INDIVIDUAL

ASSIGNMENT
CARDIOVASCULAR
nd th
2 year / 4 Semester / 2018 / FMUI 2017
Gde Ngurah Irfan Bhaskara
1706067790– Group B

Diagnosis

Physical Examination and EKG

Introduction

In the trigger, a 20 years old female student was sent to the outpatient clinic due to
the complaint of exhaustion that occur easily ever since 6 months before she came there.
There were bluish transformation in the extremities specifically on her hands and toe nails,
or is called as cyanosis in the extremities.1 From history taking from her mother, it was found
that she was diagnosed with a congenital heart defect which was recommended with a
surgery, but her parents refused it. She had a normal growth, however her growth stopped
during elementary school which made her appear stunted or shorter than other girls at her
age.

From the physical examination provided in the trigger, we were able to reach a
hypothesis that the girl is having congenital ventricular septal defect, due to it’s unique clinical
manifestation of cyanosis and clubbing fingers, pan-systolic murmur, and right ventricular
hypertrophy. In this paper we would like to help confirm that by understanding the method
of diagnosis and is interpretation. I will be focusing on discussing the physical examination
and electrocardiography result.

Physical Examination

In this trigger, the physical examination includes; inspection, auscultation, blood

pressure measurement, heart rate measurement, body temperature, and peripheral
saturation. But according to Cardiology Explained textbook, it is mentioned that there should
also be measurement of jugular venous pressure measurement.2

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Anamnesis and Inspection

Anamnesis makes up for 80% of our diagnosis, in this phase we try to dig in into the
patient’s history regarding the chief complaint, history of illness, family history of illness,
nutrition, risk factors, and a lot more. Relating to congenital heart defect, we can find out the
what underlying condition that can possibly link the symptoms to the working diagnosis.2 In
this case, a patient with down’s syndrome is usually accompanied with atrial or ventricular
septal defect.2 And the rest is mentioned in Table 1 below.

Table 1: The genetic disorder correlated with the possible congenital heart defect.2

From inspection we will be able to find out clues about what the patient is going
through, for example patients who are acutely ill will present cyanosis, sweatiness, dyspnea,
and pallor which signs for danger.2 From inspection we can also find out what to do and not
to do during palpation, for example if there are burn marks we should not palpate the area
as it will result in pain, and if possible edema is seen, we can palpate the area to confirm it. 2
And note that pitting edema is a symptom of cardiovascular problem which is heart failure.3
The trigger also mentioned about cyanotic clubbing fingers and it is something that can be
observed by inspection. Clubbing fingers occurs due to the proliferation of the connective
tissues in the distal phalanges which increases the length and width of the nail.4 It has many
causes of underlying disease from most of our systems; respiratory system, cardiovascular
system, gastrointestinal system, endocrine system, and others. But regarding the
cardiovascular disease, the clubbing of fingers are
associated with cyanotic congenital disease and
sometimes infective endocarditis can manifest this
although milder.4
Fig. 1: The difference in Interphalangeal depth and
distal phalangeal depth of clubbing finger (b) and
normal finger(a).4

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Palpation

In palpation we are looking for apex beat or ictus kordis. Usually we can just put our
palm in an area around the 5th intercostal space and midclavicular line There can be
abnormalities found in the palpation of apex beat that signifies a problem in the heart. For
example, heaving or wavy movement usually signifies high afterload, lifting or thrusting
usually signifies for high preload or aortic regurgitation. While doing this with your right hand,
you can place your left hand on the sternum of the same level to check for right ventricular
heaving which shows right ventricular hypertrophy or thrilling which shows septal defect or
aortic stenosis.2

Pulse

Pulse is observed to obtain heart rate to identify tachycardia or bradycardia, strength

of pulse, and pattern. We can usually use the brachial or carotid artery as they are large
arteries which is easier to palpate and be observed.2 Usually checking radial arteries of both
hands is useful to do gross screening test for aortic dissection. Also peripheral pulses on
femoral, popliteal, posterior tibial, and dorsalis pedis is a good indicator for peripheral
vascular disease and predictor for coronary artery disease.2

Table 2: Type of pulses, it’s characteristics, and it’s possible causes.2

Jugular Venous Pressure

This is a test to find out the central venous pressure. Although the internal jugular vein
is the ideal one to be measure as it has direct connection towards the superior vena cava, the
external jugular vein is used since it is more observable as it is more superficial. 5 The central
venous pressure has a reference range of 4-10 cmH2O when it is larger it, signifies a problem.2
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Fig. 2: The position of patient to take the JVP.2

