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Cardiac Failure
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Cardiac Failure
The failure of the heart to pump enough blood to satisfythe needs of the body.
Also known as the Heart Failure.
The cause is usually a decrease in contractility of the
myocardium resulting from diminished coronary bloodflow.
Other causes areDamaged heart valves
-External pressure around the heart.
-Vitamin B deficiency. -Primary cardiac muscle disease
-other conditions that makes the heart ahypoeffective pump.
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Progressive Changes After Myocardial
Infarction 1 / 5
Reduced Cardiac Output
Damming of the blood in the veins - Venous Pressure
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Progressive Changes After Myocardial
Infarction 2 / 5
Immediate response
Baroreceptor response
Chemoreceptor Response
CNS ischemic response
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Progressive Changes After Myocardial
Infarction 3 / 5
Sympathetic stimulation
Strengthens the heart
Raises the Psf
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Progressive Changes After Myocardial
Infarction 4 / 5
Increased fluid retention by the Kidneys
Progressive recovery of the heart
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Progressive Changes After Myocardial Infarction 4 / 5
A low cardiac output has a profound effect on renal function, sometimes
causing anuria when the cardiac output falls to one-half to two-thirdsnormal.
Low cardiac output + Low arterial pressure = low urine output.
Moderate increase in body fluid and blood volume is an important factor inhelping to compensate for the diminished pumping ability of the heart byincreasing the venous return. The increased blood volume increases venousreturn in two ways(1) it increases the mean systemic filling pressure, whichincreases the pressure gradient for causing venous flow of blood towards theheart, (2) it distends the veins which reduces the venous resistance andallows even more ease of flow of blood to the heart.
Detrimental effects of excess fluid retention in severe cardiac failure, whichinclude
1)Overstretching the heart ,thus weakening the heart still more.
2)Filtration of fluid into the lungs causing pulmonary oedema and consequentdeoxygenation of the blood.
3)Development of excessive oedema in most parts of the body.
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Progressive Changes After Myocardial
Infarction 5 / 5
Compensated Heart Failure
Increased Rt. Atrial Pressure
No cardiac reserve
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Decompensated Heart Failure
But, if the heart is severely damaged, no
amount of compensation by:
The Sympathetic Nervous System Kidneys
can restore the normal Cardiac Output.
Fluid continues to be retained leading to moreand more edema and.. finally death.
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As more & more fluid is retained, the Psf goes on rising,
& the Right Atrial pressure goes on rising.
Decompensated Heart Disease With Increase
In Right Atrial Pressure
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Soon, the rising edema causes edema of the heart muscle
& stretching of the myocardium further deterioration of
cardiac functionclinicallythis is seen as Pulmonary
edema
Decompensated Heart Disease With Increase
In Right Atrial Pressure
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Decompensated Heart Disease With Increase In
Right Atrial Pressure
The main cause of decompensated heart
failure is failure of the heart to pump
sufficient blood to make the kidneys excretedaily the necessary amounts of fluids.
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Vicious Cycle Of Cardiac Deterioration
The low Arterial pressure consequent to CardiacShock results in reduced coronary supply.
This is confounded with the already existingCoronary
blockage. The cardiac muscle becomes weaker and the arterial
pressure falls further.
Hence when treating Myocardial Infarction it is
important to avoid even brief moments ofHypotension.
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Treatment Of Heart Failure
Propped up position
Oxygen
Edema relieving drugs like Diuretics
ACE inhibitors
Cardiotonic drugs like Digitalis,
Inodilators like Amrinone, Milrinone
Salt restriction
Digitalisstrengthens the heart, so that the heartbecomes strong enough to pump adequatequantities of blood required to make the kidneys
function normally again.
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Progressive Changes In Mean Aortic Pressure,
Capillary Pressure & Right Atrial Pressure
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Causes Of Fluid Retention
Lowered Glomerular filtration (Kidneys) Reduced arterial pressure.
Sympathetic vasoconstriction (afferent arterioles).
Activation of the Renin Angiotensin system and
increased reabsorption of water and salt by the renaltubules.
Increased Aldosterone secretion
ADH (Posterior Pituitary)
Countered by: Atrial Natriuretic Factor
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Causes Of Fluid Retention
Even a slight decrease in glomerular filtration often markedly decreasesurine output. When the cardiac output falls to about one-half normal,this can result in almost complete anuria.
In chronic stage of heart failure, large quantities of aldosterone are
secreted by the adrenal cortex. Excess potassium is one of the mostpowerful stimuli known for aldosterone secretion and potassiumconcentration rises in response to reduced renal function in cardiacfailure.
Atrial natriuretic factor is a hormone released by the atrial walls of theheart when they become stretched. The ANF then has direct effect onthe kidneys to increase greatly their excretion of salt and water,therefore playing a natural role to help prevent extreme congestivesymptoms during cardiac failure.
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Cardiac Reserve
The maximum percentage that the Cardiac
Output can increase above the normal level is
called the Cardiac Reserve
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Cardiac Reserve
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Cardiac Reserve
No cardiac reserve in heart failure.
