & SCIENCES

AFPMC V. Luna General Hospital Medical Intensive Care Unit (MICU) NMC 204 (2008 - 2009)

CASE STUDY

MYOCARDIAL

INFARCTION GROUP D1 BELTRAN, JHON MARC MARIANO, RYAN TADIFA, JOLEEN

MR. EPHRAIM MIRAFUENTES Clinical Instructor

CONTENTS OF CASE STUDY.

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I. Introduction a. Background b. General Objective c. Importance of the study II. Data Base a. Client’s Profile b. History 1. History of Present Illness 2. Past Medical History 3. Family Medical History 4. Social History 5. 11 Functional Health Pattern (Gordons) c. Physical Assessment 1. Physical assessment (head to toe) 2. Diagnostic procedure done and to be done. III. Anatomy and physiology 1. Laboratory Result and significances IV. Pathophysiology and schematic diagram V. Drugs study VI. Nursing care management 1. Problem list 2. Nursing care plan (3 action and 3 potential) 3. Discharge Planning (M-E-T-H-O-D-S) VII. References VIII. Evaluation

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I. Introduction a. Background An intensive care unit (ICU), also sometimes known as a critical care unit or an intensive therapy department is a special ward found inside most hospitals. It provides intensive care (treatment and monitoring) for people who are in a critically ill or unstable condition. Patients in ICUs need constant medical support to keep their body functions going. They may not be able to breathe on their own, and may have multiple organ failure, so medical equipment takes the place of these functions while they recover.

There are several circumstances in which a person may be admitted to intensive care, for example, following surgery, or after an accident or severe illness. ICU beds are a very expensive and limited resource because they provide specialized monitoring equipment, a high degree of medical expertise and constant access to highly trained nurses (usually one nurse for each bed). Being in an ICU can be a daunting experience both for the patient and his or her friends and family. The healthcare professionals in ICUs understand this and are there to help and support both patients and their families during their time in intensive care. Myocardial infarction (MI) is the irreversible necrosis of heart muscle secondary to prolonged ischemia. This usually results from an imbalance of oxygen supply and demand. The appearance of cardiac enzymes in the circulation generally indicates myocardial necrosis. MI is considered, more appropriately, part of a spectrum referred to an acute coronary syndromes (ACSs), which also includes unstable angina and non–STelevation MI (NSTEMI). Patients with ischemic discomfort may or may not have STsegment elevation. Most of those with ST-segment elevation will develop Q waves. Those without ST elevations will ultimately be diagnosed with unstable angina or NSTEMI based on the presence of cardiac enzymes. MI may lead to impairment of systolic function or diastolic function and to increased predisposition to arrhythmias and other long-term complications.

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b. General Objective 1. Describe Critical Care as a collaborative, holistic approach that includes the patient, family and significant others 2. Established priority critical measures instituted for any patient with a critical conditions. 3. Differentiate, describe, and specify critical care measures and management for admission due to coronary artery disease (Myocardial infarction). 4. Use of a Multidisciplinary Team to Find Simple Solutions. The team determined that the following factors potentially increased a patient’s risk of infection through the central catheter: choice of insertion site, skin preparation material and technique, use of sterile barriers during insertion, dressing maintenance and change techniques, and use of aseptic technique during catheter access. 5. Have knowledge on safe drug administration (preparations/computations) and correlate drug interaction to patient’s condition. Take good performers and transform into great performers in the areas of service to patients, clinical quality, staff satisfaction. 6. Evaluate the patient’s condition and provide nursing care according to the identified needs, report unusual manifestation/ findings and complication. c. Importance of the study 1. Explain cardiac physiology in relation to cardiac anatomy and the conduction system of the heart. Describe the essential components of heart anatomy and physiology to include path of blood flow, the role of arteries, veins, and capillaries. 2. Incorporate assessment of functional health patterns and risk factors into the health history and physical assessment of the patient with coronary artery disease. 3. Outline and define the physiologic/Pathophysiology sequence of events that lead to an acute myocardial infarction (AMI). 4. List the critical parameters of assessment and treatment emergency responders must perform when first attending to a patient with an acute myocardial infarction. 5. Describe the information each of the following tests provide an critical care with physician or cardiac specialist when presented with a patient with a suspected AMI. 6. Define the following as to their prevention or treatment of an MI. 7. Describe the key roles the following health professionals provide in the care of a patient with an acute heart attack:

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II. Data Base

March 20, 2009

a. Client’s Profile Name: A.P.G

Age: 71 years old

Sex: Male

Reg. #: 901668

Address: # 405TNR, FTI Compound, Western Bicutan, Taguig City Birthday: October 2, 1937

Birthplace: Bohol

Religion: 7th Day Adventist

Status: Married

Race: Filipino

Admitted to E.R.: March 4, 2009, assisted by Maj. Benejane. Transferred to M.I.C.U.: March 7, 2009

Room #: 5

Rank: C/V/T

Diagnosis: Nosocomial Pneumonia; CAD, ACS, NSTMI, Killip II, HCVD, FC II, Intracerebral he, (L) Basal Ganglia with intraventricular extension b. History 1. History of Present Illness The patient was not able to get up at early morning, as they notice. Then after two hours he had vomited episodely and cramping, so, their relatives rush up at Fort Santiago General Hospital. Then, they transferred at AFPMC V.Luna, around 10:00 AM. 2. Past Medical History He have a high blood pressure, not complaining for almost 10 years, he only taking the drugs that given to him since the last consultation. 3. Family Medical History He had history of hypertension and Diabetes Mellitus on paternal side. 4. Social History

According to his wife, he used to smoke 8-10 sticks per day and he occasionally drinks any liquor. He sleeps 5 to 6 hours a day, irregular habit time of sleep.

