Epithelium



CVS H & P

Presenting symptoms:

Chest pain

Cause of pain of ischemic heart disease:

1) Accumulation of metabolite from ischemic muscle.

2) Complete or partial obstruction of coronary artery lead to stimulation of cardiac sympathetic nerves.

• N.B. Patient with cardiac transplantation doesn’t feel the pain of angina because the heart is denervated.

Angina

1) Character: Crushing, heaviness, discomfort or choking sensation.

2) Duration: usually short (typical duration 2 – 10 min).

3) Severity: Graded by New York Heart Association Classification (NYHAC) according to activity to the following:

Class I : angina or dyspnea during unusually intense activity.

Class II : angina or dyspnea during ordinary activity.

Class III : angina or dyspnea during less than ordinary activity.

Class IV : angina or dyspnea at rest

4) Site and radiation: Retrosternal area or the throat, central and may radiate to the jaw or the arms, rarely travel below umbilicus.

5) Aggravating and relieving factors:

Aggravating factors:

Stress ( as exercise, emotional excitement and cold weather).

Relieving factors:

A) Rest.

B) Sublingual nitrate relief the pain within minutes.

6) N.B. Angina doesn’t ( sympathetic activity and anxiety is absent or mild.

M.I

1) Character: Same of angina.

2) Duration: usually long (typical duration 30 min or more).

3) Severity: More severe and occur at rest.

4) Site and radiation: Same of angina.

5) Aggravating and relieving factors:

Often no obvious precipitant (not necessarily precipitated by exertion).

- Not relieved by rest or nitrates.

6) Associated symptoms: dyspnea, sweating, anxiety, nausea, and faintness.

7) N.B. It ( sympathetic activity and anxiety is variable and may lead to the feeling of angor amini (a sensation of impending death).

Pleuritic chest pain

• Definition: chest pain made worse by inspiration.

• Cause: movement of the inflamed pleural or pericardial surfaces on one another.

• Occur in:

1- Pleurisy . 2- Pericarditis.

• Aggravating and relieving factors:

- Not brought on by exertion but relieved by:

1- Sitting up.

2- Leaning forward.

Chest wall pain

• Localised to small area.

• Sharp associated with respiration or movement of shoulders rather than exertion.

• Last for few seconds or to long periods.

Disease of cervical or upper thoracic spine

• Pain is associated with movement

• Radiate from back to front of the chest.

Pain due to dissecting aneurysm of aorta

• Very severe (tearing).

• Radiate to the back.

Massive pulmonary embolism

• Sudden onset pain.

• Retrosternal.

• Associated with collapse, dyspnea and cyanosis.

• Pleuritic or angina like pain.

Spontaneous pneumothorax

• Sharp pain.

• Localized to one part of the chest.

• Associated with severe dyspnea.

Oesophageal spasm

• Retrosternal.

• Come after eating or drinking.

• Associated with Dysphagia.

• Relieved by nitrate.

Dyspnea

• Definition: Subjective awareness of breathing.

• Cause: sensation of increased forced required to respiratory muscles to produce volume change in lungs. Which is due to:

1- Reduction in lung compliance, or.

2- ( resistence to air flow.

Cardiac dyspnea :

• Chronic occurs with exertion.

• Cause: failure of left ventricle output to rise with exercise, this will lead to:

( in LV end diastolic pressure ( ( Pulmonary venous pressure (interstitial fluid leakage ( ( lung compliance (dyspnea).

Orthopnea :

• Definition: Dyspnea when the patient is in the supine position.

• Cause: In the supine position, interstitial edema of the lung is distributed in the whole lung. While in the upright position, the lower zones of the lungs become more edematous and the upper zones become less and this allow improved overall blood oxygenation.

Paroxysmal nocturnal dyspnea (PND) :

• Definition: Severe dyspnea which wakes the patient from sleep.

• Cause:

1- Sudden failure of acute ventricular output.

2- Acute ( in pulmonary venous pressure.

• - These lead to transudation of fluid into interstitial tissue which increases the work of breathing.

• N.B. Presence of orthopnea or paroxysmal nocturnal dyspnea may suggest cardiac failure more than lung disease.

Ankle swelling

• Character:

1- Symmetrical.

2- worse at evening.

3- Improvement at night.

• Occur in: (concerning CVS origin)

1- Biventricular failure.

2- Right ventricular failure secondary to chronic lung disease.

• N.B. -When the failure progress, edema could ascend to involve: legs , thighs , genitalia and abdomen.

- It’s important to know if the patient is taking drugs that cause edema in peripheries like vasodilators (e.g. calcium channel blockers).

Palpitation

• Definition: Unsuspected awareness of heartbeat.

• Cause: The occurrence of atrial or ventricular premature contraction (which produce little cardiac output) followed by compensating paulse and then a normally conducted beat (which is more forceful than usual because there has been a longer diastolic filling period for the ventricles).

• Some of the differential diagnosis:

A) Cardiac arrhythmias ( instantaneous in onset.

B) Sinus tachycardia ( gradual in onset.

C) Atrial fibrillation ( irregular rhythm.

D) Ventricular tachycardia ( rapid palpitation followed by syncope.

• Associated symptoms: pain, dyspnea and faintness.

