A Case of Ruptured Coronary Sinus of Valsalva

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63 rd Critical Care Course A Case of Ruptured Sinus of Valsalva Page 1

Philippine Heart CenterDepartment of Nursing Education and Research

A Case Study onRuptured Sinus of Valsalva, with Ventricular Septal Defect, with Severe Mitral andTricuspid Regurgitation, Moderate Pulmonic Regurgitation and Moderate Pleural

Effusion

Submitted in Partial Fulfillment of the RequirementsFor the 63 rd Batch Post-Graduate Course in Critical Care Nursing

Submitted to:Ma. Lilibeth Q. Icasiano, RN

Course Coordinator

Submitted by:

Carmelita O. Abulencia, RNAprille Hershey R. Agustin, RN

Amphi Joy A. Andaya, RNPaul Ryan I. Anido, RN

Reigner Jireh D. Antiquera, RNEvan Harold Q. Antonio, RNAngela Socrates A. Baron, RN

Arlene B. Basa, RNCharisse D. Belasa, RNJu-en B.Blasurca, RN

Ryan P. Bon, RNRhonalyn S. Bravo, RN

Elieza E. Bruzo, RN

May 28, 2010


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TABLE OF CONTENTS

I. Introduction 1II. Statement of Objectives 7III. Patients Profile 8

a. Biographic Data 8b. History 8c. Prenatal and Post Natal History 9d. Gordons Health Pattern 10

e. Physical Assesment 12IV. Pathophysiology 14V. Course in the Ward 15VI. Diagnostics and Laboratory Results


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Introduction

Congenital Heart Defect (CHD) refers to a problem with the heart's structure andfunction due to abnormal heart development before birth. It is a broad term that can describea number of different problems affecting the heart. The usual cause of a congenital heartdisorders is failure of a heart structure to progress beyond an early stage of embryonicdevelopment. According to the Department of Health, approximately 8 out of 1,000newborns are affected with Congenital Heart Defect.

Congenital sinus of Valsalva aneurysm was first described 1839. This first publishedaccount describes rupture of a sinus of Valsalva, which is the most feared complication. Soonafterwards, clinicians described other cases of unruptured aneurysms and applied anatomicdescriptions. The condition may have been clinically described for the first time in 1883.

Aneurysm of a sinus of Valsalva is a rare congenital cardiac defect that can rupture,causing heart failure or other catastrophic cardiac events. If the aneurysm remainsunruptured, it occasionally causes obstruction of cardiac flow resulting from compression of normal structures. Dissection of the aneurysm into the cardiac tissues may occur, causingobstruction or destruction of local structures. Sinus of Valsalva aneurysms are uncommonclinical entities but are known to be associated with up to 0.5-1.5% of patients. They developas a result of a separation of the aortic media of the sinus from the ventricular fibrousstructures leading to a progressive protrusion into the low-pressure chamber due to thepressure differential. Most often the aneurysm begins in the right coronary sinus (80%) andterminates in the right ventricle (72%) but up to 15% of cases originate in the non-coronarysinus, which usually leads to a termination in the Right Atrium.

Sinus of Valsalva aneurysms can be congenital or acquired as a result of injury,infection, or be related to Marfan syndrome or Behcet disease. Up to 47% of patients withsinus of Valsalva aneurysms are found to have an associated congenital defect. In one seriesan associated ventricular septal defect was most common (49.3%), followed by aorticinsufficiency (23.4%), tricuspid regurgitation, infundibular pulmonary stenosis, patent ductusarteriosus and patent foramen ovale (each 1.9%). An association with bicuspid aortic valvesand aortic coarctation has also been described.

A ventricular septal defect (VSD) is a defect in the septum between the right and leftventricle. The septum is a wall that separates the hearts left and right sides. Septal defects aresometimes called a hole in the heart. Its the most common congenital heart defect in thenewborn; its less common in older children and adults because some VSDs close on their own.