The patient is positioned at 0o at first, and is asked to face to the left and tilt the head
to expose and distend the external jugular vein but be careful not to tilt too much as it can
tighten the sternocleidomastoid muscle which can make the distension disappear.5 Additional
adjustments can be applied to expose the external jugular vein further.2 Then incline the
patient to 45o, the length of the “distended” jugular vein will be reduced, then draw a
horizontal imaginary line from the end of the “distended” jugular vein to the sternal angle
then measure the vertical distance between the imaginary endpoint with the sternal angle in
cm. then add 5cm because that is the distance between the sternal angle to the right atrium.5
the total represents the CVP.2 When it is above 10cmH2O, it is possible there is heart failure,
pulmonary embolism and hypovolemia.5

Fig. 3: The waveform of jugular vein pulsation.2

The pulsation pattern of the JVP can be

interpreted into a graph as it is biphasic.2 Each wave
represents a cardiac event just as described in figure 3.2
The changes in each waves can also signify different
problems which is shown in figure 4.

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Fig. 4: The abnormalities in JVP waveform and it’s possible causes.2

Auscultation

This was actually discussed before so I will only be explaining it briefly. Using the
stethoscope we can hear the heart sounds and at different locations we can hear different
sounds. It can either be the tricuspid valve closing, bicuspid valve closing, the aortic valve
closing or others. There are variations of heart sounds which is caused by not only the closure
of valves but also abnormal flow of blood or even valve prolapse. 2

Fig. 5 : the variations of heart sounds.2

S1 is caused by the closing of mitral and tricuspid valve, S2 is caused by closing of

semilunar valves. These are described as lub-dub sounds which are normal. The S2 can be
divided into 2 sounds pulmonic and aortic, it is a physiologic split when the patient fully
inhales causing the difference of the semilunar valves closure time. 2 MSC (Midsystolic click)
is heard when there is mitral valve prolapse. S3 gallop is caused by increased flow of blood
into the ventricle which maybe caused by dilated cardiomyopathy or something else. S4 is
almost impossible to distinguish, but when it is found, it usually belongs to athletes whom
have left ventricular hypertrophy.2

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 Murmurs are different it is formed when there is disturbance in the flow of blood, can
be caused by stenosis or regurgitation depending on the phase (systole or diastole) and it’s
location.2

In this trigger, it is mentioned that pansystolic murmur or holosystolic murmur is

observed. It can be due to tricuspid regurgitation, it can be due to tricuspid regurgitation or
ventricular septal defect. In VSD, it is heard because the blood travels from the left ventricle
into the right ventricle by the pressure gradient thus producing a holosystolic murmur.
Usually VSD is followed by a normal S2 which differentiate it from pulmonary stenosis where
there is splitting of S2.6 When it becomes Eisenmenger syndrome the holosystolic murmur is
replaced with midsystolic murmur or just a prominent S2 with no splitting even during
inspiration.6

Electrocardiography

In this trigger there is an alteration of QRS complex. In right ventricular hypertrophy there will
be a very high peak of R segment in precordial electrode (V1) which will decrease as it goes
towards V5.7 So the patient has hypertrophy of the right ventricle. Also there is T wave
inversion that suggests left ventricular hypertrophy and maybe a sign of ischemia if there are
ST elevation or depression. So it might be left ventricular hypertrophy, however the criteria
of LVH is that the sum of amplitude of S segment in V1 and R segment of V5 must be more
than 35mm in which in this case is just approximately 15mm.6 so it may be caused by ischemia
instead.6

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Conclusion

VSD can be confirmed for this patient from the result of history taking, auscultation
and support examination which is the EKG that shows right ventricular hypertrophy. However
the T inversion is yet to be explained because it still doesn’t match either LVH or ischemia.

References

1. Dorland’s pocket medical dictionary. 29th ed. Philadelphia: W. B. Saunders; 2013.

Cyanosis; P. 192
2. Ashley EA, Niebauer J. Cardiology explained. London: Remedica; 2004. Chapter 2;
Cardiovascular examinations.
3. Hayn, D., Fruhwald, F., Riedel, A., Falgenhauer, M., & Schreier, G. Leg edema
quantification for heart failure patients via 3D imaging. Sensors (Basel, Switzerland).
2008; 13(8);10584–10598.
4. Sarkar, M., Mahesh, D. M., & Madabhavi, I. Digital clubbing. Lung India : official organ
of Indian Chest Society. 2012; 29(4); 354–362.
5. Applefeld M M. Clinical methods: the history, physical, and laboratory examinations.
The jugular venous pressure and pulse contour. 3rd ed. Boston: Butterworths; 1990.
Chapter 19; The jugular venous pressure and pulse contour.
6. Walker HK, Hall WD, Hurst JW. clinical methods: The History, physical, and laboratory
examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 26; Systolic murmurs.
7. Dublin D. Rapid interpretation of ekg. 6th ed. 2000.