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5. 11 Functional Health Pattern (Gordons) in NANDA 1. Health perception-Health Management Pattern The patient was never ask a consultation at the Physician as long as he can stand alone and can walk. Until he woke up with vulnerable condition, the reason to seek a health management. 2. Nutritional-Metabolic Pattern He doesn’t care, too much, what should be the food to be intake, and what not should be, too. He always telling his wife “ano na lang ang kakainin ko?!”. And now he is feeding thru NGT with low salt, low cholesterol and 1,800kCal. 3. Elimination Pattern He used to commode at least once a day before he admit MICU, according to his wife. The physician ordered a Lactulose 30 cc to help him in bowel movement. 4. Activity-Exercise Pattern The patient working as a carpenter, before his condition getting bad. At the MICU, helping the patient turning side-to-side every two hours, ordered by the physician, and do the passive R.O.M. 5. Sleep-Rest Pattern According to his wife, he sleep for almost 5-6 hour with irregular habit time of sleep. The patient had never awake, since he transferred at MICU. 6. Cognitive-Perceptual Pattern He perform self-care within the level of ability to do the ADL and other activity. Since he got an Intracerebral hemorrhage, he had disturbed perceptual abilities due to neurological illness. 7. Self-Perception/self-concept Pattern He took a healthy body for granted, a kind of denial of the eventuality of aging and illness. Due to the threats to self-concepts about the self these condition may pose. 8. Role-Relationship Pattern He was hardworker and good father to his family. Because of his condition, he is now lying at room # 5, MICU. His family involved in decision making processes directed at appropriate solution for the situation crisis 9. Sexuality-reproductive Pattern He had children by their own. Since, he got CAD, less frequency and satisfaction their sexual activity 10. Coping-Stress Tolerance Pattern. When the patient felt stress, he used to smoke. Although he know there is other way to move the stress away. 11. Value-belief Pattern They do visit their church together with their family aside from his son, working on weekends. All we know, Adventist should not eat pork, but he still doing it.

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c. Physical Assessment

March 20, 2009

1. Physical Assessment (head-to-toe) perform the latest assessment

General Survey: Vital Signs

BP – 110/80 RR - 40 Temp. 37.4˚C PR – 101 bpm Unconscious patient lying on bed, with the position of semi-fowlers Integument Cold skin, from the body to lower extremity. The head, right and left arm are enough heat skin. Nails, delayed refill capillary Moist skin on his face and neck Head and neck Skull and face, shape symmetry Neck, no presence of contusions. Eyes, yellow conjunctiva, unequal pupil 2-3 mm pupil on left and 3-4 pupil on right Ears, lesion on auricle of the Left ear Nose, nasal flaring; placing an NGT (French 18) on his Left. Mouth, placing an Endotracheal tube with 7.0, plastering on his right lips; dry lips, yellowish teeth Chest RR- 40, auscultated chest with crackles sounds Extra sounds on Heart sounds Apical pulse rate: 101 bpm Abdomen no contour, no lesions tympany over the stomach and gas Extremity Left arm infused IV Fluid Right arm, no muscle tone, no strength muscle, +1 edema scale Left and Right leg, are pale, cold & dry skin, delayed capillary refill Genital Penis, placing a foley catheter in orange. Urine, yellow-orange, 200 cc at 4 hours. Neurological Glasgow Coma Scale: total score of 6 Eye: 2, he slightly his upper eyelid on pain Motor: 3, flexes abnormally Verbal: 1, no response Level of conciousness: comatose

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2. Diagnostic procedure done, and possible to be done to the patient Persistent chest pain, ST- segment changes on the electrocardiogram (ECG), and elevated levels of total creatinine kinase (CK) and the CK-MB isoenzyme over a 72 hour usually confirm an MI. Cardiac troponins are useful in differentiating an MI from skeletal muscle injury, or when CK-MB measurements are low and a small MI has actually occurred. Auscultation may reveal diminished heart sounds, gallops, and, in papillary dysfunction, the apical systolic murmur of mitral valve area. When signs and symptoms are equivocal, assume that the patient has had an MI until tests rule it out. Diagnostic test results include the following:

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Serial 12-lead ECG: ECG abnormalities may be absent or inconclusive during first few hours following an MI. When present, characteristics abnormalities include serial ST-segment depression in subendocardial MI and ST-segment elevation in a transmural MI.

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Coronary Angiography: visualization reveals which vessels have been affected and the extent of damage.

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Serial serum enzyme levels: CK levels are elevated ; specifically, CK-MB or troponin levels.

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Myoglobin: because myoglobin always rises within 3-6 hours after an MI, lack of an increase within 6 hours indicates that an MI hasn’t occurred.

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Echocardiography: may show ventricular-wall motion abnormalities in patients with a transmural MI.

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Nuclear ventriculography (multigated acquisition scan or radionuclide ventriculography) scanning: Nuclear scanning can identify acutely damaged muscle by picking up radioactive nucleotide, which appears as a “hot spot” on the film. It’s useful in localizing a recent MI.