Tricuspid regurgitation is leakage of blood backward through the tricuspid valveeach time the right ventricle contracts. Tricuspid regurgitation usually results when the rightventricle enlarges and resistance to blood flow from the right ventricle to the lungs isincreased. Resistance may be increased by a severe, long-standing lung disorder, such as
http://www.medscape.com/resource/heartfailurehttp://www.medscape.com/resource/heartfailure


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emphysema or pulmonary hypertension, by disorders involving the left side of the heart, orrarely by narrowing of the pulmonary valve (pulmonic stenosis). To compensate, the rightventricle enlarges, stretching the tricuspid valve and causing regurgitation. Tricuspidregurgitation affects about 4 out of 100,000 people. It may be found in those with a type of

congenital heart disease called Ebstein's anomaly .

Mitral regurgitation is a disorder of the heart in which the mitral valve does not closeproperly when the heart pumps out blood . It is the abnormal leaking of blood from the leftventricle , through the mitral valve, and into the left atrium , when the left ventricle contracts,i.e. there is regurgitation of blood back into the left atrium.

The mitral valve is composed of two valve leaflets, the mitral valve annulus (whichforms a ring around the valve leaflets), the papillary muscles (which tether the valve leafletsto the left ventricle, preventing them from prolapsing into the left atrium), and the chordae

tendineae (which connect the valve leaflets to the papillary muscles). A dysfunction of any of these portions of the mitral valve apparatus can cause mitral regurgitation.The most commoncause of mitral regurgitation is mitral valve prolapse (MVP), which in turn is caused bymyxomatous degeneration . The most common cause of primary mitral regurgitation in theUnited States (causing about 50% of primary mitral regurgitation) is myxomatousdegeneration of the valve. Myxomatous degeneration of the mitral valve is more common infemales, and is more common in advancing age. This causes a stretching out of the leaflets of the valve and the chordae tendineae . The elongation of the valve leaflets and the chordaetendineae prevent the valve leaflets from fully coapting when the valve is closed, causing the

valve leaflets to prolapse into the left atrium, thereby causing mitral regurgitation.

Pulmonic regurgitation, also known as pulmonary regurgitation, is the backward flowof blood from the pulmonary artery , through the pulmonary valve , and into the right ventricle of the heart during diastole . While a small amount of pulmonic regurgitation may occur inhealthy individuals, it is usually detectable only by an echocardiogram and is harmless. Morepronounced regurgitation that is noticed through a routine physical examination is a medicalsign of disease and warrants further investigation.

Pleural effusion is excess fluid that accumulates in the pleural cavity, the fluid-filled

