MYOCARDIAL INFARCTION (HEART ATTACK) A Case Study By Rolly M. Policarpio RN I. INTRODUCTION The numerous numbers of literary works that drew inspiration from the work of the heart demonstrate the magnificent and life-sustaining function of this organ. More than a metaphor of love, it is a metaphor of life. indeed heart maintains life by keeping the blood dynamic at all times even without our conscious awareness. But the hear itself has a life that need to be sustained and maintained. This is possible because of the networks of blood vessels specially the coronary artery, that nourish every single cell of the heart. Sometimes, the coronary artery become inadequate by the formation of blockage from a complex process brought about by conglomeration of differen factors. This can lead to coronary artery diseases and worst to myocardial infarction. Myocardial infarction, sometimes called as Acute Myocardial Infarction(AMI) or Myocardial Ischemia is also known as heart attack, coronary occlusion, or simply "coronary," which is a life-threatening condition characterized b! the formation of localized necrotic areas within the myocardium (Black, 2005) and occurs when myocardial tissue it abruptly and severed deprived of oxygen. Angina pectoris is characterized by a chest pain resulting from reducer coronary blood flow, which causes a temporary imbalance between myocardial blood supply and demand. Moreover it is a chest pain resulting from myocardial ischemia (inadequate blood supply to the myocardium), (Black, 2005). Worldwide, heart diseases and stroke are also found to be the leading causes of death. It is estimated tha 7.1 million people worldwide die of heart disease each year. In 2008, almost 48% of all continental deaths were dun to cardiovascular disease (Billiones, 2008). In the United Stated of America (USA), 7,900,000 had heart attack (American Heart Association), about one of every five dies from Myocardial infarction.. Incidence is 1,260,000 new and recurrent coronary attacks per year (National Heart, Lung, and Blood institute's Atherosclerotic Risk in Communities PANICS Study and Cardiovascula Health Study (CHS). About 37 percent of people who experience a coronary attack in a given year die from it. In the Philippines. as to the 10 leadings causes of Mortality in the Philippines (2008), Heart Diseases rank< 1^S^t. On the other hand, as to the 10 leading causes of Morbidity in the Philippines (2008), Hypertension and Hear Diseases ranks, 5th and 8th, respectively. The region with the highest morbidity for CVD is Region 7, followed b! Regions 1, CAR, 2 and 6, (NSO, Philippines, 2008). One of the major technological breakthroughs regarding the treatment of acute myocardial infarction is the development of hybrid stent called Stentys. The new capabilities of this stent is self-expanding platform, solving Stent-malapposition. Two patients were successfully treated during acute myocardial infarction procedures by Drs. S Verheye (Antwerp, Belgium) and K. E. Hauptmann (Trier, Germany). The problem with the old stent used is the malposition of the device several days after it was placed to the affected artery. One of the greatest problems ir myocardial infarction is the urgent diagnosis of the disease condition. Usually, the patient is diagnosed of having myocardial infarction after being positive with troponin T marker and significant ECG(electrocardiagram) tracin^( pattern. The problem is the Troponin T marker will only be evident in the blood 3 hours after the myocardial infarction. This delayed some important medical interventions which greatly improve the patient's diagnosis. Thi problem is solved by a new sensitive cardiac troponin assays and copeptin, a marker of endogenous stress, i^l combination with standard cardiac troponin. Both approaches seem to largely overcome the sensitivity deficit o current standard cardiac troponin. With the sensitive cardiac troponin assays, the time to detect the troponin T marks is greatly reduced to one hour. This is very significant because life saving measures can be iniated early. Both marke need to be presents in order to diagnosed myocardiakl infarction. Being an ICU nurse trainee before in a tertiary private hospital in Angeles City, the nurse researche encountered many patients suffered from myocardial infarction. This study is very essential in the sense that, i empowers the nurse to give appropriate nursing interventions in the prevention and management of patients havin^( myocardial infarction. This case study will serve as a tool to broaden up the knowledge of the researcher and all the people who are involve in this study. This study will also serve as a reference for the future researcher who will goin to indulge in the same topic. The researcher made this case study to meet the following objectives. Objectives Nurse Centered After the completion of the study, the nurse researcher will be able to: perform a comprehensive assessment of the patient with myocardial infarction. enumerate the signs and symptoms of myocardial infarction identify the diagnostic procedures that would help in the diagnosis of myocardial identify nursing problems utilizing the subjective cues and objective cues of myocardial infarction. perform appropriate therapeutic interventions for each of the formulated nursing diagnosis. evaluate the effectiveness of nursing care for myocardial infarction formulate conclusion based on findings and enumerate recommendations concerning myocardial infarction. Client Centered After the completion of the study, the client will be able to maintain functional health status and progress within client's own limit through the application of the nursing process. After the completion of the study, the client's significant others will be able to increase awareness on the different predisposing factors that can cause myocardial infarction, gain knowledge on the different signs and symptoms of myocardial infarction, gain knowledge on the course of myocardial infarction and will be able to state the importance of proper diet, activity in the prevention of heart problem specially myocardial infarction After the completion of the study, other patients who suffer from myocardial infarction and their significant other will be able to have increase knowledge on the course myocardial infarction, prevention and management. II. NURSING ASSESSMENT 1. PERSONAL DATA a. Demographic Data Mang Undoy is a 51-year-old male patient, a Filipino, and a member of the Catholic religion. He currently resides in Pulong Maragul, Angeles City. He was born on August 10, 1958 in Angeles City Pampanga. Mang Undo was admitted last October 07, 2009 at 3:00pm in a secondary hospital situated in Angeles City with the chief complaint of chest pain which is heavy, substernal, radiating to the left arm and unrelieved by rest. He was initiall diagnosed of to consider Acute Myocardial Infacrtion. He was discharged on October 16, 2009 with the fine diagnosis of Acute Myocardial Infacrtion. b. Socio - Economic and Cultural Factors Mang Undoy belongs to a nuclear family. He is married for 30 years with Aling Fujiwara and has 6 children Mang Undoy and his wife and 4 children live in a 3m x 4m shanty made from galvanized iron scraps and semi woods. The house has two windows (2ft by 2 ft) made from galvanized iron fastened by woods. Mang Undoy finished 2nd year high school. When he was 20 yrs old, he started working as a pig agent. Non he earns 50Phplpig sold with an average of 2000 php per week. He usually works from 8am till 9pm looking for pig t sell. The monthly breakdown of their expenses are as follows: water bill: Php 400, electric bill: Php 600, food: Ph 5,000. He smokes 1 pack of cigarette per day for 30 years now. He occasionally drinks alcohol about 5 bottles of bee per week 500mllbottle. The family believe in witchcraft and sorcery. His elder sister works as a fortune teller. They do consult to the alternative forms of medicines such as traditional healers (albularyo and manghihilot) if illnesses arises but also reso^l to the hospital to seek medical attention and assistance as necessary. The family uses common herbal plants sucl as vitex negundo (lagundi) for fever through decoction preparation (3-51eaves), and sidium guava (bayabas) fo cleaning wounds, decoction preparation as well (3-5 leaves). The family also uses over the counter (OTC) drugs to manage common illness like Paracetamol for fever, Loperamide for diarrhea, Robitusin for cough and coulds and Mefenamic acid for pain such as headache. The patient loves to eat fatty foods; his favorite food actually is ~bulalo~ and "chicharo~ He is also love drinking coffee, usually 2-3cups of coffee within a day. He eats 2-3 times a day, usually large meals. He love! drinking siftdrinks as well about 500ml/day. As to the routine activities of daily living of the patient, his usual routine are the following. At about 6:00 am the patient wakes up, do morning care, and eat his breakfast. By 8:00, he will meet his other friend and start going house to house to find pigs that can be sold. At around 11:30am, he will go home and eat his lunch. By 12:00nn-3pm he would take a rest, watch t.v. or take a nap. reading newspapers, and listening to radio and take his lunch z around 12:00-1:00pm. By 3:30pm the patient resumes roaming around until 9pm. And at around 10pm, the patient retires from the whole day's activities and usually wakes up at around 6am in the morning. As to the urinar elimination and bowel elimination of the patient, he usually urinates 5-6 times within a day and defecates 1-2 times; day. The patient lives in community which he described as polluted. Houses are not properly spaced and people usually dump their trashes almost anywhere. 2. FAMILY - HEALTH ILLNESS HISTORY (Refer to schematic diagram below) Mang Undoy belongs to a nuclear type of family wherein he lives with his wife and six children. The patien has no information on the medical history of their grandparents on both sides. His father died from heart attack hi mother has a DM and died from the complications. They all have diabetes meliitus and his 3 older brothers and sister died also from complications of DM AMI/DM 54y/o 51y/o 49y/o 48 y/o yo yo yo 3. HISTORY OF PAST ILLNESS When the patient was young, he suffered from occasional cough and cot, measles, mumps and fever. At the age of 27 (1985), he was diagnosed of having DM II and was prescribed oral medications. At the age of 47 (2005), hi had ameobiasis and was prescribed metronidazole 500mg capsules twice a day for 7 days. 4. History of Present illness January-August 2009: Patient experienced chest pain which is bearable and can be relieved by rest. He also experienced occasional headaches and difficulty of breathing. He never sought professional advices for these symptoms because he usually manages them with paracetamol for headache and rest for the other symptoms. October 7, 2009: at about 10:00 am, while the patient is drinking a glass of water inside their house, hi suddenly experienced ch~stpain. He rested for a while and after about 6 minutes the pain disappeared. At 2:00 pm while the patient is watching t.v. the chest pain recurred, the patient felt weird because he has not done anything tha usually provoke the(~ccg*nce of the pain. He became so worried because after 10 minutes of resting and nc moving at all the pain did not disappear. After 20 minutes, the pain became worst. He described the pain as Shari stabbing pain. He felt the pain becoming worst and radiating to his left amn. He had also difficulty of breathing. Hi quickly called the attention of his wife and together with his sister living nearby went to a secondary public hospital ir Angeles City. He was admitted at 3:00 pm with primary diagnosis of to consider acute myocardial infarction. 5. PHYSICAL EXAMINATION Day 1: Upon Admission (Intensive Care Unit): October 07, 2009 at 3:00pm (Lifted from the chart) Vital signs: BP: 140/100mmHg Temp: 37.5°C/axilla P R: 109bpm R R: 38bpm 02 Sat: 97% General Survey: Patient is conscious and coherent, appears weak and with guarded behaviours. Review of System: HEENT: anicteric sclerae, pale palpebral conjunctive. Chest/Lungs: Symmetrical chest expansion SCE, (-) retractions, (+1 basal rales (BLF),with orthopnea when in low fowlers position, difficulty of breathing, use of accessory muscles in breathing, chest pain scale of 10/10. Abdomen: flabby, normal abdominal bowel sounds, soft (-) abdominal pain Genitourinary: (-)dysuria, (-) changes in bowel movement. Extremities: - cyanosis, full and equal peripheral pulses Neurological: Glasgow Coma Scale (GCS) 15 Day 1 :(lntensive Care Unit): October 07, 2009 Nurses Notes (Lifted from the chart) Vital signs: BP: 140/100mmHg Temp: 36.5°C/axilla P R: 109bpm R R: 36bpm 02 Sat: 97% The patient appears weak; guarded behaviours noted; pale paipebral conjunctive; bibasal rales noted; wit orthopnea when in low fowlers position; difficulty of breathing; use of accessory muscles in breathing; coughing; chef pain scale of 10/10; Glasgow Coma Scale (GCS) 15 Day 2 :(lntensive Care Unit): October 08, 2009 Vital signs: BP: 140/100mmHg Temp: 36.9°C/axilla P R: 106bpm R R: 38bpm 02 Sat: 98% The patient appears weak; guarded behaviours noted; pale palpebral conjunctive; bibasal tales noted; Ate orthopnea when in low fowlers position; difficulty of breathing; use of accessory muscles in breathing; coughing; chest pain scale of 6/10; Glasgow Coma Scale (GCS) 15 Day 3 :(lntensive Care Unit): October 09, 2009 Vital signs: BP: 130/100mmHg Temp: 38.1°C/axilla P R: 107bpm R R: 34bpm 02 Sat: 97% General Survey: The patient was wearing white t-shirt and shorts and was sited on the bed. He appears weak wit easy fatigability at times as noted during the interview (pauses at times during conversation) but oriented a to time, place, name and person. a. Skin: Has brown complexion, no lesions, cysts or nodules and edema noted. He has good skin turgor. b. Head/Scalp: Hair is thin, curly and short with some white hairs generally black in color equally distribute upon inspection. No pediculosis, dandruff, scratches, lesions, swelling or depressions. No abnormal masses, cysts, nodules and pain felt upon palpation of scalp. c. Eyes: Eyebrows and eyelashes are black in color, thin and evenly distributed, anicteric sclera and pal, palpebral conjunctive noted. Pupils are equally round and reactive to light and accommodation. The eye are able to move in cardinal directions and with (+) blinking reflex. Upon palpation of the eyeballs, no pal is elicited. d. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was observed in the auditor canal upon inspection. Pain is not felt upon palpation of ears. e. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted.. Nasal septum is intac and at the midline. f. Mouth: With dark colored lips without cracks, dryness and smooth texture. Can purse lips, with teeth siightl yellow in color without dental caries. Gums are dark in color and tongue is pink and moist upon inspection Tonsils are not inflamed and uvula is located at the midline under lighted penlight upon inspection. 