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CARDIODYNAMICS ABNORMAL HEART SOUNDS

Lecturer: Dr. Edmee Young-Martinez  Called MURMURS produced by:

HEART SOUNDS a) Blood flowing rapidly in usual direction through an


abnormally narrowed valve (produced by valvular
 The closure of valves and the rushing of blood through the stenosis)
heart
b) By blood flowing backward through a damage
 Gives rise to the characteristics of heart sounds heard during leaky valve insufficiency
auscultation
STENOSIS
 Stethoscope - used to detect these sounds
 Or narrowing can happen in heart disease to a valve when
HEARTBEAT the valve is stiff and can’t open all the way. The result is that
the heart must work harder to move blood.
 Consists of a ´LUB AND DUB´counted as heartbeat
 Defined as an abnormal narrowing in a blood vessel or other
 LUB AND DUB – measure the duration of ventricular systole tubular organ or structure

4 HEART SOUNDS
1. S1 – LUB  Commonly heard
VALVULAR INSUFFICIENCY
 Beginning of ventricular systole
 Associated with the closure of
AV valves at the onset of systole  Inability of valves to close completely resulting to backflow of
and isovolumetric ventricular blood causing murmurs  by blood flowing between 2 atria
contraction or 2 ventricle thru a small hole in the wall separating them in
 Slightly prolonged, soft, low- cases of congenital heart diseases
pitched
 Duration: MURMURS
 Heard best at mitral and
tricuspid area  seen in person with congenital abnormalities of heart
2. S2 - DUB  Commonly heard
 End of ventricular systole  soft murmur is seen in the presence of severe anemia
 Closure of semilunar valves –
occurs at the end of systole as HEART MURMURS
pulmonary and aortic valves
closed VALVE ABNORMALITY TIMING OF
 Shorter, louder, high pitched MURMUR
 Duration- 0-12 sec
 Heard best at pulmonic and Aortic or pulmonary stenosis systolic
aortic area
3. S3  Rapid ventricular filling Insufficiency Diastolic
 May not be heard but it can be
recorded in an <ECG Mitral or tricuspid Stenosis Diastolic
 Associated with rapid rush of
blood during rapid ventricular insufficiency Systolic
filling in opening of AV valves
 Soft-low-pitched
 Duration:
 Recordable in from 26-85% of
normal person CLINICAL AREAS OF AUSCULTATION
 Abnormal cases: may be heard
in the presence of mitral Aortic area 2nd intercostal space Right sterna border
stenosis (mitral valve´s inability
to open completely Pulmonic area 2nd intercostals space Left sterna border
4. S4  May be normal or abnormal
 Heard in children during atrial Tricuspid area 4th intercostals space Left sterna border
systole
 Associated with the contraction Mitral area 5th intercostals space Left midclavicular line
of the atrium
 Recorded in 2% of normal
person
a) Maybe audible or STROKE VOLUME
heard in people – left
ventricular  volume of blood ejected by the ventricle per beat by opening
hypertrophy of semilunar valves in circulation/ systole
b) Atrial pressure is high
 normally: 70-90 ml or average stroke volume of 80ml

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 directly related to the force generated by the myocardium  refers to volume of blood in the ventricle at the end of systole
during systole after contraction/ opening of semilunar valves

 greater force of contraction, greater stroke volume  50 ml/ beat = what is left in ventricle during diastole

 An increase in ESV = decrease in SV which is not good


CO = SV (ml) X HR (beats/
min) POINTS TO REMEMBER:

 chamber of the heart is not emptied of blood even


Where: CO = cardiac output, SV = after systole
stroke volume, HR = heart rate
 for a heart to become an effective pump, there
should be adequate EDV

CARDIAC OUTPUT (CO)


 ultimate goal of the heart  to have a sufficient
SV to have sufficient CO that will supply tissues
 volume of blood ejected in circulation per minute
for tissue perfusion
 shows direct relationship, an increase in stroke volume in an
 2 determinants of CO:
increase in cardiac output and increase in heart rate

 If SV remains constant, CO increases in proportion to HR up a) stroke volume


to about 180 bts/min
b) Heart rate
 normal CO: 5-6 L/min (8% of TBW)
FACTORS THAT WILL GIVE ADEQUATE END DIASTOLIC
VOLUME (EDV)
 CO = SV is always true  if CO increases, SV will also
increase 1. Filling time

 CO = HR, not always true  Related to HR/ CR

a) Highly tachycardic heart  Increase in HR (not tachycardic) = increase in SV


= increase in CO = increase in EDV
 if HR remains constant, CO increase in
preparation to SV, thus factors that 2. Distensibility of the ventricle
increase SV can increase CO =
increase SV, increase CO, increase HR
 If ventricles is ischemic, it cannot contract
except tachycardic if > 180 bts/min thus
forcefully thus will result to inadequate EDV
increase in HR will decrease CO

b) Moderate bradycardia  If ventricle is less distensible, the less blood


received from atrium  less EDV
 Decrease HR may increase CO by
Frank Starling’s Law Bec longer  If ventricles is more distensible, increase filling,
duration of diastole (more filling time) contraction