space that surrounds the lungs. Excessive amounts of such fluid can impair breathing bylimiting the expansion of the lungs during inhalation. Pulmonic regurgitation, also known aspulmonary regurgitation, is the backward flow of blood from the pulmonary artery, throughthe pulmonary valve, and into the right ventricle of the heart during diastole. While a smallamount of pulmonic regurgitation may occur in healthy individuals, it is usually detectableonly by an echocardiogram and is harmless. More pronounced regurgitation that is noticedthrough a routine physical examination is a medical sign of disease and warrants furtherinvestigation.
http://www.righthealth.com/topic/tricuspid_Regurgitation/overview/adam20?fdid=Adamv2_007321http://www.righthealth.com/topic/tricuspid_Regurgitation/overview/adam20?fdid=Adamv2_007321http://www.righthealth.com/topic/tricuspid_Regurgitation/overview/adam20?fdid=Adamv2_007321http://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Regurgitation_%28circulation%29http://en.wikipedia.org/wiki/Regurgitation_%28circulation%29http://en.wikipedia.org/wiki/Regurgitation_%28circulation%29http://en.wikipedia.org/wiki/Fibrous_rings_of_hearthttp://en.wikipedia.org/wiki/Fibrous_rings_of_hearthttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/United_Stateshttp://en.wikipedia.org/wiki/United_Stateshttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_valvehttp://en.wikipedia.org/wiki/Pulmonary_valvehttp://en.wikipedia.org/wiki/Pulmonary_valvehttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Echocardiogramhttp://en.wikipedia.org/wiki/Echocardiogramhttp://en.wikipedia.org/wiki/Echocardiogramhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Pleural_cavityhttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Inhalationhttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Pulmonary_valvehttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Echocardiogramhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Echocardiogramhttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Pulmonary_valvehttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Inhalationhttp://en.wikipedia.org/wiki/Lunghttp://en.wikipedia.org/wiki/Pleural_cavityhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Medical_signhttp://en.wikipedia.org/wiki/Physical_examinationhttp://en.wikipedia.org/wiki/Echocardiogramhttp://en.wikipedia.org/wiki/Diastolehttp://en.wikipedia.org/wiki/Hearthttp://en.wikipedia.org/wiki/Right_ventriclehttp://en.wikipedia.org/wiki/Pulmonary_valvehttp://en.wikipedia.org/wiki/Pulmonary_arteryhttp://en.wikipedia.org/wiki/Chordae_tendineaehttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/United_Stateshttp://en.wikipedia.org/wiki/Myxomatous_degenerationhttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Mitral_valve_prolapsehttp://en.wikipedia.org/wiki/Fibrous_rings_of_hearthttp://en.wikipedia.org/wiki/Regurgitation_%28circulation%29http://en.wikipedia.org/wiki/Left_atriumhttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Left_ventriclehttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Mitral_valvehttp://en.wikipedia.org/wiki/Hearthttp://www.righthealth.com/topic/tricuspid_Regurgitation/overview/adam20?fdid=Adamv2_007321


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Figure 1: Illustration of a Ruptured Sinus of Aneurysm

Figure 2: Illustration of a Ruptured Sinus of Aneurysm

Figures show the TEE and Doppler examination. The 4 chamber view at 0 degree(Panel A) shows an aneurysmal sac protruding into the right atrium from the aortic root (openwhite arrows). Green arrows indicate tricuspid valve. Color Doppler shows turbulent flow(solid white arrows) from the aorta through the pouch into the right atrium (Panel B). Thesame saccular-like structure in the RA is seen in short axis view at 59 degrees with turbulentflow by color Doppler (Panels C & D). Interrogation by CW Doppler revealed continuousturbulent flow in systole and diastole (Panel E).


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Figure 3: Ventricular Septal Defect

Figure 4: Mitral Regurgitation


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Figure 5: Tricuspid Regurgitation

Figure 6: Pulmonary Regurgitation


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Figure 7: Pleural Effusion


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Statement of Objectives

Upon accomplishment of this case study, the participant should be able to:

1. Recognize and understand the disease condition;2. Identify predisposing and precipitating factors that could possibly contribute to the

occurrence of the disease;3. Understand the normal anatomy and physiology of the affected organs that are

affected by the underlying disease condition;4. Identify specific theoretical causes and clinical manifestations, and trace the

pathophysiology of the involved disease entity;5. Identify nursing problems and construct nursing care plans specifically;6. Identify ways of preventing the occurrence of the disease or problem by providing

health teachings upon the recommendation of the study.


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Patients Profile

I. Biographic Data

Name: Dora Age: 12 years old Date of Birth: 10/13/1997Sex: Female Address: Alaminos, Laguna Religion: Roman CatholicMarital Status: Single Occupation: Student

Chief Complaint: Nahihirapan po ako huminga at masakit po dibdib ko

Diagnosis: Ruptured Sinus of Valsalva and Ventricular Septal Defect withSevere Tricuspid and Mitral Valve Regurgitation, and Moderate PleuralEffusion.

II. HistoryA. Past Health History

An interview with t he mother was done to obtain the patients pasthealth history. Dora is the third child among the 6 siblings, who was born,term via normal spontaneous vaginal delivery at home by the local hilot or midwife. The patient was noted to be small for gestational age. Obstetricshistory as per the mothers information shows no consistent prenatal checkup

for all six offspring. The mother states that for the patient specifically, sheonly went on her third trimester to have a checkup. The mother also added thatshe usually use birth control pills but would often miss a dose.