• N.B. Some manoeuvres return the rhythm of palpitation to normal[1]. e.g. in case of supraventricular tachycardia, It could be terminated by:

1- ( vagal tone with valsalva manoeuvre.

2- Cough, or.

3- Swallowing cold water or ice cubs.

Syncope and dizziness

• Syncope: is a transient loss of consciousness resulting from cerebral anoxia usually due to inadequate blood flow.

• N.B.

- It may be simple faint or a symptom of cardiac or neurological disease.

- It could be preceded by dizziness or palpitation.

-Types of syncope:

1- Postural syncope : on standing for prolong period or standing suddenly.

- This may occur due to the uses of antihypertensive or antianginal drugs.

2- Micturation syncope : when passing urine.

3- Tussive syncope : on coughing.

4- Vasovagal syncope : with sudden emotional stress.

- It may occur because something unpleasant like sight of blood or the presence in a crowded hot room[2].

• Recovery may be:

1- Spontaneous.

2- by attention from bystanders (he must tell if he saw any abnormal movement which may indicates epilepsy).

• Some cardiac causes of syncope:

1)Arrhythmia : cause sudden syncope (regardless of the patient’s posture).

2) Exertional syncope occurs in:

1- Obstruction of left ventricular outflow by aortic stenosis.

2- Hypertrophic cardiomyopathy.

Dizziness

• definetion: a sensation of faintness or an inability to maintain normal balance in a standing or seated position.

• Tachyarrhythmiasis could cause dizziness at any position.

• We should decide weather dizziness is:

1- Vertigious.

2- Presyncopal.

Intermittent Claudication

• Definition: Pain in one or both calves, thighs or buttocks when walking more than a certain distance (claudication distance).

• The most important risk factor is SMOKING and history of vascular disease (CVA and IHD).

Types of claudication:

| |Arterial |Neurogenic |Venous |

|1) Pathology |Stenosis or occlusion of major LL |Lumber nerve or cauda equina compression |Occlusion of iliofermoral veins. |

| |arteries |(spinal stenosis) | |

|2) Site of pain |Muscles, usually calf and may involve |Ill defined, Whole leg. May associates |Whole leg |

| |thigh and buttocks |with numbness and tingling | |

|3) Onset |Gradual |Often immediate |Gradual |

|4) Colour |Normal or pale |Normal |Cyanosed |

|5) Edema |Absent |Absent |Always present |

|6) Pulses |( or absent |Normal |Present but my be difficult to |

| | | |feel owing to edema |

Fatigue

Common symptom of cardiac failure.

Past history

-If there is history of angina or MI ( ( IHD.

• You must know from the patient something like:

A) Previous diagnosis of CVS diseases.

B) If any exercise testing or coronary angiogram he made.

C) If he has rheumatic fever in his childhood.

D) If he is in bed for long time in childhood.

• Genetically determined CVS disorders includes (some of it):

1) HTN.

2) Hyperlipidemia.

3) Hypertrophic cardiomyopathy.

4)Marfan’s syndrome .

5)IHD.

6)Diabetes.

Social history

• IHD + RHD are chronic conditions that affect the patient’s ability to function normally.

• So you must know if the disease prevent the patient from working or changes his life style activities.

Begging a physical examination

(1) introduction ,privacy & positioning: (alwys tell the PT what you are doing).

(2) General inspection ł (appearance):

- appearance: well or ill (face, foot, hand, eye ,mouth, Higden, dental care).

- body built: obese, thin, cachexic

- color : pale, cyanotic, jaundice.

- Distreast: respiratory And cardic (stridulous , tachypnoic , upset, comfortable)

- environment: IV line ,BP, catheter, and ECG.

NOTE: the general inspection ∏-which is related to the ill system- could be done here also.

(3) Vital singes: BP, Temp, respiratory rate, pulse ( regulatory, rate.

(4) exposure of the needed area: this could be done after the general inspection ∏

.

(5)on the ill system :general inspection ∏ (related to the ill system), inspection, palpation, precaution auscultation

CVS examination

Positioning of the patient

• Position the patient at 45 degrees. usual position for assessment of JVP.

General appearance

Look for the following:

1) Dyspnea.

2) Cachectic.

Definition: severe loss of weight and muscle wasting.

Cause:

1- severe malignancy.

2- Severe cardiac failure (cardiac cachectic).

- This result from:

1- Anorexia : due to congestive enlargement of the liver.

2- Impaired intestinal absorption : due to congestive intestinal veins.

3) Some syndrome which are associated with specific cardiac diseases as:

A- Marfan syndrome.

B- Down syndrome.

C- Turner syndrome.

The hands…

1) Clubbin :.

Definition: increase in the soft tissue of distal part of the fingers or toes.

Causes of clubbing:

1) Common:

CVS :

1- Cyanotic congenital heart disease.

2- Infective endocarditis.

Respiratory :

1- Lung carcinoma.

2- Chronic pulmonary suppuration:

- Bronchiectasis.

- Lung abscess.

- Empyema.

- Idiopathic pulmonary fibrosis.

2) Uncommon:

Respiratory :

1- Cystic fibrosis.

2- Asbestosis.

3- Pleural mesothelioma.

GIT:

1- Cirrhosis

2- Inflammatory bowel disease.

3- Celiac disease.