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Chest X-ray: venous congestion, cardiomegaly, and kerley’s B lines

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Cardiac catheterization: show decrease cardiac output, increase in Pulmonary arterial pressure, pulmonary artery wedge pressure and central venous pressure.

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Auscultation: reveals holosystolic murmur and thrill. And also reveals a friction rub.

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ABG Analysis: reduced partial pressure of arterial oxygen.

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III. Anatomy and Physiology. ANATOMY

1. Right Coronary 2. Left Anterior Descending 3. Left Circumflex 4. Superior Vena Cava 5. Inferior Vena Cava 6. Aorta 7. Pulmonary Artery 8. Pulmonary Vein 9. Right Atrium 10. Right Ventricle 11. Left Atrium 12. Left Ventricle 13. Papillary Muscles 14. Chordae Tendineae 15. Tricuspid Valve 16. Mitral Valve Coronary Arteries. Because the heart is composed primarily of cardiac muscle tissue that continuously contracts and relaxes, it must have a constant supply of oxygen and nutrients. The coronary arteries are the network of blood vessels that carry oxygen- and nutrient-rich blood to the cardiac muscle tissue. The blood leaving the left ventricle exits through the aorta, the body’s main artery. Two coronary arteries, referred to as the "left" and "right" coronary arteries, emerge from the beginning of the aorta, near the top of the heart. The initial segment of the left coronary artery is called the left main coronary. This blood vessel is approximately the width of a soda straw and is less than an inch long. It branches into two slightly smaller arteries: the left anterior descending coronary artery and the left circumflex coronary artery. The left anterior descending coronary artery is embedded in the surface of the front side of the heart. The left circumflex coronary artery circles around the left side of the heart and is embedded in the surface of the back of the heart. Just like branches on a tree, the coronary arteries branch into progressively smaller vessels. The larger vessels travel along the surface of the heart; however, the smaller branches penetrate the heart muscle. The smallest branches, called capillaries, are so narrow that the red blood cells must travel in single file. In the capillaries, the red blood cells provide oxygen and nutrients to the cardiac muscle tissue and bond with carbon dioxide and other metabolic waste products, taking them away from the heart for disposal through the lungs, kidneys and liver. When cholesterol plaque accumulates to the point of blocking the flow of blood through a coronary artery, the cardiac muscle tissue fed by the coronary artery beyond the point of the blockage is deprived of oxygen and nutrients. This area of cardiac muscle tissue ceases to function properly. The condition when a coronary artery becomes blocked causing damage to the cardiac muscle tissue it serves is called a myocardial infarction or heart attack.

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Superior Vena Cava. The superior vena cava is one of the two main veins bringing deoxygenated blood from the body to the heart. Veins from the head and upper body feed into the superior vena cava, which empties into the right atrium of the heart. Inferior Vena Cava. The inferior vena cava is one of the two main veins bringing de-oxygenated blood from the body to the heart. Veins from the legs and lower torso feed into the inferior vena cava, which empties into the right atrium of the heart. Aorta. The aorta is the largest single blood vessel in the body. It is approximately the diameter of your thumb. This vessel carries oxygen-rich blood from the left ventricle to the various parts of the body. Pulmonary Artery. The pulmonary artery is the vessel transporting de-oxygenated blood from the right ventricle to the lungs. A common misconception is that all arteries carry oxygen-rich blood. It is more appropriate to classify arteries as vessels carrying blood away from the heart. Pulmonary Vein. The pulmonary vein is the vessel transporting oxygen-rich blood from the lungs to the left atrium. A common misconception is that all veins carry de-oxygenated blood. It is more appropriate to classify veins as vessels carrying blood to the heart. Right Atrium. The right atrium receives de-oxygenated blood from the body through the superior vena cava (head and upper body) and inferior vena cava (legs and lower torso). The sinoatrial node sends an impulse that causes the cardiac muscle tissue of the atrium to contract in a coordinated, wave-like manner. The tricuspid valve, which separates the right atrium from the right ventricle, opens to allow the de-oxygenated blood collected in the right atrium to flow into the right ventricle. Right Ventricle. The right ventricle receives de-oxygenated blood as the right atrium contracts. The pulmonary valve leading into the pulmonary artery is closed, allowing the ventricle to fill with blood. Once the ventricles are full, they contract. As the right ventricle contracts, the tricuspid valve closes and the pulmonary valve opens. The closure of the tricuspid valve prevents blood from backing into the right atrium and the opening of the pulmonary valve allows the blood to flow into the pulmonary artery toward the lungs. Left Atrium. The left atrium receives oxygenated blood from the lungs through the pulmonary vein. As the contraction triggered by the sinoatrial node progresses through the atria, the blood passes through the mitral valve into the left ventricle. Left Ventricle. The left ventricle receives oxygenated blood as the left atrium contracts. The blood passes through the mitral valve into the left ventricle. The aortic valve leading into the aorta is closed, allowing the ventricle to fill with blood. Once the ventricles are full, they contract. As the left ventricle contracts, the mitral valve closes and the aortic valve opens. The closure of the mitral valve prevents blood from backing into the left atrium and the opening of the aortic valve allows the blood to flow into the aorta and flow throughout the body. Papillary Muscles. The papillary muscles attach to the lower portion of the interior wall of the ventricles. They connect to the chordae tendineae, which attach to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. The contraction of the papillary muscles opens these valves. When the papillary muscles relax, the valves close.