During infancy, the patient was noted with diaphoresis when feeding,but no other symptoms were noted. After the third month of life, the patientwas left under the care of her paternal grandparents. As claimed, there was nohistory of recurrent respiratory tract infections. The mother however noted thather daughter had poor weight gain around that time. She also stated that she

cannot remember if her daughter had any vaccinations, except for polio givenat the local community center. The patient stayed with her grandparents untilthe age of 9, and moved back to her parents when the former passed away.


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B. History of Present Illness

A month and a half prior to her admission, Dora experienced fever andcough. By the end of March, the mother reported that her daughter had

episodes of dyspnea, easy fatigability, on and off fever, and progressive twopillow orthopnea. She also had episodes of bipedal edema, which on somedays are present and will disappear in a matter of weeks. This prompted themother to bring her to the local physician, who suggested to have a 2D Echodone. The result of the test was: Ruptured Sinus of Valsalva, SevereTricuspid Regurgitation, Severe Mitral Regurgitation, Mild PleuralRegurgitation, Moderate Pleural Effusion and Mild Pulmonary Hypertension.They were advised to seek consult at Philippine Heart Center but were notable to comply due to financial constraints. No other medications were takenand no other consults were done.

Persistent episodes of dypsnea, and chest plain prompted consult atPhilippine Heart Center.

C. Prenatal History

The mother is currently 43 years old with an obstetric scoring of Gravida 6, Para 6 with three Term, and three Preterm. She was 31 years oldwhen she gave birth to the patient. All were delivered via normal spontaneousvaginal delivery at home with the local hilot practitioners. She decided topractice artificial family planning on her second child using birth control pillsbeing given at the local community health center, but was not able to followher schedule properly. The mother admits that her third child up to the sixthwere results of missed doses. She does not remember any specific vaccinationsgiven to her during her childhood. The mother also states that she does notattend any prenatal checkup and would usually rely on local practices andprocedures.

Post Natal History

The patient was born term, with no noted abnormalities. The patienthas not undergone any newborn screening. The mother recalled she hadbreastfed the patient for a month before she was transferred to hergrandparents. Foods were introduced beginning on the sixth month. Themother stated that the patient seems too small on her sixth month. Regularvaccinations were not followed. At 10 years old, the patient began manifestingsize of easy fatigability, dyspnea and generalized weakness.

Episodes of dypsnea and fatigability would usually manifest when she engages

herself in high levels of activity. When symptoms became present, they areusually addressed by rest, and sleep in a side-lying position. Two months prior


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to admission, symptoms were becoming more frequent, thus prompting theparents to seek consultation for their daughter

D. Familial History

The patient states that both her parents were diabetic and hypertensive andthe same applies for her husband. Coronary Artery Diseases were also presentat the patients father side. The mother also noted that there is also a presenceof a congenital heart defect on the patients father side. However, the mother is not aware of the specific defect.

No other siblings have manifested any symptoms indicating congenitalheart problem, aside from the patient being presented.

E. Gordons Health Pattern

A. Health Perception and Health Management Pattern

The patient understands that she is not well, and she is willing to cooperateso that she can get better. The mother of the patient also understands herdaughters condition and would like to be a part of her health management inany way possible.

B. Nutritional and Metabolic Pattern

The patient states that her usual diet contains rice and vegetables,specifically kangkong or water spinach. On some occasions, she is able toeat chicken and pork. She does not take any supplemental vitamins. Thepatient is at present, 21 kilos.

C. Elimination Pattern

The mother recalls that prior her daughters admission, her daughter isurinating and voiding well, usually 2 to 3 times a day. The patient did notnotice anything significant in her elimination as well.

D. Activity-Exercise PatternThe patient states that her usual activity months prior to her admission

involves doing household chores, going to school, and helping out her parentssell figurines. She used to play together with kids of her own age, not until amonth prior to her admission when it became difficult to breathe and she getstired easily.

