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Examination of CVS

Pulse rate

Pressure distension wave generated during each systole transmit heal along arterial wall and palpable in supe, picial arteries.


Normal pulse rate

New born 110 – 150 beats/min
2 year 85 – 125 beats/min
4 year 75 – 115 beats/min
>6 year 60 – 100 beats/min


Persistent tachycardia


>200 beats / min



>150 beats / min


Older children

>120 beats / min


New born

<90 beats / min


Infants / older children

< 60 beats / min


In adult

Sinus bradycardia  -   pulse rate    -     < 60 /min

Sinus tachycardia   -   pulse rate    -     > 100/ min


Causes of sinus bradycardia

  1. Physiological                
    1. Athletes                
    2. Sleep
  2. Pathological          
    1. Hypothermia        
    2. Myxedema            
    3. Acute inferior wall myocardial infarction
    4. ICT 

Causes of sinus Tachycardia

  1. Physiological                
    1. Infants                  
    2. Emotion                        
    3. Exertion
  2. Pathological          
    1. High output states         
    2. Acute Anterior wall MI
    3. Hypovolemia                        
    4. Tachyarrhythmia 

2. Rhythm is defined as regularity of pulse by which one peak follows another.

  1. Regularly irregular Rhythm
    1. Atrial tachyrhythmias    
    2. Fixed AV block              
    3. Ventricular bigemini, trigemini  
  2. Irregularly irregular Rhythm
    1. Atrial or ventricular ectopics                  
    2. Atrial fibrillation
    3. Atrial flutter                                
    4. Varying Heart block  

3. Pulse Volume

The pulse pressure (difference between systolic and diastolic BP) gives an accurate measure of pulse volume. When pulse pressure is between 30 and 60 mm Hg pulse volume is normal.

Cardiac lesion High output state
Aortic Regurgitation Anemia
PDA Beriberi
Collateral Thyrotoxicosis
A-V fistula Paget's disease
  1. Features Of a Normal Pulse
    1. The upstroke is abrupt and without any secondary wave on it.
    2. The down stroke in the middle has a sharp depression called dicrotic notch which is immediately followed by a small wave, the dicrotic wave both of which are not normally palpable.
    3. Peak of upstroke is percussion wave which is felt by the palpating finger.
    4. The wave from the beginning of the tracing up to the dicrotic notch corresponds to ventricle systole.
    5. The dicrotic notch is due to the sharp fall of pressure caused by the rolling back of aortic blood towards the left ventricle at the beginning of diastole.
    6. The dicrotic wave is caused by the return of the same blood column being reflected back by the closed semilunar valves.
    7. In the central arterial pulse (Central aorta and innominate and carotid arteries), the rapidly transmitted impact of the left ventricular ejection results in a peak in early systole referred to as the percussion wave, a second small peak the tidal wave presented to represent reflected wave from the periphery can often be recorded but is not normally palpable.
    8. In peripheral arteries the pulse wave normally has a single sharp peak.  
  2. Types of Pulse
    1. Anacrotic Pulse
      1. Slow rising twice beating pulse where both the waves are felt during systole. The waves that are felt are anacrotic and percussion wave.
      2. It is best felt in carotid in Aortic stenosis.  
    2. Pulsus Bisferiens
      1. Rapid rising twice beating pulse both waves are palpable in systole.
      2. First wave palpable is percussion wave a brief decline in pressure follows because of the sudden midsystolic decrease in rate of the left ventricle ejection when severe obstruction develops. This is followed by a smaller and more slowly rising positive pulse wave (tidal wave) produced by continued ventricular ejection and by reflected wave from the periphery.
      3. E.g. Severe aortic regurgitation
      4. Moderate AS with severe AR
      5. HOCM. 
    3. Dicrotic Pulse.
      The dicrotic pulse is a twice peaked pulse with one peak in systole and second peak in diastole. The first is percussion wave and second is diacrotic wave. e. g.        
      1. Severe LV dysfunction
      2. Cardiac tamponade.
      3. Typhoid fever.
      4. Immediate post operative period during aortic valve replacement.  
    4. Pulsus alternans
      1. This is characterized by a regular sinus. Rhythm with alternate strong and weak beat due to alternation in ventricular contractility.