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Chordae Tendineae. The chordae tendineae are tendons linking the papillary muscles to the tricuspid valve in the right ventricle and the mitral valve in the left ventricle. As the papillary muscles contract and relax, the chordae tendineae transmit the resulting increase and decrease in tension to the respective valves, causing them to open and close. The chordae tendineae are string-like in appearance and are sometimes referred to as "heart strings." Tricuspid Valve. The tricuspid valve separates the right atrium from the right ventricle. It opens to allow the de-oxygenated blood collected in the right atrium to flow into the right ventricle. It closes as the right ventricle contracts, preventing blood from returning to the right atrium; thereby, forcing it to exit through the pulmonary valve into the pulmonary artery. Mitral Value. The mitral valve separates the left atrium from the left ventricle. It opens to allow the oxygenated blood collected in the left atrium to flow into the left ventricle. It closes as the left ventricle contracts, preventing blood from returning to the left atrium; thereby, forcing it to exit through the aortic valve into the aorta. Pulmonary Valve. The pulmonary valve separates the right ventricle from the pulmonary artery. As the ventricles contract, it opens to allow the de-oxygenated blood collected in the right ventricle to flow to the lungs. It closes as the ventricles relax, preventing blood from returning to the heart. Aortic Valve. The aortic valve separates the left ventricle from the aorta. As the ventricles contract, it opens to allow the oxygenated blood collected in the left ventricle to flow throughout the body. It closes as the ventricles relax, preventing blood from returning to the heart. PHYSIOLOGY. The heart is the muscular organ of the circulatory system that constantly pumps blood throughout the body. Approximately the size of a clenched fist, the heart is composed of cardiac muscle tissue that is very strong and able to contract and relax rhythmically throughout a person's lifetime. The heart has four separate compartments or chambers. The upper chamber on each side of the heart, which is called an atrium, receives and collects the blood coming to the heart. The atrium then delivers blood to the powerful lower chamber, called a ventricle, which pumps blood away from the heart through powerful, rhythmic contractions. The human heart is actually two pumps in one. The right side receives oxygen-poor blood from the various regions of the body and delivers it to the lungs. In the lungs, oxygen is absorbed in the blood. The left side of the heartreceives the oxygen-rich blood from the lungs and delivers it to the rest of the body. Systole. The contraction of the cardiac muscle tissue in the ventricles is called systole. When the ventricles contract, they force the blood from their chambers into the arteries leaving the heart.

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The left ventricle empties into the aorta and the right ventricle into the pulmonary artery. The increased pressure due to the contraction of the ventricles is called systolic pressure. Diastole. The relaxation of the cardiac muscle tissue in the ventricles is called diastole. When the ventricles relax, they make room to accept the blood from the atria. The decreased pressure due to the relaxation of the ventricles is called diastolic pressure.

1. 2. 3. 4.

Sinoatrial node (SA node) Atrioventricular node (AV node) Common AV Bundle Right & Left Bundle Branches

The Sinoatrial Node (often called the SA node or sinus node) serves as the natural pacemaker for the heart. Nestled in the upper area of the right atrium, it sends the electrical impulse that triggers each heartbeat. The impulse spreads through the atria, prompting the cardiac muscle tissue to contract in a coordinated wave-like manner. The impulse that originates from the sinoatrial node strikes the Atrioventricular node (or AV node) which is situated in the lower portion of the right atrium. The atrioventricular node in turn sends an impulse through the nerve network to the ventricles, initiating the same wave-like contraction of the ventricles. The electrical network serving the ventricles leaves the atrioventricular node through the Right and Left Bundle Branches. These nerve fibers send impulses that cause the cardiac muscle tissue to contract. A. Laboratory Result and significant HEMATOLOGY Lab Hemoglobin . Hematocrit . Red Blood Cell (RBC) Leukocytes (WBC) Platelet Blood Indices MCV MCH MCHC RBW

March 04, 2009 (11:45)

March 07, 2009 (17:30)

March 19, 2009 (05:35)

March 19, 2009 (17:35)

M:13-18 gm/dL F:1216 gm/dL

14.4

16.0

13.2

13.3

M:42-52% F:35%-47%

44%

39%

37%

40%

M:4.6-6.2 mill/mm3 F:4.2-5.2 mill/mm3

4.99

5.11

5.01

4.35

4,500-11,000 x109/L

12.6

16.5

13.6

17.5

150-450 x109/L

241

212

356

532

84-96 cu µm 28-33 µµg/cell 33%-35%

88.6 28.9 32.6 15.4

96.6 31.2 32.3 16.1

84.0 29.2 34.8 13.3

92.4 30.5 33.0 13.9

Normal value

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COAGULATION (March 18, 2009) Time : 14:30 Determination

Time : 15:00 Lab.Result

PT % activity INR

Lab.Result

12.4 86.9 1.09

Normal Value

Deteminatio n aPTT Clotting time Bleeding time

Result

18.4 3 1

Norml value

12.4 86.9 1.09

10-14 sec. 67-142% 2-3

22-35 sec 2-7 min 2-4 min

March 4,2009

March 7,2009

March 8,2009

March 11,2009

March 13,2009

March 15,2009

March 21,2009

79

65

137.3

52

109

40

117

4.25

3.8

3.72

4.0

3.5

3.7

3.07

142.3

137

123.4

103

121

SERUM ENZYME LEVELS Serum Enzyme

Nomal Value

Na+

135-145 mEq/L K+ 3.5-5.0 mEq/L Cl+ 100-106 mEq/L Creatinine 62-124

42

µmol/L

Troponin

(-)