E. Sleep-Rest Pattern

The patient stated that she gets around 6 to 7 hours of sleep. A month priorto her admission, she stated it became difficult to sleep due to shortness of


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breath, which is usually resolved by lying on her left side and by usingpillows. Two days prior to her admission, she hardly gets any sleep at all dueto episodes of chest pain.

F. Cognitive- Perceptual Pattern

The patient has a good sense of vision, hearing, taste, touch and smell. Shehas no difficulty talking or remembering things. She is also oriented to timeand place.

G. Self-Perception and Self-Concept Pattern

The patient is concern about her current hospitalization and states that sheis afraid of the outcome of her present hospitalization and the implications of any treatment in her future activities. During the interview, the patient cannot

maintain good eye contact and would often hesitate expressing herself verbally.

H. Role-Relationship Pattern

Dora is the third child among the six siblings. Her mother and father areboth Highschool graduates, and earn their daily living by selling figurines at apublic market nearby. The mother stated that there are no issues regarding herfamily, and they are satisfied with what they currently have. She admits thaton some occasions, conflict would arise due to financial reasons but gets

easily resolved as well.

I. Sexuality-Reproductive Pattern

The patient has not experienced her menarche.

J. Coping-Stress Tolerance Pattern

The patient stated that by watching television and doing some activitiessuch as coloring books, playing jack stone would usually lessen the pain. Hermother is supportive as well, and is always present whenever she has shortnessof breath or an episode of pain begins.

K. Value-Belief Pattern

The patient and her family are all Roman Catholic who occasionallyattends Sunday services. The mother stated that their current socio-economiccondition has made them closer to their faith.


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Physical Assessment

(Done on May 17, 2010 5th day in the Pediatric Intensive Care Unit)

A. Vital Signs

Heart Rate: 126 beats per minuteRespiratory Rate: 32 breaths per minuteTemperature: 37.8 CBlood Pressure: 120/30(Arterial Line) 110/0 BP cuff Weight: 21 kg Height: 150 cm BMI: 9.33 (Underweight) Allergies: No known allergies

B. Central Nervous System

Dora is awake, ambulatory and coherent with a Glasgow Coma Scale of 15 (EyeResponse: 4, Verbal Response: 5, Movement: 6). No alteration in sensory status.

C. Cardiovascular System

The patient has an abnormal heart sound (thrill) heard at the 6 th Intercostal Space Leftanterior axillary line, with regular heart rhythm. The patient still presents SinusTachycardia. She also presents with dynamic precordium and suprasternal pulsation.The upper and lower peripheral pulses are also present. The sclerae are white, and shealso has a pink palpebral conjunctivae. Capillary refill is 2 3 seconds.

D. Respiratory System

The patient has an irregular breathing pattern with subcostal retractions and dyspnea.There is a decreased breath sound in the left lower lung, as well as the presence of crackles in the bibasal lung fields. The patient also prefers to sit up as this helps herbreathe easier. Uses of accessory muscles were also noted.

E. Gastro-Intestinal System

The patient has a flabby abdomen, with normoactive bowel sounds ranging from 8 to10 sounds in each quadrant. She also has a regular bowel pattern, with one bowelmovement in the morning and another in the evening.

F. Urinary System

The patient has a normal urine pattern with no bladder distensions. The 7 am to 3 pmIntake and output shows an output of 800 cc, whereas the input on the same timelinewas noted at 400 cc. The color of the urine is yellow; however, lab results revealed


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that there are traces of blood in the urine graded as +2, indicating hematuria and tracesof protein, graded as +2, indicating proteinuria.

G. Musculoskeletal System

The patient presents generalized body weakness and looks cachexic. She also presentsgrossly normal extremities with no deformities. The patient also scores a 3 out 5 inmuscle strength in all extremities, with good coordination. The patient needs someassistance in performing her activities in the hospital.

H. Integumentary System

The patient presents poor skin turgor and dry lips. No other deviations were observed.

