Recognition of Cardiovascular Disorders



Recognition of Cardiovascular Disorders


Daniel J. Murphy Jr.



HEART MURMURS

Auscultation is a critical component of the physical examination of the infant or child. A proper examination is conducted in a quiet environment so that the examiner’s attention is focused entirely on the auscultatory findings. In general, a “pediatric” stethoscope is not necessary, and in some cases “neonatal” stethoscopes with long tubing and a small head may be inferior to an “adult” stethoscope, which transmits sounds more reliably. It is important to examine all areas of the body and listen over the precordium in addition to the right side of the chest and both sides of the back. Finally, the examiner should note any changes in the heart sounds caused by respiration or a change in the patient’s position. Children should be examined in the supine and standing positions so that the effect of a change in position on murmurs can be appreciated.

In addition to noting the characteristics of any murmurs, the examiner should assess the patient’s overall clinical condition, measure the heart rate and blood pressure,
and palpate the pulses in all the four extremities. The strength of the precordial impulse and the presence or absence of a thrill should also be noted. Finally, the first and second heart sounds (S1 and S2) should be characterized. Split heart sounds and the effect of respiration on the S2 should be noted. A split S1 is normal. The S2 normally splits variably with respiration. A fixed split of the S2 is characteristic of atrial septal defect. Any additional sounds—for example, clicks—should also be noted.

Most murmurs in infants and children are innocent murmurs that are not caused by any structural abnormality or pathologic flow (Table 24.1). The most common murmur in the newborn is a pulmonary branch stenosis murmur resulting from the relatively small size of the branch pulmonary arteries at birth. This is a systolic ejection murmur heard over the precordium and also in the right side of the chest and both sides of the back. The presence of a systolic ejection murmur in the right and left axillae is characteristic of a pulmonary branch stenosis murmur. This type of murmur is generally inaudible after the age of 4 months.

The Still murmur is a vibratory, musical, or buzzing noise heard during ejection, generally along the left sternal border. It can be heard at any age and is more prominent during an increase in cardiac output (e.g., fever, exercise). The Still murmur is loudest when the patient is in a supine position and becomes attenuated or inaudible when the patient stands. Any ejection murmur that increases in intensity when the patient is standing is likely pathologic and should prompt further investigation.

A venous hum is commonly heard in younger children in the upright position. This murmur is a continuous blowing sound created by the flow of blood in the large veins from the neck into the thorax. The murmur of a venous hum can be abolished by compressing the jugular veins on the ipsilateral side or by turning the patient’s head. This murmur could be confused with a patent ductus arteriosus.








TABLE 24.1 INNOCENT MURMURS IN INFANTS AND CHILDREN














































































Neonatal


Still


Venous Hum


Pulmonary Flow


Pitch


Medium to high


Low


High


Medium


Intensity


1-2/6


1-3/6


1-3/6


1-3/6


Time in cycle


Midsystolic


Midsystolic


Continuous


Midsystolic


Quality


Soft ejection


Vibratory, musical, buzzing


Soft blowing


Soft blowing


Location


1st and 2nd ICS, RSB, LSB, back


LLSB


Right and Left infraclavicular areas


2nd LICS


Increased by


Increased cardiac output


Supine, fever, exercise


Sitting, standing


Supine, expiration, ↑CO


Decreased by


Decreased cardiac output


Standing, valsalva


Supine, head turn, jugular compression


Upright, inspiration, ↓CO


Age appears


Birth-1 week


1-10 years


2-5 years


7-10 years


Age disappears


3-4 months


Puberty


7-10 years


Persists in adults


Produced by


Relatively small pulmonary arteries


Vibration in LVOT


Flow in jugular veins


Flow in RVOT


Confused with


Pulmonary branch stenosis


Hypertrophic cardiomyopathy


PDA


ASD or mild PS


ASD, atrial septal defect; CO, cardiac output; ICS, intercostal space; LICS, left intercostal space; LLSB, lower left sternal border; LSB, left sternal border; LVOT, left ventricular outflow tract; PDA, patent ductus arteriosus; PS, pulmonary stenosis; RSB, right sternal border; RVOT, right ventricular outflow tract.


Physiologic changes, especially in the perinatal period, affect the clinical examination findings, especially the features of murmurs. At birth, because the pulmonary artery resistance is elevated, the right ventricular and left ventricular pressures are nearly equal. Therefore, little blood flows from the left ventricle to the right ventricle in an infant with a ventricular septal defect immediately after birth, so that the holosystolic murmur of ventricular septal defect is rare during the first several days of life. As the pulmonary vascular resistance decreases during the first week, the volume and velocity of the flow through the ventricular septal defect increase to produce the typical holosystolic, harsh murmur associated with ventricular septal defect. On the other hand, stenotic lesions (e.g., aortic stenosis, pulmonary stenosis) are associated with high-velocity, disturbed flow during the systolic ejection period and cause systolic ejection murmurs immediately after birth.

