CARDIOLOGY

DANIL HAMMOUDI.MD

 

 

 

 

 

 

 

Tips for clinical examination

§          Always introduce yourself and be courteous to the patients

§         Ask for permission before examination

§         Avoid hurting the patient

§         Listen to the instruction carefully

§         Do not forget to observe the patient first for examples hearing aid or dermatitis etc.

§         Learn to describe the physical findings before giving the likely diagnosis

§         Do not rush in the examination. Remember more than one signs may be present. (This may be associated or coincidental)

§         Do not panic if you do not know the diagnosis. Give the physical findings and provide a list of differential diagnosis (you may want to classify the pathology as congenital or acquired; congenital may be inherited or non-inherited and acquired may be traumatic, nepotistic, inflammatory, iatrogenic etc.)

§         Present your findings confidently and look the examiner in the eyes. Avoid using words "may be, I think, could be"

§          Treat each case as new and do not let a bad case affect your subsequent examination

§         Avoid derogatory such as syphilis, cancer or multiple sclerosis. Use euphemism or medical jargons instead such as St.Louise's disease, neoplasm or demyelinating diseases

§         Thank the patients and examiners at the end of the examination even if the whole thing go badly.

 

Most cases have vascular diseases involving the eye or the visual pathway. Therefore, look for abnormal rhythm and left sided valvular disorders. The most likely cases are:

 

  1.  
    1. Vascular Exam (Arterial Bruits or diminished pulses)
      1. Abdominal aorta
      2. Iliac artery
      3. Femoral artery
      4. Carotid artery
      5. Subclavian artery
    2. Local Signs of Peripheral Vascular Disease
      1. Decreased skin temperature
      2. Shiny skin
      3. Skin hairless over lower extremity (e.g. shin)
      4. Dystrophic Toenails
      5. Distal extremity color change with position
        1. Skin pallor when leg elevated
        2. Skin rubor when leg dependent

 

 

 

MURMURS

BASAL SYSTOLIC MURMUR:

 

 

MIDPRECORDIAL MURMUR:

 

APICAL SYSTOLIC MURMUR

 

SYSTOLIC CLICK

1.      ANEURYSM IN ASCENDING AORTA,

2.      COARTATION OF AORTA,

3.       HTA WITH AORTIC DILATION,

4.      VALVULAR AORTIC STENOSIS,

5.       AORTIC REGURGITATION

 

·        PULMONARY VALVE STENOSIS

·        PULMONARY ARTERY DILATION

·        [DECREASE OR DISAPPEARS WITH INSPIRATION

·        INCREASED WITH EXPIRATION

 

 

 

 

APICAL SYSTOLIC MURMUR WITH MIDSYSTOLIC CLICK:

·        MITRAL LEAFLET PROLAPSE

 

 

Areas of the heart

Mitral
Tricuspid
Pulmonary
Aortic

Heart Sounds

1st Heart Sound, S1

This signals the onset of systole and is caused by the closure of the mitral and tricuspid valves with concomitant tensing of the left ventricular wall. The mitral valve closes slightly before the tricuspid valve but the two sounds are usually merged. Splitting is marked in tricuspid stenosis or right bundle branch block. NB The 1st sound can be identified by palpating the carotid pulse while auscultating - the upstroke of the carotid pulse closely follows the 1st heart beat.

2nd Heart Sound, S2

This separates systole and diastole. The sound is made by the closure of aortic and pulmonary valves. The aortic valve closes before the pulmonary valve and this splitting of the second sound is heard particularly during inspiration, as more blood is drawn into the right ventricle, a normal phenomenon. (This occurs because right heart venous return varies with respiration). During expiration the split sounds of S2 resynchronise. The sound of pulmonary valve closure (P2) is best heard over the pulmonary area as it is much quieter than that of aortic valve closure (A2).

3rd & 4th Heart Sounds

These are low pitched (so heard best with the bell) and not usually heard.

If either S3 or S4 is very loud a gallop/triple rhythm will result.

Loud S3 rhythm = S1----S2--S3 ie crotchet-quaver-quaver

Loud S4 rhythm = S4-S1-----S2 ie semiquaver-crotchet-crotchet

3rd Heart Sound, S3

This is produced by rapid ventricular filling and occurs in early-mid diastole ie soon after S2

Occurs normally in young fit adults with bradycardia eg athletes

Occurs abnormally in

4th Heart Sound, S4

This is an atrial sound, occurring just before S1. It is always abnormal as it represents atrial contraction against a stiffened ventricle eg due to aortic stenosis or hypertensive heart disease. It may also occur in heart failure.

Added Sounds

Ejection systolic clicks - usually due to aortic stenosis and systemic hypertension but can be to pulmonary stenosis or pulmonary hypertension.

