NurulHidayu: Medical state of mind

DOCTORS

6:02:00 PM
0 Comments

Congenital cardiovascular defects, also known as congenital heart defects, are structural problems that arise from abnormal formation of the heart or major blood vessels. ICD-9 lists 25 congenital heart defects codes, of which 21 designate specified anatomic or hemodynamic lesions. Defects range in severity from tiny pinholes between chambers that may resolve spontaneously to major malformations that can require multiple surgical procedures before school age and may result in death in utero, in infancy, or in childhood.

The common complex defects include the following:

Tetralogy of Fallot (TOF)
Transposition of the great arteries
Atrioventricular septal defects (ASD)
Coarctation of the aorta
Hypoplastic left heart syndrome

Incidence

Congenital heart defects are serious and common conditions that have significant impact on morbidity, mortality, and healthcare costs in children and adults.
The most commonly reported incidence of congenital heart defects in the United States is between 4 and 10 per 1,000, clustering around 8 per 1,000 live births.
Continental variations in birth prevalence have been reported, from 6.9 per 1000 births in Europe to 9.3 per 1000 in Asia.
An estimated minimum of 40,000 infants are expected to be affected each year in the United States. Of these, about 25%, or 2.4 per 1,000 live births, require invasive treatment in the first year of life.

Mortality

Mortality related to congenital cardiovascular defects in 2013 was 3,051. Any-mention mortality related to congenital cardiovascular defects in 2013 was 4,916.

Risk Factors

Numerous intrinsic and extrinsic non-genetic risk factors contribute to congenital heart defects.

Known maternal risks include maternal smoking during the first trimester of pregnancy. Exposure to secondhand smoke has also been implicated as a risk factor.
Maternal binge drinking is also associated with an increased risk of congenital cardiac defects, and the combination of binge drinking and smoking may be particularly dangerous.
A greater risk of congenital heart defects is also seen in women who both have a high BMI. Gestational DM has also been associated with cardiac defects, both isolated and multiple.
Folate deficiency is a well-accepted risk for congenital defects, including congenital heart defects, and folic acid supplementation is recommended during pregnancy

Congenital Heart Defects #NCLEXprep #NursingStudent:

Cyanotic vs Acyanotic Congenital Heart Disease:

cyanotic and acyanotic heart defects - Google Search:

acyanotic heart defects in neonates - Google Search:

Educating parents about congenital heart defects (Infographic):

1:52:00 AM
0 Comments

Physiological Changes during Pregnancy

3rd year medical student

8:32:00 PM
0 Comments

All About Heart !

3rd year medical student

F E T A L

C I R C U L A T I O N

M U R M U R S

What is murmurs?

When normal laminar blood flow within the heart is disrupted, an audible sound is created by turbulent blood flow. Outside of the heart, audible turbulence is referred to as a bruit, whereas inside the heart it is called a murmur.

There are four major causes of cardiac murmurs:

Valvular stenosis: If blood is forced through a tight area, turbulent blood flow ensues, as is the case in valvular stenosis. Generally, the worse the stenosis, the louder the murmur; however, if heart failure develops, adequate pressures to create turbulent blood flow may not be able to be achieved, and the murmur may lessen or even disappear. Thus, the intensity of a murmur is not used to indicated severity of disease.
Valvular insufficiency: Blood abnormally travels backward through an incompetent valve in valvular insufficiency, causing turbulence when it meets normal, forward blood flow.
Congenital anomaly: If blood is forced through a congenital anomaly from one chamber to another, as in an atrial septal defect (ASD) or ventricular septal defect (VSD), a murmur is produced — again due to turbulence.
Increased blood flow: Yet another cause of cardiac murmurs is increased flow of blood through a normal valve. In high-output states such as anemia, thyrotoxicosis or sepsis, a large volume passes through the cardiac valves, and the normal laminar blood flow may be disturbed. Still's murmur is a normal aortic flow murmur frequently heard in childhood that frequently disappears over time.

Murmurs

by American Family Physician

Precordial Palpation

The cardiac examination begins with palpation to assess precordial activity and femoral pulses. Increased precordial activity is commonly felt in patients with increased right or left ventricular stroke volume. Increased pre-cordial activity occurs in patients with an atrial septal defect, a moderate or large ventricular septal defect or significant patent ductus arteriosus. This increased activity should raise the possibility that the auscultatory findings may be pathologic. Other explanations for increased precordial activity include patient anxiety, anemia and hyperthyroidism.