3) Rare:

1- Neurogenic diaphragmatic tumours.

2- Pregnancy.

Unilateral clubbing :

1- Bronchial arteriovenous aneurysm.

2- Axillary artery aneurysm.

Pathogenesis:

In response to arterial hypoxemia, unknown humoral substance causes dilatation of the vessels of the fingertips or toes.

Grades of clubbing:

1- Bogginess at the nail base.

2- Increased transverse diameter than the AP diameter.

3- Parrot beak appearance.

4- HPOA - Hypertrophic Pulmonary Osteo Arthropathy.

• Examination for clubbing involves:

1. Inspection the finger and toe nails from the side to determine if there is any loss of the angle between the nail bed and the finger.

2. A stable sign may be an increased sponginess of the proximal nail bed.

3. Compression the nail bed and rocking it with one’s finger.

2) Splinter Hemorrhage:

• Definition: linear hemorrhages lying parellel to the long axis of the nail.

• Causes:

1- Trauma (mostly).

2- Infective endocarditis due to vasculitis in the nail bed.

3- Other rare causes:

A) Vasculitis.

B) Rheumatoid arthritis.

C) Polyarteritis nodosa.

D) Sepsis.

E) Hematological malignancy.

F) Profound anemia.

3)Osler’s nodes: (fig 3.4)

• Definition: These are red raised tender nodules on the pulps of the fingers or toes or in the thenar or hypothenar eminence.

• They are rare manifestation of infective endocarditis.

4) Janeway lesions :

• Definition: Non tender erythromatous maculopopular lesions containing bacteria occur rarely in palms or pulps of the fingers in patient with infective endocarditis.

5) Tendon xanthomata :

• Definition: Yellow or orange deposits of lipid in tendons of the hand or arms which occur in type II hyperlipidemia.

6) Palmar xanthomata and tuboeruptive xanthomata.

• Occur in the elbow and knee and it’s character of type III hyperlipidemia.

The arterial pulse…

Method : palpate the radial artery of the wrist. The pulse usually felt medial to the radius using forefinger and middle finger pulps of the examining hand.

* For Brachial and carotid arteries use the thumbs.

* Brachial artery ( medial to biceps muscle.

* Carotid artery ( between the larynx and the anterior border of sternocleidomastoid muscle. NEVER palpate both carotid arteries simultaneously.

Determine the following

A) Rate of the pulse :

• Method: Count the rate over 30 seconds then multiply it by 2 to obtain the rate per min.

• Normal resting heart rate: about 60 – 100 beats per min.

Bradycardia ( HR < 60 beats/min.

Tachycardia ( HR > 100 beats/min.

• The cause of bradycardia and tachycardia in table (3.5) p41.

B) Rhythm :

Refer to the book table 3.5 P 41.

C) Radiofemoral delay and radial-radial delay :

• Method : While palpating the radial pulse one place the fingers of the other hand over the femoral pulse (below inguinal ligament 1/3 of the way up from pubic tubercle).

• Radiofemoral delay occurs in : when there is coarctation of the aorta.

• Radial-radial delay occurs in : large arterial occlusion by an atherosclerosis plaque or aneurysm.

D) Character and volume :

• Method: Use the brachial and carotid arteries[3] for determine the volume and character.

Pulsus alternans : (rare)

Definition: A regular alternate of strong and weak beats (in volume).

Mechanism: unknown.

Occur in: Severe myocardial disease and heart failure.

Pulsus paradoxus :

Definition: A pulse that increases in volume on expiration and decreases in volume in inspiration.

Note: This phenomenon is physiological and not detectable in normal individuals. It is considered abnormal if the pulse pressure decrease, on inspiration, below 10 mmHg.

Mechanism: During inspiration, the systolic and diastolic blood pressure normally decrease (because intrathoracic pressure becomes more negative, blood pools in the pulmonary vessels, so left heart filling is reduced).

Occur in: constrictive pericarditis, pericardial effusion and severe asthma.

Collapsing (bounding) pulse :

Definition: High volume but ill sustained pressure wave form.

Occur in: Aortic regurgitation.

Examination: Raise the arm while feeling across the pulse with the fingers of the other hand (Macleod, fig3.12B, p 83).

Bisferiens pulse:

Definition: Slow rise, with normal or high volume, with sudden collapse.

Occur in: combined aortic stenosis and regurgitation.

E) Condition of the vessel wall :

• Only changes in the medial layer of radial artery can be assessed by palpation.

• N.B. Thickening (tortuousity) is common in arteries of elderly people.

The blood pressure…

• Systolic blood pressure: The peak pressure occurs in the artery following ventricular systole.

• Diastolic blood pressure: The level to which the arterial blood pressure falls during ventricular diastole.

• Normal BP ( systole ( 140 mmHg, diastole ( ( 90 mmHg.

• N.B. In some cases like pregnancy, There is a lower BP which is considered normal.

Measuring the blood pressure with the sphygmomanometer[4] :

Method:

1- For systolic blood pressure only:

- The cuff wrapped around the upper arm with bladder centered over the brachial artery.

- The cuff is fully inflated and then deflated slowly (3 to 4 mmHg per seconds) until radial pulse returns.

2- For both systolic and diastolic blood pressure:

- The same manoeuvre is repeated with the diaphragm of the stethoscope placed over the brachial artery slipped underneath the distal end of the cuff’s bladder.