(-)

Significances: Hematology: Hgb: still at normal ranges. Hct: acute massive blood loss RBC: decreasing due to side effects of the drugs. WBC: Increasing due to immunocompromised, immune responses. Platelet: increasing the fibrin that attract the platelet to increased Blood indices: MCHC: decreased in severe hypochromic anemia. Coagulation: Bleeding time: defective in platelet function INR: prolonged in deficiency of fibrinogen; used to standardized the prothrombin time and anti-coagulation therapy. Serum enzyme levels: Na+ : decreased; myxedema K+ : decreased; GI losses, Vitamin D Deficiency Cl+ : decreased; pneumonia, febrile condition. Creatinine: decreased; check the status of the kidney Troponin: negative; if increased the patient may experience myocardial infarction.

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`IV. Pathophysiology & Schematic Diagram. In an MI, an area of the myocardium is permanently destroyed; a condition in which the blood supply to the heart muscle is partially or completely blocked. The heart muscle needs a constant supply of oxygen-rich blood. The coronary arteries, which branch off the aorta just after it leaves the heart, deliver this blood. MI is usually caused by the reduced blood flow in a coronary artery of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus. Coronary artery disease can block blood flow, causing chest pain. In unstable angina and acute MI are considered to be the same process but different appoints along a continuum. specifically coronary atherosclerosis (literally “hardening of the arteries,” which involves fatty deposits in the artery walls and may progress to narrowing and even blockage of blood flow in the artery., As an atheroma grows, it may bulge into the artery, narrowing the interior (lumen) of the artery and partially blocking blood flow. With time, calcium accumulates in the atheroma. As an atheroma blocks more and more of a coronary artery, An atheroma, even one that is not blocking very much blood flow, may rupture suddenly. The rupture of an atheroma often triggers the formation of a blood clot (thrombus), the supply of oxygen-rich blood to the heart muscle (myocardium) can become inadequate. The blood supply is more likely to be inadequate during exertion, when the heart muscle requires more blood. An inadequate blood supply to the heart muscle (from any cause) is called myocardial ischemia. If the heart does not receive enough blood, it can no longer contract and pump blood normally. Other causes of MI include vasospasm, (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (e.g. from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (e.g. rapid heart rate, thyrotoxicosis, or ingestion of cocaine). In each case, a profound imbalance exists between myocardial oxygen supply and demand. The area of infarction develops over minutes to hours. As the cells are deprived of oxygen, ischemia develop, cellular injury occurs,, and the lack of oxygen results in infarction, or the death of cells. The area of the heart muscle supplied by the blocked artery dies.

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V. DRUG STUDY Brand Name Generic Name Classification Action Pt. dosage ordered by Physician Indication Adverse reaction Nursing consideration

Metoprolol Lopressor Antihypertensives A selective beta blocker that selectively blocks beta1 receptors; decreases cardiac output , peripheral resistance, and cardiac oxygen consumption; and depressed renin secretion 100 mg tab, every 6 hours Hypertension, initially 100 mg P.O. once daily; then up to 100 mg to 450 mg daily divided in two or three doses. CNS: fatigue, dizziness, depression. CV: hypotension, bradycardia, heart failure, AV block, edema. GI: nausea, diarrhea. Respiratory: dyspnea. Skin: rashes Always check patient’s apical pulse rate before giving drug. Monitor blood pressure frequently. Beta blockers may mask tachycardia caused by hyperthyroidism. In patients with suspected thyrotoxicosis, taper off beta blocker to avoid thyroid storm. When stopping therapy, taper dose for 1-2 weeks. Beta selectively is lost at higher doses. Watch for peripheral side effects. Take drugs exactly as prescribed with meals. Avoid driving and other task requiring mental alertness. Inform the Health provider before procedures or surgery Alert, if have a shortness of breath occurs Notify the prescriber, if you stop taking medication.

Brand Name Generic Name Classification Action Pt. dosage ordered by Physician Indication

Adverse reaction Nursing consideration

Simvastatin Zocor Antilipemics Inhibits HMG-CoA reductase, an early (and rate-limiting) step in cholesterol biosynthesis. 40 mg tab OD HS

To reduce risk of death from CV disease and CV events in patients at high-risk for coronary events. To reduce total and LDL cholesterol levels in patients with homo-zygous familial hyper- cholesterolemia. CNS: Asthenia, Headache. GI: Abdominal pain, Constipation, Diarrhea, Nausea. Musculoskeletal: Myalgia. Respiratory: upper respiratory tract infection Use drug only after diet and other non-drug therapies prove ineffective. Patient should follow a standard low-cholesterol diet during therapy. Obtain liver function test results at start of therapy and then periodically. A liver biopsy maybe performed if enzyme elevations persist.

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40 mg daily significantly reduces risk of death from coronary heart disease, non fatal MIs, stroke, and revascularization procedures. take drug with meals proper dietary management of cholesterol and triglycerides inform patients, adverse reaction occur, particularly muscles aches.