Once both brachial pulses have been palpated, the right brachial pulse should then be palpated simultaneously with the femoral pulse. If the timing and intensity of the two pulses are equal and blood pressure in the right arm is normal, coarctation of the aorta is unlikely.

Precordial palpation is also necessary to feel “thrills,” which are the palpable consequence of blood flowing rapidly from high pressure to lower pressure. Some ventricular septal defects result in thrills at the lower left sternal border. Moderate to severe pulmonary valve stenosis may cause a thrill at the upper left sternal border. A thrill resulting from aortic stenosis is frequently palpable in the suprasternal notch.

Auscultation of First and Second Heart Sounds

Precordial palpation is followed by auscultation. This part of the examination entails separate evaluation of each heart sound and each phase of the cardiac cycle.

FIRST HEART SOUND

Auscultation begins with listening for the first heart sound (S1) at the lower left border of the sternum. The S1 is caused by closure of the mitral and tricuspid valves and is normally a single sound. An inaudible S1 indicates that some sound is obscuring the closure sound of these valves. The differential diagnosis for murmurs that obscure S1 includes ventricular septal defects, some murmurs caused by atrioventricular valve regurgitation, patent ductus arteriosus and, occasionally, severe pulmonary valve stenosis in a young child. These S1-coincident murmurs are also known as “holosystolic” murmurs.

CLICKS

If S1 is audible but appears to have two components at some spots in the precordium, the patient has either a click or an asynchronous closure of the mitral and tricuspid valves. Clicks may originate from any valve in the heart. Depending on their origin, clicks have different identifying characteristics.

Ejection clicks originating from the pulmonic valve begin shortly after the atrioventricular valves close, vary with respiration and are best heard at the upper to middle area of the left sternal border. Aortic valve ejection clicks begin shortly after S1 and are best heard at the apex. They do not vary with respiration.

Systolic clicks originating from the mitral valve are best heard at the apical area when the patient is standing. Occasionally, the tissue closing a ventricular septal defect can pop or click early in systole.

SECOND HEART SOUND

After auscultation for clicks throughout the four listening areas, the next step is to return to the upper left sternal border and listen to the second heart sound (S2). This sound is caused by closure of the aortic and pulmonic valves.

The S2 should split into two components when the patient inspires. The first component, aortic second sound (A2), is closure of the aortic valve. The second component, pulmonic second sound (P2), is caused by closure of the pulmonary valve. The splitting of S2 occurs because inspiration brings more blood into the right ventricle. Right ventricular ejection is prolonged, and the pulmonary valve closes later. An awareness of this phenomenon is helpful in understanding the physical examination features of the patient with an atrial septal defect. A loud, single S2 indicates either pulmonary hypertension or congenital heart disease involving one of the semilunar valves.

Murmurs

Systolic murmurs have only a few possible causes: blood flow across an outflow tract (pulmonary or aortic), a ventricular septal defect; atrioventricular valve regurgitation, or persistent patency of the arterial duct (ductus arteriosus). Systolic murmurs can also be functional (benign).

GRADES

Systolic murmurs are graded on a six-point scale. A grade 1 murmur is barely audible, a grade 2 murmur is louder and a grade 3 murmur is loud but not accompanied by a thrill. A grade 4 murmur is loud and associated with a palpable thrill. A grade 5 murmur is associated with a thrill, and the murmur can be heard with the stethoscope partially off the chest. Finally, the grade 6 murmur is audible without a stethoscope. All murmurs louder than grade 3 are pathologic.

TIMING

Systolic murmurs may be timed as early, middle or late systolic. They can also be timed as holosystolic.

VENOUS HUMS

Many children with functional murmurs have venous hums. These sounds are caused by the flow of venous blood from the head and neck into the thorax. They are heard continuously when the child is sitting. The sounds should disappear when light pressure is applied over the jugular vein, when the child's head is turned or when the child is lying supine. Venous hums are common and are not pathologic. Patients with venous hums do not require pediatric cardiology referral. All other diastolic murmurs are pathologic and therefore warrant referral.

DESCRIPTION OF CHARACTER

The character, or tone, of a murmur may aid in the diagnosis. Words such as “harsh,” “whooping,” “honking,” “blowing,” “musical” and “vibratory” may be useful, albeit somewhat subjective, in describing murmurs.