Korotkoff sounds : (heard during the procedure, fig 3.8 p 42).

* K I : the first heard sound.

* K II : The sound increase in intensity ( a blowing or swishing sound).

* K III : the sound then decrease (A softer thud than K I).

* K IV : A softer blowing sound that disappears.

* K V : The last heard sound.

Note:

-In severe aortic regurgitation, K IV is more accurate indication.

- K V is absent in some normal people and K IV must be used.

-Auscultatory gap (occasionally occur): the sound disappears just below the systolic pressure and then reappear before diastolic pressure in healthy people.

- Systolic BP varies between the arms by up to 10 mmHg.

-In the legs BP is > BP in the arms.

Postural blood pressure :

• Take BP of the patient on lying and standing positions.

• Postural hypotension is considered when :

1- Systolic fall more than 15 mmHg or

2- Diastolic fall more than 10 mmHg.

• Causes of postural hypotension (table 3.6 P 44).

The face….

Look for the following :

1) Jaundice (CHF, hepatic congestion or prosthetic heart valve[5]).

2) Xanthelasma:

Definition: An intracutaneous yellow cholesterol deposit around the eye.

* Occur: as normal variant or in type II or III hyperlipidemia.

3) Corneal arcus:

Cause: Precipitation of cholesterol crystals at the periphery of the cornea.

4) Mitral faces (Malar flush):

Appearance: Rosy cheeks with bluish tinge.

Cause: dilatation of malar capillaries.

Occur in:

1) pulmonary HTN.

2) low cardiac output as in mitral stenosis.

5) The mouth:

A) for any high arched palate. This occurs in Marfan’s syndrome which is associated with congestive heart disease.

B) The teeth, notice if they are diseased as they can be source of organisms responsible for infective endocarditis.

C) Tongue and lips for central cyanosis.

D) The mucosa for petechiae that may indicate infective endocarditis.

The neck….

Carotid arteries :

• Importance: tell about the aorta and left ventricular function.

• It’s medial to sternomastoid muscle.

• Never palpate both carotid arteries together (it will lead to syncope).

• You must evaluate the pulse wave form :

1- amplitude.

2- Shape.

3- Volume.

• Carotid wave forms (table 3.7 p 46).

Jugular venous pressure (JVP)

Meaning:

Pulsation (which is seen in the internal jugular vein) reflects movements of the top of a column of blood which extends into the right atrium. This column enables us to observe pressure changes in the right atrium. By convention, the sternal angle is taken as the Zero point and the maximum height of pulsation in the vein indicates the JVP.

- The center of the right atrium lies 5 cm below the zero point.

• Importance: tell about right arterial and right ventricular function.

• Normal JVP: < 3-4 cm above sternal angle.

• Method:

A) Position the patient reclining supine at 45° in good light.

Note: We neither position the patient in the supine nor upright position because:

- In supine: the vein is distend.

- In upright: the vein is collapsed and the transition points obscured by sternum.

B) Ensure the neck muscles are relaxed by resting the back of the head on a pillow.

C) Identify the internal jugular pulsation[6], if necessary, by means of hepatojugular reflex.

Hepatojugular reflux:

is done by applying a firm pressure over the center of the abdomen for 5 – 10 seconds. This (venous return which leads to transient ( in right atrial pressure.

D) Identify the height and character of the pulsation.

Difference between carotid and jugular pulsation

|Carotid |Jugular |

|1) Rapid outward movement |Rapid inward movement |

|2) One peak per heartbeat |2 peaks per heartbeat |

|3) Palpable |Impalpable |

|4) Independent of respiration, position or abdominal pressure |Dependent of respiration (( during inspiration), position and |

|(no hepatojugular reflux). |abdominal pressure. |

Height :

• Causes of raised JVP ( table 3.8 P 47).

Character (The patterns of the waves): (fig 3.12 p 46)

There are 2 positive waves in normal JVP:

1- a wave:

Coincides : with right atrial systole. Also coincides with 1st heart sound and precedes the carotid pulsation.

Cause: atrial contraction.

2- v wave:

Coincides: with ventricular systole.

Cause: atrial filling in the period when the tricuspid valve remains closed during ventricular systole.

There are 2 decents in normal JVP:

1- X decent :

* Caused by atrial relaxation.

2- Y decent:

* Caused by rapid ventricular filling when the tricuspid valve open.

• N.B. c wave: (not usually visible)

Cause: a transmitted pulsation from the carotid artery.

Abnormal pattern of the wave : (Table 3.8 P 47)

1) Cannon a wave : (see Kumar for the figures)

occurs when the right atrium contract against the closed tricuspid valve (in complete heart block).

2) Giant a wave :

These are large but not explosive a wave with each beat. It occurs when the right atrial pressure raised because of the:

1- Obstruction in the outflow (tricuspid stenosis).

2- Elevated pressure in pulmonary circulation.

3) Large v wave :

Occur in tricuspid regurgitation.

Kussmaul’s sign:

Definition: an increased JVP during inspiration.

Cause: Any condition in which right ventricular filling is limited can cause elevation of the JVP and this is more marked on inspiration (because increased venous return). These conditions are:

1) Constrictive pericarditis.