9. Neck: Midline position, no deformities noted. With palpable carotid pulse, with minimal jugular distensio^l noted. There is no weakness noted on sternocleidomastoid as evidenced by head turning, neck flexior and extension. No abnormal mass, cysts, nodules noted upon neck muscle palpation. h. Chest and Lungs: With symmetrical chest expansion. No lesions and masses noted. Heart: Adynamic precordium and heart rate is of normal rate and rhythm. No murmurs or abnormal hear sounds heard upon auscultation such as S3 and S4 gallop. j. Abdomen: Has normal contour, flabby. No lesions, masses, cysts, nodules and deformities noted. Witl normal abdominal bowel sounds 10-15bowels sounds in all quadrants, no masses, cysts nodules ant tenderness noted upon palpation. k. Back and Spine: With normal curvature of the back and spinal column is straight. No report of pain upo introduction of direct hit to the costovertebral area. I. Upper and Lower Extremities: No clubbing of fingers and toes and cyanosis noted however. All joints both upper and lower extremities are within normal limits, pain free, passively and actively. Neurological Assessment: a. GCS Eye opening: 4 Verbal Response: Motor Response: Total: 15 b. Deep Tendon Reflex Finding: intact sense of smell CN II (Optic): Testing device: newspaper print Finding: The patient was able to read newspaper print at 14inches distance. CN 111 (Oculomotor): Testing device: pencil to track object in upward and downward movement Finding: The patient was able to track the object without difficulty. CN IV (Trochlear): Testing device: pencil to track object in diagonal movements Finding: The patient was able to track the object. CN V (Trigeminal): Testing device: food for chewing, cotton for blinking reflex and sensation for face Finding: The patient was able to chew, with blinking reflex and was able to feel light touch. CN Vi (Abducens): Testing device: pencil to track object in lateral eye movement Finding: The patient was able to track the object. CN Vll (Facial): Testing technique: ask the patient to do facial expression and use of vinegar, salt, sugar and coffee to assess for taste sensation Finding: The patient was able to smile, frown, grimace and pout. He was able to identify the different tastes. CN Vlll (Vestibulocochlear): Testing device: Whisper test; Watch tick test. Finding: The patient was able to repeat the whispered phrase and heard the watch ticking. CN IX (Glossopharyngeal): Testing device: food for swallowing Finding: The patient was able to swallow foods and fluids. CN X (Vagus): Testing device: tongue depressor Finding: The patient gagged after the introduction of tongue depressor to posterior third of the tongue. CN Xl (Accessory): Testing technique: ask the patient to do shoulder shrug. Finding: The patient was able to do shoulder shrug with muscle grade of 5/5. CN Xll (Hypoglossal): Testing technique: ask the patient to move tongue in all directions Finding: Patient was able to moved tongue in all directions. 2nd Nurse-Patient interaction (Medicine Ward) October 14, 2009 Vital signs: BP: 100/80mmHg Temp: 36.8°C/axilla PR: 88bpm RR: 20bpm 02 Sat: 97% General Survey: The patient was wearing white t-shirt and shorts and was sited on the bed. He appears weak witl easy fatigability at times as noted during the interview (pauses at times during conversation) but oriented a to time, place, name and person. m. Skin: Has brown complexion, no lesions, cysts or nodules and edema noted. He has good skin turgor. n. Head/Scalp: Hair is thin, curly and short with some white hairs generally black in color equally distributed upon inspection. No pediculosis, dandruff, scratches, lesions, swelling or depressions. No abnorm^E masses, cysts, nodules and pain felt upon palpation of scalp. o. Eyes: Eyebrows and eyelashes are black in color, thin and evenly distributed, anicteric sclera and pall palpebral conjunctive noted Pupils are equally round and reactive to light and accommodation. The eye are able to move in cardinal directions and with ~+) blinking reflex. Upon palpation of the eyeballs, no pail is elicited. p. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was observed in the auditor canal upon inspection. Pain is not felt upon palpation of ears. q. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted.. Nasal septum is intac and at the midline. r. Mouth: With dark colored lips without cracks, dryness and smooth texture. Can purse lips, with teeth slightly yellow in color without dental caries. Gums are dark in color and tongue is pink and moist upon inspectior Tonsils are not inflamed and uvula is located at the midline under lighted penlight upon inspection. s. Neck: Midline position, no deformities noted. With palpable carotid pulse, with minimal jugular distensio^l noted. There is no weakness noted on sternocleidomastoid as evidenced by head turning, neck flexior and extension. No abnormal mass, cysts, nodules noted upon neck muscle palpation. t. Chest and Lungs: With symmetrical chest expansion. No lesions and masses noted. u. Heart: Adynamic precordium and heart rate is of normal rate and rhythm. No murmurs or abnormal heal sounds heard upon auscultation such as S3 and S4 gallop. v. Abdomen: Has normal contour, flabby. No lesions, masses, cysts, nodules and deformities noted. Witl normal abdominal bowel sounds 10-15bowels sounds in all quadrants, no masses, cysts nodules and tenderness noted upon palpation. w. Back and Spine: With normal curvature of the back and spinal column is straight. No report of pain UpOI introduction of direct hit to the costovertebral area. x. Upper and Lower Extremities: No clubbing of fingers and toes and cyanosis noted however. All joints both upper and lower extremities are within normal limits, pain free, passively and actively. Neurological Assessment: c. GCS Eye opening: 4 Verbal Response: 5 Motor Response: 6 Total: 15 d. Deep Tendon Reflex Finding: intact sense of smell CN II (Optic): Testing device: newspaper print Finding: The patient was able to read newspaper print at 14inches distance.CN 111 (Oculomotor): Testing device: pencil to track object in upward and downward movement Finding: The patient was able to track the object without difficulty. CN IV (Trochlear): Testing device: pencil to track object in diagonal movements Finding: The patient was able to track the object.CN V (Trigeminal): Testing device: food for chewing, cotton for blinking reflex and sensation for face Finding: The patient was able to chew, with blinking reflex and was able to feel light touch. CN Vl (Abducens): Testing device: pencil to track object in lateral eye movement Finding: The patient was able to track the object.CN Vll (Facial): Testing technique: ask the patient to do facial expression and use of vinegar, salt, sugar and coffee to assess for taste sensation Finding: The patient was able to smile, frown, grimace and pout. He was able to identify the different tastes. CN Vlll (Vestibulocochlear): Testing device: Whisper test; Watch tick test.Finding: The patient was able to repeat the whispered phrase and heard the watch ticking. CN IX (Glossopharyngeal): Testing device: food for swallowing Finding: The patient was able to swallow foods and fluids. CN X (Vagus): Testing device: tongue depressorFinding: The patient gagged after the introduction of tongue depressor to posterior third of the tongue. CN Xl (Accessory): Testing technique: ask the patient to do shoulder shrug. Finding: The patient was able to do shoulder shrug with muscle grade of 515.CN Xll (Hypoglossal): Testing technique: ask the patient to move tongue in all directions Finding: Patient was able to moved tongue in all directions. 3rd Nurse-Patient interaction (Medicine Ward) October 14, 2009 Vital signs: BP: 100/80mmHg Temp: 36.7°C/axilla PR: 89bpm RR: 22bpm 02 Sat: 98% General Survey: The patient was wearing white t-shirt and shorts and was sited on the bed. He appears weak witl easy fatigability at times as noted during the interview (pauses at times during conversation) but oriented a! to time, place, name and person. a. Skin: Has brown complexion, no lesions, cysts or nodules and edema noted. He has good skin turgor. b. Head/Scalp: Hair is thin, curly and short with some white hairs generally black in color equally distribute upon inspection. No pediculosis, dandruff, scratches, lesions, swelling or depressions. No abnorrna masses, cysts, nodules and pain felt upon palpation of scalp. c. Eyes: Eyebrows and eyelashes are black in color, thin and evenly distributed, anicteric sclera and pall palpebral conjunctive noted. Pupils are equally round and reactive to light and accommodation. The eye! are able to move in cardinal directions and with (+) blinking reflex. Upon palpation of the eyeballs, no pail is elicited. d. Ears: Symmetrical and no abnormal discharges noted. No excess cerumen was observed in the auditor canal upon inspection. Pain is not felt upon palpation of ears. e. Nose: No nasal deviation. No nasal discharges, deformities and obstruction noted.. Nasal septum is intac and at the midline. f. Mouth: With dark colored lips without cracks, dryness and smooth texture. Can purse lips, with teetl slightly yellow in color without dental caries. Gums are dark in color and tongue is pink and moist upon inspection. Tonsils are not inflamed and uvula is located at the midline under lighted penlight UpOI inspection. g. Neck: Midline position, no deformities noted. With palpable carotid pulse, with minimal jugular distension noted. There is no weakness noted on sternocleidomastoid as evidenced by head turning, neck flexio~ and extension. No abnormal mass, cysts, nodules noted upon neck muscle palpation. h. Chest and Lungs: With symmetrical chest expansion. No lesions and masses noted. i. Heart: Adynamic precordium and heart rate is of normal rate and rhythm. No murmurs or abnormal hear j. Abdomen: Has normal contour, flabby. No lesions, masses, cysts, nodules and deformities noted. With normal abdominal bowel sounds 10-15bowels sounds in all quadrants, no masses, cysts nodules and tenderness noted upon palpation. k. Back and Spine: With normal curvature of the back and spinal column is straight. No report of pain upon introduction of direct hit to the costovertebral area 1. Upper and Lower Extremities: No clubbing of fingers and toes and cyanosis noted however. All jolts of both upper and lower extremities are within normal limits, pain free, passively and actively Neurological Assessment: m. GCS Eye opening: 4 Verbal Response: Motor Response: Total: 15 n. Deep Tendon Reflex Finding: Intact sense of smell CN 11 Optic): Testing device: newspaper print Finding: The patient was able to read newspaper print at Winches distance. CN 111 (Oculomotor): Testing device: pencil to track object in upward and downward movement Finding: The patient was able to track the object without difF culty. CN IV (Trochlear) Testing device: pencil to track object in diagonal movements Finding: The patient was able to track the object. CN V (Trigeminal): Testing device: food for chewing, cotton for blinking reflex and sensation for face Finding: The patient was able to chew, with blinking reflex and was able to feel light touch. CN Vl (Abducens): Testing device: pencil to track object in lateral eye movement Finding: The patient was able to track the object. CN Vll (Facial): Testing technique: ask the patient to do facial expression and use of vinegar, salt, sugar and coffee to assess for taste sensation Finding: The patient was able to smile frown, grimace and pout. He was able to identify the different tastes. CN Vlll (Vestibulocochlear): Testing device: Whisper test; Watch tick test. Finding: The patient was able to repeat the whispered phrase and heard the watch ticking. CN IX (Glossopharyngeal): Testing device: food for swallowing Finding: The patient was able to swallow foods and fluids. CN X (Various): Testing device: tongue depressor Finding: The patient gagged after the introduction of tongue depressor to posterior third of the tongue. CN Xl (Accessory): Testing technique: ask the patient to do shoulder shrug. Finding: The patient was able to do shoulder shrug with muscle grade of 515. CN Xll (Hypoglossal): Testing technique: ask the patient to move tongue in all directions Finding: Patient was able to moved tongue in all directions. 6. DIAGNOSTICS AND LABORATORY FlNDlNGS 1 . Complete Blood Cou nt (CBC) DIAGNOSTIC/ DATE ORDERED(DO) INDICATION/PURPOSE RESULTS NORMAL ANALSYS AND LABORATORY DATE DONE (DD) VALUES INTERPRETATION PROCEDURE DATE RESULTS IN (DRI) OF RESULTS Complete Blood NDICATION/S OR Count PURPOSE' It is an important screening t that includes RBC cot hemoglobin, hematocrit, R indices, with or without differen count and platelet count. Hemoglobin DO: 10-07-09 Total hemoglobin 143g/L 140-180g/L The result is within DD: 10-07-09 measures amount of normal values, hemoglobin present a which indicates that DO: 10-11-09 deciliter (dL or 100mL) 143g/L there is adequate DD: 10-11-09 of wh blood. It is oxygen carrying indicated for the pati to capacity of help evaluate iron status erythrocytes to be c oxygen carrying delivered to the capacity of R B I different parts of the body. Hematocrit DO: 10-07-09 It measures the 0.40 0.40-0.54 The result is within DD: 10-07-09 percentage volume of normal values, packed red blood Cal in which indicates that DO: 10-11-09 a whole blood sample 0.40 there is adequate DD: 10-11-09 determine the oxygen carrying percentage RBC's in the capacity of plasma. It indicated for erythrocytes to be the patient to h evaluate delivered to the iron status and ^O^Xy^s different parts of carrying capacity of the body. This RBC z hydration status could mean also of the patient. that there is no alteration of hydration status. Leukocytes DO: 10-07-09 The leukocytes count 8x109/L 5-10x109/L The result is within DD: 10-07-09 measu the number of normal values, WBC's in a cu millimeter which indicates that of blood. It is indical for there is no the patient to detect and presence of evaluate presence of infection as infection and or evidenced by no inflammation and tissue signs and necrosis. symptoms of infections such as fever and chills. Lymphocytes DO: 10-07-09 Lymphocytes produces 0.42 0.22-0.37 The result is above DD: 10-07-09 antibodies responsible the normal values, for allergic reaction. which means that Monocytes have there is phagocytic actions by inflammation removing dead and since myocardial injured cells, cell cells are denied of fragments and adequate 02 and microorganisms. It was nutrients leading to indicated for the patient hypoxemic to determine degree of damage causing inflammation. cellular death and tissue necrosis, part of the mechanism is inflammatory response. Lymphocytes, monocytes and count are within normal values. Nursing Responsibilities: Before: Tell the patient that the test requires a blood sample. Explain who will perform the yenipuncture and when. Explain to the patient that he may feel discomfort from the tourniquet and needle puncture. Instruct the patient need no to restrict food and fluids During: Handle the sample gently to prevent hemolysis. Send sample to the laboratory immediately. After: Apply direct pressure to the venipuncture site until bleeding stops. DIAGNOSTIC/ DATE INDICATION/PURPOSE RESULTS NORMAL ANALSYS AND LABORATORY ORDERED(DO) VALUES INTERPRETATION PROCEDURE DATE DONE (DD) OF RESULTS DATE RESULTS IN (DRI) Creatinine DO: 10-07-09 A routinary exam done 0.9 0.4-1.4 The result is within DD: 10-07-09 upon admission to assess the normal values, glomerular filtration and to which indicates that screen for renal damage. the kidneys are Serum creatinine levels functioning well and provide a more sensitive there is no apparent measure of renal damage evidence of than do blood urea inadequate renal nitrogen. It has also a perfusion. direct measurement of glomerular filtration rate. Creatinine is excreted entirely by the kidneys and therefore is directly proportional to renal excretory function. It is indicated to the patient to evaluate if there is renal dysfunction already in which a large number of nephrons have been destroyed due to inadequate renal perfusion secondary to decreased cardiac output as brought about by decreased contractility of the heart due to infarction. It measures serum of sodium in relation to amount of water in the body, it reflects water balance. It is lso useful to evaluate fluid, electrolyte, Sodium DO: 10-07-09 ~ hypernatremiat 140.8 mmol/L 135-150 mmol/L The result is within DD: 10-07-09 hyponatremia) and acid- normal range base balance and related which~ii~ the renal and adrenal patient does not functions. have sodium excess or This is indicated to the depletion, more so, patient to determine if no further evidence there is water, electrolyte of acidbase and acid-base balance imbalances as well since the patient is as signs and suffering from pulmonary symptoms of congestion. hyponatremia neither It measures serum levels hypernatremia of potassium, a major Potassium DO: 10-07-09 intracellular cation that 4.2 mmol/L 3,50-5.5mmol/L The result is within DD: 10-07-09 helps maintain cellular normal limits, osmotic equilibrium; which indicates regulates muscles activity, absence of and aci-base; influences electrolyte renal function imbalance. This also suggests that It is indicated to the the kidneys are patient since with functioning myocardial infarction, the properly. The necrotic cells become patient didn't electrically inactive and experience their membranes become arrhythmias/ disrupted, such that their intracellular contents, dysrhythmias within including potassium, are period of released into the hospitalization. surrounding extracellular fluid. This causes local areas of hyperkalemia, which can affect the resting membrane potentials of functioning myocardial cells which may cause arrhythmias/dysrhythmias. Nursing Responsibilities: Before: Explain to the patient that the serum creatinine test evaluates kidney function. Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when Explain to the patient that he may feel discomfort from the tourniquet and needle puncture. · Instruct the patient need no to restrict food and fluids During: Handle the sample gently to prevent hemolysis. Send sample to the laboratory immediately. After: After: Apply direct pressure to the venipuncture site until bleeding stops. 3. Lipid Profile DATE ORDERED(DO); DIAGNOSTIC/ ANALYSIS AND DATE DONE INDICATION/S OR NORMAL LABORATORY RESULTS INTERPRETATION OF (DD); DATE PURPOSES VALUES PROCEDURE RESULTS RESULTS IN (DRI) Lipid Profile Lipid profile measures the circulating levels of free cholesterol and cholesterol esters; it reflects the level of the two forms in which this biochemical compound in the body. It is indicated to the patient to assess the risk for Coronary Artery Diasease (CAD) and to A. Cholesterol DO: 10-07-09 5.8 (Increased) Less than The result is above the screen for hyperlipidemia. DD: 10-07-09 5.18 mmol/L normal range. Increased Cholesterol, a sterol cholesterol level could found in animal tissue, lead to development of circulates in the blood in atheroma. Once there is combination with endothelial injury excess triglycerides and protein- fats and cholesterol bound phospholipids. could assimilate at the This complex is called a injured site together with lipoprotein. monocytes, macrophages and To assess the risk of platelets forming foam Coronary Artery Disease cells. Foam cells (CAD) and evaluation of engulfed the lipids and fat metabolism smooth muscle cells developed. Consequently, these smooth muscle cells reproduce themselves and synthesize the connective tissues while they subsequently proliferate (intimal proliferation) making the intima thick, thus, plaque formation/atheroma Less than 1.26 mmol/L developed which increases the risk of B. Triglycerides DO: 10-07-09 1.54(Increased) developing MI. DD: 10-07-09 Serum triglycerides The result exceeds the provides quantitative normal limits. Increased analysis of triglycerides, triglycerides level could the main storage form of initiate development of lipids, which constitute atheroma. Injury to the about 95% of fatty tissue. blood vessel cause Indicated to patient to attraction of excess fats screen for hyperlipidemia and cholesterol, and to assess Coronary macrophages, Artery Disease. monocytes and platelets leading to foam cells development that is responsible for atherogenesis posing the risk of MI to occur. 29 >35mmol/L HDL is responsible for DO: 10-07-09 The result is normal, that C. High Density “reverse cholesterol DD: 10-07-09 means, at any rate, the Lipoprotein (HDL) transport,” which return HDL could participate in excess cholesterol from endothelial repair and the tissues to the liver decreases formation of metabolism. It also thrombosis. More so, participates in endothelial within normal levels or repair and decreases more importantly high thrombosis. levels of HDL maybe more protective for the It is indicated to development of patient to screen for atherosclerosis than low hyperlipedemia and to levels of HDL. assess Coronary Artery Disease. LDL is responsible for The result is above the DO: 10-07-09 5.67 2.10 – 4.90 D. Low Density the delivery of cholesterol normal range. This DD: 10-07-09 (Increased) mmol/L Lipoprotein (LDL) to the tissues. Serum signifies that an level of LDL are normally increased serum controlled by hepatic concentration of LDL is a receptors for LDL that strong indicator of bind LDL and limit liver coronary risk. LDL synthesis of this particles are the most lipoprotein. atherogenic since they play a role in endothelial It is indicated to injury, inflammation, and patient to screen for immune responses that hyperlipedemia and to have been identified as assess Coronary Artery being important in Disease. atherogenesis. More so, when an excess of LDL is produced, LDL particles adhere to vulnerable points in arterial endothelium. Here macrophages ingest them, leading to formation of foam cells and the beginning of plaque formation. In addition, elevated levels of LDL combined with low levels of HDL increase the risk for MI. Nursing Responsibilities: Before: Explain to the patient the purpose of the procedure. Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when. Explain to the patient that he/she may experience slight discomfort from the tourniquet and needle puncture. Instruct patient to fast for 12 to 14 hours before the test. Notify the laboratory and physician of medications the patient is taking that may affect test results; it may be necessary to restrict them. During: Perform a venipuncture and collect the sample in a 5 ml clot-activator tube. Send the sample to the laboratory immediately. Handle the sample gently to prevent hemolysis. Be aware that hemolysis caused by rough handling of the sample may influence test results. Be aware that hemolysis may elevate results. After: Apply direct pressure to the venipuncture site until bleeding stop 4. Fasting Blood Sugar (FBS) DATE ORDERED(DO) DIAGNOSTIC/ ; DATE DONE INDICATION/S OR NORMAL ANALYSIS AND INTERPRETATION OF LABORATORY RESULTS (DD); DATE PURPOSES VALUES RESULTS PROCEDURE RESULTS IN (DRI) Glucose (FBS) DO: 10-07-09 The fasting 6.81 4.20 – The result is above the normal range. DD: 10-07-09 blood sugar or (Increased) 6.40 Imbalance between coronary supply and fasting plasma mmol/L myocardial demand secondary to coronary glucose test is used occlusion will lead to myocardial O2 deficit to measure plasma which causes myocardial damage-death and glucose levels after necrosis. The myocardial cells significantly a 12-to 14hour fast. release catecholamines and norepinephrine. Catecholamines mediate the release of This is indicated glycogen, glucose, and stored fat from body to patient to screen cells. Therefore, plasma concentrations of free for diabetes fatty acids and glycerol rise within 1 hour after mellitus, in which onset of acute myocardial infarction. In absence or addition, norepinephrine elevates blood sugar deficiency of insulin levels through stimulation of liver and skeletal allows persistently muscle cells. It also suppresses pancreatic B high glucose levels. cell activity which reduces insulin secretion and elevates blood glucose further. Not surprisingly, hyperglycemia is noted approximately 72 hours after an acute myocardial infarction. In the case of the patient, increased glucose was noted on the 2nd day of hospitalization (05-07-08). Nursing Responsibilities: Before: Explain to the patient that this test detects disorders of the glucose metabolism and aids in the diagnosis of diabetes. Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when. Explain to the patient that he may experience slight discomfort from the tourniquet and needle puncture. Instruct to the patient to fast for 12 hours to 14 hours before the test. Notify the laboratory and physician of medications the patient is taking that may affect test results; it may be necessary to restrict them. During: Assist in performing a venipuncture and collect the sample in a 5 ml clot-activator tube. Send the sample to the laboratory immediately. After: Apply direct pressure to the venipuncture site until bleeding stops. Provide a balanced meal or snack. Instruct the patient that he may resume his usual medications that were stopped before the test. 5. Troponin (Cardiac T) DATE DIAGNOSTIC/ ORDERED(DO); ANALYSIS AND INDICATION/S OR NORMAL LABORATORY DATE DONE (DD); RESULTS INTERPRETATION PURPOSES VALUES PROCEDURE DATE RESULTS OF RESULTS IN (DRI) Troponin (Cardiac DO: 10-07-09 The cardiac Troponin T is a Positive negative The resultis positive, T) DD: 10-07-09 protein in striated is extremely though there is specific cardiac damage evident increase of markers that is released into Creatinine Kinase the bloodstream after an injury. Myocardial Muscles Elevation in Troponin T level (CKMB), troponin T can be seen within 1 hour of on the other hand is myocardial infarction (MI) and on its normal limits. will persist for 1 week or longer. This signifies that there is no significant It is indicated to the patient reinfarction event that to detect and diagnose acute happened since myocardial infarction and troponin assays reinfarction. (Troponin I and Troponin T) are more capable of detecting episodes of myocardial reinfarction. They rises more slowly than myoglobin and maybe useful for diagnosis of reinfarction, even up to 3 to 4 days. Nursing Responsibilities: Before: Explain to the patient that this test helps assess myocardial injury and that multiple samples may be drawn to detect fluctuations in serum levels. Tell the patient that the test requires a blood sample. Explain who will perform the venipuncture and when. Inform the patient that he need not restrict food and fluids, and instruct him to maintain his prescribed medications and diet regimen. Explain to the patient that he may experience slight discomfort from the tourniquet and the needle puncture. During: Perform a venipuncture and collect the specimen in a 7-ml clot-activator tube. Obtain each specimen on schedule and note the date and collection time one each. After: Apply direct pressure to venipuncture site until bleeding stops. 6. Chest X-ray (Sitting) DATE ORDERED(DO); DIAGNOSTIC/ ANALYSIS AND DATE DONE INDICATION/S NORMAL LABORATORY RESULTS INTERPRETATION OF (DD); DATE OR PURPOSES VALUES PROCEDURE RESULTS RESULTS IN (DRI) Chest X-ray AP DO: 10-07-09 To detect the 1.Atherosclerotic Chest films show There is (Sitting) DD: 10-07-09 status of aorta. the bony atherogenesis at the respiratory structures (ribs, aorta since the patient system. A chest x- 2. Cardiomegaly sternum, has increased ray can be used to with left ventricular clavicles, cholesterol level, wherein define prominence. scapulae and excess lipids could abnormalities of upper portion of accumulate within the the lungs such as 3. Pulmonary the humerus). vessel wall and coalesce excessive fluid, congestion. The vertebral into a pool called the lipid pneumonia, column is visible core to form bronchitis, asthma, vertically through atherosclerotic plaque. cysts, and cancers the middle of the Furthermore, as well as exact thorax. The two cardiomegaly with left location and size hemidiaphragms ventricular prominence of the organs such normally appear occurred since the as heart. rounded, smooth patient had infarction, it and sharply loses its contractility at It is indicated to defined; the right some degree because of the patient to hemidiaphragm is lack of response to determine and slightly higher electrical impulses, evaluate if there than the left. The eventually the heart work is/are junction of the rib hard to meet the complication(s) cage and the demand, it will enlarge brought about by diaphragm called significantly (hypertrophy myocardial the costophrenic of the heart) as well as infarction. angle, is normally thickening of the clearly visible and ventricles as a angled. Heart compensatory tissue is dense mechanism. Moreso, and appears cardiac tissue white but less surrounding the area of intensely white infarction also undergoes than bone. changes such as Normally the myocardial remodeling, a heart shadow is process mediated by clearly outlined, angiotensin II, extends primarily aldosterone, on to the left side catecholamines, of the thorax, and adenosine, and occupies no more inflammatory cytokines than one third of which causes the chest width. hypertrophy of the Close observation myocardial cells and shows the sustained activation of trachea in the neurohormonal upper middle compensatory chest almost mechanism which superimposed eventually increases wall above the cervical stress in the ventricle and thoracic and thus to reduce wall vertebra. The stress, the myocardial trachea bifurcates cells hypertrophy at the level of the (Laplace’s Law). On the fourth thoracic other hand, pulmonary vertebra into the congestion developed, left mainstem since there is bronchi. The cardiomegaly imparing pulmonary blood cardiac pumping leading vessels, bronchi, to decreased cardiac lymph nodes are output. In return, left located in the ventricular hypertrophy hilum on both the occurred as a right and left compensatory sides of the mid- mechanism. The right thorax. Lung side of the heart tissue appears continuously propel black on x-ray blood to the lungs, film. Vascular thereby, the left ventricle lung structures is unable to fully eject the are visible as returning blood to white, thin, wispy systemic circulation strings fanning leading to congestion. out from the hilum. Nursing Responsibilities: Before: Make sure the patient has signed an appropriate consent form. Explain that the patient will be asked to a deep breath and hold it momentarily during the X-ray. Explain that the test takes less than 5 minutes. During: The patient is instructed to sit in front of a stationary radiography machine. Post-anterior and left lateral views are obtained. After: Check that no tubes have been dislodged during positioning. Whenever possible, place a lead apron over the patient’s abdomen to protect from exposure to radiation. To avoid radiation exposure, leave the area or wear lead shielding while the films are being taken. 