        Example :
         Left ventricular failure produce by severe hypertension, aortic valve disease or coronary artery disease.

    5. Pulsus Paradoxus.
      1. Normally systolic pressure falls by 3 - 10 mm Hg. During inspiration when the systolic blood pressure falls more than 10 mm Hg during inspiration the pulse is called pulsus paradoxus. Although it merely is an exaggeration and not a reversal of the normal.
      2. Causes
        1. Cardiac
        • Cardiac tamponade
        • Constrictive pericarditis (less frequently) Lung conditions
        2. Lung conditions
        • Acute severe bronchial asthma
        • Emphysema
        3. Superior vena caval obstruction  
    6. ​​Reversed Pulsus Paradoxus


      a. IPPV → Intrathoracic pressure is higher in inspiration and lower in expiration.
      b. HOCM

    7. Water Hammer Pulse
      It is a large bounding pulse associated with increased stroke volume of the left ventricle and decrease in the peripheral resistance leading to a wide pulse pressure.
      1. ​​​High output states
        1. Anemia                      
        2. Beriberi              
        3. Thyrotoxicosis
        4. Paget's disease            
        5. A- V fistula
      2. ​​Cardiac lesion
        1. Aortic regurgitation      
        2. PDA            
        3. Collateral          
        4. AV - fistula 
    8. Bigeminal Pulse
      1. Alternating strong and weak pulses occurring with an irregular rhythm seen in supra ventricular or ventricular bigemini.
      2. The weak beat is prematurely close to the previous normal beat and weak beat is followed by a long pause. The strongest beat correlates with preceding longer diastole due to post extrasystolic pause resulting in greater left ventricular end diastolic volume.

Jugular Venous pulse

  1. Jugular venous pulse is defined as the oscillating top of the column of blood in the proximal portion of the Internal Jugular Vein and represents volumetric changes that reflects phasic pressure changes in the right atrium. Internal jugular vein is preferred to External jugular vein for measurement of JVP.
  2. Normal wave pattern in JVP.
  3. It consists of three positive waves a, c, v and two negative waves n, y.

a wave  due to right atrial contraction.


c wave  movement of Tricuspid valve cusps into the RA as RV pressures increases. Coincides with the onset of ventricular systole. C wave in JVP probably results from transmission of the adjacent carotid artery pulsation.


x wave  right atrial relaxation


v wave  indicates a passive rise in pressure as venous return to the atrium continues during ventricular systole while the tricuspid valve is closed.


y wave  tricuspid valve opens; Blood enters the RV rapidly and there is consequently lowering of RA pressure


Temporal sequence with cardiac cycle.

  1. A wave occurs just before S1 / Carotid upstroke.
  2. X wave just before S2
  3. Y wave after S2
  4. V wave after carotid upstroke.  

Abnormalities of JVP

  1. a wave absent   Atrial fibrillation
  2. Prominent a wave -
    1. when RVH leads to resistance to filling
    2. PS/PAH
    3. TS
  3. Cannon wave [Giant a wave]  seen in complete heart block, AV dissociation.
  4. V wave prominent  TR
  5. Rapid y descent   Constrictive pericarditis
  6. Kussmaul’s sign   is an inspiratory rise in JVP
    e.g. - Constrictive cardiomyopathy
    Restrictive cardiomyopathy 

Normal Heart Sound

  1. At the onset of ventricular systole the mitral and tricuspid valve close consecutively to give the first heart sound
  2. Opening of pulmonary and aortic valves occur next and is normally inaudible
  3. The closure of the aortic and pulmonary valves gives rise to the two components of the second sound
  4. After a brief period the mitral and tricuspid valve open normally inaudible  