2) Cardiac temponade.

3) Right ventricular infarction.

Examination: This sign is best examined with the patient sitting up at 90° and breathing quietly through his mouth.

Summery of the conditions: (Macleod: Table 3.21 P 89)

|Condition |JVP |

|- Heart failure |( |

|- SVC obstruction | |

|* Constrictive pericarditis |Kussmaul’s sign |

|* Cardiac tamponade | |

|* Right ventricular infarction | |

|Atrial fibrillation |Absent a wave |

|Tricuspid stenosis |Giant a wave |

|Tricuspid regurgitation |Giant v wave |

|Complete heart block |Cannon a wave |

The precordium….

Inspection :

1) Scars: -These are previous cardiac operations.

-The position of the scar can be a clue to the valve lesion that has been operated, e.g.

A) Valve surgery (cardiopulmonary bypass) : median sternotomy and usually hidden under the chest hair.

B) Previous closed mitral valvotomy : left or even right sided lateral thoractomy scars.

2 Some skeletal abnormalities:

A) Pectus excavatum (funnel chest).

B) Kyphoscoliosis (curvature of the vertebral column) which may be part of Marfan’s syndrome.

These can cause distortion of position of the heart and great vessels in the chest and this alter the position of the apex beat.

NOTE: The normal position of apex beat is in the 5th left intercostal space 1 cm medial to the midclavicular line.

Palpation :

1) Apex beat must be palpable.

• The position of apex beat is defined as the most lateral and inferior point at which the palpating fingers are raised with each systole.

Types of abnormal apex beats:

1) The pressure loaded (hyperdynamic or systolic overload) forcefull apex beat.Occurs with aortic stenosis or hypertension.

2) The volume loaded (hyperkinetic or diastolic overloaded) uncoordinated impulse. Occurs with left ventricular dysfunction.

3) The double impulse apex beat, where 2 distinct impulses are felt with each systole. Occurs with hypertrophic cardiomyopathy.

4) The tapping apex beat will be felt when the 1st heart sound is actually palpable (heart sounds are NOT palpable in healthy people). Occur with mitral or rarely tricuspid stenosis.

• Note: In some cases the apex beat may not be palpable due to:

1- Thick chest wall.

3- Pericardial effusion.

4- Shock (or death).

2- Emphysema.

5- Rarely to dextrocardia (where there is inversion of heart and great vessels). The apex beat will be palpable to the right of the sternum in many cases of dextrocardia.

2) Thrills :

• Definition: These are palpable murmurs.

• Cause: Turbulent blood flow of cardiac murmurs.

3) Apical thrills :

• Can be more easily felt with the patient rolled over to the left side as this brings the apex closer to the chest wall. Thrills may also be palpable over the base of the heart.

• Types of thrills :

1) Systolic thrill : a thrill which coincides in time with apex beat.

2) Diastolic thrill : one which doesn’t coincides with the apex beat. (The presence of thrill usually indicates an organic lesion).

4) Heaves :

• Definition: These are palpable impulses from either the right or left ventricle.

• Note: A pulsation over the left parasternal area (right ventricular heave) is usually due to right ventricular hypertrophy (as of pulmonary hypertension).

Percussion :

• Not important in CVS examination.

Auscaltation :

The stethoscope

1-The bell:

Designed for amplifying low pitched sounds[7].

Examples :

1- diastolic murmur of mitral stenosis.

2- 3rd heart sound.

2-The diaphragm:

Designed for higher pitched sounds.

Examples:

1- Systolic murmur of mitral regurgitation.

2- 4th heart sound. (never occur physiologically)

Examination Sequence :

1) Mitral area with the bell and then by the diaphragm.

2) Tricuspid area with the diaphragm.

3) Pulmonary area with the diaphragm.

4) Aortic area with the diaphragm.

Heart sounds

Normal findings[8]

1st heart sound (S1)

-Has 2 components:

1- Mitral valve closure.

2- Tricuspid valve closure.

-It indicates the beginning of systole.

-Heard as: lub.

2nd heart sound (S2)

-Has 2 components:

1- Pulmonary valve closure (P2).

2- Aortic valve closure (A2).

-It indicates the beginning of diastole.

-Heard as: dub…

( so 1st and 2nd ( lub dub).

Physiological splitting (the closure of the aortic valve earlier than the pulmonary valve) occurs because the pressure of systemic circulation is higher than the pressure of pulmonary circulation.

- This splitting is increased by inspiration (because increased venous return to the right ventricle which further delay pulmonary valve closure).

- It disappears on expiration.

- Heard as: lub d/dub (inspiration), lub dub (expiration).

Simultaneous palpation of the carotid pulse

This aids in distinguishing b/w the 1st and 2nd heart sounds.

1st heart sound ( precedes the pulse.

2nd heart sound ( follows the pulse.

3rd heart sound (S3)

-It is a low pitched mid-diastolic sound.

-It leads to the impression of gallop rhythm (resembling a galloping horse) which is a triple rhythm consists of 3 heart sounds.

Cause: rapid filling of the ventricles after opening of AV valves.

Occurs in (physiologically):

1- Children 2- Young adults 3- pregnancy 4- Athletes. 5- Fever.

Heard as: lub dub dum.

Abnormalities of the heart sounds

Alterations in intensity

The cause: Forcefull closure of the valves.