7. Twelve (12) Lead Electrocardiogram (ECG) DIAGNOSTIC/ DATE INDICATION/S OR NORMAL ANALYSIS AND RESULTS LABORATORY ORDERED(DO); PURPOSES VALUES INTERPRETATION PROCEDURE DATE DONE (DD); OF RESULTS DATE RESULTS IN (DRI) Twelve (12) Lead DO: 10-07-09 To determine any ST-segment ST segment is Electrocardiogram DD: 10-07-09 abnormal pumping elevation elevated since there (ECG) action of the heart is alteration and Rate: A: 90/min and to indicate Rate: delay of V: 90/min presence of A:60100/min repolarization and arrythmias V:60-100/min depolarization properties of the P: 0.08 P: heart due to less than 0.11 impairement or even sec. lack of response to P-R: 0.20 P-R: electrical impulses 0.12 to 0.20 sec. secondary to QT:0.36 QT: prolonged up to 0.42 sec. ischemia/infarction of QRS: 0.06 QRS: the myocardial cells 0.04-0.11 including all the layers of the heart. It also signifies that the area of infarction extends to the zone of injury which is significantly developed, wherein ischemic tissues produces an elevation in the ST segment. More so, there is prolonged period of decreased blood supply to the heart causing an infarction. Nursing Responsibilities: Before: Check doctor’s order. Verify patient’s name in the chart with the actual patient. Explain that the procedure is done to detect abnormalities in the electrical activity of the heart. Reassure the client that he will not receive any electrical shock or impulses. Remove any metal object from the patient (e.g. belt buckle, coins, zipper). During: Provide privacy to the patient. Secure electrodes to appropriate locations on chest and extremities. Instruct the patient to remain still during the procedure. After: Secure results. Write the patient’s name, age and diagnosis in the result and attach it to his chart. Document the time and the procedure done. Refer results to the physician. ANATOMY AND PHYSIOLOGY OF THE HEART AND BLOOD VESSEL SIZE, FORM, and LOCATION of the HEART The adult heart is shaped like a blunt cone is approximately the size of a closed fist. Its larger in physcically active adults than in less active but otherwise healthy adults, and it generally decreases in size after approximately age 65, especially in those who are not physically active. The blunt, rounded point of the cone is the apex: and the larger; flat part at the opposite end of the cone is the base. Figure 1. Location of the Heart in the Thorax The heart is located in the thoracic cavity between the two pleural cavities, which surround the lungs. The heart, trachea, esophagus, and associated structures from a midline partition the mediastinum (see figure 1). The heart is surrounded by its own cavity, the pericardial cavity. The heart lies obliquely in the mediastinum, with its base directed posteriorly and slightly superiorly and the apex directed anteriorly and slightly inferiorly. The apex is also directed to the left so that approximately two-thirds of the heart’s mass lies to the left of the midline sternum. (see figure 1.). The base of the heart is located deep to the sternum and extends to the second intercostals space. The apex is located deep to the left fifth intercostals space, approximately 7-9centimeters (cm) to the left of the sternum near the midclavicular line, which is perpendicular line that extends down from the midline of the clavicle (see figure 1.). ANATOMY OF THE HEART The heart is surrounded by the pericardial cavity. The pericardial cavity is formed by the pericardium, or pericardial sac, which surrounds the heart and anchors it within the mediastinum (see figures 1 and 2). The pericardium consists of two layers. The tough, fibrous connective tissue outer layer is called the fibrous pericardium and the inner layer of flat epithelial cells, with a thin layer of connective tissue, is called the serous pericardium. The portion of the serous pericardium lining the fibrous pericardium is the parietal pericardium, whereas the portion covering the heart surface is the visceral pericardium, or epicardium. The parietal and visceral pericardium are continuous with each other where the great vessels enter or leave the heart. The pericardial cavity, located between the visceral and parietal pericardia, is filled with a thin layer of pericardial fluid produced by the serous pericardium. The pericardial fluid helps reduce friction as the heart moves within the pericardial sac. EXTERNAL ANATOMY The right and left atria are locate at the base of the heart, and the right and left ventricles extend from the base of the heart toward the apex (figure 3). A coronary sulcus extends around the heart, separating the atria from the ventricles. In addition, two grooves, or sulci, which indicate the division between the right and left ventricles, extend inferiorly from the coronary sulcus. The anterior interventricular suclus extends inferiorly from the coronary sulcus. The anterior interventricular sulcus extends inferiorly from the coronary sulcus on the anterior surface of the heart, and the posterior interventricular sulcus extends inferiorly from the coronary sulcus on the posterior surface of the heart (see figure 3). Figure 3. Anterior and Posterior Surface View of the Heart Six large veins carry blood to the heart (see figure 3); the superior vena cava and inferior vena cava carry blood from the body to the right atrium, and four pulmonary veins carry blood from the lungs to the left atrium. Two arteries, the pulmonary trunk and the aorta, exit the heart. The pulmonary trunk, arising from the right ventricle, splits into the right and left pulmonary arteries, which carry blood to the lungs. The aorta, arising from the left ventricle, carries blood to the rest of the body. Blood Supply to the Heart Coronary Arteries Cardiac muscle in the wall of the heart is thick and metabolically very active. Two coronary arteries supply blood to the wall of the heart (figure 5). The coronary arteries originate from the base of the aorta, just above the aortic semilunar valves. The left coronary artery originates on the left side of the aorta. It has three major branches: The anterior interventricular artery lies in the anterior interventricular sulcus, the circumflex artery extends around the coronary sulcus on the left to the posterior surface of the heart, and the left marginal artery extends inferiorly along the wall the lateral wall of the left ventricle from the circumflex artery. The branches of the left coronary artery supply much of the anterior wall of the heart and most of the left ventricle. The right coronary artery originates on the right side of the aorta. It extends around the coronary sulcus on the right to the posterior surface of the heart and give rise to the posterior interventricular artery, which lies in the posterior interventricular artery, which lies in the posterior interventricular sulcus. The right marginal artery extends inferiorly along the lateral wall of the right ventricle. The right coronary artery and its branches supply most of the wall of the right ventricle. Cardiac Veins The cardiac veins drain blood from the cardiac muscle. Their pathways are nearly parallel to the coronary arteries and most drain blood into the coronary sinus, a large vein located within the coronary sulcus on the posterior aspect of the heart. Blood flows from the coronary sinus into the right atrium (see figure 4). Some small cardiac veins drain directly into the right atrium. Heart Chambers and Internal Anatomy The heart is a muscular pump consisting of four chambers; two atria and two ventricles (figure 6). Right and Left Atria The right atria of the heart receive blood from veins. The atria function primarily as reservoirs; where blood returning from veins collects before it enters the ventricles. Contraction of the atria forces blood into the ventricles to complete ventricular filling. The right atrium receives blood through three major openings. The superior vena cava and the inferior vena cava drain blood from most of the body (see figure 6), and the smaller coronary sinus drains blood from most of the heart muscle. The left atrium receives blood through the four pulmonary veins (see figure 6), which drain blood from the lungs. The two atria are separated from each other by a partition called the interatrial (between the atria) septum. Right and Left Ventricles The ventricles of the heart are its major pumping chambers. They eject blood into the arteries and force it to flow though the circulatory system. The atria open into the ventricles, and each ventricle has one large outflow route located superiorly near the midline of the heart. The right ventricle pumps blood into the pulmonary trunk, and the left ventricle pumps blood into the aorta. The two ventricles are separated from each other by the muscular interventricular (between the ventricles) septum (see figure 6). The wall of the left ventricle is thicker than the wall of the right ventricle, and the wall of the left ventricle contracts more forcefully and generates a greater blood pressure than the wall of the right ventricle. When the left ventricle contracts, the pressure increases to approximately 120mmHg. When the right ventricle contracts, the pressure increases to approximately one-fifth of the pressure in the left ventricle. However, the left and right ventricles pump nearly the same volume of blood. The higher pressure generated by the left ventricle moves blood through the larger systemic circulation, whereas the lower pressure generated by the right ventricle moves blood through the smaller pulmonary circulation (see figure 6). Heart Valves The atrioventricular (AV) valves are located between the right atrium and the right ventricle and the left atrium and the left ventricle. The AV valve between the right atrium and the right ventricle has thee cusps and is called the tricuspid valve (see figure 7). The AV valve between the left atrium and left ventricle has two cusps and is called the bicuspid, or mitral valve (resembling a bishop’s miter, a two-pointed hat) valve (see figures 7). These valves allow blood to flow from the atria into the ventricles but prevent it from flowing back into the atria. When the ventricles relax, the higher the pressure in the atria forces the AV valves to open and blood flows from the atria into the ventricles (figure 7). In contrasts, when the ventricles contract, blood flows toward the atria and causes the AV valves to close (figure 7). Figure 7. Function of the Heart Valves Each ventricle contains cone-shaped muscular pillars called papillary muscles are attached by thin, strong connective tissue strings called chordae tendineae to the free margins of the cusps of the atrioventricular valves. When the ventricles contract, the papillary muscles contract and prevent the valves from opening into the atria by pulling on the chordae tendineae attached to the valve cusps (see figure 7). The aorta and pulmonary trunk posses aortic and pulmonary semilunar(halfmoon-shaped) valves, respectively (see figure 7). Each valve consists of three pocketlike semilunar cusps (see figure 7). When the ventricles relax, the pressure in the aorta is higher than in the ventricles and pulmonary trunk. Blood flows back from the aorta or pulmonary trunk toward the ventricles, and enters the pockets of the cusps, causing them to bulge toward and meet in the center of the aorta or pulmonary trunk, thus closing the vessels and blocking blood flow back into the ventricles (see figure 7). A plate of fibrous connective tissue, sometimes called the cardiac skeleton, consisting mainly of fibrous rings around the atrioventricular and semilunar valves, provides a solid support for the valves (see figure 7). This connective tissue plate also serves as electrical insulation between the atria and the ventricles and provides a rigid site of attachment for cardiac muscle. Route of Blood Flow Through the Heart The route of blood flow through the heart is depicted in figure 8. Even though blood flow through the heart is described for the right and then left side of the heart, it is important to understand that both atria contract at the same time, and both ventricles contract at the same time. This concept is most important when the electrical activity, pressure changes, and heart sounds are considered. Blood enters the right atrium from the systemic circulation through the superior and inferior vena cava, and from heart muscle through the superior and inferior vena cava, and from the heart muscle through the coronary sinus (see figure 8). Most of the blood flowing into the right atrium flows into the right ventricle while the right ventricle relaxes following the previous contraction. Before the end of ventricular relaxation, the right atrium contracts, and enough blood is pushed from the right atrium into the right ventricle to complete right ventricular filling. Figure 8: Blood Flow Through the Heart Following right atrial contraction, the right ventricle begins to contract. Contraction of the right ventricle pushes blood against the tricuspid valve, forcing it closed. After pressure within the right ventricles increases, the pulmonary semilunar valve is forced open, and blood flows into the pulmonary trunk. As the right ventricle relaxes, its pressure falls rapidly, and pressure in the pulmonary trunk becomes greater than in the right ventricle. The back-flow of blood forces the pulmonary semilunar valve to close. The pulmonary trunk branches to form the right and left pulmonary arteries, which carry blood to the lungs, where carbon dioxide is released and oxygen is picked up. Blood returning from the lungs enters the left atrium through the four pulmonary veins (see figure 8). Most of the blood flowing into the left atrium passes into the left ventricular while left ventricle relaxes following the previous contraction. Before the end of ventricular relaxation, the left atrium contracts, and enough blood is pushed from the left atrium into the left ventricle to complete left ventricular filling. Following left atrial contraction, the left ventricle begins to contract. Contraction of the left ventricle pushes blood against the bicuspid valve, forcing it closed. After pressure within the left ventricle increases, the aortic semilunar valve is forced open, and blood flows into the aorta (see figure 8). Blood flowing through the aorta is distributed to all parts of the body, except to that part of the lung supplied by the pulmonary blood vessels. As the left ventricle relaxes, its pressure falls rapidly, and pressure in the aorta becomes greater than in the left ventricle. The back-flow of blood forces the aortic semilunar valve to close. Histology of the Heart Heart Wall The heart wall is composed of three layers of tissue: the epicardium, the myocardium, and the endocardium (figure 9). The epicardium, is also called visceral epicardium, a thin serous membrane forming the smooth outer surface of the heart. It consists of simple squamous epithelium overlying a layer or loose connective tissue and fat. The thick middle layer of the heart, the myocardium, is composed of cardiac muscle cells and is responsible for the ability of the heart to contract. The smooth inner surface of the heart chambers is endocardium, which consists of simple squamous epithelium over a connective tissue. The endocardium allows blood to move easily through the heart. Each heart valve is formed by a fold of endocardium which connective tissue between two layers. The surfaces of the interior walls of the ventricles are modified by ridges and columns of cardiac muscle. Smaller muscular ridges are found in portions of the atria. Figure 9: Heart Wall Cardiac Muscle Cardiac muscles are elongated, branching cells that contain one, or occasionally two, centrally located nuclei (figure 10). The cardiac muscle cells contain actin and myosin myofilaments organized to form sacromeres, which are joined end-to-end to form myofibrils. The actin and myosin myofialments are responsible for muscle contraction, and their organization gives cardiac muscle a (branded) appearance. The striations are less regularly arranged and less numerous than is the case in skeletal muscle. Adenosine triphosphate (ATP) provides the energy for cardiac muscle contraction, and, as in other tissues, ATP production depends on oxygen availability. Cardiac muscle cells are rich in mitochondria, which produce ATP at a rate rapid enough to sustain the normal energy requirements of cardiac muscles. An extensive capillary network provides an adequate oxygen supply to cardiac muscle cells. Unlike skeletal muscle, however, cardiac muscle cannot develop a significant oxygen debt. Development of large oxygen debt could result in muscular fatigue and cessation of cardiac muscle contraction. Figure 10. Cardiac Muscle Cells Cardiac muscle cells are organized into spiral bundles or sheets. The cells are bound end-to-end and laterally adjacent cells by specialized cell-to-cell contracts called intercalated disks (see figure 10). The membranes of the intercalated disks are highly folded, and the adjacent cells fit together, greatly increasing contract between them. Specialized cell membrane structures in the intercalated disks called gap junctions reduce electrical resistance between cells, allowing action potentials to pass easily from one cell to adjacent cells. The cardiac muscle cells of the atria or ventricles, therefore, contract at nearly the same time. The highly coordinated contractions of heart depend on this characteristics. Electrical Activity of the Heart Action Potential in Cardiac Muscles Figure 11: Comparison of Action Potentials in Skeletal and Cardiac Muscle Like action potential muscle and neurons, those in cardiac muscle exhibit depolarization followed by repolarization of the resting membrane potential. In cardiac muscle, however, the plateau