I. Psychosocial and Cognitive Development

Under Ericsons Psychosocial Development, Dora is under the Identity vs. RoleConfusion and under Piagets Cognitive Development, she is under the FormalOperational Stage. Under the former, she has good interpersonal relationship withher parents as well as her siblings and friends. She misses her friends as well hersiblings. Even though there are some restrictions due to her health condition, she stillfinds time to do her household chores as well as her studies. Under the latter, sheenjoys doing different tasks such as coloring, reading, as well as answering

mathematical equations.


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Formation of weak aortic structures Ventricular septaldefect

Modifiable Factors:

Exposure to Teratogens: Father is an active smoker (3 packs per day) andexposure to passive smoking during pregnancy can increase the risk. Alcoho ldrinking of the mother may also contribute to the development of birthdefects.

Lifestyle: Attitude towards prenatal and newborn checkups was notprioritized. Health-seeking behavior such as knowledge about vaccinationsand family planning may also contribute as well.

Organogenesis

Development of the heart septum and valves occurs on the 6 th and 7 th week of pregnancy.

Allows progressive dilatation of the sinus eventuallyleads to Aneurysm of the Right Sinus .Continues Fillingand stagnation of blood. Aneurysm protrudes to the rightatrium and right ventricle.

Highlyturbulent bloodflow causesendothelial damagewhichpredisposestothe creationof lesions

Increasedsusceptibilityof infectionandmigration of bacteria to theheart, whichcausesinflammation.

EndocarditisNeutrophil: 42% and highlymphocytes: 48%(due toacitiveinfectious process: endocarditis),lowEosinophils: 1%ESR 40 mm/hr

Pathophysiology

Strain of aortic pressure. Aortic medial is defective andfragile. The sinus gradually weakens.

Separation of the media from the attachment of the leaflets,results into aortic media retraction.

Non-Modifiable Factors:

Genetics: As stated by the mother, there is history of Congenital Heart of the patients father si de.

Race: Asians (Filipino) Shows increased to acquire Aneurysm of the Sinusof Valsalva.

Age: 11 67 years old (Patient is 12 years old). Aneurysm and Ruptureincreases within this age group.

This causes obstruction on the ventricular outflow tract.Instability and progressive distortion of the right sinusleads to the compression of the chambers of the heart.

Alteration in electrical activity of the heart (SVT (on theECG reading on the 13 th of May, 2010 ,and SinusTachycardia with episodes of PVCs soon afterwards )

The progressive increase pressure on theright side of the heart, eventually to therupture of the sinus.

Sudden gush of blood will affect all chambers of theheart

Aortic Insufficiency(widened pulse pressure)


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Decreased Circulation to the Brain:

Signs and Symptoms:Occasional headache, Restless, syncope

Effects on the Right side of the heart:

Tricuspid valve regurgitation and Pulmonic Regurgitation

Signs and Symptoms:Jugular vein distention, Bipedal edema, increase blood pressure, increase pressureon the veins of the nasal area that leads to epistaxis (during hospitalization)

Effects on the Left side of the heart:

Mitral Regurgitation. Increase pressure and volume will leadto backflow from Left atrium to Pulmonary veins to the lungs,leading to pleural effusion.Signs and Symptoms:Crackles and Difficulty of Breathing (upon admission)

Progressive congestion leads to increased cardiac workload,thus leading to ineffective contractility of the heart.

Multi chamber hypertrophy

Decreased Cardiac Output

Decreased Circulation to the Kidney:

Signs and Symptoms:Altered function of the kidneyproteinuria and hematuria

Altered nutrition and decrease in appetite increases the risk andsusceptibility to infection. Easy fatigability due to decrease energysource.

Signs and Symptoms:BMI: 15.3


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63 rd Critical Care Course A Case of Ruptured Sinus of Valsalva

Narrative Pathophysiology

The Ruptured Sinus of Valsalva is caused by modifiable factor such as exposure toteratogens (father is an active smoker consuming 3 packs per day thus exposed to passivesmoking during pregnancy and non-modifiable factors namely; genetics (as stated by themother, there was a history of Congenital Heart Defect paternal side), race (asians showsincreased to acquire Aneurysm of the Sinus of Valsalva), Age aneurysm and Ruptureincreases within 11-67 age group).