In General:

* Stenosis + Tachycardia ( loud sound.

* Regurgitation + bradycardia ( soft sound.

Special consideration:

1st heart sound :

Loud: Any case of short AV conduction time (short P-R interval) , mitral stenosis and tachycardia .

Soft: Any case of long AV conduction time (long P-R interval).

_ first degree heart block ( prorlonged diastolic filling time ) .

_ left bundle branch block ( delayed onset of left ventricular systole ) ..

_ mitral regurgitation ..

2nd heart sound :

Loud: Systemic HTN (loud A2) or pulmonary HTN (loud P2).

Soft: Calcific aortic stenosis (the leaflet movement is reduced).

Splitting…

1st heart sound :

-Not detectable clinically.

-Occurs in complete right bundle branch block.

2nd heart sound :

Occurs in 3 patterns

1) Increased normal splitting (wider on inspiration) :

When there is any delay in right ventricular emptying. Examples:

A) Right bundle branch block (delayed right ventricular depolarization).

B) Pulmonary stenosis (delayed right ventricular ejection).

C) Ventricular septal defect (increased right ventricular volume).

D) Mitral regurgitation (because of earlier aortic valve closure due to more rapid left ventricular emptying)

2) Fixed splitting :

i.e. There is no respiratory correlation.

Example:

Atrial septal defect where equalization of volume loads b/w the 2 atria occurs through the defect (atria acting as a common chamber).

3) Reversed splitting :

i.e. P2 occurs first and splitting occurs in expiration. Examples:

A) Left bundle branch block (delayed left ventricular depolarization).

B) Aortic stenosis (delayed left ventricular ejection).

C) Large patent ductus arteriosus (increased left ventricular volume).

Pathological extra heart sounds

3rd heart sound

Usually pathological after the age of 40.

Cause: poor contracting ventricle (although diastolic filling is not especially rapid).

Left ventricular S3:

- Louder at the apex and on expiration.

-Occurs in:

1- Left ventricular failure (an important sign).

2- Aortic or mitral regurgitation.

3- VSD.

4- Patent ductus arteriosus.

Right ventricular S3:

- Louder at the left sternal edge.

-Occurs in:

1- Right ventricular failure.

2- Constrictive pericarditis.

4th heart sound

-It is a low pitched presystolic sound.

-It also leads to the impression of triple (gallop) rhythm.

Cause: high pressure atrial wave reflected back from a poor compliant[9] ventricle.

Left ventricular S4: occurs whenever left ventricular compliance is reduced as in:

1- Aortic stenosis

2- Acute mitral regurgitation.

3- Systemic hypertension.

4- IHD (the sound may be the only physical sign in angina or MI).

5- Advanced age.

Right ventricular S4: occurs whenever right ventricular compliance is reduced as in:

1- Pulmonary stenosis. 2- Pulmonary hypertension.

Heard as: da lub dub.

Summation gallop

-The combining of S3 and S4 to one sound.

-It may occur if the heart rate is greater than 120/min.

Quadruple rhythm

-When both S3 and S4 are present.

-It indicates severe ventricular dysfunction.

Additional Sounds

Opening snap

Definition: A high pitched sound occurs after S2.

Cause: Sudden opening of the valve.

Occurs in: Mitral (rarely tricuspid) stenosis.

Best heard in: lower left sternal edge[10].

Systolic ejection click[11]

Definition: A high pitched early systole sound.

Cause: sudden opening of the valve.

Ocurrs in: Congenital aortic or pulmonary stenosis[12].

Best heard in: aortic, pulmonary or left sternal edge area.

Non-ejection systolic click.

Definition: A high pitched systolic sound.

Cause: prolapse of one or more redundant mitral valve leaflets.

Occurs in: mitral valve prolapse and may be heard in ASD.

Best heard in: mitral area (apex).

Pericardial rub

Definition: It is a characteristic physical sign of pericarditis which is described as superficial scratching sound with systolic and diastolic components.

Characteristic: Vary in intensity from hour to hour and with alter in the position of the patient.

Cause: Movement of inflamed pericardial surfaces.

Occurs in: pericarditis.

Best heard in: lower left sternal edge when the patient is sitting up and breathing out using the diaphragm.

Prosthetic (mechanical) heart sound

It is a high pitched “metallic” sound, commonly palpable and often audible without a stethoscope. It occurs during both the opening and closure of the valve.

Murmurs of the heart

In deciding the origin of murmur, the following should be considered:

1) Associated features ( peripheral signs).

2) Timing (systolic or diastolic).

3) Area of greatest intensity + radiation.

4) Grade.

5) Dynamic manoeuvres.

Timing

A) Systolic murmurs (Occurs during ventricular systole)

1) Pansystolic :

Character: Extend throughout systole beginning with 1st heart sound till the 2nd heart sound.

Cause: leakage of the blood from the ventricle to a lower pressure chamber or vessel[13].

Occur in: 1) Mitral regurgitation[14],

2)tricuspid regurgitation and VSD.

2) Mid systolic (ejection) murmur = crescendo-decrescendo murmur:

Character: Doesn’t begin right at 1st heart sound, its intensity is greatest in midsystole and then decreases again in late systole.