phase. Which is period of slow repolarization, greatly prolongs the action potential (see figure 11). In contrast to action potentials in skeletal muscle, which take less than 2 miliseconds (ms) to complete, action potentials in cardiac muscle take approximately 200 to 500 ms to complete. Unlike in skeletal muscle, action potentials in cardiac muscles are conducted from cell to cell. Not only does the action potential take longer, but the rate of conduction in cardiac muscle cells is slower than the rate of conduction of action potential in skeletal muscle cells and neurons. In cardiac muscle each potential consists of a rapid depolarization phase followed by a rapid, but partial early repolarization phase. Then a longer period of slow repolarization, called the plateau phase, occurs. At the end of the plateau phase, a more rapid final repolarization phase takes place. During the final repolarization phase the membrane potential returns to its resting level (see figure 11). Changes in membrane channels are responsible for the changes in the permeability of the cell membrane that produce action potentials. The depolarization phase of the action potential results from three permeability changes. Voltage-gated sodium channel open, increasing the permeability of the cell membrane to sodium. Sodium ions then diffuse into cell, causing depolarization. Voltage-gated potassium channels quickly close, decreasing the permeability of the cell membrane to potassium. The decreased diffusion of potassium out the cell also causes depolarization. Voltage-gated calcium channels slowly open, increasing the permeability of the cell membrane to calcium. Calcium ions then diffuse into cell and cause depolarization. It is not until the plateau phase that most of the voltage-gated calcium channels are opened. Early repolarization occurs when the voltage-gated sodium channels close and a small number of voltage-gated potassium channels open. Diffusion of sodium into cells stops, and there is some movement of potassium out of the cell. These changes in ion movement result in an early, but small repolarization. The plateau phase occurs as voltage-gated calcium channels continue to open, and the diffusion of calcium into the cell counteracts the potential change produced by the diffusion of potassium out of the cell. The plateau phase ends and final repolarization begins as the voltage-gated calcium channels close, and many voltage-gated potassium channels open. Diffusion of calcium into the cell decreases and diffusion of potassium out of the cells increases. These changes cause the membrane potential to return to resting level. Action potentials in cardiac muscle exhibit a refractory period, like that of action potentials in skeletal muscle and in neurons. The refractory period lasts about the same length of time as the prolonged action potential in cardiac muscle. The prolonged action potential and refractory period allow cardiac muscle to contract and almost complete relaxation to take place before another action potential can be produced. Also, the long refractory period in cardiac muscle prevents titanic contractions from occurring, thus ensuring a rhythm of contraction and relaxation for cardiac muscle. Therefore, action potentials in cardiac muscle are different from those in skeletal muscle because of the plateau phase, which makes the action potential and its refractory period last longer. The sinoartial (SA) node, which functions as the pacemaker of the heart, is located in the superior wall of the right atrium and initiates the contraction of the heart. The SA node is the pacemaker because it produces action potentials at a faster rate than other areas of the heart. The action potential of the SA node acts as a stimulus to adjacent areas of the heart. Also, the SA node action potentials have characteristics that are somewhat different from action potentials in the rest of the cardiac muscles. The SA node has a larger number of voltage- gated calcium channels than other areas of the heart. As soon as the resting membrane potential is reestablished after an action potential, some of the voltage-gated calcium channels open spontaneously. As they open, Calcium begin to diffuse into the cell and cause depolarization. The depolarization stiumulates additional voltage-gated calcium channels to open and voltage-gated sodium to open. Thus, additional calcium and sodium diffuse into the cell and cause further depolarization. Quickly, threshold is reached and another action potential is produced. Drugs called calcium channel blocking agents are used to treat some types of tachycardia (rapid heart rate) and arrhythmia (abnormal rhythm) because they block calcium channels and slow the rate of action potential production. Conduction System of the Heart Contraction of the atria and ventricles is coordinated by specialized cardiac muscles cells in the wall of the heart that form the conduction system of the heart (see figure 12). Action potentials originate in the SA node and spread over the right and left atria, causing them to contract. A second are of the heart, called atrioventricular (AV) node, is located in the lower portion of the right atrium. When action potentials reach the AV node, they spread slowly through it and then into a bundle of specialized cardiac muscle called the atrioventricular bundle. The slow rate of action potential conduction in the AV node allows the atria to complete their contraction before the action potentials are delivered to the ventricles. Figure 12: Conduction System of the Heart After action potentials pass through the AV node, they are transmitted though the AV bundle, which projects through the fibrous connective tissue plate that separates the atria from the atria from the ventricles (see figure 12). The AV bundle then divides into two branches of conducting tissue called the left and right bundle branches (see figure 12). At the tips of the left and right bundles branches, the conducting tissue forms many small of Purkinje fibers. The Purkinje fibers pass to the apex of the heart and then extend to the cardiac muscle of the ventricle walls. The AV bundle, the bundle branches and the Purkinje fibers are composed of specialized cardiac muscles fibers that conduct action potentials more rapidly than do other cardiac muscles fibers. Consequently, action potentials are rapidly delivered to all cardiac muscle of the ventricles. The coordinated contraction of the ventricles depends on the conduction of action potentials by the conduction system. Following their contraction, the ventricles begin to relax. After the ventricles have completely relaxed, another action potential originates in the SA node to begin the next cycle of contractions. The SA node is the pacemaker of the hart, but other cardiac muscle cells also are capable of producing action potentials spontaneously. For example, if the SA node is unable to function, another of the heart, such as the AV node, becomes the pacemaker. The resulting heart rate is much slower than normal. When action potentials originate in an area of the heart other than the SA node, the result is called an ectopic beat. The major events of the cardiac cycle are: 1. As systole begins, contraction of the ventricles pushes blood toward the atria, causing the AV valves to close. When the pressure in the ventricles exceeds the pressure in the pulmonary trunk and aorta, the seminulunar valves are forced open, and blood is ejected into the pulmonary trunk and aorta (see figure 14). 2. At the beginning of ventricular diastole, the pressure in the ventricules decreases. The semilunar valves close and prevent blood from flowing back into the ventricles. The pressure continues to decline in the ventricles until finally the AV valves open and blood flow directly from the atria into the relaxed ventricles. During the previous ventricular systole, the atria were relaxed and blood collected in them. When the ventricles relax and the AV valves open, blood flows into the ventricles (see figure 14, step 2) and fills them to approximately 70% of their volume. 3. At the end of ventricular diastole, the atria contract and then relax. Atrial systole forces additional blood to flow into the ventricles to complete their filling (see figure 14, step 3). The semilunar valves remain closed. Figure 15. Displays the interval the main events of the cardiac cycle in the graphic form and should be examined from the top to bottom for each period of the cardiac cycle. The ECG indicates the electrical events that cause contraction and relaxation of the atria and ventricles. The pressure graph shows the pressure changes within the left atrium, left ventricle, and aorta resulting from the atrial and ventricular contraction and relaxation. The pressure changes on the right side of the heart are not shown here, but are similar to those in the left side, only lower. The volume graph presents the changes in ventricular volume as blood flows into and out of the left ventricle as a result of the pressure changes. The sound graph records the closing of the valves caused by blood flow. See figure 14 for illustration of the valves and blood flow. Events Occurring During the Cardiac Cycle Heart Sounds A stethoscope was originally developed to listen to the sounds of the lungs and heart and is now used to listen to other sounds of the body. There are two main heart sounds. The first heart sound can be represented by the syllable lubb, and the second heart sound can be represented by dubb. The first heart sound has a lower pitch than the second. The first heart sound occurs at the beginning of ventricular systole and results from closure of the AV valves (see figure 14 step 1 and 15). The second heart sound occurs at the beginning of ventricular diastole and results from closure of the semilunar valves (see figure 14 step 2 and 15). The valves usually do not make sounds when they open. Clinically, ventricular systole occurs between the first and second heart sounds. Ventricular diastole occurs between the second heart sound and the first heart sound of the next beat. Abnormal heart sounds called murmurs are usually a result of faulty valves. For example, an incompetent valve fails to close tightly and blood leaks through the valve makes a swishing sound immediately after closure of the valve. For example, an incompetent bicuspid valve results in a swishing sound immediately after the first heart sound. When the opening of a valve is narrowed, or stenosed, a swishing sound precedes closure of the stenosed valve. For example, when the bicuspid valve is stenosed, a swishing sound precedes the first heart sound. Regulation of the Heart Function Cardiac Output (CO) is the volume of blood pumped by either ventricle of the heart each minute. Cardiac output can be calculated by multiplying the stroke volume times the heart rate. Stroke volume (SV) is the volume of blood pumped per ventricle each time the heart contracts, and the heart rate (HR) is the number of times the heart contracts each minute. CO = SV X HR (mL/min) (mL/beat) (beats/min) Under resting conditions, the heart rate is approximately 72 beats/min (or bpm) and the stroke volume is approximately 70 mL/beat. Consequently, the cardiac output is slightly more than 5 L/min: CO = SV X HR = 70 mL/beat X 72 bpm = 5040 mL/min (approximately 5 L/min) The heart rate and the stroke volume vary considerably among people. Athletes tend to have a larger stroke volume and lower heart rate at rest because exercise has increased the size of their hearts. Nonathletes are more likely to have a higher heart rate and lower stroke volume. During exercise the heart in a nonathelete can increase to 190 bpm and the stroke volume can increase to 115mL/beat. Therefore, the cardiac output increases to approximately 22 L/min: CO = SV X HR = 115 mL/beat X 190 bpm = 21,850 mL/min (approximately 22 L/min) This produces a cardiac output that is several times greater than the cardiac output under a resting conditions. Athletes can increase their cardiac output to a greater degree than nonathletes. The control mechanisms that modify the stroke volume and the heart rate are classified as intrinsic and extrinsic mechanisms. Intrinsic Regulation of the Heart Intrinsic regulation of the heart refers to the mechanisms contained within the heart itself. The force of contraction produced by cardiac muscle is related to the degree of stretch of cardiac muscle fibers. The amount of blood in the ventricles at the end of ventricular diastole determines the degree to which cardiac muscle fibers are stretched. Venous return is the amount of blood that returns to the heart, and the degree to which the ventricular walls are stretched at the end of diastole is called preload. If venous return increases, the heart fills to greater volume and stretches cardiac muscle fibers, producing and increased preload. In response to the increased preload, cardiac muscle fibers contract with a greater force. The greater force of contraction causes an increased volume of blood to be ejected from the heart, resulting in resulting in an increased stroke volume. As venous return increases, resulting in an increased preload, cardiac output increases. Conversely, if venous return decreases, resulting in a decreased preload, the cardiac output decreases. The relationship between preload and stroke volume is called Starling’s law of the heart. Because venous return is influenced by many conditions, Starling’s law of the heart has a major influence on cardiac output. For example, muscular activity during exercise caused increased venous return, resulting in an increased preload, stroke volume and cardiac output. This is beneficial because an increased cardiac output is needed during exercise to supply oxygen to exercising skeletal muscles. Afterload refers to the pressure against which the ventricles must pump blood. People suffering from hypertension have an increased afterload because they have an elevated aortic pressure during contraction of the ventricles. The heart must do more work to pump blood from the left ventricle into the aorta, which increases the workload on the heart and can eventually lead to heart failure. A reduced afterload decreases the work the heart must do. People who have a lower blood pressure have a reduced afterload and develop heart failure less often than people who have hypertension. The afterload, however, influences cardiac output less than preload influences it. The afterload must increase substantially before it decreases the volume of blood pumped by a healthy heart. Extrinsic Regulation of the Heart Extrinsic regulation refers to the mechanisms external to the heart, such as either hormonal or nervous regulation (see figure 16). Nervous influences are carried through the autonomic nervous system. Both sympathetic and parasympathetic nerve fibers innervate the heart, and have a major effect on the SA node. Stimulation by sympathetic nerve fibers causes the heart rate and the stroke volume to increase, whereas stimulation by parasympathetic nerve fibers causes the heart rate to decrease. Figure 16. Baroreceptors and Chemoreceptor Reflexes The baroreceptor reflex plays an important role in regulating the function of the heart. Baroreceptors are stretch receptors that monitor blood pressure in the aorta and in the wall of internal carotid arteries, which carry blood to the brain (see figure 16). Changes in blood pressure result in changes in the stretch of the walls of these blood vessels. Thus, changes in blood pressure cause changes in the frequency of action potentials produced by the baroreceptors. The action potentials are transmitted along nerve fibers from the stretch receptors to the medulla oblongata of the brain. Within the medulla oblongata of the brain is a cardiogulatory center, which receives and integrates action potentials from the baroreceptors. The cardioregulatory center controls the action potential frequency in sympathetic and parasympathetic nerve fibers that extend from the