These factors contribute to the malformation of heart structure during theorganogenesis period specifically on the 6 th to 7 th week of pregnancy .Generally, the defect isfocused at the aortic structure specifically the sinus which is one of the anatomic dilations of the ascending aorta, which occurs just above the aortic valve and is associated withventricular septal defect.

Aneurysms typically develop as a discrete flaw in the aortic media within one of thesinuses of Valsalva. Under the strain of aortic pressure, the sinus gradually weakens anddilates, causing the formation of an aneurysm. Lack of supporting tissue (eg, ventricularseptal defect) may contribute to instability and progressive distortion of the aortic sinus, oftenwith associated aortic insufficiency. Deficiency of the aortic media where it attaches to theaortic annulus produces dilation of the aortic sinuses over many years.

Distortion and prolapse of the sinus and aortic valve tissue leads to progressive aorticvalve insufficiency as manifested by widened pulse pressure. Continues filling and stagnation

of blood predisposes the aneurysm to shift to the right ventricle then the right atrium. Thiswill lead to obstruction of the right ventricular outflow and causes further compression. Itwill lead to altered electrical activity of the heart as manifested by sinus tachycardia,Supraventricular tachycardia, Atrial Fibrillation, Premature Ventricular Contractions andVentricular Tachycardia o n clients ECG strip.

Furthermore, it increases pressure on the Right and Left side of the heart. With thiscase, the right portion would have the initial affectation. First, the force exerted results to therupture of the sinus. There would be a sudden gush of blood that causes the pulmonary andtricuspid valve to regurgitate. On the other hand, the left side wound manifest mitral valveregurgitation and further destruction of the aortic valves happens. The pressure also causes

the backflow of blood to the left atrium to the pulmonary system thus formation of cracklesand fluid shift to the pleural space occur.

As the manifestations progress, cardiac workload also increases, ineffectivecontractility takes place and multi-chamber hypertrophy happens thereby leading tocardiomegaly. This causes compression of the diaphragm and becomes a contributory factorto the development of dyspnea, Further to this, decreased cardiac output in systemiccirculation occurs. In order for the body to compensate tachypnea and tachycardia aremanifested. Since oxygenation is compromised, two main body structures namely the brain(headache and syncope) and kidneys (proteinuria and hematuria) are affected.

On the other hand, the highly turbulent blood flow in the ventricular septal defectcauses endothelial damage which predisposes to the creation of lesion that increases
http://www.answers.com/topic/ascending-aortahttp://www.answers.com/topic/aortic-valvehttp://www.answers.com/topic/aortic-valvehttp://www.answers.com/topic/ascending-aorta


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63 rd Critical Care Course A Case of Ruptured Sinus of Valsalva

susceptibility of infection and migration of bacteria to the heart. Inflammation on theendometrium (endocarditis) causes fever and increased WBC.

Moreover, the hypermetabolic state occurs as well as insensible fluid loss causesincrease in energy consumption. This results to easy fatigability, powerlessness, and activity

intolerance. Appetite would also be decreased with the additional depression of the satietycenter as evidenced by weight loss, low body mass index and cachexia.

To further confirm the disease process, different lab examinations were conductedwhich revealed low HgB: 113g/L, HcT: 0.36, MCH: 25.5 pg, and MCHC: 318 g/L (related todecreased blood supply, active blood loss due to epistaxis, hematuria and nutritionalimbalance). Low Neutrophil: 42% and Eosinophils: 1%,high lymphocytes: 48% , plateletcount: 520 monocyte 8%, ESR: 40mm/hr and CRP: 51.4 mg/ml are due to the inflammatoryand infectious process in the endometrium. Lastly, because of the congestion and the rupture,chest x-ray and 2DECHO revealed valvular and heart structure problems.

A Case of Ruptured Coronary Sinus of Valsalva

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