Cause: turbulent flow through aortic or pulmonary valve orifices or increased flow through a normal sized orifice.

Occur in: 1) Aortic stenosis, 2)pulmonary stenosis

3)hypertrophic cardiomyopathy.

3) Late systolic murmur :

Character: It could be distinguished from midsystolic murmur by the presence of a gap between the 1st heart sound and the murmur which then continues right up to the 2nd heart sound.

Occur in: Mitral valve prolapse or papillary muscle dysfunction where mitral regurgitation begins in mid-systole.

B) Diastolic murmurs (occurs during ventricular diastole)

1) Early diastolic murmur:

Character: A high pitched sound begin immediately with the 2nd heart sound and has a decrescendo quality.

Cause: Regurgitation through leaking aortic or pulmonary valves.

Occur in: Aortic or pulmonary regurgitation.

2) Mid-diastolic murmur:

Character: Begin later in diastole and may be short or extend right up to the 1st heart sound.

Cause: Impaired flow during ventricular filling.

Occur in: mitral or tricuspid stenosis and atrial myxoma (rarely occur, where the tumour obstructs the valve orifice).

3) Presystolic murmur:

Character: These are extension of the mid-diastolic murmurs of the mitral or tricuspid stenosis and usually don’t occur when atrial systole is lost in atrial fibrillation.

Cause and Occurence: the same of mid-diastolic murmur.

C) Continuous murmur[15]:

Character: Extend throughout systole and diastole.

Cause: the presence of communication between 2 parts of the circulation with a permenant pressure gradient so that blood flow occurs continuously.

Occur in: Patent ductus arteriosus, arteriovenous fistula (coronary, pulmonary or systemic).

Area of greatest intensity and radiation (see fig 3.19, p 57)….

The place on the precordium usually indicates the origin of the murmur (but this is not always true) For example: mitral regurgitation murmurs are usually loudest at the mitral area but it may also radiate and heard in the axilla or even over the back.

Loudness and pitch

Classified into 6 grades:

* Grade 1/6 ( very soft and not heard at first.

* Grade 2/6 ( soft.

* Grade 3/6 ( moderate without thrill.

* Grade 4/6 ( loud; thrill just palpable.

* Grade 5/6 ( very loud; thrill easily palpable.

* Grade 6/6 ( very very loud; can be heard even without stethoscope!!.

Note:

- The loudness of murmurs is often not helpful in deciding the severity of the valve lesion. E.g. the severest form of valvular stenosis murmurs may be soft or inaudible.

- In general, low pitched murmurs indicate turbulent flow under low pressure as in mitral stenosis and high pitched murmurs indicate a high velocity of flow, as in mitral regurgitation.

Dynamic manoeuvres

These aids in determining the nature of the murmur:

1) Respiration :

-Murmurs that arise on the right side of the heart tend to be louder during inspiration.

-Cause: increased venous return and therefore blood flow to the right side of the heart.

-Expiration has the opposite effect.

2) Leaning forward :

-The patient should lean forward in full expiration.

- This is done to make the base of the heart closer to the chest wall.

- It aids in determining the mitral regurgitation murmurs (which may not be detected only by this manoeuvre).

3) Valsalva manoeuvre : (see table 3.10 p 61)

Mechanism: It is a forcefull expiration against a closed glottis. The patient should hold the nose with his/her fingers, close the mouth, breath out hard and completely so as to pop the eardrums, and hold this for as long as possible.

Mostly useful for:

1- Systolic murmur of hypertrophic cardiomyopathy heard over the left sternal edge.

2- Mitral valve prolapse heard over the apex.

Phases of Valsalva manoeuvre:

1- Phase 1 (beginning the manoeuvre) :

- There is increased intrathoracic pressure and transient increase in left ventricular output.

2- Phase 2 (Straining phase) :

- ( Systemic venous return ( ( filling of right side of the heart ( ( filling of left side ( ( stroke volume and blood pressure while ( heart rate.

- Here most cardiac murmurs become softer but systolic murmur of hypertrophic cardiomyopathy becomes louder.

3- Phase 3 (The release of the manoeuvre) :

- Right sided and then left sided heart murmurs become louder briefly before returning to normal.

4) Squatting or leg raised:

There is ( venous return and systemic arterial resistance ( ( stroke volume and arterial pressure.

Its effect on murmurs:

A) Most murmurs ( louder.

B) systolic murmur of hypertrophic cardiomyopathy ( softer (because left ventricular size is increased during the manoeuvre and this reduces the obstruction to outflow)

C) Mid-systolic click and murmur of mitral valve prolapse ( delayed.

5) Isometric exercise : (Occasionally used)

Mechanism: Patient should perform a sustained hand grip for 20 or 30 seconds ( ( venous return and systemic arterial resistance.

Its effect on murmurs: The same of squatting manoeuvre.

The back…

Physical signs to be noticed :

A) Percussion and Auscaltation of the lung bases (they are part of CVS examination) ( for signs of cardiac failure.

B) Pitting edema of the sacrum ( for signs of severe right cardiac failure.

The abdomen..

Physical signs to be noticed:

1) Enlarged tender liver : in the presence of Right heart failure.

2) Pulsatile liver :in tricuspid regurgitation (because the right ventricular systolic pressure wave is transmitted to the hepatic veins).