Alteration in Intensity

  1. Loud S1
    1. Mitral stenosis              
    2. Tricuspid stenosis
    3. High output state
    4. Short PR interval
    5. Ebstein anomaly  
    6. Myxoma                
    7. Thin chest wall 
  2. Soft S1      
    1. Mitral regurgitation              
    2. Tricuspid regurgitation
    3. Prolonged PR interval            
    4. Calcified mitral and tricuspid valve
    5. Depressed LV contractility            
    6. Thick chest wall                    
    7. Emphysema
  3. Loud S2    
    1. Systemic Hypertension
    2. Pulmonary Hypertension
    3. Coarctation of aorta
  4. Soft S2      
    1. AR, PR  


  1. Normally M1 precedes T1 is narrowly split which is difficult to appreciate.
  2. Pathological split Of S1 occurs in
    1. RBBB
    2. Ebstein Anomaly.
  3. Splitting of the second sound is much easier to appreciate because the aortic and pulmonary valve closure sounds A2 and P2 are more widely separated during inspiration and narrowest in expiration (Physiological splitting).
  4. Splitting of 0.06 seconds during inspiration and 0.02 seconds in expiration would be considered as normal or physiological splitting. 

Mechanism of splitting


During inspiration due to - ve pressure blood is drawn into the thorax and the RV stroke volume increases. The duration of RV systole therefore lengthens and P2 is slightly delayed conversely the left ventricular stroke volume falls during inspiration because the greater negative pressure with in the thorax enlarges the capacity of left atrium and pulmonary veins and reduces the LA pressure and hence LV systole is shortened and A2 occurs earlier. 

  1. Wide & variable splitting of S2
    Wide splitting of second  heart sound during expiration due to early A2 or late P2 which is further increased during inspiration
    1. Pulmonary stenosis      
    2. Complete RBBB 
  2. If A2- P2 interval is the same in expiration and inspiration, it is called wide and fixed split.
    1. ASP                      
    2. ​TAPVC 
  3. Paradoxical splitting or reversed splitting
    This occurs when maximal split occurs on expiration and narrows or fuses during inspiration. This is generally due to delay in A2.
    e.g. LBBB, AS, Hypertensive Heart disease, PDA  

Third Heart Sound


Rapid ventricular filling occur early in diastole when atrioventricular valves are open completely. Third heart sound (S3) occurs due to sudden cessation of filling of blood from the atria to the ventricles resulting in distension and vibration of the ventricular wall, papillary muscles and character. S3 can be heard normally in children; young adult and high cardiac output states but when heard in subject over the age of 10 years. It is usually a sign of heart failure.



  1. L  R shunt ASD, VSD, PDA
  2. Mitral regurgitation
  3. Tricuspid regurgitation  

Fourth Heart Sound


It is due to a bolus of blood delivered into the ventricle from atrial contraction. When atria contract against rigid non-compliant ventricle which causes resistance in ventricle filling.


  1. Systemic Hypertension        
  2. Ischemic Heart disease
  3. HOCM                          
  4. Severe Aortic stenosis  

Additional Sound

  1. Ejection clicks
    1. Normally opening of semilunar valves produces no sound unless valves are abnormal.
    2. Aortic ejection sounds occur in association with a deformed but mobile aortic valve and with aortic root dilation. Thus it presents in AS, bicuspid aortic valve, AR, aneurysm of the ascending aorta.
    3. In congenital aortic valve stenosis, an ejection sound is always associated with systolic murmur. This physical sign is absent in both subvalvular and supravalvular stenosis, thus helping to identify the site of obstruction at the level of the aortic valve.
    4. The findings of aortic ejection sound with out an associated systolic murmur indicates the presence of non stenotic bicuspid aortic valve.  

Mechanism of production.