A “harsh” murmur is consistent with high-velocity blood flow from a higher pressure to a lower pressure. “Harsh” is often appropriate for describing the murmur in patients with significant semilunar valve stenosis or a ventricular septal defect.

“Whooping” or “blowing” murmurs at the apex occur with mitral valve regurgitation. The term “flow murmur” is often used to describe a crescendo/decrescendo murmur that is heard in patients with a functional murmur. However, similar systolic ejection murmurs may be heard in patients with atrial septal defect, mild semilunar valve stenosis, subaortic obstruction, coarctation of the aorta or some very large ventricular septal defects.

Many functional or innocent murmurs are “vibratory” or “musical” in quality. Still's murmur is the innocent murmur most frequently encountered in children. This murmur is usually vibratory or musical.

LOCATION OF HIGHEST INTENSITY

The location of the highest intensity of a murmur is also important (Table 1). A murmur caused by aortic stenosis is often best heard at the upper sternal border, usually on the right side. A murmur resulting from pulmonary stenosis is heard best at the upper left sternal border. A murmur caused by a ventricular septal defect or tricuspid valve insufficiency is heard at the lower left sternal border. A murmur resulting from mitral valve regurgitation is best heard at the apex.

TABLE 1

Listening Areas for Common Pediatric Heart Murmurs

AREA	MURMUR
Upper right sternal border	Aortic stenosis, venous hum
Upper left sternal border	Pulmonary stenosis, pulmonary flow murmurs, atrial septal defect, patent ductus arteriosus
Lower left sternal border	Still's murmur, ventricular septal defect, tricuspid valve regurgitation, hypertrophic cardiomyopathy, subaortic stenosis
Apex	Mitral valve regurgitation

POSITION CHANGES IN THE DIFFERENTIATION OF MURMURS

Position changes are very helpful in differentiating functional and pathologic murmurs. The vibratory functional murmur heard in a young child (Still's murmur) decreases in intensity when the patient stands.

Most pathologic murmurs do not change significantly with standing. An important exception is the murmur of hypertrophic cardiomyopathy, a potentially life-threatening condition. This murmur increases in intensity when the patient stands. In the upright position, venous return to the heart is reduced, decreasing the left ventricular end diastolic volume. As left ventricular size decreases, the left ventricular outflow tract narrows, and the systolic outflow obstruction increases. This narrowing increases the intensity of the murmur. Overall, hypertrophic cardiomyopathy is rare; however, it is one of the leading causes of sudden death in athletes.

Atrial Septal Defect

Perhaps the best way to decide whether a patient needs to be referred to a pediatric cardiologist is to know confidently the clinical findings of the atrial septal defect. The abnormal findings in patients with atrial septal defects are often quite subtle and thus are easily confused with the physical findings in patients with functional or innocent murmurs (Table 2). Loud murmurs from ventricular septal defects or significant aortic or pulmonic stenosis are not subtle and are not often confused with innocent murmurs.

TABLE 2

Physical Findings in Functional (Innocent) Heart Murmur and Atrial Septal Defect

PHYSICAL FINDING	INNOCENT MURMUR	ATRIAL SEPTAL DEFECT
Precordial activity	Normal	Increased
First heart sound (S1)	Normal	Normal
Second heart sound (S2)	Splits and moves with respiration	Widely split and fixed (i.e., does not move with inspiration)
Systolic murmur (supine)	Crescendo/decrescendo	Crescendo/decrescendo
	Possibly vibratory at lower left sternal border	“Flow” at upper left sternal border
Systolic murmur (standing)	Decreases in intensity	Does not change
Diastolic murmur	Venous hum	Inflow “rumble” across tricuspid valve area

The first step in the examination is palpation for the precordial activity at the left sternal border, feeling for increased activity that may be present from right ventricular enlargement. The examination is performed with the patient in a supine position.

Auscultation at the lower left sternal border should reveal a normal, single and easily audible S1. Listening at the upper left sternal border for S2 should reveal variable splitting with respiration. A widely split S2 that does not change with respiration indicates either complete right bundle branch block or an atrial septal defect.

Because of the increased volume of blood in the right ventricle in the patient with an atrial septal defect, the S2 always sounds as if the patient has taken a deep breath. This means that the volume of blood in the right ventricle is increased and it takes longer for the ventricle to eject its contents, thus leading to a fixed, widely split S2.