brain and spinal cord to the heart. The cardioregulatory center also influences sympathetic stiumulation of the adrenal gland (see figure 16). Epinephrine and norepinenephrine, released from the adrenal gland increase the stroke volume and heart rate. When the blood pressure increases, the barorecptors are stiumulated. There is increased frequency of action potentials, sent along the nerve fibers to the medulla oblongata of the brain. This prompts the cardioregulatory center to increase parasympathetic stimulation and to decrease sympathetic stimulation of the heart. As a result, the heart rate and stroke volume decrease, causing blood pressure to decline. When the blood pressure decreases, there is less stimulation of the baroreceptors. A lower frequency of action potentials is sent to the medulla oblongata of the brain and this triggers a response in the cardioregulatory center. The cardioreulatory center responds by increasing sympathetic stimulation of the heart and decreasing parasympathetic stimulation. Consequently, the heart rate and stroke volume increase. If the decrease in blood pressure is large, sympathetic stimulation of the adrenal medulla also increases. The epinephrine and norepinephrine secreted by the adrenal medulla increase the heart rate and stroke volume, also causing the blood pressure to increase toward its normal value. Emotions integrated in the cerebrum of the brain can influence the heart. Excitement, anxiety, or anger can affect the cardioregulatory center, resulting in increased cardiac output. Depression, on the other hand, can increase parasympathetic stimulation of the heart and an increased cardiac output. Epinephrine and small amounts of norepinephrine released from the adrenal medulla in esponse to exercise, emotional excitement, or stress also influence the heart’s function (see figure 16). Epinephrine and norepinephrine bind to receptor molecules on cardiac muscle and cause increased rate and stroke volume. The medulla oblongata of the brain also contains chemoreceptors that are sensitive to changes in pH and carbon dioxide levels (see figure 6). A decrease in pH, often caused by an increase in carbon dioxide, results in sympathetic stimulation of the heart. Changes in the extracellular concentration of potassium, calcium, and sodium, which influence other electrically excitable tissues, also affect cardiac muscle function. Excess extracellular potassium causes the heart rate and stroke volume to decrease. If the extracellular potassium concentration increases further, normal conduction of action potentials through the cardiac muscle is blocked, and death can result. An excess of extracellular calcium causes the heart to contract arrythmically. Reduced extracellular calcium cause both the heart rate and stroke volume to decrease. Effects of Aging on the Heart Gradual changes in the function of the heart are associated with aging. These changes are minor under resting conditions, but become more obvious during exercise and in response to age-related diseases. By the age 70 cardiac output often decreases by approximately one-third. Because of the decrease in the reserve strength of the heart, many elderly people are limited in their ability to respond to emergencies, infections, blood loss, or stress. Hypertrophy (enlargement) of the left ventricle is common age –related change. This appears to result from a gradual increase in the pressure in the aorta (afterload) against which the left ventricle must pump. The increased aortic pressure results from gradual decrease in the elasticity of the aorta, and there is an increased stiffness of the cardiac muscle. The enlarged left ventricle has a reduced ability to pump blood out of the left ventricle. This can cause an increase in left atrial pressure, which can result in increased pulmonary edema. Consequently, there is an increased tendency for people to feel out of breath when they exercise strenuously. Aging cardiac muscle require muscle requires a greater amount of time to contract and relax. Thus, there is a decrease in the maximum heart rate. Both the resting and maximum cardiac output slowly decrease as people age, and by 85 years old, the cardiac output is decreased by 30-60%. Age-related changes in the connective tissue of the heart valves occur. The connective tissue becomes less flexible, and calcium deposits develop in valves. As a result, there is an increase tendency for the aortic semilunar valve to become stenosed or incompetent. There is an age-related increase in cardiac arrhythmias as a consequence of a decrease in the number of cardiac cells. In the Sa node and because of the replacement of cells of the AV bundle. The development of coronary artery disease and heart failure also are age-related. Approximately 10% of elderly people over age 80 have heart faiulure, and major contributing factor is coronary heart disease. Advanced age, malnutrition, chronic infections, toxins, severe anemias, hyperthyroidism, and hereditary factors can lead to heart failure. Exercise has many beneficial effects on the heart. Regular aerobic exercise improves the functional capacity of the heart at all ages, providing there are no conditions that cause the increased workload of the heart to be harmful ANATOMY AND PHYSIOLOGY OF THE BLOOD VESSELS General Features of Blood Vessel Structure Arteries are blood vessels that carry blood away from the heart. Blood is pumped from the ventricles of the heart into the large elastic arteries, which branch repeatedly to form progressively smaller arteries. As they become smaller, the arteries undergo a gradual transition from having walls containing more elastic tissue than smooth muscle to having walls with more smooth muscle than elastic tissue (figure 17). The arteries are normally classified as (1) elastic arteries, (2) muscular arteries, or (3) arterioles, although they form a continuum from the largest to the smallest branches. Figure 17. Blood Vessel Structure Blood flows from arterioles into capillaries, where exchange occurs between the blood and tissue fluid. Capillaries have thinner walls. Blood flows through them more slowly, and there are far more of them than any other blood vessel type. From the capillaries, blood flows into veins. Veins are blood vessels that carry blood toward the heart. Compared with arteries, the walls of veins are thinner and contain less elastic tissue and fewer smooth muscles cells. Going from capillaries toward the heart, small-diameter veins come together to form larger diameter veins, which are fewer in number. Veins increase in diameter and decrease in number as they project toward the heart, and their walls increase in thickness. Veins are classified as (1) venules, (2) small veins, (3) medium-sized veins, or (4) large veins (see figure 17). Blood vessel walls consist of three layers, except in capillaries and venules. The relative thickness and composition of each layer varies with the type and diameter of the blood vessel. From the inner to the outer wall of the blood vessels, the layers, or tunics, are (1) the tunica intima, (2) the tunica media, and (3) the tunica adventitia, or tunica externa (see figure 17). The tunica intima consists of an endothelium composed of simple squamous epithelial cells, a basement membrane, and a small amount of connective tissue. In muscular arteries, the tunica intima also contains a layer of thin elastic connective tissue. The tunica media, or middle layer, consists of smooth muscle cells arranged circularly around the blood vessel. It also contains variable amounts of elastic and collagen fibers, depending on the size and type of the of the vessel. In muscular arteries, there is a layer of elastic connective tissue at the outer margin of the tunica media. The tunica adventitia composed of connective tissue. It is a denser connective tissue adjacent to the tunica media that becomes loose connective tissue toward the outer portion of the blood vessel wall. Arteries Elastic arteries are the leargest diametr arteries and have the thickest walls (see figure 13.1a). A greater proportion of their walls is elastic tissue, and a smaller proportion is smooth muscle compared with other arteries. Elastic arteries are stretched when the ventricles of the heart pump blood into them. The elastic recoil of the elastic arteries prevents blood pressure from falling rapidly and maintains blood flow while the ventricles are relaxed. The muscular arteries include medium-sized and small-diameter arteries. The walls of medium-sized arteries are relatively thick compared with the diameter. Most of the thickness of the walls results from smooth muscle cells of the tunica media (see figure 13.1b). Medium-sized arteries are frequently called distributing arteries because the smooth muscle tissue enables these vessels to control blood flow to different regions of the body. Contraction of the smooth muscle in blood vessels, which is called vasoconstriction, decreases blood vessel diameter and blood flow. Relaxation of the smooth muscle in blood vessels, which is called vasodilation, increases blood vessel diameter and blood flow. Medium-sized arteries supply blood to small arteries. Small arteries have about the same structure as the medium-sized arteries, except that small arteries have a smaller diameter and their walls are thinner. The smallest arteries have only three of four layers of smooth muscle in their walls. Arterioles transport blood from small arteries to capillaries and are the smallest arteries in which the three tunics can be identified. The tunica media consists of only one or two layers of circular smooth muscle cells. Small arteries and arterioles are adapted for vasodilation and vasoconstriction. B. BOOK – BASED SYNTHESIS OF THE DISEASE 1. Definition of the Disease Coronary Artery Disease Coronary Artery Disease (CAD) is a broad term that includes stable angina pectoris and acute coronary syndrome, (Ignatavicius, 2006). Nonetheless, Coronary Artery Disease (i.e. Coronary Heart Disease, Coronary Atherosclerosis, Ischemic Heart Disease) results from focal narrowing of large and medium-sized coronary arteries due to intimal plaque formation (atherosclerosis), (Hargrove-Huttel, 2005). It may also refers to the diseases of the heart that may result from an impaired blood flow to the myocardium usually due to accumulation of atherosclerotic plaque (Suddarth and Brunner, 2008). Coronary Atherosclerosis is also a progressive disease characaterized by atheroma (plaque) formation, which affects the intimal and medial layers of large and midsize arteries and results to the occlusion of the coronary arteries (Black, 2005). In addition, Coronary Artery Disease is simply atherosclerosis of the coronary arteries. Atherosclerosis occurs when the arteries become clogged and narrowed, restricting blood flow to the heart. Without adequate blood, the heart becomes starved of oxygen and vital nutrients it needs to work properly. When the blood flow is slowed the heart doesn't get enough oxygen and nutrients. This can cause chest pain called angina. When one or more of the coronary arteries are completely blocked, the result is a heart attack (injury to the heart muscle), (Cleveland Clinic, 2008). Acute Coronary Syndrome Acute Coronary Syndromes (ACS) has recently been accepted to describe spectrum of acute ischemic heart diseases that include unstable angina, non-ST- segment elevation (non Q wave) myocardial infarction (NSTEMI), and ST-segment elevation (Q-wave) myocardial infarction (STEMI). Persons with an ACS are routinely classified as low risk or high risk based on presenting charcterisctics, ECG variables, serum cardiac markers, and the timing of presentation. Persons with ST-segment elevation on ECG are usually found to have complete coronary occlusion on angiography, and many ultimately have Q-wave myocardial infarction. This type of ACS has been labeled reperfusion elgible acute myocardial infarction(AMI). Persons without ST-segment elevation or non ST-segment elevation usually represent a group in whom thrombotic coronary occlusion is subtotal or intermittent, and most experience unstable angina or are found on the basis of elevated cardiac markers to have non-ST-segment elevation AMI (Porth, 2007). Acute Coronary Syndrome is a term used to describe disorders that include unstable angina, subendocardial MI, and MI. In acute coronary syndrome, it is believed that the atherosclerotic plaque in the coronary artery ruptures, resulting in platelet aggregation (“clumping”), thrombus (clot) formation, and vasoconstriction. The amount of disruption of the atherosclerotic plaque determines the degree of obstruction of the coronary artery and the specific disease process (unstable angina or myocardial infarction [MI]), (Ignatavicius, 2006). In addition, ACS is an umbrella term used to cover any group of clinical symptoms compatible with acute myocardial ischemia, (AHO, 2008), thus include those whose clinical presentations cover the following range of diagnoses: unstable angina, non–ST-elevation myocardial infarction (NSTEMI), and ST-elevation myocardial infarction (STEMI) (Fenton, 2008). In other cases, the blood clot (coronary thrombus) may totally block the blood supply to the heart muscle (coronary occlusion), causing one three serious conditions, called acute coronary syndromes: This is actually a name given to three serious conditions: Forms of acute coronary syndrome may include the following (WebMD, 2008): 1. Unstable angina: This may be a new symptom or a change from stable angina. The angina may occur more frequently occur more easily at rest, feel more severe, or last longer. Although this can often be relieved with oral medications, it is unstable and may progress to a heart attack. Usually more intense medical treatment or a procedure is required to treat this acute coronary syndrome (WebMD, 2008). 2. Non-ST segment elevation myocardial infarction (NSTEMI): This heart attack, or MI, does not cause changes on an electrocardiogram (ECG). However, chemical markers in the blood indicate that damage has occurred to the heart muscle. In NSTEMI, the blockage may be partial or temporary, and so the extent of the damage is relatively minimal (WebMD, 2008). 3. ST segment elevation myocardial infarction (STEMI): This heart attack, or MI, is caused by a prolonged period of blocked blood supply. It affects a large area of the heart muscle, and causes changes on the ECG and chemical markers in the blood (WebMD, 2008). Myocardial Infarction Myocardial infarction, sometimes called as Acute Myocardial Infarction(AMI) or Myocardial Ischemia is also known as heart attack, coronary occlusion, or simply “coronary,” which is a life-threatening condition characterized by the formation of localized necrotic areas within the myocardium (Black, 2005) and occurs when myocardial tissue is abruptly and severed deprived of oxygen. When blood flow if acutely reduced by 80% to 90%, ischemia develops. Ischemia can lead to injury and necrosis (infarction) of myocardial tissue if blood flow is not restored (Ignatavicius, 2006). Myocardial ischemia develops if the supply of coronary blood cannot meet the demand of the myocardium for oxygen and nutrients. Imbalances between coronary blood supply and myocardial demand can result from a number of conditions. The most common cause of decreased coronary blood flow and resultant myocardial ischemia is the formation of atherosclerotic plaques in the coronary circulation (Porth, 2007). Often MIs begin with infarction (necrosis) of the subendocardial layer of cardiac muscle. This layer has the longest myofibrils in the heart, the greatest oxygen demand, and the poorest oxygen supply. Around the initial area of infarction (zone of necrosis) in the subendocardium are two other zones: (1) the zone of injury, tissue that is injured but not necrotic, and (2) the zone of ischemia, tissue that is oxygen deprived (Ignatavicius, 2006). TYPES OF MYOCARDIAL INFARCTION AS TO DEPTH OF INFARCTION 1. Transmural Infarction 2. Intramural Infarction 3. Subepicardial Infarction 4. Subendocardial Infarction Classification of Myocardial Infarction by Location The clients response to an MI also depends on which coronary artery or arteries were obstructed or arteries were obstructed and which part of the left ventricle wall damaged: 1. Posterior (Inferior) MI – Occlusion of Right coronary artery (RCA) -Obstruction of the right coronary artery often have inferior wall MIs. Inferior wall MIs (IWMIs) account for about 17% of all MIs and have a mortality rate of about 10%. Up to 50% of all inferior wall MIs are associated with an occlusion of the right coronary artery causing significant damage to the right ventricle (Ignatavicius, 2006). 