In the newborn, in whom the pulmonary resistance and right ventricular pressure are elevated, moderate tricuspid regurgitation is common. In this setting, the jet of tricuspid regurgitation produces at the lower left sternal border a holosystolic murmur that is indistinguishable from the typical murmur of a ventricular septal defect. As the pulmonary resistance decreases, the murmur of the tricuspid regurgitation becomes less intense, lower in pitch, and eventually inaudible, usually during the first day or two after birth.


In the normal newborn, systolic ejection murmurs can be caused by:



  • Patent ductus arteriosus


  • Peripheral pulmonary stenosis


  • Flow through the right ventricular outflow tract (pulmonary flow murmur)


  • Vibration in the left ventricular outflow tract (Still murmur)

In comparison with innocent murmurs, pathologic murmurs tend to be louder, usually grade 3 or higher, and harsher. Holosystolic murmurs are always pathologic, as are murmurs associated with systolic clicks or an abnormal S2. Further evaluation is recommended for all children with a:



  • Diastolic murmur


  • Holosystolic or pansystolic murmur


  • Late systolic murmur


  • Very loud murmur


  • Continuous murmur, except for a venous hum

Most studies have shown that a pediatric cardiology consultation is more cost-effective than echocardiography performed without consultation as an initial step in the evaluation of a heart murmur.


SYNDROMES AND CONGENITAL HEART DISEASE

Congenital heart defects are a prominent feature of many chromosomal and genetic disorders (Table 24.2). The most commonly encountered syndromes are Down, Turner, Noonan, Williams, and DiGeorge. Each has a 33% to 90% incidence of associated congenital cardiac defects, and the spectrum of heart defects is unique for each syndrome. Fetal or postnatal screening with echocardiography is reasonable for these syndromes and others associated with multiple congenital anomalies.


FAMILIAL CARDIOVASCULAR DISEASE

There are a number of familial cardiovascular disorders that pose a significant risk to children and adolescents. A careful family history is essential and a family history positive for the following should prompt the practitioner to pursue further cardiac evaluation:



  • Dilated cardiomyopathy


  • Hypertrophic cardiomyopathy


  • Marfan syndrome


  • Muscular dystrophy


  • Long QT syndrome (congenital deafness, familial seizures, or syncope)


  • Sudden or premature death








TABLE 24.2 SYNDROMES AND CONGENITAL HEART DISEASE






















































































Syndrome


Congenital Heart Disease


Down (40%-50%)


AV canal defect, VSD, TOF


Turner (35%)


Coarctation, bicuspid aortic valve, AS


Noonan (80-90%)


Pulmonary stenosis, ASD, HCM


Williams (60%)


Supravalvar aortic stenosis, coarctation


DiGeorge (35%)


Conotruncal malformations (interrupted aortic arch, truncus arteriosus, TOF)


Alagille (95%)


Pulmonary artery stenosis, TOF, PS


Asplenia


Complex cyanotic CHD


CHARGE


VSD, ASD


Cri-du-chat (5p-)


Various congenital cardiac defects


De Lange


TOF, VSD


Diabetes (maternal)


Hypertrophic cardiomyopathy, VSD, TGA


Ellis van Creveld


Common atrium (ASD)


Fanconi


PDA, VSD


Fetal alcohol


VSD, ASD, TOF


Fetal hydantoin


ASD, VSD, coarctation


Goldenhar


TOF


Holt-Oram


ASD, VSD


Laurence-Moon-Biedl


TOF, VSD


Marfan


Aortic root aneurysm, mitral prolapse


Multiple lentigines (leopard)


Pulmonary stenosis


Polysplenia


Complex CHD


Rubella


PDA, peripheral pulmonary stenosis


Rubinstein-Taybi


PDA


Smith-Lemli-Opitz


VSD, PDA


Thrombocytopenia-absent radius


ASD, TOF


Tuberous sclerosis


Cardiac rhabdomyomas


AS, aortic stenosis; ASD, atrial septal defect; AV, atrioventricular; CHARGE, coloboma of the eye, heart defects, atresia of the choanae, renal anomalies and retardation of growth and/or development, genital anomalies in moles and ear abnormalities or deafness; CHD, congenital heart disease; HCM, hypertrophic cardiomyopathy; PDA, patent ductus arteriosus; PS, pulmonary stenosis; TGA, transposition of the great arteries; TOF, tetralogy of Fallot; VSD, ventricular septal defect.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jul 5, 2016 | Posted by in CRITICAL CARE | Comments Off on Recognition of Cardiovascular Disorders

Full access? Get Clinical Tree

Get Clinical Tree app for offline access