3) Ascites : may occur in severe right heart failure.

4) Splenomegaly : may indicates infective endocarditis.

5) Implanted cardioverter-defibrillator.

The lower limb

Physical signs to be examined

1- Arteries :

Palpate the following:

1) Femoral arteries and then ausculation.

Check for Bruits which may be heard if the artery is narrowed.

2) Popliteal artery (behind the knee).

3) Posterior tibial (under the medial malleolus).

4) Dorsalis pedis (on the forefoot).

2- Edema :

Technique:

1- palpate the distal shaft of tibia by compressing the area for at least 15 seconds with the thumb.

2- Determine the type of edema and its upper level.

Types of edema and their causes:

1- Pitting lower limb edema: (the skin is indented and only slowly refills).

A) Cardiac : CHF, constrictive pericarditis.

B) Drugs : Calcium antagonists.

C) Hepatic : cirrhosis.

D) Renal : nephrotic syndrome

E) GIT : Malabsorption, starvation.

2- Pitting unilateral lower limb edema:

A) DVT.

B) Tumour or lymph nods compressing a large vein.

3- Non-pitting lower limb edema:

A) Hypothyroidism.

B) Lymphedema due to:

i- Infection. ii- Malignancy. iii- Allergy iv- Milroy’s disease (unexplained lymphedema which appears at puberty and is more common in females).

3- Achilles tendon xanthomata (Which is due to hyperlipidemia).

4- Cyanosis and clubbing .

5- Peripheral vascular disease :

Signs of this disease are:

1- Absent pulses.

2- Femoral systolic bruits.

3- Marked leg pallor.

4- Absence of hairs.

5- Cool skin.

6- Reduced capillary return (compress the toe nails – the return of the normal red colour is slow).

Buerger’s Test : (to confirm the presence of the disease)

Elevate the leg to 45 degrees ( a rapid appearance of pallor (indicates poor arterial supply).

-Then place them dependent over the edge of the bed at 90 degrees ( cyanosis occurs (indicates impaired arterial supply).

Deep Venous Thrombosis (DVT)

Physical signs to be examined

1) Swelling of the calf and the leg.

2) Dilated superficial veins.

3) Feel for increased warmth.

4) Squeeze the calf gently to determine if the area is tender.

Varicose veins

Squence of examination

1) Ask the patient to stand with the legs fully exposed.

2) Inspect :

A) the front of the whole leg for tortuous, dilated branches of the long saphenous vein (below the femoral vein in the groin to the medial side of the lower leg).

B) The back of the calf for varicosities of the short saphenous vein (from the popliteal fossa to the back of the calf and lateral malleolus).

3) Palpate the veins.

A) Hard veins : suggest thrombosis.

B) Tenderness : suggest thrombophlebitis.

4) Perform Cough impulse test[16].

Technique: Put the fingers over the long saphenous vein opening in the groin[17]. Ask the patient to cough, a fluid thrill is felt if the saphenofemoral valve is incompetent.

-----------------------

[1] Some patients may have learned these manoeuvres.

[2] Those patients usually have similar episodes before especially during adolescence and young adulthood.

[3] They are more better in determining the character and volume than radial artery. But for collapsing pulse and pulsus alternans, used the radial artery.

[4] Note that there are large cuff (for obese people) and small cuff (for children).

[5] It induce hemolysis due to excessive turbulence (uncommon cause of jaundice).

[6] Note:

* The internal jugular is medial to sternomastoid but external jugular is lateral.

* We didn’t use the external jugular vein because it has tortuous course.

[7] It must applied lightly bec forcefull application will stretch the skin under the bell so it forms a diaphragm.

[8] Note that 4th heart sound never occur physiologically.

[9] Compliance of the ventricle means the condition of the ventricle that lead to decreased ventricular ejection.

[10] Macleod: best heard in the apex…

[11] Macleod: systolic ejection click ( ejection click, non-ejection systolic click ( midsystolic click.

[12] Note it doesn’t occur in rigid valves as in case of calcific aortic stenosis (the valves should be mobile).

[13]

!,U¹ÀìïðW X Y ìãϾ¨˜‡˜p]˜P8.hàEÄhB\ 5?>*B*CJ$OJ\?^JaJ$ph™3fhàEÄh‹iNCJ ^JaJ $hàEÄh‹iN5?6?CJ \?]?^JaJ -hàEÄh‹iN5?6?B*

CJ \?]?^JaJ ph€!hàEÄhB\ 6?>*[pic]CJ ]?^JaJ -hàEÄh‹iN6?CJ ]?^JaJ +hàEÄh‹iN5?B* I.e. Since there is a pressure gradient from the moment the ventricle begins to contract (S1), blood flow and the murmur begin at the 1st heart sound and continue until the pressure equalise (S2).

[14] The term incompetence is synonymous with regurgitation, but the latter describes the pathophysiology.

[15] Note the combined murmurs of aortic stenosis and aortic regurgitation, or mitral stenosis and mitral regurgitation, may sound as if they fill the entire cardiac cycle, but are not continuous murmurs by definition.

[16] There are other tests (Trendelenburg test and Perthes’ test) in the book which are more concerned in the surgery… and they are occasionally helpful.

[17] NB. Femoral vein (medial), artery (your landmark), nerve (lateral).

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