2. Massive anterolateral MI – Occlusion of Left coronary artery (LCA) (Ignatavicius, 2006). 3. Anteroseptal MI – Occlusion of Left anterior descending artery (LAD) -Obstruction of the LAD causes anterior or septal MIs because LAD artery perfuses the anterior wall and most of the septum of the left ventricle. Anterior wall MIs (AWMIs) account for 25% of all MIs and have the highest mortality rate. Clients with anterior MIs are most likely to experience left ventricular heart failure and ventricular dysrhythmias because large segment of the left ventricle wall may have been damaged (Ignatavicius, 2006). 4. Lateral MI – Occlusion of Left circumflex coronary artery (LCX) -Clients with obstruction of the circumflex artery may experience a lateral wall MI (LWMIs) and sinus dysrhythmias since the circumflex artery supplies the lateral wall of the left ventricle and possibly portions of the posterior wall or the sinoatrial (SA) or atrioventricular (AV) nodes (Ignatavicius, 2006). ANGINA PECTORIS Chest pain resulting from reduced coronary blood flow, which causes a temporary imbalance between myocardial blood supply and demand. More over, it is a chest pain resulting from myocardial ischemia (inadequate blood supply to the myocardium), (Black, 2005). Patterns of Angina 1. Stable Angina -a.k.a Exertional Angina is stable angina is paroxysmal chest pain or discomfort triggered by a predictable degree of exertion (e.g. walking 20feet) or emotion. Characteristically, a stable pattern of onset, duration, severity, and relieving factors is present, normally stable angina is relieved with rest or nitroglycerin, or both (Black, 2005). 2. Unstable Angina -a.k.a. Preinfarction angina, crescendo angina or intermittent coronary syndrome) is paroxysmal chest pain triggered by an unpredictable degree of exertion or emotion which may occur at night. Unstable angina attacks characteristically increase in number, duration. And severity over time. If unstable angina occurs, it must be treated as a medical emergency with the client receiving immediate medical attention (Black, 2005). 3. Prinzmental’s Angina -a.k.a Variant Angina, is chest discomfort similar to classic angina but of longer duration; it may occur while the client is at rest. These attacks tend to happen between midnight and 8 AM. Variant angina results from coronary artery spasm and may be associated with elevation of the ST segment on the electrocardiogram (ECG) (Black, 2005). 4. Nocturnal Angina -Nocturnal Angina is possibly associated with rapid eye movement (REM) sleep during dreaming (Black, 2005). 5. Angina Decubitus -Paroxysmal chest pain that occurs when the client reclines and lessens when the client sits or stands up (Black, 2005). 5. Intractable Angina -Is chronic incapacitating angina that is unresponsive to intervention. 6. Postinfarction Angina -Pain occurs after MI, when residual ischemia may cause episodes of angina (Black, 2005). The Killip classification is a system used in individuals with an acute myocardial infarction (heart attack), in order to risk stratify them. Individuals with a low Killip class are less likely to die within the first 30 days after their myocardial infarction than individuals with a high Killip class. Killip Classification of Heart Failure Class Description I Absent crackles and S3 II Crackles in the lower half of the lung fields and possible S3 III Crackles more than halfway up the lung fields and frequent pulmonary edema IV Cardiogenic Shock Source (Ignatavicius, 2006) 2. Non-Modifiable Factors and Modifiable Factors Non-Modifiable Factors 1. Increasing Age Age influences both the risk and the severity of CHD. Symptomatic CHD appears predominantly in people older than 40 years of age, and four of five people who die of CHD are age 65years or older . Angina and MI, however, can occur in a person’s 30s and even in one’s 20s. At older ages women who have heart attacks are twice as likely as men to die of heart attack (Black, 2005). 2. Gender (Men develop CAD at an earlier age than women) Coronary heart disease is the number-one killer of both men and women. In 1999 mortality from CHD was almost equal for men and women. Although men are at higher risk for heart attacks at younger ages, the risk for women increases significantly at menopause, so that CHD rates in women after menopause are two or three times that of women the same age before menopause. Women with an early menopause are also at higher risk than are women with a normal or late menopause (Black, 2005). 3. Family history of coronary artery disease Children whose parents had heart disease are at higher risk for CHD. This increased risk is related to genetic predisposition to hypertension, elevated lipid levels, diabetes, and obesity; all of these conditions increase the risk of CHD (Black, 2005). In addition, primary or familial dyslipidemia result from genetic defects causes abnormalities in lipid-metabolizing enzymes and abnormal cellular lipid receptors (MacCance, 2006). In addition, particular genotype patterns also may place individuals at risk of CAD/MI. For example, recent studies of a few families with high rates of CAD/MI have identified mutations in a gene known as MEF2A, which codes for one of the transcription factors known as myocyte enhancer factor-2. In its normal expression, this protein is involved in the early stages of vasculogenesis (formation of new blood vessels); mutations may compromise its ability to perform this function, resulting in increased susceptibility to heart disease (Corwin, 2008). 4. Race/Ethnicity African-American women face the highest risk for death from heart disease, and their rate of heart attacks is increasing. (Mortality rates in men do not differ much by race.) Native American men have a lower risk for heart disease than Caucasian men, and Hispanics have the lowest risk for heart disease of all major American population groups.African-Americans face a number of biologic and social dangers to their hearts, including; They have a higher prevalence of diabetes and hypertension than do Caucasians. They tend to have poorer diets, higher stress levels, and less access to health care. Some African-Americans with coronary artery disease appear to have a genetic trait that increases the danger of triglycerides, which may be particularly hazardous for women (Simon, 2008). Modifiable Factors a. Hyperlipidemia An increased serum concentration of LDL is a strong indicator of coronary risk. High dietary intake of cholesterol and fats, often in combination with a genetic predisposition to accumulations of LDL in the serum (e.g. dysfunction of the hepatic LDL receptor), results in high levels of LDL in the bloodstream. The term LDL actually describes several types of LDL molecules; the small dense LDL, particles are the most atherogenic. LDL oxidation, migration into the vessel wall, and phagocytosis by macrophages are key steps in the pathogenesis of atherosclerosis. LDL also plays a role in endothelial injury, inflammation, and immune responses that have been identified as being important in atherogenesis (McCance, 2006). b. Hypertension High blood pressure afflicts nearly 50 million American Adults and children. It increases the workload of the heart by increasing afterload, enlarging and weakening of the left ventricle over time. As blood pressure increases, the risk of serious cardiovascular event escalates. When clients have hypertension, obesity, tobacco use, high cholesterol levels and dibetes, the risk of heart attack increases significantly (Black, 2005). In addition, it is responsible for a twofold to threefold increased risk of atherosclerotic cardiovascular disease. It further contributes to endothelial injury, a key step in atherogenesis and causes myocardial hypertrophy, which increases myocardial demand for coronary flow (McCance, 2006). c. Cigarette smoking Cigarette smoking contributes to the development and severity of CAD in the following three ways. First, the inhalation of smoke increases the blood carbon monoxide level, and hemoglobin, the oxygen-carrying component of blood, combines more readily with carbon monoxide than with oxygen (Suddarth and Brunner, 2008). More over, carbon monoxide in cigarette smoke reduces the oxygen content of arterial blood. Hypoxemia (insufficient oxygen in arterial blood) may promote atherosclerosis by deceasing the availability of oxygen to the vessel walls and increasing vessel wall permeability. More so, a decreased amount of available oxygen may decrease the heart’s ability to pump (McCance, 2006). Second, the nicotine stimulates the release of cathecholamines (epinephrine and norepinephrine), which increase heart rate and peripheral vascular constriction. As a result, blood pressure increases, as do cardiac workload and oxygen demand. Elevated catecholamines also stimulate release of free fatty acids (McCance, 2006). In addition, the nicotinic acid in cigarette can also cause the coronary arteries to constrict. Smokers have a tenfold increase in risk for sudden cardiac death. The increase in catecholamines maybe a factor in sudden cardiac death (Suddarth and Brunner, 2008). More so, nicotine activates platelets and stimulates smooth-muscle-cell proliferation in the arterial walls (Black, 2005). Third, use of cigarette causes a detrimental vascular response and increases platelet adhesion, leading to a higher probability of thrombus formation (Suddarth and Brunner, 2008). More so, Cigarette smoking is associated with an increase in LDL, a decrease in HDL, and induction of a prothrombotic state, as well as increases in inflammatory markers of CAD such as C-reactive protein and fibrinogen. In addition, the cadmium in cigarette smoke maybe related to elevations in blood pressure. In addition, passive smoking from “second-hand smoke” substantially reduces blood flow velocity in the coronary arteries of healthy young adults (Ignatavicius, 2006). d. Obesity Obesity places an extra burden on the heart, requiring the muscle to work harder to pump enough blood to support added tissue mass. In addition, obesity increases the risk for CHD because it is often associated with elevated serum cholesterol and triglyceride levels, high blood pressure, and diabetes (Black, 2005). More so, It is estimated that 65% of the adult population in the United States is overweight or obese resulting in a much increased risk for CAD and stroke. An estimated 47million U.S. residents have a combination of obesity, dyslipidemia, and hypertension called the metabolic syndrome, which is associated with an even higher risk for CAD events. In addition, abdominal obesity has the strongest link with increased CAD risk and is related to insulin resistance, decreased HDL, increased blood pressure, and decreased levels of recently described cardioprotective protein called adiponectin (McCance, 2006). e. Physical Inactivity/Sedentary Lifestyle The Framingham Study demonstrated an inverse relationship between exercise and reduce their risk of CHD because they (1) higher HDL levels; (2) lower LDL cholesterol, triglyceride, and blood glucose level; (3) greater insulin sensitivity; (4) lower blood pressure; and (5) lower body mass index (Black, 2005). A sedentary life-style not only increases the risk of obesity but also has an independent effect on increasing CAD risk (McCance. 2006). More so, physical inactivity may be the most important risk factor for the general population. Less active, lest-fit persons have a 30% to 50% greater risk of developing high BP, which predisposes to CAD, (Ignatavicius, 2006). f. Response to Stress (Occupational Stress) A persons’ response to stress may contribute to the development of CHD. Some researchers have reported a relationship between CHD risk and stress levels, health behaviors, and socioeconomic status. Stress appears to increase CHD risk through its effects in major risk factors. (Black, 2005). Severe emotional stress cause surge in adrenaline, which causes the blood to clot readily increasing the risk of heart attacks. British investigators have shown that chronic work stress can produce chronic increases in adrenaline levels, and have related those changes to an increased risk of heart disease (Fogoros, 2009). For example, some people respond to stress by overeating or by starting or increasing smoking. Stress is also associated with elevated blood pressure. Although stress is unavoidable in modern life, an excessive response to stress can be a health hazard. Significant stressors include major changes in residence, occupation, or socioeconomic status (Black, 2005). g. Diet Increased dietary intake of foods high in sodium, fats and cholesterol predisposes a person to cardiovascular disoders (Udan, 2005). Engaging in eating too much fatty foods (atherogenic diet) could cause increase cholesterol level in the blood wherein elevated serum lipid level is one of the four most firmly established risk factors for Coronary Artery Disease (Mantitz, 2004). h. Amphetamine Use Young adults who abuse amphetamines may be at greater risk of suffering a heart attack. Amphetamine also acts in this way with norepinephrine (noradrenaline) and to a lesser extent serotonin. Thus, the physical effects of amphetamine could include reduced appetite, dilated pupils, flushing, loss of coordination, restlessness, dry mouth, headache, tachycardia, increased breathing rate, increased blood pressure, fever, sweating, diarrhea, constipation, blurred vision, impaired speech, dizziness,uncontrollable movements, insomnia, numbness, palpitations, arrhythmia. In high doses or chronic use convulsions, dry or itchy skin, acne, pallor can occur (Ignatavicius, 2006). Since amphetamine use releases cathecolamines (norepinephrine and epinephrine) it therefore increases peripheral vasoconstriction which increases the cardiac workload and oxygen demand. It also stimulates the release of free fatty acids. i. History of Diabetes Mellitus Diabetes Mellitus is an extremely important risk factor for CAD. Diabetes is associated with a two-fold increase in the risk for CAD death and up to a sixfold risk for stroke. Diabetes and insulin resistance have multiple effects on the cardiovascular system through the production of toxic reactive species (ROS) that alter vascular cell function. These effects can include endothelial damage, thickening of the vessel wall, increased inflammation and leukocyte adhesion, increased thrombosis, glycation of vascular proteins, and decreased production of endothelial-derived vasodilators such nitric oxide. It is also associated with dyslipidemia because of resulting alteration of hepatic lipoprotein synthesis and increases in LDL oxidation. Aggressive management of this additional risk factor can significantly improve CAD risk in individuals with diabetes (McCance, 2006). j. Menopause The incidence of CHD markedly increases among women after menopause. Before menopause estrogen is thought to protect against CHD risk by raising HDL and lowering LDL levels. Epidemiologic studies have shown that the loss of natural estrogen as women age may be associated with increase in total and LDL cholesterol and a gradually increasing CHD risk. If menopause is caused by surgical removal of the uterus and ovaries, the risks of CHD and MI increase (Black, 2005). k. Behavior Pattern (Type A Personality) The type A personality may not be as significant as was once thought; evidence of its precise role remains inconclusive. Current predictors of coronary events focus on physiologic factors. However, it has been long been recognized that emotional stress can lead to release of catecholamines and subsequent coronary ischemia. Thus, people with type A traits are advised to alter behaviors and responses to triggering events and to reduce risk factors (Suddarth and Brunner, 2008). l. Inflammatory Response A newly identified risk factor currently being researched is the presence of any chronic inflammatory state that leads to an increase in body’s production of CRP. Too much CRP tends to destabilize plaque inside artery walls. When plaque lesions crack or break, a clot is formed and this may lead to heart attack. Researchers have discovered that a high CRP is a marker for coronary disease. This means that clients with chronic inflammatory diseases, such as arthritis, lupus, and autoimmune deficiency, may be at higher risk for heart attack (Black, 2005). m. Increase homocysteine Levels Hyperhomocysteinemia occurs because of genetic lack of enzyme that breaks down homocysteine (an amino acid) or because of a nutritional deficiency of folate, cobalamin (vitamin B12), or pyridoxine (vitamin B6). It has been identified as a risk factor for CAD, although its significance in CAD and stroke continues to be explored. Mechanisms by which it contributes to coronary disease include associated increases in LDL, decreases in endogenous vasodilators, and an increased tendency for thrombosis. Routine serum measurement of homocysteine is not currently recommended and prevention and management are focused on increasing the dietary intake of folate and B vitamins (McCance, 2006). n. Infection Emerging is evidence that infection may play a role in atherogenesis and CAD risks. Studies have found that several microorganisms, especially Chlamydia pneumonae and Helicobacter pylori are often present in atherosclerotic lesions. Serum antibodies to microorganisms have been linked to an increased risk for CAD as has the presence of periodontal disease (McCance, 2006). 