Mid-systolic clicks occur in mitral valve prolapse.

Opening snap may occur in mitral or tricuspid stenosis.

Prosthetic valves make noises on opening and closing.

A pericardial friction rub is a creaking sound heard in systole or diastole which suggests pericarditis (could be viral, post MI, due to CTdisease, trauma or uraemia) so look for an associated pericardial effusion.

Murmurs

Murmurs are caused by turbulent blood flow; this may be due to a stenotic or regurgitant valve producing a high velocity jet; alternatively it may be due to increased flow velocity in a normal vessel or to normal velocity flow in a dilated or distorted vessel; non-pathological causes include the murmur of the hyperdynamic system in pregnancy or a minor anatomical distortion with no pathological consequences (innocent murmur).

Bell is good when listening to low-pitched sounds eg mitral stenosis. Diaphragm is good when listening to high-pitched sounds eg aortic regurgitation.

How to amplify murmurs

Left heart murmurs are accentuated in expiration; right heart murmurs are accentuated in inspiration

Performing the Valsalva manoeuvre (get patient to strain silently)

NB Sudden squatting has the opposite set of effects to performing the Valsalva manoeuvre.

Mitral stenosis will be heard better if the patient rolls into the left lateral position.

Aortic regurgitation will be heard better if the patient leans forward.

Murmurs are also amplified by exercise due to increase in cardiac output.

Systolic murmurs

1) Ejection systolic murmur = crescendo-decrescendo murmur

This originates from the outflow tract, waxing and waning with changing intra-ventricular pressure.

It may be a flow murmur, common in childhood and pregnancy, or a pathological murmur as in

2) Pansystolic murmur

Of uniform intensity and merges with S2 although it may obscure both S1 and S2. It is usually caused by jets passing from a high pressure chamber to a low pressure chamber during systole ie mitral or tricuspid regurgitation. A pansystolic murmur also occurs when there is a ventricular septal defect.

3) Late systolic murmur

This is caused by mitral valve prolapse or papillary muscle dysfunction. It is a high-pitched murmur of even intensity which starts halfway through systole with a mid-systolic click and terminates with A2. NB If the papillary muscle rupture has occurred posteriorly then this murmur will be loudest in the aortic area (instead of the mitral area where it is heard most of the time).

Diastolic murmurs

1) Early diastolic murmur

This is high-pitched and usually only heard as the "absence of silence" in early diastole.

It occurs due to aortic or pulmonary regurgitation. The aortic regurgitation murmur is usually soft and is best heard with the patient leaning forward and in expiration.

NB When pulmonary regurgitation is due to pulmonary hypertension caused by mitral stenosis then the early diastolic murmur is called a Graham-Steel murmur.

2) Mid-diastolic murmur

This is low-pitched and rumbling; it starts after an opening snap.

Caused by

Other murmurs

1) Continuous, machinery murmur of patent ductus arteriosus.

2) Musical or "mewing" murmurs - characteristic of a hole in an aortic valve cusp due to endocarditis

3) Innocent murmur

 

 

Hands
Radial pulse - for rate and rhythm
Carotid pulse - for character
Face
Eyes
Mouth
JVP
Inspection of precordium
Palpation
Auscultation
Chest
Sacral oedema
Abdomen
Peripherally
Finally

The Signs of Different Conditions

Aortic Stenosis (Uncomplicated)
Mitral Regurgitation (Uncomplicated)

 

Abnormalities of the JVP

1) Raised JVP with normal waveform

2) Raised JVP with absent pulsation

3) Large a wave

4) Extra-large a wave = Cannon wave

Occurs when atrium contracts against closed tricuspid eg

ie any condition in which the atria and the ventricles are not conducting in appropriate rhythm

5) Absent a wave

6) Systolic waves = combined c-v waves = big v waves

7) The slow y descent occurs in tricuspid stenosis (if the HR is so low as to allow the length of descent to be appreciated!)

8) Paradoxical JVP = Kussmaul's sign

Normally the JVP should rise on expiration and fall on inspiration.

When the JVP rises on inspiration it indicates

Right Ventricular Failure

·         R side heart failing

·         Pooling blood IVC< V

·         Raised JVP

·         Hepatomegaly

·         Ankle oedema

·         Cyanosis

·         Signs of what caused it

Pericardial Disease

·         Pericarditis

o        friction rub

·         Tamponade

o        JVP raised

o        very reduced heart sounds

§         apex beat impalpable

o        hypotension

Aortic Stenosis

·         Narrowing imposes a pressure load on LV

·         Restricts LV outflow

·         Midsystolic harsh ejection murmur

·         Max at aortic area

·         Loudest sitting and expiration

Blood Pressure Classification in Adults

Category

Systolic

Diastolic

Normal

<130

<85

High Normal

130-139

85-89

Mild Hypertension

140-159

90-99

Moderate Hypertension

160-179

100-109

Severe Hypertension

180-209

110-119

Crisis Hypertension

>210

>120

 

What does a blood pressure of 170/80 indicate?