Any factor that prevents the heart from pumping blood
satisfactorily will decrease the cardiac reserve- ischemic
heart disease, primary myocardial disease, vitamin
deficiency that affects the cardiac muscle, physicaldamage to the myocardium, valvular heart disease.
Diagnosis of Low Cardiac Reserve can be easily made by
making the person exercise on a treadmill
or
by walking up and down the steps.
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Cardiac Reserve
It may result in:
Immediate and extreme shortness of breath.
Extreme muscle fatigue. Excessive rise in heart rate.
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Decompensated Heart And Digitalis
F
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Mechanism Of Action Of Digitalis
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High Cardiac Output FailureAV Fistula & Beriberi
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High Cardiac Output FailureAV Fistula & Beriberi
In AV fistula-there is overloading of the heartbecause of excessive venous return , eventhough the pumping capability of the heart is
not depressed. In Beriberi heart disease( lack of thiamine)-
the venous return is greatly increased becauseof diminished systemic vascular resistance butat the same time, the pumping capability ofthe heart is depressed.
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Progressive Changes In Cardiac Output &
Right Atrial Pressure In Cardiac Failure
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Decompensated Heart With Shift In Venous
Return Curves
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Valvular and Congenital heartdefects
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Learning Objectives
Students should
1. Know the factors that contribute to the formation
of turbulent flow.
2. Describe the timing and causes of the four heartsounds.
3. Describe the expected auscultation sounds that
define mitral stenosis, mitral insufficiency, aortic
stenosis, and aortic insufficiency.
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Normal Heart Sounds
Ordinarily, no sound occurs when the valves
open.
Closure of the A V valves produces the First
Heart Sound.
Closure of the Semilunar valves produces the
second heart sound.
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Normal Heart Sounds
The 1st& 2ndHeart sounds were believed to beproduced due to the
Slapping together of the valve leaflets.
But instead are mostly due to:
Vibration of the taut closed valves.
Vibration of The adjacent blood. The walls of the heart.
The major blood vessels.
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Normal Heart Sounds
The 3rdHeart Soundis:
Produced at the beginning ofmiddle third of
the diastole.
Due to swirling of the blood in the partially
filled ventricle.
Not of audible frequency (only
recorded on Phonocardiography).
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Normal Heart Sounds
The 4th Heart Sound(Atrial Heart Sound):
Due to the contraction of the Atrium and
inrushing of the blood into the ventricle.
Not audible (only
recordable on the Phonocardiogram).
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Amplitude Of Different Vibrations In Heart
Sounds & Murmurs
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Auscultation Of Heart Sounds
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Phonocardiograms
V l l L i
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Valvular Lesions
The left heart valves have higher incidence of
valvular lesions than the right heart valves becauseof the higher pressures on the left side compared to
the right side.
The left heart valve lesions can be classified as: Aortic valve
Aortic stenosis
Aortic insufficiency or aortic regurgitation
Mitral valve
Mitral stenosis
Mitral insufficiency or mitral regurgitation 38
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Valvular Lesions
Stenosed valve is one in which the leaflets
adhere to one another so extensively that
blood cannot flow through it normally.
Regurgitation (back-flow) can occur when the
valve edges are so destroyed by scar tissue
that they cannot close as the ventricles
contract
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Valvular Lesions
Rheumatic valvular lesions
Rheumatic fever is an autoimmune disease in which the
heart valves are likely to be damaged or destroyed.
Usually initiated by streptococcal toxin from group Ahaemolytic streptococci.
Large haemorrhagic ,fibrinous, bulbous lesions grow along
the inflamed edges of the heart valves.
The mitral valve most often seriously damaged, followedby aortic valve.( high pressure stresses responsible for
frequency on the left heart )
Aortic valvular disease
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Aortic valvular disease
In aortic stenosis, the contracting left ventricle fails to
empty adequately, whereas in aortic regurgitation, bloodflows backward into the ventricle from the aorta after the
ventricle has just pumped the blood into the aorta.
Therefore, in either case, the net stroke volume outputof
the heart is reduced.
In both aortic stenosis and aortic regurgitation, the left
ventricular musculature hypertrophies because of the
increased ventricular workload. In regurgitation, the left ventricular chamber also enlarges
to hold all the regurgitant blood from the aorta.
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A ti l l di
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Aortic valvular disease
In the early stages of aortic stenosis or aortic regurgitation,compensatory mechanisms prevent significant
abnormalities in circulatory function in the person during
rest.
Beyond a critical stage in these aortic valve lesions, the leftventricle finally cannot keep up with the work demand. As
a consequence, blood dams up in the left atrium and in the
lungs behind the failing left ventricle. The left atrial
pressure rises progressively leading to development of
serious edema in the lungs which is known as the
pulmonary edema which would lead to death unless
treated aggressively and immediately. 42
Aortic valvular disease
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Aortic valvular disease
Aortic stenosis
a nozzle effect is created during systole, with bloodjetting at tremendous velocity through the smallopening of the valve leading to a loud, harsh, ejectionsystolic murmur and thrill (palpable murmur) due to theturbulence.