Brand Name Generic Name Classification Action

Pt. dosage ordered by Physician Indication Adverse reaction

Nursing consideration

Brand Name Generic Name Classification Action Pt. dosage ordered by Physician Indication Adverse reaction

Captopril Capoten Antihypertensives Inhibits ACE, preventing conversion of angiotensin I to angiotensin II, a potent vasoconstrictor. Less angiotensin II decrease peripheral arterial resistance, decreasing aldosterone secretion, which reduces secretion, which reduces sodium and water retention and lower blood pressure. 50 mg P.O. TID Left ventricular ventricular dysfunction after acute MI CNS: dizziness, fainting, headache, malaise, fatigue, fever. CV: tachycardia, hypotension, angina pectoris Hematologic: abdominal pain, anorexia, constipation, diarrhea, dry mouth, dysgeusia, nausea, vomiting Metabolic: hyperkalemia Respiratory: dry, persistent, nonproductive cough, dyspnea Skin: urticarial rash, maculopapular rash, pruritis, alopecia Other: angioedema Monitor blood pressure and pulse rate frequently. Elderly patient may be more sensitive to hypotensive effects. Assess patient for signs and symptoms of angioedema. drug causes the most frequent occurrence of cough, compared with other ACE inhibitors. take drugs one hour before the meal patient that have light-headedness is possible, especially during the first few days of therapy. If fainting occurs, he should stop drug and call prescriber immediately. tell patient to use caution in hot weather and during exercise, it can lead to lightheadedness and syncope. urge patient to promptly report swelling of his face, lips, or mouth, or difficulty of breathing.

Isosorbide Dinitrate Isordil Antianginals Thought to reduce cardiac oxygen demand by decreasing preload and after load and afterload. Drug also may increase blood flow through the collateral coronary vessels. 10 mg tab TID 5mg tab SL – PRN in chest pain Acute anginals attacks; to prevent situations that may cause anginal attacks. CNS: headache, dizziness, weakness CV: orthostatic hypotension, tachycardia, palpitations, ankle edema, flushing, fainting EENT: S.L. burning GI: nausea, vomiting

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Nursing consideration

Brand Name Generic Name Classification Action

Pt. dosage ordered by Physician Indication Adverse reaction Nursing consideration

Skin: cutaneous vasodilation, rash monitor blood pressure and intensity and duration of drug response. drug may cause headache, especially at the beginning of therapy. Dosage may reduced temporarily, but tolerance usually develops. Treat headache with aspirin and acetaminophen. methemoglobinemia has been seen with nitrates. Symptoms are those of impaired oxygen delivery despite adequate cardiac output and adequate partial pressure of oxygen. caution patient to take drug regularly, as prescribed. Patient stopping the drugs may cause spasm of the coronary arteries with increased angina symptoms and potential risk of heart attack. take drugs 30 minutes before the meals or 1-2 hours after meals. avoid alcohol because it may worsen blood pressure effects. instruct patient to store drug in a cool place, in a tightly container.

Tylenol Acetaminophen Nonopioid analgesics and antipyretics Thought to produce analgesia by blocking pain impulses by inhibiting synthesis of prostaglandin in the CNS or of other substances that sensitize pain receptors to stimulation. The drug may relieve fever through central action in the hypothalamic heat-regulating center. 300 mg/ amp mild pain and fever Hematologic: hemolytic anemia, leucopenia, neutropenia, pancytopenia Hepatic: jaundice Metabolic: hypoglycemia Skin: rash, urticaria Alert: many OTC and prescription products contains acetaminophen; be aware of this calculating total daily dosage. tell patient not to use for marked fever a (temperature higher than 39.5C) warn patient that high doses or unsupervised long term used can liver damage.

VI. NURSING CARE MANAGEMENT a. Problem List

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b. Nursing Care Plan Action problem ASSESSMENT Subjective: “hindi normal yung vital signs niya” as verbalized by the relative of the patient. Objective: Auscultated heart have extra sound shortness of breath cool & pale skin

NURSING DIAGNOSIS Ineffective cardiac tissue perfusion related to reduced coronary blood flow.

PLAN OF CARE The patient will alleviate and appears comfortable and is free of pain and other sign and symptoms: respiratory rate, cardiac rate, and blood pressure return to prediscomfort level.

INTERVENTION

RATIONALE

EVALUATION

initially assess, document, and report to the physician the following: the patient’s description of chest discomfort, the effect of it on cardiovascular perfusion change in blood pressure and heart sounds, changes in LOC, decrease in urine output and to the skin temperature, nad other symptoms such as nausea, increase sweating, or complaints of unusual fatigue.

assist in determining cause and effect of the chest discomfort and provide a baseline data for characteristics findings of ischemic pain and symptoms.

After rendering of nursing intervention, the patient had appears comfortable and is free from pain. Blood pressure is 110/80. Temperature of 37.1˚C. But the RR 40 and PR 101 bpm are still compensating to maintain cardiac output. The goal is partially met.

obtain a 12 –lead ECG recording the symptomatic event, as prescribed by physician, to determine extension of infarction.

An ECG during symptoms may be useful in the diagnosis of an extension of MI.

administer oxygen at the level of prescribed.

Oxygen therapy increases the oxygen supply to the

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myocardium if actual oxygen saturation is less than normal. administer medication therapy as prescribed, and evaluate the patient’s response continuously.

ensure physical rest; use the bedside commode with assistance; backrest elevated to promote comfort; diet as tolerated; arms supported during upper extremity activity; use of stool softener to straining stool. Provide a restful environment.