3. Atrial contraction

SV = EDV – ESV  minor role because because it can only elicit 30%
of blood so it needs stronger atrial contraction
Where: SV = stroke volume, EDV =
end diastolic volumen, ESV = end  its contribution is important in stenotic AV valve 
because of high atrial pressure, atrial contraction
systolic volume will have major role in ventricular filling
END DIASTOLIC VOLUME (EDV)
 MODERATE TACHYCARDIA
 Refers to the volume of blood in the ventricle at the end of
diastole Diastasis is shortened (reduced filling)

 Ventricular filling during diastole = 180 ml/ min In this case, atrial contraction will play a major role and maybe
substantial
 Increase in EDV = increase SV  this is needed for good
and strong tissue perfusion 4. Effective filling pressure (EFP)

END SYSTOLIC VOLUME (ESV)  Distending pressure of the ventricle

 residual volume

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 Difference in pressure between inside central  Area of higher pressure to an area of lower
venous pressure (CVP) and outside intrathoracic pressure favors venous return thus improves heart
pressure function

 Before inspiration: diaphragm (dome-shaped) in a


EFP = CVP – ITP relaxed position assumes a flattened position 
VR enhanced
Where: EFP = effective filling
 Increased volume of thorax will result to decrease
pressure, CVP = central venous pressure transmitted into thoracic vein
pressure, ITP = intrathoracic pressure
 Decreased volume of the abdominal cavity is
transmitted in abdominal veins  valsalva´s
CENTRAL VENOUS PRESSURE maneuver

 Represents pressure in right atrium 3. SKELETAL MUSCLE PUMP

 0-4 mmHg  Compression of veins during muscular activity


(especially in extremities) as it contracts will open
INTRATHORACIC PRESSURE (ITP) venous valve that favors blood return to the heart

 Pressure inside the thoracic cavity  Varicosities  weakening of the venous valves

 ¨distending pressure¨ 4. POSTURE

 Has a subatmospheric pressure (lower than atmospheric  Suppresses venous return


pressure)
 Ex: standing decreases venous return
 Expire against close glottis is VALSALVA maneuver  applicable to heart patients which is advised to
pressure in the thorax will increase (constipation) have a complete bed rest without bathroom
privileges because the moment the patient stands-
 Lung collapse happens when intrathoracic pressure is up there will be less VR therefore decrease CO
and decrease blood supply to the heart
equal or greater to atmospheric pressure seen in stab
wound patients
5. VENOUS CONSTRICTION/ VENODILATION
5. Intrapericardial Pressure (IPP)
 Increase venous tone/ increase constriction of the
vein
 Pressure inside the pericardium
 VENOCONTSRICTION, increase VR, less venous
 IPP = limits ventricular filling = decreased EDV =
pulling
decreased SV = decreased CO
 VENODILATION, decrease VR, greater venous
 Example: pericardial effusion  presence of fluid pulling
in pericardium, the heart muscles can not stretch
enough

6. Venous Return (VR) END SYSTOLIC VOLUME (ESV)

 Flow of blood from the periphery back to the heart


(right atrium)
 POINT TO REMEMBER: increase in ESV (can not eject
normal SV) will result to decrease CO
 Volume of blood ejected from the CO should
return to the heart with the same volume  2 factors in ESV:

 Main determinant of CO 1. Afterload

 During contraction

FACTORS THAT INFLUENCE VENOUS RETURN  All forces against which cardiac muscles
must contract to generate pressure and
1. BLOOD VOLUME (BV)
 L ventricle, afterload is equal to all the forces the
 In cases of acute blood loss = decreased in BV, muscle must overcome to eject at given volume of
VR, EDV, SV, CO blood

2. THORACO-ABDOMINAL PUMP OR REPIRATORY PUMP  Aortic pressure – major contributor to


afterload in the heart
 Favors venous return therefore increases CO
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b) Parasympathetic (major effect)

2. Contractility of the myocardium  R Vagus to SA Node (vagal tone)

 Refers to load, work or tension placed on the  L Vagus to AV node


myocardium during contraction/ systole
 Ach reduces rate
 During contraction: the myocardium has to
contract/ work to overcome the pressure in aorta
open the semilunar valve so that it can be ejected
into the circulation 3. Temperature

 Dependent upon 2 factors: a) Warm temperature = increases HR

a) State of semilunar valve  Except for typhoid fever

 No increase in load if the b) Cold Temperature = decreases HR


state of semilunar valves are
closed

b) Aortic pressure FACTORS THAT AFFECT THE CARDIAC OUTPUT (CO)