Murmurs heard in patients with atrial septal defects are often of low pitch and intensity. However, the intensity of the murmur is not a reliable basis for the diagnosis. The systolic murmur is caused by an increased volume of blood coursing across the right ventricular outflow tract. If the murmur is audible, it can be heard at the upper left sternal border.

Patients with atrial septal defects may also have a diastolic murmur. In this situation, increased diastolic blood flow across the tricuspid valve may cause a soft, often barely audible low-frequency “diastolic rumble.” This sound is heard best with the bell of the stethoscope placed at the lower left sternal border. Pushing down with the bell causes the skin beneath the stethoscope to act as a diaphragm. Consequently, only the high-frequency sounds are heard. Releasing the tension on the bell allows the low-frequency rumbling sound to become audible at the lower left sternal border.

After the supine examination, the examination should be repeated with the patient standing. If the patient has an atrial septal defect, the features of increased precordial activity, a widely split S2, a systolic murmur at the upper left sternal border and a diastolic rumble should still be present when the patient is standing. If the patient has an innocent or functional murmur, the precordial activity should be normal, the S2 should split and move with respiration, the systolic murmur should decrease in intensity and no diastolic murmur should be present in the tricuspid valve area.

If no symptoms are present, the S1 is normal, the S2 splits and is of normal intensity, and no clicks are heard, the differential diagnosis of a grade 1 to grade 2 systolic murmur is frequently a choice between an atrial septal defect and a functional murmur.

In young children, it can be difficult to confidently distinguish the respiratory variation of S2 splitting in the patient with a normal murmur from the fixed S2 splitting in the patient with an atrial septal defect. Because the patient with an asymptomatic atrial septal defect will not develop pulmonary hypertension or other permanent sequelae early in life, careful yearly follow-up examination by the primary care physician can be recommended. By the time a child reaches preschool age, the normal or abnormal splitting of the S2 usually becomes clear (Table 3).

TABLE 3

Features That Increase the Likelihood of Cardiac Pathology

Symptoms such as chest pain

Family history of Marfan syndrome or sudden death in young family members

Malformation syndrome (e.g., Down syndrome)

Increased precordial activity

Decreased femoral pulses

Abnormal second heart sound

Clicks

Loud or harsh murmur

Increased intensity of murmur when patient stands

The Authors

MICHAEL E. MCCONNELL, M.D., is associate professor of pediatrics at East Carolina University School of Medicine, Greenville, N.C. Dr. McConnell received his medical degree from the University of Alabama School of Medicine, Birmingham. He completed a pediatric residency at Children's Hospital, Birmingham, Ala., and a fellowship in pediatric cardiology at Children's Hospital Medical Center, Cincinnati.

SAMUEL B. ADKINS III, M.D., is assistant residency director and director of primary care sports medicine for the family practice residency program at East Carolina University School of Medicine. Dr. Adkins graduated from the University of Pittsburgh School of Medicine and completed a residency in family practice at St. Margaret Memorial Hospital, Pittsburgh.

DAVID W. HANNON, M.D., is associate professor of pediatrics at East Carolina University School of Medicine. Dr. Hannon received his medical degree from the University of South Florida College of Medicine, Tampa, and completed a pediatric residency and a cardiology fellowship at Children's Hospital Medical Center, Cincinnati.

REFERENCES

hide references

1. Rosenthal A. How to distinguish between innocent and pathologic murmurs in childhood. Pediatr Clin North Am. 1984;31:1229–40.

2. McCrindle BW, Shaffer KM, Kan JS, Zahka KG, Rowe SA, Kidd L. Factors prompting referral for cardiology evaluation of heart murmurs in children [Letter]. Arch Pediatr Adolesc Med. 1995;149:1277–9.

3. Danford DA, Nasir A, Gumbiner C. Cost assessment of the evaluation of heart murmurs in children. Pediatrics. 1993;91:365–8.

4. Hurwitz RA, Caldwell RL. Should pediatric echocardiography be performed in adult laboratories? [Abstract] Pediatrics 1998;102:390. Complete text at e15 at: www.pediatrics.org.