ASSESSMENT adventitious breath sounds changes in respiratory rate and rhythm

NURSING DIAGNOSES Ineffective airway clearance related to copious tracheobronchial secretions.

PLAN OF CARE After of nursing intervention the patient will clear the airway patency.

medication therapy is the first line of defense in preserving myocardial tissue. The side effects of the medications can be hazardous and the patient’s status must be assessed. physicals rest reduces myocardial oxygen consumption. Stress response, this results, this result, increase myocardial oxygen consumption.

INTERVENTION

RATIONALE

EVALUATION

assess, document & report to the physician on abnormal breath sound

can be used as a guide for activity prescription and a basis for patient health management.

After of nursing intervention the patient will clear the airway patency.

maintain the patency of oxygenation therapy

to provide an oxygen needed by the physiologic need of the body.

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Monitor Arterial Blood Gases Analysis

to indicate the effectiveness of oxygenation therapy and changes that need to improve gas exchange. retention of secretions lead to decrease of oxygen supply

suction tracheobronchial secretion established the turning patient as and “tapping back” , as prescribed by the physician.

ASSESSMENT Objective: >cold clammy skin > prolonged capillary refill >crackles sounds on chest

NURSING DIAGNOSES Decreased Cardiac Output related to alteraion of stroke volume

PLAN OF INTERVENTION CARE >take vital signs After of 8 hours of >Auscultate heart nursing sounds: intervention the patient will be display hemodynamic stability. Note development of S3, S4;

Presence of murmurs/rubs.

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help to loosen the secretions.

RATIONALE >for bseline data. >Decreased cardiac output results in diminished weak/thready pulses. Irregularities suggest dysrhythmias, which may require further evaluation/monitoring. S3 is usually associated with HF, but it may also be noted with the mitral insufficiency (regurgitation) and left ventricular overload that can accompany severe infarction. S4 may be associated with myocardial ischemia, ventricular stiffening, and pulmonary or systemic hypertension. Indicates disturbances of normal blood flow within the heart, e.g., incompetent valve, septal defect, or vibration of papillary muscle/chordae tendineae

EVALUATION After of 8 hours of nursing intervention the patient should be display hemodynamic stability. The goal is partially met.

(complication of MI). Presence of rub with an infarction is also associated with inflammation, e.g., pericardial effusion and pericarditis. >Auscultate breath sounds.

>Monitor heart rate and rhythm

>Administer supplemental oxygen, as indicated.

Measure cardiac output and other functional parameters as appropriate.

review serial ECGs.

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Crackles reflecting pulmonary congestion may develop because of depressed myocardial function. >Heart rate and rhythm respond to medication, activity, and developing complications. Dysrhythmias (especially premature ventricular contractions or progressive heart blocks) can compromise cardiac function or increase ischemic damage. Acute or chronic atrial flutter/fibrillation may be seen with coronary artery or valvular involvement and may or may not be pathological. >Increases amount of oxygen available for myocardial uptake, reducing ischemia and resultant cellular irritation/dysrhythmias. Cardiac index, preload/afterload, contractility, and cardiac work can be measured noninvasively with thoracic electrical bioimpedance (TEB) technique. Useful in evaluating response to therapeutic interventions and identifying need for more aggressive/emergency care. Provides information regarding progression/resolution of infarction, status of ventricular function, electrolyte balance, and effects of drug therapies.

May reflect pulmonary edema related to ventricular dysfunction. Review chest xray.

ASSESSMENT Objectives: physical immobilization prolonged bed pressure

Enzymes monitor resolution/extension of infarction. Presence of hypoxia indicates need for Monitor laboratory supplemental oxygen. Electrolyte imbalance, e.g., data, e.g., cardiac hypokalemia/hyperkalemia enzymes, ABGs, , adversely affects cardiac electrolytes. rhythm/contractility. NURSING PLAN OF INTERVENTION RATIONALE EVALUATION DIAGNOSES CARE impaired skin After After rendering of assess, document for guiding integrity rendering of the skin patient. data. nursing care related to nursing intervention the prolonged bed intervention patient will not be ask the physician if to avoid pressure. the patient will the patient will possible that can able to get a bed sore. not be able to allowed to turn the trigger to his get a bed sore. patient on side-to disease. side and the time interval. do the skin care

ASSESSMENT

NURSING DIAGNOSES

Objective:

risk for excess fluid volume, decreased organ perfusion

>Decreasing urinary output >abnormal breath sounds, crackles >dyspnea

PLAN OF CARE After of 8 hours of nursing intervention the patient will monitor fluid status and reduce occurrence of fluid excess.

to avoid possible complication on skin.

INTERVENTION

RATIONALE

>Auscultate breath sounds for presence of crackles.

> May indicate pulmonary edema secondary to cardiac decompensation.

> Measure I&O, noting decrease in output, concentrated appearance. Calculate fluid balance.

> Decreased cardiac output results in impaired kidney perfusion, sodium/water retention, and reduced urine output.

>assess for edema and weigh daily.

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> Sudden changes in weight reflect alterations in fluid

EVALUATION After of 8 hours of nursing intervention the patient had monitor fluid status and reduce occurrence of fluid excess. the goal is met.

balance.\

>Provide lowsodium diet/beverages.

>Sodium enhances fluid retention and should therefore be restricted during active MI phase and/or if heart failure is present.