 Increase after load is seen in Level of activity of the body


cases of aortic or arterial
hypertension
 Ex. Strenuous exercise = CO may go as high as
 An increase in arterial 35L/ min
pressure increases afterload
 The entire blood volume pumped around the
CONTRACTILITY OF THE MYOCARDIUM circuit is inanimate, if heart is functioning normally

1. Heteromaregulation  CARDIAC RESERVE = is the difference between


cardiac output at rest and the maximum volume of
blood the heart is capable of pumping per minute
 FRANK STARLING´s LAW OF THE HEART  (express in percentage)
greater stretch  when the muscle is stretched
(within the optimal range), sarcomere length
increases, and range of contraction increases:
greater strength of contraction Size of the body (surface area)

2. Intrinsic ability of the heart to contract  Refers t the surface area and not the weight

 Amount of catecholamines  CO is increased in proportion to surface area of


the body
 Parasympathetic and sympathetic effect to heart
 direct sympathetic effect to heart is excitatory  Also refers to CARDIAC INDEX
thus increases the force of contraction
CARDIAC INDEX (CI) = refers to the cardiac
POINT TO REMEMBER: Weak or ischemic heart cannot contract output per square meter of body’s surface area
forcefully because it is severely dilated. Greater stroke volume may be
greater than stroke volume (huh…confusing, pls check)  no force of 10 yrs old CI = 4L/min/sq m2
contraction  increase ESV
30 yrs old CI = 2.4L/min/sq m2

Normal CI adults = 3L/min/sq m2


HEART RATE

 Dictated by SA Node
EFFECT OF VARIOUS CONDITIONS ON CARDIAC OUTPUT
 Factors that control the heart rate:
NO CHANGE  Sleep
1. Chemical factors
 Moderate changes in environmental
2. Nervous system temperature

a) Sympathetic INCREASE  Exercise (CO=up to 7.0%)


CO
 NE at nodes  Anxiety and excitement (CO=50-100%)

 Opens fast Ca channels

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 Eating (CO=30%)  ESV – volume of blood in ventricle at the end of ventricular
contraction no matter how forceful, certain volume of blood
 High environmental temperature is left in the ventricle (Residual volume)

 Pregnancy AFTERLOAD

 Epinephrine  All the forces against which cardiac muscle must contract to
generate pressure to shorten
 Hyperventilation
 Refers to all forces that cardiac muscles must overcome to
 Fever
eject a given blood volume  aortic pressure
 Hyperthyroidism
 Resistance against which blood is ejected
 Anoxia
 Aortic pressure – major contributory factor to afterload
DECREASE  sitting or standing from lying (CO=20- INOTROPIC STATE
CO 30%)
INOTROPIC EFFECT OF INCREASE HR
 rapid arrhythmias (irregular)
FUNCTION OF VENTRICLES IS DECRIBED BY 3 PARAMETERS:
 heart diseases
1. STROKE VOLUME
 valvular lesions/ insufficiencies
 Volume of blood ejected on one
 hemorrhage ventricular contraction of the volume
ejected on one beat (ml/beat)

 SV = ESV – EDV
STROKE WORK (SW)
 Equal to 70 ml/ beat
 refers to work that the heart performs on each beat
 Difference between the volume of blood
 is equal force (aortic pressure) X distance (SV) in the ventricle before ejection and the
volume remaining in the ventricle after
 SW = AORTIC PRESSURE X STROKE VOLUME ejection

FACTORS THAT INFLUENCE CONTRACTILE STRENGTH OF  Increase SV, increase EDV


HEART MUSCLES
 Decrease SV, increase ESV
PRELOAD
2. EJECTION FRACTION
 Before contraction
 refers to the ratio of SV to EDV and
 Initial length to which the muscle is stretched before normally equal to 65%
contraction
 the fraction of the EDV that is ejected in
 Increased ventricular filling each SV

 Whole heart, passive stretch or preload is proportional to the  valuable index of ventricular function
(contractility)
amount of filling of the heart during diastole. Thus increase
filling, increase contractile force in the heart  as you
 lungs receive 100% of CO in the right
stretch the muscle, you increase the fore of contraction 
ventricle
Frank Starling’s Law
 inversely proportional to EDV
 Release of preload and developed tension or pressure is
based on degree of overlap of thick and thin filaments  increase in EF = increase contractility

 Preload for L ventricle and L ventricular EDV/ EDV fiber


length EJECTION FRACTION = STROKE
 Preload – resting length from which muscle contracts
VOLUME

 Preload = EDV EDV


POINT TO REMEMBER: when strength of
 EDV - the volume in the ventricle before ejection (ml) contraction increases without increasing the fiber
length then, more blood in the ventricles is

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expelled therefore ejection fraction increases and
EDV decreases (opposite effect)

Disclaimer: This is a compilation of the previous year’s trans.

ice.soria 092909.10a