Aortic regurgitation
during diastole, blood flows backward from the high-pressure aorta into the left ventricle, causing a "blowing"
murmur of relatively high pitch with a swishing qualityheard maximally over the left ventricle (diastolicmurmur)
Very much increased pulse pressure
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Mitral valvular disease
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Mitral valvular disease
In mitral stenosis, blood flow from the left atrium into the
left ventricle is impeded, and in mitral regurgitation, muchof the blood that has flowed into the left ventricle during
diastole leaks back into the left atrium during systole rather
than being pumped into the aorta. Therefore, either of
these conditions reduces net movement of blood from theleft atrium into the left ventricle.
The buildup of blood in the left atrium causes progressive
increase in left atrial pressure, and this eventually results in
development of serious pulmonary edema.
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Mitral valvular disease
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Mitral valvular disease
The high left atrial pressure in mitral valvular disease also
causes progressive enlargement of the left atrium, whichincreases the distance that the cardiac electrical excitatory
impulse must travel in the atrial wall and which eventually
leads to atrial fibrillation.
As the left atrial pressure rises, blood begins to dam up in
the lungs, eventually all the way back to the pulmonary
artery leading to increased systolic pulmonary arterial
pressure and also right ventricular pressure to almostdouble the normal pressures
This, in turn, causes hypertrophy of the right side of the
heart, which partially compensates for its increased
workload. 45
Mitral valvular disease
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Mitral valvular disease
Mitral stenosis
blood passes with difficulty through the stenosed mitral
valve from the left atrium into the left ventricle;
During the diastole, after partial filling, the ventricle has
stretched enough for blood to reverberate and a lowrumbling murmur begins (mid-diastolic murmur with
opening snap)
Mitral regurgitation
blood flows backward through the mitral valve into the
left atrium during systole
causes a high-frequency "blowing," swishing sound
(pan/holo systolic murmur) 46
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Congenital Anomalies
They are usually categorized under the followingheadings:
Valvular stenosis
Aortic stenosis Coarctation of the Aorta
Left to right shunts
Patent Ductus Arteriosus Right to left shunts
Tetralogy of Fallot
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Congenital Anomalies
An anomaly that allows blood to flow backwardfrom the left side of the heart or aorta to the right
side of the heart or pulmonary artery, thus failing to
flow through the systemic circulationcalled a left-
to-right shunt.
An anomaly that allows blood to flow directly from
the right side of the heart into the left side of the
heart ,thus failing to flow through the lungs is calledright-to left shunt.
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Fetal Circulation
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Fetal Circulation
Lungs are collapsed and the elastic compression of thelungs that keeps the alveoli collapsed keeps most of the
lung blood vessels collapsed as well.
Resistance to blood flow through the lungs is so great that
the pulmonary arterial pressure is high in the fetus.
Low resistance to blood flow from the aorta through the
large vessels of the placenta, the pressure in the aorta of
the fetus is lower than normal-in fact ,lower than in thepulmonary artery.
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Fetal Circulation
Almost all the pulmonary arterial blood flow through a
special artery present in the fetus that connects the
pulmonary artery with the aorta called the Ductus
arteriosus thus bypassing the lungs. This allowsimmediate recirculation of the blood through the systemic
arteries of the fetus without the blood going through the
lungs.
The lack of blood flow through the lungs is not
detrimental to the fetus because the blood is oxygenated
by placenta.
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AT BIRTH
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AT BIRTH Resistance to blood flow through the pulmonary vascular
tree decreases tremendously, allowing the pulmonary
arterial pressure to fall. Aortic pressure rises because of sudden cessation of blood
flow from the aorta through the placenta. Pulmonary
arterial pressure falls.
Forward Blood flow through the ductus arteriosus ceases
suddenly at birth.
Ductus is believed to close because the oxygen
concentration of the aortic blood now flowing through it istwice as high as that of the blood flowing from the
pulmonary artery into the ductus during foetal life. Oxygen
presumably constricts the muscle in the ductus wall.52
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Fetal Circulation
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Patent Ductus Arteriosus
PDA
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PDA
Persistence of patent ductus arteriosus is known as
Patent Ductus Arteriosus. People with PDA do not show cyanosis until later in
life when the heart fails or the lungs become
congested. The major effects of PDA on patient is decreased
cardiac and respiratory reserve.
Machinery murmur is heard . To close the ductus arteriosus, first give Aspirin,
then Steroids, and as a last resort perform Surgery
(ligation) to close PDA.55
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Tetralogy Of Fallot
Tetralogy of Fallot
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Tetralogy of Fallot
Tetralogy of Fallot:- Right ventricular hypertrophy,
pulmonary artery stenosis, overriding aorta, and ventricular
septal defect.
Most common cause of blue baby. Most of the blood
bypasses the lungs, so the aortic blood is mainly
unoxygenated venous blood. Diagnosis based on
1)babys skin -cyanotic (blue).
2)Measurement of high systolic pressure in the right ventricle
3)Enlarged right ventricle (on Chest X-ray findings)
4)Angiograms showing abnormal blood flow through the
interventricular septal hole and into the overriding aorta,