5. Pelech AN. The cardiac murmur: when to refer? Pediatr Clin North Am. 1998;45:107–22.

6. Maron BJ, Epstein SE, Roberts WC. Causes of sudden death in competitive athletes. J Am Coll Cardiol. 1986;7:204–14.

Findings

Cyanotic Congenital Heart Defects... A single S2 can be caused by Transposition of the Great Vessels, Tricuspid atresia, and truncus arteriosus... A single S2 with NO murmur = TRANSPOSITION OF THE GREAT VESSELS... This is the most common congenital cyanotic heart defect:

8:54:00 PM
0 Comments

3rd week of Paediatric Posting

3rd year medical student

2:20:00 AM
0 Comments

The formula of studying is equal to 'student' plus 'dying' - make sense!

assignments

Now only I knew how hard the student in Malaysia tried to survive in medicine. What happen to our student in Egypt?

Serious talk, Egypt was toooooo lenient. I live in Egypt for almost 3 years. Some of them are excellent students, but some of them just 'cukup cukup makan' like I used to be. Haha. In Egypt, there are no such things as assignments or homework that have carry marks.

We have holidays and we make of the holiday really well. Because we already living in other people's country, we're dying to enjoy their sceneries and cultures as much as we can before going back to Malaysia and Instagram seems to be really useful to share the moments.

In Malaysia, especially when you're a medicine student.. you will never had chances to watch RunningMan. Kalau ada masa pun, confirm tak dapat tengok sampai habis. Presentations and assignments are piled over. Haha sampai naik pening tak tahu nak buat yang mana satu dulu. Semua pun due hari dekat dekat.

Push yourself because no one else is going to do it for you.

So macam mana aku study kat Malaysia? Kerja memang bertimbun and assignments jadi berganda sebab aku kena juga buat assignment yang sebelum ni and due untuk hantar pun sama dengan assignment yang baru. Dulu kat Mesir aku selalu tidur awal, sebab kelas aku pagi je and setiap hari only one hour class. Now? Dengan assignment bertimbun, weekends pun tak rasa macam weekends. Aku sekarang tidur pun paling lewat pkul 1 pagi, kadang tu pukul 3 pagi. Library Lincoln tu dah macam tempat lepak aku lepas kelas. Assignment semua at least suku pun jadilah dapat siapkan kat library tu. Penat memang penat. Tapi at least aku nampak kat mana hardwork aku en? Kalau kat Mesir satu hari tu boleh marathon RunningMan sampai 4-5 episodes weh! Nak sentuh buku international pun malas sebab tak ada keperluan. Semua bergantung pada buku ghamaah.

Sampai sini, first thing doktor bagitahu ialah jenis buku rujukan yang dia selalu pakai, which is memang aku dah pinjam kat library.

Biochemistry - Harper's

Physiology - Guyton's

Anatomy - Snell's

Physiology kalau nak baca Gannong's pun boleh sebab aku minat lagi Gannong's dari Guyton's. Untuk Anatomy, aku beli dah Gray's Anatomy kat Maarub khutub, Cairo. Tapi kat sini dia nak Snell's pulak dah. First time aku dengar lecturer nak guna buku international, I was like... speechless for 10 secs. I dont even know how to understand the International books. I used to bergantung pada slides the doctors gave to us. But, it was too brief and I need to access internet and look out of the reference book. Nak beli agak mahallah kalau yang original. Harper's aku pinjam library since library ada plenty of it. Guyton's aku tak jumpa lagi. Haih.

Sempat jugaklah aku pergi jalan jalan kat Paradigm. Yeah, being a medicine student bukan senang. Tapi, sebab kau dah pilih bidang ni, bukan senang nak give up and start fresh bidang lain. I walk slowly, but I'll never walk backward. Try survive kayy, future doctors?

Sometimes, kau need to step outside, hirup udara segar and remind yourself of who you are and who you want to be. Keep going. No matter what you do, no matter how many times you screw up and think to yourself,"there's no point to carry on", no matter how many people tell you that you can't do it - keep going. Don't quit.

Don't quit, because a month from now you will be that much closer to your goal than you are now. Yesterday you said tomorrow. Make today count.

Okay, if nothing's going right.. then go left! Hahaha, just kidding.

Bila ada assignments, terus buat. Jangan tangguh, jangan postpones. Ntah ntah esk lusa doktor tambah lagi kerja. Setiap minggu pun jadual betukar kalau kat Malaysia ni. Have faith guys. Tak ada siapa kata medicine ni mudah. I'm not telling you it is going to be easy, I'm telling you it's going to be worth.

Tapi kau kena kuat, physically and mentally. There's is no elavator to success, you need to take the stairs.