  1. Ejection click is produced due to abrupt stoppage of doming valve in systole when it reaches its maximum excursion causes abrupt deceleration of the oncoming column of blood sets the entire cardiohemic system into vibration.
  2. Aortic ejection click not vary with respiration (Constant ejection click)
  3. Pulmonary ejection clicks have decreased intensity during inspiration and loud and clear during expiration. (Phasic ejection click) 
  1. Opening Snap
    1. Normally mitral and tricuspid valve open silently but when the valve leaflets are abnormal as in rheumatic mitral or tricuspid stenosis a sound is associated with the opening movement. This sound is analogous to systolic clicks of the aortic or pulmonary valve opening but by tradition the sounds are known as Opening snap. When related to mitral or tricuspid valve.
    2. The presence of an opening snap is indicative of thickened but mobile leaflets
    3. The severity of mitral stenosis can be assessed by noting the interval between A2 & the Opening Snap. The shorter the A2-0pening Snap interval, the more severe is the mitral stenosis.  


  1. Systolic Murmur
    1. Ejection Systolic
      e.g. Aortic stenosis Pulmonary Stenosis  
    2. Pan systolic
      e.g. Mitral regurgitation Tricuspid regurgitation Ventricular septal defect  
    3. Early Systolic
      1. MR              
      2. TR                
      3. VSD with PAH                
      4. Small VSD
    4. Late Systolic
      1. HOCM  
      2. MVP 
  2. Diastolic Murmur:
    1. Early diastolic
      e.g. * Aortic regurgitation
            * Pulmonary regurgitation
    2. Mid - Diastolic
      e.g. - Mitral stenosis
            - Tricuspid stenosis  
  3. Continuous murmur
    1. Patent Ductus Arteriosus
    2. Arteriovenous fistulas → Congenital
    3. Systemic to pulmonary shunts.
      e.g. - Blalock Taussig
    4. Rupture of sinus of Valsalva
    5. Narrowing of an artery :
      • Coarctation of aorta
      • Renal artery stenosis
      • Peripheral pulmonary stenosis 
  4. Venus hum
    Increased blood flow to an organ
       • Mammary souffle
       • Hemangioma 



Rough murmurs are associated with obstruction to flow through a narrow valve - Blowing murmur are more typical of an incompetent valve.


Point of maximum intensity and direction of selective propagation.


Murmur due to pulmonary and tricuspid valve lesions are generally well localized to their respective area of pericardium but aortic and mitral murmurs however may radiate extensively.


Dynamic Auscultation


Effect of physiological / pharmacological maneuvers on the intensity of heart murmur.

  1. Standing Most murmurs decrease in Length and intensity.
    Two exceptions H.O.C.M., MVP
  2. Valsalva Maneuvers Most murmurs decrease in Length nd Intensity.
    Two exceptions HOCM, MVP
  3. Squatting
    Most murmurs become louder but those of HOCM and MVP usually soften or disappear.
  4. Hand grip exercise Murmur of MS, PS, MR, A V, VSD increases with hand grip exercise.
       AS, HOCM murmur decrease.  



Standing →  Venous return to heart


Valsalva  Rt and Lt ventricular diastolic volume

             ↓ Arterial pressure.



Handgrip  ↑ Systemic vascular resistance Vasopressor

                   ↑ Arterial pressure

                   ↑ Cardiac output

                   ↑ Left ventricular volume


The behavior of the murmur during respiration :-


The stroke output of the right heart increases during inspiration while that of the left heart is reduced so a murmur originating on the right side of the heart will become louder during inspiration and on left side of the heart will become louder during expiration.


Other Murmurs

  1. Carey - Coombs MurmurQ  
    1. Mid diastolic murmur of mitral valvulitis in Rheumatic Fever. It can be late diastolic also.
    2. One of the few murmurs that is never accompanied by a thrill
    3. Murmur usually varies from day to day  
  2. Austin Flints MurmurQ  
    1. Mid diastolic murmur heard over apex in patient with severe aortic regurgitation which may occur with a normal heart valve  
  3. Graham Steel Murmur Q
    1. Early diastolic murmur of pulmonary regurgitation which is due to pulmonary hypertension  
  4. Rytands MurmursQ
    1. Mid diastolic flow murmur occurs intermittently in complete heart block. When atrial contraction coincides with the phase of rapid filling
    2. These murmurs are believed to result from antegrade flow across A-V valve that are closing rapidly during filling of the recipient ventricle.

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