Potential problem POTENTIAL CONSIDERATIONS following discharge from care setting (dependent on patient’s age, physical condition/presence of complications, personal resources, and life responsibilities) Activity intolerance —imbalance between myocardial oxygen supply/demand. Grieving, anticipatory—perceived loss of general well-being, required changes in lifestyle, confronting mortality. Decisional Conflict (treatment)—multiple/divergent sources of information, perceived threat to value system, support system deficit. Family Processes, interrupted—situational transition and crisis. Home Management, impaired—altered ability to perform tasks, inadequate support systems, reluctance to request assistance. c. Discharge Planning use METHODS Medications  Promotes adherence measures by thoroughly explaining the prescribed medication regimen and other treatment measures.  Warn the patients together with relatives about adverse reaction to drugs, and advise them to watch the sign and symptoms of toxic (nausea, anorexia, vomiting, and yellow vision) Exercises  Organize patient care and activities to maximize periods of uninterrupted rest.  Assist with range-of-motion exercise. And turn him, every two hours, as ordered by physician.  Don’t stress yourself, too much exercise. Enough, walk for 15 minutes. Treatment  Antiembolism stockings help prevent venostasis and thromboplebitis.  Encourage participation in a cardiac rehabilitation program. Health teaching

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 Watch for sign and symptoms of fluid retention (crackles, cough, tachypnea, and edema), which may indicate impending HF. Carefully monitor daily weight, intake and output, respiration, serum enzyme level and blood pressure. Oxygenation and OPD follow up  Oxygen administration at a modest flow rate for 3-6 hours. Diet of the patient  Review dietary restriction with the patient. A low sodium, low fat, or low cholesterol diet and caffeine-free may be ordered, provide a list of food that he should avoid. Provide a clear liquid diet until nausea subsides. Ask dietitian to speak to the patient’s family. Spiritual and sexual teaching  Counsel patient to resume sexual activity progressively.  Encourages the family to seek out religious activities, pertaining to spiritual issues. VII. Referreces Medical-Surgical Nursing, 11th edition, Brunner & Suddarth’s (Smeltzer, Bare, Hinkle, Cheever) Handbook of Diseases, 3rd edition, Sarah Y. Yuan Nursing Drug Handbook 2008, 28th edition, Wolter Kluwer/Lippincott William & Williams http://www.cardioconsult.com http://www.aacn.org VIII. Evaluation Mr. Ephraim Mirafuentes & Staff Nurse (MICU): BELTRAN, JHON MARC Highly competitive critical care nurse, that know how to assess, monitor and treat a critically ill patient, the better that patient’s chances are for early intervention. All of them excellence in the work environment. Their team using a method of habitual concentration our staff nurses could develop qualities of excellence for an improved outlook toward themselves, their work environment, and their profession. This improved outlook would lead to improved morale followed by an increase in retention within the unit, as well as progress in meeting our other goals. We recognized that our patient care, the attitudes of our nurses and staff, the helpfulness of peers, and even the cleanliness of the unit were based on tradition. During orientation, we learned what was expected of them in their individual units, and they continued this process by orienting others to the

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same routines. As we recognized, we needed to improve ourselves in reality, in the world of Intensive care unit. Because we must aware that our work was in critical situation. As we are the nursing student that would be excited to us learning to do many activities in the role they accept, their life, around the Intensive care unit. We learned some nursing skills that we can used in critical situation. We, my group, are glad to be your nursing student. Thanks you so much. Mariano, Ryan Medical Intensive Care Unit provides comprehensive and continuous care for patients who suffer from a serious illness or medical problem as well as social and psychological support for patients and their families. Their team includes board-certified, critical care physicians , highly trained nurses and other specialists who are specifically trained in critical care and provide round-the-clock care. We learned some nursing skills using their equipment in an intensive care unit (ICU) includes mechanical ventilation to assist breathing through an endotracheal tube or a tracheotomy; intravenous lines for drug infusions fluids, nasogastric tubes, suction pumps, drains and catheters; and a wide array of drugs including their medication management. Tadifa, Joleen In MICU, patients are given 24-hour assessments by the healthcare team. Preparatory orders for the ICU generally vary from patient to patient since treatment is individualized. The initial workup should be coordinated by the attending ICU staff (intensiv and ICU nurse specialist), pharmacists (for medications and IV fluid therapy), and respiratory therapists for stabilization, improvement, or continuation of cardiopulmonary care. Well-coordinated care includes prompt consultation with other specialists soon after the patient is admitted to the ICU. The patient is connected to monitors that record his or her vital signs (pulse, blood pressure, and breathing rate). Orders for medications, laboratory tests, or other procedures are instituted upon arrival. The staff are highly skilled for critically ill patients. Using their advanced patient monitoring technology and sophisticated medical equipment, as providing continuous, comprehensive care for patients with serious conditions. providing expert healthcare and to treating patients with the compassion and respect they deserve. Patients requiring intensive care usually require support for airway or respiratory compromise (such as ventilator support), potentially lethal cardiac dysrhythmias. Critical care nurse are giving their intensive care to the patient, support for the above are usually admitted for intensive/invasive monitoring. Ideally, intensive care is usually only offered to those whose condition is potentially reversible and who have a good chance of surviving with intensive care support. Since the critically ill are so close to dying, the outcome of this intervention is difficult to predict.

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