Pure Systolic Hypertension

Murmurs and Extra Sounds


Systolic Ejection

Innocent/Physiologic
Aortic/Pulmonic Stenosis


Pansystolic

Mitral/Tricusp Regurgitation
 

Systolic Click
Late Systolic

Mitral Valve Prolapse
 


Early Diastolic

Aortic Regurgitation


Mid Diastolic

Mitral/Tricusp Stenosis

Opening Snap
Diastolic Rumble

Mitral Stenosis


Ejection Sound

Aortic Valve Disease
 


S3

Normal in Children
Heart Failure


S4

Physiologic
Various Diseases

 

Murmur Grades

Grade

Volume

Thrill

1/6

very faint, only heard with optimal conditions

no

2/6

loud enough to be obvious

no

3/6

louder than grade 2

no

4/6

louder than grade 3

yes

5/6

heard with the stethoscope partially off the chest

yes

6/6

heard with the stethoscope completely off the chest

yes

 

  1. Occlusion Location
    1. Aortoilliac Occlusive Disease (Leriche's Syndrome)
      1. Bilateral leg diminished pulses throughout
      2. Slow wound healing legs
      3. Impotence
    2. Iliofemoral Occlusive Disease
      1. Unilateral leg diminished pulses throughout
      2. Buttock claudication may be present
    3. Femoropopliteal Occlusive Disease
      1. Thigh and calf claudication
      2. Normal femoral pulses in groin
    1. Ankle-Brachial ratio > 0.9: Normal
    2. Ankle-Brachial ratio 0.5 to 0.9: Claudication
    3. Ankle-Brachial ratio < 0.5: Resting ischemic pain

Chronic Venous Insufficiency

Venous Insufficiency

Venous Stasis

Risk Factors

    1. Obesity
    2. Congestive Heart Failure
    3. Diabetes Mellitus
  1. Symptoms and Signs
    1. Initial Changes
      1. Varicose veins
      2. Tan or reddish brown skin color changes
      3. Weeping and excoriated skin
      4. Pedal edema
    2. Later Changes
      1. Lipodermatosclerosis
        1. Induration at medial ankle to mid-leg
    3. Advanced Changes
      1. Brawny edema above and below fibrotic area
      2. Ulcerations
  2. Complications
    1. Venous Stasis Ulcers
      1. More common in older women
      2. Chronic and often recurrent
    2. Postphlebitic Syndrome
      1. Chronic leg edema
      2. Deep Venous Thrombosis
      3. Pigmentation
      4. Ulceration
  3. Diagnosis

 

 

Abdominal Aortic Aneurysm

Causes

    1. Associated with Atherosclerosis in only 25% of patients
    2. Aortic Dissection
    3. Mycotic Infection
    4. Cystic Medial Necrosis
    5. Ehlers-Danlos Syndrome

 

    1. Asymptomatic in 75% of AAA
    2. Abrupt onset severe pain unrelieved by position change
      1. Suggestive of aneurysm enlargement or rupture
    3. Aortic Rupture (20% present ruptured)
      1. Free Intraperitoneal Rupture (Catastrophic)
        1. Acute pain
        2. Cardiovascular Collapse
        3. Sudden Death
      2. Sentinal Bleed (small posterolateral wall tear)
        1. Acute pain (constant)
        2. Syncope
        3. Pulsatile abdominal mass
        4. Hemodynamically stable with tachycardia
        5. Needs Emergent Intervention before full rupture

Findings suggestive of occlusion

    1. Proximal lower extremity pressures less than arms
    2. Proximal femoral pressure <20 mmHg over brachial
    3. Drop in doppler pressures between segments >20-30 mmHg

Edema evaluation

Pitting edema

Dependent edema

Brawny edema

Non-Pitting edema

  1.  
    1. Examiner impresses thumb into skin over bony surface
      1. Tibia
      2. Fibula
      3. Sacrum
    2. Withdraw thumb
    3. Measure depth of pit and record in millimeters
  2. Interpretation
    1. Pitting Edema
    2. Non-Pitting edema (Brawny edema)
      1. Myxedema
      2. Chronic inflammation
      3. Chronic Venous Stasis
  3. Edema Distribution
    1. Dependent Edema (fluid shift in response to gravity)
      1. Standing patient accumulates fluid in feet and ankles
      2. Bed-bound patient collects fluid posteriorly (sacrum)
    2. Chronic Leg edema (Brawny edema)
      1. Tissue becomes fibrotic and fails to pit

Chest Pain