3. Clinical manifestations with Rationale SIGNS AND SYMPTOMS RATIONALE Atherosclerosis plaques are initiated by injury to the coronary artery endothelium. The specific cause of endothelial dysfunction maybe attributed to the non-modifiable factors and modifiable factors. Once the injury occurs the endothelium may become more permeable and recruit leukocytes. LDLs leak through the endothelium and into the vessel wall (insudation) where they are oxidized by endothelial cells and macrophages. Oxidized lipids are Atherosclerosis damaging to the endothelial and smooth muscle (Plaque Formation) cells, and stimulate the recruitment of macrophages into the vessel wall where they engulf the lipids. Lipid-filled macrophages are called foam cells. The macrophages and foal cells release inflammatory mediators and growth factors that attract more leukocytes and stimulate smooth muscle proliferation. Excess lipid and debris begins to accumulate within the vessel wall and coalesce into a pool called the lipid core. Atherosclerotic plaques with large lipid cores are fragile and prone to rupture. Due to obstruction of blood flow to the coronary arteries there will imbalance between coronary supply and demand, as a result myocardial O2 deficit will occur. Since myocardial cells are denied of adequate O2 and nutrients resulting from myocardial ischemia (inadequate blood supply to the myocardium) may result to myocardial cell death Angina Pectoris/Chest Pain which in turn will lead to accumulation of metabolic acid within ischemia part (necrotic part) of the myocardium, thus anaerobic metabolism is established leading to increase production of lactic acid. Lactic acid causes irritation to the myocardial fibers/nerve endings thus causing pain along the chest wall ranging from a sensation of heaviness or pressure to moderately severe pain. Prolonged ischemia will lead to myocardial cell death causing accumulation of lactic acid due to anaerobic metabolism. Lactic acid causes pain as it irritates myocardial fibers/nerve endings. Discomfort (+) Levine’s Sign may radiate to the neck, lower jaw, left arm, and left shoulder or, occasionally, to the back or down the right arm causing a Levine’s sign (Individuals often describe the sensation by clenching a fist over the left sternal border). Continued ischemia due to coronary obstruction will cause myocardial cell/tissue necrosis. Necrosis Elevated Cardiac Enzymes of myocardial tissue results in the release of certain intracellular enzymes (CK-MB, Troponin I, Troponin (CK-MB, Troponin I, Troponin T, T, Myoglobin) through the damaged cell Myoglobin) membranes into the interstitial spaces. The lymphatics pick up the enzymes and transport them into the bloodstream, where they can be detected by serologic tests. Imbalance between coronary supply and myocardial demand secondary to coronary occlusion will lead to myocardial O2 deficit which causes death of the myocyte, Prolonged ischemia ST-segment elevation, T wave causes myocardial infarction. Since there is death Inversion, on myocardium electrical impulses is impaired or pathologic Q wave even lack of response to electrical impulses may occur causing alteration and delay of repolarization and depolarization properties of the heart. This is evidently reflected on ECG (Electrocardiogram) showing ST-segment elevation, T wave inversion and pathologic Q wave. Due to infarcted myocardium, heart loses contractility and lack of responses to electrical Dysrhythmias/Arrhythmias impulses. This activity of the heart will eventually lead to dysrhythmias/arrhythmias which is very fatal to the individual and if not attended immediately may result to sudden death. Imbalance between coronary supply and myocardial demand secondary to coronary occlusion will lead to myocardial O2 deficit which causes myocardial damage-death and necrosis. Elevated Glucose Level The myocardial cells significantly release catecholamines and norepinephrine. Catecholamines mediate the release of glycogen, glucose, and stored fat from body cells. Therefore, plasma concentrations of free fatty acids and glycerol rise within 1 hour after onset of acute myocardial infarction. In addition, norepinephrine elevates blood sugar levels through stimulation of liver and skeletal muscle cells. It also suppresses pancreatic B cell activity which reduces insulin secretion and elevates blood glucose further. Not surprisingly, hyperglycemia is noted approximately 72 hours after an acute myocardial infarction. Obstruction of blood flow to the coronary artery because of occlusion could cause imbalance between coronary supply and myocardial demand leading to myocardial O2 deficit. In return, myocardial cells are denied of with adequate O2 and nutrients leading to O2, glycogen and ATP Increased WBC (Leukocytosis) stores depletion causing irreversible hypoxemic damage causing cellular death and tissue necrosis, as part of the response, there will be also inflammation as evidenced by attraction of increased WBCs near the injured area. Infarcted myocardium as brought about by prolonged ischemia due to imbalance between coronary supply and myocardial demand stimulates the vasovagal reflexes affecting the gastrointestinal Nausea, Vomiting, Epigastric Pain tract causing nausea and vomiting. These events is also brought by increased production of lactic acid which stimulate pain fibers at the vomiting center, which in turn triggered Medulla Oblongata causing nausea and vomiting. When heart loses its contractility and lack of response to electrical impulses due to myocardial infarction, the compensatory mechanism of the heart will work hard to increase its workload. Eventually, as the heart works hard to meet the demand, it will enlarge significantly (hypertrophy of the heart) as well as thickening of the ventricles resulting to cardiomegaly. In addition, cardiac tissue surrounding the area of infarction also undergoes changes such as myocardial remodeling, a process Cardiomegaly mediated by angiotensin II, aldosterone, catecholamines, adenosine, and inflammatory cytokines which causes hypertrophy of the myocardial cells and sustained activation of nuerohormonal compensatory mechanism which eventually increases wall stress in the ventricle and thus to reduce wall stress, the myocardial cells hypertrophy (Laplace’s Law). As a result there will be thickening of the ventricular wall which contributes to cardiomegaly. Due to obstruction of blood flow to the coronary arteries there will imbalance between coronary supply and demand, as a result myocardial O2 deficit will occur. Since myocardial cells are denied of adequate O2 and nutrients resulting from myocardial ischemia (inadequate blood supply to the myocardium) may result to myocardial cell death which in turn will lead to accumulation of metabolic Pallor, diaphoresis, dyspnea, body acid within ischemia part (necrotic part) of the weakness/easy fatigability, myocardium, thus anaerobic metabolism is headache, sense of impending established leading to increase production of lactic doom acid. Lactic acid causes irritation to the myocardial fibers/nerve endings thus causing pain along the chest wall ranging from a sensation of heaviness or pressure to moderately severe pain. As a result, the body will respond, thus there will be pallor, diaphoresis, dyspnea, body weakness/easy fatigability, headache, sense of impending doom. Due to obstruction of blood flow to the coronary arteries there will imbalance between coronary supply and demand, as a result myocardial O2 deficit will occur. Since myocardial cells are denied of adequate O2 and nutrients resulting from myocardial ischemia (inadequate blood supply to the myocardium) may result to myocardial cell death which in turn will lead to accumulation of metabolic acid within ischemia part (necrotic part) of the myocardium, thus anaerobic metabolism is Stimulation of SNS established leading to increase production of lactic Increased VS acid will lead to acidosis. In return, myocardial cells (-)Bowel Movement will become sensitive to changes in pH and become ↑O2 needs and demands less functionsal leading to conduction system disorder decreasing myocardial contractility stimulating the sympathetic nervous system causing increased vitals signs and no bowel movement and increased O2 needs and demands. Blood pressure is increased also because of decreased arterial pressure due to decreased cardiac output, therby, stimulating barorecptors causing peripheral vasoconstriction. Due to myocardial infarction, different mechanisms will occur such as heart loses contractility and lack of response to electrical ↓Hemoglogbin, ↓hematocrit, impulses, myocardial remodelling and myocardial delayed capillary refill time, pallor, dysfunction, all of which actions will lead to heart failure. As a result, there will be decreased cardiac output leading to decreased systemic circulation decreasing blood carrying O2 to peripheral parts of the body hence there will be ↓hemoglogbin, ↓hematocrit, delayed capillary refill time, pallor. Due to myocardial infarction, different mechanisms will occur such as heart loses contractility and lack of response to electrical impulses, myocardial remodeling and myocardial dysfunction, all of which actions will lead to heart Weakness/restlessness, easy failure. As a result, there will be decreased cardiac fatigability, fatigue, output leading to decreased systemic circulation redirecting of blood away from the skin to major organs, thus the body feels weakness/restlessness, easy fatigability, fatigue. Since there is heart failure, there is also decreased in cardiac output. As a result, symphathetic receptors are stimulated increasing Left ventricular hypertrophy heart rate or pumping action as a compensatory Decrease Ejection fraction mechanism, which leads to left ventricular hypertrophy eventually heart’s ability to pump will deteriorate thus leading to moderate left ventricular failure which decreases ejection fraction Coronary occlusion will lead to ischemia of the heart muscles (myocardial infarction), one of the complications of MI is heart failure which consequently decreases the cardiac output, since there is apparent decreased in cardiac output as a compensatory mechanism of the heart, it increases its pumping action. In return, it will eventually lead to Pulmonary Congestion ventricular failure (left ventricle), the right side of the heart continuously propel blood to the lungs since left ventricle is unable to fully eject the returning blood to the systemic circulation, there will be pooling of blood to the lungs which consequently lead to pulmonary congestion. Heart failure leads to decreased in cardiac output. As a result, symphathetic receptors are Fine crackles on BLF (bibasal stimulated increasing heart rate or pumping action rales), wheezes, S3 gallop as a compensatory mechanism, which leads to left Edema ventricular hypertrophy eventually heart’s ability to Jugular Distension pump will deteriorate thus leading to moderate left Dyspnea (Difficulty of breathing) ventricular failure which decreases ejection fraction. Body Weakness/Easy fatigability Still, the right side of the heart continuously propel blood to the lungs, in return, left ventricle is unable to fully eject the returning blood to systemic circulation thus, there will be pooling of blood resulting to pulmonary congestion. Since there is congestion, there will be stasis of fluid leading to formation of exudates in the alveoli and bronchioles forming consolidation of exudates as manifested by fine crackles (bibasal rales on BLF), edema, and jugular distension. As a result of pulmonary congestion, the body responded by my using accessory muscles, difficulty of breathing as compensated by orthopnea, easy fatigability or body weakness. Since there is pulmonary congestion, there will be fluid stasis leading to formation of exudates in the alveoli and bronchioles. The consolidated exudates irritate pulmonary sensory receptors and Cough action potentials are carried and conducted to medulla oblongata, in return, productive cough reflex is initiated. Because of heart failure, there is decreased in cardiac output which eventually leads to inadequate cerebral perfusion, since the brain is depleted of Lost of consciousness, dizziness, supply of O2, the body responds to this event fainting, sense of impending doom through loss of consciousness, dizziness, fainting, sense of impending doom. Imbalance between coronary supply and myocardial demand secondary to coronary occlusion will lead to myocardial O2 deficit which causes myocardial damage-death and necrosis. In Ventricular Aneurysm, Perforation return, these there will be scar tissue formation of the Ventricular Septum which apparently replaces by new tissues, as a result, tissues become weak and soft leading to ventricular aneurysm or perforation of the ventricular septum. Lack of O2 supply because of coronary occlusion could lead to myocardial infarction, Valve Regurgitation complications may include ischemia of the valve leaflets/papillary muscles leading to valve regurgitation. XIV. BIBLIOGRAPHY A. Books Black, Joyce M. and Hawks, Jane Hokanson. Medical-Surgical Nursing Clinical Management for Positive Outcomes. 7th Edition. Elsevier Saunders, USA, 2005. Copstead Lee-Ellen C. et.al. Pathophysiology. 3rd Edition. Elsevier Saunders, St. Louis, Missouri. 2005. Corwin, E.J. Handbook of Pathophysiology. 3rd Edition. Lippincott Williams and Wilkins. Philadelphia. 2008 Doenges, Marilynn E., et.al. Nurses Pocket Guide: Diagnoses, Interventions and Rationales. 8th Edition. F.A. Davis Company. Philadeplhia, U.S.A. 2006. Doenges, Marilynn E., et.al. Nursing Care Plans: Guidelines for Individualizing Patient Care Actions Across the Life Span. 7th Edition. F.A. Davis Company. Philadeplhia, U.S.A. 2006. Doyle, Rita M., et.al. 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